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Prodigy > Apex Unit 2 Flashcards ANS > Flashcards

Apex Unit 2 Flashcards ANS

1
Q

What are the 4 classifications of receptors?

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:
Ion channel
G-protein coupled receptor
Enzyme linked receptor
Intracellular receptor
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2
Q

Describe the general architecture of the G protein second messenger system

A

This is one area where it’s easy to get lost in the details. Your life will be easier if you understand the general architecture of the G protein system BEFORE trying to memorize the specifics about each receptor.

1st messenger (extracellular signal)
Receptor (responds to the extracellular signal)
G protein (turns on or turns off an effector)
Effector (activates or inhibits the second messenger)
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 cell type.

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3
Q

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

What other receptors share a similar pathway?

A

A1 = IP3, Ca, DAG (see photo)

Other receptors that share a similar 2nd messenger pathway:

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

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

What other receptors share a similar pathway?

A

G Inhibitory stops ATP & cAMP (see photo)

Other receptors that share a similar 2nd messenger pathway:

Muscarininc-2
Dopamine-2 (presynaptic)

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5
Q

What second messenger system is associated with the beta-1 AND beta-2 receptor?

What other receptors share a similar pathway?

A

G-stimulatory produces ATP cAMP

Other receptors that share a similar 2nd messenger pathway:

Histamine-2
Vasopressin-2 (renal)
Dopamine-1 (postsynaptic)

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6
Q

Describe the autonomic innervation of the heart.

A

SNS: The cardiac accelerator fibers arise from T1-T4
PNS: Vagus nerve (CN X)

myocardium & conduction system B1 = increased contractility, increased HR, increased conduction speed

M2 = decreased contractility, HR & CV

See photo

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7
Q

Describe the autonomic innervation of the vasculature.

A

arteries A1>A2 vasoconstrict
Veins A2 > A1 vasoconstrict

myocardium vascular bed B2
skeletal muscle B2
Renal DA
Mesenteric DA all vasodilate

see photo

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8
Q

Describe the autonomic innervation of the bronchial tree.

A

Beta-2 receptors are not innervated. Instead, the respond to catecholamines in the systemic circulation or in the airway (inhaled).

bronchial tree B2 = bronchdilation
M3 = bronchconstriction

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9
Q

Describe the autonomic innervation of the kidney.

A

renal tubules = A2 = diuresis ( ADH inhibition)

Renin release = B1 = increased renin release

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10
Q

Describe the autonomic innervation of the eye.

A

sphincter muscle (iris) = M = contraction = miosis

Radial Muscle (IRIS) = A2 = Contraction ( mydriasis)

Ciliary Muscle = B2 = relaxation ( far vision)
M = contraction (near vision)

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11
Q

Describe the autonomic innervation of the GI tract.

A 
Sphincters = A1 = contraction, 
M = relaxation

Motility / Tone = A1,A2,B1,B2, decrease,
M = Increase

Salivary glands = A2 = decrease
M = Increase

Galbladder/ Ducts = B2 = relaxation ,
M = Contraction

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12
Q

Describe the autonomic innervation of the pancreas.

A

Islet B cells = A2 = decrease insulin release

B2 = increase insulin release

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13
Q

Describe the autonomic innervation of the liver.

A

A1/B2 = increase serum glucose

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14
Q

Describe the autonomic innervation of the uterus.

A 
A1 = contraction
B2 = Relaxation
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15
Q

Describe the autonomic innervation of the bladder.

A

Trigone / Sphincter = A1 = Contraction
M = relaxation

Detrusor = B2 = Relaxation
M = Contraction
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16
Q

Describe the autonomic innervation of the sweat glands.

A 
A1 = Increase secretion
M = increase secretion
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17
Q

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

A

See photo) - tyrosine -> DOPA -> dopamine -> Ne -> Epi.

Tyrosine to DOPA by tyrosine hydroxylate is rate limiting step

Norepinephrine is the primary neurotransmitter in the sympathetic nervous system.

Notice how and where EPI is synthesized.

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18
Q

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

A

NE is removed from the synaptic cleft in 1 of 3 way:

Reuptake into the presynaptic neuron (accounts for 80%)
Diffusion away from the synaptic cleft
Reuptake by extraneural tissue

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19
Q

What enzymes metabolize NE and EPI?

What is the final metabolic byproduct?

A

There are 2 metabolic pathways for norepinephrine and epinephrine:

Monoamine oxidase (MAO)
Catechol-O-methyltransferase (COMT)

The final byproduct of NE and EPI metabolism is vanillylmandelic acid (VMA). Another name for this compound is 3-methoxy-4-hydroxymandelic acid. An elevated level of VMA in the urine aids in the diagnosis of pheochromocytoma.

