Resp Flashcards
Asthma What? Presentation? Common allergens? Drug cautions?
Chronic inflammatory airway disease characterised by intermittent obstruction and hyperreactivity
Recurrent wheezing, breathlessness, chest tightness, coughing
Allergic: house dust mite, pet fur, grass pollen -> IgE
Non: exercise, cold air, stress, strong emotion, viral infx, smoking
Beta blockers - B2 cause airway constriction
NSAIDS or aspirin block COX-1 -> decrease prostaglandins + overproduction of pro-inflammatory leukotrienes
Pathophysiology of asthma
Early phase
Exposure to allergen in presensitised individual
X-link IgE on mast cells
Release inflammatory mediators histamine, leukotrienes and TNFa ->
Increase in vascular permeability and autonomic hypersecretion of mucus -> airway oedema
Increase in airway tone and increased smooth muscle responsiveness
Both lead to narrowed airways
Constriction at 30 mins, inflammation at 3 hours
Late phase: eosinophil mediated (recruited by IL4 and IL5) at 6 hours
Increased goblet cells
Epithelial denudation -> airway hyperresponsiveness
Deposition of matrix proteins and swelling -> airway remodelling and smooth muscle hyperplasia
Presentation of Asthma
Worse at night and early morning Wheeze (polyphonic and expiratory) Episodic SOB Chest tightness Cough - *worse at night FHx atopy/nasal polyposis Diurnal variation - *worse in morning
Assessment of asthma control
How often felt SOB? How often woken from sleep? How often used reliever? How often interfered with normal activities e.g. school/work? How rate asthma control? Asthma control questionnaire Inhaler technique
Ix for asthma
PEFR (peak flow rate) - diurnal variation >20%, according height/weight
Reversibility testing FEV1 improves by 15% with SABA (or PEF - 20%)
Spirometry
FEV1 < 80% + *FEV1/FVC < 70% = obstructive
CXR: normal or hyperinflation
Step wise management of asthma
SABA \+ low ICS (800ug) \+ LTRA (montelukast) \+LABA (May remove or keep LTRA) \+ Higher does of ICS (200ug) \+ 40mg Pred Hospital admission
Antimuscarinic agents - Ipratropium/Triotopium can be used as adjuctive therapy.
Acute asthma management
Moderate - PEF 50-75%
Severe - PEF 33-50%, RR>25, HR>110, inability to complete sentences (one of)
Life threatening - PEF<33%, SpO2 <92%, PaO2 < 8kPa, silent chest, exhaustion
Steroids within 1 hour
O2 aim 94-98%
Nebulised salbutamol
Reassess severity -> repeat salbutamol (every 20 mins) up to 3
If poor response add nebulised ipratroprium bromide up to 3
Within 1 hour: oral pred (mild) or IV hydrocortisone (sev/lt)
If PEF < 50% IV MgSO4 IV theophylline IV salbutamol Intubate + ventilate if exhaustion
COPD
What?
Pathophysiology (2 parts)?
Aetiology
Chronic obstruction with irreversible airflow obstruction -> air trapping and hyperinflation
Narrowing of airways and mucosal oedema -> mucus hypersecretion -> cough and excessive mucus for 3M per year for >2y
Elastin breakdown: Permanent destruction and enlargement of alveoli
Cigarette smoking -> inactivation of A1AT
Occupational (particles and gases)
A1ATD
COPD
Symptoms
Signs
Pink puffer vs Blue bloater
SOB (initially with exercise but progresses) + cough (morning)
Barrel chest, CO2 flap, hyperresonant percussion, distant breath sounds (over bullae, hyperinflation and trapping), coarse crackles (exacerbation), wheeze (exacerbation)
Pink puffer: emphysema -> CO2 retention -> old and thin, use of accessory muscles
Blue bloater: peripheral oedema and overweight from RHF
COPD complications
Cor pulmonale - RHF secondary to long standing COPD - raised JVP, distended neck veins, hepatomegaly - Rx: LTOT + loop diuretic
Pneumonia - pneumococcal vaccine and yearly influenza vaccine
Depression*
Polycythaemia
Respiratory failure:
T1: PaO2 < 8 (Ventilation/perfusion mismatch)
T2: PaO2 < 8 + PaCO2 > 6.0 (Alveolar hypoventilation)
Ix of COPD
4 x ray changes.
