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MOD Midterm > Cell Inflammation And Repair - Dobson (Ch3) > Flashcards

Cell Inflammation And Repair - Dobson (Ch3) Flashcards

1
Q

Acute infection

A

Mostly N
Exam date fluid + plasma , dilate small a, increase permeability, accumulation of N
Innate

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2
Q

Chronic inflammation

A

Adaptive
Mostly M and Lymphocytes
Deposited CT, new BVs, more tissue destruction

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3
Q

Pus

A

Exaudate fluid

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4
Q

Histamine

A

Vasodilation

Also caused by microbes, burns (can cause severe fluid loss in huge burns)

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5
Q

Vasodilation and increased permeability during acute inflammation causes what

A

Increased Blood viscosity
High RBC left in the small arteries
= this causes vascular congestion and redness in tissue = STASIS**

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6
Q

What happens to endothelium when there is stasis

A

It gets activated allowing N to enter

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7
Q

Immediate transient response

A

BV get leaky by endothelial contractions and happens fast

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8
Q

Lymphangitis

A

Inflamed Lymph vessels

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9
Q

Lymohadenitis

A

Inflamed Lymph nodes , due to hyperplasia of LN

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10
Q

Stasis and erythema caused by

A

Histamine

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11
Q

Vascular permeability caused by

A

Histamine and kin in

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12
Q

Neutrophils do what to enter the site of where it is needed

A
  1. N (integrin) Binds to activated endothelium (P and E selectin)
  2. N does rolling until (intergrin, and selectins) bind to an ICAM integrin on endothelium
  3. Transmigration through endothelium (CD31, PECAM-1)
  4. Chemotaxis to right tissue
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13
Q

What activated the endothelium

A

TNF, IL1secreted from local M

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14
Q

Where are P and E selectins stored

A

In granules called Weibel-Palade Bodies

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15
Q

Transmigration of N

A

Also called Diapedesis

Postcapillry venoules

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16
Q

How is chemotaxis working for the N
Endogenous
Exogenous

A

Endogenous : cytokines (IL8), arachadonic acid, leukotriene B4 (LTB4)
Exogenous: bacteria toxins (N-formylmethionone on N-terminal)

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17
Q

When N get chemotaxis signal what happen

A

It grows filopedia

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18
Q

Drug that manages chronic inflammation

A

TNF blocker

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19
Q

N phagocytosis uses what

A

Mannose receptor for bacteria, scavenger receptor (on M for LDL)
IgG

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20
Q

N engulfment uses what

A

Pseudopods making a phagosome around particle , fusing with lysosome

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21
Q

What do lysosomes have

A

ROS and NO

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22
Q

What do N have to kill

A

Azurophilic granules with MPO making halogenation for bacteria and lipid peroxidase for proteins and lipids oxidation

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23
Q

What cytokines activated N and M

A

INF-g

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24
Q

N NETs are depended on what

A

Platelet activation

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25
Q

What secretes Histamine

Function

A

Mast , B, Platelets

Vasodilation, in crease permeability, activate endothelium

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26
Q

What secretes Prostaglandins

Function

A

Mast, Leukocyte

Vasodilation, fever, pain

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27
Q

What secretes Leukotriens

Function

A

Mast, Leukocytes

Increase permeability, chemotaxis, leukocyte adhesion + activation

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28
Q

What makes Aracidonic acid

A

Phospholipases in leukocytes and mast cells

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29
Q

What 2 things does aracidonic acid make

A

Cyclooxygenase ——> Prostaglandins

5-Lipoxygenase ——> 5-HPETE ——> leukotriens

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30
Q

Cycloogygenase makes what 3 things downstream

A
  1. Prostacyclin PGl2 = vasodilation + inhibit platelets aggregation
  2. Thromboxane A2 TXA2= vasoconstriction + platelets aggregation
  3. PGD2 and PGE2 = vasodilation + permeability
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31
Q

What inhibits cyclooxygenase

A

COX 1 and COX 2 inhibitors like aspirin

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32
Q

What inhibits phospolipase

A

Steroids

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33
Q

What does a 5-Lipoxygenase make

A
  1. 5- HPETE (chemotaxis) ——> Leukotrien A4, B4, C4, D4, E4

2. 12-Lipoxygenase ——> Lipoxin A4, B4

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34
Q

Leukotriene A4

A

Becomes B4 = chemotaxis, N adhesion

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35
Q

Leukotriene C4, D4, E4

A

Bronchospasm (constriction), permeability , vasoconstriction

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36
Q

Lipoxin A4, B4

A

Inhibits inflammation

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37
Q

5-Lipoxygenase or its receptor inhibitor

A

Zileuton or Montelukast , medication for asthma

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38
Q

TNF and IL1

A 
From M and DC
Promoting N adhesion and transmigration 
Activate endothelium 
Fever (infection, injury)
Sepsis (bacteria)
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39
Q

