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Patho Fall 2019 > Ex2L4 > Flashcards

Ex2L4 Flashcards

1
Q

Pathogen will encounter _____ first when entering body

A

Innate immunity

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2
Q

Pathogens are detected first by

A

Tissue macrophage

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3
Q

Tissue macrophages are

A

Phagocytic cells

Start off as monocytes

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4
Q

Most likely group of cells that take up vaccine

A

Macrophage

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5
Q

One of most important lines of defense in innate immune system

A

Inflammatory response

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6
Q

Two events that lead to inflammatory response

A

Tissue injury

Presence of pathogen

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7
Q

Once inflammatory response occurs, what happens next?

A

Macrophage exits tissue, enters interstitial space, enter lymphatic system, travel thru until finds CD4 T cell (T Helper cell). CD4 T cell (general) is given antigen by macrophage, T helper cell begins adaptive immune response

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8
Q

Cytokine

A

“Cyto”- cell
“Kine” - circulatory protein that signals something
* cell derived signaling proteins

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9
Q

IL-1

A

Proinflammatory cytokine

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10
Q

Cytokine relevant to septic shock

A

TNF-a (alpha)

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11
Q

Strong immune system leads to

A

Allergies, hypersensitivity

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12
Q

What type of immune system is ideal

A

Not strong, but one that has “been around the block”

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13
Q

Chemical barriers of innate immune system

A

Normal flora (microbiome), mucous membrane enzymes, acid in stomach

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14
Q

Immune System - First line of defense

A

Barriers (chemical/physical/microbial)

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15
Q

Immune system - Second line of defense

A

Inflammation

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16
Q

Phagocytic cells

A

Macrophage
Dendritic cells
Neutrophils

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17
Q

Responsible for effect in plasma protein systems

A

Last protein in cascade

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18
Q

Outcomes of complement system

A
  1. Triggers inflammation
  2. Creates proteins that opsinize (tag) pathogens
  3. Membrane attack complex
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19
Q

Most effective portion of complement system

A

Membrane attack complex (forms hole in pathogen, pathogen dies)

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20
Q

Produces pro-inflammatory mediators (bradykinin)

A

Kinin system

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21
Q

Acute phase response results in

A

Prodromal s/s infxn

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22
Q

Events that guarantee inflammatory response

A

Cell/tissue injury OR

Presence of pathogen

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23
Q

Typical inflammatory response

A

Redness, swelling, pain

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24
Q

Swelling during inflammation is d/t

A
  • increased Capillary permeability

- leaking of albumin

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25
Q

Redness is d/t

A

Vasodilation, increased BF

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26
Q

Pain during inflammatory response is d/t

A
  1. Injury

2. Inflammatory mediators increase sensitivity of pain nerve fibers in area

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27
Q

Once cytokines send message to body, what occurs next

A

Phagocytes migrate to area of inflammation

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28
Q

First responder to inflammation site

A

Neutrophils

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29
Q

Second responder to site of inflammation

A

Macrophages

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30
Q

Once phagocytes arrive to area of inflammation, what occurs?

A
  1. Adhere to endothelial lining
  2. Transmigration
  3. Engulf bacteria - make mess/damage area
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31
Q

Transmigration

A

Phagocytic cells squeeze thru pores to get to interstitial space

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32
Q

Difference between neutrophil and macrophage at inflammation

A

Neutrophils die, cause damage at site
Macrophage do same + eat dead neutrophils, enter lymphatic system, node —> node, find appropriate CD4 T Cell to present to

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33
Q

Inflammation occurs as a response to

A
  1. Injured tissue releases cytokines
  2. Injury activates mast cells
  3. Macrophages detect pathogen
34
Q

Important players in activating inflammatory response

A

Macrophages

Mast cells

35
Q

Why does blood flow become sluggish during inflammation?

