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PT 2 > Block 9 - L1 > Flashcards

Block 9 - L1 Flashcards

1
Q

List the major homeostatic functions regulated by the HPA axis.

A
  1. Metabolic changes
  2. Growth
  3. Reproduction and fertility
  4. Lactation
  5. Response to stress
  6. Water homeostasis
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2
Q

The anterior pituitary is derived from ___ tissue.

A

Ectodermal

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3
Q

Which nuclei in the hypothalamus release hormones that bind to the anterior pituitary? To the posterior pituitary?

A

AP - paraventricular and acurate nuclei

PP - paraventricular and supraoptic nuclei

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4
Q

Discuss the steps of the HPA axis for the anterior pituitary.

A
  1. Neuroendocrine cells in the paraventricular and acurate nuclei synthesize and secrete releasing-hormones (often pulsatile).
  2. Releasing-hormones are released into the hypothalamic-pituitary portal system and transported to the AP
  3. Release-hormones act on specific cells of the AP, triggering release of trophic hormones
  4. Trophic hormones are released into the blood, where they act on peripheral endocrine organs (stimulate end-stage hormone) and target tissues.
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5
Q

Discuss the steps of the HPA axis for the posterior pituitary.

A
  1. Neurosecretory cells in the supraoptic and paraventricular nuclei synthesize ADH and oxytocin.
  2. ADH and oxytocin are transported down neuronal axons and stored in vesicles in nerve terminals of the PP.
  3. In response to appropriate neuronal inputs, these hormones are secreted into the bloodstream, to act on their target.
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6
Q

What are the 5 cell types in the AP?

A
  1. Somatotroph
  2. Lactotroph
  3. Thyrotroph
  4. Gonadotroph
  5. Corticotroph
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7
Q

What are the stimulatory hypothalamic factors acting on each AP cell type?

A
  1. Somatotroph - GHRH and Grehlin
  2. Lactotroph - TRH
  3. Thyrotroph - TRH
  4. Gonadotroph - GnRH (pulsatile)
  5. Corticotroph - CRH
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8
Q

What are the anterior pituitary hormones produced from the 5 cell types in the AP?

A
  1. Somatotroph - GH
  2. Lactotroph - PRL
  3. Thyrotroph - TSH
  4. Gonadotroph - FSH and LH
  5. Corticotroph - ACTH
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9
Q

What are the inhibitory hypothalamic factors regulating AP hormone secretion?

A
  1. Somatostatin (inhibits GH and TSH release)

2. Dopamine (tonically inhibits PRL release)

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10
Q

What is the target organ and effect of GH?

A

Liver, muscle, bone, and adipose tissue

Production of IGF-1, leading to increased muscle mass and bone growth

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11
Q

What is the target organ and effect of PRL?

A

Mammary gland

Lactation

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12
Q

What is the target organ and effect of TSH?

A

Thyroid gland

Production of TH

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13
Q

What is the target organ and effect of LH and FSH?

A

Gonads (testes and ovaries)

Production of Testosterone, Estrogen, Progesterone

Sperm maturation or follicle development

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14
Q

What is the target organ and effect of ACTH?

A

Adrenal cortex

Production of cortisol and aldosterone

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15
Q

What are the stimulating factors acting on the hypothalamus in the HPG axis?

A
  1. Hypoglycemia
  2. Fasting/starvation
  3. Puberty
  4. Exercise
  5. Stress
  6. Sleep
  7. Alpha-adrenergic agonists
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16
Q

What are the inhibitory factors acting on the hypothalamus in the HPG axis?

A
  1. Hyperglycemia
  2. Obesity
  3. Old age
  4. Sleep deprivation
  5. Poor nutritional status
  6. Beta-adrenergic agonists
  7. GH/IGF-1
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17
Q

What are the stimulating and inhibitory factors regulating GH directly?

A

Stimulatory - ghrelin (hunger hormone from the stomach)

Inhibitory - somatostatin

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18
Q

GH has both direct and indirect effects. What mediates the indirect effects and what is the outcome?

A

IGF-1 (from the liver); leads to linear growth

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19
Q

List the organs/systems upon which GH has a direct effect.