Acute inflammation cytokines

A

TNF, IL1, IL6, IL17, chemokines

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40
Q

Chronic inflammation cytokines

A

IL12, IL17, IFN-g

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41
Q

Prolonged TNF can lead to

A

Cachexia

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42
Q

Nest antinflammatory for chronic infections

A

TNF antagonist

43
Q

CXC chemokine
CX3C
CC

A

IL8
Fractalkine
MCP-1

44
Q

Homeostatic chemokines

A

Those that are always produced by the tissue

45
Q

Classical pathway

A

IgM and IgG to C1

46
Q

Alternative pathway

A

By microbial urbane like polysaccharides, toxins

47
Q

Leptin pathway

A

By MBL activating C1

48
Q

MAC complex formed on

A

Bacteria like Neisseria

49
Q

Anaphylactic mediators

50
Q

Opsonizing mediators

A

C3b, promote phagocytosis by N or M

51
Q

X C1 inhibitor

A

Cant stop CP

= Hereditary Angioedema

52
Q

DAF and CD59

And what happens if you have X of these

A

DAF : ——I
CD59 : ——I MAC
= if X DAF and CD59 = paroxysmal nocturnal hemoglobinuria

53
Q

PAF

A

Platelet activating factor

Vasoconstriction, bronchoconstriction, platelet aggregation

54
Q

Bradykinin

A

Vasodilation, permeability, SM contractions, pain

= similar to histamine

55
Q

Pain is due to

A

Bradykinin and prostaglandins (also fever and vasodilation)

56
Q

Axz```¸

57
Q

Serous Inflammation

A 
Exaudate fluid (in peritoneum pericardium pleura)
= local irritation, effusion, heart failure, skin blister (usually not inflammatory)
58
Q

Fibrinoid inflammation

A

Fibrinogen and fluid pass out (fibrous exudate)
= pro-coagulation stimulus, pericardium, meningies, pleura
= can lead to scarring

59
Q

Purulent = Suppurative Inflammation

A

Abscess, PUS, exudate with N, liquefied debris from necrotic cells, edema fluid
= Liquefactive tissue (bacteria like staph, pyogenic*)
= inflammation happens here

60
Q

Ulcers

A

Surface of organ or tissue shedding necrotic cells or defected
= mouth mucosa, stomach (peptic ulcer), GI, GU, skin (esp lower extremities)

61
Q

3 outcomes of acute inflammation

A
  1. Complete resolution
  2. Healing by CT (scarring)
  3. Becomes chronic inflammation
62
Q

Organization in this chapter means

A

Exudate becomes fibrous tissue = fibrosis

63
Q

3 types of chronic inflammation

A
  1. Persistent infection (shows granulomatuous reaction)
  2. Hypersensitive disease (autoimmune, allergies)
  3. Prolonged exposure to toxin (endogenous ——> lipids and cholesterol leading to atherosclerosis, and exogenous ——> silica leading to silicosis)
64
Q

3 things that are hallmarks of chronic inflammation

A
  1. Mononuclear cells come (M, Lymphocytes, plasma cells)
  2. Tissue Destruction (persistent stimulus)
  3. Healing attempts (CT, angiogenesis of small BV, fibrosis)
65
Q

M come form

A

Hematopoietic stem cells in BM and embryonic yolk sac and fetal liver

66
Q

2 major ways to activate M

Classical

A
  1. Endotoxins or microbe ——> TLR, IFN-g from T-cells ——> activation
  2. Make ROS and NO, lysosomes, secrete IL1, IL12, IL23
    * ***M1
67
Q

2 major ways to activate M

Alternative

A
  1. IL4, IL13 made by T-cells, and E activate M
  2. Secrete TGF-B, IL10, growth repair, anti inflammatory, angiogenesis, collagen
    * ***M2
68
Q

Th1
Th2
TH17

A

Th1 : IFN-g ——> M1
Th2 : IL4, IL5, IL13 ——> E——> M2
TH17 : IL17——> IL8 to get N

69
Q

Tertiary Lymphoid Organs

What is it and where do you usually see it

A

Accumulation of lymphocytes, APCs, Plasma cells in LN
= lymphoid organogenesis
1. chronic RA
2. Hashimoto’s Thyroiditis

70
Q

What to eosinophils have

A

Major Basic Protein

71
Q

Mast cells have what

A

FceRI receptors that bind to Fc of IgE

= release of PGD +Histamines = anaphylactic shock

72
Q

N is chronic inflammation

A

Can persist for months

73
Q

Granulomatous inflammation

A

Chronic
Accumulation of M (giant and epithelioid), T-cells
Central necrosis, caseous necrosis
1. Foreign body granulomas = X t-cells, from foreign body (IV drug, sutures, M eat the body and no inflammation
2. Immune granulomas = T-cells make there due to persistent microbe or autoimmune (IL2 ——> IFN-g——> M)

74
Q

Epithelioid cell

A

M that has taken in so much cytoplasm that it looks epithelial like

75
Q

Giant cells

A

M that fuse and are nultinucleated = Langerhans giant cells

76
Q

Types of diseases that have granulomatous inflammation

A 
TB
Leprosy
Syphilis
Cat-scratch D
Sarcoidosis
Crohns (IBD)
77
Q

Acute phase reactions

3 types

A 
Inflammation that involves cytokines induced systemic response 
IL1, IL6, TNF
1. Fever
2. Acute phase Proteins
3. Leukocytosis
78
Q

