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YR5 Histopathology > Crash course: Liver, Cardiac, GI > Flashcards

Crash course: Liver, Cardiac, GI Flashcards

1
Q

Describe blood flow in the liver

A

Hepatic artery + portal vein bring blood to liver

Blood travels through sinusoids, O2 absorbed by hepatocytes along the way

pO2 much lower when blood reaches zone 3 where cells are most metabolically active - problem in alcoholics

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2
Q

Give 3 features of zone 1 hepatocytes

A

closest to portal triad
most oxygenated
first affected in viral hepatitis + toxic substance ingestion

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3
Q

Give 3 features of zone 3 hepatocytes

A

Most functional hepatocytes
Most liver enzymes- most sensitive to metabolic toxins
Least oxygenated: most affected by ischaemia

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4
Q

What is the portal triad composed of?

A

Hepatic artery
Portal vein
Bile ductule

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5
Q

What are the causes of acute hepatitis?

A

Viral (A+E)- faeco-oral route

Drugs

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6
Q

What pattern of inflammation is seen in acute hepatitis?

A

Spotty necrosis
Small foci of inflammation + necrosis with inflammatory infiltrates

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7
Q

What are the causes of chronic hepatitis?

A

Viral: B + C
Drugs
PBC, PSC, Wilson’s + Haemochromatosis

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8
Q

What is the pattern of inflammation in chronic hepatitis?

A

Piecemeal necrosis / interface hepatitis: Loss of border between portal tract + surrounding parenchyma

Bridging fibrosis from portal triad → central vein: Signals evolution to cirrhosis

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9
Q

Describe the pathogenesis of cirrhosis

A
  1. Hepatocyte damage leads to necrosis
  2. Fibroblasts replace hepatocytes + some areas of regenerating hepatocytes remain
  3. Increased resistance to blood flow within liver leads to portal HTN
  4. Increased resistance causes fibrotic bridges to form between portal triad + central vein (path of least resistance – intrahepatic shunting), bypassing hepatocytes
  5. Portal HTN causes extrahepatic shunting due to backlog of blood
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10
Q

Give 3 forms of extra hepatic shunting

A

Oesophageal varices
Anorectal varices
Caput medusae

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11
Q

How is cirrhosis classified?

A

According to aetiology
1. Alcohol/ insulin resistance (usually micro nodular)
2. Viral hepatitis etc. (usually macro nodular)

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12
Q

Which 4 features define cirrhosis?

A

Whole liver involved

Fibrosis

Nodules of regenerating hepatocytes

Distortion of liver vascular architecture: intra- + extra-hepatic shunting of blood (e.g. gastro-oesophageal)

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13
Q

Give 3 clinical complications of cirrhosis

A

Portal HTN
Hepatic encephalopathy
Liver cell cancer

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14
Q

How does the histology differ in acute and chronic hepatitis?

A

Acute: most inflammation in lobules
Chronic: most inflammation in or around portal tract

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15
Q

Once a patient has developed bridging fibrosis, what are they at increased risk of?

A

Cirrhosis
Hepatocellular carcinoma
Liver transplantation
Death

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16
Q

What are the 3 patterns of alcoholic liver disease?

A

Fatty liver: metabolic change, reversible
Alcoholic hepatitis: inflammation
Cirrhosis

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17
Q

Describe the micro and macro-nodular histology of fatty liver (hepatic steatosis)

A

Fully reversible if avoid EtOH

Macro: Large, pale, yellow, greasy

Micro: Fat droplets in hepatocytes

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18
Q

Give 4 histological features of alcoholic hepatitis

A

Macro: Large, fibrotic

Micro:
Ballooning (+/- Mallory Denk bodies)
Apoptosis
Pericellular fibrosis
Mainly seen in Zone 3

