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Pharmacotherapy II > Hypertension Barker Exam 3 > Flashcards

Hypertension Barker Exam 3 Flashcards

1
Q

What pulse pressure threshold is a very important indicator for CV risk?

A

> 65mmHg

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2
Q

Blood pressure = __ x __

A

CO x PVR

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3
Q

Which blood vessels do organic nitrates affect more–veins or arteries?

A

Veins

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4
Q

What two classes of drugs block compensatory responses like tachycardia and Na/H2O retention?

A

Diuretics (block kidney compensation) and beta blockers (block both kidney and heart compensation)

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5
Q

How does a catecholamine depleter like reserpine work?

A

Blocks monoamine transport into vesicles for release–depletes pool of NE in vesicles. Slow onset and terrible SE, but minimal compensatory response.

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6
Q

How do a2 agonists like clonidine, methyldopa, guanabenz, and guanfacine work to reduce BP?

A

They act at a central a2 GPCR (and some other imidazoline receptor?) to stimulate Gi, decreasing cAMP and causing hyperpolarization–leads to less sympathetic output (decrease HR, decrease contractility, decrease renin release, vasodilation–decrease CO and PVR both).

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7
Q

Rank the half lives of clonidine, guanabenz, and guanfacine from shortest to longest.

A

Guanabenz, guanfacine, clonidine

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8
Q

What side effects are common with a2 agonists?

A

Dry mouth, sedation, depression, withdrawal syndrome, Na+/H2O retention. (lactation + positive coombs test for hemolytic anemia with methyldopa as well).

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9
Q

Rank the half lives of the a1 antagonists from shortest to longest acting.

A

Prazosin, terazosin, doxazosin

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10
Q

What is the main mechanism of action of a1 antagonists?

A

Dilate both arteries (decrease PVR) and veins (decrease CO). More often for BPH.

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11
Q

What side effects are associated with the -zosins?

A

First-dose orthostatic hypotension, Na/H2O retention, slight tachycardia.

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12
Q

What was the first beta blocker, and as such has less preferrable properties such as non-selectivity, high lipophilicity, and higher side effects?

A

Propranolol (Inderal)

Side effects include negative lipid impact, inhibited hypoglycemia reaction, and bronchial airway resistance.

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13
Q

What cardioselective beta blocker must be given multiple times per day or as an extended release formulation due to its short half life?

A

Metoprolol tartrate

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14
Q

What cardioselective beta blocker may be given once a day due to its longer half life?

A

Atenolol–its a 10!

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15
Q

Metoprolol help to slow progression in early stages of this disease, but contraindicated in later stages of this disease. What disease?

A

Congestive heart failure–blocks renin-induced damage

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16
Q

What is the main mechanism of beta-blocker activity?

A

They block beta-1 induced release of renin from the kidney.

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17
Q

What beta blocker works through producing NO in addition to the normal beta blocker actions?

A

Nebivolol (Bystolic)

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18
Q

What are the general side effects of beta blockers? Contraindications?

A

SE: Bradycardia, AV block, sedation, withdrawal, mask hypoglycemia.
CI: Asthma, COPD, CHF type IV

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19
Q

What beta blocker has the additional activity of a1 antagonism (mixed adrenergic antagonist), may be given parenterally, and has only one isomer that posesses a1 blocking activity?

A

Labetalol (Trandate)

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20
Q

What mixed adrenergic antagonist can block a1 receptors with either enantiomer?

A

Carvediolol (Coreg)

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21
Q

Why should labetalol and carvediolol never be given to a patient with COPD or asthma?

A

Because both have nonselective B blocking activity.

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22
Q

What general feature of diuretics leads to potassium loss?

A

Increased sodium delivery to the collecting tubule–K+ and Na+ are exchanged.

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23
Q

How do diuretics affect hypertension over the long term?

A

They somehow decrease total peripheral resistance. Plasma volume is only decreased acutely but remains unchanged long-term.

24
Q

How and where do thiazide diuretics function?

A

They work in the distal convoluted tubule by targeting the Na+/Cl- symporters. This also enhances calcium reabsorption.

25
Q

What two diseases are thiazides used for clinically?

A

HTN, CHF

26
Q

What are side effects of thiazides?

A

Hypokalemia, hyponatremia, hyperuricemia, hypercalcemia, hyperlipidemia, impaired carb tolerance, hypokalemic metabolic alkalosis, ED.
Do NOT use with sulfa allergies.

27
Q

How do the loop diuretics work?

A

They inhibit the Na/K/Cl transporter in the thick ascending limb, reducing NaCl, K, Ca, and Mg absorption.

28
Q

How are loop diuretics used in practice?

A

Edematous conditions like acute pulmonary edema. Only used in HTN when CrCl under 30mL/min

29
Q

What side effects are associated with loop diuretics?

A

Dehydration, hypokalemic metabolic alkalosis, hyperuricemia, hypomagnesemia, ototoxicity.
Do NOT use with sulfa allergies.

