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4 CSIM2 > respiratory > Flashcards

respiratory Flashcards

1
Q

describe escalating management options according to BTS guidelines for asthma in adults

A
  1. SABA
  2. SABA + low dose ICS
  3. SABA + low dose ICS + LABA
  4. SABA + high dose ICS + LABA (or 4th drug e.g LRTA, theophylline or LAMA)
  5. oral CS
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2
Q

what to do if oral CS do not work for asthma

A

if IgE mediated, add in e.g. Omalizumab

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3
Q

what kind of drug is salmeterol?

A

long acting beta2 agonist

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4
Q

5 areas in the chest/lung/pulmonary that can cause conditions and examples of them

A

airways - copd, asthma, bronchiecstasis

parenchyma - pulm fibrosis, emphysema, hypersen pneumonitis

pleura - pleural effusion, pleural malignancy, pleural thickening

vascular - PE, pulm hypertension

ventilation - sleep apnea, obesity hypoventilation, neuromuscular dz, thoracic cage abnormality

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5
Q

examples of obstructive and restrictive pulmonary conditiosn

A

obstructive - copd, asthma, bronchiecstasis

restrictive - pulm fib, neuromuscular abnormalities, thoracic cage abnormalities, obesity

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6
Q

what is the shape of a flow volume loop showing large airway obstruction and diffuse small airway obstruction

A

large obs - hamburger shape

small obs - large spike and quick drop

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7
Q

what can cause large airway obs and what can cause small airway obs

A

large - tracheal collapse

small - copd/asthma

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8
Q

what is transfer factor

A

how well alveoli are at transferring gas to caps

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9
Q

difference between TLCO and KCO

A

tlco tells whole lung

kco tells per unit of lung vol

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10
Q

difference between hrct and spiral/helical ct

A

hrct is high res, can see small detail

helical shows continuously, can spot small things

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11
Q

generally what conditions can be picked up on hrct and helical ct

A

hrct - pul fibrosis, bronchiecstasis

helical - PE

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12
Q

e.g. of occupational pneumoconiosis

A

silicosis from silica, coal, and asbestos

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13
Q

what is the lung function pattern of pneumoconiosis

A

restrictive

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14
Q

what is the effect of pneumoconiosis

A

small diffuse nodules that progresses to massive large fibrosis

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15
Q

how to diagnosis pneumoconiosis

A

imaging, biopsy

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16
Q

what is the difference between asbestos pleural plaques and pleural thickening

A

pleural plaques usually asymptomatic, does not progress

diffuse plueral thickening has effusion, symptoms of sob and restrictive lung function.

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17
Q

what is asbestosis

A

interstitial fibrosis due to asbestos inhalation

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18
Q

what are signs of asbestosis

A

fine inspiratory crackles
basal reticular shadowing on cxr
restrictive lung function

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19
Q

difference between occupational asthma and work aggravated asthma

A

aggravated asthma happens in pre-existing asthma, aggravated by exposure in work place

occupational asthma is new onset asthma, due to sensitisation of allergen encountered in work place

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20
Q

what are 3 pathological characteristics of asthma

A

chronic airway inflammation
hyperresponsiveness
reversible

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21
Q

difference between sensitiser induced occupational asthma and irritant induced occupational asthma

A

sensitiser - most common, symptoms occur 1-2 years after sensitisation, immunologically driven

irritant-induced – reaction to exposure to irritant gas, fumes, vapours,

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22
Q

common causative agents of occupational asthma

A 
flour
dust
isocyanate (paints)
cleaning products
enzymes
animals
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23
Q

difference between high molecular weight and low molecular weight allergens

A

high molecular weight allergens are usually proteins that trigger an IgE response.

low molecular weight agents are usually chemicals with no specific IgE antibody

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24
Q

examples of LMW allergen

A

isocyanates

acrylates (glue)

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25
Q

risk factors for occupational asthma

A

history of atopy.

smoking

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26
Q

history indications of occupational asthma

A

new work place - 1-2 years
symptoms better when away from work
other workers affected as well

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27
Q

what are the goals of investigation of occupational asthma

A

to find relationship between symptoms and occupation

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28
Q

what are some investigations that can be done to investigate occupational asthma

A 
spirometry
inhaler reversibility
IgE tests, skin prick
daily PEFR
challenge tests
FeNO tests
sputum eosinophils
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29
Q

what does PD20 tell in challenge testing

A

the dose of stimulant needed to cause 20% drop in FEV1

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30
Q

management in occupational asthma

A

standard asthma guidelines
avoidance of allergen
Anti-IgE drug if appropriate

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31
Q

2 types of coal workers pneumoconiosis

A

simple and progressive massive fibrosis

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32
Q

describe simple pneumoconiosis

A

coal deposits in lungs, visible on CXR. symptoms depend on severity

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33
Q

what are 3 categories of simple pneumoconiosis

A

category 1 - few small nodular markings on CXR, lung field normal, no symptoms

category 2 - more small nodular opacities, some symptoms, can progress to PMF

category 3 - many small nodular opacities, lung markings partly or completely obscured. high risk of progression to PMF

