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MHD Exam 1 > Chronic Inflammation > Flashcards

Chronic Inflammation Flashcards

1
Q

chronic inflammation is characterized by…

A
  • accumulation of lymphocytes, plasma cells, and macrophages
  • proliferating blood vessels
  • formation of CT
  • significant collateral damage
  • repair processes occurring in parallel with persistent inflammation
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2
Q

what tends to cause acute inflammation

A
  • infarction
  • bacteria
  • toxins
  • trauma
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3
Q

what causes chronic inflammation

A
  • viruses
  • chronic infections
  • persistent injury
  • autoimmune disease
  • genetic inability of the host to mount an appropriate response
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4
Q

the lack of resolution in chronic inflammation may be caused by…

A
  • inability to get rid of the pathogen
  • pathogen resistance to antimicrobials
  • degradation resistant foreign body
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5
Q

chronic high levels of inflammatory cytokines cause

A
  • increased rates of hepatic production of defense proteins
  • increased hepcidin production
  • increased growth factors for platelets and monocytes
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6
Q

what is the signature cell of chronic inflammation

A

M1 macrophages

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7
Q

what is hepcidin

A

it increases iron accumulation in macrophages and reducs iron absorption in the stomach so that there is less available iron for microbes to use but there is also less iron for pt so anemia is possible

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8
Q

M1s produce…

A
  • ROS, NO, lysosomal enzyme for microbial actions and phagocytosis
  • IL-1, IL-12, IL-23, and chemokines for inflammation
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9
Q

M2s produce…

A
  • growth factors and TGF-B for tissue repair and fibrosis

- IL-10 and TGF-B for anti-inflammatory effects

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10
Q

what turns on M1s and turns off M2s?

A

microbes and IFN-y

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11
Q

What turns off M1s and turns on M2s?

A

IL-13 and IL-4

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12
Q

granulomatous inflammation

A
  • associated with persistent T-cell activation
  • common with persistent microbial intracellular infection
  • common with macrophage uptake of poorly degradable foreign bodies
  • found in sarcoidosis (granulomas without microbes), Inflammatory Bowel Disease, and Crohns
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13
Q

morphology of granuloma

A
  • central portion is necrotic debris
  • activated macrophages and multinucleated giant cells are in the periphery
  • Cuff of T-cells, the vast majority of which are CD3+/CD4+
  • the entire granuloma is rimmed by proliferating fibroblasts
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14
Q

what type of granulomas are seen in TB

A

caseous or necrotizing

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15
Q

what T cells are involved in granulomas

A

Th1- intracellular organisms

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16
Q

the Tcells in granulomas let out what cytokines?

A

IL-2 to promote more Th1 cells and INF-y to the APC

17
Q

The APC lets out what cytokine in granulomas

A

IL-12 to the Th1 cell

18
Q

frustrated macrophages in granulomas let out what cytokines

A

TNF-a, IL-1, IL-6, and IL-8

19
Q

what is the logic of the granuloma

A

wall off the infecting organism- good but can cause collateral damage by progressive tissue necrosis and fibrosis

20
Q

clinical differences in inlfammation are based solely upon _______ and _____

A

intensity and duration of the stimulus

21
Q

biochemical changes in inflammation

A
  • increased hepatic production of fibrinogen, ceruloplasmin, and complement components (C3)
  • reciprocal decrease in albumin synthesis with duration of inflammation
  • increased hepatic production of hepcidin
  • growth factors stimulate marrow to increase production of leukocytes and platelets (can be shown clinically in blood counts)
22
Q

C-Reactive Protein (CRP)

A
  • production is stimulated by inflammation ad is tightly linked to IL-6 levels
  • easily measured clinically— when it’s normal, it can exclude the presence of significant inflammation
  • obesity can cause a false elevation of CRP
23
Q

Erythrocyte sedimentation rate (ESR)

A
  • chronic inflammation causes clinically detectable Ab sysnthesis of IgG
  • IgG and fibrinogen coat RBCs which then fall more rapidly through a column of plasma (ESR)
  • not a common because can be falsely elevated because of other reasons for higher IgG
24
Q

What increases with chronic inflammation

A
  • highest = CRP and ESR
  • middle- platelets
  • least- IgG
25
Q

what decreases with chronic inflammation

A
  • most = albumin

- least = hemoglobin

26
Q

TNF

A
  • acute inflammation
  • macrophages, mast cells, and Tcells
  • stimulates expression of endothelial adhesion molecules and secretion of other cytokines
  • systemic effects
27
Q

IL-1

A
  • acute inflammation
  • macrophages, endothelial cells, some epithelial cells
  • stimulates expression of endothelial adhesion molecules and secretion of other cytokines
  • systemic effects
  • greater role in fever
28
Q

IL-6

A
  • macrophages, other cells
  • systemic effects (acute phase response)
  • acute inflammation
29
Q

chemokines

A
  • macrophages, endothelial cells, T cells, mast cells, other
  • recruitment of leukocytes to sites of iflammation
  • migration of cells in normal tissues
  • acute inflammation
30
Q

IL-17

A
  • acute inflammation
  • T cells
  • recruitment of neutrophils and monocyte
31
Q

IL-12

A
  • chronic inflammation
  • dendritic cells, macrophages
  • increased production of IFN-y
32
Q

IFN-y

A
  • chronic inflammation
  • T cells, NK cells
  • Activation of macrophages (increased ability to kill microbes and tumor cells)
33
Q

IL-17

A
  • chronic inflammation
  • T cells
  • Recruitment of neutrophils and monocytes
34
Q

systemic protective effects of inflammation

A
  • brain- fever from TNF, IL-1, and IL-6
  • Liver- acute phase proteins from IL-1 and IL-6
  • bone marrow- leukocyte production from TNF, IL-1, and IL-6
35
Q

systemic pathologic effects of inflammation

A
  • heart- low output from TNF
  • Thrombus formation in blood vessels from TNF
  • Insulin reisistance in multiple tissues from TNF and IL-1
36
Q

Scar formation occurs when there is damage to _____

A

the underlying connective tissue under the epithelium

MHD Exam 1 (6 decks)

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