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Bloc B - Respiration > Drugs for asthma and COPD Oct18 M2 > Flashcards

Drugs for asthma and COPD Oct18 M2 Flashcards

1
Q

side effects origin

A

action of the drug on unwanted targets

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2
Q

asthma 2 components

A

bronchoconstriction

inflammation

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3
Q

intermittent asthma (least severe, episodic crises) treatment

A

SABA (rescue inhaler)

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4
Q

Mild, persistent asthma treatment

A

SABA + low dose ICS

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5
Q

Moderate, persistent asthma treatment

A

SABA + low dose ICS + LABA

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6
Q

Severe persistent asthma treatment

A

SABA + medium/high dose ICS + LABA

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7
Q

alternative treatments with persistent, refractory (doesn’t respond to treatment) disease

A

leukotriene modifiers, theophylline, muscaranic antagonists (anti cholinergics), IgE Ab

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8
Q

important principle about asthma treatment

A

flexibility to treatment at all severities

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9
Q

remain uncontrolled: treatment

A

oral CS: prednisone (systemic effects bc by mouth)

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10
Q

specific receptors beta agonists and antimuscarinic agents act on

A

B2 adrenergic receptor on SM of bronchioles

M3 muscarinic receptor on SM of bronchioles

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11
Q

B2 adrenergic receptor type of protein

A

7 transmembrane, G protein coupled receptor (GS coupled)

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12
Q

B2 adrenergic receptor: what happens after substrate binds it

A

conformational change activates beta alpha subunit which changes GDP to GTP and frees alpha subunit

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13
Q

B2 adrenergic receptor: what happens when alpha subunit-GTP is free

A

binds adenylyl cyclase: activates it to produce cAMP

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14
Q

B2 adrenergic receptor: what cAMP does

A

binds protein kinase A (cyclin dependent prot kinase). Shape change to separate 2 regulatory and 2 catalytic subunits

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15
Q

B2 adrenergic receptor: what activated protein kinase A does

A

2 catalytic subunits go phosphorylate an enzyme

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16
Q

M1/M3 musc receptor type of protein

A

7 transmembrane protein, Gq (G alpha q or G alpha 11 coupled)

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17
Q

M1/M3 musc receptor: what happens when ligand binds it

A

activation of beta-gamma/alpha q protein, which converts GDP to GTP, releasing alpha q-GTP protein

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18
Q

M1/M3 musc receptor : what alpha q-GTP does

A

activates phospholipase C

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19
Q

M1/M3 musc receptor: what activated phospholipase C does

A

Cleaves PIP2 into DAG and IP3

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20
Q

M1/M3 musc receptor: what IP3 does

A

soluble so goes to bind sarco reticulum in SM to release stored Ca in cytoplasm.

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21
Q

M1/M3 musc receptor: what free Ca in smootj muscle does

A

activates processes leading to SM contraction (e.g. activates Ca dependent prot kinase)

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22
Q

what regulates balance in M3 and beta2 receptor signals

A

Ultimate signaling to myosin light chain kinase (MLCK)

23
Q

what MLCK does

A

phosphorylates myosin light chain to activate it and let it couple to actin

24
Q

how MLCK activate

A

when unphosphorylated. if phosphorylated by PKA, is inactive

25
Q

how beta2 receptor modulates MLCK

A

Protein kinase A phosphorylates MLCK to inhibit it (no SM contraction)

26
Q

how M3 receptor modulates MLCK

A

increased IC calcium, Ca binds calmodulin. Calmodulin-Ca activates MLCK

27
Q

what theophylline does

A

acts on phosphodiesterase (PDE) to stop if from changing cAMP to AMP.

28
Q

ultimate effect of blocking PDE

A

more cAMP in cell, more PKA activated, more MLCK inactivated

29
Q

SABA molecule name and drug name

A

albuterol/salbutamol (Ventolin), isoproteranol, terbutaline

30
Q

SABA mode of action

A

similar molecules to epinephrine, bind at its site to activate the B2 receptor (orthosteric binding)

31
Q

What is drug tolerance

A

desensitization of receptor. More occupancy of receptor downregulates its activity or amount of this receptor on membrane

32
Q

inhaled drug delivery: most common inhaler + 2 others

A

metered dose inhaler (with or withotu spacer)
dry powder inhalers
nebulizers

33
Q

trick for beta agonist names

A

end in ol

34
Q

CS molecular ‘‘shape’’

A

ressemble shape of cortisol (4 cycles)

35
Q

CS why slow onset of activity

A

act on gene transcription

36
Q

CS: 2 names

A

fluticasone, budesonide

37
Q

ICS mode of action in general

A

regulate airway inflammation. act on many processes that influence that

38
Q

ICS 3 examples of effects

A
  • promote eosinophils apoptosis
  • decrease cytokine (IL,inflam mediator) release
  • increase beta 2 R number on SM
39
Q

ICS why synergistic effect with beta agonist

A

increases number of B2R which will then receive beta agonist

40
Q

4 adverse effects of ICS

A

oral candidiasis (thrush)/yeast in mouth bc ICS has immunosuppressive action and some of it goes to mouth

  • HPA axis suppression
  • Growth inhibition
  • Decreased bone density
41
Q

LABAs: 2 important things to note

A

1) not for acute bronchospasm

2) never taken alone, always with ICS

42
Q

2 drugs name where LABA contained and name of molecules inside

A

Advair: salmaterol/fulticasone
Symbicort: Formoterol/budesonide

43
Q

important molecule from which PG and leukotrienes come from

A

arachidonic acid

44
Q

what NSAIDs (ibuprofen, aspirin) do

A

inhibit cyclooxygenase 1 and COX2 production of PG from AA

45
Q

why leukotrienes important in asthma (4)

A
  • SM contraction
  • bronchovascular leakage
  • mucous gland secretion
  • leukocyte infiltration
46
Q

how leukotriens produce

A

Lipooxygenases convert AA to leukotrienes

47
Q

2 ways to inhibit leukotriene effect

A
  • inhibit lipooxygenases

- inhibit leukotriene receptors

48
Q

most common way of inhibiting leukotriene effect and 2 drugs

A

inhibit leukotriene receptor
Montelukast
Zafirlukast
(end with kast)

49
Q

leukotriene modifying agents vs ICS what’s best

A

are less effective than ICS

50
Q

2 classes of muscarinic antagonists

A

short acting (ipratropium) and long acting (triotropium)

51
Q

PSS spine origins + important one in bronchial tree

A

cranial nerves (not cervical!) (vagus in resp) and sacral

52
Q

main diff between asthma and COPD and consequence

A

COPD less inflammatory so ICS used in later stages only

53
Q

order of drug implementation in COPD

A

SABA, SAMA, LABA or LAMA or both.

ICS+LABA/ICS+LAMA, ICS+LABA+LAMA

54
Q

SABA vs SAMA (ipratropium)

A

SAMA has slower onset and acts longer than SABA

Bloc B - Respiration (36 decks)

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