Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Histopathology > Liver pathology > Flashcards

Liver pathology Flashcards

1
Q

Anatomy of the liver

A

Basic structural unit is the hepatic lobule – thought of as a hexagon. At the centre are the terminal
branches of the hepatic vein (= centrilobular vein). The points of the hexagon are formed by the
portal tracts, which contain 3 structures (portal triad): branches of the bile ducts, hepatic artery
and portal vein.
The liver cells can be split into three zones.
• Zone 1 (closest to the portal triad) – periportal hepatocytes receive more oxygen and
• Zone 2 – mid zone
• Zone 3 (close to terminal hepatic vein) – perivenular hepatocytes are the most mature
and metabolically active. Zone 3 has most liver enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Functions of the liver

A
  1. Metabolism – involved in glycolysis, glycogen storage, glucose synthesis, amino acid
    synthesis, fatty acid synthesis and lipoprotein metabolism. Drug metabolism.
  2. Protein synthesis – makes all circulating proteins (except gamma globulins) including
    albumin, fibrinogen, and coagulation factors.
  3. Storage – glycogen, vitamins A, D and B12 in large amounts, small amounts of vitamin K,
    folate, iron and copper
  4. Hormone metabolism – Activates vitamin D. Conjugation and excretion of steroid
    hormones (oestrogen/glucocorticoids). Peptide hormone metabolism (insulin, GH, PTH)
  5. Bile synthesis – 600-1000ml daily
  6. Immune function – antigens from gut reach liver via portal circulation. Phagocytosed by
    Kupffer cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Histopathology of liver injury

A
  • A normal liver has hepatocytes with microvilli and stellate cells which lie quiescent in the space of Disse (space between hepatocytes and sinusoid)
  • Chronic inflammation causes the loss of microvilli and activation of stellate cells, which produce collagen.
  • They become myofibroblasts that initiate fibrosis by deposition of collagen in the space of Disse.
  • Myofibroblasts contract constricting sinusoids and increasing vascular resistance.
  • Undamaged hepatocytes regenerate in nodules between fibrous septa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Features of acute hepatitis

A

Can either be caused by viruses (A to E) or by drugs.

Histopathology - SPOTTY NECROSIS (small foci of inflammation and infiltrates)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Features of chronic hepatitis

A 
The severity of inflammation = grade
The severity of fibrosis = stage
Histopathology:
1. Portal Inflammation 
2. Interface hepatitis (PEICEMEAL NECROSIS) – cannot see the border between the portal tract 
and parenchyma 
3. Lobular inflammation
4. Bridging from the portal vein to central vein (critical stage in the evolution of hepatitis to 
cirrhosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Definition and features of cirrhosis

A

Diffuse abnormality of liver architecture that interferes with blood flow and liver function.

There is a disruption of liver architecture - ↑resistance to blood flow through liver portal
hypertension. Fibrotic bridges form between the portal triad and central vein – extra hepatic
shunting results in anastomoses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Histopathology of a cirrhotic liver

A

Hepatocyte necrosis
Fibrosis
Nodules of regenerating hepatocytes
Disturbance of vascular architecture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

List major causes of cirrhosis

A
  1. Alcoholic liver disease
  2. Non-alcoholic fatty liver disease
  3. Chronic viral hepatitis (hep B+/-D and C)
  4. Autoimmune hepatitis
  5. Biliary causes: Primary biliary cirrhosis & Primary sclerosing cholangitis
  6. Genetic causes:
    a) Haemochromatosis- HFE gene Chr 6
    b) Wilson’s disease- ATP7B gene Chr 13
    c) Alpha 1 antitrypsin deficiency (A1AT)
    d) Galactosaemia
    e) Glycogen storage disease
  7. Drugs e.g. methotrexate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Classification of cirrhosis

A

MICRONODULAR (nodules < 3mm). Uniform liver involvement.
• Caused by: alcoholic hepatitis, biliary tract disease
MACRONODULAR (nodules > 3mm). Variable nodule size.
• Caused by: viral hepatitis, Wilson’s disease, alpha1 antitrypsin deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Scoring system of cirrhosis

