lecture 8 nature of airways obstruction Flashcards

1
Q

what is the bronchialwall mainly made up of

A

smoooth muscle

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2
Q

3 ways the airway bronchial lumen decrease

A

excess mucus
contraction of the smooth muscle
loss of outward traction

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3
Q

what are the bronchi party held open by

A

alveoli mesh

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4
Q

asthma colour of the airways, why

A

red

inflammation

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5
Q

main immune cell in asthma

A

eosinophil

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6
Q

feature of asthma

A

airways constrict to a very small amount of histamine and acetylcholine

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7
Q

what does Th1 inflammation drive

A

gamma interferon production

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8
Q

what does Th2 inflammation drive

A

production of IL4 and IL5

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9
Q

in asthmatics what type of inflammation takes over

A

Th2

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10
Q

how does the release of histamine come about

A

dendritic cells present the antigen to the T cell
T cell makes B cell produce antibodies
IgE binds to mast cells = degranulation

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11
Q

what happens after mast cell degranulation

A

eosinophils are attracted to the area

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12
Q

how would you measure how much eosinophil was in the airways

A

measure the nitric oxide exhaled

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13
Q

problems with measureing nitric oxide for asthmatics

A

reduces in smoking
increases with some foods
increases with bronchitis

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14
Q

chronic airway changes in asthma

A

smooth muscle hypertrophy

subepithelial fibrosis

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15
Q

what is COPD

A

bronchiectasis and emphysema

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16
Q

biggest risk factorfor COPD

A

smoking

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17
Q

who is genetically more prone to COPD

A

people with alpha 1 antitrypsin disease

18
Q

mucus and bronchitis

A

mucus gland hypertrophy
excess mucus
goblet cell hyperplasia

19
Q

other changes in bronchitis

A

inflammatory cell infiltration

smooth muscle hypertrophy

20
Q

what is chronic bronchitis

A

having cough and sputum for 3 months

21
Q

do you get airway obstruction with chronic bronchitis

A

no

22
Q

emphysema

A

abnormal enlargement of airspace distal to the terminal bronchiole accompanied by destruction of their walls and without obvious fibrosis

23
Q

types of emphysema

A

normal, centrilobular and panlobular

24
Q

who does emphysema affect

A

chronic smokers

25
Q

occupations assosiated with COPD

A

coal minors
welders
biomass

26
Q

where does airway obstruction need to be for the patient to complain earlier

A

bigger airway

27
Q

blue bloater

A

chronic bronchitic
cough and sputum
cyanosed
swollen legs

28
Q

pink puffer

A

emphysema

cachexic

29
Q

cachexic

A

wasting syndrome

30
Q

cor pulmonale

A

ventilation perfusion mixmatch
vasoconstriction
chronic hypertension causes right heart hypertrophy
heart failure

31
Q

what will present with corpulmonale

A

leg oedema

32
Q

what part of the lobe is more affected by COPD

A

upper

33
Q

what can happen with an emphysematic upper lobe

A

squash the lower lobe

34
Q

how can you deal with a problematic upper lobe

A

surgery removal

one way valves

35
Q

how do valves in the upper lobe work

A

air can get in but not out

36
Q

bronchiectasis

A

dilation of the airways
recurrent infection
purulent sputem

37
Q

purulent

A

pus containing

38
Q

CF mucus

A

abnormally thick and sticky

39
Q

what happens in CF over time

A

scarring of the lungs

40
Q

in CF what is the mutation

A

CFTR

41
Q

what is the CF gene for

A

chloride channel

42
Q

what else does CF affect

A

pancreatic duct