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VBMS 325 > module 3- endocrine > Flashcards

module 3- endocrine Flashcards

1
Q

hormone function

A

allow cells that are not beside each other to communicate in synchronized functions

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2
Q

paracrine vs neurotransmitter communication

A

P- short, local
N- long, distant

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3
Q

endocrine cells function

A

dump message into blood & only effector will be the cell that has a receptor for that message

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4
Q

neurohormone

A

nerve cell that drops a neurhormone into blood & communicates with faw away cells

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5
Q

parahormone function

A

messages to another animal

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6
Q

3 types of hormones

A

1) peptides & proteins
2) amines
3) steroids

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7
Q

amines are derived from

A

tyrosine

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8
Q

steroids

A

neutral lipids derived from cholesterol

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9
Q

peptides

A

chains of amino acids- long or short

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10
Q

what are all steroids derived from?

A

cholesterol

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11
Q

T or F: steroid structures are similar but have very different affects on the body

A

T

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12
Q

4 types of steroids & what they are

A

1) testosterone- male
2) estradiol- fermale
3) corticosterone- stress
4) aldosterone- water retention

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13
Q

why does insulin get injected, not taken in pill form

A

b/c peptides get denatured in the stomach

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14
Q

why can estrogen for birth control be taken using pills?

A

estrogen does not get denatured in the stomach

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15
Q

peptides & catecholamines are ( ) and steroids & thyroid hormones are ( )

A

hydrophilic, lipophilic

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16
Q

where are peptides produced

A

ribosomes on rough endoplasmic ret

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17
Q

preprohormone

A

long chain of amino acids

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18
Q

how are peptides synthesized steps

A

1) preprohormone is synthesized
2) pruned to prohormone
3) cut to active hormone in golgi complex
4) gets concentrated in golgi complex & packaged into vesicles to be ready for use
5) released into body via exocytosis when stimulated

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19
Q

where do the bits from cutting of the peptide hormone go?

A

used to make other things from POMC

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20
Q

steroid hormone synthesis steps

A

1) cholesterol from diet or LDL
2) enzymes modify cholesterol into hormone
3) steroid hormone is produced & secreted right away b/c they cannot be stored
4) diffuse through membrane into blood & some undergo further modifications

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21
Q

amine hormone synthesis

A

1) derived from tyrosine
2) undergoes modification
3) stored until needed
4) thyroid hormone undergoes further processing after release

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22
Q

peptides, steroids & thyroid hormone transport

A

peptides: freely in plasma or bound to carrier
steroids & thyroid hormones: dragged by plasma protein b/c they cannot dissolve

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23
Q

T or F: only free lipophilic hormones are active

A

T

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24
Q

what is the goal of hormone transport?

A

maintain hormonal equilibrium through feedback loops

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25
Q

what occurs after a free hormone has interacted with its target cell

A

it gets inactivated

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26
Q

tropic vs non-tropic hormones & their targets

A

tropic- regulate production/secretion of another hormone by acting on it
target: endocrine tissues

non-tropic: final product, acts on regular cells & does not regulate other hormones
target: non-endocrine tissue

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27
Q

T or F: hormones act like key & lock system

A

T

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28
Q

2 categories of receptor & hormone interactions

A

1) membrane receptors
2) internal receptors

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29
Q

membrane receptors

A

bind a receptor outside plasma membrane to start a chain of reactions

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30
Q

internal receptors

A

bind to specific receptors inside the cell, often produce new protein

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31
Q

where does hormone binding occur?

A

HRE (hormone response element)

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32
Q

hormone effects on transcription steps

A

1) hormone gets dropped & tries to leave cell
2) finds specific receptor & binds = activates it
3) goes to nucleus & finds HRE to activate some gene
4) cell makes a new protein

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33
Q

negative feedback loops

A

counteracts any change

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34
Q

TRH, TSH, TH- tropic or non-tropic

A

TRH & TSH= tropic
TH= non-tropic

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35
Q

when are neuroendocrine reflexes used for hormonal regulation?

A

to produce a sudden increase in hormone secretion in response to an external stimulus

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36
Q

catecholamine vs cortisol release time

A

cat- released within seconds, very fast so cannot measure

cort- peaks after 1 hour

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37
Q

what is circadian control and when is it used to regulate hormone secretion?

A

anticipatory regulation allows your body to adjust cyclical changes

example- cortisol cycle

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38
Q

when is cortisol the highest?