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34
Q

what is progressive massive fibrosis

A

more severe coal workers pneumoconiosis

several round fibrotic masses, usually in upper lobes. some with necrotic cavities

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35
Q

what are 2 serum markers that are positive in coal workers pneumoconiosis

A

rheumatoid factor

anti-nuclear antibodies

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36
Q

what does CXR look like in coal workers pneumoconiosis

A

destruction of lung apices
emphysema
lung airway damage

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37
Q

what do respiratory investigations look like in coal workers pneumoconiosis

spirometry
flow volume loop
gas transfer

A

spirometry shows mixed restrictive and obstructive pattern

irreversible airflow limitation shown

reduced gas transfer

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38
Q

symptoms of progressive massive fibrosis in coal workers pneumoconiosis

A

moderate to severe dyspnea
cough (may be black)
respiratory failure

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39
Q

describe the pathophysiological characteristics of COPD

A

chronic airway inflammation
over production of mucus in airways
infiltration of lymphocytes
emphysema - alveoli destruction

40
Q

describe the effects of cor pulmonale

A

right ventricle hypertrophy
ECG changes
peripheral edema
polycythaemia

41
Q

why does cigarette smoking cause COPD

A

due to increased infiltration of neutrophil granulocytes caused by smoke. tips the balance towards protease production by neutrophils

42
Q

why is alpha1 antitrypsin important in preventing COPD

A

it is an importan anti-protease that prevents destruction of airways

43
Q

non-respiratory manifestation of COPD

A 
cardiovascular effects 
hypertension
osteoporosis
metabolic disorders
depression
44
Q

signs of COPD

A 
wheeze, tachypnea
increased work of breathing
hyperinflated chest
poor chest expansion
polycythaemia
coarse flapping tremor
45
Q

explain respiratory drive in COPD patients

A

in long standing COPD, patients body gets used to elevated CO2 levels, thus becoming dependant on hypoxaemia as a ventilary drive.

46
Q

how is cor pulmonale treated

A

LTOT

47
Q

how is COPD investigated and diagnosed

A 
spirometry
reversibility with inhalers
CXR, CT
haemoglobin levels
ECG
echo
48
Q

what must be done in non-smokers when investigating copd

A

alpha1 antitrypsin levels

49
Q

what can be seen on a CXR of a COPD patient

A

flattened diaphragm, bullae, overinflation of lungs

50
Q

inhaler management of COPD

A

give SABA (salbutamol)
give LAMA or LABA
give ICS

51
Q

other management in COPD

A

mucolytics
LTOT
annual flu vaccines
pulmonary rehab

52
Q

how to treat excr of COPD

A

oxygen
antibiotics
oral steroids (short course)
neb bronchodilators

53
Q

why does COPD cause hypoventilation?

A

because after prolonged periods of hypercapnia, body gets used to high CO2 levels. this causes a switch in ventilatory drive from the normal (high co2 levels), to the secondary drive which is hypoxaemia.

so in prolonged COPD, body stops hyperventilating because it is used to high CO2 levels. if too much oxygen is given, then central ventilatory drive is switched off, causing hypoventilation.

54
Q

cause of obstructive sleep apnea

A

airway narrowing during REM sleep due to relaxed muscles

55
Q

causes/risk factors of obstructive sleep apnea

A

pharyngeal narrowing - obesity, acromegaly, enlarged tonsils

nasal obstruction - nasal polyps, adenoids, rhinitis

respiratory depressant drugs - alcohol, sedatives, strong analgesics

56
Q

symptoms of obstructive sleep apnea

A 
sleepiness
fatigue
poor concentration
snoring
resuscitative grunts during sleep
57
Q

process of diagnosis/investigations for obstructive sleep apnea

A 
collateral history
epworth sleepiness scale
overnight pule oximetry
inpatient studies 
blood gases
58
Q

how many apneac episodes per hour would be diagnstic of obstructive sleep apnea?

