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Gastrointestinal tract > Histology/Pathology > Flashcards

Histology/Pathology Flashcards

1
Q

Where is skeletal muscle present in the GIT?

A

Top 3rd of oesophagus, mixed 3rd mixed with smooth.

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2
Q

What is the epithelium in the GIT?

A

Stratified squamous in oesophagus and rectum.

Columnar everywhere else.

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3
Q

Where are gastric glands and what are some of the cell types present in them?

A

At the bottom of gastric pits in the stomach (pits in rugae), pits open to 3-5 glands.
Glands have mucus, stem, parietal and chief cells present

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4
Q

How are the muscle layers so strong?

A

Thick muscularis mucosae, thick submucosa and 3rd oblique musclularis external layer

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5
Q

Where does pepsinogen come from and how is it activated?

A

From chief cells, activated to pepsin by the low pH

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6
Q

How is the surface area of the small intestine increased?

A

On the epithelium there is:

  • Microvilli
  • Villi
  • Plica circulares
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7
Q

Where are crypts of leiberkuhn and what are in them? What is the significance in terms of cancer?

A

At base of villi in SI.
Contain goblet cells and secretory cells.
Also have stem cells in base–> can go to cancer

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8
Q

What is inside the lamina propria of the villi? How does this contribute to movement and digestion?

A
  • Muscularis mucosae in the LP so villi can move and stir contents
  • Blood vessels and lymphatics present for absorption of products and fluid
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9
Q

What are some differences between the duodenum and jejunum/ileum in terms of plica and goblet cells?

A

duodenum has low plica and few goblet cells.

rest of SI has lots of goblet cells and more plica (but shortest villi)

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10
Q

Does the colon have villi?

What about glands?

A

No villi, surface smooth.

Looots of glands, crypts of leiberkuhn secreting lots of mucus

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11
Q

What connective tissue supports the liver?

A

Glissons capsule surrounds the liver and its blood vessels and ducts,
Also reticular fibres forming delicate framework around hepatocytes

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12
Q

What space do the sinusoids create in the liver?? How? Whats within it?

A

Space of Disse
Bathes the hepatocytes in plasma
As the sinusoids are fenestrated so it leaks out.

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13
Q

What is the hepatic acinus? What characterises zone 1 vs zone 3?

A

Functional unit of liver, organised around blood vessels.
Zone 1 is high in O2, toxins and metabolites.
Zone 3 is low in O2, toxins and metabolites

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14
Q

What are some histological characteristics of the gall bladder?

A

Simple columnar epithelium
Smooth muscle layer
Thick outer serosa

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15
Q

What is a pancreatic acini? What do the cells contain?

A

A ball of exocrine cells with a duct in the middle.

Cells have zymogen granules with the enzymes

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16
Q

What is the difference between gastric erosion, acute ulcer and chronic ulcer in terms of the layers it penetrates?

A

Gastric erosion just effects first 1/4 of LP in mucosa
Acute ulcer in muscularis mucosae
Chronic ulcer in series with fibrosis

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17
Q

What characterises autoimmune gastritis?

A
  • Destruction of parietal cells in corpus–> get atrophy of mucosa and achlorhydria
  • Leads to hypergastrinaemia
  • Can get intestinal metaplasia which can become a carcinoid
  • Pernicinous anemia
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18
Q

What is chemical gastritis? What is one compensation?

A

Reflex of bile or alkaline duodenal juice due to altered motility.
Leads to direct mucosal injury.
Mucus neck cells undergo hyperplasia to compensate and gastric pits get more tortuous and elongated

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19
Q

In antrum predominant H. pyloric gastritis what happens to the acid output, duodenal pathology and ulcer risk?

A

Gastric pathology: chronic inflammation and polymorphs
Hyperacidity
In duodenal: gastric metaplasia and chronic inflammation, leads to duodenal ulcer risk

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20
Q

In pan-gastritis predominant H. pyloric gastritis what happens to the gastric pathology, acid output, duodenal pathology and ulcer risk?

A

Gastric path: Chronic inflam, polymorphs, atrophy, intestinal metaplasia
Hypoacidity
No duodenal pathology
Gastric ulcer risk

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21
Q

What are some possible complications of peptic ulcer disease?

A
  • Perforation > peritonitis
  • Haemorrhage from eroding into near by artery
  • Penetration into adjacent organ
  • Stenosis from contraction of radial fibrous tissue eg at pylorus or end of oesophagus
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22
Q

How does the following contribute to coeliac pathogenesis?

