NR 341 EXAM 3 STUDY NOTES
Exam 3
Adrenal Crisis “Addisonian Crisis” p. 1178-1179
- A condition in which the pituitary gland doesn’t make enough
adrenocorticotropic hormone or ACTH
- A medical emergency and potentially life-threatening situation and
require immediate emergency treatment
- Causes of Adrenal Crisis
When the body cannot produce sufficient amounts of cortisol
Caused by either previously undiagnosed or untreated Addison’s
disease
Suddenly stopping intake of glucocorticoids
- Signs and Symptoms of Adrenal Crisis
Weakness
Mental confusion – loss of consciousness
Dizziness
N/V
Extreme low BP
Chills
Rash
Sweating
High HR
- Diagnosis and Treatment of Adrenal Crisis
Cosyntropin stimulation test
Cortisol level test
Immediate injection of hydrocortisone
- Kidneys filter blood and regulate blood pressure
Acute Kidney Injury p. 1070-1074
- Acute kidney injury (acute renal failure – ARF)
Sudden deterioration of renal function
Changes in the vital signs
Signs of hypo- or hypervolemia
Patient history
o Predisposing factors
Disease states
o HTN
o DM
o Immunologic disease
o Hereditary disorders
Hypotensive episodes
Exposure to nephrotoxic agents
- Clinical Presentation of AKI
1
, Vital signs may be altered
o BP changes depending on etiology
o Hyperventilation to compensate for metabolic acidosis
o Body temperature may be altered
Assess for volume depletion and volume overload
- Laboratory Test of AKI
Serum creatinine
Serum BUN
o Affected by catabolism, bleeding, and dehydration
BUN: Creatinine ration
o Normal 10:1 to 20:1
o More than 20:1, suspect non-renal causes of laboratory
abnormalities
Urine creatinine clearance
o Estimate of GFR
o 24-hour urine; specific collection protocol
o Normal 84-138 mL/min
o Can calculate an estimated value with serum lab values
(Cockroft and Gault formula)
Urine electrolytes
Urine specific gravity
Urine osmolarity
- Hyperkalemia
Due to decreased GFR
Reduced content
o Kayexalate
o Mineralocorticoids
o Diuretics
Shift intracellularly
o Glucose and insulin
o Alkali (sodium bicarbonate)
Antagonize cellular membrane effect
o Calcium gluconate
- Hyponatremia
Related to fluid overload
Salt wasting can occur as nephron are damaged
Treatment – fluid and sodium restriction
- AKI – Acid Base Imbalances
Metabolic acidosis
o Treatment based on severity of imbalance
o May need IV bicarbonate
o Monitor ionized calcium as hypocalcemia can occur as pH
is corrected
- Fluid and Electrolyte Imbalances
Hyperkalemia
2
, o Low excretion
Hyponatremia
o Fluid retention
Hypocalcemia
o Low excretion of phosphorus
o Decreased level of vitamin D
Hyperphosphatemia
o Low excretion
Hypermagnesium
o Low excretion
- AKI – Diagnostic Studies
Non-invasive tests
o X-ray of kidneys, ureter, and bladder (KUB)
Size, shape, and position of kidneys
Calculi, cysts, and tumors
o Renal ultrasound
Size of kidneys
Obstruction
Invasive tests
o IV pyelogram
o Computed tomography
Structures, accumulation of fluid
o Renal angiography
Abnormalities in blood flow; infarction, masses
o Renal scan
Renal uptake of isotopes
o Renal biopsy
Histologic changes
- AKI Course (slide 12 – didn’t talk about)
Initiation Phase
o Time from event to signs of decreased renal perfusion
Few hours to 2 days
o Potentially reversible
Maintenance Phase (oliguric / anuric)
Recovery Phase
- AKI – Diuretic Therapy
Controversial
o Convert oliguria to non-oliguric state
Hypovolemia corrected first
Loop (furosemide)
Osmotic (mannitol)
- AKI – Drug therapy
Dopamine
o May increase renal blood flow
o Efficacy questioned in current research
3
, Acetylcysteine (antidote for Tylenol)
o Prevent contrast-induced acute renal failure
Epoetin alfa
o Treat anemia
Must adjust dosages and timing of medication if client on dialysis
- AKI – Dietary Management
Higher than normal basal requirement
Provide adequate energy, protein, and micronutrients
25-35 kcal.kg of ideal body weight per day
Restricted
o Protein
o Sodium
o Potassium
o Fluid intake (output +600-1000mL)
- AKI – Causes
Pre-renal
o Diminished blood flow; hypoperfusion of the kidney
Volume depletion
Vasodilation
Decreased cardiac output
o Can progress to intra-renal damage
o Increased BUN/creatinine ratio to greater than 20:1
Post-renal
o Obstruction of flow
o Increased intratubular pressure leading to decreased GFR
o Reverses when obstruction is removed
Intra-renal
o Kidney tissue affected directly
o Glomerular, vascular, and/or hematologic problem
o Acute tubular necrosis (ATN)
Ischemia
Nephrotoxic agents
o Antibiotics – aminoglycosides
o NSAIDs
Contrast – induced
Rhabdomyolysis
Nervous System p. 1306-1311, p. 1314-1334
- Cerebral Perfusion Pressure
CPP=MAP-ICP
Normal CPP= 60-100
Low CPP results in loss of autoregulation and hypoxic insult to
brain tissue
- Increased ICP s/s:
Changes in LOC; most often first sign
