Apex Unit 2 ANS Flashcards
Match each chemical signal with the type of receptor to which it binds.
Acetylcholine at neuromuscular junction
Insulin at skeletal muscle
Norepinephrine at vascular smooth muscle
Ion channel
G-protein coupled receptor
Tyrosine kinase linked receptor
Acetylcholine at neuromuscular junction + Ion channel
Norepinephrine at vascular smooth muscle + G-protein coupled receptor
Insulin at skeletal muscle + Tyrosine kinase linked receptor
Signal transduction is the process by which a cell converts an extracellular signal into an intracellular response.
There are 4 categories of signal transduction mechanisms:
Ion channels
G-protein coupled receptors
Enzyme linked receptors
Intracellular receptors
Let’s explore each of these in greater detail.
All of the following are examples of second messengers EXCEPT: inositol triphosphate. glutamate. cyclic adenosine monophosphate. calcium.
Glutamate
First messengers are extracellular chemicals (neurotransmitters, hormones, or drugs) that stimulate a receptor. Second messengers are intracellular chemicals (usually enzymes) that instruct the cell to do something.
Glutamate is the first messenger for the NMDA receptor.
Calcium, cyclic adenosine monophosphate, and inositol triphosphate are second messengers.
Stimulation of which receptors increases phospholipase C? (Select 2.) Vasopressin-1 Alpha-1 Muscarinic-2 Beta-1
Alpha-1
Vasopressin-1
Alpha-1 and vasopressin-1 stimulation increases phospholipase C.
Beta-1 stimulation increases adenylate cyclase.
Muscarinic-2 receptor decreases adenylate cyclase.
Match each receptor with its physiologic action.
α2
β1
β2
M3
Bronchoconstriction
Increased automaticity
Skeletal muscle vasodilation
Diuresis
α2 + Diuresis
β1 + Increased automaticity
β2 + Skeletal muscle vasodilation
M3 + Bronchoconstriction
Match each receptor with its physiologic action.
M
α1
α2
β2
Mydriasis
Decreased insulin release
Increased insulin release
Miosis
M + Miosis
α1 + Mydriasis
α2 + Decreased insulin release
β2 + Increased insulin release
Stimulation of the alpha-2 receptor reduces: (Select 2.) sympathetic tone. shivering. platelet aggregation. serum glucose.
Shivering
Sympathetic tone
Hopefully you already know that alpha-2 receptor stimulation reduces SNS outflow and produces sedation, hypnosis, and analgesia.
In addition to these effects, alpha-2 receptor stimulation also:
Produces an antishivering effect
Depresses level of consciousness
Inhibits insulin release → hyperglycemia (not hypoglycemia)
Promotes (not inhibits) platelet aggregation
Which enzyme metabolizes cyclic adenosine monophosphate? Protein kinase A Phospholipase C Phosphodiesterase III Adenylate cyclase
Phosphodiesterase III
Adenylate cyclase is an effector that converts ATP to cAMP (the second messenger).
cAMP activates protein kinase A, which initiates a variety of phosphorylation reactions inside the cell.
Phosphodiesterase III essentially “turns off” cAMP by metabolizing it to AMP.
We know this is confusing stuff. The explanation on the next page will bring all of this into focus.
Select the true statements regarding norepinephrine synthesis and release. (Select 2.)
Tyrosine hydroxylase catalyzes the rate limiting step in norepinephrine synthesis.
The adrenal medulla releases 80% norepinephrine and 20% epinephrine.
Norepinephrine in the synaptic cleft inhibits its release.
Norepinephrine is converted to epinephrine in sympathetic post-ganglionic nerves.
Tyrosine hydroxylase catalyzes the rate limiting step in norepinephrine synthesis.
Norepinephrine in the synaptic cleft inhibits its own release.
What was wrong with the other answer choices?
Norepinephrine is converted to epinephrine in the adrenal medulla (not in sympathetic post-ganglionic nerves).
The adrenal medulla releases 80% epinephrine and 20% norepinephrine (the answer choice was reversed).
What is the PRIMARY mechanism for the termination of action of norepinephrine in the synaptic cleft?
