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
polypeptide based, steroid, or amino acid/fatty acid hormone: transported transporter proteins
steroid and fatty/amino; (hydrophobic cant freely circulate in da blood)
26
polypeptide based, steroid, or amino acid/fatty acid hormone: uptake by diffusing through membrane - receptors are inside the cell
steroid and fatty/amino;
27
4 major kinds of receptors
- ligand gated ion/ channel receptors - GPCR - Enzyme linked/Catalytic Receptors - Cytokine family
28
Tyrosine kinase receptors: | cytoplasmic domains have _________ kinase activity
specific tyrosine
29
Tyrosine kinase receptors: | will phosphorylate ___________
proteins and self
30
Tyrosine kinase receptors: | The signal is terminated how?
receptor internalization
31
Tyrosine kinase receptors: | are receptors for what things?
insulin; GROWTH FACTORS (insulin-like, epidermal, platelet derived)
32
which receptor use SH2 domain
tyrosine kinase
33
List parts of the structure of a steroid hormone receptor
- Activation domain - N-Term - C-Term - DNA-binding domain - Ligand binding domain
34
Hormone binds to a hormone receptor and a ________ dissociates;
HSP (heat shock protein)
35
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
nucleus; dimer
36
HRE stands for ?
Hormone response elements
37
______ is found on DNA and is upstream from the steroid responsive genes and will alter the rate of transcription
HRE
38
How to end hormone stimulation: | Halting _____________ and __________
production of hormone; Response of receptor
39
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
negative; change in concentration; CNS
40
HPA Axis = H = ? P =? A = ?
Hypothalmic pituitary adrenal axis
41
HPA: Stress causes hypothalamus to release _________
CRH
42
HPA: CRH causes ________ gland to release _______
pituitary; ACTH
43
HPA: ACTH causes ________ to release _______
adrenal gland; cortisol
44
steroid hormones made from _________
cholesterol
45
steroid hormones are hydrophobic, rigid and ______
planar
46
2 classes of Steroid Hormones
Sex/Progestational and Adrenocortical
47
Cortisol is (anti stress or stress) and (anti inflammation or inflammation)
anti stress and anti inflammation
48
Glucocorticoid is ______
cortisol
49
Mineralcorticoid is _______
aldosterone
50
which steroid hormone has an aromatic ring
17B-Estradiol
51
A 11 -OH group is found on which compounds? | Progesterone, Estradiol, testosterone, cortisol, and aldosterone
cortisol and aldosterone have the 11-OH group. | this is what distinguishes between sex hormones and adrenal hormones
52
Synthesis of Steroid Hormones: | Cholesterol is made into ___________ by this enyzme __________
pregneolone; CYP11A1
53
Is estradiol made from testosterone or is testosterone made from estradiol?
estradiol is made from testosterone
54
what enzyme is needed to make estradiol from testosterone?
Aromatase
55
21-hydroxylase deficiency - what kind high or low levels of cortisol, aldosterone, and sex hormones
low levels of cortisol and aldosterone; | can have high levels of sex hormones
56
what two enzymes are needed to change progesterone to aldosterone
21- hydroxylase and 11B-hydroxylase (aka they are adding -OH groups)
57
DHEA gets made into adrenocorticoids or sex hormones?
Sex hormones
58
in 21-hydroxylase deficiency - they have low cortisol levels which has what kind of symptom
enlargement of adrenal glands
59
in 21-hydroxylase deficiency - they have low aldosterone levels and leads to what kind of symptom
hyponatremia (low Na+ levels which can be life threatening)
60
in 21-hydroxylase deficiency - they can have preamature androgen exposure can lead to what in females
ambigous genitalia, Hirsutism (very hairy), early epiphyseal closure (leads to short stature)
61
in 17a hydroxylase deficiency what kind high or low levels of cortisol, aldosterone, and sex hormones
lots of mineralcorticoids, low corticosteroids and sex hormones
62
what are symptoms of 17a hydroxylase deficiency
hypocortisolism = enlargment of adrenal gland; ambigous genitalia HYPERtension due to hyperaldosteronism
63
steroids are excreted in the ______ or ______
bile or urine
64
steroids are metabolized in the ______ by becoming ________
liver; hydrophillic
65
ketoconazole and steroid interaction
blocks cortisol and aldosterone production
66
ketoconazole or aminoglutethimide? | can treat hyperglucorticoid states
ketoconazole
67
ketoconazole or aminoglutethimide? | inhibits aromatase
aminoglutethimide
68
Does the anterior pituitary control synthesis of glucocoritcoids or mineralcorticoids
glucocorticoids
69
_________ comes from the liver to stimulate the adrenal gland to create aldosterone
Angiotensin II
70
Regulation of Testosterone Synthesis: | Hypothalamus releases ________ and works on __________
GnRH; Ant. Pituitary
71
Regulation of Testosterone Synthesis: | Anterior pituitary releases what two hormones?
