Mcphs - Mmd - Hyperprolactinemia, Disorders Of Growth Hormone, And Diabetes Insipidus

Front 1

This is when there is elevated serum prolactin.

Back 1

Hyperprolactinemia

Front 2

This is the most common pituitary hypersecretion syndrome in both men and women.

Back 2

Hyperprolactinemia

Front 3

What are 9 causes of Hyperprolactinemia?

Back 3

1. Decreased dopaminergic inhibition

2. Hypothyroidism

3. Lacotroph adenoma (Prolactinoma)

4. Estrogen

5. Stress

6. Nipple Stimulation

7. Idiopathic

8. Macroprolactinemia

9. Chronic renal failure

Front 4

The following are responsible for what kind of cause of hyperprolactinemia?

Hypothalamic or pituitary disease or trauma

Drugs: antipsychotics, antidepressants, opiates, cimetidine, certain antihypertensives

Back 4

Decreased dopaminergic inhibition

Front 5

Correction of this cause of hyperprolactinemia can result in prolactin levels normalizing.

Back 5

Hypothyroidism

Front 6

This accounts for 30-40% of pituitary adenomas, and about 10% co-secrete growth hormone.

May be micro- (slight elevation of PRL) or macroadenomas (significant elevation of PRL)

Back 6

Lactotroph Adenoma (Prolactinoma)

Front 7

This is when hyperprolactinemia is caused by pregnancy of OCP, women have greater PRL response to stress than men, may directly affect transcription in lactotroph.

Back 7

Estrogen

Front 8

This can be either physical or psychological and it is a cause of hyperprolactinemia.

Back 8

Stress

Front 9

This can cause hyperporlactinemia and can be from sucking, injury, shingles, trauma etc.

Back 9

Nipple Stimulation

Front 10

This is a cause of hyperprolactinemia that may be associated with non-visible microadenomas.

Back 10

Idiopathic

Front 11

This is when there is big PRL leading to decreased clearance of PRL causing hyperprolactinemia.

Back 11

Macroprolactinemia

Front 12

This is when there is decreased clearance of prolactin as the cause of hyperprolactinemia.

Back 12

Chronic Renal Failure

Front 13

What are the manifestations of excess prolactin?

Back 13

Hypogonadotropic Hypogonadism

Mammary Gland Effects

Front 14

When you have enlargement of the pituitary associated with hyperprolactinemia, this can manifest as what?

Back 14

Headache and visual changes, ie. bitemporal hemianopsia

Front 15

Abnormal prolactin levels associated with hyperprolactinemia can manifest as what in pregnancy?

Back 15

Cardiomyopathy

Front 16

The excess prolactin in hyperprolactinemia that manifest as hypogonadotropic hypogonadism can do what in men?

Back 16

Decreaed libido, erectile dysfunction, infertility, decreased muscle mass, osteoporosis

Front 17

The excess prolactin in hyperprolactinemia that manifest as hypogonadotropic hypogonadism can do what in pre-menopausal women?

Back 17

Amenorrhea, infertility, osteoporosis

Front 18

The excess prolactin in hyperprolactinemia that manifest as hypogonadotropic hypogonadism can do what in post-menopausal women?

Back 18

Already hypogonadal, so wouldn't notice it.

Front 19

With the manifestations of hyperprolactinemia, what are the mammary gland effects in men?

Back 19

Gynecomastia or galactorrhea (rarely)

Front 20

With the manifestations of hyperprolactinemia, what are the mammary gland effects in pre-menopausal women?

Back 20

May get galactorrhea

Front 21

With the manifestations of hyperprolactinemia, what are the mammary gland effects in post menopausal women?

Back 21

most do not get galactorrhea because also hypoestrogenic.

Front 22

When you are measuring serum prolactin this can happen if there is a macroprolactinoma, ultimately resulting in test disruption, but visual field defects will still usually show up.

Back 22

Hook effect with extreme elevations of prolactin

Front 23

When you do an MRI in the presence of hyperprolactinemia, what are the two options you are looking for?

Back 23

1. If mass is present - check levels of all other pituitary hormones

2. If no mass and no other apparent cause then make diagnosis of idiopathic hyperprolactinemia.

Front 24

What is the first line tx of hyperprolactinemia?

Back 24

Dopamine agonist - ex. carbergolide

Always try this first
Adenoma may shrink
Prolactic levels often come down
Fertility may return - let patient know pregnancy may occur

Front 25

If there is no effect from using a dopamine agonist to tx hyperprolactinemia what is the next step?

Back 25

Trans-sphenoidal surgery.

Front 26

What are the three main metabolic actions of growth hormone?

Back 26

1. Increase fat breakdown

2. Decrease glucose uptake by skeletal muscles, resulting in glucose for the brain.

3. Increased gluconeogenesis by the liver.

Front 27

What are the three growth promoting actions of IGF-1?

Back 27

1. Increased cell division

2. Increased protein synthesis

3. Increased bone growth (thickness and length)

Front 28

What are three main causes of growth hormone deficiency?

Back 28

1. Hypothalamic dysfunction (lack of GHRH, so GH low)

2. Pituitary defect (lack of GH, so GH low)

3. Unresponsiveness to GH (GH high)

Front 29

What are the effects of growth hormone deficiency?

Back 29

Dwarfism if prior to growth plate fusion

May be symptomatic in an adult.

Front 30

If this is congenital it will show up as low birth size, hypoglycemia, prolonged jaundice, length 3-4 standard deviations below mean at 6-12 months.

In Adults, this is seen as increased fat, decreased lean body mass, decreased bone minteral density and possibly cardiovascular disease, impaired psychological function.

