HTN: Diuretics Flashcards Preview

Clinical Pharmacology > HTN: Diuretics > Flashcards

Flashcards in HTN: Diuretics Deck (33)
Loading flashcards...

What is mannitol MOA? What are the clinical indications?

MOA: diuretic working on Proximal Tubule & Loop of Henle
- relative H2o diuresis


1. DEC ICP associated with cerebral edema**
- maintain serum osm 310 to < 320

2. GU irrigate in TURP or other transurethral surgical procedures**


How can mannitol increase plasma osmolality? Two mechanisms.

1. Water diuresis leading to water deficit & hypernatremia

2. Hypertonic mannitol may be retained in AKI pts


What are the interactions and ADRs for mannitol and acetazolamide?

Interactions: anti-HTN & Vasodilators --> additive effective

- fluid/'lyte imbalance
- hypovolemia* or dehydration secondary to rapid diuresis


What is acetazolamide MOA? What's indication for use?

MOA: reversible inhibition of carbonic anhydrase
- produces both NaCl & NaHCO3 loss


1. prevention or amelioration of acute mountain sickness**

2. edematous pt w/metabolic alkalosis - lose excess bicarb can restore acid-base


What's the MOA of loop diuretics? Which drug is the big loop banger?

MOA: interferes with Na/K exchange in Thick Segment of Loop of Henle

Furosemide** (Lasix)


What are clinical indications for loop diuretics?

- acute pulmonary edema & other edematous states**

- acute hypercalcemia**


What do you need to monitor for your pt on loop, thiazide diuretics?

BMP - first few weeks, then periodically

Ca & Mg - as needed


Why are loops better than thiazides for HF?

More Na excretion*

"double the dose until the urine flows"

- if more is needed, add aldosterone AAG
- if sxs persist, add thiazide


Besides HF, what else are loops better than thiazides at?

Loops work better than thiazides for GFR < 30**


How do loops impact calcium?

enhances calcium excretion --> improvement in hypercalcemia**


What are three things to know about Ethacrynic acid (loop) ?

1. may be useful for pt who have not responded to other diuretics
2. causes most ototoxicity
3. only loop that is not a sulfonamide


There are 6 specific drug interactions of loop diuretics. What are they?

1. NSAIDs antagonize diuretic effect** [via Na retention]

2. Antagonizes DM meds** [via hypoK]

3. Anti-arrhythmic toxicity [via hypoK]

4. Li tox [DEC excretion]

5. Antagonize gout meds [via urate reabsorption]

6. Anti-HTN & VD [additive effect]


What are loop diuretic ADRs?

1. Hypokalemia** / hypomagnesemia *
2. Hyperglycemia** [hypoK involved in dysglycemia]
3. Volume depletion [orthostatics, AKI]
4. hyperuricemia
5. SNHL "ringing"
6. rash - sulfa


What are the three bolded thiazide diuretics?

1. Hydrochlorothiazide
2. Chlorthalidone
3. Metolazone


What is the only thiazide available as IV?

Outside of knowing the IV, it is not really used clinically.



What are thiazide MOA?

Interfere with K/Na exchange in Early Distal Convoluted Tubule

Effects of most thiazides is an overall DEC in SVR**


Compare and contrast Chlorthalidone to Hydrochlorothiazide in terms of efficacy and general use

Chlorthalidone is 2x as potent w/a much longer duration of action (d/t creating a RBC "depot")

Despite superiority of chlorthalidone, most fixed-dose combo that include a diuretic use HCTZ**


Which is the main thiazide used in context of altered renal function [CrCl < 30]


- other Thiazides are less effective with this renal level


What effects may thiazide diuretics have on calcium?

All enhance Ca2+ reabsorption**

Improvement in hypercalciuria = DEC kidney stones **

May be beneficial in osteoporosis


Which thiazide may be used with a loop diuretic for synergy in refractory edematous states?



What are ADRs of thiazides?

Hypokalemia / hypomagnesemia --> hyperglycemia **

For the most part otherwise, at the low dose used for thiazides, you don't really get many ADRs.
[The others listed are the same as loop diuretics]


What is the unique thiazide ADR related to skin?

Increased risk of nonmelanoma skin CA w/HCTZ*


There are two "classes" of K-sparing diuretics. List the class MOA and the two drugs for each class.

1. Anti-aldosterone drug
- MOA: antagonize mineralocorticoid receptors at Cortical Collecting Tubule --> DEC transcription of gene for Na/K ATPase
- Spironolactone** and Eplerenone

2. MOA: interferes with K/Na exchange
- Amiloride** and triamterene


What is the major difference between spironolactone and eplerenone in terms of action

Spironolactone - nonselective

Eplerenone - more selective for aldo than androgen and progesterone
- less gynecomastia and breast tenderness


What is the clinical use of amiloride and triamterene?

Used with other diuretics to prevent or correct hypokalemia

Overall weak diuretic / BP lowering

Less use now as most diuretics combined with ACE/ARB


What is the clinical use of spironolactone and eplerenone?

Mineralocorticoid excess

1. Primary aldosteronism*

2. Secondary aldosteronism**
- HFrEF, hepatic cirrhosis, nephrotic syndrome

3. Off-label
- acne vulgaris, hirsutism


As a class, what is the clinical use for Potassium-sparing diuretics?

Relatively weak natiuretic effect --> primarily used in combination with a loop or thiazide diuretic**

DEC degree of K loss or may INC net diuresis in pt w/refractory edema


What monitoring is required with K-sparing diuretics? What are some C.I. values?

Don't use for K > 5.5 or eGFR < 30

- K and BUN/Cr: baseline, w/in 1wk, monthly x3, quarterly for 1yr, then q 6mo


What are the 3 main drug interactions with potassium-sparing diuretics?

1. Avoid K supplements / salt substitutes
2. Additive effect with Anti-HTN & vasodilators
3. Careful with drugs retaining K
- B-blockers


Class ADR of potassium-sparing diuretics?