Antihypertensives and Diuretics Study Guide Flashcards Preview

Anesthesia Pharm II > Antihypertensives and Diuretics Study Guide > Flashcards

Flashcards in Antihypertensives and Diuretics Study Guide Deck (53)
Loading flashcards...
1

Describe the mechanism of action of ACE inhibitors?

- ACE inhibitors block the conversion of angiotensin I to angiotensin II

(angiotensin II is a potent vasoconstrictor responsible for arterial smooth muscle constriction, increased aldosterone secretion , and sympathetic nervous system stimulation)

2

Describe the renin-angiotensin-aldosterone system. (a good explanation, but kind of long)

A decrease in GFR slows the rate of infiltrate through the ascending loop of Henle which causes increased reabsorption of sodium and chloride ions.

The reduced concentration of sodium is sensed by the macula densa-a thick short segment of the ascending limb.

Sensing this change, the macula densa does 2 things: 1) decreases resistance to blood flow in the afferent arterioles which raises glomerular hydrostatic pressure and
2) increases renin released from the juxtaglomerular cells.

Renin acts as an enzyme to increase the formation of angiotensin I an inactive polypeptide.

Two amino acids are split from Angiotensin I to form angiotensin II. This action occurs almost entirely in the lungs by the converting enzyme. Angiotensin II is a very potent vasoconstrictor with duration of action of 1-2 minutes because of rapid inactivation by angiotensinases.

Vasoconstriction occurs intensely in the arterioles and much less in the veins.

Angiotensin acts directly on the kidneys to cause salt and water retention and causes the adrenal glands to secrete Aldosterone with also increases salt and water reabsorption by the kidneys.

3

What is the role of angiotensin converting enzyme?

to convert angiotensin I to angiotensin II

...hopefully we'll get questions like this on the test...

4

What are the CV effects of captopril? What are the side effects?

CV effects:
- captopril lowers systemic BP without alterations in cardiac output or heart rate

(d/t decreases in sodium and water retention)

side effects:
- Rash or pruritus (10%)

- loss of taste

- hyperkalemia.

- angioedema (rare, but the worst side effect)

5

Describe the pharmacokinetics of nipride.

- nipride interacts with oxyhemoglobin, dissociating immediately and forming methemoglobin while releasing cyanide and NO.

- NO activates the enzyme guanylate cyclase present in vascular smooth muscle, resulting in increased intracellular concentrations of cGMP.

- cGMP inhibits calcium entry into vascular smooth muscle cells and may increase calcium uptake by the smooth endoplasmic reticulum to produce vasodilation.

- As such, NO is the active mediator responsible for the direct vasodilating effect of nipride.

- nipride spontaneously generates NO, thus it functions as a prodrug .

6

What is an angiotensin receptor blocker? How does it work and where? Name one.

- ARB’s produce antihypertensive effects by blocking the vasoconstrictive actions of angiotensin II without affecting ACE activity.

- It blocks the binding of angiotensin II to the AT₁ receptors found principally in vascular smooth muscles.

- Losartan is an ARB

7

What is the MOA of hydrochlorothiazide?

inhibition of sodium reabsorption in the distal tubule

8

What is the site of action for hydrochlorothiazide?

distal renal tubule

9

What is the clinical use of hydrochlorothiazide?

lowers blood pressure by reducing extracellular fluid volume (edema)

10

What are side effects of hydrochlorothiazide?

- hypochloremic metabolic acidosis

- dysrhythmias

- skeletal muscle weakness

- ileus

- potentiation of NDNMB

11

Hydrochlorothiazide is what type of diuretic?

a thiazide diuretic

12

What is the MOA of furosemide?

inhibits the reabsorption of sodium and chloride

13

What is the site of action of furosemide?

- the medullary and ascending limbs of the loops of Henle

- distal renal tubule

14

What is the clinical use of furosemide?

- diuresis with subsequent mobilization of excess fluids (edema, plural effusions, and ascites)

- reduction in blood pressure

15

What are side effects of furosemide?

- ototoxicity (hearing loss or tinnitis)

- hypotension

- large loss of electrolytes (K, Cl, Mg, Na, Ca)

16

Furosemide is what type of diuretic?

a loop diuretic

17

What is the MOA of ethacynic acid?

inhibits the reabsorption of sodium and chloride

18

What is the site of action of ethacynic acid?

- medullary and ascending lims of the loop of Henle

- distal renal tubule

19

What is the clinical use for ethacynic acid?

diuresis with subsequent mobilization of excess fluids (edema, pleural effusions, ascites

*(alternative diuretic for patients with allergy to sulfonamides)*

[only starred that last line cause i thought it was pretty cool]

20

What are the side effects of ethacynic acid?

- GI reactions with oral med (abdominal pain, anorexia, N/V, diarrhea, dry mouth) (pretty common)

- ototoxicity (hearing loss or tinnitis)

- hypotension

- large loss of electrolytes (K, Cl, Mg, Na, Ca)

basically the same as with lasix, except for the GI complications with the oral version.

21

Ethacynic acid is what type of diurectic?

a loopy diuretic

22

What is the MOA of mannitol?

- increases plasma osmolarity which draws intracellular fluid to the extracellular spaces

- results in acute expansions of intravascular volume

23

What is the clinical use for mannitol?

- prophylaxis against acute renal failure

- acute oliguria

- increased ICP

- increased IOP (intraocular pressure)

24

What is the site of action for mannitol?

- typically used to decrease brain bulk or to increase renal blood flow to the medulla

- i suppose the site is everywhere

25

What are the side effects of mannitol?

- may cause pulmonary edema in patients with oliguria secondary to heart failure

- prolonged use may cause hypovolemia, electrolyte disturbances, and plasma hyperosmolarity

26

Mannitol is what type of diuretic?

an osmotic diuretic

27

What is the MOA of urea?

its small molecular size causes reabsorption of more than 60% of urea filtered by the glomerulus

28

What are side effects of urea?

- crosses the BBB and can cause rebound increases in ICP

- high incidence of thrombosis and tissue necrosis at injection site

(sounds like a great drug...)

29

Urea is what type of diuretic?

an osmotic diuretic

30

What is the MOA of potassium-sparing diuretics, such as triamterene or amiloride?

- acts directly on renal tubular transport mechanisms in the distal convoluted tubules, independent of aldosterone, to produce diuresis

- causing an increase in urinary excretion of Na, Cl, and bicarb, and increases urine pH

- inhibits potassium secretion in the distal renal tubules