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Acute viral hepatitis time frame

What types of hepatitis are generally chronic

What can chronic hepatitis lead to: (3 things)

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Acute viral hepatitis time frame

What types of hepatitis are generally chronic

What can chronic hepatitis lead to: (3 things)

Acute viral hepatitis time frame: < 6 months

What types of hepatitis are generally chronic: B, C, D

What can chronic hepatitis lead to (3 things): Cirrhosis, ESLD, and hepatocellular carcinoma

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Clinical presentation of hepatitis:

Most people are generally symptomatic

Flu-like symptoms, fatigue, anorexia, NVD, dark urine, pale stools, abdominal pain

Jaundice, splenomegaly, and extra-hepatic symptoms

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Transmission of viral hepatitis: A B C D E

A - fecal/oral B - blood and bodily fluids (perinatal, percutaneous, or sexual) C - Parenteral (contaminated needles/syringes) D - blood and bodily fluids (perinatal, percutaneous, or sexual) E - fecal/oral

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Who should be screened for Hep A?

International travelers Contact with an infected person (sex, household, daycare) IVDUs Zookeepers with monkeys Hx clotting factor disorders

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Hepatitis B/D - Who should be screened?

International travelers MSM/Multiple heterosexual partners IVDU Healthcare providers/safety workers Residents and staff of facilities for developmentally disabled Hemodialysis Infants born to infected mothers

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Hepatitis C - who should be screened?

Everyone > 18 years of age at least once in their lifetime IVDU as yearly HD as yearly Women during each pregnancy

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Hepatitis E - who should be screened?

international travelers Ingestion of food/drink contaminated with bodily waste

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Vaccinations for hepatitis A

HAVRIX and VAQTA (VAQTA is 2 injections 6 months apart)

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vaccines for Hepatitis B/D

Recombivax HB Engerix - B (3 doses at 0, 1, and 6 months) Heplisav - B (adults only)

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Vaccine for Hepatitis A/B

Twinrix (usually a 3 dose series)

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How is acute hepatitis primarily managed?

Supportive care

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Hepatitis A Prevention measures

Good hand washing/proper disposal of waste Vaccination: Lifelong immunity Immunoglobulin IM: passive immunity (Pre-exposure and post-exposure)

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Hepatitis A prevention:

  • Pre-exposure: What age ranges can you give IGIM to unvaccinated people to promote passive immunity? What conditions may they have?

-Post-exposure: How long after exposure must it be? Age ranges? Conditions that may be occurring?

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Hepatitis B serology: HBsAg

Present on virus cells (indicating virus is currently present) Used to make vaccines

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Hepatitis B serology: HBsAb (aka Anti-HBs)

Means your body is mounted a response either to the virus itself OR to the vaccine

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Hepatitis B serology: Anti-HBc

You can only have this if you were infected with the virus at some point

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Hepatitis B serology: IgM anti-HBc

This is present ONLY during an acute hepatitis infection

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Hepatitis B Prevention

Vaccination or HBIG for post-exposure prophylaxis

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Treatment for an exposed unvaccinated patient with: HBsAG Positive

Administer HBIG and Hep B vaccine

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Treatment for an exposed unvaccinated patient with: HBsAg Unknown

Administer Hep B vaccine

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Treatment for an exposed vaccinated patient with: HBsAg Positive

Vaccine booster dose

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Treatment for an exposed vaccinated patient with: HBsAg unknown

No Treatment

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All oral HBV agents have what BBW?

Lactic acidosis and hepatomegaly

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treatment of Chronic HBV: Indicated when: Always test for: Monitoring:

Indicated when: ALT persistently >2x ULN or significant histological disease AND HBV DNA >20,000 IU/mL

Always test for: HIV before treating HBV

Monitoring: LFTs must be monitored if Treatment is discontinued. (severe acute hepatitis exacerbations may occur)

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1st line HBV agents: Pegasys (Pegylated IFN-a2a) What does it do: How is it administered: ADRs: CI: How long is treatment?

Effective in suppressing and often ceasing viral replication without resistance

SUBQ administration

ADRs: flu-like symptoms, psych abnormalities, thrombocytopenia/neutropenia

CIs: autoimmune disorders, uncontrolled psych issues, uncontrolled seizures, decompensated cirrhosis

48 week tx course

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What does a pegylated IFN mean

A pegylated form increases half-life and allows for less frequent dosing

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1st line HBV agents: Baraclude What is it? Approval tx age? Administration? Is it well tolerated?

