Assessing severity of asthma ``` Confusion - AMT 7 Resp rate - >30 BP - home treatment 2 -> hospital treatment 3 -> ?ITU

Respiratory Flashcards by abc xyz

Features and stages of clubbing

1) Bogginess / fluctuance of nail bed
2) Loss of concave nail fold angle
3) ↑ longitudinal and transverse curvature
4) Soft tissue expansion at distal phalanx (drumstick)

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Respiratory causes of clubbing

Carcinoma

Bronchial
Mesothelioma

Chronic lung suppuration

Empyema, abcess
Bronchiectasis, CF

Fibrosis

Idiopathic pulmonary fibrosis / CFA
TB

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Cardiac causes of clubbing

Infective endocarditis
Congenital cyanotic heart disease
Atrial myxoma

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GI causes of clubbing

Cirrhosis
Crohn’s, UC
Coeliac
Cancer - GI lymphoma

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Definition of cyanosis

Blue discolouration of mucosal membranes or skin

- Deoxygenated Hb >5g/dl

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Respiratory causes of cyanosis

Hypoventilation - COPD, musc
↓ diffusion: pulm oedema, fibrosing alveolitis
V/Q mismatch: PE, AVM (e.g. HHT)

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Cardiac causes of cyanosis

Congenital - Fallot’s, TGA

↓ CO: MS, systolic LVF

Vascular: Raynaud’s, DVT

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CURB 65 score

Assessing severity of asthma

Confusion - AMT<8
Urea - >7
Resp rate - >30
BP - <90/60
65 yo or older

Score
0-1 -> home treatment
2 -> hospital treatment
3 -> ?ITU

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Empirical abx treatment for mild/mod/severe CAP

Mild - amox 500mg TDS for 5 days or clari 500mg BD for 7 days

Moderate - both as above for 7 days unless pen allergy, consider IV

Severe - co-amoxiclav 1.2g TDS IV / cefuroxime 1.5g TDS IV
AND clari 500MG BD IV for 7-10 days. Add fluclox if staph suspected.

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Empirical therapy for atypical CAPs

Chlamydia - tetracycline

PCP - Co-trimoxazole

Legionella - clari and rifampacin

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Empirical abx therapy for HAP

Mild / <5 days - co-amox 625mg PO TDS for 7 days

Severe / >5 days - Tazocin +/- Vanc +/- Gent for 7 days

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Definition of type 1 and type 2 respiratory failure

Both - PaO2 <8

Type 1 - PaCO2 <6
Type 2 - PaCO2 >6

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Causes of lung abscess

Aspiration
Bronchial obstruction: tumour, foreign body
Septic emboli: sepsis, IVDU, RH endocarditis
Pulmonary infarction
Subphrenic / hepatic abscess

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Features of lung abscess

Swinging fever
Cough, foul purulent sputum, haemoptysis
Malaise, wt. loss
Pleuritic pain
Clubbing
Empyema (pus in the plural cavity)

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Systemic Inflammatory Response Syndrome

Inflammatory response to a variety of insults manifested by 2 or more of:

Temp >38 or <36
HR >90
RR > 20 or PaCO2 <4.6
WCC >12 or <4 or >10% bands

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Pathophysiology of bronchiectasis

Chronic infection of bronchi/bronchioles -> permenent dilatation

Retained inflammatory secretions and microbes -> airway damage and recurrent infection

Common organisms of infection in bronchiectasis

H. influenza
Pneumococcus
S. aureus
Pseudomonas

Congenital causes of bronchiectasis

CF (mainly upper lobe inflitration)

Kartagener’s / Primary Ciliary Dyskinesia

Young’s syndrome (azoospermia + bronchiectasis)

Causes of post-infectious bronchiectasis

Measles
Pertussis
Pneumonia
TB
Bronchiolitis

Immunodeficiency causes of bronchiectasis

Bruton’s X-linked agammaglobinaemia

Common Variable Immunodeficiency

IgG subclass deficiency
IgA deficiency

signs and symptoms of bronchiectasis

Persistent cough with purulent sputum
Haemoptysis
Fever and weight loss
Clubbing
Coarse inspiratory creps

Complications of bronchiesctasis

Pneumonia
Pleural effusion
Pneumothorax
Pulmonary HTN
Massive haemoptysis
Cerebral abcess
Amyloidosis

Pathogenesis of CF

Mutation in CFTR gene on Chromosome 7 (commonly ∆F508)

↓ luminal Cl secretion and ↑ Na reabsorption → viscous secretions.

In sweat glands, ↓ Cl and Na reabsorption → salty sweat

Clinical features of CF in neonates

Failure to thrive
Meconium ileus
Rectal prolapse

Clinical features of CF in children and young adults

Nose: nasal polyps, sinusitis Resp: cough, wheeze, infections, bronchiectasis, haemoptysis, pneumothorax, cor pulmonale GI: Pancreatic insufficiency (DM and steatorrhoea), Distal Intestinal Obstruction Syndrome, Gallstones, Cirrhosis Male infertility, osteoporosis, vasculitis

Types of lung cancer

Small-cell and non-small-cell (squamous cell carcinoma, adenocarcinoma, large-cell)

Lung squamous cell carcinoma

35% of lung cancer M>F Smokers Radon gas Centrally located Keratinisation Locally invasive Metastasise late via LN PTH releasing -> ↑Ca

Lung adenocarcinoma

25% of lung cancer Females Non-smokers Far East Peripherally located Glandualar differentiation Extrathoracic mets common and early -> 80% present with mets

Large cell lung cancer

10% of lung cancer Peripheral or central Large, poorly differentiated cells Poor prognosis

Small-cell lung carcinoma

20% of lung cancer Smokers Central location, near bronchi Small, poorly differentiated cells 80% present with advanced disease v. chemo sensitive but poor prognosis Ectopic hormone secretion

Clinical features of ARDS

Tachypnoea Cyanosis Bilateral fine creps SIRS

Pulmonary causes of ARDS

Pneumonia Aspiration Inhalation injury Contusion

Systemic causes of ARDS

``` Shock Sepsis Trauma Haemhorrage and multiple transfusions Pancreatitis Acute liver failure DIC ```

Definintion of chronic asthma

Episodic, reversible airway obstruction due to bronchial hyper-reactivity to a variety of stimuli.

Definition of COPD

- Airway obstruction: FEV1 <80%, FEV1:FVC <0.70 - Chronic bronchitis: cough and sputum production on most days for 3mo of 2 successive years. - Emphysema: histological diagnosis of enlarged air spaces distal to terminal bronchioles c¯ destruction of alveolar walls.