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year 1 > resp pharmacology quick > Flashcards

resp pharmacology quick Flashcards

1
Q

what does ACh on M3 receptors in the airway cause

A

Gq
stimulates phospholipase C
contraction

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2
Q

what does adrenaline on B2 receptors in airway cause

A 
Gs
stimulates adenylyl cyclase
ATP --> cAMP
--> PKA
PKA phosphorylates 
\+ inhibits MLCK
\+ stimulates myosin phosphatase 
relaxation
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3
Q

how does calcium initiate relaxation in a SMC

A

joins with calmodulin to form Ca2+-calmodulin

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4
Q

what does ca2+-calmodulin do

A

converts inactive MLCK into active MLCK

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5
Q

what does active MLCK do

A

converts inactive myosin cross bridge into phosphorylated myosin cross bridge (binds actin)

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6
Q

phosphorylation of regulatory MLC in the presence of elevated intracellular Ca2+ and ATP —->

A

contraction

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7
Q

dephosphorylation of MLC by myosin phosphatase —>

A

relaxation

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8
Q

in the presence of elevated intracellular Ca2+, what is greater - the rate of phosphorylation or the rate of dephosphorylation

A

rate of phosphorylation

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9
Q

true/false

relaxation requires return of intracellular Ca2+ to basal level

A

true - primary and secondary active transport

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10
Q

what does myosin light chain kinase do

A

dephosphorylated inactive MLC —> phosphorylated active MLC
relaxation —> contraction

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11
Q

what does myosin phosphatase do

A

phosphorylated active MLC —> dephosphorylated inactive MLC

contraction —> relaxation

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12
Q

give 5 characteristics of chronic asthma

A 
increased mass of SM (hyperplasia and hypertrophy)
accumulation of interstitial fluid
increased secretion of mucus
epithelial damage
sub-epithelial fibrosis
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13
Q

what does epithelial damage cause

A

exposed sensory nerve endings (c-fibres) - hypersensitivity

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14
Q

what kind of hypersensitivity is asthma

A 
Type 1
(delayed phase is type 4 but in general type 1)
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15
Q

what is the immediate phase of asthma

A

bronchoconstriction - hyperresponsiveness

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16
Q

what is the delayed phase of asthma

A

inflammation

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17
Q

what happens when a non-atopic individual encounters an allergen

A

phagocytosis of allergen by dendritic cell

low level Th1 response

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18
Q

what kind of immunity is it when a non-atopic individual meets an allergen

A

cell mediated

IgG and macrophages

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19
Q

what happens when an atopic person encounters an allergen

A

phagocytosis by dendritic cell

strong Th2 response

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20
Q

what kind of immunity is it when an atopic individual meets an allergen

A

anti-body mediated

IgE

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21
Q

what happens in severe asthma

A

Th1 also contributes

22
Q

how does the antigen presenting cell present to Th cells

A

MHC class II

23
Q

what does Th2 produce that activates B cells

A

IL4

also by binding to them

24
Q

what do the activated B cells do

A

mature to plasma cells that secrete IgE

25
Q

what IL activates eosinophils

A

IL5

26
Q

what IL activates mast cells to express Fc receptors

A

IL4 and IL13

27
Q

what does cross linking of IgE receptors cause

A

Ca2+ entry into mast cell and release of Ca2+ from intracellular stores

28
Q

what does Ca2+ entry into mast cell and release of Ca2+ from intracellular stores cause

A

release of secretory granules containing preformed histamine
release of LTC4 and LTD4
release of LTB4, PAF, PGD2

29
Q

what do LTC4 and LTD4 cause

A

airway smooth muscle contraction
increased vascular permeability
mucous secretion

30
Q

what do LTB4, PAF and PGD2 cause

A

attract cells causing inflammation e.g. eosinophils, lymphocytes,

31
Q

what do glucocorticoids do

A

basically decrease everything inflammatory

increase B2 receptors

32
Q

how do glucocorticoids increase transcription of anti-inflammatory genes

A

HATs (histone acetyl transferases)

33
Q

how do glucocorticoids decrease the transcription of inflammatory genes

A

HDACs (histone deacetyl transferases)

34
Q

where are M1 found

A

ganglia

35
Q

where are M2 found

A

post ganglionic neurone terminals

36
Q

where are M3 found

A

ASM

mucus secreting cells

37
Q

what M receptor

facilitates fast neurotransmission mediated by ACh acting on nicotinic receptors

A

M1

38
Q

what M receptor

mediates contraction due to ACh

A

M3

39
Q

what M receptor

evokes increased mucus secretion

A

M3

40
Q

what M receptor

is an inhibitory auto receptor reducing release of ACh

A

M2

41
Q

what would a blockade of M2 cause

A

increase ACh release

42
Q

what immune cells are involved in COPD

A

neutrophils
CD8+ t cells
increased macrophage numbers

43
Q

what do the immune cells in COPD cause

A

release of matrix metalloproteins

e.g. elastase, free radicals

44
Q

what does smoking/air pollutants cause

A

stimulation of resident alveolar macrophages –> cytokine production

45
Q

where is the synapse of the vago-vagal reflex and what nerve is involved

A

CNX

brainstem

46
Q

what causes the immediate phase response of asthma attack

A

release of spasmogens from mast cells

47
Q

what causes the delayed phase response in asthma attack

A

release of substances that attract inflammatory cells

LTB4, PAF and PGD2

48
Q

where are glucocorticoids released from

A

zona fasiculata

49
Q

true/false

glucocorticoids can resolve established inflammation

A

true

50
Q

where are mineral corticoids released from

A

zona glomerulosa

51
Q

what is the term for distension and damage to alveoli, destruction of acinal pouching in alveolar salsa and loss of elastic recoil in COPD

A

emphysema

year 1 (45 decks)

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