Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm > Block 2 Drugs > Flashcards

Block 2 Drugs Flashcards

1
Q

aspirin MOA

A

inhibit COX 1 (acetyaltes COX)–>inhibit TXA2 synthesis–> inhibit platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

diphenhydramine

  1. receptor
  2. what generation?
  3. use
  4. AE
A
  1. H1 receptor
  2. 1st generation drug
  3. use in allergic reactions, motion sickeness, EPS caused by antipsychotics
  4. AE: anticholinergic affects (dry mouth, blurred vision, urinary hesitancy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

eptafibatide MOA

A

inhibit fibrinogen receptor

ie GpIIb/IIIa receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

cetirizine

A
  1. H1 receptor
  2. 2nd generation drug
  3. Use: allergic reactions; motion sickness, EPS caused by antipsychotics
  4. AE: no sedation; no anticholinergic side effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

This drug causes neutropenia & TCP and is used as an alternative to aspirin

A

Ticlopidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Dipyrimadole MOA

A

Inhibit PDE –> Inceases cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

abciximab MOA & uses

A

inhibit fibrinogen receptor

ie GpIIb/IIIa receptors

use: in coronary angioplasty with aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

tirofiban MOA

A

inhibit fibrinogen receptor

ie GpIIb/IIIa receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Promethazine

  1. receptor
  2. what generation?
  3. use
  4. AE
A
  1. H1 receptor
  2. 1st generation drug
  3. use in allergic reactions, motion sickeness, EPS caused by antipsychotics
  4. AE: anticholinergic affects (dry mouth, blurred vision, urinary hesitancy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

sumatriptan: type; receptor; use

A

AGONIST
5HT1D
receptor: 5HT1
use: acute migraine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

tegaserid use

A

irritable bowel syndrome with constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

chlorpheniramine

  1. receptor
  2. what generation?
  3. use
  4. AE
A
  1. H1 receptor
  2. 1st generation drug
  3. use in allergic reactions, motion sickeness, EPS caused by antipsychotics
  4. AE: anticholinergic affects (dry mouth, blurred vision, urinary hesitancy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

streptokinase MOA & use & AE

A

plasminogen–>plasmin–>fibrin

binds to free plasminogen. Very effective if given within 12-24h

AE: bleeding, treat by aminocaproic acid, tranexemic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

cimetidine
type of drug
use
A/E

A

H2 receptor agonist
use: peptic ulcers; ZE syndrome; GERD
A/E: CYP enzyme inhibitor–>drug interactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

buspirone

A

agonist
5HT1a
use: anxiety disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Clopidogrel MOA

A

Inhibit ADP receptors–> increases cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

fexofenadine

  1. receptor
  2. what generation?
  3. use
  4. AE
A
  1. H1 receptor
  2. 2nd generation drug
  3. Use: allergic reactions; motion sickness, EPS caused by antipsychotics
  4. AE: no sedation; no anticholinergic side effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

alprostadil

A

PGE1
vasodilation
use: erectile dysfunction; potency of the ductus arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

aminocaproic acid, tranexemic acid

A

used to treat bleeding caused by streptokinase or alteplase (tPA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

LSD

A

5HT1 receptor agonist
is an ergot alkaloid
use: hallucinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ticlopidine MOA & side effects

A

Inhibit ADP receptors–> increases cAMP

AE: can cause neutropenia & TCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

carboprost

A

PGF2alpha

effect: contraction of uterine muscle
use: abortifacent; postpartum bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

ketanserine

A

5HT2 receptor antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

alteplase (tPA)

A

binds to fibrin bound plasminogen

Very effective if given within 12-24h

AE: bleeding, treat by aminocaproic acid, tranexemic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

dinoprostone

A

PGE2

effect: contraction of uterine muscle
use: abortifacient; cervical ripening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

ranitidine

A

H2 receptor agonist

use: peptic ulcers; ZE syndrome; GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

cyproheptadine

A

5HT2 receptor antagonist

use: carcinoid tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Hydroxyzine

  1. receptor
  2. what generation?
  3. use
  4. AE
A
  1. H1 receptor
  2. 1st generation drug
  3. use in allergic reactions, motion sickeness, EPS caused by antipsychotics
  4. AE: anticholinergic affects (dry mouth, blurred vision, urinary hesitancy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

epoprostenol

A

PGI2

effect: vasodilation
use: pulmonary hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

famotidine

A

H2 receptor agonist

use: peptic ulcers; ZE syndrome; GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Loratidine