  • Genetics
  • Environment
  • T cells
A

Genetics: HLA DQ2 or DQ8 genes present in 99.6%

Environment: Early infant env. including breast feeding (protective) and when introduced to gluten. Infections can also affect (e.g. gastroenteritis)

T cells: HLA DQ2/8 restricted CD4 tells resident in SI mucosa.
CD8+ accumulate in epithelium and part of innate response

23
Q

What is coeliac disease?

A

An immunologically mediated disease in response to gluten that causes chronic inflammation of the SI mucosa

24
Q

What is the order of cell types in the gastric glands of the stomach?

A
  • Surface epithelium
  • Regenerative stem cell in neck
  • Mucus neck cells
  • Parietal cells
  • Chief cells
  • ECL cells
25
Q

Compare stage 1, 2 and 3 in coeliac disease in terms of

  • IEL
  • Villus to crypt ratio
A

Stage 1

  • Excess of CD8 IEL
  • Still 4:1 normal ratio

Stage 2

  • Marked excess of CD8 IEL
  • Crypt hyperplasia
  • 1:1

Stage 3

  • Marked excess of CD8 IEL
  • Villus atrophy
  • Crypt hyperplasia
  • 4:1
26
Q

What are some clinical presentations of coeliac?

A

GIT: diarrhoea, bloating, flatulence
Anemia and other vitamin deficincies
Malabsorption and so failure to thrive

27
Q

What is the mechanism of gluten beginning the inflammation? How does it get through the epithelium? What is the main cytokine that damage the enterocytes?

A

Gliadin has a high proline and glutamine content which confers resistance to digestive enzymes.
This means some peptides can pass through epithelium in tact.
Intact peptides then deaminated by tissue transglutaminase (tTG) making glutamate (negative).
Neg charge now allows peptide to fit in APC HLADQ2/8
Presents to CD4+ T cells
TNFa causing damage

28
Q

How can we diagnose coeliac? What is a possible immune related consequence if left untreated?

A
  • Serological testing for tTG and DGP antibodies
  • HLA-DQ haplotyping
  • SI biopsy

Risk of small bowel lymphoma from all the CD8 proliferation and mutations (EATL)

29
Q

What takes a photo-oncogene to an oncogene?

What do oncogenes do?

A

An activating mutation (one hit) e.g. in a growth factor receptor or kinase.
They accelerate cell division

30
Q

What has to happen for a tumor suppressor gene to cause cancer?

A

Loss of function of them by both chromosomes being hit by mutation.

31
Q

What occurs in the cervical transformation zone? What virus is it susceptive to and what cancer type can occur as a result? How genetically does it cause this cancer?

A

Transition zone between the glandular columnar epithelium of the endocervix and the squamous ectocervix.
Susceptible to HPV.
Can cause squamous cell carcinoma
It causes over expression of oncogenes which inhibit tutor suppressor genes

32
Q

What happens in Barrett’s oesophagus?
What cancer can it predispose to?
What are some histological features in terms of glands the nucleus of cells of this cancer?

A

From chronic reflux oesophagitis
Get glandular columnar metaplasia
Can get mutations and adenocarcinoma as a result
Can see surface maturation of glandular epithelium, but glands are crowded with differing shape. If they fuse together sign of malignancy
Nucleus of proliferating cells show atypic and loss of polarity

33
Q

What is the clinical definition of acute hepatitis?

What are some symptoms they might present with?

A

Raised serum transaminases for period of less than 6 months without history of chronic liver disease.
Malaise, jaundice, nausea

34
Q

Describe the reversible and irreversible hepatocyte changes in necrosis?

A

Reversible: swelling and cholestasis
Irreversible: apoptosis of single cells and necrosis or groups of adjacent hepatocytes

35
Q

Describe the steps of necrosis in hepatitis and how they present instead of the expected coagulative necrosis

A

Zonal: around zone 3 and the central vein
Bridging: goes from central vein to portal triad
Multi-acinar: spreading throughout lobule and
Will see the result of their osmotic lysis: breakdown of reticulin framework and scavenger macrophages

36
Q

How does paracetamol induced liver necrosis differ from acute viral hepatitis in terms of necrosis location, what the necrosis looks like and inflammation?

A 
Involves zone 3 and lobular disarray not seen (vs pan lobular necrosis)
Coagulative necrosis (vs lytic)
Minimal inflammation (vs inflammation)
37
Q

What is familial adenomatous polypsis?
What can it lead to?
What gene is deleted?

A

Inherited condition in which polyps form in colon.
Big cause of early onset colorectal carcinoma
Caused by APC gene deletion, a tumour suppressor gene/

38
Q

What is lynch syndrome?
What does it cause?
Is it a bigger cause of colorectal carcinomas then FAP?
What type of gene is mutated?

