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Flashcards in Block 2 Drugs Deck (132):
1

aspirin MOA

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

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diphenhydramine
1. receptor
2. what generation?
3. use
4. AE

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)

3

eptafibatide MOA

inhibit fibrinogen receptor

ie GpIIb/IIIa receptors

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cetirizine

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

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

Ticlopidine

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Dipyrimadole MOA

Inhibit PDE --> Inceases cAMP

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abciximab MOA & uses

inhibit fibrinogen receptor

ie GpIIb/IIIa receptors

use: in coronary angioplasty with aspirin

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tirofiban MOA

inhibit fibrinogen receptor

ie GpIIb/IIIa receptors

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Promethazine
1. receptor
2. what generation?
3. use
4. AE

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)

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sumatriptan: type; receptor; use

AGONIST
5HT1D
receptor: 5HT1
use: acute migraine

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tegaserid use

irritable bowel syndrome with constipation

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chlorpheniramine
1. receptor
2. what generation?
3. use
4. AE

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)

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streptokinase MOA & use & AE

plasminogen-->plasmin-->fibrin

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

AE: bleeding, treat by aminocaproic acid, tranexemic acid

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cimetidine
type of drug
use
A/E

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

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buspirone

agonist
5HT1a
use: anxiety disorder

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Clopidogrel MOA

Inhibit ADP receptors--> increases cAMP

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fexofenadine
1. receptor
2. what generation?
3. use
4. AE

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

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alprostadil

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

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aminocaproic acid, tranexemic acid

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

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LSD

5HT1 receptor agonist
is an ergot alkaloid
use: hallucinogen

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Ticlopidine MOA & side effects

Inhibit ADP receptors--> increases cAMP

AE: can cause neutropenia & TCP

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carboprost

PGF2alpha
effect: contraction of uterine muscle
use: abortifacent; postpartum bleeding

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ketanserine

5HT2 receptor antagonist

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alteplase (tPA)

binds to fibrin bound plasminogen

Very effective if given within 12-24h

AE: bleeding, treat by aminocaproic acid, tranexemic acid

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dinoprostone

PGE2
effect: contraction of uterine muscle
use: abortifacient; cervical ripening

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ranitidine

H2 receptor agonist
use: peptic ulcers; ZE syndrome; GERD

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cyproheptadine

5HT2 receptor antagonist
use: carcinoid tumor

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Hydroxyzine
1. receptor
2. what generation?
3. use
4. AE

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)

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epoprostenol

PGI2
effect: vasodilation
use: pulmonary hypertension

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famotidine

H2 receptor agonist
use: peptic ulcers; ZE syndrome; GERD

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Loratidine
1. receptor
2. what generation?
3. use
4. AE

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

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NO donors & use

sodium nitroprusside, nitrates

use: hypertensive emergency, angina (respectively)

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fluoxetine

5HT1 agonist
SSRI
use: depression

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latanoprost

PGF2alpha
effect: increase in aqueous humor outflow
use: glaucoma

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azelastine
1. receptor
2. what generation?
3. use
4. AE

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

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drug that inhibits phospholipase A1

prednisolone

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drug that inhibits leukotriene receptors

monteleukast

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alosetron

5HT3 CTZ vomiting center antagonist
use: irritable bowel syndrome with diarrhea

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misoprostol

PGE1
effect: gastric cytoprotection
use: gastric & duodenal ulcers induced by use of NSAIDs

40

NO action & use

increases cGMP-->causes vasodilation

use: pulmonary artery hypertension, ARDS

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dipyridamole action & use

inhibit PDE-->increases cAMP

use: as antiplatelet

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olanzapine

5HT2 antagonist
use: schizophrenia

43

drug that inhibits lipooxygenase

zileuton

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sildenafil action & use

inhibits PDE-->increases cGMP

use: erectile dysfunction

never use along with nitrates; leases to vasodilation & hypotension

45

granisetron

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

46

ticlopidine action & use

inhibit ADP-->cAMP

use: as antiplatelet

47

drug that inhibits cyclooxygenase

all NSAIDS & corticosteroids

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barbiturates

phenobarbital
pentobarbital
thiopentone (ULTRA short acting)

