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PHCOL 401 > Midterm #2 (11/4-11/9) > Flashcards

Midterm #2 (11/4-11/9) Flashcards

1
Q

General feedback control of the hypothalamus axis

A

sensory input from the environment acts on the CNS which acts onto the hypothalamus. The hypothalamus secretes hypothalamic releasing hormones which act at the anterior pituitary. The anterior pituitary releases anterior pituitary hormones into the blood which can act at target glands. The target gland will release the ultimate hormone which will cause an ultimate hormonal response. The ultimate hormone can provide positive/negative feedback at the CNS, hypothalamus, or anterior pituitary.

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2
Q

Anterior Pituitary Hormones: Growth Hormone

A

GH, somatotropin. Stimulates secretion of IGF-1 and IGF-2 to regulate body growth and metabolism.

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3
Q

Anterior Pituitary Hormones: Thyroid stimulating hormone

A

TSH. Stimulates secretion of thyroid hormone and growth of thyroid gland.

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4
Q

Anterior Pituitary Hormones: Adrenocorticotropic hormone (ACTH): stimulates secretion of cortisol by the adrenal cortex and promotes growth of the adrenal cortex.

A

Adrenocorticotropic hormone (ACTH): stimulates secretion of cortisol by the adrenal cortex and promotes growth of the adrenal cortex.

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5
Q

Anterior Pituitary Hormones: Follicle-secreting hormone

A

(FSH): stimulates growth and development of ovarian follicles, promotes secretion of estrogen by ovaries and is required for sperm production

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6
Q

Anterior Pituitary Hormones: Luteinizing hormone

A

(LH): responsible for ovarian secretion of sex hormones, corpus luteum formation and responsible for ovulation. Is required for testosterone production in testes.

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7
Q

Growth Hormone

A

Direct effect on muscle, live, adipose to promote skeletal growth and accumulation of lean muscle mass. Somatomedins IGF-1 is the primary and found in adults and IGF-2 is the secondary and only found in developing fetus.

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8
Q

Growth Hormone: Feedback Control

A

GHRH is released from the hypothalamus and acts on the anterior pituitary. The anterior pituitary releases growth hormone (GH) to act on the liver to release IGF-1 and IGF-2.

IGFs stimulate release of somatostatin from the hypothalamus. Somatostatin inhibits GHRH. IGF also negatively feedbacks on GHRH and GH.

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9
Q

Cytokine Mechanism

A

cytokines interact with the cytokine receptor family, these receptors activate JAK tyrosine kinases which leads to the phosphorylation of STAT transcription factors. The STATs dimerize and translocate to the nucleus where they activate gene transcription.

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10
Q

Growth Hormone Disorders, Site of of defect: Hypothalamus

A

caused by dysplasia, trauma, surgery, hypothalamic tumors, genetic defects in GHRH or GHIH genes

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11
Q

Growth Hormone Disorders, Site of of defect: Pituitary gland

A

caused by dysplasia, trauma, surgery, pituitary tumors and genetic defects in GH gene

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12
Q

Growth Hormone Disorders, Site of of defect: Sites of IGF production

A

Caused by GH receptor defect. Full defect causes Laron’s dwarfism, with high [GH] but low [IGF]. Partial defect causes pygmies with normal [GH] and low [IGF].

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13
Q

Growth Hormone Disorders, Site of of defect: Cartilage

A

caused by resistance to IGF-1

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14
Q

Idiopathic GH Deficiency

A

Characterized by low GH levels that do not rise after provocative testing.

symptoms: short stature, cherubic appearance, obesity, delayed skeletal age.

Provocative testing: IV administration of insulin or arginine should increase levels of GH. If GH levels do not increase to a level greater than 10 ng/mL that indicates deficiency.

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15
Q

Laron Syndrome

A
  1. Genetic mutation in GH receptor
  2. High incidence in Ecuador
  3. Short stature, hypoglycemia, poor muscle development, obesity and osteoporosis
  4. Patients are long-lived and resistant to cancer and diabetes.

5 .Treated with IGF-1 to correct growth and certain metabolic changes.

