• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/124

Click to flip

124 Cards in this Set

  • Front
  • Back
Adrenal cortex and medulla: what is the cortex derived from
mesoderm
Adrenal cortex and medulla: what is the medulla derived from
neural crest
Adrenal cortex and medulla: what are the 3 layers of the cortex and what does each make?
"GFR… it gets sweeter the deeper you go"
G = zone glomerulosa = mineralcorticoids = aldosterone (salt)
F = zona fasiculata = glucocorticoids = cortisol (sugar)
R = zona reticularis = androgens = DHEA (sex)
Adrenal cortex and medulla: what axis controls aldodterone?
Renin-angiotensin
Adrenal cortex and medulla: what axis controls cortisol?
CRH from the HT - ACTH from the ant. pituitary
Adrenal cortex and medulla: what axis controls DHEA?
CRH from the HT - ACTH from the ant. pituitary
Adrenal cortex and medulla: what cell type is in the medulla that produces a hormone and what is it?
Chromaffin cells in the medulla produce cetacholamines
Adrenal cortex and medulla: what stilumates the medulla?
preganglionic sympathetic fibers THAT SECRETE ACH
Adrenal cortex and medulla: what is the most common adrenal medulla tumor in both adults and children? 2
1. Adults = pheochromocytoma (rare overall)
2. Kiddies = adrenal medulla (common overall)
What is the main presentation difference between a pheochromocytoma and a neuroblastoma?
Pheochromosytoma cuases HTN, neuroblastoma does not
Adrenal cortex and medulla: what are they derived from ? 2
1. Adrenal cortex = mesoderm
2. Adrenal medulla = neural crest
Adrenal gland drainage: left adrenal gland 4
1. Left adrenal gland
2. Left adrenal vein
3. Left renal vein
4. IVC
Adrenal gland drainage: right adrenal gland 3
1. Right adrenal gland
2. Right adrenal vein
3. IVC
Adrenal gland drainage: how does this layout compare to the gonadal drainage.
It's the same: the left drainage goes to the left renal vein, but the right drainage does not
Pituitary gland: what two hormones are released by the posterior pituitary and where are they made?
ADH and oxytocin
They are actually made in the HT (ADH = supra optic, oxy = paraventricular) and the shipped through axons where they are stored in the posterior pituitary until they are released.
Pituitary gland: what is the posterior pit derived from
neuroectoderm
Pituitary gland: what is the anterior pit derived from
oral ectoderm
Pituitary gland: what are the hormones that are released from the ant. pit. 7
1. FSH
2. LH
3. ACTH
4. TSH
5. prolactin
6. GH
7. melantotropin (MSH)
Pituitary gland: what are the two subunits and what does each do? 2
1. The alpha subunit is the same for: TSH, FSH, LSH and beta-HCG. The alpha subunit activates adenylyl cyclase to raise cAMP
2. The beta subunit is different for each hormone and it determines the type of hormone
Pituitary gland: describe the staining patterns of hormone making cells and what hormones come from each.
Hormones that come from basophils: "B-FLAT" FSH, LH, ACTH, TSH
Hormones that come from acidophils: prolactin and GH
Endocrine pancreas: what 3 cell types are found in the islets of langerhans, what hormone is secreted by each and where is each cell type found in the islet? 3
1. Alpha = glucagon = periphery
2. Beta = insulin = central
3. Delta = somatostatin = interspersed
Endocrine pancreas: how can you remember the location in the islet of each cell type?
"INSulin = INSide"
Endocrine pancreas: where are the islets most numerous.
In the pancreatic tail
Endocrine pancreas: from what structure do islets arise?
pancreatic buds
Insulin: describe the steps of insulin release
1. Glucose enters the beta cell via the GLUT2 transporter
2. Glucose inside the beta-cell undergoes glycolysis to raise intracellular ATP levels
3. High ATP/ADP ratio causes K+ efflux channels to close
4. Beta cell depolarizes
5. Voltage gated Ca2+ influx channels open and intracellular calcium levels rise.
6. Rising calcium levels trigger the Qs pathway to raise calcium levels even more (via IP3 DAG)
7. Super high calcium levels lead to exocytosis of insulin secretory vescicles.
Insulin: which tissues require insulin in order to take up glucose and what transporter do they use?
Skeletal muscle and adipose tissue both require insulin which activates their GLUT4 trasporter to uptake glucose
Insulin: how does insulin affect other islet cells
Insulin inhibits alpha-cell release of glucagon
Insulin: describe insulin synthesis 6
1. Proinsulin is made in the RER - circle with the two ends overlapping and sealed by cysteine side chain disulfide bonds.
