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Advanced Pharm > Anti-hypertensives > Flashcards

Anti-hypertensives Flashcards

1
Q

How does the RAAS system work?

What are the ultimate functions of Angiotensin II?

A
  • Low renal perfusion causes release of Renin
  • Renin activates angiotensinogen to angiotensin I
  • ACE activated angiotensin I into angiotensin II
  • Angiotensin II causes:
    • increased sympathetic activity
    • tubule Na and Cl reabsorption and K excretion; H2O retention
    • Adrenal glad to secrete aldosterone
    • arterial vasoconstriction, increasing BP
    • pituitary gland to secrete ADH
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2
Q

ACE inhibitors are the first line therapy for what diseases?

They also delay the progression of what disease?

A
  • First line therapy:
    • HTN
    • CHF (post MI wil reduce progression of CHF)
    • Migral regurgitation
  • Delay progression of renal desease
    • Most effective in diabetic patients
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3
Q

What is the MOA of ACE Inhibitors?

A
  • MOA- block the conversion of angiotensin I to angiotensin II in the vascular endothelium
    • this is done by an interaction with the zinc ion of angiotensin converting enzyme (peptidyl- dipeptidase)
  • Causes a fall in arterial pressure and reduces the cardiac workload of the heart
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4
Q

What role do Bradykinins play in relation to BP and ACE?

A
  • ACE inhibitors increase the amount of bradykinin
    • This helps ACE inhibitors be more effective in decreasing BP than ARBS because the bradykinin is a vasodilator, further lowering the BP
  • Increase in Bradykinin causes:
    • vasodilation
    • cough
    • Angioedema
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5
Q

What effects does the decrease in Angiotensin II (caused by ACE inhibitors) have?

A
  • Decreased Ang II causes:
    • vasodilation
    • decreased blood volume
    • decreased cardiac and vascular remodeling
    • potassium retention
    • fetal injury
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6
Q

What receptor does Angiotensin II mostly interact with?

What are the effects of this receptor?

A
  • Angiotensin II mostly interactics with AT-1 (GCPR)
    • it signals increased Ca++ release from the SR
  • AT-1 receptor effects:
    • generalized vasoconstriction- especially in the afferent arterioles of renal glomeruli
    • increased NE release
    • Proximal tubule reabsorption of Na
    • Secretion of aldosterone from adrenal cortex
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7
Q

What are the side effects of ACE inhibitors?

A
  • Cough
  • hyperkalemia
  • Intra-op hypotension (hold am of surgery)
  • Granulocytopenia
  • Angiodema
  • Minimal side effects, so there is usually pretty good patient compliance
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8
Q

What are the different ACE inhibitors available?

How can you easily tell that a drug is an ACEI?

A
  • Drugs that end in -pril are ACE inhibitors
  • Captopril
  • enalapril
  • Ramipril
  • benazepril
  • lisinopril
  • Moexipril
  • Quinapril
  • Fosinopril
  • Trandorapril
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9
Q

What drugs will interact with ACE inhibitors?

A
  • NSAIDS will antagonize the effects because of the decrease in prostaglandins
  • Anti-hypertensives will have an additive effect
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10
Q

When are ACE inhibitors contraindicated?

A
  • Pregnancy
  • Renal artery stenosis- pts may develop renal failure due to impaired efferent arteriole constriction
    • if the efferent arteriole can’t constrict, they will not be able to maintain GFR with low flow
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11
Q

From the Table in the powerpoint, which ACE inhibitors are prodrugs and what are their duration of effects?

Captopril

Enalapril

Lisinopril

Ramipril

Do they have more effect on the Venous system or arterial system?

A
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12
Q

Angiotensin II Receptor Blockers (ARBS)

MOA?

Side effects?

Contraindication?

A
  • MOA: Competitive binding to inhibit the action of angiotensin II at its receptor (AT-1)
    • blocks the vasoconstrictive actions of Ang II without affecting ACE activity
  • Side effects- similar to ACE inhibitors
    • NO cough because there is no bradykinin accumulation
  • Contraindication
    • renal artery stenosis
    • pregnancy
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13
Q

How can you know a drug is an ARB?

A

The drug name ends in -artan

Losartan

Valsartan

Irbesartan

etc…

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14
Q

Hydralazine:

MOA

A
  • Activates guanylate cyclase causing hyperpolarization and vasodilation
    • direct relaxant effect of vascular smooth muscles, decreasing SVR
    • arteries > veins
    • alters Ca transport in vascular smooth muscles
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15
Q

Hydralazine Pharmacokinetics:

metabolism

onset

E1/2t

A
  • metabolism:
    • Extensive hepatic first pass metabolism
    • Acetylated in liver and excreted in urine (15% unchanged)
  • Onset: 15 minutes- give slowly, wait for effect
  • E1/2t- 4 hours
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16
Q

Hydralazine:

Side effects

A
  • Angina with EKG changes
    • DBP reduced > SBP
  • Reflex increase in HR, SV, CO
  • tolerance and tachyphylaxis
  • Na and H2O retention
  • Systemic lupus-like syndrome
  • Cannot be used long term b/c of body’s compensatory mechanisms
17
Q

What is Minoxidil used for clinically?

How does it work?

