Summary
Summary Nur 265 GU Study Guide
- Course
- ATI NUR265
- Institution
- Galen College Of Nursing
This is a comprehensive and detailed study guide on Genitourinary System for Nur 265.
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GUNephron: functional unit of the kidney, forms urine by filtering waste products and water from
blood.
Glomerular filtration: first process in urine formation
GFR: Normal 90-120 when b/p is below 65-70 self-regulation processes do not maintain GFR.
Decrease in renin(enzyme) and aldosterone(holds on to fluid) causes: an excretion of na,
dilution of urine, a decreased thirst.
Acute Kidney Injury:
Rapid reduction is kidney function: resulting in failure to maintain fluid and acid based balance.
Unable to maintain waste elimination, electrolyte balance, acid base balance. Occurs in a few
hours and days.
*reversible
*Causes:
Prerenal: anything before it gets to the kidney: Issue with perfusion to kidney= decrease
function to kidney, decrease of amount of blood to kidney to filter and deprives kidney= leads to
Intrarenal injury – issues with cardiac(blood/fluid loss, hypotension, Infection) chart 68-4
decrease in b/p 65 cause renal problem
Intrarenal-damage to nephrons- within kidney, problem with nephron= decrease ability to filter
blood- excessive waste build, excessive water, not able to maintain electrolyte, from
nephrotoxic drugs(NSAIDS, Vanc, Contrast dye, renal drugs, Pyelonephritis)
Postrenal: Lower in urinary system, blockage in tract, after the kidney, Prevents urine draining
out of system, High pressure in kidney and high in waste decreases kidney function
Causes: renal calculi, enlarged prostate, Stroke “bladder doesn’t empty”
In any acute kidney injury- reduce urine to increase blood volume and improve kidney
elimination
Oliguria: urine output less than 400/day
Azotemia: retention and buildup of nitrogenous wastes in blood
+all healthcare providers be alert for signs of AKI, Interventions early to prevent ESKD
Encourage 2-3L water daily
- Evaluate I/O, fluid status, foul odor.
- Report urine output less than 0.5 ml/kg/hr that persists for more than 2 hours. After 6
hours of oliguria= progression of kidney damage
- Monitor increase in creatinine (0.6-1.2) over hours of days
- Bun (10-20)
- Potassium (3.5-5)
- Urine specific (1.005-1.030)
- Decreased GFR (less than 90) bad on kidneys
, Assessment: ask about recent surgery, trauma, transfusions, drugs history (NSAIDS) Contrast
dye? HTN, NPO(can cause AKI) IV vasopressor
START with oral fluids before IV
Foley- check output every hour after surgery till stable
Anasarca(edema)
SIGNS: Tachy, thready pulse, decrease LOC, edema, increase in daily wt, reduced urine output
Diagnostic: IVP( Contrast dye), U/S, CT, KUB
Onset of polyuria= recovery of AKI
Phases of AKI:
Onset phase: from time of event to manifestations, up to a week after event (slight increase in
BUN,CREAT, normal or decrease in urine output- may not know something wrong
Oliguric stage: can last 1-8 weeks, longer=worse prognosis, Urine output decreases to 400ml or
less/day -400 in a shift (8 hours)
Diuretic stage: gradual or abrupt return of GFR, urine output increase 1-2l day, BUN creat
decrease
Recovery stage: everything back to normal last 3-12 months
Treatment: diuretics(increase urine output)
Hemodialysis: temporary to pull off fluid and toxins, 3 days a week, 3-6 hours, creates shifts of
fluid and electrolytes and may be tolerated by critically ill patients= hypotension and can
worsen renal function, fluid restriction
Hemodialysis can cause disequilibrium syndrome: mental status changes, seizures, coma
Parenteral: AT home, 4 exchanges per day, move around, 7-10 hours at night, no PD if a lot of
abdominal surgeries, don’t have to have fluid restriction
CRRT: unstable patient, ICU, cant tolerate changes in blood pressure, removes 1L/hour OK with
b/p being in 80’s
Chronic renal failure: serum creat level is the most accurate measure of renal function
Low fat, low protein, low NA diet
Metabolic acidosis= increase rate, depth breathing, kussmaul respirations
No NSAIDS, Tylenol, naproxen
Main causes: HTN, DM- African am. More likely to develop ESKD
HTN, HLD,
Decrease Ca= Increase Phos
IRREVERSIABLE, kidneys do not recover
11% increase d/t obesity, HTN, DM
Azotemia: build up nitrogen waste in blood
Uremia (build up): metallic taste, anorexia, n/v, muscle cramps, uremic frost, itching, fatigue,
hiccups, edema, Uremic frost, dyspnea- coma, seizures, decrease LOC= need dialysis ASAP
Stages of CKD:
Stage 1: may have normal GFR greater than 90, may have abn. Urine findings, structural abn,
traits: Uncontrolled HTN, DM, Congenital, Family hx, exposed nephrotoxic drugs
Stage 2: GFR: 60-89, kidney nephron damage occurred, slight elevations in metabolic waste in
blood, Increase output of dilute urine may occur, (BUN,Creat, uric acid, phos may be normal)
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