• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/89

Click to flip

89 Cards in this Set

  • Front
  • Back
Angiotensin converting enzyme inhibitors
ACEi
captopril (Capoten)
enalapril (Vasotec)
lisinopril (Prinivil, Zestril)
quinapril (Accupril)
ramipril (Altace)
benazepril (Lotensin)
etc…
ACEi
MOA
Highly selective drugs that inhibit the conversion of Ang. I (Inactive) to Ang II (Active) which interferes with aldosterone & renin release


All have similar therapeutic indications (CHF and Hypertension), ADR, and contraindications
ACEi
Effects
Reduce angiotensin II and aldosterone levels = Reduced vasoconstriction

Systemic arteriolar dilation & increase compliance of larger arteries which lowers systemic vascular resistance and (mean, diastolic and systolic) BP
ACEi
Clinical applications
Hypertension

Heart failure, diabetes
ACEi
Uses in HTN
Monotherapy in mild-moderate (50%).

Combo with BB, CCB, or diuretics (90%)
ACEi
Side Effects
HAD NAB
Hypotension (High Plasma Renin Activity and CHF)
Angioedema
Dry cough due to increase bradykinin levels (5-20%)

Not during pregnancy
Acute renal failure
Bilateral renal artery (or solitary) stenosis (can lead to acute renal failure)
ACEi
DDI
Hyperkalemia:
Especially if used in conjunction with K+ sparing, K+ supplements, NSAIDS, Beta Blockers
Angiotensin II-receptor antagonists
ARBs
losartan
candesartan
irbesartan
valsartan, etc…
ARBs
MOA
Competitive binding but often insurmountable antagonism.

Slow dissociation

ARB-induced receptor internalization

Allosteric antagonism
ARBs
Effects
Same as ACEi but with no increase in bradykinin
ARBs
Clinical applications
Hypertension

Heart failure
ARBs
Uses in HTN
All ARBs are approved for hypertension treatment (Combination with hydrochlorothiazide)

A number of studies suggest that ARBs are just as good as ACE inhibitors (No cough and less incidence of angiodema than ACE inh.)
ARBs
Side Effects
Not given during pregnancy (teratogenic potential)

Careful in Renal Stenosis
ARBs
DDI
Hyperkalemia
Diuretics
Thiazides

chlorthalidone
hydrochlorothiazide
metolazone, etc…
Why use thiazides for HTN?
Thiazides and related diuretics are the most frequently used class of antihypertensive agents in the US

Antihypertensive effects when used alone (monotherapy) occurs with small doses

Enhance antihypertensive effects of virtually all other drugs and can be used to prevent/reverse the salt and water retention caused by other antihypertensive drugs
Thiazides
MOA
Block of NCC1 (Na/Cl transporter) in DCT & prevents Na+ from being reabsorbed.
Water stays with Na+, so diuresis occurs.
Thiazides
Effects
Reduce blood volume plus poorly understood vascular effects
Thiazides
Clinical applications
Hypertension

Mild heart failure
Thiazides
Side effects/ADR
Hypokalemia (Urinary K+ Loss)- Fatal arrhythimias

Erectile Dysfunction

Gout due to hyperuricemia (rare)

Hydrochlorothiazide rapid hyponatremia

Hypercalcemia

Changes in plasma lipids (increase LDL) and glucose intolerance
Thiazides DDI
NSAIDS: Inhibit synthesis of prostaglandin synthesis and decrease antihypertensive effect

Quinidine- Torsade de Points

Digitalis toxicity- arrhythmias

Corticosteroids- Amplify the hypokalemia effects

Li+- Decrease clearance and increase toxicity
Loop Diuretics MOA
Block of NKCC2 in Loop of Henle & prevents Na+ from being reabsorbed. Water stays with Na+, so diuresis occurs.

Decrease in electrical potential, therefore lose Na+, Ca++, and K+

Less effective for BP & possibly detrimental
Loop Diuretics
Effects
Like thiazides except with greater efficacy
Loop Diuretics
Clinical applications
Severe hypertension

Heart Failure
Loop Diuretics
Side effects/ADR
Toxicity:
Hypokalemic metabolic alkalosis
Ototoxicity (dose related)
Hyperuricemia (can trigger gout)
Hypomagnesemia
Allergic reactions (for ones that are sulfonamides)
Dehydration

Contraindications:
Allergy to sulfonamides
Loop Diuretics DDI
Co administration with aminoglycosides may increase ototoxicity
Aldosterone Receptor Antagonists
(K+ Sparing)
MOA
Reduce kaliuresis and potentiate the hypotensive effects

