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Therapeutics 2 - Fall 2017 > Park's Endocrine Lectures > Flashcards

Park's Endocrine Lectures Flashcards

1
Q

________ cell - cell signaling has direct physical contact

A

juxtacrine

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2
Q

__________ cell - cell signaling travels very far in the body/blood to a target organ

A

endocrine

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3
Q

__________ cell - cell signaling generally has LOW concentration and HIGH affinity

A

Endorcrine

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4
Q

__________ cell - cell signaling generally has HIGH concentration and LOW affinity

A

paracrine

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5
Q

__________ cell - cell signaling typically travels short distances to neighboring cells

A

paracrine

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6
Q

__________ cell - cell signaling use neurotransmitters

A

synaptic, neuronal

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7
Q

__________ cell - cell signaling travels VERY short distance and is supa fast (millisecond)

A

synaptic

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8
Q

__________ cell - cell signaling very high local concentration/dissociates rapidly

A

synaptic

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9
Q

__________ cell - cell signaling affect same cell

A

Autocrine

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10
Q

3 main chemical families of hormones

A

polypeptide-based hormones; steroid hormones; amino acid or fatty acid derived hormones

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11
Q

is this chemical signal a polypeptide based, steroid, or amino acid/fatty acid:

Insulin

A

polypeptide

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12
Q

is this chemical signal a polypeptide based, steroid, or amino acid/fatty acid:

estradiol

A

steroid

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13
Q

is this chemical signal a polypeptide based, steroid, or amino acid/fatty acid:

cortisone

A

steroid

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14
Q

is this chemical signal a polypeptide based, steroid, or amino acid/fatty acid:

epinephrine

A

amino acid/fatty acid

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15
Q

is this chemical signal a polypeptide based, steroid, or amino acid/fatty acid:

prostaglandin

A

amino acid/fatty acid

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16
Q

is this chemical signal a polypeptide based, steroid, or amino acid/fatty acid:

oxytocin

A

polypeptide based hormones

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17
Q

polypeptide based, steroid, or amino acid/fatty acid:

which ones gets translated into itself/has post translational modifications

A

polypeptide based..

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18
Q

polypeptide based, steroid, or amino acid/fatty acid hormone:

made from cholesterol

A

steroid

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19
Q

polypeptide based, steroid, or amino acid/fatty acid hormone:

made by ribosomes

A

polypeptide

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20
Q

polypeptide based, steroid, or amino acid/fatty acid hormone:

require multiple steps catalyzed by enzymes

A

steroid; amino acid/fatty acid

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21
Q

polypeptide based, steroid, or amino acid/fatty acid hormone:

secreted by exocytosis

A

polypeptide (they are hydrophillic and cannot move through membrane without vesicles)

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22
Q

polypeptide based, steroid, or amino acid/fatty acid hormone:

transports freely/circulates freely

A

polypeptide based

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23
Q

polypeptide based, steroid, or amino acid/fatty acid hormone:

uptaken via cell surface receptors or transporters

A

polypeptide (hydrophillic so dont go inside cell)

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24
Q

polypeptide based, steroid, or amino acid/fatty acid hormone:
secreted by diffusion

A

steroid and fatty/amino; (hydrophobic so just goes through membrane

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25
Q

polypeptide based, steroid, or amino acid/fatty acid hormone:
transported transporter proteins

A

steroid and fatty/amino; (hydrophobic cant freely circulate in da blood)

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26
Q

polypeptide based, steroid, or amino acid/fatty acid hormone:
uptake by diffusing through membrane - receptors are inside the cell

A

steroid and fatty/amino;

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27
Q

4 major kinds of receptors

A
  • ligand gated ion/ channel receptors
  • GPCR
  • Enzyme linked/Catalytic Receptors
  • Cytokine family
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28
Q

Tyrosine kinase receptors:

cytoplasmic domains have _________ kinase activity

A

specific tyrosine

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29
Q

Tyrosine kinase receptors:

will phosphorylate ___________

A

proteins and self

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30
Q

Tyrosine kinase receptors:

The signal is terminated how?

A

receptor internalization

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31
Q

Tyrosine kinase receptors:

are receptors for what things?

