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PHGY 210 > endocrinology > Flashcards

endocrinology Flashcards

1
Q

what is essential between the physiological processes which take place simultaneously?

A

coordination between these processes

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2
Q

how is long distance communication achieved?

A

through a number of chemical substances,

which are secreted by the releasing cells and interact with specific receptors on the distant target cells.

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3
Q

what does endocrine signalling involve?

A

Involves hormone secretion into the blood by an endocrine gland.

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4
Q

what are neurohormones?

A

Hormones involved are initially released by neurones

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5
Q

how is the hypothalamus linked to the pituitary gland

A

by a portal blood system

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6
Q

how does the portal blood system between the hypothalamus and the pituitary gland function?

A

Hormone A by the hypothalamus triggers the release of hormone B by the anterior pituitary gland. Hormone B then activates a target site (often another endocrine organ).

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7
Q

identify the type of signalling; Cell signals to adjacent target cells. No transport through blood?

A

Paracrine signaling

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8
Q

what is autocrine signalling?

A

Cell signals to self by producing hormones that interact with its own receptors.

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9
Q

what are the main steps involved in hormonal communication?

A
  • synthesis of hormone
  • release of hormone
  • transport of hormone to target site
  • detection of hormone by specific receptor
  • change in cellular metabolism
  • removal of hormone
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10
Q

what endocrine hormones are found in the brain?

A

hypothalamus

pituitary

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11
Q

what part of the pituitary gland is the extension of the hypothalamus?

A

posterior

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12
Q

which of the pituitary is neuronal?

A

posterior

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13
Q

what constitutes the hypothalamic-hypophyseal portal system

A

blood vessels of the pituitary stalk

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14
Q

what is the function of the hypothalamic-hypophyseal portal system?

A

allow Neurohormones from the hypothalamus reach the APG through these vessels.

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15
Q

how are peptide hormone synthesized?

A

synthesized by ribosomes and RNA pulled directly from the individual’s genes.

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16
Q

how are steroid and amine hormones synthesized?

A

they are not coded by DNA, but the enzymes required for their biosynthesis is coded

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17
Q

what is the other name given to protein hormones?

A

secreted protein

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18
Q

what is the additional sequence generally added to protein hormones

A

pre pro sequence

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19
Q

what is the function of the endoplasmic reticulum in sequencing of peptide hormones?

A

it Disposes of the pre sequence.

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20
Q

what is the function of the golgi apparatus in sequencing of peptide hormones?

A

Packs hormones into secretory vesicles. Disposes of

the pro sequence.

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21
Q

give a common glucocorticoid?

A

cortisol

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22
Q

give a common mineralocorticoid?

A

aldosterone

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23
Q

where are glucocorticoid and mineralocorticoids produced?

A

adrenal cortex

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24
Q

is the first ring of testosterone aromatic?

A

no

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25
Q

what is the precursor to estradiol?

A

testosterone

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26
Q

what does aromatase do?

A

it removes the methyl group from testosterone and converts it to estradiol

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27
Q

what are thyroid hormones produced from?

A

tyrosine

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28
Q

what are the main thyroid hormones?

A

T3 and T4

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29
Q

how do hormone receptors function?

A

through lock and key mechanisms –> complimentary binding

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30
Q

what are some properties of hormone receptors?

A

specificity
affinity
saturable
measurable biological effects

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31
Q

how are hormone receptors regulated?

A

up regulated: increased activity or synthesis

downregulated: decreased activity or synthesis

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32
Q

what are the 3 ways for hormones to exert effects on a target cell?

A
  1. Direct effects on function at the cell membrane.
  2. Intracellular effects mediated by second messenger systems.
    ‣ G protein coupled receptors that produce cAMP is a common type of second messenger system.
  3. Intracellular effects mediated by genomic or nuclear action.
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33
Q

which type of hormone generally exerts effect on cell mediated by genomic nuclear action?

A

steroid hormones

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34
Q

how does it function for the effect of cell to be mediated by genomic nuclear action?

