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Question 1

Define Asthma

Answer 1

reversible, obstructive. CO2 retention. Can be response to exercise, allergens, stress or idiopathic.
Atopic features
Expiration wheeze, dyspnoea (diurnal)

Variable

Chronic sputum, dizziness, chest pain and inspiratory wheeze make asthma less likely

Question 2

Specific asthma triggers vs non specific

Answer 2

Only affect some patients (pets, pollen)
Non specific triggers (viral infection, cigarette smoke, pollution, cold weather, emotion, exercise) affect some patients

Question 3

Atopy

Answer 3

Allergic rhinitis, eczema and asthma

Question 4

Asthma diagnosis in under 5

Answer 4

Treat symptoms based on obs/clinical judgement. Review regularly and get objective testing ASAP

Question 5

Asthma diagnosis in 5-16

Answer 5

Spirometry (reversibility is key - if not reversible then FeNO test (NO raised in asthma)

Question 6

Asthma diagnosis in 17+

Answer 6

Spirometry for reversible obstruction (if not, then FeNO) and variable Peak Flow. Can also to histamine/methalcholine challenge - specialist test

Question 7

Asthma Tx

Answer 7

SABA
Add ICS
Add LRTA
LABA+ICS+SABA

MART has LABA as ICS as reliever and preventer

Question 8

Moderate Acute Asthma

Answer 8

Increasing symptoms
PEFR >50-75% predicted
No acute severe asthma features

Question 9

Acute Severe Asthma

Answer 9

One of:
PEF 33-50% predicted
RR>25
HR>110
Inability to complete sentences in 1 breath

Question 10

Life threatening Asthma

Answer 10

Any one of:
PEF<33% pred.
SpO2 <92%
PO2 <8kPa
Normal CO2 (4.6-6)
Silent chest
Cyanosis
Poor resp effort
Arrythmia
Exhaustion
Hypotension

Question 11

Emergency Asthma management

Answer 11

Salbutamol neb (children can use inhalor). Can add ipratropium if no response. give oxygen if hypoxic. Steroids, IV mag sulphate .

Question 12

COPD Definition

Answer 12

Progressive non fully reversible airflow obstruction.
Get mucus hypersecretion, ciliary disfunction, airflow limitation and hyperinflation. Impaired gas exchange and pulmonary HT (V/Q mismatch

Question 13

COPD RF

Answer 13

Smoking, indoor air pollution, occupational toxins, outdoor pollution, genetic factors, infections, socioeconomic factors, asthma

Question 14

COPD features and examination

Answer 14

Often asymptomatic until exertion. Chronic cough, chronic progressive dyspnoea, regular sputum, wheeze, chest tightness. Can lead to weight loss, anorexia, cough syncope and depression.
O/E: hyperinflated chest, wheeze, quiet breath sounds, pursed lip breathing, accessory muscle use, paradoxical movement of lower ribs, peripheral oedema, cyanosis, raised JVP, cachexia.

Question 15

Difference between pink puffer and blue bloater

Answer 15

Pink puffer is more emphasematous presentation. Tends to be thin, pursed lip breathing, maintains co2 level.
blue bloater is more chronic bronchitis, larger, prone to hypercapnia

Question 16

COPD investigations

Answer 16

CXR, FBC, BMI, spirometry, peak flow, alpha 1 anti-trypsin, CO transfer factor, oxygen sats, CT thorax, ECG, echo, ABGs, sputum culture.

Question 17

COPD management

Answer 17

Empirical with SABA/SAMA
Can add LAMA (tiotropium) an can use LABA/LAMA combos
For frequent (2+/12 months) and steroid sensitivity features then ICS + LABA
If severe then ICS+LAMA+LABA combo
Mucolytics adjunct
ABx in acute exacerbation
Smoking cessation

Question 18

Chronic Bronchitis definition

Answer 18

Cough productive of sputum on most says for 3 months of at least 2 successive years.
Due to chronic irritation leading to defensive increase in mucus (through goblet hyperplasia). Increased sputum production increases infection risk. This process is not necessarily inflammatory. Mucus hypersecretion occurs in the proximal airspaces

Question 19

Emphysema definition

Answer 19

Distal airspace disease where terminal bronchiole airspace is increased through balance between proteases and antiproteases is disturbed. Macrophages and neutrophils recruited. Alveoli dilated. Occurs without fibrosis.

