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GI II Exam 2 > DSA: Approach to Hepatobiliary Patient - Chronic Liver Disease (McGowan) > Flashcards

DSA: Approach to Hepatobiliary Patient - Chronic Liver Disease (McGowan) Flashcards

1
Q

What are two associations with HBV and HCV infection, and what are two non-invasive ways to identify presence/absence of fibrosis in Chronic Hepatitis?

A

HBV: polyarteritis nodosa
HCV: mixed cryoglobulinemia

ID: serum FibroSure and US elastography

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2
Q

Chronic HBV vs Chronic HVC

A

HBV: endemic in Asia/sub-Saharan Africa

  • 90% of infants with maternal transmission
  • inc. risk in males, high chronicity with younger age
  • asymptomatic healthy carrier state (75%)

HCV: cirrhosis inc. in males, heavily EtOH, tobacco, infection after 40 yrs

  • coffee slows progression; HCC has high risk
  • can have normal AST/ALT
  • HCV Ab + HCV RNA needed for chronic diagnosis
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3
Q

Autoimmune Hepatitis

What is the difference between Type I and Type II, how does it clinically manifest, and what are diagnostic findings for each type?

How can it be treated?

A

Type I: classic, anti-SM, or antinuclear Ab (ANA)
- MOST COMMON
Type II: anti-liver/kidney microsomal Ab (anti-LKM)

CM: progressive jaundice, epistaxis, amenorrhea (healthy young female with stigmata of cirrhosis)

D: serum aminotransferase lvls may be > 1000, total bilirubin usually inc; Type I hypergammaglobulinemia/SM Ab (SMA), ANA; Type II anti-LMK Ab

treat with glucocorticoids

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4
Q

Alcohol Liver Disease

What is it, what does it cause, and how does it present?

A
  • excessive alcohol causing fatty liver, alcoholic hepatitis, cirrhosis (exceeds 80g/day in males and 30-40 g/day in females x 10 yrs)
  • causes Fatty Liver (Steatosis) = asymptomatic hepatomegaly and mild elevations in liver tests

P: anorexia, nausea, vomiting, fever, jaundice, tender hepatomegaly, RUQ pain

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5
Q

Alcohol Liver Disease

What labs are associated with it (4), what are 3 imaging options, and what is seen on liver biopsy?

A

L: AST 2x > ALT, bilirubin inc. (>10 mg/dL), anemia (usually macrocytic –> folic acid deficiency), marked prolongation of PROTHROMBIN time

I: US, CT w/intravenous contrast/MRI, US elastography

LBx: Mallory-Dank bodies (alcoholic hyaline)

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6
Q

Alcohol Liver Disease

How is it treated (non-severe vs severe) and what are 2 complications it can lead to (WE/KS)?

A

Tx: abstinence from alcohol, thiamine 100 mg, folic acid 1 mg, zinc

  • give thiamine with or before glucose
  • glucose can precipitate Wernicke-Korsakoff
  • for severe (DF > 32, MELD > 21, GAW > 9)
    • steroid and pentoxifylline
    • liver transplant (abstain from EtOH for 6 months)
  • can cause Wernicke Encephalopathy, Korsakoff Syndrome (permanent)
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7
Q

What are Wernicke Encephalopathy and Korsakoff Syndrome?

What 4 things is severe alcoholic hepatitis characterized by? (B/P/H/A)

A

WE: confusion, ataxia, abnormal eye movements
- treat with Thiamine

KS: severe memory issues, confabulation

SAH: total bilirubin > 8-10 mg/dL, PTT > 6 sec, hypoalbuminemia, azotemia
- critically ill = 30 day mortality of > 50%

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8
Q

What is the threshold for alcohol consumption in female and male patients with Non-alcoholic Fatty Liver Disease (NAFLD)?

A

Female: < 20 g EtOH/day

Male: < 30 g EtOH/day

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9
Q

Non-Alcoholic Fatty Liver Disease

What is it, what causes it, what labs are associated with it and how can it be viewed?

How is it treated?

A
  • MOST COMMON cause of chronic liver disease in US
  • caused by Metabolic Syndrome (obesity, DM, hypertriglyceridemia = inc. risk of disease)

L: mild AST/ALT elevation (can be normal in up to 80%)

I: Ultrasound elastography (assess fibrosis) and Liver Biopsy (diagnostic) –> NASH

T: lifestyle modifications, liver transplant (if fibrosis)
- physical activity and coffee protect against it

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10
Q

Alpha-1 Antitrypsin Deficiency

What is it, what two findings are diagnostic for it (A/P), how is it treated, and what are two complications of disease?

