NR 341 COMPLEX ADULT HEALTH MIDTERM EXAM 2025/2026
EVALUATION QUESTIONS WITH ANSWERS GRADED A+
Calcium Gluconate - Prevents and treats cardiac toxicity related to
increased K+ levels
What is the purpose of Continuous Renal Replacement Therapy (CRRT)? -
Dialysis
This is a blood filtering therapy that replaced the normal blood-filtering
function of the kidneys in patients with renal failure and acute kidney
injuries.
The prerenal system - Delivers blood to the kidneys.
A prerenal block is: - An interruption on the way to the kidneys.
The intrarenal system - Processes ultra-filtrate by tubular secretion & re-
absorption.
An intrarenal block is: - Direct damage to the kidneys.
The postrenal system - Excretes kidney waste products through the
ureters, bladder, and urethra.
A postrenal block is: - Obstruction of urine output.
Causes:
Enlarged prostate
Kidney stones
Bladder tumor
Bladder injury
S/SX of the oliguric phase of acute kidney injury (AKI): - <400 mL/24hr
Increase BUN, Cr, uric acid, K, Mg
Metabolic Acidosis
S/SX of the diuretic phase of acute kidney injury (AKI): - Urine output 1-
3L/day
Decreased K & Na
S/SX of the risk stage of acute kidney injury (AKI): - Cr >1.5xbaseline
,Urine output <0.5ml/kg/hr for 6+ hours
S/SX of the injury stage of acute kidney injury (AKI): - Cr >2xbaseline
Urine output <0.5ml/kg/hr for 12+ hours
S/SX of the risk failure of acute kidney injury (AKI): - Cr >3xbaseline
Urine output <0.3ml/kg/hr for 12+ hours
Priority assessment findings of acute kidney injury (AKI): - Respiratory:
Crackles
Pleural Effusion
Kussmaul respirations
Cardiovascular:
CHF, hypo/hypertension
Cardiac dysrhythmias
Pericarditis, pericardial effusion
Neurologic:
Altered mentation, confusion, lethargy
Decreased seizure threshold
S/SX of hypovolemic shock: - Elevated HR, decreased BP, tachypnea,
oliguria, cool pale skin, decreased mental status, flat neck veins, decreased
CO CI RAP PAP PAOP, elevated SVR, decreased SvO2.
Dehydration causes elevated HCT
Blood loss causes decreased HCT
Possible causes of hypovolemic shock: - External loss of blood
External loss of fluid
Internal sequestration of blood fluid (3rd spacing)
Management of hypovolemic shock: - Eliminate and treat the cause
Replace lost volume with appropriate fluid (NS or LR)
Initial shock - Inadequate intravascular volume
Initial shock clinical presentation: - There are no obvious clinical indications
of hypoperfusion seen in this stage of shock
May see a drop in cardiac output
Compensatory shock - Inadequate myocardial contractility
, Compensatory shock neural compensation S/SX: - HR & contractility
increase
Systemic vasoconstriction and redistribution of blood occurs
Venous vasoconstriction augments venous return to the heart
Blood is shunted from the kidneys, GI tract, and skin
Respiratory rate and depth are increased
Increased blood glucose levels
Dilated pupils, peripheral vasoconstriction, Sweat gland activity causing
cool moist skin
Compensatory shock endocrine compensation S/SX: - Increased blood
glucose
Reabsorbtion of salt and water increasing intracascular volume and BP
RAAS >Renin > Angiotensinogen > Angiotensinogen 1 > Angiotensinogen
2 > increases BP and venous return to the heart
Angiotensinogen 2 activates the adrenal cortex for the release of
aldosterone
Compensatory shock chemical compensation S/SX: - Perfusion begins to
decline
Rate and depth of respiration increase
Hyperventillation >CO2 is released > Respiratory alkalosis occurs
Vasoconstriction of cerebral blood vessels occurs > Cerebral hypoxia &
ischemia may result
Compensatory shock clinical presentation: - Elevated HR
Narrowed pulse pressure
Rapid, deep respirations causing respiratory alkalosis
Thirst
Cool, moist skin
Oliguria
Diminished bowel sounds
Restlessness > confusion
Hyperglycemia
Increased urine specific gravity
Decreased creatinine clearance
Progressive shock S/SX: - Ischemia in extremities
Weak or absent peripheral pulses
EVALUATION QUESTIONS WITH ANSWERS GRADED A+
Calcium Gluconate - Prevents and treats cardiac toxicity related to
increased K+ levels
What is the purpose of Continuous Renal Replacement Therapy (CRRT)? -
Dialysis
This is a blood filtering therapy that replaced the normal blood-filtering
function of the kidneys in patients with renal failure and acute kidney
injuries.
