ANS Pharm: ACEIs, ARBs, Anesthetic Agents Flashcards

1
Q

dry cough from ACEI

A
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2
Q

Which effects of the volatiles are:
ANS mediated?
spinal cord mediated?

A
  • ANS: amnesia, sedation, unconsiousness
  • spinal cord: immobility (MAC)
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3
Q

Which locals are antiarrhythmics?

A

1A: procainamide
1B: Lidocaine

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4
Q

RAAS starts with renin secretion by renal cortical juxtaglom. cells. What causes this?

A

decreased renal perfusion d/t hemorrhage or SNS activation

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5
Q

synthesizes angiotensinogen

A

liver

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6
Q

renin acts on ___ to produce ___

A

cleaves angiotensinogen to produce angiotensin 1

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7
Q

Angiotensin 2 is a potent vasoconstrictor of kidney and mesenteric arterioles via its action on….

A

the angiotensin receptor, type 1 (AT 1).

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8
Q

angiotensin receptor, type 2 (AT2)

A

regulates vascular response, cardiac growth response, and fibrotic response in other tissues

type 1: angiotensin 2 acts there to vasoconstrict

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9
Q

RAAS
role in HTN

A
  • HTN involves RAAS dysfxn
  • RAAS modules NT release (influences SNS outflow)
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10
Q

Actions of angiotensin II

A
  • triggers release of norepi & epinephrine from the adrenal medulla
  • acts on renal tubules to decrease both Na & water elimination while increasing K excretion.
  • stimulates Aldosterone production (amplifies Na retention & K excretion)
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11
Q

T/F:
The result of RAAS is an elevation of venous blood pressure and an increased intravascular volume.

A

false
arterial BP

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12
Q

RAAS

Which hormones come from the adrenal cortex vs the medulla

A

cortex: aldosterone

medulla: epi, norepi

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13
Q

T/F:
Angiotensin 1 and 2 cause vasoconstriction.

A

False
only 2

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14
Q

Although ACEi drugs are potent, they are devoid of the many side effects of other antihypertensives such as…

A

bradycardia, bronchospasm, and rebound hypertension when acutely discontinued

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15
Q

ACEi drugs are best for HTN from increased renin & are first-line therapy for…

A

HTN, CHF, mitral regurgitation, LV dysfunction

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16
Q

ACEI effects

A
  • Decrease angiotensin (↓ aldosterone)
  • Reduce LV afterload
  • reduce arterial tone
  • ↓ water and Na retention
  • decrease bradykinin breakdown (endogenous vasodilator)
  • lowers LDL
  • Do not impair baroreceptors, thus orthostatic hypotension is not an issue.
  • renal protection in diabetics
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17
Q

ACEI prevent bradykinin breakdown. This contributes to 2 important side effects

A

cough
angioedema

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18
Q

ACEIs + vasodilating GA can cause hypoTN that is not responsive to …., so use ___

A

neo, ephedrine, norepi

use vaso (V1)

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19
Q

ACEIs can cause renal dysfxn and this electrolyte imbalance

A

hyperK

my also see fatigue

20
Q

Which ACEI is a prodrug?

21
Q

Which ACEI is excreted unchanged in the urine?

A

lisinopril

22
Q

T/F:
Angioedema from ACEIs is thought t be genetically linked.

A

True
Black people 4.5x more likely

23
Q

the only ACEI available IV

24
Q

Why do ARBs have less SEs than ACEIs?

A

ACEI impair activity at both AT 1 & AT 2 receptors

ARBs only AT1 receptor (more selective)

ARBS have similar SE to ACEi but milder and no dry cough
primary outcome is also similar

25
Q

ARBs receptor activity

A
  • great affinity for AT1r
  • inhibit angiotensin 2 @ AT1r
  • better at inhibiting angiotensin 2 than ACEi
26
Q

T/F:
ACEi provides renal protection for DM, unlike ARBs.

A

False
both can

27
Q

T/F:
Volatiles have anti-seizure activity.

28
Q

primary inhibitory & excitatory NT in CNS

A

GABA

glutamate

29
Q

common anesthetics that enhance GABA

A
  • volatiles
  • prop
  • etomidate
  • BZDs
  • Barbs
30
Q

What explains the CV, respiratory and neuroendocrine effects of anesthetics?

A

they alter neurotransmission

31
Q

GABAr structure

A

ligand gated ion channel

Cl- influx hyperpolarizes = inhibits neuronal cells

32
Q

ANS modification by volatile inhaled agents:

A
  • ↓ BP, CO, Cl, SVR
  • ♡ depressant & vasodilates (Alters Ca fxn)
  • Depress baroreceptor reflex (HD instability)
  • Antagonizes SA node automaticity (nodal rhythm) & prolong QT interval (inhibition K efflux which repolarizes)
  • Impairs ventilatory response to CO2 and O2. Low Minute ventilation for a given blood gas tension.
  • Uncoupling of cerebral blood flow autoregulation (> 0.5 MAC).
33
Q

Volatiles primary receptor target

34
Q

Volatiles uncouple CBF autoregulation, usually above 0.5 MAC. What does this mean?

A
  • blood flow will be higher than metabolic need
  • the ability to maintain a consistent blood flow despite changes in blood pressure is disrupted
35
Q

Which anesthetics target GABA A?

A
  • volatiles
  • Propofol
  • Etomidate
  • BZDs
36
Q

T/F:
Etomidate blocks the SNS response to laryngoscopy.

37
Q

How does etomidate affect CBF?

A

cerebral vasoconstrictor
reduces CBF & ICP

38
Q

Ketamine is a/w CV stability and works to treat depression and pain. What are the limiting SEs?

A
  • emergence delirium
  • secretions
  • nystagmus
  • hallucinations
39
Q

Precedex can decrease MAC by how much?

40
Q

Lidocaine is a class 1B antiarrhythmic. How do they work?

A
  1. suppress automaticity by increasing stimulation threshold of the ventricle & His-Purkinje
  2. inhibiting spontaneous depolarization during diastole
41
Q

longest doA LAs

A

bupi & ropi

42
Q

most potent LA

A

tetracaine

followed by chloroprocaine, bupi, ropi

43
Q

What rhythms can lidocaine treat?

A
  • AFIB
  • PVCs
  • VTach
44
Q

fast onset LAs

A
  • lidocaine
  • chloroprocaine
  • cocaine
45
Q

Why is cocaine unique as a LA?

A

increases endothelin (vasconstrictor)
&
impairs nitric oxide production

46
Q