A

insulin; GROWTH FACTORS (insulin-like, epidermal, platelet derived)

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32
Q

which receptor use SH2 domain

A

tyrosine kinase

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33
Q

List parts of the structure of a steroid hormone receptor

A
  • Activation domain
  • N-Term
  • C-Term
  • DNA-binding domain
  • Ligand binding domain
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34
Q

Hormone binds to a hormone receptor and a ________ dissociates;

A

HSP (heat shock protein)

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35
Q

Hormone is bound to HR and HSP has left - the hormone bound to hormone receptor go to the _________ to form a ________ to become a transcription factor

A

nucleus; dimer

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36
Q

HRE stands for ?

A

Hormone response elements

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37
Q

______ is found on DNA and is upstream from the steroid responsive genes and will alter the rate of transcription

A

HRE

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38
Q

How to end hormone stimulation:

Halting _____________ and __________

A

production of hormone; Response of receptor

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39
Q

ways to stop production of hormone:

  • trigger by ________ feedback loops
  • endocrine organs sense ___________ of a marker and shuts down production of hormone
  • ______ sense change in concentration of a marker and sends message to endocrine organ to stop production
A

negative; change in concentration; CNS

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40
Q

HPA Axis = H = ? P =? A = ?

A

Hypothalmic pituitary adrenal axis

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41
Q

HPA: Stress causes hypothalamus to release _________

A

CRH

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42
Q

HPA: CRH causes ________ gland to release _______

A

pituitary; ACTH

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43
Q

HPA: ACTH causes ________ to release _______

A

adrenal gland; cortisol

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44
Q

steroid hormones made from _________

A

cholesterol

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45
Q

steroid hormones are hydrophobic, rigid and ______

A

planar

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46
Q

2 classes of Steroid Hormones

A

Sex/Progestational and Adrenocortical

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47
Q

Cortisol is (anti stress or stress) and (anti inflammation or inflammation)

A

anti stress and anti inflammation

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48
Q

Glucocorticoid is ______

A

cortisol

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49
Q

Mineralcorticoid is _______

A

aldosterone

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50
Q

which steroid hormone has an aromatic ring

A

17B-Estradiol

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51
Q

A 11 -OH group is found on which compounds?

Progesterone, Estradiol, testosterone, cortisol, and aldosterone

A

cortisol and aldosterone have the 11-OH group.

this is what distinguishes between sex hormones and adrenal hormones

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52
Q

Synthesis of Steroid Hormones:

Cholesterol is made into ___________ by this enyzme __________

A

pregneolone; CYP11A1

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53
Q

Is estradiol made from testosterone or is testosterone made from estradiol?

A

estradiol is made from testosterone

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54
Q

what enzyme is needed to make estradiol from testosterone?

A

Aromatase

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55
Q

21-hydroxylase deficiency - what kind high or low levels of cortisol, aldosterone, and sex hormones

A

low levels of cortisol and aldosterone;

can have high levels of sex hormones

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56
Q

what two enzymes are needed to change progesterone to aldosterone

A

21- hydroxylase and 11B-hydroxylase (aka they are adding -OH groups)

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57
Q

DHEA gets made into adrenocorticoids or sex hormones?

A

Sex hormones

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58
Q

in 21-hydroxylase deficiency - they have low cortisol levels which has what kind of symptom

A

enlargement of adrenal glands

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59
Q

in 21-hydroxylase deficiency - they have low aldosterone levels and leads to what kind of symptom

A

hyponatremia (low Na+ levels which can be life threatening)

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60
Q

in 21-hydroxylase deficiency - they can have preamature androgen exposure can lead to what in females

A

ambigous genitalia, Hirsutism (very hairy), early epiphyseal closure (leads to short stature)

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61
Q

in 17a hydroxylase deficiency what kind high or low levels of cortisol, aldosterone, and sex hormones

A

lots of mineralcorticoids, low corticosteroids and sex hormones

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62
Q

what are symptoms of 17a hydroxylase deficiency

A

hypocortisolism = enlargment of adrenal gland;
ambigous genitalia
HYPERtension due to hyperaldosteronism

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63
Q

steroids are excreted in the ______ or ______

A

bile or urine

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64
Q

steroids are metabolized in the ______ by becoming ________

A

liver; hydrophillic

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65
Q

ketoconazole and steroid interaction

A

blocks cortisol and aldosterone production

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66
Q

ketoconazole or aminoglutethimide?

