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					GROUP H – OBJECTIVES MANDATORY SELECTIVES

10247 - Review the general host responses to injury and understand the pathogenesis, morphological features and
functional alterations attributable to these processes: cellular injury, inflammation and repair, disorders of growth,
and fluid and hemodynamic disturbances.




Trois composantes principales de la réponse inflammatoire aigue:
    1. Altération du calibre vasculaire (vasodilatation) entraînant une augmentation du flot sanguin :
            a. Vasoconstriction initiale transitoire et généralement de courte durée.
            b. Période de vasodilatation artériolaire produisant la chaleur et l’érythème local.
            c. Stase vasculaire relative due à l’augmentation de la perméabilité vasculaire.


    2. Augmentation de la perméabilité de la microvasculature permettant aux protéines plasmatiques et aux
        leucocytes de quitter les vaisseaux :
            a. Ceci se produit surtout au niveau des veinules post - capillaires.
            b. C’est la rétraction des cellules endothéliales qui permet l’augmentation de la perméabilité vasculaire.
            c. L’altération des Forces de Starling entraîne soit un transsudat (dommage léger) ou un exudat (dommage
                sévère ).
d. Dépendamment du type de dommage le degrés de perméabilité varie:
1. Des dommages causés par l’effet histaminique vont entraîner des changements immédiats mais transitoires.
2. Des dommages causant de la nécrose endothéliale vont entraîner des changements immédiats mais soutenus.
3. Des dommages causant une atteinte endothéliale sous - létale vont entraîner des changements retardés mais
    prolongés.
3. Migration des leucocytes a travers la microcirculation, accumulation au site de dommage et leur activation pour
    éliminer l’agent nocif :
•   Margination et roulement: C’est la disposition des neutrophiles le long de la paroi vasculaire en contact avec
    l’endothélium.
•   Adhésion : Les neutrophiles adhèrent à l’endothélium en utilisant des molécules d’adhésion spécifiques. Ceci
    survient seulement si l’endothélium est activee et non a l’etat normal.
•   Trans Migration (diapedese): les pseudopodes des neutrophiles s’infiltrent entre les cellules endothéliales avant de
    se glisser hors des vaisseaux.
•   Migration: dans le tissue interstitiel vers le stimuli chimiotactique
10248 - Recognize the morphology of malignant cells and the characteristic features of common neoplasms.

Morphology of malignant cells:
- Less differentiated
- Pleomorphic cell:
- Abnormally large nuclei
- Altered nuclear/cytoplasmic ratio




- Hyperchromatism and altered nucleoli
- Abnormal mitoses




Characteristic features of common neoplasms:
                                 Benign Neoplasms          Malignant Neoplasms

                           Slow growth               Rapid growth

                           Expansive growth          Invasive growth

                           Exophytic growth          Endophytic growth

                           Well-demarcated           Poorly-demarcated

                           No invasion               Invasion

                           No metastases             Metastases

                           No anaplasic              Anaplasia


10249 - Démontrer une connaissance des techniques courantes employées en anatomo-pathologie et connaître leurs
limites.

    -   Examen macroscopique
            o   Œil
            o   Balance

    -   Examen microscopique
           o Microscopes photoniques et électroniques
           o Microtome (étude des cellules)
           o «Tissus processor» (pour le traitement et la protection des tissus à analyser)
           o Immunofluorescence, immunohistochimie et hybridation in situ pour approfondir le diagnostic


10250- Demonstrate familiarity with the formulation of cytopathology, surgical pathology and provisional/final
autopsy reports and recognize the importance of a clear, concise, organized and accurate report as an effective
vehicle of communication

Cytopathology
Most cytopathology reports include the following elements:
-the source of specimen
-statement on adequacy of the specimen
-a general categorization of the diagnosis (ie within normal limits or other)
-the descriptive diagnosis
-summary of the clinical diagnosis

Surgical Pathology report:
Most pathology reports include the following elements:
-Identification (patient and doctor)
-Specimen identification: biopsy or surgery performed, type of tissue obtained
-Gross description: describe the specimen as seen with the naked eye (color, weight, size, consistency)
-Microscopic description: details the cells’ characteristics viewed under a microscope and how they relate to normal
cells, mitotic rate, invasion, type of cancer, describe the margine (ie positive), spread of cancer to lymph node or other
organs, stage of cancer
-Diagnosis
-Sampling differences (ie difference from initial report)

Final Autopsy reports
Most pathology reports include the following elements:
-Autopsy Face Sheet (final anatomic diagnosis): list the autopsy diagnosis + patient demographic data
-Historical Summary: statement of the patient medical history, laboratory, imaging studies + historical circumstances
-Examination Type (ie complete or partial autopsy), Date, Time, Place, Assistants, Attendees
-Presentation, Clothing, Personal Effects, Associated Items
-Evidence of Medical Intervention: listing of all medical devices placed in the course of medical therapy
-Postmortem Changes (ie rigor mortis, livor mortis, skin slippage, discoloration, malodor)
-Postmortem Imaging Studies
-Identification: marks, scars, body weight, body length, hair color, condition of dentition
-Evidence of Injury
-External Examination: body height, weight, nutrition, body symmetry, eyes, nose, ears, mouth, teeth, neck, chest,
abdomen, genitalia, extremities
-Internal Examination: all internal organs are inspected, weighed + described
-Histology Cassette Listing
-Microscopic Descriptions
-Toxicology Results, Laboratory Results, Ancillary Procedure Results
-Pathologic Diagnoses
-Summary and Comments: summarize gross and microscopic findings, along with history and pertinent imaging +
laboratory test results
-Cause of Death Statement

10251 - Discuss the quantitation of turnover time and recognize the fixed (processing/technical) and flexible
(manpower dependent) components of this measure of quality of service regarding cytopathology, surgical pathology
and provisional/final autopsy reports.

10252 - Explain to the patient in rehabilitation the importance and role of each member of the multidisciplinary team
in the care of his/her condition.
10265 - Distinguish inguinal hernias from hydroceles by the end of the rotation.
Hydrocele                                           Inguinal hernia

Definition                                          Definition
     collection of fluid within the tunica         An inguinal hernia is a protrusion of abdominal-
        vaginalis                                   cavity contents through the inguinal canal.
     most often seen surrounding the testis,            Indirect: protrudes through the inguinal
        may occur within the spermatic cord                 ring and is ultimately the result of the
                                                            failure of embryonic closure of the internal
                                                            inguinal ring after the testicle passes
                                                            through it

                                                           Direct: enters through a weak point in the
                                                            fascia of the abdominal wall
Etiology                                            Etiology
     usually idiopathic                                 Congenital:
     found in 5-10% of testicular tumours                  All hernias in infants and children are
     associated with trauma, orchitis,                     indirect and occur as a result of the failure
        epididymitis                                        of the processus vaginalis to undergo
                                                            apoptosis.

                                                          Acquired:
                                                        In patients over the age of 25 the most
                                                    common cause of inguinal hernia is attenuation or
                                                    degeneration and fatty transformation of the
                                                    aponeurotic tissues of the inguinal floor, leading
                                                    either to direct weakness and bulging of the
                                                    inguinal floor, dilation of the internal ring, or both.
                                                    This is not work or activity related.

                                                            Relationship to "lifting" at work or other
                                                             activity:
                                                       Lifting and straining make patients aware that
                                                    they have a bulge. Lifting and straining do not
                                                    cause the attenuation or degeneration of the
                                                    inguinal floor, which is the underlying cause of the
                                                    hernia.
Investigations
     usually a non-tender cystic intrascrotal          Investigation:
        mass which transilluminates                            On physical exam, look for a buldge in the
     ultrasound (definitive), especially if <40                groin area that disappears when the
        years of age (rule out tumour)                          patient lies on his back and reappears in
                                                                valsalva.
Treatment                                               Treatment:
     nothing if tolerated and no complications         Surgery
     needle drainage ± instillation of a
       sclerosing agent to prevent recurrence
     surgical
Complications                                           Complications
     hemorrhage into hydrocele sac following               recurrence
       trauma                                               infection post-surgery
     may prevent palpation of testicular mass              seromas and hematomas
     compression of testicular blood supply                pain and neuralgia



10266 Advise parents of babies with umbilical hernias regarding the evolution and management.

Because the natural course of the umbilical ring is eventual closure, most umbilical hernias will spontaneously resolve. In
general, asymptomatic children with an umbilical ring that continues to decrease can be observed. Surgical intervention
is required only in a minority of patients:

- Incarcerated umbilical hernia in children is an absolute indication for surgical repair to avoid strangulation.

- Children with large, proboscoid (trunk-like) hernias without any decrease in the size of the umbilical ring defect over
the first two-three years of life, generally require surgery, because their hernias will fail to close spontaneously.

- Other relative indications for surgical repair include defects that cease decreasing in size, are symptomatic, or create
significant behavioral problems.

(www.uptodate.com)

10270 - Aborder les pathologies chirurgicales les plus courantes p.ex. l’appendicite, en participant aux visites des
patients hospitalisés avec les résidents en chirurgie.

Appendicites
   - Generalized abdominal pain to RIQ
   - Children with local or general peritonitis rarely display the board-like rigidity so often found in adulte
   - Histoire - Ne pas oublier de demander à propos...
           o Fever/Chills
           o Urinary symptoms
           o Joint swellen
           o Rash
           o Bumps (car) are bugging the patient?
           o Sick contact
           o Blood problem in family
           o Anesthetic problem in family
   - Physical exam
           o Abdominal tenderness, percussion tenderness, guarding
                    Guarding = Involuntary increased muscle resistance
          o    Scrotal examination
                    Torsion of the testis occasionnally presents with referred pain in the iliac fossa, and can be
                       mistaken for appendicitis
   -   Tests
           o   McBurney
                    Appendicite inférieure
                    Douleur QID
           o Rebond
           o Psoas
                    Appendicite rétrocecal
                    Flexion résistée ou hyperextension hanche
           o Obturateur
                    Appendicite pelvienne
                    Rotation interne et externe de la hanche
   -   Investigations: CBC, U/S
   -   Diagnostic differential
           o Mesenteric adenitis
           o Right testicular torsion
           o Right lower lobe pneumonia
           o Infections in the lower urinary tract
           o Une gastro-entérite peut devenir une appendicite
   -   Traitement
           o Adequate preoperative IV correction of fluid and electrolyte deficits
           o Surgical removal of the appendix
           o Irrigation of the peritoneal cavity to remove pus and contaminated free peritoneal fluid
           o Effective antibiotic treatment to cover aerobic and anaerobic organisms commencing before surgery

NEC
   -   Sick premature neonates can develop necrosting enterocolotis as a further complications
   -   Souvent iléum et colon
   -   Combinaison ischémie + infection (klebsiella) du bowel wall
           o Ischémie à cause qu,en cas de stress/hypoxie, le sang aime mieux aller au coeur et au cerver, at the
               expense of the splanchnic circulation, skin and muscle
   -   Présentations
           o Presents with abdominal distension and bile-stained vomiting
           o Sang dans le rectum (loose stool)
           o The infant is ill, lethargic, febrile and not interested in feeds
           o When complicated py peritonitis, the anterior abdominal wall becomes oedematous and red, with
               dilated veins and palpation causes pain
   -   Investigations
           o Bébé en acidose
           o Plaquettes, globules blancs et Hb dimininuent si sévère
           o X-Ray
                     Dilated loops of bowel + intramural bubbbles of gas (pneumatosis intestinaly)
   -   Traitement
           o Most babies with NEC respond to supportive treatment consisting of adequate ventilatroy care, support
               of their circulation, resting the GI tract and the administration of antibiotics.
                     Stop oral feeds, decompression of the intestine by suction through a nasogastric tube and
                        parenteral administration of fluids
           o Some patients require surgery for full-thickness necrosis of the intestine, as revealed by free
               intraperitoneal gas on x-ray or by continued clinical deterioration despite intesive supportive care
                     Clinical deterioration
                       Perforation

Intussuception
    - One segment of the bowel passes onwards inside the adjacent distal bowel. Intestinal obstruction follows.
    - Causes: Inconnue
            o In older children, there is more likely to be a pathological lesion at the lead point of the intussusceptu
                    Meckel's diverticulum
                    Polyp
                    Duplication cyst
    - Présentation
            o Typically a 3 months - 3 years old who has a sudden onset of severe abdominal pain with his legs drawn
               up to the chest followed by a period of almost complete resolution. There may be a history of recent
               URI/adenitis
    - Symptômes
            o 1. Colicky pain lasting 2-3 min
            o 2. Spasms occur at intervals of 15-30 min
            o 3. After 12h, pain more continuous
            o Vomiting
            o Stools/diarrhea with mucus and blood (jello)
            o Intermitenly pale and clammy, exhausted and lethargic, tachycardia
            o Masse palpable au début, avant la distension abdominale
                    Souvent right hypochondrium, but may be anywhere between the line of the colon and
                       umbilicus
    - Diagnostic
            o Abdominal X-Ray peut être normal
            o U/S
            o Air/barium contrast
    - Traitement
            o Air/barium contrast (air surtout)
            o Chirurgie

Hirschsprung's disease
    - Génétique?
    - Lack of ganglion cells
    - Thickened abnormal cholinergic nerve fibres are found in the affected segment
    - Constant state of spasm and won't relax
    - Functionnal obstruction
    - Suspect this disease in a newborn who fails to pass meconium in the first 24 hours
    - Étendue: Canal anal -- Rectum -- Colon sigmoïde...
    - Investigation
           o X-Ray
                     Gaseous distension
                     Air-fluid levels
           o Contrast enema: Constriction of the segment of bowel affected
    - Diagnostic par Rectal suction biopsy
           o Constrast enema will show continuous of the segment affected
    - Traitement
           o Décompression par saline enemas
           o Colostomy

Malrotation with midgut volvulus
   - In the case of malrotation, the duodenal-jéjunal junction and the ileo-caecal junction lie side by side
   - 360° twist: May cause venous and lymphatic engorgement with bile stained vomiting
    -   720° twist: Arterial ischemia of the gut from the duodenum to the mid tranverse colon
    -   Présentation
            o Healthy full term baby who is well for the frist few days and develop feeding difficulties with bile-stained
                vomiting or coffee-ground emesis
            o Présentation tardive
                      Blood in rectum + abdominal distension
                      Major gut ischemia
            o Occurs at any age, but is more likely in the neonatal period
    -   Diagnostic
            o UGI: Demonstrate the abnormal poistion of the duodeno-jejunal flexure
            o X-Ray
    -   Traitement
            o Chirurgie – Laparotomie
                      Urgent! Risque de gangrène!
                      Détwister
                      Ladd's operation
                               Réparer la malfixation du gut

Vous pouvez aussi aller lire sur ces maladies:
   - Diaphragmatic hernia
   - Neuroblastoma
   - Inguinal Hernia
   - Imperforate anus
   - Abdominal wall defect : Gastroschisis, Omphalocele
   - Pyloric stenosis
   - Foreign bodies
   - Esophageal atresia/trachosophageal fistula
   - Wilm’s tumor (nephroblastoma of the kidney)


10271- Discuss the basic principles in fluid management on patients with frequently encountered surgical pathologies
by the end of the rotation.

There are 2 components of fluid management:
-Maintenance therapy replaces the ongoing losses of water and electrolytes under normal physiologic conditions via
urine, sweat, respiration, and stool.
-Replacement therapy corrects any existing water and electrolyte deficits. These deficits can result from gastrointestinal,
urinary, or skin losses, bleeding, and third-space sequestration.

Maintenance fluid therapy
In the presence of normal or near-normal kidney function, maintenance fluid therapy is usually undertaken when the
patient is not expected to be able to eat or drink normally for a prolonged period of time (eg, perioperatively or on a
ventilator). The goal of maintenance fluid therapy is to preserve water and electrolyte balance and to provide nutrition.
The serum sodium concentration provides the best estimate of water balance in relation to solute. A normal serum
sodium concentration implies that the patient is in water balance in relation to sodium but does not provide any
information on volume status. Weighing the patient daily provides the best means for estimating net gain or loss of
fluid, since gastrointestinal, urine, and insensible losses in hospitalized patients are unpredictable and difficult to
monitor. The patient should also be monitored for clinical signs of either volume excess (edema) or volume depletion
(eg, reduced skin turgor, fall in blood pressure).

Water — Hospitalized patients who are afebrile, not eating, and physically inactive require less than one liter of
electrolyte (sodium and potassium)-free water as maintenance fluid. Maintenance water requirements can be increased
or decreased by a number of factors:

Increased water intake is required if the patient has fever, sweating, burns, tachypnea, surgical drains, polyuria, or
ongoing significant gastrointestinal losses.

Decreased water intake is required in a number of clinical settings, including oliguric renal failure, the use of humidified
air, edematous states, and hypothyroidism.

Electrolytes — The majority of electrolyte losses (primarily sodium and potassium salts) are in the urine, with a lesser
contribution from the skin and gastrointestinal tract. Electrolyte balance can be maintained over wide range of intakes
due to appropriate changes in urinary electrolyte excretion.
Since maintenance electrolyte-free water intake is less than one liter per day, a reasonable approach is to begin with
two liters per day of one-half isotonic saline to which 20 meq of potassium chloride is added per liter. This regimen
provides 9 g of sodium chloride (3.4 g of sodium), which is similar to the sodium content of a hospital diet. Patients with
gastrointestinal or third-space losses may require a higher rate of saline (or blood) administration to maintain volume
balance. In patients with normal or near normal renal function, hyperkalemia is a rare problem.

Replacement Fluid Therapy

Volume deficit — There is no formula that can be used to accurately estimate the total fluid deficit. If pre- and post-
deficit body weight is known, then weight loss provides a reasonable estimate of fluid losses. If the degree of weight loss
is not known, then the fluid deficit cannot be estimated. Clinical and laboratory parameters can be used to assess the
possible presence of volume depletion, including the blood pressure, jugular venous pressure, urine sodium
concentration, urine output, and, if baseline values are available and bleeding has not occurred, the hematocrit. Use of
the urine sodium concentration does not apply to edematous patients with heart failure or cirrhosis in whom the urine
sodium concentration is a marker of effective circulating volume depletion but not of the need for more fluid or more
salt.

Rate of repletion — The rate of correction of volume depletion depends upon its severity. With severe volume depletion
or hypovolemic shock, at least 1 to 2 liters of isotonic saline are generally given as rapidly as possible in an attempt to
restore tissue perfusion, Fluid repletion is continued at a rapid rate until the clinical signs of hypovolemia improve (eg,
low blood pressure, low urine output, and/or impaired mental status. In comparison, rapid fluid resuscitation is not
necessary in patients with mild to moderate hypovolemia. To avoid worsening of the volume deficit, the rate of fluid
administration must be greater than the rate of continued fluid losses, which is equal to the urine output plus estimated
insensible losses (usually 30 to 50 mL/h) plus any other fluid losses (eg, gastrointestinal losses) that may be present.

Choice of replacement fluid — The composition of fluid that is given is largely dependent upon the type of fluid that has
been lost and any concurrent electrolyte disorders.
As examples, hypotonic solutions should be used in hypernatremia, isotonic or, in symptomatic patients, hypertonic
saline should be used in hyponatremia, and isotonic saline and/or blood should be used in patients with blood loss.

Hypernatremia — Water deficits resulting in hypernatremia should almost always be corrected slowly, since overly rapid
correction is potentially harmful.
Avoidance of overly rapid correction can be achieved by calculating how much dilute fluid (eg, 5 percent dextrose in
water) should be given to raise the sodium at the desired rate. Dextrose in water can be given alone in patients with
diabetes insipidus who have lost only water, but will not correct all of the hypovolemia if there has also been salt and
water loss due, for example, to concurrent diarrhea. Sodium and/or potassium can be added to the intravenous fluid as
necessary to treat concurrent volume depletion and/or hypokalemia (due, for example, to diarrhea). However, the
addition of sodium and/or potassium decreases the amount of free water that is being given.

Hyponatremia — As with hypernatremia, overly rapid correction of hyponatremia is potentially harmful. In this setting,
water retention leading to hyponatremia results from nonosmotic stimulation of antidiuretic hormone (ADH) secretion.
The administration of isotonic saline will initially tend to raise the serum sodium, since it has a higher sodium
concentration than the serum. However, once the volume deficit is largely repaired, the stimulus to ADH secretion will
be removed, resulting in the excretion of a maximally dilute urine and possible overly rapid correction of the
hyponatremia that can lead to severe neurologic dysfunction.

Addition of potassium — Concurrent potassium replacement is indicated in patients who have developed potassium
depletion as typically manifested by hypokalemia.

Addition of bicarbonate — A more complex solution may be required in patients with metabolic acidosis. In this setting,
sodium bicarbonate may be added, particularly if the acidemia is severe (arterial pH less than 7.15 to 7.20 or less than
7.0 in diabetic ketoacidosis) or bicarbonate losses persist (as with severe diarrhea).

Saline alone vs with dextrose— There is little evidence that a dextrose-saline solution has any benefit or harm compared
to a saline solution alone for most patients. However, there are some exceptions to this general rule:

-Dextrose-containing solutions should be used in patients with hypoglycemia or alcohol or fasting ketoacidosis, and
should be given with insulin in patients with hyperkalemia and no hyperglycemia since insulin-mediated entry of
potassium into cells will lower the serum potassium concentration.
-Dextrose-containing solutions should not be used in patients with uncontrolled diabetes mellitus or hypokalemia. With
respect to hypokalemia, the administration of dextrose stimulates the release of insulin, which promotes potassium
entry into cells with possible worsening of the hypokalemia.
10272 - Demonstrate the ability to work and interact (as a collaborator and professional) with the surgical team.

10273 - Discuss the assessment and investigation of common geriatric problems: dementia/delirium, depression, falls,
dizziness, hypertension in the elderly and polypharmacy.

