Resp Flashcards
what is COPD
poorly reversible airflow obstruction usually progressive assoc w persistent inflam
consists of emphysema and chronic bronchitis
define emphysema
dilation and destruction of lung tissue distal to the terminal bronchiole and destruction of alveolar walls
how does smoking lead to COPD
smoke leads to mucus gland hypertrophy and increase in neutrophils, macrophages and lymphocytes - these release inflam mediatiors leading to structural changes and connective tissue breakdown
smoking also inhibits a1-AT which is a protease inhibitor
characteristic clinical features of COPD
chronic productive cough (for >3m for 2 consec years)
wheeze and breathlessness
- above 2 w hx of smoking
others: recurrent chest infs, pursed lips on expiration, poor chest expansion - hyperinflation of lungs (barrel-shaped chest), increased work of breathing - leaning forward and use of accessory muscles
most important factor in COPD mx
smoking cessation!
first line bronchodilator in COPD
antimuscarinic eg tiotropium bromide
why must you be careful giving O2 to COPD pts
in some pts hypoxia is only respiratory drive so if you correct hypoxia they lose any resp drive and can go into resp arrest
3 key characteristics of asthma pathology
REVERSIBLE AIRFLOW LIMITATION
airway hyperresponsiveness
inflam of bronchi
define atopy
the tendency to form IgE Ab against common (non-harmful) environmental agents
triad of atopy
asthma, eczema, hayfever
airway remodelling in asthma
SM undergoes hypertrophy and hyperplasia –> increased muscle in airway wall
also get collagen deposition in repair processes - further thickens wall
both lead to decrease in lumen size
columnar ciliated epi also replaced by squamous metaplasia and increased goblet cells
asthma precipitants/triggers
HOUSE DUST MITE AND ITS FAECES, cold, exercise, car fumes/perfumes/smoke, emotion, drugs (NSAIDs and BB) and occupational exposure
clinical presentation
wheezing attacks SOB chest tightness cough DIURNAL VARIATION and provoked by triggers
steowise mx of asthma
1 - SABA eg salbutamol/terbutaline 2 - add ICS eg beclametasone 3 - add SABA ed formoterol/salmeterol 4 - either: increase ICS, add leukoterine agonist eg montelukast, or oral B agonist 5. add oral steroid - prednis
emergency mx of asthma
high flow 02, nebulised SABA - salbutamol, IV hydrocortisone
what is EAA
= extrinsic allergic alveolitis - widespsread granulomatous inflam of lung parenchyma, alveoli and small airways
type III hypersensitivity reaction (immune-complex mediated)
3 subtypes of EAA
farmers, pigeon-fanciers, malt-workers
RF for EAA
preexisting lung condition
occupational exposures
bird-keeping
hot-tub use
key features of chronic exposure in EAA
GRANULOMA and OBLITERATIVE BRONCHIOLITIS
others: clubbing, cyanosis, SOBOE, type 1 resp failure, cor pulmonale, crackles
IPF - w HONEYCOMB LUNG
CXR findings in EAA
fluffy nodular shadows
ground glass appearance (fibrosis)
HONEYCOMB LUNG if severe
mx of EAA
REMOVE offending agent (if not possible - ie occupation, advise on protective equipment eg facemasks)
oral steroids (prednis)
COMPENSATION
(O2 in acute)
what is bronchiectasis
abnormal and permanent dilation of the bronchial airways w impaired clearance or bronchial secretions and subsequent recurrent infs and bronchial inflam
characteristic feature of bronchiectasis
Chronic PRODUCTIVE cough with COPIOUS amounts of discoloured sputum (and recurrent chest infections)
most common causes of bronchiectasis
CF or post-inf (pneumonia, whopping cough, TB, measles)
many cases idiopathic
symptoms of bronchiectasis
(chronic productive cough with LOTS OF SPUTUM and recurrent infs)
halitosis
febrile w malaise
episodes of pneumonia
severe disease = foul-smelling, khaki/green mucus
clubbing and coarse crackles
haemoptysis (may be MASSIVE haemorrhage - life threatening)
breathlessness, wheeze, chest pain
DDX for bronchiectasis
COPD, CF, TB
most useful ix in bronchiectasis and what does it show
CT of chest = gold standard - bronchial dilation and wall thickening (airways bigger than corresponding artery)
major causative organisms of bronchiectasis
staph. a, pseudomonas aureginosa, h. influenzae, anaerobes
others: strep and klebsiella
mx of bronchiectasis
POSTURAL DRAINAGE = essential, PT teach pt to tip themselves 3x/day
ABX for inf/cause - flucloxacillin if staph a
bronchodilators
ICS/oral steroid - delay progression
surgery in few pts
prevention/supportive - annual flu vac/pneumococcal, smoking cessation, prompt ABX in inf
what is CF
= autosomal recessive condition
mutation (deletion of phenylalanine)in signle gene on chromosome 7 resulting in mutation in CFTR
deletion most commonly at △F508
alteration of CFTR –> deranged transport of Cl –> alterations to composition of secretions (viscosity and tenacity changed)
where are CFTRs found
in epi cells of lungs, pancreas, GI and reproductive tracts
what is CFTR
chloride channel and regulatory protein (=cystic fibrosis transmembrane conductance regulator)
CF syndrome characterised by?
