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GI/Hepatic > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

(G) Pancreatitis: Endocrine function

A

Glucose homeostasis regulation
- Beta cells (insulin), alpha cells (glucagon), D cells (somatostatin)

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2
Q

(G) Pancreatitis: Exocrine function

A

Acinar cells: digestive enzymes (lipases, carbohydrase, peptidase)

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3
Q

(G) What is acute pancreatitis?

A

Painful episodic inflammation
- may lead to chronic pancreatitis

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4
Q

(G) What is chronic pancreatitis?

A

Inflammatory condition affecting the pancreas and involves progressive, irreversible damage to the pancreatic tissue

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5
Q

(G) Chronic pancreatitis results in ___, ____, and ____

A

Loss of glandular function (endo/exo), fat malabsorption (steatorrhea), and protein maldigestion

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6
Q

(G) CP treatment: loss of function

A

Pancreatic enzymes (lipase, amylase, and proteases) insulin

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7
Q

(G) CP treatment: pain

A

Delivery of active proteases to the duodenum to repress CCK secretion

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8
Q

(St) What causes acute pancreatitis (AP)?

A
  • Gallstones
  • Chronic alcohol abuse
  • Pancreatic cancer
  • Hypertriglyceridemia
  • Drugs (rare)
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9
Q

(St) S/S, lab tests of AP

A
  • Abrupt onset of severe persistent epigastric or LUQ pain that typically radiates to back
  • N/V
  • Voluntary guarding
  • Elevated amylase and lipase
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10
Q

(St) How is AP diagnosed?

A

At least 2 of the following:
1. Characteristic abdominal pain
2. Serum amylase >= 3x ULN (N: 0-130): not pancreatitis specific: increased by renal, hepatic, cancer
3. Serum lipase >= 3x ULN (N: 20-180): pancreatitis specific

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11
Q

(St) Characteristic findings on CECT or MRI with AP (2 types of AP)

A
  • Interstitial edematous AP: focal or diffuse pancreatic edema
  • Necrotizing AP: focal or diffuse areas of pancreatic necrosis
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12
Q

(St) Severity of AP: Mild
- Characteristics
- Local complications

A
  • No organ failure
  • No local complications
  • Generally marked improvement ( & return to oral feeding) w/i 48 hrs
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13
Q

(St) Severity of AP: Moderately Severe
- Characteristics
- Local complications

A
  • Local complications &/or transient organ failure (<48 hrs)
  • Fluid collections, pseudocysts, sterile/infected necrosis
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14
Q

(St) Severity of AP: Severe
- Characteristics
- Local complications

A
  • Persistent organ failure (> 48 hrs)
  • Early severe (=< 7 d): SIRS &/or organ failure, GI bleed, serum Cr >=2
  • Late severe (> 7 d): sepsis
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15
Q

(St) Severity of AP: Determine SIRS criteria

A

2 or more of the following
- Fever >38.3 C (100.9F) or <36 C (96.8 F)
- HR > 90 bpm
- Respiratory Rate > 20 bpm or PaCO2 < 32 mmHg
- WBC > 12,000/mm3 or < 4,000 mm3 or >10% bands

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16
Q

(St) Indications of ICU admissions for AP

A
  • Age > 55
  • BMI > 30 kg/m2
  • APACHE-II >8 during first 24 hr
  • SIRS for >48 hr
  • Pleural effusions or infiltrates
  • Decr mental status
  • Underlying cardiac/pulmonary disease
  • BUN > 20mg/dL, Hct >44%, or serum Cr > 1.8 mg/dL
  • HR <40 or >150
  • SBP <80, MAP <60, or DBP >120
  • RR >35
  • PaO2 <50
  • Arterial pH <7.1 or >7.7
  • Serum Na <110 or >170, K <2 or >7, glucose >800, or Ca >15
  • Anuria
  • Coma
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17
Q

(St) Treating ICU AP patients (4)

