Antihypertensive agents & angina pectoris Flashcards by Marah Joy M. FLORES

Systolic blood pressure of 140 or greater or diastolic blood pressure of 90 or greater.

Risk factors:
•Smoking
•Metabolic syndrome
•Manifestations of end organ damage at the time of diagnosis
•Family history

HYPERTENSION

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Classification of Hypertension:

<120/80 - Normal
120-139/80-89 - Prehypertension
>= 140/90 - Hypertension
140-159/90-99 - Stage 1
>=160/100 - Stage 2

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Hypertension Etiology

Essential/primary Hypertension
Secondary Hypertension

Contributing Factors:
- Genetic factors
- Physiological stress
- Environmental & dietary factors

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Anatomic sites of blood pressure control

Resistance - Arterioles
Capacitance - Venules
Pump output - Heart
Volume - Kidneys

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BASIC PHARMACOLOGY OF ANTIHYPERTENSIVE AGENTS:

•DRUGS THAT ALTERS SODIUM & WATER BALANCE: DIURETICS
•DRUGS THAT ALTER SYMPATHETIC NERVOUS SYSTEM FUNCTION: SYMPATHOPLEGIC AGENTS
•DIRECT VASODILATORS:
•AGENTS THAT BLOCK PRODUCTION OR ACTION OF ANGIOTENSIN

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lowers BP by depleting the body of sodium stores and reducing blood volume or other mechanisms.
Increase urine excretion
Reduce the circulating fluid volume to treat edema and hypertension.

Agents used:
Thiazide
Loop diuretics
Potassium-sparing diuretics
Osmotic diuretics

DIURETICS

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For mild to moderate hypertension and normal renal and cardiac function.

•Hydrochlorothiazide
•Chlorthalidone

Uses:
-Hypertension
-Edema
-Prophylaxis of calculu formation

Side effects:
-Hypokalemia
-Muscle weakness
-Postural hypotension Hyperglycemia
-Increase uric acid level

Thiazides (Diuretics)

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-Acts directly on the loop of Henle in the kidney to inhibit sodium and chloride reabsorption which in turn inhibits water reabsorption back into the bloodstream leading to increased urine formation.
• Furosemide
• Bumetanide

Uses:
-Edema
-Pulmonary edema
-Ascites
-Hypertension combined with antihypertensives especially in patients with kidney disease.

Side Effects:
-Fluid & electrolyte imbalance -Hypotension
-Hyperglycemia & increase uric
acid level

Loop Diuretics

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-Prevent potassium depletion and enhance the natriuretic effects of other diuretics,
-Counteracts the increase of glucose and uric acid levels
•Spironolactone
•Triamterene

Uses:
-Used in combination with thiazide diuretics
-To increase the diuretic and hypotensive effects and reduce the dangers of hyperkalemia.

Side Effects:
Hyperkalemia
Fatigue, lethargy
Hypotension
Gynecomastia

Potassium-Sparing Diuretics

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Used to reduce intracranial pressure (ICP) or intraocular pressure (IOP). - Used in emergency cases that involves cranial or spinal trauma & used to reduce the risk ofnnervous system damage from swelling.
• Mannitol

Side Effects:
- fluid & electrolyte imbalance
- CNS symptoms
- Gl symptoms
- Tachycardia
- Allergic reactions
- Pulmonary edema

Osmotic Diuretics

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Used for the treatment of hypertension during pregnancy.
-Lowers BP by reducing peripheral vascular resistance with a variable reduction in heart rate and cardiac output.

Pharmacokinetics:
half-life: 2 hours
bioavailability: 25%
initial dose: 1g/day

Toxicity:
Sedation
Mental lassitude & impaired mental
concentration.
Nightmares
Mental depression
Vertigo
EPS

Methyldopa (CENTRALLY ACTING SYMPATHOPLEGIC DRUGS)

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used in the treatment of hypertension.
Lowers BP in the supine position and rarely causes postural hypotension.