LH, FSH
72
Regulation of Testosterone Synthesis: | LH works on what cells in the testis?
Leydig cells ("L"H on "L"eydig)
73
Regulation of Testosterone Synthesis: | FSH works on what cells in the testis?
Sertoli cells (F"S"H on "S"ertoli cells)
74
Regulation of Testosterone Synthesis: | What do Sertoli Cells do?
Spermatogenesis
75
Regulation of Testosterone Synthesis: | What do Leydig cells do?
make testosterone
76
is it better to supplement LH, FSH, or Testosterone?
testosterone! hella lot cheaper
77
what are activin and inhibin?
peptide hormones
78
where are activin and inhibin made?
sertoli cells in the testis
79
what does activin do?
stimulates pituitary FSH release (acts as POSITIVE FEEDBACK)
80
what does inhibin do?
inhibits pituitary FSH release in conjunction with testosterone
81
what is 5a-reductase's role with testosterone
makes testosterone into 5a-dihydrotestosterone which is a more potent/more active androgen
82
How dose testosterone get excreted
in LIVER - gets oxidized (-OH to =O)
83
Adrenal Androgens: | __________ of the testosterone synthesis pathway
intermediate
84
Adrenal Androgens: | a lot of these are made; largely in the ___________
adrenal gland
85
Adrenal Androgens: | do they have weak or strong effects
WEAK
86
Physiological Effects of Testosterone: - creates changes of puberty - ________ promoting properties - stimulate/maintain sexual function - decrease (_____) level - stimulates __________ production
growth; HDL; erythrocyte
87
When testosterone is taken orally - it is (not/readily) absorbed but inactivated (slowly/quickly)
readily; quickly
88
to make testosterone more active orally; make it a _______ form
17 alkyl
89
Synthetic Androgens: _____ forms of testosterone increase absorption time and greater activity for IM administration
ester
90
why should testosterone should not be used in infants or pregnant women...
disturbances in sexual development may occur
91
Adverse effects of testosterone in women
- hirsutism - acne - amenorrhea - clitoral enlargement - deepening of the voice
92
Adverse effects of testosterone in men
- acne - sleep apnea - gynecomastia - azoospermia/testicular atrophy - increased aggressiveness and psychotic symptoms
93
antiandrogens = _________ inhibitor or _____________ inhibitor
5a reductase; androgen receptor
94
why are 5a-reductase inhibitors helpful?
block the conversion of testosterone to 5a-dihydrotestosterone (the super potent version)
95
examples of drugs: 5a reductase inhibitors
finasteride; dutasteride
96
examples of drugs: Steroidal androgen receptor inhibitors
cyproterone/cyporterone ester; Spironolactone
97
examples non-steroidal androgen receptor inhibitors
flutamide; enzalutamide
98
Regulation of Estrogen Synthesis: | Hypothalamus produces ________
GnRH
99
Regulation of Estrogen Synthesis: | Anterior Pituitary produces _______/______
FSH/LH
100
Regulation of Estrogen Synthesis: | Ovaries produce ________/_______
estrogen;progesterone
101
Regulation of Estrogen Synthesis: | FSH/LH go to the ______ to produce a signal
Ovaries
102
Regulation of Estrogen Synthesis: | GnRH goes to the _______ to create a response
Anterior pituitary
103
Menstrual Cycle: | Order of Follicle Maturing
1) Primordial 2) Primary Follicle 3) Secondary Follicle 4) Graafian Follicle
104
What is the name of a fully mature follicle?
Graafian Follicle
105
The fully mature follicle will fuse with _________ and the _____ breaks out and goes down the _________
organ membrane; egg; fallopian tube
106
Menstrual Cycle: | which comes first? Follicular phase or luteal phase?
Follicular! (Days 1 - 14) Luteal (14 - 28) (Follicular - broken up to Early and Late phases)
107
When does menstruation occur? Follicular or Luteal Phase?
