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Pharmacology > Exam 6 > Flashcards

Exam 6 Flashcards

1
Q

Acetazolamide

A

DIURETIC
1. carbonic anhydrase inhibitor (membrane bound and cytoplasmic)
2. excreted by renal tubular secretion (organic acid sites)
3. acts in proximal convoluted tubule
4. effect= inhibit NaHCO3 reabsorption, decrease Na-H exchange, no significant excretion of Cl- (hyperchloremia, metabolic acidosis)
7. also works in eye, stomach, CNS (topicals used to treat glaucoma (decrease IOP))
8. treat respiratory alkalosis, cerebral edema dt mountain sickness (decrease CSF production), epilepsy, causes urinary alkalinization (to excrete acid toxins..ASA)
9. SE: hyperchloremic metabolic acidosis, kidney stones (due to increased precipitation of calcium phosphate dt alkaline urine), hypokalemia (increased K excretion, sulfonamide hypersensitivity
DONT USE WITH HEPATIC CIRRHOSIS–>prevention of ammonium secretion
DONT USE IN NA OR K DEPLETED PATIENT

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2
Q

Mannitol

A

DIURETIC
1. Osmotic Diuretic
2. less irritating, less likely to cause thrombosis
3. doesn’t cross BBB
4. filtered by glomeruli (minimal action in tubules)
5. oral mannitol used to eliminate GI toxins
6. decreased reabsorption of h20 in nephron
7. inhibits renin release due to increased renal blood flow
8. NOTE: excretion of all electrolytes
9. USES: Oliguric acute renal failure, to decrease IOP and ICP, to increase excretion of toxins, tx peripheral edema alone/in combo with other drugs
10. SE: if in blood too long–>pulmonary edema in CHF pt, hyponatremia, HYPERGLYCEMIA
CONTRAINDICATE WITH RENAL DISEASE, CRANIAL BLEEDING

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3
Q

Furosemide

A

DIURETIC
1. loop diuretic/high ceiling diuretic
2. inhibits Na/K/2Cl symport
3. sulfonamide derivative
4. bound by plasma proteins
5. secreted by organic acid secretion mechanism in PCT
6. acts in thick ascending limb (here blocks symport)
7. decrease LV filling pressure (dt increased renal BF and increased systemic venous capacitance)
8. USES: abolishes drive force for paracellular reabsorption of Ca–>lumen positive potential, tx of edema of nephrotic syndrome, liver cirrhosis, renal elimination of drugs, paradoxical tx of hyponatremia with hypertonic saline
9. SE:
-increased Na & HCO3 reabsorption in PCT
-increased Na and Cl delivery to collecting duct system–>increased secretion of K and H
-gout: decreased excretion of uric acid (competition for organic acid secretion system)
-ototoxicity: tinnitus, impairment, vertigo (reversible)-less common with furosemide
-sulfonamide hypersensitivity
-hyperglycemia, increased LDL and triglycerides
-hypomagnesia
NSAIDS CAN DECREASE ANTIHYPERTENSIVE RESPONSE
CAN INCREASE PLASMA LITHIUM

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4
Q

Ethacrynic acid

A

DIURETIC
1. loop diuretic/high ceiling diuretic
2. inhibits Na/K/2Cl symport
3. phenooxyacetic acid derivative
4. bound by plasma proteins
5. secreted by organic acid secretion mechanism in PCT
6. acts in thick ascending limb (here blocks symport)
7. decrease LV filling pressure (dt increased renal BF and increased systemic venous capacitance)
8. USES: abolishes drive force for paracellular reabsorption of Ca–>lumen positive potential, tx of edema of nephrotic syndrome, liver cirrhosis, renal elimination of drugs, paradoxical tx of hyponatremia with hypertonic saline
9. SE:
-increased Na & HCO3 reabsorption in PCT
-increased Na and Cl delivery to collecting duct system–>increased secretion of K and H
-gout: decreased excretion of uric acid (competition for organic acid secretion system)
-ototoxicity: tinnitus, impairment, vertigo (reversible)–more common with Ethacrynic acid!!
-sulfonamide hypersensitivity
-hyperglycemia, increased LDL and triglycerides
-hypomagnesia
NSAIDS CAN DECREASE ANTIHYPERTENSIVE RESPONSE
CAN INCREASE PLASMA LITHIUM

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5
Q

Hydrochlorothiazide

A

DIURETIC
1. thiazide (like) diuretic
2. inhibitor of apical Na/Cl symport-early DCT
3. sulfonamide derivative (benzothiadazide)
4. secreted by organic acid secretory system in PCT
5. parental only in emergent situations
RELATIVE POTENCY: 1, excreted by kidney
6. increase excretion of Na, CL K, H. decrease excretion of Ca
7. K wasting diuretic. increase Na conductance=negative voltage. indirectly promotes K excretion. Na conductance faster than paracellular Cl leaves negative charge
8. compensatory increase in RAAS (can contribute to K wasting)
9. USES: edema of heart failure, HTN, to decrease excretion of Ca in Ca nephrolithiasis and osteoporosis, NEPHROGENIC DIABETES INSIPIDUS (paradoxical antidiuretic. decrease GFR will increase proximal tubular reabsorption), ascites dt liver cirrhosis
SE: Hypokalemia, metabolic alkalosis (excretion of K and H in DCT), skeletal muscle cramps, potentiate arrhythmias, Vtach–>Vfib, gout (due to decreased excretion, increase comp for receptor in prox. tubule), sulfonamide hypersensitivity, SJS SKIN LESIONS, hyperglycemia (decreased insulin secretion), increased LDL, Triglycerides), lithium toxicity, CNS and impotence

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6
Q

Chlorothiazide

A

DIURETIC
1. thiazide (like) diuretic
2. inhibitor of apical Na/Cl symport-early DCT
3. sulfonamide derivative (benzothiadazide)
4. secreted by organic acid secretory system in PCT
5. parental only in emergent situations
RELATIVE POTENCY: 0.1, excreted by kidney
6. increase excretion of Na, CL K, H. decrease excretion of Ca
7. K wasting diuretic. increase Na conductance=negative voltage. indirectly promotes K excretion. Na conductance faster than paracellular Cl leaves negative charge
8. compensatory increase in RAAS (can contribute to K wasting)
9. USES: edema of heart failure, HTN, to decrease excretion of Ca in Ca nephrolithiasis and osteoporosis, NEPHROGENIC DIABETES INSIPIDUS (paradoxical antidiuretic. decrease GFR will increase proximal tubular reabsorption), ascites dt liver cirrhosis
SE: Hypokalemia, metabolic alkalosis (excretion of K and H in DCT), skeletal muscle cramps, potentiate arrhythmias, Vtach–>Vfib, gout (due to decreased excretion, increase comp for receptor in prox. tubule), sulfonamide hypersensitivity, SJS SKIN LESIONS, hyperglycemia (decreased insulin secretion), increased LDL, Triglycerides), lithium toxicity, CNS and impotence

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7
Q

Chlorthalidone

A

DIURETIC
1. thiazide (like) diuretic
2. inhibitor of apical Na/Cl symport-early DCT
3. sulfonamide derivative (benzothiadazide)
4. secreted by organic acid secretory system in PCT
5. parental only in emergent situations
RELATIVE POTENCY: 1, excreted by kidney
6. increase excretion of Na, CL K, H. decrease excretion of Ca
7. K wasting diuretic. increase Na conductance=negative voltage. indirectly promotes K excretion. Na conductance faster than paracellular Cl leaves negative charge
8. compensatory increase in RAAS (can contribute to K wasting)
9. USES: edema of heart failure, HTN, to decrease excretion of Ca in Ca nephrolithiasis and osteoporosis, NEPHROGENIC DIABETES INSIPIDUS (paradoxical antidiuretic. decrease GFR will increase proximal tubular reabsorption), ascites dt liver cirrhosis
SE: Hypokalemia, metabolic alkalosis (excretion of K and H in DCT), skeletal muscle cramps, potentiate arrhythmias, Vtach–>Vfib, gout (due to decreased excretion, increase comp for receptor in prox. tubule), sulfonamide hypersensitivity, SJS SKIN LESIONS, hyperglycemia (decreased insulin secretion), increased LDL, Triglycerides), lithium toxicity, CNS and impotence

