DIABETES

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PNEUMOTHORAX Persistent obstruction of nostrils with

Def Collection of air b/w visceral and parietal pleura sniffing, sneezing, and nasal discharge.

PP 20 000 spontaneous ./ year  Allergic Conjunctivitis- redness / swelling,

o

1 Spontaneous- tall, thin, male, smoker, 20-40 During summer (Hayfever) or throughout the

o

2 Spontaneous- COPD, male, >40 year (Perennial rhinitis).

Cause

o

1 SPONTANEOUS  NB: Most atopic pts have +ve skin tests to

Most common type common allergens (house dust mite, pollen,

Tx recommended after 2nd time animal danders), eosinophilia,  IgE.

 Med- insertion of Bleomycin / Talc Paeds Moderate if:

  - Abrasion of Pleural lining Aged 92%

> Serious than Primary due to  respiratory reserve Severe if:

TRAUMATIC / IATROGENIC   RR 50 / min, HR 140, PF 50% predicted.

Trauma- RTA, Stabbing, Rib Fracture  Too breathless to speak / feed.

Iatrogenic- Pleural Aspiration, Bx, Central Line Insert  Sats: 5.

ECG  Tachycardia, T wave inversion CXR  Hyperinflation, Exclude Pneumothorax

Tx O2 + Analgesia ABGs (acute)  Resp Alkalosis (Due to  PCO2)

SMALL CXR in week  Severe =  PO2

50% hemithorax Check CXR afterwards  Salbutamol (Neb)  Bronchodilation

LARGE Chest Tube  Hydrocortisone/ Prednisolone (IV)  Inflammation

TENSION Immediate needle decompression  Ipratropium Bromide  Muscle spasm

Chest Tube  Mg Sulphate  Bronchodilation

 Antibiotics) If signs of infection

ASTHMA  (Aminophylline #...)  Bronchoconstriction

Def Chronic airway inflammation characterised by 3 elements:  Intubate If still failure to respond

 Chronic airway secretions and inflammation NB: Nebulise with O2 for Asthma, with Air for COPD

 Bronchial hyperactivity As with any O2 [except*], after starting O2, ABGs / oximetry should be

 Reversible airway obstruction repeated adjusting inspired oxygen concentration to achieve PaO2

PP  FHx; 7% adults, 15% children; >59mmHg (7.8kPa) / SaO2 > 90%.

 Childhood: ♂>♀. Adolescence ♂=♀.  *COPD: Hypoxic drive

 10-20% Acute Paediatric (1-16) admissions  *Premature Infants: Risk of retrolental fibroplasias, which may

 15 child deaths / year.  blindness. Condition is caused by blood vessels growing

 Prevalence  if:  weight / passive smoking / bottle fed. into vitreous  fibrosis. Low birth weight v. premature infant is

 Geography: > in NZ, Australia, UK. severe if # …if failure to respond to

 …pollen, dust mites  Pulse > 110 bronchodilator: ECG & Electrolyte

 Intrinsic- Non immune triggers:  RR > 25 monitoring needed since S/Es

 …aspirin (10%), pollution, cold, stress, exercise, B-  PEFR 3x/52, waking

 , exacerbation in last 2 yrs  2)

Bronchial Hyperactivity + TRIGGER FACTORS STEP 2: REGULAR PREVENTER THERAPY: All

(Mast cells [via IgE mech]  Histamine + prostaglandins)  1 + Low dose steroid-Beclomethasone (Bd 200mcg adults/ Bd

 100mcg children)

Bronchoconstriction STEP 3: ADD ON THERAPY: Adults / children > 5

 Capillary Permeability (oedema) 

st

(1 ) 1 to B2 agonist: Long acting- Salmetarol (Bd 400mcg

 Mucous production adults/ Bd 200mcg children >5 +/- spacer)

  (2nd) No response  +/- LABA (depending if helping or not) +

Airway narrowing  2 (800mcg, 400mcg / day)

  (3rd) Still No response  Leukotriene R antagonist /

Symptoms Theophylline / Slow release B2 tabs (Latter: Adults only)

  > 2  Leukotriene R antagonist

S&S NORMAL Wheeze, SOB, Cough (Esp ), Tight chest,   50mmHg

smoking). FEV1 is liable to Dyspnoea, abnormal S&S.

collapse during expiration. 60 Dyspnoea on exertion, Inh Anticholinergic + PRN B2

S&S: (Blue Bloaters: Blue from hypoxia, bloater from ascites -RHF) Cough & Sputum, Some agonist

Main Pc is SOB as opposed to Asthma where the complaint is cough. COPD 50 abnormal S&S. Reg B2 agonist. Flu vacc

patients are used to coughing due to smoking. 40 Dyspnoea on mild exertion, Pulmonary Rehab. ID and

Predominant PINK PUFFERS- BLUE BLOATERS- Hyperinflation & cyanosis, TxObesity,  nutrition,

Disease Emphysema Chronic Bronchitis Wheeze & Cough. depression, social isolation

Body Size Thin Obese 20 Death Amb O2 + inh steroids

Hyperinflation Marked + barrel chest Present Comp  Bullae (Thin walled air spaces caused by rupture of alveolar

Post mortem Panacinar Centrilobar emphysema walls), Pneumothorax (Rupture of bullae), Respiratory Failure,

finding emphysema Cor Pulmonale

Cor pulmonale Absent Present Prog  Inversely related to age

2o Polycythaemia  Directly related to post bronchodilator FEV1.

Cyanosis Absent Centrally  Poor prognostic conditions: Pulmonary HT, PaCO2 that

Corpulmonale No Yes- oedema reverts to N on recovery (assoc with survival of 3 years).