A
  1. Bone
  2. Muscle
  3. Liver
  4. Adipose tissue
  5. Carbohydrate metabolism
  6. Heart
  7. Brain
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20
Q

What are the physiological effects of GH on bone?

A

Increased cartilage, bone density, bone growth, and strength

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21
Q

What are the physiological effects of GH on muscle?

A

Decreased glucose uptake, increased protein synthesis, increased lean musclemass

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22
Q

What are the physiological effects of GH on the liver?

A

Increased gluconeogenesis, glycogenolysis, and blood glucose

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23
Q

What are the physiological effects of GH on adipose tissue?

A

Increased lipolysis, decreased lipogenesis, glucose uptake, and adiposity

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24
Q

What are the physiological effects of GH on carbohydrate metabolism?

A

Decreased peripheral glucose uptake, increased insulin resistance and blood glucose

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25
Q

What are the physiological effects of GH on the heart?

A

Increased myocardial function

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26
Q

What are the physiological effects of GH on the brain?

A

Neural growth and development, protects the CNS from injury, increased sense of well-being and cognitive function

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27
Q

Upon which organs does IGF-1 act?

A

Bone and muscle (anabolic effects)

+/- brain and heart (?)

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28
Q

What causes GH deficiency in children?

A

Mutations in genes involved in GHRH response, pituitary development, or GH expression

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29
Q

What causes GH deficiency in adults?

A

Pituitary adenoma or effects related to surgery or radiotherapy of a pituitary tumor

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30
Q

What are the symptoms of GH deficiency in children?

A
  1. Abnormal postnatal growth
  2. Short stature, delayed bone age, low age-adjusted growth velocity
  3. Mild adiposity and hypoglycemia
  4. Micropenis and delayed puberty (sometimes)
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31
Q

What are the symptoms of GH deficiency in adults?

A
  1. Decreased lean muscle mass and increased adiposity
  2. Decreased exercise capacity
  3. Decreased bone density/increased frequency of bone fractures
  4. Fatigue, weakness, poor memory, depression, overall malaise
  5. Cardiovascular changes - decreased cardiovascular function and atherogenic lipid profiile
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32
Q

How is GH deficiency diagnosed?

A

Determination of IGF-1 levels (GH has a short half-life and is difficult to measure)

GH stimulation test (use clonidine or glucagon to stimulate GHRH/GH production)

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33
Q

What is the treatment for GH deficiency?

A

Somatropin (recombinant human GH, aka rhuGH)

Administered subQ once a day

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34
Q

What is the MOA of somatropin?

A

Directly activates the GH receptor expressed on target tissue

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35
Q

What are the indications of somatropin?

A
  1. Children with GH deficiency
  2. Other conditions affecting children associated with short stature (Prader-Willi, Turner, Noonan, chronic renal insufficiency, small-for-gestational age with failure to catch up by age 2, idiopathic short stature)3
  3. Adults with GH deficiency in childhood that persists into adulthood
  4. Adult onset GH deficiency (controversial - high cost, daily injects, modest benefit)
  5. AIDS-associated wasting syndrome
  6. Short bowel syndrome w/malabsoprtion
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36
Q

Why is somatropin indicated for AIDS-associated wasting syndrome?

A

GH promotes maintenance of lean muscle mass

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37
Q

Why is somatropin indicated for short bowel syndrome?

A

GH promotes intestinal growth and adaptation

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38
Q

How is the clinical efficacy of somatropin monitored in children?

A

Increased growth
IGF-1 levels within the normal range

Discontinue treatment when linear growth is <2-25.cm/year

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39
Q

How is the clinical efficacy of somatropin monitored in adults?

A

Improved body composition, muscle mass, lipid profile, cardiac function, sense of well-being

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40
Q

What are the AE of somatropin in children?

A

Idiopathic intracranial HTN, increased intraocular pressure, development of insulin resistance (only a slightly increased risk)

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41
Q

What are the AE of somatropin in adults?

A 
Peripheral edema
Arthralgias
Carpal tunnel syndrome
parathesis
Worsening glucose intolerance
Acute pancreatitis
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42
Q

What are the contraindications of somatropin?

A 
Active malignancy
Uncontrolled diabetes
Proliferative retinopathy
Pediatric patients with closed epiphyses
Prader-Willi with severe obesity and/or respiratory obstruction (can lead to death)
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43
Q

True or false - there is no evidence that GH increases muscle strength or aerobic exercise capacity in normal healthy individuals.

