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Biochem Final > Endocrine > Flashcards

Endocrine Flashcards

1
Q

what is an endocrine hormone?

A

hormone released by gland into blood

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2
Q

what is a paracrine hormone?

A

hormone released by neighboring cell effecting neighboring cell

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3
Q

what is an autocrine hormone?

A

hormone made by that cell that acts on itself

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4
Q

what are some examples of polypeptide hormones?

A

ACTH
angiotensin II
calcitonin
glucagon
insulin
GH
PTH
ADH

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5
Q

What are some examples of steroid hormones?

A

Aldosterone
Cortisol
Calcitrol
estradiol
progesterone
testosterone

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6
Q

what are some examples of amine hormones?

A

epinephrine
norepinephrine
T4
T3
Melatonin

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7
Q

epinephrine is syn from which amino acid?

A

tyrosine

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8
Q

thyroid hormone (T3/4) are derived from?

A

tyrosine

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9
Q

what ion do you need to make thyroid hormone?

A

iodide

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10
Q

how are peptide hormones synthesized?

A

in inactive form as pre-prohormone

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11
Q

where are peptide hormones made?

A

RER

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12
Q

increase in what ion stimulates the release of peptide hormones?

A

Ca

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13
Q

how are steroid hormones made?

A

cholesterol

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14
Q

how are steroid hormones released?

A

biosynthetic pathway
–enzyme expression
–acute regulation via protein phosphorylation

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15
Q

all biosynthetic androgens have ___ carbons, a biosyn estrogens have ____ carbons

A

19, 18

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16
Q

what is the more potent form of testosterone called?

A

DHT

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17
Q

testosterone is the precursor to what other hormone?

A

17-b–estradiol

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18
Q

what is the rate limiting step of steroid hormone synthesis?

A

pregnenolone

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19
Q

what is the first step or steroid hormone syn?

A

cholesterol cleaved by CYP11A1 gene to convert cholesterol into pregnenolone
**stAR

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20
Q

how is stAR reguated?

A

protein phosphorylation

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21
Q

pregnenolone is the precursor for which hormones?

A

mineralocorticoids
glucocorticoids
Androgens
Estrogen

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22
Q

what is needed for gucocorticoid and androgen syn

A

P450c17

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23
Q

what are some characteristics of steroid hormones?

A

-lipid soluble
-carrier protein in blood
hours/days
intracellular receptor
receptor-hormone

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24
Q

what are some characteristics of peptide hormones?

A

water sol
no carrier protein
lasts mins in plasma
cell surface receptor
2nd messenger syst

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25
Q

what effect does the stroid hormone carrier protein have on the hormone?

A

influences potency and lifetime

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26
Q

where do steroid hormone receptors bind?

A

hormone response elements on DNA (increase or decrease transcription)

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27
Q

how is the equilibrium relationship of steroid hormone and receptorexpressed?

A

Kd

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28
Q

a steroid hormone with higher affinity will have what Kd?

A

lower Kd
less likely to dissociate from the carrier protein and enter the cell

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29
Q

What changes does carrier protein binding effect?

A

prolongs half life
buffers
controls potency

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30
Q

what happens if more free protein enters the cell?

A

more hormone is released from HP?

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31
Q

on a nuclear receptor, activation domain 1 and 2 interact with:

A

co- repressors and co activators

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32
Q

on nuclear receptors DNA binding domain contains:

A

zinc fingers that interact with DNA

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33
Q

in the hormone binding domain what happens?

A

recognition of specific hormones biding induces dimerization

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34
Q

what are examples of hormones that use a tyrosine kinase receptor?

A

insulin, GH, PR

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35
Q

what are some examples of hormones that use G protein receptors?

A

cAMP, IP3, DAG/ Ca

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36
Q

apha is a _____

A

GTPase (inactive with GDP, active with GTP)

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37
Q

what are some key features of 2nd messenger systems?