A

early morning

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39
Q

hasimotos disease

A

destroys thyroid hormone =no thyroid hormones

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40
Q

hormone elimination is primary through

A

urinary excretion

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41
Q

human chorionic gonadotropin hormone (hCG)

A

detecting hormone produced by the fetus

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42
Q

the response of a cell to hormone is correlated with

A

number of receptors

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43
Q

downregulation of hormones & example

A

presence of hormones reduces number of receptors on the cell

example-type II dabetes

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44
Q

type II diabetes

A

too much insulin so your cells stop responding

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45
Q

pineal gland

A

controls circadian rhythm via light/dark and secretes melatonin

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46
Q

in low light ( ) melatonin is produced

A

more

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47
Q

melatonin effects

A

sleep, blood pressure, & anti-imflammatory

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48
Q

ADH & oxytocin are released by the ( ) but produced in the ( )

A

posterior pit, hypothalamus

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49
Q

what type of diabetes is caused by ADH deficiency

A

diabetes insipidus

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50
Q

central vs nephrogenic diabetes insipidus

A

c: no ADH secretion
n: kidneys do not respond to ADH

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51
Q

prolactin vs oxytocin in relation to milk

A

p- milk production
o- milk delivery

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52
Q

what 2 hormones stop milk from being produced when not needed

A

progesterone & estrogemn

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53
Q

what hormone increases during pregancy

A

prolactin

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54
Q

how many hormones does the anterior pit produce?

A

6

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55
Q

portal system

A

2 capillary beds back to back without going through the heart

how hormones travel

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56
Q

portal system pathway

A

heart, artery, capillaries in hypothalamus (picks up hormone), veins, capillaries in anterior pit (drops hormone & picks up new one, veins, heart

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57
Q

if hypothalamus drops TRH, the anterior pit stimulates ( ) TSH

A

release of

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58
Q

hypothalamus secretes its own tropic hormone in response to

A

stress

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59
Q

what occurs if you do not have stress

A

corticosteroids have antigrowth effects

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60
Q

when does GH get released

A

when body is running out of glucose

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61
Q

overall effect of GH on metabolism

A

mobilize fat stores & keep glucose for the brain

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62
Q

indirect effect of GH on growth

A

effects are mediated by IFGs

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63
Q

how are IGF-1 stimulated

A

by GH

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64
Q

what is the most important IGF for growth

A

IGF 1

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65
Q

IGF-2 is important for

A

muscle growth

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66
Q

T or F: IGF-2 is independent of GH

A

T

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67
Q

hyperplasia

A

increase number of cells

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68
Q

hypertrophy

A

increase in the size of the cells

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69
Q

IGF-1 is important for

A

soft tissue and bone growth

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70
Q

T or F: bone is a living tissue

A

T

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71
Q

what are the 2 components of bone

A

cells & extracellular matrix

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72
Q

why is a bone strong

A

it is calcified

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73
Q

what is a long bone made of?

A

diaphysis, epiphysis & epiphyseal plate

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74
Q

long bone formation steps

A

1) cylindrical shaft- diaphysis
2) articulating knobs at both end- epiphysis
3) layer of cartilage separating the 2- epiphyseal plate

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75
Q

how do bones grow thicker vs longer

A

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

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76
Q

T or F: thickness of cartilage reflects how much growth you have left

A

T

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77
Q

what is the epiphyseal plate made of

A

chondrocytes (non-calcified)

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78
Q

how does a bone grow?

A

1) chondrocytes divide & start creating a new layer
2) everything gets pushed down to grow the knob
3) calcification of extracellular matrix
4) dead chrondocytes are cleared by osteoblasts
5) osteoblasts deposit bone over top of everything, die & become regulate bones
6) plate shifts up & bone gets longer

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79
Q

osteoblast vs osteoclasts

A

osteoblasts- builds
osteoclasts- blasts

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80
Q

GNRH vs GHIH stimulatory or inhibitory? where do they come from?

