Inflammation Flashcards
(94 cards)
1
Q
Is a sistemic and local reaction of tissues and microcirculation to a pathogenic insult
A
inflammation
2
Q
Mention the 5 key signs of inflammation
A
Heat Pain Redness Swelling Fuctio Laesa
3
Q
When the 4 key signs of inflammation combined, that produces a
A
Temporary loss of function (Functio Laesa)
4
Q
Goals of inflammation are
A
Respond to stimuli Restore balance Eliminate the cause Clearing out necrotic cells Tissue repair
5
Q
Types of trigger factors of inflammation
A
External or internal factors
6
Q
Types of external trigger factors of inflammation
A
Non microbial
Microbial
7
Q
What are the non microbial external factors of inflammation?
A
Allergens
Irritants
Toxins
8
Q
What are the microbial external factors of inflammation?
A
Virulence factors
PAMPs
9
Q
PAMPs
A
Pathogen Associated Molecular Patterns
10
Q
Help pathogen to colonize tissues and cause and infection
A
virulence factors
11
Q
Are recognized by our inmune system and trigger and inflammatory response
A
PAMPs and DAMPs
12
Q
DAMPs
A
Damage Associated Molecular Paterns
13
Q
DAMPs released when
A
plasma membrane injured or cell dies
14
Q
PAMPs and DAMPs are recognized by PRRs as ____ and activate the inflammatory response
A
Toll Like Receptors (TLRs)
15
Q
PAMPs could be
A
Polysaccharide
Peptidoglycan
RNA segment
16
Q
DAMPs appears when the cell is in
A
danger
17
Q
Characteristics of PRRs
A
Activate cell
Spark inflammatory response
Non specific
18
Q
Types of leukocytes
A
Granulocytes
Agranulocytes
19
Q
Mention the granulocytes
A
Neutrophil
Eosinophil
Basophil
Mast cells
20
Q
Mention the agranulocytes
A
Monocyte
Lymphocyte
21
Q
Mention the monocytes
A
Macrophages
Dendritic cells
22
Q
Are the first cells who phagocyte the pathogens
A
Neutrophils
23
Q
Control mechanisms associated with allergy
A
Eosinophil
24
Q
Basophils contain
A
histamine and heparin
25
Granulocytes that secrete an antibody
Lymphocyte
26
Eat a pathogen and present to T lymphocyte to activate the adaptive inmune system
Dendritic cells
27
Granules has inflammatory mediators which are
Histamine
Serotonin
Cytokines
Eicosanoids
28
Which are the eicosanoids?
Prostaglandins
| Leukotrienes
29
Describe the process of inflammation
The tissue got injured
Macrophages phagocyte the pathogen
The endothelial cells separate and the vascular permeability increased and there is a vasodilation
30
Vasodilation is produced by an increased in
Nitric oxide
31
Is when the macrophage squeeze him between endothelium cells and arrive to injured tissue
Extravasation
32
Complement system are activated in presence of
pathogens
33
Function of complement system
Attract leukocytes
Help with opsonization
Kill pathogens
34
In tissue repair growth factors released to _____
angiogenesis
35
Synthesize collagen and helps with wound healing
Fibroblasts
36
Is the creation of new blood vessels
Angiogenesis
37
What happen after the neutrophil phagocyte the pathogen?