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16
Q

Hypersecretion of GH

A

usually due to a pituitary tumor

Pre-puberty = gigantism. increased bone growth and > 7 feet tall

Post-puberty = acromegaly. Some tissues still grow, including the cartilage in the nose, hands, feet, ridges of eyebrow, chin and tongue.

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17
Q

GH deficiency Treatment

A

GH was extracted from cadavers, however patients began contracting Creutzfeld-Jakob disease. FDA then approved a recombinant GH. Main goal of treatment is to monitor serum IGF-1 levels, and it is used until the epiphyses are fused (puberty) or into adulthood. Causes metabolic effects including acceleration of puberty, pancreatitis, intercranial hypertension, may increase the risk of leukemia and stroke.

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18
Q

Small for gestational age (SGA) Treatment

A

smaller than most babies after the same number of weeks of pregnancy. GH is used when there is no catch-up growth by age 2.

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19
Q

Prader-Willi syndrome (PWS) Treatment

A

causes short stature, polyphagia, obesity, hypogonadism, and mild mental retardation. Affects newborns. GH supports growth, increased muscle mass, lessens polyphagia and obesity.

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20
Q

Turner syndrome (TS) Treatment

A

affects girls. There are lots of symptoms but short stature is the main, and GH supports growth.

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21
Q

Idiopathic Short stature (ISS) Treatment

A

shorter than 98.8% of children (2 SD), growing at a rate that will not allow them to reach normal adult height, and growth plates haven’t fused. GH supports growth, but requires higher doses of GH than GH deficient patients. Genetic factors influence dose.

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22
Q

Recombinant human IGF-1

A

used if patient has GH receptor mutants (Laron dwarfism)

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23
Q

Sermorelin

A

synthetic GHRH. less effective than GH, and won’t work if the defect is in pituitary production of GH.

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24
Q

GH excess Treatment

A

Surgery: effective 50% of time

Bromocriptine: dopamine agonist. paradoxical because dopamine normally stimulates GH release

Octreotide: somatostatin analog.

Pegvisomant: GH receptor antagonist.

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25
Q

Vasopressin Receptors

A

V1 receptors: Gq coupled to increase vascular smooth muscle contraction (increases blood pressure), increase liver glycogenolysis, increase ACTH release and increase prostaglandin synthesis.

V2 receptors: Gs coupled to increase water resorption in the kidney by increasing water permeability of aquaporin-2 water channels in renal luminal membranes

V3 receptors: in pituitary and act like V1.

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26
Q

Vasopressin Function in Kidney

A

Vasopression binds receptors in the distal or collecting tubules of the kidney to promote reabsorption of water. The tubules are impermeable to water without vasopression. MOA is to insert aquaporins into the membranes of the kidney tubule, causing decrease in plasma osmolarity and an increase in urine osmolarity

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27
Q

Aquaporins

A

Aquaporin 2: regulated by V2R. Phosphorylation causes fusion to the apical membrane when stimulated by vasopressin

Aquaporin 3: resides constitutively on the basolateral membrane. Allows water to flow out of the cell after entering through AQP2 channels

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28
Q

Regulation of vasopressin Release

A
  1. hypothalamic osmoreceptors detect plasma osmolarity. With dehydration (high osmolarity) vasopressin secretion is increased. With overhydration (low blood osmolarity) vasopressin secretion is decreased.
  2. Decreases in blood pressure and volume increases vasopressin secretion. These stretch receptors are not as sensitive as changes in osmolarity.
  3. Nausea and vomiting increase secretion of vasopressin. 1
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29
Q

neurogenic diabetes insipidus

A

deficiency in secretion of vasopressin from the posterior pituitary. Caused by head trauma, infections or tumors involving the hypothalamus, or genetic mutations to the vasopressin gene

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30
Q

nephrogenic diabetes insipidus

A

kidney is unable to respond to vasopressin. Commonly caused by renal disease and less common are mutations in the vasopressin receptor gene or the aquaporin-2 gene

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31
Q

Syndrome of inappropriate antidiuretic hormone (SIADH)