Spirometry: Classification based upon FEV1 Obstructive pattern: FEV1/FVC < 0.7 Non-reversible Decreased pulse oximetry ABG: may see hypoxia +- hypercapnia CXR: Flattened diaphragm Increased intercostal spaces Hyperlucent lungs Increased AP diameter FBC: may see polycythaemia (HCT > 0.55) + Hb rise
Management of COPD
Patient education + vaccination + depression screen + COPD nurse
Smoking cessation, exercise, obesity mgmt (pulmonary rehabilitation)
Inhaled therapy
LTOT (*15hrs) IF PaO2 <7.3 or 7.3-8 with SaO2 < 88 or CHF or oedema or PCV
Inhalers if no significant improvement.
Infective exacerbation of COPD
Management
SABA + SAMA neb (salbuamol + ipratropium) + O2 (24% venturi aim for 88-92%)
Oral corticosteroid (prednisolone) - prevents recurrence
Airway clearance - mucolytics + physio
BIPAP if respiratory insufficiency
Blood culture and sputum culture + gram stain
Community (less severe)
Narrow spectrum: amoxicillin or doxycycline
Hospital
Broad spectrum: ?IV vancomycin or tazocin
Cell differences in COPD vs Asthma
Neutrophils + macrophages = COPD
Mast cells + eosinophils = Asthma
CURB 65
CURB 65 Confusion Urea > 7 RR > 30 BP < 90 or < 60 diastolic 65
Score
0-1 - low risk, recommend outpatient care
2 - moderate risk - to hospital
3-5 - high risk = to ITU (30 day mortality = 15-40%)
Pneumonia Ix & Chest xray changes
FBC, CRP (raised WCC, raised CRP)
ABG: may be low oxygenation
Sputum culture and sensitivity - for causative
CXR - lobar
Air bronchograms
Consolidation: homogenous opacification in lobe
Atelectasis if small airway obstruction (incomplete obstruction)
If atypical = diffuse reticular or reticulonodular opacities (affects interstitium)
Blood culture - for causative organism
*Urinary antigen: for legionella and pneumococcus
Pneumonia management Low/Mod/Severe Hospital aq Legionella Chlamydia
O2 if needed + IV fluids if needed +
Low risk (0-1) CAP: Oral 5 day amoxicillin
Mod (2) CAP: Oral 7-10 days amoxicillin + clarithromycin (doxycycline if allergic)
Mod and high risk (2+) CAP: 7-10 day dual therapy:
Co-amoxiclav + clarithromycin (IV) if penicillin allergic = cefotaxime
HAP: IV cefotaxime + gentamicin
Legionella: Clarithromycin + fluoroquinolone
Chlamydia: Doxycycline
Complications of Pneumonia
Septic shock
ARDS - non-cardiogenic pulmonary oedema
Pleural effusion (50%) + empyema
*Hepatisation (histologically)
Bilateral hilar lymph enlargement
Sarcoid
TB
Lymphoma
TB aetiology
Risk factors
Organisms
Birth endemic (asia etc), immunocompromised (e.g. HIV), exposure (v.infective)
Poor nutrition, overcrowding, IVDU, homeless, prisons
M. tuberculosis, m. bovis
TB Pathophysiology
MP @ midzone of lun engulfs bacteria
MP + LC -> granuloma -> Ghon Focus
MP presents antigen to T cell -> caseation
Caseation heals and calcifies -> some bacilli -> regional LN (mediastinal) -> Ghon complex (calcified focus + associated LN)
Secondary lesions form @lung apices -> fewer WBC (usually at year 1 or 2)
TB Presentation
Cough (+haemoptysis) + fever + weight loss + night sweats + weight loss + RF
Pleuritic chest pain + erythema nodosum
Crackles, bronchial breathing
Ix for TB
CXR:
Primary: consolidation + ipsilateral hilar enlargement (lymphadenopathy)
Healed primary: Ghon focus: large round calcified lesion near hilum
Post primary: fibronodular upper zone opacities with cavitation + calcification + consolidation to hilum
3 x sputum acid fast bacilli smear Ziehl-Neelsen stain - pink Sputum culture No growth or solid medium = 4-8 weeks or liquid medium = 1-3 weeks FBC - leukocytosis and anaemia NAAT - +ve for m.tuberculosis
Medical TB management
Infectivity TB management
6M Rifampicin: liver tox, orange secretions, induces hepatic enzymes (accelerate oestrogens, steroids, anticoagulants, phenytoin)
