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APEX Study Guide > Unit 2: ANS > Flashcards

Unit 2: ANS Flashcards

1
Q

What are the four classifications of receptors?

A
  • Ion channel
  • G protein coupled receptor
  • Enzyme linked receptor
  • Intracellular receptor
  • receptor receives the signal and instructs the cell to perform a specific function
  • signal transduction = cell converts this extracellular signal into an intracellular response
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2
Q

What is the general architecture of the G protein second messenger system?

A
  • 1st messenger (extracellular signal)
  • Receptor (responds to extracellular signal)
  • G protein (turns on or off an effector)
  • Effector (activates or inhibits 2nd messenger)
  • 2nd messenger (primary intracellular signal)
  • Enzymatic cascade
  • Cellular response (causes physiologic change)

*2nd messengers are tissue specific

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3
Q

What 2nd messenger system is associated with the alpha-1 receptor? What other receptors share a similar pathway?

A

Alpha-1 Gq -> stimulates Phospholipase C production -> IP3, Calcium, DAG

Others that share similar pathway:

  • Histamine-1
  • Muscarinic-1
  • Muscarinic-3
  • Muscarinic-5
  • Vasopressin-1 (vascular)
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4
Q

What 2nd messenger system is associated with the alpha-2 receptor? What other receptors share a similar pathway?

A

Alpha-2 Gi -> inhibits Adenylate Cyclase -> ATP, cAMP

Others that share similar pathway:

  • Muscarinic-2
  • Dopamine-2 (presynaptic)
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5
Q

What 2nd messenger system is associated with the beta-1 AND beta-2 receptor? What other receptors share a similar pathway?

A

Beta-1 and Beta-2 Gs -> stimulate Adenylate Cyclase -> ATP, cAMP

Others that share similar pathway:

  • Histamine-2
  • Vasopressin-2 (renal)
  • Dopamine-1 (postsynaptic)
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6
Q

Describe the autonomic innervation of the heart

A

SNS: cardiac accelerator fibers arise from T1-T4
PNS: vagus nerve

Myocardium: beta-1 increases contractility – M2 decreases contractility
Conduction System: beta-1 increases HR and conduction speed – M2 decreases HR and CV

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7
Q

Describe the autonomic innervation of the vasculature

A
  • Arteries: alpha-1 > alpha-2 –> vasoconstriction
  • Veins: alpha-2 > alpha-1 –> vasoconstriction
  • Myocardium: beta-2 –> vasodilation
  • Skeletal muscle: beta-2 –> vasodilation
  • Renal: dopamine –> vasodilation
  • Mesenteric: dopamine –> vasodilation
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8
Q

Describe the autonomic innervation of the bronchial tree

A

beta-2 receptors are not innervated – instead they respond to catecholamines in the systemic circulation or in the airway (inhaled)

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9
Q

Describe the autonomic innervation of the kidney

A

Renal Tubules: alpha-2 –> diuresis (ADH inhibition)

Renin Release: beta-1 –> increased renin release

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10
Q

Describe the autonomic innervation of the eye

A

Sphincter Muscle (iris): muscarinic –> contraction (miosis)

Radical Muscle (iris): alpha-1 –> contraction (mydriasis)

Ciliary Muscle: beta-2 –> relaxation (far vision) – muscarinic –> contraction (near vision)

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11
Q

Describe the autonomic innervation of the GI tract

A

Sphincters: alpha-1 –> contraction – muscarinic –> relaxation
Motility & Tone: alpha-1, alpha-2, beta-1, beta-2 –> decreases – muscarinic –> increases
Salivary Glands: alpha-2 –> decreases – muscarinic –> increases
Gallbladder & Ducts: beta-2 –> relaxation – muscarinic –> contraction

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12
Q

Describe the autonomic innervation of the pancreas

A

Islet (beta cells):

  • alpha-2 –> decreases insulin release
  • beta-2 –> increases insulin release
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13
Q

Describe the autonomic innervation of the bladder

A

Trigone & Sphincter:

  • alpha-1 –> contraction
  • muscarinic –> relaxation

Detrusor:

  • beta-2 –> relaxation
  • muscarinic –> contraction
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14
Q

What are the steps of norepinephrine synthesis? What is the rate limiting step?

