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Pharm SJSM > Receptors simplified & all drugs for B2 (BBH's notes) > Flashcards

Receptors simplified & all drugs for B2 (BBH's notes) Flashcards

1
Q

Describe the following for 2nd generation H1 blockers (antihistamines):

What drugs do they include?

What are their clinical uses?

What are the adverse effects?

A

Drugs:
LoratADINE
FexofenADINE
DesloratADINE
Cetirizine

Clinical use:
1) Allergic rhinitis

Adverse effects:
Fewer side effects because it doesn’t enter the CNS

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2
Q

Drugs:
LoratADINE
FexofenADINE
DesloratADINE
Cetirizine

Clinical use:
1) Allergic rhinitis

Adverse effects:
Fewer side effects because it doesn’t enter the CNS

Describes which type of drug?

A

2nd generation H1 Blockers (antihistamines)

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3
Q

Describe the following for Misoprostol:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
PGE1 analog

MOA:
It increases the production & secretion of gastric mucus while reducing the production of gastric acid

Clinical use:
1) Prevent NSAID-induced peptic ulcers (protective)
2) An off-label labor inducer (ripens the cervix)

Adverse effects:
1) Nausea/vomiting/diarrhea
2) May cause abortion
3) Vaginal bleeding
4) Uterine cramping
5) Flushing
6) Tachycardia

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4
Q

Drug type:
PGE1 analog

MOA:
It increases the production & secretion of gastric mucus while reducing the production of gastric acid

Clinical use:
1) Prevent NSAID-induced peptic ulcers (protective)
2) An off-label labor inducer (ripens the cervix)

Adverse effects:
1) Nausea/vomiting/diarrhea
2) May cause abortion
3) Vaginal bleeding
4) Uterine cramping
5) Flushing
6) Tachycardia

Describes which drug?

A

Misoprostol:

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5
Q

Describe the following for Alprostadil:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
PGE1 analog

MOA:
It relaxes smooth muscle in the ductus arteriosus

Clinical uses:
1) Keep the PDA open
2) Impotence

Adverse effects:
1) Hypotension
2) Nausea/vomiting/diarrhea
3) Vaginal bleeding
4) Flushing
5) Tachycardia

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6
Q

Drug type:
PGE1 analog

MOA:
It relaxes smooth muscle in the ductus arteriosus

Clinical uses:
1) Keep the PDA open
2) Impotence

Adverse effects:
1) Hypotension
2) Nausea/vomiting/diarrhea
3) Vaginal bleeding
4) Flushing
5) Tachycardia

Describes which drug?

A

Alprostadil:

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7
Q

Describe the following for 1st generation H1 blockers (antihistamines):

What are the drugs?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Diphenhydramine
Dimenhydrinate
Doxylamine
Chlorpheniramine

Clinical uses:
1) Allergies
2) Motion sickness
3) Vomiting in pregnancy
4) Sleep aid

Adverse effects:
1) Sedation
2) Antimuscarinic effects
3) Anti a adrenergic effects

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8
Q

Diphenhydramine
Dimenhydrinate
Doxylamine
Chlorpheniramine

Clinical uses:
1) Allergies
2) Motion sickness
3) Vomiting in pregnancy
4) Sleep aid

Adverse effects:
1) Sedation
2) Antimuscarinic effects
3) Anti a adrenergic effects

Describes which kind of drugs?

A

1st generation H1 blockers (antihistamines):

“all it takes is 1 daffodile or dog to cause drowsiness & Congestion”

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9
Q

Describe the following for acetaminophen:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
NSAID

MOA:
It reversibly inhibits cyclooxygenase in the CNS (mostly) & it’s activated peripherally meaning it’s not great as an anti-inflammatory

Clinic uses:
1) Antipyretic
2) Analgesic (acts on the cannabinoid receptors)

Adverse effects:
1) Hepatic necrosis (OD)

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10
Q

Drug type:
NSAID

MOA:
It reversibly inhibits cyclooxygenase in the CNS (mostly) & it’s activated peripherally meaning it’s not great as an anti-inflammatory

Clinic uses:
1) Antipyretic
2) Analgesic (acts on the cannabinoid receptors)

Adverse effects:
1) Hepatic necrosis (OD)

Describes which drug?

A

Acetaminophen

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11
Q

Describe the following for indomethacin:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
NSAID

MOA:
It reversibly inhibits COX1 & COX2 to block prostaglandin synthesis (pro-inflammatory)

Clinical uses:
1) Antipyretic
2) Analgesic
3) Anti-inflammatory
4) Close a PDA

Adverse effects:
1) Interstitial nephritis
2) Gastric ulcers
3) Renal ischemia
4) Aplastic anemia

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12
Q

Drug type:
NSAID

MOA:
It reversibly inhibits COX1 & COX2 to block prostaglandin synthesis (pro-inflammatory)

Clinical uses:
1) Antipyretic
2) Analgesic
3) Anti-inflammatory
4) Close a PDA

Adverse effects:
1) Interstitial nephritis
2) Gastric ulcers
3) Renal ischemia
4) Aplastic anemia

Describes which drug?

A

Indomethicin

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13
Q

Indomethacin
Acetaminophen

Are examples of which type of drug?

A

NSAIDS

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14
Q

Describe the following for Colchicine:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
Acute gout drug

MOA:
It binds & stabilizes tubulin to inhibit microtubule polymerization resulting in impaired neutrophil chemotaxis & degranulation causing decreased leukotriene (LTB4), leukocyte, & granulocyte migration

Clinical uses:
1) Acute gout & gout prophylaxis

Adverse effects:
1) Diarrhea
2) Acute Gi pain
3) Hematuria
4) Myelosuppression
5) Gastritis
6) Peripheral neuropathy (with long-term use)

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15
Q

Drug type:
Acute gout drug

MOA:
It binds & stabilizes tubulin to inhibit microtubule polymerization resulting in impaired neutrophil chemotaxis & degranulation causing decreased leukotriene (LTB4), leukocyte, & granulocyte migration

Clinical uses:
1) Acute gout & gout prophylaxis

Adverse effects:
1) Diarrhea
2) Acute Gi pain
3) Hematuria
4) Myelosuppression
5) Gastritis
6) Peripheral neuropathy (with long-term use)

Describes which drug?

A

Colchicine

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16
Q

Describe the following for Sulfinpyrazone:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
Chronic anti-gout

MOA:
It inhibits renal reabsorption of uric acid AVOID in acute gout cases (it’ll make it worse!)

Clinical uses:
1) Chronic gout

Adverse effects:
1) Precipitate uric acid calculi (kidney stones)
2) Nephrotic syndrome
3) Aplastic anemia
4) Allergy

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17
Q

Drug type:
Chronic anti-gout

MOA:
It inhibits renal reabsorption of uric acid AVOID in acute gout cases (it’ll make it worse!)

Clinical uses:
1) Chronic gout

Adverse effects:
1) Precipitate uric acid calculi (kidney stones)
2) Nephrotic syndrome
3) Aplastic anemia
4) Allergy

Describes which drug?

A

Sulfinpyrazone

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18
Q

Describe the following for Probenecid:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
Chronic gout drug

MOA:
It inhibits the reabsorption of uric acid in the PCT & it inhibits penicillin secretion from the DCT (promotes retention) AVOID in acute gout (it will get worse!)

Clinical uses:
1) Chronic gout
2) Prophylaxis of chronic gout

Adverse effects:
1) Precipitate uric acid calculi (kidney stones)
2) Nephrotic syndrome
3) Aplastic anemia
4) Allergy

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19
Q

Drug type:
Chronic gout drug

MOA:
It inhibits the reabsorption of uric acid in the PCT & it inhibits penicillin secretion from the DCT (promotes retention) AVOID in acute gout (it will get worse!)

Clinical uses:
1) Chronic gout
2) Prophylaxis of chronic gout

Adverse effects:
1) Precipitate uric acid calculi (kidney stones)
2) Nephrotic syndrome
3) Aplastic anemia
4) Allergy

Describes which drug?

A

Probenecid

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20
Q

Describe the following for Ergotamine:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
An ergot alkaloid

MOA:
It acts as a partial agonist at 5-HT2 (serotonin) receptors in the vasculature & maybe the CNS resulting in vasoconstriction & reduced pulsation in the cerebral vessels

Clinical uses:
1) Acute migraine attacks

Adverse effects:
1) Gi distress
2) Ischemia/gangrene (if vasoconstriction is prolonged)
3) Abortion near term (avoid in preggos)

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21
Q

Drug type:
An ergot alkaloid

MOA:
It acts as a partial agonist at 5-HT2 (serotonin) receptors in the vasculature & maybe the CNS resulting in vasoconstriction & reduced pulsation in the cerebral vessels

Clinical uses:
1) Acute migraine attacks

Adverse effects:
1) Gi distress
2) Ischemia/gangrene (if vasoconstriction is prolonged)
3) Abortion near term (avoid in preggos)

Describes which drug?

