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BOARDS > Endocrine ABIM > Flashcards

Endocrine ABIM Flashcards

1
Q

Hypopituitarism causes (3 most common)

A
  • Pituitary Tumor
  • Pituitary surgery
  • Cranial irradiation
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2
Q

Hypopituitarism:

Pituitary Apoplexy (bleeding within organ):

cause, symptoms, treatment

A
  • Cause: Pituitary hemorrhage or infarction
  • Sx: sudden headache, visual change, opthalmoplegia, AMS
  • Tx: Acute admin of glucocorticoids until adrenal insuffiency r/o; May also require neurosurgical decompression
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3
Q

Hypopituitarism:

Postpartum pituitary necrosis (Sheehan syndrome)

~ cause, symptoms

A
  • Cause: silent pituitary infarction usually associated with obstetric hemorrhage and hypotension.
  • Sx: Acutely, vascular collapse.
  • More commonly, amenorrhea, inability to lactate, fatigue.
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4
Q

Hypopituitarism:

Lymphocytic hypophysitis: what is it?

A
  • It causes hypopituitarism, and possibly sx of mass lesion.
  • Most cases occur during or after pregnancy.
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5
Q

Hypopituitarism:

Signs of pituitary mass effect

A
  • Headache
  • Loss of peripheral vision
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6
Q

Hypopituitarism: Symptoms of anterior hypopituitarism

FSH/LH deficiency - symptoms/testing/findings

A
  • FSH/LH: amenorrhea, loss of libido, ED
  • Test: depressed FSH, LH, estradiol or testosterone
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7
Q

Hypopituitarism:

Symptoms of anterior hypopituitarism:

ACTH deficiency -symptoms/tests/findings

A
  • Sx: fatigue, N/V, Wt loss, Abd pain
  • Tests: Low cortisol/depressed ACTH;
  • depressed response of 11-deoxycortisol and cortisol to metyrapone
  • positive cortisol response to ACTH
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8
Q

Hypopituitarism: Symptoms of anterior hypopituitarism:

  • TSH deficiency - symptoms/tests/findings
A
  • TSH: cold intolerance, weight gain, constipation
  • Tests: depressed free T4 and TSH
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9
Q

Hypopituitarism: Symptoms of anterior hypopituitarism

  • GH deficiency - symptoms/tests/findings
A
  • GH: loss of muscle mass
  • Tests: depressed IGF-1 (serum marker of GH)
  • diminished response to insulin tolerance test ~ insulin induced hypoglycemia
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10
Q

Hypopituitarism: Symptoms of anterior hypopituitarism:

  • DI secondary to ADH deficiency
    • Symptoms
    • Tests
A
  • ADH/DI: polyuria, polydypsia, nocturia
  • Tests: Urine osmo < 200 does not increase with water deprivation test
  • Positive desmopressin challenge (urine concentrates)
  • If positive, order MRI of pituitary
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11
Q

Hypopituitarism: Symptoms of anterior hypopituitarism

Visual Changes

A
  • Bitemporal loss of vision
    • (mass effect on optic chiasm)
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12
Q

Hypopituitarism: Symptoms of anterior hypopituitarism: prolactin level

A

Level may be elevated from loss of tonic inhibition ~ hyperprolactinemia

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13
Q

Hypopituitarism Treatment

A
  • Replace hormone deficiency appropriately
  • Hydrocortisone for adrenal insufficiency
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14
Q

Hypopituitarism Treatment:

  • Central Hypothyroid Tx
A
  • Thyroxine dosing based on serum T4 rather than TSH level
  • T4 replacement only after hypoadrenalism r/o or treated
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15
Q

Pituitary Adenoma: micro vs macro

A

benign tumors; microadenoma < 10mm; macroadenoma > 10mm

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16
Q

Pituitary Adenoma: 2 ways they become symptomatic

A
  1. mass effect causing hypopituitarism ~ ant pit hormone deficiencies + headaches/visual field disturbances, CN dysfn.
  2. endocrine hyperfunction caused by excess secretion by the tumor
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17
Q

Pituitary gland is diffusely enlarged in these 2 situations

A

Normal Pregnancy & Untreated Primary Hypothyroidism

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18
Q

Pituitary Adenoma: Galactorrhea/Amenorrhea -

  1. Think this
  2. Order this…
A
  1. Think this: Prolactinoma
  2. Order this: Serum Prolactin Level
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19
Q

Pituitary Adenoma:

Enlargement of hands, feet, nose, lips, or tongue; increased spacing between teeth

  1. Think think
  2. Order this…
A
  1. Think this: Acromegaly
  2. Order this: Serum IGF-1, OGTT (fails to suppress GH)
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20
Q

Pituitary Adenoma:

Proximal muscle weakness, facial rounding, centripetal obesity, purple striae, diabetes mellitus, and hypertension

  1. Think this
  2. Order this
A
  1. Think this: Cushing Disease
  2. Order this:
  • 24-hour urine cortisol excretion
  • dexamethasone (manmade cortisol) suppression test (suppresses)
  • late night salivary cortisol level (elevated)
  • serum ACTH level (elevated or inappropriately normal)
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21
Q

Pituitary Adenoma: Goiter and Hyperthyroidism

  1. Think this
  2. Order this
A
  1. Think this: TSH-secreting adenoma (rare)
  2. Order this: TSH normal or elevated; increased T4
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22
Q

Pituitary Adenoma: General Testing Rules

  1. Who to test?
  2. If pituitary source indicated, what do you order?
  3. If mass effect, what do you order?
  4. What syndrome do you always eval for?
A
  1. Test all patients w/incidentally discovered pituitary adenoma for hormone hypersecretion
  2. Order MRI if testing indicates hormonal hypersecretion from pituitary source
  3. If mass effect is presenting sx, obtain MRI first, endocrine testing later (headache/visual)
  4. Eval pts with at least 1 component of MEN1 and family hx of MEN1 for a pituitary adenoma (usually hyperparathyroidism)
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23
Q

Pituitary Adenoma:

Nonprolactinoma causes of hyperprolactinemia

A
  • Usually level < 150ng/mL
  • Psychotropic agents, TCAs, Antiseizure meds, Metoclopramide, Domperidone, CCBs, Methyldopa, Opiates, Protease Inhibitors
  • Check TSH level (hypothyroidism can cause it)
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24
Q

Pituitary Adenoma:

Treatment for:

  1. women with microprolactinoma/normal menses
  2. patients with nonfunctioning microadenomas (< 10mm)
A

Observation

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25
Q

Pituitary Adenoma:

  • Treatment for symptomatic prolactinoma
A
  • Dopamine Agonist (cabergoline preferred to bromocriptine)
    • consider withdrawal of RX if prolactin level normalized and mass no longer visible on imaging
  • Close follow up ~ recurrence rates up to 50%
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26
Q

Pituitary Adenoma:

Treatment for adenomas secreting GH, ACTH, TSH; Tx for adenomas w/mass effect, visual field disturbance, Tx for hypopituitarism and Tx for prolactinomas unresponsive to dopamine agonist

