DM complications Flashcards

1
Q

microvascular complications

A

-eye:
-retinopathy
-cataracts
-glaucoma
-> blindness

-kidney:
-nephropathy- microalbuminuria and gross albuminuria
-> kidney failure

-nerves:
-neuropathy- peripheral and autonomic
-> amputation

-all can lead to death and/or disability

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2
Q

diabetic retinopathy

A

-Diabetic retinopathy is MC cause of new cases of blindness among adults 20-74 years of age.
-Each year, between 12,000-24,000 people lose their sight because of diabetes.
-During the first 2 decades of disease, nearly all patients with type 1 diabetes and over 60% of patients with type 2 diabetes have retinopathy
-develops in some degree in nearly all pts
-MC cause of new cases of blindness in adults
-most predominant cause of vision loss are clinically significant macular edema and proliferative diabetic retinopathy
-proper ophthalmic care and exam to identify retinopathy in early stages

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3
Q

screening for diabetic retinopathy

A

-type 2- initial dilated and comprehensive eye exam by ophthalmologist at time of diabetes dx
-If no evidence of diabetic retinopathy (DR) for 1 or more annual eye exams and glycemia is well controlled, then screening every 1–2 years may be considered
-If any level of DR is present -> dilated retinal exam should be repeated at least annually
-If DR is progressing or sight-threatening, then exam required more frequently
-Programs that use retinal photography (with remote reading or use of a validated assessment tool) to improve access to DR screening can be appropriate screening strategies for DR
-Such programs need to provide pathways for timely referral for a comprehensive eye examination when indicated

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4
Q

risk of diabetic retinopathy related vision loss

A

-Duration of diabetes disease
-Type 1 patients experience a 25% rate of retinopathy after 5 years of disease, and 80% at 15 years of disease
-Up to 21% of newly diagnosed type 2 patients have some degree of retinopathy at time of diagnosis
-Puberty
-Pregnancy- GDM doesnt tend to have eye problems -> dont need to fu as often
-Lack of appropriate ophthalmic examination

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5
Q

retinopathy

A

-Diabetes accounts for 8% of all legal blindness in the US
-Tight control – delays onset and progression of retinopathy
-Proteinuria, elevated blood urea nitrogen, and elevated blood creatinine
-Cataract: 5x more common among people with diabetes
-Glaucoma- Glaucoma occurs with increased frequency in people with diabetes

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6
Q

natural hx of diabetic retinopathy

A

-from most mild to severe
-Mild nonproliferative diabetic retinopathy (NPDR)
-Moderate NPDR
-Severe NPDR
-Very Severe NPDR
-Proliferative diabetic retinopathy (PDR)- new vessels are being formed bc less O2 -> fragile and bleed easily

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7
Q

mild NPDR

A

-Clinical Findings
-Increased vascular permeability
-Microaneurysms
-Intraretinal hemorrhages
-Clinically Significant Macular Edema (CSME) possible

-Management/Treatment
-Annual follow-up
-If CSME present: color fundus photography, fluorescein angiography, and photocoagulation

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8
Q

moderate NPDR

A

-Clinical Findings
-Venous caliber changes
-Intraretinal Microvascular Abnormalities (IRMAs)
-CSME possible

-Management/Treatment
-6-12 month follow-up without CSME
-Color fundus photography
-CSME present: color fundus photography, fluorescein angiography, focal photocoagulation*, 3-4 month follow-up

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9
Q

severe/very sever NPDR

A

-Clinical Findings
-Retinal ischemia
-IRMAs
-Extensive hemorrhage and microaneurysms
-CSME possible

-Management/Treatment
-3-4 month follow-up
-Color fundus photography
-Possible panretinal photocoagulation
-CSME present: color fundus photography, fluorescein angiography, focal photocoagulation* (clotting off the blood vessels), 3-4 month follow-up

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10
Q

proliferative diabetic retinopathy

A

-Clinical Findings
-Ischemia induced neovascularization
-at the optic disk (NVD)
-elsewhere in the retina (NVE)

-Vitreous hemorrhage
-Retinal traction, tears, and detachment
-CSME possible

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11
Q

normal retinopathy

A

-Color yellowish orange to creamy pink
-Disc vessels tiny
-Disc margins sharp (except perhaps nasally)
-The physiologic cup is located centrally or somewhat temporally.
-It may be conspicuous
-or absent. Its diameter from side to side is usually less than half that of the disc.

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12
Q

micoaneurysms

A

-Tiny, round, red spots seen commonly but not exclusively in and around the macular area.
-They are minute dilatations of very small retinal vessels, but the vascular connections are too small to be seen ophthalmoscopically.

