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Flashcards in Inflammation Deck (52)
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1
Q

leukocytes

A
white blood cells:
neutrophils
lymphocytes
monocytes
eosinophils
2
Q

4 cardinal signs of acute inflammation

A
  1. redness/rubor
  2. swelling/ tumor
  3. calor/ heat
  4. dolor/ pain
3
Q

distinct patterns that trigger acute inflammation

A

pathogen associated molecular patterns - PAMPs - like bacterial cell wall
Damage Associated molecular patterns - DAMPs- like fragments of necrotic cells

4
Q

step one in acute inflammation

A

hyperemia - dilation of blood vessels - increases blood flow to the area. accounts for the rubor/redness and calor/heat at site of inflammation

5
Q

histamine and serotonin

A

VASOACTIVE AMINES -mediators of increased blood flow
FIRST MEDIATORS released
Stored in mast cells, basophils, and platalets and is released in response to trauma, heat, or immune reactions
Serotonin - similar effects of histamine - pre-formed in platalets

6
Q

Cyclooxygenase

A

produces AA metabolites

7
Q

Arachidonic acid (AA) metabolites

A

include prostaglandins, leokotrienes, lipoxins - VASODILATION

8
Q

arachidonic acid metabolites

A

prostaglandins - involved in vasodilation
example is prostaglandins
enzyme cyclooxygenase produces the AA metabolites
inhubited by aspirin and NSAIDs

9
Q

nitric oxide

A

NO acts on smooth muscle relaxant causing vasodilation - by endothelial cells

10
Q

platalet activating factor

A

from cell membranes- causes platalet aggregation, in addition to vascoconstriction, bronchoconstriction, and leokocyte activation

11
Q

bradykinin

A

kinina are vasoactive peptides from plasma proteins called kininogens
increased vascular permeability and contraction of smooth muscle, dilation of blood vessles and pain when injected into the skin

12
Q

step 2 in acute inflammation

A

increase in vascular permeability

13
Q

where does the increased vascular permeability occur?

A

post capillary venules - NOT LARGE ARTERIES OR VEINS - venules between endothelial cells
many factors that increase hyperemia- increased blood flow/dilation of blood vessels also increase the vascular permeability

14
Q

transudate

A

fluids low in protein concentration and cell numbers - released across capillary beds and usually reabsorbed on the venous side or by lymphatics

15
Q

exudate

A

fluid higher concentration of proteins and inflammatory response

16
Q

edema

A

interstitial fluid accumulation - can be either of transudate or exudate

17
Q

effusion

A

accumulation of fluid in A SEALED BODY CAVITY (can be removed/ directly aspirated with needle or catheter where edema cannot)
example- between the lung and chest wall is a pleural effusion

18
Q

purulent exudate

A

large concentration of neutrophils usually due to bacteria that attracts the neutrophils - results in a cloudy appearance
example - pus

19
Q

hemmorrhagic exudate

A

contains red blood cells due to capillary damage

20
Q

third step in acute inflammation

A

emigration, accumulation, and activation of leukocytes

21
Q

sequence of leukocyte recruitment

A

margination
rolling
tight adhesion
migration across vessel wall

22
Q

margination

A

in order for leukocytes to exit the blood stream - they must accumulate to the margin of the bloodstream and come INTO CONTACT WITH VASCULAR WALL

23
Q

rolling

A

after they have marginated - may physically contact the endothelial cells. at first it is a lose connection and interaction with adherence molecules occurs - then when appropriate adherence occurs with the endothelial cell - the leuokocyte can migrate out of the blood stream

24
Q

tight adhesion

A

part of step 3 - integrin molecules to increase their affanity for integrin ligands on the endothelial cell surface
when tightly adhered - no more rolling

25
Q

migration across the vessel wall

A

leuokocyte will migrate between two endothelial cell - briefly breaking the junction between the two

26
Q

migration into the tissue

A

neutrophils will move towards specific molecules called CHEMOTACTIC FACTORS

27
Q

chemotactic factors

A

molecules that neutrophils are attracted to when migrating into the tissue - can be proteins and lipids

28
Q

pyrogens

A

collection of these causes fever
bacteria not directly causing the fever
stimulate the production of prostaglandins synthesis in the hypothalamic regulatory centers thus altering the thermostat controlling body temperature

29
Q

tachychardia

A

increased heart rate

30
Q

tachypnea

A

increase in respiratory rate

31
Q

acute phase reactants

A

chronic inflammation

32
Q

benefits of acute inflammation

A

remove invading pathogens or clear necrotic tissue

33
Q

C3a and C5a

A

involved in the complement cascade system

34
Q

skin blister is an example of

A

a serous exudate

fluid and a few cells underneath the skin

35
Q

integrin activation by?

A

chemokines

36
Q

microbe binding to CD14?

A

microbe direct binding to CD14 causes increase in the inflammatory pathway

37
Q

superoxide (o2), hydrogen peroxide (h202), hydrogen radical (OH), peroxinitrite (OONO-)

A

oxygen derivatives - reactive oxygen and nitrogen metabolites
main source is from leukocytes

38
Q

generation of reactive oxygen and nitrogen species

A

mitochondria + phagosome

39
Q

NETs - neutrophil extracellular trap

A

extruded DNA from neutrophils that trap bacteria

histones on DNA are toxic to the bacteria

40
Q

three outcomes of acute inflammation

A
  1. complete resolution
  2. fibrosis
  3. chronic inflammation
41
Q

chronic inflammation

A

persists for more than a few days

42
Q

causes of chronic inflammation

A

prolonged exposure to the injury/irritation
immune mediated disease (autoimmune, allergies)
persistent infections - granulomatous inflammation

43
Q

cells with chronic inflammation

A

monocyte - macrophage when in the tissue
lymphocytes - T,B, natural killer
Eosinophils

44
Q

acute phase proteins

A

increase in acute inflammation but stay chronically elevated unless the inflammation subsidies

45
Q

examples of acute phase proteins

A

Interleukins 1 and 6
Tumor necrosis Factor
molecules/proteins promote the synthesis of these proteins in the liver

46
Q

type 1 hypersensitivity

A

immediate hypersensativity

47
Q

type II hypersensitivity

A

antibody-mediated hypersensitivity

48
Q

type III hypersensitivity

A

immune complex hypersensitivity

49
Q

type IV hypersensitivity

A

T-cell mediated hypersensitivity

50
Q

stimuli for histamine release

A

Physical injury: trauma, cold, heat
Binding antibodies to mast cells
Fragments of complement C3a, C5a

51
Q

therapy for acute inflammation

A

block histamine receptors

52
Q

neutrophil chemotactic factors

A

CXC chemokines - IL8
C5a
Bacterial products
Platalet activating facor (PAF)