A

10-15

59
Q

management for obstructive sleep apnea

A

correct modifiable factors - weight, drugs

cpap, ent surgery

60
Q

causes of hypoventilation

A 
decreased central drive
respiratory muscle weakness
obstructive sleep apnea
thoracic cage dysfunction
obesity related
61
Q

what can cause central alveolar hypoventilation

A

any neurological conditions, trauma, space occuyping lesions, CNS degenerative diseases, drugs

62
Q

what is obesity hypoventilation syndrome

A

abnormal ventilatory drive, associated with BMI>30

63
Q

what are features of obesity hypoventilation syndrome

A

awake hypercapnia
obesity
exclusion of other causes

64
Q

consequences of obesity hypoventilation syndrome

A

blunted ventilatory drive
chronic hypercapnia
polycythaemia
right sided heart strain/failure (and complications)

65
Q

e.g. of neuromuscular disorders causing hypoventilation

A

myaesthenia gravis, ALS, GBS, muscular dystrophy

66
Q

people with neuromuscular disorders also have central drive dysfunction - T or F

A

F, usually intact

67
Q

symptoms of hypercapnia

A 
headaches - similar to raised ICP
sleepiness
altered GCS
poor concentration
Co2 retention flap
68
Q

what is hypersensitivity pneumonitis

A

inflammatory response to inhaled antigens

69
Q

what are some associations/causes of hypersensitivity pneumonitis

A

farmers lungs
bird fanciers
cheese worker
mushroom workers

70
Q

what is the pathophysiology of hypersensitivity pneumonitis

A

inhalation of antigen into alveoli and small airways causes inflammatory recruitment of neutrophils, macrophages, lymphocytes. this causes granulomas and focal inflammation.

eventually leading to fibrosis and lung dysfunction

71
Q

symptoms of hypersensitivity pneumonitis

A

systemic symptoms - fever, weight losss, fatigue, anorexia

dry cough, breathlessness,

72
Q

signs of hypersensitivity pneumonitis

A

dry cough, wheeze, squeak, lung crackles

73
Q

radiological findings in hypersensitivity pneumonitis

A

CXR - fluffy nodular shadowing with streaky shadows

HRCT - reticular, nodular and ground glass opacities

74
Q

pulmonary function tests findings in hypersensitivity pneumonitis

A

restrictive with reduced TLCO

75
Q

what other investigations can be done in hypersensitivity pneumonitis

A

FBC - raised PMNs
bronchoalveolar lavage - lymphocytes and granulocytes
antibody testing

76
Q

differentials of hypersensitivity pneumonitis

A

occupational asthma

77
Q

treatment of hypersensitivity pneumonitis

A

avoidance, steroids

78
Q

what is sarcoidosis

A

multisystemic granulomatous disease of unkown cause, frequently affecting the lung

79
Q

how is sarcoidosis often picked up

A

incidental on CXR

80
Q

symptoms of sarcoidosis

A

often asymptomatic
can affect any system and cause any local symptoms

systemic - fatigue, weight loss, fever, night sweats, peripheral lymphadenopathy

respiratory - cough, breathlessness, chest pain

81
Q

lung function tests signs in sarcoidosis

A

mixed restrictive and obstruction picture, often variable

82
Q

what is a classical CXR finding of sarcoidosis

A

bilateral hilar lymphadenopathy

83
Q

what would HRCT show in sarcoidosis

A

opacities around lung fissures, hilar and diffused micronodular opacities “starry sky”

84
Q

how to diagnose sarcoidosis

A

biopsy through EBUS

85
Q

differentials of blateral hilar lymphadenopathy

A

sarcoid
TB
lymphoma
carcinoma

86
Q

idiopathic pulmonary fibrosis is an inflammatory process - T or F

A

F

87
Q

how does IPF happen

A

unkown cause, but injury/insult cause fibrogenic secretions of alveoli causing fibrosis.

88
Q

history pattern in IPF

A

often no PMH, no occupational exposure, progressive breathlessness.

89
Q

what other conditions is IPF associated with

A

coeliac, UC, renal tubular acidosis

90
Q

symptoms of IPF

A

dry cough, breathlessness, advanced cases lead to cor pulmonale

91
Q

signs of IPF

A

finger clubbing, peripheral cyanosis, bi-basal fine crackles, reduced lung expansion, pattern

92
Q

what is the classical CXR finding in IPF

A

ground glass appearance - reticular opacities

93
Q

lung function testing picture in IPF

A

restrictive with reduced TLCO

94
Q

what would ABG look like in IPF

A

type 1 respiratory failure

95
Q

what can be found on HRCT of IPF

A

lower lobe reticular opacities

traction bronchiecstasis

96
Q

treatment for IPF

A

none, supportive, oxygen, pulmonary rehab, transplant

4 CSIM2 (11 decks)

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