inflam

Question 1

what is inflammation

Answer 1

Inflammation is a protective biological process designed to remove damaged cells and clear threats such as infections and toxins.
non-specific response to cellular injury

Question 2

how is it initiated

Answer 2

when cellular damage (non-apoptotic cell death) leads to the release of damage associated molecular patterns (DAMPs) or the body detects pathogen associated molecular patterns (PAMPs)

Question 3

what to those cause

Answer 3

This causes the cells in the damaged tissue to secrete a range of signals designed to induce inflammation including molecules that alter the structure of nearby blood vessels and chemokines that promote the recruitment of immune cells to the site of injury

Question 4

what is the function of the immune cells

Answer 4

The aim of immune cell recruitment is to clear the source of the initial inflammatory signal, and eventual resolution and repair of the inflamed tissue. As a result inflammation has a characteristic pathology associated with the presence of increased fluid and leukocyte numbers.

Question 5

what happens to the blood vessels

Answer 5

thickening of the blood vessels.

Question 6

what happens if the acute inflammation can’t remove the inflammatory stimuli

Answer 6

adaptive immune cells are recruited and a state of chronic inflammation can occur.

Question 7

harmful effects of chronic inflammation

Answer 7

chronic inflammation can lead to repetitive rounds of inflammation, tissue damage and repair, resulting in scarring and loss of tissue function.

Question 8

what are the 5 canonical cardinal features of inflammation

Answer 8

redness
heat
pain
swelling

Question 9

what are some causes of inflammation

Answer 9

pathogens
allergy
extreme temp

Question 10

describe acute inflammation

Answer 10

Inflammation is a rapid response non-specific response to cellular injury

Question 11

why is there swelling

Answer 11

Change in local blood flow
Structural changes in the microvasculature
Recruitment/accumulation of immune cells and proteins

Question 12

what happens when you get a break in the skin

Answer 12

non-apoptotic cell death- release signals that cause immune response
Detection of foreign material

Question 13

which cells release vasodilators

Answer 13

mast cells degranulate releasing vasodilators causing increased blood flow which results in the classic warmth (calor) and redness (rubor) seen in inflammation.

Question 14

what are the vasodilators

Answer 14

Histamine

Nitric Oxide

Question 15

What are the vascular changes following vasodilator release

Answer 15

Increased permeability
Dilation
Reduced flow
plasma leakage

Question 16

what does the increase in permeability do

Answer 16

allows movement of proteins and immune cells from the blood into the tissue as well as causing movement and build up of fluid into the affected tissues leading to another classical sign of inflammation, swelling (tumor)

Question 17

benefits of increase permability

Answer 17

more protiens
more antibodies
leukocytes
form barrier

Question 18

histamine production and action

Answer 18

mast cells, basophil, platelets

vasodialtion, i^ vascular permeability, endothelial activation

Question 19

prosatgalndin action and source

Answer 19

Mast cells, leukocytes

Vasodilation, pain, fever

Question 20

what is exudate

Answer 20

luid, proteins and cells that have seeped out of a blood vessel

acts as a barrier between inflammation and healthy tissue

Question 21

how are immune cells recruited

Answer 21

chemokines produce inflammational signal
diffuse to form a gradient
leukocytes with complementary receptors
migrate towards the chemokine source

Question 22

what are the stages to acute inflammation

Answer 22

steady state
damage
immune cell requirement
neutrophil Extravasation

Question 23

what are the 4 steps to neutrophil Extravasation

Answer 23

chemo attraction
rolling adhesion
tight adhesion
transmigration

Question 24

describe chemo attraction

Answer 24

secretion of chemokine act on endothelial layer cause upregulation of adhesion molecules e.g. selectins

Question 25

describe rolling adhesion

Answer 25

Carbohydrate ligands in a low affinity state on neutrophils bind selectins

Question 26

describe tight adhesion

Answer 26

Chemokines promote low to high affinity switch in integrins

Question 27

what is mac 1

Answer 27

enhance binding to ligands | enhance binding of nuetrophil to endothelial walls

Question 28

what is transmigration

Answer 28

Cytoskeletal re-arrangement and extension of pseudopodia

Question 29

what is it mediated by

Answer 29

pecam on both cells

Question 30

function of nuetrophil in inflammation

Answer 30

Pathogen recognition Pathogen clearance Cytokine secretion phagocytosis

Question 31

pathogen recognition describe

Answer 31

identify lipopolysaccharides (LPS) present in gram-negative bacteria

Question 32

what are the 2 types of pathogen clearance

Answer 32

Phagocytosis | Netosis

Question 33

what does cyotokine secreation do

Answer 33

Recruitment and activation of other immune cells

Question 34

describe pahgocytosis mechanism

Answer 34

Large particles engulfed into membrane bound vesicles (phagosomes) Phagosome fuses with lysosome (vesicles containing enzymes e.g. elastase and lysozyme) -> phagolysosome Ractive oxygen species (ROS) – phagocyte NADPH oxidase Antimicrobial peptides – e.g. defensins.

