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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
Q

what are possible consequences of chronic inflammation?

A
  1. scarring
  2. tissue destruction
  3. development of cancer
  4. diversion of nutrients
  5. amyloidosis
26
Q

what is granulomatous inflammation?

A

A specific type of chronic inflammation. A granuloma is an aggregate of activated macrophages

27
Q

what are possible causes of granulomatous inflammation?

A

infections
sarcoidosis
crohns disease

28
Q

what is the flow chart for inflammation in TB?

A

After a few weeks T cell immunity is established –> macrophages activate CD4 via MHC II –> Th1 T cells produce interferon g

29
Q

in TB Th1 helper cells produce interferon g, what is the effcet of this?

A

it’s a powerful activator of macrophages promoting increased levels of intracellular killing

30
Q

in TB what do the activated macrophages do?

A

Form granulomas by aggregating around the mycobacteria

31
Q

who is at risk of active TB?

A 
immunocomprimised patients
HIV (infects CD4)
people living in places with high rates
elderly
alcoholics
D.M
32
Q

what happens if in TB instead of a Th1 response there is a th2 response?

A

the wrong immune cells are recruited meaning the organism can survive and it may become active

33
Q

what are features of active pulmonary TB?

A 
feeling unwell for weeks/months
persistant cough
fever
night sweats
loss of appetite
34
Q

what is the definition of active tuberculosis disease?

A

Infection with M/tuberculosis where mycobacteria are growing and causing symptoms and signs of disease

35
Q

what is latent infection?

A

infection with m.tuberculosis where mycobacteria are alive but not currently causing active disease

36
Q

what are the lab features of active pulmonary TB?

A
  • staining ith ziehl neelson stain

- cultures take 3-6 weeks to grow due to the slow growing nature of the organism.

37
Q

what are the most common sites of involvement for extra pulmonary TB?

A

kidneys and lymph nodes

38
Q

what are the important steps to take once TB has been diagnosed?

A

quadriple therapy with rifampicin, isoniazid, pyrazinamide, ethambutol
a notifiable disease
contact tracing

39
Q

what is atherosclerosis?

A

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
Q

what are modifiable risk factors for the development of atherosclerosis?

A

Smoking, hypertension, diabetes mellitus, dyslipidaemia.

41
Q

what do damaged endothelial cells become dysfunctional?

A

Increased permeability

adhesion molecules and cytokines and produced

42
Q

what does vascular cell adhesion molecule 1 bind?

A

monocytes and T cells

43
Q

in atherosclerosis what are the effects of macrophages?

A

produce free radicals leading to oxidised LDL production

Formation of foam cells

44
Q

How do macrophages form foam cells in atherosclerosis?

A

they engulf oxidised LDL and cholesterol.

45
Q

what do foam cells produce?

A

growth factors

46
Q

what are non-modifiable risk factors for atherosclerosis?

A

family history

Male gender

47
Q

in atherosclerosis what is a fatty streak?

A

Collections of lipid full macrophages sit in the intimal layer and become visible.

48
Q

what is an atherosclerotic plaque?

A

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
Q

what three hallmarks of a chronic inflammatory process does atherosclerosis show?

A
  • persistant injury
  • on going inflammation
  • repair with scarring

T IoD cellular pathology (10 decks)

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