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8
Q

Indapamide

A

DIURETIC
1. thiazide (like) diuretic
2. inhibitor of apical Na/Cl symport-early DCT
3. sulfonamide derivative (benzothiadazide)
4. secreted by organic acid secretory system in PCT
5. parental only in emergent situations
RELATIVE POTENCY: 20, metabolized
6. increase excretion of Na, CL K, H. decrease excretion of Ca
7. K wasting diuretic. increase Na conductance=negative voltage. indirectly promotes K excretion. Na conductance faster than paracellular Cl leaves negative charge
8. compensatory increase in RAAS (can contribute to K wasting)
9. USES: edema of heart failure, HTN, to decrease excretion of Ca in Ca nephrolithiasis and osteoporosis, NEPHROGENIC DIABETES INSIPIDUS (paradoxical antidiuretic. decrease GFR will increase proximal tubular reabsorption), ascites dt liver cirrhosis
SE: Hypokalemia, metabolic alkalosis (excretion of K and H in DCT), skeletal muscle cramps, potentiate arrhythmias, Vtach–>Vfib, gout (due to decreased excretion, increase comp for receptor in prox. tubule), sulfonamide hypersensitivity, SJS SKIN LESIONS, hyperglycemia (decreased insulin secretion), increased LDL, Triglycerides), lithium toxicity, CNS and impotence
-useful when GFR falls too much (as well as meolazone)
-presence of methylindoline ring–>increases lipid solubility. does not increase LDL, triglycerides

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9
Q

Triamterene

A

DIURETIC

  1. K-sparing diuretic
  2. inhibitor of renal Na channels
  3. secreted by organic base system
  4. metabolized in liver to 4 hydroxytriamterene (equally potent), then excreted in liver
  5. Block liminal Na channels in principal cells of collecting duct (decreased K secretion)
  6. decreased H secretion b/c lumen stays positive
  7. USES: mostly used in combo with other drugs to tx edema dt CHF, hepatic cirrhosis, hyperaldosteronism, HTN, USED TO COUNTERBALANCE HYPOK DT OTHER DRUGS, Liddle’s syndrome (pseudohyperaldosteronism
  8. SE: hyperK, cardiac arrhythmias, muscle weakness, DO NOT ADMINISTER WITH ALDOSTERONE RECEPTOR BLOCKERS, caution with RAAS blockers, TRIAMTERENE IS POORLY soluble–KIDNEY STONES
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10
Q

Amiloride

A

DIURETIC

  1. K-sparing diuretic
  2. inhibitor of renal Na channels
  3. secreted by organic base system
  4. renal excretion of intact drug. longer half life.
  5. Block liminal Na channels in principal cells of collecting duct (decreased K secretion)
  6. decreased H secretion b/c lumen stays positive
  7. USES: mostly used in combo with other drugs to tx edema dt CHF, hepatic cirrhosis, hyperaldosteronism, HTN, USED TO COUNTERBALANCE HYPOK DT OTHER DRUGS, Liddle’s syndrome (pseudohyperaldosteronism)
    - used to inhibit NA absorption in respiratory tract, promotes hydration of respiratory secretions-tx of cystic fibrosis
  8. SE: hyperK, cardiac arrhythmias, muscle weakness, DO NOT ADMINISTER WITH ALDOSTERONE RECEPTOR BLOCKERS, caution with RAAS blockers, TRIAMTERENE IS POORLY soluble–KIDNEY STONES
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11
Q

Spironolactone

A

DIURETIC
1. K-sparing diuretic
2. aldosterone antagonist
3. synthetic steroid, metabolized in liver
4. Canrenone is active metabolite of SPIRINOLACTONE
5. excretion in urine and biliary fecal elimination
6. 3rd day of tx is max effect
7. antagonist at mineralocorticoid receptor–>prevents gene transcription
8. INTRACELLULAR SITE OF ACTION.
10. USES: with loop/thiazide to tx edema and HTN, give 2-3d prior to thiazide in cirrhosis pt, tx hyperaldosteronism (1* or 2*)
11. SE: hyperK, antiandrogen effects (gynecomastia, impotence, menstrual irregularities) SPIRINOLACTONE-interacts with other steroid hormone receptors (progesterone, androgen)–>used for precocious puberty and hirsutism)
CONTRAINDICATED IN HYPERK PTS AND K SUPPLEMENTS, AND OTHER K SPARING DIURETICS
-CAUTION WITH DRUGS THAT BLOCK RAAS (HYPER K)

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12
Q

Eplerenone

A

DIURETIC
1. K-sparing diuretic
2. aldosterone antagonist
3. synthetic steroid, metabolized in liver
5. excretion in urine and biliary fecal elimination
6. 3rd day of tx is max effect
7. antagonist at mineralocorticoid receptor–>prevents gene transcription
8. INTRACELLULAR SITE OF ACTION.
10. USES: with loop/thiazide to tx edema and HTN, give 2-3d prior to thiazide in cirrhosis pt, tx hyperaldosteronism (1* or 2*)
11. SE: hyperK, antiandrogen effects (gynecomastia, impotence, menstrual irregularities) SPIRINOLACTONE-interacts with other steroid hormone receptors. progesterone, androgen)–>used for precocious puberty and hirsutism) EPLERENONE is more selective antagonist at just mineralcorticoid receptors
CONTRAINDICATED IN HYPERK PTS AND K SUPPLEMENTS, AND OTHER K SPARING DIURETICS
-CAUTION WITH DRUGS THAT BLOCK RAAS (HYPER K)-

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13
Q

Drospirenone

A

DIURETIC
1. K-sparing diuretic
2. aldosterone antagonist
3. synthetic steroid, metabolized in liver
5. excretion in urine and biliary fecal elimination
6. 3rd day of tx is max effect
7. antagonist at mineralocorticoid receptor–>prevents gene transcription
8. INTRACELLULAR SITE OF ACTION.
10. USES: with loop/thiazide to tx edema and HTN, give 2-3d prior to thiazide in cirrhosis pt, tx hyperaldosteronism (1* or 2*)
11. SE: hyperK, antiandrogen effects (gynecomastia, impotence, menstrual irregularities) SPIRINOLACTONE-interacts with other steroid hormone receptors (progesterone, androgen)–>used for precocious puberty and hirsutism)
CONTRAINDICATED IN HYPERK PTS AND K SUPPLEMENTS, AND OTHER K SPARING DIURETICS
-CAUTION WITH DRUGS THAT BLOCK RAAS (HYPER K)-Yasmin-combo of OCP and drospirenone. help counterbalance fluid retention of ethinyl estradiol. also has antiandrogen activity.

