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*ANS > ANS Pharmacology & Pathophysiology > Flashcards

ANS Pharmacology & Pathophysiology Flashcards

1
Q

How is phenylephrine metabolized?

A

monoamine oxidase (MAO)

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2
Q

How is dexmedetomidine metabolized?

A

Liver -CYP450

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3
Q

Alpha 2 agonism in the vasculature results in what?

A

Vasoconstriction

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4
Q

Which receptor is responsible for inhibiting ADH (diuresis)?

A

Alpha-2

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5
Q

Which receptor is responsible for decreasing insulin release from the pancreatic ___________cells.

What increases insulin secretion from these cells?

A

Alpha-2

(Islets/B-Cells)

M3 increases insulin (DM3)

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6
Q

What adrenergic receptor increases platelet aggregation?

A

Alpha 2

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7
Q

Agonism of which adrenergic receptors produce an antishivering effect?

A

alpha 2

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8
Q

Where does dexmedetomidine produce its analgesic effects?

A

alpha-2 receptors in the dorsal horn of the spinal cord

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9
Q

Alpha 2: Alpha 1 binding of clonidine vs precedex

A

clonidine 200:1

precedex 1600:1

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10
Q

What happens with abrupt clonidine withdrawal?

A

Rebound HTN and tachyarrythmias

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11
Q

3 Endogenous catecholamines

A
  1. Epi
  2. Norepi
  3. Dopamine
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12
Q

What systemic effects do endogenous catecholamines have on GI tract, lungs, heart, liver, and BP

A

GI- decreased digestion
Lungs- bronchodilation
Heart- increased HR
Liver- converts glycogen to glucose
Increased BP

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13
Q

Epi may cause (hyper/hypo) glycemia and (hypo/hyper) kalemia and why?

A

hyperglycemia (stimulation of B2 receptors)
hypokalemia 2nd to transcellular K shift

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14
Q

Norepinephrine affects which receptors the most?

A

Alpha 1 and Beta 1

(Low doses = beta 1- increased HR, CO, inotropy, dromotropy
High doses = alpha 1 - systemic vasoconstriction [minus coronaries] and decreased HR)

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15
Q

Norepi at high doses causes systemic vasoconstriction by agonizing alpha 1 receptors. Why is the baroreceptor response of bradycardia not as clinically significant as neosynephrine?

A

Because Norepi also has inherent B1 agonizing properties which limits the BRR of bradycardia secondary to alpha-1.

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16
Q

Does Norepi cause elevations in glucose?

A

No- or very minimally (minimal effects at b2)

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17
Q

What is 1st line therapy in distributive shock states refractory to hypotension?

A

Norepi

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18
Q

Low/Moderate/High dose dopamine
-dosages and effects

A

Low 1-2mcg/kg/min : D1 receptors (vasodilation: increased renal and splanchnic blood flow)

Mod 2-10: alpha 1 & beta 1 (increased HR, contractility, and BP)

High 10-20: pure alpha 1 agonism (vasoconstriction)

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19
Q

Which dopamine receptors cause direct vasodilation of the renal, GI, coronary, and cerebral blood vessels?

A

Post-synaptic D1

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20
Q

Which dopamine receptors inhibit Norepi release causing systemic vasodilation?

A

Pre-synaptic D2

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21
Q

3 Places D2 receptors are found

A
  1. Pituitary gland
  2. Emetic center
  3. Kidney
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22
Q

Which dopamine receptors are responsible for inducing nausea and vomiting?

A

D2 - chemoreceptor trigger zone

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23
Q

Main concern with Levophed

A

Extravasation and skin necrosis
*Central line

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24
Q

How do you treat extravasation caused by Levophed? (2 ways)

A

Phentolamine (2.5-10mg diluted in 10mls) > vasodilate
(keep it simple 10mg diluted in 10mls)

Stellate ganglion block (improve blood flow to extremity

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25
Q

Where are B3 receptors primarily found and what are they primarily responsible for?

A

Apidose tissue - thermoregulation and lipolysis

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26
Q

What is isoproterenol derived from?

