Neuroendocrine Control, Hormones And Growth

Front 1

Regarding the hypothalamus- pituitary-thyroid axis, what are the features of:
A. primary hypothyroidism
B. secondary hypothyroidism
C. primary hyperthryoidism
D. secondary hyperthyroidism

Back 1

A. primary hypothyroidism: high TSH, low T4
B. secondary hypothyroidism: normal or low TSH, low T4
C. primary hyperthryoidism: low TSH, high T4
D. secondary hyperthyroidism: normal or high TSH, high T4

* serum TSH is the best thyroid screening test but it will miss patients with secondary causes of hypo or hyperthyroidism

Front 2

What is the best thyroid screening test? What is it's con?

Back 2

Serum TSH is the best thyroid screening test but it will miss patients with secondary causes of hypo or hyperthyroidism

Front 3

Diagram the hypothalamus- pituitary-thyroid axis with its appropriate feedback loops.

Back 3

See back of p.133 syllabus page.

Front 4

What hormones are secreted in a pulsatile manner? (6)

Back 4

LH & FSH, ACTH & cortisol, GH

Front 5

Regarding exogenous GnRH, if administered acutely, what is the effect on LH and FSH? What about if administered constantly in a chronic fashion?

Back 5

GnRH, if administered acutely is able to stimulate LH and FSH secretion. If constantly stimulated though, will actually suppress LH and FSH secretion!

Front 6

Diagram the hypothalamus- pituitary-gonadal axises (testes and ovaries) with its appropriate feedback loops.

Back 6

See back of p.133 syllabus page.

Front 7

Mineralocorticoids are under control of RAA system. Thus, patients lacking ACTH gets treated with ........ while patients packing adrenal glands need to be treated with ......... .

Back 7

Patients lacking ACTH get treated with glucocorticoids; but patients lacking adrenal glands need to be treated with glucocorticoids AND mineralocorticoids.

Front 8

Cortisol is pulsatile in dispension and has diurnal rhythm that actually "dampens" ________ spikes.

Back 8

ACTH

Front 9

If ACTH insufficiency is suspected, what test is done and what do the results mean?

Back 9

If ACTH insufficiency is suspected, can do an ACTH stimulation test. If no increase in cortisol is seen, then it is primary and also called Addison's dz. If there IS a rise in cortisol then you know the adrenals are indeed working and it thus is it a secondary ACTH stimulation test.

Front 10

True or False:
Cortisol decreases in hypoglycemic situations.

Back 10

FALSE. Cortisol INCREASES in hypoglycemic situations.

Front 11

This hormone is stimulated by sleep, stress, hypoglycemia, exercise. Decreased by hyperglycemia and aging.
A. TSH
B. LH, FSH
C. ACTH
D. GH

Back 11

D. GH

Front 12

Some effects of this hormone are mediated by IGF-1, which feeds back to hypothalamus to stimulate SRIF secretion.

Back 12

GH (growth hormone)

Front 13

If you suspect a deficiency in GH, what can you stimulate it with?

Back 13

insulin, arginine, L-dopa, clonidine or exercise

alternatively when you suspect a GH deficiency, you can measure the IGF-1 serum levels

Front 14

If you suspect a deficiency in GH, what can you measure in the serum?

Back 14

IGF-1

alternatively, you can try to stimulate GH levels by administering insulin, arginine, L-dopa, clonidine or exercise.

Front 15

Prolactin is under inhibitory control via what hormone?

Back 15

Dopamine!

Sever connection from hypothalamus to pituitary and all hormones except prolactin decrease.

Front 16

Diagram the hypothalamus- pituitary-GH axis with its appropriate feedback loops.

Back 16

See back of p.134 syllabus page.

Front 17

Diagram the hypothalamus- pituitary-prolactin axis with its appropriate feedback loops.

Back 17

See back of p.134 syllabus page.

Front 18

Excess prolactin decreases _________ secretion.
A. CRH
B. GnRH
C. SRIF

Back 18

B. GnRH

Front 19

Metabolic abnormalities due to biochemical effects of ____ include hyperglycemia, HTN, galactorrhea, hypercalciuria, myopathy.

