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SMUSPG-PHY1 > ENDO-Pituitary > Flashcards

ENDO-Pituitary Flashcards

1
Q

What occurs in the hypothalamus-pituitary axis?

A 
Negative Feedback-reverses of current reaction, NOT Down,
Hypothalmus release TRH hormone 
anterior pituitary hormone TSH, LH, FSH
peripheral endocrine gland
 targets
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2
Q

What is Primary endocrine disorder?

A

Defect at producing gland

Ex. Thyroid gland

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3
Q

What is a Secondary endocrine disorder?

A

Producing gland normal, defect in stimulation

Usually next step up-Pitutary

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4
Q

What is a tertiary endocrine disorder?

A

Defect of hypothalamic dysfunction (two glands removed from target organ)

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5
Q

List the hormones in the anterior pituitary?

A 
FLAT PiG
FSH- sperm and egg producing
LH- luetenzing (ovulation)
ACTH- adrenocorticotripic hormone
Prolacin
GH-growth hormone
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6
Q

What provides linear growth of bones?

A 
GH
AKA- Somatotropin, 
produces somatotropes cells w/in the anterior pituitary
necessary for growth and maintenance, 
 linear bone growth in children
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7
Q

What are the effects of growth hormone on the liver?

A

Wide spread, no truly organ
Fat cells and LIVER =”peripheral gland”
Effects through secondary hormones called somatomedins,
Liver- releases insulin-like growth factors produced by liver

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8
Q

What tissues are affected by growth hormone

A

effects on carbohydrates, lipids and protein metabolism

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9
Q

Describe the effects of growth hormone on adipose tissue

A

Reduces body fat mass by 1] Increases Lipolysis (HSL) 2] Reduce glucose uptake, 3] Reduce lipogenesis, 4] Reduces re-esterification of FFA

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10
Q

Describe the MOA of GH on adipocytes

A

GH acts on B3 adrenergic receptors -> Gs proteins -> Adenylate cyclase -> cAMP -> HSL -> triglycerides -> glycerol + FFA

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11
Q

Describe the effects of growth hormone on skeletal muscle

A

Increase Beta-oxidation by 1] Reduces glucose uptake and 2] Increases LPL activity

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12
Q

Describe the effects of growth hormone on liver

A

Increase production and uptake of IDL, LDL, HDL by 1] Increasing VLDL secretion, 2] HL activity, 3] Reduces PARalpha expression

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13
Q

Describe the metabolic effects of GH

A

1] Inhibition of glucose utilization, by increased insulin resistance, 2] Promotion of fatty acid metabolism for fuel

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14
Q

Describe the half-life of GH

A

Short half-life – unbound in plasma

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15
Q

Describe what controls the release of Growth hormone

A

1] GHRH – releasing hormone, 2] Somatostatin – inhibitory, 3] Ghrelin newly identified, unknown action

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16
Q

What is the primary causes the short statue in children?

A

growth hormone deficiency, but many factors affect GH, so broad testing must be done to determine cause of short stature/growth delay

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17
Q

What causes Growth Hormone Deficiency

A

1] Idiopathic – lack of GHRH from hypothalamus for undefined reason, 2] Primary causes include pituitary tumors and pituitary agenesis, Consider panhypopituitarism

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18
Q

How is growth hormone deficiency determined?

A

Chart growth conscientiously, Look for deviations across growth lines vs consistent trajectory

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19
Q

Describe congential growth hormone deficiency

A

usually children of normal size at birth expressing delayed growth over first 1-2 years

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20
Q

What are the associated features of growth hormone deficiency

A

intelligence normal, short, obese, immature fascies, delayed skeletal growth and sexual maturation, hypoglycemia and seizures in neonate

