D/C when pregnancy is detected. Drugs that act directly on the renin-angiotensin system (RAS) can cause injury/death to the developing fetus.
ACE inhibitor/thiazide diuretic
Treatment of HTN.
BP Uncontrolled w/ Lisinopril/HCTZ Monotherapy:
10mg/12.5mg or 20mg/12.5mg qd, depending on current monotherapy dose
If possible, d/c diuretic 2-3 days prior to therapy. If BP is controlled w/ lisinopril alone, then diuretic therapy may be resumed
Titrate: Base further increases on clinical response
May increase HCTZ dose after 2-3 weeks
May reduce lisinopril dose after addition of diuretic
BP Controlled on HCTZ 25mg qd w/ Hypokalemia: Switch to 10mg/12.5mg qd
Replacement Therapy: May substitute for the titrated individual components
Start at lower end of dosing range
Tab: (Lisinopril/HCTZ) 10mg/12.5mg, 20mg/12.5mg, 20mg/25mg
History of ACE inhibitor-associated angioedema, hereditary or idiopathic angioedema, anuria, hypersensitivity to other sulfonamide-derived drugs. Coadministration with aliskiren in patients with diabetes.
Not for initial therapy of HTN. Not recommended with severe renal impairment (CrCl ≤30mL/min). Caution in elderly. Lisinopril: Head/neck angioedema reported; promptly d/c and administer appropriate therapy. Higher rate of angioedema in blacks than nonblacks. Intestinal angioedema reported; monitor for abdominal pain. Anaphylactoid reactions reported during desensitization with hymenoptera venom, dialysis with high-flux membranes, and LDL apheresis with dextran sulfate absorption. Excessive hypotension may occur in salt/volume-depleted persons (eg, patients treated vigorously with diuretics or on dialysis). Excessive hypotension, which may be associated with oliguria and/or progressive azotemia, and rarely with acute renal failure and/or death, may occur in patients with severe CHF; monitor closely during first 2 weeks of therapy and whenever dose is increased. Caution with ischemic heart or cerebrovascular disease in whom an excessive fall in BP could result in a MI or cerebrovascular accident. Leukopenia/neutropenia and bone marrow depression may occur. Associated with a syndrome that starts with cholestatic jaundice or hepatitis and progresses to fulminant hepatic necrosis and sometimes death (rare); d/c if jaundice or marked elevations of hepatic enzymes develop. Caution with left ventricular outflow obstruction. May cause changes in renal function; in patients with severe CHF whose renal function is dependent on the RAS system, oliguria and/or progressive azotemia, and (rare) acute renal failure and/or death may occur . May increase BUN and SrCr in patients with renal artery stenosis or with no preexisting renal vascular disease; monitor renal function during the 1st few weeks of therapy in patients with renal artery stenosis. Hyperkalemia and persistent nonproductive cough reported. Hypotension may occur with major surgery or during anesthesia. HCTZ: May cause idiosyncratic reaction, resulting in acute transient myopia and acute angle-closure glaucoma; d/c as rapidly as possible. May precipitate azotemia in patients with renal disease. Caution with hepatic dysfunction or progressive liver disease; may precipitate hepatic coma. Sensitivity reactions may occur. May cause exacerbation or activation of systemic lupus erythematosus (SLE), hyperuricemia or precipitation of frank gout, manifestation of latent diabetes mellitus (DM), hypomagnesemia, and hypercalcemia. Observe for signs of fluid or electrolyte imbalance. Hypokalemia may sensitize or exaggerate the response of the heart to toxic effects of digitalis. Enhanced effects in postsympathectomy patients. D/C or withhold if progressive renal impairment becomes evident. D/C before testing for parathyroid function. Increased cholesterol and TG levels reported.
Dizziness, headache, cough, fatigue, orthostatic effects.
See Contraindications. NSAIDs, including selective COX-2 inhibitors, may reduce effects of diuretics and ACE inhibitors, and may deteriorate renal function. Increased risk of lithium toxicity; avoid with lithium. Lisinopril: Dual blockade of the RAS is associated with increased risks of hypotension, hyperkalemia, and changes in renal function (including acute renal failure); avoid combined use of RAS inhibitors, or closely monitor BP, renal function, and electrolytes with concomitant agents that also affect the RAS. Avoid with aliskiren in patients with renal impairment (GFR <60mL/min). Hypotension risk, and increased BUN and SrCr with diuretics. Increased risk of hyperkalemia with K+-sparing diuretics (eg, spironolactone, eplerenone, triamterene, amiloride), K+ supplements, or K+-containing salt substitutes; use with caution and monitor serum K+. Nitritoid reactions reported with injectable gold. HCTZ: Potentiation of orthostatic hypotension may occur with alcohol, barbiturates, or narcotics. Dosage adjustment of antidiabetic drugs (oral agents, insulin) may be required. Additive effect or potentiation with other antihypertensives. Anionic exchange resins (cholestyramine, colestipol) may impair absorption. Corticosteroids and adrenocorticotropic hormone may intensify electrolyte depletion, particularly hypokalemia. May decrease response to pressor amines (eg, norepinephrine). May increase responsiveness to nondepolarizing skeletal muscle relaxants (eg, tubocurarine).
PREGNANCY AND LACTATION
Category D, not for use in nursing.
MECHANISM OF ACTION
Lisinopril: ACE inhibitor; decreases plasma angiotensin II, which leads to decreased vasopressor activity and decreased aldosterone secretion. HCTZ: Thiazide diuretic; not established. Affects distal renal tubular mechanism of electrolyte reabsorption. Increases excretion of Na+ and Cl-.
Absorption: Lisinopril: Tmax=7 hrs. Distribution: Crosses placenta. HCTZ: Found in breast milk. Elimination: Lisinopril: Urine (unchanged); T1/2=12 hrs. HCTZ: Kidneys (≥61% unchanged); T1/2=5.6-14.8 hrs.
Assess for hereditary/idiopathic angioedema, anuria, DM, volume/salt depletion, CHF, ischemic heart or cerebrovascular disease, collagen vascular disease, left ventricular outflow obstruction, SLE, history of ACE inhibitor-associated angioedema, hypersensitivity to drug or sulfonamide-derived drugs, renal/hepatic dysfunction, postsympathectomy status, pregnancy/nursing status, and possible drug interactions.
Monitor for signs/symptoms of angioedema, anaphylactoid/idiosyncratic/hypersensitivity reactions, exacerbation/activation of SLE, hyperuricemia or precipitation of gout, latent DM, fluid/electrolyte imbalance, and other adverse reactions. Monitor BP, renal/hepatic function, serum electrolytes, cholesterol, and TG levels. Consider periodic monitoring of WBCs in patients with collagen vascular disease and renal disease.
Inform about fetal risks if taken during pregnancy and discuss treatment options in women planning to become pregnant; instruct to report pregnancy to physician as soon as possible. Instruct to d/c therapy and to immediately report signs/symptoms of angioedema. Instruct to report lightheadedness, especially during the 1st few days of therapy; advise to d/c therapy and consult with a physician if actual syncope occurs. Inform that excessive perspiration, dehydration, and other causes of volume depletion (eg, diarrhea, vomiting) may lead to fall in BP; advise to consult with physician. Advise not to use salt substitutes containing K+ without consulting physician. Advise to promptly report any indication of infection (eg, sore throat, fever).
20-25°C (68-77°F). Protect from excessive light and humidity.
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