  1. receptor
  2. what generation?
  3. use
  4. AE
A
  1. H1 receptor
  2. 2nd generation drug
  3. Use: allergic reactions; motion sickness, EPS caused by antipsychotics
  4. AE: no sedation; no anticholinergic side effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

NO donors & use

A

sodium nitroprusside, nitrates

use: hypertensive emergency, angina (respectively)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

fluoxetine

A

5HT1 agonist
SSRI
use: depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

latanoprost

A

PGF2alpha

effect: increase in aqueous humor outflow
use: glaucoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

azelastine

  1. receptor
  2. what generation?
  3. use
  4. AE
A
  1. H1 receptor
  2. 2nd generation drug
  3. Use: allergic reactions; motion sickness, EPS caused by antipsychotics
  4. AE: no sedation; no anticholinergic side effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

drug that inhibits phospholipase A1

A

prednisolone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

drug that inhibits leukotriene receptors

A

monteleukast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

alosetron

A

5HT3 CTZ vomiting center antagonist

use: irritable bowel syndrome with diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

misoprostol

A

PGE1

effect: gastric cytoprotection
use: gastric & duodenal ulcers induced by use of NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

NO action & use

A

increases cGMP–>causes vasodilation

use: pulmonary artery hypertension, ARDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

dipyridamole action & use

A

inhibit PDE–>increases cAMP

use: as antiplatelet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

olanzapine

A

5HT2 antagonist

use: schizophrenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

drug that inhibits lipooxygenase

A

zileuton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

sildenafil action & use

A

inhibits PDE–>increases cGMP

use: erectile dysfunction

never use along with nitrates; leases to vasodilation & hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

granisetron

A

5HT antagonist
5HT3, CTZ vomiting center antagonist
use: chemotherapy induced vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

ticlopidine action & use

A

inhibit ADP–>cAMP

use: as antiplatelet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

drug that inhibits cyclooxygenase

A

all NSAIDS & corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

barbiturates

A

phenobarbital
pentobarbital
thiopentone (ULTRA short acting)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

ondansetron

A

5HT antagonist
5HT3, CTZ vomiting center antagonist
use: chemotherapy induced vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

clopidogrel action & use

A

inhibit ADP–>cAMP

use: as antiplatelet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

HYPOLIPIDEMIC DRUGS

A
  1. statins
  2. bile acid binding resins: cholestyramine, cholesterol
  3. nicotinic acid: niacin
  4. fibric acid derivatives: gemfibrozil and fenofibrate
  5. ezetimibe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

dyslipidemia

A

term associated with high cholesterol and/or high triglyceride (TG) levels in plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

combined dyslipidemias

A

where both cholesterol (>200) and TGs are elevated

54
Q

2 major sequelae of hyperlipidemia

A
  1. acute pancreatitis

2. atherosclerosis

55
Q

chylomicrons

A
  • largest of the lipoproteins
  • formed in the intestines
  • carry TG of dietary origin
56
Q

bile acid binding resins

A

cholestyramine

colestipol

57
Q

fabric acid derivatives

A

gemfibrozil

fenofibrate

58
Q

VLDL

A

very low density lipoproteins

  • secreted by liver
  • provide means for TG From liver to be exported to peripheral tissues (mostly TGs)
  • liver synthesizes cholesterol and secretes it as VLDL )–> IDL–> LDL)
59
Q

Niacin

  1. MOA
  2. effect
  3. side effects
A
  1. decrease synthesis of VLDL
  2. decrease TG and LDL (hyperglycemia)
  3. flushing, diarrhea, hepatic dysfunction, nausea, pruritus (itching), gout
60
Q

?

A

?

61
Q

?

A

?

62
Q

?

