ADVANCED PATHOPHYSIOLOGY EXAM 1 NEWEST 2024
ACTUAL EXAM 200 QUESTIONS AND CORRECT DETAILED
ANSWERS WITH RATIONALES (VERIFIED ANSWERS)
|ALREADY GRADED A+
what is the anion gap - answer-Concentration of anions (Cl and HCO3) to cations (Na and K) in the ECF,
by rule, the concentrations should be relatively equal
relationship of anion gap and metabolic acidosis - answer--metabolic acidosis is characterized as either
normal anion gap metabolic acidosis or elevated anion gap metabolic acidosis
-MA elevated gap - we know abnormal anions
-MA normal gap - we know that the cause is loss of bicarbonate
What are the causes of elevated anion gap in metabolic acidosis - answer-P - paraldehyde
L - lactic acidosis
U - uremia
M - Methanol
S - Salicylates
E - Ethanol
E - Ethylene Glycol
D - DKA
S - Starvation
calculate the anion gap - answer-AG = (Na + K) - (Cl + HCO3)
relationship between metabolic alkalosis and hydrogen - answer--bicarb generation is coupled with
hydrogen secretion
-increase in bicarb can be due to loss of hydrogen ions - usually from GI losses or shift from ECF to ICF
explain buffers in metabolic acidosis - answer--buffer systems compensate for excess acid and attempt
to maintain pH.
,-H+ into cell, K+ out
-acidosis severe then buffers depleted cannot compensate and pH continues to decrease
-there is also an increase in Ca because acidosis decreases the amount of Ca bound to albumin
What is compensation in ABG's - answer--metabolic (renal) and respiratory (pulmonary) counter
adjustments to try to fix pH imbalance in ABG's ex. metabolic alkalosis means high bicarb, respiratory
will try to compensate by retaining CO2 into blood
partial compensation - answer-systemic arterial blood pH is still lower than 7.35
example - respiratory acidosis, renal system tries to balance by reabsorbing bicarb (bc high bicarb will
raise pH) but is not enough to reach WDL
full compensation - answer-pH is normal, pCO2 and HCO3 are abnormal
3 pathophysiolgical types of AKI - answer-prerenal
intrarenal (intrinsic) postrenal
nonoliguria vs oliguria vs anuria - answer-nonoliguria - daily volume >500
oliguria - daily volume <500 anuria <100
prerenal AKI etiologies - answer--hypovolemia
-hemorrhagic blood loss (trauma, GI bleeding, complications of childbirth)
-loss of plasma volume (burns, peritonitis)
-water and electrolyte losses (severe vomiting, diarrhea, obstruction, diabetes, diuretics)
-hypotension or hypoperfusion
-septic shock
-cardiac failure
-massive pulmonary embolism
-stenosis
,-increased intraabdominal pressure
intrarenal AKI etiologies - answer--acute tubular necrosis
-glomerulopathies
-acute interstitial necrosis (tumors or toxins)
-vascular damage
-malignant HTN, vasculitis
-coagulation defects
-renal artery/vein occlusion
-bilateral acute pyelonephritis
postrenal AKI etiologies - answer--obstructive uropathies (usually bilateral - fibrosis)
-ureteral destruction (edema, tumors, stones, clots)
-bladder neck obstruction (enlarged prostate)
-neurogenic bladder
how does urinary sediment differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN), and
postrenal AKI - answer-normal - bland prerenal - bland intrarenal (G) - active (hallmark) intrarenal (ATN)
- muddy brown casts, renal tubular epithelial cells postrenal - bland
how does urine sodium differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN), and
postrenal AKI - answer-normal - 20 mEq/L prerenal - <10 mEq/L intrarenal (G) - <20 mEq/L
intrarenal (ATN) - >40 mEq/L postrenal
- usually low
how does urine osmolality differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN) -
answer-normal - 300 - 900 mOsm prerenal - > 500 mOsm (high) intrarenal (G) - > 500 mOsm
intrarenal (ATN) - <300 mOsm postrenal -
, how does proteinuria differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN), and
postrenal AKI - answer-normal - 0 - 20 mg/dL prerenal - 5 - 20 mg/dL intrarenal (G) - > 100 mg/dL
presence of proteinuria intrarenal (ATN) - 5-20 mg/dL postrenal - 5-20 mg/dL
how does specific gravity differentiate prerenal, intrarenal (ATN) - answer-normal - 1.00 - 1.03
prerenal - >1.020 intrarenal (ATN) - 1.010 - 1.012 (low)
how does BUN/Cr ratio differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN), and
postrenal AKI - answer-normal - 10 - 20:1 prerenal - >20:1 intrarenal (G) - 10 - 20:1 intrarenal (ATN)
- 10 - 20:1 postrenal - >20:1
glomerulonephritis - answer-injury to the glomeruli typically from systemic disease usually immunologic
in etiology
what distinguishes glomerulonephritis from pre-renal AKI - answer-azotemia (BUN and Cr will be
elevated active urinary sediment proteinuria
acute tubular necrosis - answer-damage to the renal tubules due to presence of toxins in the urine or to
ischemia most common cause of hospital acquired ARF
distinguish ATN from prerenal - answer-UA: granular muddy brown casts
no significant increase in protein urine sodium is >20 (FE NA >3%)
FeUrea is elevated BUN/CR is normal
does not respond to volume replacement
GFR - answer-the filtration of plasma per unit of time the
sum of the filtration rate of all the functioning nephrons
normal value - 90 - 120
ACTUAL EXAM 200 QUESTIONS AND CORRECT DETAILED
ANSWERS WITH RATIONALES (VERIFIED ANSWERS)
|ALREADY GRADED A+
what is the anion gap - answer-Concentration of anions (Cl and HCO3) to cations (Na and K) in the ECF,
by rule, the concentrations should be relatively equal
relationship of anion gap and metabolic acidosis - answer--metabolic acidosis is characterized as either
normal anion gap metabolic acidosis or elevated anion gap metabolic acidosis
-MA elevated gap - we know abnormal anions
-MA normal gap - we know that the cause is loss of bicarbonate
What are the causes of elevated anion gap in metabolic acidosis - answer-P - paraldehyde
L - lactic acidosis
U - uremia
M - Methanol
S - Salicylates
E - Ethanol
E - Ethylene Glycol
D - DKA
S - Starvation
calculate the anion gap - answer-AG = (Na + K) - (Cl + HCO3)
relationship between metabolic alkalosis and hydrogen - answer--bicarb generation is coupled with
hydrogen secretion
-increase in bicarb can be due to loss of hydrogen ions - usually from GI losses or shift from ECF to ICF
explain buffers in metabolic acidosis - answer--buffer systems compensate for excess acid and attempt
to maintain pH.