A

Ergotamine

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22
Q

Describe the following for Sumatriptan:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
A triptan aka serotonin agonist

MOA: An agonist at 5-HT(B1/D1) to inhibit the trigeminal nerve affects via vasoactive peptide release to induce vasoconstriction

Clinical uses:
1) Acute migraine
2) Cluster headache attacks

Adverse effects:
1) Coronary vasospasms (AVOID in CAD or vasospastic angina)
2) Mild paresthesia
3) Serotonin syndrome

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23
Q

Drug type:
A triptan aka serotonin agonist

MOA: An agonist at 5-HT(B1/D1) to inhibit the trigeminal nerve affects via vasoactive peptide release to induce vasoconstriction

Clinical uses:
1) Acute migraine
2) Cluster headache attacks

Adverse effects:
1) Coronary vasospasms (AVOID in CAD or vasospastic angina)
2) Mild paresthesia
3) Serotonin syndrome

Describes which drug?

A

Sumatriptan

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24
Q

Sumatriptan
Ergotamine

Are both used to treat which conditions

A

Migraines (both)
Cluster headache attacks (S)

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25
Q

Describe the following for warfarin toxicity:

What are the symptoms?

What are the treatments/antidotes?

A

Signs:
1) Bleeding
2) Skin necrosis (if there’s low protein C)

Rx:
Fresh frozen plasma (acutely)
Vitamin K (not acutely)

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26
Q

Signs:
1) Bleeding
2) Skin necrosis (if there’s low protein C)

Rx:
Fresh frozen plasma (acutely)
Vitamin K (not acutely)

Indicate which type of toxicity?

A

Warfarin toxicity

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27
Q

Describe the following for Heparin toxicity:

What are the symptoms?

What are the treatments/antidotes?

A

Signs:
1) Bleeding

Rx:
Protamine sulfate (it’s a +ve charged molecule that binds -ve charged heparin)

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28
Q

Signs:
1) Bleeding

Rx:
Protamine sulfate

Describes which type of toxicity?

A

Heparin toxicity

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29
Q

Describe the following for digoxin toxicity:

What are the symptoms?

What are predisposing factors/risks?
- factors associated with a poor prognosis

What are the treatments/antidotes?

A

Signs:
1) Cholinergic effects (nausea, vomiting, diarrhea)
2) blurry yellow vision
3) Arrythmias
4) AV block

Risks:
1) Renal failure

2) Hypokalemia (ass with poor prognosis)

3) Drugs that displace digoxin from its tissue binding sites (i.e verapamil, amiodarone, quinidine)

Poor prog:
- Hypokalemia
- Hypomagnesemia
- Hypercalcemic

Rx:
1) anti-digoxin Fab fragments ***
2) Slowly normalize K+
3) Antiarrhythmic drugs
4) Cardiac pacer (in severe cases)
5) Mg2+ supplement
6) Block the vagus nerve (propranolol or atropine)

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30
Q

Signs:
1) Cholinergic effects (nausea, vomiting, diarrhea)
2) blurry yellow vision
3) Arrythmias
4) AV block

Risks:
1) Renal failure

2) Hypokalemia (ass with poor prognosis)

3) Drugs that displace digoxin from its tissue binding sites (i.e verapamil, amiodarone, quinidine)

Poor prog:
- Hypokalemia
- Hypomagnesemia
- Hypercalcemic

Rx:
1) anti-digoxin Fab fragments ***
2) Slowly normalize K+
3) Antiarrhythmic drugs
4) Cardiac pacer (in severe cases)
5) Mg2+ supplement
6) Block the vagus nerve (propranolol or atropine)

Describes which type of toxicity?

A

Digoxin toxicity

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31
Q

Describe the following for Aspirin/Salicylate poisoning:

What happens?

What are the symptoms?

What are predisposing factors/risks?
- factors associated with a poor prognosis

What are the treatments/antidotes?

A

Patho:
Toxic doses cause respiratory alkalosis early on that then turns into a mixed metabolic acidosis/respiratory alkalosis later on

Signs:
1) Confusion/Stupor
2) Lethargy
3) Ataxia
4) Nystagmus
5) Hypothermia
6) Respiratory failure
7) Coma/death

Rx:
1) NaHCHO3 (bicarbonate to alkalize the urine)
2) Dialysis
3) Electrolytes

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32
Q

Patho:
Toxic doses cause respiratory alkalosis early on that then turns into a mixed metabolic acidosis/respiratory alkalosis later on

Signs:
1) Confusion/Stupor
2) Lethargy
3) Ataxia
4) Nystagmus
5) Hypothermia
6) Respiratory failure
7) Coma/death

Rx:
1) NaHCHO3 (bicarbonate to alkalize the urine)
2) Dialysis
3) Electrolytes

Describes which type of toxicity/poisoning?

A

Aspirin/Salicylate poisoning

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33
Q

Describe the following for Atropine poisoning:

What are the symptoms?

What are the treatments/antidotes?

A

Aka Belladona or deadly nightshade berries

Signs:
1) Tachycardia
2) Hypertension
3) Hyperthermia
4) Delirium
5) Mydriasis

Rx:
1) Physostigmine (an indirect M agonist to inhibit AChE & increase the available Ach to control the symptoms)

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34
Q

Aka Belladona or deadly nightshade berries

Signs:
1) Tachycardia
2) Hypertension
3) Hyperthermia
4) Delirium
5) Mydriasis

Rx:
1) Physostigmine (an indirect M agonist to inhibit AChE & increase the available Ach to control the symptoms)

Describes which type of poisoning?

A

Atropine poisoning

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35
Q

Describe the following for iron poisoning:

What are the symptoms?

What are the complications?

What are the treatments/antidotes?

A

Sigs:
1) Severe Gi distress
2) Dyspnea
3) Shock
4) Coma

Comps:
Necrotizing gastroenteritis
Hematemesis & bloody diarrhea

Rx:
1) Deferoxamine, Deferasirox, & Deferiprone (iron chelators)
2) Gastric aspiration
3) Carbonate lavage

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36
Q

Sigs:
1) Severe Gi distress
2) Dyspnea
3) Shock
4) Coma

Comps:
Necrotizing gastroenteritis
Hematemesis & bloody diarrhea

Rx:
1) Deferoxamine, Deferasirox, & Deferiprone (iron chelators)
2) Gastric aspiration
3) Carbonate lavage

Describes which type of poisoning?

A

Iron poisoning

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37
Q

Describe the following for Acetaminophen poisoning:

What happens?

What are the symptoms?

What are the complications?

What are the treatments/antidotes?

A

Patho:
Acetaminophens metabolite (NAPQI) depletes all the glutathione & it forms toxic tissue byproducts in the liver (hepatic necrosis)

Signs:
1) Hepatic & renal failure
2) Mild anorexia
3) Delayed jaundice
4) Nausea/vomiting

Rx:
1) N-acetylcysteine (to replenish the glutathione to break down acetaminophens byproduct)

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38
Q

Patho:
metabolite (NAPQI) depletes all the glutathione & it forms toxic tissue byproducts in the liver (hepatic necrosis)

Signs:
1) Hepatic & renal failure
2) Mild anorexia
3) Delayed jaundice
4) Nausea/vomiting

Rx:
1) N-acetylcysteine (to replenish the glutathione)

A

Acetaminophen poisoning

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39
Q

Describe the following for Organophosphate poisoning:

What predisposes/risks?

What happens?

What are the symptoms?

What are the complications?

What are the treatments/antidotes?

A

Risk:
Insecticides (usually farmers)

Patho:
The organophosphates irreversibly bind AChE which can then only be freed by dephosphorylation from atropine or pralidoxime

Signs:
Muscarinic (DUMBBELLSS)
1) Diarrhea (colic)
2) Urination
3) Miosis
4) Bronchospasms (constriction)
5) Bradycardia
6) Emesis
7) Lacrimation
8) Sweating/Salivation

Nicotinic (CNS effects)
1) Seizures
2) Lethargy
3) Coma
4) Respiratory/CNS depression

Rx:
Atropine (antagonizes M receptors)
Pralidoxime (dephosphorylation to regen AChE if given early)

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40
Q

Risk:
Insecticides (usually farmers)

Patho:
irreversibly bound AChE which can then only be freed by dephosphorylation from atropine or pralidoxime

Signs:
Muscarinic (DUMBBELLSS)
1) Diarrhea (colic)
2) Urination
3) Miosis
4) Bronchospasms (constriction)
5) Bradycardia
6) Emesis
7) Lacrimation
8) Sweating/Salivation

Nicotinic (CNS effects)
1) Seizures
2) Lethargy
3) Coma
4) Respiratory/CNS depression

Rx:
Atropine (antagonizes M receptors)
Pralidoxime (dephosphorylation to regen AChE if given early)

Describes which type of poisoning?

