Diuretic Classes Flashcards
(42 cards)
Thiazide Meds and prototype
chlorthiazide, hydrochlorothiazide, chlorthalidone, indapamide, metolazone
PROTOTYPE: Hydrochlorothiazide
Thiazide MOA
- 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)
Indications for thiazide
- 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
CI to thiazide
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
AE to thiazide
- GI upset, fluid, and e- imbalances
- Labs : Hypercalcemia, hypokalemia, hyperglycemia, hyperuricemia (gout)
- Cardio : hypotension
- GU : UTI d/t alkalization of urine
S/S hypokalemia
weakness, muscle cramps, trembling, nausea, vomiting, diarrhea, and arrhythmias
DDI thiazide
- 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.
Important AE of Hydrochlorothiazide
- 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
Loop diuretics MEDS and prototype
- bumetanide (Bumex), furosemide (Lasix), torsemide (Soaanz), ethacrynic acid (edecrin)
- Prototype: Furosemide
Loop diuretics MOA
- Blocks chloride pump in ascending loop of Henle. Decreases reabsorption of Na+ and Cl-. Causes Na+, Cl- and K+ rich urine
Indications of loop diuretics
- 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.
Additional info on loop diuretics
- 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
CI to loop diuretics
- 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
AE loop diuretics
- 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
DDI loop diuretics
- 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
What additional AE can furosemide cause
- Urinary bladder spasm, vomiting, paresthesia
Nursing interventions for loop diuretics
- VS, CMP, I&Os
- Administer potassium supplementation (K+ bolus) ; monitor hypokalemia symptoms
- Potassium given piggyback d/t extreme burning (let pt know about discomfort)
Carbonic Anhydrase Inhibitors MEDS and prototype
(-mide)
- acetazolamide, dichlorphenamide (Keveyis), methazolamide
Prototype: Acetazolamide
MOA CAI
Block carbonic anhydrase. Slow movement of hydrogen ions. Increase Na+ and HCO3
in urine
Indications CAI
- Edema
- Glaucoma
CI to CAI
- 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.
AE CAI
- Labs – metabolic acidosis (kussmaul respirations) , hypokalemia (potassium lost in order to retain Na being excreted)
- CV – paresthesia of extremities, confusion, drowsiness
DDI CAI
- Salicylates (aspirin): increased risk of salicylate toxicity d/t metabolic acidosis
- Meds that cause metabolic acidosis or lower K+
Nursing implications CAI
- Monitor CNS for confusion and paresthesia
- VS, CMP, I&Os