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MCM Week 1 - Leesy > Inflammation > Flashcards

Inflammation Flashcards

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

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
Q

What are the steps of microbial killing

A
  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
Q

What are the 3 major methods of microbial killing

A
  1. reactive oxygen species
  2. nitric oxide
  3. Lysosomal enzymes and proteins
27
Q

How do ROS kill microbes

A 
NADPH oxidase (phagocyte oxidase) generates superoxide anion
Superoxide anion generates H2O2 which works with myeloperoxidase and Cl- to generate OCl2-
28
Q

How does NO kill microbes

A

Inducible nitric oxide synthase (iNOS) generates NO in activated neutrophils and macrophages
This works with superoxide anon to generate peroxynitrite (ONOO-)

29
Q

How do Lysosomal enzymes and proteins kill microbes

A

Lysozomes, collagenase, elastase, acid hyrolase degrade bacteria and can cleave complement components and other proteins

30
Q

What are some protective mechanisms against microbial killing pathways

A
  1. Location - limited to lysosome, phagolysosome
  2. Antioxidants
  3. Antiproteases
31
Q

Mediators of Acute Inlammation

A
  1. Vasoactive amines
  2. Aarachidonic acid metabolites
  3. Ctyokines and chemokines
  4. Complement system
32
Q

What is a powerful target for therapeutic agents to block inflammation?

A

Block the inflammation cascade

33
Q

Examples of vasoactive amines and their source

A

Histamine, Serotonin - preformed in mast cells and basophils - rapid release and action. Associated with vasodilation and increased vascular permeability

34
Q

Serotonin

A

Preformed in GI endocrine cells and platelets, its a neurotransmitter

35
Q

Arachadonic acid metabolites - where are they derived from and what do they do

A

Derived from cell membrane phospholipids

They bind to G-protein coupled receptors.

36
Q

Downstream effects of AA mediators

A

Vasodilation, Vasoconstricton, increased vascular permeability and chemotaxis and leukocyte adhesion

37
Q

Cell membrane phospholipids combine with phospholipases to form

A

Arachadonic acid

38
Q

What are two mediators of arachadonic acid

A

Cyclooxygenase, 5-Lipoxygenase

39
Q

how do steroids affect inflammation

A

Blocking phospholipases and preventing the downstream effects of arachodonic acids

40
Q

Examples of cytokines

A

TNF and IL-1

41
Q

What do cytokines do

A

recruit neutrophils and monocytes, recruit leukocytes, systemic effects

42
Q

Local inflammation caused by cytokines is regulated by what

A

TNF, IL-1
They increase permeability of blood vessels by increasing gaps between endothelial cells by increasing the expression of adhesion molecules

43
Q

Systemic protective effects of cytokines

A

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
Q

Systemic pathological effects of cytokines

A

TNF - in heart - Low output
TNF - in Blood vessels - increased permeability
TNF, IL-1 - in skeletal muscles - insulin resistance

45
Q

What is the complement system

A

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
Q

Complement system begins with

A

C3 thats cleaved into C3a and C3b

47
Q

name the 3 complement system pathways

A

Alternative, classical, lectin

48
Q

Describe the alternative pathway of the complement system

A

Microbe, C3 binds to microbe

49
Q

Describe the classical pathway of the complement system

A

Antibodies bind to a microbe and then C3 binds

50
Q

Describe the lectin pathway of the complement system

A

Mannose binding lectin binds to a microbe which then binds to C3

51
Q

Describe a MAC

A

Membrane attack complex, a tube that allows for the contents of the microbe cell to exit the cell leading to its lysis

52
Q

What are the roles of C5a and C3b

A

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
Q

Causes of chronic inflammation

A
  1. persistent infections
  2. hypersensitivity diseases
  3. prolonged exposure to toxins
54
Q

Morphologic features of chronic inflammation

A

mononuclear cell infiltration - macrophages, lymphocytes, plasma cells

tissue destruction

Attempts at healing

55
Q

What is granulomatous inflammation

A

Special form of chronic inflammation

56
Q

What cells are associated with granulomatous inflammation

A

Macrophages, giant cells, T lymphocytes ,variable necrosis

57
Q

Etiology of granulomatous inflammation

A
  1. foreign material
  2. infection - mycobacterial, fungal
  3. immune reactions
58
Q

Systemic effects of inflammation

A
  1. Fever
  2. Leukocytosis
  3. Sepsis and septic shock
59
Q

Diagnostic proteins of inflammation

A

C-reactive protien (most common), fibrinogen, serum amyloid A, hepcidin

MCM Week 1 - Leesy (4 decks)

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