Resp Flashcards
how do asthma + COPD differ
asthma - obstructive airway disease with paroxysmal/reversible bronchocontriction
COPD - irreversible obstructive airway disease
how are bronchi in asthma
inflamed, hyper-responsive
what is immunology of asthma
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
what remodelling occurs in asthma
inflammation causes airway remodelling
bronchial smooth muscle hypertrophy, bronchoconstriction
higher vascular permeability
mucous gland hypertrophy
how does asthma present
wheeze, SOB
diurnal variation - cough worse at night
symptoms worse with exercise or after NSAID
PMH/FH of atopy: asthma, allergic rhinitis, eczema
how does acute asthma attack present
high RR, worsening SOB
hyper-resonant
wheeze, chest tightness
what are different severities of asthma attack
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)
what are diagnostic criteria for asthma
PEFR variability >20%
FeNO >40ppb in adult, >35ppb in child
spirometry shows obstructive pattern FEV1/FVC <0.7, with bronchodilator reversibility
how is acute asthma attack managed
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
how is chronic asthma managed
conservative = stop smoking, weight loss, avoid triggers, review inhaler technique
medical = SABA -> ICS -> ICS + LTRA -> ICS + LABA -> MART -> specialist referral
what are pink puffer + blue bloater in COPD
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
what is pathology of COPD
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)
how does alpha-1 antitrypsin deficiency cause asthma
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
how does cigarette smoke affect the airway
stops cilia moving, so noxious chemicals not swiped away
prevents WCC from removing bacteria
how does COPD present
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
why are COPD patients prone to chest infections
damaged lung tissue and obstructive lung disease makes it harder to ventilate lungs
so pathogens are trapped
what are signs of cor pulmonale
R-sided HF secondary to COPD
raised JVP, hepatomegaly, peripheral oedema
chronic hypoxia causes pulmonary artery vasoconstriction, leading to pulmonary HTN
how is COPD classified
depends on FEV1 - 4 stages ranging from <30-80%
what are RF for COPD
smoker, old, male
FH/PMH of A1AT deficiency (autosomal recessive)
what is FEV1/FVC <0.7 with chronic cough but no wheeze/SOB
bronchiectasis - dilated airways that allow pathogen to be trapped in
how is COPD diagnosed + what are investigation results
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
how is COPD managed
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
what additional medications can be given for COPD
PO carbacystine - break down mucus
azithromycin - long term ABx to prevent infections
what are target O2 sats for COPD
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)
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
can COPD pt have surgery for condition
YES - lung volume reduction surgery (remain breathless despite maximal medical therapy)
upper lobe predominant emphysema, FEV1 >20%
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)
what are RF for TB
close contact with infected individuals
homeless, IVDU, immunocompromised - HIV
south-asia + sub-saharan
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
how do secondary + military TB differ
secondary = latent TB eactivates
miliary = primary TB bacteria spread via blood
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
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)
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
what does CXR for TB show
calcified granulomas - ghon focus
pulmonary consolidation, pleural effusion
upper lobe cavitation
if miliary TB, millet seeds spread evenly
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
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
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
what type of TB does BCG not protect against
pulmonary TB
what are the 3 most common cancers
breast, prostate, lung
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
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
which lung cancer metastasises early + late
early: large cell, small cell
late: squamous
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
where do lung cancers metastasise to
bone, brain, adrenal glands, liver
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
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
what is mesothelioma
malignancy of mesothelial cells of pleura
associated with asbestos exposure
v.poor prognosis, treat with palliative chemo
when to do 2WW referral for lung cancer
aged 40yr+ with unexplained haemoptysis
when to order urgent CXR in 2weeks
aged 40yr with
recurrent chest infection, clubbing, lymphadenopathy
or 2 of: cough/SOB/fatigue/weight loss
what is main RF for lung cancer + mesothelioma
SMOKING
mesothelioma - asbestos exposure
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
when to do lung function test for lung cancer
if non small cell
pre-existing lung disease + before surgical resection
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
