Pit H.
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| What is growth hormone called | Somatotropin
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| What regulates secretion of GH | GHRH (positive) and Somatostatin (negative)
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| What is interesting about the release of GHRH | Pulsile
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| What is activated by GH | (include receptor, and one hormone, and one location) In the liver, GH binds a JAK-STAT receptor and leads to the release of IGF-1
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| Who has high level of GH | (4 – random mix) 1.Kids, 2.Hypoglycemia, 3.Long sleep, 4.Ppl that exercise
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| Other than GH what leads to increase IGF-1 | Eating/nutrition
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| How does IGF-1 feedbacks on the growth hormone pathway | 1.inhibitis the release of GHRH and 2.promote the release of somatostatin
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| What are three causes of GH deficiency/malfunction | 1.Laron’s syndrome, 2.Dwarfism, 3.Pit Adenomas
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| What is dwarfism due to | Hypothalamic defect (can't make GHRH)
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| What are the tx for dwarfism | (2) (which one works better) 1.recombinant GH (better), 2.synthetic GHRH
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| what is synthetic GHRH called | sermorelin
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| What are the side effects of dwarfism tx | (2) 1.Intracranial hypertension, 2.Scoliosis: due to too fast growth (+maybe leukemia)
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| What is somatrem | A derivative of GH with a methionine (can be used to tx dwarfism)
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| What are the tx of Laron’s | (drug also called) IGF-1 (mecasermin)
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| Why can’t one use GH or GHRH to tx Laron’s | Receptors don’t work
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| What are the 3 Sx of GH deficiency in adults (due to pit adenoma) | 1. fat distribution, 2. Decrease muscle, 3.impaired psychosocial
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| How is GH deficience due to pit adenoma txed | (1) GH/Somatotropin
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| What are the AE of Somatotropin in adults | (4) Edema, and carpal tunnel , arthalgia, myalgia
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| How is GH deficiency dxed | (2) 1.Induced hypoglycemia using insulin (should raise GH), 2.Give sermorelin (should raise GH)
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| Why can’t GH deficiency not be dxed by looking at serum GH levels | Not consistent (pulsile)
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| How is GH deficience tx, monitored | IGF-1 serum levels
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| Is hGH effective at increasing muscle strength | No (not proven)
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| What are the side effects of hGH in athletes | (5) Edema, and carpal tunnel , arthalgia, myalgia + ACROMEGALY
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| Why aren’t athletes tested for hGH | Can’t (remember the pulsile thing)
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| 3 other medical uses of GH | (all related to decrease growth or maintenance of weight) 1.AIDS wasting, 2.Short bowel syndrome, 3.Intrauterine growth retard
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| What are the 2 GH excess disorders | (which one is after puberty
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| Causes of GH excess disorders | (1) Pit adenoma
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| How are GH excess disorders dx | (2) Sx and IGF-1
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| 3 Tx for GH excess disorders | 1.Pit surgery, 2.Octreotide (synthetic somatostatin), 3.Pegvisomant (GH-receptor antagonist)
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| What is the advantage of octreotide, what is the advantage of pegvisomant | Octreotide: targets the tumor, can make it smaller, Pegvisomant: treat Sx better
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| What is a major problem (not AE) of octreotide | Many tumors do not respond
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| AE of octreotide | (1) Gallstones
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| AE of pegvisomant: (1) Abnormal liver test (reversible) |
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| what is the function of prolactin | (1~2) 1.breast development, 2.lactation
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| Who has low level of prolactin | (1) Males
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| Who has high levels of prolactin | (3) 1.cycling females, 2.early pregnancy, 3.lactation
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| what can lead to increase serum levels of prolactin | (4) 1.Hypoglycemia, 2.Deep sleep, 3.excercise, 4.children
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| Prolacting inhibitis: _____________ (~1) Gonadotropins release |
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| What regulates the release of prolactin | (2) 1.TRH increases the release of prolactin, 2.Dopamine inhibitis the release of prolactin
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| What are the 4 causes of hyperprolactinemia | 1.Pit adenoma, 2.Hypothalamus problems, 3.Renal failure (decrease excretion), 4.Chest trauma (autonomic response)
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| what are the Sx of hyperprolactinemia | (males: 4, women: 3) Males: infertility, impotence, loss of libido, breasts; Females: infertility, amenorrhea, milk secretion when non-pregnant
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| What are the Tx of hyperprolactinemia | (4) 1.Surgery, 2.Radiation, 3.Bromocriptine, 4.Pergolide
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| How do bromocriptine and pergolide work | (what is important to note) They are dopamine agonist, thus inhibit the production of prolactin. It is important to note, that if Tx is stopped, tumor will resume.
