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71 Cards in this Set

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What are the three primary effects of thyroid hormone?
1: increase BMR
2. induce gluconeogenesis
3. coordinate normal growth and development
How do thyroid hormones increase BMR?
generate futile cycles where triglycerides are being made and broken down at the same time

increase the expression of Beta adrenergic receptors
What kind of a drug could you use to treat overproduction of thyroid hormones?
beta adrenergic antagonist
What disease state results if hypothyroidism is left untreated in the first weeks of birth?
Cretinism-irreversible mental retardation
Explain thyroid hormone control?
TRH-(+)->TSH(+)-->T3/T4(-)->TRH
Explain the purpose of using the Radioactive Iodine uptake test?
Because the thyroid is one of the few places where iodine is absorbed you can trace it to the follicles.

If the thyroid is enlarged (graves) you see a bigger dark shape

a hot spot means one area is unresponsive to TSH and is constitituively active
What will the size of the colloid be in a person with graves disease?
Very tiny follicles with tall columnar epithelium b/c it is awlays active
Explain the production of thyroid hormones
a) iodine from the diet is actively transported across the cell membrane

b) trapped iodine is transfered across the cell into the lumen where it is linked to tyrosine to form MIT and DIT (in thyroglobulin)

c) MIT and DIT are convered to T3 and T4 with the aid of peroxidase and transaminase

d) T4 and T3 are reabsorbed into the cell in the form of colloid droplets

e) T4 and T3 are separated from thyroglobulin

f) T4 and T3 are secreted into the circulation. Any uncoupled MIT and DIT are diodinated to release tyrosine and iodine
What converts thyroxine to active T3 inside of cells?
5'-iodinase (3-4x more potent than T4)
What class of drug could prevent thyroid hormones from being produced?
A thyroid peroxidase blocker (makes the DIt and the MIT) eg propylthiouracil
In what form is most of the thyroid hormone stored?
Thyroxine (90% is T4)
Why does a patient with hypothyroidism or hyperthyroidism develop a goiter?
sustained high levels of TSH from lack of negative feedback from T4/t3 or from the trophic effects of TSI in graves disease cause hyperplasia of the thyroid
What is the mechanistic cause of Hashimoto's thyroiditis?
autoantibodies against thyroid peroxidase and antithyroglobulin
What is the mechanism of Graves disease?
thyroid stimulating immunoglobulin are produced by the immune system it is an analog of TSH
What are the 4 roles of parathyroid hormone?
1. Stimulates bone resorption
2. Decrease in renal calcium excretion
3. Increase in renal phosphate excretion
4. Final step in vitamin D synthesis in the kidney
What 3 factors regulate the secretion of PTH?
1. Plasma free calcium levels (decrase = pth secretion-sensed through CaSR receptors in cheif cells)

2. Plasma [phosphate]-increase = increased PTH secretion

3. VItamin D-PTH stimulate vitamin D synthesis which exerts negative feedback on PTH
What form is most phosphate in?
alkaline phosphate 4:1
What role does vitamin D play in the body?
regulates calcium/phosphate homeostasis
How is vitamin D made?

Which step is regulated?
7 dihydrocholesterol is exposed to light to become cholecalciferol (or it comes from th ediet) which the liver makes into 25 hydroxycalciferol then the kidney makes it into 1,25 (calcitrol) the active form

hydroxylation in the kidney is the regulated step that is stimulated by PTH
What controlsl Vitamin D production?
PTH

phosphate inhibits vitamin D synthesis even though it does increase PTH

low calcium stimulate vitamin D synthesis
What kind of hormones does the adrenal cortex secrete?
Steroid hormones
What kind of catecholamine predominates adrenal medullary secretions?
EPINEPHRINE; nor epi is for NEURons
How do adrenal cortex hormones have an effect on adrenal medulla secretions?
The adrenal medulla receives high concentrations of adrenal steroids b/c there is a portal venous blood supply.

The adrenal cortex hormones (cortisol) stimulate release of the medulla catecholamines
What substrate and enzyme is necessary for steroid production?
LDL cholesterol

Desmolase
What enzyme is necessary for adolsterone creation and in what cell?
Glomerulosa cells have adlosterone synthase
What enzyme is necessary for cortisol creation and in what cell does this occur?
17 alpha hydroxylase in the fasciulata
Why is lack of cortisol potentially fatal?
Hypotension results due to lack of sympathetic stimulation
What enzyme is unique to the reticularis and the fasciculata that allows them to secrete cortisol?
17 alpha hydroxylase
What part of the renal cortex has aldosterone synthase?
Glomerulosa
What are 3 roles of cortisol?
mobilize glucose, amino acids, and fatty acids

resist inflammatory and immune responses

increase blood glucose
When are cortisol levels the highest?
highest in the morning and lower during late afternoon and prior to sleep.
What other hormone is created upon synthesis of adrenalcorticotrophic hormone?
Melanocyte stimulating hormone!!
In a case of ACTh insufficiency why would aldosterone continue to be produced?
B/c it is stimulated by angiotensin 2 and only weakly by ACTH
Why does excess ACTH cause hyperpigmentation?
B/c when cortisol is produced so is melanocyte stimulating hormone
What enzyme allows the precursors for both androgens and mineralcorticoids and glucocorticoids to become corticosteroids?
21 alpha hydroxylase.!! w/o this you get congenital adrenal hyperplasia
What is 11 beta hydroxysteroid dehydrogenase and what can inhibit it?
It deactivates cortisol and is expressed in addition to aldosterone which prevents cortisol from blocking aldosterone receptors.

