Vascular complications of DM-2 Flashcards
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: HTN MI TIAs and strokes platelets hypersensitivity PVD
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?
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)
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
Mononeuropathies?
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?
70-80%
What are the 3 macrovascular complications?
- CVD
- Cerebrovascular disease
- PAD
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
- HTN
- 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
- HTN
- 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
