INSTANT PDF DOWNLOAD — This comprehensive review resource for the NR 574 Acute Care Practicum I Final Exam at Chamberlain University features verified questions and answers with detailed rationales aligned with the AG-ACNP curriculum and acute care management standards. It includes 450+ exam-style questions covering Weeks 5-8 content, clinical decision-making, diagnostic interpretation, and evidence-based interventions for complex patient presentations.
Rhabdomyolysis Management – Diagnostic criteria include dark urine OR acute neuromuscular illness without other symptoms PLUS acute elevation in serum CK (at least 5x upper limit of normal). The most reliable test for diagnosis is CK, which typically exceeds 1000 and rises within 2-12 hours, peaking around 24-72 hours following injury. Electrolyte imbalances commonly seen include hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia. Treatment includes isotonic IVF at 400 cc/hr ASAP titrated to maintain urine output of at least 200 cc/hr; CK 15,000 requires 6+ liters to prevent acute renal failure. Treat hyperkalemia with IV glucose, insulin, sodium bicarbonate, or sodium polystyrene sulfonate; hemodialysis for severe refractory cases. Consult nephrology for AKI, orthopedics for suspected compartment syndrome requiring fasciotomy.
Burn Management and Parkland Formula – Parkland formula: TBSA (%) x weight (kg) x 4 mL = total fluids in first 24 hours; half given in first 8 hours. Example: 75% TBSA x 80 kg x 4 = 24L total; 12L given in first 8 hours. Applies to patients with burns 20% TBSA, 2nd-degree or higher. Indications for transfer to certified burn center include burns 20% TBSA, burns to face/head/neck/genitals, circumferential extremity or chest burns, full-thickness burns 5%, burns over joints, burns with inhalation injury, electrical burns. Rule of Nines for adults (age 14): anterior head 9%, chest 9%, abdomen 9%, right arm 9%, left arm 9%, perineum 1%, front right leg 9%, front left leg 9%, posterior upper back 9%. Absolute indications for endotracheal intubation in burns include stridor and circumferential burns to the neck. Priority diagnostic studies for burn patients with head/neck/face involvement include carboxyhemoglobin (CO) level and ABGs. Decreased urine output in burn injury within first 24 hours generally indicates need for fluid challenge; provide 1L rapid bolus of lactated Ringers.
Hepatorenal Syndrome (HRS) – Functional form of renal failure occurring primarily in patients with cirrhosis and ascites. Subjective presentation: known diagnosis of acute or chronic liver disease presenting with dysgeusia (altered taste perception), malaise, fatigue, decreased urine output. Diagnostic criteria include: cirrhosis with ascites; increase in Cr 0.3 mg/dL within 48 hours or 50% increase from baseline within 7 days; no response to 2-day diuretic withdrawal and volume expansion with albumin 1g/kg body weight; absence of shock; no nephrotoxic drug use; no macroscopic signs of structural kidney injury (proteinuria 500 mg/dL, microhematuria 50 RBCs per high-power field, and/or abnormal renal ultrasonography). Surgical intervention for HRS is TIPS procedure.
Acute Intestinal Obstruction – Risk factors include adhesions from previous abdominal surgeries, internal or external hernias, foreign bodies, feces, congenital issues (atresia, stenosis, cyst formation, intestinal duplication, malrotation), trauma (hematoma formation), inflammation (IBD, diverticulitis, radiation, TB), volvulus, ischemic injury, intussusception, intraperitoneal abscess, endometriosis, neoplasms. Subjective findings: colicky abdominal pain (crampy, umbilical initially; later becomes constant and diffuse), vomiting (more significant with proximal obstruction), abdominal bloating, obstipation. Objective findings: fever, high-pitched tinkling bowel sounds (may be hypoactive or absent with complete obstruction), abdominal distention (more significant with distal obstruction), mild abdominal tenderness with no peritoneal findings, tender abdominal or groin masses (incarcerated hernia), signs of shock (tachycardia, hypotension, oliguria).
Acute Mesenteric Ischemia (AMI) – Oral contrast should be avoided in suspected AMI as it can obscure bowel wall enhancement and mesenteric vessels. CT abdomen and pelvis with IV contrast is usually the first imaging to evaluate patients with severe acute abdominal pain; may show SMV or SMA thrombosis, portal venous gas, intestinal pneumatosis, ischemia of other organs, lack of bowel enhancement, thickened bowel wall, mesenteric fat stranding, or pneumoperitoneum.