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19
Q

Describe the micro and macro-nodular histology of alcoholic cirrhosis

A

Macro: shrunken brown orange

Micro: micro nodular cirrhosis

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20
Q

Give 3 features of NAFLD

A

Histologically similar to alcoholic liver disease

Distinguished based on hx

Cause: insulin resistance a/w raised BMI + diabetes

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21
Q

What are the 3 stages of NAFLD

A

Hepatic steatosis
Non alcoholic steato-hepatitis
Cirrhosis

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22
Q

Give 4 features of primary sclerosing cholangitis

A

M > F

Fibrotic: periductal intra + extra hepatic bile duct fibrosis

a/w UC + risk of cholangiocarcinoma

pANCA-associated

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23
Q

Give 3 features of primary biliary cholangitis

A

F > M
a/w other AI conditions e.g. Sjogrens, Hashimoto’s thyroiditis
Inflammatory: Bile duct chronic inflammation with GRANULOMAs

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24
Q

What antibody is present in Primary Biliary Cholangitis?

A

Anti-mitochondrial antibodies

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25
Q

In which populations is AI hepatitis most commonly seen?

A

Young/ post menopausal women
with other AI conditions e.g. Hashimoto’s thyroiditis, UC, T1DM, Graves

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26
Q

What antibodies are associated with AI hepatitis?

A

TI: Anti-smooth muscle antibodies

TII: Anti-liver-kidney-microsomal (LKM) antibodies

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27
Q

What is Haemochromatosis?

A

Autosomal recessive
Genetically determined increased gut iron absorption (Chr 6)
Parenchymal damage to organs secondary to iron deposition

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28
Q

Give 3 clinical manifestations of Haemochromatosis

A

In liver: fibrosis - cirrhosis
In skin: bronze pigmentation
In pancreas: severe pancreatitis, islet damage + DM

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29
Q

What stain is used for liver biopsies in patients with Haemochromatosis?

A

Prussian blue iron stain

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30
Q

What is Wilson’s disease? Give 2 clinical manifestations

A

Autosomal recessive
Accumulation of copper due to failure of excretion by hepatocytes into bile

Deposits in CNS: lenticular degeneration- psych disturbances

Deposits in cornea: kayser fleishcer rings on slit lamp

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31
Q

What stain is used for liver biopsies with Wilson’s disease?

A

Rhodanine stain

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32
Q

What is seen on bloods in Wilson’s disease?

A

Low serum caeruloplasmin
Low serum copper

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33
Q

What is alpha-1 antitrypsin deficiency?

A

Autosomal dominant
Failure to secrete alpha-1 antitrypsin (in blood)

Excess alpha 1 antitrypsin in hepatocytes causes misfolding of proteins + intra-cytoplasmic inclusions

Causes hepatitis + cirrhosis

a/w emphysema

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34
Q

Why is alpha 1 antitrypsin deficiency associated with emphysema?

A

Alpha 1 antitrypsin usualy dampens inflammation
Without this, inflammation in lung is prolonged, allowing more lung destruction

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35
Q

What is seen on histology in alpha 1 antitrypsin deficiency?

A

Periportal red hyaline globules using Periodic Acid Schiff stain

36
Q

Give 3 benign liver tumours

A

Haemangioma: most common benign

Liver cell adenoma: a/w OCP

Bile duct adenoma

37
Q

Give 3 malignancies of the liver

A

Secondary metastases: most common

Hepatocellular carcinoma

Cholangiocarcinoma

38
Q

What tumour marker is seen in hepatocellular carcinoma?

A

AFP

39
Q

Hepatocellular carcinoma is associated with which 5 conditions/ exposures

A

Viral hepatitis
Alcoholic cirrhosis
NAFLD
Aflatoxin
Haemochromatosis

40
Q

Cholangiocarcinoma can be associated with which 3 conditions? From which bile ducts can it arise?

A

PSC
Worm infections
Cirrhosis
Can arise from intra-hepatic + extra-hepatic ducts (inc. gall bladder)

41
Q

What is seen on histology in cholangiocarcinoma?

