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MHD II Test 3 > Hypothalamic and Pituitary Hormones PHARM > Flashcards

Hypothalamic and Pituitary Hormones PHARM Flashcards

1
Q
  1. What is the communication between the hypothalamus and the anterior pituitary?
  2. What happens normally in the posterior pituitary?
  3. What do most Pituitary Hormones act on?
  4. What is the exception?
A
  1. vascular link: hypothalamic-pituitary-portal system
  2. hormones of the posterior lobe of pituitary are synthesized in the hypothalamus, transported to the posterior pituitary, and released into circulation in response to specific physiologic signals
  3. most act on an endocrine gland before affecting target tissue
  4. Prolactin
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2
Q

Anterior Pit Secretion

  1. Hypothalamus creates what?
  2. What do these do?
  3. Long Loop Inhibition
  4. Short Loop Inhibition
  5. Ultra-short Loop Inhibition
A
  1. specific releasing or inhibiting factors/hormones that are released into portal system
  2. signal release of other hormones from AP that then act on a peripheral endocrine gland or the liver
  3. end product/ far downstream product acts as inhibitor on pituitary and hypothalamus
  4. Pituitary hormone inhibits hypothalamus
  5. Hypothalamus product inhibits its own release
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3
Q

Hypothalamic-Pituitary-Growth Hormone (GH) Axis

  1. Hypothalamic Homones (2) and action
  2. Ant Pit Hormone (1)
  3. Major Target Tissue
  4. Effects?
A
  1. GHRH- releases GH from AP; Somatostatin (SS)- inhibits GH release
  2. Growth Hormone
  3. Liver;
  4. releases IGF-1
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4
Q

Physiological Actions of GH

  1. In childhood (4)
  2. In Adulthood (5)
  3. How is it released?
  4. How is its secretion affected by age?
  5. How does it transmit its effects to cells?
  6. What mediates its effects?
A
  1. promotes linear growth: growth of long bones, cartilage, muscle, organ systems
  2. increases protein synthesis and bone density; promotes lipolysis and inhibits lipogenesis; promotes gluconeogenesis and glucose release; opposes insulin-induced glucose uptake in adipose tissue, reduces insulin sensitivity
  3. pulsatile manner, mostly during sleep; interplay of GHRH and SS
  4. decreases
  5. binds to its receptor and activates cascade mediated by JAK tyrosine kinases and STATs;
  6. IGF-1
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5
Q

GH Deficiency

  1. In children
  2. In Adults
A
  1. short stature and adiposity, hypoglycemia (most commonly deficiency of GHRH)
  2. changes in body composition, increased generalized adiposity; decreased skeletal muscle mass and strength, decreased bone density; CV changes, cardiac muscle atrophy, atherogenic blood lipid profile; fatigue, weakness, depression, overall malaise
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6
Q

Drugs Used in GH Deficiency

  1. Synthetic GHRH
  2. Recombinant Growth Hormone (2)
  3. Recombinant IGF-1
A
  1. Sermorelin- used in diagnosis
  2. Somatropin, Somatrem
  3. Mecasermin (used where the deficiency is due to mutation of GH receptor)
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7
Q

Somatropin and Somatrem

  1. Difference between the two
  2. Mechanism
  3. Indications for children (3)
  4. Indications for adults (3)
A
  1. 1 amino acid; somatropin is identical to hGH
  2. replaces GH
  3. documated growth failure in peds pts associated with: GH deficiency, chronic renal failure, Prader-Willi, Turner syndrome
  4. Small for gestational age condition w/ failure to catch up by age 2
  5. Idiopathic short stature, non GH-deficient (>2.25 SD below mean)
  6. GH deficiency in Adults
  7. Wasting pts w/ AIDS
  8. Short bowel syndrome in pts who are also receiving specialized nutritional support
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8
Q

Somatropin and Somatrem

  1. Controversies
  2. What do they do in children?
  3. What do they do in adults?
  4. Side Effects (5)
A
  1. Anti-aging remedies; use by athletes
  2. increases linear growth and weight gain to low normal range; increases muscle mass, organ size, RBCs
  3. increases bone mineral density, normalizes body composition (decreased central adiposity); increases muscle mass and strength, improves lipid profile and cardiac function, improves psychological symptoms and sense of well being
  4. Leukemia, rapid growth of melanocytic lesions; hypothyroidism, insulin resistance, arthralgia, increase in CYP450 activity
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9
Q