can treat hyperglucorticoid states

A

ketoconazole

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67
Q

ketoconazole or aminoglutethimide?

inhibits aromatase

A

aminoglutethimide

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68
Q

Does the anterior pituitary control synthesis of glucocoritcoids or mineralcorticoids

A

glucocorticoids

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69
Q

_________ comes from the liver to stimulate the adrenal gland to create aldosterone

A

Angiotensin II

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70
Q

Regulation of Testosterone Synthesis:

Hypothalamus releases ________ and works on __________

A

GnRH; Ant. Pituitary

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71
Q

Regulation of Testosterone Synthesis:

Anterior pituitary releases what two hormones?

A

LH, FSH

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72
Q

Regulation of Testosterone Synthesis:

LH works on what cells in the testis?

A

Leydig cells (“L”H on “L”eydig)

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73
Q

Regulation of Testosterone Synthesis:

FSH works on what cells in the testis?

A

Sertoli cells (F”S”H on “S”ertoli cells)

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74
Q

Regulation of Testosterone Synthesis:

What do Sertoli Cells do?

A

Spermatogenesis

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75
Q

Regulation of Testosterone Synthesis:

What do Leydig cells do?

A

make testosterone

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76
Q

is it better to supplement LH, FSH, or Testosterone?

A

testosterone! hella lot cheaper

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77
Q

what are activin and inhibin?

A

peptide hormones

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78
Q

where are activin and inhibin made?

A

sertoli cells in the testis

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79
Q

what does activin do?

A

stimulates pituitary FSH release (acts as POSITIVE FEEDBACK)

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80
Q

what does inhibin do?

A

inhibits pituitary FSH release in conjunction with testosterone

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81
Q

what is 5a-reductase’s role with testosterone

A

makes testosterone into 5a-dihydrotestosterone which is a more potent/more active androgen

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82
Q

How dose testosterone get excreted

A

in LIVER - gets oxidized (-OH to =O)

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83
Q

Adrenal Androgens:

__________ of the testosterone synthesis pathway

A

intermediate

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84
Q

Adrenal Androgens:

a lot of these are made; largely in the ___________

A

adrenal gland

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85
Q

Adrenal Androgens:

do they have weak or strong effects

A

WEAK

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86
Q

Physiological Effects of Testosterone:

  • creates changes of puberty
  • ________ promoting properties
  • stimulate/maintain sexual function
  • decrease (_____) level
  • stimulates __________ production
A

growth; HDL; erythrocyte

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87
Q

When testosterone is taken orally - it is (not/readily) absorbed but inactivated (slowly/quickly)

A

readily; quickly

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88
Q

to make testosterone more active orally; make it a _______ form

A

17 alkyl

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89
Q

Synthetic Androgens: _____ forms of testosterone increase absorption time and greater activity for IM administration

A

ester

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90
Q

why should testosterone should not be used in infants or pregnant women…

A

disturbances in sexual development may occur

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91
Q

Adverse effects of testosterone in women

A
  • hirsutism
  • acne
  • amenorrhea
  • clitoral enlargement
  • deepening of the voice
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92
Q

Adverse effects of testosterone in men

A
  • acne
  • sleep apnea
  • gynecomastia
  • azoospermia/testicular atrophy
  • increased aggressiveness and psychotic symptoms
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93
Q

antiandrogens = _________ inhibitor or _____________ inhibitor

A

5a reductase; androgen receptor

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94
Q

why are 5a-reductase inhibitors helpful?

A

block the conversion of testosterone to 5a-dihydrotestosterone (the super potent version)

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95
Q

examples of drugs: 5a reductase inhibitors

A

finasteride; dutasteride

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96
Q

examples of drugs: Steroidal androgen receptor inhibitors

A

cyproterone/cyporterone ester; Spironolactone

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97
Q

examples non-steroidal androgen receptor inhibitors

A

flutamide; enzalutamide

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98
Q

Regulation of Estrogen Synthesis:

Hypothalamus produces ________

A

GnRH

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99
Q

Regulation of Estrogen Synthesis:

Anterior Pituitary produces _______/______

100
Q

Regulation of Estrogen Synthesis:

Ovaries produce ________/_______

A

estrogen;progesterone

101
Q

Regulation of Estrogen Synthesis:

FSH/LH go to the ______ to produce a signal

102
Q

Regulation of Estrogen Synthesis:

GnRH goes to the _______ to create a response

A

Anterior pituitary

103
Q

Menstrual Cycle:

Order of Follicle Maturing

A

1) Primordial
2) Primary Follicle
3) Secondary Follicle
4) Graafian Follicle

104
Q

What is the name of a fully mature follicle?