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14
Q

Desmopressin acetate

A

ANTIDIURETIC
1. antidiuretic drug
2. similar structure to ADH
3. increase h20 reabsorption in collecting duct system
binds G protein coupled V2 vasopressin receptor
4. net: increased cAMP and increased insertion of h2o channels in apical membrane
5. greater antidiuretic activity than ADH, but less cardiovascular vasopressor activity.
USES: Nocturnal enuresis, central diabetes insipidus (due to lack of vasopression secretion)
SE: water intoxication: careful in pts with angina, HTN, heart failure

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15
Q

Hydrochlorothiazide

A

ANTIHYPERTENSIVE
Thiazide diuretic
1. recommended for initial tx of HTN
2. may activate RAAS-can limit its effectiveness
3. with continued use, decrease peripheral vascular resistance..CO back to normal. CONTINUED ANTIHYPERTENSIVE EFFECT dt auto regulatory phenomenon
4. general 10mmHg fall in DBP maximally
5. most effect achieved with low/intermediate doses
6. volume dependent HTN’s respond well (low renin is sign)
7. SE: poor response? lots of dietary Na or impaired renal capacity to excrete Na; overly vigorous tx leads to activation of RAAS (more vasoconstriction, Na retention, K wasting), HypoK (weakness, cramps), arrhythmias), Hypercholesterolemia, glucose intolerance with hyperglycemia

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16
Q

Chlorthalidone-HTN

A

ANTIHYPERTENSIVE
Thiazide diuretic
1. recommended for initial tx of HTN
2. may activate RAAS-can limit its effectiveness
3. with continued use, decrease peripheral vascular resistance..CO back to normal. CONTINUED ANTIHYPERTENSIVE EFFECT dt auto regulatory phenomenon
4. general 10mmHg fall in DBP maximally
5. most effect achieved with low/intermediate doses
6. volume dependent HTN’s respond well (low renin is sign)
7. SE: poor response? lots of dietary Na or impaired renal capacity to excrete Na; overly vigorous tx leads to activation of RAAS (more vasoconstriction, Na retention, K wasting), HypoK (weakness, cramps), arrhythmias), Hypercholesterolemia, glucose intolerance with hyperglycemia

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17
Q

Indapamide-HTN

A

ANTIHYPERTENSIVE
Thiazide diuretic
1. recommended for initial tx of HTN
2. may activate RAAS-can limit its effectiveness
3. with continued use, decrease peripheral vascular resistance..CO back to normal. CONTINUED ANTIHYPERTENSIVE EFFECT dt auto regulatory phenomenon
4. general 10mmHg fall in DBP maximally
5. most effect achieved with low/intermediate doses
6. volume dependent HTN’s respond well (low renin is sign)
7. SE: poor response? lots of dietary Na or impaired renal capacity to excrete Na; overly vigorous tx leads to activation of RAAS (more vasoconstriction, Na retention, K wasting), HypoK (weakness, cramps), arrhythmias), Hypercholesterolemia, glucose intolerance with hyperglycemia
8. decreased propensity to increase serum cholesterol
9. longer duration of action
10. CCB’s cause direct relaxation of vasculature over time (specific to Indapamide)

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18
Q

Furosemide-HTN

A

ANTIHYPERTENSIVE
Loop diuretic
1. sulfonamide derivative
2. more powerful than thiazides
3. block NaCl reabsorption in thick ascending limb of loop of Henle
4. for patients with DECREASED RENAL EXCRETORY FUNCTION (thiazides are ineffective)
5. SE: hypokalemia, hypercholesterolemia, glucose intolerance with hyperglycemia, gout, ototoxicity, sulfonamide allergic rxns
6. LOOP DIURETIC

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19
Q

Triamterene-HTN

A

ANTIHYPERTENSIVE
1. K-sparing diuretic. Inhibitor of renal Na channels
2. limited natriuretic and BP lowering effectiveness on its own
3. SE: Hyperkalemia
DONT GIVE TO PTS WITH K SUPPLEMENTS

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20
Q

Spironolactone-HTN

A

ANTIHYPERTENSIVE

  1. K-sparing diuretic
  2. block binding of aldosterone to receptors
  3. Tx of HTN due to aldosterone excess
  4. SE: Hyperkalemia, inhibits sex steroid hormone receptors
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21
Q

Eplerenone-HTN

A

ANTIHYPERTENSIVE

  1. more selective aldosterone antagonist (less likely to cause sex steroid hormone receptor issues)
  2. K-sparing diuretic
  3. block binding of aldosterone to receptors
  4. tx of HTN secondary to aldosterone excess
  5. SE: hyperkalemia
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22
Q

Reserpine

A

ANTIHYPERTENSIVE

  1. Adrenergic neuron blocker-PERIPHERAL
  2. depletes storage of NE in symp nerve endings
  3. BP lowering may persist for some time after discontinuing (irreversible depletion)
  4. Decrease BP dt decreased CO and TPR
  5. SE: sedation, migraine by effects on serotonin, nasal congestion, POSTURAL HYPOTESNTION, BRADYCARDIA, FLUID RETENTION, diarrhea, peptic ulcer exacerbation
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23
Q

Methyldopa

A

ANTIHYPERTENSIVE
1. Adrenergic neuron blockers-CENTRAL
2. a2 receptor agonists in vasomotor centers (decrease symp outflow)
3. decrease renal renin, CO, TPR
4. prodrug. converted to methynorepinephrine
5. DOESNT HARM FETUS. HTN DURING PREGNANCY
6. SE: peripheral fluid retention, sedation, dry mouth, autoimmune disorders, parkinsonian signs
LESS LIKELY TO GET REBOUND HTN BC DRUG TAKES TIME TO DEPLETE

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24
Q

Clonidine

A

ANTIHYPERTENSIVE

  1. Adrenergic neuron blocker-CENTRAL
  2. a2 receptor agonist in vasomotor centers (decrease symp outflow)
  3. decrease renal renin, CO, TPR
  4. may influence imidazoline receptors
  5. PATCH for transdermal absorption-smooth BP control with fewer side effects
  6. only small dose needed
  7. SE: rebound HTN when stopped quickly (less w/ patch)
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25
Q

Prazosin

A

ANTIHYPERTENSIVE
1. a1 adrenergic receptor blocker
2. inhibits binding of NE. blunts vasoconstriction
3. decreases BP by decreasing TPR
4. dilation of both resistance and capacitance vessels
5. dosage should be slowly increased
6. USES: may improve glucose tolerance (BUT dont use with diabetics with impaired postural reflex function), CHOLESTEROL AND TRIGLYCERIDE LEVELS LOWERED AND HDL RAISED
SE: postural hypotension (minimize by initial low dose), stress induced incontience, reflex tachycardia and fluid retention

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26
Q

Doxazosin

A

ANTIHYPERTENSIVE
1. a1 adrenergic receptor blocker
POSTURAL HYPOTENSION LESS SEVERE
2. inhibits binding of NE. blunts vasoconstriction
3. decreases BP by decreasing TPR
4. dilation of both resistance and capacitance vessels
5. dosage should be slowly increased
6. USES: may improve glucose tolerance (BUT dont use with diabetics with impaired postural reflex function), CHOLESTEROL AND TRIGLYCERIDE LEVELS LOWERED AND HDL RAISED
SE: postural hypotension (minimize by initial low dose), stress induced incontience, reflex tachycardia and fluid retention

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27
Q

Terazosin

A

ANTIHYPERTENSIVE
1. a1 adrenergic receptor blocker
POSTURAL HYPOTENSION LESS SEVERE
2. inhibits binding of NE. blunts vasoconstriction
3. decreases BP by decreasing TPR
4. dilation of both resistance and capacitance vessels
5. dosage should be slowly increased
6. USES: may improve glucose tolerance (BUT dont use with diabetics with impaired postural reflex function), CHOLESTEROL AND TRIGLYCERIDE LEVELS LOWERED AND HDL RAISED
SE: postural hypotension (minimize by initial low dose), stress induced incontience, reflex tachycardia and fluid retention

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28
Q

Propanolol

A

ANTIHYPERTENSIVE
1. B adrenergic receptor blocker B1, B2
HIGH LIPID SOLUBILITY
2. lowers arterial BP by decreasing CO, contractility and HR
3. inhibits release of renin from renal JG cells
4. removes B2 mediated vasodilation in peripheral vessels (offsets decrease in TPR-less antihypertensive effect)
5. the more lipid soluble, the more metabolized on first pass thru liver (enters brain)..less lipid soluble excreted thru kidneys–>fewer CNS effects
6. LESS EFFECTIVE IN ELDERLY AND AA patients
7. Good for tx of HTN with tachycardia and high CO, HTN associated with angina, arrhythmia
8. SE: bradycardia, decrease exercise ability, rebound HTN with sudden withdrawl, bronchoconstriction (with nonselective), hypoglycemia (diabetics should only be given non-selective agents. warning signs are diminished), hypertriglyceridemia, fall in HDL, bad dreams, hallucinations with lipid soluble agents

