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Fisiopatología > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Is a sistemic and local reaction of tissues and microcirculation to a pathogenic insult

A

inflammation

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2
Q

Mention the 5 key signs of inflammation

A 
Heat 
Pain
Redness
Swelling
Fuctio Laesa
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3
Q

When the 4 key signs of inflammation combined, that produces a

A

Temporary loss of function (Functio Laesa)

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4
Q

Goals of inflammation are

A 
Respond to stimuli 
Restore balance
Eliminate the cause
Clearing out necrotic cells 
Tissue repair
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5
Q

Types of trigger factors of inflammation

A

External or internal factors

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6
Q

Types of external trigger factors of inflammation

A

Non microbial

Microbial

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7
Q

What are the non microbial external factors of inflammation?

A

Allergens
Irritants
Toxins

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8
Q

What are the microbial external factors of inflammation?

A

Virulence factors

PAMPs

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9
Q

PAMPs

A

Pathogen Associated Molecular Patterns

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10
Q

Help pathogen to colonize tissues and cause and infection

A

virulence factors

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11
Q

Are recognized by our inmune system and trigger and inflammatory response

A

PAMPs and DAMPs

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12
Q

DAMPs

A

Damage Associated Molecular Paterns

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13
Q

DAMPs released when

A

plasma membrane injured or cell dies

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14
Q

PAMPs and DAMPs are recognized by PRRs as ____ and activate the inflammatory response

A

Toll Like Receptors (TLRs)

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15
Q

PAMPs could be

A

Polysaccharide
Peptidoglycan
RNA segment

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16
Q

DAMPs appears when the cell is in

A

danger

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17
Q

Characteristics of PRRs

A

Activate cell
Spark inflammatory response
Non specific

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18
Q

Types of leukocytes

A

Granulocytes

Agranulocytes

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19
Q

Mention the granulocytes

A

Neutrophil
Eosinophil
Basophil
Mast cells

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20
Q

Mention the agranulocytes

A

Monocyte

Lymphocyte

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21
Q

Mention the monocytes

A

Macrophages

Dendritic cells

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22
Q

Are the first cells who phagocyte the pathogens

A

Neutrophils

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23
Q

Control mechanisms associated with allergy

A

Eosinophil

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24
Q

Basophils contain

A

histamine and heparin

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25
Q

Granulocytes that secrete an antibody

A

Lymphocyte

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26
Q

Eat a pathogen and present to T lymphocyte to activate the adaptive inmune system

A

Dendritic cells

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27
Q

Granules has inflammatory mediators which are

A

Histamine
Serotonin
Cytokines
Eicosanoids

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28
Q

Which are the eicosanoids?

A

Prostaglandins

Leukotrienes

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29
Q

Describe the process of inflammation

A

The tissue got injured
Macrophages phagocyte the pathogen
The endothelial cells separate and the vascular permeability increased and there is a vasodilation

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30
Q

Vasodilation is produced by an increased in

A

Nitric oxide

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31
Q

Is when the macrophage squeeze him between endothelium cells and arrive to injured tissue

A

Extravasation

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32
Q

Complement system are activated in presence of

A

pathogens

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33
Q

Function of complement system

A

Attract leukocytes
Help with opsonization
Kill pathogens

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34
Q

In tissue repair growth factors released to _____

A

angiogenesis

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35
Q

Synthesize collagen and helps with wound healing

A

Fibroblasts

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36
Q

Is the creation of new blood vessels

A

Angiogenesis

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37
Q

What happen after the neutrophil phagocyte the pathogen?

A

the neutrophil die by itself (like suicide)

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38
Q

Mention the 4 steps for the modulation of inflammatory response

A
  1. Initiation
  2. Amplification
  3. Destruction
  4. Termination
39
Q

Is the step for the modulation of inflammatory response where cells are released by trigger factors and circulate inflammatory cells producing an acute inflammation

A

Initiation

40
Q

Cells which are released to an inflammatory response

A

Cytokines
Chemokines
Platelets
Neutrophils

41
Q

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

A

Amplification

42
Q

Is the step for the modulation of inflammatory response where the enzymatic digestion, phagocytosis and damaged tissue is removed

A

Destruction

43
Q

Is the step for the modulation of inflammatory response where the damage to normal cells is prevent

A

Termination

44
Q

Principle which explains the pression between extravascular and intravascular space

A

Starling principle

45
Q

Components of the Starling Principle

A

Hydrostatic pressure
Oncotic pressure
Osmotic pressure
Lymph flow

46
Q

Accumulation of fluid in the extravascular space and interstitial tissues

A

Edema

47
Q

Types of edema

A

Non inflammatory edema

Inflammatory edema

48
Q

Types of non inflammatory edema

A

Lymphedema

Thrombosis

49
Q

Type of edema which disrupt the lymphatic flow

A

Lymphedema

50
Q

Obstruction of venous outflow

A

Thrombosis

51
Q

Characteristics of an inflammatory edema (triple response)

