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Pathology > Exam 1 Path (Inflammation and tissue repair) > Flashcards

Exam 1 Path (Inflammation and tissue repair) Flashcards

1
Q

What are the 5 Rs of the inflammatory response?

A
  • Recognition of the injurious agent
  • Recruitment of leukocytes
  • Removal of agent
  • Regulation (control) of the response
  • Resolution (repair)
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2
Q

What is the first cell type to come in during inflammation?

A

-Neutrophils

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3
Q

What are the vascular reactions that occur with acute inflammation?

A
  • Arteriolar vasodilation with engorgement of downstream capillaries (redness and warmth) (may follow initial vasoconstriction)
  • Increase in vascular permeability (protein-rich fluid exits vascular compartment into surrounding tissue spaces and causes swelling)-exudate
  • Viscosity increase results in stasis with leukocytes settling out and accumulating on endothelial surfaces (margination)
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4
Q

What are the sequence of events that occur in acute inflammatory response?

A

1) Margination and rolling of the cells
2) Adhesion onto the endothelium
3) Transmigration
4) Migration in interstitial tissues (chemotaxis)

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5
Q

Explain acute inflammation

A
  • Relatively short duration (minutes to days)
  • neutrophil accumulation
  • fluid and plasma protein exudation
  • process is designed to deliver leukocytes and plasma proteins to the sites of injury (clear invading microbes)
  • stimulated by infection, tissue necrosis, foreign bodies
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6
Q

explain chronic inflammation

A
  • longer duration (days to years)
  • lymphocytes, macrophages
  • vascular proliferation ans car tissue accumulation
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7
Q

What cells recruit white blood cells?

A

Capillary cell walls

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8
Q

What are the mechanisms of permeability?

A

Endothelial recontraction:
–occurs mainly in venules
–induced by histamine, NO, other mediators
–rapid and short lived (minutes)
Direct endothelial injury (due to trauma, microbes, leukocytes)
–occurs in arterioles, capillaries, venues
–caused by burns, some microbial toxins
–rapid: may be long-lived (hours to days)
Increased transcytosis:
–occurs in venues
–induced by VEGF
Leukocyte mediated vascular injury:
–occurs in venues, pulmonary capillaries
–associated with late stages of inflammation
–long lived (hours)

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9
Q

What are some examples of inflammatory signals that activated endothelium which increases the number and activity of surface adhesion molecules

A
  • Selectins (relatively loose and transient (rolling))
  • CD34 (rolling) (help WBC stick)
  • Ig superfamily adhesion molecules (ICAM, VCAM) interact with interns on leukocyte surface (firm adhesion) (really stick so it can get through capillary wall)
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10
Q

After edema what is the first cell you see and last cell you see?

A
  • Neutrophils

- Monocytes/Macrophages

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11
Q

What are some mechanisms of leukocytes at the site of injury?

A
  • Phagocytosis and elaboration of degradative enzymes

- Neutrophils predominate in first 6 to 24 hours, replaces by monocytes at 24 to 48 hours

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12
Q

What are the three distinct steps of phagocytosis?

A

1) recognition and attachment to antigen
2) Engulfment
3) Killing/degradation of ingested material

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13
Q

What are some leukocyte-induced tissue injury?

A

1) Collateral damage to native tissue
- TB and associated lung injury
- long term issues
2) Inappropriate targeting of the immune response
- autoimmune conditions
3) excessive reaction by host tissue to harmless antigens
- allergies

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14
Q

What are some outcomes of acute inflammation?

A

1) Resolution
- short-lived, no residual tissue injury
- normal histology and function restored
2) Scarring (fibrosis)
- significant tissue destruction or inability to regenerate
- unable to restore normal histology
- collagen deposition
3) Progression to chronic inflammation
- if injury persists through acute inflammatory response

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15
Q

What are some of the morphology that occurs with the inflammatory response?

A

1) Serous-accumulation of serous fluid
- blister, sunburn
2) Fibrinous-fibrin deposits in extracellular space
- pericarditis
3) Supporative-production of pus/purulent exudate
- abscess, zit
4) Ulcer

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16
Q

What is the job of the chemical mediators of inflammation?

A
  • Direct the vascular and cellular events of the acute inflammatory response
  • Tight regulation is important!
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17
Q

What is the job of vasoactive amines as chemical mediators?

A 
1) Affect vasculature by inducing contraction and dilation and altering vascular permeability (affected by drugs) 
Histamine 
-Mast cells
-Basophils
-Platelets
Serotonin (platelets)
-released during platelet aggregation 
-effector similar to histamine
18
Q

What is the job of Arachidonic acid metabolites as chemical mediators?

A

Derived from metabolism of arachidonic acid (AA)

  • AA metabolites also referred to as eicosanoids
  • Part of lipid bilayer
  • Metabolized via two major pathways
    1) Cyclooxyrgenase acts on AA to produce
  • Prostaglandins–>vasodialation, inhibit platelets, increased vascular permeability
  • ->these can also cause vasoconstriction and promote platelets
    2) Lipoxygenase acts on AA to produce Leukotrienes
  • ->vasoconstriction, bronchospasm, increased vascular permeability
19
Q

Why would you want to inhibit AA?

A
  • because it is responsible signals that produce
    1) vasconstircition
    2) Increased vascular permeability
    3) Vasodilaiton
    4) Inhibit neutrophil adhesion and chemotaxis
20
Q

Explain Platelet activating factor (PAF) in chemical mediated inflammation

A
  • Bioactive phospholipid derived mediator form a variety of cell types
  • multiple inflammatory effects through a G-protein couple receptor
  • 100 to 10,000 more potent than histamine
  • no drugs that affect PAF yet
21
Q

What are the actions of cytokines in chemical mediated inflammation?