A

Organophosphate poisoning

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41
Q

Describe the following for
Clopidogrel
Prasugrel
Ticagrelor
Ticlopidine:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
ADP receptor antagonists

MOA:
They reduce ADP-induced expression of GpIIb/IIa

Clinical uses:
1) Aspirin-like effects (anti-inflammatory)
2) Antiplatelet treatment

Adverse effects:
1) Neutropenia (ticlopidine)
2) Thrombotic thrombocytopenic purpura (TTP)

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42
Q

Drug type:
ADP receptor antagonists

MOA:
They reduce ADP-induced expression of GpIIb/IIa

Clinical uses:
1) Aspirin-like effects (anti-inflammatory)
2) Antiplatelet treatment

Adverse effects:
1) Neutropenia
2) Thrombotic thrombocytopenic purpura (TTP)

Describes which drugs?

A

Clopidogrel
Prasugrel
Ticagrelor
Ticlopidine

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43
Q

Describe the following for Heparin:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

Avoid use in which conditions?

A

Durg type:
An antithrombin 3 activator

MOA:
It activates antithrombin 3 to reduce the action of thrombin (IIa) & factors resulting in a conformational change in antithrombin that makes reactive sites more accessible to proteases

Clinical uses:
1) Immediate anticoagulation for pulmonary embolism
2) Acute coronary syndrome
3) MI
4) DVT (safe in preggos)

Adverse effects:
1) Bleeding
2) Thrombocytopenia/thrombosis
3) Osteoporosis
4) Drug-drug interactions (warfarin)
5) Hyperkalemia

AVOID:
1) Hypersensitivities
2) Active bleeding
3) Active TB inf
4) Significant thrombocytopenia
5) Advanced hepatic/renal disease
6) Hemophilia
7) GIT ulcers
8) Infective endocarditis

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44
Q

Durg type:
An antithrombin 3 activator

MOA:
It activates antithrombin 3 to reduce the action of thrombin (IIa) & factors resulting in a conformational change in antithrombin that makes reactive sites more accessible to proteases

Clinical uses:
1) Immediate anticoagulation for pulmonary embolism
2) Acute coronary syndrome
3) MI
4) DVT (safe in preggos)

Adverse effects:
1) Bleeding
2) Thrombocytopenia/thrombosis
3) Osteoporosis
4) Drug-drug interactions (warfarin)
5) Hyperkalemia

AVOID:
1) Hypersensitivities
2) Active bleeding
3) Active TB inf
4) Significant thrombocytopenia
5) Advanced hepatic/renal disease
6) Hemophilia
7) GIT ulcers
8) Infective endocarditis

Describes which drug?

A

Heparin

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45
Q

Describe the following for Enoxaparin:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

Avoid use in which conditions?

A

Drug type:
Low molecular weight heparin

MOA:
It binds to antithrombin 3 to reduce thrombin similar to heparin but it has a much longer 1/2 life & it doesn’t need to be monitored as much because it’s more predictable & has less risk of adverse effects

Clinical uses:
1) Anticoagulant

Adverse effects:
1) Bleeding
2) Thrombocytopenia/thrombosis (Less risk)
3) Osteoporosis
4) Drug-drug interactions
5) Hyperkalemia

AVOID:
not for patients with renal failure

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46
Q

Drug type:
Low molecular weight heparin

MOA:
It binds to antithrombin 3 to reduce thrombin similar to heparin but it has a much longer 1/2 life & it doesn’t need to be monitored as much because it’s more predictable & has less risk of adverse effects

Clinical uses:
1) Anticoagulant

Adverse effects:
1) Bleeding
2) Thrombocytopenia/thrombosis (Less risk)
3) Osteoporosis
4) Drug-drug interactions
5) Hyperkalemia

AVOID:
not for patients with renal failure

Describes which drug?

A

Enoxaparin

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47
Q

Which drugs are mainly used for asthma?

A

Zileuton & Montelukast

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48
Q

Zileuton & Montelukast

Are drugs often used to treat which condition?

A

bronchial asthma

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49
Q

Describe the following for Zileuton:

What is the drug type?

What is the MOA?

What is the clinical use?

What is an adverse effect?

A

Drug type:
An antileukotriene

MOA:
It inhibits the 5-lipoxygenase pathway to block the conversion of arachnoid acid into leukotrienes reducing the levels of leukotrienes (LTB4 (chemotactic) & LTC4/D4 (bronchoconstriction))

Clinical use:
1) Prophylaxis of asthma

Adverse effects:
1) Hepatotoxicity

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50
Q

Drug type:
An antileukotriene

MOA:
It inhibits the 5-lipoxygenase pathway to block the conversion of arachnoid acid into leukotrienes reducing the levels of leukotrienes (LTB4 (chemotactic) & LTC4/D4 (bronchoconstriction))

Clinical use:
1) Prophylaxis of asthma

Adverse effects:
1) Hepatotoxicity

Describes which drug?

A

Zileuton

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51
Q

Describe the following for Montelukast:

What is the drug type?

What is the MOA?

What is the clinical use?

What is an adverse effect?

A

Drug type:
An antileukotriene

MOA:
An antagonist at leukotriene receptors (LTD4/C4 involved in bronchoconstriction), it’s safe to use in preggos

Clinical uses:
1) Prophylaxis for aspirin or exercise induced asthma (added with an inhaled corticosteroid & B2 blocker)

Adverse effects:
1) hepatotoxicity

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52
Q

Drug type:
An antileukotriene

MOA:
An antagonist at leukotriene receptors (LTD4/C4 involved in bronchoconstriction), it’s safe to use in preggos

Clinical uses:
1) Prophylaxis for aspirin or exercise induced asthma (added with an inhaled corticosteroid & B2 blocker)

Adverse effects:
1) hepatotoxicity

Describes which drug?

A

Montelukast

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53
Q

Describe the following for Pralidoxime:

What is the drug type?

What is the MOA?

What is the clinical use?

What is an adverse effect?

A

Drug type:
A quaternary amine & chemical antagonist of organophosphates

MOA:
It regenerates AChE by dephosphorylation if given early enough

Clinical use:
1) Organophosphate poisoning

Adverse effect:
1) Muscle weakness

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54
Q

Drug type:
A quaternary amine & chemical antagonist of organophosphates

MOA:
It regenerates AChE by dephosphorylation if given early enough

Clinical use:
1) Organophosphate poisoning

Adverse effect:
1) Muscle weakness

Describes which drug?

A

Pralidoxime

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55
Q

Describe the following for Epoetin alfa (Erythropoietin):

What drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
An erythropoiesis-stimulating agent

MOA:
It is an erythropoietin receptor agonist that is expressed on RBC progenitors

Clinical uses:
1) Anemias (from chronic renal failure, HIV, cancer, or premature birth)
2) Prevent anemias during transfusions

Adverse effects:
1) Hypertension
2) Thrombotic complications
3) Pure RBC aplasia

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56
Q

Drug type:
An erythropoiesis-stimulating agent

MOA:
It is an erythropoietin receptor agonist that is expressed on RBC progenitors

Clinical uses:
1) Anemias (from chronic renal failure, HIV, cancer, or premature birth)
2) Prevent anemias during transfusions

Adverse effects:
1) Hypertension
2) Thrombotic complications
3) Pure RBC aplasia

Describes which drug?

A

Epoetin alfa (erythropoietin)

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57
Q

Describe the following for Thiazide diuretics:

What are the drugs included?

What is the MOA?
- effects

What are the clinical uses?

What are the adverse effects?

A

Drugs:
Hydrochlorothiazide
Chlorthalidone
Metolazone

MOA:
They inhibit NaCl resorption in the early DCT resulting in reduced diluting capacity of the nephron causing more Ca2+ retention

Effects:
1) Na/Cl-/K+ excretion
2) Ca2+ retention
3) Alkalemia (HCO3) retention

Clinical uses:
1) Hypertension
2) Heart failure
3) Idiopathic hypercalcemia
4) Nephrogenic diabetes insipidus
5) Osteoporosis

Adverse effects:
1) Hypokalemic metabolic alkalosis
2) Hyponatremia
3) Hyperglycemia
4) Hyperuricemia
5) Hypercalcemia
6) Sulfa allergy
7) Hyperlipidemia

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58
Q

Drugs:
Hydrochlorothiazide
Chlorthalidone
Metolazone

MOA:
They inhibit NaCl resorption in the early DCT resulting in reduced diluting capacity of the nephron causing more Ca2+ retention

Effects:
1) Na/Cl-/K+ excretion
2) Ca2+ retention
3) Alkalemia (HCO3) retention

Clinical uses:
1) Hypertension
2) Heart failure
3) Idiopathic hypercalcemia
4) Nephrogenic diabetes insipidus
5) Osteoporosis

Adverse effects:
1) Hypokalemic metabolic alkalosis
2) Hyponatremia
3) Hyperglycemia
4) Hyperuricemia
5) Hypercalcemia
6) Sulfa allergy
7) Hyperlipidemia

Describes which group of diuretics

A

Thiazide diuretics

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59
Q

Hydrochlorothiazide
Chlorthalidone
Metolazone

Are examples of which type of diuretics that act on which part of the nephron?