A

Transient vasoconstriction of arterioles
Vasodilation of precapillary arterioles
Increase in endothelial cells barriers permeability

52
Q

Accumulation of fluid in some body spaces

A

Effusion

53
Q

Types of effusion

A

Transudative

Exudative

54
Q

Effusion that occurs due to increased hydrostatic pressure or low plasma oncotic pressure

A

Transudative

55
Q

Effusion that occurs due to inflammation and increased capillary permeability

A

Exudative

56
Q

Difference between transudative and exudative

A

Transudative–>low in protein and LDH

Exudative–>high in protein and LDH

57
Q

If we have 1 or more of this 3 criteria is an exudate

A

Serum protein >0.5
Serum LDH >0.6
LDH > 2/3 upper limit normal for serum

58
Q

Types of exudate

A

Serous exudate
Serosanguineous
Fibrinous exudate
Suppurative inflammation

59
Q

Inflammation purulent exudate with significant liquefactive necrosis

A

suppurative inflammation

60
Q

Exudate with large amounts of fibrins due to inflammation

A

Fibrinous exudate

61
Q

Exudate with an infusion with blood

A

Serosanguineous

62
Q

Exudate color white with yelow

A

Serous exudate

63
Q

Factor XII is also known as

A

Hageman Factor

64
Q

Function of factor XII

A

Converts plasminogen to plasmic
Activate the Kallikrein
Activation of Coagulation System

65
Q

There are 2 routes to synthesize arachidonic acid

A

Phosphatidylcholine

Phosphatidylinositol-P2

66
Q

Etiology of chronic inflammation

A

Failure of eliminating
Exposure to irritants
Autoimmune disorder
Oxydative stress

67
Q

Risk factors associated with chronic inflammation

A 
Age
Obesity
Diet
Smoking
Low sex hormones
Stress and sleep disorders
68
Q

Management for chronic inflammation

A 
Low glycemic diet 
Metformine
Reduce intake of fats
Statins
NSAIDs 
Corticosteroids
69
Q

Could the NSAIDs be used in every inflammatory process? Why?

A

No, because they can interfere delay with the healing process

70
Q

Which could be the consequences of using NSAIDs during an inflammatory process?

A

Production of prostaglandins

Increase local blood flow and vascular permeability

71
Q

The _______ phase is an important part of healing and, without it, healing would not occur

A

inflammatory

72
Q

Do NSAIDs interfere with healing?

A

Yes, inhibiting the COX

73
Q

When the COX is inhibited, we are also blocking the production of

A

prostaglandin

74
Q

NSAIDs have a _____ effect on wound healing

A

depressant

75
Q

When do we have to use cold therapy?

A

Accute pain

76
Q

Why do we use cold therapy in the first 48 hrs?

A

To reduce blood flow and slow inflammation

Decrease swelling and pain

77
Q

When do we have to use heat therapy?

A

Chronic pain

78
Q

Why do we use heat therapy for chronic pain?

A

Will dilate the blood vessels, Promote blood flow

79
Q

Ice therapy is most effective when applied early and frequently during the first ____ after an acute injury

A

48 hrs

80
Q

Cold therapy should not be used for a chronic injury because it can increase

A

stifness

81
Q

Is a disorder that causes immunodeficiency, resulting in recurrent bacterial and fungal infections. This patient have granulomas in various tissues

A

Granulomatous Disease

82
Q

Pathophysiology of GD

A

Inability to phagocytes kill microbes caused by several defects in NADPH

83
Q

Most patients of GD are males who has mutations on the gene coding for

A

gp91phox

84
Q

Patients with GD are susceptible to _____ organisms

A

catalase-positive

85
Q

Collections of immune cells that cluster when the can’t kill pathogens

A

granulomas

86
Q

Mention 2 classical mutations in GD in genes for NADPH oxidase

A

Autosomal recessive

X-linked recessive

87
Q

Mention the 2 pathways of arachidonic acid

A

Cyclooxigenase pathway

5-lipooxygenase pathway

88
Q

COX1 and COX2 produce

A 
Prostaglandin E2 (PGE2)
Prostaciclin (PGI2)
89
Q

Pathophysiology of Rheumatoid Arthritis

A

Hyperplasia of synovial membrane

90
Q

____ and ____ stimulate the expresión of adhesion molecules on endothelial cells and increase the recruitment of neutrophils into the joint is RA

A

IL-1

TNF-a

91
Q

Neutrophils release ____ and ____ which degrade proteoglycan in the superficial layer of cartilage in RA

A

elastase and proteases

92
Q

Chronic autoimmune inflammatory disease that results in progressive destruction of articular cartilage

A

Rheumatoid Arthritis

93
Q

Mention the autoantibodies that produce RA

A 
Rheumatoid factor (RF) 
Anti CCP
94
Q

In RA, T cells stimulate B and secrete cytokines such as _______ and macrophages such as ____ which are pro inflammatory cells

A

INF gamma and IL-17

IL-1 and IL-6

Fisiopatología (12 decks)

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