endocrinología 3

7/28/2019 Endocrinologa 3

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Recopilacin realizada por: Dr. Ren Njera Alvarado - Neurlogo

Endocrinologa 3

41.- La estimulacin simptica del pncreas exocrino provoca:

a) Dilatacin del conducto pancretico principalb) Aceleracin del vaciamiento de los acinos pancreaticosc) Supresin de la secrecin de jugo gstricod) Incremento en la liberacin de tripsinae) Supresin de la activacin del tripsinogeno

El pncreas excrino es la principal glndula digestiva del organismo, secreta alrededor de un litro deun lquido claro rico en bicarbonato cada da al intestino delgado. Este lquido, el jugo pancretico,contiene las enzimas digestivas necesarias para la hidrlisis intraluminal (dentro de la luz del intestino)de los macronutrientes de la dieta (protenas, almidn, grasas, y cidos nucleicos) y de las vitaminasliposolubles a molculas ms pequeas que pueden absorverse directamente en los enterocitos(clulas del intestino delgado) o seguir actuando formando parte de enzimas presentes en la bilis parapermitir su posterior absorcin. En los humanos el jugo pancretico tiene una concentracin deprotenas del 1 al 10 %. La mayor parte de estas protenas son enzimas digestivas o cofactores, queincluyen 20 isozimas de 12 diferentes enzimas. El resto est formado por la secrecin de un inhibidorde tripsina (que tiene una funcin protectora para evitar el dao al pncreas debido a una activacinprematura de la tripsina en el tejido o en el jugo pancretico) y otras enzimas similares a la tripsina queno tienen una funcin primaria en la digestin, protenas plasmticas y glicoprotenas. Las cuatroprincipales categoras de las enzimas digestivas son las proteasas (digieren protenas y pptidos)amilasa (digiere almidn), lipasas (digieren triglicridos y fosfolpidos) y nucleasas (digieren cidosnucleicos). Todas la proteasas como tambin la fosfolipasa son secretadas por el pncreas comoproenzimas (zimogenos) inactivas. Luego de llegar al lumen intestinal, el tripsingeno es convertido atripsina por las enteropeptidasas, enzima que se encuentra en el ribete de la clula del intestino. Latripsina puede activar a otras proenzimas como as tambin al tripsingeno. De manera diferente a lasotras enzimas digestivas, la amilasa, la lipasa y la ribonucleasa se secretan en su forma activa. Elpancreas excrino tiene una reserva de enzimas mucho mayor de las necesarias para la digestin de

los alimentos. La mayor reserva es de las enzimas necesarias para digerir los azcares (carbohidratos)y las protenas. Las reservas para la digestin de las grasas (lpidos) particularmente para la hidrlisisde triglicridos es ms limitada. Los estudios realizados en personas sometidas a una reseccinparcial del pncreas demostraron que la insuficiencia digestiva para las grasas no se produce hastaque se pierde la capacidad del rgano en un 80 % al 90% Esta observacin tiene implicancia clnicaspues indica que la costumbre de ingerir tabletas rotuladas como digestivos que contienen enzimaspancreticas no tiene racionalidad teraputica. Una vez que el jugo pancretico entra en el intestino, eltripsingeno es activado a tripsina por la enterokinasa en forma tan rpida y completa que la relativapequea cantidad del inhibidor de tripsina presente no interfiere con el proceso digestivo normal. Otromecanismo protector adicional contra el efecto potencialmente perjudicial de la activacin prematurade tripsina dentro del pncreas, es la habilidad de diversas molculas similares a la tripsinasintetizadas por la clula acinosa y de la misma tripsina para destruir las molculas nocivas de tripsina

y tripsingeno. Durante el estado basal o sea en ayuno, el volumen del jugo pancretico secretado alduodeno es bajo, con una secrecin de enzimas de alrededor del 10 % de su nivel mximo y debicarbonato solo un 2% del mximo. Existen breves perodos en el que aumenta la secrecin deenzimas y bicarbonato cada 60-120 minutos asociados con una actividad motora del estmago y elintestino entre las comidas. Los nervios colinrgicos (parasimptico) son los que regulan elaumento de la actividad secretora. Los nervios adrenrgicos (simptico) actan como inhibidorde la secrecin pancretica en ayunas.Luego de una ingestin de una comida el pncreas excrinosegrega bicarbonato y enzimas a un nivel del 60-75% del que podra obtenerse luego de una


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administracin endovenosa mxima de una dosis de secretina y CCK (colecistokinina) principalesestimulantes de la secrecin del pncreas. La secrecin estimulada por la comida, al igual que en elestmago tambin puede dividirse en fases ceflicas, gstricas e intestinal aunque puedensobreponerse en parte. La fase ceflica es estimulada por el pensamiento, la visualizacin, ladegustacin o el olfato a comida. Puede producir una respuesta secretora del 25 al 50 % del mximo yest regulada primordialmente por una inervacin vagal colinrgica. La fase gstrica no ha sido muy

estudiada, pero la distensin del estmago produce un pequeo aumento en la secrecin del pncreastambin mediada por reflejos vagales colinrgicos. Durante la fase intestinal se libera secretina a lasangre desde el duodeno en respuesta a la presencia de cido en el mismo. Los cidos grasos y labilis tambin pueden estimular la liberacin de secretina. Es interesante tener presente que solo senecesita un 10 % de accin de la lipasa (encargada de digerir sustancias grasas de nuestra dieta).Esto significa la natural sobreabundancia de enzimas digestivas por lo que es poco razonable laautomedicacin con "as llamados digestivos" para intentar favorecer el proceso de la digestin.

42.- Para efectuar la deteccin temprana de la diabetes mellitus en personas que tienen factoresde riesgo se debe practicar:

a) Determinacin anual de hemoglobina glucosilada

b) Curva de tolerancia a la glucosa cada seis mesesc) Vigilancia anual mediante la determinacin de la glicemia en ayunod) Determinacin de la glucemia con carga oral cada dos aose) Control diettico y la cuantificacin de la glucemia en ayuno cada semestre

Al identificar factores de riego se debe recomendar la glicemia en ayuno, que si es negativa sedebe realizar cada ao, se recomienda el cambio de los hbitos dietticos + actividad fsica.

