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Clin Med III > Liver disorders > Flashcards

Liver disorders Flashcards

1
Q

cirrhosis pathophys

A
  • injury to hepatocytes -> fibrosis and nodular regeneration -> scarring
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2
Q

stages of cirrhosis

A
  • compensated: managed in clinic
  • compensated with varices
  • decompensated: ascites, variceal bleeding, encephalopathy, jaunce
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3
Q

common complications of cirrhosis

A
  • ascites
  • hepatorenal syndrome
  • portal HTN
  • hepatic encephalopathy
  • spontaneous bacterial peritonitis (SBP)
  • coagulopathy
  • gastroesophageal varices
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4
Q

main causes of cirrhosis

A
  • hep C
  • alcoholic liver disease
  • Hep C + alcoholic liver disease
  • NAFLD -> NASH
  • Hep B (may be coincident with hep D)
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5
Q

pathophys of NAFLD

A
  • excess fat deposition in liver -> proinflammatory state -> hepatocellular injury -> NAFLD -> NASH -> cirrhosis
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6
Q

common causes of NAFLD

A
  • DM2
  • obesity
  • typer TG
  • metabolic syndrome
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7
Q

si/sx of cirrhosis

A
  • 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
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8
Q

what skin changes are assoc with cirrhosis?

A
  • spider telangiectasis
  • caput medusa
  • palmar erythema
  • dupuytren contracture
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9
Q

PE findings for cirrhosis

A
  • findings are LATE
  • appearance of chronic illness
  • palpable firm liver
  • splenomegaly
  • ascites
  • jaundice/ icterus
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10
Q

common lab findings for cirrhosis

A
  • often absent or minimal abnormalities
  • anemia
  • WBC low
  • thrombocytopenia*
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11
Q

imaging/diagnosis for cirrhosis

A
  • US
  • CT/ MRI
  • liver biopsy- “imperfect” gold std
  • EGD for varices
  • fibroscan- best and easiest
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12
Q

MELD score

A
  • 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
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13
Q

what is included in the MELD score

A
  • total bili
  • age
  • sodium
  • INR
  • creatinine
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14
Q

portal HTN

A
  • portal vein pressure > 10-12 mmHg

- collateral BF begins to develop

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15
Q

portal HTN pathophys

A
  • pressure increases -> BF decreases -> mmHg transferred to portal vein tributaries with dilation -> collateral formation
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16
Q

sequelae of portal HTN

A
  • ascites
  • esophageal and gastric varices
  • hepatic encephalopathy
  • splenomegaly and thrombocytopenia
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17
Q

prophylactic treatment for portal HTN

A
  • nonselective BB: nadolol or propranolol
  • reduce first bleed likelihood of 50%
  • screening EGD for varices
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18
Q

most common causes of portal HTN

A
  • portal vein thrombosis
  • cirrhosis- ETOH or chronic hepatitis
  • RHF
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19
Q

ascites

A
  • pathologic accumulation of excessive fluid in peritoneal cavity
  • pts have large, distended but non-tympanitic abdomens
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20
Q

causes of ascites

A
  • cirrhosis- 80% of all cases
  • neoplasm
  • CHF
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21
Q

PE for ascites

A
  • need 1500 mL of fluid for dx so relatively inaccurate
  • abd distension
  • bulging flanks
  • shifting dullness to percussion
  • fluid wave
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22
Q

diagnosis of ascites

A
  • US

- can also do guided paracentesis for drainage and fluid analysis

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23
Q

treatment for ascites

A
  • Na restriction first line (<1.5 g/day)
  • fluid restriction (< 1.5 L/day)
  • diuretics second line: spironolactone or furosemide
  • surgical options
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24
Q

surgical treatment for ascites

A
  • large volume paracentesis
  • TIPS procedure
  • liver transplant
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25
Q

hepatic encephalopathy

A
  • 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
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26
Q

ammonia theory of encephalopathy

A
  • ammonia produced by bacteria in GIT is detoxified in liver to urea
  • in cirrhosis ammonia accumulates which is neurotoxic
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27
Q

GABA theory of encephalopathy

A
  • GABA increases neurotransmitter inhibition
  • ETOH increases GABA
  • more gut GABA made -> increased cognitive suppression
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28
Q

sx of hepatic encephalopathy

A
  • sx range in severity
  • minor impairment
  • memory impairment
  • coordination issues and falls
  • cognitive issues
  • coma
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29
Q

PE findings for hepatic encephalopathy

A
  • asterixis- hand flapping when pts are in “stop” position

- twitchiness

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30
Q

EEG findings for encephalopathy

A
  • high amplitude low frequency waves

- triphasic waves

31
Q

common causes of encephalopathy in pts with cirrhosis

A
  • infection- SBP
  • diuretic therapy
  • hypovolemia
  • renal failure
  • GI bleed
  • constipation
32
Q

treatment for hepatic encephalopathy

A
  • 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
33
Q

where do esophageal varices occur?

