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Patho Fall 2019 > Ex2L4 > Flashcards

Ex2L4 Flashcards

(81 cards)

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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
Redness is d/t
Vasodilation, increased BF
26
Pain during inflammatory response is d/t
1. Injury | 2. Inflammatory mediators increase sensitivity of pain nerve fibers in area
27
Once cytokines send message to body, what occurs next
Phagocytes migrate to area of inflammation
28
First responder to inflammation site
Neutrophils
29
Second responder to site of inflammation
Macrophages
30
Once phagocytes arrive to area of inflammation, what occurs?
1. Adhere to endothelial lining 2. Transmigration 3. Engulf bacteria - make mess/damage area
31
Transmigration
Phagocytic cells squeeze thru pores to get to interstitial space
32
Difference between neutrophil and macrophage at inflammation
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
33
Inflammation occurs as a response to
1. Injured tissue releases cytokines 2. Injury activates mast cells 3. Macrophages detect pathogen
34
Important players in activating inflammatory response
Macrophages | Mast cells
35
Why does blood flow become sluggish during inflammation?
Vascular stasis - helps keep mediators in area and Isolate possible area of infxn
36
Cellular migration towards chemical mediatory
Chemotaxis
37
Normal inflammation
ACUTE - short lived
38
Chronic inflammation is
Always pathogenic
39
Cytokines released when macrophage senses pathogen —> acute vascular effects/cellular effects
IL-1 TNFa IL-6
40
All cytokines released from activated macrophage is responsible for
Fever
41
2 cellular initiators of inflammation
Macrophage | Mast cell
42
Mast cell
Lives in tissue among capillaries, packed with histamine
43
Mast cell triggers inflammation d/t
Injury in area IL-1 IgE Compliment proteins
44
Hypersensitivity reaction is d/t
IgE antibody
45
Mast cell activation causes
1. Degranulates: spits out contents (histamine, chemotaxis factors) 2. Synthesize prostaglandin/leukotreines
46
Site of vascular events during inflammation
Microvasculature (venule, capillary, arterioles)
47
Cellular events of inflammation
Chemotaxic migration Adhesion Transmigration
48
Vascular events of inflammation
Increased permeability, vasodilation, delayed vascular stasis
49
Adhesion proteins
1. Endothelial cells express adhesion protein on surface | 2. WBCs get to area - bind to adhesion protein
50
What ensures that WBCs don’t get swept past area of injury?
Adhesion proteins on endothelial wall
51
WBC squeezes through gaps of endothelium to get to interstitial space
Transmigration
52
Complement system purposes
Promotes inflammation Kill pathogen Opsonization
53
Opsonization
Tap pathogen for later killing
54
Activation of complement system
1. Presence of pathogen (bloodstream) 2. Systemic inflammatory response 3. Adaptive immunity (antibody-mediated)
55
2 proteins that stick to pathogen surface
C-Reactive Protein Manosbinding Lectin (MBL) *produced by liver
56
Kinin system is composed of
Inactive proteins (kininogens) —> convert into inflammatory mediators (kinins) in presence of kallikrein (Factor 12)
57
What releases Factor 12
Neutrophils | *F12=kallikrein
58
Activated kinin result in
- complement system activation - localized vasodilation/cap permeability - activate pain receptors - chemotaxins
59
Determines when inflammation should go on /healing response turns on
Macrophages
60
Clotting cascade goal
Form thrombin in order to convert fibrinogen | —>fibrin
61
Protein strands in bloodstream are formed into clot by
+thrombin =fibrin Protein strands form into cross links, net that suspends RBCs
62
Blood clot
Gelatinous state of fibrin suspending RBCs
63
Increases risk for blood clot
Inflammation
64
Thrombin promotes
Kinin activation | Inflammation
65
No sign of original injury
Complete resolution
66
Ideal circumstance of inflammation
Injury —> acute inflammation —> complete resolution
67
Dysfunctional healing occurs d/t
1. Infection (inflammation ruins healed tissue — scar/fibrosis) 2. Chronic inflammation
68
Problem with Fibrosis
Increased collagen, inelastic, scar tissue, LOST FUNCTION
69
Occurs when source of injury persists/does not go away
Chronic inflammation
70
Chronic inflammation is also known as
Frustrated repair
71
Example of chronic inflammation - viral infection
Hepatitis of liver (fibrosis of liver)
72
Example of chronic inflammation - autoimmune disease
YOU do not go away
73
End point of dysfunctional healing
Fibrosis + loss of function
74
How is inflammation blocked?
1. Steroids | 2. NSAIDS
75
Adverse effect of steroids
Children - stunt growth
76
Last resort of autoimmune diseases
Immunosuppressant - risk for infxn + cancer
77
Primary or secondary intention - which more likely = complete resolution?
Primary
78
Causes of chronic inflammation
1. Persistent infxn 2. Prolonged exposure to toxic agents (endo/exogenous—HTN, elevated HDL, smoking for atherosclerosis) 3. Autoimmunity
79
Cell that directs healing or dysfunctional healing
Macrophage
80
Primary intention of healing
1. Minimal tissue loss, clean approximation 2. Involves sealing- epithelialization 3. Wound shrinkage - contraction that pulls wound back together
81
Secondary intention of healing
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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