43.- La prueba especfica para establecer el diagnstico de diabetes gestacional es la:

a) Glucemia postprandialb) Glucemia postrcarga de 50 g

c) Glucemia en ayunod) Determinacin de hemoglobina glucosiladae) Curva de tolerancia a la glucosa

Se recomienda la seleccin selectiva de mujeres de 30 aos de edad y mayores con una carga oral deglucosa de 50 g entre las 24 y 28 semanas de la gestacin. Las enfermas cuyos valores de glucemiason de 140 mg/dL o mayores deben valorarse con una prueba de tolerancia a la glucosa oraldiagnstica de tres horas.

44.- La funcin metablica de la somatotropina consiste en:

a) Disminuir la utilizacin celular de glucosa

b) Disminuir la liberacin de cidos grasos hacia la sangrec) Incrementar el volumen de los depositos corporales de tejido adiposod) Aumentar la sntesis celular de protenase) Promover la utilizacin de glucosa por las clulas

La hormona del crecimiento moviliza los FFA del tejido adiposo, lo que favorece la cetognesis.Disminuye la captacin de glucosa dentro de ciertos tejidos (accin antiinsulnica), aumenta la salidade glucosa heptica y puede disminuir la unin de la insulina a los tejidos.


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45.- La anovulacin crnica hipotalamica funcional es consecuencia de:

a) Reduccin de la secrecin de hormona liberadora de gonadotropinasb) Niveles sricos bajos de estradiolc) Concentraciones sricas aumentadas de hormona luteinizanted) Descenso del tono dopaminergico

e) Niveles sricos elevados de hormona fliculoestimulante

La anovulacin puede deberse a disfuncin en cualquier nivel del eje hipotlamo-hipfisis-ovario. Lasaberraciones de la liberacin intermitente de hormona liberadora de gonadotropina (GnRH) delhipotlamo dan por resultado una deficiencia de la secrecin hipofisiaria de hormonaestimulante del folculo (FSH) y hormona luteinizante (LH). Sin la estimulacin apropiada por lasgonadotropinas, no se lleva a cabo la foliculognesis ovrica ni la ovulacin. Una interrupcin de estasecuencia de fenmenos en cualquier etapa inhibe la ovulacin.

46.- La destruccin del ncleo supraptico puede dar lugar a:

a) Incremento del volumen urinario y disminucin de la densidad

b) Aumento del volumen urinario y orina concentradac) Orina escasa e hipotenuricad) Disminucin del volumen urinario y orina muy diluidae) Disminucin del volumen urinario y orina concentrada

La hormona antidiurtica, llamada tambin vasopresina, se sintetiza en el ncleo supraptico, por loque la eventual destruccin del mismo causara aumento en la diuresis y disminucin de la densidadurinaria. Como dato adicional la oxitocina se sintetiza en el ncleo paraventricular.

47.- La paratohormona estimula la absorcin de calcio en:

a) Porcin ascendente del asa de Henle

b) Porcin descendente del asa de Henlec) Tbulo contorneado proximald) Tbulo contorneado distale) Tbulo colector

La PTH acta de modo directo en el hueso aumentando su resorcin y movilizando Ca+. Adems deincrementar el calcio y deprimir el fosfato plasmticos, la PTH aumenta la excrecin de fosfato en laorina; esta accin fosfatrica se debe a una disminucin en la resorcin d fosfato en los tbulosproximales. La PTH tambin incrementa la resorcin de calcio en los tbulos dstales aunque laexcrecin de calcio frecuentemente est elevada en el hiperparatiroidismo debido a que el aumento enla cantidad filtrada sobrepasa a los efectos sobre la reabsorcin. La PTH tambin incrementa laformacin de 1,25 dihidrocolecalciferol, qu a su vez aumenta la absorcin intestinal de calcio. En una

escala de tiempo ms prolongada, la PTH estimula a los osteoclastos y a los osteoblastospredominando el efecto sobre los osteoclastos de tal modo que hay una mayor movilizacin de calciodesde el hueso.


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48.- En trminos fisiolgicos la paratohormona ejerce su efecto directamente sobre:

a) Plaquetas, mdula sea y eritrocitosb) Plaquetas, sistema nervioso central y tejido muscularc) Tejido seo, mucosa intestinal y tejido renald) Cerebro, msculo estriado y msculo cardaco

e) Tejido heptico, estomago y eritrocito

La PTH acta de modo directo en el hueso aumentando su resorcin y movilizando Ca+. Adems deincrementar el calcio y deprimir el fosfato plasmticos, la PTH aumenta la excrecin de fosfato en laorina; esta accin fosfatrica se debe a una disminucin en la resorcin d fosfato en los tbulosproximales. La PTH tambin incrementa la resorcin de calcio en los tbulos dstales aunque laexcrecin de calcio frecuentemente est elevada en el hiperparatiroidismo debido a que el aumento enla cantidad filtrada sobrepasa a los efectos sobre la reabsorcin. La PTH tambin incrementa laformacin de 1,25 dihidrocolecalciferol, qu a su vez aumenta la absorcin intestinal de calcio. En unaescala de tiempo ms prolongada, la PTH estimula a los osteoclastos y a los osteoblastospredominando el efecto sobre los osteoclastos de tal modo que hay una mayor movilizacin de calciodesde el hueso.

49.- Para efectuar la deteccin temprana de la diabetes mellitus tipo 2 en personas que tienenfactores de riesgo se debe practicar:

a) Determinacin semestral de hemoglobina glucosiladab) Curva de tolerancia a la glucosa cada 6 mesesc) Vigilancia anual mediante la determinacin de la glucemia en ayunod) Medicin de pptido C cada seis mesese) Control diettico y la cuantificacin de glucemia en ayuno cada semestre

La pesquisa debe realizarse en todos los individuos hispanos con o sin factores de riesgo para DM, sies normal y no hay factores de riesgo se debe realizar cada 3 aos, si la prueba es negativa pero tiene

factores de riesgo debe realizarse la pesquisa de forma anual con una glucemia plasmtica en ayunaso una glucemia capilar en ayunas.

