Pathophysiology Final Study Guide
Patho Section 1
Cell & Tissue Function/Dysfunction
Atrophy: decrease in size of cells.
Hypertrophy: increase in cell size.
Hyperplasia: increase in number of cells.
Metaplasia: mature cell type is replaced by a different mature cell type.
Dysplasia: cells vary in size & shape within a tissue.
Anaplasia: undifferentiated cells with variable nuclear & cell structure.
Ischemia: oxygen deficit due to respiratory or circulatory problems.
Hypoxia: reduced oxygen in tissue.
Oxygen Deficit: decreased energy production, loss of Na pump ↑ intracellular Na.
Temperature: inactivation of some enzymes, damages organelles, protein coagulation,
disruption of cell membrane.
Abnormal Metabolites: caused by genetic disorders or altered metabolism.
Apoptosis:programmed cell death controlled by genetics.
Necrosis:lysis of a cell, cell components leak into blood.
Liquification:dead cells liquefy due to release of enzymes.
Coagulation:cell proteins are altered or denatured causing coagulation.
Caseous:form of coagulation necrosis, thick, yellowish, cheesy.
Fat: fatty tissue is broken down into fatty acids.
Tissue Damage from Chemicals
Exogenous: from environment.
Endogenous: from inside the body,
Tissue Damage from Physical Agents
Hypothermia: vasoconstriction, ↑ blood viscosity, hypovolemic shock ↓ blood
Hyperthermia: causes general vasodilatation, decrease in circulating blood
Radiation: primarily affects actively dividing cells
Insects/Animals: direct injection of toxin, transmission of infectious agent,
allergic reaction to insect proteins.
Normal Defenses of the Body
1st Line Defense
Physical Barriers: unbroken skin, mucous membranes, nasal hair, clots.
Fluids: may contain enzymes or chemicals:saliva, tears, gastric, sweat.
2nd Line Defense-non-specific
Phagocytosis:neutrophils & macrophages engulf cells, debris, foreign mat.
Inflammation: automatic response to cell injury.
3rd Line Defense-specific defense produced by
Cell Mediated Immunity
Mast Cells: located in tissue & release histamine & bradykinin.
Macrophages: monocytes that enter tissue & act as phagocytes.
Interferons: small proteins made by lymphocytes to prevent virus replication.
White Blood Cells
Neutrophils: work by phagocytosis.
Basophils: release histamine leading to inflammation.
Eosinophils:combat the effects of histamine.
Monocytes:can enter tissue to become macrophages which
function as phagocyte.
Lymphocytes: B & T
Vascular Response: vasodilatation & increased capillary permeability.
Cellular Response: migration of inflammatory cells through chemotaxis to injury site to
destroy ineffective organism, remove damaged cells, released inflammation mediators.
Serous: watery, mostly fluids, some proteins and WBC’s.
Fibrinous: thick, sticky, high fibrin content.
Purulent: thick, yellow-green, contains leukocytes, cell debris & microorganisms.
Abscess: Pocket of purulent exudates or pus in a solid tissue.
Local Effects of Inflammation-Cardinal Signs of Inflammation
Redness & Warmth: due to increased blood flow to area.
Swelling: shift of protein & fluid into interstitial space.
Pain: pressure on free nerve endings, chemical mediators irritate nerves.
Loss of Function: edema may restrict movement.
Systemic Effects of Inflammation
Mild Fever: due to resetting of hypothalamic thermoregulatory set point, release of
Treatment of Inflammation: drugs may decrease capillary permeability, reduce number of
leukocytes & mast cells.
Types of Healing
Resolution: minimal tissue damage, cells can repair themselves.
Regeneration: damaged tissue is replaced by identical tissue.
Replacement: functional tissue replaced by scar or fibrous tissue.
1st Intention: wound is clean, edges are close together with minimal gap.
2nd Intention: large break in tissue, longer healing process with more scar tissue.
Scar Formation: fibroblasts proliferate, abnormal amount of collagen.
Hypertrophic: overgrowth of fibrous tissue, keloid.
Ulceration: blood supply around scar is impaired resulting in tissue
1. Partial thickness ulcer-red or pink ie. Sunburn.
2. Partial thickness ulcer-blister, scrape, abrasion.
3. Full thickness ulcer- through dermis.
4. Full thickness ulcer that includes muscle or bone.
Transudate: clear & watery.
Serosanginous: clear w/ tinge of red/brown. Contains serum/blood thin & watery.
Exudate: creamy yellowish. Contains proteins & WBC’s Thick.
Purulent: yellowish. Contains leukocytes and necrotic debris, thick.
Infected Pus: hues of yellow, green or blue. Contains pathogens, thick.
Venous Insufficiency Clinical Presentation
Incompetent Valves medial leg area
Inefficient Calf Pump edema
Distended Capillary Bed wet wound
Decreased Fibrolysis scaring, red base
Fibrin Leakage hemosiderin deposits(purple/brown on leg)
Documentation of Pulses
Arterial Insufficiency: decreased arterial blood supply.
Acute(thrombosis) vs Chronic(arteriosclerosis)
Dry Gangrene: nonviable dry tissue.
Wet Gangrene: tissue necrosis + bacterial infection. Drainage w/ odor.
Black Gangrene: gangrenous borders, mummified skin.
Pain w/ walking=Claudication
Skin is atrophic(no hair) slow nail growth & Diminished Pulse
Ankle Pressure Index: SBP LE/SBP UE
>1 no arterial occlusive disease
.9-1 min sx in LE
.5-.9 claudication pain(leg pain w/ walking)
.3-.5 ischemic rest pain
<.3 ischemic w/ tissue necrosis
Assessment of arterial flow, skin color w/ elevation/dependency
1. LE Elevation to 60º for 1 minute. Normal=no color change.
2. Lower the LE & record time for color to return.>30seconds
means arterial insufficiency. Will look hyperemic(bright red).
Immune Response-Third Body Defense
Humeral Immunity: antibodies are produced to protect body & stored in blood.
Cell Mediated Immunity:lymphocytes are programmed to attack non-self cells.
Antigens:immunogens, proteins, polysaccharides, glycoproteins on cell surface.
Macrophages:present throughout the body, derived from monocytes,
initiate immune response, engulf foreign materialprocess & display
foreign antigens & present them to lymphocytes, secrete monokines &
Lymphocytes:primary cell in immune response,
T: has 3 subgroups made in bone marrow & differentiate in
thymus, cell mediated immunity, can target certain cells.
1.Cytotoxic T:cells destroy cells bind to antigen & release enzymes
2.Helper T: facilitate immune response by activating & regulating
3.Memory T: remember antigens.
B:Made in bone marrow, located in spleen & lymphoid tissue,
Natural Killer:kill tumor or virus infected cells w/o prior exposure
IgG:most common, can activate compliment, cross placenta, primary &
secondary immune response.
IgM:can activate compliment, natural antibodies ie. Involved in blood type
IgA:not in blood, is in tears, saliva & colostrums.
Compliment System:antigen-antibody complex, activated during immune rxn w/ IgG or
IgM. Causes cell damage when activated, causes macrophages to release enzymes.
Primary: 1st exposure to antigen, 1-2 weeks needed for effective antibodies
Secondary:repeat exposure to same antigen, effective response in 1-3 days
Immunity: Innate-always present. Or acquired.
Type 1 Hypersensitivity:allergic rxn, exposed to allergen causes development of
IgE’s,activate mast cells and causes inflammation. Ie. Hay fever, allergies, asthma
Type 2 Hypersensitivity:cytotoxic hypersensitivity. Antigen on cell membrane reacts
w/ circulating IgG’s, activates compliment, cells w/ antigen destroyed. Ie incompatible blood
Type 3: Immune complex hypersensitivity-antigen & antibody combine forming
immune complexes that cause inflammation & tissue destruction.
Type 4:Cell Mediated or delayed response by T-lymphocytes. No antibodies
present. Ie. Tb test, contact dermatitis.
Immune System Malfunction
Hypersensitivity: full system immune response to non-noxious stimulus.
Asthma: central windpipe or airway disorder.
Interventions/Treatment:avoid triggers, medicate. Peak flow 50-80% of
person’s best signal moderate attack, >50% below best PF = major attack.
Multiple Sclerosis: autoimmune demyelinization of nerves in brain &CNS
Clinically Isolated Syndrome-only suffer 1 attack.
MS-multiple attacks at least 1 month apart & damage to at
least 2 separate CNS areas & r/o all other possible causes.
Tests & Measures: MRI, visual evoked potentials, CSF analysis.
Interventions: modify disease course, treat attacks, manage sx.
Myasthenia Gravis: antibodies destroy Ach receptors at NM junction.
Guillen Barre Syndrome: demyelination of peripheral nerves.
Fibromyalgia: generalized musculoskeletal pain > 3 months, multiple
tender points affecting all 4 quadrants, 11/18 points, 4Kg force painful
Rheumatiod Arthritis:autoimmune destruction of joints affects multiple
joints in symmetrical pattern, inflammation can affect organs.
Scleroderma:affects microvessels causing hypoxia in all tissue. Skin &
organs commonly affected.
Sjogren’s Syndrome: autoimmune disease » loss of fluid for tears/saliva
Hashimoto’s Disease: autoimmune thyroid disease, causes hypothyroidism
Graves Disease: hyperthyroidism,
Type 1 Diabetes: autoimmune destruction of pancreas cells » no insulin.
Inflammatory Bowel Disease: group of disorders with inflammation of
Crohn’s: ulcers throughout intestines, except rectum.
Ulcerative Colitis: ulcers in lower intestines, may begin in rectum.
