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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
What are the 4 main causes of hyperprolactinemia?
Lack of dopamine Adenoma Hypothyroidism (excess TRH --> lactotroph stimulation) Antipsychotics (block D2 receptors)
26
What are the Symptoms of hyperprolactinemia?
Galactorrhea Gynecomastia Amenorrhea Loss of vision (macro adenomas)
27
What are the treatments of hyperprolactinemia?
``` Surgery Bromocriptine (long-acting D2 agonist) or Cabergolin ```
28
What is a major side effect of Cabergolin?
Valvular heart disease
29
When is surgical removal of pituitary gland absolutely contraindicated?
Pregnancy (loss of fetus)
30
What is the Hardy-Weinberg formula?
p^2 + 2pq + q^2 = 1
31
What is the disease incidence in an Autosomal Dominant disease?
2pq
32
What is the ratio of affected males to females in an x-linked recessive disease?
1/q, where q = the number of affected males
33
How do you calculated if a population is in HW equilibrium?
p + q = 1
34
What is the founder effect?
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
What are the 5 assumptions of the HW principle?
Large population, Random mating, No: mutation, migration or selection.
36
What are the requirement for balanced polymorphisms?
Homozygous mutant = low fitness Homozygous normal = reduced fitness Heterozygous = highest fitness
37
What is the function of osteoblasts?
Bone deposition
38
What is the function of osteocytes?
Maintain bone
39
What is the function of osteoclasts?
Break down bone
40
What are the embryonic origin of the superior and inferior parathyroids and the thyroid?
4th and 3rd pharyngeal pouches | Foramen cecum
41
What is reverse triiodothyronine?
Inactive form of TH formed when abundance of T3 is present.
42
What enzyme is responsible for the formation of T3 and T4 and what else is required for it to work?
Thyroid peroxidase needs H2O2 to make T3 and T4
43
Where is thyroid peroxidase located?
Apical surface of thyrocyte (thyroid epithelium)
44
Where in the thyroid are T3 and T4 stored?
Follicles
45
Where in the pituitary and by what cell is TSH produced?
Anterior lobe, Basophils (B-FLAT)
46
Draw out the figure from Guyton 76-2
Do it!!!
47
How do the thyrocytes change in shape when active?
They become taller
48
What are the three types of goiters?
Grave's disease, Hashimoto's, Nontoxic
49
What do the parafollicular (C) cells do?
secrete calcitonin --> reduce blood Ca++
50
What is the embryologic origin of C cells?
Neural crest
51
What is the effect of calcitonin?
Increase osteoblasts and class --> increase bone formation
52
What gland is responsible for blood Ca++ monitoring?
Thyroid monitors fee Ca++ (50% of total)
53
What is the result of an absence of a parathyroid gland?
DEATH
54
What are the predominant cells of the Parathyroid and their function?
Chief cells make PTH
55
What stimulates the release of PTH and its result?
Low calcium levels, PTH stimulates bone resorption and retention of Ca in the gut and kidney
56
What is the result of Vitamin D?
Increase intestinal resorption of Ca
57
What is the result of PTH?
Bone resorption, increase Vit D activation, increase renal Ca reabsorption
58
What is the RANK, RANK-L, OPG relationship?
https://www.youtube.com/watch?v=VwCkyf0lQwo
59
What is the target of Denosumab?
RNAK-L antibody
60
How is RANK-L influenced by PTH?
Increased RANK-L --> osteoclast formation
61
How does PTH influence Ca levels in the body?
Osteoclast activation --> resorption Increase 1-hydroxylase --> active Vit D Increase renal reabsorption of Ca
62
How does Vit D influence Ca levels?
Increase intestinal absorption | Increase bone resorption
63
How does calcitonin influence Ca levels?
Decrease by inhibiting bone resorption
64
Where are the body's serum calcium sensors?
Parathyroid - C cells
65
What is the pathway for activation and deactivation of Vit D?
https://orthojournal.wordpress.com/2011/11/13/osteoblast-progenitor-cells/
66
What are the primary regulators of Vit D?
1-Hydrox: PTH, Estrogen, low PO4 | 25-Hydrox: hypercalcemia
67
What are the primary sites of osteoporosis in men and women?
Men: Hip and wrist (Colles') Women: Hip, wrist, vertebrae
68
How are osteoporosis and post menopause related?
Low estrogen --> low activation of 1-Hydroxylase and OPG
69
What is the best way to prevent osteoporosis?
Build as much bone as possible at an early age (teens)
70
How are RANKL and OPG related to osteoporosis?
RANKL increase bone reabsorption | OPG protects against bone reabsorption
71
What is defective in X-linked Hypophosphatemic VDRR?
Phosphate is trapped in renal cells due to a defect in the transport protein
72
What is the underlying cause of Vitamin D dependent Ricket's?
Mutation of 1-Hydroxylase prevents activation of Vitamin D (25-OH-D3 --> 1, 25-(OH)2-D3
73
How is Vitamin D dependent Ricket's treated?
Vit D supplementation
74
What is the underlying cause of Vit D Dependency Rickets Type II?
Vit D receptor on target tissue defective (lethal)
75
What is the MoA of bisphosphates?
Inhibition of osteoclasts
76
What is the MoA of Denosumab?
Neutralize RANKL --> inhibit osteocalsts, Prevent osteoclast differentiation
77
What are the 2 major risks of hormone replacement therapy (estrogen) for post menopausal women?
Thromboembolism (enhanced clotting) | Cancer (esp. breast)

Endo / Repro (15 decks)

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