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
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
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
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
5
Q
Pathophysiology of cardiac failure and liver
A
- sinusoidal congestion
- cholestatic picture (elevated ALP, GGt, bili)
- Hypotension - ischemic hepatitis (shock liver)
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
7
Q
Symptoms of jaundice
A
- pruritis
- anorexia
- sleep
- dyspepsia
- encephalopathy
- pain
- nausea
8
Q
Investigations for jaundice
A
- History
- Physical
- Drugs
- Portal hypertension
- intrabdominal malignancy
- encephelopathy (LOC, confusion, asterixis)
- Labs: cbc, lytes, LFTS, INR, albumin)
9
Q
Isolated ALP increase
A
- bone disease
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
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
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
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
14
Q
Intrahepatic cholstasis VS post hepatic cholestasis
A
- palpable GB
- INR corrects with vit K
- dilated bile ducts on US
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
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
