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87 Cards in this Set
- Front
- Back
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Adrenal cortex and medulla
embryological origins? |
cortex - mesoderm
medulla - neural crest |
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Zona glomerulosa
a. primary regulatory control b. secretory products |
a. RAAS
b. Aldosterone |
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Zona fasciculata
a. primary regulatory control b. secretory products |
a. ACTH, hypothelamic CRH
b. coritsol, sex hormones |
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Zona Reticularis
a. primary regulatory control b. secretory products |
a. ACTH, hypothelamic CRH
b. sex hormones (androgens) |
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Medulla
a. primary regulatory control b. secretory products |
a. Preganglionic sympathetic fibers
b. catecholamines (NE, E) |
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Most common tumor of adrenal medulla in adults?
Most common in kids? How do you tell difference? |
Pheochromocytoma
Neuroblastoma Pheo causes episodic HTN, neuroblastoma does not |
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Neuroendocrine cells of adrenal medulla responsible for releasing catecholamines sytemically
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chromaffin cells
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Adrenal gland drainage
a. left adrenal b. right adrenal Similar drainage as what other organ |
a. Left adrenal --> L adrenal vein --> L renal vein --> IVC
b. R adrenal --> R adrenal vein --> IVC Same as L and R gonadal vein |
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Posterior pituitary (neurohypophysis)
2 things it releases Where are they made and how do they get to pituitary |
Oxytocin, Vasopressin (ADH)
Made in hypothalamus, shipped to pituitary |
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What are Neurophysins
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Carrier proteins that carry hormones from posterior pituitary to systemic circulation
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Embryological derivation of posterior pituitary
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Neruoectoderm
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Anterior pituitary (adenohypophysis)
7 things it excretes |
FLAT PiG M
FSh LH ACTH TSH Prolactin GH MSH (melanotropin) |
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Adenohypophysis
from where is it derived? |
oral ectoderm (Rathke's pouch)
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strucutre of anterior pituitary hormones
a. what is alpha subunit b. what is beta subunit |
a. common subunit in TSH, LH, FSH, and hCG
b. determines hormone specificity |
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Pituitary gland
a. acidophils b. basophils |
a. GH, PRL
b. B-FLAT = FSH LH ACTH TSH |
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What are islets of langerhans?
where are they most common? From what structure did they derive? |
areas of pancreas where alpha, beta, and gamma endocrine cells reside
tail of pancreas derived from pancreatic buds |
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Pancreatic cell types - what do the following secrete and where are they in the islet?
a. alpha b. beta c. delta |
a. glucagon, peripheral
b. insulin, central c. somatostatin, interspersed INSulin is INSide |
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What is 1 signal for insulin secretion by beta cells?
Pathway? |
ATP from glucose metabolism
Glucose brought into beta cell by GLUT-2 --> aerobic respiration --> ATP --> Closes K channels --> depolarizes cell --> Ca channel opens --> exoctyosis |
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Protein required for adipose and skeletal muscle uptake of glucose
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insulin
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Effect of insulin on glucagon
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inhiits glucagon release from alpha cells
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How can you tell the difference between endogenous and exogenous insulin?
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exogenous insulin does not have C-peptide
endogenous insulin has C peptide (Proinsulin --> insulin + C-peptide) |
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1. Increases glucose transport
2. Increases glycogen synth and storage 3. Increases TG synth and storage 4. Increases Na retention (kidneys) 5. Increases protein synth (muscles) 6. Increases cellular uptake of K and amino acids what causes this? |
insulin
INsulin moves glucose INto cells |
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5 organs that do not need insulin for glucose uptake
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BRICK L
Brain RBCs Intestine Cornea Kidney Liver |
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2 places where you find GLUT-1 transporters
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RBCs, brain
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beta islet cell
liver kidney type of glucose transporter? Type of diffusion? |
GLUT-2 (bidirectional)
Facilitated diffusion |
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Adipose tissue
Skeletal muscle Type of glucose transporter? Responsive to what? |
GLUT -4
Insulin responsive |
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2 organs that depend on insulin
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Skeletal muscle and adipose tissue
need insulin for GLUT-4 transporters to bring in glucose |
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2 organst that take up glucose independent of insulin
What do these use for fuel? |
Brain (glucose, ketone bodies in starvation)
RBCs (glucose) |
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Hypothalamic-Pituitary axis
Effect of TRH |
stimulates TSH, PRL
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Hypothalamic-Pituitary axis
effect of dopamine |
inhibits PRL
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Hypothalamic-Pituitary axis
effect of CRH |
stimulates ACTH
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Hypothalamic-Pituitary axis
effect of somatostatin |
Inhibits GH, TSH
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Hypothalamic-Pituitary axis
effect of PRL |
inhibits GnRH
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How is PRL secretion regulated
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1. Tonic inhibition by dopamine
2. PRL stimulates dopamine production and release from hypothalamus 3. TRH stimulates release of PRL |
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2 functions of PRL
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1. stimulates milk production in breast
2. Inhibits GnRH --> inhibits ovulation and spermatogenesis |
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Effect of bromocriptine on a prolactinoma
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Dopamine agonist --> inhibits PRL secretion --> good treatment for prolactinoma
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Effect of antipsychotics on PRL
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Dopamine antagonists --> releases tonic inhibition --> increases PRL secretion
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Cholesterol --> pregnenolone
What enzyme? What activates? inhibits? |
Desmolase
ACTH Ketoconazole |
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17 hydroxylase
where is it found? What is it important for making? |
Fasciculata and Reticularis
Cortisol and sex steroids |
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21 hydroxylase
where is it found? what is it important for making? |
fasciculata and glomerulosa
aldosterone and cortisol |
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11B hydroxylase
where is it found? what is it important for making? |
glomerulosa and fasciculata
aldosterone and cortisol |
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final enzyme in the aldosterone synthesis pathway?
