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56 Cards in this Set
- Front
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Key Roles T3, T4 Mechanism |
Regulation of body development Govern rate at which metabolism occurs in individual cells. Mechanism: Since they are hydrophobic (bind to receptors), they easily diffuse through and bind to cytosolic and nuclear receptors, forming Thyroid hormone-receptor complex and function as a TF to perform transcription and translation (long, long half life) Influence gene expression |
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What contains the major cells for T3, T4 synthesis. |
Thyroid follicular cells |
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Structure thyroid follicular cells |
Tight junctions, preventing leakage Microvilli line apical area of lumen Pseudopods extend into lumen |
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Structure colloid |
Thick proteinaceous gel like substance, colloid, composed primarily of thyroglobulin. |
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What are thyroid colloid cells composed primarily of? |
Thyroglobulin |
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General formation of T3, T4 |
Iodination of tyrosine residues on thyroglobulin Thyroglobulin -- 3 iodinations --> T3 Thyroglobulin -- 4 iodinations --> T4 T3, T4 -- pinocytosis from colloid into follicular cells --> finalize Thyroid hormone production |
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Mechanism T3, T4 transport |
When needed, TG pinocytoszed back into follicular cells. Bind to lysosome, peroxidase activity removes T3, T4 from TG > DIT, MIT recycled (I recycled) > T3 T4 released and bind to Thyroxine binding globulin (TBG) (80% T3 bound, 70% T4 bound) > T3, T4 reaches site, ~ 40% T4 converted to T3 > T3 main physiological function |
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Function T3, T4 |
Important role CNS development during fetal and neonatal life and developing nerve cells in brain In adults: Brain cells show little responsiveness to metabolic regulatory activities of t thyroid hormones |
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Thyroid hormone function, mechanism |
Mechanism: T4, T3 enter cell. T4 > T3 T3 binds to Thyroid receptor (TR) T3-TR complex recruits RXR (9-cis retinoid acid receptor) and TR-T3-RXR complex binds to thyroid hormone response element (TRE) Binding of TR-T3-RXR complex to TRE causes displacement of corepressor and recruitment of coactivator. This results in transcription via RNA polymerase 2 to form proteins relevant to thyroid hormone Function: Normal body growth in children Basal energy metabolism Brain maturation during fetal growth (2nd trimester - birth) Normal cell differentiation, development, body growth |
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What happens with a drenalectomy. |
Blood glucose supply diminishes, ATP generation declines. Loss Na+, H2O causing circualtory collapse |
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Embryonic development of parts adrenal gland |
Cortex: mesoderm Medulla: ectoderm |
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Function glucocorticoids (types, functions) |
Types: Cortisol, corticosterone Function: adjusting metabolism carbohydrates, lipids, proteins, ensure glucose, FA supply for energy metabolism despite absence of food cope with physical stress |
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Function mineralocorticoids (function) |
Na+, H2O conservation, K+ secretion @ DCT (late CD) |
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Zones adrenal cortex |
80-90%
3 histologically distinct cortical zones of adenral gland: GFR Zona glomerulosa: mineralocorticoids (aldosterone) Zona fasciculata: glucocorticoids Zona reticularis: sex hormones |
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Ability produce cholesterol in adrenal cortex . |
Cholesterol esters present in droplets as lipid droplets as an important source of cholesterol used as precursor for tsyntehsisof steroid hormones |
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Adrenal medulla structure, function |
Modified sympathetic ganglions that secretes NE stored in granules from chromatin cells when stimulated via sympathetic cholinergic innervation (Ach) |
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Concentration glucocorticoid hormones |
10x more cortisol concentration (physiologically important glucocorticoid) corticosterone 1/5 of cortisol's glucocorticoid activity |
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Mechanism for cholesterol utilziation for steroid biosynthesis |
