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BOARD REVIEW > Autonomic Nervous System > Flashcards

Autonomic Nervous System Flashcards

1
Q

What is a receptor and what are the 4 classifications of receptors? (4)

A

A receptor receives the signal and instructs the cell to perform a specific function. Signal transduction is the process by which a cell converts this extracellular signal into an intracellular response.

Receptor classifications:

  1. Ion channel
  2. G-protein coupled receptor
  3. Enzyme linked receptor
  4. Intracellular receptor
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2
Q

Describe 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)
  • second messenger (primary intracellular signal)
  • enzymatic cascade (a bunch of steps you don’t have to worry about)
  • cellular response (causes a physiologic change)

**remember that second messengers are tissue specific. For example, cAMP may cause a response in one cell type while causing a different response in a different cll type

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3
Q

What second messenger system is associated with the alpha-1 receptor?

A
  • Gq > phospholipase C (IP3, Ca+, DAG)
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4
Q

What other receptors share a similar pathway as the alpha-1 receptor? (5)

A
  1. Histamine-1
  2. Muscarinic-1
  3. Mauscarinic-3
  4. Muscarinic-5
  5. Vasopressin-1 (vascular)
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5
Q

What second messenger system is associated with alpha-2 receptor?

A
  • Gi > adenylate cyclase (ATP, cAMP)
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6
Q

What other receptors share a similar pathway as alpha-2 receptor? (2)

A
  1. Muscarinic-2

2. Dopamine-2 (presynaptic)

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7
Q

What second messenger is associated with beta-1 AND beta-2 receptors?

A
  • B1&2 > Gs > adenylate cyclase (ATP, cAMP)
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8
Q

What other receptors share a similar pathway as beta-1 and beta-2? (3)

A
  1. Histamine-2
  2. Vasopressin-2 (renal)
  3. Dopamine-1 (postsynaptic)
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9
Q

Describe the autonomic innervation of the heart (myocardium and conduction system)

A

Beta-1

  • myocardium: increased contractility
  • conduction system: increased heart rate and increased conduction speed

Muscarinic 2

  • myocardium: increased contractility (0/or decreased)
  • conduction system: decreased HR and CV
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10
Q

What specific autonomic nerves innervate the heart?

A
  1. SNS: the cardiac accelerator fibers arise from T1-T4

2. PNS: vagus nerve (CN X)

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11
Q

Describe the autonomic innervation of the vasculature of the heart

A
  1. Vasculature:
    - arteries: a1 > a2 (vasoconstriction)
    - veins: a2 >a1 (vasoconstriction)
  2. Specific vascular beds:
    - myocardium: B2 (vasodilation)
  3. Skeletal muscle: B2 (vasodilation)
  4. Renal: DA (vasodilation)
  5. Mesenteric: DA (vasodilation)
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12
Q

Describe the autonomic innervation of the bronchial tree

A

Bronchial tree:

  • B2 > bronchodilation
  • M3 > bronchoconstriction

**Beta-2 receptors are NOT innervated; instead, they respond to catecholamines in the systemic circulation or in the airway (inhaled)

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13
Q

Describe the autonomic innervation of the kidney

A

Kidney:

  • renal tubules > a2 > diuresis (ADH inhibition)
  • renin release > B1 > increased renin release
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14
Q

Describe the autonomic innervation of the eye

A

Eye:

  • sphincter (iris) > M > contraction (miosis)
  • radial muscle > a1 > contraction
  • ciliary muscle > B2 > relaxation (far vision); M > contraction (near vision)
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15
Q

Describe the autonomic innervation of the GI tract

A

GI:

  • sphincters > a1 > contraction; M > relaxation
  • motility & tone: a1 / a2 / B1 / B2 > decrease; M > increase
  • salivary glands: a2 > decrease; M > increase
  • gallbladder & ducts: B2 > relaxation; M > contraction
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16
Q

Describe the autonomic innervation of the pancreas

A

Pancreas:

  • islet (Beta cells): a2 > decrease insulin release
  • islet (B cells): B2 > increase insulin release
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17
Q

Describe the autonomic innervation of the liver

A

Liver:

- a1 / B2 > increase serum glucose

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18
Q

Describe the autonomic innervation of the uterus

A

Uterus:

  • a1 > contraction
  • B2 > relaxation
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19
Q

Describe the autonomic innervation of the bladder

A

Bladder:

  • trigone & sphincter: a1 > contraction; M > relaxation
  • detrusor: B2 > relaxation; M > contraction
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20
Q

Describe the autonomic innervation of sweat glands

A

Sweat glands

- a1 > increase secretion; M > increase secretion

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21
Q

List the steps of norepinephrine synthesis. What is the Rate limiting step?