A

Graafian Follicle

105
Q

The fully mature follicle will fuse with _________ and the _____ breaks out and goes down the _________

A

organ membrane; egg; fallopian tube

106
Q

Menstrual Cycle:

which comes first? Follicular phase or luteal phase?

A

Follicular! (Days 1 - 14)
Luteal (14 - 28)
(Follicular - broken up to Early and Late phases)

107
Q

When does menstruation occur? Follicular or Luteal Phase?

A

Follicular (being of cycle is start of menstruation)

108
Q

What day of the cycle is the egg released?

A

day 14! - middle of cycle = ovulation

109
Q

Menstrual Cycle:

Menstrual Phase –> _____ Phase –> _______ Phase

A

Proliferative; Secretory

110
Q

in the Luteal Phase - what is the role of estrogen and progesterone

A

suppress the production of LH and FSH

111
Q

If pregnancy dose not occur - the ________ degenerates and production of estrogen and progesterone (decreases or increases) and leads to __________

A

corpus luteum; decreases; menstruation

112
Q

If pregnancy occurs, the fertilized egg/emybro will produce hCG. hCG acts like ____ hormone which causes the corpus luteum to produce _________

A

Luteual (LH); progesterone

113
Q

High (Estrogen or Progesterone) levels are good for the maintenance of endometrium

A

Progesterone!

114
Q

What are the 4 types of estrogens

A

1) Natural
2) Synthetic
3) Phytoestrogens
4) Environmental

115
Q

What are the 3 types of natural estrogens

A

17B- Estradiol; Estrone; Estriol

116
Q

Which one of the natural estrogens is the most potent

A

17B Estradiol

117
Q

what notable enzymes are needed to make aldosterone

A

the dehygrodenase/isomerase; 21 hydroxylase; 11B hydroxylase

118
Q

what notable enzymes are needed to make cortisol

A

the dehygrodenase/isomerase; 21 hydroxylase; 11B hydroxylase; 17a hydroxylase

119
Q

what notable enzymes are needed to make testosterone

A

17a hydroxylase; 17,20 lyase; 17B hydorxysteroid dehydrogenase

120
Q

what notable enzymes are needed to make estrogen

A

17 a hydroxylase; 17,20 lyase; 17b hydroxysteroid dehydrogenase; AROMATASE

121
Q

how do glucocorticoids cause immunosuppression?

A

the activated glucocorticoid receptor will bind to NfKB - which prevents NFkB from being a transcription factor to make cytokines

122
Q

Physiologic Effects of Glucocorticoids:

at the Liver it will —–

A

increase gluconeogenesis; increase glycogen storage

123
Q

Physiologic Effects of Glucocorticoids:

in the muscle it will ——-

A

increase protein degradation; decrease protein synthesis; decrease sensitivity for insulin

124
Q

Physiologic Effects of Glucocorticoids:

in adipose tissue it will ——

A

promote lipolysis; decrease sensitivity to insulin

125
Q

Physiologic Effects of Glucocorticoids:

will cause the immune system to ——-

A
  • block cytokine synthesis (immunosuppression)

- inhibit eicoasanoids (anti-inflammation)

126
Q 
In Primary Adrenal Insufficiency (aka Addisions Disease)
what are the levels?
CRH (low or high)
ACTH (low or high)
Cortisol (low or high)
Aldosterone (low or high)
A

CRH: high
ACTH: high
cortisol: LOW
aldosterone: LOW

127
Q

Is aldosterone or cortisol controlled by ACTH?

