Anatomy, Histology, and Cell Biology PreTest Self-Assessment by Robert Klein, George Enders

By Robert Klein, George Enders

This distinct try prep consultant enables you to try out your wisdom of crucial anatomy, histology and telephone biology recommendations for the USMLE Step 1; perform with 500 USMLE Step 1-style questions with referenced solutions; evaluate motives for correct and mistaken answers;and construct self belief, talents, and information.

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Additional info for Anatomy, Histology, and Cell Biology PreTest Self-Assessment and Review, Third Edition (PreTest Basic Science)

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The ureteric bud induces surrounding intermediate mesoderm to form the metanephric cap, which forms the excretory units of the kidney. The ureteric bud will form the collecting ducts. During kidney development, epithelial-mesenchymal interactions occur reciprocally between the epithelium of the ureteric bud and the mesenchyme of the metanephric cap (blastema) to convert the mesenchyme of the metanephric cap into an epithelium. , collecting ducts, calyces, and pelves) of the developing kidney. The epithelial lining (transitional epithelium) of the ureters, as well as their muscular and connective tissue components, are derived from intermediate mesoderm.

Collecting ducts, calyces, and pelves) of the developing kidney. The epithelial lining (transitional epithelium) of the ureters, as well as their muscular and connective tissue components, are derived from intermediate mesoderm. The transitional epithelium of the bladder and most of the urethra are derived from hindgut endoderm of the urogenital sinus. Connective tissue and muscle are derived from splanchnic lateral plate mesoderm. DEVELOPMENT OF THE REPRODUCTIVE SYSTEMS Intermediate mesoderm forms the epithelia, connective tissues, and smooth muscle of the indifferent sex cords and their ducts.

Infiltrating T cells and autoantibodies destroy the thyroid follicular cells resulting in hypothyroidism. In Hashimoto’s thyroiditis autoantibodies are also produced to the thyroidstimulating hormone (TSH) receptor. In that case, the autoantibody recognizes an epitope which results in blocking the activity of TSH. In contrast, in Graves’ disease autoantibodies are produced to the TSH receptor, but they are long-acting thyroid stimulating (LATS) antibodies. The result is unregulated activation of the receptor and overproduction of thyroid hormones (hyperthyroidism).

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