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21
Q

Describe the cause of acquired defiency later in life

A

usually tumor related

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22
Q

What if growth is reduced by growth hormone levels are normal

A

Consider IGF deficiency

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23
Q

Why is growth hormone important in adults

A

GH still important for maintenance

24
Q

Describe causes of adult GH deficiency

A

May be carry-over from childhood or new onset – related to tumor or treatment

25
Q

What are the associated risk factors with adult GH deficiency

A

Cardiac risk, central obesity, atherosclerosis, metabolic syndrome

26
Q

How is adult GH deficiency diagnosed

A

Test with stimulation studies

27
Q

Describe what results in excess GH

A

Excessive bone growth caused by IGF stimulation

28
Q

Describe what occurs if the excess GH is before closure of epiphyses

A

gigantism

29
Q

Describe what occurs if the excess GH is after closure of epiphyses

A

circumferential bone growth (widened, rather than longer) and acromegaly

30
Q

What usually causes gigantism and acromegaly

A

1] somatotrope adenoma, 2] Some caused by hypothalamic and other tumors

31
Q

What are the metabolic changes due to excess GH

A

increased FA metabolism, increased ketone production, decreased glucose uptake, gluconeogenesis by liver, increased insulin from pancreas (insulin resistance syndrome, ultimately DM)

32
Q

Describe the associated adenoma causing GH excess

A

HA, visual field defects, CN III, IV, VI palsies, secondary deficiency of other pituitary hormones

33
Q

Describe the associated symptoms in GH excess

A

Excessive sweating, oily skin, wt gain, weakness, fatigue, menstrual changes, decreased libido, HTN, apnea

34
Q

What are the associated risk due to GH excess

A

Increased risk of colonic polyps and colorectal cancer

35
Q

Describe the treatment of GH excess

A

surgery, reversal of GH/IGF effects

36
Q

Describe the function of Prolactin

A

stimulates milk production by the female breast during pregnancy. Drop of estrogen at birth triggers let down.

37
Q

Why don’t post-partum women ovulate

A

Due feedback that suppresses FSH & LH after childbirth that drops estrogen at birth triggers let down.

38
Q

What hormone causes milk gland growth?

A

progesterone

39
Q

What hormone causes milk production?

A

prolactin

40
Q

What is the most common type of pituitary tumor

A

Prolactinoma

41
Q

Describe the incidence rate of Prolactinoma

A

1] F>M, 2] May be familial as part of MEN-1 syndrome, 3] Most are microadenomas which rarely grow

42
Q

What is MEN syndrome?

A

Multiple endocrine neoplasia syndrome, endocrine tumors that are usually associated with each other

43
Q

What is the result of hyperprolatinemia

A

Hypogonadotropic hypogonadism - term used to define low sex hormone production by the gonads as a result of low production of FSH/LH from the pituitary (gonadotropic hormones)

44
Q

Describe Hypogonadotropic hypogonadism in Women

A

Oligomenorrhea or amenorrhea, galactorrhea common, increased risk of osteoporosis

45
Q

Describe Hypogonadotropic hypogonadism in Men

A

ED, diminished libido, gynecomastia classic but not 100%, never with galactorrhea.

46
Q

What are the hallmarks for prolactinoma

A

a man or woman comes in with breast sx

47
Q

What should you do with hyperprolactinemia

A

1] Rule out secondary causes, 2] MRI

48
Q

If the MRI show microadenomas with regular menses what is the next step

A

No treatment

49
Q

If the MRI show microadenomas with infertility what is the next step

A

Bromocriptine (pariodel)

50
Q

If the MRI show microadenomas with Amenorrhea what is the next step

A

Dopamine agonist or estrogen progesterone

51
Q

If the MRI show macroadenoma intrasellar with infertility what is the next step

A

Bromocriptine (pariodel)

52
Q

If the MRI show macroadenoma intrasellar with Amenorrhea what is the next step

A

Dopamine agonist

53
Q

If the MRI show macroadenoma suprasellar with infertility what is the next step

A

Bromocriptine (pariodel), surgery or both

54
Q

If the MRI show macroadenoma suprasellar with Amenorrhea what is the next step

A

Dopamine agonist, surgery or both

55
Q

What the most common cause Hyperprolactinemia

A

Pregnancy

56
Q

What are the other causes of Hyperprolactinemia

A

1] Hypothyroidism, 2] Renal failure, 3] Cirrhosis, 4] SLE, 5] Drugs: psychotropic agents, cimetidine, TCAs, OCP

57
Q

What are the treatments for Hyperprolactinemia

A

1] stop offending agents, 2] dopamine agonists first line, 3] surgery for large or unresponsive tumors, 4] radiation tends to cause global loss of pituitary function and should be used cautiously

SMUSPG-PHY1 (15 decks)

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