Question 20

Comparison of chronic bronchitis and emphysema

Answer 20

Bronchitis onset is often 40-45, emphysema is 50-75
Dyspnoea is milder and later in bronchitis
Infections are more common in bronchitis
Respiratory failure and cor pulmonale is more common throughout bronchitis, but terminal in emphysema
Airway resistance increased in bronchitis, but normal or slight increase in emphysema
Elastic recoil normal in bronchitis, low in emphysema

On CXR, bronchitis is prominent vessels and large heart. Emphysema is hyperinflation and small heart

Question 21

Comparison of COPD and asthma

Answer 21

COPD nearly always smoker or ex smoker
COPD is rare under 35
Chronic productive cough is common in COPD but uncommon in asthma
Dyspnoea is persistent and progressive in COPD, variable in asthma
Night time waking dyspnoea is rare in COPD but common in asthma
Asthma shows diurenal/day-to-day variation

Question 22

Main haemoptysis differentials

Answer 22

Lung cancer, TB, bronchiectasis. Not a common COPD feature

Question 23

Lung cancer RF

Answer 23

Smoking, age (75+), air pollution, occuputation risk, FHx of asbestos exposure
Emphysema is bigger risk factor than chronic bronchitis

Question 24

Lung cancer Symptoms

Answer 24

Dry cough 3 weeks +
Haemoptysis
Chest pain (esp radiating to shoulder, pain on coughing)
Recurrent chest infection
Cervical lymphadenopathy
Exertional dyspnoea
Fatigue
Weight loss
Thrombocytosis
Bone pain
Hoarseness
Fever
Dysphagia

Question 25

SCLC

Answer 25

Rare Associated with smoking Grows quick, mets early Very poor prognosis, often metastasised by diagnosis Can cause cavitating lesions and paraneoplastic syndromes. Generally centrally located.