A
  • AR defective a1-antitrypsin that accumulates in hepatocytes and causes liver damage (protease activity NOT inhibited)

MC inherited hepatic disorder in children/infants

D: low a1-antitrypsin, check phenotype, PiZZ genes

T: no smoking, liver transplant

C: emphysema at young age, micronodular cirrhosis (risk of HCC)

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11
Q

Primary Biliary Cholangitis

What is it, what are 4 common risk factors of disease (U/S/HR/HD), and how does it clinically present?

What molecule has isolated increase?

A
  • chronic liver disease; autoimmune destruction of small intrahepatic bile ducts and cholestasis (F > 50 yo)
    • asymptomatic isolated inc. in ALP

RF: UTI, smoking, hormone replacement, hair dye

C: pruritus, fatigue, progressive jaundice, XANTHELASMA; associated with other autoimmune disease

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12
Q

Primary Biliary Cholangitis

What are 3 diagnostic findings of disease (A/A/M), how is it treated (U), and what complication does it lead to?

A

D: AMA Abs (90-95%), inc. ALP, inc. IgM lvls (get liver biopsy if AMA (-))

T: ursodeoxycholic acid

C: cirrhosis –> liver failure

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13
Q

Hemochromatosis

What is it, what is the classic tetrad it presents with (C/SP/DM/HF), what are 4 diagnostic findings, and how can it be visualized (3)?

A
  • AR HFE gene mutation leading to inc. iron absorption in the duodenum (hemosiderin in liver, pancreas, heart, testes, kidneys of MALES)

T: cirrhosis/hepatomegaly, skin pigment (bronze), diabetes mellitus, heart failure (cardiac dysfunction)

D: HFE gene mutation, inc. plasma iron w/> 45% transferrin, inc. serum ferritin, mildly abnormal liver test

V: MRI, CT, liver biopsy (is cirrhosis present)

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14
Q

Hemochromatosis

Who should get screening, how is disease treated/managed, and what 3 organisms are pts at inc. risk of infection from (VV/LM/YE)?

A
  • screen all first-degree family members w/iron studies and HFE testing (evidence of iron overload)

T: phlebotomy therapy (deplete iron stores), avoid iron-rich food, monitor, PPIs, possible liver transplant
- if anemia/thalassemia = DEFEROXAMINE

  • inc. risk of Vibrio vulnificus, Listeria monocytogenes, Yersinia enterocolitica
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15
Q

Wilsons Disease

What is it, how does it present, what are diagnostics of disease, and how can it be treated (OP/LT)?

A
  • AR disorder of Chromosome 13 (ATP7B) in persons < 40 yo causing impaired copper excretion into bile and failure to incorporate in ceruloplasmin
    • liver, brain, eye accumulations (also Hemo Anemia)
    • excessive absorption and dec. excretion of copper

P: kids w/hepatitis, Coombs (-) hemolytic anemia, portal hypertension, hypersplenism, psychiatric abnormalities

D: Kayser-Fleischer rings, inc. urine copper, low serum ceruloplasmin, inc. hepatic copper, inc. copper in brain

T: oral penicillamine and liver transplant

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16
Q

How does Heart Failure affect the liver?

What molecular marker is elevated?

What is the hallmark finding if ischemia is involved?

A
  • pts w/right heart failure cause passive congestion of the liver = “Nutmeg” liver –> ischemic hepatitis
  • hepatojugular reflux is present and tricuspid regurgitation can cause pulsatile liver (jaundice in worse outcomes)
  • marked elevated serum N-terminal-proBNP or BNP

Hallmark: “Shock Liver” - elevated serum aminotransferases > 5000 units/L and early rapid rise in LDH levels (ALP/bilirubin elevation is mild)

17
Q

What is the peak time of incidence for Cirrhosis and what are the 3 most common causes?

What does cirrhosis due to the liver and what can help protect against development?

A
  • peaks around ages 40-60

CC: Hepatitis C, alcoholic liver disease, NAFLD

  • causes fibrosis that replaces normal liver and can lead to formation of regenerative nodules (destroys livers vascular and lobular architecture)

P: higher coffee and tea consumption

18
Q

Liver Cirrhosis

What is Dupuytren’s Contracture and Muehrcke/Terry Nails?

A

DC: pts. ring and pinky finger are contracted on hand

Muehrcke lines: double white lines at base of nail
Terry nails: dark line at tip of nail
- both are problems associated with low albumin
- commonly seen in pts with cirrhosis

19
Q

What is Abdominal Paracentesis used for?

What findings would lead you to find Portal Hypertension vs SBP?