A
  1. Common in hospital population
  2. Characterized by excessive release of vasopressin
  3. Leads to hyponatremia, and hyper-osmolality
  4. Caused by CNS injuries and malignancies or psychotropic drugs (haloperidol, TCAs, alkaloids, sulfonylureas).
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32
Q

Vasopressin Uses

A

neurogenic diabetes insipidus, acute bleeding due to esophageal varices or colonic diverticula, CPR as a first line alternative to epinephrine and vasodilatory shock

33
Q

Desmopressin uses

A

Desmopressin: nocturnal enuresis (bedwetting), and treatment of mild to moderate hemophilia including hemophilia A and von Willebrand Syndrome.

34
Q

Vasopressin, Desmopressin Cautions and contraindications

A
  1. conditions aggrevated by water retention: HF, hypertension, raised intracranial pressure, renal failure,
  2. elderly
  3. cardiac insufficiency and diuretics
  4. cystic fibrosis
  5. vascular disease due to vasoconstriction
  6. renal impairment
  7. pregnancy: oxytocic effects in 3rd trimester
35
Q

Vasopressin and desmopressin interactions

A

acetaminophen and indomethacin: increase response to vasopressin

lithium: antagonizes effect of vasopressin
demeclocycline: antagonizes vasopressin

36
Q

Vasopressin and desmopressin receptor antagonists

A
  1. Used to treat SIADH, CHF, cirrhosis-induced edema
  2. V1a/V2R antagonist: conivaptan
  3. V2R specific antagonists: tolvaptan, lixivaptan
37
Q

Oxytocin Functions

A
  1. during labor
  2. stimulates contraction of myoepithelial cells causing milk to be ejected into the ducts and cisterns. Acts through a positive feedback mechanism
  3. Maternal bonding behavior: increased in CSF during birth and continued suckling by infant releases oxytocin. Effects are due to release from centrally projecting hypothalamic neurons
38
Q

Oxytocin MOA

A

oxytocin, released from the posterior pituitary, acts through the oxytocin receptor which is a Gq receptor to mobilize calcium. Increase in calcium causes uterine and mammary smooth muscle contraction. Contraction positively feedbacks on the hypothalamus to increase oxytocin secretion from the posterior pituitary.

39
Q

Oxytocin Regulation

A
  1. Acute stress: catecholamines decreases oxytocin neurons
  2. Sex steroids: modulate production of oxytocin and response to oxytocin.
  3. Enzymes: in a variety of tissues, act to degrade oxytocin.
40
Q

synthetic oxytocin analogs

A

carbetocin, demoxytocin. IM or IV. Used to induce labor and support labor in case of non-progression birth

41
Q

Ergometrine

A
  1. chemically similar to LSD, used to facilitate delivery of the placenta and to prevent bleeding after childbirth. Causes smooth muscle in blood vessels to narrow, reducing blood flow. Usually combined with oxytocin as syntometrine
  2. advantages: low price, lasts 2-4 hours
  3. disadvantages: takes 6-7 minutes to become effective, IM or IV only, tonic uterine contraction, increased risk hypertension, vomiting, headache, contraindicated in women with hypertension or heart disease
42
Q

Misoprostol

A
  1. prostaglandin analog. commonly used to induce labor, causes uterine contractions and ripening of the cervix.
  2. Advantages: shorter time from induction to birth, low cost, oral/vaginal/rectal administration, heat stable
  3. disadvantages: possible to tear uterus when used for labor and delivery, rare amniotic fluid embolism
43
Q

Oxytocin as a drug

A
  1. advantages: causes uterus to contract, IM acts within 2.5 minutes, no side effects
  2. disadvantages: more expensive than ergometrine, IM or IV only, not heat stable
44
Q

Syntometrine

A
  1. combination of oxytocin and ergometrine
  2. advantages: combined effect of rapid action of oxytocin and sustained action of ergometrine
  3. disadvantages: increased risk of hypertension, N/V, not heat stable.
45
Q

Steroid biosynthesis

A

rate limiting step is the steroidogenic acute regulatory protein (StAR) which facilitates cholesterol crossing the aqueous inner membrane space. Unknown mechanism

