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** Board Exam ** > ANS > Flashcards

ANS Flashcards

1
Q

What is signal transduction?

A

Process by which a cell converts an extracellular stimulus to an intracellular response

Usually by

1) Altering enzymatic activity within the cell
2) Opening or closing an ion channel

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2
Q

First messengers that affect ion channels and G proteins

A

Ion channels: Glutamate, GABA, and Ach at the nicotinic receptor

G proteins: NE, phenylephrine, and Ach at the MUSCARINIC receptor

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3
Q

Describe G proteins

A
  • 7 transmembrane segments with external N terminus and internal C terminus
  • G protein becomes activated when a ligand binds the receptor it’s attached to
  • G protein goes on to either activate OR inhibit an effector (either an enzyme or an ion channel)
  • G protein has 3 subunits: alpha, beta, and gamma. When ligand binds to the receptor, the alpha subunit detaches. If the G protein is stimulatory, the alpha subunit will activate an effector. If it’s inhibitory, the alpha subunit will inhibit an effector.
  • Stimulatory G proteins are Gs and Gq
  • Inhibitory G protein is Gi
  • Once the first messenger dissociates from the receptor, the alpha unit returns to to the G protein (rejoining the beta and gamma subunits), and it’s effect on the effector ends.
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4
Q

What is the purpose of the effector?

A

To turn on the second messenger

- The effector is either an enzyme or ion channel

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5
Q

Examples of enzymatic and ion channel effectors

A

Enzymatic:

  • Adenylate cyclase
  • Phospholipase C

Ion channel effectors:

  • GABA-A
  • NMDA
  • nAchR
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6
Q

The intracellular response to a second messenger is ____

A

Tissue specific

  • Ex- cAMP may cause different effects in different cell types
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7
Q

5 second messengers we should be familiar with

A

1) Cyclic adenosine monophosphate (cAMP)
2) Cyclic guanosine monophosphate (cGMP)
3) Inositol triphosphate (IP3)
4) Diacylglycerol (DAG)
5) Ca+2

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8
Q

Stimulation of alpha-1 receptor, results in this

A

Stimulation of the effector Phospholipase C, which then activates DAT, IP3, and Ca+2

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9
Q

Stimulation of alpha-2 receptor results in

A

inhibition of the effector adenylate cyclase. As a result, ATP is not converted to cAMP

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10
Q

Stimulation of Beta 1 and 2 receptors results in

A

Stimulation of the effector adenylate cyclase. As a result, ATP is converted to cAMP.

This is the opposite of the effects of Alpha 2 receptor activation.

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11
Q

Where are Beta 2 receptors located?

A

Muscles and other vascular beds

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12
Q

Where are Beta 1 receptors located?

A

The heart

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13
Q

What does cAMP do?

A

It turns on a variety of protein kinases that instruct the cell to perform a specific function.

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14
Q

How is cAMP metabolized?

A

Phosphodiesterase III (3) (PDE III)metabolizes cAMP to just AMP. This inactivates cAMP, thus inactivating the protein kinases it had been working on, and tells the cell to stop performing that function.

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15
Q

What will happen if phosphodiesterase III (PDE III) is inhibited?

A

cAMP will not be metabolized. So cAMP will continue to keep the protein kinases in the “turned on” state

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16
Q

PDE III inhibitors are also called

A

Inodilators
This is due to their effects on cAMP
cAMP in the heart causes increased inotropy and lusitropy.
cAMP in the vessels causes dilation and decreased SVR.

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17
Q

This medication is a PDE III inhibitor

A

Milrinone

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18
Q

This is the primary NT in the SNS

A

NE

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19
Q

Termination of action for NE is due to

A

1) Reuptake (80%)
- PRIMARY mechanism
- 80% of NE released undergoes reuptake. Most NE is then repackaged into vesicles to be used again, although some gets metabolized by MAO in the terminal.
- Reuptake is blocked by TCAs and cocaine

2) Reuptake by extraneural tissues
- These tissues contain MAO and COMT which metabolize NE

3) Diffusion away from the synapse
- NE enters circulation and is metabolized in the liver and kidney by MAO and COMT
- The kidneys and liver are the primary sites of catecholamine metabolism

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20
Q

The final byproduct of Epi and NE metabolism is

A

Vanillylmandelic acid (VMA)

This can be measured in the urine as a general measure of SNS activity (used in the diagnosis of pheochromocytoma)

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21
Q

This is the primary NT in the PSNS

A

Ach

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22
Q

When is Ach used by the SNS?

