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Pharm- Pit. H.
Pit H.
| Question | Answer |
|---|---|
| What is growth hormone called | Somatotropin |
| What regulates secretion of GH | GHRH (positive) and Somatostatin (negative) |
| What is interesting about the release of GHRH | Pulsile |
| 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 |
| Who has high level of GH | (4 – random mix) 1.Kids, 2.Hypoglycemia, 3.Long sleep, 4.Ppl that exercise |
| Other than GH what leads to increase IGF-1 | Eating/nutrition |
| How does IGF-1 feedbacks on the growth hormone pathway | 1.inhibitis the release of GHRH and 2.promote the release of somatostatin |
| What are three causes of GH deficiency/malfunction | 1.Laron’s syndrome, 2.Dwarfism, 3.Pit Adenomas |
| What is dwarfism due to | Hypothalamic defect (can't make GHRH) |
| What are the tx for dwarfism | (2) (which one works better) 1.recombinant GH (better), 2.synthetic GHRH |
| what is synthetic GHRH called | sermorelin |
| What are the side effects of dwarfism tx | (2) 1.Intracranial hypertension, 2.Scoliosis: due to too fast growth (+maybe leukemia) |
| What is somatrem | A derivative of GH with a methionine (can be used to tx dwarfism) |
| What are the tx of Laron’s | (drug also called) IGF-1 (mecasermin) |
| Why can’t one use GH or GHRH to tx Laron’s | Receptors don’t work |
| What are the 3 Sx of GH deficiency in adults (due to pit adenoma) | 1. fat distribution, 2. Decrease muscle, 3.impaired psychosocial |
| How is GH deficience due to pit adenoma txed | (1) GH/Somatotropin |
| What are the AE of Somatotropin in adults | (4) Edema, and carpal tunnel , arthalgia, myalgia |
| How is GH deficiency dxed | (2) 1.Induced hypoglycemia using insulin (should raise GH), 2.Give sermorelin (should raise GH) |
| Why can’t GH deficiency not be dxed by looking at serum GH levels | Not consistent (pulsile) |
| How is GH deficience tx, monitored | IGF-1 serum levels |
| Is hGH effective at increasing muscle strength | No (not proven) |
| What are the side effects of hGH in athletes | (5) Edema, and carpal tunnel , arthalgia, myalgia + ACROMEGALY |
| Why aren’t athletes tested for hGH | Can’t (remember the pulsile thing) |
| 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 |
| What are the 2 GH excess disorders | (which one is after puberty |
| Causes of GH excess disorders | (1) Pit adenoma |
| How are GH excess disorders dx | (2) Sx and IGF-1 |
| 3 Tx for GH excess disorders | 1.Pit surgery, 2.Octreotide (synthetic somatostatin), 3.Pegvisomant (GH-receptor antagonist) |
| What is the advantage of octreotide, what is the advantage of pegvisomant | Octreotide: targets the tumor, can make it smaller, Pegvisomant: treat Sx better |
| What is a major problem (not AE) of octreotide | Many tumors do not respond |
| AE of octreotide | (1) Gallstones |
| AE of pegvisomant: (1) Abnormal liver test (reversible) | |
| what is the function of prolactin | (1~2) 1.breast development, 2.lactation |
| Who has low level of prolactin | (1) Males |
| Who has high levels of prolactin | (3) 1.cycling females, 2.early pregnancy, 3.lactation |
| what can lead to increase serum levels of prolactin | (4) 1.Hypoglycemia, 2.Deep sleep, 3.excercise, 4.children |
| Prolacting inhibitis: _____________ (~1) Gonadotropins release | |
| What regulates the release of prolactin | (2) 1.TRH increases the release of prolactin, 2.Dopamine inhibitis the release of prolactin |
| What are the 4 causes of hyperprolactinemia | 1.Pit adenoma, 2.Hypothalamus problems, 3.Renal failure (decrease excretion), 4.Chest trauma (autonomic response) |
| 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 |
| What are the Tx of hyperprolactinemia | (4) 1.Surgery, 2.Radiation, 3.Bromocriptine, 4.Pergolide |
| 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. |
| what are 2 AE of bromocriptine and pergolide | 1.rare CNS effects, 2.insomnia |
