Microvascular Complications Flashcards

1
Q

Mechanism for hyperglycemia induced tissue damage

A

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

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2
Q

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

A

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

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3
Q

Molecular pathways implicated in pathogenesis of diabetic tissue damage - polyol

A

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

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4
Q

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

A

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

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5
Q

Molecular pathways implicated in pathogenesis of diabetic tissue damage - PKC

A

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

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6
Q

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

A

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

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7
Q

Diabetic retinopathy

A

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

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8
Q

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

A

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

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9
Q

Pathophysiology of diabetic retinopathy

A

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

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10
Q

Two categories of retinopathy

A

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

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11
Q

Macular edema

A

can occur at any stage of retinopathy –> “clinically significant macular edema”

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12
Q

Clinical findings of mild retinopathy

A

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

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13
Q

Clinical findings of moderate/severe retinopathy

A

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

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14
Q

dot hemmorhage

A

mild retinopathy

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15
Q

cotton wool spot

A

moderate/severe retinopathy

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16
Q

Defining feature of proliferative retinopathy vs non-proliferative retinopathy

A

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

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17
Q

Prevention of retinopathy

A

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

18
Q

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

A

prevention –> less pronounce in slowing

19
Q

Tx of NPDR/CSME

A

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

20
Q

Tx of high risk/severe PDR

A

panretinal photocoagulation, intravitreal glucocorticoids, VEGF inhibitor

21
Q

Indications for vitrectomy

A

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

22
Q

Diabetic nephropathy

A

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

23
Q

Pathologic changes of nephropathy

A

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

24
Q

Prevention of nephropathy

A

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

25
Q

Tx of nephropathy

A

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

26
Q

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

A

F

27
Q

Mx of action of ACE inhibitors and ARB

A

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

28
Q

Diabetic neuropathy

A

most common microvascular complication –> polyneuropathy is most common

29
Q

Peripheral neuropathy

A

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

30
Q

Clinical findings of polyneuropathy

A

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

31
Q

diff dx of polyneuropathy

A

alcohol, b12, uremia, hypothyroidism

32
Q

Tx of painful neuropathy

A

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

33
Q

CV autonomic neuropathy

A

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

34
Q

GI autonomic neuropathy

A

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

35
Q

Gastroparesis

A

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

36
Q

Tx of gastroparesis

A

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

37
Q

Genitourinary autonomic neuropathy

A

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

38
Q

Peripheral autonomic neuropathy/sudomotor neuropathy

A

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

39
Q

T/F neuropathy in diabetes can affect single nerves

A

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

40
Q

Diabetic amyotrophy

A

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

41
Q

Truncal polyradiculopathy

A

sever abdominal pain in band like pattern T4-T12

42
Q

Tx of NPDR without CSME

A

risk factor management