A

Released by postganglionic fibers on muscarinic receptors that are located at the sweat glands, piloerector muscle, some BVs, and by preganglionic fibers in the adrenal medulla

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23
Q

Ach synthesis

A
  • Choline is transported from the blood into the nerve terminal
  • Mitochondria make Acetyl CoA, which is released into the cytoplasm
  • In the presence of choline acetyltransferase, Choline + Acetyl CoA = Ach
  • Ach is then packaged into vesicles
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24
Q

This is an antagonist of Ca+2 at the presynaptic nerve terminals

A

Magnesium

This is why Mg can cause muscle weakness. It antagonizes the Ca+2 channels, preventing Ca from entering the cell and releasing Ach to elicit a muscle response.

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25
Q

Type of fiber that pre-ganglionic SNS neurons are

A

Myelinated B fibers

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26
Q

Type of fiber that post-ganglionic SNS neurons are

A

Unmyelinated C fiber

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27
Q

Origin of SNS signals

A 
Thoracolumbar output (Sympathetic Chain)
T1-L3****

Cell bodies arise from the intermediolateral region of the spinal cord, and axons exit via the ventral root

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28
Q

Origin of PSNS signals

A

Craniosacral output

  • CN X
  • S2-4
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29
Q

For each pre-ganglionic neuron in the SNS, there are this many postganglionic

A

30

Results in signal amplification that contributes to mass response

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30
Q

For each pre-ganglionic neuron in the PSNS, there are this many postganglionic

A

3

Allows for precise control of each organ

31
Q

What does the stellate ganglion do?

A

Provides SNS innervation to the ipsilateral extremity and portion of the head and neck

May be blocked to treat complex regional pain syndrome, upper extremity sympathetic dystrophy, or to increase blood flow to that extremity

32
Q

2 areas of the adrenal gland and what they make

A

1) Medulla
- Secretes catecholamines

2) Cortex
- Makes hormones (cortisol, aldosterone, and androgens)

33
Q

Do catecholamines stay longer in the synaptic cleft or the bloodstream?

A

5-10x longer in the bloodstream

34
Q

Function of alpha 2 receptors

A

Most are on presynaptic nerve terminals and modulate NE release.

However, there are also some located on effector organs.

35
Q

MOA of alpha 2 receptors

A

1) Decrease Ca+2 conductance to decrease NT release

2) Increase K+ conductance to cause hyper polarization

36
Q

BP and Precedex

A

Precedex will work alpha 2 receptors in both the brain and in the periphery.

Rapid administration will stimulate the post-ganglionic alpha 2 receptors in the arterial and venous circulations leading to vasoconstriction and HTN.

The effect in the brain is what causes vasodilation. This effect is slower, but once it kicks in, it overpowers the effect in the periphery.

37
Q

Are beta 2 receptors innervated?

A

As a general rule, no.

They respond to circulating epinephrine in the blood stream

38
Q

How does beta 2 stimulation by EPI affect the liver?

A

Stimulating B2 receptors in the hepatocyte results in release of GLUCOSE and POTASSIUM into circulation.

39
Q

Effect of beta 2 stimulation by EPI on potassium levels

A

Overall, it causes hypokalemia

There are two phases to potassium response:

1) Initial K+ release from the cell, causing serum levels to rise (very short lived)
2) Epi then binds to beta 2 receptors on skeletal muscle and erythrocytes. This activates the Na/K pump, bringing K+ into the cell.

40
Q

Baroreceptor reflex

A

Increase in BP causes:
- Decreased HR, contractility, and SVR

Decrease in BP causes
- Increased HR, contractility, and SVR

Overall, an increase in BP will result in a decrease in SNS output and an increase in PSNS output

41
Q

Where is the main control center for the baroreceptor reflex?

A

Vasomotor center in the pons and medulla

42
Q

4 Key functions of the vasomotor center

A

Vasoconstriction and dilation

Cardiac stimulation and inhibition

43
Q

Sevoflurane and the baroreceptor reflex

A

Sevo decreases the effectiveness of the baroreceptor reflex in a dose dependent fashion
This can result in hemodynamic instability (body unable to compensate for the low BP caused by the VA)

Iso has some mild B-1 stimulation, so it impairs baroreceptors the least

44
Q

Congestion on the R side of the heart leads to these hormonal changes

A

1) Decrease in ADH release

2) Release of ANP –> diuresis

45
Q

These factors will worsen the severity of the OCR

A

Hypercarbia, hypoxia, and light anesthesia

46
Q

Muscarinic receptors and their effectors

A

Even ones (2&4) inhibit adenylate cyclase

Odd ones (1, 3, & 5) stimulate phospholipase

47
Q

This muscarinic receptor causes bronchial constriction

A

M3

48
Q

This muscarinic receptor causes decreased chronotropy

A

M2

49
Q

How does the bainbridge reflex work?

