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Pathology > Liver Histopath > Flashcards

Liver Histopath Flashcards

1
Q

Major causes of cirrhosis (3) & less common causes (3)

A
  1. Alcoholic fatty liver disease
  2. Non alcoholic fatty liver disease
  3. Chronic hepatitis infection

Autoimmune hepatitis

Drugs e.g. Methotrexate

Biliary causes: PBC & PSC

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2
Q

Genetic causes of cirrhosis (5)

A

1) haemochromatosis - HFE gene chr 6
2) Wilson’s disease - ATP7B gene chr 13
3) alpha 1 anti-trypsin deficiency (pulmonary & hepatic dysfunction)
4) galactosaemia
5) Glycogen storage disease

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3
Q

Difference between micronodular & macronodular cirrhosis & 2 examples of each

A

Micronodular indicates regenerating nodules (of regenerating hepatocytes) < 3mm e.g. alcoholic & biliary tract disease

Macro > 3mm e.g. Viral, Wilson’s

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4
Q

Briefly describe pathophysiology of cirrhosis (Refer to picture)

A

1) chronic inflammation activates the normally quiescent stellate cells
2) convert to myofibroblasts and deposit collagen in space of disse
3) when myofibroblasts contract they cause constriction of the sinusoids - increasing vascular resistance
4) undamaged hepatocytes regen in nodules between fibrous septa

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5
Q

5 criteria of the child’s Pugh score - indicates prognosis of cirrhosis

A

Ascites (none, mild, severe)

Encephalopathy (none, mild, severe)

Bilirubin (<34, 34-50, >50)

Albumin (>35, 28-35, 6)

PTT (seconds more than normal) (<4, 4-6, >6)

Score 1,2 & 3 respectively

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6
Q

Score boundaries for Child Pugh A, B & C (Indicates cirrhosis prognosis)

A
  • < 7 (A) = 45% 5 yr survival
  • 7-9 (B) = 20% 5 yr survival
  • 10+ (C) = <20% 5 yr survival
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7
Q

Portal htn (>10-12mmHg) venous system dilates, where do collateral vessels form? (6)

A

1) gastro-oesophageal
2) Rectal
3) Umbilical
4) retroperotneal
5) diaphragm
6) left renal vein

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8
Q

Causes of portal HTN (pre hepatic, hepatic & post hepatic)

A

Pre-hepatic: portal vein thrombosis (e.g, Factor V Leiden)

Hepatic:

  • Pre sinusoidal: schistomasis, PBC, Sarcoidosis
  • Sinusoidal: Cirrhosis
  • Post-sinusoidal: veno-occlusive disease Post-hepatic: Budd-Chiari syndrome
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9
Q

Give some causes of Budd-Chiari & treatment

A

Occlusion of hepatic vein!

Causes: 30% idiopathic, thrombophilia, OCP, leukaemias, compression by renal tumours etc.

Treatment: Thrombolytic, treat underlying cause, TIPS (transjugular intrahepatic portosystemic shunt)

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10
Q

Triad of Budd Chiari

A

Pain + ascites + hepatomegaly

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11
Q

3-4 features of cirrhosis

A

1) hepatocyte necrosis
2) nodules of regenerating hepatocytes
3) fibrosis
4) disrupted liver architecture> increased resistance to blood flow through liver > portal hypertension

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12
Q

Microscopic characteristics of hepatic steatosis (fatty liver)

A

Steatosis - fatty droplets in hepatocytes. Fibrosis in late stage if chronic exposure reversible if alcohol avoided

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13
Q

microscopic characteristics of alcoholic cirrhosis

A

MICRONODULAR cirrhosis - small nodules + bands of fibrous tissue

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14
Q

Microscopic characteristics of alcoholic hepatitis (2)

A

Hepatocyte BALLOONING & necrosis due to accumulation of fat, water & proteins

MALLORY BODIES (damaged intermidiate filaments within hepatocytes)

fibrosis

seen acutely after night of heavy drinking

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15
Q

What antibodies are present in Type 1 autoimmune hepatitis? (4)

A

ANA (anti nuclear ab), anti-SMA (anti smooth muscle ab), anti-actin ab, anti-soluble liver antigen ab

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16
Q

What antibody is present in Type 2 autoimmune hep?

A

Anti-LKM Ig (anti-liver-kidney-microsomal Ig)

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17
Q

How is autoimmune hepatitis managed?

A

Immune suppression until transplant, (but disease returns in up to 40%)

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18
Q

Associations of autoimmune hepatitis: Who gets it? M or F? HLA association?

A

People with autoimmune conditions females (78%) HLA-DR3

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19
Q

What is main tissue destroyed by autoimmune inflammation in PBC?

A

medium sized INTRAHEPATIC bile ducts (this leads to cholestasis which very SLOWLY leads to development of cirrhosis over many years)

20
Q

Ratio of F:M in PBC

A

10:1

21
Q

What will the investigations/ histology show in PBC? (4)

A

High ALP, high cholesterol, high IgM, ANTI-MITOCHONDRIAL Abs in 90%

US - NO bile duct dilatation

histology - bile duct loss with GRANULOMA formation

22
Q

Presentation of PBC?

