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week 9 Patho
urinary stuff
| Question | Answer |
|---|---|
| what is the pathophysiology of UROLITHIAS and what is another name for it? | form when: ○ there are excessive amounts of insoluble salts in the filtrate ○ insufficient fluid intake creates a highly concentrated filtrate Also known as Kidney stones |
| How can calculi lead to infection? | bc they cause urinary Stais and tissue irritation |
| What does hydronphrosis lead to? | dilation of the calyces and trophy of Renal tissue due to back pressure of urine behind the stone |
| what is calculi composed of? | 75% is formed of calcium salts, remainder is usual of uric acid and other breakdown products |
| what is the ethology of calculi? | hypercalcemia, hyperparathyroidism, highly alkaline uric, inadequate fluid intake, high oxalate diets |
| what are the signs and symptoms of urolirhias or kidney stones? | people may be asymptomatic, flank pain, renal colic (nausea, vomiting, cool, moist skin, and rapid pulse) |
| what causes renal colic and what causes the severe pain accompanied? | Caused by obstruction of the ureter, which causes intense spasms of flank radiating into the groin Pain is caused my vigorous contractions of the ureter in effort to push stone out |
| What is the pathophysiology of hydronphrosis? | Obstruction in urine flow leads to back flow of urine which then causes dilation or enlargement of renal pelves and calyces If urine continues build tissue necrosis can occur due to pressure and compression of blood vessels |
| what is the ethology go hydronephrosis? | secondary problem of calculi, tumors, scar tissue, |
| what are some signs and symptoms of hydronephrosis? | Frequently asymptomatic particularly unilateral Potential ↑in BUN & Creatinine Palpable enlarged kidney Mild flank pain If cause not removed, bilateral hydronephrosis → chronic renal failure |
| How can hydronephrosis be treated? | Remove the cause Depends on location of obstruction- higher then nephrostomy tube Treat any secondary infections |
| What is glomerulonephritis? | inflammation of the tiny filters in your kidneys |
| What is the etiology of glomerulonephritis? | follows an infection caused by group A beta-hemolytic Streptococcus |
| what are some signs and symptoms? | Dark, cloudy urine Facial and periorbital edema, followed by generalized edema Elevated blood pressure Flank pain or back pain Malaise, fatigue, headache, nausea, anorexia Oliguria |
| what is the rationale of dark cloudy urine | because the protein and red blood cells that have leaked into it |
| what is the rationale of Facial and periorbital edema, followed by generalized edema | colloid osmotic pressure of the blood drops and sodium and eater are retained |
| what is the rationale of Elevated blood pressure | increased renin secretion and decrease GFR |
| what is the rationale of Flank pain or back pain | develops when kidney tissue swells and stretches the capsule |
| what is the rationale of Malaise, fatigue, headache, nausea, anorexia | general signs of inflammation |
| what is the rationale of Oliguria | GFR declines |
| what are some diagnostic test for glomerulonephritis? | Blood tests show elevated serum urea and creatinine as GFR decreases. |
| what is acute renal failure? | rapid deterioration (within hours to days) of renal function with rising levels of urea and other nitrogenous wastes in the blood (azotemia) and fluid and electrolyte imbalance |
| what is the pathophysiology for acute renal failure? | kidneys may fail to function due to: Directly reduced blood flow into the kidney or inflammation Necrosis of the tubules cause obstruction and back pressure, leading to greatly reduced GFR and oliguria (reduced urine output) or anuria (no urine output |
| what is the etiology of acute renal failure? | Prerenal acute renal failure • results from conditions that affect renal blood flow and perfusion Intrinsic or Intrarenal acute renal failure • acute damage to the renal parenchyma and nephrons Acute tubular necrosis (ATN) ○ prolonged ischemia, such |
| What are the phases of ARF due to ATN? | initiation, maintenance, and recovery phase |
| What happens in the initiating phase? | begins with the initiating event, such as hypovolemia ,and ends when tubular injury occurs few symptoms |
| What happens in the maintenance phase? | Salt and water retention, Azotemia, Hyperkalemia, dec erythropoietin, depressed immune function |
| what happens in recovery phase? | repair and regeneration of tubular cells ○ gradual return of GFR to normal or pre-ARF levels |
| what are some of the diagnostic tests that can be done ? | urinalysis, serum creatinine and blood urea nitrogen, serum electrolytes, cbc (reduces rbcs and hematocrit) |
| what is chronic renal failure? | the presence of kidney damage for three or more months gradual, irreversible destruction of the kidneys over a long period of time |
| what is the etiology of chronic renal failure? | diabetic nephropathy hypertensive nephrosclerosischronic glomerulonephritis chronic pyelonephritis |
| what is the pathophysiology of chronic renal failure? | Glomerulosclerosis Interstitial inflammation and fibrosis Entire nephron units are gradually destroyed Remaining functional nephrons hypertrophy Glomerular capillary flow and pressure increase in these nephrons |
| What is the first stage of chronic kidney disease and explain | decreased renal reserve (60% nephron loss) ○ slightdecreaseinGFR ○ serumcreatininehighnormal ○ normalserumurea ○ noapparentclinicalsigns |
| What is the second stage of chronic kidney disease and explain | renal insufficiency (75% nephron loss) ○ GFR reduced to approximately 20% of normal ○ high levels of urea and creatinine in blood ○ tubule function is decreased = failure to concentrate urine ○ failure to control the secretion and exchange of acid san |
| What is the third stage of chronic kidney disease and explain | uremia or end-stage renal failure (more than 90% nephron loss) ○ GFR is negligible ○ fluids, electrolytes and wastes are retained ○ all body systems are affected ○ marked oliguria or anuria |
| what is epoetin alfa (Eprex®)? | stimulate erythropoiesis functionally identical to human erythropoietin. |
Created by:
Omyy
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