Endo Test 2

  1. What is the BMI for normal weight, overweight, class I, II, and III obesity?
    • Normal: 18.5-24.9
    • Overweight: 25-29.9
    • Class I: 30-34.9
    • Class II: 35-39.9
    • Class III: >40
  2. What are the pros of using the BMI system?
    • BMI can be easily looked up on a chart.
    • Studies have identified health risks associated with night AND low BMI.
  3. What are the cons of using the BMI system?
    • May misclassify 25% of people.
    • Does not take into account location of body fat.
    • May not be accurate for frail, sedentary, elderly OR body builders.
    • Does NOT distinguish between body fat and lean body mass.
  4. What is the minimum percentage of body fat a female must have for regular menstruation? What are the adverse effects of amenorrhea due to low weight?
    • 13-17%
    • Leads to infertility and earlier onset of osteoporosis.
  5. What is the percentage of body fat considered essential for males? What are the adverse effects of body fat below this point?
    • 3%
    • Males may suffer from chronic fatigue and increased susceptibility to illness if BF is <3%.
  6. What are the locations of body fat that can accumulate within the abdomen? Which is more hazardous to health?
    • Visceral fat (more hazardous)
    • Subcutaneous abdominal fat
  7. What are the etiologies for obesity?
    • High fat/caloric intake
    • Increased amount of food eaten (obese pts underestimate kcals by 30-40%)
    • Decreased physical activity (increased reliance on cars, remote control, elevators, etc)
    • Genetic risk (weight & metabolism are genetically predetermined)
  8. What is the most common genetic cause of MARKED obesity and occurs in 0.01% of the population?
    Prader-Willi syndrome
  9. What are some condition for obesity is a major risk factor?
    • Hypertension
    • Diabetes (type 2)
    • Coronary heart disease
    • Hyperlipidemia
    • Osteoarthritis/gout
    • sudden death
    • CHF
    • All cause mortality
    • Thromboembolic disease (stroke, DVT)
    • Low HDL-C
    • Gallstones
    • Sleep apnea
    • Restrictive lung disease
    • Colo-rectal cancer
    • Endometrial/breast cancer
  10. What should be included in the work-up of an overweight/obese patient?
    • Good family hx, age of onset, recent wt changes, occupational history, eating & exercise behavior, previous wt loss.
    • Assess degree and distribution of body fat.
    • Develop a wise food plan by having pt keep a food diary as part of the assessment of present behavior, and refer to dietician (MNT).
    • Check for secondary causes for obesity (TSH, FT4, cortisol/adrenal overactivity).
  11. How should overweight/obese patients be managed?
    • Exercise is a must.
    • Modify behavior with goal-directed behavior therapy (grp therapy may be helpful to some).
    • Medication use if there has been little or no progress after AGGRESSIVE attempts to lose excess weight AND the pt has a BMI that justifies medication use.
  12. What should the initial weight loss goal be? What is the rate in which weight should be lost?
    • 10% initially
    • Rate of 1-2 lbs per week in 10 lb increments
  13. What are some of the barriers to successful weight loss that need to be overcome?
    • "too tired"
    • "not enough time"
    • "nobody to exercise with"
    • reducing fast food consumption
  14. What type of interaction between the patient and physician, or patient and educator is the most effective in accomplishing weight loss maintenance than any other method?
    Brief monthly personal contact.
  15. What are the treatment options for overweight/obese patients?
    • Diet (MNT)
    • Exercise
    • Behavioral changes
    • Weight loss medications
    • Bariatric surgery
  16. As a family medicine provider what should you talk to your overweight/obese patients about when discussing diet modifications?
    • Maintenance calories (current wt X 13)-500 kcal/day= 1 lb per week wt loss
    • Identifying sources of concentrated carbohydrates
    • Identifying sources of saturated fat
    • Low carbohydrate diets (atkins, protein power, the zone, sugarbusters)
  17. What are the American Heart Association warnings on low carb diets?
    • Wt loss is temporary
    • Vitamin & mineral deficient
    • CI in heart, liver and kidney disease and diabetes (proteinuria)
  18. When do nutrition or weight loss specialists use low calorie diets? What are the basic details of this diet?
    • If BMI is >25 with comorbidities.
    • 800-1000 kcals/day, balanced diet overall
  19. When do nutrition or weight loss specialists use very low calorie diets? What are the basic details of this diet?
    • If BMI is >35 with or without comorbidities (pts at least 30% overweight).
    • High protein, no fat, maintained for 4-6 months, must be monitored due to side effects, consists of 600-800 kcals/day.
  20. What does the incorporation of exercise in an overweight/obese patient's treatment do for them?
    • Signals commitment
    • Accelerates calorie consumption when combined w/ a reduced caloric intake
    • Reduces risk of developing CVD and/or type 2 DM
    • Improves immunity
    • Creates awareness of how food influences weight loss (1 cookie=3 miles)
  21. What do positive behavioral changes do for overweight/obese patients?
    • Influences stimulus control
    • Provides positive reinforcement/increased self esteem
    • Enhances stress management
    • Is essential if weight loss is to be permanent
  22. When assisting overweight/obese pts with weight loss, you should emphasize that the goal weight should be what?
    NOT lower than the pts lowest weight since age 21 (set realistic goals).
  23. What do many obese females typically have in common as a reason to their obesity? How is this treated?
    • Present or past hx or physical, emotional, or sexual abuse and/or depression.
    • Consider SSRI therapy for these pts (Zoloft, Prozac).
  24. What are the guidelines for weight-loss medication use?
    • If used, should be part of a complete program
    • Buys time for change in habits
    • Usual wt loss is about 10%
    • Eval pts within 4-6 weeks of initiating therapy
    • If meds are stopped wt may be regained
    • 1998 NIH guidelines for med use: BMI >/= 30 or BMI >/= 27 w/ obesity related risk factors.
  25. What are the contraindications for the use of weight loss medications?
    • Uncontrolled cardiovascular disease (including HTN)
    • Pregnancy and/or lactation
    • Hx of psychiatric disease
    • Age <18 yrs
    • Concurrent use of certain incompatible meds (MAOIs/SSRIs)
  26. What are the medication options for overweight/obese patients?
    • Noradrenergic anoretics (Phentermine): act at norepinephrine synapses within the brain to suppress appetite, approved for 3 month use, high abuse potential (schedule IV)
    • Adrenergic-Serotonergic reuptake inhibitors (sibutramine "meridia"): prevents reuptake of serotonin and norepinephrine in the CNS, carbs don't taste good, banned from use
    • Lipase inhibitors (Orlistat "xenical"): inhibits gastric and pancreatic lipase, decreases fat absorption by 30%, recommend multivitamin
    • Fat substitutes: Olestra "olean"
  27. In which patient population should bariatric surgery be considered?
    • BMI >40
    • BMI >35 with comorbidities
  28. Which bariatric procedure resects the distal stomach, anastomosing it to a retrocolic segment of jejunum, resulting in gastric remnant capacity of 30-50 ml?
    Roux-en-Y gastric bypass (RYGB)
  29. What are the pro's of bariatric surgery procedures?
    • May be performed laparoscopically.
    • Wt loss of 40-75% of pre-op wt possible.
    • Low mortality rate (0-2.5%)
  30. What are the con's of bariatric surgery procedures?
    • Peptic ulceration: 1-11%
    • Outlet stenosis: 3.5-22%
    • Leakage and sepsis: 0-2.5%
    • Staple disruption: 1.6-48%
    • Need for surgical revision: 17-45%
    • Wound problems, thromboembolism
    • Abdominal wall hernias
    • Gallstones
    • "Dumping Syndrome"
    • Pulmonary edema
    • **complications can occur in up to 50% of pts**
  31. Which bariatric procedure uses a prosthetic band that is positioned on the stomach to decrease size of the gastric outlet, and provides benefits of surgery with less complications?
    Vertical banded gastroplasty (VBG)- requires more frequent follow-ups
  32. What is the excessive growth of terminal hairs in androgen-dependent regions of the body in an adult female referred to as?
  33. What kind of hormone acts on sex-hormone responsive hair follicles on the chin, upper lip, chest, axillae, abdomen, pubic region, convert vellus hairs to terminal hairs and may cause acne?
  34. What are two ways in which androgens can cause hirsutism?
    • Elevated levels of circulating hormone
    • Increased sensitivity of hair follicles to normal levels of hormone
  35. What are the differential diagnosis to be considered when suspecting hirsutism?
    • Idiopathic/familial cause
    • Pharmacological cause
    • Hirsutism with UNLIKELY neoplastic potential
    • Hirsutism WITH adrenal or ovarian neoplastic potential
  36. What are the major sources for testosterone in females?
    • Ovary (60%)
    • Peripheral conversion of androstenedione (40%)
  37. How much of testosterone is bound to sex-hormone binding globulin (SHBG)? How much is bound to albumin? How much circulates free?
    • 65% SHBG
    • 33% albumin
    • 1% free
  38. How long does testosterone circulate before it becomes "fixed" to tissues or gets degraded and excreted? What is "fixed" testosterone converted to and what does it stimulate?