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29
Q

Nadolol

A

ANTIHYPERTENSIVE
1. B adrenergic receptor blocker B1, B2
LOW LIPID SOLUBILITY
2. lowers arterial BP by decreasing CO, contractility and HR
3. inhibits release of renin from renal JG cells
4. removes B2 mediated vasodilation in peripheral vessels (offsets decrease in TPR-less antihypertensive effect)
5. the more lipid soluble, the more metabolized on first pass thru liver (enters brain)..less lipid soluble excreted thru kidneys–>fewer CNS effects
6. LESS EFFECTIVE IN ELDERLY AND AA patients
7. Good for tx of HTN with tachycardia and high CO, HTN associated with angina, arrhythmia
8. SE: bradycardia, decrease exercise ability, rebound HTN with sudden withdrawl, bronchoconstriction (with nonselective), hypoglycemia (diabetics should only be given non-selective agents. warning signs are diminished), hypertriglyceridemia, fall in HDL, bad dreams, hallucinations with lipid soluble agents

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30
Q

Timolol

A

ANTIHYPERTENSIVE
1. B adrenergic receptor blocker B1, B2
MODERATE LIPID SOLUBILITY
2. lowers arterial BP by decreasing CO, contractility and HR
3. inhibits release of renin from renal JG cells
4. removes B2 mediated vasodilation in peripheral vessels (offsets decrease in TPR-less antihypertensive effect)
5. the more lipid soluble, the more metabolized on first pass thru liver (enters brain)..less lipid soluble excreted thru kidneys–>fewer CNS effects
6. LESS EFFECTIVE IN ELDERLY AND AA patients
7. Good for tx of HTN with tachycardia and high CO, HTN associated with angina, arrhythmia
8. SE: bradycardia, decrease exercise ability, rebound HTN with sudden withdrawl, bronchoconstriction (with nonselective), hypoglycemia (diabetics should only be given non-selective agents. warning signs are diminished), hypertriglyceridemia, fall in HDL, bad dreams, hallucinations with lipid soluble agents

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31
Q

Pindolol

A

ANTIHYPERTENSIVE
1. B adrenergic receptor blocker B1 B2
PARTIAL AGONIST- lower BP without as much reduction in CO and renin but with decrease in TPR by partially stimulating B2 receptors vascularly
MODERATE LIPID SOLUBILITY
2. lowers arterial BP by decreasing CO, contractility and HR
3. inhibits release of renin from renal JG cells
4. removes B2 mediated vasodilation in peripheral vessels (offsets decrease in TPR-less antihypertensive effect)
5. the more lipid soluble, the more metabolized on first pass thru liver (enters brain)..less lipid soluble excreted thru kidneys–>fewer CNS effects
6. LESS EFFECTIVE IN ELDERLY AND AA patients
7. Good for tx of HTN with tachycardia and high CO, HTN associated with angina, arrhythmia
8. SE: bradycardia, decrease exercise ability, rebound HTN with sudden withdrawl, bronchoconstriction (with nonselective), hypoglycemia (diabetics should only be given non-selective agents. warning signs are diminished), hypertriglyceridemia, fall in HDL, bad dreams, hallucinations with lipid soluble agents

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32
Q

Atenolol

A

ANTIHYPERTENSIVE
1. B adrenergic receptor blocker B1 only
LOW LIPID SOLUBILITY
2. lowers arterial BP by decreasing CO, contractility and HR
3. inhibits release of renin from renal JG cells
4. removes B2 mediated vasodilation in peripheral vessels (offsets decrease in TPR-less antihypertensive effect)
5. the more lipid soluble, the more metabolized on first pass thru liver (enters brain)..less lipid soluble excreted thru kidneys–>fewer CNS effects
6. LESS EFFECTIVE IN ELDERLY AND AA patients
7. Good for tx of HTN with tachycardia and high CO, HTN associated with angina, arrhythmia
8. SE: bradycardia, decrease exercise ability, rebound HTN with sudden withdrawl, bronchoconstriction (with nonselective), hypoglycemia (diabetics should only be given non-selective agents. warning signs are diminished), hypertriglyceridemia, fall in HDL, bad dreams, hallucinations with lipid soluble agents

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33
Q

Metoprolol

A

ANTIHYPERTENSIVE
1. B adrenergic receptor blocker B1 only
MODERATE LIPID SOLUBILITY
2. lowers arterial BP by decreasing CO, contractility and HR
3. inhibits release of renin from renal JG cells
4. removes B2 mediated vasodilation in peripheral vessels (offsets decrease in TPR-less antihypertensive effect)
5. the more lipid soluble, the more metabolized on first pass thru liver (enters brain)..less lipid soluble excreted thru kidneys–>fewer CNS effects
6. LESS EFFECTIVE IN ELDERLY AND AA patients
7. Good for tx of HTN with tachycardia and high CO, HTN associated with angina, arrhythmia
8. SE: bradycardia, decrease exercise ability, rebound HTN with sudden withdrawl, bronchoconstriction (with nonselective), hypoglycemia (diabetics should only be given non-selective agents. warning signs are diminished), hypertriglyceridemia, fall in HDL, bad dreams, hallucinations with lipid soluble agents

34
Q

Acebutolol

A

ANTIHYPERTENSIVE
1. B adrenergic receptor blocker B1 only
PARTIAL AGONIST
LOW LIPID SOLUBILITY
2. lowers arterial BP by decreasing CO, contractility and HR
3. inhibits release of renin from renal JG cells
4. removes B2 mediated vasodilation in peripheral vessels (offsets decrease in TPR-less antihypertensive effect)
5. the more lipid soluble, the more metabolized on first pass thru liver (enters brain)..less lipid soluble excreted thru kidneys–>fewer CNS effects
6. LESS EFFECTIVE IN ELDERLY AND AA patients
7. Good for tx of HTN with tachycardia and high CO, HTN associated with angina, arrhythmia
8. SE: bradycardia, decrease exercise ability, rebound HTN with sudden withdrawl, bronchoconstriction (with nonselective), hypoglycemia (diabetics should only be given non-selective agents. warning signs are diminished), hypertriglyceridemia, fall in HDL, bad dreams, hallucinations with lipid soluble agents

35
Q

Labetolol

A

ANTIHYPERTENSIVE
1. a1/B blocker and NO releasing B1 blocker
2. ISA at B2
3. decrease BP dt decreased TPR (a-block) partial vascular stimulation (B2 stimulation), less renin release, decrease in CO
4. ORAL LABETOLOL for SEVERE 1* HTN
IV LABETOLOL FOR HTN EMERGENCY
5. SE: a-block: postural dizziness, b-block: bradycardia, AV block at high doses

36
Q

Nebivolol

A

ANTIHYPERTENSIVE
1. a1/B blocker and NO releasing B1 blocker
2. ISA at B2
3. decrease BP dt decreased TPR (a-block) partial vascular stimulation (B2 stimulation), less renin release, decrease in CO
4. ORAL LABETOLOL for SEVERE 1* HTN
IV LABETOLOL FOR HTN EMERGENCY
5. SE: a-block: postural dizziness, b-block: bradycardia, AV block at high doses

37
Q

Hydralazine

A

ANTIHYPERTENSIVE

  1. direct arteriolar dilators
  2. decrease BP by decreasing TPR
  3. release of NO
  4. marked 1st pass effect (dt acetylation in liver)
  5. USES: increase capillary hydrostatic pressure–edema. renal retention of h20 and Na
  6. SE: release of renin, tachycardia, edema, loss of HTN efficacy IF NOT USED WITH B BLOCKER AND DIURETIC
    - -LUPUS LIKE RXN
38
Q