A
  1. Tyrosine (tyrosine hydroxylase) >
  2. DOPA (DPOA decarboxylase) >
  3. Dopamine (Dopamine B-hydroxylase) >
  4. Norepinephrine (phnenylethanolamine N-methyltransferase) >
  5. Epinephrine (step #5 occurs in the adrenal medulla)

**rate limiting step is tyrosine to DOPA via tyrosine hydroxylase

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22
Q

What are the 3 ways that NE can be removed from the synaptic cleft? Which is the most important?

A
  1. Reuptake into the presynaptic neuron (accounts for 80%; MOST important)
  2. Diffusion away from the synaptic cleft
  3. Reuptake by the extraneural tissue
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23
Q

What enzymes metabolized NE and Epi? What is the final metabolic byproduct?

A

Metabolic pathways:

  1. Monoamine oxidase (MAO)
  2. Catechol-O-methyltransferase (COMT)

Final byproduct of NE and Epi is vanillylmandelic acid (VMA); and elevated VMA in the urine aids in the dx of pheochromocytoma

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24
Q

List the 3 types of cholinergic receptors and where each of them is found in the body

A
  1. Nicotine type M (muscle):
    - neuromuscular junction
  2. Nicotinic type N (nerve):
    - preganglionic fibers at autonomic ganglia (SNS & PNS)
    - central nervous system
  3. Muscarinic:
    - postganglionic PNS fibers at effector organs
    - central nervous system
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25
Q

List the 5 components of the autonomic reflex arc

A
  1. Sensor
  2. Afferent pathway
  3. Control center
  4. Efferent pathway
  5. Effector
26
Q

Describe the architecture of the SNS efferent pathways

A
  • preganglionic: short, myelinated, B-fibers, releases Ach
  • postganglionic: long, unmyelinated, C-fiber, releases NE (*Ach is released in sweat glands, piloerector muscles, and some vessels
27
Q

Describe the architecture of the PNS efferent pathway

A
  • preganglionic: long, myelinated, B-fiber, releases ACH

- postganglionic: shot, unmyelinated, C-fiber, releases Ach

28
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)
29
Q

What is the origin of the efferent PNS pathways?

A

Craniosacral:

  • CN 3, 7, 9, 10
  • S2-S4
  • preganglionic fibers synapses with postganglionic fibers near or in such effector organ (precise control of each organ)
30
Q

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

A
  • the innervation of the adrenal medulla is unique because there are NO postganglionic fibers
  • the preganglionic fibers release Ach onto the chromaffin cells, and the chromaffin cells release Epi and NE into the systemic circulation at a ratio of 80% and 20% respectively
  • you can think of the adrenal medulla as an autonomic ganglion that is in direct communication with the bloodstream
31
Q

Describe the hemodynamic management of the pt with pheochromocytoma

A
  • MUST block alpha before beta

Commonly used alpha antagonists includes:

  1. Non-selective: phenoxybenzamine and phentolamine
  2. Alpha-1 selective: doxazosin and prazosin

Problems that arise from blocking the beta receptor first:

  • Beta-2 blockade inhibits skeletal muscle vasodilation and increases SVR
  • Beta-2 blockade reduces inotropy and can precipitate CHF in the setting of increased SVR
32
Q

What is the transcellular potassium shift?

A

The transcellular K+ shift describes of processes that alter serum K+ by shifting K+ Into or out of cells

33
Q

What things cause K+ To shift into the cells (hypokalemia)? (4)

A
  1. Alkalosis
  2. Beta-2 agonists
  3. Theophylline
  4. Insulin
34
Q

What things cause K+ to move out of the cells (hyperkalemia)? (4)

A
  1. Acidosis
  2. Cell lysis
  3. Hyperosmolarity
  4. Succinylcholine
35
Q

What does the baroreceptor regulate? Describe the anatomy and physiology of the baroreceptor reflex

A
  • the baroreceptor reflex regulates short term blood pressure control
  • when the blood pressure rises, the baroreceptor reflex decreases HR, contractility, and SVR
  • when blood pressure falls, the baroreceptor increases HR, contractility and SVR
36
Q

What controls long term regulation of blood pressure?