Meningitis: photophobia is red flag.
Toxoplasmosis: parasitic infection. Contaminated cat feces in 1st trimester.
Histoplasmosis: fungal infection diagnoses based on organ involved
Bacteria-unicellular organisms, no nucleus, divide by binary fission.
Cocci-staph, strep, diplococci-pneumococcus
Gram Positive: doesn’t retain crystal violet, has outer membrane layer.
Gram Negative: retains crystal violet, no outer layer, thick peptidoglycan layer
Exotoxins: produced by gram+ bacteria.
Endotoxins: gram- bacteria. Released when bacteria die causing shock.
Active Viral Infection: virus attacks host cell injects genetic material, uses
host cell to produce viral proteins & nucleic acids. New viruses made in
cytoplasm & released by lysis or budding from host cell.
Latent Viral Infection: virus enters cell similar to active infection, replicates slowly
or delays replication, viral proteins are inserted into cell membrane of host cell causing
immune response. Ie. Herpes virus.
Fungi: eukaryotic organisms, primarily affect skin or mucous membranes.
Protozoa: eukaryotic organisms, usually parasites. Ie. Malaria, dysentary
Prions: protein like agent that can change shape of proteins in host cell. Mad Cow.
Modes of Transmission
Nosocomial Infections: infections that occur in healthcare setting.
Development/Stages of Infection
Incubation Period: time of organism entering body to appearance of clinical signs
Prodromal Period: infection is developing, nonspecific symptoms.
Acute Infection: fully developed infectious disease with peak clinical signs.
Chronic Infection: microorganism continues to replicate in body, sx milder.
Subclinical Infection: Microbe can reproduce in body but no signs present.
Septicemia: bacteria reproducing & circulating in bloodstream.
Red Flags: refer to Dr.
Chest pain/discomfort, unusual SOB w/ acute pain in chest, arm, throat or jaw,
unexplained dizziness, persistent hoarseness or cough, difficulty swallowing,
persistent abdominal pain/discomfort, coughing up blood, unexplained weight
gain/loss, persistent unexplained fatigue, changes in a mole, change in bowel/bladder
habits, blood in stool, unexplained vaginal bleeding, lump in breast or discharge or
change in size or shape, changes in testicles, severe HA, blurred vision, sores that don’t heal,
persistent unexplained lumps/swelling, persistent back pain even w/ rest, unexplained leg
Absent Lunula: anemia, malnutrition.
Pyramidal Luluna: trauma or excessive manicures.
Red Luluna: cardiovascular disease, collagen disease of vessels, blood CA
Mee’s Lines: metal toxicity, chemotherapy exposure.
Longitudinal Lines: Addison’s disease, breast CA, melanoma, trauma.
Splinter Hemorrhages bacterial endocarditis, lupus, renal failure, psoriasis
Terry’s Nails:half& half appearance:edema & anemia »renal/liver disease.
Cancerous Moles-asymmetry, border, color, diameter
PATHO TEST 2 REVIEW
General Cancer Info
General Genetics Info
Bladder Cancer : -Early stages bleeding in urine but little no pain
-Hematuria 1 sign with changes in urination
Breast Cancer: -New lump is most common symptom
-Manual palpation better catch than mammogram
Cervix cancer: -often asymptomatic
-vaginal discharge, abnormal bleeding, pain during intercourse
Colorectal cancer: -change in bowel habits most common
-Diarrhea, constipation, more narrow stools, blood in stool
-Bright blood-lower GI, Dark/black blood-Upper GI
Lung cancer: -persistent cough with or w/o chest pain
-Feeling of an infection that just won’t go away
Prostate cancer: -weak interrupted urine flow, frequent urination esp. @ night
Renal cancer: -low back pain, especially if pain not assoc. w/ injury
Skin Cancer: -Any new growth on skin should be examined
-Spot or bump that changes size, irregular borders
-Sore that will not heal
Change in bowel/other habits
A sore that does not heal
Unusual bleeding or discharge
Thickening or lump in breast
Indigestion or difficulty swallowing, unexplained weight loss
Obvious change in wart or mole
Water -60% adult body wt, 70% infants, higher % in females
-Intracellular 2/3 water in body -ECF 1/3
*Interstitial 3/4, Intravascular 1/4, Cerebro Spinal Fluid 1%
Control Fluid Balance->Thirst mechanism
-Antidiuretic Hormone (ADH): fluid output
-Aldosterone: Reabsorption of water and sodium
-Atrial Natriuretic Peptide (ANP): lowers BP by controlling blood volume
EDEMA: fluid excess in interstitial compartment
DEHYDRATION: Signs-decreased skin turgor, sunken eyes, low BP, rapid weak pulse, high temp
Intracellular electrolytes: potassium, phosphate, magnesium
Blood electrolytes: sodium, calcium, less extent bicarbonate
EXCESS/DEFICIENT ELECTROLYTE CAUSES of EFFECTS of
Excessive sweating, vomiting, Impaired nerve conduction, fatigue,
HypoNatremia diarrhea, insufficient aldosteerone, mm cramps, Abdom issues,
kidney failure, excessive water- decreased Osmotic pressure in ECF-
intake THUS fluid into cells
Insufficient ADH, loss of thirst Fluid shift out of cells, weakness, dry
HyperNatremia mechanism, watery diarrhea, rapid tongue mucous membranes,
respiration, increased BP
Diarrhea, diuresis, excessive Cardiac Dysrythmias, interference
HypoKalemia aldosterone, low dietary intake, with neuromm junc, decreased dig.
Insulin forces K+ into cell Tract motility
Renal failure, deficit aldosterone, Cardiac dysrythmias, mm weakness
HyperKalemia leakage of K+ from ICF into ECF, common progressing to paralysis,
prolonged acidosis (H+ replaces) respiratory arrest
HypoCalcemia Hypothyroidism, malabsorption Increased permeability/ --
syndrome, deficient serum albumin, excitability of nerve
increased serum pH membranes,spont stim of skeletal
mm, Tetany, weak Heart
HyperCalcemia Uncontrolled release from bones - Depressed neuromm activity
demineralization from immobil. -interference with ADH function
-increased intake -increased strength cardiac
HypoMagnesmia Malabsorption of assoc with Neuromuscular hyperirritability -
alcoholism, use of diuretics heart arrythmia
HyperMagnesmia Renal failure Depressed neuromm funct
GENETIC DISORDERS CAUSE(S) CHARACTERISTICS
Flat head. PROTUDING TONGUES
Angelman syndrome X-linked, lose “bit” of chromosome odd bouts of Laughter, Balance
Missing part chromosome 5, Hi “CAT-like” cry, webbed toes &
Cri du Chat mutation at fingers, DOWNward slant to wide
set eyes, skin tags ant. ears
Flat face, Upward slanted eyes,
Downs syndrome Trisomy 21 single DEEP crease palm of hand,
HYPOtonia (low muscle tone),
Large head w/ prominent forehead,
Fragile X syndrome Fragile x retardation protein boys develop long face, tactile
Esp. effects nervous syst and skin,
Neurofibromatosis Autosomal dominant, birthmarks called café-au-lait,
freckles in armpits and groin,
purplish RUBBERY lesions on skin
GENETIC DISORDERS CAUSE(S) CHARACTERISTICS
Prader Willi syndrome Chromosome XV obsessed w FOOD, temper
tantrums, violent outbursts, @ 1
Y.O. become ravenously hungry
Broad nasal bridge, PROTRUDING
Smith-Magenis Syndrome Deletion @ XVII jaw, ear anomalies, SPEECH &
middle ear problems, SLEEP
Sudden Mood changes
Teenagers less developed,
Klinefelter’s Syndrome Men w/ extra X chromosome prepubescent testosterone helps,
testosterone levels to diagnose,
WEBBED neck!! Underdeveloped
Turner Syndrome Females w/ only 1 X chromosome BREASTS
High BP, Type II diabetes
Triple X syndrome Extra X chromosome Girls TALL, often not diagnosed, no
long term problems
Williams syndrome 50% retardation, PUFFINESS around
Random mutation chrom. 4 eyes, long neck, sloping shoulders,
Poor DEPTH perception
Cystic Fibrosis Life limiting (30s), frequent
Single point mutation CFTR coughing w/ thick sputum, salty-
skin, frequent lung infections,
-Duschenne most common (missing
Muscular Dystrophy Dystrophin-over 30 different genetic dystrophin), affects skeletal &
diseases cardiac Muscle
-Myotonic; congenital, juvenile,
adult, late onset-over 50
ACID-BASE Imbalance -> Normal 7.4, ranges from 7.35 to 7.45
o Enzymes act in narrow pH range
20:1 base to acid ratio
Respiratory system- alters carbonic acid levels Acidosis-> CO2 up
Kidneys- modifies excretion rates of acids, Most effective control system
Acidosis: excess Hydrogen ions
Alkalosis: deficit in Hydrogen ions
Acidosis HCO3- down Alkalosis HCO3- down
**compensation occurs to balance relative ratio (20:1), NOT total concentration
Hemocrit - proportion of cells (RBC)
-indicates viscosity & inc or dec in hydration
Hemoglobin: Tetramer-> 4 hemes which carry 1 oxygen each
Hemophilia A: 90% of cases, deficit of clotting FACTOR III, an X-linked recessive trait
Hemophilia B: Xmas disease, deficit FACTOR IV
Hemophilia C: factor XI, milder form
o Whole blood: for severe anemia
o Artificial EPO (stimulates RBC production)
o Bone marrow Transplants: some cancers, immune deficiencies, blood cell disease
ANEMIAS- can lead to ANGINA or CHF
Hemoglobin deficit= reduction in oxygen transport
Fatigue, pale face, dyspnea, tachycardia
Impaired bone marrow
Blood loss or excessive destruction of RBCs
Iron deficiency: impairs hemoglobin, very common, usually underlying CAUSE
