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Pharm of Non-anesthetic agents Test #2

Pharm Of Non-Anesthetic Agents Test #2

by waterlilly1962, Feb. 2010

Subjects: 2010 adrenergic anti-hypertensives cholinergic coyle vasodilators

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198 Cards in this Set

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	Cholinergic drugs act on receptors that are activated by a) Norepinephrine b) Acetylcholine	Acetylcholine
	In the sympathetic nervous system AcH binds with _______________ receptors at the pre/post synaptic ganglion	Nicotinic Pre-synaptic
	In the adrenal medulla AcH binds at the pre/post synaptic and the receptor is muscarinic/nicotinic	Pre-synaptic Nicotinic
	The nicotinic receptor is an example of a(n) a) ion channel b) g-protein linked c) steroid d) enzyme	ion channel
	In the parasympathetic nervous system (choose all that apply) a) AcH binds to muscarinic receptors pre-synaptically b) AcH binds to muscarinic receptors post-synaptically c) Has AcH binding both pre-synaptically & post-synaptically d) AcH binds only at the post-synaptic nicotinic receptor	AcH binds to muscarinic receptors post-synaptically Has AcH binding both pre-synaptically & post-synaptically
	Cholinergic drugs that are indirect acting (choose all that apply) a) bind & activate the receptor b) inhibit breakdown of AcH by cholinesterase c) are also called anticholinesterase drugs	inhibit breakdown of AcH by cholinesterase are also called anticholinesterase drugs
	Clinical uses for cholinergic agonists include (choose all that apply) a) reversal of neuromuscular blockade b) management of dementia c) Management of myastenia gravis d) treatment of glaucoma	a) reversal of neuromuscular blockade b) management of dementia c) Management of myastenia gravis d) treatment of glaucoma
	Synthesis of acetylcholine is a made possible by (choose all that apply) a) Ca voltage channels once the reach threshold b) A Na concentration gradient c) Choline Acetyltransferase which catalyzes the reaction of choline with Acetyl CoA d) a negative feedback process	b) A Na concentration gradient c) Choline Acetyltransferase which catalyzes the reaction of choline with Acetyl CoA d) a negative feedback process
	Release of AcH is facilitated by (choose any that apply) a) action potential at Ca voltage gated channel b) Elevated intracellular Ca c) Elevated intracellular Na	a) action potential at Ca voltage gated channel b) Elevated intracellular Ca
	When M1 or M3 receptors are activated a) increase IP3 DAG b) decrease IP3 DAG c) increase cAMP d) decrease cAMP	increase IP3 DAG
	Cholinergic drugs act on receptors that are activated by a) Norepinephrine b) Acetylcholine	Acetylcholine
	In the sympathetic nervous system AcH binds with _______________ receptors at the pre/post synaptic ganglion	Nicotinic Pre-synaptic
	In the adrenal medulla AcH binds at the pre/post synaptic and the receptor is muscarinic/nicotinic	Pre-synaptic Nicotinic
	The nicotinic receptor is an example of a(n) a) ion channel b) g-protein linked c) steroid d) enzyme	ion channel
	In the parasympathetic nervous system (choose all that apply) a) AcH binds to muscarinic receptors pre-synaptically b) AcH binds to muscarinic receptors post-synaptically c) Has AcH binding both pre-synaptically & post-synaptically d) AcH binds only at the post-synaptic nicotinic receptor	AcH binds to muscarinic receptors post-synaptically Has AcH binding both pre-synaptically & post-synaptically
	Cholinergic drugs act on receptors that are activated by a) Norepinephrine b) Acetylcholine	Acetylcholine
	In the sympathetic nervous system AcH binds with _______________ receptors at the pre/post synaptic ganglion	Nicotinic Pre-synaptic
	In the adrenal medulla AcH binds at the pre/post synaptic and the receptor is muscarinic/nicotinic	Pre-synaptic Nicotinic
	The nicotinic receptor is an example of a(n) a) ion channel b) g-protein linked c) steroid d) enzyme	ion channel
	In the parasympathetic nervous system (choose all that apply) a) AcH binds to muscarinic receptors pre-synaptically b) AcH binds to muscarinic receptors post-synaptically c) Has AcH binding both pre-synaptically & post-synaptically d) AcH binds only at the post-synaptic nicotinic receptor	AcH binds to muscarinic receptors post-synaptically Has AcH binding both pre-synaptically & post-synaptically
	M1 receptors are found a) CNS b) bronchial/smooth c) skeletal muscle d) stomach	CNS (nerves) stomach (parietal cells)
	M2 receptors are found a) Cardiac b) bronchial/smooth c) skeletal muscle d) bladder	Cardiac bronchial/smooth SPASM (MOSTLY) skeletal muscle
	M3 receptors are found a) Cardiac b) smooth muscle c) skeletal muscle d) bladder	smooth muscle bladder (MOSTLY)
	Cholinergic agonists cause a) decreased HR & BP b) bronchospasm c) midrasis d) miosis e) increased GI motility	a) decreased HR & BP b) bronchospasm d) miosis e) increased GI motility
	T/F Muscarinic agonists release Nitric Oxide in the presence of endothelium and cause Vasodilation	TRUE, Nitric Oxide is an endothelial relaxing factor which causes VASODILATION in presence of endothelium
	T/F When Muscarinic agonists cause release of Nitric Oxide in absence of endothelium there is Vasoconstriction	TRUE! In absence of endothelium Nitric Oxide causes VASOCONSTRICTION!!