Back 30

Effects of GH deficiency

Front 31

How do you evaluate for GH deficiency?

Back 31

There is no gold standard

Rule out other causes of growth failure (ex. hypothyroidism)

Obtain IGF-1 level (decreased)

Perform GH stimulation test

MRI

Front 32

How do you TX GH deficiency in children?

Back 32

Once diagnosis is confirmed begin treatment with growth hormone replacement and continue until linear growth ceases.

Front 33

How do you treat GH deficiency in adults?

Back 33

Growth hormone replacement is usually reserved for patients with severe symptoms.

GH repalcement leads to decreased fat, increased lean body mass, and increased bone mineral density in men (but not in women)

Front 34

What are four causes of growth hormone excess?

Back 34

1. Pituitary adenoma (macroadenoma in acromegaly)

2. GHRH excess (gigantism)

3. Ectopic GH or GHRH

4. Disruption of neuroendocrine control of GH

Front 35

What are the effects of GH excess?

Back 35

Pituitary gigantism if prior to growth plat closure.

Acromegaly if after growth plate closure.

Front 36

This may occur at any age, rare, typically sporadic. Growth in height typically preceded by weight gain. Height exceeds +3 to +4 standard deviations from mean, and may grow taller than 8ft. May also see thickening of bones in face or extremities (but more common in acromegaly). Rule out other causes of rapid growth (ex. hyperthyroidism).

Back 36

Pituitary gigantism.

Front 37

How do you diagnose pituitary gigantism?

Back 37

1. Screen with IGF-1 (will be increased)
2. Gold standard for making diagnosis is GH suppression test - measure GH response to oral glucose load.
3. Confirm with MRI
4. Trans-sphenoidal surgery is tx of choice.
5. Meds include somatostatin analogs (octreotide), dopamine agonists (bromocriptine), and GH receptor antagonist (pegvisomant)

Front 38

What is the major cause of mortality in acromegaly?

Back 38

Hypertension, Cardiomegaly, CHF

Front 39

How do you diagnose acromegaly?

Back 39

Screen with IGF-1:
IGF-1 normal then active acromegaly is ruled out.
IGF-1 elevated then move to GH suppression test.

GH suppression test (oral glucose)
-GH suppressed lead to active acromegaly ruled out.
-GH inadequately suppressed leads to a move to MRI.

Pituitary MRI
Adenoma leads to treat
Normal, small, or hyperplastic leads to check for extrapituitary acromegaly lead to CT of chest and abdomen and measure GHRH levels.

Front 40

How do you TX acromegaly?

Back 40

1. Transphenoidal surgery is tx of choice.

2. Meds alone or with surgery - somatostatin analogs work best: Octreotide, lanreotide. Dopamine agonists: Cabergoline, bromocriptine. GH receptor antagoinst (Pegvisomant) - For inadequate response to drug intolerance.

Repeat surgery or radiotherapy if still inadequate response.

Front 41

What is involved with the long term monitoring of acromegaly?

Back 41

Every 3-4 months following initial tx - clinical exam, IGF-1, GH suppression test.

MRI - yearly for several years

Visual field assessment

Colonoscopy every 3-4 years for patients over 50 or patients with over 3 skin tags.

Front 42

This is a partial or complete deficiency of or resistance to antidiuretic hormone - ADH - Vasopressin

Back 42

Diabetes insipidus

Front 43

This is when you have polyuria with large volume of dilute urine. Nocturia may be noticed first, and then new onset nocturia in absence of another cause could be the first clue to this.

Polydipsia

If fluid intake is inadequate leads to hypernatremia.

Hyperuricemia (due to decreased clearance)

Back 43

Diabetes insipidus (DI)

Front 44

This is when there is complete or partial absence of ADH - it is idipathic (autoimmune - accounts for 30% of cases), Familial DI, Wolfram syndrome, Anorexia nervosa, post Supra ventricular tachycardia, and damage to hypothalamus from neurosurgery, other trauma, tumor, hypoxia, or infiltrative disease.

Back 44

Central Diabetes insipidus

Front 45

This is when you have vasopressinase being secreted by the placenta during pregnancy, breaks down ADH.

Back 45

Vasopressinase induced DI

Front 46

This can be hereditary - mutation in gene for the vasopressin receptor or the vasopressin sensitive aquaporin.

This can be acquired - Chronic lithium therapy, persistant hypercalcemia or hypokalemia, post op craniopharyngeoma, drugs-demeclocycline, cidofovir, foscarnet, kidney disease - obstruction, infection, sickle cell disease/trait, amyloidosis, myeloma, Sjogren's syndrome.

Back 46

Nephrogenic DI

Front 47

How do you diagnose central DI?

Back 47

Water restriction leads to increase in plasma osomolarity but there is no ADH, so uring osmolarity is inappropriately low. DdAVP leads to complete or partial improvement.

Front 48

How do you diagnose Nephrogenic DI?

Back 48

Water restriction leads to increase in plasma osmolarity, plasma ADH is high but urine osmolarity is inappropriately low. DdAVP lead to either no improvement or only partial improvement.

Front 49

What is the TX for central DI?

Back 49

Desmopressin is most effective

IV Fluids - must give desmopressin before giving IV fluids

Front 50

What is TX for vasopressinase induced DI?

Back 50

dDAVP

Front 51

What is TX for nephrogenic DI?

Back 51

Correct underlying cause if identified.

Low solute diet - decrease solute excretion - in adults low Na-low protein diet, in kids, low Na diet.

Prevention of urinary tract dilation

Children with complex congenital syndrome start with NSAIDS

All other children and adults start with a thiazide.