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86 Cards in this Set
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ADH -
ACTH- CRH - D-receptors- DA - FSH - GH - SST - GHRH- |
ADH antidiuretic hormone,vasopressin
ACTH adrenocorticotropic hormone CRH corticotropin-releasing hormone D-receptors dopamine receptors (1,2 etc.) DA dopamine FSH follicle-stimulating hormone GH growth hormone SST somatostatin GHRH growth hormone-releasing hormone |
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GnRH -
IGF-1 - IGF-1 BP - LH - PRL - TRH - TSH - VIP - V–receptors- |
GnRH gonadotropin-releasing hormone
IGF-1 insulin-like growth factor 1 IGF-1 BP insulin-like growth factor binding protein 3 LH luteinizing hormone PRL prolactin TRH thyroid-releasing hormone TSH thyroid –stimulating hormone VIP vasoactive intestinal peptide V–receptors vasopressin receptors (1,2 etc.) |
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pituitary anatomy:
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*intermediate lobe (IL) is vestigial
*Note anatomic locations of hormone production--neurosurgical applications |
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Normal Hypothalamus-Pituitary: gross-
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Normal Hypothalamus-Pituitary: MRI-
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*optic chiasm just dorsal (above) the pit
*sphenoid sinus just ventral (below) pit |
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Overview of pituitary/hypothalamus disorders:
what clinical clue might differentiate the two? |
*Most commonly, clinical syndromes involving the hypothalamus present as neurologic injury caused by inflammation, infiltration, or tumor and are characterized by pituitary hormone dysfunction and OFTEN ACCOMPANIED by diabetes insipidus.
*Clinical syndromes involving the pituitary gland may causes XS HORMONE SECRETION as in acromegaly and excess ACTH secretion in Cushing’s Disease and rarely central hyperthyroidism due to excess TSH release. *Increased prolactin secretion directly and indirectly causes hypogonadism. *Pituitary tumors often cause local compressive effects and hypopiuitarism but diabetes insipidus is UNCOMMON. |
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Disorders of the Hypothamus:
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*Hypothalamus:
Tumors (e.g. craniopharyngioma) Inflammation ( lymphocytic hypophysitis) Infiltration (sarcoidosis, histiocytosis) Metastatic tumor (breast, lung) *Often associated with loss of posterior pituitary function i.e central diabetes insipidus |
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Causes of Central Diabetes Insipidus:
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*Idiopathic: 30 – 50% (? autoimmune/inflamatory)
*CNS/pituitary surgery, trauma, anoxic encephalopathy *Primary tumors, craniophyrngioma, suprasella germinoma, pinealoma *Metastatic tumors , leukemia and lymphoma *Granulomatous Disease (e.g. TB) *Hereditary: Autosomal dominant (onset at months to years) *Pregnancy: unmasking of partial central diabetes or nephrogenic insipidus; -markedly increased levels and activity of vasopressinase (oxytocinase) |
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arrow points to?