The prerenal system - Delivers blood to the kidneys.
A prerenal block is: - An interruption on the way to the kidneys.
The intrarenal system - Processes ultra-filtrate by tubular secretion & re-
absorption.
An intrarenal block is: - Direct damage to the kidneys.
The postrenal system - Excretes kidney waste products through the
ureters, bladder, and urethra.
A postrenal block is: - Obstruction of urine output.
Causes:
Enlarged prostate
Kidney stones
Bladder tumor
Bladder injury
S/SX of the oliguric phase of acute kidney injury (AKI): - <400 mL/24hr
Increase BUN, Cr, uric acid, K, Mg
Metabolic Acidosis
S/SX of the diuretic phase of acute kidney injury (AKI): - Urine output 1-
3L/day
Decreased K & Na
S/SX of the risk stage of acute kidney injury (AKI): - Cr >1.5xbaseline
,Urine output <0.5ml/kg/hr for 6+ hours
S/SX of the injury stage of acute kidney injury (AKI): - Cr >2xbaseline
Urine output <0.5ml/kg/hr for 12+ hours
S/SX of the risk failure of acute kidney injury (AKI): - Cr >3xbaseline
Urine output <0.3ml/kg/hr for 12+ hours
Priority assessment findings of acute kidney injury (AKI): - Respiratory:
Crackles
Pleural Effusion
Kussmaul respirations
Cardiovascular:
CHF, hypo/hypertension
Cardiac dysrhythmias
Pericarditis, pericardial effusion
Neurologic:
Altered mentation, confusion, lethargy
Decreased seizure threshold
S/SX of hypovolemic shock: - Elevated HR, decreased BP, tachypnea,
oliguria, cool pale skin, decreased mental status, flat neck veins, decreased
CO CI RAP PAP PAOP, elevated SVR, decreased SvO2.
Dehydration causes elevated HCT
Blood loss causes decreased HCT
Possible causes of hypovolemic shock: - External loss of blood
External loss of fluid
Internal sequestration of blood fluid (3rd spacing)
Management of hypovolemic shock: - Eliminate and treat the cause
Replace lost volume with appropriate fluid (NS or LR)
Initial shock - Inadequate intravascular volume
Initial shock clinical presentation: - There are no obvious clinical indications
of hypoperfusion seen in this stage of shock
May see a drop in cardiac output
Compensatory shock - Inadequate myocardial contractility
, Compensatory shock neural compensation S/SX: - HR & contractility
increase
Systemic vasoconstriction and redistribution of blood occurs
Venous vasoconstriction augments venous return to the heart
Blood is shunted from the kidneys, GI tract, and skin
Respiratory rate and depth are increased
Increased blood glucose levels
Dilated pupils, peripheral vasoconstriction, Sweat gland activity causing
cool moist skin
Compensatory shock endocrine compensation S/SX: - Increased blood
glucose
Reabsorbtion of salt and water increasing intracascular volume and BP
RAAS >Renin > Angiotensinogen > Angiotensinogen 1 > Angiotensinogen
2 > increases BP and venous return to the heart
Angiotensinogen 2 activates the adrenal cortex for the release of
aldosterone
Compensatory shock chemical compensation S/SX: - Perfusion begins to
decline
Rate and depth of respiration increase
Hyperventillation >CO2 is released > Respiratory alkalosis occurs
Vasoconstriction of cerebral blood vessels occurs > Cerebral hypoxia &
ischemia may result
Compensatory shock clinical presentation: - Elevated HR
Narrowed pulse pressure
Rapid, deep respirations causing respiratory alkalosis
Thirst
Cool, moist skin
Oliguria
Diminished bowel sounds
Restlessness > confusion
Hyperglycemia
Increased urine specific gravity
Decreased creatinine clearance
Progressive shock S/SX: - Ischemia in extremities
Weak or absent peripheral pulses