What is it? Guanosine nucleoside analog Approval tx age? >2 years old Administration? 0.5-1.0mg PO QD on empty stomach Is it well tolerated? Well tolerated

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1st line agent: How does Tenofovir work?

Acyclic adenine nucleotide reverse transcriptase inhibitor

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First line agent: Tenofovir Disoproxil fumarate (Viread) Dose? Age? RISK:

Dose: 300mg PO QD Age: ≥2 years old RISK: Rare but serious risk of renal toxicity and osteomalacia

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First line agent HBV: Tenofovir Alafenamide (Vemlidy) Dose? Age? RISK:

Dose: 25mg PO daily Age: ≥12 years old RISK: Less risk of osteomalacia and renal toxicity than Tenofovir Disoproxil fumarate (Viread)

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2nd line HBV treatment: Adefovir dipivoxil (Hepsera) How does it work? Administration Age risks:

How does it work: Adenosine nucleotide analog inhibits DNA Polymerase Administration: 10mg PO QD Age: >12 years risks: Nephrotoxicity, Fanconi syndrome, HIGH RATES OF RESISTANCE

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2nd line HBV treatment: Lamivudine (Epivir-HBV) How does it work: Dose Age Benefit Risk

How does it work: Cytosine nucleoside analog Dose: 100mg PO QD (HBV only) for adults Age: approved for >2 years old Benefit: Also effective for HIV Risk: High rates of resistance

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Hepatitis C are there vaccines? who is a candidate? Is there a cure?

are there vaccines? No vaccines, no IG products who is a candidate? EVERYONE IS A CANDIDATE FOR Is there a cure? Sustained virological cures exist

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Treatment options for Hep C Interferon/ribavirin: Ribavirin is associated with:

Associated with hemolytic anemia, dematological effects, and significant teratogenicity

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When using second generation direct-acting antiviral agents EPCLUSA, MAVYRET, and VOSEVI are all _____ and before use you must test for:

EPCLUSA, MAVYRET, and VOSEVI are all pangenotypic

and you must first test for HBV prior to use

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Drugs that can interfere with direct acting antivirals

PPIs, Statins, amiodarone, statins, immunosuppressive agents, antimicrobials, St John's wort, antiepileptic agents, Highly active antiretroviral therapy (HAART)

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1st line treatment for HCV: Harvoni How does it work: What Genotypes does it work on: What Genotype can is be used on with decompensated cirrhosis? How long is the treatment depending on prior treatment hx, cirrhosis status, genotype, and baseline viral load? Contraindications?

NS5B polymerase inhibitor and a NS5A inhibitor

Genotype 1, 4, 5, and 6

Can be used in type 1 with decompensated cirrhosis

8-24 week treatment depending on prior treatment history, cirrhosis, status, genotype, and baseline viral load

Contraindicated with amiodarone and PPIs

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1st line treatment for HCV: Zepatier How does it work? Genotypes When using... test for ____ and you may need to add __


Works by NS5A and NS3/4A protease inhibitor

Genotypes 1 or 4

Test for polymorphisms in 1a disease and you may need to add ribavirin

Do not use in patients with Child-Pugh B or C

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1st line treatment for HCV: EPCLUSA How does it work? administration therapy length Can it be used with compensated cirrhosis When should you add ribavirin Contraindications

Works by NS5B polymerase inhibition and NS5A inhibition

PO QD with or without food

12 week therapy

Can be given with or without compensated cirrhosis

Add ribavirin in patients with decompensated Child-pugh B or C cirrhosis

Contraindicated in patients on amiodarone or PPI therapy

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1st line treatment for HCV: Vosevi How does it work? Administration and therapy length? Can it be taken with compensated cirrhosis Can it be used in patients with decompensated child-pugh B or C? Contraindications:

Combination drug of Epclusa and voxilaprevir (NS3/4A protease inhibitor) Taken PO QD with food for 12 weeks

Can be taken with or without compensated cirrhosis

Do NOT use in decompensated cirrhosis B or C

CIs: amiodarone and PPI therapy

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1st line treatment for HCV: Mavyret How does it work? Administration and therapy length? Can it be used with decompensated child-pugh B and C?

NS3/4A protease inhibitor + NS5 inhibitor

3 tablets PO QD with mod/high fat meal; 8 wk therapy

Do not use in patients with a Child-pugh B or C cirrhosis

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NS3/4A PROTEASE inhibitors end in

NS5A inhibitors end in

NS5B inhibitors end in




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Summary for Harvoni: Is it Pangenotypic? Can it be used in decompensated cirrhosis? Approved in HIV coinfection?


