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Phase 2A HT > Resp > Flashcards

Resp Flashcards

1
Q

what is COPD

A

poorly reversible airflow obstruction usually progressive assoc w persistent inflam
consists of emphysema and chronic bronchitis

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2
Q

define emphysema

A

dilation and destruction of lung tissue distal to the terminal bronchiole and destruction of alveolar walls

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3
Q

how does smoking lead to COPD

A

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

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4
Q

characteristic clinical features of COPD

A

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

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5
Q

most important factor in COPD mx

A

smoking cessation!

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6
Q

first line bronchodilator in COPD

A

antimuscarinic eg tiotropium bromide

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7
Q

why must you be careful giving O2 to COPD pts

A

in some pts hypoxia is only respiratory drive so if you correct hypoxia they lose any resp drive and can go into resp arrest

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8
Q

3 key characteristics of asthma pathology

A

REVERSIBLE AIRFLOW LIMITATION
airway hyperresponsiveness
inflam of bronchi

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9
Q

define atopy

A

the tendency to form IgE Ab against common (non-harmful) environmental agents

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10
Q

triad of atopy

A

asthma, eczema, hayfever

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11
Q

airway remodelling in asthma

A

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

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12
Q

asthma precipitants/triggers

A

HOUSE DUST MITE AND ITS FAECES, cold, exercise, car fumes/perfumes/smoke, emotion, drugs (NSAIDs and BB) and occupational exposure

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13
Q

clinical presentation

A 
wheezing attacks
SOB
chest tightness
cough
DIURNAL VARIATION and provoked by triggers
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14
Q

steowise mx of asthma

A 
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
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15
Q

emergency mx of asthma

A

high flow 02, nebulised SABA - salbutamol, IV hydrocortisone

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16
Q

what is EAA

A

= extrinsic allergic alveolitis - widespsread granulomatous inflam of lung parenchyma, alveoli and small airways
type III hypersensitivity reaction (immune-complex mediated)

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17
Q

3 subtypes of EAA

A

farmers, pigeon-fanciers, malt-workers

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18
Q

RF for EAA

A

preexisting lung condition
occupational exposures
bird-keeping
hot-tub use

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19
Q

key features of chronic exposure in EAA

A

GRANULOMA and OBLITERATIVE BRONCHIOLITIS
others: clubbing, cyanosis, SOBOE, type 1 resp failure, cor pulmonale, crackles
IPF - w HONEYCOMB LUNG

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20
Q

CXR findings in EAA

A

fluffy nodular shadows
ground glass appearance (fibrosis)
HONEYCOMB LUNG if severe

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21
Q

mx of EAA

A

REMOVE offending agent (if not possible - ie occupation, advise on protective equipment eg facemasks)
oral steroids (prednis)
COMPENSATION
(O2 in acute)

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22
Q

what is bronchiectasis

A

abnormal and permanent dilation of the bronchial airways w impaired clearance or bronchial secretions and subsequent recurrent infs and bronchial inflam

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23
Q

characteristic feature of bronchiectasis

A

Chronic PRODUCTIVE cough with COPIOUS amounts of discoloured sputum (and recurrent chest infections)

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24
Q

most common causes of bronchiectasis

A

CF or post-inf (pneumonia, whopping cough, TB, measles)

many cases idiopathic

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25
Q

symptoms of bronchiectasis

A

(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

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26
Q

DDX for bronchiectasis

A

COPD, CF, TB

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27
Q

most useful ix in bronchiectasis and what does it show

A

CT of chest = gold standard - bronchial dilation and wall thickening (airways bigger than corresponding artery)

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28
Q

major causative organisms of bronchiectasis

A

staph. a, pseudomonas aureginosa, h. influenzae, anaerobes

others: strep and klebsiella

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29
Q

mx of bronchiectasis

A

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

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30
Q

what is CF

A

= 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)

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31
Q

where are CFTRs found

A

in epi cells of lungs, pancreas, GI and reproductive tracts

32
Q

what is CFTR

A

chloride channel and regulatory protein (=cystic fibrosis transmembrane conductance regulator)

33
Q

CF syndrome characterised by?

