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Block 13 - The Development of Cardiorespiratory Disease > Block 13 Pharmacology DONE > Flashcards

Block 13 Pharmacology DONE Flashcards

1
Q

paclitaxel class (2)

A

microtubule stabilisation, taxoid antineoplastic agent

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2
Q

paclitaxel use (2)

A

ovarian, breast cancer

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3
Q

paclitaxel MOA (5 steps)

A
  1. binds B subunit of tubulin
  2. hyper stabilises microtubule
  3. prevents cell from disassembly
  4. prevents microtubule reorganisation
  5. ruins cell function as chromosomes can’t move
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4
Q

as well as its main MOA, how else does paclitaxel tackle cancer? (4 steps)

A
  1. binds to B-cell leukaemia 2
  2. blocks its anti-apoptotic function
  3. cell apopotosis
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5
Q

cisplatin class (1)

A

antineoplastic alkylating agent

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6
Q

cisplatin use (1)

A

cancer

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7
Q

cisplatin 3 main mechanisms

A
  1. alkyl groups attach to DNA bases, DNA fragmentation, prevents DNA synthesis/RNA transcription
  2. damages DNA by cross-linking, prevents synthesis
  3. nucleotide mispairing so mutations
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8
Q

cisplatin MOA summary (4 steps)

A
  1. affect DNA so it can’t uncoil
  2. no DNA replication
  3. no cell proliferation
  4. cell death
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9
Q

isoniazid class (2)

A

bactericidal agent, highly specific

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10
Q

isoniazid use (4)

A

Mycobacterium tuberculosis, M. bovis, M. kansaii

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11
Q

isoniazid is bactericidal to

A

rapidly dividing mycobacteria

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12
Q

isoniazid is bacteriostatic to

A

slow growing mycobacteria

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13
Q

isoniazid is a _____ that must be _____

A

prodrug, activated

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14
Q

isoniazid is activated by

A

bacterial catalase

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15
Q

isoniazid MOA (2 steps)

A
  1. prodrug activated by bacterial catalase
  2. inhibits synthesis of mycoloic acids, essential part of cell wall
  3. disrupts DNA, lipids, carbs, nicotinamide adenine dinucletoide (NAD) synthesis
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16
Q

ethambutol class

A

bactericidal, oral chemotherapeutic agent

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17
Q

ethambutol is specifically active against

A

actively growing Mycobacterium, e.g. M. tuberculosis

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18
Q

ethambutol MOA is not fully understood but it is thought to… (5 steps)

A
  1. inhibit arabinosyl transferase involved in cell wall synthesis
  2. cell wall production inhibited
  3. increased cell wall permeability
  4. inhibits RNA synthesis
  5. decreases tubercle bacilli replication
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19
Q

rifampicin class

A

broad spectrum antibiotic

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20
Q

rifampicin targets what kind of bacteria?

A

gram positive, gram negative

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21
Q

rifampicin advantages

A

easily absorbed and distributed

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22
Q

rifampicin MOA (3 steps)

A
  1. inhibits DNA-dependent RNA polymerase
  2. decreased RNA synthesis
  3. cell death
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23
Q

rifampicin can target ____ but not _____ versions of the DNA-dependent RNA polymerase enzyme

A

bacterial, but not mammalian

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24
Q

rifampicin is restricted to use mainly on

A

Mycobacterium

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25
Q

rifampicin is restricted to use mainly on mycobacterial infections because of

A

emergence of resistant bacteria

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26
Q

rifampicin is metabolised where?

A

liver

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27
Q

rifampicin is eliminated in

A

bile, urine

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28
Q

pyrazinamide use

A

with other drugs, TB

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29
Q

pyrazinamide is active only against

A

M, tuberculosis

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30
Q

pyrazinamide is only active in what conditions?

A

slightly acidic pH

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31
Q

pyrazinamide MOA (4 steps)

A
  1. activated to Pyrazinoic acid in bacilli
  2. interfere with fatty acid synthesis so growth and replication
  3. disrupt membrane potential and energy production needed for survival in acidic infection
  4. binds to ribosomal protein S1, inhibits trans-translation (so can effect dormant mycobacteria)
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32
Q

ciprofloxacin class

A

broad-spectrum antibiotic, quinolone

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33
Q

ciprofloxacin targets what kind of bacteria?