A
  • Tyrosine –> DOPA via Tyrosine Hydroxylase (rate limiting step)
  • DOPA –> Dopamine via DOPA decarboxylase
  • Dopamine –> Norepinephrine via Dopamine B-hydroxylase

*norepi –> epi via phenylethanolamine N-methyltransferase in the adrenal medulla

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15
Q

What are the three ways that Norepi can be removed from the synaptic cleft? Which is the most important?

A
  • Reuptake into presynaptic neuron (accounts for 80%)
  • Diffusion away from synaptic cleft
  • Reuptake by extraneural tissue
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16
Q

What enzymes metabolize Norepi and Epi? What is the final metabolic byproduct?

A
  • Monoamine Oxidase (MAO)
  • Catechol-O-methyltransferase (COMT)

-final byproduct = vanillylmandelic acid (VMA)

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17
Q

What are the three types of cholinergic receptors? Where are each found in the body?

A

1.Nicotinic Type M (muscle):
- neuromuscular junction

2.Nicotinic Type N (nerve):
- preganglionic fibers at autonomic ganglia (SNS & PNS)
- CNS

3.Muscarinic:
- postganglionic PNS fibers at effector organs
- CNS (M1,3,5 activates Phospholipase C; M2,4 inhibits Adenylyl Cyclase)

** Nicotinic = ion channel
** Muscarinic = G-protein coupled

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18
Q

How is Acetylcholine synthesized, released, and metabolized?

A

Synthesized in pre-synaptic nerve terminal – Acetyl Coenzyme A + Choline –(ChAT)–> Acetylchoine + Coenzyme A + H2O

Released after an action potential acts on the preganglionic neuron

Metabolized by Acetylcholinesterase into Acetate and Choline

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19
Q

What are the five components of the autonomic reflex arc?

A

Sensor –> Afferent Pathway –> Control Center –> Efferent Pathway –> Effector

20
Q

What type of nerve fibers make up the PNS and SNS?

A

PNS:

  • preganglionic = long, myelinated B-fibers – releases ACh
  • postganglionic = short, unmyelinated C-fibers – releases ACh

SNS:

  • preganglionic = short, myelinated B-fibers – releases ACh
  • postganglionic = long, unmyelinated C-fibers – releases NE
  • ACh is released at sweat glands, piloerector muscles, and some vessels
21
Q

What is the origin of the efferent SNS pathways?

A

Thoracolumbar

  • T1-L3
  • Cell bodies arise from the intermediolateral region of the spinal cord and axons exit via the ventral nerve roots
  • Preganglionic fibers usually synapse with postganglionic fibers in the 22 paired sympathetic ganglia (mass effect)
22
Q

What is the origin of the efferent PNS pathways?

A

Craniosacral

  • CN 3, 7, 9, 10
  • S2-S4
  • Preganglionic fibers synapse with postganglionic fibers near or in each effector organ (precise control of each organ)
23
Q

How is the innervation of the adrenal medulla different than the typical SNS efferent architecture?

A

There are no postganglionic fibers

  • preganglionic fibers release ACh onto the chromaffin cells, which release Epi (80%) and NE (20%) into systemic circulation
  • adrenal medulla = autonomic ganglion that is in direct communication w/ the bloodstream
24
Q

Describe the hemodynamic management of a pt with pheochromocytoma

A

Must alpha block BEFORE beta block

Alpha Antagonists:

  • Phenoxybenzamine and Phentolamine (non-selective)
  • Doxazosin and Prazosin (alpha-1 selective)
25
Q

What is the transcellular potassium shift? What causes it to occur?

