Presentation is loading. Please wait.

Presentation is loading. Please wait.

ENDOCRINOLOGY BOARD REVIEW Presented by Med/Peds PGY III Class.

Similar presentations


Presentation on theme: "ENDOCRINOLOGY BOARD REVIEW Presented by Med/Peds PGY III Class."— Presentation transcript:

1 ENDOCRINOLOGY BOARD REVIEW Presented by Med/Peds PGY III Class

2 ENDOCRINOLOGY Disorders of the Hypothalamic – Pituitary Axis K. Dionne Posey, MD, MPH

3 ENDOCRINOLOGY Pituitary Disorders Thyroid Disorders Adrenal Disorders Gonadal Disorders Calcium Disorders Lipid Disorders

4

5 Hypothalamic–Pituitary Axis

6 Pituitary Gland Located within the sella tursica Contiguous to vascular and neurologic structures –Cavernous sinuses –Cranial nerves –Optic chiasm Hypothalamic neural cells synthesize specific releasing and inhibiting hormones –Secreted directly into the portal vessels of the pituitary stalk Blood supply derived from the superior and inferior hypophyseal arteries

7

8 Pituitary Gland Anterior pituitary gland –Secrete various trophic hormones –Disease in this region may result in syndromes of hormone excess or deficiency Posterior pituitary gland –More of a terminus of axons of neurons in the supraoptic and paraventricular nuclei of the hypothalamus –Storehouse for the hormones –The main consequence of disease in this area is disordered water homeostasis

9 Anterior Pituitary Gland Anterior Pituitary “Master gland” –Major blood source: hypothalamic-pituitary portal plexus Allows transmission of hypothalamic peptide pulses without significant systemic dilution Consequently, pituitary cells are exposed to sharp spikes of releasing factors and in turn release their hormones as discrete pulses –Production of six major hormones: Prolactin (PRL) Growth hormone (GH) Adrenocorticotropin hormone (ACTH) Luteinizing hormone (LH) Follicle-stimulating hormone (FSH) Thyroid-stimulating hormone (TSH)

10

11 Anterior Pituitary Gland Anterior Pituitary “Master gland” –Secreted in a pulsatile manner –Elicits specific responses in peripheral target tissues –Feedback control at the level of the hypothalamus and pituitary to modulate pituitary function exerted by the hormonal products of the peripheral target glands –Tumors cause characteristic hormone excess syndromes –Hormone deficiency may be inherited or acquired

12

13 Hypopituitarism

14 Gonadotropin Deficiency Women Oligomenorrhea or amenorrhea Loss of libido Vaginal dryness or dyspareunia Loss of secondary sex characteristics (estrogen deficiency) Men Loss of libido Erectile dysfunction Infertility Loss of secondary sex characteristics (testosterone deficiency) Atrophy of the testes Gynecomastia (testosterone deficiency)

15 ACTH Deficiency Results in hypocortisolism –Malaise –Anorexia –Weight-loss –Gastrointestinal disturbances –Hyponatremia Pale complexion –Unable to tan or maintain a tan No features of mineralocorticoid deficiency –Aldosterone secretion unaffected

16 TSH Deficiency Hypothyroidism Atrophic thyroid gland

17 Prolactin Deficiency Inability to lactate postpartum Often 1 st manifestation of Sheehan syndrome

18 Growth Hormone Deficiency Adults –Often asymptomatic –May complain of –Fatigue –Degrees exercise tolerance –Abdominal obesity –Loss of muscle mass Children –GH Deficiency –Constitutional growth delay

19

20 Hypopituitarism Etiology Anterior pituitary diseases –Deficiency one or more or all anterior pituitary hormones Common causes: –Primary pituitary disease –Hypothalamic disease –Interruption of the pituitary stalk –Extrasellar disorders

21 Hypopituitarism –Primary pituitary disease Tumors Pituitary surgery Radiation treatment –Hypothalamic disease Functional suppression of axis –Exogenous steroid use –Extreme weight loss –Exercise –Systemic Illness –Interruption of the pituitary stalk –Extrasellar disorders Craniopharyngioma Rathke pouch

