Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

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

Give 3 features of zone 1 hepatocytes

A

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

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

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

What is the portal triad composed of?

A

Hepatic artery
Portal vein
Bile ductule

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

What are the causes of acute hepatitis?

A

Viral (A+E)- faeco-oral route

Drugs

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

What pattern of inflammation is seen in acute hepatitis?

A

Spotty necrosis
Small foci of inflammation + necrosis with inflammatory infiltrates

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

What are the causes of chronic hepatitis?

A

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

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

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

Give 3 forms of extra hepatic shunting

A

Oesophageal varices
Anorectal varices
Caput medusae

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

How is cirrhosis classified?

A

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

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

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

Give 3 clinical complications of cirrhosis

A

Portal HTN
Hepatic encephalopathy
Liver cell cancer

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

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

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

A

Cirrhosis
Hepatocellular carcinoma
Liver transplantation
Death

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

What are the 3 patterns of alcoholic liver disease?

A

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

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

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

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

Describe the micro and macro-nodular histology of alcoholic cirrhosis

A

Macro: shrunken brown orange

Micro: micro nodular cirrhosis

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

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

What are the 3 stages of NAFLD

A

Hepatic steatosis
Non alcoholic steato-hepatitis
Cirrhosis

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

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

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

What antibody is present in Primary Biliary Cholangitis?