A

?

63
Q

?

A

?

64
Q

?

A

?

65
Q

statins

  1. MOA
  2. effect
  3. side effects
A 
1. decrease cholesterol synthesis
increase LDL receptor
2. decrease TG and LDL
3. hepatotoxicity (increase AST/ALT)
myopathy
66
Q

?

A

?

67
Q

?

A

?

68
Q

?

A

?

69
Q

?

A

?

70
Q

Fibrates

  1. MOA
  2. effect
  3. side effects
A 
1. increase LPL and TG hydrolysis
PPAR stimulant
2. decrease TG and increase HDL
3. hepatotoxicity (increase AST/ALT)
nausea, myositis
71
Q

Used along with GA to achieve skeletal m relaxation during surgeries

A

Succinylcholine: rapid onset and short DOA (rapidly hydrolyzed by plasma pseudocholinesterase)

and and D-tubocurarine

and vecuronium
pancuronium
doxacurium
rocuronium

72
Q

Other effects of Succinylcholine

A

Stimulates autonomic ganglia –> cardiac arrhythmia

73
Q

D- Tubocurarine

A

Competitive neuromuscular blocker

competitive ANTAGONIST at Nm receptor!

74
Q

How can you overcome blockade by D- Tubocurarine

A

Neostigmine

75
Q

?

A

?

76
Q

Ezetimibe

  1. MOA
  2. effect
  3. side effects
A
  1. decrease intestinal absorption of cholesterol
  2. decrease TG and LDL
  3. GI disturbances
77
Q

?

A

?

78
Q

?

A

?

79
Q

?

A

?

80
Q

?

A

?

81
Q

?

A

?

82
Q

bile acid binding resins

  1. MOA
  2. effect
  3. side effects
A
  1. interrupts enterohepatic circulation of bile acids and
    increases synthesis of bile acids and LDL receptors
  2. decrease LDL and Increase HDL
  3. constipation, bloating, nbausea, fat soluble vitamin deficiency
    (LOOK UP FAT SOLUBLE VITAMINS)
83
Q

Succinylcholine

A

Depolarizing Neuromuscular Blocker

Rapidly hydrolyzed by plasma pseudocholinesterase

puts with congenital deficiency of plasma pseudocholinesterase–> shock &

84
Q

Succinylcholine MOA

A

Phase 1: agonist at N receptor–> Na channel opens for a LONGER period than with ACH

depolarization–> contractions (fasciculations) –> there is no repolarization–>flaccid paralysis

Leads to a characteristic reduction in contractile response (with no fade) during the train of four stimuli

Phase 2: initial depolarization decreases–> depolarization

membrane becomes desensitized and CAN’T be depolarized again

Causes a “fade” pattern during “train of four” stimuli

85
Q

How do you augment Phase 1 depolarization caused by Succinylcholine?

A

Neostigmine

Leads to a characteristic reduction in contractile response (with no fade) during the train of four stimuli

86
Q

Succinylcholine toxicity

A
  • hyperkalemia
  • increased intraocular pressure
  • myalgias
  • SCh apnea
  • malignant hyperthermia
87
Q

a) What drug blocks autonomic ganglia and causes histamine release?
b) What’s the effect of histamine release by this drug?

A

a) D-Tubocurarine

b) HYPOtension and Bronchospasm

88
Q

Competitive antagonists at NM receptors

A

end in “curium” or “-curonium” or D-Tubocurarine

Vecuronium
Pancuronium
Rocuronium
Doxacurium

89
Q

Toxicities of D-Turbocurarine

A
  • Hypotension (from histamine release)
  • tachycardia
  • bronchospasm (from histamine release)
  • anaphylaxis
90
Q

?

A

?

91
Q

?

A

?

92
Q

?

A

?

93
Q

?

A

?

94
Q

The following are symptoms of toxicity associated with what drug:

  • Hypotension (from histamine release)
  • tachycardia
  • bronchospasm (from histamine release)
  • anaphylaxis
A

D-tubocurarine

competitive NM blocker (competitive antagonist at Nm receptor)

95
Q

?

A

?

96
Q

?

