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ABIM Board Review Endocrinology

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ABIM Board Review Endocrinology Endocrine Top 10 Pituitary Disease Thyroid Function Testing Thyroid Nodules Adrenal hyper/hypofunction Adrenal incidentalomas ... – PowerPoint PPT presentation

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Title: ABIM Board Review Endocrinology


1
ABIM Board ReviewEndocrinology
2

Cardiovascular Disease 14
Gastroenterology 10
Pulmonary Disease 10
Infectious Disease 9
Rheumatology/Orthopedics 8
Endocrinology/Metabolism 7
Oncology 7
Hematology 6
Nephrology/Urology 6
Allergy/Immunology 5
Psychiatry 4
Neurology 4
Dermatology 3
Obstetrics/Gynecology 2
Ophthalmology 2
Miscellaneous 3
Total 100













3
Endocrine Top 10
  1. Pituitary Disease
  2. Thyroid Function Testing
  3. Thyroid Nodules
  4. Adrenal hyper/hypofunction
  5. Adrenal incidentalomas
  6. Amenorrhea
  7. Diabetes
  8. Bone and Calcium Disorders
  9. SIADH
  10. Lipids

4
PITUITARY
5
  • With exception of PRL, all anterior hormones are
    regulated by hypothalamic releasing hormones (via
    the stalk) and feedback by peripheral hormones
  • AVP regulated by serum Osm, BP
  • PRL unique because under tonic inhibition by
    Dopamine

6
Pituitary Key Points
  • Presentation of pituitary masses (hormone
    changes, mass effect, invasion, differences in
    men and women)
  • Work-up suspected pituitary deficiency
  • Distinguish prolactinoma hyperprolactinemia
  • Factors that can elevate PRL
  • Medical vs. surgical management of tumors
  • Principles of panhypopituitarism
  • Complications of acromegaly

7
Anatomical Relationships
8
THYROID
9
Thyroid Physiology
  • Uptake and concentration of Iodide ion
  • Stimulated by TSH, Inhibited by perchlorate
  • Thyroglobulin made in follicular cells,
  • secreted into lumen, stored as colloid.
  • In lumen, thyroid peroxidase oxidizes
  • iodide and incorporates it into tyrosine
  • residue of thyroglobulin protein
  • The joining of mono and diiodotyrosine
  • makes T4 and T3
  • Under TSH, thyroglobulin molecules are
  • retrieved via endocytosis into the follicular
  • cell. There, lysosomal proteases release
  • free T4 and T3 (101), which enter capillaries

10
Euthyroid Sick
  • Mild-moderate illness
  • T3 decreases as a result of reduced conversion of
    T4 to T3 in peripheral tissues
  • Serum free T4 usually normal TSH normal or
    elevated
  • rT3 increases
  • Severe illness
  • T3 levels decrease further
  • T4 also decreases because of decreased binding
    proteins and decreased TSH secretion
  • How can euthyroid sick be distinguished from
    hypothyroidism?
  • In hypothyrodism, both T4 and T3 will be low rT3
    is low
  • In euthyroid sick, T3ltltT4 and rT3 is elevated
  • Do not treat euthyroid sick. In hospitalized
    patients w/ abnormal TFTs,
  • repeat approximately 6 weeks after discharge

11
Radioiodine Uptake vs. Scan
  • Tissues that take up trap iodine can be
    visualized and/or treated w/ RAI
  • Although other tissues can take up I- , only
    differentiated thyroid tissue (normal or
    metastatic) can trap the RAI
  • RAIU gives a number () of I- uptake. Used to
    determine whether patients with thyrotoxicosis
    have a high RAIU or a low RAIU disorder.
  • A scan gives a picture of the I- distribution in
    the gland. Used to distinguish among the three
    types of high-RAIU thyrotoxicosis and to
    determine whether thyroid nodules are
    nonfunctioning (cold), or hyperfunctioning (hot)

12
Radioiodine Uptake and Scan
  • Only done when theres hyperthyrodism
  • If low
  • Thyroiditis
  • Exogenous T4 ingestion
  • Struma ovarii
  • If high
  • Graves, HCG, TSH adenoma
  • Toxic nodule
  • Multinodular goiter

13
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14
Thyroid Nodules
  • Always get TSH and FT4
  • If TSH suppressed, do RAIU and scan to r/o a hot
    nodule
  • If TSH normal or elevated, then biopsy
  • For boards, biopsy all palpable nodules and
    incidentalomas gt1.5 cm
  • Hot nodules are virtually all benign
  • Cancers are cold, although most cold nodules are
    benign

