Pharmacy Chapter 32 & 40 Highlights

Diuretics (Chapter 32)

• Fluid overload/edema can stem from heart failure, endocrine disorders, kidney disease, liver disease.
• A diuretic ↑ urinary output, ↓ excess tissue fluid.

Loop Diuretics

• Mechanism: inhibit re-absorption of $Na^+$ and $Cl^-$ in the ascending Loop of Henle.
• Large % of filtered $Na^+$ is normally reclaimed here → blocking this site makes loop agents very potent.

Thiazide & Related Diuretics

• Act in early distal tubule → block $Na^+$/$Cl^-$ re-uptake.
• Result: ↑ excretion of $Na^+$, $Cl^-$, H(_2)O.
• Often first-line for hypertension.

Potassium-Sparing (Potassium-Saving) Diuretics

• Reduce renal loss of $K^+$.
• Block $Na^+$ re-absorption in collecting tubules → more $Na^+$/H(_2)O in urine, less $K^+$ lost.
• Hyperkalemia risk, especially when fluid intake/urine output are low, in diabetes, renal disease, older & severely ill pts.

Spironolactone Specifics

• Aldosterone antagonist in distal convoluted tubule.
• Aldosterone (adrenal cortex hormone) normally ↑ $Na^+$ re-absorption.
• Inhibits testosterone secretion → used for feminizing hormone therapy (male→female).
• Adverse: gynecomastia in male pts (usually reversible after drug cessation).

Electrolyte Issues & Prevention

• Loop agents: hypokalemia + possible Mg(^{2+}) deficiency.
• Imbalance depends on volume/electrolyte losses vs replacement (e.g., poor diet + low fluid intake → high risk).
• High-potassium foods to replete $K^+$ when needed: white beans, dark leafy greens, baked potato (skin on), dried apricots, acorn squash, plain low-fat yogurt, salmon, avocado, mushrooms, bananas, sun-dried tomatoes.

Patient/Family Education

• Weigh weekly; report change > $3-5$ lb/week.
• On potassium-sparing agents: avoid high-$K^+$ foods, salt substitutes containing $K^+$; scrutinize food labels.

Contraindications for Diuretics

• Known drug hypersensitivity.
• Pre-existing electrolyte imbalance.
• Severe renal/hepatic damage.
• Anuria.

Diabetes Mellitus (Chapter 40)

• Insulin deficiency → hyperglycemia → ↑ risk of MI, stroke, blindness, nephropathy, vascular & neurologic damage, limb compromise.

Type 1 Diabetes (Formerly "IDDM")

• Autoimmune β-cell destruction → little/no insulin production → exogenous insulin required.
• Rapid onset, usually < age 20.
• More severe symptoms & harder to control vs Type 2.

Type 2 Diabetes (Formerly "NIDDM")

• $90-95\%$ of all DM cases.
• Pathophysiology: ↓ β-cell insulin output and/or insulin resistance.
• Typical onset ≥ 40 y; symptoms milder than Type 1.

Risk Factors for Type 2

• Obesity.
• Advancing age.
• Family history.
• Prior gestational DM.
• Impaired glucose tolerance.
• Ethnicity: African American, Hispanic/Latino, Native American, etc.

Management Spectrum

• Diet + exercise ± oral agents; ~$40\%$ eventually need insulin due to poor oral response.

Insulin Fundamentals

• Insulin facilitates glucose entry into striated muscle & adipose cells.

Timing of Common Preparations

• Regular insulin: give $30{-}60$ min pre-meal.
• Aspart: immediately before meal.
• Lispro: right before or right after meal.
• Many pts maintained on a single morning dose of intermediate-acting insulin (e.g., NPH) SQ.

Oral Antidiabetic Agents

Biguanides – Metformin (only US agent)

• Actions:
– Sensitizes liver to circulating insulin.
– ↓ intestinal glucose absorption.
– ↓ hepatic gluconeogenesis.
• Adverse: nausea, vomiting, diarrhea → take with food.
• Contraindicated in renal insufficiency.
• Hold on day of iodinated contrast studies & for $48$ h post-procedure (renal failure/lactic acidosis risk).

Sulfonylureas

• Lower glucose by stimulating pancreatic β-cells to release insulin.

Monitoring Glycemic Control

• Glycosylated hemoglobin (HbA(_1c)) reflects average blood glucose ≈ 3 months.

Glucagon

• Endogenous hormone from pancreatic α-cells; clinically used to treat severe hypoglycemia when pt cannot take oral glucose.