A

Surgery

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27
Q

DI: what is it? central vs nephrogenic

A

Inability to concentrate urine due to insufficient arginine vasopressin (AVP, ADH) release (central) or activity (nephrogenic)

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28
Q

DI: patient history includes…(6 likely scenarios)

A
  1. recent head trauma 2. pituitary mass lesion 3. evidence of anterior hypopituitarism 4. h/o infiltrative disorder (such as sarcoidosis) 5. kidney disease (tubulointerstitial disease) 6. meds such as lithium
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29
Q

DI: symptoms/signs of central DI

A

cravings for water or cold liquids, urinary frequency, nocturia, and, depending on mass effect of pituitary tumor, visual field deficits

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30
Q

DI: initial testing/confirmation testing

A

Initial: 1. urine osmo < 200 mOsm/kg 2. inability to concentrate urine during water deprivation test Confirmation: 1. desmopressin challenge test (+) urine concentrates = central, order MRI of pituitary; (-) urine does not concentrate = nephrogenic, order u/s kidneys

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31
Q

DI: Tx DI after neurosurgery or head trauma

A

If unable to drink, 5% dextrose in 0.45% sodium chloride IV; Add desmopressin if urine output high or hypernatremia develops

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32
Q

DI: Tx DI Chronic Central DI

A

Intranasal or oral desmopressin

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33
Q

DI: Lithium Induced nephrogenic DI

A

Stop lithium or add amiloride (diuretic)

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34
Q

DI: Non-drug induced nephrogenic DI

A

Thiazide diuretic and salt restriction

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35
Q

Empty Sella Syndrome: diagnosis

A

MRI: pituitary gland not visualized or is excessively small

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36
Q

Empty Sella Syndrome: causes

A

increased CSF entering and enlarging sella; tumor; previous pituitary surgery, radiation, infarction

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37
Q

Empty Sella Syndrome: testing in asymptomatic, testing in symptomatic

A

Asymptomatic: obtain cortisol, TSH, and free or total T4 Symptomatic: testing of all pituitary hormones

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38
Q

Hyperthyroidism: Thyrotoxicosis

A

any cause of hormone excess, including primary, secondary, destructive thyroiditis, excessive exogenous ingestion

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39
Q

Hyperthyroidism: destructive thyroiditis causes & testing

A

causes: subacute (de Quervain), silent (painless), postpartum ~ permanent hypothyroidism may follow all; testing: decreased TSH, normal T3 and T4, no symptoms, decreased or no RAIU uptake

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40
Q

Hyperthyroidism: Subacute (de Quervain): presentation, testing

A

nonautoimmune inflammation presents with firm and painful thyroid gland

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41
Q

Hyperthyroidism: Postpartum

A

painless autoimmune occurring within a few months of delivery

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42
Q

Hyperthyroidism: defined (* = most common)

A

disorders of increased thyroid hormone production and release ~ destructive thyroiditis, *Graves disease, *thyroid nodules, toxic multinoduar goiter

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43
Q

Hyperthyroidism: signs/symptoms

A

nervousness, emotional lability, increased sweating, heat intolerance, palpitations, increased defecation, weight loss, menstrual irregularity, tachycardia, lid lag, fine tremor, muscle wasting, proximal muscle weakness, hyperreflexia

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44
Q

Hyperthyroidism: Graves specific findings

A

goiter, opthalmopathy (proptosis, chemosis, extraocular muscle palsy) and pretibial myxedema; TSH receptor abs - do not need checked unless diagnosis unclear

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45
Q

Hyperthyroidism: Thyroid Storm - what? why? testing?

A

what? life threatening hyperthyroidism associated with cardiac decompensation, fever, delirium, and psychosis. why? following surgery, infection, iodine load (contrast), untreated grave’s. diagnosis? clinical diagnosis; levels are not indicative

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46
Q

Hyperthyroidism: surreptitious use of thyroid hormone

A

Suppresses thyroglobulin levels (useful measurement to r/o this cause)

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47
Q

Hyperthyroidism: testing - what to order?

A

order TSH, Free T4 levels; it TSH suppressed but T4 is normal, order free T3 to diagnose T3 toxicosis (rare)

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48
Q

Hyperthyroidism: testing - 1: tsh low; free T4 high; 2: tsh low; T3 high; normal fT4 3: low TSH, normal T3 and free T4, w/o sx 4: high TSH, high T3, high free T4

A
  1. Primary hyperthyroidism 2. Primary hyperthyroidism w/T3 toxicosis 3. Subclinical hyperthyroidism 4. Secondary hyperthyroidism from pituitary tumor
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49
Q

Hyperthyroidism testing - RAUI uptake: 1. diffuse homogenous increased uptake 2.patchy areas of increased uptake 3.focal increased uptake with decreased uptake elsewhere in gland 4.decreased or no uptake

A
  1. Grave’s 2.Toxic Multinodular Goiter 3.Solitary adenoma 4. Iodine load (IV contrast or Amiodarone), Thyroiditis (silent, subacute, postpartum, amiodorone induced), Serruptitious ingestion of excessive thyroid hormone
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50
Q

Hyperthyroidism: Treatment options (3)

A
  1. Radioactive iodine therapy (may lead to painful radiation thyroidits and sialadenitis, not used during pregnancy or breastfeeding), frequently restores euthyroidism 2. Antithyroid drugs (may lead to drug free remission in 30-50% of Grave’s or bridge to more definitive therapy), 3. Thyroidectomy (when definitive therapy required in patient with severe graves opthalmopathy or if RAI or antithyroid drugs can’t be given or aren’t tolerated or if large goiter causing local sx)
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51
Q

Hyperthyroidism: Antithyroid drugs ~ 1. Methimazole - used for/watch for 2. Propylthiouracil - used for/watch for

A
  1. Methimazole: 1st line antithyroid for most pts; watch for agranulocytosis, drug rash, hepatotoxicity 2. PPU: 1st trimester, thyroid storm (inhibits T4 to T3 conversion); watch for: agranulocytosis, drug rash, frequent hepatotoxicity
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52
Q

Hyperthyroidism: Treatment 1. Sympathetic nervous system symptoms 2. Prep for thyroidectomy 3. Severe Graves opthalmopathy 4. Pregnancy 1st trimeser; 2nd/3rd trimester

A
  1. SNS: Atenolol or Propanolol 2. Thyroidectomy Prep: Methimazole 3. Severe Graves optho: MMZ or Thyroidectomy *Avoid RAI (may worsen unless pretreated with glucocorticoids) 4. Pregnancy: 1st trimester PPU; 2nd/3rd trimester: MMZ (RAI contraindicated)
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53
Q

Hyperthyroidism: Treatment 5. Subclinical Hyperthyroidism 6. Subacute Thyroiditis 7. Suspicious Nodule (malignancy) 8. Thyroid Storm

A
  1. Methimazole if TSH < 0.1 6. NSAIDS, glucocorticoids for pain mgmt; atenolol or propanolol for sx; levothyroxine for sx hypothyroidism; repeat thyroid studies 4-6 mos; 50% normalize without treatment
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54
Q

Hyperthyroidism: Treatment 7. Suspicious Nodule (malignancy) 8. Thyroid Storm

A
  1. FNAB followed by thyroidectomy if malignant 8. PPU (preferred) or MMZ, idoine-potassium solutions, glucocorticoids and B blockers
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55
Q

Hyperthyroidism: PPU or MMZ + fever or sore throat?