6M Isoniazid: liver tox, peripheral neuropathy (give w/ pyridoxine B6)
2M Pyrazinamide: liver tox, hepatitis
2M Ethambutol: *visual disturbance: optic neuritis, loss of acuity
Isolate patient e.g. negative pressure room
Contact tracing and treatment
Decreased infectivity after 2 weeks of treatment + 3 consecutive -ve AFB smears
Screen household and close contacts
Extra pulmonary TB (8)
Pleura - pleural TB leads to pleural effusion
LN - scrofula - swelling and discharge
GU - frequency/dysuria/haematuria
Bone - osteomyelitis starting in growth plates of bone Pott’s disease - vertebral fracture associated with TB
Brain - TB meningitis - Rich foci
Abdomen - ascites (peritoneal) and abdominal LN
Miliary TB: millet seed appearance on CT: liver/spleen/lung - by haematogenous spread
DVT
Clot forming triad
Risk Factors
Virchow’s triad: venous stasis, vessel injury, activation of clotting system (hypercoaguable state)
Thromboembolic risk factors:
Cancer, trauma, major surgery, hospitalisation, immobilisation, oral contraception, obesity/preg (high oestrogen), recent flight (immobilisation)
Genetic risk factors: (Family history)
Factor V leiden, protein C deficiency, protein S deficiency, antithrombin deficiency, antiphospholipid
Wells scoring for DVT Ix pathway
0 or 1 = D dimer If D dimer negative = No DVT. D dimer positive/2 or more Wells = USS <4hours If positive = Treat. If negative = Repeat @6-8 days
Types of pulmonary embolism
Thrombus formation in distal veins -> 50% will embolise Amniotic fluid embolus Fat embolus (at long bone fracture) Air embolus Tumour embolus
X ray appearance of PE
Wedged shaped opacity set against the pleura.
PE Wells scores
DVT = 3 Most likely = 3 TachyC (>100) = 1.5 Immobilisation (bed > 3 days or surg in 4 weeks) = 1.5 Hx DVT/PE = 1 Haemoptysis = 1 Malig (6 months) = 1 4 points = PE likely
Ix for PE
ECG: sinus tachycardia, S1Q3T3, RBBB D dimer + CTPA CXR: Decreased vascular markings, atelectasis, small pleural efusion Late sign: wedge shape infarction ABG: reduced PaO2, high lactate
PE management
Haemodynamically stable: LMWH (dalteparin) or fondaparinux (10a inhibitors) then switch to warfarin
Haemodynamically unstable (?renal fail): UFH ± thrombolysis (alteplase)
For 5 days OR till INR > 2 for 24 hours (longer)
Unprovoked - Warfarin/ NOACfor 3 months
Provoked - As above but lifelong
DVT management
LMWH or fondaparinux (5d) with warfarin (3 months) or LMWH (6 months) *if unprovoked = 6M
Pulmonary fibrosis
What?
FVC? FEV1/FVC?
Presentation?
Restrictive interstitial lung damage and fibrosis leading to decreased compliance
FVC low, FEV1/FVC high
4Ds: dry cough, dyspnoea, digital clubbing, diffuse inspiratory crackles
Types of pulmonary fibrosis (3)
Replacement fibrosis - secondary to lung damage -
Infarction, tuberculosis, pneumonia
Focal fibrosis: due to irritants
Coal dust, silica, aspestosis
DPLD: diffuse parenchymal lung disease
IPF, Hypersensitivity pneumonitis (Bird fanciers, Farmers, cheese workers)
Causes of pul fibrosis (5)
Presentation
Connective tissue disease: RA, SLE, SS, Sjogren’s
Occupational exposure: asbestos, coal dust, silica
Medication: amiodarone, bleomycin, methotrexate
Inhalation of irritants: hypersensitivity pneumonitis, birds, mould
Radiation
Progressive SOB, non productive cough, finger clubbing, cor pulmonale, fine end inspiratory crackles in bases.
Imaging of Idiopathic pulmonary fibrosis
CXR: reticular shadowing (net-like) of lung peripheries + bases, shaggy heart border, ground glass and honeycombing appearance.
HRCT:
Honeycombing, reticular pattern, and reticular septal thickening, no micronodules or cysts
Idiopathic pulmonary fibrosis treatment
Pirfenidone - Antifibrotic.