A

GNRH- stimulatory
GHIH- inhibitory

comes from hypothalamus

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81
Q

high amino acid concentration & low fatty acid concentration does what to GH

A

increase

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82
Q

growth hormone deficiency
- cause
- effect on newborn vs adult
- treatment

A

caused by pituitary issues or congential

newborn: dwarfism
adult: no effects on growth, but see effects on soft tissues

treatment: injection of GH

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83
Q

provacative test

A

tests for GH deficiency
injects insulin & if peaks then normal, but if no peak then GH problems

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84
Q

growth hormone hyperproduction
- cause
- effect on children vs adults
- treatment
- how to diagnose

A

cause: pit issues or congenital

children: gigantism
adults: acromegaly - soft tissue overgrowth

treatment: injection of GHIH

diagnose: if given glucose, GH will not drop

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85
Q

acromegaly

A

constant production of GH & causes soft tissue to continue growing

86
Q

what is considered gigantism

A

over 2.2 meters

87
Q

T or F: HGH (human growth hormone) does not have performance enhancement

A

T

88
Q

thyroid gland shape/location

A

sits like a bowtie down the front of the neck

1 gland- 2 lobes

89
Q

follicular cells

A

spheres full of fluid that stores TH

90
Q

what is the backbone to TH

A

thyroglobulin

91
Q

where is iodine stored

A

colloid of thyroid gland

92
Q

follicular cells produce what 2 iodine containing hormones?

A

T3 & T$

93
Q

to make TH, you need

A

tyrosine & iodine

94
Q

what form of TH is the major biologically active form?

A

T3

95
Q

T or F: most TH is bound to plasma proteins

A

T

96
Q

3 main things TH are supposed to do:

A

metabolic effects, cardiovascular effects & growth/nervous system effects

97
Q

what can be used to measure BMR

A

O2 consumption

98
Q

endotherms vs ectotherms TH levels

A

en- high
ec- low

99
Q

3 cardiovascular effects of TH

A

increase HR, cardiac output & heat production

100
Q

T or F: GH cannot be secreted properly if not enough TH

A

T

101
Q

T or F: AP transmission can be slowed down if not enough TH

A

T

102
Q

dwarfism on GH levels

A

GH is normal, but b/c there is not enough TH, the GH could not do its job

103
Q

T or F: hair loss occurs with low TH

A

T

104
Q

SNS effect on TH

A

increase

105
Q

T or F: TH controls metamorphosis

A

T

106
Q

what is the most important regulator of the TH secretion

A

TSH (thyroid stimulating hormone)

107
Q

how to increase TH

A

size & number of cells

108
Q

T or F: TH release is slow

A

T

109
Q

why does TRH production increase in cold newborn mammals?

A

kickstarts negative feedback loops to increase TH b/c they cannot thermoregulate on their own

110
Q

hypothyroidism
- what is it
- causes
- symptoms

A

low TH levels
not enough TRH, damage to thyroid gland itself, no iodine
cold, weight gain, hair loss
goiter

111
Q

disease formed when hypothyroidism from birth

A

cretinism

112
Q

why does hypothyroidism from birth lead to cretinism

A

GH needs enough TH to do its job so with too little TH=GH cannot do its job

113
Q

cretinism

A

physical & mental growth impairment

114
Q

treatment to hypothyroidism

A

thyroxine & iodine supplement

115
Q

hyperthyroidism

A

too much TH, more signalling for TSH which causes thyroid gland to grow = goiter

116
Q

how to treat hyperthyroidsm

A

remove thyroid gland & low iodine diets

117
Q

2 layers of adrenal glands

A

1) outer: adrenal cortex- secretes steroids
2) inner: adrenal medulla - secretes catecholamines

118
Q

3 layers to adrenal cortex

A

1) zona glomerulosa (outermost)
2) zona fasiculata (middle & largest)
3) zona reticularis (inner)

119
Q

3 main jobs of the adrenal glands

A

salt, sugar, sex

120
Q

3 main categories of steroids

A

1) mineralocorticoids
2) glucocorticoids
3) sex steroids

121
Q

mineralcorticords

A

electrolyte balance, aldosterone, produced by glomerulosa

122
Q

glucocorticoids

A

glucose, lipid & protein metabolism
- cortisol & corticosterone
- produced by fasicultata & reticularis

123
Q

most important sex steroid

A

DHEA
- produced by fasiculata & reticularis

124
Q

what carries only glucocorticoids

A

transportin

125
Q

4 metabolic effects of glucocorticoids

A

1) stimulate gluconeogenesis
2) inhibit glucose uptake
3) stimulate protein degradation
4) facilitate lipolysis

126
Q

permissiveness

A

one hormone must be present in adequate amount for full exertion of another hormones effect

127
Q

lack of cortisol can cause

A

hypovolemia = not enough blood flow

128
Q

stress

A

generalized response to any factor that overwhelms the bodys ability to maintain homeostasis

