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180 Cards in this Set
- Front
- Back
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Where is Ach a NT?
(select all) A. Preganglion B. Postganglion C. Parasympathetic D. Sympathetic |
B. Postanglion
C. Parasympathetic Also: A. Preganglion (Symp & Para) D. Sympathetic (sweat glands) |
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Where is NE a NT?
(select all) A. Preganglion B. Postganglion C. Parasympathetic D. Sympathetic |
B. Postganglion
D. Sympathetic |
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What kind of NT is at muscarinic tissue synapses?
A. Ach B. NE C. Dopamine |
A. Ach
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What kind of NT is at adrenergic tissue synapses?
A. Ach B. NE C. Dopamine |
B. NE
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What kind of NT is at nicotinic tissue synapses?
A. Ach B. NE C. Dopamine |
A. Ach
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What kind of NT is at dopaminergic tissue synapses?
A. Ach B. NE C. Dopamine |
C. Dopamine
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Where does CHOLINERGIC transmission occur in SYMPATHETIC systems?
(select all) A. ganglia B. NMJ C. sweat glands D. adrenal medulla E. renal blood vessels |
A. ganglia
C. sweat glands D. adrenal medulla |
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Where does DOPAMINERGIC transmission occur in SYMPATHETIC systems?
(select all) A. ganglia B. NMJ C. sweat glands D. adrenal medulla E. renal blood vessels |
E. renal blood vessels
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Sympathetic nervous system includes:
A. NE B. Ach C. Dopamine D. A & C E. All of the Above |
D. All of the Above
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Parasympathetic nervous system includes:
A. NE B. Ach C. Dopamine D. A & C E. All of the Above |
B. Ach
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What does Choline acetyltransferase do?
A. Degrade Ach B. Synthesize Ach |
B. Synthesize Ach
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What does acetylcholinesterase (AchE) do?
A. Degrade Ach B. Synthesize Ach |
A. Degrade Ach
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What is the rate-limiting step in neurotransmission?
A. synthesis & storage B. release C. metabolism D. recognition |
A. synthesis & storage
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Prevention of which step of neurotransmission causes an increase in effective NT concentrations?
A. synthesis & storage B. release C. metabolism D. recognition |
C. metabolism
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Intervening of which step of neurotransmission is most effective and most rapid?
A. synthesis & storage B. release C. metabolism D. recognition |
B. release
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Dopamine is a precursor of:
A. Ach B. NE |
B. NE
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What amino acid is a precursor of catecholamines?
A. lysine B. serine C. tyrosine D. glycine |
C. tyrosine
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Regardless of the pathway, what enzyme(s) degrade catecholamines (Epi, NE, Dopamine)?
(select all) A. AchE B. MAO C. COMT D. VMA |
B. MAO
C. COMT |
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What is the rate-limiting step of Cholinergic neurotransmission?
A. release of choline B. precursor transport into neurons C. metabolism D. synthesis of choline |
B. precursor transport into neurons
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In NE synthesis, what enzyme converts Tyrosine into Dopa?
A. Tyrosine hydroxylase B. Dopa decarboxylase C. Dopamine β-hydroxylase D. PNMT |
A. Tyrosine hydroxylase
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In NE synthesis, what enzyme converts Dopa into Dopamine?
A. Tyrosine hydroxylase B. Dopa decarboxylase C. Dopamine β-hydroxylase D. PNMT |
B. Dopa decarboxylase
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In NE synthesis, what enzyme converts Dopamine into NE?
A. Tyrosine hydroxylase B. Dopa decarboxylase C. Dopamine β-hydroxylase D. PNMT |
C. Dopamine β-hydroxylase
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What enzyme converts NE into Epi?
A. Tyrosine hydroxylase B. Dopa decarboxylase C. Dopamine β-hydroxylase D. PNMT |
D. PNMT
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T/F
If Ach is not degraded, it can be taken back up by the pre-synaptic neuron. |
False
(NE can be taken back up) |
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A ligand that activates a receptor
A. Agonist B. Antagonist |
A. Agonist
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A ligand that prevents the action of another molecule.
A. Agonist B. Antagonist |
B. Antagonist
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A molecule that binds to a target for an effect
A. direct-acting B. indirect-acting |
A. direct-acting
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A molecule that interacts with another molecule to create an effect on a target
A. direct-acting B. indirect-acting |
B. indirect-acting
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Describe the intervention of Ach degradation.
