Z2. Pharmacology p300
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- Ganciclovir (DHPG dihydroxy-2-propoxymethyl guanine)
- p300
- Mechanism of action of Ganciclovir.
- Phosphorlation by viral kinase; perferentially inhibits CMV DNA polymerase.
- Clinical use of Ganciclovir.
- CMV, especially in immunocompromised patients.
- Symptoms of Ganciclovir toxicity.
- Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.
- Foscarnet
- p300
- Mechanism of action of Foscarnet.
- Viral DNA polymerase inhibitor that binds to the pyrophophate binding site of the enzyme. Does not require activation by viral kinase. "FOScarnet = pyroFOSphate analog."
- Clinical use of Foscarnet.
- CMV retinitis in immunocompromised patients when ganciclovir fails.
- Symptoms of Foscarnet toxicity.
- Nephrotoxicity.
- HIV therapy
- p300
- Saquinavir, ritonavir, indinavir, nelfinavir, amprenavir are example of this type of anti-HIV drug.
- Protease inhibitor.
- Mechanism of action of protease inhibitors.
- Inhibit assembly of new virus by blocking protease enzyme.
- Symptoms of protease inhibitor toxicity.
- GI intolerance (nausea, diarrhea), hyperglycemia, lipid abnormalities, thrombocytopenia (indinavir).
- Reverse transcriptase inhibitors:
- Zidovudine (AZT), didanosine (ddI), zalcitabine (ddC), stavudine (d4T), lamivudine (3TC), and abacavir are examples of --------- reverse transcriptase inhibitors.
- Nucleoside.
- Nevirapine, delavirdine, and efavirenz are examples of --------- reverse transcriptase inhibitors.
- Non-nucleoside.
- Mechanism of action of reverse transcriptase inhibitors.
- Preferentially inhibit reverse transcriptase of HIV; prevent incorporation of viral genome into host DNA.
- Symptoms of reverse transcriptase inhibitor toxicity.
- Bone marrow supression (neutropenia, anemia), periphral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (AZT).
- Highly active antiretroviral therapy (HAART) generally entails combination therapy with ---------- and -----------.
- Protease inhibitors, reverse transcriptase inhibitors.
- When should HIV therapy be initiated?
- When patients have low CD4 counts (<500 cells/mm3) or high viral load.
- -------- is used during pregnancy to reduce risk of fetal transmission.
- AZT.
- Interferons
- p300
- Mechanism of action of Interferons.
- Glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis.
- Clinical use of Interferons.
- Chronic hepatitis B and C, Kaposi's sarcoma.
- Symptoms of Interferon toxicity.
- Neutropenia.
- Antiparasitic drugs
- p301
- Clinical uses of Ivermectin.
- Onchocerciasis "rIVER blindness treated with IVERmectin".
- Clinical uses of Mebendazole / thiabendazole.
- Nematode/roundworm (e.g., pinworm, whipworm) infections.
- Clinical uses of Pyrantel pamoate.
- Giant roundworm (Ascaris), hookworm (Necator/Ancylostoma), pinworm (Enterobius).
- Clinical uses of Praziquantel.
- Trematode/fluke (e.g., schistosomes, Paragonimus, Clonorchis) and cysticercosis.
- Clinical uss of Niclosamide
- Cestode/tapeworm (e.g., Diphyllobothrium latum, Taenia species) infections except cysticercosis.
- Clinical uses of Pentavalent antimony.
- Leishmaniasis.
- Clinical uses of Chloroquine, quinine, mefloquine, atovaquone, proguanil.
- Malaria.
- Clinical uses of Primaquine.
- Latent hypnozoite (liver) forms of malaria (Plasmodium vivax, P.ovale).
- Clinical uses of Metronidazole.
- Giardiasis, amebic dysentery (Entamoeba histolytica), bacterial vaginitis (Gardnerella vaginalis), Trichomonas.
- Clinical uses of Pentamidine.
- Pneumocystis carinii pneumonia prophylaxis.
- Clinical uses of Nifurtimox.
- Chagas' disease, American trypanosomiasis (Trypanosoma cruzi).
- Clinical uses of Suramin.
- African trypanosomiasis (sleeping sickness).