A

-specificity
-amputation
augmentation
-rapid signal termination

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38
Q

what does alpha i do?

A

decrease adenylate cyclase, decreases cAMP

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39
Q

what does alpha q do?

A

stimulated phospholipase C, increase IP3, DAG, Ca2, PKC activated

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40
Q

what does alpha s do?

A

stimulates adenylate cyclase
increase cAMP, PKA activated

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41
Q

Which of the following is most likely to occur in hepatocytes, if the Gas subunit is constitutively active?
A. Decreased conversion of ATP to cAMP.
B. Inhibition of protein kinase A.
C. Increased glycogen synthesis.
D. Unregulated release of blood glucose.
E. Decreased glycogenolysis.

A

D. Unregulated release of blood glucose.

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42
Q

what are the steps for the DAG, Ca second messenger system?

A

–Hormone binding to the
receptor activates Gaq
–Gaq-GTP activates PLC
–PLC generates IP3 and DAG.
–IP3 binding to its receptor
causes release of Ca2+ from
ER
–DAG and Ca2+ activate protein kinase C

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43
Q

The IP3 Receptor is a _________ Calcium channel

A

Ligand Gated

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44
Q

____ binding causes the ____ receptor to open

A

IP3, IP3
(ca flows from ER to cytosol)

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45
Q

what are some examples of episodic hormone fluctuation levels?

A

sucking, food intake, exercise

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46
Q

what is an example of a pulsatile hormone?

A

lutinizing hormone

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47
Q

where do steroid hormones degrade?

A

outside of cell, dependent on lifetime of carrier-protein hormone complex

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48
Q

how are conjugated steroids excreted?

A

70% in urine
20% feces

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49
Q

how are peptide hormones degraded?

A
  • Proteases in the blood
  • Proteases in the cell surface
  • Receptor-mediated endocytosis
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50
Q

what type of regulation occurs with steroid hormones

A

feedback inhibition

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51
Q

Big Concept: cortisol, thyroid hormone, sex
steroid hormones inhibit their production at the
level of the hypothalamus and anterior pituitary.
(Examples of long-feedback loop)

A

know this

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52
Q

what are the categories for hormone function?

A

1) utilization and storage of fuels; 2) maintenance of complex internal environment;
3) reproduction;
4) growth and development

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53
Q

Amines synthesized from tyrosine are:

A

epinephrine, norepinephrine; thyroxine/T4; triodothyronine/T3

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54
Q

are steroid hormones stored?

A

no

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55
Q

how are polypeptides and glycoproteins made?

A

synthesized from transcription and translation of genes

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56
Q

how are polypeptide hormones secreted?

A

inactive, as pre-pro-hormone, stored in membrane

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57
Q

Describe effects of plasma binding proteins on hormone levels and actions on target cells.

A

a. Steroid and steroid related proteins are bound to carrier proteins in the blood. The steroid carrier proteins buffer changes in blood steroid levels and modulate biological availability.
b. Some peptide hormones (like IGFs) are also bound to carrier proteins

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58
Q

what is the posterior pituitary called? why?

A

neurohypophysis- contains nerve termina endings whose cells ie in the hypothalamus

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59
Q

what is the anterior pituitary called?

A

adenophyopsisis

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60
Q

which part of the pituitary is considered a true endocrine gland?

A

anterior

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61
Q

what is the hypothalamus?

A

collection of neurons that synthesize and secrete peptide hormones in PUSATIE fashion

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62
Q

where do hypothalamic hormones act and how to they get there?

A

released to hypophyseal portal system and act on cells of the AP

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63
Q

what kind of hormones are released from the hypothalamus?

A

peptide

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64
Q

hypothalamic hormones are produced in and released from where?

A

neurons

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65
Q

how are peptide hormones produced in HTs?

A

An influx of Ca2+ through voltage-gated calcium channels
stimulates exocytosis of membrane vesicles containing
the peptide hormone

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66
Q

how are HP hormones released?