Dyspnoea Severe Exertional

Cough  Productive- esp mornings PNEUMONIAS

due to regen of cilia Df Lower respiratory tract infection associated with

Blood gases  PCO2 / N  PCO2  Inflammation, Alveolar exudates, Consolidation

Severe: Reflect … P  10% pts admitted to H RISK FACTORS:

I …Pulmonary hyperinflation, hypoxaemia, cor pulmonale, polycythaemia. P  Incidence:1-3/1000 Immunosupression

INSPECTION Neurological impairment of cough reflex

C COMMUNITY ACQUIRED (Dysphagia, OH, Epilepsy  Aspiration)

F  Flapping tremor (Hypercapnia)

1. Strep pneumoniae (65%) Secretion retention

 Pursed lip breathing- physiological response to  air trapping

A 2. Haemophilus influenzae Pulmonary Oedema

  JVP

3. Mycoplasma Pneumonia I

 Accessory muscles of respiration: Sternomastoid, Scalenes.

U 4. Staphylococcus Aureus Resp Tract Infection

 Excavation of Suprasternal fossae, Supraclavicular fossae.

 Tracheal tug on inspiration Antibiotics

S  Indrawing of Costral margins, Intercostal spaces. S Tracheal instrumentation (Surgery)

  AP diameter of chest relative to lateral diameter loss of cardiac HOSPITAL ACQUIRED Impaired alveolar macrophages

E dullness on CXR E 1. Staphylococcus Aureus Other eg Age (Elderly, Children Tracheal Deviation Away from Effusion if large

common bronchial. DDx

Tachypnoea, Chest dull on percussion,  Tactile & Vocal fremitus / Inv / Only detected: CXR when volume > 300 ml; Clinically when >500 ml

resonance, Pleural rub, Bronchial Breathing, Cyanosis, Confusion, Dx CXR Effusions (dense uniform opacities) at costophrenic angles

Hypotension,  Expansion (sign of consolidation) US Examination for tumours and diaphragm

DDx Asp Pleural Aspiration + Bx (US guided). As well as determining

Inv / CXR  Consolidation, Shadowing, Pleural Effusions, protein levels, Test for Glucose, Cytology, Culture. Glucose

Dx Petchy Shadows, Pneumatoceles, Lung Cavitation, may be  in RA / SLE / TB / Malignancy.

Lobar / Multilobar More ESR, Amylase, Albumin, TFTs, BC,

FBC   WCC ( WCC = poor prognosis) Tx  Drain or Repeated Tap (+ CXR to check for iatrogenic

LFTs  Legionella / Mycoplasma infection pneumothorax). Don’t’ remove > 1000 ml at one time.

CRP   Pleurodesis e.g. Bleomycin if malignant effusion.

ABGs   PO2 Mx 

Serol  Sputum gram stain Comp

B Cult 

PULMONARY OEDEMA

RADIOGRAPHIC FEATURES OF PNEUMONIA Def  1 of 3 forms of cardiac dyspnoea (2 others: Angina & CHF)

 Diffuse extravascular accumulation of fluid in pulmonary tissues

and air spaces due to changes in hydrostatic forces in

Homogenous Patchy shadows capillaries or to  capillary permeability.

(lobar) seen in many PP

consolidation as pneumonias but Cause  Capillary  LHF: Atrial, e.g. MS; Ventricular, e.g. MI, HT

seen in 80% Strep especially Pressure  Pulmonary venous obstruction

Pneumoniae Mycoplasma  IV fluid overload, e.g. from blood transfusion

pneumoniae  Capillary  Pneumonia, DIC, Renal F, ARDS

(50%) Permeability  Toxins (inh) e.g. Chlorine, Mustard Gas

 Toxins (circ) e.g. Histamine, Septicaemia

Progression of  Oncotic  Any cause of hypoalbuminaemia e.g. Nephrotic

shadowing to both Pneumatocoeles Pressure Syndrome, Liver Cirrhosis

lungs especially in as seen with Lymphatic  Any Obstruction e.g. Tumour,Parasitic Infections

Strep pneumoniae Staph aureus Other Causes   ICP, PE, PIH, High Altitude, Heroin OD

and Legionella infection Path  In Left ventricular diastolic pressure

pneumophillia



LHF  Pressure in LA, Pulmonary veins, Pulmonary capillaries.



Pleural effusions Lung cavitation When hydrostatic pressure of pulmonary capillaries > oncotic

as in any often in pressure of plasma (25-30mmHg), fluid moves from capillaries to

pneumonia but pneumonia causes alveoli

especially Staph by Staph aureus 

aureus and Strep and aspergillus Vagus nerve and Hering Breuer reflex

pneumoniae 

Rapid shallow respiration

Tx Admit if > CURB-65: Confusion (Mental Test score 7), RR  (>30), BP, >65 Years.

congestion at apices of lungs), Orthopnoea, PND.

 Unable to speak, distressed, agitated.

 O2

 Cyanosed, sweaty, pale.

 Antibiotics….… Amoxicillin (Community)

 Respiration:  + Use of accessory muscles.

 Antibiotics….… Cefotaxime (Hospital)

 Coughing, Wheezing.

 IV fluids………..if anorexia / dehydration / shock

 Sputum: Profuse, Frothy, Pink / Blood stained.

 Analgesia……..Paracetamol

 Extensive crepitations and rhonchi.

Mx PREVENTION: Offer pneumococcal vaccine to those with:

 Signs of Right heart failure e.g.  JVP

 Chronic heart conditions, Lung conditions, Cirrhosis,  Cheyne stokes if severe: waxing and waning ventilation,

Nephrosis, Dm, Immunosuppression

sometimes with periods of apnoea, that occur in cycles. Due to

Comp Pleural Effusions, Empyema, Lung Abscesses, Meningitis,

delay in medullary chemoreceptor response to blood gas .

Respiratory F, Septicaemia, Pericarditis, Cholestatic Jaundice

DDx

Inv CXR Ground glass appearance: alveolar oedema

PLEURAL EFFUSIONS

ECG MI?

Def  Fluid in the pleural space

U&Es

 TRANSUDATIVE (Protein content than normal.