o Large, immature, nucleated erythrocytes(RBCs)
o SYMPTOMS-> Tongue large, RED, sore, shiny
o Temporary or permanent impairment or failure of bone marrow
o Bone marrow cells replaced by FAT
o Cause must be ID’d for prompt treatment & marrow recover or is LIFE threatening
o CAUSE: excessive destruction of RBCs via many causes
Sickle Cell Anemia-> abnormal hemoglobin
o Genetic condition; autosomal rec., heterozygous R carrier
More common n AFRICAN ancestry
o Sickle cell crisis occurs when LOW O2 levels
When deoxygenated HbS is unstable and crystallizes=sickle shape
o Most common blood disorder in world
o Abnormal hemoglobin due to missing genes
o Primary polycythemia->Increased rate of RBC production
Secondary polycythemia-> Increased RBC production due to prolonged Hypoxia
o Concerns for both:
Category Sytemic disease Musculoskeletal
Sluggish blood flow
Increased BP & hypertrophied heart
Indications of Blood clotting Disorders
o Persistent bleeding in gums & nose bleeds, bleeding into joint, coughing up/vomiting blood,
blood in feces, vomiting, low BP
Causes of clotting disorders
o Defective platelet function
o Long term use of warfarin
Hemophilia A (classic)
o Most common inherited clotting disorder
o Varying severity
o Spontaneous bleeding into joints
Disseminated Intravsascular Coagulation
o Excessive clotting & excessive bleeding in circulation
o Clotting factors reduced to dangerous level
o Widespread uncontrollable bleeding
o HIGH fatality rate
Acute High proportion of IMMATURE, nonfunctional cells in marrow and circulation
Onset is abrupt
SIGNS: Frequent uncontrolled infections ,BONE PAIN, Weight loss, fatigue, drowsiness, vomiting
Chronic Higher proportion of MATURE cells
Mild signs & better prognosis
Diagnostics for all leukemias
Peripheral blood smears
Bone marrow biopsy confirmation
Treatment-> Chemo, Biologic therapy using INTERFERONS, Can stimulate immune system
Differential diagnosis of Systemic Pain versus Musculoskeletal
Course/duration Cyclic, progressive symptoms Sudden (gradual when related to
Constant or may come & go overuse)
Usually NONE : if relieved by rest Decrease with Rest
Relieving Factors or position, there is typically cyclic
progression of increasing frequency,
intensity, or duration until
rest/position doesn’t work
Aggravating Factors None specific Increase with use affected region
Quality DEEP, ACHING, throbbing SHARP
DIFFUSE or waves/spasm
Intensity Severe if cancer spread to nerves Depends on if acute, subacute, or
surrounding a visceral organ chronic
From Upper back, middle to low Located over injury sight.
Location back regions. May also be in front If severe may also refer proximal
of trunk frequently in abdomen over and distal to injury sight
Associated signs & symptoms Jaundice, skin rash, weight loss, Usually none- trigger pts may be
fatigue, low-grade fever, muscular accompanied by nausea/sweat
weakness, frequent infections
Cardiovascular Disorders - Gould Ch. 18
-Low Na+, fat ->Decrease weight
-exercise – Increase HDL, decrease LDL (high and low density lipoproteins)
-Vasodilators, (e.g. nitroglycerin for coronary a.’s)
-Beta-blockers – prevent CNS stimulation of heart
-Ca2+ channel blockers – decrease contractility of heart
- anti-hypertensives – ACE inhibitors (angiotensin converting enzyme – work via renal
system), diuretics, cholesterol decreasing drugs, anticoagulates to prevent clots
Arteriosclerosis – hardening, narrowing of arteries – fibrous tissue formation (tunica adventicia
-caused by hypertension
Atherosclerosis – plaque buildup in arteries, “atheromas”
-coronary occlusion angina, MI
-clot to brain TIA or stroke
-clot in periphery can lead to aneurysm
-HDL – mostly protein, little fat – carries lipids to liver for excretion
-LDL – mostly fat, little protein – carries lipids to cells of body
-largely responsible for atheroma formation
Risk factors for cardiovasc problems – age, heredity, obesity, sedentary lifestyle, smoking,
glycemic control, serum lipids
Angina Pectoris – O2 low in heart muscle severe, crushing chest pain, “angere”= “to choke”
Myocardial infarction – cell death from O2 deprivation replaced with fibrous tissue
-majority occur in left ventricle
Congestive Heart Failure
-Forward effect – Not enough blood going out, pump FAILURE
-Backward effect – CONGESTION of blood behind failing ventricle
-One side fails first, ultimately leads to failure of other side
-Decreased CO (cardiac output) one side compensation mechanisms –
vasoconstriction, water & sodium retention, increased blood volume increased
work for the heart
-Eventually muscles of affected side weaken congestion behind affected side
unaffected side pumps against increased resistance Previously unaffected side
Right side failure – systemic congestion
Left side failure – pulmonary congestion
-pericarditis effusion fibrous adhesions
-endocarditis infection of heart valves can lead to fibrosis
Dx tests for heart diseases
-auscultation – listen to valves
-exercise stress test
-doppler blood flow
-blood test – can detect enzymes release from infracted myocytes
EKG – usually 12 leads – at least 3
The basics –
-P wave – depolarization of atria
-QRS complex – depolarization of ventricles
-T wave – Repolarization of ventricles
-PAC –premature atrial contrx – slight flutter, benign
-PVC – premature ventricular contrx – many times benign, can lead to ventricular fib
-atrial flutter – atria contract quickly, but in rhythm – P waves not always followed by
-atrial fibrillation – atria quiver ineffectually (can live without coordinated atrial
-ventricular fibrillation – will die without swift intervention
Heart block – problem with SA node communication with AV node
-1st degree AV block – long PR interval – slow communication
-2nd – Missing QRS after P wave
-3rd – 2 consecutive missing QRS after P waves
-Sound 1 = tricuspid and mitral valves
-Sound 2 = semilunar valves
Nervous control of heart
-medulla of brain stem – control center of heart
-baroreceptors in aorta and internal carotid (peripheral a’s - stretch recepts for BP
-Autonomic system – increase and decrease HR
-tunica intima –endothelial cells
-endothelial cells respond to hormones, signal smooth muscle to contract, relax
-tunica media – muscle cells
-tunica externa (adventicia) – connective tissue
Venous return – thinner walls, valves prevent backflow
-can cause endothelial cells to shear off
-epinephrine in blood stream = inhibitory for endothelial cells, excitatory for
smooth muscle underneath vasoconstriction and incr. BP
-fat deposits in hole in intima atheroma
-blood can begin running between tunica intima and media dissecting aneurysm
Angiotensin Renin complex
+ACE (angiotensin converting enzyme)
**ACTION = angiotensin II receptor vasoconstriction, incr. BP
-fusiform – bulge in all directions
-saccular – sac forms on one side – pooling of blood causing clotting thrombus formed
-dissecting – most dangerous – blood runs between tunica intima and media – dissecting
aortic aneurysm =ticking time bomb
Circulatory shock – severe hypotension
-causes = hypovolemic, cardiogenic, septic, distributive (vasogenic, neurogenic,
-compensations – SNS incr. HR, force of heart contraction; kidneys release renin,
-antibod’s produced against endothelial cells and smooth mm
-Presentation – red tongue, rash @ distal extremity, skin sloughing, edema
-recovery usually spontaneous
-insufficient blood supplied to distal phalanges – Women>men
-prolonged ischemia can gangrene.
-valves fail due to age, injury, sendentary life, obesity
-chronic pooling of blood in LE
-brown, blue, purple skin in feet and toes – waste accumulation!
-minor trauma large wound! Hard to treat
Lymphomas – cancer of T-cells and B-cells
-Hodgkins – Tcell; Non-Hodgkins- B-cell
-large lymph nodes and spleen
-good prognosis if tx’d before metastasis
Respiratory Disorders – Gould Ch. 19
How to Breathe – the basics
-respiratory muscles contract & thoracic cage expands, creating negative pressure in
-air goes in
-elastic fibers around alveoli passively contract
-air goes out
-Sympathetic activation smooth mm relaxation, bronchodilation
-alveoli = squamous epithelium – maximizes gas exchange
-covered with surfactant – reduce surface tension of fluid, prevent collapse
-intrapleural pressure a shade under atmospheric pressure
-feeling when you hold breath due to chemoreceptors for CO2.
Hypercapnia – Increased CO2 in blood – compensate with hyperventilation
Hypocapnia – decr. CO2 – compensate with hypoventilation
Hyper/hypoxemia – O2 sats
-As more O2 binds to hemoglobin, affinity for O2 rises – aids in acquisition and release
-viral, bacterial, or fungal; 1 lobe or both lungs
-spread by oral droplet, can survive in dry sputum
-TB takes root in primary infection stage, symptoms present in reinfection stage
-can go dormant for long periods, bacilli walled off in localized area of lung
- resurfaces when immune compromised
-tissues of lung die in active infection
-dx with skin test, chest x-ray, sputum culture
-Long multidrug treatment, 6 mos- 1 yr.
-grown more resistant to drugs in recent years.
