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Pathoma Chapter 2 > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

Inflammation

A

Allows inflammatory cells, plasma proteins & fluid to exit blood vessels & enter interstitial space

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2
Q

Acute inflammation is the response to

A

Infection
OR
Tissue Necrosis

Goal is to eliminate pathogen or clear necrotic debris

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3
Q

Acute inflammation is characterized by

A 
Edema
Neutrophils
Immediate response (peaks within 24 hours)
Innate immunity
Limited specificity
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4
Q

24 hours after infarction, which inflammatory cells do you see?

A

Neutrophils

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5
Q

Components of Innate Immunity

A 
Epithelium
Mucus
Complement System
Mast Cells
Macrophages
Eosinophils, etc
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6
Q

Adaptive Immunity

A

Lymphocytes
More Specific
Takes Longer

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7
Q

Where is LPS located?

A

On the outer membrane of gram negative bacteria

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8
Q

Toll-Like Receptors

A

Present on Macrophages & Dendritic Cells
Recognize PAMPs
Also present on Lymphocytes
Mediate chronic inflammation too

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9
Q

CD14

A 
CD14 = TLR on Macrophage
Recognizes LPS
Activates NF-κB
Activates immune response genes
Increases production of multiple immune mediators
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10
Q

NF-κB

A

Molecular “on” switch for acute inflammation response
Activates immune response genes
Increases production of multiple immune mediators

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11
Q

Arachidonic Acid

A 
Released from Phospholipid Cell Membrane by Phospholipase A2
Undergoes:
COX Pathway
vs.
5-Lipooxygenase Pathway
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12
Q

Cyclooxygenase Arachidonic Acid Pathway

A

Produces prostaglandins
PGI2 (Vasodilation, leaky vessels)
PGD2 (Vasodilation, leaky vessels)
PGE2 (Vasodilation, leaky vessels, pain, fever)

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13
Q

Vasodilation occurs at the level of the

A

Arterioles

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14
Q

Increased vascular permeability occurs at the level of the

A

Post-capillary venule

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15
Q

5-Lipooxygenase Pathway

A

Produces Leukotrienes
LTB4 (Attracts & activates PMNs)
LTC4, LTD4, LTE4 (Contract smooth muscle: Vasoconstriction, Bronchospasm, Leaky Capillaries via pericyte contraction)

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16
Q

Which substances attract and activate PMNs?

A

LTB4
C5a
IL-8
Bacterial Products

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17
Q

LTB4

A

Attracts & activates PMNs

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18
Q

LTC4

A

Smooth Muscle Contraction:
Vasoconstriction
Bronchospasm
Leaky Capillaries via Pericyte Contraction → Windows between pericyte-bound endothelial cells

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19
Q

LTD4

A

Smooth Muscle Contraction:
Vasoconstriction
Bronchospasm
Leaky Capillaries via Pericyte Contraction → Windows between pericyte-bound endothelial cells

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20
Q

LTE4

A

Smooth Muscle Contraction:
Vasoconstriction
Bronchospasm
Leaky Capillaries via Pericyte Contraction → Windows between pericyte-bound endothelial cells

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21
Q

PGI2

A

(Vasodilation, leaky vessels)

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22
Q

PGD2

A

(Vasodilation, leaky vessels)

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23
Q

PGE2

A

(Vasodilation, leaky vessels, pain, fever)