              Assessment                                                            Investigations
Dementia      History                                                               Investigations
              o Geriatric giants
                      o incontinence/falls/polypharmacy                                depend on suspected etiologies
                      o memory and safety (wandering, leaving doors                     (see Tables 13 and 14)
                        unlocked, leaving stove on, dressing Shopping losing            o CBC (note MCV), glucose,
                        objects)                                                            TSH, B12, folateˇ
                      o Behavioural (mood, anxiety, psychosis, suicidal                     electrolytes LFTs renal
                        ideation, personality changes, aggression)                          function
              o cardiovascular, endocrine, neoplastic                                   o CT head if Hx of TIA, stroke,
              o EtOH, smokingˇ                                                              focal neurological deficit,
              o OTCs, herbal remedies, compliance, accessibility                            <65 years old, rapid
              o collateral history is usually very helpful                                  progression (weeks to
              o history of vascular disease                                                 months),
                                                                                            immunocompromised, Hx of
              Physical Examination                                                          neoplasm that can
               o   hearing and vision                                                      metastasize to brain,
               o   neurological exam                                                       anticoagulant use
               o   as directed depending on risk factors and history                   o   MRI as indicated
               o   MMSE                                                                o   as clinically indicated -VDRL,
                       o clock drawing                                                     HlV, ANA, anti-dsDNA,
                       o frontal lobe testing (go/no-go, word lists,                       ANCA, ceruloplasmin,
                           similarities, proverb)                                          copper, cortisol, toxicology,
                       o Baycrest NeurocognitiVE' Assessment                               heavy metals
                                                                                       •   indications for CT head, as
                                                                                           in Delirium section plus: age
                                                                                           <60, rapid onset
                                                                                           (unexplained decline in
                                                                                           cognition or function over
                                                                                           1-2 months), dementia of
                                                                                           relatively short duration «2
                                                                                           years), recent Significant
                                                                                           head trauma, unexplained
                                                                                           neurological symptoms
                                                                                           (new onset of severe
                                                                                           headache/seizures)

                                                                                      Issues to consider
                                                                                       o failure to copeˇ fitness to
                                                                                           driveˇ
                                                                                       o caregiver education and
                                                                                           stress
                                                                                       o power of attorneyˇ willsˇ
                                                                                       o advanced directives (DNR)

Delirium
           Clinical Presentation and Assessment                                       standard: CBC + cliff,
                                                                                       electrolytes, calcium,
           • common symptoms                                                           phosphate, magnesium,
           •       wandering attention                                                 glucose, ESR, LFTs (AST, ALT,
           •       distractibility                                                     ALP, albumin, bilirubin), RFTs
           •       disorientation (time, place, rarely person)                         (Cr, BUN), TSH, vitamin BIz,
           •       misinterpretations, illusions, hallucinations                       folate, albumin, urine C&S, R&M
           •       speech!language disturbances (dysarthria, dysnomia,                as indicated: ECG, OCR, CT head,
           dysgraphia)                                                                 toxicology/heavy metal screen,
           •       affective symptoms (anxiety, fear, depression, irritability,        VDRL, HIV, LP, LE preparation,
           anger, euphoria, apathy)                                                    EEG (typically abnormal:
           •       shifts in psychomotor activity (groping/picking at clothes,         genpralized slowing or fast
           attempts to get out of bed when unsafe, sudden movements,                   activity), blood cultures
           sluggishness, lethargy)                                                    indications for raJiological
           •       Folstein exam is helpful to assess baseline of altered              intervention: focal neurological
           mental state -i.e. score will improve as symptoms resolve                   deficit, acute change in status,
                                                                                       anticoagulant use, acute
           Risk Factors                                                                incontinence, gait abnormality,
                hospitalization (incidence 10-40%)                                    history of cancer
                nursing home residents (incidence 60%)
                childhood (e.g. febrile illness, anticholinergic use) • old age
                   (especially males)
                severe illness (e.g. cancer, AIDS)
                   pre-existing cognitive impairment or brain pathology
                   recent anesthesia
                   substance abuse

Depression   Exemples de présentations atypiques pour une dépression :     Quand procéder au dépistage :
                                                                              • Symptômes :
                   Irritabilité
                                                                                     • Importantes
                   Anxiété
                                                                                         préoccupations
                   Apathie
                   Éthylisme                                                            somatiques (poids,
                   Exacerbation de douleur chronique                                    sommeil, énergie)
                   Pseudodémence                                                    • Apparition récente
                   Symptômes psychotiques                                               d’anxiété
                   Alcoolisme                                                       • Difficultés à dormir
                                                                                         qui persistent
                                                                                     • Refus de manger ou
                                                                                         négligence des soins
                                                                                         personnels
                                                                              • Événement
                                                                                     • Deuil récent (avec
                                                                                         Sx inhabituels ou de
                                                                                         3 à 6 mois après la
                                                                                         perte)
                                                                                     • Récente maladie
                                                                                         physique grave
                                                                                     • Placement récent
                                                                                         en établissement de
                                                                                         soins de longue
                                                                                         durée (SLD)
                                                                                     • Hospitalisation
                                                                                         récurrente ou
                                                                                         prolongée
                                                                              • Autres
                                                                                     • Maladie chronique
                                                                                         invalidante
                                                                                     • Isolement social
                                                                                     • Alcool

                                                                           Outils de dépistage

                                                                              •   Échelle de dépression
                                                                                  gériatrique (GDS)
                                                                                      – Échelle d’auto-
                                                                                           évaluation à 30
                                                                                           items
                                                                                      – Valeur seuil de 11
                                                                                      – Sensibilité de 84 %
                et spécificité de 95
                %
           – Version abrégée à
                15 items avec une
                valeur seuil de 7,
                sensibilité et
                spécificité
                semblables (voir
                présentation pour la
                liste de questions)
    •   Échelle de dépression de
        Cornell pour la démence
           – Échelle à 19 items
           – Nécessite une
                entrevue de 20
                minutes avec le
                fournisseur de soins
                et une entrevue de
                10 minutes avec le
                patient

Mini-GDS (4 questions rapides
posées par le généraliste)

        • Avez-vous le sentiment
        que votre vie est vide ? (O)
        • Êtes-vous heureux(se),
        bien la plupart du temps ?
        (N)
        • Vous sentez-vous souvent
        découragé(e) et triste ? (O)
        • Avez-vous l’impression
        que votre situation est
        désespérée ? (O)

(N) signifie que la réponse négative
cote 1 point. (O) signifie que la
réponse affirmative cote 1 point
1 point seulement nécessaire pour
indiquer la pertinence d’une
entrevue complète pour la
dépression

Le diagnostic se fait à l’aide d’une
entrevue complète avec le patient.
(GDS, version abrégée du GDS et
                                                                                 Mini-GDS ne sont que des outils de
                                                                                 DÉPISTAGE)

Falls       Causes :                                                                Direct by Hx or Physical Exam
                                                                                    CBC, electrolytes, BUN,
            •   Multifactoriel                                                       creatinine, glucose, Ca, TSH,
            •   Extrinsinc                                                           Bl21 urinalysis, cardiac
                     • Accidental                                                    enzymes, ECG, CThead
                     • Environemental (e.g. home layout, lighting, stairs,          Test du lever de la chaise
                          footwear)                                                  (Version chronométrée de
                     • Abuse                                                         Mathias)
                     • Medications
                                                                                    Échelle d’équilibre de Berg
                              • Opioids, Steroids, Benzos, TCAs
                                                                                    Épreuve de Tinetti
                              •   4-A’s : Anticonvulsants, Antihypertensives,
                                                                                    Échelle de confiance dans
                                  Anticholinergics, Alcohol
                                                                                     l’équilibre particulier pour
                              •   Cardiac (digoxin, Nitrates)
                                                                                     certaines activités (ABC Scale)
                              • NSAIDS
                                                                                 
                              • Insulin
                     • Illness/Recent Illness/Excaberation of chronic illness
            •   Intrinsic
                     • Syncope/Hypotension (orthostatic, post-prandial)
                     • Sensory (Visual, proprioception, vestibular -
                          étourdissements/vertiges)
                     • Metabolic (glucose, electrolytes)
                     • Cognitive (depression, dementia, delirium, anxiety)
                     • Neurological (Stroke, ↓ LOC, ataxia)
                     • Cardiovascular (CAD, MI, arrhythmia, MI)
                     • MSK (arthritis, muscle weakness –drop attack)



Polypharm   1. Faites comme si chaque médicament que vous prescrivez est         
acy            un essai clinique avec N=1.
            2. Pensez toujours aux médicaments comme un diagnostic pour
               un nouveau symptôme.
            3. La seule règle que vous avez apprise à l’école de médecine au
               sujet des personnes âgées et des médicaments: «
               COMMENCEZ À DE FAIBLES DOSES ET LENTEMENT » était
               seulement à moitié vraie. Vous devez pousser / ajuster la
               posologie jusqu’à :
                        1.ce que les buts thérapeutiques soient atteints;
                        2.l’apparition d’effets secondaires;
                        3.l’obtention d’un dosage maximal satisfaisant
                                • Avoid maximizing dose- Increased side
                                     effects, Less efficacy
            4. Vous n’avez besoin que d’une petite PHARMACOPÉE.
               Apprenez-en une petite quantité, mais apprenez-la bien.
            5. Passez en revue régulièrement les traitements
               médicamenteux de vos patients et prenez le risque de réduire
               les médicaments régulièrement.
            6. Évitez les nouveaux médicaments qui « font boule de neige » à
               moins qu’ils aient fait l’objet de recherche chez les personnes
               âgées ou qu’ils soient considérablement utilisés ailleurs.
             7. C’EST VOTRE RESPONSABILITÉ DE VOUS INFORMER:
                    a. Essais cliniques chez les personnes âgées
                    b. Contre-indications absolues/relatives
                    c. Effets indésirables majeurs et mineurs
                    d. Interactions médicamenteuses et interactions
                       médicament/maladie,
                    e. Instauration de doses habituelles/maximales
                    f. Coûts

             8. Sous-traitement:
                   a. Anticoagulation chez les personnes souffrant de FA
                        (Afib)
                   b. HTA (surtout systolique)
                   c. DÉMENCE (e.g. Inhibiteurs de la cholinestérase)
                   d. Douleur (e.g. crainte particulière des narcotiques chez
                        les personnes âgées)

             9. Il s’agit d’une arme à DEUX TRANCHANTS!
                       Over -med VS under-med
                              o Au Canada, on estime qu’il y a :
                                       200 000 effets indésirables graves
                                           d’un médicament/année
                                       10 000 décès/année
                              o Mais, il y a aussi la sous-médication.
             10. La non observance du traitement médicamenteux est un
                 ÉNORME PROBLÈME
                      (75 % des antihypertenseurs à 1 an)
                          KISS
                          Flacons non à l’épreuve des enfants
                          Étiquettes claires et de gros format
                          Explications aux patients, éducation
                          Pharmaciens – soins pharmaceutiques totaux


Hypertensi      Isolated systolic HTN (ISH) = Systolic ≥140mmHg and Diastolic
on               < 90mmHg
                Accounts for 60-75% of cases of HTN in the elderly
             •   Systolic and pulse pressures may be the major predictors of
                 outcome in the elderly
             •   ISH a/w 2-4 X ↑ in the risk of:
                     • MI, LVH, Cardiovascular mortality, CVA, Renal
                          dysfunction
             •   Even in patients who also have diastolic hypertension, the
                 cardiovascular risk is a/w more closely with the systolic than
                 the diastolic BP
             •   The ↑ in SBP (and Pulse Pressure) is due to stiffening of the
                 arterial circulation (increase peripheral resistance)
             •   SBP ↑ and the DBP ↓ after age 60 in both normotensive and
                 untreated HTN subjects
             •   BP reduction should always be gradual in elderly patients
             •   ARBs = ACE inhibitors for most indications
             •   Combination therapy will likely be required
             •   ACE/CCB combination > ACE/Diuretic combination
                •   Increased risk of orthostatic hypotension OR postprandial
                    hypotension
                        • Before initiating treatment, check their orthostatic
                            vitals
                                 – 20% of ISH pts have orthostatic hypotension
                                     OR postprandial hypotension
                        • Orthostatic hypotension:
                                 – If w/in 2-5 min. of quiet standing (after being
                                     supine), ONE or MORE of the following is
                                     present:
                                                 • ≥20 mmHg fall in SBP
                                                 • ≥ 10 mmHg fall in DBP
                                                 • Symptoms of cerebral
                                                     hypoperfusion (e.g. dizziness,
                                                     confusion,blurred vision)
                •   Patient self monitoring optimizes control and reduces excess
                    hypotension
                •   Avoid maximizing drug doses
                        • Increased side effects
                        • Less efficacy
                •   -blockers should only used for compelling indications like
                    (but even then we can use ACE-I):
                        • Angina (???), MI, Systolic dysfunction,LV
                            dysfunction,AFib rate control,(side-effect profile and
                            potential for worse CVA event rates C/W other agents)
                •



10274 - Describe the special assessment tools that are used to perform a comprehensive functional assessment of an
elderly patient, i.e.mini-mental status examination of Folstein/activities of daily living/instrumental activities of daily
living.
MMSE: The Mini-Mental State Exam (MMSE) is the most widely used cognitive test for dementia in clinical practice. The
examination takes approximately seven minutes to complete. It tests a broad range of cognitive functions including
orientation, recall, attention, calculation, language manipulation, and constructional praxis.
Activities of daily living: Routine activities that people tend do everyday without needing assistance. There are six basic
ADLs: eating, bathing, dressing, toileting, transferring (walking) and continence. An individual's ability to perform ADLs is
important for determining what type of long-term care (e.g. nursing-home care or home care) and coverage the
individual needs.
          Evaluation based on 6 criteria


                      1.   Bathing with sponge, bath, or shower
                      2.   Dressing
                      3.   Toilet Use
                      4.   Transferring (in and out of bed or chair)
                      5.   Urine and Bowel Continence
                      6.   Eating
        Each criteria is graded on level of dependence

                             Performs independently
                             Performs with assistance
                             Unable to perform

Instrumental activities of daily living: the activities often performed by a person who is living independently in a
community setting during the course of a normal day, such as managing money, shopping, telephone use, travel in
community, housekeeping, preparing meals, and taking medications correctly. Increasing inability to perform IADLs may
result in the need for care facility placement.


        Based on 7 criteria

            1.   Use of the telephone (look up numbers, dial, answer)
            2.   Traveling via car or public transportation
            3.   Food or clothes shopping (regardless of transport)
            4.   Meal preparation
            5.   Housework
            6.   Medication use (Preparing and taking correct dose)
            7.   Management of money (write checks, pays bills)

        Each criteria is graded on 3 part scale

                 1. Independent
                 2. Assistance needed
                 3. Dependent

        Two separate surveys completed

               1. Patient
               2. Informant (nurse, caregiver or family member)
10275 Demonstrate appropriate history taking of elderly patients, with particular emphasis on the medical,
functional, mental status and psychosocial evaluation of the patient.

Comprehensive geriatric assessment (CGA) is defined as a multidisciplinary diagnostic and treatment process that
identifies medical, psychosocial, and functional limitations of a frail elderly person in order to develop a coordinated
plan to maximize overall health with aging
MAJOR COMPONENTS — Core components of CGA that should be evaluated during the assessment process are as
follows:
- Functional capacity
          Activities of daily living
- Fall risk
- Cognition
- Mood
- Polypharmacy
- Social support
- Financial concerns
- Advanced care preferences
Additional components may also include evaluation of the following:
- Nutrition/weight change
- Urinary continence
- Sexual function
- Vision/hearing
- Dentition
- Living situation
- Spirituality

10276 - Décrire les modifications pharmacocinétiques liées au vieillissement et comment elles modifient le choix des
médicaments et les doses des médicaments sur ordonnance et des médicaments sans ordonnance chez les personnes
âgées.

Changements pharmacocinétiques (effet du corps sur le med)
   - Absorption
         o Augmentation du pH gastrique
                   Diminution du fer et B12
         o Diminution de la motilité gastrique
                   On absorbe moins de lévodopa et plus de digoxine
   - Distribution
         o Changements au niveau d’albumine
                   Phenytoin, warfarin, digoxine sont très liés aux protéines (et sont ainsi inactifs)
                         S'il y a moins de protéines, alors il y a plus de médicament libre/actif dans le sang!
         o Diminution de l’eau corporelle totale (en raison d’une diminution de la masse musculaire)
                   Médicaments hydrosolubles s'acummulent (concentration augmentée)
                         Lithium, aminosides, alcool, digoxine
         o Augmentation de la masse adipeuse totale agissant sur le volume de distribution
                   Médicaments liposolubles se concentrent dans les lipides
                         Effet prolongé et élimination longue pour diazépam, thiopental, trazodone
                         Augmentation de la demi-vie en présence d’une masse adipeuse augmentée (reservoir)
   - Métabolisme
         o Changements variables dans l’effet de premier passage en raison du déclin variable du débit sanguin
             hépatique
                   Les personnes âgées peuvent avoir un effet de premier passage moindre que les personnes plus
                    jeunes, mais il est extrêmement difficile de le prédire
   - Élimination
         o Élimination peut être soit hépatique ou rénale
         o Fonction rénale (DFG) diminue avec l'âge, mais très variable
                   Effet accru des médicaments avec élimination rénale
                   Important de vérifier la créatinine sérique (taux élevé = problème!)
                   Dosage de la CrCl est plus exacte
                   Équation Cockroft et Gault n'est pas suffisante dans les extrêmes d'âge et de poids
                         Surestime CrCl chez les personnes âgées frêles

Changements pharmacodynamiques (effet du med sur le corps)
    Effet sur le corps est additif
         o Effet cognitif, effet cardiaque, etc
    Médicament et déficience cognitive
         o Cause courante de déficience cognitive possiblement réversible
         o Les patients atteints de démence sont particulièrement exposés à un delirium causé par les
              médicaments
                      Benzodiazépines
                      Les anticholinergiques sont souvent en cause (ATC, Benadryl et d’autres antihistaminiques, et
                       beaucoup d’autres médicaments)
10277- Discuss the atypical presentation of illnesses in the elderly patient.

While both acute and chronic illnesses may, and often do, present with "classic" signs and symptoms, age-related
changes and coexisting conditions may combine to obscure these classic presentations in older persons. Manifestations
of clinically important disease may be attenuated in older persons, particularly those who are frail. Another common
phenomenon is that symptoms in one organ system may reflect disease in another system.

Examples:
Acute abdomen: constipation and decreased appetite instead of severe pain
Pneumonia with vague chest pain, confusion, anorexia or dry cough rather than fever
Infection with falls rather than fever or elevated white count
UTI with behavioral or functional changes
Depression with agitation rather than dysphoria
Sepsis with functional decline and generalized weakness rather than fever
MI with dyspnea and confusion rather than chest pain
Heart failure with fatigue rather than dyspnea
Arthritis limiting physical activity may mask the presence of cardiovascular disease

10278 - Demonstrate the accurate use of problem oriented medical records for following the patient’s progress.

10279 - Demonstrate effective communication skills and professional behaviour when dealing with the elderly and
their caregiver, particularly those who suffer from cognitive impairment.

10280 - Perform a thorough physical examination with special emphasis on blood pressure, gait and balance, and
neurological and musculoskeletal exams.

1028 - Work effectively with a multidisciplinary team in assessing the management of an elderly patient.

CONDUCTING THE ASSESSMENT
Framework — Conceptually, Comprehensive geriatric assessment (CGA) involves several processes of care which are
shared over several providers in the assessment team. The overall care rendered by CGA teams can be divided into six
steps:
1) Data gathering
2) Discussion among the team
3) Development of a treatment plan
4) Implementation of the treatment plan
5) Monitoring response to the treatment plan
6) Revising the treatment plan

Each of these steps is essential if the process is to be successful at achieving maximal health and functional benefits.
Several different models for CGA have been implemented in various health care settings. An increasing number of CGA
programs are relying on post-discharge assessment due to the decrease in length of hospital stay. Furthermore, while
most of the early CGA programs focused on restorative or rehabilitative goals (tertiary prevention), many newer
programs are aimed at primary and secondary prevention.
10282 - Reconnaître le rôle et l’importance de la famille et des soignants dans la prestation de soins au patient
(gériatrie).

10283- Demonstrate attentiveness to the emotional aspects of the family and the caregiver when dealing with a
patient suffering from dementia.

Most elders with functional impairment live in the community with the help of an "informal" caregiver, most commonly
a spouse or daughter. The health and well being of the patient and caregiver are closely linked. High levels of functional
dependency place an enormous burden on a caregiver, and may result in caregiver "burnout," depression, morbidity,
and even increased mortality.

An older patient’s need for nursing home placement is often better predicted from assessment of the caregiver
characteristics and stress than the severity of the patient’s illness. Therefore, part of caring for a frail elder involves
paying attention to the well being of the caregiver. The older patient who is also a caregiver is at risk for depression and
should be screened for it. For the stressed caregiver, a social worker may help identify programs such as caregiver
support groups, respite programs, adult day care, or hired home health aides.


10284 - Recognize the importance of working with a multidisciplinary team and how each member contributes to the
assessment and care of the elderly.

10285 - Recognize the complex ethical issues of balancing end of life issues involving investigation and treatment in
elderly patients.


10286 - Discuss the factors that are related to dependence on tobacco and the factors that assist patients to stop
smoking.
Facteurs relies à la dépendance au tabac:
                     1) Éducation : Les patients ayant un niveau d’éducation équivalent à un diplôme d’étude
                         secondaire ou inférieur à ce niveau compose près de la moitié des fumeurs. (d’après uptodate)
                     2) Revenue : Les gens ayant un revenu faible sont plus à risque de développer une dépendance au
                         tabac. (uptodate)
                     3) Race : La prévalence de tabagisme chez les amérindiens (32.4%) est la plus haute et est la plus
                         basse chez les asiatiques (9.9%). La prévalence est similaire chez les blancs, les afro-américains
                         et les hispaniques (autour de 20%) (uptodate).
Facteur affectant l’arret du tabagisme : d’après santé-canada
    1) Statut socio-économique : le taux de cessation du tabagisme chez les femmes enceintes et notamment plus bas
        chez les femmes ayant un bas statut socio-éoconomique.
    2) Reseau social : l’influence et le support du réseau social est un déterminant important du succès ou non de
        l’arrêt du tabagisme.
    3) Degré de dépendance à la nicotine : Le degré de difficulté lié à l’abandon du tabac est influencé par la durée de
        l’exposition à la nicotine.
    10287 - Discuss the stages through which a person typically progresses in attempting to stop smoking.
10288 - Discuter des divers niveaux d’interventions offerts pour aider une personne qui souhaite arrêter de fumer.

      Soutien par un parrain/marraine
      Aide pharmacologique
           o Les thérapies de remplacement de la nicotine (TRN)
                    Sous forme de timbres, de gommes, de pastilles ou d’inhalateur (comme Habitrol, NicoDerm,
                        Thrive et Nicorette).
                    Aident le corps à s’habituer à vivre sans tabac en lui fournissant une partie de la dose de
                        nicotine à laquelle il est accoutumé
           o Comprimés de varénicline (Champix)
                    Sous ordonnance
                    Ne contient pas de nicotine
                    Agit sur les récepteurs nicotiniques dans le cerveau
           o Comprimés de bupropion (Zyban)
                    Sous ordonnance
                    Ne contient pas de nicotine
                    Anti-dépresseur
      Aide alternative
           o Acupuncture
           o Hypnose
           o Cures de déconditionnement
           o Phytothérapie
           o Homéopathie
10289- Demonstrate the ability to assess a patient's readiness to stop smoking.

Assessing a smoker's interest in stopping allows for categorization of smokers which is useful for establishing if the
counseling strategy is appropriate and to set achievable goals. Although the clinician's overall goal is to assist the smoker
to stop permanently, a realistic goal for a single office visit is to move the smoker to the next stage of readiness to stop.

The stages of change are an important component to any behavioral change:

Pre-contemplation: not seriously thinking about quitting

Contemplation: thinking about quitting in the next six months

Preparation: preparing to quit in the nest month and possibly has already tried to quit in the past year

Action: receptive to cessation advice. Actively trying to quit

Maintenance: continues to remain smoke free for more than six months. May slip and have occasional cigarette

Example of University of Ottawa Heart Institute questionnaire:




Also you can ask:

-How important is it for you to quit smoking on a scale of 1 to 5?

-How confident are you that you could succeed in quitting for good on a scale of 1 to 5?

If the patient is ready to quit within 30 days = develop a quit plan, if the patient is not ready to quit = provide self help
and follow up.
10290 - Demonstrate the ability to appropriately advise and assist patients who are ready for change.

10291 - Demonstrate motivation and commitment to helping patients with an addictive behaviour.

10292 - Demonstrate empathy and understanding regarding patients who are attempting to stop smoking.

10293 - Discuss typical challenges in delivering quality health care to recent immigrants.

(From an article in CMAJ: Providing health care to medically uninsured immigrants and refugees)

…Physicians in this country may be surprised to know that, despite Canada's universal health care system, many who
reside here legally are never granted public health insurance. Other immigrants and refugees are granted coverage, but
only after long delays: 4 provinces impose a mandatory 3-month waiting period — but in our experience, our patients'
wait has averaged 2.1 years. Many others reside in limbo: between 1997 and 2004 Canada's Immigration and Refugee
Board adjudicated 228 000 refugee claims, approving only 40%. Rejected refugee claimants who continue to reside in
Canada while they pursue legal avenues of appeal lose their eligibility for public insurance, either provincial or federal.
Up to 15% of the 29 000 claims backlogged during the same period are abandoned annually because of cost and delay
(www.irb-cisr.gc.ca), which again leads to losses of Interim Federal Health Benefits.

Our patients (at the Scarborough Hospital) regularly report being turned away by community health clinics because they
do not meet enrolment requirements such as possession of identifying documents or evidence that they reside within
the clinic's prescribed area. Such problems are common among people who are homeless or underhoused, or have lost
their identifying documents or had them destroyed. In Toronto, many community health clinics have capacity
restrictions that resulted in waiting lists to enroll. Some of our pregnant patients have reported being turned away when
presenting at an advanced gestational age.

Delayed health care or denial of care at emergency departments because of inability to pay are also common themes. …

…Others who are entitled to health benefits lack the knowledge, documentation or means to secure them: 5% of our
uninsured youth, mostly children born in Canada to uninsured newcomers, are in fact Canadian citizens.

More research is urgently needed to facilitate policy initiatives and solutions. Meanwhile, our preliminary research
points to remedies that should be considered now. These include elimination of 3-month waiting periods in the
provinces that require it; facilitation of health coverage for those who are eligible; improvements to the refugee claims
process; implemention of emergency health insurance coverage for those in need while their claims are in process
(pregnancy and newborn care, for example, are covered in Québec); and at community health clinics, increases in
capacity and relaxion of enrolment criteria. If universal health insurance is a core Canadian value, we need to ensure
that it is, indeed, universal.