    • 30-60 minutes
    • DHT (active form) by 5-alpha-reductase in the skin
    • Stimulates androgen-dependent hair follicles
  39. What are the sources of androstenedione in females?
    • Ovary
    • Adrenal gland
  40. What is the source of dehydroepiandrosterone sulfate (DHEAS) in females?
    Adrenal gland
  41. What are the major androgens in females?
    • Testosterone
    • Androstenedione
    • Dehydroepiandrosterone sulfate (DHEAS)
  42. What are the characteristics of idiopathic/familial hirsutism?
    • Normal androgen levels
    • More common in Mediterranean and Middle Eastern ethnic groups
    • Onset usually in the peri-pubertal period
    • Slow progression of hair growth
    • Menses are regular
    • PE otherwise normal (no other signs of increased androgens noted)
  43. Name the pharmacologic etiologies of hirsutism.
    • Minoxidil
    • Cyclosporine
    • Dilantin (phenytoin)
    • Anabolic steroids
    • Certain progestins in oral contraceptives
  44. What are the characteristics in hirsutism with an UNLIKELY neoplastic etiology?
    • Irregular menses since menarche
    • Gradual onset of hirsutism
    • Congenital adrenal hyperplasia (CAH, 21-hydroxylase deficiency)
    • Cushing's syndrome
    • Polycystic ovary syndrome (PCOS): accounts for 50% of hirsutism cases
  45. What is polycystic ovary syndrome (PCOS) and how does it cause hirsutism?
    • Common functional disorder of the ovaries
    • Excess LH acts on thecal cells of ovaries causing excess androgen production
    • Sign and symptoms include hirsutism, amenorrhea, oligomenorrhea, infertility, obesity, insulin resistance
  46. What are the characteristics in hirsutism WITH the possibility of adrenal or ovarian neoplasm?
    • Onset of hirsutism is outside peri-menarchal period
    • Rapid progression of hair growth
    • Hirsutism is SEVERE
    • Recent onset of menstrual irregularity
    • Other signs of virulization present: temporal hair recession, crown balding, deepened voice, lost female body contour/breast tissue, increased muscle mass (esp upper shoulder girdle), clitorimegaly
  47. When evaluating for hirsutism, what should be performed BEFORE proceeding to imaging studies?
    Laboratory tests
  48. What are the laboratory tests used to evaluate hirsutism?
    • Free and total testosterone: TT >200 ng/dl or FT >40 ng/dl warrants pelvic exam and ultrasound for polycystic ovaries, if negative perform bilateral adrenal CT scan
    • Serum androstenedione: >1000 ng/dl indicates ovarian or adrenal neoplasm
    • Serum DHEAS: >600 mcg/dl indicates adrenal source of androgen (hyperplasia/carcinoma), perform bilateral adrenal CT scan
  49. What is the treatment for hirsutism of neoplastic origin?
    Surgical/medical treatment of lesion.
  50. What is the treatment for hirsutism of idiopathic origin, PCOS or CAH (unlikely neoplastic origin)?
    • Oral contraceptive with low-androgenic progestins: suppresses LH/FSH production
    • GnRH analogs + estrogen/progesterone: decreases LH/FSH production
    • Weight loss
    • CAH specific: glucocorticoids (consider long term effects) which inhibit ACTH production, or laparoscopic bilateral adrenalectomy
  51. What is an anti-androgen that is commonly prescribed with oral contraceptives when treating hirsutism?
    Spironolactone (Aldactone)
  52. What are some cosmetic therapies one can use to treat the effects of hirsutism?
    • Vaniqa cream
    • Bleaching
    • Tweezing
    • Waxing
    • Electrolysis
    • Shaving
    • Laser therapy
  53. What is the presence of palpable glandular breast tissue in the male called?
  54. How much breast tissue needs to be present in a male for it to be considered gynecomastia?
    >4cm of glandular breast tissue
  55. What condition in males is often caused by an imbalance of the estrogen-androgen ratio?
  56. What are the causes of gynecomastia?
    • Idiopathic/familial
    • Physiologic
    • Endocrine disease
    • Systemic disease
    • Neoplasms
    • Medications
  57. Explain gynecomastia due to idiopathic or familial causes.
    • Breast tissue is extremely sensitive to estrogens.
    • There is excess conversion of estrogen precursors to estrogen.
  58. What are the physiologic reasons for gynecomastia?
    • Neonatal: reflects high lvl of estrogens in maternal-fetal unit
    • Pubertal: affects up to 60% of normal teens (esp tall/obese ones)
    • Aging: occurs in 1/3+ of males 50-80 yrs old
    • Obesity: increased fat causes increased aromatase activity (more testosterone converted to estradiol)
  59. What type of gynecomastia reflects the imbalance between estrogen and androgen action on the breasts caused by increased sex steroid production, may be unilateral/bilateral, presents as a tender discoid enlargement of breast tissue 2-3 cm in diameter beneath the areola, and usually subsides within a year?
    Pubertal gynecomastia
  60. How does aging cause gynecomastia?
    • Testosterone levels decrease
    • Sex hormone biding globulin levels increase
    • This process reduces the amount of free testosterone levels
  61. What are the endocrine causes for gynecomastia?
    • Androgen resistance syndromes (testicular feminization)
    • Aromatase excess syndrome
    • Hyperprolactinemia
    • Klinefelter's syndrome
    • Hypogonadism
  62. What systemic diseases cause gynecomastia?
    • Chronic liver disease
    • Renal disease
  63. What are the neoplasms that can develop that cause gynecomastia?
    • Steroid-producing neoplasms (estrogen-producing neoplasms of the adrenal glands/testes)
    • hCG-producing neoplasms of the testes or lung
    • Breast cancer (unilateral, irregular, painless, firm/hard mass fixed to underlying tissue...higher incidence in men with Klinefelter's syndrome)
  64. What are medications that can cause gynecomastia?
    • Marijuana
    • Amphetamines
    • Type I and II 5-alpha-reductase inhibitors for BPH (proscar, avodart)
    • Exogenous steroids and androgens (50% of athletes abusing androgens and/or steroids develop gynecomastia)
  65. What are the initial laboratory tests to perform when investigating the cause of gynecomastia?
    • Prolactin and beta-hCG: elevated lvls indicate testicular tumor/other malignancy (lung/liver), low levels of hCG indicate primary hypogonadism
    • LH and testosterone: diagnoses primary and secondary hypogonadism
    • Estradiol: usually normal, increased in testicular tumors, liver disease, obesity and with increased beta-hCG
  66. What tests would be performed when evaluating prolonged or concerning cases of gynecomastia?
    • Karyotype for Klinefelter's syndrome: cases of persistent gynecomastia without identifiable etiology
    • Chest X-ray: in unclear cases, may reveal bronchogenic/metastatic carcinoma
    • Needle biopsy: suspicious unilateral/asymmetric enlargment
  67. How is idiopathic or pubertal gynecomastia treated?
    Observe and reassure: follow-up visit at 6 months is appropriate to check for resolution
  68. How is medication induced gynecomastia treated?
    Stop offending drug if possible.
  69. How is painful gynecomastia treated?
    • Tamoxifen (antiestrogen)
    • Danazol (testosterone derivative)
  70. How is gynecomastia due to hypogonadism treated?
    Dihydrotestosterone (not aromatized to estradiol)
  71. When should surgery be used to treat gynecomastia?
    In cases of persistent or severe gynecomastia.
  72. Is GnRH released in a pulsatile manner?
  73. Which hormone binds to specific receptors on Leydig cells in the testes? What does it stimulate?
    • LH
    • Stimulates production of testosterone.
  74. Which hormone binds to receptors on Sertoli cells of the seminiferous tubules? What is this hormone necessary for?
    • FSH
    • Necessary for spermatogenesis.
  75. What is the clinical manifestation of early prenatal testosterone deficiency?
    • Ambiguous genitalia
    • Pseudohermaphroditism (either testes or ovaries, not both)
    • Accessory sex organs and/or external genitalia not completely developed or inappropriate for chromosomal sex
  76. What is the clinical manifestation of later prenatal testosterone deficiency?
    • Micropenis
    • Cryptorchidism (failure of one or both testes to descend)
  77. What is the clinical manifestation of testosterone deficiency in puberty (delayed puberty)?
    • Poor muscle development
    • Decreased strength and endurance
    • High-pitched voice
    • Sparse axillary and pubic hair
    • Absence of facial and body hair
    • Long bones may continue to grow under influence of GH, causing eunuchoidal proportions (testosterone closes epiphyses)
  78. What is the clinical manifestation of post-pubertal testosterone?
    • Decreased libido
    • Impotence
    • Low energy
    • Fine wrinkling around the eyes and mouth
    • Diminished facial and body hair
    • Testes may be small/normal size
  79. What are the 3 types of hypogonadism?
    • Primary: defect of the testes (low testosterone, elevated LH/FSH
    • Secondary: hypothalamic-pituitary defect (low testosterone, low LH/FSH)
    • Defect in androgen action: elevated testosterone, elevated LH/FSH (insensitivity)
  80. What laboratory tests should be performed when evaluating hypogonadism?
    • Serum total testosterone: 60-75% bound to sex-hormone binding globulin (SHBG)
    • Serum free testosterone: 1-2% of total testosterone lvl (biologically active portion)
    • LH and FSH: low lvls warrant further evaluation of pituitary function
  81. What are the levels of testosterone by age group?
    • 20-30 yrs: highest
    • 30-40 yrs: lvls begin to decrease
    • >40 yrs: lvls continue to fall gradually
  82. What are the causes of primary hypogonadism?
    • Klinefelter's syndrome: most common congenital cause of hypogonadism (seminiferous tubule dysgenesis)
    • Cryptorchidism
    • Bilateral anorchia
    • Acquired gonadal failure
    • Other etiologies: lymphoma, anti-tumor chemo, radiation therapy, testicular trauma
