Liver disorders Flashcards
cirrhosis pathophys
- injury to hepatocytes -> fibrosis and nodular regeneration -> scarring
stages of cirrhosis
- compensated: managed in clinic
- compensated with varices
- decompensated: ascites, variceal bleeding, encephalopathy, jaunce
common complications of cirrhosis
- ascites
- hepatorenal syndrome
- portal HTN
- hepatic encephalopathy
- spontaneous bacterial peritonitis (SBP)
- coagulopathy
- gastroesophageal varices
main causes of cirrhosis
- hep C
- alcoholic liver disease
- Hep C + alcoholic liver disease
- NAFLD -> NASH
- Hep B (may be coincident with hep D)
pathophys of NAFLD
- excess fat deposition in liver -> proinflammatory state -> hepatocellular injury -> NAFLD -> NASH -> cirrhosis
common causes of NAFLD
- DM2
- obesity
- typer TG
- metabolic syndrome
si/sx of cirrhosis
- sx ONLY in late stages
- fatigue, sleep disturbances
- weight loss/ wasting/ anorexia
- skin changes
- abd pain
- ascites
- hematemesis
- coagulopathies
- jaundice, icteric sclera, pruritis
- GYN dysfunction
- encephalopathy
what skin changes are assoc with cirrhosis?
- spider telangiectasis
- caput medusa
- palmar erythema
- dupuytren contracture
PE findings for cirrhosis
- findings are LATE
- appearance of chronic illness
- palpable firm liver
- splenomegaly
- ascites
- jaundice/ icterus
common lab findings for cirrhosis
- often absent or minimal abnormalities
- anemia
- WBC low
- thrombocytopenia*
imaging/diagnosis for cirrhosis
- US
- CT/ MRI
- liver biopsy- “imperfect” gold std
- EGD for varices
- fibroscan- best and easiest
MELD score
- measure mortality risk and prognosis of live disease
- scored 4-40, higher meld score= higher placement on transplant list
- 16-20= 56% mortality
- > 26= 85% mortality in 90 days
what is included in the MELD score
- total bili
- age
- sodium
- INR
- creatinine
portal HTN
- portal vein pressure > 10-12 mmHg
- collateral BF begins to develop
portal HTN pathophys
- pressure increases -> BF decreases -> mmHg transferred to portal vein tributaries with dilation -> collateral formation
sequelae of portal HTN
- ascites
- esophageal and gastric varices
- hepatic encephalopathy
- splenomegaly and thrombocytopenia
prophylactic treatment for portal HTN
- nonselective BB: nadolol or propranolol
- reduce first bleed likelihood of 50%
- screening EGD for varices
most common causes of portal HTN
- portal vein thrombosis
- cirrhosis- ETOH or chronic hepatitis
- RHF
ascites
- pathologic accumulation of excessive fluid in peritoneal cavity
- pts have large, distended but non-tympanitic abdomens
causes of ascites
- cirrhosis- 80% of all cases
- neoplasm
- CHF
PE for ascites
- need 1500 mL of fluid for dx so relatively inaccurate
- abd distension
- bulging flanks
- shifting dullness to percussion
- fluid wave
diagnosis of ascites
- US
- can also do guided paracentesis for drainage and fluid analysis
treatment for ascites
- Na restriction first line (<1.5 g/day)
- fluid restriction (< 1.5 L/day)
- diuretics second line: spironolactone or furosemide
- surgical options
surgical treatment for ascites
- large volume paracentesis
- TIPS procedure
- liver transplant
hepatic encephalopathy
- late cirrhosis induced mental status changes
- personality changes
- intellectual impairment
- depressed level of consciousness
- occurs in up to 70% of pts with cirrhosis- liver loses ability to detoxify
ammonia theory of encephalopathy
- ammonia produced by bacteria in GIT is detoxified in liver to urea
- in cirrhosis ammonia accumulates which is neurotoxic
GABA theory of encephalopathy
- GABA increases neurotransmitter inhibition
- ETOH increases GABA
- more gut GABA made -> increased cognitive suppression
sx of hepatic encephalopathy
- sx range in severity
- minor impairment
- memory impairment
- coordination issues and falls
- cognitive issues
- coma
PE findings for hepatic encephalopathy
- asterixis- hand flapping when pts are in “stop” position
- twitchiness
EEG findings for encephalopathy
- high amplitude low frequency waves
- triphasic waves
common causes of encephalopathy in pts with cirrhosis
- infection- SBP
- diuretic therapy
- hypovolemia
- renal failure
- GI bleed
- constipation
treatment for hepatic encephalopathy
- lactulose (laxative)- titrate up to 3-4 BM per day
- lactulose stimulates ammonia from tissues to gut to get passed in stool
- xifaxan (abx)- targets bacteria in gut that are amoniagenic so absorbed in gut and passed out in stool
where do esophageal varices occur?
