Diuretics, RAAS

Question 1

What are the two major applications of Diuretics?

Answer 1

-Hypertension
-Mobilization of edematous fluid to prevent renal failure

Question 2

Diuretics
Mechanism of Action

Answer 2

Blockade of sodium and chloride

Question 3

Diuretics
Adverse effects

Answer 3

Hypovolemia
Acid-base imbalance
Electrolyte imbalances

Question 4

Thiazides and loop diuretics ____ K

Answer 4

decrease

Question 5

Aldesterone blockers ______ K

Answer 5

increase

Question 6

Furosemides (Lasix)
Mechanism of action

Answer 6

Acts on ascending loop of Henle to block reabsorption of sodium, chloride, potassium

Question 7

Furosemide onset

Answer 7

IV - 5 mins
Oral - 60 mins

Question 8

Furosemide
Therapeutic uses

Answer 8

Pulmonary edema
Edematous states
Hypertension

Question 9

Signs of pulmonary embolism

Answer 9

SOB
Cough/wheeze/crackles
O2 low
RR elevated

Question 10

Furosemide adverse effects

Answer 10

Hyponatremia (low sodium)
Hypochloremia
Hypokalemia
Hypotension
Hypocalcemia
Hypomagnesemia
Hyperuricemia (too much uric acid in the blood)

Ototoxicity
**May raise blood sugar and cholesterol **

Question 11

In terms of adverse effects, how do you loops diuretics vs. thiazides differ?

Answer 11

Loop diuretics may cause ototoxicity, while thiazides do not

Question 12

Furosemide
Drug interactions

Answer 12

Digoxin
Ototoxic drugs (like aminoglycoside abx “-micin”)
Lithium
Antihypertensive agents
NSAIDs

Question 13

Bumetanide is a ____ diuretic

Answer 13

high-ceiling loop

Question 14

Which causes more diuresis - thiazides or loop diuretics?

Answer 14

Loop diuretics

Question 15

When are thiazides ineffective?

Answer 15

-Oliguria (reduced urine output)
-When GFR is low

Question 16

Hydrochorothiazide
Therapeutics uses

Answer 16

Essential hypertension
Edema

Question 17

What kind of diuretics do you use for pulmonary edema?

Answer 17

Loop diuretics - faster onset of action compared to thiazides (thiazides peak in 4-6 hours)

Question 18

How do loop diuretics and hydrochlorothiazide differ in terms of drug interactions?

Answer 18

Hydrochlorothiazides do not cause ototoxity, so they can be combined with other drugs that are ototoxic like the mycin ABX (Gentamycin)

Question 19

Spironolactone
Class

Answer 19

Potassium-sparing antidiuretic

Question 20

Spironolactone
Mechanism of Action

Answer 20

Aldosterone antagonist
Retention of potassium
Increased excretion of sodium

Question 21

Triamterene and Amiloride
Class

Answer 21

Potassium-sparing diuretics

Question 22

Triamterene and Amiloride
Mechanism of action

Answer 22

-Block the exchange pump instead of the aldosterone receptor
-Decrease sodium reuptake

Question 23

Spironolactone
Therapeutic uses

Answer 23

HEART FAILURE
-Hypertension (not first line)
-Edematous states
-Primary hyperaldosteronism
-PMS
-PCOS
-Acne in young women

Question 24

Spironolactone
Adverse effects

Answer 24

Hyperkalemia
Benign and malignant tumors
Endocrine effects

Question 25

Spironolactone Drug interactions

Answer 25

-Thiazide and loop diuretics -Agents that raise potassium levels

Question 26

Triamterene (Dyrenium) & Amiloride Therapeutic uses

Answer 26

Hypertension Edema Counteract potassium loss caused by more powerful diuretic

Question 27

Triamterene (Dyrenium) Adverse effects

Answer 27

-Hyperkalemia -Leg cramps -N/V, dizziness -Blood dyscrasias (rare)

Question 28

Amiloride Adverse effects

Answer 28

Hyperkalemia

Question 29

Amiloride Drug interactions

Answer 29

-ACE inhibitors -Other drugs that can cause hyperkalemia

Question 30

Mannitol (Osmitrol) Mechanism of action

Answer 30

-Promotes diuresis by creating osmotic force within lumen of nephron

Question 31

Mannitol Route of administration

Answer 31

IV

Question 32

Mannitol therapeutic uses

Answer 32

Prophylaxis of renal failure Reduction of intracranial pressure/ intraocular pressure

Question 33

Mannitol Adverse effects

Answer 33

-Edema- pulmonary edema -Headache -N/V

Question 34

What does RAAS stand for?