A

-pull in inflammatory cells
5 classes
1) Regulate lymphocyte function (IL-20
2) Innate immunity (TNF and IL-1)
3) Inflammatory cell activation (IFN-y and IL-12)
4) Chemokines -promote chemotaxis
5) Stimulate hematopoiesis (IL-3, GM-CSF)

22
Q

What are lysosomal components and oxygen free radicals chemical mediators of inflammation?

A
  • Forms hydrogen peroxide and bleach to kill bacteria
  • Designed to kill microbes
  • Likely responsible for tissue destruction associated with inflammation, including endothelial cell damage and parenchymal cell damage
  • Held in check by system of antiproteases and antioxidants
23
Q

What is the job Nitrous Oxide as a chemical mediator of inflammation?

A
  • produced by endothelial cells and macrophages
  • potent vasodilator
  • NO-derived free radicals are microcidal
  • may modulate (reduce) the effects of inflammation
24
Q

What is the job of plasma proteins as a chemical mediator of inflammation?

A

-Kinin system (repercussions similar to histamine
-clotting system
-fibrinolytic system
(LINKED BY THE ACTIVATION OF HANGMAN FACTOR)
Complement system
-20 proteins
-innate and adoptive immunity functions
-attaches on to cell and kills it
-Activation: Vascular phenomenon, leukocyte adhesion/chemotaxis and activation, phagocytosis, Cell lysis (membrane attack complex)
-C3 and C5 are the most important inflammatory mediators

25
Q

What protein is responsible for initiating the kinin, complement, clotting and fibrinolytic systems?

A

Hangman factor

26
Q

What are the common features of chronic inflammation?

A

-prolonged duration
-inflammation, tissue injury, and healing are occurring simultaneously
Characterized by:
-mononuclear cell infiltrate (macrophages, lymphocytes, plasma cells)
-tissue destruction
-tissue repair

27
Q

What are the typical clinical settings of chronic inflammation?

A
  • Viral infection (intracellular)
  • Persistent microbial infections
  • Prolonged exposure to toxic agents (non-degradable material)
  • Autoimmune tissue injury (rheumatoid arthritis, MS)
28
Q

What are the key cell player in chronic inflammation?

A

Macrophage

  • 24-48 hrs post injury
  • as they enter the tissues, they undergo transformation into larger tissue macrophages capable of phagocytic activity
  • exposure to cytokines also triggers macrophage activation
29
Q

What are common macrophage products during chronic inflammation?

A
  • proteases (breakdown proteins)
  • complement compotes
  • ROS
  • Eicosaniods
  • Cytokines (IL-1, TNF, and tissue growth factors)
30
Q

What are cell types besides macrophages involved in chronic inflammation?

A
  • Lymphocytes (T and B cells)
  • Plasma cells
  • Eosinophils
  • Mast cells
31
Q

What creates the distinctive pattern of chronic inflammation?

A
  • Aggregates of activated macrophages
  • Does not often lead to eradication of offending agent, but does effectively walls off the agent from other healthy tissues
32
Q

What pathologic conditions cause Granulomas?

A
  • TB
  • Fungal infection
  • Foreign body (suture, breast implants)
33
Q

What is the difference between repair and regeneration?

A

Repair: begins early in the inflammatory process and involves two mechanisms
-remaining tissue tries to re-grow
-endothelial cells re-grow (new blood vessel formation - angiogenesis)
-fibroblasts fill in defects with fibrous tissue
Regeneration only occurs in cells where stem cells can remake same cells–liver

34
Q

What types of tissues repair well?

A

-continuously dividing tissue (mucosa)
-stable tissue (organs) (liver)
-permanent tissue (brain and heart)
(related to stem cell pool)

35
Q

What are the two basic forms of ECM?

A 
Interstital matrix (presents in spaces between cells in connective tissues)
Basement membrane (sits beneath epithelial surfaces)
36
Q

What are the components of ECM?

A
  • Collagen
  • Elastin
  • Proteoglycans
  • Hyaluronan
37
Q

What are the 4 components in repairing connective tissue?

A

1) hemostasis and formation of new blood vessels
2) fibroblast and leukocyte recruitment/migration and proliferation of fibroblasts (scar tissue/collagen)
3) Deposition of ECM
4) maturation and re-organization of fibrous tissue

38
Q

What does stimulation of PDGH, FGF, and TGF-B produced by macrophages and endothelial cells ?

A

It helps the emigration and proliferation of fibroblasts into site of injury

39
Q

What causes the formation of scar tissue?

A

Over time, number of vessels and fibroblasts decreases, but collagen synthetic activity increases and remains high for weeks

40
Q

Differentiate between the 3 different intentions of would healing

A

Primary: reapproxiamte edges with sutures, staples (clean and recent wounds)
Secondary: pack would with gauze–>big scar
Tertiary: allow wound to close by itself because dirty or delayed presentation for treatment (REALLY FUCKING BIG)

41
Q

How much tensile strength does a properly closed wound have?

A

only 70% after 3 months

42
Q

What are factors influencing wound healing?

A 
Infection
Nutritional status
Corticosteroids (inhibit AA(cut off the help me I'm dying signal))
Mechanical stress
Poor perfusion
Size of injury
Location of injury

Pathology (4 decks)

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