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DIsease and Defense > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Early morphological changes in cell injury (reversible)

A 
swelling (membrane damage)
Mitochondrial swelling (Hypoxia)
Endoplasmic Reticulum swelling - polyribosomes detach
Nucleolus changes
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2
Q

Two examples of metaplasia

A

Columnar epithelium in bronchus –> squamous epithelium in response to smoking

Squamous epithelium –> columnar epithelium in esophagus from GERD (Barrett’s esophagus)

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3
Q

Classic Necrosis

A
  • Ca leaks into the cell and is released from organelles, activating enzymes and proteases and opening the mitochondrial membrane permeability transition pore (MTP)
  • Cell loses ability to make ATP, and everything swells and the membrane blebs, loss of membrane integrity
  • Nonspecific degradative smear of DNA fragments
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4
Q

Classic Apoptosis

A

Programmed cell death, activated by extracellular ligand binding (Fas/FasR) and cytochrome c release from mitochondria activates caspases
Cytoplasm shrinks, cytoplasm buds and forms apoptotic bodies that are taken up by macrophages.
-Internucleosomal DNA breakage

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5
Q

Coagulative necrosis

A

Characteristics of infarcts
Architecture preserved for several days (proteins AND enzymes damaged)
Dead cells remain pale and white
Leukocytes digest dead cells

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6
Q

Liquefactive necrosis

A
  • Focal bacterial or fungal infections because microbes stimulate inflammatory cells
  • Leukocyte enzymes “liquefy” (digest) tissue
  • Hypoxic cell death in CNS –> liquefactive necrosis
  • Dead cells are completely digested and removed by phagocytes
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7
Q

Caseous necrosis

A
  • TB infection
  • Central portion of infected tissue is necrotic (toxic mycobacteria effects)
  • Fragmented cells and amorphous debris are surrounded by granulomatous inflammation
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8
Q

Fat necrosis

A
  • Areas of fat destruction, resulting from release of activated pancreatic lipases following acute pancreatitis or trauma
  • Fats are hydrolyzed into free fatty acids and precipitate with Ca++ to make a chalky grey material
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9
Q

7 causes of cell/tissue injury

A

1) physical agents (heat, trauma)
2) Chemical and drugs (toxicity, poisoning)
3) Infection
4) Immunologic insults (anaphylaxis, autoimmunity)
5) Genetic derangement (CF, PKU)
6) nutritional imbalance (atherosclerosis, vitamin deficiency)
7) Hypoxia

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10
Q

Reversible changes due to hypoxia (Cell swelling)

A

1) ↓ ATP
2) ↓ Na pump (cell swelling)
3) ↑ glycolysis, ↓ pH
4) ↓ protein synthesis

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11
Q 
Irreversible changes
(Membrane damage)
A

1) Activation of lysosomal enzymes
2) DNA, protein degradation
3) ↑ Ca 2+ influx

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12
Q

Secondary injury from oxygen radicals

A

1) O2 therapy produces high levels of O2 radicals, esp. in lung
2) Inflammation - PMN’s have enzymes like myeloperoxidase which make O2 radicals
3) Reperfusion - in hypoxia, xanthine dehydrogenase is proteolytically converted to xanthine oxidase, and this will create o2 radicals once hypoxia is fixed

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13
Q

Oxygen free radicals

A

O2- (superoxide) and •OH

-Generated by intrinsic oxidases and radiation

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14
Q

Free Radical removal

A

Superoxide removed by SOD making H202
-If H202 isn’t sufficiently removed by catalase, hydroxyl radical forms
Antioxidants, catalase, and glutathione peroxidase remove these radicals

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15
Q

4 key features of acute inflammation

A

fast; neutrophils, mild/self limited tissue injury/fibrosis, prominent local and systemic signs

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16
Q

4 key features of chronic inflammation

A

Slow (days)
Monocytes/macrophages and lymphocytes
severe/progressive tissue injury/fibrosis
Less local/systemic signs

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17
Q

Major causes of acute inflammation

A 
trauma
infection
any cause of necrosis
foreign material (splinter, suture)
immune reactions (allergies)
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18
Q