(select all) A. stimulatory B. inhibitory C. agonistic D. antagonistic |
B. inhibitory
C. agonistic (activation of Anti-ChE to inhibit AchE) (leads to increased [Ach]) |
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Describe the activity of the following organs upon SYPMATHETIC stimulation
- Heart - Blood vessels - Lungs - GI - Genitourinary tract - Glands - Eye |
- Heart = ↑ activity
- Blood vessels = vasoconstriction - Lungs = bronchodilation - GI = ↓ activity - Genitourinary tract = ↓ activity - Glands = (salivary) secretion - Eye = dilation (mydriasis) & aqueous humor production |
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Describe the activity of the following organs upon PARASYPMATHETIC stimulation
- Heart - Blood vessels - Lungs - GI - Genitourinary tract - Glands - Eye |
- Heart = ↓ activity
- Blood vessels = vasodilation - Lungs = bronchoconstriction - GI = ↑ activity - Genitourinary tract = ↑ activity - Glands = secretion - Eye = constriction (myosis) & aqueous humor outflow (near vision) |
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What are the predominant innervations of the following organ systems?
(sympathetic or parasympathetic) - Heart - Blood vessels - Lungs - GI - Genitourinary tract - Glands - Eye |
- Heart = parasympathetic
- Blood vessels = parasympathetic - Lungs = parasympathetic - GI = parasympathetic - Genitourinary tract = parasympathetic - Glands = parasympathetic - Eye = sympathetic |
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Nicotinic cholinergic receptors are found at:
(select all) A. ganglia B. glands C. adrenal medulla D. NMJ E. heart F. vascular smooth muscle |
A. ganglionic
C. adrenal medulla D. NMJ |
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Muscarinic cholinergic receptors are found at:
(select all) A. ganglia B. glands C. adrenal medulla D. NMJ E. heart F. vascular smooth muscle |
B. glands
E. heart F. vascular smooth muscle |
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What do activation of Muscarinic cholinergic receptors cause?
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- Defecation
- Urination - Miosis - Bronchoconstriction - Emesis - Lacrimation - Salivation (DUMBELS) |
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Put the α-adrenergic receptor agonist potency in order of most potent to least potent:
- Epi - Iso - NE |
For α:
NE > Epi > Iso |
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Put the β-adrenergic receptor agonist potency in order of most potent to least potent:
- Epi - Iso - NE |
For β:
Iso > Epi > NE |
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Describe α1 adrenergic receptors.
(select all) A. excitatory B. inhibitory C. Gi D. Gq E. Gs |
A. excitatory
D. Gq |
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Describe α2 adrenergic receptors.
(select all) A. excitatory B. inhibitory C. Gi D. Gq E. Gs |
B. inhibitory
C. Gi |
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These adrenergic receptors are found at post-synaptic effector cells (esp. smooth muscle) and stimulation usually produces vasoconstriction.
A. α1 B. α2 C. β1 D. β2 E. β3 |
A. α1
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These adrenergic receptors are found at pre-synaptic nerve terminals (autoreceptor) and stimulation usually produces inhibition of NT release and platelet aggregation.
A. α1 B. α2 C. β1 D. β2 E. β3 |
B. α2
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These adrenergic receptors are found at post-synaptic effector cells (esp. heart) and stimulation usually produces ↑ heart rate & force.
A. α1 B. α2 C. β1 D. β2 E. β3 |
C. β1
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These adrenergic receptors are found at post-synaptic effector cells (esp. smooth muscle) and stimulation usually produces bronchodilation and vasodilation.
A. α1 B. α2 C. β1 D. β2 E. β3 |
D. β2
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These adrenergic receptors are found at post-synaptic effector cells (esp. adipose tissue) and stimulation usually produces lipolysis.
A. α1 B. α2 C. β1 D. β2 E. β3 |
E. β3
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List the 3 most common receptors for NE
- α1/2 - β1 - β2 - D1/2 |
α1/2 > β1 > β2
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List the 3 most common receptors for Epi
- α1/2 - β1 - β2 - D1/2 |
β1/2 > α1/2
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List the 3 most common receptors for Dopamine
- α1/2 - β1 - β2 - D1/2 |
D1/2 > β1 > α1/2
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What effect will a substitution at the α-carbon of NE have?
A. increase α activity B. increase β activity C. decrease metabolism by COMT D. decrease metabolism by MAO E. increase β2 selectivity |
D. decrease metabolism by MAO
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What effect will adding an -OH group to C3 & C5 of NE have?
A. increase α activity B. increase β activity C. decrease metabolism by COMT D. decrease metabolism by MAO E. increase β2 selectivity |
E. increase β2 selectivity
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What effect will substitution of -OH on C3 and/or C4 of NE have?
A. increase α activity B. increase β activity C. decrease metabolism by COMT D. decrease metabolism by MAO E. increase β2 selectivity |
C. decrease metabolism by COMT
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What effect will an alkyl substitution of -NH₂ of NE have?