15
Thyroid Cancer
  1. Thyroidectomy
  2. Suppression of TSH w/ Synthroid
  3. RAI ablation of remnant thyroid tissue
  4. Whole body scan w/ I131 6 months later
  5. Periodic surveillance with thyroglobulin
    measurements

16
ADRENAL
17
Cushings
  • All of my patients look like they have Cushings!
    Are some
  • clinical findings more specific than others?
  • Sign/symptom Sensitivty () Specificity ()
  • Hypokalemia 25 96
  • Ecchymoses 53 94
  • Osteoporosis 26 94
  • Weakness 65 93
  • DBP gt105 39 83
  • -If clinically suspected, then confirm
    biochemically w/
  • 24-hr urinary cortisol. (Elevated if 3x normal)
  • -If ACTH is suppressed, then cause is either an
    adrenal
  • neoplasm or exogenous steroids

18
What if both Cortisol and ACTH are Elevated ?
  • ACTH should normally be suppressed when Cortisol
    is high.
  • If ACTH is detectable, then its either from
    pituitary or ectopic secretion
  • In order to determine the source, do high-dose
    overnight Dex suppression. If AM cortisol
    decreases by 50 from baseline, then likely
    pituitary Cushings. Order MRI next.
  • If cortsiol remains elevated, search for ectopic
    ACTH (lung cancer, carcinoid)

19
Adrenal Insufficiency
  • In primary AI, mineraldocorticoids,
    glucocorticoids and adrenal androgens are lost
  • In secondary AI, mineraldocorticoids are
    preserved because they are under control of
    renin-angiotensin axis.
  • Most commonly caused by exogenous steroids
  • Other causes include pituitary adenomas,
    panhypopit, stalk disruption
  • Diagnose primary AI with cosyntropin stim test
    (gt20ug/mL excludes diagnosis)
  • Diagnose secondary AI with CRH stim test,
    metapyrone test or insulin-induced hypoglycemia

20
Adrenal Incidentalomas
  • Determine whether the lesion is hormonally active
    or nonfunctioning and
  • whether it is malignant or benign.
  • Size is best predictor of malignancy. Tumors gt6
    cm have high risk of malignancy lt4 cm rarely
    malignant.
  • Most common hormonal disorder is subclinical
    Cushings
  • All patients with an incidentaloma should have a
    1-mg dexamethasone suppression test and a
    measurement of plasma-free metanephrines.
  • Patients with hypertension should also undergo
    measurement of serum potassium and plasma
    aldosterone concentration/plasma renin activity
    ratio.
  • Indications for surgery
  • Functional tumors
  • All tumors gt6cm
  • Tumors 4-6cm w/ features suggestive of cancer or
    rapid growth

21
AMENORRHEA
22
Amenorrhea
  • Pregnancy
  • Pituitary/hypothalamic
  • -Prolactin (impairs GnRH)
  • -Hypothyrodism (raises PRL)
  • -GnRH deficiency or loss of pulsatility
    (anorexia, female athletic triad)
  • -Gonadotropin deficiency (Kallmans syndrome)
  • PCOS
  • -increased LH/FSH
  • Primary ovarian problem
  • -Estrogen or progestin deficiency (diagnose by
    withdrawal testing)
  • -Polyglandular deficiency (DM, Graves, vitiligo,
    AI)
  • -Chemotherapy, XRT
  • Plumbing
  • -Anatomic problem (Ashermans syndrome)

23
DIABETES
24
Outpatient Diabetes
  1. Screening
  2. Current guidelines
  3. Use of oral agents
  4. Insulin regimens
  5. Gestational diabetes

25
Who Should be Screened for Diabetes?
  • ?45 years old repeat q 3 years
  • Overweight (BMI gt25 kg/m2)
  • Physically inactive
  • Have a first-degree relative with diabetes
  • High-risk ethnic population
  • h/o GDM or baby gt9 lbs
  • HTN
  • Hyperlipidemia
  • PCOS
  • Other sx of insulin resistance (acanthosis)
  • h/o vascular disease

26
Criteria for the diagnosis of diabetes
  • Symptoms of diabetes and a casual plasma glucose
    200 mg/dl or..
  • FPG 126 mg/dl ( no caloric intake for at least 8
    hr) or
  • BS 200 mg/dl after OGTT (2 hr after 75 gm
    glucose).
  • In the absence of unequivocal hyperglycemia,
    these
  • criteria should be confirmed by repeat testing on
    a different
  • day.
  • OGTT is not recommended for routine clinical
  • use, but may be required in the evaluation of
    patients with
  • IFG or when diabetes is still suspected despite a
  • normal FPG as with the postpartum evaluation of
    women
  • with GDM.