Median survival 2-5 years
RA lung disease (4)
Interstitial lung disease in middle aged men
Rheumatoid nodules may lead to small effusion
Methotrexate associated pneumonitis -> stop and Rx with steroids
Caplan’s syndrome - pulmonary fibrosis in coal workers with RA
Scleroderma lung disease (3)
Antibody detected
Chest wall fibrosis -> restrictive ventilatory defects
Diffuse fibrosis of alveolar walls
Pneumonia from aspiration from stiff oesophagus
ANA - 95%
Sarcoidosis lung changes
Treatment
Multisystem granulomatous disorder (non-caseating)
Pulmonary fibrosis + BHL
Oral prednisolone if BHL persists past 6 months
Hypersensitivity pneumonitis
Pathology
Examples
Non-IgE mediated widespread inflammation of alveoli and distal bronchioles
Cellular infiltrate -> *non-caseating granulomas (reticulo-nodular)
Farmer’s lung (hay), pigeon fancier’s lung (droppings protein), maltworker’s lung, cheese maker’s lung
Clinical features of Sarcoidosis (7)
Chest - Cough, SOB, Wheeze, inspiratory crackles
Skin - Erythema nodosum, infiltration of scars with sarcoid
Eye - Anterior &; Posterior uveitus, conjunctivial nodules
Bone - Arthralgias, bone cysts
Metabolic - Hypercalcaemia
Neuro - Meningeal inflammation, mass lesions, seizures, diffuse sensoryneuropathy
Cardio - Ventricular arrythmia, conduction defects
Hypersensitivity pneumonitis Ix
CXR: diffuse micronodular interstitial shadowing - upper zone
CT: reticulo-nodular shadowing, ground glass, micronodules
LuFT: restrictive, decreased DLco (diffusing lung capacity of carbon monoxide), decreased SpO2
Nodular pattern in upper lung zones & Black sputum
Coal workers pneumoconiosis & Silicosis
Asbestosis
Time delay
Presentation
Ix
20 - 40 years
Dry cough, dyspnoea, diffuse inspiratory crackles: velcro, digital clubbing
LuFT: restrictive
CXR: ground glass opacification, small nodular opacities (asbestos bodies - in alveoli at lung bases), shaggy cardiac sillhouette
Sputum microscopy: asbestos bodies
Biopsy
Effects of asbestos on the lung
Pleural effusions
Plerual thickening - Parietal and viseral.
Pleural plaques (benign)
Mesothelioma
Asbestosis - Breathless, finger clubbing, fine inspiratory crackles
Lung cancer
Mesothelioma
Presentation (4)
Stageing
Hx of asbestos exposure, aged 60-85
Dry cough, dyspnoea, dig club + pleuritic chest pain (*recurrent pleural effusion)
Symp of pleural effusion: diminished breath sounds, dull to percuss
Constitutional symptoms: weight loss, fatigue, fever, night sweats
1a: ipsilateral parietal pleura
1b: ipsilateral visceral pleura
2: diaphragm or lung involvement
3: ipsilateral bronchopulmonary or hilar LN
4: contralateral or distant mets
Mesothelioma
Ix
Management
CXR - Irregular pleural thickening, reduced lung vol, ev asbestosis, unilateral pleural effusion
CT - Pleural thickening, pleural plaques, hilar or mediastinal LN enlargement
Thoracocentesis - Exudate with malignant cells
Pleural biopsy (*epithelioid mesothelioma)
Operable: only curative at stage 1
Inoperable: Chemoradio
Survival = 1 year
Pleural effusion
What?
Types & Egs
Excessive fluid in the potential space between visceral and parietal pleura
Transudate (low protein <30g/L): disruption of hydrostatic and oncotic forces across pleural membranes,
- Heart failure, cirrhosis, hypoalbuminaemia, nephrotic syndrome, Meig’s = right pleural effusion + ovarian fibroma + ascites
Exudate (high protein >30g/L): increased permeability of pleura from inflammation
- Infection (pneumonia, TB, emyema), malignancy, PE, AI disease (RA) comp of MI (Dressler’s)
Pleural effusion signs (5)
Reduced chest wall movment Dull to percussion Absent breath sounds Reduced vocal resonance Mediastinum shift
Unilateral pleural effusion management
Clinical picture transudate?