A. increase α activity B. increase β activity C. decrease metabolism by COMT D. decrease metabolism by MAO E. increase β2 selectivity |
B. increase β activity
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The main function of α1 receptors is
A. smooth muscle contraction (arteries) B. smooth muscle relaxation (lungs) C. decrease of presynaptic terminal NE release D. increase heart activity E. vasodilation of renal & splanchnic arteries |
A. smooth muscle contraction (arteries)
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The main function of α2 receptors is
A. smooth muscle contraction (arteries) B. smooth muscle relaxation (lungs) C. decrease of presynaptic terminal NE release D. increase heart activity E. vasodilation of renal & splanchnic arteries |
C. decrease of presynaptic terminal NE release
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The main function of β1 receptors is
A. smooth muscle contraction (arteries) B. smooth muscle relaxation (lungs) C. decrease of presynaptic terminal NE release D. increase heart activity E. vasodilation of renal & splanchnic arteries |
D. increase heart activity
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The main function of β2 receptors is
A. smooth muscle contraction (arteries) B. smooth muscle relaxation (lungs) C. decrease of presynaptic terminal NE release D. increase heart activity E. vasodilation of renal & splanchnic arteries |
B. smooth muscle relaxation (lungs)
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The main function of Dopamine receptors is
A. smooth muscle contraction (arteries) B. smooth muscle relaxation (lungs) C. decrease of presynaptic terminal NE release D. increase heart activity E. vasodilation of renal & splanchnic arteries |
E. vasodilation of renal & splanchnic arteries
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After administration of NE, an increase in MAP causes:
(select all) A. increased NE B. decreased NE C. increased Ach D. decreased Ach E. reflex bradycardia F. reflex tachycardia |
B. decreased NE
C. increased Ach E. reflex bradycardia |
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High doses of Epi activate ___ receptors and cause ______.
A. α1; vasoconstriction B. α1; vasodilation C. β2; vasoconstriction D. β2; vasodilation |
A. α1; vasoconstriciton
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Low doses of Epi activate ___ receptors and cause ______.
A. α1; vasoconstriction B. α1; vasodilation C. β2; vasoconstriction D. β2; vasodilation |
D. β2; vasodilation
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Isoproterenol only uses __ receptors
(select all) A. α1 B. α2 C. β1 D. β2 E. Dopamine |
C. β1
D. β2 |
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α activation on blood vessels causes:
A. vasoconstriction B. vasodilation |
A. vasoconstriction
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β activation on blood vessels causes:
A. vasoconstriction B. vasodilation |
B. vasodilation
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D1 activation on blood vessels causes:
A. vasoconstriction B. vasodilation |
B. vasodilation
(of splanchnic/renal arteries) |
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α activation of the radial pupillary dilator muscle (in the eye) causes:
A. contraction B. relaxation |
A. contraction
(leads to mydriasis = dilation) |
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Metyrosine, Tyramine, Phenelzine, and α-methyl dopa indirectly act on _____ of adrenergic neurons.
A. Metabolism B. Release C. Vesicular transport & storage D. Uptake |
A. Metabolism
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Cocaine and imipramine indirectly act on _____ of adrenergic neurons.
A. Metabolism B. Release C. Vesicular transport & storage D. Uptake |
D. Uptake
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Reserpine indirectly acts on _____ of adrenergic neurons.
A. Metabolism B. Release C. Vesicular transport & storage D. Uptake |
C. Vesicular transport & storage
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Amphetamine, guanethidine, and bretylium indirectly act on _____ of adrenergic neurons.
A. Metabolism B. Release C. Vesicular transport & storage D. Uptake |
B. Release
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Clonidine is a(n):
A. α1 agonist B. α2 agonist C. α1 antagonist D. α2 antagonist E. β agonist F. β antagonist |
B. α2 agonist
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β2 activation of the uterus causes:
A. contraction B. relaxation |
B. relaxation
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What kind of receptors does Ach bind?
(select all) A. Adrenergic B. Muscarinic C. Nicotinic E. All of the Above |
B. Muscarinic
C. Nicotinic |
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Muscarinic receptors are:
A. G-Protein linked receptors B. Ion-channel linked receptors |
A. G-Protein linked receptors
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Nicotinic receptors are:
A. G-Protein linked receptors B. Ion-channel linked receptors |
B. Ion-channel linked receptors
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Besides Ach, what are 2 other drugs that can activate cholinergic receptors?
A. Bethanachol B. Atropine C. Scopolamine D. Carbachol |
A. Bethanachol
D. Carbachol (also Pilocarpine) (Atropine & scopolamine are antagonists) |
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Why is Ach not an effective drug?
