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Endocrinología 3

41.- La estimulación simpática del páncreas exocrino provoca: a) b) c) d) e) Dilatación del conducto pancreático principal Aceleración del vaciamiento de los acinos pancreaticos Supresión de la secreción de jugo gástrico Incremento en la liberación de tripsina Supresión de la activación del tripsinogeno

El páncreas exócrino es la principal glándula digestiva del organismo, secreta alrededor de un litro de un líquido claro rico en bicarbonato cada día al intestino delgado. Este líquido, el jugo pancreático, contiene las enzimas digestivas necesarias para la hidrólisis intraluminal (dentro de la luz del intestino) de los macronutrientes de la dieta (proteínas, almidón, grasas, y ácidos nucleicos) y de las vitaminas liposolubles a moléculas más pequeñas que pueden absorverse directamente en los enterocitos (células del intestino delgado) o seguir actuando formando parte de enzimas presentes en la bilis para permitir su posterior absorción. En los humanos el jugo pancreático tiene una concentración de proteínas del 1 al 10 %. La mayor parte de estas proteínas son enzimas digestivas o cofactores, que incluyen 20 isozimas de 12 diferentes enzimas. El resto está formado por la secreción de un inhibidor de tripsina (que tiene una función protectora para evitar el daño al páncreas debido a una activación prematura de la tripsina en el tejido o en el jugo pancreático) y otras enzimas similares a la tripsina que no tienen una función primaria en la digestión, proteínas plasmáticas y glicoproteínas. Las cuatro principales categorías de las enzimas digestivas son las proteasas (digieren proteínas y péptidos) amilasa (digiere almidón), lipasas (digieren triglicéridos y fosfolípidos) y nucleasas (digieren ácidos nucleicos). Todas la proteasas como también la fosfolipasa son secretadas por el páncreas como proenzimas (zimogenos) inactivas. Luego de llegar al lumen intestinal, el tripsinógeno es convertido a tripsina por las enteropeptidasas, enzima que se encuentra en el ribete de la célula del intestino. La tripsina puede activar a otras proenzimas como así también al tripsinógeno. De manera diferente a las otras enzimas digestivas, la amilasa, la lipasa y la ribonucleasa se secretan en su forma activa. El pancreas exócrino tiene una reserva de enzimas mucho mayor de las necesarias para la digestión de los alimentos. La mayor reserva es de las enzimas necesarias para digerir los azúcares (carbohidratos) y las proteínas. Las reservas para la digestión de las grasas (lípidos) particularmente para la hidrólisis de triglicéridos es más limitada. Los estudios realizados en personas sometidas a una resección parcial del páncreas demostraron que la insuficiencia digestiva para las grasas no se produce hasta que se pierde la capacidad del órgano en un 80 % al 90% Esta observación tiene implicancia clínicas pues indica que la costumbre de ingerir tabletas rotuladas como ¨digestivos¨ que contienen enzimas pancreáticas no tiene racionalidad terapéutica. Una vez que el jugo pancreático entra en el intestino, el tripsinógeno es activado a tripsina por la enterokinasa en forma tan rápida y completa que la relativa pequeña cantidad del inhibidor de tripsina presente no interfiere con el proceso digestivo normal. Otro mecanismo protector adicional contra el efecto potencialmente perjudicial de la activación prematura de tripsina dentro del páncreas, es la habilidad de diversas moléculas similares a la tripsina sintetizadas por la célula acinosa y de la misma tripsina para destruir las moléculas nocivas de tripsina y tripsinógeno. Durante el estado basal o sea en ayuno, el volumen del jugo pancreático secretado al duodeno es bajo, con una secreción de enzimas de alrededor del 10 % de su nivel máximo y de bicarbonato solo un 2% del máximo. Existen breves períodos en el que aumenta la secreción de enzimas y bicarbonato cada 60-120 minutos asociados con una actividad motora del estómago y el intestino entre las comidas. Los nervios colinérgicos (parasimpático) son los que regulan el aumento de la actividad secretora. Los nervios adrenérgicos (simpático) actúan como inhibidor de la secreción pancreática en ayunas. Luego de una ingestión de una comida el páncreas exócrino segrega bicarbonato y enzimas a un nivel del 60-75% del que podría obtenerse luego de una

Recopilación realizada por: Dr. René Nájera Alvarado - Neurólogo

René Nájera Alvarado . lo que favorece la cetogénesis. gástricas e intestinal aunque pueden sobreponerse en parte. al igual que en el estómago también puede dividirse en fases cefálicas.. Es interesante tener presente que solo se necesita un 10 % de acción de la lipasa (encargada de digerir sustancias grasas de nuestra dieta).La función metabólica de la somatotropina consiste en: a) b) c) d) e) Disminuir la utilización celular de glucosa Disminuir la liberación de ácidos grasos hacia la sangre Incrementar el volumen de los depositos corporales de tejido adiposo Aumentar la síntesis celular de proteínas Promover la utilización de glucosa por las células La hormona del crecimiento moviliza los FFA del tejido adiposo. la visualización. pero la distensión del estómago produce un pequeño aumento en la secreción del páncreas también mediada por reflejos vagales colinérgicos. que si es negativa se debe realizar cada año. Durante la fase intestinal se libera secretina a la sangre desde el duodeno en respuesta a la presencia de ácido en el mismo. Puede producir una respuesta secretora del 25 al 50 % del máximo y está regulada primordialmente por una inervación vagal colinérgica. se recomienda el cambio de los hábitos dietéticos + actividad física. La secreción estimulada por la comida.. 42.La prueba específica para establecer el diagnóstico de diabetes gestacional es la: a) b) c) d) e) Glucemia postprandial Glucemia postrcarga de 50 g Glucemia en ayuno Determinación de hemoglobina glucosilada Curva de tolerancia a la glucosa Se recomienda la selección selectiva de mujeres de 30 años de edad y mayores con una carga oral de glucosa de 50 g entre las 24 y 28 semanas de la gestación. La fase cefálica es estimulada por el pensamiento. 43. Los ácidos grasos y la bilis también pueden estimular la liberación de secretina.. La fase gástrica no ha sido muy estudiada. Disminuye la captación de glucosa dentro de ciertos tejidos (acción antiinsulínica).Para efectuar la detección temprana de la diabetes mellitus en personas que tienen factores de riesgo se debe practicar: a) b) c) d) e) Determinación anual de hemoglobina glucosilada Curva de tolerancia a la glucosa cada seis meses Vigilancia anual mediante la determinación de la glicemia en ayuno Determinación de la glucemia con carga oral cada dos años Control dietético y la cuantificación de la glucemia en ayuno cada semestre Al identificar factores de riego se debe recomendar la glicemia en ayuno. Las enfermas cuyos valores de glucemia son de 140 mg/dL o mayores deben valorarse con una prueba de tolerancia a la glucosa oral diagnóstica de tres horas. aumenta la salida de glucosa hepática y puede disminuir la unión de la insulina a los tejidos.administración endovenosa máxima de una dosis de secretina y CCK (colecistokinina) principales estimulantes de la secreción del páncreas. Esto significa la natural sobreabundancia de enzimas digestivas por lo que es poco razonable la automedicación con "así llamados digestivos" para intentar favorecer el proceso de la digestión.Neurólogo . Recopilación realizada por: Dr. 44. la degustación o el olfato a comida.

