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Endocrinology > Complications of DM > Flashcards

Complications of DM Flashcards

1
Q

Pathogenesis of Diabetic Tissue Damage (4)

A
  1. Oxidative Stress
  2. Inflammation
  3. Glucotoxicity–>Advanced glycosylation end products (AGE)
  4. Vasoconstriction, angiogenesis, coagulation,
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2
Q

Retinopathy Statistics: Onset/prevalence

A

Type1DM: Onset 3-5 yr after dx; nearly all patients have it within 20 years

Type 2DM: Onset 5-7yr before dx; 20% before dx; 40-80% incidence after 20 years

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3
Q

Pathophysiology of Diabetic Retinopathy (3)

A

Hyperglycemia: dysregulated retinal blood flow, oxidative stress, increased vascular permeability, microthrombosis (ischemia), endothelial proliferation

Genetics
Hypertension

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4
Q

Mild NPDR Signs (3)

A

Microaneurysms
Dot hemorrhages
Hard exudate (lipid leakage within mø)

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5
Q

Moderate/Severe NPDR Signs (3)

A

Soft exudates: “Cotton wool spots” (nerve infarcts)
Venous beading
Intraretinal microvascular abnormalities (IRMA)–>Occluded vessels, dilated/tortuous capillaries

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6
Q

What risk increases with severity of NPDR?

A

Risk of progression to PDR

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7
Q

Macular Edema:

A

Edema and thickening of retina
Accounts for 75% of blindness

Requires special fundoscopic exam

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8
Q

Proliferative Diabetic Retinopathy Signs (4)

A

Neovascularization (new blood vessels leaky–>hemorrhage)
Preretinal and vitreous hemorrhage–>acute vision loss that resolves spontaneously
Fibrosis–>Retinal traction/detachment
Ischemia

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9
Q

Prevention of retinopathy: Cornerstones (2) and Weaker links (3)

A 
Glycemic control and antihypertensives
Weaker evidence for: 
Lipid lowering meds
Antiplatelet meds
Carbonic anhydrase inhibitors
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10
Q

Effect of Glycemic Control on Retinopathy

A

Best as primary prevention (metabolic memory)–>Favorable effects persist for up to 10 years
Positive but less pronounced effect on mild/moderate NPDR
More effective in T1DM than T2DM

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11
Q

Treatment of Retinopathy:
NPDR
High Risk/severe PDR
Vitrectomy

A

NPDR: focal photocoagulation
High-risk/severe PDR:
panretinal photocoagulation (PRP)
Meds: VEGF-inhibitors, intravitreal glucocorticoids

Vitrectomy for nonresponsive shit

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12
Q

Nephropathy: Epidemiology–Onset and Risk

A

Onset 5-20 yr after diabetes (lifetime=25-35%
More common in T2DM
Most common cause of kidney failure (40% of dialysis patients)

Risk factor for CV/overall mortality

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13
Q

Risk factors for nephropathy (8)

A

Poor glycemic control, obesity, race, hypertension, age, tobacco use, retinopathy

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14
Q

Pathologic changes of Nephropathy: Glomerular changes (3)

A

Mesangial expansion
Thickening of glomerular basement membrane
Glomerular sclerosis

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15
Q

Course of Nephropathy (6)

A

Hyperfiltration (increased kidney size)–>Microalbuminuria–>Regress to normal–>Macroalbuminuria–>Decresed GFR–>ESRF

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16
Q

Prevention of Nephropathy (3)

A

Glycemic control

Blood pressure control (

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17
Q

Treatment of Nephropathy (4)

A

ACE Inhibitors/ARB: Improves albuminuria but not prevent onset
Other hypertensive agents: diltiazem/verapamil
Dietary restriction: salt/protein
Weight loss

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18
Q

Neuropathy: Prevalence

A

50-70% lifetime

Most common microvascular complication

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19
Q

Risk Factors for Diabetic Neuropathy (big list)

A

Age, duration of diabetes, poor glucose controls, blood vessel damage, mechanical injury to nerves, genetics, HTN, dyslipidemia, tobacco use, alcohol use

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20
Q

Peripheral Neuropathy (aka distal, symmetric polyneuropathy): Symptoms (4) and Distribution

A

Stocking glove distribution

Decreased sensation, paresthesia, hyperesthesia, worse at night

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21
Q

Polyneuropathy: clinical findings
Physical exam (2)
Electrodiagnostics (2)

A

Physical exam: sensory loss (proprioception/vibration), loss of ankle reflexes
Electr Tests: Decreased nerve conduction velocity and amplitude of evoked potentials

22
Q

Treatment of painful neuropathy (6)

A 
Anticonvulsants
TCAs
SNRIs
Topical agents
Opioids
Antioxidants
TENS (nerve stim)
23
Q

