P.05 Hypothalamic & Pituitary Hormones PDF

PCC SOM 2026 PHARMACOLOGY AND THERAPEUTICS P.05 HYPOTHALAMIC & PITUITARY HORMONES PHARMACOLOGY LECTURE LECTURER: DR. SHARON GAWIGAWEN LECTURE DATE: 01/22/2024 TOPIC OUTLINE I. II. III. IV. V. ENDOCRINE SYSTEM TYPES OF HORMONES ACTION OF ENDOCRINE DRUGS HYPOTHALAMIC-PITUITARY-TARGET H-P DRUGS A. GROW...

PCC SOM 2026 PHARMACOLOGY AND THERAPEUTICS P.05 HYPOTHALAMIC & PITUITARY HORMONES PHARMACOLOGY LECTURE LECTURER: DR. SHARON GAWIGAWEN LECTURE DATE: 01/22/2024 TOPIC OUTLINE I. II. III. IV. V. ENDOCRINE SYSTEM TYPES OF HORMONES ACTION OF ENDOCRINE DRUGS HYPOTHALAMIC-PITUITARY-TARGET H-P DRUGS A. GROWTH HORMONE B. GROWTH HORMONE ANTAGONISTS C. GONADOTROPINS D. GONADOTROPIN-RH & ITS ANALOGS E. GnRH RECEPTOR ANTAGONISTS F. PROLACTIN G. DOPAMINE AGONISTS H. OXYTOCIN I. OXYTOCIN ANTAGONIST J. VASOPRESSIN K. VASOPRESSIN ANTAGONISTS Particular cell is a target cell for a hormone if it contains functional receptors for that hormone, and cells which do not have such a receptor cannot be influenced directly by that hormone. a. Hormones - chemical messengers secreted into blood or extracellular fluid by one cell that affect the functioning of other cells. - Most hormones circulate in blood, coming into contact with essentially all cells. - a given hormone usually affects only a limited number of cells, which are called target cells. b. Target cell - responds to a hormone because it bears receptors for the hormone. c. Hormone receptors - found either outside the cell (exposed on the surface of the cell) or inside/within the cell depending on the type of hormone - binding of hormone to receptor triggers a cascade of reactions within the cell that affects function. II. I. ENDOCRINE SYSTEM A. AGONISTS Endocrine disorders are unique in the sense that treatment can be targeted directly to the malfunctioning pathway. complex network of glands and organs. uses hormones to control and coordinate your body's metabolism, energy level, reproduction, growth and development, and response to injury, stress, and mood. control of metabolism, growth, and reproduction is mediated by a combination of neural and endocrine systems located in the hypothalamus and pituitary gland. N OT E TA K E R : B A C W A D E N , TYPES OF MOLECULES BASED ON ITS RECEPTOR EFFECT C U T A Y, S A N G D A A N , A B U L E N C I A induce all the post receptor events that lead to a biologic effect/ expected effect/ natural effect act like the "normal" hormone, although perhaps more or less potently. Natural hormones/ endogenous hormones are themselves agonists and, in many cases, more than one distinct hormone binds to the same receptor. For a given receptor, different agonists can have dramatically different potencies. Drugs that are agonists bind to the receptor producing a similar response to the intended chemical and receptor just like a natural hormone. , BALDOS , F E R R E R , B A S T I A N P a g e 1 | 10 PCC SOM 2026 PHARMACOLOGY AND THERAPEUTICS P.05 HYPOTHALAMIC & PITUITARY HORMONES B. ANTAGONISTS IV. HYPOTHALAMIC-PITUITARY- TARGET ORGAN block binding of the agonist, but fail to trigger intracellular signaling events. like certain types of bureaucrats – they don't themselves perform useful work, but block the activities of those that do have the capacity to contribute. widely used as drugs III. PHARMACOLOGIC ACTION OF ENDOCRINE DRUGS a. Hormone replacement: hypofunctioning diseases b. Antihormone treatment: hyperfunctioning disorders are the hallmark of endocrine treatment. Areas of Application: 1. Replacement therapy in hormonal deficiency states. 2. Antagonists of diseases caused by excess production of hormones. 