A

True

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44
Q

What is Mecasermin?

A

Recombinant human IGF-1; used to stimulate IGF-1 dependent responses by direct activation of IGF-1R

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45
Q

When is Mecasermin indicated?

A

In children with impaired growth that are non-responsive to GH (mutations in GHR, in GHR signaling pathway - both seen in Laron dwarfism, development of Ab to GH, IGF-1 gene defects)

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46
Q

What are the AE of Mecasermin?

A

Hypoglycemia due to direct effect on insulin receptors (can address with CHO meal/snack)
Intracranial HTN (possibly due to increased CSF production)
Increased liver enzymes

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47
Q

What are the contraindications of Mecasermin?

A 
Active neoplasia (growth factor effects of IGF-1)
Children with closed bone epiphyses (will not have an effect)
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48
Q

What is gigantism?

A

Excessive linear growth, tall stature, and mild to moderate obesity in children; caused by GH excess prior to closure of bone epiphyses

49
Q

What is growth hormone excess in adults?

A

Acromegaly

50
Q

What are the symptoms of acromegaly?

A

Insidious onset and slow progression of soft tissue overgrowth, skin thickening, enlargement of the jaw, hands, and feet, coarse facial features (enlargement of nose and tongue), enlargement of visceral orgoans (heart, thyroid, liver, lungs, kidneys), enlarged cartilage (hypertrophic arthropathy of the joints), increased CVD, metabolic symptoms (hyperinsulinemia, insulin resistance, diabetes)

51
Q

What are the increased risks associated with acromegaly?

A

Colon polyps and colon cancer, and increased mortality

52
Q

What are the effects of somatostatin?

A

Inhibition of GH (and TSH)

Decreased gastric acid, gastric enzymes, TSH, GI motility, and splanchnic blood flow

Decreased blood flow to the liver, bile duct secretion, and gallbladder contraction

53
Q

What are the somatostatin analogues used to treat GH excess?

A

Octreotide and Lanreotide

54
Q

What is the MOA of Octreotide/Lanreotide?

A

Long-lived analogues of somatostatin that bind the receptor and inhibit GH production

55
Q

What are the AE of Octreotide/Lanreotide?

A

GI effects (N/V, diarrhea, constipation)
Gallstones
Suppresses TSH (have to monitor for hypothyroidism)
Bradycardia

56
Q

What are other indications of Octreotide and Lanreotide?

A
  1. Bleeding esophageal varices (decreases blood flow)
  2. Carcinoid syndrome (decreases serotonin release)
  3. Gastrinoma and glucagonoma (decreases hormone release)
  4. Gi fistulae (decreased GI secretions and motility)
57
Q

What is Pegvisomant?

A

GH receptor antagonist (attenuates the effects of excess GH in gigantism/acromegaly)

58
Q

What is the MOA of Pegvisomant?

A

Normally, GH binds to 2 GHR subunits and promotes dimerization. In PegV, one GHR binding site is deleted and the other has an increased affinity for GHR. It binds to a single GHR subunit, blocking GH binding and preventing dimerization.

59
Q

What is the most common cause of hyperprolactinemia?

A

Prolactin-secreting adenoma

60
Q

What are the effects of increased prolactin?

A

Excessive milk production and lactation
Antagonizes GnRH release and decreases GnRH sensitivity (leads to reduced FSH and LH - infertility, and reduced E/T synthesis)

61
Q

What are the symptoms of hyperprolactinemia in women?

A

Hypogonadism
Infertility
Oligomenorrhea/amenorrhea
Galactorrhea

62
Q

What are the symptoms of hyperprolactinemia in men?

A 
Hypogonadism
Loss of libido
Erectile dysfunction
Infertility
Gynecomastia
63
Q

What is used to treat hyperprolactinemia and what is the outcome?

A

Dopamine agonists - high affinity for D2 receptor (Bromocriptine and Cabergoline)

Restoration of fertility
Reversal of galactorrhea

64
Q

What are the AE of Bromocriptine/Cabergoline?