,-H+ into cell, K+ out
-acidosis severe then buffers depleted cannot compensate and pH continues to decrease
-there is also an increase in Ca because acidosis decreases the amount of Ca bound to albumin
What is compensation in ABG's - answer--metabolic (renal) and respiratory (pulmonary) counter
adjustments to try to fix pH imbalance in ABG's ex. metabolic alkalosis means high bicarb, respiratory
will try to compensate by retaining CO2 into blood
partial compensation - answer-systemic arterial blood pH is still lower than 7.35
example - respiratory acidosis, renal system tries to balance by reabsorbing bicarb (bc high bicarb will
raise pH) but is not enough to reach WDL
full compensation - answer-pH is normal, pCO2 and HCO3 are abnormal
3 pathophysiolgical types of AKI - answer-prerenal
intrarenal (intrinsic) postrenal
nonoliguria vs oliguria vs anuria - answer-nonoliguria - daily volume >500
oliguria - daily volume <500 anuria <100
prerenal AKI etiologies - answer--hypovolemia
-hemorrhagic blood loss (trauma, GI bleeding, complications of childbirth)
-loss of plasma volume (burns, peritonitis)
-water and electrolyte losses (severe vomiting, diarrhea, obstruction, diabetes, diuretics)
-hypotension or hypoperfusion
-septic shock
-cardiac failure
-massive pulmonary embolism
-stenosis
,-increased intraabdominal pressure
intrarenal AKI etiologies - answer--acute tubular necrosis
-glomerulopathies
-acute interstitial necrosis (tumors or toxins)
-vascular damage
-malignant HTN, vasculitis
-coagulation defects
-renal artery/vein occlusion
-bilateral acute pyelonephritis
postrenal AKI etiologies - answer--obstructive uropathies (usually bilateral - fibrosis)
-ureteral destruction (edema, tumors, stones, clots)
-bladder neck obstruction (enlarged prostate)
-neurogenic bladder
how does urinary sediment differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN), and
postrenal AKI - answer-normal - bland prerenal - bland intrarenal (G) - active (hallmark) intrarenal (ATN)
- muddy brown casts, renal tubular epithelial cells postrenal - bland
how does urine sodium differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN), and
postrenal AKI - answer-normal - 20 mEq/L prerenal - <10 mEq/L intrarenal (G) - <20 mEq/L
intrarenal (ATN) - >40 mEq/L postrenal
- usually low
how does urine osmolality differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN) -
answer-normal - 300 - 900 mOsm prerenal - > 500 mOsm (high) intrarenal (G) - > 500 mOsm
intrarenal (ATN) - <300 mOsm postrenal -
, how does proteinuria differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN), and
postrenal AKI - answer-normal - 0 - 20 mg/dL prerenal - 5 - 20 mg/dL intrarenal (G) - > 100 mg/dL
presence of proteinuria intrarenal (ATN) - 5-20 mg/dL postrenal - 5-20 mg/dL
how does specific gravity differentiate prerenal, intrarenal (ATN) - answer-normal - 1.00 - 1.03
prerenal - >1.020 intrarenal (ATN) - 1.010 - 1.012 (low)
how does BUN/Cr ratio differentiate prerenal, intrarenal (glomerulonephritis), intrarenal (ATN), and
postrenal AKI - answer-normal - 10 - 20:1 prerenal - >20:1 intrarenal (G) - 10 - 20:1 intrarenal (ATN)
- 10 - 20:1 postrenal - >20:1
glomerulonephritis - answer-injury to the glomeruli typically from systemic disease usually immunologic
in etiology
what distinguishes glomerulonephritis from pre-renal AKI - answer-azotemia (BUN and Cr will be
elevated active urinary sediment proteinuria
acute tubular necrosis - answer-damage to the renal tubules due to presence of toxins in the urine or to
ischemia most common cause of hospital acquired ARF
distinguish ATN from prerenal - answer-UA: granular muddy brown casts
no significant increase in protein urine sodium is >20 (FE NA >3%)
FeUrea is elevated BUN/CR is normal
does not respond to volume replacement
GFR - answer-the filtration of plasma per unit of time the
sum of the filtration rate of all the functioning nephrons
normal value - 90 - 120
