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Pathology > Week 3: Inflammation > Flashcards

Week 3: Inflammation Flashcards

1
Q

Inflammation

A

Reaction of living tissue to injury

Starts with injury –> healing/repair

Immune response but MAY BE HARMFUL

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2
Q

Agents of Inflammation

A
  1. Immune reaction
  2. Trauma
  3. Anoxia
  4. Infection (other biologic agents)
  5. Physical agents
  6. Metabolic injury
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3
Q

Acute Inflammation

A

Duration: Short; minutes to days
Characteristics: Neutrophils and exudation

Pathogenesis: Vascular changes, edema, neutrophil-dominant infiltrate

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4
Q

Exudate

A

The fluid that filters from the circulatory system into lesions/areas of inflammation

HIGH PROTEIN CONTENT

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5
Q

Chronic Inflammation

A

Duration: Long; days to years
Characteristics: Lymphocytes, macrophages, plasma cells

Tissue repair

Clinically: 2 weeks or longer
Pathogenesis: mononuclear-predominant inflammatory infiltrate, tissue destruction, tissue replacement by proliferative connective tissue

Can occur without preceding acute inflammation

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6
Q

Vascular Events of Acute Inflammation

A
  1. Transient Vasoconstriction of arterioles (not important)
  2. Vasodilation - redness (rubor) and heat (calor)
  3. Permeability changes - swelling (tumour)
    ^Cells and proteins lost from intravascular compartment, blood viscosity increases
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7
Q

Describe endothelial cell contraction

A

An immediate transient response
Occurs in SMALL VENULES ONLY
Mediated by histamine, bradykinins, leukotrienes

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8
Q

Describe junctional disruption

A

A delayed prolonged response
Occurs in all VENULES
Structural reorganization of cell’s cytoskeleton, disruption of intercellular junctions
Mediated by cytokines (TNF, IL1)

4-6 hours after stimulus

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9
Q

Direct endothelial injury

A

Immediate sustained response in severe injuries (burns, infections, cuts, abrasions)
The prolonged response can be delayed (sunburns)

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10
Q

Leukocyte dependent endothelial injury

A

Delayed prolonged response
VENULES
During the cellular phase, leukocytes adhere to the endothelium and may become activated in the process, releasing ROS and proteolytic enzymes that damage the endothelium
-Activated while still within vessels

This only happens in vascular beds where leukocytes adhere for longer periods of time (Lung, glomeruli in kidneys)

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11
Q

Increased Transcytosis

A

VENULES
VEGF and other chemical mediators increase permeability

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12
Q

New blood vessel formation

A

New blood vessels are leaky until they form intercellular junctions Increased receptors for VEGF and histamine)

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13
Q

Starling’s Hypothesis

A

Normal fluid balance is maintained by TWO opposing sets of forces from the intravascular AND interstitial

HYDROSTATIC PRESSURE and OSMOTIC PRESSURE

Net movement is small and outward under normal conditions because any excess interstitial fluid will drain into the lymphatic system

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14
Q

Transudative Edema

A

Low level of proteins and cells in the interstitium

Factors that increase intravascular hydrostatic pressure (vasodilation) or decrease intravascular osmotic pressure (decreased albumin) = INCREASE in interstitial fluid and edema (transudate)

Heart Failure (Pleural Effusion) - heart does not pump well, backup of blood in the venous system

Liver failure, kidney failure, malnutrition

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15
Q

Transudate

A

Fluid that filters from circulatory system into lesions/areas of inflammation

LOW PROTEIN CONTENT

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16
Q

Exudative Edema

A

High level of proteins and cells in the interstitium

Leaky endothelium causes loss of high protein fluid and nucleated cells with a reduction of intravascular osmotic pressure and increased interstitial osmotic pressure

Fluid cannot return to blood vessels

Produces inflammatory edema

Pneumonia, cancer

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17
Q

Vasodilation

A

Causes INCREASED intravascular hydrostatic pressure

Rudor, calor (red and heat)

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18
Q

Increased permeability

A

Causes INCREASED OP of interstitial proteins + DECRASED OP of plasma proteins

Tumour (swelling)