Minoxidil

A

ANTIHYPERTENSIVE

  1. direct arteriolar dilators
  2. act via sulfate metabolite–opens ATP sensitive K channels in aa. DECREASE IN BP BY DECREASE IN TPR
  3. FOR SEVERE HTN (when renal insufficiency)
  4. USES: increase capillary hydrostatic pressure–edema. renal retention of h20 and Na
  5. SE: release of renin, tachycardia, edema, loss of HTN efficacy IF NOT USED WITH B BLOCKER AND DIURETIC
    - -HAIR GROWTH!!
39
Q

bumetanide

A

ANTIHYPERTENSIVE

  1. loop diuretic for hypertension
  2. short acting
  3. given BID/TID
40
Q

torsemide

A

ANTIHYPERTENSIVE

  1. loop diuretic for hypertension
  2. longer acting
  3. sustained effect with one dose/day
41
Q

verapamil

A

ANTIHYPERTENSIVE
1. ca-channel blocker
2. decrease ventricular contractility by decrease ca entry thru ventricular L type channels (decreases CO)
3. some decrease in HR and arterial tone dt channels in SA node and aa
4. SLOW RELEASE FORMULATIONS
5. DECREASE BP WELL IN ELDERLY AND AA HTN PTS
VERAPAMIL SPECIFIC SE: NAUSEA, HA, CONSTIPATION
MOST LIKELY TO CAUSE MYOCARDIAL DEPRESSION (bradycardia, AV nodal dysfunction)

42
Q

diltiazem

A

ANTIHYPERTENSIVE
1. ca-channel blocker
2. decrease ventricular contractility by decrease ca entry thru L type channels (decreases CO)
3. some decrease in HR and arterial tone dt channels in SA node and aa
4. SLOW RELEASE FORMULATIONS
5. DECREASE BP WELL IN ELDERLY AND AA HTN PTS
DILTIAZEM SE: NAUSEA, HA

43
Q

nifedipine

A

ANTIHYPERTENSIVE
1. ca-channel blocker
2. decrease Ca entry in arterial SM cells thru arterial L type channels–decrease in vascular tone. decrease TPR and BP
3. little effect on ventricles
4. INTRINSIC NATRIURETIC CAPABILITY
5. SLOW RELEASE FORMULATIONS
6. APPROVED TO TX PRIMARY PULMONARY HTN
5. DECREASE BP WELL IN ELDERLY AND AA HTN PTS
6: SE: increase HR dt peripheral vasodilation, ANKLE EDEMA
NO LONG TERM USE DT MIs

44
Q

amlodipine

A

ANTIHYPERTENSIVE
1. ca-channel blocker
2. decrease Ca entry in arterial SM cells thru arterial L type channels–decrease in vascular tone. decrease TPR and BP
3. little effect on ventricles
4. INTRINSIC NATRIURETIC CAPABILITY
5. LONGER ACTING WITH SLOW ONSET
5. DECREASE BP WELL IN ELDERLY AND AA HTN PTS
6: SE: increase HR dt peripheral vasodilation, ANKLE EDEMA
NO LONG TERM USE DT MIs

45
Q

captopril

A

ANTIHYPERTENSIVE
1. ACE inhibitor (no conversion of A-1 to A-2)
2. prototype
CAPTOPRIL SE: rash, loss of taste, renal abnormalities
3. A-2 mediated vasoconstriction is overcome (TPR, BP falls)
4. synthesis of ADH is inhibited. Na and H20 retention reduced
5. NOTE: ACE-inactivates bradykinin–>increased bradykinin is vasodilator–decreased TPR (NOT IN ARBS)
6. inhibit relase of NE from symp nerve endings. prevents reflex tachy with drop in TPR.
USES: all RAAS inhibitors work in normal and high renin patients. good for HTN dt DM nephropathy
SE: BAD FOR FULLY ESTABLISHED BILATERAL RENOVASCULAR HTN–may have more loss of GFR with these drugs, hyperkalemia, HIGHER BRADYKININ ONLY WITH ACE inhibitors–>non productive cough, angioedema
ACES, ARBS and renin inhibitor can harm fetal development
hepatotoxicity
NSAIDS may impair ACEs by blocking bradykinin mediated vasodilation

46
Q

enalapril

A

ANTIHYPERTENSIVE
1. ACE inhibitor
2. prodrug. activated by desterifacation to enalaprilat
3. A-2 mediated vasoconstriction is overcome (TPR, BP falls)
4. synthesis of ADH is inhibited. Na and H20 retention reduced
5. NOTE: ACE-inactivates bradykinin–>increased bradykinin is vasodilator–decreased TPR (NOT IN ARBS)
6. inhibit relase of NE from symp nerve endings. prevents reflex tachy with drop in TPR.
USES: all RAAS inhibitors work in normal and high renin patients. good for HTN dt DM nephropathy
SE: BAD FOR FULLY ESTABLISHED BILATERAL RENOVASCULAR HTN–may have more loss of GFR with these drugs, hyperkalemia, HIGHER BRADYKININ ONLY WITH ACE inhibitors–>non productive cough, angioedema
ACES, ARBS and renin inhibitor can harm fetal development
hepatotoxicity
NSAIDS may impair ACEs by blocking bradykinin mediated vasodilation

47
Q

lisinopril

A

ANTIHYPERTENSIVE
1. ACE inhibitor
2. active derivative of enalaprilat
3. A-2 mediated vasoconstriction is overcome (TPR, BP falls)
4. synthesis of ADH is inhibited. Na and H20 retention reduced
5. NOTE: ACE-inactivates bradykinin–>increased bradykinin is vasodilator–decreased TPR (NOT IN ARBS)
6. inhibit relase of NE from symp nerve endings. prevents reflex tachy with drop in TPR.
USES: all RAAS inhibitors work in normal and high renin patients. good for HTN dt DM nephropathy
SE: BAD FOR FULLY ESTABLISHED BILATERAL RENOVASCULAR HTN–may have more loss of GFR with these drugs, hyperkalemia, HIGHER BRADYKININ ONLY WITH ACE inhibitors–>non productive cough, angioedema
ACES, ARBS and renin inhibitor can harm fetal development
hepatotoxicity
NSAIDS may impair ACEs by blocking bradykinin mediated vasodilation

48
Q

fosinopril

A

ANTIHYPERTENSIVE
1. ACE inhibitor
2. LONG ACTING
3. activated by liver
4. ROUTE OF ELIMINATION SHIFTS TOWARDS LIVER IN RENAL IMPAIRMENT
3. A-2 mediated vasoconstriction is overcome (TPR, BP falls)
4. synthesis of ADH is inhibited. Na and H20 retention reduced
5. NOTE: ACE-inactivates bradykinin–>increased bradykinin is vasodilator–decreased TPR (NOT IN ARBS)
6. inhibit relase of NE from symp nerve endings. prevents reflex tachy with drop in TPR.
USES: all RAAS inhibitors work in normal and high renin patients. good for HTN dt DM nephropathy
SE: BAD FOR FULLY ESTABLISHED BILATERAL RENOVASCULAR HTN–may have more loss of GFR with these drugs, hyperkalemia, HIGHER BRADYKININ ONLY WITH ACE inhibitors–>non productive cough, angioedema
ACES, ARBS and renin inhibitor can harm fetal development
hepatotoxicity
NSAIDS may impair ACEs by blocking bradykinin mediated vasodilation

