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int med exam 0828 > Endocrinology - Thyroid, pituitary > Flashcards

Endocrinology - Thyroid, pituitary Flashcards

1
Q

with regards to glandular abnormality, primary refers to ?

A

refers to the gland that secretes the hormone

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2
Q

With regards to glandular abnormalities, secondary refers to?

A

refers to the disease of the gland that controls the primary gland

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3
Q

With regards to glandular abnormalities, tertiary refers to?

A

the disease of the gland that controls the gland that controls the primary gland

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4
Q

what is the difference between the anterior and posterior pituitary control?

A
  • the hypothalamus uses hormones to control the anterior pituitary
  • hypothalamus uses direct nerve stimulation to control the posterior pituitary.
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5
Q

what hormones does the posterior pituitary contain?

A

It stores and releases oxytocin and ADH (vasopressin).

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6
Q

what is the formula for serum osmolality?

A

2Na + glucose/18 + BUN/2.8

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7
Q

what triggers ADH to be released?

A
  • volume contraction
  • nausea
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8
Q

what decreases the threshold for ADH to be released?

A

pregnancy and pre-menses

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9
Q

what increases the threshold set for ADH to be released?

A
  • chronic hypervolemia
  • acute hypertension
  • corticosteroids
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10
Q

what hormones does the anterior pituitary contain?

A
  • FSH
  • LH
  • ACTH
  • TSH
  • Prolactin
  • Growth Hormone
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11
Q

what are the two types of signals that control the release of anterior pituitary hormones?

A
  1. stimulatory hormones produced by the hypothalamus
  2. target organ hormone feedback
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12
Q

basics of ACTH? peaks?

A
  • diurinary variation with peak 3-4AM and nadir at 10-11pm
    ACTH increase in response to CRH and stress
  • ACTH stimulates the adrenal gland to produce corticosteroids and androgens
  • stimulates adrenal cortex which produces glucocorticoids
  • cortisol inhibits CRH and ACTH
    *
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13
Q

basics of GH?

A
  • pulsatile fashion
  • regulated by GHRH and somatostatin
  • GHRH cause release of GH from the pituitary
  • somatostatin/GHIH inhibits the release of GH from the pituitary
  • somatostatin/GHIH also inhibit release of TSH from pituitary
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14
Q

basics of LH and FSH?

A
  • produced by gonadotrophs, regulated by pulsatile secretion of GnRH from the hypothalamus
  • LH stimulates the secretion of sex steroids from gonads. In testes, LH binds to Leydig cell receptors to produce and secrete testosterone. THeca cells in ovary respond to LH by secretion of testosterone, which is converted into estrogen by adjacent granulosa cells.
  • FSH stimulates maturation of ovarian follices and helps for sperm production.
  • testosterone, estrogen and progesteorne both inhibit pituitary LH and FSH and hypothalamus GNRH
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15
Q

basics of prolactin regulation?

A
  • under tonic inhibition by hypothalamic dopamine, only secreted when brake is released.
  • positively regulated by TRH, GRH, and VIP. Estrogens too. (VEG-T)
  • stimulation of nipples and mammary gland stimulates prolactin-stimulating hormones from the hypothalamus too.
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16
Q

basics of TSH regulation?

A

TSh secretion stimulated by hypothalamic TRH and inhibited by T3/T4 and somatostatin/GHIH

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17
Q

what is the first step to determine a pituitary tumor?

A
  1. if it is functionally abnormal
  2. if it is secreting abnormal amount of any hormone
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18
Q

what are the mass effect symptoms of pituitary tumor?

A

headache, diplopia, or visual field defects (bitemporal hemianopsia), and seizures.

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19
Q

you suspect pituitary tumor, what test/lab are you going to order?

A
  1. MRI to see tumor
  2. Prolactin
  3. IGF_1 to screen for acromegaly
  4. 24-hour urine free cortisol concentration or 1 mg overnight dexamethasone (if cortisol excess) or ACTH stim (if cortisol deficiency)
  5. TSH and T4
  6. alpha subunit, FSH, and LH
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20
Q

what is alpha subunit for pituitary tumor?

