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Endocrine Week 1 > ICL 13.2: Pituitary Disorders > Flashcards

ICL 13.2: Pituitary Disorders Flashcards

1
Q

what is the embryologic origin of the anterior vs. posterior pituitary gland?

A

anterior = oral ectoderm

posterior = neural ectoderm

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2
Q

what is the blood supply of the anterior pituitary gland?

A

superior hypophyseal artery from the external carotid gland

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3
Q

how does the hypothalamus communicate with the posterior pituitary?

A

neurons!

neurons travel from the supraoptic and paraventricular nuclei of the hypothalamus to the posterior pituitary

hormones are produced in the hypothalamus and stored in the posterior pituitary

vs. the anterior pituitary communicates with the hypothalamus via the hypopheaseal portal system and it produces and stores hormones! it doesn’t just store them like the posterior pituitary

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4
Q

which hormones are secreted by the posterior pituitary?

A
  1. vasopressin (ADH)

2. oxytocin

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5
Q

which hormones are secreted by the anterior pituitary?

A
  1. GnRH
  2. GHRH
  3. dopamine/prolactin inhibiting hormones
  4. TRH
  5. CRH
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6
Q

which hormones does somatostatin inhibit?

A

GH and TSH secretion

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7
Q

what are the various clinical manifestations associated with hypothalamic-pituitary lesions?

A
  1. pituitary hormone hyper secretion and hyposecretion
  2. sellar enlargement
  3. visual loss
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8
Q

what is a pituitary adenoma?

A

the most common mass lesion seen in the sella and parasellar region

there are two types:
1. micro adenoma: less than 1 cm

  1. macro adenoma: 1+ cm

they may secrete a target trophic hormone and/or invade or compress neighboring structures leading to their varied clinical manifestations

the clinical classification separates adenomas into those that are hypersecretory or nonfunctioning adenomas

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9
Q

which structures are in the cavernous sinus?

A

internal carotid artery and CN VI

lateral cavernous sinus: CN III, IV, V1 and V2

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10
Q

how do you evaluate a pituitary adenoma?

A
  1. initial evaluation of any pituitary mass requires a search for hormone hypersecretion, and in the case of a macroadenoma, for pituitary hypofunction
  2. in addition larger tumors are likely to present with compressive symptoms

the onset of clinical features associated with hormone secretion is insidious and may be unnoticed for years or decades; therefore, endocrine function should always be tested

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11
Q

what are the causes of cellar masses?

A
  1. pituitary adenoma
  2. craniopharynginoma
  3. pituitary hyperplasia (ex. lactotrph hyperplasia during pregnancy)
  4. malignant tumors
  5. cysts
  6. pituitary abscess
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12
Q

what is a craniopharyngiomas?

A

suprasellar tumor that arises from remnants of Rathke’s pouch

two histological variants:
1. adamantinomatous (typically occur among children)

  1. papillary (occur almost exclusively among adults)

presentation:
1. headache

  1. bitemporal hemianopsia
  2. endocrine abnormalities (e.g.,hyperprolactinemia, hypopituitarism)
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13
Q

what is the imagining seen with craniopharyngiomas

A

radiological appearance depends on the proportion of the solid and cystic components, the content of the cyst(s) (cholesterol, keratin, hemorrhage), and the amount of calcification present

but if you see solid and cystic components + calcifications, think craniopharyngiomas

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14
Q

how do you manage pituitary adenomas?

A
  1. medical treatment
  2. surgery
  3. irradiation alone or in combination

goal of therapy is to correct hormone hyeprxsection or deficiencies, prevent tumor growth, relieve compressive symptoms and preserve normal pituitary function

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15
Q

35-year-old woman complains of recent visual problems and breast discharge. She has not had her period for the past 6 months and is upset that she has been unable to become pregnant, despite trying for the past year. She denies taking any medications. Laboratory workup reveals a negative pregnancy test, normal TSH and prolactin elevation. MRI of the head shows pituitary tumor compressing optic chiasma.

what is the diagnosis?

why does this patient have galactorrhea?

why is asking use of medications relevant?

why must hypothyroidism be evaluated?

what type of visual field defect would you expect?

A

hyperprolectinemia! probably due to prolactinoma which is the most common hormone-secreting pituitary tumors

prolactin is synthesized and secreted by lactotroph cells in the anterior pituitary and it is essential for breast milk production – elevated prolactin can lead to hypogonadism

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16
Q

what are the physiologic causes of hyperprolactinemia?

A
  1. pregnancy

2. niple stimuation during breastfeeding, physical exertion and sass

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17
Q

why do pregnant women not have galactorrhea?

A

progesterone inhibits prolactin

once the placenta is delivered, progesterone levels drop and lactation is no longer inhibited

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18
Q

what are the pathologic causes of hyperprolactinemia?

