Pathology Flashcards

1
Q

Which cells are involved in acute inflammation?

A
  • Neutrophils.

- Monocytes.

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2
Q

What are the microscopic features of acute inflammation?

A
  • Vasodilation.
  • Vascular leakage of protein rich fluid.
  • Neutrophil polymorphs migrate to the site.
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3
Q

What are the clinical (macroscopic) features of acute inflammation?

A
  • Rubor (redness)
  • Tumour (swelling)
  • Calor (hot).
  • Dolar (pain).
  • Loss of function.
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4
Q

What are the potential causes of acute inflammation?

A
  • Trauma.
  • Ischaemia.
  • Chemicals.
  • Microbial infection.
  • Hypersensitivity.
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5
Q

Which cells are involved in chronic inflammation?

A
  • Lymphocytes, macrophages and plasma cells.
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6
Q

What are the microscopic features of chronic inflammation?

A
  • Evidence of continuous destruction.

- Necrosis.

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7
Q

What are the clinical (macroscopic) features of chronic inflammation?

A
  • Chronic ulceration.
  • Chronic abscess cavity.
  • Granulomatous inflammation.
  • Fibrosis.
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8
Q

What are the potential causes of chronic inflammation?

A
  • Resistance of infective agent (e.g. TB)
  • Endogenous materials (e.g. necrotic tissue).
  • Exogenous materials (e.g. asbestos).
  • Autoimmune conditions (e.g. RA).
  • Primary granulomatous diseases (e.g. Crohn’s, sarcoidosis).
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9
Q

What is a granuloma?

A
  • An aggregation of epithelioid histiocytes.
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10
Q

What is fibrosis? Which cells are involved?

A
  • Excess deposition of ECM proteins.

- Carried out by myofibroblasts.

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11
Q

What is the process of scar tissue formation?

A
  • Fibroblasts secrete collagen.
  • The collagen cross-links and forms a pronounced alignment in a single direction.
  • New tissue appears differently and has inferior function.
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12
Q

What are the four overarching stages of atherosclerosis?

A

1) Endothelial damage.
2) Fatty streak formation.
3) Plaque growth.
4) Plaque rupture (thrombus).

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13
Q

What is the detailed process of atherosclerosis?

A

1) Endothelium of vessel damaged.
2) LDL accumulates in the arterial wall.
3) Macrophages migrate to site and take up lipids to become FOAM CELLS.
4) Fatty streak forms (containing dead foam cells).
5) Macrophages release inflammatory cytokines and GF.
6) Smooth muscle in vessel wall proliferates.
6) Fibrin forms a fibrous cap over the atheroma.
7) Plaque continues to grow.
8) Eventually, the plaque ruptures which triggers thrombosis.

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14
Q

What are the three features in Virchow’s triad?

A
  • Stasis of blood flow.
  • Endothelial injury.
  • Hypercoagulable state.
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15
Q

What is the difference between thrombosis and atherosclerosis?

A
  • Atherosclerosis - Deposition of fatty materials int he arterial wall.
  • Thrombosis - Coagulation/clotting of blood (platelet aggregation).
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16
Q

What is the process of thrombosis?

A

1) Endothelial injury.
2) Collagen exposed.
3) Platelets are activated and aggregate.
4) Clotting factors released/intrinsic pathway activated.
5) Fibrin meshwork forms and RBCs also become stuck in the atheroma.
6) Structure grows and protrudes further and further into the lumen of the vessel. This causes more turbulence of blood flow, and more platelet aggregation… (+ve feedback loop).

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17
Q

What are the 4 different fates of thrombosis?

A

1) Resolves - Body clears the thrombus/thrombus dissolves.
2) Organised - Becomes a scar.
3) Recanalisation - Intima proliferates and the thrombus becomes vascularised.
4) Embolus - Fragments of the thrombus break off into the circulation.

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18
Q

What is an embolus?

A
  • Mass of material in the circulation lodges in a vessel, occluding the lumen.
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19
Q

What is ischaemia?