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-location where vasopressin is stored
-this bright spot is NORMAL; indicates INTACT ADH -if it's not there, suspect central diabetes insipidus |
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Hypothalamic/Posterior Pituitary Hormones: vasopressin
discuss receptors |
V-1 a receptors mediate pressor activity
V-1b receptors modulate ACTH secretion V-2 receptors mediate renal handling of water excretion and promote coagulation factor VIII action |
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Hypothalamic/Posterior Pituitary Hormones
Vasopressin V- 1 agonist uses: |
*Treat systemic hypotension (e.g. septic shock)
*Decrease splanchnic blood flow in upper GI hemorrhage (e.g. post Bx, gastritis, ulcer) *Enhance coronary blood flow and myocardial oxygenation in cardiac asystole |
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Hypothalamic/Posterior Pituitary Hormones
Vasopressin V- 2 agonist uses |
*To decrease water excretion in central diabetes insipidus and nocturnal eneuresis
*To increase circulating levels of factor VIII and improve platlet responsiveness (hemophilia A, vonWilibrand’s disease, uremic coagulopathy) |
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Posterior Pituitary Hormones and Analogs: discuss Desmopressin:
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*Desmopressin (desamino, D- arginine vasopressin (DDAVP)
*Amine at 1 postiion is removed increasing half life *L-arginine at position 8 is changed to D-arginine reduicing pressor activity |
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Central Diabetes Insipidus chart:
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*lots of problems with thirst and urination
*symptoms come on really suddenly...they never relent once they start *crave cold water |
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Craniopharyngioma:
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*Most frequent sellar tumor of childhood and adolescence (3% of all brain tumors)
*Usually suprasellar but may extend into sella *Arise from Rathke’s Pouch remnants that extend into the diencephalon during development *Histology: cystic to solid-cystic filled with lipid rich viscous fluid (consistency of motor oil) *Childhood presentation : growth retardation, pubertal delay, visual field loss, vomiting |
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Functional pituitary tumors:
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-Excess growth hormone (Acromegaly)
-Pituitary dependant Cushing’s Disease (ACTH) -Prolactinomas with prolactin associated hypogonadism -Central hyperthyroidism due to TSH secretion |
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Anatomic Damage from pituitary tumors:
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-Visual field loss, cranial nerve injury etc
-Hypopituitarism -CSF leak etc -Diabetes insipidus : uncommon |
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Hypothalamic-pituitary regulation and pituitary tumor pathogenesis:
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Classification of Pituitary Tumors:
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Pituitary Tumors Genetic syndromes:
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carney syndrome
mccune-albright syndrome |
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Carney Syndrome:
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*Punctate skin pigmentation, myxomas, testicular and adrenal tumors
*Multifocal somatommamotropic hyperplasia; sublinical increases hGH, hPr *Growth hormone secreting tumors 10 – 20% *Mutation in sub-unit of Protein Kinase A may be present *Localization to 17q22-24 +/- 50%, others 2p16 |
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McCune-Albright Syndrome:
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*Patches of skin pigmentation, bone tumors
*Adrenal tumors, precocious ovarian function, GH secreting tumors *Inactivation of GTPase of Gsα with increased C-AMP |
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Genetic Associations with endocrine tumors:
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*Multiple Endocrine Adenomatosis Type 1
-Loss of function in tumor suppressor gene Men 1 -Pituitary Tumor, Hyperparathyroidism, Pancreatic Neuroendocrine Tumors (PPP) *Multiple Endocrine Adenomatosis Type 2 -Activating germ line mutation in RET proto-oncogene -Type 2a: Medullary cancer thyroid, Hyperparathroidism, Pheochromocytoma -Type 2b (previously Type 3): Marfanoid body habitus. medullary cancer thyroid, Pheochromocytoms, Mucosal gangliomatosis (no hyperpara or pituitary tumors) -Familial Isolated Medullary Thyroid carcinoma *Multiple Endocrine Adenomatosis Type 4 -Loss of function in gene CDKN1B encoding kinase p27 a regulator of G1-S1 -Pituitary tumor, Hyperparathyroidism, other tumors (renal, testis) |
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talk about the irish giant:
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*Born Northern Ireland -1762
*“Exhibited “ London – 1781 *Died 1783; HT 7 ‘ 7 “ *Death wish “to be buried at sea” *Fake burial and body stolen by Mr. John Hunter distinguished surgeon and anatomist *Skeleton eventually in the Hunterian Museum RCS *Pituitary enlargement confirmed by Harvey Cushing 1909 *Familial Pituitary Tumor marker AIP identified in tooth (Karbonits 2011) *Identical c,910 C → T mutation in 4 contemporary families in Northern Ireland with FIPA |
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Diffuse Pituitary Hyperplasia:
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*Occurs in Pregnancy
*Prolonged Primary Hypothyroidism and Hypogonadism *GhRH secreting tumors -Eutopic: hypothalamic (gangliocytomas), -Ectopic: extrahypothalamic (peripheral neuroendocrine tumors) *Somatomamatotropic Hyperplasia in Carney Syndrome |
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Discrete Pituitary Tumor:
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*Most common human neoplasm!