46
Q

pregnenolone to aldosterone

A

pregnenolone –> progesterone (3-beta dehydrogenase)

–> deoxycorticosterone (21-alpha hydroxylase)

–> corticosterone (11-beta hydroxylase)

–> aldosterone

47
Q

pregnenolone to cortisol

A

pregnenolone –> 17-hydroxy pregnenolone (17-alpha hydroxylase)

–> 17-hydroxy progesterone (3-beta dehydrogenase)

–> 11-deoxycortisol (21-alpha hydroxylase)

–> cortisol (11-beta hydroxylase)

48
Q

Alternative method for cortisol

A

progesterone to 17-hydroxy progestrone (17 alpha hydroxylase) then normal path

49
Q

pregnenolone to estradiol

A

pregnenolone –> 17-hydroxy pregnenolone (17-alpha hydroxylase)

–> dehydroepiandrosterone

–> androstenedione (3-beta dehydrogenase)

–> testosterone

–> estradiol (aromatase)

50
Q

Steroid metabolism

A
  1. inactivated by glucuronide conjugation in the liver
    converted to less active steroid. estradiol –> estrone –> estriol
  2. altered to have increased affinity or altered specificity.
  3. example is testosterone –> dihydrotestosterone.
51
Q

Agonist Steroid Interactions

A

Agonists: endogenous ligands normally upregulate gene expression. Agonists induce a receptor conformation that favors coactivator binding

52
Q

Antagonist Steroid Interactions

A

Antagonists: no effect on transcription in the absence of endogenous ligand, they block endogenous effects by competitive binding, and induce a conformation of the receptor that prevents coactivator binding and promotes corepressor binding.

53
Q

Inverse Agonist Steroid Interactions

A

Inverse agonists: receptor promotes a low level of transcription without agonist and the inverse agonist, which is normally a synthetic ligand reduces the basal level of activity.

54
Q

Selective receptor modulators (SRMs)

A

synthetic ligand that has an agonist response in some tissues and an antagonist response in other tissues. Thought they work by promoting a conformation of the receptor that is closely balanced between agonism and antagonism. Where coactivators are more abundant, the SRM behaves as an agonist, where corepressors are more abundant the SRM is an antagonist.

55
Q

Steroid Therapeutic uses

A
  1. replacement therapy: adrenal steroids for Addison’s disease, estrogen/progesterone for menopause
  2. Pharmacological: glucocorticoids, estrogen/progesteron for contraception, androgens for muscle mass, mifepristone for pregnancy termination
  3. Cancer chemotherapy: tamoxifen for breast cancer, flutamide/bicalutamide for prostate cancer
56
Q

Classic mechanism Steroids

A

Classic mechanism: Steroids interact with intracellular receptors of the nuclear receptor super family, the receptors act as transcription factors and directly activate gene transcription. Receptors must dimerize and translocate to the nucleus.

57
Q

NRE-independent mechanism Steroids

A

: DNA binding domain does not bind to DNA but rather to transcription factors on DNA to initiate transcription

58
Q

Ligand independent mechanism Steroid

A

: binding of the ligand to a tyrosine kinase causes a kinase cascade which phosphorylates the ligand binding domain of a dimerized receptor on the DNA causing transcription

59
Q

nongenomic mechanism Steroids

A

binding of the ligand in the cytoplasm causes tissue response directly in the cytoplasm.

60
Q

Genomic vs nongenomic:

A

genomic: changes in gene expression, delayed (hours-days), requires nuclear receptor, prevented by transcription and translation inhibitors.
nongenomic: changes in existing enzyme activity and/or protein structure, rapid (sec-min), unknown cytosolic mechanisms, not affected by transcription and translation inhibitors.

61
Q

Activation of nuclear receptors

A

depends on receptor subtype, dimeric form, ligand, cell or tissue type.

62
Q

Estrogen Synthesis

A

most prevalent forms are estradiol and estrone. They are produced primarily by developing ovarian follicles, the corpus luteum and the placenta

Ovary: LH catalyzes cholesterol to pregnenolone. This is converted to progesterone then to androstenedione.

