NURS 5461 FINAL QUIZ EXAM QUESTIONS AND
ANSWERS WITH COMPLETE SOLUTIONS VERIFIED
Renal issues that occur with normal aging
Decreased GFR, decreased diluting capacity, decreased concentration ability, decreased sodium
conservation (volume depletion) decreased sodium excreation (salt sensitivity/HTN), decreased
ammonium & bicarb production (metabolic acidosis)
Most accurate indicator of renal function in older adults
GFR - declines 8mls per decade starting at age 40
Small amounts of protein in urine
Chronic nephrosclerosis from HTN
renal artery stenosis
partial or complete blocking of one or both renal arteries - THIS ACTIVATES THE RENIN ANGIOTENSION
ALDOSTERONE SYSTEM AND CAUSES SYSTEMIC HYPERTENSION TO ATTEMPT TO PERFUSE THE KIDNEY -
if pt has a 30% increase in creatinine after starting an ACE or ARB - think renal artery stenosis - risk
factors include smoking, HTN, hyperlipidemia, DM, aneurysms - renal stenting isn't indicated except in
extreme cases when you can't control BP or there is progressive kidney failure.
Most common cause of AKI
Acute tubular necrosis (ATN) followed by prerenal azotemia
,Acute Tubular Necrosis (ATN)
Damage to the renal tubules due to presence of toxins in the urine or to ischemia. Results in oliguria.
Prerenal azotemia
Due to decreased blood flow to kidneys; common cause of acute renal failure - increase bun and
decreased renal flow - treat with volume resuscitation
acute tubular necrosis diagnostic criteria
DIAGNOSIS: URINE SEDIMENT WILL INCLUDE TUBULAR EPITHELIAL CELLS & GRANULAR MUDDY BROWN
CASTS - in oliguria FENa >2% - TREATMENT IS SUPPORTIVE CARE AND OFTEN TIMES REVERSIBLE
Acute interstitial nephritis
Drug-induced hypersensitivity involving the interstitium and tubules; results in acute renal failure
(intrarenal azotemia) - most commone antibiotics to cause this are PENICILLINS, CEPHLOSPORINS, AND
FLUOROQUINOLONES (floxacins)
multiple myeloma "myeloma kidney"
malignant neoplasm of bone marrow. Proteins light & heavy chains will deposit in parenchyma - pt will
present with lower back pain - seen AA women - will see sever proteinurea, low anion gap,
hypercalcemia, anemia, and bone pain - treat w chemotherapy (melphalan and prednisone)
3 types of glomerular disease
Acute nephritic syndrome
Post infection glomerulonephritis (step/staph)
IgA nephropathy
Nephrotic syndrome
, URINATING >3.5G OF PROTEIN PER DAY! WITH HYPOALBUMINEMIA, HLD, AND EDEMA - Can be from
primary glomerular disease, infection, malignancy, exposure to allergen/medication, DM, or HTN.
◦ RENAL BIOPSY IS ESSENTIAL FOR EARLY DIAGNOSIS
◦ THERAPY - CONTROLL BP, USE RASS BLOCKERS, SODIUM RESTICTION, STATINS, ANTICOAGULATION
WHEN ALBUMIN IS <2.8
What do RAAS inhibitors do?