A

ONLY cortisol

128
Q 
In secondary adrenal insufficiency
what are the levels?
CRH (low or high)
ACTH (low or high)
Cortisol (low or high)
Aldosterone (low or high)
A

CRH: high
ACTH: low
Cortisol: low
Aldosterone: not affected

129
Q 
In tertiary adrenal insufficiency
what are the levels?
CRH (low or high)
ACTH (low or high)
Cortisol (low or high)
Aldosterone (low or high)
A

CRH: low
ACTH: low
Cortisol: low
aldosterone: not affected

130
Q

For glucocorticoids - what structural things are REQUIRED for GC activity

A
  • 4/5 double bond
  • C3 ketone
  • 11-B hydroxyl group
  • C17 hydroxyl group
131
Q

for Minearlcorticoids - what structural things are REQUIRED for MC activity

A
  • 4/5 double bond

- C3 ketone

132
Q

what is the difference between cortisol and cortisone?

A

cortisol is ACTIVE (-ol means -oh group on C11- which is needed for GC activity)
cortisone has ketone at C11 = inactive
-OH to =O happens in liver

133
Q

Cortisone and liver impaired patients? why a concern?

A

impaired liver patients - will not be able to activate cortisone to cortisol….

134
Q

Fludrocortisone:

what is its “special” structural group - and thus its effect on activity

A

9a-F - causes v strong mineralcorticoid activity

135
Q

when is it appropriate to use fludrocortisone?

A

when trying to replace mineralcorticoids

136
Q

Prednisone:

what is its “special” structural group - and thus its effect on activity

A

extra double bond between C1 and C2 - more potent GC activity - leads to better bonding

137
Q

Prednisolone:

what is its “special” structural group - and thus its effect on activity

A

extra double bond b/w c1 and c2

more potent GC activity - leads to better bonding

138
Q

Difference b/w prednisone and prednisolone?

A

prednisone inactivated - must be activated by liver! (=o to -oh at C11)

139
Q

Methylprednisolone:

what is its “special” structural group - and thus its effect on activity

A

6a-methyl group
potency for GC same as prednisone
MC activity decreases

140
Q

Triamcinolone:

what is its “special” structural group - and thus its effect on activity

A

9a-F AND 16a-OH

141
Q

What is Conn’s Syndrome?

A

lack of 17a hydroxylation activity in the ADRENAL gland

142
Q

Conn’s Syndrome -
Hyper or Hypo?
- Aldosterone?

143
Q

Conn’s Syndrome -
Hyper or Hypo?
- Cortisol

144
Q

Conn’s Syndrome -
Hyper or Hypo?
- Sex hormones

A

NOT AFFECTED - because adrenal gland

145
Q

What are symptoms of Conn’s Syndrome?

A
  • Hypertension/Hypernatremia (due to hyperaldosterone)
  • Polyuria (v. thirsty –> pee a lot)
  • Alkalosis
146
Q

21-Esters = a prodrug for glucocorticoids:

Get activated through ________ by ________

A

hydrolysis; Esterases

147
Q

What are the common 21-Ester groups used for making glucocorticoids a prodrug

A
  • Acetate/Butyrate
  • Succinate
  • Phosphate
148
Q

21-Ester/Glucocorticoid:
Acetate & Butyrate:
- Increase lipophilicity or hydrophilicity?
- prolongs action upon what kind of administration?

A

LIPOphilicity; IM or Intra-Articular injection

149
Q

21-Ester/Glucocorticoid:
Succinate:
- Increase lipophilicity or hydrophilicity?
- slow or fast hydrolysis?

A

hydrophilicity(because it has a charge); SLOW hydrolysis

150
Q

21-Ester/Glucocorticoid:
Phosphate group
- increase lipophilicity or hydrophilicity

A

hydrophilicity (because it has 2 charges)

151
Q

Why are 21-Chlorocorticoids beneficial?

A

the Cl group is better than OH group (at pos 21) because it greatly enhance TOPICAL anti-inflammatory activity (Cl increases lipophilicity - bc it cant do hydrogen bonding)

152
Q

What are the Drugs that are 21-Chlorocorticoids?

A

Clobetasol propionate, Halobetasol propionate, and Halcinonide

153
Q

what topical corticosteroids have notably poor solubility?

A
  • mometasone furoate

- fluticasone propionate

154
Q

What hormones are Anterior pituitary hormones?

A

GH (growth hormone), prolactin; Thyroid Stimulating hormone (TSH), FSH, LH, ACTH

155
Q

what hormones come form the hypothalamus?

A

CRH, GnRH; TRH; GHRH; SST

156
Q

Functions of Growth Hormone:

- required during childhood and adolescence for attaining _______

A

normal adult size….