Pharmacokinetics:
half-life: 8-12 hours
bioavailability: 95%
initial dose: 0.2mg/day

Toxicity:
- Dry mouth
- Sedation
- Nervousness
- Tachycardia
- H/A
- Sweating

Clonidine (CENTRALLY ACTING SYMPATHOPLEGIC DRUGSl

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Inhibits the release of norepinephrine from the sympathetic nerve endings.
It replaces norepinephrine and causes a gradual depletion of norepinephrine stores in the nerve endings.
-It interferes with amine release.
Half-life: 5 days

Toxicity:
Symptomatic postural hypotention Delayed or retrograde ejaculation
Diarrhea

Guanethidine (ADRENERGIC NEURON-BLOCKING AGENTS)

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-Blocks the ability of aminergic transmitter vesicle to take up & store biogenic amines by interfering with the vesicular membrane associated transporter (VMAT).

-Half-Life: 24-48 hours
-Bioavailability: 50%
-Initial dose: 0.25mg/day

Toxicity:
- Sedation
- Lassitude
- Nightmares
- Severe mental depression

Reserpine (ADRENERGIC NEURON-BLOCKING AGENTS)

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Decreases BP primarily as a result of a decrease in cardiac output.
Inhibits the stimulation of renin production by caatecholamines.
Most effective in patients with high plasma renin activity.

Half-life: 3-5 hours
Bioavailability: 25%
Initial dose: 80mg/day

Propranolol (BETA-ADRENOCEPTOR-BLOCKING AGENTS)

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Less bronchial constriction than propranolol at doses that produce equal inhibition of B-adrenoceptor responses.
Metabolized by CYP2D6 with high first-pass metabolism.

Half-life: 4-6 hours

METOPROLOL (BETA-ADRENOCEPTOR-BLOCKING AGENTS)

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Less effective than metoprolol in preventing complications of hypertensions

Half-life: 6 hours

Patients with reduced renal functions should receive lower doses.

ATENOLOL (BETA-ADRENOCEPTOR-BLOCKING AGENTS)

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-Non selective B-receptor antagonist. -Not metabolized & excreted in the urine.

Nadolol & Carteolol (BETA-ADRENOCEPTOR-BLOCKING AGENTS)

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B1-selective blockers
Primary metabolized in the liver.

Betaxolol & Bisoprolol (BETA-ADRENOCEPTOR-BLOCKING AGENTS)

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These drugs are partial agonist
-Lowers BP but they are rarely used in HPN.

Pindolol, Acebutolol, & Penbutolol (BETA-ADRENOCEPTOR-BLOCKING AGENTS)

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Labetalol is useful in the treatment of hypertension of pheochromocytoma & hypertensive emergencies. Formulated as a racemic mixture of 4 isomers.
Carvedilol also administered as a racemic mixture. With a half-life of 7-10 hours.
Nebivolol is a B1-selective blocker & vasodilating property that is not mediated by alpha blockade, with a half-life of 10-12 hours.

Labetalol, Carvedilol, & Nebivolol (BETA-ADRENOCEPTOR-BLOCKING AGENTS)

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A BI-selective blocker, rapidly metabolized via hydrolysis by RBC esterases.
Short half-life: 9-10 minutes
Administered through IV infusion

Esmolol (BETA-ADRENOCEPTOR-BLOCKING AGENTS)

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Produces their antihypertensive effects by selectively blocking alpha I receptors in arterioles & venules.
Reduces arterial pressure by dilating both resistance & capacitance vessels.
More effective when used in combination with B-blockers & a diuretic.

Uses:
- Prostatic hyperplasia
- Bladder obstruction symptoms
- Hypertension
- BPH

Toxicity:
Dizziness
Palpitations
H/A
Lassitude

Prazosin, Terazosin & Doxazosin (ALPHA I BLOCKERS)

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Nonselective agents
Used in diagnosis & treatment of PHEOCHROMOCYTOMA & in other clinical situations.
used in the treatment of clonidine withdrawal syndrome in combination with B-blockers.

