Brainscape's Knowledge GenomeTM

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


See full index

Year 5 Path Histopathology > Liver > Flashcards

Liver Flashcards

1
Q

What bilirubin (conjugated/unconjugated) is measured in the direct bilirubin?

A

Direct bilirubin = conjugated

(Van den Berg reaction - direct = conjugated then something is added that measures total)

Toal- direct = indirect= unconjugated

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

How does Phototherpy as treatment for neonatal jaundice work?

A

Converts bilirubin into two other compounds, lumirubin and photobilirubin which are isomers that do not need conjugation for excretion.

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

What is the pathophystiology of Gilbert’s ?

A

UDP glucuronyl transferase activity reduced to 30%

–> decreased bilirubin (worse with fasting, stress etc.)

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

Explain Hepatitis B serology

What makers?
What do they indicate?

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

What are histologically defining features of alcoholic hepatitis?

A
  1. Ballooning degeneration +/-
  2. Mallory-Denk Bodies (marker of chronic hepatitis (hyaline inclusion in hepatocytic cytoplasim)

inflammation
fibrosis

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

What nutritinal deficiency causes Beri-Beri?

A

B1 deficiency

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

At what sites does porto-systemic anastomosis occur?

A

Oesophageal varices
Rectal varices
Umbilical vein recanalising
Spleno-renal shunt

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

What is Courvoisier’s law?

A

In the presence of jaundice, if the gall bladder is palpable, the cause is unlikely to be gall stones.

This is because a gall bladder with stones is usually small and fibrotic and incapable of being large.

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

What are the components of the hepatic lobule?

How does it grossly work?

A

Hepatic lobule = hexagonal functional structure of the liver

  1. Hepatic vein at center (central vein)
  2. Blood enters via the portal Vein in the Portal tracts, that contrain 3 structures (portal triad) (bile, vein, artrey)
  3. Goes through 3 zones:

Zone1: closest to portal triad
Zone 2 in between
Zone 3: closest to central vein

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

Where is Zone 1in the hepatic lobule located?

In what pathology does it get affected first?

A

Zone 1 = closest to portal triad: most oxygen

–> Blood flow and filtration from portal triad to central vein, bile flow in opposite direction

But also first affected in viral hepatitis

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

What is the main function of hepatocytes in Zone 3?

When do they experience damage?

A

The least oxygenated zone, and thus most susceptible to ischemia

Most sensitive to metabolic toxins as this is the most metabolically active (e.g., ethanol, CCl4, halothane, rifampin, acetaminophen)

Has the highest amount of cytochrome P-450 –> most liver metabolism happens here

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

How much bile is produced every day?

A

600-1000ml

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

What is the perisinusoidal space in the liver called?

What lie quiescently in that space and what is their function?

A
  1. space (of Disse): contains hepatic stellate cells
    - store vitamin A
    - extracellular matrix production in liver injury (formation of scar tissue → fibrosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are histological finsinds of acutet hepatitis?

A

Caused bei either viruses (Hep A-E) or Drugs

Histopathology shows spottynecrosis (small foci of inflammatiton and infiltrates)

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

What is the normal weight of the liver?

A

1500g

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

What is the blood suppy of the liver?

A

Dual blood supply –> makes ischaemia unlikey

  1. Portal vein
  2. hepatic artery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a hepatic acinus?

A

Devision of the liver lobule considering blood flow, intorhobus shaped devisins

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

What is the function of liver Kupffer cells?

Where are they located?

A

Kupffer cells (a type of macrophage) are housed in the sinusoids

These cells phagocytize foreign particles, bacteria, and damaged, old blood cells.

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

What are hepatic stellate cells?

What is their main function?

A

Usually: store Vitamin A

Otherwise
Can get activated –> become myofibroblast –> and are the main source of extracellular matrix production in liver injury (formation of scar tissue → fibrosis)

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

What are the histological changes in Liver injuries?

A
  1. Loss of hepatocyte microvilli
  2. acvication of stellate cells –> deposition of scar tissue
  3. Loss of fenestration in endothelial cells
  4. Kupffer cell activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the definition of cirrhosis?

Structural and functional abnromalities

A
  1. Whole liver involved
  2. Fibrosis (blue)
  3. Nodules of regenerating hepatocytes (centre of picture)

Leading to:
Functionally
Distortion of liver vascular architecture (obstruction of blood flow) –> inra- and extra-hepatic shunting of blood (no filtration of blood)

–> no blood to hepatocytes

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

How can liver cirrhosis be classified?

