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RC Study > Jaundice, ascites, encephalopathy > Flashcards

Jaundice, ascites, encephalopathy Flashcards

1
Q

Causes of jaundice

A

PREHEPATIC

  • Gilberts
  • hemolysis
  • hematoma

HEPATIC

  • tumour
  • viral hepatitis
  • drugs (incl etoh)
  • Cholestasis :
    • drugs
    • sepsis
    • parenteral nutrition
  • GVHD
  • Severe heart failure
  • Budd Chiari

POST HEPATIC

  • malignancy (pancreas, ampulla, cholangio, lymphadenopathy)
  • gallstones
  • pancreatitis
  • biliary stricture
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2
Q

What is Gilbert’s syndrome

A
  • inherited disorder 3-10% population
  • mild chronic uncongugated hyperbilirubinemia
  • no liver disease
  • no hemolysis
  • elevated levels in response to stress
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3
Q

Drug induced liver disease

A

Hepatocellular reactions

  • allupurinol
  • herbal remedies
  • halothane
  • minocycline
  • phenytoin

Cholestatic/mixed reactions

  • amox/clav
  • chlopromazine
  • erythromycin
  • TCA
  • fluoxetine
  • acetylcholinesterase inhibitors
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4
Q

Pathophysiology of sepsis and jaundice

A
  • cholestatic, non obstrucive jaundince in shock
  • hypotension
  • low hepatic blood flow
  • direct inhibition of bile secretion by endotoxin and cytokines
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5
Q

Pathophysiology of cardiac failure and liver

A
  • sinusoidal congestion
  • cholestatic picture (elevated ALP, GGt, bili)
  • Hypotension - ischemic hepatitis (shock liver)
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6
Q

Etiology of obstructive jaundice

A
  • obstruction from within liver to ampulla of vater
  • gallstones
  • pancreatic ca
  • cholangio ca
  • metastatic ca
  • HCC
  • not necessarily painless
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7
Q

Symptoms of jaundice

A
  • pruritis
  • anorexia
  • sleep
  • dyspepsia
  • encephalopathy
  • pain
  • nausea
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8
Q

Investigations for jaundice

A
  • History
  • Physical
  • Drugs
  • Portal hypertension
  • intrabdominal malignancy
  • encephelopathy (LOC, confusion, asterixis)
  • Labs: cbc, lytes, LFTS, INR, albumin)
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9
Q

Isolated ALP increase

A
  • bone disease
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10
Q

Clinical characteristics of HEMOLYTIC jaundice

A

Sx

  • asymptomatic, backache

Px

  • splenomegaly

LFTS

  • Bili < 100
  • normal ALT, ALP, INR

US

  • no dilated ducts on US
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11
Q

Clinical characteristics of HEPATOCELLULAR jaundice

A

Hx:

  • nausea, vx, anorexia, pyrexia

Px:

  • tender hepatomegaly

LFTS:

  • bili variable
  • ALT 5x increase
  • ALP 2-3 x increase
  • INR high

US

  • No dilated ducts
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12
Q

Clinical characteristics of INTRAHEPATIC CHOLESTATIC jaundice

A

Hx:

  • deep jaundice
  • dark urine, light stools
  • pruritis

Px:

  • tender hepatomegaly

LFTS

  • Bili > 500 ug/L
  • ALT 2-5x
  • ALP 3-5 x
  • INR high

US:

  • NO dilated ducts
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13
Q

Clinical characteristics of POSTHEPATIC CHOLESTATIC (obstructive) jaundice

A

Hx:

  • deep jaundice
  • dark urine, light stools
  • pruritis
  • cholangitis
  • biliary colic

Px:

  • hepatomegaly
  • palpaple GB, murphy’s sign

LFTS:

  • Bili > 500
  • ALT 2-5x
  • ALP 3-5x
  • INR high

US:

  • Dilated bile ducts

Vit K - Yes

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14
Q

Intrahepatic cholstasis VS post hepatic cholestasis

A
  • palpable GB
  • INR corrects with vit K
  • dilated bile ducts on US
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15
Q

Imaging for jaundice

A

US

  • cheap bedside no radiation
  • biliary duct dilatation

CT

  • staging, smaller lesions

MRCP

  • benging vs malignant lesions
  • no risks like ERCP

ERCP

  • imaging, cytology, dilatation, stents
  • risks: cholangitis, perforation, pancreatitis, bleeding
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16
Q

Biliary drains

A
  • ERCP with stent
  • Percutaneous transhepatic biliary drainage
    • proximal obstruction to CBD
    • distorted anatomy
  • Internal/external drain
    • tip lies in bowel
    • bile drains either internally into bowel or externally into bag
17
Q

