Thyroxine or T4 and Triiodothyronine or T3 are synthesized from?
tyrosine and iodine.
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Thyroid hormone synthesis
tyrosine --\> thyroglobulin (TG)
iodide pumped in via Na/cI symporter
iodiode coupled to TG by peroxidase
TG + I --\> MIT --\> DIT (iodinated thyroglobulins
TSH--\> MIT/DIT uptake into follicular cells --\> digested in lysosome to T3/4 (mostly T4)
protein TBG carries T3/4 in circulation
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deiodinase
This enzyme removes an iodine from T4, producing T3.
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What is the impact of deiodinase?
1. increasing half-lives of T4 2. provides another level of control
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Hyperthyroidism
"Graves disease" -Increased oxygen consumption (increased metabolic rate) -Sweating, warm flushed skin -Increased heart rate and increased blood pressure -Heat intolerance -Increased appetite and weight loss -Insomnia -Increased nervous system activity, hyper excitability, irritability, insomnia -Increased muscle protein catabolism resulting in muscle weakness and weight loss.
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Treatments for hyperthyroidism
beta blockers to decrease heart rate radioactive iodine to destroy some thyroid cells surgical removal of thyroid gland (followed by hormone replacement therapy)
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Hypothyroidism
"Hashimotos" -Decreased oxygen consumption (decreased metabolic rate) -Decreased HR/BP -Decreased sweating, cold skin -Intolerance to cold -Decreased appetite and weight gain -Apathy, sleepiness - brittle hair, nails, and dry skin. -puffy appearance (myxedema). -Reduced nervous system activity resulting in fatigue and slower processing.
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treatment for hypothyroidism?
synthroid, a synthetic form of thyroxine
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Adrenal gland composition
outer cortex and an inner medulla, both of which produce hormones.
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Adrenal gland production
ADRENAL steroids.
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Adrenal Cortex zones
out --\> in zona glomerulosa, zona fasiculata, and zona reticularis.
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zona glomerulosa
mineralocorticoids (aldosterone)
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zona fasiculata
glucocorticoids (cortisol)
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zona reticularis
androgens
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cortisol effects
-Gluconeogenesis -Protein catabolism -Lipid catabolism -suppress inflammation -Brain function
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Hypercortisolism
"Cushing's syndrome" hyperglycemia (too much glucose) muscle breakdown fat breakdown (deposition in face/trunk) depression and learning difficulties.
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Hypocortisolism
"Addison's disease" Total cortex loss hyperkalemia hyponatremia increased ACTH production since the normal negative feedback control is lost.
70% of islets secrete insulin activated by high glucose
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Alpha cells
30% of islets secrete glucagon activated by low glucose
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Regulation of Insulin secretion
high Plasma glucose low Plasma amino acids high Gastrointestinal hormones ANS
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Diabetes Mellitus
body's inability to process glucose correctly \= high blood glucose levels
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What happens if Diabetes Mellitus is left untreated?
diabetes can cause both acute (ketoacidosis -acidic blood pH) and chronic complications (cardiovascular disease, renal failure, blindness, infections, and nerve damage).
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Type 1 diabetes mellitus
(10%) loss of beta cells \= no insulin under 15 y.o. acute complications: acidosis polyuria polydipsia polyphagea
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Treatment of type 1 diabetes
insulin injections
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Type 2 Diabetes Mellitus
(90%) reduced response by cells to insulin over 15 y.o., genetics, lifestyle few acute complications:' increase blood sugar
change in diet and exercise drug therapy to decrease carb digestion, decrease glucose production in liver, increase target cell sensitivity insulin administration.
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Gestational diabetes
diabetes during pregnancy increases risk of type 2 diabetes