A
  1. Early aggressive hydration: 0.9% NS or lactated Ringer’s over 12-24 hrs
  2. Pain management: IV opioids hydromorphone or morphine (PCA > IVP)
  3. Nutrition
  4. IV antibiotics: empiric antibiotics indicated with necrotizing pancreatitis showing systemic signs of infection (fever, leukocytosis, organ dysfunction)
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18
Q

(St) Treating ICU AP patients:
- Nutrition for mild AP

A
  • Oral intake typically resumes in 3-7 days
  • Can start with clear liquids or solid low-fat diet
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19
Q

(St) Treating ICU AP patients:
- Nutrition for moderately severe to severe AP

A
  • Enteral feeding
  • Nasogastric/jejunal equally safe and effective
  • Start with regular formula, switch to peptide-based formula if not tolerated
  • Pancreatic enzyme supplements once enteral feeding initiated
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20
Q

(St) Treating ICU AP patients:
- Antibiotics: gram negative bacteria

A
  • Carbipenem
  • Fluoroquinolone + Metronidazole
  • 3rd/4th gen Cephalosporin + Metronidazole
  • Pip/Tazo (Zosyn)
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21
Q

(St) Treating ICU AP patients:
- Antibiotics: gram positive bacteria

A

Vancomycin

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22
Q

(St) Potential etiologies of fever and relapsing AP

A
  • Pancreatic abscess or necrosis
  • Infected pseudocyst
  • Nosocomial pneumonia
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23
Q

(St) High neutrophils (segs, bands) indicate higher chance of ____

A

Bacterial

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24
Q

(St) High lymphocytes indicate higher chance of ____

A

Viral

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25
Q

(St) Causes of Chronic Pancreatitis (CP)

A
  • Chronic alcohol abuse
  • CF, pancreatic cancer, hypertriglyceridema
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26
Q

(St) Clinical symptoms of CP

A
  • Abdominal pain (worsen after eating)
  • Fat malabsorption (steatorrhea: mild = 7-15 g/day fat, severe = >15 g/day), diarrhea, weight loss
  • Diabetes
  • Duodenal ulcers, biliary cirrhosis
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27
Q

(St) Diagnosis of CP

A
  • High serum amylase and lipase during acute, often normalize as disease progresses
  • Fecal fats: steatorrhea does not begin until disease is advanced
  • Imaging: Endoscopic retrograde cholangiopancreatography (ERCP), ultrasound/CT
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28
Q

(St) Management of CP (3)

A
  1. Chronic pain management: eliminate contributing factor -> APAP or NSAID -> opioid
  2. Dietary fat restriction: small, frequent meals, medium chain TG
  3. Pancreatic enzyme supplements
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29
Q

(St) Management of CP
- Pancreatic enzyme supplements: goal, dose, AEs

A
  • 25,000-40,000 units of lipase to duodenum with each meal or snack
  • Must be taken with each meal or snack, swallow whole with a full glass of water
  • Dose must be individualized
  • AEs: N/D, abdominal pain, constipation, bloating, hyperuricemia/uricosuria, hypersensitivity
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30
Q

HBV vs HCV
- DNA/RNA, manageable/curable

A
  • HBV: DNA, manageable
  • HCV: RNA, curable
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31
Q

HBV routes of infection

A

Parenteral, sexual, perinatal

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32
Q

HBV Physical exam

A
  • Icteric sclera, skin, secretions
  • Decreased bowel sounds, increased abdominal girth
  • Asterixis
  • Spider angiomas
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33
Q

HBV Pathology

A
  • Nodules of damaged & regenerating hepatocytes
  • Fibrous bands > cirrhosis > HCC
  • Ground-glass cytoplasm (light)
  • Bile pigment accumulation (dark)
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34
Q

HBV structure: HBsAg

A

Surface antigen
- Most abundant antigens
- Detectable at onset of clinical symptoms

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35
Q

HBV structure: HBcAg

A

Core/Capsid antigen
- Marker of viral replication

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36
Q

HBV structure: HBeAg

A

Antigen b/w nucleocapsid & lipid envelope
- Marker of viral replication

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37
Q

HBV Life cycle: 5 big steps

A
  1. Entry into hepatocytes
  2. Transcription
  3. Translation
  4. Packaging
  5. Secretion/Recycling
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38
Q

HBV Life cycle: Entry into hepatocytes (which transporter?)