Mechanism can be inhibited by NSAIDs due to their inhibition of renal prostaglandin production
Aldosterone Receptor Antagonists
Effects
Increase Na & decrease K excretion

Poorly understood reduction in heart failure mortality
Aldosterone Receptor Antagonists
Clinical applications
Hypertension

Heart failure

Aldosteronism
Aldosterone Receptor Antagonists
(K+ Sparing)
Side effects/ADR
Hyperkalemia

Hyperchloremic metabolic acidosis

Gynecomastia (with spironolactone but not eplerenone)

Acute renal failure (combine triamterene with indomethacin)

Kidney stones (triamterene)

Dosage adjustment for triamterene and spironolactone in liver disease
Aldosterone Receptor Antagonists
(K+ Sparing)
DDI
Combined use of CYP3A4 inhibitors and eplerenone
Renin Inhibitors
aliskiren
Renin inhibitor
MOA
Inhibits enzyme activity of renin

It binds with high affinity to plasma renin
Reduces PRA & concentrations of AngI, AngII and aldosterone
Renin inhibitor
Effects
Reduces angiotensin I and II and aldosterone
Renin inhibitor
Clinical applications
Hypertension
Renin inhibitor
Side effects
Skin rash, diarrhea, headache, cough, hypotension, & angioedema
Renin inhibitor
DDI
Diuretics and ARB (synergism effect)
Sympatholytics
Alpha-1 Antagonists
Prazosin
Terazosin
Doxazosin
Sympatholytics
Alpha-1 Antagonists
MOA
Selectively block alpha-1 adrenoreceptors
Sympatholytics
Alpha-1 Antagonists
Effects
Prevent sympathetic cardiac stimulation

Reduce renin secretion
Sympatholytics
Alpha-1 Antagonists
Clinical applications
Hypertension

BPH (benign prostatic hyperplasia)
Sympatholytics
Alpha-1 Antagonists
Side effects/ADR
1st Dose Effect

Reflex tachycardia

Arrhythmias

Orthostatic Hypotension & Syncope (30-90 min)

Blurred vision

Headache and dizziness

Sexual dysfunction
Sympatholytics
Alpha-1 Antagonists
DDI
Any drug that can affect BP

PDE-5 inhibitor (e.g., sildenafil)

Changes in the free fraction- Drugs that compete for the plasma protein α1-acid glycoprotein (e.g. Olanzapine, Fluoxetine)
Sympatholytics
α1 & 2 receptors irreversible antagonist
Phenoxybenzamine (Dibenzyline)
Sympatholytics
α1 & 2 receptors irreversible antagonist
MOA
Decrease Peripheral Resistance
Sympatholytics
α1 & 2 receptors irreversible antagonist
Uses
Short-Term Control of Hypertension

Pheochromocytoma

Hypertensive Crisis (MAO inhibitors)

Clonidine withdrawal
Sympatholytics
α1 & 2 receptors irreversible antagonist
Side effects/ADR
Induce reflex cardiac stimulation
Tachycardia, arrhythimias, & ischemia

Enhance Norepinephrine Secretion

GI stimulation
Sympatholytics
α1 & 2 receptors irreversible antagonist
DDI
Tadalafil (theoretical)
Sympatholytics
Selective α2 Receptor Agonist
Clonidine (Duraclon®)

Guanfacine (Wytensin)

Guanabenz (Tenex)
Sympatholytics
Selective α2 Receptor Agonist
MOA
Activate alpha-2 adrenoreceptors
Sympatholytics
Selective α2 Receptor Agonist
Effects
Suppressing Sympathetic Output in the CNS (Brainstem)

Increasing Vagal Tone

Inhibiting Release of Norepinephrine and Ach (GI)
Sympatholytics
Selective α2 Receptor Agonist
Clinical applications
Hypertension

Clonidine is also used in withdrawal from abused drugs
Sympatholytics
Selective α2 Receptor Agonist
ADR
Clonidine ADR-

CNS side effects: Nightmares, restlessness, & depression

Dry Mouth and Sedation (50% of pts)

Postural Hypotension & Marked Bradycardia

Sexual Dysfunction

Hypertensive Crisis (withdrawal)
Sympatholytics
Selective α2 Receptor Agonist
DDI
Clonidine DDI-

Pts taking other drugs that suppress AV conduction. BBB+CCB = Bradycardia & Sinus arrest