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- Ach Is polar (poor absorption)
- susceptible to AchE (highly metabolized) |
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What are the physiologic consequences of muscarinic activation in the EYE?
(select all) A. mydriasis B. myosis C. aqueous humor outflow D. aqueous humor production |
B. myosis
C. aqueous humor outflow |
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What are the physiologic consequences of muscarinic activation in the CARDIOVASCULAR SYSTEM?
(select all) A. vasoconstriction B. vasodilatation C. increased heart activity D. decreased heart activity |
B. vasodilation
D. decreased heart activity |
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What are the physiologic consequences of muscarinic activation in the GI TRACT?
A. increase activity B. decrease activity |
A. increase activity
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What are the physiologic consequences of muscarinic activation in GLANDS?
A. increased secretion B. decreased secretion |
A. increased secretion
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What are the physiologic consequences of muscarinic activation in the LUNGS?
A. bronchoconstriction B. bronchodilation |
A. bronchoconstriction
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T/F
Inhibition of AchE has the same effect as Ach "overdose" |
True
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Which drug is a muscarinic agonist that stimulates the bladder and GI tract?
A. atropine B. pilocarpine C. carbachol D. bethanechol |
D. bethanechol
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Which drug is a muscarinic agonist that stimulates salivation and can help treat glaucoma?
A. atropine B. pilocarpine C. carbachol D. bethanechol |
B. pilocarpine
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What drug can be used as an antidote for toxic use of bethanechol (or other muscarinic drugs)?
A. carbachol B. pilocarpine C. atropine D. neostigmine |
C. atropine
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T/F
Atropine can enter CNS, and scopolamine can not. |
False
(scopolamine can cross BBB, atropine can not) |
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What are 2 muscarinic ANTAGONISTS?
A. carbechol B. atropine C. scopolamine D. bethanechol |
B. atropine
C. scopolamine |
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Muscarinic antagonists _____ inhibit muscarinic receptors.
A. competitively B. non-competitively C. uncompetitively D. allosterically |
A. competitively
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T/F
The antidote to atropine poisoning is physostigmine. If true, why? |
True
can enter CNS (atropine = muscarinic cholinergic antagonist = decreases Ach) (physostigmine = anti-AchE = increases Ach) |
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T/F
Atropine is used to treat motion sickness. |
False
(SCOPOLAMINE is used to treat motion sickness) (Atropine can cause pupil dilation) |
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What is the general mechanism of diuretics?
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Lower BP by depleting Na⁺ stores
(↑ water secretion = ↓ blood volume = ↓ CO = ↑ PVR) |
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Centrally acting antihypertensive drugs are:
A. α1 agonists B. α2 agonists C. α1 antagonists D. α2 antagonists |
B. α2 agonists
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What are the common adverse effects of Centrally acting antihypertensive drugs?
A. hypokalemia B. sedation C. reflex tachycardia D. fetotoxic |
B. sedation
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β-blockers are ______ of β1 & β2 autoreceptors, thereby, __ CO
A. agonists; ↑ B. agonists; ↓ C. antagonists; ↑ D. antagonists; ↓ |
D. antagonists; ↓
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α-blockers are _____ of α autoreceptors, thereby, __ PVR
A. agonists; ↑ B. agonists; ↓ C. antagonists; ↑ D. antagonists; ↓ |
D. antagonists; ↓
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T/F
The basic mechanism of Peripherally-acting AHDs is to block one or more key steps of parasympathetic neurotransmission |
False
(block SYMPATHETIC neurotransmission) |
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____ blocks NE SYNTHESIS, thereby depleting NE, and ↓ PVR & CO
A. reserpine B. guanethidine C. hydrochlorothiazide D. nitroprusside |
A. reserpine
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____ blocks NE RELEASE, thereby depleting NE, and ↓ PVR & CO
A. reserpine B. guanethidine C. hydrochlorothiazide D. nitroprusside |
B. guanethidine
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Why are diuretics a first-line drug for hypertension?
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- safe
- effective - suitable for older adults - given orally - inexpensive |
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Which of the following drugs are direct vasodilators that stabilize membrane potential at resting level by opening K⁺ channels?
(select all) A. diazoxide B. hydralazine C. sodium nitroprusside D. minoxidil |
A. diazoxide
B. hydralazine D. minoxidil |
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Which of the following drugs is a direct vasodilator that increases cGMP levels which leads to smooth muscle relaxation?
A. diazoxide B. hydralazine C. sodium nitroprusside D. minoxidil |
C. sodium nitroprusside
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What is the clinical use of direct vasodilators?
