Block 13 Pharmacology DONE Flashcards
(123 cards)
1
Q
paclitaxel class (2)
A
microtubule stabilisation, taxoid antineoplastic agent
2
Q
paclitaxel use (2)
A
ovarian, breast cancer
3
Q
paclitaxel MOA (5 steps)
A
- binds B subunit of tubulin
- hyper stabilises microtubule
- prevents cell from disassembly
- prevents microtubule reorganisation
- ruins cell function as chromosomes can’t move
4
Q
as well as its main MOA, how else does paclitaxel tackle cancer? (4 steps)
A
- binds to B-cell leukaemia 2
- blocks its anti-apoptotic function
- cell apopotosis
5
Q
cisplatin class (1)
A
antineoplastic alkylating agent
6
Q
cisplatin use (1)
A
cancer
7
Q
cisplatin 3 main mechanisms
A
- alkyl groups attach to DNA bases, DNA fragmentation, prevents DNA synthesis/RNA transcription
- damages DNA by cross-linking, prevents synthesis
- nucleotide mispairing so mutations
8
Q
cisplatin MOA summary (4 steps)
A
- affect DNA so it can’t uncoil
- no DNA replication
- no cell proliferation
- cell death
9
Q
isoniazid class (2)
A
bactericidal agent, highly specific
10
Q
isoniazid use (4)
A
Mycobacterium tuberculosis, M. bovis, M. kansaii
11
Q
isoniazid is bactericidal to
A
rapidly dividing mycobacteria
12
Q
isoniazid is bacteriostatic to
A
slow growing mycobacteria
13
Q
isoniazid is a _____ that must be _____
A
prodrug, activated
14
Q
isoniazid is activated by
A
bacterial catalase
15
Q
isoniazid MOA (2 steps)
A
- prodrug activated by bacterial catalase
- inhibits synthesis of mycoloic acids, essential part of cell wall
- disrupts DNA, lipids, carbs, nicotinamide adenine dinucletoide (NAD) synthesis
16
Q
ethambutol class
A
bactericidal, oral chemotherapeutic agent
17
Q
ethambutol is specifically active against
A
actively growing Mycobacterium, e.g. M. tuberculosis
18
Q
ethambutol MOA is not fully understood but it is thought to… (5 steps)
A
- inhibit arabinosyl transferase involved in cell wall synthesis
- cell wall production inhibited
- increased cell wall permeability
- inhibits RNA synthesis
- decreases tubercle bacilli replication
19
Q
rifampicin class
A
broad spectrum antibiotic
20
Q
rifampicin targets what kind of bacteria?
A
gram positive, gram negative
21
Q
rifampicin advantages
A
easily absorbed and distributed
22
Q
rifampicin MOA (3 steps)
A
- inhibits DNA-dependent RNA polymerase
- decreased RNA synthesis
- cell death
23
Q
rifampicin can target ____ but not _____ versions of the DNA-dependent RNA polymerase enzyme
A
bacterial, but not mammalian
24
Q
rifampicin is restricted to use mainly on
A
Mycobacterium
25
rifampicin is restricted to use mainly on mycobacterial infections because of
emergence of resistant bacteria
26
rifampicin is metabolised where?
liver
27
rifampicin is eliminated in
bile, urine
28
pyrazinamide use
with other drugs, TB
29
pyrazinamide is active only against
M, tuberculosis
30
pyrazinamide is only active in what conditions?
slightly acidic pH
31
pyrazinamide MOA (4 steps)
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)
32
ciprofloxacin class
broad-spectrum antibiotic, quinolone
33
ciprofloxacin targets what kind of bacteria?