A

Capillary ingrowth

42
Q

What is the most common examination finding in a patient with portal hypertension?
a. Splenomegaly
b. Hepatomegaly
c. Spider naevi in the distribution of the SVC
d. Jaundice
e. Liver flap

A

a. Splenomegaly

43
Q

An 23M has just returned from Tanzania, where he swam in Lake Malawi. Following this he develops fever, rigors, hepatomegaly + haematuria. What would his blood tests most likely show?
a. Deranged U+Es
b. Deranged LFTs
c. Raised Neutrophils
d. Raised Macrophages
e. Raised Eosinophils

A

e. Raised eosinophils

Likely Schistosomiasis
Any parasitic infection will cause raised eosinophils

44
Q

When are eosinophils seen? Describe their appearance

A

Allergic reactions
Parasitic infections

Bi-lobed nuclei (blue) with red granules

45
Q

Which tumour type produces keratin and intercellular bridges?

A

Squamous cell carcinoma

46
Q

Where is transitional epithelium found? (and thus transitional cell carcinomas)

A

Kidney
Ureters
Bladder

47
Q

What is stained on haematoxylin and eosin preparations?

A

H: stains basic parts purple/blue
E: acidic parts red/pink

48
Q

A 40M presents to ED complaining of 5 hours of central, crushing chest pain. ECG shows ST elevation in leads II, III and aVF. What changes would be seen on histology?

A

None

49
Q

Describe the histopathological changes occurring after myocardial infarction

A

< 6h: Normal histology + CK-MB

6–24h: Loss of nuclei, homogenous cytoplasm, necrotic cell death.

1-4d: Infiltration of polymorphs then macrophages (clear up debris).

5-10d: Removal of debris.

1-2w: Granulation tissue, new blood vessels, myofibroblasts, collagen synthesis.

Weeks-months: Strengthening, decellularising scar.

50
Q

What are the types of cardiomyopathy?

A

Dilated: progressive loss of myocytes

Hypertrophic: LV hypertrophy

Restrictive: Impaired ventricular compliance

(Too thin, too thick, too stiff)

51
Q

Which lipids are good and which are bad?

A

LDL = BAD

HDL = GOOD

52
Q

What is the response to injury hypothesis?

A

Chronic inflammatory + healing response of arterial wall to endothelial injury.

53
Q

Describe the impact of IHD worldwide

A

Leading cause of death worldwide for M+F (7million/year).

54
Q

What is angina pectoris?

A

Transient ischaemia not producing myocyte necrosis.

55
Q

Where do plaques usually occur in IHD?

A

1st few cm of LAD or LCX

Entire length RCA

56
Q

What characterises vulnerable plaques?

A

Large lipid core

Thin fibrous cap

Large inflammatory infiltrate

57
Q

What are the acute plaque changes that can occur?

A

Rupture: Exposes prothrombogenic plaque contents

Erosion: Exposes prothrombogenic subendothelial basement membrane

Haemorrhage into plaque: Increase size

58
Q

What is stenosis?

A

Critical stenosis: demand > supply

Occurs at ~70% occlusion (or diameter <1mm)

Causes “stable” angina

Can lead to Chronic IHD

Acute plaque rupture can occur

59
Q

What is an atheromatous plaque?

A

Raised proliferation of endothelium

Soft lipid core

White fibrous cap

60
Q

A 30F is receiving the results of a colonoscopy he has had due to persistent PR bleeding. The results reveal ~75 polyps seen
in the right-sided colon. What is the mechanism by which she has an increased risk of malignancy?

A

AD mutation in DNA mismatch repair gene

(HPNCC)

61
Q

What is the aetiology of familial adenomatous polyposis? (FAP)

A

Autosomal DOMINANT mutation in APC tumour suppressor gene on Chr 5q21

62
Q

How does FAP present?

A

100s-1000s polyps
Seen in childhood

63
Q

What is the prognosis of FAP?

A

If untreated will progress to adenocarcinoma by early adulthood (within 10-15y) with cancer risk of 100%

64
Q

What is Gardner’s syndrome?