49
Q

quinapril

A

ANTIHYPERTENSIVE
1. ACE inhibitor
2. long acting
3. activated by liver
3. A-2 mediated vasoconstriction is overcome (TPR, BP falls)
4. synthesis of ADH is inhibited. Na and H20 retention reduced
5. NOTE: ACE-inactivates bradykinin–>increased bradykinin is vasodilator–decreased TPR (NOT IN ARBS)
6. inhibit relase of NE from symp nerve endings. prevents reflex tachy with drop in TPR.
USES: all RAAS inhibitors work in normal and high renin patients. good for HTN dt DM nephropathy
SE: BAD FOR FULLY ESTABLISHED BILATERAL RENOVASCULAR HTN–may have more loss of GFR with these drugs, hyperkalemia, HIGHER BRADYKININ ONLY WITH ACE inhibitors–>non productive cough, angioedema
ACES, ARBS and renin inhibitor can harm fetal development
hepatotoxicity
NSAIDS may impair ACEs by blocking bradykinin mediated vasodilation

50
Q

ramipril

A

ANTIHYPERTENSIVE
1. ACE inhibitor
2. long acting
3. activated by liver
3. A-2 mediated vasoconstriction is overcome (TPR, BP falls)
4. synthesis of ADH is inhibited. Na and H20 retention reduced
5. NOTE: ACE-inactivates bradykinin–>increased bradykinin is vasodilator–decreased TPR (NOT IN ARBS)
6. inhibit relase of NE from symp nerve endings. prevents reflex tachy with drop in TPR.
USES: all RAAS inhibitors work in normal and high renin patients. good for HTN dt DM nephropathy
SE: BAD FOR FULLY ESTABLISHED BILATERAL RENOVASCULAR HTN–may have more loss of GFR with these drugs, hyperkalemia, HIGHER BRADYKININ ONLY WITH ACE inhibitors–>non productive cough, angioedema
ACES, ARBS and renin inhibitor can harm fetal development
hepatotoxicity
NSAIDS may impair ACEs by blocking bradykinin mediated vasodilation

51
Q

losartan

A

ANTIHYPERTENSIVE
1. angiotensin II receptor blocker
2. short half life
3. 24 hr bp control with one dose
3. A-2 mediated vasoconstriction is overcome (TPR, BP falls)
4. synthesis of ADH is inhibited. Na and H20 retention reduced
5. NOTE: ACE-inactivates bradykinin–>increased bradykinin is vasodilator–decreased TPR (NOT IN ARBS)
6. inhibit relase of NE from symp nerve endings. prevents reflex tachy with drop in TPR.
USES: all RAAS inhibitors work in normal and high renin patients. good for HTN dt DM nephropathy
SE: BAD FOR FULLY ESTABLISHED BILATERAL RENOVASCULAR HTN–may have more loss of GFR with these drugs, hyperkalemia, HIGHER BRADYKININ ONLY WITH ACE inhibitors–>non productive cough, angioedema
ACES, ARBS and renin inhibitor can harm fetal development
hepatotoxicity
NSAIDS may impair ACEs by blocking bradykinin mediated vasodilation

52
Q

valsartan

A

ANTIHYPERTENSIVE
1. angiotensin II receptor blocker
2. no active metabolite
3. A-2 mediated vasoconstriction is overcome (TPR, BP falls)
4. synthesis of ADH is inhibited. Na and H20 retention reduced
5. NOTE: ACE-inactivates bradykinin–>increased bradykinin is vasodilator–decreased TPR (NOT IN ARBS)
6. inhibit relase of NE from symp nerve endings. prevents reflex tachy with drop in TPR.
USES: all RAAS inhibitors work in normal and high renin patients. good for HTN dt DM nephropathy
SE: BAD FOR FULLY ESTABLISHED BILATERAL RENOVASCULAR HTN–may have more loss of GFR with these drugs, hyperkalemia, HIGHER BRADYKININ ONLY WITH ACE inhibitors–>non productive cough, angioedema
ACES, ARBS and renin inhibitor can harm fetal development
hepatotoxicity
NSAIDS may impair ACEs by blocking bradykinin mediated vasodilation

53
Q

candesartan

A

ANTIHYPERTENSIVE
1. angiotensin II receptor blocker
2. prodrug-conversion to active from by GI tract
3. A-2 mediated vasoconstriction is overcome (TPR, BP falls)
4. synthesis of ADH is inhibited. Na and H20 retention reduced
5. NOTE: ACE-inactivates bradykinin–>increased bradykinin is vasodilator–decreased TPR (NOT IN ARBS)
6. inhibit relase of NE from symp nerve endings. prevents reflex tachy with drop in TPR.
USES: all RAAS inhibitors work in normal and high renin patients. good for HTN dt DM nephropathy
SE: BAD FOR FULLY ESTABLISHED BILATERAL RENOVASCULAR HTN–may have more loss of GFR with these drugs, hyperkalemia, HIGHER BRADYKININ ONLY WITH ACE inhibitors–>non productive cough, angioedema
ACES, ARBS and renin inhibitor can harm fetal development
hepatotoxicity
NSAIDS may impair ACEs by blocking bradykinin mediated vasodilation

54
Q

Aliskiren

A

ANTIHYPERTENSIVE

  1. renin inhibitor
  2. eliminated in feces and urine
  3. taken once daily
  4. A-II mediated vasoconstriction stopped
  5. A-II synthesis of ADH inhibitied (H20 Na retention reduced) decreased fluid retention
  6. Harmful to fetus
55
Q

felodipine

A

ANTIHYPERTENSIVE
1. ca channel blocker
2. decrease Ca entry in arterial SM cells thru arterial L type channels–decrease in vascular tone. decrease TPR and BP
3. little effect on ventricles
4. INTRINSIC NATRIURETIC CAPABILITY
5. LONGER ACTING WITH SLOW ONSET
5. DECREASE BP WELL IN ELDERLY AND AA HTN PTS
6: SE: increase HR dt peripheral vasodilation, ANKLE EDEMA
NO LONG TERM USE DT MIs

56
Q

Nitroglycerin

A

ANTIANGINAL
2. rapidly denitrated in the liver–>glyceryl denigrate
3. high first pass metabolism–>unchanged drug is main cause of therapeutic effects
4. become NO in SM cells–>increase cGMP–>SM relax
5. vv more sensitive than aa (large aa more sens)
6. peripheral dilation=decreased cardiac work (decr. preload). decrease o2 demand
7. MAIN EFFECT IS DECREASED O2 DEMAND
NOTE: NO can inhibit platelet agg.
USE: all anginas.
-SR, transdermal forms have longer duration
SE: ortho hypotension, HA, reflex increase in HR and contractility, Na/H20 retention, tolerance (rebound angina), HYPOTENSIVE INTERACTION WITH VIAGRA (phosphodiesterase 5 inhibitors)
DONT USE DURING INFERIOR WALL MI

57
Q

Isosorbide Dinitrate

A

ANTIANGINAL
2. rapidly denitrated in the liver–>glyceryl denigrate
3. high first pass metabolism–>unchanged drug is main cause of therapeutic effects
4. become NO in SM cells–>increase cGMP–>SM relax
5. vv more sensitive than aa (large aa more sens)
6. peripheral dilation=decreased cardiac work (decr. preload). decrease o2 demand
7. MAIN EFFECT IS DECREASED O2 DEMAND
NOTE: NO can inhibit platelet agg.
USE: all anginas.
-SR, transdermal forms have longer duration
SE: ortho hypotension, HA, reflex increase in HR and contractility, Na/H20 retention, tolerance (rebound angina), HYPOTENSIVE INTERACTION WITH VIAGRA (phosphodiesterase 5 inhibitors)
DONT USE DURING INFERIOR WALL MI

58
Q

Nifedipine

A

ANTIANGINAL
1. Ca channel blocker
2. act in arterial tissue. block Ca channels in SM.
aa more sensitive than vv
3. rapid short action
4. decreased afterload in pts with angina. decrease 02 demand
VASOSPASM CAN BE REVERSED.
CAN INHIBIT PLATELET AGGREGATION
USES: preventative treatment of all anginas. acute anginal attack.
SE: may reflex increase HR and contractility (more common with short acting forms)

59
Q

Amylodipine

A

ANTIANGINAL
INTRINSICALLY LONG ACTING
1. Ca channel blocker
2. act in arterial tissue. block Ca channels in SM.
aa more sensitive than vv
3. rapid short action
4. decreased afterload in pts with angina. decrease 02 demand
VASOSPASM CAN BE REVERSED.
CAN INHIBIT PLATELET AGGREGATION
USES: preventative treatment of all anginas. acute anginal attack.
SE: may reflex increase HR and contractility (more common with short acting forms)

60
Q

Propanolol

A

ANTIANGINAL
1. B1 B2 blocker. competitive antagonists
2. decrease HR, Contractility, arterial BP. DECREASE O2 DEMAND.
NOTE: PARTIAL AGONISTS NOT EFFECTIVE FOR ANGINA
USES: Preventative for anginas, especially exercise induced (not so much vasospastic form)
-TX of silent ischemia picked up by EKG
-can use with nitrates to prevent tachy
SE: bradycardia, AV block, rebound angina/MI, asthmatic attacks for NONSELECTIVE B1B2, masking of hypoglycemic symptoms, CNS: sedation, fatigue.

