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Pharm Exam 3 > 7 - Hypertension > Flashcards

7 - Hypertension Flashcards

1
Q

Diagnosis of HTN

A

Two or more Diastolics >40

Systolic >90

Pulse pressure >65

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2
Q

Stage 2 HTN

A

S >160

D>100

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3
Q

Essential HTN

A

90% of cases, no identifiable cause

Increased PVR

Normal CO

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4
Q

Diuresis

A

an increase in urine volume

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5
Q

Natriuresis

A

Increase in Renal sodium

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6
Q

Clinical uses for diuretics

A

HTN, edema, CHF

Kidney disease, cirrhosis

Hypercalcemia

Diabetes insipidus

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7
Q

Acetazolamide SOA

A

PCT

(NaHCO3)

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8
Q

Mannitol (or other osmotic agents) SOA

A

PCT – H20

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9
Q

Furosamide SOA

A

Thick ascending limb

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10
Q

Thiazides SOA

A

DCT (early)

(NaCl)

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11
Q

Aldosterone SOA

A

Collecting tubule

(NaCl)

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12
Q

ADH antagonists SOA

A

Collecting tubule

(H20)

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13
Q

Adenosine SOA

A

Affererent arteriole, PCT, Thick ascending limb, Collecting duct

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14
Q

Acetazolamide class, MOA

A

Carbonic anhydrase inhibitor

Inhibit the formation of CO2 and H20 (from H2CO3) out in the lumen

→ CO2 and H2O are excreted

Prevent the reformation of H2CO3 in the PCT cell

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15
Q

Hemodynamic effect of long-term administration of diuretics

A

HR and CO are unchanged

Plasma volume = decreased/unchanged

TPR = decreased

Renin = increased

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16
Q

Mechanism for long term vasodilation with long term diuretics

A

unknown

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17
Q

Diuretics that act in the loop of henle

A

Furosamide

Bumetanide

Ethacrynic acid

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18
Q

Loop diuretics MOA

A

Inhibit the Na-K-2Cl symporter in the lumenal membrane

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19
Q

Loop diuretics - Effect on K+ dynamics

A

No accumulation of K

No K+ outflux back into lumen

NO Mg+ and Ca++ entry

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20
Q

How and where do Mg++ and Ca++ enter the cell in response to K outflux?

A

From the lumen of the Thick Asc. Limb via the paracellular route

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21
Q

Net ionic effects of loop diuretics

A

Increases excretion of all:

Na/ Cl / K / Mg / Ca

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22
Q

Increased ____ from loop diuretics is due to PG formation

A

RBF

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23
Q

Duration of action of loop diuretics depends on ____

A

Renal function

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24
Q

Toxicities of loop diuretics

A

Dehydration

Hypokalemic Met. Acidosis

Ototoxicity

Hyperuricemia

Hypomagnesemia

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25
Q

CI’s for loop diuresis

A

Sulfa allergy

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26
Q

____ are more effective antihypertensives than loops in patients with _________

A

Thiazides

Normal renal function

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27
Q

Thiazide MOA

A

Interfere with the NCC (Na-Cl Cotransporter) in the DCT

–> net excretion of Na (with water following)

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28
Q

Thiazides reduce the formation of

A

calcium stones in idiopathic hypercalcuria

29
Q

Net ionic effects of thiazides

A

increase excretion of Cl, Na, K, and HCO3 (high doses only)

Reduce the excretion (Ca+)

30
Q

Thiazide diuretics

A

Chlorthiazide

HCTZ

Trichlormethiazide

Methylclothiazide

Polythiazide

Cyclothiazide

31
Q

Thiazide-like diuretics

A

Chlorthalidone

Indapamide

Metolazone

32
Q

Thiazides may open…

A

Ca++ activated K+ channels

(leading to vasodilation)

33
Q

Why decrease in peripheral resistance with thiazides?

