Cell death and inflammation Flashcards

(22 cards)

1
Q

Describe the nuclear changes seen in necrosis?

A

Pyknosis - DNA condenses
Karyorrhexis - Nuclear membrane ruptures and contents fragment
Karyolysis - Enzymes break down nuclear material

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the microscopic appearance of coagulative necrosis?

A

The genetic material is broken down but the tissue retains much of its cellular structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the causes of coagulative necrosis?

A

Ischaemia and haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a possible complication of coagulative necrosis?

A

Gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe gangrene

A

Bacteria invade the necrotic tissue and degrade via proteolysis. The tissue becomes black/green due to haemoglobin breakdown and smells foul.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the appearance of colliquative necrosis

A

Tissue appears as a liquid mass of dead cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the causes of colliquative necrosis?

A
  • Cerebral infarction

- Infection from pyogenic bacteria (abscess)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the appearance of caseous necrosis

A

Tissue resembles cream cheese - structure unrecognisable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What condition is caseous necrosis typically seen?

A

Tuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is amyloidosis?

A

When insoluble beta-sheets of proitein accumulate and aggregate within a tissue causing damage and impaired function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the pathophysiology of AL amyloidosis?

A

Primary amyloidosis

  • Mutations cause accumulation of immunuglobin light chains
  • e.g. multiple myeloma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the pathophysiology of AA amyloidosis?

A

Secondary amyloidosis

  • Caused by chronic inflammation
  • Aggregation of amyloid pre-cursor protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is dystrophic calcification?

A
  • Calcification of necrotic or fibrotic tissue
  • Otherwise normal calcium metabolism

e.g. atheroma of arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is metastatic calcification>

A

Calcification of normal healthy tissue due to increased calcium levels and impaired metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the production and role of histamine in the inflammatory response?

A

Produced by mast cells

  • Causes vasodilation
  • increases vascular permeability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the production and function of inflammaatory cytokines?

A

Mast cells and macrophages

  • Causes vascular endothelium to express adhesion molecules
  • Systemically causes a fever
17
Q

How do leukocytes reach the affected area in acute inflammation?

A
  • Adhere to the vascular wall via adhesion molecules (caused by inflammatory cytokines)
  • Migrate through vascular wall which is permeable due to histamine
18
Q

Summarise the process of phagocytosis

A
  • Leukocyte recognise and bind the foreign agent via receptors.
  • Agent engulfed
  • Degraded via free radicals produced by lysosome enzymes
19
Q

Describe the histopathological appearance of a granuloma/granulomatous inflammation

A

Activation and fusion of macrophages to form multinucleate giant cells

  • Strong T-lymphocyte activation and presence
  • May be central necrosis
20
Q

What conditions can cause granulomatous inflammation?

A

Tuberculosis, sarcoidosis

21
Q

What is the pathophysiology of Rheumatoid Arthritis?

A
  • Chronic inflammation of the synovium between joints
22
Q

What is the pathophysiology of atherosclerosis

A
  • Repeated injury to the vascular endothelium due to smoking/hypertension
  • Recruited macrophages become mast cells due to accumulation of lipoproteins
  • Plaque formation