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

Drugs for asthma and COPD Oct18 M2 Flashcards

(54 cards)

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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

Study These Flashcards
A

Ultimate signaling to myosin light chain kinase (MLCK)

23
Q

what MLCK does

Study These Flashcards
A

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

24
Q

how MLCK activate

Study These Flashcards
A

when unphosphorylated. if phosphorylated by PKA, is inactive

25
how beta2 receptor modulates MLCK
Protein kinase A phosphorylates MLCK to inhibit it (no SM contraction)
26
how M3 receptor modulates MLCK
increased IC calcium, Ca binds calmodulin. Calmodulin-Ca activates MLCK
27
what theophylline does
acts on phosphodiesterase (PDE) to stop if from changing cAMP to AMP.
28
ultimate effect of blocking PDE
more cAMP in cell, more PKA activated, more MLCK inactivated
29
SABA molecule name and drug name
albuterol/salbutamol (Ventolin), isoproteranol, terbutaline
30
SABA mode of action
similar molecules to epinephrine, bind at its site to activate the B2 receptor (orthosteric binding)
31
What is drug tolerance
desensitization of receptor. More occupancy of receptor downregulates its activity or amount of this receptor on membrane
32
inhaled drug delivery: most common inhaler + 2 others
metered dose inhaler (with or withotu spacer) dry powder inhalers nebulizers
33
trick for beta agonist names
end in ol
34
CS molecular ''shape''
ressemble shape of cortisol (4 cycles)
35
CS why slow onset of activity
act on gene transcription
36
CS: 2 names
fluticasone, budesonide
37
ICS mode of action in general
regulate airway inflammation. act on many processes that influence that
38
ICS 3 examples of effects
- promote eosinophils apoptosis - decrease cytokine (IL,inflam mediator) release - increase beta 2 R number on SM
39
ICS why synergistic effect with beta agonist
increases number of B2R which will then receive beta agonist
40
4 adverse effects of ICS
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
LABAs: 2 important things to note
1) not for acute bronchospasm | 2) never taken alone, always with ICS
42
2 drugs name where LABA contained and name of molecules inside
Advair: salmaterol/fulticasone Symbicort: Formoterol/budesonide
43
important molecule from which PG and leukotrienes come from
arachidonic acid
44
what NSAIDs (ibuprofen, aspirin) do
inhibit cyclooxygenase 1 and COX2 production of PG from AA
45
why leukotrienes important in asthma (4)
- SM contraction - bronchovascular leakage - mucous gland secretion - leukocyte infiltration
46
how leukotriens produce
Lipooxygenases convert AA to leukotrienes
47
2 ways to inhibit leukotriene effect
- inhibit lipooxygenases | - inhibit leukotriene receptors
48
most common way of inhibiting leukotriene effect and 2 drugs
inhibit leukotriene receptor Montelukast Zafirlukast (end with kast)
49
leukotriene modifying agents vs ICS what's best
are less effective than ICS
50
2 classes of muscarinic antagonists
short acting (ipratropium) and long acting (triotropium)
51
PSS spine origins + important one in bronchial tree
cranial nerves (not cervical!) (vagus in resp) and sacral
52
main diff between asthma and COPD and consequence
COPD less inflammatory so ICS used in later stages only
53
order of drug implementation in COPD
SABA, SAMA, LABA or LAMA or both. | ICS+LABA/ICS+LAMA, ICS+LABA+LAMA
54
SABA vs SAMA (ipratropium)
SAMA has slower onset and acts longer than SABA

Bloc B - Respiration (36 decks)

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