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Lecture 2 Flashcards

1
Q

What is inflammation?

A

Inflammation is a non-specific, predictable response
- Etiology (cause): chemical agents, physical forces, invading microbes etc.
- Can be acute or chronic
- Dependent on the duration of response
- A vital reaction that’s required for host defense and tissue repair, but can be noxious..

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2
Q

Signs of inflammation

A

Calor - heat
Rubor - redness
Tumour - swelling
Dolar - pain
Functio laesa - loss of function

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3
Q

Pathogenesis of inflammation involves…

A

1.Circulatory changes
2.Vascular changes
3.Mediators of inflammation
4.Induced cellular response

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4
Q

Circulatory changes (the first response to injury)

A

Transient vasoconstriction of arteriolar smooth muscles followed by vasodilation
- Active hyperemia: Influx of (excess) blood into inflamed area
- Increased hydrostatic pressure = edema
- Slowdown of circulation = congestion

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5
Q

Rouleaux

A

Stacks of red blood cells that form as a result of the slow blood flow caused by vasodilation

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6
Q

Changes within circulation (Circulatory changes continued)

A
  1. Margination of WBCs such as neutrophils: the WBCs move to the endothelium
  2. Adhesion of platelets to the wall
  3. Pavementing of WBCs: attachment of WBCs to the endothelium mediated by selections and integrins
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7
Q

What causes the vascular changes of inflammation

A

Vasculature changes during inflammation as a result of…
1.Increased hydrostatic pressure
2.Slowing down of the circulation
3.Adhesion of leukocytes and platelets to endothelial cells
4.Release of soluble mediators of inflammation

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8
Q

Histamine

A

Cell derived
Stored in cytoplasmic granules of platelets, basophils, eosinophils and mast cells
Stimulates retraction of endothelial cells of the venules, increasing permeability = tissue edema
Short action (immediate transient reaction)
Inactivated by local histaminase

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9
Q

How arachidonic acid derivatives are made

A
  1. Phospholipases break down membrane phospholipids to arachidonic acid (AA)
  2. Arachidonic acid feeds into either the cyclooxygenase, lipoxygenase or cytochrome P450 pathway
    Corticosteroids prevent the action of phospholipase, preventing any arachidonic acid from being made, and therefore both pathways.
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10
Q

Lipoxygenase pathway of arachidonic acid produces

A

Leukotrienes: chemotaxis & increased vascular permeability
Lipoxins: inhibit chemotaxis & negative regulator of leukotrienes

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11
Q

Cyclooxygenase pathway of arachidonic acid produces

A

Thromboxane: platelet aggregation, thrombosis, & vasoconstriction
Prostaglandins: vasodilation, increased vascular permeability, pain, & fever
Prostacyclin: opposes thromboxane

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12
Q

Bradykinin

A

Similar action to histamine, but longer lasting: Stimulates retraction of endothelial cells of the venules, increasing permeability = tissue edema
Activation: Hageman factor > kallikrein > kininogen > bradykinin
Induces pain, sensitized the nerve endings

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13
Q

What is the complement system?

A

Group of plasma proteins (C1-C9) produced by the liver, circulating in an inactive form > zymogens
- Activated in an enzymatic cascade

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14
Q

Complement system pathways

A

Classical pathway: antibody-antigen complexes
Lectin pathway: mannose-binding lectin bound to the surface of a pathogen
Alternative pathway: activated by properdin bound to pathogens, requires hydrolysis of C3

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15
Q

Complement system outcomes

A
  1. Opsonization (C3b): facilitated phagocytosis of bacteria
  2. Anaphylaxis (C3a, C5a): act on endothelial cells and cause histamine release – increase vascular permeability
  3. Chemotaxis: migration of leukocytes
  4. Cell lysis (C5-C9): formation of the membrane attack complex
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16
Q

Transudate

A

Fluid leakage low in proteins and with few cells

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17
Q

Exudate

A

Extravascular fluid with increased proteins and cells

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18
Q

Emigration of leukocytes during swelling process

A

A. Adhesion of PMNs to endothelial cells (margination)
B. Insertion of cytoplasmic pseudopods between junctions of endothelial cells
C. Passage through the basement membrane (diapedesis)
D. Amoeboid movement from the vessel to the site of inflammation (chemotaxis)
E. Phagocytosis (or other cellular functions)

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19
Q

Phagocytosis process

A
  • Opsonized bacterium binds to receptors on leukocytes
  • Bacterium (microbe) is engulfed or internalized
  • Oxygen burst and formation of ROS resulting in degradation of microbe
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20
Q

Neutrophils

A

Granulocyte
Most abundant WBC (60-70%)
1st to respond at the site of injury/infection
Segmented nucleus
Contain bactericidal granules

21
Q

Eosinophil

A

Granulocyte
2-3% total WBC
Bi-lobed nucleus
Parasites and allergic inflammation

22
Q

Basophil

A

Granulocyte
Found in circulation
<1% of WBC
Allergic reactions (IgE)
Granules contain vasoactive substances (histamine

23
Q

Mast cells

A

Granulocyte
Tissue resident
Allergic reactions (IgE)
Granules contain vasoactive substances (histamine)

24
Q

Macrophages

A

Tissue resident, precursors are circulating monocytes
Long-lived, appear 3-4 days after initial inflammatory response
Associated with chronic inflammatory responses
Secrete numerous inflammatory mediators
Antigen presenting cells – activate lymphocytes