10294 - Démontrer la capacité de discuter de leurs (immigrants) propres antécédents ethnoculturels, valeurs et
croyances.

10295- Demonstrate empathy for, and understanding of, patients and their particular ethno‐cultural circumstances.

10296 - Discuss the importance of cultural influences in the provision of care.

10297 - Discuss disability management, work fitness and public health surveillance with regard to occupational health
problems, i.e. hazard recognition, evaluation and control; occupational and environmental injury/illness.


10298 - Describe the Canadian system for occupational health problem surveillance and hazard investigation.
10299 - Elicit a patient's occupational history and possible exposures in relation to the patient’s presentation.

Systematic approach to history taking and diagnosis of occupational or environmental illness




(www.uptodate.com)

10300 – Proposer un plan de prise en charge efficace pour un patient qui a des problèmes de santé liés au travail, y
compris le counseling concernant les questions de sécurité et un rapport de constations à l’intention du patient et de
son employeur (en tenant compte des questions de confidentialité médicale).

Objectif incomplet/imparfait

Assessing occupational health and safety
     Symptoms of disease and job-related injuries
     Work description including occupational profile
     Prior or current exposure to dusts, chemicals, solvents, radiation, biological agents, loud noise, mechanical or
        psychosocial stressors
       Review of relevant workplace material safety data sheets (ask patient to provide these)
       Temporal relationship between symptoms and exposure
       Description of other environments (home, neighbourhood)
       Hobbies
       Occupation of family members

Treatment and rehabilitation
     Treat injury or illness with safe return to the workplace
           o May require…
                    Rehabilitation
                    Retraining
                    Change in job duties and/or workers' compensation involvement

Establishes Workplace Safety and Insurance Board (WSIB), an autonomous government agency which oversees
workplace safety training and administers insurance for workers and employers (previously Workers' Compensation
Board, WCB)
     Physicians are required to provide the WSIB with information about a worker's health without a medical waiver
        once a claim is made
     Physicians are required to report diseases due to exposure to a "designated substance"
            o Acrylonitrile, arsenic, asbestos, benzene, coke oven emissions, ethylene oxide, isocyanates, lead,
                mercury, silica and vinyl chloride

10301- Describe alternative models of health behavior change, including an integrated model of the determinants of
change.

The Stages of Change Model introduced the idea that people move through a succession of six relatively distinguishable
stages in making changes in behavior.

Precontemplation stage: There is little thought about the problem or its solution.

Contemplation stage: The problem and the potential methods, costs, and benefits involved in trying to address it are
explored and evaluated.

Preparation/Determination stage: Choosing and committing to a specific course of action and timetable around which to
commit energies to change.

Action stage: New behaviors are initiated and problem behaviors are replaced (e.g., following a diet and exercise
program on a consistent basis).

Maintenance stage: Successful changers begin to incorporate Action stage behaviors into a "new normal" way of living.

Relapse stage: There is a return to an earlier stage after an initial period of successful change.

Motivational Interviewing

Miller and Rollnick's Motivational Interviewing Model challenged the existing assumption that people change primarily
when they are pressured from outside.

The theory of reactance posits that individuals are strongly motivated to maintain a sense of autonomy and to resist
coercion by others. People who might otherwise have admitted their concern over a problem may instead feel
compelled to defend their behavior when criticized.

Miller and Rollnick demonstrated that the most effective way to influence patients' behavior is to build on their own
self-motivation to change. This is accomplished through an interview style that emphasizes empathy, curiosity, self-
determination, and acceptance on the clinician's part.

Example: I am concerned that you will continue to worry about another heart attack unless you can change some of the
continuing risks we have been discussing. What do you think about that?

Social Learning Theory

Describes how people learn social behaviors, evaluate the desirability of behaviors, and influence and are influenced by
others to adopt behaviors and beliefs. Conviction and confidence are continuous rather than dichotomous dimensions
(more or less rather than all or none).

Example:

How convinced are you that cigarette smoking is really hurting you?

How confident are you that you could quit smoking if you really wanted to? What gets in the way of your feeling
more confident that you could quit?

Motivational Interviewing advises the clinician to approach these tasks through empathic conversation rather than
lecturing/advising.

10302 - Demonstrate skills in assessing the barriers to behavioral changes.
10303 - Demonstrate skills in evaluating the factors that support behaviour change.

10304 - List the clinical features of common and life-threatening skin diseases.
Contact dermatitis : Contact dermatitis is a localized rash or irritation of the skin caused by contact with a foreign
substance. Only the superficial regions of the skin are affected in contact dermatitis. Inflammation of the affected tissue
is present in the epidermis and the outer dermis.

Atopic dermatitis: The skin of a patient with atopic dermatitis reacts abnormally and easily to irritants, food, and
environmental allergens and becomes red, flaky and very itchy. It also becomes vulnerable to surface infections caused
by bacteria. The skin on the flexural surfaces of the joints (for example inner sides of elbows and knees) are the most
commonly affected regions in people.

Cutanous vasculitis : Palpable purpura is the hallmark and most diagnostic feature of cutaneous vasculitis. Other
primary lesions, although less specific, may represent vasculitis of the skin; these include transient petechiae, vesicles,
bullae, necrosis, ulceration, and chronic telangiectasia, livedo reticularis and atrophic scarring, depending on the severity
and duration of damage to the vessel wall. In the absence of palpable purpura clinical diagnosis is extremely difficult and
only pathologic examination is confirmatory.


Allergic urticaria : Urticarial lesions are circumscribed, raised, erythematous plaques, often with central pallor. Individual
lesions usually appear and resolve over a few hours without leaving residual marks on the skin unless there is skin
trauma from scratching. Any area of the body may be affected. Pruritus may be severe enough to disrupt work, school,
or sleep.
Severe staphylococcal cutaenous infections and toxic shock syndrome: Toxic shock syndrome due to GAS typically
presents with pain that precedes physical findings of infection. The pain typically involves soft tissue of an extremity but
may also mimic peritonitis, pelvic inflammatory disease, pneumonia, acute myocardial infarction, cholecystitis, or
pericarditis.
Clinical signs of soft tissue infection typically consist of localized swelling and erythema followed by ecchymoses and
sloughing of skin which progresses to necrotizing fasciitis or myositis in 70 to 80 percent of cases. An influenza-like
syndrome characterized by fever, chills, myalgia, nausea, vomiting, and diarrhea is observed in about 20 percent of
patients. A diffuse, scarlatina-like erythema occurs in about 10 percent of cases.
Stevens-Johnson syndrome:


       Confluent erythema (erythroderma)
       Facial edema or central facial involvement
       Skin pain
       Palpable purpura
       Skin necrosis
       Blisters and/or epidermal detachment
       Mucous membrane erosions and crusting
       Swelling of tongue

10305 - List the differential diagnosis of common dermatological groupings (e.g. eczema, papulosquamous).

DD of Eczema (atopic dermatitis):
other eczematous disorders such as contact dermatitis,
seborrheic dermatitis,
drug reactions

In infants, considerations include
psoriasis
scabies
Wiskott-Aldrich syndrome,
hyperimmunoglobulin E syndrome
nutritional deficiencies,
acrodermatitis enteropathica
Netherton's syndrome.

The ones we saw in class:

DD of Scabies lesion:
Atopic dermatitis
Contact dermatitis
Lichen planus
Impetigo
Psoriasis (Norwegian Scabies)

DD of Lichen Planus, based on skin lesions:
Lichenoid drug eruption - usually photodistribution
        scaly, more widespread
         oral lesions absent
Pityriasis Rosea
Psoriasis
Secondary Syphilis
Tinea

DD of Lichen Planus, based on mucous membrane lesions:
Leukoplakia
Lupus
Candida
Syphilis

DD of Granuloma Annulare
Necrobiosis lipoidica diabeticorum (on shins, mostly in diabetics)
Sarcoidosis
Lichen planus
Tinea corporis
*Often misdiagnosed for ringworms or tinea corporis

DD of subcutaneous Granuloma annulare
Rheumatoid nodule
Erythema nodosum
Dermoid cyst

10306 - Décrire la pathologie, l’immunopathologie et la physiopathologie des maladies cutanées courantes et mettant
la vie en danger.

OBJECTIF BEAUCOUP TROP LONG, DÉSOLÉ ! SI VOUS AVEZ LA NAUSÉE, ABSTENEZ-VOUS!

Maladies cutanées courantes
    Contact dermatitis
           o Irritant and allergic contact dermatitis are the two major variants of this condition. Despite their
               different mechanisms, they can be difficult to distinguish at the clinical, histologic and even molecular
               levels.
           o Allergic contact dermatitis is biphasic, with an afferent (sensitization) phase and an efferent (elicitation)
               phase. Cutaneous antigen-presenting cells (for example, Langerhans’ cells) play a role in trafficking and
               presenting hapten-self complexes to T lymphocytes.
           o CD8 + T lymphocytes are thought to be the major effector cell of allergic contact dermatitis, whereas
               CD4 + T lymphocytes may play a role as regulatory cells in allergic contact dermatitis.
           o Irritant contact dermatitis is a nonimmunologic response to chemicals that are damaging to the skin
               (surfactants, solvents, hydrocarbons, strong acids/bases, and others).
    Atopic dermatitis
           o This is a complex disease process that involves polygenic inheritance as well as gene– environment
               interactions.
           o Because this condition is so common in industrialized nations, it has been hypothesized that the
               avoidance of common childhood diseases (because of hygienic conditions and vaccination) interferes
               with the normal development of the immune system.
           o A variety of factors play a role in atopic dermatitis: abnormal barrier function, neuroimmunepsychiatric
               factors, impaired innate immunity, and abnormal acquired immunity.
        o   Bacterial products, and the aberrant immune response to such products, are important pathogenic flare
            factors for eczema.
   Psoriasis
        o Psoriasis is a common, immune-mediated inflammatory papulosquamous skin disease that results in
            recurring scaly, erythematous plaques, typically in a symmetrical distribution.
        o There is strong evidence that psoriasis is determined by genetic predisposition. It is thought that there is
            not a single disease gene, but rather a complex set of gene variants that results in an abnormal response
            to environmental factors.
        o Psoriasis is now considered to be a disease caused by the infiltration of effector immunocytes in the
            epidermis and dermis.
        o Important effector cells are CD4 and CD8 conventional T-lymphocytes, as well as natural killer (NK) T
            cells, plasmacytoid dendritic cells (PDCs), TIP-DCs.
        o Other cell types that participate in this pathologic process include keratinocytes, endothelial cells,
            fibroblasts, monocytes/macrophages, and neutrophils.
        o Pathologic cytokines include inflammatory cytokines such as tumor necrosis factor-α (TNFα), interferon-
            α (IFN-α), T-helper-1 (Th1) cytokines such as IFN-γ, Th17 cytokines such as interleukin-17 (IL-17) and IL-
            22, and antigenpresenting cell (APC)-derived cytokines such as IL-12 and IL-23.
   Acne
        o Acne is a complex disease with multiple pathogenic factors.
        o Propionibacterium acnes is the trigger for inflammatory acne.
        o Acne is a complex disease with multiple pathogenic factors that act together to produce disease.
        o Dystrophic keratinization is involved in the formation of the plug in the follicle (comedo or
            microcomedo) that is the central lesion of acne.
        o Hormonal stimulation of the sebaceous gland occurs at puberty, which causes production of sebum, a
            complex mixture of lipids that is about 50% triglycerides. Triglycerides are a rich carbon source for lipase
            producing bacteria and are a powerful determinant of the skin microflora.
        o Propionibacterium acnes, an anaerobic diphtheroid, dominates the follicular microflora after puberty
            and is the trigger for inflammatory acne.
   Drug eruptions
        o Such drug eruptions, in most cases, have been demonstrated to be mediated by immunologic
            mechanisms, and can involve type I (immunoglobulin E [IgE]-mediated), type II (cytotoxic), type III
            (immune complex), type IV (cell-mediated immunity), or a combination of multiple mechanisms.
        o Certain drugs may be linked to specific types of drug eruptions (for instance, anticonvulsants are
            notorious for causing severe cutaneous reactions).
        o There are predisposing factors that place a patient at increased risk for drug eruptions (viral infections,
            past history of medicament allergies, polymorphisms in human leukocyte antigen).
   Cutaneous vasculitis
        o The diagnosis of vasculitis is confirmed unequivocally by the presence of an inflammatory infiltrate
            around and within the walls of vasculature with fibrin deposition. These areas of fibrinoid necrosis are
            accompanied by swelling and necrosis of endothelial cells, as well as secondary changes such as
            erythrocyte extravasation and necrosis leading to purpura and infarction, respectively. Apoptotic cells
            are seen frequently as well as overlying ulceration.
        o The pathogenic features of vasculitis in the skin are related to vessel wall injury, which can be toxin
            mediated, immune mediated, or from direct infection, and all three mechanisms can result in the
            histologic pattern of fibrinoid necrosis
        o Deposition of immune complexes leads to complement activation, further recruitment of inflammatory
            cells and cytokines, and expression of adhesion molecules such as E-selectin, P-selectin, and intercellular
            adhesion molecule (ICAM-1).
        o With endothelial cell retraction, there is vascular deposition of immune complexes, neutrophil
            infiltration, edema, hemorrhage, and thrombosis.
        o Immunofluorescence is an essential diagnostic tool in the evaluation of cutaneous vasculitis, especially
            in the small-vessel group. This technique consists of the detection of immunoglobulins (Igs) and
            complement deposited within tissue. Deposition of IgA, IgG, IgM, and C3 in or around vessels
                 characterizes antibody and immune complex– mediated vasculitis, and the patterns of deposition
                 further classify disease.
       Allergic urticaria
             o Urticaria can be acute or chronic, and may be allergic (mediated by immunoglobulin E) or nonallergic
                 (mediated by pharmacologic effects of drugs such as aspirin or an acute-phase response).
             o There are variants of urticaria that are caused by physical factors such as exposure of the skin to
                 pressure, vibration, cold, or even water (aquagenic urticaria).
             o Urticarial lesions are produced in the skin by the degranulation of mast cells. Urticaria can be a
                 presenting sign of urticarial vasculitis.
             o Chronic urticaria is the common presentation of this condition, and in most instances it is not possible to
                 identify an etiology (idiopathic urticaria).
             o There are a multitude of causes of urticaria, including food or medication allergies, infections, as well as
                 in association with autoimmune diseases such as thyroid disease. Histamine-releasing autoantibodies
                 are thought to be one of the possible causes of urticaria.
       Je pourrais continuer et continuer encore… Vous pouvez lire sur les infections virales, bactériennes et fongiques.
        J’ai trouvé mes informations dans le livre «Clinical Immunodermatology» (catalogue de l’Université d’Ottawa –
        Livre électronique)

Maladies cutanées mettant la vie en danger
    Purpura fulminans
           o Abnormalities in both the coagulation and fibrinolytic pathways can lead to purpura fulminans.
           o Endothelial cell dysfunction may play a major role in the pathophysiology.
           o Infections reported to cause purpura fulminans include Neisseria meningitidis, Streptococcus
               pneumoniae, Haemophilus influenzae, H. aegyptius, Staphylococcus aureus, Group A and other beta-
               haemolytic streptococci, Pseudomonas aeruginosa, Rickettsiae and Candida albicans.
    Severe infections of soft tissues (including fascitis and diabetic foot infections)
           o Erysipelas and other non-necrotizing dermal– hypodermal infections are mainly caused by streptococci,
               though other bacteria can cause such infections, which often occur in specific circumstances.
           o There is an increasing prevalence of soft-tissue infections (STIs) caused by community-acquired MRSA
               which are responsible for about half of the cases of cellulitis with purulent exudates in involved
               geographic areas. Contrary to erysipelas, the best therapeutic option will be an antibiotic that is
               effective both against streptococci and S. aureus.
           o In diabetic patients, severe STIs of the lower extremity represent a frequent and difficult problem; these
               diabetic foot infections frequently expand to bones and joints, and are associated with a poor prognosis
               of limb salvage.
           o Except diabetic foot infections, STIs are frequently due to streptococci though staphylococci, particularly
               methicillin-resistant Staphylococcus aureus (MRSA), play a growing role in dermal– hypodermal
               infections evolving into abscesses. However, numerous other bacteria (Pseudomonas aeroginusa,
               Entero-bacteriaceae, anaerobes) may also be responsible for severe STIs with local necrosis and/or
               abscess formation.
    Severe staphylococcal cutaenous infections and toxic shock syndrome
           o S. aureus is a Gram-positive cocci of the Micrococcaceae family. It is one of the most common
               pathogens in skin and soft-tissue infections, and can cause potentially serious nosocomial infections
               when acquired in the hospital setting. S. aureus has a diverse arsenal of components and products that
               contribute to the pathogenesis of infection.
           o The virulence of S. aureus infection is remarkable, given that the organism is a commensal that colonizes
               the nares, axillae, vagina, pharynx or damaged skin surfaces. Infections are initiated when a breach of
               the skin or mucosal barrier allows staphylococci access to adjoining tissues or the bloodstream.
           o Whether an infection is contained or spreads depends on a complex interplay between S. aureus
               virulence determinants and host defense mechanisms.
    Erythoderma and exfoliative dermatitis
            o   Erythroderma is conventionally defined as inflammation of at least 90% of the skin surface,
                characterized by erythema and variable scaling. When the scaling is prominent it is often called
                exfoliative dermatitis.
            o There are a multitude of possible causes which encompass virtually all inflammatory skin diseases; a
                proportion develop without any apparent trigger and remain ‘idiopathic’.
            o The commonest causes of acute erythroderma are psoriasis, atopic and other varieties of eczema,
                cutaneous T-cell lymphoma and drug reactions.
       Stevens-Johnson syndrome and toxic epidermal necrolysis
            o Stevens– Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe, druginduced skin
                reactions with a high morbidity and mortality.
            o Drugs with a high risk to induce SJS and TEN are allopurinol, antibacterial sulfonamides including
                sulfasalazine, carbamazapine, lamotrigine, nevirapine, oxicam-NSAIDs, phenobarbital, and phenytoin.
            o Drugs are the cause of the majority of all cases of SJS and TEN. However, it is not yet clear how the link
                between a certain drug and the (epidermal) necrosis is made. Several investigations have shown that T
                cells, especially CD8 + lymphocytes, play an important role in this process, which may be mediated by
                cytokines such as TNF-alpha, Fas, and Fas-ligand.
       Drug reactions with eosinophilia and systemic symptoms
            o Drug-induced hypersensitivity syndrome (DIHS/ DRESS) is an adverse drug-induced reaction of severity
                similar to that of Stevens– Johnson syndrome.
            o Human herpesvirus 6 (HHV-6) can be reactivated 2– 3 weeks after the onset of rash in the vast majority
                of DIHS patients.
       Acute generalized exanthematous pustulosis
            o The drugs with the highest risk to cause AGEP are antibacterial agents like ampicillin/amoxicillin, and
                quinolones, pristinamycin, anti-infective sulfonamides, the antimycotic drug terbinafine,
                (hydroxy)chloroquine, and diltiazem, but a large number of other drugs as well as infections have been
                reported as triggers.
            o It is obvious that neutrophils play an important role in AGEP and the role of drug specific (CD4+) T-cells
                that produce neutrophil-attracting factors like interleukin-8 (IL-8) and cytotoxic (CD8+) T-cells has been
                extensively investigated
       Autoimmune bullous diseases
            o Life-threatening autoimmune blistering disorders include bullous pemphigoid and the different subtypes
                of pemphigus: pemphigus vulgaris, pemphigus foliaceus and paraneoplastic pemphigus. Major extent of
                skin and mucosal lesions results in the failure of main skin functions.
                      Bullous pemphigoid
                              BP patients develop circulating and tissue-bound antibodies that are directed against
                                  two proteins of the hemidesmosomes.
                              The target of these antibodies are proteins and are termed bullous pemphigoid antigen
                                  1 (BPAG1), an intracellular protein of the hemidesmosome, and bullous pemphigoid
                                  antigen 2 (BPAG2), a transmembrane protein.
                              Anti-BPAG2 antibodies react with the first extra cellular domain of the molecule, and
                                  appear to be more pathogenic than anti-BPAG1 antibodies.
                              Following antibody binding to these proteins, the Fc portion of the antibody activates
                                  both the classical and alternative pathway of complement. Poly-morphonuclear cells
                                  recruited to the area release inflammatory mediators, ultimely leading to the
                                  occurrence of clinical features of BP.
       Encore là, j’aurais pu en écrire davantage. J’ai utilisé le livre électronique «Life-Threatening Dermatosis and
        Emergencies in Dermatology» via le catalogue de l’Université d’Ottawa

10307- Describe commonly used dermatological investigative and therapeutic techniques.

Investigatice techniques
-Agnification: a standard magnifying glass serves as a useful aid in the characterization of skin lesions.
-Diascopy: compress red lesions with a magnifying glass or a glass slide, to see, if they blanche indicating dilated vessels.
Extravasated blood will not blanch.

-KOH preparation: allow visualization of dermatophyte hyphae, Candida pseudohyphae and budding yeasts and the
spores and fragmented hyphae of tinea versicolor. Scrape skin scales from the lesion and place them on a glass slide.
Add 2 drops of a 10% to 20% solution of KOH to dissolve keratin, allowing the fungal elements to be more easily seen
microscopically. Gentle heating with a flame will catalyze this process, but care should be taken to avoid boiling the
solution. First, examine the slide at scanning magnification, followed by a higher power view. Hyphae appear as thin,
elongated filaments, often best seen just slightly out of the plane in which the keratinocytes are in focus. Other
confounders include hair and clothing fibers.

-Tzanck smear: to identify herpes simplex or varicella-zoster viruses in vesicular lesions, firmly scrape the base of an
unroofed early vesicle with a scalpel and air dry the specimen on a glass slide. Stain it with Wright or Giemsa stain and
examine microscopically for characteristic cytopathic changes such as multinucleated giant cells or ballooning
keratinocytes. Culture a fresh specimen for virus identification.

-Wood light: ultraviolet illumination (360 nm) demonstrates a characteristic fluorescence in scalp infections caused by
some (but not all) dermatophytes such as Microsporum canis (yellow), Pseudomonas abscesses (pale blue), or
intertriginous infections with Corynebacterium minutissimum (coral red). Keep in mind that recent bathing may decrease
the presence of the fluorescent substance and lead to falsely negative results.

-Skin biopsy: techniques include use of a skin punch, shaving with a scalpel or razor blade, and sharp excision.

-Patch test: is designed to document sensitivity to a specific antigen. In this procedure, a battery of suspected allergens
is applied to the patient's back under occlusive dressings and allowed to remain in contact with the skin for 48 h. The
dressings are removed, and the area is examined for evidence of delayed hypersensitivity reactions (e.g., erythema,
edema, or papulovesicles).

Therapeuic techniques
-Ointments: consist predominantly of water suspended in oil. This type of vehicle is an excellent lubricant, facilitates
heat retention, decreases transepidermal water loss, provides enhanced medication absorption, and is semiocclusive.
Ointments should be applied two to three times per day to dry, lichenified lesions, particularly after moistening the skin.

-Creams: are semisolid emulsions of oil in 20 to 50 percent water and can be washed off with water. They are the most
cosmetically appealing vehicle type for delivering topical medications. Creams are less potent than ointments, but are
useful in most dermatoses. For the same medication, cream formulations are usually stronger than lotions, but less
potent than ointments.

-Lotions: are the least potent topical therapies, but are useful in hairy areas and in conditions where large areas have to
be treated. They consist of powder-in-water; thus, patients must shake the container before each application to receive
the desired therapeutic concentration (and therefore the desired effect). In addition, as lotions evaporate, they provide
a cooling and drying effect, making them useful for treating moist dermatoses and/or pruritus.

-Solutions: consist of water, or water in combination with various medications or substances. Solutions such as bath
soaks and open wet dressings provide coolness and aid in drying exudative lesions by means of evaporation. In addition,
vasoconstriction results in decreased local blood flow and reduction in local edema.