A

the cell receptors goes into the nucleus to regulate gene transcription

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35
Q

how are hormonal secretions regulated?

A

through feedback mechanisms

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36
Q

what does an excess of hormone or hormone activity lead to in negative feedback loop?

A

diminished secretion of the hormone

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37
Q

what system has a double negative feedback loop?

A

the hypothalamic-pituitary end organ axis where feedback is exerted on hypothalamus and pituitary

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38
Q

whats happens if under stressful conditions there is an increase of plasma cortisol?

A

negative feedback loop will signal the hypothalamus to decrease production of CRH and the anterior pituitary will decrease ACTH production

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39
Q

what are the 2 tissues that make up the pituitary gland

A

anterior (adenohypophysis)

posterior (neurohypophysis)

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40
Q

what type of tissue is the anterior pituitary?

A

endocrine

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41
Q

what type of tissue is the posterior pituitary?

A

neural tissue

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42
Q

what do the neurohormones secreted by the hypothalamus mostly target?

A

the anterior pituitary

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43
Q

what does GnRH produced in the hypothalamus target in the anterior pituitary?

A

+ FSH and LH

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44
Q

what does GHRH produced in the hypothalamus target in the anterior pituitary?

A

+ GH

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45
Q

what does somatostatin produced in the hypothalamus target in the anterior pituitary?

A
  • GH

- TSH

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46
Q

what does TRH produced in the hypothalamus target in the anterior pituitary?

A

+ TSH

+ prolactin

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47
Q

what is Prolactin release inhibiting hormone?

A

dopamine

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48
Q

what does CRH produced in the hypothalamus target in the anterior pituitary?

A

+ACTH

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49
Q

what are the hormones secreted by the posterior pituitary?

A

Arginine vasopressin. Oxytocin.

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50
Q

what type of hormones are the hypothalamic hormones?

A

all peptide except for PIH

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51
Q

what organ do FSH and LH affect?

A

gonads

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52
Q

what role do FSH and LH play in the gonads?

A

germ cell development

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53
Q

what organs does GH affect

A

liver and many more

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54
Q

what organs does TSH affect

A

thyroid

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55
Q

what is the main function of TSH?

A

regulates secretion of T3 and T4

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56
Q

what organs does prolactin affect

A

breast

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57
Q

what is the main function of prolactin?

A

Controls breast development and milk production in females.

Facilitates reproductive function for males.

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58
Q

what does ACTH induce?

A

cortisol secretions

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59
Q

how are oxytocin and vasopressin synthesized?

A

in two hypothalamic nuclei whose axons run down the pituitary stalk and terminate in the posterior pituitary close to capillary blood vessels.

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60
Q

where are the prohormones of oxytocin and vasopressin

A

• The prohormones are processed in the secretory granules during axonal transport.

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61
Q

what is the half life of oxytocin and vasopressin? why?

A

1-3 minutes

short half life = easier to control

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62
Q

what are the functions of oxytocin in females?

A
  • uterine contractions in parturition
  • milk ejection in response to suckling
  • decreased anxiety and enhanced pro-social behaviors
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63
Q

effects of oxytocin in males?

A
  • decreased anxiety and enhanced pro-social behaviors

- ejaculation

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64
Q

how much does the thyroid gland weight

A

~15-20g

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65
Q

is the thyroid gland greater in males or females?

A

females

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66
Q

how much healthy thryoid is actually needed for proper function

A

only ~ 3g

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67
Q

what is thyroglobulin?

A

huge protein (700 000 Da) that bathes inside thyroid

68
Q

what is the function of thyroglobulin?

A

serves as a source of amine, will also function as storage for T3/T4 before released into blood

69
Q

synthesis of thyroglobulin is under control of what?

A

-TSH on pituitary

70
Q

what cells usually produce thyroglobulin and used by what cells

A

follicular cells of the thyroid and used entirely within the thyroid gland.

71
Q

how many iodines does t4 & t3 have?

A

T4: 4
T3: 3

72
Q

why is reverse T3 not a hormone

A

because it does not bind to T3/T4 receptors

73
Q

what cells are able to able to trap iodine and transport it across the cell membrane against a chemical gradient (active transport).