A 
Nausea, headache
Orthostatic hypotension
Psychiatric symptoms (DA excess)
65
Q

Why can Bromocriptine/Cabergoline be used to treat GH excess at high doses?

A

Due to shared embryology, ~20-30% of somatotrophs express D2 receptors and respond to this treatment

66
Q

Describe the normal HPG (gonadal) axis.

A

GnRH release (pulsatile) -> FSH and LH release -> Testosterone/Estrogen production (both have negative feedback + E has positive feedback at ovulation)

67
Q

What happens when GnRH is continuously released?

A

FSH and LH production is inhibited

68
Q

What is the physiological role of the HPG (gonadal) axis?

A
  1. Initiate puberty (GnRH release is low in childhood, increases/becomes pulsatile in adolescence, receptor sensitivity increases) -> elevated FSH/LH, gonadal hormone production, induction of puberty and secondary sexual characteristic development
  2. Regulation of adult sexual function (promotes spermatogenesis / oogenesis, follicular development, ovulation and testosterone / estrogen and progesterone synthesis)
69
Q

What are the physiological effects of FSH and LH in males?

A
  1. LH binds to Leydig cells and testosterone is produced
  2. Testosterone diffuses to Sertoli cells. FSH binds to Sertoli cells and increases androgen-binding protein
  3. ABP and Testosterone and other FSH-induced proteins promote spermatogenesis
70
Q

What are the physiological effects of FSH and LH in females?

A
  1. LH binds to thecal cells, increases androgen synthesis and progesterone
    1a. Progesterone causes the endometrium to switch from proliferative to secretory
  2. Androgens also diffuse to Granulosa cells. FSH binds, increases aromatase, which catalyzes conversion of androgens to estrogen.
  3. Estrogen causes endometrial proliferation/maturation, granulosa cell proliferation, positive and negative regulation of the axis, and ovulation (also increases FSHR and LHR receptors on the granulosa cell)
71
Q

Discuss the role of the HPG (gonadal) axis int the control of ovulation.

A
  1. Pulsatile GnRH induces FSH/LH during the follicular phase - FSH and LH promote growth and maturation of the ovarian follicle.
  2. Developing follicles secrete increasing levels of estrogen - estrogen increases LH/FSH receptors (# and responsiveness)
  3. Initial low levels of estrogen negatively regulate GnRH/FSH/LH secretion - most follicles degenerate, primary follicle that produces the most estrogen/most responsive to FSH and LH survives
  4. Primary follicle rapidly grows and secretes high levels of estrogen - induce GnRH, leading to LH surge
  5. Mid-cycle LH surge causes follicle rupture and ovulation
  6. Progesterone prepares the endometrium for implanation
72
Q

How does estrogen negatively regulate GnRH/FSH/LH stimulation? Positive regulation?

A

Negative - Inhibition of Kiss1+ ARC neurons

Positive - activation of Kiss1+ AVPV neurons

73
Q

What are the 4 classes of drugs targeting the HP-gonadal axis?

A
  1. Natural GnRH (no longer available in US)
  2. GnRH agonists
  3. GnRH antagonists
  4. Gonadotropin agonists
74
Q

List the 5 GnRH agonists.

A
  1. Leuprolide
  2. Goserlin
  3. Buserelin
  4. Triptorelin
  5. Naferelin
75
Q

What is the MOA of GnRH agonists?

A

Potently activate the GnRH receptor, which leads to down regulation of GnRH receptor and downstream signaling pathways. There is an initial transient flare-up of FSH/LH and gonadal hormones (first 7-10 days).

76
Q

What are the indications for GnRH agonists?

A
  1. Controlled ovarian stimulation during assisted reproduction procedures
  2. Palliative therapy of sex hormone-dependent tumors
  3. Suppress inappropriate growth of hormone-dependent tissues (endometriosis, uterine fibroids)
  4. Treatment of central precocious puberty caused by early onset of HP-gonadal axis (7-8 y/o)
  5. Suppression of endogenous puberty in adolescents with gender dysphoria
77
Q

What is the function of GnRH agonists in ovarian stimulation during assisted reproduction procedures?

A

Suppress endogenous LH surge and prevent premature luteinization of the ovarian follicle

78
Q

What are the AE of GnRH agonists?