A

support diagnosis of gonadotroph adenoma, suggest mass is the pituitary origin.

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21
Q

define hyperprolactinemia?

A

prolactin level >20 ng/ml

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22
Q

prolactin level of 21-40 can be caused by?

A
  • dopamine antagonists (antipsychotics, verpamil etc)
  • pregnancy or estrogen use
  • CKD
  • hypothyroidism
  • sarcoidosis and trauma (interfere with production/dopamine transport)
  • food intake
  • chest wall injuries/nipple stimulation in lactating women
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23
Q

describe what separates micro vs maroadenoma?

A

microadenoma<1cm; macroadenoma 1cm and higher (bigger - visual defects)

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24
Q

describe the pathophysiology of elevated prolactin level and resultant symptoms?

A
  1. elevated PRL causes decrease release of GnRH
  2. decreased GnRH causes decrease in LH and FSH
  3. Decrease LH and FSH causes ED ,amenorrhea, hirsutism
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25
Q

what is the treatment for prolactinomas?

A
  • dopamine agonists like cabergoline and bromocriptine which reduce both PRL level and tumor size.
  • transsphenoidal surgery if refractory
  • Can use both in pregnancy (1/3 of macroadenomas enlarge)
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26
Q

what are the important side effects specific to cabergoline?

A

increased cardiac valvulopathy in high doses.

contraindicated in patients with known lung, heart valve, and retroperitoneal fibrotic disease.

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27
Q

what is growth hormone suppressed by?

A

hyperglycemia, somatostatin, chronic corticosteroid use

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28
Q

what is growth hormone stimulated by?

A

hypoglycemia and estrogens

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29
Q

what is the most important long term problem associated with acromegaly?

A

cardiovascular disease, OSA, DM2, colon polyps

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30
Q

how do you screen and confirm for acromegaly? what else do you need to check?

A
  • screen by checking the adjusted IGF-1 level
  • Confirm by failure to suppress GH after 75gm OGTT
  • Post OGTT GH level>1 is dx of acromegaly.
  • check prolactin which may be elevated due to co-secretion in 25% of GH tumors
  • large tumors can disrupt thyroid and gonadotropin release, so levels may need to be assessed too.
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31
Q

how do you treat acromegaly?

A
  1. treat all patients even asymptomatic with transphenoidal surgery
  2. give somatostatin analogs (octreotide) +/- dopamine agonsits (bromocriptine or carbergoline) or GH receptor antagonists as adjuvant tx for residual tumor.
  3. Screen with colonoscopy and echocardiogram regardless of age.
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32
Q

what suggests a gonadotroph adenoma?

A

increase in free alpha subunits or high levels of FSH and/or LH

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33
Q

which cancers mets to the pituitary?

A
  • breast and lung cancer is the most common
  • lymphoma and leukemia can present as primary
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34
Q

how does pituitary cancer mets present?

A

presents as Diabetes inspidus

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35
Q

what is the work up for pituitary incidentaloma?

A
  1. test visual fields for tumors that impinge on optic nerve
  2. Measures PRL to r/o prolactinomas
  3. IGF-1 to screen for acromegaly
  4. 24 hour urine free cortisol or low dose dexa test
  5. TSH and FT4
  6. morning cortisol to assess for hyposecretion
  7. LH, FSH and testosterone
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36
Q

what is the clinical presentation fo pituitary apoplexy? labs and imaging?

A
  • pituitary bleeding
  • suspect when variable neuro symptoms with fluctuating symptoms
  • decreased ACTH and cortisol levels
  • on cosyntropin stimulation, cortisol levels increase since adrenals remain intact.
  • imaging shows a high density mass in sella
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37
Q

what are the two types of DI? Explain the difference?

A
  • nephrogenic DI - decreased ADH effect on the kidneys
  • Neurogenic DI - decreased ADH production
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38
Q

what are the main causes of nephrogenic DI?