Follicular (being of cycle is start of menstruation)
108
What day of the cycle is the egg released?
day 14! - middle of cycle = ovulation
109
Menstrual Cycle: | Menstrual Phase --> _____ Phase --> _______ Phase
Proliferative; Secretory
110
in the Luteal Phase - what is the role of estrogen and progesterone
suppress the production of LH and FSH
111
If pregnancy dose not occur - the ________ degenerates and production of estrogen and progesterone (decreases or increases) and leads to __________
corpus luteum; decreases; menstruation
112
If pregnancy occurs, the fertilized egg/emybro will produce hCG. hCG acts like ____ hormone which causes the corpus luteum to produce _________
Luteual (LH); progesterone
113
High (Estrogen or Progesterone) levels are good for the maintenance of endometrium
Progesterone!
114
What are the 4 types of estrogens
1) Natural 2) Synthetic 3) Phytoestrogens 4) Environmental
115
What are the 3 types of natural estrogens
17B- Estradiol; Estrone; Estriol
116
Which one of the natural estrogens is the most potent
17B Estradiol
117
what notable enzymes are needed to make aldosterone
the dehygrodenase/isomerase; 21 hydroxylase; 11B hydroxylase
118
what notable enzymes are needed to make cortisol
the dehygrodenase/isomerase; 21 hydroxylase; 11B hydroxylase; 17a hydroxylase
119
what notable enzymes are needed to make testosterone
17a hydroxylase; 17,20 lyase; 17B hydorxysteroid dehydrogenase
120
what notable enzymes are needed to make estrogen
17 a hydroxylase; 17,20 lyase; 17b hydroxysteroid dehydrogenase; AROMATASE
121
how do glucocorticoids cause immunosuppression?
the activated glucocorticoid receptor will bind to NfKB - which prevents NFkB from being a transcription factor to make cytokines
122
Physiologic Effects of Glucocorticoids: | at the Liver it will -----
increase gluconeogenesis; increase glycogen storage
123
Physiologic Effects of Glucocorticoids: | in the muscle it will -------
increase protein degradation; decrease protein synthesis; decrease sensitivity for insulin
124
Physiologic Effects of Glucocorticoids: | in adipose tissue it will ------
promote lipolysis; decrease sensitivity to insulin
125
Physiologic Effects of Glucocorticoids: | will cause the immune system to -------
- block cytokine synthesis (immunosuppression) | - inhibit eicoasanoids (anti-inflammation)
126
``` 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) ```
CRH: high ACTH: high cortisol: LOW aldosterone: LOW
127
Is aldosterone or cortisol controlled by ACTH?
ONLY cortisol
128
``` In secondary adrenal insufficiency what are the levels? CRH (low or high) ACTH (low or high) Cortisol (low or high) Aldosterone (low or high) ```
CRH: high ACTH: low Cortisol: low Aldosterone: not affected
129
``` In tertiary adrenal insufficiency what are the levels? CRH (low or high) ACTH (low or high) Cortisol (low or high) Aldosterone (low or high) ```
CRH: low ACTH: low Cortisol: low aldosterone: not affected
130
For glucocorticoids - what structural things are REQUIRED for GC activity
- 4/5 double bond - C3 ketone - 11-B hydroxyl group - C17 hydroxyl group
131
for Minearlcorticoids - what structural things are REQUIRED for MC activity
- 4/5 double bond | - C3 ketone
132
what is the difference between cortisol and cortisone?
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
Cortisone and liver impaired patients? why a concern?
impaired liver patients - will not be able to activate cortisone to cortisol....
134
Fludrocortisone: | what is its "special" structural group - and thus its effect on activity
9a-F - causes v strong mineralcorticoid activity
135
when is it appropriate to use fludrocortisone?
when trying to replace mineralcorticoids
136
Prednisone: | what is its "special" structural group - and thus its effect on activity
extra double bond between C1 and C2 - more potent GC activity - leads to better bonding
137
Prednisolone: | what is its "special" structural group - and thus its effect on activity
extra double bond b/w c1 and c2 | more potent GC activity - leads to better bonding
138
Difference b/w prednisone and prednisolone?
prednisone inactivated - must be activated by liver! (=o to -oh at C11)
139
Methylprednisolone: | what is its "special" structural group - and thus its effect on activity
6a-methyl group potency for GC same as prednisone MC activity decreases
140
Triamcinolone: | what is its "special" structural group - and thus its effect on activity
9a-F AND 16a-OH
141
What is Conn's Syndrome?
lack of 17a hydroxylation activity in the ADRENAL gland
142
Conn's Syndrome - Hyper or Hypo? - Aldosterone?
