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Pathology Flashcards

1
Q

What is infection from animal to human called?

A

Zoonosis

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2
Q

What is the definition of an ulcer?

A

Full thickness loss of an epithelial surface

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3
Q

What is the definition of an erosion?

A

A shallow ulcer (some loss of an epithelial surface)

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4
Q

What enzyme test is used to test for H. Pylori?

A

Urease test

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5
Q

Why does H. Pylori contain a lot of urease?

A

So it can surround itself with ammonia (from the breakdown of urea) and raise the pH around it.

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6
Q

Complications of a duodenal ulcer, and their causes?

A

Perforation - extension of ulcer to peritoneal surface

Massive GI haemorrhage - Rupture of large vessel at ulcer base

Anaemia - Chronic blood loss from surface of ulcer causing iron deficiency

Gastric outlet obstruction - fibrosis around the ulcer causing scarring

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7
Q

Two types of cancer that an H.Pylori infection can lead to?

A

Adenocarcinoma

Lymphoma

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8
Q

Process of duodenal ulcer formation?

A

Gastric H. Pylori infection

Antral gastritis

More acid secretion

Increased duodenal acid load

Gastric metaplasia in duodenal bulb, leads to Infection

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9
Q

4 virulence factors of H. Pylori?

A

Urease

LPS

IL-8

Vacuolating cytotoxin

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10
Q

What are the two strains of H.Pylori which is worse?

A

Cag A+ and Cag A-

A+ is worse

A- is mostly asymptomatic

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11
Q

What are the two things that a Cag A+ strain does that lead to a duodenal ulcer?

A

Active duodenitis and bicarbonate suppressed

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12
Q

Treatment options for Barrett’s oesophagus?

A

Oesophagectomy

Photodynamic therapy

Laser ablation

Endoscopic mucosectomy

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13
Q

What is an inlet pouch?

A

Ectopic bit of gastric mucosa that rarely leads to carcinoma, it is congenital

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14
Q

Peptic ulcer risk factors?

A 
H.Pylori infection
Low Socio-economic status
NSAIDS
Heavy drinking
Smoking
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15
Q

Complex and simple tests to diagnose H.Pylori?

A

Complex: endoscopy/culture/histology/urease test

Simple: Breath test/serology

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16
Q

Functional dyspepsia is what?

A

Dyspepsia with no evidence of structural disease at endoscopy in last 3 months

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17
Q

Dyspepsia alarm signals?

A

Weight loss

Persistent vomiting

Progressive dysphagia

Anaemia/GI bleed

Palpable mass

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18
Q

What is a hiatus hernia?

A

A hernia of the fundus of stomach pushed through the diaphragm

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19
Q

What is carnetts test and what does a positive and negative result suggest?

A

Patient lies flat and legs are lifted and then head is lifted

Positive if the pain increases or stays the same after legs are lifted

Negative if head is lifted and pain goes

Positive means likely in abdominal wall

Negative means intraabdominal

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20
Q

When should you endoscope a pt who comes in with dyspepsia?

A

True dypepsia with alarm symptoms

> 55yrs

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21
Q

Treatment for true dyspepsia?

A

Simple antacids/lifestyle changes/review medications

Full dose PPI for a month

Test and treat for H.Pylori

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22
Q

Signs of large gastric bleed?

A

Dizziness

Postural hypotension

Hypovolaemia

Weak pulse

HR >100

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23
Q

Where is calcium most likely to be deposited pathologically?

A

In necrotic tissue

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24
Q

What is steatosis?

A

abnormal deposition of lipid within cells

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25
Q

Where is the most common site for steatosis to occur?

A

The liver

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26
Q

What can cause hepatic fatty deposits to form?

A 
Alcohol
Type II diabetes
Metabolic syndrome
Hyperlipidaemia
Obesity
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27
Q

What is haemosiderosis?

A

Abnormal deposition of haemosiderin

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28
Q

What is haemosiderin?

A

An iron pigment

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29
Q

What two conditions mainly result in haemosiderosis?

A

inflammation and systemic iron overload

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30
Q

How can inflammation lead to haemosiderosis?

A

Leads to a large leakage of RBCs into tissue which are degraded by macrophages, the iron from the haemoglobin may form haemosiderin

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31
Q

What is haemochromatosis?

A

A genetic condition where large amounts of iron is absorbed from the intestine

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32
Q

How does excess systemic iron overload lead to haemosiderosis?

What other impacts does this have?

A

Excess iron is deposited in tissues and forms haemosiderin

Excess iron can cause damage to cells it is deposited in, and large amounts are deposited in the liver and pancrease leading to liver disease and diabetes respectively.

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33
Q

Avg. loss of iron from the human body daily?

A

1mg

34
Q

Common causes of liver damage?

A

Ingested substances e.g. ethanol, many prescribed drugs

Congenital accumulation of substances e.g. Iron, Copper, Alpha-1-antitrypsin

Immune mediated e.g. autoimmune

Infectious e.g. Hepatitis, EBV, CMV, bacteria e.t.c.

35
Q

Effects of liver damage?

A

Liver failure

Cholestasis

Inflammation

36
Q

Is acute liver injury likely to cause cirrhosis?

A

No, chronic will

37
Q

What are stellate cells?

A

Liver cells that produce collagen and other matrix proteins, store Vit A and control vascular tone

38
Q

What happens to blood flow in the liver during fibrosis?

What does this cause?

A

Thrombosis in sinusoids and small blood vessels

Capillarisation of sinusoids (loss of fenestrations and collagen in space of Disse)

Causes poor blood-hepatocyte change and increased vascular resistance

39
Q

How does cirrhosis form from damaged cells in the liver

A

Nodules of regenerating hepatocytes form as hepatocytes divide to replace damaged cells. these are surrounded by bands of fibrous tissue and this is cirrhosis

40
Q

Complications of liver cirrhosis?

