Thyroid & Parathyroid Flashcards
How does increased TH effect Oxygen consumption and heat production in everywhere except the brain?
INCREASE
The lumen of the thyroid cells are filled with:
Colloid (thyroid hormones attached thyroglobulins)
Where is the increased heat coming from in response to thyroid hormone?
Since it’s controlling rate of the Na/K pumps, the heat is coming from the ATP burning
Where is the site of synthesis of thyroid hormone within the thyroid cell?
The colloid - the home of thyroglobulin
Thyroid follicle has a basal membrane which is exposed to ______ and the apical membrane exposed to the _____.
blood, lumen
What is the most RELEASED form of TH?
T4
What is the most ACTIVE form of TH?
T3
What is the 3 or 4 after T in reference to?
The number of iodines attached
Is tyrosine an ESSENTIAL AA?
No, body can synthesize it
What is the LIMITING AGENT for thyroid synthesis?
Iodide (need it from diet)
What is the enzyme that removes a Iodide, creating an active T3 form?
5’ - iodinase
If a patient is HYPERTHYROID, what could be do to the enzyme creating T3 to treat?
INHIBIT it, keep more in T4 form (decreasing active T3)
How do we bring TYROSINE into the epithelium from the BL membrane?
via Na-symporter (is an AA)
How do we bring IODIDE into the epithelium from the BL membrane?
via Na-symptorter
In order to move the IODIDE into the colloid, what is necessary to do to it?
Needs to be converted to ioDINE (I2) form via peroxidase and will diffuse out into the colloid lumen
How many tyrosine’s get added to the THYROGLOBULIN molecule?
2 = creates the SCAFFOLDING for TH
What is the compound called when 1 iodine binds to tyrosine?
MIT = monoiodotyrosine
What is the compound called when 2 iodine binds to tyrosine?
DIT = diiodotyrosine
DIT + DIT + Thyroglobulin =
T4
MIT + DIT + Thyroglobulin =
T3
How does thyroid hormone get back out to the blood circulation?
Endocytosed back into epithelium and fuses with LYSOSOME and releases T3 & T4 off and then exits out to blood because lipid soluble
Once T4 reaches target cells and gets deiodinated to T3, and acts on cell nucleus to do what intracellularly?
INCREASE: mitochondria, Na/K ATPase pumps, Enzymes, O2 consumption, Metabolic rate
Since TH is the PRENATAL controller of growth, what do we see in a child born in the absence of TH?
Cretinism
What effect does TH on beta-receptors?
INCREASES them
How do epinephrine and TH work together?
Since TH increases the beta receptors it increases the effect of epinephrine – increase CO, etc
How does TH increase the kidney function?
Due to increased metabolism, have more nitrogen waste and needs to rev the kidneys up to excrete it
TSH stimulates the thyroid gland to secrete TH, where does TSH come from?
Anterior Pituitary
TRH stimulates the Anterior Pituitary to secrete TSH, where does TRH come from?
Hypothalamus
What 2 locations do high levels of TH can FEEDBACK on to decrease TH production?
Anterior Pituitary,
Hypothalamus
If the body needs TH, then what will it do to the individual follicular cells in the thyroid gland?
Increase their size and replication - can see growth of thyroid gland
How are TH levels affected with PREGNANCY?
Make more thyroglobulin when pregnant and will stimulate T3 and T4 production because lowering the levels in the blood (because it’s bound up!)
How are TH levels affected with LIVER DISEASE?
Make LESS thyroglobulin and less bound (more free), so will INHIBIT TH production
How are TH levels affected by the IMMUNE SYSTEM?
immune system can create a substance that looks just like TSH to the thyroid gland, and will STIMULATE TH production.
What is the effect of TOO MUCH Iodine?
Will down-regulate TH production
T/F. A hyperthyroid individual has symptoms similar to a person with an adrenal medullary tumor.
True (increased epinephrine production - they work in permissibly)
Most of the increased TEMP in HYPERthyroidism is produced where?
LIVER
What is an uncontrolled growth of a thyroid gland called?
GOITER
Goiter results from:
A. Hyperthyroid
B. Hypothyroid
C. Both
BOTH
What is the mechanism of HASHIMOTO’s Disease, and do we expect to feel thyroid gland on palpation?
AUTOIMMUNE destruction of thyroid gland itself/
Yes, will be firm
What effect does Low T3,4 have on TSH production?