2. Proinsulin is packaged into secretory vesicles.
3. Inside vesicles proinsulin is cleaved into insulin and C-peptide
4. C-peptide is the non-overlapping part of the circle
5. Insulin is the two overlapping ends that now look like a ladder with 2 rungs
6. Vesicles release sends equimolar portions of insulin and C-peptide into the blood stream.
Insulin: what are the affects of insulin 6
1. Increased glucose uptake into cells
2. Increased glycogen sysnthesis and storage in the liver
3. Increased triglyceride synthesis and storage
4. Increased Na+ retention in the kidneys
5. Increase protein synthesis in the muscles
6. Increased cellular uptake of K+ (also reduced K+ efflux)
Insulin: what cells use the GLUT1 transporter 2
1. RBCs
2. Brain
Insulin: what cells use the GLUT2 transporter 4
1. Beta cells
2. Liver cells
3. Kidney cells
4. Small intestine
Insulin: what is special about GLUT2 2
1. It transports glucose bidirectionally
2. It has a low affinity for glucose (high Km) and so it acts as a glucose sensor
Insulin: what cells use the GLUT4 transporter 2
1. Skeletal muscle
2. Adipose tissue
Insulin: what is special about GLUT4
It only takes up glucose when insulin is present
Insulin: what is special about GLUT1
It has a high affinity for glucose (low Km), thus is takes up glucose constantly
Insulin: name the organs which don't need insulin for glucose uptake
BRICK L
B = brain
R = RBCs
I = intestine
C = cornea
K = kidney
L = liver
Insulin: what does the brain use for energy 2
1. Uses glucose via constant uptake transporter GLUT1
2. Uses ketone bodies suring periods of starvation
Insulin: what do RBCs use for energy
RBCs always depend on glucose
HT-pit axis: name the affect of HT TRH on the pituitary
induces release of TSH (+)
HT-pit axis: name the affect of HT dopamine on the pituitary
inhibits release of prolactin (-)
HT-pit axis: name the affect of HT CRH on the pituitary
induces release of ACTH (+)
HT-pit axis: name the affect of HT GHRH on the pituitary
induces release of GH (+)
HT-pit axis: name the affect of HT somatostatin on the pituitary
inhibits release of GH and TSH (-)
HT-pit axis: name the affect of HT GnRH on the pituitary
induces release of FSH and LH (+)
HT-pit axis: name the affect of prolactin on the pituitary
inhibts release of GnRH (-)
this is what keeps breast feeding mother's from getting pregnant again
Prolactin regulation: describe the communication between the HT and prolactin secreting cells in the pituitary 2
1. Dopamine (HT) inhibits prolactin release (pit)
2. TRH (HT) induces prolactin release (pit)
Prolactin regulation: describe the feedback from the pituitary to the HT
Dopamine (pit) feeds back negatively by inducing dopamine release (HT)
Prolactin regulation: how does prolactin affect other endocrine axes?
Prolactin (pit) feeds back to inhibit GnRH release (HT)
This promotes infertility while a woman is breast feeding
Prolactin regulation: what are the functions of prolactin? 2
1. Stimulation of milk production in the breast
2. Inhibition of GnRH release causes cessation of ovulation/spermatogenesis
Prolactin regulation: what types of drugs are used to treat prolactinoma and why?
Bromocriptine is an dopamine agonist which works to inhibit prolactin release
Prolactin regulation: what drugs inidentally induce prolactin release?