what stimulates it? |
aldosterone synthase
angiotensin II |
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5a reductase
where is it found and what does it do? |
periphery
testosterone --> DHT |
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Aromatase
where is it found and what does it do? |
periphery
testosterone --> estradiol |
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What is the enzyme deficiency that causes
-decrease in sex hormones -decrease in cortisol -increase in aldo --> HTN, hypokalemia |
17 hydroxylase
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17 hydroxylase deficiency
a. effect in boys b. effect in girls |
a. no DHT --> pseudohermaphroditism (externally female, no internal reproductive structures due to Mullerian inhibiting factor)
b. Sexual infantalism = externally female with normal internal sex organs, but lacking secondary sex characteristics |
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Most common cause of congenital adrenal hyperplasia?
why do enzyme deficiencies cause hyperplasia? |
21 hydroxylase deficiency
enzyme deficiencies cause decrease cortisol --> increases ACTH stimulation --> enlarges adrenal gland |
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What is the enzyme deficiency that causes
-decreased cortisol (increased ACTH) -decrease mineralocorticoids -increased sex hormones --> Hypotension, hyperkalemia, increased plasma renin, volume depletion what can this cause in a newborn |
21 hydroxylase
can cause hypovolemic shock in newborn |
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21 hydroxylase deficiency
effect in females |
masculinization, female pseudohermaphroditism (ambiguous external genitalia)
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What enzyme deficiency causes
-decreased cortisol -decreased aldosterone and corticosterone -increased sex hormones --> hypertension why do you see HTN in this case? |
11B hydroxylase
even though aldosterone is low, you still make 11-deoxycorticosterone (now in excess), which is a mineralocorticoid |
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11b hydroxylase deficiency
symptoms in females |
masculanization - normal female internally, ambiguous externally
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Cortisol
5 functions |
BBIIG
1. Blood pressure maintenance (upregulates a1 receptors on blood vessels) 2. Bone growth decreased 3. anti-Inflammatory 4. Immune function decreases 5. Gluconeogenesis, lipolysis, proteolysis increases |
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How does cortisol circulate?
