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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
treatment of hypothyroidism
iodine
26
excess of TH
hyperthyroidism= increase in TH = increase in TSH = goiter
27
3 key steroids & functions
1) mineralcorticoids- electrolytes 2) glucocorticoids- glucose, lipid & protein metabolism 3) sex steroids- DHEA
28
most abundant hormone
DHEA
29
metabolic, anti-inflammatory & immunosuppression effects of glucocorticoids
metabolic: increase blood glucose concentration anti-inflammatory: cortisol release immunosuppression: too much stress
30
3 negative effects of glucocorticoids
immunosuppression, abortion & more infection
31
too much vs too little cortisol production disease
too much = cushings too little = addisons
32
metabolic pathways involved in anabolism vs catabolism
anabolism: glycogenesis catabolism: glycogenolysis, gluconeogenesis
33
effects of insulin on blood glucose
decrease blood glucose by facilitating uptake of glucose in muscle & adipose cells through GLUT-4 transporters & storage
34
effects of glucagon on blood glucose
increase blood glucose by promoting gluconeogenesis by increasing genolysis & inhibiting glycogenesis
35
why does AA intake trigger release of insulin & glucagon?
AA triggers release of glucagon = cancels insulin effect on glucose
36
2 types of diabetes
type 1: insulin dependent: insulin is not produced type 2: insulin independent: cells stop responding to insulin
37
consequences of failed glucose control (diabetes)
blindness & leg pain
38
how does physical activity mediate blood glucose levels?
exercise of skeletal muscles can mimic the activity of insulin & absorb all extra glucose
39
why is calcium so tightly regulated
has various physiological effects
40
long vs short term regulation of calcium
long: structural support in bones & teeth, milk & egg production short: blood clotting cascade, decrease in neuromuscular
41
how does body obtain calcium from outside its own supply?
diet & sunlight
42
what is PTH & how does it work to maintain calcium levels
PTH (parathyroid hormone): decreased plasma Ca = increase PTH calcitonin: increased plasma ca = increase calcitonin
43
osteoblasts vs osteoclasts
blasts: makes new bones, stroma cells, secrete organic matrix clasts: destroys bone, macrophages, release HCI to breakdown organic matrix
44
3 functions of vitamin D for calcium homeostasis
1) calcium absorption 2) phosphate absorption 3) bone reponsiveness
45
milk fever
hypocalemia
46
why should you feed a low Ca diet prior to calving
to trigger calcitonin pathway to avoid hypocalemia
47
PRH vs PIH on prolactin
PRH =stimulate prolactin release PIH = inhibin prolactin release
48
goiter formation on hyper vs hypothyroidism
hyper-increase TH = increase TSH = hypertrophy & hyperplasia = gland grows = goiter hypo-decreased TH = increased TSH = hypertrophy & hyperplasia = gland grows = goiter
49
fast stress response
increase CNS = increase glucagon & decrease insulin
50
synthesis of TH
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
T or F: T3 & T4 diffuse into blood
T
52
increased osteoclasts = ( ) bone mass
decreased
53
decreased osteoclasts = ( ) bone mass
increased
54
nervous vs endocrine systems
nervous: fast, precise, short, constant endocrine: slow, generalized, long, amplified
55
catecholamine vs cortisol release speeds
catecholamine- very fast, cannot measure cortisol-peaks after 1 hour
56
ADH roles (2)
1) enhanced water retention 2) contraction of arteriolar smooth muscles
57
what does a deficiency of ADH mean
large amount of very dilute urine
58
angiotension II role
increase water uptake & BP
59
ACTH role
stimulate cortisol secretion by adrenal cortex
60
LH
regulates sex hormone secretion
61
prolactin vs oxytocin
prolactin: milk production oxytocin: milk delivery
62
what hormone is high during pregnancy to cause mammary gland growth
prolactin
63
what does high progesterone levels during pregnancy cause
blocks milk production
64
overall effect of GH
mobilize fat stores as major energy source to keep glucose for the brain
65
how do bones grow thicker vs longer?
thicker- adding new bone on top larger: proliferation of cartilage cells in epiphyseal plates
66
what does the thickness of cartilage tell us
how much growth you have left, is thicker in kids
67
what does a closed growth plate indicate
no growth left
68
what is the epiphyseal plate made of
chondrocytes
69
what test is used to diagnose hyperproduction of GH
provacative test- give glucose - GH should drop - GH stays risen
70
what is the backbone of thyroid hormone
Tg
71
what is the active form of TH? why?
T3, is quicker & better at doing job than T4
72
more vs less TH produced on O2 consumption
more= higher O2 consumption bc more heat produced less= lower O2 consumption b/c less heat produced
73
how can we measure BMR
speed of which the animal is consuming O2
74
endotherms vs ecotherms- which as higher level of TH
endotherms
75
low TH triggers ( ) effects
anabolic
76
T or F: TH has permissive effects on GH
T
77
why does hypothryoidism from birth lead to cretnisim
too little TH = GH cannot do its job b/c TH has permissive effects on GH
78
inner vs outer layer of adrenal cortex- what secretes what
outer- secretes steroids inner- secretes catecholamines
79
80% of adrenal cortex in most mammals is made of the
cortex
80
3 layers of adrenal cortex
1) zona glomerulosa (outer) 2) zona fasiculata (middle) 3) zona reticularis (inner)
81
what is aldosterone release stimulated by
angiotension II
82
where are sex steroids vs glucocorticoids vs mineralcorticoids produced
sex- zona faciclata & reticularis gluco-zona faciclata & reticularis mineral-zona glomerulosa
83
what can AA be turned into
sugar
84
treatment of hyper vs hypo adrenalcorticism
hyper-destory adrenal cortex to stop cortisol production hypo-aldosterone
85
a-1 receptor causes
vasodilation
86
b-2 receptor causes
vasodilation
87
B-2 receptors are activated by
epinephrine
88
glycogen is broken down into ( ) for muscles
lactate
89
what is released during fed vs starvation state
fed- insulin starvation- glucagon
90
sorbitol
causes cataracts
91
HbA1c test
shows blood glucose level over last 3 months - lots bound = bad at controlling glucose
92
what are produced by liver during glucose sparing
ketones
93
when is the only time the brain can use ketones instead of glucose
starvation
94
beta vs alpha cells- insulin & glucagon
beta-insulin alpha-glucagon
95
when are somatostatins released in blood
when glucose & AA levels are high
96
GLUT
glucose transporter- move glucose into a cell & methylate it so its trapped
97
what GLUT is the only independent
GLUT-4
98
GLUT 1 vs 2
1- moves glucose through blood-brain barrier 2-transport glucose into neurons
99
how to manage diet with diabetes
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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