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1
Q

markers of SLE

A

IgG and postitive ANA

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2
Q

how to test for CF in newborn

A

immuno-reactive trypsin raised

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3
Q

normal position of ET tube

A

2cm above the carina

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4
Q

when is ground glass opacity seen

A

EAA

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5
Q

daltons law of partial pressure

A

at constant volume and temperature, the total pressure exerted by a mixture of gases is equal to the sum of the partial pressures of the component gases

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6
Q

boyles law

A

as volume increases, pressure decreases

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7
Q

henrys law

A

the solubility of a gas in a liquid is directly proportional to the partial pressure of that gas on the surface of the liquid

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8
Q

where are asbestosis inhaled fibred deposited

A

in the bifurcaitons of alveolar ducts

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9
Q

what happens when asbestos is deposited?

A

causes alveolar macrophage alveolitis which causes a process of fibrosis

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10
Q

why does asbestosis have pleural plaques?

A

asbestos drains via lymphatic drainage and pleural cavities - this forms pleural plaques
they are benign and asymptomatic but may lead to pleural effusion

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11
Q

which is the most carcinogenic asbestos fibre?

A

crocidolite

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12
Q

are straight or curved asbestos fibres more dangerous

A

straight

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13
Q

when is ARDS most serious?

A

secondary to sepsis

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14
Q

what is the O2 goal for ARDS?

A

88-95%

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15
Q

what drugs can be risk factors for OSA?

A

benzodiazepides. opiates and alcohol

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16
Q

what is OSA a big risk factor for

A

pulmonary hypertension

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17
Q

what is the CTFR gene?

A

an anion channel found on the apical membrane of epithelial cells

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18
Q

what are some complictions of CF

A

bronchiectaiss, pancreatic insuficiency, meconium ileus, male infertility, portal hypertension

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19
Q

how do CF affect exocrine cells of the pancreas?

A

they become blocked due to HCO3 not being produced by duct cells - this causes early activation of pancreatic enzymes - autodestruction of pancrease = malabsoption - treat with creon and ADEK supplements

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20
Q

how does CF affect enocrine cells of the pacnreas?

A

destrutcion of islets of langerhan - they are replaced by fatty tissue and so patients require insulin

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21
Q

what pattern of inheritance is CF?

A

autosomal recessive

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22
Q

why do you see signet rings in bronchiectasis on CT?

A

the bronchiole walls have thickened and widened

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23
Q

when is keratinisation lost?

A

as you go deeper into the epithelium

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24
Q

where are club cells found?

A

terminal bronchioles

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25
Q

what is the diff between terniaml and resp bronchioles?

A

resp bronchioles can gas exchnage

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26
Q

what do type 1 pneumocytes do?

A

gas exchnage

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27
Q

what are conchae?

A

fleshy bits in the nose which increase SA

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28
Q

where are seromucous glands and venous sinuses found?

A

lamina propria

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29
Q

what is the trachea made of?

A

fibrocartilage

30
Q

what changes occur going into the bronchioles?

A

loss of cartilage

columnar to cuboidal

31
Q

what type of hypersensitivity is beryllosis?

A

type 4

32
Q

what is the caplan syndrome triad?

A

pneumoconiosis, RA and pulmonary rheumatoid nodules

33
Q

what is caplans syndrome?

A

multiple lung nodules in coal workers with rheumatoid arthiritis cause by an inflammatory reaction to an external allergen
bilateral peripheral nodules

34
Q

what is the pathogenesis of latent TB?

A
  1. macrophage engulfs MB in the alveoli
  2. MB replicates and kills macrophage - becoming released
  3. this stimulates an immune response of TH1 cells and macrophages - creaating a granulomata with a caseous necrotic core surrounded by macrophages and lymphocytes
35
Q

what is the treatment for latent TB?

A

RI = 3 months

or I = 6 months

36
Q

what does primary TB look like?

A

gohn focus in mid periphery zone and large hilar nodes

37
Q

what does secondary TB look like?

A

fibrosing and containing apical lesions

38
Q

what are some paraneoplastic symptoms of lung cancer?

A

finger clubbing, hypertrophic pulmonary osteoarthopathy, thrombophlebitis, hypercalcaemia, SIADH, eaton-lambert syndrome

39
Q

are paraneoplastic symptoms from the primary tumour or the met?

A

primary tumour

40
Q

what is the most common type of lung cancer?

A

bronchial carcinoma

41
Q

what do adenocarcinomas secrete?

A

TTF

42
Q

how to diagnose bronchilitis?

A

PCR on throat or perinasal swab

43
Q

what is churg strauss syndrom?

A

eosinophilic infiltration causing vasculitis in small areas and veins - ANCA+

44
Q

what is seen on XRAY for coal workers pneumoniosis?

A

upper lobe robe opicates

45
Q

what can cause cor pulmonale?

A

acute - PE

chronic - COPD

46
Q

when to suspect empyema?

A

resolving pneumonia + feveer

47
Q

how to treat empyema?

A

amox + metro

48
Q

which bacteria causes epiglottiisi?

A

h influenza

49
Q

how to treat epiglottiis?

A

ceftiaxone

50
Q

bloody pleural fluid?

A

mesothelioma

51
Q

microorganisms causing pertussis?

A

bordatella pertussis

52
Q

first line treatment for pertussis?

A

erythromycin

53
Q

GS investigation for PE

A

severe- CTPA
pregnant - V/Q
low risk - duplex then CTPA

54
Q

what would be seen on a chest XRAY for a lung abcess

A

walled cavity often with a fluid level

55
Q

where do you aspirate for a tension pneumothroax?

A

second ICS anteriorly, mid clavicular line

56
Q

is sarcoidosis T cell mediated?

A

yes

57
Q

what is kostmann syndrome?

A

sevre neutropenia, autosomal recessive

58
Q

what is a feature of leukocyte adhesion deficiency

A

high leukocyte number during infection

59
Q

which gene is affected in leukocyte adhesion deficiency?

A

CD18

60
Q

which marker is increased in SLE?

A

ANA

61
Q

how do you measure airway hyper-reactivity?

A

methacholine, histamine or mannitol challenge testing

62
Q

how can spirometry differentiate between COPD and asthma?

A

copd - decreases FVC and FEV

asthma - decreased FEV but normal FVC

63
Q

things that shift the oxyhaemaglbobin curve left

A

reduced 2,3 DPG, hypothermia, hypocapnia, alkalosis, carbon monoxide

64
Q

things that shift the oxyhaemaglobin curve right

A

hyperthermia, hypercapnia, acidosis, sickle cell

65
Q

decreased pulmonary compliance and examples

A

greater change in pressure require to produce a change in lung volume because lungs are stiffer
SOB, pulmonary fibrosis, oedema, collapse
restrictive pattern

66
Q

increased pulmonary compliacnce and examples

A

have to work harder to get air out of the lungs
hyperinflation of lungs
eg emphysema and COPD

67
Q

TTF-1

A

adenocarcinoma and small cell

68
Q

non small cell markers

A

kras and EFGR

69
Q

pg63

A

squamous cell

70
Q

PTH

A

Squamous

71
Q

ACTH

A

small cell

Resp (30 decks)

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