129
Q

how to glucocorticoids help manage stress

A

release of them increases the availability for blood glucose to protect the brain from malnutrition

130
Q

lymphocytes release ( ) when activated

A

ACTH

131
Q

low, high, very high stress effects

A

low: no anti-inflammatory effects
high: anti-inflammatory effects
very high: immunosuppression

132
Q

glucocorticoids inhibits the secretion of ( ) and ( )

A

CRH & ACTH

133
Q

what factors influence secretion of glucocorticoids

A

stress & circadian rhythm

134
Q

HPA suppression on glucocorticoids

A

inhibits release of ATCH = adrenal gland is not stimulated = little cortisol available

135
Q

ATCH is responsible for the adrenal cortex ( )

A

size

136
Q

what can occur if a steroid drug is stopped immediately

A

vomiting, fatigue, low BP

137
Q

T or F: adrenal cortex produces androgens & estrogens in both sexes

A

T

138
Q

the only adrenal sex hormone that has significant biological effects is

A

DHEA

139
Q

what does androgens in females cause

A

pubic hair, armpit hair, sex drive & puberty growth spurt

140
Q

hyerpadrenocorticisim
- what is it
- disease example
- cause
- symptoms
- treatment

A
  • too much cortisol caused by too much CRH or ATCH
  • cushings
  • increased appetite = weight gain & high BP
  • destroy adrenal cortex to stop producing cortisol
141
Q

hypoandrenocorticism
- what is it
- disease example
- cause
- symptoms
- treatment

A

too little cortisol
- addisons disease
- aldosterone deficiency
- weak & lethargic
- glucocorticoids & mineralcorticoids (aldosterone)

142
Q

how do chromaffin cells work in the adrenal cortex

A

dump their neurohormones directly into the blood & do not send signals to other neurons

143
Q

what do chromaffin cells release

A

epinephrine & some NE

144
Q

only ( ) is released as NT from post-ganglionic fibre but ( ) and ( ) are released as hormones from adrenal medulla

A

NE, NE & epinephrine

145
Q

how is NE released from chromaffin cells

A

exocytosis

146
Q

how is catecholamine secretion from adrenal medulla controlled

A

SNS input

147
Q

5 effects of epinephrine

A

1) cardiac effects = increase CO
2) a-1 = vasoconstriction & b-2 causes selective vasoconstriction
3) respiratory effects = bronchodilation
4) metabolic = glycogenolysis & increase metabolic rate
5) less salivation = no need to digest

148
Q

catecholamine function

A

TH increase adrenergic receptors & cortisol

149
Q

T or F: everything increases blood glucose level but not insulin

A

T

150
Q

slow vs rapid stress responses

A

slow= CRH
rapid= CNS

151
Q

epigenetic effects

A

infant rearing modifies activation of HPA axis = can transfer via genetics

152
Q

the number of glucocorticoid receptors is related to

A

HPA axis

153
Q

3 fuel molecules

A

protein, carbs & fats

154
Q

2 complications to interconversion of nutrients

A

1) need energy released during fasting periods
2) brain needs continuous energy but only can use glucose

155
Q

normal range of glucose

A

70-100mg/ml

156
Q

sorbitol

A

stays in eyes & causes cataracts due to long term high concentrations of glucose

157
Q

glucose homeostasis prevents ( hypoglycemia) and ( ) hyperglycemia

A

short term, long term

158
Q

HbA1c test

A

tests blood glucose level over last 3 months

more free glucose = good at controlling glucose

159
Q

3 alternate energy sources

A

glycerol, lactate, ketones

160
Q

when is the only time the brain can use a non-glucose energy source

A

use ketones during starvation

161
Q

beta vs alpha cells

A

b- insulin synthesis & secretion
a- glucagon

162
Q

when are delta cells released

A

high glucose & AA in blood

163
Q

overall effect of insulin

A

decrease blood glucose concentration, AA & FA

164
Q

GLUT

A

glucose transporter, moves glucose into a cell so it gets methylated & trapped

165
Q

GLUT 1, 3 & 4

A

1- moves glucose through blood brain barrier (insulin-independent)
3- transport glucose into neurons (insulin-independent)
4- release via exocytosis to increase absorption when insulin is detected (insulin-dependent)

