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Cell Pathology > Cell Pathology Case studies > Flashcards

Cell Pathology Case studies Flashcards

1
Q

What are the effects of Helicobacter on the stomach

A 
Inflammation: 
acute, chronic (including ulcers)
Cell  damage: 
atrophy, metaplasia, dysplasia 
Neoplasia: 
carcinoma, lymphoma
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2
Q

What are the causes of gastritis

A 
Oxygen deprivation
Chemical agents  = drugs- common
Infectious agents  = helicobacter- common
Immunological reactions = autoimmune- common
Genetic defects
Nutritional imbalances
Physical agents
Aging
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3
Q

Describe the appearance of H.Pylori

A

Spirally, looks like a seagull

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4
Q

Describe the range of pathologies of H.Pylori

A

can produce range of pathological processes (or none at all in 80% cases) e.g. Gastritis (inflammation) in 15-20%, and cancer in 1%. May be asymptomatic, cause ulceration. Its pathology has been studied and worked out.

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5
Q

How will acute gastritis appear down an endoscope

A

Red- rubor
Swollen- tumor- oedema
It also may be painful for the patient- dolor

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6
Q

Describe the histology of acute gastritis

A

The key inflammatory cell of acute inflammation is the

neutrophil polypmorph

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7
Q

What is meant by an abscess

A

A large mass of dead and dying neutrophils.

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8
Q

What may be another feature of acute gastritis

A

Acute peptic ulcer formation
If the inflammation is severe enough it will destroy the mucosae- forming an ulcer. Can breach peritoneal cavity- acid can leak into peritoneum- dangerous.

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9
Q

Define an ulcer

A

“An open sore on an external or internal surface of the body, caused by a break in the skin or mucous membrane which fails to heal.
Ulcers range from small, painful sores in the mouth to bedsores and serious lesions of the stomach or intestine.”

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10
Q

Describe how chronic gastritis appears down an endoscope

A

Loss of rugi due to atrophy- pathological.

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11
Q

Describe the histology of chronic gastritis

A

The key inflammatory cell of chronic inflammation is the
lymphocyte
Formation of lymphoid follicles with germinal centres, the inflammation induces abnormal MALTs in the stomach (not normally present)- why there is an increased risk of lymphoma.

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12
Q

What is granulomatous gastritis

A

A sub-set of chronic inflammation

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13
Q

Describe the histology of granulomatous gastritis

A

Pale areas- indicating presence of activated macrophages

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14
Q

Describe granulomatous inflammation

A

Granuloma= collection of activated macrophages (secreting cytokines not doing phagocytosis).
Particular form of chronic inflammation showing granuloma formation
Cluster of macrophages
Involves specific immune reaction T cells.
Type 4 hypersensitivity.

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15
Q

What are the causes of granulomatous inflammation

A

Infection – TB, fungi, helicobacter
Foreign material- glass or metal
Reaction to tumours- good-shows that they have elicited an immune response
Immune diseases (sarcoid, Crohn’s)

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16
Q

Describe the differences between acute and chronic ulcer formation

A

Pattern of inflammation
Acute- will heal normally
Chronic- fibrosis- scar tissue formation- replaces specialised cells- repair but not regeneration.

17
Q

Describe acute ulcer healing

A

Parenchymal cell regeneration and RESOLUTION

= acute gastric ulcer

18
Q

Describe chronic ulcer healing

A

REPAIR by connective tissue and SCAR TISSUE FORMATION

= chronic gastric ulcer

19
Q

What is the aim of plastic surgery

A

To reduce scarring

20
Q

Describe the atrophy associated with helicobacter gastritis

A

mucosa decreases in thickness; specialised cells are lost (hence reduced function)

21
Q

Describe the metaplasia associated with helicobacter gastritis

A

goblet cells (mucous secreting cells) are not normally present (found in intestines) - but gastric mucosa has changed to small intestinal mucosa due to metaplasia

22
Q

Describe the dysplasia associated with helicobacter gastritis

A

Adenocarcinoma- may contain glands producing mucous

Lymphoma- lymphocytes attack crypts.

23
Q

Despite their names, which tumours are malignant

A

Melanomas and lymphomas

24
Q

Distinguish between grading and staging

A

Grading:
based on the degree of histological differentiation
Staging
based on how far the tumour has spread

Staging- essential for prognosis

25
Q

Describe the staging of cancers

A 
Combination of clinical, radiological and pathological findings
Main staging system = “TNM” 
Size  and spread of the primary Tumour 
Spread to regional Lymph Nodes
Presence of Metastases
26
Q

What is atherosclerosis essentially a disease of

A

the intima

27
Q

What do we look at when analysing atheromas

A

How much of the artery is occluded:
60% open- Asymptomatic stable plaque.
20% open- Symptomatic stable plaque causing inducible ischaemia OR Unstable plaque with risk of rupture and acute ischaemic events.

28
Q

What are the common sites of clinically important atheromas

A

Coronary arteries
Carotid arteries
Aorta and / or iliac arteries

29
Q

What is a consequence of plaques becoming ulcerated

A

thrombosis on top off the plaque- can break off.

30
Q

Describe the different types of atherosclerotic plaques

A

Stable atherosclerotic plaques: stable angina, dementia, chronic lower limb ischaemia
Thrombosis overlying an unstable atherosclerotic plaque: unstable angina, myocardial infarction, cerebral infarction, acute lower limb ischaemia
Weakening of arterial wall leading to aneurysm formation

31
Q

Describe myocardial scarring

A

Appears white- scarring- atrophy and death of myocytes- replaced by collagen- lower metabolic requirement-

32
Q

What can myocardial scarring lead to

A

Chronic heart failure

results from loss of muscle cells as needed to pump

33
Q

Describe infarction

A

ischaemic death of tissue leads to acute cardiac failure, due to arrhythmias. Not replaced by scar tissue

34
Q

What are the consequences of MI

A

Acute cardiac failure

Sudden death

35
Q

What is meant by an aneurysm

A

An abnormal blood-filled bulge of a blood vessel and especially an artery resulting from weakening of the vessel wall.

36
Q

What are the consequences of a coronary artery aneurysm

A

Rupture

Thrombosis- damaged endothelium- turbulent flow- 2/3 requirements for thrombosis.

37
Q

Describe haemopericardium

A

Blood leaked into pericardium- due to rupture of coronary artery from MI

38
Q

In death certificates- what should be put in category 2

A

Things relating to the death, but not the proximate cause- usually a chronic condition e.g hypertension, diabetes.

39
Q

Why can plaques lead to aneurysms

A

Inner part of blood vessel thicker (due to plaque)- less diffusion of oxygen to smooth muscle, smooth muscle atrophy- becomes thinner- more prone to rupture- law of Laplace.

Cell Pathology (6 decks)

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