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Endo / Repro > Day 1, 2 > Flashcards

Day 1, 2 Flashcards

1
Q

What are the 3 effects of Growth Hormone?

A

Fat metabolism, GNG, Stimulate IGF-1 (insulin like growth factor –> elongation of bone)

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2
Q

Draw the somatostatin / GH balance…

A

http://www.naturalheightgrowth.com/2012/09/20/increase-height-and-grow-taller-using-hypothalamic-growth-hormone-releasing-hormone/

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3
Q

What is the pathway for GH receptor hormone?

A

GHRH –> GHRH-R –> Gs –> Incr. Adrnylyl Cyclase –> Activate PKA –> GH Transcription and release

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4
Q

How does Ca++ influence GH?

A

It enhances release from the Ant. Pituitary

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5
Q

What is the pathway of Somatostatin?

A

SST –> SST-R –> Gi and Go –> Go blocks Ca++ channel, Gi blocks Adenylyl Cyclase –> No PKA activation –> No GH transcription

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6
Q

How is GH release influenced by: Hypoglycemia, Aginine, Dopamine?

A

All stimulate GH release

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7
Q

What is the pathway for GH?

A

GH causes 2 GH receptors to dimerize –> JAK 2 and receptors - P –> STAT 5 dimerizes –> STAT 5 enters nucleus –> increase in IGF-1, GNG, and fat met.

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8
Q

What are the two types of recombinant hGH and there differences?

A

Somatrem: mild allergies in 50% of pts.
Somatropin: less allergenic

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9
Q

What must be administered with hGH?

A

T3 and T4

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10
Q

For what disease is hGH appropriate?

A

Hypopituitary dwarfism

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11
Q

What is Laron syndrome?

A

Hypersomatotrophic dwarfism

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12
Q

What is defective in Laron syndrome?

A

GH receptor (no IGF-1 stimulation)

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13
Q

In which populations is Hypersomatotrophic dwarfism most prevalent?

A

Oriental Jews, African pygmies

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14
Q

How would Laron syndrome influence the GH / Somatostatin balance?

A

Increase [GH], but no GH effects

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15
Q

What is the treatment for hypersomatotrophic dwarfism?

A

Recombinant human IGF-1

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16
Q

What is the underlying cause of acromegaly?

A

Excess GH

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17
Q

What would be the result of inactive GTPase in a somatotroph cell (adenoma)?

A

Adenylyl cyclase does not shut off –> GH pathway remains active in the absence of GHRH

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18
Q

What is the DoC for GH-secreting ademona?

A

Bromochriptine

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19
Q

What is the MoA of Octreotide?

A

Somatostatin analogue

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20
Q

For what condition is Pasireotide prescribed?

A

Cushing’s that persists after ACTH-secreting tumor removal

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21
Q

What is the mechanism of Pegvisomant?

A

GH receptor antagonist (prevents dimareization of receptors)

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22
Q

What is the effect of prolactin?

A

Milk production

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23
Q

What si the primary inhibitor of prolactin?

A

Dopamine

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24
Q

To what proteins are D2 receptors coupled and their effects?

A

Gi: inhibit Adenylyl Cylcase and cAMP influence on nucleus Go: Blocks Ca++ transport into cell

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25
Q

What are the 4 main causes of hyperprolactinemia?

A

Lack of dopamine
Adenoma
Hypothyroidism (excess TRH –> lactotroph stimulation)
Antipsychotics (block D2 receptors)

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26
Q

What are the Symptoms of hyperprolactinemia?

A

Galactorrhea
Gynecomastia
Amenorrhea
Loss of vision (macro adenomas)

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27
Q

What are the treatments of hyperprolactinemia?

A 
Surgery
Bromocriptine (long-acting D2 agonist) or Cabergolin
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28
Q

What is a major side effect of Cabergolin?

A

Valvular heart disease

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29
Q

When is surgical removal of pituitary gland absolutely contraindicated?

A

Pregnancy (loss of fetus)

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30
Q

What is the Hardy-Weinberg formula?

A

p^2 + 2pq + q^2 = 1

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31
Q

What is the disease incidence in an Autosomal Dominant disease?

A

2pq

32
Q

What is the ratio of affected males to females in an x-linked recessive disease?

A

1/q, where q = the number of affected males

33
Q

How do you calculated if a population is in HW equilibrium?

A

p + q = 1

34
Q

What is the founder effect?

A

A population is founded by a carrier of a mutated gene, resulting in that new population having a disproportionally large number of the mutation.

35
Q

What are the 5 assumptions of the HW principle?

A

Large population, Random mating, No: mutation, migration or selection.

36
Q

What are the requirement for balanced polymorphisms?

A

Homozygous mutant = low fitness
Homozygous normal = reduced fitness
Heterozygous = highest fitness

37
Q

What is the function of osteoblasts?