-Wet dressings: permit the cleansing of exudate while maintaining drainage in infected lesions (eg, ulcers). Wet
dressings should be changed every six hours for two to three days before judging their effectiveness. Closed wet
dressings consist of a wet dressing covered by an impermeable substance such as a polyurethane plastic (eg, Saran
Wrap), which allows heat to be retained, prevents evaporation, and causes maceration.

-Gels: are an oil-in-water emulsion with alcohol in the base, and they dry in a thin, greaseless, nonstaining film. Gel
formulations combine the best therapeutic advantages of ointments with the best cosmetic advantages of creams. Gels
are transparent, colorless, semisolid emulsions that liquefy on contact with the skin. They are an efficient method for
delivering medications to hair-bearing areas and for treating acne.

-Foams: are pressurized collections of gaseous bubbles in a matrix of liquid film. Foam preparations spread readily and
are easier to apply than other preparations, particularly for inflamed skin and for scalp dermatoses. They are also often
more cosmetically acceptable, which can lead to higher compliance. Unlike other vehicles, foams depend on the vehicle
delivery system for the physical delivery of the drug. Because of the complexities in designing vehicle delivery systems,
foam preparations tend to be more expensive than other vehicles.

10308 - Describe the mechanism of action, side effects and how to use common dermatological therapies.

***Reference: Toronto Notes 2006***

TOPICAL THERAPY:

VEHICLES
      For acute inflammation (edema, vesiculation, oozing, crusting, infection) use aqueous drying preparation
      For chronic inflammation (scaling, lichenification, fissuring) use a greasier, more lubricating compound
Powders
Promote drying, increase skin surface area (i.e. cooling)
• used in intertriginous areas to reduce moisture and friction
• inert or contain medication
Lotions
Suspensions of powder in water
• cool and dry as they evaporate
• leave a uniform film of powder on skin
• easily applied to hirsute areas
Cream
Semisolid emulsions of oil in water
• water-soluble, containing emulsifiers and preservatives
• cosmetically pleasing
Gel
Crystalline with a lattice
• transparent, colourless, semisolid emulsion with aqueous, acetone, alcohol or propylene glycol base
• liquifies on contact with skin
• dries as a thin, greaseless, nonocclusive, nonstaining film
Ointment
Semisolid water in oil emulsions (more viscous than cream)
• inert bases - petroleum
• most effective to transport medications into skin
• retain heat, impede water loss, increase hydration
• occlusive, not to be used in oozing or infected areas
Possible side effects of topical steroids:

       Diabetes Mellitus
       Osteoporosis
       Allergic Contact Dermatitis
       Skin Atrophy
       Perioral dermatitis
       Increased Intra-ocular pressure
       Tachyphylaxis
       Facial hypertrichosis, folliculitis
10309 -Appreciate the interaction between patients with skin diseases, their families, the community and the
environment.

10310 - Recognize the various abnormalities of the diseased skin, hair, nails and visible mucosa, including how to look
for the basic lesion including its colour, location, distribution, pattern, etc.

10311 - List the medical terms used for describing the skin abnormalities in objective 10310.

Primary Lesions

      Macule - A macule is a change in surface color, without elevation or depression and, therefore, nonpalpable,
       well or ill-defined, variously sized, but generally considered less than either 5 or 10mm in diameter at the widest
       point.
      Patch - A patch is a large macule equal to or greater than either 5 or 10mm,[4] depending on one's definition of a
       macule.[1] Patches may have some subtle surface change, such as a fine scale or wrinkling, but although the
       consistency of the surface is changed, the lesion itself is not palpable.[3]
      Papule - A papule is a circumscribed, solid elevation of skin with no visible fluid, varying in size from a pinhead to
       either less than 5[6] or 10mm in diameter at the widest point.[4]
      Plaque - A plaque has been described as a broad papule, or confluence of papules equal to or greater than
       1 cm,[4] or alternatively as an elevated, plateau-like lesion that is greater in its diameter than in its depth.[3]
      Nodule - A nodule is morphologically similar to a papule, but is greater than either 5[3] or 10mm in both width
       and depth, and most frequently centered in the dermis or subcutaneous fat.[4] The depth of involvement is what
       differentiates a nodule from a papule.[6]
       Vesicle - A vesicle is a circumscribed, fluid-containing, epidermal elevation generally considered less than either
        5[6] or 10mm in diameter at the widest point.[4]
       Bulla - A bulla is a large vesicle described as a rounded or irregularly shaped blister containing serous or
        seropurulent fluid, equal to or greater than either 5[6] or 10mm[4], depending on one's definition of a vesicle.[1]
       Pustule - A pustule is a small elevation of the skin containing cloudy[3] or purulent material usually consisting of
        necrotic inflammatory cells.[4]
       Cyst - A cyst is a cavity containing liquid, semi-solid, or solid material.[6]
       Erosion - An erosion is a discontinuity of the skin exhibiting incomplete loss of the epidermis,[7] a lesion that is
        moist, circumscribed, and usually depressed.[5]
       Ulcer - An ulcer is a discontinuity of the skin exhibiting complete loss of the epidermis and often portions of the
        dermis and even subcutaneous fat.[7]
       Fissure - A fissure is a crack in the skin that is usually narrow but deep.[3]
       Wheal - A wheal is a rounded or flat-topped, pale red papule or plaque that is characteristically evanescent,
        disappearing within 24 to 48 hours.[6]
       Telangiectasia - A telangiectasia represents an enlargement of superficial blood vessels to the point of being
        visible.[3]
       Burrow - A burrow appears as a slightly elevated, grayish, tortuous line in the skin, and is caused by burrowing
        organisms.[3][4]

Secondary lesions

       Scale - dry or greasy laminated masses of keratin[4] that represent thickened stratum corneum.[3]
       Crust - dried serum, pus, or blood usually mixed with epithelial and sometimes bacterial debris.[6]
       Lichenification - epidermal thickening characterized by visible and palpable thickening of the skin with
        accentuated skin markings.[1]
       Excoriation - a punctate or linear abrasion produced by mechanical means (often scratching), usually involving
        only the epidermis but not uncommonly reaching the papillary dermis.[4]
       Induration - dermal thickening causing the cutaneous surface to feel thicker and firmer.[3]
       Atrophy - refers to a loss of tissue, and can be epidermal, dermal, or subcutaneous.[4] With epidermal atrophy,
        the skin appears thin, translucent, and wrinkled.[3] Dermal or subcutaneous atrophy is represented by
        depression of the skin.[3]

The following terms may apply to the shape or arrangement of skin lesions: linear, annular, polycyclic; aciform;
serpiginous; grouped (herpetiform and zosteriform); agminate (collected together into clusters or masses); reticular
(netlike).

The following terms are helpful in describing the distribution of skin lesions: generalized; localized; bilateral; unilateral;
symmetrical; asymmetrical; sun-exposed; intertriginous.

10312 - Faire la démonstration de techniques simples et de procédures qui ont l’avantage de mettre en évidence
diverses affections cutanées.

Biopsie cutanée
    - Acte chirurgical
    - Zone biopsée est anesthésiée avec de la lidocaïne 1%
    - La lésion cutanée à biopsier est excisée au bistouri ou à l'emporte-pièce à l'aide d'un punch
            o Biopsie à l'emporte-pièce
                    Le punch est enfoncé dans la peau en exerçant un mouvement de rotation jusqu'à ce que le
                       punch pénètre dans le tissu sous-cutané.
                    Le prélèvement circulaire est soulevé avec une pince et le fond de la pièce est coupé à l'aide de
                       ciseaux
                    Les sites de biopsies peuvent ou non être suturés en fonction de la localisation et de la taille du
                       prélèvement
Préparation à la potasse (KOH)
   - Un examen des squames après préparation à la potasse est effectué lorsqu'une étiologie fongique est suspectée
   - La potasse dissout la kératine et permet une meilleure visualisation des éléments fongiques

Cytodiagnostic de Tzanck
    - Technique cytologique
    - Utilisée pour le diagnostic des infections à l'herpèsvirus
           o De cellules géantes multinucléées sont évocatrices d’infections à herpèsvirus
                     Seule la culture et les techniques d’immunofluorescence permettent d’identifier le type
                       spécifique de virus herpès

Vitopression
    - Détermine si une lésion cutanée s'efface à la pression
    - Pour distinguer les lésions hémorragiques des lésions liées à la vasodilatation
    - Techinique: Consiste à presser une lame de microscpe ou le verre d'une loupe sur une lésion spécifique et à
        noter le degré de blanchiment

Lumière de Wood
   - Émet des ultraviolets de 360nm (lumière noire)
   - Pour certaines dermatoses (e.g. Érythasma, Vitiligo, pytiriasis versicolor)
   - Selon la pathologie, une couleur caractéristique apparait

Tests épicutanés (patch-tests)
    - Pour documenter une réaction d'hypersensibilité à un antigène spécifique
    - Dans cette technique, une batterie d'allergènes suspectés est appliquée sur le haut du dos
    - Souvent d'une aide appréciable dans la prise en charge diagnostique et thérapeutique des patients atteints
        d'eczéma chronique

10313- Demonstrate the importance of proper lighting for skin examination.

The entire surface of the skin must be examined with proper lighting which is preferably natural light or similar artificial
light. Artificial light often distorts colors and masks jaundice.


10314 - Demonstrate the ability to perform examination of the mouth, diascopy, palpation, etc.

10315 - List the cause and general features of common bacterial, viral and fungal infections affecting the skin.

Bacterial


Epidermal

                  Impetigo Vulgaris                                         Bullous Impetigo
Definition and     Acute purulent infection which appears vesicular         Scattered, thin-walled bullae containing
Clinical             and progresses to golden yellow "honey-                    clear yellow or slightly turbid fluid with
Features             crusted" lesions surrounded by erythema                    NO surrounding erythema
                   Sites: face, arms, legs and buttocks                     Sites: trunk, intertriginous areas, face
                   Age:Preschool and young adults, living in                Age: neonates and older children, can be
                     crowded conditions, poor hygiene                           epidemic
Etiology                       GAS (Group A ß Hemolytic Strep)                           S. aureus group II elaborating
                               S. aureus                                                  exfoliating toxin
                               Both

Picture




Dermal

                      Erysipelas                                                   Cellulitis
Definition and         Fever, chills, headache, weakness (more serious)            Systemic: fever, leukocytosis,
Clinical               upper dermis                                                   lymphadenopathy (less common)
Features               may be confluent, erythematous, raised, warm                Lower dermis/subcutaneous fat
                          plaque                                                    Unilateral erythematous flat lesion, often
                       very painfull (once called St-Anthony's fire)                  with vesicles poorly demarcated, no
                       Sites: Face and legs                                           tuniform-raised
                                                                                    Tender
                                                                                    Sites: commonly legs


Etiology                   GAS                                                       GAS
                                                                                      S. aureus (large sized wounds)
                                                                                      H. influenzae (periorbital)
                                                                                      Pasteurella muftocida (dog/cat bite)

Picture




Hair Follicules
                  Superficial Folliculitis                            Furuncles                          Carbuncles
                                                                      (Boils)

Definition               Superficial infection of the hair            Red, hot, tender, nodules with      Deep-seated abcess
and Clinical              follicule                                     yellowish point involving            formed by multiple
Features          Pseudofolliculitis: Infection of the        subcuteanous tissue arising              coalescing furuncles
                   hair follicule due to friction,             from hair follicule                     Lesion drains
                   irritation, occlusion                      Forms over summit and                    through multiple
                  Dome-shaped pustule at the mouth            ruptures                                 points to the
                   of the hair follicule                      Sites: Face, neck, axillae, thigh,       surface
                  Pustule ruptures to form a crust            buttocks, perineum
                  Sites: scalp, shoulders, chest, upper
                   back, any hair-bearing area

Etiology          S. Aureus (Most common)                    S. Aureus                               S. Aureus
                  Pseudomonas (hot tubs)
                  Pityrosporum
Picture




Fungal

Dermathophyte

Definition
     infection of skin, hair and nails caused by dermatophytes (fungi that live within the epidermal keratin and do not
        penetrate deeper structures)
Etiology and Pathophysiology
     Trichophyton, Microsporum, Epidermophyton species (Pityrosporum is a superficial yeast)
     digestion of keratin by dermatophytes results in scaly skin, broken hairs, crumbling nails
Treatment
     Tinea corporis/cruris/pedis (interdigital type)
            o 1st line: topical
                     Clotrimazole or Terbinafine cream applied OD or bid, until 1 week after resolution of lesions
     Onychomycosis or Tinea capitis
            o 1st line: Oral therapy
                     Terbinafine (Lamisil)
                             Liver toxicity, cyp 2D6 inhib.)
                             6 wks fingers, 12 wks toes
                     Itraconazole (Sporanox)
                             CHF reported, cyp 3A4 inhib.)
                             7 days on, then 3 off (2 pulses for fingernails, 3 for pulses toes)
Tinea capitis         Fungeal infection of scalp, eyelashes and
                       eyebrows
                      Round, scaly patches of alopecia, possible w/
                       broken-off hairs
                      Akerion (may form)
                           o Boggy, elevated, purulent inflamed
                                nodule/ plaque
                      Affects children (mainly black) and
                       immunocompromised adultsˇ
                      Very contagious:
                           o Barber
                           o Hats
                           o Theatre seats
                           o Pets
                      Site: scalp, eyelashes and eyebrows

Tinea corporis        Puritic, scaly, round/oval plaque with active
(‘Ring worm’)          erythematous margin and central clearing
                      Site: trunk, limbs, face




Tinea Cruris          scaly patch/plaque with a well-defined,
(‘Jock itch’)          curved border and central clearing on medial
                       thigh
                      pruritic, erythematous, dry/macerated
                      Sites: medial thigh, does NOT involve
                       scrotum




Tinea Pedis           pruritic scaling of the web spaces and
(Athlete’s foot)       powdery scaling of soles
                      Acute infection: interdigital (esp. 4th web
                       space) red/white psoriasis scales, vesicles,
                       bullae, often with maceration
                      may present as flare-up of chronic tinea
                       pedis
                      frequently become secondarily infected by
                        bacteria
                       Chronic: non-pruritic, pink,scaling keratosis
                        on soles and sides of foot
                       Risk Factors: heat, humidity,
                        occlusivefootwear
                       Sites: Web spaces, soles, side of foot

TIinea Manuum          Acute: blisters at edge of red areas on hand
                       Chronic: Single dry scaly patch
                       Primary fungal infection of the hand is
                        actually quite RARE  Usually a/w tinea
                        pedis
                       Sites: Hands

TInea Unguium          Crumbling, distally dystrophic nails,
(Onchomychosis)         yellowish opaque with subungual
                        hyperkeratotic debris
                       Toenail infection usually preceded fingernails
                       T. Rubrum (90% of toenail infection)
                       Sites: Toenails, fingernails




10316 - List the causes and general features of rosacea, acne vulgaris, and perioral dermatitis.
ROSACEA
    Definition:
         o capillary vasodilation, papules, and pustules

       Epidemiology:
            o 30-50 years old
            o F>M

       Pathophysiology:
            o unknown

       signs and symptoms:
            o vascular: intermittent than persistent erythema/flushing, telangiectasias
            o acneiform: papules, pustules, cysts; no comedones; symmetrical distribution
                on forehead, cheeks, nose, chin
            o ocular: conjunctivitis, blepharitis, keratitis
            o rhinophyma: progressive enlargement of nose with sebaceous hyperplasia
            o differentiated from acne by its absence of comedones

       exacerbating factors:
            o heat, cold, wind, sun, stress, drinking hot liquids, alcohol, caffeine, spices (triggers of vasodilatation)
       clinical course:
             o prolonged course common, recurrences

ACNE VULGARIS:

        Definition and Clinical Features:
            o a common inflammatory pilosebaceous disease categorized with respect to severity of acne
                     Type I – comedonal, sparse, no scarring
                     Type II – comedonal, papular, moderate +/- little scarring
                     Type III – comedonal, papular, and pustular, with scarring
                     Type IV – nodulocystic acne, risks of severe scarring
            o predilection sites: face, neck, upper chest, back
            o epidemiology
                     common during teen years
                     severe disease affects males 10x more frequently than females
                     incidence decreases in adult life

        Pathogenesis
            o increased sebum production
            o sebum is comedogenic, an irritant, and is converted to free fatty acids (FFA) by microbial lipases made
               by anaerobic diphtheroid Propionibacterium acnes
            o free fatty acids + bacteria ––> inflammation + delayed hypersensitivity reaction––> hyperkeratinization
               of follicle lining with resultant plugging

        Exacerbating Factors
            o menstruation/hormonal factors
            o oral contraceptives (OCP): specifically those containing progestins with significant androgenic effects
               (norethindrone acetate, levo/norgestrel)

            o   topical acnegenic agents
                     workplace - heavy oils, grease, tars
                     topical drugs - steroids, tars, ointment vehicles
                     cosmetics - especially those containing cocoa butter, fatty acids, isopropyl myristate
            o   systemic meds: lithium, phenytoin, steroids, halogens (chloracne), androgens, iodides, bromides,
                danazole
            o   NB: foods are not a major aggravating factor

Differential Diagnosis
     rosacea
     folliculitis
     perioral dermatitis
     keratosis pilaris (arms, face)

10317 - List the indications of an intralesional corticosteroid injection.

The rationale for intralesional therapy is simple: to deliver a medication directly into a specific skin lesion to treat local
tissues with minimal systemic effects. The skin also serves as a reservoir, allowing medication deposited in the dermis to
be delivered over a period of time, resulting in prolonged therapy while avoiding or minimizing the adverse effects of
systemic therapy.

Indications for intralesional corticosteroid therapy are acute and chronic inflammatory processes, hyperplastic and
hypertrophic skin disorders, and conditions that typically have a favorable response to systemic and topical
corticosteroids. In addition to antiinflammatory properties, the atrophogenic side effect of corticosteroids also can be
used advantageously when treating hypertrophic types of lesions, including keloids, lichen simplex chronicus,
hypertrophic lupus, and psoriasis.

Intralesional injections are not advised when the possibility of infection is present, either as the etiology of the lesion or
as a secondary sequela. Intralesional corticosteroids do have some degree of systemic absorption and, although it is rare
to have systemic effects, large amounts of corticosteroids, frequent injections, and even small amounts of
corticosteroids in diabetic patients produce unwanted systemic effects.

10318 - Énumérer les caractéristiques du psoriasis et d’autres pathologies papulosquameuses.

Lichen Planus
    - Association with hepatitis C, may be triggered by severe emotionnal stress
    - Acute or chronic inflammation of mucous membranes or skin characterized by violaceous papules, especially on
        flexural surfaces
    - Sites: Wrists, Ankle, Mucous membrane (mouth, vulva, glans), Nails, Scalp, Scarring alopecia
    - Small, polygonal, flat-topped, shiny violet papules
            o Resolves into hyperpigmented macules
    - Spontaneously resolves in weeks or lasts for years
    - Koebner phenomenon: Develops in areas of trauma

Pityriasis Rosea
    - Suspected human herpes virus 7
    - Acute, self-limiting, erythematous eruption
    - Characterized by red, oval plaques/patches with central scales that do not extend to edge of lesion
    - Most start with a «Herald» patch which precedes other lesions by 1-2 weeks
    - Sites:
             o Trunk: Long axis of lesions follows parallel to ribs producing «Christmas tree» pattern on back
             o Proximal aspects of arms and legs
    - Clears spontaneously in 6-12 weeks

Psoriasis
    - Plaque psoriasis
          o Chronic and recurrent
          o Plaque bien circonscrite, érythémateuse avec des squames argentées
          o Sites : Cuir chevelu, Extensor surfaces of elbows and knees, Trunk (Région lombosacrée et ombilic), Nails
              (Doigts>orteils), Pressure areas
          o Koebner phenomenon: Develops in areas of trauma (où il y a des cicatrices)
          o Auspitz sign: Si on gratte, il y a saignement à cause de la proximité des vaisseaux sanguins
    - Guttate psoriasis
          o Discrete, scattered salmon-pink scaling papules
          o Éruptif
          o Prurit variable
          o Sites: Generalized (Sparing palms and soles)
          o Ressemble au pityriasis rosea ou à l'eczéma
          o Often antecedent streptococcal pharyngitis
          o Éruption disparait d'elle-même en 3-4 mois
          o 1/3 développeront le psoriasis vulgaris (plaques)
    - Erythrodermic psoriasis
          o Début graduel ou rapide
          o Generalized erythema with fine desquamative scale on surface
          o With arthralgia + severe pruritus
          o Malaise systémique
            o De novo ou à la suite d'un psoriasis en plaques qui détériore
            o Aggravating factors : Lithium, bêta-bloqueurs, NSAID, Antimalarials, phototoxic reaction, infection
            o Risques : d'hypothermie, d'hypoalbuminémie, edeme des jambes, défaillance cardiaque, sepsie
    -   Pstular psoriasis
            o Début rapide
            o Érythème douloureux et généralisé avec pustules stériles
            o Erythematous macules and papules which eveolve rapidly into pustules
            o Can be generalized or localized to palms/soles
            o Fièvre et malaise systémique
            o Souvent histoire de psoriasis
            o May occur with sudden withdrawal from steroid therapy
            o Admission souvent requise
    -   Psoriatic arthritis (Spondyloarthropathie seronégative)
            o Souvent suite à un psoriasis chronique
            o Catégories
                      Asymmetric oligoarthropathy
                      DIP joint involvement (#1)
                      Rheumatoid pattern - symmetric polyarthropathy
                      Psoriatic arthritis mutilans : More severe form
                      Predominant spondylitis or sacroliitis


10319- List the indications for a punch biopsy of the skin.

Punch biopsies are useful in the work-up of:
-cutaneous neoplasms
-pigmented lesions
-inflammatory lesions
-chronic skin disorders
-all bullous disorders

Routine biopsy of skin rashes is not recommended because the commonly reported nonspecific pathology result rarely
alters clinical management.

10320 - Identify the features of a benign skin lesion and differentiate it from a malignant lesion.

***Reference: Toronto Notes 2006***

Primary Morphological Lesions (BENIGN SKIN LESIONS):
       Pustule: a vesicle containing purulent exudate (white, yellow, green)
       Cyst: a nodule containing semisolid or fluid material
       Erosion: a disruption of the skin involving the epidermis alone
       Ulcer: a disruption of the skin that extends into the dermis or deeper
       Wheal: a special form of papule or plaque that is blanchable and transient, formed by edema in the dermis (e.g.
        urticaria)
       Scar: replacement fibrosis of dermis and subcutaneous tissue

MALIGNANT SKIN LESIONS:

       Basal Cell Carcinoma: malignant proliferation of basal cells of the epidermis
           o noduloulcerative (typical)
           o skin-coloured papule/nodule with rolled, translucent (“pearly”)
                telangiectatic border and depressed/eroded/ulcerated centre
           o pigmented (variant)
                     flecks of pigment in translucent lesion with surface telangiectasia
                     may mimic malignant melanoma
           o superficial (variant)
                     scaly plaque with fine telangiectasia at margin
           o sclerosing (variant)
                     flesh/yellowish-coloured, shiny papule/plaque with indistinct borders
           o sites: sun-exposed regions (mainly head and neck)
       Squamous Cell Carcinoma: malignant neoplasm of keratinocytes
           o indurated erythematous nodule/plaque with surface scale/crust, and eventual ulceration
           o more rapid enlargement than BCC
           o sites: face, ears, scalp, forearms, dorsum of hands
       Malignant Melanoma: malignant neoplasm of pigment forming cells (melanocytes and nevus cells)
           o malignant characteristics of a mole include ( ABCDE)
                     A – Asymmetry
                     B - Border (irregular)
                     C - Colour (varied)
                     D - Diameter (increasing or > 6 mm)
                     E - Enlargement, elevation
           o sites: skin, mucous membranes, eyes, CNS

10321 - Identify the features of the common malignant skin conditions including basal cell carcinoma (BCC), squamous
cell carcinoma (SCC) and melanoma.

