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Endocrine I and II
| Question | Answer |
|---|---|
| Secretagogues | Inhibitors of positive effectors |
| Tropic factor | Hormone is released and does not have direct effect |
| Trophic factor | Hormone has direct effect |
| Describe negative feedback from T3 and T4 | T3 and T4 are secreted from thyroid and when levels rise they will send feedback for the pituitary to shut TSH release down |
| Lipophillic | It can get through the plasma membrane easily and will interact with receptors in cytoplasm or nucleus (steroid type hormones: not stored) |
| Hydrophilic hormones | Hormone has to interact with a surface receptor. In many cases they are stored in granules as pre or pro form |
| Basophils | FSH, LH, ATCH and TSH |
| Responsibilities of Pituitary/hypophysis | Water homeostasis, Blood pressure, growth, development, reproduciton |
| Downward growth of diencephalon | Responsible for forming the infundibulum and posterior region of pituitary |
| Upward growth (Rathke's pouch) | Form anterior region of pituitary |
| Which region has direct neuoronal likange? | Posterior (Pars nervosa) |
| Supraopticular nucleus and paraventricular nucleus | Cell bodies will synthesize hormones that will undergo fast axonal transport into posterior lobe of pituitary. The tract: hypothalamohypophyseal tract |
| Posterior lobe hormones | Oxytocin and ADH(vasopressin): structurally 9 amino acids differing by 2 amino acids |
| Oxytocin and ADH actions | Oxytocin is important for contraction. ADH is important for water homeostasis |
| Herring bodies | Storage sites along the tract. Neurophysin in storage vesicle which if defective can lead to defective packaging of oxytocin or vasopressin |
| Pituicytes | At the end of nerve terminal, glial cells, supporting cells that have a clamp like structure over the terminus of the axonal end. Herring bodies and pituicytes are regulating the release of granules |
| Anterior lobe hormones | Growth hormone, Prolactin, FSH, LH, ACTH, TSH |
| Acidophils | Growth hormones and Prolactin |
| Chromophobes | Resting cells that stain clear |
| Pre-cursor for ACTH and MSH | Pro-opimelanocortin |
| Control for release of hormones in Anterior lobe | Neurons sitting in the hypothalmus. Short axons that don't go all the way down. There is a capillary plexus that can take up inhibitory or releasing hormones and travel down the portal vessel |
| Portal vessel damage | Decreased release of hormones because it is under the positive regulator of gonadotropin |
| How is the thyroid gland arranged? | In follicles |
| What hormones does the thyroid produce? | T3 and T4 |
| What do follicular cells surround? | Colloid which is composed of Thgb (660 AAs) 130 of the AAs tyrosine |
| What is located at the basal surface of the thyroid? | G protein (7 transmembrane receptor). |
| Describe the mechanism for producing Thgb | G protein-TSH binds-activates adenyl kinase-cAMP- kinase-production of Thgb |
| What happens when we need thyroid hormone | It is stored in the colloid then gets endocytosed into follicular cell, chopped up then released into interstitium and then into vasculature |
| What happens when Thgb is in circulation? | Iodide gets taken up through Na/I symporter then delivered to colloid. Iodide is converted to Iodine by thyroid peroxidase |
| After Thgb is iodinated what happens? | It gets endocytosed into an endosome, fused with a lysosome and then the large Thgb is hydrolyzed into free AAs and thyroid hormone |
| T4 vs T3 | 80% T4. T3 is more potent and active |
| How is T4 converted to T3? | T4 is taken up to target tissues and there is a deiodinase enzyme which removes one of the iodines and you get T3 |
| Negative feedback of T3 and T4 | T3 and T4 send feedback to the pituitary to inhibit TSH secretion and also negative feedback to hypothalmus to inhibit TRH |
| Name ways to form a Goiter | Lack of T3/T4 production so no negative feedback. Inactive thyroid peroxidase so no iodination of Thgb. Without sufficient iodine prese |
| Congenital hypothyroidism | Defect in an iodine transporter |
| Hashimoto's Thyroiditis | Destroys thyroid peroxidase. Body tries to make more T3, T4 to make up |
| Grave's disease | Antibody forms against TSH receptors. It mimics TSH, is not regulated and constantly activates the TSH receptor |
| Adenoma of the Pituitary | Constantly producing TSH |
| Follicular cell morphology | Resting gland= squamous. Active gland=cuboidal and columnar |
| Leakage of Thgb into systemic circulation | Is minimum but in some disease states it is in increased amounts in cancers |
| Parafollicular cells (c-cells) | Clear cells because they don't pick up stain. Euchromatic nucleus. Generates calcitonin. Calcitonin responds to high calcium |
| Parathyroid glands: Chief cells | Chief cells: PTH release. Ca can inhibit PTH. If Ca is low it won't inhibit PTH. |
| Oxyphils | increases as person ages, very eosinophilic |
| Adrenal gland | Salt balance, metabolism of carbohydrates proteins and fats, secondary sex characteristics |
| Zona Glomerulosa | 15% of cortex, aldosterone |
| Zona Fasiculata | 80% of cortex, arranged in columns. Secretes cortisol in response to ACTH |
| Zona Reticularis | 5% of cortex, steroid secreting cells, mitochondria |
| Medulla | Chromaffin cells: produce catecholamins Epi and NE |
| Chromaffin cells | Post-synaptic sympathetic cells because they lack axon. Upon stimulation they secrete the granular content right into the interstitial tissue and into capillaries. Epi/NE are packaged with another carrier called chromatogranins |
| Synthesis of Epi | L-Dopa-NE-(methyl transferase)-Epi. Methyl transferase is regulated in presence of glucocorticoids/cortisol |
| Pineal Gland | In dark: Converts serotonin to melatonin. It is under control of PVN and stimulates the release of NE which leads to synthesis of Melatonin |
Created by:
Kahiranoel@gmail.com
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