A

It describes a number of processes that alter serum K+ by shifting K+ into or out of cells

  • K+ Shift In: alkalosis, beta-2 agonists, theophylline, insulin
  • K+ Shift Out: acidosis, cell lysis, hyperosmolarity, SUX
26
Q

What is the Baroreceptor reflex?

A

Regulates short term BP control

  • when BP rises, baroreceptor reflex decreases HR, contractility, and SVR
  • when BP falls, baroreceptor reflex increases HR, contractility, and SVR
27
Q

What is the Bainbridge reflex?

A

Increases HR when venous return is too high – minimizes venous congestion and promotes forward flow

  • Sensor = SA node, RV, Pulmonary veins
  • Afferent = Vagus
  • Control Center = Vasomotor center in the medulla
  • Efferent = Vagus (inhibition)
  • Effector = SA node increases HR

*ex: Autotransfusion during childbirth

28
Q

What is the Bezold-Jarisch reflex?

A

Decreases HR when venous return is too low – gives an empty heart adequate time to fill

  • Sensor = Cardiac mechanoreceptors (venous return) and Cardiac chemoreceptors (ischemia)
  • Afferent = Vagus
  • Control Center = Vasomotor center in medulla
  • Efferent = Vagus
  • Effector = SA node decreases HR and AV node decreases conduction velocity

Treatment = restore preload (IVF) and increased HR (Epi)

*ex: cardiac arrest during spinal, massive hemorrhage, MI, shoulder arthroscopy + interscalene block w/ Epi + sitting position

29
Q

What is the pathway of the Oculocardiac reflex?

A

“Five and Dime”

  • Sensor = Pressure to the eye or globe
  • Afferent = Long and short ciliary n. –> ciliary ganglion –> ophthalmic division V1 of trigeminal n. –> gasserian ganglion
  • Control Center = Vasomotor center in the medulla
  • Efferent = Vagus
  • Effector = SA node decreases HR and AV node decreases conduction velocity

*ex: strabismus surgery, ocular trauma, retrobulbar block

30
Q

What is the primary determinant of CO in a pt w/ a heart transplant? What is the consequence of this?

A
  • Transplanted heart has fixed HR so CO is dependent on Preload
  • transplanted heart is severed from autonomic influence – HR is determined by intrinsic rate of SA node (HR typically 100-120)

-Patient is very sensitive to hypovolemia

31
Q

What drugs can be used to augment HR in a heart transplant pt?

A

Drugs that directly stimulate the SA node CAN be used to increase HR: Epinephrine, Isoproterenol, Glucagon

Drugs that indirectly stimulate the SA node CANNOT be used: Atropine, Glycopyrrolate, and Ephedrine

*there is no autonomic input from the cardiac accelerator fibers (T1-T4) or vagus nerve

32
Q

What are the primary anesthetic concerns for removal of a glomus tumor?

A

Glomus tumors originate from neural crest cells and tend to grow in neuroendocrine tissues that lay close proximity to carotid artery, aorta, glossopharyngeal n. and middle ear

  • Can release several vasoactive substances that can lead to exaggerated HTN or HoTN
  • Octreotide can be used to treat carcinoid like s/sx
  • Cranial n. dysfunction (glossopharyngeal, vagus, hypoglossal) can cause swallowing impairment, aspiration, and airway obstruction
  • Surgical dissection of tumor that invaded IJ vein = risk of air embolism
33
Q

What are the anesthetic considerations for multiple system atrophy? What is another name for it?