A

Dopamine

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27
Q

Isoproterenol is how much more potent than epi?

A

2-3x

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28
Q

T/F Isoproterenol has no effect on alpha receptors

A

True!

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29
Q

S/E’s of Isoproterenol?

A

Hypotension (B2), SVTs and VTs

(has been largely replaced by transcutaneous or transvenous pacing for this reason)

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30
Q

How does isoproterenol work?

A

It agonizes B1 & B2 receptors leading to increased HR, contractility, and *vasodilation (hypotension!)

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31
Q

What can be used for bradycardia unresponsive to atropine or in a denervated heart?

A

Isoproterenol

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32
Q

How does isoproterenol treat cor-pulmonale? Are there better options?

A

By enhancing RV contraction (B1), thereby decreasing pulmonary congestion (blood can move forward more easily with a better contracting RV + B2 bronchodilator effects)

*NO & prostagadin I2 are better

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33
Q

What is dobutamine derived from?

A

Isoproterenol

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34
Q

What drug acts as a pharmacologic stress test and how?

A

Dobutamine

  • potent B1 agonist
  • increased inotropy and chronotropy
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35
Q

What 2 populations should Dobutamine be avoided in and why?

A
  1. Active MI (could extend the MI)
  2. Afib (increased conduction velocity through the AV node may trigger RVR)
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36
Q

What classification is Dobutamine?

A

Positive inotrope
*Not a pressor!
*Increase in HR, contractility, and CO

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37
Q

When is dobutamine a good choice?

A

Cardiogenic shock and CHF

*coronary artery vasodilator
*LV failure improves due to a decrease in SVR
*RV failure improves due to a decrease in PVR - allowing forward flow)

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38
Q

Why is ephedrine considered a controlled substance in some institutions?

A

It crosses the BBB and has mild stimulating effects centrally

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39
Q

What is the black box warning regarding B2 agonists?

A

The long-acting ones can lead to asthma-related death

(Salmetrol and formoterol)
*Long term use may lead to downregulation of beta2 receptors resulting in tachyphylaxis and may lead to a hyperresponsive airway

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40
Q

2 long-acting Beta 2- agonists

A
  1. Salmeterol
  2. Formoterol
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41
Q

3 Short-acting beta-2 agonists

A
  1. Albuterol
  2. Levoalbuterol
  3. Terbutaline
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42
Q

What’s the problem when people just take their rescue inhaler more instead of being put on a controller?

A

Increased B2 agonism over time, the B2 selectivity wanes and B1 predominates > tachycardia and arrhythmias

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43
Q

What is the precursor of Epinephrine?

A

Norepi

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44
Q

What adrenergic agonist is metabolized by the liver?

A

Ephedrine

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45
Q

What is the precursor of Norepi?

A

Dopamine

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46
Q

What are the two non-selective alpha antagonists?

A
  1. Phenoxybenzamine
  2. Phentolamine
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47
Q

What alpha antagonist is used almost exclusively preoperatively to treat pheochromocytoma?

A

PHEnOxybenzamine
PHEO

(think the one with benz bc you’ll need a benzo to manage pheo cases)

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48
Q

Best treatment for phenoxybenzamine-induced severe hypotension.

A

IVF and vasopressin

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49
Q

Why can phenoxybenzamine and phentolamine produce reflex tachycardia?

A

BRR + NE keeps being released but no alpha receptors to bind to > beta 1 on SA and AV node

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50
Q

Which non-selective alpha antagonist:

  1. binds reversibly/irreversibly (competitive/noncompetitive)
  2. short vs long acting
  3. IV vs PO
A

Phenoxybenzamine - PO/long/non-comp (irreversible)
Phentolamine- IV/short/competitive (reversible)

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51
Q

Which drug is used to treat IV extravasation to prevent tissue necrosis?

A

Phentolamine (2-10mg diluted in 10mls)

(keep it simple: 10mg in 10mls)

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52
Q

Why should you avoid phentolamine in pts with severe CAD?