	Carbechol a) a muscarinic/nicotinic cholinergic b) used to treat glaucoma c) causes miosis d) used to treat urinary retention	a) a muscarinic/nicotinic cholinergic b) used to treat glaucoma c) causes miosis
	Bethanechol a) a muscarinic cholinergic b) used to treat urinary/gi retention c) can cause bradycardia d) a beta blocker	a) a muscarinic cholinergic b) used to treat urinary/gi retention c) can cause bradycardia
	Of the following which drug is NOT hydrolyzed by acetylcholinesterase a) Carbechol b) Bethanechol c) Pilocarpine d) Methacholine	MethaCHOLINE
	Pilocarpine a) used to treat glaucoma b) can cause central cholinergic syndrome c) causes miosis d) crosses BBB	a) used to treat glaucoma b) can cause central cholinergic syndrome c) causes miosis d) crosses BBB (tertiary amine)
	Physostigmine a) reversibly binds to AcHase b) used to treat Central Anticholinergic Syndrome c) Can treat delirium d) is a irreversible bond at both muscarinic & nicotinic receptors	a) reversibly binds to AcHase b) used to treat Central Anticholinergic Syndrome c) Can treat delirium
	Neostigmine a) a quartenary ammonium b) higher affinity for nicotinic than muscarinic receptor c) causes tachycardia d) causes bradycardia	quartenary ammonium higher affinity for nicotinic than muscarinic receptor causes bradycardia
	Edrophonium a) used to diagnose Myasthenia Gravis b) used to treat Myasthenia Gravis c) short acting d) long acting	used to diagnose Myasthenia Gravis (because it is short acting) short acting ( 10-20 minutes)
	Pyridostigmine a) used to diagnose Myasthenia Gravis b) used to treat Myasthenia Gravis c) short acting d) long acting	used to treat Myasthenia Gravis (because it is long acting) long acting ( 3-6 hours)
	Alzheimer's Disease a) a deficit of cholinergic neurons b) an over abundance of cholinergic neurons c) treated with Donezepril d) treated with Rivastigmine	a) a deficit of cholinergic neurons c) treated with Donezepril d) treated with Rivastigmine
	Irreversible cholinergic inhibitors a) organophospates b) echothiopate c) prevent breakdown of AcH d) can be reversed with Atropine	a) organophospates b) echothiopate c) prevent breakdown of AcH d) can be reversed with Atropine
	T/F Bethanechol, Carbachol & Pilocarpine bind preferentially at muscarinic receptors	TRUE
	T/F pilocarpine & Physostigmine are uncharged tertiary amines that can penetrate CNS	TRUE
	Which of the following has the longest duration of action a) neostigmine b) physostigmine c) echothiopate d) Carbachol	echothiopate
	Other names for cholinergic antagonists include a) cholinergic blockers b) anticholinesterase drugs c) anticholinergic drugs d) parasympatholitics	cholinergic blockers anticholinergic drugs parasympatholitics
	Atropine, Scopolamine, & Ipratroium are all a) nicotinic blockers b) muscarinic blockers c) ganglionic blockers	muscarinic blockers
	Atropine a) causes midrasis b) miosis c) bradycardia d) increases salivation	causes midrasis
	Which of the following drugs crosses the CNS a) Atropine b) Scopolamine c) Glycopyrrolate	a) Atropine b) Scopolamine
	Anticholinergics side effects include a) urinary retention b) constipation c) dry mouth d) thin secretions	a) urinary retention b) constipation c) dry mouth
	Which of the following has the most antisialagogue effect a) atropine b) glycopyrrolate c) Scopolamine	Scopolamine
	Which of the following causes the most sedation a) atropine b) glycopyrrolate c) Scopolamine	Scopolamine
	When treating urinary retention disorders you want a drug that has an affinity for which receptor a) M1 b) M2 c) M3 d) M4	M3
	Non-depolarizing muscle relaxants a) competitively bind at nicotinic receptors b) competitively bind at muscarinic receptors c) can be overcome by increasing AcH at receptor site	competitively bind at nicotinic receptors can be overcome by increasing AcH at receptor site
	Examples of ganglionic blocking drugs a) Buproprion b) chantax c) Oxytrol d) Detrol	Buproprion Chantax
	T/F Ganlionic blocking drugs are nonspecific blockers of both parasympathetic and sympathetic ganglia	TRUE