A
  • Via NTCP transporter
  • Uncoat the nucleocapsid
  • Genome released into the nucleus
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39
Q

HBV Life cycle: Transcription

A
  • Relaxed circular HBV genome repaired
  • Forms covalently closed circular DNA (cccDNA)
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40
Q

HBV Life cycle: what is cccDNA?

A

Covalently closed circular DNA
- Template for the viral mRNA transcription
- Resulting DNA does not integrate; only serves as an episomal template

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41
Q

HBV Life cycle: translation

A
  • Pregenomic(pg) HBV mRNAs are translated into L/M/S surface, precore, core, polymerase, HBx proteins
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42
Q

HBV Life cycle: packaging

A

pgRNA and pol are encapsidated into the nucleocapsid
- Viral DNA is reverse-transcribed into partially double stranded DNA (+)

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43
Q

HBV Life cycle: secretion/recycling

A
  • Assembled HBV virions secreted
  • Recycled back to the nucleus for amplification of cccDNA
  • Secrete hepatitis core & envelop antigens to promote immune tolerance
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44
Q

Phases of chronic HBV infection (4)

A
  1. Immune tolerance phase
  2. Immune active/clearance phase
  3. Immune inactive/control phase
  4. Reactivation phase
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45
Q

Immune tolerance phase:
- Labs, liver histology, tx indication

A
  • Labs: HBsAg(+), HBeAg(+), HB DNA >200,000 IU/mL, ALT normal
  • Liver: minimal inflammation/fibrosis
  • No
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46
Q

Immune active/clearance phase:
- Labs, liver histology, tx indication

A
  • Labs: HBsAg(+), HBeAg(+), HBV DNA >20,000, ALT >2xULN
  • Liver: progressive inflammation/fibrosis (nodules)
  • Yes
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47
Q

Immune inactive/control phase:
- Labs, liver histology, tx indication

A
  • Labs: HBsAg(+), seroconversion to HBeAg(-)/anti-HBe(+), HBV DNA <2,000 IU/mL, ALT normal
  • Liver: minimal inflammation, fibrosis variable
  • No; up to 80% of pts remain in this phase long-term
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48
Q

Reactivation phase:
- Labs, liver histology, tx indication

A
  • Labs: HBsAg(+), HBeAg(-)/anti-HBe(+), HBV DNA >2,000 IU/mL, ALT >2xULN
  • Liver: progressive inflammation/fibrosis
  • Yes
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49
Q

HBV Pharmacology FDA approved

A
  • Interferon Alpha (IFNa)
  • Nucleos(t)ide Analogs
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50
Q

HBV IFNa signaling pathway

A
  1. JAKs cross-phosphorylate each other on tyrosines (dimerization)
  2. Activated JAKs phosphorylate receptors on tyrosines
  3. STATs dock on phosphotyrosines & JAKs phosphorylate them
  4. STATs dissociate from receptor and dimerize
  5. Move into the nucleus for gene transcription
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51
Q

HBV IFNa MoA
- ____ of NK cell
- ____ of viral cccDNA
- ____ of the pool of cccDNA
- ____ of the viral nicleocapsid

A

Innate immunity cytokine that induces gene expression via JAK-STAT signaling that involves:
- Activation of NK cell activity
- Repression of transcription of viral cccDNA
- Partial degradation of the pool of cccDNA
- Destabilization of the viral nucleocapsid

