Discuss Pathophysiology of Primary Biliary Cholangitis.

Discuss Pathophysiology of Primary Biliary Cholangitis.
Topic for pp is Unstable Angina.
Pharmacological Management PowerPoint Presentations
For this assignment, you are to complete a PowerPoint presentation addressing the specific criteria below.

The PowerPoint presentation will be based on Unstable Angina.
Assignments will be posted in announcements during Week 1. If you cannot locate your assignment contact your faculty.

Your presentation must include the following headings.

Heading – Title Page
Heading – Pathophysiology of Unstable Angina
Heading – Definitions of the Two Drug Classes for Unstable Angina
Heading – Discussion of 4 Medications (2 drugs from each drug class)
Heading – Pharmacokinetics, Pharmacodynamics, Safety/Monitoring, & Pregnancy/Lactation of the 4 Medications Discussed Earlier
Heading – Contraindications of the 4 Medications Discussed Earlier
Heading – Conclusions
Heading – References (remember to use apa style for the references and use citations not later then 5 years ago).

Please use the same exact template attached to this post. Just put in the info for my topic assigned.

Pharmacological Management Project

Student Name

NSG6005

Faculty name

Pathophysiology of assigned disease

Assigned Disease: Primary Biliary Cholangitis

Pathophysiology: Primary biliary cholangitis (PBC, formerly known as primary biliary cirrhosis) is an uncommon cholestatic liver disease characterized by immune-mediated destruction of biliary epithelial cells. PBC is female preponderant and typically presents in the fifth or sixth decade of life. The clinical presentation may include generalized pruritus, dryness of eyes and mouth, fatigue, and upper abdominal discomfort; patients may be asymptomatic. Typical laboratory findings are elevations in serum alkaline phosphatase levels, increased serum immunoglobulin M levels, and the presence of antimitochondrial antibodies or specific subtypes of antinuclear antibodies. A diagnosis of PBC is usually made without histologic examination. When used, liver biopsy typically reveals nonsuppurative granulomatous cholangitis with loss of small bile ducts and lymphocytic portal inflammation. Patients who do not achieve an adequate biochemical response to first-line therapy have a greater risk of disease progression to cirrhosis and may ultimately require liver transplantation.

Definition of the two assigned drug Classifications

Classification 1: Bile Acid Analog

Bile acids aid in the digestion and solubilization of lipophilic nutrients and drugs in the small intestine, they signal endocrine molecules that regulate the glucose, lipid, and energy metabolism through complex and intertwined pathways that are largely mediated by activation of nuclear receptor farnesoid X receptor (FXR) and cell surface G protein-coupled receptor 1, TGR5 (also known as GPBAR1).

Classification 2: Immunomodulatory therapy

Immunomodulatory drugs modify the response of the immune system by increasing (immunostimulators) or decreasing (immunosuppressives) the production of serum antibodies. Immunostimulators are prescribed to enhance the immune response against infectious diseases, tumours, primary or secondary immunodeficiency, and alterations in antibody transfer, among others. Immunosuppressive drugs are used to reduce the immune response against transplanted organs and to treat autoimmune diseases.

Discussion of 4 medications – 2 from each drug classification (you are to choose the drugs – they must belong to the drug class)

Classification 1: Bile Acid analog

Drug 1: Actigall (ursodiol)

13 – 15 mg/kg/day orally given in 2 – 4 divided doses

Give with food

Drug 2: Obeticholic acid

5 – 10 mg PO qD

Start 5mg PO qd x 3 months, then may increase to 10mg PO qd if needed

Classification 1: immunomodulatory therapy

Drug 1: prednisone

20 – 30 mg PO qd initially for one month, titrate downward according to IgG concentration

Drug 2: Mycophenolate mofetil

500 – 1000 mg PO qd BID

Pharmacokinetics, Pharmacodynamics, safety/monitoring & pregnancy/lactation of the 4 Medications you discussed earlier

Drug 1: actigall (ursodiol)

Metabolism: Liver, GI Tract, CYP450; half-life unknown

Excretion: feces primarily; urine

Mechanism of Action: decreases cholesterol synthesis, secretion, and absorption; alters bile cholesterol composition

Monitoring Parameters: liver function tests q months x 3months, then q6 months

Pregnancy: may use during pregnancy; no known risk of fetal harm based on human data

Lactation: may use while breastfeeding; no known risk of infant harm based on limited human data

Drug 1: obeticholic

Metabolism: live; no CYP450; enterohepatically recirculated; active metabolites

Excretion: feces 87%; urine <3%; half-life 24 hours Mechanism of Action: agonizes farnesoid X receptor, decreasing intracellular hepatocyte concentrations of bile acids Monitoring Parameters: liver function tests at baseline, then frequently, especially if there is an increase in risk of hepatic decompensation or before dose adjustment; lipid panel Pregnancy: caution advised during pregnancy; inadequate human data available to assess risk Lactation: caution advised while breastfeeding; no human data available to assess risk of infant harm or effects on milk production Drug 1: prednisone Metabolism: liver; CYP450 – 3A4 substrate; prodrug converted to prednisolone Excretion: urine; half-life: 2-4 hours (plasma); 18-36 hours (biological) Mechanism of Action: exact mechanism of anti-inflammatory action unknown; inhibits multiple inflammatory cytokines; produces multiple glucocorticoid and mineralocorticoid effects Monitoring Parameters: electrolytes; BP; weight; 2 hours postprandial glucose; chest x-ray if prolonged treatment; ophthalmic exam if treatment >6weeks

Pregnancy: weight risk/benefit during pregnancy, especially in 1st trimester; risk of orofacial cleft based on limited human data; possible risk of teratogenicity based on animal data

Lactation: may use while breastfeeding, consider breastfeeding at least 4 hours after high-dose prednisone use; no known risk of infant harm

Drug 1: mycophenolate mofetil

Metabolism: liver; CYP450-unknown; UGT: 1A9 substrate; info: prodrug converted to mycophenolic acid

Excretion: urine 93%, feces 6%, half-life: 17.9 hour (PO route), 16.6h (IV route)

Mechanism of Action: inhibits B- and T-lymphocyte proliferation

Monitoring Parameters: pregnancy test immediately prior to treatment start, then 8-10 days later, then continue at routine visits, creatinine at baseline, CBC qwk x 1 month, then 2x/mo x 2mo, then q month during 1st year of treatment

Pregnancy: avoid use during pregnancy; risk of fetal harm; included teratogenicity and spontaneous abortion, based on human data

Lactation: weigh risk/benefit while breastfeeding; no human data available to assess risk of infant harm though possible drug excretion into milk

Contraindications of the 4 medications discussed earlier

Actigall (ursodiol)

Hypersensitivity to drug, unremitting acute cholecystitis, acute cholangitis, biliary obstruction, gallstone pancreatitis

Obeticholic acid

Hypersensitivity to drug; complete biliary obstruction, caution if Child-Pugh Class B or C hepatic impairment, caution if prior hepatic decompensation event

prednisone

Systemic fungal infection, cerebral malaria, avoid abrupt withdrawal, caution in pediatrics, pregnancy, if immunosuppressed, if active infection, if TB infection, if hypertensive, if diabetic

Mycophenolate mofetil

Hypersensitivity to polysorbate 80, pregnancy, avoid donating blood during treatment and 6 weeks after d/c, avoid semen donation during treatment and 90 days after d/c, caution HBV or HCV infection, caution if CrCl <50 conclusion Summarize what you learned on this slide – what are the important things to know about the disease, the classifications, drugs and risks references Include all the references used following the APA 7th Edition

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