A
  1. proalactinoma
  2. ecreased dopaminergic inhibition of prolactin secretion
  3. any disease in or near the hypothalamus or pituitary that interferes with the secretion of dopamine or its delivery
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19
Q

what are the drug induced causes of hyperprolactinemia?

A
  1. antipsychotics
    ex. risperidone, haloperidol, phenothiazines
  2. SSRIs
  3. metoclopramide
  4. domperidone
  5. methyldopa
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20
Q

what other causes can cause hyperprolactinemia?

A
  1. hypothyroidism
  2. decreased clearance
  3. chest wall injuries
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21
Q

what is the clinical presentation of hyperprolactinemia?

A

WOMEN
1. hypogonadism

  1. infertility
  2. oligomenorrhea/amenorrhea
  3. galactorrhea

MEN
1. hypogonadotropic hypogonadism is manifested by decreased libido

  1. infertility
  2. gynecomastia
  3. galactorrhea
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22
Q

what is the diagnostic evaluation done ofor hyperprolactinemia?

A
  1. pregnancy should be ruled out in women of childbearing age
  2. TSH and free T4 since hypothyroidism can cause hyperprolactinemia since increased TRH levels stimulate prolactin production
  3. asses renal and hepatic function

diagnosis of hyeprprolactinemia is made by a serum prolactin concentration that is well about the normal range: over 20 for men and postmenopausal women and over 30 in premenopausal women

once other causes of elevated prolactin levels have been ruled out, do an pRI

23
Q

how do you manage hyperprolactinemia?

A

dopamine agonists like bromocriptine and cabergoline are first line therapy

they decrease prolactin secretion and reduce size of the lactotroph adenoma in more than 90% of patients!

surgery is only considered if they fail to respond to medical treatment

24
Q

38-year-old man came to see you complaining he cannot wear wedding ring anymore. Looking at his driver’s license picture from 15 years ago for comparison, his facial features have coarsened.
Laboratory evaluation shows mildly elevated plasma glucose levels, MRI images done in ER when he went complaining of a headache showed a mass.

diagnosis?

A

acromegaly

25
Q

what is acromegaly? what is the most common cause?

A

Aromegaly is usually caused by GH secretion from pituitary adenoma and very rarely by secretion of GH by ectopic tumor

GH is increased and its dynamic control is abnormal

most of the deleterious effects of chronic GH hypersecretion are causes by its stimulation of excessive amount of IGF-1

the most common cause of acromegaly is an adenoma of the anterior pituitary

26
Q

what is the effect of GH?

A

stimulates liver to breakdown glycogen to glucose

liver is also going to release IGF-1 which further stimulates growth

27
Q

what are the clinical manifestations of acromegaly?

A
  1. coarse facial features
  2. enlarged nose and tongue
  3. increased interdental separation
  4. enlarged hands and feet
  5. increased headaches
  6. sweating
  7. fatigue
  8. carpal tunnel syndrome
  9. systemic: CVD, sleep apnea, metabolic disorders, colon neoplasia
28
Q

what are the diagnostic evaluation tests done to test for for acromegaly?

A
  1. elevated serum IGF-1 levels
  2. inability to suppress serum GH during an oral glucose tolerance test to less than 1 ng/mL
  3. pituitary MRI once GH hypersecretion has been confirm
29
Q

how do you manage acromegaly?

A

removal or destruction of the pituitary tumor, reversal of the GH hypersecretion and maintenance of normal anterior and posterior pituitary secretion

  1. surgery (first line to get rid of tumor and mass effect)
  2. radiotherapy
  3. medical therapy
30
Q

what medical therapy is used for acromegaly?

A
  1. somatostatin receptor ligands like octreotide and lanreotide
  2. GH receptor antagonists
31
Q 
61-year-old female patient who presented with a history of palpitations, weight loss, sweating for few months. She also complained of enlargement of her hands, increased shoe size, as well as coarse facial features. She has been on Synthroid for few years for elevated levels of TSH. 
Labs:
TSH 5.55 (0.4-4.5)
Free T4 2.88 (0.82-1.77)
Free T3 11.1 (2.0 – 4.4)
Alpha subunit 18
GH 19.4 (0-7ng/ml)
IGF1 616 ng/mL (75-212)
Prolactin 16.7 (4.8-23.3 ng/ml)
LH 27.1 mIU/ml, FSH 61.5 mIU/ml.

MRI of the brain showed a 2.1x1.9x2.2 cm pituitary mass with superior extension into the optic chiasm, lateral extension into cavernous sinus and left internal carotid artery.

