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Advanced Pharm COPY COPY > Anti-hypertensives Part II > Flashcards

Anti-hypertensives Part II Flashcards

1
Q

Nitroglycerin

MOA

E1/2t

A
  • Generates NO through a glutathione-dependent pathway which involves glutathione S-transferase
  • NO then stimulates cGMP to cause peripheral vasodilation
  • E1/2- 1.5 minutes
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2
Q

How does nitroglycerin cause methemoglobinemia?

How is metHgb treated?

A
  • Nitrite metabolite oxidizes ferrous ion in Hgb to ferric form which leads to the formation of metHgb
  • Caution with high doses
  • Treated with methylene blue 1-2 mg/kg IV over 5 min to reconvert metHgb to Hgb
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3
Q

What are the CV effects of Nitroglycerin?

A
  • venodilation
    • decreased venous return (preload)
  • decrease L and R ventricular end-diastolic pressure
  • decrease CO
  • no change, or slight change to HR
    • b/c drop in BP is not as significant so the baroreceptors dont respond
  • No change to SVR
  • Increase in coronary blood flow to ischemic subendocardial areas (opposite of SNP)
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4
Q

Nitroglycerin systemic effects:

CNS

Pulm

Heme

GI

A
  • CNS- vasodilation, increased ICP, HA
  • Pulm
    • decreased PVR
    • bronchial dilation
    • inhibits hypoxic pulmonary vasoconstriction
  • Heme- inhibits platelet aggregation causing dose related prolonged bleeding time
  • GI- relaxes smooth muscles of GI tract
    • this is why it is one of the treatment options for SOO spasm
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5
Q

What are the clinical uses of nitroglycerin?

A
  • Angina
    • venodilation and increased venous capacitance decreases venous return to the heart which reduces RVEDP and LVEDP
    • reduces myocardial O2 requirements by reducing cardiac work
  • Cardiac failure
    • decreases preload
    • relieves pulmonary edema
    • limits damage of MI
  • Controlled hypotension
    • less potent than SNP, better choice
  • Sphinctor of Oddi spasm
    • during laparoscopic cholecystectomy or opioid use
    • bolus 200 mcg (1 ml) at a time
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6
Q

What is the dose if you are using Nitroglycerin for controlled hypotension?

when is it NOT recommended?

A
  • start at 10-20 mcg/min
  • titrate by increasing 5-10 mcg/min every 5-10 min
  • usual dosage 50-200 mcg/min; max 500 mcg/min
  • NOT recommended in cranial surgery prior to opening the dura
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7
Q

Isosorbid Dinitrate

Use

administration

How does it work?

SE

Active metabolite

A
  • used to treat angina
  • Administered PO (DOA 6 hours) or SL (DOA 2 hours)
  • Works predominantly on venous circulation, improves regional distribution of myocardial blood flow in patients with CAD
  • Side effects: Orthostatic hypotension
  • Active metab: isosorbid-5-mononitrate
    • more active than parent drug
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8
Q

Trimethaphan

what does it do?

dose

onset

SE

A
  • Ganglionic blocker and peripheral vasodilator
    • blocks the ANS and relaxes capacitance vessels
    • lowers SVR,BP, CO
    • Can have increased HR d/t PNS blockade, not becasue of baroreceptors
  • Dose: 10-200 mcg/kg/min IV
  • Onset: rapid onset, must be given continuously
  • Side effects:
    • mydriasis, decreased GI activity, urinary retention
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9
Q

What are the three major classes of Ca channel blockers?

What drugs belong to each class?

A
  • Dihydropyridines- more effect on Ca channels in vasculature (-pine)
    • Nifedipine
    • Amlodipine
    • Nicardipine
    • Felodipine
  • Phenylalkylamines- more effect on Ca channels on the heart
    • Verapamil
  • Modified Benzothiazepines- works on both heart and vasculature
    • Diltiazem
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10
Q

Why do the different classes of CCBs work in different places?

A
  • Because the different classes bind to different places on the Ca channels
  • Dihydropyridines- cause extracellular allosteric modulation of the channel at the binding site
  • Phenylalkylamine- pore blocker of channel at the binding site
  • Benzothiazepine- mechanism unclear
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11
Q

Where are L-type Ca channels found?

A
  • vascular smooth muscle- predominatlye arterial
  • SA node
  • AV node
  • Cardiac myocytes
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12
Q

Which CCBs block entry of Ca, and what does that cause?

A
  • All classes block entry of Ca
  • Causes:
    • decreased contractility in cardiac muscle
    • Coronary vascular dilation (good choice in variant angina)
    • Systemic arterial diltation (artery > vein) causing decreased afterload, wall tension and BP
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13
Q

Which CCBs slow Ca channel recovery?

What does this cause?

Who should you avoid these drugs in?

A
  • Phenylalkylamines
  • Causes:
    • SA node: chronotropic effect, decreasing HR
    • AV node: dromotropic effect, decreasing conductivity and HR
  • **Avoid in pt with uncompensated HF, bradycardia, or heart block
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14
Q

During what part of the ventricular action potention do CCBs have effect?

A
  • Ventricular cardiomyocyte (pic below)
    • During plateau phase, which is why it decreases contractility
  • SA/AV node (front pic)
    • During the initial depolarization in phase 0, slowing the depolarizing rate and lengthening the recovery phase to decrease HR
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15
Q

What are some anesthetic specific drug interactions with CCBs?

A
  • Myocardial depression and vasodilation with IA
  • Can potentiate NMB
  • Verapamil contraindicated with Beta blockers
  • Verapamil increases risk of LA toxicity
    • cardiac toxic?
  • Verapamil and dantrolene can cause hyperkalemia due to slowing of inward movement of K ions can result in cardiac collapse
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16
Q

What are some general (non anesthetic) drug interactions with CCBs?