	Adrenergic agonists a) sympathomimetic drugs b) bind to alpha receptors c) bind to beta receptors	a) sympathomimetic drugs b) bind to alpha receptors c) bind to beta receptors
	The neurotransmitter found at adrenergic receptors a) AcH b) NE c) Epi	NE Epi
	The second messenger associated with Beta adrenergic receptors a) adenlyl-cyclase b) phospholipase-C c) guanlyl-cyclase	adenlyl-cyclase
	The second messenger associated with Alpha 1 adrenergic receptors a) adenlyl-cyclase b) phospholipase-C c) guanlyl-cyclase	phospholipase-C
	Alpha 1 receptors a) found on vascular smooth muscle b) cause vasodilation c) cause vasoconstriction d) found post-synaptically e) found pre-synaptically	found on vascular smooth muscle cause vasoconstriction found post-synaptically
	Activation of Alpha 1 receptors a) decreases production of cAMP b) inhibits release of norepinephrine from neuron c) increase production of DAG & IP3 d) causes an increase in intracellular calcium e) found on post synaptic membrane of effector organ	a) decreases production of cAMP c) increase production of DAG & IP3 d) causes an increase in intracellular calcium e) found on post synaptic membrane of effector organ END RESULT CONSTRICTION OF SMOOTH MUSCLE
	Alpha receptors a) more responsive to epinephrine b) more responsive to isuprel	more responsive to epinephrine >norepinephrine>isuprel
	Dopamine receptors a) found in peripheral mesenteric vascular beds b) found in renal vascular beds c) found in CNS d) all of the above	a) found in peripheral mesenteric vascular beds b) found in renal vascular beds c) found in CNS
	T/F Alpha 2 receptors use feedback inhibition and decrease adenyl-cyclase activity	TRUE
	Activation of the dopaminergic receptor a) causes vasodilation b) causes vasoconstriction c) increases GFR d) decreases GFR	causes vasodilation increases GFR
	T/F Dopamine receptors are found in CNS effecting movement, affect, and nausea centers	TRUE
	The precursor to endogenous catecholamines is ________________	Tyrosine DOPA Dopamine Norepi
	T/F Alpha 2 receptor drugs can cause sedating effects	True, such as clonidine, because of the release of opiods
	Beta 1 receptors ( choose all that apply) a) cause tachycardia b) vasodilation c) increased renin release d) bronchodilation e) increased myocardial contractility	cause tachycardia increased renin release increased myocardial contractility
	Beta 2 receptors (choose all that apply) a) cause vasodilation b) bronchodilation c) vasodilate vasculature in skeletal muscles d) decrease K, Ca, Mg, increase glucose r/t glycogen metabolism e) relaxed uterine smooth muscle	cause vasodilation bronchodilation vasodilate vasculature in skeletal muscles relaxed uterine smooth muscle decrease K, Ca, Mg, increase glucose r/t glycogen metabolism
	T/F Beta arrestin turns g-protein coupled receptors off to decrease # of receptors	True, causes the receptor to migrate to pits in cell membrane to be recycled
	D1 receptors (choose all that apply) a) renal dilators b) splanchnic dilators c) modulate CNS	renal dilators splanchnic dilators
	D2 receptors a) renal dilator b) splanchnic dilator c) modulate neurotransmitters in CNS	modulate neurotransmitters in CNS
	Prolonged exposure to catechols a) decreases number (downregulated) b) increases number (upregulated)	decreases number (downregulated)
	Lack of exposure to catechols a) decreases number (downregulated) b) increases number (upregulated)	increases number (upregulated)
	The fundamental underlying mechanism for increasing contractility is a) an increase in intracellular Calcium influx b) an increase in Na moving out of cell through slow Na channels	an increase in intracellular Calcium influx
	Beta 1 stimulation increases/decreases renin production	increases
	Alpha 2 stimulation increases/decreases renin production	decreases
	Which receptor causes an increase in platelet aggregation a) Alpha 1 b) Alpha 2 c) Beta 1 d) Beta 2	Alpha 2 Epinephrine, this is a good drug for pt coming of coronary bypass pump
	T/F Catecholamines are polar and do not readily penetrate the CNS	TRUE
	Which of the following drugs are considered catecholamines a) epinephrine b) isoproterenol c) ephedrine d) phenylephrine	epinephrine isoproterenol