40. - Hypercalcemia occurs as a paraneoplastic manifestation of cancer:

a) Gastricb) Prostatec) Liverd) Renale) Thyroid

Hematuria is present in 60% of patients with renal cell carcinoma. Paraneoplastic syndromes are not

uncommon in renal cell carcinoma. Erythrocytosis from increased erythropoietin production occurs in5%, though anemia is far more common; hypercalcemia may be present in up to 10% of patients.Stauffers syndrome is a reversible syndrome of hepatic dysfunction in the absence of metastaticdisease.


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41.- La hormona necesaria para el desarrollo del sistema nervioso central es:

a) Somatotropinab) Lactogeno placentarioc) Lipotropinad) Levotiroxina

e) Adrenocorticotropina

La T3 es fundamental para el desarrollo del sistema nervioso central durante la embriognesis.

42.- El medicamento til para tratar la manifestacin ms peligrosa de la tormenta tiroidea enpocas horas es:

a) Yodurob) Tionamidac) Propanolold) Dexametasonae) Metimazol

El metimazol es una tionamida (antitiroideo); una est incluida en la otra, as que eliminamos las dos.El resto de opciones nos presentan frmacos que se usan en una crisis de hipertiroidismo. Pero, tal ycomo se plantea el enunciado, parece que estn preguntndonos por el betabloqueante que, no sloproduce una rpida mejora de la sintomatologa adrenrgica del cuadro (peligro de arritmias), sino queadems inhibe la conversin perifrica de T4 a T3: PROPRANOLOL.

43.- Una de las posibles causas de bocio simple es:

a) Tiroiditisb) Deficiencia de yodoc) Exceso en la ingesta de yodo

d) Pobre produccin de hormona estimulante del tiroidese) Ausencia de hormonas tiroideas

El bocio simple es un bocio difuso con funcin tiroidea normal. Es decir, los niveles de hormonastiroideas (T3 y T4), as como la TSH son normales. Las causas, aparte del dficit de yodo, son laingesta de bocigenos (antitiroideos, litio, compuestos yodados) y los defectos en la sntesis dehormonas tiroideas (generalmente de la organificacin).

44. - The main objective of the screening test for congenital hypothyroidism is avoided:

a) Risks of generalized hypotoniab) Progression of umbilical hernia

c) Progression of jaundiced) Mental retardatione) Macroglossia

Primary hypothyroidism occurs in approximately 1/4,000 births. Because most of these infants areasymptomatic at birth, all states screen for this serious and treatable disease. Thyroid deficiency mayalso be apparent at birth in genetically determined cretinism or in infants of mothers treated withthiouracil or its derivatives during pregnancy. Constipation, prolonged jaundice, goiter, lethargy, or poorperipheral circulation as shown by persistently mottled skin or cold extremities should suggest


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cretinism. Early diagnosis plus treatment of congenital deficiency of thyroid hormone improvesintellectual outcome and is facilitated by screening all newborn infants for this deficiency. Transienthypothyroxinemia of prematurity is most common in ill infants of very low birthweight. These infants areprobably chemically euthyroid as suggested by normal levels of serum thyrotropin and other tests of thepituitary-hypothalamic axis. Because the relationship between low thyroid levels andneurodevelopmental outcome is unclear, it remains uncertain whether premature infants with this

transient problem should be treated with thyroid hormone.

45.- Exceso de produccin de la hormona del crecimiento despus de la pubertad:

a) Gigantismob) Sndrome de Chiari-Frommelc) Acromegaliad) Panhipopituitarismoe) Sndrome de Sheehan

La acromegalia es una enfermedad crnica del adulto, que viene causada por la hipersecrecin de la

hormona hipofisaria del crecimiento y que se caracteriza por un agrandamiento de muchas partes delesqueleto, especialmente de las porciones distales o prominentes: nariz, orejas, mandbula, dedos delas manos y de los pies, etc. Es el fenmeno opuesto a la acromicria. La causa de esta enfermedad esun aumento de la secrecin de la hormona del crecimiento (debida, generalmente, a un tumorhipofisario), despus de la pubertad. Se manifiesta con dolor en las articulaciones, como consecuenciade la osteoporosis y de la artrosis.

46. - Leading Cause of Addison's disease:

a) Tuberculosisb) An autoimmune diseasec) Anticoagulation

d) Traumae) Bilateral infarction

Addison's disease is an uncommon disorder caused by destruction or dysfunction of the adrenalcortices. It is characterized by chronic deficiency of cortisol, aldosterone, and adrenal androgens andcauses skin pigmentation that can be subtle or strikingly dark. Volume and sodium depletion andpotassium excess eventually occur in primary adrenal failure. In contrast, if chronic adrenalinsufficiency is secondary to pituitary failure (atrophy, necrosis, tumor), mineralocorticoid production(controlled by the renin-angiotensin system) persists and hyperkalemia is not present. Furthermore, if

ACTH is not elevated, skin pigmentary changes are not encountered.Autoimmune destruction of theadrenals is the most common cause of Addison's disease in the United States (accounting forabout 80% of spontaneous cases). It may occur alone or as part of a polyglandular autoimmune

(PGA) syndrome. Type 1 PGA is also known as autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APCED) syndrome and is caused by a defect in T cell-mediated immunityinherited as an autosomal recessive trait. It usually presents in early childhood with mucocutaneouscandidiasis, followed by hypoparathyroidism and dystrophy of the teeth and nails; Addison's diseaseusually appears by age 15 years. Partial or late expression of the syndrome is common. A variedspectrum of associated diseases may be seen in adulthood, including hypogonadism, hypothyroidism,pernicious anemia, alopecia, vitiligo, hepatitis, malabsorption, and Sjogren's syndrome. Type 2 PGAusually presents in adulthood with autoimmune adrenal insufficiency (no hypoparathyroidism) that isHLA-related. It is associated with autoimmune thyroid disease (usually hypothyroidism, sometimes


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hyperthyroidism), vitiligo, type 1 diabetes, alopecia areata, or celiac sprue. Autoimmune Addison'sdisease can also be associated with primary ovarian failure (40% of women before age 50), testicularfailure (5%), and pernicious anemia (4%). The combination of Addison's disease and hypothyroidism isknown as Schmidt's syndrome. Tuberculosis was formerly a leading cause of Addison's disease.The association is now relatively rare in the United States but common where tuberculosis ismore prevalent. Bilateral adrenal hemorrhage may occur during sepsis, heparin-associated

thrombocytopenia or anticoagulation, or with antiphospholipid antibody syndrome. It may occur inassociation with major surgery or trauma, presenting about 1 week later with pain, fever, and shock. Itmay also occur spontaneously. Adrenoleukodystrophy is an X-linked peroxisomal disorder causingaccumulation of very long chain fatty acids in the adrenal cortex, testes, brain, and spinal cord. It maypresent at any age and accounts for one-third of cases of Addison's disease in boys. Aldosteronedeficiency occurs in 9%. Hypogonadism is common. Psychiatric symptoms often include mania,psychosis, or cognitive impairment. Neurologic deterioration may be severe or mild (particularly inheterozygote women), mimics symptoms of multiple sclerosis, and can occur years after the onset ofadrenal insufficiency. Rare causes of adrenal insufficiency include lymphoma, metastatic carcinoma,coccidioidomycosis, histoplasmosis, cytomegalovirus infection (more frequent in patients with AIDS),syphilitic gummas, scleroderma, amyloid disease, and hemochromatosis. Familial glucocorticoiddeficiency is caused by a mutation in the gene encoding the adrenal ACTH receptor. Triple A

(Allgrove's) syndrome is characterized by variable expression of the following: adrenal ACTHresistance with cortisol deficiency, achalasia, alacrima, nasal voice, and neuromuscular disease ofvarying severity (hyperreflexia to spastic paraplegia). Cortisol deficiency usually presents in infancy butmay not occur until the third decade of life. Congenital adrenal hypoplasia causes adrenal insufficiencydue to absence of the adrenal cortex; patients may also have hypogonadotropic hypogonadism,myopathy, and high-frequency hearing loss. Patients with hereditary defects in adrenal enzymes forcortisol synthesis develop congenital adrenal hyperplasia due to ACTH stimulation. The most commonenzyme defect is P450c21 (21-hydroxylase). Patients with severely defective P450c21 enzymesmanifest deficiency of mineralocorticoids (salt wasting) in addition to deficient cortisol and excessiveandrogens. Women with milder enzyme defects have adequate cortisol but develop hirsutism inadolescence or adulthood and are said to have "late-onset" congenital adrenal hyperplasia. Isolatedhypoaldosteronism can be caused by various conditions. Hyporeninemic hypoaldosteronism can be

caused by renal tubular acidosis type IV and is commonly seen with diabetic nephropathy, hypertensivenephrosclerosis, tubulointerstitial diseases, and AIDS; patients present with hyperkalemia,hyperchloremia, and metabolic acidosis. Hyperreninemic hypoaldosteronism can be seen in patientswith myotonic dystrophy, aldosterone synthase deficiency, and congenital adrenal hyperplasia. Somepatients with congenital adrenal hyperplasia (CYP17 deficiency) may present in adulthood withhyperkalemia, hypertension, and hypogonadism; cortisol deficiency is also usually present but may notbe clinically evident.

47. - An adverse effect may occur if administered growth hormone before puberty is:

a) Premature closure of the metaphysisb) Hyperlipoproteinemia

c) Appearance of diabetesd) Gigantisme) Acromegaly

Excessive GH causes tall stature and gigantism if it occurs before closure of epiphyses. Afterward,acromegaly develops. The term "acromegaly," meaning extremity enlargement, seriously understatesthe manifestations. The hands enlarge and a doughy, moist handshake is characteristic. The fingerswiden, causing patients to enlarge their rings. Carpal tunnel syndrome is common. The feet also grow,particularly in width. Facial features coarsen since the bones and sinuses of the skull enlarge; hat size


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increases. The mandible becomes more prominent, causing prognathism and malocclusion. Toothspacing widens. Macroglossia occurs, as does hypertrophy of pharyngeal and laryngeal tissue; thiscauses a deep, coarse voice and sometimes makes intubation difficult. Obstructive sleep apnea mayoccur. A goiter may be noted. Hypertension (50%) and cardiomegaly are common. At diagnosis, about10% of acromegalic patients have overt heart failure, with a dilated left ventricle and a reduced ejectionfraction. Weight gain is typical, particularly of muscle and bone. Insulin resistance is usually present

and frequently causes diabetes mellitus (30%). Arthralgias and degenerative arthritis occur. Overgrowthof vertebral bone can cause spinal stenosis. Colon polyps are common, especially in patients with skinpapillomas. The skin may also manifest hyperhidrosis, thickening, cystic acne, and areas of acanthosisnigricans. GH-secreting pituitary tumors usually cause some degree of hypogonadism, either bycosecretion of prolactin or by direct pressure upon normal pituitary tissue. Decreased libido andimpotence are common, as are irregular menses or amenorrhea. Secondary hypothyroidism sometimesoccurs; hypoadrenalism is unusual. Headaches are frequent. Temporal hemianopia may occur as aresult of the optic chiasm being impinged by a suprasellar growth of the tumor. Endoscopic transnasal,transsphenoidal pituitary microsurgery removes the adenoma while preserving anterior pituitaryfunction in most patients. Surgical remission is achieved in about 70% of patients followed over 3 years.GH levels fall immediately; diaphoresis and carpal tunnel syndrome often improve within a day aftersurgery. Transsphenoidal surgery is usually well tolerated, but complications occur in about 10% of

patients, including infection, cerebrospinal fluid leak, and hypopituitarism. Hyponatremia can occur 4-13days postoperatively and is manifested by nausea, vomiting, headache, malaise, or seizure. It isprudent to monitor serum sodium levels postoperatively. Dietary salt supplements for 2 weekspostoperatively may prevent this complication. Patients who fail to have a clinical or biochemicalremission after surgery are treated with a dopamine agonist (eg, cabergoline), octreotide, pegvisomant,or a combination of these medications. Cabergoline may be used first, since it is an oral medication.Cabergoline therapy is most successful for tumors that secrete both prolactin (PRL) and GH, but canalso be effective for patients with normal serum PRL levels. Therapy with cabergoline will shrink one-third of such tumors by more than 50%. Cabergoline is administered orally, starting with 0.25 mg twiceweekly. If the patient tolerates cabergoline, the dosage may be increased gradually, based upon serumGH and IGF-I levels; the maximum dosage is 1 mg orally twice weekly. Side effects of cabergolineinclude nausea, fatigue, constipation, abdominal pain, and dizziness. Cabergoline is expensive.

Somatostatin analogs may be used to treat patients who have persistent acromegaly despite pituitarysurgery. Octreotide and lanreotide are somatostatin analogs that are given by subcutaneous injection.Short-acting octreotide acetate in doses of 50 mcg is injected subcutaneously three times daily.Responders who tolerate the drug are switched to long-acting octreotide acetate injectable suspensionin a dosage of 20 mg intragluteally per month. The dosage may be adjustedup to a maximum of 40mg monthlyto maintain the serum GH between 1 and 2.5 ng/mL, keeping IGF-I levels normal.Lanreotide SR (not available in the United States) is given by subcutaneous injection at a dosage of 30mg every 7-14 days. Lanreotide Autogel (not available in the United States) is a newer formulation thatis administered by deep subcutaneous injection in doses of 60-120 mg every 28 days; this preparationis better tolerated than lanreotide SR. All somatostatin analogs are expensive and must be continuedindefinitely or until other treatment has been effective. Octreotide long-acting release (LAR)preparations (Sandostatin LAR depot) are superior to shorter-acting octreotide, ultimately achieving

serum GH levels under 2 ng/mL in 79% of patients and normal serum IGF-I levels in 53% of patients.Headaches often improve, and tumor shrinkage of about 30% may be expected. Acromegalic patientswith pretreatment serum GH levels exceeding 20 ng/mL are less likely to respond to octreotide therapy.Side effects are experienced by about one-third of patients and include injection site pain, loose acholicstools, abdominal discomfort, or cholelithiasis. Pegvisomant is a GH receptor antagonist that blocks theeffects of GH. Pegvisomant therapy produces symptomatic relief and normalizes serum IGF-I levels inover 90% of acromegalic patients. The starting dosage is 10 mg subcutaneously daily. Themaintenance dosage can be increased by 5-10 mg every 4-6 weeks, based upon serum IGF-I levelsand liver transaminase levels; the maximum dosage is 30 mg subcutaneously daily. Pegvisomant does


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not shrink GH-secreting tumors. Patients need to be monitored carefully with visual field examinations,GH levels, and MRI scanning of the pituitary. Side effects of pegvisomant can include injection sitereactions, hepatitis, edema, flu-like syndrome, nausea, and hypertension. In acromegalic diabetics,hypoglycemic drugs are reduced to avoid hypoglycemia during pegvisomant therapy. The effectivenessof pegvisomant is reduced by coadministration of opioids or propoxyphene. Pegvisomant isextraordinarily expensive. Acromegalic patients who have not had a complete remission with

transsphenoidal surgery or medical therapy may be treated with stereotactic radiosurgery administeredby gamma knife, heavy particle radiation, or adapted linear accelerator. Radiosurgery precisely radiatesthe pituitary tumor in a single session and reduces radiation to the normal brain. However, it cannot beused for pituitary tumors with suprasellar extension due to the risk of damaging the optic chiasm.Radiosurgery can be used for pituitary tumors invading the cavernous sinus, since cranial nerves III, IV,V, and VI are less susceptible to radiation damage. Compared to conventional radiation therapy,radiosurgery is more effective and carries a lower risk of hypopituitarism, cerebral necrosis,psychological impairment, and small vessel stroke. Radiosurgery can also be used for patients whohave failed conventional radiation therapy.

En el control del tratamiento antituberculosis, con una muestra mensual de expectoracin con apoyode los mtodos convencionales (puo y palmo-percusin), toda muestra de control

independientemente de la calidad y apariencia macroscpica debe ser procesada, principalmente alfinal del tratamiento.

48. - Physical feature of acromegaly:

a) Micrognathiab) Prognathismc) Reducing the size of the sinusesd) Hypotelorisme) Microglosia

Excessive GH causes tall stature and gigantism if it occurs before closure of epiphyses. Afterward,

acromegaly develops. The term "acromegaly," meaning extremity enlargement, seriously understatesthe manifestations. The hands enlarge and a doughy, moist handshake is characteristic. The fingerswiden, causing patients to enlarge their rings. Carpal tunnel syndrome is common. The feet also grow,particularly in width. Facial features coarsen since the bones and sinuses of the skull enlarge; hat sizeincreases. The mandible becomes more prominent, causing prognathism and malocclusion.Tooth spacing widens. Macroglossia occurs, as does hypertrophy of pharyngeal and laryngeal tissue;this causes a deep, coarse voice and sometimes makes intubation difficult. Obstructive sleep apneamay occur. A goiter may be noted. Hypertension (50%) and cardiomegaly are common. At diagnosis,about 10% of acromegalic patients have overt heart failure, with a dilated left ventricle and a reducedejection fraction. Weight gain is typical, particularly of muscle and bone. Insulin resistance is usuallypresent and frequently causes diabetes mellitus (30%). Arthralgias and degenerative arthritis occur.Overgrowth of vertebral bone can cause spinal stenosis. Colon polyps are common, especially in

patients with skin papillomas. The skin may also manifest hyperhidrosis, thickening, cystic acne, andareas of acanthosis nigricans. GH-secreting pituitary tumors usually cause some degree ofhypogonadism, either by cosecretion of prolactin or by direct pressure upon normal pituitary tissue.Decreased libido and impotence are common, as are irregular menses or amenorrhea. Secondaryhypothyroidism sometimes occurs; hypoadrenalism is unusual. Headaches are frequent. Temporalhemianopia may occur as a result of the optic chiasm being impinged by a suprasellar growth of thetumor.


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49. - Most common menstrual pattern in hypothyroidism:

a) Hypermenorrhoeab) Menorrhagiac) Oligomenorrhead) Metrorrhagia

e) Amenorrhoea

- Weakness, fatigue, cold intolerance, constipation, weight change, depression, menorrhagia,hoarseness- Dry skin, bradycardia, delayed return of deep tendon reflexes- Anemia, hyponatremia- T4 and RAI uptake usually low- TSH elevated in primary hypothyroidism

50.- Lugar donde actua la paratohormona:

a) Medula sea, eritrocitos y plaquetas

b) Sistema nervioso central, tejido musclar y plaquetasc) Tejido renal, tejido seo y mucosa intestinald) Msculo cardaco, cerebro y msculo estriadoe) Eritrocito, tejido hepatico y estomago

La parathormona, tambin denominada hormona paratiroidea, PTH o paratirina, es una hormonapeptdica secretada por la glndula paratiroides que interviene en la regulacin del metabolismo delcalcio y del fsforo.

La parathormona regula la concentracin de iones calcio en el lquido extracelular mediante el controlde la absorcin de calcio por el intestino, de la excrecin de calcio por los riones y de la liberacin decalcio procedente de los huesos. Adems, regula los niveles de iones fsforo en la sangre, de tal forma

que hace descender la concentracin de ellos en este medio al aumentar su excrecin renal. En elcaso de iones calcio, lo que hace es aumentar la resorcin de estos iones procedentes del hueso,principalmente, para as aumentar los niveles de calcio en sangre. Por tanto, tiene un efecto contrario ala calcitonina.

El dficit de esta hormona produce hipocalcemia (niveles bajos de calcio en sangre) que puedeconducir a la tetania; el aumento de la secrecin de parathormona provoca hipercalcemia (niveleselevados de calcio en sangre).

Esta se produce en base a la cantidad de calcio en el organismo.

* Ante el descenso de Calcio:

o Se incrementa la sntesis de PTHo Se incrementa el tamao y cantidad de clulas (en hipocalcemias prolongadas)o Disminuye la degradacin de PTHo Aumenta la degradacin de proPTH

* Ante el aumento de Calcio:o Aumenta la cantidad de vitamina D, la cual inhibe la produccin de PTHo Disminuye la degradacin de proPTH


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El calcio ionizado circulante acta directamente en las clulas paratiroideas unindose a un receptoren serpentina para calcio asociado a una protena G. La activacin de este receptor inhibe la secrecinde PTH. De esta forma el calcio acta mediante una retroalimentacin negativa para mantenerconstantes los niveles sricos de calcio. Cuando hay concentraciones altas se inhibe la secrecin dePTH y el calcio se deposita en los huesos. Cuando la concentracin es baja, la secrecin de PTHaumenta y el calcio se moviliza de los huesos y se reabsorbe en el rin.

La PTH se une a un receptor asociado a proteina G en la membrana plasmatica, y tras una serie depasos activa genes y enzimas que median la accin biolgica. Por ejemplo, puede inducir la propialiberacion de calcio intracelular.

51. - Pathophysiology of type 2 diabetes mellitus:

a) Resistance to insulin but hyperinsulinismb) Decreased insulin resistancec) Decreased glycogenolysisd) Increased production of hepatic glycogene) Decreased gluconeogenesis

DM2 is a complex of polygenic disorders. Certain families show an autosomal dominance. The geneticdefects differ and many mutations are known. One is the gene on chromosome 7, which code forglucokinase. Identical twins show almost absolute concordance in development of DM2. The muchmore frequent type 2 diabetes is the result of insulin resistance and b-cell defects. Type 2diabetes also occurs in younger persons, especially in persons with a high fat-low muscle mass. Astrong genetic element is always present, but inactivity and stress (an inactive life style with a lowendurance capacity) seems to be involved in the development of type 2 diabetes. Lack of exercisepredisposes one to obesity, a condition that greatly decreases insulin sensitivity of the target cells(adipocytes, heart and skeletal muscle tissues). Reduced glucose combustion creates hyperglycaemia.The hyperglycaemia elicits insulin secretion from defective b-cells in some patients, resulting in raisedserum [insulin]. Since insulin is present, the acute complications such as ketonaemia and metabolic

acidaemia are rare in these patients. The high serum insulin may further down-regulate the activity oftheir insulin receptors. The insulin secreted in DM2 patients does not increase the uptake ofglucose as in normal persons. Many DM2 patients need much more insulin for a given test effectsthan DM1 patients and healthy people. An inactive life style for years, with redundant food intake,seems to be involved in the development of DM2 in persons with a genetic predisposition. Lack ofregular physical activity with development of overweight, increases the incidence if DM2. The impairedglucose tolerance is demonstrated by a glucose tolerance test. The insulin secretion is abnormal in

patients with DM2, although they typically possess half of their b-cell mass at autopsy. The destroyedb-cells is filled with amyloid material (islet amyloid polypeptide, IAPP). IAPP is a possible antagonistto insulin, and explain some cases of insulin resistance. Many older patients with DM2 have nosymptoms, but a routine examination reveals glucosuria or a raised blood glucose. Other patients aretired, have minor genital infections or sugar spots on their underwear. Some patients present with

established late-complications such as retinopathy (blindness), nephropathy, arteriosclerotic disorders(cerebrovascular insults, myocardial infarction, intermittent claudication, gangrene), susceptibility toinfection or neuropathy. DM2 can be caused, theoretically, by 1) b-cell defects including geneticdefects, resulting in abnormal insulin production, or by 2) target cell defects including receptorfailure. The possible defective sites in 1 and 2 have one common denominator. They are all keyproteins (hormone, receptors and transporters). Muscular activity is required to stimulate the normalproduction of key proteins. DM2 relates to inactive life style. The basic problem is therefore possibly agenetically and activity dependent defect in key protein production in the cell interior. Actually, a genetic


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defect has just been demonstrated at certain steps of insulin action in a subset of patients of late-onsetDM2.

52.- Tratamiento urgente de la crisis corticosuprarrenal:

a) Reposicin de lquidos y ACTH

b) Glucanato de calcio y aldosteronac) Reposicin de lquidos y vasopresinad) Solucin mixta y somatostatinae) Solucin salina e hidrocortisona

Acute adrenal insufficiency is an emergency caused by insufficient cortisol. Crisis may occur in thecourse of chronic treated insufficiency, or it may be the presenting manifestation of adrenalinsufficiency. Acute adrenal crisis is more commonly seen in primary adrenal insufficiency (Addison'sdisease) than in disorders of the pituitary gland causing secondary adrenocortical hypofunction.

Adrenal crisis may occur in the following situations: (1) following stress, eg, trauma, surgery, infection,or prolonged fasting in a patient with latent insufficiency; (2) following sudden withdrawal ofadrenocortical hormone in a patient with chronic insufficiency or in a patient with temporary

insufficiency due to suppression by exogenous glucocorticoids or megestrol; (3) following bilateraladrenalectomy or removal of a functioning adrenal tumor that had suppressed the other adrenal; (4)following sudden destruction of the pituitary gland (pituitary necrosis), or when thyroid is given to apatient with hypoadrenalism; and (5) following injury to both adrenals by trauma, hemorrhage,anticoagulant therapy, thrombosis, infection, or, rarely, metastatic carcinoma. The patient complains ofheadache, lassitude, nausea and vomiting, abdominal pain, and often diarrhea. Confusion or coma maybe present. Fever may be 40.6C or more. The blood pressure is low. Patients with preexisting type 1diabetes may present with recurrent hypoglycemia and reduced insulin requirements. Other signs mayinclude cyanosis, dehydration, skin hyperpigmentation, and sparse axillary hair (if hypogonadism is alsopresent). Meningococcemia may be associated with purpura and adrenal insufficiency secondary toadrenal infarction (Waterhouse-Friderichsen syndrome). The eosinophil count may be high.Hyponatremia or hyperkalemia (or both) are usually present. Hypoglycemia is frequent. Hypercalcemia

may be present. Blood, sputum, or urine culture may be positive if bacterial infection is the precipitatingcause of the crisis. The diagnosis is made by a simplified cosyntropin stimulation test, which isperformed as follows: (1) Synthetic ACTH1-24 (cosyntropin), 0.25 mg, is given parenterally. (2) Serumis obtained for cortisol between 30 and 60 minutes after cosyntropin is administered. Normally, serumcortisol rises to at least 20 mcg/dL. For patients receiving glucocorticoid treatment, hydrocortisone mustnot be given for at least 8 hours before the test. Other glucocorticoids (eg, prednisone,dexamethasone) do not interfere with specific assays for cortisol. Plasma ACTH is markedly elevated ifthe patient has primary adrenal disease (generally > 200 pg/mL). If the diagnosis is suspected, draw ablood sample for cortisol determination and treat with hydrocortisone, 100-300 mg intravenously, andsaline immediately, without waiting for the results. Thereafter, give hydrocortisone phosphate orhydrocortisone sodium succinate, 100 mg intravenously immediately, and continue intravenousinfusions of 50-100 mg every 6 hours for the first day. Give the same amount every 8 hours on the

second day and then adjust the dosage in view of the clinical picture. Since bacterial infectionfrequently precipitates acute adrenal crisis, broad-spectrum antibiotics should be administeredempirically while waiting for the results of initial cultures. Hypoglycemia should be vigorously treatedwhile serum electrolytes, BUN, and creatinine are monitored. When the patient is able to take food bymouth, give oral hydrocortisone, 10-20 mg every 6 hours, and reduce dosage to maintenance levels asneeded. Most patients ultimately require hydrocortisone twice daily (AM, 10-20 mg; PM, 5-10 mg).Mineralocorticoid therapy is not needed when large amounts of hydrocortisone are being given, but asthe dose is reduced it is usually necessary to add fludrocortisone acetate, 0.05-0.2 mg daily. Somepatients never require fludrocortisone or become edematous at doses of more than 0.05 mg once or


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twice weekly. Once the crisis has passed, the patient must be investigated to assess the degree ofpermanent adrenal insufficiency and to establish the cause if possible.

53. - Male patient aged 17 presented with sweating, pallor, hypertension, nausea and vomiting.The most likely diagnosis is:

a) Glomerulonephritisb) Pheochromocytomac) Nephrotic syndromed) Adrenal insufficiencye) Renal tumor

Pheochromocytomas are rare, being found in less than 0.3% of hypertensive individuals. The incidenceis higher in patients with moderate to severe hypertension. Pheochromocytomas can be lethal unlessthey are diagnosed and treated appropriately. They typically cause attacks of severe headache (80% ofpatients), perspiration (70% of patients), and palpitations (60% of patients); other symptoms mayinclude anxiety (50% of patients), a sense of impending doom, or tremor (40% of patients). Vasomotorchanges during an attack cause mottled cyanosis and facial pallor; as the attack subsides, facial

flushing may occur as a result of reflex vasodilation. Other findings may include tachycardia, precordialor abdominal pain, vomiting, increasing nervousness and irritability, increased appetite, and loss ofweight. Anginal attacks may occur. Physical findings usually include hypertension (90% of

patients), which may be sustained (20% of patients), sustained with paroxysms (50% of patients), orparoxysmal only (25% of patients). There may be cardiac enlargement and cardiomyopathy, posturaltachycardia (change of more than 20 beats/min) and postural hypotension, and mild elevation of basalbody temperature. Retinal hemorrhage or cerebrovascular hemorrhage occurs occasionally.Catastrophic hypertensive crisis and fatal cardiac arrhythmias can occur spontaneously or may betriggered by intravenous contrast dye or glucagon injection, needle biopsy of the mass, anesthesia, andsurgical procedures. The manifestations of pheochromocytoma are quite varied and mimic otherconditions. Some patients are normotensive and asymptomatic. In addition to the above symptoms,some patients can present with psychosis or confusion, seizures, hyperglycemia, bradycardia,

hypotension, constipation, paresthesias, or Raynaud's phenomenon. Other patients may havepulmonary edema and heart failure due to cardiomyopathy. Epinephrine secretion may cause episodictachyarrhythmias, hypotension, or syncope. Some patients may be entirely asymptomatic despite highserum levels of catecholamines. Others may present with abdominal discomfort from a largehemorrhagic pheochromocytoma, or with pain from metastatic disease. In addition to catecholaminesand their metabolites, pheochromocytomas secrete a wide range of other peptides that can sometimescause symptoms of Cushing's syndrome (ACTH), erythrocytosis (erythropoietin), or hypercalcemia(PTHrP). Hypermetabolism is present; thyroid function tests are normal, including serum T4, FT4, T3,and TSH. Hyperglycemia is present in about 35% of patients but is usually mild. Leukocytosis iscommon. The ESR is sometimes elevated. Plasma renin activity may be increased by catecholamines.

Assay of urinary catecholamines and metanephrines (total and fractionated) and creatinine detectsmost pheochromocytomas, especially when samples are obtained during or immediately following an

episodic attack. A 24-hour urine specimen is usually obtained, although an overnight or shortercollection may be used; patients with pheochromocytomas generally have more that 2.2 mcg of totalmetanephrine per milligram of creatinine, and more than 135 mcg total catecholamines per gramcreatinine. Urinary assay for total metanephrines is about 97% sensitive for detecting functioningpheochromocytomas. Urinary assay for vanillylmandelic acid (VMA) is about 89% sensitive and is notusually required.


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54.- El colesterol es el precursor de todas las hormonas:

a) Tiroideasb) Hipofisiariasc) Pancreticasd) Esteroideas

e) Hipotalamicas

El colesterol es un alcohol esteroide con aspecto de grasa, presente en grasas animales, aceites, bilis,sangre, huevo (yema), etc. Es precursor de los cidos biliares y constituye la materia prima para lasntesis de las hormonas esteroides.

55. - The principal circulating precursor for placental estrone and 17-estradiol is:

a) Sulfate dehydroisoandrosteroneb) Testosteronec) Androsteroned) Dehydroisoandrosterone

e) Pregnanediol

The naturally occurring estrogens are 17b-estradiol, estrone, and estriol. They are C18 steroids; ie,they do not have an angular methyl group attached to the 10 position or a D-3-keto configuration in the

A ring. They are secreted primarily by the granulosa cells of the ovarian follicles, the corpus luteum,and the placenta. The biosynthetic pathway involves their formation from androgens(testosterona). They are also formed by aromatization of androstenedione in the circulation.

Aromatase (CYP19) is the enzyme that catalyzes the conversion of androstenedione to estrone and theconversion of testosterone to estradiol.

56. - The most important adverse effect of propylthiouracil is presenting:

a. Agranulocytosis.b. Acute renal failure.c. Hypoglycemia.d. Pseudotumor cerebri.e. Hyponatremia.

Agranulocytosis is an uncommon complication, but serious, treatment with thiourea, which has reportednearly 0.1% of patients taking methimazole and about 0.4% of those who ingest propylthiouracil. Theagrunolocitosis is usually reversible and can be treated with filgrastim (G-CSF).

57. - In the first stage of the biosynthesis of steroid hormones is given:

a. Conversion of steroids C-21 C-19 steroids.b. Hydroxylation of steroids at C-21.c. Conversion of cholesterol to pregnenolone.d. Reduction of steroids at C-5 alpha.e. Conversion of androstenedione to 17 - hydroxyprogesterone.

Adrenal steroid hormones are synthesized from cholesterol that is derived mostly from plasma, but asmall portion of what is in situ from acetyl-CoA via mevalonate and squalene. Much of the cholesterol inthe adrenal is esterified and stored in cytoplasmic lipid droplets. Under adrenal stimulation by ACTH (or


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cAMP) is activated and free cholesterol esterase formed is transported into the mitochondria where anenzyme side chain cleavage cytochrome P450 (P450 scc) converts cholesterol to pregnenolone . Thefirst step in steroidogenesis is the conversion of cholesterol to pregnenolone catalyzed by a complexenzyme system (mixed function oxidase) called desmolase cholesterol oxidase.

58. - The first cause of hyperthyroidism in adolescents is:

a) Tiroditis subacuteb) Diffuse toxic goiter (Graves disease)c) Toxic nodular goiterd) Toxic Adenoma

Thyrotoxicosis is the hypermetabolic condition associated with elevated levels of free thyroxine (FT4),free triiodothyronine (FT3), or both. Hyperthyroidism includes diseases that are a subset ofthyrotoxicosis (excludes exogenous thyroid hormone intake and subacute thyroiditis) that is caused byexcess synthesis and secretion of thyroid hormone by the thyroid. Most clinicians, exclusive ofendocrinologists, use the terms hyperthyroidism and thyrotoxicosis interchangeably. The most commonforms of hyperthyroidism include diffuse toxic goiter (Graves disease), toxic multinodular goiter

(Plummer disease), and toxic adenoma. The most common cause of thyrotoxicosis is Gravesdisease (50-60%). Graves disease is an organ-specific autoimmune disorder characterized by a varietyof circulating antibodies, including common autoimmune antibodies, antithyroperoxidase (anti-TPO),and antithyroglobulin (anti-TG) antibodies. The most important autoantibody is thyroid-stimulatingimmunoglobulin (TSI). TSI is directed toward epitopes of the thyroid-stimulating hormone (TSH)receptor and acts as a TSH-receptor agonist. Similar to TSH, TSI binds to the TSH receptor on thethyroid follicular cells to activate thyroid hormone synthesis and release and thyroid growth(hypertrophy). This results in the characteristic picture of Graves thyrotoxicosis, with a diffuselyenlarged thyroid, very high radioactive iodine uptake, and excessive thyroid hormone levels comparedto a healthy thyroid with subacute thyroiditis, these conditions constitute 85-90% of all causes ofthyrotoxicosis.

59.- En que capa de la glndula suprarrenal se produce el cortisol:

a) Glomerularb) Fasciculadac) Reticulard) Medula

La corteza suprarrenal est situada rodeando la circunferencia de la glndula suprarrenal. Su funcines la de regular varios componentes del metabolismo con la produccin de mineralcorticoides y


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glucocorticoides que incluyen a la aldosterona y al cortisol. La corteza suprarrenal tambin es un lugarsecundario de sntesis de andrgenos.La corteza suprarrenal puede dividirse en tres capas diferentes de tejido basado en los tipos celularesy la funcin que realizan.

a) Zona glomerular: Produccin de mineralcorticoides, sobre todo, aldosterona.b) Zona fascicular: Produccin de glucocorticoides, principalmente cortisol, cerca del 95%.

c) Zona reticular: Produccin de andrgenos, incluyendo testosterona.

60.- La disminucin de este disminuye la reabsorcin osea:

a) Paratohormonab) Calcitoninac) Osteoclastosd) Osteoblastos

La PTH segregada por las glndulas paratiroides que acta manteniendo una concentracin constantede calcio en el lquido extracelular. Regula la absorcin de calcio a partir del tracto GI, la movilizacindel calcio seo, el depsito de calcio en los huesos y la excrecin de calcio en la leche materna, en las

heces, en el sudor y en la orina

endocrinología 3

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