Pharm Ch 11 Antihypertensive Agents

Front 1

Thiazide diuretics are used for what kind of hypertension, and work in which portion of the kidney?

Back 1

used to treat mild hypertension, work in the early portion of the distal convoluted tubules

Front 2

Maximum hypertensive effects of thiazides are achieved at what dose levels?

Back 2

due to compensatory effects, doses lower than diuretic doses are best

Front 3

What are the loop diuretics, and how do they work?

Back 3

furosemide. bumetanide, and torsemide. they work in the thick ascending loop of Heinle. more powerful antihypertensive effects, inhibit the Na+/K+/2Cl- cotransport mechanism

Front 4

Toxic effects of loop diuretics:

Back 4

hypokalemic metabolic alkalosis, severe K+ wasting, hypovolemia, and ototoxicity

Front 5

What are the toxic effects of thiazides?

Back 5

can cause K+ wasting in chronic therapy, may cause significant hyperglycemia in diabetic patients

Front 6

Sympathoplegic drugs interfere with the sympathetic (SANS) control of cardiovascular function, through reduction in at least one of the following:

Back 6

venous tone, heart rate, cardiac output, contractility, and total peripheral resistance

Front 7

These drugs cause a decrease in sympathetic outflow by activation of A2 receptors in the CNS

Back 7

A 2 selective agonists: Clonidine and Methyldopa

Front 8

Method of administration of both methyldopa and clonidine, that facilitate entry into CNS

Back 8

oral

Front 9

Methods by which Clonidine and Methyldopa reduce blood pressure:

Back 9

cardiac output, vascular resistance, or both

Front 10

Methyldopa is a prodrug that is converted to what in the brain?

Back 10

methylnorepinephrine

Front 11

Major side effects/toxicities of Clonidine:

Back 11

severe rebound hypertension if abruptly stopped,(treat with phentolamine) causes compensatory salt retention, and may cause sedation

Front 12

Major side effects/toxicities of Methyldopa:

Back 12

Causes CNS depression, hematologic immunotoxicity (+ coombs test) sedation

Front 13

Ganglion acting drugs that are very efficacious but due to toxic effects are now obsolete

Back 13

Nicotinic blockers: Hexamethonium and Trimethaphan

Front 14

Major toxicities in Ganglion blocking drugs:

Back 14

sympathetic blockade (sexual dysfunction, ortho HTN) and parasymp blockade (const, blurred vision, urinary hesitancy, sex dysfunction) effects, salt retention

Front 15

Postganglionic sympathetic nerve terminal blockers act by what two mechanisms to lower blood pressure:

Back 15

depleting adrenergic nerve terminal of its norepinephrine stores (respirine), and those that deplete or block release of the stores (guanethidine)

Front 16

Major toxicities of Guanethidine, leading to its removal from the US Market

Back 16

orthostatic hypotension and sexual dysfunction. Cocaine and TCA inhibited the norepinephrine pump, interfering with guanedithidine action

Front 17

Most serious side effect of Respirine is what:

Back 17

behavioral depression

Front 18

Mechanism of action of MAOI's that led to their use in hypertension:

Back 18

formed a false transmitter octopamine in sympathetic postganglionic neuron terminals. this transmitter had a much lower efficacy, leading to decreased exciting

Front 19

Reason MAOI's are no longer used to treat hypertension:

Back 19

large doses of indirect acting sympathomimetics (tyramine) cause release of high amounts of norepinephrine with the octopamine, resulting in a hypertensive crisis

Front 20

Adrenoceptor blockers that reduce vascular resistance and venous return. Used in Hypertension

Back 20

A1 receptor blockers: Prazosin, Doxazosin, Terazosin

Front 21

Nonselective A blockers with no value in Hypertension due to excessive compensatory responses:

Back 21

Phenoxybenzamine and Phentolamine

Front 22

Common Side effect of A1 selective blockers:

Back 22

orthostatic hypotension with first few doses

Front 23

Side effect of some A1 selective blockers that makes them useful in BPH

Back 23

smooth muscle relaxation. decreases urinary stasis, increases flow. (Tamsulosin)

Front 24

Mechanism of action of B blockers in treatment of hypertension

Back 24

Initially reduce cardiac output, but eventually reduce vascular resistance as well

Front 25

What is a new B Blocker with a direct vasodilating effect?