- Pharmacology - CNS / Neurologic drugs
- p301
- Parasympathetic preganglionic neurons release the neurotransmitter -------- which act on -------- receptors.
- Ach, nicotinic.
- Parasympathetic postganglionic neurons release the neurotransmitter -------- which act on ------- receptors.
- Ach, muscarinic.
- Sympathetic preganglionic neurons to sweat glands release the neurotransmitter ------- which act on ------- receptors.
- Ach, nicotinic.
- Sympathetic postganglionic neurons to sweat glands release the neurotransmitter ------- which act on ------- receptors.
- Ach, muscarinic.
- Sympathetic preganglionic neurons to glands, cardiac and smooth muscles release the neurotransmitter ------- which act on ------- receptors.
- Ach, nicotinic.
- Sympathetic postganglionic neurons to glands, cardiac and smooth muscles release the neurotransmitter ------- which act on ------- receptors.
- NE, alpha and beta
- Sympathetic preganglionic neurons to renal vascular smooth muscle release the neurotransmitter ------- which act on ------- receptors.
- Ach, nicotinic.
- Sympathetic postganglionic neurons to renal vascular smooth muscle release the neurotransmitter ------- which act on ------- receptors.
- Dopamine, D1
- Sympathetic preganglionic neurons to the adrenal medulla release the neurotransmitter ------- which act on ------- receptors.
- Ach, nicotinic.
- Sympathetic preganglionic neurons to the adrenal medulla synapse directly on ------- cells of the adrenal medulla.
- Chromaffin.
- Somatic neurons synapse directly on -------- muscle and release the neurotransmitter ------- which act on ------- receptors.
- skeletal muscle, Ach, nicotinic.
- Autonomic drugs
- p302
- Cholinergic:
- Ach is synthesized from acetyl-CoA and choline by the enzyme ---------.
- Choline acetyltransferase.
- The transport of choline into the nerve terminal can be inhibited by --------.
- Hemicholinium.
- The release of transmitter from vesicles in the nerve ending require the entry of ------ into the neuron.
- Calcium.
- #NAME?
- Botulinum toxin.
- The action of Ach in the synapse is terminated by its metabolism to acetate and choline by the enzyme ---------.
- Acetylcholinesterase.
- Noradrenergic:
- In the noradrenergic nerve terminal, tyrosine is hydroxylated to -------, which is decarboxylated to --------, which is finally hydroxylated to NE.
- DOPA, dopamine.
- Dopamine is transported into vesicles for hydroxylation to NE. This transport can be blocked by the drug --------.
- Reserpine.
- The action of NE and DA is terminated by --------- and ----------.
- Reuptake, diffusion (different than for Ach).
- --------- inhibits the release of the stored NE.
- Guanethidine.
- The --------- drugs promote catecholamine release.
- Amphetamine.
- The drugs --------- and ---------- inhibit the reuptake of NE.
- Cocaine, TCA.
- The release of NE from a sympathetic nerve ending is modulated by ---------, --------- and ---------.
- NE, Ach, angiotensin II.
- NE inhibits its own release at the noradrenergic nerve terminal through --------- receptors.
- Alpha 2.
- Angiotensin II --------- (inhibits / stimulates) the release of NE from the noradrenergic nerve terminal.
- Stimulates.
- Ach inhibits the release of NE from the noradrenergic nerve terminal by binding to --------- receptors.
- M1.
- Cholinomimetics
- p303
- Direct agonists:
- Clinical application and action of Bethanechol.
- Postoperative and neurogenic ileus and urinary retention. / Activates bowel and bladder smooth muscle.
- Clinical application and action of Carbachol and Pilocarpine.
- Glaucoma. / Activates ciliary muscle of eye (open angle), pupillary sphincter (narrow angle).
- Indirect agonists (anticholinesterases):
- Clinical application / action of Neostigmine.
- Postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (postoperative). / Increase endogenous Ach.
- Clinical application / action of Pyridostigmine.
- Myasthenia gravis. / Increase Ach; increase strength.
- Clinical application / action of Edrophonium.
- Diagnosis of myasthenia gravis (extremely short acting). / Increase endogenous Ach.
