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BPK 375 > Hormones > Flashcards

Hormones Flashcards

1
Q

Define autocrine

A

the cell that produces and releases the hormone is acted on by the hormone

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2
Q

Define paracrine

A

The cell produces a signal to alter the behavior of nearby cells

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3
Q

Define Endocrine

A

Hormones that travel via circulatory system to influence cells further away

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4
Q

What does the anterior pituitary originate from

A

oral ectoderm

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5
Q

What does the posterior pituitary originate from

A

neuroectoderm

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6
Q

What is the name of the capillary system which hypothalamic hormones are secreted

A

hypothalamic-hypophyseal portal system

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7
Q

What 5 hormones are synthesized and secreted by the anterior pituitary; what causes the release of these hormones, what inhibits the release

A

1) Growth hormone (aka, somatotropin); released by hypothalamic growth hormone releasing factor; inhibited by hypothalamic somatostatin
2) Thyroid stimulating hormone; released by hypothalamic thyrotropin releasing factor; inhibited by somatostatin
3) Adrenocorticotropic hormone; released by hypothalamic corticotropin releasing factor
4) Luteinizing hormone; released by gonadotropin releasing hormone
5) Follicle stimulating hormone; released by gonadotropin releasing hormone

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8
Q

What are the three ligands involved in the insulin-like growth factor system

A
  • IGF-1: somatomedin
  • IGF2
  • insulin
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9
Q

When are HGH levels the highest?

A
  • deep sleep; phase 4
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10
Q

What type of stress increases/decreases HGH secretion

A
  • physical stress; increases

- psychological; decreases due to an increase in glucocorticoid (also reduces bone/collagen formation

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11
Q

What does HGH do?

A
  • increased DNA synthesis and cell multiplication
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12
Q

What hormone is involved in a permissive relationship with HGH

A
  • thyroid hormone is needed for HGH to work
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13
Q

What three things does HGH directly effect

A
  • Adipose tissue; decrease glucose uptake, increases lipolysis, decreases adiposity
  • Liver; increases RNA synthesis, protein synthesis, gluconeogenesis, IGF-1
  • Muscle; decreased glucose uptake, increased AA uptake, protein synthesis and lean body mass
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14
Q

how does the local production of IGF-1 affect other systems

A
  • bones/heart/lungs; increased AA uptake, protein synthesis, RNA synthesis, DNA synthesis, organ size/fxn
  • Chondrocytes; increased AA uptake, protein synthesis, RNA synthesis, DNA synthesis, collagen, chondroitin sulphate, cell #/size, increased linear growth
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15
Q

How do IGF-1 and growth hormone interact in long bones

A
  • GH stimulates proliferation of chondrocyte precursors > expands proliferative chondrocyte pool & the production of IGF-1
  • IGF-1 stimulates clonal expansion via auto/paracrine mechansims & therefore promotes chondrocytet hypertrophy
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16
Q

what does hypopituitarism result in

A
  • stunted growth

- ex, height, penis

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17
Q

what is acromegaly, what does it result from

A
  • enlarged extremities

- hyperpituitarism

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18
Q

at how many weeks of gestation does the thyroid appear

A

3-4 weeks it appears as an epithelial proliferation at the base of the tongue, it then migrates to the base of the neck

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19
Q

when are TRF and TSH secreted in the fetus

A
  • 18-20 weeks gestation
20
Q

when does thyroxine/triiodothyronine reach clinically significant levels

A
  • T4; 18-20 weeks

- T3; 30 weeks

21
Q

what is the purpose of fetal thyroid hormones

A

to protect against brain development abnormalities caused by maternal hypothyroidism

22
Q

How does T3/T4 form

A
  • iodide and thyroglobulin combine to form DIT and MIT

- DIT + MIT = T3 ; DIT + DIT = T4

23
Q

What causes goiter; Derbyshire neck

A
  • lack of iodine in diet

- rare

24
Q

what is the function of thyroid hormones

A
  • RNA synthesis, increased metabolic rate, stimulated o2 uptake and NRG expenditure
25
Q

what causes cretinism, what are the symptoms

A
  • hypothyroidism

- leads to impaired bone growth at birth & irreparable brain damage

26
Q

What causes grave’s disease, what are the symptoms

A
  • hyperthyroidism

- exopthalmus (bugg eyed), high metabolic rate, early death due to heart attack

27
Q

What causes hashimoto’s disease; what are the symptoms

A
  • both hyper/hypothyroidism
  • antibodies destroy the thyroid; first released thyroid hormones, but then they are depleted and can no longer be stimulated
28
Q