Basal Cell Carcinoma (BCC)

Definition
    1. Malignant proliferation of basal cells of the epidermis (primarily tangential growth)

Differential Diagnosis
    • Intradermal melanocytic nevus
    • Sebaceous hyperplasia
    • SCC
    • Nodular malignant melanoma
Epidemiology
     Most common cancer worldwide --75% of all malignant skin tumours >40 years
     Increased prevalence in the elderly
     M>F
     usually due to UV light, therefore >80% on face (e.g. Nose, forehead, behind ears for men)
Risk Factors
     Chronic cumulative sun exposure
     May also be caused by:
            o Genetic Predispostion (Grolin syndrome)
            o Scar formation
            o Radiation
            o Trauma
            o Arsenic exposure

Signs and Symptoms

Subtype         Morphology                                          Picture



Papulonodulo-       Skin-coloured papule/nodule with:
ulcerative               o Rolled, translucent ("pearly")
(typical)                    telangiectatic border and
                         o Depressed/eroded/ulcerated centre




Pigmented           flecks of pigment in translucent lesion with
variant              surface telangiectasia
                    may mimic malignant melanoma




Superficial
variant         • Scaly plaque with fine telangiectasia at margin
Sclerosing         Flesh/yellowish-coloured, shiny deep
variant             sclerosing (‘scar-like’)papule/plaque with
                    indistinct borders




Squamous Cell Carcinoma (SCC)

Definition
    2. Malignant neoplasm of keratinocytes (primarily vertical growth)
Differential Diagnosis
    • Bowen's disease (SCC in situ - evolves to SCC in 10-20% of skin lesions, >20% in mucosal lesions)
    • Nummular eczema
    • Psoriasis
    • BCC
    • Melanoma
Epidemiology
     Primarily on sun-exposed skin in the elderly
     M>F
Risk Factors
     Chronic sun exposure
     Predisposing factors include:
             o Atrophic skin lesion
             o Radiation
                     Radiation UV radiation
                     ionizing radiation therapy/exposure
                     PUVA
             o Immunosuppression
             o Chemical carcinogens such as arsenic, tar and nitrogen mustards

Signs and Symptoms
     Indurated erythematous nodule/plaque with surface scale/crust, and eventual ulceration
     more rapid enlargement than BCC
     Sites: face, ears, scalp, forearms, dorsum of hands
Treatment
     Surgjcal excision with primary closure, skin flaps or grafting
     Lifelong follow-up (more aggressive treatment than BCC)

Prognosis
    Prognostic factors include: immediate treatment, negative margjns, and small lesions
    SCCs that arise from AK metastasize less frequently (~1%) than other SCCs (e.g. arising in old burns) (2-5% of
       cases)
    Overall control is 75% over 5 years, 5-10% metastasize

Malignant Melanoma

Definition
 malignant neoplasm of pigment forming cells (melanocytes and nevus cells)
 several different subtypes based on pathology (see below)

Epidemiology
     incidence 1:100
     Risk factors (SP2F is a SIN):
          o Sun exposure
          o Pigmentation traits (fair skin, blue/green eyes, red hair, freckles)
          o Personal history
          o Familial dysplastic nevus syndrome (100%)
                    100 % lifetime risk with 2 blood relatives with melanoma (0.8% risk for general population)
          o Skin reaction to sunlight (increased incidence of sunburn)
          o Immunossupression (e.g. renal transplant)
          o Nevi ( dysplatic nevi, increased number of benign melanocytic moles, large congenital nevi, large/giant
               congenital hairy nevi )
     most common sites: back (M), calves (F)
     worse prognosis if: male, on scalp, hands, feet, late lesion, no pre-existing nevus present

Signs and Symptoms
o malignant characteristics of a mole: see mnemonic"ABCDE"
         Asymmetry
         Border (irregularl)
         Colour (varied, multicolor)
         Diameter (increasing or >6 mm)
         Enlargement, elevation
        Sensitivity 92%, Specificity 100%
o Sites:
            o Skin
            o Mucous membranes
            o   Eyes
            o   CNS

Prognostic Indicators
    sentinel node status (MOST IMPORTANT for recurrence &survival)
    number of nodes more important than size of
    ulceration or microulceration upstages risk


Lentigo maligna (premalignant lesion)
    malignant melanoma in situ (normal and malignant melanocytes confined to the epidermis)
    2-6 cm, tan/brown/black uniformly flat macule or patch with irregular borders
    lesion grows radially and produces complex colours
    sites: face, sun exposed areas
    1/3 evolve into lentigo maligna melanoma

Lentigo maligna melanoma (15% of all melanomas)
    malignant melanocytes invading into the dermis
    flat, brown, stain-like lesion that gradually enlarges with loss of skin surface markings
    with time, colour changes from uniform brown to dark brown with black and blue hues
    found on all skin surfaces, especially those chronically exposed to sun
    not associated with preexisting acquired nevi

Superficial spreading melanoma (60-70% of all melanomas)
    atypical melanocytes initially spread laterally in the epidermis then invade the dermis
    irregular, indurated, enlarging plaques with red/white/blue discolouration, focal papules and nodules
    ulcerate and bleed with growth


Nodular melanoma (30% of all melanomas)
    atypical melanocytes that initially grow vertically with little lateral spread
    uniformly ulcerated, blue-black, and sharply delineated plaque or nodule
    rapidly fatal

Acrolentiginous melanoma (5% of all melanomas)
    ill-defined dark brown, blue-black macule
    palmar, plantar, subungual skin
    melanomas on mucous membranes have poor prognosis


10322 - Discuss the pathology, immunopathology, clinical features and treatment of erythema multiforme, bullous
pemphigoid, pemphigus, and dermatitis herpetiformis.
                Erythema multiforme:


Lesion                Macules/papules with central vesicles
                      Classic bull’s-ey pattern of concentric light and dark
                       rings (target lesion)
                      Bilateral and symmetric
                        Erythema multiform minor: no mucosal involvement,
                         bullae, or systemic symptoms
                        Erythema multiform major: mucosal involvement,
                         bullae, systemic symptoms, usually drug induced
                        Nikolsky sign
Site                    Mucous membrane involvement (oral, genital,
                         conjunctival)
                        Extrimities with face more than trunk
                        Involvement of palms and soles
Other                   Corneal ulcers, keratitis, anterior uveitis, stomatitis,
organs/com               vulvitis, balanitis
plications              Lesion in trachea, pharynx, larynx
Constitution            Fever, weakness, malaise
al symptoms
Etiology                Drug : sulfonamides, NSAIDs, anticonvulsants,
                         penicillin, allopurinol
                        Infection: herpes, mycoplasma
                        Idiopatic: more then 50%
Pathology/p             Perivascular PMN infiltrate in the dermis and
athophysiol              epidermis with edema in upper dermis.
ogy
Ddx                     EM minor: urticaria, viral exanthems
                        EM major: Staphylococcal Scalded Skin Syndrome,
                         pemphigus bulgaris, bullous pemhigoid
Course and              Lesion last 2 wks.
prognosis
Tx                      Prevention: drug avoidance
                        Symptomatic treatment
                        Corticosteroids in severely ill



Bullous pemphigoid:

           definition
               o chronic autoimmune bullous eruption characterized by pruritic, tense, subepidermal bullae on an
               o erythematous or normal skin base
           epidemiology
            o 60-80 years old
       etiology
            o autoimmune
            o associated with malignancy in some
       pathophysiology
            o IgG produced against dermal-epidermal basement membrane
       signs and symptoms
            o sites: flexor aspect of forearms, axillae, medial thighs, groin, abdomen, mouth (33%)
       investigations
            o direct immunofluorescence shows deposition of IgG and C3 at basement membrane
            o anti-basement membrane antibody (IgG)
       clinical course
            o generalized bullous eruption
            o healing without scars if no infection
       management
            o prednisone 50-100 mg/day (to clear) +/– steroid sparing agents such as azathioprine
            o tetracycline 500-1 000 mg/day +/– nicotinamide

Pemphigus:

       definition
            o autoimmune blistering disease characterized by flaccid, non-pruritic bullae/vesicles on an erythematous
                 or normal skin base
       epidemiology
            o 40-60 years old, patients are often Jewish or Mediterranean
       etiology
            o autoimmune
            o associated with thymoma, myasthenia gravis, malignancy, D-penicillamine
       pathophysiology
            o IgG produced against epidermal desmoglein 3 leads to acantholysis (epidermal cells separated from
                 each other) which produces intraepidermal bullae
       signs and symptoms
            o may present with erosions and secondary bacterial infection
            o sites: mouth (90%), scalp, face, chest, axillae, groin, umbilicus
            o Nikolsky’s sign: pressure on skin induces lesion
            o Asboe-Hanson sign: bulla extends with finger pressure
       investigations
            o immunofluorescence shows IgG and C3 deposited in epidermal intercellular spaces
       clinical course
            o initially mouth lesions, followed by skin lesions
            o first localized (6-12 months) then generalized
            o lesions heal with hyperpigmentation but no scar
            o may be fatal unless treated with immunosuppressive agents
       management
            o prednisone 2.0-3.0 mg/kg until no new blisters, then 1.0-1.5 mg/kg until clear, then taper
            o steroid sparing agents - azathioprine, methotrexate, gold, cyclophosphamide, cyclosporin, IV
                 immunoglobulin (IVIG)
            o plasmapheresis for acutely high antibody levels

Dermatitis herpetiformis:

       definition
             o intensely pruritic grouped papules/vesicles/urticarial wheals on an erythematous base
        etiology
             o 90% have HLA B8, DR3, DQWZ
             o 90% associated with gluten sensitive enteropathy (80% are asymptomatic), 30% have thyroid disease,
                  and some have intestinal lymphoma
             o iron or folate deficiency
        epidemiology
             o 20-60 years old, M:F = 2:1
        signs and symptoms
             o sites: extensor surfaces of elbows/knees, sacrum, buttocks, scalp
             o lesions grouped in bilateral symmetry
             o pruritus, burning, stinging
        investigations
             o immunofluorescence: granular IgA and complement deposition in dermis
        clinical course
             o lesions last days - weeks
        management
             o dapsone 50-200 mg/day for pruritus, multiple side effects include hemolytic anemia, peripheral
                  neuropathy, toxic hepatitis, aplastic anemia
             o gluten free diet

10323 Describe the most common types of drug eruptions and the common drugs that cause them.

**If you want to breeze through this, just read what's in bold: the type of drug eruption and the drugs that cause them. I
added the rest to explain what these terms actually mean.

Most common types:

- Drug induced exanthems: 75% of all drug rashes, The rashes are referred to as exanthems, morbilliform, and macular
and papular eruptions.

Drugs: the most commonly prescribed medications (eg, antibiotics, sulfa) are implicated most often.

- Urticaria/angioedema:

        Urticaria, or hives, is characterized by an intensely pruritic, circumscribed, raised, and erythematous eruption
        with central pallor, mediated by the cutaneous mast cell in the superficial dermis.

        Angioedema is swelling of the deeper dermis and subcutaneous tissues, which may coexist with urticaria in as
        many as 50 percent of cases. Angioedema may be disfiguring if it involves the face and lips, or life-threatening if
        airway obstruction occurs from laryngeal edema or tongue swelling.

Drugs: Antibiotics (especially penicillins, cephalosporins, and sulfonamides) are common causes of IgE-mediated drug
allergy. Other drugs may cause urticaria due to mast cell degranulation by a non-IgE mediated mechanism. The most
frequently implicated are the opiate analgesics morphine and codeine. The concomitant use of opiates and vancomycin
may increase the frequency of reactions to the latter. The intense flushing of "Red man syndrome" seen after rapid
vancomycin infusion also is due to direct mast cell activation and may have accompanying urticaria.

- Anaphylaxis — The most severe form of immediate type I hypersensitivity is anaphylaxis, which is characterized by
symptoms affecting multiple organ systems, including but not limited to pruritus, urticaria, angioedema, laryngeal
edema, wheezing, nausea, vomiting, tachycardia, sense of impending doom, and occasionally shock
- Hypersensitivity vasculitis: AKA serum sickness. The major clinical findings, in addition to the skin lesions, palpable
purpura and/or petechiae, include fever, urticaria, arthralgias, lymphadenopathy, low serum complement levels, and an
elevated erythrocyte sedimentation rate

Drugs: caused by drugs that probably act as haptens to stimulate an immune response. The penicillins, cephalosporins,
sulfonamides (including most loop and thiazide-type diuretics), phenytoin, and allopurinol have been most often
implicated

- Exfoliative dermatitis/erythroderma — Erythroderma is a cutaneous reactional state defined as chronic erythema and
scale involving greater than 50 percent of the body surface area

Drugs: implicated drugs include penicillins, barbiturates, gold salts, arsenic, and mercury

- Stevens-Johnson syndrome and toxic epidermal necrolysis — Children with fever, stomatitis, severe ocular
involvement, and a disseminated cutaneous eruption of discrete dark red macules were described in 1922 by Stevens
and Johnson (Stevens-Johnson syndrome) [12]. Adults with rapid, extensive, epidermal necrolysis and marked erythema
resembling scalding were described by Lyell in 1956 (Toxic epidermal necrolysis)

- Erythema multiforme — Erythema multiforme (EM) major is sometimes used as a synonym for SJS but is probably a
different condition. It is an acute eruption characterized by distinctive target skin lesions and diagnostic histology that is
often caused by infections (typically Herpes virus or Mycoplasma) and has a benign clinical course. Lesions tend to affect
the distal extremities, including the palms and soles.

- Hypersensitivity syndrome — The hypersensitivity syndrome, also described as drug reaction with eosinophilia and
systemic symptoms (DRESS), is characterized by a severe idiosyncratic reaction including rash and fever, often with
associated hepatitis, arthralgias, lymphadenopathy, or hematologic abnormalities

Drugs: The aromatic antiepileptic agents (phenytoin, carbamazepine and phenobarbital) and the sulfonamides are the
most frequently implicated causes of this disorder

- Fixed drug eruption — A fixed drug eruption is a distinctive reaction characterized acutely by erythematous and
edematous plaques with a grayish center or frank bullae, and chronically by a dark postinflammatory pigmentation
(picture 9A-C). Favored sites include the mouth (lips and tongue), genitalia, face, and acral areas [2]. The defining
features of this eruption include the postinflammatory hyperpigmentation and the recurrence of lesions at exactly the
same site with drug reexposure [2].

Drugs: The drugs commonly involved include phenolphthalein (laxatives), tetracyclines, barbiturates, sulfonamides,
NSAIDs, and salicylates [2,23].

- Phototoxic eruptions — Phototoxic eruptions are by far the most common drug-induced photoeruption. They are
caused by absorption of ultraviolet light by the causative drug, which releases energy and damages cells. Ultraviolet A
light (UVA) is the most common wavelength implicated; ultraviolet B light (UVB) and visible light can elicit reactions with
some drugs.

The eruption is typically an exaggerated sunburn, often with blisters.

Drugs: NSAIDs, quinolones, tetracyclines, amiodarone, and the phenothiazines

- Photoallergic eruptions — Photoallergy is a lymphocyte-mediated reaction caused by exposure to UVA. It is postulated
that the absorbed radiation converts the drug into an immunologically active compound that is then presented to
lymphocytes by Langerhans cells, causing a spongiotic dermatitis (eczema). The eruption is characterized by widespread
eczema in the photodistribution: face; upper chest; and back of hands (picture 11).

Drugs: Most photoallergic reactions are caused by topical agents including biocides added to soaps (halogenated
phenolic compounds) and fragrances such as musk ambrette and 6-methyl coumarin [24]. Systemic photoallergens such
as the phenothiazines, chlorpromazine, sulfa products, and NSAIDs can produce photoallergic reactions, although most
of their photosensitive reactions are phototoxic [24].

10324 - Démontrer les habiletés requises pour faire l’anamnèse appropriée d’un patient ayant un problème
ophtalmique.

    -    In addition to general history taking, aspects of the ophtalmological history include
             o Ocular symptoms
                       Loss of visions: sudden vs gradual, transient vs prolonged, central vs peripheral field loss
                       Pain
                       Redness
                       Double vision (diplopia)
                       Tearing
                       Dryness (sicca)
                       Foreign body sensation
                       Itchy (pruritis)
                       Discharge
                       Eyelid crusting
                       Eyelid swelling
                       Drooping eyelid (ptosis)
                       Floaters
                       Flashes (photopsia)
                       Haloes
                       Sensitivity to light (photophobia)
                       Headache
             o Past ocular history (e.g. corrective lens use, prior trauma, surgery, infections, eye diseases)
             o Past medical history (for ocular effects of systemic diseases)
             o Family history of eye disease
             o Ocular and systemic medications


10325- Demonstrate the approach to a systematic eye exam.

Vision

-Testing Central Vision: central visual acuity is measured with a display of different-sized targets shown at a standard
distance from the eye. For example, the familiar "Snellen chart" is composed of a series of progressively smaller rows of
random letters used to test distance vision. By convention, vision can be measured either at a distance of 20 feet (6
meters) or near, 14 inches away. For diagnostic purposes, distance acuity is the standard for comparison and is always
tested separately for each eye. Acuity is scored as a set of two numbers (eg, "20/40"). The first number represents the
testing distance in feet between the chart and the patient, and the second number represents the smallest row of
letters that the patient's eye can read from the testing distance. Normal vision is 20/20; 20/60 vision indicates that the
patient's eye can only read from 20 feet letters large enough for a normal eye to read from 60 feet. Uncorrected visual
acuity is measured without glasses or contact lenses. Corrected acuity means that these aids were worn. Since poor
uncorrected distance acuity may simply be due to refractive error, corrected visual acuity is a more relevant assessment
of ocular health.
-Pinhole Test: if the patient needs glasses or if his or her glasses are unavailable, the corrected acuity can be estimated
by testing vision through a "pinhole."

-Testing Peripheral Vision: since the visual fields of the two eyes overlap, each eye must be tested separately. The
patient is seated facing the examiner with one eye covered while the examiner closes the opposite eye (eg, the patient's
left eye is covered and the examiner's right eye is closed so that the patient's right eye looks into the examiner's left
eye). Presentation of targets at a distance halfway between the patient and the examiner allows direct comparison of
the field of vision of each eye of the patient and the examiner. Since the patient and examiner are staring eye to eye,
any loss of fixation by the patient will be noticed.

Pupils

-Basic Examination: the pupils should be symmetric, and each one should be examined for size, shape (circular or
irregular), and reactivity to both light and accommodation. Swinging Penlight

-Test for Marcus Gunn Pupil: as a light is swung back and forth in front of the two pupils, one can compare the reactions
to stimulation of each eye, which should be equal.

Ocular Motility

-Testing Alignment: a simple test of binocular alignment is performed by having the patient look toward a penlight held
several feet away. A pinpoint light reflection, or "reflex," should appear on each cornea and should be centered over
each pupil if the two eyes are straight in their alignment..

-The cover test: a more accurate method of verifying normal ocular alignment. The test requires good vision in both
eyes. The patient is asked to gaze at a distant target with both eyes open. If both eyes are fixating together on the
target, covering one eye should not affect the position or continued fixation of the other eye.

-Testing Extraocular Movements: the patient is asked to follow a target with both eyes as it is moved in each of the four
cardinal directions of gaze. The examiner notes the speed, smoothness, range, and symmetry of movements and
observes for unsteadiness of fixation (eg, nystagmus).

External examination

A general external examination of the ocular adnexa (eyelids and periocular area) is performed. Skin lesions, growths,
and inflammatory signs such as swelling, erythema, warmth, and tenderness are evaluated by gross inspection and
palpation.

The positions of the eyelids are checked for abnormalities, such as ptosis or lid retraction. Asymmetry can be quantified
by measuring the central width (in millimeters) of the "palpebral fissure"—the space between the upper and lower lid
margins. Abnormal motor function of the lids, such as impairment of upper lid elevation or forceful lid closure, may be
due to either neurologic or primary muscular abnormalities. Palpation of the bony orbital rim and periocular soft tissue
should always be done in instances of suspected orbital trauma, infection, or neoplasm.

Slitlamp examination

The slitlamp is a table-mounted binocular microscope with a special adjustable illumination source attached. A linear slit
beam of incandescent light is projected onto the globe, illuminating an optical cross section of the eye. Since the slitlamp
is a binocular microscope, the view is "stereoscopic," or three-dimensional. Using the slitlamp alone, the anterior half of
the globe—the "anterior segment"—can be visualized. Details of the lid margins and lashes, the palpebral and bulbar
conjunctival surfaces, the tear film and cornea, the iris, and the aqueous can be studied. Through a dilated pupil, the
crystalline lens and the anterior vitreous can be examined as well.

Lid eversion

Lid eversion to examine the undersurface of the upper lid can be performed either at the slitlamp or without the aid of
that instrument. It should always be done if the presence of a foreign body is suspected. Following topical anesthesia,
the patient is positioned at the slitlamp and instructed to look down. The examiner gently grasps the upper lashes with
the thumb and index finger of one hand while using the other hand to position an applicator handle just above the
superior edge of the tarsus. The lid is everted by applying slight downward pressure with the applicator as the lash
margin is simultaneously lifted.

Fluorescein staining

Fluorescein is a specialized dye that stains the cornea and highlights any irregularities of its epithelial surface. Sterile
paper strips containing fluorescein are wetted with sterile saline or local anesthetic and touched against the inner
surface of the lower lid, instilling the yellowish dye into the tear film. The illuminating light of the slitlamp is made blue
with a filter, causing the dye to fluoresce. A uniform film of dye should cover the normal cornea. If the corneal surface is
abnormal, excessive amounts of dye will absorb into or collect within the affected area.

Tonometry

Tonometry is the method of measuring intraocular pressure using calibrated instruments. The normal range is 10 to 21
mm Hg.

In applanation tonometry, intraocular pressure is determined by the force required to flatten the cornea by a standard
amount. The force required increases with intraocular pressures.

The Schiotz tonometer, now rarely used, measures the amount of corneal indentation produced by preset weights. Less
corneal indentation is produced as intraocular pressure rises. Since both methods employ devices that touch the
patient's cornea, they require topical anesthetic and disinfection of the instrument tip prior to use.

10326 - Discuss the principle of pinhole vision.




Each perforation (pinhole) allows only a very narrow beam of light to enter the eye which reduces the size of the circle
of confusion on the retina and increases depth of field. Because light passes only through the center of the eye's lens,
defects in the shape of the lens (errors of refraction) have no effect while the occluder is used. In this way the
ophthalmologist can estimate the maximum improvement in a patient's vision that can be attained by lenses to correct
errors of refraction.

10327- Demonstrate the ability to use direct ophthalmoscopy.
10328 - Demonstrate the ability to use a slit lamp.

10329 - Describe the different strabismus conditions.

Strabismus is the term used to describe an anomaly of ocular alignment. Strabismus can occur in one or both eyes, and
in any direction. The terms used to describe strabismus depend upon the direction of deviation, the conditions under
which it is present, and whether it changes with the position of gaze.

- Nasal deviation (relative to the fixating eye) is described with the prefix "eso," and temporal deviation with the prefix
"exo." As a general rule, the prefix "hyper" is applied to the eye that is more superior in vertical deviations, regardless of
which eye is fixating. However, the prefix "hypo" is sometimes used to denote an eye that is depressed relative to the
fixing eye.

- A "latent" strabismus is present only when fixation is interrupted and is known as a "phoria" (eg, esophoria, exophoria).
In children with this condition, ocular alignment is maintained by fusion as long as fixation is uninterrupted. Strabismus
that is present without interruption of the visual axis is "manifest" and described as a "tropia."

- Manifest strabismus can be intermittent, occurring only when fusional capabilities are exceeded (eg, when the child is
tired) or constant [1].

- Manifest strabismus can be monocular, when deviation always involves the same eye, or alternating, when either eye
may deviate.

- Deviation that is the same in all positions of gaze is described as "comitant." Deviation that changes depending upon
the position of gaze is "incomitant" and usually is present with paralytic or restrictive strabismus.

- Unsteady ocular alignment is often present in normal newborns during the first few months of life [2] and can be
described as "ocular instability of infancy."

10330 - Discuter des indications du test de l’écran en cas de strabisme et de la façon de l’effectuer.