 SVC Obstruction, Cons Pericarditis, Hypothyroidism

Mx  SIT UP PATIENT

 EXUDATIVE (Protein content > 25 g / L)

 O2: High flow 100% (So long as no COPD)

  Microvascular permeability due to disease of  MORPHINE: Alleviates SOB. Reverses peripheral

pleural surface itself / injury in adjacent lung… vasoconstriction reflex (so long as no COPD)

 Infective: Pus / Pneumonia  DIURETIC: Furosemide (Vasodilating action)

 Inflammatory: TB / SLE / RA / PAN.  NITRATE: GTN until clinical improvement or BP  by 10mm.

 Malignant: Bronchial / Mesothelioma / Myeloma / HL  If above Fails:

 Misc: Pulmonary Infarct / Pancreatitis / Uraemia.  Inotropic agents: To stimulate heart…or

 Drugs: Methotrexate, Sulphonamides  Vasodilators (more powerful):  Left ventricular load.

 UNILATERAL Prog

 BILATERAL often occurs in: Cardiac failure, Connective tissue

disorders, Hypoproteinuria. PULMONARY EMBOLISM

CAUSE TYPE OF FLUID PREDOMINANT FLUID CELLS Def Occurs when clot from vein, originating in venous sinuses of calf /

CARDIAC Transudate Few serosal cells femoral vein / pelvis, detaches  Lodged in pulmonary arterial tree.

TB Exudates Lymphocytes PP  Present in 60-80% with DVT, even though > ½ asymptomatic.

MALIGNANT Exudates (+ Blood) Serosal cells & lymphocytes  Third most common cause of death in hospitalized patients

Often clumps of malignant cells Cause

PULMONARY Exudate (rarely RBCs, Eosinophils

INFARCTION transudate) (+/- Blood)

RA Exudates Lymphocytes

SLE Exudates Lymphocytes and serosal cells

PANCREATITIS Exudates (+/- Blood) No cells predominate

Path 

S&S Asymptomatic, SOB (related to size), Pleuritic chest pain

Chest Expansion  on Affected side

(Often Percussion Stony dullness over Effusion



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CHANGES IN THE VESSEL WALL: ECG  Arrhythmias, Bundle BB.

 Previous thrombo-embolism PFTs  May be N. May show  lung volumes, impaired gas

 > 40 years transfer and restrictive ventilator defect.

 Smoking Bx  Dx: Shows noncaseating granulomata (May be

 Local trauma taken from lung, liver, lymph nodes, skin nodules,

 Obesity lacrimal glands).

Lavage  Bronchoalveolar Lavage: Shows  lymphocytes

inactive disease.  Neutrophils with pulm fibrosis

 BLOOD COAGULABILITY  BLOOD FLOW / STASIS

 Malignancy  Surgery US  Nephrocalcinosis, Splenomegaly

 Oestrogen:  Immobility Bone  XR: Punched out lesions at terminal phalanges

 OCP, HRT  Bed rest RadioA  Gallium, Thallium Scans may indicate distribution of

 Pregnancy  Paralysis active granulomata

 Blood disorders:  Obesity CT/MR  Assessing severity of pulmonary disease or

 Polycythaemia  Cardiac failure neurosarcoidosis.

 Thrombocythaemia  Dehydration Opthal  Slit lamp / Flurescein angiography in ocular disease.

 Anti-phospholipid syndrome Mx  BHL needs no Tx as most recover spontaneously.

 Acute: Bed rest, NSAIDS, Corticosteroids.

S&S SOB, Pleuritic Chest Pain, Haemoptysis, Dizziness, Syncope  Indications for corticosteroid Tx: Parenchymal Lung disease,

Right Ventricular Strain:  JVP, Central Cyanosis, RV heave, Uveitis, Hypercalcaemia, Neurological / Cardiac involvement.

Tachycardia, Hypotension, AF Prog  60%: Pts with thoracic sarcoidosis  spontaneous resolution

Pleural effusion:  AE, Crackles; Pyrexia, Pleural Rub within 2 years. 20%: Respond steroid Tx. 20%:  Improvement.

DDx CHF, Aortic dissection, Pericarditis, Cardiac Tamponade, Pneumonia,  Likelihood of regression for pulmonary disease correlates with

Bronchitis, COPD, Asthma, Pleural Effusions, Pneumothorax, MS extent of parenchymal disease, as noted by CXR stage.

Chest pain, Anxiety, GORD

Inv / FBC  HB? Need to know if anticoagulant Tx TUBERCULOSIS

Dx  Platelets:  clotting? Def  Disease caused by infection with mycobacterium tuberculosis

 WBC: Cellulitis? PP  WORLDWIDE: 1.7 B infections, and 2M deaths / year.

U&E   PREVALENCE: Countries of Asia e.g. India, China, Indonesia,

CXR  Dilated pulmonary A, small pleural effusions, Pakistan and Bangladesh have largest number of cases.

Wedge shaped infarct  INCIDENCE:  in parallel with a global epidemic of HIV.  in

ECG  Often No Change! May only be Tachycardia. UK from 120, 000 in 1913  5,000 in 1987  7000 in 2002.

 V1: Tall R Waves  RISK IN DEVELOPED WORLD: Alcoholics, Undernourished,

 V1-3: T Wave Inversion Ethnic Communities, Elderly, HIV, Pts after gastrectomy for PU.

 Inf: P Pulmonale (Peaked P Waves)  SEX: Young: F>M. Older: M>F

 RBBB, R axis deviation  AGE: > 60% aged 25-64 years but risk highest in over 65s.

 Deep waves in: Si / Qiii / T(inversion) iii Path  ORG: Mycobacterium tuberculosis (Humans are only known

ABGs   PO2,  PCO2, ( pH) reservoir)

D Dimers  Use to Exclude PE / DVT. Also DIC, Post OP  SPREAD: Airborne droplet

  In many situations  RESIDENCE: Droplets deposited within terminal airspaces.