A

Thiazide diuretics that act on the early DCT

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60
Q

Thiazide diuretics that act on the early DCT include which drugs?

A

Hydrochlorothiazide
Chlorthalidone
Metolazone

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61
Q

Describe the following for Loop diuretics:

What are the drugs?

What is the MOA?
-effects

What are the clinical uses?

What are the adverse effects?

A

Drugs:
Furosemide
Bumetanide
Torsemide

MOA:
These are sulfonamide loop diuretics that act on the thick ascending loop of Henle to inhibit Na+, K+, & Cl- co-transporters resulting in:

Effects:
1) Ca2+/K+/NaCl excretion
2) Alkalemia (HCO3) retention
3) Abolished hypertonicity of the medulla
4) Elevated PGE (vasodilation of afferent arteriole

Clinical uses:
1) Edematous states (HF, Cirrhosis, Nephrotic syndrome, Pulmonary edema)
2) Hypertension
3) Hypercalcemia/kalemia/natremia

Adverse effects:
1) Ototoxicity
2) Hypokalemia
3) Hypomagnesemia
4) Dehydration
5) Allergy (Sulfa)
6) Alkalosis (metabolic)
7) Nephritis
8) Gout
“OHH DAANG!”

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62
Q

Drugs:
Furosemide
Bumetanide
Torsemide

MOA:
These are sulfonamide loop diuretics that act on the thick ascending loop of Henle to inhibit Na+, K+, & Cl- co-transporters resulting in:

Effects:
1) Ca2+/K+/NaCl excretion
2) Alkalemia (HCO3) retention
3) Abolished hypertonicity of the medulla
4) Elevated PGE (vasodilation of afferent arteriole

Clinical uses:
1) Edematous states (HF, Cirrhosis, Nephrotic syndrome, Pulmonary edema)
2) Hypertension
3) Hypercalcemia/kalemia/natremia

Adverse effects:
1) Ototoxicity
2) Hypokalemia
3) Hypomagnesemia
4) Dehydration
5) Allergy (Sulfa)
6) Alkalosis (metabolic)
7) Nephritis
8) Gout
“OHH DAANG!”

Describes which drug type?

A

Loop diuretics

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63
Q

Drugs:
Furosemide
Bumetanide
Torsemide

Are examples of which type of diuretics that act on what part of the nephron?

A

Loop diuretics that act on the thick ascending limb of the loop of Henle

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64
Q

Loop diuretics that act on the thick ascending limb of the loop of Henle, include which drugs?

A

Furosemide
Bumetanide
Torsemide

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65
Q

Describe the following for potassium sparring diuretics:

What are the drugs?

What is the MOA?

What are the effects?

What are the clinical uses?

What are the adverse side effects?

A

Drugs:
Spironolactone
Eplerenone
Amiloride
Triamterene

MOA:
1) Spironolactone & Eplerenone (are competitive antagonists in the cortical collecting tubule
2) Amiloride & Triamterene (are Na channel blockers in the cortical collecting tubule)

Effects:
1) Acidemia (K+ & H+ retention)
2) NaCl excretion

Clinical uses:
1) Hyperaldosteronism
2) Hypokalemia
3) Heart failure
4) Nephrogenic Diabetes Insipidus
5) Anti-Androgenics

Adverse effects:
1) Hyperkalemia & arrythmia
2) Endocrine symptoms (Gynecomastia)
3) Metabolic acidosis

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66
Q

Drugs:
Spironolactone
Eplerenone
Amiloride
Triamterene

MOA:
1) Spironolactone & Eplerenone (are competitive antagonists in the cortical collecting tubule
2) Amiloride & Triamterene (are Na channel blockers in the cortical collecting tubule)

Effects:
1) Acidemia (K+ & H+ retention)
2) NaCl excretion

Clinical uses:
1) Hyperaldosteronism
2) Hypokalemia
3) Heart failure
4) Nephrogenic Diabetes Insipidus
5) Anti-Androgenics

Adverse effects:
1) Hyperkalemia & arrythmia
2) Endocrine symptoms (Gynecomastia)
3) Metabolic acidosis

Describes which group of diuretics?

A

K+ sparring diuretics that act in the Cortical collecting tubule

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67
Q

Spironolactone
Eplerenone
Amiloride
Triamterene

Are examples of which type of diuretics?

A

K+ sparring that act in the cortical collecting tubules

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68
Q

K+ sparring that act in the cortical collecting tubules, include which drugs?

A

Spironolactone
Eplerenone
Amiloride
Triamterene

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69
Q

Describe the following for carbonic anhydrase inhibitors:

What are the drugs?

What is the MOA?

What are the effects?

What are the clinical uses?

What are the Adverse effects?

A

Drugs:
Acetazolamide

MOA:
It causes self limiting NAHCO3 diuresis & reduced total body HCO3 stores

Effects:
1) Alkalinize the urine

Clinical use:
1) Glaucoma
2) Metabolic alkalosis
3) Altitude sickness
4) Idiopathic intracranial hypertension

Adverse effects:
1) Proximal renal tubular acidosis
2) Paresthesia
3) NH3 toxicity
4) Sulfa allergy
5) Hypokalemia
6) Calcium phosphate stone formation (kidney stones)

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70
Q

Drugs:
Acetazolamide

MOA:
It causes self limiting NAHCO3 diuresis & reduced total body HCO3 stores

Effects:
1) Alkalinize the urine

Clinical use:
1) Glaucoma
2) Metabolic alkalosis
3) Altitude sickness
4) Idiopathic intracranial hypertension

Adverse effects:
1) Proximal renal tubular acidosis
2) Paresthesia
3) NH3 toxicity
4) Sulfa allergy
5) Hypokalemia
6) Calcium phosphate stone formation (kidney stones)

Describes which diuretic type?

A

Carbonic anhydrase inhibitor

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71
Q

What are the antihypertensives deemed safe for use during pregnancy?

A

Hydralazine
Labetalol
Methyldopa
Nifedipine

“He Likes My Neonate”

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72
Q

Hydralazine
Labetalol
Methyldopa
Nifedipine

Describes drugs that can be used for what condition?

A

Hypertension during pregnancy

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73
Q

Describe the following for oprelvekin (IL-11):

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
A megakaryocyte growth factor

MOA:
It activates IL-11 receptors to stimulate the growth of primitive megakaryocytic progenitors & increase the number of peripheral platelets

Clinical uses:
1) A secondary prevention of thrombocytopenia in patients undergoing cytotoxic chemotherapy for non-myeloid cancer

Adverse effects:
1) Fatigue
2) Headache
3) Dizziness
4) Anemia
5) Plural edema
6) Transient atrial arrythmias

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74
Q

Drug type:
A megakaryocyte growth factor

MOA:
It activates IL-11 receptors to stimulate the growth of primitive megakaryocytic progenitors & increase the number of peripheral platelets

Clinical uses:
1) A secondary prevention of thrombocytopenia in patients undergoing cytotoxic chemotherapy for non-myeloid cancer

Adverse effects:
1) Fatigue
2) Headache
3) Dizziness
4) Anemia
5) Plural edema
6) Transient atrial arrythmias

Describes which drug?

A

Oprelvekin (IL-11)

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75
Q

Describe the following for folic acid:

What is the MOA?

What is the clinical use?

What is an adverse effect?

A

MOA:
A precursor of an essential donor of methyl groups used to make amino acids, purines, & deoxynucleotides

Clinical uses:
1) Folic acid deficiency (megaloblastic anemia) to prevent NTD

Adverse effects:
1) Masks B12 deficiency when given in large doses

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76
Q

MOA:
A precursor of an essential donor of methyl groups used to make amino acids, purines, & deoxynucleotides

Clinical uses:
1) Folic acid deficiency (megaloblastic anemia) to prevent NTD

Adverse effects:
1) Masks B12 deficiency when given in large doses

Describes which drug?

A

Folic acid

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77
Q

Describe the following for Cyanocobalamin (vit B12):

What is the MOA?

What are the clinical uses?

A

MOA:
A cofactor that is needed for essential enzymatic reactions that form tetrahydrofolate which converts monocysteine into methione & metabolizes methyl-malonyl-CoA

Clinical uses:
1) Vit B12 deficiency (megaloblastic anemia)
2) Pernicious anemia

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78
Q

MOA:
A cofactor that is needed for essential enzymatic reactions that form tetrahydrofolate which converts monocysteine into methione & metabolizes methyl-malonyl-CoA

Clinical uses:
1) Vit B12 deficiency (megaloblastic anemia)
2) Pernicious anemia

Describes which drug?

A

Cyanocobalamin (vit B12)

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79
Q

Which drugs are considered Ca2+ channel blockers?

A

Amlodipine
Clevidipine
Nicardipine
Nifedipine
Diltiazem
Verapamil

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80
Q

Amlodipine
Clevidipine
Nicardipine
Nifedipine
Diltiazem
Verapamil

Are all considered which type of drug?

