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VBMS 325 > module 3-endocrine review > Flashcards

module 3-endocrine review Flashcards

1
Q

steroids

A

derived from cholesterol, bound to plasma protein, not stored, lipophillic

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2
Q

3 classes of hormones

A

1) peptides
2) amines
3) steroids

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3
Q

peptides

A

derived from preprohormones, hydrophillic, free floating

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4
Q

amines

A

derived from tyrosine, stored until needed, bound to plasma proteins

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5
Q

tropic vs non-tropic hormone

A

tropic- regulates secretion of another hormone by acting on it

non-tropic: final product, does not regulate secretion of other hormones

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6
Q

how are hormone levels regulated (4)

A

1)rate of secretion
2) control of H transport
3) metabolism & excretion
4) control of hormone receptors

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7
Q

pineal gland

A

controls circadian rhythm, secretes melatonin

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8
Q

what 2 hormones are produced by posterior pituitary

A

ADH & oxytocin

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9
Q

what controls release of ADH & oxytocin

A

ADH- increase in plasma osmolarity
oxytocin: cervix nerves detecting stretch or suckling

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10
Q

what hormones are produced by the anterior pituitary gland? what controls their relase

A

GH, THS, ATCH, FHS, LH, prolactin
produced by hypothalamus

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11
Q

what is the hypothalamys-hypohyseal portal

A

2 capillary beds back to back without going through heart

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12
Q

3 factors effecting growth

A

diet, stress & normal levels of other hormones

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13
Q

differences between IGF-1 vs IGF-2

A

1- most important for growth, soft tissue & bone growth, stimulated by GH, produced everywhere

2-independent of GH, produced continuously throughout life, muscle growth

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14
Q

hyperplasia vs hypertrophy

A

plasia- increase in cell numbers
trophy- increase in size

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15
Q

3 steps of elongation of lone bones

A

1) diaphysis- shaft
2) epiphsysis- knobs
3) epiphyseal plate- layer of cartilahge

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16
Q

what causes GH deficiency

A

pituitary issues or congential

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17
Q

GH deficiency effects on newborn vs adult

A

newborn-dwarfism
adult-soft tissue overgrowth

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18
Q

treatment of GH deficiency

A

GH injection

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19
Q

excess GH condition cause

A

pituitary issues or congenital

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20
Q

excess GH conditions on children vs adult

A

children- gigantism
adult-acromegaly-soft tissue overgrwoth

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21
Q

what test is used to diagnose GH deficiency disorders

A

provocative test
- give massive injection of insulin, if no peak = GH disorder

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22
Q

metabolic, cardiovascular & growth effects of TH

A

metabolic: modulate BMR
cardiovascular: increase HR
growth: AP transmission slowed

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23
Q

lack of TH

A

hypothyroidism= lack of TH = increase TSH = goiter

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24
Q

cretnism

A

too little TH = GH cannot do its job

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25
Q

treatment of hypothyroidism

A

iodine

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26
Q

excess of TH

A

hyperthyroidism= increase in TH = increase in TSH = goiter

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27
Q

3 key steroids & functions

A

1) mineralcorticoids- electrolytes
2) glucocorticoids- glucose, lipid & protein metabolism
3) sex steroids- DHEA

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28
Q

most abundant hormone

A

DHEA

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29
Q

metabolic, anti-inflammatory & immunosuppression effects of glucocorticoids

A

metabolic: increase blood glucose concentration
anti-inflammatory: cortisol release
immunosuppression: too much stress

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30
Q

3 negative effects of glucocorticoids

A

immunosuppression, abortion & more infection

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31
Q

too much vs too little cortisol production disease

A

too much = cushings
too little = addisons

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32
Q

metabolic pathways involved in anabolism vs catabolism

A

anabolism: glycogenesis
catabolism: glycogenolysis, gluconeogenesis

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33
Q

effects of insulin on blood glucose

A

decrease blood glucose by facilitating uptake of glucose in muscle & adipose cells through GLUT-4 transporters & storage

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34
Q

effects of glucagon on blood glucose

A

increase blood glucose by promoting gluconeogenesis by increasing genolysis & inhibiting glycogenesis

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35
Q

why does AA intake trigger release of insulin & glucagon?

A

AA triggers release of glucagon = cancels insulin effect on glucose

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36
Q

2 types of diabetes

A

type 1: insulin dependent: insulin is not produced
type 2: insulin independent: cells stop responding to insulin

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37
Q

consequences of failed glucose control (diabetes)

A

blindness & leg pain

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38
Q

how does physical activity mediate blood glucose levels?

A

exercise of skeletal muscles can mimic the activity of insulin & absorb all extra glucose

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39
Q

why is calcium so tightly regulated

A

has various physiological effects

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40
Q

long vs short term regulation of calcium

A

long: structural support in bones & teeth, milk & egg production
short: blood clotting cascade, decrease in neuromuscular

41
Q

how does body obtain calcium from outside its own supply?