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| what are 2 AE of bromocriptine and pergolide | 1.rare CNS effects, 2.insomnia
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| what are the causes of decrease FSH or LH | (2 vague) 1.hypothalamic, 2.pituitary
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| What are the Sx of FSH deficiency | (3 women, 2 men) Women: amenorrhea, infertility, decrease breast development; Men: decreased testis size, oligospermia
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| What are the Sx of LH deficiency | (3 women, 2 men) Women: amenorrhea, infertility, cystic ovaries; Men: infertility, no puberty
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| what are the tx used in hypogonodotropism | (5 – which ones is not used anymore) They are all about hormone replacement: 1.Chorionic gonadotropin (CG) – mimics LH, 2. Menotropins (urinated FSH and LH from postmenopausal women), 3.Urofollitropin (FSH - menotropins with LH removed), 4.recombinant FS
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| What are the AE of gonadotropim tx | (2) 1.Multiple births, 2.Ovarian hyperstimulation syndrome (OHSS): ovaries start secreting substances that increase permeability and you get systemic edema (including lungs)
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| What are the causes of hypergonadotropism | (1- who gets it) Males can get LH receptor which are always active (dominant disease)
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| What are the Sx of hypergonadotropism | (2) 1.Precocious puberty, 2.Testicular tumor
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| What is the Tx of hypergonadotropism | (vague) Steroid synthesis inhibitors
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| How are gonadotropic disease dx | (2~3) 1.FSH and LH levels, 2.give GnRH (if LH goes up: it is a hypothalamic problem, if it does not: it is a pit problem)
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| 2 other uses of gonadotropins | CG can be used for undescended testes, FSH and CG can be used for In Vitro Fertilization (IVF)
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| What is addison’s | Low cortisol
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| How is addison’s txed | Cortisol
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| What is cushing’s syndrome | High cortisol
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| How is cushing’s txed | ketoconazole (suppress corticosteroid synthesis)
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| What is the precursor of ADH | Vasopressin
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| What are the receptors for ADH | (2 – their function) V1 (sm. Muscle contraction) and V2 (conservation of water by the kidney)
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| How does ADH work at the cellular level | (2) 1.binds receptor, thus leading to increase in cAMP, 2.aquaporins go from inside the cell to binding the plasma membrane
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| ADH leads to increase or decrease permeability | Increase
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| What makes ADH | Hypothalamus
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| From where is ADH released | Post. Pit.
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| What controls the release of ADH | (3) Osmoreceptors in the hypothalamus, heart, and aorta
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| Other than osmoreceptors what can lead to increase ADH | (3) Pain, nausea, hypoxia
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| What are the 2 diseases of decrease ADH | 1.Diabetes insipidus, 2.Nephrogenic diabetes insipidus
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| What are the 2 causes of DI | 1.autosomal dominant due to misfolding of vasopressin prohormone (lead to neuronal death), 2.autosomal recessive due to misfolding of vasopressin
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| What are the 3 Sx of DI | 1.Polyuria, 2.Polydipsia, 3. Dehydration
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| How are DI and NDI DDxed from polydipsia | High osmolarity
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| How are DI and NDI DDxed | DI responds positively to desmopressin
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| What are the 2 tx of DI | Vasopressin or desmopressin (analog vasopressin)
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| AE of Vasopressin or Desmopressin | (for each receptors) (5) V1 (most): intestinal cramping & vasoconstriction/pallor/MI – V2: water intoxication, seizures, dizziness (brain swelling)
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| Who cannot receive vasopressin or desmopressin | (2) Heart problem patients, Renal failure
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| What are the 3 causes of NDI | 1.X-linked NDI-V2 receptor defect, 2.autosomal recessive or dominant mutations in aquaporins 2, 3.Drug/Lithium induced inhibition of V2
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| What are the Sx of NDI | (general) Same as DI (1.Polyuria, 2.Polydipsia, 3. Dehydration)
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| Tx of NDI | (2, one drug, one behavioral) 1.Increase water intake, 2.Thiazide diuretics (paradoxical, MOA:
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| What disease is linked with increased ADH | SIADH
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| What can cause SIADH | (5) Cerebellar disease, pulmonary disease, cancer, head trauma, drugs
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| What are the tx of SIADH | (3, only 1 drug) 1.water restriction, 2.IV saline, 3.demeclocycline
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| MOA of demeclocycline | Inhibitis decrease cAMP in the collecting duct
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| What drug is known to increase ADH | NSAIDs
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| How come many drugs seem to influence the level of ADH | Might influence pain and nausea
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| what are the 2 functions of oxytocin | 1.milk ejection, 2.uterine contraction
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| Where is oxytocin made | Hypothalamus
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| What leads to oxytocin release | (2) 1.suckling on breast, 2.uterine stretching
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| Where are receptors for oxytocin found | (3) 1.epithelial of mammary glands, 2.oviducts, 3.uterus
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| what is oxytocin used for | (2) 1.induce labor/initiate contraction/ enhance contraction, 2.inducte lactation
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| What form is oxytocin given in when used to induce lactation | 1.nasal spray
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| 3 AE of oxytocin | 1.fatal hypoxia, 2.excessive contraction, 2.uterine rupture
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| What is used to tx preterm labor | (to suppress it) Atosiban, an oxytocin antagonist
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