A

thyroid follicular cells

74
Q

what is the rate of synthesis of T3/T4 increased by?

A

TSH

75
Q

what is the release of TSH controlled by?

A

TRH

76
Q

what is the function of TSH

A

increases the production of T3/T4

77
Q

what happens when T3/T4 in blood increases?

A

negative feedback decreases secretions of TRH and TSH

78
Q

what happens in cases of iodine deficiency to T3/T4?

A

Levels in circulation decreases

79
Q

what happens to TSH under iodine deficiency?

A

it is constantly stimulated causing for thyroid to enlarge

80
Q

what are some of the effects of thyroid hormones?

A 
stimulation of calorigenesis
increase of glucose uptake in muscles
promotes glycogen
increased lipid synthesis
stimulate protein synthesis
stimulate GH secretion, 
maturation of nervous system
81
Q

does thyroid hormones increased BMR?

A

yes thus greater need for oxygen as well

82
Q

do thyroid hormones affect growth?

A

yes, growth of various organs and tissues along with development of the brain

83
Q

what may absence of thyroid hormones lead to?

A
  • Absence of thyroid hormones leads to decreases neuronal development.
  • Absence of thyroid hormones at early stages of life leads to irreversible mental retardation.
84
Q

how does the mechanism of action of thyroid hormones function?

A

same as steroid hormones

bind to target cell cognat receptors and alter transcription of the specific genes

85
Q

what type of iodine is used in radioactive plants

A

stable iodine. it limits the amount of radioactive iodine that enters the thyroid

86
Q

what type of iodine is used to treat thyroid cancers?

A

radioactive iodine

87
Q

what are some of the consequences of hypothyroidism?

A

decreased levels of T3/T4
low BMR
goiter (not always present)

88
Q

what are some of the consequences of hyperthyroidism?

A

elevated T3/T4
elevated BMR
goiter (primary or secondary origin)

89
Q

what is myxedema?

A

it is the inability to synthesize active thyroid hormones (primary hypothyroidism)

90
Q

what may be the causes to myxedema?

A
  • athrophy of thyroid
  • hasimoto’s disease (destruction of cellular compartment by antibodies)
  • non toxic goiter
91
Q

when do symptoms for infantile hypothyroidism appear and why?

A

after a few month of birth, before in belly, thyroid hormones are supplied from the mother via placenta

92
Q

what may infantile hypothyroidism lead to?

A

growth and mental retardation leads to

cretinism.

93
Q

what is Secondary hypothyroidism.?

A

Failure to synthesizes TSH in the pituitary gland.

94
Q

what is teritary hypothyroidism?

A

Failure to synthesizes TRH in the hypothalamus.

95
Q

how can hypotheroidism be treated?

A

administration of synthroid

96
Q

what is graves disease?

A

toxic diffuse goiter/ a form of hyperthyroidism

97
Q

how is graves disease caused?

A

autoimmune disease where LATS mimic the action of TSH and constantly stimulate the release of T3/T4

98
Q

what are the forms of primary hyperthryroidism?

A

graves disease and thyroid adenoma

99
Q

what happens in secondary hypothyroidism?

A

No negative feedback from increased levels of T3/T4. TSH synthesis is autonomous.

100
Q

what causes secondary hypothyroidism?

A

often a tumor to the pituitary

101
Q

what causes tertiary hypothyroidism?

A

hypothalamic tumor

102
Q

what happens in tertiary hypothyroidism?

A

No negative feedback from high T3/T4 to decrease thyrotropin releasing hormone secretions (TRH).

103
Q

what treatments can be used for hyperthyroidism?

A

surgery
remplacement therapy
use drugs that block thyroid hormone synthesis

104
Q

what are the main functions of CA2+

A

◦ Essential structural component of the skeleton.
◦ Normal blood clotting.
◦ Maintenance of the transmembrane potential with Na+ and K+.
◦ Excitability of nervous tissue.
◦ Muscle contraction.
◦ Release of hormones and neurotransmitters.

