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Urinary Patho

BMS263

QuestionAnswer
Glomerular Disease Damage to filtration membrane. Increased permeability. Decreased GFR & increased reabsorption (Increased BV & BP). Inflam. Abnormal cell prolif. Increase in EXC material different parts of corpuscle. Thickening of basement membrane. Fusion of podocytes.
Causes of Glomerular Disease Autoimmune disease (SLE), Infections, Diabetes, Hypertension, Toxic stresses (drugs & chemicals)
Diabetes Resulting In Glomerular Disease 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
Tubulointerstitial Disorders Nephron tubules (& often surrounding tissue) affected. Often caused by infections, drugs, & toxins. Hypertension can cause nephron tubule necrosis. Disrupt normal electrolyte and pH balance
Obstructive Urinary Disorders 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
Cystic Diseases 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
Kidney Stones (Renal Caliculi) 1. Calcium oxalate 80%. 2. Magnesium 15% (pH >7). 3. Uric Acid 7% (pH <7). Causes: Pregnancy, bladder stones or cancer, colon cancer, hyperplasia, infection. <5mm passed in urine. >1cm intervention. Treatment: High fluid intake, alter pH, ultrasound
Acute Renal Failure Rapid decline renal function. Decrease GFR. Inability to maintain fluid, electrolyte, pH balance, & get rid of wastes sufficiently. Accumulation of nitrogenous wastes in blood
Causes of Acute Renal Failure Acute decrease renal BF (Prerenal -> hypovolaemia, cardiac failure, anaphylactic shock). Structural damage to kidney (intrinsic). Difficulties eliminating urine from the kidney (postrenal). Extreme exercise, infections, genetics, dehydration, statins, etc
Chronic Kidney Disease (CKD) Permanent loss of nephrons & gradual decline in renal function leading to renal failure. Aging population, hypertension,diabetes, autoimmune diseases. Symptoms change as disease progresses. Early is mild. Usually advanced before diagnosis
Effects During Stages of CKD 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
Detecting CKD Serum creatinine levels are often used as an indicator of GFR. RBC or WBC in urine. Proteinuria (Albumin & Globulins)
CKD Pathophysiology Will disrupt fluid balance, electrolyte balance, pH balance (acidosis), mineral metabolism (osteodystrophy), RBC numbers (anaemia), nitrogenous waste excretion & drug excretion. May cause coagulation disorders & CV complications
Treatment of End-Stage CKD Artificial dialysis (Haemodialysis or peritoneal dialysis. Haemodialysis requires anticoagulation drugs e.g. Heparin). Renal transplantation, which requires immunosuppressant drugs
Effect Of CKD On Hypertension Hypertension will develop from renal failure. Hypertension can cause renal damage & renal failure. Anti-hypertensive drugs are important to both treatment & prevention of CKD
Effect of Hyperphosphataemia From CKD 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
CKD Effects Bones 1. Decreased (DC) phosphate excretion > hyperphosphataemia > DC Ca2 levels lead to bone reabsorption. 2. Active vit D synthesized in kidneys > DC in CKD > DC absorption of Ca2+ from GIT-Blood > Hypocalcemia > PTH > Bone resorption replace Ca2+ in blood
Osmotic Diuretics 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
Loop Diuretics Most powerful diuretics. Cause ‘torrential urine flow’. Act upon the thick ascending limb of LOH. Inhibit Na+ carrier in lumenal membrane of tubal cells. Usually only used for Acute pulmonary oedema, chronic heart failure & renal failure (not severe)
Effect of Loop Diuretics on pH 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
Loop Diuretics Pharmacokinetics Readily absorbed across GI tract. Usually given orally (act within 1 h). Can be given by IV (act within 30’) for severe cases. Does not pass through GF membrane, but pass into tubule lumen. Excreted from urine. Metabolised in liver
Loop Diuretics Unwanted Effects 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)
Thiazides 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)
Action Of Thiazides 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)
Thiazides Pharmacokinetics All different kinetics. Absorbed across GI tract well. Given orally. Tubular secretion causes all to be excreted in urine. Compete for uric acid secretion
Unwanted Effects of Thiazides 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
Thiazide Common Uses Given alone for hypertension. If used in combination with loop diuretics usually for severe resistant oedema
Aldosterone Antagonists Act on intercalating disks of CD (only 2% of Na reabsorption). Relatively weak diuretics. Will increase Na+ excretion. Effective anti-hypertensive drugs. Decrease K+ secretion. K+ sparing diuretic
Aldosterone Antagonist Unwanted Effects Hyperkalaemia. GI disturbances are common. Can affect reproductive systems (some also interact with receptors for sex hormones). Oestrogen-like side effects. Can be used with other diuretics to avoid hypokalemia
Aldesterone Antagonist Common Uses 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
Other Renal Drugs Other drugs used to: Alter urine pH (decreased urinary stones, burning during urination, UTI & increase excretion of weak acid or basic drugs), excretion of uric acid (gout) & excretion of other drugs
Treatment of Urinary Incontinence Smooth muscle in wall urinary bladder contracts during urination. Acetylcholine (ACh) stimulates bladder SM contraction Blocking ACh reduces contraction. ACh acts on muscarinic receptors in SM. Muscarinic receptor anatagonists used to treat condition
Created by: Mandyrox300
 

 



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