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T IoD cellular pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are the two types of inflammation?

A

Acute

Chronic

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2
Q

What are the two major events in acute inflammation?

A

Vascular Changes

Neutrophil leukocytosis and accumulation in the area of damage

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3
Q

what vascular changes occur in acute inflammation?

A

Dilatation of the blood flow allowing increased flow to the injury site.
Endothelial activation increases capillary permeation
Activation of the coagulation cascade to form fibrin

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4
Q

what happens in the neutrophils leukocytosis and accumulation stage of acute inflammation?

A

increased neutrophil production

endothelial activation leading to upregulation of adhesion moeclules so neutrophils can migrate to the area of damage

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5
Q

what does acute inflammatory exudate consist of?

A

fluid, fibrin and neutrophils

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6
Q

what are the five local effects of acute inflammation?

A

1, warmth

  1. redness
  2. swelling
  3. pain (due to inflammatory mediators activating pain endings)
  4. loss of function
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7
Q

What causes the systemic effects of acute inflammation?

A

1IL 1, IL6, TNF-a

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8
Q

what are the systemic effects of acute inflammation?

A

fever
increased acute phase proteins from the liver
hormone production of ADH, cortisol and adrenaline leading to weakness and appetite loss

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9
Q

what is CRP produced in response to?

A

IL 6 which is secreted by macrophages

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10
Q

CRP is an opsonin, what does this mean?

A

It can coat a particle so it becomes a target for phagocytosis, CRP binds to bacterial cell walls

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11
Q

what is a raised CRP a risk factor for?

A

atherosclerosis

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12
Q

what are the three possible outcomes of acute inflammation?

A

1, regeneration
2. repair
3, chronic inflammation

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13
Q

what is the best outcome of acute inflammation?

A

Regeneration which is resolution

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14
Q

what is the repair outcome of acute inflammation?

A

fibrous scar formation.

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15
Q

what are the two steps to repair after acute inflammation?

A

organisation

scar formation

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16
Q

what happens in the ‘organisation’ stage of repair after acute inflammation?

A

replacement of inflammatory exudate by granulation tissue. macrophages phagocytose debris

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17
Q

what happens in the scar formation stage of repair after acute inflammation?

A

granulation tissue is replaced by a scar which is laid down by fibroblasts. a scar is mainly fibrous tissue.

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18
Q

what is an abscess?

A

a localised collection of pus in a newly formed cavity in a tissue.

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19
Q

what are the clearly defined zones of an abscess?

A
  1. the cavity
    2, a layer of neutrophils and fibrin
  2. a wall
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20
Q

what is in the abscess cavity?

A

Pus which is liquified tissue with dead and dying neutrophils, fibrin and oedema fluid.

21
Q

what are the two zones of an abscess wall?

A

an inner layer of granulation tissue containing new capillaries
an outer layer of fibroblastic tissue laying down scar tissue.

22
Q

what is an empyema?

A

an accumulaiton of pus in a pre-existing cavity (an abscess is in a newly formed cavity)

23
Q

what three processes occur in chronic inflammation?

A

persistant tissue injury and destruction
an ongoing inflammatory response
healing by fibrosis

24
Q

what are the main inflammatory cells in chronic inflammation?

A

macropahges, lymphocytes and plasma cells

25
what are possible consequences of chronic inflammation?
1. scarring 2. tissue destruction 3. development of cancer 4. diversion of nutrients 5. amyloidosis
26
what is granulomatous inflammation?
A specific type of chronic inflammation. A granuloma is an aggregate of activated macrophages
27
what are possible causes of granulomatous inflammation?
infections sarcoidosis crohns disease
28
what is the flow chart for inflammation in TB?
After a few weeks T cell immunity is established --> macrophages activate CD4 via MHC II --> Th1 T cells produce interferon g
29
in TB Th1 helper cells produce interferon g, what is the effcet of this?
it's a powerful activator of macrophages promoting increased levels of intracellular killing
30
in TB what do the activated macrophages do?
Form granulomas by aggregating around the mycobacteria
31
who is at risk of active TB?
``` immunocomprimised patients HIV (infects CD4) people living in places with high rates elderly alcoholics D.M ```
32
what happens if in TB instead of a Th1 response there is a th2 response?
the wrong immune cells are recruited meaning the organism can survive and it may become active
33
what are features of active pulmonary TB?
``` feeling unwell for weeks/months persistant cough fever night sweats loss of appetite ```
34
what is the definition of active tuberculosis disease?
Infection with M/tuberculosis where mycobacteria are growing and causing symptoms and signs of disease
35
what is latent infection?
infection with m.tuberculosis where mycobacteria are alive but not currently causing active disease
36
what are the lab features of active pulmonary TB?
- staining ith ziehl neelson stain | - cultures take 3-6 weeks to grow due to the slow growing nature of the organism.
37
what are the most common sites of involvement for extra pulmonary TB?
kidneys and lymph nodes
38
what are the important steps to take once TB has been diagnosed?
quadriple therapy with rifampicin, isoniazid, pyrazinamide, ethambutol a notifiable disease contact tracing
39
what is atherosclerosis?
A chronic inflammatory process affecting the intima of the arteries. it is characterised by the formation of lipid rich plaques in the vessel wall
40
what are modifiable risk factors for the development of atherosclerosis?
Smoking, hypertension, diabetes mellitus, dyslipidaemia.
41
what do damaged endothelial cells become dysfunctional?
Increased permeability | adhesion molecules and cytokines and produced
42
what does vascular cell adhesion molecule 1 bind?
monocytes and T cells
43
in atherosclerosis what are the effects of macrophages?
produce free radicals leading to oxidised LDL production | Formation of foam cells
44
How do macrophages form foam cells in atherosclerosis?
they engulf oxidised LDL and cholesterol.
45
what do foam cells produce?
growth factors
46
what are non-modifiable risk factors for atherosclerosis?
family history | Male gender
47
in atherosclerosis what is a fatty streak?
Collections of lipid full macrophages sit in the intimal layer and become visible.
48
what is an atherosclerotic plaque?
A core of lipid debris forms when the foamy macrophage die and the lipid in them is released. a fibrous cap is formed due to smooth muscle cells secreting collagen.
49
what three hallmarks of a chronic inflammatory process does atherosclerosis show?
- persistant injury - on going inflammation - repair with scarring

T IoD cellular pathology (10 decks)

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