| what are the causes of decrease FSH or LH | (2 vague) 1.hypothalamic, 2.pituitary |
| What are the Sx of FSH deficiency | (3 women, 2 men) Women: amenorrhea, infertility, decrease breast development; Men: decreased testis size, oligospermia |
| What are the Sx of LH deficiency | (3 women, 2 men) Women: amenorrhea, infertility, cystic ovaries; Men: infertility, no puberty |
| 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 |
| 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) |
| What are the causes of hypergonadotropism | (1- who gets it) Males can get LH receptor which are always active (dominant disease) |
| What are the Sx of hypergonadotropism | (2) 1.Precocious puberty, 2.Testicular tumor |
| What is the Tx of hypergonadotropism | (vague) Steroid synthesis inhibitors |
| 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) |
| 2 other uses of gonadotropins | CG can be used for undescended testes, FSH and CG can be used for In Vitro Fertilization (IVF) |
| What is addison’s | Low cortisol |
| How is addison’s txed | Cortisol |
| What is cushing’s syndrome | High cortisol |
| How is cushing’s txed | ketoconazole (suppress corticosteroid synthesis) |
| What is the precursor of ADH | Vasopressin |
| What are the receptors for ADH | (2 – their function) V1 (sm. Muscle contraction) and V2 (conservation of water by the kidney) |
| 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 |
| ADH leads to increase or decrease permeability | Increase |
| What makes ADH | Hypothalamus |
| From where is ADH released | Post. Pit. |
| What controls the release of ADH | (3) Osmoreceptors in the hypothalamus, heart, and aorta |
| Other than osmoreceptors what can lead to increase ADH | (3) Pain, nausea, hypoxia |
| What are the 2 diseases of decrease ADH | 1.Diabetes insipidus, 2.Nephrogenic diabetes insipidus |
| 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 |
| What are the 3 Sx of DI | 1.Polyuria, 2.Polydipsia, 3. Dehydration |
| How are DI and NDI DDxed from polydipsia | High osmolarity |
| How are DI and NDI DDxed | DI responds positively to desmopressin |
| What are the 2 tx of DI | Vasopressin or desmopressin (analog vasopressin) |
| AE of Vasopressin or Desmopressin | (for each receptors) (5) V1 (most): intestinal cramping & vasoconstriction/pallor/MI – V2: water intoxication, seizures, dizziness (brain swelling) |
| Who cannot receive vasopressin or desmopressin | (2) Heart problem patients, Renal failure |
| 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 |
| What are the Sx of NDI | (general) Same as DI (1.Polyuria, 2.Polydipsia, 3. Dehydration) |
| Tx of NDI | (2, one drug, one behavioral) 1.Increase water intake, 2.Thiazide diuretics (paradoxical, MOA: |
| What disease is linked with increased ADH | SIADH |
| What can cause SIADH | (5) Cerebellar disease, pulmonary disease, cancer, head trauma, drugs |
| What are the tx of SIADH | (3, only 1 drug) 1.water restriction, 2.IV saline, 3.demeclocycline |
| MOA of demeclocycline | Inhibitis decrease cAMP in the collecting duct |
| What drug is known to increase ADH | NSAIDs |
| How come many drugs seem to influence the level of ADH | Might influence pain and nausea |
| what are the 2 functions of oxytocin | 1.milk ejection, 2.uterine contraction |
| Where is oxytocin made | Hypothalamus |
| What leads to oxytocin release | (2) 1.suckling on breast, 2.uterine stretching |
| Where are receptors for oxytocin found | (3) 1.epithelial of mammary glands, 2.oviducts, 3.uterus |
| what is oxytocin used for | (2) 1.induce labor/initiate contraction/ enhance contraction, 2.inducte lactation |
| What form is oxytocin given in when used to induce lactation | 1.nasal spray |
| 3 AE of oxytocin | 1.fatal hypoxia, 2.excessive contraction, 2.uterine rupture |
| What is used to tx preterm labor | (to suppress it) Atosiban, an oxytocin antagonist |
Created by:
mcafej02
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