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inflam Flashcards

1
Q

what is inflammation

A

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

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2
Q

how is it initiated

A

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)

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3
Q

what to those cause

A

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

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4
Q

what is the function of the immune cells

A

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.

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5
Q

what happens to the blood vessels

A

thickening of the blood vessels.

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6
Q

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

A

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

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7
Q

harmful effects of chronic inflammation

A

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

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8
Q

what are the 5 canonical cardinal features of inflammation

A

redness
heat
pain
swelling

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9
Q

what are some causes of inflammation

A

pathogens
allergy
extreme temp

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10
Q

describe acute inflammation

A

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

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11
Q

why is there swelling

A

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

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12
Q

what happens when you get a break in the skin

A

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

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13
Q

which cells release vasodilators

A

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

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14
Q

what are the vasodilators

A

Histamine

Nitric Oxide

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15
Q

What are the vascular changes following vasodilator release

A

Increased permeability
Dilation
Reduced flow
plasma leakage

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16
Q

what does the increase in permeability do

A

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)

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17
Q

benefits of increase permability

A

more protiens
more antibodies
leukocytes
form barrier

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18
Q

histamine production and action

A

mast cells, basophil, platelets

vasodialtion, i^ vascular permeability, endothelial activation

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19
Q

prosatgalndin action and source

A

Mast cells, leukocytes

Vasodilation, pain, fever

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20
Q

what is exudate

A

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

acts as a barrier between inflammation and healthy tissue

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21
Q

how are immune cells recruited

A

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

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22
Q

what are the stages to acute inflammation

A

steady state
damage
immune cell requirement
neutrophil Extravasation

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23
Q

what are the 4 steps to neutrophil Extravasation

A

chemo attraction
rolling adhesion
tight adhesion
transmigration

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24
Q

describe chemo attraction

A

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

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25
Q

describe rolling adhesion

A

Carbohydrate ligands in a low affinity state on neutrophils bind selectins

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26
Q

describe tight adhesion

A

Chemokines promote low to high affinity switch in integrins

27
Q

what is mac 1

A

enhance binding to ligands

enhance binding of nuetrophil to endothelial walls

28
Q

what is transmigration

A

Cytoskeletal re-arrangement and extension of pseudopodia

29
Q

what is it mediated by

A

pecam on both cells

30
Q

function of nuetrophil in inflammation

A

Pathogen recognition
Pathogen clearance
Cytokine secretion
phagocytosis

31
Q

pathogen recognition describe

A

identify lipopolysaccharides (LPS) present in gram-negative bacteria

32
Q

what are the 2 types of pathogen clearance

A

Phagocytosis

Netosis

33
Q

what does cyotokine secreation do

A

Recruitment and activation of other immune cells

34
Q

describe pahgocytosis mechanism

A

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.

35
Q

how is acute inflammation resolved

A

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

36
Q

what is macrophages role in the resolution

A

clear apoptotic cells

produce anti inflammatory mediaters

37
Q

last step

A

wound is healed

38
Q

what is an antigen

A

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

39
Q

what is a foriegn antigen

A

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

40
Q

Self antigen:

A

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

41
Q

Immunogen:

A

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

42
Q

Hapten

A

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

43
Q

chronic inflammation initial

A

have the same initial phase with acute

44
Q

difference between chrinuc and acute

A

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

45
Q

macrophages in inflammaton are recruited as whatg

A

monocytes

46
Q

why are they good

A

PHAGOCYTIC
ANTI INFLAMMTORY
WOUND REPAIR
cytoxic

47
Q

bad

A

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

48
Q

what is granulomatous inflammation

A

Chronic inflammation with distinct pattern of granuloma formation

49
Q

what is granuloma formation

A

disruption of surrounding tissue with clear distinc scaring

50
Q

function

A

Aggregation of activated macrophages. A barrier designed for clearance.

51
Q

what are they triggered by

A

Triggered by strong T cell responses.

52
Q

form against what

A

Resistant agents

53
Q

DIFFERENCE BETWEEN ACUTE AND CHRONIC INFLAM

A 
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
54
Q

CHRONIC IS WHAT

A 
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
55
Q

what is the outcome of inflammation linked to

A

site
type
length

56
Q

positive outcome of inflammation

A

clear inflam agent
remove damage cell
restore normal function

57
Q

negative

A

excess tissue damage
scarring
loss of organ function
so organ failure

58
Q

what is the scar

A

unremoved collagen deposition

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

59
Q

what causes teh sweling

A

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

60
Q

redness

A

ccumulation of blood contents including red blood cells (redness

61
Q

HEAT

A

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.

62
Q

loss in function

A

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.

63
Q

pain

A

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

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