 +PV: 44%, -PV: 98% Upon encountering bacilli, macrophages ingest & transport

VQ / Spiral CT / (CTPA: not used so much anymore) bacteria to regional lymph nodes.

Tx  O2 & IV Access  FATE OF TB- One of four choices:

 Morphine  1) Killed by immune system

 LMW Heparin  2) Multiply and cause primary TB

 Immediate Surgery: If severe causing CV Collapse.  3) Become dormant and remain asymptomatic, or

 BP: 90: Warfarin disease). Reactivation may occur following 2 or 3.

Mx  Don’t fly / dive for 2 weeks  GROWTH: Slow-growing, requiring 4-8 /52 for visible growth on

 Wear Thromboembolism Stockings solid medium

 Stop Hep when INR > 2  INFECTIVITY:

 Continue Warfarin for 3-6/12 –Aim for INR of 2-3 Prev BCG vaccination  80% protection 15 years when given in schools

Comp programme, but in older patients there is White. M>F (2:1) T TUBERCULOUS MENINGITIS:

Path  O  Headache- Intermittent / Persistent for 2-3 weeks.

S&S AYSYMPTOMATIC: M  Mental status changes  Coma over days to weeks.

 20-40%...Dx incidentally on CXR S  Fever may be low-grade or absent

ACUTE SARCOIDOSIS: SKELETAL TB:

 Erythema nodosum +/- polyarthralgia.  Spine is most common site (Pott disease). Back Pain Or

PULMONARY DISEASE: Stiffness. Lower extremity paralysis (50%)

 90% abnormal Xray with bilateral hilar lymphadenopathy (BHL)  Arthritis: Usually involves 1 joint only. Hip / Knee > Ankle,

+/- Pulmonary infiltrates, Fibrosis. elbow, wrist, and shoulder

 S&S: Dry cough, Progressive SOB,  Exercise tolerance,  Pain may precede XR  by weeks - months.

chest pain. GENITOURINARY TB:

 In 10-20%, S&S progress with deterioration in lung function.  Flank pain, dysuria, frequency.

NONPULMONARY MANIFESTATIONS  In men, genital TB S&S: Epididymitis or scrotal mass.

SWOLLEN Lymphadenopathy, Hepatomegaly, Splenomegaly  In women, genital TB S&S may mimic PID. TB  10% sterility

EYES Uveitis, Conjunctivitis, Keratoconjuctivitis sicca, in women worldwide and 1% in industrialized countries.

Glaucoma GASTROINTESTINAL TB:

BONE Terminal phalangeal bone cysts  Any site along GI Tract may be infected. S&S relate to site.

 Nonhealing ulcers of mouth or anus;

GLANDS Enlarged lacrimal / parotid glands; Pituitary

 Difficulty swallowing with oesophageal disease;

dysfunction

 Abdo pain mimicking PUD with stomach / duodenal infection;

NEURO Bell’s palsy, Neuropathy, Meningitis, Brainstem /

 Malabsorption with infection of small intestine;

Spinal syndromes, Space occupying lesion

 Pain, diarrhoea, or hematochezia with infection of colon.

SKIN Erythema nodosum, Lupus pernio, Subcut nodules

TUBERCULOUS LYMPHADENITIS (scrofula):

HEART Cardiomyopathy, Arrhythmias

 Most common site is in neck along sternocleidomastoid muscle.

RENAL Hypercalcaemia, Renal Stones  Usually unilateral, with little or no pain.

DDx  Advanced disease may suppurate and form draining sinus.

Inv / Bloods   ESR, Lyphopenia, Abnormal LFTs,  ACE,  Igs CUTANEOUS TB:

Dx Urine   Ca  Direct inoculation may  Ulcer or wartlike lesion.

CXR  Abnormal in 90%. Staging as follows:  Contiguous spread from infected lymph node  Draining sinus.

 0: Normal  Haematogenous spread  Reddish brown plaque on face /

 1: BHL (Bilateral Hilar Lymphadenopathy) extremities (lupus vulgaris) / tender nodules or abscesses.

 2: BHL + Peripheral Pulmonary Infiltrates S  PULMONARY TB: Abnormal breath sounds, esp over upper

 3: Only Peripheral Pulmonary Infiltrates I lobes or areas involved.

 4: Progressive pulmonary fibrosis; bullae formation G  EXTRAPULMONARY TB: Differ depending on tissues involved.

(honeycoming); pleural involvement. N May include confusion, coma, neurologic deficit, chorioretinitis,

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S lymphadenopathy, cutaneous lesions (as described above).  Organisms most commonly involved are aerobic and

DDx Bronchiectasis, Crohn Disease, Histoplasmosis, Lung Abscess, Lung anaerobic streptococci, Staphylococcus aureus and variety of

Cancer, Miliary TB, Pericarditis- Constrictive, Pneumonia- Fungal, different gram-negative organisms.

Sarcoidosis.  Anaerobes normally found in oral cavity occur exclusively in

Inv / Hx Suspect Pulmonary TB with >3/52 unexplained cough esp if 60% of cases - inc Bacteroides, Fusobacterium, Peptococcus.

Dx additional: Haemoptysis, SOB, Appetite , Weight , Fever Organisms may be introduced through:

& Sweats (Nocte), Fatigue, Swollen glands… URGENT…  Aspiration (Most common cause. See risks.)

CXR  Antecedent primary bacterial infection (Pneumonia, TB)

Always compare previous XR if possible:  Septic emboli (Endocarditis, Thrombophlebitis from systemic)

 Primary TB: F (2:1)

abscess. Most pts with severe disease  Respiratory failure. Cause Unknown: But thought there is alteration in cell-mediated immunity,

LUNG ABSCESS perhaps activated T lymphocytes  fibroblastic activity

Def  Confined area of suppuration within lung parenchyma. It is Assoc  Polyarthritis - 10% of cases have RA (RF +ve in 35%).

