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1
Q

how do asthma + COPD differ

A

asthma - obstructive airway disease with paroxysmal/reversible bronchocontriction
COPD - irreversible obstructive airway disease

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2
Q

how are bronchi in asthma

A

inflamed, hyper-responsive

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3
Q

what is immunology of asthma

A

type 1 hypersensitivity reaction - involves IgE
causes mast cell degranulation, releasing histamine

allergen stimulates Th2 cells to produce cytokines (hygiene hypothesis - too clean, immune system not strong)
IL4 = class switch to IgE
IL5 = eosinophil release
IL13 = stimulate mucus secretion

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4
Q

what remodelling occurs in asthma

A

inflammation causes airway remodelling

bronchial smooth muscle hypertrophy, bronchoconstriction
higher vascular permeability
mucous gland hypertrophy

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5
Q

how does asthma present

A

wheeze, SOB
diurnal variation - cough worse at night

symptoms worse with exercise or after NSAID

PMH/FH of atopy: asthma, allergic rhinitis, eczema

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6
Q

how does acute asthma attack present

A

high RR, worsening SOB
hyper-resonant
wheeze, chest tightness

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7
Q

what are different severities of asthma attack

A

moderate, severe, life-threatening

moderate: PEFR 50-75%

severe: PEFR 33-50%, RR >25, HR >110, can’t complete sentences

life-threatening: PEFR <33%, O2 <92% or PO2 <8kPa, silent chest (as airways too tight, so no air entry), exhaustion (normal CO2 or hypercapnia)

fatal if T2RF (hypoxia + hypercapnia)

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8
Q

what are diagnostic criteria for asthma

A

PEFR variability >20%
FeNO >40ppb in adult, >35ppb in child
spirometry shows obstructive pattern FEV1/FVC <0.7, with bronchodilator reversibility

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9
Q

how is acute asthma attack managed

A

O SHIT ME

oxygen if O2 <92% or PO2 <8kPa (aim for 94-98%)
salbumatol + ipatropium bromide nebulised

if severe:
IV hydrocortisone
IV MgSO4
(theophylline - if severe and inadequate response from nebulisers)

escalate

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10
Q

how is chronic asthma managed

A

conservative = stop smoking, weight loss, avoid triggers, review inhaler technique

medical = SABA -> ICS -> ICS + LTRA -> ICS + LABA -> MART -> specialist referral

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11
Q

what are pink puffer + blue bloater in COPD

A

pink puffer:
emphysema - enlarged air spaces distal to terminal bronchioles due to destroyed alveolar walls as less elastin
so less SA for gas exchange

blue bloater:
chronic bronchitis - chronic productive cough for 3+ months
mucus gland hypertrophy/hyperplasia, small airway disease

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12
Q

what is pathology of COPD

A

chronic exposure to noxious chemicals (smoke, air pollution) causes mucus secretion in large+small bronchi

airways narrow from inflammation and fibrosis
chronic bronchitis - neutrophils, CD8-T, macrophages
goblet cell hyperplasia, mucus gland hypertrophy

emphysema from loss of elastin (as excess elastase protein made)
reduces integrity causing alveolar collapse, so dilated airways distal to terminal bronchioles + bullae form (fused alveoli)

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13
Q

how does alpha-1 antitrypsin deficiency cause asthma

A

alpha-1 antitrypsin acts to inhibit neutrophil elastase

since there is A1AT deficient, there is no elastase inhibition
so more elastin destroyed causing alveolar collapse -> emphysema

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14
Q

how does cigarette smoke affect the airway

A

stops cilia moving, so noxious chemicals not swiped away
prevents WCC from removing bacteria

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15
Q

how does COPD present

A

chronic bronchitis - chronic productive cough for 3+ months
sputum
SOB on exertion

wheeze, pursed-lip breathing, intercostal recession
hyper-inflated chest, reduced expansion, coarse crackles