A

thickened secretions –> bronchopulm inf andpancreatic insufficiency w increased sodium and cl conc in sweat

34
Q

resp symps of CF

A 
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
35
Q

GI/alimentary effects of CF

A

pancreatic insufficiency –> steatorrhoea (85%) and DM
meconium ileus
cholesterol gallstones
cirrhosis/hepatic failure

36
Q

Nutritional effects of CF

A

malabsorption, deficiency states, WL, poor growth, malnutrition

37
Q

urogenital effects of CF

A

in male - atrophy of vas leads to 98% infertile
women - able to conceive but often get secondary amenorrhoea
renal impairment

38
Q

waht sodium level in swaet is diagnostic of CF

A

> 60mmol/L

39
Q

what infections do you have to especially careful with in regards to CF

A

pseudomonas aureginosa
burkholderia cepecia complex
MYCOBACTERIA ABSCESSUS
–> poor prognosis and multiresistant to ABX

40
Q

waht drug can be used in CF to inhibit sodium transport

A

amiloride

41
Q

what is sarcoidosis

A

a multisystem granulomatous chronic inflam condition characterised by epithelioid non-caseating granuloma formation at various sites in the body
unknown aetiology

42
Q

4 resp s and s of sarcoidosis

A

breathlessness, wheeze, chronic non-productive cough, coarse crackles, pulm infiltrates

43
Q

4 skin s and s of sarcoidosis

A

erythema nodosum, lupus pernio, waxy maculopapular lesions, granulomas infiltrating scars

44
Q

4 eye s and s of sarcoidosis

A

ant and post uveitis, conjunctivitis, lacrimal gland enlargement
later on: glaucoma and dry eyes

45
Q

liver s and s of sarcoidosis

A

granulomatous hepatitis, hepatomegaly

46
Q

4 neurological s and s of sarcoidosis

A

bell’s palsy, facial nerve palsy, dysphasia, hoarseness, seizures, mass lesions, visual defects

47
Q

bone involvement in sarcoidosis

A

arthralgias, bone cysts, bone and joint pain and inflam arthritis

48
Q

Common sites for bx in sarcoidosis

A

enlarged LN
TBBx
skin lesions

49
Q

when would you give steroids (prednis) in sarcoid

A

2/3 remit spontaneously, give steroids if:
lung infil/abnormal function persists for 6m
or hypercalcaemia
neurological/myocardial/optic involvement

50
Q

define pulm HTN

A

mPAP>25mmhg at rest measured on R heart catheterization

51
Q

three early symps of pulm HTN and why do you get them

A

dyspnoea, fatigue, weakness - due to inability to increase CO on exercise

52
Q

features of advanced pulm HTN

A 
= features of R HF
increased JVP
hepatomegaly
ascites
pleural effusion
periph oedema
pulsatile liver
53
Q

s and s of R heart hypertrophy in pulm HTN

A

angina, syncope, periph oedema and abdo distension (due to hepatic congestion), lethargy

54
Q

best ix in pulm HTN

A

r heart catheterization = gold standard

55
Q

what would an ECG show in pulm HTN

A

right heart hypertrophy and p pulmonale

56
Q

clinical presentation of pneumothorax

A

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

57
Q

typical signs of pleural effusion

A

reduced chest expansion
reduced breathing sounds
stony dull to percussion

58
Q

define pneumothorax

A

air in the pleaural space leading to partial or complete collapse of lung (primary/secondary)
unilateral increase in pleural pressure

59
Q

mx of pneumothorax

A

PRIMARY: needle aspiration, if lung fails to reexpand - intercostal tube drainage nad if pneumothorax reamins a 48hrs –> surgery - pleurectomy/pleurodesis
SECONDARY: if

60
Q

name three pleurodesis agents

A

talc, tetracycline, bleomycin

61
Q

what lung cancer is most associated with asbestos exposure

A

adenocarcinoma (no small cell) local and distant mets

62
Q

what it the most common form of lung cancer

A

squamous cell carcinoma (NSCLC) local spread common, widespread mets late

63
Q

what LC do you get in non smokers

A

adenocarcinoma

64
Q

what cell type do SCLC arise from

A

endocrine cells (kulchitsky cells) – secrete polypeptide hormones

65
Q

4 most common causes of pneumonia

A

strep pneumoniae (most common), h influenzae, influenza A, mycoplasma pneumoniae

66
Q

treatment of TB

A 
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
67
Q

3 components of global strategy to reduce TB prevalence

A

contact tracing
identification and tx of dormant phase
screening of healthcare proffessionals/new entries to country

68
Q

tx for mild CAP

A

amoxicillin/clarythromycin

69
Q

tx for moderate CAP

A

amox and claryth

70
Q

tx for severe CAP

A

IV coamoxiclav and clarythromycin/cefuoxime

71
Q

tx for HAP

A

gentamycin and meropenam

72
Q

tx for HAP caused by MRSA

A

VANCOMYCIN

73
Q

two tests specific to TB

A

TST (Mantoux) and Interferon gamma release assays (IGRAs)

74
Q

complications of pneumonia

A

empyema and lung abscess

75
Q

how do you predict mortality in CAP

A 
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

Phase 2A HT (11 decks)

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