Back 19

GH (acromegaly)

Front 20

What testing can you do to diagnose acromeglay? (3)

Back 20

1. Serum GH after glucose load (gold standard)
2. Serum IGF-1 level
3. Serum IGF-BP3 levels

Front 21

What are some common causes of galactorrhea? (5)

Back 21

Prolactinoma, Acromegaly (GH is lactogenic), Pituitary stalk compression (decreases dopamine, inhibitor of prolactin), primary hypothyroidism (increases TRH to make more TSH due to low T4 but TRH additionally stimulates prolactin), drugs (esp. antipsychotics since they use up dopamine, and also estrogen drugs like contraceptives)

Front 22

What is included in the differnetial diagnosis of galactorrhea? (5)

Back 22

Pituitary adenoma, drug-induced hyperprolactinemia, idiopathic hyperprolactinemia, primary hypothyroidism, renal failure (PRL catabolized by kidney)

Front 23

Why is it that women with excess prolactin present with amenorrhea and men present with decreased libido?

Back 23

Excess prolactin decreases GnRH pulsation, leading to hypogonadism.

Front 24

What is the better surgical treatment for pituitary tumor: transsphenoidal hypohysectomy or transfrontal craniotomy?

Back 24

transsphenoidal hypophysectomy

the other one is classical approach but should be avoided if possible because there are many complications.

Front 25

Regarding medical therapy for pituitary tumors, __________ agonists can be given for prolactinomas and __________ analogs can be given for acromegaly.

Back 25

dopamine agonists like bromocriptine and cabergoline (decrease PRL, allow GnRH pulsatile secretion and reduction of symptoms)

somatostatin analogs for acromegaly

Front 26

Which would be used to treat someone with a prolactinoma?
A. Octreotide or lanreotide
B. Bromocriptine and cabergoline
C. Metiropone or ketoconazole

Back 26

B. Bromocriptine and cabergoline

these are dopamine agonists

Front 27

Which would be used to treat someone with acromegaly?
A. Octreotide or lanreotide
B. Bromocriptine and cabergoline
C. Metiropone or ketoconazole

Back 27

A. Octreotide or lanreotide

these are somatostatin analogs

Front 28

Which would be used to treat someone with Cushing's syndrome?

A. Octreotide or lanreotide
B. Bromocriptine and cabergoline
C. Metiropone or ketoconazole

Back 28

C. Metiropone or ketoconazole

these decrease cortisol synthesis

Front 29

What are some causes of pituitary deficiencies? (7)

Back 29

- Hypothalamic tumors
- granulomatous dz like sarcoidosis which is usually in the hypothalamus or pituitary stalk
- Sheehan's Syndrome (post-partum pituitary necrosis)
- autoimmune lymphocytic hypophysitis
- pituitary tumors and/or treatment thereof
- traumatic brain injury
- functional hypopituitarism caused by opiates

Front 30

When replacing a deficiency of ACTH, what do you administer?

Back 30

Glucocorticoid rather than ACTH! Use dexamethasone or prednisone at bedtime, and if needed hydrocortisone in mid afternoon.

Front 31

True or False:
If have a deficient ACTH patient, treat with glucocorticoid replacement rather than ACTH replacement.

Back 31

TRUE

Front 32

When treating hypothalamic or pituitary deficiency of TRH and TSH, which test do yo use to adjust dosage and monitor replacement: Free T4 levels or TSH level?

Back 32

Free T4 levels

replacement itself is with L-thyroxine

Front 33

For hypothalamic and or pituitary deficiencies of each of the following, what do you administer?
A. TR/TSH/T4
B. GnRH/LH , FSH/Sex steroids - for fertility
C. GnRH/LH , FSH/Sex steroids - for maintenance
D. CRH/ACTH/Cortisol
E. GHRH/GH
F. PRL

Back 33

A. TR/TSH/T4 : use L-thyroxine
B. GnRH/LH , FSH/Sex steroids - for fertility : use pulsatile GnRH
C. GnRH/LH , FSH/Sex steroids - for maintenance : estrogen and progesterone for females, testosterone for males
D. CRH/ACTH/Cortisol : cortisol (hydroortisone) or substitutes
E. GHRH/GH : GH
F. PRL : none available

Front 34

What is Sheehan's syndrome and what does it cause?

