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MD2 Foundation > Asthma and COPD > Flashcards

Asthma and COPD Flashcards

1
Q

what is asthma

A

recurrent episodes of airway obstruction due to chronic inflammatory hypersensitivity and hyperresponsiveness of airways

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2
Q

symptoms of asthma and signs

A 
wheeze (due to turbulent flow)
cough
SOB
atopy
family history of asthma, atopy
worse at night
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3
Q

kind of inflammation in asthma (cell)

A

eosinophilic inflammation leadig to bronchospasma and mucosal inflammation

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4
Q

diagnosis of asthma

A

FEV1/FVC salbutamol test

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5
Q

treatment of acute asthma attack

A

oxygen, nebulised salbutamol, tiotropium

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6
Q

asthma management

A

salbutamol (SABA) <3 times per week

otherwise manage with LABA, inhaled steroids/preventers (fluticasone, budesonide)

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7
Q

complications of asthma

A

acute attack
collagen deposition/fibrosis
smooth muscle cell hyperplasia, goblet cell hyperplasia

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8
Q

salbutamol side effects

A

tremor

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9
Q

steroid complications in asthma

A

appettie/weight gain, interrption of sleep

oral thrush, dysphonia (hoarse voice)

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10
Q

prednisolone side effects

A

weight gain/appetie
mood change
can raise blood sugar

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11
Q

pathology of COPD

A

chronic bronchial inflammation/obstruction
loss of cilia
mucus hypersecretion
loss of A-C units, gas exchange surface area, loss of elastic support for airways

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12
Q

what is tiotropium

A

a long acting anticholinergic used in COPD to reduce mucus, reduces exacerbations

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13
Q

treatments available for COPD

A

anticholinergics (tiotropiums)
SABA
inhaled steroids +- LABA
oxygen if PaO2<55

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14
Q

vaccinations for COPD patients

A

yearly influenza

5 yearly pneumococcal

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15
Q

what is pneumonia

A

infection of alveolar units leading to VQ mismatch, diffusion impairment and increased work of breathign

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16
Q

what is the rationale behind empiric antibiotics for community acquired pneumonia?

A

cover both typical and atypical organisms
outcomes are worse if we wait
usually start with penicillin and doxycyline

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17
Q

antibiotics for TB

A

INAH, rifampicin, pyrazinamide, ethambutol

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18
Q

findings on examination in asthma attack

A 
tachypnoea
anxiety
wheeze
prolonged expiratory phase
cyanosis
use of accessory muscles
19
Q

types of inflammation in COPD

A

neutrophilic, macrophages

proteinase-antiproteinase imbalance destroying alveolar connective tissue

20
Q

changes in lung parenchyma in COPD

A

loss of alveolar-capillary membrane so loss of surface area for gas exchange
loss of elastic support
lose oxygenation capacity

21
Q

mechanism of emphseama

A

protease/antiprotease imablance digest elastin and other structureal proteins in alveolar wall
macrophages and t cell inflammation

22
Q

function of alpha1antitrypsin

A

degrade proteases in the lung and the liver

23
Q

why might you use slow vitgal capacity in assessing COPD

A

forced vital cpacity can cause airway collapse, trapping air and giving an underestimate of vital capacity

24
Q

what should the forced expiratory ratio be below to indicate obstruction

A

<0.7

25
Q

what kind of inflammation is asthma?

A

eosinophilic

26
Q

COPD goals of treatment

A

control symptoms
improve lung function
prevent exacerbations/deterioiration
smoking cessation

27
Q

COPD treatment plan? side effeects?

A

mild: treat symptoms with short and long beta 2 agonist (salbutamol) but get tremor
more: add tiotropium/anticholinergic to lower SOB, but get anti-SLUD
severe: inhaled steroids (fluticasone) but get increased pneumonia risk

also pulmonary rehabilitation couse (8 week exercise class)
low dose theophylline may be antiinflammatory
VACCINES: influenza and twice pneumoccocal 5 years apart
HOME OXYGEN THERAPY

28
Q

requirements for home oxygen therapy

A

PaO2<55mmHg

smoking cessation

29
Q

what is lung volume reduction surgery

A

resection of emphysematous lung to decompress areas of functional lung

30
Q

what is a COPD exacerbation and how should it be treated

A

change in patients baseline SOB, sputum amount/colour, coough beyond normal day-day variations with acute onset.
usually infectious, treat with doxycyline

31
Q

what happens to pulmonary pressures as CO increases

A

it stays the same by recruiting pulmonary vessels

32
Q

causes of pulmonary hypertension

A

increased Left atrial pressure
increased pulmonary flow (fluid overload, left to right shunt)
increased pulmonary vascular resistance (vasoconstriction in hypoxia etc)

33
Q

consequences of pulmonary hypertension

A

right ventricular dilation/hypertrophy can lead to systemic venous pressure elevation

34
Q

symptoms of pulmonary vascular disease

A 
SOB
syncope
tiredness
ankle swelling
cough
pleuritic pain
haemoptysis
35
Q

signs of pulmonary vascular disease

A

right ventriucular heave
loud P2
elevated JVP
ascites

36
Q

what criteria dow e use to grade likeliness of PE

A

wells criteria

37
Q

PE diagnosis

A

D-dimer: negative result excludes PE
CTPA
VQ scan

38
Q

treatment for PE

A

supportive oxygen

anticoagulation (heparin and warfarin)

39
Q

causes of clubbing

A

NSCLC, bronchiectasis, fibrosis, SBE, biliary cirrhosis

40
Q

why do we do metabolic flap in resp exam

A

can be caused by hypercapnoea

41
Q

what lobe are we listening to on the back and why?

A

the oblique fissure goes up high posteriorly so it is the lower lobe

42
Q

what causes crackles physiologically? (2 things)

A

bubbling of air through secretions

sudden opening of small airways with equalisation of pressure (at end of inspiration)

43
Q

percussion and breath soudns in pleural effusion?

A

decreased percussion and breath sounds

44
Q

percussion and breath sounds in consolidation?

A

increased breath sounds and decreased percussion

MD2 Foundation (10 decks)

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