A

Vascular stasis - helps keep mediators in area and Isolate possible area of infxn

36
Q

Cellular migration towards chemical mediatory

A

Chemotaxis

37
Q

Normal inflammation

A

ACUTE - short lived

38
Q

Chronic inflammation is

A

Always pathogenic

39
Q

Cytokines released when macrophage senses pathogen —> acute vascular effects/cellular effects

A

IL-1
TNFa
IL-6

40
Q

All cytokines released from activated macrophage is responsible for

A

Fever

41
Q

2 cellular initiators of inflammation

A

Macrophage

Mast cell

42
Q

Mast cell

A

Lives in tissue among capillaries, packed with histamine

43
Q

Mast cell triggers inflammation d/t

A

Injury in area
IL-1
IgE
Compliment proteins

44
Q

Hypersensitivity reaction is d/t

A

IgE antibody

45
Q

Mast cell activation causes

A
  1. Degranulates: spits out contents (histamine, chemotaxis factors)
  2. Synthesize prostaglandin/leukotreines
46
Q

Site of vascular events during inflammation

A

Microvasculature (venule, capillary, arterioles)

47
Q

Cellular events of inflammation

A

Chemotaxic migration
Adhesion
Transmigration

48
Q

Vascular events of inflammation

A

Increased permeability, vasodilation, delayed vascular stasis

49
Q

Adhesion proteins

A
  1. Endothelial cells express adhesion protein on surface

2. WBCs get to area - bind to adhesion protein

50
Q

What ensures that WBCs don’t get swept past area of injury?

A

Adhesion proteins on endothelial wall

51
Q

WBC squeezes through gaps of endothelium to get to interstitial space

A

Transmigration

52
Q

Complement system purposes

A

Promotes inflammation
Kill pathogen
Opsonization

53
Q

Opsonization

A

Tap pathogen for later killing

54
Q

Activation of complement system

A
  1. Presence of pathogen (bloodstream)
  2. Systemic inflammatory response
  3. Adaptive immunity (antibody-mediated)
55
Q

2 proteins that stick to pathogen surface

A

C-Reactive Protein
Manosbinding Lectin (MBL)
*produced by liver

56
Q

Kinin system is composed of

A

Inactive proteins (kininogens) —> convert into inflammatory mediators (kinins) in presence of kallikrein (Factor 12)

57
Q

What releases Factor 12

A

Neutrophils

*F12=kallikrein

58
Q

Activated kinin result in

A
  • complement system activation
  • localized vasodilation/cap permeability
  • activate pain receptors
  • chemotaxins
59
Q

Determines when inflammation should go on /healing response turns on

A

Macrophages

60
Q

Clotting cascade goal

A

Form thrombin in order to convert fibrinogen

—>fibrin

61
Q

Protein strands in bloodstream are formed into clot by

A

+thrombin
=fibrin
Protein strands form into cross links, net that suspends RBCs

62
Q

Blood clot

A

Gelatinous state of fibrin suspending RBCs

63
Q

Increases risk for blood clot

A

Inflammation

64
Q

Thrombin promotes

A

Kinin activation

Inflammation

65
Q

No sign of original injury

A

Complete resolution

66
Q

Ideal circumstance of inflammation

A

Injury —> acute inflammation —> complete resolution

67
Q

Dysfunctional healing occurs d/t

A
  1. Infection (inflammation ruins healed tissue — scar/fibrosis)
  2. Chronic inflammation
68
Q

Problem with Fibrosis

A

Increased collagen, inelastic, scar tissue, LOST FUNCTION

69
Q

Occurs when source of injury persists/does not go away

A

Chronic inflammation

70
Q

Chronic inflammation is also known as

A

Frustrated repair

71
Q

Example of chronic inflammation - viral infection

A

Hepatitis of liver (fibrosis of liver)

72
Q

Example of chronic inflammation - autoimmune disease

A

YOU do not go away

73
Q

End point of dysfunctional healing

A

Fibrosis + loss of function

74
Q

How is inflammation blocked?

A
  1. Steroids

2. NSAIDS

75
Q

Adverse effect of steroids

A

Children - stunt growth

76
Q

Last resort of autoimmune diseases

A

Immunosuppressant - risk for infxn + cancer

77
Q

Primary or secondary intention - which more likely = complete resolution?

A

Primary

78
Q

Causes of chronic inflammation

A
  1. Persistent infxn
  2. Prolonged exposure to toxic agents (endo/exogenous—HTN, elevated HDL, smoking for atherosclerosis)
  3. Autoimmunity
79
Q

Cell that directs healing or dysfunctional healing

A

Macrophage

80
Q

Primary intention of healing

A
  1. Minimal tissue loss, clean approximation
  2. Involves sealing- epithelialization
  3. Wound shrinkage - contraction that pulls wound back together
81
Q

Secondary intention of healing

A
  1. Large wound, not approximated
  2. More extensive/prolonged epithelialization, likely looks different (scar)
  3. More contraction of underlying tissue

Patho Fall 2019 (13 decks)

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