  83. What is the most common genotype in Klinefelter's syndrome? What is the phenotype?
    • 47 XXY
    • Male
  84. What are the puberty findings in a pts with Klinefelter's syndrome?
    • Small, firm testes <2cm
    • Testes were normal size during childhood
    • Body hair & external genitalia mature to varying degrees
    • Gynecomastia, impotence, infertility
    • Testosterone decreased, estradiol increased
    • Eunuchoidal proportions, tall stature
    • 47 XXY may be fertile
    • Osteopenia/osteoporosis if not treated
    • Karyotype required to confirm dx
  85. What are the characteristics of cryptorchidism?
    • Undescended testes
    • Occurs in 3% of full-term male infants
    • 0.75% are still affected after 1 yr of age
    • Undescended testes may become cancerous after several years if not removed
  86. What are the characteristics of bilateral anorchia (vanishing testicle syndrome)?
    • Testes are present 1st 14-16 weeks of gestation
    • Scrotum is empty at birth
    • Growth & development normal until secondary sexual development fails to occur @ puberty
    • Diagnose with hCG stimulation test: no increase in testosterone after injection with hCG confirms dx
  87. What causes acquired gonadal failure at the level of the seminiferous tubules and Leydig cells?
    • Seminiferous tubules:
    • Mumps, gonorrhea, leprosy
    • Irradiation
    • Vascular injury
    • Trauma
    • Alcohol ingestion
    • Chemotherapy
    • FSH level is usually elevated, but may be normal
    • Leydig cells: same as above plus aging (LH lvl usually elevated)
  88. What is the treatment for primary hypogonadism?
    • Testosterone IM every 2-3 weeks: transdermal patches (testoderm, androderm) used on scrotal and non-scrotal areas (shoulder, upper arm/ abdomen); 1% testosterone gel (androgen) on same areas as patch; or oral agents (methyltestosterone, fluoxymesterone) just not as effective as IM therapy
    • Prostate cancer screening prior to therapy is appropriate for older men (DRE & PSA)
  89. What are the contraindications to using IM testosterone for primary hypogonadism treatment?
    • Prostate hyperplasia
    • Prostate cancer
    • Boys <13 y/o to avoid premature epiphyseal closure and short stature
  90. What are the side effects if IM testosterone therapy?
    • acne
    • decreased HDL levels
    • gynecomastia
  91. What is the follow-up procedure when treating primary hypogonadism?
    • Check testosterone @ 1 month, then every 6 months
    • Check lipid levels and Hgb/Hct at 3 months
    • DRE every 6 months, PSA
  92. What are the causes of secondary hypogonadism?
    • Kallmann's syndrome
    • Panhypopituitarism
    • Hyperprolactinemia
    • Other etiologies
  93. What is the most common form of secondary hypogonadism?
    Kallmann's syndrome
  94. What are the characteristics of Kallmann's syndrome?
    • Secondary hypogonadism
    • X-linked inheritance- isolated gonadotropin deficiency
    • Associated with the inability discriminate odors
    • Individual has prepubertal testes, eunuchoidal proportions, and gynecomastia
  95. What is the pathophysiology of Kallmann's syndrome?
    Defective development of hypothalamic cells that secrete GnRH (these cells are near the olfactory bulbs).
  96. What are the etiologies of panhypopituitarism?
    • Congenital disorders
    • Tumors
    • Infarction from vascular insufficiency
    • Autoimmune diseases
    • Trauma
    • Infections
  97. What is the cause of hyperprolactinemia and what does it do?
    • Pituitary adenoma
    • Inhibits normal GnRH release, inhibits action of testosterone, and decreases effectiveness of LH
  98. What are other etiologies for secondary hypogonadism?
    • ETOH abuse
    • Chronic illnesses (renal failure, CHF, etc)
    • Obesity (BMI >40 kg/m)
    • Marijuana use
    • Idiopathic
    • Cushing's syndrome
    • Hypothyroidism
    • Cancer, AIDS
  99. What is the treatment for secondary hypogonadism?
    • Treated based on the location of the disorder (hypothalamus/pituitary) OR is focused on underlying etiology.
    • Various hormones are utilized when treating hypothalamic or pituitary etiology (testosterone plus other hormone therapy selected based on man's desire for fertility).
  100. What are the causes of hypogonadism due to a defect in androgen action?
    • Testicular feminization: complete androgen insensitivity
    • Incomplete testicular feminization: incomplete androgen insensitivity
    • 5-alpha-reductase deficiency: variable degrees of gynecomastia, hypospadias, cryptorchidism
  101. What are the characteristics of testicular feminization (genetic male)?
    • Testes function normally but are located intra-abdominally
    • Abnormal receptors in the pituitary gland don't recognize testosterone, development proceeds is if there is a lack of testosterone
    • External female genitalia observed with no uterus or fallopian tubes
    • No male accessory sex organs
    • Testes are cryptorchid
    • Child has appearance of normal pre-pubertal girl
    • At puberty testes secrete large amounts of testosterone that gets converted into estrogens by adipose tissue resulting in a phenotypic female with well developed breasts that never menstruates
  102. What are the characteristics of incomplete testicular feminization?
    Mixed pattern of virilization and feminization.
  103. What is the treatment for testicular feminization?
    • There are NO treatments that can restore androgen receptors.
    • Pt's phenotype and gender assignment are female.
    • Intra-abdominal testes must be removed to avoid malignancy.
    • Estrogen treatment is provided to develop secondary female sexual characteristics.
  104. What are the characteristics of 5-alpha-reductase deficiency (DHT deficiency)?
    • LH, FSH & testosterone levels are normal
    • Internal sex organ develop normally
    • Cryptorchid (intra-abdominal) testes present
    • Dihydrotestosterone-dependent structures fail to develop (prostate, external genitalia are poorly developed)
    • Individual appears female or has ambiguous genitalia at birth
    • At puberty testosterone levels rise dramatically to overcome the defect and secondary sexual characteristics develop (external genitalia becomes masculinized, penis develops, "guevedoce"=penis at 12)
  105. What do osteoclasts and osteoblasts do?
    • -clasts: dissolve bone
    • -blasts: build new bone
  106. How much of the total body calcium circulates in the blood? Of that how much calcium circulates as free (ionized) calcium, how much bound to proteins and how much bound to bicarb, citrate and phosphate?
    • 1% total body calcium circulates in blood
    • 50% circulates as free/ionized (active) calcium
    • 40% is bound to proteins (albumin, globulin)
    • 10% is bound to bicarb, citrate, phosphate
  107. What are the primary regulators of serum calcium?
    • Parathyroid Hormone (PTH)
    • Vitamin D
    • Calcitonin
  108. What is a very potent hormone that exerts major control over the plasma calcium concentration?
    Parathyroid hormone
  109. What are the actions of parathyroid hormone?
    • Stimulates resorption (or dissolution) of bone by osteoclasts, increasing delivery of calcium and phosphorus to the circulation.
    • Increases renal tubular reabsorption of calcium.
    • Stimulates renal activation of vitamin D which enhances intestinal absorption of calcium.
  110. What stimulates PTH secretion from the parathyroid?
    • Falling free (ionized) calcium levels.
    • Stimulating suppressed by rising free (ionized) calcium levels.
  111. How is vitamin D synthesized by the action of sunlight on the skin?
    • 7-DHC (dehydrocholesterol) present in the epidermis is exposed to UV B light.
    • UV B-exposed 7-DHC continues to be transformed by the liver and kidney into the active form of vitamin D.
  112. What is the action of vitamin D on calcium levels?
    Vitamin D increases calcium and phosphate absorption from the intestines.
  113. What hormone is produced by the parafollicular cells of the thyroid gland in response to an elevated serum calcium level and plays a minor role in plasma calcium concentration?
  114. What is the action of calcitonin in regards to calcium levels?
    • Inhibits calcium resorption from bone (inhibits osteoclasts).
    • Increases calcium storage in bone.
    • Increases renal excretion of calcium.
  115. When the serum calcium level decreases, what response will you see with PTH and calcitonin?
    • Increased PTH
    • Decreased calcitonin
  116. When the serum calcium level increases, what response will you see with PTH and calcitonin?
    • Decreased PTH
    • Increased calcitonin
  117. What are the three failures of calcium homeostasis?
    • Hypercalcemia
    • Hypocalcemia
    • Failure to maintain normal bone
  118. What are reasons for hypercalcemia?
    • Increased PTH: primary hyperparathyroidism (women>men)
    • Normal or minimally increased PTH: familial hypocalcuiric hypercalcemia (FHH)
    • Suppressed PTH: malignancy, vitamin D excess, high bone turnover (thyrotoxicosis), immobilization
  119. What is the best assy for evaluating serum calcium level?
    Free (ionized) calcium
  120. If a free calcium assay is not available what should you do?
    • Calculate corrected total calcium level
    • +/- 0.8 mg/dL per each gram of album over (subtract) or under (add) 4.0 g/dL
  121. What is the clinical presentation of hypercalcemia?
    • Stones: kidney stones, nephrocalcinosis, thirst, polyuria, metabolic acidosis
    • Bones: bone pain and fracture
    • Groans: anorexia, dyspepsia, constipation
    • Moans: myalgia, proximal muscle weakness, joint pain
    • Overtones: depression, memory loss, confusion, lethargy, coma
  122. What are the etiologies of primary hyperparathyroidism?
    • Benign parathyroid adenoma (80%)
    • Parathyroid hyperplasia (20%)
  123. What is the pathophysiology of primary hyperparathyroidism?
    • Excess PTH causes hypercalcemia
    • Much of the excess calcium is present in the glomular filtrate
    • Much of the excess in the glomular filtrate is excreted due to overwhelming the renal tubular reabsorption capacity resulting hypercalciuria
  124. What are the signs and symptoms of hyperparathyroidism?
    • Most pts are asymptomatic
    • Total serum calcium >10.5 mg/dl (corrected)
    • Free (ionized) calcium level is elevated (>5.3 mg/dl)
    • Serum phosphate level is low (<2.5 mg/dl)
    • Hypercalciuria or normal urine calcium excretion occurs
    • Shortened QT interval on ECG may be observed
    • If total calcium is >14 mg/dl, pt may be confused, weak, and lethargic
  125. What are the characteristics of parathyroid adenoma?
    • Common, esp in middle-aged women
    • Most presentations are mild/asymptomatic
    • 24-hr urine calcium and phosphorus is increased
    • 20% of pts develop kidney stones
    • X-rays are not required for diagnosing hypercalcemia but instead to check cortical bone mineral density (may be low) or to observe possible changes in distal finger tufts
  126. How is hypercalcemia associated with a parathyroid adenoma treated?
    • Maintain good hydration
    • Surgery considered if: serum calcium is markedly elevated w/ symptoms, there is hx of prior life-threatening hypercalcemia, kidney stones present by abdominal Xray, 30% reduced creatinine clearance, 24-hr urine calcium >400 mg/24 hours, evidence of severe osteoporosis, pt is less than 50 yrs old, pregnancy (2nd tri), medical follow-up or pt compliance issues present.