gram positive, gram negative
34
bacteria that are resistant to other antibiotics such as beta-lactams, macrolides, tetracyclines, or aminoglycosides may be susceptible to ciprofloxacin as it has a
different MOA
35
ciprofloxacin MOA (2 steps)
1. inhibits topoisomerase 2 (DNA gyrase) and topoisomerase 4
| 2. bacteria can't replicate, repair or recombinate
36
B2 receptor (agonist) stimulation in the lung causes
relaxation of bronchial smooth muscle, bronchodilation, increased airflow
37
B2 receptor agonists uses (2)
asthma, COPD
38
salbutamol class
B2 adrenergic agonist
39
salbutamol has
2 isomers
40
2 isomers of salbutamol
- R-isomer, levalbuterol
| - S-isomer
41
R-isomer, levalbuterol of salbutamol is responsible for
bronchodilation
42
S-isomer of salbutamol is responsible for
increasing bronchial reactivity
43
salbutamol MOA (7 steps)
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
44
salmeterol class
B@ adrenergic agonist, LABA
45
salmeterol has a (structure)
long, lipophilic side chain
46
salmeterol MOA (5 steps)
1. side chain binds near receptors so active part can keep binding/unbinding for more stimulation
2. relaxes smooth muscle, bronchodilation
47
salmeterol should be used
regularly
48
if used regularly, salmeterol decreases the
number and severity of asthma attacks
49
salmeterol is not for use in an
asthma attack already started
50
salmeterol duration of action
12hrs
51
salbutamol duration of action
4-6hrs
52
salmeterol is similar in action to
formoterol
53
although salmeterol is similar in action to formoterol, formoterol is (2)
faster, more potent
54
budesonide class
anti-inflammatory corticosteroid
55
budesonide has a high what effect?
glucocorticoid
56
budesonide has a weak what effect?
mineralocorticoid
57
budesonide's binding affinity to the glucocorticoid receptor is higher than (2)
cortisol, prednisolone
58
precise mechanism of corticosteroid action on inflammation in asthma, crohn's and ulcerative colitis is
unknown
59
corticosteroid anti-inflammatory action is most likely due to inhibition of (6)
mast cells, eosinophils, neutrophils, macrophages, lymphocytes, mediators (histamine, leukotrienes, cytokines, eicosanoids) involved in allergic reaction and inflammation
60
budesonide undergoes significant
first-pass elimination
61
because budesonide undergoes significant first-pass elimination, oral preparations are
extended release tablets, delaying release until small intestine
62
montelukast class
leukotriene receptor antagonist
63
montelukast is used as an alternative to
anti-inflammatory meds in asthma and exercise-induced bronchospasm
64
montelukast MOA (1 step)
selectively antagonises leukotriene D4 (LTD4) at cysteinyl leukotriene receptor (CysLT1)
65
montelukast prevents (3)
airway oedema, smooth muscle contraction, mucus secretion
66
ipratropium bromide class
anticholinergic bronchodilator
67
ipratropium use (3)
cholinergic-mediated bronchospasm in COPD, rhinorrhoea, rhinitis
68
ipratropium bromide MOA (3 steps)
1. non-selectively inhibits muscarinic cholinergic receptors
2. decreased cGMP
3. decreased smooth muscle contraction as cGMP effects calcium or myosin
69
verapamil class
class IV anti-arrhythmic
70
verapamil inhibits
voltage-dependent calcium channels
71
verapamil MOA (3 steps)
1. blocks L-type calcium channels in heart
2. decreased ionotropy, chronotropy
3. reduced heart rate and blood pressure
72
verapamil has
2 enantiomers
73
verapamil 2 enantiomers
R-enantiomer, S-enantiomer
74
verapamil R-enantiomer is more effective at what than the S-enantiomer?
reducing bp
75
the verapamil S-enantiomer is 20x more potent than the R-enantiomer at what?
prolonging PR interval, arrhythmias
76
verapamil is given
IV
77
what non-dihydropyridine calcium channel blocker is used more commonly than verapamil?
diltiazem
78
diltiazem class
non-dihydropyridine calcium channel inhibitor
79
how does diltiazem work?
inhibits influx of Ca2+ across cell membranes
80
what are the 3 possible mechanisms for how diltiazem inhibits influx of Ca2+?