A

Ca2+ channel blockers

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81
Q

Describe the following for Amlodipine:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
Ca2+ channel blocker

MOA:
It blocks voltage dependent L-type Ca2 channels of vascular smooth muscle resulting in relaxation

Clinical use:
1) Hypertension
2) Angina
3) Raynaud syndrome

Adverse effects:
1) Ankle edema (peripheral)
2) Gingival hyperplasia
3) Flushing
4) Dizziness

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82
Q

Drug type:
Ca2+ channel blocker

MOA:
It blocks voltage dependent L-type Ca2 channels of vascular smooth muscle resulting in relaxation

Clinical use:
1) Hypertension
2) Angina
3) Raynaud syndrome

Adverse effects:
1) Ankle edema (peripheral)
2) Gingival hyperplasia
3) Flushing
4) Dizziness

Describes which drug?

A

Amlodipine

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83
Q

Which Ca2+ channel blockers are considered dihydropyridines?

A

Amlodipine
Clevidipine
Nifedipine
Nimodipine

They act on relaxing the vascular smooth muscle

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84
Q

Amlodipine
Clevidipine
Nifedipine
Nimodipine

They act on relaxing the vascular smooth muscle are considered to be which type of Ca2+ channel blockers?

A

Dihydropyridines

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85
Q

Nimodipine is used to treat which condition?

A

Subarachnoid hemorrhage

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86
Q

Nicardipine & Clevidipine are used to treat which condition?

A

Hypertension urgency or emergency

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87
Q

What are the non-dihydropyridines & what do they treat?

A

Diltiazem & Verapamil

They act on the heart

Rx:
1) Hypertension’
2) Angina
3) A fibrillation
4) A flutter

Adverse effects:
1) Cardiac depression
2) AV block
3) Hyperprolactinemia (verapamil)
4) Constipation

88
Q

Non-dihydropyridines that act on the heart

Rx:
1) Hypertension’
2) Angina
3) A fibrillation
4) A flutter

Adverse effects:
1) Cardiac depression
2) AV block
3) Hyperprolactinemia (verapamil)
4) Constipation

Describes which 2 drugs?

A

Diltiazem & Verapamil

89
Q

Describe the following for Sildenafil:

What is the drug type?

What is the MOA?

What are the clinical uses?

What are the adverse effects?
- Avoid giving which drugs?

A

Drug type:
A PDE-5 inhibitor (phosphodiesterase)

MOA:
It inhibits PDE-5 to increase available cGMP to prolong the vasodilatory effects of nitric oxide

Clinical use:
1) Erectile dysfunction’
2) Pulmonary hypertension

Adverse effects:
1) Headache
2) Flushing
3) Transient blue-green tinted vision

Avoid giving with nitroglycerines or nitrates otherwise you risk severe hypotension

90
Q

Drug type:
A PDE-5 inhibitor (phosphodiesterase)

MOA:
It inhibits PDE-5 to increase available cGMP to prolong the vasodilatory effects of nitric oxide

Clinical use:
1) Erectile dysfunction’
2) Pulmonary hypertension

Adverse effects:
1) Headache
2) Flushing
3) Transient blue-green tinted vision

Avoid giving with nitroglycerines or nitrates otherwise you risk severe hypotension

Describes which drug?

A

Sildenafil

91
Q

Describe the following for Dobutamine:

What is the drug type?

What are the effects of the drug?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
A B1 selective agonist (B1>B2>a) sympathomimetic

MOA:
It stimulates B1 receptors to activate Gs path to increase adenylate cyclase & cAMP resulting in increased CO without significantly raising the HR

Effects:
1) Increased CO

Clinical uses:
1) Cardiogenic shock
2) Heart failure
3) Cardiac stress test

Adverse effects:
1) Hypertension
2) Tachycardia
3) PVC’s
4) Arrythmias

92
Q

Drug type:
A B1 selective agonist (B1>B2>a) sympathomimetic

MOA:
It stimulates B1 receptors to activate Gs path to increase adenylate cyclase & cAMP resulting in increased CO without significantly raising the HR

Effects:
1) Increased CO

Clinical uses:
1) Cardiogenic shock
2) Heart failure
3) Cardiac stress test

Adverse effects:
1) Hypertension
2) Tachycardia
3) PVC’s
4) Arrythmias

Describes which drug?

A

Dobutamine

93
Q

Describe the following for nitrates:

What are the drugs?

What is the MOA?

What are the clinical uses?

What are the adverse effects?

A

Drugs:
Nitroglycerin
Isosorbide dinitrate
Isosorbide mononitrate

MOA:
They increase NO & cGMP in smooth muscle & veins resulting in vasodilation & reduced preload in the heart

Clinical uses:
1) Angina
2) Acute coronary syndrome
3) Pulmonary edema

Adverse effect:
1) Reflex tachycardia
2) Methemoglobinemia
3) Hypotension
4) flushing
5) Headache
6) Monday syndrome (exposure during the work week causes sensitization but re-exposure after the weekend makes headache, tachycardia, & dizziness worse)

94
Q

Drugs:
Nitroglycerin
Isosorbide dinitrate
Isosorbide mononitrate

MOA:
They increase NO & cGMP in smooth muscle & veins resulting in vasodilation & reduced preload in the heart

Clinical uses:
1) Angina
2) Acute coronary syndrome
3) Pulmonary edema

Adverse effect:
1) Reflex tachycardia
2) Methemoglobinemia
3) Hypotension
4) flushing
5) Headache
6) Monday syndrome (exposure during the work week causes sensitization but re-exposure after the weekend makes headache, tachycardia, & dizziness worse)

Describes which drug type?

A

Nitrates

95
Q

People with which conditions do you NOT want to give nitrates?

A

Right ventricular infarction
Hypertrophic cardiomyopathy
People taking PDE-5 inhibitors (Sildenafil)

96
Q

Describe the RAAS pathway & where each of these drugs inhibit the steps:

1) Mineralcorticoid antagonists (Spironolactone & Eplerenone)
2) ACE inhibitors (-Prils)
3) Direct renin inhibitor (Aliskiren)
4) Angiotension II receptor blockers (-sartans)
5) Aldosterone antagonists

A

Angiotensin

(Renin) *3) Direct renin inhibitor

angiotensin I

(ACE) *2) ACE inhibitors

Angiotensin II

*4) Angiotensin II receptor blockers

Aldosterone

*5) Aldosterone antagonists

Adrenals

*1) Mineralcorticoid antagonists

Target tissues

97
Q

Describe the following for procainamide:

What is the drug type?

What is the MOA?

What are the effects?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
Na channel blocker (antiarrhythmic)

MOA:
A moderate Na channel blocker to increase AP duration to increase the effective refractory period ventricular action potential & it’s metabolized by N-acetyltransferase.

Effects:
1) Increased AP duration
2) Increased QT interval
3) Block some K+

Clinical uses:
1) Atrial & ventricular arrythmias
2) Re-entrant/ectopic SVT & VT

Adverse effects:
1) SLE-like symptoms (SHIPPD acetylation metabolism)
2) thrombocytopenia
3) Torsade’s de points (QT interval)

98
Q

Drug type:
Na channel blocker (antiarrhythmic)

MOA:
A moderate Na channel blocker to increase AP duration to increase the effective refractory period ventricular action potential & it’s metabolized by N-acetyltransferase.

Effects:
1) Increased AP duration
2) Increased QT interval
3) Block some K+

Clinical uses:
1) Atrial & ventricular arrythmias
2) Re-entrant/ectopic SVT & VT

Adverse effects:
1) SLE-like symptoms (SHIPPD acetylation metabolism)
2) thrombocytopenia
3) Torsade’s de points (QT interval)

Describes which drug?

A

Procainamide

99
Q

Describe the following for statins:

What are the drugs?

What is the MOA?

What are the effects of the drug?

What adverse effects?

A

What are the drugs:
Atorvastatin
Simvastatin

MOA:
They inhibit conversion HMG-CoA to mevalonate (a cholesterol precursor)

Effects:
1) Very low LDL (more LDL receptor recycling & increased expression on hepatocytes to up catabolism)

2) High HDL
3) Low triglycerides (less intrahepatic fat)

Adverse effects:
1) Hepatotoxicity
2) Statin-induced myopathy (especially when given fibrates or niacin)

100
Q

What are the drugs:
Atorvastatin
Simvastatin

MOA:
They inhibit conversion HMG-CoA to mevalonate (a cholesterol precursor)

Effects:
1) Very low LDL (more LDL receptor recycling & increased expression on hepatocytes to up catabolism)

2) High HDL
3) Low triglycerides (less intrahepatic fat)

Adverse effects:
1) Hepatotoxicity
2) Statin-induced myopathy (especially when given fibrates or niacin)

Describes which type of drug?

A

Statins

101
Q

Describe the following for niacin:

What is the drug type?

What is the MOA?

What are the effects?

What are the adverse effects?