PP  More common in: Alcoholics, Elderly, Debilitated (prone to  Autoimmune chronic hepatitis in 5 - 10% of cases

aspiration), IV Drug abusers. M>F (Slight)  Thyroid disease, SLE, Systemic Sclerosis, Dermatomyositis

 Incidence  due to ABx Tx of Lower RTI,  Childhood TB. S&S  Panting SOB

Cause  Infection and necrotic tissue  Development of abscess.

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 Exhaustion on effort (amount needed decreases)  Giant cell carcinoma

 Dry cough  Clear cell carcinoma

 S&S: Hypoxia, Cardiac F, Bronchopulmonary infection  MISCELLANEOUS TUMOURS

 Terminal Stages: Respiratory failure and pulmonary embolism  Bronchial carcinoid carcinoma

 Dyspnoea And Tachypnoea (Cyanosis if severe)  Bronchial gland carcinomata:

 Clubbing (> 50% cases)  Adenoid cystic carcinoma

 Auscultation: Fine Crepitations marked at end of inspiration  Muco-epidermoid carcinoma

('velcro-like' crackles). Wheezes are rare.  Others

DDx Bronchiectasis: Longstanding productive cough + purulent sputum. Stage  Staging important in determining: Prognosis, Appropriate Tx

Transfer factor is not . Usually airway obstruction and dyspnoea.  Non-small cell lung tumours staged using TNM model.

Causes of Upper Zone Fibrosis…BREAST! Most important are S&T:  Small cell lung tumours are staged differently:

 Berylliosis, Radiation, Extrinsic Allergic Alveolitis (e.g. Stage 0: Carcinoma In Situ I.e.

Farmer’s Lung): Hx of exposure to organic dusts, Ankylosing Stage IA: T1N0M0

Spondylitis, Sarcoid, TB No Nodes

Stage IB: T2N0M0

Causes of Lower Zone Fibrosis…Connective Tissue Disorders: Stage IIA: T1N1M0

 SLE, RA, Sceroderma. Nodes

stage IIB: T2N1M0, T3N0M0

 Drugs: Cytotoxics, Amiodarone, Nitrofurantoin. Stage IIIA: T3N1M0, T1N2M0, T2N2M0, T3N2M0

 Occupational lung diseases: Silicosis, Asbestosis. > Growth.

Stage IIIB: T4N0M0, T4N1M0, T4N2M0,

Inv / CXR  Main: Ground glass haze at lung bases. > Nodes

T1N3M0, T2N3M0, T3N3M0, T4N3M0

Dx  Others: Streaky wisps of shadow with elevation of Stage IV: M1 with any T or N Mets

diaphragms suggesting basal collapse. Miliary mottling.

S&S  Lung  should be suspected in any pneumonia which is slow to

Honeycomb lung develops as condition progresses

resolve / recurrent, or who presents with a pyrexia of unknown origin.

and lung function lost

LOCAL EFFECTS:

Bloods  ESR , Gamma-globulin 

 INTRA-PULMONARY: Invasion of Tissue…

 Anti-nuclear factor +ve in 45%, RF in 35%

 Cough, Poorly localised chest pain, Haemoptysis

CT  Sensitive for diagnosis and monitoring

 INTRA-PULMONARY: Airway Obstruction…

Bronch-  Neutrophils +/or Eosinophils 

 Dyspnoea, Wheeze / stridor, Pneumonia,

oscopy  Lymphocytes may also 

Bronchiectasis, Lung abscess, Lobar collapse

PFTS &  RESTRICTIVE DEFECT  INTRA-THORACIC INFILTRATION: Apex

 Lung Volumes . Lung Compliance 

 Horner's syndrome due to sympathetic ganglion

ABGs  Blood Gases N until advanced disease when there invasion by pancoast's tumour

may be arterial hypoxaemia and hypocapnia

 Rib destruction

Tx  OXYGEN: Palliates S&S of breathlessness.

 Arm pain & weakness due to brachial plexus invasion

 STEROIDS (Prednisolone): S&S in ½.  Lung function in ¼.

 INTRA-THORACIC INFILTRATION: Left hilum:

 IMMUNOSUPPRESSIVE Tx (Azathioprine)

 Hoarseness due to recurrent laryngeal nerve invasion

 LUNG TRANSPLANT: Consider is no response to above

 INTRA-THORACIC INFILTRATION: Mediastinum:

steps. Survival after 1 year: 80%; Survival after 3 years: 55%

 ANTIFIBROTICS (pirfenidone): May improve survival but more  Cardiac tamponade or pericardial invasion

evidence needed.  Arrhythmias

 Dysphagia due to oesophageal invasion

LUNG CARCINOMA  Diaphragmatic palsy due to phrenic nerve invasion

Def  Bronchial carcinomata so common that lung  & bronchial  Central chest pain due to chest wall invasion

 INTRA-THORACIC INFILTRATION: Chest wall invasion:

carcinoma appear synonymous. Further confusion due to fact that not

all bronchial carcinomata derived from bronchi, e.g.  Pleural effusion, Pleuritic chest

bronchioloalveolar carcinomata found peripherally and derived from  INTRA-THORACIC INFILTRATION: Right paratracheal:

bronchioles. Clinically lung  divided: Small cell & Non-small cell.  Superior VC obstruction (SVC compression / invasion)

PP  Common: Accounts for 1 in 8 cases and 17% of cancer deaths. EXTRA-THORACIC METASTASES

 Relative risk of death related to no of cigarettes smoked / day:  Anorexia, Weight  and Lethargy frequently indicate

 Non-smokers: 0.07 lung cancer deaths/year/1000 disseminated disease. Distant metastasis is…

 > Common with, SCC followed by

 1-14 cig/day: 0.78 lung cancer deaths/year/1000

adenocarcinoma & LCC.

