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

(30 cards)

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
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?
- 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
What is a SAAG Score and what can it tell us?
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
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)?
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
What is Hepatic Encephalopathy and what is it caused by?
- 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
Hepatocellular Carcinoma Who is most at risk, how is it screened, how is it diagnosed, and how can it be treated (S/A/TACE)?
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
Liver Transplant When should it be considered, what are considerations for pts. with alcoholism, and what is needed after transplant?
- 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