A

Subtype of FAP (autosomal dominant) with extra-intestinal features

65
Q

List 4 extraintestinal features of Gardner’s syndrome

A

Osteomas of skull
Epidermoid cysts
Dermoid tumours
Dental caries

66
Q

What is the aetiology of hereditary non-polyposis colorectal carcinoma (HPNCC), aka Lynch syndrome?

A

Autosomal dominant mutation in DNA mismatch repair gene

67
Q

Describe the characteristics of HPNCC

A

Less polyps than FAP but increased chance of any individual polyp progression to cancer due to inability to correct errors

68
Q

Give 4 extra-colonic cancers associated with HPNCC

A

Endometrial (most common)
Ovarian
Small bowel
Gastric

69
Q

What is the mainstay of management in familial GI cancer syndromes?

A

Monitoring +/- total colectomy

70
Q

Which 4 features indicate higher risk of cancer in GI polyps?

A

Larger polyps
More polyps
Higher villous component
Dysplastic features

71
Q

What is the sequelae of disease progression to neoplasia in oesophageal and gastric cancers?

A

“Flat pathway”

Squamous

Metaplastic glandular epithelium- Intestinal type

Dysplasia: Changes showing some cytological + histological features of malignancy but no invasion through BM

Adenocarcinoma: Invasion through BM

72
Q

What is the most important risk factor for carcinoma in the colon?

A

Polyps

73
Q

Give 3 features of adenocarcinoma of the oesophagus

A

Commonest oesophageal carcinoma in Developed countries

A/w reflux

Lower oesophagus (where most reflux affects)

74
Q

What is gastric cancer and how can it be split?

A

95% of stomach cancers are adenocarcinoma.

Split morphologically into:

Intestinal: Well differentiated.
Diffuse: Poorly differentiated (Linitis plastica), inc. signet ring cell carcinoma

75
Q

What will be seen on duodenal biopsy in coeliac disease?

A

Gluten rich diet: villous atrophy

GF: Normal villi

76
Q

What are the 3 types of neoplastic polyps of the colon and rectum?

A

Tubular adenoma

Tubulovillous adenoma

Villous adenoma

77
Q

What is villous carcinoma?

A

Sessile growths lined by dysplastic glandular epithelium
Risk of malignancy is esp. high up to 50%.

78
Q

What is tubular carcinoma?

A

most common type of adenoma in the colon/ rectum
Considered benign, or noncancerous.

79
Q

What sort of colon polyps most commonly predispose to adenocarcinoma of the colon?

A

Villous adenoma

80
Q

A 64F who has been diagnosed with MEN2A presents with a thyroid lump. Further Ix reveals a malignancy, which hormone would be measured to assess response to Tx?

A

Calcitonin

81
Q

Give 3 features of MEN 1

A

Pituitary adenoma
Parathyroid hyperplasia
Pancreatic tumours

82
Q

Give 3 features of MEN 2A

A

Parathyroid hyperplasia
Medullary thyroid carcinoma
Phaeochromocytoma

83
Q

Give 4 features of MEN 2B

A

Mucosal neuromas
Marfanoid body habits
Medullary thyroid carcinoma
Phaeochromocytoma

84
Q

What is medullary thyroid carcinoma?

A

Cancer of the parafollicular C cells
Measure calcitonin to assess response to Tx

85
Q

How do you remember the features of MEN conditions?

A

3P → 2P → 1P

0M → 1M → 3M

86
Q

Describe Prostate cancers

A

Most commonly adenocarcinoma in the peripheral area of the gland
Staging based on histology of biopsy

87
Q

How is the Gleason score calculated?

A

Score 1-5 based on differentiation (5 is worst– least differentiated + most aggressive)

Take a biopsy + classify the most common pattern seen (X) + the worst pattern seen (Y)

Add these 2 numbers together to get a result out of 10

Expressed as X+Y=Z

YR5 Histopathology (27 decks)

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