Obstructive Pulmonary Disorders – impaired ability to push air out of lungs
-Single gene mutation
-increased mucus in the lungs, increased risk of infections
-90% smoking related, 3rd most common cancer
-can be result of metastasis
-inflammation and bleeding in lungs cough blood
-pleural effusion, pneumothorax
-can secrete hormones –“paraneoplastic syndrome”
-Type 1 hypersensitivity – IgE formed in response to allergen
-inflammation of mucosa bronchoconstriction, obstructive mucus
-can cause atelectasis –collapse of lung because of airway blockage
(-pneumothorax involves a collapsed lung caused by mechanical damage or a
rupture of a small airsac or “bleb” on outside of lung)
-presents with hypoxia, respiratory alkalosis (initially due to hyperventilation), cyanosis,
cough, tightness in chest, thick mucus, tachycardia
-treat with inhalers and glucocorticoids
COPDs –progressive degeneration
-Emphysema –“pink puffers” – red face, overinflation
-destruction of alveolar walls permanent inflation
-smoking eliminates anti-trypsin that inhibits enzyme that destroys elastin elastin of
alveoli destroyedloss of septae between alveolar sacs decreased surface area for gas
-presents with “barrel chest” – ribs fixed in inspiration position
-Chronic Bronchitis – “blue bloater”
-inflammatory obstruction repeat infections, progressive, irreversible damage of
-hypertrophy, hyperplasia of mucus glands, fibrosis
-Present with constant cough, SOB, cyanosis
-treat by Stopping Smoking, O2 supplementation, available vaccinations for at risk
Emphysema Chronic Bronchitis
Alveoli affected Bronchioles affected
Septae walls destroyed Increased secretions
Some cough Lots of coughing
Little sputum Lots of sputum
No cyanosis Cyanosis
Some infections Frequent infections
-permanent dilation of medium-to-large-sized bronchi
-caused by recurrent inflammation
Restrictive Pulmonary Disorders – impaired lung expansion
-often abnormal chest wall or lung inself
-exposure to irritants – coal workers
-inflammationfibrosis, “stiff lung”
- insidious onset
-Fluid collects in alveoli and interstitial fluid
-lung expansion decr, O2 in blood decr,
-leads to pulmonary hypertension and edema
-blood clot from veins pumped to lungs – deadly
-collapse of lung caused by: obstructed airway, compression (tumor), increased surface
tension preventing expansion
-small areas asymptomatic, large areas –dyspnea and chest pain
-Pleural effusion – “hydrothorax”
-fluid in pleural cavity protiens and WBCs follow, respond to inflammation
-Incr pressue in pleural cavity, layers separate, prevent expansion
-presents with incr RR and HR, cyclic chest pain
-air in chest cavity, lung collapse
-open – air enters through hole in chest cavity;
-closed – air in chest cavity from rupture on inside
-tension – air allowed to enter cavity, no natural way to remove it
-Adult Respiratory Distress Syndrome
-rapid, shallow resp, incr HR, confusion
-caused by shock, sepsis, burns, multiorgan failure
-yellow-green = infection
-rusty-dark = pneumonia
-purulent and foul odor = bronchiectasis
-labored breathing – obstruction
-wheezing, whistling – obstruction of small airways
-stridor – high crowing noise – obstruction of small airways
Digestive System Overview
5 layers of gut wall (inner to outer): mucosa, submucosa, circular muscle layer, longitudinal muscle layer, serosa
*Peristalsis (involuntary contractions) occurs in circular and longitudinal smooth muscle layers
Gastrin cells (G cells): initiated by food entering stomach, stimulates chief and parietal cells
Intrinsic factor (parietal cells): needed for absorption of vitamin B12
HCL (parietal cells): activates pepsinogen, creates optimal pH ~2, denatures proteins
Pepsinogen (chief cells): pepsin not activated until pH of 6
Liver “Metabolic factory of the body”
1)Storage of nutrients 2) Maintains blood glucose 3) Blood reservoir 4) Produces bile, plasma proteins,
blood clotting factors, cholesterol/lipoproteins 5) Metabolic processes (detoxification, conversions)
Glucose -> Glycogen = Glycogenesis (when glycogen supply low)
Protein, Fat -> Glycogen = Glyconeogenesis
Glycogen -> Glucose = Glycogenolysis (maintains blood glucose levels)
Exocrine (secreting digestive enzymes and electrolytes) and endocrine organ
Trypsin, chymotrypsin, carboxypeptidase-break proteins
Ribonuclease-break nucleic acids
Pancreatic amylase-break starch
Ileum=major site of nutrient absorption, villi (folds of mucosa)
Large intestine=fluid and electrolyte reabsorption, movement slow to allow absorption of water, vitamin K
synthesis (essential for blood clotting)
Neural and hormonal control
PNS (vagus mainly): increased motility and secretions, SNS: inhibits GI activity
Gastrin: increases gastric motility and promotes stomach entering, Secretin: decreases gastric secretions,
Cholecystokinin: inhibits gastric emptying
Upper GI Tract Disorders (includes differential diagnosis)
Disorder Description Causes
Dysphagia Difficulty swallowing 1) Neurological deficit
2) Muscular disorder
3) Mechanical obstruction
Esophageal Squamous cells in distal esophagus, Chronic irritation
Cancer poor prognosis -chronic esophagitis
Hiatal hernia Part of stomach protrudes into thoracic
Gastroesophag Gastric substances reflux into distal Decreased competence of lower
eal Reflux esophagus,often seen with hiatal esophageal sphinctor
Gastritis Stomach mucosa inflamed (either Acute: Infection, allergies to food,
acute or chronic) spicy food, excessive alcohol,
*Helicobacter pylori infection typically ulgerogenic drugs
present w/ chronic Chronic: Most idiopathic
Gastroenteritis Inflammation of stomach AND Usually an infection
Peptic Ulcers Erosion in mucosa 1) H. pylori infection
(gastric and Common in proximal duodenum and 1) Increased acid-pepsin
duodenal) antrum of stomach (ulcers in general secretions
rarely found in large intestine) 2) Inadequate blood supply
3) Excessive glucocorticoid
4) Ulcerogenic subtances
Stress Ulcers Rapid onset, may form within hours of Severe trauma: Burns (curling’s
precipitating event ulcers), head injury (cushing’s
Systemic: hemorrage, sepsis
Gastric Cancer Primarily in mucous glands and in Gone down bc we have
antrum or pyloric area, poor prognosis preservatives w/ food
Pyloric Stenosis Narrowing and obstruction of pyloric May be developmental anomaly or
sphinctor acquired later in life
Liver and Pancreas Disorders (includes differential diagnosis)
Cholelithiasis Formation of gallstones*
Cholecystitis Inflammation of gallbladder and cystic
Cholangitis Inflammation related to infection of bile
Choledocholithiasis Obstruction of biliary tract by
gallstones (due to larger stones)
*Risk factors for developing gallstones: Women (2x more likely), high cholesterol, obesity, multi parity (several
children), use of oral contraceptives or estrogen supplements, hemolytic anemia, alcoholic cirrhosis
Disorder Description Causes
Jaundice Yellowish color of skin (not disease itself but Prehepatic: excessive
sign of other disorders) destruction of RBCs
Prehapatic: unconjugated bilirubin elevated Intrahepatic: disease or damage
Intrahepatic: unconjugated and conjugated to hepatocytes
bilirubin elevated Posthepatic: obstruction of bile
Posthepatic: conjugated bilirubin elevated flow into gallbladder or
Hepatitis Inflammation of liver 1) Idiopathic (fatty liver)
Mild: impaired hepatocyte function 2) Infection (viral or non-viral)*
Severe: necrosis and obstruction of blood/bile
flow along w/ impaired hepatocyte function
Cirrhosis Progressive destruction of liver 1) alcohol (most common)
Stage 1=fatty liver (asymptomatic & reversible) 2) biliary: obstruction of bile flow
Stage 2= alcoholic hepatitis (irreversible) 3) post-necrotic: linked w/
Stage 3=end stage cirrhosis (liver failure when chronic hepatitis or long-term
80-90% of liver destroyed) toxic exposure
Liver Initial signs mild, diagnosis occurs with Hepatocellular carcinoma (most
Cancer advanced stages common primary tumor of liver)
(arises from areas served by
Acute Chronic or acute(medical emergency for acute) Results from auto digestion of
Pancreat Spreads to tissue surrounding the pancreas the tissue (Premature activation
itis Very painful (different than pancreatic cancer) of pancreatic proenzymes)
Chronic in 15% of cases Precipitating factors=alcohol
(most common), biliary tract
obstruction, gallstones, mumps
Pancreat Adenocarcinoma-most common form Risk factors=smoking,
ic cancer Asymptomatic until advanced (metastasizes pancreatitis, and dietary factors
Hepatitis A: Infectious hepatitis, RNA virus, transmitted by fecal-oral route in areas of inadequate sanitation, no
carrier or chronic stage, vaccine available
Hepatitis B: Serum hepatitis, DNA virus, incubation period of 2 months, primarily transmitted by infectious blood
(may also be sexual transmission or from mother to fetus), carriers asymptomatic but contagious, vaccine available,
chronic hepatitis B (ascites) =engorgement of blood vessels, can’t filter toxins anymore
Hepatitis C: RNA virus, most common type transmitted by blood transfusion, has carrier state, increases risk of
Hepatitis D: Delta virus, incomplete RNA virus (needs hepatitis B to produce active infection), transmitted by blood
Hepatitis E: RNA virus, transmitted by oral-fecal route, no chronic or carrier state
Lower GI tract disorders (includes differential diagnosis)
Disorder Description Causes
Celiac disease Malabsorption syndrome: prevents Autoimmune disease (1% of
further digestion of gliadin US population)
(breakdown product of gluten) -defect in intestinal enzyme
Atrophy of villi
Primarily a childhood disorder
Crohn’s disease Progressive inflammation and fibrosis Genetic factor (often occurs
(included in cause obstructed areas during adolescence)
chronic Normally affects small intestines (but
Inflammatory may affect any part of GI tract)
Bowel Disease) Inflammation occurs in “skip lesions”
Ulcerative Colitis Blood and mucous in stool Genetic factor (often occurs
(included in Inflammation starts in rectum and during 2nd or 3rd decade)
chronic IBD) progresses to colon
Appendicitis Obstruction of appendiceal lumen, Fecalith, gallstone, or foreign
wall inflamed as fluid builds in object cause obstruction
Occurs in 10% of population
tenderness, periumbilical pain
Diverticular Diverticulum=outpouching of mucosa May be genetic link
Disease through muscular layer of colon
diverticula (very painful)
nausea, fever, elevated WBC, do
NOT see blood in stool
Colorectal Cancer Early diagnosis essential Most from adenomatous polyps
Symptoms=alternating diarrhea and (polyp does not always mean
constipation, bleeding,weight loss, cancer!)
anemia, fatigue, red blood in stool, Risk factors: familial multiple
pain doesn’t often occur polyps, long-term ulcerative
Most diagnosed cancer next to skin colitis, diet low in fiber (why
cancer susceptibility has increased)
Intestinal Lack of movement of intestinal Mechanical obstruc.