A. CHF B. severe hypertension C. angina D. MI |
B. severe hypertension
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Why are direct vasodilators not used as first-line drugs?
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Adverse side effects:
- reflex tachycardia - sodium retention - cyanide ion production - body hair growth |
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What are the 2 actions of ACE Inhibitors?
A. competitively inhibit ACE B. ↑ angiotensin II C. ↑ bradykinin D. ↓ aldosterone |
A. competitively inhibit ACE (↓ AT-II formation)
C. ↑ bradykinin |
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What are the 2 actions of Angiotensin-II receptor antagonists?
A. competitively inhibit AT-II receptor B. ↑ vasoconstriction C. ↑ bradykinin D. ↓ aldosterone release |
A. competitively inhibit AT-II receptor (↓ vasoconstriction)
D. ↓ aldosterone release |
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What is the major difference between ACE inhibitors & AT-II receptor inhibitors?
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- ACE Inhibitors = ↑ bradykinin
- AT-II receptor inhibitors = ↓ aldosterone release |
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What are the major adverse effects of ACE inhibitors & AT-II receptor inhibitors?
A. hypokalemia B. sedation C. reflex tachycardia D. fetotoxic |
D. fetotoxic
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What AHDs should be avoided during pregnancy?
(select all) A. ACE inhibitors B. β-blockers C. Verapamil D. AT-II receptor inhibitors |
A. ACE inhibitors
D. AT-II receptor inhibitors |
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What are the 5 categories of diuretics?
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1. Carbonic Anhydrase Inhibitors
2. Loop 3. Thiazides 4. Osmotic 5. K⁺ sparing (Na⁺ channel inhibitors & Aldosterone antagonists) |
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Name an example of a CA-Inhibitor diuretic
A. furosemide B. hydrochlorothiazide C. spironolactone D. acetazolamide E. amiloride |
D. acetazolamide
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Name an example of a Loop diuretic
A. furosemide B. hydrochlorothiazide C. spironolactone D. acetazolamide E. amiloride F. mannitol |
A. furosemide
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Name an example of a thiazide diuretic
A. furosemide B. hydrochlorothiazide C. spironolactone D. acetazolamide E. amiloride F. mannitol |
B. hydrochlorothiazide
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Name an example of a Na⁺ Channel Inhibitor diuretic (K⁺ sparing)
A. furosemide B. hydrochlorothiazide C. spironolactone D. acetazolamide E. amiloride F. mannitol |
E. amiloride
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Name an example of a aldosterone antagonist diuretic (K⁺ sparing)
A. furosemide B. hydrochlorothiazide C. spironolactone D. acetazolamide E. amiloride F. mannitol |
C. spironolactone
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Name an example of an osmotic diuretic
A. furosemide B. hydrochlorothiazide C. spironolactone D. acetazolamide E. amiloride F. mannitol |
F. mannitol
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Which diuretic's mechanism of action inhibits the Na⁺-K⁺-2Cl⁻ symport?
A. CA-Inhibitor B. Loop C. Thiazide D. Na⁺ channel inhibitor E. aldosterone antagonist |
B. loop
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Which diuretic's mechanism of action inhibits the Na⁺-Cl⁻ symport?
A. CA-Inhibitor B. Loop C. Thiazide D. Na⁺ channel inhibitor E. aldosterone antagonist |
C. thiazide
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T/F
CA-inhibitors inhibit carbonate excretion and proton reabsorption. |
False
(inhibit carbonate REABSORPTION and proton EXCRETION) (↓ carbonate reabsorption = ↓ Na⁺ reabsorption = ↓ water reabsorption) |
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Osmotic diuretics inhibit reabsorption of water by osmotic force. They also expand volume of extracellular compartment and may increase heart burden.
A. The first statement is true, the second statement is false. B. The first statement is false, the second statement is true C. Both statements are true D. Both statements are false |
C. both statements are true
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T/F
Furosemide and ethacrynic acid (loop diuretics) are sulfonamide derivatives |
False
- Furosemide = sulfonamide - ethacrynic acid = non-sulfondamide |
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Where do Loop diuretics act?
A. proximal tubule B. thin descending limb C. thick ascending limb D. distal tubule E. collecting duct |
C. thick ascending limb
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Which ions do loop diuretics prevent the reabsorption of?
(select all) A. Na⁺ B. K⁺ C. Cl⁻ D. Mg²⁺ E. Ca²⁺ |
A. Na⁺
B. K⁺ C. Cl⁻ D. Mg²⁺ E. Ca²⁺ |
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Where do thiazide diuretics act?
