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Flashcards in Vascular complications of DM-2 Deck (55):

Where are DM complications occuring in body and why?

- nerves, skin, retina, kidney, heart, brain, arms and legs
- common to all of these are: blood vessels


fatty streaks appear when?

0-10, part of natural aging process


What pts will be bypassed instead of stented?

- diabetics (multiple vessel disease) and pts with Left main artery disease


Microvascular complications?

- nephropathy
- retinopathy
- neuropathy


Macrovascular complications?

- cardiovascular and cerebrovascular:
TIAs and strokes
platelets hypersensitivity


What is diabetic nephropathy the leading cause of in US? other numbers?

- 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


What is pathophys of nephropathy?

- 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


Lesions encountered in diabetic nephropathy?

- 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)


What is microalbuminuria?

- 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


Nephropathy progression to macroalbuminuria?

- greater than 300 g/24 hr
- steady drop in GFP
- ESRD leading to dialysis


How can decline of nephropathy be slowed?

- tight glucose control
- BP control
- protein restriction in diet to decrease proteinuria
- smoking cessation


What drugs help nephropathy?

- 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)


When should ACEI not be used?

- in renal artery stenosis, pregnant women (category x)
- otherwise it should be used in every diabetic pt


Screening protocol for nephropathy?

- 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


Diabetic retinopathy numbers?

- 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


Nonproliferative retinopathy?

- 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


Proliferative retinopathy?

- 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


Screening guidelines for retinopathy?

- 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


Tx of retinopathy?

- 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


What is peripheral neuropathy?

- 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


What sensation do you lose first in peripheral neuropathy?

- 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


Somatic neuropathy: peripheral polyneuropathy?

- 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


What will you see in diabetic neuropathy?

- abnormal gait, drag their feet
- hammer toes
- abnormal pressures on feet
- trauma and fracture
- soft tissue atrophy d/t arterial insufficiency
- foot ulcers that never heal
- osteomyelitis and gangrene


What should be done on each exam on diabetic pt?

- detailed foot exam with each visit:
color, sores, pressure areas, feel for pulses, cap refill
- neuro exam of foot: monofilimant test, reflextes, vibratory sensation, proprioception


Tx of neuropathy?

- pain and sensory issues: TCAs work well
- Elavil (Amitryptilene)
- ASA, tylenol, NSAIDS (watch out for kidneys)
- tegretol (Carbamazapine)
- neurontin (Gabapentin): best result
- Lyrica (Pregabalin)
- cymbalta (Duloxitine) SNRI: less hyperawareness of pain


Pt education on neuropathy?

- prevention of foot ulcers
- daily foot inspection
- approprate footwear
- drying and nail cutting
- podiatry visit annually


Autonomic neuropathy? GI

- gastric dysmotility: gastroparesis
going to have delayed emptying, constipation, N/V, diarrhea, all can lead to ***hyperglycemia


What cranial nerves can be affected in diabetic neuropathy?

- CN 3, 4, 6 (mostly 6 - lateral gaze)
- even 7: facial


Autonomic neuropathy?

- orthostatic hypotension: elevate HOB, gradual position change from supine to upright, support stockings
- cardiac rhythm disturbances
- bladder involvement: retention: diuretics, self cath, incontinence: detrol
- ***erectile dysfunction


Tx of autonomic neuropathy?

- orthostatic hypotension: Florinef (fludrocortisones) and Midodrine (ProAmatine)
- gastraparesis: metocloperamide (carbamazepine), erythromycin, imodium (Loperamide)
- erectile dysfunction: Viagra or cialis



focal limb or cranial nerve:
- present acutely and are self limiting
- cranial nerves commonly involved
- CN 3,4, 6, 7
- limb commonly femoral, sciatic, or peroneal
- diabetic amyotrophy: muscle atrophy and weakness: anterior thigh and pelvic girdle


What percentage of diabetics will die from a macrovascular event?



What are the 3 macrovascular complications?

- Cerebrovascular disease


What is atherosclerosis?

- fibrofatty lesions in intimal lining of large and medium sized arteries such as aorta, coronary arteries, and large vessels that supply the brain
- heart attack, stroke, AAA


Process of atherosclerosis formation?

- chronic inflammatory disorder of the intima of large blood vessels characterized by formation of fibrofatty plaques called atheroma
- develop into foam cells
- LDLs become oxidized and release more inflammatory mediators -> forms clumps of lipids
- body tires to correct inflammatory process- leading to fibrous scar tissue and ectracellular tissue is covered with connective tissue, this bleeds, and attracts more inflammatory mediators - then ulcerates, hemmorhages and could flick off and lodge downstream , pt will present with angina while exercising
- in diabetes: more sugar so more inflammation and fatty streaks


Timeline of atheroscelrosis?

