Vascular complications of DM-2 Flashcards
1
Q
Where are DM complications occuring in body and why?
A
- nerves, skin, retina, kidney, heart, brain, arms and legs
- common to all of these are: blood vessels
2
Q
fatty streaks appear when?
A
0-10, part of natural aging process
3
Q
What pts will be bypassed instead of stented?
A
- diabetics (multiple vessel disease) and pts with Left main artery disease
4
Q
Microvascular complications?
A
- nephropathy
- retinopathy
- neuropathy
5
Q
Macrovascular complications?
A
- cardiovascular and cerebrovascular: HTN MI TIAs and strokes platelets hypersensitivity PVD
6
Q
What is diabetic nephropathy the leading cause of in US? other numbers?
A
- ESRD (end stage renal disease)
- 40% of new cases and growing
- 33% of people in US who seek renal replacement have DM
- both type 1 and II since 80s predominantly type 2
- higher prevalence in certain ethnic and racial groups: American Indians, Hispanics, and African Americans
7
Q
What is pathophys of nephropathy?
A
- lesions occurring in diabetic kidney, hammers on glomeruli, basement membrane thickens leading to glomerular scelrosis and nodular glomerulosclerosis (specific to diabetics)
- all cause impaired blood flow, nodular lesions in glomerular capillaries of kidneys, and the kidneys will slowly die
- proteins leak through damaged membrane
- kidneys and nephrons hypertrophy, hyperfiltration occur early in disease suggesting increased work on the kidneys, difficult to reabsorb excessive amounts of glucose
- then comes the microalbuminuria (first sign)
- decline in GFR and leads to ESRD
- not really reversible
8
Q
Lesions encountered in diabetic nephropathy?
A
- glomerularsclerosis (Kimmelstiel-Wilson) disease: specific to diabetes, much higher in native americans, hispanics, african americans. Causes impaired blood flow and loss of fxn
- renal vasculature - renal artery stenosis: losing blood flow to kidneys, kidneys sense low oxygen and release renin, lungs release angiotensin - creaetes increased volume and constricts vessels in periphery to increase blood prussure
(if on ACEI: been stable and then all of sudden feels crappy - check creatinine levels - could be renal artery stenosis (ACEI blocking renin)
9
Q
What is microalbuminuria?
A
- refers to appearance of small but abnormal amounts of albumin in the urine: leading indicator of developing nephropathy, 30-300 mg/24 hours
- strongest independent risk factor of CVD
- risk increased by
duration of diabetes, high blood pressure, and smoking
10
Q
Nephropathy progression to macroalbuminuria?
A
- greater than 300 g/24 hr
- steady drop in GFP
- ESRD leading to dialysis
11
Q
How can decline of nephropathy be slowed?
A
- tight glucose control
- BP control
- protein restriction in diet to decrease proteinuria
- smoking cessation
12
Q
What drugs help nephropathy?
A
TOCS:
- ACEI
- ARBs: have marked antiproteinuric effect, used even if pt is normotensive, these are cardioprotective as well, possibly prevent or reverse progresion towards renal failure
- may consider nondihydropyyidine Ca channel blockers (Cardizem) and B blockers (Lopressor, and Tenormin)
13
Q
When should ACEI not be used?
A
- in renal artery stenosis, pregnant women (category x)
- otherwise it should be used in every diabetic pt
14
Q
Screening protocol for nephropathy?
A
- annual screening:
type 1 starting 5 years after dx
type 2 starting at time of dx (don’t know how long they have had this) - random spot urine: measure ratio of protein (albumin) to creatinine) - closeley reflects 24 hr urinary protein estimations
15
Q
Diabetic retinopathy numbers?
A
- leading cause of acquired blindness b/t ages 20-65 in US
- 20 years after onset, 100% Type 1 and 60% type 2 have some degree of retinopathy
- proliferative and nonproliferative
16
Q
Nonproliferative retinopathy?
A
- increased capillary permeability
- dilation of venules
- presence of microaneurysms
- appear as dots
- hard exudates: yellow deposits of proteins and lipids
- superficial retinal microinfarcts: cotton wool spots
17
Q
Proliferative retinopathy?
A
- neovascularization
- extend b/t retina and vitreous: can lead to sudden vision loss, neovascular glacoma, blind painful eye, retinal detachment (floaters), senile cataracts (snowflake lens opacities) - progress to blindness
18
Q
Screening guidelines for retinopathy?
A
- annual dilated fundoscopic exams by an ophtho
- pregnant ladies need to be extra careful, dilated fundoscopic exam before conception and every 4-8 weeks (high risk pregnancy)
- key is strict BP and glucose control early on
19
Q
Tx of retinopathy?
A
- tight glucose control
- aggressive tx of HTN
- Vit C, E, and beta carotene have not shown to be protective
- statins decrease lipid deposition (want LDL to be less than 70)
- laser photocoagulation
- vitrectomy for severe macular edema
20
Q
What is peripheral neuropathy?
A
- pathophys changes including thickening of walls of nutrient vessels that supply the nerve leading to assumption that vessel ischemia plays a major role
- 2nd finding: segmental demyelination process that affects the schwann cells which slows nerve conduction
21
Q
What sensation do you lose first in peripheral neuropathy?
A
- vibratory sensation: good early indicator
- pain comes next - werid, like a burning and shocking pain, really difficult to tx
- temp: predispose diabetics to sig complications - stepping on nails, glass, hot or cold surfaces
- effects schwann cells -> progresses distally to proximal (demyelination) - dragging their feet
22
Q
Somatic neuropathy: peripheral polyneuropathy?
A
- most common
- have a glove and stocking distribution:
pain, numbness, hyperethesias which increase in sensitivity, paresthesias: burning, itching, and tingling - eventual sensory loss: loss of proprioception, and loss of vibratory sense