4
Exam 3
Adrenal Crisis “Addisonian Crisis” p. 1178-1179
- A condition in which the pituitary gland doesn’t make enough
adrenocorticotropic hormone or ACTH
- A medical emergency and potentially life-threatening situation and
require immediate emergency treatment
- Causes of Adrenal Crisis
When the body cannot produce sufficient amounts of cortisol
Caused by either previously undiagnosed or untreated Addison’s
disease
Suddenly stopping intake of glucocorticoids
- Signs and Symptoms of Adrenal Crisis
Weakness
Mental confusion – loss of consciousness
Dizziness
N/V
Extreme low BP
Chills
Rash
Sweating
High HR
- Diagnosis and Treatment of Adrenal Crisis
Cosyntropin stimulation test
Cortisol level test
Immediate injection of hydrocortisone
- Kidneys filter blood and regulate blood pressure
Acute Kidney Injury p. 1070-1074
- Acute kidney injury (acute renal failure – ARF)
Sudden deterioration of renal function
Changes in the vital signs
Signs of hypo- or hypervolemia
Patient history
o Predisposing factors
Disease states
o HTN
o DM
o Immunologic disease
o Hereditary disorders
Hypotensive episodes
Exposure to nephrotoxic agents
- Clinical Presentation of AKI
1
, Vital signs may be altered
o BP changes depending on etiology
o Hyperventilation to compensate for metabolic acidosis
o Body temperature may be altered
Assess for volume depletion and volume overload
- Laboratory Test of AKI
Serum creatinine
Serum BUN
o Affected by catabolism, bleeding, and dehydration
BUN: Creatinine ration
o Normal 10:1 to 20:1
o More than 20:1, suspect non-renal causes of laboratory
abnormalities
Urine creatinine clearance
o Estimate of GFR
o 24-hour urine; specific collection protocol
o Normal 84-138 mL/min
o Can calculate an estimated value with serum lab values
(Cockroft and Gault formula)
Urine electrolytes
Urine specific gravity
Urine osmolarity
- Hyperkalemia
Due to decreased GFR
Reduced content
o Kayexalate
o Mineralocorticoids
o Diuretics
Shift intracellularly
o Glucose and insulin
o Alkali (sodium bicarbonate)
Antagonize cellular membrane effect
o Calcium gluconate
- Hyponatremia
Related to fluid overload
Salt wasting can occur as nephron are damaged
Treatment – fluid and sodium restriction
- AKI – Acid Base Imbalances
Metabolic acidosis
o Treatment based on severity of imbalance
o May need IV bicarbonate
o Monitor ionized calcium as hypocalcemia can occur as pH
is corrected
- Fluid and Electrolyte Imbalances
Hyperkalemia
2
, o Low excretion
Hyponatremia
o Fluid retention
Hypocalcemia
o Low excretion of phosphorus
o Decreased level of vitamin D
Hyperphosphatemia
o Low excretion
Hypermagnesium
o Low excretion
- AKI – Diagnostic Studies
Non-invasive tests
o X-ray of kidneys, ureter, and bladder (KUB)
Size, shape, and position of kidneys
Calculi, cysts, and tumors
o Renal ultrasound
Size of kidneys
Obstruction
Invasive tests
o IV pyelogram
o Computed tomography
Structures, accumulation of fluid
o Renal angiography
Abnormalities in blood flow; infarction, masses
o Renal scan
Renal uptake of isotopes
o Renal biopsy
Histologic changes
- AKI Course (slide 12 – didn’t talk about)
Initiation Phase
o Time from event to signs of decreased renal perfusion
Few hours to 2 days
o Potentially reversible
Maintenance Phase (oliguric / anuric)
Recovery Phase
- AKI – Diuretic Therapy
Controversial
o Convert oliguria to non-oliguric state
Hypovolemia corrected first
Loop (furosemide)
Osmotic (mannitol)
- AKI – Drug therapy
Dopamine
o May increase renal blood flow
o Efficacy questioned in current research
3
, Acetylcysteine (antidote for Tylenol)
o Prevent contrast-induced acute renal failure
Epoetin alfa
o Treat anemia
Must adjust dosages and timing of medication if client on dialysis
- AKI – Dietary Management
Higher than normal basal requirement
Provide adequate energy, protein, and micronutrients
25-35 kcal.kg of ideal body weight per day
Restricted
o Protein
o Sodium
o Potassium
o Fluid intake (output +600-1000mL)
- AKI – Causes
Pre-renal
o Diminished blood flow; hypoperfusion of the kidney
Volume depletion
Vasodilation
Decreased cardiac output
o Can progress to intra-renal damage
o Increased BUN/creatinine ratio to greater than 20:1
Post-renal
o Obstruction of flow
o Increased intratubular pressure leading to decreased GFR
o Reverses when obstruction is removed
Intra-renal
o Kidney tissue affected directly
o Glomerular, vascular, and/or hematologic problem
o Acute tubular necrosis (ATN)
Ischemia
Nephrotoxic agents
o Antibiotics – aminoglycosides
o NSAIDs
Contrast – induced
Rhabdomyolysis
Nervous System p. 1306-1311, p. 1314-1334
- Cerebral Perfusion Pressure
CPP=MAP-ICP
Normal CPP= 60-100
Low CPP results in loss of autoregulation and hypoxic insult to
brain tissue
- Increased ICP s/s:
Changes in LOC; most often first sign
4