Back 34

Post-partum pituitary necrosis. Is a cause pituitary deficiency along with things like hypothalamic tumors, granulomatous dzs, autoimmune lymphocytic hypphysitis, pituitary tumors, treatment of pituitary tumors, TBI, and opiates

Front 35

What is THE most important hormone to replace in pituitary deficiencies? (Without this, you DIE)
A. TRSH/TSH/T4
B. GnRH/LH and FSH/Sex Steroids
C. CRH/ACTH/Cortisol
D. GHRH/GH
E. PRL

Back 35

C. CRH/ACTH/Cortisol , namely the end product, CORTISOL

Front 36

GH action is primarily mediated through ______ which stimulate cell proliferation in target tissues. These come in two types (1 and 2). Which is relatively stable in blood throughout the day?

Back 36

IGF, or insulin-like growth factors. There are IGF-1 and IGF2. Blood levels of IGF-1 are relatively stable throughout the day.

Front 37

IGFs circulate and exert their biologic effects through interactions with lare binding proteins called IGFBPs. The major IGF binding protein is _________.

Back 37

IGF-BP3

IGF-BP3 production occurs in the liver and is highly GH-dependent. It is less dependent on nutritional status as IGF-1 is.

Front 38

What hormones act to (1) enahance pituitary GH secretion in response to GHRH and (2) have a direct stimulatory effect of cartilage growth by actin gin concert with IGFs?
A. Insulin
B. Thyroid hormones
C. Sex steroids
D. Glucocrticoids

Back 38

B. Thyroid hormones

These are actually essential for normal postnatal growth and brain development for these two very reasons!

Front 39

Which of the following does NOT apply to androgens?
A. Responsible for increasing amplitude of pituitary pulses of GH secretion
B. appear to be mediated by estradiol, which is produced from testosterone by aromatase enzymes
C. responsible for advancing skeletal age and epiphyseal fusion
D. play an important role in mediating pubertal growth spurt.

Back 39

C. responsible for advancing skeletal age and epiphyseal fusion

that is mostly estrogen mediated

Front 40

True or False:
Supraphysiologic doses of glucocorticoids inhibit growth centrally by stimulating somatostatin secretion and through a direct inhibitor effect on cartilage.

Back 40

TRUE

Front 41

GH and thyroid hormones exert major influences on the process of growth during:
A. fetal development
B. childhood

Back 41

B. childhood

Front 42

During childhood,, growth occurs at a relatively constant rate of ____ cm/year and once puberty hits, growth rates are approximately ___ cm/year.

Back 42

5-6 cm/ year during childhood; 9 cm/year during puberty

Front 43

Growth ultimately ceases following puberty as a result of _______ -induced epiphyseal closure in both sexes.

Back 43

estrogen

Front 44

Although children and their parents often focus on absolute height, evaluation of WHAT is the most critical factor in evaluating the growth of a child.

Back 44

Growth velocity

Front 45

Which of the following statements is FALSE?
A. Evaluation of growth velocity is the most critical factor in evaluating the growth of a child
B. Most children whose heights are below the 3rd or 5th percentile do NOT have pathalogic conditions
C. The absolute height of a child should always be evaluated in context of his or her genetic potential
D. Most children achieve an adult stature within 10 cm of their targeted height
E. Endocrine disorders tend to affect weight more substantially than height such that the child will be underweight for height

Back 45

E. Endocrine disorders tend to affect HEIGHT more substantially than WEIGHT such that the child will be OVERweight for height

Front 46

[ Endocrine / Other systemic ] disorders are more likely to affect height more than weight thus yielding [ underweight for height / overweight for height ] individuals.

Back 46

ENDOCRINE disorders affect height more than weight --> overweight for height individuals

Front 47

[ Endocrine / Other systemic ] disorders are more likely to affect weight more than height thus yielding [ underweight for height / overweight for height ] individuals.

Back 47

Other systemic disorders affect weight more than height, thus yielding underweight for height individuals.

Front 48

What is the most common "growth disorder"?
A. Constitutional delay of growth and adolescence (CDGA)
B. Familial short stature
C. Primary growth disorders

Back 48

A. Constitutional delay of growth and adolescence (CDGA) , or more colloquially called "late bloomer"

Front 49

Differentiate between primary growth disorders and secondary growth disorders and endocrine disorders.

Back 49

Primary growth disorders are due to intrinsic defects in growing tissues, have prenatal onset and can be broadly classified into: maternal factors, skeletal dysplasias, genetic conditions like Down Syndrome, Prader-Willi syndrome, Noonan syndrome.