Toll-like receptors

A

10 forms in humans
Recognize microbial materials
Activate transcription factors that upregulate inflammatory mediators, interferons (interfere with infectious agents), and promote lymphocyte activation

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19
Q

Inflammasome

A

Complex of many receptors that stimulate inflammation by activating caspase 1
Receptors recognize microbial components and pieces of dead cells (ATP just floatin)

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20
Q

Caspase 1 action

A

-Forms active Interleukin 1 beta
-IL-1ß recruits leukocytes to clean up dead cells
(activated by inflammasome)

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21
Q

Exudate

A

High protein content and may contain some white and red cells
Allowed by increased vasodilation and permeability during inflammation

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22
Q

Transudate

A

low protein content, few cells

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23
Q

Vasodilation in acute inflammation

A

Arterioles swell flooding effected capillary beds (rubor and calor)
As fluid leaves vessels, cells are left behind (slow blood flow and stasis)

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24
Q

Increased permeability in acute inflammation (3 mxns)

A

(1) endothelial cell contraction
(2) Injury of endothelial cells (activated leukocytes may release toxic compounds to injure endothelial cells)
(3) Transcytosis - vesicular transport accross membrane

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25
Q

Chemical mediators for Endothelial cell contraction

A

Histamine - quick, fleeting (minutes)

TNF and IL-1 - longer term, slower (hours)

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26
Q

Leukocyte recruitment: Margination/rolling

A

Margination - Heavy leukocytes are slowed by vasodilation in postcapillary venules and head to edge of vessel
Rolling - Endothelial cell adhesion molecules are upregulated and make surface “sticky” P-selectin and E- selectin

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27
Q

Signals that upregulate Selectins

A

Histamine releases P-selectin from Weibel Palade bodies

TNF and IL-1 induce E-Selectin

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28
Q

Leukocyte recruitment: Adhesion

A

Integrins cluster on leukocyte surface and bind CAM’s on endothelial cells resulting in stable attachment

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29
Q

Signals that upregulate integrins on endothelial cells

A

IL-1 and TNF

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30
Q

Leukocyte recruitment: Transmigration

A

Leukocytes push between endothelial cells (“diapedesis”)_ in postcapillary venules
Leukocytes secrete collagenases to break down basement membrane

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31
Q

Leukocyte recruitment: Chemotaxis

A

Leukocytes diapedese to follow certain chemicals, and they continue to follow them extracellularly.
Contractile elements in leukocytes have receptors for chemotactic chemicals (**Memorize C5a from complement system)

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32
Q

Phagocytosis in Inflammation

A

(cells recognize opsonins (IgG+ C3b) or have affinity for specific microbial components)

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33
Q

Killing phagocytosed material (O2 dependent)

A

ROS!
NADPH is oxidized by phagocyte oxidase to superoxide ion.
Superoxide dismutase makes it into H202
Myeloperoxidase with chloride converts hydrogen peroxide to HOCl (bleach!)

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34
Q

Killing phagocytosed material (O2 independent)

A

Lysosomal enzymes (elastase, lysozyme)

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35
Q

Secretion of microbicidal compounds by leukocytes

A

-It happens.
They also produce “Neutrophil extracellular traps” which make a scaffolding to embed antimicrobial compounds.
Microbes are trapped in “NETs”

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36
Q

Outcomes of acute inflammation

A

1) Resolution (minimal damage)
2) Chronic inflammation - when acute can’t do the job
3) scarring - too much destruction for complete regeneration (connective tissue fils void = fibrosis)

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37
Q

Chédiak-Higashi syndrome

A

Genetic deficit in proteins responsible for organelle traficcing (phagosomes and lysosomes can’t fuse)

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38
Q

Host tissue damage due to acute inflammation

A
  • Infections resistant to extermination (TB)
  • Cleaning up necrotic tissue
  • Inflammation directed against host tissues
39
Q

3 main processes of chronic inflammation

A

(1) mononuclear cell infiltrate
(2) Tissue destruction
(3) Tissue repair (inc neovascularization and fibrosis)_