A

Generally well-tolerated
Initial flare-up - initial worsening of symptoms
Long term - hot flashes, decreased bone density, vaginal dryness/atrophy, ED

79
Q

What are the contraindications of GnRH agonists?

A

Pregnancy

80
Q

List the GnRH antagonists.

A

Ganirelix, Cetrorelix, Degarelix

81
Q

What is the MOA of GnRH antagonists?

A

Competitive inhibition of the binding of endogenous GnRH to its receptor leading to suppression of production of endogenous gonadotropins

82
Q

Compare GnRH agonists and antagonists.

A

Antagonists have an immediate effect and NO transient flare-up of gonadotropins; there is more complete inhibition and it is more readily reversible

83
Q

What are the indications of GnRH antagonists?

A
  1. Controlled ovarian stimulation during assisted reproduction producedures (Ganirelix/Cetrorelix)
  2. Treatment of advanced prostate cancer (Degarelix - decrease in androgen production decreases growth of prostate cancer)
84
Q

What are the AE of GnRH antagonists?

A

Side effects associated with gonadal hormone deprivation

85
Q

What are the contraindications of GnRH antagonists?

A

Pregnancy

86
Q

What is human chorionic gonadotropin?

A

Hormone produced by the trophoblast/placenta following fertilization; signals to the corpus luteum that pregnancy has occurred, promotes E and P synthesis to maintain the endometrium for implantation, structurally similar to LH, binds and activates LH receptor

87
Q

Discuss the composition of FSH, LH, and HCG.

A

All are composed of alpha-beta heterodimers (share identical alpha chains); beta chain determines binding - LH and HCG share homologous beta chains and bind to the same receptor

88
Q

What are the available gonadotropin formulations?

A
  1. Menotropins (hMG) - combined human FSH and LH
  2. FSH (uFSH - urofollitropin, rFSH - recombinant, shorter half life, lower potency than uFSH)
  3. LH (no longer commercially available in the US)
  4. HCG (rHCG or HCG)
89
Q

What are the clinical uses of gonadotropins?

A
  1. Treatment of female infertility in anovulatory women
  2. Ovarian hyperstimulation in assisted reproduction procedures
  3. Treatment of male infertility in men with hypogonadotropic hypogonadism
90
Q

When can gonadotropins be used to treat female infertility in anovulatory women?

A
  1. Hypogonadotropic hypogonadism secondary to hypothalamic/pituitary dysfunction
  2. Hypothalamic amenorrhea due to excessive exercise or low body weight
  3. Women with PCOS who have failed to ovulate with other treatments
91
Q

What is the goal of gonadotropin use in infertile anovulatory women?

A

To induce the formation and ovulation of a single dominant follicle to allow for pregnancy

92
Q

Describe the treatment regimen with gonadotropins in female infertility/anovulatory women.

A
  1. Gonadotropins (FSH or hMG) during pre-peak to promote follicle development (increasing dose)
  2. Detect <2 follicles >17 mm with ultrasound
  3. Administer HCG to trigger LH receptors/promote ovulation
  4. Intercourse or artificial insemination within 36 hours
93
Q

Describe the treatment regimen with gonadotropins in assisted reproduction procedures.

A
  1. High doses of gonadotropins (rFSH or hMG) administered to stimulate maturation of multiple ovarian follicles
  2. GnRH agonists or antagonists are administered in parallel to suppress endogenous LH surge and prevent ovulation/premature luteinization of the ovarian follicles
  3. Monitor production of healthy follicles by ultrasound
  4. Trigger ovulation by HCG, harvest eggs 36 hours later
  5. Oocytes are fertilized in vitro and transferred to a prepared uterus for implantation
94
Q

Compare ovarian hyperstimulation protocols using agonists vs. antagonists.

A

Agonist long protocol: give GnRH agonist during luteal phase to suppress LH surge/ovulation through to ovulation vs. Antagonist short protocol: give GnRH antagonist midway through pre-peak

95
Q

What are the symptoms of hypogonadotropic hypogonadism in males?

A

Delayed or absent puberty
Under-developed testes
Infertility

96
Q

How are gonadotropins used to treat male infertility in men with hypogonadotropic hypogonadism?

