Block 2 Drugs Flashcards
aspirin MOA
inhibit COX 1 (acetyaltes COX)–>inhibit TXA2 synthesis–> inhibit platelet aggregation
diphenhydramine
- receptor
- what generation?
- use
- AE
- H1 receptor
- 1st generation drug
- use in allergic reactions, motion sickeness, EPS caused by antipsychotics
- AE: anticholinergic affects (dry mouth, blurred vision, urinary hesitancy)
eptafibatide MOA
inhibit fibrinogen receptor
ie GpIIb/IIIa receptors
cetirizine
- H1 receptor
- 2nd generation drug
- Use: allergic reactions; motion sickness, EPS caused by antipsychotics
- AE: no sedation; no anticholinergic side effects
This drug causes neutropenia & TCP and is used as an alternative to aspirin
Ticlopidine
Dipyrimadole MOA
Inhibit PDE –> Inceases cAMP
abciximab MOA & uses
inhibit fibrinogen receptor
ie GpIIb/IIIa receptors
use: in coronary angioplasty with aspirin
tirofiban MOA
inhibit fibrinogen receptor
ie GpIIb/IIIa receptors
Promethazine
- receptor
- what generation?
- use
- AE
- H1 receptor
- 1st generation drug
- use in allergic reactions, motion sickeness, EPS caused by antipsychotics
- AE: anticholinergic affects (dry mouth, blurred vision, urinary hesitancy)
sumatriptan: type; receptor; use
AGONIST
5HT1D
receptor: 5HT1
use: acute migraine
tegaserid use
irritable bowel syndrome with constipation
chlorpheniramine
- receptor
- what generation?
- use
- AE
- H1 receptor
- 1st generation drug
- use in allergic reactions, motion sickeness, EPS caused by antipsychotics
- AE: anticholinergic affects (dry mouth, blurred vision, urinary hesitancy)
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
cimetidine
type of drug
use
A/E
H2 receptor agonist
use: peptic ulcers; ZE syndrome; GERD
A/E: CYP enzyme inhibitor–>drug interactions
buspirone
agonist
5HT1a
use: anxiety disorder
Clopidogrel MOA
Inhibit ADP receptors–> increases cAMP
fexofenadine
- receptor
- what generation?
- use
- AE
- H1 receptor
- 2nd generation drug
- Use: allergic reactions; motion sickness, EPS caused by antipsychotics
- AE: no sedation; no anticholinergic side effects
alprostadil
PGE1
vasodilation
use: erectile dysfunction; potency of the ductus arterioles
aminocaproic acid, tranexemic acid
used to treat bleeding caused by streptokinase or alteplase (tPA)
LSD
5HT1 receptor agonist
is an ergot alkaloid
use: hallucinogen
Ticlopidine MOA & side effects
Inhibit ADP receptors–> increases cAMP
AE: can cause neutropenia & TCP
carboprost
PGF2alpha
effect: contraction of uterine muscle
use: abortifacent; postpartum bleeding
ketanserine
5HT2 receptor antagonist
alteplase (tPA)
binds to fibrin bound plasminogen
Very effective if given within 12-24h
AE: bleeding, treat by aminocaproic acid, tranexemic acid
dinoprostone
PGE2
effect: contraction of uterine muscle
use: abortifacient; cervical ripening
ranitidine
H2 receptor agonist
use: peptic ulcers; ZE syndrome; GERD
cyproheptadine
5HT2 receptor antagonist
use: carcinoid tumor
Hydroxyzine
- receptor
- what generation?
- use
- AE
- H1 receptor
- 1st generation drug
- use in allergic reactions, motion sickeness, EPS caused by antipsychotics
- AE: anticholinergic affects (dry mouth, blurred vision, urinary hesitancy)
epoprostenol
PGI2
effect: vasodilation
use: pulmonary hypertension
famotidine
H2 receptor agonist
use: peptic ulcers; ZE syndrome; GERD
Loratidine
- receptor
- what generation?
- use
- AE
- H1 receptor
- 2nd generation drug
- Use: allergic reactions; motion sickness, EPS caused by antipsychotics
- AE: no sedation; no anticholinergic side effects
NO donors & use
sodium nitroprusside, nitrates
use: hypertensive emergency, angina (respectively)
fluoxetine
5HT1 agonist
SSRI
use: depression
latanoprost
PGF2alpha
effect: increase in aqueous humor outflow
use: glaucoma
azelastine
- receptor
- what generation?
