B2.050 Chronic Complications of Diabetes Mellitus Flashcards

1
Q

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

A

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

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2
Q

what is the difference between tissue regeneration and tissue repair?

A

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

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3
Q

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

A

angiogenesis
granulation tissue
remodeling

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4
Q

why does angiogenesis produce leaky vessels?

A

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

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5
Q

what are the components of granulation tissue?

A

fibroblasts
loose connective tissue
leukocytes
leaky vessels

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6
Q

what is remodeling?

A

reorganization of college and increased cross linking as wound healing progresses

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7
Q

why is there contraction in scar remodeling?

A
  1. as collagen cross links, collagen pulls tissue together

2. fibroblasts have contractile properties due to presence of actin (myofibroblasts)

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8
Q

what are the 3 components of angiogenesis?

A

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

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9
Q

what is the function of growth factors in angiogenesis?

A

migration and proliferation of endothelial cells

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10
Q

what is the function of notch signaling?

A

regulates sprouting and branching of vessels

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11
Q

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

A

interact with integrin receptors on endothelial cells

enzymatic remodeling allows growth

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12
Q

how is extracellular matrix degradation controlled in remodeling?

A

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

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13
Q

how does wound strength change over time?

A

increases

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14
Q

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

A

appears lighter due to increased fluid and edema

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15
Q

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

A

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

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16
Q

characterize healing by first intention

A

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

17
Q

what is wound dehiscence?

A

edges of a wound come apart

18
Q

what is ulceration?

A

wound heal from the bottom up; some may never epithelialize

19
Q

what is fibromatosis?

A

semiautonomous proliferation of fibroblasts beyond what is required
difficult to control

20
Q

what kinds of factors negatively affect would healing?

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