PHIS 206 1st EditionLecture 32Outline of Last Lecture I. Location + Anatomy of PituitaryII. Blood Supply in Anterior Pituitary GlandIII. Mammals (except humans)IV. 2 Kinds of Hormones of Posterior PituitaryV. Anterior LobeVI. Secretions of Anterior Pituitary VII. Hormones of Anterior LobeVIII. Growth HormoneOutline of Current Lecture I. Thyroid GlandII. 2 Thyroid HormonesIII. Follicular CellsIV. T4 v. T3V. Major Effect of Thyroid HormoneVI. Anabolic ProcessesVII. Fat-Mobilizing VIII. Thyroid HormoneIX. TSH (Thyroid-Stimulating Hormone)X. TRHXI. Causes of HypothyroidismXII. Symptoms of HypothyroidismXIII. Causes of HyperthyroidismXIV. Symptoms + Effects of Grave’s DiseaseXV. Another Cause of HyperthyroidismXVI. GoiterCurrent LectureI. Thyroid Gland-consists of 2 bulbs connected by a narrow connective tissue-cells have sacs surrounded by a one-layer with liquid in the inside-Follicle cell: outside-colloid: “like glue”; inside of follicle cellII. 2 Thyroid Hormones-T4: Tetraiodothyronine -T3: TriiodothyronineThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.-Major effect: increase basal metabolic rate (increase rate at which cells use oxygen)III. Follicular Cells-vigorous active systems that allow them to take up tyrosine and iodide from plasma tyrosine: amino acid some tyrosine: material to synthesize thyroglobino on ribosomes, E.R., golgi body, etc… thyroglobin is synthesized in tyrosine cells but secreted into colloids iodide diffuses into colloid-loads of thyroglobin = high concentration of iodide in follicular cells -you can iodinate proteins easily-tyrosines which thyroglobin is loaded with wind up with iodide ions attached 1 I: monoiodotyrosine 2 I: diiodotyrosine-iodinated tyrosines spontaneously react with one another and attach 2 I + 2 I: tetraiodotyrosine 2 I + 1 I: triiodotyrosince 1 I + 1I: diiodotyrosine (no endocrine property of thyroid)o diiodotyrosine more reactive than monoiodotyrosineo all occurs when thyroglobin is in colloids -endocytosis (drink) and lysozomes break thyroglobin into amino acids -derivatives are T4 and T3 (fat-soluble) NOT PEPTIDES OR STEROIDS behave as steroids (diffuse out before synthesis) bind to proteinsIV. T4 v. T3-90% of what is released: T4-5 times more potent (gives response): T3-T4 converted to T3 when passing kidneys and liver-90-95% response comes from T3V. Major Effect of Thyroid Hormone-increase basal metabolic rate (oxidation of substrates) generates heat: calorigenic effectVI. Anabolic Processes-protein process that will not proceed in the absence of the thyroid hormone-normal physiological catabolic: needs to break down-increases metabolism decreases fat, glycogen, protein result: reduce muscle massVII. Fat-Mobilizing-thyroid hormone increases receptors of norepinephrine makes cells more sensitive to stimuli responses are exaggerated sympathomimetic: dramatic effect that the thyroid hormone has-other effects of high levels of thyroidism increase cardiac output increase blood pressureVIII. Thyroid Hormone-essential to growth-essential to normal function of CNSIX. TSH (Thyroid-Stimulating Hormone)-stimulated to take up more tyrosine and iodide and make thyroglobin-TSH increases thyroid hormone-TSH deficiency thyroid gland doesn’t make much thyroglobin, so bulk of follicle cells have atrophy -TSH excess hypertrophy of thyroid gland follicles bigger, thyroid gland biggerX. TRH (from hypothalamus)-stimulates TSH-negative feedback in which thyroid hormone inhibits TRH + TRH decreases TSH stimulationXI. Causes of Hypothyroidism-defect in follicular cells-reduced pathological secretion of TRH-anterior pituitary disorder-iodide deficiency XII. Symptoms of Hypothyroidism-basal metabolic rate decreases-person gains weight-intolerance to cold-fatigue easily-low blood pressure-reflexes low-slow-thinking-sluggish-myxedema: accumulation of fluid subcutaneously (ADULTS) edema means swelling myxedema: swelling of ankles-cretinism: retarded growth, profoundly retarded (NEWBORNS) no survival chance as dwarfXIII. Causes of Hyperthyroidism-Grave’s Disease: production of abnormal antibody that fools thyroid gland into thinking it is TSH stimulates follicular cells into doing job, but NOT subject to negative feedback increased circulating levels of thyroid hormoneXIV. Symptoms + Effects of Grave’s Disease-weight loss -muscle weakness-heart rate increases, blood pressure increases, cardiac output increases-Central Nervous System hyperactivity-reduced emotional control-irritable, paranoia, anxiety-exophtalmos: bulgy eyes dues to accumulation of fluid behind eyesXV. Another Cause of Hyperthyroidism-Thyroid-Stimulating TumorXVI. Goiter-enlarged thyroid cannot tell by looking whether it is hypo- or hyper- thyroidism does not enlarge thyroid under stimulated (hyperthyroidism)o no goitero iodine deficiency: goiter with
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