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Flashcards in Deck 3 Deck (21)
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1

Q. Name two signs of idiopathic pulmonary fibrosis, how can diagnosis occur?

A. Cough, shortness of breath
B. Constitutional symptoms
C. Clubbing, crackles (fine end inspiratory crepitations), skin/eyes/joints
D. Pulmonary function tests – restrictive patterns, reduced gas transfer, low/normal paO2
E. Blood tests – eosinophils, total IgE
F. High res CT – different distributions depending on diagnosis

2

Q. What are the 5 major categories of interstitial lung diseases?

Diseases affecting the interstitium i.e. tissue and space around air sacs: concerns alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues.

A. Systemic – rheumatological, vasculitis
B. Environmental – dust, fungal, dust
C. Granulomatous – sarcoid, wegener’s
D. Idiopathic - Idiopathic pulmonary Fibrosis
E. Other - lymphangiolyomyomatosis, eosinophilic pneumonia

3

Q. Name two rare lung diseases

A. Lymphangiolyomyomatosis – benign proliferation of lymphatic smooth muscle cells – often presents in pregnancy
B. Langerhans cell histiocytosis –proliferation of histiocytes (tissue macrophages) affecting multi-systems
C. Pulmonary alveolar proteinosis – stimulation of alveolar macrophages, abnormal accumulation of pulmonary surfactant

4

Q. What is sarcoidosis? Which systems does it affect?

A. A multi-system disease of unknown aeitiology
B. Affecting any organ system, but predominantly the lymph nodes and lung
C. Typical granulomatous histology

5

Q. What are the three main disorders of pulmonary vasculature?

A. Pulmonary embolism
B. Pulmonary hypertension
C. Pulmonary vasculitis

6

Q. Name three predisposing factors for acute myocardial infarction

A. Fracture, knee surgery, bed rest, increasing age, obesity

7

Q. Name three investigations appropriate for MI diagnosis?

A. Chest X-ray
B. ECG
C. D-dimer (coag cascade)
D. Scoring system
E. CTPA (CT pulmonary angiogram) or ventilation-perfusion scan (V/Q)

8

Q. Name two treatment options for pulmonary embolism

A. Heparin
B. Novel oral anticoag (NOAC)
C. Reperfusion – thrombolysis, interventional radiology, embolectomy

9

Q. Name three features of pulmonary hypertension presentation, which investigation is appropriate?

A. Dyspnoea
B. Ankle swelling
C. Chest pain
D. Syncope
E. ECHO
F. (Many different forms of PH, associated with various conditions)

10

Q. Describe the pathophysiology of pulmonary vasculitis

A. Destruction of blood vessels
B. Number of different disorders defined by size, type and location
C. Diagnosis hard due to overlapping of signs and symptoms – all rare

11

Q. Describe the pathophysiology of asthma

A. Bronchial hyper-responsiveness
B. Inflammation = lumen becomes narrower
C. Excessive contraction of smooth muscle
D. Hypertrophy and proliferation of smooth muscle = further narrowing
E. Airway odema = airway remodelling

12

Q. What are the two main types of asthma? Which cell types are associated with each type?

A. Eosinophilic – associated with allergy, (also non allergic) –fungal, common aeroallergens, occupation (lab workers, vet staff, animal breeders, bakers, paint sprayers), pets, exposures. (25% are atopic – IgE mediated)
B. Non-eosinophilic - non-smoking/smoking/obesity related
Associated with monocytes, macrophages, neutrophils

13

Q. Name three factors that may affect the severity of asthma

A. Smoking, exercise, weight, dysfunctional breathing,
B. Inhaler technique, adherence to medication, additional diagnoses
C. How to grade the level – ask about number of inhalers/medication, A&E attendances/admissions, ventilation, antibiotics and steroid usage, nocturnal waking, prev pneumonias?

14

Q. What signs and symptoms are suggestive of asthma?

A. Episodic wheeze
B. Cough
C. SOB
D. Diurnal variation (worse in the morning)
E. Brittle disease (type 1, chronic severe; type 2 sudden dips)
F. Provoking factors – allergens, infections, menstrual cycle, exercise, occupation, birth
G. Age of conset
H. FHx (hay fever, asthma, eczema)

15

Q. What differences can be seen between COPD and asthma

A. COPD – associated with smokers, more relentless progressive SOB, less variation
B. Asthma – variable, early onset, often FHx of asthma/hay fever/eczema
C. Overlap does occur

16

Q. What investigations may be carried out for asthma diagnosis?

A. Examination – wheeze, polyphonic, expiratory, widespread, sputum
B. Lung function – airway obstruction – variable – reduced FEV1, reduced FEV1/FVC ratio
C. FBC – eosinophils
D. Tests for atopy/allergy – skin prick tests and RAST
E. Chest XR
F. Oxygen sats
G. Reversibility with bronchodilators or anti-inflammatory treatment
H. Exhaled nitric oxide – test for airway inflammation

17

Q. Name two classes of drugs that can be used to treat asthma

A. Bronchodilators: beta agonists, leukotriene receptor antagonists, theophyllines, long acting beta agonists, anticholinergics – treats the symptoms by causing smooth muscle to relax
e.g. Salbutamol neb 5mg – short acting beta2-agonist (1-2 puffs 33-4 times a day, PRN)
B. Anti-inflammatory drugs: steroids – reduces airway inflammation
e.g. Clenil modulate – preventer inhaler – prophylaxis - corticosteroid

18

Q. Which patients should not take oral steroids?

A. Systemic: diabetes, cataracts, osteoporosis, hypertension, skin thinning, easy bruising, growth retardation
B. Topical: hoarse voice, oral candida, skin thinning, easy bruising, cataracts

19

Q. Name two differential diagnoses for asthma signs/symptoms

A. COPD, Bronchiolitis, bronchiectasis, CF, pulmonary embolism, CEA, CFA, hyperventilation, bronchial obstruction – foregin body, tumour etc

20

Q. Which cells are important in immune response? Briefly outline their function

A. Alveolar macrophage:phagocytic, polarise into M1- inflammatory and M2- repair, APCs
B. B-cell: antibody formation, opsonisation of bacteria
C. T-cell: CD8 – T cells kill viral-infected cells directly, CD4-T cells augement the function of macrophages, B cells and neutrophils

21

Q. Name some causes of cellular immune compromise

A. Primary immune deficiency: common variable immune deficiency (PIID), X-linked agammaglobulinaemia (XLA), severe combined immune deficiency (SCID), chroic granulomatous disease (CGD)
B. Secondary immune deficiency: immunosuppressant treatment (transplant recipients, cancer chemotherapy, inflammatory diseases), haematological malignancy (CLL, lymphoma), HIV infection (mostly untreated), non-specific (malnutrition, co-existing illness, alcohol)