A

Longer term BP is mediated by the RAAS and ADH

37
Q

Describe the anatomy and physiology of the Bainbridge reflex

A

The Bainbridge reflex increases HR when venous return is too high. This is beneficial because it minimizes venous congestion and promotes forward flow

  • sensor: SA node, RV, pulmonary veins
  • afferent: vagus
  • control: vasomotor center in the medulla
  • efferent: vagus (inhibition)
  • effector: SA node increases HR
  • treatment: none required
  • ex: autotransfusion during childbirth
38
Q

Describe the anatomy and physiology of the Bezold-Jarisch reflex

A

The Bezold-Jarisch reflex decreases HR when venous return is too low; this gives an empty heart adequate time to fill

  • sensor: cardiac mechanoreceptors (VR) & cardiac chemoreceptors (ischemia)
  • afferent: vagus
  • control: vasomotor center in the medulla
  • efferent: vagus
  • effector: SA node decreases HR & AV node decreases conduction velocity
  • treatment: restore preload (IVF and leg elevation) and increases HR (Epi is BEST)

ex:

  • Cardiac arrest during spinal anesthesia
  • massive hemorrhage
  • myocardial ischemia
  • shoulder arthroscopy + interscalene block w/ Epi + sitting position
39
Q

Describe the anatomy and physiology of the oculocardiac reflex

A

Think five (V) and dime reflex (X)

  • sensor: pressure to the eye or globe
  • afferent: long and short ciliary n. > ciliary ganglion > opthalmic division V1 of trigeminal n. (CN V) > Gasserian ganglion
  • control: vasomotor center in the medulla
  • efferent: vagus
  • effector: SA node decreases HR and AV node decreases conduction velocity

Treatment:

  • ask the surgeon to remove the stimulus
  • administer 100% O2, ensure proper ventilation, and deepen the anesthetic
  • administer an anticholingeric (atropine or glyco)

Ex:

  • strabismus surgery
  • ocular trauma
40
Q

What is the primary determinant of CO in the pt with heart transplant? What is the consequence of this?

A
  • the transplanted heart is severed from autonomic influence, so the HR is determined by the intrinsic rate of the SA node. This explains when these pts often have resting tachycardia (HR = 100-120 bpm)
  • if CO is the product of HR x SV (and the HR is fixeD), then CO becomes dependent on preload. Indeed CO is highly dependent on filling. This feature makes theses pts very sensitive to hypovolemia
41
Q

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

A
  • remember, there is NO autonomic input from the cardiac accelerator (T1-4) or the vagus nerve
  • drugs that directly stimulate the SA node can be used to increase HR (Epinephrine, isoproterenol, glucagon)
  • drugs that indirectly stimulate the SA node can NOT be used (atropine, glyco and ephedrine)
42
Q

A pt presents for removal of a glomus tumor. What are your primary concerns when planning you anesthetic?

A

Glomus tumors (glomangiomas) originate from neural crest cells. They tend to grow in the neuroendocrine tissues that lay in close proximitry to the carotid artery, aorta, glosspharyngeal nerve and the middle ear. These tumors are NOT usually malignant.

  • They can release several vasoactive substances that can lead to exaggerated hyper or hypotension (NE, 5-HT, histamine, bradykinin)
  • Octreotide can be used to tread carcinoid like s&sx
  • cranial nerve dysfncation (glossopharyngeal, vagus, hypoglossal) can cause swallowing impairment, aspiration of gastric contents and airway obstruction
  • surgical dissection of a glomus tumor that has invaded the internal jugular vein increases the risk of air embolism
43
Q

What are the anesthetic considerations for multiple system atrophy?

A

Multiple system atrophy (previously known as Sky-Drager sundrome) causes degeneration of the locus coeruleus, intermediolaterl column of the spinal cord (where the cell bodies for the SNS efferent nerves live)., and the peripheral autonomic nerves

  • autonomic dysfunction (orthostatic hypotension)
  • treat hypotension with volume and direct acting sympathomimetics
  • exaggerated hypertension response to ephedrine and possible ketamine
44
Q

Describe the effects of low does epinephrine

A
  • low dose epi: 0.01-0.03 mcg/kg/min
  • at low doses, non-selective beta effects predominate Beta-1 stimulation incrases HR and contractility, while Beta-2 stimulation mediates vasodilation in the skeletal muscle.
  • the net effect is typically an increased CO witha reduction in SVR and possible a slight reduction in blood pressure; pulse pressure is increased (widened)
45
Q