A

Drug type:
A hormone-sensitive lipase inhibitor

MOA:
It inhibits lipolysis in fat to reduce VLDL synthesis in the liver

Effects:
1) Very low LDL
2) Very high HDL
3) Low Triglycerides

Adverse effects:
1) Flushed face
2) Hyperglycemia
3) Hyperuricemia

102
Q

Drug type:
A hormone-sensitive lipase inhibitor

MOA:
It inhibits lipolysis in fat to reduce VLDL synthesis in the liver

Effects:
1) Very low LDL
2) Very high HDL
3) Low Triglycerides

Adverse effects:
1) Flushed face
2) Hyperglycemia
3) Hyperuricemia

Describes which drug?

A

Niacin

103
Q

Describe the following for fibrates:

What are the drugs included?

What is the drug type?

What is the MOA?

What are the effects?

What are the adverse effects?

A

Drugs:
Gemfibrozil
Bezafibrate
Fenofibrate

Drug type:
PPAR-a activator

MOA:
They activate PPAR-a (peroxisome proliferative factor) to upregulate LPL & increased triglyceride clearance resulting in induced HDL synthesis

Effects:
1) Low LDL
2) High HDL
3) Very low Triglycerides

Adverse effects:
1) Myopathy (especially given with statins)
2) Cholesterol gallstones

104
Q

Drugs:
Gemfibrozil
Bezafibrate
Fenofibrate

Drug type:
PPAR-a activator

MOA:
They activate PPAR-a (peroxisome proliferative factor) to upregulate LPL & increased triglyceride clearance resulting in induced HDL synthesis

Effects:
1) Low LDL
2) High HDL
3) Very low Triglycerides

Adverse effects:
1) Myopathy (especially given with statins)
2) Cholesterol gallstones

Describes which type of drug?

A

Fibrates

105
Q

Gemfibrozil
Bezafibrate
Fenofibrate

Are all examples of which type of drug that works in what way?

A

Fibrates aka PPAR-a activators that work to reduce LDL & triglycerides & raise HDL

106
Q

Fibrates aka PPAR-a activators that work to reduce LDL & triglycerides & raise HDL

A

Gemfibrozil
Bezafibrate
Fenofibrate

107
Q

Describe the following for digoxin:

What is the drug type?

What is the MOA?

What are the effects?

What are the clinical uses?

What are the adverse effects?

A

Drug type:
An indirect Na/K+ ATPase inhibitor

MOA:
It inhibits Na+/K+ ATPase meaning there is no Na+ for the Na/Ca2+ exchanger resulting in less available Ca2+ for cardiomyocytes & a stimulated vagus nerve causing reduced HR

Effects:
1) Lower HR, Conduction & Contractility

Clinical uses:
1) Heart failure
2) A fibrillation (reduces conduction at the AV/SA nodes)

Adverse effects:
1) Cholinergic effects (N/V/D)
2) Yellow tinged vision
3) Arrythmias
4) AV block
5) Hypokalemia (poor prognosis)

108
Q

Drug type:
An indirect Na/K+ ATPase inhibitor

MOA:
It inhibits Na+/K+ ATPase meaning there is no Na+ for the Na/Ca2+ exchanger resulting in less available Ca2+ for cardiomyocytes & a stimulated vagus nerve causing reduced HR

Effects:
1) Lower HR, Conduction & Contractility

Clinical uses:
1) Heart failure
2) A fibrillation (reduces conduction at the AV/SA nodes)

Adverse effects:
1) Cholinergic effects (N/V/D)
2) Yellow tinged vision
3) Arrythmias
4) AV block
5) Hypokalemia (poor prognosis)

Describes which drug?

A

Digoxin (cardiac glycoside)

109
Q

Describe the following for Digoxin toxicity::

What are the predisposing factors/risks?

What is the antidote?

A

Risks:
1) Renal failure
2) Hypokalemia
3) Drugs that displace digoxin from tissues (Verapamil, Amiodarone, Quinidine)

Rx:
Anti-digoxin Fab fragments
Slowly normalize K+
Cardiac pacer (in severe cases)
Mg2+ Supplements

110
Q

Risks:
1) Renal failure
2) Hypokalemia
3) Drugs that displace digoxin from tissues (Verapamil, Amiodarone, Quinidine)

Rx:
Anti-digoxin Fab fragments
Slowly normalize K+
Cardiac pacer (in severe cases)
Mg2+ Supplements

Describes which type of toxicity?

A

Digoxin toxicity

111
Q

Describe the following for ACE inhibitors:

What are the drugs included?

What is the MOA?

What are the effects?

What are the clinical uses?

What are the adverse effects?

A

Drugs:
Lisinopril*
Ramipril*
Captopril
Enalapril

MOA:
Inhibit ACE to reduce angiotensin II levels resulting in dilation of blood vessels like the efferent arteriole to reduce GFR & BP

Effects:
1) Increase Bradykinin
2) Increase renin
3) Increase K+
4) Increase angiotensin I
5) Reduce Aldosterone
6) Reduce Angiotensin II

Clinical uses:
1) Hypertension
2) Heart failure
3) Proteinuria
4) Diabetic neuropathy
5) Prevent cardiomyopathies via chronic HTN

Adverse effects:
1) Cough
2) Angioedema
3) Teratogenic (Hypoplastic digits, Oligohydramnios, Renal dysplasia)
4) Hyperkalemia
5) Hypotension

“CATCHH”

112
Q

Drugs:
Lisinopril*
Ramipril*
Captopril
Enalapril

MOA:
Inhibit ACE to reduce angiotensin II levels resulting in dilation of blood vessels like the efferent arteriole to reduce GFR & BP

Effects:
1) Increase Bradykinin
2) Increase renin
3) Increase K+
4) Increase angiotensin I
5) Reduce Aldosterone
6) Reduce Angiotensin II

Clinical uses:
1) Hypertension
2) Heart failure
3) Proteinuria
4) Diabetic neuropathy
5) Prevent cardiomyopathies via chronic HTN

Adverse effects:
1) Cough
2) Angioedema
3) Teratogenic (Hypoplastic digits, Oligohydramnios, Renal dysplasia)
4) Hyperkalemia
5) Hypotension

“CATCHH”

Describes which type of drug?

A

ACE inhibitors

113
Q

Describe the following for Sartans:

What are the drugs included?

What is the type of drug?

What are the effects?

What are the clinical uses?

What are the adverse effects?

A

Drugs:
Losartan**
Candesartan
Valsartan

Drug type:
Selective angiotensin receptor blockers (ARBs)

Effects:
1) NO change in bradykinin
2) Reduced Aldosterone
3) Increased K+
4) Increased Renin
5) Increased Angiotensin I & II

Clinical uses:
1) HTN
2) HF
3) Proteinuria
4) Chronic kidney disease (diabetic neuropathy with intolerance to ACE inhibitors)

Adverse effects:
1) Hyperkalemia
2) Reduced GFR
3) Hypotension
4) Teratogenic effects

114
Q

Drugs:
Losartan**
Candesartan
Valsartan

Drug type:
Selective angiotensin receptor blockers (ARBs)

Effects:
1) NO change in bradykinin
2) Reduced Aldosterone
3) Increased K+
4) Increased Renin
5) Increased Angiotensin I & II

Clinical uses:
1) HTN
2) HF
3) Proteinuria
4) Chronic kidney disease (diabetic neuropathy with intolerance to ACE inhibitors)

Adverse effects:
1) Hyperkalemia
2) Reduced GFR
3) Hypotension
4) Teratogenic effects

Describes which type of drugs?

A

Sartans

115
Q

Which two drugs inhibit norepinephrine reuptake?

A

Cocaine & Imipramine

116
Q

Which drug is used to treat BPH & HTN?

A

Tamsuloin

117
Q

An irreversible alpha blocker used to treat pheochromocytoma followed by a B-blocker to avoid a hypertensive crisis & arrythmia

A

Phenoxybenzamine

118
Q

Nicotinic receptors target which tissues?

A

CNS & skeletal muscles (ligand-gated ion channels)

119
Q

M1 & M3 receptors target which secondary messenger pathway?

A

Gq to increase phospholipase C & IP3, DAG, & Ca2+

120
Q

M2 & M4 receptors target which secondary messenger pathway?

A

Gi to decrease adenylate cyclase & cAMP levels

121
Q

M1 targets which tissues?

A

CNS
Ganglia
Gastric parietal cells

122
Q

CNS
Ganglia
Gastric parietal cells

Are all acted upon by which receptor?

A

M1

123
Q

M2 targets which tissues?

A

Heart

124
Q

Heart

is acted upon by which receptor?

A

M2

125
Q

M3 targets which tissues?

A

Smooth muscle
Eye
GIT
Bronchus
Bladder

126
Q

Smooth muscle
Eye
GIT
Bronchus
Bladder

Are all acted upon by which receptor?

A

M3

127
Q

Describe the following for Albuterol & Salbutamol:

What are the drug types?

What are they clinically used for?