A

release from hypothalamic neurons is coordinated and
pulsatile TO HYPOSEA PORTA SYSTEM.

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67
Q

Hormones released into the hypophyseal portal system act on cells of the

A

anterior pituitary (adenohypophysis)

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68
Q

how are posterior pit hormones synthesized and reIeased?

A
  1. **OT and VP are synthesized in neuronal cell bodies in the hypothalamus (either paraventricular nuclei or supraoptic nucleus)
  2. **OT and VP are released from nerve terminal endings in the posterior pituitary.
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69
Q

what does oxytocin do?

A

**Uterine contractions
**Milk secretion
(mammary myoepithelia)

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70
Q

what does vasopressin do?

A

**Water resorption (kidney) ACTH release (AP)
**Vasoconstriction (vascular s.m.)

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71
Q

what are some other names for vasopressin?

A
  1. Antidiuretic Hormone (ADH)
  2. Vasopressin (VP)
  3. Arginine vasopressin (AVP)
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72
Q

what increases OT secretion?

A

ESTROGEN
suckling
cervical stretch

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73
Q

what is benefit of breast feeding after birth?

A

promotes uterine contractions to get placenta and other things out

74
Q

what decreases OT secretion?

A

progesterone

75
Q

what stimulates VP?

A

❑ >2% increase in osmolality of
ECF, (Osmoreceptors in the brain)
❑ >10-15% decrease in blood
volume (BP), Low pressure receptors in the left atrium of the heart
❑ Sensitivity to osmolality
increases with decreasing
blood volume.

76
Q

what does VP do?

A

makes you retain water to add back to blood

77
Q

what receptors does vasopressin trigger to hep retain water?

A

AQP2 (adds them to Lumina membrane, VP bind requires VP 2 receptor)

78
Q

what happens in absence of VP?

A

AQP2 removed by endocytosis

79
Q

what can occur with inadequate secretion or utilization of VP?

A

diabetes incipitus (excessive thirst and urination)

80
Q

what are some genetic causes for issues with vasopressin?

A

➢ Neurogenic DI: vasopressin deficiency
❖Mutations in neurophysin II
➢ Nephrogenic DI: kidney resistant to vasopressin
❖Mutations in VP V2 receptor
❖Mutations in AQP2 channe

81
Q

what are the two AP hormones that can make direct changes to target organ?

A

Growth hormone and prolactin

82
Q

CRH stimulates corticotropes to produce POMC and release its major product _____.

A

ACTH

83
Q

GHRH (somatocrinin) stimulates
sommatotropes to release ____

A

GH

84
Q

TRH stimulates thyrotropes
to release

A

TSH

85
Q

GnRH stimulates gonadotropes to release _____

A

FSH and LH

86
Q

GHRIH (somatostatin) inhibits
the release of ____

A

GH

87
Q

what is the AP hormone that is under tonic inhibition from the hypothalamus? (what controls it)

A

prolactin (dopamine)

88
Q

memorize hormone chart on side 309

A

put some in cards

89
Q

What does ACTH act on and what does it do?

A

Adrenal Cortisol
Chronic stress

90
Q

What does TSH act on and what does it do?

A

Thyroid, T3, T4
Energy production
(fuel metabolism, BMR)

91
Q

What does LH, FSH act on and what does it do?

A

gonads (test/est/prog)
Reproduction
Sperm production
Ovulation, Menstrual Cycle
Pregnancy

92
Q

What does GH and -GH act on and what does it do?

A

IGF-1
Increases: blood glucose,
lipolysis adipose (GH)
Cell Growth (GH, IGF1)

93
Q

What does - GH act on and what does it do?

A

Mammary Gland
Milk production

94
Q

what does Proopiomelanocortin (POMC) do?

A

an Anterior Pituitary Pro-Hormone also present in
Neurons, Melanocytes and Keratinocytes

95
Q

corticotropes express what and what is their products?