A

bc of the BRR resulting in tachycardia

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53
Q

Prazosin

  • competitive/noncompetitive
  • selective/nonselective
A

competitive
selective- alpha 1

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54
Q

What is the only commonly used beta-blocker that is dependent on the kidneys as its primary route of elimination AND metabolism and can accumulate in renal failure?

A

Atenolol

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55
Q

What is the only beta-blocker metabolized by RBC esterases?

A

Esmolol

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56
Q

Treatment of betablocker overdose? (6)

A
  1. Glucagon
  2. Calcium
  3. PDE III inhibitors
  4. Epi
  5. Isoproterenol
  6. Cardiac pacing
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57
Q

Beta-1 selective Betablockers (6)

A

Metoprolol
Atenolol
Betaxolol
Esmolol

Acebutolol
Bisoprolol

“MAyBE AB”

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58
Q

Nonselective Betablockers (6)

A

Cardivelol
Labetalol

Timolol
Propanolol
Pindolol
Nadolol

(the two with mixed alpha and beta + TPPN)

59
Q

Half life of labetalol

A

6 hours

60
Q

beta: alpha ratio of labetalol vs carvedilol

A

labetalol 7:1
carvedilol 10:1

61
Q

Metoprolol bolus dosing and max dose

A

2.5-5mg

Max 15mg

62
Q

Esmolol duration of action

A

<15 minutes

63
Q

Esmolol bolus dosing and infusion dose

A

10-80mg
50-300mcg/kg/min

64
Q

Which betablocker has intrinsic sympathomimetic effects?

A

Labetalol

65
Q

Which betablocker has membrane stabilizing effects

A

Propanolol

(inhibits AP propagation across the cell membrane - kind of like local anesthetics, so has antidysthrymic properties to it)

66
Q

What does abrupt betablocker withdrawal result in?

A

HTN, tachycardia, myocardial ischemia, and an increase in 1-year mortality

(due to upregulation of receptors)

67
Q

What does nicotine do to acetylcholine?

A

It enhances its effect

(Cholinomimetic)

68
Q

What cholinergic agonist is used to identify reactive airway disease in those who don’t have clinically apparent signs of asthma?

A

methaCHOLINE

69
Q

What cholinergic agonist is used selectively for M3 receptors in the GI and urinary tracts and is used to treat non-obstructive urinary retention?

A

BethanaCHOL

70
Q

Mneumonic for anticholinergic syndrome (5)

A

Dry as a bone
Red as a beat
Blind as a bat
Hot as a hare
Mad as a hatter

71
Q

What drugs would cause central anticholinergic syndrome and what drug reverses it?

A

Atropine & Scopolamine
Reverse with PHYSostigimine 1-2mg

72
Q

What are the 3 classes of calcium channel blockers?

A
  1. Dihydropyridines
  2. Benzothiazepines
  3. Phenylalkyamines

(Ni’s & clevidipine)
(Diltazem)
(Verapamil)

73
Q

Which CCBs are best for reducing HR in patients with tachycardia, afib, or aflutter?

A

Diltiazem & Verapamil

(benozthiazepine & phenylalkyamine)

74
Q

Which CCB would you want to use in a patient with a tachyarrhythmia and a reduced EF? (with the goal of lowering HR will preserving myocardial contractility)

A

Diltiazem

75
Q

Rank the CCBs in order of greatest impairment of contractility to least:

Nifedipine, Diltiazem, Verapamil, Nicardipine

A
  1. Verapamil
  2. Nifedipine
  3. Diltiazem
  4. Nicardipine
76
Q

Which two CCBs are the best vasodilators for the treatment of HTN from an elevated SVR?

A

Nifedipine & Nicardipine

77
Q

Which CCB is useful for coronary vasospasm?

A

Nicardipine

78
Q

Which is the only CCB proven to decrease M&M from cerebral vasospasm?

A

Nimodipine (PO)

79
Q

What are two class-4 antiarrhythmics?

A

Verapamil and Diltiazem

>decrease electrical impulses in the SA and AV nodes

80
Q

What could happen if you give verapamil to a patient on betablockers?