	Direct acting adrenergic agonists a) block uptake of norephinephrine b) cause the release of norephinephrine c) produce sympathetic effects	produce sympathetic effects
	Indirect acting adrenergic agonists a) block uptake of norephinephrine b) cause the release of norephinephrine c) produce sympathetic effects	cause the release of norephinephrine
	T/F Catecholamines are polar and do not readily penetrate the CNS	TRUE
	Which of the following drugs are considered catecholamines a) epinephrine b) isoproterenol c) ephedrine d) phenylephrine	epinephrine isoproterenol
	Direct acting adrenergic agonists a) block uptake of norephinephrine b) cause the release of norephinephrine c) produce sympathetic effects	produce sympathetic effects
	Indirect acting agonists a) block uptake of norephinephrine b) cause the release of norephinephrine c) produce sympathetic effects	cause the release of norephinephrine
	Examples of direct acting adrenergic agonists are a) Ephedrine b) Dobutamine c) Norepinephrine d) Cocaine e) Phenylephrine	Dobutamine Norepinephrine Phenylephrine
	Examples of indirect acting adrenergic agonists a) Amphetamine b) Dobutamine c) Norepinephrine d) Cocaine e) Phenylephrine	Amphetamine Cocaine
	Which of the following is a mixed direct/indirect adrenergic agonist a) Ephedrine b) Dobutamine c) Norepinephrine d) Cocaine e) Phenylephrine	Ephedrine
	What are the two types of cholinergic receptors?	nicotinic, muscarinic
	Muscarinic receptors are found a) pre-ganglionically in the PSNS neurons, but post-ganglionically in the SNS neurons b) post-ganglionically in the PSNS neurons, and not found in the SNS neurons c) post synaptically in the somatic neurons, and not found in the PSNS neurons	post-ganglionically in the PSNS neurons, and not found in the SNS neurons
	You have just given a cholinergic, muscarinic agonist a) the sphincter of the iris will contract and cause miosis b) the sphincter of the iris will contract and cause mydriasis c) the sphincter of the iris will relax and cause miosis d) the sphincter of the iris will relax and cause mydriasis	the sphincter of the iris will contract and cause miosis
	T/F Cholinergic agonists will cause dilation of both arterial & venous dilation in low doses	True
	M1 receptors are found a) in the heart, smooth muscle b) in the lungs (bronchospasm) c) in the bladder, glands d) in the nerves, parietal cells	in the nerves, parietal cells
	M3 receptors are found a) in the heart, smooth muscle b) in the lungs (bronchospasm) c) in the bladder, glands d) in the nerves, parietal cells	in the bladder, glands
	When an M1 receptor is stimulated what 2nd messenger(s) are activated and is there an increase or decrease in the 2nd messenger a) ↑ IP3, DAG b) ↓ IP3, DAG c) ↓ cAMP d) ↑ cAMP	↑ IP3, DAG
	When an M2 receptor is stimulated what 2nd messenger(s) are activated and is there an increase or decrease in the 2nd messenger a) ↑ IP3, DAG b) ↓ IP3, DAG c) ↓ cAMP d) ↑ cAMP	↓ cAMP
	. When an M3 receptor is stimulated what 2nd messenger(s) are activated and is there an increase or decrease in the 2nd messenger a) ↑ IP3, DAG b) ↓ IP3, DAG c) ↓ cAMP d) ↑ cAMP	↑ IP3, DAG
	. The effect that cholinergic agonists has on the bladder & sphincter a) contraction of detrusor muscle b) relaxation of detrusor muscle c) contraction of sphincter d) relaxation of sphincter	contraction of detrusor muscle relaxation of sphincter
	. T/F GI motility is increased with cholinergic agonists	True
	Nicotinic receptors are ___________receptors Muscarinic receptors are ___________ receptors	ion channel g-protein
	. Bethanechol, Carbachol, and Pilocarpine a) direct acting cholinergic agonists b) indirect acting cholinergic agonists c) act on muscarinic receptors d) act on nicotinic receptors	direct acting cholinergic agonists act on muscarinic receptors
	Direct acting cholinergic drugs act by a) increasing AcH by inhibiting hydrolysis of AcH b) decreasing AcH by increasing hydrolysis of AcH c) mimic effects of AcH by binding directly to the cholinergic receptor	mimic effects of AcH by binding directly to the cholinergic receptor