A

Corticotropes express PC1
Products: ACTH, B-lipotropin

96
Q

Corticotropes express _____ which contains ______
what does it do?

A

ACTH
a-MSH
✓ Stimulates cortisol synthesis in adrenal gland
✓ In excess, stimulates melanin production in melanocytes

97
Q

Melanocytes and Keratinocytes express what?

A

a-MSH
✓ Stimulates melanin production via MC1 receptor
✓ Melanin produced provides protection from u.v. radiation

98
Q

what is important about the glycoprotein family of anterior pit hormones?

A
  • TSH, FSH, LH (pituitary basophils); hCG Placenta
  • Two subunits  + 
  • Both required for activity
  •  subunits same
  •  subunits confer specific biological function
99
Q

what is significant about the growth/prolactin family?

A
  • GH/PRL/hPL family similar structure and sequence identity
  • GH most abundant pituitary hormone
  • GH species specific
    ✓ GH from other non-primates no effect on humans (imp cause issues with it cant be supplemented by other animas)
100
Q

what is the most abundant AP hormone?

A

GH

101
Q

Describe the relationship between pro-opiomelanocortin (POMC) and the hormones derived from it.

A
  • POMC is the prohormone for ACTH, a-melanocyte stimulating hormone (a-MSH). ACTH contains amino acids encoding a-MSH which stimulates melanin production in melanocytes and can lead to hyperpigmentation of the skin.
102
Q

what stimulates GH release?

A
  • Hypoglycemia
  • Decreased FA’s
  • AA’s (arginine)
  • Exercise
  • Sleep Stages
  • Estradiol
  • Required (thyroid hormone
103
Q

if you are conceted a patient has not enough GH how can you test?

A

give sugar drink and see what happens

104
Q

what conditions inhibit GH release?

A
  • Hyperglycemia
  • Elevated FA’s
  • IGF-1
105
Q

how does IGF get through ECF?

A

on binding protein, not free fIoat, this ensured targeted delivery of free igf to igf receptors

106
Q
  • _____ is the major source
    of IGF-1 in the blood.
A

Liver

107
Q

what stim growth in bone?

A

GH and locally produced IGF-1 stimulate growth in bone

108
Q

______ stimulates prechondrocyte in germinal zone to differentiate into chondrocytes and secrete _____

A

GH, IGF-1

109
Q

what stim chondrocytes to proliferate?

A

Local IGF-1 stimulates
chondrocytes to proliferate

110
Q

what prevents growth in long bones?

A

epiphyseal pate closure

111
Q

somatostatin is stimulated by

A

glucose and fatty acids

112
Q

GH stimulates_____ synthesis
and secretion.

A

IGF-1

113
Q

_____ is the main
source of IGF-1 in the blood

A

Liver

114
Q

IGF-1 inhibits ____

A

GH release

115
Q

what stimuates somatocrinin or GHRH?

A

Stress*
Exercise
Sleep stages
Decreased glucose
Increased a.a.’s

116
Q

Which hormone could restore growth when the GH receptor does not respond to GH?

A

IGF-1

117
Q

too much GH in aduts causes

A

acromegaly (enarged tounge

118
Q

Which hormones are peptide hormones synthesized in cell bodies in the hypothalamus; released from nerve terminal endings in the posterior pituitary

A

Oxytocin and vasopressin

119
Q

oxytocin:

A

stimulates uterine contractions during parturition and contraction of myoepithelia and milk ejection during lactation. Release stimulated by suckling, “let down” reflex, cervical stretch from uterine contraction (positive feedback loop).
Estrogen stimulates OT release; progesterone inhibits OT release

120
Q

vasopressin: adh or antiduretic hormone:

A

Humans require arginine vasopressin.
ADH decreases osmolality of the ECF by increasing water resorption in the kidney by
stimulating Vasopressin V2 GPCR receptors, increase in cAMP/PKA and increase in insertion of aquaporin 2 channels into the luminal plasma membrane of kidney collecting duct cells. Stimuli: ≥2% increase in osmolality (i.e. NaCl) of ECF, ≥10%
decrease in BP. Sensitivity to osmolality increases with decreased BP.