Obstruction contents (most common in small -tumors, adhesions, etc
intestine) Functional obstruc.
-impairment of peristalsis
-Ex: spinal cord injury
Peritonitis Inflammation of peritoneal 1) Chemical peritonitis: caused
membranes by foreign chemical in
Symptoms: sudden severe and peritoneal (bile, chyme, etc)
generalized abdominal pain, 2) Bacterial peritonitis: direct
abdominal distention, dehydration, trauma affecting intestines,
low blood pressure,tachycardia, ruptured appendix
vomiting 1) Abdominal surgery
(infection may develop)
2) Pelvic inflammatory disease
Irritable Bowel 1) Change in bowel motility that is
Syndrome associated with pain
2) Must be there 12 weeks out of the
3) Do NOT see blood in stool
Urinary System Overview
Nephron=functional unit of the kidney (>1 million), consists of renal corpuscle (filtration unit) and renal
ADH-prevents water loss (increases reabsorption of water in distal convoluted tubules and collect. duct)
Aldosterone-prevents water loss (increases sodium reabsorption in distal convoluted tubules)
ANP-allows water loss in response to high blood pressure
Glomerular rate: 1)afferent arteriole dilation=increased filtrate 2) efferent arteriole constriction=increased
filtrate 3) afferent arteriole constriction=decreased filtrate
Renin (kidney) ACE (lung)
Angiotensinogen → Angiotensin I → Angiotensin II
(Renin secreted in response to reduced afferent arteriole blood flow)
Cloudy-presence of large amounts of protein, blood, bacteria, and pus
Blood: if large amount=increased glomerular permeability or hemorrhage, if small amount=infection,
inflammation or tumors in urinary tract
Dark color-hematuria, excessive bilirubin, highly concentrated urine
Unusual smell or odor-infection, diet, or medication
Elevated BUN and creatine=failure to excrete nitrogen waste
Metabolic acidosis (low pH, low bicarbonate)=failure of tubules to control acid/base balance
Urinary System Disorders (includes differential diagnosis)
Disorder Description Cause
Urinary Tract Infection Lower=cystitis and urethritis E.coli
(hyperactive bladder and reduced Predisposing
capacity), may have systemic signs factors=incontinence,
w/ painful urination retention of urine, direct
Upper=pyelonephritis (in one or both contact w/ fecal material
kidneys: purulent exudate and
abscess block blood and urine flow),
systemic sign of high fever *can lead
to renal failure*
Glomerulonephritis Decreased GFR rate (decreased Acute poststreptococcal
urine output, elevated blood glomerulonephritis caused by
pressure and edema) presence of anti-streptococcal
Metabolic acidosis antibodies
Bloody, foamy urine and pain
Nephrotic Syndrome Increased permeability in glomerular
aldosetrone, severe edema
Bladder cancer Often develops as multiple tumors Predisposing factors: working
Early signs:hematuria and dysuria w/ chemicals (analine dyes,
rubber, aluminum), smoking,
recurrent infections, heavy
Vascular Disorders Thickening/hardening of walls and Some normal w/ aging
Reduces blood to kidney-stimulation
of renin (increases blood pressure)
Adult Polycystic kidney Manifests around 40 Autosomal dominant gene on
disease Multiple cysts in both kidneys-leads chromosome 16
to chronic renal failure
Polycystic disease in Manifested at birth, child dies in first Autosomal recessive mutation
children month or is stillborn
Acute Renal Failure Rapid onset 1) Acute bilateral kidney
Metabolic acidosis and diseases
hyperkalemia 1) Prolonged/severe
Ogliuria, increased serum urea circulatory shock or heart
3) Mechanical obstruction
Chronic Renal Failure Gradual, irreversible destruction of 1) Chronic kidney disease
kidneys (<10%=end stage) 2) Polycystic disease
Asymptomatic w/ up to 40% left 3) Systemic disorders
Symptoms later on=polyuria with 4) Low-level nephrotoxin
dilute urine, anemia, fatigue exposure over long time
Kidney Stones Calcium (sharp),magneisum, uric
1-5mm can be passed
Wilms Tumor Usually unilateral and gives purely Most common tumor in
kidney symptoms children, defects in tumor-
suppressor on chromosome
Diabetic Neuropathy Leading cause of chronic renal
1/3 ppl on dialysis have Type 1
diabetes, 2/3 have Type 2
Reflux Neuropathy Flow of urine from bladder to upper Primary (congenital)
tract Secondary (obstruction)
Can lead to end stage renal disease Associated with hypertension
Incontinence 1)Stress: most common Ex:sneeze Associated w/ aging, most
2)Urge: spasm common in women
3)Overflow: can’t fully empty bladder
4)Functional: bladder normal,
something else keeps them from
going to bathroom Ex: spinal cord
Dialysis-provides filtration and reabsorption (hemodialysis=blood moves from shunt into machine, 3x per week for
4 hours)(Peritonal dialysis= peritoneal membrane serves as semipermiable membrane, usually done at home
Endocrine System Differential Diagnosis
Acromagly- thicker skull and jaw (occurs after joint plates fuse)
Common cause=Grave’s disease
Common symptoms=exopthalmos, goiter, heat intolerance, and anxiety
Very familial, 4X more likely in women
Common symptoms=weight gain, cold intolerance, fatigue
Myxedema- lots of fluid (would not pit), can look like fibromyalgia bc of muscle aches and trigger point
tenderness, sparse hair, brittle nails, may have buffalo hump
Thyroid storm-dumps T3 and T4 into system -> causes tachycardia, fever, and agitation
Very treatable, most are benign (only 5% malignant and they normally dont metastasize)
Palpation will be painless, unilateral, and in one spot
Maintain calcium levels between bone and blood
Parathyroid cancer=can’t easily be distinguished from thyroid cancer
Release epinephrine and aldosterone
Trousseau’s sign- positive sign would be tremors and twitching bc of nerve or muscle irritability (Non specific sign)
Chvostek’s sign-elicit this by having the patient relax face and then the therapist taps the facial nerve, watch for
twitch of mouth or side of face
Addison’s Diseases (hypoadrenal)- autoimmune, skin changes color to a slight grey
Cushing’s Syndrome (hyperadrenal)- too much glucocorticoids in system, can cause muscle wasting, bone
demineralization, and ligaments to be lax, might see buffalo hump on back (does NOT feel like fluid)
Diabetes (fasting plasma glucose >126mg/dL)
Action of insulin-when insulin gets to cell, it makes glucose transporters close to membrane (Below 100
mg/dL is normal for FPG)
Type 1=autoimmune (insulin producing B cell destruction), typically under age 20
Risk factors: sibling has Type 1, parents have type 1
Type 2=obesity (insulin resistance...receptor not binding to insulin as well, pancreas intact), hyperglycemia
develops slowly, may have genetic predisposition, 85-90% of all diabetes
Risk factors: overweight, over 45 yrs old, inactive, women who had a baby over 9ilbs, low HDL
Gestational=associated with type 2, glucose intolerance w/ pregnancy, increased risk of diabetes later on, if
continues >6 weeks after pregnancy...no longer GDM
Early signs: blood sugar >180mg/dL, blurred vision, thirsty, ketones,dry skin, increased urination, tired
Late signs: blood sugar >240mg/dL, nausea/vomiting, deep/rapid breathing, large ketones in urine, fruity
breath, some diabetes pts don’t sense changes bc of neuropathy
Caused by: over treatment w/ insulin, missed meal, exercising when insulin peaking, stress
Early signs: tachycardia, hunger, headache, dizziness, sweating, shaking, pale skin, tingling around mouth,
Late signs: slurred speech, confusion, sudden moodiness, clumsy or jerky movements, seizures, pass out
Treatment: Act quickly! Test blood sugar after attempting to raise it with 15 grams of fast acting sugar...if
<70 repeat, if >70 eat meal/snack (always assume they will drop 50 mg/dL while exercising)
Obesity **Nursing/Allied health professions have greater risk of injury due to rising obesity trends**
Underweight = <18.5 Normal weight = 18.5-24.9 Overweight = 25-29.9 Obesity = BMI of 30 or greater
Subcutaneous vs. Intra-abdominal fat
Subcutaneous fat needed for thermal control
Abdominal obesity=most important factor in determining pre-diabetic state (1 out of 5 US adults have
metabolic syndrome), want to avoid fat around organs (especially liver)
Fat=largest/most active endocrine organ, releases 50 hormones, Adiponectin=hormone that signals brain we
are full (as fat cell gets bigger, releases less of this)
More macrophages recruited with obesity, causing chronic inflammation
Lifestyle=big factor (obesity trends with US Pima Indians vs Mexican Pima Indians)
Epigenetics= We can change which genes we turn on and off by our activitity
Pathophysiology Exam 5 Review
Acute Neurologic Disorders
Neurons and Conduction of Impulses
Neurons: highly specialized, non-mitotic cells which conduct impulses through the CNS and PNS
Myelin sheath: insulates, speeds up conduction, formed by Schwann cells, Nodes of Ranvier
Glial cells: astroglia, oligodendroglia, microglia, ependymal cells
Regeneration of Neurons: neuronal cell body damaged = death of neuron; CNS = neurons do
NOT regenerate; PNS = neurons may be able to
Conduction of impulses: depolarization (sodium influx) generation of action potential
repolarization (outward movement of potassium) sodium – potassium pump moves ions into