Nutrition and cholestasis

A
  • chronic cholestasis
  • malabsorption of fat soluble vitamins
  • Vit K deficiency
  • prlonged INR
18
Q

Presentation of pruritis

A
  • itch does not correlate with bili level
  • palms/soles –> generalized
  • circadian rhythm worst 12:00-18:00
19
Q

Pathophysiology of Pruritus

A
  • Opioids system
    • endogenous opioids increased in cholestatic disease
    • kappa and mu opioid receptors
    • naloxone
  • Serotonergic system
    • sertraline
  • Gabaergic system
  • Lysophosphatidic autotaxin
20
Q

Management of Pruritis

A
  • Mild
    • emollients
    • warm bath
    • antihistamines but not effective
  • Moderate to severe
    • bile acid sequestrants (cholestyramine 4-16g)
    • rifampin 150-300 mg po bid (reduces autotaxan expression, MOA unknown)
    • naltrexone 12.5-50 mg po od
    • sertraline 75 mg po od
21
Q

Non pharmacological management of pruritis

A
  • cut fingernails short
  • wear cotton gloves at night
  • stay cool
  • lessen sweating
22
Q

Ascites

A
  • 85% cirrhosis
  • 10% malignancy
  • ovarian, urothelial, peritoneal mesothelioma
  • colon, breast, gastric, pancreatic, lung
  • lymphoma
23
Q

Prognosis of malignancy related ascites

A
  • non ovarian cancer - < 3 months
  • epithelial ovarian cancer - much longer
24
Q

Peritoneovenous shunts and TIPS

A
  • treats medically refractory ascites
  • shunt : transfers fluid via one way valve from peritoneum to venous circulation
  • TIPS : trasnjugular intrahepatic portosystemic shunt
    • wire, mesh coil stent into hepatic vein
    • expanded
    • shunt bypasses liver, reduces portal pressure
  • longer prognosis
  • complications: fluid overload, bleeding, infection, vte, vena caval thrombosis
  • peritonitis, HE
  • CI: loculated ascites, hemorrhagic/chylous ascites, poor cardiac or renal function
25
Q

Hepatic Encephelopathy : definition and pathophys

A
  • neuropsych disturbance from progressive liver disease
  • abnormal cognitive, motor, psychiatric disturbances
  • cirrhosis
  • malignancy (rare)
  • sign of decompenastion
  • shunting or damaged hepatocytes unable to metabolise ammonia
26
Q

Causes of HE

A
  • ammonia build up (generated in small intestine by bacteria)
  • normally transport by portal vein to liver where it is metabolized and excreted
  • Impaired by portosystemic shunting or hepatocyte dysfunction
  • ammonia accumulates in systemic circulation, crosses BBB
  • increased GABA activity
  • increased osmotic pressure in astrocytes
27
Q

Precipitants of HE in liver disease

A
  • ETOH
  • Infection
  • Sedating drugs
  • Dehydration
  • Constipation
  • Anemia
  • GI Bleeding
28
Q

Diagnosis of HE

A
  • Diagnosis of exclusion
  • r/o CVA, space occupying lesion
  • r/o metabolic encephalopathy (lytes, uremia, etc)
  • Blood ammonia level

clinical findings

  • fetor hepaticus
  • asterixis
  • jaundice
  • EPS (tremor, bradykinesia, cog wheel, shuffling gait)
29
Q

West Haven Criteria for HE

A
  • Stage 0
    • impairment on psychomotor testing only
    • no asterixis
  • Stage 1
    • mild lack of attention
    • altered sleep pattern
    • mild asterixis/tremor
  • Stage 2
    • lethargy, disorientation
    • slurred speech
    • asterixis
  • Stage 3
    • somnolent, but rousable
    • disoriented
    • bizarre behaviour
    • no asterixis, high muscle tone, hyperreflexia
  • Stage 4
    • coma
    • decrebrate posturing
30
Q

Management of HE

A
  • Diet
    • high protein, vegetable protein
  • Disaccharides
    • lactulose preferentially consumed by intestinal bacteria
    • competitively reduces ammonia production
    • increases BMs and exretion of toxins
    • Titrate to 2-3 BM/day
    • weak evidence
  • Antibiotics
    • rifaximin
    • reduce urease-producing bacteria in gut
    • poorly absorbed PO, effective at reducing ammonia
    • use in addition to lactulose if needed
  • Euvolemia / avoid dehydration
31
Q

Acute management of HE

A
  • Identify and treat underlying cause
    • para for SBP
    • cbc, lytes, ammonia, Cr, CT head, CXRAy pna, pan culture
    • recent meds, intoxication
    • GI bleeding
    • constipation
  • Lower blood ammonia
    • Lactulose and titrate
    • lactulose enemas
  • In no improvement in 48 hours, start rifaximin po

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