157
Q

Functions of Growth Hormone:

has (anabolic or catabolic) effects in the muscle which leads to increasing __________

A

ANABOLIC! (Growth - building muscle, duh)

lean body mass

158
Q

Functions of Growth Hormone:

has (anabolic or catabolic) effects in lipid cells which leads to __________

A

CATABOLIC! (break down fat - aka like losing baby fat in growth spurt…); Reduces “central adiposity”

159
Q

Functions of Growth Hormone:

Mediated primarily via increasing production of ________ in the liver, bone, cartilage, and muscle

A

IGF-1 (insulin like growth factor 1)

160
Q

Functions of Growth Hormone:

Reduce or Increase insulin sesnsitivity

A

reduces! (ok tho bc its compensated by IGF (insulin like growth factor)

161
Q

Growth hormone deficiency - what kind of body type would a kid have

A

short stature, adiposity

162
Q

how is Growth Hormone cleared?

A

by da liver

163
Q

what kind of receptors/pathway foes Growth Hormone (GH) activate?

A

JAK/STAT pathway

164
Q

If growth hormone deficient -

Hypo or Hyper - glycemia? and WHY

A

HYPO(glycemia) bc NO opposed action to insulin is present

165
Q

what are the posterior pituitary hormones?

A

Vasopression and Oxytocin

166
Q

where are vasopressin and oxytocin made?

A

the HYPOTHALAMUS’s neuronal cell bodies (but transported to post. pituitary via axons!)

167
Q

what is mecasermin?

A

recombinant human IGF-1 (aka rhIGF-1)

168
Q

what are the two groups of growth hormone antagonists?

A
  • GH receptor antagonist

- Somatostatin analogs

169
Q

What are the somatostatin analogs?

A

octreotide; lanreotide

170
Q

what does somatostatin do?

A

inhibits release of GH, glucagon, insulin, and gastrin

171
Q

why is somatostatin not therapeutically useful?

A

it has a rapid clearance (like 1 -3 mins)

172
Q

___________ is also known as ADH (antidiuretic hormone)

A

Vasopressin

173
Q

where is vasopressin released from?

A

posterior pituitary

174
Q

when is vasopressin release from the posterior pituitary

A
  • rising plasma tonicity

- falling blood volume

175
Q

Physiological Functions of Vasopressin:

increases ________ of water from ________ by increasing water permeability in the cells in ___________

A

reabsorption; tubular filtrate; renal collecting tubules

176
Q 
Physiological Functions of Vasopressin:
Increases or Decreases -?
\_\_\_\_\_\_\_\_\_ urine volume
\_\_\_\_\_\_\_\_\_ blood volume
\_\_\_\_\_\_\_\_\_ blood pressure
A

decreases; increases; increases

keep more water in the body….

177
Q

Physiological Functions of Vasopressin:

(relaxes or constricts) blood vessels

A

Constricts! (why BP goes up….)

178
Q

Vasopressin will increase the levels of __________ and _______ factors

A
  • VonWillebrand

- Coagulation (factor) VIII

179
Q

what is the structural difference in vasopressin and oxytocin?

A

amino acid sequence is different at position 3 and 8!

180
Q

What is the structure of vasopressin and oxytocin?

A

9 -amino acid peptide hormone with ring formed by disulfide bond

181
Q

________ is a long-acting synthetic analog of vasopression

A

desmopressin

182
Q

what receptors does vasopressin work on?

183
Q

Vasopressin Receptors:
V1 or V2?
which one mediates vasoconstriction (via GPCR/Ca2+/smooth muscle)

184
Q

Vasopressin Receptors:
V1 or V2?
which one cause water resorption (via GPCR/cAMP/renal tubule cells/more aquaporins/ more water permeability)

185
Q

Desmopressin has much more activity on which receptor? V1 or V2?

A

V2! (much more ADH activity) than vasopressor activity)

186
Q

what are the adverse effects of Vasopressin

A 
- WATER INTOXICATION 
(WATCH  FLUID INTAKE)
- Hyponatremia (^)
- drowsiness, HA, 
- Abdominal cramping
-(rare allergic reaction)
187
Q

Vasopressin (not so much desmopressin) should be used with EXTREME CAUTION in persons with _________ disease

188
Q

when to use Vasopressin antagonists?