Yes -> treat cause (LVF, hypoalbuminaemia)
No -> USS guided pleural aspiration/thoracentesis
Pleural fluid for: cytology, MC+S, AFB stain, LDH, protein, glucose, amylase, RF
PH - normal = 7.6, <7.2 = empyema, RA, SLE, TB, malignancy
Glucose < 3.3 = empyema, RA, SLE, TB, malignancy
Types of pneumothorax (3)
Primary spontaneous: tall thin males, smoking, Marfan’s, family history
Secondary spontaneous: pre-existing lung disease: COPD (bullae), CF, TB, Pneumocystis Pneumonia
Traumatic
Pneumothroax presentation
X ray changes
Pleuritic CP + dyspnoea (size and sev)
Hyper-resonant
Reduced expansion
Decreased breath sounds
Visceral pleural line identified
Dark area with no lung markings
Diaphragm pushed downwards
Tension pneumothorax
Signs
Management
Respiratory distress with rapid shallow breathing Distended neck veins Tracheal deviation away Hyperexpanded ipsilateral hemithorax TachyC/TachyP Hyper-resonant Reduced expansion Decreased breath sounds
Immediate needle thoracostomy: 2nd IC mid clavicular
100% O2
Pneumothorax maagement
O2
If haemodynamically unstable insert chest drain
Primary
>2cm/SOB - Fine needle aspiration - No success then chest drain and admit.
<2cm - Discharge, review in 2 weeks, avoid strenuous
Secondary
>2cm/SOB - Chest drain and admit
1-2cm - Fine needle aspritation
1cm - Admit, O2 and observe for 24 hours
Chest drain placment
Lateral border pectoralis major
Anterior border latissimus dorsi
Horizontal line at nipples
Mid axillary IC 4-6 with pain relief
Pleuritic chest pain DDx
ACS Aortic dissection Pneumothorax PE Pneumonia Malignancy
Bronchiectasis
Pathology
Presentation
Causes (5)
Failure of mucociliary clearance and impaired immune function -> continued insult to bronchial wall -> chronic inflammation -> Permanent dilatation and thickening
Recurrent (chronic daily) cough, excessive sputum, bacterial colonisation, recurrent infection
Post infectious: measles/flu/pertussis, aspergillus fumigatus (ABPA), pneumonia Immunodeficiency: HIV, Ig deficiency Genetic: CF, ciliary dyskinesia, A1ATD Connective tissue disease: RA, Sjogren’s IBD: CD, UC
Early inspiratory: airway disease
Late inspiratory: interstitial disease
Early - Bronchiectasis
Late - IPF
Bronchiectasis
Symptoms/Signs
Sputum culture and sensitivity
Chest X ray
Cough and daily sputum Intermittent haemoptysis Obstructive symptoms: dyspnoea + wheeze Weight loss and fatigue Inspiratory coarse crackles (shift on cough), high pitched inspiratory squeaks and pops, low pitched rhonci (snoring sounds), clubbing
G- = pseudomonas aeruginosa (high risk if CF) G+ = s.aureus, s.pneumonia
Normal/dilated bronchi with thickened walls + cysts (cystic shadows)
Cystic fibrosis pathology
Genetic disease with mutations in CFTR gene, a Cl channel in Lungs, bowel, pancreatic duct, sweat glands, reproductive organs
Failure of Cl channel opening in response to cAMP in epithelial cells
Decreased excretion of Cl to lumen, increased reabsorption of Na to cells
Decreased excretion of H20
Thick, sticky secretions
Cystic fibrosis
Screening
Presentation
Serum immunoreactive trypsinogen on 5d heel prick (Guthrie).