Describe the effects of intermediate dose epinephrine

A

Intermediate dose epi: 0.03-0.15 mcg/kg/min

  • this dose range is characterized by mixed beta and alpha effects
46
Q

Describe the effects of high does epinephrine

A

High dose epi: >0.15 mcg/kg/min

  • in this dose range, the alpha effects prevail and BP rises
  • supraventricular tachyarrythmias are common and these limit the usefulness of high dose epi
47
Q

What is isoproterenol? Describe the cardiovascular effects of isoproterenol

A

Isproterenol is a synthetic catecholamine that stimulates B1 and B2 receptors

  • it decreases HR, contractility and myocardial O2 demand
  • it decreases SVR, which reduces diatolic BP; this may reduce coronary perfustion pressure (CPP = AoDB - LVEDP)
  • it causes severe dysrhythmias and tachycardia
  • it vasodilates nonessential vascular beds, such as those in muscle and skin; b/c of this, it preludes its use in septic shock
48
Q

List 4 clinical indications for isoproterenol

A
  1. Chemical pacemaker for bradycardia unresponsive to atropine
  2. Heart transplant
  3. Bronchoconstriction
  4. Co pulmonale
49
Q

How does ephedrine work and in what situations should ephedrine NOT be used to treat hypotension? (3)

A

Ephedrine uses endogenous catecholamines stores from presynaptic nerve. Multiple doses can cause tachyphylaxis

  1. When neuronal chatecholamine stores are depleted (sepsis) or absent (heart transplant)
  2. Risk of hypertensive crisis in pts on MAO inhibitors
  3. Conditions where increased HR or contractility is detrimental to hemodynamics
50
Q

How does vasopressin increase BP?

A

Vasopressin restores BP in two ways:

  1. V1 receptor stimulation causes intense vasoconstriction
  2. V2 receptor stimulation increases intravascular volume by stimulating the synthesis and insertion of aquaporins into the walls of the collecting ducts. This increases water (but not solute) reabsorption and lowers serum osmolarity

Aldosterone increases water AND sodium reabsorption (serum osmolarity is unchanged). This is an important difference btw vasopressin and aldosterone

51
Q

What is the best tx for vasoplegic syndrome?

A

Refractory hypotension is also called vasoplegic syndrome. The key here is that hypotension does not respond to conventional therapies such as adrenergic agonists, hydration, and reducing depth of anesthesia

  • vasopressin is the best treatment (0.5-1 unit IV bolus followed by an infusion of 0.03 units/min)
  • the incidence of vasoplegic syndrome is increased by ACE inhibitors or angiotensin receptor antagonist
  • methylene blue is the next best choice
52
Q

List 6 drugs that are selective for the beta-1 receptor

A
  1. Atenolol
  2. Acebutolol
  3. Betaxolol
  4. Bisprolol
  5. Esmolol
  6. Metoprolol
53
Q

List 6 non-selective beta blockers - they antagonize beta-1 and beta-2 receptors

A
  1. Carvedilol
  2. Labetalol
  3. Nadolol
  4. Pindolol
  5. Propranolol
  6. Timolol
54
Q

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

A

Most beta-blockers depend on the liver as their primary site of metabolism (ex: propranolol, metoprolol, labetalol, and carvedilol)

2 exceptions:
1. Esmolol is metabolized by RBC esterases (NOT pseudocholinesterase)

  1. Atenolol is eliminated by the kidneys (caution in renal failure)
55
Q

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

A

Membrane stabilizing properties is another way of saying that a drug has local anesthetic-like effects.

This effect reduces the rate of rise of the cardiac action potential, however it probably only occurs when these drugs reach toxic levels. Ex:

  • propranolol
  • acebutolol
56
Q

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

A

Beta blockers that exert a partial agonist effect, while simultaneously blocking other agonists that have a higher affinity for the beta receptor are said to have intrinsic sympathomimetic activity.

Ex:

  • labetalol
  • pindolol
57
Q

What is the MOA of alpha antagonists?

A

They reduce BP by causing vasodilation (decreased SVR)

58
Q

What is the drug class and MOA of Phenoxybenzamine?

A

Phenoxybenzamine is a long-acting, non-selective, noncompetitive antagonist of the alpha-1 and alpha-2 receptor

59
Q

What is the drug class and MOA of Phentolamine?

A

Phentolamine is a short, non-selective, competitive antagonist of the alpha-1 and alpha-2 receptor

60
Q

What is the drug class and MOA of Prazosin?

A

Prazosin is a selective alpha-1 antagonist

BOARD REVIEW (3 decks)

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