Test de l'écran simple
    - Chaque oeil est couvert séparément
    - Observation de l'oeil qui n'est pas masqué pour détecter le mouvement
    - Pour détecter les tropies seulement (Déviation oculaire manifeste ou intermittente)

Test de l'écran alterné
    - Cache-oeil placé alternativement sur un oeil puis sur l'autre
    - Observation d'un mouvement de refusion quand le cache-oeil est enlevé complètement
    - Pour détecter les phories

Test de l'écran et prisme
    - Par un ophtalmologiste
    - Prisme utilisé pour neutraliser la déviation oculaire et la mesurer

10331- Discuss the eight steps for assessing a red eye and differentiate between what is serious and what is not.
Assess: Visual acuity
                Extraocular movements
                Pupil reactivity
                Pupil shape
                Tests for direct and consensual photophobia
                Slit lamp examination of the cornea for edema, defects, or opacification with and without fluorescein
                Anterior chamber evaluation for depth cells and flare
                Intraocular pressure (IOP) measurements
                Eyelid inspection with eversion

Serious symptoms:
Sudden, severe pain and vomiting (suggestive of acute angle closure glaucoma)
Zoster skin rash
Decreased visual acuity
Corneal crater (suggestive of ulcer related to bacterial keratitis)
Branching, dendritic corneal lesion
Ocular pressure > 40 (suggestive of acute angle closure glaucoma)
Failure to blanch with phenylephrine eye drop

10332 - Differentiate between major and minor eye injuries and know when to refer.

BLUNT TRAUMA
    E.g. fist, squash ball
    History: injury, ocular history, drug allergy, tetanus status
    Exam: VA first, pupil size and reaction, EOM (diplopia), external and slit lamp exam, ophthalmoscopy
    If VA normal or slightly reduced, globe less likely to be perforated
    If VA reduced, may be perforated globe, corneal abrasion, lens dislocation, retinal tear
    Bone fractures
           o Blow out fracture: restricted upgaze, diplopia
           o Ethmoid fracture: subcutaneous emphysema of lid
    Lids (swelling, laceration, emphysema)
    Conjunctiva (subconjunctival hemorrhage)
    Cornea (abrasions - detect with fluorescein and cobalt blue)
    Anterior chamber (assess depth, hyphema, hypopyon)
    Iris (prolapse, iritis)
    Lens (cataract, dislocation)
    Refer if you observe any of these signs of ocular trauma: decreased VA, shallow anterior chamber, hyphema,
       abnormal pupil, ocular misalignment or retinal damage

PENETRATING TRAUMA
    Include ruptured globe +/– prolapsed iris, intraocular foreign body
    Be suspicious if history of "metal striking metal"
    Initial management: refer immediately
          o ABCs
          o Don't press on eyeball!
          o Check vision, diplopia
          o Apply rigid eye shield to minimize further trauma
          o Keep head elevated 30-45 degrees to keep IOP down

CHEMICAL BURNS
      Alkali burns have a worse prognosis vs. acid burns because acids coagulate tissue and inhibit further corneal
       penetration
      Poor prognosis if cornea opaque, likely irreversible stromal damage
      Even with a clear cornea initially, alkali burns can progress for weeks (thus, very guarded prognosis)

OCCULAR EMERGENCIES
These require urgent consultation to an ophthalmologist for management
    Trauma, especially intraocular foreign bodies, lacerations
    Corneal ulcer
    Gonococcal conjunctivitis
    Orbital cellulitis
    Chemical burns
    Acute iritis
    Acute angle closure glaucoma
    Central retinal artery occlusion (CRAO)
    Retinal detachment
    Endophthalmitis
    Giant cell arteritis

10333 -Describe the common types of uveitis: anterior and posterior and their different etiologies.

General
    uveal tract = iris, ciliary body, and choroid
    vascularized, pigmented middle layer of the eye, between the sclera and the retina


              Anterior Uveitis/Iritis                                     Posterior Uveitis
Definition     inflammation of iris, usually accompanied by cyclitis     o Inflammation of choroid
                 (inflammation of ciliary body)
               when both = iridocyclitis
               usually unilateral

Etiology         Idiopathic (usually)                                       Bacterial:
                 Connective diseases:                                            o Syphilis
                      o HLA-B27: Reiter’s Syndrome, Ankylosing                    o TB
                          Spondylitis (AS), IBD                              Viral:
                      o Non-HLA-B27: JRA                                          o HSV
                 Infectious:                                                     o CMV
                      o Syphillis                                                 o HIV
                      o Lyme                                                 Fungal:
                      o Toxoplasmosis                                             o Histoplasmosis
                      o TB                                                        o Candidiasis
                      o HSV/Zoster                                           Parasitic:
                 Other:                                                          o Toxoplasmosis (Most common
                      o Sacroidosis                                                    cause)
                      o Trauma                                                    o Toxocara
                      o Large Abraison                                       Autoimmune:
                      o Post-ocular surgery                                       o Bechet's disease (triad of
                                                                                       aphthous ulcers, genital ulcers,
                                                                                       and posteriorˇ uveitis)ˇ
                                                                             Malignancies (masquerade syndrome):
                                                                                  o Metastatic lesions
                                                                                  o   Malignant melanoma

Clinical         Decreased visual acuity                                    Decreased visual acuity
Features         Photophobia (reactive spasm from inflamed muscle)          Painless (choroid - no sensory
                 Ocular pain                                                 innervation)
                 Tenderness of globe                                        No conjunctival/scleral injection
                 Brow ache (ciliary muscle spasm)                            (frequently)
                 Tearing
                 Ciliary flush (perilimbal conjunctival injection)
                 Miosis (spasm of sphincter muscle)
Slit-Lamp        AC "cells"                                                 Floaters (debris and inflammatory cells)
                       o WBC in AC due to anterior segment inflam.           Vitreous cells and opacities
                 "Flare"                                                    Hypopyon formation
                       o Protein precipitates in AC sec. to inflam)
                 Hypopyon
                       o Neutrophilic exudates inferiorly in AC
                            chamber
                 Keratitic precipitates (Occasionally )
                       o clumps of cells on corneal endothelium)
                 Note: Iritis typically reduces IOP b/c of decreased
                  aqueous production in light of ciliary body
                  inflammation. However, severe iritis, or iritis from
                  HSV and zoster may cause an inflammatory glaucoma

Treatment        Mydriatics:                                                steroids: retrobulbar or systemic if
                      o Prevent formation of posterior synechiae              indicated (e.g. threat of vision loss)
                      o Decrease pain from ciliary spasm
                 Steroids: topical, subconjunctival or systemic
                 systemic analgesia
                 medical workup may be indicated to determine
                  etiology


10334- Discuss the different glaucomas (congenital, acute angle, angle closure, and secondary) in terms of their
etiologies, manifestations, treatment and prognosis.

Glaucoma (General)

Definition:
 progressive optic neuropathy involving characteristic structural changes to optic nerve head with associated visual
    field changes
 commonly associated with high intraocular pressure (lOP) although not required for diagnosis

Background
 aqueous is produced by the ciliary body and flows from the posterior chamber to the anterior chamber through the
   pupil, and drains into the episcleral veins via the trabecular meshwork and the canal of Schlemm
 an isolated increase in IOP is termed ocular hypertension (or glaucoma suspect) and these patients should be
   followed for increased risk of developing glaucoma:
        o ~10% if IOP 20-30 mrnHg
        o ~ 40% if IOP 30-40 mmHg
        o Most if IOP >40 mm Hg
 average lOP is 15 ± 3 mm Hg (diurnal variation, higher in a.m.)
   pressures >21 mmHg more likely to be associated with glaucoma, however, up to 50% of patients with glaucoma do
    not have lOP >21mmHg
   normal CD (cup:disc) ratio <0.4
   Be suspicious of glaucoma if:
        o C:D ratio >0.6
        o CD ratio difference between eyes >0.2 or cup approaches disc margin
   Sequence of events:
        o Gradual pressure rise
        o Increased C:D ratio
        o Visual field loss
        o Central loss
   Screening tests should include:
        o medical and family history
        o visual acuity testing
        o slit lamp exam to assess anterior chamber depthˇ
        o ophthalmoscopy to assess the disc featuresˇ
        o tonometry by applaI1ation or indentation to measure the lOP
        o visual field testing

               POAG                                               PACG
General         Most common form, >95% of all glaucoma            5% of all glaucoma cases
                  cases                                            Peripheral iris bows forward in an already
                Due to obstruction of aqueous drainage within       susceptible eye with a shallow anterior chamber
                  the trabecular meshwork and its drainage into      obstructing aqueous access to the trabecular
                  the Canal of Schlemm                               meshwork
                Insidious and asymptomatic, so screening is       sudden shifting forward of the lens-iris
                  critical for early detection                       diaphragm = pupillary block, results in inability
                                                                     of the aqueous to flow from the posterior
                                                                     chamber to the anterior chamber and a sudden
                                                                     rise in lOP

Risk factors   Major Risk Factors                                    family history
                Familial (2-3x increased risk); polygenic           Asians and Inuits
                Black race                                          age >70
                age: prevalence in 40 y.o. is 1-2% and in 80        Female
                  y.o. 10%                                           Hyperopia: small eye, big lens -large lens crowds
                Elevated IOP (>21 mm Hg)                             the angle
                                                                     Mature cataracts
               Minor Risk Factors                                    Shallow anterior chamber
                Myopia                                              pupil dilation (topical and systemic
                anemia/hemodynamic crisis (ask about blood           anticholinergics, stress, darkness)
                  transfusions in past)
                HTN
                Diabetes
                Hyperthyroidism (Graves' disease)
                Chronic topical ophthalmic steroid use on eyes
                  in steroid responders
                       o Yearly eye exams recommended if >4
                           weeks steroid use
                Previous ocular trauma

Clinical          Onset: Gradual (chronice)                          •   Onset: acute
Features       Sx:                                                 •   Sx:
                        o     Asymptomatic initially (painless                 Symptomatic (painful red eye = RED
                              eye w/o redness)                                  FLAG)
                         o Bilateral, but usually asymmetric                 unilateral, but other eye
               IOP: Moderately elevated                                        predisposed
               Cornea: Normal                                      •   IOP: Extermely elevated (> 40mmHg)
               Pupil: Normal                                       •   Cornea: Hazy
               GI: No N/V                                          •   Pupil: Mid-dilated, unreactive to light
               Light: No halos around light                        •   GI: Presence of N/V, abdominal pain
               AC: Normal                                          •   Light: Halos around light
               Earliest signs are optic disc changes (safe to      •   AC: shallow anterior chamber ± cells in
                dilate pupil)                                           anterior chamber
                o Increased C:D (>0.6)
                o Significant CD asymmetry between eyes
                     (>0.2 difference)
                o Thinning, notching of the neuroretinal rim
                o flame shaped disc hemorrhage
                         0
                o 360 of peripapillary atrophy
                o Nerve fibre layer defect
                o large vessels become nasally displacedˇ
               Visual field loss
                o Slow, progressive, irreversible loss of
                     peripheral vision
                o Paracentral defects, arcuate scotoma and
                     nasal step are characteristic
                o Central vision loss (late) if untreated



Treatment   Principles: ↓ IOP by:                                Refer to ophthalmologist
                • ↑drainage and/or                                                   • laser iridotomy
                • ↓ the production of aqueous                                        • aqueous suppressants and
                                                                                         hyperosmotic agents
            Medical treatment:                                   Immediate treatment important to
                1)increases aqueous outflow                       preserve vision
                        • topical cholinergics                    prevent adhesions of peripheral iris to
                        • topical prostaglandin agonist              trabecular meshwork (peripheral anterior
                        • topical alpha-adrenergics                  synechiae) resulting in permanent closure of
            •            2)decreases aqueous production              angle
                        • topical beta-blockers                  Medical treatment:
                        • topical and oral carbonic               Miotic drops (pilocarpine) to reverse pupillary
                            anhydrase inhibitor                      block
                        • topical alpha-adrenergics               ↓ IOP
            Surgical treatment:                                          o topical b-blockers
            • Laser trabeculoplasty                                      o topical adrenergics
                        • cyclophotocoagulation = selective              o topical cholinergics
                            destruction of ciliary body (for                     - pilocarpine 1-4% q15min, up to
                            refractory cases)                                        q5min)
            • Trabeculectomy (filtering bleb)                            o systemic carbonic anhydrase inhibitor
                        • shunts fluid from AC to under                          - IV acetazolamide 250-500 mg
                            conjunctiva and fibrosis prevented           o Systemic hyperosmotic agents
                            with mitomycin C or 5-FU injection                   - oral glycerine, 1.0 g/kg
                               during surgery; if extensive                          -   Mannitol IV 1.0 g/kgˇ
                               fibrosis after surgery can use tube
                               shlmt placement as alternative

Prognosis                                                            Complications
                   Optic nerve head examination                      irreversible loss of vision if untreated, within
                   IOP measurement                                     hours to days
                   Visual field testing                              permanent peripheral anterior synechiae



Secondarv Open Angle Glaucoma
Steroid-induced            • due to topical/systemic corticosteroid use
Glaucoma                   • Rule of 4: ¼ population after 4 weeks (or less) of topical steroid use
                              4x/day (higher in 5% of population are super-responders

Traumatic Glaucoma            hyphema-induced increase in lOP
                              angle recessiun glaucoma occurs with blunt, non-p'enetrating trauma to
                               globe and orbit, causing ledr.~ in trabecular meshwork and Clliary body
                               with secondary scarring

Pigmentary Dispersion      •      iris pigment cl?gs trabecular meshwork
Syndrome                   •      typICally seen m younger myope

Pseudoexfoliation          •       systemic disease, abnormal basement membrane-like material clogs
Syndrome                   trabecular meshwork
                           •       seen mostly in the elderly



Secondary Angle Closure Glaucoma
Uveitis                 •inflamed iris adheres to lens (posterior synechiae)
(posterior)
Neovascular Glaucoma  abnormal blood vessels develop on surface of iris (rubeosis iridis), into the
                            angle, and withm the trabecular meshwork
                         due to retinal ischemia associated with proliferative diabetic retinopathy
                            and CRVO
                         treatment with laser therapy to retina, to reduce neovascular stimulus to
                            iris vessels


Congenital Glaucoma

Pathophysiology
 The main pathology is malformation of the trabecular meshwork and iris (iridotrabeculodysgenesis) or iridocorneal
   dysgenesis.
 Isolated trabeculodysgenesis is the usual finding in primary congenital glaucoma.
 Primary congenital glaucoma is characterized by improper development of the eye's aqueous outflow system,
   leading to increased intraocular pressure (IOP), with consequent damage to ocular structures, resulting in loss of
   vision.
 Symptoms:
        o Triad
                 Epiphora
                 Photobphobia
                 Blepharospasm
        o    Cornea
                 Larger diameter (> 12 mm)
                 Tears (Haab striae represent tears in the Descemet membrane)
                 Edema, haze, opacity
        o    Deep AC

10335 - Distinguish between orbital and periorbital cellulitis and describe the four important signs.

Periorbital cellulitis: infection of soft tissue anterior to orbital septum
Orbital cellulitis: ocular and medical emergency, inflammation of orbital contents posterior to orbital septum

Clinical manifestations of orbital cellulitis, but not preseptal cellulitis, include:
    - Proptosis
    - Globe displacement
    - Limitation of eye movements
    - Double vision
    - Vision loss (indicates orbital apex involvement)




Orbital septum:
10336 - Décrire l’utilisation de base des médicaments à des fins diagnostiques et thérapeutiques en ophtalmologie.

À des fins diagnostiques
    - Agents anesthésiques topiques
             o Diminuent la sensibilité cornéenne
             o Ex : proparacaïne et tétracaïne
             o Ne pas utiliser de manière continue
                      Très toxique pour la cornée
                      Provoqueront un ulcère cornéen cécitant
                      Ne jamais prescrire pour utilisation à domicile!
    - Fluorescéine
             o Colorant végétal orange
             o Propriétés
                      Colle à la cornée et à la conjonctive à l'endroit endommagé
                      Apparence verte lorsque exposée à de la lumière bleue (fluorescence)
             o Permet de visualiser les érosions cornéennes et autres pathologies à la surface oculaire
    - Gouttes mydriatiques
             o Permettent la dilatation de la pupille pour visualiser le fond de l'œil
             o Muscle dilatateur
                      Phényléphrine stimule le muscle dilatateur (imite le système sympathique)
             o Muscle sphincter
                      Si la phényléphrine n'est pas suffisante
                      Tropicamide ou cyclopentolate décontracte le muscle sphincter de l'iris en bloquant le système
                         parasympathique
                      Vision trouble temporaire
             o Durée de quelques heures, parfois quelques jours
             o Faible risque de déclencher crise de glaucome à angle fermé

À des fin thérapeutiques
    - Cycloplégiques
             o Dilatation thérapeutique de la pupille
             o Prévention des synéchies postérieurs (iris se colle au cristalin)
             o Paralysent le muscle ciliaire réduisant la douleur oculaire ou les céphalée dues aux spasmes de ce
                muscle
             o Ex : homatropine et atropine
    - Stéroïdes
             o Sont utilisés de manière topique pour contrôler l'inflammation (ex : ulcère cornéen bactérien)
             o Risques
                     Immunosuppression oculaire
                     Augmentation de la pression intraoculaire et glaucome lors d'utlisation prolongée (plusieurs
                        semaines)
                     Cataracte lors d'utilisation prolongée
             o Nécessitent un suivi étroit par un ophtalmologiste
             o Ex : suspension d'acétate de prednisolone
    - Anti-inflammatoires non stéroïdiens (AINS)
             o Pour inflammation intraoculaire et douleur de la surface oculaire
             o Utilisé en pré-op (cataracte) pour mainternir la pupille dilatée
             o Surveillance nécessaire pour prévenir complications
             o Ex : diclofénac, flubiprofène et kétorolac
    - Antibiotiques
             o Antibactériens
                     Grande variété
                     Traitent efficacement la conjonctivite bactérienne de routine
                     Ex : sulfate de polymyxine B + zinc de bacitracine; acide fusidique; fluroquinolones (si sévère)
            o   Antiviraux
                     Pour traiter infection par l'herpès (Infection à l'herpès peuvent causer un cécité (mort oculaire))
                     Bloquent la réplication virale
                     Ex : trifluridine
    -   Agents anti-glaucomateux
           o Collyres qui diminuent la production aqueuse (usage courant)
                     Bêta-bloquants (timolol)
                            Peuvent provoquer l’aggravation de la pathologie réactive des voies respiratoires
                            Effets secondaires
                                     o Exacerbation d’asthme
                                     o Bradycardie
                                     o Hypotension
                                     o Diminution de libido
                                     o Depression
                     Agonistes alpha-2 (brimonidine)
                            Effets secondaires
                                     o Conjonctivite allergique
                                     o Léthargie, confusion
                                     o Bouche sèche
                                     o Fatigue
                                     o Contrindication chez les enfants (Risque de dépression respiratoire)
                     Inhibiteurs de l’anhydrase carbonique (dorzolamide)
                            Contre-indiqué si allergie au sulfa
                            Effets secondaires
                                     o A: Fréquence urinaire, Diminution de l'appétit, Nausée, Dépression, Fatigue /
                                        Malaise, Diminution du goût
                                     o B: Neuropathie périphérique, Formation de calculs rénaux, Anémie aplasique,
                                        Baisse du taux de potassium
           o Collyres qui augmentent la production aqueuse
                     Analogues des prostaglandines (latanoprost - très fréquemment utilisé)
                     Effets secondaires
                            Rougeur de la conjonctive
                            Sensation de brûlure
                            Iris, les cils et les paupières plus foncés
                            Oedème maculaire cystoïde
                     Myotiques (pilocarpine - rarement utilisés)


10337- Recognize issues in medical ophthalmology by describing when it is appropriate to refer a patient to an
ophthalmologist.

-cataracts: refer if vision in either eye is worst than 6/12. Ideally a recent optometrical assessment (within six months)
done prior to referral.

-diabetics: DM type 1 refer 5 years after diagnosis for photoscreening, DM type 2 refer for photoscreening, promt
referra for following cases: progressive/intermittent loss of vision, pregnancy, multiple risk factors

-diplopia: acute painless refer urgently, acute painful refer immediately, chronic diplopia refer non-urgent (if
troublesome)

-eye infection/inflammation: red eye with reduced vision, suspected iritis, suspected corneal ulcer, suspected herpes
simplex infections, herpes zoster ophthalmicus with eye involvement or Acute dacryocystitis refer immediately/urgently,
Drug Allergy: If unresponsive and severe refer immediately, Vernal Catarrh (children) refer immediately, contact lens
wearer: if subacute, optometrical management preferred. If acute, or associated conjunctivitis, refer
immediately/urgently

-eyelids/malposition: severe and persistent blepharitis with secondary ocular lid changes refer non-urgent, trichiasis
refer non-urgent if unresponsive or recurrent, ectropion refer non urgent if sever symptoms, entropion prompt referral,
peri orbital cellulitis prompt refferal or immediate if children, chronic recurrent chalazia refer non-urgent

-glaucomas: refer immediately

-intra ocular foreign bodies: refer immediately

-loss of vision: arterial occlusions, retinal detachment or optic neuritis refer urgently, optic swelling or pathology refer
immediately

-orbital: acute proptosis discuss with opthalmologist

-pediatric squint/vision problem: age less than 8 years refer immediately, age more than 8 years non-urgent referral,
white pupil refer urgently

-trauma: refer as appropriate

-watery eye: congenital refer non-urgent, pediatrics acquired refer immediately/urgently, adult refer non-urgent

10338 - Demonstrate the ability to perform a good physical examination in otolaryngology.

10339 - Demonstrate the ability to perform good history for both pediatric and adult otolaryngology patients.

10340 - Discuss the interpretation of audiograms (air conduction, bone conduction, degree of hearing loss, and type of
hearing loss).
10341 - Describe the diagnosis and treatment of acute otitis media.

Diagnosis — Examination with a hand-held otoscope is the standard method of diagnosis of AOM. Examination typically
demonstrates tympanic membrane redness, opacification, bulging (picture 1), and poor mobility when pneumatic
pressure is applied using a pneumatic otoscope (picture 2). In addition, there may be purulence in the ear canal if there
is an associated tympanic membrane rupture.

A tuning fork examination (512 Hz) may demonstrate conductive hearing loss.

AOM can usually be differentiated from otitis externa in that the latter tends to be more painful, especially with mild
traction on the outer ear, and there is a normal-appearing ear drum on examination.

Treatment — Antibiotics are the mainstay of treatment of uncomplicated acute otitis media in adults.

In 2004 the American Academy of Pediatrics and the American Academy of Family Physicians proposed a protocol for
withholding antimicrobial therapy for children who were older than two years of age, whose diagnosis was uncertain,
and who did not have severe disease (eg, moderate to severe otalgia with fever ≥39C) *34+. There are no data about
withholding antimicrobial drugs from adult patients with AOM. At this time, it is prudent to treat adults with antibiotic
therapy for a diagnosis of AOM.

Antibiotic Tx:

Amoxicillin, 40mg/kg/day, 10 day course

Prevention:




10342 - Décrire le traitement de l’otite moyenne avec épanchement.

Aiguë
    - Antibiotiques
          o Amoxicillin : Streptococcus, Pneumococcus, H.influenza, Proteus coverage
          o Ciprofloxacin : Pseudomonas, MRSA, Streptococci, Gram-négatifs (no anaerobic coverage)
          o Erythromycin: Alternative to penicillin
    - Prévention : Vaccin antipneumococcique conjuguée heptavalent (prevnar)

Chronique
   - Rarement des antibiotiques
          o No statistical proof that antihistamines, decongestants, antibiotics clear disease faster
   - Changer les facteurs modifiables
          o Éviter d'aller à la garderie (+ de virus qui va obstruer la trompe d'Eustache)
          o Éviter la fumée à la maison (+ d'épanchement et plus de problèmes de fonction de la trompe
            d'Eustache)
          o Risques modifiables
                         S'endormir avec un biberon ou boire un biberon en étant coucher sur le dos (prédispose au
                          reflux dans la trompe d'Eustache)
                      Fumeurs dans la maison
                      Poêle à bois, chat
                      Garderie comptant plus de 6 enfants (prédispose à plus d'infections d'oreilles)
                      Sucette
    -   Envisager les stéroïdes nasaux en cas de congestion
    -   Maîtriser les allergies
    -   Effectuer un test auditif
    -   Approche plus énergique en cas de retard du langage
    -   Envisager la mise en place de tubes de ventilation
            o Surgery: Myringotomy +/- ventilating tubes +/- adenoidectomy (if enlarged)
            o Ventilating tubes to equalize pressure and drain ear
    -   Disparition en 3 mois (90%)


10343- Describe the diagnosis and treatment of acute otitis externa.