A

Also known as Shy-Drager Syndrome

Causes degeneration of the locus coeruleus, IML column of spinal cord, and peripheral autonomic nerves

  • autonomic dysfunction – orthostatic HoTN
  • treat HoTN w/ volume and direct acting sympathomimetics
  • exaggerated HTN response to ephedrine and possibly ketamine
34
Q

Compare and contrast low, intermediate, and high dose epinephrine

A

LOW dose Epi: 0.01-0.03 mcg/kg/min

  • non-selective beta effects predominate
  • beta-1 stimulation increases HR and contractility, while eta-2 mediates vasodilation in skeletal muscle = net effect of increased CO w/ reduction in SVR

INTERMEDIATE dose Epi: 0.03-0.15 mcg/kg/min
-mixed beta and alpha effects

HIGH dose Epi: > 0.15 mcg/kg/min

  • alpha effects dominate and BP rises
  • supraventricular tachyarrhythmias are common – limit the usefulness of high dose epi
35
Q

What are the CV effects of isoproterenol?

A

it is a synthetic catecholamine that stimulates beta-1 and beta-2

  • increases HR, contractility, and myocardial oxygen consumption
  • decreases SVR (reduces DBP) – may reduce CPP
  • causes severe dysrhythmias and tachycardia
  • vasodilates nonessential vascular beds (i.e. in the muscle and skin) – precludes its use in septic shock
36
Q

What are the four clinical indications for isoproterenol?

A
  • Chemical pacemaker for bradycardia unresponsive to atropine
  • Heart transplant
  • Bronchoconstriction
  • Cor pulmonale
37
Q

In what situations should ephedrine NOT be used to treat hypotension?

A
  • Doesn’t work well when neuronal catecholamine stores are depleted (sepsis) or absent (heart transplant)
  • Pt is on MAO inhibitors – risk of hypertensive crisis
  • Conditions where increased HR or contractility is detrimental to hemodynamics
38
Q

How does vasopressin increase BP?

A

V1 receptor stimulation: causes intense vasoconstriction

V2 receptor stimulation: increases intravascular volume by stimulating synthesis and insertion of aquaporins into the walls of collecting ducts – increases water (but not solute) reabsorption and lowers serum osmolarity

39
Q

What is vasoplegic syndrome? What is the best treatment?

A

Also known as Refractory Hypotension

  • hypotension doesn’t respond to conventional therapies such as adrenergic agonists, hydration, and reducing depth of anesthesia
  • incidence is increased by ACE inhibitors or ARBs

Vasopressin (0.5-1 unit IV bolus followed by an infusion of 0.03 units/min) = best treatment
Methylene blue = next best choice

40
Q

What six drugs are beta-1 selective?

A
  • Atenolol
  • Acebutolol
  • Betaxolol
  • Bisoprolol
  • Esmolol
  • Metoprolol
41
Q

What six drugs are non-selective beta antagonists?

A
  • Carvedilol
  • Labetalol
  • Nadolol
  • Pindolol
  • Propranolol
  • Ttimolol
42
Q

What is the primary site of metabolism of the commonly used beta blockers? What are two exceptions?

A

Dependent on LIVER as primary site of metabolism
-propranolol, metoprolol, labetalol, carvedilol

Exceptions = Esmolol (metabolized by RBC esterases) and Atenolol (metabolized by kidneys)

43
Q

What beta blockers have local anesthetic properties? What is another name for this?

A

Propranolol and Acebutolol
-effect reduces the rate of rise of the cardiac action potential (only occurs when reach toxic levels)

Also known as Membrane stabilizing properties

44
Q

What is intrinsic sympathomimetic activity? Which drugs exert this effect?

A

Intrinsic Sympathomimetic Activity = Beta blockers that exert a partial agonist effect, while simultaneously blocking other agonists that have a higher affinity for beta receptor

ex: Labetalol and Pindolol

45
Q

What are three alpha antagonists? What is the MOA for each?

A

Alpha antagonists reduce BP by causing vasodilation (decreased SVR)

  • Phenoxybenzamine: long acting, non-selective, noncompetitive antagonist of alpha-1 and alpha-2
  • Phentolamine: short acting, non-selective, competitive antagonist of alpha-1 and alpha-2
  • Prazosin: alpha-1 selective antagonist

APEX Study Guide (13 decks)

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