A
  • Used in combination with BB and diuretic to treat the most severe forms of HTN caused by:
    • renovascular disease
    • renal failure
    • transplant rejection
  • Works by directly relaxing the arteriolar smooth muscle. Has little effect on venous
    • Orally active
18
Q

Minoxidil:

MOA

absorption

peak

E1/2t

A
  • MOA: Opens K channels, resulting in hyperpolarization and vasodilation
  • 90% of oral dose is absorbed from the GI tract
  • Peak levels in 1 hour
  • E1/2 t 4 hours
19
Q

Minoxidil:

Side effects

A
  • Marked increase in HR and CO
  • increased plasma concentration of NE and Renin
    • compensatory retention of Na and H2O
    • weight gain
    • edema
    • hypertrichosis (hair growth)
    • pulmonary HTN
    • pericardial effusion or tamponade
  • abnormal EKG
    • flat or inverted T wave, increased voltage of QRS complex
  • **May want EKG or CXR if pt is on Minoxidil; lower threshold to send to cardiologist
20
Q

What is the most potent vasodilator used in the OR?

A
  • Sodium Nitroprusside
  • Direct acting
  • non-selective: artery and vein
  • lacks significant effects on non-vascular smooth muscle and cardiac muscle
21
Q

Sodium nitroprusside (SNP)

MOA

A
  • SNP interacts with oxyhemoglobin and dissociates immediately to form methemoglobin and release NO and cyanide
    • NO activates guanylate cyclase in the vascular muscle, thus increasing cGMP
    • cGMP inhibits Ca entry into vascular smooth muscle and increases uptake of Ca into the smooth endoplasmic reticulum
  • Results in vasodilation via NO
22
Q

How is Sodium nitroprusside metabolized?

A
  • Transfer of an electron from the Iron of oxyhemoglobin to SNP yields methemoglobin and an unstable SNP radical where all 5 cyanide ions are released
  • One of these cyanide ions reacts with the methemoglobin to form cyano-methemoglobin (non-toxic)
    • the remainder are metabolized in the liver and kidney and converted to thiocyanate
    • this can be a problem if there is too much thiocyanite to metabolize (larger doses) and can lead to cyanide toxicity
23
Q

Cyanide toxicity with Sodium Nitroprusside:

When is it a risk?

When should you start to suspect it?

A
  • At risk when rates are > 2 mcg/kg/min for long periods of time
  • Suspect Cn toxicity when pt who was previously responsive to the antihypertensive effects of the SNP is no longer responsive (tachyphylaxis)
  • Cn toxicity may precipitate tissue anoxia, anaerobic metabolism, and lactic acidosis
  • Caution in pregnancy
24
Q

How do you treat SNP toxicity?

A
  • Immediate d/c of SNP
  • 100% FiO2 even if pt has normal O2 sat
  • Sodium bicarb to correct metabolic acidosis
  • Sodium thiosulfate 150 mg/kg over 15 min (drug of choice)
  • Sodium nitrate 5 mg/kg if toxicity is severe
25
Q

Sodium thiosulfate:

use

dose

MOA

A
  • Used to treat SNP toxicity
    • drug of choice!
  • 150 mg/kg over 15 minutes
  • MOA: actus as a sulfur donor to convert cyanide to thiocyanate
26
Q

Sodium nitrate:

use

dose

MOA

A
  • Used to treat very severe SNP toxicity
  • 5 mg/kg
  • MOA: Converts hemoglobin to metHgb which converts cyanide to cyanomethemoglobin
27
Q

What is thiocyanate toxicity?

Symptoms?

A
  • SNP toxicity
  • rarely seen b/c thiocyanate is cleared by the kidney in 3-7 days
  • less toxic than cyanide
  • Symptoms:
    • N/V
    • tinnitus
    • fatigue
    • CNS hyperreflexia
    • confusion/psychosis
    • miosis
    • sz/coma
28
Q

What are the other two toxicities seen with SNP?

A
  • MetHgb
    • rare
    • should be considered in pts with impaired oxygenation despite adequate CO and arterial oxygenation
  • Phototoxicity
    • If SNP is exposed to light, it will be converted to aquapentacyanoferrate and hydrogen cyanide will be released
    • wrap solution and tubing in foil or dark plastic bag
    • SNP should be mixed with 5% glucose in water
29
Q

SNP

dose

onset

DOA

monitoring

A
  • 0.3 -10 mcg/kg/min IV
  • >2 mcg/kg/min = increased toxicity risk
    • max dose should not be infused > 10 min
  • Onset: immediate
  • DOA: short
    • requires continuous IV to maintain therapeutic effect
  • Art line REQUIRED b/c SNP is extremely potent
30
Q

What are the CV effects of SNP?

A
  • direct venous and arterial vasodilation
    • increased venous capacitance due to decreased venous return
  • Increased HR d/t baroreceptor reflex
  • decreased SBP, SVR, PVR; increased Contractility
    • causes intracoronary steal in areas of damage associated with MI. (Because it dilates everywhere, less will go where it is really needed)
31
Q

What are the other effects of SNP?

CNS

Pulm

Heme

A
  • CNS- Increased CBF and ICP
  • Pulm- attenuation of hypoxic vasoconstriction
  • Heme- increases in intracellular GMP inhibits platelet aggregation and increases bleeding time
32
Q

What are the clinical uses for SNP?

A
  • Controlled hypotension (rarely used, maybe for ENT surgeries)
    • 0.3-0.5 mcg/kg/min, not to exceed 2 mcg/kg/min
  • Hypertensive crisis
    • 1-2 mcg/kg IV; can be given as a bolus
  • Cardiac disease- decreases LV afterload, managing mitral or aortic regurgitation, CHF, and HF
    • consider coronary steal

Advanced Pharm (27 decks)

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