	. Bethanechol (choose all that apply) a) structurally related to AcH b) hydrolyzed by acetylcholinesterase c) lacks nicotinic actions d) acts on the smooth musculature of bladder & gi tract	structurally related to AcH lacks nicotinic actions acts on the smooth musculature of bladder & gi tract
	. Indirect acting cholinergic drugs act by a) increasing AcH by inhibiting hydrolysis of AcH b) decreasing AcH by increasing hydrolysis of AcH c) mimic effects of AcH by binding directly to the cholinergic receptor	increasing AcH by inhibiting hydrolysis of AcH
	. Physostigmine (choose all that apply) a) direct acting cholinergic agonist b) indirect acting cholinergic agonist c) effects both muscarinic & nicotinic receptors d) enters the CNS	indirect acting cholinergic agonist effects both muscarinic & nicotinic receptors enters the CNS
	. Physostigmine used to treat (choose all that apply) a) central cholinergic syndrome b) central anticholinergic syndrome c) atonic bladder or bowel d) glaucoma	central anticholinergic syndrome atonic bladder or bowel glaucoma
	T/F Physostigmine reversibly binds to acetylcholinesterase and inhibits its action	True
	Which of the following drugs would be used to diagnose Myasthenia Gravis, and why? a) Pyridostigmine b) Neostigmine c) Edrophonium	Edrophonium, because it is short acting vs pyridostigmine and neostigmine
	Alzheimer’s Disease increased/decreased cholinergic receptors in CNS	decreased
	Which of the following drugs would be used to treat Alzheimer’s Disease (choose all that apply) a) Donezepril b) Captopril c) Rivastigmine d) Glantamine	Donezepril Rivastigmine Glantamine
	How are irreversible cholinesterase inhibitors treated?	with atropine
	Match the dose of Atropine with the expected effect 0.03mg ..............................↓gi/bladder 0.8 -1mg ............................ bradycardia 2-3mg .................................tachycardia, mydrasis, bronchodilation 4-5mg .................................dry mouth, ↓ bronchial secretions	0.03 bradycardia 0.8-1mg tachycardia, mydriasis, bronchodilation 2-3mg dry mouth, ↓bronchial secretions 4-5mg ↓ gi/bladder
	. Adverse effects of cholinergic antagonists include (choose all that apply) a) CNS toxicity b) constipation c) urinary retention d) bronchospasm	CNS toxicity constipation urinary retention
	Your pt is on an Epi drip at 1mcg/kg/min, you give 1mg of Propanolol and continue the drip you would expect a) HR to decrease, contractility to decrease, BP to decrease b) HR to increase, contractility to decrease, BP to increase c) HR to decrease, contractility to decrease, BP to increase	HR to decrease, contractility to decrease, BP to increase
	Prior to giving Isuprel your pt was α-blocked what would the BP do? increase/decrease/stay the same	stay the same (because Isuprel is strictly a beta drug)
	Prior to giving some Epi your pt was α-blocked what would the BP do? increase/decrease/stay the same	decrease
	Prior to starting your pt on a levo drip he was α-blocked what would the BP do? increase/decrease/stay the same	decrease (levophed is both alpha and beta)
	Clonidine (choose all that apply) a) α1 agonist b) α2 agonist c) exerts its effect both peripherally & centrally d) inhibits sympathetic tone e) inhibits NE release	α2 agonist exerts its effect both peripherally & centrally inhibits sympathetic tone inhibits NE release
	Drugs used to treat bronchospasms a) β2-blockers b) β2 agonists	β2 agonists
	Albuterol, Metaproterenol short acting/ medium acting/ long acting	medium acting
	. What is the problem with using short acting/ medium acting adrenergics for bronchospasm?	(think receptors) using short acting causes up & down regulation of receptors, and so are not effective in long term treatment
	Match the receptor type with its location in the body (may be more than one answer for some) α1 ........................lungs β2........................ Smooth vascular α2 ........................ heart β3.......................CNS D1 ....................... Renal D2...................... adipose tissue β1...................... Nerve endings ...........................Splanchnic ...........................uterine	Smooth vascular α1 β2 Lungs β2 Heart β1 CNS α2 Renal D1 vascular skeletal β2 Nerve endings D2 Splanchnic D1 Uterine β2 Adipose tissue β3
