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UNIT 5 SIGS 4-6
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Explain the pathogenesis of hepatitis B virus
transmitted by blood/sexual contact/transplacentally->hepatocytes->dsDNA->mRNA viral proteins->dsDNA packaged->viral antigens attached by CTL-> acute hepatitis
Compare and Contrast the clinical features and Anatomy of Ulcerative Colitis and Chron Disease
UC: continuous colonic involved; bloody diarrhea, smoking helps it, tenesmus; CD: skip lesions mouth to anus; gingival ulcers, kidney stones, erythema nodosum
Compare and contrast the histological findings of Ulcerative Colitis (UC) and Chron Disease (CD)
UC: loss of hostra, pseudopolyp, ulcers, crypt distortion; CD: transmural inflammation,ulcerations,fissures; cobblestoning, thickened wall
Mesalamine (5-aminosalicylic acid (5-ASA): drug class, MOA, indication, side effect
Sulfasalazine; inhibit production of inflammatory mediators from both cyclooxygenase & lipoxygenase pathways; induce/remission UC+CD; sulfonamide toxicity
Adalimumab - Drug Class, MOA, Indication, Side effect
Anti-TNF IgG1 Antibody; binds TNF-α + blocks interaction w/ surface TNF receptors; for UC/CD diseases; side effect-serious infection
Describe the pathophysiology, risk factors, and clinical features of celiac disease
genetic(HLA DQ 2,8)+exposure to prolamins->TTG alter + gliadin w/ zonulin -> IgA against TTG + tight junctions open = inflammation GI ->malabsorption-diarrhea
Identify the utility of serologic and endoscopic evaluation in the diagnosis and management of celiac disease.
Serology: Anti-TTG; Endoscopic-histologically see vilious atrophy+crypt hypertrophy+increased IEL
Describe the role of gliadin, zonulin, and tight junctions in maintenance of the intestinal barrier
Zonulin regulate tight junctions leakiness; Tight junctions regulate paracellular movement; gliadin modifies paracellular permeability
In celiac disease, explain how malabsorption can result in osmotic diarrhea
damaged villi + mucosa --> Osmotic diarrhea=osmotically active, poorly absorbed solutes in the bowel lumen->inhibit normal water + electrolyte absorption
Describe the immunologic mechanisms resulting in hepatic injury from hepatitis
immune system–mediated cytotoxicity: (HLA) class I–restricted CD8 CTL's recognize hepatitis B core antigen + e antigen on infected hepatocytes->inflammation
Explain the use of osmotic laxatives (lactulose) to manage hepatic encephalopathy.
colonic acidifier that works by decreasing the amount of ammonia in the blood (decrease intestinal production/absorption of ammonia) -> less toxin to brain
Describe life-threatening complications from cirrhosis including hepatic encephalopathy (HE), spontaneous bacterial peritonitis (SBP), and esophageal varices (EV)
HE: toxin build up in blood->brain damage; SBP: infection of ascitic fluid in peritoneum; EV: blood flow to liver blocked->enlarged esophageal veins
Define shifting dullness, palmar erythema, and asterixis (reference: Alcoholic Cirrhosis Physical Exam)
shifting dullness: ascites sign, Percuss across abdomen-transition tympany to dull; palmar erythema: red palms from oestradiol; asterixis: negative myoclonus
Discuss the Batts-Ludwig grading and staging criteria
Grade-amount of necroinflammatory activity; Stage-amount of fibrosis
Explain the rationale for utilizing sofosbuvir-velpatasvir in previously untreated hepatitis C
Velpatasvir: NS5A inhibitor; Sofosbuvir: NS5B polymerase inhibitor; both work by weakening the activity of proteins needed by hepatitis C
Explain the pathogenesis of hepatitis C virus
human reservoir→transmission by blood, semen, in utero→infects hepatocytes→immune response by CTLs kills infected hepatocytes=acute hepatitis
Describe specific dietary modifications and medicinal foods (soy, green tea, flax, olive oil) for dyslipidemia.
soy-reduces HMG-CoA reductase; Green Tea Extract and Green Tea-reduces FA gene expression, inhibits HMG-CoA reductase; flax-reduce LDL
Explain the pathogenesis of dyslipidemia
Primary: Genetic - over production/defective LDL or over-clearance HDL; Secondary: lifestyle + other factors -high free fatty acids + high VLDL =excessive fats
Describe the therapeutic benefits and potential adverse effects associated with HMG-CoA reductase inhibitors
Pleiotropic effects: NO synthesis, LDL lower, Inflammatory down; Adverse: myopathy; decrease Coenzyme Q10 -> impair energy in muscles = myalgia
Elaborate the role of statin in the regulation of intracellular cholesterol synthesis
Statins inhibit HMG-CoA reductase->reduce cellular cholesterol synthesis->Lower intracellular cholesterol->over-expression of the LDL receptors=lower plasma LDL
Identify the spectrum of disorders of NAFLD
NAFD --> NASH --> Fibrosis --> Cirrhosis
Identify common comorbidities of NAFLD
hepatic manifestation of metabolic syndrome linked with insulin resistance; obesity, dyslipidemia, diabetes
Explain how hepatocellular oxidative injury can result in hepatic inflammation and necrosis
Reactive oxygen species produced in mitochondria + ER of hepatocytes via cytochrome P450-> imbalance oxidants/antioxidants=structural & functional abnormality
Explain how insulin resistance can lead to the development of hepatic steatosis
skeletal resistance -> glucose to liver; adipose resistance -> lipolysis = glycerol + Fatty acids -> fats deposited in liver


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