What is the role of the parathyroid

A
  • regulates Ca2+ and phosphate metabolism, therefore it’s important for normal bone/tooth development
  • maintains plasma calcium concentrations by stimulating osteoclastic activity
  • Thyrocalcitonin has the opposite effect
29
Q

What is the role of the pancreas

A
  • regulates glucose uptake & the mobilization of energy

- via insulin

30
Q

How does insulin affect protein metabolism

A
  • increased rate of transport of AA
  • increased formation of RNA
  • increased formation of ribosomes
31
Q

How does protein intake affect HGH/Insulin interactions

A
  • protein > ^ HGH, ^IGF-1, ^ insulin > ^ protein synthesis/growth, ^/decreased caloric storage
32
Q

How does carb intake affect HGH/Insulin interactions

A

carbs > dc HGH, ^/dc IGF-1, ^ insulin > ^/dc. protein synthesis/growth, ^ caloric storage

33
Q

How does fasting affect HGH/Insulin interactions

A

fasting> ^ HGH, dc IGF-1, dc insulin > dc. protein synthesis/growth, ^ caloric mobilization

34
Q

Differentiate insulin deficiency/hyperinsulinism

A
  • slows growth almost as much as GH deficiency

- hyper: results in accelerated growth and maturity

35
Q

where are androgens produced; differentiate this in males/females

A
  • Adrenals and testicles
  • Females: adrenals/liver (testosterone)
  • Males: testes (also secrete estrogen)
36
Q

Describe the sexual development of the fetus; at what week can we determine sex based on external appearance

A
  • M/F follow the same growth pattern until 6 weeks of gestation
  • at 12 weeks sex can be determined externally
37
Q

differentiate Mullerian and wolfian characterisitcs

A
  • W: Male characteristerics due to androgens

- Mullerian: Female charactersitics due to less androgens

38
Q

what causes the release of testosterone

A
  • follicle stimulating hormone
39
Q

what are the metabolic effects of testosterone

A
  • increased protein formation
  • increased cholesterol, triglycerides and FFA production
  • decreased phospholipids
  • increased retention of Na, Cl and K- increased muscle development
  • increased rate of skeletal maturation/closure of epiphyses
  • facial development
  • spermatogenesis (2-3 yrs after puberty)
40
Q

What are the effects of adrenal hyperplasia

A
  • increased bone age
  • enlarged clitoris
  • pubic hair
41
Q

what is androgen insensitivity syndrome

A
  • androgen receptors are insensitive to testosterone due to a gene mutation of AR protein located on proximal long arm of the X chromosome
  • 46 XY always show the mutant effect
42
Q

describe stage 1, 6 and 7 of Androgen insensitivity syndrome based on the CA Quigley 7-class system

A

1) Fully male external genitalia
6) Fully female genitalia
7) equivalent to 6 but no secondary terminal hair after puberty

43
Q

what is alpha 5 reductase deficiency, what causes it, what are the symptoms

A
  • autosomal recessive disorder; alpha 5 reductase converts testosterone to DHT
  • caused a gene mutations
  • only affects 46, XY
  • external genetalia appear female
  • condition becomes apparent at puberty
44
Q

what are the symptoms of male pseudohermaphroditism

A
  • gonads = testes but with massive hypertrophy of Leydig cells
  • but np uterus or fallopian tubes
45
Q

what is the most prevalent intersex individual

A
  • XY-female
46
Q

what condition occurs when excess testosterone is produced & there’s an enzyme deficiency

A
  • Congenital adrenal hyperplasia
47
Q

term for too high of androgen level

A
  • hyperandrogenism

BPK 375 (6 decks)

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