  127. How should you observe a parathyroid adenoma in an otherwise asymptomatic patient?
    • Follow up every 6 months
    • Ask about symptoms of hypercalcemia at each visit
  128. What are some complications associated with hypercalcemia with increased PTH?
    • Pathologic fractures (more common)
    • Urinary tract infections from stones/obstruction may lead to renal failure and uremia
  129. Parathyroid hyperplasia may be associated with what other endocrine disorder?
    Multiple Endocrine Neoplasia (MEN) types 1, 2a and 2b (familial disorders).
  130. What is the clinical/lab presentation and treatment of parathyroid hyperplasia?
    • Presentation: same as parathyroid adenoma
    • Treatment: subtotal parathyroidectomy
  131. What is the presentation of hypercalcemia with parathyroid cancer? How is it treated?
    • Severe hypercalcemia with very high PTH levels
    • Tumor resection along with affected thyroid lobe
  132. What conditions cause hypercalcemia with increased PTH?
    • Primary hypercalcemia
    • Parathyroid adenoma
    • Parathyroid hyperplasia
    • Parathyroid cancer
  133. What conditions cause hypercalcemia with suppressed PTH?
    • Malignancies (other than parathyroid)
    • Excess vitamin D
    • High bone turnover
    • Immobilization
  134. What are some other malignancies besides parathyroid cancer that can cause hypercalcemia?
    Squamous cell cancer of lung, esophagus, head and neck, renal, bladder, ovarian, breast cancer.
  135. What are the major mechanisms of malignancies that cause hypercalcemia?
    • Tumor production of PTHrP (PTH related protein)
    • Localized bone destruction (multiple myeloma, breast cancer, lymphoma)
    • Tumors may produce calcitriol causing hypercalcemia (Hodgkin's disease, non-Hodgkin's lymphoma)
  136. How does PTHrP produced by malignancies cause hypercalcemia?
    Causes bone resorption and hypercalcemia similar to the action of PTH.
  137. High doses of exogenous vitamin D or excess endogenous production of vitamin D (excess vitamin D) cause hypercalcemia with suppressed PTH. What are some diseases that cause excess vitamin D production?
    • Lymphomas
    • Granulomatous diseases (sarcoidosis, TB, histoplasmosis, coccidiomycosis)
  138. How does hyperthyroidism or excess exogenous thyroid hormone cause hypercalcemia with suppressed PTH?
    They cause high bone turnover.
  139. What is a cause of hypercalcemia with normal or minimally elevated PTH?
    Familial hypocalciuric hypercalemia.
  140. What are the characteristics of familial hypocalciuric hypercalemia?
    • Autosomal dominant disorder, benign
    • There is lifelong hypercalcemia and hypocalciuria
    • Patients are usually asymptomatic
    • There are defective calcium receptors on parathyroid cells
  141. How is hypercalcemia generally treated and managed?
    • Hydration
    • Furosemide to promote calciuresis (increases CA excretion through urine)
    • Avoid immobilization (stay active)
    • Avoid thiazide diuretics, vitamins A&D, calcium containing supplements and antacids
    • Dialysis (pts w/ renal failure, hyperkalemia, CHF)
    • Parathyroidectomy (severe/symptomatic parathyroid adenoma/parathyroid hyperplasia)
    • Bisphosphonates (inhibits bone resorption by osteoclasts, used on hyperparathyroidism, malignancy, prolonged immobilization)
    • Check serum calcium and albumin twice/year (asymptomatic pts)
    • Check renal function & urine calcium once/year (asymptomatic pts)
    • Check bone mineral density of distal radius every 2 years (asymptomatic pts)
    • Consider estrogen replacement therapy for postmenopausal women
  142. What are the signs and symptoms of hypocalcemia?
    • Paresthesias
    • Muscle cramps
    • Tingling of hands, feet, and circumoral area
    • Irritability, confusion
    • Seizures
    • Tetany
    • Laryngospasm, bronchospasm
    • Prolonged QT interval
    • Coma
    • Chvostek's sign (tapping on facial nerve causes facial spasm)
    • Trousseau's sign (carpal spasm occurs when BP cuff is inflated to above systolic pressure for up to 3 minutes)4
  143. What are the etiologies of decreased total calcium?
    • Hypoalbuminemia: total calcium decreased but free (ionized) calcium normal
    • Hypomagnesemia: impairs PTH synthesis and release, causes resistance to PTH, must correct magnesium deficiency to correct calcium deficiency
  144. What is the process of the step-wise approach to the laboratory evaluation of hypocalcemia?
    • If total calcium level is low, check free calcium level if available. If free calcium is NOT available...
    • Check albumin level, correct total calcium level if necessary utilizing formula given. If albumin level is normal...
    • Check magnesium level, correct if necessary. If magnesium is normal...
    • Check the PTH level
    • Check vitamin D level
  145. What are other common causes of hypocalcemia besides hypoalbuminemia and hypomagnesemia?
    • PTH deficiency (hypoparathyroidism)
    • PTH resistance (pseudohypoparathyroidism)
    • Vitamin D deficiency
    • Vitamin D resistance
  146. What conditions cause hypocalcemia with elevated PTH levels?
    • PTH resistance
    • Albright's hereditary osteodystrophy
    • Vitamin D deficiency
    • Vitamin D resistance
  147. What is the pathophysiology of PTH resistance?
    • Defects in the renal parathyroid hormone receptors cause increased urine calcium excretion.
    • PTH receptors in bone are not affected so bone changes due to increased PTH level may be seen (cystic lesion, pathologic fractures, diffuse demineralization)
  148. What are the signs/symptoms of Albright's hereditary osteodystrophy?
    • Patients my have resistance to TSH, FSH, LH
    • Patients have short stature, rounded faces, and short 4th and 5th metacarpals
  149. What can cause vitamin D deficiency?
    • Defective supply: inadequate intake, exposure to sunlight, and malabsorption syndromes
    • Defective processing: liver and kidney disease, medication used (isoniazid, rifampin, phenytoin)
    • Childhood vitamin D deficiency (rickets): poor bone formation at epiphyseal growth plates, poor bone mineralization
    • Adult vitamin D deficiency (osteomalacia): abnormal bone mineralization, BONE PAIN, xray of long bones reveal thin radiolucent lines perpendicular to the cortex (Looser's lines)
  150. What are the characteristics of vitamin D resistance?
    • Vitamin D level is elevated
    • Genetic defects in vitamin D metabolism
    • Severe resistance: childhood rickets
    • Mild resistance: osteomalacia
  151. What are the etiologies for PTH deficiency (hypocalcemia with low PTH)?
    • Surgical damage during any neck surgery: esp thyroid surgery/removal of parathyroid glands.
    • Hypomagnesemia: chronic alcoholism, malabsorption
    • Autoimmune/idiopathic hypoparathyroidism
    • Congenital absence of parathyroid glands
  152. How is chronic hypocalcemia from any cause treated?
    • Oral calcium supplements
    • Oral vitamin D supplements (resistant pts will not benefit)
    • Increase exposure to sunlight
    • Goal is to keep serum calcium in the low-normal range
  153. What is a medical emergency that may be observed after a parathyroidectomy in which there is a decreased level of circulating PTH, causing decreased serum calcium levels?
    Hypoparathyroid tetany (acute hypocalcemia), other signs of hypocalcemia are also commonly present.
  154. How is hypoparathyroid tetany treated in-patient?
    • Airway maintenance
    • Magnesium sulfate for hypomagnesemia (IV)
    • Calcium gluconate for hypocalcemia (10-20 ml of 10% solution by IV slowly till tetany ceases)
    • Transplantation of cryopreserved parathyroid tissue (restores normocalcemia in about 1/4 pts)
    • Oral calcium and vitamin D after pt stabilizes
  155. How is hypoparathyroid tetany prevention therapy maintained out-patient?
    • Maintain serum total caclium in slightly low but asymptomatic range to minimize risk of hypercalciuria and development of renal stones.
    • Calcium & vitamin D supplements
    • Monitor calcium levels every 3 months
    • "Spot" urine calcium assays to check for hypercalciuria
    • HCTZ with potassium supplement as needed for hypercalciuria
  156. What is the pathophysiology of Paget's disease?
    • Excess bone lysis followed by replacement with vascular fibrous connective tissue, then bone formation with disorganized structure.
    • May be consequence of viral infection.
