Lecture 83 - Pituitary Disorders Flashcards

1
Q

why is random plasma hormone testing not helpful?

what other tests should you consider if you suspect a deficiency in a hormone ?

If you suspect an excess of a hormone what should you consider?

A

hormones are cycling throughout the day (cortisol is lowest at midnight, peaks at 8am);

When suspecting hormone deficiencies, consider stimulation testing

For suspected hormone excess, consider suppression testing

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2
Q

inputs to the HPA axis that stimulates cortisol

what is the HPA axis?

A

Pain, pleasure, fear, anxiety, inflammation, hypoglycemia, depression

Hypothalamus –> CRH –> Pit —>ACTH –> Adnrenal —> Cortisol

Cortisol has negative feedback on levels of CRH and ACTH

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3
Q

what tests are are used to stimulate cortisol

A

cosyntropin (ACTH analog) test –

insulin tolerance test (ITT) – induces hypoglycemia which stimulates CRH

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4
Q

what the difference between primary and secondary adrenal insufficiency?

how can you differentiate between the two based on labs?

what is the best test for secondary hypothyroidism ?

A

Primary – due to direct adrenal failure (will have low cortisol, but high ACTH)

secondary – problem at the Pit or Hypothalamus (will have low CRH/ACTH + low cortisol)

secondary: ITT

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5
Q

Suspected Results for ITT and Cosyntropin tests for primary vs secondary adrenal insufficiencies?

A

Cosyntropin –
Primary – abnormal
Secondary - normal

ITT –
Primary – abnormal
secondary - abnormal

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6
Q

Cushing’s syndrome

whats the ddx for the etiology?

whats the most common exogenous etiology vs endogenous etiology

A

cortisol excess

Pitutiary adenoma (most common from endogenous)

Exogenous steroids (most common exogenous + overall cause) (such as those given for inflammatory)

Adrenal Tumor

Ectopic – Lung cancer (Small cell), carcinoid tumor

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7
Q

three bests diagnostic tests for hypercortisolism?

A

24 hour urine free cortisol (most specific)

Overnight 1 mg dexamethasone suppression test – should be low the next morning; but if Cushing’s state, then the cortisol will still be high

Midnight salivary free cortisol

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8
Q

tests for localization of the tumor

A

ACTH

if Adrenal – too much cortisol = negative feedback = low ACTH
If central/ectopic = normal or high ACTH

MRI - of brain

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9
Q

effects of too much cortisol

A
Cushing's features
obesity
moon facies 
poor bone and muscle strength
Buffalo hump 
etc
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10
Q

what is Psueo-cushing state?

what can cause it?

A

Mild hypercortisolism in patients who have features of cushing’s
Hypercortisolism often seen in patients with clinical features

and
Generalized obesity
Active alcohol abuse
Depression

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11
Q

what is the thyroid axis

A

TRH –> TSH –> T3, T4

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12
Q

what is the most common cause of hypothyroid?
what is the level of TSH and T3/4?

in what other setting is the axis depressed?

how do you differentiate between primary and secondary hypothyroid based on labs ?

A

Hashimoto’s Disease

High TSH (b/c no neg feedback) 
Low T3, T4 

Commonly depressed in very ll patients (neuro-endocrine response to severe illness)

Central (secondary) = low TRH, low T3, T4

Thyroid (primary) = low T3, T4 but high TRH

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13
Q

central vs primary hyperthyroidism:

how to you use labs to differentiate

whats the most common cause of primary hyperthyroid?

A

Central = High TSH, High T3, T4

Primary hyperthyroid (graves) = Low TSH, High t4, T3

Most common Primary = Graves Disease

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14
Q

what is Laron dwarfism? what are the GH labs?

what can these patients be treated with?

A

Normal GH levels

form of dwarfism in which the receptor is defective (therefore “effective” GH)

IGF1 (insulin like growth factor) is a possible treatment

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15
Q

beneficial effects of GH therapies for adults with GH deficeincy

A

Decreases in total and visceral body fat

Increase in muscle mass and bone density

Improved CV performance

Can help prevent HTN, Dyslipidemia, Insulin resistance, vascular effects, inflammation, osteoporesis

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16
Q

what is used as the surrogate marker for GH? when does it peak

A

IGF 1
rises up until ~20
then declines throughout life

17
Q

why is it stupid to draw single dose of GH in the dx of GH disordres ?

A

GH secretion is pulsatile

18
Q

for GH deficiency suspicion

describe the GH secretion test for the level of the pitutiary?

what is the stimulus at the level of the hypothalamus ?

A

Test Pituitary Function: block Somatostatin with Arginine;
stimulate GH with GHRH

Test Hypothalamic function:
ITT – in the stting of hypoglycemia;

19
Q

acromegaly –

best diagnostic tests?

A

IGF1 levels

Glucose tolerance test (making the patient hyperglycemic should drop GH levels)

20
Q

acromegaly –

Tx

A

□ Surgery
□ Radiation
□ Ocreotide (SST analog)

GH Antagonist: Pegvisomant (somavert)

21
Q

prolactin – what inhibitors proflacin release?

A

Dopamine inhibits Prolactin

22
Q

what factors promote the release of GH from the pituitary?

what factors inhibit it?

A

GHRH (from the hypothalamus) and Ghrelin (from the stomach) promote GH release

Somatostatin – inhibits GH release

23
Q

GH excess before puberty is called _______

GH excess after puberty is called _____

A

Gigantism

Acromegaly

24
Q

DDx of hyperprolactiemia

A

§ Dopamine Antagonists

§ Stalk effect – (anatomic/physiologic) block of dopamine

§ Hypothyrodism –> High TRH is a stimulator of prolactin

25
Q

A clinical

tx of prolactinemia

A

§ Dopamine agonists – (cabergoline, bromocriptine)

26
Q

Clinical consequences of hyper-prolactin

tx of prolactinemia

A

Clinical Consequences:
Amenorrhea in females (body things it might be pregnant)
hypogonadism in men

Dopamine agonists – (cabergoline, bromocriptine)

27
Q

Clinical consequences of hyper-prolactin

tx of prolactinemia

A

Clinical Consequences:
Amenorrhea in females (body things it might be post partum)
hypogonadism in men

Dopamine agonists – (cabergoline, bromocriptine)