30
Q

What are the two types of potassium sparing diuretics?

A

Both work in the collecting duct. Amiloride (Midamor) and triamterene (Dyrenium) block sodium reabsorption so it won’t be exchanged with potassium (potassium sparing diuretics) and spironlactone (Aldactone) and Eplerenone (Inspra) antagonize the aldosterone receptor.

31
Q

What contraindication does triamterene have in addition to contraindicated use with potassium supplements and ace inhibitors?

A

Kidney stones

32
Q

What are two potential side effects of amiloride and triamterene?

A

Hyperkalemia, hyperchloremic metabolic acidosis

33
Q

Which potassium sparing diuretic (amiloride or triamterene) has some efficacy in reducing BP by itself?

A

Amiloride

34
Q

How do the aldosterone antagonists function?

A

Blocking the aldosterone receptor leads to decreased numbers of sodium channels in the collecting duct, reducing sodium reabsorption and potassium excretion.

35
Q

What side effects are associated with aldosterone antagonists?

A

Hyperkalemia, genecomastia/impotence/BPH (spironlactone), hypertriglycemidemia (eplerenone), hypercholremic metabolic acidosis (spironlactone)

36
Q

What should potassium sparing diuretics never be used with?

A

ACE inhibitors, ARBs, potassium supplements, other potassium sparing diuretics.

37
Q

What is the first molecule in the renin-angiotensin system and what enzyme acts on it?

A

Angiotensinogen; renin cleaves last four amino acids to produce angiotensin I.

38
Q

What enzyme acts on angiotensin I and is stopped by the penultimate proline to produce angiotensin II?

A

Angiotensin converting enzyme (ACE)

39
Q

What other peptide (besides angiotensin I) does angiotensin converting enzyme cleave?

A

Bradykinin–breaks it down into inactive metabolites.

40
Q

Where are angiotensin II type 1 (AT1) receptors located?

A

Blood vessels, brain, adrenal, kidney, and heart.

41
Q

What is a primary mechanism of renin release from the kidney? What are the two secondary mechanisms of renin release?

A

Primary: The macula densa senses the reabsorption of NaCl from the distal convoluted tubule and can enhance or suppress renin release from the juxtaglomerular cells.
Secondary: Baroreceptor sensing of blood pressure and B1 receptor activation of JGCs.

42
Q

What are the three ways that angiotensin II acts?

A

Rapid pressor response (direct vasoconstriction, increased sympathetic stimulation), slow pressor response (Na reabsorption thru aldosterone release), vascular and cardiac hypertrophy/remodeling (proto-oncogene and growth factor expression–increased afterload and tension)

43
Q

What are the three subtypes of ACE inhibitors?

A

Sulfhydryl-containing, dicarboxyl-containing, and phosphorous-containing

44
Q

How do NSAIDS interfere with ACE inhibitors?

A

They inhibit prostaglandin synthesis so they stop production of prostaglandins that mediate vasodilation through bradykinin. Effect on kidney as well.

45
Q

What ACEI has a short half life and contains a sulfur group?

A

Captopril (Capoten)

46
Q

What dicarboxyl ADEI is a prodrug?

A

Enalapril (Vasotec)

47
Q

What dicarboxyl ACEI is best in patients with compromised renal function?

A

Moexipril (Univasc)

48
Q

What dicarboxyl ACEI is not a prodrug and has a long half life?

A

Lisinopril (Prinivil, Zestril)

49
Q

What is the only phosphinate containing ACEI?

A

Fosinopril–prodrug! hepatic metabolism.

50
Q

What are the four major indications for ACEI therapy?

A

HTN, MI, diabetic nephropathy, left ventricular systolic dysfunction.

51
Q

What are potential side effects of ACEIs?

A

Hypotension, dry cough (bradykinin-mediated), hyperkalemia, acute renal failure (renal artery stenosis especially), skin rash (captopril), angioedema (life-threatening but rare)

52
Q

What patients should never receive ACEIs?

A

Pregnant patients

53
Q

Name major drug interactions with ACEIs

A

Antacids (decreased F), NSAIDS, K supplements, digoxin/lithium (increased plasma levels)

54
Q

How do the -sartans function?

A

They selectively block AT1 receptors, blocking pressor effects, stimulation of NE, secretion of aldosterone, effect on renal vasculature, and hypertrophy/remodeling effects.

55
Q

Why do ARBs provide more complete inhibition of the action of Angiotensin II compared to ACEIs?

A

Because they block all AT1 receptors, whereas ACEIs only block production of ang II through one pathway.

56
Q

What are the four main indications for ARB use?

A

HTN, CHF, diabetic nephropathy, stroke prophylaxis

57
Q

What is the only renin inhibitor and what is its unique side effect?

A

Aliskiren (Tekturna)–diarrhea

Pharmacotherapy II (15 decks)

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