A

Increased venous return stretches the RA.
Info goes to the vasomotor center in the medulla.
PSNS tone to the heart is reduced, resulting in increased HR.

50
Q

This is the only commonly used beta blocker that uses the kidneys as it’s primary route of elimination

A

Atenolol

Most others depend on the liver. Think about how so many liver patients are on atenolol (for varices –> liver is shot, so use the one that’s eliminated via kidneys)

51
Q

Vasopressin and seizures

A

Overdose of vasopressin can lead to hyponatremia and resultant seizures

52
Q

TCAs have this effect on NE

A

They decrease the repute of NE –> can lead to excessive SNS activation

53
Q

Epi dose ranges

A

Low dose epi

  • 0.01-0.03 mcg/kg/min
  • B1 and B2 stimulation results in decreased SVR and increased CO

Intermediate epi

  • 0.01-0.15 mcg/kg/min
  • Mixed alpha and beta effects

High Dose Epi

  • > 0.15 mcg/kg/min
  • Mostly alpha effects
  • SVT can also occur here (limits it’s usefulness)
54
Q

This BB has great membrane stabilizing properties

A

Propanolol

55
Q

This BB has intrinsic sympathomimetic properties

A

Labetalol

56
Q

What does it mean to say that a medication has membrane stabilizing properties?

A

Means that the drug has local anesthetic-type effects

Includes propanolol and acebutolol

57
Q

S/S of central anticholinergic syndrome

A 
Sedation
Stupor 
Coma
Restlessness
Anxiety 
Hallucinations
Confusion
Flushed skin
Dry mouth
Blurred vision
Fever

Diphenhydramine and promethazine both have anticholinergic qualities and can cause central anticholinergic syndrome (I believe atropine and scopolamine can also do this)

58
Q

These are selective beta 1 blockers

A 
Atenolol
Acebutolol
Betaxolol
Bisprolol
Esmolol
Metoprolol
59
Q

These are some non-selective BBs

A 
Carvedilol
Labetalol
Nadolol
Timolol
Propanolol
Pindolol
60
Q

2 Types of MAO and what they metabolize

A

1) MAO-A
- Metabolizes catecholamines (EPI, NE, DA, and Serotonin)

2) MAO-B
- Metabolizes tyramine, DA, and phenylethylamine

Dopamine is metabolized by both forms of MAO

61
Q

Name 3 drugs that block nicotinic Ach receptors at autonomic ganglia

A

Trimethephan
D-Tubocurarine
Metocurine

62
Q

What happens in response to blocking nicotinic autonomic receptors?

A

Hypotension 2/2 arterial and venodilation

This occurs because sympathetic impulses are blocked

63
Q

How does EPI increase BP?

A

1) Arterial and venoconstriction
2) Increased HR
3) Increased contractility

64
Q

This dose of EPI is very good for producing bronchodilation

A

LOW dose EPI is the most effective bronchodilator available

025-0.50 mcg/min

65
Q

Effect of cocaine on SNS

A

Increases SNS activity by blocking reuptake of EPI and NE

66
Q

Effect of phenylephrine

A

Activates A1 and A2 receptors
Veins > arteries
Stimulates baroreceptor reflex (will decrease HR and CO)

67
Q

Effects of Dobutamine

A

Mostly B1 Stimulation
Minimal B2 and Alpha stimulation

Overall, produces increased contractility and CO with minimal increases in HR and BP

68
Q

Effects of isoproterenol

A

Works on B1 and B2
Causes increased contractility and HR and thus CO
Also decreases BP 2/2 B2 effects.
Can cause dysrhythmias and increased O2 demand, resulting in MI.

Good clinical use as chemical pacemaker for complete HB

69
Q

What is the most common clinical use of dopamine?

A

For it’s positive inotropic effects

70
Q

Where are B2 receptors most commonly found?

A

In the SM of blood vessels in skeletal muscle

71
Q

Receptors that phentolamine blocks

A

A1 and A2

72
Q

Receptors blocked by labetalol

A

B1, B2, and A1

73
Q

Avoid labetalol in these isorders

A

Asthma and CHF (will further decrease inotropy and CO)

74
Q

Risk of giving a BB to a diabetic patient

A

Beta blockade may mask the s/s of hypoglycemia

** Board Exam ** (22 decks)

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