Diuretic Classes Flashcards

(42 cards)

1
Q

Thiazide Meds and prototype

A

chlorthiazide, hydrochlorothiazide, chlorthalidone, indapamide, metolazone

PROTOTYPE: Hydrochlorothiazide

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2
Q

Thiazide MOA

A
  • Blocks chloride pump in distal convoluted tubule. Blocks reabsorption of Na+ and Cl- (thus urine becomes rich in Na+, Cl-, and K+)
  • Potassium is lost at distal tubule b/c of actions on the pumping mechanism, causing hypokalemia. The change in K levels keeps glucose out of the cells and can cause elevated blood glucose levels
  • Patient’s look like they’re DM but they’re not (would be monitored, not tx)
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3
Q

Indications for thiazide

A
  • essential htsn
  • Edema caused by CHF, liver, or renal disease
  • For use on clients when kidney function is not impaired
    Additonal info: Uric acid excretion is decreased, resulting in gout flare ups if they have it
  • less effective than loop b/c of site of action but usually effective enough for CV purposes
  • Patient’s with sulfa allergy will be allergic to these agents
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4
Q

CI to thiazide

A

Allergy to sulfonamides
- Severe renal disease : azotemia (increased BUN/CRT)
- SLE (lupus) :dx causes glomerular changes and renal dysfunction that could precipitate
renal failure
- Diabetes mellitus: which is worsened by the glucose-elevating effects of many diuretics
- Bipolar :exacerbated d/t changes in Ca levels
- Uric acid excretion is decreased, resulting in gout (hyperuricemia)
- GU : UTI – d/t alalinized urine
- hyperparathyroidism

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5
Q

AE to thiazide

A
  • GI upset, fluid, and e- imbalances
  • Labs : Hypercalcemia, hypokalemia, hyperglycemia, hyperuricemia (gout)
  • Cardio : hypotension
  • GU : UTI d/t alkalization of urine
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6
Q

S/S hypokalemia

A

weakness, muscle cramps, trembling, nausea, vomiting, diarrhea, and arrhythmias

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7
Q

DDI thiazide

A
  • Dig : risk of toxicity d/t changes in K levels
  • Antidiabetic agents : decreased effectiveness d/t changes in glucose metabolism
  • Lithium : risk of toxicity d/t change in Na levels
  • Quinidine: toxicity increases due to decreased quinidine excretion with an alkaline urine
  • Antihypertensive medications: additive hypotensive eect and should be monitored.
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8
Q

Important AE of Hydrochlorothiazide

A
  • Anorexia, dry mouth, muscle cramps, ortho hypotsn (only effects when dehydrated
  • can be used in small doses because it is more potent than chlorothiazide, the oldest
    drug of this class
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9
Q

Loop diuretics MEDS and prototype

A
  • bumetanide (Bumex), furosemide (Lasix), torsemide (Soaanz), ethacrynic acid (edecrin)
  • Prototype: Furosemide
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10
Q

Loop diuretics MOA

A
  • Blocks chloride pump in ascending loop of Henle. Decreases reabsorption of Na+ and Cl-. Causes Na+, Cl- and K+ rich urine
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11
Q

Indications of loop diuretics

A
  • Essential HTN
  • Edema caused by heart failure, liver or renal disease
  • Heart failure / severe pulmonary Edema
  • Can be used in patients with acid-base disturbances, renal insufficiency and electrolyte
    imbalances.
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12
Q

Additional info on loop diuretics

A
  • strongest b/c of site of action; in high doses they can produce a loss of fluid of up to 20 lbs per day, loop diuretics are the drug of choice for rapid and extensive diuresis (high ceiling)
  • B/C these drugs have an effect ONLY on the blood that reaches the nephrons, if a person isn’t perfusing the kidney d/t HF or vascular disease, these drugs will not work.

*Potassium is lost at distal tubule b/c of actions on the pumping mechanism, causing hypokalemia. The change in K levels keeps glucose out of the cells and can cause elevated blood glucose levels. Uric acid excretion is decreased, resulting in gout

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13
Q

CI to loop diuretics

A
  • Severe renal disease (anuria) : azotemia (increased BUN/CRT)
  • SLE : dx causes glomerular changes and renal dysfunction that could precipitate renal
    failure
  • DM d/t hyperglycemia effects
  • GU / UTI : d/t alkalinized urine
  • hepatic encephalopathy, which could be exacerbated by the fluid shift associated with
    drug use
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14
Q

AE loop diuretics

A
  • Labs : Hypocalcemia (tetany), hypokalemia (extreme), hyperglycemia, hyperuricemia,
    alkalosis, hypomagnesemia
  • Card – hypotension, dizziness,
  • Ototoxicity even deafness have been reported with too rapid IV pushing
  • Alkalosis: may occur if more chloride is excreted in the urine compared to bicarbonate
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15
Q

DDI loop diuretics

A
  • Ototoxicity with aminoglycosides
  • Anticoagulant
  • Salicylates/NSAIDs/ibuprofen: Loss of NA and decreased antihypertensive effects if
    given with Dig : risk of toxicity d/t changes in K levels
  • Antidiabetic agents : decreased effectiveness d/t changes in glucose metabolism
  • Lithium : risk of toxicity d/t change in Na levels
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16
Q

What additional AE can furosemide cause

A
  • Urinary bladder spasm, vomiting, paresthesia
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17
Q