3. Regulate normal endocrine function to achieve a desired effect. E.g., inhibition of ovulation 4. Diagnostic tools for identifying endocrine abnormalities. The H and P gland is connected by a stalk of neurosecretory fibers and blood vessels, including a portal venous system that drains the hypothalamus and perfuses the anterior pituitary. Portal venous system carries small regulatory or releasing hormones from the hypothalamus to the anterior pituitary. Releasing hormones stimulate anterior pituitary cells to produce their corresponding hormones compared to the posterior lobe hormones, they are produced in the hypothalamus and transported via the neurosecretory fibers in the stalk of the pituitary to the posterior lobe from there they are stored and released into the circulation. Posterior Pituitary Hormones Oxytocin Anti-diuretic Hormone Target Organs Breast, Uterus Kidneys A. HYPOPITUITARISM a. b. c. d. e. f. N OT E TA K E R : B A C W A D E N , C U T A Y, S A N G D A A N , A B U L E N C I A disorders from hypothalamus and/or pituitary gland causing deficiency in one or more pituitary hormones GH deficiency o short stature, micropenis (children), fatigue, decreased sense of well-being (adults) TSH deficiency o low T4 and T3 – short stature, mental retardation, fatigue, weight gain ACTH deficiency o Low cortisol- adrenal crisis (hypotension, vomiting, low blood sugar, shock) LH, FSH deficiency o low estrogen and testosterone (delayed puberty, micropenis, undescended testis) Vasopressin (ADH) deficiency o D. insipidus (polyuria, hypotension, shock) Oxytocin deficiency o like inability to lactate, vaginal dryness, decreased libido, etc. , BALDOS , F E R R E R , B A S T I A N P a g e 2 | 10 PCC SOM 2026 PHARMACOLOGY AND THERAPEUTICS P.05 HYPOTHALAMIC & PITUITARY HORMONES  CAUSES OF HYPOPITUITARISM ✓ tumors ✓ infiltrative diseases ✓ hydrocephalus ✓ genetic mutations ✓ chromosomal disorders 1. Growth hormone (GH; somatotropin) 2. Somatropin B. HYPERPITUITARISM primary hypersecretion of pituitary hormones, typically from pituitary adenoma a. PHARMAKOKINETICS i. HYPOTHALAMIC- PITUITARY HORMONES/DRUGS PHARMACOLOGIC APPLICATION Frequently used as treatment ✓ GH, somatostatin ✓ LH, FSH ✓ GnRH, ✓ dopamine ✓ analogs of these hormones the recombinant form of GH, has a 191- amino-acid sequence that is identical with the predominant native form of human GH. Creutzfeldt-Jakob Disease In the past, medicinal GH was isolated from the pituitaries of human cadavers. However, this form of GH was found to be contaminated with prions that could cause this disease. For this reason, it is no longer used. a. High GH level o acromegaly and gigantism b. High prolactin o galactorrhea, infertility, oligomenorrhea, amenorrhea c. High ACTH o high cortisol (Cushing syndrome) V. 191-aminoacid peptide with two sulfhydryl bridges. Closely resembles that of prolactin. Infrequently used as treatment ✓ TRH, TSH ✓ GHRH ✓ CRH and ACTH used for specialized diagnostic testing for stimulation in some hypo/hyperfunctioning endocrine disorders ii. Circulating endogenous GH secretion: pulsatile (approx. 10 pulses per day) lasting approximately 90 minutes and separated by approximately 128 minutes. half-life: 20 minutes Clearance: liver Recombinant human GH (rhGH) Administration: subcutaneously 6–7x /week Peak levels: 2–4 hours, and active blood levels persist for approximately 36 hours. Usually at bedtime since high GH secretion at night or during sleep b. PHARMACODYNAMICS A. GROWTH HORMONE: SOMATOTROPIN GH mediates its effects via cell surface receptors of the JAK/STAT cytokine receptor superfamily GH has complex effects: i. Growth mediated principally, but not solely, through an increase in the production of IGF-I. Majority of IGF-1 is produced by the liver. o In liver disease, short stature may be seen Gh has autocrine or paracrine roles tha stimulates production of IGF-1 in bone, cartilage, muscle, kidney, and other tissues, It stimulates longitudinal bone growth until the epiphyseal plates fuse—near the end of puberty. N OT E TA K E R : B A C W A D E N , C U T A Y, S A N G D A A N , A B U L E N C I A , BALDOS , F E R R E R , B A S T I A N P a g e 3 | 10 PCC SOM 2026 PHARMACOLOGY AND THERAPEUTICS P.05 HYPOTHALAMIC & PITUITARY HORMONES  GIGANTISM When a GH-secreting adenoma occurs before the long bone epiphyses close Vertical growth ii. Body composition in both children and adults, GH has anabolic effects in muscle and catabolic effects in adipose cells that shift the balance of body mass to an increase in muscle mass and a reduction in adiposity.  