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19
Q

Cellular Events of Acute Inflammation

A
  1. Margination - WBCs pushed to vessel periphery
  2. Rolling - WBCs briefly attach to endothelium with selectin
  3. Adhesion - WBCs adhere to endothelium using VCAM, ICAM, integrins
  4. Transmigration/diapedesis - WBCs dissolve basement membrane, squeeze through endothelial cells using PEDCAM1/CD31
  5. Chemotaxis - chemotactic agents bind to GPCR –> cascade –> actin –> movement toward gradient
  6. Activation - WBC’s receptors meet offender + is activated
  7. Phagocytosis - recognition/attachment, engulfment, killing

Mice really are the coolest animals present

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20
Q

Migration (Cellular Event 1)

A

When blood is viscous, WBCs are pushed to vessel periphery because of sludging RBCs

Rouleaux formation

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21
Q

Rolling (Cellular Event 2)

A

WBCs tumble and briefly adhere to the endothelium using SELECTIN molecules

22
Q

Adhesion (Cellular Event 3)

A

WBCs firmly stick to endothelial surfaces using

VCAM1, ICAM1 (endothelial cells)

INTEGRINS (leukocytes - must be activated by chemicals)

23
Q

Transmigration/Diapedesis (Cellular Event 4)

A

Leukocytes (WBCs) squeeze through endothelial cells at intercellular junctions + penetrate the basement membrane

Uses PEDCAM1/CD31 (on both leukocytes AND endothelial cells)

24
Q

Chemotaxis (Cellular Event 5)

A

WBCs migrate (unidirectional) to an attractant (chemotactic factors) along a chemical gradient

Chemotactic factors bind to GPCR receptors on WBCs, activate cascade, induce polymerization of actin = increases calcium

Factors: exogenous (bacterial proteins), endogenous (cytokines)

25
Q

Activation (Cellular Event 6)

A

WBC surface receptors recognize offending agents (necrotic tissue, microbes) which triggers intracellular signaling pathways within WBCs that activate them

26
Q

Phagocytosis (Cellular Event 7)

A

WBC mops up the foreign tissue

  1. Recognition and attachment: microorganisms are coated with serum factors (opsonins - IgG, C3b)
  2. Engulfment: pseudopods flow around organisms –> phagolysosome. Enzymes/metabolic products (H2O2) leak into the compartment (it’s like a stomach)

Ca++ and Mg++ are required.

  1. Killing/Degradation:
    a. Oxygen dependent: burst of oxygen use –> ROS (H2O2) –> hypochlorite using enzyme MPO, or hydroxyl radical without MPO
    b. Oxygen independent: H+ ion from lactate –> lowered pH OR WBC granules can harm microbes
27
Q

Chemical Mediators of Inflammation

A

Direct vascular and cellular events

Produced LOCALLY at site of injury or CIRCULATE as precursors in the plasma

Mediators may stimulate target cells to release secondary effector molecules.

Mediators may act on only one or a very few targets, or they may have widespread activity; there may be widely differing outcomes depending on which cell type they affect.

Mediator function is generally TIGHTLY REGULATED.
A major reason for the checks and balances is that most mediators have the potential to have harmful effects.

28
Q

Local Mediators

A
  1. Histamine and serotonin: vasodilation and inc. vascular permeability through endothelium contraction
  2. Prostaglandins: vasodilation
    -fever and pain (dolor)
    -inhibited by NSAIDs (aspirin, ibuprofen)
  3. Leukotrienes: inc. vascular permeability (endothelial contraction), chemotaxis, WBC activation
  4. Cytokines (TNF, IL1): vasodilation, inc. vascular permeability (junctional retraction), adhesion
    -fever, pain, anorexia
  5. Chemokines: chemotaxis

His penis looked corn cob

29
Q

Systemic Mediators

A
  1. Bradykinin (from factor 12): inc. vascular permeability (endothelial contraction)
    -pain at injury site
  2. Thrombin: inc. rolling, adhesion (VCAM/ICAM), cytokines/chemokines
  3. Complement products: vasodilation, inc. vascular permeability, chemotaxis, WBC activation, phagocytosis

Brad the cat

30
Q

Vasodilation (chemical mediators)

A

-histamine/serotonin
-prostaglandin
-complement products

31
Q

Vascular permeability (chemical mediators)

A

-histamine/serotonin
-leukotrienes
-cytokines
-complement products
-bradykinins

32
Q

Rolling (chemical mediators)

