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my1 resp > pharmacology > Flashcards

pharmacology Flashcards

1
Q

what controls the airways para or sympathetic

A

parasympathetic

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2
Q

is parasympathetic preganglionic Cholinergic or nitrergic

A

cholinergic

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3
Q

where do parasympathetic preganglionic fibres come from

A

brainstem

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4
Q

where do parasympathetic post ganglionic fibres act on

A

bronchioles

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5
Q

what are the neurotransmitters and receptors of the cholinergic fibres and what do they do

A

ACh and M3, M3 increases phospho C which converts IP2 to PIP3 which opens calcium channels

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6
Q

what are the neurotransmitters of the non-cholinergic fibres and what do they do

A

NO and VIP, dilation

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7
Q

what do sympathetic post ganglionic fibres act on

A

submucosal glands and smooth muscles of arterial vessels (a1)

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8
Q

what do sympathetic post ganglionic fibres act on, causing what to be released

A

adrenal glands, adrenaline

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9
Q

what receptors does adrenaline act on and what does this cause

A

B2, dilation, decreased mucous secretion, increased mucociliary clearance

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10
Q

which 2 ways can cause contraction in airway smooth muscle

A

hormonal (ACh on m3, causing IP3) and depolarisation (calcium influx), both cause Ca influx

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11
Q

how does calcium cause contraction

A

Ca binds to calmodium which activates myosin light chain kinase (MLCK), MLCK used ATP to phosphorylate MLC and myosin slides past actin

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12
Q

what caused relaxation of MLC

A

dephosphorylation of MLC by myosin phosphate (MP),

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13
Q

is asthma obstructive or restrictive and reversible or irreversible

A

obstructive, reversible

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14
Q

what are pathological changes of asthma

A

1) increased smooth muscle mass, 2) accumulation of interstitial fluid 3) increased mucous secretion 4) epithelial damage 5) sub epithelial fibrosis

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15
Q

What happens to FEV1 and peak flow in asthamtics

A

decrease

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16
Q

what causes hypersensitivity of airways

A

epithelial damage exposing nerve endings

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17
Q

what is the difference between mild and severe asthma

A

mild = hypersensitivity and minor hyperactivity, severe = hypersensitivity and hyper activity

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18
Q

why does hypersensitivity to an allergen mean

A

when allergen eg pollen is inhaled, there is a very strong immune inflammatory response

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19
Q

in non-atopic individuals what happens when pollen is inhaled

A

dendritic cell phagotyoses and TH0 cells produce TH1 (normally IgG

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20
Q

in atopic individuals what happens when pollen is inhaled

A

strong TH2 response, release interleukins (IL4) and activate B cells producing IgE

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21
Q

in severe asthma what T cells are involved

A

TH2 and TH1

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22
Q

what does IgE bind to

A

FcE on mast cells and eisonophils

23
Q

what do mast cells and eisonophils release

A

leukotrienes, histamina and chemokines

24
Q

what are the 2 components of an asthma attack

A

initial phase (bronchospasm and early inflammation), followed by delayed stage (inflammation and bronchospasm)

25
Q

what cells cause early stage

A

mast cells

26
Q

what cells cause late stage

A

eosinophils

27
Q

what are the main relievers in asthma - bronchodilators

A

SABA’s, LABA’s, CysLT1 antagonist

28
Q

what are the main controllers in asthma - anti-inflammatory

A

glucocorticoids and cromoglicate

29
Q

what is both a controller and reliever

A

methylxanthines

30
Q

what action to beta2 adrenoreceptor agonists have on ASM

A

cause relaxation by stimulating adenyly cylcase to increase cAMP which activates PKA which inhibits MCLK and activates MP

31
Q

what are the types of beta2 adrenoreceptor agonists

A

SABA’s eg salbutamol, LABA’s eg salmenterol and formoterol, ultra-LABA

32
Q

what is CysLT1 used for and an example

A

acute bronchospasm, taken orally, not for severe asthma. eg Montelukast, orally

33
Q

what is known about methylxanthines

A

very narrow therapeutic window and lots of side affects eg Theophylline, orally

34
Q

what are the 2 main classes or corticosteroids

A

glucocorticoids and mineralocorticoids, inhaled

35
Q

what does cortisol do

A

decreased inflammatory and immunological response

36
Q

what do mineralocorticoids do

A

salt and water retention

37
Q

what is the action mechanism of glucocorticoids

A

bind to GRa and alter transcription of anti-inflammatory proteins, not bronchodilators

38
Q

for chronic and severe asthma what is the last step before hospitalisation

A

prednisolone, orally, is a glucocorticoids

39
Q

what are cromones used for

A

mast cell stabilisation, reduces inflammatory response, eg sodium cromoglicate

40
Q

is COPD obstructive or restrictive and irreversible or reversible

A

obstructive, irreversible (sometimes reversible eg exacerbations)

41
Q

COPD often branches into what 2 conditions

A

emphysema and chronic bronchitis

42
Q

what is emphysema

A

Collapsing alveoli and loss of elastic recoil, losing SA for gas exchange, can cause SOB

43
Q

what is chronic bronchitis

A

inflammation of bronchioles and bronchi, increased sputum production, can cause coughing and SOB

44
Q

what does M1 do

A

allow transmission of ACh from pre to post ganglionic fibres (this allows contriction)

45
Q

what does M3 do

A

allows ACh to activate constriction of ASM

46
Q

What does M2 do

A

inhibits further release of ACh, (aids broncodilation)

47
Q

what does SAMA act on and give an example

A

non selective of M1, M2 and M3, is inhaled, ipratropium

48
Q

what does LAMA act on and give an example

A

inhaled, acts on M3, eg tiotropium

49
Q

give an example of an ultra-LABA

A

Indacaterol

50
Q

what does a PDE4 inhibitor do

A

supresses inflammation by acting on eosinophils eg Rofumilast

51
Q

what is rhinitis

A

inflammation of nasal mucosa causing sneezing, rhinorrhoea (runny nose) and a blocked nose (common cold, hay fever)

52
Q

what antibody is produced in allergic rhinitis

A

IgE

53
Q

what drugs can be given for rhinitis

A

H1 and CysLT1 receptor antagonists, sodium chromoglicate and Glucocorticoids

54
Q

what are H1 receptor antagonists more commonly known as

A

anti-histamines

my1 resp (16 decks)

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