Yes +/- ribavirin


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Summary for Zepatier: Is it Pangenotypic? Can it be used in decompensated cirrhosis? Approved in HIV coinfection?




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Summary for Epclusa: Is it Pangenotypic? Can it be used in decompensated cirrhosis? Approved in HIV coinfection?


Yes +/- Ribavirin


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Summary for Vosevi: (combination of Epclusa and voxilaprevir) Is it Pangenotypic? Can it be used in decompensated cirrhosis? Approved in HIV coinfection?




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Summary for Mavyret: Is it Pangenotypic? Can it be used in decompensated cirrhosis? Approved in HIV coinfection?


No it cannot


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What does only have a IgM (+) mean?

Acute infection

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What does (+) HBSAB and (-) Anti-HBc mean?

Immune by vaccination

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What does (+) HBSAB and (+) HBCAB mean?

Immune by natural infection or virus

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What does (+) HBSAg and (+) Anti-HBC indicate?

Chronic infection

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What does it mean if all serology tests come back negative for a patient?

They are susceptible for HBV

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IgM anti-HBC (+) occurs only during

Acute infection

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What two times does HBSAg occur in the body?

Vaccination and when virus is alive and active

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What does it mean that you have HBSAb?

Resolved infection or mounted immune response from vaccine

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What does having anti-HBC in you mean?

HepB virus was or IS in you

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6 things that can lead to cirrhosis?

What is the outcome of having cirrhosis?

What is a consequence (3) of liver fibrosis?

Alcohol, HCV, Metabolic liver disease, immunologic disease, vascular damage, or drugs

Having cirrhosis can lead to an advanced stage of liver fibrosis

Advanced stage liver fibrosis can lead to impaired hepatocyte function, Portal HTN, and hepatocellular carcinoma

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(Pathophysiology of Cirrhosis) activation of _____ cells

_____ cells lose vitamin A, proliferate, and synthesize __________

Fibrosis results in loss of hepatocyte _____ and deterioration of hepatocyte _____

If fibrosis progresses, _____ occurs

activation of stellate cells

stellate cells lose vitamin A, proliferate, and synthesize fibrotic scar tissue

Fibrosis results in loss of hepatocyte microvilli and deterioration of hepatocyte function

If fibrosis progresses, cirrhosis occurs

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Hepatic fibrosis leads to (4 things)

Splanchnic vasodilation Decreased responsiveness of vasoconstrictors Formation of new blood vessels Portal-systemic shunting

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Portal Hypertension is classified by (4 things):

Hypervolemia Increased cardiac index (relation of output to BSA) Hypotension Decreased systemic vascular resistance

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5 classifications of the Child-Pugh score

Does it:

Excrete bilirubin Metabolize drugs make clotting factors make thrombopoeitin make albumin

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Symptoms of cirrhosis

Asymptomatic enlarged liver or spleen Laundice, spider angiomata, hyperpigmentation Gynecomastia, reduced libido Ascites, edema, pleural effusion Malaise, anorexia, weight loss, encephalopathy

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Lab values to watch with cirrhosis

prothrombin time thrombocytopenia elevated alkaline phosphatase elevated AST, ALT, or GGT

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Define the 3 types of hepatic encephalopathy: Episodic HE Recurrent HE Persistent HE

Episodic HE: refers to precipitated, spontaneous, or recurrent acute episodes of HE

Recurrent HE: refers to episodes of HE that occur within a time interval of 6 months or less

Persistent HE: a pattern of behavioral alterations that are always present (treatment dependent) and are interspersed with relapses of overt HE

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Clinical presentation of HE: what 3 things are we looking for?

Level of consciousness changes Personality/intellect changes Neurological abnormalities (tremor, incoordination, abnormal reflexes, etc.)

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Generalized treatment goals for hepatic encephalopathy (3 generalized things)

Decrease ammonia blood concentrations by reducing the nitrogenous load from the gut

identify and correct precipitating factors

nutritional management (protein restrictions)

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Hepatic encephalopathy: first line drugs and second line drugs

First line drugs: Lactulose and rifaximin

Second line: Metronidazole and neomycin

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Mainstay of HE treatment: Lactulose How does it work? Dosing? How should it be titrated? How can it ALSO be given?