A

Hereditary non-polyposis colorectal cancer
Early onset colorectal cancer
Yes
A DNA mismatch repair gene

39
Q

What are some histological features of a adenomatous polyp? Is there invasion of the muscularis mucosae?

A
  • Abnormal crypt architecture (villous or tubular)
    Dysplasia
  • Nuclear atypia e.g increased nucleus to cytoplasmic ratio and irregular contours
    *Crowded cells
  • Hyperchromatic pseudostratified nuclei
  • Abnormal complexity to glandular architecture
  • Decreased goblet cells
  • Abnormal mitosis
    NO invasion
40
Q

What are some differences in growth pattern of carcinomas between the proximal and distal colon?

A

Proximal
- Bulky, polyps, exophytic (growing outward)
Distal/rectum
- Annular, stenosing, ulcerated

41
Q

How do we stage colorectal cancers?

What is a main feature in grading?

A

Tumor invasion
Lymph node metastasis
Distant metastasis

How differentiated, glands a good way to tell so stage 1 still has glands but by 3 or 4 not really a gland in site

42
Q

What are two histological features of adenocarcinoma that differ from adenoma?

A
  • Invasion to submucosa so can access blood vessels and lymphatics
  • Desmoplasia as the storm becomes reactive and inflamed
43
Q

What type of genes are K-RAS and B-RAF?

Does EGFR therapy in cancer therefore work if they are mutated?

A

They are oncogenes, which is an activating mutation so no an EGFR therapy won’t work as mutation downstream from that.

44
Q

What is the clinical definition of chronic hepatitis?

What are the most common causes?

A

Persistence of liver injury and raised serum aminotransferases for >6 months
Hep B and C (80% get chronic in Hep C, acute v. rare)

45
Q

What is the main difference between acute and chronic hepatitis in terms of their location across hepatocytes?
What about fibrosis? What induces fibrosis?

A

Acute- pan lobular
Chronic- portal and periportal

No fibrosis in acute, fibrosis in chronic which can progress to cirrhosis.
Cytokine induces hepatic satellite cells which become myofibroblasts

46
Q

What is interface hepatitis?

A

Periportal hepatocyte injury with lymphoplasmacytic inflammation.

47
Q

What determines the grade and stage of chronic hepatitis?

What are the 4 stages?

A 
Grade: degree of interface hepatitis
Stage: degree of fibrosis 
1. Portal triads enlarged 
2. Septa but portal tracts not linked
3. Portal tracts linked
4. Cirrhosis
48
Q

What causes alcoholic liver disease?

A

Acetaldhyde causes hepatocyte damage, oxidative stress, impaired fat and CHO metabolism, genetic susceptibility

49
Q

ALD can cause steatosis, steatohepatitis then fibrosis. What are the histological characteristics of each?

A

Steatosis
- Accumulation of lipid in hepatocyte

Steatohepatitis

  • Steatosis
  • Hepatocyte damage–> inflammation
  • Mallory-Denk bodies
  • Hepatocyte ballooning degeneration
  • Neutrophils

Fibrosis

  • Chicken wire, surrounding the hepatocytes
  • Starts around central vein
50
Q

What are the main causes of non alcoholic fatty liver disease?
What is the main histological difference to ALD?
What are the two main pathways it can lead to?

How do they generally distinguish between is and ALD?

A

Metabolic syndrome and diabetes.
It doesn’t generally have severe steatohepatitis (v. unlikely to see M-D bodies)
Generally clinical distinction

Isolated fatty liver or NASH (non alcoholic steatohepatitis) which can lead to cirrhosis.

51
Q

What is the main difference in autoimmune hepatitis compared to normal hepatitis?

A

It has the same early destruction of liver cells but fibrosis develops really quickly opposed to normal hepatitis where it develops slowly

52
Q

What are the 5 steps in the new model of liver scarring?

A
  1. Early parenchymal extinction
  2. Veno-portal approximation
  3. Formation of fibrous septa
  4. Elongation of septa
  5. Resorptions of septa
53
Q

What are the two clinical definitions of portal hypertension?

A

Increase in pressure in portal vein of >8 mmHg

Difference in pressure between portal vein and hepatic vein of >5 mmHg

54
Q

What are the 4 main consequences of portal hypertension?

A
  1. Porto-systemic anastamoses
  2. Hepatic encephalopahy
  3. Congestive splenomegaly
  4. Ascites

Gastrointestinal tract (6 decks)

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