61
Q

Nadolol

A

LESS CNS EFFECTS-less lipid soluble
ANTIANGINAL
1. B1 B2 blocker. competitive antagonists
2. decrease HR, Contractility, arterial BP. DECREASE O2 DEMAND.
NOTE: PARTIAL AGONISTS NOT EFFECTIVE FOR ANGINA
USES: Preventative for anginas, especially exercise induced (not so much vasospastic form)
-TX of silent ischemia picked up by EKG
-can use with nitrates to prevent tachy
SE: bradycardia, AV block, rebound angina/MI, asthmatic attacks for NONSELECTIVE B1B2, masking of hypoglycemic symptoms, CNS: sedation, fatigue.

62
Q

Timolol

A

ANTIANGINAL
1. B1 B2 blocker. competitive antagonists
2. decrease HR, Contractility, arterial BP. DECREASE O2 DEMAND.
NOTE: PARTIAL AGONISTS NOT EFFECTIVE FOR ANGINA
USES: Preventative for anginas, especially exercise induced (not so much vasospastic form)
-TX of silent ischemia picked up by EKG
-can use with nitrates to prevent tachy
SE: bradycardia, AV block, rebound angina/MI, asthmatic attacks for NONSELECTIVE B1B2, masking of hypoglycemic symptoms, CNS: sedation, fatigue.

63
Q

Atenolol

A

LESS CNS EFFECTS-less lipid soluble
ANTIANGINAL
1. B1 ONLY blocker. competitive antagonists
2. decrease HR, Contractility, arterial BP. DECREASE O2 DEMAND.
NOTE: PARTIAL AGONISTS NOT EFFECTIVE FOR ANGINA
USES: Preventative for anginas, especially exercise induced (not so much vasospastic form)
-TX of silent ischemia picked up by EKG
-can use with nitrates to prevent tachy
SE: bradycardia, AV block, rebound angina/MI, masking of hypoglycemic symptoms, CNS: sedation, fatigue.

64
Q

Metoprolol

A

ANTIANGINAL
1. B1 ONLY blocker. competitive antagonists
2. decrease HR, Contractility, arterial BP. DECREASE O2 DEMAND.
NOTE: PARTIAL AGONISTS NOT EFFECTIVE FOR ANGINA
USES: Preventative for anginas, especially exercise induced (not so much vasospastic form)
-TX of silent ischemia picked up by EKG
-can use with nitrates to prevent tachy
SE: bradycardia, AV block, rebound angina/MI, masking of hypoglycemic symptoms, CNS: sedation, fatigue.

65
Q

Ranolazine

A

ANTIANGINAL
“fatty acid oxidation inhibitor”
1. inactivated by hepatic metabolism
2. MECHANISM: shift fuel of heart from fa–>glucose. demands less o2 to produce same energy level. OR inhibition of late inward directed Na current caused by ischemia. better Na/Ca exchange occurs. decreased ca overload and resultant o2 demand
USES: combo with other antianginals for stable angina
SE: dizziness, HA, constipation. USE WITH VERAPAMIL AND DILTIAZEM INCREASE PLASMA CONC. can prolong QT interval

66
Q

Verapamil

A

ANTIANGINAL
1. Ca channel blocker-Cardiac muscle
2. rapid short action (unless slow release)
3. decrease HR and contractility. decrease O2 demand
4. inhibit platelet aggregation
5. prevent anginas
6. USEFUL WITH NITRATES TO PREVENT TACHYCARDIA OF NITRATES
SE: CHF, AV block, too much sinus depression

67
Q

Diltiazem

A

ANTIANGINAL
1. Ca channel blocker-Cardiac muscle
2. rapid short action (unless slow release)
3. decrease HR and contractility. decrease O2 demand
4. inhibit platelet aggregation
5. prevent anginas
6. USEFUL WITH NITRATES TO PREVENT TACHYCARDIA OF NITRATES
SE: CHF, AV block, too much sinus depression

68
Q

Ezetimibe

A

ANTILIPID
1. Cholesterol absorption inhibitor
2. uptake by intestine-converted to glucoronide metabolite. RECIRCULATION=more active metabolite
3. inhibits dietary and biliary cholesterol across brush border thru chylomicrons (protein mediated transport)
4. decrease delivery to liver–>increase uptake of LDL from circulation
5. used in combo with statins
SE: diarhhea and abdominal pain, fibrates increase bile acid binding resins–decrease availability of drug, increased LFTs

69
Q

Cholestyramine

A

ANTILIPID
1. Bile acid binding resin. ion exchange capacity Cl
2. not digested from lumen of small intestine
3. excreted directly to feces
4. more cholestorol must be converted to bile acid. thru serum LDL. may initially increase VLDL
5. tx high LDL
SE: NO SYSTEMIC TOXICITY, bloating, nausea, constipation
CAN INHIBIT ABSORPTION OF THIAZIDE DIURETICS, ABS, BARBITURATES, EZETIMIBE, STATINS, fat soluble vitamins and iron
can cause malabsorption

70
Q

Colestipol

A

ANTILIPID
1. Bile acid binding resin. ion exchange capacity Cl
2. not digested from lumen of small intestine
3. excreted directly to feces
4. more cholestorol must be converted to bile acid. thru serum LDL. may initially increase VLDL
5. tx high LDL
SE: NO SYSTEMIC TOXICITY, bloating, nausea, constipation
CAN INHIBIT ABSORPTION OF THIAZIDE DIURETICS, ABS, BARBITURATES, EZETIMIBE, STATINS, fat soluble vitamins and iron
can cause malabsorption

71
Q

Colesevelam

A

LESS GI EFFECTS
ANTILIPID
1. Bile acid binding resin. ion exchange capacity Cl
2. not digested from lumen of small intestine
3. excreted directly to feces
4. more cholestorol must be converted to bile acid. thru serum LDL. may initially increase VLDL
5. tx high LDL
SE: NO SYSTEMIC TOXICITY, bloating, nausea, constipation
CAN INHIBIT ABSORPTION OF THIAZIDE DIURETICS, ABS, BARBITURATES, EZETIMIBE, STATINS, fat soluble vitamins and iron
can cause malabsorption

72
Q

Lovastatin

A

ANTILIPID
1. HMG CoA reductase inhibitors (statins)
2. First pass hepatic metabolism
- can be inhibited by gemfibrozil and grapefruit
3. excreted in feces by bile
PRODRUG
4. Acts at liver. inhibits HMG coA reductase from conversion to of HMG coA to mevolonate. RATE LIMITING STEP in synth of cholesterol
5. increase LDL receptors. less LDL
USES: MORE EFFECTIVE THAN ALL OTHER DRUGS and decrease LDL. aniatherosclerotic benfits: antiinflammatory
SE: constipation, diarrhea, HA, dizziness, rash, blurred vision, INCREASED SERUM TRANSAMINASE, Myopathy (increase CK levels)–muscle weakness, cramps, pain–RABDOMYOLYSIS–urine turns dark (caused due to DECREASED COENZYME Q10 levels in skeletal muscle mitochondria, exercise may make worse
CONTRAINDICATIONS: active liver disease, pregnancy, lactation

