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SC BIOL 460 - Adrenal and thyroid Glands

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BIOL 460 1nd Edition Lecture 9 Outline of Last Lecture I. Pituitary Glanda. Embryology b. Hormonesi. Adenohypophysis ii. Neurohypophysis II. Adrenal GlandOutline of Current Lecture I. Adrenal Gland (End of Exam Two Material)a. Three regions II. Thyroid Gland (begins Exam Three Material)a. Composition b. Hormonesi. T3 ii. T34c. DiseasesCurrent LectureAdrenal Gland1. Cortex- corticosteroidsa. Formed from mesodermb. 3 regions- each secrete specific hormone with some overlapi. Zona glomerulosa 1. Mineralocorticoids (electrolyte balance)2. Secretes aldosteronea. Causes kidneys to reabsorb sodium ions b. Excrete K+ into filtratec. Increases blood volume These 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.d. Triggers for secretionsi. High potassium (hyperkalemia)ii. Renin/angiotensin/aldosterone system 1. Renin released due to low blood pressure2. Causes angiotensin released (vasoconstriction)3. Angiotensin causes adrenal cortex to secrete aldosteroneii. Zona fasciculate1. Glucocorticoids (glucose metabolism)2. Secretes cortisol3. Response of ACTH release 4. Causes body to conserve glucosea. Inhibits cells form using glucoseb. Triggers gluconeogenesis→ produce glucose from novel sources c. Lipolysis5. Suppress immune response6. Too much cortisol→ hyperglycemia7. Norepinephrine/epinephrine act on receptors in live r (alpha 2)a. Raise glycogenolysis (short term response)b. Also deal with long term stressc. General adaptation syndrome (GAS)i. Alarm (activate adrenal glands)ii. Resistance- body adjusts to stress, glucocorticoids released in response to ACTHiii. Exhaustion- illness or deathiv. Causes hypertrophy of adrenal cortex and lymphoidtissue atrophyv. Stress stimulates pituitary/adrenal axis vi. Keeps immune system in checkiii. Zona retiuclaris1. Secretes small amounts of weak androgens (sex steroids)**END of Material for Exam TwoExam Three Material 1. Thyroid Glanda. Largest pure endocrine glandb. Composed of thyroid follicles c. Colloid is suspension of proteins in middle from which thyroid hormones are producedd. Parafollicular cells produce calcitonin (regulate Ca++ in blood)i. Lowers amount of Ca++ in bloodii. Causes kidney to excrete more Ca++ in urineiii. Inhibits osteoclasts from degrading bone matrixe. Thyroid colloidi. Suspension of proteins in fluid of thyroid follicles ii. Most important protein is thyroglobuliniii. Figure 11.231. Plasma iodide taken up by thyroid follicle cells 2. Enters colloid3. Combines with tyrosine residues of thyroglobulin4. Produces monoiodotyrosin (MIT) and diiodotyrosine (DIT)5. MIT+DIT= triiodothyronine6. DIT+DIT= tetraiodothronine (thyroxin)7. T3 and T4 still bound to thyroglobulin8. TSH stimulates movement of T3 and T4 and release into bloodstreamiv. Thyroid hormones have genomic action1. Promote protein synthesis2. Promote maturation of nervous tissue3. Regulate metabolisma. Basal metabolic rate (BAR)- rate at which cells use calories when restingb. Hypothyroidism- less thryroid hormone than there should be c. Hyperthyroidism- more thyroid hormone than there should be v. Endemic Goiter1. Iodine deficiency2. Figure 11.253. Cant make T3 or T44. No negative feedback, TSH still being released- causes hypertrophy of thyroid gland 5. Also exhibit hypothyroid symptomsvi. Hyperthyroidism1. Inflamed thyroid gland causes some2. Mostly caused by grave’s disease 3. Autoimmune disease 4. Exposed to pathogen→ antibodies produced5. Antibodies adhere to cells of thyroid follicles (autoantibody), have TSH-life effects 6. Negative feedback loop turns off release of TSH, but the antibodies still cause the effects7. Enormous amounts of T3 and T4, hypertrophy of thyroidvii. Symptom of hypothyroidism- myxedema- buildup of fluid and mucoproteins in connective tissues under skin 1. No TSH 2. Not TSH-RH 3. No T3 and T4viii. Cretinism- hypothyroidism in


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SC BIOL 460 - Adrenal and thyroid Glands

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