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Physio > Endocrine-2 > Flashcards

Endocrine-2 Flashcards

1
Q

tropic hormones refers to

A

hormones released by the ant pit

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2
Q

hypothalamic hormones

A

trh, crh, gnrh, ghrh, prl inhibitory, somatostatin

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3
Q

trh

A

causes ant pit to release tsh

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4
Q

crh

A

stimulates release of acth

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5
Q

gnrh

A

stimulates release of lh & fsh

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6
Q

ghrh

A

stimulates release of gh

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7
Q

prl inhibitory

A

inhibits release of prl

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8
Q

somatostatin

A

inhibits release of gh & digestive hormone

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9
Q

endocrine axes

A

end products feed back to inhibit regulators of own secretion

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10
Q

castration results in an increase of __ BECAUSE you wouldn’t produce

A

lh & fsh secretion; testosterone

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11
Q

if person can’t produce thyroid hormone, their tsh & trh levels are

A

HIGH

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12
Q

secretion of acth inhibited by

A

corticosteroids

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13
Q

describe thyroid axes

A

trh -> tsh -> th -> feedback inhibits tsh & trh

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14
Q

can corticosteroids be stopped abruptly? why?

A

no. body can’t tell difference between drug taken & cortisol it produces; body thinks cortisol levels are high -> shuts off prod of acth & crh

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15
Q

glucocorticoids suppress the

A

hypothalamus & ant pit

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16
Q

why must you taper person off drugs slowly

A

to give axes time to start producing acth & crh again

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17
Q

abruptly withdrawing drug can be fatal because

A

aldosterone can’t be released w/o presence of acth

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18
Q

adrenal medulla

A

modified sympathetic ganglion

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19
Q

adrenal cortex

A

endocrine tissue

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20
Q

adrenal medulla releases __ in response to

A

epi & norepi; sns

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21
Q

adrenal cortex releases __ in response to

A

aldosterone, cortisol, & weak androgens; ant pit producing acth

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22
Q

all hormones produced in the adrenal cortex are __ hormones; derived from __

A

steroid hormones; cholesterol

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23
Q

cortisol is a __ hormone

A

stress

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24
Q

why is cortisol considered a stress hormone

A

it tries to make nutrients available so you have energy source

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25
Q

cortisol disorders

A

cushing’s syndrome & addison’s disease

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26
Q

cause of cushing’s syndrome

A

over secretion of acth from ant pit or too much hormone produced from adrenal cortex

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27
Q

effect of cushing’s syndrome

A

changes in carbohydrate & protein metabolism

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28
Q

result of cushing’s syndrome

A
  1. cortisol elevates blood sugar -> hyperglycemia
  2. defect in metabolism -> abnormal fat deposition, moon face, etc.
  3. muscle breakdown & muscle weakness
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29
Q

cause of addison’s disease

A

inadequate secretion of glucocorticoids (cortisol) & mineralcorticoids (aldosterone)

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30
Q

why can addison’s disease be fatal?

A

lack of aldosterone production which is essential for life

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31
Q

main effect of addison’s disease

A

darkening of skin (bc trying to prof a lot of acth = producing msh)

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32
Q

cushing’s disease mimics someone who is on

A

high dose of prednisone

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33
Q

symptoms: euphoria, psychotic, poor wound healing, bruising, prone to infection

A

cushing’s syndrome

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34
Q

why is it bad to place cortisol near bone frequently

A

cortisol stimulates osteoclast activity -> lead to osteoporosis

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35
Q

adrenal medulla releasing epi & norepi is similar to that of the NS however it

A

lasts longer (put straight into bloodstream)

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36
Q

adrenal medullary tumor (pheochromocytoma) symptoms

A

epi & norepi high, hr high, high bp, blood sug, nervousness, digestive probs, glycosuria, thin

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37
Q

stress releases

A

cortisol

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38
Q

why does increased stress increase illness

A

glucocorticoids inhibit immune responses

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39
Q

chronically elevated cortisol ->

A

atrophy of hippocampus (defects in learning & memory)

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40
Q

glucocorticoids (stress hormone) stimulate

A

catabolism

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41
Q

catabolism

A

breakdown

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42
Q

ex of catabolism

A

protein -> amino acids

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43
Q

anabolism

A

building

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44
Q

why do glucocorticoids stimulate catabolism

A

they try to provide nutrients to be used as energy sources

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45
Q

gluconeogenesis

A

production of glucose from non-carbohydrate sources

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46
Q

what do glucocorticoids stimulate to provide nutrients

A

gluconeogenesis, fat & protein breakdown, elevation of blood sugar, & opposition of insulin effects

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47
Q

stress complicates diabetes tx? why?

A

t; stress -> glucocorticoids -> aggravate insulin resistance

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48
Q

spherical hollow sacs

A

follicles

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49
Q

follicles lines with __ that secrete __

A

follicular cells; thyroxine

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50
Q

protein rich fluid inside thyroid follicles

A

colloid

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51
Q

where is thyroid hormone stored

A

w/in colloid

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52
Q

parafollicular cells secrete

A

calcitonin

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53
Q

calcitonin

A

lowers blood calcium

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54
Q

pth

A

increases blood calcium

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55
Q

what does thyroid hormone do?