 14-24 cig/day: 1.27 lung cancer deaths/year/1000

 24 cig/day: 2.51 lung cancer deaths/year/1000

 Secondary spread may occur to virtually any part of

 M>F (7:1); Ratio  as incidence of bronchial C in ♀ .

body. Most common sites are: Brain BALL: Brain,

 Peak in 70s (♂) & 80s (♀). Rare 90% Patients are symptomatic at Dx.

 Marrow involvement occurs in 10-20% of cases of

Cause  SMOKING: Most important cause: 90% ♂ & 80% ♀. Others…

advanced small cell carcinoma and may  leuco-

 ASBESTOS: Blue asbestos (Crocidolite) poses greatest risk.

erythroblastic anaemia. However, anaemia in lung 

Assoc with pleural mesothelioma and bronchial carcinoma

 DUST: Containing arsenics, dichromates, chromates, nickel is usually due to due to non-specific effects of

malignancy.

 COAL: Tar and products of coal combustion

 CHRONIC INFLAMMATION: NON - METASTATIC : ENDOCRINE

 Predisposes to Alveolar cell carcinoma

Small  Hypercalcaemia: 6-7% tumours. Usually  Ca of

 malignancy. In squamous cell carcinoma, may be due

 Associated with adenocarcinoma of the lung

ADH, to PTH-like peptides

 IONISING RADIATION

 Tumours assoc occupational factors are > likely adenocarcinomas.

ACTH  Dilutional hyponatraemia: 10% of small cell

carcinoma. Due to ADH-like peptides

Path  Lungs are common site for met spread from distant 1o neoplasms.

&  1o Tumours of lung divided into following however to simplify…

(Think  Cushing's syndrome: Ectopic ACTH-like peptide

AA tits commonly produced by small cell tumours but

Class Small Cell (SCLC.. 70% Mets) / Non Small Cell (NSCLC..40% Mets): are

 BENIGN TUMOURS symptomatic 50% of squamous cell tumours. Unusual

Sqam in small cell tumours.

diameter, ‘coin lesion’]. Mesenchymal in 

origin & usually composed of mature, hyaline  Hypertrophic pulmonary osteoarthropathy

PTH

cartilage. PP: Middle / Elderly Men.  Gynaecomastia

 Rarely symptomatic. Tx: Sx- Resection. NON - METASTATIC : NEUROLOGIC

Prog: V Good  Uncommon, occurring in Common: Peripheral neuropathy, Cerebellar

 Squamous cell carcinoma (40 % of all lung cancers): degeneration / ataxia

 Spindle cell (squamous) carcinoma  Rare: Encephalomyositis, polymyositis /

 Small cell carcinoma (20-30 %): dermatomyositis, Lambert-Eaton myasthenia gravis

 Oat cell carcinoma DERMATOLOGIC Associations

 Intermediate cell type  Erythema gyratum repens (Irregular wavy bands)

 Combined oat cell carcinoma  Acanthosis nigricans (Dark hyperplasia of creases)

 Adenocarcinoma (20%):  Erythroderma (Generalised redness of the skin)

 Bronchial derived adenocarcinoma:  SUMMARY LOCAL:

 Acinar adenocarcinoma  Hoarseness

 Papillary adenocarcinoma  Cough

 Solid carcinoma with mucus formation  SOB (obstruction / pleural effusion)

 Bronchioloalveolar carcinoma  Haemoptysis

 Þ Large cell carcinoma (10-15%):

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 SUMMARY PARANEOPLASIA:  Pneumonia

 Neuro  Aspiration

 Skin  Congestive HF

 Weight , Bone pain, Seizure, Ascites,  Pulmonary embolism

Lymphadenopathy CHRONIC COUGH

DDx  Post nasal drip secondary to nasal or sinus disease.

Inv / CXR Posteroanterior and lateral films.  Asthma

Dx Histo / Cyt Confirmation of diagnosis: Histological diagnosis;  GORD: May require ambulatory pH monitoring / anti reflux Tx.

Cytology of sputum and bronchoscopic washings  Pertussis

Bx Confirmation of diagnosis:  Intrabronchial tumour

 Proximal lesions - Bronchoscopy  Foreign body

 Peripheral lesions - Percutaneous biopsy C Serous Pulmonary Oedema

 Pleural effusions - Aspiration and biopsy O Bronchoalvelola cell carcinoma

 Lymph nodes L Mucoid Chronic Bronchitis

Tissue Dx required in majority, esp those under 70 yr, O COPD

in order that appropriate Tx can be given. U Asthma

Confirmation of diagnosis: R Purulent Infection

CT scan - Assessment of spread: Useful for showing  in Rusty Pneumococcal Pneumonia

mediastinum, e.g. local spread of tumour, enlarged Assoc Stridor Indicates partial obstruction of major airway. Eg.

o

lymph nodes, and for showing 2 spread to opposite Laryngeal oedema / Tumour / Inhaled foreign body

lung which may be too small to see on CXR

Barium Assessment of spread: May show oesophageal HAEMOPTYSIS

Swallow compression by enlarged mediastinal nodes Def  A clear Hx must be taken to maintain that there is true

Bone scan Assessment of spread haemoptysis and NOT epitaxis (nosebleed).

Bloods:  May help to indicate disseminated disease  Always assume there is a serious cause until following have

FBC, U+E,  Small cell tumours may secrete substances e.g. been ruled out: Bronchial , Thromboembolic disease, TB etc

2+ Causes *: More Common Causes

LFTs, Ca ADH  hyponatraemia…ACTH  Cushing's.