27
Recommendations for Adults w/ DM
  • A1Clt7.0 (q 3 mo if uncontrolled twice yr if at
    goal)
  • Preprandial BS 80-110 mg/dl (60-90 if pregnant)
  • Postprandial BSlt140 mg/dl (lt120 if pregnant)
  • Blood pressurelt130/80 mmHg
  • LDLlt100 mg/dl
  • Triglycerides lt150 mg/dl
  • HDLgt40 mg/dl
  • Annual influenza vaccine
  • Pneumococcal vaccine for adults with diabetes
  • Revaccination is for individuals gt64 if vaccine
    was administered gt5 years ago. Other indications
    for repeat vaccination include nephrotic
    syndrome, chronic renal disease, and other
    immunocompromised states, such as after
    transplantation.

28
Health Maintainance
  • SMBG TID w/ DM1 and GDM
  • BP each visit
  • Annual urinary microalbumin (lt30ug/mg)
  • Annual lipids
  • Annual optho exam starting 3-5 yrs after onset w/
    DM1, and upon diagnosis in DM 2
  • Visual foot exam each visit. Comprehensive exam
    yearly (sensation, biomechanics, foot structure,
    vascular status and skin integrity)

29
Mnemonic for Diabetes Office Visits
30
Screening for Gestational Diabetes
  • Risk assessment at first prenatal visit
  • Low-risk status requires no glucose testing
  • Age lt25 years
  • Weight normal before pregnancy
  • Member of an ethnic group with low prevalence
  • No known diabetes in first-degree relatives
  • No history of abnormal glucose tolerance
  • No history of poor obstetric outcome
  • High risk features (obesity, h/o GDM, glycosuria,
    or FH) should undergo glucose testing as soon as
    possible

31
Diagnosis of GDM
  • FPG 126 mg/dl or a casual plasma glucose 200
    mg/dl meets the threshold for the diagnosis of
    diabetes (confirm on subsequent day)
  • High-risk women not found to have GDM at initial
    screening and average-risk women should be tested
    between 24 and 28 weeks of gestation. Testing
    should follow one of two approaches
  • One-step approach 100-g OGTT
  • 95 mg/dl fasting
  • 180 mg/dl at 1 h
  • 155 mg/dl at 2 h and 140 mg/dl at 3 h.
  • Two or more of the plasma glucose values must be
    met or exceeded for a positive diagnosis
  • Two-step approach perform an initial screening
    by measuring the plasma or serum glucose
    concentration 1 h after a 50-g oral glucose load
    and perform a diagnostic 100-g OGTT on that
    subset of women exceeding 140 mg/dl

32
Oral Hypoglycemic Agents
Drug Class Mechanism of Action Side Effects
Sulfonylureas/ secretagogues ?insulin secretion weight gain, hypoglycemia
Metformin ?hepatic glucose output GI upset, lactic acidosis,
TZDs ? peripheral glucose disposal fluid retention, weight gain
Alpha-glucosidase inhibitors ? intestinal carbohydrate absorption flatulence, diarrhea

Each will lower A1c by 1-2 compared to placebo.
When combined, efficacy typically is additive
33
FDA-Approved Combination Therapies
  • Sulfonylurea Metformin
  • Sulfonylurea a-glucosidase inhibitors
  • Sulfonylurea TZD
  • Metformin Secretagogues
  • Metformin TZD
  • Insulin Sulfonylurea
  • Insulin Metformin
  • Insulin TZD

34
Insulin
  • Know the types of insulin and onset
  • Know how to adjust insulin
  • All regimens include basal and bolus

35
Adjusting Insulin
  • Make changes slowly, taking into account diet,
    activity, stress
  • Asses the effectiveness of insulin at its peak
    time of action
  • Increase short/rapid insulin based on
    post-prandial readings
  • Increase long-acting when BG high fasting or
    throughout day
  • Inject into subcutaneous abdomen and rotate sites