- from first decade: start making foam cells and fatty streaks, then from third decade intermediate lesion then atheroma, and fourth decade: fibrous plaque and complicated lesion and rupture - thrombosis and hematoma


Endothelial dysfunction leads to imbalance of factors resulting in vascular disease, what are these factors?-

- increased LDLs
- diabetes
- smoking
all lead to dysfunction:
vasoconstriction, increased platelet and leukocyte adhesion, SMC migration and growth, and increased lipid deposit and decreased clearance


Mechanisms of atherogenesis in diabetes?

- abnormal lipoproteins
- insulin resistance and hyperinsulinemia
- procoagulant state
- hormones, Growth factor, cytokines enhanced SMC proliferation and foam cell formation


Clinical manifestations of diabetes and atherosclerosis?

- depend on vessel invovled and extend of obstruction
- narrowing of vessel and producing ischemia
- sudden vessel obstruction due to plaque rupture
- thrombosis and formation of emboli
- aneurysm formation due to weakening of vessel wall


Final manifestations of atherosclerosis?

- aorta: complications are those of thrombus and weakening of vessel wall
- coronary, peripheral, and cerebral arteries: ischemia, and infarction due to vessel occlusion
- if there is disease in one vascular bed, don't forget about the others


loss of Endothelium structure due to?

- constriction
- growth promotion
- prothrombotic
- proinflammatory
- pro-oxidant


Coronary artery disease?

- leading cause of death of men and women in US
- insidious process
- almost all of us have early fibrous plaques in coronary arteries


HTN as risk factora and tx?

- detrimental RF with diabetes
- tx: control HTN: below 120/80
- ACEI (lisinopril, enalapri, captopril)
- ARBs (losartan, valsartan)
- b-blockers: lopressor, atenolol, nadolol
use cautiously - may mask warning signs of hypoglycemia (adrenergic blunting)
- most will require a combo of meds for control


Improving cardiovascular, peripheral and cerebral vessel health?

- smoking cessation
- management of obesity
- hyperlipidemia
- lifestyle modifications
- exercise
- glycemic control


Blood pressure goals?

- check at every visit
- optimal is less than 120/80
- minimal goal: 130/80
- take meds as prescribed
- advise not to smoke, smoking cessation counseling for those who smoke
- diabetics: strive for near normal blood glucose levels: monitor blood glucose levels regularly, take meds as Rx


Guidelines for reducing risk of CVD?

- diet: limit sat. fats to less than 7% of total calories
limit dietary cholesterol to less than 200 mg
limit intake of trans fatty acids, DASH diet
- lipids: LDL less than 100, less than 70 ideally, HDL in men greater than 40 and in women greater than 50, TGs less than 150, and non-HDL cholesterol is less than 130, take meds as Rx


Physical activity guidelines for reducing risk of CVD?

- 30 minutes of moderate intensity activity on most days of the week


Wt management recommendations?

- BMI: 18.5-24.9
waist circumference less than 35 in women, and less than 40 in men


Antiplatelt agents in guidelines for reducing risk of CVD?

- consider low dose aspirin in those over age 40
- consider other antiplatelet agents if CI to aspirin


PVD hx?

- every office intake form should include:
pain/cramping in legs when walking or walking uphill or in a hurry
- does the pain improve sitting or standing still?
- pain improves within 10 min of resting?


Primary sites of PVD?

- femoral and popliteal arteries: 80-90%
- tibial and peroneal: 40-50%
- aorta and iliac: 30%


Dx of PVD?

- history taking
- careful exam of leg and feet
- pulse eval
- ABI (SBP in ankle/ SBP in upper arm)


Normal ABI?

- greater than 0.90
claudication: 0.5-0.9
** diabetics may give false reading


Who should get screened for PAD?

A screening ABI should be performed in pts with diabetes
- those greater than 50: if normal an exercise test should be carried out, the ABI test should be repeated every 5 years
- those younger than 50 who have other risk factors associated with PAD: smoking, HTN, hyperlipidemia diabetes for more than 10 years


Who should be a part of the diabetes management team?

- PA-C
- endocrinologist
- podiatrist
- ophtho
- dentist
- vascular surgeon
- Registered dietician/nurse
- educate the person
- mental health specialist