ADH,  Squamous cell carcinomas may secrete PTH- BRONCHIAL  Carcinoma*- (Hx & appears streaky)

ACTH like substances producing hypercalcaemia DISEASE  Acute bronchitis*

Mx: Treatment for NSCLC: Sx Excision:  Bronchiectasis*(may cause catastrophic bronchial

NICE  Lobectomy [I-II] hemorrhage)

 Pneumonectomy [II-III])  Bronchial adenoma

 +/- Radiotherapy [I-III]  Foreign body

 +/- Chemotherapy [III - IV]. PARENCHYMAL  Tuberculosis* (& chronic fever & weight loss)

DISEASE  Trauma

 Limited Resection / Radical Radio Tx for pts who would not tolerate  Suppurative pneumonia (rusty coloured sputum)

lobectomy due to comorbid disease or pulmonary compromise.  Actinomycosis

Treatment for SCLC: SCLC metastasise early  Sx not indicated.  Lung abscess

 Radiotherapy and Combo Chemotherapy is indicated.  Aspergilloma (may cause catastrophic bronchial

 For most cases treatment is palliative: hemorrhage)

 RadioTx used to ease pain / bronchial obstruction.  Parasites (e.g. hydatid disease, flukes)

 Pleurodesis indicated for recurrent pleural effusions. LUNG  Pulmonary infarction*

 Palliative endoscopic laser Tx of obstructive lesions of VASCULAR  Idiopathic pulmonary

large airways may also be effective. DISEASE  Polyarteritis nodosa

Prog  80% 1 year mortality from lung cancer after Tx.  Haemosiderosis

 5 year survival is only about 5%.  Goodpasture’s syndrome

 5-year survival after Sx of NSMLC is ~ 25%. CARDIO-  Acute left ventricular failure*

 Small cell tumours carry the worst prognosis: VASCULAR  Aortic aneurysm

 Untreated - 1-2 months median survival

DISEASE  Mitral stenosis

 Treated - 12 months median survival BLOOD  Leukaemia

 Untreated median survival times for other tumours include: DISORDERS  Anticoagulants

 Haemophilia

 Adenocarcinoma: 12 months

Risk Immobilisation, Malignant disease of any organ, CF, Pregnancy

 Squamous carcinoma: 8 months

 TNM Prognosis: S&S  Melaena if enough blood swallowed.

 Clubbing: bronchial carcinoma & bronchiectasis.

 Stage I: 80-90% 5 yr survival

 Cachexia, Hepatomegaly, Lymphadenopathy: 

 Stage II: 40-50% 5 yr survival

 Fever, Signs Of Consolidation, Pleurisy: Pneumonia /

 Stage IIIA: 30-40% 5 yr survival

Pulmonary Infarct

 Stage IIIB: 9-12 months median survival  DVT In Legs: Pulmonary Infarct

 Stage IV: 6-9 months median survival  Rash, Purpura, Haematuria, Splinter haemorrhages, Lymphad-

enopathy, Splenomegaly: Uncommon systemic disease.

COUGH DDx

Def Tussis Inv / CATASTROPHIC ACUTE HAEMOPTYSIS

Path Form of violent exhalation by which irritant particles in airways may Mx Haemodynamic resuscitation

be expelled. Stimulation of cough reflexes  epiglottis being kept Bronchoscopy  Rigid- allows optimal bronchial suction.

shut until a high expiratory pressure has built up which is then under GA: Allows adequate ventilation during GA

suddenly released.  May be need for: Angiography, Bronchial arterial embolization,

Cause Stimulation of sensory nerves in mucosa of: Pharynx, Larynx, Emergency pulmonary surgery.

Trachea, Bronchi MAJORITY OF CASES, NOT SERIOUS

Cause  S&S CXR  May give clear evidence of lesion including:

ORIGIN COMMON CAUSES NATURE Pulmonary infarct, Tumour- malignant or

Pharynx Post Nasal Drip Usually persistent benign, Pneumonia, TB

Larynx Laryngitis, tumour, Harsh, barking, painful, persistent, FBC and other blood tests including clotting screen

whooping cough, associated with stridor Bronchoscopy  Necessary to exclude bronchial carcinoma

croup (invisible on CXR)

Trachea Tracheitis Painful  Provides tissue diagnosis in other cases of

Bronchi Bronchitis & acute Dry or productive, worse in morning suspected bronchial neoplasia.

COPD V/Q scan  Helpful in establishing Dx of suspected

Asthma Dry or productive, worse in night pulmonary thromboembolytic disease.

Bronchial carcinoma Persistent- often with haemoptysis.  CT pulmonary angiography may be

Lung TB Productive- often with haemoptysis. necessary with pre existing lung disease

Parenchyma Pneumonia Dry initially, productive later (interpretation of VQ scan can be difficult).

Bronchiectasis Productive, changes in posture CT  Particularly useful in Inv peripheral lesions

induce sputum production seen on CXR which may not be accessible to

Pulmonary Oedema Often at night, may be pink frothy bronchoscopy & facilitates accurate

sputum percutaneous needle Bx where indicated

Interstitial Fibrosis Dry, irritant, distressing

Onset ACUTE COUGH DYSPNOEA

 Viral induced lower respiratory tract infection Def  Shortness of breath, difficult or laboured breathing

 Post nasal drip from rhinitis or sinusitis  Unpleasant subjective awareness of the sensation of breathing

 Throat clearing secondary to laryngitis or pharyngitis

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PP   Asthma, Respiratory tract infection, Lung tumours, Pleural

Path Pts usually perceive discomfort from either: effusions, Metabolic acidosis.

