DM Complications Flashcards

1
Q

4 mechanisms of hyperglycemia induced damage

A
  1. Increased polyol pathway influx
  2. Increased intracellular formation of AGE
  3. Activation of protein kinase C
  4. Increased hexosamine pathway influx
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2
Q

Mononeuropathy of this nerve is the least likely associated with DM

A

4th cranial nerve

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3
Q

CSME definition

Clinically significant macular edema

A

Retinal thickening within 500 um of the the fovea, hard exudates at or within 500 um of the fovea

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4
Q

DCCT results on retinopathy ang glycemic control

A

Intensive insulin therapy prevented the development of retinopathy by 27%

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5
Q

Treshold for treatment of eyes with DME

A

Presence of thickening of the central 1 mm diameter retinal subfield

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6
Q

Severe NPDR bu american academy of ophthalmology

A

More than 20 intraretinal hemorrhages in each of the four retinal quadrants
Definite venous beading in two or more retinal quadrants
Prominent intraretinal microvascular abnormalities in one or more retinal quardrants
No PDR

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7
Q

Definition of PDR by the american college of ophthalmology

A
  1. One or mor retinal neovascularization
  2. Vitreous hemorrhage
  3. Preretinal hemorrhage
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8
Q

% of EOM palsies attributable to DM

A

4.5-6%

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9
Q

Does BP control help reduce diabetic retinopathy?

A

Yea. UKPDS demonstrated a 34% and 47% reduction in risk of DM retinopathy progression in those assigned to intensive BP control

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10
Q

Strong predictor of incipient DM nephropathy, first ever CB event and all cause mortality in patients with T1DM

A

Serum OPN

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11
Q

Single upstream process that links different hyperglycaemia induced pathogenic mechanisms

A

Overproduction of superoxide by the mitochondrial electron transport chain

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12
Q

Explain the hexosamine pathway influx (4th hypothesis)

A

Fructose 6 phosphate diverted from glycolysis to the hexosamine pathway, it orocudes substrate for reactions that require UDP-GlcNac I

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13
Q

What is the rate llimiting step of the conversion of glucose to glucosamine

What mechanism for hyperglycemia induced damaged?

A

GFAT

hexosamine pathyway

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14
Q

Explain increased polyol pathyway flux (mech #1)

A

Aldose reductose converts glucose to sorbitol

Sorbitol is oxidized to fructose by sorbitol dehydrogenase

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15
Q

Accounts for almost all of the hyperglycemia induced increase in reactive AGE precursors

A

Methylglyoxal

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16
Q

Earliest morphologic changes in the diabetic retinal capillaries

A

1) Pericyte loss

2) Acellular capillary formation

17
Q

Voltage gated sodium channel expressed exclusively in the unmyelinated sensory C fibers, responsible for the painful diabetic neuropathy

18
Q

Anti atherogenic enzymes inactivated by ROS

A

Prostacycline synthase

eNOS

19
Q

Most common cause of vision loss from diabetes

A

Macular disease/ macular edema

20
Q

Current first line therapy for most etes with center involved DME

A

Intravitreal injections of VEGF inhibitors

21
Q

Clinical triad of DM nephropathy

A

Hypertension
Proteinuria
Renal impairment

22
Q

5 stages of diabetic nephropathy in T1 DM patients

A
  1. Hyperfiltration
  2. Silent stage
  3. Microalbuminuria/ incipient nephropathy
    4: macroalbuminuria
  4. Uremia
23
Q

EM abnormalities of diabetic renal disease

A

Glomerular basement membrane thickening

Mesangial expansion

24
Q

Thiamine derivative that inhibits the downstream effects of mirochondrial ROS production

A

Benfotiamine

25
The most important single intervention to prevent progressive nephropathy in T1DM and T2DM
Sustained reduction in BP
26
2 landmark studies performed in T2DM patients for DM nephropathy
RENAAL Losartan | IDNT Irbesartan
27
Signs and symptoms of large fiber neuropathy
Impaired vibration perception and position sense Depressed tendon reflexes Sensory ataxia
28
Describe Ao (aloha delta) fiber pain
Deep seated gnawing dull like a toothache in the bones of the feet or even crushing or cramplike pain
29
Tuning fork required to measure vibration perception
128 Hz
30
Pharmacologic therapy of Diabetic neuropathy
1. Aldose reductase inhibitors 2. A-lipoic acid 3. Y-linolenic acid 4. Protein kinase C-B inhibition 5. Benfotiamine 6. Metanx 7. Human intravenous Ig
31
Management of C fiber pain
1. Capcaisin | 2. Clonidine/ phenyolamine
32
The greatest predictor of CVD as well as increased risk of death
Autonomic nerve dysfunction
33
According ti NCEP ATP guidelines DM pxs are candidates for cholesterol lowering therapy if LDL cholesterol is higher than
130 mg/dL | Goal of therapy is less than 100