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13
Q

deep retinal hemorrhages

A

-Small, rounded, slightly irregular red spots that are
sometimes called dot or blot hemorrhages.
-They occur in a deeper layer of the retina than flame shaped hemorrhages.
-Diabetes is a common cause

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14
Q

neovascularization

A

-Refers to the formation of new blood vessels.
-They are more numerous, more tortuous, and narrower than other blood vessels in the area and form disorderly looking red arcades.
-A common cause is the late, proliferative stage of diabetic retinopathy.
-The vessels may grow into the vitreous, where retinal detachment or hemorrhage may cause loss of vision
-Neovascularization with fibrous proliferations,
distortion of the macula, and reduced visual acuity

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15
Q

PDR management and tx

A

-2-4 month follow-up
-Color fundus photography
-Panretinal photocoagulation (3-4 month follow-up)
-Vitrectomy
-CSME present: focal photocoagulation, fluorescein angiography

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16
Q

diabetic neuropathy

A

-About 60-70% of people with diabetes have mild to severe forms of nervous system damage, including:
-Impaired sensation or pain in the feet or hands -> check feet at every visit
-Slowed digestion of food in the stomach
-Carpal tunnel syndrome
-Other nerve problems
-More than 60% of nontraumatic lower-limb amputations in the United States occur among people with diabetes

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17
Q

risk factors of neuropathy

A

-Glucose control
-Duration of diabetes
-Damage to blood vessels
-Mechanical injury to nerves
-Autoimmune factors
-Genetic susceptibility
-Lifestyle factors
-Smoking
-Diet

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18
Q

pathogenesis of diabetic neuropathy

A

-Linked to duration of diabetes and level of glucose control
-May affect any part of the nervous system - cranial, peripheral, and autonomic
-Mainly starts at and affects lower limbs
-Often causes paresthesias of extremities
-Symptoms are symmetric and associated with intense burning

-Metabolic factors
-High blood glucose
-Advanced glycation end products
-Sorbitol - breakdown product
-Abnormal blood fat levels
-Ischemia
-Nerve fiber repair mechanisms

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19
Q

screening for diabetic neuropathy

A

-may not have neuropathy in type 1 because they present much earlier
-All people with diabetes should be assessed for diabetic peripheral neuropathy (DPN) starting at dx of type 2 diabetes and 5 years after dx of type 1 diabetes and every visit after
-check every visit after and with evidence of other microvascular complications, particularly kidney disease and DPN
-Screening can include asking about orthostatic dizziness, syncope, or dry cracked skin in the extremities.
-Signs of autonomic neuropathy include orthostatic hypotension, a resting tachycardia, or evidence of peripheral dryness or cracking of skin

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20
Q

dx test for neuropathy

A

-Assess symptoms - muscle weakness, muscle cramps, prickling, numbness or pain, vomiting, diarrhea, poor bladder control and sexual dysfunction

-Comprehensive foot exam:
-Skin sensation and skin integrity:
-Temperature/pinprick sensation [small fibers]
-Vibration with 128Hz tuning fork [large fibers]
-Quantitative Sensory Testing (QST)
-Monofilaments [10-g] for risk for ulceration and amputation

-Nerve conduction studies
-Electromyographic examination (EMG)
-Ultrasound

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21
Q

tx of neuropathy pain

A

-Gabapentinoids, serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants, and sodium channel blockers are recommended as initial pharmacologic treatments for neuropathic pain in diabetes.
-Refer to neurologist or pain specialist

22
Q

classification of diabetic neuropathy

A

-Symmetric polyneuropathy
-Autonomic neuropathy
-Polyradiculopathy
-Mononeuropathy

23
Q
A

longest nerves are most affected
-stocking

24
Q

symmetric polyneuropathy

A

-MC form of diabetic neuropathy
-Affects distal lower extremities and hands (“stocking-glove” sensory loss)
-Symptoms/Signs
-Pain
-Paresthesia/dysesthesia
-Loss of vibratory sensation
-Symptoms generally begin distally in the toes and feet and move upward toward the calf
-not uncommon for symptoms to also begin to appear in the hands, and the patient develops what is known as “stocking-glove” sensory loss.
-Symptoms include pain, abnormal sensation in the affected areas, and loss of vibratory sensation. Thermal sensation is also affected.