A. proximal tubule B. thin descending limb C. thick ascending limb D. distal tubule E. collecting duct |
D. distal tubule
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Which ions do thiazide diuretics prevent the reabsorption of?
(select all) A. Na⁺ B. K⁺ C. Cl⁻ D. Mg²⁺ E. Ca²⁺ |
A. Na⁺
C. Cl⁻ |
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What is the major side effect of Na⁺ channel inhibitors & aldosterone antagonsits?
A. hyponatremia B. hyperkalemia C. hypocalcemia D. hypokalemia |
B. hyperkalemia
(Na⁺ not reabsorbed, so K⁺ not excreted) |
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What is the key role of angiotensin?
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Stimulates release of aldosterone
↓ Increased Na⁺ retention ↓ Increased BP |
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Which drugs control blood volume?
(select all) A. ACE Inhibitors B. diuretics C. Inotropics D. β-blockers |
A. ACE Inhibitors
B. diuretics |
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Which drugs control cardiac contractility?
(select all) A. ACE Inhibitors B. diuretics C. Inotropics D. β-blockers |
C. Inotropics
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Why is control of volume and afterload one key to controlling symptoms of CHF?
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↑ afterload causes ↓ CO, which ↑ afterload more (vicious spiral)
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What is the major adverse side effect of loop diuretics & thiazides?
A. hyponatremia B. hyperkalemia C. hypocalcemia D. hypokalemia |
D. hypokalemia
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Which drugs are inotropic agents?
(select all) A. furosemide B. digoxin C. milrinone D. dobutamine |
B. digoxin (glycoside)
C. milrinone (PDE-III inhibitor) D. dobutamine (β1 agonist) |
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What are the 4 classes of antiarrhythmic agents?
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1. Na⁺ channel blockers
2. β-blockers 3. prolong refractory period 4. Ca⁺ channel blockers |
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What is the major side effect of overdosing of antiarrhythmic agents?
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arrhythmia
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What do Group I antiarrhythmic agents treat?
A. ventricular tachycardia B. supraventricular tachycardia C. ventricular bradycardia D. supraventricular bradycardia |
A. ventricular tachycardia
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What do Group II antiarrhythmic agents treat?
A. ventricular tachycardia B. supraventricular tachycardia C. ventricular bradycardia D. supraventricular bradycardia |
B. supraventricular tachycardia
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What do Group III antiarrhythmic agents treat?
A. ventricular tachycardia B. supraventricular tachycardia C. ventricular bradycardia D. supraventricular bradycardia |
A. ventricular tachycardia
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What do Group IV antiarrhythmic agents treat?
A. ventricular tachycardia B. supraventricular tachycardia C. ventricular bradycardia D. supraventricular bradycardia |
B. supraventricular tachycardia
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Quinidine, procainamide, lidocaine, and phenytoin are ____ antiarrhytmic drugs.
A. Class I B. Class II C. Class III D. Class IV |
A. Class I
(Na⁺ channel blockers) |
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Propranolol is a ____ antiarrhytmic drug.
A. Class I B. Class II C. Class III D. Class IV |
B. Class II
(β-blockers) |
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Verapamil is a ____ antiarrhytmic drug.
A. Class I B. Class II C. Class III D. Class IV |
D. Class IV
(Ca²⁺ channel blockers) |
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What are the 3 types of anti-angina agents?
|
1. Nitrates/nitrites
2. Ca²⁺ channel blockers 3. β-blockers |
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Which of the following drugs are nitrates/nitrites that treat angina?
(select all) A. verapamil B. propranolol C. nitroglycerin D. nifedipine |
C. nitroglycerin
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Which of the following drugs are Ca²⁺ channel blockers that treat angina?
(select all) A. verapamil B. propranolol C. nitroglycerin D. nifedipine |
A. verapamil
D. nifedipine |
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Which of the following drugs are β-blockers that treat angina?
(select all) A. verapamil B. propranolol C. nitroglycerin D. nifedipine |
B. propranolol
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Restore O₂ supply-demand balance through redistribution of coronary flow, ↓ in preload, afterload, and TPR.
This describes what class of anti-angina drugs? A. Nitrates/nitrites B. Ca²⁺ channel blockers C. β-blockers D. Na⁺ channel blockers |
A. nitrates/nitrites
- vasodilation - ↓ TPR - ↓ afterload - venodilation - ↓ preload - redistribution of coronary flow (to larger coronary vessels) - ↑ blood to ischemic areas |
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Reduces cardiac contractility and HR by antagonizing β-effects of endogenous catecholamines, thus resulting in ↓ myocardial O₂ consumption.
