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Hypothalamic Pit-axi
Chapter 64 Cecils
| Question | Answer |
|---|---|
| Location of the pituitary gland | It lies at the base of the skull in the sella turcica within the sphenoid bone |
| Anterior Pituitary Hormones | ACTH, GH, PRL, TSH, LH, FSH |
| Posterior Pituitary Hormones | ADH and Oxytocin |
| Most common pituitary tumor | Prolactinomas |
| The earliest clinical manifestation of pituitary tumors are | the characteristitc signs and symptoms caused by hormone hypersecretion. Headache is a frequent symptom. Lateral extension can result in opthalmoplegia, diplopia, ptosis |
| Growth Hormone is inhibited by which hormone? | Somatostatin |
| What is the MOA of GH? | Binds to receptors in the liver and induces secretion of insulin-like growth factor I (IGF-I). IGF-I mediates most of the growth-promoting effects of GH. GH also affects carbohydrate metabolism |
| What is the gold standard test for assessing GH reserve? | Insulin-Induced hypoglycemia (Insulin tolerance test: ITT) |
| ________is a potent stimulus for GH secretion, and a normal response is a peak GH level in exress of 5ng/mL at 60minutes | Hypoglycemia |
| _________can be used as a screening test for GH deficiency | IGF-I. Low IGF-I levels indicate the need to perform provocative testing of GH secretion |
| Gh deficiency during infancy and childhood is exhibited as... | growth retardation, short stature, and fasting hypoglycemia. |
| Adult GH deficiency is exhibited as... | high abdominal fat, total fat mass. low muscle strength, lean body mass, bone density. Glucose intolerance and insulin resistance |
| GH hormone deficiency treatment | Administered in adulthood as a subcutaneous daily injection |
| GH hypersecretion in childhood leads to | Gigantism |
| GH hypersecretion in adulthood leads to | Acromegaly; adults have fused long bone epiphyses, so overgrowth of acral bone will occur |
| GH hypersecretion is almost always caused by __________ | a GH-secreting pituitary adenoma |
| Treatment of GH hypersecretion | Trans-sphenoidal microsurgery is the initial therapy of choice, resulting in rapid reduction of GH levels with a low rate of surgical morbidity. |
| Somatic Changes of Acromegaly | Acral: Enlarged hands and feetMusculoskeletal: Arthralgias, prognathism, malocclusion, carpal tunnel syndrome, proximal myopathySkin: sweatingColon: polyps, CarcinomaCV: cardiomegaly, HTNVisceromegaly: tongue, thyroid, liver |
| Endocrine-Metabolic Changes of Acromegaly | Reproduction: menstrual abnormalities, Galactorrhea, Decreased libidoCarbohydrate Metabolism: Impaired glucose tolerance, DMLipids: Hypertriglyceridemia |
| Prolactin is synthesized and secreted by __________ | pituitary lactotrophs |
| Hypothalamic _________ provides predominantly inhibitory control of PRL secretion, allowing only a low basal rate of secretion | Dopamine |
| Hyperprolactinemia in women can cause hypogonadotropic hypogonadism, resulting in _______ deficiency | estrogen. In men who have hyperprolactinemia, testosterone levels are usually suppressed. |
| Clinical features of prolactinomas in women | menstrual irregularities, infertility, galactorrhea |
| Clinical features of prolactinomas in men | decreased libido and impotence |
| Estrogen deficiency can cause | osteopenia, vaginal dryness, hot flashes, and irritability |
| PRL stimulates adrenal androgen production, and androgen excess can cause | weight gain and hirsutism |
| _______ is the test used to confirm the diagnosis of prolactinoma | MRI |
| Medical management of hyperprolactinemia | A dopamine agonist restores gonadal function and fertility in the majority of patients. Dopamine agonists cause tumor shrinkage in a significant number of patients with macroadenomas. |
| TSH stands for | Thyroid-stimulating hormone. |
| TSH secretion is stimulated by the hypothalamic tripeptide ______ | TRH |
| TSH acts upon which gland? | Thyroid, stimulating iodine uptake and the synthesis and release of the thyroid hormones T4 and T3 |
| What provides negative feedback inhibition on pituitary TSH and hypothalamic TRH secretion? | T3 and T4 |
| What method is used to measure TSH levels? | ultrasensitive TSH assay |
