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MSN570 STUDY GUIDE 2026
COMPREHENSIVE ANSWER DIGEST
◉hemophilia labs. Answer: - Normal PT with prolonged PTT**
- Decreased Factor VIII in Hemophilia A
- Decreased Factor IX in B
- Normal platelet count in both ◉hemophilia genetics. Answer: Females carriers, males exclusively affected Long arm of X chromosome Unaffected mothers give to 50% of sons ◉hemophilia complications. Answer: Intracranial hemorrhage in neonates Joint bleed (hemarthrosis)- pain Anemia Early/infant death, increasing death risk with age Blood-borne infection Pseudotumors
◉hemophilia treatment. Answer: clotting factor transfusions, recombinant clotting factors, desmopressin (DDAVP), and bleed precautions ◉gallbladder role. Answer: stores and concentrates bile ◉cholecystitis. Answer: inflammation of the gallbladder ◉cholelithiasis. Answer: gallstones ◉cholecystitis referred pain. Answer: right shoulder from stimulation of phrenic nerve ◉cholesterol gallstone. Answer: most common type of gallstone ◉What are pigmented gallstones composed of?. Answer: Calcium bilirubinate, bilirubin polymers, bile acids, iron, and phosphorus ◉What colors can pigmented gallstones be?. Answer: Black, dark brown, yellow, or green ◉gallstone imaging. Answer: ultra sound
◉What is central diabetes insipidus (CDI) characterized by?. Answer: Lack of ADH production ◉What causes central diabetes insipidus (CDI) in terms of hormone production?. Answer: Absolute ADH deficiency ◉Nephrogenic diabetes insipidus (NDI). Answer: results when ADH secretion is normal but the ADH receptor, or the response to ADH, in the kidney is abnormal. ◉How does central diabetes insipidus (CDI) typically present in terms of blood ADH levels?. Answer: Presents with low blood ADH ◉Nephrogenic diabetes insipidus (NDI) treatment. Answer: desmopressin ◉Central diabetes insipidus (NDI) treatment. Answer: vasopressin ◉antidiuretics are released from. Answer: posterior pituitary gland ◉BUN normal ranges. Answer: 10- 20 ◉creatinine normal ranges. Answer: 0.6-1.
◉Normal urinary output. Answer: 0.5 ml/kg/hr ex: 130 lb/2.2 lb/kg = 59 kg 0.5 mL/kg/hr * 60 kg = 30 mL/hr ◉causes of tubular necrosis. Answer: Ischemia- Inadequate blood flow to kidneys Nephrotoxic-exposure to kidney toxins sepsis-reduced blood flow from hypotension ◉pathophysiology tubular necrosis. Answer: - ischemia or nephrotoxin exposure occurs to the renal tubules
- inflammation and tubular injury occur
- cast formation and tubular obstruction occurs
- tubular injury, leakage, increased glomerular pressure causes decreased capillary perfusion further decrease in GFR occurs
- oliguria results ◉What are the signs of tubular necrosis related to urine output?. Answer: Decreased urine output or oliguria
◉tubular necrosis treatments. Answer: u Addressing the underlying cause (BP, infection, nephrotoxic medications) u Fluid and electrolyte management u Diuretics (Furosemide) u Dialysis (RRT) ◉acute renal failure diagnosis. Answer: Measure levels of creatinine in your blood used to calculate your GFR ◉Normal GFR. Answer: * GFR > ◉kidney disease GFR. Answer: * GFR < ◉kidney failure. May need dialysis or kidney transplant.. Answer: * GFR < ◉Renal failure urine test. Answer: Albumin is a protein normally found in your blood > Healthy kidneys do not let albumin pass into the urine ◉What are the leading causes of renal failure?. Answer: Diabetes and high blood pressure
◉What percentage of new renal failure cases do diabetes and high blood pressure account for?. Answer: 75% ◉What are some other common risk factors for renal failure?. Answer: Heart disease, obesity, family history of CKD ◉renal failure pathophysiology. Answer: low GFR, Juxtaglomerular cells feel low filtrate, stim RAAS system, inc in Na and water retention by aldosterone. Causes inc in BP =Causes edema. The more pressure we have in body, the more fluid leaks outside vessels and goes to cells. Low Na also gives us pitting edema. ◉renal failure sings and symptoms. Answer: fatigue, nausea, confusion, and difficulty concentrating. edema, cramps, and dry or itchy skin can also occur. In addition, poor appetite or food or beverage may taste metallic. In addition, chest pain and shortness of breath are non-specific symptoms of kidney disease. These are also caused by other conditions. Since the kidneys can still make up for lost functions, patients do not experience any of these symptoms until they have irreversible damage.