Somatropin and Somatrem

  1. Contraindications (4)
  2. Considerations
  3. Drug Interaction (1)
A
  1. Pediatric pts w/ closed epiphyses
    Active underlying intracranial lesion
    Active malignancy
    Proliferative diabetic retinopathy
  2. Cautin in diabetics and in children whose GH deficiency results from an intracranial lesion
  3. Glucocorticoids inhibit growth promoting effect of somatropin
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10
Q

GH Excess

  1. Usually due to what?
  2. What does it cause in children?
  3. What does it cause in adults?
A
  1. benign anterior pituitary tumor
  2. gigantism (occurs before closure of epiphyses)
  3. acromegaly (occurs after closure of epiphyses): thickening of bones, esp face, hands; large facial structure; increased soft tissue growth; enlarged, arthritic joints; headache, sleep apnea, excessive sweating; increased risk of CV disease, GI cancers,
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11
Q

Medical Treatment for GH Excess

  1. Somatostatin Analogues
  2. GH receptor antagonist
  3. Dopamine receptor agonist
A
  1. Octreotide, Lanreotide (used in Europe)
  2. Pegvisomant
  3. Bromocriptine
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12
Q

Octreotide

  1. Describe the drug
  2. Mechanism
  3. Indications (4)
A
  1. somatostatin analogue, long lasting peptide that is far more potent than SS
  2. inhibits GH secretion
  3. used to control pituitary adenoma growht in acromegalic pts
  4. Carcinoid crisis (flushing, diarrhea, and all symptoms of carcinoid syndrome)
  5. Secretory diarrhea from vasoactive intestinal peptide (VIP) secreting tumors
  6. Control acute GI bleeding
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13
Q

Octreotide

  1. Side Effects (4)
  2. Contraindications
  3. What drug levels does it decrease?
  4. What drug levels does it increase?
A
  1. N/V, abdominal cramps, GI discomfort
    Cardiac Effects (sinus bradycardia and conduction disturbances)
    Hypoglycemia
    Gallstones
  2. Hypersensitivity
  3. Decreases cyclosporin levels
  4. concomitant administration w/ bromocriptine increases availability of bromocriptine
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14
Q

Pegvisomant

  1. Describe the drug
  2. Mechanism
  3. Indication (1)
A
  1. recombinant protein, polyethylene glycol residues prolong half life; GH w/ several amino acid substitutions
  2. competitive antagonist of GH activity; decreases serum IGF-1 levels
  3. treatment of acromegaly that is refractory to other modes of surgical, radiologic, or pharmacologic intervention
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15
Q

Pegvisomant

  1. Side Effects (2)
  2. Contraindication
  3. What tests should be performed regularly? (2)
A
  1. increased pituitary adenoma size, elevated serum aminotransferase levels
  2. hypersensitivity rxn
  3. yearly MRI to exclude enlarging adenoma; liver function tests should be performed periodically
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16
Q

Hypothalamic Pituitary Reproductive Axis

  1. Role of Continuous GnRH
  2. Role of Pulsatile GnRH
  3. Role of Estrogen/Testosterone on Axis
A
  1. inhibits LH/FSH release
  2. activates LH/FSH release
  3. inhibits LH/FSH release
17
Q

Hypothalamic Pituitary Reproductive Axis: In Women

  1. FSH function
  2. What happens in follicular stage of menstrual cycle?
  3. What happens in luteal stage of menstraul cycle?
A
  1. ovarian follicle development
  2. LH stimulates androgen production in ovary (theca cells); FSH stimulates conversion of androgens to estrogens (Granulosa cells)
  3. estrogen and progesterone production is mainly controlled by LH; in pregnancy, these are controlled by hCG made by placenta
18
Q

Hypothalamic Pituitary Reproductive Axis: In Men

  1. FSH function
  2. LH function
  3. What does FSH do in Sertoli cells?
A
  1. regulates spermatogenesis
  2. stimulates production of testosterone by the testicular Leydig cells
  3. produces androgen binding protein, which helps maintain high levels of testosterone
19
Q

Hypothalamic Pituitary Reproductive Axis: Pharm

  1. In order for pharm therapy to work in infertility, what must be normal?
  2. What drugs are used to stimulate Axis?
  3. What drugs are used to inhibit Axis?
A
  1. ability of gonads to competently respond to neuroendocrin factors
  2. Gonadotropins (human menopausal gonadotropins or menotropins, hCG, urofollitropin, follitropin); Gonadotropin Releasing Hormone (GnRH) or its analogue Gonadorelin
  3. Synthetic analogues of GnRH w/ longer half lives (Goserelin, Histrelin, Leuprolide, Nafarelin, Triptorelin); GnRH receptor antagonists (Ganirelix, Cetrorelix, Abarelix)
20
Q