1. channel deformation
2. inhibition of channel ion gating
3. inhibits release of Ca2+ from sarcoplasmic reticulum
81
the decrease in intracellular Ca2+ caused by diltiazem inhibits
contractile process of myocardial smooth muscle cells
82
diltiazem's inhibition of myocardial muscle contraction causes (5)
artery dilation, increased O2 to heart tissue, decreased total peripheral resistance, decreased bp, decreased afterload
83
diltiazem use
hypertension, stable angina, prinzmetal's variable angina
84
b-adrenergic antagonists compete with
sympathomimetic neurotransmitters, e.g. catecholamines
85
b-adrenergic antagonists compete to bind with what receptor?
B1-adrenoreceptor
86
where are B1-adrenoreceptors found?
heart, smooth muscle
87
b-adrenergic antagonists result in (4)
reduction in resting heart rate, cardiac output, blood pressure, reflex orthostatic hypotension
88
atenolol class
B1-selective antagonist
89
higher doses of atenolol also competitively block
B2-adrenergic responses in bronchial and vascular smooth muscle
90
b-adrenergic antagonists is not
commonly used
91
what drug is used more commonly than atenolol?
bisoprolol
92
atropine class
antimuscarinic agent
93
atropine MOA (1)
binds to and inhibits muscarinic (M2) acetylcholine receptor
94
adequate doses of atropine abolish various types of (2)
reflex vagal cardiac slowing, asystole
95
atropine also stops what effect produced by injection of choline esters, anticholinesterases or other parasympathomimetic drugs? (2)
bradycardia, asystole
96
atropine also stops what effect produced by stimulation of the vagus? (1)
cardiac arrest
97
atropine may also lessen he degree of what?
partial heart block due to vagal activity
98
glyceryl trinitrate (GTN) class
vasodilator
99
glyceryl trinitrate (GTN) uses
angina, perioperative hypertension
100
glyceryl trinitrate (GTN) is used to try and produce
controlled hypotension
101
glyceryl trinitrate (GTN) MOA (7 steps)
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
amiodarone class
class 3 antiarrhythmic, antianginal
103
amiodarone 2 possible MOAs (2)
1. prolongs myocardial action potential (phase 3) by blocking K+ channels refractory period
2. a non-competitive A and B-adrenergic inhibitor
104
amiodarone can also have what activity on SA and AV nodes? (2)
B-blocker, calcium channel blocker
105
amiodarone can also have B-blocker and calcium channel blocker-like actions on what? (2)
SA and AV nodes
106
amiodarone increases the refractory period via what effects? (2)
sodium and potassium channel
107
amiodarone does what via sodium-channel effects?
slows intra-cardiac conduction of cardiac action potential
108
adenosine class
endogenous nucleotide
109
adenosine MOA (4 steps)
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
adenosine slows conduction time through
AV node
111
as adenosine slows conduction time through the AV node, it interrupts re-entry pathways through the AV node, resulting in
restoration of normal sinus rhythm in paroxysmal SVT
112
adenosine also increases
blood flow in coronary arteries
113
adenosine produces a relative difference in what uptake in the myocardium?
thallous (thallium) chloride TI 201
114
adenosine is antagonised competitively by
methylxanthines (e.g. caffeine, theophylline)
115
adenosine is potentiated by blockers of
nucleoside transport (e.g. dipyridamole)
116
lidocaine class
class 1b anaesthetic
117
lidocaine MOA (3 steps)
1. blocks voltage-sensitive Na+ channels
2. during phase 0 of cardiac action potential
3. slows and depresses impulse conduction
118
lidocaine dissociates
rapidly from channel, almost completely between APs
119
in depolarised tissues or firing at a high frequency lidocaine dissociation is _____, so (3)
decreased, promoting channel blockade, conduction depression
120
lidocaine is used to treat
venrticular tachyarrhythmias from MI
121
lidocaine does not affect the
SA node
122
lidocaine depresses
ventricular excitability
123
lidocaine increases the stimulation threshold of the ventricle during
diastole