Lactulose reduces ammonia production by the small intestine and leaches ammonia from circulation into the colon for excretion

start at 45 mL PO Q1H until catharsis, decrease dose as time goes on to 15-45mL every 8-12 hours

Titrated to produce 2-3 stools per day

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How does Rifaximin work? Pro and con of it

It inhibits bacterial RNA synthesis by binding to bacterial DNA-dependent RNA polymerase

It has a favorable side effect profile but it is more expensive than lactulose

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Second line options for HE: Metronidazole/Neomycin

How do they work?

Neomycin: ADE and monitoring

Metronidazole: ADE

Inhibit the activity of urease-producing bacteria and decreases production of ammonia

Neomycin: ototoxicity and nephrotoxicity (annual auditory and periodic renal monitoring)

Metronidazole: Neurotoxicity

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Cirrhosis/portal HTN can lead to ascites due to an increase in nitric oxide causing systemic/splanchnic vasodilation.

Decreased effective arterial blood volume occurs and the RAAS system gets activated.

What does this cause in relation to ascites?

Hyperdynamic circulation, sodium and water retention, renal vasoconstriction

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We should consider paracentesis if the patient has:

New onset ascites Tense ascites Refractory ascites

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When should albumin replacement be considered in patients undergoing paracentesis

When more than >5L are removed from the body.

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Treatment of ascites: -fluid -diet -drug -procedure

-fluid: culture the fluid pulled from paracentesis to assess bacterial risk -diet: restrict sodium to less than 2000mg/day -drug: Spironolactone:Furosemide. 100:40 ratio -procedure: Transjugular intrahepatic portosystemic shunt can be considered in refractory patients

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Spontaneous Bacterial Peritonitis can result from increased intestinal wall permeability, translocation of bacteria into mesenteric lymph nodes, and seeding into ascitic fluid

What are the primary bacteria that occur in SBP

What should we use to treat SBP

Escherichia Coli, Klebsiella Pneumonia, and Streptococcus Pneumoniae

Empiric treatment with third-generation cephalosporins like Ceftriaxone and Cefotaxime

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Long term SBP prophylaxis should be done if the patient has a history of SBP or low-protein ascites with lab of SCr >1.2, BUN >25, Na

Sulfamethoxazole/trimethoprim (Bactrim) Ciprofloxacin

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Primary prevention of esophageal varices drug options: What they do:

Non-selective beta-blockers: Propranolol and Nadolol Decrease CO and decrease splanchnic blood flow

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Another primary prophylactic measure: Endoscopic variceal ligation can be considered for _____

patients with contraindications to beta-blockers or high-risk medium to large varices

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What medication choice should you use small varices or risk factors

Beta Blockers

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Acute Variceal Hemorrhage: 3 main things Stabilize the patient Control hemorrhage Prevent complications (SBP)

Stabilize the patient: normalize HR, BP, Hgb >7, avoid aggressive resus with NS

Control hemorrhage: pharmacologic plus endoscopic therapy, correct coagulopathy

Prevent complications (SBP): Ceftriaxone and Ciprofloxain

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Octreotide: how does it work where does it work what does it cause DOSING

how does it work: Inhibits release of vasodilatory peptides (more potent, longer DOA)

where does it work: binds selectively to splanchnic vasculature

what does it cause: Reduction in portal pressure and port-collateral blood flow

DOSING: 50 mcg IV bolus followed by 50 mcg/hr

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Octreotide side effects:

bradycardia, hyperglycemia, vomiting, hypertension

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Secondary Prophylaxis Combination therapies: Heart rate range for beta blockers: TIPS should be considered for ____

Combination therapies: combination of non-selective beta-blockers plus EVL is preferred (Primarily Nadolol and propranolol)

Heart rate range for beta blockers: 55-60 BPM

TIPS should be considered for: Child-Pugh A/B who are refractory to Beta Blockers plus EVL

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Hepatorenal syndrome: What is it drugs to stop drugs to use Only definitive treatment

Intense renal vasoconstriction caused by systemic vasodilation Discontinue diuretics Use: Octeotide and midodrine Liver transplant is the only definitive treatment

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Terlivaz (terlipressin): how should it be adjusted Most common side effect and BBW: Contraindications

how should it be adjusted: By SCr response Most common side effect and BBW: Respiratory failure Contraindications: Do not use in patients with SCr >5 or hypoxic

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Systemic complications: Hepatopulmonary syndrome

defect in arterial oxygenation caused by systemic vasodilation supportive therapy with oxygen Liver transplant is only definitive cure

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Systemic complications: Coagulopathy

Impaired synthesis of clotting factors, excessive fibrinolysis, etc. Usually only corrected during active bleeding

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Systemic complications: Endocrine disorders

hypogonadism DM Osteoporosis Thyroid disorders

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Consequences of PK/PD changes in liver cirrhosis (4 things)

Reduction in intrinsic metabolic activity reduction in delivery of blood to the liver Decreased protein binding increased interstitial fluid

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PK/PD Changes in the body are _____ through out the whole disease course


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NASH (Non-alcohol Steatohepatitis) What is it? Risk factors? Treatments?

