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MCM Week 1 - Leesy > Inflammation > Flashcards

Inflammation Flashcards

(59 cards)

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1
Q

What is inflammation

A

Host defense response to infection and tissue damage intended to eliminate offending agents.

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2
Q

Causes of inlammation

A

Infections, Tissue Necrosis, Foreign bodies, immune reactions

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3
Q

Features of Acute Inflammation

A

Initial rapid response
Develops within minutes-hours
Features: Redness, swelling, heat,

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4
Q

Cells involved in acute Inflammation

A

Neutrophils, other phagocytes

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5
Q

Outcome of acute inflammation

A

Complete resolution, resolution with fibrosis (usually mild) or progression to chronic inflammation

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6
Q

Characteristics of Chronic Inflammation

A

Longstanding injury with tissue damage

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7
Q

How long does chronic inflammation last?

A

Develops over days to months

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8
Q

Local features of Chronic inflammation

A

Variable, related to extent and type of tissue damage

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9
Q

Cells involved in chronic inflammation

A

lymphocytes, plasma cells, monocytes, macrophages, fibroblasts

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10
Q

Outcome of chronic inflammation

A

Progressive and sometimes severe tissue damage with fibrosis

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11
Q

Acute inflammation phases

A
  1. Blood vessel changes
  2. Leukocyte recruitment
  3. Phagocytosis
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12
Q

During acute inflammation what happens with the blood vessel changes

A

Increased flow due to vasodilation, increased permeability

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13
Q

During acute inflammation what happens with leukocyte recruitment

A

Margination, rolling, adhesion
Diapedesis
Chemotaxis

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14
Q

During acute inflammation what happens with phagocytosis

A

receptor binding, engulfment and intracellular destruction

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15
Q

What does exudate mean

A

Leakage of fluid and proteins from blood vessels

Caused by increased interedothelial space

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16
Q

What does Transudate mean

A

Leakage of fluid from blood vessels

Caused by increase in hydrostatic pressure common in congestive heart failure

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17
Q

Phases to getting leukocyte out of the blood vessel

A
  1. Rolling
  2. Integrin activation by chemokines
  3. Stable adhesion
  4. Migration through endothelium
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18
Q

How does your body go about slowing down the leukocytes in your blood stream to get them out of the blood vessels?

A

Activation of P-selectin and E-selectin attach to proteins on the surface of the leukocyte cell, the cell attaches and then rolls along the endothelium

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19
Q

Once it starts rolling how does the leukocyte slow down?

A

Attaching to Integrin (in its high affinity state) which is when its considered to be in stable adhesion

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20
Q

What is the process of the leukocyte moving through the endothelium to exit the blood stream called

A

diapedesis

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21
Q

What happens after diapedesis?

A

The leukocyte has proteins on the outside that use chemotaxis to move towards the site of inflammation

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22
Q

What is chemotaxis

A

migration along a chemical gradient (chemoattractants). It can be exogenous (bacterial products like peptids and lipids) or endogenous (chemical mediators)

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23
Q

What are some of the chemicals that can aid in the chemotaxis of leukocytes?

A

C5a - part of the complement cascade
Aarachadonic acid metabolites like Leukotriene B4
Cytokines like IL-8

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24
Q

Cellular Infiltrate in acute inflammation

Study These Flashcards
A

Neutrophils - 6-24 hours
Monocytes - 24-48 hours and thereafter (when they persist as macrophages)
*Infiltrate may be mixed if tissue injury is ongoing