25
complication of polyneuropathy
-Ulcers -Charcot arthropathy -Dislocation and stress fractures -Amputation - Risk factors include: -Peripheral neuropathy with loss of protective sensation -Altered biomechanics (with neuropathy) -Evidence of increased pressure (callus) -Peripheral vascular disease -History of ulcers or amputation -Severe nail pathology
26
treatment of symmetric polyneuropathy
-Glucose control -Pain control: -Tricyclic antidepressants -Topical creams -Anticonvulsants -Foot care: Screening and referral to a podiatrist
27
foot problems
-annual incidence of foot ulcers among people with diabetes is 2.5-10.7%, and the annual incidence of amputation is 0.25-1.8% * -Charcot's foot: -Acutely swollen foot with negative radiographic changes may represent the early stage of Charcot's foot -Requires careful observation, appropriate rest, elevation and immobilization, and referral to a professional -Distinguishing Charcot's foot from infection or monarticular arthritis may be difficult, and careful follow-up is required
28
essentials of foot care
-comprehensive vascular, neurologic, musculoskeletal, skin, and soft-tissue evaluation should be done annually and at every visit -Examination: -Annually for all patients -Patients with neuropathy - visual inspection of feet at every visit with a health care professional -Including between the toes and the posterior aspect of the heels -Musculoskeletal evaluation should include foot and ankle joint range of motion and inspection for bone abnormalities -Observe for abnormal gait or stance (with and without shoes) and abnormal wear patterns of his/her shoes
29
diabetic foot ulcers
-Prompt and proper care of diabetic foot ulcers is essential -Exclude systemic infection -Infection and/or inflammation may result in widely fluctuating blood glucose levels -Surgical and antibiotic treatment of abscesses or deep infection -> may control the infection and also help bring blood glucose levels under better control -Patients with severe hyperglycemia may have decreased ability to fight infection -Poor nutritional status may hinder the healing process and must be corrected promptly -usually locations: pad of foot, heel, knuckles (metatarsal heads), dorsal toe
30
nylon monofilament test
-There is a risk of ulcer formation if the patient is unable to feel the monofilament when it is pressed against the foot with just enough pressure to bend the filament. -The patient is asked to say “yes” each time he or she feels the filament. -Failure to feel the filament at four of 10 sites is 97 percent sensitive and 83 percent specific for identifying loss of protective sensation.
31
general guidelines for foot care
-Advise patients to: -Use lotion to prevent dryness and cracking -File calluses with a pumice stone -Cut toenails weekly or as needed (go to podiatric)- always cut toenails straight -Always wear socks and well-fitting shoes -Notify their health care provider immediately if any foot problems occur
32
autonomic neuropathy
-Affects the autonomic nerves controlling internal organs -Peripheral -Genitourinary -Gastrointestinal -Cardiovascular- diabetics may not even feel chest pain! -Is classified as clinical or subclinical based on the presence or absence of symptoms
33
peripheral autonomic dysfunction
-Contributes to the following symptoms/signs: -Neuropathic arthropathy (Charcot foot) -Aching, pulsation, tightness, cramping, dry skin, pruritus, edema, sweating abnormalities -Weakening of the bones in the foot leading to fractures -Testing: -Direct microelectrode recording of postglanglionic C fibers -Galvanic skin responses -Measurement of vascular responses
34
peripheral autonomic dysfunction treatment
-Foot care/elevate feet when sitting -Eliminate aggravating drugs -Reduce edema: -midodrine -diuretics -Support stockings -Screen for CVD
35
genitourinary autonomic neuropathy
-bladder dysfunction -> tx- voluntary urination; catheterization (if retention) -retrograde ejaculation -> tx- antihistamine -erectile dysfunction -> tx- sildenafil, tadalafil -dyspareunia (decrease vaginal secretion) -> lubricants; estrogen creams
36
gastrointestinal autonomic neuropathy
-Symptoms/Signs: -Gastroparesis resulting in anorexia, nausea, vomiting, and early satiety -Diabetic enteropathy resulting in diarrhea and constipation; nocturnal diarrhea -Treatment: -Other causes of gastroparesis or enteropathy should first be ruled out -Gastroparesis - Small, frequent meals, metoclopramide, erythromycin -> make sure this due to diabetes and not atherosclerosis, tumor, etc. -Enteropathy - loperamide (anti-diarrheals), antibiotics, stool softeners or dietary fiber
37
cardiovascular autonomic neuropathy
-Symptoms/Signs -Exercise intolerance -Postural hypotension -Treatment: -Discontinue aggravating drugs -Change posture (make postural changes slowly, elevate bed)- prevents syncope, orthostatic hypotension -Increase plasma volume
38
polyradiculopathy