22 Hypopituitarism

23 Hypopituitarism Developmental and genetic causes –Dysplasia Septo-Optic dysplasia –Developmental hypothalamic dysfunction Kallman Syndrome Laurence-Moon- Bardet-Biedl Syndrome Frohlich Syndrome (Adipose Genital Dystrophy) Acquired causes: –Infiltrative disorders –Cranial irradiation –Lymphocytic hypophysitis –Pituitary Apoplexy –Empty Sella syndrome

24 Hypopituitarism: Developmental and Genetic causes Septo-Optic dysplasia Kallman Syndrome Laurence-Moon-Bardet-Biedl Syndrome Frohlich Syndrome (Adipose Genital Dystrophy)

25 Hypopituitarism: Genetic –Septo-Optic dysplasia –Hypothalamic dysfunction and hypopituitarism »may result from dysgenesis of the septum pellucidum or corpus callosum –Affected children have mutations in the HESX1 gene »involved in early development of the ventral prosencephalon –These children exhibit variable combinations of: »cleft palate »syndactyly »ear deformities »hypertelorism »optic atrophy »micropenis »anosmia –Pituitary dysfunction »Diabetes insipidus »GH deficiency and short stature »Occasionally TSH deficiency

26 Hypopituitarism: Developmental Kallman Syndrome Defective hypothalamic gonadotropin-releasing hormone (GnRH) synthesis Associated with anosmia or hyposmia due to olfactory bulb agenesis or hypoplasia May also be associated with: color blindness, optic atrophy, nerve deafness, cleft palate, renal abnormalities, cryptorchidism, and neurologic abnormalities such as mirror movements GnRH deficiency prevents progression through puberty characterized by –low LH and FSH levels –low concentrations of sex steroids

27 Hypopituitarism: Developmental Kallman Syndrome Males patients –Delayed puberty and hypogonadism, including micropenis »result of low testosterone levels during infancy –Long-term treatment: »human chorionic gonadotropin (hCG) or testosterone Female patients –Primary amenorrhea and failure of secondary sexual development –Long-term treatment: »cyclic estrogen and progestin Diagnosis of exclusion Repetitive GnRH administration restores normal pituitary Fertility may also be restored by the administration of gonadotropins or by using a portable infusion pump to deliver subcutaneous, pulsatile GnRH

28 Hypopituitarism: Developmental Laurence-Moon-Bardet-Biedl Syndrome Rare autosomal recessive disorder Characterized by mental retardation; obesity; and hexadactyly, brachydactyly, or syndactyly Central diabetes insipidus may or may not be associated GnRH deficiency occurs in 75% of males and half of affected females Retinal degeneration begins in early childhood –most patients are blind by age 30

29 Hypopituitarism: Developmental Frohlich Syndrome (Adipose Genital Dystrophy) A broad spectrum of hypothalamic lesions –hyperphagia, obesity, and central hypogonadism Decreased GnRH production in these patients results in –attenuated pituitary FSH and LH synthesis and release Deficiencies of leptin, or its receptor, cause these clinical features

30 Hypopituitarism Acquired causes: –Infiltrative disorders –Cranial irradiation –Lymphocytic hypophysitis –Pituitary Apoplexy –Empty Sella syndrome

31 Hypopituitarism: Acquired Lymphocytic Hypophysitis –Etiology Presumed to be autoimmune –Clinical Presentation Women, during postpartum period Mass effect (sellar mass) Deficiency of one or more anterior pituitary hormones –ACTH deficiency is the most common –Diagnosis MRI - may be indistinguishable from pituitary adenoma –Treatment Corticosteroids – often not effective Hormone replacement

32

33 Hypopituitarism: Acquired Pituitary Apoplexy – Hemorrhagic infarction of a pituitary adenoma/tumor –Considered a neurosurgical emergency –Presentation: Variable onset of severe headache Nausea and vomiting Meningismus Vertigo +/ - Visual defects +/ - Altered consciousness –Symptoms may occur immediately or may develop over 1-2 days