A
  • diagnostic and therapeutic procedure done on all pts with new onset ascites to determine cause (want to rule out Spontaneous Bacterial Peritonitis)
  • check fluid lvls for albumin, WBC w/diff, culture and gram staining (due blood culture of fluid)

PH: SAAG > 1.1
SBP: > 250 PMNs/mL

20
Q

What are two non-invasive predictive indices for hepatic fibrosis? (UE/F)

A
  1. Ultrasound Elastography
  2. Fibrosure (more specific serum diagnostics)
    • non-invasive blood test for markers of fibrosis
    • high = advanced fibrosis/low = no advanced fibrosis
21
Q

What are 3 complications that liver cirrhosis can lead to?

A

Hepatocellular carcinoma, HIV co-infection, decompensated cirrhosis

22
Q

How much acetaminophen should a patient with liver disease take to help manage cirrhosis?

What should be checked and how often to help screen for Hepatocellular Carcinoma in a pt. with cirrhosis?

A
  • max 2 grams every 24 hours

- check Alpha fetoprotein (AFP) and ultrasound every 6 months for HCC screening

23
Q

What would you use to treat Spontaneous Bacterial Peritonitis?

A

Ceftriaxone or cefotaxime

  • consider IV albumin to help with renal perfusion pressure
24
Q

MELD/MELD-Na (B/C/S/I) and Child-Turcotte-Pugh (B/A/P) Scoring for Cirrhosis

What do you order for each (4/3) and what scores are associated with worse prognosis?

A

M: order bilirubin, creatinine, sodium (check CMP), order INR, check for recent dialysis

  • > 10 = worsening condition
  • > 14 = needs to be on transplant list

CTP: order bilirubin, albumin (check CMP/hepatic function panel), order PT/INR, check for ascites/encephalopathy

  • reported usually A, B, C w/C being the most severe
  • > 7 indicates higher severity if numerical
25
Q

Ascites

What is the most common cause, what are two physical exam findings seen in patients with it, and what laboratory testing should be done?

A
  • MCC is PORTAL HYPERTENSION secondary to chronic liver disease (80%)

PE: asterixis secondary to encephalopathy may be present, “shifting dullness” - change in percussion based on position (need 1500 mL of fluid)

L: Abdominal US w/Doppler (vascular evaluation) and Abdominal Paracentesis

  • check cell count (< 500 leukocytes, < 250 PMN)
  • check albumin/total protein
  • culture and Gram stain
26
Q

What is a SAAG Score and what can it tell us?

A

SAAG = serum albumin - ascites albumin
- used to determine cause of ascites in pt.

SAAG > 1.1 g/dL
- portal hypertension, nonperitoneal cause of ascites

SAAG < 1.1 g/dL
- ascites caused by peritoneal cause

27
Q

What are 5 conditions related to SAAG score of < 1.1 g/dL (BL/NS/P/PC/TB) and what are 6 conditions related to SAAG score of > 1.1 g/dL(C/BC/LM/C/IO/SO)?

A

SAAG < 1.1 g/dL

  • biliary leak, nephrotic syndrome, pancreatitis
  • peritoneal carcinomatosis, tuberculosis

SAAG > 1.1 g/dL

  • cirrhosis, Budd-Chiari, massive liver metastasis
  • CHF, IVC obstruction, sinusoidal obstruction
28
Q

What is Hepatic Encephalopathy and what is it caused by?

A
  • alteration in mental status in the presence of liver failure (ammonia lvls typically elevated, but do not correlate with severity of liver disease)

PE: asterixis (flapping tremor), confusion, slurred speech, being sleeping/difficult arousal

mild confusion –> drowsy –> stupor –> COMA

29
Q

Hepatocellular Carcinoma

Who is most at risk, how is it screened, how is it diagnosed, and how can it be treated (S/A/TACE)?

A

RF: 50-60 yo M w/cirrhosis from Asia/Africa (AFLATOXIN EXPOSURE)

S: AFP/US every 6 months, Hep B vaccine

D: pt. w/liver disease with abnormality on ultrasound or rising alpha fetoprotein (AFP)
- also abnormal liver function tests/enzymes

T: surgical resection/transplant, radiofrequency ablation, transcatheter arterial embolization (TACE)

30
Q

Liver Transplant

When should it be considered, what are considerations for pts. with alcoholism, and what is needed after transplant?

A
  • considered in pts. with irreversible, progressive CLD, ACLF, and certain metabolic diseases
    • check MELD/MELD-Na score
    • > 14 should be on transplant listing
  • pts. with alcoholism should abstain for 6 months
  • need immunosuppression after transplant

GI II Exam 2 (8 decks)

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