endocrine lectures Flashcards

1
Q

neural communication?

A

neurotransmitters released act on post-synaptic cell

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2
Q

paracrine communication?

A

cell products diffuse in extracellular fluid to affect the same or neighbouring cells

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3
Q

endocrine communication?

A

hormones reach their target cells through blood circulation

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4
Q

ligand, source and target?

A
ligand = chemical messenger
source = cells that produce the ligand
target = cell with receptors to respond to ligand
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5
Q

lipophobic ligand?

A

not lipid soluble, but is water soluble. doesn’t easily cross the cell membrane, may need pumps or channels.
receptors on cell membrane. response often enzyme activation or membrane permeability changes

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6
Q

lipophilic ligand?

A

lipid soluble, not water soluble.
easily cross the cell membrane.
receptor usually located within the cell.
target response usually gene expression.

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7
Q

amines as chemical messengers?

A

most are lipophobic.

made or derived from amino acid.

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8
Q

example amine messengers?

A

catecholamines are derived from tyrosine - dopamine, epinephrine.
serotonin made from tryptophan

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9
Q

peptide/ protein messengers?

A
  • most abundant type
  • lipophobic
  • made of chains of amino acids. (>50 is protein ligand,
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10
Q

steroid ligands?

A
  • lipophilic
  • derived from cholesterol
  • all steroid ligands function as hormones.
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11
Q

lipophilic ligand synthesis and release?

A

synthesized on demand, released immediately.

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12
Q

lipophobic ligand synthesis and release?

A

synthesis is independent of demand. stored in vesicles until needed. released by exocytosis.

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13
Q

amine synthesis?

A

-produced in cytosol of source

amine product is dependent on enzymes present

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14
Q

transport of ligands?

A
  • interstitial fluid if source and target are close. ligand then quickly degraded
  • blood borne transport if source and target are a distance apart. lipophobic dissolve in plasma, lipophilic bind to carrier protein
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15
Q

half life of dissolved and protein bound messeengers?

A

dissolved relatively short

bound is relatively long

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16
Q

strength of ligand response depends on?

A
  • concentration of ligands
  • number of receptors on target cell
  • receptor ligand affinity
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17
Q

down-regulation?

A
  • receptor number on target decreases
  • may result from excess messenger
  • sensitivity to messenger decreases
  • tolerance to messenger develops
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18
Q

up-regulation?

A
  • receptor number on target increases
  • may result from too little messenger
  • sensitivity to messenger increases
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19
Q

agonist and antagonist?

A

agonist - chemical that binds to a receptor and mimics the normal response
antagonist - chemical which binds to a receptor but binding has no effect - it competes with the ligand.

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20
Q

enzyme linked membrane receptor?

A

receptor and enzyme are same protein - ligand binding activates the enzyme and target response occurs.

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21
Q

G protein linked receptor/ channel?

A

binding of ligand activates G protein which activates channel. this process is slow. change in transport of ions through the channel causes a target response.

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22
Q

second messenger systems?

A

binding of first messenger to a receptor leads to production of second messenger.
Gs activates amplifier enzyme
Gi inhibits amplifier enzyme

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23
Q

cholera and G proteins?

A

cholera toxin binds ganglioside in small intestine. G protein activates cAMP. protein kinases lead to increased secretion of chloride ions out of the cell and sodium follows then water and severe diarrhoea occurs

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24
Q

primary endocrine glands?

A

pineal gland, hypothalamus, pituitary gland, thyroid gland, parathyroid gland, thymus, adrenal gland, pancreas, ovaries, testes

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25
Q

secondary endocrine glands?

A

heart, stomach, liver, kidney, small intestine, skin

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26
Q

infundibulum?

A

stalk that connects pituitary to brain

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27
Q

posterior pituitary?

A

extension of the neural tissue

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28
Q

anterior pituitary

A

true endocrine of epithelial origin

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29
Q

2 hormones of the posterior pituitary?

A

ADH - water balance and osmolarity

oxytocin - milk ejection

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30
Q

tropic hormones?

A

affect the release of another hormone

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31
Q

hypothalamic tropic hormones?

A

1) blood with tropic hormones enters portal vein
2) hypothalamic tropic hormones access anterior pituitary secretory cells through capillary beds
3) anterior pituitary tropic hormone release altered
4) anterior P. tropic H’s enter bloodstream through capillary bed
5) travel to distant endocrine gland where they trigger releas

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32
Q

melatonin derivative and function?

A

tryptophan. secreted at night when we sleep, transmits information about light-dark cycles and governs bodies biological clock

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33
Q

pineal gland

A

secretes melatonin. believed to be involved in circadian rhythms.

34
Q

two thyroid homrones?

A

T4, T3 regulate metabolism

calcitonin regulates calcium levels in the blood

35
Q

parathyroid hormone?

A

regulates calcium levels in the blood

36
Q

thyroid hormones made of?

A

iodine and tyrosine

37
Q

thymosin?

A

regulates T cell function. is secreted by the thymus

38
Q

location of adrenal gland?

A

on top of kidney

39
Q

androgens?