their normal position; myelinated fibers: salutatory conduction = rapid conduction
Chemical neurotransmitters: stimulated released into synaptic cleft; inactivated by enzymes
or reuptake; postsynaptic neuron dendrites or cells body depolarizes depending on
o Acetylcholine: (excitatory and inhibitory) located: neuromuscular junction, autonomic
nervous system (SNS and PNS), peripheral nervous system, CNS
o Catecholamines: (excitatory) present in the brain, norepinephrine: neuromuscular
junction and SNS, epinephrine: SNS, dopamine
o Seratonin: (excitatory) located in the CNS (brain) and GI; regulates behavior, attention,
digestive processes; implicated in mood changes
o Glutamate: (excitatory)
o Y-Aminobutyric acid (GABA): (inhibitory) located in brain
Autonomic Nervous System:
o Involuntary, motor and sensory innervation: cardiac muscle, smooth muscle, glands,
sympathetic/parasympathetic, neural pathway: preganglionic fibers (in brain or spinal
cord) postganglionic fibers (outside CNS)
Sympathetic Nervous System:
o “Fight or flight”; stress response, increase general level of activity: cardio, respiratory,
neurologic, Neurotransmitters: preganglionic fibers release acetylcholine (cholinergic);
postganglionic fibers release norepinephrine (adrenergic)
Parasympathetic Nervous System:
o Dominates digestive system, aids recovery after sympathetic activity, vagus N:
innervates heart and GI, neurotransmitter: acetylcholine; receptors (cholinergic):
nicotinic and muscarinic
Acute Neurologic Disorders
Problem/Disorder Description Treatment
Increased Intracranial Pressure Expansion of fluids/tissue
Increase in pressure
Ischemia and infarction
Herniation Displacement of brain tissue
caused by large mass
Brain Tumors Lesions that cause increased ICP If accessible then removal
Vascular Disorders Hemorrahagic (increased ICP) or
Transient Ischemic Attacks Temporary reduction of blood
flow in the brain
Small mini-strokes occurring
Connected to dementia
Cerebrovascular Accidents Infarction of the brain due to Clot busting agents, surgery,
lack of blood glucocorticoids, team approach
Cerebral Aneurysms Localized dilation in the wall of Surgery before rupture,
an artery antihypertensive drugs
Meningitis Bacterial infection of the Antimicrobial therapy,
meninges of the CNS glucocorticoids, vaccines
Brain Abscess Localized infection; necrosis of Surgical drainage, antimicrobial
Encephalitis Infection of the parenchymal or Antimicrobial therapy, antiviral
conn tissue in the brain and drugs (depends on the type of
spinal cord encephalitis)
Rabies Viral transmitted by bite of rabid Prophylactic immunization
animal or transplantation of
Tetanus Infection by puncture wound Immunizations advised
Poliomylitis Polio virus; attacks motor Immunization available
neurons of the spinal cord and
Herpes – Zoster (shingles) Caused by varicella – zoster in Vaccine available for ages 60+
Post-polio syndrome Occurs 10 – 40 years after initial
Reye Syndrome Viral infection linked to children No immediate cure
treated with aspirin
Guillain – Barre syndrome Inflammatory condition of the Recovery usually spontaneous;
PNS supportive treatment
Chronic Neurologic Disorders
Problem/Disorder Description Treatment
Hydrocephalus Excess CSF within the skull
Non-communicating (flow of
CSF through ventricular
system is blocked)
Communicating: absorption of
CSF through subarachnoid
Spina Bifida Failure of the posterior Diagnostic Tests: alpha –
spinous processes to fuse fetoprotein (AFP) elevated,
meninges and spinal cord ultrasound
herniated Surgical repair, OT/PT
Cerebral Palsy Motor impairment due to brain Speech, PT/OT, assistive
damage: intellectual function, devices, monitor
behavior, communication / hearing/vision, alternate
speech, seizures, visual or modes of communication
Causes: genetic mutations,
abnormal fetal formation,
brain damage, difficult
delivery, hypoxia (ischemia)
Dyskinetic: loss of
coordination with fine
Ataxic: loss of balance and
Multiple Sclerosis (MS) Progressive demyelination of MRI for diagnosis and
neurons in brain, spinal cord, monitoring
and cranial nerves Research treatments:
Cause: unknown interferon beta – 1b,
S&S: blurred vision, diplopia, glucocorticoids
scotoma, weakness in legs, PT/OT
progressive weakness and Muscle relaxants
dysarthria, loss of
coordination, bladder / bowel /
sexual dysfunction, chronic
Parkinson’s Disease Progressive degeneration in Removal of cause if known
basal nuclei; imbalance Dopamine replacement
between excitation and therapy
inhibition Anticholinergic drugs
Excess stimulation affects Speech/language, PT/OT
movement and posture Treatment of respiratory or
S&S: resting tremors (“pill urinary tract infections
rolling”), muscular rigidity,
difficulty initiating movement,
postural instability, decreased
flexibility, fatigue, lack of
facial expressions, propulsive
Amyotrophic Lateral Sclerosis Muscle wasting, progressive Stem cell therapy under
(ALS) degenerative disease affecting investigation
motor neurons Moderate exercise and rest
Cause: unknown Electronic communication
Cognition, sensory neurons, devices
neurons of eye are unaffected Team approach
Loss of upper motor neurons: No specific treatment to slow
spastic paralysis and degeneration
Loss of lower motor neurons:
Flaccid paralysis, decreased
muscle tone and reflexes
Myasthenia Gravis (MG) Autoimmune disorder: auto- Diagnostic tests: EMG, serum
antibodies to acetylcholine antibody test, acetylcholine
receptors at NMJ esterase inhibitor
S&S: muscle weakness in Treatment: antiacetylcholine
face/eyes, weakness in esterase agents,
arms/trunk, impaired vision gludocorticoids,
and speech, difficulty chewing plasmaphoresis, thymectomy
and swallowing, head droops,
upper respiratory infections
Huntington’s Disease Rapid, jerky movements, Diagnositc test: DNA analysis
chronic progressive Treatment: no therapy to slow
neurodegenerative chorea, progress, only symptomatic
hereditary, autosomal therapy
dominant (~40 years of age)
Progressive atrophy of brain
S&S: mood swings,
movements in arms and face,
Dementia Intellectual deterioration that
interferes with occupational or
S&S: impaired cognitive
skills, impaired thinking,
judgment, and learning,
memory loss, confusion,
behavioral and personality
Causes: vascular disease,
infections, toxins, genetic
Alzheimer’s Disease Progressive cortical atrophy: 1st stage: short term memory
neurofibrillary tangles and loss, social withdrawal, no
amyloid plaques sense of humor
Cause: unknown 2nd stage: general confused
S&S: onset insidious, stage, wandering (sundown
behavioral changes syndrome)
(irritability, hostility, mood 3rd stage: terminal stage,
swings), gradual loss of incontinent, apathetic,
memory and lack of institutionalized
concentration, impaired No diagnostic tests available
learning, poor judgment, Treatment: anti-acetylcholine
decline in cognitive function, esterase drugs, OT/PT,
memory and language, change psychologists, speech
in food intake, inability to therapists, team approach
recognize family, environment
Creutzfeld – Jacob Disease Rapidly progressive Diagnosis: blood tests
(Mad Cow Disease) Cause: prion ingested or Fatal: within 6 months = dead
S&S: memory loss, behavioral
changes, motor dysfunction,
AIDS Dementia Common in later stages of
AIDS, virus invades brain
Gradual loss of memory and
cognitive ability, impaired
Complex Regional Pain Syndrome (CRPS)
Pathogenesis: abnormal activity of the SNS, gate control theory, reflexive muscle spasm
Stages of CRPS:
o Stage 1 (acute): right after injury, weeks to 3 mo., excess sympathetic activity, persistent
burning pain and swelling, hyperesthetic, hyperhidrosis, increased nail/hair growth, pain
will be severe
o Stage 2: dystrophic stage, 3 – 6 mo., persistent pain and stiffness, trophic skin changes,
muscle atrophy, flexion contractures, pain exacerbated by stimulus, limb: edematous,
cool, cyanotic, mottled, hair loss, cracked brittle nails, skin cool to touch
o Stage 3: atrophic stage, ~6 mo., pain can increase or decrease, progressive atrophy of
skin, subcutaneous tissue, muscle, and bone, bone demineralization, skin: cool, thin and
o Stage 4: existence of stage 4 is questionable, 2+ years, psychosocial level, swelling is
gone, atrophy is permanent (muscle, bone, skin), no NOC firing now
Definite CRPS: pain and tenderness in extremity, S&S of vasomotor instability, swelling,
dystrophic skin changes
Probable CRPS: pain and tenderness OR swelling, dystrophic skin changes often present
Possible CRPS: vasomotor instability AND/OR swelling, NO pain but tenderness, dystrophic skin
Doubtful CRPS: unexplained pain and tenderness in an extremity
How we interpret pain: NOC perception interpretation emotions social
Pain: the perception of nociception that is not directly measurable
Pain behavior: the observed consequence of a painful experience (distress response); Pain
behaviors: verbal, vocal, facial expressions, physical actions, function, social actions
Benign pain: not associated with terminal illness vs. Malignant: associated with terminal disease
Acute Pain Chronic Pain
Recent onset (<3 mo.) >3 mo.
