Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Histopathology > Liver and biliary pathology > Flashcards

Liver and biliary pathology Flashcards

1
Q

Deescribe the basic structure 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

Which zone receives the most oxygen?

A

Zone 1- closest to the portal triad

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

Which zone is the most metabolically active?

A

Zone 3- closest to the central vein

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

Which protein is NOT synthesised by the liver?

A

Gamma globulin

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

Where is the space of Disse?

A

Between the hepatocytes and endothelieal cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where are the stellate cells?

A

In the space of disse

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

What is the function of stellate cells?

A

store vitamin A

Usually lie quiescent in the space of disse

when activated due to injurt to the hepatocytes, they produce collagen

They become myofibroblasts–>deposit collagen in the space of disse

Myofibroblasts contract constricting sinusoids and increasing vascular resistance

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

What causes acute hepatitis? + define acue hepatitis

A

Viruses or drugs

Hepatitis last <6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Histology of acute hepatitis

A

Spotty necrosis

small foci of inflammation + infiltration

lymphocytes and macrophages with damaged hepatocytes

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

Grade vs stage of chronic inflammation

A

Grade- severity of inflammation

Stage - severity of fibrosis - this is more important in chronic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Histopathology of chronic hepatitis

A
  1. Portal Inflammation: inflammation has not crossed the limiting plate
  2. Interface hepatitis (PEICEMEAL NECROSIS) – cannot see the border between the portal tract and parenchyma
  3. Lobular inflammation- looks similar to spotty necrosis in acute hepatitis
  4. Fibrosis: Bridging from the portal vein to central vein due to fibrosis- intraheptic shunting- (critical stage in the evolution of hepatitis to cirrhosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the key stage in evolution of hepatitis to cirrhosis?

A

Bridging between the portal vein and central vein

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

Histopathology of cirrhotic liver

A

whole liver is affected

Hepatocyte necrosis

Fibrosis

Nodules of regenerating hepatocytes with surrouding fibrosis

Disturbance of vascular architecture (formation of intrahepatic and extrahepatic shunts)

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

Explain intrahepatic and extrahepatic shunting

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

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
16
Q

Haemochromatosis gene mutation

A

HFE gene Ghr 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Wilson’s disease mutation

A

ATP7B gene Chr 13

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Alpha 1 antitrypsin: gene mutation

A

A1At gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Micronodular vs macronodular cirrhosis

A

Micro: <3mm and uniform nodules throughout the liver

Maco: >3mm, variable nodule size throughout the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What causes micronodular cirrhosis?

A

alcoholic hepatitis, biliary tract disease

(a, b)

non alcoholic Fatty liver disease

Haemchromatosis

**think haemachromatosis is bronzed diabetes; diabetes, NAFLD all similar pathology…**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Causes of macronodular cirrhosis

A

viral hepatitis, Wilson’s disease, alpha1 antitrypsin deficiency

VWA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Outline the child’s pugh score

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Outline the spectrum of alcoholic liver disease

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What type of cirrhosis is alcoholic cirrhosis?