A

Thrombin

33
Q

Adhesion (chemical mediators)

A

-thrombin
-cytokines

34
Q

Chemotaxis (chemical mediators)

A

-chemokines
-leukotrienes
-complement products

35
Q

Leukocyte activation (chemical mediators)

A

-leukotrienes
-complement products

36
Q

Phagocytosis (chemical mediators)

A

complement products

37
Q

Defects in Leukocyte Function

A
  1. Number of leukocytes
  2. Leukocyte adhesion (diabetes, alcohol, inherited)
  3. Leukocyte migration/chemotaxis (C5 deficiency, diabetes, drugs)
  4. Phagocytosis and microbicidal (MPO deficiency, leukemia, sepsis, diabetes, malnutrition)
38
Q

Serous Inflammation

A

Due to mild injuries

Outpouring of thin fluid from PLASMA or MESOTHELIAL CELLS lining cavities

Skin blister from burn, pleural effusion from early pneumonia

39
Q

Fibrinous Inflammation

A

Severe inflammations, typically in body cavities.

Vessels are so damaged that large molecules (fibrin) can pass through + deposited in extracellular space

Fibrinous exudate = inflammation in body cavity linings

Gross appearance; deeply acidophilic; can scar if not removed

40
Q

Suppurative/Purulent Inflammation/Abscess

A

From bacterial infections

Accumulate pus/purulent exudate (neutrophils, liquefactive necrosis, edema fluid)

Must be DRAINED (not enough just to have antibiotics)

41
Q

Pyogenic bacteria

A

Characteristically produce pyogenic infections (pus-producing)

42
Q

Abscess

A

Localized collection of purulent exudate (pus) in TISSUE

43
Q

Empyema

A

Localized collection of purulent exudate in PLEURAL CAVITY

44
Q

Ulcer

A

Defect of organ/tissue surface with EPITHELIAL LINING

The surface is eroded and necrotic with chronic inflammation

Peptic ulcers, skin, mouth, stomach, intestines, TI tract

NOT liver (no lining)

BOTH chronic and acute process

45
Q

Chronic Inflammation Causes

A

Viral infections
Persistent microbial infections by organisms of low direct pathogenicity
Prolonged exposure to non-degradable material
Autoimmune diseases

46
Q

Nonspecific Chronic Inflammation

A

Mononuclear inflammation (lymphocytes, plasma cells, macrophages)
Tissue destruction
Replacement by connective tissue.

47
Q

Granulomatous Chronic Inflammation

A

A special type of tissue reaction

Often an attempt to wall-off and isolate the affected site
The granuloma is composed of a central focus (usually but not always) of (nidus of) necrotic tissue surrounded circularly by macrophages/histiocytes (usually modified to epithelioid cells), which in turn are surrounded by a rim of lymphocytes.

Necrotic tissue –> macrophages/histiocytes –> lymphocytes

Often giant cells (multinucleated histiocytes) are in the inner epithelioid cells.

Certain infections (TB, syphilis, cat-scratch, fungal, protozoan)

Foreign body inflammations (foreign body granuloma, pneumoconiosis, inhaled metals)

Some inflammatory conditions of unknown etiology (Rheumatoid Arthritis, sarcoidosis, granuloma annular of skin, Crohn’s disease)

48
Q

Local Clinical Manifestations of Inflammation

A
  1. Calor - heat
  2. Tumour - swelling
  3. Dolor - pain
  4. Functio Laesa - Impaired Function
  5. Rubor - redness
49
Q

Systemic Clinical Manifestations of Inflammation

A

Systemic Inflammatory Response Syndrome (SIRS)

  1. Fever
  2. Acute Phase Reactants (proteins)
  3. Leukocytosis (high WBC count)
  4. Other (increase HR, BP, less sweating, rigot, anorexia, somnolence)

In response to infection = septic shock

50
Q

Pyrogen (LPS)

A

Any substance capable of producing fever

Bacterial, chemical, endogenous

Stimulates TNF and IL1

51
Q

TNF and IL1

A

Cytokines that act on the thermoregulatory center of the hypothalamus –> prostaglandin –> reset body temperature to higher

Cause the release of WBCs from the bone marrow

52
Q

Left Shift

A

When immature precursors of WBCs are released (usually by TNF and IL1 in response to inflammation)

Pathology (7 decks)

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