A
  1. Androgen therapy provided initially to stimulate secondary sexual characteristic development.
  2. HCG injections 3x/week for 8-12 weeks to stimulate LH responses and induce T synthesis (monitor levels)
  3. Lower HCG dose and provide FSH treatment 3x/week (hMG or rFSH)
  4. Monitor sperm count
97
Q

What are AE of gonadotropins in women?

A
  1. Multiple pregnancies
  2. Ovarian hyperstimulation syndrome (OHSS) - potentially life-threatening, results from ovarian secretion of factors that promote vascular permeability
98
Q

What is seen in OHSS?

A

Rapid accumulation of fluid in the peritoneal cavity, thorax, and pericardium, hypovolemia and electrolyte abnormalities, ARDS, ovarian enlargement, ascites, hepatic dysfunction, and thromboembolic events

99
Q

What are AE of gonadotropins in men?

A

Gynecomastia due to elevated estrogen synthesis

100
Q

What is oxytocin?

A

Nonapeptide that stimulates the frequency and force of uterine contractions and plays a role in milk ejection from the breast

101
Q

What is the MOA of oxytocin?

A

Acts through G-protein coupled receptors on uterine SMC and breast myoepithelium

102
Q

What are the indications of oxytocin?

A
  1. Induce labor (IV infusion) under conditions requiring expedited vaginal delivery (uncontrolled maternal diabetes, worsening pre-eclampsia, intrauterine infection, ruptured membrane, protracted labor)
  2. Treat uterine atony (failure to contract after delivery) - compressed blood vessels to prevent hemorrhage
103
Q

What are the AE of oxytocin?

A

Rare with correct use

Excessive stimulation of the uterus prior to delivery can cause fetal distress, placental abruption, or uterine rupture

High concentrations can activate vasopressin receptors leading to excessive fluid retention, hyponatremia, heart failure, seizures, and death

104
Q

Describe the role of ADH on the cardiovascular system.

A

Stimulates V1 vasopressin receptors on peripheral arterioles, promotes vasoconstriction, increases arterial BP

105
Q

Describe the role of ADH on the kidney.

A

Stimulates V2 vasopressin receptors in the DCT and CD, induces expression of water channels, and increases water reabsorption from the nephron

106
Q

How is ADH release triggered?

A

Reduced plasma volume activates low pressure baroreceptors in veins OR increased plasma osmolality activates osmoreceptors

107
Q

What is the main ADH agonist?

A

Desmopressin

108
Q

What is the MOA of Desmopressin?

A

Selective agonist of the V2 receptor, promotes water reabsorption in the kidney; also activates V2 on endothelial cells, promote release of VW factor and blood coagulation

109
Q

What are the indications of Desmopressin?

A
  1. Neurogenic diabetes insipidus (ADH secretion deficiency)
  2. Nocturnal enuresis
  3. Minor bleeding in patients with mild hemophilia and VW disease
110
Q

What are the AE of Desmopressin?

A

Headache, hyponatremia, acute thrombotic events (rare)

111
Q

What is the MOA of vasopressin?

A

Synthetic full agonist of V1 and V2 receptors, promotes vasoconstriction and BP

112
Q

What is the indication of Vasopressin?

A

Second line agent in treatment of refractory vasodilatory shock (unresponsive to EPI)

113
Q

What are the AE of Vasopressin?

A

CV (Afib, low CO, arrhythmia) and hyponatremia

114
Q

What are the two vasopressin receptor antagonists?

A

Conivaptan and Tolvaptan

115
Q

What is the MOA of Conivaptan?

A

Antagonist of both V1 and V2, blocks ADH, promotes increased water excretion and raises serum Na+

116
Q

What are the indications of Conivaptan?

A

Treatment of hypervolemic hyponatremia associated with SIADH

117
Q

What is hte MOA of Tolvaptan?

A

Selective antagonist of ADH at V2, promotes increased water excretion and raises serum Na+

118
Q

What are the indications of Tolvaptan?

A

Treatment of hypervolemic hyponatremia associated with SIADH

119
Q

What are the AE of Conivaptan and Tolvaptan?

A

Conivaptan - none
Tolvaptan - hepatotoxicity (contra in liver disease), osmotic demylination syndrome (overly rapid correction of hyponatremia)

PT 2 (15 decks)

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