Androstenedione forms estrone through aromatase, catalyzed by FSH

Androstenedione forms testosterone. Through aromatase, catalyzed by FSH this forms 17-beta estradiol.

63
Q

Progestagen synthesis

A

: precursors to all other steroids, so all steroid-producing tissues produce progestagens. Progesterone is the major progestagen

64
Q

Feedback Control Estrogen and Progestagen

A

: GnRH is released from the hypothalalmus to stimulate the anterior pituitary to release LH and FSH. These act on the ovary to release estradiol and progesterone. Estrogen and progesterone negatively feedback on the hypothalamus and anterior pituitary. Inhibin is also released from the ovary and it negatively feedbacks on the anterior pituitary.

65
Q

Hormone Replacement Therapy (HRT)

A

: Estrogen and progesterone levels decline usually in late 40s or early 50s. Many systems become affected and symptoms include hot flashes, changing sleep patterns, emotional changes (mood swings), headaches, heart palpitations, and generalized itching

66
Q

Perimenopause

A

: fluctuation in hormone levels lasting 2-8 years

67
Q

Menopause

A

: estrogen levels drop occurs 1 year after cessation of menstrual cycle

68
Q

Postmenopause

A

: estrogen levels continue to drop, miscellaneous health concerns begin

69
Q

Beneficial effects of HRT

A

: strengthen bones, lowers LDL cholesterol, raises HDL, reduces menopause symptoms, may reduce risk of Alzheimer’s

70
Q

Detrimental effects of HRT

A

: increases breast cancer risk, increases uterine cancer risk, increases blood clot risk, and increases risk of heart attack and stroke

71
Q

Raloxifene

A

: selective ER modulators. Reduced risk of vertebral fractures, did not increase bone density but showed a decrease in breast cancer. Side effects include heart risk, blood clots, leg cramps, hot flashes but these went away with time

72
Q

Dyspareunia

A

(painful intercourse)

Causes: hormone imbalance, infection, injury, anatomic variations, cysts/tumors/fibroids, bladder irritation, psychologic

Treatment: Prempro vaginal cream, Ospemifene (Osphena) oral SERM

73
Q

Infertility

A

Clomiphene: partial agonist/antagonist of estrogen acting at both the pituitary and hypothalamus. Blocks estrogen feedback to increase GnRH, LH, FSH.

Pulsatile GnRH pump for 2 weeks followed by human chorionic gonadotropin (similar to LH)

74
Q

Cancer Chemotherapy Treatment

A
  1. Tamoxifen: Selective ER modulator. Effective in treatment of ER or PR positive. Adjuvant therapy with chemotherapy or radiation or treatment for advanced metastatic breast cancer. Can be used as preventative treatment for women at high risk for breast cancer. Resistance usually develops in 5 years.
  2. In the breast tamoxifen inhibits gene transcription through the classical mechanism. In the uterus tamoxifen increases gene expression.
  3. Aromatase Inhibitors: Aromatase converts androestenedione to estrone and testosterone to estradiol in the ovary. Aromatase inhibitors are second line treatment for breast cancer in patients when tamoxifen therapy is unsuccessful.
75
Q

Birth Control Methods:

A
  1. Feedback Inhibition: prevents LH surge, causing ovulation or follicular growth
  2. Alter endometrial lining of uterus: prevents implantation
  3. Alter cervical mucosa: secrete mucous that is hostile to sperm
  4. BC lowers LH and FSH levels to lower estradiol
76
Q

Beneficial effects of BC

A

: nearly 100% effective, protects against ectopic pregnancy, protects against iron deficiency, decrease in benign breast tumors, decrease in endometrial cancer, decrease in ovarian cancer and decrease in pelvic inflammatory disease

77
Q

Pregnancy termination

A

Emergency contraception side effects: N/V, abdominal pain, fatigue, HA, dizziness, breast tenderness, disruption of menstrual cycle. Usually do not occur for more than a few days after treatment.

78
Q

Endometriosis:

A

ectopic implantation of endometrial cells outside the uterus. Cells remain responsive to steroid treatment.

PHCOL 401 (9 decks)

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