Block 2 Drugs Flashcards
(132 cards)
1
Q
aspirin MOA
A
inhibit COX 1 (acetyaltes COX)–>inhibit TXA2 synthesis–> inhibit platelet aggregation
2
Q
diphenhydramine
- receptor
- what generation?
- use
- AE
A
- H1 receptor
- 1st generation drug
- use in allergic reactions, motion sickeness, EPS caused by antipsychotics
- AE: anticholinergic affects (dry mouth, blurred vision, urinary hesitancy)
3
Q
eptafibatide MOA
A
inhibit fibrinogen receptor
ie GpIIb/IIIa receptors
4
Q
cetirizine
A
- H1 receptor
- 2nd generation drug
- Use: allergic reactions; motion sickness, EPS caused by antipsychotics
- AE: no sedation; no anticholinergic side effects
5
Q
This drug causes neutropenia & TCP and is used as an alternative to aspirin
A
Ticlopidine
6
Q
Dipyrimadole MOA
A
Inhibit PDE –> Inceases cAMP
7
Q
abciximab MOA & uses
A
inhibit fibrinogen receptor
ie GpIIb/IIIa receptors
use: in coronary angioplasty with aspirin
8
Q
tirofiban MOA
A
inhibit fibrinogen receptor
ie GpIIb/IIIa receptors
9
Q
Promethazine
- receptor
- what generation?
- use
- AE
A
- H1 receptor
- 1st generation drug
- use in allergic reactions, motion sickeness, EPS caused by antipsychotics
- AE: anticholinergic affects (dry mouth, blurred vision, urinary hesitancy)
10
Q
sumatriptan: type; receptor; use
A
AGONIST
5HT1D
receptor: 5HT1
use: acute migraine
11
Q
tegaserid use
A
irritable bowel syndrome with constipation
12
Q
chlorpheniramine
- receptor
- what generation?
- use
- AE
A
- H1 receptor
- 1st generation drug
- use in allergic reactions, motion sickeness, EPS caused by antipsychotics
- AE: anticholinergic affects (dry mouth, blurred vision, urinary hesitancy)
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
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
15
Q
buspirone
A
agonist
5HT1a
use: anxiety disorder
16
Q
Clopidogrel MOA
A
Inhibit ADP receptors–> increases cAMP
17
Q
fexofenadine
- receptor
- what generation?
- use
- AE
A
- H1 receptor
- 2nd generation drug
- Use: allergic reactions; motion sickness, EPS caused by antipsychotics
- AE: no sedation; no anticholinergic side effects
18
Q
alprostadil
A
PGE1
vasodilation
use: erectile dysfunction; potency of the ductus arterioles
19
Q
aminocaproic acid, tranexemic acid
A
used to treat bleeding caused by streptokinase or alteplase (tPA)
20
Q
LSD
A
5HT1 receptor agonist
is an ergot alkaloid
use: hallucinogen
21
Q
Ticlopidine MOA & side effects
A
Inhibit ADP receptors–> increases cAMP
AE: can cause neutropenia & TCP
22
Q
carboprost
A
PGF2alpha
effect: contraction of uterine muscle
use: abortifacent; postpartum bleeding
23
Q
ketanserine
A
5HT2 receptor antagonist
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
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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
42
olanzapine
5HT2 antagonist
| use: schizophrenia
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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
50
clopidogrel action & use
inhibit ADP-->cAMP
use: as antiplatelet
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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)
59
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
73
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
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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
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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
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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