- Clinical application / action of Physostigmine.
- Glaucoma (crosses blood-brain barrier) and atropine overdose. / Increase endogenous Ach.
- Clinical application / action of Echothiophate.
- Glaucoma. / Increase endogenous Ach.
- Symptoms of cholinesterase inhibitor poisoning.
- Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, Salivation (also abdominal cramping). "DUMBBELSS".
- Cholinesterase inhibitor poisoning may be caused by ---------.
- Parathion and other organophosphates.
- The cholinesterase regenerator ------- can be used as an antidote for cholinesterase inhibitor poisoning.
- Pralidoxime.
- Mechanism of action of Pralidoxime.
- Regenerates active cholinesterase, chemical antagonist, used to treat organophosphate exposure.
- Cholinoreceptor blockers:
- p303
- Clinical uses of the muscarinic antagonist Atropine.
- Dilate pupils, decrease acid secretion in peptic ulcer disease, decrease urgency in mild cystitis, decrease GI motility, reduce airway secretions, and treat organophosphate poisoning. "Blocks SLUD: Salivation, Lacrimation, Urination, Defecation."
- Side effects of Atropine.
- Increase body temp, rapid pulse, dry mouth, dry/flushed skin, disorientation, mydriasis with cycloplegia, and constipation. "Atropine parasympathetic block side effects: Blind as bat, Red as a beet, Mad as a hatter, Hot as a hare, Dry as a bone."
- Hexamethonium (ganglionic blocker) blocks -------- receptors.
- Nicotinic.
- AUTHOR
- Tzivia Moreen
- antimuscarinic drugs
- p. 304
- tropi are anti-muscarinic
- while vacationing in the tropics you lie on a beach and your muscles waste away!
- benztropine is used to treat
- Parkinson's disease
- scopolamine is used to treat
- motion sickness
- scopolamine is an antimuscarinic that does not convert to the mnemonic!
- name 2 antimuscarinic drugs that act on the CNS
- benztropine, scopolamine
- name a muscarinic used to treat motion sickness
- scopolamine
- name a muscarinic used to treat Parkinson's disease
- benztropine
- mechanism of action of benztropine
- antimuscarinic
- mechanism of action of scopolamine
- antimuscarinic
- name three antimuscarinics that act on eye
- atropine, homatropine, tropicamide
- the action of atropine is ______
- produce mydriasis, cycloplegia
- mechanism of atropine is
- antimuscarinic
- the action of homatropine is ______
- produce mydriasis, cycloplegia
- mechanism of homatropine is
- antimuscarinic
- the action of tropicamide is
- produce mydriasis, cycloplegia
- mechanism of tropicamide is
- antimuscarinic
- ipatropium is used to treat
- asthma, COPD
- mechanism of ipatropium is
- antimuscarinic
- name an antimuscarinic used to treat asthma and COPD
- ipatropium
- neuromuscular blocking drugs
- p. 304
- neuromuscular blocking drugs are used for
- muscle paralysis in surgery or mechanical ventilation
- name a depolarising neurmuscular blocking drug
- succinylcholine
- name 6 nondepolarizing neuromuscular blocking drugs
- tubocurarine
- *mnemonic -- the "cur" drugs are nondepolarizing neuromuscular blocking agents
- atracurium
- is succinylcholine depolarizing or nondepolarizing?
- depolarizing
- is tubocurarine depolarizing or nondepolarizing?
- nondepolarizing
- is atracurium depolarizing or nondepolarizing?
- nondepolarizing
- is mivacurium depolarizing or nondepolarizing?
- nondepolarizing
- is pancuronium depolarizing or nondepolarizing?
- nondepolarizing
- is vacuronium depolarizing or nondepolarizing?
- nondepolarizing
- is rapacuronium depolarizing or nondepolarizing?
- nondepolarizing
- what is tubocurarine used for
- nondepolarizing neuromuscular blockade
- what agents are used to reverse neuromuscular blockade by succinylcholine?
- cholinesterase inhibitors in phase II (ex -- neostigmine)
- what phase of succinylcholine neuomuscular bloackade is reversible?
- phase II (repolarized but blocked)
- what agents are used to reverse pahse I neuromuscular blockade by succinylcholine?