25
What are the steps of microbial killing
1. recognition and attachment where the microbes bind to phagocyte receptors 2. engulfment - phagocyte membrane zips up around microbe 3. killing and degradation - killing of microbes by ROS and NO, degradation of microbes by lysosomal enzymes in phagolysosome
26
What are the 3 major methods of microbial killing
1. reactive oxygen species 2. nitric oxide 3. Lysosomal enzymes and proteins
27
How do ROS kill microbes
``` NADPH oxidase (phagocyte oxidase) generates superoxide anion Superoxide anion generates H2O2 which works with myeloperoxidase and Cl- to generate OCl2- ```
28
How does NO kill microbes
Inducible nitric oxide synthase (iNOS) generates NO in activated neutrophils and macrophages This works with superoxide anon to generate peroxynitrite (ONOO-)
29
How do Lysosomal enzymes and proteins kill microbes
Lysozomes, collagenase, elastase, acid hyrolase degrade bacteria and can cleave complement components and other proteins
30
What are some protective mechanisms against microbial killing pathways
1. Location - limited to lysosome, phagolysosome 2. Antioxidants 3. Antiproteases
31
Mediators of Acute Inlammation
1. Vasoactive amines 2. Aarachidonic acid metabolites 3. Ctyokines and chemokines 4. Complement system
32
What is a powerful target for therapeutic agents to block inflammation?
Block the inflammation cascade
33
Examples of vasoactive amines and their source
Histamine, Serotonin - preformed in mast cells and basophils - rapid release and action. Associated with vasodilation and increased vascular permeability
34
Serotonin
Preformed in GI endocrine cells and platelets, its a neurotransmitter
35
Arachadonic acid metabolites - where are they derived from and what do they do
Derived from cell membrane phospholipids They bind to G-protein coupled receptors.
36
Downstream effects of AA mediators
Vasodilation, Vasoconstricton, increased vascular permeability and chemotaxis and leukocyte adhesion
37
Cell membrane phospholipids combine with phospholipases to form
Arachadonic acid
38
What are two mediators of arachadonic acid
Cyclooxygenase, 5-Lipoxygenase
39
how do steroids affect inflammation
Blocking phospholipases and preventing the downstream effects of arachodonic acids
40
Examples of cytokines
TNF and IL-1
41
What do cytokines do
recruit neutrophils and monocytes, recruit leukocytes, systemic effects
42
Local inflammation caused by cytokines is regulated by what
TNF, IL-1 They increase permeability of blood vessels by increasing gaps between endothelial cells by increasing the expression of adhesion molecules
43
Systemic protective effects of cytokines
TNF, IL-1,6 - in brain --> fever IL-1,6 in liver --> acute phase proteins TNF, IL-1,6 - in bone marrow --> leukocyte production
44
Systemic pathological effects of cytokines
TNF - in heart - Low output TNF - in Blood vessels - increased permeability TNF, IL-1 - in skeletal muscles - insulin resistance
45
What is the complement system
Has to do with the activation of normally present proteins in the blood stream that become activated and then cause a cascade to amplify its effects ending in inflammation
46
Complement system begins with
C3 thats cleaved into C3a and C3b
47
name the 3 complement system pathways
Alternative, classical, lectin
48
Describe the alternative pathway of the complement system
Microbe, C3 binds to microbe
49
Describe the classical pathway of the complement system
Antibodies bind to a microbe and then C3 binds
50
Describe the lectin pathway of the complement system
Mannose binding lectin binds to a microbe which then binds to C3
51
Describe a MAC
Membrane attack complex, a tube that allows for the contents of the microbe cell to exit the cell leading to its lysis
52
What are the roles of C5a and C3b
C5a (and C3a) recruit and activate leukocytes that lead to inflammation and destruction o f microbes by those leukocytes C3b leads to phagocytosis of microbe
53
Causes of chronic inflammation
1. persistent infections 2. hypersensitivity diseases 3. prolonged exposure to toxins
54
Morphologic features of chronic inflammation
mononuclear cell infiltration - macrophages, lymphocytes, plasma cells tissue destruction Attempts at healing
55
What is granulomatous inflammation
Special form of chronic inflammation
56
What cells are associated with granulomatous inflammation
Macrophages, giant cells, T lymphocytes ,variable necrosis
57
Etiology of granulomatous inflammation
1. foreign material 2. infection - mycobacterial, fungal 3. immune reactions
58
Systemic effects of inflammation
1. Fever 2. Leukocytosis 3. Sepsis and septic shock
59
Diagnostic proteins of inflammation
C-reactive protien (most common), fibrinogen, serum amyloid A, hepcidin

MCM Week 1 - Leesy (4 decks)

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