Most anti-psychotics are dopamine antagonists and this stimulate prolactin secretion
Adrenal steroids: describe the layout of androgen synthesis
Made up of 4 columns:
1. Column 1 = glomerulosa = mineralocorticoids = aldosterone
Column 2 = fasciculata = glucocorticoids = cortisol
Column 3 = reticulata = androgens = DHEA
Column 4 = periphery = estrogens/androgens
Adrenal steroids: what conversion starts this all out and what things induce/inhibit this step? 3
1. It all starts out with conversion of cholesterol to prenenolone (via desmolase) - pregnenlone puts you at the top of the 1st column
2. ACTH induces desmolase
3. Ketoconazole inhibits desmolase
Adrenal steroids: what is the enzyme that does the first conversion in all 3 columns
3-beta-hydroxysteroid dehydrogenase (3-beta-HSD)
Adrenal steroids: recite the first column 4
1. Prenenolone to progesterone (via 3-beta-HSD)
2. Progesterone to 11-deoxycorticosterone (via 21-hydroxylase)
3. 11-deoxycorticosterone to corticosterone (via 11-beta-hydroxylase)
4. Corticosterone to aldosterone (via aldosterone synthase)
Adrenal steroids: how do you cross from the first column to the second column 2
1. Pregnenelone to 17-hydroxypregnenolone (via 17-alpha-hydroxylase)
2. Progesterone to 17-hydroxyprogesterone (via 17-alpha-hydroxylase)
Adrenal steroids: recite the second column 3
1. 17-hydroxypregnenolone to 17-hydroxyprogesterone (via 3-beta-HSD)
2. 17-hydroxyprogesterone to 11-deoxycortisol (via 21-hydroxylase)
3. 11-dexycortisol to cortisol (via 11-beta-hydroxylase)
Adrenal steroids: how do you cross from the second column to the third column 2
1. 17-hydroxypregnenolone to DHEA
2. 17-hydroxyprogesterone to andro
Adrenal steroids: recite the third column 2
1. DHEA to andro (via 3-beta-HSD)
2. andro to testosterone
Adrenal steroids: how do you cross from the third column to the fourth column 3
1. Andro to estrone
2. Testosterone to estradiol (via aromatase)
3. Testosterone to DHT
Adrenal steroids: what conversion does 17-alpha-hydroxylase mediate? 2
1. Pregnenolone to 17-hydroxypregnenelone (first to second column)
2. Progesterone to 17-hydroxyprogesterone (first to second column)
Adrenal steroids: what conversion does 21-hydroxylase mediate? 2
1. Progesterone to 11-deoxycorticosterone (first column)
2. 17-hydroxyprogesterone to 11-deoxycortisol (second column)
Adrenal steroids: what conversion does 11-beta-hydroxylase mediate? 2
1. 11-deoxycorticosterone to corticosterone (first column)
2. 11-deoxycortisol to cortisol (second column)
Adrenal steroids: where does angiotensin II fit into all this drama?
Angiotensin II induces aldosterone synthase to convert corticosterone to aldosterone
Adrenal steroids: what is altered in 17-alpha-hydroxylase deficiency 3
1. Decreased DHEA and andro
2. Decreased cortisol (with increased ACTH)
3. Increased aldosterone
Adrenal steroids: what are the sx of 17-alpha-hydroxylase deficiency 4
1. Increased aldosterone leads to HTN with hypokalemia/hypernetremia
2. Increased ACTH leads to hyperpigmenation and adrenal hyperplasia
3. XY males: decreased DHT leads to pseudohemaphrodism
4. XX females: normal external phenotype but no secondary sexual characteristics (aka sexual infantilism)
Adrenal steroids: describe XY pseudohermaphrodism of 17-alpha-hydroxylase deficiency
External genitalia is feminine
Internal reproductive structures are missing (due to presence of MIF)
Adrenal steroids: what is altered in 21-hydroxylase deficiency 3
1. Decreased cortisol (with increased ACTH)
2. Decreased aldosterone
3. Increased DHEA and andro
Adrenal steroids: what are the sx in 21-hydroxylase deficiency 5
1. Decreased aldosterone leads to hypotension with hyperkalemia/hyponetremia
2. Decreased aldosterone leads to increased plasma renin levels
3. Decreased aldosterone leads to salt and volume wasting - possibly hypotensive shock in newborns
4. Increased ACTH can cause hyperpigmentation and adrenal hyperplasia
5. XX females are virilized (female pseudohemaphrodites)
Adrenal steroids: what is altered in 11-beta-hydroxylase deficiency 3
1. Decreased cortisol (with increased ACTH)
2. Decreased aldosterone
3. Increased DHEA and andro
Adrenal steroids: what are the sx of 11-beta-hydroxylase deficiency 3
1. Although aldosterone production is decreased, 11-corticosterone production is severely elevated and this is a mineralocorticoid that acts very similarly to aldosterone - so HTN with hypokalemia/hypernatremia.
2. Increased ACTH can cause hyperpigmentation and adrenal hyperplasia
3. XX females are virilized (female pseudohemaphrodites)
Adrenal steroids: which of the CAH syndromes is most common
21-hydroxylase deficiency
Adrenal steroids: what feature is common to all CAH syndromes?
They all have decreased cortisol which leads to increased ACTH.