ACROMEGALY characterized by abnormal growth of cartilage and bone tissue, and many organs including skin, muscle, heart, liver, and the gastrointestinal tract Seen in adults Lateral growth iii. Carbohydrate, protein, and lipid metabolism B.1. SOMATOSTATIN c. TOXICITY Children generally tolerate GH treatment well Adverse events are relatively rare pseudotumor cerebri slipped capital femoral epiphysis progression of scoliosis edema, hyperglycemia increased risk of asphyxiation in severely obese patients with Prader-Willi syndrome (GH is an anabolic steroid that can cause further obesity) upper airway obstruction or sleep apnea B. GROWTH HORMONE ANTAGONISTS used to reverse the effects of GH producing cells in the anterior pituitary (GH-secreting pituitary adenomas) = ↑ GH levels N OT E TA K E R : B A C W A D E N , C U T A Y, S A N G D A A N , a 14-amino-acid peptide found in the hypothalamus, other parts of the central nervous system, the pancreas, and other sites in the gastrointestinal tract primarily acts as an inhibitory paracrine factor and inhibits the release of GH, TSH, glucagon, insulin, and gastrin rapidly cleared from the circulation half-life: 1–3 minutes. B.2. PEGVISOMANT GH receptor antagonist used to treat acromegaly Polyethylene glycol (PEG) derivative of a mutant GH. B.3. LANREOTIDE octapeptide somatostatin analog approved for the treatment of acromegaly B.4. OCTREOTIDE A B U L E N C I A most widely used somatostatin analog 45X more potent than somatostatin in inhibiting GH release half-life: about 80 minutes, 30 times longer than that of somatostatin indications: hormone-secreting tumors:acromegaly, carcinoid syndrome, gastrinoma, glucagonoma, insulinoma, VIPoma, and ACTH-secreting tumor. other therapeutic use: ✓ include diarrhea—secretory, HIV associated, diabetic, chemotherapy, or radiation induce. ✓ For acute control of bleeding from esophageal varices (portal hypertension) , BALDOS , F E R R E R , B A S T I A N P a g e 4 | 10 PCC SOM 2026 PHARMACOLOGY AND THERAPEUTICS P.05 HYPOTHALAMIC & PITUITARY HORMONES a. PHARMACODYNAMICS FSH, LH and hCG exert their effects through G protein coupled receptors C. GONADOTROPINS: FSH, LH, HCG C.1. GONADOTROPINS (FSH & LH) ✓ in women: FSH: stimulates ovarian follicle development LH: critical for ovulation, stimulation of androgens (the estradiol precursors) from theca cells, and maintenance of the corpus luteum ✓ in men: FSH: primary regulator of spermatogenesis LH: stimulates testosterone production from the Leydig cells in the testes for virilization (developing male fetus) ✓ Important for sexual development during puberty serve complementary functions in the reproductive process b. CLINICAL INDICATIONS: 1. Ovulation induction- in women with hypogonadotropic hypogonadism, polycystic ovarian syndrome *hypogonadotropic hypogonadism: decreased hormone secretion in hypothalamus and pituitary gland 2. Controlled ovarian stimulation- in assisted reproductive technology procedures 3. Male infertility/ hypogonadism (micropenis; delayed puberty) 4. Prepubertal cryptorchidism- hCG induces testicular descent; not recommended at present for treatment of cryptorchidism because long term efficacy is much lower than that of surgical treatment 5. Stimulation test in the diagnosis of hypogonadism primary vs secondary/central C.2. HUMAN CHORIONIC GONADOTROPIN (hCG) placental glycoprotein nearly identical with LH its actions are mediated through LH receptors high hCG = high testosterone i. PHARMACOKINETICS heterodimers, share an identical α subunit LH and hCG have nearly identical β subunit Administration: subcutaneous or I.M. Half-lives vary by preparation and route of injection: 10-40 hrs c. TOXICITY/ COMPLICATIONS 1. Ovarian hyperstimulation syndrome (OHSS) ovarian enlargement, intravascular depletion, ascites, liver dysfunction, pulmonary edema, thromboembolic events self-limited with spontaneous resolution within a few days severe disease may require hospitalization and intensive care C.3. MENOTROPINS OR HUMAN MENOPAUSAL GONADOTROPIN (HMG) first commercial gonadotropin containing both LH and FSH extracted from urine of postmenopausal women 1960’s: for stimulation of follicle development in women C.i. Follicle stimulating hormone UROFOLLITROPIN from urine of postmenopausal women recombinant forms: follitropin alfa and follitropin beta C.ii. Luteinizing hormone LUTROPIN ALFA first and only