Cardio VI Flashcards

1
Q

What are the three prototypical Thiazide diuretics?

A

Chlorthalidone
Hydrochlorothiazide
Metolazone
Indapamide

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2
Q

What is the MOA of thiazide diuretics like chlorthalidone?

A

block the Na/Cl cotransporter in the distal collecting ducts

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3
Q

What is the effect of thiazide diuretics on Ca?

A

Increase reabsorption (therefore decreasing excretion)

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4
Q

What is the effect of thiazide diuretics on the vasculature? How?

A

Vasodilation

Increased Ca leads to increase NO synthesis

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5
Q

What are the drugs that cause Ca loss? Ca reuptake?

A
Loss = loop diuretics
Uptake = thiazide diuretics
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6
Q

Thiazide diuretics are indicated with edema caused by what?

A

CHF
Hepatic cirrhosis
Renal disease

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7
Q

When are thiazide diuretics contraindicated for edema?

A

if GFR is less than 30-40 ml/min

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8
Q

Why are thiazide diuretics used to treat HTN?

A

Inexpensive, well tolerated

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9
Q

Why are thiazide diuretics used in treating renal stones?

A

Increase Ca uptake= decrease in urine

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10
Q

Why are thiazide diuretics used to treat nephrogenic DI?

A

reduce urine volume and increase Na reabsorption

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11
Q

Do thiazide diuretics cause hypokalemia?

A

Yes

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12
Q

What is the cause of nephrogenic DI?

A

Loss of aquaporins

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13
Q

What are the major adverse effects of thiazide diuretics?

A

Hypokalemia

Metabolic acidosis

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14
Q

How do thiazide diuretics cause hyperglycemia?

A

Impairment of pancreatic insulin secretion

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15
Q

What is the relationship between thiazide diuretics and hyperlipidemia?

A

increases total serum cholesterol

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16
Q

How do thiazide diuretics cause hyponatremia?

A

increased Na excretion

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17
Q

What drug class share cross-reactivity with thiazide diuretics?

A

sulfa drugs

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18
Q

What are the two prototypical inhibitors of renal epithelial Na channels?

A

Amiloride

Triamterene

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19
Q

What is the MOA of amiloride?

A

Inhibit renal epithelial Na channels in the late distal tubule and collecting duct by competing with Na for the channel

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20
Q

What group of diuretic drugs have to be used in combination with another diuretic class?

A

epithelial Na channel inhibitors

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21
Q

True or false: Na channel inhibiting diuretics have only a weak diuretic effect on their own

A

True

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22
Q

How is it that Na channel inhibitors are K sparing diuretics?

A

If you inhibit the Na channel, K will not flow out of the cell

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23
Q

What is the main use of Na channel inhibitors?

A

used in combination with loop diuretics to prevent hypokalemia

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24
Q

What is the MOA of chlorthalidone?

A

Thiazide diuretic

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25
Q

What is the MOA of hydrochlorothiazide?

A

thiazide diuretic

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26
Q

What is the MOA of metolazone?

A

Thiazide diuretic

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27
Q

What is the MOA of indapamide?

A

Thiazide diuretic

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28
Q

What is the MOA of triamterene?

A

Renal epithelial Na channel inhibitor

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29
Q

Which type of diuretic is K sparing?

A

Inhibitors of renal epithelial Na channels (amiloride/triamterene)

Aldosterone blockers

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30
Q

What is the MOA of spironolactone?

A

Aldosterone receptor antagonist

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31
Q

What is the MOA of eplerenone?

A

Aldosterone receptor antagonist

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32
Q

What is the effect of activation of the aldosterone receptor on renal epithelial cells?

A

Increase Na/K pump on basolateral side, and increased channels on the lumenal side.

Causes increased K excretion, decreased Na excretion

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33
Q

What part of the renal tubule are aldosterone receptors found?

A

distal tubule and collecting duct

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34
Q

What happens when you block aldosterone?

A

Decreased K loss
Increased Na loss
Increased water loss

35
Q

Which type of diuretic does not require access to the tubular lumen to induce diuresis?

A

Aldosterone receptor antagonists

36
Q

Are spironolactone and Eplerenone competitive or noncompetitive aldosterone receptor antagonists?

A

Competitive

37
Q

How do aldosterone receptor blockers like spironolactone prevent LV remodeling and cardiac fibrosis?

A

Inhibit matrix metalloproteases

Inhibit protein kinase C

38
Q

How do aldosterone receptor blockers like spironolactone prevent sudden cardiac death? (3)

A
  • improve HR variability
  • Reduce QT dispersion
  • Prevent severe hypokalemia
39
Q

What are the hemodynamic effects of aldosterone inhibitors?