A

gram positive, gram negative

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34
Q

bacteria that are resistant to other antibiotics such as beta-lactams, macrolides, tetracyclines, or aminoglycosides may be susceptible to ciprofloxacin as it has a

A

different MOA

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35
Q

ciprofloxacin MOA (2 steps)

A
  1. inhibits topoisomerase 2 (DNA gyrase) and topoisomerase 4

2. bacteria can’t replicate, repair or recombinate

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36
Q

B2 receptor (agonist) stimulation in the lung causes

A

relaxation of bronchial smooth muscle, bronchodilation, increased airflow

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37
Q

B2 receptor agonists uses (2)

A

asthma, COPD

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38
Q

salbutamol class

A

B2 adrenergic agonist

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39
Q

salbutamol has

A

2 isomers

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40
Q

2 isomers of salbutamol

A
  • R-isomer, levalbuterol

- S-isomer

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41
Q

R-isomer, levalbuterol of salbutamol is responsible for

A

bronchodilation

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42
Q

S-isomer of salbutamol is responsible for

A

increasing bronchial reactivity

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43
Q

salbutamol MOA (7 steps)

A
  1. stimulates B2 adrenoreceptor’s adrenergic receptor
  2. activates adenyl cyclase
  3. increases cAMP and cAMP-dependent protein kinase A (PKA)
  4. PKA modulates myosin and lowers Ca2+
  5. relaxes smooth muscle, bronchodilation
  6. inhibits release of bronchoconstricting agents
  7. enhances mucociliary clearance
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44
Q

salmeterol class

A

B@ adrenergic agonist, LABA

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45
Q

salmeterol has a (structure)

A

long, lipophilic side chain

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46
Q

salmeterol MOA (5 steps)

A
  1. side chain binds near receptors so active part can keep binding/unbinding for more stimulation
  2. relaxes smooth muscle, bronchodilation
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47
Q

salmeterol should be used

A

regularly

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48
Q

if used regularly, salmeterol decreases the

A

number and severity of asthma attacks

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49
Q

salmeterol is not for use in an

A

asthma attack already started

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50
Q

salmeterol duration of action

51
Q

salbutamol duration of action

52
Q

salmeterol is similar in action to

A

formoterol

53
Q

although salmeterol is similar in action to formoterol, formoterol is (2)

A

faster, more potent

54
Q

budesonide class

A

anti-inflammatory corticosteroid

55
Q

budesonide has a high what effect?

A

glucocorticoid

56
Q

budesonide has a weak what effect?

A

mineralocorticoid

57
Q

budesonide’s binding affinity to the glucocorticoid receptor is higher than (2)

A

cortisol, prednisolone

58
Q

precise mechanism of corticosteroid action on inflammation in asthma, crohn’s and ulcerative colitis is

59
Q

corticosteroid anti-inflammatory action is most likely due to inhibition of (6)

A

mast cells, eosinophils, neutrophils, macrophages, lymphocytes, mediators (histamine, leukotrienes, cytokines, eicosanoids) involved in allergic reaction and inflammation

60
Q

budesonide undergoes significant

A

first-pass elimination

61
Q

because budesonide undergoes significant first-pass elimination, oral preparations are

A

extended release tablets, delaying release until small intestine

62
Q

montelukast class

A

leukotriene receptor antagonist

63
Q

montelukast is used as an alternative to

A

anti-inflammatory meds in asthma and exercise-induced bronchospasm

64
Q

montelukast MOA (1 step)

A

selectively antagonises leukotriene D4 (LTD4) at cysteinyl leukotriene receptor (CysLT1)

65
Q

montelukast prevents (3)

A

airway oedema, smooth muscle contraction, mucus secretion

66
Q

ipratropium bromide class

A

anticholinergic bronchodilator

67
Q

ipratropium use (3)

A

cholinergic-mediated bronchospasm in COPD, rhinorrhoea, rhinitis

68
Q

ipratropium bromide MOA (3 steps)

A
  1. non-selectively inhibits muscarinic cholinergic receptors
  2. decreased cGMP
  3. decreased smooth muscle contraction as cGMP effects calcium or myosin
69
Q

verapamil class

A

class IV anti-arrhythmic

70
Q

verapamil inhibits

A

voltage-dependent calcium channels

71
Q

verapamil MOA (3 steps)

A
  1. blocks L-type calcium channels in heart
  2. decreased ionotropy, chronotropy
  3. reduced heart rate and blood pressure
72
Q

verapamil has

A

2 enantiomers

73
Q

verapamil 2 enantiomers

A

R-enantiomer, S-enantiomer

74
Q

verapamil R-enantiomer is more effective at what than the S-enantiomer?

A

reducing bp

75
Q

the verapamil S-enantiomer is 20x more potent than the R-enantiomer at what?

A

prolonging PR interval, arrhythmias

76
Q

verapamil is given

77
Q

what non-dihydropyridine calcium channel blocker is used more commonly than verapamil?

78
Q

diltiazem class

A

non-dihydropyridine calcium channel inhibitor

79
Q

how does diltiazem work?

A

inhibits influx of Ca2+ across cell membranes

80
Q

what are the 3 possible mechanisms for how diltiazem inhibits influx of Ca2+?

