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Inflammation and Infection Case Studies
Human Pathophysiology (NUR 252)
Creighton University
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Inflammation and Infection Case Studies (KEY)
- Mr. Davis is a 65-year-old male who presents to the emergency department (ED) with jaundice, ascites, and shortness of breath. He has a history of heavy alcohol consumption over the past 15 years. His wife recently died of cancer and he has stopped attending family functions.
A. What exemplar do you suspect Mr. Davis will be diagnosed with and why? Cirrhosis, based on the listed symptoms and history of heavy alcohol use.
B. What are risk factors for developing this condition, in addition to what the patient presents with in the case study? Heavy alcohol consumption, history of other liver disease/injury including hepatitis, biliary disease which can be caused by an autoimmune disorder or blockage of the bile duct.
C. Detail/diagram the pathophysiology of how the symptoms of jaundice, ascites, and complications of portal hypertension develop.
Jaundice - Bilirubin is the waste product of red blood cell destruction. This form of bilirubin is lipid soluble and must be transformed to a water-soluble product to be excreted. Albumin carries unconjugated bilirubin to the liver, where it detaches from the albumin and is then conjugated to a water-soluble product. Removal of this conjugated bilirubin is accomplished with bile salts that enter the intestine from the common bile duct. From the intestines, the bilirubin is broken down to urobilinogen, which is mostly eliminated in the feces (40–280 mg/day). A small part of the urobilinogen is directed back to the blood, where it is either eliminated in the urine (0–1 mg/day) or moved back to the liver. In liver disease, there is a deficiency of albumin to accomplish this task and the liver cells are damaged.
Ascites - Albumin, which is produced in the liver, is essential for maintenance of the oncotic pressure, thus helping to maintain the vascular system. With liver damage, albumin production stops, resulting in fluid leaking out of the vessels into the interstitial spaces and peritoneal cavity, causing edema and ascites. Reduced albumin causes the capillary hydrostatic pressure to exceed the osmotic pressure – this pushes the fluid into the peritoneal cavity.
Portal hypertension - The fibrous connective tissue of cirrhosis becomes damaged with the constriction of blood and bile flow in the liver lobules. This constriction forces blood out of the liver in vessels that have a lower pressure, thus contributing to portal hypertension. Blood is shunted to the spleen, causing splenomegaly. White blood cells (WBCs), red blood cells, and platelets are damaged in this engorged spleen, contributing to systemic effects from leukopenia, anemia, and thrombocytopenia, respectively.
D. What other complications can result from this exemplar? Anemia, hepatic encephalopathy, peritonitis, bleeding due to decrease in fat-soluble vitamins
E. What diagnostics tests would you anticipate being done to confirm the diagnosis? Bilirubin levels, AST, ALT, clotting factors/bleeding time, albumin, total protein, and ammonia levels.
- Mrs. Smith brings her 10-year-old son, Christopher, to the provider’s office. She states Christopher has had some swelling start around his face, he complains of fatigue often, and he recently recovered from a strep throat infection.
A. What exemplar do you suspect Christopher will be diagnosed with and why? Glomerulonephritis based on the symptom of edema and recent streptococcal infection.
B. What are risk factors for developing this condition, in addition to what the patient presents with in the case study? Recent strep infection, presence of other chronic disease including autoimmune disorders such as SLE
C. Detail/diagram the pathophysiology of how the symptoms of edema, hypovolemia, and hyperlipidemia develop in this exemplar.
Edema - The increased glomerular membrane permeability found in nephrotic syndrome is responsible for the massive excretion of protein in the urine. This results in decreased serum protein and subsequent edema formation.
Hypovolemia - Increased permeability due to glomerular damage allows RBCs and protein to leak out into the urine, this leads to decreased oncotic pressure and hypovolemia. With a lack of protein, vessels become more permeable and fluid leaks into vascular space.
Hyperlipidemia - The diminished plasma oncotic pressure from the decreased serum proteins stimulates hepatic lipoprotein synthesis, which results in hyperlipidemia. Initially, cholesterol and low- density lipoproteins are elevated. Later the triglyceride level is also increased. Fat bodies (fatty casts) commonly appear in the urine.
D. What other complications can result from this exemplar? Can lead to chronic renal failure if not treated
E. What diagnostics tests would you anticipate being done to confirm the diagnosis? Albumin, BUN, Creatinine, Total Protein, Urinalysis
- Mrs. Jones presents to the emergency department (ED) with abdominal pain in her abdomen rated as a 10/10, a fever, and jaundice. She has a history of gall stones (cholelithiasis/cholecystitis).