Build up of of extra fat in liver cells leading to a fatty liver and swelling causing cirrhosis

Risk factors: overweight/obese, DM, high colesterol/HyperTG

There are no current treatments - just control underlying causes

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Lobule in the liver is made up of what? Whats in the corners? what do we call cells close to the center of the lobule? How does blood flow from the heart/body to and through the liver? What do Reticuloendothelial cells (Kupffer cells) do in the lobule?

Many cells surrounding a central vein in the middle of the hexagon.

In the corners are portal triads with: a bile duct, a branch of the hepatic portal vein, and a branch of the hepatic artery

Central lobular hepatocytes exist close to the center of a lobule

Blood flows from the outside (triads) inward toward the central veins of the lobules. This mixes nutrient-rich blood from the GI and Oxygen-rich blood from the heart

They break down old RBCs and act as minor immune cells

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How does blood move through the liver and how does bile move through the liver?

Blood flows from the hepatic artery (oxygen rich) and the hepatic portal vein (GI rich) to the liver sinusoids, to the central vein, to the hepatic veins, inferior vena cava, right atrium

Bile from the left and right hepatic duct mix in the common hepatic duct of the liver, and cystic duct from the gallbladder mixes in, then to the common bile duct. The pancreatic duct mixes in. Then into the duodenum

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Most common agents that cause hepatotoxicity?

APAP, anti-infectives, antiepileptics, and isoniazid

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Define the following:

Intrinsic hepatotoxicity: Idiosyncratic hepatotoxicity: Chronic DILI:

Intrinsic hepatotoxicity: toxicity with potential to affect all individuals to varying degrees. Reactions typically stereotypic and dose dependent (acetaminophen)

Idiosyncratic hepatotoxicity: toxicity that affects only rare susceptible individuals. Reaction is less dose-dependent and more varid in larency, presentation, and course

Chronic DILI: failure of liver enzymes or bilirubin to return to pre-DILI baseline and/or other signs/symptoms of ongoing liver disease 6 months after DILI onset.

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pathophysiology of Centrilobular necrosis: Pathophysiology of steatohepatitis/steatonecrosis: ---- what interesting drugs can cause this? Pathophysiology of phospholipidosis: Pathophysiology of generalized hepatocellular necrosis: Pathophysiology of toxic cirrhosis

direct tissue damage permanent or reversible that results from introduction of agent

Accumulation of fatty acids in hepatocytes via reduction in oxidation rate within mitochondria of hepatocyte interrupting homeostasis ----- ethanol and tetracyclines (IV doses >1/5g QD)

Accumulation of phospholipids in the hepatocyte engorge lysosomal bodies, leading to disruption in mitochondrial or lysosomal activity

Non-toxic metabolites undergo bioactivation in the liver binding to proteins and creating haptens that trigger an immune response leading to an immune response damaging the liver

Hepatitis causes scar tissue to develop ultimately leading to a reduction in liver function

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Pathophysiology of cholestatic injury ---- what can cause this? Pathophysiology of Mixed hepatocellular injury Pathophysiology of Liver vascular disorders

disturbance of subcellular actin filaments preventing movement of bile through the canalicular system ----TPN >1 week, augmentin

Combination of any hepatocellular/cholestatic process

Focal lesions in hepatic venules, sinusoids, and portal veins occur with drug administration. Occlusion, hemorrhaging, or compromised patency are common manifestations

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Diagnosis of DILD --Gold standard? --when should it be considered and how can it be found?

gold standard: consensus of expert opinion

it should always be considered and things might have to be rechallenged in order to find it.

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Clinical presentation of DILD? (4 things)

Asymptomatic transaminitis Malaise, abd pain, nausea, anorexia Jaundice Acute Liver failure symptomatology

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Clinical presentation of acute liver failure: (5 things)

Jaundice INR >1.5 while not on anticoagulation Hypo/hyperglycemia Pruritus Hepatic encephalopathy

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