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52
Q

HBV Nucleoside/tide Analogs MoA

A
  • Potent inhibitors of the reverse transcriptase activity of the HBV pol
  • Incorporated into the growing DNA chain leading to chain termination and decreasing the amount of viral DNA
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53
Q

HBV nucleosides vs nucleotide

A
  • Nucleoside: sugar, base
  • Nucleotide: sugar, base, phosphate
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54
Q

HBV L-Conformation nucleosides

A

Direct chain terminator
- Lamivudine: high resistance
- Telbivudine

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55
Q

HBV D-Cyclopentane Sugar/nucleoside drug & MoA

A

Entecavir
- Deoxyguanosine analog: competitive inhibitor (Not a direct inhibitor)
- Inhibits HBV pol/reverse transcriptase
1. Base priming
2. Reverse transcription of (-) strand from the pgmRNA
3. Synthesis of (+) HBV DNA
- Most potent inhibitor

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56
Q

HBV Acyclic phosphnates/nucleotides

A
  1. Adefovir: prodrug for acyclic 2’-deoxyAMP (diphosphate active form), undergoes de-esterification, direct chain terminator
  2. Tenofovir: MoA similar but preferred due to more favorable safety and resistance
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57
Q

HBV Tx goals: HBeAg(+) vs HBeAg(-)

A
  • HBeAg(+): HBeAg seroconversion, loss of serum HBV DNA, normalization of ALT, loss of serum HBsAg
  • HBeAg(-): same except HBeAg seroconversion
58
Q

HBV Peg IFNa (+), (-)

A
  • (+): finite tx course (48 weeks), no resistance
  • (-): more AEs, cannot administer to pt with decompensated cirrhosis
59
Q

HBV Nucleoside/tide analogues (NAs) (+), (-)

A
  • (+): oral dosing, fewer AEs, pts with decompensated cirrhosis qualify for tx
  • (-): viral resistance, require indefinite tx, severe ALT flare upon discontinuation
60
Q

HBV IFNa monotherapy BBW

A

May cause or aggravate fatal or life-threatening neuropsychiatric, autoimmune, ischemic, and infectious disorders

61
Q

HBV Peg IFNa AEs

A
  • Hepatic decompensation in pts with compensated cirrhosis
  • Flu-like symptoms when starting tx
  • Psychiatric: depression, aggressive behavior, psychosis, hallucinations, suicidal ideation
  • Anemia, neutropenia, lymphopenia
  • Autoimmunity
  • Retinopathy
  • Stroke
  • Dyspnea, pneumonia
  • UC, ischemic colitis
  • Pancreatitis
  • Growth retardation in pts 5-17 yrs
62
Q

HBV Peg IFNa absolute C/I

A
  • Decompensated cirrhosis
  • Pregnancy
  • Hx of severe depression or schizophrenia
  • Uncontrolled epilepsy
  • Uncontrolled autoimmune disease
  • HF or COPD
  • Retinal disease
63
Q

HBV Peg IFNa recommended dose & dose adjustments

A
  • Recommended: 48 weeks, should NOT exceed 96 weeks
  • Adjustment: neutropenia (ANC <1,000) or thrombocytopenia (PLT <50,000), CrCL <30, moderate or severe depression
64
Q

HBV Nucleoside/tide analogues (NAs) preferred agents

A
  • Nucleoside: Entecavir
  • Nucleotide: TAF > TDF
65
Q

HBV Entecavir AEs

A

Elevated glucose, lipase, liver enzymes, creatinine

66
Q

HBV TDF vs TAF: AEs, DDIs

A
  • TDF: renal dysfunction, decreased bone mineral density
  • TAF: less renal and bone toxicity => first-line, DDI: Pgp inducers (carbamazepine, oxcarbazepine, phenobarbital, phenytoin, rifampin, rifabutin, rifapentine, St. John’s wort)
67
Q