34 Hypopituitarism: Acquired Pituitary Apoplexy –Risk factors: Diabetes Radiation treatment Warfarin use –Usually resolve completely –Transient or permanent hypopituitarism is possible undiagnosed acute adrenal insufficiency –Diagnose with CT/MRI –Differentiate from leaking aneurysm –Treatment: Surgical - Transsphenoid decompression –Visual defects and altered consciousness –Medical therapy – if symptoms are mild Corticosteroids

35 MedStudy Endocrine Quiz!!! Quick Quiz!!! When should you suspect pituitary apoplexy?

36 Answer Suspect in patient presenting with Variable onset of severe headache Nausea and vomiting Meningismus Vertigo +/ - Visual defects +/ - Altered consciousness

37 Hypopituitarism: Acquired Empty Sella Syndrome –Often an incidental MRI finding – Usually have normal pituitary function Implying that the surrounding rim of pituitary tissue is fully functional –Hypopituitarism may develop insidiously –Pituitary masses may undergo clinically silent infarction with development of a partial or totally empty sella by cerebrospinal fluid (CSF) filling the dural herniation. –Rarely, functional pituitary adenomas may arise within the rim of pituitary tissue, and these are not always visible on MRI

38 Hypopituitarism Clinical Presentation Can present with features of deficiency of one or more anterior pituitary hormones Clinical presentation depends on: –Age at onset –Hormone effected, extent –Speed of onset –Duration of the deficiency

39 Hypopituitarism Diagnosis Biochemical diagnosis of pituitary insufficiency –Demonstrating low levels of trophic hormones in the setting of low target hormone levels Provocative tests may be required to assess pituitary reserve

40 Hypopituitarism Treatment Hormone replacement therapy –usually free of complications Treatment regimens that mimic physiologic hormone production –allow for maintenance of satisfactory clinical homeostasis

41 Hormone Replacement Trophic Hormone DeficitHormone Replacement ACTHHydrocortisone (10-20 mg A.M.; 10 mg P.M.) Cortisone acetate (25 mg A.M.; 12.5 mg P.M.) Prednisone (5 mg A.M.; 2.5 mg P.M.) TSHL-Thyroxine ( mg daily) FSH/LHMales Testosterone enanthate (200 mg IM every 2 wks) Testosterone skin patch (5 mg/d) Females Conjugated estrogen ( mg qd for 25days) Progesterone (5-10 mg qd) on days Estradiol skin patch (0.5 mg, every other day) For fertility: Menopausal gonadotropins, human chorionic gonadotropins GHAdults: Somatotropin ( mg SC qd) Children: Somatotropin [ (mg/kg per day)] VasopressinIntranasal desmopressin (5-20 ug twice daily) Oral ug qd

42 Take home points: Remember that the cause may be functional –Treatment should be aimed at the underlying cause Hypopituitarism may present –Acutely with cortisol deficiency –After withdrawal of prolonged glucocorticoid therapy that has caused suppression of the HPA axis. –Post surgical procedure –Post trauma Hemorrhage Exacerbation of cortisol deficiency in a patient with unrecognized ACTH deficiency –Medical/surgical illness –Thyroid hormone replacement therapy

43 Pituitary Tumors

44

45 Microadenoma < 1 cm Macroadenoma > 1 cm Is the tumor causing local mass effect? Is hypopituitarism present? Is there evidence of hormone excess? Clinical presentation: –Mass effect Superior extension –May compromise optic pathways – leading to impaired visual acuity and visual field defects –May produce hypothalamic syndrome – disturbed thirst, satiety, sleep, and temperature regulation Lateral extension –May compress cranial nerves III, IV, V, and VI – leaning to diplopia Inferior extension –May lead to cerebrospinal fluid rhinorrhea

46 Pituitary Tumors Diagnosis –Check levels of all hormones produced –Check levels of target organ products Treatment –Surgical excision, radiation, or medical therapy –Generally, first-line treatment surgical excision –Drug therapy available for some functional tumors –Simple observation Option if the tumor is small, does not have local mass effect, and is nonfunctional Not associated with clinical features that affect quality of life