105
Q

what is the general concentration of calcium intra/extracellular?

A

10mg/100 mL

106
Q

how are plasma levels maintaiuned?

A

exchanges between bones and plasma

107
Q

what hormones greatly impact levels of circulating calcium?

A

parathyroid hormone
calcitonin
vitamin D

108
Q

which hormones increase levels of circulating calcium? which decreases?

A

parathyroid and vit D increase

decrease: calcitonin

109
Q

calcium from diet is obtained through where?

A

duodenum and upper jejunum

110
Q

what hormone increases calcium deposition in bones?

A

calcitonin

111
Q

what hormone increases Ca2+ loss via kidneys?

A

calcitonin

112
Q

what happens if plasma calcium is below 10mg/100mL

A

the parathyroid homrone will stimulate the
Reabsorption of Ca++ from the kidney.
◦ Removal of Ca++ from bones (bone resorption).

113
Q

how many parathyroid glands do we have?

A

4

114
Q

what happens if a parathyroid gland is removed?

A

will cause a severe drop in plasma calcium levels.

A Drop in plasma [Ca++] causes tetanic convulsions and death.

115
Q

what is the structure of parathyroid hormone? what is needed for its full function?

A

84 AA but only the 34 from N terminal are needed for full activity

116
Q

what is the name given to Parathyroid hormone before it is proteolytically cleaved?

A

preproparathyroid hormone

117
Q

what is the half life of parathyroid hormone?

A

3-18 minutes

118
Q

how does PTH increases levels of plasma calcium?

A
  • bone resortion; increases demineralization of the bone
  • kidney reabsorption from proximal convoluted tubules
  • stimualtes synthesis of vitamin D (Active form)
  • along with Vit D they increase absorption of Ca2+ in the gut
119
Q

where does vitamin D synthesis take place?

A

kidneys

120
Q

what controls PTH levels?

A

levels of circulating ca2+

121
Q

what symptoms are associated with hypoparathyroidism?

A

Low plasma Ca++ (hypocalcemia).
‣ Production of biologically active vitamin D is decreased.
‣ More serious clinical problems - Tetany & convulsions.
• Ca++ < 7mg/100ml leads to increased neural overexcitability = muscle spasms.
• Spasms of laryngeal muscles may lead to death by asphyxiation.

122
Q

how can hypoparathyroidism be treated?

A

administration of active vitamin D and Ca2+ supplements

123
Q

what is hyperfunction of parathyroids generally caused by?

A

parathyroid adenoma

124
Q

what symptoms are associated with hyperparathyroidism?

A
  • high vitamin D
  • high bone resorption and kidney reabsorption
  • high ca2+ in circulation (kidney stones)
125
Q

what serious problems can arise from hyperparathyroidism?

A
  • cardiac arythmias
  • depreessed neuromuscular excitability
  • calcium deposition on the walls of the blood vessels
126
Q

what treatment is used for hyperparathyroidism?

A

Surgery to remove the affected parathyroid glands & replacement therapy (1,25,D3 + Ca++).

127
Q

what sources of food can vitamin D be found in?

A

cod liver oil

fatty fish

128
Q

why is vitamin D technically not a vitamin?

A

because it can be synthesized from cholesterol

129
Q

how is vitamin D synthesized?

A

UVB light + 7-dehydrocholesterol in skin.
◦ 25-hydroxylation in the liver (
◦ 1-hydroxylation in the kidney and several
peripheral tissues (PTH controlled).
‣ The end result is 1,25-
dihydroxyvitamin D3.

130
Q

what functions does vitamin D have?

A 
Increase Ca++ absorption from the
intestine.
◦ Regulates the immune system - Anti-
inflammatory.
◦ Anticancer properties.
131
Q

what happens to vit D synthesis if calcium is low?high?

A

low: increased production of Ca2+ along with PTH
high: depressed synthesis

132
Q

what will low levels of vitamin D cause?

