Flashcards in Diabetes Microvascular Complications (half of one lecture) Deck (40):
Name some things diabetes is the most common cause of...
-Blindness in ages 20-74
-Non-traumatic leg amputations
-2-4x higher death rates due to heart disease
-7th leading cause of death in USA
What are the 3 most common microvascular complications of diabetes?
retinopathy, nephropathy, neuropathy
-->result of hyperglycemia
What is the mechanism for hyperglycemia-induced tissue damage?
Not completely understood. Involves genetic factors, repeated acute changes in cellular metab and cumulative long-term changes in stable macromolecules due to hyperglycemia, leading to tissue damage. Also involves independent accelerating factors like hypertension, hyperlipidemia etc
What are the 2 major categories of diabetic retinopathy?
1. Non-proliferative (NPDR)
2. Proliferative (PDR)
When is the ave onset of retinopathy in type 1 vs type 2?
Type 1: obset 2-5 yrs after diagnosis, nearly everyone affected by 20 yrs
Type 2: 20% at the time of diagnosis, obset 4-7 years prior to diagnosis. 50-80% incidence at 20 yrs
Describe the pathophys of retinopathy
Hyperglycemia-->dysreg retinal blood flow-->inc inflammation/oxidative stress, edema (inc vasc permeability), ischemia (microthrombosis), proliferation of new bvs
-hypertension, dyslipidemia and meds are also risk factors
Describe the genetics of retinopathy
Inc incidence in 1st deg relatives, associated with nephropathy in T1D pts
-Thickening of the retina
-Accounts for 75% of vision loss due to diabetes
-Can occur at any stage of retinopathy and is clinically significant
What is mild NPDR?
-Microaneurysms (small areas of dilated arteries), dot hemorrhages, and/or hard exudates (lipid leakage from within macrophages in the retina)
-5% annual progression to PDR
What is moderate/severe NPDR?
-Findings of mild NPDR plus...
-Soft exudates (cotton wool spots caused by nerve fiber layer infarcts), venous beading, intraretinal microvascular abnormalities (occluded vessels, dilated and tortuous capillaries)
-Moderate: 15% annual progression PDR
-Severe: 50-75% progression
How do we diagnose macular edema?
Req specialized fundoscopic exam
What is the key characteristic of PDR?
-new bvs are fragile and can easily rupture. Rupture results in hemorrhage
What can proliferative retinopathy lead to?
2. Preretinal and vitreous hemorrhage
-Acute vision loss, often resolves spontaneously
-Retinal traction and detachment
How should retinopathy be prevented?
-Glycemic control (highly effective in primary prevention--T1D--via metabolic memory as well, somewhat helpful at slowing progression of NPDR in T2D, more helpful with T1D)
-Maybe with lipid lowering, antiplatelet agents or carbonic anhydrase inhibitors
How do we treat retinopathy ?
-NPDR with clinically significant macular edema (CSME): focal laser photocoagulation
-High-risk and severe PDR: panretinal photocoagulation and medical therapy: Intravitreal glucocorticoids, VEGF inhibitors
-Vitrectomy indications: nonclearing vitreous hemorrhage, traction retinal detachment involving fovea, severe PDR not responsive to PRP
Describe epidemiology of nephropathy
Most common cause of kidney failure in US
-Onset 5-20 yrs after diabetes
-Independent risk factor for both CV and overall mortality
What are the risk factors for nephropathy?
-Poor glycemic control
-Race (AAs, Pima Indian, Mexican-American)
-Other microv disease like retinopathy
What are the pathologic changes in nephropathy?
-mesangial expansion, basement membrane thickening, sclerosis
Albuminuria (protein in urine)
-Microalbuminuria (high albuminuria)-->>30-300mg/g creatinine
-Proteinuria (macro/very high albuminuria)-->>300mg/g creatinine
How does nephropathy progress?
First, inc glomerular filtration. Then microalbuminuria develops with progression to proteinuria or, if control it, regression to normoalbuminuria. If didn't control it, net result is a decrease in kidney fxn/GFR and progression to end=stage kidney failure
How do we prevent nephropathy?
-Treatment of dyslipidemia
-Measurement of spot urine microalbumin to creatine ratio
What is the treatment of nephropathy?
-ACE inhibitor/Angiotensin II receptor blocker (first line, dilate efferent arteriole to reduce glomerular pressure)
-Other antihypertensive agents
-Dietary restriction (no sodium, protein)
-All in addition to glucose control
Epi of neuropathy
-Most common microvascular complication
-50-70% lifetime incidence of at least one form of neuropathy
Most common type of diabetic neuropathy?
-Diabetic polyneuropathy (peripheral neuropathy) is the most common type
List the risk factors for neuropathy
-Duration of dis
-Poor glucose control
-Mechanical injury to nerves
-Excessive alc use
List the 4 types of diabetic neuropathy
1. Distal symmetric sensorimotor polyneuropathy
2. Autonomic neuropathy
3. Polyradiculopathy (diabetic amyotrophy)
4. Mononeuropathy (cranial, peripheral, mononeuritis multiplex)
What are the symptoms of peripheral neuropathy?
-Worse at night
-Sensory symptoms worse than motor
-Axonal mostly (hands and toes)
Treatment of peripheral neuropthay
What are the 4 types of autonomic neuropathy
Describe cardiovascular autonomic neuropathy
-Resting tachycardia (loss of parasymp tone)
-Exercise intolerance (fixed HR, dec CO)
-Postural hypotension (orthostatic and post prandial
Describe GI autonomic neuropathy
-Gallbladder atony and elargement
Describe gastropareiss autonomic neuropathy
-Delayed gastric emptying (issue with timing insulin injections)
-Symptoms: early satiety, nausea, vomiting, worse glycemic control or none
-Treatment: glycemic control, dietary mods, prokinetic agents
Describe genitourinary autonomic neuropathy
Describe peripheral autonomic neuropathy
-aka Sudomotor neuropathy
-Callus formation (ulcers)
-May contribute to neuroarthropathy (charcot joint, foot anatomy changes to create weird pressure pts)
How do we prevent neuropathy?
-Dec alc intake
Diabetic foot ulcers
-MAjor cause of amputations, sepsis, death
What are the risk factors for diabetic foot ulcers
-Neuropathy (dec pain, dry skin and callus, abnormal weight bearing pressure pts)
-Foot deformity (charcot)
-Peripheral vasc dis
-Poor glycemic control-->impaired wound healing
Prevention of foot ulcers?
-Proper fitting shoes
-Trimmed toenails, avoid sharp edges
-Daily foot inspection
-Daily foot washing
Treatment of NPDR without CSME
Risk factor mamagement
Treatment of PDR or CSME