Monoamine oxidase
Diffusion
Catechol-O-methyltransferase
Reuptake
Reuptake
Approximately 80% of the NE released into the synaptic cleft undergoes reuptake into the presynaptic neuron. This explains why reuptake is the primary mechanism of NE’s termination of action.
Most of the NE that doesn’t undergo reuptake diffuses into the systemic circulation, where it is subject to metabolism by COMT and MAO in the liver and kidneys. Additionally, a small amount of NE undergoes reuptake into extraneural tissue.
What is the end product of norepinephrine metabolism? Normetanephrine Vanillylmandelic acid Metanephrine Tyrosine
Vanillylmandelic acid
Metabolites of norepinephrine:
Intermediate: metanephrine and normetanephrine
Final end product: vanillylmandelic acid
Tyrosine is a precursor of NE synthesis.
Select the true statements regarding acetylcholine. (Select 3.)
Hypomagnesemia decreases acetylcholine release from the presynaptic nerve.
It stimulates N-type cholinergic receptors in the sympathetic ganglia.
Pseudocholinesterase hydrolyzes acetylcholine in the synaptic cleft.
Coenzyme A is produced in the mitochondria.
Acetate is a metabolite of acetylcholine metabolism.
Reuptake is the primary mechanism for acetylcholine’s termination of action.
Ach stimulates N-type cholinergic receptors in the sympathetic ganglia.
Acetate is a metabolite of acetylcholine metabolism.
Coenzyme A is produced in the mitochondria.
What was wrong with the other answer choices?
Acetylcholinesterase (not pseudocholinesterase) hydrolyzes acetylcholine in the synaptic cleft.
Hypermagnesemia (not hypomagnesemia) decreases acetylcholine release from the presynaptic nerve.
Metabolism (not reuptake) is the primary mechanism for acetylcholine’s termination of action.
Preganglionic nerve fibers in the sympathetic nervous system are: myelinated B-fibers. unmyelinated C-fibers. myelinated C-fibers. unmyelinated B-fibers.
Myelinated B-fibers
The efferent limb of the ANS reflex arc consists of 2 nerve fibers:
Preganglionic fiber = myelinated B-fiber
Postganglionic fiber = unmyelinated C-fiber
Which statements BEST characterize the architecture of the parasympathetic nervous system? (Select 3.)
Postganglionic fibers release acetylcholine
Myelinated postganglionic fibers
Synapse in the stellate ganglion
Short postganglionic fibers
Post- to preganglionic nerve ratio of 30 : 1
Cell bodies arise from S2 – S4
Cell bodies arise from S2-S4
Short postganglionic fibers
Postganglionic fibers release acetylcholine
What was wrong with the other answer choices?
The SNS (not PNS) has a post- to preganglionic nerve ratio of 30:1.
The stellate ganglion is part of the SNS (not PNS).
Autonomic postganglionic fibers are unmyelinated (not myelinated).
Click on the white ramus.
In the sympathetic nervous system, the preganglionic sympathetic fibers exit the spinal cord via the ventral nerve roots of the spinal nerves. These fibers enter the sympathetic chain by way of the white communicating rami.
Sympathetic nerves that directly innervate the adrenal medulla are: B-fibers that release norepinephrine. B-fibers that release acetylcholine. C-fibers that release norepinephrine. C-fibers that release acetylcholine.
B-fibers that release acetylcholine
There are no ganglia between the spinal cord and the adrenal medulla. In essence, the adrenal medulla is directly innervated by a “preganglionic” nerve (myelinated B-fiber).
Stimulation of which receptors results in a transcellular potassium shift?
Alpha-1
Alpha-2
Beta-1
Beta-2
Beta-2
Stimulation of the beta-2 receptor drives potassium into cells. This explains why drugs like albuterol produce hypokalemia.
Which surgical procedures are MOST likely to activate the baroreceptor reflex? (Select 2.)
Cesarean section
Carotid endarterectomy
Mediastinoscopy
Strabismus repair
Carotid endarterectomy
Mediastinoscopy
Mechanical stimulation of the baroreceptors in the carotid sinus and transverse aortic arch can activate the baroreceptor reflex (bradycardia + hypotension).