Licorice blocks it.-results in hypertension etc why?
Why does synthetic glucocorticoid therapy result in water retention?
It overwhelms the ability of 11 beta hydroxysteroid dehydrogenase which means that cortisol agonizes the receptors for the mineralcorticoids causing increased sodium and therefore water retention in the kidney.
What are the three stimuli for the release of renin?
1. reduced distension of the afferent arteriole

2. tubuloglomerular feedback

3. stimulation of renal sympathetic nerves (baroreceptor reflex)
What is addison's disease?
primary failure of the entire adrenal cortex

symptoms are:

hypoglycemia-cortisol
hypotension-cortisol
Weakness and fatigue-cortisol
Hypovolemai-aldo
increased pigmentation-too much ACTH = alpha melanocyte
Reduced libido in FEMALES
What is Cushing's syndrome? not to be confused with Cushing's disease.
Too much cortisol maybe from corticosteroids;

Hyperglycemia, muscle wasting, truncal obesity, hypertension -mineralcorticoids
What is Conn's syndrome?
Hyperaldosteronism-hypertenion, hypokalemia, metabolic alkalosis

things that prevent blood flow to the kidney can cause 2ndary hypoaldosteronism.
What is the rate limiting enzyme of making catecholamines?
Tyrosine hydroxylase
What does the final conversion from norepinephrin to epinephrine and *only* occurs in chromaffin cells?
Phenylethanolamine N methyltransferase
What controls release of catecholamines from the adrenal medulla?
CNS
What stimulates Phenyl N methyltransferase to convert nor epi to epi?
Cortisol!
Why would you want to give someone with tachycardia a epinephrine antagonist rather than a norepinephrine antagonist?
B/c epinephrine like Beta receptors more than norepinephrine

(closer in the alphabet)
Name the major effectors of the following receptor subyptes:

alpha 1

beta 1

beta 2
alpha 1 -vasodilator

beta 1-heart contractile

beta 2-relaxes smooth muscle of the lungs
What can be measured in the urine to determine the amount of catecholamines being produced by the adrenal medulla?
VMA-vanillymlmandelic acid -is created by MAO using epinephrine
What is a pheochromocytoma?
a secretory tumor of the adrenal medulla
When is GH secretion the highest?
during the first 2 hours of sleep
What factors results in increased GH secretion?
Acute stress

hypoglycemia through ghrelin

starvation
What are the 2 functions of growth hormone?
Stimulates lineal growth through IGF (somatomedin)

Metabolic effects that oppose insulin
What is the largest source of plasma IGf1
Liver also secreted in many tissue
What controls the secretion of GH?
IGF-1
What is the advantage of having plasma proteins bound to IGF1 even though it is a peptide hormone?
It allows for a more stable amount of IGF1 to circulate.
Explain feedback in GH IGF axis?
GH inhibits its own secretion

IGF-1 inhibits GH secretion directly at somatotropes

IGF-1 inhibits hypothalamic GHRH

IGF1 stimulates hypothalamic somatostatin
What is the main regulator of glucagon levels and why?
Insulin, it has to flow from the center toward the periphery and suppresses glucagon secretion as it goes into the blood.
What is the first screening method for diabetes?
microalbuminuria
What mediates the effects of insulin in a cell?
Receptor tyrosine kinases (number of receptors is important for determining response-obesity lowers the number of receptors)
Explain the mechanism of insulin secretion:
Glucose is taken up by glut 2 to produce Atp

Inhibits atp sensitive potassium channel which depolarizes the membrane

Depolarization activates voltage sensitive calcium channels causing and influx of calcium

Calcium induced calcium release triggers exocytosis of secretory granules continaing insulin.
What is an incretin? Name one example?
GIP GLP1 (glucagon like peptide)-

incretins are GI peptide hormones that stimulate insulin secretion that are secreted in response to eating

allows an increase in plasma insulin levels ONLY when in conjunction with high blood glucose levels
What is the Wolff Chaikoff effect?
Too much iodine actually causes hypothyroidism
What is the main function of glucagon?
Makes the liver perform gluconeogenesis and make ketone bodies (beta hydroxybutyrate and acetoacetic acid) from acetyl coA

increase lipolysis and proteolysis
What is the effect on glucagon and insulin of eating a protein rich meal?
It increases both glucagon and insulin secretion, minimizing the change in the concentrations and preventing the development of hypoglycemia
What is the short term reaction to hypoglycemia, what is the long term reaction to starvation?
Short term-glucagon/catecholamines

Long term-cortisol and GH
DIagnose the following glucose levels:

70-99
100-125
126+
Normal
prediabetes
diabetic

nonfasting over 200 is diagnostic if they have the 3 Ps
What is one major difference in the symptoms between Type 1 and Type 2 diabetes?
Type 2 does not produce ketoacidosis b/c there is still enough hepatic resposne to insulin to prevent ketogenesis
Primary hyperparathyroidism
Stones, bones, groans, psychiatric overtones
What is metabolic syndrome?
Increased risk of both cardiovascular disease and type 2 diabetes
What causes the following forms of dwarfism?

Achondroplasia-
Pituitary Dwarfism
Laron Dwarfism
Cretinism-
Achondroplasia-gene defect for cartilage FGF receptor

Pituitary dwarfism-GRH, GH, IGF1 deficiency

Laron dwarfism-unresponsive GH receptors

Cretinism: hypothyroidism in children-thyroid hormones are permissive for action of GH
What hormone results in pubic hair development in women?
DHEA (weak adrogens)