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302 review > Resp > Flashcards

Resp Flashcards

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
Q

when is LTOT given for COPD

A

only if stopped smoking

chronic hypoxia, PaO2 <7.3kPa
OR PaO2 7.3-8kPa + polycthaemia, HF, peripheral oedema, pulmonary HTN

26
Q

can COPD pt have surgery for condition

A

YES - lung volume reduction surgery (remain breathless despite maximal medical therapy)

upper lobe predominant emphysema, FEV1 >20%

27
Q

what type of bacteria is TB

A

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
Q

what are RF for TB

A

close contact with infected individuals

homeless, IVDU, immunocompromised - HIV

south-asia + sub-saharan

29
Q

how is TB spread

A

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
Q

how do secondary + military TB differ

A

secondary = latent TB eactivates

miliary = primary TB bacteria spread via blood

31
Q

how does TB present

A

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
Q

how to investigate TB

A

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
Q

how are sputum samples taken for TB

A

at least 3 (may need bronchoscopy/lavage)
lymph node aspiration, MTB blood cultures

if CNS involved, do CSF - high protein, low glucose, lymphocytosis

34
Q

what does CXR for TB show

A

calcified granulomas - ghon focus
pulmonary consolidation, pleural effusion
upper lobe cavitation

if miliary TB, millet seeds spread evenly

35
Q

how is active TB managed

A

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
Q

what are side effects of TB drugs

A

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
Q

what are key facts of BCG vaccine

A

need to do matoux skin test before administering

BCG = live attenuated vaccine (weakened form of TB)
doesn’t provide immunity against pulmonary TB

38
Q

what type of TB does BCG not protect against

A

pulmonary TB

39
Q

what are the 3 most common cancers

A

breast, prostate, lung

40
Q

what are the different types of lung cancer

A

80% non-small cell:
most common adenocarcinoma (esp non-smoker)
squamous cell carcinoma, large cell

20% small cell

41
Q

how do the different non-small cell lung cancers differ

A

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
Q

which lung cancer metastasises early + late

A

early: large cell, small cell
late: squamous

43
Q

what are features of small cell carcinoma

A

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
Q

where do lung cancers metastasise to

A

bone, brain, adrenal glands, liver

45
Q

how does lung cancer present

A

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
Q

what additional syndromes are seen with small cell + squamous carcinoma

A

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
Q

what is mesothelioma

A

malignancy of mesothelial cells of pleura
associated with asbestos exposure

v.poor prognosis, treat with palliative chemo

48
Q

when to do 2WW referral for lung cancer

A

aged 40yr+ with unexplained haemoptysis

49
Q

when to order urgent CXR in 2weeks

A

aged 40yr with
recurrent chest infection, clubbing, lymphadenopathy

or 2 of: cough/SOB/fatigue/weight loss

50
Q

what is main RF for lung cancer + mesothelioma

A

SMOKING

mesothelioma - asbestos exposure

51
Q

what investigations done for lung cancer

A

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
Q

when to do lung function test for lung cancer

A

if non small cell
pre-existing lung disease + before surgical resection

53
Q

how does management of NSCLC + small cell differ

A

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

302 review (14 decks)

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