- junction of portal and systemic venous system
- distal esophagus and proximal stomach
variceal bleeds
- 5-10% of all UGIB
- causes severe bleeding
- tendency to bleed directly related to portal mmHg
- 15% mortality per episode
risk factors for variceal bleeds
- anything that increases portal HTN
- ETOH
- large varices
- severe cirrhosis and/or liver failure
- red wale sign
red wale sign
- red marks on varices
si/sx of esophageal varices
- hematemesis*- large volumes
- melena, hematochezia
- pale, hypotensive, lightheaded, syncope, orthostatic, tachycardic
- any si/sx of hemorrhagic shock
- liver disease/ cirrhosis signs
- can cause hepatic encephalopathy
treatment for esophageal varices
- 2 large bore IV access/ central access
- PRBC txn hb > 7
- vit k/ FFP if significant coagulopathy
- NTG with lavage
- octreotide
- tamponade
- endoscopy- ligation/ banding, injection, sclerotherapy
- TIPS
- angiotherapy
- surgery last line
prevention of rebleed for varices
- non selective BB: nadolol
- titrate to max tolerated dose
endoscopic prevention for variceal rebleeds
- band ligation tx of choice
- conact thermal modality +/- epi injection
- epi injection
- sclerosant inj
- hemoclip
infectious causes of acute hepatitis
- viral > 50%- usually hep B or C
- CMV, EBV, HSV
- fungal, bacterial, parasitic causes much less common
non-infectious causes of hepatitis
- alcohol
- autoimmune
- toxins/ drugs
- metabolic diseases
si/sx of hepatitis
- variable presentation
- fatigue/ malaise/ anorexia
- n/v/f
- enlarged tender liver
- jaundice
- normal to low WBC
- markedly elevated transaminases
- hyperbili
- elevated PT/ INR
- encephalopathy
hep A
- uncommon in US
- assoc with crowding and poor sanitation
- transmitted fecal- orally
- vaccine avail
mortality and progression of acute hep A to chronic
- mortality very low
- fulminant hepatitis uncommon unless pt already has HCV
- more severe in adults than kids
- clinical recovery usually within 3 mo
acute hep B
- variable presentation
- rarely dev into fulminant disease or chronic HBV in adults
- 90% of infants dev infection and half dev chronic infection
- vaccine available
exposure to hep B
- exposure to needle sticks, sex exposure, newborns
- HBIG within 7 days of exposure followed by HBV vaccine series
- newborns at risk= vaginal delivery, get HBIG and HBV vaccine within 12 hours of birth
- mom may need antiviral tx in 3rd trimester if viral load is high
risk factors for acute hep C
- IVDU- 30% coinfection with hep c and HIV
- body piercings
- tattoos
- hemodialysis
- very low transmission sexually or maternally
- pre-1992 blood transfusion
how often does acute hep c become chronic?
