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Pathology > Lecture 3 Acute & chronic inflam > Flashcards

Lecture 3 Acute & chronic inflam Flashcards

1
Q

What does inflammation do?

A

Remove/contain cause. Initiate repair. Reinstate useful function. Stops when agent is eliminated

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2
Q

5 reasons for inflammation?

A

Foreign body, infection, ischaemia/infarction, physical/chemical injury, immune reactions

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3
Q

Define acute inflammation?

A

Rapid host response triggering vascular and cellular reaction

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4
Q

What induces vasodilation?

A

Histamine and nitric acid

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5
Q

Result of increased permeability?

A

Fluid leaking into extravascular tissues -> oedema

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6
Q

Define blood stasis?

A

Pooling the blood at inflammation site

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7
Q

What triggers endothelial cells of vessel wall to contract? (4)

A

Histamine, bradykinin, leukotriens, substance P.

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8
Q

Define immediate transient response

A

Endothelial cells of vessel wall triggered to contact-> ^ interendothelial spaces

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9
Q

What does endothelial injury lead to?

A

endothelial cell death -> vessel wall damaged -> immediate extravascular leakage

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10
Q

Define transcytosis

A

^ transport of fluids/proteins through cell channels.

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11
Q

Define VEGF

A

Vascular endothelial growth factor (new blood vessels)

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12
Q

Define transcytosis

A

through the cell in and out

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13
Q

Main aim of inflammation is to recruit…

A

leucocytes to area of damage

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14
Q

What do neutrophils and macrophages do?

A

Ingest and kill bacteria and necrotic cells AND promote repair

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15
Q

What are 5 steps of cellular reaction?

A

Margination. Rolling. Adhesion. Transmigration. Chemotaxis

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16
Q

Define margination

A

Red blood cells flow in centre, WBC flow peripherally. In stasis more WBC fall to peripheral flow

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17
Q

Define rolling

A

Increased amount of leucocytes roll along edge of damaged endothelium (mediated by selectins)

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18
Q

Define adhesion

A

Leucocytes stop and adhere to endothelium.

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19
Q

What encourages the adhesion of leucocytes?

A

Cytokines from injured cells

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20
Q

Define transmigration

A

Leucocyte encouraged to pass through endothelium to extravascular space.

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21
Q

What is PECAM-1?

A

Platelet endothelial cell adhesion molecule

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22
Q

Define chemotaxis

A

Exogenous (bacteria) and endogenous (cytokines/complement) substances attract leucocytes

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23
Q

When do neutrophils appear?

A

6-24 hours

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24
Q

When do monocytes appear?

A

24-48 hours

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25
Q

Are neutrophils or monocytes more common in circulating blood and respond to chemokines?

A

Neutrophils

26
Q

What do leucocytes do?

A

Recognise foreign microbes

27
Q

What receptors do leucocytes have?

A

Toll like, G-protein coupled receptors and, opsonin receptors and cytokine receptors

28
Q

What do toll like receptors do?

A

Attach to bacteria products

29
Q

What do G-protein coupled receptors recognise?

A

N-formymethionyl of bacteria & chemokine breakdown

30
Q

What do opsonin receptors recognise?

A

microbes that have been coated with proteins (antibodies/compliment) or opsonins. (opsonisation). Targets them for phagocytosis

31
Q

What do cytokine receptors do?

A

respond to cytokines.

32
Q

After substantial tissue destruction, X regeneration, what replaces damaged area?

A

Connective tissue

33
Q

Chronic inflammation is caused by?

A

Persistent infection (parasite), immune mediated, prolonged exposure to toxic agent (asbestos, lipids).

34
Q

With chronic inflammation what is normally seen?

A

Show infiltration of mononuclear cells (macrophages), Tissue destruction following prolonged inflam, signs of attempts at healing.

35
Q

Define granulomas

A

Cellular attempt to contain offending agent that it cannot remove. Macrophages &T-lymphocutes cause injury. (Tuberculosis.

36
Q

Damaged tissues release…

A

histamine that ^ blood flow to area

37
Q

What do histamines do?

A

cause capillaries to leak releasing phagocytes & clotting factors.

38
Q

What can cause acute inflam?

A

infarction, bacterial infection, trauma, burn

39
Q

What can cause chronic inflam?

A

virus, autoimmune

40
Q

What can acute inflam result in?

A

resolution, abscess, fibrosis

41
Q

What can chronic inflam result in?

A

Fibrosis

42
Q

Clinical cardinal signs of inflam

A

Redness (rubor), heat (calor), swelling (tumor), pain (dolor) and loss of function

43
Q

Signs and symptoms of inflam?

A

fever, tachy, hypotension, ^ WCC, ^CRP.

Weight loss, malaise, sepsis -> CV failure (septic shock)

44
Q

Numbers for CRP

A

> 10 means inflam. Not worried about 15 but will in 100’s

45
Q

Examples of exagerated or inappropriate inflam response?

A

Allergies, hypersensitivity & autoimmune diseases

46
Q

What can we do for inflam?

A

NSAIDs, antihistamines, steroids, targeted biologics (anti TNF)

47
Q

What happens if there is no inflam response?

A

^ chance of infection, delayed wound healing, tissue damage

48
Q

Acute appendicitis notes

A

10-30 years old. Pain localised to right iliac fossa. Worse on movement. N/V. Pyrexia. Tachy. ^WCC. ^CRP.

49
Q

Management of acute appendicitis?

A

Appendicectomy

50
Q

Complications of appendicitis?

A

Performation leading to peritonitis & abscess formation

51
Q

Septic arthritis notes

A

Red, hot, swollen joints, unable to move. Pyrexia, tachy, ^WCC, ^CRP.

52
Q

Risk factors for septic arthritis?

A

prosthetic joint, recent surgery/trauma. age. RA.

53
Q

Treatment of septic arthritis?

A

Joint aspirate. IV antibiotics. Sepsis 6.

54
Q

Minor injury inflam response

A

has no benefit. Rest prevents further injury.

55
Q

RA notes

A

Chronic autoimmune inflam. Warm, swollen, stiff and painful joints. Immune sees host as foreign -> healthy joint destroyed.

56
Q

Complications with RA.

A

Vessels can become involved- vasculitis -> circulatory problems

57
Q

Treatment of RA

A

Steroids, DMARDS, biologics

58
Q

Peptic ulcers notes

A

Acute inflam response (hpylori/excess acid). Necrotic inflamed mucose falls away. Does not repair.

59
Q

Complications of peptic ulcers

A

developing bleed/perforation

60
Q

Treatment of peptic ulcers

A

PPIs/ histamine receptor agonist/ antibiotics.

Pathology (25 decks)

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