Cell Inflammation And Repair - Dobson (Ch3) Flashcards
(104 cards)
1
Q
Acute infection
A
Mostly N
Exam date fluid + plasma , dilate small a, increase permeability, accumulation of N
Innate
2
Q
Chronic inflammation
A
Adaptive
Mostly M and Lymphocytes
Deposited CT, new BVs, more tissue destruction
3
Q
Pus
A
Exaudate fluid
4
Q
Histamine
A
Vasodilation
Also caused by microbes, burns (can cause severe fluid loss in huge burns)
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**
6
Q
What happens to endothelium when there is stasis
A
It gets activated allowing N to enter
7
Q
Immediate transient response
A
BV get leaky by endothelial contractions and happens fast
8
Q
Lymphangitis
A
Inflamed Lymph vessels
9
Q
Lymohadenitis
A
Inflamed Lymph nodes , due to hyperplasia of LN
10
Q
Stasis and erythema caused by
A
Histamine
11
Q
Vascular permeability caused by
A
Histamine and kin in
12
Q
Neutrophils do what to enter the site of where it is needed
A
- N (integrin) Binds to activated endothelium (P and E selectin)
- N does rolling until (intergrin, and selectins) bind to an ICAM integrin on endothelium
- Transmigration through endothelium (CD31, PECAM-1)
- Chemotaxis to right tissue
13
Q
What activated the endothelium
A
TNF, IL1secreted from local M
14
Q
Where are P and E selectins stored
A
In granules called Weibel-Palade Bodies
15
Q
Transmigration of N
A
Also called Diapedesis
Postcapillry venoules
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)
17
Q
When N get chemotaxis signal what happen
A
It grows filopedia
18
Q
Drug that manages chronic inflammation
A
TNF blocker
19
Q
N phagocytosis uses what
A
Mannose receptor for bacteria, scavenger receptor (on M for LDL)
IgG
20
Q
N engulfment uses what
A
Pseudopods making a phagosome around particle , fusing with lysosome
21
Q
What do lysosomes have
A
ROS and NO
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
23
Q
What cytokines activated N and M
A
INF-g
24
Q
N NETs are depended on what
A
Platelet activation
25
What secretes Histamine
| Function
Mast , B, Platelets
| Vasodilation, in crease permeability, activate endothelium
26
What secretes Prostaglandins
| Function
Mast, Leukocyte
| Vasodilation, fever, pain
27
What secretes Leukotriens
| Function
Mast, Leukocytes
| Increase permeability, chemotaxis, leukocyte adhesion + activation
28
What makes Aracidonic acid
Phospholipases in leukocytes and mast cells
29
What 2 things does aracidonic acid make
Cyclooxygenase ——> Prostaglandins
| 5-Lipoxygenase ——> 5-HPETE ——> leukotriens
30
Cycloogygenase makes what 3 things downstream
1. Prostacyclin PGl2 = vasodilation + inhibit platelets aggregation
2. Thromboxane A2 TXA2= vasoconstriction + platelets aggregation
3. PGD2 and PGE2 = vasodilation + permeability
31
What inhibits cyclooxygenase
COX 1 and COX 2 inhibitors like aspirin
32
What inhibits phospolipase
Steroids
33
What does a 5-Lipoxygenase make
1. 5- HPETE (chemotaxis) ——> Leukotrien A4, B4, C4, D4, E4
| 2. 12-Lipoxygenase ——> Lipoxin A4, B4
34
Leukotriene A4
Becomes B4 = chemotaxis, N adhesion
35
Leukotriene C4, D4, E4
Bronchospasm (constriction), permeability , vasoconstriction
36
Lipoxin A4, B4
Inhibits inflammation
37
5-Lipoxygenase or its receptor inhibitor
Zileuton or Montelukast , medication for asthma
38
TNF and IL1
```
From M and DC
Promoting N adhesion and transmigration
Activate endothelium
Fever (infection, injury)
Sepsis (bacteria)
```
39
Acute inflammation cytokines
TNF, IL1, IL6, IL17, chemokines
40
Chronic inflammation cytokines
IL12, IL17, IFN-g
41
Prolonged TNF can lead to
Cachexia
42
Nest antinflammatory for chronic infections
TNF antagonist
43
CXC chemokine
CX3C
CC
IL8
Fractalkine
MCP-1
44
Homeostatic chemokines
Those that are always produced by the tissue
45
Classical pathway
IgM and IgG to C1
46
Alternative pathway
By microbial urbane like polysaccharides, toxins
47
Leptin pathway
By MBL activating C1
48
MAC complex formed on
Bacteria like Neisseria
49
Anaphylactic mediators
C3a C5a
50
Opsonizing mediators
C3b, promote phagocytosis by N or M
51
X C1 inhibitor
Cant stop CP
| = Hereditary Angioedema
52
DAF and CD59
| And what happens if you have X of these
DAF : ——I
CD59 : ——I MAC
= if X DAF and CD59 = paroxysmal nocturnal hemoglobinuria
53
PAF
Platelet activating factor
| Vasoconstriction, bronchoconstriction, platelet aggregation
54
Bradykinin
Vasodilation, permeability, SM contractions, pain
| = similar to histamine
55
Pain is due to
Bradykinin and prostaglandins (also fever and vasodilation)
56
Axz```¸
Åvbfew
57
Serous Inflammation
```
Exaudate fluid (in peritoneum pericardium pleura)
= local irritation, effusion, heart failure, skin blister (usually not inflammatory)
```
58
Fibrinoid inflammation
Fibrinogen and fluid pass out (fibrous exudate)
= pro-coagulation stimulus, pericardium, meningies, pleura
= can lead to scarring
59
Purulent = Suppurative Inflammation
Abscess, PUS, exudate with N, liquefied debris from necrotic cells, edema fluid
= Liquefactive tissue (bacteria like staph, pyogenic*)
= inflammation happens here
60
Ulcers
Surface of organ or tissue shedding necrotic cells or defected
= mouth mucosa, stomach (peptic ulcer), GI, GU, skin (esp lower extremities)