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24
Q

Mast Cells are Activated By

A

Tissue Trauma
C3a & C5a
Cross-linking of cell-surface IgE by Ag

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25
Mast Cell Immediate Response
Release of histamine granules (similar effect to prostaglandins): Vasodilation Increased vascular permeability
26
Mast Cell Delayed Response
``` Production of Arachidonic Acid Metabolites Especially Leukotrienes (2nd phase of mast cell response) ```
27
Complement
Pro-inflammatory serum proteins, circulate as inactive precursors
28
3 Complement Activation Pathways
Classical: C1 binds IgG or IgM, bound to Ag Alternative: Microbial Products directly activate complement Mannose-Binding Lectin (MBL): MBL binds mannose on microorganisms, activates complement
29
Complement Activation (Broad Strokes)
C3 Convertase C5 Convertase MAC Formation
30
C3a
Triggers Mast Cell Degranulation
31
C3b
Opsonin | Contributes to C5 Convertase
32
C5a
Triggers Mast Cell Degranulation | Chemotactic Agent for PMNs
33
C5b
Teams up with C6 - C9 to form MAC
34
MAC
Membrane Attack Complex | Perforates and Lyses
35
Hageman Factor
AKA Factor XII ``` Inactive proinflammatory protein Produced in the liver Activated by exposure to subendothelial collagen or tissue collagen Activated by GN Organisms Activates Coagulation & Fibrinolytic Systems Activates Complement Activates Kinin System Important in DIC & Severe GN Sepsis ```
36
High MW Kininogen
Cleaved to Bradykinin
37
Bradykinin Causes
Vasodilation Leaky capillaries Pain
38
Symphony of Inflammation
``` Rubor Calor Tumor Dolor Fever ```
39
What mediates Rubor & Calor?
Histamine (Most important) Prostaglandins (PGI2, PGD2, PGE2) Bradykinin These lead to vasodilation & increased blood flow through relaxation of arteriolar smooth muscle
40
What mediates Tumor?
Histamine Tissue Damage These lead to leakage of fluid from postcapillary venule into interstitium
41
What mediates Dolor?
Bradykinin PGE2 These lead to sensitized nerve endings
42
What mediates Fever?
Macrophages release IL-1 & TNF → Perivascular COX Activity → PGE2 PGE2 in the hypothalamus raises temperature set point
43
What is the first phase of Acute Inflammation?
Fluid Phase | Peaks at 12h
44
What is the second phase of Acute Inflammation?
Neutrophil Phase | Peaks at 24h
45
What is the third phase of Acute Inflammation?
Macrophage Phase | Peaks at 2 - 3 days
46
What is contained in storage granules of endothelial cells?
Weibel-Palade Bodies containing: Von Willebrand Factor P-Selectin Histamine induces their release.
47
Overarching steps of Neutrophil Phase of Acute Inflammation
``` Margination Rolling Adhesion Transmigration & Chemotaxis Phagocytosis Destruction of Phagocytosed Materials ```
48
Neutrophil Phase - Margination
Vasodilation of arterioles slows blood flow in the post-capillary venules. Heavy particles (normally in the center of the lumen) move to the periphery of the vessel.
49
Neutrophil Phase - Rolling
Selectins (speed bumps) upregulated on endothelial cells: P-Selectins (Released from Weibel-Palade bodies, mediated by Histamine) E-Selectins (Induced by TNF & IL-1) Sialyl Lewis X binds these selectins Cells roll along vessel wall
50
Sialyl Lewis X
Glycoprotein on Leukocytes | Binds to selectins on endothelial cells for leukocyte rolling
51
Neutrophil Phase - Adhesion
TNF & IL-1 → Upregulation of ICAM & VCAM (Cellular adhesion molecules) on endothelium C5a & LTB4 → Upregulation of integrins on leukocytes ICAM/VCAM interaction with Integrins → Adhesion
52
Neutrophil Phase - Transmigration & Chemotaxis
Leukocytes transmigrate across endothelium of post-capillary venules ``` Chemotactic Attractants for PMNs: IL-8 C5a LTB4 Bacterial Products ```
53
Neutrophil Phase - Phagocytosis
Consumption of pathogens or necrotic tissue Enhanced by opsonins IgG & C3b Pseudopods from leukocytes extend to form phagosomes (vesicle) Phagosomes merge with lysosomes → Phagolysosome
54
IgG & C3b
Opsonins for phagocytosis
55
Neutrophil Phase - Oxygen-Dependent Destruction of Phagocytosed Material
Most effective killing | HOCl generated by oxidative burst in phagolysosome
56
Neutrophil PHase - Oxygen-Independent Destruction of Phagocytosed Material
Less effective killing | Enzymes present in leukocyte secondary granules (Lysozyme, Major Basic Protein)
57
In which leukocytes can Major Basic Protein be found?
Eosinophils
58
Marginated Pool of PMNs
Normal PMNs Hang out like bats on vessel walls of lungs via integrins Wait for recruitment
59
Leukocyte Adhesion Deficiency
Autosomal Recessive Deficit of CD18 subunit of integrins Clinical Findings (based on lack of marginated pool of PMNs): Delayed separation of umbilical cord Increased circulating PMNs Recurrent bacterial infections (lacking pus formation)
60
Chediak-Higashi Syndrome
Autosomal Recessive Protein-Trafficking Deficit Microtubule railroad tracksdefective, so phagosome can't be brought to lysosome. Phagolysosome is not formed. Clinical Findings: Increased risk of pyogenic infections Neutropenia (from impaired mitosis) Giant granules in leukocytes (exported proteins can't be trafficked once left the Golgi) Defective primary hemostasis Albinism (melanocytes typically form melanin and hand it off to surrounding keratinocytes) Peripheral neuropathy (can't traffic proteins from ganglion to nerve ending)
61
Resolution of Acute Inflammation
PMNs undergo apoptosis | Disappear within 24h after resolution of inflammatory status
62
Oxidative Burst in Phagolysosome
O2 ↓ NADPH Oxidase Superoxidase Radical ↓SOD H2O2 ↓MPO HOCl
63
Chronic Granulomatous Disease
X-Linked Recessive or Autosomal Recessive NADPH Oxidase Defect Poor O2-dependent Killing Leads to infections & granuloma formation w/ Catalase (+) organisms Nitroblue Tetrazolium Test (NBT Test)
64
NBT Test
Nitroblue Tetrazolium Test Screen for Chronic Granulomatous Disease Turns blue if NADPH Oxidase turns O2 → Superoxidase Remains colorless if NADPH is defective
65
Catalase (+) Organisms
``` Staph Aureus (Classic!) Pseudomonas Cepacia (Now called Burkholderia cepacia) Serratia Marcescens Nocardia Aspergillus Other things less high yield ```
66
MPO Deficiency
Most patients asymptomatic Increased risk for candida infections Normal NBT Test H202 never be comes HOCl
67
Why do Chronic Granulomatous Disease patients have trouble with Catalase (+) Organisms
Most bacteria have an alternative source of H2O2 (with lesser stores), so the host can bypass their NADPH Oxidase defect and still generate HOCl from bacterial H2O2 reserves. Catalase (+) organisms break down H2O2 In those infections, there is no way for a Chronic Granulomatous Disease patient to make HOCl
68
Acute Inflammation - Macrophage Phase
Peaks 2 - 3 days after inflammation begins Monocytes arrive and start calling themselves macrophages Macrophages phagocytose & destroy material using enzymes in secondary granules (lysozyme) Not much O2-dependent killing Macrophages also manage next step of inflammatory process
69
What is the mechanism for arrival of Monocytes in the Macrophage Phase of Acute Inflammation?
Margination Rolling Adhesion Transmigration
70
How do Macrophages induce resolution of Acute Inflammation?
IL-10 TGF-β Anti-inflammatory
71
How do Macrophages induce the continuation of Acute Inflammation?
IL-8 Calls in new PMNs Pus = Sign of CONTINUED acute inflammatory response, not CHRONIC.
72
Who induces the formation of Abscesses?
Macrophages

Pathoma Chapter 2 (3 decks)

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