HCV route of infection

A

Parenteral, sexual

68
Q

HCV structure

A
  • Positive-sense, single-stranded RNA
  • Untranslated regions at each end (5’UTR), Structural proteins (Core/Capsid & Envelope E1,E2), Nonstructural (NS) proteins
69
Q

HCV NS proteins: NS1

A

Viroporin and assembly factor

70
Q

HCV NS proteins: NS2

A

Transmembrane protein with Cys-protease activity

71
Q

HCV NS proteins: NS3/4A dimer

A

Serine protease (cleave precursor polyprotein into structural/nonstructural proteins) and cofactor

72
Q

HCV NS proteins: NS4B

A

Replication complex that anchors to host ER and induces morphological changes in the ER forming a membranous web structure

73
Q

HCV NS proteins: NS5A

A

Viral replication and assembly, will bind to host ER

74
Q

HCV NS proteins: NS5B

A

RNA-dependent RNA polymerase

75
Q

HCV Life cycle 9 steps

A
  1. Receptor binding
  2. Endocytosis
  3. Fusion and uncoating: fusion of endosome and viral envelope, acidification of endosome, release of +sense ssRNA
  4. RNA translation: host ER translates a single protein with 3000+ AA
  5. Cleavage: proteolysis by NS3/4A
  6. Membranous web formation: NS4B, conceal viral replication from pattern recognition receptors (PRRs) in the cytoplasm that could trigger host cell immune activation
  7. Transcription: (-) RNA template for new +strand viral genome
  8. Assembly
  9. Budding/Release: VLDL secretion
76
Q

HCV entry into the cell

A

NPC1L1, SR-B1, occludins, claudins

77
Q

HCV MoA of drugs

A
  1. Immune system boost: Peg IFNa, Ribavirin
  2. Direct-Acting antivirals (DAA): protease/replicase/polymerase inhibitors
78
Q

HCV Peg IFNa MoA

A

Innate immunity cytokine that activates JAK-STAT signal transduction, nuclear translocation, gene transactivation
- Degrade HCV viral RNA
- Block HCV RNA translation
- Induce mutations during HCV RNA replication
- Interfere with HCV viral assembly/release

79
Q

HCV Ribavirin is a synthetic ____ analog and are _______ by host enzymes

A

Guanosine (purine), phosphorylated

80
Q

HCV Ribavirin MoA

A
  1. Competitively inhibit cellular IMP dehydrogenase & interferes with the synthesis of GTP and nucleic acids (translation)
  2. Competitively inhibits GTP-dependent 5’ capping of viral mRNA
  3. Induce differentiation of activated CD4+ T cells from Th-2 to Th-1
  4. Restore IFNa responsiveness
81
Q

HCV Protease inhibitors: drugs, MoA

A
  • ‘-previr’
  • Potent inhibition of the HCV NS3/4A serine protease -> prevent processing the HCV polyprotein into constituent proteins
82
Q

HCV Replicase inhibitors: drugs, MoA, 2 forms when existing

A
  • ‘-asvir’
  • Inhibit NS5A viral RNA replication and virion assembly
  • Unphosphorylated: replication mode, phosphorylated: particle assembly mode (recruitment of lipid droplets)
83
Q

HCV Polymerase inhibitors: drugs, MoA

A
  • ‘-buvir’
  • Inhibit the NS5B RNA-dependent RNA polymerase by binding the catalytic site of the HCV pol or near the active site of the enzyme
84
Q

HCV Sofosbuvir activity

A
  • Prodrug uptake by hepatocyte
  • Carboxylesterase cleave off and reveal hidden phosphate
  • Adds two more phosphates = active
  • Inhibit NS5B polymerase
  • Dephosphorylation/inactivation
85
Q

HCV Child-Pugh Scoring System

A
  • Clinical scoring system
  • A: 5-6 points, compensated
  • B: 7-9 points, decompensated
  • C: 10-15 points, decompensated
86
Q