Secondary growth disorders are non-intrinsic growth issues that present with decreased weight-to-height ratio. Most common cause is malnutrition.

Endocrine disorders is a secondary cause of growth failure that is associated with an increased weight to height ratio. Can manifest as hypothyroidism, Cushing syndrome, GH deficiency,

Front 50

This etiology of short stature is characterized by normal or near normal growth velocity during the prepubertal years with delayed BA and pubertal maturation despite being in normal range. Adult height is within normal range. May eventually when all is said and done, just be called a "late bloomer".

A. Constitutional Delay of Growth and Adolescence (CDGA)
B. Familial (genetic) short stature (FSS)
C. Primary growth disorder
D. Secondary growth disorder

Back 50

A. Constitutional Delay of Growth and Adolescence (CDGA)

Front 51

This etiology of short stature is characterized by normal growth velocity during prepubertal years. BA is not delayed. Normal onset and progression of puberty. Adult height is short but appropriate for parental heights.

A. Constitutional Delay of Growth and Adolescence (CDGA)
B. Familial (genetic) short stature (FSS)
C. Primary growth disorder
D. Secondary growth disorder

Back 51

B. Familial (genetic) short stature (FSS)

Front 52

What is the most common chromosomal disorder associated with growth failure?
A. Trisomy 21
B. Turner's Syndrome
C. Prader-Willi syndrome
D. Noonan Syndrome

Back 52

A. Trisomy 21

Front 53

Short stature is the single most common feature of this genetic condition, occuring more frequently than delayed puberty, cubitus valgus, or webbing of the neck.
A. Trisomy 21
B. Turner's Syndrome
C. Prader-Willi syndrome
D. Noonan Syndrome

Back 53

B. Turner's Syndrome

Front 54

This genetic condition should be considered in any phenotypic female with unexplained growth failure.

A. Trisomy 21
B. Turner's Syndrome
C. Prader-Willi syndrome
D. Noonan Syndrome

Back 54

B. Turner's Syndrome

Front 55

This genetic condition is associated with deletions of the short arm of chromosome 15 and parental imprinting. Presents as hypotonia and in male cryporchidism and microphallus in the neonatal period.

A. Trisomy 21
B. Turner's Syndrome
C. Prader-Willi syndrome
D. Noonan Syndrome

Back 55

C. Prader-Willi syndrome

Hyperphagia and obesity become prominent with increasing age.

Front 56

This genetic condition is associated with an autosomal dominant disorder mutation in PTPN11 gene on chromosome 12. Characterized by minor facial dysmorphism, short stature and congenital heart dz.

A. Trisomy 21
B. Turner's Syndrome
C. Prader-Willi syndrome
D. Noonan Syndrome

Back 56

D. Noonan Syndrome

Front 57

Categorize the following into either primary or secondary causes of growth disorders
Cyanotic heart dz
congestive heart failure
osteochondroplasias
chronic renal dz
Sickle-cell dz
Turner Syndrome
uncontrolled DM
maternal drug ingestion

Back 57

PRIMARY:
osteochondroplasias
Turner Syndrome
maternal drug ingestion

SECONDARY:
Cyanotic heart dz
congestive heart failure
chronic renal dz
Sickle-cell dz
uncontrolled DM

Front 58

_____________ if left untreated, results in severe mental retardation and growth failure.
A. Congenital hypothyroidism
B. Glucocorticoid excess
C. Growth Hormone deficiency

Back 58

A. Congenital hypothyroidism

Front 59

True or False:
Most cases of acquired GH deficiency is idiopathic.

Back 59

TRUE

Though they can indeed be associated with other pituitary hormone deficiencies like tumors, TBI, CNS infection or irradiation or surgical damage to hypothalamus or pituitary.

Front 60

What is the treatment for Growth Hormone deficiency?

Back 60

Patients are given recombinant human GH (rhGH). These are daily subcutaneous injections with weight based dosing.

SE: edema, slipped capital femoral epiphysis (SCFE), worsening of preexisting scoliosis, gynecomastia, hyperglycemia

Front 61

Besides GH deficiency, what are the other conditions for which GH is an appropriate therapy?

Back 61

Turner Syndrome, adults with HIV wasting, Prader-WIlli Synrome, Noonan Syndrome, children with intrauterine growth retardation