A

Agranulocytosis until proven otherwise

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56
Q

Hypothyroidism: Signs/Symptoms

A

weakness, lethargy, fatigue, depression, poor concentration, myalgia, cold intolerance, constipation, weight gain, menstrual irregularity or menorrhagia, carpal tunnel syndrome

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57
Q

Hypothyroidism: Exam findings

A

Bradycardia, Hypothermia, diastolic hypertension, husky voice, goiter, cool dry skin, brittle hair, edema, delayed relaxation phase of DTRs

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58
Q

Hypothyroidism: Causes (6)

A
  1. chronic lymphocytic thyroiditis (Hashimotos) 2.thyroidectomy 3.previous radioactive iodine ablation 4.history of external beam radiation to the neck 5.medication induced (lithium, interferon alfa, ILK2, amiodarone) 6.central (pituitary disease, previous surgery, radiation to sella)
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59
Q

Hypothyroidism: Myxedema coma - defined - caused by - precipitated by

A

defined: severe hypothyroidism leading to decreased mental status, hypothermia, hypotension, bradycardia, hyponatremia, hypoglycemia, hypoxemia, hypoventilation. occurs with: severe, long-standing, untreated hypothyroidism; may pre precipitated by: acute medical or surgical event or administration of opiates

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60
Q

Hypothyroidism: Testing

A

TSH, free T4; T3 usually not necessary; Antithyroid peroxidase associated w/hashimotos

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61
Q

Hypothyroidism: Non thyroidal illness

A

Low/Normal Free T4 Low TSH (initially) then elevated TSH (recovery phase) Normalization of levels 4-8 weeks after recovery No treatment required

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62
Q

Hypothyroidism: 1. High TSH; Low free T4 2. High TSH; Normal T4 3. Low TSH, Low free T4

A
  1. Primary hypothyroidism 2. Subclinical hypothyroidism 3. Secondary (central) hypothyroidism; hypopituitarism
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63
Q

Hypothyroidism: How do you treat? Who do you treat?

A

Levothyroxine; treat subclinical w/serum TSH > 10 or who are pregnant or are trying; Also thyroxine demand increases by 30-50% during pregnancy

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64
Q

Hypothyroidism: 4 causes of decreased levothyroxine absorption

A
  1. Celiac disease 2. Calcium 3. Iron 4. PPIs
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65
Q

Hypothyroidism: Levothyroxine dosing 1. Age < 60 2. Age > 60 3. Heart disease

A
  1. < 60: Begin full dose 2. > 60: Begin at 25 - 50; increase by 25 q6 weeks 3. <3: Begin at 12.5 - 25
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66
Q

Hypothyroidism: Levothyroxine dosing 4. Myxedema coma 5. Pregnancy

A
  1. Begin levothyroxine & hydrocortisone ~ give until adrenal insufficiency ruled out 5. increased by 30% initially; check levels frequently
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67
Q

Thyroid nodules: 1st step; what does normal mean? what does low mean? 2nd step; 3rd step

A

1st: TSH level; commonly normal aka not helpful 2nd: Low TSH level suggests benign 3rd: If low, order radioisotope scan to confirm diagnosis and r/o additional non functioning nodules w/i a multinodular goiter

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68
Q

Thyroid nodules: Eval MNGoiter for compressive symptoms (name 3) and further testing as needed (name 4)

A
  1. Dysphagia 2. Hoarseness 3. Dyspnea (tracheal compression from substernal goiter) Testing: Barium Swallow; direct visual cord visualization, spirometry w/flow volume loops and/or CT chest
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69
Q

Thyroid nodules: FNAB is indicated for…

A
  1. All thyroid nodules > 1 cm with suspicious features & normal TSH 2. Nodules < 1 cm with risk factors for thyroid cancer or suspicious u/s characteristics
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70
Q

Thyroid nodules: Management/Treatment 1. Observe who? how? 2. RAI or surgery for who? 3. Surgery for who?

A
  1. Observation: periodic u/s for benign nodules 2. RAI or surgery: hyperfunctioning solitary thyroid nodules with RAI ablation or hemithyroidectomy 3. Surgery: continued nodule growth, malignant cytology, large MN goiters w/compressive sx
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71
Q

Hypercortisolism Syndrome: what is it? most common causes?

A

defined: Ongoing exposure to excessive glucocorticoids MCC: iatrogenic, endogenous (ACTH dependent or non)

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72
Q

Hypercortisolism: ACTH dependent

-defined

causes

A

defined by: inappropriately elevated or normal ACTH levels in relation to cortisol level

  1. ACTH secreting pituitary adenoma (cushing disease)
  2. ACTH secreting carcinomas and carcinoid tumors
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73
Q

Hypercortisolism: ACTH independent

A

defined by: low or normal ACTH levels in relation to cortisol level | 1. adrenal adenoma 2. adrenal carcinoma

74
Q

Hypercortisolism: Clinical Findings highly specific for Cushing Syndrome

A

centripetal obesity

facial plethora

supraclavicular or dorsocervical (buffalo hump) fat pads

wide > 1 cm violaceous striae

75
Q

Hypercortisolism: Testing

First Line Diagnostic Studies

A
  • 1mg overnight dexamethasone suppression test (failure to suppress serum cortisol to < 3)
    • if failure to suppress, order ACTH level
  • 24 hour urine cortisol level (elevated)
  • late night salivery cortisol level (elevated
76
Q

Hypercortisolism:

1mg overnight dexamethason suppression test fails to suppress serum cortisol > 3, what’s next?

A
  • Order ACTH level to differentiate ACTH-dependent from ACTH-independent hypercortisolism
  • If Morning ACTH elevated > 20:
    • Order Pituitary MRI or CT
  • If Morning ACTH suppressed or normal (<5):
    • Order Adrenal CT
77
Q

Hypercortisolism:

Treatment for Cushing Syndrome

Treatment of low bone density caused by hypercortisolism

A
  • Treatment for Cushing Syndrome: Surgical resection or adrenal gland, pituitary gland, or ectopic tumor
  • Treatment for low bone density: Bisphosphanates
78
Q

What do you do if

  • 1mg Dexamethasone fails to suppress serum cortisol < 3
  • ACTH is evelated > 20
  • MRI or CT shows no pituitary tumor
A
  1. Order high dose (8mg) dexamethasone suppression test to differentiate between pituitary and ectopic tumor ACTH production
  2. If high dose does not suppress cortisol production: ectopic tumor is releasing ACTH ~ SCLC, bronchial carcinoid, pheochromocytoma, medullary thyroid carcinoma. ​
    1. Order Chest CT
  3. If high dose does suppress pituitary ACTH production and adrenal cortisol secretion: the source is pituitary
    1. Obtain intrapetrosal sinus sampling
79
Q

