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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

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