This describes what class of anti-angina drugs? A. Nitrates/nitrites B. Ca²⁺ channel blockers C. β-blockers D. Na⁺ channel blockers |
C. β-blockers
- ↓ sympathetic stimulation - ↓ heart action - ↓ afterload - ↑ O₂ supply |
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Reduce cardiac contractility and HR by blocking Ca²⁺ channels, thus resulting in ↓ contractility & afterload and thereby ↓ O₂ demand of the heart.
This describes what class of anti-angina drugs? A. Nitrates/nitrites B. Ca²⁺ channel blockers C. β-blockers D. Na⁺ channel blockers |
B. Ca²⁺ channel blockers
- ↓ Ca into cell - ↓ contraction (vasodilation) - ↓ TPR - ↓ afterload - ↑ O₂ supply |
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Where in the body is histamine found in high concentrations?
(select all) A. brain B. gut C. skin D. lungs |
A. brain
B. gut C. skin D. lungs |
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What are the main cell types that contain histamine?
(select all) A. epithelial B. mast cells C. neurons D. mucosal cells E. enterochromaffin-like cells F. parietal cells |
B. mast cells
C. neurons E. enterochromaffin-like cells |
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Describe the major effects of histamine on the following tissues:
- Lungs - Vascular smooth muscle - Vascular endothelial cells - Nerves - Stomach - CNS |
- Lungs = bronchoconstriction
- Vascular smooth muscle = vasodilation Vascular endothelial cells = ↑ permeability (edema) - Nerves = itchiness/pain - Stomach = ↑ acid secretion - CNS = wakefullness, emesis |
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Where are H1 receptors located?
A. CNS B. Vascular smooth muscle C. Stomach D. Nerves E. Vascular endothelial cells F. Lungs |
B. Vascular smooth muscle
D. Nerves E. Vascular endothelial cells F. Lungs |
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Where are H2 receptors located?
A. Lungs B. Vascular smooth muscle C. Vascular endothelial cells D. Nerves E. Stomach F. CNS |
E. stomach
(also in heart) |
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Where are H3 receptors located?
A. Lungs B. Vascular smooth muscle C. Vascular endothelial cells D. Nerves E. Stomach F. CNS |
F. CNS
(act as neurotransmitter) |
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What are 2 drugs that indirectly counteract histamine?
A. Diphenhydramine B. cromolyn C. ranitidine D. Epi E. NE |
B. cromoylin
D. Epi |
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What is cromolyn's anti-histamine action?
A. counteracts histamine's physiological activity B. histamine receptor antagonist C. prevents mast cell degranulation D. all of the above |
C. prevents mast cell degranulation
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What is Epi's anti-histamine action?
A. counteracts histamine's physiological activity B. histamine receptor antagonist C. prevents mast cell degranulation D. all of the above |
A. counteracts histamine's physiological activity
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What is diphenhydramine's anti-histamine action?
A. counteracts histamine's physiological activity B. histamine receptor antagonist C. prevents mast cell degranulation D. all of the above |
B. histamine receptor antagonist
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What are 2 drugs that directly counteract histamine?
A. Diphenhydramine B. cromolyn C. ranitidine D. Epi E. NE |
A. Diphenhydramine
C. ranitidine |
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What is the major difference in the side effects of 1st & 2nd generation H1 antagonists?
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1st generation = sedation, anti-emetic
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What is the main use of H2 antagonists?
|
↓ stomach acid secretion
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T/F
Asthma is an acute inflammatory disease of the airways |
False
(it is CHRONIC) |
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How do β-agonists treat asthma?
A. stimulate adenylyl cyclase to ↑ cAMP, which leads to bronchodilation B. inhibits the action of inflammatory cytokines C. Inhibits phosphodiesterase to ↑ cAMP, which causes bronchodilation D. Inhibits Ach to prevent bronchoconstriction E. Blocks Cl⁻ & Ca²⁺ channels in mast cell to prevent degranulation F. Inhibit 5-lipoxygenase on arachidonica acid, or blocks leukotriene D4 receptors |
A. stimulate adenylyl cyclase to ↑ cAMP, which leads to bronchodilation
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How do inhaled corticosteroids treat asthma?
A. stimulate adenylyl cyclase to ↑ cAMP, which leads to bronchodilation B. inhibits the action of inflammatory cytokines C. Inhibits phosphodiesterase to ↑ cAMP, which causes bronchodilation D. Inhibits Ach to prevent bronchoconstriction E. Blocks Cl⁻ & Ca²⁺ channels in mast cell to prevent degranulation F. Inhibit 5-lipoxygenase on arachidonica acid, or blocks leukotriene D4 receptors |
B. inhibits the action of inflammatory cytokines
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How does theophylline treat asthma?