HYPER
143
Conn's Syndrome - Hyper or Hypo? - Cortisol
HYPO
144
Conn's Syndrome - Hyper or Hypo? - Sex hormones
NOT AFFECTED - because adrenal gland
145
What are symptoms of Conn's Syndrome?
- Hypertension/Hypernatremia (due to hyperaldosterone) - Polyuria (v. thirsty --> pee a lot) - Alkalosis
146
21-Esters = a prodrug for glucocorticoids: | Get activated through ________ by ________
hydrolysis; Esterases
147
What are the common 21-Ester groups used for making glucocorticoids a prodrug
- Acetate/Butyrate - Succinate - Phosphate
148
21-Ester/Glucocorticoid: Acetate & Butyrate: - Increase lipophilicity or hydrophilicity? - prolongs action upon what kind of administration?
LIPOphilicity; IM or Intra-Articular injection
149
21-Ester/Glucocorticoid: Succinate: - Increase lipophilicity or hydrophilicity? - slow or fast hydrolysis?
hydrophilicity(because it has a charge); SLOW hydrolysis
150
21-Ester/Glucocorticoid: Phosphate group - increase lipophilicity or hydrophilicity
hydrophilicity (because it has 2 charges)
151
Why are 21-Chlorocorticoids beneficial?
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
What are the Drugs that are 21-Chlorocorticoids?
Clobetasol propionate, Halobetasol propionate, and Halcinonide
153
what topical corticosteroids have notably poor solubility?
- mometasone furoate | - fluticasone propionate
154
What hormones are Anterior pituitary hormones?
GH (growth hormone), prolactin; Thyroid Stimulating hormone (TSH), FSH, LH, ACTH
155
what hormones come form the hypothalamus?
CRH, GnRH; TRH; GHRH; SST
156
Functions of Growth Hormone: | - required during childhood and adolescence for attaining _______
normal adult size....
157
Functions of Growth Hormone: | has (anabolic or catabolic) effects in the muscle which leads to increasing __________
ANABOLIC! (Growth - building muscle, duh) | lean body mass
158
Functions of Growth Hormone: | has (anabolic or catabolic) effects in lipid cells which leads to __________
CATABOLIC! (break down fat - aka like losing baby fat in growth spurt...); Reduces "central adiposity"
159
Functions of Growth Hormone: | Mediated primarily via increasing production of ________ in the liver, bone, cartilage, and muscle
IGF-1 (insulin like growth factor 1)
160
Functions of Growth Hormone: | Reduce or Increase insulin sesnsitivity
reduces! (ok tho bc its compensated by IGF (insulin like growth factor)
161
Growth hormone deficiency - what kind of body type would a kid have
short stature, adiposity
162
how is Growth Hormone cleared?
by da liver
163
what kind of receptors/pathway foes Growth Hormone (GH) activate?
JAK/STAT pathway
164
If growth hormone deficient - | Hypo or Hyper - glycemia? and WHY
HYPO(glycemia) bc NO opposed action to insulin is present
165
what are the posterior pituitary hormones?
Vasopression and Oxytocin
166
where are vasopressin and oxytocin made?
the HYPOTHALAMUS's neuronal cell bodies (but transported to post. pituitary via axons!)
167
what is mecasermin?
recombinant human IGF-1 (aka rhIGF-1)
168
what are the two groups of growth hormone antagonists?
- GH receptor antagonist | - Somatostatin analogs
169
What are the somatostatin analogs?
octreotide; lanreotide
170
what does somatostatin do?
inhibits release of GH, glucagon, insulin, and gastrin
171
why is somatostatin not therapeutically useful?
it has a rapid clearance (like 1 -3 mins)
172
___________ is also known as ADH (antidiuretic hormone)
Vasopressin
173
where is vasopressin released from?
posterior pituitary
174
when is vasopressin release from the posterior pituitary
- rising plasma tonicity | - falling blood volume
175
Physiological Functions of Vasopressin: | increases ________ of water from ________ by increasing water permeability in the cells in ___________
reabsorption; tubular filtrate; renal collecting tubules
176
``` Physiological Functions of Vasopressin: Increases or Decreases -? _________ urine volume _________ blood volume _________ blood pressure ```
decreases; increases; increases | keep more water in the body....