HCV Metavir Scoring System

A
  • Liver biopsy
  • F1: portal fibrosis
  • F2: portal fibrosis with few septa
  • F3: septal fibrosis
  • F4: cirrhosis
87
Q

HCV testing criteria

A
  • Born 1945-1965
  • Hx of IV Drug Abuse (IVDA)
  • Hx of incarceration
  • Tattoo in unregulated setting
  • Clotting factor concentrate prior to 1987
  • Blood transfusion or solid organ transplant prior to 1992 or from an HCV+ donor
  • Long-term hemodialysis
  • Exposure to HCV-infected blood
  • HIV+
  • Unexplained S/S of CLD (ALT)
  • Born to HCV+ mother
88
Q

HCV Ribavirin (RBV) BBW

A
  • Monotherapy not effective for chronic HCV -> combination with IFNa or DAA
  • C/I in CD due to toxicity leading to hemolytic anemia
  • C/I in pregnancy, 6 months post tx follow-up, contraception must be utilized during tx & post tx
89
Q

HCV RBV C/I

A
  • Pregnancy
  • Autoimmune hepatitis
  • Hemoglobinopathies
  • CrCl <50 mL/min
  • Concomitant use of didanosine (HIV+)
90
Q

HCV RBV AEs

A
  • Flu-like symptoms on start
  • Psychiatric: depression, relapse, aggressive behavior, psychosis, hallucinations, suicidal/homicidal ideation
  • CV: HTN, chest pain, supraventricular arrhythmias, acute MI
  • Hemolytic anemia
91
Q

HCV DAAs: prior use, preferred agents

A
  • All pts should be tested for HBV coinfection prior to starting tx
  • Epclusa (NS5B pol & NS5A inhibitor)
  • Mavyret (Protease & NS5A inhibitor)
  • Harvoni (NS5A & NS5B inhibitor)
92
Q

HCV Epclusa w or w/o compensated cirrhosis: genotype, dose, duration

A
  • All genotypes 1-6
  • 1 T po QD
  • 12 weeks
93
Q

HCV Epclusa AEs, DDIs

A
  • AEs: well-tolerated
  • DDIs: Pgp and BRCP inducers (rifampin, St. John’s wort, carbamazepine), CYP2B6 inducers
94
Q

HCV Mavyret treatment-naive, w or w/o compensated cirrhosis: genotype, dose, duration

A
  • All genotypes 1-6
  • 3 T po QD
  • 8 weeks
95
Q

HCV Mavyret AEs, DDIs

A
  • well tolerated
  • Strong CYP3A4 inducers (carbamazepine, efavirenz, St. John’s wort)
96
Q

HCV Harvoni AEs, DDIs

A
  • Well tolerated
  • Strong Pgp inducers (carbamazepine, phenytoin, phenobarbital, rifampin, rifabutin, St. John’s wort)
  • H2RAs, PPIs, antacids decrease absorption
  • Amiodarone: severe bradycardia
  • Digoxin: toxicity
  • Rosuvastatin: rhabdomyolysis
97
Q

HCV preferred regimens for tx-naive : G1a
- No cirrhosis vs compensated cirrhosis

A
  • Epclusa 12 wks
  • Mavyret 8 wks
  • Harvoni 12 wks

-Same

98
Q

HCV preferred regimens for tx-naive : G1b
- No cirrhosis vs compensated cirrhosis

A
  • Epclusa 8 wks (No cirrhosis), 12 wks (cirrhosis)
  • Mavyret 8 wks
  • Harvoni 12 wks
  • Zepatier 12 wks
99
Q

HCV preferred regimens for tx-naive : G2
- No cirrhosis vs compensated cirrhosis

A
  • Epclusa 12 wks
  • Mavyret 8 wks

Same

100
Q

HCV preferred regimens for tx-naive : G3
- No cirrhosis vs compensated cirrhosis

A
  • Epclusa 12 wks
  • Mavyret 8 wks

Same

101
Q

HCV preferred regimens for tx-naive : G4
- No cirrhosis vs compensated cirrhosis

A
  • Epclusa 12 wks
  • Mavyret 8 wks
  • Harvoni 12 wks
  • Zepatier 12 wks

Same

102
Q

HCV preferred regimens for tx-naive : G5 or 6
- No cirrhosis vs compensated cirrhosis