A

Negative Na balance

34
Q

What effect does K have on vascular state

A

K outflow hyperpolarizes the vascular smooth muscle –> increases vasodilation

35
Q

In patients with renal insufficiency, thiazides…

A

lose the anti-hypertensive effect

36
Q

Thiazide diuretics may cause these conditions

A
  • Hypokalemia, Hyponatremia, Hypochloremic Alkalosis
  • Hyperuricemia, Hyperlipidemia, Hypercalcemia
  • Erectile dysfunction
37
Q

CI’s for thiazides

A

sulfa allergies

38
Q

Diuretics that act on the collecting tubule

A

Potassium-sparing

Amiloride

Trimterene

Eplerenone

Spironolactone

39
Q

Amiloride MOA

A

Inhibit apical Na channels in collecting tubule

**Reduced Na entry also reduces K+ excretion

40
Q

Clinical use for amiloride

A

Adjunct Tx with Thiazide or Loop for CHF or HTN

has some efficacy in reducing BP

Also used in Cirrhosis and edema due to secondary hyperaldosteronism

41
Q

Amiloride toxicities

A

Hyperkalemia

Hyperchloremic met. acidosis

42
Q

CI’s for amiloride

A

K+ supplementation

ACE inhibitors

43
Q

Triamterene MOA

A

Inhibit apical Na+ channels in collecting tubule

also reduces K excretion (d/t reduced sodium entry)

44
Q

Clinical use for triamterene

A

Edema associated with CHF, Cirrhosis, nephrotic symdrome, or hyperaldosteronism

45
Q

Triamterene does not have efficacy in…

A

lowering BP when used as monotherapy

use in combo!

46
Q

Toxicities for triamterene

A

Hyperkalemia, Hyperchloremic metabolic acidosis

47
Q

CI’s for triamterene

A

Kidney stones

K supplementation

ACE inhibitors

48
Q

Both triamterene and Amiloride are secreted in the

A

PCT

49
Q

____ increases urinary excretion of Mg++ but ____ does not.

A

Triamterene does

Amiloride doesn’t

50
Q

Other class of drugs that act on the collecting ttubule

A

Aldosterone antagonists

51
Q

Counteract thiazide postassium loss with

A

amiloride or triamterene

52
Q

Drug that controls the number of Na channels in the membrane

A

antagonist

53
Q

Aldosterone works in the

A

nucleus to alter gene transcription

54
Q

AIP

A

aldosterone induced proteins

upregulated with increased aldosterone

55
Q

Function of AIP’s

A

controls proteins that traffic Na channels in and out of the membrane

Influences the amount of channels in membrane

56
Q

Aldosterone antagonists downstream effects

A

Block aldosterone from binding receptor and inducing AIPs and downregulate Na channels for reabsorption from the lumen

LESS REABS. OF SODIUM FROM LUMEN

57
Q

Aldosterone antagonists

A

aldosterone

spironolactone

58
Q

Spironolactone MOA

A
  • blocks acions of aldosterone
  • blocks 5a reductase

(5a-reductase creates active metabolites of aldosterone)

59
Q

Clinical use of spironolactone

A

HTN or CHF with other diuretics

60
Q

Aldosterone and RAAS play a role in pathogenesis of

A

CHF

61
Q

Tox’s with spironolactone

A

Hyperkalemia

HyperCL met acidosis

Gynecomastia, impotence, BPH

62
Q

CI’s for spironolactone

A

K supplements, ACE inhibitors (promote K retention)

Chronic renal insufficiency

63
Q

More selective mineralocorticoid receptor antagonist

A

Eplerenone

64
Q

Eplerenone MOA

A

selective antag of MCR in kidney heart BV and brain

65
Q

Eplerenone uses

A

HTN alone or combo

66
Q

Eplerenone therapeutic effect should be observed within

A

4 weeks

67
Q

Tox’s for eplerenone

A

hyperkalemia

Hypertriglyceridemia

68
Q

CI’s for eplerenone

A

K supps, K sparing diuretics, ACE inhibitors

Chronic renal insufficiency

Diabetes associated with microalbuminemia

CYP450 3A4 inhibitors (ketoconazole)

Pharm Exam 3 (11 decks)

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