121
Q

Diabetes incipidus is caused by

A

inadequate production or utilization of ADH

122
Q

neurogenic DI is caused by

A

vasopressin deficiency, mutations in neurophysin 2 part of ADH prohormone; Nephrogenic DI kidney resistant to ADH, causes mutations in either vasopressin V2 receptor or the AQP2 channel.

123
Q

Hypothalamic hormones are ____ released from neurons in coordinated ____
secretion pattern

A

peptide, pulsatile

124
Q

TSH (AP): stimulates
what inhibits this?

A

thyroid gland to produce T3/T4 which increase fuel metabolism
and basal metabolic rate (BMR). Feedback inhibited by T3.

125
Q
  • ACTH (AP): stimulates
    what inhibits this?
A

the adrenal gland to produce cortisol which raises blood
glucose. Feedback inhibited by cortisol.

126
Q
  • FSH/LH (AP): stimulates
    what inhibits?
A

estradiol/testosterone production in ovary and testes. LH stimulates progesterone in ovary. Feedback inhibited by estradiol

127
Q

GH stimulates lipolysis of TGs in adipose and release of insulin like growth factor 1 (IGF1), it inhibits glucose uptake in muscle. Together GH and IGF1 promote growth in all tissues. GH release is stimulated by low blood glucose via somatocrinin release from the hypothalamus

A
128
Q

what are the effects of thyroid hormone in adults?

A
  • Increase BMR
  • Increase O2 consumption
  • Increase cardiac output
  • Stimulates metabolism of fat, carb. and proteins
  • Induces many enzymes
129
Q

what does thyroid hormone do in children?

A
  • Growth and maturation of skeletal bone
  • Vital for development of the CNS
    – Deficiency, untreated immediately after birth, leads to
    irreversible brain damage.
130
Q

thyroid hormone is derived from

A

tyrosine and iodide

131
Q

TSH stimulates synthesis of:

A

T3 and T4

132
Q

what transports iodide into the lumen?

A

pendrin

133
Q

thyroid hormone synthesis requires?

A

thyroglobulin and iodide

134
Q

how can iodide be transported against its electrochemical gradient

A

Na/I symporter

135
Q

____________ incorporates I- into Tyr on intact Tgb to form DIT

A

Thyroid peroxidase

136
Q

Thyroid peroxidase couples
two _____ to make _____

A

DIT to make T4 on Tgb

137
Q

what is one difference between T3 and T4?

A

T4 is not as potent as T3

138
Q

what is tertiary hypothyroidism

A

defect in hypothalamus

139
Q

what is secondary hypothyroidism?

A

defect in pituitary

140
Q

what is primary hypothyroidism?

A

defect in thyroid gland

141
Q

Predict the TSH and T3/T4 levels for Primary Hypothyroidism

A

TSH: high
T3/4: low

142
Q

Predict the TSH and T3/T4 levels for Secondary Hypothyroidism

A

TSH: low
T3/4: low

143
Q

Predict the TSH and T3/T4 levels for Tertiary Hypothyroidism

A

TSH: low
T3/4: low

144
Q

what does TRH test measure?

A

increase in pituitary TSH

145
Q

in a 1* hypothyroidism TRH dependent stimulation testing what is the result?

A

TSH elevated before TRH;
normal pituitary response

146
Q

in a 2* hypothyroidism TRH dependent stimulation testing what is the result?

A

TSH suppressed/undetectable;
no pituitary response.

147
Q

in a 3* hypothyroidism TRH dependent stimulation testing what is the result?

A

delayed TSH pituitary response

148
Q

Name possible causes for primary hypothyroidism

A

iodide def
def of thyroid peroxidase

149
Q

what is the Rate-limiting step of adrena cortica steroid hormones?