A. What exemplar do you suspect Mrs. Jones will be diagnosed with and why? Acute pancreatitis due to her presenting symptoms and history of gallbladder issues.
B. What are risk factors for developing this condition, in addition to what the patient presents with in the case study? Alcohol abuse, gallstones, viral infections, trauma, and abdominal surgery
C. Detail/diagram the pathophysiology of how the symptoms of pain, fever, and jaundice develop from this condition.
Pain - Pancreatitis that results from gallstone obstruction of the pancreatic ducts causes trapped digestive enzymes, usually trypsin, to autodigest the pancreatic tissue, activating an acute inflammatory response. Trypsin activates other enzymes, including lipase, elastase, and chymotrypsin.
- Mrs. Clark, a 52-year-old female presents to her provider with a large, reddened area on her left calf. She stated she scraped her leg on a tree branch when walking her dog a week ago. The redness has increased, the area is now painful, and she has a low-grade fever. Mrs. Clark also has a history of Type 2 diabetes mellitus.
A. What exemplar do you suspect Mrs. Clark will be diagnosed with and why? Cellulitis due to her presenting symptoms and risk factor of diabetes mellitus.
B. What are risk factors for developing this condition, in addition to what the patient presents with in the case study? The people who are most at risk for developing cellulitis include athletes, children, prisoners, residents of long-term care facilities, intravenous drug users, and individuals who have had prior MRSA exposure. In addition, individuals who are immunosuppressed, who have chronic liver or kidney disease, or who sustain animal or human bites are at higher risk.
C. Detail/diagram the pathophysiology of how the symptoms of redness, swelling, pain, and fever present in this condition.
Pain - release of chemical mediators including histamine, bradykinin, and prostaglandins stimulates nerve endings to produce pain
Redness - Injury to, or death of, tissue and release of chemical mediators leads to vasodilation and increased blood flow to the small vessels surrounding the area of injury; histamine plays a role in this process
Swelling - Injury to, or death of, tissue and release of chemical mediators occurs; swelling and partial retraction or separation of activated endothelial cells; increased vascular permeability and leakage of water, salts, fibrinogen (later becoming fibrin), and other small plasma proteins into the surrounding tissue; histamine plays a role in this process
Fever - Exogenous pyrogens (those of external origin) include bacterial endotoxins, viruses, antigen- antibody complexes, etc. Endogenous pyrogens are produced by phagocytic white blood cells as part of the immune response and include interleukin-1, interleukin-6, tumor necrosis factor, and interferon. When exogenous pyrogens invade the body, endogenous pyrogens are released that trigger the production of prostaglandin E2, which in turn elevates the thermal set point and increases core body temperature.
D. What other complications can result from this exemplar? Sepsis and septic shock if not treated; could ultimately lead to MODS and death
E. What diagnostics tests would you anticipate being done to confirm the diagnosis? WBC with differential, anticipate shift to the left, skin/wound culture
- Mr. Brown, a 75-year-old male presents to the emergency department (ED) with a cough, high fever, and chills that has been occurring for five days and getting worse. He did state he was recently at a family gathering and other family members had the same symptoms. Three of the family members, including Mr. Brown, have not had their influenza vaccine since last year.
A. What exemplar do you suspect he will be diagnosed with and why? Influenza due to symptoms and lack of vaccination.
B. What are risk factors for developing this condition, in addition to what the patient presents with in the case study? No vaccination, exposure to ill individuals, age, history of chronic disease, immunosuppression, other chronic lung condition.
C. Detail/diagram the pathophysiology of how the symptoms of cough and fever occur in this condition
Cough - a protective reflex as the body tries to rid itself of the microorganism; since this is the path of entry, this is also how the disease is spread to others
Fever - Exogenous pyrogens (those of external origin) include bacterial endotoxins, viruses, antigen- antibody complexes, etc. Endogenous pyrogens are produced by phagocytic white blood cells as part of the immune response and include interleukin-1, interleukin-6, tumor necrosis factor, and interferon. When exogenous pyrogens invade the body, endogenous pyrogens are released that trigger the production of prostaglandin E2, which in turn elevates the thermal set point and increases core body temperature.
D. What other complications can result from this exemplar? Secondary bacterial pneumonias, sepsis, death.
E. What diagnostics tests would you anticipate being done to confirm the diagnosis? WBC with differential, possible sputum culture, swab for influenza
Inflammation and Infection Case Studies
Course: Human Pathophysiology (NUR 252)
University: Creighton University
