EXAM #2: CV PHARM V Flashcards Preview

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Flashcards in EXAM #2: CV PHARM V Deck (37):
1

What is the mechanism of action of the Thiazide diuretics?

Block the NaCl Cotransporter (NCC) in the distal collecting tubule

Recall that NKCC inhibitors are LOOP diuretics, NOT thiazide diuretics

2

What are the major side effects of NCCs?

- Ca++ reabsorption
- Vasorelaxation

3

Why is there reduced Ca++ excretion with the NCC's?

- Ca++ in the DCT is under the control of parathyroid hormone (PTH)
- Thiazide stimulates PTH to cause increased Ca++ reabsorption

4

Why is there loss of K+ with NCC's?

Increased solute concentration in the lumen stimulates K+ excretion

5

What are the clinical indications for NCC Inhibitors?

1) HTN (note that K+ loss in these patients can be bad)
2) CHF
3) Hypercalciuria
4) Nephrolithiasis (calcium renal stones)
5) Nephrogenic Diabetes Insipidus

****Note that hypercalciuria increases the likelihood of kidney stones

6

What is Nephrogenic Diabetes Insipidus?

Decreased expression of aquaporins that would normally cause water-reuptake leads to water LOSS

7

Why are Thazide DIURETICS used in Nephrogenic Diabetes Insipidus?

1) Increased renal Na+ reabsorption in patients with DM-Insipidus
2) Recovery of aquaporin 2 abundance
3) Recovery of NCC, ENaC

8

List the thiazide diuretics.

Chlorathalidone
Hydrochlorothiazide
Metolazone
Indapamide

9

What is the mechanism of action of the inhibitors of renal epithelial Na+ channels?

- Normally in the DCT, Na+ is absorbed via epithelial channels in the apical membrane of the lumen; K+ is secreted

*****Block epithelial Na+ channels on principle cells in the late DCT and K+ is not longer secreted*****

10

Why are the epithelial Na+ channel blockers K+ sparing?

*****Block epithelial Na+ channels on principle cells in the late DCT and K+ is not longer secreted*****

11

What are the clinical indications for epithelial Na+ channel blockers?

1) Hypokalemic alkalosis
2) Used in combination with other diuretics to PREVENT HYPOKALEMIA

12

List the K+ sparing diuretics.

Amiloride
Triamterene

13

What is the mechanism of action of the aldosterone-receptor antagonsists?

1) Recall that aldosterone stimulates Na+ reabsorption in renal collecting tubules; water following
2) ANTAGONIZE aldosterone receptors in collecting tubules and DECREASE Na+ reabsorption

*****Note that K+ loss if also limited in these diuretics.*****

14

What are the pleotropic effects of the aldosterone receptor antagonists?

1) Prevention of LV remodeling and cardiac fibrosis
2) Prevention of sudden cardiac death
3) Anti-hypertensive
4) Reduces the generation of ROS

Thus, these drugs are commonly given to patients with CHF, post-MI.

15

Why is cardiac remodeling negative?

This is the process that leads to hypertrophy and hyperplasia of the cardiac tissue that happens in patients s/p MI that eventually leads to DEATH

16

What are the clinical indications for Aldosterone receptor antagonisnts?

1) Edema and HTN
2) CHF
3) Primary hyperaldosteronism
4) Refractory edema with secondary aldosteronism

17

What causes secondary aldosteronism?

- HF
- Hepatic cirrhosis
- Nephrotic syndrome
- Severe ascites

*****These are associated with an increase in aldosterone b/c the body thinks that it doesn't have enough water and increases the secretion of aldosterone*****

18

What are the adverse effects of the aldosterone receptor antagonists?

1) Hyperkalemia
2) Metabolic acidosis in cirrhotic patients
3) Hormonal effects including
- Gynecomastia
- Impotence
- Decreased libido
- Hirsutism
- Deepening of the voice
- Menstrual irregularity

19

List the aldosterone receptor antagonists.

Spironolactone
Eplerenone

20

What is the definition of chronic systemic arterial hypertension?

140/90 mmHg

21

What is a hypertensive crisis?

BOTH urgency and emergency

22

What is hypertensive urgency?

Systolic BP > 180
Diastolic BP > 120

WITH NO associated acute end organ damage; decrease BP within a few minutes to hours

23

What is a hypertensive emergency?

Markedly elevated BP with acute end organ damage

****Decrease blood pressure within minutes to an hour*****

24

What are the organs that are specific to end organ damage?

Heart
Kidney
Brain
Retina

25

What is resistant HTN?

Blood pressure that is uncontrolled despite 3+ anti-hypertensive drugs, one of which is a diuretic

26

What is pseudo-resistant HTN?

Uncontrolled BP that can be attributed to:
- "White coat" effect
- Poor compliance
- Incorrect measurement techniques

27

Why are females at risk for resistant HTN?

Loss of estrogen post-menopause

28

What is primary/essential HTN?

- Idopathic
- Genetic based

29

What is secondary HTN?

HTN secondary to:
1) Renal parenchymal disease
2) Sleep apnea
3) Renal artery stenosis
4) Primary aldosteronism

30

Outline the principles of treatment for HTN.

1) Treat with intent of reducing CV risk factors
2) JNC8
- Less than 150/90 greater than 60 y/o
- Less than 140/90 under 60 y/o

31

What are the non-pharmacological modifications to treat HTN?

1) Reduce weight
2) Adopt DASH diet
3) Lower Na+ intake
4) Physical activity
5) Moderation of alcohol consumption

32

What are the important considerations that you need to consider prior to starting HTN therapy?

1) Life-long ordeal
2) Cost
3) Side effects and drug interactions

33

What do you need to consider with anti-hypertensive medications and the baroreceptor reflex?

Anti-HTN meds will activate the baroreceptor reflex to RAISE pressure

34

What is the formula for MAP?

CO x TPR

35

What is the formula for CO?

HR x SV

36

List the general principles of the HTN treatment algorithm.

1) ACEIs/ARB are the first line therapy for all comorbid conditions

CAD= add beta-blocker
LV dysfunction= add diuretic and beta-blocker

37

Outline the renin-angiotensin-aldosterone system.

N/A

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