Microvascular Complications of DM Flashcards
There's a lot of detail in this lecture...
4 molecular pathways implicated in pathogenesis of diabetic tissue damage?
Polyol pathway (involves oxidative stress).
Advanced glycosylation end-products (AGE) -> inflammation.
Protein Kinase C (PKC) activation.
Hexosamine pathway.
What are the big 3 areas of microvascular complications of DM?
Retinopathy, nephropathy, and neuropathy.
What has hyperglycemia got to do with retinopathy? (5 processes)
Causes altered blood flow, inflammation, edema, ischemia, and proliferation.
Two major categories of diabetic retinopathy?
Non-proliferative diabetic retinopathy (NPDR)
Proliferative diabetic retinopathy (PDR)
What’s the most common cause of vision loss of diabetes?
Macular edema.
3 signs of mild edema?
Microaneurysms
Dot hemorrhages
Hard exudates (macrophages leaking lipids)
3 signs of moderate/severe retinopathy?
Soft exudates (“cotton wool spots”)
Venous beading
Intraretinal microvascular abnormalities (messed up, dilated, tortuous vessels)
What’s the main characteristic of proliferative diabetic retinopathy (PDR)? Why is that bad?
Neovasculariztion.
Bad because new vessels are fragile and prone to hemorrhage, fibrosis, and ischemia.
Can cause retinal detachment.
2 main ways to prevent retinopathy in diabetes?
3 treatments with less evidence?
“Cornerstones”: Glycemic control, antihypertensives.
Less evidence: Lipid lowering, antiplatelets, carbonic anyhydrase inhibitors.
Is glycemic control better for primary prevention or delaying progression of retinopathy?
Primary prevention, unsurprisingly.
3 treatments for severe PDR?
Panretinal photocoagulation (PRP). Medical Tx: intravitreal steroids, VEGF-inhibitors. Vitrectomy (only for very severe cases).
3 pathological changes in glomerular disease (of diabetes)?
Mesangial (i.e. stromal) expansion.
Basement membrane thickening.
Sclerosis.
What’s the difference between microalbuminuria and proteinuria?
Proteinuria is more. ( > 300 mg/g Creatinine)
Microabuminuria is 30-300 mg/g Creatinine.
5 stages in the natural history of diabetic nephropathy? At what point is this most likely still reversible?
Glomerular hypefiltration (w/ enlarged kidneys).
Microalbuminuria.
Macroalbuminuria.
Decreased GFR.
End stage kidney failure.
This is most likely still reversible at the microalbuminuria stage.
4 ways to prevent nephropathy?
Glycemic control.
Blood pressure control.
Treat dyslipidemia <- note this helps nephropathy, less clear for retinopathy.
Monitor urine microalbumin:creatinine ratio.
When should screening for nephropathy start in T1D vs. T2d?
T1D: annually starting 5 years after Dx.
T2D: right away.
2 medical treatments for diabetic nephropathy?
2 behavioral changes?
ACE inhibitors.
Angiotensin II receptor blocker.
Restrict sodium and protein intake. Lose weight.
Why do antihypertensives help nephropathy?
Efferent arteriole from glomerulus is dilated, reducing glomerular pressure.
Where does diabetic neuropathy first present?
Usual in hands in feet.
4 types of diabetic neuropathy?
Distal symmetric sensorimotor polyneuropathy (i.e. peripheral/diabetic neuropathy).
Autonomic neuropathy.
Polyradiculopathy.
Mononeuropathy.
Symptoms of peripheral neuropathy?
What’s lost first in peripheral neuropathy?
Decreased sensation, paraesthesia, or hyperesthesia.
Vibration and proprioception are lost first?
Motor stuff is lost later.
2 physical exam findings in polyneuropathy?
Sensory loss.
Loss of ankle reflexes.
4 things on DDx of polyneuropathy? (other than diabetes-related)
Alcohol, B12 deficiency, Uremia (from kidney disease), hypothyroidism.
Treatment of painful neuropathy?
Lots of things: Anticonvulsants, TCAs, SNRIs, opioids, topical stuff…
4 types of autonomic neuropathy?
Cardiovascular
GI
GU
Peripheral (sudomotor)
4 CV manifestations of autonomic neuropathy?
Resting tachycardia. Exercise intolerance (HR won't increase). Orthostatic hypotension. Silent MI. (can be fatal)
Big picture of GI autonomic neuropathy? What 4 things can this lead to?
Loss of smooth muscle tone.
Lower esophageal sphincter relaxed -> GERD.
Gastroparesis.
Diabetic enteropathy. (Constipation / diarrhea / fecal incontience).
Gall bladder atony and enlargement (increased risk of stone formation).
Treatment of gastroparesis secondary to diabetic autonomic neuropathy? (3 things)
Glycemic control
Diet modification: less fat, more fiber.
Prokinetic agents: Eg. erythromycin, metoclopramide (Reglan)
How does delayed gastric empyting mess up glycemic control?
People take insulin with meals, but if food doesn’t get absorbed quickly, people will have a period of hypoglycemia followed by hyperglycemia.
4 GU manifestations of autonomic neuropathy?
Urinary retention -> UTIs + overflow incontinence. Erectile dysfunction. Retrograde ejacuation (internal urethral sphincter not closing). Female sexual dysfunction (pain, no lube).
Skin changes secondary to peripheral autonomic neuropathy?
Less sweating -> dry, itchy skin.
Peripheral edema.
Biomechanical changes -> callus and ulceration.
Can the neuropathy from diabetes be acute?
Yes. Can manifest as sudden weakness and pain in single nerve. (doesn’t look like stroke, because it’s more LMN than UMN)
Presentation of acute-onset radculopathy aka diabetic amyotrophy?
Pain followed by weakness… often of L2-L4 -> legs, hips, buttocks.
Can be truncal and happen in a dermatomal pattern.
Why are foot ulcers bad?
Amputations, sepsis, death.
4 risk factors for diabetic foot ulcers?
Neuropathy (can't feel pain, skin changes) Foot deformity -> pressure points Peripheral vascular disease Poor glycemic control (the latter 2 impair wound healing)
What is Charcot arthropathy?
In diabetes, loss of arch of foot. Can predispose to ulcers.
