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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
Chemical mediators for Endothelial cell contraction
Histamine - quick, fleeting (minutes) | TNF and IL-1 - longer term, slower (hours)
26
Leukocyte recruitment: Margination/rolling
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
27
Signals that upregulate Selectins
Histamine releases P-selectin from Weibel Palade bodies | TNF and IL-1 induce E-Selectin
28
Leukocyte recruitment: Adhesion
Integrins cluster on leukocyte surface and bind CAM's on endothelial cells resulting in stable attachment
29
Signals that upregulate integrins on endothelial cells
IL-1 and TNF
30
Leukocyte recruitment: Transmigration
Leukocytes push between endothelial cells ("diapedesis")_ in postcapillary venules Leukocytes secrete collagenases to break down basement membrane
31
Leukocyte recruitment: Chemotaxis
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)
32
Phagocytosis in Inflammation
(cells recognize opsonins (IgG+ C3b) or have affinity for specific microbial components)
33
Killing phagocytosed material (O2 dependent)
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!)
34
Killing phagocytosed material (O2 independent)
Lysosomal enzymes (elastase, lysozyme)
35
Secretion of microbicidal compounds by leukocytes
-It happens. They also produce "Neutrophil extracellular traps" which make a scaffolding to embed antimicrobial compounds. Microbes are trapped in "NETs"
36
Outcomes of acute inflammation
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)
37
Chédiak-Higashi syndrome
Genetic deficit in proteins responsible for organelle traficcing (phagosomes and lysosomes can't fuse)
38
Host tissue damage due to acute inflammation
- Infections resistant to extermination (TB) - Cleaning up necrotic tissue - Inflammation directed against host tissues
39
3 main processes of chronic inflammation
(1) mononuclear cell infiltrate (2) Tissue destruction (3) Tissue repair (inc neovascularization and fibrosis)_
40
3 main settings of chronic inflammation
(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
Granulomatous inflammation
-Enlarged macrophages forma nodule surrounded by lymphocytes May partially contain infection, and be surrounded by fibrosis over time
42
Possible etiologies for granulomatous inflammation
- Organisms not eradicated by inflammatory rxn (TB, leprosy, fungi) - immune-mediated disease (Crohn's) - Foreign material (stitch) - Sarcoidosis
43
Macrophage in the liver
Kupffer Cell
44
Roles of Macrophages
- Ingest microbes and necrotic debris - Initiate tissue repair and scarring - Secrete inflammatory mediators - Present antigens!
45
Classical Macrophage activation (M1)
Endotoxin, IFN-gamma (from T-Cells), foreign material
46
M1 Macrophage products
ROS's, Nitrous oxide, Lysosomal enzymes, proinflammatory cytokines
47
M1 Macrophage main functions
kill microbes, chronic inflammation
48
Alternative macrophage activation (M2)
IL-4, IL-13 (From T-Cells, eosinophils, Mast cells)
49
M2 Products
Growth factors for new vessel growth and fibroblast activation
50
M2 Functions
Tissue repair and fibrosis
51
Th1 proinflammatory cytokines
IFN-γ, which activates classical pathway macrophages
52
Th2 proinflammatory cytokines
IL-4, IL-5, IL-13 --> activates alternative pathway macrophages and eosinophils
53
Th17
IL-17 --> eventuates recruitment of neutrophils and monocytes
54
Eosinophils
- Recruited by Eotaxin - Notable in parasitic infections (Major basic protein is toxic to parasites! ~and epithelial cells) - Allergic reactions mediated by IgE
55
Mast Cells
- Acute and chronic inflammation - Widely distributed and quickly release inflammatory mediators (Histamine and arachidonic acid) - Coated with IgE to trigger release
56
Pyrexia (fever)
Pyrogens stimulate PGE2 to cause increase of body temperature in hypothalamus Exogenous pyrogens (lipopolysaccharide) release endogenous pyrogens (IL-1, TNF) and act directly
57
Acute Phase proteins in blood
IL-6 stimulates hepatocytes to make new proteins: - C-Reactive protein, serum amyloid A (Opsonins?) - Fibrinogen - causes RBC's to form stacks
58
Leukocytosis
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
Rule of thumb: Neutrophilia
Bacterial infection
60
Rule of thumb: Lymphocytosis
Viral infection
61
Rule of thumb: eosinophilia
asthma | parasitic infections
62
Leukopenia
specific infections (eg typhoid fever)
63
Physiologic effects during acute phase reaction:
tachycardia, hypertension, | hypohidrosis, rigors, chills, anorexia, somnolence, malaise
64
Vasoactive amines
Histamine and serotonin Stored in mast cells, basophils, platelets, quick release inactivated by histaminase Serotonin - vasoconstriction aids in clotting (platelets)
65
Factors that promote Mast cell degranulation
(1) Tissue trauma (2) C3a and C5a (3) IgE (4) IL1 and IL8
66
AA sources and inactivation
From membrane phospholipids in leukocytes, mast cells, endothelium, and platelets Inactivated by spontaneous decay and enzymes
67
Arachadonic acid pathways
(1) COX --> prostaglandins and thromboxanes | (2) Lipoxygenase - > leukotrienes and lipoxens
68
Where do meds interact with arachadonic acid pathways
NSAIDs block COX | Glucocorticoids block PLA2
69
Which COX products are produced in a cell?
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
Leukotriene activity
LTB4 - chemotactic for neutrophils | LTC4, D4, E4 cause vascular permeability
71
LIpoxin activity
Generated as leukocytes enter tissues | Antagonize leukotrienes and are anti-inflammatory (inhibit neutrophil chemotaxis and endothelial adhesion.)
72
Platelet Activating Factor
wide variety of effects including platelet aggregation, vasodilation, vascular permeability, bronchoconstriction, and platelet stimulation Production like AA: PLA2 cleaves lipids from cell membranes
73
TNF and IL-1
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
Chemokines
2 groups: CXC attracts neutrophils (Ex. IL-8) | CC attracts multiple cells (Ex. Eotaxin for eosinophils)
75
Interferon gamma
stimulates classical macrophage activation
76
IL-12
Stimulate the growth and function of T-cells
77
Important chronic inflammatory cytokines
IFN-gamma, IL-12
78
myeloperoxidase
Converts hydrogen peroxide to a hypochlorous radical
79
Endogenous antioxidant
superoxide dismutase
80
Nitric Oxide
Free radical that kills microbes Vasodilation antagonizes platelets reduces leukocyte recruitment
81
NO synthesis and types
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
Lysosomal enzymes
-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
Are granules in neutrophils all the same?
No
84
Substance P
Secreted by nerves and inflammatory cells Binds neurokinin-1 receptor Proinflammatory effect
85
Alternative pathway complement activation
Microbe cell wall components combine with plasma proteins (factor B, D)
86
C3a, C5a
increase vascular permeability and stimulate histamine release
87
C5a
activates lipogenous pathway for AA metabolism
88
C5a, C4a, C3a
activate leukocytes, increasing endothelial adhesion
89
C3b
opsonin
90
Factors limiting C3/C5 convertase formation
DAF and Factor H
91
Factor XII
activates kinin system, leading to bradykinin (vascular permeability, dilation, and pain)
92
Thrombin
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
Anti inflammatory agents
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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