A

Drug type:
B2 agonist (bronchodilation via M3 receptors)

Clinical use:
1) Acute bronchial asthma
2) Hyperkalemia (B2 causes K+ uptake into SM)

128
Q

Drug type:
B2 agonist (bronchodilation via M3 receptors)

Clinical use:
1) Acute bronchial asthma
2) Hyperkalemia (B2 causes K+ uptake into SM)

Describes which 2 drugs?

A

Albuterol & Salbutamol:

129
Q

Pilocarpine is a direct Muscarinic agonist that can treat which conditions?

A

Closed-angle glaucoma
Xerostomia (sjogrens)
Miosis (side effect)

130
Q

Which 2 drugs are the go to when treating open-angle glaucoma’s?

A

1) Latanoprost (PGF2a receptor to increase uveoscleral outflow)

2) Timolol (non-selective B-blocer that reduced aqueous humor production by blocking B2 receptors)

131
Q

Which drugs are considered cardio selective B-blockers?

  • What are their effects?
  • What conditions should you avoid giving them in?
A

Atenolol & Metoprolol the lol’s

Effects:
1) Bradycardia
2) Fatigue
3) Masked hypoglycemia

Avoid in:
1) Diabetes
2) Asthma/COPD
3) CHF
4) Heart block

132
Q

What is the first line choice rx for Alzheimer’s & what is the alternative?

A

1 Rivastigmine (because it has fewer drug interactions)

Alternative:
Donepezil an indirect muscarinic agonist

133
Q

Describe the following for Atropine:

What is the drug type?

What are the effects?

What is the clinical use?

A

Drug type:
A direct muscarinic antagonist

Effects: anticholinergic
1) CNS stimulation
2) Raised temperature
3) Mydriasis
4) Dry mouth/flushed dry skin

Rx:
Organophosphate poisoning (insecticides)

134
Q

Drug type:
A direct muscarinic antagonist

Effects: anticholinergic
1) CNS stimulation
2) Raised temperature
3) Mydriasis
4) Dry mouth/flushed dry skin

Rx:
Organophosphate poisoning (insecticides)

Describes which drug?

A

Atropine

135
Q

Describe the following for Physostigmine:

What is the drug type?

What is the clinical use?

A

Drug type:
An indirect muscarinic agonist (AChE inhibitor)

Rx:
Atropine poisoning

136
Q

Drug type:
An indirect muscarinic agonist (AChE inhibitor)

Rx:
Atropine poisoning

Describes which drug?

A

Physostigmine

137
Q

Which drugs would you give a farmer showing signs of organophosphate poisoning?

A

Atropine & Pralidoxime

138
Q

Describe the following for clonidine:

What is the drug type?

What are the effects?

What are the adverse effects?

A

Drug type:
a2 agonist at prejunctional synapses

Effects:
1) Decreased sympathetic outflow & relaxation of SM/BVs

Adverse effects:
1) Rebound HTN when medication is discontinued

139
Q

Drug type:
a2 agonist at prejunctional synapses

Effects:
1) Decreased sympathetic outflow & relaxation of SM/BVs

Adverse effects:
1) Rebound HTN when medication is discontinued

Describes which drug?

A

Clonidine

140
Q

Describe the following Bethanechol:

What is the drug type?

What is the clinical use?

A

Drug type:
A direct muscarinic agonist (M3) that frees the pee!

Rx urine retention (contracts bladder wall detrusor)

141
Q

Drug type:
A direct muscarinic agonist (M3) that frees the pee!

Rx urine retention (contracts bladder wall detrusor)

Describes which drug?

A

Bethanechol

142
Q

Describe the following for Oxybutynin:

What is the drug type?

What are the effects?

What is the clinical use?

A

Drug type:
Muscarinic antagonist (M3)

Effects (relaxes detrusor/bladder wall)

Rx Overactive bladder/incontinence

143
Q

Drug type:
Muscarinic antagonist (M3)

Effects (relaxes detrusor/bladder wall)

Rx Overactive bladder/incontinence

Describes which drug?

A

Oxybutynin

144
Q

M1, M4, M5

A

Influences neurologic function (e.g., cognitive impairment)

145
Q

M2

A

↑ Heart rate
Increases AV-node conduction (may lead to tachyarrhythmia)

146
Q

M3

A
  1. Gastrointestinal tract
    ↓ Intestinal peristalsis
    ↓ Salivary and gastric secretions
  2. Urinary tract:
    ↓ Bladder contraction (↓ detrusor muscle tone, ↑ internal urethral sphincter tone)
  3. Airway
    Bronchodilation
    ↓ Bronchial secretions
  4. Eye
    Mydriasis → narrowing of the iridocorneal angle & Impaired accommodation
  5. Blood vessels minimal effect
  6. Exocrine ↓ Secretions (sweat)
147
Q

Ipratropium bromide
Tiotropium bromide

A

List of antimuscarinic agents that are Quarternary amines
Hydrophilic (poor oral bioavailability and CNS penetration)

148
Q

Atropine
Scopolamine
Homatropine
Tropicamide
Benzotropine
Biperiden
Trihexyphenidyl
Oxybutynin
Tolterodine
Solifenacin
Dicyclomine
Hyoscyamine
Darifenacin

All represent

A

antimuscarinic agents

List the Tertiary amines that are
Lipophilic (good oral bioavailability and CNS penetration)

149
Q

Nebivolol (most)
Bextaxolol
Bisoprolol
Acebutolol
Esmolol
Atenolol
Metoprolol
Celiprolol

Are examples of which type of drug that have what effect?

A

Cardio-selective beta blockers (B1 selective) -lol

Reduces heart rate, contractility, and myocardial oxygen
consumption

150
Q

What are the adverse effects of cardio selective B-blockers?

A

Adverse effects
1) Bradycardia*
2) Masks hypoglycemia*
3) fatigue
4) cold extremities
5) sleep disturbances
6) depression

151
Q

Adverse effects
1) Bradycardia*
2) Masks hypoglycemia*
3) fatigue
4) cold extremities
5) sleep disturbances
6) depression

Are all adverse effects of which type of drug?

A

Cardioselective B-blockers

152
Q

Which conditions should you avoid giving cardioselective B-blockers to?

A

Contraindications
1) Asthma/COPD
2) diabetes
3) heart block/CHF

153
Q

List the types of drugs that cause Miosis (constriction)

A

1) Sympatholytic (a2 agonists)
2) Heroin/opioids
3) Parasympathomimetic (pilocarpine)

154
Q

List the types of drugs that cause Mydriasis (dilation)

A

1) Anticholinergics
(atropine, TCAs, tropicamide, antihistamines)

2) Drug abuse (amphetamines, cocaine, LSD)

3) Sympathomimetics (Cyclopentolate, homatropine, scopolamine and tropicamide)

155
Q

What is the MOA of Donepezil

A

Ach esterase inhibitor
- Increase acetylcholine levels in synaptic cleft

156
Q

Wha) are the signs of an atropine OD (CNS stimulant)

A

o Hot as a hare: increased temperature

o Blind as a bat: mydriasis (dilated pupils)

o Dry as a bone: dry mouth, dry eyes, decreased sweat

o Red as a beet: flushed face

o Mad as a hatter: delirium

157
Q

What is the drug used to treat an atropine OD & why?

A

Physostigmine (because it crosses the BBB to increase Ach availability to bind muscarinic receptors

158
Q

What is the presentation of organophosphate poisoning?

What is the treatment?

A

Insecticides Poisoning (farmers)

Muscarinic effect like dumbbells –
diarrhea, urination, miosis, bradycardia,
bronchoconstriction, lactation, sweating

Treatment –
atropine (lifesaving; crosses BBB)
or
pralidoxime

159
Q

What is the MOA of clonidine & what is its effect?

What is an adverse effect?

A

a2 agonist (presynaptic) that reduces of sympathetic outflow from CNS

Antihypertensive effect: can cause rebound hypertension when discontinued

160
Q

What drug is used to treat urinary retention & why?

A

Muscarinic agonist like bethanechol that Activates M3 receptor to contract the detrusor smooth muscle & increase bladder emptying

161
Q

What drug is used to treat urgency incontinence & why?

A

Muscarinic antagonists LIKE Oxybutynin by Inhibits M3 receptor to relax the detrusor smooth muscle & decrease
overactivity

162
Q

Sympathomimetics that inhibit synthesis of norepinephrine block which step (& what process is prevented?)

A

Step A where the hydroxylation of tyrosine is prevented (RLS)

163
Q

Sympathomimetics that inhibit Uptake of dopamine into storage vesicles block which step (& what process is prevented?)

A

Step B, drugs like reserpine inhibits transport of dopamine into the vesicles & prevent it from being converted into norepinephrine & being protected from degradation

164
Q

Sympathomimetics that inhibit Release of neurotransmitter block which step (& what process is prevented?)

A

Step C, drugs like guanethidine & bretylium block the influx of Ca2+ & exocytosis of norepinephrine

165
Q

Sympathomimetics that inhibit Binding to receptor block which step (& what process is prevented?)

