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Pathology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Inflammation

A
  1. response to cell & tissue injury by vascularized tissue
  2. elicted to protect host
  3. By eliminating necrotic debris
  4. By eliminating initial cause
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2
Q

Features of Inflammation

A
  • protective response
  • Vascular= vasodilation & perm
  • Cell= inflammatory cells (neutrophils, macrophages & lymphocytes)
  • Via plasma proteins & cytokines
  • Outcome elimination or persistence= chronic inflammation
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3
Q

Steps in Inflamm Response

A
  1. recognize injurious agent
  2. recruit leukocytes
  3. remove agent
  4. regulation of response
  5. resolution & repair
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4
Q

Acute inflammation

A
  1. heat
  2. redness
  3. swelling
  4. pain
  5. loss of function
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5
Q

Acute Inflammation

A
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6
Q

Vascular events in acute inflamm

A

alter vascular caliber & increase BF

Extravasation of plasma fluid & protein (leakage)

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7
Q

Cell events in acute inflamm

A

Leukocyte immigration & phagocytosis

*neutrophils first then macrophages*

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8
Q

Etiology of Inflammation

A
  1. microorg- bac, viral, fungal, parasitic
  2. tissue necrosis- uric acid, ATP, DNA, DNA binder HMGB-1
  3. hypoxia- mediatoer HIF1-a, effectors eg VEGF
  4. physical- trauma, thermal, chem
  5. foreign- splinter, dirt, suture
  6. immune- hypersensitivity, inappropriate immune rxn
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9
Q

Normal/Transudate/Exudate

A
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10
Q

Mechanism of Increased vascular perm

A
  1. Endothelial contraction- via his, bradykinin, leukotrienes, NO, SP. 15-30 min or 2-12 hr (sunburn)
  2. direct endothe injury- burns, UV, neutrophil damage
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11
Q

Increase Transcytosis

A

in venules

induced by VEGF

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12
Q

Exudate

A

Vasodilation

Increase blood viscosity

Decrease Colloid osmotic P

increased vascular perm

  • transport
  • nutrition
  • make appropriate ground for neutrophils
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13
Q

Exudate

A
  1. fluid of acute inflammation
  2. high protein
  3. contain cell debris
  4. sp gravity >1.02

abscess

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14
Q

Transudate

A
  1. ultrafiltrate of blood plasma; increase hydrostatic P
  2. low protein
  3. no cells
  4. sp gravity <1.012

ascites

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15
Q

Lymphatics

A
  • lymph flow increased to drain edema from extravascular space
  • lymph drainage can also transport microbes in extensive inflammation

Lymphangitis- inflammation of lymph channels

lymphadenitis- inflammation of draining LN

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16
Q

Neutrophils

A
  1. from BW
  2. highly motile
  3. in tissue 24-48 hours
  4. high phagocytic capacity
  5. effective killers of bac
  • use NADPH/Phagocyte oxidase= makes O2-*
  • Myeloperoxidase= makes HOCl*
  • NO oxidase= makes OONO-*
  • Fenton= makes OH*
17
Q

Leukocytes in inflammation Steps

A
  1. margination
  2. rolling
  3. activation
  4. adhesion
  5. pavementing
  6. emigration
  7. diapedesis
  8. chemotaxis
  9. phagocytosis
18
Q

Leukocytes

A
19
Q

P selectin on Endothelial Mem

A

Allows for rolling when bound; neutrophols, lymph & monocytes:

  • to Sialyl Lewis X modified proteins on leukocytes
20
Q

E selectin on endothelial mem

A

Allows for rolling & adhesion; neutrophils, T lymphocytes & monocytes, when:

  • bound to sialyl lewis X modified prot on leukocyte
21
Q

GlyCam-1, CD34 on endothelial

A

Allows for rolling, neutrophils & monocytes :

  • when bound to L-selectin on leukocyte
22
Q

ICAM-1 on endothe

A

Adhesion, arrest, transmigration; neutrophils, mono & lymphocytes

  • when bound to CD11/CD18 integrins (LFA-1, Mac-1) on leukocyte

TNF & IL-1 activation of neutrophils

23
Q

VCAM-1 on endothelial

A

Adhesion of eosinophils, moncytes & lymphocytes

  • when bound to VLA-4 integrin on leukocyte
24
Q

CD31 on endoth

A

Transmigration of all leukocytes aided by PECAM-1 on endothelial cell as well:

