Diabetes Microvascular Complications (half of one lecture) Flashcards Preview

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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
-Kidney failure
-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


Macular edema

-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?

1. Neovascularization

2. Preretinal and vitreous hemorrhage
-Acute vision loss, often resolves spontaneously

3. Fibrosis
-Retinal traction and detachment

4. Ischemia


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)
-Antihypertensive therapy
-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
-Genetic factors
-Race (AAs, Pima Indian, Mexican-American)
-Tobacco use
-Other microv disease like retinopathy


What are the pathologic changes in nephropathy?

Glomerular disease
-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?

-Glycemic control
-BP control
-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)
-Weight loss
-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
-BV damage
-Mechanical injury to nerves
-Genetic susceptibility
-Tobacco use
-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?

-Decreased sensation
-Worse at night
-Sensory symptoms worse than motor
-Axonal mostly (hands and toes)


Treatment of peripheral neuropthay

-Topical agents


What are the 4 types of autonomic neuropathy

1. Cardiovascular
2. Gastrointestinal
3. Genitourinary
4. Peripheral/sudomotor


Describe cardiovascular autonomic neuropathy

-Resting tachycardia (loss of parasymp tone)
-Exercise intolerance (fixed HR, dec CO)
-Postural hypotension (orthostatic and post prandial
-Silent MI


Describe GI autonomic neuropathy

-Esophageal enteropathy
-Diabetic enteropathy
-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

-Urinary retention
-Erectile dysfxn


Describe peripheral autonomic neuropathy

-aka Sudomotor neuropathy
-Impaired perspiration
-Peripheral edema
-Callus formation (ulcers)
-May contribute to neuroarthropathy (charcot joint, foot anatomy changes to create weird pressure pts)


How do we prevent neuropathy?

-Glucose control
-BP control
-Dyslipidemia control
-Smoking cessation
-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?

-Avid barefoot
-Proper fitting shoes
-Trimmed toenails, avoid sharp edges
-Daily foot inspection
-Daily foot washing
-Moisturizing cream


Treatment of NPDR without CSME

Risk factor mamagement


Treatment of PDR or CSME



Treatment of nephropathy

Renin-angiotensin inhibition
-note microalbuminuria