A
  • junction of portal and systemic venous system

- distal esophagus and proximal stomach

34
Q

variceal bleeds

A
  • 5-10% of all UGIB
  • causes severe bleeding
  • tendency to bleed directly related to portal mmHg
  • 15% mortality per episode
35
Q

risk factors for variceal bleeds

A
  • anything that increases portal HTN
  • ETOH
  • large varices
  • severe cirrhosis and/or liver failure
  • red wale sign
36
Q

red wale sign

A
  • red marks on varices
37
Q

si/sx of esophageal varices

A
  • 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
38
Q

treatment for esophageal varices

A
  • 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
39
Q

prevention of rebleed for varices

A
  • non selective BB: nadolol

- titrate to max tolerated dose

40
Q

endoscopic prevention for variceal rebleeds

A
  • band ligation tx of choice
  • conact thermal modality +/- epi injection
  • epi injection
  • sclerosant inj
  • hemoclip
41
Q

infectious causes of acute hepatitis

A
  • viral > 50%- usually hep B or C
  • CMV, EBV, HSV
  • fungal, bacterial, parasitic causes much less common
42
Q

non-infectious causes of hepatitis

A
  • alcohol
  • autoimmune
  • toxins/ drugs
  • metabolic diseases
43
Q

si/sx of hepatitis

A
  • variable presentation
  • fatigue/ malaise/ anorexia
  • n/v/f
  • enlarged tender liver
  • jaundice
  • normal to low WBC
  • markedly elevated transaminases
  • hyperbili
  • elevated PT/ INR
  • encephalopathy
44
Q

hep A

A
  • uncommon in US
  • assoc with crowding and poor sanitation
  • transmitted fecal- orally
  • vaccine avail
45
Q

mortality and progression of acute hep A to chronic

A
  • mortality very low
  • fulminant hepatitis uncommon unless pt already has HCV
  • more severe in adults than kids
  • clinical recovery usually within 3 mo
46
Q

acute hep B

A
  • variable presentation
  • rarely dev into fulminant disease or chronic HBV in adults
  • 90% of infants dev infection and half dev chronic infection
  • vaccine available
47
Q

exposure to hep B

A
  • 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
48
Q

risk factors for acute hep C

A
  • IVDU- 30% coinfection with hep c and HIV
  • body piercings
  • tattoos
  • hemodialysis
  • very low transmission sexually or maternally
  • pre-1992 blood transfusion
49
Q

how often does acute hep c become chronic?

A
  • 85% of pts that are infected
50
Q

treatment for acute HCV

A
  • 8-12 weeks of harvoni
  • clinically recover in 3-6 mo
  • low overall mortality
51
Q

acute hep D infection

A
  • 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
52
Q

acute hep D infection

A
  • 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
53
Q

autoimmune hepatitis

A
  • 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
54
Q

treatment for autoimmune hepatitis

A
  • steroids

- +/- azathioprine

55
Q

alcoholic hepatitis

A
  • 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
56
Q

sx of alcoholic hepatitis

A
  • may be asymptomatic esp with fatty liver
  • recent pd of heavy drinking usually precedes hepatitis sx
  • n/v
  • abdominal pain
  • anorexia
  • jaundice
57
Q

dx of alcoholic hepatitis

A
  • 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
58
Q

treatment for alcoholic hepatitis

A
  • alcohol cessation
  • correct nutritional deficiency- folate, thiamine, zinc
  • assist with abstinence
  • liver transplant only if abstinence for 6 mo
59
Q

what are the most common causes of drug induced hepatitis

A
  • macrobid
  • minocycline
  • most commonly abx
60
Q

chronic HBV

A
  • 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
61
Q

extrahepatic manifestations of chronic HBV

A
  • glomerulonephritis- mostly in kids

- polyarteritis nodosa- diffuse vasculitis

62
Q

risk factors for chronic HBV to progress to cirrhosis, liver failure, and HCC

A
  • persistently elevated HBV DNA or ALT
  • older, male
  • family hx of HCC
  • AFP elevated
  • co-infection with any hepatitis
63
Q

when is treatment for chronic HBV indicated

A
  • elevated transaminases
  • elevated HBV DNA
  • cirrhotic liver
  • acute liver failure
64
Q

treatment for chronic HBV

A
  • 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
65
Q

where are most new cases of chronic HCV

A
  • africa
  • central and east asia
  • back on the rise in the US due to opioid epidemic
66
Q

what is the 20/20 rule

A
  • 20 years of HCV disease= 20% risk of cirrhosis
67
Q

increased risk factors for cirrhosis in pts with HCV

A
  • chronic alcohol ingestion
  • male
  • HCV > 40 years old
  • co-infection with HIV and/or HBV
68
Q

prevention of chronic HCV

A
  • needle exchange programs
  • tx of substance abuse
  • blod donor screenings
  • universal precautions
69
Q

treatment for chronic HCV

A
  • 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
70
Q

why has HCC dropped in US

A
  • screen pts in U.S. with cirrhosis every 6 mo
71
Q

clinical presentation of HCC

A
  • insidious onset
  • weakness, weight loss, anorexia
  • ascites
  • jaundice, icterus, pruritis
  • enlarged tender liver +/- mass
72
Q

work up for HCC

A
  • 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
73
Q

biopsy for HCC

A
  • risk of seeding
  • < 1 cm mass: CT/MRI f/u every 3 mo
  • 1-2 cm- perform biopsy
  • 2+ cm- biopsy not needed
74
Q

treatment for HCC

A
  • 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

Clin Med III (26 decks)

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