A
  1. electrolytes: hypercalcemia, hypokalemia
  2. Medications: loops diuretics, lithium
  3. interstitial: sickle cell, Sjogren’s
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39
Q

what are the important causes of neurogenic DI?

A
  • genetic (50%)
  • Acquired: hypopituitarism, CNS injury,
  • infiltrative diseases (sarcoidosis, wegners, eosinophilic grnuloma etc)
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40
Q

what are the symptoms of DI?

A
  • polyuria (high urinary output)
  • polydypsia (excessive thirst)
  • nocturia is usually the first symptom
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41
Q

what do you see on labs for DI?

A
  • low urine osm
  • normal to high serum osmolality
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42
Q

how do you differentiate neurogenic vs nephrogenic DI with water deprivation?

A
  • with water deprivation, measure ADH and plasma osmolality
  • If ADH does not increase with increase plasma osmolality, this is neurogenic DI
  • If ADH increases with but no increase in urine osm, this is nephrogenic DI.
  • If urine fails to concentrate with water restriction and desmopressin, this is also nephrogenic DI.
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43
Q

how do you treat nephrogenic DI?

A

low sodium diet and thiazide diuretics +/- amiloride

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44
Q

how do you treat neurogenic DI?

A

desmopressin

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45
Q

high TSH, low FT4 ddx?

A
  1. primary hypothyroidism
  2. chronic lymphocytic thryoiditis (hashimotos)
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46
Q

high TSH, high FT4 ddx

A
  1. Pituitary (secondary; TSH induced)
  2. hyperthyroidism
  3. thyroid hormone resistance syndromes
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47
Q

Low TSH, high FT4 ddx?

A
  1. Euthyroid sick syndrome (primary hyperthyroidism)
  2. subacute or silent thyroiditis
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48
Q

Low TSH, normal FT4 ddx?

A
  1. Euthyroid sick syndrome
  2. subclinical hyperthyroidism
  3. multinodular goiter with autonomous production
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49
Q

Low TSH, low FT4 ddx?

A

pituitary hypothryoidism

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50
Q

when is RAIU increased?

A
  1. Graves disease
  2. TSH pituitary tumor
  3. Hot nodules (solitary, TMN)
  4. HcG secreting tumor
  5. Iodine deficiency
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51
Q

when is RAIU decreased?

A
  1. Thryoiditis
  2. excess exogenous T4 or T3
  3. iodine excess (contrast, dye, diet, amiodarone)
  4. Factitious hyperthyroidism
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52
Q

what is the purpose of a thyroid scan?

A
  • Scintigraphy where you can see isotopes localize in the thyroid.
  • used in the work up for hyperthyroidism
  • shows hot - hyperfunctioning vs cold (underfunctioning).
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53
Q

what is the difference between thyroid uptake vs thyroid scan vs US?

A
  • thyroid RAIU - gives you a number
  • Thyroid scan assess for goiter and nodular disease (hot vs. cold)
  • US determines size and number of nodules - cystic vs solid
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54
Q

when do you suspect secondary or tertiary hypothyroidism?

A
  • low or inappropriately normal TSH with low FT4 except in hospitalized patients with multiple hormone deficiencies
  • Differentiate secondary and tertiary by imaging the sella.
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55
Q

what conditions/drugs interfere with absorption of thyroxine?

A
  • these cause increased TBG or increase the metabolism of T4, which can cause elevated TSH
  • malabsorption syndromes
  • estrogens
  • cholestyramine
  • iron/calcium/aluminum supplements
  • resin binders
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56
Q

what are the two thyroid emergencies?

A
  • myxedema coma
  • thyroid storm
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57
Q

what signs and symptoms are suggestive of myxedema coma?

A
  • decreased mentation and hypothermia
  • Slowing of systemic processes (hypoventilation, hypoglycemia, bradycardia, hypoventilation)
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58
Q

what labs are suggestive of hypothyroidism outside of TSH?