Gonadotropins: Describe

  1. Menotropins
  2. hCG
  3. Urofollitropin
  4. Follitropin
  5. Mechanism
  6. Indications (3)
A
  1. contain LH and FSH, obtained from urine of menopausal women
  2. placental hormone and LH agonist
  3. purified FSH from urine of menopausal women
  4. recombinant form of human FSH
  5. Replaces FSH and LH
  6. Ovulation induction in women w/ anovulation due to hypogonadotropic hypogonadism. polycystic ovary syndrome, obesity
  7. Controlled ovarian hyperstimulation in assisted reproductive technology procedures (eg IVF)
  8. Infertility in male hypogonadotropic hypogonadism
21
Q

Gonadotropins

1. Side Effects (5)

A
  1. Ovarian hyperstimulation syndrome (associated w/ ovarian enlargement, ascites, hydrothorax, hypovoluemia, may result in shock);
  2. increase in multiple pregnancies
  3. increased risk of gynecomastia in men
  4. Ovarian cancer
  5. Ovarian cysts and hypertrophy (hypertrophy subsides after time)
22
Q

Gonadotropins

1. Contraindications (5)

A
  1. Any endocrine disorder other than anovulation
  2. Primary gonadal failure
  3. Pituitary tumor or sex-hormone dependent tumors
  4. Ovarian cyst or enlargement
  5. Pregnancy
23
Q

Pulsatile GnRH Agonist

  1. Describe GnRH
  2. Describe Gonadorelin
  3. Mechanism
  4. Indications (3)
A
  1. obtained from hypothalamus
  2. synthetic human GnRH (short half life)
  3. pulsatile GnRH secretion or Gonadorelin stimulates LH and FSH release (mimicks physiology)
  4. Diagnosis of hypogonadism; stimulate ovulation (less cost effective); Infertility in men w/ hypothalamic hypogonadotropic hypogonadism (less cost effective, occasional use)
24
Q

Pulsatile GnRH Agonist

1. Side Effects (3)

A
  1. Anaphylaxis w/ mutliple administrations
  2. Light headedness, flushing
  3. Generalized hypersensitivity dermatitis
25
Q

Sustained GnRH Agonists

  1. What drugs are synthetic analogs of GnRH?
  2. What are some advantages to using drugs over native GnRH or gonadorelin?
A
  1. Goserelin, Histrelin, Leuprolide, Nafarelin, Triptorelin

2. more potent, longer-lasting

26
Q

Sustained GnRH Agonists

  1. Mecahnism
  2. Describe the response to these drugs
A
  1. Sustained nonpulsatile administration inhibits release of FSH and LH in men and women –> inhibition of gonadal axis;
    This desensitizes GnRH receptors.
  2. produces biphasic response:
    transient flare for 7-10 days (increase in gonadal hormone levels)- agonist effect
    Long-lasting suppression of gonadotropins and gonadal hormones - inhibitory action
27
Q

Sustained GnRH Agonists

How is the flare prevented/minimized?

A

With co-administration of an androgen antagonist

28
Q

Sustained GnRH Agonists: Indications (5 + which drugs are indicated for which)

A
  1. Keep LH surge low in controlled ovarian hyperstimulation that provides multiple mature oocytes for assisted reproductive technologies (Leuprolide, nafarelin, goserelin)
  2. Endometriosis and Uterine fibroids (leuprolide, nafarelin, goserelin)
  3. Adjunctive in prostate cancer (leuprolide, goserelin, histrelin, triptorelin)
  4. Central precocious puberty (leuprolide, nafareling)
  5. Others (advanced breast and ovarian cancer, amenorrhea and infertility in women w/ polycystic ovary disease)
29
Q

Sustained GnRH Agonists

  1. Side Effects (4)
  2. Contraindications (3)
A
  1. Symptoms of menopause (hot flashes, sweats, headache); Osteoporosis; Urogenital atrophy; Temporary worsening of precocious puberty during the initial weeks of treatment
  2. Hypersensitvity; pregnancy; breast feeding
30
Q