Otitis externa is a clinical diagnosis:
History of 1-2 days of progressive ear pain
History of exposure to or activities in water, such as swimming, surfing, and kayaking
Pruritus within the ear canal
Purulent discharge
Conductive hearing loss
Feeling of fullness or pressure

On physical examination:
The sine qua non of otitis externa is pain on gentle traction of the external ear structures.
Periauricular adenitis may occur but is not necessary for the diagnosis.
Erythema, edema, and narrowing of the external auditory canal.
Accumulation of moist debris is observed in the external canal.
The tympanic membrane may be difficult to visualize and may be mildly inflamed, but it should be normally mobile on
insufflation.
Spores and hyphae may be seen in the external canal if the etiology is fungal.
Eczema of the pinna may be present.

Treatment:
-For an edematous canal: foam or gauze wick may be inserted in canal to facilitate delivery of medications
-Topical antibiotics: aminoglycoside combined with 2nd antibiotic and topical steroids (ex: neomycin-polymyxin B-
hydrocortisone)
-For a perforated tympanic membrane: it is critical to avoid using the otic solution, which increases the risk of
aminoglycoside ototoxicity. In this setting, suspension drops are safer to use (ex: fluoroquinolones)
-Mild fungal infections: acetic acid solution
-Severe fungal infections: topical antifungal (ex: 1% clotrimazole)
-Analgesics, antipruritics, and antihistamines may be indicated

10344 - Discuss the differential diagnosis for adult conductive hearing loss

DDx - Conductive Hearing Loss
       Congenital
            o Atresia of auditory canal
            o Ossicular abnormalities
       Neoplasm
            o Glomus tumour
       Otologic (adult, with intact TM)
            o Otosclerosis
                     Most common cause of conductive hearing loss with an intact TM in adults
                     Progressive hearing loss
                     Disease of the otic capsule and the ossicles
                     Abnormal bone resorption/deposition in the labyrinthine capsule and middle ear
            o Acute Otitis Media (AOM)
            o Otitis Media Effusion (OME)
            o Otitis Externa (OE)
            o Middle Ear Effusion (MEE)
       Tympanic Membrane (TM) perforation
            o Traumatic
            o Cholesteatoma
            o Chronic Otitis Media (COM)
       Foreign Body in Ear Canal or Cerumen

DDx- Unilateral Sensorineural Hearing Loss

       Idiopathic (Sudden Sensorineural Hearing Loss)
            o Viral infection
            o TIA/CVA
            o Inner ear membrane rupture
       Congenital
            o Genetic
            o Ischemia
            o Prenatal infection (e.g. TORCH))
       Neoplasm
            o Vestibular Schwannoma (aka Acoustic Neuroma)
                      Benign Neoplasm of the myelin sheath of CN VIII
                      5-10% of Intracranial Neoplasia
       Otologic
            o Degenerative (presbycusis)
            o Menieres Disease
                      Episodic Vertigo, Fluctuating Hearing Loss, Aural Fullness, Tinnitus
                      Unilateral usually (up to 30% bilateral)
       Trauma
            o (Temporal Bone Fracture, perilymph fistula)
            o Noise Induced (acute vs. chronic)
       Otoxins (ASA/NSAIDS, aminoglycosides, chemotherapy, diuretics)

NOTE: All unilateral hearing loss and/or unilateral tinnitus needs to be investigate = Audiogram, MRI

10345 - Discuss the differential diagnosis for pediatric conductive hearing loss.

Hearing loss in Children (Conductive + sensorineural hearing loss)
                              1/1 000 né sourd


       50 % héréditaire-génétique                50 % acquit durant la période
                                                 prénatale ou périnatale
1/3 syndromique          2/3 non syndromique        50 % idiopathique
                                                    Infection intra-utérine (TORCH)
                                                    Faible poids à la naissance
                                                    Hypoxie
 Dominant                        23 % dominant
                                                    Hyperbilirubinémie
    syndrome de Waardenburg 75 % récessif
                                                    Syndromes non génétiques
    syndrome branchio-oto-rénal 2 % lié à l’X
                                                        syndrome de Goldenhar
    syndrome de Stickler         1 % mitochondrial
                                                        syndrome d’alcoolisme fœtal
    neurofibromatose de type 2
    syndrome de Treacher-Collins
 Récessif
      syndrome de Usher
      syndrome de Pendred
      syndrome de Jervell et Lange-Nielsen
 Lié à l’X
     syndrome d’Alport




Transmission:

      Méningite – cause une ossification du cochlée
      Syndrôme de Waardenburg (unilatéral ou bilatéral)
      TORCHS
            o Rubella
            o CMV
Perception :

   -    Usher`s syndrome (1% of the perceptual hearing losses are causes)
   -    TORCHS
           o Toxoplasmosis
           o Encéphalite herpétique
           o Congenital syphilis


10346 - Describe the possible complications of acute otitis media.
Complications of AOM
    extracranial
           o chronic suppurative otitis media
           o acute mastoiditis
           o facial nerve paralysis
           o febrile seizures
           o nystagmus - bacterial labyrinthitis
           o TM perforation
    intracranial
           o meningitis
           o extradural, subdural, cerebral abscess
           o petrositis
           o lateral sinus thrombosis

Complications of Otitis Media with Effusion (OME)
    hearing loss, speech delay, learning problems in young children
    chronic mastoiditis
    ossicular erosion
    cholesteatoma especially when retraction pockets involve pars flaccida or postero-superior TM
       retraction of tympanic membrane, atelectasis, ossicular fixation

10347 - Describe the treatment of a tympanic membrane perforation (either acute or traumatic).

       The following findings warrant prompt involvement of an otolaryngologist after middle ear trauma once life-
        threatening conditions are addressed :
                 - Hearing loss ≥40 dB, or a subjectively decreased ability to hear a whisper or asymmetric
                     appreciation of sounds between the two ears
                 - Basilar skull fracture
                 - Otorrhea or rhinorrhea
                 - Facial nerve paralysis
                 - Vestibular symptoms (nausea, vomiting, nystagmus, ataxia)
       Patients with isolated tympanic membrane perforation and minimal hearing loss (<40 dB, decreased perception
        of whisper or minor asymmetry) may be managed with water precautions (keeping water out of the ear),
        antibiotic otic drops (for contaminated wounds), recommendation for audiometry within 24 hours if not
        previously obtained, and follow-up in four weeks to ensure that the perforation is closed and hearing deficit has
        resolved. Otolaryngological follow-up should occur in patients with persistent tympanic membrane perforation.
       We suggest that patients with middle ear trauma and hearing loss ≥40 dB, vestibular signs (eg, nystagmus,
        vomiting, ataxia), findings that indicate basilar skull fracture, or facial nerve injury undergo evaluation by an
        otolaryngologist emergently if possible, but at least within 48 hours of injury (Grade 2C). Definitive treatment
        depends on the specific injury that is identified (ex: surgery for ossicle injury).

10348 - Décrire le diagnostic et le traitement de la sinusite aiguë.

    -   Acute infection and inflammation of the paranasal sinuses
    -   Surtout au niveau du sinus maxillaire

    -   Clinical diagnosis requiring at least 2 major symptoms or 1 major + 2 minor symptoms
             o Major symptoms
                      Facial pain/pressure
                      Facial fullness/congestion
                      Nasal obstruction
                      Purulent/discoloured nasal discharge
                      Hyposmia/anosmia
                      Fever
             o Minor symptoms
                      Headache
                      Halitosis
                      Fatigue
                      Dental pain
                      Cough
                      Ear pressure/fullness
    -   Virus ou bactérie (enfant)
             o Rhinovirus, influenza, parainfluenza (virus)
             o S.pneumoniae, H.influenzae, M.catarrhalis, anaerobes (bactéries)

    -   Management
           o Anterior rhinoscopy
           o Xray/CT scan for complications
           o Antibiotics +/- nasal saline irrigation +/- topical/systemic decongestants
            o   Symptoms improving within 5 days
                     Symptomic relief and expectant management
            o   Moderate symptoms that worsen or persist beyond 5 days
                     Institute an intranasal
            o   Severe symptoms that worsen or persist beyond 5 days and refractory to intranasal corticosteroid
                     Clarithromycin or Clavulin
            o   Surgery if medical therapy fails (and complications)


10349- Discuss the possible complications of acute sinusitis.

Treatment fails in 10-25% of patients. Untreated, inadequately treated, or partially treated rhinosinusitis may lead to
chronic rhinosinusitis, meningitis, brain abscess, or other extra-sinus complications.

-Orbital or periorbital infections are the most common complications

-Meningitis usually occurs by extension of infection from the ethmoid or sphenoid sinuses

-Epidural abscess is a collection of purulent material between the bone of the skull and the dura, typically in relation to
frontal sinusitis. The further spread of infection, either by direct extension or by hematogenous seeding, may lead to
subdural empyema and eventually to brain abscess.

-Cavernous sinus thrombosis: septic emboli may flow posteriorly through the ophthalmic venous system to the
cavernous sinus, causing infection, inflammation, and eventually thrombosis of the sinus.

-Pott puffy tumor: infection in the frontal sinus spreads to the marrow of the frontal bone, localized osteomyelitis with
bone destruction can result in a doughy swelling of the forehead.

10350 - Discuss the diagnosis and treatment of chronic sinusitis.

Irreversible changes in lining membrane of one or more sinuses due to
• Neglect of acute and subacute phase
• Recurrent attacks or obstruction of osteomeatal complex (by polyp, deviated septum, FB, allergic rhinitis, or anatomic
narrowing)
Presentation
     chronic nasal obstruction
     pain over sinus or headache
     halitosis
     yellow-brown post-nasal discharge
Treatment
     dependent upon involved sinus, as confirmed by coronal CT of head
     decongestants, antibiotics, steroids; if fails, then surgery
Surgical Treatment
     removal of all diseased soft tissue and bone, post-op drainage and obliteration of pre-existing sinus cavity
     Functional Endoscopic Sinus Surgery (FESS)

10351- Describe the treatment of epistaxis.

1.First-aid
    • ABC’s
    • Patient leans forward to minimize swallowing blood nasopharynx
    • Firm pressure applied for 20 min on soft part of nose (not bony pyramid)
2.Assess Blood Loss (can be potentially fatal hemorrhage)
    • pulse, blood pressure, and other signs of shock
    • IV NS, cross match for 2 units packed RBCs if significant
3. Determine Site of Bleeding
    • insert cotton pledget of 4% topical lidocaine ± topical decongestant cocaine
    • visualize nasal cavity with speculum and aspirate excess blood and clots
    • anterior/posterior hemorrhage defined by location in relationship to bony septum
    • if suspicion, coagulation studies (e.g. Hemophilias, Von Willbrand’s)
4.Control bleeding
    • First line: Otrivin™, cocaine (topical vasoconstrictors)
    • Second line: Cauterize with silver nitrate (if first line fails and bleeding adequately visualized)
                           Note: do not attempt to cauterize both sides of the septum due to risk of septal perforation
    • Anterior hemorrhage treatment
            a. if fail to achieve hemostasis with cauterization
                      i. anterior pack with half inch Vaseline™ and ribbon gauze strips or absorbable packing (i.e.
                          Gelfoam™) layered from nasal floor toward nasal roof extending to posterior choanae for 2 to 3
                          days
                     ii. can also attempt packing with MeroceFM or nasal tampons of different shapes
    • Posterior hemorrhage treatment
            a. if unable to visualize bleeding source, then usually posterior source
            b. different ways of placing a posterior pack with a Foley catheter, gauze pack or Epistat™ balloon
            c. bilateral anterior pack is layered into position
            d. antibiotics for any posterior pack or any pack in longer than 48 hours
            e. admit to hospital with packs in for 3 to 5 days
            f. watch for complications: hypoxemia (naso-pulmonic reflex), toxic shock syndrome (Rx: remove packs
               immediately), pharyngeal fibrosis/ stenosis, alar/septal necrosis, aspiration
    • If anterior/posterior packs fail to control epistaxis
            a. elective catheterization and embolization of branches of external carotid artery
            b. ± septoplasty
            c. vessel ligation of
                      i. anterior/posterior ethmoid artery
                     ii. internal maxillary
                    iii. external carotid
5. Prevention
    • prevent drying of nasal mucosa with humidifiers, saline spray, or topical ointments
    • avoidance of irritants
    • medical management of hypertension and coagulopathies

10352 - Discuss the differential diagnosis of vertigo.
10353 - Describe the treatment regimen for the following: acute vestibular neuronitis, Meniere’s disease, benign
positional vertigo and multisensory deficits.

BPPV:




Menieres:




Vestibular neuronitis:




Multisensory deficits:

Treatment: Reassurance, Prevention, Life style review, Review of medication

10354 - Décrire l’approche du diagnostic d’une masse au cou.

    -   History and physical (dont nasopharynx et larynx)
            o Duration of symptoms
                     7 days: Inflammatory
                     7 months: Neoplastic
                     7 years: Congenital
            o À demander
                     Dyspnea or stridor (Postitional vs non-positional)
                     Hoarseness or dysphonia
                     Otalgia
                     Aural fullness
                     Dysphagia

    -   Laboratory
           o WBC
            o   Distinction infection – lymphoma
            o   Mantoux TB test
            o   Thyroid function tests and scan

    -   Imaging
           o Neck U/S
           o CT scan
           o Angiography (Vascularity and blood supply to mass)
           o Radiologic exam of stomach, bowel and sinuses

    -   Biopsy
            o Fine needle aspiration (Le moins invasive)
            o Needle biopsy
            o Open biopsy (Pour un lymphoma)

10355- Describe the differential diagnosis for an adult neck mass.




Rapid growth and tenderness suggest an inflammatory process, while firm, painless, and slowly enlarging masses are
often neoplastic. In young adults, most neck masses are benign (branchial cleft cyst, thyroglossal duct cyst, reactive
lymphadenitis), although malignancy should always be considered (lymphoma, metastatic thyroid carcinoma).
Lymphadenopathy is common in HIV-positive persons, but a growing or dominant mass may well represent lymphoma.
In adults over age 40, cancer is the most common cause of persistent neck mass. A metastasis from SCC arising within
the mouth, pharynx, larynx, or upper esophagus should be suspected, especially if there is a history of tobacco or
significant alcohol use. Especially among patients younger than 30 or older than 70, lymphoma should be considered.

10356 - Discuss the differential diagnosis for a pediatric neck mass.
   Branchial cleft cysts are the most common congenital lesions. They represent epithelial cysts, which arise on the
    lateral part of the neck from a failure of obliteration of the second branchial cleft in embryonic development.
    They are smooth, nontender, fluctuant masses, which occur along the lower one third of the anteromedial
    border of the sternocleidomastoid muscle between the muscle and the overlying skin.
   Thyroglossal duct cysts are the second most common type of congenital paediatric neck mass. They most
    commonly occur in the midline and elevate with swallowing. Occasionally, they will swell after an infection,
    bringing them to clinical attention.
   Dermoid cysts are composed of both ectoderm and mesoderm. They are thought to arise when a fold of the
    endoderm and ectoderm produces a cyst. In this sense they are similar to branchial cleft cysts in that they both
    form from “folds” in embryological tissue. Treatment of dermoid cysts is complete excision.
Inflammatory lesions are the second most common category of paediatric neck masses. Children commonly may have
lymph nodes which remain enlarged for months due to infectious etiologies. Children with benign reactive lymph nodes
do not require biopsies. However, other diseases such as lymphoma, may also present with lymph node enlargement.
History and physical is paramount in deciding whether to pursue further workup of a pediatric neck mass. One indication
for fine needle aspiration (FNA) or biopsy can be a mass that does not resolve after seemingly appropriate treatment.
Another can be an enlarging mass, a suspicious clinical course, unusual image findings or systemic symptoms. FNA can
allow for gram stain, culture, acid fast stain, imunocytochemistry and cytogenetics. All FNAs have two inherent
weaknesses: 1) the needle may miss the lesion of interest and 2) an FNA cannot appreciate histological architecture.




Inclusion cysts are akin to an “acquired dermoid cysts.” Inclusion cysts are believed to result from part of the skin being
traumatically implanted in the deeper layers. This can result in the ectopic formation of a dermal cyst lined with
squamous epithelium. In contrast, congenital inclusion dermoid cysts form along the lines of embryologic fusion and
contain both dermal and epidermal derivatives. Many inclusion cysts originate from the infundibular portion of the hair
follicle, and the more general term, epidermoid cyst, is favored today.
Injuries, especially of the crushing type, such as the slamming of a car door on a finger, are frequently reported in
association with epidermoid cysts. Theoretically, any surgical procedure may result in epidermoid cysts, and it is
surprising that they are not a more common occurrence. Epidermoid cysts are treated by surgical excision.
       Neurofibromas may present as either a solitary lesion or part of a generalized syndrome of neurofibromatosis.
        Neurofibromas are believed to be arise from Schwann cells. Central low T2 signal on MRI is characteristic of
        neurofibromas.
       Lipomas, though more common in the adult population, also occur in children. In addition to lipomas, pediatric
        patients can also have a lipoblastoma. A lipoblastom is a rare benign mesynchymal tumor of embryonal fat.
        Clnically and radiologically, a lipoblastoma may mimic a hemangioma. On histology a lipoblastoma appears as
        acollection of multivuolated cells with round nuclei which resembryological adipose tissue.




Lymphoma was the most common diagnosis of the malignancies. Lymphoma is in general the third most common
pediatric cancer. It affects 11-20 per million children per year worldwide, with a male predominance of 2.5 to 1. Wide
geographical variance exists. Lymphoma represents 50% of all childhood cancers in equatorial Africa due to a high
incidence of Burkitt’s lymphoma.

10357 - Discuss the differential diagnosis of adult upper airway obstruction (stridor).
Stridor
          o   High pitched sound resulting from turbulant air flow in the upper airway.
          o   It is primarily inspiratory
          o   Note quality, timing
          o   body position important
                     lying prone: subglottic hemangioma, double aortic arch
                     lying supine: laryngomalacia, glossoptosis
          o   site of stenosis
                     vocal cords or above: inspiratory stridor
                     subglottis and extrathoracic trachea: biphasic stridor
                     distal tracheobronchial tree: expiratory stridor

DDx Stridor (Children and Adults)
 congenital
        o Lingual thyroid/tonsil
 neoplastic
        o Squamous cell carcinoma (SCC) (adults): larynx, hypopharynx
        o Retropharyngeal: lymphoma, neuroblastoma
        o Nasopharyngeal: carcinoma, rhabdomyosarcoma
 infection
        o Ludwig's angina
        o Peritonsillar-parapharyngeal abscess
        o Retropharyngeal abscess
 allergic
        o angioneurotic edema
        o Polyps (suspect cystic fibrosis in children)
 trauma
        o laryngeal fracture, facial fracture
        o bums and lacerations
        o post-intubation
        o caustic ingestion
        o
10358 - Discuss the differential diagnosis of pediatric upper airway obstruction (stridor)

Neonates (obligate nose breathers)           2 to 3 Months                                   Infants – Sudden Onset


•Extralaryngeal                                 Congenital                                     Foreign body
o       Choanal atresia                             o Laryngomalacia                             aspiration
    o Nasopharyngeal dermoid                        o Vascular:                                 Caustic ingestion
    o Glioma                                                 Subglottic hemangioma             Croup
o       Encephalocele                                           (more common)                   Bacterial tracheitis
    o Glossoptosip: Pierre-Robin                             Innominate artery                 Epiglottitis
    sequence,                                                   compression
         Down syndrome,                                      Double aortic arch
    lymphangioma, hemangioma                        o laryngeal papilloma
                                                Acquired
•Laryngeal                                          o Subglottic stenosis -post intubation
    o Laryngomalacia - most common                  o tracheal granulation -post
o      Laryngocele                                      intubation
o       Vocal cord palsy (Amold-Chiari              o Tracheomalacia -post tracheotomy
malformations)                                      o Tracheoesophageal fistula (TEF)
o      Glottic web                                      repair
o       subglottic stenosis
o       Laryngeal cleft

•Tracheal
o      tracheoesophageal fistula
o      tracheomalacia
o      vascular rings


10359 - Recognize the common features of the following conditions on chest radiographs: pneumonia, pulmonary
edema, primary and secondary neoplasms, pneumothorax and solitary pulmonary nodule.

Pulmonary edema:
    Enlarged cardiac silhouette
    Kerley B lines (fluid in the interlobular septae)
    Peribronchial cuffing
    Indistinctness of the pulmonary vessels
    Pleural effusion

Pneumonia:
- Lobar pneumonia:
Consolidation (white) and air bronchograms
Involves single area, usually a lobe
Bloodborn pathogen
Unilateral
Commonest pathogen:Strept Pneumonia
- Bronchopneumonia:
Central bronchi involved
Inhaled pathogen
Patchy bilateral disease
Asymetrical
Peribronchial Cuffing
Commonest pathogen: Staph aureus
- Interstitial pneumonia:
Involves interstitial space, not airways
“ground glass” appearance
Bilateral, symetrical
If severe, involves airspace
Commonest pathogen: PCP, mycoplasma

Pneumothorax:

The main radiologic feature of a pneumothorax is a white visceral pleural line, which is either straight or convex towards
the chest wall, separated from the parietal pleura by an avascular collection of gas. In most cases, no pulmonary vessels
are visible beyond the visceral pleural edge.
Deep sulcus sign:

       pneumothorax on supine films

       especially seen in ICU patients




Neoplasms and Pulmonary nodules:

Radiographic features — Radiographic features that can be used to predict whether a nodule is malignant include size,
border, calcification, density, growth, ground glass appearance, and metabolic activity.

      Size — Larger lesions are more likely to be malignant than smaller lesions..)
      Border — Malignant lesions tend to have more irregular and spiculated borders, whereas benign lesions often
       have a relatively smooth and discrete border.
      Calcification — The presence of calcification does not exclude malignancy. As an example, "eccentric"
       calcification (ie, asymmetric calcification) should raise concern about carcinoma arising in an old granulomatous
       lesion (ie, a "scar" carcinoma).
Certain patterns of calcification, however, strongly suggest that a SPN is likely benign. These patterns include "popcorn"
calcification (picture 3), laminated (concentric) calcification, central calcification (picture 4), and diffuse, homogeneous
calcification (picture 5).

       Density — Increased density of a SPN argues against malignancy.
       Growth — A SPN whose size has increased very rapidly or has remained stable for a prolonged duration is likely
        benign.
       Ground glass appearance — SPNs that have a ground glass appearance are frequently malignant.

10360 - Reconnaître les caractéristiques courantes suivantes sur des radiographies abdominales : air libre,
calcifications anormales, contour des organes et schémas des gaz intestinaux.

Air libre (anormal)
     - Extraluminal
             o Intraperitoneal (pneumoperitoneum)
                      Upright film: Air under diaphragm
                      LLD film: Air between liver and abdominal wall
                      Supine film: Gas outlines of structures not normally seen
                               Inner and outer bowel wall
                               Falciform ligament
                               Peritoneal cavity
             o Retroperitoneal
                      Psoas shadows
                      Renal shadows
     - Intramural: Pneumatosis intestinalis
     - Intralumina
             o Dilated lopps of bowel
             o Air-fluid levels
     - Loculated: Mottled, localized in abnormal position without normal bowel features
     - Biliary: Air centrally over liver
     - Portal venous: Air peripherally over liver in branching pattern

Calcifications anormales
    - RUQ
             o Renal stone
             o Adrenal calcification
             o Gallstone
             o Porcelain gallbladder
    - RLQ
             o Ureteral stone
             o Appendicolith
             o Gallstone ileus
    - LUQ
             o Renal stone
             o Adrenal calcification
             o Tail of pancreas
    - LLQ
             o Ureteral stone
    - Central
             o Aorta/aortic aneurysm
             o Pancreas
             o Lymph nodes
    -   Pelvis
            o Phleboliths (calcified veins)
            o Uterine fibroids
            o Bladder stones

Contour des organes
   - Outlines can occasionally be identified because they are surrounded by more lucent fat
           o Kidney
           o Liver
           o Gallbladder
           o Spleen
           o Pancreas
           o Urinary bladder
           o Psoas shadow

Schémas des gaz intestinaux
   - Adynamic ileus
          o Air throughout GI tract generalized or localized
                    In a localized ileus (pancreatitis, appendicitis), dilated sentinel loop remains in the same location
                       on serial films, usually adjacent to the area of inflammation
   - Mechanical obstruction
          o Dilated bowel up to the point of obstruction (transition point)
          o No air distal to obstructed segment

10361- Recognize various fractures and dislocations visible on x-ray and their clinical implications, as well as the basics
of bone neoplasms and articular pathology.

