BMS263
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Glomerular Disease | show 🗑
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Causes of Glomerular Disease | show 🗑
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show | 3 ways. 1. High BGL --> inflamm --> damage. 2. High BGL --> Alter renal vasculature --> Afferent arteriole loses ability to regulate BF into glomerulus. Blood rushes in causing damage. 3. Glucose causes basement membrane to thicken = Lower GFR
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show | Nephron tubules (& often surrounding tissue) affected. Often caused by infections, drugs, & toxins. Hypertension can cause nephron tubule necrosis. Disrupt normal electrolyte and pH balance
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show | Obstruction of urinary system ducts. Increase UTI risk. Can cause renal damage & atrophy. Causes: Kidney stones. Compression of ducts due to pregnancy or tumours. Congenital duct disorders. Bladder stones. Bladder cancer. Prostatic hyperplasia or cancer
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show | Renal cysts = epithelial-lined cavities filled with fluid or semisolid material. Single or multiple. Microscopic to several cm diameter. Most hereditary. Can develop with age, dialysis, or conditions affecting tubular function. Can lead to renal failure
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Kidney Stones (Renal Caliculi) | show 🗑
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show | Rapid decline renal function. Decrease GFR. Inability to maintain fluid, electrolyte, pH balance, & get rid of wastes sufficiently. Accumulation of nitrogenous wastes in blood
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Causes of Acute Renal Failure | show 🗑
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Chronic Kidney Disease (CKD) | show 🗑
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show | Early CKD causes polyuria & increases dehydration. Later decrease in GFR & increased risk oedema & hypertension. ‘salt wasting’ also occur --> loss of functional nephron tubules for reabsorption
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Detecting CKD | show 🗑
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CKD Pathophysiology | show 🗑
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Treatment of End-Stage CKD | show 🗑
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show | Hypertension will develop from renal failure. Hypertension can cause renal damage & renal failure. Anti-hypertensive drugs are important to both treatment & prevention of CKD
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show | CKD causes hyperphosphataemia, leads to decreased Ca2 levels in blood lead to bone resorption, can cause calcification in aortic semilunar valve > Undue pressure on LV > hypertrophy > heart failure
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CKD Effects Bones | show 🗑
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show | Used in acute renal failure. Stop nephrons drying up when severe GFR reduction occurs. Inhibit excessive reabsorption. Pass easily through GF membrane, not reabsorbed. Increase solute concent inside tubular fluid. Pharmacologically inert. E.g. Mannitol
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Loop Diuretics | show 🗑
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show | Loop diuretics impact pH balance. H+ excretion in urine increase causing pH to rise in body fluid. HCO3 levels remain same, but BV will be decreased. Can cause alkalosis > impact electrical signalling of NS & skeletal muscle. Severe > convulsions & death
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Loop Diuretics Pharmacokinetics | show 🗑
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show | Frequent urination. High loss of Na+ (and therefore H20) cause hypovolaemia & hypotension. Hypokalaemia. Increase effects & toxicity of other drugs patient may take. Alkalosis. Hyperuricaemia, resulting in gout. Hearing loss (rare)
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show | Block Na+ (& Cl-) reabsorption in DCT. Inhibit action of Na+/Cl- co-transporter. Less powerful than loop diuretics. Preferred drugs for treating hypertension if no no renal complications)
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show | Limited by action homeostatic control mechanisms (RAA system). Increase K+, H+Mg2+ excretion. Decrease uric acid secretion & Ca2+ excretion (less risk osteoporosis). Vasodilator. Synergistic effect with loop diuretics (Increase Na+ excretion & H2O loss)
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Thiazides Pharmacokinetics | show 🗑
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show | Reversible erectile dysfunction. Can cause hyperglycaemia (act on pancreas to decrease insulin). Lot of same problems as loop diuretics, but risk lower. Urinate more frequently. Hyponatremia. Hypotension. Hypokalaemia. Alkalosis. Hyperuricaemia & gout
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show | Given alone for hypertension. If used in combination with loop diuretics usually for severe resistant oedema
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Aldosterone Antagonists | show 🗑
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Aldosterone Antagonist Unwanted Effects | show 🗑
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show | Often prescribed with K + losing diuretics to prevent K + loss, where hypoklaemia is hazardous (also taking digoxin). For Hyperaldosteronism and some cases of hypertension and heart failure
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Other Renal Drugs | show 🗑
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Treatment of Urinary Incontinence | show 🗑
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