How can CCB toxicity be reversed?

A
  • Digoxin- CCBs can increase the plasma concentration of digoxin by decreasing its plasma clearance
  • H2 antagonists- ranitidine and cimetidine alter hepatic enzyme activity and thus could increase plasma levels of CCB
  • CCB toxicity can be reversed with IV Calcium or dopamine
17
Q

Verapamil

Classification

primary site of acction

effects

A
  • Phenylalkylamine; synthetic derivative of papaverine
    • levoisomer is specific to the slow Ca channel
  • Primary site of action is the AV node
    • depresses the AV node
    • negative chronotropic effect on SA node
    • negative inotropic effect on myocardial muscle
    • moderate vasodilation on coronary as well as systemic arteries
18
Q

What are the clinical uses of verapamil?

A
  • SVT
  • vasospastic angina
  • HTN
  • hypertrophic cardiomyopathy
  • maternal and fetal tachydysrhythmias
  • premature onset of labor
19
Q

Verapamil Pharmacokinetics:

PB

absorption

metabolite

peak

E1/2t

A
  • 90% PB; presence of other agents such as lidocaine, diazepam, propranolol will increase activity
  • Orally almost completely absorbed with extensive hepatic first pass metabolism
    • PO dose 10x higher than IV dose
  • Active metabolite: norverapamil
  • Oral peak: 30-45 minutes; IV peak 15 minutes
  • E1/2t = 6-12 hours
20
Q

Nifedipine

CCB class

clinical uses

Primary site of action/effect

A
  • Dihydropyridine derivative
  • Clinical uses
    • angina
    • HTN
  • Primary site of action: peripheral arterioles
    • coronary and peripheral vasodilator properties > verapamil
    • little to no effect on SA or AV node
    • decrease SVR and BP
    • reflex tachycardia
    • can produce myocardial depression in pts with LV dysfunction or on BBs
21
Q

Nifedipine pharmacokinetics

route

PB

metabolism

E1/2

A
  • IV, oral or SL
    • Oral effects seen in 20 minutes, peak in 60-90 min
  • 90% PB
  • Nearly completely hepatically metabolised and metabolites excreted in urine
  • E1/2t is 3-7 hours
22
Q

Nifedipine Side effects

A
  • vertico
  • HA
  • flushing
  • hypotension
  • paresthesias
  • muscle weakness
  • can induce renal dysfunction
  • coronary vasospasm with abrupt d/c
23
Q

Diltiazam

CCB class

principle site of action

uses

A
  • Benzothiazepines derivative
  • Principle site of action is the AV node
  • Uses
    • 1st line tx for SVT
    • HTN
  • Intermediate potency between verapamil and nifedipine
  • minimal CV depressant effects
    • do not combine with BB
24
Q

What are some other clinical uses of Diltiazam?

Route

Dose

A
  • Vasospastic angina
  • hypertrophic cardiomyopathy
  • maternal and fetal tachydysrhythmias
  • Route: PO or IV
  • Dose: 0.25-0.35 mg/kg over 2 min; can repeat in 15 min
25
Q

Diltiazem pharmacokinetics

oral onset

PB

E1/2t

A
  • Oral onset is 15 min and peaks in 30 min
  • 70-80% PB
  • Excreted in the bile and urine
  • E1/2t is 4-6 hours
  • Liver disease may require a decrease in dose
26
Q

Chart comparing the prototypes of the three classes of CCBs

Selectivity

Adverse effects

contraindications

drug interactions

A
27
Q

What are the two centrally acting anti-hypertensive agents?

MOA?

Clinical uses?

A
  • Clonidine and dexmedetomidine
  • MOA: selective alpha-2 agonist that reduces sympathetic outflow from vasomotor centers in the brain stem
  • Clonidine site of action: Alpha-2 receptors in CNS
  • Clinical uses:
    • hypertension
    • sedation
    • decrease anesthetic requirements
    • improve peri-op hemodynamics
    • analgesia
28
Q

Clonidine results in ______

Rebound hypertension can be caused by ______.

A
  • clonidine results in BP reduction from decreased CO d/t decreased HR and peripheral resistance
  • Rebound HTN can be caused by abrupt cessation (withdrawal)
29
Q

What are the side effects of the centrally acting agents?

A
  • bradycardia
  • sedation
  • xerostomia (dry mouth)
  • impaired concentration
  • nightmares
  • depression
  • vertigo
  • EPS
  • lactation in men
30
Q

Pharmacokinetics of centrally acting agents

route

metab

A
  • Available as PO or transdermal patch
  • 50/50 hepatic metabolism and renal excretion
31
Q

When does withdrawal syndrome occur with patients on centrally acting agents?

A
  • Occurs in pts on doses of >1.2 mg/day
  • Occurs 18 hours after acute d/c of drug
  • lasts 24-72 hours
  • Can be treated by rectal or transdermal clonidine
32
Q

Which anti hypertensives do you have the pt continue before surgery?

Which ones do you hold?

why?

A
  • Give BB- b/c it reduces peri-op MI
  • Give CCBs- benefits outweigh risks unless severe LV dysfunction
  • Hold ACE inhibitors- for one or two dose intervals, depending on DOA of drug
    • will cause labile BPs during procedure
33
Q

What is considered a hypertensive crisis?

How can you treat it?

A
  • DBP > 120 mmHg with evidence of end organ failure
  • Goal to decrease DBP to 100-105 mmHg ASAP
  • Treatment:
    • NTP- most effective, first choice
    • NTG
    • Labetalol

Advanced Pharm COPY COPY (27 decks)

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