177
Physiological Functions of Vasopressin: | (relaxes or constricts) blood vessels
Constricts! (why BP goes up....)
178
Vasopressin will increase the levels of __________ and _______ factors
- VonWillebrand | - Coagulation (factor) VIII
179
what is the structural difference in vasopressin and oxytocin?
amino acid sequence is different at position 3 and 8!
180
What is the structure of vasopressin and oxytocin?
9 -amino acid peptide hormone with ring formed by disulfide bond
181
________ is a long-acting synthetic analog of vasopression
desmopressin
182
what receptors does vasopressin work on?
V1 and V2
183
Vasopressin Receptors: V1 or V2? which one mediates vasoconstriction (via GPCR/Ca2+/smooth muscle)
V1
184
Vasopressin Receptors: V1 or V2? which one cause water resorption (via GPCR/cAMP/renal tubule cells/more aquaporins/ more water permeability)
V2
185
Desmopressin has much more activity on which receptor? V1 or V2?
V2! (much more ADH activity) than vasopressor activity)
186
what are the adverse effects of Vasopressin
``` - WATER INTOXICATION (WATCH FLUID INTAKE) - Hyponatremia (^) - drowsiness, HA, - Abdominal cramping -(rare allergic reaction) ```
187
Vasopressin (not so much desmopressin) should be used with EXTREME CAUTION in persons with _________ disease
CV
188
when to use Vasopressin antagonists?
- when trying to treat hyponatremia | - usually given in acute care settings (seen in acute heart failure)
189
What drugs are Vasopressin antagonists
Conivaptan; Talvaptan
190
How is oxytocin relevant to mothers?
- uterine contraction in labor and delivery | - milk ejection in lactating women
191
Oxytocin - in labor/delivery | - stimulates the release of ________ and _______ that augment uterine contraction
prostaglandins; leukotrienes
192
Oxytocin - lactating women: | - contracts ________ cells surrounding mammary _______
myoepithelial; alveoli
193
Oxytocin acts through what kind of signal pathway?
GPCR/Ca2+ - smooth muscle contraction
194
Brand names for Oxytocin?
Pitocin; Syntoncinon
195
Clinical Uses for Oxytocin?
- induction/stimulation of labor - enhancement of milk ejection - control of uterine hemorrhage after delivery
196
CONTRAINDICATIONS for Oxytoxin?
- fetal distress - abnormal fetal presentation - cephalopelvic disproportion
197
Adverse effects of Oxytocin? (related to delivery)
TOO MUCH STIMULATION OF UTERINE CONTRACTION leads to - fetal distress - placental abruption - uterine rupture - trauma to birth canal
198
Adverse Effects of Oxytocin? (related to cross reactivity)
OVERDOSE OF OXYTOCIN CAN LEAD TO VASOPRESSIN RECEPTORS BEING ACTIVATED and lead to - excessive fluid retention - water intoxication - hyponatremia
199
what is a GH receptor antagonist?
Pegvisomant
200
when do you use Growth hormone antagonists?
in GH-secreting pituitary adenomas | acromegaly - abnormal growth of cartilage, bone and other organs
201
Structure of Gonadotropins: | FSH, LH, hCG are all __________ proteins
heterodimeric
202
Structure of Gonadotropins: | FSH, LH, hCG all share the same _______ but are distinguished by their ______
alpha chain; beta chain
203
(FSH or LH) beta chain is almost identical to hCG's beta chain
LH
204
There are 6 preparations of gonadotropins used clinically - what are they?
- Menotropins - Urofollitropin (uFSH) - Follitropin alpha and Follitropin beta - Lutropin alpha - hCG - Choriogondotropin a (rhCG)
205
What are the desired properties for topical glucocorticoids?
- high lipophilicity for fast absorption - minimal systemic effect - prolonged action
206
__________ is a 4th generation progestin - has relatively weak androgenic properties and has ANTIMINERALCORTICOID activity
Drosperinone
207
What is the nickname for progestins used in oral contraceptives?