A

diet & sunlight

42
Q

what is PTH & how does it work to maintain calcium levels

A

PTH (parathyroid hormone): decreased plasma Ca = increase PTH
calcitonin: increased plasma ca = increase calcitonin

43
Q

osteoblasts vs osteoclasts

A

blasts: makes new bones, stroma cells, secrete organic matrix
clasts: destroys bone, macrophages, release HCI to breakdown organic matrix

44
Q

3 functions of vitamin D for calcium homeostasis

A

1) calcium absorption
2) phosphate absorption
3) bone reponsiveness

45
Q

milk fever

A

hypocalemia

46
Q

why should you feed a low Ca diet prior to calving

A

to trigger calcitonin pathway to avoid hypocalemia

47
Q

PRH vs PIH on prolactin

A

PRH =stimulate prolactin release
PIH = inhibin prolactin release

48
Q

goiter formation on hyper vs hypothyroidism

A

hyper-increase TH = increase TSH = hypertrophy & hyperplasia = gland grows = goiter

hypo-decreased TH = increased TSH = hypertrophy & hyperplasia = gland grows = goiter

49
Q

fast stress response

A

increase CNS = increase glucagon & decrease insulin

50
Q

synthesis of TH

A

1) Tg is formed in follicular cells & dumped into colloid by exocytosis
2) iodide moves from blood to follicular cells
3) iodide is oxidized to active form by TPO
4) TPO attaches iodide to tyrosine
5) coupling to form hormones
6) follicular cells engulf colloid
7) lyzosomes spilt Tg into T3 & T4 = diffuse into blood

51
Q

T or F: T3 & T4 diffuse into blood

A

T

52
Q

increased osteoclasts = ( ) bone mass

A

decreased

53
Q

decreased osteoclasts = ( ) bone mass

A

increased

54
Q

nervous vs endocrine systems

A

nervous: fast, precise, short, constant
endocrine: slow, generalized, long, amplified

55
Q

catecholamine vs cortisol release speeds

A

catecholamine- very fast, cannot measure
cortisol-peaks after 1 hour

56
Q

ADH roles (2)

A

1) enhanced water retention
2) contraction of arteriolar smooth muscles

57
Q

what does a deficiency of ADH mean

A

large amount of very dilute urine

58
Q

angiotension II role

A

increase water uptake & BP

59
Q

ACTH role

A

stimulate cortisol secretion by adrenal cortex

60
Q

LH

A

regulates sex hormone secretion

61
Q

prolactin vs oxytocin

A

prolactin: milk production
oxytocin: milk delivery

62
Q

what hormone is high during pregnancy to cause mammary gland growth

A

prolactin

63
Q

what does high progesterone levels during pregnancy cause

A

blocks milk production

64
Q

overall effect of GH

A

mobilize fat stores as major energy source to keep glucose for the brain

65
Q

how do bones grow thicker vs longer?

A

thicker- adding new bone on top
larger: proliferation of cartilage cells in epiphyseal plates

66
Q

what does the thickness of cartilage tell us

A

how much growth you have left, is thicker in kids

67
Q

what does a closed growth plate indicate

A

no growth left

68
Q

what is the epiphyseal plate made of

A

chondrocytes

69
Q

what test is used to diagnose hyperproduction of GH

A

provacative test- give glucose
- GH should drop
- GH stays risen

70
Q

what is the backbone of thyroid hormone

A

Tg

71
Q

what is the active form of TH? why?

A

T3, is quicker & better at doing job than T4

72
Q

more vs less TH produced on O2 consumption

A

more= higher O2 consumption bc more heat produced

less= lower O2 consumption b/c less heat produced

73
Q

how can we measure BMR

A

speed of which the animal is consuming O2

74
Q

endotherms vs ecotherms- which as higher level of TH

A

endotherms

75
Q

low TH triggers ( ) effects

A

anabolic

76
Q

T or F: TH has permissive effects on GH

A

T

77
Q

why does hypothryoidism from birth lead to cretnisim

A

too little TH = GH cannot do its job b/c TH has permissive effects on GH

78
Q

inner vs outer layer of adrenal cortex- what secretes what

A

outer- secretes steroids
inner- secretes catecholamines

79
Q

80% of adrenal cortex in most mammals is made of the

A

cortex

80
Q

3 layers of adrenal cortex

A

1) zona glomerulosa (outer)
2) zona fasiculata (middle)
3) zona reticularis (inner)

81
Q

what is aldosterone release stimulated by

A

angiotension II

82
Q

where are sex steroids vs glucocorticoids vs mineralcorticoids produced

A

sex- zona faciclata & reticularis
gluco-zona faciclata & reticularis
mineral-zona glomerulosa

83
Q

what can AA be turned into

A

sugar

84
Q

treatment of hyper vs hypo adrenalcorticism

A

hyper-destory adrenal cortex to stop cortisol production
hypo-aldosterone

85
Q

a-1 receptor causes

A

vasodilation

86
Q

b-2 receptor causes

A

vasodilation

87
Q

B-2 receptors are activated by

A

epinephrine

88
Q

glycogen is broken down into ( ) for muscles

A

lactate

89
Q

what is released during fed vs starvation state

A

fed- insulin
starvation- glucagon

90
Q

sorbitol

A

causes cataracts

91
Q

HbA1c test

A

shows blood glucose level over last 3 months
- lots bound = bad at controlling glucose

92
Q

what are produced by liver during glucose sparing

A

ketones

93
Q

when is the only time the brain can use ketones instead of glucose

A

starvation

94
Q

beta vs alpha cells- insulin & glucagon

A

beta-insulin
alpha-glucagon

95
Q

when are somatostatins released in blood

A

when glucose & AA levels are high

96
Q

GLUT

A

glucose transporter- move glucose into a cell & methylate it so its trapped

97
Q

what GLUT is the only independent

A

GLUT-4

98
Q

GLUT 1 vs 2

A

1- moves glucose through blood-brain barrier
2-transport glucose into neurons

99
Q

how to manage diet with diabetes

A

low glycemic index diets- short & complex fibers that are absorbed & broken down slowly to ensue stable blood glucose levels

VBMS 325 (17 decks)

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