recombinant form of human LH C.iii. Human chorionic gonadotropin PREGNYL produced by human placenta and excreted in the urine where it is extracted and purified N OT E TA K E R : B A C W A D E N , C U T A Y, S A N G D A A N , 2. Multiple pregnancies 5-10% risk during ovulation induction A B U L E N C I A D. GONADOTROPIN- RELEASING HORMONE (GnRH) AND ITS ANALOGS Endogenous GNRH causes the pituitary gland to secrete gonadotropins (LH, FSH). In childhood, GNRH levels are normally low. As puberty begins, GNRH levels will start to rise and secondary sexual development will start When the testes and ovaries are fully developed, GNRH, LH and FSH production is being controlled by the level of testosterone, estrogen and progesterone , BALDOS , F E R R E R , B A S T I A N P a g e 5 | 10 PCC SOM 2026 PHARMACOLOGY AND THERAPEUTICS P.05 HYPOTHALAMIC & PITUITARY HORMONES b. PHARMACODYNAMICS GnRH binds to specific G protein coupled receptors in the pituitary – stimulating gonadotropin secretion and synthesis GnRH agonists induce an initial gonadotropin hypersecretion (flare-up), followed by pituitary desensitization and profound suppression of LH and FSH. Prolonged activation of GnRH receptors by GnRH leads to desensitization and consequently to suppressed gonadotropin secretion. This is the primary mechanism of action of agonistic GnRH analogues. c. GNRH CLINICAL INDICATIONS 1. Stimulation o Female infertility o Male infertility o Diagnosis of LH responsiveness in cases of GnRH is a decapeptide found in all mammals. delayed puberty D1. Gonadorelin 2. Suppression of gonadotropin production is an acetate salt of synthetic human GnRH. o Controlled ovarian stimulation Substitution of amino acids at the 6 position or o Endometriosis replacement of the C-terminal glycine amide - defined as the presence of estrogenproduces synthetic agonists. sensitive endometrium outside the uterus Both modifications make them more potent and that results in cyclical abdominal pain in longer lasting than native GnRH premenopausal women. D2. GnRH analogs: - pain of endometriosis is often reduced by goserelin, buserelin, histrelin, leuprolide, abolishing exposure to the cyclical changes nafarelin, and triptorelin. in the concentrations of estrogen and a. PHARMACOKINETICS progesterone that are a normal part of the menstrual cycle Administration o Gonadorelin: intravenously or subcutaneously - ovarian suppression induced by continuous o Nafarelin: nasal spray treatment with a GnRH agonist greatly o Other GnRH agonists can be administered reduces estrogen and progesterone subcutaneously, intramuscularly, via nasal spray, concentrations and prevents cyclical or as a subcutaneous implant. changes. o Uterine leiomyomata/fibroids Half-life o subcutaneous and intranasal: 3 hours - benign, estrogen-sensitive, smooth muscle o intravenous: 4 minutes tumors in the uterus that can cause Duration of clinical uses menorrhagia, with associated anemia and o varies from a few days for controlled ovarian pelvic pain. stimulation to a number of years for - Treatment for 3–6 months with a GnRH treatment of metastatic prostate cancer. agonist reduces fibroid size and, when Preparations combined with supplemental iron, improves o developed with a range of durations of action anemia. from several hours (for daily administration) - effects of GnRH agonists are temporary, to 1, 4, 6, or 12 months (depot forms) with gradual recurrent growth of N OT E TA K E R : B A C W A D E N , C U T A Y, S A N G D A A N , A B U L E N C I A , BALDOS , F E R R E R , B A S T I A N P a g e 6 | 10 PCC SOM 2026 PHARMACOLOGY AND THERAPEUTICS P.05 HYPOTHALAMIC & PITUITARY HORMONES leiomyomas to previous size within several months after cessation of treatment. - GnRH agonists have been used widely for preoperative treatment of uterine leiomyomas, both for myomectomy and hysterectomy. o Prostate cancer - androgen deprivation therapy is the primary medical treatment o Central precocious puberty - onset of puberty before 8 years old in girls and 9 years old in boys - Androgen deprivation therapy is the primary medical therapy for prostate cancer - Combined antiandrogen therapy with continuous GnRH agonist and an androgen receptor antagonist