Types of autonomic neuropathy (4)

A

CV, GI, genitourinary, peripheral

24
Q

CV Neuropathy Symptoms (4): P-MET

A

Postural hypertension
MI
Exercise intolerance
Tachycardia

25
Q

GI Autonomic Neuropathy: Esophageal enteropathy (2)

A

Gastro-esophageal reflux disease

Transient Lower Esophageal Sphincter relaxation

26
Q

GI Autonomic Neuropathy: Diabetic enteropathy (3)

A

Small bowel dysfunction: diarrhea, steatorrhea
Colonic dysfunction: constipation
Anorectal dysfunction: fecal incontinence

27
Q

GI Neuropathy: Gastroparesis–Symptoms (2)

A

Early satiety, nausea, vomiting

Worsening of glycemic control

28
Q

GI Neuropathy: Gastroparesis–treatment (3)

A

Glycemic control
Diet (decrease fat/fiber)
Prokinetic agents: erythromycin/azithromycin

29
Q

Genitourinary Autonomic Neuropathy: Px (2)

A

Urinary retention: UTIs and incontinence

ED

30
Q

Peripheral Autunomic Nueorpathy (sudomotor neuropathy): Presentation (4)

A

Impaired perspiration: dry skin, itchiness
Peripheral edema
Callus formation (can form ulcers)
Neuroarthropathy

31
Q

Describe Acute Onset Mononeuropathy: Onset and resolution

A

Sudden weakness or pain in single nerve that resolves spontaneously

32
Q

How does acute onset mononeuropathy present? CN and Peripheral locations

A

CN: Opthalmoplegia (CN III,IV,VI) or Bell’s Palsy (CNVII)
Peripheral: Carpal tunnel or foot drop

33
Q

Acute Onset Radiculopathy: Types (2), location and px

A

Diabetic amyotrophy: L2-L4
Acute asymmetric pain and weakness in proximal legs, hips and butt
Truncal polyradiculopathy: T4-T12
Severe abdominal pain in band-like patter

34
Q

Prevention of Neuropathy (5)

A 
Glucose control
BP control
Treatment of dyslipidemia
Smoking cessation
Decreased alcohol intake
35
Q

Diabetic Foot Ulcers: Risk factors (4)

A

Neuropathy: decreased pain sensation/dry skin/calluses
Foot deformity
Peripheral vascular disease
Poor glycemic control (impaired wound healing)

36
Q

Prevention of Foot Ulcers (6)

A

Avoid walking barefoot, proper fitting shoes, trim toe nails, daily foot inspection, daily foot washing, moisturizer

37
Q

What are main chronic macrovascular complications? (3)

A

Coronary artery disease
Cerebrovascular disease
Peripheral vascular disease

38
Q

CVD in DM Stats:

A

75% all diabetes deaths
2-4x risk of CVD
Disease more likely to be asymptomatic and more likely to have worse outcomes than non-DM

39
Q

Risk factors for CVD (big list)

A

age, duration of DM, poor glucose control, HTN, dyslipidemia, renal disease/albuminuria, Women, obesity, smoking, sedentary lifestyle

40
Q

What is most important factor for microvascular disease in T1DM? When is risk highest?

A

Duration of diabetes– risk highest after 20-25 years

41
Q

What are factors for microvascular disease in T2DM?

A

Usually pre-existing–insulin resistance and presence of multiple other risk factors

42
Q

Prevention of microvascular disease (7)

A

Glucose control, BP control lipid control, reduction of microalbuminuria, weight loss/exercise, smoking cessation, aspirin

43
Q

What are results of DCCT for T1DM?

A

Intensive therapy reduces retinopathy, nephropathy and neuropathy
Nonsignificant decrease in CVD

44
Q

What are results of EDIC for DCCT follow up?

A

A1c converged
Metabolic memory: risk reduction persisted
Reduction in CVD and death

45
Q

What are results of UKPDS for T2DM?

A

Intensive therapy reduces microvascular diseases

No difference in CV outcomes

46
Q

What are results of BP control in UKPDS?

A

Reduction in retinopathy and loss of visual acuity

47
Q

What are results of monitoring post-trial for UKPDS?

A

Decrease in MI, diabetes-related death

Metabolic memory: decreased risk of microvascular complications persisted

48
Q

Retinopathy Screening

A

Annual dilated eye: T1DM (5 years) T2DM (at dx)

Counsel preggers on risk

49
Q

Nephropathy Screening

A

Annual urine microalbumin: T1DM (5 years) T2DM (at dx)

Confirm abnormal tests and initiate ACE inhibitor

50
Q

Neuropathy Screening

A

Annual exam : T1DM at 5yr T2DM at dx

51
Q

CV Screening

A

Check BP at first visit (goal

Endocrinology (26 decks)

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