A

sex hormones, secreted by adrenal gland, regulate reproductive function.

40
Q

Adrenal medulla?

A

chromaffin cells are the secretory cells.

  • 80% epinephrine
  • 20% noradrenaline
41
Q

Addisons disease?

A

The inability to produce adrenaline. caused by a mutation leading to a defective adrenal medulla.

42
Q

endocrine function of pancreas?

A
islets of langerhans:
-alpha cells - glucagon
-beta cells - insulin
delta cells- somatostatin
-F cells - pancreatic polypeptide
43
Q

testes hormones?

A

testosterone

androstenedione

44
Q

ovaries hormones?

A

estradiol

progesterone

45
Q

suprachiasmatic nucleus?

A

part of hypothalamus

46
Q

sites of hormone metabolism?

A

target cell, blood, liver.

47
Q

primary and secondary secretion disorders?

A

primary - abnormality in endocrine organ secreting hormone

secondary - abnormality in tropic hormone

48
Q

exogenous medication issue?

A

replaces and exceeds normal, causes atrophy of gland.

49
Q

permissiveness?

A

one hormone needed for another to exert its effects

50
Q

glycogen?

A

stores glucose

51
Q

energy output?

A

heat - 60%

work - 40%

52
Q

metabolic rate?

A

energy expended per unit time

53
Q

basal metabolic rate?

A

rate of energy expenditure or a person awake, resting, lying down and fasted for 12 hours.
represents minimum energy necessary to maintain body functions

54
Q

absorptive state?

A

energy input> output as nutrients have been absorbed.

glucose is the primary energy source for the cell

55
Q

excess nutrient storage in absorptive state?

A

liver and muscle store glycogen

adipose tissue stores triglycerides

56
Q

postabsorptive state?

A

energy input

57
Q

insulin?

A

peptide hormone

secreted from beta cells of islets of langerhans (pancreas)

promotes synthesis of energy storage molecules (anabolic)

promotes glucose uptake by body cells

58
Q

glucagon?

A

peptide hormone

secreted from alpha cells of islets of langerhans (pancreas)

promotes breakdown of energy storage molecules

promotes sparing of glucose for nervous system by diverting body cells to utilizing other energy sources

59
Q

type 1 diabetes?

A

plasma glucose levels rise, but no insulin is released.

60
Q

type 2 diabetes?

A

accounts for 90% of all diabetes

insulin resistance

therapy is diet and exercise as well as some drugs.

61
Q

3 blood glucose states and levels?

A

normal - 70-100mg/dL

hyperglycemia > 140mg/dL

hypoglycemia

62
Q

hormones of growth?

A

growth hormone

somatomdins (insulin like growth factors)

insulin

thyroid hormones

sex hormones

63
Q

hypertrophy and hyperplasia?

A

increase in cell size and increase in cell number respectively

64
Q

somatomedins (insulin-like growth factors)?

A

GH stimulates IGF release from liver

IGFs have direct effect on target cells as hormones and paracrines.

65
Q

growth hormone secretion?

A

GHRH in hypothalamus stimulates GH release from anterior pituitary.

66
Q

GH inhibition?

A

GHIH (somatostatin) inhibits GH release from anterior pituitary

67
Q

Bone is?

A

calcium phosphate crystals

68
Q

bone makers, bone breakers and bone maintainers?

A

osteoblasts

osteoclasts

osteocytes

69
Q

formation of bone?

A

osteoblasts lay down osteoid which then undergoes calcification (depositing of calcium phosphate).
osteoblast becomes immobilised then becomes osteocyte, this maintains the surrounding osteoid

70
Q

resorption of bone?

A

osteoclasts secrete acid and enzymes

acid dissolved the calcium phosphate crystals

enzymes degrade osteoid

calcium + phosphate released into blood

71
Q

increase in bone width?

A

osteoblasts lay down osteoid on outer surface meanwhile osteoclasts resorb bone in inner surface of cavity to minimize weight gain

72
Q

increase in bone length?

A

osteoblasts lay down osteoid at epiphyseal plates

73
Q

epiphyseal plate?

A

cartilage between the epiphysis and diaphysis

74
Q

long bone growth?

A

chondrocytes produce new cartilage at epiphyseal plate, this widens so bone grows.
chondrocytes then die and osteoblasts replace and lay down bone.

at puberty epiphyseal plates close and no further length increase is possible

75
Q

acromegaly?

A

increased GH secretion in adults

76
Q

thyroid hormones (T4 and T3)?

A

T4 most abundant, last active, provides long loop negative feedback

T3 not as much made, more active at target tissue.

77
Q

exopthalmus?

A

caused by hypertrophy of tissues in the eye socket, it is a sign of hyperthyroidism

78
Q

treating excess thyroid hormone secretion?

A

surgical removal of portion of oversecreting thyroid gland

treatment with radioactive iodine - gets concentrated in thyroid gland and selectively destroys thyroid tissue

anti-thyroid drugs

79
Q

cortisol?

A

hormone of stress

mobilises energy stores

suppresses immune system

80
Q

hypersecretion of glucocorticoid?

A

cushing’s syndrome - protein depletion.