Diuretics and other anti-hypertension agents
Sympatholytics
Beta Blockers
Non-selective b1/b2
1st Generation
Nadolol (Corgard)
Propranolol (Inderal)
Pindolol [ISA] (Visken)
Penbutolol [ISA] (Levatol)
TImolol (Blocadren)
Sympatholytics
Beta Blockers
Selective b1 (cardioselective)
2nd Generation
Acebutolol (Sectral)
Atenolol (Tenormin)
Bisoprolol (Zebeta)
Esmolol (hospital setting)
Metoprolol (cardioselective at lower doses b1 heart and kidneys..loses selectivity with increase in dose)
Sympatholytics
Beta Blockers
Selective b1
3rd Generation
Betaxolol
Celiprolol
Nebivolol
Sympatholytics
Beta Blockers
Non-subtype
3rd Generation
Carvidolol (b1,b2,a1, antioxidant)
Coreg used for HTN,CHF, patients with left ventricular dysfunction post MI

Carteolol (Cartrol)

Bucindolol (b1,a1,b2 agonist)

Labetolol (Trandate, Normodyne) (b1,b2,a1,ISA b2)
use for HTN during pregnancy
Sympatholytics
Beta Blockers
MOA
Blockade of β1-Receptors of the Juxtaglomerular Complex

Reduce renin secretion & production of Ang. II

Other BB may decrease CO or decrease peripheral vascular resistance to various degrees depending on cardioselectivity
Sympatholytics
Beta Blockers
Effects
Reduction in:

Myocardial contractility Heart Rate
Cardiac Output
CNS sympathetic output
Firing of peripheral adrenergic neurons
Sympatholytics
Beta Blockers
Clinical Applications
Mild to moderate HTN

Useful in preventing reflex tachycardia in SEVERE HTN from other HTN meds

Reduce mortality in post MI and HF patients
Sympatholytics
Beta Blockers
ADR/SE
Careful in pts with:
1. Reactive airway disease (asthma)
2. Sinoatrial or atrioventricular nodal dysfunction
3. Patients with bradycardia
4. Patients with insulin-dependent diabetes

BB without ISA increase concentration of triglycerides and lower HDL

Sudden discontinuation lead to rebound hypertension

Tissue sensitivity to endogenous catecholamines
-Epinephrine: hypertension & bradycardia
Sympatholytics
Beta Blockers
DDI
Not used in combination with drugs that:

Inhibit AV conduction (verapamil)

Nonsteroidal antiinflammatory drugs (e.g. indomethacin)

Additive antihypertensive effects in conjunction with Diuretics

Administration of Epinephrine can produce severe hypertension and bradycardia..alpha 1 are not being blocked will get innervated
Beta Blocker
Sympatholytic Effects
Blocking a1,b1,b2
a1: lowers HR, SV, TPR

b1: heart increases HR and contractile force and rate of relaxation

b2-pulmonary: bronchial smooth muscle contraction

b2-brain: decrease sympathetic flow

b2-vasculature: cause dilation
Calcium Channel Blockers
Dihydropyridines
& Clinical Applications
Amlodipine (Norvasc)
Nifedipine (Adalat, Procardia)
Felodipine (Plendil)

Hypertension
Calcium Channel Blockers
Non-dihydropyridines
& Clinical Applications
Verapamil (Calan, Isoptin)
Diltiazem (Cardizem)

Hypertension, angina, arrhythmias
CCC: Dihydropyrines
MOA & Effects
Block vascular calcium channels more so than cardiac calcium channels

Reduce arterial vascular tone (afterload)
CCC: Non-dihydropyridines
MOA & Effects
Non-dihydropyridines:
Prevent calcium influx into myocytes AND smooth muscle lining arteries and arterioles by blocking L-type calcium channels

Reduce arterial vascular tone (afterload)

Reduce HR + contractility → reduce O2 requirement

Verapamil & Diltiazem have direct negative chronotropic effects.
Inhibition of transmembrane movement of Ca++ through voltage sensitive Ca++ channels.
1. Effects on the vasculature
2. Effects on the Heart (non-dihyropyridines)
3. Uses
CCB lower BP by relaxing ARTERIOLAR smooth muscle and decreasing peripheral vascular resistance

Effects on the Heart:
Have no effect on the AV node but Non-dihyropyrines effect Ca-channels in the heart

Mild to moderate hypertension in the elderly & African Americans
CCC
ADR/Side effects
Ankle edema, headache, flushing, palpitation

Headache, dizziness and flushing

Peripheral Edema

Increased hydrostatic pressure in lower extremities due to precapillary dilation and reflex postcapillary constriction