what is the effect of chronic stress on cortisol levels? |
bound to corticosteroid binding globulin
chronic stress --> prolonged secretion |
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Regulation of Cortisol
a. release b. feedback |
a. CRH (hypothalamus) --> ACTH (pituitary) --> cortisol (fasciculata)
b. cortisol inhibits CRH, ACTH, and cortisol secretion |
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PTH
source? |
Chief cells of parathyroid
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4 functions of PTH
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1. increases bone resorption of Ca
2. increases kidney reabsorption of Ca in DCT 3. decreases kidney reabsorption of phosphate 4. stimulates kidney 1a-hydroxylase --> increases 1,25(OH)2 vitamin D (calcitriol) --> increases intestinal absorption of Ca |
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Ultimate of PTH on
a. serum Ca b. serum phosphate c. urine phosphate |
a. increase
b. decrease c. increase PTH = Phosphate trashing hormone |
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4 effects of PTH on bone
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1. increases Ca release from bone mineral compartment
2. stimulates production of M-CSF and RANK-L in osteoBlasts --> stimulates osteoClasts 3. Osteoclast effect --> bone resorption 4. enhances bone matrix degradation |
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4 effects of PTH on kidney
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1. stimulates Ca reabsorption
2. Inhibits phosphate reabsorption 3. increases urinary cAMP 4. Stimulates production of active vit D (1,25-(OH)2D) --> increases GI absorption of Ca |
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Effect of decreased free serum Ca on PTH
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increases PTH
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Effect of
-diarrhea -aminoglycosides -diuretics -alcohol abuse on PTH |
these all cause decreased free Mg --> decrease PTH
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Phosphate homeostasis
effect of low serum phosphate on kidney, GI, bone |
increases kidney conversion to active vitamin D -->
increases GI absorption of Ca and phosphate releases phosphate from bone matrix |
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2 sources of vitamin D
how is it converted to active form (2 conversions) |
D3 (sun), D2 (plant ingestion)
converted to 25-OHD in liver, then 1,25-(OH)2D in kidney (active) |
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2 functions of Vitamin D (cholecalciferol)
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1. increases absorption of dietary phosphate and Ca
2. increases bone resorption of Ca and phosphate |
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Increased PTH
Decreased Ca Decreased phosphate effect on active vitamin D production |
Increase vitamin D production
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How is production of active vitamin D inhibited
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neg. feedback by active vit. D
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Effect of vitamin D deficiency in
a. adults b. kids |
a. osteomalacia
b. rickets |
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How is the effect of PTH different from active vitamin D
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PTH --> increases Ca reabsorption, decreases phosphate (renal)
Vitamin D --> increases both Ca and Phosphate absorption (GI) |
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Calcitonin
source? function? how is it regulated? |
a. parafollicular (C cells) from thyroid
b. decreases bone resorption of Ca "CalciTONin TONes down Ca" c. increase serum Ca --> calcitonin secretin |
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Endocrine hormones that signal by cAMP
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FLAT CHAMP +CGG
FSH LH ACTH TSH CRH hCG ADH (V2 receptor) MSH PTH + calcitonin, GHRH, glucagon |
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2 Endocrine hormones that signal by cGMP
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ANP, NO (EDRF)
Think "vasodilators" |
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4 endocrine hormones that signal by IP3 pathway
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GOAT
GnRH, Oxytocin, ADH (V1 receptor), TRH |
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6 endocrine hormones that bind to cytosolic steroid receptors
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VET CAP
Vitamin D Estrogen Testosterone Cortisol Aldosterone Progesterone |
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1 endocrine hormone that binds to nuclear steroid receptos
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T3/T4
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Insulin
IGF-1 FGF PDGF what pathway do these all work on? |
Intrinsic tyrosine kinase (MAPK)
think "growth factors" |
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GH, PRL, IL-2
what type of signaling pathway do these all use |
Receptor-associated tyrosine kinase
JAK/STAT |
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Steroid/thyroid hormone
a. how do they circulate and why b. speed of onset |
a. circulate bound to binding globulin (like SHBG) to increase their solubility and delivery to target organ
b. Slow because they must induce transcription and translation |
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Effect of increased SHBG in men
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increased SHBG --> decreased free testosterone --> gyncecomastia
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EFfect of decreased SHBG in women
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decreased SHBG --> increased free testosterone --> hirsutism
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Thyroid hormone
5 functions |
4 B's + G
1. Brain maturation - CNS maturation 2. Bone growth - synergistic with GH 3. Beta-adrenergic effects - increases B1 receptors in heart --> increases CO, HR, SV, contractility 4. BMR increases - increases Na/K ATPase activity --> increases O2 consumption, RR, body temp 5. Increases serum glucose - gluconeogenesis, glycogenolysis, lipolysis increased |
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Regulation of Thyroid hormone
a. factors affecting release b. factors inhibiting release |
a. TRH (hypothalamus) --> TSH (pituitary) --> stimulates follicular cells
b. neg. feedback by free T2 to anterior pituitary --> decreases sensitivity to TRH |
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Effect of Thyroid stimulating immunoglobulin in Graves' disease
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stimulates follicular cells to secrete T3/T4
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Effect of hepatic failure on T3/T4
EFfect of pregnancy or OCP use |
hepatic failure --> decrease in Thyroid binding globulin (TBG) --> increased free, active T3/T4
these induce estrogen --> upregulates TBG --> decreases free, active thyroid hormone |
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T3 vs. T4
which has higher affinity for receptors? What happens because of this? |
T3 has higher affinity
T4 --> T3 in peripheral tissues |
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Enzyme responsible for oxidation and organification of iodide, as well as coupling of MIT and DIT
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peroxidase
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2 inhibitors of Iodine oxidation by follicular cell of thyroid
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perchlorate, pertechnetate (anions)
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2 drugs that inhibit MIT and DIT formation/fusion
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Propylthiouracil, methimazole
(antithyroid drugs) |