A

BP reduction

Moderate diuresis and natriuresis

40
Q

What are the vascular effects of aldosterone inhibitors?

A

Decrease vascular NAD(P)H oxidase activity

41
Q

What are the clinical uses of aldosterone inhibitors?

A

Edema and HTN

heart failure

42
Q

What is the diuretic of choice when treating hepatic cirrhosis?

A

Aldosterone inhibitors

43
Q

What is the most severe adverse effect of aldosterone inhibitors?

A

Hyperkalemia

44
Q

What is the diuretic treatment of choice for primary hyperaldosteronism?

A

Aldosterone antagonists

45
Q

What are the two main mechanisms by which diuretics lower BP?

A

Decrease TPR and Na/water

46
Q

What is the upper limits of normal BP?

A

120/80

47
Q

What is the range of high-normal BP?

A

120-140 /80-90

48
Q

What is the range of BP for stage 1 HTN? What medication should you consider using? How often should you recheck?

A

140-160 / 90-100
Thiazide
3 months

49
Q

What is the range of BP for stage 2 HTN? What medication should you consider using?

A

> 160 / >100
Thiazide and ACEI
2-4 weeks

50
Q

What is the range of BO to diagnose isolated systolic HTN?

A

> 140 /

51
Q

What are HTN crises?

A

High blood pressure and/or organ damage

52
Q

What is a HTN urgency?

A

NO associated end organ damage

Have hours/days to treat

53
Q

What is a HTN emergency?

A

Markedly elevated BO WITH end organ damage

have minutes/hours to treat

54
Q

What are the four end organs in HTN emergencies?

A

Kidney
Brain
Heart
Retina

55
Q

What is resistant HTN?

A

BP that is uncontrolled despite the use of three or more anti-HTN drugs (one of which is a diuretic)

56
Q

What is pseudo-resistant HTN?

A

Uncontrolled HTN d/t white coat effect or poor adherence to HTN meds

57
Q

Who is more at risk for HTN, females or males? Why?

A

Females–loss of estrogen

58
Q

Which ethnicity is at higher risk of HTN?

A

African-americans

59
Q

What is primary HTN?

A

Idiopathic rise in BP

60
Q

What are the causes of secondary HTN?

A

Renal disease

Primary aldosteronism

61
Q

What are some of the uncommon causes of secondary HTN?

A

Pheochromocytoma
Cushing syndrome
Hyperparathyroidism
Coarctation of the aorta

62
Q

What should be you intent when treating HTN?

A

Treat with the intent of reducing CV events

63
Q

What is the BP goal of treating pts

A

140/90

64
Q

What is the BP goal of treating pts > 60 yo?

A

150/90

65
Q

What medication should you consider adding if treating a stage 1 HTN pt for more than 3 months without a significant drop in BP?

A

Add ACEI

66
Q

What is the diet for HTN?

A

DASH diet

67
Q

How much EtOH is helpful with HTN?

A

2 drinks / day

68
Q

True or false: once initiated, HTN is a lifelong disease

A

True

69
Q

Why is it that there is no baroreceptor reflex in HTN?

A

Chronic HTN resets the reflex

70
Q

Mean arterial pressure = ?

A

CO * TPR

71
Q

CO = ?

A

HR * SV

72
Q

What is the drug that is indicated for HTN secondary to another disease?

A

ACEI

73
Q

What are the drugs that should be used to treat HTN with coronary artery disease?

A

Beta blocker

ACEI

74
Q

What is the first line regimen for left ventricular dysfunction?

A

ACEI
Diuretic
Beta blockers

75
Q

What is the first line regimen for HTN with previous ischemic stroke?

A
ACEI
Thiazide diuretic (?)
76
Q

What are the drugs that should be added on to HTN w/ DM?

A

thiazide
Beta blocker
CCB

77
Q

What are the drugs that should be added on to HTN w/ coronary artery disease?

A

Aldosterone antagonist
CCB
thiazide

78
Q

What are the drugs that should be added on to HTN w/ left ventricular dysfunction?

A

Aldosterone antagonist

Hydralazine

79
Q

What enzyme is released by the kidneys to cleave angiotensinogen to angiotensin I?

A

Renin

80
Q

What is the effect of angiotensin II?

A

Vasoconstriction and aldosterone release

Release vasopressin

81
Q

What is the effect of aldosterone?

A

Increase Na reuptake

Increase K output

82
Q

What is the enzyme that cleaves angiotensin I to angiotensin II?

A

ACE

83
Q

What is the effect of increased Na at the tubular macula densa?

A

Vasoconstriction

84
Q

Which are the three MOA of treating HTN via the angiotensin pathway?

A

Inhibit renin
Inhibit ACE
Inhibit angiotensin receptor