A
  1. Nodule size (micronodular vs macronodular) –> not super useful
  2. Aetiology of cirrhosis –> useful
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the main complicatios of cirrhosis?

A
  1. Portal HTN
  2. Hepatic encephalopathy
  3. Hepatocellular carcinoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Is cirrhosis reversible?

A

It sometimes can be

(e.g. with good treatment of viral hepatitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the main reasons of acute heaptitis?

A
  1. Drugs
    Alcohol
    Paracetamol
  2. Viruses (Hepatitis A-E)
26
Q

What are the histological features of acute hepatitis?

A

Spotty necrosis
( Inflammaiton in he liver lobule vs around the portal tract in chronic hepatitis

–> usually caused by Drugs of Viruses

27
Q

What is the aetiology of chronic hepatitis?

A
  1. Viral hepatitis
  2. Drugs
  3. Auto-immune
28
Q

What is the difference between stage and grade in chronic hepatitis on histology?

A
  1. Grade: severity of inflammation
  2. Stage: severity of fibrosis
29
Q

What are the histological findings of chornic hepatitis relating to grade?

A

Grade = degree of inflammation

Usually inflammaiton in or around the portal tract (but can extend to lobule)

  1. Portal inflammation
  2. interface hepatitis –> piecemeal necrosis (important as this causes hepatocyte damage + symptoms)
30
Q

What are the histological findings of chornic hepatitis relating to stage?

A

Stage = degree of fibrosis

Fibrosis –> initially bridging fibrosis spanding from portal triad to central vein –> direct way for erythrocytes passing into central vein without entering hepatocytes –> mechanism of intra-hepatic shunting

(Once bridging there–> increased risk of cancer)

31
Q

What are the 3 patterns that contribute to alcoholic liver disease?

A

Can be progressive but also co-exist with each other

  1. Fatty liver –> reversible and metabolic process (picture –> fat in hepatocytes, large droplet fatty change)
  2. Alcoholic hepatitis
  3. Cirrhosis
32
Q

What are the histological changes of alcoholic hepatitis?

A

Mainly in Zone 3

  1. Ballooning –> swelling of hepatocytes because of Acetaldehyde (damage to cytoskeleton)
  2. (+/- Mallory Denk bodies –> damaged cytoskeleton)
  3. Apoptosis
  4. Pericellular fibrosis (characteristic of alcoholic liver disease)
33
Q

What is the usually macroscopic appearance of alcoholic cirrhosis?

A

Usually micronodular

34
Q

What is the aetiology of Non-alcoholic fatty liver disase?

What is the epidemiology?

A

Due to insulin resistance
–> high BMI
Diabetes (type II)

–> most common cause of liver disease worldwide (and increasing)

35
Q

What are the histological changes of NAFLD/ NASH?

A

Looks exactly like alcoholic hepatitis

36
Q

What is PBC? What is the pathophysiology + histological changes ?

A

Primary Biliary Cholangitis

progressive destruction of bile duct due to (periductal granulomatous inflammation) –> chronic cholestasis –> hepatocyte damage due to increased accumulation of toxins –> + fibrotic changes –> might lead to cirrhosis in 50% of patients

37
Q

What is the epidemiolgoy of Primary Biliary cirrhosis?

A

Female > Male

38
Q

What is the diagnostic test for primary biliary choloangitis?

A

Anti-mitochondrial antibodies
(NOT biopsy)

39
Q

What is PSC?

Explain the pathophysiology + histological changes

A

Primary Sclerosing Cholangitis

Periductal fibrosisleading to bile duct loss (squeezing of bile ducts) (inrahepatic + extrahepatic)

40
Q

What is the epidemiolgoy of PSC and its associated risk?

A

Male> Femlaes
strong associated with UC
Increased risk of cholangiocarcinoma

41
Q

What is the diagnostic test for PSC?

A

Bile duct imaging ERCP/MRCP
(not biopsy)

42
Q

What is the pathophyiology of Haematomachrosis

A
  1. Mutation of Gene on chromosome 6 (HFe)
  2. Genetically determined increased GI iron absorption
  3. –> parenchymal damge to organs due to iron organ deposition
43
Q

What are the histological liver changes occuring with Haemochomatosis?

