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kidney and urinary 2
patho exam 2
| Question | Answer |
|---|---|
| nephrolithiasis (kidney stone) | results from formation of urinary crystals into larger stones, common obstruction |
| Who do nephrolithiasis (kidney stones) most commonly affect? | white males |
| nephrolithiasis risk factors | previous stones, dehydration, hypercalcuria, hyperoxaluria, high sodium diet |
| nephrolithiasis composition | majority are calcium based, less common: uric acid, struvite, cysteine stones |
| nephrolithiasis stone formation | damage to lining of the urinary tract, crystal aggregation, slow urine flow to allow crystallization, excretion of large amounts of calcium |
| Clinical menifestations renal calculi (kidney stones) | acute, unilateral flank pain, nausea, vomiting, severe pain that comes and goes (renal colic) |
| renal calculi diagnosis | based on clinical symptoms, ultrasound, x-ray |
| renal calculi treatment | thiazide diuretic or allopurinol, percutaneous nephrolithotomy (PCNL), surgery as needed |
| who is urinary incontinence most common in? | caucasian women |
| urinary incontinence risk factors | pregnancy, older age, obesity, hypertension, smoking, alcohol consumption, postmenopausal diabetes, neurogenic bladder |
| types of incontinence | stress, urgency, postural, nocturnal enuresis, mixed, continuous, insensible, coital |
| stress inctoninence | physical activity, sneezing, coughing |
| urgency incontinence | feeling urgency with loss of urine |
| postural incontinence | position change |
| nocturnal enuresis | during sleep |
| continuous incontinence | continuous loss of urine |
| insensible incontinence | unawareness of loss of urine |
| coital inconctinence | occurs with coitus |
| urinary incontinence diagnosis | report of loss of urine in various situations |
| urinary incontinence treatment | weight loss, bladder training, pelvic floor muscle training, pessary, surgery, antimuscarinics/ anticholinergics |
| Chronic kidney disease etiology and pathogenesis | either kidney damage or GFR <60 mL/min/1.73 m2 for 3 months or more, incidence continues to rise |
| What happens to people with CKD within the first year of starting dialysis? | 25% die |
| etiology of CKD | diabetic nephropathy, hypertensive, nephrosclerosis, chronic glomerulonephritis, polycystic kidney disease |
| diabetic nephropathy pathogenesis | most frequent cause of CKD in ESRD, moderate albuminuria=early indicator, basement membrane thickening, mesangial expansion, increased glomerular permeability, decreased GFR |
| hypertensive nephrosclerosis pathogenesis | increased pressure in the glomerulus-> damage of glomerular cells-> glomerulosclerosis; damage of small vessels in kidneys-> inadequate blood supply-> decreased BP to glomeruli-> glomerulosclerosis; hyperfiltration-> thickening of glomerular vessels |
| chronic glomerulonephritis pathogenesis | direct injury to glomerulus, pathogenesis similar to diabetic nephropathy, antibody deposition-> glomerular inflammation; chemokines and cytokine-> mesangial cells promote inflammation |
| when polycystic kidney disease onset begin | at 30 years of age |
| polycystic kidney disease pathogenesis | cysts develop from collecting duct of nephron, cysts increase in number and size with age; macrophage infiltration, neurovascularization, progressive fibrosis, and decreased renal function |
| What is 90% of polycystic kidney disease caused by? | mutation of the PKD1 gene |
| complications of CKD | cardiovascular disease, metabolic acidosis, chronic kidney disease-mineral and bone disorder (CKD-MBD), anemia, hyperkalemia, hypervolemia, uremia |
| CVD as a complication of CKD | most common cause of death in CKD, HTN, dyslipidemia, and chronic inflammatory state |
| metabolic acidosis as a complication of CKD | In CKD, kidneys retain H+ ions; decreased kidney function leads to decreased ammonia and retained H+ ions, decreased kidney function decreases resorption of sodium bicarbonate |
| chronic kidney disease-mineral and bone disorder as a complication of CKD | bone diseases in CKD resulting from mineral and hormonal changes; causes bone pain, deformities, and fractures; results from abnormal bone turnover, hypocelcemia, hyperphospatemia, and hyperparathyroidism |
| anemia as a complication of CKD | decreased erythropoietin, worsens with worsening CKD; leads to increased cardiac preload, decreased afterload, and increased cardiac output |
| hyperkalemia as a complication of CKD | develops as oliguria develops, results from decreased aldosterone secretion and decreased excretion of potassium |
| hypervolemia as a complication of CKD | once GFR falls, renal secretion of sodium and water decreases, exacerbates CVD and LVH |
| uremia as a complication of CKD | results from waste product accumulation |
| diagnosis of CKD | national kidney foundation guidelines, blood and urine tests, additional laboratory tests |
| additional lab tests for diagnosis of CKD | liver profile, thyroid function tests, electrolyte panel, imaging- KUB, renal ultrasound, arteriogram, CT, MRI |
| What happens as GFR decreases? | severity of kidney disease increases, stage number increases |
| treatment of CKD | anti-hypertensives, lipid lowering agents, hemodialysis, peritoneal dialysis, renal transplantation |
| anti-hypertensives for CKD | ACE/ARB medications |
| lipid lowering agents for CKD | statin therapy |
| hemodialysis for CKD | removal of toxins and excess fluid from the blood |
| peritoneal dialysis for CKD | removal of toxins and excess fluid by utilizing the peritoneum |
| renal transplantation for CKD | encouraged in those who have the potential of a good quality of life after transplantation |
Created by:
camrynfoster