A

increases bmr

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56
Q

as a result of an increase of bmr ->

A

o2 consumption (generates heat), thyroid hormone secretion (in cold weather), hr + force of contraction, & resp rate ALL RAISED

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57
Q

what else does thyroid hormone do?

A

stimulates appetite, accelerates breakdown of macromolecules, & for NS maturation

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58
Q

which hormone if not produced in infancy can affect brain development

A

thyroid hormone

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59
Q

person with too much thyroid hormone is

A

thin, gittery, hr racing, high bp, sweating, constantly hungry

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60
Q

person with too little thyroid hormone

A

overweight, tired, lethargic, cold

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61
Q

calcitonin secreted by

A

parafollicular cells of thyroid

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62
Q

calcitonin lowers blood calcium levels by

A

inhibiting osteoclast activity & by stimulating renal calcium excretion

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63
Q

iodine deficiency goiter cause

A

inadequate thyroid hormone produced

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64
Q

iodine deficiency goiter results in

A

increased tsh -> but since don’t have thyroid hormone = hypertrophy of gland

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65
Q

grave’s disease caused by

A

autoantibodies against thyroid gland

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66
Q

grave’s disease results in

A

hypertrophy & toxic goiter or thyrotoxicosis

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67
Q

mechanism of grave’s disease

A

autoantibodies look like tsh -> bind to tsh receptor -> stimulate thyroid hormone & gland growth

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68
Q

what determines if they have goiter

A

whether tsh receptor is being stimulated or not

69
Q

iodine deficiency stimulated by

A

tsh

70
Q

grave’s disease stimulated by

A

antibodies

71
Q

grave’s disease: patient also develops

A

exopthalmia (antib’s bind to recep’s behind orbits->eyes bulge)

72
Q

grave’s disease: patient actual tsh levels very

A

LOW (tsh stops bc have tons of thyr horm)

73
Q

grave’s disease: patient bmr & bp

A

high

74
Q

hypothyroidism in adults aka

A

myxedema

75
Q

hypothyroidism in adults can also result in

A

swelling of hands & feet

76
Q

hypothyroidism in children aka

A

cretinism

77
Q

pth raises blood calcium by

A
  1. stimulating osteoclast activity
  2. prod. vit d
  3. increasing renal reabsorption of ca
78
Q

pancreas is a mixed gland

A

t

79
Q

islets are __ structures

A

endocrine

80
Q

alpha cells ->

beta cells ->

A

glucagon

insulin

81
Q

insulin secreted in response to a

A

rise in plasma glucose

82
Q

insulin binds receptors in target cells ->

A

results in translocation of glucose transporters -> glucose taken up by ADIPOSE tissue -> stimulates glycogen prod -> fat deposition -> storage of hormone

83
Q

insulin effects

A
  1. inhibits lipolysis
  2. induces prod of fat-forming enzymes
  3. inhibits protein breakdown
84
Q

ketogenesis

A

when you use FATS as energy source -> prod ketones

85
Q

testosterone produced by

A

interstitial cells of leydig

86
Q

ovarian follicles release

A

estrogen

87
Q

estrogen produced by

A

granulosa cells

88
Q

cells that surround developing oocyte

A

granulosa cells

89
Q

what converts testosterone to estrogen

A

aromatase

90
Q

you must have __ to make estrogen

A

testosterone

91
Q

progesterone produced by

A

corpus luteum

92
Q

keeps uterine lining in tact to continue pregnancy

A

placenta

93
Q

placenta releases

A

estrogen & progesterone

94
Q

insulin rises during __ state

A

absorptive (following a meal) aka postprandial phase

95
Q

insulin falls during __ state

A

postabsorbative (fasting)

96
Q

hormonal regulation of metabolism primarily via

A

plasma glucose levels & amino acid levels

97
Q

if can’t use glucose as energy source & must use fat breakdown you produce __ as a biproduct

A

ketoacids

98
Q

result of ketoacids accumulating

A

ketoacidosis

99
Q

ketoacidosis usually only occurs in

A

untreated type 1 diabetes

100
Q

high blood glucose stimulates insulin to get

A

stored

101
Q

glucagon stimulated by

A

fall in blood glucose

102
Q

glucagon inhibited by

A

rise in blood glucose

103
Q

glucagon increases blood glucose during

A

fasting

104
Q

type 1 diabetes you do produce insulin

A

f; don’t

105
Q

type 1 diabetes __ cells not functional

A

beta

106
Q

type 1 diabetes tx

A

give insulin

107
Q

insulin overproduction type __

A

2 diabetes

108
Q

cause of type 2 diabetes

A

either cells aren’t responding OR down regulating receptors; have insulin resistance

109
Q

can end up w/ islet cell failure -> islet cells can’t produce insulin (BIG PROBLEM) -> characteristic of