"19-nor-17-ethynl" steroids
208
"19-nor-17-ethynl" - which part increase oral bioavailability
17-Ethynl (C- triple bond-C)
209
The optimal progestin will minimize ___________ and _______ properties
androgenic; antiestrogenic
210
Pharmacological Effects of Oral Contraceptive: | Inhibits _______; and Effects ______, ______, and ______
ovulation; breast; uterus; ovary
211
Pharmacological Effects of Oral Contraceptive: | How does it inhibit ovulation
estrogen and progestin levels selectively inhibit pituitary function
212
Pharmacological Effects of Oral Contraceptive: | What are the effects on the ovary
suppresses ovary function;
213
Pharmacological Effects of Oral Contraceptive: | What are the effects on the uterus
change in cervical mucus and in uterine endometrium | mucus thicker and endometrium is not ready/prepped for implantation
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Pharmacological Effects of Oral Contraceptive: | effects on the breast
stimulation of breasts(enlargement) and suppression of lactation
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Drug Interactions with Oral Contraceptive: | OC's and Steroids
Oral Contraceptives will increase the blood levels of other steroids by interfering their metabolism
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Drug Interactions with Oral Contraceptive: | OC's and anticonvulsants
phenytoin - induces drug-metabolizing enzymes in the liver (aka BC less effective bc BC is metabolized faster by the liver)
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Drug Interactions with Oral Contraceptive: | Antibiotics and OC's
Rifampin ( induces metabolism in the liver) | Tetracycline (suppress gut flora that particpates in enterohepatic recycling)
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which drug can be used for post-cotal contraceptive for 5 DAYS after
Ella (or ulipristal acetate)
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How does Ella (ulipristal acetate) work?
SPRM (selective progesterone receptor modulator)
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what is Mifepristone?
- progesterone antagonist | - poistcoital contraceptive/abortifacient (with misopristol)
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what is Danazol used for?
for Endometriosis
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How does danazol work?
inhibits surges of LH/FSH and suppresses ovarian function & causes atrophy of endometrium
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What are the adverse effects for Danazol?
- weight gain; decreased breast size; acne; oily skin; hirstusim (aka things that arise from weak androgenic effects)
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What are the contraindications for Danazol?
hepatic dysfunction; pregnancy; breast feeding
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Possible side effect of recombinant IGF-1
hypoglycemia
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Using GnRH agonist and want to stimulate gonadotropin release - how must GnRH be administered?
in a pulsatile way - to prevent receptor down regulation
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Using GnRH agonist and want to suppress gonadotropin release - how must GnRH be administered?
give it continuously - will down regulate the receptors - less gonadotropins will be released
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Clinical Uses can you use to a GnRH agonist to stimulate Gonadotropin release
Female infertility or Male infertility
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Clinical Uses can you use to a GnRH agonist to suppress Gonadotropin release
- To control ovarian hyperstimulation - Endometriosis - Prostate cancer - Central Precocioius puberty
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Menstrual Cycle: | When estrogen peaks ~ Day 12 - it triggers the hypothalamus to release ________ aka the "_________"
LH and FSH; LH SURGE
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``` Progestin - Physiological Effects: Menstruation Participates in the preovulation _______ and causes maturation/secretory changes in __________ ```
LH surge; endometrium
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Progestin: Physiological Effects: Metabolic Effects Increases _______ levels and ______ response to ______
basal insulin levels; insulin; glucose
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Progestin: Physiological Effects: Metabolic Effects Promotes __________ in the liver
glycogen storage
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Progestin: Physiological Effects: | Interference with aldosterone? Explain
competes w/ aldosterone for MC receptor --> will decrease Na reabsorption --> increase aldosterone by adrenal cortex
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_________ suppress the growth of endometrial cells
Progestins
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What structure things are required for progestins?
C3 Ketone; C-18 Me(or ethyl) group; | 17B-OH will increase bioavail.
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what are the 1st generation of progesterones
Norethidrone, Etyhnodiol diacetate; medroxyprogesterone
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2nd generation progestins?
Levonorgestrel; Norgestimate
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3rd generation progestins?
Desogestrel; Etonogestrel
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ADE's of Oral Contraceptives | Estrogen - mild Side Effects
- nausea - HTN - edema - breast fullness
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ADE's of Oral Contraceptives | Progestins - mild Side Effects
increased appetite, Fatigue, breast regression
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What are some moderate ADE's of oral contraceptives
irregularities in menstruation, weight gain, acne, hirsutism, amenorrhea
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Severe ADE's of Oral Contraceptives
- Venous thromboembolic disease - MI - Dangerous for women over 35
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what is Danazol used for?
endometriosis
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how does Danazol work
inhibits surges of LH/FSH/suppress ovarian function | cause atrophy of endometrium
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ADE from Danazol
comes from weak androgenic activity (wt gain,decreased breast size, acne, oily skin, hirsutism)