Phentolamine & Phenoxybenzamine (ALPHA ADRENOCEPTOR-BLOCKING AGENTS)

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Oral vasodilators for long-term therapy of HPN.

HYDRALAZINE & MINOXIDIL (VASODILATORS)

Parenteral vasodilators for hypertensive emergencies

NITROPRUSSIDE & FENOLDOPAM (VASODILATORS)

-used in ischemic heart disease & hypertensive emergencies

CALCIUM CHANNEL BLOCKERS & NITRATES (VASODILATORS)

- Useful in combination therapy in the treatment of severe HPN.. - Hydralazine in combination with nitrates is effective in heart failure. - Dilates arterioles but not veins. - Well-absorbed & well metabolized in the liver. Availability: 25% Half-life: 1.5 to 3 hours Dose: 40 to 200mg/day Toxicity: H/A Anorexia Palpitations Sweating Flushing Peripheral neuropathy Drug fever

HYDRALAZINE (VASODILATORS)

- The effect results from the opening of potassium channels in smooth muscle membranes by minoxidil sulfate (active metabolite). - Increase potassium permeability stabilizes the membrane at its resting potential and makes contraction less likely. - Dilates arterioles but not veins Half-life: 4 hours Bioavailability:90% Initial dose: 5-10mg/day - Used in combination with B-blocker & a loop diuretic. Toxicity: Tachycardia Palpitations Angina Edema H/A Sweating Hypertrichosis

MINOXIDIL (VASODILATORS)

- Hypertensive emergencies & for severe heart failure. - Dilates both the arterioles and venous vessel - The action of sodium nitroprusside results from the activation of granylyl cyclase, either via the release of nitric oxide or by direct stimulation of the enzyme. - Rapidly metabolized by uptake into RBC with release of nitric oxide & cyanide. - Lowers BP rapidly & its effect disappear 1-to 10 minutes after discontinuation. Toxicity: excessive BP lowering accumulation of cyanide metabolic acidosis arrythmias death

SODIUM NITROPRUSSIDE (VASODILATORS)

- Long-acting potassium channel opener that causes hyperpolarization in smooth muscle and pancreatic B-cells. - Dilates the arterioles - Used in the treatment of hypoglycaemia in hyperinsulinism. Half-life: approx. 24 hours - Partially metabolized Toxicity: Excessive hypotension Angina Ischemia Cardiac failure

DIAZOXIDE (VASODILATORS)

- A peripheral arteriolar dilator for hypertensive emergencies & postoperative HPN. - Acts primarily as an agonist of dopamine DI receptors, resulting in dilation of peripheral arteries & natriuresis. -;Rapidly metabolized by conjugation Half-life: 10 minutes Toxicity: Reflex tachycardia H/A Flushing Increase intraocular pressure

FENOLDOPAM (VASODILATORS)

Uses: -Angina -Anti-arrythmic effects -Reduces peripheral resistance and BP Moa: Inhibits calcium influx into arterial smooth muscle cells. Ex Verapamil, Diltiazem, Dihydropyridine family NIFEDIPINE & other dihydropyridine - are more selective as vasodilators & less cardiac depressant effects than Verapamil & Diltiazem,

CALCIUM CHANNEL BLOKERS

Lisinopril, Enalapril, Captopril - Inhibition of ACE lowers BP by decreasing vasoconstriction. - First or second line agents in the treatment of HPN are excellent alone, but can also be used in combination with diuretics & calcium channel blocker. Side effects: Rash/photosensitivity Severe hypotension Chronic dry cough or nasal congestion hyperkalemia