- use
- AE
- H1 receptor
- 2nd generation drug
- Use: allergic reactions; motion sickness, EPS caused by antipsychotics
- AE: no sedation; no anticholinergic side effects
drug that inhibits phospholipase A1
prednisolone
drug that inhibits leukotriene receptors
monteleukast
alosetron
5HT3 CTZ vomiting center antagonist
use: irritable bowel syndrome with diarrhea
misoprostol
PGE1
effect: gastric cytoprotection
use: gastric & duodenal ulcers induced by use of NSAIDs
NO action & use
increases cGMP–>causes vasodilation
use: pulmonary artery hypertension, ARDS
dipyridamole action & use
inhibit PDE–>increases cAMP
use: as antiplatelet
olanzapine
5HT2 antagonist
use: schizophrenia
drug that inhibits lipooxygenase
zileuton
sildenafil action & use
inhibits PDE–>increases cGMP
use: erectile dysfunction
never use along with nitrates; leases to vasodilation & hypotension
granisetron
5HT antagonist
5HT3, CTZ vomiting center antagonist
use: chemotherapy induced vomiting
ticlopidine action & use
inhibit ADP–>cAMP
use: as antiplatelet
drug that inhibits cyclooxygenase
all NSAIDS & corticosteroids
barbiturates
phenobarbital
pentobarbital
thiopentone (ULTRA short acting)
ondansetron
5HT antagonist
5HT3, CTZ vomiting center antagonist
use: chemotherapy induced vomiting
clopidogrel action & use
inhibit ADP–>cAMP
use: as antiplatelet
HYPOLIPIDEMIC DRUGS
- statins
- bile acid binding resins: cholestyramine, cholesterol
- nicotinic acid: niacin
- fibric acid derivatives: gemfibrozil and fenofibrate
- ezetimibe
dyslipidemia
term associated with high cholesterol and/or high triglyceride (TG) levels in plasma
combined dyslipidemias
where both cholesterol (>200) and TGs are elevated
2 major sequelae of hyperlipidemia
- acute pancreatitis
2. atherosclerosis
chylomicrons
- largest of the lipoproteins
- formed in the intestines
- carry TG of dietary origin
bile acid binding resins
cholestyramine
colestipol
fabric acid derivatives
gemfibrozil
fenofibrate
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)
Niacin
- MOA
- effect
- side effects
- decrease synthesis of VLDL
- decrease TG and LDL (hyperglycemia)
- flushing, diarrhea, hepatic dysfunction, nausea, pruritus (itching), gout
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statins
- MOA
- effect
- 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
- MOA
- effect
- side effects
1. increase LPL and TG hydrolysis PPAR stimulant 2. decrease TG and increase HDL 3. hepatotoxicity (increase AST/ALT) nausea, myositis
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
Other effects of Succinylcholine
Stimulates autonomic ganglia –> cardiac arrhythmia
D- Tubocurarine
Competitive neuromuscular blocker
competitive ANTAGONIST at Nm receptor!
How can you overcome blockade by D- Tubocurarine
Neostigmine
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Ezetimibe
- MOA
- effect
- side effects
- decrease intestinal absorption of cholesterol
- decrease TG and LDL
- GI disturbances
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bile acid binding resins
- MOA
- effect
- side effects
- interrupts enterohepatic circulation of bile acids and
increases synthesis of bile acids and LDL receptors - decrease LDL and Increase HDL
- constipation, bloating, nbausea, fat soluble vitamin deficiency
(LOOK UP FAT SOLUBLE VITAMINS)
Succinylcholine
Depolarizing Neuromuscular Blocker
Rapidly hydrolyzed by plasma pseudocholinesterase
puts with congenital deficiency of plasma pseudocholinesterase–> shock &
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
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
Succinylcholine toxicity
- hyperkalemia
- increased intraocular pressure
- myalgias
- SCh apnea
- malignant hyperthermia
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
Competitive antagonists at NM receptors
end in “curium” or “-curonium” or D-Tubocurarine
Vecuronium
Pancuronium
Rocuronium
Doxacurium
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
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
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
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