    • Occurs in 1-2% of the population >40 years old
  157. What is the clinical presentation of Paget's disease?
    • Asymptomatic: usually discovered incidentally (73%)
    • Bone pain: 1st symptom, usually constant, worse at night, not precipitated by weight bearing/exercise, not relieved by rest
    • May involve one/several bones
    • Bone deformities may be present
    • Increased warmth over bones may be present (increase bone vascularity)
  158. What are complications associated with Paget's disease?
    • "High output" cardiac failure: increase skeletal vascularity
    • Osteoarthritis of adjacent joints
    • Hypercalcemia if immobilized which may lead to kidney stones
    • Osteosarcoma (uncommon): suspect with severe, intractable pain (occurs in 1-3% of pts)
    • Frequent fractures w/ minimal trauma
    • Spinal cord compression from vertebral fractures
    • Deafness secondary to excess bone formation in auditory region
  159. What are the some of the xrays findings in a patient with Paget's disease?
    • Lytic lesions and multiple fissure fractures of long bones
    • Increased bone density & expansion
    • Radionuclide bone scan reveals diffuse uptake in the skull, pelvis, and long bones
  160. What will lab test show in a patient with Paget's disease?
    • Elevated serum alkaline phosphatase level
    • Normal serum calcium, phosphorus, and PTH levels (resorption matches deposition, calcium may be elevated in immobilized pts)
    • Elevated urinary hydroxyproline (bone resorption marker)
  161. How is Paget's disease treated?
    • If pt is asymptomatic: annual alkaline phosphatase level and X-rays of lytic lesions
    • Treat complications (orthotics as needed)
    • Medications to decreased bone resorption by osteoclasts: bisphosphonates (tx of choice) given clinically until alkaline phosphatase level normalizes then is discontinued for 3 months, nasal calcitonin-salmon (not used often but still effective for some pts)
  162. What is the leading cause of blindness in adults?
  163. What is the normal fasting glucose range?
    • <100 mg/dl
    • 140 mg/dl on 2 hr OGTT
  164. What is the impaired fasting glucose (IFG) range?
    100-125 mg/dl
  165. What is the impaired glucose tolerance (IGT) range?
    OGTT level >/= 140-199 mg/dl @ 2 hr
  166. What is the general age, weight, insulin requirement, ketone prone-ness, pathogenesis, fasting C-peptide level and percentage affected in type 1 diabetes mellitus?
    • Age: young
    • Weight: thing
    • Insulin required: yes
    • Ketosis prone: yes
    • Pathogenesis: autoimmune (90%) beta cell destruction
    • Fasting C-peptide: very low
    • % affected: about 10%
  167. What is the general age, weight, insulin requirement, ketone prone-ness, pathogenesis, fasting C-peptide level and percentage affected in type 2 diabetes mellitus?
    • Age: older
    • Weight: obese
    • Insulin required: no
    • Ketosis prone: no
    • Pathogenesis: peripheral resistance to insulin, beta cell dysfunction
    • Fasting C-peptide: normal/high concentration
    • % affected: about 90%
  168. What are the signs and symptoms of diabetes mellitus?
    • Polyuria
    • Polydipsia
    • Polyphagia (type 1)
    • Weight loss (type 1)
    • Peripheral neuropathy
    • Fatigue, weakness
    • Frequent infections (candidiasis)
    • Slow wound healing
    • Recurrent blurred vision
    • Asymptomatic (type 2)
  169. What are the causes for secondary hyperglycemia?
    • Disorders affecting insulin action or insulin secretion
    • Endocrine disorders (excess GH, hypercortisolism, glucagons/somatostatin)
    • Medication induced (high-dose glucocorticoids, diuretics, phenytoin, niacin)
  170. What are the characteristics of "pre-diabetes"?
    • Pts have IFG, IGT, or HgA1C 5.7-6.4%
    • Increased risk of developing DM and/or cardiovascular disease
    • Is associated w/ metabolic syndrome (insulin resistance syndrome)
    • Pts w/ IFG and/or IGT may have normal HgA1C
  171. How can development of type 2 diabetes be prevented or delayed in some pre-diabetic patients with IGT?
    Use of medical nutrition therapy (MNT) to decrease body weight by 5-10% + exercise + pharmacologic agents.
  172. What are clinical abnormalities associated with metabolic syndrome (insulin resistance syndrome, syndrome X)?
    • Insulin resistance
    • Dyslipidemia: elevated trig, decreased HDL, increased LDL
    • Hypertension: >130/85
    • Hypercoagulable state: elevated plasminogen activator inhibitor-1, hyperfibrinogenemia, increased platelet aggregation)
    • Proinflammatory state: elevated C-reactive protein, endothelial dysfunction
    • Hyperuricemia
    • Hyperinsulinemia
    • Abdominal obesity: waist circumference >40" (males) and >35" (females) w/ BMI of 25-34.9 kg/m
  173. In order for a patient to be diagnosed with metabolic syndrome, they must have 3 out of what 5 clinical abnormalities?
    • Central adiposity
    • IFG or IGT
    • Increased triglyceride level
    • Decreased HDL-C level
    • Hypertension
  174. What is the level of blood glucose directly proportional to?
  175. What is the goal for HbA1C level? Why?
    • <7%
    • Associated with decreased micro/macrovascular complications.
  176. What is the HBA1C for the average American?
  177. What does HbA1C reflect, and how often should it be checked?
    • Glucose control over past 8-12 weeks
    • Should be checked every 3 months in pts w/HbA1C >/= 7% or with change in therapy and checked every 6 months in pts w/HbA1C <7%
  178. What are the advantages of using HbA1C as a screening lab and evaluation tool for diabetics?
    • Measure over 2-3 month, not day to day
    • Provides better indicator of severity and presence of disease
    • A1C levels are relatively stable
    • Ease and convenience of sample collecting (no fast required)
  179. What are some limitations to using HbA1C?
    • Hemoglobinopathies may interfere with results
    • Conditions that cause RBC turnover can cause false positives (anemias, blood transfusions, blood loss, pregnancy)
    • Not useful for acute elevations (DM Type 1)
  180. What are risk factors for developing type 2 diabetes mellitus?
    • Age >/= 45 years
    • Low HDL cholesterol (<35 mg/dl) and/or high triglycerides (>250 mg/dl)
    • Family history of diabetes (1st/2nd degree relative)
    • Overweight or obesity (BMI >/= 25 kg/m)
    • Ethnicity (native american, african american, latino, asian american, pacific islander)
    • Previously identified IFG or IGT
    • HTN
    • Habitual physical inactivity
    • Hx of gestational diabetes mellitus/delivery of baby weighing >9 lbs
    • Polycystic ovarian syndrome (PCOS)- insulin resistance
    • Hx of vascular disease
  181. What are the labs used for screening for type 2 diabetes mellitus in an adult?
    • Fasting plasma glucose (FPG)
    • A1C
    • OGTT
  182. How often should adults be screened for type 2 DM without risk factors? With risk factors?
    • Without: every 3 years for pts >45 yrs
    • With: adults any age with BMI >25, repeat annually if initial fasting glucose is 100-125 mg/dl (IFG), repeat every 3 years if normal
  183. What labs are used to screen for type 2 DM in children?
    Fasting plasma glucose is the preferred test.
  184. When should children be screened for type 2 DM and how often?
    • If the individual is overweight and has one or more risk factors.
    • Test every 2 years starting at age 10 or at the onset of puberty.
  185. What are the three tests used to determine criteria for diagnosis of diabetes mellitus and what is the criteria?
    • Fasting blood sugar (FBS): >/= 126 mg/dl with no caloric intake for at least 8 hours (run HbA1C in conjunction, >6.5% is diagnostic for DM)
    • Random (casual) glucose: >200mg/dl with symptoms of diabetes
    • Oral glucose tolerance test (OGTT): 2 hr plasma glucose >/= 200 mg/dl 
    • **any of the diagnostic criteria above must be confirmed on a different day to make the diagnosis**
  186. Out of the three main lab tests used to diagnose diabetes mellitus, which is recommended as the confirmatory test?
    Fasting blood sugar (FBS)
  187. What is the presentation of patients diagnosed with diabetes mellitus that have a mild case, and how should it be treated?
    • Mild sx/asymptomatic AND negative ketones AND no acute current illness
    • Start MNT and physical activity, if target isn't met in 6-8 weeks start on oral agent therapy
  188. What is the presentation of patients diagnosed with diabetes mellitus that have a moderate case, and how should they be treated?
    • FBS >200 mg/dl OR random >300 mg/dl AND does not meet criteria for mild or severe DM
    • Start oral agent therapy
  189. What is the presentation of patients diagnosed with diabetes mellitus that have a severe case, and how should they be treated?
    • Marked hyperglycemia OR significant weight loss OR severe/significant symptoms OR 2+ or greater ketonuria OR DKA, hyperosmolar state OR severe current illness or surgery
    • Start insulin immediately!!
  190. How do patients perform self-monitoring of their diabetes?
    Blood glucose testing (may need to test 3 x/day or more if they use on insulin pump or are on insulin therapy).
  191. What are some resources available to patients that help them monitor their blood glucose levels appropriately?
    • Diabetes educators: assist w/ patient education of blood glucose self-monitoring (method, frequency, recording)
    • Provider: ensure patient is educated on calibrating and using their insulin pump machine
  192. How is diabetes mellitus generally treated?
    • Diet (MNT): a fundamental element
    • Exercise: ideally 150 min/week of aerobic activity + resistance training 3 times per week
    • Medications: glycemic controlling agents, ASA therapy (75-162 mg/day), lipid control agents, blood pressure control agents
    • Immunizations: annual flu, pneumococcal vaccine
    • Bariatric surgery: if BMI >35
    • Diabetes self management education (DSME): done @ time of diagnosis and annually
  193. What percentage of diabetic patients will adhere to a diet? What percentage of total calories should be saturated fat? What about their beer?