*Malignancy quite rare *Monoclonal origin except in rare conditions *Gsα (gsp)alteration in 40 % of sporadic GH secreting neoplasm *Pituitary transforming gene expression common |
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Pituitary Tumors Manifestatons:
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*Intrasellar: Headache, Pituitary hypofunction
*Tumor associated loss: GH>LH/FSH>TSH>ACTH *Suprasellar: Impingement on Optic Chiasm Other Mass Effects: obstruction of 3rd ventricle, hydrocephalus, altered sensorium *Lateral Extension: Impingement on Cr N iii, iv, vi *Inferior Erosion: Spinal Fluid Leak, Meningitis |
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optic effects from pituitary tumors:
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Pituitary Tumor
*bitemporal hemianopsia look out |
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Neurologic Effects: Pituitary- Hypothalamic Lesions:
effect if there's a tumor at the arrow? |
Tumor erosion with CSF leak
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*Pituitary Tumor Pressure Effects--tumor is extending laterally
*Look for IIId or VIth palsies |
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classification of pituitary tumors:
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Pituitary Incidentaloma:
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*Pituitary Incidentaloma
*Prevalence: Autopsy: 11% (90 % stain for prolactin) MRI: 10% *Hormonal Activity: none *Clinical Presentation: Incidental (by definition) *Management: Prolactin measurement (normal by definition) *Prognosis: Generally < 0.5% chance of subsequent significant clinical events *Recommendation: measure prolactin, if wnl < 5mm no additional study required 6- 9mm repeat MRI over subsequent 2 years |
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*Pituitary Incidentaloma (dark round mass dorsal to sphenoid sinus)
*About 5% of pts who get an MRI will have these *usually no clinical significance *MEASURE PROLACTIN, GH, AND ACTH |
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classification of prolactinomas:
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Prolactinoma: clinical effects in women--
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*Clinical effects in Women
-Microadenomas most common -Infertility, oligomenorrhea, common -Occur in 20% of patients with amenorrhea *Galactorhea: 30 – 40 % women with prolactinoma -(50 % patients with galactorrhea no increase in prolactin) *Galactorrhea uncommon with high levels of hPr 20 to hypogonadism |
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Prolactinoma: clinical effects in men--
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*Macroadenomas most common
*Longstanding erectile dysfunction at presentation *Headaches, visual field impairment common *Hormonal deficiencies (TSH & ACTH) |
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Causes of Increased Prolactin:
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*Hypothalamic
-Diminished synthesis or release of dopamine -Structural: tumors, sarcoidosis, hemochromatosis -Drugs: methyldopa, reserpine *Pituitary Stalk Impairment: -Impaired transport of dopamine -Structural: damage, compression, blood supply injury *Lactotroph Insensitivity to Dopamine -Drugs: dopamine receptor blocking effects e.g. benzamides (metoclopromide), butyrphrenones (haloperidol), phenothiazines (chlorpromazine) *Increased lactotroph number or secretion -Tumor: pituitary tumor lactotroph or mixed or pluripotetial -Estrogen effects: pregnancy, drugs (e.g. BCP) -Increased TRH (hypothyroidism) -Chest wall injury (rare); pseudosuckling response *Decreased prolactin disposal -Renal Failure (also associated with increased ) -Macroprolactinemia (raremolecular genetic variation) |
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Significance of Dopamine as a Prolactin Inhibitory Factor:
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*Dopamine is catechol neurotransmitter
*Low dose (2-3 mcg/min) dilates splachnic bed and increases renal blood flow *Moderate dose (4-8 mcg/min) activates cardiac β-1 receptors to increase cardiac contractility *High dose (> 10 mcg/min) acts as a pressor by activating peripheral α- receptors *Prolactin is under tonic inhibitory control and predominant inhibitor is dopamine *D2 receptors are coupled to G-proteins and increase intracellular C-AMP *Growth hormone secreting tumors may also express D2 receptors |
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drug of choice for prolactinomas:
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dopamine
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Dopamine Agonists:
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*Dopamine agonists may have dramatic effects on prolactin secreting tumors
*Macroadenomas often shrink *Decrease in size may be detectable within 24 hours *Microadenomas respond dramatically; often with resumption of menses and restoration of fertility |
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2 examples of dopamine agonists you may prescribe:
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*bromocriptine: excellent drug with strong record of clinical success; drug of choice in INFERTILITY; troublesome side effects can occur
*cabergoline: most tolerable preparation with less side effects; biweekly dosing; expensive *NB: High doses of cabergoline and pergolide( in Parkinsonism) are associated with valvular heart disease due to activation of valvular serotinin receptors |
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Prolactinoma-- Indications for Treatment:
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*Mass Effets
Hypopiuitarism Visual Field Defects Cranial Nerve Defects Headaches *Consequences of IncreAsed Prolactin Effects of Hypogonadism Amenorhea or Oligomenorrhea Infertility Impotence Osteoporosis *Relative Indications Bothersome Hirsuitism Bothersome Galactorrhea |
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A) PRL 6800
B) PRL 5 after bromocriptine RX *take away: the drugs work in treating prolactinomas |
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Classification of somatotroph adenomas:
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Pituitary Gigantism:
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*Excessive linear growth due to excess growth hormone secretion in infants, children and adolescents who have open epiphiseal growth plates; often accompanied by obesity, acral enlargement, etc.
*Causes: Growth hormone secreting tumors GhRH secreting tumors ? Somatostatin dysregulation ? |
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Acromegaly:
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*Clinical syndrome of hypertrophic and degenerative injury to soft tissues, joints, the heart and cardiovascular system accompanied by disturbances in respiration and intermediary metabolism.
*Macroadenoma in > 70 % *Onset of Sx 10 – 12 years before diagnosis |
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Acromegaly – what gets enlarged?
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*Visceromegaly of the:
-Tongue -Liver -Spleen -Thyroid -Salivary Glands -Kidney -Prostate *Pulmonary Abnormalities -Obstructive Sleep Apnea -Narcolepsy *Mineral and Electrolyte Abnormalities -Low Renin and Increased Aldosterone -Hypercalciuria -Herpervitimonisis 25 D |
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Acromegaly Somatic Symptoms:
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*Acral Enlargement including Soft Tissues of Hands and Feet
*Frontal Bossing *Prognathism and Jaw Malocclusion *Arthragias and Arthritis *Carpal Tunnel Syndrome *Proximal Myopathy *Acroparasthesisas |
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Acromegaly Skin and Gastrointestinal symptoms:
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Hyperhidrosis
Oily Skin Skin Tags Colonic Polyps |
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Acromegaly Cardiovascular Symptoms:
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Cardiomyopathy
Congestive Failure Ventricular Hypertrophy Hypertension |
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Acromegaly reproductive and CHO/Lipid abnormalities:
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*Reproductive Abnormalities
-Menstrual Abnormalities -Galactorrhea -Hirsuitism -Decreased Libido and Erectile Dysfunction *Carbohydrate and Lipid Abnormalities -Insulin Resistance and Impaired Glucose Tolerance -Diabetes Mellitus -Hypertriglyceridemia |
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L: Acromegalic hands
R: Distal tufting of the terminal phalanges in acromegaly |
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Acromegaly pictures 1:
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Acromegaly pictures 2:
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Acromegaly pictures 3:
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flowchart for diagnosing acromegaly:
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Discuss Somatostatin and Somatostatin Analogues:
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*Initial identification as inhibitor of growth hormone
*Widespread neuroendocrine, gastroendocrine, and neurologic transmitter activity *Cleaved from pro-hormone to 28 AA and 14 AA forms *GI tract: 28 AA peptide; CNS: 14 AA peptide *5 different somatostatin receptors (SST1-5) *Analogues have selective activity due to different receptor affinity/activity |
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Uses of Somatostatin and Somatostatin Analogues:
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*Suppress growth hormone secretion and tumor growth in acromegaly
*Suppress hepatic synthesis of IGF1 *Suppress TSH secretion in TSH secreting tumors *Suppress GI hormone secretion in GI endocrine tumors e.g. VIP, carcinoid, glucagonoma, etc. *20% of patients develop gall stones or “sludge” with long term use |
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Somatostatin Analog
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3 somatostatin analogs you may Rx:
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*octreotide: short acting somatostatin analogue interacts with SST1 and SST5 which are expressed in 90% of growth hormone secreting tumors
*octreotide LAR: long acting release preparation given monthly *lanreotide gel: now available in US similar activity to octreotide |
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Newer Pharmacologic Interventions that may be better than somatostatin analogs:
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*Classic SST analogs, octreotide and lanreotide have potent effects limited to SST 2
*Pasireotide is an newly developed SST analog which has activity at SST 1,2,3, and 5 and is emerging as especially helpful in tumors resistant to surgery and pharmacologic intervention (especially in hGH and ACTH tumors expressing SST 5) *Clinical use is limited by effects on SST 5 which impairs insulin release causing hyperglycemia *Somatoprim a specific SST 3 analog is also in development and is not likely to cause hyperglycemia *pituitary tumors other than prolactinomas often also express D2 receptors *the use of dopamine agonist may be efficacious in some hGH and ACTH secreting tumors *“Dopastatins” which are chimeric compounds designed to have both dopaminegic agonist and somatostatin-like effects are in trials |
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Discuss Growth Hormone Receptor Antagonists:
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*Receptor dimerization leads to cascade of intracellular kinase/phosphorylase activity with ultimately increased IGF-1 secretion
*Growth hormone interacts with two separate distinct binding sites to promote intracellular phosphorulation *Antagonists with enhanced binding to a portion of receptor binding site and inability to bind to the other receptor block GH induced activity |
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IGF- 1 Receptor
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treatment for prolactinoma:
treatment for acromegaly: |
treatment for prolactinoma: dopamine
treatment for acromegaly: 1) surgery 2) if not successful, somatostatin analogs 3) if SST analogs fail, GH receptor antagonists |
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Classification of corticotroph adenomas:
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Classification of gonadotroph adenomas, null cells, and thyrotroph adenomas:
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*gonadotroph adenomas make but don't secrete FSH/LH
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Structural similarities between FSH/LH/TSH/HCG
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*FSH/LH/TSH/HCG all have a common alpha subunit and different beta subunits
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Surgical Treatment of Pituitary and Hypothalamic Tumors:
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*Microadenomas (<10 mm) may be completely removed with Transphenoidal Surgery (except prolactinoma...use dopamine)
*Macroadenomas (>10 mm) with suprasellar extension surgical cure less likely *Hypothalamic Tumors (Craniopharyngioma) TSS or Transfrontal approach may be necessary for complete removal |
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2 approaches for surgery of Pituitary and Hypothalamic Tumors:
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*Transphenoidal Hypophysectomy
Direct or Endoscopic approach from below through the sphenoidal sinus *Transfrontal open-craniotomy--Major intracranial surgery anteriorly through the frontal araea of the skull |
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Transphenoidal Surgery
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Radiation and drug therapy for Pituitary and Hypothalamic Tumors:
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-Not the first choice treatment for these tumors (it's usually surgery except for prolactinomas)
*RADIATION THERAPY -Conventional Supervoltage Radiation -Stereotactic Radiosurgery (Gamma Knife): Highly focused single dose radiation *PHARMACOLOGIC THERAPY -Somatostatin Analogues (Acromegaly, TSH Secreting tumors) -Dopaminergic Agonists (Prolactinoma, Acromegaly) |
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Hypopituitarism Clinical Features:
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*The hallmarks of hypopituitarism are often abnormal growth in children and abnormalities of menstruation in women
*Losses of pituitary function are those of end-organ failure often of a gradual and progressive nature *Patients are often slightly overweight, pale, with fine wrinkled skin with atrophic genitalia and diminished axilary and pubic hair |
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Genetic Causes of Hypopituitarism:
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*Structural defect e.g. pituitary aplasia
*Isolated defect in hypophysiotropic hormone or pituitary hormone e.g. GnRH in Kallman’s syndrome (Anosmia and Hypogonadism) *Isolated defect in hormone receptors e.g.CRH *Isolated hormone mutation etc. |
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Causes of Hypopituitarism:
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*Intrapituitary tumor (e.g. Prolactinoma)
*Extrapituitary (e.g craniophyngioma, rathke’s cleft cyst) *Vascular -Sheehan’s Syndrome (pituitary infarction at delivery) -Pituitary apoplexy (sudden pituitary hemorrhage) -Ischemic infarction e.g. coronary bypass *Injury: damage to stalk, pituitary, hypothalamus *Immunologic: inflammatory lymphocytic damage “lymphocytic hypophysitis “ *Iatrogenic: surgery and radiation treatment *Infectious: tuberculosis, syphilis, mycoces *Idiopathic: isolated or familial *TBI |
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Discuss invasive, infarction, and infiltration causes of Hypopituitarism:
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*Invasive: CNS ,pituitary and metastatic tumors e.g. craniophayngioma, meningiomas
*Infarction: Postpartum ischemic injury (Sheehan), pituitary apoplexy (hemorrhagic infarction of pituitary tumor) *Infiltration: (hypothalimic injury most prominent) e.g. sarcoidosis, hemochromatosis, histiocytosis |
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Discuss Traumatic Brain Injury Hypopituitarism:
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*A traumatically induced structural injury
and/or physiological disruption of brain function as a result of an external force that is indicated by new onset or worsening of at least one of the following clinical signs, immediately following the event: (1) any period of loss of or decreased level of consciousness (2) any loss of memory for events immediately before or after the injury (3) any alteration in mental state at the time of the injury, (4) neurological deficits (5) intracranial abnormalities *Military service members with traumatic brain injury may have some combination of loss of anterior pituitary functions constituting hypopitutarism in 30 to 80 % with detection rates at 24 to 32 months *High incidences of similar finding may occur in patients suffering non-military TBI and also in patients with the occurence of subarachnoid hemorrhage *A high index of suspicion is needed in these patients due to the often subtle manifestations of hormonal failure |
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Human Recombinant Growth Hormone--USES to be Discouraged:
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Anti-aging…”fountain of youth”
To enhance athletic performance In the critically ill (worsened survival) (N.B. use in wasting of HIV/Aids is approved) |
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what happens to the hypothalamus/pituitary with age?
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*they slow down a bit, especially testosterone.
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Growth Hormone and Aging:
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*Aging blunts the amplitude and decreases the frequency of GH secretion
*IGF-1 levels are 20 -70 % lower in healthy aging adults than young controls *GH treatment has no impressive additive benefits to exercise on muscle strength, bone density, etc. *Side effects including carpal tunnel sx, fluid retention, hyperglycemia occur *Theoretical concern re GI and other malignancies |
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SIADH:
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*ADH leads to inappropriate volume expansion due to water retention
*Volume expansion over-rides sodium handling with inappropriate urinary sodium loss *Clinical hallmark is hyponatremia (<135 meq) with evidence of relative water excess |
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Syndrome of Inappropriate ADH Causes:
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*Ectopic Production:
-Malignancy: Small Cell Lung, GI, GU, Oropharnyx, etc *Baroreceptor Dysregulation: (loss of inhibitory input) -Central Nervous System: Infection, Masses, Hemorrhage, Multiple Sclerosis etc. -Pulmonary: Pneumonia, Abscess, TB, etc (thoracic baroreceptor network) -Transient: Pain, Nausea , etc. *Multifactorial (central and peripheral): -Drugs: Antidepressants, Antipsychotics, Narcotics, Cancer chemotherapies etc. |
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siadh
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Clinical Features of SIADH:
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*“Euvolemia” - i.e. no edema, no signs of dehydration
*Decreased serum sodium and osmolality with apparent relative increase water to solute *Inappropriate i.e. less than maximal urine dilution despite dilutional hypo-osmolality *Inappropriate (increased) urine sodium loss despite low serum sodium |
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Treatment of SIADH:
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*Basic approach is to restrict fluid intake (problem is excess volume)
*Gentle administration of hypertonic fluids used to reverse symptoms (e.g. seizures) *Drugs which impair renal responses to ADH i.e. demeclocline and lithium *Vasopressin antagonists |
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Discuss Vasopressin Antagonists:
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*Targeted to block VP action at V2 receptor and promote water diuresis without direct effects on electrolyte metabolism or additional kidney functions
*Conivaptan (IV) and Tolvapaptan (oral): only agents currently available in US; multiple other drugs in development *These aren't first line treatments--restrict fluid intake! |