A
  • Epclusa 12 wks
  • Mavyret 8 wks
  • Harvoni 12 wks

Same

103
Q

HCV preferred regimens for decompensated cirrhosis: No RBV C/I

A
  • Epclusa/Harvoni + low-dose RBV (600mg/d increased as tolerated to goal of 1000mg/d) for 12 wks
  • G3: only Epclusa + RBV (no Harvoni)
104
Q

HCV preferred regimens for decompensated cirrhosis: RBV C/I

A

Epclusa or Harvoni 24 weeks

105
Q

Metabolic functions of liver

A
  • CHO, protein, hormone metabolism
  • Synthesis of fatty acids, lipoproteins, cholesterol, plasma proteins, urea
  • RBC production
  • Ketogenesis
106
Q

Storage functions of liver

A

Glycogen, ADEK/B12 vitamins, iron, copper

107
Q

Excretory/Secretory functions of liver

A

Bile, IGF-1, most blood proteins, cholesterol, fatty acids

108
Q

Protective functions of liver

A
  • Purification, transformation, clearance: endo/exogenous
  • Kupffer cell: bacteria, foreign materials
109
Q

Circulatory function of liver

A

Antechamber of the heart: collect portal blood from the GI tract

110
Q

Coagulation function of liver

A

Fibrinogen I, prothrombin II, factors V, VII, IX, X, XI, protein C/S, antithrombin

111
Q

Liver enzymes

A
  • Transaminases (hepatocytes): AST, ALT
  • Cholestatic enzymes (epithelial): ALP, GGT
112
Q

Liver: bile vs blood flow

A
  • Bile: central to portal triad to portal circulation
  • Blood: portal triad to portal vein to hepatic artery to hepatocytes to central
113
Q

Acute vs Chronic hepatitis characteristics

A
  • Acute: inflammatory infiltrate, MP aggregates
  • Chronic: fibrosis
114
Q

What is MASH?

A
  • Metabolic dysfunction-associated with steatohepatitis
  • Non-alcoholic fatty liver disease
115
Q

Characteristics of MASH & ASH

A
  • Macrovesicular steatosis + inflammation
  • Infiltration of both lymphocytes and Kupffer cells
  • Ballooned hepatocytes that also contain Mallory-Denk bodies
  • Perivenular/cellular “chicken wire” fibrosis
116
Q

Liver lipid homeostasis to increase fat

A
  1. De novo fatty acid synthesis
  2. Long chain FFA uptake transporter
117
Q

Two-hit or multi-hit theory of MASH

A
  • First hit: fat accumulation in the liver (obesity, long-term fasting)
  • Second hit: injury leads to inflammation (drugs, pathogens, leaky gut, genetic abnormalities, oxidative stress)
118
Q

What is AUD?

A
  • Alcohol Use Disorder
  • ASH: alcoholic steatohepatitis
119
Q

AUD/ASH pathophysiology

A
  • Hepatic fat storage
  • Inflammation: trigger Kupffer cell and leakage
  • Oxidation: CYP2E1
  • ER stress: ethanol-mediated, protein mis-folding
120
Q

Mechanism of AUD/ASH inflammation

A
  • Alcohol intake leads to activation of innate & adaptive immunity
  • Leads to inflammation and fibrosis
121
Q

Cirrhosis induced by MASH

A

¼ of pts never develop cirrhosis and straight to HCC

122
Q

Treatment for MASH/ASH

A
  • Reduce weight
  • Lifestyle modification: exercise, diet
  • Reduce or no ethanol
  • Avoid drugs or toxins with liver injury
  • Avoid pathogens or drugs with gut injury
  • No FDA approved drug
123
Q

