Inflammation

Question 1

5 steps of inflammatory response

Answer 1

recognition
recruitment
removal
regulation
resolution

Question 2

signs of inflammation

Answer 2

dolor
calor
rubor
tumor
functio laesa (loss of function)

Question 3

acute inflammation

Answer 3

minutes or hours
mainly neutrophils
usually mild
prominent

Question 4

chronic inflammation

Answer 4

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

Question 5

monocyte

Answer 5

large cell with a nucleus that does not fill cell space

Question 6

lymphocyte

Answer 6

cell with a nucleus that mostly fills cell space

Question 7

stimuli for acute inflammation

Answer 7

infection, trauma, necrosis, foreign bodies, immune reactions

Question 8

vascular reaction (acute inflammation)

Answer 8

increased vasodilation and vascular permeability

Question 9

cell response (acute reaction)

Answer 9

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

Question 10

pattern recognition receptors

Answer 10

receptors that sense infectious pathogens and substances

Question 11

inflammasome

Answer 11

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

Question 12

hydrostatic pressure

Answer 12

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

Question 13

oncotic pressure

Answer 13

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

Question 14

edema

Answer 14

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

Question 15

major mediator of vessel changes

Answer 15

histamine

Question 16

difference between mast cell and basophil

Answer 16

mast cell is a lot bigger

basophil has smaller nucleus and a ton of granulocytes

Question 17

how do leukocytes get to the site of inflammation?

Answer 17

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

Question 18

first cell to respond to inflammation

Answer 18

neutrophil (6-24 hrs), then monocyte

Question 19

how do leukocytes destroy a pathogen

Answer 19

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

Question 20

classical pathway

Answer 20

activated by antibody immune complexes

Question 21

non classical pathway

Answer 21

activated by LPS

Question 22

cyclooxygenase

Answer 22

will turn arachidonic acid into prostaglandins, prostacyclins, and thromboxanes

Question 23

prostaglandins

Answer 23

inflammation, clotting, thermoregulation

Question 24

prostacyclins

Answer 24

vasodilation, inhibit platelet activation, reduces clotting

Question 25

thrombaxanes

Answer 25

platelet activation and stickiness

Question 26

lipoxygenase

Answer 26

will turn arachidonic acid into leukotrienes

Question 27

leukotrienes

Answer 27

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

Question 28

where do anti inflammatory steroids act?

Answer 28

phospholipase A2 - turns membrane phospholipid to arachidonic acid

Question 29

where does aspirin act?

Answer 29

cox

Question 30

how can omega 3s help inflammation?

Answer 30

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

Question 31

cell derived mediators for acute inflammation

Answer 31

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

Question 32

plasma protein mediators for acute inflammation

Answer 32

complement activation | factor 7 activation

Question 33

morphology of acute inflammation

Answer 33

serous, fibrinous, purulent, abcess

Question 34

serous inflammation

Answer 34

watery, fluid filled space | burns and viral infections

Question 35

fibrinous inflammation

Answer 35

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

Question 36

purulent inflammation

Answer 36

purulent exudate | infection with a specific pathogen (pyogenic)

Question 37

abscess

Answer 37

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

Question 38

ulcer

Answer 38

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

Question 39

stimuli for chronic inflammation

Answer 39

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

Question 40

cell mediators for chronic inflammation

Answer 40

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

Question 41

classic activation (chronic)

Answer 41

microbial actions | inflammation

Question 42

alternative activation (chronic)

Answer 42

tissue repair, fibrosis | anti inflammatory actions

Question 43

cd4 T cell

Answer 43

promotes inflammation by secreting cytokines

Question 44

cd4 T cell mediation

Answer 44

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

Question 45

causes of a granuloma

Answer 45

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

Question 46

noncaseating granulomas

Answer 46

shaumann bodies - calcium and protein | asteroid bodies - stellate inclusion

Question 47

risk factors of noncaseating granulomas

Answer 47

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

Question 48

amyloidosis

Answer 48

aggregation of misfolded proteins | alzheimers is most common form

Question 49

risk factors of ammyloidosis

Answer 49

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

Question 50

systemic effects of chronic inflammation

Answer 50

fever, acute phase proteins, leukocytosis

Question 51

diet and inflammation (pathway)

Answer 51

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)

Question 52

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

Answer 52

true

Question 53

problematic waist to hip ratios

Answer 53

men - more than 1 | women - more than .8

Question 54

which type of body fat is pro inflammatory

Answer 54

visceral

Question 55

two types of tissue repair

Answer 55

regeneration | scar formation

Question 56

labile tissues

Answer 56

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

Question 57

stable tissues

Answer 57

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

Question 58

permanent tissues

Answer 58

cells are totally out of cell cycle | neurons, cardiac muscle

Question 59

incision wound

Answer 59

longer than they are deep

Question 60

stab wound

Answer 60

deeper than they are long

Question 61

puncture wound

Answer 61

caused by shapr point, not sharp edge

Question 62

chopping wounnd

Answer 62

combination of blunt and sharp characteristics

Question 63

first intention

Answer 63

healing incision wounds | regeneration

Question 64

second intention

Answer 64

healing wider wounds | scar

Question 65

two sections of ECM to repair

Answer 65

basement membrane | interstitial matrix

Question 66

fuctions of ecm

Answer 66

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

Question 67

steps for scar formation

Answer 67

angiogenesis migration and proliferation (granulation tissue) remodeling - scar

Question 68

factors that influence tissue repair (6)

Answer 68

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