73
Q

Pravastatin

A

ANTILIPID
1. HMG CoA reductase inhibitors (statins)
ACTIVE AS INGESTED
2. First pass hepatic metabolism
- can be inhibited by gemfibrozil and grapefruit
3. excreted in feces by bile
4. Acts at liver. inhibits HMG coA reductase from conversion to of HMG coA to mevolonate. RATE LIMITING STEP in synth of cholesterol
5. increase LDL receptors. less LDL
USES: MORE EFFECTIVE THAN ALL OTHER DRUGS and decrease LDL. aniatherosclerotic benfits: antiinflammatory
SE: constipation, diarrhea, HA, dizziness, rash, blurred vision, INCREASED SERUM TRANSAMINASE, Myopathy (increase CK levels)–muscle weakness, cramps, pain–RABDOMYOLYSIS–urine turns dark (caused due to DECREASED COENZYME Q10 levels in skeletal muscle mitochondria, exercise may make worse
CONTRAINDICATIONS: active liver disease, pregnancy, lactation

74
Q

Simvastatin

A

ANTILIPID
1. HMG CoA reductase inhibitors (statins)
PRODRUG
2. First pass hepatic metabolism
- can be inhibited by gemfibrozil and grapefruit
3. excreted in feces by bile
4. Acts at liver. inhibits HMG coA reductase from conversion to of HMG coA to mevolonate. RATE LIMITING STEP in synth of cholesterol
5. increase LDL receptors. less LDL
USES: MORE EFFECTIVE THAN ALL OTHER DRUGS and decrease LDL. aniatherosclerotic benfits: antiinflammatory
SE: constipation, diarrhea, HA, dizziness, rash, blurred vision, INCREASED SERUM TRANSAMINASE, Myopathy (increase CK levels)–muscle weakness, cramps, pain–RABDOMYOLYSIS–urine turns dark (caused due to DECREASED COENZYME Q10 levels in skeletal muscle mitochondria, exercise may make worse
CONTRAINDICATIONS: active liver disease, pregnancy, lactation

75
Q

Atorvastatin

A

ANTILIPID
1. HMG CoA reductase inhibitors (statins)
ACTIVE AS INGESTED
COMBINED WITH CCB amlodipine (Caduet) to treat high cholesterol and BP
2. First pass hepatic metabolism
- can be inhibited by gemfibrozil and grapefruit
3. excreted in feces by bile
4. Acts at liver. inhibits HMG coA reductase from conversion to of HMG coA to mevolonate. RATE LIMITING STEP in synth of cholesterol
5. increase LDL receptors. less LDL
USES: MORE EFFECTIVE THAN ALL OTHER DRUGS and decrease LDL. aniatherosclerotic benfits: antiinflammatory
SE: constipation, diarrhea, HA, dizziness, rash, blurred vision, INCREASED SERUM TRANSAMINASE, Myopathy (increase CK levels)–muscle weakness, cramps, pain–RABDOMYOLYSIS–urine turns dark (caused due to DECREASED COENZYME Q10 levels in skeletal muscle mitochondria, exercise may make worse
CONTRAINDICATIONS: active liver disease, pregnancy, lactation

76
Q

Rosuvastatin

A

ANTILIPID
1. HMG CoA reductase inhibitors (statins)
ACTIVE AS INGESTED
2. First pass hepatic metabolism
- can be inhibited by gemfibrozil and grapefruit
3. excreted in feces by bile
4. Acts at liver. inhibits HMG coA reductase from conversion to of HMG coA to mevolonate. RATE LIMITING STEP in synth of cholesterol
5. increase LDL receptors. less LDL
USES: MORE EFFECTIVE THAN ALL OTHER DRUGS and decrease LDL. aniatherosclerotic benfits: antiinflammatory
SE: constipation, diarrhea, HA, dizziness, rash, blurred vision, INCREASED SERUM TRANSAMINASE, Myopathy (increase CK levels)–muscle weakness, cramps, pain–RABDOMYOLYSIS–urine turns dark (caused due to DECREASED COENZYME Q10 levels in skeletal muscle mitochondria, exercise may make worse
CONTRAINDICATIONS: active liver disease, pregnancy, lactation

77
Q

Gemfibrozil

A

ANTILIPID
1. fibrate
2. inactivated by hepatic metabolism and renal excretion
3. enterohepatic recycling
4. increase VLDL clearance via INCREASED LIPOPROTEIN LIPASE ACTIVITY (increased activity of PPAR-a). increased enzymes for oxidation of ffa’s in liver. less available for VLDL production.
May increase HDL moderately (HDL apolipoprotein A1 and 2)
USES: primary hyperlipidemias with high VLDL, hypertriglyceridemia dt defect in apolipoprotein E
SE: gallstones, GI upset, nausea, myopathy when combined with STATINS–gemfibrozil in particular

78
Q

fenofibrate

A

ANTILIPID
1. fibrate-prodrug
2. inactivated by hepatic metabolism and renal excretion
3. enterohepatic recycling
4. increase VLDL clearance via INCREASED LIPOPROTEIN LIPASE ACTIVITY (increased activity of PPAR-a). increased enzymes for oxidation of ffa’s in liver. less available for VLDL production.
May increase HDL moderately (HDL apolipoprotein A1 and 2)
USES: primary hyperlipidemias with high VLDL, hypertriglyceridemia dt defect in apolipoprotein E
SE: gallstones, GI upset, nausea, myopathy when combined with STATINS–gemfibrozil in particular

79
Q

niacin

A

ANTILIPID
1. metabolized to nicotinamide. inactive
2. short duration
3. Inhibits intracellular lypolysis (inhibits lipase)
4. decrease source of fa for triglyceride biosynthesis
5. lower VLDL secretion as well
6. increase VLDL catabolism by not changing extraceullular lipoprotein lipase
7. Decrease levels of lipoprotein A
CONSIDERABLY INCREASES HDL-MOST EFFECTIVE DRUG (HDL apolipoprotein A1)
USES: least expensive of all drugs. most effective HDL increaser, use for all types of primary hyperlipids. Decrease VLDL and LDL
SE: flushing, itching/burning (dilation of skin vessels dt prostaglandin release–can stop by giving ASA first), less severe if taken with meals
HYPOTENSION, increased LFTS, hyperglycemia and glucose intolerance, GI disturbances, glucose intolerance when combined with RESIN, increase plasma uric acid.

80
Q

omega 3 acid ethyl esters

A

ANTILIPID
1. EPA and DHA thought to inhibit hepatic synthesis of triglycerides from endogenous ffas. many different mechanisms possible.
2. adjuct to diet. decrease VLDL like fibrates. LDL not decreased. (less risk of myopathy)
ANTIINFLAMMATORY ACTION
SE: sx of flue or infections, GI distress, fish taste, inhibit platelet aggregation
Drug interactions: prolonged bleeding times if taken with anticoagulants

81
Q

mipomerson

A

ANTILIPID
1. decrease VLDL and LDL by inhibiting formation of apolipoprotein B containing lipoproteins in GI and liver
2. oligonucleotide type inhibitor
3. adjucts to diet. for HOMOZYGOUS familial hypercholesterolemia
SE: liver toxicity
REMS programs give restricted use

82
Q

lomitapide

A

ANTILIPID
1. Microsomal triglyceride transfer protein type inhibitor
2. decrease VLDL and LDL by inhibiting formation of apolipoprotein B containing lipoproteins in GI and liver
3. adjucts to diet. for HOMOZYGOUS familial hypercholesterolemia
SE: liver toxicity
REMS programs give restricted use

Pharmacology (6 decks)

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