Aggravate gastroesophageal reflux

Inhibition of smooth muscle contraction of the esophageal sphincter

Constipation (common for verapamil)

Bradycardia & sinoatrial node arrest (verapamil & diltiazem)
CCC
DDI
Verapamil blocks the P-glycoprotein drug transport. Thus it will affect any drug that is eliminated by this mechanism

Increase plasma concentration of Digoxin

CCB and Quinidine (Na+, K+, α, M2) can cause excessive hypotension

Verapamil or Diltiazem and β-blockers
Vasodilators
Never 1st line
Diazoxide
Hydralazine (Apresoline)
Methyldopa (Aldomet)
Minoxidil
Nitroprusside
Vasodilators
Minoxidil
MOA
Opens K+ channels in vascular smooth muscle

Not 1st choice; 3rd or later
Vasodilators
Minoxidil
Effects
K + efflux and Hyperpolarization, cant depolarize & not much vasoconstriction..only works on arterial side

Increase blood flow to skin, skeletal muscle, the GI and heart more than to the CNS

It enhances venous return to the heart and SNS output, which leads to an increase in CO

It only works in the ARTERIOLES NOT VEINS
Vasodilators
Minoxidil
Clinical Applications
Efficacious in pts with the most severe and drug resistant forms of hypertension
Vasodilators
Minoxidil
ADR/Side effects
1. Fluid and Salt Retention
2. Increased proximal renal tubular reabsorption
3. Reduced renal perfusion and stimulation of α adrenergic receptor
4. Can be given with a loop diuretic

Cardiovascular
1. Baroreceptor-mediated activation of SNS
2. Increase HR, myocardial contractility, and myocardial O2 consumption
3. Can be given with a β-blocker

Hypertrichosis- Growth of hair in the face, back, arms, and legs
Vasodilators
Hydralazine
MOA & Effects
Direct relaxation of arteriolar smooth muscle via nitric oxide release. Doesn't effect veins

Reduces vascular resistance
Vasodilators
Hydralazine
Clinical Applications
Severe Hypertension or hypertensive emergencies (e.g. preeclampsia)
Vasodilators
Hydralazine
ADR/Side effects
Headache, Nausea, flushing, Hypotension, palpitations, reflex tachycardia, dizziness, Salt Retention and ANGINA PECTORIS.

Not given to pts with coronary artery disease

Combine with a β-blocker and a diuretic
Vasodilators
Hydralzaine
DDI
Drug induced lupus syndrome and other autoimmune reactions (e.g. serum sickness, vasculitis, glomerulonephritis, etc…)

Dose dependent, Acetylator Phenotype, and Race
Vasodilators
Nitroprusside
MOA & Effects
Powerful nitrovasodilator that acts by releasing nitric oxide (NO)

Mimic the production of NO by vascular endothelial cells

Increase in intracellular cGMP

Dilates both arterioles and venules (non-selective)

Modest increase in HR

Overall reduction in myocardial demand for oxygen
Vasodilators
Nitroprusside
Clinical Applications
Hypertensive emergencies
Vasodilators
Nitroprusside
ADR/Side effects
Due to excessive vasodilation

Conversion of nitroprusside to cyanide and thiocyanate

Given with sodium thiosulfate
Vasodilators
Diazoxide
MOA & Effects
Vasodilates arteriolar smooth muscle vessels by activating K+ channels (Hyperpolarization)
Vasodilators
Diazoxide
Clinical Applications
IV only for the treatment of severe hypertension (rarely used)
Vasodilators
Diazoxide
ADR/Side effects
Salt and water retention

Tachycardia and myocardial ischemia

Hyperglycemia (inhibit the excretion of insulin from pancreatic β cells)

Hypertrichosis (excessive hair growth includes the face)
Vasodilators
Methyldopa
MOA & Effects
Prodrug (analog of dopa)

Stimulates CENTRAL (acting) alpha adrenoreceptors by alpha-methylnorepinephrine or alpa-methyldopamine

Reduces vascular resistance by decreasing sympathetic tone
Vasodilators
Methyldopa
Clinical Applications
Hypertension during pregnancy
Vasodilators
Methyldopa
ADR/Side Effects
CNS effects
Sedation, depression, reduction in libido, Parkinsonian signs and hyperprolactinemia
Dry mouth

ADR’s unrelated to its pharmacology
1. Hepatotoxicity (rare but serious SE)
2. Hemolytic anemia (20%)
3. Autoantibodies directed at the Rh antigen on erythrocytes
4. Treat with glucocorticoids to alleviate symptoms