All individuals in MESHD
| Label | Id | Description |
|---|---|---|
| Glycogen Storage Disease Type VIII | D006015 | [An x-linked recessive hepatic glycogen storage disease resulting from lack of expression of phosphorylase-b-kinase activity. Symptoms are relatively mild; hepatomegaly, increased liver glycogen, and decreased leukocyte phosphorylase are present. Liver shrinkage occurs in response to glucagon.] |
| Glycosuria | D006029 | [The appearance of an abnormally large amount of GLUCOSE in the urine, such as more than 500 mg/day in adults. It can be due to HYPERGLYCEMIA or genetic defects in renal reabsorption (RENAL GLYCOSURIA).] |
| Glycosuria, Renal | D006030 | [An autosomal inherited disorder due to defective reabsorption of GLUCOSE by the PROXIMAL RENAL TUBULES. The urinary loss of glucose can reach beyond 50 g/day. It is attributed to the mutations in the SODIUM-GLUCOSE TRANSPORTER 2 encoded by the SLC5A2 gene.] |
| Gnathostomiasis | D058429 | [Infections with nematodes of the genus GNATHOSTOMA, superfamily THELAZIOIDEA. Gnathostomiasis is a food-borne zoonosis caused by eating undercooked or raw fish or meat.] |
| Goat Diseases | D015511 | [Diseases of the domestic or wild goat of the genus Capra.] |
| Goiter | D006042 | [Enlargement of the THYROID GLAND that may increase from about 20 grams to hundreds of grams in human adults. Goiter is observed in individuals with normal thyroid function (euthyroidism), thyroid deficiency (HYPOTHYROIDISM), or hormone overproduction (HYPERTHYROIDISM). Goiter may be congenital or acquired, sporadic or endemic (GOITER, ENDEMIC).] |
| Goiter, Endemic | D006043 | [A form of IODINE deficiency disorders characterized by an enlargement of the THYROID GLAND in a significantly large fraction of a POPULATION GROUP. Endemic goiter is common in mountainous and iodine-deficient areas of the world where the DIET contains insufficient amount of iodine.] |
| Goiter, Nodular | D006044 | [An enlarged THYROID GLAND containing multiple nodules (THYROID NODULE), usually resulting from recurrent thyroid HYPERPLASIA and involution over many years to produce the irregular enlargement. Multinodular goiters may be nontoxic or may induce THYROTOXICOSIS.] |
| Goiter, Substernal | D006045 | [An enlarged THYROID GLAND with at least 50% of the gland situated behind the STERNUM. It is an unusual presentation of an intrathoracic goiter. Substernal goiters frequently cause compression on the TRACHEA leading to deviation, narrowing, and respiratory symptoms., A goiter that grows behind the STERNUM and CLAVICLE.] |
| Goldenhar Syndrome | D006053 | [Mandibulofacial dysostosis with congenital eyelid dermoids.] |
| Gonadal Disorders | D006058 | [Pathological processes of the OVARIES or the TESTES.] |
| Gonadal Dysgenesis | D006059 | [A number of syndromes with defective gonadal developments such as streak GONADS and dysgenetic testes or ovaries. The spectrum of gonadal and sexual abnormalities is reflected in their varied sex chromosome (SEX CHROMOSOMES) constitution as shown by the karyotypes of 45,X monosomy (TURNER SYNDROME); 46,XX (GONADAL DYSGENESIS, 46XX); 46,XY (GONADAL DYSGENESIS, 46,XY); and sex chromosome MOSAICISM; (GONADAL DYSGENESIS, MIXED). Their phenotypes range from female, through ambiguous, to male. This concept includes gonadal agenesis., The complete failure of gonadal development.] |
| Gonadal Dysgenesis, 46,XX | D023961 | [The 46,XX gonadal dysgenesis may be sporadic or familial. Familial XX gonadal dysgenesis is transmitted as an autosomal recessive trait and its locus was mapped to chromosome 2. Mutation in the gene for the FSH receptor (RECEPTORS, FSH) was detected. Sporadic XX gonadal dysgenesis is heterogeneous and has been associated with trisomy-13 and trisomy-18. These phenotypic females are characterized by a normal stature, sexual infantilism, bilateral streak gonads, amenorrhea, elevated plasma LUTEINIZING HORMONE and FSH concentration.] |
| Gonadal Dysgenesis, 46,XY | D006061 | [Defects in the SEX DETERMINATION PROCESS in 46, XY individuals that result in abnormal gonadal development and deficiencies in TESTOSTERONE and subsequently ANTIMULLERIAN HORMONE or other factors required for normal male sex development. This leads to the development of female phenotypes (male to female sex reversal), normal to tall stature, and bilateral streak or dysgenic gonads which are susceptible to GONADAL TISSUE NEOPLASMS. An XY gonadal dysgenesis is associated with structural abnormalities on the Y CHROMOSOME, a mutation in the GENE, SRY, or a mutation in other autosomal genes that are involved in sex determination.] |
| Gonadal Dysgenesis, Mixed | D006060 | [A type of defective gonadal development in patients with a wide spectrum of chromosomal mosaic variants. Their karyotypes are of partial sex chromosome monosomy resulting from an absence or an abnormal second sex chromosome (X or Y). Karyotypes include 45,X/46,XX; 45,X/46,XX/47,XXX; 46,XXp-; 45,X/46,XY; 45,X/47,XYY; 46,XYpi; etc. The spectrum of phenotypes may range from phenotypic female to phenotypic male including variations in gonads and internal and external genitalia, depending on the ratio in each gonad of 45,X primordial germ cells to those with normal 46,XX or 46,XY constitution.] |
| Gonadoblastoma | D018238 | [A complex neoplasm composed of a mixture of gonadal elements, such as large primordial GERM CELLS, immature SERTOLI CELLS or GRANULOSA CELLS of the sex cord, and gonadal stromal cells. Gonadoblastomas are most often associated with gonadal dysgenesis, 46, XY.] |
| Gonorrhea | D006069 | [Acute infectious disease characterized by primary invasion of the urogenital tract. The etiologic agent, NEISSERIA GONORRHOEAE, was isolated by Neisser in 1879.] |
| Gout | D006073 | [Metabolic disorder characterized by recurrent acute arthritis, hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of URIC ACID calculi.] |
| Graft Occlusion, Vascular | D006083 | [Obstruction of flow in biological or prosthetic vascular grafts.] |
| Graft vs Host Disease | D006086 | [The clinical entity characterized by anorexia, diarrhea, loss of hair, leukopenia, thrombocytopenia, growth retardation, and eventual death brought about by the GRAFT VS HOST REACTION.] |