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20
Q

List the 3 types of cholinergic receptors. Where are each of these found inside the body?

A

Nicotinic type M (muscle):
Neuromuscular junction

Nicotinic type N (nerve):
Preganglionic fibers at autonomic ganglia (SNS & PNS)
Central nervous system

Muscarinic:
Postganglionic PNS fibers at effector organs
Central nervous system

SEE PHOTO

21
Q

Describe the synthesis, release, and metabolism of acetylcholine.

A

see photo

choline + Acetyl CoA -> Ach then AchE breaks down to Acetate + choline (which is reused)

22
Q

List the 5 components of the autonomic reflex arc.

A

sensor -> afferent pathway to control center –> efferent pathway to effector

23
Q

Compare and contrast the architecture of the SNS and PNS efferent pathways.

A

Both pathways contain a pre- and postganglionic nerve fiber.

PNS:
Preganglionic: Long, myelinated, B-fiber, releases Ach
Postganglionic: Short, unmyelinated, C-fiber, releases Ach

SNS:
Preganglionic: Short, myelinated, B-fiber, releases Ach
Postganglionic: Long unmyelinated, C-fiber, releases NE (*Ach is released at sweat glands, piloerector muscles, and some vessels)

24
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).

25
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).

26
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.; 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.

SEE PHOTO

27
Q

Describe the hemodynamic management of the patient with pheochromocytoma.

A

Understanding the hemodynamic management of this patient is critical to the success of your anesthetic. You must alpha block before you beta block! Just remember that A comes before B.

Commonly used alpha antagonists include:

Non-selective: phenoxybenzamine and phentolamine
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-1 blockade reduces inotropy and can precipitate CHF in the setting of increased SVR.

28
Q

What is the transcellular potassium shift, and what causes it to occur?

A

The transcellular K+ shift describes a number of processes that alter serum K+ by shifting K+ into or out of cells.

Things that shift K+ into cells (ICF) leads to hypokalemia. (Alkalosis, B2 Agonists, Theophylline, Insulin)

Things that shift K+ into the ECF lead to hyperkalemia. (acidosis, Cell Lysis, Hyperosmolarity, Succinylcholine)

SEE PHOTO

29
Q

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 heart rate, contractility, and systemic vascular resistance.
When blood pressure falls, the baroreceptor reflex increases heart rate, contractility, and systemic vascular resistance.

Longer term blood pressure control is mediated by the RAAS and ADH.

SEE PHOTO

30
Q

Describe the anatomy and physiology of the Bainbridge reflex.

A

The Bainbridge reflex increases heart rate 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

Example:
Autotransfusion during childbirth

31
Q

Describe the anatomy and physiology of the Bezold-Jarisch reflex.

A

The Bezold-Jarisch reflex decreases heart rate when venous return is too low. This gives an empty heart adequate time to fill.

Sensor: Cardiac mechanoreceptors (venous return) & cardiac chemoreceptors (ischemia)
Afferent: Vagus
Control: Vasomotor center in the medulla
Efferent: Vagus
Effector: SA node decreases heart rate & AV node decreases conduction velocity

Treatment:  
Restore preload (IVF and leg elevation) and increase heart rate (EPI is best)
Examples:
Cardiac arrest during spinal anesthesia
Massive hemorrhage
Myocardial ischemia
Shoulder arthroscopy + interscalene block w/ EPI + sitting position
32
Q

Describe the anatomy & physiology of the oculocardiac reflex.

A

The oculocardiac reflex as the five (V) and dime (X) reflex.

Sensor: Pressure to the eye or globe
Afferent: Long and short ciliary n. → ciliary ganglion → ophthalmic division V1 of trigeminal n. (CN V) → Gasserian ganglion
Control: Vasomotor center in the medulla
Efferent: Vagus
Effector: SA node decreases heart rate & AV node decreases conduction velocity

Treatment:
Ask the surgeon to remove the stimulus. This is usually enough to terminate the reflex.
Administer 100% oxygen, ensure proper ventilation, and deepen the anesthetic.
Administer an anticholinergic (atropine or glycopyrrolate).

Examples:
Strabismus surgery
Ocular trauma
Retrobulbar block (can cause or prevent the OCR)

33
Q

What is the primary determinant of cardiac output in the patient with a heart transplant? What is the consequence of this?

A

The transplanted heart is severed from autonomic influence, so the heart rate is determined by the intrinsic rate of the SA node. This explains why these patients often have a resting tachycardia (HR = 100 - 120 bpm).

If cardiac output is the product of heart rate and stroke volume (and the heart rate is fixed), then cardiac output becomes dependent on preload. Indeed, CO is highly dependent on cardiac filling. This feature makes these patients very sensitive to hypovolemia.