A
  • when trying to treat hyponatremia

- usually given in acute care settings (seen in acute heart failure)

189
Q

What drugs are Vasopressin antagonists

A

Conivaptan; Talvaptan

190
Q

How is oxytocin relevant to mothers?

A
  • uterine contraction in labor and delivery

- milk ejection in lactating women

191
Q

Oxytocin - in labor/delivery

- stimulates the release of ________ and _______ that augment uterine contraction

A

prostaglandins; leukotrienes

192
Q

Oxytocin - lactating women:

- contracts ________ cells surrounding mammary _______

A

myoepithelial; alveoli

193
Q

Oxytocin acts through what kind of signal pathway?

A

GPCR/Ca2+ - smooth muscle contraction

194
Q

Brand names for Oxytocin?

A

Pitocin; Syntoncinon

195
Q

Clinical Uses for Oxytocin?

A
  • induction/stimulation of labor
  • enhancement of milk ejection
  • control of uterine hemorrhage after delivery
196
Q

CONTRAINDICATIONS for Oxytoxin?

A
  • fetal distress
  • abnormal fetal presentation
  • cephalopelvic disproportion
197
Q

Adverse effects of Oxytocin? (related to delivery)

A

TOO MUCH STIMULATION OF UTERINE CONTRACTION leads to

  • fetal distress
  • placental abruption
  • uterine rupture
  • trauma to birth canal
198
Q

Adverse Effects of Oxytocin? (related to cross reactivity)

A

OVERDOSE OF OXYTOCIN CAN LEAD TO VASOPRESSIN RECEPTORS BEING ACTIVATED and lead to

  • excessive fluid retention
  • water intoxication
  • hyponatremia
199
Q

what is a GH receptor antagonist?

A

Pegvisomant

200
Q

when do you use Growth hormone antagonists?

A

in GH-secreting pituitary adenomas

acromegaly - abnormal growth of cartilage, bone and other organs

201
Q

Structure of Gonadotropins:

FSH, LH, hCG are all __________ proteins

A

heterodimeric

202
Q

Structure of Gonadotropins:

FSH, LH, hCG all share the same _______ but are distinguished by their ______

A

alpha chain; beta chain

203
Q

(FSH or LH) beta chain is almost identical to hCG’s beta chain

204
Q

There are 6 preparations of gonadotropins used clinically - what are they?

A
  • Menotropins
  • Urofollitropin (uFSH)
  • Follitropin alpha and Follitropin beta
  • Lutropin alpha
  • hCG
  • Choriogondotropin a (rhCG)
205
Q

What are the desired properties for topical glucocorticoids?

A
  • high lipophilicity for fast absorption
  • minimal systemic effect
  • prolonged action
206
Q

__________ is a 4th generation progestin - has relatively weak androgenic properties and has ANTIMINERALCORTICOID activity

A

Drosperinone

207
Q

What is the nickname for progestins used in oral contraceptives?

A

“19-nor-17-ethynl” steroids

208
Q

“19-nor-17-ethynl” - which part increase oral bioavailability

A

17-Ethynl (C- triple bond-C)

209
Q

The optimal progestin will minimize ___________ and _______ properties

A

androgenic; antiestrogenic

210
Q

Pharmacological Effects of Oral Contraceptive:

Inhibits _______; and Effects ______, ______, and ______

A

ovulation; breast; uterus; ovary

211
Q

Pharmacological Effects of Oral Contraceptive:

How does it inhibit ovulation

A

estrogen and progestin levels selectively inhibit pituitary function

212
Q

Pharmacological Effects of Oral Contraceptive:

What are the effects on the ovary

A

suppresses ovary function;

213
Q

Pharmacological Effects of Oral Contraceptive:

What are the effects on the uterus

A

change in cervical mucus and in uterine endometrium

mucus thicker and endometrium is not ready/prepped for implantation

214
Q

Pharmacological Effects of Oral Contraceptive:

effects on the breast

A

stimulation of breasts(enlargement) and suppression of lactation

215
Q

Drug Interactions with Oral Contraceptive:

OC’s and Steroids

A

Oral Contraceptives will increase the blood levels of other steroids by interfering their metabolism

216
Q

Drug Interactions with Oral Contraceptive:

OC’s and anticonvulsants

A

phenytoin - induces drug-metabolizing enzymes in the liver (aka BC less effective bc BC is metabolized faster by the liver)

217
Q

Drug Interactions with Oral Contraceptive:

Antibiotics and OC’s

A

Rifampin ( induces metabolism in the liver)

Tetracycline (suppress gut flora that particpates in enterohepatic recycling)

218
Q

which drug can be used for post-cotal contraceptive for 5 DAYS after

A

Ella (or ulipristal acetate)

219
Q

How does Ella (ulipristal acetate) work?