What is important mediators in fever

A

IL1 TNF, LPS on bacteria = PYROGENS which increase cyclooxygenase to make
Prostaglandins

79
Q

What is important mediators in making acute phase proteins

3 types

A

IL6 ——> CRP and fibrinogen
IL1 +TNF ——> SAA
1. CRP = breaks down nuclear contents and opsonizing
2. Fibrinogen : cause RBC to stack (ROULEUX*)
3. SAA (serum amyloid A) : chronic inflammation

80
Q

Chronic CRP can cause

A
  1. MI due to activating plaques more easily

2. Anemia due to ACPs increase hepcidin

81
Q

What is important mediators in Leukocytosis

A

Bacteria infection
TNF And IL1 cause release of cells from BM = more immature N in blood = LEFT SHIFT
(Eosinophilia, neutrophilia)

82
Q

Erythrocytes sedimentation rate

A

Higher rate = more stacked RBCs = good indicator that inflammation is happening

83
Q

Regeneration in tissue repair
What is it
3 things it needs

A

Cell proliferation from stem cells that are quiescent and the ECM helps

  1. Remnants of old tissue to restore it
  2. Angiogenesis to get nutrients needed for repair
  3. Fibroblasts to make scar tissue in areas that are unrepairable
84
Q

Labile tissues

A

Continuously dividing lost and replaced
Hematopoietic cells, skin , vagina, GI
= CSFs

85
Q

Stable tissues

A

Quiescent cells in G0
= divide for repair
= usually in parenchyma (kidney, pancreas, liver. Lung, thyroid)
= fibroblasts , endothelial , SM cells

86
Q

Permanent tissues

A

Terminally differentiated postnatal life (brain and heart)

= scar is made and irreversible damage

87
Q

Regeneration of the liver is done by

A

proliferation of the hepatocytes and repopulation of progenitor cells
By cytokines and polypeptide GFs

88
Q

Steps in regeneration of the liver

A
  1. Priming : Kupffer secretes IL6—-> hepatocytes to make activating of parenchyma cells possible
  2. GF : HGF and TGF-B ——> primed hepatocytes
  3. Hepatocytes leave G0 and enter cell cycle
  4. Hepatocytes return to quiescent state
89
Q

When can hepatocytes not regenerate

What happens then

A

During chronic liver injury or chronic inflammation

= depends on progenitor cells becoming hepatocytes

90
Q

Steps in scar formation

A
  • CT deposition*
    1. angiogenesis (VEGF signal, Ang1 and2)
    2. Granulation tissue forms (loose CT) with some M2 (FGF2)
    3. Remodeling : CT reorganized and matures making scar
91
Q

What degrades the ECM to allow for vascular remodeling

92
Q

What recruits SM

93
Q

Deposition of CT needs what factors

A
  1. TGF-B**, makes scar and from M2
  2. FGF-2
  3. PDGF
94
Q

What helps with contraction of scar over time

A

Myofibrils = fibrinogen with SM and actin

95
Q

What shuts MMPs down after remodeling is done

A

TIMPs from mesenchyme last cells

96
Q

Drug that inhibits collagen and CT deposition

A

Steroids (anti-inflammatory)

97
Q

Healing with first intention happens when

A

Injury to only the first layer
= inflammation ——> epithelial regeneration and proliferation happens——> CT maturation
EX : Surgical incision healing

98
Q

Healing with first intention

Steps

A
  1. vasodilation (VEGF)
  2. N
  3. M + fibroblasts + new capillaries
  4. Fibrous union formed and normal tissue thickness and epithelium
99
Q

Healing with second intention happens when

A

Large wounds, ulcers, abscesses, ischemic necrosis(MI), in parenchymal organs

100
Q

Healing with second intention

Steps

A
  1. ECM and granulation tissue accumulation = large scar
  2. Type 3 collagen
  3. Type 1 collagen replaces it
  4. Myofibroblasts, wound contraction (tissue has smaller thickness)
101
Q

Not good scar tissue formation can lead to what 2 complications

A
  1. Dehiscence (rupture of wound form cough, V, D, increase P, usually after GI surgery)
  2. Ulceration : low vascularization and BF to the scar area during healing
102
Q

Excessive scar tissue made can lead to what 2 things

A
  1. Hypertrophic scar: a lot of collagen = raised scar (burn or deep injury)
  2. Keloid scar : if the above does not regress and grows beyond boundary (common in AAs)
  3. Exuberant granulation : a lot of granulation tissue so epithelium can regrow, needs to be surgically removed
103
Q

Desmoids and aggressive fibromatoses

A

When the exuberant granulation tissue and fibroblasts keep growing after surgical removal - tumor like

104
Q

Contracture

A

Too much contraction of a scar (usually palms, soles, anterior thorax)from burns usually
Can compromise joint movement

MOD Midterm (9 decks)

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