	The 2nd messenger for α1 receptor a) adenyl cyclase b) phospholipase C	phospholipase C
	α1 receptors a) vasoconstriction b) vasodilation c) ↑ peripheral resistance d) mydriasis e) miosis	vasoconstriction ↑ peripheral resistance mydriasis
	α2 receptors a) inhibit NE release b) inhibit insulin release c) tachycardia d) sedation e) ↓ renin release	inhibit NE release inhibit insulin release sedation ↓ renin release
	β1 receptors a) tachycardia b) vasodilation c) ↑ renin release d) metabolism changes ( ↑ glucose, ↓ K, Ca, Mg)	tachycardia ↑ renin release
	β2 receptors a) vasodilation b) bronchodilation c) increased muscle/liver glycogenolysis d) relax uterine muscle	vasodilation bronchodilation increased muscle/liver glycogenolysis relax uterine muscle
	What cholinergic antagonist is also a ganglionic blocker & is used to treat HTN	Trimethaphan
	Aldomet (Methyldopa) a) a dopaminergic drug b) α2 agonist c) converted to methylnorepinephrine & diminishes adrenergic outflow in the CNS d) ↓ peripheral resistance & ↓ BP	α2 agonist converted to methylnorepinephrine & diminishes adrenergic outflow in the CNS ↓ peripheral resistance & ↓ BP
	. Aldomet a) ↓ CO b) does not ↓ CO c) good drug for renal pts d) side effects of sedation, drowsiness	does not ↓ CO good drug for renal pts side effects of sedation, drowsiness
	. Hydralazine a) direct vasodilation b) indirect vasodilation c) causes reflex tachycardia d) ↑ renin release → Na & H2O retention e) used in combination with β-blockers (propanolol)	direct vasodilation causes reflex tachycardia ↑ renin release → Na & H2O retention used in combination with β-blockers (propanolol)
	T/F Hydralazine increases myocardial contractility, HR, and MVO2	True
	α-blockers a) arterial/venous dilation b) prevent HTN when exposed to catecholamines c) ↑ HR, renin, ADH d) reverse vasoconstriction caused by Epinephrine	arterial/venous dilation prevent HTN when exposed to catecholamines ↑ HR, renin, ADH reverse vasoconstriction caused by Epinephrine
	T/F Angiotensin Blockers will allow renin release, but not Na & H2O retention	True
	Which Ca Channel blockers are more active in the heart vs vascular smooth muscle a) Nifedipine b) Diltiazem c) Nicardipine d) Verapamil	Diltiazem Verapamil
	Which Ca Channel blockers are more active in the vascular smooth muscle vs heart a) Nifedipine b) Diltiazem c) Nicardipine d) Verapamil	Nifedipine Nicardipine
	Your pt has SVT which Ca Channel blockers would you use a) Nifedipine b) Diltiazem c) Nicardipine d) Verapamil	Diltiazem Verapamil
	ACE Inhibitors a) ↓ SNS output b) ↓ aldosterone c) ↑ aldosterone d) ↑ bradykinin	↓ SNS output ↓ aldosterone ↑ bradykinin
	Which Ca Channel blockers have some effect on coronary vasodilation a) Diltiazem b) Nicardipine c) Nifedipine d) Verapamil	Diltiazem Nifedipine Verapamil
	T/F Dihydropyridines cause reflex sympathetic activation & edema	True
	Nicardipine a) has a ceiling effect b) can be rapidly titrated in HTN emergency c) can not be rapidly titrated d/t long ½ life d) good drug for Neuro-anesthesia (only minimal ↑ CBF) e) causes coronary vasodilation	has a ceiling effect can not be rapidly titrated d/t long ½ life good drug for Neuro-anesthesia (only minimal ↑ CBF) causes coronary vasodilation
	β-blockers ↓ BP by a) ↓ stress related to HTN b) ↓ renin production c) ↑ aldosterone d) block β adrenoreceptors on heart	↓ stress related to HTN ↓ renin production block β adrenoreceptors on heart
	The administration of Nitrates a) ↑ cGMP b) ↓ cGMP c) ↑ Nitric Oxide d) ↑ dephosphorylation of light chain myosin e) ↓ dephosphorylation of light chain myosin	↑ cGMP ↑ Nitric Oxide ↑ dephosphorylation of light chain myosin
	Molecule is made up of Fe, Cyanide (CN), Nitric Oxide a) Nitroglycerin b) Nitroprusside	Nitroprusside
	You are administering a nitrate to your patient and notice a ↓ LOC and upon drawing some labs see that he is in metabolic acidosis. This drug is rapidly metabolized by RBC’s the drug is a) Nitroprusside b) Nitroglycerin	Nitroprusside