34
Q

What drugs can be used to augment heart rate in the patient with a heart transplant?

A

Central to understanding this is knowing that there is no autonomic input from the cardiac accelerator fibers (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, glycopyrrolate, and ephedrine).

35
Q

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

A

Glomus tumors (glomangiomas) originate from neural crest cells. They tend to grow in the neuroendocrine tissues that lay in close proximity to the carotid artery, aorta, glossopharyngeal nerve, and the middle ear. These tumors usually aren’t 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 treat carcinoid-like s/sx.
Cranial nerve dysfunction (glossopharyngeal, vagus, and 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.

36
Q

What are the anesthetic considerations for multiple system atrophy?

A

Multiple system atrophy (previously known as Shy-Drager syndrome) causes degeneration of the locus coeruleus, intermediolateral 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 hypertensive response to ephedrine and possibly ketamine

37
Q

Compare and contrast low, intermediate, and high dose epinephrine.

A

Low Dose Epi (0.01 - 0.03 mcg/kg/min):
At low doses, non-selective beta effects predominate. Beta-1 stimulation increases heart rate and contractility, while beta-2 stimulation mediates vasodilation in the skeletal muscle. The net effect is typically an increased cardiac output with a reduction in SVR and possibly a slight reduction in blood pressure. Pulse pressure is increased (wider).

Intermediate Dose Epi (0.03-0.15 mcg/kg/min):
This dose range is characterized by mixed beta and alpha effects.

High Dose Epi (> 0.15 mcg/kg/min):
In this dose range, the alpha effects prevail and blood pressure rises. Supraventricular tachyarrhythmias are common, and these limit the usefulness of high dose EPI.

38
Q

Describe the cardiovascular effects of isoproterenol.

A

Isoproterenol is a synthetic catecholamine that stimulates β1 and β2 receptors.

It increases heart rate, contractility, and myocardial oxygen consumption.
It decreases SVR, which reduces diastolic blood pressure. This may reduce coronary perfusion pressure (CPP = AoDB - LVEDP).
It causes severe dysrhythmias and tachycardia.
It vasodilates nonessential vascular beds, such as those in the muscle and skin. This characteristic precludes its use in septic shock.

39
Q

List 4 clinical indications for isoproterenol.

A
  1. Chemical pacemaker for bradycardia unresponsive to atropine
  2. Heart transplant
  3. Bronchoconstriction
  4. Cor pulmonale
40
Q

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

A

Uses endogenous catecholamine stores from the presynaptic sympathetic nerve. Multiple doses can cause tachyphylaxis (progressively smaller response to a given dose after multiple administrations).

Ephedrine doesn’t work well when neuronal catecholamine stores are depleted (sepsis) or absent (heart transplant).
Risk of hypertensive crisis in patients on MAO inhibitors.
Conditions where increased HR or contractility is detrimental to hemodynamics.

41
Q

How does vasopressin increase blood pressure?

A

Vasopressin restores blood pressure in two ways:

V1 receptor stimulation causes intense vasoconstriction.
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 between vasopressin and aldosterone.

42
Q

What is the best treatment 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 antagonists.
Methylene blue is the next best choice.

43
Q

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

A

These drugs are beta-1 selective:

Atenolol
Acebutolol
Betaxolol
Bisoprolol
Esmolol
Metoprolol

Knowing what you know about the beta-1 and beta-2 receptor, you should be able to predict their side effects.

44
Q

List 6 non-selective beta antagonists.

A

These drugs are non-selective beta blockers - they antagonize beta-1 and beta-2 receptors:

Carvedilol
Labetalol
Nadolol
Pindolol
Propranolol
Timolol

Knowing what you know about the beta-1 and beta-2 receptor, you should be able to predict their side effects.

45
Q

What is the primary site of metabolism of the commonly used beta blockers? What are 2 exceptions?

A

Most beta blockers depend on the liver as their primary site of metabolism. Examples include: propranolol, metoprolol, labetalol, and carvedilol.

There are 2 exceptions:
Esmolol is metabolized by RBC esterases (not pseudocholinesterase)
Atenolol is eliminated by the kidneys (caution in renal failure)

46
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. Examples include:

Propranolol
Acebutolol

47
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.

Examples: labetalol and pindolol

48
Q

List 3 alpha antagonists. What is the MOA for each?

A

Alpha antagonists reduce BP by causing vasodilation (decreased SVR).

Phenoxybenzamine is a long acting, non-selective, noncompetitive antagonist of the alpha-1 and alpha-2 receptor.
Phentolamine is a short acting, non-selective, competitive antagonist of the alpha-1 and alpha-2 receptor.
Prazosin is a selective alpha-1 antagonist.

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