A

large hands and shoe size + coarse facial features = acromegaly

elevated TSH, sweating, weight loss, sweating = hyperthyroidism but it’s weird because TSH is high AND so are T3/4 which doesn’t make sense

so she has a TSH-secreting adenoma

32
Q

what is TSH-secreting adenoma?

A

super rare but it manifests as hyperthyroidism with goiter in the presence of elevated TSH

patient may also have symptoms related to the expanding tumor pass

33
Q

what lab results will you get with a TSH-secreting adenoma?

A
  1. normal or high serum TSH
  2. elevated alpha subunit
  3. high serum total and free T4 and T3

MRI of the pituitary usually shows macro adenoma

34
Q

what is the management for a TSH-secretin adenoma?

A

surgical resection

radiotherapy and medical treatment can also be used if surgery is contraindicated or deiced

35
Q

26-year-old female with history of hypertension, presented to the hospital because of diarrhea and vomiting.
She had a fall a day prior to admission because of dizziness. Patient had been complaining of severe weakness.
On arrival to the emergency department she was hypotensive, BP was 80/40 and after 4 litters of intravenous fluids BP 85/30.

Random cortisol level: 0.6 ug/dL (5-25)

ACTH stimulation test showed inadequate response 0.7  3.5 5.0

ACTH was very low <1.1 (7.2-63.3 pg/mL)

TSH 0.861 (0.400-4.00)

FT4 0.19 (0.80-1.40),

prolactin level was low <0.2 (1.9 -25)

diagnosis?

A

hypopituitarism

36
Q

what is hypopituitarism?

A

manifested by diminished or absent secretion of one or more pituitary hormones

development of signs and symptoms is often slow-depends on factors that are influenced by the underlying pathogenesis

damage to the anterior pituitary can occur suddenly or slowly, can be mild or severe, and can affect the secretion of one, several, or all of its hormones; clinical presentation of anterior pituitary hormone deficiencies varies

in general, acquired loss of anterior pituitary function follows the sequence of GH –> LH/FSH –> TSH –> ACTH and PRL
(Go Look For The Adenoma Please)

37
Q

what is the clinical manifestations of hypopituitarism?

A

low cortisol

  1. hypoglycemia
  2. vomiting
  3. malaise

low T3/T4:

  1. fatigue
  2. constipation
  3. low HR
  4. cold interlace

low sex steroids:

  1. delayed puberty
  2. amenorrhea
  3. micropenis

low GH:

  1. hypoglycemia
  2. short stature

low ADH:

  1. polyuria
  2. polydipsia
  3. high Na
  4. lethargy
  5. dehydration
38
Q

how do you diagnose hypotuituarism

A

baseline investigation of:
1. adrenocortical axis: serum cortisol

  1. thyroid axis: free T3/T4
  2. gonadal axis: men - testosterone (9 am and fasting), SHBG, albumin, LH, FSH; women-estradiol, LH, FSH, progesterone (Day 21 if menstruating)
  3. prolactin
  4. insulin-like growth factor-1, growth hormone
  5. paired plasma and urine osmolality
39
Q

how do you treat hypopituitarism?

A

lac of ACTH causes primarily cots defieicny: hydrocoritson

TSH deficiency: treated with T4; BUT show not be given till adrenal function has been evaluation

  1. testosterone replacement for gonadotropin deficiency in men
40
Q

43-year-old man, previously healthy, was complaining of polydipsia, polyuria, and nocturia during the previous 3 months. DM was excluded. Water deprivation test was positive for CDI. Pituitary MRI was normal, with normal signal of high intensity in the neurohypophysis. He had no other hormonal deficits. Autoimmune and infectious diseases were excluded. After initiation of oral desmopressin, the symptoms disappeared.

diagnosis?

A

central diabetes insipidus

41
Q

what is central diabetes insidious?

A

excess production of dilute urine

AVP is synthesized in the cell bodies in the paraventricular (PVN) and supraoptic (SON) nuclei, then transported down the axons of the pituitary stalk and released from the neuron terminals in the posterior pituitary

if there’s a tumor effecting hypothalamus or the pituitary stalk, then the hormones from the hypothalamus through the pituitary stalk could get inhibited

42
Q

what are the causes of central DI?

A
  1. hypothalamic lesions (40-50%)
  2. pituitary lesions are generally not sufficiency to cause DI
  3. idiopathic (20-30%)
  4. genetic (<5%)
  5. trauma: head injury, post-surgery
  6. tumors: craniopharyngioma, germinoma, metastatic disease, pituitary macro adenoma
  7. inflammatory: sarcoidosis, histiocytosis, meningitis
43
Q

what are the clinical manifestations fo DI?