Increased ACTH causes hyperpigmentation and hyperplasia of the adrenal glands (hence the name)
Cortisol: where does cortisol come from?
Zona fasciculata in the adrenal gland
Cortisol: what are the functions of cortisol? 7
1. Acts on alpha-1 receptors to maintain vascular tone (and thus maintain BP)
2. Decreases bone formation
3. Anti-inflammatory
4. Decreases immune function
5. Increases gluconeogenesis
6. Increases lipolysis
7. Increases proteolysis (protein breakdown)
Cortisol: describe cortisol regulation
CRH (HT) induces ACTH (ant. pit.) release induces cortisol release (reticulata)
Cortisol feeds back negatively to the ant pit and the (maybe) HT
Cortisol: how does cortisol travel in the blood
It travels in the blood bound to the cortisol binding globulin (CBG)
Cortisol: what else induces cortisol release
Chronic stress induces prolonged cortisol release
PTH: where does it come from?
chief cells of the parathyroid
PTH: what alters PTH secretion
PTH hormone changes primarily due to calcium levels
1. Increased blood calcium decreases PTH
2. Decreased blood calcium incerases PTH
PTH: what is the role of Mg in PTH secretion
In contrast to most cells, chief cells don't use calcium to secrete PTH. Instead they use magnesium. Thus, low blood magnesium leads to deacreased PTH secretion
PTH: what is the affect of PTH on the kidney 5
1. Stimulates reabsoprtion of calcium in the distal tubule and TAL
2. Stimulates reabsoprtion of magenesium in the distal tubule and TAL
3. Inhibits phosphate reabsorbtion
4. Increased urinary cAMP levels
5. Induces 1-alpha-hydroxylase to convert 25-hydroxy vitamin D to 1,25-dihydroxy vitamin D
PTH: what is the affect of PTH on serum calcium
increased
PTH: what is the affect of PTH on serum phosphate 3
1. decreases via urinary excretion
2. increases via bone breakdown
3. The net effect is to lower serum phosphate though
PTH: what is the affect of PTH on urine phosphate
increased
PTH: what is the affect of PTH on bone?
PTH binds to osteoblasts which output RANKL which tells activates osteoclasts
Activated osteoclasts degrade bone, thus releasing both calcium and phosphate into the blood.
PTH: why does PTH regulate calcium and phosphate inversely?
PTH releases both phosphate and calcium from bone. When these to ions are together they tend to precipitate. Thus, it makes sense that in order to make more free calcium available in the blood, PTH tells the kidneys to keep calcium and get rid of phosphorus.
PTH: how does phosphate get regulated
Low phosphorous/phosphate causes the kidneys to ramp up conversion of 25-hydroxy vitamin D to 1,25-dihydroxyvitamin D
What is the formula for phosphate ions
(PO4)3-
Vitamin D: what is another name
cholecalciferol
Vitamin D: what are the 2 types of vitamin D and where does each come from?
Vitamin D3 comes from sun exposure in skin
Vitamin D2 comes from ingested plant matter
Vitamin D: what happens to both Vitamin D2 and D3? 2
Both are:
1. Converted to 25-OH vitamin D in the liver
2. Converted to 1,25-diOH vitamin D in the kidneys
Vitamin D: what is the active form of vitamin D
1,25-diOH vitamin D
Vitamin D: what does vitamin D deficiency lead to in kids and adults?
Kids: rickets
Adults: osteomalacia
Vitamin D: what is an inactive form of vitamin D and where does it come from?
24,25 diOH vitamin D is inactive and it is a metabolite of Vitamin D metabolism but I don't know where
Vitamin D: what is the function of vitamin D 3
1. Increase GI absorption of dietary calcium
2. Increase GI absoprtion of dietary phosphate
3. Increase bone breakdown which increases blood levels of both calcium and phosphate
Vitamin D: compare and contrast the effect of PTH and vitamin D on calcium and phosphate 2
1. PTH: increases blood clacium, decreases blood phosphate
2. Vitamin D: increases both blood calcium and phosphate
Vitamin D: name 3 things that increase production of 1,25 diOH viatmin D 3
1. high PTH
2. low calcium - via high PTH
3. low phoasphate - independent of PTH
Vitamin D: describe 1,25 diOH vitamin D feedback
1,25 diOH vitamin D feeds back negatively to the kidney to decrease it's production
Calcitonin: what is the source
parafollicular cells (aka C cells) of the thyroid
Calcitonin: function 2
Acts to decrease blood calcium levels by:
1. Inhibiting osteoclasts
2. Decreasing gut absorption of calcium
Calcitonin: what make it get secreted
high calcium
Calcitonin: what is notable about the calcitonin axis?