A

Step D, it blocks the Postsynaptic receptor from being activated by binding of
neurotransmitter

166
Q

Sympathomimetics that inhibit Removal of norepinephrine block which step (& what process is prevented?)

A

Step E, drugs like cocaine & imipramine inhibit norepinephrine reuptake

167
Q

Norepinephrine is metabolized by which factors?

A

Norepinephrine is methylated by COMT and oxidized by MAO

168
Q

Tamsulosin is used to treat which condition

A

BPH

169
Q

Phenoxybenzamine is used to treat which condition & prep for what?

A

used to treat pheochromocytoma
(Beta blockers need to be used secondary to alpha blockers, A then B; Phenoxybenzamine + atenolol to avoid hypertensive crisis)

Used to treat patient preparation for surgery

170
Q

Nicotinic vs muscarinic receptors

A

Nicotinic receptors:
– limited to CNS and skeletal muscle (Ligand-gated ion channels)

Muscarinic receptors:
widely distributed (G protein – coupled receptors)

171
Q

M1 & M3 receptor

A

Gq coupled – increase
phospholipase C &increase IP3, DAG, and Ca2+

M1 receptors: CNS, ganglia, and gastric parietal cells

M3 receptors: smooth muscle and secretory cells (eye, GIT, bronchus, bladder)
1) Increases contractions and secretory activity of GIT & parasympathetic response

2) In respiratory system & increase tracheobronchial secretion and
bronchoconstriction

172
Q

M2 and M4

A

Gi coupled – decrease
adenylyl cyclase & decrease cAMP

M2 receptors: myocardium
1) Decrease rate of conduction in SA & AV nodes

173
Q

What is the MOA of Zilueton?
What step does it inhibit?

A

Step C, 5-lipoxygenase pathway inhibitor (HPX)

that blocks the conversion of arachidonic acid into hydroperoxides

174
Q

What is the MOA of Montelukast? What step does it inhibit?

A

Step G, a leukotriene receptor antagonist that blocks leukotriene receptors to reduce bronchoconstriction in asthma (HPX)

175
Q

Treatment of acute bronchial asthma & hyperkalemia

A

Albuterol and Salbutamol (B2 agonist)

  • Question will be presented with potassium levels greater than 5
176
Q

What are the Bronchodilators uses in asthma

A

1) Sympathomimetics
Salbutamol, albuterol, terbutaline, orciprenaline, bambuterol

2)Anti-cholinergic (atropine derivatives)
Ipratropium bromide, oxitropium, tiotropium

177
Q

Carbonic anhydrase inhibitor -ide effects which part of the nephron

A

In the PCT
o Acetazolamide

178
Q

Osmotic diuretic includes which drug?

A

Mannitol

179
Q

Loop diuretics effects which part of the nephron

A

thick ascending LoH (loop loses calcium)

Furosemide is given in cases of hypercalcemia; reduces calcium

Increased sodium, potassium, and calcium excretion

180
Q

Thiazide diuretics effects which part of the nephron

A

In the DCT

1) Hydrochlorothiazide which given in case of renal stones

181
Q

Potassium sparing diuretics effects which part of the nephron

A

In the collecting duct

Amiloride, spironolactone

182
Q

Digoxin acts on the which transporter to reduce heart contractility?

A

sodium/potassium

183
Q

What is the MOA of Lisinopril & what are the effects on lab values

A

ACE inhibitor
- Increases bradykinin, renin, and AT1
- Low aldosterone and high potassium

184
Q

What is the MOA of Losartan & what are the effects on lab values

A

angiotensin receptor blockers

  • No effect on bradykinin
  • Increases renin, AT1, AT2
  • Low aldosterone and high potassium
185
Q

What is the MOA of Statin & what are the effects on lab values, & adverse effect?

A

inhibiting HMG-CoA reductase therefore decreasing cholesterol

  • Increasing LDL receptor expression on hepatocytes; high LDL clearance
  • Statin-induced myopathy
  • Highly hepatotoxic drug
186
Q

What is a side effect of niacin?

A

Flushed face

187
Q

What is the MOA of fibrates?

A

stimulates PPR-a – stimulates lipoprotein lipase (significantly decreases TG)

188
Q

What is a side effect of procainamide?

A

drug-induced lupus (SLE) – SHIPD

189
Q

What is the MOA of Sildenafil

A

Classification: PDE-5 inhibitor
Mechanism of Action: inhibits PDE-5 leading to increased cGMP resulting in prolonged vasodilatory effect of NO –– pulmonary artery relaxation

190
Q

What is Dobutamine used to treat & why?

A

It treats cardiogenic shock because it’s a beta1 specific agonist to Increases heart contraction

191
Q

What are nitrates used to treat & why?

A

angina because they cause venous dilation which decreases preload and high doses can reduce the afterload

192
Q

What is a side effect of Amlodipine?

A

Ankle edema

193
Q

What is the MOA of Labetalol & what can it be used to treat in pregnancy?

A

Antihypertensive drug safe in pregnancy (methyl dopa and hydralazine) HLMN

  • Both alpha and beta blocker activity
194
Q

What is the MOA of Oprelvekin & what is it to used to prevent?

A

IL-11 (secondary prevention of thrombocytopenia)

195
Q

signs of pallor and neurological symptoms (tingling or loss of sensation) indicates which deficiency?

A

Cyanocobalamin/Vit B12 deficiency

196
Q

What is the MOA of erythropoietin & what are the adverse effects?

A

MOA: agonist of erythropoietin receptors expressed by red cell progenitors

AE: hypertension, thrombotic complication

197
Q

What is the MOA of heparin?

A

binds to antithrombin III to inhibit factor Xa and IIa (thrombin)

causing excessive bleeding, allergy (anaphylaxis), & thrombocytopenia if toxic (protamide sulphate)

198
Q

What is the MOA of Enoxaparin? What is it contraindicated in?

A

activate antithrombin III; inhibiting factor Xa and IIa (thrombin)

Contraindicated in renal failure

199
Q

What drug type is clopidogrel?

A

An ADP receptor antagonist

200
Q

Rx:

  1. OP poisoning
  2. Atropine poisoning
  3. Iron poisoning
A
  1. OP poisoning =
    atropine or pralidoxime
  2. Atropine poisoning = physostigmine
  3. Iron poisoning = deferoxamine or deferasirox
201
Q

Rx:

  1. Aspirin poisoning
  2. Acetaminophen poisoning
  3. Digoxin toxicity
A
  1. Aspirin poisoning =
    sodium bicarbonate; alkalizing urine
  2. Acetaminophen poisoning = acetylcysteine
  3. Digoxin toxicity =
    Digiband antibodies; present with visual changes
202
Q

Rx:

  1. Heparin toxicity
  2. Warfarin
A
  1. Heparin toxicity = protamine sulfate
  2. Warfarin=
    Fresh plasma protein or vitamin K
203
Q

What drug for acute migraine attacks

A

Sumatriptan

204
Q

acute attack of gout

A

Colchicine

205
Q

What is the MOA of Colchicine & what is it used to treat?

A

MOA: binds and stabilizes tubulin to inhibit microtubule polymerization

acute attack of gout

206
Q

closure of PDA

A

Indomethacin

207
Q

What is the MOA of Misoprostol & what is it used to prevent?

A

PGE1 agonist
- Prevention of NSAID-induced peptic ulcers

208
Q

What is the MOA of Alprostadil & what is it used to prevent?

A

PGE1 agonist
- Relaxes smooth muscle in ductus arteriosus (maintenance of PDA)

209
Q

Which uricosuric agents are used to treat chronic gout?

A

probenecid & sulphinpyrazone (chronic gout)

210
Q

probenecid & sulphinpyrazone (chronic gout) are both uricosuric agents that are used to treat which condition?

A

Chronic gout

211
Q

What is the drug used to treat Allergic rhinitis

A

second generation antihistamine drug -adine: Loratadine

212
Q

ALBUTEROL = SABA.

A

A short-acting β2agonist

that causes relaxation of bronchial smooth muscle. Used as a bronchodilator.

β2 agonist activates Na+/K+ ATPase channel = help treat hyperkalemia.

213
Q

SALMETEROL = LABA.

A

A long-acting β2 adrenergic agonist used to treat COPD and moderate/severe chronic asthma.

214
Q

Methylxanthines, what is their MOA & effects?

A

Methylxanthines like theophylline

it causes bronchodilation by inhibiting phosphodiesterase but it has a narrow rx window (neuro/cardio toxicity)

215
Q
  • Hydrochlorothiazide acts on which part & has what effect on Na/K+/Ca2+ excretion?
A

4 DCT

Decreased Ca2+ excretion

216
Q

*Furosemide acts on which part & has what effect on Ca2+ excretion?

A

3 Thick ascending limb of loop of henle

Na/K+/Ca2+ excretion increased

Pharm SJSM (23 decks)

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