 VENTILATORY RATE, PROVOKED BY: CHRONIC (MONTHS- YEARS)

  Pa CO2 eg. COPD  COPD, Cardiac failure, Fibrosing alveolitis, Anaemia,

  Pa O2 eg. Cyanotic congen heart disease, asthma, COPD Arrhythmia, Valvular heart disease, Chest wall derformities,

 Exercise Neuromuscular disorders, Cystic fibrosis, Pulmonary

 Fever hypertension

 VENTILATORY RATE, PROVOKED BY: Inv / 

  Lung vol (Restrictive lung disease) eg Pneumonia, Dx 

Pulmonary oedema, Interstitial lung disease Mx

 Pleural pain Prog

 RESISTANCE TO AIR FLOW:

 eg. Asthma, COPD, Upper airway or laryngeal obstruction. CAUSES OF DYSPNOEA BY SYSTEM

S&S ASSESS SEVERITY, RATE OF ONSET: ACUTE DYSPNOEA AT REST CHRONIC EXERTIONAL

 Consciousness DYSPNOEA

 Central Cyanosis (degree) C  Pulmonary Oedema  Chronic heart failure

 Anaphylaxis (angioedema, Urticaria) V  Ischaemia (angina  Myocardial ischaemia

 Patency of Upper airway. equivalent (angina equivalent

 Ability to speak R  Asthma (Acute severe)  *COPD

PMH OF: E  COPD (Acute  *Chronic asthma

 LHF, Asthma, COPD S exacerbation)  Bronchial carcinoma

ALSO: P  Pneumothorax  Interstitial lung disease

 Renal disease, Dm, Anaemia  Pneumonia (sarcoidosis, fibrosing

 Inhaled foreign body?  Pulmonary embolus alveolitis, extrinsic allergic

 Acute epiglottitis?  Acute RDS alveolitis, pneumoconiosis)

CARDIOVASCULAR STATUS:  Inhaled foreign body  Chronic pulmonary

 SYMPTOMS: Chest pain, Palpitations, Sweating, Nausea (especially in the child) thromboembolism

 SIGNS: Rate and rhythm, BP, Peripheral perfusion, Leg  Lobar collapse  Lymphatic carcinomatosis

swelling may indicate CF or venous thrombosis.  Laryngeal oedema (e.g. (may cause intolerable

RESPIRATORY SYSTEM: anaphylaxis) dyspnoea)

 SYMPTOMS: Cough, Wheeze, Haemoptysis, Stridor  Large pleural effusion(s)

 SIGNS: Rate, Evidence of CO2 retention, Breathing pattern, O  Metabolic acidosis (e.g.  Severe anaemia

Tracheal position, Chest expansion (Degree, Symmetry) T diabetic ketoacidosis  Obesity

Percussion (Hyper resonant, Dull), Breath sounds (Chest, H  Lactic acidosis, uraemia,

Bases), PEFR measured if possible. E overdose of salicylates,

 Digital clubbing: Anaemia, Polycythaemia R ethylene glycol poisoning)

 Clinical features of: Dm, Renal failure, Other chronic disease  Phsychogenic

DDx SUDDEN (SECS- MINS) hyperventilation (anxiety

 Pneumothorax, Pulmonary oedema, Pulmonary embolism, or panic-related

Aspiration, Anaphalaxis, Anxiety, Chest trauma

ACUTE (HOURS-DAYS)



DIFFERENTIAL DIAGNOSIS OF ACUTE SEVERE DYSPNOEA: * denotes a valuable discriminatory feature;  = Hypoxia,  = Hypercapnea =  Plasma bicarbonate



CONDITION Hx SIGNS CXR ABGs ECG OTHER

LEFT Central cyanosis JVP  or  ) Cardiomegaly

Chest pain Sinus tachycardia

VENTRICULAR Murmurs *Upper zone vessel Echo ( left

Orthopnoea  Pa02 *Signs of

FAILURE *Sweating enlargement ventricular

Palpitations or N Pa CO2 MI

Cool extremities *Overt oedema/ pleural function)

*Previous cardiac history Arrhythmia

*Dullness and Crepitations at bases effusions

MASSIVE Severe central cyanosis Sinus tachycardia

Recent surgery or other risk factors May be subtle changes *Echo

PULMONARY *Elevated JVP S1Q2T3 pattern

Chest pain Previous pleurisy only Prominent hilar  Pa02 *V/Qscan

*Absence of S&S in lung (unless  T (V1—V4)

EMBOLUS *Syncope vessels  Pa CO2 *CT pulmonary

previous pulmonary infarction) Shock Right bundle- Branch

*Dizziness *oligaemic lung fields angiography

(tachycardia,  blood pressure) block

ACUTE SEVERE Tachycardia and pulsus paradoxus Sinus tachycardia

*Hyperinflation only  PaO2

ASTHMA *History of previous Cyanosis (late) (bradycardia with

(unless complicated PaCO2

episodes, asthma medications, wheeze *JVP  severe hypoxaemia

by pneumothorax) (until late)

 peak flow, rhonchi —late)

ACUTE Cyanosis

*Hyperinflation  or  Pa02

EXACERBATION *Signs of COPD Nil, or signs of

*Previous Episodes (Admissions) Signs of In type II failure

(barrel chest, intercostal indrawing, right ventricular

OF COPD If in type II respiratory failure, may not Emphysema. Signs of PaCO2 , with

pursed lips, tracheal tug) failure (in cor

be distressed events precipitating  [H+] and

*Signs of CO2 retention (warm periphery, pulmonale)

exacerbation  bicarbonate

flapping tremor, bounding pulses)

PNEUMONIA *Prodromal illness  CRP

Fever, confusion

*Fever *Pneumonic PaCO2  WCC

*Pleural rub Tachycardia

*Rigors consolidation  PaO2 Sputum & Blood

*Consolidation Cyanosis (only if severe)

*Pleurisy culture

METABOLIC Fetor (ketones)

ACIDOSIS *Evidence of diabetes/renal disease *Hyperventilation without physical signs *PaO N

in heart or lungs Normal  PaCO2

*Overdose of aspirin or ethylene glycol *Dehydration   pH (H+)

Air hunger (Kussmaul’s respiration)

PSYCHOGENIC *Pao N

*Not cyanosed End-tidal PaCO2

(A Dx Previous episodes  PaCO2

*No heart signs Normal *Low exercise

Symptoms mainly at rest, but not sleep. *pH N or

OF EXCLUSION) *No lung signs Carpopedal spasm tolerance test

 (H+ )









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