A

SPRM (selective progesterone receptor modulator)

220
Q

what is Mifepristone?

A
  • progesterone antagonist

- poistcoital contraceptive/abortifacient (with misopristol)

221
Q

what is Danazol used for?

A

for Endometriosis

222
Q

How does danazol work?

A

inhibits surges of LH/FSH and suppresses ovarian function & causes atrophy of endometrium

223
Q

What are the adverse effects for Danazol?

A
  • weight gain; decreased breast size; acne; oily skin; hirstusim (aka things that arise from weak androgenic effects)
224
Q

What are the contraindications for Danazol?

A

hepatic dysfunction; pregnancy; breast feeding

225
Q

Possible side effect of recombinant IGF-1

A

hypoglycemia

226
Q

Using GnRH agonist and want to stimulate gonadotropin release - how must GnRH be administered?

A

in a pulsatile way - to prevent receptor down regulation

227
Q

Using GnRH agonist and want to suppress gonadotropin release - how must GnRH be administered?

A

give it continuously - will down regulate the receptors - less gonadotropins will be released

228
Q

Clinical Uses can you use to a GnRH agonist to stimulate Gonadotropin release

A

Female infertility or Male infertility

229
Q

Clinical Uses can you use to a GnRH agonist to suppress Gonadotropin release

A
  • To control ovarian hyperstimulation
  • Endometriosis
  • Prostate cancer
  • Central Precocioius puberty
230
Q

Menstrual Cycle:

When estrogen peaks ~ Day 12 - it triggers the hypothalamus to release ________ aka the “_________”

A

LH and FSH; LH SURGE

231
Q 
Progestin - Physiological Effects:
Menstruation  
Participates in the preovulation \_\_\_\_\_\_\_
and
causes maturation/secretory changes in \_\_\_\_\_\_\_\_\_\_
A

LH surge; endometrium

232
Q

Progestin: Physiological Effects:
Metabolic Effects
Increases _______ levels and ______ response to ______

A

basal insulin levels; insulin; glucose

233
Q

Progestin: Physiological Effects:
Metabolic Effects
Promotes __________ in the liver

A

glycogen storage

234
Q

Progestin: Physiological Effects:

Interference with aldosterone? Explain

A

competes w/ aldosterone for MC receptor –> will decrease Na reabsorption –> increase aldosterone by adrenal cortex

235
Q

_________ suppress the growth of endometrial cells

A

Progestins

236
Q

What structure things are required for progestins?

A

C3 Ketone; C-18 Me(or ethyl) group;

17B-OH will increase bioavail.

237
Q

what are the 1st generation of progesterones

A

Norethidrone, Etyhnodiol diacetate; medroxyprogesterone

238
Q

2nd generation progestins?

A

Levonorgestrel; Norgestimate

239
Q

3rd generation progestins?

A

Desogestrel; Etonogestrel

240
Q

ADE’s of Oral Contraceptives

Estrogen - mild Side Effects

A
  • nausea
  • HTN
  • edema
  • breast fullness
241
Q

ADE’s of Oral Contraceptives

Progestins - mild Side Effects

A

increased appetite, Fatigue, breast regression

242
Q

What are some moderate ADE’s of oral contraceptives

A

irregularities in menstruation, weight gain, acne, hirsutism, amenorrhea

243
Q

Severe ADE’s of Oral Contraceptives

A
  • Venous thromboembolic disease
  • MI
  • Dangerous for women over 35
244
Q

what is Danazol used for?

A

endometriosis

245
Q

how does Danazol work

A

inhibits surges of LH/FSH/suppress ovarian function

cause atrophy of endometrium

246
Q

ADE from Danazol

A

comes from weak androgenic activity (wt gain,decreased breast size, acne, oily skin, hirsutism)

Therapeutics 2 - Fall 2017 (22 decks)

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