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Pharmacology for Amjad > EXAM #2: CV PHARM V > Flashcards

EXAM #2: CV PHARM V Flashcards

1
Q

What is the mechanism of action of the Thiazide diuretics?

A

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

Recall that NKCC inhibitors are LOOP diuretics, NOT thiazide diuretics

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2
Q

What are the major side effects of NCCs?

A
  • Ca++ reabsorption

- Vasorelaxation

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3
Q

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

A
  • Ca++ in the DCT is under the control of parathyroid hormone (PTH)
  • Thiazide stimulates PTH to cause increased Ca++ reabsorption
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4
Q

Why is there loss of K+ with NCC’s?

A

Increased solute concentration in the lumen stimulates K+ excretion

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5
Q

What are the clinical indications for NCC Inhibitors?

A

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

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6
Q

What is Nephrogenic Diabetes Insipidus?

A

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

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7
Q

Why are Thazide DIURETICS used in Nephrogenic Diabetes Insipidus?

A

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

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8
Q

List the thiazide diuretics.

A

Chlorathalidone
Hydrochlorothiazide
Metolazone
Indapamide

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9
Q

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

A
  • 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

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10
Q

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

A

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

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11
Q

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

A

1) Hypokalemic alkalosis

2) Used in combination with other diuretics to PREVENT HYPOKALEMIA

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12
Q

List the K+ sparing diuretics.

A

Amiloride

Triamterene

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13
Q

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

A

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.

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14
Q

What are the pleotropic effects of the aldosterone receptor antagonists?

A

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.

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15
Q

Why is cardiac remodeling negative?

A

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

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16
Q

What are the clinical indications for Aldosterone receptor antagonisnts?

A

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

17
Q

What causes secondary aldosteronism?

A
  • 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
Q

What are the adverse effects of the aldosterone receptor antagonists?

A

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

19
Q

List the aldosterone receptor antagonists.

A

Spironolactone

Eplerenone

20
Q

What is the definition of chronic systemic arterial hypertension?

A

140/90 mmHg

21
Q

What is a hypertensive crisis?

A

BOTH urgency and emergency

22
Q

What is hypertensive urgency?

A

Systolic BP > 180
Diastolic BP > 120

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

23
Q

What is a hypertensive emergency?

A

Markedly elevated BP with acute end organ damage

Decrease blood pressure within minutes to an hour*

24
Q

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

A

Heart
Kidney
Brain
Retina

25
Q

What is resistant HTN?

A

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

26
Q

What is pseudo-resistant HTN?

A

Uncontrolled BP that can be attributed to:

  • “White coat” effect
  • Poor compliance
  • Incorrect measurement techniques
27
Q

Why are females at risk for resistant HTN?

A

Loss of estrogen post-menopause

28
Q

What is primary/essential HTN?

A
  • Idopathic

- Genetic based

29
Q

What is secondary HTN?

A

HTN secondary to:

1) Renal parenchymal disease
2) Sleep apnea
3) Renal artery stenosis
4) Primary aldosteronism

30
Q

Outline the principles of treatment for HTN.

A

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
Q

What are the non-pharmacological modifications to treat HTN?

A

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

32
Q

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

A

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

33
Q

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

A

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

34
Q

What is the formula for MAP?

A

CO x TPR

35
Q

What is the formula for CO?

A

HR x SV

36
Q

List the general principles of the HTN treatment algorithm.

A

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

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

37
Q

Outline the renin-angiotensin-aldosterone system.

A

N/A

Pharmacology for Amjad (64 decks)

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