A

Fatigue, pruritis, abdo discomfort

23
Q

Secondary symptoms of PBC (give 3)

A

xanathelasma, skin pigmentation, steatorrhoea, inflammatory arthropathy

24
Q

Treatment of PBC

A

Ursodeoxychilic acid (slows down absorption of cholesterol from intestine) in early phase (25% remission)

25
Q

Briefly describe the pathophysiology of PSC

A

inflammation & obliterative fibrosis of EXTRA & INTRAHEPATIC bile ducts > leads to multi focal STRICTURE FORMATION & dilatation

26
Q

What autoimmune condition is PSC particularly associated with?

A

IBD - esp UC

27
Q

what will the investigations// histology show in PSC?

A

i_ncreased serum ALP,_ several auto abs- esp p-ANCA

US - bile duct DILATATION

ERCP - BEADING OF BILE DUCTS (due to multifocal strictures) increased incidence of CHOLANGIOCARCINOMA

28
Q

Main differences between PBC & PSC:

A

PSC more common in males, PBC in females

PSC associated with UC, PBC not as much

PSC both intra & extra hepatic bile ducts affected, in PBC only intra Therefore in PSC you get bile duct dilatation, in PBC you dont

29
Q

Pathophysiology of Haemochromatosis

A

Inheritance - autosomal recessive Mutate HFE gene at chr 6(p21.3) > increased Fe absorption from gut > deposition everywhere > eventually leads to fibrosis

30
Q

Histology of Haemochromatosis (which stain used)

A

Fe deposits in liver, stains with PRUSSIAN blue

31
Q

Signs/symptoms of haemochromatosis (at least 3)

A

Skin pigmentation

Diabetes

Hepatomegaly

pseudogout

32
Q

Investigations

A

Fe high,

Transferrin saturation high (>45%),

Ferritin high,

TIBC low (transferrin transports iron, it has binding sites normally only a third are occupied - more iron = more transferritin saturation. TIBC is total iron binding capactiy )

33
Q

Pathophysiology of Wilson’s disease

A

autosomal recessive Mutation in ATPB7 gene - encodes Cu transporter protein on cannilicular membrane > so reduced biliary Cu excretion > deposition in liver, CNS, iris

34
Q

Histology of Wilson’s (2)

A

Cu stains on Rhodanine stain

Mallory bodies (damaged IFs) & fibrosis on microscopy

35
Q

Signs/ symptoms of Wilson’s (neuro, hepatic, eyes)

A

Neuro: parkinson’s, dementia (if basal ganglia involved), psychosis

Hepatic: acute hep, cirrhosis, liver failure

Eyes: Kayser Fleischer rings: copper deposits in Descemet’s membrane in cornea

36
Q

Investigations Wilsons (3)

A

reduced serum caeruloplasmin,

reduced serum copper,

increased urinary copper

37
Q

Alpha 1 antitrypsin deficiency pathophysiology

A

A1AT is produced in liver and normally 1 of its functions is protection of lungs from neutrophil esterase.

In A1AT deficiency the mutation results in defective A1AT > accumulates in liver & causes cirrhosis (cannot be secreted properly) and because it cannot protect lungs > emphysema

38
Q

Histology of Alpha 1 antitrypsin deficiency (2)

A

INTRACYTOPLASMIC INCLUSIONS OF A1AT which stain with PERIODIC ACID SCHIFF

39
Q

Signs and symptoms of A1AT def (kids and adults)

A

Kids - neonatal jaundice

Adults - emphysema & chronic liver disease

40
Q

Investigations of Alpha 1 antitrypsin deficiency (2)

A

low A1AT

Absent alpha globulin bands on electrophoresis

41
Q

Treatment of Haemochromatosis

A

VENESECTION

DESFERRIOXAMINE (siderophore - chelates Fe)

42
Q

Treatment of Wilson’s disease

A

Life long PENICILLAMINE - chelates coppper (good prog with early treatment, but any neuro damage is permanent)

43
Q

Clinical features of Hepatic adenoma & how to treat

A

Benign hepatic tumour, associated with OCP presents with

Abdo pain + intraperitoneal bleeding

Resect if symptomatic or > 5 cm or if doesnt shrink after stopping OCP

44
Q

Clin features of Haemangioma

A

most common benign lesion - doesnt require treatment

45
Q

Hepatocellular carcinoma causes (4) & investigations (2)

A

Causes: chronic hep B + C, alc cirrhosis, NAFLD, Steroids

Ix: AFP, USS

46
Q

Cholangiocarcinoma: what is it? prognosis? causes (3)

A

Adenocarcinoma arising from bile ducts poor prognosis

Causes: PSC Chronic liver disease Lynch syndrome type 2

Pathology (20 decks)

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