B2.050 Chronic Complications of Diabetes Mellitus Flashcards Preview

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Flashcards in B2.050 Chronic Complications of Diabetes Mellitus Deck (20)
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1

how is it that diabetics are in a proinflammatory state but are also more prone to infection?

the proinflammatory state is due to release of cytokines and a nonspecific rise in inflammation throughout the body
this state reduces the efficacy of first responders to actual infections, leading to the increased risk of infection

2

what is the difference between tissue regeneration and tissue repair?

regeneration has a superior functional outcome- don't easily in epithelium due to epithelial stem cells, but difficult in infrastructure wounds
repair of tissues usually comes with scarring and structural and functional consequences

3

what are the 3 primary steps to repair by connective tissue deposition

angiogenesis
granulation tissue
remodeling

4

why does angiogenesis produce leaky vessels?

partially by default and the virtue of the formation process- they're being developed piece by piece so can't be immediately structurally sound
also allows inflammatory cells easier passage between intra/extracellular compartments

5

what are the components of granulation tissue?

fibroblasts
loose connective tissue
leukocytes
leaky vessels

6

what is remodeling?

reorganization of college and increased cross linking as wound healing progresses

7

why is there contraction in scar remodeling?

1. as collagen cross links, collagen pulls tissue together
2. fibroblasts have contractile properties due to presence of actin (myofibroblasts)

8

what are the 3 components of angiogenesis?

growth factors (VEGF, FGF, angioprotein)
notch signaling
ECM proteins and enzymes

9

what is the function of growth factors in angiogenesis?

migration and proliferation of endothelial cells

10

what is the function of notch signaling?

regulates sprouting and branching of vessels

11

what is the function of ECM proteins and enzymes in angiogenesis?

interact with integrin receptors on endothelial cells
enzymatic remodeling allows growth

12

how is extracellular matrix degradation controlled in remodeling?

matrix metalloproteinases
inactive zymogens, activated by proteases like plasmin
inactivated by tissue inhibitors of metalloproteinases

13

how does wound strength change over time?

increases

14

how does new collagen appear different from old collagen on a slide?

appears lighter due to increased fluid and edema

15

how do the leading edges of benign and malignant neoplasms differ?

malignant- always has young collagen deposits due to constant tissue injury due to invasion and the resulting inflammation in host tissue
benign- capsule of well developed collagen at edge due to lack of invasion

16

characterize healing by first intention

minimizes time of healing
limited connective tissue
limited scarring, but limited strength

17

what is wound dehiscence?

edges of a wound come apart

18

what is ulceration?

wound heal from the bottom up; some may never epithelialize

19

what is fibromatosis?

semiautonomous proliferation of fibroblasts beyond what is required
difficult to control

20

what kinds of factors negatively affect would healing?

infection
nutritional status (vitamin C)
steroids
mechanical factors
poor perfusion
foreign bodies
type and extent of injury
location of injury