- phase I Succinylcholine neuromuscular blockade cannot be reversed
- what phase of succinylcholine neuomuscular bloackade is irreversible?
- phase I Succinylcholine neuromuscular blockade cannot be reversed
- what is atracurium used for
- nondepolarizing neuromuscular blockade
- what is the effect of cholinesterase inhibitors on succinylcholine neuromuscular blockade?
- phase I: cholinesterase inhibitors potentiates the blockade phase II: cholinesterase inhibitors reverse the blockade
- what cholinesterase inhibitor is used to reverse phase II of succinylcholine neuromuscular blockade?
- neostigmine
- what is mivacurium used for
- nondepolarizing neuromuscular blockade
- Dantrolene
- p. 304
- what is dantrolene used for
- neuroleptic malignant syndrome
- what causes malignant hyperthermia
- use inhalation anesthetics and succinylcholine together
- what inhalation anesthetic DOES NOT cause malignanat hyperthermia?
- N2O
- what is neuroleptic malignant syndrome
- a toxicity of antipsychotic drugs
- what drug is used to treat malignant hyperthermia
- dantrolene
- what is the mechanism of dantrolene
- prevents release of Ca++ from saarcoplasmic reticulum of skeletal muscle
- Sympathomimetics
- p. 305
- epinephrine, NE, isoproterenol, dopamine, and dobutamine are all________________
- catecholamines
- catecholamines are_____________________
- sympathomimetics
- name 5 catecholamines
- EPI, NE, Isoproterenol, dopamine, dobutamine
- what receptors does epinephrine act on?
- alpha-1, alpha-2, beta-1, beta-2 adrenergics
- what receptors does NE work on?
- alpha-1, alpha-2, beta-1 adrenergics
- what receptors does isoproterenol work on?
- beta-1 = beta-2 adrenergics
- what receptors does dopamine work on?
- D1 = D2, D1 and D2 more than beta, beta more than alpha
- what receptors does dobutamine work on?
- beta-1 > beta-2
- which catecholamines are agonists to alpha-adrenergic receptors
- EPI, NE > dopamine
- which catecholamines are agonists to beta-1 adrenergic receptors
- EPI, NE, Isoproterenol, dopamine, dobutamine
- which catecholamines are agonists to beta-2 adrenergic receptors
- EPI, isoproterenol, dopamine and dobutamine (less)
- what is epinephrine used to treat?
- anaphylaxis, open-angle glaucoma, asthma, hypotension
- what is norepinephrine used to treat?
- hypotension (but decreases renal perfusion)
- what is isoproterenol used to treat?
- AV block
- what is dopamine used to treat
- shock with renal failure, heart failure
- what is dobutamine used to treat
- shock, heart failure
- what catecholamine is used to treat anaphylaxis
- epinephrine ("EPI-pen")
- what catecholamines are used to treat hypotension
- EPI, NE
- what catecholamine is used to treat asthma
- epinephrine
- what catecholamine is used to treat AV block
- isoproterenol
- what catecholamines are used to treat shock
- doapmine, dobutamine
- what is the action of amphetamine
- indirect general adrenergic agonist, releases stored catecholamines
- what is the action of ephedrine
- indirect general adrenergic agonist, releases stored catecholamines
- what is amphetamine used to treat
- narcolepsy, obesity, attention deficit disorder
- what is ephedrine used to treat
- nasal decongestion, urinary incontinence, hypotension
- name three sympathomimetic drugs used to treat hypotension
- epinephrine, norepinephrin, ephedrine
- what is the action of phenylephrine
- adrenergic agonist, alpha-1 > alpha-2
- what is the action of albuterol
- adrenergic agonist, beta-2 >beta-1
- what is the action of terbutaline
- adrenergic agonist, beta-2 >beta-2
- what is phenylephrine used for?