A

Complete heart block or profound myocardial depression

81
Q

Why is nimodipine useful in cerebral vasospasm and not the other CCBs?

A

It is more lipophilic and crosses the BBB
>cerebral vasodilation

82
Q

Which type of calcium channels to calcium-channel blockers target?

A

L-type calcium channels

83
Q

How does Nitroglycerine work?

A

It’s a direct vasodilator – dilates coronary arteries and reduces systemic BP (preload>afterload), supplying more blood flow and less workload

*liberates nitric oxide from the vascular smooth muscle walls

84
Q

How is nitro metabolized?

A

by the liver

85
Q

Before giving nitro, what should you think of?

A

Are they on viagra/sildenafil? >will become profoundly hypotensive.

86
Q

Dosing of nitro gtt

A

5-100mcg/min

87
Q

Which nitrodilator primarily reduces preload

A

Nitroglycerin

88
Q

Which nitrodilator reduces both preload and afterload?

A

Nitroprusside

89
Q

Which nitrodilator affects mainly arterial smooth muscle?

A

Hydralazine

90
Q

Why is Sodium Nitroprusside not used in MI?

A

It will induce coronary steal and redistribute blood flow away from the ischemic tissue

91
Q

What total dose and rate should sodium nitroprusside not exceed and why?

A

Cyanide toxicity
total dose < 500mcg/kg
no faster than 2mcg/kg/min

92
Q

How does Hydralazine produce vasodilation?

A

It activates potassium ATP channels which reduces intracellular calcium.

93
Q

Which nitrodilator preserves preload?

A

Hydralazine - it doesn’t dilate veins

94
Q

Which drug causes hypertrichosis and what is that?

A

Minoxidil > Hair growth

95
Q

Where is vasopressin stored and released?

A

Posterior pituitary

96
Q

Where is vasopressin synthesized?

A

Hypothalamus

97
Q

What do V1 receptors produce?

A

intensive vasoconstriction

98
Q

What do V2 receptors produce?

A

increases ADH and creates more aquaporin channels which insert themselves into the walls of collecting ducts to increase water (not solute) reabsorption

(lowers serum os)

99
Q

Where are V3 receptors located?

A

Pituitary gland

100
Q

What is first-line therapy for ACE or ARB-induced vasoplegia?

What would be the next best drug after that?

A

Vasopressin

Methylene Blue

101
Q

What can vasopressin OD cause?

A

hyponatremia and seizures

(holding onto water, getting rid of solute)

102
Q

Vasopressin bolus dose

A

1-2 units

103
Q

Infusion rate of vasopressin

A

0.01-0.1 units/min

104
Q

How long does vasopressin last?

A

10-30 minutes

105
Q

Two PDE3 inhibitors

A
  1. Milrinone
  2. Cilostazol
106
Q

How many moles of ATP can be produced from one mole of glucose?

A

38

107
Q

What do phosphodiesterases usually do?

A

Break down cAMP and cGMP

108
Q

How do PDE inhibitors work in general?

A

They prevent the breakdown of cAMP and cGMP
>increased concentrations in the cell
>increased inotropy in the heart
>vasodilation in lungs and smooth muscle

109
Q

What are the PDE5 inhibitors (3)?

A
  1. sildenAFIL
  2. tadalAFIL
  3. vardenAFIL

varmints slide in, ta-da! (Dont know how i’m going to remember the whole 5 part with that but ok)

110
Q

Which drug class treats pulmonary HTN and ED?

A

PDE5 inhibitors

(increases cGMP in the lungs and penis > smooth muscle relaxation > increased blood flow)

111
Q

Suffix for PDE4 inhibitors

A

-ilast

Romflumilast, Apremilast, Ibudilast

112
Q

What are theophylline and methylxanthine classified as?

A

Nonspecific PDE ihibitors

>relax airway smooth muscle
>decrease inflammation
>Asthma/COPD

113
Q

PDE inhibitors affect what two 2nd messengers?