    • <50% adhere to a diet
    • <7% total calories of saturated fat
    • Beer/ETOH in moderation: men not more than 2/day, women not more than 1/day (2 fat exchanges per drink)
  194. What should type 1 diabetes be warned about in regards to exercise?
    Risk of hypoglycemia (exercise decreases blood glucose).
  195. Graded exercise stress tests or radionuclide stress test should performed by which diabetic patients?
    • Diabetic pts >35 yrs
    • Pts with type 2 disease >10 yrs duration
    • Pts with type 1 disease >15 yrs duration
    • Pts with any other risk factor for CAD
    • + presence of microvascular disease (retina 1st thing to go)
    • + presence of peripheral vascular disease
    • + presence of autonomic neuropathy
  196. What are the risk factors that warrant ASA therapy as a primary preventative strategy for coronary artery disease (CAD)?
    • HTN
    • Increased lipid levels (dyslipidemia)
    • Family hx of premature CAD
    • Micro/macroalbuminuria
    • Smoking
  197. What conditions warrant the use of ASA therapy as secondary preventative strategy for diabetics?
    • Transient ischemic attacks (TIA)
    • Peripheral vascular disease (PVD)
    • Non-hemorrhagic stroke
    • MI, angina, or documented CAD (add BB unless contraindicated)
  198. If a patient is allergic to ASA what alternative can you consider?
    Clopidogel (Plavix) 75 mg/day
  199. What are the goals for lipid control in diabetic patients?
    • LDL <100 (<70 if overt CVD present)
    • Trig <150
    • HDL >50
    • **values should be checked annually at minimum by a cardiologist)**
  200. Statins for lipid control should be added to patients with what condition regardless of lab values?
    • Overt CVD
    • Without CVD, >40 yrs with one or more CVD risk factors
  201. What are the goals for blood pressure control in diabetic patients? How often should it be checked?
    • <130/<80
    • Should be checked at each visit.
  202. How long are lifestyle modifications acceptable when treating blood pressure in diabetics? When are lifestyle modifications alone used and when are medications added to therapy? What meds are used?
    • First 3 months only if BP is 130-139/80-89
    • Lifestyle mod AND meds used if BP is >140/>90 
    • Treat with ACE/ARB as first line
  203. When should the pneumococcal vaccine be used for diabetic patients?
    • At time of diagnosis.
    • Repeat dose at age 65 if received prior to 65.
  204. What are the general mechanisms of action for oral type 2 diabetic agents?
    • Stimulate pancreatic insulin secretion (secretagogues): sulfonylureas, meglitinide analogs, D-phnylalanine dervative
    • Alter insulin action: metformin, thazolidinediones
    • Affect absorption of glucose: alpha-glucosidase inhibitors
  205. What are the secretagogue agents used to treat type 2 diabetes?
    • Sulfonylureas: Glipizide (Glucotrol), Glyburide (DiaBeta, Micronase)
    • Meglitinide analogs: Repaglinide (Prandin), Nateglinide (Starlix)
  206. In which pt population are secretagogues used? What are the advantages, disadvantages and contraindications for using these agents?
    • Non-obese/mildly obese, repaglinide and nateglinide are useful for pts with postprandial hyperglycemia.
    • Advantages: long use hx, inexpensive, addresses FPG
    • Disadvantages: hypoglycemia, wt gain, lack of durable glycemic response over time
    • CI: sulfonylureas in severe liver or renal disease
  207. In which pt population is metformin (a biguanide) used? What are the advantages, disadvantages and contraindications for using these agents?
    • Obese pts w/ normal renal/liver function.
    • Advantages: improves lipid profile, no hypoglycemia, wt neutral (most lose wt), address FPG, inexpensive
    • Disadvantages: dose related GI side effects, lactic acidosis occurs with renal insufficiency or after use of IV contrast agents (50% mortality rate)
    • CI: serum creatinine >1.4 mg/dl (female), >1.5 mg/dl (male), concurrent use of IV contrast agents, alcoholics, >/= 80 yrs old unless creatinine normal, CHF
  208. What is the mechanism of action for metformin (a biguanide)?
    Suppresses hepatic gulconeogenesis, increases hepatic insulin sensitivity.
  209. What are the thiazoladinedione oral agents for treating type 2 diabetes mellitus?
    • Rosiglitazone (Avandia)
    • Pioglitazone (Actos)
  210. What is the mechanism of action for thazoladinediones?
    • Sensitizes peripheral tissues to insulin.
    • Decreases FFA release.
    • Increases muscle insulin sensitivity.
  211. In which pt population are thiazoladinediones used? What are the advantages, disadvantages and contraindications for using these agents?
    • Obese with signs of insulin resistance, normal liver function and renal impairment.
    • Advantages: improves lipid profile, address FPG (Pioglitazone)
    • Disadvantages: may take 2-4 months to see effects of therapy, fluid retention (edema/CHF), expensive
    • CI: NYHA Class III or IV CHF, LFTs >2.5 times the upper limit of normal
  212. What are the alpha-glucosdiase inhibitor oral agents used to treat type 2 diabetes mellitus?
    • Acarbose (Precose)
    • Miglitol (Glyset)
  213. What is the mechanism of action for alpha-glucosidase inhibitors?
    • Inhibits alpha-glucosidase activity in the intestinal tract, delaying absorption of carbohydrates.
    • Decreases postprandial hyperglycemia.
  214. In which pt population are alpha-glucosidase inhibitors used? What are the advantages, disadvantages and contraindications for using these agents?
    • Milder presentation of diabetes, no GI symptoms/disease, predominant postprandial hyperglycemic pattern.
    • Advantages: wt neutral, may have preventative tx value, address PPG
    • Disadvantages: GI side effect (flatulence, diarrhea), small effects on HbA1C
    • CI: chronic intestinal disorders, cirrhosis (Acarbose), renal impairment- serum creatinine >2.0 mg/dl (Acarbose, Miglitol)
  215. What are the dipeptidyl peptidase-4 (DPP-4) inhibitor oral agents used to treat type 2 DM?
    • Sitagliptin (Januvia)
    • Saxagliptin (Onglyza)
  216. What is the mechanism of action for dipeptidyl peptidase-4 (DPP-4) inhibitors?
    • Stabilize insulin secretion and decrease glucagon release.
    • Decrease fasting and postprandial glucose levels.
    • Inhibits degradation of endogenous incretin hormones like GLP-1.
  217. What are the advantages, disadvantages and contraindications for using dipeptdyl peptidase-4 (DPP-4) inhibitor agents?
    • Advantages: NOT an injection, no wt gain
    • Disadvantages: minimal GI disturbances, hypoglycemia, HA
    • Precautions: renal impairment- have to adjust the dose, cannot be used on children
  218. What is the incretin mimetic agent used to treat type 2 DM?
    Byetta (Exenatide) Injection
  219. What is the mechanism of action for the incretin mimetic agent (Byetta) used to treat type 2 DM?
    • GLP-1 agonist
    • Enhances glucose-dependent insulin secretion (FPG and PPG improvement)
    • Restores 1st phase insulin response usually absent in type 2 diabetics (increases beta cell response and decreases beta cell workload)
    • Decreases glucagon concentration
    • Decreases gastric emptying time
    • Decreases food intake (promotes satiety, reduces appetite-CNS effects)
  220. In which pt population is an incretin mimetic agent used? What are the advantages, disadvantages and contraindications for using these agents?
    • Adjunct therapy for pts on metformin and/or a sulfonylurea but have not yet achieved glycemic control.
    • Advantages: NOT an insulin substitute, restores 1st line insulin response, decreases food intake
    • Disadvantages: not a treatment for DKA, not approved for monotherapy or in combination with insulin, GI side effects
    • CI: type 1 diabetics
  221. How is oral agent therapy administered?
    • Usually one agent is selected but 2 may be selected for initial therapy if there is evidence of MARKED hyperglycemia after MNT and exercise.
    • Titrate dose over 2-4 months, reinforce MNT and exercise.
  222. What lab values indicate the need to add a second oral drug in a different class to a diabetic patient's therapy after 2-4 months?
    If fasting plasma glucose is >140 mg/dl OR postprandial glucose is >180 mg/dl OR HbA1C is >/= 7.0
  223. After adding a second oral agent to a diabetic patient's therapy, titrating over 2-4 months and re-checking lab values, you decide to add a third oral agent or insulin. Why?
    • Fasting plasma glucose is >140 mg/dl OR postprandial glucose is >180 mg/dl OR HbA1C is >/= 7.0
    • Third oral agent should be of a different class than the other 2 already in use.
  224. What is normal average FPG (mg/dl) or preprandial glucose? What is the goal of glycemic control for diabetes? At what levels should action be initiated?
    • Normal: <100
    • Diabetic Goal: 90-130
    • Initiate action: <80, >140
  225. What is normal average postprandial 2 hr glucose (mg/dl)? What is the goal of glycemic control for diabetes? At what levels should action be initiated?
    • Normal: <140
    • Diabetic Goal: <160
    • Initiate action: >180
  226. What is normal average bedtime glucose (mg/dl)? What is the goal of glycemic control for diabetes? At what levels should action be initiated?
    • Normal: <120
    • Diabetic Goal: 110-150
    • Initiate action: <110, >160
  227. What is normal sustained HbA1C? What is the goal sustained HbA1C for diabetes? At what levels should action be initiated?