Adrenal Incidentaloma: Diagnosis

VS

Adrenal malignancy

A

Mass > 1 cm discovered incidentally

VS

Adenomas > 6cm; common in patients with known

nonadrenal malignancy

80
Q

Adrenal Incidentaloma:

  • Testing goals
  • Asymptomatic patients
  • Patients with HTN and hypoK
A

Goals:

  1. Is adenoma functioning? Is it malignant?
  • Asymptomatic patients: 1mg dexamethasone suppression test and measurement of 24 hour urine levels of metanephrines and chatecholamines
  • Htn & HypoK: above plus plasma aldosterone and plasma renin activity
81
Q

Adrenal Incidentaloma: Treatment

A

Treatment:

  • Adrenal masses < 4cm: monitored radiographically; repeat imaging in 6-12 months and screen for hormonal hypersecretion
  • Adrenal masses > 4cm or hyperfunctioning tumors: surgery may be recommended
82
Q

Hypoadrenalism: Diagnosis

  • Primary
  • Secondary
A

Diagnosis

  1. Primary: caused by disease of adrenal glands (Addisons)
    * loss of cortisol, aldosterone, adrenal androgens
  2. Secondary: caused by disease of pituitary gland
    * loss of cortisol and adrenal androgen deficiencies (aldosterone synthesis is not ACTH-dependent)
83
Q

Hypoadrenalism: Causes

  1. Most common cause of primary insufficiency
  2. Most common cause of secondary insufficiency
A
  1. MCC Primary insuffiiciency: Autoimmune adrenalitis
    * also look for type 1 diabetes, hypothyroidism, and vitiligo
  2. MCC Secondary insufficiency: Glucocorticoid use

(hypothalamic-pituitary suppression)

  • look for patients who recently discontinued glucocorticoid therapy or did not increase glucocorticoid dose in times of stress
84
Q

Hypocortisolism: Testing

A
  • 8AM serum cortisol < 3ug/dL diagnoses cortisol deficiency
    • ACTH level to differentiate primary vs secondary
    • Morning ACTH > 20: Adrenal CT
    • Morning ACTH < 5: Pituitary MRI
  • 8AM serum cortiosl > 18ug/dL excludes diagnosis
  • For nondiagnostic values, select stimulating testing with ACTH (cosynotropin).
  • A stimulated serum cortisol > 18 excludes adrenal insufficiency.
85
Q

Hypocortisolism: Treatment

  1. Acute Adrenal Insuffiency
  2. Standard Treatment
  3. Stress/Surgery dosing
  4. Primary Adrenal Insufficiency
A
  1. Acute: high dose (4mg) dexamethasone and IV saline before obtaining cortisol, ACTH levels (dexa does not effect serum cortisol assay)
  2. Standard: Hydrocortisone 10-30mg/d
  3. Increase dose 2-10 times standard replacement
  4. Primary: Fludrocortisone; not reqd if hydrocortisone dose is >40
86
Q

Pheochromocytoma: Diagnosis

  1. What is it?
  2. What do they secrete?
  3. SIgns/Symptoms
A
  1. Rare tumors arising from chromaffin cells of adrenal medulla
  2. They secrete biogenic amines: norepinephrine, epinephrine, dopamien and their metabolites
  3. Htn, Headache, Hypermetabolism

Hyperhidrosis, Hyperglycemia, Hypocalcemia

Hypotension during anesthesia induction

87
Q

Pheochromocytoma:

Associations

A
  • MEN2
  • Von Hippel-Lindau
  • Neurofibromatosis 1
88
Q

Pheochromocytoma: Testing

  • Low clinical suspicion
  • High clinical suspicion
  • If biochemical tests are positive
A
  • Low pretest probability: 24 hour measurements of metanephrines and chatecholamines
  • Higher clinical suspicion: Plasma measurements of metanephrines
  • If positive, MRI or CT of abd/pelvis
  • If scans MRI or CT neg 131I or 123 I-MIBG scan may aid in localization
89
Q

Pheochromoctyoma: Treatment

  1. Treatment of choice
  2. To control BP preoperatively
  3. To maintain intravascular volume
  4. Treatment for intraoperartive hypertensive crisis
A
  1. Surgery
  2. Phenoxybenzamine
  3. IV NS
  4. Nitroprusside or Phentolamine
90
Q

Primary Hyperaldosteronism:

Characteristic findings/scenarios

A
  1. difficult-to-treat or resistant hypertension
  2. unprovoked or difficult to treat hypokalemia
  3. family history of hyperaldosteronism
91
Q

Hyperaldosteronism: Testing

A
  1. Simultaneous measurements of plasma aldosterone and renin
    * Plasma aldosterone-plasma renin >20 with plasma aldosterone > 15 strongly suggests primary hyperaldosteronism
92
Q

Hyperaldosteronism: Confirmation Testing

A
  • Diagnosis confirmed by demonstrating nonsuppressibility of elevated plasma aldosterone in response to high salt load given IV or PO
  • In patients w/o adneoma: aldostrone level is supporessed < 5
  • Once autonomous hyperaldosteronism is diagnosed, order CT or MRI of adrenal glands
  • Adrenal V sampling is needed before surgery

* Testing can be done in pts receiving treatment with all antihypertensives except spironolactone and eplerenone (antagonize aldosterone recepter)

93
Q

Hyperaldosteronism: Treatment

A
  • Adrenal Hyperplasia: Spironolactone or Eplerenone
  • Aldosterone producing adenoma: Laprascopic adrenalectomy
  • Additional HTN control: Add thiazide diuretic
94
Q

Primary Amenorrhea: definition

  • 50% due to?
  • 15% due to?
  • 4 most common causes of primary amenorrhea
A

definition: failure of menstruation (never occured)

  • 50% due to chromosomal disorders
  • 15% have anatomic abnormality
  1. Turner syndrome,
  2. Hypothalamic/pituitary disorders
  3. Androgen-resistnace syndromes
  4. PCOS
95
Q

Primary Amenorrhea: TESTING

A

Most important studies:

  1. Pregnancy Test
  2. Karyotype
  3. FSH, LH, TSH, Prolactin Level
  4. Pelvic ultrasound
96
Q

Primary Amenorrhea: 4 MCCs

Turner Syndrome

  • Karyotype
  • Characteristics
A
  • Karyotype: 45 XO
  • Lack of secondary sexual characteristics
  • Growth Retardation
  • Webbed Neck
  • Frequent Skeletal abnormalities
97
Q

Primary Amenorrhea: 4 MCCs

Hypothalamic/Pituitary disorders

A

Functional: stress, excessive exercise, weight loss

Developmental defects of cranial midline structors, tumors, or infiltrative disorders (sarcoidosis)

98
Q

Primary Amenorrhea: 4 MCCs

Androgen-resistance syndromes

  • Karyotype
  • Characteristics
A
  • XY Karyotype
  • Absence of or minimal pubic and axillary hair
  • Shallow vagina
  • Labial Mass (testes)
99
Q

Primary Amenorrhea: 4 MCCs

PCOS

A

most commonly causes secondary ammenorrhea but may cause primary amenorrhea

100
Q

Secondary Amenorrhea:

Diagnosis

A
  • Look for abscence of menstruation for three cycles
  • or 6 consecutive months in women with previous menstrual flow
101
Q

Secondary Amenorrhea: Testing

  • Test all women for
  • Look for:
  • Assess hormonal status with:
A
  • Test all women with secondary amenorrhea for pregnancy (most commong cause)
  • Look for: structural causes (such as Asherman syndrome)
  • If no structural cause, asess hormonal status with: estradiol, FSH, LH, TSH and prolactin levels
102
Q

Secondary Amenorrhea:

Hypogonadotrophic Hypogonadism

  • Estradiol level
  • FSH level
  • LH level
  • 4 Causes
A
  • Low estradiol
  • Low or inappropriately normal FSH and LH
  1. Hypothyroidism
  2. Hyperprolactinemia
  3. Hypothalamic (stress, weight loss, exericse)
  4. Pituitary (tumor, sheehan syndrome)
103
Q

Secondary Amenorrhea: Hypogonadotrophic hypogonadism

What test is performed in these patients?

A

Progesterone Challenge Test

  • No bleeding following a progesterone challenge indicates low estrogen because of hypothalamic hypogonadism
    • Measure estradiol to confirm
  • Bleeding followign progesterone challenge indicates a normal estrogen state and suggests possible hyperandrogenism (e.g. PCOS)
104
Q
  1. Low estradiol + Low/Normal FSH and LH =
    1. 4 causes
  2. Low estradiol and Elevated FSH and LH =
    1. 3 causes
A
  1. Hypogonadatrophic Hypogonadism
    1. hypothyroidism, hyperprolactinemia, hypothalamic (stress, weight loss, exercise)
  2. Hypergonadotrophic Hypogonadism
    1. premature ovarian insuffiency (autoimmune), chemotherapy, pelvic radiation
105
Q

Common Causes of Secondary Amenorrhea:

PCOS

  • characteristics
  • evaluation
A
  • characteristics:
    • ovulatory dysfunction
    • evidence of hyperandrogenism
    • polycystic ovaries on ultrasonagraphy
  • evaluation:
    • mild elevation in testosterone & DHEAS
    • (not needed for diagnosis)
106
Q

Common causes of Secondary Amenhorrhea

Hyperprolactinemia

  • Characteristics:
    • May be associated with:
    • Related to/Causes
  • Evaluation
    • Rule out
    • Order
A
  • Associated with galactorrhea
  • Related to medications, tumors that secrete prolactin or compress pituitary stalk, h/o cranial radiotherapy
  • First rule out hypthyroidism
  • If TSH is normal and serum prolactin level > 100, obtain MRI to diagnose tumor
107
Q

Common causes of Secondary Amenhorrhea

Hypothalamic Amenorrhea

  • Characteristics/causes
  • Evaluation
A

Characteristics:

  • Most commonly functional (related to stress, weight loss, excessive exercise)
  • Low or normal LH level, and low estradiol level
108
Q

Common Causes of Secondary Amenorrhea

Hypothyroidism

  • Cause
  • Evaluation
A

Causes secondary increase in serum prolactin levels

High TSH, high prolactin

109
Q

Secondary Amenorrhea

Adrenal Tumor

  • Signs
  • Evaluation
A
  • Signs of hyperandrogenism and virilzation, usually acute onset and severe
  • Decreased LH and FSH, increased or normal estradiol, and increased testosterone and DHEAS levels
110
Q

Secondary Amenorrhea

Sheehan Syndrome

  • History of
  • Eval
A
  • History of difficult delivery (blood loss, hypotension) and inability to breastfeed
  • Varying levels of panhypopituitarism
111
Q

Secondary Amenorrhea

Asherman Syndrome

(Uterine adhesions)

  • History of
  • Eval
A
  • previous d&c amenorrhea caused by fibrous uterine scarring
  • normal LH and estradiol levels
  • no response to estrogen and progesterone challenge
112
Q

Secondary Amenorrhea:

  • Treatment
  • Prevent osteoporosis
  • Hypothalamic amenorrhea
A
  • Treat underlying disorder
  • Prevent osteoporosis with estrogen/progesterone replacement until menstruation returns to normal or age 50 years
  • For hypothalamic anemorrhea: reduced exercise, improved nutrition, attention to emotional needs
113
Q

PCOS

  • Most common cause of ___ with ___
  • Diagnosis requires two of the following:
A
  • most common cause of hirsutism with oligomenorrhea
  1. ovulatory dysfunction (amenorrhea, oligomenorrhea, infertility)
  2. labratory or clinical evidence of hyperandrogenism (hirsutism, acne)
  3. ultrasonagraphic evidence of polycystic ovaries
114
Q

PCOS: Testing

A
  • PCOS IS A CLINICAL DIAGNOSIS
  • Insulin resisrance is an important features of this disorder as is being overweight or obese
  • Mild elevation in testosterone and DHEAS levels and LH/FSH ratio greater than 2:1 are typical

* do not routinely order testosterone or DHEAS b/c PCOS is a clinical diagnosis and lab eval is only necessary when androgen producing neoplasm must be ruled out (androgen secreting ovarian or adrenal tumor)

* this should be suspected in rapidly progressive hirsutism or virilization

115
Q

PCOS: Treatment

A
  • Lifestyle modification: reduce weight, control abdominal obesity, restore insulin sensitivity
  1. If fertility is not desired: first line treatment of hirsutism and regulation of menses is OCP. Spironolactone can be added if hirsutism remains problem.
  2. If fertility is disired, ovluation induction can be brought about with clomiphene citrate or letrozole
116
Q

Infertility: Diagnosis

A

Defined: inability to conceive after 1 year of intercourse without contraception < 35 years and after 6 months in women > or = 35

  • Regular menses is correlated with regular ovulation
  • If oligomenorrhea is present, eval like secondary amenorrhea
  • Consider structural abnormalities and eval with pelvic u/s
  • Semen analysis can be perforemd at any time
117
Q

Male Hypogonadism: Diagnosis

  • Decreased production of
  • May be ___ or ___
  • Characteristic findings
A
  • Defined: When sperm or testosterone production is decreased
  • May be primary or secondary
  • Characteristic findings: fatigue, decreased strength, poor libido, ED, gynecomastia
118
Q

Male Hypogonadism: Causes/Testing

Testosterone deficiency diagnosis

  • What if it is equivocal?
  • What if it is low?
A
  • Diagnosis: two 8am total testosterone levels below reference range
  • If it is equivacol, measure free testosterone level by equilbirum dialysis or mass spectrometry
  • If it is low, measure LH, FSH, prolatin levels
119
Q

Male Hypogonadism: Causes/Testing

  • Primary testicular failure diagnosis
  • Some causes include (name 5)
A
  • Elevated LH and FSH level

Causes:

  • klinefelter syndrome (check karyotpe, 47XXY)
  • atrophy secondary to mumps orchitis
  • autoimmune destruction
  • previous chemotherapy or pelvic irraditaion
  • hemochromatosis
120
Q

Male Hypogonadism: Causes/Testing

  • Secondary hypogonadism diagnosis
  • Some causes include (name 4)
A
  • Low or normal LH and FSH
  • If confirmed: measure prolactin, iron studies, MRI

Causes:

  • Sleep apnea
  • Hyperprolactinemia
  • Hypothalamic or Pituitary disorders (hemochromatosis, pituitary/hypothalamic tumor)
  • Use of opiates, anabolic steroids, or glucocorticoids
121
Q

Male Hypogonadism: Treatment

A
  • Testosterone: transdermal (preferred but expensive), buccal, implantable, or IM prep
  • Before initiating and during therapy: monitor hematocrit, PSA to screen for development of erythrocytosis and prostate cancer
  • Testosterone replacement and anabolic steroid use results in small testicles and male infertility
122
Q

Hypercalcemia/Hyperparathyroidism

  • MCC in outpatients
    • Commonly presents as:
    • Less common presentations are:
    • PTH level
    • Phos level
    • XRAY features (possible)
A

Most common cause in outpatients: Primary hyperparathyroidism

  1. Common: asymptomatic
  2. Less common: kidney stones, osteoporosis, pancreatits, fractures
  3. PTH elevated (80%) or inappropriately normal (20%)
  4. Phosophrous low
  5. Xrays may show: chondrocalcinosis or osteitis fibrosa cystica (rare)
123
Q

Hypercalcemia

Most common cause in hospitalized patients

  • PTH level
  • Phosphorous level
  • PTH related protein
A

Most common cause in hospitalized patients: Malignancy

  • PTH level: suppressed
  • Phosphorous level: normal or low
  • PTH related protein may be elevated but is not needed for diagnosis
124
Q

Hypercalcemia and Hyperparathyroidism:

  • Ingestion of these 4 agents causes hypercalcemia
A
  1. Lithium (PTH mediated)
  2. Thiazide diuretics (non PTH mediated)
  3. Excessive vitamin D ingestion
  4. Excessive calcium ingestion
125
Q

Hypercalcemia

  • This disease may be associated with
    • Hypercalcemia (10%)
    • Hypercalciuria (50%)
A

Sarcoidosis

126
Q

Hypercalcemia causes:

Local Osteolytic Lesions

  • PTH level
  • Phospohorous level
  • How?
A
  • PTH suppressed
  • Phosphorous normal or low
  • Lytic bone metastasis result in increased mobilization of calcium from bone
127
Q

Hypercalcemia causes:

Multiple Myeloma

  • PTH level
  • Phospohorous level
  • Presentation
  • Diagnose with
A
  • PTH suppressed
  • Phosophrous elevated
  • Look for patients presenting with new kidney injury & anemia
  • Diagnose with serum and urine protein immunoelectrophoresis
128
Q

Hypercalcemia causes:

Granulomatous disease (sarcoidosis and TB)

& B Cell Lymphoma

  • PTH level
  • Phosophorous level
  • Calcitriol level
A
  • PTH suppressed
  • Phosphorous elevated
  • Calcitriol evelated (particularly in sarcoidosis)
129
Q

Hypercalcemia causes:

Milk Alkali Syndrome

  • PTH level
  • Phosphorous level
  • Creatinine level
  • Carbon dioxide level
  • Consider in healthy persons when ____ has been excluded
  • Excessive ingestion of _____ is a cause (rare)
A
  • PTH level suppressed
  • Phosphorous, Creatinine, Carbon dioxide levels elevated
  • Consider in healthy person when primary hyperparathyroidism excluded
  • Excessive ingestion of calcium containing antacids is a cause
130
Q

Hypercalcemia causes:

Hyperthyroidism

  • Frequent incidental finding in hyperthyroidism
  • Caused by…
A
  • Caused by direct simultation of osteoclasts by thyroid hormone
131
Q

Hypercalcemia: Acute intervention

  • When is acute intervention needed?
    • Serum calcium level:
    • Symptoms may include:
    • Most common in setting of:
A
  • with rapid rise in calcium level
    • serum calcium > 14mg/dL
    • symptoms may include: mental status change and coma
    • most commong in setting of malignancy
132
Q

Hypercalcemia and Hyperparathyroidism: Testing

  • Measure ___ to exclude ___
  • If hypercalcemia confirmed, check these 5 levels
  • If PTH is elevated or inappropriately normal w/increased calcium, most likely?
A
  • Measure ionized calcium to exclude pseudohypercalcemia
    • Pseudohypercalcemia: total calcium increased; ionized normal
  • Hypercalcemia confirmed, check:
    • calcium, PTH, phosphate
    • creatinine and 25 hydroxyvitamin D
  • If PTH elevated or inappropriately normal w/increased calcium: most likely cause is primary hyperparathyroidism
133
Q

Hypercalcemia:

Hypercalcemia + Normal PTH levels

  • What do you do next?
  • What needs to be excluded?
A

​

  • Measure urinary calcium excretion
  • To exclude familial hypocalciuric hypercalcemia
134
Q

Hypercalcemia and Hyperparathyroidism

  1. If hyperparathyroidism is confirmed and surgery is indicated, what do you do next?
A

Sestamibi parathyroid Scan

To look for an Adenoma

135
Q

What is the most common manifestation of MEN I?

A

Primary Hyperparathyroidism

136
Q

Hypercalemia:

Two treatments plus

Treatment if cause is MM or Sarcoid

A
  1. Volume Resuscitation with normal saline
  2. IV bisphosphanates and serum calcitonin
  3. oral glucocorticoid therapy (if caused by multiple myeloma or sarcoidosis)
137
Q

Multiple Endocrine Neoplasia

MEN I vs MEN 2

A

MEN 1 vs MEN 2

  • multigland hyperparathyroidism: MC manifestation vs LC manifestation
  • pituitary neoplsms vs medullary thyroid cancer
  • Pancreatic NETs vs Pheochromocytoma
138
Q

MEN 1

  • most common manifestation
  • most common neoplasms
  • most common NETs
A
  • most common manifestation: multigland hyperparathyroidism
  • pituitary neoplasms: prolactinoma, acromegaly, Cushing disease
  • pancreatic NETs: gastrinoma, insulinoma, vip-oma, carcinoid syndrome
139
Q

MEN 2

  • Least common manifestation
  • Most common manifestation
  • Most common NET
A
  • least common manifestation: multigland hyperparathyroidism
  • most common manifestation: medullary thyroid cancer (may be associated with a palpable neck mass)
  • NET: pheochromocytoma (hypertension and palpitations)
140
Q

What level should you check in ALL patients with hyperparathyroidism???

A

Serum Vitamin D levels

  • about 50% have coexisting vitamin D deficiency
  • serum and urine calicum levels may be decreased
141
Q

MEN: Treatment

  1. Primary hyperparathyroidism and hypercalcemic complications (kidney stones, bone diease, hypercalcemic crisis)?
  2. Asymptomatic patients are surgical candidiates if they have any of the following?
A

Parathyroidectomy for:

  1. primary hyperparathyroid + complications
  2. asymptomatic + any of the following:
    1. serum calcium > 1 above UNL
    2. estimated GFR < 60
    3. reduction in bone mineral density
    4. age < 50 years
142
Q

MEN: Treatment

  • Fall in calcium ater parathyroidectomy is due to?
    • What do you monitor?
    • How do you treat?
A
  • Due to relative hypoparathyroidism “hungry bone syndrome”
  • Monitor serum calcium after surgery
  • If mild hypocalcemia develops, give oral calcium
143
Q

MEN

How do you treat patients who are not candidates for surgery?

A

Cinacalcet or Bisphosphonates

144
Q

Hypocalcemia

  • most cases caused by?
  • what is ical in these cases?
  • what is the formula?
A
  • low serum albumin levels
  • ionized calcium is normal
  • total calcium declines by 0.8 for each 1g/dL decrement in serum albumin
145
Q

Hypocalcemia

  • Symptoms/Signs: Name 4
A
  • circumoral and acral parasthesias
  • carpal-pedal spasm
  • positive trousseau sign (blood pressure cuff carpopedal spasm)
  • positive chvostek sign (contraction of ipsilateral facial muscles elicited by tapping facial nerve)
146
Q

Hypocalcemia:

  1. Most common cause of acquired hypocalcemia?
  2. Name 5 other causes
A
  • Surgical excision of or vascular injury to parathyroid glands
  • Other causes include:
    • neck irradiation
    • congenital hypoparathyroidism (DiGeorge syndrome)
    • autoimmune destruction
    • infiltrative disease
    • complication of plasmapheresis
147
Q

Hypocalcemia:

Name 7 causes aside from hypoparathyroidism

A
  1. hypomagnesemia
  2. pancreatitis
  3. pseudohypoparathyroidism
  4. vitamin d deficiency
  5. rhabdomyolysis
  6. kidney injury
  7. tumor lysis syndrome
148
Q

Hypocalcemia:

Tests to order in evaluation

A
  • Calcium
  • Phosphate
  • Magnesium
  • Creatinine
  • PTH
  • 25-hydroxyvitamin D
  • albumin
  • ionized calcium
  • EKG to evaluate for QTc prolongation
149
Q
  1. Hypocalcemia due to Hypoparathyroidism
  2. Hypocalcemia due to psuedohyoparathyroidism (resistance to PTH)

Phosphate Level

  • Phosphate Level
  • PTH Level
  • Vitamin D Level
A
  1. ​Hypoparathyroidism
  • PO4 elevated
  • Low PTH
  • Variable Vit D
  1. Pseudohypoparathyroidism
  • PO4 elevated
  • PTH elevated
  • Normal Vit D
150
Q

Hypocalcemia due to psuedohyoparathyroidism (resistance to PTH)

  • Phosphate Level
  • PTH Level
  • Vitamin D Level
A
  • Elevated PO4
  • Elevated PTH
  • Normal Vitamin D
151
Q
  1. Hypocalcemia due to CKD
  • Phosphate Level
  • PTH Level
  • Vitamin D Level
  1. Hypocalcemia due to Vitamin D deficiency
  • Phosphate level
  • clinical signs
A
  1. CKD
  • Elevated PO4
  • Elevated PTH
  • Low 1, 25 hydroxyvitamin D levels
  1. Vitamin D deficiency
  • Low PO4
  • bone tendernress or fibromyalgias like syndrome, weakness, gait difficulty, osteomalacia
152
Q

Hypocalcemia causes: Key Features

  1. Impaired PTH secretion and PTH resistance
  2. “Hungry Bone” Syndrome
A
  1. Impaired PTH secretion and PTH resistance:
    • Magnesium deficiency
    • (small bowel bypass, diarrhea, alcoholism, diuretic therapy)
  2. Hungry Bone Syndrome
    • Recent parathyroidectomy
153
Q

Hypocalcemia: Treatment

  • Acute symptomatic hypocalcemia
  • Chronic hypocalcemia
A
  • Acute: IV calcium gluconate and vitamin D
  • Chronic: oral calcium supplements and vitamin D
154
Q

Hypocalcemia:

How do you choose the type of Vitamin D for supplementation?

A
  • kidney disease: calcitriol (1,25 dihydroxyvitamin D)
  • liver disease: 25-hydroxycholecalciferol
  • any other cause of hypocalcemia: cholecalciferol
155
Q

Osteoporosis: Screening

  • Who do you screen BDM with DEXA in?
A
  • Women >/= 65 years old
  • Postmenopausal women < 65 yo who are at increased risk per formal clinical risk assessment tool such as FRAX
    • increased risk defined by using the FRAX tool as a predicted 10-year fracture risk > 8.4%
  • Screen men and women with risk factors for secondary osteoporosis (glucocorticoid use, hyperparathyroidism, ADT, malabsorption)

* most experts recommend 10 to 15 years as screening interval for women with normal or slightly low BMD with no risk factors

156
Q

Osteoporosis: Diagnosis

  • what is it?
  • what is DEXA?
  • what is T score?
    • T score: osteopenia
    • T score: osteoporosis
      • also defined by history of:
A
  • Defined: silent skeletal disorder characterized by compromised bone strength and increased predisposition to fractures
  • Dexa is machine used to determine BMD
  • T score: comparison of healthy persons BD to yours
    • Osteopenia: dexa T score -1 to 2.4
    • Osteoporosis: dexa T score < or = 2.5
      • Osteoporosis also diagnosed by history of fragility fracture (fracture from a fall at standing height or lower)
157
Q

Osteoporosis: causes

  • Most common cause in women/men
  • Secondary causes (name 7)
A
  • MCC in women: estrogen deficiency
  • MCC in men: testosterone deficiecy
  • Secondary causes:
    • hyperthyroidism, hyperparathyroidism, Cushing syndrome
    • malabsorption (crohn disease, intestinal resection, celiac)
    • rheumatoid arthritis
    • medications (excessive glucocorticoids, thyroid hormone, phenytoin)
    • multiple myeloma
    • CKD, chronic liver disease
    • vitamin D deficiency
158
Q

Osteoporosis Treatment

  • Lifestyle
  • Indications for antiresorptive therapy
A

Lifestyle:

  • stop smoking, reduce alcohol intake, begin resistance exercises
  • exposure to sunlight
  • supplement calcium and vitamin D intake

Indications for antiresorptive therapy

  • osteoporosis
  • osteopenia (if additional high risk factors present)
  • previous fragility fracture
  • vertebral or hip fracture
159
Q

Osteoporosis Treatment:

  • Antiresporptive treatment is cost effective when
    • risk of major osteoporotic fracture is ? per FRAX
    • risk of hip fracture is ? per FRAX
A

​10 year probablity

  • > or = to 20%
  • > or = to 3%
160
Q

Osteoporosis: Treatment

  • Antiresorptive drugs:
    • First line
    • Patients with CKD 4 or intolerant to 1st line
    • Approved for: glucocorticoid induced osteoporosis with high risk of fracture, postmenopausal women, men with hypogonadism related osteoporosis at high risk of fracture
    • Pain for osteoporosis high risk fracture
A
  • Antiresorptive drugs:
    • First Line: aldrenoate or risedronate
      • IV zoledronate once yearly
      • ALL contranindicated in patients with CKD or esophageal disease
    • Denosumab
    • Teriparatide
    • Calcitonin
161
Q

Osteoporosis:

When is it reasonable to stop therapy?

A
  • No recommended duration of therapy is specified
  • Stopping therapy after 5 years is reasonable in women who have
    • stable BMI
    • no history of fracture
    • are at low risk of fracture
162
Q

Osteoporosis: Adverse effects of drugs used

  • oral bisphosphonate
  • IV bisphosphonate and denosumab
  • teriparatide
A
  • oral bisphosphonate: erosive esphagitis and atypical hip fracture
  • IV bisphosphonate and denosumab: osteonecrosis of the jaw
  • teriparatide: osteosarcoma
    • limit to 2 years
163
Q

Osteoporosis

When do you do a follow up DEXA after beginning therapy for osteoporosis?

A

No concesus exists.

24 months after beginning therapy is reasonable.

164
Q

Osteomalacia:

What is it?

A
  • A metabolic bone disease resulting from failure of organic matrix to mineralize because of lack of available calcium or phosphorous
  • Many cases are realted to abnormalities in Vitamin D
  • May also result from lack of calcium or phosphate.
165
Q

Osteomalacia: Signs and Symptoms

A
  • Fatigability, malaise, bone pain
  • Generalized bone tenderness
  • Proximal muscle weakness
  • Looser zones (bands perpendicular to the bone surface visible on x rays)
  • Hypocalcemia and Hypophosphatemia
  • elevated serum alkaline phosphotase level
166
Q

Osteomalacia:

Testing

Diagnosis

A

Testing:

Evaluate for underlying conditions that may lead to malabsorption of Vitamin D, such as celiac disease, or abnormalities in vitamin D metabolism,

such as liver and kidney disease.

Diagnosis:

Confirmed with bone biopsy

167
Q

Osteomalacia: Treatment

A

If osteomalacia is secondary to vitamin D deficiency -

  • treat with oral ergocalciferol 1000 to 2000 U/d and
  • elemental calcium 1g/d
168
Q

Vitamin D Deficiency:

  • Screening
  • Diagnosis
  • Testing
  • Population with lower levels
  • Treatment of deficient patient
A
  • Screening: Not enough evidence to screen
  • Diagnosis: Prolonged, severe defieincy will cause secondary hyperparathyroidism, osteomalacia and symptoms of bone pain, muscle weakness and fracture
  • Testing: 25 hydroxyvitamin D best inidicator of status
  • Lower levels: obestiy, glucocorticoids, orlistat, malabsoprtion
  • Treatment: 50,000 U ergocalciferol of cholecalciferol is recomended, followed by maintenance of 1500-2000 U/d
169
Q

Paget Disease:

What is it?

How is it usually suspected?

A

Focal disorder of bone remodeling that leads to greatly accelerated rates of bone turnover, disruption of the normal architecture of bone, and sometimes gross defomities of large bone

Most patients are asymptomatic and the disease is suspected with an isolated alkaline phosphotase level in the absence of liver disease

170
Q

Paget Disease:

  • Symptoms and Signs
A

​Signs/Symptoms:

  • Bone pain, fractures
  • Cranial nerve compression syndromes, spinal stenosis, nerve root syndromes
  • high-output cardiac failure
  • angioid retinal streaks
171
Q

Paget Disease:

Testing

A

Asymptomatic Patient

  • With elevated Alkaline Phosphatase (bone)
  • Order bone scan and follow up X rays in areas that localize radionucleotide

Symptomatic Patient

  • Obtain X rays of painful area
  • Xrays will reveal pathognomonic pagetic lesions: focal osteolysis with coarsening of trabecular pattern, cotton wool skull, and cortical thickening
172
Q

Paget Disease:

Treatment

A
  • Indidications to treat Paget Disease include bone pain, radiculopathy, involvement of weight bearing bone or joint, regardless of symptoms
  • Bisphosphonates are first line agents
173
Q

Diabetes Mellitus Type 1 Diagnosis:

  • Initial confirmation testing
  • 20% develop…
A
  • GAD65 and IA-2 antibodies
  • 20% develop organ-specific autoimmune diseases, such as celiac disease, Grave’s disease, hypothyroidism, addison disease, pernicious anemia and vitiligo
174
Q

Diabetes Type 1: Treatment

  • Basal dose accounts for what % of daily total insulin?
    • examples
  • The remaining % covers?
    • examples
A
  • Basal dose: covers 40-50% total daily dose
    • Insuline glargine, detemir, degludec
    • 10pm dose covers noctural plasma glucose levels and levels between meals; counters dawn phenomenon
    • NPH intermediate: morning and evening to provide basal levels to suppress hepatic gluconeogenesis
  • Remaining insulin cover preprandial doses
    • insulin aspart, glulisine, lispro. Rapid acting 5-15 mins before meals to modulate postprandial rise in glucose level.
    • Regular insulin: 30 mins before meals to prevent postprandial elevations
175
Q

Diabetes: How do you resttore sensitivity to hypoglycemia?

A

Lowering insulin dose and allowing average plasma glucose level

to increase for several weeks

176
Q

Type 2 Diabetes:

Characteristic findings of long standing disease

A
  • polyria, polyphagia, polydypsia
  • retinal microaneurysms, dot and blot hemorrahges, macular edema
  • symmetric sensory stocking glove peripheral neuropathy
  • cardiovascular and kidney disease
177
Q

Diabetes Type 2: Risk Factors

A
  • positive family history
  • history of gestational diabetes or PCOS
  • member of certain racial or ethnic groups
    • AA, American Indian, Alaskan Native, Asian American, Hispanic, Latino, Native Hawaiian or Pacific Islander
178
Q

Type 2 Diabetes: Screening

USPSTF recommends

  • Screen for abnormal blood glucose as part of cardiovascular risk assessment in adults aged ___who are ___
  • Also consider screening in___

ADA recommends

  • Screen overweight adults with ____
  • Screen all patients >__yo
A

USPSTF

  • Aged 40-70yo who are overweight or obese
  • Earlier if one or more risk factors for diabetes

ADA

  • overweight adults with at least one additional risk factor
  • and all patients > 45 yo
179
Q

DM 2

What tests do you use to screen?

A
  • fasting plasma glucose
  • 2 hour postprandial glucose during oral glucose tolerance test
  • hemoglobin A1c
    • if two seperate tests are done simultaneously and both are abnormal, diagnose diabetes
    • if one of the two tests is abnormal, repeat the abnormal test
180
Q

DM 2

  • Increased risk for diabetes
  • Diabetes
    • fasting glucose
    • random glucose
    • 2 hour glucose during OGTT
    • hgbA1c
A

Increased risk:

  • FG: 100-125
  • RG: 140-199
  • 2HR: 140-199
  • HgbA1c: 5.7-6.4%

Diabetes

  • FG: >126
  • RG: >200 w symptoms (diagnostic w/o repeat measurement)
  • 2HR: >200
  • > 6.5%
181
Q
A

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