A

Bone deposition

38
Q

What is the function of osteocytes?

A

Maintain bone

39
Q

What is the function of osteoclasts?

A

Break down bone

40
Q

What are the embryonic origin of the superior and inferior parathyroids and the thyroid?

A

4th and 3rd pharyngeal pouches

Foramen cecum

41
Q

What is reverse triiodothyronine?

A

Inactive form of TH formed when abundance of T3 is present.

42
Q

What enzyme is responsible for the formation of T3 and T4 and what else is required for it to work?

A

Thyroid peroxidase needs H2O2 to make T3 and T4

43
Q

Where is thyroid peroxidase located?

A

Apical surface of thyrocyte (thyroid epithelium)

44
Q

Where in the thyroid are T3 and T4 stored?

A

Follicles

45
Q

Where in the pituitary and by what cell is TSH produced?

A

Anterior lobe, Basophils (B-FLAT)

46
Q

Draw out the figure from Guyton 76-2

A

Do it!!!

47
Q

How do the thyrocytes change in shape when active?

A

They become taller

48
Q

What are the three types of goiters?

A

Grave’s disease, Hashimoto’s, Nontoxic

49
Q

What do the parafollicular (C) cells do?

A

secrete calcitonin –> reduce blood Ca++

50
Q

What is the embryologic origin of C cells?

A

Neural crest

51
Q

What is the effect of calcitonin?

A

Increase osteoblasts and class –> increase bone formation

52
Q

What gland is responsible for blood Ca++ monitoring?

A

Thyroid monitors fee Ca++ (50% of total)

53
Q

What is the result of an absence of a parathyroid gland?

A

DEATH

54
Q

What are the predominant cells of the Parathyroid and their function?

A

Chief cells make PTH

55
Q

What stimulates the release of PTH and its result?

A

Low calcium levels, PTH stimulates bone resorption and retention of Ca in the gut and kidney

56
Q

What is the result of Vitamin D?

A

Increase intestinal resorption of Ca

57
Q

What is the result of PTH?

A

Bone resorption, increase Vit D activation, increase renal Ca reabsorption

58
Q

What is the RANK, RANK-L, OPG relationship?

A

https://www.youtube.com/watch?v=VwCkyf0lQwo

59
Q

What is the target of Denosumab?

A

RNAK-L antibody

60
Q

How is RANK-L influenced by PTH?

A

Increased RANK-L –> osteoclast formation

61
Q

How does PTH influence Ca levels in the body?

A

Osteoclast activation –> resorption
Increase 1-hydroxylase –> active Vit D
Increase renal reabsorption of Ca

62
Q

How does Vit D influence Ca levels?

A

Increase intestinal absorption

Increase bone resorption

63
Q

How does calcitonin influence Ca levels?

A

Decrease by inhibiting bone resorption

64
Q

Where are the body’s serum calcium sensors?

A

Parathyroid - C cells

65
Q

What is the pathway for activation and deactivation of Vit D?

A

https://orthojournal.wordpress.com/2011/11/13/osteoblast-progenitor-cells/

66
Q

What are the primary regulators of Vit D?

A

1-Hydrox: PTH, Estrogen, low PO4

25-Hydrox: hypercalcemia

67
Q

What are the primary sites of osteoporosis in men and women?

A

Men: Hip and wrist (Colles’)
Women: Hip, wrist, vertebrae

68
Q

How are osteoporosis and post menopause related?

A

Low estrogen –> low activation of 1-Hydroxylase and OPG

69
Q

What is the best way to prevent osteoporosis?

A

Build as much bone as possible at an early age (teens)

70
Q

How are RANKL and OPG related to osteoporosis?

A

RANKL increase bone reabsorption

OPG protects against bone reabsorption

71
Q

What is defective in X-linked Hypophosphatemic VDRR?

A

Phosphate is trapped in renal cells due to a defect in the transport protein

72
Q

What is the underlying cause of Vitamin D dependent Ricket’s?

A

Mutation of 1-Hydroxylase prevents activation of Vitamin D (25-OH-D3 –> 1, 25-(OH)2-D3

73
Q

How is Vitamin D dependent Ricket’s treated?

A

Vit D supplementation

74
Q

What is the underlying cause of Vit D Dependency Rickets Type II?

A

Vit D receptor on target tissue defective (lethal)

75
Q

What is the MoA of bisphosphates?

A

Inhibition of osteoclasts

76
Q

What is the MoA of Denosumab?

A

Neutralize RANKL –> inhibit osteocalsts, Prevent osteoclast differentiation

77
Q

What are the 2 major risks of hormone replacement therapy (estrogen) for post menopausal women?

A

Thromboembolism (enhanced clotting)

Cancer (esp. breast)

Endo / Repro (15 decks)

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