A

Micronodular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Most common cause of chronic liver disease in the West
NAFLD
26
Spectrum of NAFLD
a) simple steatosis - fatty change b) non-alcoholic steatohepatitis (NASH) - progressed to inflammation
27
HLA association of Autoimmune hepatitis
HLA-DR3
28
Antibodies seen in autoimmune hepatitis
**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)
29
PBC biochemical features
↑serum ALP, ↑cholesterol, ↑IgM, hyperbilirubinaemia (late)
30
Anti-mitochondrial antibodies
PBC
31
Bile duct loss with granulomas secondary to chronic inflammation
PBC * Hallmark: **granulomatous inflammatory destruction of bile ducts.**
32
signs & symptoms of PBC
Fatigue, pruritis, abdominal discomfort skin pigmentation, xanthelasma (part. eyelid), steatorrhoea, vitamin D malabsorption, inflammatory arthropathy.
33
Which bile ducts are affected in PBC vs PSC?
PBC- intrahepatic PSC- intrahepatic and extrahepatic
34
Treatment of PBC
ursodeoxycholic acid
35
Male vs female incidence of PBC vs PSC
PBC: F\>M PSC: M\>F
36
Association of PSC
UC
37
Biochemical features of PSC
↑ serum ALP, several associated auto-Ig, particularly p-ANCA
38
USS of PSC vs PBC
PBC- no dilatation of bile ducts PSC - dilatation of bile ducts: **beading of the bile ducts** (multi-focal strictures with dilation of preserved segments)
39
ERCP findings of PSC
beading of bile ducts (due to multifocal strictures)
40
What type of fibrosis do you get in PSC?
Onion skinning - concentric fibrosis
41
Which cancer is associated with PSC?
Cholangiocarcinoma
42
What is the most common benign liver lesion?
Haemangioma
43
3 benign liver tumours
Liver cell adenoma Bile duct Adenoma Haemangioma
44
What is the main risk factor of hepatic adenoma?
OCP use, associated with to oestrogen levels Treated with stopping OCP; if doesn't resolve --\> resection
45
Malignant liver lesions
HCC Chlangiocarcinoma Haemangiosarcoma Hepatoblastoma Secondary tumours
46
Causes of HCC
Most commonly occurs in patients with chronic liver disease – closely linked with viral hepatitis, alcoholic cirrhosis, haemochromatosis, NAFLD, Aflatoxin, androgenic steroids
47
IVx of HCC
AFP and USS
48
RF for cholangiocarcinoma
primary sclerosing cholangitis (worm)parasitic liver disease chronic liver disease-Cirrhosis congenital liver abnormalities Lynch syndrome type II
49
when are hepatic adenomas resected
when symptomatic \>5mm non shrinkage despite stopping OCP
50
Most common malignant liver lesion
Secondary tumours - GI tract, breast or bronchus
51
Genetic causes of cirrhosis
haemochromatosis Wilson's Alpha 1 antitrypsin deficiency
52
Haemochromatosis mode of inheritance
Autosomal recessive mutation of HFE gene on chrmosome 6
53
Wilson's disease mode of inheritance
Autosomal recessive mutation of ATP7B gene on chr 13
54
Alpha 1 antitrypsin deficiency mode of inheritance
Autosomal dominant mutation of A1AT
55
Histology of haemochromatosis
Fe deposits in liver – stains with Prussian blue stai micronodular cirrhosis Liver turns chocolatey brown colour
56
Wilson's disease histology
Cu stains with **Rhodanine stain** Mallory bodies and fibrosis on microscopy
57
A1AT deficiency histology
Intracytoplasmic inclusions of A1AT which stain with **Periodic acid Schiff**
58
Ivx of haemochromatosis
↑ Fe, ↑ Ferritin ● Transferrin saturation \> 45% ● ↓ TIBC
59
Treatment of haemochromatosis + prognosis
Venesection iron chelation Desferrioxamine 30% with cirrhosis → HCC
60
Biochemical findings of wilson's disease
↓ serum caeruloplasmin ● ↓ serum copper (as it's depositing everywhere else) ↑ urinary copper
61
Treatment of wilson's disease
Lifelong pencillamine
62
Absent α-globulin band on electrophoresis
Alpha 1 antitrypsin deficiency
63
in drug injury which zone of the liver is most affected/damaged
* The **_damaged hepatocytes are in zone 2 and 3- mostly zone 3_** Zone 3 is most affected because that is where the most drug metabolising hepatocytes are so where most of the toxic metabolites of drug metabolism is formed
64
Difference between PBC and PSC
PBC: intrahepatic and bile duct loss secondary to **_inflammation_** PSC: Extrahepatic and intrahepatic: bile duct loss due to peridcutal **_fibrosis_**
65
which liver conditions cause granulomas
PBC Drugs
66
sturcture of hepatic adenoma
round circumscribed lesion ## Footnote **_Sharply demarcated borders_**
67
HCC- main causes in the west and developing countries
west- cirrhosis developing countries -viruses
68
difference between haemchromatosis and haemsiderosis
haemchromatosis: Fe accumulation in hepatocytes, develops into cirrhosis and HCC HAemosiderosis: Fe accumulation in macrophages, does not develop into cirrhosis, secondary to repeated blood transfusions, not somethign to be worried about
69
whihc malignancy is common in thailand and due to worms
cholangiocarcinoma
70
**Which of these is NOT associated with fatty change in the liver?** * Diabetes * Hepatitis B * Hepatitis C * Alcohol
* Answer: Hep B * Diabetes and alcohol are classic causes of fatty change * There is a genotype of Hepatitis C which can cause fatty change so it is also technically correct
71
3 Cirrhosis defining features
WHOLE liver is involved Characterised by scarring and fibrosis surrounding nodules of regenerating hepatocytes Distortion of liver vascular architecture: development of intra- and extrahepatic shunts
72
**3 Complications of Cirrhosis**
Portal hypertension:oesophageal varices + splenomegaly: palpable slpeen due to backlog of blood into spleen Hepatic encephalopathy Liver cell cancer
73
is cirrhosis reversible
cirrhosis may be REVERSIBLE If the underlying cause is aggressively treated
74
which stages of alcoholic liver disease are reversible and irreversible
Fatty liver disease- reversible Alocohlic hepatits- irreversible
75
in alcolhilic liver disease, which zone is alcoholic hepatits mostly affecting
changes are MAINLY seen in Zone 3 cells that get damaged are the ones that contain the most alcohol dehydrogenase that convert alcholic in toxic metabolise of acetaladehyde
76
what type of firbosis is very characteristic of alcoholic liver disease and what else do you see (cell types)
**Pericellular fibrosis**: Fibrosis around individual cells **inflammation**: lots of inflammatory cells will be seen but the most characteristic inflammatory cell seen is the **_neutrophil_ polymorph** but can be lymphocytic too.
77
features of haemchromatosis
**deposition in:** testes: fertility pancreas: Bronzed diabetes Liver: hepatocyte damage \>\> HCC cardiovascular: cardiomyopathy skin: tanned complexion
78
what is **Haemosiderosis**
is **_a type of iron overload_** **accumulation of iron _in macrophages_** usually occurs as a result from repeated blood transfusion
79
presentation of Wilson's disease
depositio of copper in: lentiform nucleus of the basal ganglia: Parkinsonian features, dementia, psychosis iris- Kayser-Fleischer rings liver- liver disease: : acute hepatitis, fulminant liver failure or cirrhosis
80
other associated conditons of autoimmune hepatits:
**autoimmune conditions: SLE, rheumatoid arthritis, thyroiditis, UC** etc.
81
what type of cell accumulaiton do you find in autoimmune hepatitis + why
active form of chronic hepatits: lots of inflammatory cells + plasma cells lots of plasma cells **Lots of _plasma cells because lots of autoantibodies_ are secreted**
82
treatment for autoimmune hepatits:
Responds to STEROIDS
83
**a****1-Antitrypsin Deficiency clinical features:**
hepatocyte can make a1-antitrypsin but cannot secrete it so deficinecy in blood but excess in liver causes: emphysema in the lung COPD in NON SMOKERS A1AT: deficiency can present in neonates as giant cell hepatitis (giant cell hepatocytes are multinuclear)
84
what can the skin look like in haemochromatosis?
bronzed or **slate grey**

Histopathology (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions