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Med Study > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Causing Hyperprolactinemia?

A
  • Pituitary tumor
  • 1° hypothyroidism
  • Pregnancy
  • Renal insufficiency
  • Chest trauma
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2
Q

Medications that Cause of Hyperprolactinemia

A
  • Metoclopramide ***
  • Risperidone ***
  • Phenothiazine ***
  • Butyrophenones • SSRI • Tricyclics • Opiates • Verapamil • Estrogen • ? H2 blockers
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3
Q

PRL - Effects on LH / FSH

A
  • Decreases LH, FSH
  • lowers estradiol/tetstosterone
  • Increases galactorrhea + hypogonadism + bone loss
    • amanorrhea
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4
Q

Women with Elevated PRL / how do they present:

A

31-year-old female with PRL 60

  • Amenorrhea
  • Galactorrhea
  • Infertility
  • Microadenoma, PRL corresponds to tumor size
  • Hypopituitarism rare
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5
Q

Male with Elevated PRL / how do they present:

A

52 yo male w PRL 2000

  • Diplopia
  • Headache
  • Macroadenoma
  • Hypopituitarism
  • Galactorrhea / gynecomastia rare
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6
Q

Macroadenoma

A

>= 10 mm in size

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7
Q

Prolactinomas Tx

A
  • Transsphenoidal surgery associated with recurrent hyperprolactinemia (high rate)
    • Long-term remission of hyperprolactinemia uncommon
  • Cabergoline more potent, better tolerated
  • BromocriPtine preferred when Pregnancy desired
  • Neither drug teratogenic
  • Microadenomas rarely grow / Macroadenomas require long-term therapy to prevent growth
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8
Q

GH Secretion (origin / agonist / antagonist / effect)

A

Hypothalamus

+ GHRH -Somatostatin

Pituitary

GH

Liver

IGF

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9
Q

Acromegaly

A
  • Coarse facial features / does not have to be bone growth
  • Soft tissue thickening
  • “Spade-like” hands
  • Excessive sweating / Body odor
  • Goiter
  • Macroglossia / may require trach
  • Impaired glucose tolerance / DM
  • PRL co-secretion
  • Cardiac hypertrophy main cause of mortality
  • Colonic polyps
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10
Q

Dx of Acromegaly

A
  • High IGF-1
  • GH not suppressed after glucose
  • Macroadenomas / radiographic confirmation
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11
Q

Acromegaly Treatment

A
  • Transsphenoidal surgery - 70-80% success rate
  • Medical therapy
    • Somatostatin | octreotide (Sandostatin) or lanreotide (Somatuline).
    • Dopamine agonist is less effective | Bromocriptine (Parlodel) or Cabergoline.
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12
Q

Nonfunctioning Pituitary Tumor - Treatment

A
  • Most common Macroadenomas no evident hormone excess
  • Elevated LH, FSH sometimes
  • Alpha subunit glycoprotein hormone
  • In men, clinical picture similar to that of a prolactinoma
  • Hypopituitarism (partial or complete)
  • Treatment is surgery, no effective medical therapy
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13
Q

Evaluation of Pituitary Function

FLAT GP

A

Testosterone/estradiol

FSH/LH

Cortisol (ACTH)

FT4 (TSH)

(GH/IGF-1)

PRL

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14
Q

Stalk compression leads to

?ADH, ? PRL, ? anterior pituitary hormones

A
  • Decrease ADH / pituitary hormones
  • Increase PRL
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15
Q

Hypopituitarism

A
  • Pituitary thyroid axis
    • FT4, TSH
  • Pituitary adrenal axis
    • cortisol, ACTH
  • Pituitary gonadal axis
    • testosterone/estradio LH, FSH
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16
Q

Causes of Hypopituitarism

A
  • Infiltrative processes
  • Sarcoidosis
  • Hemochromatosis
  • Metastases
  • Pituitary apoplexy
  • Sheehan Syndrome
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17
Q

Replacement Therapy for Hypopitiutarism

A
  • Thyroid - Levothyroxine - Monitor with FT4
  • Adrenal - Prednisone usually OK
  • Gonadal - Oral contraceptive - Androgen
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18
Q

Empty Sella

A
  • Normal pituitary function
  • May be associated with benign intracranial hypertension
  • Random findings on Imaging
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19
Q

Pituitary apoplexy

A
  • Severe headache / Neurosurgical emergency /ACTH deficiency common
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20
Q

Sheehan Syndrome

A

Enlarged pituitary and tenuous blood supply with loss post hemorrhage

  • One or more pituitary hormones affected
    • Failure to lactate (PRL)
    • Amenorrhea (LH)
    • Loss of axillary/pubic hair (ACTH)
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21
Q

Pituitary incidentolomas

A

If large need to follow up in 6-12 months with imaging

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22
Q

Posterior Pituitary

A

ADH** and **oxytocin are synthesized in brain and transported to posterior pituitary and released directly

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23
Q

Diabetes Insipidus Nephrogenic DI

-Treatments

A

Nephrogenic Dl

  • Normal ADH levels
  • Renal resistance to H2O retaining effect
  • Lithium
  • Hypercalcemia

TX: Low Na diet/ Thiazide or Amiloride

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24
Q

Diabetes Insipidus Central DI Treatments:

A
  • Lack of ADH
  • Idiopathic
  • Pituitary surgery
  • Trauma
  • TX: Intranasal Or Oral Desmopression
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25
Q

Diabetes Insipidus

A
  • Polyuria - Dilute urine - Hypernatremia
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26
Q

TEST for DI

A

H2O deperivation Rasing Plasma Osmolality leads to increase in ADH and urine osmolality (once 300) give Desmopression Central DI will have 50% incrase in Urine osmolality

  • Nephrogenic will see no change.
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27
Q

Assessment of Thyroid Function

A
  • Free T4 (FT4)
  • TSH
  • Antithyroid antibodies
  • 24-hr iodine uptake
  • Technetium or iodine scan
  • Ultrasound
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28
Q

Primary Hypothyroidism

A
  • Ab to thyroid microsomes, thyroglobulin, and TSH receptor / however could be negative does not mean anything.
  • With or without goiter
  • More common in women
  • Other autoimmune disease
  • Low FT4, High TSH due to Hashimatos / autoimmune thyroiditis
  • Anti-thyroid peroxidase / Thyroid Microsomal Ab (anti-TPO) - Hashimatos 90%
  • Thyroglobulin antibodies - Hashimatos
  • TSH receptor antibodies - Graves (eye dz)
  • Thyroid-stimulating hormone - Graves
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29
Q

Secondary Hypothyroidism

A
  • Pituitary/hypothalamic disease
  • Look for other signs of pituitary dysfunction
  • FT4 low, TSH low
  • Don’t use TSH to monitor therapy - Due to pituitary tumors / hypothelamic dz, trauma etc
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30
Q

Thyroid Hormone Replacement

A
  • OK to start full replacement dose except in elderly and in patients with CV disease
  • Levothyroxine best choice / Normal 1.7 mcg/kg
  • Repeat TFTs in 8-10 weeks
  • Annual visits after levels are normal
  • Avoid T3 and T4/T3 combinations
  • Conversions 200 mcg levothyroxin = 25 mcg liothyronin = 60-65 thyroid (porcine)= 1 grain liotrix
  • T4 Levothyroxin has longer half life
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31
Q

Suppressive doses of T4

A
  • Its done in some patients with history of Thyroid cancer but must becareful with
    • Cardiomyopathy
    • Bone loss
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32
Q

T4 Replacement in Pregnancy

A
  • Need levothyroxine increases by about 50% / This is due to increase in Protien leves (Thyroglobulin )
  • Increased need persists throughout pregnancy
  • Hypothyroidism is mild
  • TSH returns to normal after delivery
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33
Q

DDx Hyperthyroidism

                          FT4            TSH   / High or low  Graves  Hot nodule  Thyroiditis  Toxic goiter

How to differentiate ?

A

FT4 TSH
Graves High Low
Hot nodule High Low
Thyroiditis High Low
Toxic goiter High Low

A thyroid scan and RAIU can help determine etiology.

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34
Q

Hyperthyroidism Sx

A
  • Clinical features
    • Weight loss, tremor, fatigue, amenorrhea,palpitations, heat intolerance, hyperdefecation
  • Apathetic thyrotoxicosis in elderly
  • FT4 levels do not always correlate with symptoms
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35
Q

Graves Disease

A
  • Graves Disease
  • Autoimmune
  • Thyroid stimulating antibodies bind to TSH receptors
  • Diffuse thyroid enlargement
  • Orbitopathy
  • Increase RAI uptake
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36
Q

Treat Graves

A
  • Antithyroid Drugs
  • Radioactive iodine
  • Surgery
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37
Q

Treat Graves

Antithyroid drugs

A
  • Antithyroid drugs
    • Methimazole (once a day)
    • Propylthiouracil (TID / 1st Trimaster of Pregnancy / advantage it also inhibits T4 to T3 conversion)
    • PTU is associated with high liver toxicity during pregnancy after first trimaster
  • Decrease TSIG (Thyroid stimulating IG) and block T4 synthesis
  • 30-50% have spontaneous remission after year of therapy
  • Agranulocytosis rare
  • Rash
  • Rare cholestatic hepatitis
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38
Q

Treat Graves

Radioactive Iodine

A
  • Gland destruction
  • TSH receptor antibodies persist after treatment
  • Avoid RAI in patient with severe Graves ophthalmopathy
  • 90% success rate after a single dose
  • Slow process // some patients stay euthyroid
  • post RAI / do free T4 as TSH does not come down for a while
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39
Q

Graves Treatment

Surgery

A
  • Recurrence is possible
  • Potential hypocalcemia and recurrent laryngeal nerve damage
  • Use for nodules or extremely large glands
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40
Q

Hyperthyroidism in Pregnancy

A
  • Keep FT4 at upper limit of normal range
  • Use PTU in first trimester
  • Radioactive iodine contraindicated

Propylthiouracil (TID / 1st Trimaster of Pregnancy / advantage it also inhibits T4 to T3 conversion)
PTU is associated with high liver toxicity during pregnancy after first trimaster

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41
Q

Thyroid Storm

A
  1. BBlk / Give Methimazole high dose / 100 mg hydrocortisone as well
  2. Cold Iodine
  • Exaggerated symptoms of hyperthyroidism
  • Surgery, infection, iodine load
  • First block T4 synthesis then block T4 release
  • Glucocorticoids and PTU decrease T4 -> T3 conversion
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42
Q

Random crap

  1. Surreptitious Use of Thyroid hormone and Thyroglobulin hormone level

2 Graves disease and lenght of dz

3 Subacute thyroiditis and palpation

  1. Toxic multinodular goiter and palpation
A
  1. Thyroglobulin would be low / acute settings
  2. Graves would be more chronic type of picture lenght wise
  3. could be tender with high thyroglobulin levels
  4. should palpate more nodules
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43
Q

Subacute or Painless Thyroiditis

A
  • Painful gland, ear pain
  • Elevated ESR
  • Mild hyperthyroidism
  • Hyperthyroid phase followed by transient hypothyroidism
  • Usually resolves without Rx
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44
Q

Graves vs Thyroiditis

A

Graves
TSIG
I
thyroid hormone synthesis (seen on scan)
I
high T4 and T3
I
suppressed TSH

Thvroiditis
inflammation
I
release of thyroid hormone (no synthesis and not seen on scan)
I
high T4 and T3
I
suppressed TSH
I
Lower thyroid hormone synthesis

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45
Q

Postpartum Thyroiditis

A
  • Silent, painless
  • Hyperthyroid phase followed by hypothyroidism
  • Decreased RAI uptake
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46
Q

A healthy 24 yo noted a thyroid nodule last week.
It is nontender; she feels great, and her exam is
normal. What is next?

Who is at a higher risk with malignant nodules?

A

TSH T4 levels & U/S

Higher risk for malignant nodules

  • History of radiation exposure
  • Family history
  • Male
  • Nodule t* in size
  • Age < 20 or > 70
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47
Q

What to expect after U/S FNA

A
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48
Q

Management after FNA

A

Management after FNA
• Malignant
- Surgery and RAI ablation
• Follicular neoplasm/nondiagnostic
- Surgery
• Benign
- Yearly follow-up / if has grown over 50% then fna

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49
Q

Thyroid Nodules Discovered Incidentally

A

• Ultrasound
- Cystic vs. solid
- Number and size of nodules
• Refer for ultrasound guided FNA if nodule(s)
> 1 cm or suspicious characteristics

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50
Q

Multinodular Goiter

A
  • Surgery if symptomatic
  • Suppressive therapy not uniformly effective
  • Thyroid cancer risk is the same in solitary nodules and multinodular goiter
  • Usually euthyroid
  • Dysphagia, hoarseness with substemal extension
  • Nodule size and characteristics determine whether FNA is necessary
  • Heterogeneous uptake on scan
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51
Q

Myxedema Coma?

Treatment:

A

• Rare with Extreme hypothyroidism
• Preexisting thyroid disease likely
• Stroke, infection may precipitate coma
• Mental status changes and hypothermia
Tx: with IV levothyroxine until oral is tolerated (usually with half the recommended)
- Glucocorticoid coverage
- Avoid T3 especially in elderly

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52
Q

Adrenal Disorders

A
  • Gushing syndrome
  • Adrenal insufficiency
  • Adrenal incidentalomas
  • Hyperaldosteronism
  • Pheochromocytoma
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53
Q

Gushing Syndrome

A
  • ACTH-secreting pituitary tumor
  • Adrenal adenoma/carcinoma
  • EctopicACTH production
  • Exogenous glucocorticoid

Cushing Dz - relates to pituitary Dz

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54
Q

Cushings Features

A
  • Centripetal obesity
  • Violaceous striae
  • Proximal muscle weakness
  • Amenorrhea
  • Thin skin/ Bruising
  • Weight gain
  • Glucose intolerance
  • Hypertension
  • Hypokalemia
  • Edema
  • Best two predictors : proximal weakness (cant do squads) Amenorrhea for women, Very thin skin (steriods breakdown collagen under the skin / easy to break)
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55
Q

Ectopic ACTH

A

• Small cell lung cancer
• Lack classic stigmata
• Hypokalemia
• Metabolic alkalosis
• Muscle weakness
• Hyperpigmentation

They will not be obese

Tiad : Hyperpigmented / hypokalemia refractory / muscle weakness

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56
Q

Screening for Cortisol Excess?

A

• 1 mg DST
-1 mg Dex at 11 p.m. then 8 a.m. cortisol
- If cortisol < 2 meg Cushing’s is excluded
• Urinary free cortisol
- Most sensitive

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57
Q

1 mg Dex test False positives ?

A
  • False positives / Because these guys will not suppress
  • Dilantin®, estrogen, obesity, stress, depression
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58
Q

Flow chart for Excess Glucocorticoid work up

A
  1. Screening Test (1 mg Dex suppression test)
    - Stop if negative
  2. Confirm Test (increase dose)
    - Stop if negative
  3. Get ACTH
    - If ACTH Undetectable (Adrenal)

If ACTH is Lelevated (Pituitary vs Ectopic ) will Need DST to differentiate

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59
Q

Elevated Cortisol levels

A

Patients with Adrenal Adenoma will not suppress and ACTH undectable

Patients with Ectopic ACTH will not suppress and have very High ACTH

Pateints with pituitary hyperfunction will suppress still elevated cortisol level and ACTH is elevated

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60
Q

Pituitary Tumor Treatment

  1. Cushing
  2. Prolactinomas
  3. Acromegaly
A
  1. Surgery TSS
  2. Medical therapy
  3. Surgery TSS
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61
Q

Treatment of Cushing’s

  1. Pituitary tumor
  2. Adrenal adenoma/carcinoma
  3. Ectopic ACTH
A

• Pituitary tumor
- Transsphenoidal surgery
• Adrenal adenoma/carcinoma
- Adrenalectomy
• Ketoconazole, aminoglutethimide for ectopic ACTH
or if surgery not feasible

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62
Q

Primary Adrenal Insufficieny

What is it?

Clinical Features of Primary Al?

Causes?

A

Laboratory Features of Primary Al
Hypo-Na, hyper-K, 4, hypo-CO2
hypoglycemia
low cortisol, high ACTH

Causes of 1°AI
• Autoimmune
• Adrenal hemorrhage
• Tuberculosis
• HIV associated
• Medication
- Ketoconazole / Megase

Clinical Features of Primary Al
• Fatigue and weakness
• Hyperpigmentation
• Hypotension
• Postural dizziness
• Abdominal pain

•Weight loss

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63
Q

Autoimmune dz

A

Polyendocrine Failure
• Hashimoto’s
• Addison disease
• Diabetes
• Hypogonadism
• Hypoparathyroidism
• Pernicious anemia
• Vitiligo

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64
Q

How to test for primary adrenal Def

A

Short Cortrosyn Stimulation is much better then just sending levels

65
Q

Therapy of 1° Adrenal Insufficiency

Treatment

A

Addison’s

  • Hydrocortisone ± fludrocortisone
  • Prednisone and dexamethasone have no mineralocorticoid activity
  • Monitor therapy clinically (BP) and with electrolytes / you can not measure cortisol / ACTH (usually stays high and does not come down)
  • Add mineralocorticoid if K remains elevated or CO2 not improved
  • Can’t use ACTH or cortisol to monitor therapy
  • Consider later onset of other autoimmune disease
66
Q

2° Adrenal Insufficency

Features ?

A

Features of 2° Al

  • • Fatigue
  • • Weight loss
  • • Loss of axillary and groin hair
  • • Normal lytes
  • • Normal BP
67
Q

2° Adrenal Insufficency

Causes?

A
  • Pituitary tumor
  • Sarcoidosis
  • Hemochromatosis
  • Glucocorticoid therapy
  • Megestrol acetate

• Cortisol deficiency is due to absent ACTH, not to adrenal dysfunction
• Symptoms nonspecific
- Fatigue prominent
• No hyperpigmentation
• Normal electrolytes and B/P
• Cortisol Low , ACTH Low

68
Q

2° Adrenal Insufficency
Test?
Treatment?

A

Test Cortrosyn Simulation /

  • Glucocorticoid only usually
  • Prednisone OK
  • Monitor clinically not with cortisol or ACTH
  • Be sure to address thyroid function
69
Q

Dexamethasone suppression test

A

The test is given at low (usually 1–2 mg) and high (8 mg) doses of dexamethasone and the levels of cortisol are measured to obtain the results

To Differentiate between cushing’s

  • Primary Adrenal Cushing syndrome is likely.

ACTH: undetectable or low Cortisol: Not suppressed by high or low doses.

  • Ectopic ACTH syndrome

_ACTH: _normal to elevated _Cortisol: _ is not suppressed by high or low doses

If an adrenal tumor is not apparent, a chest CT and abdominal CT is indicated to rule out a different tumor secreting ACTH.

  • Cushing’s disease should be considered.

ACTH: elevated Cortisol: is not suppressed by low doses, but is suppressed by high doses

A pituitary MRI would be needed to confirm.

70
Q

Cortrosyn Stimulation

A

Cosyntropin stimulation test

if > 18 AI ruled out //// If < 18 then ACTH level

If ACTH Low/Normal - Secondary or Tertiary AI

IF Elevated ACTH then Primary AI

71
Q

Secondary AI

What else should wathc out for?

A

• May be accompanied by global pituitary
dysfunction
• 2° hypothyroidism
- Low FT4, Low TSH
• Hypogonadism
-Low T or E, Low FSH

72
Q

Adrenal Incidentaloma

Size?

Active hormones to watch for?

A
  • *• Size?**
  • > 4 cm send to surgery
  • *• Hormonally active?**
  • Glucocorticoid excess
  • Mineralocorticoid excess
  • Adrenal androgen excess
  • Catecholamine excess
73
Q

What to screen for in All Adrenal Incidentalomas?

A

1 and 2 are important

1. Pheochromocytoma
- Urine or plasma catecholamines
2. Do a 1 mg DST to screen for Cushing’s 8 a.m.
cortisol < 2 normal / This is to rule out subclinical cushings

Screen for mineralocorticoid excess if
• Patient is hypertensive
- Measure potassium and plasma renin/aldo ratio
• Screen for androgen excess in hirsute woman
- DHEA-S
- Androstenedione

Follow-Up
• Repeat CT 6-12 months
• Surgery if mass increases in size
• No consensus on need or timing of repeat hormone testing

74
Q

Pheochromocytoma

A
  • Plasma-free metanephrines (if negative your free to go but if positive you need to do Urine)
  • Fractionated urine metanephrines and catecholamines
  • CT scan with contrast
  • May be hyperintense on T2 weighted MRI
  • Surgery definitive treatment, pretreat with _phenoxybenzamine _
  • Most secrete norepinephrine
  • 90% arise in adrenal
  • 90% of patients have sustained hypertension
  • Triad of headache, diaphoresis, palpitations classic
  • Avoid B-blocker until adequate a blockade

MEN IIb (2Ms,1P) - Medullary Thyroid Ca, Marfanoid habitus/mucosal neuroma, Pheochromocytoma

75
Q

MEN I

MEN II a

MEN II b

A
  • *MEN I (3 Ps)** - Pituitary, Parathyroid, Pancreas
  • *MEN IIa (1M,2Ps)** - Medullary Thyroid Ca, Pheochromocytoma, Parathyroid
  • *MEN IIb (2Ms,1P)** - Medullary Thyroid Ca, Marfanoid habitus/mucosal neuroma, Pheochromocytoma
76
Q

Primary Aldosteronism

Test:

Treatment:

A
  • Hypertension / Hypokalemia / Low Renin
  • Plasma _aldo/renin ratio > 20 _
  • Bilateral hyperplasia or single adenoma
  • If PAC/renin ratio is high, see if the elevated aldosterone can be suppressed using an IV or oral saline load
  • If can not suprress then get CT

Treatment

  • *• Bilateral hyperplasia**
  • Spironolactone or eplerenone
  • *• Adenoma**
  • Surgery
77
Q

Gonadal Disordersl

A

primary or secondary Amenorrhea

Androgen excess
PCOS
Male hypogonadism
Gynecomastia

78
Q

Amenorrhea

Primary / Secondary

Tests used

A

• Primary

  • No menses by age 16
  • Gonadal or pituitary origin

• Secondary (More common)

  • Absence of periods for 6 months
  • Gonadal or pituitary origin

Tests:

• Pregnancy test
• Estradiol / will be low
• LH/FSH
• Prolactin / causes amenorrhea
• Free T4/TSH
• Progesterone challenge test

79
Q

Causes

Central

Gonadal/other

A
  • Central Causes of Amenorrhea*
  • Hypothalamic
  • Pituitary tumor
  • Craniopharyngioma
  • Kallmann syndrome
  • Gonadal/Other Causes of Amenorrhea*
  • Turner’s
  • Premature ovarian failure
  • Androgen excess
  • **Central **
    • Low, LH, FSH
    • Low, estradiol
  • Ovarian
    • High LH, FSH
    • Low, estradiol
80
Q

Ovarian Failure and younger than 30

A

Ovarian Failure
• If woman younger than 30, do karyotype even if
classic stigmata of Turner’s are lacking.

81
Q

Turner Syndrome

A

Turner Syndrome
• XO gonadal dysgenesis
• Bicuspid aortic valve
• Hypertension
• 1° hypothyroidism
• Glucose intolerance
• Short stature
• Estrogen and GH

82
Q

Causes of 2° Amenorrhea

A

Causes of 2° Amenorrhea
• PCOS
• Prolactinoma
• Cushing’s
• Hypothalamic
- Tumor
- Infiltrative
• Chemotherapy

83
Q

Premature Ovarian Failure

A

Premature Ovarian Failure
• Secondary amenorrhea before menopause
• Generalized ovarian sclerosis and decreased follicles
• Irradiation, chemotherapy
• Autoimmune dysfunction
• Look for other autoimmune disease —thyroid/adrenal

84
Q

Hypothalamic Amenorrhea

A

Hypothalamic Amenorrhea / Athletics usualy
• Low body wt
• Low body fat
• I GnRH secretion from hypothalamus

85
Q

Kallmann Syndrome

A
  • Rare / Hypogonadism + Anosmia (hypothalamus)
  • Isolated GnRH deficiency
  • Mid line defects (cleft palets)
  • Anosmia
  • Low Estradiol, Low LH, Low FSH
86
Q

Polycystic Ovarian Syndrome

A
  • Amenorrhea/oligomenorrhea
  • Hirsutism / Acne / Obesity / Insulin resistance
  • High LH:FSH ratio (Diagnostic with PCOS)
  • Testosterone mildly Elevated
  • DHEA-S mildly Elevated

PCOS Treatment
• Weight loss
• Oral contraceptive (hair growth)
- Low androgen progestin
• Metformin
- Lowers testosterone
• Medroxyprogesterone (every three months they need provera)
- Endometrial protection

87
Q

Spironolactone

A

Remember Oral Contraceptives have same effect

  • lowers Testosterone synthesis
  • Competes with testosterone at receptor / DHT at hair follicles
  • 9-12 months to see an effect
  • Contraindicated in pregnancy
88
Q

Causes of Androgen Excess

A

Causes of Androgen Excess
• Ovarian tumor ( most important not to miss / causes virilization / increase testostrone)
• Adrenal tumor
• PCOS
• Congenital adrenal hyperplasia (21 hydroxylase def)

• Drugs

  • Danazol
  • Cyclosporine
  • Last onset Congenital Adrenal Hyperplasia / 20’s hair growth / menstral issues
89
Q

Hirsutism vs Virilization

A

Hirsutism: Excessive growth of hormone dependent
pubic, axillary, abdominal, chest, and facial hair
Virilization: Clitoromegaly
temporal balding
hirsutism
Increase muscle mass

Virilization (ovarian vs Adrenal)

Will need a Pelvic exam.

90
Q

Diagnostic Studies

A

• Adrenal androgens
- DHEA-S
- Androstenedione
• Testosterone
- Derived from ovaries and conversion from androstenedione

91
Q

Ovarian tumor vs Adrenal tumor

A
  • Virilization represents serious cause of androgen excess
  • Ovarian tumor, very high testosterone
  • Adrenal tumor, very high DHEA-S
  • Transvaginal ultrasound and/or abdominal CT
92
Q

Congenital Adrenal Hyperplasia

A

• 21-hydroxylase deficiency
• Rare: 0.1-1% of women
• Hirsutism at menarche, oligo, oramenorrhea in early adulthood
• 17-OH progesterone before and after ACTH
Treat with glucocorticoid to suppress ACTH stimulation of adrenal

93
Q

Menopausal Issues

A
  • Hot flashes occur in 75%
  • Sleep and mood disturbances
  • Short-term estrogen treatment of choice
  • SSRI effective — use with caution in breast cancer
  • Gabapentin (not very well tested)
  • Progesterone (not as effective)
  • Efficacy of alternative therapy not established
94
Q

Male Hypogonadism

A

Central
• Hypothalamic
• Pituitary tumor
• Craniopharyngioma
• Kallmann syndrome
Gonadal
• Chemotherapy
• Injury
• Klinefelter’s

95
Q

Klinefelter’s Syndrome

A
  • Low Testosterone, High LH/FSH
  • XXY karyotype
  • Arm span > height
  • Eunuchoid habitus
  • Atrophic testicles
  • Infertility
  • Gynecomastia
96
Q

Gynecomastia

Causes?

Workup?

A

• Causes: Puberty (upto 60%) , old age, estrogen
hyperthyroidism / testicular tumors
Klinefelter syndrome
androgen therapy (testostrone therapy)
estrogen, spironolactone, digoxin

Gynecomastia Workup
• B-HCG (testicular Ca) / • Estradiol / • Prolactin / • Testosterone / •FT4

97
Q

Testosterone Replacement

A

To deferintiate between central or gonadal low testostrone do FSH levels

• Testosterone enanthate/cypionate
- Injection q 2-3 weeks
• Daily topical androgen
• Adverse events
- Gynecomastia
- increases PSA
- increases Hct
- Prostatic enlargement
- Increase HDL
- Worsens sleep apnea

  • Use with caution in elderly and those with
    heart disease
  • Don’t use in individuals with obstructive
    sleep apnea
98
Q

Calculate LDL

A

LDL = TC - HDL - TG/5

99
Q

ATPIII Guidlines:

Major Risk Factors CAD/

When to start therapy LDL

A
  • Smoking
  • BP> 140/90
  • Men > 35, women > 55
  • HDL < 40
  • Family history of premature CAD (male < 55, female < 65)
100
Q

Statins

A
  • Block HMG Co-A reductase
  • Lowering CHD events mortality by 25%
  • Myalgias rarely
  • Myopathy worse with gemfibrozil / Niacin

USE pravastatin on Elderly

101
Q

Statins and TLC in All Diabetics

A

Any DM has to be on a STATING
• Overt CVD
• With no overt CVD and age < 40 consider statin if
LDL > 100 with multiple CVD risk factors
• With no overt CVD primary goal is LDL < 100
• With overt CHD a goal of < 70 is an option

102
Q

Triglycerides and HDL Targets

A

• Triglycerides
-
• HDL
- > 40 in men
- > 50 in women
• LDL is primary target

103
Q

Nicotinic Acid

A
  • Blocks LDL synthesis
  • Lower LDL
  • Increase HDL **
  • Lower TG
  • Flushing, hyperuricemia, hepatotoxicity / Try to not use with DM
104
Q

Fibrates

A

• Gemfibrozil
- Lower TG ***
- Increase HDL
-Lower LDL
• Fenofibrate best combination with a statin

105
Q

A 50 yo had the lipid profile below at a recent office
visit. She does not smoke, takes no medications,
and herBPis 119/80.
TC 220, HDL 40, LDL 125, TG 250

A

When TG is 200-250, estimate non-HDL
cholesterol.
Non-HDL = TC - HDL
non-HDL goal is 30 mg/dL higher than LDL goal

non-HDL = 220-40 = 180

106
Q

CVA - LDL treatment goals

A

Coronary artery equivalent disease. The goal is
< 100, and a statin would be first-line therapy.

107
Q

Diagnosis of Diabetes

A

• A1c>6.5%
or
• FPG>126
or
• 2-hr glucose > 200 on 75 gm OGTT
or
• Random glucose > 200** and **symptoms

108
Q

Prediabetes

A

• FBG 100-125
or
• A1c 5.7-6.4%
or
• 2-hr glucose 140-199 on 75 gm OGTT

109
Q

Pramlintide

A
  • Synthetic amylin
  • Use with insulin before meals
  • Prolongs gastric emptying
  • Reduces postprandial glucose
  • Appetite suppression
  • Hypoglycemia

Mechanism of Action: amylin, a small peptide hormone that is released into the bloodstream by the β-cells of the pancreas along with insulin, after a meal.[1] Like insulin, amylin is completely absent in individuals with Type I diabetes.[2]

110
Q

Testing in Asymptomatic / SCREENING

A

Testing in Asymptomatic
• Adults with BMI > 25 and 1 other risk factor
- Family history
- Gestational DM
- Hypertension
-CVD
• In others, test at 45 and then at 3-year intervals
if normal

111
Q

Glycemic Control and Complications / Studies

A
  • DCCT and UKPDS
    • 60% and 25% reduction in microvascular complications (eye and Kidney can be improved)
  • ACCORD (NEJM 2009)
    • Increased mortality, no CV benefit / A1C lowered but no macrovascular
  • ADVANCE and VADT (NEJM 2008)
    • No increase in mortality, no CV benefit / lower levels of A1C but no improvement
112
Q

DM Retinopathy Screening / Neuropathy / Nephropathy

A

Retinopathy Screening

  • Adults with Type 1 within 5 years after onset
  • Type 2 shortly after diagnosis
  • Retinal photography is a screen not an eye exam
113
Q

DM Targets

A

• Blood pressure -< 130/80
- When RX necessary, use ACE inhibitor or ARB
- Pregnant patients 110-129/65-79
- No ACE or ARB in pregnancy
Aspirin (75-162 mg/day)
• Primary prevention in those with increased CV risk (10-yrrisk> 10%)
• Risk of bleeding may offset beneficial effects for those with DM and low CVD risk
• Secondary prevention in those with DM and history of CVD
• For ASA allergy, use clopidogrel

114
Q

/ Neuropathy screening in DM

A
  • Screen annually with simple clinical tests
  • Electrophysiologic testing rarely needed
  • Optimize sugar control, use medication to improve QOL
115
Q

Nephropathy in DM /Screening

A

• Urine albumin annually
- Type 1 after 5 years
- All Type 2 at diagnosis
• Serum creatinine and estimated GFR annually
• ACEI and ARBs delay progression of nephropathy

116
Q

Insuline and Surgery

A

Pt with Type I never stop long acting insuline / can stop Lispro

Type I in MICU / Gtt keep sugars between 140-180

117
Q

Effectiveness Lowering A1c

A
  • Metformin 1.0-2.0%
  • Sulfonylurea 1.0-2.0%
  • Thiazolidinediones 0.5-1.4%
  • Acarbose 0.5-0.8%
  • Meglitinide 0.5-2.0%
118
Q

Metformin

A
  • No weight gain or hypoglycemia
  • Start with 500 mg daily, increase slowly to 2,500 mg maximum
  • Renal/Liver function
  • Takes 8-12 weeks to see effect

Renal function cr > 1.4 / CHF / Elderly

Mechanism of action: primarily by suppressing glucose production by the liver (hepatic gluconeogenesis)

119
Q

Sulfonylureas / Glipizide, Glibenclamide (glyburide), Glimepiride

A
  • Effectiveness decreases over time
  • All cause hypoglycemia
  • Use short-acting ones to reduce hypoglycemia
  • Glipizide half-life 14-16 hours
  • Glimepiride and glyburide half-life 24 hours

Mechanism of action: They act by increasing insulin release from the beta cells in the pancreas.

120
Q

Meglitinides / nateglinide (Starlix) , repaglinide (Prandin)

A
  • Repaglinide, nateglinide
  • Rapid acting, short half-life
  • Effect on postprandial glucose

Mechanism of Action: bind to an ATP-dependent K+ (KATP) channel on the cell membrane of pancreatic beta cells in a similar manner to sulfonylureas but at a separate binding site.

121
Q

Thiazolidinediones (Rosiglitazone (Avandia), Pioglitazone (Actos))

A

• Enhance insulin secretion
• Weight gain, edema
• CHF (FDA warning)
• Myocardial ischemia
• Fractures / bladder cancer
Arch Intern Med 169, 2009

122
Q

When to initiate insulin therapy

A
  • A1c>10%
  • Severe symptoms of hyperglycemia
  • Consistently high glucose
123
Q

Exenatide (Byetta, Bydureon)

A
  • GLP agonist (glucagon-like peptide-1 agonist )
  • Weight Reduction
  • Increases Insulin secretion
  • Lowers Gastric emptying (becareful with Gastroparesis)
  • Lowers Glucagon
  • Pancreatitis?
  • Thyroid C cell tumors?
124
Q

DPP-IV Inhibitors / Dipeptidyl peptidase-4 inhibitors /

Vildagliptin
Sitagliptin (Januvia)
Saxagliptin (Onglyza)
Berberine

A
  • Raise endogenous GLP-1
  • No weight change
  • Nasopharyngitis
  • ? Effect on (3-cell apoptosis)

Mechnism of Action: Inhibition of the DPP-4 enzyme prolongs and enhances the activity of incretins that play an important role in insulin secretion and blood glucose control regulation.

125
Q

FYI

A

A1C Cost/Yr
Exenatide 0.5-1.0% $2,800
Sitagliptin 0.5-0.8% $1,700
Pramlintide 0.2-0.5% $2,556

126
Q

Pramlintide

A
  • Synthetic amylin
  • Use with insulin before meals
  • Prolongs gastric emptying
  • Reduces postprandial glucose
  • Appetite suppression
  • Hypoglycemia

a small peptide hormone that is released into the bloodstream by the β-cells of the pancreas along with insulin, after a meal. Reduction in glycated hemoglobin and weight loss have been shown in insulin-treated patients with type 2 diabetes taking pramlintide as an adjunctive therapy.

127
Q

Hypoglycemia

A

A. Insulinoma
B. Surreptitious use of insulin
C. Surreptitious use of Oral meds

Tests

  • Drug levels
  • if sugar is low and insulin is low its most likely normal
  • C-peptide levels / insulin levels after fasting 72 hrs once drops > 50 need to do levels
128
Q

Hyperosmolar Nonketotic State

A
  • Glucose > 600
  • pH>7.3, CO2>15
  • Minimal ketonemia/ketonuria
  • Correct Na for hyperglycemia (for each 100 mg/dL glucose > 100 add 1.6 mg to serum sodium)
  • If K is < 3.3, hold insulin and give K
129
Q

DKA

A

IVF

K Keep > 3.3

IV insulin once K > 3.3

Once glucose 200 can reduce IV insulin 50% and change to d5W1/2

Adjunct KCL / Vasopressors / Bicarb / phosphate (no definite benefit found)

130
Q

Calcium and Bone

A
  • Hyper and hypocalcemia
  • Vitamin D deficiency
  • Osteomalacia
  • Osteoporosis
  • Paget disease
131
Q

PTH

A

Increases (Renal) Ca absorption - PO4 secretion

Conversion of 1,25 OH2-D which increases (GI ) Ca and PO4 absorption

Also increases Ca and PO4 levels from bone

132
Q

DDx Hypercalcemia

A
  1. Primary hyperparathyroidism
  2. Malignancy (Squamous / small C Ca )
  3. Lithium, thiazides (dont test if they are on these meds)
  4. Vitamin D excess
  5. Hyperthyroidism / Adrenal insuff
  6. Sarcoidosis 10% patients will have it / because macrophages make vitD
  7. Multiple myeloma
133
Q

1° Hyperparathyroidism

A
  • high Ca / PTH, low P04
  • Hypercalciuria
  • Common in elderly women
  • 85% single adenoma, 15% bilateral hyperplasia
  • Usually asymptomatic

MEN I / MEN IIa

134
Q

Treatment of 1° HPT

A

• Parathyroidectomy
- 95% cure rate
- Pre-op localization
- Hypoparathyroidism rare
• No effective medical Rx
• Treat symptomatic patients

135
Q

Ordering Dexa in hyper PTH patients

A

Must order a Radius + Hip and spine

136
Q

When to Operate in Asymptomatic Patients

A

• Calcium > 1 mg/dL above normal
• GFR < 30 mL/min
• Age < 50
• T-score < -2.5 hip, spine, or forearm

137
Q

MEN 1

Multiple Endocrine Neoplasia

A

3 P’s | if so it will be very hard to do surgery

  • 1° HPT (parathyroid hyperplasia)
  • Pituitary tumor
  • Pancreatic tumor (gastrin)
  • Gene maps to chromosome 11q13
  • Autosomal dominant
138
Q

MEN II

A
  • 1° HPT (parathyroid hyperplasia)
  • Medullary thyroid cancer (Calcitonin levels are the markers)
  • Pheochromocytoma
  • Chromosome 10
  • RET proto oncogene
  • Genetic testing for presymptomatic individuals
139
Q

Hypercalcemia of Malignancy

A

• High levels lead to obtundation, coma, lethargy
• Treat volume depletion
- Loop diuretic not necessary (no benefit)
• IV bisphosphonate / Zoledronic acid more potent
• Response in 2-4 days

  • Calcitonin is not as effective very short acting
  • Glucocorticoids would be beneficial in Vit D toxicity / lymphoma
140
Q

Hypercalcemia of Malignancy

A
  • high Ca, low PO4, low PTH, high PTHrP
  • Lung (squamous cell) - PTHrP
  • Renal cell - PTHrP
  • Lymphoma, leukemia
  • Multiple myeloma -OAF
  • Metastatic disease
141
Q

Sarcoid

A
  • Some other granulomatous diseases
  • Macrophages make vitamin D
  • high Ca, Low PO4, Low PTH (its low because Ca is high)
  • T 1,25(OH)2 vitamin D

GENERAL RULE when PTH is low with high CA look for other reasons CA is high

142
Q

Hypocalcemia

A
  • Hypoparathyroidism (autoimmune / like pts with hashimatos)
  • Vitamin D deficiency (usually must be very sever)
  • Hypomagnesemia — Low PTH release
  • Anticonvulsants (Dilantin and phenobarb - excelerate vit D metabolism)
  • Malabsorption
  • Gastric bypass
143
Q

Symptoms of Hypocalcemia

A
  • Asymptomatic
  • Paresthesias
  • Perioral numbness
  • Chvostek/Trousseau signs
  • Tetany
  • Laryngeal spasm
144
Q

Acute Treament of Hypocalcemia

A
  • Calcium gluconate
  • Vitamin D / and Ca combo
  • Maintain Ca in range of 8-8.5 as over-replacement can lead to hypercalciuria
  • Vitamin D and calcium need careful titration
145
Q

Laboratory Diagnosis of Hypocalcemia

A

• Hypoparathyroidism (autoimmune)
low Ca, high PO4, low PTH
• Hypomagnesemia (alcohol)
low Ca, high P04, low PTH

146
Q

2° Hyperparathyroidism

A
  • Clinical picture is classic anticonvulsant, elderly, minimal sun exposure, bone pain
  • Vitamin D replacement should restore PTH to normal
147
Q

IOM Recommendations

A

IOM Recommendations
Age IU/dav

  • 19-70(M / F) 600
  • > 71 800
148
Q

Osteomalacia

A

Osteomalacia
• Inadequate bone mineralization
• Vitamin D deficiency
• Malabsorption
• Anticonvulsant therapy
• Renal tubular acidosis
• Chronic renal failure
• Hypophosphatemia
• Bone pain
• Proximal myopathy
• Low Ca
• Low PO4
• high PTH
• Low Vitamin D

149
Q

Paget Disease

A
  • Usually asymptomatic
  • high Bone turnover -> structurally weak bone
  • very high Alkaline phosphatase 100’s
  • Treat if pain is severe, pagetic lesions in_ weight-bearing_ areas, or _lytic lesions_

So do not treat if not symptomatic / first step to go to NSAIDs then Bisphosphonates/Calcitonin

150
Q

Familial Hypocalciuric Hypercalcemia

A
  • Rare
  • Lower Sensitivity of Ca-sensing receptor and higher Ca levels are needed to suppress PTH
  • Familial /Autosomal Dominnant
  • 24-hr urine calcium < 100

Will have a very low urine calcium | Ca / ratio < 0.01

Treatment not recommended

151
Q

Panretinal laser photocoagulation

A

results in retained central vision but poorer peripheral and night vision

152
Q

adrenal incidentalom

A

metastatic cancer is nearly 2% for tumors less than 4 cm in diameter but increases to 25% for tumors 6 cm or larger

Hounsfield units > 10-12 we start to worry

153
Q

Evaluate secondary amenorrhea

A

Question: menarche at age 13 years and had normal menstrual cycles until 6 months ago.

Pregnancy test

FSH (> 35 ovariand insufficiency |

PRL /T4 and TSH normal

Progestrone withdrawal is last / if no bleed must look at central causes of low estrogen

154
Q

tuberculosis-induced hypercalcemia.

A

excessive production of 1,25-dihydroxyvitamin D by the tuberculous granulomas. The granulomas of tuberculosis (and other granulomatous diseases, such as sarcoidosis, Crohn disease, and leprosy) are composed of macrophages that possess the 1α-hydroxylase enzyme needed to convert 25-hydroxyvitamin D to its active form, 1,25-dihydroxyvitamin D.

Low PTH, PO4 high

with Malignancy Hypercalcemia High PTH /prPTH and low PO4

155
Q

Graves ophthalmopathy.

A

Luedde Exophthalmometer - to measure extend of dz

The medical treatment for ophthalmopathy trial of corticosteroids. In sever cases thyroid surgery (this is in pts intolerance to iodine or antithyroid drugs, large or obstructive goiters, or ophthalmopathy).

Pathology: lid changes, proptosis or exophthalmos, and inflammatory eye changes, such as chemosis, conjunctival injection, periorbital edema, or iritis. Extraocular muscle involvement can result in double vision, whereas optic nerve compression can result in reduced visual acuity and even blindness.

156
Q

Woman with low bone mass. How to treat?

A

The NOF recommends antiosteoporotic therapy for persons whose risk of major osteoporotic fracture over the next 10 years is 20% or greater or whose risk of hip fracture over the next 10 years is 3% or greater.

Denosumab, osteoclast formation, reserved for patients with a high risk of fracture, including those with multiple risk factors for fracture or a history of previous fractures.

Estrogen is contradicted in this patients with dx of breast cancer.

Raloxifene, a selective estrogen receptor modulator, approved for osteoporosis prevention by the FDA. However, significant hot flushes.

Teriparatide (recombinant human parathyroid hormone) is also contraindicated in persons with malignancy involving bone, Paget disease, or existing hyperparathyroidism or hypercalcemia.

Bispho alendronate is the most appropriate drug to use for osteoporosis prevention in patients with osteopenia and a history of radiation therapy

157
Q

Sestamibi parathyroid scintigraphy

A

parathyroid adenoma

158
Q

Thyroid Scan

A

123-Iodine

  • Patient needs fast
  • Amount of radioactivity documented, the patient swallows the tracer
  • Imaging about 4-6 hours after the tracer is swallowed.
  • Repeat in 24 hrs

99m-Technetium

  • No special prep instructions
  • The tracer is injected about 15-30 minutes after imaging starts
159
Q
A

Med Study (2 decks)

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