llamada también vasopresina. la PTH aumenta la excreción de fosfato en la orina. por lo que la eventual destrucción del mismo causaría aumento en la diuresis y disminución de la densidad urinaria. no se lleva a cabo la foliculogénesis ovárica ni la ovulación.La destrucción del núcleo supraóptico puede dar lugar a: a) b) c) d) e) Incremento del volumen urinario y disminución de la densidad Aumento del volumen urinario y orina concentrada Orina escasa e hipotenurica Disminución del volumen urinario y orina muy diluida Disminución del volumen urinario y orina concentrada La hormona antidiurética. Sin la estimulación apropiada por las gonadotropinas. Las aberraciones de la liberación intermitente de hormona liberadora de gonadotropina (GnRH) del hipotálamo dan por resultado una deficiencia de la secreción hipofisiaria de hormona estimulante del folículo (FSH) y hormona luteinizante (LH). René Nájera Alvarado . Además de incrementar el calcio y deprimir el fosfato plasmáticos. Una interrupción de esta secuencia de fenómenos en cualquier etapa inhibe la ovulación.45. qué a su vez aumenta la absorción intestinal de calcio. se sintetiza en el núcleo supraóptico. La PTH también incrementa la resorción de calcio en los túbulos dístales aunque la excreción de calcio frecuentemente está elevada en el hiperparatiroidismo debido a que el aumento en la cantidad filtrada sobrepasa a los efectos sobre la reabsorción.La anovulación crónica hipotalamica funcional es consecuencia de: a) b) c) d) e) Reducción de la secreción de hormona liberadora de gonadotropinas Niveles séricos bajos de estradiol Concentraciones séricas aumentadas de hormona luteinizante Descenso del tono dopaminergico Niveles séricos elevados de hormona fóliculoestimulante La anovulación puede deberse a disfunción en cualquier nivel del eje hipotálamo-hipófisis-ovario.. la PTH estimula a los osteoclastos y a los osteoblastos predominando el efecto sobre los osteoclastos de tal modo que hay una mayor movilización de calcio desde el hueso.Neurólogo . esta acción fosfatúrica se debe a una disminución en la resorción d fosfato en los túbulos proximales. Recopilación realizada por: Dr. Como dato adicional la oxitocina se sintetiza en el núcleo paraventricular.25 dihidrocolecalciferol. 47. 46. En una escala de tiempo más prolongada. La PTH también incrementa la formación de 1.La paratohormona estimula la absorción de calcio en: a) b) c) d) e) Porción ascendente del asa de Henle Porción descendente del asa de Henle Túbulo contorneado proximal Túbulo contorneado distal Túbulo colector La PTH actúa de modo directo en el hueso aumentando su resorción y movilizando Ca+...

Paraneoplastic syndromes are not uncommon in renal cell carcinoma.. esta acción fosfatúrica se debe a una disminución en la resorción d fosfato en los túbulos proximales. la PTH estimula a los osteoclastos y a los osteoblastos predominando el efecto sobre los osteoclastos de tal modo que hay una mayor movilización de calcio desde el hueso. René Nájera Alvarado . La PTH también incrementa la resorción de calcio en los túbulos dístales aunque la excreción de calcio frecuentemente está elevada en el hiperparatiroidismo debido a que el aumento en la cantidad filtrada sobrepasa a los efectos sobre la reabsorción. la PTH aumenta la excreción de fosfato en la orina.25 dihidrocolecalciferol. músculo estriado y músculo cardíaco Tejido hepático. 40. Erythrocytosis from increased erythropoietin production occurs in 5%. si es normal y no hay factores de riesgo se debe realizar cada 3 años. Stauffer´s syndrome is a reversible syndrome of hepatic dysfunction in the absence of metastatic disease. qué a su vez aumenta la absorción intestinal de calcio.Para efectuar la detección temprana de la diabetes mellitus tipo 2 en personas que tienen factores de riesgo se debe practicar: a) b) c) d) e) Determinación semestral de hemoglobina glucosilada Curva de tolerancia a la glucosa cada 6 meses Vigilancia anual mediante la determinación de la glucemia en ayuno Medición de péptido C cada seis meses Control dietético y la cuantificación de glucemia en ayuno cada semestre La pesquisa debe realizarse en todos los individuos hispanos con o sin factores de riesgo para DM. La PTH también incrementa la formación de 1.Neurólogo .En términos fisiológicos la paratohormona ejerce su efecto directamente sobre: a) b) c) d) e) Plaquetas. En una escala de tiempo más prolongada. si la prueba es negativa pero tiene factores de riesgo debe realizarse la pesquisa de forma anual con una glucemia plasmática en ayunas o una glucemia capilar en ayunas.. Recopilación realizada por: Dr. . though anemia is far more common. 49. hypercalcemia may be present in up to 10% of patients. mucosa intestinal y tejido renal Cerebro. Además de incrementar el calcio y deprimir el fosfato plasmáticos. estomago y eritrocito La PTH actúa de modo directo en el hueso aumentando su resorción y movilizando Ca+. sistema nervioso central y tejido muscular Tejido óseo. médula ósea y eritrocitos Plaquetas.48.Hypercalcemia occurs as a paraneoplastic manifestation of cancer: a) Gastric b) Prostate c) Liver d) Renal e) Thyroid Hematuria is present in 60% of patients with renal cell carcinoma.