thickened secretions –> bronchopulm inf andpancreatic insufficiency w increased sodium and cl conc in sweat
resp symps of CF
babies born with structurally normal lungs --> recurrent infs --> inflam damage --> bronchiectasis --> airflow limitation and resp failure recurrent infs (presenting feature) sinusitis and nasal polyps breathlessness and haemoptysis spontaneous pneumothorax cor pulmonale eventually
GI/alimentary effects of CF
pancreatic insufficiency –> steatorrhoea (85%) and DM
meconium ileus
cholesterol gallstones
cirrhosis/hepatic failure
Nutritional effects of CF
malabsorption, deficiency states, WL, poor growth, malnutrition
urogenital effects of CF
in male - atrophy of vas leads to 98% infertile
women - able to conceive but often get secondary amenorrhoea
renal impairment
waht sodium level in swaet is diagnostic of CF
> 60mmol/L
what infections do you have to especially careful with in regards to CF
pseudomonas aureginosa
burkholderia cepecia complex
MYCOBACTERIA ABSCESSUS
–> poor prognosis and multiresistant to ABX
waht drug can be used in CF to inhibit sodium transport
amiloride
what is sarcoidosis
a multisystem granulomatous chronic inflam condition characterised by epithelioid non-caseating granuloma formation at various sites in the body
unknown aetiology
4 resp s and s of sarcoidosis
breathlessness, wheeze, chronic non-productive cough, coarse crackles, pulm infiltrates
4 skin s and s of sarcoidosis
erythema nodosum, lupus pernio, waxy maculopapular lesions, granulomas infiltrating scars
4 eye s and s of sarcoidosis
ant and post uveitis, conjunctivitis, lacrimal gland enlargement
later on: glaucoma and dry eyes
liver s and s of sarcoidosis
granulomatous hepatitis, hepatomegaly
4 neurological s and s of sarcoidosis
bell’s palsy, facial nerve palsy, dysphasia, hoarseness, seizures, mass lesions, visual defects
bone involvement in sarcoidosis
arthralgias, bone cysts, bone and joint pain and inflam arthritis
Common sites for bx in sarcoidosis
enlarged LN
TBBx
skin lesions
when would you give steroids (prednis) in sarcoid
2/3 remit spontaneously, give steroids if:
lung infil/abnormal function persists for 6m
or hypercalcaemia
neurological/myocardial/optic involvement
define pulm HTN
mPAP>25mmhg at rest measured on R heart catheterization
three early symps of pulm HTN and why do you get them
dyspnoea, fatigue, weakness - due to inability to increase CO on exercise
features of advanced pulm HTN
= features of R HF increased JVP hepatomegaly ascites pleural effusion periph oedema pulsatile liver
s and s of R heart hypertrophy in pulm HTN
angina, syncope, periph oedema and abdo distension (due to hepatic congestion), lethargy
best ix in pulm HTN
r heart catheterization = gold standard
what would an ECG show in pulm HTN
right heart hypertrophy and p pulmonale
clinical presentation of pneumothorax
sudden onset pleuritic chest pain and breathlessness
if large: decreased breath sounds and hyper-resonant percussion
others: pallor, tachycardia, decreased chest expansion and deviated trachea
typical signs of pleural effusion
reduced chest expansion
reduced breathing sounds
stony dull to percussion
define pneumothorax
air in the pleaural space leading to partial or complete collapse of lung (primary/secondary)
unilateral increase in pleural pressure
mx of pneumothorax
PRIMARY: needle aspiration, if lung fails to reexpand - intercostal tube drainage nad if pneumothorax reamins a 48hrs –> surgery - pleurectomy/pleurodesis
SECONDARY: if
name three pleurodesis agents
talc, tetracycline, bleomycin
what lung cancer is most associated with asbestos exposure
adenocarcinoma (no small cell) local and distant mets
what it the most common form of lung cancer
squamous cell carcinoma (NSCLC) local spread common, widespread mets late
what LC do you get in non smokers
adenocarcinoma
what cell type do SCLC arise from
endocrine cells (kulchitsky cells) – secrete polypeptide hormones
4 most common causes of pneumonia
strep pneumoniae (most common), h influenzae, influenza A, mycoplasma pneumoniae
treatment of TB
RIPE rifampicin isoniazid pyrizinamide ethambutol (first 2 for 6m second 2 only for first 2m) add corticosteroid and tx for 12m if CNS involvement DOTS -- better prognosis
3 components of global strategy to reduce TB prevalence
contact tracing
identification and tx of dormant phase
screening of healthcare proffessionals/new entries to country
tx for mild CAP
amoxicillin/clarythromycin
tx for moderate CAP
amox and claryth
tx for severe CAP
IV coamoxiclav and clarythromycin/cefuoxime
tx for HAP
gentamycin and meropenam
tx for HAP caused by MRSA
VANCOMYCIN
two tests specific to TB
TST (Mantoux) and Interferon gamma release assays (IGRAs)
complications of pneumonia
empyema and lung abscess
how do you predict mortality in CAP
CURB65 c-confused u-urea>7 r-RR>30 b-BP -- SBP65yrs
1 point for each - score of 0-1 = outpt tx, 2 = closely supervised outpt tx, 3-5 = admission