is as effective as surgical castration in reducing serum testosterone concentration and effects o Others: advanced breast and ovarian cancer d. Toxicity Headache, light-headedness, nausea and flushing Local swelling at injection site Osteoporosis and reduced bone mineral density Clinical Indications 1. Suppression of gonadotropin production - Controlled ovarian stimulation 2. Advance prostate cancer - degarelix and abarelix; reduce concentrations of gonadotropins and androgens more rapidly than GnRH agonists Toxicity: nausea and headache F. PROLACTIN Prolactin is a 198-amino-acid peptide hormone produced in the anterior pituitary. Its structure resembles that of GH. Prolactin is the principal hormone responsible for lactation. Milk production is stimulated by prolactin when appropriate circulating levels of estrogens, progestins, corticosteroids, and insulin are present. ❖ Hyperprolactinemia from pituitary prolactin-secreting adenoma G. DOPAMINE AGONISTS E. GnRH RECEPTOR ANTAGONISTS suppress prolactin release very effectively in patients with hyperprolactinemia; GH release is also reduced in patients with acromegaly, although not as effective as the somatostatins G.1. BROMOCRIPTINE AND CABERGOLINE, QUINAGOLIDE 4 SYNTHETIC DECAPEPTIDES Ganirelix | Cetrorelix | Abarelix |Degarelix Inhibit the secretion of FSH and LH in a dosedependent manner Administration: subcutaneous injection N OT E TA K E R : B A C W A D E N , C U T A Y, S A N G D A A N , Administration: All are active as oral preparations all are eliminated by metabolism can also be absorbed systemically after vaginal insertion of tablets to avoid nausea due to oral administration. After vaginal administration, serum levels peak more slowly Half-life Cabergoline- 65 hrs. - longest duration of action Quinagolide- 20 hrs. Bromocriptine- 7 hrs. A B U L E N C I A , BALDOS , F E R R E R , B A S T I A N P a g e 7 | 10 PCC SOM 2026 PHARMACOLOGY AND THERAPEUTICS P.05 HYPOTHALAMIC & PITUITARY HORMONES Clinical Indications 1. Hyperprolactinemia - dopamine agonist is the first-line treatment, and shrinks pituitary prolactin-secreting tumors 2. Physiologic lactation 3. Acromegaly - alone or in combination with pituitary surgery, radiation therapy or octreotide Toxicity nausea, headache, light-headedness, orthostatic hypotension and fatigue H. OXYTOCIN secreted by the posterior pituitary. stimulates muscular contractions in the uterus and myoepithelial contractions in the breast involved in parturition and the milk letdown. During the second half of pregnancy, uterine smooth muscle shows an increase in the expression of oxytocin receptors and becomes increasingly sensitive to the stimulant action of endogenous oxytocin. (In preparation for parturition or labor) Structure 9-amino-acid peptide with an intrapeptide disulfide cross-link. Its amino acid sequence differs from that of vasopressin at positions 3 and 8. Pharmacokinetics Administration: Intramuscular - Control of postpartum bleeding Elimination: Kidneys & Liver Half-life: 5 minutes Clinical Indication 1. Induction of labor - for conditions requiring expedited vaginal delivery (worsening pre-eclampsia, ruptured membranes after 34 weeks gestation, uncontrolled maternal diabetes, intrauterine infection) 2. Immediate postpartum period to stop vaginal bleeding due to uterine atony. Toxicity I. B A C W A D E N , C U T A Y, S A N G D A A N , rare, when used judiciously Contraindications – fetal distress, fetal malpresentation, placental abruption OXYTOCIN ANTAGONIST G.1. ATOSIBAN antagonist of the oxytocin receptor that has been approved outside the United States as a treatment (tocolysis; anticontraction) for preterm labor. modified form of oxytocin that is administered by intravenous infusion for 2–48 hours. In a small number of published clinical trials, atosiban appears to be as effective as βadrenoceptor-agonist tocolytics and to produce fewer adverse effects. In 1998, however, the FDA decided not to approve atosiban based on concerns about efficacy and safety. Pharmacodynamics Oxytocin acts through G protein-coupled receptors and the phosphoinositide-calcium second-messenger system to contract uterine smooth muscle. N OT E TA K E R : stimulates the release of prostaglandins and leukotrienes that augment uterine contraction. causes contraction of myoepithelial cells surrounding mammary alveoli, which leads to milk letdown. Without oxytocin-induced contraction, normal lactation cannot occur. A B U L E N C I A J. VASOPRESSIN (ANTIDIURETIC HORMONE, ADH) released by the posterior pituitary in response to rising plasma tonicity or falling blood pressure. possesses antidiuretic and vasopressor properties. , BALDOS , F E R R E R , B A S T I A N P a g e 8 | 10 PCC SOM 2026 PHARMACOLOGY AND THERAPEUTICS P.05 HYPOTHALAMIC & PITUITARY HORMONES Structure H.1. DESMOPRESSIN ACETATE (DDAVP, 1-desamino-8-darginine vasopressin) long-acting synthetic analog of vasopressin with minimal pressor activity and an antidiuretic-topressor ratio 4000 times that of vasopressin. modified at position 1 contains a d-amino acid at position 8. Like vasopressin and oxytocin, desmopressin has a disulfide linkage between positions 1 and 6. Toxicity Headache, nausea, abdominal cramps, agitation, and allergic reactions occur rarely. OVERDOSAGE can result in hyponatremia and seizures because of water intoxication. When vasopressin is given (anti-diuretic) ► no urine output for hours ► yet the patient keeps drinking ► WATER OVERLOAD ► dilution of sodium in the blood ► HYPONATREMIA and SEIZURES Vasopressin (but not desmopressin) can cause vasoconstriction and should be used cautiously in patients with coronary artery disease. K. VASOPRESSIN ANTAGONIST Drugs Vasopressin Desmopressin Administration I.V , I.M I.V , Sub Q, intranasal, oral Half-life 15 mins 1.5- 2.5 hours Pharmacodynamics Vasopressin activates two subtypes of G protein– coupled receptors V1 receptors: - vascular sm. muscle cells ► vasoconstriction V2 receptors: - on renal tubule cells ► reduce diuresis through increased water permeability and water resorption in the collecting tubules Extrarenal V2-like receptors: - regulate the release of coagulation factor VIII and von Willebrand factor, which increases platelet aggregation. Clinical Indication 1. Central diabetes insipidus treatment of choice deficiency of vasopressin (tumors compressing the pituitary stalk, infiltrative diseases destroying the pituitary stalk, transection of pituitary stalk after surgery) causing polyuria. 2. Esophageal variceal bleeding and colonic diverticular bleeding 3. Treatment of coagulopathy in Hemophilia A and von Willebrand disease N OT E TA K E R : B A C W A D E N , C U T A Y, S A N G D A A N , K.1 CONIVAPTAN | TOLVAPTAN used in patients with hyponatremia or acute heart failure, which is often associated with elevated concentrations of vasopressin e.g. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) They promote excretion of free water, relieve symptoms, and reduced objective signs of hyponatremia and heart failure. ❖ Conivaptan- intravenous ❖ Tolvaptan- oral CHECKPOINT ! 1. The increase of this molecule is the primary action of growth hormone to stimulate growth. 2. What gonadotropin is responsible for spermatogenesis? 3. This is an acetate salt of synthetic human GnRH produced by the substitution of amino acids at the 6 position or replacement of the C-terminal glycine amide. 4. What is the use of oxytocin when treating preterm labor? 5. Desmopressin is a long-acting synthetic analog of vasopressin modified at what position? 6. What vasopressin receptor causes an increase in platelet aggregation? 7. How does Conivaptan differ from Tolvaptan with regard to their administration? 8. The agonist of this hormone is used for the treatment of hyperprolactinemia. 9. What do you call the condition with increased cortisol? 10.What condition is characterized by adrenal insufficiency? A B U L E N C I A , BALDOS , F E R R E R , B A S T I A N P a g e 9 | 10 PCC SOM 2026 PHARMACOLOGY AND THERAPEUTICS P.05 HYPOTHALAMIC & PITUITARY HORMONES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. N OT E TA K E R : B A C W A D E N , C U T A Y, S A N G D A A N , A B U L E N C I A IGF-I FSH Gonadorelin Tocolytic/ anticontraction Position 1 Extrarenal V2-like receptor Conivaptan: Intravenous , Tolvaptan: oral Dopamine Cushing’s Syndrome Addison’s Disease , BALDOS , F E R R E R , B A S T I A N P a g e 10 | 10