	How is cyanide toxicity from Nitroprusside treated a) Vit B 12 b) Thiosulfate	Vit B 12
	Systemic effects of Nitroprusside a) ↑ cerebral blood flow b) inhibits platelet aggregation c) ↑ platelet aggregation d) blocks hypoxic pulmonary vasoconstriction reflex	↑ cerebral blood flow inhibits platelet aggregation blocks hypoxic pulmonary vasoconstriction reflex
	Vasodilators work by a) ↑ LV afterload b) ↓ LV afterload c) venous decompression d) venous pooling e) improving RV function thru pulmonary vasodilation	↓ LV afterload venous decompression improving RV function thru pulmonary vasodilation
	How does Vit B12 work when used for cyanide poisoning?	displacing the drug from the receptor
	Nitroprusside or Nitroglycerin which one dilates coronary’s and can be used for vasospasm in the uterus?	Nitroglycerin
	T/F Nitroglycerin exerts it’s effect on smooth muscle relaxation by release of endothelial Nitric Oxide	True
	Nitroglycerin a) ↓ cGMP b) ↓ preload c) ↑ preload d) dilates lg coronary arteries e) ↓ LVEDP	↓ preload dilates lg coronary arteries ↓ LVEDP cGMP would increase because cGMP vasodilates
	Your pt has Torsades de Pointe what would you treat it with?	Mg or Phenytoin or propanolol or lidocaine
	Trimethaphan a) blocks SNS ganglia only b) blocks SNS & PSNS ganglia c) ↓ BP by ↓ preload (CO & SVR) d) reflex tachy e) binds to nicotinic receptors f) can be used to ↓ intraoperative bleeding	blocks SNS & PSNS ganglia ↓ BP by ↓ preload (CO & SVR) binds to nicotinic receptors can be used to ↓ intraoperative bleeding
	What vasodilator causes lupus like syndrome (Steven-Johnson’s) and may be a problem in slow acetylators a) Nitroprusside b) Hydralazine c) Fenoldopam d) Nicardipine	Hydralazine
	T/F Enalaprit (Vasotec) causes ↑ renin release and ↑ bradykinin	True
	. Fenoldopam a) α agonist b) D1 agonist c) renal artery dilation d) natiuretic	D1 agonist renal artery dilation natiuretic
	Brain Natiuretic Peptide, pulmonary vasodilator, used to treat CHF, Pulmonary Edema a) Diazoxide b) Nesiritide c) Phentolamine d) Enalaprit	Nesiritide
	Side effects of vasodilators include a) reflex tachy b) Na & H2O retention c) ↓ aldosterone d) HOTN	reflex tachy Na & H2O retention HOTN
	Which drug could be used to treat dig toxicity a) Amiodorone b) Phenytoin c) Quinidine d) Flecinide	Phenytoin
	Nitric Oxide causes vasodilation in a) all alveoli b) only ventilated alveoli	only ventilated alveoli
	Nitric Oxide a) ↓ PA pressures b) endothelial-derived relaxing factor c) only approved in PPH (neonates) d) cause pulmonary edema	↓ PA pressures endothelial-derived relaxing factor only approved in PPH (neonates) cause pulmonary edema
	50% of people don’t respond to Nitric Oxide therapy but may if what drugs are added to the therapy?	Nitroprusside or Nitroglycerin
	T/F Nitric Oxide inhalation therapy is beneficial in ARDS, RV failure after cardiac surgery & sickle cell crisis	True
	Nitric Oxide is delivered in parts/million, if delivered at a rate 20 parts/million what could result?	Methemoglobinemia d/t free radicals
	T/F Rebound Pulmonary HTN can occur after withdrawing Nitric Oxide therapy	True, need to withdraw slowly
	Which of the following drugs produces CYP itself a) Phenytoin b) Amiodorone c) Procainamide d) Quinidine	Phenytoin
	Which anti-dysrrhythmic drug could be a problem in pts who are slow acetylators a) Phenytoin b) Amiodorone c) Procainamide d) Quinidine	Procainamide
	Which of the following anti-dysrrhythmic drugs are considered “membrane stabilizers” a) Procainamide b) Propanolol c) Propafenone d) Lidocaine	Procainamide Propanolol Propafenone Lidocaine
	Which of the following drugs is both a class II & class III anti-dysrrhythmic drug a) Amiodorone b) Sotolol d) Mexilitine e) Adenosine	Sotolol
	Class IA anti-dysrrhythmics a) prolong the action potential b) have no effect on the action potential c) slows phase 0 depolarization d) suppresses phase 4 depolarization	prolong the action potential slows phase 0 depolarization
	Class IB anti-dysrrhythmics a) decrease the duration of the action potential b) have no effect on the action potential c) shorten phase 3 repolarization d) prolong phase 3 repolarization	decrease the duration of the action potential shorten phase 3 repolarization