A

DI is the excretion of a large volume of urine that is HYPOTONIC, DILUTE and TASTELESS

patients with untreated central diabetes insipidus (CDI) typically present with polyuria, nocturia, and, due to the initial elevation in serum sodium and osmolality, polydipsia

the serum sodium concentration in untreated CDI is often in the high normal range, which is required to provide the ongoing stimulation of thirst to replace the urinary water losses

moderate to severe hypernatremia can develop when thirst is impaired or cannot be expressed

44
Q

how do you diagnose DI?

A

history and examination may reveal important clinical information:
1. features of systemic disease

  1. associated endocrinopathy: suggestive of additional hypothalamic or pituitary dysfunction
  2. neuro-ophthalmic problems suggestive of structural disease
  3. evidence of drug toxicity (e.g. lithium, phenytoin)
  4. confirmation of true polyuria: over 50 mL/kg in 24 hrs with low osmolarity and absence of solute diuresis

If polyuria is confirmed and simple causes are excluded, the clinician should proceed to a diagnostic Water Deprivation Test

45
Q

how do you treat DI?

A

mild forms of HDI may not require treatment

significant polyuria and polydipsia are treated effectively with DDAVP in divide doses

46
Q

A 48-year-old female presents to the emergency room with mental status changes. Laboratory analysis of the patient’s serum shows:Na+122 mEq/L,K+3.9 mEq/L,HCO3-24 mEq/L, BUN 21 mg/dL, Creatinine 0.9 mg/dL, Ca2+8.5 mg/dL, Glucose 105 mg/dL. Urinalysis shows: Osmolality 334 mOsm/kg,Na+45 mEq/L

diagnosis?

A

SIADH

47
Q

what is SIADH?

A

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a disorder of impaired water excretion caused by the inability to suppress the secretion of antidiuretic hormone (ADH)

if water intake exceeds the reduced urine output, the ensuing water retention leads to the development of hyponatremia

the SIADH should be suspected in any patient with:
1. hyponatremia

  1. hypoosmolality
  2. a urine osmolality above 100mosmol/kg
48
Q

what is the criteria for diagnosing SIADH?

A
  1. true plasma hypoosmolality
  2. urine concentration inappropriate for plasma osmolality (Uosm >100 mOsm/kg/H20)
  3. clinical euvolemia, no diuretic therapy
  4. bsent renal sodium conservation (UNa >30 mmol/L)
  5. normal thyroid, adrenal and renal function
49
Q

what is the clinical presentation of SIADH?

A
  1. headache
  2. irritability
  3. nausea and vomitng
  4. mental slowing
  5. unstable gate/falls
  6. confusion/delireu/disorientation
  7. stupor/coma
  8. convulsions
  9. respiratory arrest
50
Q

what are the causes of SIADH?

A
  1. CNS disturbance
  2. malignancies
  3. drugs
  4. surgery
  5. pulmonary disease
  6. idiopathic
51
Q

how do you treat SIADH?

A

severe symptoms: hypertonic NaCl following by fluid restriction –> coma, obtundation, seizures, respiratory distress

moderate symptoms: solute repletion, captain, fluid restriction –> altered mental status, disorientation, naeusea

no or minimal symptoms: fluid restriction but consider pharmacologic therapy under select circumstances

52
Q

A 12-year-old boy is brought to the clinic because of “growing pains” for the past several years. He recently emigrated from another country and has no available medical records. His temperature is 37.0°C (98.6°F), pulse is 82/min, respirations are 14/min, and blood pressure is 132/84 mm Hg. Height is 203 cm (6 ft 8 in) tall and weight is 130-kg (286-lb). Physical examination shows a male of tall stature in no apparent physical distress. He has large hands and feet, and coarse facial features. Karyotypic analysis shows normal X and Y chromosomes.

which laboratory tests Is most likely to confirm the diagnosis?

A

insulin-like growth factor-1

you don’t do GH or GHRH levels because pattern for GH changes throughout the day; that’s just its pattern of secretion

IGF-1 is elevated all day long so if it’s elevated, it will always be elevated

oral glucose tolerance test can be used to confirm and at that point you’d test GH levels – so load them up with glucose and check GH levels and if they dont drop below 1 then it confirms acromegaly

53
Q

A 26-year-old woman complains of fatigue and malaise. She gave birth to a healthy infant 3 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’s thyroiditis. Pregnancy test negative, prolactin level is low. Of interest, TSH is 0.9 mIU/L (normal, 0.3-5.0) and free thyroxine is 0.6 ng/dL (normal, 0.8-1.4). The results of MRI of the pituitary are reported as normal. The next step would be to:

A

perform ACTH stimulation test to confirm Sheehan syndrome

TSH should be really high since her T3/T4 is low so she has hypothyroidism post-partum but you dont want to treat for this because you could cause severe adrenal failure if you do that before you check cortisol levels

Endocrine Week 1 (11 decks)

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