liver pathology Flashcards

1
Q

liver functions

A

energy metabolism = stores glycogen, synth glucose + cholesterol
protein synth
solubilisation of fats
protective + clearance functions eg conversion of ammonia to urea

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2
Q

describe bile production + secretion

A

bile = secreted by liver + stored in gall bladder to be injected into small intestine
water, bile salts, cholesterol, bilirubin
eliminates bilirubin (+non water soluble things)
promote emulsification + absorption

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3
Q

describe acute and chronic hepatitis

A
acute = inflam <6 months -= anorexia, nausea, jaundice, right upper quandratn pain 
chronic = >6 months = asymptomatic or vauge sumptoms  (poor appetite)
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4
Q

describe acute fulminant hepatitis

A

liver failure
underlying is not affected
hyperbilirubinarmia (jaundice), hepatic ecenphalopathy

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5
Q

describe steatosis

A

accumulation of lipid in
hepatocytes
white blobs histologically
can be bc obesity or metabolic syndrome, or alcohol, drugs/toxins

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6
Q

describe steatohepatitis

A

accumulation fat + inflam
hepatocyte death
chronic alcohol consumption + NASH

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7
Q

describe cirrhosis

A

end stage liver disease
scar tissue, liver failure, portal hypertension
irreversible
distorted bile ducts + bv

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8
Q

describe cirrhosis patho

A

injury + loss hepatocytes = inflam mediators -> hyperplasia + angiogenesis -> impinge normal structures -> stellate cells -> dec vit A + proliferative + scar tissue in sinusoidal space -> detioration of hepatocyte function -> fibrosis

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9
Q

clinical presentiation about cirrhosis

A

jaundice, hepatic encephalopathy, coagulability, increased oestrogen,

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10
Q

describe jaundice

A

yellow discolouration bc deposition of bile pigment
inc breakdown rbc
failure liver uptake bilirubin from blood
failure liver conjugate or excretion
obstruction biliary excretion into intestine

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11
Q

describe hyperoestrogenism

A

MEN = gynaecomastia
women = menstrual irregularities
spider noevi = dilated small bv

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12
Q

describe portal hypertension

A

scarring distorts vascular architecure = blood cant flow from portal -> hepatic vein = inc pressure

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13
Q

describe porto-systemic anastomoses

A

compensate for portal hypertension => inc blood flow through veins
causes: oesphageal varices, dilations of umbilical veins, haemorrhoids

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14
Q

what is caput medusae

A

appearance of distended + engorged superficial epigastric veins
radiating from umbilicus across abdomen

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15
Q

what is oesophageal varices

A

dilates oes. veins

common comp = bleeding, exacerabted by coagulopathy from cirrhosis

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16
Q

describe splenomegaly

A

inc pressure prevents draining og splenic cein => engorged spleen with blood
=> hypersplenism => inc removal platelets, inc rbc, dec wbc

17
Q

describe ascites

A

Increased extravascular fluid accumulates in the peritoneal
cavity
inc presure in caps -> dec albumin = dec oncotic pressure
big bloating of stomach

18
Q

describe hepatic encephalopathy

A

inc ammonia w/bloodstream
bc dec functon hepatocutes => shunting ammonia from intestine to circulation
ammonia -> BBB -> atrocyte process to glutamine -> ICP ->inc distance between caps and neuorons => preventing nutrients reaching -> glutamine = ntsm imbalance

19
Q

waht are the symptoms of encephalopathy

A

astrerixis (flapping hand motion)

imbalance, cant concentrate, mood change, disordered sleep

20
Q

describe cirrhosis and heaptocellular carcinoma

A

primary risk factor

repeated hepatocyte damage -> cirrhosis -> HCC

21
Q

describe hep A

A

faecal oral
acute
anorecia, nausea, jaundiace
benign + self limiting

22
Q

describe hep B

A

Blood, semen, vaginal fluid Perinatal (through deliery)
acute or chronic
asymptomatic but infectious
ground glass cytoplasmic inclusions

23
Q

describe hep C

A

Blood
acute
progress to chronic hep
inflammation, variable steatosis, progressive fibrosis
highly variable, hard for immune system to respond

24
Q

describe hep D

A
blood 
HBV to enter hepatocytes 
coinfection = HBV + HDV 
superinfection = chronic HBV then HDV 
bad prognosis -> cirrhosis
25
Q

describe hep E

A

faecal-oral (water-borne)
rare
acute
can cause fulminant hep when assoiciated with pregnancy

26
Q

effects of excess alcohol intake

A

metabolism process alcohol -> accumulation of fat in hepatocytes (steatosis) -> damage protein export -> inflam cells -> stellate cells -> fibrosis -> steatohepatitis -> cirrhosis

27
Q

what is the progression of alcoholic liver disease

A

chronic alcohol consumption -> healthy liver -> alcoholic fatty liver -> alcoholic steatohepatitis -> (can get alcoholic hepatitis) -> alcoholic cirrhosis -> hepatocellular cancer

28
Q

describe non-alcoholic steatohepatitis (NASH)

A

metabolic syndrome associated
- obesity, hyperlipidaemia, hypertension, insulin resistance
lipid accumulation liver => hepatocellular lipotoxicity -> inflam response
10-30% develop cirrhosis