ViA LDL > LDL with cholesterol with ApoB-100 receptor binds to adrenal > Endocytosis of cholesterol > Cholesterol ester removed > Cholesterol ester -- CEH --> FA + Cholesterol * > * De novo: Acetate -- HMG COA --> Cholesterol > Cholesterol --> steroids > Cholesterol --ACAT --> Choesterol ester > Cholesterol ester stored as lipid droplets |
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What convert cholesterol esters into cholesterol. |
CEH |
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What converts cholestero to cholesterol esters to be stored in lipid droplets. |
ACAT |
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What is the LDL receptor. |
APO B 100 |
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What is the enzyme to convert acetate to cholesterol |
ACAT |
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What enzyme adds iodine to tyrosine to form T3, T4 and couples? |
Thyroid peroxidase |
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Process of releasing T3, T4 from thyroglobulin |
Lysosomes of follicular cells, enzymes will cleave the 2 peptide bonds releasing thyroid |
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Process iodine uptake into follicular cells |
Iodine uptake from blood via NIS (Na+/I- simperer) Iodine transport from follicular cells to colloid (Pendrin) |
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Formuals T3, T4 formation Properties of both, differences |
MIT + DIT = T3 (Thyroxine) DIT + DIT = T4 (Tetraiodothyronine) Long half life since bound proteins (Long latent periods) Several hours to see effects |
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If liver dysfunctional what will happen? |
Reduced thyroxine binding globulin, Increase free, increase thyroxine |
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What are D1-D3. |
D1-D2: Remove I from T4 to form active T3 D3: Degradation process making T3 inactive |
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Transport forms thyroid hormoen |
Majority thyroid binding globulin (TBG) 30%: Transthyretin, albumin |
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Properties TRH |
Tonic release Negative feedback |
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Stimuli thyroid hormoen (stimualtors, inhibitors) |
Stimulators: Cold Low metabolism Inhibitors: Excitement Anxiety (sympathetic) Starvation > TSH inhibitions: Dopamine Somatostatin |
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Dopamine functino |
Inhibit Prolactin, TSH |
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Somatostatin function |
Inhibit TSH Inhibit GHRH |
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TSH function, mechanism |
Increase thyroid hormone Increase growth thyroid gland (also ACTH) (can be pathological) Result: Increase NIS (Na+/I- simperer) Increase TPO Increase thyroglobulin Increased endocytosis (colloid) Mechanism: cAMP PLC (with high TSH) |
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Mechanism Thyroid hormone (what was the lecture thought) |
t3, t4 enters via facilitated through thyroid receptors T4 > T3 (5' Deiodinate) T3 binds TR T3-TR complex deterodimerizes with RXR T3-T4-RXR complex is a TF that binds to TRE on DNA, displacing corepressor, brings coactivator increasing transcription Lecture thought * Thought that T3 can do things directly, without changing protein expression, having rapid responses |
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Function thyroid hormone (overview) |
Overview: Therogetnic effect of heat production Thyroid receptors really determine the effectiveness Increase BMR > Incraase O2 consumption, heat production > Oxidative phosphorylation > result heat production > Na+/K ATPase : Hydrolyzes ATP (7.3 kcal, -33kcal), releasing energy, and release Growth muscles, bone, fetal brain > Thyroid hormone differentiates and matures, inhibiting nerve cell replication (NOT INCREASING CELL GROWTH)* > Other > decrease plasma cholesterol* marker, increase vitamin utilization Other Systemic effects > Increase CV > Increase Respiratory > Nervous system: regulates development, increases synaptic firing, enhances wakefulness, alertness > Musculoskeletal: more activity small rise thyroid |
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What is the prime determinant of thyroid hormone |
# Thyroid receptors and whether it works |
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Role thyroid hormone in fetal development |
Differentiation and maturation of nerve cells, inhibiting nerve cell replication, NOT INCREASING NERVE CELLS If not thyroid hormone: Mental retardation (cretinism, congenital hypothyroidism) |
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Graves disease labs, S&S, mechanism |
Mechanism: Antibodies (Thyroid stimulating immunoglobins: TSI) stimulating TSH receptors on thyroid
Labs: High T3, T4 Low TSH Low TRH S&S: Exophthalmos Goiter (enlarged thyroid/neck) |