47

48

49

50

51 Craniopharyngioma –Derived from Rathke's pouch. –Arise near the pituitary stalk extension into the suprasellar cistern common –These tumors are often large, cystic, and locally invasive –Many are partially calcified characteristic appearance on skull x-ray and CT images –Majority of patients present before 20yr usually with signs of increased intracranial pressure, including headache, vomiting, papilledema, and hydrocephalus

52 Craniopharyngioma Associated symptoms include: – visual field abnormalities, personality changes and cognitive deterioration, cranial nerve damage, sleep difficulties, and weight gain. Children –growth failure associated with either hypothyroidism or growth hormone deficiency is the most common presentation Adults –sexual dysfunction is the most common problem –erectile dysfunction –amenorrhea

53 Craniopharyngioma Anterior pituitary dysfunction and diabetes insipidus are common Treatment –Transcranial or transsphenoidal surgical resection followed by postoperative radiation of residual tumor This approach can result in long-term survival and ultimate cure most patients require lifelong pituitary hormone replacement. If the pituitary stalk is uninvolved and can be preserved at the time of surgery –Incidence of subsequent anterior pituitary dysfunction is significantly diminished.

54

55

56 Quiz!!! Quick Quiz!!! How does prolactin differ from LH/FSH in regard to hypothalamic control?

57 Answer Tonic hypothalamic inhibition by Dopamine

58 Prolactinoma Most common functional pituitary tumor Usually a microadenoma Can be a space occupying macroadenoma – often with visual field defects Although many women with hyperprolactinemia will have galactorrhea and/ or amenorrhea –The absence these the two signs do not excluded the diagnosis GnRH release is decreased in direct response to elevated prolactin, leading to decreased production of LH and FSH

59 Prolactinoma Women –Amenorrhea – this symptom causes women to present earlier –Hirsutism Men –Impotence – often ignored –Tend to present later –Larger tumors –Signs of mass effect

60 Prolactinoma Essential to rule out secondary causes!! –Drugs which decrease dopamine stores Phenothiazines Amitriptyline Metoclopramide –Factors inhibiting dopamine outflow Estrogen Pregnancy Exogenous sources –Hypothyroidism If prolactin level > 200, almost always a prolactinoma (even in a nursing mom) Prolactin levels correlate with tumor size in the macroadenomas –Suspect another tumor if prolactin low with a large tumor

61 Prolactinoma Diagnosis –Assess hypersecretion Basal, fasting morning PRL levels (normally <20 ug/L) –Multiple measurements may be necessary Pulsatile hormone secretion levels vary widely in some individuals with hyperprolactinemia –Both false-positive and false-negative results may be encountered May be falsely lowered with markedly elevated PRL levels (>1000 ug/L) –assay artifacts; sample dilution is required to measure these high values accurately May be falsely elevated by aggregated forms of circulating PRL, which are biologically inactive (macroprolactinemia) –Hypothyroidism should be excluded by measuring TSH and T4 levels

62 Prolactinoma Treatment –Medical Cabergoline – dopamine receptor agonist Bromocriptine - dopamine agonist –Safe in pregnancy –Will restore menses Decreases both prolactin and tumor size (80%) –Surgical Transsphenoidal surgery – irridation (if pt cannot tolerate rx)

63

64

65 MedStudy Endocrine Quiz!!! Quick Quiz!!! What type of tumors are most prolactinomas? Prolactin levels >200 almost always indicate what? Do prolactin levels correlate with tumor size?

66 Answer What type of tumors are most prolactinomas? Microadenomas Prolactin levels >200 almost always indicate what? Almost always indicates prolactinoma Do prolactin levels correlate with tumor size? Yes, in macroadenomas

67

68 Growth Hormone Tumors Gigantism –GH excess before closure of epipheseal growth plates of long bones Acromegaly –GH excess after closure of epipheseal growth plates of long bones –Insidious onset Usually diagnosed late

69 Growth Hormone Tumors May have DM or glucose intolerance Hypogonadism Large hands and feet Large head with a lowering brow and coarsening features Hypertensive – 25% Colon polyps –3-6 more likely than general population Multiple skin tags