Una de las posibles causas de bocio simple es: a) Tiroiditis b) Deficiencia de yodo c) Exceso en la ingesta de yodo d) Pobre producción de hormona estimulante del tiroides e) Ausencia de hormonas tiroideas El bocio simple es un bocio difuso con función tiroidea normal. Because most of these infants are asymptomatic at birth.. aparte del déficit de yodo. 43. lethargy. sino que además inhibe la conversión periférica de T4 a T3: PROPRANOLOL. or poor peripheral circulation as shown by persistently mottled skin or cold extremities should suggest Recopilación realizada por: Dr. René Nájera Alvarado . así como la TSH son normales. tal y como se plantea el enunciado.000 births.. Pero.41. Las causas. 42. Es decir. prolonged jaundice. all states screen for this serious and treatable disease. litio. Thyroid deficiency may also be apparent at birth in genetically determined cretinism or in infants of mothers treated with thiouracil or its derivatives during pregnancy.La hormona necesaria para el desarrollo del sistema nervioso central es: a) b) c) d) e) Somatotropina Lactogeno placentario Lipotropina Levotiroxina Adrenocorticotropina La T3 es fundamental para el desarrollo del sistema nervioso central durante la embriogénesis. . una está incluida en la otra. 44.The main objective of the screening test for congenital hypothyroidism is avoided: a) Risks of generalized hypotonia b) Progression of umbilical hernia c) Progression of jaundice d) Mental retardation e) Macroglossia Primary hypothyroidism occurs in approximately 1/4. Constipation.El medicamento útil para tratar la manifestación más peligrosa de la tormenta tiroidea en pocas horas es: a) b) c) d) e) Yoduro Tionamida Propanolol Dexametasona Metimazol El metimazol es una tionamida (antitiroideo).Neurólogo . parece que están preguntándonos por el betabloqueante que. son la ingesta de bociógenos (antitiroideos. El resto de opciones nos presentan fármacos que se usan en una crisis de hipertiroidismo. no sólo produce una rápida mejoría de la sintomatología adrenérgica del cuadro (peligro de arritmias). los niveles de hormonas tiroideas (T3 y T4).. goiter. compuestos yodados) y los defectos en la síntesis de hormonas tiroideas (generalmente de la organificación). así que eliminamos las dos.

La causa de esta enfermedad es un aumento de la secreción de la hormona del crecimiento (debida. mineralocorticoid production (controlled by the renin-angiotensin system) persists and hyperkalemia is not present. pernicious anemia.Exceso de producción de la hormona del crecimiento después de la pubertad: a) b) c) d) e) Gigantismo Síndrome de Chiari-Frommel Acromegalia Panhipopituitarismo Síndrome de Sheehan La acromegalia es una enfermedad crónica del adulto. In contrast. tumor). aldosterone. hypothyroidism. Early diagnosis plus treatment of congenital deficiency of thyroid hormone improves intellectual outcome and is facilitated by screening all newborn infants for this deficiency. sometimes Recopilación realizada por: Dr. vitiligo. . if ACTH is not elevated. mandíbula.cretinism. Type 2 PGA usually presents in adulthood with autoimmune adrenal insufficiency (no hypoparathyroidism) that is HLA-related. generalmente.Leading Cause of Addison's disease: a) Tuberculosis b) An autoimmune disease c) Anticoagulation d) Trauma e) Bilateral infarction Addison's disease is an uncommon disorder caused by destruction or dysfunction of the adrenal cortices. Partial or late expression of the syndrome is common. Es el fenómeno opuesto a la acromicria. como consecuencia de la osteoporosis y de la artrosis. orejas. alopecia. después de la pubertad. These infants are probably chemically euthyroid as suggested by normal levels of serum thyrotropin and other tests of the pituitary-hypothalamic axis.. Because the relationship between low thyroid levels and neurodevelopmental outcome is unclear. and Sjogren's syndrome. necrosis. 45. including hypogonadism. It is characterized by chronic deficiency of cortisol. malabsorption.Neurólogo . 46. que viene causada por la hipersecreción de la hormona hipofisaria del crecimiento y que se caracteriza por un agrandamiento de muchas partes del esqueleto. etc. It may occur alone or as part of a polyglandular autoimmune (PGA) syndrome. It usually presents in early childhood with mucocutaneous candidiasis. a un tumor hipofisario). Autoimmune destruction of the adrenals is the most common cause of Addison's disease in the United States (accounting for about 80% of spontaneous cases). Transient hypothyroxinemia of prematurity is most common in ill infants of very low birthweight. skin pigmentary changes are not encountered. It is associated with autoimmune thyroid disease (usually hypothyroidism. hepatitis. A varied spectrum of associated diseases may be seen in adulthood. Addison's disease usually appears by age 15 years. especialmente de las porciones distales o prominentes: nariz. it remains uncertain whether premature infants with this transient problem should be treated with thyroid hormone. Type 1 PGA is also known as autoimmune polyendocrinopathy-candidiasisectodermal dystrophy (APCED) syndrome and is caused by a defect in T cell-mediated immunity inherited as an autosomal recessive trait. René Nájera Alvarado . dedos de las manos y de los pies. Se manifiesta con dolor en las articulaciones. if chronic adrenal insufficiency is secondary to pituitary failure (atrophy. Volume and sodium depletion and potassium excess eventually occur in primary adrenal failure. Furthermore. followed by hypoparathyroidism and dystrophy of the teeth and nails. and adrenal androgens and causes skin pigmentation that can be subtle or strikingly dark.