	Class IC anti-dysrrhythmics a) decrease the duration of the action potential b) have no effect on the action potential c) slow phase 0 depolarization d) supress phase 4 depolarization	have no effect on the action potential slow phase 0 depolarization
	Class I drugs a) Na channel blockers b) Ca channel blockers c) β-blockers d) K channel blockers	Na channel blockers
	Class II drugs a) Na channel blockers b) Ca channel blockers c) β-blockers d) K channel blockers	β-blockers
	Class III drugs a) Na channel blockers b) Ca channel blockers c) β-blockers d) K channel blockers	K channel blockers
	Class IV drugs a) Na channel blockers b) Ca channel blockers c) β-blockers d) K channel blockers	Ca channel blockers
	Procainamide, Quinidine, Disopyramide all a) Class IA drugs b) Class II drugs c) Class IB drugs d) Class IV drugs	Class IA drugs
	Lidocaine, Mexiletine a) Class IA drugs b) Class II drugs c) Class IB drugs d) Class IV drugs	Class IB drugs
	Flecainide a) Class IC drugs b) Class III drugs c) Class IB drugs d) Class IV drugs	Class IC drugs
	Esmolol, Propanolol, Sotolol a) Class IA drugs b) Class II drugs c) Class IB drugs d) Class IV drugs	Class II drugs
	Amiodorone, Sotolol a) Class III drugs b) Class II drugs c) Class IB drugs d) Class IV drugs	Class III drugs
	Diltiazem, Verapamil a) Class IA drugs b) Class II drugs c) Class IB drugs d) Class IV drugs	Class IV drugs
	Which drug crosses all four anti-arrhythmic classes a) Procainamide b) Amiodorone c) Disopyramide d) Sotolol	Amiodorone
	Propafenone, Procainamide, Amiodorone which drug has the following adverse effects - Hyper &/or Hypo thyroidism - dig toxicity - blue skin coloring - inhibits CYP - pulmonary alveolitis	Amiodorone
	Increased levels of Flecainide can be seen when given in combination with (choose all that apply) a) digoxin b) amiodorone c) propanolol d) Phenytoin	digoxin amiodorone propanolol
	Which of the following prostanoids are vasoconstrictors a) TXA2 b) PGE1 c) PGE2 d) PGI2 e) PGF2α	TXA2 PGE2 PGF2α
	Which of the following prostanoids are vasodilators a) TXA2 b) PGE1 c) PGE2 d) PGI2 e) PGF2α	PGE1 PGI2
	Hemabate a) PGF2α b) PGE1 c) used for post partum hemorrhage d) should not be used in a pt with asthma	PGF2α used for post partum hemorrhage should not be used in a pt with asthma
	Alprostadil a) will close the PDA b) will keep the PDA open c) PGE1 d) PGE2	will keep the PDA open PGE1
	Epoprostanol (Flolan) a) treat Pulm HTN b) PGI2 c) PGF2α d) requires continuous infusion d/t short ½ life	treat Pulm HTN PGI2 requires continuous infusion d/t short ½ life
	Iloprost a) PGI2 b) PGI1 c) ↓ plt aggregation d) ↑ plt aggregation	PGI2 ↓ plt aggregation
	Thromboxane a) PGI2 b) TXA2 c) ↑ plt aggregation d) ↓ plt aggregation	TXA2 ↑ plt aggregation
	Misoprostol (Cytotec) a) PGE1 b) PGI2 c) ↑ gi motility d) proton pump inhibitor	PGE1 ↑ gi motility proton pump inhibitor
	Digoxin a) increases Na+/K+ exchange b) decreases Na+/K+ exchange c) increases intracellular Ca++ d) decreases intracellular Ca++	decreases Na+/K+ exchange increases intracellular Ca++
	Digoixin a) ↑ protein binding b) narrow therapeutic window c) ↑ duration of action potential d) ↓ duration of action potential e) ↑ PSNS activity on SA node f) increased conduction on rest of heart	↑ protein binding narrow therapeutic window ↓ duration of action potential ↑ PSNS activity on SA node (which slows heart rate) increased conduction on rest of heart
	Hypokalemia/Hyperkalemia causes dig toxicity	Hypokalemia
	Hypercalcemia/Hypocalcemia causes dig toxicity	Hypercalcemia
	Spironolactone a) aldosterone antagonist b) K+ sparing c) loop diuretic d) aldosterone agonist	aldosterone antagonist K+ sparing
	Angiotensin Inhibitors a) Captopril b) Losartan c) ↓ aldosterone d) ↓ angiotensin II e) ↑ bradykinin	Losartan ↓ aldosterone ↓ angiotensin II ↑ bradykinin
	Bipyridines a) Milrinone b) Eplerone c) phosphodiesterase inhibitors d) ↑cGMP e) ↑ cAMP	Milrinone phosphodiesterase inhibitors ↑cGMP (vasodilation) ↑ cAMP (contraction)

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