70 Growth Hormone Tumors Diagnosis –Screen: Check for high IGF-I levels (>3 U/ml) Remember, levels very high during puberty –Confirm: 100gm glucose load Positive: GH levels do not increase to <5ng/ml Treatment –Surgical –Radiation –Bromocriptine - temporizing measure May decrease GH by 50% –Octreotide For suboptimal response to other treatment

71

72

73 MedStudy Endocrine Quiz!!! Quick Quiz!!! How do you screen for acromegaly?

74 Answer Check for high IGF-I levels (>3 U/ml)

75 Pituitary Gland Anterior pituitary gland –Secrete various trophic hormones –Disease in this region may result in syndromes of hormone excess or deficiency Posterior pituitary gland –More of a terminus of axons of neurons in the supraoptic and paraventricular nuclei of the hypothalamus –Storehouse for the hormones –The main consequence of disease in this area is disordered water homeostasis

76 Posterior Pituitary Gland The Neurohypophysis Major blood source: the inferior hypophyseal arteries Directly innervated by hypothalamic neurons –(supraopticohypophyseal and tuberohypophyseal nerve tracts) via the pituitary stalk Sensitive to neuronal damage by lesions that affect the pituitary stalk or hypothalamus

77 Posterior Pituitary Gland Production of –Vasopressin (antidiuretic hormone; ADH; AVP ) –Oxytocin Vasopressin (antidiuretic hormone; ADH; AVP ) –Acts on the renal tubules to reduce water loss by concentrating the urine –Deficiency causes diabetes insipidus (DI), characterized by the production of large amounts of dilute urine –Excessive or inappropriate production predisposes to hyponatremia if water intake is not reduced in parallel with urine output Oxytocin –Stimulates postpartum milk letdown in response to suckling

78 Posterior Pituitary Gland Vasopressin (Anti Diuretic Hormone) –Some control via anterior hypothalamus Contains separate osmoreceptors which aid in ADH release and thirst regulation –Osmotic stimulus Sodium Mannitol –Non osmotic factors Blood pressure and volume at extremes Nausea Angiotensin II Insulin induced hypoglycemia Acute hypoxia Acute hypercapnia

79 Posterior Pituitary Gland Rapidly secreted in direct proportion to serum osmolality –Increased with Aging Hypercalcemia Hypoglycemia Lithium treatment Volume contraction –Decreased with Hypokalemia Threshold set point –Increased Hypervolemia, Acute hypertension, Corticosteroids –Decreased Pregnancy, Pre-menses, Volume contraction

80

81 Diabetes Insipdus Etiology –Deficient AVP can be primary or secondary The primary form –Deficiency in secretion »Agenesis or irreversible destruction of the neurohypophysis »Malformation or destruction of the neurohypophysis by a variety of diseases or toxins »Neurohypophyseal DI, Pituitary DI, or Central DI –Deficiency in action »Can be genetic, acquired, or caused by exposure to various drugs »Nephrogenic DI –It can be caused by a variety of congenital, acquired, or genetic disorders »50% idiopathic

82 Diabetes Insipdus Gestational DI –Primary deficiency of plasma AVP –Result from increased metabolism by an N-terminal aminopeptidase produced by the placenta –Signs and symptoms manifest during pregnancy and usually remit several weeks after delivery

83 Diabetes Insipdus Secondary deficiencies of AVP –Results from inhibition of secretion by excessive intake of fluids Primary polydipsia –Dipsogenic DI »characterized by an inappropriate increase in thirst »caused by a reduction in the "set" of the osmoregulatory mechanism. »association with multifocal diseases of the brain such as neurosarcoid, tuberculous meningitis, or multiple sclerosis but is often idiopathic. –Psychogenic polydipsia »is not associated with thirst »polydipsia seems to be a feature of psychosis –Iatrogenic polydipsia »results from recommendations of health professionals or the popular media to increase fluid intake for its presumed preventive or therapeutic benefits for other disorders

84 Diabetes Insipdus Secondary deficiencies of AVP –Antidiuretic response to AVP Results from polyuria Caused by washout of the medullary concentration gradient and/or suppression of aquaporin function. Usually resolves 24 to 48 h after the polyuria is corrected –Often complicate interpretation of tests commonly used for differential diagnosis