A
  1. channel deformation
  2. inhibition of channel ion gating
  3. inhibits release of Ca2+ from sarcoplasmic reticulum
81
Q

the decrease in intracellular Ca2+ caused by diltiazem inhibits

A

contractile process of myocardial smooth muscle cells

82
Q

diltiazem’s inhibition of myocardial muscle contraction causes (5)

A

artery dilation, increased O2 to heart tissue, decreased total peripheral resistance, decreased bp, decreased afterload

83
Q

diltiazem use

A

hypertension, stable angina, prinzmetal’s variable angina

84
Q

b-adrenergic antagonists compete with

A

sympathomimetic neurotransmitters, e.g. catecholamines

85
Q

b-adrenergic antagonists compete to bind with what receptor?

A

B1-adrenoreceptor

86
Q

where are B1-adrenoreceptors found?

A

heart, smooth muscle

87
Q

b-adrenergic antagonists result in (4)

A

reduction in resting heart rate, cardiac output, blood pressure, reflex orthostatic hypotension

88
Q

atenolol class

A

B1-selective antagonist

89
Q

higher doses of atenolol also competitively block

A

B2-adrenergic responses in bronchial and vascular smooth muscle

90
Q

b-adrenergic antagonists is not

A

commonly used

91
Q

what drug is used more commonly than atenolol?

A

bisoprolol

92
Q

atropine class

A

antimuscarinic agent

93
Q

atropine MOA (1)

A

binds to and inhibits muscarinic (M2) acetylcholine receptor

94
Q

adequate doses of atropine abolish various types of (2)

A

reflex vagal cardiac slowing, asystole

95
Q

atropine also stops what effect produced by injection of choline esters, anticholinesterases or other parasympathomimetic drugs? (2)

A

bradycardia, asystole

96
Q

atropine also stops what effect produced by stimulation of the vagus? (1)

A

cardiac arrest

97
Q

atropine may also lessen he degree of what?

A

partial heart block due to vagal activity

98
Q

glyceryl trinitrate (GTN) class

A

vasodilator

99
Q

glyceryl trinitrate (GTN) uses

A

angina, perioperative hypertension

100
Q

glyceryl trinitrate (GTN) is used to try and produce

A

controlled hypotension

101
Q

glyceryl trinitrate (GTN) MOA (7 steps)

A
  1. nitroglycerin converted to nitric oxide (NO)
  2. NO activates guanylate cyclase
  3. stimulates synthesis of cGMP
  4. activates protein kinase G (PKG)
  5. dephosphorylation of myosin of smooth muscle fibres
  6. decreased Ca2+
  7. relaxed smooth muscle, vasodilation
102
Q

amiodarone class

A

class 3 antiarrhythmic, antianginal

103
Q

amiodarone 2 possible MOAs (2)

A
  1. prolongs myocardial action potential (phase 3) by blocking K+ channels refractory period
  2. a non-competitive A and B-adrenergic inhibitor
104
Q

amiodarone can also have what activity on SA and AV nodes? (2)

A

B-blocker, calcium channel blocker

105
Q

amiodarone can also have B-blocker and calcium channel blocker-like actions on what? (2)

A

SA and AV nodes

106
Q

amiodarone increases the refractory period via what effects? (2)

A

sodium and potassium channel

107
Q

amiodarone does what via sodium-channel effects?

A

slows intra-cardiac conduction of cardiac action potential

108
Q

adenosine class

A

endogenous nucleotide

109
Q

adenosine MOA (4 steps)

A
  1. activates A1 and A2 adenosine receptors
  2. inhibition of inward Ca2+
  3. and activation of adenylate cyclase
  4. relaxation of vascular smooth muscle
110
Q

adenosine slows conduction time through

111
Q

as adenosine slows conduction time through the AV node, it interrupts re-entry pathways through the AV node, resulting in

A

restoration of normal sinus rhythm in paroxysmal SVT

112
Q

adenosine also increases

A

blood flow in coronary arteries

113
Q

adenosine produces a relative difference in what uptake in the myocardium?

A

thallous (thallium) chloride TI 201

114
Q

adenosine is antagonised competitively by

A

methylxanthines (e.g. caffeine, theophylline)

115
Q

adenosine is potentiated by blockers of

A

nucleoside transport (e.g. dipyridamole)

116
Q

lidocaine class

A

class 1b anaesthetic

117
Q

lidocaine MOA (3 steps)

A
  1. blocks voltage-sensitive Na+ channels
  2. during phase 0 of cardiac action potential
  3. slows and depresses impulse conduction
118
Q

lidocaine dissociates

A

rapidly from channel, almost completely between APs

119
Q

in depolarised tissues or firing at a high frequency lidocaine dissociation is _____, so (3)

A

decreased, promoting channel blockade, conduction depression

120
Q

lidocaine is used to treat

A

venrticular tachyarrhythmias from MI

121
Q

lidocaine does not affect the

122
Q

lidocaine depresses

A

ventricular excitability

123
Q

lidocaine increases the stimulation threshold of the ventricle during

Block 13 - The Development of Cardiorespiratory Disease (14 decks)

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