A

Modified Child’s Pugh score (ABCDE)

Albumin
Bilirubin
Clotting - PT
Distention - ascites
Encephalopathy
  • Total Score <7 = Child’s Pugh A (45% 5yr survival)
  • Total Score 7-9 = Child’s Pugh B (20% 5yr survival)
  • Total Score 10+ = Child’s Pugh C (<20% 5yr survival)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe progression of alcoholic liver disease

A

Hepatic steatosis (fatty liver)
Alcoholic hepatitis
Alcoholic cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Features of hepatic steatosis

A

Macroscopic
Large, pale, yellow and greasy liver

Microscopic
Accumulation of fat droplets in hepatocytes (=steatosis)
Chronic exposure -> fibrosis (late stage)
Fully reversible if alcohol avoided

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Features of alcoholic hepatitis

A

Macroscopic
Large, fibrotic liver

Microscopic
Hepatocyte ballooning and necrosis due to accumulation
of fat, water and proteins
Mallory Denk Bodies
Fibrosis
Seen acutely after night of heavy drinking. Ranges from
asymptomatic to fulminant liver failure. Each episode has
10-20% mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Features of alcoholic cirrhosis

A 
Macroscopic
Yellow-tan, fatty, 
enlarged. 
Transforms into 
shrunken, non-fatty, brown organ.

Microscopic
Micronodular cirrhosis – i.e. small nodules + bands of
fibrous tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Features of non-alcoholic fatty liver disease

A

● = hepatic steatosis in non-alcoholics – histologically looks very similar to alcoholic hepatitis
● Most common cause of chronic liver disease in West
● Mainly in obese individuals with hyperlipidaemia/metabolic syndrome. Diabetes is also a risk
factor.
● NAFLD includes:
o Simple steatosis: fatty infiltration, relatively benign
o Non-alcoholic steatohepatitis (NASH)
▪ Steatosis + hepatitis (fatty infiltration + inflammation)
▪ Can progress to cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Features of autoimmune hepatitis

A

● Common with other autoimmune diseases e.g. coeliac, SLE, RA, thyroiditis, Sjögren’s, UC
● 78% female– young and postmenopausal.
● Associated with HLA-DR3
● Type 1: ANA (antinuclear Ig), anti-SMA (anti-smooth muscle Ig), anti-actin Ig, anti- soluble
liver antigen Ig
● Type 2: Anti-LKM Ig (anti liver-kidney-microsomal Ig)
● Treatment: Immune suppression until transplant, BUT disease returns in up to 40%

17
Q

What are the biliary causes of cirrhosis

A

Primary biliary cirrhosis (PBC)

Primary sclerosing cholangitis

18
Q

Features of primary biliary cirrhosis

A

● Autoimmune inflammatory destruction of medium sized intrahepatic bile ducts à
cholestasis à SLOW development of cirrhosis over many years
● F > M 10:1
● Peak incidence at 40-50yrs
● ↑serum ALP, ↑cholesterol, ↑IgM, hyperbilirubinaemia (late)
● Anti-mitochondrial antibodies in > 90%
● US scan shows no bile duct dilatation
● Histology: bile duct loss with granulomas
● Presents with fatigue, pruritus and abdominal discomfort
● Secondary symptoms incl: skin pigmentation, xanthelasma (part. eyelid),
steatorrhoea, vitamin D malabsorption, inflammatory arthropathy.
● Can treat with ursodeoxycholic acid in early phase à remission in 25%

19
Q

Features of primary sclerosing cholangitis

A

● Inflammation and obliterative fibrosis of extrahepatic and intrahepatic bile ducts
à multi-focal stricture formation with dilation of preserved segments
● M > F
● Peak incidence at 40-50yrs
● Associated with IBD (especially UC)
● ↑ serum ALP, several associated auto-Ig, particularly p-ANCA
● US scan: bile duct dilatation
● ERCP: shows beading of bile ducts (due to multifocal strictures)
● Histology: onion skinning fibrosis – concentric fibrosis
● ↑ incidence of cholangiocarcinoma

20
Q

Genetic causes of cirrhosis?