Close link with pain generator Loose link with pain generator
Not a learned response even though there will be Learned behavior, positive reinforcement for pain
pain behavior behavior
Objective findings coincide with generator No lab or clinical findings to support pain
Unlikely to have errors in stimulus discrimination Pt. may confuse pain with other forms of
Brief in nature lengthy
Differential Diagnosis of Chronic Pain
Wadell’s Signs Distracted SLR, rotation of back, superficial
tenderness, regional pain, migrating trigger
points, sham axial loading of spine, regional
Mankopf’s Test Pain should raise pulse rate of person by 5% +
O’ Donoghue’s Maneuver AROM > PROM = + sign
McBride’s Test Stand on one leg and raise other leg to chest =
should decrease LBP
Hoover’s Test Supine, hold pt.’s heels off table and have
them raise one leg, feel downward pressure if
they try to lift the leg
Symptom magnifier: magnifying their symptoms vs. Malingerer: knowingly manipulating the
system for their own gain, purposely deceiving the health care providers
Look at pt’s work history
Review types of seizure table
Seizure: abnormal discharge of a group of cortical or subcortical neurons
Epilepsy: syndrome characterized by experience of recurrent seizures
Aura: subjective sensation or motor phenomenon that precedes a seizure (pre-ictal/prodomal)
Ictal period: period of abnormal EEG activity; seizure S&S are evident
Post-ictal period: period following acute seizure, time of confusion, EEG activity = normal
Status epilepticus: series of rapidly repeated epileptic convulsions without any period of
consciousness between them
Inappropriate electrical activity Recurrent seizures or neurological syndrome
associated with seizures
Transient neurological signs (seizure) Seizures occurring with little or no provocation
Altered consciousness, involuntary movements, Individual or multiple seizure types; characteristics
and disturbed perception often occur may change with age
Defined by neurological S&S and EEG patterns Spectrum of seizure types, EEG, clinical settings
Etiology: genetic (inherited metabolic abnormalities, lowered threshold to electrical activity of
the brain), structural (disturbed cerebral flow, disorders of blood composition), environmental
(anoxia, toxins, drug withdrawal), head trauma, idiopathic causes
Triggering mechanisms: visually induced, movement induced, hyperventilation, trauma,
emotions, hydration/electrolyte imbalance, fever, alcohol or drug withdrawal, premenstrual
period, lack of sleep, illness
Diagnosis: medical history, diagnostic tests (lab studies, x-rays, lumbar puncture, CT, MRI, EEG),
Treatment: drugs, surgery, diet, microcomputers, education
Differentiate from: disorders of cerebral blood flow or blood constitution, structural, psychiatric
conditions, and migraine headaches
Mental Health Disorders of Children
Autism Spectrum Disorder
Autistic disorder, pervasive developmental disorder, and Asperger’s disorder: differ in when the
symptoms start, how fast they appear, and severity
Cause is unknown; genetic and environmental factors; structural brain abnormalities: larger
total brain mass, smaller frontal cortex, abnormal cerebellum
S&S: lack of social skills, avoid eye contact and physical contact, echolalia, don’t listen,
aggressive or passive (may switch), inflict self injury, resistant to change, diff in expressing
Early indications: no babbling or pointing, no single words, no response to name, loss of
language or social skills, poor eye contact, excessive lining of objects, no social responsiveness
Later indicators: impaired ability to make friends or initiate conversation, impaired play,
echolalia, preoccupation with objects, inflexible adherence to routines and rituals
Screening tests: Childhood Autism Rating Scale (CARS), Checklist for Autism in Toddlers (CHAT),
Autism screening questionnaire, screening test for autism in 2 year olds
Treatment: intensive behavior therapy
Attention Deficit Hyperactivity Disorder (ADHD)
Inability to focus on one thing in all aspects of life impairing function; diagnosis (must have all 3):
inattention, hyperactivity, and impulsivity
Characterized by tics; tics: involuntary, rapid, repetitive, and stereotyped movements of
individual muscle groups
Transient tic disorder: do not persist for more than 1 year vs. chronic tic disorder: duration over
many years (unchanging character) vs. chronic multiple tics: several chronic motor tics vs.
Tourettes: multiform frequently changing motor and phonic tics, unknown cause
Combination of euphoria and depression; in kids: continuous, rapid-cycling, irritable, and mixed
symptom state that may co-occur with disruptive behavior disorders
Refuse to go to school on a regular basis or problem staying in school once there
Separation Anxiety Disorder
Extreme anxiety when away from home or separated from parents
Fail to speak in situation where speech is expected or necessary
Oppositional Defiant Disorder (ODD)
Persistent / consistent pattern of defiance, disobedience, and hostility towards authority figures
Fighting, bullying, intimidating, physically assaulting, sexually coercing, cruel to people and
animals, vandalism, theft, truancy, drug and alcohol abuse, precocious sexual activity
Adult Mental Health Disorders
Dementia, Alzheimer’s, Vascular Dementia (TIAs), Creutzfeld – Jakob, Huntington’s refer to table
General Anxiety Disorder
Excessive worry for 6+ mo., focus of worry will shift between things
Obsessive-Compulsive Disorder (OCD)
Persistent, recurring thoughts and obsessions, obsessive behavior with repeated behavios
3 types of attacks: unexpected, situational, and situationally predisposed
Post Traumatic Stress Disorder
Follows exposure to a traumatic event; 3 symptoms: relive the disaster, avoidance behavior,
emotional detachment from others
Social Anxiety Disorder
Extreme anxiety about being judged by others or being embarrassed, cause avoidance behavior
Fear is at a level that is inappropriate and recognized as irrational
Combination of symptoms that interfere with work, sleeping, eating, and social activities
Less severe form of depression, chronic, doesn’t interfere with everyday activities
Cyclic mood swings with mania and depression
Paranoid Personality Disorder
Continual mistrust, view everyone as an enemy, hypersensitive, defensive and antagonistic
Delusional Paranoid Disorder
Persistent non-bizarre delusions without symptoms of any other mental disorder, delusions of
Extremely bizarre delusions or hallucinations; hear voices or believe thoughts are controlled
Antisocial Personality Disorder
Long-standing pattern of a disregard for other people’s rights, can only be diagnosed in ages 18+
Avoidant Personality Disorder
Long-standing & complex pattern of feelings of inadequacy, extreme sensitivity, social inhibition
Borderline Personality Disorder
Labile interpersonal relationships characterized by instability, shallow, impulsive behaviors
Narcissistic Personality Disorder
Pervasive pattern of grandiosity, need for admiration, lack of empathy
Schizoid Personality Disorder
Detachment from social relationships and a restricted range of expression of emotion in
Bones classified by shape: long, short, blat, irregular
Bone tissue: intercellular matrix (fibers, calcium phosphate, strong/rigid structure) and cells
-cytes (mature cells), -blasts (producing cells), -clasts (resorption cells)
Bone remodeling: regulated by stress (weight bearing, mm tension) & hormones (growth, PTH)
Osteoblasts: make collagen/proteins of matrix; osteoclasts: secrete collagenase/degrading
enzymes (regulated by PTH)
Bone tissue: compact: outer covering of bone; cancellous (spongy) interior of bone
Periosteum: fibrous conn tissue cover over bone; endosteum: osteoblast rich lining of medullary
Functions: body movement, body position, stabilize joints, maintain body temp.
Skeletal Muscle: bundles of protein fibers covered by conn tissue, striated, voluntary,
respiration: aerobic and anaerobic, glycogen for energy
Joints: synarthroses (immovable), amphiarthroses (slightly moveable), diarthroses (freely
Disorder Description Treatment
Fracture Bleeding, local inflammation,
necrosis of tissue at the end of
the broken bone
Osteoporosis Decrease in bone mass and Dietary supplements (calcium,
density, loss of bone matrix and vitamin D), weight bearing
mineralization activities, PT, fluoride,
Predisposing factors: 50+ yrs., bisphosphonates, calcitonin
sedentary, hormonal, low BMI,
diet, Asian/European ancestry
Rickets and Osteomalacia Deficit of vitamin D and
phosphates, kids = weak bones,
adults = soft bones
Paget’s Disease Excessive bone destruction with
replacement by fibrous tissue
and abnormal bone
Tumors Common site of secondary Excision of tumor if possible
tumors, majority of primary Surgical amputation
tumors are malignant Chemotherapy
Osteosarcoma: bone pain at rest
Chondrosarcoma: cartilage cells
Ewing’s sarcoma: shaft of long
Muscular Dystrophy (MD) Autosomal recessive disorders, Diagnostic tests: ID genetic
degeneration of skeletal mm, abnormalities, elevated creatine
Duchenne MD most common kinase levels, EMG, muscle
(boys): deficit of dystrophin, biopsy, blood test
skeletal mm replaced by fat and Treatment: no curative
fibrous conn tissue treatment, moderate exercise,
assistive devices, PT/OT,
Osteoarthritis (OA) Degenerative, “wear and tear”, Treatment: assistive devices,
result of increased weight mild exercise program, orthotics,
bearing or lifting, articular massage therapy, PT/OT,
cartilage damage, surface = acupuncture, glucosamine-
rough and worn, bone spurs, chondroitin suppletments,
narrow joint space, injection of synthetic synovial
inflammation, lack of ROM, pain, fluid, NSAIDS, analgesics,
predisposition of falls arthrotomy, jt. replacement
Rheumatoid Arthritis Autoimmune, chronic systemic Treatment: rest/moderate
inflammatory, rheumatoid factor activity, heat/cold, NSAIDS,
(RF), synovitis, red, swollen, glucocorticoids, analgesics,
painful jt., pannus formation, surgery, Drugs
cartilage erosion, fibrosis,
ankylosis, atrophy of mm.,
muscle spasms, contractures,
bilateral joint involvement, jt.
