Exam 4 part 4

Question 1

pyelonephritis

Answer 1

• upper uti
• must have cystitis before developing
• infection moves up to kidneys (can effect 1 or 2 kidneys), ureter, renal pelvis, medullary tissue

Question 2

pyelonephritis pathophysiology

Answer 2

ascending infection
- Usually caused by e-coli
- purulent exudate fills the kidney pelvis and the medullary tubules are inflamed with necrosis
- if the infection is severe it can compress the renal artery and vein and obstruct urine flow

Question 3

pyelonephritis s/s

Answer 3

a) similar to those of cystitis
b) urinary casts consisting of leukocytes or renal epithelial cells
c) dull, aching pain in the lower back resulting from stretching of the renal capsule
d) Chills with moderate to high fever

Question 4

calcium stones

Answer 4

• most common
• caused by high oxalate or phosphate
• spinach and leafy greens contain these ^

Question 5

magnesium ammonium phosphate stones

Answer 5

• struvite stones
• softest stones
• often seen in bladder infection pts

Question 6

uric acid stones

Answer 6

gouty arthritis

Question 7

cystine stones

Answer 7

• from the amino acid cystine
• hardest stones

Question 8

how stones damage the kidney

Answer 8

back pressure builds up behind the stone (the stone itself usually isn’t causing the damage)

Question 9

prerenal acute kidney injury

Answer 9

Blood supply decreased
Shock, dehydration, vasoconstriction

Question 10

Postrenal acute kidney injury

Answer 10

Urine flow blocked
Stones, tumors, enlarged prostate

Question 11

Intrinsic acute kidney injury

Answer 11

Kidney tubule function decreased
Ischemia, toxins (nephrotoxic drugs), intratubular obstruction

Question 12

acute renal injury - acute tubular necrosis

Answer 12

Intrarenal injury
Destruction of tubular cells
- Ischemia
- Nephrotoxic drugs
– Gentamicin, radiocontrast agents
- Obstruction
- Sepsis
- Myoglobin (rhabdomyolysis), hemoglobin in urine
Renal tubule can recover is agent is removed and removal of damaged cells and regeneration of tubular cells

Question 13

S/S of Acute Renal Injury - acute tubular necrosis

Answer 13

Initiation phase: last several hours to days: from event (ischemia, toxins) to tubular injury
Maintenance phase: nonoliguric -> oliguric phase
- Decrease in GFR, retention of metabolic wastes, fluid retention, edema, uremia which has neurological issues
Recovery phase: repair of renal tubule takes place
- Gradual increase in urine formation and fall in creatinine
- Diuresis even though you might still have increased in metabolic wastes
- Return to normal function

Question 14

how to know if patient has moved from maintenance to recovery in acute tubular necrosis

Answer 14

diuresis - they have began increased urine production

Question 15

NSAIDS and nephrotoxicity

Answer 15

can be nephrotoxic - kidney disease pts should not take NSAIDs - acetaminophen does not count (its removed by the liver, not the kidney)

Question 16

treatment of acute tubular necrosis

Answer 16

To treat you need to identify the cause, use of diuretics, dialysis
- Hemodialysis
- Continuous renal replacement therapy, give kidneys time to recover

Question 17

electrolyte imbalances in renal failure

Answer 17

• Sodium decreases
• Potassium increases
• Calcium decreases
• Phosphate increases
• Magnesium increases
• H+ increases
• blood volume increases (but this is not an electrolyte)

Question 18

peritoneal dialysis

Answer 18

done at home - pt uses own peritoneal membrane to dialyze their blood, entry point is in peritoneal cavity

Question 19

hemodialysis

Answer 19

a fistula is created (usually in the arm) to allow direct entry to a high blood flow artery to dialyze. bicarbonate moves from the solution (also containing medication and erythropoetin to combat anemia) into blood.

Question 20

creatinine

Answer 20

• determines level of renal function
• increases with kidney failure
• nitrogenous compound/metabolic waste
• have to lose 75% of renal function before seeing increase in creatinine (about a kidney and a half)

Question 21

blood urea nitrogen (BUN)

Answer 21

• nitrogenous compound
• increases with kidney failure
• not as good an indicator as creatinine

Question 22

urinary retention

Answer 22

inability to empty the bladder; spinal damage at the sacral level or after anesthesia, the micturition reflex is blocked (ureter doesn’t close off, urine backflows) - retention of urine/failure to void
- straight cath to see amount
- bladder scan

Question 23

chronic kidney disease / chronic renal failure

Answer 23

• gradual irreversible damage to kidney
• fewer nephrons, remaining ones hypertrophy bc they have to do more work
• 75% of kidney function lost before s/s

Question 24

chronic kidney disease / chronic renal failure s/s

Answer 24

Uremic state (increase in metabolic waste like bun and creatinine)
- Altered neuromuscular function
- Fatigue
- Peripheral neuropathy
- Restless leg syndrome
- Uremic encephalopathy (build up of bun in brain cells)
Gastrointestinal issues
- Anorexia
- Nausea
WBC and immune dysfunction
Uremic bleeding - impaired platelet function
Uremic frost

Question 25

Stage 1

Answer 25

Kidney damage is present but undetected Normal GFR - normal levels of creatinine and BUN

Question 26

Stage 2

Answer 26

GFR is decreased slightly No recognized markers of kidney damage; no s/s

Question 27

Stage 3

Answer 27

Moderate decrease in GFR - increased creatinine and BUN. See complication such at hypertension, anemia (late stage 3)

Question 28

Stage 4

Answer 28

severe decrease in GFR - further increase in creatinine and BUN . Dialysis or transplant in near future (prepare pt for dialysis)

Question 29

Stage 5

Answer 29

kidney have failed must be on dialysis

Question 30

osteodystrophy in CKD

Answer 30

Hyperphosphatemia -> hypocalcemia > increased PTH > calcium resorption from bone > bone loss Decreased vitamin D activation > increased PTH, impaired osteoblasts