GnRH Receptor Antagonists

  1. Name the drugs (3)
  2. Mechanism
  3. What do these lack that GnRH receptor agonists have?
A
  1. Ganirelix, Cetrorelix, Abarelix; G and C produce immediate antagonistic effects
  2. competitive antagonists of GnRH receptors, inhibits secretion of FSH and LH in dose dependent manner
  3. flare effect
31
Q

GnRH Receptor Antagonists: Indications

  1. Ganirelix and Cetrorelix
  2. Abarelix
A
  1. keeps LH surge low in controlled ovarian hyperstimulation for assisted reproductive technologies resulting in improved rates of implantation and pregnancy
  2. metastatic prostate cancer in pts with extensive metastases or tumor encroaching on the spinal cord
32
Q

GnRH Receptor Antagonists

  1. Side Effects in general
  2. Side Effect of Abarelix
  3. Side Effects of Ganirelix (3)
  4. Side Effect of Cetrorelix
  5. Contraindications (4)
A
  1. ovarian hyperstimulation syndrome;
  2. QT interval prolongation
  3. Ectopic pregnancy, thrombotic disorder, spontaneous abortion
  4. Anaphylaxis
  5. Pregnancy, lactation, ovarian cysts or other enlargement;
    Primary ovarian failure;
    Thryoid or adrenal dysfunction;
    Vaginal bleeding of unknown etiology
33
Q

Hypothalamic-Pituitary-Prolactin Axis

  1. What cell type in AP produces and secretes prolactin?
  2. What inhibits Prolactin release?
  3. What increases Prolactin release?
  4. Describe negative feedback
  5. What is the role of estrogen?
  6. What is a powerful stimulus for release?
A
  1. Lactotrophs
  2. dopamine
  3. thyrotropin-releasing hormone
  4. There is none, because prolactin does not stimulate hormone secretion
  5. stimulates prolactin release, but antagonizes prolactin action; prevents lactation until after parturition
  6. suckling
34
Q

Physiologic Actions of Prolactin (3)

A
  1. regulates mammary gland development,
  2. milk protein biosynthesis and secretion
  3. inhibits GnRH release, suppresses ovulation during lactation
35
Q

Disorders of Hyperprolactinemia

  1. Destruction of what can cause it?
  2. How is it commonly caused?
  3. Symptoms of Hyperprolactinemia (3)
A
  1. hypothalamic destruction
  2. prolactin secreting adenomas
  3. amenorrhea, galactorrhea, and infertility in women
  4. Loss of libido and infertility in men
  5. can compress optic nerves and cause visual changes
36
Q

Pharmacology of hyperprolactinemia

  1. Drugs Used
  2. What is used to treat prolactin deficiency?
A
  1. Dopamine Receptor Agonists: Bromocriptine, Cabergoline, Pergolide (all are D2 receptor agonists)
  2. nothing, yet
37
Q

Bromocriptine, Cabergoline, Pergolide

  1. Mechanism
  2. Indications (3 + drugs)
A
  1. Inhibit pituitary prolactin release; GH release is reduced in pts w/ acromegaly, less effective
  2. Amenorrhea, galactorrhea, infertility from hyperprolactinemia, premenstrual syndrome (Bromocriptine, Cabergoline)
  3. Acromegaly (Bromocriptine- requires high doses)
  4. Parkinson’s Disease (Bromocriptime, Pergolide, Cabergoline)
38
Q

Bromocriptine, Cabergoline, Pergolide

  1. Side Effects of all of them
  2. Side Effects of Bromocriptine
  3. Side Effects of Pergolide
  4. Side Effects of Cabergoline
A
  1. Orthostatic hypotension
  2. Cerebral vascualr accidnet, seizure, acute MI
  3. Arrhythmia, MI, heart failure
  4. Pulmonary fibrosis and pleural effusion
39
Q

Bromocriptine, Cabergoline, Pergolide

  1. Contraindications (3)
  2. Which causes less nausea?
  3. What route of administration can reduce nausea but cause local irritation?
  4. Intolerance to what may occur?
  5. What potentiates hypotension?
  6. What drugs have additive effects?
A
  1. Hypersensitivity to ergot derivatives
  2. Uncontrolled HTN
  3. Toxemia of Pregnancy/Ecclampsia (Bromo)
  4. Cabergoline
  5. Intravaginal
  6. alcohol
  7. antihypertensives
  8. CNS depressants

MHD II Test 3 (14 decks)

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