A

type 2 diabetes

110
Q

patients w/ type2 diabetes usually develop keto acids

A

f; rarely bc have insulin working to some degree so ARE pulling in some glucose

111
Q

are beta cells functional in type 2 diabetes

A

yes

112
Q

type2 tx

A

diet & exercise

113
Q

what is the hallmark of glycosuria

A

hyperglycemia

114
Q

the word diabetes refers to

A

freq urination

115
Q

the word mellitus refers to

A

honeyed/sweet

116
Q

which type of diabetes is insulin dependent

A

1

117
Q

what gets used up trying to neutralize ketoacids

A

bicarb buffers

118
Q

ketone bodies & glycosuria results in

A

osmotic diuresis

119
Q

osmotic diureses ->

A

severe dehydration -> severe electrolyte disturbances & acidosis -> comma & death

120
Q

loss of insulin sensitivity/ insulin resistance characteristic of

A

type2

121
Q

down regulation of receptors or loss of receptor sensitivity, down regulation of glucose transporters characteristics of

A

type2

122
Q

in the early stages of type2, patient produces normal-slightly elevated insulin

A

t

123
Q

type2 has a gradual progression

A

t

124
Q

what up-regulates glucose transporters on skeletal m

A

exercise

125
Q

if lifestyle modification alone can’t control type2 ->

A

oral hypoglycemic agents added

126
Q

what do oral hypoglycemic agents do

A

help body use glucose

127
Q

oral hypoglycemic agents only work well with

A

diet & exercise

128
Q

why are insulin levels high in patient w pre diabetes

A

body not responding to insulin so puts more out to get a response

129
Q

obesity kills more than smoking & drinking combined

A

t

130
Q

what happens over time if body not responding to insulin & keeps putting more out to get a response

A

islet cells can get exhausted & stop producing insulin

131
Q

catecholamines

A

epi & norepi

132
Q

catecholamines stimulate

A

glycogenolysis, release of glucose from liver, lypolysis

133
Q

glucocorticoids promote

A

lypolysis, ketogenesis, gluconeogenesis, & protein breakdown

134
Q

what does thyroxine do

A

increases bmr

135
Q

what promotes heat generation which is important to cold adaptation

A

thyroxine

136
Q

why is cornoary art disease associated w type 2

A

high blood sugar causes tears in endothel -> makes it easier for lipids to deposit

137
Q

what condition goes hand in hand with type 2

A

dyslipidemia

138
Q

gucocorticoids cause protein synthesis to go

A

down

139
Q

glucocorticoids cause blood glucose, glycogen, & gluconeogenesis to go

A

up

140
Q

the skeleton is a huge __ & __ reservoir

A

ca & phosphate

141
Q

bone resorption done by

A

osteoclasts

142
Q

bone resorption returns __ & __ to blood

A

ca & phosphate

143
Q

what stimulates osteoclast apoptosis

A

estrogen

144
Q

why are women more prone to osteoporosis after menopause

A

estrogen stimulates osteoclast apoptosis

145
Q

what increases absorption of ca & phosphate from gut

A

vit d

146
Q

what must be present for pth to stimulate osteoclast activity

A

vit d

147
Q

bone remodeling important for

A

stress adaptation

148
Q

__ is secreted in response to low blood ca

A

pth

149
Q

how does pth raise blood calcium

A
  1. stimulating osteoclast activity
  2. increasing renal reabsorption while inhibiting phosphate reabsorption
  3. increasing formation of vit d
150
Q

regulators of pth

A
  1. ca levels
  2. vit d levels
  3. glucocorticoids
151
Q

vit d production beings in the

A

skin

152
Q

vit d is protective against certain cancers

A

t

153
Q

raises plasma concentrations of ca & phosphate

A

vit d

154
Q

how does vit d raises plasma concentrations of ca & phosphate

A

by increasing intestinal reabsorption of ca & phosphate & from gut & by being permissive to osteoclast activity

155
Q

vit d results in increased

A

pth

156
Q

vit d results in low

A

plasma phosphate

157
Q

vit d decreased by

A

elevated plasma phosphate

158
Q

pth stimulates excretion of __ so that the net effect is an increase in blood ca

A

phosphate

159
Q

osteoblast

A

bone forming

160
Q

widow’s hump a result of

A

spinal compression

161
Q

breakdown occurs faster than formation

A

t

162
Q

__ is inhibited when ca levels are high

A

pth

163
Q

elevation in vit d levels will inhibit

A

pth

164
Q

glucocorticoids stimulate pth production

A

t

165
Q

glucocorticoids cause osteoporosis

A

t; bc pth stimulates osteoclast activity

166
Q

sunlight far more protective at increasing vit d

A

t

167
Q

how does pth cause the production of vit d

A

pth stimulates kidneys to perform last hydroxylation for active form of vit d

168
Q

what does vit d do

A

raises plasma concentrations of ca & phosphate

169
Q

vit d promotes osteoclast activity

A

f; in order to pth to stim osteoclast activity, vit d must be present

Physio (14 decks)

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