Becomes fixed and deformed,
systemic: fatigue, anorexia, mild
fever, generalized aching
Gout Deposits of uric acid and crystals Diagnosis: examination of
in jt. Causing local inflammation, synovial fluid and blood tests
affects single jt. (hallux), redness, Treatment: reduce uric acid
swelling, pain levels by drugs and dietary
Ankylosing Spondylitis Joint fixation, inflammation of a Treatment: relieve pain and
spinal joint, SI and maintenance of mobility: anti-
costovertebral joints and inflammatory drugs, analgesics,
intervertebral spaces of axial daily exercise, PT/OT
skeleton, fibrosis and
calcification of jts., S&S: LBP,
pain when supine, rigid spine;
systemic: fatigue, fever, weight
Patho Test 6 Review
Skin- body’s largest organ
*Thickest on scalp, palms soles and back (1.4 to 4mm)
*Function:barrier, temp regulation, secretion/excretion, vita D production, immunologic,
Superficial burn- epidermis only
Partial thickness- papillary layer of dermis
Deep partial- damage to reticular layer of dermis
Full thickness- entire thickness to subcutaneous tissue
Subdermal- beyond skin to bone, fat of muscle
Histological Assesment of burn wound:
Zone of coagulation (necrosis)
Zone of stasis (injury)
Zone of hyperemia
Begin in 24-48 hours after burn
Epithelial cells detach from basale layer and migrate toward wound, proliferate by
mitosis and differentiate into mature epidermal cells
Contact guidance and contact inhibition
Rule of nines: front of leg, front upper torso, front lower torso, entire head, entire arm, each are
9% of body when estimating burn coverage. (Genital area 1%)
Treatment of burns:
Silicone pressure garments
Allograft, xenograft, cultured skin, dermal substitutes, synthetic skin
***Never put legs in dependent position without compression. Initially don’t move graft
site! Ambulation guided by physician.
Dermis: made of connective tissue (flexible/ strong), contains nerves(sensory receptors)
and blood vessels.
Skin accessory structures: hair follicles, sebaceous glands, sweat glands, nails.
Subcutanous tissue: below skin includes connective tissue, fat cells, macrophages,
fibroblasts, large blood vessels and nerves.
Contact dermatitis: exposure to allergen (soap), sensitization on first exposure.
Chemical irritation: doesn’t involve immune response.
Urticara (Hives): Type 1 hypersensitivity. Ingestion of substance (shellfish). Lesion pruritic, part
of anaphylaxis (check airway for breathing).
Atopic dermatitis (eczema)- inherited allergy, moist pruritic rash on face/chest in infants. Dry,
scaly in adults. Type 1 hypersensitivity. Treatment: glucocorticoids
Psoriasis- chronic inflam. skin disorder, abnormal T- cell activation, excess keratinocytes.
Lesions on face scalp elbow and knees. Treatment: gluco. Anti-metabolites, UV light
Scleroderma: systemic skin disorder, increased collagen/ inflam. Shiny tight hard areas of skin.
May lead to renal failure, intestinal obstruction, respiratory failure.
Keratoses: Benign lesion assoc. w/ aging/ skin damage.
Seborrheic keratoses- proliferation of basal cells, painless, round, dark, elevated
Actinic keratoses- on UV exposed skin, common in fair skinned, looks scaly and may
develop into squamous cell carcinoma.
Squamous cell carcinoma- painless, malignant tumor of epidermis. From sun, smoking. Slow
growing. Good prognosis with early removal.
Malignant melanoma: highly metastic skin cancer, multicolored w/ irregular border, grows
quickly and changes in appearance.
ABC’s of melanoma: increase in Area. Change in Border. Change in Color. Increase in
Karposi’s sarcoma- occurs in AIDS and other immunocompromised pt.s Purple skin spots.
Senescence: biological processes that lead to aging, begins prior to birth. Also the period from
onset of old age to death.
Cardio changes w/ aging: size/ # of cardiac muscle fibers decrease. Fatty tissue and collagen
accumulate. Reduced strength in contraction. Heart valve thickens, less flexible. Less oxygen to
heart, cardiac reserve diminished.
Arteriosclerosis: loss of elasticity, accumulation of collagen, thickening of arteries
Atherosclerosis- hyperlipidemia, accumulation of cholesterol. Common cause of heart attack.
Osteoarthritis: degeneration of cartilage in joints. Associated with sports injury
Neuro changes with aging: reduction in neurons, lipid accumulation in neurons, loss of myelin,
slower response time.
Vision changes with aging: lens less flexible, yellow, night/ color vision reduced.
Falls account for 70% of all deaths in those over 75. 90% of hip fractures due to fall.
Fall intervention: exercise, decrease meds, pressure stockings, gait training, balance exe.
Geriatric physical exam should include: Up and Go Test, Tinetti gait and balance test.
Amenorrhea: no menstruation
Dysmenorrhea: painful menstruation due to excess release of prostaglandins.
Menorrhagia: increase flow
Metrorrhagia: bleeding btwn cycles
Polymenorrhea: short cycles less than 3 wks
Oligomenorrhea: long cycle more than 6 wks.
Endometriosis: endometrial tissue occurs outside uterus. Bleeding/ pain
Candidiasis: not sexually transmitted. Caused by fungus. Opportunistic infection by normal flora
of vagina. White curdlike discharge. Antifungal treatment.
Pelvic Inflammatory disease: infection of uterus, fallopian tubes or ovaries. Originates from
lower reproductive tract. Arises from STD, non sterile abortion or postpartum. Potential
complications: peritonitis, pelvic abcesses, septic shock.
Signs: pain, high temp, guarding, nausea, leukocytosis, purulent discharge. Rx: antibiotic
therapy in hospital.
Leiomyoma: benign tumor of myometrium, well defined encapsulated masses. Surgery or
hormonal therapy for treatment.
Ovarian cysts: last 8-12 wks. Multiple small fluid filled sacs requiring surgical removal if
bleeding is present. ID with ultrasound.
Polycystic ovarian disease: fibrous capsule thickens around follicles of ovary. Hereditary,
absence of ovulation and infertility. Hormonal imbalance, amenorrhea, hirstuism. Rx: surgical
wedge resection of pharmacology.
Fibrocyctic breast disease: cyclic occurrence of nodules or masses in breast tissue
Carcinoma of breast: increase after age 20, usually unilateral, metastasis via lymph nodes.
Predisposing factors: family hx, BRACA gene, late 1st pregnancy, sedentary lifestyle,
smoking, high fat diet.
Cervical cancer: usually due to HPV, Pap Smear can ID early.
Carcinoma of uterus: vaginal bleeding early sign.
Risk factors: over 50 y.o., high dose estrogen without progesterone, obesity, diabetes.
Pap smear down not detect. Slow growing but invasive.
Ovarian Cancer: no reliable screening, detected by pelvic exam.
Risk factors: BRACA gene, early menarche, obesity, late first pregnancy, fertility drugs.
Oral contraceptives are protective.
Pregnancy terminology: number of term infants, pre- term, abortions, kids currently alive (3-0-0-
Avoid modalities on pregnant women.
Ectopic pregnancy: implantation outside the uterus
Prostatitis: inflammation of prostate.
Acute bacterial: gland swollen, tender, bacteria in urine.
Non-bacterial: urine has leukocytes
Chronic bacterial- gland slightly enlarged, dysuria, frequency/ urgency.
Bacterial infection- from e-coli
Occurs in: young men w UTI’s, old men w/ prostatic hypertrophy, w/ STD’s,
through a catheter and bacteria.
Signs: low back pain, decrease urinary stream, muscle aches, anorexia, fever etc.
Benign prostatic hypertrophy: signs- obstructed urinary flow, dribbling, nocturia etc.
Cancer of prostate: often androgen dependent. Hard nodule on periphery of gland, hesitancy in
urinating, recurrent UTI, etc. Diagnosis by serum marker: PSA, prostate specific antigen and
prostatic acid phosphatase.
Testicular cancer: most common solid tumor cancer in young men. Self exam preventative.
Biopsy not performed. Tumor markers: hCG and AFP. Ultrasound
Chlamydia: most common STD.
Males: itchy, white discharge, painful swollen scrotum.
Females: no symptoms until PID or infertility. May infect newborn.
Gonorrhea: males: inflammation of urethra
Females: asymptomatic until PID. May cause blindness in newborns.
Syphillis: chancre at site of infection. Painless firm ulcerated nodule, 3 wks after exposure. If
untreated flu like illness with rash. Tertiary stage: dementia blindness. Rx: antimicrobials.
Genital herpes: blisters on genitals, itching, painful. Antivirals.
Genital warts: HPV, incubation up to 6 months, asymptomatic, may predispose to cervical or