Nursing interventions for loop diuretics

A
  • VS, CMP, I&Os
  • Administer potassium supplementation (K+ bolus) ; monitor hypokalemia symptoms
  • Potassium given piggyback d/t extreme burning (let pt know about discomfort)
18
Q

Carbonic Anhydrase Inhibitors MEDS and prototype

A

(-mide)
- acetazolamide, dichlorphenamide (Keveyis), methazolamide

Prototype: Acetazolamide

19
Q

MOA CAI

A

Block carbonic anhydrase. Slow movement of hydrogen ions. Increase Na+ and HCO3
in urine

20
Q

Indications CAI

A
  • Edema
  • Glaucoma
21
Q

CI to CAI

A
  • Allergy to sulfonamides/thiazides
  • Pregnancy/lactation
  • Chronic angle-closure glaucoma: diuretic could mask warning symptoms that glaucoma
    is worsening
  • renal/hepatic disease, adrenocortical insufficiency, respiratory acidosis, COPD could be
    exacerbated by the uid and electrolyte changes caused by these drugs.
22
Q

AE CAI

A
  • Labs – metabolic acidosis (kussmaul respirations) , hypokalemia (potassium lost in order to retain Na being excreted)
  • CV – paresthesia of extremities, confusion, drowsiness
23
Q

DDI CAI

A
  • Salicylates (aspirin): increased risk of salicylate toxicity d/t metabolic acidosis
  • Meds that cause metabolic acidosis or lower K+
24
Q

Nursing implications CAI

A
  • Monitor CNS for confusion and paresthesia
  • VS, CMP, I&Os
25
Additional info for CAI
(weakest b/c of site of action, used mainly for glaucoma) * Carbonic anhydrase inhibitors are mild diuretics. For this reason, they are mainly used to treat edema and open-angle glaucoma (decrease amounts of aqueous humor of the eye) *Carbonic anhydrase is a catalyst for sodium bicarb. These agents slow movement of hydrogen ions, causing NA and HCo3 to be lost in urine
26
Additional AE of Acetazolamide
- Renal calculi: d/t bicarb in urine (usually in pt that already have it or in those that are dehydrated and have perfusion probs) - Bone marrow suppression (watch CBC)
27
Potassium sparring MEDS and prototype
amiloride (Midamor), spironolactone (Aldactone), triamterene (Dyrenium), eplerenone (Inspra) Prototype: Spironolactone
28
MOA K+ sparing
Block actions of aldosterone in distal tubule or block K+ secretion through tubule. Cause a loss of Na+ while promoting retention of K+ (low Na+, normal/high K+)
29
Indications K+ sparing
- Edema - CHF (heart failure) - Clients at risk for or chronically hypokalemia (ic) - Spironolactone: treats hyperaldosteronism (cirrhosis of the liver and nephrotic syndrome) or excessive output of aldosterone from the adrenal gland = increased Na and water retention and loss of K+
30
CI K+ sparing
- Pregnancy/lactation - Hyperkalemia - Severe renal disease / anuria
31
AE K+ sparing
- Hyperkalemia ( lethargy, confusion, ataxia, muscle cramps, cardiac arrhythmia) - hyponatremia - GU (spironolactone) – decreased libido, hirsutism, gynecomastia, irregular menses, deepening of the voice, gynecomastia - Because spironolactone blocks androgen production and alters the testosterone estrogen ratio, it is associated with hormonal changes
32
DDI K+ sparing
- Salicylates: Diuretic effect is decreased - Antihypertensives (ACE/ ARBS) cause hypotension - Meds that block renin-angiotensin aldosterone pathway= hyperkalemia
33
Additional AE of Spironolactone
- Big hormonal influence - Deepening of voice, irregular menses
34
Nursing implications of K+ sparring
- VS (b/p, HR), CMP, I&Os - Edu about low K+ - CNS effects
35
Potassium rich foods
- Avocado - Banana - Broccoli - Cantaloupe / Watermelon - Grapefruit / Orange - Peach - Tomato - Potato - Spinach - Lima / Navy Beans - Decaffeinated Coffee - Sunflower seeds - Dried fruits
36
Osmotic diuretics MED and what is it
Mannitol - sugar that is not well reabsorbed by the tubules, it pulls large amounts of fluid into the urine d/t the osmotic pull exerted by the large sugar molecule. The tubule cannot reabsorb all of the sugar and large amounts of urine are lost in the urine. It pulls fluid from the extravascular spaces, including aqueous humor.
37
MOA osmotic diuretic
- pull water into renal tubule w/o Na+ loss (also pulls from extravascular spaces)
38
Indications OD
- Increased ICP - Acute attacks of glaucoma - Acute renal failure - Shock, drug OD, trauma
39
CI to OD
- Pregnancy/lactation - Pulmonary congestion - Intracranial bleed (risk vs benefit) - Dehydration / CHF - Severe renal disease / anuria large shifts in fluid related to these drugs can exacerbate
40
AE of OD
- Fluid shift - Will cause HF, pulmonary edema, dehydration, hypotension, h/a, lightheadedness - Electrolyte imbalance d/t fluid shift - CNS toxicity (confusion, lethargy, coma) - Dry mouth/ thirst/ diuresis
41
DDI to OD
none (since it’s just sugar)
42
NI to OD
- Monitor cardio and CNS, visual changes, I&Os