  • when bound to CD31 on leukocyte
25
Q

Chemotaxis

A

Escaped leukocytes reach injury site

Chemoattractans

  • exogenous- bac agents N-formylmethionine terminal aa
  • endogenous- chemokines, C5a, leukotriene B4
26
Q

Inflammation

A
27
Q

Recognition & Attachment

A
  • C3b & IgG= opsonins
  • Aid in phagocytosis
28
Q

Phagocytosis

A

Bidn to R on leukocyte

Engulf

Fusion of lysosome with phagocytic vacuole

Destroy ingested particles- enz, ROS & nitrogen species

Use O2-*, HOCl* and OH* and OONO*

Granule contents may be exocytosed

Imp enz= MPO, iNOS and Phagocyte oxidase!

29
Q

Phagocytosis

A
30
Q

O2 indep mechanisms of killing

A
  1. lysozymes- from neutrophil granules destroy microbe mem
  2. major basic prot- from eosinophil granule kill prasite
  3. bactericidal perm increasing prot BP- cationic prot that strongly increases cell wall permeability
  4. defensins- in primary granules of neutrophils, can kill fungi & viruses & bac
31
Q

Activated Macrophages

A
  1. Microbial prod- cytokines, IFNg, TLR ligands activate M1 (clasically activated macrophage)
  • show inflamation!
  • IL-1,12-23, chemolines
  • ROS, NO, lysosomal enz
  1. helminths, IL-13 and IL-4 activate alternatively activated macrophage M2
  • anti inflammtory & woulnd repair
  • IL-10, TGFB
32
Q

Leukocyte Induced injury

A
  • tissues around leukocytes get injured
  • reperfusion injury in MI
  • autoimune & allergic responses
  • activated luekocytes that don’t distinguish self/non self
  1. lysosomal enz
  2. ROS
  3. cytokines
33
Q

Acute Leukocyte Induced Injury Inflamm Disorders

A
  1. acute resp distress yndrome- neutrophils
  2. acute transplant rejection- lymphocytes, Y & complement
  3. Asthma- eosinophils & IgE
  4. Glomerulonephritis- Y & complement, neutrophils & monocytes
  5. Septic shock- cytokines
  6. vasculitis- Y & complement, neutrophils
34
Q

Chronic Leukocyte Induced Injury Inflamm Disorders

A
  1. Arthritis- lymph, macrophages & Y
  2. asthma- eosinophils, IgE & other leukocytes
  3. atherosclerosis- macrophages
  4. chronic transplatn rejection- lymphocytes & cytokines
  5. pulm fibrosis- macrophages & fibroblasts
35
Q

Genetic Defects In Leukocyte function

A
  1. leukocyte adhesion def 1- defective leukocyte adhesion due to CD11/CD18 B chain mutation
  2. def 2- def leukocyte adhesion due to mut in fucosyl transferase needed for ligand syn for selectins
  3. chronic granulomatous disease- decrease ox burst
  4. x-linked- phagocyte oxidase in mem
  5. autsomal recessive- phagocyte oxidase in cytoplasm
  6. MPO def- decreased microbe killing, no H2O2 sys
  7. Chediak-Higashi syndrome- decreased due to mut affecting prot of lysosomal mem traffic.
36
Q

Chediak Higashi Syndrome

A

LYST

albinism

n. defects

neutropenis

defective degranulation

Leukocyte giant observed

37
Q

Acquired Defects

A
  1. BM suppression: tumors, radiation & chemotherapy- defect in producing leukocytes
  2. Thermal injury, diabetes, malignancy, sepsis, immunodef- defect in chemotaxis
  3. Hemodialysis, DM- defect in adhesion
  4. Leukemia, anemia, sepsis, diabetse, neonates, malnutrition- defect in phagocytosis & microbicidal activity
38
Q

Inflammation

A

Pathology (8 decks)

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