166
Q

why does exercise help with managing diabetes

A

it can mimic activity of insulin & absorb all the extra glucose

167
Q

insulin control of beta cells for high vs low glucose

A

high: activates beta cells = release insulin
low: inhibits beta cells = no insulin release

168
Q

glucagon has ( ) effects of insulin

A

opposite

169
Q

glucagon control on alpha cells for high vs low blood glucose

A

high: inhibits alpha cells = no glucagon secretion
low: activates alpha cells = glucagon secretion

170
Q

diabetes mellitus

A

elevated blood glucose levels

171
Q

type 1 vs 2 diabetes

A

1) insulin dependent
- no insulin produced
- genetic

2) insulin independent
- insulin produced but cells stop responding
- mature onset

172
Q

chances of getting diabetes increases after the age of

A

40

173
Q

long term effects of diabetes

A

blindness & leg pain

174
Q

prevention of diabetes

A

avoid sugar spikes, work out, lose weight

175
Q

how can fiber diets help with preventing diabetes

A

can slow down rate your body produces sugar

176
Q

what is one of the most tightly controlled variable

A

calcium

177
Q

short vs long term calcium homeostasis

A

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

178
Q

where is 99% of Ca found

A

bones & teeth

179
Q

bone fluid

A

liquid layer around hard layer so need to decrystalize it to get ions

180
Q

2 timescales of Ca regulation

A

short- give ions of Ca to bones
long- control how much Ca to keep & excrete

181
Q

primary scale of short term vs long term calcium regulation

A

short: rapid exchange between bone & ECF and via urine

long: diet & reabsorption

182
Q

parathyroid gland function & secretion

A

control Ca regulation & release parathyroid hormone (PTH)

183
Q

effect of PTH

A

increase Ca in plasma

184
Q

what happens if you have no PTH

A

asphyxia

185
Q

how do Ca pumps work

A

parathyroid gland detects low Ca, PTH goes to Ca pump & the pump grabs Ca from bone & pumps it out to plasma

186
Q

fast vs slow exchange of Ca from bone fluid

A

fast: Ca pump takes Ca from bone fluid & into plasma

slow: bone must be dissolved by osteoclasts= Ca produced for bone fluid to store

187
Q

osteoblasts are derived from ( ) once trapped inside bone they become ( )

A

stroma cells, osteocytes

188
Q

osteoclasts are derived from ( )

A

macrophages

189
Q

bone spurs

A

natural bone growth in response to tension & creates a bump

190
Q

estrogen increases ( ) apoptosis

A

osteoclast

191
Q

T or F: adults cannot deposit Ca into bones anymore, just strengthen the outside layer

A

T

192
Q

osteoporosis

A

taking all Ca away from bone

193
Q

<6 vs >6 phosphorus levels & bone

A

<6= liquid form
>6= crystalizes

194
Q

if phosphate increass = plasma calcium ( )

A

decreases

195
Q

hypocalcemia

A

try lower plasma phosphate & increase plasma calcium concentrations

196
Q

T or F: you need P & Ca to make bones

A

T

197
Q

calcitonin

A

produced by C cells in the thyroid, decreases Ca plasma concentration

198
Q

short vs long term calcitonin

A

short- decreased Ca movement into plasma
long- inhibits osteoclasts

199
Q

T or F: vitamin D is an essential nutrient

A

T

200
Q

2 ways vitamin D gets activated

A

sunlight or diet

201
Q

3 steps to activate vitamin D

A

1) sunlight
2) liver (add HO group)
3) kidney (add another HO group)

202
Q

vitamin d3 requires two ( ) groups to be activated

A

hydroxyl

203
Q

calbindin

A

transporter for Ca

204
Q

3 functions of vitamin D

A

1) Ca absorption
2) phosphate absorption
3) bone responsiveness to PTH

205
Q

overall function of vitamin D

A

long term calcium balance

206
Q

hyperparathyroidism
- what is it
- cause
- symptoms

A

excess secretion of PTH
low Ca & vitamin D diets or tumor of parathryoid gland
kidney stones, weak bones

207
Q

vitamin D deficiency
- cause
- symptoms

A

not enough sun exposure or low diet supplementation
- low absorption of Ca
- rickets

208
Q

rickets

A

soft bones that bend under pressure of body weight = arched legs

209
Q

milk fever & treatment

A

hypocalcemia
IV or sub-q calcium

210
Q

milk fever prevention

A

high Ca diets to trigger calcitonin pathway

VBMS 325 (17 decks)

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