A

Liver failure

Portal hypertension

Hepatocellular carcinoma

41
Q

Consequences of portal hypertension?

A

Oesophageal and Rectal varices

Caput medusae

Ascites

Splenomegaly

Toxins bypass liver, can reach the brain

42
Q

How do ascites form in liver failure? all factors

A

Portal hypertension increases the hydrostatic pressure

Liver failure leads to less proteins produced and reduces the oncotic pressure

Both Lead to exudate in peritoneal cavity

The reduced plasma volume can then lead to activation of the RAAS pathway and retention of salt and water leading to further development of ascites

43
Q

Symptoms of acute hepatitis?

A

Jaundice, pale stools

Weight loss

itching

Fatigue

44
Q

What are the five Hepatitis viruses?

A

A, B, C, D and E

45
Q

What are the differences in acute and chronic hepatitis? Which Hep viruses cause which?

A

Diffuse inflammation of the liver - A,B,C and E

Persistent, has lasted for more than 6 months - B, C and D

46
Q

How is Hep A transmitted?

A

Faecal-oral route

47
Q

How is Hep B transmitted?

A

Through contact with the blood

48
Q

What hepatitis infection is self-limiting, and what percentages of cases do not resolve by themselves?

A

Hep B, 5-10% do not resolve

49
Q

What Hep virus has lots of carriers?

A

Hep B

50
Q

What is special about Hepatitis D?

A

Only associated with Hep b it is a delta agent (genome coated in hepatitis delta antigen)

51
Q

How is Hep D transmitted?

A

Parenterally

52
Q

Features of Hep C virus?

A

Has a variable incubation period 15-150 days

60-70% infected do not show symptoms

80% develop a chronic infection

53
Q

Features of Hep E virus?

A

High mortality, 20% in pregnant women

Associated with middle age men and swine in UK

54
Q

Route of transmission of Hep E virus?

A

Faecal-oral route

55
Q

What hepatitis viruses have vaccines?

A

A and B

56
Q

Pancreatitis causes?

A

Ethanol

Obstruction e.g. gallstone

Infections, Trauma, Autoimmune

Idiopathic

57
Q

What happens in acute inflammation of the pancreas?

A

Activation of digestive enzymes

Damage to cells

Cell death

58
Q

Acute and chronic complication of pancreatitis?

A

Acute:

  • SIRS - multiorgan failure
  • Necrotizing pancreatitis

Chronic:

  • Destruction of pancreas (steatorrhoea)
  • Diabetes
  • Pancreatic pseudocyst
59
Q

Whats more common ulcerative colitis or Crohns disease?

A

Ulcerative colitis

60
Q

Clinical features of IBD?

A

Chronic and relapsing conditions

Diarrhoea, change in bowel habit/melaena

Abdominal pain

Fever

61
Q

Where does ulcerative colitis affect?

A

Limited to the colon

More severe in the distal colon

62
Q

Macroscopic features of ulcerative colitis?

A

Superficial mucosal ulceration

Normal serosa

Inflammation evenly distributed

63
Q

Where does Crohns disease normally affect?

A

Can involve entire GI tract

Classically the terminal ileum

64
Q

Macroscopic features of Crohns?

A

Deep ulceration

Bowel wall thickening and strictures

abnormal serosa (fat wrapping)

65
Q

Microscopic features of UC?

A

Distortion of glands

66
Q

Microscopic features of Crohns disease?

A

Transmural inflammation

Fissuring ulceration

Neuronal hyperplasia

Granulomas

67
Q

Differential diagnoses for IBD?

A

Infective colitis

Diverticular disease

Ischaemic colitis

Pouchitis

TB

68
Q

Ulcerative colitis complications?

A

Toxic megacolon

Dysplasia

Malignancy

69
Q

Crohn’s disease complications?

A

Fistula formation

Abscess formation

Bowel obstruction

Malignancy

70
Q

Aetiology of IBD

A

Mostly unknown

Infective agents e.g. mycobacteria, rotavirus, chlamydia

Genetic influences

Cigarette smoking: increases CD risk, decreased UC risk

71
Q

IBD therapies?

A

Infliximab - TNF alpha antibody

72
Q

Genetics of Crohns disease?

A

Quite a strong genetic link

NOD2 gene - recognises gram positive bacterial cell wall

IL23R gene

73
Q

What cytokine is particularly increased in crohns disease?

A

TNF

74
Q

How does blocking TNF-a work in crohns disease?

A

Inhibitor binds to TNF-a Preventing it from activating it’s receptors

Foxp3 expression is upregulated

This down-regulates inflammatory reactions associated with autoimmune diseases

75
Q

Whats a T-reg cell?

A

A T cell that has been activated by a dendritic cell in a peyers patch, to produce an anti-inflammatory response to some antigens by secreting IL-10

76
Q

What colour is collagen in an H&E stain?

A

Pink

77
Q

How are tissues processed to produce slides?

A

Either:

  1. Embedded with paraffin wax
  2. Frozen

And then encapsulated in paraffin wax and cut

78
Q

What type of lymphocyte dominates germinal centres in lymph nodes?

A

B cells

79
Q

Common presentations of colorectal cancer?

A

Change in bowel habit
Anaemia
Bleeding
Obstruction

80
Q

3 main ways colorectal carcinoma spreads?

A

Lymphatic vessels

Blood vessels (haematogenous spread)

Trans-coelomic

81
Q

What is dukes staging and the four stages?

A

A B C and D, corresponds to TNM I to IV

A: Limited to wall, nodes clear
B: penetrated wall, nodes clear
C: nodes positive
D: distant metastases

GI (11 decks)

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