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16
Q

why are COPD patients prone to chest infections

A

damaged lung tissue and obstructive lung disease makes it harder to ventilate lungs
so pathogens are trapped

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17
Q

what are signs of cor pulmonale

A

R-sided HF secondary to COPD
raised JVP, hepatomegaly, peripheral oedema

chronic hypoxia causes pulmonary artery vasoconstriction, leading to pulmonary HTN

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18
Q

how is COPD classified

A

depends on FEV1 - 4 stages ranging from <30-80%

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19
Q

what are RF for COPD

A

smoker, old, male
FH/PMH of A1AT deficiency (autosomal recessive)

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20
Q

what is FEV1/FVC <0.7 with chronic cough but no wheeze/SOB

A

bronchiectasis - dilated airways that allow pathogen to be trapped in

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21
Q

how is COPD diagnosed + what are investigation results

A

history/exam + spirometry (FEV1/FVC <0.7 without SABA reversibility)

CXR = hyperinflation, flattened diaphragm, few peripheral vascular markings, bullae
CT chest done if suspecting bronchiectasis or cancer

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22
Q

how is COPD managed

A

conservative: smoking cessation, pulmonary rehab (physiotherapy to clear sputum)
annual flu + 1-off pneumococcal vaccine

medical: SABA or SAMA -> LABA
-> LABA + ICS if asthmatic features present (eosinophil, steroid responsive)
OR LABA + LAMA
-> trimbo inhaler LABA + ICS + LAMA -> specialist

23
Q

what additional medications can be given for COPD

A

PO carbacystine - break down mucus
azithromycin - long term ABx to prevent infections

24
Q

what are target O2 sats for COPD

A

88-92%
as COPD CO2 retainers rely on hypercapnic drive instead of hypoxic (ABG shows high CO2 + high HCO3, so chronic compensation to increase pH levels)

