PHM 146 Exam Questions And Answers
What are two different types of neuromuscular blockers? - Answer Non-depolarizing
groups (tubocurarine)
Depolarizing groups (succinylcholine)
What is the effect of non-depolarizing neuromuscular blockers? - Answer Antagonize
nicotinic receptors, prevent depolarization
What is the effect of depolarizing neuromuscular blockers? - Answer Activate nicotinic
receptors constantly, neuromuscular end plate can't recover.
Succinylcholine only broken down by plasma cholinesterases
What can reverse the effects of non-depolarizing drugs? - Answer High ACh release can
overcome the competitive inhibitor.
Cholinesterase inhibitors increase levels of ACh
Describe the phases of depolarizing drugs. - Answer *Phase I - Depolarizing*:
succinylcholine binds nicotinic receptor, causes it to open until broken down by plasma
cholinesterases. End plate is non-responsive to subsequent action potentials causing
flaccid paralysis
*Phase II - Desensitizing*: an un-excitable area develops around the motor end plate
What are the clinical uses of depolarizing drugs? - Answer Muscle relaxation for surgery
What are the adverse effects of depolarizing drugs? - Answer Hyperkalemia (increased
K+ in circulation could lead to cardiac arrest)
Increase in intraocular pressure (transient)
Increase in intragastric pressure
,Muscle pain
Malignant hyperthermia
What are toxins that affect the neuromuscular junction? - Answer Botulinum Toxin
(non-dep)
Bungarotoxins (non-dep)
Black Widow Spider Venom (latrotoxin) (dep)
Conium Alkaloids (dep)
Curare (non-dep)
What are the effects of botulinum toxin? What is it produced by? - Answer Prevents
prejunctional release of ACh, causes muscle weakness, respiratory paralysis, and
death.
Produced by Clostridium botulinum bacteria.
What are the uses of botulinum toxin? - Answer *Cosmetically*: induce local muscle
relaxation in certain areas
*Therapeutically*: Ocular conditions, hemifacial spasms, various dystonias, spasms,
certain dermatological abnormalities
What are the effects of bungarotoxins? What is it produced by? - Answer *Alpha
bungarotoxin* targets nicotinic receptor, produces a neuromuscular blockade.
*Beta bungarotoxin* induces rapid release of acetylcholine, depleting stores, also
inhibits choline transporter in presynaptic membrane.
Produced in *krait venom*
What are the effects of latrotoxin? What is it produced by? How is it treated? - Answer
Release of acetylcholine from motor neurons in neuromuscular junction - depletion of
ACh and depolarizing blockade.
Produced in black widow spider venom.
Treated symptomatically (pain medication, muscle relaxants)
, What are the effects of coniceine (conium alkaloid) toxicity? Where is it produced? -
Answer Stimulates nicotinic receptors (resembles nicotine).
Toxicity (resembles nicotine toxicity): CNS stimulation including headaches, ataxia,
sweating, salivation and tachycardia; prolonged toxicity - depressant stage that leads to
death.
Produced in *poison hemlock* plants
What are the effects of tubocurarine? - Answer Respiratory depression - activity at
nicotinic receptors in autonomic ganglia
Fall in blood pressure - release of histamine from mast cells
What are catecholamines?
Examples? - Answer Catecholamines are adrenergic receptor agonists that are subtype
specific.
(Noradrenaline, dopamine, adrenaline)
What are sympathomimetic drugs? - Answer Drugs that mimic the effects of
noradrenaline and adrenaline
How does signal transduction occur in α1 receptors? - Answer α1 receptors are coupled
to Gq. This stimulates phospholipase C (PLC) which leads to an increase in Ca2+,
resulting in mucle contraction.
How does signal transduction occur in α2 receptors? - Answer α2 receptors are coupled
to Gi. This inhibits AC and reduces cAMP levels.
how does signal tranduction occur in β receptors? - Answer β receptors are coupled to
Gs which stimulates AC and increases cAMP levels.