A

cAMP & cGMP

(prevent their metabolism/breakdown)

114
Q

What drug is frequently used for weaning pt’s off cardiopulmonary bypass?

A

Milrinone

115
Q

Which specific PDE inhibitor prevents platelet aggregation?

A

PDE3

116
Q

List the Gq receptors

A

Alpha-1
Vasopressin-1
Histamine-1
M1/3/5

117
Q

List the Gs receptors

A

Beta 1 & 2
Vasopressin-2
Histamine-2

Post-synaptic Dopamine 1

118
Q

List the Gi receptors

A

Alpha-2
Presynaptic Dopamine 2
M2/M4

119
Q

Where is aldosterone secreted by and what does it do?

A

The adrenal cortex

  • sodium and water reabsorption
  • K+ excretion
120
Q

ACE inhibitors are 1st line therapies for what 4 conditions?

A
  1. HTN
  2. CHF
  3. MR
  4. LV dysfunction
121
Q

Which drug class is renal protective in diabetics?

A

ACE inhibitors

122
Q

Why do ACE inhibitors elicit a cough in some people?
What about angioedema?

A

Because ACE breaks down bradykinins (pro-inflammatory mediator in the lungs)

  • ACE inhibitors prevent this breakdown
  • more bradykinin = more pulm inflammation = cough

-in most people bradykinin can be broken down by other pathways, but those who do not (possibly genetic component) will develop angioedema

123
Q

Which people are at most risk for angioedema from ACE inhibitors?

A

African Americans - 4-5x more likely

124
Q

Which ace inhibitor undergoes hepatic metabolism?

A

Captopril

125
Q

Which ACE inhibitor is a prodrug?

A

Enalapril

126
Q

What receptor do ARBs target?

A

AT1 (prevents binding of angiotensin II at that receptor)

127
Q

What happens when an agonist binds to the GABA-A receptor?

A

An influx of chloride hyperpolarizes the cell membrane and APs aren’t generated

128
Q

What receptor do volatile agents primarily target?

A

GABA-A

129
Q

By which mechanism do volatile anesthetics produce myocardial depression and vasodilation?

A

By blocking calcium channels in cardiac and VSM.

130
Q

By which mechanism do volatile agents prolong the QT interval?

A

by inhibiting potassium efflux which normally causes repolarization

131
Q

What enzyme converts angiotensinogen to angiotension I?

A

Renin

132
Q

What is cardiac output dependent on in the denervated heart?

A

Stroke volume (Preload)

HR is fixed

133
Q

Which ANS reflex remains intact in the denervated heart and why?

A

Bainbridge - bc stretch of the SA node directly increases the SA node firing rate

134
Q

What agent can be used to treat carcinoid-like symptoms?

A

Octreotide

135
Q

What are carcinoid-like symptoms?

A

bronchoconstriction, diarrhea, headache, flushing, HTN

(think need to emergently have diarrhea but can’t bc your in public so you start freaking out and getting HTN, flushed, headache, and then you cant breathe bc u cant hold it in any longer….and your thinking why does this always happen to me- do i have cancer?/carcinoid

136
Q

What is Shy-Drager syndrome now referred to as?

A

Multiple system atrophy

137
Q

2 Metabolites of ephedrine?

A

Noreipi & Benzoic acid

138
Q

What drug is a selective alpha-2 receptor ANTAGONIST

A

Yohimbine

139
Q

How does Methylene Blue produce widespread vasoconstriction?

A

Bc it inhibits the nitric oxide pathway

140
Q

Max dose of methylene Blue

A

7mg/kg

141
Q

What is central anticholinergic syndrome treated with?

A

Physostigmine (Anticholinesterase, inhibits the breakdown of acetylcholine allowing it to build up)

-tertiary amine

142
Q

6 drugs that can induce carcinoid syndrome.

A
  1. Sux
  2. Atracurium
  3. Thiopental
  4. Epi
  5. NE
  6. Isoproterenol
143
Q

What is carcinoid syndrome?

A

A life-threatening event seen in patients with carcinoid tumors that release GI peptides and vasoactive substances.

*ANS (4 decks)

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