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Flashcards in Microvascular Complications Deck (42):
1

Mechanism for hyperglycemia induced tissue damage

hyperglycemia --> repeated acute changes in cellular metabolism + cumulative long-term changes in stable macromolecules --> tissue damage + accelerating factors (e.g. hypertension)

2

Molecular pathways implicated in pathogenesis of diabetic tissue damage (4)

polyol pathway, advanced glycosylation end products (AGE), pKC activation, hexosamine pathway

3

Molecular pathways implicated in pathogenesis of diabetic tissue damage - polyol

decreased NADPH due to altered function of aldose reductase --> decreased glutathione --> oxidative stress

4

Molecular pathways implicated in pathogenesis of diabetic tissue damage - advanced glycosylation end-products (AGE)

modification of intra/extracellular proteins resulting in increased cytokines and growth factors

5

Molecular pathways implicated in pathogenesis of diabetic tissue damage - PKC

decreased endothelial nitric acid synthase, increased endothelin1,tgfbeta,pai1,vegf,nfkb --> vasoconstriction, coagulation, angiogenesis, inflammation

6

Molecular pathways implicated in pathogenesis of diabetic tissue damage - hexosamine pathway

diversion from glycolysis --> increased nacetyl glucosamine --> altered gene expression of cytokines

7

Diabetic retinopathy

most common cause of blindness in US --> most t1d affected at 20 years, 50-80% of t2d at 20 years

8

T/F diabetic retinopathy tends to onset after diagnosis of t2d

F --> before diagnosis of t2d and after diagnosis of t1d

9

Pathophysiology of diabetic retinopathy

dysregulated retinal blood flow, oxidative stress and inflammation, edema, microthrombosis, growth factors leading to proliferation, genetic, hypertension, dyslipidemia, medications

10

Two categories of retinopathy

non proliferative (mild/moderate/severe) + proliferative (early/high-risk/severe)

11

Macular edema

can occur at any stage of retinopathy --> "clinically significant macular edema"

12

Clinical findings of mild retinopathy

microaneurysms, dot hemorrhages, hard exudate (lipid leakage within macrophages)

13

Clinical findings of moderate/severe retinopathy

soft exudate (cotton wool spots - nerve fiber layer infarct), venous beading, intraretinal microvascular abnormalities (tortuous capillaries, occluded vessels)

14

dot hemmorhage

mild retinopathy

15

cotton wool spot

moderate/severe retinopathy

16

Defining feature of proliferative retinopathy vs non-proliferative retinopathy

neovascularization --> new vessels are fragile and can hemorrhage (also has preretinal and vitreous hemorrhage, fibrosis, ischemia)

17

Prevention of retinopathy

glycemic control, antihypertensive therapy (maybe lipid lowering, antiplatelet, and carbonic anhydrase inhibitors)

18

Glycemic control is highly effective in prevention/slowing of retinopathy in t1d

prevention --> less pronounce in slowing

19

Tx of NPDR/CSME

NPDR with CSME (non prolif + clinically sig macular edema) = focal laser photocagulation

20

Tx of high risk/severe PDR

panretinal photocoagulation, intravitreal glucocorticoids, VEGF inhibitor

21

Indications for vitrectomy

non clearing vitreous hemorrhage, traction retinal detachment involving fovea, non responsive pdr

22

Diabetic nephropathy

most common cause of kidney failure in US, independent risk factor for cv and overall mortality

23

Pathologic changes of nephropathy

glomerular disease (mesangial expansion, glomerular basement thickening, glomerular sclerosis) + albuminuria (micro or protein/macro)

24

Prevention of nephropathy

glycemic control, bp control, tx of dyslipidemia, measurement of spot urin microalbum/creatinine ratio

25

Tx of nephropathy

ace inhibitor/angiotensin ii receptor blocker (improves or normalizes), hypertensive agents, dietary restriction, weight loss

26

T/F ace inhibitors and angiotensin ii receptor blockers can prevent onset of microalbuminuria

F

27

Mx of action of ACE inhibitors and ARB

dilation of efferent arteriole --> reduction of glomerular pressure --> decreased urinary protein

28

Diabetic neuropathy

most common microvascular complication --> polyneuropathy is most common

29

Peripheral neuropathy

most common diabetic neuropathy --> distal, symmetric (stocking glove distribution) sensory loss > motor loss, worse at night

30

Clinical findings of polyneuropathy

sensory loss, loss of ankle reflexes/ vibration loss> pain/temp loss

31

diff dx of polyneuropathy

alcohol, b12, uremia, hypothyroidism

32

Tx of painful neuropathy

anticonvulsants, tca's, snris, topical agents, opioids, antioxidants, tens

33

CV autonomic neuropathy

resting tachycardia/loss of ps tone, exercise intolerance, postural hypertension, silent MI

34

GI autonomic neuropathy

esophageal enteropathy (GERD, LES relaxation), gastroparesis, diabetic enteropathy, gallbladder atony and enlargement

35

Gastroparesis

delayed gastric emptying/symptoms = early satiety, vomiting, nausea, worsening of glycemic control, asymptomatic

36

Tx of gastroparesis

glycemic control, eating less fat and non-digestible fiber, prokinetic agents

37

Genitourinary autonomic neuropathy

urinary retension (utis and overflow incontinence), ED, retrograde ejaculation, female sexual dysfunction

38

Peripheral autonomic neuropathy/sudomotor neuropathy

impaired perspiration, peripheral edema, callus formation/ulcers, contributor to neuroarthropathy

39

T/F neuropathy in diabetes can affect single nerves

T --> cranial nerves (e.g. bells palsy), peripheral nerves (e.g. carpal tunnel), or mononeuritis multiplex (multiple nerves)

40

Diabetic amyotrophy

an example of radiculopathy with motor neuropathy of l2-l4- -> acute, asymmetric pain followed by weakness of butt and proximal leg

41

Truncal polyradiculopathy

sever abdominal pain in band like pattern T4-T12

42

Tx of NPDR without CSME

risk factor management