- 85% of pts that are infected
treatment for acute HCV
- 8-12 weeks of harvoni
- clinically recover in 3-6 mo
- low overall mortality
acute hep D infection
- ONLY assoc with HBV
- HBsAg present
- usu percutaneous blood exposure
- in combo with HBV carries worse short term prognosis with rapid fulminant hepatitis/ cirrhosis
- more common in africa, cnetral asia, e europe, amazon
acute hep D infection
- waterborne, only transmitted fecal orally
- very rare
- usu only in immunocomp
- can be spread by pig so consuming undercooked meats or pet is RF
- no chronic state
- tx- sofosbuvir
- more common in central and SE asia, middle east, north africa
autoimmune hepatitis
- usu in young or middle aged women
- insidious onset
- 40% have acute hepatitis presentation following viral illness or drug exposure
- elevated transaminases, pos ANA, elevated IgG
- liver bx
treatment for autoimmune hepatitis
- steroids
- +/- azathioprine
alcoholic hepatitis
- acute or chronic inflammation and necrosis of liver
- reversible inflammation- stop drinking
- women more susceptible
- 10-15% of people who consume > 50g alcohol/day for ten years will dev cirrhosis
sx of alcoholic hepatitis
- may be asymptomatic esp with fatty liver
- recent pd of heavy drinking usually precedes hepatitis sx
- n/v
- abdominal pain
- anorexia
- jaundice
dx of alcoholic hepatitis
- macrocytic anemia
- thrombocytopenia*
- AST/ ALT ratio 2:1 and mildly elevated
- total bili elevated
- PT/ INR elevated
- US, CT/MRI
- prognosis assessed with MELD score and glasgow alcoholic hepatitis score
treatment for alcoholic hepatitis
- alcohol cessation
- correct nutritional deficiency- folate, thiamine, zinc
- assist with abstinence
- liver transplant only if abstinence for 6 mo
what are the most common causes of drug induced hepatitis
- macrobid
- minocycline
- most commonly abx
chronic HBV
- dominant cause of cirrhosis and HCC
- half of HCC cases world wide due to HBV
- transmitted sexually and hematogenously
- half of infants with HBV dev chronic infection
- higher HBV DNA= better predictor of cirrhosis and HCC
extrahepatic manifestations of chronic HBV
- glomerulonephritis- mostly in kids
- polyarteritis nodosa- diffuse vasculitis
risk factors for chronic HBV to progress to cirrhosis, liver failure, and HCC
- persistently elevated HBV DNA or ALT
- older, male
- family hx of HCC
- AFP elevated
- co-infection with any hepatitis
when is treatment for chronic HBV indicated
- elevated transaminases
- elevated HBV DNA
- cirrhotic liver
- acute liver failure
treatment for chronic HBV
- entecavir and tenofovir
- may be life long treatment
- want to convert pt from hep B envelope antigen to antibody
- d/c treatment after 6 mo of seroconversion
where are most new cases of chronic HCV
- africa
- central and east asia
- back on the rise in the US due to opioid epidemic
what is the 20/20 rule
- 20 years of HCV disease= 20% risk of cirrhosis
increased risk factors for cirrhosis in pts with HCV
- chronic alcohol ingestion
- male
- HCV > 40 years old
- co-infection with HIV and/or HBV
prevention of chronic HCV
- needle exchange programs
- tx of substance abuse
- blod donor screenings
- universal precautions
treatment for chronic HCV
- goal= cure, prevent cirrhosis and HCV
- treatment recommended for everyone
- usually treated with harvoni
- 12 weeks tx without cirrhosis
- 24 weeks of treatment with cirrhosis
why has HCC dropped in US
- screen pts in U.S. with cirrhosis every 6 mo
clinical presentation of HCC
- insidious onset
- weakness, weight loss, anorexia
- ascites
- jaundice, icterus, pruritis
- enlarged tender liver +/- mass
work up for HCC
- CBC, CMP, lipase, PT/INR
- alpha fetoprotein
- HCV, HBV testing
- alpha 1 antitrypsin
- alcohol
- US and CT for screening
- MRI best for small lesions
- biopsy may or may not be needed
biopsy for HCC
- risk of seeding
- < 1 cm mass: CT/MRI f/u every 3 mo
- 1-2 cm- perform biopsy
- 2+ cm- biopsy not needed
treatment for HCC
- surgical= only long term cure
- resecetion of tumor < 5 cm and minimal/ no cirrhosis
- liver transplants highly successful
- medical/ palliative tx if dont meet transplant criteria
- chemo and radiation both ineffective