- pupil dilator, vasoconstriction, nasal decongestion
- what sympathomimetics are used to treat nasal congestion
- ephedrine, phenylephrine
- what is the mechanism of cocaine
- indirect general adrenergic agonist, catecholamine uptake inhibitor
- what is the action of cocaine
- vasoconstriction, local anesthesia
- what is the mechanism of clonidine
- centrally acting alpha-adrenergic agonist, decreases central adrenergic outflow
- what drug has the same mechanism as amphetamine
- ephedrine
- what is the mechanism of alpha-methyldopa
- centrally acting alpha-adrenergic agonist, decreases central adrenergic outflow
- what drug has the same mechanism as clonidine
- alpha-methyldopa
- what are clonidine and alpha-methyldopa used to treat
- hypertension, especially in renal disease because they do not decreased blood flow to the kidney
- what sympathomimetic is used to treat urinary incontinence
- ephedrine
- what sympathomimetic is used to treat attention deficit disorder
- amphetamine
- what sympathomimetic is used to treat narcolepsy
- amphetamine
- alpha-blockers
- p. 306
- name a nonselective irreversible alpha blocker
- phenoxybenzamine
- name a nonselective reversible alpha blocker
- phentolamine
- what is the mechanism of phenoxybenzamine
- nonselective irreversible alpha blocker
- what is the mechanism of phentolamine
- nonselective reversible alpha blocker
- what are phenoxybenzamine and phentolamine used for
- pheochromocytoma
- what are the side effects of nonselective alpha blockers
- orthostatic hypotension, reflex tachycardia
- name 3 alpha-1 selective adrenergic blockers
- prazosin, terazosin, doxazosin
- what is the mechanism of prazosin
- alpha-1 selective adrenergic blocker
- what is the mechanism of terazosin
- alpha-1 selective adrenergic blocker
- what is the mechanism of doxazosin
- alpha-1 selective adrenergic blocker
- what are alpha-1 selective adrenergic alpha blockers used for
- hypertension, urinary retention in BPH
- what are the side effects of alpha-1 blockers
- orthostatic hypotension, dizziness, headache
- what is prazosin used for?
- hypertension, urinary retention in BPH
- what drugs have the same action as prazosin
- terazosin, doxazosin
- what are the side effects of terazosin?
- orthostatic hypotension, dizziness, headache
- what selective alpha blockers cause orthostatic hypotension
- phenoxybenzamine, phentolamine, terazosin, prazosin, doxazosin
- name an alpha-2 selective adrenergic blocker
- yohimbine
- what is yohimbine used for
- impotence (effectiveness controversial)
- what alpha blockers are used to treat pheochromocytoma
- phenoxybenzamine, phentolamine
- beta-blockers ("lol"s)
- p. 307
- name some beta-blockers
- propranolol, metoprolol, atenolol, nadolol, timolol, pindolol, esmolol, labetalol
- what is the mechanism of propanolol
- selective beta-adrenergic blocker
- what is the mechanism of metoprolol
- selective beta-adrenergic blocker
- what is the mechanism of esmolol
- selective beta-adrenergic blocker
- what is the mechanism of pindolol
- selective beta-adrenergic blocker
- what are beta-blockers used to treat
- hypertension, angina, MI, SVT, CHF, glaucoma
- how do beta blockers treat hypertension
- decrease cardiac output, decrease renin secretion
- how do beta blockers treat angina
- decrease heart rate, decrease cardiac contractility, decreased O2 consumption
- why are beta blockers used to treat MI
- decrease MI mortality
- which beta blockers are used to treat SVT
- propanolol, esmolol
- how do propanolol and esmolol treat SVT
- decrease AV conduction velocity
- how do beta blockers treat CHF
- slow progression of chronic failure
- which beta blocker is used to treat glaucoma
- timolol
- what is timolol used to treat glaucoma
- decrease secretion of aqueous humor
- what are the toxic effects of beta blockers
- impotence, exacerbation of asthma, caution in diabetes
- what are the cardiovascular toxic effects of beta blockers
- bradychardia, AV block, CHF
- what are the CNS adverse effects of beta blockers
- sedation, sleep alterations
- which beta blockers are beta-1 selective
- acebutolol, betaxolol, esmolol, atenolol, metaprolol (A BEAM of beta-1 blockers)
- which beta-1 blocker is short-acting
- esmolol
- which beta blockers are non-selective
- propanolol, timolol, pindolol, nadolol, labetalol
- which beta blocker also blocks alpha receptors
- labetalol (all others are spelled "olol")