Endocrine Flashcards
Hypothalamus and Pituitary secretions
Post pituitary - secretes directly to post pit which flows directly to blood (ADH and Oxy)
Ant Pit - Hypothalamus to Hypothalmic - hypophyseal portal veins to tropic cells which stim release of hormones to blood
Draw Overall hormone flow chart
On paper
What controls concentration of Free hormone
Rate of secretion is primary determinant
Degradation is at constant rate and is not regulated nor responsible for normal fluctuations
Dose threshold curve
SD50 is concentration of hormone that elicits half maximal response
Threshold is the minimum amount of hormone that produces a response
Sensitivity and effect on dosage curve
Decreased sensitivity shifts curve to the right, this effect can be overcome with concentration. Due to decreased receptors, affinity, increased degradation
Capacity and dosage curve
Decreased capacity will decrease maximal response and cannot be overcome with more H.
This is caused by a decrease in reacting cells or substrate available
Somatotrophs
Secretes GH
Thyrotrophs
Secrete TSH
Corticotrophs
Secrete ACTH
Lactotropes
Secretes PRL
Gonadotrophs
Secrete FSH and LH
Glycoprotein family
2 subunits: alpha is conserved and beta unique
FSH, LH, TSH
Somatomammotropin family
GH and PRL
POMC family
Single gene and CRH cleaves product to what is needed
ACTH
Hypo-Pit GH axis
GH stim by GHRH and in turn stims IGF 1
GH and IGF-1 stim Somatostatin to inhib GH secretion. They also neg feedback on GHRH and GH
Direct effects of GH
Increases IGF-1
Increases lipolysis by adipocytes
Inhibits glucose uptake
Indirect effects of GH
Through IGF 1, Induces skl growth through proliferation of chondrocytes and osteoblast proginator
Increases AA uptake and protein synth
Insulin like activity
Which zone of adrenal gland produces what hormones
ZG - mineralcorticoids (Aldosterone)
ZF - glucocorticoids (cortisol)
ZR - Androgens (DHEA and androstenedione)
Medulla - Epi
Blood flow of adrenal glands
Cortisol is secreted in artery in cortex which then flows to medulla to influence chromaffin cells and therefore epi secretion
Draw Steroidgenic adrenal pathway
On paper
Role of star
Steroidgenic acute regulatory protein transports chol to inner mito membrane to be altered by P450 scc
Actions of ACTH on adrenocorticol cells
Binds to receptor activating cAMP pathway
Increases hydrolysis of chol esters, increases star protein, increases growth and proliferation of ZF and ZR, increases steroidgenic enzymes (LDL-R and p450s)
Biological effects of Cortisol
- Carbohydrate, protein, and fat intermediary metabolism ie increases their blood levels by appropriate mechanisms
- Protective during acute stress: increases raw materials for correct response
- Anti-inflamm and immunosuppressive - via glucocorticoids and blocks all steps in inflamm pathway
- Permissive for other hormones by enhancing their effects
Chromaffin cells
Modified SNS ganglion
Adrenergic receptors
alpha 1 - increases IP3, Ca, and DG
Alpha 2 - decreases cAMP
Beta - Increase cAMP
alpha receptors
Affinity for NE>E, respond to acute stress: vasocons of skin GI kidney, intestinal relax, constricts intestinal sphincters, dilates pupils, piloerection
beta 1 receptors
NE=E affinity, increase heart rate, increase cardiac contraction, increase lipolysis
Beta 2 receptor
E>NE, Intestinal relax, bladder wall relax, airway dilation, glycogenlysis
Synergism
Hormones are often synergistic which increase their effectiveness over the sum
ACTH stim test
Measure effect of adding ACTH, change of cortisol should be over 200. Impaired = adrenal insuff of impaired adrenal glands
Thyroid follicle
responsible for secreting and synth thyroid hormone
C cells
secrete calcitonin
Colloid
glycoprotein = thyroglobulin
TH synth
I pumped in by Na/I cotransporter
I pumped into colloid via pendrin (I/cl) after oxidized by peroxidase
I binds to TG and endocytosed to lysosomal digestion
Regulation of TH
autoreg by lvls of I, low levels of I increases transport into follicular cell
hypo and pit - TRH and TSH
Conversion of T4 to T3
Via 5prime deiodinase in most tissue (also to rT3 which is bio inactive)
Type 2 in pit for neg feedback on TSH
T3 and cell effect mech
THR and Retinoid X = TRE
TH effects
Increases Oxygen consumption and BMR
TH and metabolism
Increases glucose absorb in gut, increases glucose production and oxidation. Increases lipolysis. Catabolic therefore thermogenic.
TH and heart
Increases cardiac output and ventilation
TH and growth
Promotes bone formation and bone maturation
PTH general info
secreted by chief cells of parathyroid and is 84 AA long. Intraglandular degradation is control mech for intact PTH released.
Hypercalcemia and PTH
decreases intact PTH and favors C-term fragments
Hypocalcemia and PTH
Increases intact PTH and decreases C-term fragments
PTH and Ca sensing control
Secretion is controlled by ca-sensing receptors. Decreased Ca increases PTH secretion.
If calcium is high, G proteins activated by sensor to: inhibit PKA (decreases secretion), increase PLC to IP3 which along with activation of intracell Ca pore leads to more cleavage and decreased secretion.
Effect of PTH
- Increases Renal reabsorb of Ca
- Increases bone calcium mobilization
- Increases kidney activation of Vit D leading to increased Ca absorb in intestines
Actions of Vit D on bone
Acts synergistically with PTH to promote bone mobilization and has indirect stim effects on bone mineralization
Actions of Vit D on parathyroid gland
Feedback suppresion of PTH release
Modulates chief cell response to Ca and Vit D
Actions of Vit D on Kidney
Stimulates synth of calbindin for intestinal Ca grab
Neg feedback on 25-hydroxycholecalciferol to 1,25 dihydroxy …
Nuclear action of D3
Binds VDR in nucleus which dimerizes with RXR with CoA to attach to response element leading to transcription complex
Cells of endocrine pancreas
beta cells = insulin
alpha cells = glucagon
Both go through pancreatic vein to liver to hepatic vein to elicit responses
Actions of Insulin and glucagon
Insulin activated by high plasma glucose
Glucagon by low plasma glucose
Norm glucose is 70-110
Mechanism of Ins Sec
Glucose binds to Glut 2 on beta cells. Glucose enters cell and is oxidized to ATP closing K channels leading to depol of beta cells. Depol opens Ca channels leading to Insulin secretion
Incretin and insulin
GLP-1 Incretni activates Gs protein leading to camp to PKA to insulin secretion, similar to alpha 2 induction of insulin
Blocked by epi
AA and endocrine pancreas
AA activates both insulin and glucagon pathways so blood glucose stays normal but insulin still promotes AA uptake
Insulin and Skl M and Adipocytes
Insulin recruits Glut 4 uptake of glucose in these cells
ADH origin
Originates in supraoptic nuclei of hypo
Factors that increase ADH
Increased serum osmolarity, volume contraction, pain, nausea, hypoglycemia, nicotine
ADH role
Increases water permeability of late distal tubule and collecting duct so more water reabsorption
Constricts vascular smooth muscle
Control of ADH secretion
Hypothalmic osmoreceptors react to osmolarity greater than 280 mOsm
Atrial stretch receptors react to decreased stretch due to low blood volume
Carotid and aortic baroreceptors react to decreased blood pressure
All work to synth ADH and its effect on collecting duct epi
