Cirrhosis, Portal HTN, etc. Flashcards
(37 cards)
Patho cirrhosis
- end result of hepatocellular injury–>slow fibrosis and nodular regeneration throughout the liver
- hepatocyte injury due to cytokine release and inflammatory response–> hepatocyte/bile duct cell/ vascular endothelial cell death
Is cirrhosis reversible?
No, only the initial fibrosis is via removal
Complications of cirrhosis
ascites portal htn hepatorenal syndrome hepatic encephalopathy spontaneous bacterial peritonitis coagulopathy GI varices
Cause cirrhosis
hepatitis c alcoholic liver disease hep c + alcoholic liver disease Non-alcoholic fatty liver dz (obesity, DM, hyperTG) Hep B hemochromatosis wilson dz alpha 1 antitrypsin deficiency
Clinical Cirrhosis
- asymptomatic till late stage
- fatigue
- sleep disturbance
- muscle cramps
- weight loss/wasting
- spider telangiectasias on face
- abdominal and thoracic superficial veins are dilated
- palmar erythema
- peripheral edema
- splenomegaly
- liver enlargement; palpable and firm
- ascites
- hematemesis
- icteric sclera
- pruritis with no rash
- encephalopathy (confusion/altered mental status)
Labs cirrhosis
macrocytic anemia due to ETOH suppression of EPO
low WBC
Thrombocytopenia
Imaging cirrhosis
US/CT- nodular liver
The imperfect gold standard for cirrhosis
liver biopsy
Fibrosure test
- biomarker test that uses the results of 6 serum tests to generate a score which is equivalent to the predictive value of liver biopsy
- replaces liver biopsy
Transient elastography
- used at the bedside, non-invasive test
- ultrasound passes a vibratory wave through the liver and measure hepatic fibrosis/liver stiffness
- limitations ascites, chest wall fat, obesity, and severe liver inflammation
MELD score
- prognostic scoring system for cirrhosis
- measure mortality risk and predict short and intermediate survival and complication of cirrhosis
- how bad is my disease and where am I on the transplant list
MELD score includes what
total bilirubin age sodium INR creatinine
Scores of MELD score
6= 90 mortality of 40%
16-20= 90 mortality of 56%
more than 26= 90 mortality of 85%
Patho portal HTN
- increased hydrostatic pressure within the portal vein; more than 10-12mmhg –> collaterals develop
- progressive increase in peripheral resistance to portal venous flow
- as mmhg increases blood flow decreases and then mmhg is transferred to portal vein tributaries with subsequent dilation –> collateral formation
Sequelae of portal HTN
ascites
esophageal and gastric varices
splenomegaly and thrombocytopenia
Prophylactic tx for portal HTN
non-selective beta blocker (nadolol)
Cause portal HTN
portal/splenic vein thrombosis cirrhosis(mc) acute hepatitis schistosomiasis budd-chiari R. HF
Patho Ascites
pathologic accumulation of excess fluid in the peritoneal cavity
Causes of ascites
cirrhosis
neoplasms
CHF
Clinical ascites
- abdominal distention
- bulging flanks
- shifting dullness to percussion
- fluid wave
- *need 1500ml of fluid to see this
Dx ascites
US
paracentesis
Tx ascites
Na+ (<1.5g) and water restriction (<1.5L)- first line
Diuretic- 2nd line (spironolactone and furosemide): make sure not water restricted–> dehydration
Surgery
- large volume paracentesis (5-7L)
- Transjugular inrahepatic portosystemic shunt (TIPS)- need MELD<18 and total bilirubin <3 –> serious complications
- liver transplant
What is hepatic encephalopathy
late cirrhosis induced mental status change
- personality change
- intellectual impairment
- depressed level of consciousness
Patho hepatic encephalopathy
bacteria in gut produces ammonia and the liver usually detoxifies it but due to cirrhosis the liver cannot detoxify the ammonia–> accumulation
GABA increase neurotransmitter inhibition–> ammonia accumulation
