Complications of DM Flashcards
Pathogenesis of Diabetic Tissue Damage (4)
- Oxidative Stress
- Inflammation
- Glucotoxicity–>Advanced glycosylation end products (AGE)
- Vasoconstriction, angiogenesis, coagulation,
Retinopathy Statistics: Onset/prevalence
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
Pathophysiology of Diabetic Retinopathy (3)
Hyperglycemia: dysregulated retinal blood flow, oxidative stress, increased vascular permeability, microthrombosis (ischemia), endothelial proliferation
Genetics
Hypertension
Mild NPDR Signs (3)
Microaneurysms
Dot hemorrhages
Hard exudate (lipid leakage within mø)
Moderate/Severe NPDR Signs (3)
Soft exudates: “Cotton wool spots” (nerve infarcts)
Venous beading
Intraretinal microvascular abnormalities (IRMA)–>Occluded vessels, dilated/tortuous capillaries
What risk increases with severity of NPDR?
Risk of progression to PDR
Macular Edema:
Edema and thickening of retina
Accounts for 75% of blindness
Requires special fundoscopic exam
Proliferative Diabetic Retinopathy Signs (4)
Neovascularization (new blood vessels leaky–>hemorrhage)
Preretinal and vitreous hemorrhage–>acute vision loss that resolves spontaneously
Fibrosis–>Retinal traction/detachment
Ischemia
Prevention of retinopathy: Cornerstones (2) and Weaker links (3)
Glycemic control and antihypertensives Weaker evidence for: Lipid lowering meds Antiplatelet meds Carbonic anhydrase inhibitors
Effect of Glycemic Control on Retinopathy
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
Treatment of Retinopathy:
NPDR
High Risk/severe PDR
Vitrectomy
NPDR: focal photocoagulation
High-risk/severe PDR:
panretinal photocoagulation (PRP)
Meds: VEGF-inhibitors, intravitreal glucocorticoids
Vitrectomy for nonresponsive shit
Nephropathy: Epidemiology–Onset and Risk
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
Risk factors for nephropathy (8)
Poor glycemic control, obesity, race, hypertension, age, tobacco use, retinopathy
Pathologic changes of Nephropathy: Glomerular changes (3)
Mesangial expansion
Thickening of glomerular basement membrane
Glomerular sclerosis
Course of Nephropathy (6)
Hyperfiltration (increased kidney size)–>Microalbuminuria–>Regress to normal–>Macroalbuminuria–>Decresed GFR–>ESRF
Prevention of Nephropathy (3)
Glycemic control
Blood pressure control (
Treatment of Nephropathy (4)
ACE Inhibitors/ARB: Improves albuminuria but not prevent onset
Other hypertensive agents: diltiazem/verapamil
Dietary restriction: salt/protein
Weight loss
Neuropathy: Prevalence
50-70% lifetime
Most common microvascular complication
Risk Factors for Diabetic Neuropathy (big list)
Age, duration of diabetes, poor glucose controls, blood vessel damage, mechanical injury to nerves, genetics, HTN, dyslipidemia, tobacco use, alcohol use
Peripheral Neuropathy (aka distal, symmetric polyneuropathy): Symptoms (4) and Distribution
Stocking glove distribution
Decreased sensation, paresthesia, hyperesthesia, worse at night
Polyneuropathy: clinical findings
Physical exam (2)
Electrodiagnostics (2)
Physical exam: sensory loss (proprioception/vibration), loss of ankle reflexes
Electr Tests: Decreased nerve conduction velocity and amplitude of evoked potentials
Treatment of painful neuropathy (6)
Anticonvulsants TCAs SNRIs Topical agents Opioids Antioxidants TENS (nerve stim)
Types of autonomic neuropathy (4)
CV, GI, genitourinary, peripheral
CV Neuropathy Symptoms (4): P-MET
Postural hypertension
MI
Exercise intolerance
Tachycardia
GI Autonomic Neuropathy: Esophageal enteropathy (2)
Gastro-esophageal reflux disease
Transient Lower Esophageal Sphincter relaxation
GI Autonomic Neuropathy: Diabetic enteropathy (3)
Small bowel dysfunction: diarrhea, steatorrhea
Colonic dysfunction: constipation
Anorectal dysfunction: fecal incontinence
GI Neuropathy: Gastroparesis–Symptoms (2)
Early satiety, nausea, vomiting
Worsening of glycemic control
GI Neuropathy: Gastroparesis–treatment (3)
Glycemic control
Diet (decrease fat/fiber)
Prokinetic agents: erythromycin/azithromycin
Genitourinary Autonomic Neuropathy: Px (2)
Urinary retention: UTIs and incontinence
ED
Peripheral Autunomic Nueorpathy (sudomotor neuropathy): Presentation (4)
Impaired perspiration: dry skin, itchiness
Peripheral edema
Callus formation (can form ulcers)
Neuroarthropathy
Describe Acute Onset Mononeuropathy: Onset and resolution
Sudden weakness or pain in single nerve that resolves spontaneously
How does acute onset mononeuropathy present? CN and Peripheral locations
CN: Opthalmoplegia (CN III,IV,VI) or Bell’s Palsy (CNVII)
Peripheral: Carpal tunnel or foot drop
Acute Onset Radiculopathy: Types (2), location and px
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
Prevention of Neuropathy (5)
Glucose control BP control Treatment of dyslipidemia Smoking cessation Decreased alcohol intake
Diabetic Foot Ulcers: Risk factors (4)
Neuropathy: decreased pain sensation/dry skin/calluses
Foot deformity
Peripheral vascular disease
Poor glycemic control (impaired wound healing)
Prevention of Foot Ulcers (6)
Avoid walking barefoot, proper fitting shoes, trim toe nails, daily foot inspection, daily foot washing, moisturizer
What are main chronic macrovascular complications? (3)
Coronary artery disease
Cerebrovascular disease
Peripheral vascular disease
CVD in DM Stats:
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
Risk factors for CVD (big list)
age, duration of DM, poor glucose control, HTN, dyslipidemia, renal disease/albuminuria, Women, obesity, smoking, sedentary lifestyle
What is most important factor for microvascular disease in T1DM? When is risk highest?
Duration of diabetes– risk highest after 20-25 years
What are factors for microvascular disease in T2DM?
Usually pre-existing–insulin resistance and presence of multiple other risk factors
Prevention of microvascular disease (7)
Glucose control, BP control lipid control, reduction of microalbuminuria, weight loss/exercise, smoking cessation, aspirin
What are results of DCCT for T1DM?
Intensive therapy reduces retinopathy, nephropathy and neuropathy
Nonsignificant decrease in CVD
What are results of EDIC for DCCT follow up?
A1c converged
Metabolic memory: risk reduction persisted
Reduction in CVD and death
What are results of UKPDS for T2DM?
Intensive therapy reduces microvascular diseases
No difference in CV outcomes
What are results of BP control in UKPDS?
Reduction in retinopathy and loss of visual acuity
What are results of monitoring post-trial for UKPDS?
Decrease in MI, diabetes-related death
Metabolic memory: decreased risk of microvascular complications persisted
Retinopathy Screening
Annual dilated eye: T1DM (5 years) T2DM (at dx)
Counsel preggers on risk
Nephropathy Screening
Annual urine microalbumin: T1DM (5 years) T2DM (at dx)
Confirm abnormal tests and initiate ACE inhibitor
Neuropathy Screening
Annual exam : T1DM at 5yr T2DM at dx
CV Screening
Check BP at first visit (goal
