Lecture 3 Acute & chronic inflam Flashcards Preview

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Flashcards in Lecture 3 Acute & chronic inflam Deck (60):
1

What does inflammation do?

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

2

5 reasons for inflammation?

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

3

Define acute inflammation?

Rapid host response triggering vascular and cellular reaction

4

What induces vasodilation?

Histamine and nitric acid

5

Result of increased permeability?

Fluid leaking into extravascular tissues -> oedema

6

Define blood stasis?

Pooling the blood at inflammation site

7

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

Histamine, bradykinin, leukotriens, substance P.

8

Define immediate transient response

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

9

What does endothelial injury lead to?

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

10

Define transcytosis

^ transport of fluids/proteins through cell channels.

11

Define VEGF

Vascular endothelial growth factor (new blood vessels)

12

Define transcytosis

through the cell in and out

13

Main aim of inflammation is to recruit...

leucocytes to area of damage

14

What do neutrophils and macrophages do?

Ingest and kill bacteria and necrotic cells AND promote repair

15

What are 5 steps of cellular reaction?

Margination. Rolling. Adhesion. Transmigration. Chemotaxis

16

Define margination

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

17

Define rolling

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

18

Define adhesion

Leucocytes stop and adhere to endothelium.

19

What encourages the adhesion of leucocytes?

Cytokines from injured cells

20

Define transmigration

Leucocyte encouraged to pass through endothelium to extravascular space.

21

What is PECAM-1?

Platelet endothelial cell adhesion molecule

22

Define chemotaxis

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

23

When do neutrophils appear?

6-24 hours

24

When do monocytes appear?

24-48 hours

25

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

Neutrophils

26

What do leucocytes do?

Recognise foreign microbes

27

What receptors do leucocytes have?

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

28

What do toll like receptors do?

Attach to bacteria products

29

What do G-protein coupled receptors recognise?

N-formymethionyl of bacteria & chemokine breakdown

30

What do opsonin receptors recognise?

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

31

What do cytokine receptors do?

respond to cytokines.

32

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

Connective tissue

33

Chronic inflammation is caused by?

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

34

With chronic inflammation what is normally seen?

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

35

Define granulomas

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

36

Damaged tissues release...

histamine that ^ blood flow to area

37

What do histamines do?

cause capillaries to leak releasing phagocytes & clotting factors.

38

What can cause acute inflam?

infarction, bacterial infection, trauma, burn

39

What can cause chronic inflam?

virus, autoimmune

40

What can acute inflam result in?

resolution, abscess, fibrosis

41

What can chronic inflam result in?

Fibrosis

42

Clinical cardinal signs of inflam

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

43

Signs and symptoms of inflam?

fever, tachy, hypotension, ^ WCC, ^CRP.
Weight loss, malaise, sepsis -> CV failure (septic shock)

44

Numbers for CRP

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

45

Examples of exagerated or inappropriate inflam response?

Allergies, hypersensitivity & autoimmune diseases

46

What can we do for inflam?

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

47

What happens if there is no inflam response?

^ chance of infection, delayed wound healing, tissue damage

48

Acute appendicitis notes

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

49

Management of acute appendicitis?

Appendicectomy

50

Complications of appendicitis?

Performation leading to peritonitis & abscess formation

51

Septic arthritis notes

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

52

Risk factors for septic arthritis?

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

53

Treatment of septic arthritis?

Joint aspirate. IV antibiotics. Sepsis 6.

54

Minor injury inflam response

has no benefit. Rest prevents further injury.

55

RA notes

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

56

Complications with RA.

Vessels can become involved- vasculitis -> circulatory problems

57

Treatment of RA

Steroids, DMARDS, biologics

58

Peptic ulcers notes

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

59

Complications of peptic ulcers

developing bleed/perforation

60

Treatment of peptic ulcers

PPIs/ histamine receptor agonist/ antibiotics.