A

Anti-mitochondrial antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
In which populations is AI hepatitis most commonly seen?
Young/ post menopausal women with other AI conditions e.g. Hashimoto's thyroiditis, UC, T1DM, Graves
26
What antibodies are associated with AI hepatitis?
TI: Anti-smooth muscle antibodies TII: Anti-liver-kidney-microsomal (LKM) antibodies
27
What is Haemochromatosis?
Autosomal recessive Genetically determined increased gut iron absorption (Chr 6) Parenchymal damage to organs secondary to iron deposition
28
Give 3 clinical manifestations of Haemochromatosis
In liver: fibrosis - cirrhosis In skin: bronze pigmentation In pancreas: severe pancreatitis, islet damage + DM
29
What stain is used for liver biopsies in patients with Haemochromatosis?
Prussian blue iron stain
30
What is Wilson's disease? Give 2 clinical manifestations
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
31
What stain is used for liver biopsies with Wilson's disease?
Rhodanine stain
32
What is seen on bloods in Wilson's disease?
Low serum caeruloplasmin Low serum copper
33
What is alpha-1 antitrypsin deficiency?
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
34
Why is alpha 1 antitrypsin deficiency associated with emphysema?
Alpha 1 antitrypsin usualy dampens inflammation Without this, inflammation in lung is prolonged, allowing more lung destruction
35
What is seen on histology in alpha 1 antitrypsin deficiency?
Periportal red hyaline globules using Periodic Acid Schiff stain
36
Give 3 benign liver tumours
Haemangioma: most common benign Liver cell adenoma: a/w OCP Bile duct adenoma
37
Give 3 malignancies of the liver
Secondary metastases: most common Hepatocellular carcinoma Cholangiocarcinoma
38
What tumour marker is seen in hepatocellular carcinoma?
AFP
39
Hepatocellular carcinoma is associated with which 5 conditions/ exposures
Viral hepatitis Alcoholic cirrhosis NAFLD Aflatoxin Haemochromatosis
40
Cholangiocarcinoma can be associated with which 3 conditions? From which bile ducts can it arise?
PSC Worm infections Cirrhosis Can arise from intra-hepatic + extra-hepatic ducts (inc. gall bladder)
41
What is seen on histology in cholangiocarcinoma?
Capillary ingrowth
42
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. Splenomegaly
43
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
e. Raised eosinophils Likely Schistosomiasis Any parasitic infection will cause raised eosinophils
44
When are eosinophils seen? Describe their appearance
Allergic reactions Parasitic infections Bi-lobed nuclei (blue) with red granules
45
Which tumour type produces keratin and intercellular bridges?
Squamous cell carcinoma
46
Where is transitional epithelium found? (and thus transitional cell carcinomas)
Kidney Ureters Bladder
47
What is stained on haematoxylin and eosin preparations?
H: stains basic parts purple/blue E: acidic parts red/pink
48
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?
None
49
Describe the histopathological changes occurring after myocardial infarction
< 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
What are the types of cardiomyopathy?
Dilated: progressive loss of myocytes Hypertrophic: LV hypertrophy Restrictive: Impaired ventricular compliance (Too thin, too thick, too stiff)
51
Which lipids are good and which are bad?
LDL = BAD HDL = GOOD
52
What is the response to injury hypothesis?
Chronic inflammatory + healing response of arterial wall to endothelial injury.
53
Describe the impact of IHD worldwide
Leading cause of death worldwide for M+F (7million/year).
54
What is angina pectoris?
Transient ischaemia not producing myocyte necrosis.
55
Where do plaques usually occur in IHD?
1st few cm of LAD or LCX Entire length RCA
56
What characterises vulnerable plaques?
Large lipid core Thin fibrous cap Large inflammatory infiltrate
57
What are the acute plaque changes that can occur?
Rupture: Exposes prothrombogenic plaque contents Erosion: Exposes prothrombogenic subendothelial basement membrane Haemorrhage into plaque: Increase size
58
What is stenosis?
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
What is an atheromatous plaque?
Raised proliferation of endothelium Soft lipid core White fibrous cap
60
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?
AD mutation in DNA mismatch repair gene (HPNCC)
61
What is the aetiology of familial adenomatous polyposis? (FAP)
Autosomal DOMINANT mutation in APC tumour suppressor gene on Chr 5q21
62
How does FAP present?
100s-1000s polyps Seen in childhood
63
What is the prognosis of FAP?
If untreated will progress to adenocarcinoma by early adulthood (within 10-15y) with cancer risk of 100%
64
What is Gardner's syndrome?
Subtype of FAP (autosomal dominant) with extra-intestinal features
65
List 4 extraintestinal features of Gardner's syndrome
Osteomas of skull Epidermoid cysts Dermoid tumours Dental caries
66
What is the aetiology of hereditary non-polyposis colorectal carcinoma (HPNCC), aka Lynch syndrome?
Autosomal dominant mutation in DNA mismatch repair gene
67
Describe the characteristics of HPNCC
Less polyps than FAP but increased chance of any individual polyp progression to cancer due to inability to correct errors
68
Give 4 extra-colonic cancers associated with HPNCC
Endometrial (most common) Ovarian Small bowel Gastric
69
What is the mainstay of management in familial GI cancer syndromes?
Monitoring +/- total colectomy
70
Which 4 features indicate higher risk of cancer in GI polyps?
Larger polyps More polyps Higher villous component Dysplastic features
71
What is the sequelae of disease progression to neoplasia in oesophageal and gastric cancers?
“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
What is the most important risk factor for carcinoma in the colon?
Polyps
73
Give 3 features of adenocarcinoma of the oesophagus
Commonest oesophageal carcinoma in Developed countries A/w reflux Lower oesophagus (where most reflux affects)
74
What is gastric cancer and how can it be split?
95% of stomach cancers are adenocarcinoma. Split morphologically into: Intestinal: Well differentiated. Diffuse: Poorly differentiated (Linitis plastica), inc. signet ring cell carcinoma
75
What will be seen on duodenal biopsy in coeliac disease?
Gluten rich diet: villous atrophy GF: Normal villi
76
What are the 3 types of neoplastic polyps of the colon and rectum?
Tubular adenoma Tubulovillous adenoma Villous adenoma
77
What is villous carcinoma?
Sessile growths lined by dysplastic glandular epithelium Risk of malignancy is esp. high up to 50%.
78
What is tubular carcinoma?
most common type of adenoma in the colon/ rectum Considered benign, or noncancerous.
79
What sort of colon polyps most commonly predispose to adenocarcinoma of the colon?
Villous adenoma
80
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?
Calcitonin
81
Give 3 features of MEN 1
Pituitary adenoma Parathyroid hyperplasia Pancreatic tumours
82
Give 3 features of MEN 2A
Parathyroid hyperplasia Medullary thyroid carcinoma Phaeochromocytoma
83
Give 4 features of MEN 2B
Mucosal neuromas Marfanoid body habits Medullary thyroid carcinoma Phaeochromocytoma
84
What is medullary thyroid carcinoma?
Cancer of the parafollicular C cells Measure calcitonin to assess response to Tx
85
How do you remember the features of MEN conditions?
3P → 2P → 1P 0M → 1M → 3M
86
Describe Prostate cancers
Most commonly adenocarcinoma in the peripheral area of the gland Staging based on histology of biopsy
87
How is the Gleason score calculated?
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)

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