| In a patient with hypothyroidism, a suppressed TSH level indicates... | central (secondary) hypothyroidism |
| In a patient with hypothyroidism, an elevated TSH level indicates.. | primary hypothyroidism |
| Patients with central (secondary) hypothyroidism are treated with | Thyroxine. TSH levels are low-to-normal in central hypopituitarism, thus TSH levels cannot be used to monitor thyroid hormone replacement dosage in secondary hypothyroidism |
| Adrenocorticotrpic hormone secretion is stimulated by | Hypothalamic corticotropin-releasing hormone (CRH) and to a lesser extent, ADH |
| ACTH stimluates | cortisol synthesis and secretion from the adrenal gland. Cortisol exerts a negative feedback on ACTH and CRH secretion |
| ACTH daily patterns | ACTH reaches maximal levels in the last hours before awakening, followed by a steady decline to a nadir in the evening. |
| Excess ACTH results in hypercortisolemia, which may be caused by | an ACTH-secreting pituitary adenoma (Cushing's disease) or by ectopic ACTH secretion |
| ACTH deficiency results in | adrenocortical insufficiency, with decreased secretion of cortisol. Aldosterone secretion is largley regulated by the renin-angiotensin axis and therefore remains intact |
| How to measure ACTH levels | Because ACTH regulates cortisol secretion, plasma cortisol levels better reflect hypothalamic-pituitary-adrenal function. An 8am cortisol less than 3mcg/dL suggests adrenal insufficiency |
| In primary adrenal disorder ACTH levels are | normal to high |
| In adrenal insufficiency secondary to hypothalamic pituitary dysfunction | ACTH levels are low to absent |
| To assess the adequacy of ACTH reserve under conditions of stree, _________testing is performed | provocative; Insulin-induced hypoglycemia test. |
| Prolonged ACTH deficiency results in | adrenal atrophy, and thus ACTH status can be assessed indirectly by measuring adrenal cortisol reserve |
| ACTH deficiency signs and symptoms | results in adrenal failure, causing lethargy, weakness, nausea, vomiting, dehydration, orthostatic hypotension, com, and, if untreated, death |
| Treatment for ACTH deficiency | Hydrocortisone; the dose should be increased 5-10x in times of stress (surgery). If minor illness, then double |
| ACTH-secreting pituitary tumors result in hypercorticosolemia with the following associated signs and symptoms | obesity, moon facies, cevicodorsal dysplasia, striae, thinning of the skin, hirsutism, HTN, menstrual irregularities, glucose intolerance, mood changes, proximal myopathy, and osteopenia |
| Treatment for ACTH hypersecretion | in Cushing's disease: trans-sphenoidal resection, radiation therapy and medical theraphyin Ectopic tumor: remove tumor |
| Gonadotroph secretion of LH and FSH is regulated by | hypothalamic gonadotropin-releasing hormone (GnRH) |
| ________ release determines the onset of puberty and generates the midcycle gonadotropin surges necessary for ovulation | GnRH |
| LF and FSH bind to the receptors in the ______ and ________ and timulate sex steroid secretion as well as gametogenesis | ovaries and testes |
| Prepubertal gonadotropin levels are ___, and menopausal women have ____ levels | low; elevated |
| Central hypogonadism during childhood results in | failure to enter normal puberty. Gilrs have delayed breast development, scant pubic and axillary hair, and primary amenorrhea. |
| Central hypogonadism in boys results in | small phallus and testes, sparse body hair |
| In isolated gonadotropin deficiency in childhood, the result is... | growth continues and epiphyseal fusion fails (b/c sex steroids are need for closure of epiphyses of the long bones), resulting in tall adolescents |
| In adult women hypogonadism results in | breast atrophy, loss of pubic and axillary hair, and secondary amenorrhea |
| In adult men hypogonadism results in | testicular atrophy, decreased libido, impotence, decreased muscle mass and bone-mineral density, loss of body hair, elevated LDL cholesterol levels |
| Treatment for central hypogonadism in men | Androgen replacement therapy such as testosterone |
| Treatment for central hypogonadism in women | estrogen replacement therapy if premenopausal. If they have a uterus they should receive progesterone to protect uterine lining. |
| In young children and adults, the most common cause of hypothalamic dysfunction is | craniopharyngioma |
| Clinical manifestations of tumors that can cause hypothalamic dysfunction include | visual loss, sx of raised intracranial pressure (HA, Vomiting), hypopituitarism (including growth failure), and diabetes insipidus |
| Hypothalamic disturbances include | disorders of thirst (polydipsia, polyuria, dehydration), appetite (hyperphagia, obesity), termperature regulation, and consciousness (somnolence, emotional lability) |
| What test confirms the diagnosis of hypothalamic dysfunction? | MRI |
| Because hypopituitarism occurs frequently with hypothalamic lesions,________ should be assessed | anterior pituitary function |
| Craniopharyngioma is treated with | surgical resection |
| Hypopituitarism results from | diminished secretion of one or more pituitary hormones; results from either anterior pituitary destruction or dysfunction secondary to deficient hypothalamic stimulatory-inhibitory factors that normally regulate pituitary function. |
| Pituitary insufficiency is an insidious/rapid onset disorder | insidious. Also, pituitary lesions may result in single or multiple hormone losses |
| Treatment of panhypopituitarism | adequate replacement of T4, glucocorticoids, and appropriate sex steroids. |
| Children with GH deficiency should receive | GH replacement. The safety and efficacy of GH replacement therapy for adults who develop GH deficiency is being evaluated. |
| Testosterone therapy in men results in | restored libido and potency, growth of body hair and muscle strength |
| Estrogen therapy in women results in | secondary sex characteristics and prevents hot flashes |
| In patients with combined TSH and ACTH deficiency, _______ should be replaced before T4 and T3 b/c T4 may aggravate adrenal insufficiency and may precipitate acute adrenal failure | glucocorticoids |
| The posterior pituitary secretes ADH and Oxytocin both of which are produced in the | hypothalamic nuclei that extend from the hypothalamus to the posterior pituitary |
| ADH MOA | facilitates reabsorption of water and concentration of urine. ADH also binds to peripheral arteriolar receptors, causing vasoconstriction and resultat increase in BP. ADH also causes bradycardia and the inhibition of sympathetic nerve activity. |
| Deficiency of ADH or insensitvity of the kidneys to ADH results in | Diabetes insipidus, which is exhibited as polyuria, polydipsia and nocturia |
| Inappropriate secretion of ADH in excess amounts results in | SIADH and causes a hyponatremic state |
| Oxytocin MOA | causes uterine smooth muscle contraction |
| Causes of hypopituitarism | Congenital, Tumors, Infiltrative, Infectious, Physical Trauma, Vascular |
| In diabetes insipidus (central or nephrogenic), inappropriate diuresis results in a urine osmolarity that is ____than that of plasma osmolarity | less |
| In primary polydipsia, both plasma and urine are ______ | dilute |
| The primary test used to differentiate the causes of polyuria is | the water deprivation test. The pt is denied fluids for 12 to 18 hours and body weight, bp, urine volume, urine-specific gravity, and plasma and urine osmolarity are measured every 2 hours |
| Normal response to water deprivation test | low urine output |
| Diabetes Insipidus response to water deprivation test | high urine output is maintained which continues to be dilute |
| Primary Polydipsia response to water deprivation test | Urine osmolarity incrases to values greater than plasma osmolarity |
| Treatment of DI | Desmopressin acetate (DDAVP), a synthetic analog of ADH, is usually administered intranasally or orally. Frequency of administration is determined by the severity of the disease |
| Measuring adequacy of DI treatment | regular measurement of serum osmolarity and sodium |
| Treatment of Nephrogenic DI | Goal is to maintain a state of mild sodium depletion with reduction in teh solute loadon the kidneys and subsequent increased proximal tubular reabsorption. Diuretics coupled with dietary salt restriciton can be used to acheive this goal. |
Created by:
ltm12