To ? pre-dinner BG.?AM intermediate-acting
(e.g., NPH) To ? fasting BG.. ?PM
long/intermediate-acting insulin (e.g., glargine,
NPH) To ? pre-lunch BG..?AM short/rapid-acting
insulin (e.g., regular, lispro, aspart) To ?
bedtime BG....?PM short/rapid-acting insulin
(regular, lispro, aspart)
36
DKA
  • Decreased insulin, high counterregulatory
    hormones (catecholamines, glucagon, GH,
    cortisol), leading to hyperglycemia, proteolysis,
    lipolysis ketone production
  • Diagnostic Criteria
  • hyperglycemia glucosegt250 mg/dl
  • acidosis pH lt7.35 HCO3 lt 18
  • ketosis (blood /or urine)
  • Therapeutic Goals
  • Improve circulating volume tissue perfusion
  • Identify precipitating factors
  • FLUIDS restores intravascular volume, decreases
    counterregulatory hormones and lowers glucose
    levels
  • Reduce Gluc. serum osmolarity lytes q2,
    glucose q1
  • Clear ketones, fix electrolytes

37
Diagnostic Criteria for Metabolic Syndrome
(National Cholesterol Education Program)
  • Risk Factor
  • Abdominal obesity (waist circumference) gt 102 cm
    (gt 40 in) for men
    gt 88 cm (gt 35 in)
    for women
  • Triglyceride 150 mg/dL
  • High-density lipoprotein-cholesterollt 40 mg/dL
    for men
    lt 50 mg/dL for women
  • Blood pressure 130 / 85 mm Hg
  • Fasting glucose 110 mg/dL
  • Diagnosis is established when three of more of
    these risk factors are present.
  • Adapted from Expert Panel on Detection,
    Evaluation, and Treatment of High Blood
    Cholesterol in Adults. JAMA. 20012852486-2497.

38
BONE AND CALCIUM DISORDERS
39
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40
Hypercalcemia
41
Treatment of Hypercalcemia
  • Fluids then lasix once euvolemic
  • Search for causes
  • Antiresorptive therapies
  • (Bisphosphonates, Calcitonin) if caused by high
    bone turnover
  • Steroids if due to extra-renal vitamin D
    production (Sarcoidosis, lymphoma, TB)

42
Indications for Parathyroidectomy
  • Serum Ca ?1.0 mg/dL above the upper limit of
    normal
  • Hypercalciuria (urinary Ca excretion gt400 mg/day
  • Cr clearance ?30 of age-matched controls
  • BMD T score lt-2.5
  • Patients who are less than 50 years old
  • Patients in whom periodic follow-up will be
    difficult
  • 2002 NIH Workshop

43
Osteoporosis
  • Standard deviationdistribution about the mean in
    a set of data.
  • T-score is the number of SD above/below mean for
    sex-matched, young adults for the site measured
    2.5 means 2.5 SD below the mean
  • Z-score is the number of SD above/below mean for
    sex and age-matched controls
  • Osteoporosis defined by T-score of -2.5 or lower,
    ie. 2.5 SD below the mean Osteopenia is -1.0-2.5
  • Z-scores used to r/o accelerated osteoporosis
    such as w/ secondary causes

44
Causes of Osteoporosis
  • 1. Failure to achieve peak bone mass
  • 2. Increased bone resorption
  • 3. Inadequate replacement of lost bone
  • Primary Osteoporosis bone loss that occurs
  • during the normal aging process
  • Secondary Osteoporosis due to a specific
  • clinical disorder which decreases BMD

45
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46
Predictors of Low Bone Mass
  • Female sex
  • Advancing age
  • Sex steroid deficiency
  • White race
  • Low body weight and BMI
  • Family history
  • Low calcium intake
  • Smoking or excessive alcohol intake
  • Low level of physical activity
  • Chronic glucocorticoid use
  • History of fracture

47
Who Should be Worked up for Secondary Causes?
  • No clear guidelines
  • Suspect in younger patients with low trauma
    fracture or low BMD
  • Common causes
  • Hyperthyroidism
  • Vitamin D deficiency
  • Steroids

48
Glucocorticoids
  • Bone loss occurs w/ sustained doses (5 mg/day
    Predisone)
  • Greater effects on axial skeleton (vertebral fx)
  • Excessive inhaled steroids can decrease BMD
  • Cause accelerated bone loss by increasing bone
    resorption and decreasing formation
  • Decreased muscle mass contributes to falls

