Linger CIS Clinical Pharm of Antihypertensives Flashcards
Benefits of antihypertensive therapy relative risk reduction
Heart Failure
Stroke
MI
50%
30-40%
20-25%
Carbonic anhydrase Inhibitors prototype
acetazolamide
Carbonic anhydrase Inhibitors MOA
inhibits the membrane-bound and cytoplasmic forms of carbonic anhydrase
Carbonic anhydrase Inhibitors Results in
↓ H+formation inside PCT cell
↓ Na+/H+antiport
↑ Na+and HCO3-in lumen
↑ diuresis
Carbonic anhydrase Inhibitors PH results
Urine pH is increased and body pH is decreased
Loop Diuretics prototypes
furosemideand ethacrynicacid
Loop Diuretics moa
inhibit the luminal Na+/K+/2Cl-cotransporter(NKCC2) in the TAL of the loop of Henle
Loop Diuretics results in
↓ intracellular Na+, K+, Cl-in TAL
↓ back diffusion of K+ and positive potential
↓ reabsorption of Ca2+and Mg2+
↑ diuresis
Loop Diuretics facts
- Ion transport is virtually nonexistent
* Among the most efficacious diuretics available
Thiazide Diuretics prototype
hctz/chlorthalidone
Thiazide Diuretics moa
cause inhibition of the Na+/Cl-cotransporter(NCC) and block NaClreabsorption in the DCT
Thiazide Diuretics results in
↑ luminal Na+and Cl-in DCT
↑ diuresis
Thiazide Diuretics facts
- Enhance the reabsorption of Ca2+in both DCT and PCT
- Largest class of diuretic agents
- More hyponatremiceffects than loop diuretics
- Use with caution in patients with diabetes mellitus
K+ sparing diuretics
Mineralocorticoid receptor (MR) antagonists
- Spironolactoneand eplerenone
- Uses include hyperaldosteronism, adjunct to K+-wasting diuretics, antiandrogenicuses (female hirsutism), heart failure (reduces mortality)
- Do not require access to the tubular lumen to induce diuresis
- Adverse effects include hyperkalemia, acidosis, and antiandrogeniceffects
K+ sparing diuretics
Na+channel (ENaC) inhibitors
- Amilorideand triamterene
- Uses include adjunct to K+-wasting diuretics and lithium-induced nephrogenicdiabetes insipidus (amiloride)
- Adverse effects include hyperkalemia and acidosis
Thiazide Diuretics used for
hypertension, mild heart failure, nephrolithiasis (calcium stones), nephrogenicdiabetes insipidus
Thiazide Diuretics adverse effects
hypokalemia, alkalosis, hypercalcemia, hyperuricemia, hyperglycemia, hyperlipidemia, sulfonamide hypersensitivity
Beside thiazide diuretics what other class of diuretics can be used to treat calcium stones
loop bc they flush everything out
A 42 y/o male presents to the ED complaining of sharp flank pain radiating to the groin, gross hematuria, and dysuria. A urine sample is obtained. Microscopy identifies a large amount of calcium oxalate crystals in the urinary sediment. He has a history of untreated hypertension and previous episodes of nephrolithiasis. Which agent would be most appropriate in this setting?
Chlorthalidone–thiazide-like diuretic, increase ca reabsorption
A 53 y/o female presents with BP of 155/90. She has a history of diabetes with hypertension currently treated with insulin and hydrochlorothiazide. Laboratory results indicate reduced GFRand proteinuria. Which drug is indicated for additional blood pressure control at this time?
Enalapril–ACE inhibitor, renoprotective by dialating the efferent arteriole
Which finding, if present, would contraindicate the use of angiotensin converting enzyme inhibitors?
Bilateral renal artery stenosis
Renal Considerations with ACEIs
- ACEIs prevent/delay the progression of renal disease in type 1 diabetics and in patients with nondiabeticnephropathies (results mixed in type 2 diabetics)
- ACEIs vasodilateefferent arterioles > afferent arterioles
- Reduces back pressure on the glomerulus and reduces protein excretion
- ACEIs usually improve renal blood flow and Na+excretion rates in CHF
- In rare cases, ACEIs can cause a rapid decrease in GFR, leading to acute renal failure (ARF)
- Can occur anytime during therapy, even after months or years of uneventful ACEI treatment
Risk Factors for ACEI-Induced ARF
- MAP insufficient for adequate renal perfusion
- Poor cardiac output
- Low systemic vascular resistance
- Volume depletion (diuretic use)
- Renal vascular disease
- Bilateral renal artery stenosis
- Stenosis of dominant or single kidney
- Afferent arteriolar narrowing (HTN, cyclosporinA)
- Diffuse atherosclerosis in smaller renal vessels
- Vasoconstrictor agents (NSAIDs, cyclosporine)
- All cause renal hypoperfusion
A 51 y/o male presents with difficulty breathing. The patient is afebrile and normotensive, but tachypneic. Auscultation of the chest reveals diffuse wheezes. The physician provisionally makes the diagnosis of bronchial asthma and administers epinephrine by intramuscular injection, improving the patient’s breathing over several minutes. A normal chest X-ray is subsequently obtained, and the medical history is remarkable only for mild hypertension that was recently treated with propranolol. The physician instructs the patient to discontinue use of propranolol, and change the patient’s antihypertensive medication to verapamil.
Why is the physician correct to discontinue propranolol?
Why is verapamil a better choice for managing hypertension in this patient?
you dont want to block b2 bc you will bronchoconstrict and exacerbate asthma
nondihyropyridine ccb, dont effect bronchoconstriction