A

osteomalacia in adults

rickets in growing individuals

133
Q

what can absence of UVB cause?

A

VIT D deficency which may lead to bone demineralization

134
Q

is a certain skin tone more prone to being vit D deficenct?

A

darker skin tones

135
Q

what happens to patient with renal failture?

A

tends to have vit D deficency since 1-hydroxylase is not produced

136
Q

what are the 2 causes to congenital rickets?

A
  • lack of enzymes to produce vit D

- lack of VDR (bald)

137
Q

what is calcitonin?

A

a 32 SS peptide

138
Q

what manufactures calcitonin?

A

parafollicular C cell of the thyroid gland

139
Q

is calcitonin as important as vit D and PTH on calcium homeostasis?

A

no, unless thyroid gland is removed

140
Q

where are the adrenal glands located?

A

above kidney

141
Q

are the adrenal glands heavier in males or females?

A

males

142
Q

under the microscope, what does the adrenal cortex look like?

A

large lipid containing endothelial cell

143
Q

under the microscope, what does the adrenal medulla look like?

A

chromaffin cells- fine brown granules when fixed with potassium
bichromate.

144
Q

what part of the adrenal is derived from the mesoderm?

A

cortex

145
Q

what part of the adrenal is derived from the neural crest?

A

medulla

146
Q

what is produced by the adrenal cortex?

A

glucocorticoids, mineralocorticoids, progestins

147
Q

what is produced by the adrenal medulla?

A

catecholamines & some peptide hormones

148
Q

the cortex is composed of 3 distinct layers which are?

A

zona glomerulosa
zona fasciculata
zona reticularis

149
Q

what is produced in the zona glomerulosa?

A

mineralocorticoids due to presence of 18-hydroxylase

150
Q

what is produced in the zona fasciculata

A

mainly glucocorticoids due to presence of 17a-hydroxylase

151
Q

what is produced in the zona reticularis

A

glucocorticois, progestins, androgens, estrogens

152
Q

where do steroid hormones interact with steroid hormone receptors?

A

in the cytoplasm

153
Q

do steroid need active transport to travel across the cell membrane?

A

no

154
Q

where does regulation of transcription of steroid hormones take place?

A

inside the nucleus

155
Q

what are the main roles of mienralocorticoids?

A
  • Controls sodium metabolism by increasing the reabsorption of Na+ by the kidney.
  • Affects the plasma concentration of K+ and H+.
156
Q

what needs to be done in order to attain balance when pumping out certain ions?

A

balance is achieved as other ions get pumped in

157
Q

what happens if aldosterone is in hypofunction?

A

High [H+] in circulation

158
Q

what are some of the effects of glucocorticoids?

A
  • salt retention (less than mineralocorticoids)
  • effect on protein and cho metabolism
  • effect on lipid metabolism
  • antiinflammatory and immunosupressive properties
  • decrease of protein matrix of the bone
159
Q

how do glucocorticoids impact CHO and proteins?

A

increase break down of proteins into CHO along with decrease glucose uptake in muscles rapidly causes increase of blood sugar. if prolonged it may cause adrenal diabetes

160
Q

how do glucocorticoids impact lipid metabolism?

A

FFA become the primary source of energy, but isn’t fully oxidized which leads to ketosis (acetone breathe) and may also lead to hyperlipidemia and hypercholesterolemia.

161
Q

don glucocorticoid decrease or increase histamine production?

A

decrease; good for allergic reactions

162
Q

what happens to wounds under high levels of glucocorticoids?

A

do not properly heal since inflammatory response is reduced

163
Q

how are secretions of glucocorticoids controleled?

A

negative feedback on hypothalamus and anterior pituitary

164
Q

what is ACTH?

A

a 39 AA peptide hormone produced by anterior pituitary

165
Q

what may cause for adrenal hyperplasia?

A

11B- hydroxylase deficency causes for cortisol not to be produced and ACTH is left uncheck

166
Q

how can adrenal hyperplasia be treated?

A

the deficency needs to be corrected and the ACTH levels need to be restored

PHGY 210 (11 decks)

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