Where are α1 receptors found?
What are two different types of neuromuscular blockers? - Answer Non-depolarizing
groups (tubocurarine)
Depolarizing groups (succinylcholine)
What is the effect of non-depolarizing neuromuscular blockers? - Answer Antagonize
nicotinic receptors, prevent depolarization
What is the effect of depolarizing neuromuscular blockers? - Answer Activate nicotinic
receptors constantly, neuromuscular end plate can't recover.
Succinylcholine only broken down by plasma cholinesterases
What can reverse the effects of non-depolarizing drugs? - Answer High ACh release can
overcome the competitive inhibitor.
Cholinesterase inhibitors increase levels of ACh
Describe the phases of depolarizing drugs. - Answer *Phase I - Depolarizing*:
succinylcholine binds nicotinic receptor, causes it to open until broken down by plasma
cholinesterases. End plate is non-responsive to subsequent action potentials causing
flaccid paralysis
*Phase II - Desensitizing*: an un-excitable area develops around the motor end plate
What are the clinical uses of depolarizing drugs? - Answer Muscle relaxation for surgery
What are the adverse effects of depolarizing drugs? - Answer Hyperkalemia (increased
K+ in circulation could lead to cardiac arrest)
Increase in intraocular pressure (transient)
Increase in intragastric pressure
,Muscle pain
Malignant hyperthermia
What are toxins that affect the neuromuscular junction? - Answer Botulinum Toxin
(non-dep)
Bungarotoxins (non-dep)
Black Widow Spider Venom (latrotoxin) (dep)
Conium Alkaloids (dep)
Curare (non-dep)
What are the effects of botulinum toxin? What is it produced by? - Answer Prevents
prejunctional release of ACh, causes muscle weakness, respiratory paralysis, and
death.
Produced by Clostridium botulinum bacteria.
What are the uses of botulinum toxin? - Answer *Cosmetically*: induce local muscle
relaxation in certain areas
*Therapeutically*: Ocular conditions, hemifacial spasms, various dystonias, spasms,
certain dermatological abnormalities
What are the effects of bungarotoxins? What is it produced by? - Answer *Alpha
bungarotoxin* targets nicotinic receptor, produces a neuromuscular blockade.
*Beta bungarotoxin* induces rapid release of acetylcholine, depleting stores, also
inhibits choline transporter in presynaptic membrane.
Produced in *krait venom*
What are the effects of latrotoxin? What is it produced by? How is it treated? - Answer
Release of acetylcholine from motor neurons in neuromuscular junction - depletion of
ACh and depolarizing blockade.
Produced in black widow spider venom.
Treated symptomatically (pain medication, muscle relaxants)
, What are the effects of coniceine (conium alkaloid) toxicity? Where is it produced? -
Answer Stimulates nicotinic receptors (resembles nicotine).
Toxicity (resembles nicotine toxicity): CNS stimulation including headaches, ataxia,
sweating, salivation and tachycardia; prolonged toxicity - depressant stage that leads to
death.
Produced in *poison hemlock* plants
What are the effects of tubocurarine? - Answer Respiratory depression - activity at
nicotinic receptors in autonomic ganglia
Fall in blood pressure - release of histamine from mast cells
What are catecholamines?
Examples? - Answer Catecholamines are adrenergic receptor agonists that are subtype
specific.
(Noradrenaline, dopamine, adrenaline)
What are sympathomimetic drugs? - Answer Drugs that mimic the effects of
noradrenaline and adrenaline
How does signal transduction occur in α1 receptors? - Answer α1 receptors are coupled
to Gq. This stimulates phospholipase C (PLC) which leads to an increase in Ca2+,
resulting in mucle contraction.
How does signal transduction occur in α2 receptors? - Answer α2 receptors are coupled
to Gi. This inhibits AC and reduces cAMP levels.
how does signal tranduction occur in β receptors? - Answer β receptors are coupled to
Gs which stimulates AC and increases cAMP levels.
Where are α1 receptors found?