Question 26

Squamous cell

Answer 26

``` Non small cell. 50% of lung cancers. Often Central and close to carina. Gives obstructive symptoms Relatively slow growing and may be resectable Associated with smoking Can cause cavitating lesions ```

Question 27

Adenocarcinoma

Answer 27

20% of lung cancers. Equal gender distribution. Less association with smoking. Can rise at existing lung scarring (scar cancerS). If no mets then can have good prognosis.

Question 28

Superior sulcus tumour

Answer 28

Occurs in lung apex (e.g. pancoast tumour). | T3 tumour.

Question 29

Hilar mass

Answer 29

Common presentation of squamous cell and small cell carinomas (but can also be due to nodal mets). Tumous can compress/narrow broncus (tapered bronchus is specific for lung cancer)

Question 30

How does tobacco smoke damage lungs?

Answer 30

Benzoayrine damages DNA at cancer protecting parts, Chromium allows other harmful chemicals to bind to DNA, increasing their toxicity Alcohol and tobacco give synergistic effect by reducing CYP450 effectiveness and exposure to more toxins

Question 31

Lung cancer genetics

Answer 31

Loss of Rb, P53 and P3 is common. RAS proteins mutated in 1/5 of NSCLC and carry poorer prognosis. EGF overexpression common

Question 32

Transudate causes

Answer 32

Think FAILURE! | Heart failure, liver failure , but can also occur in nephrotic syndrome, peritoneal dialysis and hypothyoidism

Question 33

Exudate causes

Answer 33

Occur due to increased permeability of microcirculation, or alteration to pleural drainage to lymph nodes. Examples are cancers, PE, pneumonia, TB, mesothelioma, Rheumatoid arthritis, sLE, lymphoma

Question 34

Differentiating transuldate and exudate

Answer 34

Transudates have lower LDH and protein than exudates. Lights criteria is: - Effusion protein: serum protein >0.5, -LDH effusion: serum >0.6 - Effusion LDH is greater than 2/3 of lab upper reference for serum LDH If any of these is true then it is an exudate. Transudates tend to be bilateral

Question 35

Effusion diagnosis

Answer 35

Signs include dullness to percussion and quieter breath sounds on CXR can see indications once >250mL (initialy costophrenic angle blunting). If larger then see fluid in hosizonal and oblique fissures If massive effusion then meniscus sign with mediastinal shift Chest tap can be performed, but Hx might indicate cause and resolution. If no known Hc then chest tap and broncoscopy

Question 36

Bronchiectasis definition and pathophysiology

Answer 36

Airway widening. Diagnosis of structural pathology Permanent dilation of subsegmental airways (bronchi and bronchioles) - causes surface/volume ratio decrease and also causes gaps that fill with thick mucus (limits gas exchange - widened anatomical and physiological space) Cole's viscious cycle hypothesis: initial insult causes blockage, neutrophils infiltrate and elastases damage parenchyma. Mucus stasis leads to opportunistic colonisation. RF: Congenital (CF, primary ciliary dyskinesias), infective, fungal, obstruction, irritants, idiopathic, tertiary due to primary diseases like hypogammaglobulinaemia, RA.

Question 37

Cylindrical bronchiectasis

Answer 37

More common, airways widen but structure remains.

Question 38

Varicose bronchiectasis

Answer 38

Tortuous airways

Question 39

Cystic bronchiectasis

Answer 39

Outpouchings, less common but most severe. Associated with CF.

Question 40

Distinction between COPD and bronchiectasis

Answer 40

COPD is functional/physiological diagnosis (poorly reversible airflow obstruction) while bronchiectasis is structural (see airway dilatation on CT) - although bronchiectasis progresses to obstructive and restrictive pitcure

Question 41

Bronciectasis S+S+ examination

Answer 41

SOB, fatigue, cupfuls of sputum (generally green, may have blood), recurrent pneumonias. Can get pneumothorax through lung lining damage. Can het massive haemoptysis if larger blood vessels eroded Amyloidosis can occur (autoimmune response to chronic inflammation causes protein deposits) Cor pulmonale can occur Rarely, bacteria get into blood and brain (cerebral abscess) Can also get dry bronchiectasis (no sputum) and idopathic (no PMHx of lung disease) O/E: Ronchi, loud expiratory wheeze, mid inspiratory squeak, coarse crackles, clubbing, right heart failure.

Question 42

Bronchiectasis investigations

Answer 42

FBC U&E CRP Coagulation screen (bleeding risk factors) Sputum (causative/propagating organisms: H. influenzae, S. pneumoniae and P. aeruginosa are common but can get mycobacterium). If culture negative, consider fungal cause. Bronchoscopy can be done if culture is negative or no sputum. Broncho alveolar lavage can also be used if no sputu,. CXR: pneumonia, effusion, bronchial thickening Spirometry: obstructive Peak flow is not appropriate High Res CT shows Signet Ring Pattern (widening around inflamed bronchiole) May also want to test immunoglobulins, functional antibodies and aspergillus serology

Question 43

Pneumonia symptoms

Answer 43

Fever, productive cough, SOB, hypoxia, tachypnoea, confusion

Question 44

CAP definition and assessment

Answer 44

LRTI+ new pneumonic changes on CXR in community or within 48h of admission. Peak age is 50-70, more in winter/early spring Commonly Strep pneumonia, H influenzae, and moraxella catarrhalis. MRSA more common after viral pneumonia Can also get group A strep Atypical causes: mycoplasma, legionella, chlamydia. ``` Can ID pathogen by sputum or urinary antigens. CURB 65: Confusion (new onset) Urea >7mmol/L Resp rate >30 BP <90 sys <60dias 65 years + ``` Low risk is 0-1 Mod is 2 (?hospital) 3-5 is hospital with IV abx

Question 45

HAP

Answer 45

LRTI symptoms +pneumonic changes on CXR after 48h admission or within 7 days of previous stay. Risk increases with longer stay, poor mobility, reduced cough, over 70 and severe underlying disease Common causes: enteric gram negatives (enterobacteria, pseudomonas) but can be S. pneumoniae, H, influenzae and S aureus

Question 46

Aspiration pneumonia

Answer 46

May not show on CXR Consider if low GCS, evidence of vomiting, stroke survivor. If suspected then add metronidazole to cover for anaerobics

Question 47

Pneumonia complications

Answer 47

1) sepsis/septic shock (can show as AKI, new confusion, hypoxia, high RR, deranged clotting, deranged LFT. Septic shock is sepsis plus regractory hypotension and raised lactate 2) Lung abscess (more common with S aureus, can cause pus in parenchyma) - suspect if swinging pyrexia and rising CRP 3) empyema (parapneumonic effusion stasis, more common with streptococcus pneumoniea)

Question 48

Factors determining TB transmission probability

Answer 48

Susceptility (immune status of exposed person) Infectiousness (number of tubercle bacilli expelled into air) Environment (enclosed spaces, away from UV light) Exposure (proximity, frequency and duration of exposure)

Question 49

Extrapulmonary TB

Answer 49

Less common. Sites include larynx, pleura, brain, kidneys and bone. Generally not infectious unless also have pulmonary TB or if in larynx/pharynx. In miliary TB, disseminates into blood stream

Question 50

TB exposure pathway

Answer 50

80% eliminate with no infection 20% don't eliminate and get primary disease. Often asymptomatic. Macrophages take up TB droplets but fail to kill them. TB multiplies inside macrophages (which can then spread TB around body or to lymph nodes). HIV+ patients more likely to disseminate TB inside macrophages causes granulomatous lesion in lungs - either heals by fibrosis, invades locally or disseminates. 2-6 weeks for adaptive response, T cells involved and allow granuloma formation. Granuloma can contain TB for life or can be reactivated

Question 51

TB investigation

Answer 51

Culture and test for AFB(sputum , or extrapulmonary site if needed) Histology (caseating granuloma) Imaging: CXR can show caseating granulomas (calcifies to Ghon focus, if lymphadenopathy then Ghon complex). May see lobar/patchy consolidation, effusions, lymphadenopathy, miliary TB. May see necrosis and cavitation (esp in apex). Latent TB CXR should be normal. Mantoux test shows TB exposure, but FP with BCG and FN in HIV Can do IGRA test to comfirm (don't get FP with BCG and don't get FN with HIV)

Question 52

Management of TB

Answer 52

``` Quadrupole therapy: RIPE Rifampicin (R) Isoniazid (H) (with pyroxidine to prevent peripheral neuropathy) Pyrazinamide (Z) Ethambutol (E) R and H for 6/12, Z and E 2/12 ```

Question 53

Definition of restrictive lung disease

Answer 53

physical reduction in potential max lung volume.