49
Screening Guidelines
50
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51
Treatment Indications
52
Treatment Options
  • Should address the 3 causes
  • of osteoporosis
  • peak bone mass
  • increased bone resorption
  • inadequate replacement of lost bone)

53
Calcium and Vitamin D
  • Reduces rate of hip fractures in nursing home
    patients
  • Indicated for all postmenopausal women and anyone
    at risk for osteoporosis
  • Given along with any other osteoporosis treatment
  • Dosages of 1000-1500mg/day of calcium and 400-800
    U of Vitamin D
  • Calcium citrate may be more effective than
    carbonate and is preferred in patients with a
    history of renal stones

54
Bisphosphonates
  • Potent inhibitors of osteoclasts
  • Reduce the rate of bone turnover
  • Proven in prospective randomized trials to
    prevent bone loss, increase BMD at spine and hip
    and reduce fractures
  • Prolonged action (weekly dosing)
  • GI side effects

55
Bisphosphonates
56
Calcitonin
  • Inhibits osteoclast-mediated bone resorption
  • Increased BMD of spine and reduced incidence of
    new vertebral fractures by 33 in postmenopausal
    women with osteoporosis (5-year study)
  • Has not been demonstrated to reduce hip and
    nonvertebral fractures
  • Side effects include rhinitis, nose bleeding

57
Raloxifine
  • SERM (Selectieve Estrogen Receptor Modulator)
  • Agonist in bone and lipoprotein antagonist in
    breast and uterus
  • Indicated for prevention or treatment of
    osteoporosis
  • Increases spine and femoral BMD
  • Shown to reduce vertebral fractures in
    postmenopausal women

58
Teriparatide
  • Recombinant PTH
  • Paradoxically increases BMD when given in pulse
    injections
  • Stimulates new bone formation
  • Increases spine and hip BMD
  • Reduces risk of vertebral and nonvertebral
    fractures in postmenopausal women
  • Risk of osteosarcoma in animal studies
  • Contraindicated in children, adolescents,
    pregnancy, hypercalcemia and Pagets disease
  • Only approved for 2 years

59
Estrogen
  • Suppresses osteoclast activity
  • WHI showed estrogen plus progesterone increased
    BMD and reduced fractures in postmenopausal women
  • Because of WHI, HRT is no longer recommended for
    prevention or treatment
  • Ongoing studies looking at ultralow-dose estrogen
    and combination of low dose estrogen with
    bisphosophonates
  • Stay tuned....

60
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61
Treatment Summary
  • Post-menopausal women
  • Alendronate and risedronate reduce hip and
    vertebral fracture risk
  • Raloxifene and calcitonin reduce vertebral
    fracture risk
  • Hormone replacement therapy reduces vertebral and
    hip fracture risk
  • Men with osteoporosis
  • Alendronate reduces vertebral fracture risk
  • In glucocorticoid use
  • Risedronate (and perhaps alendronate) reduces
    vertebral fracture risk

62
Osteomalacia
  • Poorly mineralized bone matrix caused by
    deficiency of Ca or PO42-
  • Usually from vitamin D deficiency or phosphaturia
  • Bone pain, muscle weakness
  • Multiple fractures
  • Diagnose w/ bone biopsy
  • Vitamin D deficiency from low sun exposure, or
    malabsorption

63
SIADH
SIADH
64
SIADH
  • Euvolemic hyponatremia
  • Caused by ectopic secretion of ADH or diffuse
    input into the hypothalamus
  • Must rule out other causes of free-water
    retention (adrenal insuff, hypothyroidism)
  • Distinguish from psychogenic polydipsia by urine
    Osm (concentrated in SIADH)
  • Can do a diagnostic volume stimulation test w/
    normal saline
  • ?UNa ?PNa SIADH
  • ?UNa ?PNa Dehydration

65
SIADH Treatment
  • Treatment depends on chronicity.
  • If acute and severe symptoms, slowly raise Na w/
    3
  • If chronic, then fluid restrict
  • Demeclocycline inhibits activity of ADH
    (nephrotoxic)
  • V2 antagonists currently in Phase 3 trials
  • Greatest risk is central pontine demyelinosis
    from rapid correction
  • Symptoms occur several days after correction.
  • Fluctuating consciousness, convulsions,
    hypoventilation

66
LIPIDS
67
LDL Goals Based on Risk
68
Criteria for Metabolic Syndrome
69
Lipid Drugs
70
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