85 Diabetes Insipdus Pathophysiology –When secretion or action of AVP is reduced to  80 to 85% of normal urine concentration ceases and the rate of output increases to symptomatic levels –Primary defect (pituitary, gestational, or nephrogenic DI) Polyuria results in a small (1 to 2%) decrease in body water and a commensurate increase in plasma osmolarity and sodium concentration that stimulate thirst and a compensatory increase in water intake Overt signs of dehydration do not develop unless the patient also has a defect in thirst or fails to drink for some other reason

86 Diabetes Insipdus Pathophysiology –Primary polydipsia Pathogenesis of the polydipsia and polyuria is the reverse of that in pituitary, nephrogenic, and gestational DI –Excessive intake of fluids slightly increases body water, thereby reducing plasma osmolarity, AVP secretion, and urinary concentration. –Results in a compensatory increase in urinary free-water excretion that varies in direct proportion to intake –Clinically appreciable overhydration uncommon »unless the compensatory water diuresis is impaired by a drug or disease that stimulates or mimics endogenous AVP

87 Diabetes Insipdus Clinical Presentation –Production of abnormally large volumes of dilute urine The 24-h urine volume is >50 mL/kg body weight and the osmolarity is <300 mosmol/L. –The polyuria produces symptoms of urinary frequency, enuresis, and/or nocturia, which may disturb sleep and cause mild daytime fatigue or somnolence. –It is also associated with thirst and a commensurate increase in fluid intake (polydipsia). –Clinical signs of dehydration are uncommon unless fluid intake is impaired.

88 Diabetes Insipdus Diagnosis –Verify polyuria a 24-h urine output collection > 50 mL/kg per day (>3500 mL in a 70-kg man). –Check osmolarity >300 mosmol/L –due to a solute diuresis and the patient should be evaluated for uncontrolled diabetes mellitus or other less common causes of excessive solute excretion <300 mosmol/L –Due to water diuresis and should be evaluated further to determine which type of DI is present

89 Diabetes Insipdus Diagnosis –Water deprivation test If does not result in urine concentration before body weight decreases by 5% or plasma osmolarity/sodium exceed the upper limit of normal –(osmolarity 300 mosmol/L, specific gravity 1.010) –Primary polydipsia or a partial defect in AVP secretion or action are largely excluded –Severe pituitary or nephrogenic DI are the only remaining possibilities

90 Diabetes Insipdus Diagnosis: Neurogenic vs Nephrogenic Administer Desmopressin (DDAVP) 1  g 0.03 ug/kg subcutaneously or intravenously Measure urine osmolality –(30,60,120 min) –1 to 2 h later An increase of >50% indicates severe pituitary DI Smaller or absent response is strongly suggestive of nephrogenic DI

91 Diabetes Insipdus Treatment –Neurogenic DI DDAVP Chlorpropamide (Diabinese) –Antidiuretic effect can be enhanced by cotreatment with a thiazide diuretic –SE: hypoglycemia, disulfiram like reaction to ethanol –Contraindicated in Gestional DI –Nephrogenic DI Not affected by treatment with DDAVP or chlorpropamide May be reduced by treatment with a thiazide diuretic and/or amiloride in conjunction with a low-sodium diet Inhibitors of prostaglandin synthesis (e.g., indomethacin) are also effective in some patients –Psychogenic or dipsogenic DI there is no effective treatment

92

93 Syndrome of Inappropriate ADH secretion Etiology –CNS Lesions, Inflammatory disease Trauma, psychosis –Drugs Stimulate AVP release –Nicotine, phenothiazines, TCAs, SSRIs Chlorpropamide, clofibrate, carbamazepine, cyclophosphamide, vincristine –Pulmonary Infection Mechanical/ventilatory issue

94 Syndrome of Inappropriate ADH secretion Pathophysiology –Excessive AVP production resulting in decreased volume of highly concentrated urine –Water retention –Decreased plasma osmolarity –Decreased plasma Na

95 Syndrome of Inappropriate ADH secretion Clinical Presentation –Acute Water intoxication Headache, confusion Nausea, vomiting Anorexia Coma, convulsions – Chronic May be asymptomatic