Question 54

Restrictive lung disease causes

Answer 54

Compliance issues (e.g. fibrosis), increase in dead space (effusion/pus) Occupational lung disease lobectomy obesity pregnancy neuromuscular disease (affecting diaphragm) Kyphoscoliosis

Question 55

S+S of restrictive lung disease

Answer 55

SOB, cough, wheeze, chest pain, fatigue, anxiety, depression, Ronchie, wheeze, cyanosis, clubbing, right side heart failure Coarse crackles in fibrosis Fine crackles in fluid pathology Spirometry shows FEV1 <80%, FVC <80%, but FEV1/FVC >0.7

Question 56

Spirometry contrast between restrictive and obstructive

Answer 56

Obstructive: FEV1<80%, FVC >80%, FEV1/FVC <0.7 Restrictive FEV1<80%, FVC <80%, FEV1/FVC <0.7

Question 57

Classification of restrictive lung disease | E.g. focal, interstitial, replacement.

Answer 57

Focal is generally occupational lung disease (affects lymphoid tissue, inflammation derived fibrosis) Interstitial is diffuse, affects parenchyma (seen in extrinsic allrgeric alveolitis as type 3 H/S) Replacement is sequalae of RA, TB, CT disease

Question 58

Basal or Apical Fibrosis

Answer 58

``` Apical: Allergic bronchopulmonary Aspergillosis TB Extrinsic allergic alveolitis Ankylosing spondylitis Sarcoid Histiocytosis Occucational (berylliosis/silicosis) ``` ``` Basal: Drug induced (amiodarone, bleomycin, methotrexate, vincristine, nitrofurantoin) RA CT disease Idiopathic pulmonary fibrosis Asbestosis ``` However, occupational causes (asbestosis, silicosis, berylliosis) can affect upper or lower, and RA and anklyosing spondylosis can affect both. Drugs tend to affect the lower lobes.

Question 59

Extrinsic allergic alveolitis (tertiary fibrosis)

Answer 59

``` Bird droppings Hay mou dHop mould M avium from hot tub mist Mixed fungi from uncleaned musical instruments ```

Question 60

Pulmonary fibrosis investigations

Answer 60

ABG (t2Resp failure), CRP (superimposed infection), special tests (Antinuclear antibody, Rheumatoid factor) Imaging: honeycomb on CT Lung biopsy if doubt exists

Question 61

Pulmonary fibrosis investigations

Answer 61

Slow progression Pirfenidone (downregs procollagens 1 and II) Nintedanib (TK inhibitor, anti fibrotic) Lung transplant

Question 62

Differentials for dyspnoea with wheeze

Answer 62

Asthma, COPD, heart failure, anaphylaxis

Question 63

Dyspnoea with stridor

Answer 63

Upper airway obstruction. | Foreign body, tumour, acute epiglottitis, anaphylaxis

Question 64

Dyspnoea with creps

Answer 64

Heart failure, pneumonia, bronchiectasis, fibrosis

Question 65

Dyspnoea with clear chest

Answer 65

PE, hyperventilation, anaemia, DKA, drugs (e.g. aspirin), central cause

Question 66

Dyspnoea with dullness

Answer 66

pneumonia, consolidation, collapse, pleural effusion, haemothorax(Stony)

Question 67

Dysnpnoea with increased resonance

Answer 67

Pneumothorax

Question 68

Phases of lobal pneumonia

Answer 68

1) Congestion (24h, alveoli fill with fluid/bacteria) 2) Red hepatisation (airless. Alveolar capillaries dilate. Fibrin strands extend between alveoli. Neutrophils infiltrate. Exudate in pleura) 3) Gray hepatisation (less hyperaemia. Macrophages, neutrophils and fibrin) 4) Resolution (lysis of fibrin, removal by sputum/lymphatics. Starts at 8-9 days without Abx)

Question 69

Bronchopneumonia

Answer 69

More affects infants, young children, elderly and often secondary to other conditions (influenza/measles) or aspiration pneumonia, bronchus obstruction, inhalation of gaseous irritants, major surgery or chronic illness. Shows diffuse opacity on CXR as inflammation of bronchioles (and more proximal)