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ondansetron

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

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clopidogrel action & use

inhibit ADP-->cAMP

use: as antiplatelet

51

HYPOLIPIDEMIC DRUGS

1. statins
2. bile acid binding resins: cholestyramine, cholesterol
3. nicotinic acid: niacin
4. fibric acid derivatives: gemfibrozil and fenofibrate
5. ezetimibe

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dyslipidemia

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

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combined dyslipidemias

where both cholesterol (>200) and TGs are elevated

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2 major sequelae of hyperlipidemia

1. acute pancreatitis
2. atherosclerosis

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chylomicrons

-largest of the lipoproteins
-formed in the intestines
-carry TG of dietary origin

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bile acid binding resins

cholestyramine
colestipol

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fabric acid derivatives

gemfibrozil
fenofibrate

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VLDL

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)

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Niacin
1. MOA
2. effect
3. side effects

1. decrease synthesis of VLDL
2. decrease TG and LDL (hyperglycemia)
3. flushing, diarrhea, hepatic dysfunction, nausea, pruritus (itching), gout

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statins
1. MOA
2. effect
3. side effects

1. decrease cholesterol synthesis
increase LDL receptor
2. decrease TG and LDL
3. hepatotoxicity (increase AST/ALT)
myopathy

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Fibrates
1. MOA
2. effect
3. side effects

1. increase LPL and TG hydrolysis
PPAR stimulant
2. decrease TG and increase HDL
3. hepatotoxicity (increase AST/ALT)
nausea, myositis

71

Used along with GA to achieve skeletal m relaxation during surgeries

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

and and D-tubocurarine

and vecuronium
pancuronium
doxacurium
rocuronium

72

Other effects of Succinylcholine

Stimulates autonomic ganglia --> cardiac arrhythmia

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D- Tubocurarine

Competitive neuromuscular blocker

competitive ANTAGONIST at Nm receptor!

74

How can you overcome blockade by D- Tubocurarine

Neostigmine

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Ezetimibe
1. MOA
2. effect
3. side effects

1. decrease intestinal absorption of cholesterol
2. decrease TG and LDL
3. GI disturbances

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bile acid binding resins
1. MOA
2. effect
3. side effects

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

Succinylcholine

Depolarizing Neuromuscular Blocker

Rapidly hydrolyzed by plasma pseudocholinesterase

puts with congenital deficiency of plasma pseudocholinesterase--> shock &

84

Succinylcholine MOA

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

How do you augment Phase 1 depolarization caused by Succinylcholine?

Neostigmine

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

86

Succinylcholine toxicity

- hyperkalemia
- increased intraocular pressure
- myalgias
- SCh apnea
- malignant hyperthermia

87

a) What drug blocks autonomic ganglia and causes histamine release?

b) What's the effect of histamine release by this drug?

a) D-Tubocurarine
b) HYPOtension and Bronchospasm

88

Competitive antagonists at NM receptors

end in "curium" or "-curonium" or D-Tubocurarine

Vecuronium
Pancuronium
Rocuronium
Doxacurium

89

Toxicities of D-Turbocurarine

- Hypotension (from histamine release)
- tachycardia
- bronchospasm (from histamine release)
- anaphylaxis

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The following are symptoms of toxicity associated with what drug:
- Hypotension (from histamine release)
- tachycardia
- bronchospasm (from histamine release)
- anaphylaxis

D-tubocurarine

competitive NM blocker (competitive antagonist at Nm receptor)

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Vecuronium

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

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Pancuronium

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

Spasmolytics
a) names
b) MOA
c) Uses

- 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

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doxacurium

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

Dantrolene

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

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Botox

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

rocuronium

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

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

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

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Tizanidine

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

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Baclofen

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