Surgical procedures that might elicit this response include:
Carotid endarterectomy / stenting
Mediastinoscopy
There are a variety of other surgical procedures that can predictably activate other cardiovascular reflexes:
Strabismus repair can evoke the oculocardiac reflex.
Cesarean section requires neuraxial blockade to ~ T4. This inhibits the cardioaccelerator nerves (increased vagal tone).
Which drugs are MOST likely to impair the integrity of the baroreceptor reflex. (Select 3.)
Norepinephrine Hydralazine Labetalol Thiopental Propofol Sevoflurane
Propofol
Sevoflurane
Labetalol
Preservation of the baroreceptor reflex means that the heart rate will adjust appropriately when the blood pressure changes. Hypotension increases the heart rate, while hypertension reduces the heart rate.
Drugs that decrease BP and increase HR (BRR is preserved):
Hydralazine
Thiopental
Drugs that increase BP and decrease HR (BRR is preserved):
Norepinephrine
Drugs that decrease BP and HR (BRR is inhibited):
Labetalol
Sevoflurane
Drugs with variable response (HR can increase, decrease, stay the same, or even stop entirely):
Propofol
Activation of the Bezold-Jarisch reflex manifests as: (Select 3.) hypotension. coronary artery vasoconstriction. hypertension. coronary artery vasodilation. tachycardia. bradycardia.
Bradycardia
Hypotension
Coronary artery vasodilation
The Bezold-Jarisch reflex slows the heart in the setting of profound hypovolemia. The idea is that the heart slows down to allow itself adequate time to fill.
Risk factors that contribute to the manifestation of the oculocardiac reflex include all of the following EXCEPT:
strabismus surgery.
retrobulbar block.
old age.
hypercarbia.
Old age
The oculocardiac reflex is otherwise known as the five & dime reflex.
Afferent limb = CN V (trigeminal nerve)
Efferent limb = CN X (vagus nerve)
The OCR is more likely to occur (or is made worse by) in the following situations:
Traction to the extraocular muscles (particularly the medial rectus)
Pressure on the eye or orbital tissue
Strabismus surgery (particularly in children)
Hypercarbia
Hypoxemia
Light anesthesia
Identify the BEST agents to augment the heart rate in the patient with a heart transplant. (Select 2.)
Isoproterenol
Epinephrine
Atropine
Phenylephrine
Isoproterenol
Epinephrine
The transplanted heart is severed from autonomic influence, so the heart rate is dependent on the intrinsic rate set by the SA node. Said another way, the transplanted heart is NOT under the influence of the vagus nerve or the cardiac accelerator fibers.
Direct acting agents (isoproterenol and epinephrine) may be used to augment the HR, while indirect acting agents (atropine and ephedrine) will be ineffective.
Phenylephrine can cause reflex bradycardia in the patient with an intact SNS. This would not be expected to occur in the patient with a denervated heart.
Which agent reduces coronary artery perfusion pressure the MOST?
Dopamine
Isoproterenol
Phenylephrine
Dobutamine
Isoproterenol
Isoproterenol is a synthetic catecholamine that stimulates beta-1 and beta-2 receptors.
Because of its potent beta-2 effect (vasodilation in skeletal muscle), SVR may fall significantly.
This reduces diastolic blood pressure, which can impair coronary perfusion pressure (CPP = AoDB - LVEDP).
Which beta blockers antagonize the alpha-1 receptor? (Select 2.) Atenolol Carvedilol Labetalol Propranolol
Labetalol
Carvedilol
Labetalol and carvedilol are mixed alpha and beta antagonists. In addition to their beta effects, these agents produce vasodilation via alpha-1 blockade.
Beta to alpha block ratios:
Labetalol = 7:1
Carvedilol = 10:1
Match each drug with its mechanism of action.
Phenoxybenzamine
Phentolamine
Prazosin
Phenoxybenzamine + Noncompetative and nonselective alpha antagonist
Phentolamine + Competitive and nonselective alpha antagonist
Prazosin + Competitive and selective alpha-1 antagonist