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Growth hormone secretion (rate, times, times in life) Reason possible changes. |
Secretion in periodic bursts Times: mainly at morning and night, mainly at NIGHT (within 1st hour of sleep) Ages: Adolescence (late puberty) Decline in adults due to reduced GH secretory bursts, not # pulses Reason decline with age: No change in secretion, rate but smaller pulse width (P. 616) |
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What is primary thyroid disease |
Disorder in thyroid gland |
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What is secondary thyroid disease |
PG disorder |
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What is tertiary thyroid disease |
Hypothalamic disorder |
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Hyperthyroidism S&S |
Heat interlace Weight loss High state excitability Muscle weakness (too much protein catabolism) Increase CV stimulation Fatigue Exophthalmos (swelling in eye orbital), reason infiltrations come in sockets, causing protrusion of eyes Diarrhea * Constantly high state metabolism . . |
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What does TSH at 0 means? |
Primary thyroid hyperthyroidism |
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Distintuish grave |
Immunological measurements to TSI High TSH, TRH as usual Clinical observations: goiter, ophthalmic |
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What can occur if you consume Cruciferous food (vegetables) |
Result: Decrease T3, T4 Mechanism: Decreased NIS S&S: |
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Considerations thyroid administration |
Good short term But long term, T3, T4, TSH, TRH all decline. |
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Affect lack 11 b hydroxylase |
High G, R Low F |
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Affect lack 21 b hydroxylase |
Low GF High R (Viralism) |
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Affect lack 17 alpha hydroxylase |
High G only (hypertension) Low F Low L (Affect males more) |
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Importance of zone glomerulosa mechanism in producing hormone |
21 B hydroxylase 11 B hydroxylase If 21 B OH deficiency, still produce 11-deoxycorticosterone, which is a weak aldosterone, but still will maintain BP. If 11 b oh deficient, no aldosteorne, glucocorticoid production. |
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Function cortisol |
Overview: Survive hormone Increase epinephrine activity > Ino/chrono HR effect > Increase gluconeogenesis, lipolysis Increase glucose ('need to survive') to be available to brain > via gluconeogenesis > Block glucose uptake into adipose + muscles Slight increase glycogenesis Increase AA (decrease aa increase protein in Growth hormone) FA via lipolysis |
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Function epinephrine |
Gluconeogenesis No affect protein (vs. protein degradation cortisol, protein synthesis GH) |
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Low thyroid hormones, other possible signs. |
Low T3, T4 (Low GH as well) Rationale: Low thyroid usually related to low GH gene expression High TRH, TSH |
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Phases stress. |
Alarm: Increase catecholamines (Sympathetic stimulation) > Result: Increase chronotropic, inotropic HR (Increased SV, BP, CO, beta 1), Vasoconstriction (non-skeletal muscle tissue, alpha 2), Vasodilation (skeletal muscle, alpha 2), increase RR Alertness, mobilization resources Resistance: Prolonged stress > Sympathetic stimulation Release: RAAS activation: mineralocorticoids, ADH ACTH: mineralocorticoids, glucocorticoids Mineralocorticoids Glucocorticoids Glucagon Growth hormone Result: Aldosterone: Increase Na+(Cl-), H2O reabsorption, K+ secretion Glucocorticoids: Increase free glucose, gluconeogenesis, Increase free FA (lipolysis), Increase glycogen synthesis slightly, immune suppression Glucagon: Increase free glucose, gluconeogenesis, glycogenolysis, Increase free FA(Lipolysis) Growth hormone: Increase free glucose (diabetogenic effect), increase free FA, No change in protein metabolism (increase protein formation) Exhaustion: Effects prolonged stress: prolonged sympathetic stimulation Prolonged RAAS: Prolonged Angiotensin II, Aldosterone Prolonged ADH Prolonged ACTH: Prolonged Aldosterone (ADH) Prolonged Glucocorticoids Prolonged glucagon Prolonged gH Effects: Decreased proteins (prolonged catabolic hormones: Glucagon, glucocorticoids, x GH) Decreased fats (prolonged catabolic hormones: GLucagaon, glucocorticoids, GH) decreased glucose (less available brain): prolonged glucagon, glucocorticoids, GH decreased immunity (prolonged glucocorticoids) Decreased blood volume (blood pressure): decreased ADH, Aldosterone > eventual circulatory collapse |