A. stimulate adenylyl cyclase to ↑ cAMP, which leads to bronchodilation B. inhibits the action of inflammatory cytokines C. Inhibits phosphodiesterase to ↑ cAMP, which causes bronchodilation D. Inhibits Ach to prevent bronchoconstriction E. Blocks Cl⁻ & Ca²⁺ channels in mast cell to prevent degranulation F. Inhibit 5-lipoxygenase on arachidonica acid, or blocks leukotriene D4 receptors |
C. Inhibits phosphodiesterase to ↑ cAMP, which causes bronchodilation
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How does cromolyn treat asthma?
A. stimulate adenylyl cyclase to ↑ cAMP, which leads to bronchodilation B. inhibits the action of inflammatory cytokines C. Inhibits phosphodiesterase to ↑ cAMP, which causes bronchodilation D. Inhibits Ach to prevent bronchoconstriction E. Blocks Cl⁻ & Ca²⁺ channels in mast cell to prevent degranulation F. Inhibit 5-lipoxygenase on arachidonica acid, or blocks leukotriene D4 receptors |
E. Blocks Cl⁻ & Ca²⁺ channels in mast cell to prevent degranulation
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How do anti-muscarinic agents treat asthma?
A. stimulate adenylyl cyclase to ↑ cAMP, which leads to bronchodilation B. inhibits the action of inflammatory cytokines C. Inhibits phosphodiesterase to ↑ cAMP, which causes bronchodilation D. Inhibits Ach to prevent bronchoconstriction E. Blocks Cl⁻ & Ca²⁺ channels in mast cell to prevent degranulation F. Inhibit 5-lipoxygenase on arachidonica acid, or blocks leukotriene D4 receptors |
D. Inhibits Ach to prevent bronchoconstriction
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How do leukotriene inhibitors treat asthma?
(select all) A. block receptors B. block release C. block synthesis D. block storage |
A. block (D4) receptors
C. block synthesis (inhibit 5-lipoxygenase on arachidonic acid) - both prevent bronchoconstriction, bronchial reactivity, mucosal edema, and mucus secretion |
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What are the 2 main side effects of β-agonsts?
|
1. tremor
2. tachycardia |
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T/F
Cromolyn & nedocromil have NO bronchodilator or antihistamine activity |
True
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NSAIDs are:
(select all) A. antipyretic B. anti-inflammatory C. analgesic |
A. antipyretic (↓ temperature)
B. anti-inflammatory C. analgesic (↓ pain) |
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Acetaminophen is:
(select all) A. antipyretic B. anti-inflammatory C. analgesic |
A. antipyretic
C. analgesic (NOT anti-inflammatory) |
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Inhibition of ____ causes gastric distress
A. COX-1 B. COX-2 C. COX-3 D. All of the Above |
A. COX-1
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NSAIDS inhibit:
(select all) A. COX-1 B. COX-2 C. COX-3 |
A. COX-1
B. COX-2 |
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NSAIDs are metabolized by:
A. kidney B. albumin C. liver D. stomach |
C. liver
(CYP3A of cytochrom P450) |
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T/F
Aspirin gets metabolized into Acetic acid & salicylic acid |
False
Aspirin → acetic acid + SALICYLATE (Salicylate is converted into salicylic acid) |
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T/F
Acetaminophen toxicity is due to of N-acetyl-p-benzoquinone imine not being inactivated by glutathione |
True
|
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How does Allopurinol treat gout?
A. ↑ uric acid excretion B. inhibits leukocyte migration into joints C. inhibit xanthine oxidase to ↓ uric acid |
C. inhibit xanthine oxidase to ↓ uric acid
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How does colchicine treat gout?
A. ↑ uric acid excretion B. inhibits leukocyte migration into joints C. inhibit xanthine oxidase to ↓ uric acid |
B. inhibits leukocyte migration into joints
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How do uricosuric agents treat gout?
A. ↑ uric acid excretion B. inhibits leukocyte migration into joints C. inhibit xanthine oxidase to ↓ uric acid |
A. ↑ uric acid excretion
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T/F
NSAIDs and DMARDs stop the progress of arthritis. |
False
- NSAIDs = DON'T stop progress – just reduce symptoms - DMARDs = DO stop progress |
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How are immunosuppressant drugs used to treat arthritis?
(select all) A. inhibit IL-2 B. inhibit DNA synthesis C. Inhibit cytokine gene expression D. scavenge toxic O₂ metabolites produced by neutrophils E. bind & inhibit TNFα |
A. inhibit IL-2
B. inhibit DNA synthesis C. Inhibit cytokine gene expression |