psychosis. René Nájera Alvarado .Neurólogo . Familial glucocorticoid deficiency is caused by a mutation in the gene encoding the adrenal ACTH receptor. Some patients with congenital adrenal hyperplasia (CYP17 deficiency) may present in adulthood with hyperkalemia." meaning extremity enlargement. vitiligo. tubulointerstitial diseases. and hypogonadism. nasal voice.An adverse effect may occur if administered growth hormone before puberty is: a) Premature closure of the metaphysis b) Hyperlipoproteinemia c) Appearance of diabetes d) Gigantism e) Acromegaly Excessive GH causes tall stature and gigantism if it occurs before closure of epiphyses. Hyperreninemic hypoaldosteronism can be seen in patients with myotonic dystrophy. Cortisol deficiency usually presents in infancy but may not occur until the third decade of life. The fingers widen. and neuromuscular disease of varying severity (hyperreflexia to spastic paraplegia). patients may also have hypogonadotropic hypogonadism. The association is now relatively rare in the United States but common where tuberculosis is more prevalent. The feet also grow. Tuberculosis was formerly a leading cause of Addison's disease. myopathy. It may also occur spontaneously. type 1 diabetes. hyperchloremia. cytomegalovirus infection (more frequent in patients with AIDS). amyloid disease. and high-frequency hearing loss. and spinal cord. hypertensive nephrosclerosis. Bilateral adrenal hemorrhage may occur during sepsis. fever. and hemochromatosis. seriously understates the manifestations. or with antiphospholipid antibody syndrome. Facial features coarsen since the bones and sinuses of the skull enlarge. histoplasmosis. aldosterone synthase deficiency. Neurologic deterioration may be severe or mild (particularly in heterozygote women). Psychiatric symptoms often include mania. Afterward. Hypogonadism is common. Patients with hereditary defects in adrenal enzymes for cortisol synthesis develop congenital adrenal hyperplasia due to ACTH stimulation. . Rare causes of adrenal insufficiency include lymphoma. Triple A (Allgrove's) syndrome is characterized by variable expression of the following: adrenal ACTH resistance with cortisol deficiency. hypertension. 47. Congenital adrenal hypoplasia causes adrenal insufficiency due to absence of the adrenal cortex. presenting about 1 week later with pain. Patients with severely defective P450c21 enzymes manifest deficiency of mineralocorticoids (salt wasting) in addition to deficient cortisol and excessive androgens. cortisol deficiency is also usually present but may not be clinically evident. It may present at any age and accounts for one-third of cases of Addison's disease in boys. testes. Isolated hypoaldosteronism can be caused by various conditions. or cognitive impairment. and shock. patients present with hyperkalemia. testicular failure (5%). acromegaly develops. alacrima. and metabolic acidosis. syphilitic gummas. causing patients to enlarge their rings. and pernicious anemia (4%). brain. particularly in width. Hyporeninemic hypoaldosteronism can be caused by renal tubular acidosis type IV and is commonly seen with diabetic nephropathy. coccidioidomycosis. Autoimmune Addison's disease can also be associated with primary ovarian failure (40% of women before age 50). The combination of Addison's disease and hypothyroidism is known as Schmidt's syndrome. metastatic carcinoma. alopecia areata. moist handshake is characteristic. or celiac sprue. Women with milder enzyme defects have adequate cortisol but develop hirsutism in adolescence or adulthood and are said to have "late-onset" congenital adrenal hyperplasia. achalasia. scleroderma. The most common enzyme defect is P450c21 (21-hydroxylase). It may occur in association with major surgery or trauma. and can occur years after the onset of adrenal insufficiency. Aldosterone deficiency occurs in 9%.hyperthyroidism). hat size Recopilación realizada por: Dr. Adrenoleukodystrophy is an X-linked peroxisomal disorder causing accumulation of very long chain fatty acids in the adrenal cortex. The term "acromegaly. heparin-associated thrombocytopenia or anticoagulation. and congenital adrenal hyperplasia. The hands enlarge and a doughy. and AIDS. Carpal tunnel syndrome is common. mimics symptoms of multiple sclerosis.

Colon polyps are common. hypoadrenalism is unusual. diaphoresis and carpal tunnel syndrome often improve within a day after surgery. and hypopituitarism. Tooth spacing widens. If the patient tolerates cabergoline. cerebrospinal fluid leak. malaise. the dosage may be increased gradually. as does hypertrophy of pharyngeal and laryngeal tissue. abdominal pain. including infection. At diagnosis. and dizziness. Headaches often improve. the maximum dosage is 30 mg subcutaneously daily. and tumor shrinkage of about 30% may be expected. thickening. Somatostatin analogs may be used to treat patients who have persistent acromegaly despite pituitary surgery.Neurólogo . Patients who fail to have a clinical or biochemical remission after surgery are treated with a dopamine agonist (eg. Acromegalic patients with pretreatment serum GH levels exceeding 20 ng/mL are less likely to respond to octreotide therapy. but can also be effective for patients with normal serum PRL levels. Cabergoline is administered orally. or seizure. since it is an oral medication. but complications occur in about 10% of patients. The dosage may be adjusted¾up to a maximum of 40 mg monthly¾to maintain the serum GH between 1 and 2. the maximum dosage is 1 mg orally twice weekly. coarse voice and sometimes makes intubation difficult. keeping IGF-I levels normal. Dietary salt supplements for 2 weeks postoperatively may prevent this complication. The skin may also manifest hyperhidrosis. pegvisomant. Pegvisomant does Recopilación realizada por: Dr. Obstructive sleep apnea may occur. vomiting. constipation. Headaches are frequent. The mandible becomes more prominent. especially in patients with skin papillomas. Octreotide long-acting release (LAR) preparations (Sandostatin LAR depot) are superior to shorter-acting octreotide. Overgrowth of vertebral bone can cause spinal stenosis. this causes a deep. starting with 0. Pegvisomant is a GH receptor antagonist that blocks the effects of GH. or a combination of these medications. Hyponatremia can occur 4-13 days postoperatively and is manifested by nausea. Short-acting octreotide acetate in doses of 50 mcg is injected subcutaneously three times daily. René Nájera Alvarado . It is prudent to monitor serum sodium levels postoperatively. GH levels fall immediately. cystic acne. Lanreotide Autogel (not available in the United States) is a newer formulation that is administered by deep subcutaneous injection in doses of 60-120 mg every 28 days. Temporal hemianopia may occur as a result of the optic chiasm being impinged by a suprasellar growth of the tumor. All somatostatin analogs are expensive and must be continued indefinitely or until other treatment has been effective. this preparation is better tolerated than lanreotide SR. Insulin resistance is usually present and frequently causes diabetes mellitus (30%). Octreotide and lanreotide are somatostatin analogs that are given by subcutaneous injection. based upon serum IGF-I levels and liver transaminase levels. GH-secreting pituitary tumors usually cause some degree of hypogonadism. Endoscopic transnasal. Macroglossia occurs. and areas of acanthosis nigricans. Surgical remission is achieved in about 70% of patients followed over 3 years. particularly of muscle and bone. cabergoline). Transsphenoidal surgery is usually well tolerated. Hypertension (50%) and cardiomegaly are common. abdominal discomfort. The maintenance dosage can be increased by 5-10 mg every 4-6 weeks. as are irregular menses or amenorrhea. or cholelithiasis. Cabergoline may be used first. Pegvisomant therapy produces symptomatic relief and normalizes serum IGF-I levels in over 90% of acromegalic patients. Responders who tolerate the drug are switched to long-acting octreotide acetate injectable suspension in a dosage of 20 mg intragluteally per month. based upon serum GH and IGF-I levels. ultimately achieving serum GH levels under 2 ng/mL in 79% of patients and normal serum IGF-I levels in 53% of patients. A goiter may be noted. Cabergoline is expensive. Side effects of cabergoline include nausea. fatigue. Lanreotide SR (not available in the United States) is given by subcutaneous injection at a dosage of 30 mg every 7-14 days. Side effects are experienced by about one-third of patients and include injection site pain. Decreased libido and impotence are common. Cabergoline therapy is most successful for tumors that secrete both prolactin (PRL) and GH. headache. causing prognathism and malocclusion.increases. octreotide. loose acholic stools. either by cosecretion of prolactin or by direct pressure upon normal pituitary tissue. Weight gain is typical. Secondary hypothyroidism sometimes occurs. about 10% of acromegalic patients have overt heart failure. with a dilated left ventricle and a reduced ejection fraction. transsphenoidal pituitary microsurgery removes the adenoma while preserving anterior pituitary function in most patients.5 ng/mL. The starting dosage is 10 mg subcutaneously daily. Therapy with cabergoline will shrink onethird of such tumors by more than 50%. Arthralgias and degenerative arthritis occur.25 mg twice weekly.

hypoadrenalism is unusual. and VI are less susceptible to radiation damage. Radiosurgery can also be used for patients who have failed conventional radiation therapy. Colon polyps are common. cystic acne. GH-secreting pituitary tumors usually cause some degree of hypogonadism. IV. thickening. Patients need to be monitored carefully with visual field examinations. hypoglycemic drugs are reduced to avoid hypoglycemia during pegvisomant therapy. or adapted linear accelerator. radiosurgery is more effective and carries a lower risk of hypopituitarism. heavy particle radiation. as does hypertrophy of pharyngeal and laryngeal tissue. . However. Headaches are frequent. Pegvisomant is extraordinarily expensive. The term "acromegaly. Radiosurgery precisely radiates the pituitary tumor in a single session and reduces radiation to the normal brain. The feet also grow. Insulin resistance is usually present and frequently causes diabetes mellitus (30%). and hypertension. Obstructive sleep apnea may occur.Physical feature of acromegaly: a) Micrognathia b) Prognathism c) Reducing the size of the sinuses d) Hypotelorism e) Microglosia Excessive GH causes tall stature and gigantism if it occurs before closure of epiphyses. Secondary hypothyroidism sometimes occurs. hepatitis. Radiosurgery can be used for pituitary tumors invading the cavernous sinus. Tooth spacing widens. GH levels. Afterward. Facial features coarsen since the bones and sinuses of the skull enlarge. Side effects of pegvisomant can include injection site reactions. cerebral necrosis. The skin may also manifest hyperhidrosis. psychological impairment. con una muestra mensual de expectoración con apoyo de los métodos convencionales (puño y palmo-percusión). Arthralgias and degenerative arthritis occur. and MRI scanning of the pituitary. In acromegalic diabetics. The hands enlarge and a doughy. 48. it cannot be used for pituitary tumors with suprasellar extension due to the risk of damaging the optic chiasm. with a dilated left ventricle and a reduced ejection fraction. this causes a deep. causing prognathism and malocclusion. acromegaly develops. Acromegalic patients who have not had a complete remission with transsphenoidal surgery or medical therapy may be treated with stereotactic radiosurgery administered by gamma knife. Compared to conventional radiation therapy. hat size increases. The effectiveness of pegvisomant is reduced by coadministration of opioids or propoxyphene. either by cosecretion of prolactin or by direct pressure upon normal pituitary tissue. Carpal tunnel syndrome is common. Macroglossia occurs. Hypertension (50%) and cardiomegaly are common. moist handshake is characteristic. V. as are irregular menses or amenorrhea. principalmente al final del tratamiento. edema.Neurólogo . Overgrowth of vertebral bone can cause spinal stenosis. particularly of muscle and bone. seriously understates the manifestations. nausea. Weight gain is typical. coarse voice and sometimes makes intubation difficult. The mandible becomes more prominent. At diagnosis. flu-like syndrome. En el control del tratamiento antituberculosis.not shrink GH-secreting tumors. especially in patients with skin papillomas. Temporal hemianopia may occur as a result of the optic chiasm being impinged by a suprasellar growth of the tumor. causing patients to enlarge their rings. since cranial nerves III. René Nájera Alvarado . Recopilación realizada por: Dr. and small vessel stroke. The fingers widen. about 10% of acromegalic patients have overt heart failure. Decreased libido and impotence are common. particularly in width. A goiter may be noted. and areas of acanthosis nigricans. toda muestra de control independientemente de la calidad y apariencia macroscópica debe ser procesada." meaning extremity enlargement.

Anemia.T4 and RAI uptake usually low . weight change. * Ante el descenso de Calcio: o Se incrementa la síntesis de PTH o Se incrementa el tamaño y cantidad de células (en hipocalcemias prolongadas) o Disminuye la degradación de PTH o Aumenta la degradación de proPTH * Ante el aumento de Calcio: o Aumenta la cantidad de vitamina D. bradycardia. de la excreción de calcio por los riñones y de la liberación de calcio procedente de los huesos. principalmente. lo que hace es aumentar la resorción de estos iones procedentes del hueso. Además. tejido musclar y plaquetas Tejido renal.TSH elevated in primary hypothyroidism 50. para así aumentar los niveles de calcio en sangre. la cual inhibe la producción de PTH o Disminuye la degradación de proPTH Recopilación realizada por: Dr. fatigue.Dry skin. eritrocitos y plaquetas Sistema nervioso central. tejido óseo y mucosa intestinal Músculo cardíaco. tejido hepatico y estomago La parathormona. hyponatremia .. La parathormona regula la concentración de iones calcio en el líquido extracelular mediante el control de la absorción de calcio por el intestino. de tal forma que hace descender la concentración de ellos en este medio al aumentar su excreción renal. El déficit de esta hormona produce hipocalcemia (niveles bajos de calcio en sangre) que puede conducir a la tetania. René Nájera Alvarado . . cold intolerance. es una hormona peptídica secretada por la glándula paratiroides que interviene en la regulación del metabolismo del calcio y del fósforo. constipation.49.Most common menstrual pattern in hypothyroidism: a) Hypermenorrhoea b) Menorrhagia c) Oligomenorrhea d) Metrorrhagia e) Amenorrhoea . menorrhagia. el aumento de la secreción de parathormona provoca hipercalcemia (niveles elevados de calcio en sangre). hoarseness . Esta se produce en base a la cantidad de calcio en el organismo. también denominada hormona paratiroidea.Lugar donde actua la paratohormona: a) b) c) d) e) Medula ósea. regula los niveles de iones fósforo en la sangre. tiene un efecto contrario a la calcitonina. depression. delayed return of deep tendon reflexes . En el caso de iones calcio. cerebro y músculo estriado Eritrocito. PTH o paratirina.Weakness.Neurólogo . Por tanto.

The high serum insulin may further down-regulate the activity of their insulin receptors. Reduced glucose combustion creates hyperglycaemia. Lack of exercise predisposes one to obesity. DM2 can be caused. They are all key proteins (hormone. The insulin secreted in DM2 patients does not increase the uptake of glucose as in normal persons. 51. Other patients are tired.Pathophysiology of type 2 diabetes mellitus: a) Resistance to insulin but hyperinsulinism b) Decreased insulin resistance c) Decreased glycogenolysis d) Increased production of hepatic glycogen e) Decreased gluconeogenesis DM2 is a complex of polygenic disorders. La activación de este receptor inhibe la secreción de PTH. IAPP is a possible antagonist to insulin.El calcio ionizado circulante actúa directamente en las células paratiroideas uniéndose a un receptor en serpentina para calcio asociado a una proteína G. Por ejemplo. or by 2) target cell defects including receptor failure. Cuando hay concentraciones altas se inhibe la secreción de PTH y el calcio se deposita en los huesos. The hyperglycaemia elicits insulin secretion from defective b-cells in some patients.Neurólogo . The impaired glucose tolerance is demonstrated by a glucose tolerance test. One is the gene on chromosome 7. and explain some cases of insulin resistance. DM2 relates to inactive life style. Since insulin is present. Type 2 diabetes also occurs in younger persons. la secreción de PTH aumenta y el calcio se moviliza de los huesos y se reabsorbe en el riñón. The insulin secretion is abnormal in patients with DM2. Muscular activity is required to stimulate the normal production of key proteins. nephropathy. intermittent claudication. a condition that greatly decreases insulin sensitivity of the target cells (adipocytes. the acute complications such as ketonaemia and metabolic acidaemia are rare in these patients. Many DM2 patients need much more insulin for a given test effects than DM1 patients and healthy people. theoretically. De esta forma el calcio actúa mediante una retroalimentación negativa para mantener constantes los niveles séricos de calcio. by 1) b-cell defects including genetic defects. René Nájera Alvarado . The possible defective sites in 1 and 2 have one common denominator. have minor genital infections or sugar spots on their underwear. The genetic defects differ and many mutations are known. arteriosclerotic disorders (cerebrovascular insults. . increases the incidence if DM2. y tras una serie de pasos activa genes y enzimas que median la acción biológica. with redundant food intake. Certain families show an autosomal dominance. but a routine examination reveals glucosuria or a raised blood glucose. receptors and transporters). heart and skeletal muscle tissues). a genetic Recopilación realizada por: Dr. Many older patients with DM2 have no symptoms. IAPP). but inactivity and stress (an inactive life style with a low endurance capacity) seems to be involved in the development of type 2 diabetes. which code for glucokinase. seems to be involved in the development of DM2 in persons with a genetic predisposition. susceptibility to infection or neuropathy. The much more frequent type 2 diabetes is the result of insulin resistance and b-cell defects. resulting in raised serum [insulin]. La PTH se une a un receptor asociado a proteina G en la membrana plasmatica. resulting in abnormal insulin production. Some patients present with established late-complications such as retinopathy (blindness). Cuando la concentración es baja. gangrene). The basic problem is therefore possibly a genetically and activity dependent defect in key protein production in the cell interior. The destroyed b-cells is filled with amyloid material (islet amyloid polypeptide. although they typically possess half of their b-cell mass at autopsy. especially in persons with a high fat-low muscle mass. A strong genetic element is always present. Lack of regular physical activity with development of overweight. An inactive life style for years. puede inducir la propia liberacion de calcio intracelular. Actually. myocardial infarction. Identical twins show almost absolute concordance in development of DM2.

PM. and (5) following injury to both adrenals by trauma. hemorrhage. nausea and vomiting. The blood pressure is low. prednisone. 52. or prolonged fasting in a patient with latent insufficiency.. and reduce dosage to maintenance levels as needed. and continue intravenous infusions of 50-100 mg every 6 hours for the first day. Hypoglycemia is frequent. draw a blood sample for cortisol determination and treat with hydrocortisone. Hypercalcemia may be present. 5-10 mg). without waiting for the results. Blood. anticoagulant therapy. which is performed as follows: (1) Synthetic ACTH1-24 (cosyntropin). 100 mg intravenously immediately. or when thyroid is given to a patient with hypoadrenalism. Since bacterial infection frequently precipitates acute adrenal crisis. 10-20 mg every 6 hours. Other signs may include cyanosis. Adrenal crisis may occur in the following situations: (1) following stress. Acute adrenal crisis is more commonly seen in primary adrenal insufficiency (Addison's disease) than in disorders of the pituitary gland causing secondary adrenocortical hypofunction.05-0. infection. The diagnosis is made by a simplified cosyntropin stimulation test. (2) following sudden withdrawal of adrenocortical hormone in a patient with chronic insufficiency or in a patient with temporary insufficiency due to suppression by exogenous glucocorticoids or megestrol. is given parenterally. Hypoglycemia should be vigorously treated while serum electrolytes. Other glucocorticoids (eg. (3) following bilateral adrenalectomy or removal of a functioning adrenal tumor that had suppressed the other adrenal. When the patient is able to take food by mouth. dehydration. and creatinine are monitored. Some patients never require fludrocortisone or become edematous at doses of more than 0. 100-300 mg intravenously. infection. René Nájera Alvarado . broad-spectrum antibiotics should be administered empirically while waiting for the results of initial cultures. Thereafter. Plasma ACTH is markedly elevated if the patient has primary adrenal disease (generally > 200 pg/mL). or urine culture may be positive if bacterial infection is the precipitating cause of the crisis. rarely. dexamethasone) do not interfere with specific assays for cortisol.defect has just been demonstrated at certain steps of insulin action in a subset of patients of late-onset DM2. hydrocortisone must not be given for at least 8 hours before the test. trauma. serum cortisol rises to at least 20 mcg/dL. Give the same amount every 8 hours on the second day and then adjust the dosage in view of the clinical picture. 0.Neurólogo . or.2 mg daily. and saline immediately. and often diarrhea. sputum. eg. Fever may be 40. but as the dose is reduced it is usually necessary to add fludrocortisone acetate. thrombosis.05 mg once or Recopilación realizada por: Dr. The eosinophil count may be high. skin hyperpigmentation. Meningococcemia may be associated with purpura and adrenal insufficiency secondary to adrenal infarction (Waterhouse-Friderichsen syndrome). Confusion or coma may be present. Normally. For patients receiving glucocorticoid treatment. BUN. Most patients ultimately require hydrocortisone twice daily (AM. (2) Serum is obtained for cortisol between 30 and 60 minutes after cosyntropin is administered. If the diagnosis is suspected.Tratamiento urgente de la crisis corticosuprarrenal: a) b) c) d) e) Reposición de líquidos y ACTH Glucanato de calcio y aldosterona Reposición de líquidos y vasopresina Solución mixta y somatostatina Solución salina e hidrocortisona Acute adrenal insufficiency is an emergency caused by insufficient cortisol. Patients with preexisting type 1 diabetes may present with recurrent hypoglycemia and reduced insulin requirements. Mineralocorticoid therapy is not needed when large amounts of hydrocortisone are being given. (4) following sudden destruction of the pituitary gland (pituitary necrosis). Crisis may occur in the course of chronic treated insufficiency. The patient complains of headache. or it may be the presenting manifestation of adrenal insufficiency.25 mg.6°C or more. give oral hydrocortisone. metastatic carcinoma. lassitude. Hyponatremia or hyperkalemia (or both) are usually present. abdominal pain. 10-20 mg. and sparse axillary hair (if hypogonadism is also present). 0. give hydrocortisone phosphate or hydrocortisone sodium succinate. surgery.

Pheochromocytomas can be lethal unless they are diagnosed and treated appropriately. nausea and vomiting. seizures. and TSH. Anginal attacks may occur. or hypercalcemia (PTHrP). constipation. or paroxysmal only (25% of patients). Some patients may be entirely asymptomatic despite high serum levels of catecholamines. and more than 135 mcg total catecholamines per gram creatinine. precordial or abdominal pain. sustained with paroxysms (50% of patients). other symptoms may include anxiety (50% of patients). The ESR is sometimes elevated. 53. Other findings may include tachycardia. as the attack subsides. needle biopsy of the mass. They typically cause attacks of severe headache (80% of patients). and palpitations (60% of patients). hypotension. patients with pheochromocytomas generally have more that 2. Once the crisis has passed. a sense of impending doom. Catastrophic hypertensive crisis and fatal cardiac arrhythmias can occur spontaneously or may be triggered by intravenous contrast dye or glucagon injection. Some patients are normotensive and asymptomatic. thyroid function tests are normal. There may be cardiac enlargement and cardiomyopathy. especially when samples are obtained during or immediately following an episodic attack.Neurólogo . including serum T4. Recopilación realizada por: Dr.Male patient aged 17 presented with sweating. Retinal hemorrhage or cerebrovascular hemorrhage occurs occasionally. pheochromocytomas secrete a wide range of other peptides that can sometimes cause symptoms of Cushing's syndrome (ACTH). postural tachycardia (change of more than 20 beats/min) and postural hypotension. FT4. hypertension. increased appetite. Epinephrine secretion may cause episodic tachyarrhythmias. perspiration (70% of patients). paresthesias. being found in less than 0. and loss of weight. pallor.3% of hypertensive individuals. facial flushing may occur as a result of reflex vasodilation. vomiting. Hypermetabolism is present. . or tremor (40% of patients). hyperglycemia. Plasma renin activity may be increased by catecholamines.twice weekly. T3. Other patients may have pulmonary edema and heart failure due to cardiomyopathy. although an overnight or shorter collection may be used. Leukocytosis is common. In addition to the above symptoms. Assay of urinary catecholamines and metanephrines (total and fractionated) and creatinine detects most pheochromocytomas. René Nájera Alvarado . anesthesia. and surgical procedures. and mild elevation of basal body temperature. increasing nervousness and irritability. or Raynaud's phenomenon. Hyperglycemia is present in about 35% of patients but is usually mild. erythrocytosis (erythropoietin). or syncope. Urinary assay for vanillylmandelic acid (VMA) is about 89% sensitive and is not usually required. The most likely diagnosis is: a) Glomerulonephritis b) Pheochromocytoma c) Nephrotic syndrome d) Adrenal insufficiency e) Renal tumor Pheochromocytomas are rare. The manifestations of pheochromocytoma are quite varied and mimic other conditions. some patients can present with psychosis or confusion. which may be sustained (20% of patients). The incidence is higher in patients with moderate to severe hypertension. bradycardia. Physical findings usually include hypertension (90% of patients). Urinary assay for total metanephrines is about 97% sensitive for detecting functioning pheochromocytomas. hypotension. A 24-hour urine specimen is usually obtained. or with pain from metastatic disease. Vasomotor changes during an attack cause mottled cyanosis and facial pallor.2 mcg of total metanephrine per milligram of creatinine. Others may present with abdominal discomfort from a large hemorrhagic pheochromocytoma. the patient must be investigated to assess the degree of permanent adrenal insufficiency and to establish the cause if possible. In addition to catecholamines and their metabolites.

They are C18 steroids. Hypoglycemia.hydroxyprogesterone. ie. Conversion of steroids C-21 C-19 steroids. and estriol.The principal circulating precursor for placental estrone and 17-estradiol is: a) Sulfate dehydroisoandrosterone b) Testosterone c) Androsterone d) Dehydroisoandrosterone e) Pregnanediol The naturally occurring estrogens are 17b-estradiol. but serious. Conversion of cholesterol to pregnenolone. . Es precursor de los ácidos biliares y constituye la materia prima para la síntesis de las hormonas esteroides. but a small portion of what is in situ from acetyl-CoA via mevalonate and squalene. Conversion of androstenedione to 17 . treatment with thiourea. d. presente en grasas animales.The most important adverse effect of propylthiouracil is presenting: a.1% of patients taking methimazole and about 0. which has reported nearly 0. Hydroxylation of steroids at C-21.4% of those who ingest propylthiouracil. aceites. The agrunolocitosis is usually reversible and can be treated with filgrastim (G-CSF). 57. Agranulocytosis is an uncommon complication. estrone. etc. they do not have an angular methyl group attached to the 10 position or a D-3-keto configuration in the A ring.Neurólogo . Aromatase (CYP19) is the enzyme that catalyzes the conversion of androstenedione to estrone and the conversion of testosterone to estradiol. Adrenal steroid hormones are synthesized from cholesterol that is derived mostly from plasma. Agranulocytosis. René Nájera Alvarado . the corpus luteum. 55. They are secreted primarily by the granulosa cells of the ovarian follicles. Under adrenal stimulation by ACTH (or Recopilación realizada por: Dr. c. Much of the cholesterol in the adrenal is esterified and stored in cytoplasmic lipid droplets. 56. Acute renal failure. bilis. . The biosynthetic pathway involves their formation from androgens (testosterona). Pseudotumor cerebri. c.. and the placenta. b. Hyponatremia. . Reduction of steroids at C-5 alpha. huevo (yema). e. sangre. b. e.El colesterol es el precursor de todas las hormonas: a) Tiroideas b) Hipofisiarias c) Pancreáticas d) Esteroideas e) Hipotalamicas El colesterol es un alcohol esteroide con aspecto de grasa. d.54. They are also formed by aromatization of androstenedione in the circulation.In the first stage of the biosynthesis of steroid hormones is given: a.

and toxic adenoma. Su función es la de regular varios componentes del metabolismo con la producción de mineralcorticoides y Recopilación realizada por: Dr..cAMP) is activated and free cholesterol esterase formed is transported into the mitochondria where an enzyme side chain cleavage cytochrome P450 (P450 scc) converts cholesterol to pregnenolone . The most common cause of thyrotoxicosis is Graves disease (50-60%). . including common autoimmune antibodies. Hyperthyroidism includes diseases that are a subset of thyrotoxicosis (excludes exogenous thyroid hormone intake and subacute thyroiditis) that is caused by excess synthesis and secretion of thyroid hormone by the thyroid. 59. and antithyroglobulin (anti-TG) antibodies. antithyroperoxidase (anti-TPO). use the terms hyperthyroidism and thyrotoxicosis interchangeably. toxic multinodular goiter (Plummer disease). and excessive thyroid hormone levels compared to a healthy thyroid with subacute thyroiditis. TSI is directed toward epitopes of the thyroid-stimulating hormone (TSH) receptor and acts as a TSH-receptor agonist.En que capa de la glándula suprarrenal se produce el cortisol: a) b) c) d) Glomerular Fasciculada Reticular Medula La corteza suprarrenal está situada rodeando la circunferencia de la glándula suprarrenal.The first cause of hyperthyroidism in adolescents is: a) Tiroditis subacute b) Diffuse toxic goiter (Graves disease) c) Toxic nodular goiter d) Toxic Adenoma Thyrotoxicosis is the hypermetabolic condition associated with elevated levels of free thyroxine (FT4). René Nájera Alvarado . Graves disease is an organ-specific autoimmune disorder characterized by a variety of circulating antibodies. free triiodothyronine (FT3). Most clinicians. The most common forms of hyperthyroidism include diffuse toxic goiter (Graves disease). The first step in steroidogenesis is the conversion of cholesterol to pregnenolone catalyzed by a complex enzyme system (mixed function oxidase) called desmolase cholesterol oxidase. or both. This results in the characteristic picture of Graves thyrotoxicosis. The most important autoantibody is thyroid-stimulating immunoglobulin (TSI). exclusive of endocrinologists. 58. TSI binds to the TSH receptor on the thyroid follicular cells to activate thyroid hormone synthesis and release and thyroid growth (hypertrophy).Neurólogo . Similar to TSH. these conditions constitute 85-90% of all causes of thyrotoxicosis. very high radioactive iodine uptake. with a diffusely enlarged thyroid.

principalmente cortisol. sobre todo. La corteza suprarrenal puede dividirse en tres capas diferentes de tejido basado en los tipos celulares y la función que realizan. 60. en las heces. Regula la absorción de calcio a partir del tracto GI.. aldosterona. el depósito de calcio en los huesos y la excreción de calcio en la leche materna.Neurólogo . a) Zona glomerular: Producción de mineralcorticoides. incluyendo testosterona. la movilización del calcio óseo.La disminución de este disminuye la reabsorción osea: a) b) c) d) Paratohormona Calcitonina Osteoclastos Osteoblastos La PTH segregada por las glándulas paratiroides que actúa manteniendo una concentración constante de calcio en el líquido extracelular. René Nájera Alvarado . cerca del 95%. c) Zona reticular: Producción de andrógenos.glucocorticoides que incluyen a la aldosterona y al cortisol. b) Zona fascicular: Producción de glucocorticoides. en el sudor y en la orina Recopilación realizada por: Dr. La corteza suprarrenal también es un lugar secundario de síntesis de andrógenos.