A

cholesterol to pregnenolone
catalyzed by p450scc,
regulated by STAR
VERY IMP

150
Q

________________________is required for synthesis of cortisol and DHEA

A

p450c17 hydroxylase lyase

151
Q

_______ is required for synthesis of aldosterone and cortisol

A

p450c21

152
Q

what can happen with a p450c21 deficiency?

A
  • impaired aldosterone and cortisol synthesis
  • elevated DHEA
153
Q

Glucocorticoids named for ?

A

their ability to raise blood glucose

154
Q

In absence of cortisol, even short periods of fasting result in ___________

A

catastrophic hypoglycemia

155
Q

In liver, cortisol:

A
  • Stimulates GN
  • Stimulates glycogen synthesis
156
Q

Glycerol used by liver as a precursor for

A

gluconeogenesis

157
Q

In adipose:
Cortisol stimulates

A

lipolysis of TGs

158
Q

In muscle, cortisol:

A
  • Stimulates protein degradation
  • Decreases glucose uptake
159
Q

what is the chain of rxn for cortisol release?

A

CRH, ACTH, cortisol from adrenal gland

160
Q

what does cortisol inhibit?

A

CRH and ACTH

161
Q

Primary hypocortisolism causes increase or decrease in what?

A

ACTH: high
Cor: ow

162
Q

hypercortisoism from oray administed cortiso causes what change?

A

inc cort
dec ATCH

163
Q

what happens with cushing syndrome?

A

weight gain, rounding face, muscle weakness, thin fragile skin, high BP (cause corto)

164
Q

what does Aldosterone do?

A

Stimulates Na+ resorption and
K+ excretion

165
Q

what triggers synthesis of Aldosterone?

A

✓ Angiotensin (AII)
✓ Elevated K+ in ECF.

166
Q

What does RAAS do?

A

Increases Na+ & BP, Decreases K+

167
Q

what activates RAAS?

A

K+, decrease in BP, Na+ levels

168
Q

ANG II stimuates:

A

✓ Increases BP
✓ Stimulates aldosterone
synthesis/release
✓ Stimulates ADH release

169
Q
  • Aldosterone stimulates
A

✓ Na+ resorption, K+ excretion
* Low BP stimulates renin release
from kidney
* Renin converts Angiotensinogen to A-I
* ACE converts A-I to A-II K+

170
Q

what is Addison’s disease?

A

adrenal insufficiency
causes weakness, dec BP, dec bood sugar

171
Q

what are eicosanoids?

A

–Derived from essential fatty
acids: w6, linoleic acid & w3,
linolenic acid.
–Regulate inflammatory response, smooth muscle contraction, hemostasis

172
Q

Linoleic acid is converted to ______ and stored in phospholipid membranes

A

arachidonic acid (AA)

173
Q

PLA2 activity is decreased by

A

glucocorticoids
(inc by cytosol Ca and protein kinase C)

174
Q

Cyclo-oxygenase converts AA into
PGH2 a precursor for:

A

prostaglandins and thromboxanes (TXA2).

175
Q

Cyclo-oxygenase is inhibited by:

A
  • Irreversibly inhibited by aspirin
  • Reversibly inhibited by non-
    steroidal anti-inflammatory
    drugs (NSAIDs)
176
Q

____ converts AA into
PGH2 a precursor for prostaglandins
and thromboxanes (TXA2)

A

Cyclo-oxygenase

177
Q

Aspirin as an ________

A

anti-thrombotic agent.

178
Q

Thromboxanes DO WHAT?

A

increase platelet
aggregation; are synthesized by
platelets. (platelets lack nuclei and cannot make new proteins)

179
Q

Prostacyclin (PGI2) DOES WHAT?

A

decreases platelet aggregation; is synthesized by endothelial cells of blood vessels

180
Q

aspirin irreversibly inhibits?

A

COX

Biochem Final (6 decks)

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