Liver pathology Flashcards

1
Q

Why is vascular pathology rare in liver disease?

A

Dual blood supply - hepatic artery (oxygenated blood) + portal vein (deoxygenated blood drained from intestine)

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2
Q

Liver anatomy

A

Cells are arranged into hepatic lobules, which are hexagonal structures with portal triads (hepatic artery branch, bile duct branch, hepatic portal vein branch) at each vertice and a central vein. Hepatic arteries supply oxygenated blood into the sinusoid (and form metabolic zones (1, 2 and 3) with increasing distance from the hepatic artery); hepatic portal vein supplies deoxygenated blood, which travel along hepatic sinusoids to the central vein; bile duct forms bile canaliculi that radiate into the centre. Blood mixes within the sinusoid – oxygenated blood from artery and deoxygenated blood from vein. It is lined with discontinuous, fenestrated endothelium. Hepatocytes are separated from the endothelium of sinusoids by the space of DIsse, which contains Kupffer cells (hepatic macrophages). Hepatic stellate cells are also present here and are involved in scar formation in response to liver damage. Bile released from hepatocytes flows into the bile canaliculi and travels in the opposite direction back to the portal triad biliary duct branch.

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3
Q

REALLY IMPORTANT

Cellular change in liver injury

A
  • Healthy liver - endothelial cells discontinuous with spaces between them - blood easily passes between endothelial cells to get to hepatocytes
  • Liver injury - Kupffer cells in sinusoids activate - endothelial cells stick together - blood passes less easily to get to hepatocytes

Basically liver injury = harder for blood to get from capillaries to hepatocytes

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4
Q

4 features of cirrhosis

A
  1. Whole liver involved
  2. Fibrosis (collagen deposition)
  3. Nodules of regenerating hepatocytes
  4. Distorted vasculature (intra-hepatic and extra-hepatic shunting)
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5
Q

End-point of liver injury

A

Acute hepatitis –> Chronic hepatitis –> Cirrhosis

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6
Q

How is cirrhosis classified?

A
Alcohol/insulin resistance - fatty changes - micronodular (smaller) regenerating nodules
Viral hepatitis (BCD) - macronodular (bigger) regenerating nodules
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7
Q

Micronodular (small) regnerating nodules

Fatty changes

A

Alcohol / insulin resistance causing cirrhosis

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8
Q

Macronodular (large) regenerating nodules

A

Virus (chronic only - BCD) causing cirrhosis

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9
Q

3 key complications of cirrhosis

A

Portal hypertension (extra-hepatic shunting = varices, splenomegaly)
Hepatic encephalopathy
Liver cell cancer

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10
Q

Spotty necrosis w/ small inflammatory foci

2 main causes: Hepatitis (A + E), drugs

A

Acute hepatitis

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11
Q

Chronic inflammation + fibrosis (blue strands of collagen)

3 main causes: Hepatitis (BCD), AI, Drugs

A

Chronic hepatitis

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12
Q

Grade of chronic hepatitis = ?

Stage of chronic hepatitis = ?

A
Grade = degree of inflammation (i.e. hepatocyte damage)
Stage = Degree of fibrosis
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13
Q

Active chronic hepatitis
ASMA antibodies in serum
Responds well to steroids
Flooding with plasma cells + big Golgi

A

AI hepatitis

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14
Q

Pale yellow liver

A

Alcoholic liver disease

Fat = yellow

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15
Q

3 patterns of alcoholic liver disease

A
  1. Fatty liver
  2. Alcoholic hepatitis
  3. Cirrhosis
    (Increasing inflammation + fibrosis down list)
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16
Q

Reversible fat infiltration

Drinking excess alcohol

A

Fatty liver

17
Q

Balloon cells containing Mallory Denk bodies
Apoptosis
Pericellular fibrosis
Zone 3 - most metabolically active cells (alcohol breakdown happens here)

A

Alcoholic hepatitis

18
Q

Micronodular regenerating

nodules containing fat

A

Alcohol related cirrhosis

19
Q

Alcoholic liver disease type picture without alcohol drinking
Insulin resistance - raised BMI, DM

A

NASH

20
Q

Females
AMA diagnostic
Risk of cirrhosis
Granulomatous bile duct destruction

A

Primary biliary cholangitis (PBC)

Previously primary biliary cirrhosis

21
Q

Males, UC
ERCP / MRCP diagnostic ‘Beaded appearance’
Risk of cirrhosis, cholangiocarcinoma
Fibrotic bile duct destruction (onion skinning around duct)

A

Primary sclerosing cholangitis (PSC)

22
Q

GENETIC - HFe gene on chromosome 6
Iron deposition in HEPATOCYTES, pancreas, heart
Cirrhosis, HF, bronzed diabetes
Prussian blue stain
Elevated serum iron + ferritin, redued TIBC

A

Hereditary haemochromatosis

23
Q

Iron accumulation in MACROPHAGES (Kupffer cells)
Blood transfusion
NOT GENETIC - blood transfusion

A

Haemosiderosis

24
Q

Cu accumulation in basal ganglia (LN) + eye
Kayser-Fleischer Rings
Parkinsonism
Rhodanine stain

A

Wilson’s disease

25
Q

Pink alpha1-antitrypsin globules in hepatocytes

Low alpha1-antitrypsin in blood

A

Alpha1-antitrypsin deficiency

26
Q

Commonest liver cancer

A

Metastastic

27
Q

Collection of macrophages in chronic inflammation

A

Granuloma

28
Q

Causes of hepatic granuloma

A

Liver specific - PBC, drugs

General - TB, sarcoid

29
Q

3 types of benign liver tumour

A

Liver cell adenoma (hepatocytes)
Bile duct adenoma (bile duct cells)
Hemangioma (endothelial cells)

30
Q

Commonest benign liver tumour

A

Hemangioma

31
Q

Multiple malignant lesions

A

Secondary (metastatic) cancer

32
Q

Single malignant lesion

A

Primary

33
Q

Malignancy associated with:
Chronic HepB/HepC infection
Cirrhosis

A

HCC

34
Q

Malignancy associated with:
PSC
Worm infections
Cirrhosis

A

Cholangiocarcinoma

35
Q

Abdo pain, nausea + vomiting
Tender hepatomegaly + ascites
CT = hepatic vein occlusion, diffuse abnormal parenchyma
Hepatic vein thrombosis

A

Budd-Chiari syndrome

36
Q

‘After a fall’

A

Alcohol