A
  • hyponatremia,
  • normocytic anemia,
  • hyperlipidemia (increased TC, LDL)
  • pericardial effusions (rare)
  • increased prolactin level (<100)
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59
Q

patient has elevated prolactin and amenorrhea, what do you need to check?

A
  • check thyroid function as if hypothyroid, it will resolve with treatment.
  • If not hypothryoid, do prolactin work up.
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60
Q

if you suspect myxedema coma, what labs do you need to draw?

A
  • TSH and Ft4
  • baseline cortisol and ACTH to rule coincident adrenal insufficiency
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61
Q

what is the empiric treatment for myxedema coma?

A
  • Treat with either T3 as possible rapid onset and decrease conversion to T4 to T3 or T4
  • empiric glucocorticoids until stim testing available
  • empiric broad spectrum abx until the infection is excluded.
  • passive rewarming if needed.
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62
Q

outside of TSH, what are abnormal labs/studies for hyperthyroidism?

A
  • low TC and LDL
  • normocytic/normochromic anemia
  • hypercalcemia with increased bone alk phos
  • osteopenia/osteoperosis
  • increased CO, DCM, any tachyarrhythmia
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63
Q

what is apathetic hyperthyroidism?

A

commonly seen in elderly patients, new onset Afib or depression.

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64
Q

what specific findings for graves disease?

A
  • diffuse, soft symmetric goiter
  • exophthalmos and periorbital edema
  • pretibial myxedema (thickening and reddening fo dermis due to lymphocytic infiltrate)
  • immune-mediated hematologic abnormalities such as pernicious anemia and Idiopathic thrombotic purpura.
65
Q

what labs/studies is abnormal in Graves disease? (8)

A
  1. low TSH
  2. elevated Ft3 and FT4
  3. increased diffuse uptake on thyroid uptake scan
  4. hypercalcemia
  5. elevated alk phos
  6. thrombocytopenia
  7. thyroid-stimulating immunoglobulins
  8. normocytic anemia
66
Q

how do you treat graves disease? how about in pregnancy?

A
  • PTU (in thyroid storm or pregnancy)
  • MMI in nonpregnancy due to lower toxicity
  • thyroid ablation or surgery
  • beta blockers to help with adrenergic symptoms or pre-treatment for iodine ablation
67
Q

what are the most serious side effects of graves disease treatments? do you need screening labs?

A
  • hepatic toxicity and agranulocytosis
  • check LFTs and CBC if symptomatic (jaundice, dark urine, prolonged fever/sore throat)
68
Q

what are the precipitating events to thyroid storm?

A
  • surgery
  • infections
  • iodine load such as amniodarone or contrast dye
69
Q

what is the treatment for thyroid storm?

A
  1. beta blockers (propanolol/esmolol) to interrupt physiologic response of thyroid hormone
  2. PTU or MMI to block new hormone synthesis
  3. iodine to block release of preformed hormone from the gland
  4. glucocorticoids to prevent adrenal crisis
  5. broad spectrum abx until infection excluded
  6. supportive care
70
Q

what are the 3 categories of thyroidits?

A
  • acute - a bacterial infection of gland
  • subacute - caused by viruses (also called granulomatous)
  • chronic (autoimmune mediated disease Hashimoto’s), painless, postpartum
71
Q

what is the most common presentation for subacute thyroiditis?

A

30-50 year olds, females >males with a tender neck with pain that may radiate to teh ear +/- fever

72
Q

what is the pathophys of subacute thyroidits?

A

viral infection that results in granulomas in the thyroid gland which becomes fibrotic but returns to normal months later.

73
Q

what lab studies are suggestive of subacute thyroiditis?

A
  1. Initially, T3 and T4 increased, TSH depressed, with RAIU initially decreased.
  2. Overtime, overt hypothyroidism develops with low T4 and increased TSH
  3. RAIU returns to normal, then T4 and TSH normalize
74
Q

treatment for subacute thyroiditis?