Acetaminophen Overdose – Treatment includes activated charcoal given within first 4 hours of intentional overdose. Serial monitoring of liver enzymes (AST, ALT), coagulation parameters (INR, factor V levels), arterial pH, and serial assessment of mental status to determine stage of encephalopathy. N-acetylcysteine (NAC) provides protection from hepatotoxicity if given within 12 hours of non-staggered ingestion; IV NAC dosing: loading dose 150 mg/kg in D5W, then 50 mg/kg over 4 hours, followed by 100 mg/kg over 16 hours.
Hypothermia Management – Hypothermia can mimic clinical death; remember "you are not dead until you are warm and dead." Patients with hypothermia are extremely sensitive to movement; sudden movement can precipitate ventricular fibrillation.
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NR 574 Final Acute Care Practicum Review
Study Questions with Verified Answers and
Detailed Rationales Chamberlain
1. What are common trauma-related risk factors for rhabdomyolysis?
Correct Answer: Trauma, muscle compression, or ischemia.
Rationale:
1. Direct muscle injury from trauma releases intracellular contents into the
bloodstream.
2. Muscle compression (crush injuries) causes ischemia and cell death.
3. Prolonged ischemia leads to muscle necrosis and rhabdomyolysis.
2. What are examples of trauma-related causes of rhabdomyolysis?
Correct Answer: Compartment syndrome, crush injuries, lightning
strike, near-drowning, significant burns, blunt force trauma, high-
voltage electrical injuries, prolonged immobilization following a fall.
Rationale:
1. Compartment syndrome increases pressure within a muscle compartment,
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causing ischemia.
2. Crush injuries cause direct muscle cell death and release of myoglobin.
3. Electrical injuries and lightning strikes cause massive muscle necrosis.
4. Prolonged immobilization leads to pressure necrosis of muscle tissue.
3. What heat-related conditions can lead to rhabdomyolysis?
Correct Answer: Heatstroke, malignant hyperthermia, and neuroleptic
malignant syndrome.
Rationale:
1. Heatstroke causes systemic inflammation and muscle breakdown.
2. Malignant hyperthermia is a genetic reaction to anesthesia causing muscle
rigidity and breakdown.
3. Neuroleptic malignant syndrome is a reaction to antipsychotic medications
causing fever and muscle breakdown.
4. What infections can directly attack muscle and cause rhabdomyolysis?
Correct Answer: Epstein-Barr virus (EBV), cytomegalovirus (CMV),
adenovirus, human immunodeficiency virus (HIV), coxsackievirus,
influenza A/B, herpes simplex virus (HSV), Varicella-zoster virus (VZV),
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E. coli, C. perfringens, Legionella, Rickettsia, Group B beta-hemolytic
streptococci, S. pneumoniae, S. pyogenes.
Rationale:
1. Viral myositis from influenza, EBV, CMV, and HIV can cause muscle
breakdown.
2. Bacterial infections (C. perfringens, Group B strep, S. pneumoniae) can cause
necrotizing myositis.
3. Rickettsia and Legionella are associated with rhabdomyolysis in severe cases.
5. What metabolic factors can contribute to rhabdomyolysis?
Correct Answer: Electrolyte imbalances (hypocalcemia,
hypophosphatemia, hypokalemia, hypo- and hypernatremia),
hypothyroidism, hyperglycemic hyperosmolar nonketotic syndrome.
Rationale:
1. Hypokalemia impairs muscle blood flow and predisposes to necrosis.
2. Hypophosphatemia depletes ATP, leading to muscle cell injury.
3. Hypothyroidism can cause a myopathy that predisposes to rhabdomyolysis.
6. What are the genetic risk factors for rhabdomyolysis?
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Correct Answer: Phosphofructokinase deficiency, myoadenylate
deaminase deficiency, phosphoglycerate kinase deficiency,
mitochondrial respiratory chain enzyme deficiencies, sickle cell trait,
etc.
Rationale:
1. Metabolic myopathies impair energy production in muscle cells.
2. Sickle cell trait can cause exertional rhabdomyolysis in athletes.
3. These genetic defects predispose to muscle breakdown with exercise or stress.
7. What medications may cause direct myotoxicity leading to
rhabdomyolysis?
Correct Answer: HMG-CoA reductase inhibitors (statins), cyclosporin,
corticosteroids, zidovudine, colchicine, itraconazole.
Rationale:
1. Statins are the most common medication cause of rhabdomyolysis.
2. Colchicine toxicity causes neuromyopathy and muscle breakdown.
3. Zidovudine (AZT) causes mitochondrial toxicity in muscle.
8. What toxins may cause indirect myotoxicity leading to
rhabdomyolysis?