RNSG 2539 2539 Exam 1 Study Guide with
Complete Solutions | 2026 Update | Graded A+
Acute Kidney Injury Types and causes x2 - ANSWERS Prerenal failure:
(hypoperfusion of kidney) most common leads to decrease in gfr
Volume depletion resulting from:
•Gastrointestinal losses (vomiting, diarrhea, nasogastric suction)
•Hemorrhage
•Renal losses (diuretic agents, osmotic diuresis)
•Impaired cardiac efficiency resulting from:
•Arrhythmias
•Cardiogenic shock
•Heart failure
•Myocardial infarction
•Vasodilation resulting from:
•Anaphylaxis
•Antihypertensive medications or other medications that cause vasodilation
•Sepsis
Intrarenal Failure (actual damage to kidney tissue) s/s: tubular back leak,
vasocnstriction
,•Prolonged renal ischemia resulting from:
•Hemoglobinuria (transfusion reaction, hemolytic anemia)
•Pigment nephropathy (associated with the breakdown of blood cells containing
pigments that in turn occlude kidney structures)
•Rhabdomyolysis/myoglobinuria (trauma, crush injuries, burns)
•Nephrotoxic agents such as:
•Aminoglycoside antibiotics (gentamicin, tobramycin)
•Angiotensin-converting enzyme inhibitors
•Heavy metals (lead, mercury)
•Nonsteroidal anti-inflammatory drugs
•Radiopaque contrast agents
•Solvents and chemicals (ethylene glycol, carbon tetrachloride, arsenic)
•Infectious processes such as:
•Acute glomerulonephritis
•Acute pyelonephritis
Postrenal Failure (obstruction to urine flow)
•Urinary tract obstruction, including:
•Benign prostatic hyperplasia
•Blood clots
•Calculi (stones)
•Strictures
•Tumors
, AKI Diagnostic Findings - ANSWERS In AKI, urine output varies from scanty to a
normal volume, hematuria may be present, and the urine has a low specific
gravity
One of the earliest manifestations of tubular damage is the inability to
concentrate the urine
Patients with prerenal azotemia have a decreased amount of sodium in the urine
Patients with intrarenal azotemia usually have increased urinary sodium levels
greater than 40 mEq/L with urinary casts and other cellular debris.
metabolic acidosis occurs because patients cannot eliminate acid-type substances
normal valuesGFR:90-120BUN: 7-20creatinine: .6-1.2USG:1.010- 1.030
AKI- Hyperkalemia/ clinical manifestations - ANSWERS With a decline in the
GFR, oliguria, and anuria, patients are at high risk for hyperkalemia. Protein
catabolism results in the release of cellular potassium into the body fluids, causing
severe hyperkalemia (high serum potassium levels). Hyperkalemia may lead to
cardiac arrhythmias, such as ventricular tachycardia and cardiac arrest. Sources of
potassium include normal tissue catabolism, dietary intake, blood in the GI tract,
or blood transfusion and other sources (e.g., IV infusions, potassium penicillin,
and extracellular shift in response to metabolic acidosis).
irritability, abdominal cramping, diarrhea, paresthesia, and generalized muscle
weakness. Muscle weakness may present as slurred speech, difficulty breathing,
Complete Solutions | 2026 Update | Graded A+
Acute Kidney Injury Types and causes x2 - ANSWERS Prerenal failure:
(hypoperfusion of kidney) most common leads to decrease in gfr
Volume depletion resulting from:
•Gastrointestinal losses (vomiting, diarrhea, nasogastric suction)
•Hemorrhage
•Renal losses (diuretic agents, osmotic diuresis)
•Impaired cardiac efficiency resulting from:
•Arrhythmias
•Cardiogenic shock
•Heart failure
•Myocardial infarction
•Vasodilation resulting from:
•Anaphylaxis
•Antihypertensive medications or other medications that cause vasodilation
•Sepsis
Intrarenal Failure (actual damage to kidney tissue) s/s: tubular back leak,
vasocnstriction
,•Prolonged renal ischemia resulting from:
•Hemoglobinuria (transfusion reaction, hemolytic anemia)
•Pigment nephropathy (associated with the breakdown of blood cells containing
pigments that in turn occlude kidney structures)
•Rhabdomyolysis/myoglobinuria (trauma, crush injuries, burns)
•Nephrotoxic agents such as:
•Aminoglycoside antibiotics (gentamicin, tobramycin)
•Angiotensin-converting enzyme inhibitors
•Heavy metals (lead, mercury)
•Nonsteroidal anti-inflammatory drugs
•Radiopaque contrast agents
•Solvents and chemicals (ethylene glycol, carbon tetrachloride, arsenic)
•Infectious processes such as:
•Acute glomerulonephritis
•Acute pyelonephritis
Postrenal Failure (obstruction to urine flow)
•Urinary tract obstruction, including:
•Benign prostatic hyperplasia
•Blood clots
•Calculi (stones)
•Strictures
•Tumors
, AKI Diagnostic Findings - ANSWERS In AKI, urine output varies from scanty to a
normal volume, hematuria may be present, and the urine has a low specific
gravity
One of the earliest manifestations of tubular damage is the inability to
concentrate the urine
Patients with prerenal azotemia have a decreased amount of sodium in the urine
Patients with intrarenal azotemia usually have increased urinary sodium levels
greater than 40 mEq/L with urinary casts and other cellular debris.
metabolic acidosis occurs because patients cannot eliminate acid-type substances
normal valuesGFR:90-120BUN: 7-20creatinine: .6-1.2USG:1.010- 1.030
AKI- Hyperkalemia/ clinical manifestations - ANSWERS With a decline in the
GFR, oliguria, and anuria, patients are at high risk for hyperkalemia. Protein
catabolism results in the release of cellular potassium into the body fluids, causing
severe hyperkalemia (high serum potassium levels). Hyperkalemia may lead to
cardiac arrhythmias, such as ventricular tachycardia and cardiac arrest. Sources of
potassium include normal tissue catabolism, dietary intake, blood in the GI tract,
or blood transfusion and other sources (e.g., IV infusions, potassium penicillin,
and extracellular shift in response to metabolic acidosis).
irritability, abdominal cramping, diarrhea, paresthesia, and generalized muscle
weakness. Muscle weakness may present as slurred speech, difficulty breathing,
