Inflammation

Question 1

leukocytes

Answer 1

white blood cells:
neutrophils
lymphocytes
monocytes
eosinophils

Question 2

4 cardinal signs of acute inflammation

Answer 2

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

Question 3

distinct patterns that trigger acute inflammation

Answer 3

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

Question 4

step one in acute inflammation

Answer 4

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

Question 5

histamine and serotonin

Answer 5

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

Question 6

Cyclooxygenase

Answer 6

produces AA metabolites

Question 7

Arachidonic acid (AA) metabolites

Answer 7

include prostaglandins, leokotrienes, lipoxins - VASODILATION

Question 8

arachidonic acid metabolites

Answer 8

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

Question 9

nitric oxide

Answer 9

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

Question 10

platalet activating factor

Answer 10

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

Question 11

bradykinin

Answer 11

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

Question 12

step 2 in acute inflammation

Answer 12

increase in vascular permeability

Question 13

where does the increased vascular permeability occur?

Answer 13

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

Question 14

transudate

Answer 14

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

Question 15

exudate

Answer 15

fluid higher concentration of proteins and inflammatory response

Question 16

edema

Answer 16

interstitial fluid accumulation - can be either of transudate or exudate

Question 17

effusion

Answer 17

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

Question 18

purulent exudate

Answer 18

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

Question 19

hemmorrhagic exudate

Answer 19

contains red blood cells due to capillary damage

Question 20

third step in acute inflammation

Answer 20

emigration, accumulation, and activation of leukocytes

Question 21

sequence of leukocyte recruitment

Answer 21

margination
rolling
tight adhesion
migration across vessel wall

Question 22

margination

Answer 22

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

Question 23

rolling

Answer 23

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

Question 24

tight adhesion

Answer 24

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

Question 25

migration across the vessel wall

Answer 25

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

Question 26

migration into the tissue

Answer 26

neutrophils will move towards specific molecules called CHEMOTACTIC FACTORS

Question 27

chemotactic factors

Answer 27

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

Question 28

pyrogens

Answer 28

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

Question 29

tachychardia

Answer 29

increased heart rate

Question 30

tachypnea

Answer 30

increase in respiratory rate

Question 31

acute phase reactants

Answer 31

chronic inflammation

Question 32

benefits of acute inflammation

Answer 32

remove invading pathogens or clear necrotic tissue

Question 33

C3a and C5a

Answer 33

involved in the complement cascade system

Question 34

skin blister is an example of

Answer 34

a serous exudate | fluid and a few cells underneath the skin

Question 35

integrin activation by?

Answer 35

chemokines

Question 36

microbe binding to CD14?

Answer 36

microbe direct binding to CD14 causes increase in the inflammatory pathway

Question 37

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

Answer 37

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

Question 38

generation of reactive oxygen and nitrogen species

Answer 38

mitochondria + phagosome

Question 39

NETs - neutrophil extracellular trap

Answer 39

extruded DNA from neutrophils that trap bacteria | histones on DNA are toxic to the bacteria

Question 40

three outcomes of acute inflammation

Answer 40

1. complete resolution 2. fibrosis 3. chronic inflammation

Question 41

chronic inflammation

Answer 41

persists for more than a few days

Question 42

causes of chronic inflammation

Answer 42

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

Question 43

cells with chronic inflammation

Answer 43

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

Question 44

acute phase proteins

Answer 44

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

Question 45

examples of acute phase proteins

Answer 45

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

Question 46

type 1 hypersensitivity

Answer 46

immediate hypersensativity

Question 47

type II hypersensitivity

Answer 47

antibody-mediated hypersensitivity

Question 48

type III hypersensitivity

Answer 48

immune complex hypersensitivity

Question 49

type IV hypersensitivity

Answer 49

T-cell mediated hypersensitivity

Question 50

stimuli for histamine release

Answer 50

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

Question 51

therapy for acute inflammation

Answer 51

block histamine receptors

Question 52

neutrophil chemotactic factors

Answer 52

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