Je n’ai pas inclu de photos puisque cela aurait fait un très gros documents mais il y a plusieurs cas avec explications sur
ce site web http://bubbasoft.org/Clinical_Radiology/ et le livre radiology made ridiculously simple est un bon outils.

Fracture patterns:
-simple: bone is in 2 pieces (transverse, oblique, spiral, vertical)
-comminuted: bone broken in more than 2 pieces
-compound: fracture fragment extend through skin or adjacent organ

Deformity:
-translation
-angulation
-rotated
-impaction (body fragment driven into another)
-dislocation (misaligment of articular surface)

Cervical spine fractures
Approximately 5-10% of unconscious patients who present to the ED as the result of a motor vehicle accident or fall
have a major injury to the cervical spine. Most cervical spine fractures occur predominantly at 2 levels. One third of
injuries occur at the level of C2, and one half of injuries occur at the level of C6 or C7. Most fatal cervical spine injuries
occur in upper cervical levels, either at craniocervical junction C1 or C2.

-flexion teardrop: anterior-inferior portion of vertebral body is broken off and a posterior displacement
-Hangman’s: bilateral C2 pedicule fracture with anterior displacement of anterior part of C2
-Hyperflexion fracture-dislocation: slight anterior vertebral subluxation with complex fracture
-Burst: compression of vertebral body = loss of anterior and posterior vertebral body height
-Jefferson’s: 2 fractures or more of C1
-Clay-Shovelers: avulsion of piece of spinous process
-Wedge: compression of anterior part of vertebral body
-Extension teardrop: avulsion of a piece of anterioinferior portion of vertebrae

For pictures http://emedicine.medscape.com/article/824380-media

Skull fractures
A blow to a stationary but moveable head causes acceleration, and the brain floating in CSF lags behind, sustaining an
injury directly underneath the point of impact (coup injury). When a moving head hits the floor, sudden deceleration
results in an injury to the brain on the opposite side (countercoup injury).

-Blow out orbital fracture: fracture of the orbital floor (bony fragments in superior aspects of maxillary sinuses, air in
orbit, fluid in sinuses)
-Zygomatic arch fracture: simple or tripod fractures
-Nasal fracture: fracture fragments are displaced towards the nasal cavity
-Le fort fracture: type 1 = floating palate = maxillary bone + nasal septum fracture
                    type 2 = floating maxilla = maxillary sinuses, orbital sinuses + nose fracture
                    type 3 = floating face = zygomatic arches, orbital rims + nose fracture
-Mandibular fracture

For pictures http://emedicine.medscape.com/article/391129-media

Thoracolumber spine fractures
Fracture of the lumbar spine, can occur whenever forces applied to the lower spinal column exceed the strength and
stability of the spinal column unit. Common injuries resulting in fractures of the lumbar spine include fall from a height;
motor vehicle and motor vehicle and pedestrian accidents; and penetrating trauma, including gunshot wounds and
stabbings. Unstable injuries to the pelvis often are associated with injury to the sacral plexus and the lower lumbar
spine. 


-chance fracture: horizontal severing of vertebrae
-burst fracture: collapse of an entire vertebral body
-wedge fracture: collapse of anterior vertebral body
-spinous process fracture
-spondylosis: defect in par interarticularis (collar on scottie dog) most common L4,L5
-spondylolisthesis: bilateral par intercularis defect, superior vertebral body slips forward in the inferior one

For pictures http://emedicine.medscape.com/article/396016-media

Pelvis Fractures
Pelvic fracture is a disruption of the bony structures of the pelvis. In elderly persons, the most common cause is a fall
from a standing position. However, fractures associated with the greatest morbidity and mortality involves significant
forces such as from a motor vehicle crash or fall from a height.
-malgaigne fracture: fracture through ishiopubic rami + SI joint of same side
-open book fracture: fracture through ishiopubic rami + SI joint on both sides
-bucket handle fracture: fracture through ishiopubic rami on one side + SI joint on opposite side
-straddle fracture: fracture through both ishiopubic rami + both SI joints
-rami fractures: both ishial rami + public rami
-avulsion fracture: small chip of bone pulled off at origin site of tendon

Shoulder fractures
-proximal humeral fracture
-glenohumeral joint dislocation (more common anterior)
-acromioclavicular joint seperation
-clavicular fracture (more common middle third of bone)
-humeral shaft fracture (associated with radial nerve injury)

Elbow fractures
-distal humeral fracture: supracondylar, transcondylar, intercondylar
-proximal ulnar fracture (olecran fracture)
-elbow dislocation (more common posterior dislocation)
-radial head fracture (indirect sign = positive anterior and posterior fat pads on x-ray)

Forearm fractures
-monteggia fracture dislocation: fracture of ulna + dislocation of radial head
-galeazzi fracture dislocation: fracture of distal radius + dislocation of distal radio-ulnar joint at wrist

Wrist fractures
-colle’s fracture: fracture distal radius + dorsal displacement of distal fragments with apex palmar angulation
-smith’s fracture: opposite of colle’s = apex dorsal angulation
-scaphoid fracture (only blood supply to scaphoid is distal to proximal- may cause avascular necrosis)
-wrist dislocation: perilunate (dorsal dislocation of capital bone), lunate (palmar dislocation of lunate bone)

Had fractures
-1st metacarpal base fracture
-bennett’s fracture: single intraarticular fracture of base of 1st metacarpal bone
-rolando’s fracture: comminuted bennett’s fracture
-skier’s thumb: fracture of base of proximal phalanx of thumb
-boxer’s fracture: fracture of 5th metacarpal neck
-baseball finger: avulsion of extensor tendon

Hip fractures
-hip fracture: subcapital, intertrochanteric, subtrochanteric
-hip dislocation

Femoral shaft fractures

Knee fractures
-tibial plateau fracture
-patellar fracture

Tibial and Fibular fractures

Ankle fractures
-Type A: below tibiofibular ligament
-Type B: through ligament
-Type C: above ligament

Foot fractures
-calcaneal fracture: angle of less then 28 degrees, associated with thoracolumbar fracture
-march fracture: stress fracture of 2nd or 3rd metatarsal bone
-joint fracture: stress fracture of base of 5th metatarsal

Bone neoplasm
Bone tumors are usually lytic lesions darker than normal. Some tumors such as breast and prostate metastasis can be
sclerotic.
         -Malignant: wide area of transition between lesion and normal bone, cortical destruction, periosteal reaction
         and soft tissue mass
         -Benign: sharp area of transition between lesion and normal bone. No cortical destruction.

Articular pathology
-Septic arthitis: joint effusion and swelling of adjacent soft tissue. Bone on each side may become demineralized (focal
osteopenia). Destruction of articular cartilage.
-Osteoarthritis: caused by wear and tear of articular cartilage. Mostly weight barring joints: knees, hips, spine. Bone
near joint reacts and forms osteophytes. Areas of bony degeneration form cysts in subarticular bone. Look for:
asymmetric joint space narrowing, periarticular sclerosis, osteophytes and subarticular cysts.
-Rheumatoid arthritis: inflammatory process of synovium. Soft tissue swelling, articular cartilage destruction,
periarticular demineralization and bony erosion. Usually symmetrical and no osteophytes.
-ankylosing spondylosis: inflammatory process that causes sclerosis and fusion of SI joint. Vertebrae become bridged by
ligamentous calcification (syndesmophytes) = bamboo stick apperance of the spine.

10362 - Recognize the following common features and conditions on CT of the head: basic anatomy, subarachnoid,
subdural and epidural hemorrhage, infarction, infection and neoplasm.

Basic Anatomy: There are too many slices for me to include in this document. I’m attaching a link that has all the slices
with all of the anatomy clearly marked.

http://www.urmc.rochester.edu/smd/Rad/neuroanatomy/headCT_anatomy.htm

Subarachnoid hemorrhage/Subdural hemorrhage/Epidural hemorrhage:
Infarction:

http://www.radiologyassistant.nl/en/484b8328cb6b2

ACA infarct:




MCA infarct:
PCA infarct:




PICA infarct:
Infection:
Neoplasm:

Astrocytoma:




Multiforme glioblastoma:
Medulloblastoma:




MRI of medulloblastoma:




Meningioma:
11034 - Describe the structure, funding and roles of the various components of the public health system in Canada.

11035 - List the functions of the public health department in disease prevention and control (population health
assessment & surveillance, health protection and promotion, and prevention).

11036 - Define and differentiate between: outbreak, epidemic, endemic and pandemic.

Endemic: Present in a community at all times but in relatively low frequency. Something that is endemic is typically
restricted or peculiar to a locality or region.

Epidemic: A sudden severe outbreak within a region or a group, as with AIDS in Africa or AIDS in intravenous drug users.
Pandemic: An epidemic (a sudden outbreak) that becomes very widespread and affects a whole region, a continent, or
the world.

Outbreak: a sudden, violent, or spontaneous occurrence

11037 - Décrire et expliquer la raison d’être des principales étapes de la lutte contre les éclosions et de la gestion des
éclosions.

    1. Define the problem: Is it an outbreak?
           a. Outbreak: Occurrence of new cases clearly in excess of the baseline frequency of the disease in a
               defined community or population over a given period of time.
                     i. Synonymous with epidemic although generally considered to be an epidemic that is localized,
                        has an acute onset or is relatively short in duration.
    2. Appraise existing data and institution of a surveillance system
           a. Case definition: From the most common symptoms or signs, including the likely date of onset of illness
               of the first case. Laboratory confirmation via culture or serology can help to define a case more
               precisely.
           b. Active surveillance: Identify those who may have been exposed to the infectious agent and who fit the
               case definition
    3. Formulate hypothesis and implementation of initial control measures: Depends on symptoms, suspected agent,
       population at risk
    4. Test the hypothesis through analysis of surveillance data or special studies
    5. Draw conclusions, re-adjust hypothesis and control measures
    6. Write report, make recommendations of long-term prevention and surveillance
           a. Modify control measures to stop the outbreak
                     i. Remove/neutralize agent (isolating residents in a facility)
                    ii. Strenghten resistance of hosts (immunization)
           b. Communicate outbreak information to the public in an effective manner
                     i. Provide education
                    ii. Recommend specific prevention and control strategies clearly
                   iii. Deliver a unifed message

But de la Lutte Contre les Maladies et de leur Contrôle
Les Centers for Disease Control (CDC) d’Atlanta et le Centre de prévention et de contrôle des maladies infectieuses
(CPCMI) au Canada cherchent à combattre les maladies d’aujourd’hui et à prévenir celles de demain. Ils ont établi une
hiérarchie de buts et objectifs, soit :
    - Premier but : Surveillance et réponses
            o Les programmes de surveillance détectent, analysent et surveillent les pathogènes qui émergent, les
                 maladies qu’ils causent et d’autres facteurs influant sur leur émergence, puis acheminent les réponses
                 aux problèmes, dès qu’ils sont cernés.
            o Objectifs :
                      A. Renforcer la surveillance des maladies infectieuses et les réponses trouvées.
                      B. Améliorer les méthodes de collecte et d’évaluation des données de la surveillance.
                      C. Assurer l’utilisation des données de la surveillance pour améliorer la pratique de la santé
                         publique et les traitements médicaux.
                      D. Consolider la capacité globale à surveiller et à répondre aux maladies infectieuses
                         émergentes.
    - Deuxième but : Recherche appliquée
            o Intégrer la science de laboratoire et l’épidémiologie pour optimiser la pratique de la santé publique.
            o Objectifs :
                      A. Élaborer, évaluer et diffuser les outils permettant de cerner et de comprendre les maladies
                         infectieuses émergentes.
                        B. Déterminer les comportements, environnement et facteurs de l’hôte qui font que les gens
                         risquent davantage de contracter des maladies infectieuses et de souffrir de leurs séquelles.
                      C. Mener une recherche en vue d’élaborer et d’évaluer des stratégies de lutte et de prévention
                         dans les neuf domaines visés.
    -   Troisième but : Infrastructure et formation
            o Consolider les infrastructures de santé publique en vue d’appuyer la surveillance et la recherche ainsi
                que de mettre en œuvre les programmes de prévention et de lutte.
            o Objectifs :
                      A. Renforcer la capacité épidémiologique et des laboratoires.
                      B. Rehausser l’habileté du CDC à communiquer électroniquement avec les départements de
                         santé locaux et d’états, postes de quarantaine américains, les professionnels de la santé et les
                         autres intervenants.
                      C. Améliorer la capacité nationale à répondre aux menaces de maladie infectieuse complexe aux
                         États-Unis et à l’échelle internationale, incluant les éclosions qui peuvent découler du
                         bioterrorisme.
                      D. Offrir des possibilités de formation en épidémiologie et en diagnostic des maladies
                         infectieuses, aux États-Unis et à l’échelle internationale.
    -   Quatrième but : Prévention et maîtrise
            o Assurer une mise en œuvre rapide des stratégies de prévention et améliorer la communication de
                l’information sur la santé publique sur les nouvelles maladies.
            o Objectifs
                      A. Instaurer, appuyer et évaluer les programmes de prévention et de contrôle des nouvelles
                         maladies infectieuses.
                      B. Élaborer, évaluer et promouvoir des stratégies visant à aider les prestateurs de soins de santé
                         et d’autres intervenants à modifier les comportements qui favorisent la transmission des
                         maladies.
                      C. Appuyer et promouvoir la prévention et la lutte des maladies à l’échelle internationale.

11427- Define and differentiate the 5 strategies of the Ottawa Charter for Health Promotion. Illustrate each of these
strategies in improving the health of a population.

1.Build healthy public policy:

Health promotion policy combines diverse but complementary approaches including legislation, fiscal measures,
taxation and organizational change. It is coordinated action that leads to health, income and social policies that foster
greater equity. Joint action contributes to ensuring safer and healthier goods and services, healthier public services, and
cleaner, more enjoyable environments. Health promotion policy requires the identification of obstacles to the adoption
of healthy public policies in non-health sectors, and ways of removing them. The aim must be to make the healthier
choice the easier choice for policy makers as well.

2.Create supportive environments for health:

The overall guiding principle for the world, nations, regions and communities alike, is the need to encourage reciprocal
maintenance - to take care of each other, our communities and our natural environment. The conservation of natural
resources throughout the world should be emphasized as a global responsibility.

Changing patterns of life, work and leisure have a significant impact on health. Work and leisure should be a source of
health for people. The way society organizes work should help create a healthy society. Health promotion generates
living and working conditions that are safe, stimulating, satisfying and enjoyable.Systematic assessment of the health
impact of a rapidly changing environment - particularly in areas of technology, work, energy production and
urbanization - is essential and must be followed by action to ensure positive benefit to the health of the public. The
protection of the natural and built environments and the conservation of natural resources must be addressed in any
health promotion strategy.

3.Strenghten community action for health:

Health promotion works through concrete and effective community action in setting priorities, making decisions,
planning strategies and implementing them to achieve better health. At the heart of this process is the empowerment of
communities - their ownership and control of their own endeavours and destinies.

Community development draws on existing human and material resources in the community to enhance self-help and
social support, and to develop flexible systems for strengthening public participation in and direction of health matters.
This requires full and continuous access to information, learning opportunities for health, as well as funding support.

4.Develop personal skills:

Health promotion supports personal and social development through providing information, education for health, and
enhancing life skills. By so doing, it increases the options available to people to exercise more control over their own
health and over their environments, and to make choices conducive to health.

Enabling people to learn, throughout life, to prepare themselves for all of its stages and to cope with chronic illness and
injuries is essential. This has to be facilitated in school, home, work and community settings. Action is required through
educational, professional, commercial and voluntary bodies, and within the institutions themselves.

5.Re-orient health services:

The responsibility for health promotion in health services is shared among individuals, community groups, health
professionals, health service institutions and governments. They must work together towards a health care system
which contributes to the pursuit of health.

The role of the health sector must move increasingly in a health promotion direction, beyond its responsibility for
providing clinical and curative services. Health services need to embrace an expanded mandate which is sensitive and
respects cultural needs. This mandate should support the needs of individuals and communities for a healthier life, and
open channels between the health sector and broader social, political, economic and physical environmental
components.

Reorienting health services also requires stronger attention to health research as well as changes in professional
education and training. This must lead to a change of attitude and organization of health services which refocuses on the
total needs of the individual as a whole person.

11428 - Demonstrate skills in advocating for the promotion of vaccination, physical activity, and uptake of
evidence‐based periodic health examinations.

11429 - Demonstrate skills in risk assessment and risk communication.

11430 - Identify steps in determining whether work‐place or environmental conditions are potentially hazardous.

11431 - Recommend appropriate preventive approaches to common occupational health risks.

Here is a good website: http://www.preventionbestpractices.org/index.html

Is important to consider whether others have been exposed and need to be evaluated and treated once the diagnosis of
a work- or environment-related illness has been made. It may be necessary to make an intervention to decrease or
eliminate exposures in order to prevent illness in others. The physician may find it necessary to alert the company
medical department, a company health and safety committee, or the state public health or labor department. OSHA
performs work site inspections routinely on a priority basis, or at the request of a current worker or management. Fines
may be levied in some cases if OSHA standards are violated.

The National Institute for Occupational Safety and Health (NIOSH) can provide the practitioner with toxicological
information and perform health hazard evaluations of workers to detect work-related health problems. Industrial
hygienists from private consulting groups or from workers' compensation carriers can conduct worksite evaluations and
monitoring and advise about interventions. The practitioner may find it useful to contact the local state Department of
Environmental Protection or city departments of public health for environmental problems.

Efforts to control home environmental exposures can also be helpful. As an example, practitioners can advise asthmatic
patients on measures to reduce environmental triggers. In a study of children with asthma, interventions that resulted in
reducing levels of cockroach allergen and dust mite allergen in the bedroom were significantly correlated with reduced
complications from asthma [79].

11432 - Mettre en évidence les façons dont les patients peuvent percevoir et mal interpréter les risques liés aux
dangers environnementaux.

11433- List common diseases associated with environmental exposures (including exposures to biological, chemical
and physical hazards in air, water, soil and food).

-Lead poisoning caused by paint
        sxs: abdominal pain
-Carbon monoxide poisoning caused by faulty furnace
         sxs: headache
-Cholinesterase inhibitor: organophosphate pesticide, sarin nerve gas
        sxs: miosis, dim vision, eye pain, rhinorrhea, headache, sweating, diarrhea
-Toluene diisocyanate found in chemical car lacquer
        sxs: dry hacking cough (bronchospasm)
-Chlorine gas, Sulfur dioxide
        sxs: reactive airway disease syndrome (dry cough, SOB)
-Repetitive wrist flexion and pinching
        sxs: Carpal tunnel syndrome
-Asbestosis
        sxs: lung cancer, mesothelioma
-Nylon flocking plant
        sxs: flock workers lung
-Diacetyl (butter flavoring additive)
        sxs: popcorn lung = bronchiolitis obliterans
-Radon
        sxs: lung cancer

11434 - Demonstrate skill in eliciting an environmental exposure history (e.g. for allergic reactions or respiratory
conditions).

11435 - Explain safety labeling and identify sources of information on environmental hazards (including Material
Safety Data Sheets (MSDSs), poison control centers, etc.).
11436 - Develop an effective management plan for patients with a possible environmental exposure.

11437 - Identify the appropriate steps to take in reporting an environmental hazard and in protecting the public.

DOCUMENTING AND QUANTIFYING EXPOSURE — If the history raises concerns about exposures, it is usually necessary
to measure the exposure in order to assess the level of risk and/or relationship to any symptoms. Documenting and
quantifying exposures can involve performing biological monitoring tests of the affected person as well as evaluating the
work or environmental site. The practitioner may find it helpful to seek assistance from specialists such as
occupational/environmental medicine specialists, toxicologists, governmental agencies, and industrial hygienists.

Within the office setting the patient can be tested for evidence of exposure in body fluids (biological monitoring) or of
adverse health effects upon target organs. The practitioner must know what agent to look for, the desirable test
medium (urine, blood, hair, tissue), appropriate timing, and influences upon test results [63].

Examination of the environmental or occupational site can be performed by governmental agencies, such as the
Occupational Safety and Health Administration (OSHA) or the Environmental Protection Agency (EPA), or by private
consultants such as certified industrial hygienists. Air sampling is performed with area or personal sampling devices to
get results that can lead to estimates of exposure based upon an average eight-hour exposure. Many regulatory
standards such as OSHA permissible exposure limits (PELs) are based upon eight-hour, time-weighted averages. Toxins
can be measured in air, water, soil, and from surfaces.
Assessment of musculoskeletal stresses can be performed qualitatively by observing the workers performing job tasks,
and more quantitatively with biomechanical analyses performed by an ergonomics expert.

11438 - Décrire les enjeux auxquels les médecins font face relativement aux industries pharmaceutiques et du
matériel médical.

How trustworthy is the information provided by a pharmaceutical representative?
Does seeing a rep influence prescribing practices?
What are the implications for patient care?
How do I know the info presented is accurate?
Is the information coming directly from an industry employee or is it through a physician?
Some of the issues related to doing clinical studies funded by industry?
      What phase is the project?
             o Phase 1 -3 – Medical division controlled
             o Phase 4 – Marketing division controlled
      Who determines the research questions?
      Who analyzes the data? Who writes the publications?
      Is it an unrestricted grant?
      Who is paid what for what roles?

The AAMC (Association of American Medical Colleges) report recommends prohibiting drug industry gifts and services to
physicians, faculty, residents, and students, and the curtailment of industry involvement in continuing medical education
activities.

Academic medical centers should make clear to their faculty, students, and staff that to the extent certain interactions
with industry are prohibited within academic medical centers, they are also prohibited off-site.

Academic medical centers should develop mechanisms whereby industry representatives who wish to provide
educational information on their products may do so by invitation in faculty-supervised structured group settings that
provide the opportunity for interaction and critical evaluation. Highly trained industry representatives with M.D., Ph.D.,
or Pharm.D. degrees would be best suited for transmitting such scientific information in these settings.

Academic medical centers should prohibit their faculty, students, and trainees from:
    1. Attending non-ACCME accredited industry events billed as continuing medical education;
    2. Accepting payment for attendance at industry-sponsored meetings; and
    3. Accepting personal gifts from industry at such events.


11439 - Discuss ethical and practical realities that contribute to choosing whether or not to participate in
industry‐funded activities.

As opportunities for commercial ties continue to grow, physicians should be increasingly wary of threats to their
professionalism and independent judgment about patient care.

Industry gifts, hospitality, services, and subsidies

The acceptance of individual gifts, hospitality, trips, and subsidies of all types from industry by an individual physician is
strongly discouraged. Physicians should not accept gifts, hospitality, services, and subsidies from industry if acceptance
might diminish, or appear to others to diminish, the objectivity of professional judgment. Helpful questions for gauging
whether a gift relationship is ethically appropriate include 1) What would my patients think about this arrangement?
What would the public think? How would I feel if the relationship was disclosed through the media? 2) What is the
purpose of the industry offer? 3) What would my colleagues think about this arrangement? What would I think if my
own physician accepted this offer?

Recommendations

The inherent difficulty in defining what makes a gift appropriate has, to an extent, contributed to lapses in judgment by
otherwise ethical persons. It is difficult to set with any precision a monetary value that would render a gift unacceptable.
There is no consensus model for determining relative value. Some specific guidance is offered in the following examples
of generally acceptable industry gifts: inexpensive gifts for office use (such as pens and calendars), low-cost gifts of an
educational or patient-care nature (such as medical books), and modest (such as a reception or other food and drink)
that is connected with a legitimate educational program. Understandably, even these “generally acceptable” examples
are subject to interpretation. It is unethical for physicians to accept any industry gift or subsidy that is predicated on
recommending a particular product or taking a particular clinical action.

Financial relationships between physicians and industry

Physicians who have financial relationships with industry, whether as researchers, speakers, consultants, investors,
owners, partners, employees, or otherwise, must not in any way compromise their objective clinical judgment or the
best interests of patients or research subjects. Physicians must disclose their financial interest in any medical facilities or
office-based research to which they refer or recruit patients.

For more information guidelines for physicians in interactions wih industry visit this web site from cma
http://www.cma.ca/ppi.htm

				
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