Back 25

Nebivolol

Front 26

B Blocker also used to treat migraine, tremor, and stagefright

Back 26

Propanolol

Front 27

B1 Specific blockers that have more effect on heart than lungs, and can be used in asthmatic patients

Back 27

Metoprolol, atenolol, Acebutolol, and Esmolol

Front 28

Side effects/ toxicities of B Blockers

Back 28

elevated glucose, LDL, and triglycerides, and lower HDL in the blood. sexual dysfunction,

Front 29

Four main mechanisms of vasodilators:

Back 29

release of NO, opening of K+ channels (hyperpolarization), block of Ca++ channels, and activation of dopamine D2 receptors

Front 30

Mechanism of Hydralazine:

Back 30

causes epithelial cells to release nitric oxide, works more on arterioles than veins

Front 31

Toxicity of Hydralazine

Back 31

Drug induced SLE, compensatory salt and water retention

Front 32

Prodrug who's metabolite is a K+ channel opener, that hyperpolarizes and relaxes vascular smooth muscle

Back 32

Minoxidil. used only in hypertensive emergencies do to extreme efficacy.

Front 33

Side effects and toxicities of minoxidil:

Back 33

excessive hypotension, severe compensatory response, and hirsutism.

Front 34

Oral acting, vasodilating drugs effective for hypertension of any severity:

Back 34

Calcium Channel Blockers: Nifedipine, verapamil, diltiazam

Front 35

Calcium channel blockers that reduce cardiac output and therefore are contraindicated in preexisting cardiac or renal disease

Back 35

Verapamil and Diltiazam

Front 36

Prototype Dihydropyridine, calcium channel blocker, and other analogs:

Back 36

Nifedipine, amlodipine, felodipine, isradipine.

Front 37

Toxicities of Calcium Channel Blockers:

Back 37

constipation, pre tibial edema, nausea, flushing, and dizziness

Front 38

Short acting IV infused vasodilator that release nitric oxide itself

Back 38

Nitroprusside

Front 39

Toxicity of nitroprusside:

Back 39

hypotension and tachycardia. if infused for several days, could cause cyanide or thiocyanate in blood

Front 40

Thiazide derivative without diuretic effects, given in IV bolus, or infused, to open K+ channels, hyperpolarizing and relaxing the smooth muscle cell

Back 40

Diazoxide. also reduces insulin release, so can be used to treat hypoglycemia caused by insulin producing tumors

Front 41

Toxicities of Diazoxide

Back 41

hypotension, hyperglycemia, and salt and water retention

Front 42

Dopamine D1 receptor activation by this IV infused drug causes prompt, marked, and short lived arteriolar vasodilation. Is used for hypertensive emergencies

Back 42

Fenoldopam

Front 43

Drugs that inhibit the action of angiotensin converting enzyme. Used in hypertension

Back 43

Captopril, enalapril, lisinopril, and Benazopril

Front 44

Side effects with ACE inhibitors:

Back 44

dry cough, due to increase in bradykinin, and renal damage

Front 45

ACE inhibitors are absolutely contraindicated in?

Back 45

pregnancy

Front 46

Drugs that have a protective effect of the kidney in Diabetes

Back 46

ACE inhibitors

Front 47

Drugs that block the Angiotensin II receptors, used in hypertension

Back 47

Losartan, candesartan, irbesartan, and Valsartan

Front 48

Toxicities and contraindications

Back 48

cause fetal renal toxicity and are still contraindicated in pregnancy

Front 49

Drug that inhibits renin's effect on angiotensin I, used to treat hypertension

Back 49

Aliskiren

Front 50

Toxicity of Aliskiren:

Back 50

causes headache and diarrhea. could cause marked K+ retention, especially in renal impairment.

Front 51

In stepped care for patients with severe hypertension, what are the five steps?

Back 51

1) reduce salt and weight 2) diuretics (thiazide) 3) sympathoplegics (B blocker) 4) ACE inhibitors 5) vasodilators (1st is CCB)

Front 52

Combinations of drug therapy so that the effects of one drug can control the compensatory responses of the others, cite one example:

Back 52

propanolol (B Blocker) would reduce the tachycardia caused by hadralazine (step 5), and the thiazide (step 2) would reduce the salt and water retention

Front 53

Older patients respond better to which two classes of drugs than ACE inhibitors?

Back 53

B Blockers and diuretics

Front 54

In a case of malignant hypertensive emergency, what would be the best treatment?

Back 54

powerful vasodilators (nitroprusside, fenoldopam, or diazoxide) combined with a powerful diuretic (furosemide), and B blockers to promptly lower pressure to the 140/90-160/110 range