25
when is LTOT given for COPD
only if stopped smoking chronic hypoxia, PaO2 <7.3kPa OR PaO2 7.3-8kPa + polycthaemia, HF, peripheral oedema, pulmonary HTN
26
can COPD pt have surgery for condition
YES - lung volume reduction surgery (remain breathless despite maximal medical therapy) upper lobe predominant emphysema, FEV1 >20%
27
what type of bacteria is TB
mycobacterium TB acid fast bacillus (rod shaped) obligate aerobe = needs O2 facultative intracellular = prefers to grow inside cell resistant to gram staining due to waxy coat stain with ziehl-neesn (bright red against blue)
28
what are RF for TB
close contact with infected individuals homeless, IVDU, immunocompromised - HIV south-asia + sub-saharan
29
how is TB spread
mycobacterium TB spread by droplet infection (via cough) usually latent TB - as immune system strong enough to contain infection macrophages engulf bacteria, localised to hisar lymph nodes bacteria engulfed by granulation tissue (if calcified, appears as Ghon focus on CXR) if latent TB re-activates = secondary TB (usually at lung apices) if primary infection not contained, bacteria spreads via blood = miliary TB
30
how do secondary + military TB differ
secondary = latent TB eactivates miliary = primary TB bacteria spread via blood
31
how does TB present
fever, lethargy, appetite/weight loss night sweats chronic productive cough +/- haemoptysis lymphadenopathy = palpable, enlarged, firm superficial lymph nodes erythema nodosum if CNS involved - headache, meningism, focal neurological signs
32
how to investigate TB
only investigate if showing signs Mantoux skin test = sees previous immune response to TB intradermal tuberculin injection (contains purified mycobacterium TB proteins) +ve means previous exposure (immunised, latent/active TB) delayed type 4 hypersensitivity reaction - after 72hr see if bleb under skin (induration 5mm+) IGRA interferon gamma release assay = see immune response to TB +ve means latent or active TB (unaffected by prior BCG)
33
how are sputum samples taken for TB
at least 3 (may need bronchoscopy/lavage) lymph node aspiration, MTB blood cultures if CNS involved, do CSF - high protein, low glucose, lymphocytosis
34
what does CXR for TB show
calcified granulomas - ghon focus pulmonary consolidation, pleural effusion upper lobe cavitation if miliary TB, millet seeds spread evenly
35
how is active TB managed
notify PHE 2 months: rifampicin, isoniazid, pyrazinamide, ethambutamol extra 4 months: rifampicin, isoniazid if latent TB - R/I for 3 months, extra 6 months of I
36
what are side effects of TB drugs
R - red/orange tears, urine, sweat + hepatotoxicity I - peripheral neuropathy (supplement VitB6/pyridoxine) + hepatotoxicity P - gout (hyperuraemia) + hepatotoxicity E - vision changes (colour blind, reduced acuity), CKD
37
what are key facts of BCG vaccine
need to do matoux skin test before administering BCG = live attenuated vaccine (weakened form of TB) doesn't provide immunity against pulmonary TB
38
what type of TB does BCG not protect against
pulmonary TB
39
what are the 3 most common cancers
breast, prostate, lung
40
what are the different types of lung cancer
80% non-small cell: most common adenocarcinoma (esp non-smoker) squamous cell carcinoma, large cell 20% small cell
41
how do the different non-small cell lung cancers differ
adenocarcinoma - peripheral affects mucus secreting cells (most common overall, esp non smoker) squamous carcinoma - central presents with pneumonia 2ndary to obstructed bronchus releases ectopic PTHrP histopathology shows keratin metastasises late large cell metastasises early
42
which lung cancer metastasises early + late
early: large cell, small cell late: squamous
43
what are features of small cell carcinoma
affects APUD neuroendocrine cells of lung causes paraneoplastic syndromes (SIADH, Cushing syndrome, LEMS, limbic encephalitis) most aggressive lung cancer common in smokers metastasises early
44
where do lung cancers metastasise to
bone, brain, adrenal glands, liver
45
how does lung cancer present
SOB, cough, haemoptysis recurrent chest infections - pneumonia (in squamous carcinoma, 2ndary to obstructed bronchus) fever, appetite/weight loss finger clubbing, lymphadenopathy, wheeze/stridor pleural effusion plethoric face as SVC obstruction - swollen, SOB, distended veins if cyanosis = Pemberton sign, medical emergency Horner syndrome (ptosis, meiosis, anhydrosis) - pan coast tumour in lung apex causing cervical SNS chain compression hoarse voice as recurrent laryngeal nerve palsy SOB, weak diaphragm as phrenic nerve palsy
46
what additional syndromes are seen with small cell + squamous carcinoma
small cell = SIADH (euvolaemic hypoNa), Cushing syndrome, LEMS, limbic encephalitis squamous = hyperCa (as ectopic PTHrP) causes bone pain, renal stone, abdo pain, psych moan
47
what is mesothelioma
malignancy of mesothelial cells of pleura associated with asbestos exposure v.poor prognosis, treat with palliative chemo
48
when to do 2WW referral for lung cancer
aged 40yr+ with unexplained haemoptysis
49
when to order urgent CXR in 2weeks
aged 40yr with recurrent chest infection, clubbing, lymphadenopathy or 2 of: cough/SOB/fatigue/weight loss
50
what is main RF for lung cancer + mesothelioma
SMOKING mesothelioma - asbestos exposure
51
what investigations done for lung cancer
initial = CXR hilar enlargement, wide mediastinum as enlarged lymph nodes focal lesion - peripheral if adenocarcinoma, central in squamous unilateral pleural effusion lung collapse diagnostic = EBUS + biopsy CT TAP to check for metastasis PET-CT to see lymph node involvement
52
when to do lung function test for lung cancer
if non small cell pre-existing lung disease + before surgical resection
53
how does management of NSCLC + small cell differ
for both - smoking cessation NSCLC = surgical resection with VATS + adjuvant chemo or radiotherapy if early stage NSCLC small-cell = chemo (with cisplatin) + radio as worse prognosis

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