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PATH 300 (Xavier) > Class #4 - Inflammation (part 2) > Flashcards

Class #4 - Inflammation (part 2) Flashcards

1
Q

Granulocyte?

a) Definition
b) other name
c) Eg

A

a) WBC containing granules in their cytoplasm
b) polymorphonuclear leukocytes (b/c varying shapes of nucleus)
c) Neutrophiles, Eosinophiles, Basophiles, Mast cells

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2
Q

Female mosquito saliva contains? causes?

A

Anticoagulants; Enz. to dissolve tissue

Inflammation due to release of histamine by body

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3
Q

Two major sources of inflammatory mediators?

A

1- Cell derived: Either preformed stocked in granules and secreted or de novo produced
2-Plasma p+-derived: Major source is the liver

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4
Q

Cell derived inflam. mediators?

A

HIstamine, serotonin, prostanglandins, leukotrienes, plt-activating factor, ROS, Nitric Oxide, cytokines, chemokines

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5
Q

Plasma p+-derived inflam. mediator?

A

Complement, Kinins, clotting system

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6
Q

Vasoactive inflam. mediators? Mostly by…cell

A

Histamine/prostanglandins/Nitric Oxide/plt activating factors = vasodilatation
Serotonin = Vasoconstriction

Mast cells

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7
Q

Complement system role (3)?

A
  • Lysis of B
  • Chemotaxis
  • Opsonization
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8
Q

Activation of complement system (3 pathways)?

A
  • Classical : 2IgG activating C1
  • Alternative: ON its own
  • Lectin:
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9
Q

All three pathways of complement activation leads to?

A

Activation of C3 => Formation of C3 convertase that cleave C3 to C3a and C3b

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10
Q

Complement role, chemotaxis, how?

A

C5a and C3a: Recruitment and activation of leuko. (also increase adhesion to endothelium)

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11
Q

Complement osponization effect?

A

C3b bound on bacteria attracts phagocytes.

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12
Q

Vasodilating effect of complement system by?

A

C3a and C5a

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13
Q

Lysis of bacteria by complement, how?

A

C5b to C9 create the membrane attack complex (MAC) that put a hole on B membrane.

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14
Q

Kinin system activation leads to?

Role?

A

Bradykinin

a) Bind to GCPR on nociceptor causing pain and
b) increase vascular permeability, arteriolar dilation

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15
Q

*Most important mediators that cause pain at site of injury

A

Histamine, prostaglandins, Bradykinins

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16
Q

Prostanglandins formation and actions?

A

Phospholilase A-2 (Enz.) that liberates Arachidonic acid from membrane ->Cyclooxygenase (COX1 and 2) type 2 more involved in inflam. -> Prostaglandin
Functions: Vasodilation and increase vascular permeability and causes pain

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17
Q

Cytokines role?

A

Orchestrate systemic effect of inflammation

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18
Q

Interleukins and TNFs effects?

A

Cause fever

19
Q

What are chemokines?

A

Cytokines that attract cells.

20
Q

Chemokines receptor family?

A

CXCR and CCR

21
Q

Plt activating factors actions?

A

Vascular permeability, vasoconstriction, growth factors, clotting, chemotaxis.

22
Q

Nitric oxide action?

A

Relaxation of smooth musc.

23
Q

Resolution of inflammation?

A

Edema draines by lymph, neutro. die by apoptosis, macrophage get rid of debris, after macrophage goes away.

24
Q

Abces definition?

A

Hole in tissue with collection of pus: NET

25
Q

2 types of macrophages?

A

Classic (M1) - attack microbes

Alternatively (M2) - Tissue repair

26
Q

Chronic inflammation results in?

A

a) Angiogenesis: continuous new vessels formed
b) Monocytes continuously getting activated
c) Fibrosis

27
Q

Chronic inflammation causes?

A

Persistent injury

28
Q

Granuloma definition?

A

Center: macrophage, some multinucleated giant cells around object of injury.
Surround: T-cells

29
Q

Granuloma Eg.

A

Splinter

Tuberculosis

30
Q

Morphologic patterns of inflammation?

A 
1-Serous: blisters
2-Fibrinous: Deposition of fibrin due to more severe injury
3-Abces (purulent/suppurative)
4-Ulcer
5-Membranous
31
Q

Eg of fibrinous inflammation?

A

a) Streptococcal inflammation: Fibrin removed at the end

b) Legionnaires’ disease: Fibrin not removed = dead alveoli

32
Q

Membranous inflamm. Eg.

A

Diphtheria: membrane in throat

33
Q

Systemic effects of inflammation (3) with cause?

A

1-Fever: Due to prostaglandins, reason b/c leukocytes speed increases
2-Leukocytis: Increase prod. in bone marrow
3-Acute phase response by liver: Increase mediators prod. Eg. C-Reactive p+ ->Opsonin, chemotactic

34
Q

Tissue regeneration 3 major types of cells and their reaction to injury?

A

1) Labile cells: Turning over all the time (Eg. Keratinocytes)
2) Stable cells: Not turning over all the time, but they can (Eg. Hepatocytes, however if architecture damaged, results in scaring)
3) Permanent cells: Cant be replaced (Eg.Neurons, if cell body still alive, can repair)

35
Q

What is Wallerian degeneration?

A

Regeneration of myelinated axons by Schwann cells (they normally myelinate axons) guidance.

36
Q

If repair is impossible?

A

replacement happens

37
Q

Granulation tissue contains?

A

Macrophage, fibroblast, necrotic cells, new blood vessels

38
Q

Macrophage stimulate…(2) in tissue replacement?

A

Angiogenesis

Fibrogenesis: prod scar tissue

39
Q

Fibroblast role?

A
  • Lay down collagen for formation of Extra-Cellular Matrix (ECM)
  • transform into myofibroblast and are contractile
40
Q

Wound contraction occurs b/c?

A

fibroblast ->myofibroblast->contract

41
Q

Explain: Wound -> Inflammation -> Proliferation -> Tissue remodeling

A

a) Inflam: 1-5 days
b) Proliferation: Granulation tissue (3-21days)
c) wound contraction, reepithelialization, scar tissue formation (14 days-2years)

42
Q

Different intention repairs?

A

Primary: surgical with suture
Secondary: Large wound ->granulation tissue->large scar

43
Q

Keloid tissue?

A

Too much secretory fibroblast, produce large scar tissue.

Improve with age

PATH 300 (Xavier) (34 decks)

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