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Immunology > Lecture 3-Inflammation > Flashcards

Lecture 3-Inflammation Flashcards

1
Q

What are the types of inflammation?

A

Acute

Chronic

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2
Q

What are the characteristics of acute inflammation?

A

Beneficial
Directs immune components to infection
Eliminates infection with rapid resolution
Increases blood supply, capillary permeability, WBC migration
30-60 min: Influx of neutrophils
4-6h: Influx of monocytes/macrophages and lymphocytes

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3
Q

What are the characteristics of chronic inflammation?

A

Harmful
Tries to wall off infection that cannot be eliminated
Granulométrie
Tissue destruction or fibrosis
Macrophages, epithelia cells, lymphocytes predominate
Contributes to heart disease, Alzheimer’s, diabetes, arthritis, cancer

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4
Q

What are the inducers of inflammation?

A 
infections
Allergies
Burns
Ischemia
Cut
Fractures 
Cuts
Neoplasms
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5
Q

What are the local signs off inflammation?

A 
Classic triad is:
Pain
Heat
Redness
Other signs are:
Edema
Loss of function
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6
Q

What are the systemic signs of inflammation?

A

Fever
Cytokine release
Acute phase protein release from liver

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7
Q

what are the characteristics of pathogen recognition by local macrophages?

A

PAMPS are expressed on microbes
Phagocytes bind to PAMPS via PRR
PRR-PAMP interactions:
Enhance phagocytosis
Up regulate adhesion molecule expression to id leukocyte extravasation and migration
Enhance cytokine production by phagocytes

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8
Q

Examples of PRR and PAMP?

A

PRR: fMet-Leu-Phe receptor
PAMP: fMet-Leu-Phe
Chemotactic for macrophages and neutrophils
PRR: TLR4 + CD14
PAMP: LPS (endotoxin)-outer membrane of gram negative
PRR: TLR2 + CD14
PAMP: Lipoteichoic acid- gram positive cell wall

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9
Q

What are the actions of some NLRs?

A

Assemble into the inflammasome

Inflammasome activates cas passé 1 that cleaves the precursor of interleukin 1 beta into its active IL-1 beta

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10
Q

What are the pro-inflammatory cytokines synthesized by PRR-PAMP interactions?

A

IL-1
Il-6
TNF-alpha

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11
Q

What actions are induced by pro inflammatory cytokines?

A

Septic shock
Fever
Acute phase protein release from the liver
ROS generation by phagocytes
Leukocyte extravasation through up regulation of adhesion molecule expression

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12
Q

What are the characteristics of septic shock?

A 
TNF alpha is most potent
Drop in blood pressure 
Hyper or hypothermia
Shaking chills
Weakness
Tachypnea and tachycardia
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13
Q

What are the characteristics of fever?

A

IL-1 is most potent
IL-1 induces central and peripheral synthesis of PGE2
Central PGE2 raises hypothalamic set point
IL-1=endogenous pyrogens
LPS, lipoteichoic acid= exogenous pyrogens

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14
Q

What are the characteristics of acute phase protein (APP) release from the liver?

A 
IL-6 is most potent inducer
APPS aid host defense through opsonins, clots, tissue repair
Positives APPs can induce:
Complement
CRP
Serum amyloid A
Clot buster precursor plasminogen
Coagulation factors
Ferritin
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15
Q

What are the characteristics of enhanced adhesion molecule expression, extravasation?

A

TNF alpha, IL-1 in importance

Extravasation/diapedesis: movement of leukocytes out of blood vessels and into tissues

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16
Q

What are the steps in extravasation of leukocytes?

A

Endothelial cells start expressing E- selection and ICAM-1 in response to TNF alpha and IL-1
Tethering and rolling via Sialyl Lewis X (CD15) on PMN binds to E-selection on endothelium
Adhesion/pavementing: IL-8 regulates LFA-1 expression on PMN,LFA-1 binds to ICAM-1 on endothelial cell
Transendothelial migration-PMN moves through endothelium
Chemotaxis-PMN moves up the concentration gradient of chemotaxins (IL-8, C5a, fMet-Leu-Phe)

17
Q

What are the characteristics of leukocyte adhesion deficiency?

A

LAD1-no CD18 so no LFA-1
LAD2- no sialyl Lewis X
No extravasation
Leukocytosis (too many WBCs), especially neutrophilia
No pus, poor healing
Chronic/repeated bacterial infections of mouth and GI

18
Q

Characteristics of the stimulation of the respiratory burst?

A

Respiratory/oxidative burst in macrophages and PMNs generates ROS
ROS damage proteins, lipids, DNA
IFN gamma, TNF alpha, GM-CSF stimulate respiratory burst in macrophages and PMNs

19
Q

What are the steps in respiratory burst?

A

NADPH oxidase generates superoxide
Superoxide dismutase destroys superoxide, catalysés formation of hydrogen peroxide
Myeloperoxidase generates hypochlorite from hydrogen peroxide
CVatalasse reduces hydrogen peroxide to water and oxygen

20
Q

What are the results of NADPH oxidase deficiency?

A

Chronic granulométrie disease (CGD)
Marked by repeated infections by catalase positive microbes
Pneumonia, lymphadenitis, abscesses in skin and viscera

21
Q

What are the tests for CGD?

A

NBT reduction test- CGD phagocytes cannot reduce NBT to blue formatant dye (not used much now)
Dihydrorhodamine (DHR) test-normal phagocytes reduce DDHR to fluorescent rhodamine, quantified by flow cytometry
Genetic tests

Immunology (8 decks)

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