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Pathology Flashcards

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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
Where is the most common site for steatosis to occur?
The liver
26
What can cause hepatic fatty deposits to form?
``` Alcohol Type II diabetes Metabolic syndrome Hyperlipidaemia Obesity ```
27
What is haemosiderosis?
Abnormal deposition of haemosiderin
28
What is haemosiderin?
An iron pigment
29
What two conditions mainly result in haemosiderosis?
inflammation and systemic iron overload
30
How can inflammation lead to haemosiderosis?
Leads to a large leakage of RBCs into tissue which are degraded by macrophages, the iron from the haemoglobin may form haemosiderin
31
What is haemochromatosis?
A genetic condition where large amounts of iron is absorbed from the intestine
32
How does excess systemic iron overload lead to haemosiderosis? What other impacts does this have?
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.
33
Avg. loss of iron from the human body daily?
1mg
34
Common causes of liver damage?
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
Effects of liver damage?
Liver failure Cholestasis Inflammation
36
Is acute liver injury likely to cause cirrhosis?
No, chronic will
37
What are stellate cells?
Liver cells that produce collagen and other matrix proteins, store Vit A and control vascular tone
38
What happens to blood flow in the liver during fibrosis? What does this cause?
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
How does cirrhosis form from damaged cells in the liver
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
Complications of liver cirrhosis?
Liver failure Portal hypertension Hepatocellular carcinoma
41
Consequences of portal hypertension?
Oesophageal and Rectal varices Caput medusae Ascites Splenomegaly Toxins bypass liver, can reach the brain
42
How do ascites form in liver failure? all factors
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
Symptoms of acute hepatitis?
Jaundice, pale stools Weight loss itching Fatigue
44
What are the five Hepatitis viruses?
A, B, C, D and E
45
What are the differences in acute and chronic hepatitis? Which Hep viruses cause which?
Diffuse inflammation of the liver - A,B,C and E Persistent, has lasted for more than 6 months - B, C and D
46
How is Hep A transmitted?
Faecal-oral route
47
How is Hep B transmitted?
Through contact with the blood
48
What hepatitis infection is self-limiting, and what percentages of cases do not resolve by themselves?
Hep B, 5-10% do not resolve
49
What Hep virus has lots of carriers?
Hep B
50
What is special about Hepatitis D?
Only associated with Hep b it is a delta agent (genome coated in hepatitis delta antigen)
51
How is Hep D transmitted?
Parenterally
52
Features of Hep C virus?
Has a variable incubation period 15-150 days 60-70% infected do not show symptoms 80% develop a chronic infection
53
Features of Hep E virus?
High mortality, 20% in pregnant women Associated with middle age men and swine in UK
54
Route of transmission of Hep E virus?
Faecal-oral route
55
What hepatitis viruses have vaccines?
A and B
56
Pancreatitis causes?
Ethanol Obstruction e.g. gallstone Infections, Trauma, Autoimmune Idiopathic
57
What happens in acute inflammation of the pancreas?
Activation of digestive enzymes Damage to cells Cell death
58
Acute and chronic complication of pancreatitis?
Acute: - SIRS - multiorgan failure - Necrotizing pancreatitis Chronic: - Destruction of pancreas (steatorrhoea) - Diabetes - Pancreatic pseudocyst
59
Whats more common ulcerative colitis or Crohns disease?
Ulcerative colitis
60
Clinical features of IBD?
Chronic and relapsing conditions Diarrhoea, change in bowel habit/melaena Abdominal pain Fever
61
Where does ulcerative colitis affect?
Limited to the colon More severe in the distal colon
62
Macroscopic features of ulcerative colitis?
Superficial mucosal ulceration Normal serosa Inflammation evenly distributed
63
Where does Crohns disease normally affect?
Can involve entire GI tract Classically the terminal ileum
64
Macroscopic features of Crohns?
Deep ulceration Bowel wall thickening and strictures abnormal serosa (fat wrapping)
65
Microscopic features of UC?
Distortion of glands
66
Microscopic features of Crohns disease?
Transmural inflammation Fissuring ulceration Neuronal hyperplasia Granulomas
67
Differential diagnoses for IBD?
Infective colitis Diverticular disease Ischaemic colitis Pouchitis TB
68
Ulcerative colitis complications?
Toxic megacolon Dysplasia Malignancy
69
Crohn's disease complications?
Fistula formation Abscess formation Bowel obstruction Malignancy
70
Aetiology of IBD
Mostly unknown Infective agents e.g. mycobacteria, rotavirus, chlamydia Genetic influences Cigarette smoking: increases CD risk, decreased UC risk
71
IBD therapies?
Infliximab - TNF alpha antibody
72
Genetics of Crohns disease?
Quite a strong genetic link NOD2 gene - recognises gram positive bacterial cell wall IL23R gene
73
What cytokine is particularly increased in crohns disease?
TNF
74
How does blocking TNF-a work in crohns disease?
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
Whats a T-reg cell?
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
What colour is collagen in an H&E stain?
Pink
77
How are tissues processed to produce slides?
Either: 1. Embedded with paraffin wax 2. Frozen And then encapsulated in paraffin wax and cut
78
What type of lymphocyte dominates germinal centres in lymph nodes?
B cells
79
Common presentations of colorectal cancer?
Change in bowel habit Anaemia Bleeding Obstruction
80
3 main ways colorectal carcinoma spreads?
Lymphatic vessels Blood vessels (haematogenous spread) Trans-coelomic
81
What is dukes staging and the four stages?
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

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