61
3 outcomes of acute inflammation
1. Complete resolution
2. Healing by CT (scarring)
3. Becomes chronic inflammation
62
Organization in this chapter means
Exudate becomes fibrous tissue = fibrosis
63
3 types of chronic inflammation
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
3 things that are hallmarks of chronic inflammation
1. Mononuclear cells come (M, Lymphocytes, plasma cells)
2. Tissue Destruction (persistent stimulus)
3. Healing attempts (CT, angiogenesis of small BV, fibrosis)
65
M come form
Hematopoietic stem cells in BM and embryonic yolk sac and fetal liver
66
2 major ways to activate M
| Classical
1. Endotoxins or microbe ——> TLR, IFN-g from T-cells ——> activation
2. Make ROS and NO, lysosomes, secrete IL1, IL12, IL23
* ***M1
67
2 major ways to activate M
| Alternative
1. IL4, IL13 made by T-cells, and E activate M
2. Secrete TGF-B, IL10, growth repair, anti inflammatory, angiogenesis, collagen
* ***M2
68
Th1
Th2
TH17
Th1 : IFN-g ——> M1
Th2 : IL4, IL5, IL13 ——> E——> M2
TH17 : IL17——> IL8 to get N
69
Tertiary Lymphoid Organs
| What is it and where do you usually see it
Accumulation of lymphocytes, APCs, Plasma cells in LN
= lymphoid organogenesis
1. chronic RA
2. Hashimoto’s Thyroiditis
70
What to eosinophils have
Major Basic Protein
71
Mast cells have what
FceRI receptors that bind to Fc of IgE
| = release of PGD +Histamines = anaphylactic shock
72
N is chronic inflammation
Can persist for months
73
Granulomatous inflammation
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
Epithelioid cell
M that has taken in so much cytoplasm that it looks epithelial like
75
Giant cells
M that fuse and are nultinucleated = Langerhans giant cells
76
Types of diseases that have granulomatous inflammation
```
TB
Leprosy
Syphilis
Cat-scratch D
Sarcoidosis
Crohns (IBD)
```
77
Acute phase reactions
| 3 types
```
Inflammation that involves cytokines induced systemic response
IL1, IL6, TNF
1. Fever
2. Acute phase Proteins
3. Leukocytosis
```
78
What is important mediators in fever
IL1 TNF, LPS on bacteria = PYROGENS which increase cyclooxygenase to make
Prostaglandins
79
What is important mediators in making acute phase proteins
| 3 types
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
Chronic CRP can cause
1. MI due to activating plaques more easily
| 2. Anemia due to ACPs increase hepcidin
81
What is important mediators in Leukocytosis
Bacteria infection
TNF And IL1 cause release of cells from BM = more immature N in blood = LEFT SHIFT
(Eosinophilia, neutrophilia)
82
Erythrocytes sedimentation rate
Higher rate = more stacked RBCs = good indicator that inflammation is happening
83
Regeneration in tissue repair
What is it
3 things it needs
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
Labile tissues
Continuously dividing lost and replaced
Hematopoietic cells, skin , vagina, GI
= CSFs
85
Stable tissues
Quiescent cells in G0
= divide for repair
= usually in parenchyma (kidney, pancreas, liver. Lung, thyroid)
= fibroblasts , endothelial , SM cells
86
Permanent tissues
Terminally differentiated postnatal life (brain and heart)
| = scar is made and irreversible damage
87
Regeneration of the liver is done by
proliferation of the hepatocytes and repopulation of progenitor cells
By cytokines and polypeptide GFs
88
Steps in regeneration of the liver
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
When can hepatocytes not regenerate
| What happens then
During chronic liver injury or chronic inflammation
| = depends on progenitor cells becoming hepatocytes
90
Steps in scar formation
* ***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
What degrades the ECM to allow for vascular remodeling
MMPs
92
What recruits SM
TGF-B
93
Deposition of CT needs what factors
1. TGF-B****, makes scar and from M2
2. FGF-2
3. PDGF
94
What helps with contraction of scar over time
Myofibrils = fibrinogen with SM and actin
95
What shuts MMPs down after remodeling is done
TIMPs from mesenchyme last cells
96
Drug that inhibits collagen and CT deposition
Steroids (anti-inflammatory)
97
Healing with first intention happens when
Injury to only the first layer
= inflammation ——> epithelial regeneration and proliferation happens——> CT maturation
EX : Surgical incision healing
98
Healing with first intention
| Steps
1. vasodilation (VEGF)
2. N
3. M + fibroblasts + new capillaries
4. Fibrous union formed and normal tissue thickness and epithelium
99
Healing with second intention happens when
Large wounds, ulcers, abscesses, ischemic necrosis(MI), in parenchymal organs
100
Healing with second intention
| Steps
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
Not good scar tissue formation can lead to what 2 complications
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
Excessive scar tissue made can lead to what 2 things
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
Desmoids and aggressive fibromatoses
When the exuberant granulation tissue and fibroblasts keep growing after surgical removal - tumor like
104
Contracture
Too much contraction of a scar (usually palms, soles, anterior thorax)from burns usually
Can compromise joint movement