Cirrhosis: HVPG >10 to 12 indicates

A

Clinically significant portal HTN: formation of varices, high risk of progression to decompensation & HCC

124
Q

Cir: HVPG >12 indicates

A

Decompensation: high risk of variceal bleeding, formation of ascites

125
Q

Cir: lab results

A
  • Low: BUN, albumin, RBC, WBC, Plts
  • High: ammonia
126
Q

Cir: management

A
  • Definitive: only liver transplantation
  • Supportive care
127
Q

Cir: prognosis stages 1-5

A
  1. Compensated with no varices
  2. Compensated with varices
  3. Decompensated with ascites
  4. Decompensated with GI bleeds
  5. Infection or renal failure
128
Q

Cir: what are ascites?

A

Increased portal venous pressure (water out) and decreased plasma oncotic pressure (water in)

129
Q

Cir: drugs to avoid in ascites

A
  • Nonselective beta blockers should be stopped in pts with advanced cirrhosis/progressively declining BP (refractory ascites)
  • ACEi, ARBs, NSAIDs, nephrotoxic drugs
130
Q

Cir: What indicates Spontaneous Bacterial Peritonitis (SBP)?

A

Ascitic fluid neutrophil count (ANC) >250/mm3

131
Q

Cir: primary prophylaxis of SBP use vs avoid

A
  • Bactrim or Ciprofloxacin
  • Avoid PPIs (increase risk of SBP and C. diff)
132
Q

Cir: tx of SBP

A
  • Ceftriaxone IV x5 days
  • Albumin
133
Q

Cir: Secondary prophylaxis of SBP

A

Bactrim or Ciprofloxacin

134
Q

Cir: diuretic tx for ascites

A
  • Must be added if Na excretion =< 50 mEq/day
  • Na >30: spironolactone
  • Na 10-30: spironolactone + furosemide (100:40 ratio)
  • Na <10: refractory, so other options LVP, TIPS
135
Q

Cir: risk factors for variceal bleeding

A
  • HVPG >12 mmHg
  • Medium-large varices, small varices with red wale signs
136
Q

Cir: primary prevention of medium-large varices & absolute C/I

A
  • Nonselective beta blocker: propranolol, nadolol, carvedilol
  • Endoscopic variceal ligation (EVL): 2nd line for refractory pts or who cannot take nonselective bb
  • COPD, CHF
137
Q

Cir: primary prevention of small varices with red wale signs

A

Nonselective beta blocker: propranolol, nadolol, carvedilol

138
Q

Cir: tx of active variceal bleeding

A
  1. Oxygenation and hemodynamic stability
  2. NG tube: antibiotic for SBP prophylaxis
  3. Octreotide 3-5 days
  4. EVL combo more effective
139
Q

Cir: variceal rebleeding or high rebleeding risk pts management

A

Rescue TIPS: lowers portal pressure by shunting blood from portal vein directly into hepatic vein

140
Q

Cir: secondary prevention of variceal bleeding mangement

A
  • Nonselective bb + EVL
  • TIPS if refractory: bridging therapy for good liver transplant candidates
141
Q

Cir: what is the cause of hepatic encephalopathy

A
  • Ammonia produced by intestinal bacteria that breaks down blood or urea
  • Systemic absorption is pH dependent
  • At low pH, NH3 gets ionized to NH4+ -> not able to cross membrane easily -> not absorbed efficiency -> :) !!!
142
Q

Cir: hepatic encephalopathy tx

A
  1. Nutrition
  2. Lactulose: non-absorbable disaccharide converted to lactic/formic/acetic acid by gut bacteria, so lowers pH (dose= 30-50 mL PO Q2-3H titrated to 3-4 loose stools daily)
  3. Rifaximin: antibiotic that inhibits growth of ammonia-producing gut bacteria

GI/Hepatic (2 decks)

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