A
  • Reduced blood flow to a tissue or body part caused by constriction or blockage of the vessels supplying it.
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20
Q

What is infarction?

A
  • Necrosis of a tissue or body part when blood supply is compromised.
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21
Q

Is ischaemia reversible or non-reversible?

A
  • Reversible.
22
Q

Is infarction reversible or non-reversible?

A
  • Non-reversible.
23
Q

What is apoptosis?

A
  • Controlled cell-death.
24
Q

What are the two pathways for apoptosis?

A
  • Extrinsic. Involves ligand binding (TNF/receptor binding)

- Intrinsic. Involves P53.

25
Q

What is necrosis?

A
  • Traumatic cell death.

- Triggers inflammation/repair.

26
Q

What is hypertrophy?

A
  • Increase in cell SIZE.
27
Q

What is hyperplasia?

A
  • Increase in cell NUMBER.
28
Q

What is atrophy?

A
  • Decrease in cell SIZE AND/OR NUMBER.
29
Q

What is metaplasia?

A

Conversion of one fully differentiated cell type into another fully differentiated cell type.

30
Q

What is a good example of metaplasia?

A

Barrett’s oesophagus.

Stratified squamous epithelium to simple columnar epithelium.

31
Q

What is dysplasia?

A

Morphological cell changes seen in the early stages of cancer formation.
Not yet cancer, but could become cancer.

32
Q

What is carcinogenesis?

A

Conversion of normal cells to neoplastic cells via genetic mutation.

33
Q

What is a neoplasm?

A
  • A genetically abnormal mass of cells.
34
Q

What is a tumour?

A
  • Any abnormal swelling.
35
Q

What are the features of benign/malignant tumours?

A

Benign:

  • Clearly differentiated border.
  • Low rate of cell division.
  • No basement membrane involvement.
  • Necrosis/ulceration is rare.

Malignant:

  • Poorly differentiated border.
  • High rate of cell division.
  • Basement membrane involvement.
  • Necrosis/ulceration common.
36
Q

What is a carcinogen?

A
  • An environmental agent that participates in causation of a tumour.
37
Q

What is a sarcoma?

A
  • Malignant cancer of connective tissue.
38
Q

What is a carcinoma?

A
  • Malignant cancer of epithelial cells.
39
Q

What is an adenocarcinoma?

A
  • Malignant cancer of glandular/secretory cells.
40
Q

What is an adenoma?

A
  • Benign cancer of glandular/secretory cells.
41
Q

What is metastasis?

A
  • Spread of malignant tumour cells from origin to form other tumours at different sites.
42
Q

What are the two methods of metastatic spread?

A
  • Lymphatic.

- Haematogenous.

43
Q

What are the different types of hypersensitivity and what do they involve?

A

Type 1 - Mediated by IgE
Type 2 - Mediated by IgG/IgM
Type 3 - Mediated by immune complexes (Antibodies).
Type 4 - Mediated by T cells (delayed reaction).

44
Q

What is the pneumonic for hypersensitivity?

A

“ACID”

Type 1 - Anaphylaxis.
Type 2 - Cytotoxic.
Type 3 - Immune complex (antigen/antibody).
Type 4 - Delayed.

45
Q

What are some examples of type 3 hypersensitivity?

A
  • Rheumatoid arthritis.

- SLE.

46
Q

What are some examples of type 1 hypersensitvity?

A
  • Allergic asthma.
  • Rhinitis.
  • Anaphylaxis.
47
Q

What are some examples of type 2 hypersensitivity?

A
  • Blood transfusion reactions.

- Organ transplant rejections.

48
Q

What is an example of type 4 hypersensitivity?

A
  • Contact dermatitis.
49
Q

What is innate immunity?

Which cells are involved?

A
  • Non specific immune response.
  • Immediate.
  • Neutrophils, macrophages, monocytes, eosinophils.
50
Q

What is adaptive immunity?

What cells are involved?

A
  • Specific immune response.
  • Delayed.
  • B lymphocytes, T lymphocytes, plasma cells.