ACE INHIBITORS

- Inhibit the converting enzymes peptidyl dipeptidase, that hydrolyzes angiotensin I to angiotensin II & inactivates bradykinin, a potent vasodilator that works at least in part by stimulating release of nitric oxide & prostacyclin. - Enalapril - prodrug - Good choice for patients with other serious conditions: •Heart failure •Following myocardial infarction •When high coronary disease risk exists •Diabetes •Renal disease and cardiovascular disease - Useful in treating patients withbchronic kidney disease because they diminish proteinuria & stabilize renal function. Drug of Choice: For hypertensive patients with nephropathy- they slow the progression of renal disease

ACE INHIBITORS

- The first marketed blockers of angiotensin II type I receptor. - They have no effect on bradykinin metabolism therefore more selective blockers of angiotensin effects than ACE inhibitors. - Commonly used in patients who have had adverse reactions to ACE inhibitors.

Losartan & Valsartan (ANGIOTENSIN RECEPTOR-BLOCKING AGENTS(ARB))

The primary symptom of ischemic heart disease is _______ which is the most common form of angina.

Ischemic Heart Disease....ANGINA PECTORIS

Chest pain resulting from decreased blood supply to the heart. Caused by transient episodes of myocardial ischemia which are due to imbalance in the myocardial oxygen supply.

Angina Pectoris

If there's an inadequate blood flow in the presence of CAD. Diagnosis is usually made on the basis of history and stress testing.

Classic/Effort Angina

• Caused by spasm in the coronary arteries (at rest). • Usually occurs in younger patient • Diagnosis is made on the basis of history

Vasospastic/Variant/Prinzmetal Angina

• Episodes of angina occurs at rest. • Caused by episodes of increased epicardial coronary artery resistence or small platelet clots occurring in the vicinity of an atherosclerotic plague. • Can happen without physical exertion.

Unstable Angina

• Occurs when heart is working harder than usual. • When a patient has brief episodes of pain, squeezing pressure or tightness in the chest. Occurs with activity or emotional stress.

Stable Angina

These drugs are used for the treatment and prophylactic management of angina. •Nitrates •Beta-blockers •Calcium Channel blockers

CORONARY VASODILATORS (TREATMENT)

Inhibition of ACE lowers blood pressure by

Decreasing vasoconstriction

Nitrates are used in hypertensive emergencies. Vasodilators works best in combination with other antihypertensive drugs that oppose the compensatory cardiovascular response. All vasodilators are useful in hypertension, relaxes smooth muscle arterioles, thereby decreasing systemic vascular resistance

True

Diltiazem is classified as

Calcium channel blocker

Produces competitive antagonism of catecholamine by a blockade of alpha 1 receptors

Phentolamine

Sympatholegic agent lowers blood pressure by

Reducing peripheral vascular resistance, inhibiting cardiac function and increase venous pooling

Contributing factors to the development of hypertension: 1.Genetic factors 2.Increase salt, decrease K or Ca intake 3. Psychological stress 4. Exposure to chronic stress

True

This drug is sensitive to light and must be prepared fresh when administered. This deug lowers blood pressure rapidly and its effect disappear 1 to 10 minutes after discontinuation.

Sodium nitroprusside

Most common side effects of antihypertensive agents: l. Postural hypotension II. Muscle weakness III. Bradycardia IV. K deficiency

"True or F"

A cardioselective beta blocker used for the treatment of hypertension

Metoprolol Atenolol Esmolol

An adverse effect of ace inhibitor

Dry cough

In case of acute angina, which of the following route of administration is appropriate?

Sublingual

The following are used to treat methemoglobinemia as a toxic effect of nitrites:

Hydroxocobalamin Methylene blue

A pFOX inhibitor which partially inhibit the fatty acid oxidation pathway in myocardium:

Trimetazidine

used as an inhalant?

Amyl nitrite

First line of choice in the treatment of chronic effort angina

Beta blockers

Drugs best for intermittent claudication

Pentoxifylline

Coronary vessels letters are used for the

Treatment of angina

Nitroglycerin is classified as

Anti-angina