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Flashcards in Inflammation Deck (68):
1

5 steps of inflammatory response

recognition
recruitment
removal
regulation
resolution

2

signs of inflammation

dolor
calor
rubor
tumor
functio laesa (loss of function)

3

acute inflammation

minutes or hours
mainly neutrophils
usually mild
prominent

4

chronic inflammation

days
monocytes/macrophages and lymphocytes
often severe and progressive
less prominent; subtle

5

monocyte

large cell with a nucleus that does not fill cell space

6

lymphocyte

cell with a nucleus that mostly fills cell space

7

stimuli for acute inflammation

infection, trauma, necrosis, foreign bodies, immune reactions

8

vascular reaction (acute inflammation)

increased vasodilation and vascular permeability

9

cell response (acute reaction)

emigration of leukocytes from the circulation and accumulation at the focus of injury followed by activation of leukocytes

10

pattern recognition receptors

receptors that sense infectious pathogens and substances

11

inflammasome

a cytoplasmic complex that identifies products of damaged cells and activated capsase-1

12

hydrostatic pressure

pressure due to the water molecules being pushed slightly close together by the heart beating
higher at arterial end of the capillaries

13

oncotic pressure

large amounts of protein in the blood exerts an osmotic pressure that pulls water into the blood
constant pressure

14

edema

accumulation of free fluid in interstitial spaces
increased hydrostatic pressure
loss of plasma protein
increased capillary permeability
lymphatic obstruction

15

major mediator of vessel changes

histamine

16

difference between mast cell and basophil

mast cell is a lot bigger
basophil has smaller nucleus and a ton of granulocytes

17

how do leukocytes get to the site of inflammation?

1. margination and rolling
2. adhesion
3. transmigration
4. chemotaxis

18

first cell to respond to inflammation

neutrophil (6-24 hrs), then monocyte

19

how do leukocytes destroy a pathogen

1. recognition and attachment to pathogen (pattern recognition receptors, opsonins, cytokine receptors)
2. engulfment of pathogen (when opsonins are sensed)
3. killing and degradation of pathogen

20

classical pathway

activated by antibody immune complexes

21

non classical pathway

activated by LPS

22

cyclooxygenase

will turn arachidonic acid into prostaglandins, prostacyclins, and thromboxanes

23

prostaglandins

inflammation, clotting, thermoregulation

24

prostacyclins

vasodilation, inhibit platelet activation, reduces clotting

25

thrombaxanes

platelet activation and stickiness

26

lipoxygenase

will turn arachidonic acid into leukotrienes

27

leukotrienes

causes most of the inflammation in asthma and allergic rhinitis
smooth muscle contraction in the trachea

28

where do anti inflammatory steroids act?

phospholipase A2 - turns membrane phospholipid to arachidonic acid

29

where does aspirin act?

cox

30

how can omega 3s help inflammation?

block the actions of arachidonic acid metabolites by competitively binding
inhibit cox; activate resolvins (anti inflammatory)

31

cell derived mediators for acute inflammation

performed granules (histamine and serotinin)
newly synthesized molecules (aa, ROS, PAF, cytokines, NO)

32

plasma protein mediators for acute inflammation

complement activation
factor 7 activation

33

morphology of acute inflammation

serous, fibrinous, purulent, abcess

34

serous inflammation

watery, fluid filled space
burns and viral infections

35

fibrinous inflammation

fibrinous exudate
more serious for prolonged injuries/inflammation that increase blood flow

36

purulent inflammation

purulent exudate
infection with a specific pathogen (pyogenic)

37

abscess

focal collection of pus with a necrotic region surrounded by neutrophils
can be replaced with CT (scar)

38

ulcer

local defect on the surface of the tissue from necrosis and shedding
mucosa and skin

39

stimuli for chronic inflammation

persistent infections
immune mediated inflammatory diseases
prolonged exposure to toxic agents
metabolic inflammation

40

cell mediators for chronic inflammation

microbes (LPS) and IFN-gamma for classic activation - M1
cytokines other than IFN gamma for alternative activation

41

classic activation (chronic)

microbial actions
inflammation

42

alternative activation (chronic)

tissue repair, fibrosis
anti inflammatory actions

43

cd4 T cell

promotes inflammation by secreting cytokines

44

cd4 T cell mediation

cd4 cell will release 3 subsets of cytokines, one being IFN gamma which will activate M1 and will release M1 cytokines
positive feedback

45

causes of a granuloma

persistent t cell response
certain immune mediated diseases
sarcoidosis (non caseating)

46

noncaseating granulomas

shaumann bodies - calcium and protein
asteroid bodies - stellate inclusion

47

risk factors of noncaseating granulomas

below the age of 40
black is more susceptible than white
can affect lungs, heart, skin, spleen

48

amyloidosis

aggregation of misfolded proteins
alzheimers is most common form

49

risk factors of ammyloidosis

older aged
males more than females
family history
kidney dialysis
can affect heart, kidneys, liver, spleen, nervous sys

50

systemic effects of chronic inflammation

fever, acute phase proteins, leukocytosis

51

diet and inflammation (pathway)

SFA, LPS, TNF can all activate TLR4 which is activated as an innflammatory pathway
TLR4 will activate ceramine which will lead to insulin resistance (lipotoxicity)

52

t/f. foods that increase insulin also increase sfa in the blood

true

53

problematic waist to hip ratios

men - more than 1
women - more than .8

54

which type of body fat is pro inflammatory

visceral

55

two types of tissue repair

regeneration
scar formation

56

labile tissues

cells are always proliferating
bone marrow, skin, gi tract, oral mucosa

57

stable tissues

cells usually in resting phase, can proliferate if necessary
liver, kidney, pancreas

58

permanent tissues

cells are totally out of cell cycle
neurons, cardiac muscle

59

incision wound

longer than they are deep

60

stab wound

deeper than they are long

61

puncture wound

caused by shapr point, not sharp edge

62

chopping wounnd

combination of blunt and sharp characteristics

63

first intention

healing incision wounds
regeneration

64

second intention

healing wider wounds
scar

65

two sections of ECM to repair

basement membrane
interstitial matrix

66

fuctions of ecm

mmechanical support
control of cell proliferation
scaffolding for tissue renewal
establishment of tissue microenviornments

67

steps for scar formation

angiogenesis
migration and proliferation (granulation tissue)
remodeling - scar

68

factors that influence tissue repair (6)

infection, nutrition, gucocorticoids, poor perfusion, foreign bodies, location