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
Q

complication of polyneuropathy

A

-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
Q

treatment of symmetric polyneuropathy

A

-Glucose control
-Pain control:
-Tricyclic antidepressants
-Topical creams
-Anticonvulsants

-Foot care: Screening and referral to a podiatrist

27
Q

foot problems

A

-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
Q

essentials of foot care

A

-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
Q

diabetic foot ulcers

A

-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
Q

nylon monofilament test

A

-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
Q

general guidelines for foot care

A

-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
Q

autonomic neuropathy

A

-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
Q

peripheral autonomic dysfunction

A

-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
Q

peripheral autonomic dysfunction treatment

A

-Foot care/elevate feet when sitting
-Eliminate aggravating drugs
-Reduce edema:
-midodrine
-diuretics

-Support stockings
-Screen for CVD

35
Q

genitourinary autonomic neuropathy

A

-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
Q

gastrointestinal autonomic neuropathy

A

-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
Q

cardiovascular autonomic neuropathy

A

-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
Q

polyradiculopathy

A

-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
Q

mononeuropathy

A

-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
Q

cranial mononeuropathy

A

-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
Q

mononeuropathy: treatment

A

-foot care
-glucose control
-pain control

42
Q

other tx options

A

-aldose reductase inhibitors
-ACE inhibitors- doesnt need to be HTN
-weight control
-exercise

43
Q

diabetic nephropathy

A

-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
Q

5 stages of kidney disease

A

-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
Q

tx of diabetic nephropathy: htn

A

-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
Q

tx of diabetic nephropathy: glycemic control

A

-<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
Q

tx of end-stage renal disease (ESRD)

A

-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
Q

hemodialysis procedure

A

-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
Q

hemodialysis diet and complications

A

-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
Q

peritoneal dialysis procedure

A

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
Q

kidney transplant

A

-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