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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
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
26
ammonia theory of encephalopathy
- ammonia produced by bacteria in GIT is detoxified in liver to urea - in cirrhosis ammonia accumulates which is neurotoxic
27
GABA theory of encephalopathy
- GABA increases neurotransmitter inhibition - ETOH increases GABA - more gut GABA made -> increased cognitive suppression
28
sx of hepatic encephalopathy
- sx range in severity - minor impairment - memory impairment - coordination issues and falls - cognitive issues - coma
29
PE findings for hepatic encephalopathy
- asterixis- hand flapping when pts are in "stop" position | - twitchiness
30
EEG findings for encephalopathy
- high amplitude low frequency waves | - triphasic waves
31
common causes of encephalopathy in pts with cirrhosis
- infection- SBP - diuretic therapy - hypovolemia - renal failure - GI bleed - constipation
32
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
33
where do esophageal varices occur?
- junction of portal and systemic venous system | - distal esophagus and proximal stomach
34
variceal bleeds
- 5-10% of all UGIB - causes severe bleeding - tendency to bleed directly related to portal mmHg - 15% mortality per episode
35
risk factors for variceal bleeds
- anything that increases portal HTN - ETOH - large varices - severe cirrhosis and/or liver failure - red wale sign
36
red wale sign
- red marks on varices
37
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
38
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
39
prevention of rebleed for varices
- non selective BB: nadolol | - titrate to max tolerated dose
40
endoscopic prevention for variceal rebleeds
- band ligation tx of choice - conact thermal modality +/- epi injection - epi injection - sclerosant inj - hemoclip
41
infectious causes of acute hepatitis
- viral > 50%- usually hep B or C - CMV, EBV, HSV - fungal, bacterial, parasitic causes much less common
42
non-infectious causes of hepatitis
- alcohol - autoimmune - toxins/ drugs - metabolic diseases
43
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
44
hep A
- uncommon in US - assoc with crowding and poor sanitation - transmitted fecal- orally - vaccine avail
45
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
46
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
47
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
48
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
49
how often does acute hep c become chronic?
- 85% of pts that are infected
50
treatment for acute HCV
- 8-12 weeks of harvoni - clinically recover in 3-6 mo - low overall mortality
51
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
52
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
53
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
54
treatment for autoimmune hepatitis
- steroids | - +/- azathioprine
55
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
56
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
57
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
58
treatment for alcoholic hepatitis
- alcohol cessation - correct nutritional deficiency- folate, thiamine, zinc - assist with abstinence - liver transplant only if abstinence for 6 mo
59
what are the most common causes of drug induced hepatitis
- macrobid - minocycline - most commonly abx
60
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
61
extrahepatic manifestations of chronic HBV
- glomerulonephritis- mostly in kids | - polyarteritis nodosa- diffuse vasculitis
62
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
63
when is treatment for chronic HBV indicated
- elevated transaminases - elevated HBV DNA - cirrhotic liver - acute liver failure
64
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
65
where are most new cases of chronic HCV
- africa - central and east asia - back on the rise in the US due to opioid epidemic
66
what is the 20/20 rule
- 20 years of HCV disease= 20% risk of cirrhosis
67
increased risk factors for cirrhosis in pts with HCV
- chronic alcohol ingestion - male - HCV > 40 years old - co-infection with HIV and/or HBV
68
prevention of chronic HCV
- needle exchange programs - tx of substance abuse - blod donor screenings - universal precautions
69
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
70
why has HCC dropped in US
- screen pts in U.S. with cirrhosis every 6 mo
71
clinical presentation of HCC
- insidious onset - weakness, weight loss, anorexia - ascites - jaundice, icterus, pruritis - enlarged tender liver +/- mass
72
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
73
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
74
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

Clin Med III (26 decks)

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