It acts oppositely of PTH but it is not a significant component of normal calcium regulation
Endocrine signalling pathways: name the hormones that elevate cAMP
"GC FLAT CHAMPS"
G = glucagon
C = calcitonin
F = FSH
L = LH
A = ACTH
T = TSH
C = CRH
H = hCG
A = ADH at the V2 receptor
M = MSH
P = PTH
Endocrine signalling pathways: name the hormones that elevate cGMP 2
"Think vasodilators"
1. ANP
2. NO
What's another name for NO?
Endothelium derived relaxing factor (EDRF)
Endocrine signalling pathways: name the hormones that use IP3 DAG
"G GOAT"
G = GnRH
G = GHRH
O = oxytocin
A = ADH at the V1 receptor
T = TRH
Endocrine signalling pathways: name the hormones that bind to steroid receptors 6
1. Glucocorticoid
2. Estrogen
3. Progesterone
4. Testosterone
5. Aldosterone
6. Vitamin D
7. T3/T4
Endocrine signalling pathways: name the hormones that use tyrosine kinase receptors 3
1. Insulin
2. IGF-1
3. FGF = fibroblast growth factor
4. PDGF = platelet dervied growth factor
5. Prolactin
6. GH
What is another name for tyrosine kinase receptors?
JAK-STAT where:
JAK = janus kinase
STAT = signal transducer and activator of transcription
Steroid mechanisms: describe the process that steroids do at their target cells 4
1. Steroid enters the cell
2. Steroid binds to a cytosolic or nuclear receptor
3. Hormone-receptor complex transforms to expose DNA binding area of the receptor
4. Hormone-receptor complex acts as a transcription factor
Steroid mechanisms: how do steroids get carried in the blood and why?
Steroids are lipophilic and so they need to be carried on specific binding globulins
Steroid mechanisms: what happens to free testosterone if it's carrier globulin levels are altered?
Increased SHBG decreases levels of free testoseterone
Men: increased SHBG leads to decreased free testosterone leads to gynecomastia
Women: decreased SHBG leads to increased free testosterone leads to hirsutism
Steroid mechanisms: are steroid hormone pathways fast or slow
They are slow because it takes time to alter gene expression
Thyroid hormone: what is the basic function and description?
these are iodine containing hormones that control the body's basal metabolic rate
Thyroid hormone: where is it produced
T3/T4 are made in thyroid follicles (surrounded by follicular cells that govern transport).
These cells mostly secrete T4 which is then converted to T3 in the periphery
T3 is the active version compared to T4
Thyroid hormone: what are the functions 7
1. Brain growth which is synergistic with GH
2. CNS maturation
3. Increased beta 1 receptors in the heart
4. Increased BMR by increasing Na/K pump activity (leads to increased O2 consumption, RR and temp)
5. Increased gluconeogenesis
6. Increased glycogenolysis
7. Increased lipolysis
Thyroid hormone: whats the mnemonic for the effects of T4/T3 4
"the 4 B's" 1. Brain maturation
2. Bone growth
3. Beta-adrenergic effects
4. BMR goes up
Thyroid hormone: how is T4/T3 carried in the blood?
carried on thyroxine binding globulin (TBG)
Thyroid hormone: what are some things that chage TBG levels?
Hepatic failure: decreased TBG, thus more free T3/T4
Pregnancy, OCP and other estrogenic states: increased TBG, thus less T3/T4
Thyroid hormone: what does thyroperoxidase do? 3
1. Oxidates iodide (iodide to I2)
2. Organifies iodide (I2 + thyroglobulin to MIT or DIT)
3. Couples MIT and DIT to make T3/T4 (MIT + DIT = T3, DIT + DIT = T4)
Thyroid hormone: what are 2 anti-thyroid drugs and where do they act 3
1. Propylthiouracil and methimazole
3. Both inhibit thyroperoxidase from linking MIT and DIT
Thyroid hormone: desribe the regulation
HT secrete TRH which stimulates anterior pituitary to secrete TSH which stimulates thyroid to make T4/T3
Free T3 feeds back negatively to the anterior pituitary to decrease it's senstivity to TRH
Thyroid hormone: what is TSI
Thyroid stimulating immunoglobulin: this is created in Grave's disease. It binds to TSH receptors in the thyroid and activates them, so hyperthyroidism ensues