A

?

97
Q

?

A

?

98
Q

Vecuronium

A

Competitive NM blocker (competitive antagonist of Nm receptor)

blockade can be overcome by Neostigmine

Cause a “fade” in contractile responses seen during “train of four” stimuli

99
Q

?

A

?

100
Q

?

A

?

101
Q

?

A

?

102
Q

?

A

?

103
Q

?

A

?

104
Q

?

A

?

105
Q

?

A

?

106
Q

Pancuronium

A

Competitive NM blocker (competitive antagonist of Nm receptor)

blockade can be overcome by Neostigmine

Cause a “fade” in contractile responses seen during “train of four” stimuli

107
Q

Spasmolytics

a) names
b) MOA
c) Uses

A
  • Diazepam
  • Baclofen
  • Tizanidine
  • Dantrolene
  • Gabapentin
  • Botulism

b) depress the spinal and supra spinal reflexes in the SC–> decreases the muscle tone WITHOUT causing paralysis

c)
- acute muscle spasm
- sprain
- ligament tear
- backache
- torticollis
- tetanus
- cerebral palsy
- MS
- stroke

108
Q

?

A

?

109
Q

?

A

?

110
Q

?

A

?

111
Q

?

A

?

112
Q

doxacurium

A

Competitive NM blocker (competitive antagonist of Nm receptor)

blockade can be overcome by Neostigmine

Cause a “fade” in contractile responses seen during “train of four” stimuli

113
Q

Dantrolene

A

Spasmolytic.

MOA: depress the spinal and supra spinal reflexes in the SC–> decreases the muscle tone WITHOUT causing paralysis

How: Inhibits the release of calcium from the SR during excitation/contraction coupling

Also inhibits the ryanodine receptor and calcium channel in skeletal muscle

Use: malignant hyperthermia

114
Q

?

A

?

115
Q

?

A

?

116
Q

?

A

?

117
Q

Botox

A

Spasmolytic.

MOA: depress the spinal and supra spinal reflexes in the SC–> decreases the muscle tone WITHOUT causing paralysis

HOW: Acts at vesicles in cholinergic nerves–> prevents fusion of vesicles to membrane–>prevents Ach release

Use:

  • cerebral palsy
  • blepharospasm (involuntary tight closure of the eyelids)
  • strabismus
  • cosmetics
118
Q

rocuronium

A

Competitive NM blocker (competitive antagonist of Nm receptor)

blockade can be overcome by Neostigmine

Cause a “fade” in contractile responses seen during “train of four” stimuli

119
Q

?

A

?

120
Q

?

A

?

121
Q

Gabapentin

a) What is it?
b) MOA
c) Use

A

Spasmolytic

MOA: depress the spinal and supra spinal reflexes in the SC–> decreases the muscle tone WITHOUT causing paralysis

Use:

  • acute muscle spasm
  • sprain
  • ligament tear
  • backache
  • torticollis
  • tetanus
  • cerebral palsy
  • MS
  • stroke
122
Q

?

A

?

123
Q

?

A

?

124
Q

?

A

?

125
Q

?

A

?

126
Q

Tizanidine

A

Spasmolytic

MOA: depress the spinal and supra spinal reflexes in the SC–> decreases the muscle tone WITHOUT causing paralysis

How: alpha 2 agonist!! (note: -idine)

Use:

  • acute muscle spasm
  • sprain
  • ligament tear
  • backache
  • torticollis
  • tetanus
  • cerebral palsy
  • MS
  • stroke
127
Q

?

A

?

128
Q

?

A

?

129
Q

?

A

?

130
Q

?

A

?

131
Q

?

A

?

132
Q

Baclofen

A

Spasmolytic

MOA: depress the spinal and supra spinal reflexes in the SC–> decreases the muscle tone WITHOUT causing paralysis

How: GABA B agonist

increases K+ flow –> hyper polarization–> reduces release of excitatory NTs

Use:

  • acute muscle spasm
  • sprain
  • ligament tear
  • backache
  • torticollis
  • tetanus
  • cerebral palsy
  • MS
  • stroke

Pharm (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions