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Patho Exam 2 > Inflammation and repair. > Flashcards

Inflammation and repair. Flashcards

1
Q

What is the general reaction pattern of cellular pathology?

A
  1. Degeneration and atrophy
  2. apoptosis and necrosis
  3. inflammation and immunity
  4. regenearation, hypertrophy, hyperplasia
  5. dysplasia, atypia, neoplasia
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2
Q

Degeneration & Atrophy

A
  • Degeneration
    • Reversible cell response to injury
      • cellular swelling
        • proteinaceious –> leaking of the cell.
    • Fatty degeneration
      • fatty change
      • steatosis ie fatty liver
  • Atrophy
    • catabolic metabolism of cell, not immediately lethal to the cell
    • cells/organs shrink with or without accumulation of metabolic products
    • Can be symmetric atrophy - of old age - reduced blood supply
    • asymmetric - due to a decreased workload, nutrional deficiencies, nuero endocrine, chronic low level injury (radiation, chemical toxins)
    • Cachexia - symmetric atrophy of entire body
      • due to tumors, aids, TB
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3
Q

Hypoplasia & apoptosis

A

Hypoplasia - less cell growth, less coloration

  • Apoptosis
    • programmed cell death
    • serves purpose of natural cell turnover in development and aging
    • serves as disposal for damaged or dysfunctional cells
    • macrophages are ultimately involved in “clean up” of degraded cellular material
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4
Q

What does necrosis involve? Coagulation necrosis vs liquefaction necrosis. Autolysis vs heterolysis

A
  1. A process that follows irreversible cell and tissue injuries (frostbite) (Decreased blood flow)
    1. ischemia, trauma, toxin, infection, immunologic factors.
  2. Starts with cell membrane damage –> swelling –> denaturation –> coagulatoin of intracellular protein
  • Coagulative necrosis - tissue with normal protien content
  • liquefaction necrosis - tissue in poor protein (brain and fat)
  • Autolysis - self destruction,
  • heterolysis - digestion for adjacent cells and tissues by enzymes released from dying cells.
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5
Q

What does inflammation involve?

A
  • Involves acute and chronic classifications
  • It is a mechanism for coping with damagin agents
    • It is a protective response to rid body of cause of cell injury and resultant necrosis
  • Process in itself in potentially damaging
  • Changes occur locally through vasodilation and increased vascular permability.
    • allows for white blood cell accumulation at the site - chemotaxis
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6
Q

What is the process of acute inflammation? Main cell involved?

A
  • This is rapid onset inflammation
    • characterized by exudative fluid and protein (serous fluid)
  • Due to alterations in microvascular circulation
  • Main cell involved is neutrophils
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7
Q

Stages of Acute inflammation

A
  1. Vasodilation
    1. Occurs through cellular release of mediators
      1. histamine, prostacyclin, nitric oxide
    2. increases the hydrostatic pressure by slowing of blood flow- causes margination of leukocytes along the vessel wall
  2. Increased vascular permeability
    1. increased leakiness of vessles - histamine, leukotrienes
    2. occurs through release of mediators from cells
    3. allows fluid to cross interstital tissue, increase protein at interstitial tissue –> decreasing osmotic pressure in the blood and increasing osmotic pressure in tissue = get edema of interestitial tissue.
      1. In short increase protein in tissue –> get edema in tissue.
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8
Q

What are the ways you can increase vascular permeability?

A
  1. Endothelial contraction - short lived
    1. immediate transient response
    2. Histamine, bradykinin and leukotriene mediated
    3. MOA: acts on postcapillary venules
  2. Endothelial retraction - long lived
    1. TNF and interleukin mediated
    2. MOA: structural rearrangement of cytoskeleton
  3. Direct endothelial injury
    1. bacterial enzyme mediated
    2. all vessels affected
    3. MOA: enothelial cell necrosis
  4. Delayed prolonged response - UV light, xray, mild thermal injury
  5. Leukocyte mediated damage.
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9
Q

Increased vascular permeability allows macrophages to?

A

squeeze through the endothelial and become tissue macrophages.

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10
Q

How do white blood cells get from the blood vessel to the site of inflammation? 3 ways

A
  1. Rolling
    1. loose, intermittenet conact of WBC with endothelial
    2. due to margination of WBC from stasis of blood
  2. Pavementing
    1. tight, constant contact of WBC with endothelial
  3. Transmigration
    1. WBC crossing through endothelial layer
    2. platelet adhesion molecule mediated.
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11
Q

What is chemotaxis? What are two mediators?

A

The process that draws WBC to the site of inflammation

  • Exogenous: bacterial polysaccharides
  • endogenous: leukotriene, IL-8
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12
Q

What is the role of leukocytes in inflammation?

A

Recognize foreign particles through mannose and scavenger receptors

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13
Q

What are opsonins? What are 3 opsonins?

A

Particles that bind to foregin material for better WBC recognition

igG-FC receptor recognition on WBC

C3b

Collectins

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14
Q

What are the two ways that white blood cells can kill foreign substance?

A

Reduced NADPH oxidase - Uses two oxygen molecules to produce superoxide radical which then converts to hydrogen peroxide

Myeloperoxidase- converts hydrgeon peroxide and halogen (Cl-) to HOCl which causes lipid or protein peroxidation –> breaksdown the cell wall of bacteria

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15
Q

What are the types of acute inflammation?

A
  • Serous inflammation
    • relatively clear, watery fluid
    • transudative- few cells, protein poor, specific gravity less than 1.012
    • viral infections and burns
  • Fibrinous inflammation
    • finely particulate, thick fluid
    • exudative- protein rich fluid, specific gravity greater than 1.020
    • postmyocardial infarction pericarditis
  • purulent inflammation
    • pus
    • neutrophil, protein rich exudative
    • bacterial and fungal infections
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16
Q

What is an abscess?

A

walled off collectin of pus

can occur in any organ

cannot rid of inciting agent or surrounding tissue repair quicker than site of abscess

17
Q

what is an ulcer

A

loss of mucosa and deeper tissue

microscopy shows 4 layers of superficial to deep fibrin, neutrophils, granulation tissue, and fibrosis

18
Q

What is a fistula?

A

Connection between 2 organs, most commonly, organs with a lumen, ie bladder and colon

inflammtory process involving full thickness of wall of organ, duct, or blood vessel, wall adheres to adjacent organs wall which allows for communication between organs.

19
Q

What is the process of chronic inflammation? Causes?

A

Inflammation and repair resulting in activation of immune system and phagocytosis. (over a period of time)

  • Usually involves lymphocytes and macrophages
    • activated lymphocytes produce collagen = leads to scarring
    • activated macrophages produce proteaes, IL-1, TNF - can cause inflammation
    • angiogenesis and growth factors result.

Results in proliferation of new capillaries and fibroblasts, collagen production, and scarring.

  • Lymphohistioloytic infiltration with increasing fibroblasts = granulation tissue
  • T cell immune response predominant - granuloma formation may result
    • TB

Causes

  • Viral, persistent microbial infection, prolonged exposure to toxin, autoimmune dysfunction
20
Q

What is granulomatous inflammation?

A

A colloection of activated macrophages. Think TB granulomas.

TB, fungi, sarcoidosis, foreign material and silica

21
Q

What is the repair phase of inflammation? When does it begin? Healing vs Regeneration

A

Repair process begins early and involves regeneration of parenchyma or replacement of damaged tissue with a scar if regeneration is not possible.

Regeneration

  • complete replacement of damaged cells - no scar formation
  • ccan occur in skin, GI tract, compensatory tissue of liver and kidney

Healing

  • regeneration of cells combined with scarring and fibrosis.
22
Q

What are the mediators of repair? (5)

A
  1. Epidermal growth factor
    1. stimulates granulation tissue formation
  2. vascular endothelial growth factor
    1. induces blood vessel formatoin
  3. platelet derived growth factor
    1. promotes migration and proliferatio of smooth muscle cells
  4. fibroblast dervied growth factor
    1. stimualtes blood vessel formation and wound repair through macropahges, fibroblast, and endothelial cell migration.
  5. Transforming grwoth favor - B
    1. acts as growth inhibitor for epithelium
23
Q

Describe the regeneration process from inflammatory response

A
  1. Inflammatory response induced to deal with source of injury
  2. Damage is contained, removing substance, remove dead tissue, start deposition of extracellular matrix
  3. New blood vessel formation
  4. Collagen production
  5. Tissue remodeling
  6. Wound contracture
  7. Increase in wound strength - placement of a scar
24
Q

What are the requirements for replacement by scar

A
  • Angiogenesis
  • migration and proliferation of fibroblasts
  • depositoin of extracellular matrix
  • maturation and reorganizatoin of fibrous tissue
  • time frame
    • 3-5 days = granulation tissue
    • week 2 = collagen deposition continues
    • 1 month = inflammatory infiltrate absent collagen starts to strengthen
25
Q

What does healing by primary intention mean?

A

Healing of the wound with clean edges, close reapproximation of margins, and minimal tissue disruption

example: healing of surgical incision

small to nonexistent scar

26
Q

what does healing by secondary intention mean?

A

Healing of a wound that has unclean edges, extensive tissue disruption and necrosis

Example: cutaneous ulcer

Results in large or prominent scar

Wound as much more necrotic debris - debridement is necessary for healing.

27
Q

Is wound healed skin as strong as the original? What are factors that impair wound healing?

A
  1. Wound strength is about 10% of normal skin at week 1, and fully healed it is about 2/3 strength of normal skin
  2. factors
    1. nutritional deficiency - protein - Vitamin C
    2. infection
    3. steroid therapy
    4. poor blood flow
    5. pressure

Patho Exam 2 (5 decks)

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