Neonates + infants: failure to pass meconium, failure to thrive, large appetite (pancreatic insufficiency), chronic wet cough
Resp - Recurrent infection, chronic cough, wheeze, thick mucus, nasal polyps
GI - Gallstones, decreased motility
Panc - Insufficiency -> bulky, greasy, foul smelling stool
Reproductive system - Absent VAS - infertility
Digital clubbing
Infective organisms in CF
Pseudomonas aeruginosa (70%) - *highly transmissible
Burkholderia cepacia
S.aureus
CF management
Oral/IV ABX (oral = co-amoxiclav, if IV = gentamicin + cover for pseudomonas/staphylococcus tazocin)
Chest physio
Inhaled bronchodilator
Inhaled mucolytic:
Segregate in hospital
Vaccination: influenza and pneumococcal
Prophylactic ABX: fluclox or amoxi
Pancreatic enzyme replacement, fat soluble vitamins DEAK, GORD = H2 antag + PPI
Treat CF diabetes, fertility and genetic counselling
Pulmonary hypertension
Definition
Presentation
Mean pulmonary artery pressure >25mmHg at rest with pulmonary capillary wedge pressure <15mmHg
Dyspnoea
Accentuated P2 (pulmonary component of second heart sound)
Tricuspid regurgitation murmur (high pitched holosystolic)
Pulmonary regurgitation murmur (Graham Steell) - high pitched early diastolic at pulm area (normally if pul HTN secondary to mitral stenosis)
RHF: oedema, exertional syncope, visible RV heave, pulsatile hepatomegaly, ascites, raised pulsatile JVP
Pul Hypertension
Management
CCB (nifedipine or amlodipine) or sildenafil (PDE5 inhibitor - augments pulmonary vascular response to nitric oxide)
Anticoagulant: warfarin target 1.5 to 2.5
Lifestyle: low level graded exercise
Oedema: furosemide and low salt diet
Supplemental O2 if needed
Types of lung cancer
Small cell (least common) 15% Non-small cell (most common) 85% -Adenocarcinoma -Squamous cell carcinoma -Large cell carcinoma
Non Small cell carcinomas (3)
Adenocarcinoma - 40% - peripheral lung
- From mucus cells at bronchial epithelium
- Mets: brain, adrenal bone
- Most common LC with aspestos
Squamous cell carcinoma - 20% - central airways, metastasise late
- Present as obstructive lesion
- Local spread common
- Well differentiated cells
Large cell carcinoma - 10% - central airways, appear undifferentiated
Metastasise early very large
LC presentation
General
Locally invasive (3)
Cough + dyspnoea + haemoptysis (new or persistent)
Requires imaging
Chest pain (lung has no pain fibres therefore this suggests invasion of pleura or chest wall)
Constitutional symptoms: Weight loss, fatigue
Local invasive symptoms
Pancoast tumour
- Invasion of brachial plexus -> weakness, parasthesia, pain in C8-T1, shoulder pain
- Invasion of sympathetic chain -> Horner’s syndrome
Ptosis, miosis, ipsilateral anhydrosis
Recurrent laryngeal nerve -> hoarseness
Mediastinal invasion/shift -> dysphagia, arrhythmia, facial swelling (compression of superior vena cava)
NSCLC staging
T1: < 3cm
T2: 3-7cm, assoc atelectasis, involves main bronchus >2cm to carina, invades visceral pleura
T3: >7cm and directly invades chest wall, diaphragm, phrenic, mediastinal pleura, parietal pericardium
T4: invasion of mediastinal organs: oesophagus, trachea, great vessels, heart, malignant pleural effusion, recurrent laryngeal
N1: ipsilateral bronchopulmonary or hilar
N2: ipsilateral mediastinal or subcarinal
N3: contralateral mediastinal, hilar or any supraclavicular
M1: mets present, contralat lung or malignant pleural effusion
Goodpasture’s
What
Presentation
Antibody
Anti-glomerular basement membrane disease
Pulmonary renal syndrome
Usually as an AKI caused by rapidly progressive glomerulonephritis.
Kidney symptoms: oedema, *reduced urine output
Lung symptoms: cough + haemoptysis + SOB + fever
AntiGBM aB: autoantibody to type IV collagen (alveoli and glomeruli)
Respiratory failure
Type 1: hypoxia (<8kPa) without hypercapnia (>6kPa)
T1: COPD (pink puffer), pneumonia, pulmonary oedema, fibrosis, asthma, PE, ARDS
Type 2 hypoxia + hypercapnia
2: COPD (blue bloater), asthma, myasthenia gravis, polyneuropathy
ARDS
What?
Cause
Dyspnoea and hypoxaemia caused by non-cardiogenic pulmonary oedema and diffuse lung inflammation which may progress to respiratory failure
Most common: SEPSIS OR PANCREATITIS
Location of pulmonary fibrosis
Upper
Lower
hypersensitivity pneumonitis (also known as extrinsic allergic alveolitis)
coal worker’s pneumoconiosis/progressive massive fibrosis
silicosis
sarcoidosis
idiopathic pulmonary fibrosis
most connective tissue disorders
drug-induced: amiodarone, bleomycin, methotrexate
asbestosis
Kelbsiella pneumonia
Causes cavitating upper lobe mass & infective symptoms
Small cell para neoplastic
ADH, ACTH, Lambert-Eaton syndrome (muscle weakness - NMJ)
SIADH - hyponatraemia
ACTH - HTN, hyperglycaemia, hypokalaemia, alkalosis, muscle weakness
LES - weakness that improves with muscle contraction
Squamous cell para neoplastic
PTH-rp, clubbing, TSH
PTHrp - bone pain and hypercalcaemia
Hyperthyroidism
Adenocarcinoma para neoplastic
Gynaecomastia