96 Syndrome of Inappropriate ADH secretion Diagnosis –Diagnosis of exclusion –AVP level inappropriately elevated relative to plasma osmolality

97 Syndrome of Inappropriate ADH secretion Treatment –Acute Fluid restriction Hypertonic saline –Central myelinolysis – Chronic Demeclocyline mg PO TID-QID –Reversible Nephrogenic DI

98 Treatment Guidelines See Handout

99 References Harrison's Principles of Internal Medicine - 16th Ed. (2005) Up to Date Med Study – Endocrine Mayo Clinic Board Review

100 Questions

101 True or False The pituitary: 1.Pituitary tumors are usually macroadenomas. 2.Lack of galactorrhea essentially rules out a prolactinoma. 3.Prolactin levels correlate with the size of a prolactinoma 4.Prolactin level of 230 in a nursing woman is probably due to a prolactinoma 5.An enlarged sella tursica can be seen in a hypothyroid patient.

102 MedStudy Endocrine Answers The pituitary: – 1.Pituitary tumors are usually macroadenomas. – True – False 2.Lack of galactorrhea essentially rules out a prolactinoma. – False – 3.Prolactin levels correlate with the size of a prolactinoma – True – 4.Prolactin level of 230 in a nursing woman is probably due to a prolactinoma – True – 5.An enlarged sella tursica can be seen in a hypothyroid patient. – True

103 A 24 year old woman complains of fatigue and malaise. She gave birth to a healthy infant 4 months before presentation. She did not breastfeed. Menses have subsequently been irregular and infrequent, representing a change from before pregnancy. The family history is notable for a sister who has Hashimoto thyroiditis. The pregnancy test is negative, and the serum level of prolactin is normal. Of interest, TSH is 0.9mIU/L (normal, ) and free thyroxine is 0.8ng/dL (normal, ). The results of MRI of the pituitary are reported as normal. The next step would be to:

104 A) Start thyroxine replacement therapy B) Request a neurosurgeon to perform a biopsy of the pituitary Perform a water deprivation test Perform a 1 µg corticotropin (ACTH) stimulation test Measure IGF-1

105 A) Start thyroxine replacement therapy B) Request a neurosurgeon to perform a biopsy of the pituitary C) Perform a water deprivation test Perform a 1 µg corticotropin (ACTH) stimulation testD) Perform a 1 µg corticotropin (ACTH) stimulation test E) Measure IGF-1

106 A 38-year-old woman is referred to you by her gynecologist. She first presented to her gynecologist 4.5 years ago with amenorrhea of 3 years’ duration and galactorrhea of 1 year’s duration. She had been taking no medications, and her initial physical examination was unremarkable except for expressible galactorrhea bilaterally. A routine chemistry screen was normal; her T4 level was 7.8 µg/dL, serum TSH was 1.4 µU/mL, and prolactin level was 48.2 ng/mL. After taking bromocriptine for 2 months, her prolactin level was 19 ng/mL, at which point her galactorrhea ceased and she had her first menstrual period in 3 years. She continued to take bromocriptine over the next 4 years; her prolactin level remained less than 20 ng/mL, and she continued to have regular periods. However, she stopped taking her bromocriptine 6 months ago and is now having progressively worse headaches.

107 Her prolactin level is now 60.5 ng/mL, and a visual field examination shows a small superotemporal field cut in the right eye. A computed tomographic (CT) scan shows a 2.4-cm ´ 1.6-cm sellar mass with considerable suprasellar extension. She is now referred to you for further management. What is the most likely diagnosis? (A) Prolactinoma (B) Clinically nonfunctioning pituitary adenoma (C) Metastatic cancer to the sella (D) Craniopharyngioma

108 What is the most likely diagnosis? (A) Prolactinoma (B) Clinically nonfunctioning pituitary adenoma (C) Metastatic cancer to the sella (D) Craniopharyngioma


Download ppt "ENDOCRINOLOGY BOARD REVIEW Presented by Med/Peds PGY III Class."

Similar presentations


Ads by Google