Question 35

how is acute inflammation resolved

Answer 35

pathogen can be recognised as the source of the inflammation signal and treated the nuetrophills then are rapidly dying as they have short half lives as are inflammatory mediaters like hiatmines and prostoglandin

Question 36

what is macrophages role in the resolution

Answer 36

clear apoptotic cells | produce anti inflammatory mediaters

Question 37

last step

Answer 37

wound is healed

Question 38

what is an antigen

Answer 38

a molecule or molecular structure that can be recognised by an antibody any substance to which your immune system can mount an antibody or adaptive immune response

Question 39

what is a foriegn antigen

Answer 39

Foreign antigen: an antigen derived from molecules not found in the body

Question 40

Self antigen:

Answer 40

Self antigen: an antigen derived from molecules produced by our bodies

Question 41

Immunogen:

Answer 41

an antigen independently capable of driving an immune response in the absence of additional substances

Question 42

Hapten

Answer 42

a small molecule that alone does not act as an antigen but when bound to a larger molecule can create an antigen

Question 43

chronic inflammation initial

Answer 43

have the same initial phase with acute

Question 44

difference between chrinuc and acute

Answer 44

persistent inflammatory e.g. our own antigen disctinct immune cell inflitrate you would have inflammatory macrophage and t cells as well as plasma a cycle no clearnce of inflammatory agent tisuue destruction

Question 45

macrophages in inflammaton are recruited as whatg

Answer 45

monocytes

Question 46

why are they good

Answer 46

PHAGOCYTIC ANTI INFLAMMTORY WOUND REPAIR cytoxic

Question 47

bad

Answer 47

cytotoxic - if they can't remove infection they damage surrounding tissue inflammatory-more neutrophils t cells at sight of infection if left unchecked pro fibrotic- they promote of collegen for repair but caan get excess

Question 48

what is granulomatous inflammation

Answer 48

Chronic inflammation with distinct pattern of granuloma formation

Question 49

what is granuloma formation

Answer 49

disruption of surrounding tissue with clear distinc scaring

Question 50

function

Answer 50

Aggregation of activated macrophages. A barrier designed for clearance.

Question 51

what are they triggered by

Answer 51

Triggered by strong T cell responses.

Question 52

form against what

Answer 52

Resistant agents

Question 53

DIFFERENCE BETWEEN ACUTE AND CHRONIC INFLAM

Answer 53

``` acute is Immediate onset; lasts a few days Vasodilation, increased vascular permeability, leukocyte response Neutrophils predominate Histamine release Prominent necrosis Outcomes include: Complete resolution Progression to Chronic Inflammation ```

Question 54

CHRONIC IS WHAT

Answer 54

``` Delayed onset; may last weeks, months or years Persistent inflammation, ongoing tissue injury, attempts at healing Monocytes / Macrophages predominate Ongoing cytokine release Prominent scarring Outcomes include: Scarring Loss of function ```

Question 55

what is the outcome of inflammation linked to

Answer 55

site type length

Question 56

positive outcome of inflammation

Answer 56

clear inflam agent remove damage cell restore normal function

Question 57

negative

Answer 57

excess tissue damage scarring loss of organ function so organ failure

Question 58

what is the scar

Answer 58

unremoved collagen deposition | bad when in the thin epithial cells are replaced by collagen not allowing gas exchange

Question 59

what causes teh sweling

Answer 59

vasodilation as a result of signalling by mast cell derived histamine and nitric oxide on the vascular endothelium leading to a breakdown in tight junctions. Vascular leakage increases blood flow into the inflamed tissue, leading to fluid build-up (swelling

Question 60

redness

Answer 60

ccumulation of blood contents including red blood cells (redness

Question 61

HEAT

Answer 61

Heat results from the increased presence of fluid at core body temperature at a site that would otherwise have a limited exposure to this. During inflammation infiltrating immune cells are also highly metabolically active, which may also contribute to the generation of heat as a by-product.

Question 62

loss in function

Answer 62

fluid build-up and immune cell infiltration often result in the inability of that area of tissue to carry out its primary function. Take for example, inflammation of the lung parenchyma during respiratory infection, if immune cells and fluid build-up in the alveoli. a barrier is created which prevents efficient gas exchange between the capillaries and the air we inhale.

Question 63

pain

Answer 63

many of the same mediators that signal to endothelial cells and other immune cells during inflammation, also signal on local nerve cells.