A
  • self-limiting
  • severe cases - ASA or NSAIDs
  • Glucorticoids taper in refractory/systemic cases.
75
Q

what is the most common thyroid problem?

A

hashimotos

76
Q

what labs do you see for hashimotos?

A
  1. incipient hypthyroidism - normal FT4, rising TSH
  2. overhypothyroidism - low Ft4, high TSH
  3. hyperthyroidism - high FT4/FT3, low TSH
77
Q

common presentation of painless thyroiditis?

A
  • complaints of hypo/hyperthyroidism where patient presents with hyperthryoid stage (2-4 weeks) and then prorgresses with hypothyroid stage (4-12 weeks)
  • diffuse, painless enlargement.
  • 50% progress to chronic autoimmune hypothyroidism
78
Q

how do you distinguish Graves disease from thyroidits? what is similar?

A
  • RAIU is high in graves and low in patients who are hyperthyroid due to others.
  • Thyroid scintigraphy are both high for graves and hyperthyroidism caused by thyroiditis
    *
79
Q

what are the labs seen in euthyroid sick syndrome? pathophys?

A
  • in illness, body does not need much T3. So body converts T4 to reverse T3 (rT3).
  • You see very low FT3, high reverse T3, and low/low-normal FT4 and TSH.
80
Q

what is a hot nodule vs cold nodule?

A

hot means increased radioactive iodine uptake, cold means decreased radioactive iodine uptake

81
Q

solitary nodule with suspicious findings on US? next step?

A

FNA independent of TSH

82
Q

solitary nodule with non-supsicious US findings. Next step?

A
  • If TSH high, high likelihood nodule is malignant, biopsy, measure free T4 and anti-TPO antibodies
  • If large >1cm, biopsy unless hot nodule
  • If TSH low, do scintigraphy. If hot, done.
  • If normal, most experts FNA.
83
Q

how do you work up multinodular goiter?

A
  • if low /low-normal TSH and a MNG, perform scintigraphy to determine which nodules are hot or cold.
  • Leave hot nodules alone, FNA on all cold nodules and suspicious nodules seen on US
  • if U/S not concerning, treat hyperthyroidism.
84
Q

what are the 4 histologic types of thyroid carcinomas?

A

papillary, follicular, anaplastic, medullary

85
Q

basics of papillary thyroid carcinoma?

A
  • most common
  • indolent
  • spreads via lymphatics to bone/lungs
86
Q

basics of follicular carcinoma?

A
  • mimics normal thyroid tissue with early hematogenous spread to bone, lungs, CNS.
  • Capsular invasion part of staging
  • total thyroidectomy needed for adequate staging.
87
Q

basics of anaplastic follicular carcinoma?

A
  • highly malignant, death within 6 months of diagnosis.
  • no good treatment.
88
Q

basics of medullary carcinoma?

A
  • hyperplasia of parafollicular cells with elevated serum calcitonin
  • associated with MEN 2A and 2B syndromes\
  • associated with point mutations in the RET proto-oncogene which causes production of kinase that phosphorylates tyrosine residues for uncontrolled cell growth
89
Q

what is the general tx for thyroid cancer?

A
  • thyroidectomy
  • some have residual thyroid tissue, with most needing postoperative RAI.
  • Suppressive thyroxine therapy later.
90
Q

what is thyroid lymphoma associated with? what type of lymphoma?

A
  • chronic autoimmune thyroiditis.
  • associated with diffuse large b-cell lymphoma
91
Q

what are the 2 main indications for the treatment of non-toxic multinodular goiter?

A
  • symptomatic compression of structures
  • cosmesis
92
Q

what is the difference between toxic and non-toxic multinodular goiter? what are the labs?

A

toxic refers to thyrotoxicosis where TSH suppressed and FT3 and FT4 are increased with thyroid scan showing 1 or more hot nodules.

93
Q

what is the clinical presentation of the following adenomas:

  1. Prolactinoma
  2. Gonadotrophs
  3. Thyrotrophs
  4. Somatotrophs
  5. Corticotrophs
  6. Mixed cell type? (which)
94
Q

MRI shows an incidential pituitary tumor <1cm, what to do next?