25
Lymphocytes (T and B cells)
T cell subsets Th1, Th2, Th17, Treg B cells differentiate into plasma cell
26
Platelets
Contain granules with coagulation proteins, histamine, cytokines and growth factors
27
Classification of inflammation: Acute inflammation
Sudden onset, lasting hours to days
28
Classification of inflammation: chronic
Lasts weeks to months Occurs when there is persistence of causative agent An extension of acute inflammation, prolonged healing, or can be a primary chronic reaction
29
Classification of inflammation: Etiology
1. Infections: living pathogens (bacterial, viral. protozoal, fungal or helminthic) 2. Chemical: organic or inorganic, industrial or medicinal 3. Physical: heat, irradiation, trauma 4. Foreign bodies: acute or chronic inflammation (silver) 5. Immune: antibody or cell mediated, hypersensitivity reactions etc.
30
Classification of inflammation: Location
Localized inflammation: •Skin boil •Infection at site of cut •Joint inflammation •Symptoms are the cardinal signs of inflammation Systemic Inflammation: •Bacteria entering the blood – bacteremia •Toxemia •Systemic shock (sepsis) – potentially fatal! •Fever, leukocytosis, fatigue, weakness
31
Serous Inflammation
• Serous exudate (serum = clear fluid) • Early stages of most inflammation • Viral infections of skin vesicles in herpesvirus infection • Joint swelling with trauma or rheumatoid arthritis • Blisters of the skin caused by 2nd degree burns
32
Fibrinous inflammation
• Exudate rich in fibrin (large plasma proteins) • Occurs through large vascular defects • Severe inflammation, bacterial infections “strep throat” • Bacterial pericarditis • Not easily resolved... macrophages invade the exudate and lyse fibrin
33
Purulent Inflammation
• Caused by pus forming bacteria • Pus: viscous, yellow, comprised of dead leukocytes (mostly neutrophils) • Pus accumulates on the mucosa, skin and internal organs • Forms abscess = localized pus in an organ or tissue • Abscess must be removed surgicall
34
Abscess
Accumulation of pus in a newly formed tissue space
35
Sinus
Cavity at the previous site of an abscess which drains to the surface of the tissue
36
Fistula
Channel formed between two pre-existing cavities, hollow organs, or pre-existing cavity and the surface of the body
37
Ulcerative inflammation
• Inflammation of body surfaces or mucosa of hollow organs (stomach) • Ulcer = defect involving the epithelium • Can extend deep into connective tissues if not dealt with appropriately = removal of stimulus
38
Psuedomembranous inflammation
• Combination of ulcerative inflammation and fibrinopurulent exudation • Exudate of fibrin, pus, and cell debris • Mucus forms a pseudomembrane on the surface of ulcers
39
Granulomatous inflammation
• Granuloma consists of lymphocytes, macrophages, & multinucleated giant cells • Occurs during chronic inflammation • Antigens evoke a cell-mediated hypersensitivity reaction or by antigens at site of inflammation
40
How granulomas form
• T-lymphocytes respond to injury, accumulate and secrete cytokines • Macrophages attracted to the site • Macrophages transform into epithelioid cells • Epithelioid cells fuse and form multinucleated giant cells • Granulomas destroy tissue
41
Participating cells in wound healing
Polymorphonuclear (PMN) leukocytes • Scavenge the initial site of injury (brief role) Macrophages • Stay long at the site of injury (long-lived cells) • Produce cytokines, growth factors and other mediators • Act on connective tissue cells
42
What macrophages act on during wound healing
1. Myofibroblasts: hybrid of smooth muscle and fibroblasts, hold tissues together 2. Fibroblasts: produce fibronectin and collagen • Fibronectin: forms a scaffold, provides tensile strength and “glues” other substances together • Collagen: forms fibers that are first to appear during healing “building blocks” of tissues 3. Angioblasts: precursors of blood vessels • Increase blood supply provides required nutrients/cell populations
43
First intention wound healing
Sharp, sterile, surgical wounds. After the incision, there is formation of scab and scavenger action of PMN leukocytes, followed by the formation of granulation tissue, and finally scarring
44
Granulation tissue
Vascularized connective tissue rich in macrophages, myofibroblasts, angioblasts and fibroblasts Temporary makeshift structure prior to scar formation
45
Secondary intention wound healing
For large defects & infected wounds • Myofibroblasts cannot close the wound and infection can be present • Granulation tissue exposed • Prolonged healing • Scaring is more prominent
46
Wound healing time course
First Intention • 24 hours – neutrophils, PMNs • 3 days – macrophages • 5 days – granulation tissue • 10 days – mature collagen • 1 month – formation of scar tissue Second Intention • Large tissue defect • Prolonged healing process of above
47
Determinants of wound healing
1. Site of wound (tissue type) 2. Size of the wound 3. Mechanical factors (margins, movement) 4. Infection 5. Circulatory status (ischemia = poor healing) 6. Nutritional and metabolic factors 7. Age
48
Deficient scar formation
• Slow granulation, inadequate collagen formation • Dehiscence: separation of tissue margins
49
Excessive scar formation
• Keloid: hypertrophic scar • Contractures: exaggeration of wound contraction

Human Pathology (9 decks)

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