40
Q

3 main settings of chronic inflammation

A

(1) Persistant infections - ex. TB
(2) Immune related diseases - autoimmune (Lupus, Crohn’s) and allergic (asthma)
(3) Prolonged exposure to toxins ex. crystalline silica (exogenous) and atherosclerosis (endogenous)

41
Q

Granulomatous inflammation

A

-Enlarged macrophages forma nodule surrounded by lymphocytes
May partially contain infection, and be surrounded by fibrosis over time

42
Q

Possible etiologies for granulomatous inflammation

A
  • Organisms not eradicated by inflammatory rxn (TB, leprosy, fungi)
  • immune-mediated disease (Crohn’s)
  • Foreign material (stitch)
  • Sarcoidosis
43
Q

Macrophage in the liver

A

Kupffer Cell

44
Q

Roles of Macrophages

A
  • Ingest microbes and necrotic debris
  • Initiate tissue repair and scarring
  • Secrete inflammatory mediators
  • Present antigens!
45
Q

Classical Macrophage activation (M1)

A

Endotoxin, IFN-gamma (from T-Cells), foreign material

46
Q

M1 Macrophage products

A

ROS’s, Nitrous oxide, Lysosomal enzymes, proinflammatory cytokines

47
Q

M1 Macrophage main functions

A

kill microbes, chronic inflammation

48
Q

Alternative macrophage activation (M2)

A

IL-4, IL-13 (From T-Cells, eosinophils, Mast cells)

49
Q

M2 Products

A

Growth factors for new vessel growth and fibroblast activation

50
Q

M2 Functions

A

Tissue repair and fibrosis

51
Q

Th1 proinflammatory cytokines

A

IFN-γ, which activates classical pathway macrophages

52
Q

Th2 proinflammatory cytokines

A

IL-4, IL-5, IL-13 –> activates alternative pathway macrophages and eosinophils

53
Q

Th17

A

IL-17 –> eventuates recruitment of neutrophils and monocytes

54
Q

Eosinophils

A
  • Recruited by Eotaxin
  • Notable in parasitic infections (Major basic protein is toxic to parasites! ~and epithelial cells)
  • Allergic reactions mediated by IgE
55
Q

Mast Cells

A
  • Acute and chronic inflammation
  • Widely distributed and quickly release inflammatory mediators (Histamine and arachidonic acid)
  • Coated with IgE to trigger release
56
Q

Pyrexia (fever)

A

Pyrogens stimulate PGE2 to cause increase of body temperature in hypothalamus
Exogenous pyrogens (lipopolysaccharide) release endogenous pyrogens (IL-1, TNF)
and act directly

57
Q

Acute Phase proteins in blood

A

IL-6 stimulates hepatocytes to make new proteins:

  • C-Reactive protein, serum amyloid A (Opsonins?)
  • Fibrinogen - causes RBC’s to form stacks
58
Q

Leukocytosis

A

WBC’s increased due to TNF and IL-1 stimulating cell release form bone marrow
Eventually, colony stimulating factors will increase bone marrow production of leukocytes

59
Q

Rule of thumb: Neutrophilia

A

Bacterial infection

60
Q

Rule of thumb: Lymphocytosis

A

Viral infection

61
Q

Rule of thumb: eosinophilia

A

asthma

parasitic infections

62
Q

Leukopenia

A

specific infections (eg typhoid fever)

63
Q

Physiologic effects during acute phase reaction:

A

tachycardia, hypertension,

hypohidrosis, rigors, chills, anorexia, somnolence, malaise

64
Q

Vasoactive amines

A

Histamine and serotonin
Stored in mast cells, basophils, platelets, quick release
inactivated by histaminase

Serotonin - vasoconstriction aids in clotting (platelets)

65
Q

Factors that promote Mast cell degranulation

A

(1) Tissue trauma
(2) C3a and C5a
(3) IgE
(4) IL1 and IL8

66
Q

AA sources and inactivation

A

From membrane phospholipids in leukocytes, mast cells, endothelium, and platelets
Inactivated by spontaneous decay and enzymes

67
Q

Arachadonic acid pathways

A

(1) COX –> prostaglandins and thromboxanes

(2) Lipoxygenase - > leukotrienes and lipoxens

68
Q

Where do meds interact with arachadonic acid pathways

A

NSAIDs block COX

Glucocorticoids block PLA2

69
Q

Which COX products are produced in a cell?