    • Normal: <6%
    • Diabetic Goal: <7%
    • Initiate action: >/= 7%
  228. What are the characteristics of medical insulin?
    • Source: recombinant DNA (human)
    • Concentration: U-100 (100 units/ml), U-500 available
    • Formulations: very rapid acting (ultra short acting), rapid-acting (short-acting), intermediate-acting, long-acting
  229. Name the insulin formulations that are very rapid-acting (ultra-short acting).
    • Humalog (lispro)
    • Novolog (aspart)
    • Apidra (glulisine)
  230. Name the insulin formulations that are rapid-acting (short acting).
    Humulin R (regular)
  231. Name the insulin formulations that are intermediate-acting.
    • Humulin N (NPH)
    • Lente
  232. Name the insulin formulations that are long-acting (ultra-lente).
    • Lantus (glargine)
    • Detemir (levemir)
  233. Which insulin is not used as often, has increased risk of delayed hypoglycemia, has a variable absorption rate, and is inexpensive?
    Humulin (rapid acting)
  234. Which insulin is not used as often and has a pronounced peak at 9 hours?
    • Humulin N (NPH) (intermediate acting)
    • Lente (intermediate acting)
  235. Which insulin is generally used as the initial choice, usually initiated at bedtime, and is titrated slowly by 1-3 U every 2-3 days?
    • Lantus (glargine)- long acting
    • Detemir (levemir)- long acting
  236. What are the usual body sites for insulin injection?
    • Abdomen: except circular area w/in 2 inches of the navel
    • Thighs: medial, anterior or lateral
    • Upper arms: near triceps or deltoid
  237. What are the type 2 DM guidelines for ADDING insulin to oral therapy?
    • Continue oral agents at the same dose
    • Add a single evening insulin dose (about 10 U): suggested starting dose 0.1-0.2 U/kg of IDEAL body wt, NPH insulin or Lantus at bedtime
    • 70/30 insulin (evening meal) (OBESE)
    • Adjust dose by monitoring fasting SMBG
    • Increase insulin dose weekly as needed: 4 U if FBS >140 mg/dl, 2 U if FBS=120-140 mg/dl
  238. What are the type 2 DM guidelines for ADVANCING insulin + oral therapy?
    • Indicated when FBS is acceptable but HbA1C >7% and/or SMBG b4 dinner >180 mg/dl.
    • Insulin options include adding AM NPH and mealtime regular insulin or lispro to bedtime NPH, or adding morning 70/30 to suppertime 70/30.
    • Oral agent options include discontinuing sulfonylurea agent, and continueing metofrmin for wt control (if applicable).
  239. Describe insulin therapy management for type 1 diabetes mellitus.
    • Regulate dose after conditions of normal daily activity and optimal diet have been achieved.
    • Once-daily and split-dose regimens are INEFFECTIVE.
    • 3 or 4 dose intensive insulin regimens are recommended.
  240. Describe intensive insulin therapy for type 1 diabetes mellitus.
    Ultra-short-acting insulin analogs (lispro) before meals (more safe and convenient than regular insulin).
  241. What is the insulin of choice for use in insulin pumps?
    Lispro (ultra-short acting)
  242. What are some barriers to insulin therapy?
    • Patient resistance: needles/injections=pain, presence of complications/comorbidities, inconvenience and feeling they "failed" therapy
    • Clinician resistance: time consuming, inadequate support/resources, belief that insulin is the "last resort"
  243. What happens in morning fasting hyperglycemia attributed to the Dawn Phenomenon?
    • Slightly/markedly elevated glucose at 0200-0300 in 75% of type 1 and many type 2 pts.
    • Reduced tissue sensitivity to insulin develops between 0500-0800.
    • Attributed to nocturnal rise in GH secretion.
    • Treat by INCREASING bedtime insulin.
  244. What happens in morning fasting hyperglycemia attributed to the Somogyi (rebound) effect (or Somogyi phenomenon)?
    • Low 0200-0300 glucose observed.
    • Nocturnal hypoglycemia stimulates a surge of epinephrine that produces high glucose levels by 0700 (glucose released by liver).
    • Treat by REDUCING bedtime insulin dose.
  245. What are some acute diabetic complications?
    • Hypoglycemia (<55 mg/dl)
    • DKA
    • Hyperosmolar nonketotic syndrome
  246. What are some chronic diabetic complications?
    • Microvascular (retina, kidney, peripheral nerves)
    • Macrovascular (coronary arteries, peripheral vasculature)
  247. What are the symptoms of hypoglycemia?
    • Neurogenic: hunger, diaphoresis, anxiety, tremors, tachycardia, palpitations
    • Neuroglycopenic: behavior/cognitive changes, drowsiness, confusion, blurred vision, HA, amnesia, seizures, coma
  248. What are the common causes for hypoglycemia?
    • Too much insulin: most common complication of insulin therapy
    • Insulinoma: otherwise healthy ppl
    • Too little food
    • Too much activity
    • ETOH
    • Oral hypoglycemic agents
    • Other meds
    • Menstrual cycle
    • Gastroparesis (nerve damage delays stomach emptying, food is absorbed slower)
  249. What is the treatment for mild to moderate hypoglycemia (BS <50)?
    • 2-3 glucose tabs/gel (dextrosol)
    • 4-6 oz OJ
    • 4-6 oz reg soda
    • 1/4-1/3 cup of raisins
    • 5 lifesaver candies
    • Follow with complex carbs (milk/sandwich)
    • Glucagon if responsive but very symptomatic
  250. What is the treatment for severe hypoglycemia/patient is unresponsive (BS <20)?
    • Home treatment glucagon kit: contains 1 ampule (1 mg), should be provided to every pt receiving insulin therapy, pt and fam/friends should be instructed on use
    • ER treatment: insure adequate airway, give IV glucose (50 ml of 50% solution), once pt is conscious they can sip fruit juice, if IV glucose isn't available, give glucagon 1 mg IM
  251. What is the incidence of DKA?
    • 5-8 episodes/1000 type 1 pts annually, may occur in type 2 esp during acute illness
    • Accounts for 20-40% of new pts
    • 50-60% of children will have at least 1 episode
    • 3-5% of events occur in infants < 1 yr
  252. What are the risk factors for diabetic pts developing DKA?
    • Infection: 30%
    • Lapse in insulin administration: 15-41%
    • Recent onset diabetes: 17-25%
    • Medical illnesses: 10%
    • Trauma, ETOH, steroid use: 10-20%
    • Idiopathic: 2-25%
  253. What are the symptoms of DKA?
    Polyuria, polydipsia for 1-2 days progressing to fatigue, nausea, vomiting, and mental stupor that can progress to coma.
  254. What are the signs of a pt suffering from DKA?
    • Dehydration in stuporous patient
    • Rapid, deep breathing (Kussmaul's respirations)
    • "Fruity" breath odor (acetone)
    • Tachycardia, HOTN
    • May have abdominal pain/tenderness
  255. What are the laboratory findings in pts with DKA?
    • Hyperglycemia (>250 mg/dl): due to decreased glucose uptake plus hepatic gluconeogenesis
    • Ketonemia (elevated serum acetone): elevated lvl of GH, catecholamines, and glucagon increase lipolysis from adipose and liver ketone production
    • Low arterial blood pH: <7.3
    • Low plasma bicarb: <15 mEq/L
    • 4+ glucosuria
    • Elevated serum potassium (may not reflect potassium depletion- dehydration)
    • Elevated serum osmolality
  256. How is DKA managed?
    • Restore circulating plasma volume: there is 4-5 liter fluid deficit in most pts, use IV NS for 4 hrs then 1/2 NS for 4 hrs then consider D5 1/2 NS (glucose <250 mg/dl), avoid excess fluid replacement (>5 L/8 hrs), can cause ARDS or cerebral edema
    • Regular insulin: 10 U IV after 30 min or 0.1 U/kg/hr, goal is to maintain glucose lvl of 250-300 mg/dl to decrease risk of cerebral edema & hypoglycemia
    • If pH <7.0 give 100 ml bicarb over 45 min
    • Give potassium chloride 10-30 mEq/L during 2nd & 3rd hrs of fluid resuscitation as acidosis starts to resolve
    • Monitor ECG
    • Monitor serum osmolality
    • Search for precipitating cause
  257. What are the sick day rule guidelines for preventing DKA?
    • Test urine ketones every 2-4 hours
    • Pt is to call if their blood glucose >250 for >6 hrs
    • Pt is to call if there are + urine ketones for >6 hrs
    • Pt is to continue taking insulin
    • Pt should eat and drink fluids if possible
    • If pt can't eat, they should drink carb containing liquids
  258. What are the characteristic of hyperglycemic hyperosmolar nonketotic syndrome?
    • Occurs in pts with mild or undiagnosed DM
    • Most pts are middle aged/elderly (type 2)
    • Underlying CHF/ renal insufficiency is common
    • Etiologies include: infection, MI, stroke, post-operative states, medications
  259. What are the signs and symptoms of hyperosmolar nonketotic syndrome?
    • Insidious onset of polyuria, polydipsia, and weakness over several days or weeks
    • Lethargy, confusion, coma
    • Profound dehydration
    • ABSENCE of Kussmall's respiration
    • NO acetone breath odor
  260. Why is there such a high mortality rate (10x mortality rate of DKA) in hyperosmolar nonketotic syndrome?
    Due to the insidiousness, organ dysfunction, and delayed diagnosis.