◉normal B12 levels. Answer: 200-900 pg/mL ◉pernicious anemia antibodies. Answer: intrinsic factor ◉megaloblastic anemia. Answer: a blood disorder characterized by anemia in which the red blood cells are larger than normal ◉megaloblastic anemia examples. Answer: pernicious anemia ◉What blood test is used to determine the type and degree of anemia in pernicious anemia?. Answer: Complete blood count (CBC) ◉Which blood test checks if the bone marrow can make new red blood cells in pernicious anemia?. Answer: Reticulocyte count ◉What does an extremely high level of LDH enzyme indicate in pernicious anemia?. Answer: Possible pernicious anemia ◉Which blood test confirms vitamin B12 deficiency in pernicious anemia?. Answer: Methylmalonic acid (MMA) levels ◉What does a high homocysteine level indicate in pernicious anemia?. Answer: It is used to test if there is a presence of the
antibodies that attack the parietal cells in the stomach and block the action of intrinsic factor. ◉What test is used to check for the presence of antibodies that attack parietal cells in the stomach in pernicious anemia?. Answer: Homocysteine level ◉What procedure is done to see if there is degeneration or atrophy of the stomach lining in pernicious anemia?. Answer: Upper endoscopy ◉What race is at higher risk for pernicious anemia?. Answer: Northern European (White) ◉What age group is more susceptible to pernicious anemia?. Answer: People over 60 years old ◉How does family history influence the risk of pernicious anemia?. Answer: Having a family history of autoimmune diseases ◉How does stomach surgery relate to pernicious anemia risk?. Answer: Having had part or all of the stomach surgically removed
Renal failure Sepsis Pseudocysts or abscesses ◉chronic pancreatitis. Answer: Persistent inflammation leads to irreversible changes Most common cause: alcohol consumption Ductal obstruction Acinar Fibrosis Atrophy ◉Acute pancreatitis symptoms. Answer: Severe midepigastric pain. Pain is frequently acute in onset, occurring 24 to 48 hours after a very heavy meal or alcohol ingestion, and it may be diffuse and difficult to localize. It is generally more severe after meals and is unrelieved by antacids. ◉Pancreatitis Clinical Manifestations. Answer: upper left to mid epigastric pain nausea vomiting low grade fever leukocytosis
hypotension tachycardia Jaundice ◉pancreatitis pathophysiology. Answer: Premature Activation of Pancreatic enzymes ◉pancreatitis treatment. Answer: fasting, TPN, advancing diet from clear liquids to low fat, low-residue pancreatic enzyme supplements maintaining hydration and fluid balance Treatment of nausea/vomiting ◉Pancreatitis treatment complications. Answer: Glucose control and insulin for hyperglycemia due to pancreatic damage dialysis for renal failure blood transfusions for hemorrhages management of Acute Respiratory Distress Syndrome (ARDS) ◉What lab tests are used in the diagnosis of pancreatitis?. Answer: Amylase and lipase levels, Liver enzymes (AST and ALT), Bilirubin
◉Wolff's Law. Answer: A bone grows or remodels in response to forces or demands placed upon it ◉myasthenia gravis. Answer: a chronic autoimmune disease that affects the neuromuscular junction and produces serious weakness of voluntary muscles ◉myasthenia gravis patho. Answer: autoantibodies against ACh receptors at the neuromuscular junction ◉What is the mechanism of action of Pyridostigmine?. Answer: Anticholinesterase - increases ACh ◉How does Pyridostigmine affect muscle strength?. Answer: Increases muscle strength ◉What condition is Pyridostigmine used for?. Answer: Myasthenia gravis (long acting) ◉proliferative phase of wound healing. Answer: Fibroblasts provide increased collagen production tensile strength inflammation and edema
4 days-1 month ◉maturation stage of wound healing. Answer: - begins 3 weeks to 6 months after injury
- collagen remodeled (scar flattens) ◉Wound Resolution. Answer: Returning injured tissue to the original structure and function ◉decubitus. Answer: bedsore ◉nociceptive pain. Answer: normal process that results in noxious stimuli being perceived as painful ◉diabetes insipidus (NDI) treatment. Answer:
