Pharmaco5_Tuft Flashcards
administration of ganglionic blocking agents will result in
• miosis
• diarrhea
• copious salivation
• orthoststic hypotension
• enhance activity of the parasympathetic nervous system
orthoststic hypotension
tachycardia in a patient administered with atropine or scopolamine results from?
• release of adrenal catecholamines
• blockade of vegus nerve activity
• blockade of the nicotinic cholinergic receptor
• stimulation of the alpha adrenergic receptor
• stimulation of the beta adrenergic receptor
blockade of vegus nerve activity - atropine and scopolamine are muscarinic cholinergic receptor blockers. Any sudden increase in heart rate usually stimulates baroreceptors to send a signal to the vagus nerve to stimulate the heart to slow it back down. This reflex is cholinergically mediated, and will be blocked by cholinergic blockers such as atropine. Even when given in the absence of higher than normal HR, atropine will block the normal cholinergic control over the heart, leaving the sympathetic system in charge with a resulting tachycardia
a paralyzing dose of succinylcholine initially alicits • CNS stimulation • CNS depression • decreased salivation • muscle fasiculation • extrapyramidal reactions
muscle fasciculation (involuntary muscle contraction and relaxation which may be visible under the skin)
based on its known mechanism and sites of action, scopolamine should theoretically be useful in
• treatment of peptic ulcer
• providing euphoria and amnesia prior to surgery
• relieving bronchoconstriction
• relieving some of the symptoms of Parkinson’s disease
• visualization of the retina
all of them
symptoms of poisoning by an organophosphate onsecticide include all of the following except • skeletal muscle fasciculation • excessive salivation • bronchoconstriction • hot, dry skin • diarrhea
hot, dry skin
all of the following symptoms are associated with neostigmine poisoning except • diarrhea • salivation • convulsion • bronchiolar constriction • skeletel muscle paralysis
skeletel muscle paralysis
symptoms of atropin poisoning in man include • decreased intraocular pressure • burning dry mouth • nausea, vomiting and diarrhea • hyperthermia • orthostatic hypotension
• burning dry mouth
• hyperthermia
“the most likely sign is CNS excitation and tachycardia”
Disorientation, confusion, and hallucinations resulting from an overdose of scopolamine are most efficaciously treated by administering
a. atropine
b. levodopa
c. acetylcholine
d. physostigmine
physostigmine
the immediate cause of death from irreversible cholinesterase inhibitors is • shock • convulsion • cardiac arrhythmia • respiratory paralysis • dehydration from vomiting and diarrhea
respiratory paralysis which results from the stimulation of nicotinic receptors at the neuromuscular junction resulting in paralysis of skeletal muscles
each of the following is a symptom of cholinergic crisis except • bradycardia • lacrimation • vasoconstriction • extreme salivation • weakness of voluntary muscles
vasoconstriction
- alpha1 stimulation
- beta 1 stimulation
- beta 2 stimulation
- alpha1 block
- beta 1 block
- beta 2 block
- alpha1 stimulation: vasoconstriction, urinary retention, mydriasis
- beta 1 stimulation:increased heart rate
- beta 2 stimulation:brochodilation, vasodilation
- alpha1 block: vasodilation
- beta 1 block: decreased heart rate
- beta 2 block: bronchoconstriction
a mechanism for the antiadrenergic action of guanethidine is
• inhibition of dopa decarboxylase
• increased rate of metabolism of NE
• depletion of NE from the nerve terminals
• substitution for NE and subsequent action as a false transmitter
• uncoupling of the action potential from the NE release mechanism
uncoupling of the action potential from the NE release mechanism (inhibits the release of catecholamine)
which of the following statements most accurately describes the effectiveness of action of methyldopa?
• it causes marked cardiac slowing
• it directly relaxes vascular smooth muscle
• it causes rapid depletion of NE from adrenergic nerve terminals
• it causes formation of a false transmitter which is released at vascular smooth muscle
• it produces a false transmitter, the effect of which is primarily at central nuclei
it produces a false transmitter, the effect of which is primarily at central nuclei (thus decreasing sympathetic activity)
the mechanism of action of reserpine is to
• inhibit monoamine oxidase
• inhibit catechole-O-methyltransferase
• block the passage of the nerve action potential in the postgalglionic nerve fibers
• stabilize the axon terminal membrane thus preventing release of NE
stabilize the axon terminal membrane thus preventing release of NE (depletes NE by inhibiting reuptake)
amphetamine acts by
• promoting storage of the mediator
• causing a rapid release of the mediator
• causing a slow depletion of the mediator
• combining with a receptor substance on the effector cell
• interfering with the response of the receptor to the mediator
causing a rapid release of the mediator (it is a indirect acting drug like tyramine and ephedrine stimulating the release of stored NE)