Less negative feedback, so TSH increased by anterior pituitary
What do we expect hormone levels to be if we have IODINE Deficiency?
LOW T3, T4
HIGH TSH
What is the mechanism of GRAVES disease? and what do we expect hormone levels to be?
Autoimmune mimicking immunoglobulin stimulates the thyroid:
HIGH T3, 4 (so high negative feedback)
LOW TSH
T/F. Graves disease is not influenced by negative feedback, from high thyroxine levels.
TRUE - is non functional feedback
What physical exam finding do you find on the face in HYPERTHYROIDISM?
Exopthalmos
Hyper or Hypo:
- weight loss
- goiter
- sweating
- more urea in urine
HYPER
Hyper or Hypo:
- weight gain
- drooping eyelids
- goiter
- brittle nails
- cold sensitivity
HYPO
Who are the “keepers of calcium”?
Parathyroid glands
Beside regulation of calcium, what else does parathyroid regulate?
Phosphate
Parathyroid glands secrete _____, the calcium regulating hormone.
PTH - parathyroid hormone
How much of total calcium is protein-bound, which protein?
40% to Albumin
Since Albumin in negatively charged, in addition to binding calcium, it also binds what?
Protons
What is the result of ACIDOSIS on Free Calcium?
Protons will outcompete Ca, and Albumin will release Ca and INCREASE levels = HYPERcalcemia
Consequence of HYPOcalcemia?
INCREASED excitability of plasma membranes
Consequence of HYPERcalcemia?
Cardiac ARRTHYMIAS and DECREASED excitability of membranes
In response to LOW calcium, the parathyroid gland INCREASES PTH secretion, which targets which 3 tissue types?
- BONE
- KIDNEYS
- INTESTINE
What effect does PTH have on BONE?
Increase RESORPTION
What effect does PTH have on KIDNEYS?
Increase Ca REABSORPTION
Increase Vit D PRODUCTION
What effect does PTH have on INTESTINES?
Increase Ca ABSORPTION from diet
What cells in the bone DISSOLVE aka resorb bone?
osteoCLASTS
What are the bone FORMING cells?
OsteoBLASTS
2/3 of bone mass is crystals of calcium and phosphate, called:
Hydroxyapatite
Hormones that favor bone FORMATION: (decrease Ca levels)
Insulin GH IGF-1 Estrogen & Testosterone Calcitonin
Hormones that favor bone RESORPTION: (decrease Ca levels)
PTH
Cortisol
TH (T3,4)
Which bone cells have the receptors for PTH?
OsteoBLASTS (formation cells)
T/F. Most of the calcium you eat is Absorbed.
False - is under hormonal control, ca absorption is vitamin D dependent
Plasma Vitamin D comes from which 2 sources?
- Diet
2. Sunlight
Plasma Vit D needs to be hydroxylated TWICE in order to be active. Where does this happen?
First in LIVER
Second in KIDNEYS (increased with PTH)
What is the mechanism for which Vit D INCREASES Ca absorption?
D generates MORE Calbindin, which binds up intracellular Ca and keep the concentration gradient up for more Ca to come in!
What is the RATE-LIMITING step in Activating Vit D?
The 2nd hydroxylation at the KIDNEYS, this enzyme is stimulated by PTH
What happens to bone REFORMATION as we age?
DECREASES - increased risk of fractures from osteoporosis
When bone is broken down to increase Ca levels, what other levels rise in the plasma?
Phosphate
How does PTH and the kidneys manage this increased rise in Phosphate after bone resorption?
PTH inhibit reabsorption of P and you pee it out!
What hormone is an ANTAGONIST of PTH at bone? What is it’s effect?
Calcitonin - inhibits osteoclasts, therefore bone resorption
A tumor in the parathyroid gland can secrete unregulated PTH levels, and not suppressed by high Ca levels, so become HYPERCALCEMIC but the excess PTH will do what?
INCREASE bone resorption + kidney absorption + vitamin D
Other causes of HYPERcalcemia?
Autoimmune - PTHrp mimicks PTH
Excessive ingestion of Vit D
What is the effect of pseudohypoparathyroidism?
in presence of normal PTH in blood (similar to insulin in type 2 diabetes) problem is in the receptors! resistance to them on bone or on blasts or proximal tubule of kidney = HYPOCALCEMIA