95
Q

MRI shows an incidental pituitary tumor >1cm, what to do next?

96
Q

if non-functional tumor, what do you do next?

97
Q

indications for surgical removal of non-prolactinoma pituitary tumor?

98
Q

what do prolatinomas cause?

99
Q

what if you see a macroadenoma with only mild hyperprolactinemia (prl<100)? Whats the hook effect?

100
Q

what is the complication of long standing hypogonadism?

101
Q

medical management of prolactinomas?

102
Q

what are the non-medical mgmt of proloactinomas?

103
Q

how about a patient who is pregnant who is on drug therapy for a prolactinoma. what do you do ?

104
Q

what is the signs and symptoms of acromegaly?

105
Q

long term complications of acromegaly?

106
Q

screening, and tests to order for acromegaly

107
Q

how do you treat acromegaly?

108
Q

how do you diagnose a gonadotroph adenoma?

109
Q

treatment of gonadotroph adenoma?

110
Q

treatment of pituitary hyperplasia?

111
Q

MC cause of metastatic cancer to the pituitary?

112
Q

what is pituitary apoplexy?

113
Q

what are the postpartum hypopituitarism conditions?

114
Q

what is the general rules for the treatment of acute hypopituitarism?

115
Q

what is DI?

116
Q

basics of neurogenic DI?

117
Q

basics of nephrogenic DI?

118
Q

what is your first step in diagnosing central vs nephrogenic DI?

119
Q

how to interpret the water restriction test in Nephrogenic vs central DI?

120
Q

how would you treat central vs nephrogenic DI?

121
Q

what are the urine osm, urine na, serum na, and serum Osm in patients with SIADH?

122
Q

whats the difference between RAIU and thyroid scan?

123
Q

when is RAIU increased or decreased?

124
Q

what does a thyroid scan give you?

125
Q

when is the thyroid RAIU and scintigraphy scan useful?

126
Q

when is thyroid US use?

127
Q

when should a RAIU and scintigraphy precede a thyroid US?

128
Q

what non-thyroid abnormal labs associated with hypothyroidism?

129
Q

diagnose primary, subclinical, secondary or tertiary hypothyroidism labs?

130
Q

what do you need to watch out for that interferes with the absorption of thyroxine?

131
Q

how do you treat pregnant hypothyroid patients?

132
Q

how do you treat subclinical hypothyroidism?

133
Q

how would you start treating hypothyroidism?

134
Q

patient has myxedema coma. what to do you do next?

135
Q

what labs are abnormal in hyperthyroidism?

136
Q

how do you diagnose graves?

137
Q

physical exam findings of Graves disease?

138
Q

Tx for Graves disease?

139
Q

treatment of thyroid storm?

140
Q

what are the phases of thyroiditis?

141
Q

what are painful and tender thyroiditis?

142
Q

what are the painless and nontender thyroiditis?

143
Q

name the 6 thyroiditis and their treatments? which are painful, painless?

144
Q

what is euthyroid sick syndrome?

145
Q

how would you do a basic eval for thyroid nodule?

146
Q

generalities of thyroid nodules?

147
Q

what are the risk factors that increase likelihood that a nodule is malignant?

148
Q

what’s the work up for thyroid nodules?

149
Q

US criteria for biopsy(FNA) high risk and low risk?

150
Q

what is a toxic thyroid adenoma?

151
Q

tx of thyroid adenoma?

152
Q

RAIU findings in hyperthyroid disorders?

153
Q

what is the 4 types of histiologic types of carcinomas?

154
Q

After thyroidectomy, what suggests a higher risk of recurrence after thyroid cancer?

155
Q

what is the treatment of thyroid cancer after thyroidectomy?

156
Q

what suggests thyroid lymphoma?

157
Q

what is nontoxic multinodular goiter? tx?

158
Q

what is toxic multinodular goiter? tx?

int med exam 0828 (24 decks)

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