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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
Q

Mast Cell Immediate Response

A

Release of histamine granules (similar effect to prostaglandins):

Vasodilation
Increased vascular permeability

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26
Q

Mast Cell Delayed Response

A 
Production of Arachidonic Acid Metabolites
Especially Leukotrienes (2nd phase of mast cell response)
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27
Q

Complement

A

Pro-inflammatory serum proteins, circulate as inactive precursors

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28
Q

3 Complement Activation Pathways

A

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

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29
Q

Complement Activation (Broad Strokes)

A

C3 Convertase
C5 Convertase
MAC Formation

30
Q

C3a

A

Triggers Mast Cell Degranulation

31
Q

C3b

A

Opsonin

Contributes to C5 Convertase

32
Q

C5a

A

Triggers Mast Cell Degranulation

Chemotactic Agent for PMNs

33
Q

C5b

A

Teams up with C6 - C9 to form MAC

34
Q

MAC

A

Membrane Attack Complex

Perforates and Lyses

35
Q

Hageman Factor

A

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
Q

High MW Kininogen

A

Cleaved to Bradykinin

37
Q

Bradykinin Causes

A

Vasodilation
Leaky capillaries
Pain

38
Q

Symphony of Inflammation

A 
Rubor
Calor
Tumor
Dolor
Fever
39
Q

What mediates Rubor & Calor?

A

Histamine (Most important)
Prostaglandins (PGI2, PGD2, PGE2)
Bradykinin

These lead to vasodilation & increased blood flow through relaxation of arteriolar smooth muscle

40
Q

What mediates Tumor?

A

Histamine
Tissue Damage

These lead to leakage of fluid from postcapillary venule into interstitium

41
Q

What mediates Dolor?

A

Bradykinin
PGE2

These lead to sensitized nerve endings

42
Q

What mediates Fever?

A

Macrophages release IL-1 & TNF → Perivascular COX Activity → PGE2

PGE2 in the hypothalamus raises temperature set point

43
Q

What is the first phase of Acute Inflammation?

A

Fluid Phase

Peaks at 12h

44
Q

What is the second phase of Acute Inflammation?

A

Neutrophil Phase

Peaks at 24h

45
Q

What is the third phase of Acute Inflammation?

A

Macrophage Phase

Peaks at 2 - 3 days

46
Q

What is contained in storage granules of endothelial cells?

A

Weibel-Palade Bodies containing:

Von Willebrand Factor
P-Selectin

Histamine induces their release.

47
Q

Overarching steps of Neutrophil Phase of Acute Inflammation

A 
Margination
Rolling
Adhesion
Transmigration & Chemotaxis
Phagocytosis
Destruction of Phagocytosed Materials
48
Q

Neutrophil Phase - Margination

A

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
Q

Neutrophil Phase - Rolling

A

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
Q

Sialyl Lewis X

A

Glycoprotein on Leukocytes

Binds to selectins on endothelial cells for leukocyte rolling

51
Q

Neutrophil Phase - Adhesion

A

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
Q

Neutrophil Phase - Transmigration & Chemotaxis

A

Leukocytes transmigrate across endothelium of post-capillary venules

Chemotactic Attractants for PMNs:
IL-8
C5a
LTB4
Bacterial Products
53
Q

Neutrophil Phase - Phagocytosis

A

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
Q

IgG & C3b

A

Opsonins for phagocytosis

55
Q

Neutrophil Phase - Oxygen-Dependent Destruction of Phagocytosed Material

A

Most effective killing

HOCl generated by oxidative burst in phagolysosome

56
Q

Neutrophil PHase - Oxygen-Independent Destruction of Phagocytosed Material

A

Less effective killing

Enzymes present in leukocyte secondary granules (Lysozyme, Major Basic Protein)

57
Q

In which leukocytes can Major Basic Protein be found?

A

Eosinophils

58
Q

Marginated Pool of PMNs

A

Normal PMNs
Hang out like bats on vessel walls of lungs via integrins
Wait for recruitment

59
Q

Leukocyte Adhesion Deficiency

A

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
Q

Chediak-Higashi Syndrome

A

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
Q

Resolution of Acute Inflammation

A

PMNs undergo apoptosis

Disappear within 24h after resolution of inflammatory status

62
Q

Oxidative Burst in Phagolysosome

A

O2

↓ NADPH Oxidase

Superoxidase Radical

↓SOD

H2O2

↓MPO

HOCl

63
Q

Chronic Granulomatous Disease

A

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
Q

NBT Test

A

Nitroblue Tetrazolium Test

Screen for Chronic Granulomatous Disease
Turns blue if NADPH Oxidase turns O2 → Superoxidase
Remains colorless if NADPH is defective

65
Q

Catalase (+) Organisms

A 
Staph Aureus (Classic!)
Pseudomonas Cepacia (Now called Burkholderia cepacia)
Serratia Marcescens
Nocardia
Aspergillus
Other things less high yield
66
Q

MPO Deficiency

A

Most patients asymptomatic
Increased risk for candida infections
Normal NBT Test
H202 never be comes HOCl

67
Q

Why do Chronic Granulomatous Disease patients have trouble with Catalase (+) Organisms

A

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
Q

Acute Inflammation - Macrophage Phase

A

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
Q

What is the mechanism for arrival of Monocytes in the Macrophage Phase of Acute Inflammation?

A

Margination
Rolling
Adhesion
Transmigration

70
Q

How do Macrophages induce resolution of Acute Inflammation?

A

IL-10
TGF-β

Anti-inflammatory

71
Q

How do Macrophages induce the continuation of Acute Inflammation?

A

IL-8

Calls in new PMNs

Pus = Sign of CONTINUED acute inflammatory response, not CHRONIC.

72
Q

Who induces the formation of Abscesses?

A

Macrophages

Pathoma Chapter 2 (3 decks)

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