Answer 34

Renin-Angiotensin-Aldosterone System

Question 35

What does ACE inhibitor stand for?

Answer 35

Angiotensin-converting enzyme inhibitors

Question 36

Which type of angiotensin is responsible for much of the damage in CV disease?

Answer 36

Angiotensin II

Question 37

What are the actions of angiotensin II?

Answer 37

-Vasoconstriction -Release of aldosterone > BP increases -Cardiac remodeling

Question 38

What are the actions of aldosterone?

Answer 38

-Regulation of blood volume and BP -Cardiac remodeling

Question 39

What ending do the ACE inhibitors have?

Answer 39

-pril

Question 40

ACE inhibitors mechanism of action

Answer 40

-Reduce levels of angiotensin II -Increase levels of bradykinin

Question 41

ACE inhibitors therapeutic uses

Answer 41

-Hypertension -Heart failure -Prevention of MI, stroke death -Nephropathy (diabetic & non-diabetic)

Question 42

ACE inhibitors reduce levels of angiotensin II. What effect does this have?

Answer 42

-Vasodilation -Reduced blood volume -Reduced remodeling -Potassium retention -Fetal injury

Question 43

ACE inhibitors raise levels of Bradykinin. What major Therapeutic effect does this have? Name 2 adverse effects.

Answer 43

-Vasodilation -Cough -Angioedema (rare)

Question 44

Aldosterone effect on sodium

Answer 44

More sodium absorbed into the blood (sodium reabsorption)

Question 45

ACE inhibitors Adverse effects

Answer 45

-First-dose hypotension -Fetal injury -Cough -Angioedema -Hyperkalemia -Renal failure

Question 46

ACE inhibitors Drug interactions

Answer 46

-Diuretics -Antihypertensive agents -Drugs that raise K levels -NSAIDs

Question 47

Salt substitutes can _____ K

Answer 47

elevate

Question 48

Angiotensin II Receptor Blockers end in _____

Answer 48

-sartan

Question 49

Angiotensin II Receptor Blockers (-sartan) cause _____ of blood vessels

Answer 49

dilation

Question 50

Angiotensin II Receptor Blockers (-sartan) Pharmacologic effects

Answer 50

Same as ACE inhibitors -Prevent cardiac remodeling -Reduce excretion of potassium -Decrease release of aldosterone -Increase excretion of sodium and water EXCEPT: -Do NOT inhibit kinase I (means less cough)

Question 51

How do ACE inhibitors and Angiotensin II Receptor Blockers differ in terms of adverse effects?

Answer 51

The only difference is that Angiotensin II Receptor Blockers (-sartans) do not inhibit kinase, and therefore do not produce cough

Question 52

A very rare but serious side effect of ARBs and ACE inhibitors. It involves swelling of the face, lips, tongue, throat, or extremities and can potentially lead to airway obstruction, requiring immediate medical attention

Answer 52

Angioedema

Question 53

Aliskiren (Tekturna) Class

Answer 53

Direct Renin Inhibitor - binds tightly with renin and inhibits the conversion angiotensinogen to angiotensin I

Question 54

Aliskiren (Tekturna) Adverse effects

Answer 54

Same as ACE Inhibitors - angioedema, cough, hyperkalemia, fetal injury

Question 55

Eplerenone (Inspra) Mechanism of action

Answer 55

Aldosterone antagonist

Question 56

Aldosterone Antagonist (Eplerenone) Therapeutic uses

Answer 56

Hypertension Heart failure

Question 57

Aldosterone Antagonist (Eplerenone) Adverse effect

Answer 57

Hyperkalemia

Question 58

Aldosterone Antagonist (Eplerenone) Drug interactions

Answer 58

Drugs that raise potassium levels

Question 59

Spironolactone (Aldacton) Adverse effects

Answer 59

Hyperkalemia Hormonal effects: Gynecomastia Menstrual irregularities Impotence Hirsutism Deepening of the voice

Question 60

Spironolactone vs Eplerenone How do they differ in terms of selectivity

Answer 60

Spironolactone is less selective, it binds with receptors for other steroid hormones as well - which results in some unusual adverse effects

Question 61

A medical condition characterized by excessive hair growth in women in areas where hair is typically more common in males.

Answer 61

Hirsutism