  261. What are the laboratory findings in a pt with hyperosmolar nonketotic syndrome?
    • Severe hyperglycemia: BS 600-2400 mg/dl common
    • No ketosis
    • No acidosis
    • Elevated serum osmolality
    • Moderate to severe dehydration common
    • Hyponatremia initially, then a gradual increase
    • Elevated serum urea nitrogen (dehydration)
  262. How are pts suffering from hyperosmolar nonketotic syndrome treated?
    • Fluid replacement (important!): 4-6 liters over 8-10 hrs, is pt is hypovolemic NS (0.9%) is used, if pt is not hypovolemic, 0.45% saline is used, once glucose level <250 mg/dl give 5% dextrose in water (D5W), 0.45% saline or 0.9% (decreases risk of cerebral edema and hypoglycemia)
    • Insulin: lower dose than DKA
    • Potassium replacement: 10 mEq/L given during initial IV fluid admin if potassium is not elevated
    • Look for underlying cause
  263. What are microvascular chronic complications of diabetes mellitus?
    • Retinopathy: leading cause of blindness ages 20-74 in developed world
    • Nephropathy: 30% of end-stage renal disease pts
    • Neuropathy: distal symmetric polyneuropathy, isolated peripheral, painful diabetic, autonomic
  264. What are macrovascular chronic complications of diabetes mellitus?
    • Coronary artery disease
    • Peripheral artery disease
    • Cerebrovascular disease
  265. What are types of chronic complications of diabetes mellitus?
    • Microvascular
    • Macrovascular (accounts for 75% of death in type 2 DM)
    • Foot problems (both micro and macro damage present)
  266. What are the types of retinopathies that affect diabetics?
    • Background retinopathy: microaneurysms, hemorrhages, exudates, edema
    • Preproliferative retinopathy: cotton-wool spots (arteriolar ischemia)
    • Proliferative retinopathy: retinal ischemia promotes neovascularization (tx with 1000-2000 laser burns which ablate the ischemia therby reducing level of growth factor and neovascularization)
    • Glaucomatous changes of the optic disc: 6% diabetics
    • Premature cataracts
  267. What are the vision screening guidelines for diabetes mellitus?
    • Pts should get comprehensive dilated fundoscopic exam by ophthalmologist/optometrist.
    • Type 1 DM: initial exam within 5 yrs after dx (>/= 10 yrs), then annually
    • Type 2 DM: initial exam at diagnosis, then annually
  268. What are the ocular complaints to worry about in pts who have had DM for more than a few years?
    • Acute loss of visual acuity
    • Diplopia
    • Fluctuating visual changes
    • Floating spots
    • Flashing lights
    • Ocular pain
    • **question pt about these symptoms at each visit**
  269. When should screening for microalbuminuria (earliest stage of diabetic nephropathy) be performed?
    • Type 1: 5 yrs after dx, then annually
    • Type 2: time of dx then annually (after BS is stabilized)
    • Annual UAE screening should be done annually in all diabetic pts until 70 yrs
    • Performed as clinically indicated in pts >70 yrs of age
  270. What is the assay of choice for performing annual screening for microalbuminuria in diabetic patients?
    • Morning spot urine screen for albumin/creatinine ratio (can be ordered as microalbumin, random)
    • Routine UA will for protein will NOT screen for microalbuminuria
    • If ratio is 30-300 mcg/mg confirm microalbuminuria w/ at least 2 of 3 positive collections within 3-6 months
  271. What is a normal result for timed overnight collection urinary albumin excretion and spot albumin:creatinine ratio?
    • Timed overnight: <15 mcg/min
    • Spot: <30 mcg/mg creatinine
  272. What results for timed overnight collection urinary albumin excretion and spot albumin:creatinine ratio indicate microalbuminuria?
    • Timed overnight: >/= 20 mcg/min
    • Spot: 30-300 mcg/mg creatinine
  273. How is microalbuminuria managed in diabetic patients?
    • ACE inhibitors (captopril): used in normotensive type 1, and in type 2 for its renal-protective effect
    • Angiotensin II receptor blockers: cozaar or hyzaar (losartan)
    • Maintain BP: <130/80, and <120/75 for pts with proteinuria >1 gm/24 hrs
    • Repeat albumin:creatinine ratio every 6 months
  274. How is progressive diabetic nephropathy managed?
    • Continued BP control
    • Protein sparing diet
    • Within 5 yrs 50% of pts have 50% decline in GFR
    • In the next 3-4 yrs, 50% will have ESRD (transplant may be required)
    • Think twice before ordering contrast radiographic studies in pts with diabetic nephropathy
  275. What are the characteristics of distal symmetric polyneuropathy (peripheral neuropathy)?
    • Bilateral, symmetrical nerve involvement
    • "Glove and stocking" distribution
    • Primarily sensory: dullness of vibration, pain, temperature perception
    • Symptoms of numbness, hyperesthesias, paresthesias, pain may progress to sensory loss
  276. How would you ensure early detection of peripheral neuropathies when talking to your diabetic patients?
    • Ask about sensation of bugs crawling on feet, burning or shooting pain.
    • Examine distal reflexes, vibratory sensation, and light touch perception.
    • Screen at diagnosis, then annually.
  277. What is the treatment for peripheral neuropathies (distal symmetric polyneuropathy)?
    Tight and stable glucose control to slow progression.
  278. What are the characteristics of isolated peripheral neuropathy?
    • May involve one or several nerves
    • Onset is acute
    • Femoral and cranial nerves are most commonly involved
    • Recovery of all or most function usually occurs in 6-12 weeks (ex. CN III palsy)
  279. What are the symptoms of painful diabetic neuropathy (autonomic neuropathies)?
    • Hypersensitivity to light touch
    • Severe burning pain, esp at night
  280. How is painful diabetic neuropathy (autonomic neuropathies) treated?
    • Elavil (amitriptyline)
    • Norpramin (desipramine)
    • Neurontin (gabapentin)
    • Capsaicin cream
  281. What systems are involved in autonomic neuropathy?
    • GI tract: dysmotility, gastroparesis (tx Reglan, Propulsid), constipation, diarrhea (tx imodium, lomotilo)
    • BP: orthostatic HOTN
    • Bladder: urinary retention or incontinence
    • Erectile dysfunction: medical therapy includes viagra (50-60% improvement) and intracavernous injection of vasoactive drugs (papaverine), mechanical therapy (external vacuum), surgical therapy (implant of penile prostheses)
  282. What are the cardiovascular (macro vascular) complications that occur with diabetes mellitus?
    • HTN
    • Myocardial ischemia/infarction: DM eliminates female advantage, dyslipidemia, obesity, hyperglycemia, HTN
  283. What are the cerebrovascular (macrovascular) complications that occur with diabetes mellitus?
    • Stroke
    • Transient ischemic attacks (TIA)
  284. How are macrovascular complications managed?
    • Keep BP less than 130/80
    • ACE inhibitor therapy
    • Angiotensin II receptor blocker (ARB)
    • BB may mask hypoglycemia!
    • Low-dose aspirin
    • Tobacco cessation
    • Manage obesity and dyslipidemia: GOALS= LDL <100 mg/dl (<70 mg/dl for pts with CAD), HDL >40 mg/dl (males) HDL >50 mg/dl (females), trig <150 mg/dl (fasting), STATINS are the drug of choice for lipid control in diabetics
    • Regular exercise program
  285. What are the factors responsible for diabetic foot problems?
    • Ischemia
    • Peripheral artery disease (PAD): often asymptomatic, sometimes presents as intermittent claudication; signs include absence of pedal pulses, poor ABI scores, absence of hair growth on lower legs
    • Peripheral neuropathy
    • Secondary infection
  286. What are the steps to take for preventing diabetic foot problems in pts?
    • Comprehensive foot exam annually: visually check skin and tissue integrity, look at shoes for wear patterns, observe biomechanical integrity (gait, deformities), check pedal pulses, test sensation (vibration/pin prick/ankle reflexes)
    • Categorize findings as "low risk" or "at risk": pt at risk with loss of protective sensation, absent pedal pulses, foot deformity, hx of foot ulcer, prior amputation, smokes, hx of retinopathy, nephropathy, those on anticoagulant, those who can't see, feel or reach their feet (refer to podiatrist)
  287. What are the essentials of patient education of foot care?
    • Shoes: wear them, diabetic shoes available through medicare, be sure shoes fit, shake them, NO SANDALS
    • Foot hygiene: wash and inspect daily, moisturize, toenail care
    • Avoid trimming corns and calluses: can cause infections or wounds (advise foot clinic!)
  288. What are skin conditions that diabetic patients develop?
    • Insulin hyperatrophy
    • Fungal infections (thrush)
    • Xanthelasma
    • Vitiligo
    • Necrobiosis lipoidica diabeticorum
    • Granulam annulare
    • Dupuytren's contracture
  289. What is the summary of "P" (diabetic management)?
    • Diabetes education classes
    • Dietary consult
    • BP, pulse, ht and wt at every visit
    • Foot exam (including pulse) at every visit, monofilament exam annually
    • FBS (110-120 mg/dl), UA, Chem 10, HbA1C (<7%, ideally <6.5%) at every visit (2-4 times yearly for stable pts)
    • Serial microalbumin at initial diagnosis and annually (type 2 DM)
    • Lipid profile annually (fasting chol, trig, LDL, HDL)
    • Ophthalmology referral at diagnosis and annually (type 2)
    • Pneumovax vaccine (once) and flu vaccine yearly
    • Meds: ACE, daily low-dose aspirin, statin, glucose lowering agent (oral/insulin), glucose monitor, strips & lancets
    • Baseline ECG
    • MedicAlert bracelet or necklace and wallet card
    • Tobacco cessation
  290. What can cause a falsely elevated urinary protein excretion when testing urinary albumin excretion?
    • Exercise
    • UTI
    • Heart failure
    • Fever
Card Set
Endo Test 2