What stain can be used to visualise them?

A
  1. Iron depositions in the hepatocytes –> chirrosis + cancer
  2. Stain with prussion blue stain
44
Q

What is haemosiderosis?

What is it associated with?

A

Accumulation of iron in macrophages –> associated with many blood transfusion

45
Q

What results on blood iron studies would you expect in a patient with Haemochromatosis?

A

↑ Fe, ↑ Ferritin
● Transferrin saturation > 45% ● ↓TIBC

46
Q

Explain the pathophysiology of Wilson’s disease

A

Genetic mutation on chromosome 13

Cupper accumulation due to failure of copper excretion into bile

–> accumulation mainly in liver and CNS incl. Kayser Fleischer rings

47
Q

What blood results would you expect in a patient with Wilson’s disease when you do copper studies?

A

↑ Transaminases (liver damage)

CBC: Coombs-negative hemolytic anemia, thrombocytopenia (hypersplenism)

↓ Serum ceruloplasmin (normal value > 20 mg/dL) (carrier of copper in blood)

↑ Free serum copper, but ↓ total serum copper (as test detect ceruloplasmin boung copper –> false negative result as often low serum ceruloplasmin )

48
Q

What stain is used in the diagnosis of Wilson’s disease?

A

Rhodanine stain

49
Q

What are the key features of autoimmuen hepatitis?
(epidemiolgoy)
Antibodies asoosiction

A
  1. usually in Females > Males
  2. Diagnosed by Anti-SM in serum
50
Q

What are the histologicla changes seen in Auto-immune hepatitis?

A

Usually very active form of hepatits
–> Interface hepatitis

51
Q

What is the pathophysiology of Alpha-1 antitrypsin deficiency

What histological changes are associated with it?

A

Failure to secret alpha-one antitrypsin –> deficiency in peripheral. blood, but accumulation in hepatocytes –> (intra-cytoplasmic inclusions due to misfolded protein)

(+ assicated with lung emphysema due to lack of anti-inflammatory effect of alpha-1-antitrypsine in lungs)

Leading to Hepatitis and Cirrhosis

52
Q

What are the histological damages seen in Paracetamol toxicity?

A

Usually damage in Zone 3. (with extention in Zone 2)

53
Q

What are the diseases that can cause non-caseatign granulomas?

A

an inflammatory condition
–> sarcoidosis and Crohn disease
–> vasculitis
– > exposure to foreign objects.

54
Q

What is a caseating granuloma?
What are the cases?

A

Granuloma with necrosis in the middle

Generally formed by infections
- TB
- fungal infection

55
Q

What is a granuloma?

A

Area of chronic inflammatiton characterised by
1. Giant cells (fused macrophages)
2. Activated macrphages around them

56
Q

The Modified Child’s Pugh Score is a way of quantifying + predicting survival of pateitns with liver disease.

What criteria are taken into consideration/ calculation?

A

ABCDE

57
Q

What are the most common benign tumours of the livers?

A
  1. Adenoma (liver cell or bile duct)
  2. haemangioma –> most common lesion of liver
58
Q

What are the most common tumours of the liver?

A

Metastasis (seconary tumours)

–> usually multiple, from GI, pancreas or bronchus

59
Q

What are the 4 primary types of malignat liver cell tumours

A
  1. Hepatocellular carcinomas
  2. Hepatoblastomas
  3. Chaloangiocarcinoma
  4. Haemangiosarcoma
60
Q

What are the risk factors/ association for the development of hepatocellular carcinoma?

A
  1. Cirrhosis –> screening via USS every 6 months in patients with cirrhosis
  2. Hepatitis B (can cause hepatocellulular carcinoma directly, without cirrhosis)
61
Q

How common are cholangiocarcinomas?

What diseases are they manly associated with?

A

Adenocarcinomas arising from bile ducts

  • 10% of liver tumours
  • Can be intra or extrahepatic
  • Poor prognosis
  • 90% Associated with gallstones

Causes:
Primary sclerosing cholangitis
parasitic liver disease (worms)
chronic liver disease (cirrhosis)
congenital liver abnormalities, Lynch syndrome type II.

62
Q

What tissue do haemangiosarcomas originate from?

What is the epiudemiology?

A

Occurs in children/infants – presents with abdominal mass

Originates from immature liver precursor cells.

Year 5 Path Histopathology (19 decks)

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