Decrease proteinuria
Chronic Kidney Disease (CKD)
progressive, irreversible loss of kidney function - RENAL GLOMERULAR AND TUBULOINTERSTITIAL
FIBROSIS INCREASES WITH AGE LEADING TO CKD - presents with a decompensation of the pts preexisting
medical problems. - HTN AND DM ARE HIGH RISK FACTORS FOR CKD
RAAS (renin-angiotensin-aldosterone system)
Renin is released by kidneys in response to decreased blood volume; causes angiotensinogen to split &
produce angiotensin I; lungs convert angiotensin I to angiotensin II; angiotensin II stimulates adrenal
gland to release aldosterone & causes an increase in peripheral vasoconstriction
Medications to avoid in CKD
-NSAIDs- block the synthesis of the renal prostaglandins that promote vasodilation, and this can worsen
renal hypoperfusion
-DEMEROL: Metabolized to normeperidine in the liver, which kidneys excrete
-AMINOGLYCOSIDES, PENICILLIN, AND TETRACYCLINES: Nephrotoxic
ANSWERS WITH COMPLETE SOLUTIONS VERIFIED
Renal issues that occur with normal aging
Decreased GFR, decreased diluting capacity, decreased concentration ability, decreased sodium
conservation (volume depletion) decreased sodium excreation (salt sensitivity/HTN), decreased
ammonium & bicarb production (metabolic acidosis)
Most accurate indicator of renal function in older adults
GFR - declines 8mls per decade starting at age 40
Small amounts of protein in urine
Chronic nephrosclerosis from HTN
renal artery stenosis
partial or complete blocking of one or both renal arteries - THIS ACTIVATES THE RENIN ANGIOTENSION
ALDOSTERONE SYSTEM AND CAUSES SYSTEMIC HYPERTENSION TO ATTEMPT TO PERFUSE THE KIDNEY -
if pt has a 30% increase in creatinine after starting an ACE or ARB - think renal artery stenosis - risk
factors include smoking, HTN, hyperlipidemia, DM, aneurysms - renal stenting isn't indicated except in
extreme cases when you can't control BP or there is progressive kidney failure.
Most common cause of AKI
Acute tubular necrosis (ATN) followed by prerenal azotemia
,Acute Tubular Necrosis (ATN)
Damage to the renal tubules due to presence of toxins in the urine or to ischemia. Results in oliguria.
Prerenal azotemia
Due to decreased blood flow to kidneys; common cause of acute renal failure - increase bun and
decreased renal flow - treat with volume resuscitation
acute tubular necrosis diagnostic criteria
DIAGNOSIS: URINE SEDIMENT WILL INCLUDE TUBULAR EPITHELIAL CELLS & GRANULAR MUDDY BROWN
CASTS - in oliguria FENa >2% - TREATMENT IS SUPPORTIVE CARE AND OFTEN TIMES REVERSIBLE
Acute interstitial nephritis
Drug-induced hypersensitivity involving the interstitium and tubules; results in acute renal failure
(intrarenal azotemia) - most commone antibiotics to cause this are PENICILLINS, CEPHLOSPORINS, AND
FLUOROQUINOLONES (floxacins)
multiple myeloma "myeloma kidney"
malignant neoplasm of bone marrow. Proteins light & heavy chains will deposit in parenchyma - pt will
present with lower back pain - seen AA women - will see sever proteinurea, low anion gap,
hypercalcemia, anemia, and bone pain - treat w chemotherapy (melphalan and prednisone)
3 types of glomerular disease
Acute nephritic syndrome
Post infection glomerulonephritis (step/staph)
IgA nephropathy
Nephrotic syndrome
, URINATING >3.5G OF PROTEIN PER DAY! WITH HYPOALBUMINEMIA, HLD, AND EDEMA - Can be from
primary glomerular disease, infection, malignancy, exposure to allergen/medication, DM, or HTN.
◦ RENAL BIOPSY IS ESSENTIAL FOR EARLY DIAGNOSIS
◦ THERAPY - CONTROLL BP, USE RASS BLOCKERS, SODIUM RESTICTION, STATINS, ANTICOAGULATION
WHEN ALBUMIN IS <2.8
What do RAAS inhibitors do?
Decrease proteinuria
Chronic Kidney Disease (CKD)
progressive, irreversible loss of kidney function - RENAL GLOMERULAR AND TUBULOINTERSTITIAL
FIBROSIS INCREASES WITH AGE LEADING TO CKD - presents with a decompensation of the pts preexisting
medical problems. - HTN AND DM ARE HIGH RISK FACTORS FOR CKD
RAAS (renin-angiotensin-aldosterone system)
Renin is released by kidneys in response to decreased blood volume; causes angiotensinogen to split &
produce angiotensin I; lungs convert angiotensin I to angiotensin II; angiotensin II stimulates adrenal
gland to release aldosterone & causes an increase in peripheral vasoconstriction
Medications to avoid in CKD
-NSAIDs- block the synthesis of the renal prostaglandins that promote vasodilation, and this can worsen
renal hypoperfusion
-DEMEROL: Metabolized to normeperidine in the liver, which kidneys excrete
-AMINOGLYCOSIDES, PENICILLIN, AND TETRACYCLINES: Nephrotoxic