the neutrophil die by itself (like suicide)
38
Mention the 4 steps for the modulation of inflammatory response
1. Initiation
2. Amplification
3. Destruction
4. Termination
39
Is the step for the modulation of inflammatory response where cells are released by trigger factors and circulate inflammatory cells producing an acute inflammation
Initiation
40
Cells which are released to an inflammatory response
Cytokines
Chemokines
Platelets
Neutrophils
41
Is the step for the modulation of inflammatory response where leukocytes and macrophages are released to continue the inflammation. Also the system of complement is active
Amplification
42
Is the step for the modulation of inflammatory response where the enzymatic digestion, phagocytosis and damaged tissue is removed
Destruction
43
Is the step for the modulation of inflammatory response where the damage to normal cells is prevent
Termination
44
Principle which explains the pression between extravascular and intravascular space
Starling principle
45
Components of the Starling Principle
Hydrostatic pressure
Oncotic pressure
Osmotic pressure
Lymph flow
46
Accumulation of fluid in the extravascular space and interstitial tissues
Edema
47
Types of edema
Non inflammatory edema
| Inflammatory edema
48
Types of non inflammatory edema
Lymphedema
| Thrombosis
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Type of edema which disrupt the lymphatic flow
Lymphedema
50
Obstruction of venous outflow
Thrombosis
51
Characteristics of an inflammatory edema (triple response)
Transient vasoconstriction of arterioles
Vasodilation of precapillary arterioles
Increase in endothelial cells barriers permeability
52
Accumulation of fluid in some body spaces
Effusion
53
Types of effusion
Transudative
| Exudative
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Effusion that occurs due to increased hydrostatic pressure or low plasma oncotic pressure
Transudative
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Effusion that occurs due to inflammation and increased capillary permeability
Exudative
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Difference between transudative and exudative
Transudative-->low in protein and LDH
| Exudative-->high in protein and LDH
57
If we have 1 or more of this 3 criteria is an exudate
Serum protein >0.5
Serum LDH >0.6
LDH > 2/3 upper limit normal for serum
58
Types of exudate
Serous exudate
Serosanguineous
Fibrinous exudate
Suppurative inflammation
59
Inflammation purulent exudate with significant liquefactive necrosis
suppurative inflammation
60
Exudate with large amounts of fibrins due to inflammation
Fibrinous exudate
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Exudate with an infusion with blood
Serosanguineous
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Exudate color white with yelow
Serous exudate
63
Factor XII is also known as
Hageman Factor
64
Function of factor XII
Converts plasminogen to plasmic
Activate the Kallikrein
Activation of Coagulation System
65
There are 2 routes to synthesize arachidonic acid
Phosphatidylcholine
| Phosphatidylinositol-P2
66
Etiology of chronic inflammation
Failure of eliminating
Exposure to irritants
Autoimmune disorder
Oxydative stress
67
Risk factors associated with chronic inflammation
```
Age
Obesity
Diet
Smoking
Low sex hormones
Stress and sleep disorders
```
68
Management for chronic inflammation
```
Low glycemic diet
Metformine
Reduce intake of fats
Statins
NSAIDs
Corticosteroids
```
69
Could the NSAIDs be used in every inflammatory process? Why?
No, because they can interfere delay with the healing process
70
Which could be the consequences of using NSAIDs during an inflammatory process?
Production of prostaglandins
| Increase local blood flow and vascular permeability
71
The _______ phase is an important part of healing and, without it, healing would not occur
inflammatory
72
Do NSAIDs interfere with healing?
Yes, inhibiting the COX
73
When the COX is inhibited, we are also blocking the production of
prostaglandin
74
NSAIDs have a _____ effect on wound healing
depressant
75
When do we have to use cold therapy?
Accute pain
76
Why do we use cold therapy in the first 48 hrs?
To reduce blood flow and slow inflammation
| Decrease swelling and pain
77
When do we have to use heat therapy?
Chronic pain
78
Why do we use heat therapy for chronic pain?
Will dilate the blood vessels, Promote blood flow
79
Ice therapy is most effective when applied early and frequently during the first ____ after an acute injury
48 hrs
80
Cold therapy should not be used for a chronic injury because it can increase
stifness
81
Is a disorder that causes immunodeficiency, resulting in recurrent bacterial and fungal infections. This patient have granulomas in various tissues
Granulomatous Disease
82
Pathophysiology of GD
Inability to phagocytes kill microbes caused by several defects in NADPH
83
Most patients of GD are males who has mutations on the gene coding for
gp91phox
84
Patients with GD are susceptible to _____ organisms
catalase-positive
85
Collections of immune cells that cluster when the can't kill pathogens
granulomas
86
Mention 2 classical mutations in GD in genes for NADPH oxidase
Autosomal recessive
| X-linked recessive
87
Mention the 2 pathways of arachidonic acid
Cyclooxigenase pathway
| 5-lipooxygenase pathway
88
COX1 and COX2 produce
```
Prostaglandin E2 (PGE2)
Prostaciclin (PGI2)
```
89
Pathophysiology of Rheumatoid Arthritis
Hyperplasia of synovial membrane
90
____ and ____ stimulate the expresión of adhesion molecules on endothelial cells and increase the recruitment of neutrophils into the joint is RA
IL-1
| TNF-a
91
Neutrophils release ____ and ____ which degrade proteoglycan in the superficial layer of cartilage in RA
elastase and proteases
92
Chronic autoimmune inflammatory disease that results in progressive destruction of articular cartilage
Rheumatoid Arthritis
93
Mention the autoantibodies that produce RA
```
Rheumatoid factor (RF)
Anti CCP
```
94
In RA, T cells stimulate B and secrete cytokines such as _______ and macrophages such as ____ which are pro inflammatory cells
INF gamma and IL-17
| IL-1 and IL-6