A

Haemochromatosis
Wilson’s disease
Alpha 1 antitrypsin deficiency

21
Q

Pathophysiology, histology of haemochromatosis

A

P - Autosomal recessive
Mutated HFE gene at 6p21.3 ↑Fe gut
absorption which deposits in liver, heart,
pancreas, adrenals, pituitary, joints, skin
fibrosis
H - Fe deposits in liver – stains with Prussian blue
stain

22
Q

Clinical features, investigations, treatment of haemochromatosis

A 
CF -  ● Skin bronzing (melanin deposition)
● Diabetes
● Hepatomegaly with micronodular cirrhosis
● Cardiomyopathy
● Hypogonadism
● Pseudogout
I - ● ↑ Fe, ↑ Ferritin
● Transferrin saturation > 45%
● ↓ TIBC
T - Venesection
Desferrioxamine
30% with cirrhosis → HCC
23
Q

Pathophysiology, histology of Wilson’s disease

A

Autosomal recessive
Mutated gene ATP7B (Chr 13): Encodes copper
transporting ATPase expressed on canalicular
membrane therefore à ↓biliary Cu excretion and
deposition in liver, CNS, iris.

Cu stains with Rhodanine stain
Mallory bodies and fibrosis on microscopy

24
Q

Clinical features, investigations, treatment of Wilson’s disease

A

CF - ● Liver disease: acute hepatitis, fulminant liver
failure or cirrhosis
● Neuro disease: parkinsonism, psychosis,
dementia (basal ganglia involvement)
● Kayser Fleischer rings: copper deposits in
Descemet’s membrane in cornea

I - ● ↓ serum caeruloplasmin
● ↓ serum copper
● ↑ urinary copper

T - Lifelong penicillamine.
Good prognosis with early treatment but any neuro
damage is permanent and may require liver
transplant

25
Q

Pathophysiology and histology of alpha 1 antitrypsin deficiency

A 
Autosomal dominant
A1AT accumulates in 
hepatocytes -> intracytoplasmic 
inclusions -> hepatitis
Lack of A1AT in lungs ->
emphysema

Intracytoplasmic inclusions of
A1AT which stain with
Periodic acid Schiff

26
Q

Clinical features and investigations for alpha 1 antitrypsin deficiency

A

Kids: neonatal jaundice
Adults: emphysema and chronic
liver disease

I - ↓A1AT
Absent α-globulin band on
electrophoresis

27
Q

What are the benign liver tumours and their clinical features?

A

Hepatic adenoma
● Associated with OCP
● Present with abdo pain/ intraperitoneal bleeding
● Resection if symptomatic, >5cm or if no shrinkage when
stopping OCP

Haemangioma
● Most common benign lesion
● No rx

28
Q

What are the malignant liver tumours

A 
Hepatocellular carcinoma
Cholangiocarcinoma
Haemangiosarcoma
Hepatoblastoma
Secondary tumours
29
Q

Features of hepatocellular carcinoma

A

● Causes: Most commonly occurs in patients with chronic liver
disease – closely linked with viral hepatitis, alcoholic cirrhosis,
haemochromatosis, NAFLD, Aflatoxin, androgenic steroids.
Screening in cirrhotic patients with 6 monthyly USS
Ix: alpha-fetoprotein, USS

30
Q

Features of cholangiocarcinoma

A

● Adenocarcinomas arising from bile ducts
● 10% of liver tumours
● Can be intra or extrahepatic
● Poor prognosis
Causes: primary sclerosing cholangitis, parasitic liver disease
chronic liver disease, congenital liver abnormalities, Lynch
syndrome type II

31
Q

Features of haemangiosarcoma

A

Cancer of the vascular epithelium - highly invasive

32
Q

Features of hepatoblastoma

A

Occurs in children/infants - presents with abdominal mass

Originates from immature liver prescursor cells

33
Q

Features of secondary tumours

A

● MOST COMMON malignant liver lesion.
● Usually from GI tract, breast or bronchus.
● Usually multiple

Histopathology (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions