Fisiopatología endocrina
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Transcript of Fisiopatología endocrina
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FISIOPATOLOGÍA ENDOCRINA
Dr. Miguel Edo. Poblete Sepúlveda
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Alteraciones de la hipófisis
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Acromegalia
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Alteraciones del tiroides
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Bocio
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Hipotiroidismo
Congénito. Adquirido:
Primario. Farmacológico. Tiroiditis
autoinmune de Hashimoto.
Secundario.
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Causas de hipotiroidismo
Primarias:- Autoimmune hypothyroidism:
Hashimoto's thyroiditis, atrophic thyroiditis.
- Iatrogenic: 131I treatment, subtotal or total thyroidectomy, external irradiation of neck for lymphoma or cancer.
- Drugs: iodine excess (including iodine-containing contrast media and amiodarone), lithium, antithyroid drugs, p-aminosalicyclic acid, interferon- and other cytokines, aminoglutethimide.
- Congenital hypothyroidism: absent or ectopic thyroid gland, dyshormonogenesis, TSH-R mutation.
- Iodine deficiency. - Infiltrative disorders:
amyloidosis, sarcoidosis, hemochromatosis, scleroderma, cystinosis, Riedel's thyroiditis.
- Overexpression of type 3 deoiodinase in infantile hemangioma
Transientes: - Silent thyroiditis, including
postpartum thyroiditis. - Subacute thyroiditis. - Withdrawal of thyroxine
treatment in individuals with an intact thyroid.
- After 131I treatment or subtotal thyroidectomy for Graves' disease
Secondary: - Hypopituitarism: tumors,
pituitary surgery or irradiation, infiltrative disorders, Sheehan's syndrome, trauma, genetic forms of combined pituitary hormone deficiencies.
- Isolated TSH deficiency or inactivity.
- Bexarotene treatment.- Hypothalamic disease:
tumors, trauma, infiltrative disorders, idiopathic
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Hipertiroidismo
Enfermedad de Basedow Graves.
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Subacute thyroiditis. Silent thyroiditis. Other causes of thyroid
destruction: amiodarone, radiation, infarction of adenoma.
Ingestion of excess thyroid hormone (thyrotoxicosis factitia) or thyroid tissue.
Graves' disease. Toxic multinodular goiter. Toxic adenoma. Functioning thyroid
carcinoma metastases. Activating mutation of the
TSH receptor. Activating mutation of Gsa
(McCune-Albright syndrome).
Struma ovarii. Drugs: iodine excess (Jod-
Basedow phenomenon)
Causas de tirotoxicosis
Hipertirodismo primarioTirotoxicosis sin hipertiroidismo
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Trastornos de las paratiroides
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Hipoparatirodismo
Hipocalcemia. Sd. Di George. Cirugía de cuello. Autoinmunidad. Otros.
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Hiperparatiroidismo
Primario. secundario.:
IRC.
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Trastornos de las suprarrenales
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21 hidroxilasa1-β-hydroxylase2
Glándula suprarrenal
Cortisol
ACTH
HIPERPLASIA ADRENAL´sobreestimulación de la producción de andrógenos adrenales
VIRILIZACIÓN (NIÑAS)MACROFALIA
HIPERPLASIA ADRENAL CONGÉNITA
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INSUFICIENCIA CORTICAL ADRENAL
Insuficiencia cortical adrenal primaria o enfermedad de Addison.
Secundaria.
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Síndrome de Cushing
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Vitiligo!!!! Marcador de endocrinopatía y/o autoinmunidad
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DIABETES MELLITUS
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DIABETES MELLITUS
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Target cell
Receptor de insulina
Dominio receptor
Dominio enzimático
insulina
Activación del dominio enzimático: tirosinquinasa
IRS
MAP-K síntesis de proteínas
GLUT-4
glucosa
Poblete S. M, Vergara S A. Complicaciones cardiovasculares en mujeres postmenopáusicas diabéticas del Hospital de Lota. Congreso nacional científico ANACEM Chile 2000
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SÍNDROME DE RESISTENCIA A LA INSULINA
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Resistencia insulinica. Hiperinsulinemia. Obesidad central. Intolerancia a la
glucosa Displipidemia. HTA. Aumento del
fibrinógeno. Aumento del factor vW. Microalbuminuria.
Disminución de NO. Disminución de la
vasodilatación. Aumento de la PCR. Hiperuricemia. SOP Hígado graso ¿aumento de
homocisteína? ¿aumento de leptina? Aumento de
dimetilarginina asimétrica?
Síndrome metabólico actual
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¿Insulinorresistencia=obesidad? En el obeso:
Factores pro resistencia: FNT-alfa. Leptina: resistencia a ella. Resistina.
Factores protectores: Adiponectina: su déficit induciría IR.
Patogénesis
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IR HIPERINSULINEMIA
Obesidad inactividad
Medicamentos-tabaco-stress
Factores genéticos
HTA
DM tipo 2Intolerancia a la glucosa
ATE
Bajo peso al nacer
Hígado graso
SOP
Durruty P, García de los Rios M, Bases bioquímicas y fisiopatológicas de la DM
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Diabetes mellitus
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Diabetes mellitus
Definición.
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Complicaciones agudas
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