A

Depends on presence of specific enzymes.
ex. Endothelial cells have prostacyclin synthase which makes PGI2 (vasodilator) + inhibits aggregation but doesn’t have enzyme to TXA2, which has opposite effects.

70
Q

Leukotriene activity

A

LTB4 - chemotactic for neutrophils

LTC4, D4, E4 cause vascular permeability

71
Q

LIpoxin activity

A

Generated as leukocytes enter tissues

Antagonize leukotrienes and are anti-inflammatory (inhibit neutrophil chemotaxis and endothelial adhesion.)

72
Q

Platelet Activating Factor

A

wide variety of effects including platelet aggregation, vasodilation, vascular permeability, bronchoconstriction, and platelet stimulation
Production like AA: PLA2 cleaves lipids from cell membranes

73
Q

TNF and IL-1

A

Produced in a range of cells, esp macrophages, mast cells, endothelial cells
Stimulated by microbial products, immune complexes, and T cells
Causes endothelial activation (leukocyte binding and recruitment)
Induces systemic effects of inflammation (fever, etc.)

74
Q

Chemokines

A

2 groups: CXC attracts neutrophils (Ex. IL-8)

CC attracts multiple cells (Ex. Eotaxin for eosinophils)

75
Q

Interferon gamma

A

stimulates classical macrophage activation

76
Q

IL-12

A

Stimulate the growth and function of T-cells

77
Q

Important chronic inflammatory cytokines

A

IFN-gamma, IL-12

78
Q

myeloperoxidase

A

Converts hydrogen peroxide to a hypochlorous radical

79
Q

Endogenous antioxidant

A

superoxide dismutase

80
Q

Nitric Oxide

A

Free radical that kills microbes
Vasodilation
antagonizes platelets
reduces leukocyte recruitment

81
Q

NO synthesis and types

A

Made by Nitric oxide synthase from L- arginine
Type 2, inducible NOS: induced in macrophages and endothelial cells (IL1, TNF, IFN gamma)
Type 3 - endothelial NOS constitutively expressed

82
Q

Lysosomal enzymes

A

-In azurophilic neutrophil granules and monocyte granules (like lysosomes)
Acid proteases active in lysosomes, neutral proteases active all over
Protease inhibitors are present in blood and body tissues to limit host tissue damage (Alpha 1 antitrypsin (neutrophil elastase inhibitor)) and alpha-2-macroglobulin (inhibits collagenase)

83
Q

Are granules in neutrophils all the same?

A

No

84
Q

Substance P

A

Secreted by nerves and inflammatory cells
Binds neurokinin-1 receptor
Proinflammatory effect

85
Q

Alternative pathway complement activation

A

Microbe cell wall components combine with plasma proteins (factor B, D)

86
Q

C3a, C5a

A

increase vascular permeability and stimulate histamine release

87
Q

C5a

A

activates lipogenous pathway for AA metabolism

88
Q

C5a, C4a, C3a

A

activate leukocytes, increasing endothelial adhesion

89
Q

C3b

A

opsonin

90
Q

Factors limiting C3/C5 convertase formation

A

DAF and Factor H

91
Q

Factor XII

A

activates kinin system, leading to bradykinin (vascular permeability, dilation, and pain)

92
Q

Thrombin

A

Activated by Hageman factor
binds protease activated receptors on endothelial cells and activates
Cleaves fibrinogen creating chemotactic peptides that increase vascular permeability
Cleaves complement factor 5

93
Q

Anti inflammatory agents

A

Lipoxins
C1 inhibitors
IL-10 (secreted by macrophages, down regulates macrophages)
TGF-beta - anti-inflammatory, promotes fibrosis

DIsease and Defense (3 decks)

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