-Lumbar polyradiculopathy (diabetic amyotrophy)-> Thigh pain followed by muscle weakness and atrophy -Polyradiculopathies are diagnosed by electromyographic (EMG) studies -Treatment: -Foot care -Glucose control -Pain control
39
mononeuropathy
-Peripheral mononeuropathy -Single nerve damage due to compression or ischemia -Occurs in wrist (carpal tunnel syndrome), elbow, or foot (unilateral foot drop*) -Symptoms/Signs: -numbness -edema -pain -prickling
40
cranial mononeuropathy
-Mononeuropathies CN III, IV, and VI (and other CN’s affected) -> causing diplopia and abnormality of visual fields -Symptoms/Signs -unilateral pain near the affected eye -paralysis of the eye muscle -double vision -Mononeuropathy multiplex
41
mononeuropathy: treatment
-foot care -glucose control -pain control
42
other tx options
-aldose reductase inhibitors -ACE inhibitors- doesnt need to be HTN -weight control -exercise
43
diabetic nephropathy
-Occurs in 20% of patients with type 2 diabetes mellitus -Develops SLOWLY (over 15-25 years), but the period may appear to be shorter in type 2 because dx is late in the course of the disease -First evidence of nephropathy is persistent albuminuria (albumin excretion 30- 299mg/24h); moderate albuminuria (microalbuminuria) -By the time a rise in serum creatinine has occurred, over 50% of renal function has been lost -first visit needs a full panel work up ->300 mg/24 h: overt proteinuria/macroalbuminuria/persistent albumin excretion -Management includes tight control of glucose, blood pressure, and protein-restricted diets* -ACE inhibitors delay the progression of microalbuminuria into overt diabetic nephropathy -> if cough sx switch to ARB
44
5 stages of kidney disease
-Stage 1: Hyperfiltration, or an increase in glomerular filtration rate (GFR) occurs. Kidneys increase in size. -Stage 2: Glomeruli begin to show damage and microalbuminuria occurs. -Stage 3: Albumin excretion rate (AER) exceeds 200 micrograms/minute, and blood levels of creatinine and urea-nitrogen rise. Blood pressure may rise during this stage -Stage 4: GFR decreases to less than 75 ml/min, large amounts of protein pass into the urine, and high blood pressure almost always occurs. Levels of creatinine and urea-nitrogen in the blood rise further. -Stage 5: Kidney failure, or end stage renal disease (ESRD). GFR < 10 ml/min. The average length of time to progress from Stage 1 to Stage 4 kidney disease is 17 years for a person with type 1 diabetes. The average length of time to progress to Stage 5, kidney failure, is 23 years.
45
tx of diabetic nephropathy: htn
-Hypertension Control - Goal: lower blood pressure to < 140/90 -<130/80 mmHg ideally if high risk of ASCVD -Antihypertensive agents -Angiotensin-converting enzyme (ACE) inhibitors -captopril, enalapril, lisinopril, benazepril, fosinopril, ramipril, quinapril, perindopril, trandolapril, moexipril -Angiotensin receptor blocker (ARB) therapy -candesartan cilexetil, irbesartan, losartan potassium, telmisartan, valsartan, esprosartan -Diuretics: (not the best) -Thiazide -Loop diuretics
46
tx of diabetic nephropathy: glycemic control
-<7 target HmgA1c -pregnancy <8 -becoming hypoglycemic is more dangerous than hyperglycemia -Preprandial plasma glucose 90-130 mg/dl -A1C <7.0% [as close to normal as possible without causing hypoglycemia] -Peak postprandial plasma glucose <140 mg/dl -Self-monitoring of blood glucose (SMBG) -Medical Nutrition Therapy -Restrict dietary protein to RDA of 0.8 g/kg body weight per day (dont need to know number)
47
tx of end-stage renal disease (ESRD)
-There are 3 primary tx options for individuals who experience ESRD: -1. Hemodialysis- fistula between artery and vein on forearm -2. Peritoneal Dialysis -3. Kidney Transplantation
48
hemodialysis procedure
-fistula or graft is created to access the bloodstream -Wastes, excess water, and salt are removed from blood using a dialyzer -Hemodialysis required approx. 3 times per week, each treatment lasting 3-5 hrs -Can be performed at a medical facility or at home with appropriate patient training
49
hemodialysis diet and complications
-Hemodialysis Diet -Monitor protein intake -Limit potassium intake -Limit fluid intake -Avoid salt -Limit phosphorus intake -Complications -Infection at access site -Clotting (at fistula), poor blood flow -if waiting for fistula to heal -> put in port -Hypotension
50
peritoneal dialysis procedure
Dialysis solution is transported into the abdomen through a permanent catheter where it draws wastes and excess water from peritoneal blood vessels. The solution is then drained from the abdomen.
51
kidney transplant
-A cadaveric kidney or kidney from a related or non-related living donor is surgically placed into the lower abdomen. -3 factors must be taken into consideration to determine kidney/recipient match: -Blood type -Human leukocyte antigens (HLAs) -Cross-matching antigens -Complications/Risk Factors -Rejection -Immunosuppressant side effects -Benefits -No need for dialysis -fewer dietary restrictions -higher chance of living longer