Endocrine ( 10% ) Flashcards
Insulin
- Is secreted by the α cells in the islets of Langerhans.
- Is a triple helical polypeptide.
- Is synthesized as a prohormone
- Binds at cytoplasmic receptor sites
- Causes K to leak out of the cells.
Is synthesized as a prohormone
Pre-proinsulin->proinsulin->insulin
- Is secreted by the beta cells in the islets of Langerhans.
- Is a double helical polypeptide.
- Binds at Cell surface - tyrosine kinase receptor
- Causes K to leak into the cells.
The pancreas
- Does not resemble the salivary glands
- Contains digestive enzymes in α granules
- Secretes 500mL of pancreatic juice/d
- Secretes trypsin which activates phospholipase A2
- Is stimulated by secretin to secrete enzyme rich pancreatic juice which is low in volume
Secretes trypsin which activates phospholipase A2
Resembles salivary glands
Digestive enzymes contained in zymogen granules
Secretes 1500mL of pancreatic juice/day
Secretin stimulates alkaline, watery juice; CCK stimulates low-volume enzyme-rich juice
All of the following increase BSL except
- T4
- Cortisol
- Growth hormone
- Somatostatin
- LH
LH
- Somatostatin inhibits insulin and glucagon secretion*
- GH and glucocorticoids are catabolic for fat*
Which statement is correct
- Serum glucose is increased by glucagon without increasing serum lactate
- Insulin increases glucose entry into the liver by increasing the number of GLUT4 transporter.
- Cortisol increases serum glucose by increasing hepatic glycogenolysis.
- Insulin secretion is inhibited by glucagons
- Glucagon secretion is stimulated by free fatty acids.
Serum glucose is increased by glucagon without increasing serum lactate
- Insulin increases glucose entry into the liver by inducing glucokinase causing an increase in the phosphorylation of glucose, increasing the concentration gradient for diffusion
- GLUT 4 in skeletal muscle and fat (stimulated by insulin)
- GLUT2 in pancreas
- Cortisol increases serum glucose by increasing hepatic gluconeogenesis and export of glucose from hepatocytes
- Insulin secretion is stimulated by glucagons
- Glucagon secretion is inhibited by free fatty acids.
With respect to insulin
- Increases ketone release in muscles.
- Synthesized in A cells.
- Increased cAMP in cell causes release of insulin by exocytosis.
- GLUT2 transporter controls the entry of glucose into the endocrine pancreas
- Increases the conversion of TG to FFA.
GLUT2 transporter controls the entry of glucose into the endocrine pancreas
- Inhibits ketone release in muscles.
- Synthesized in beta cells.
- Increased calcium in cell causes release of insulin by exocytosis.
- Decreases the conversion of TG to FFA.
Concerning the islets of Langerhan
- The B cells make up 90% of the islets
- The D cells secrete the pancreatic polypeptide.
- Beef insulin is structurally more like human insulin than pork insulin
- The release of insulin involves the depolarization of the cell membrane, causing opening of Ca channels
- High K increases the secretion of insulin
The release of insulin involves the depolarization of the cell membrane, causing opening of Ca channels
Glucose enteres cells, generates ATP which inhibitis K channels, causing cellular depolarisation. This causes a calcium influx, which causes exocytosis of granules containing insulin.
- The B cells make up ~75% of the islets
- The F cells secrete the pancreatic polypeptide
- D cells secrete somatostatin
- Hypokalaemia inhibits the secretion of insulin
regarding insulin
- α adrenergic stimulation inhibits insulin secretion
- Theophylline inhibits insulin secretion.
- Insulin has a half life of ~ 30 min in the circulation.
- Insulin inhibits K uptake into muscle and adipose cells
- Somatostatin stimulates insulin secretion.
α adrenergic stimulation inhibits insulin secretion
- Theophylline s**timulates insulin secretion
- Insulin has a half life of ~ 5 min in the circulation (most metabolic hormones are 5-10 mins)
- Insulin stimulates K uptake into muscle and adipose cells
- Which is why you use it in hyperkalaemia
- Somatostatin inhibits insulin secretion
actions of glucocorticoids include all of the following except
- gluconeogenesis in the liver
- maintenance of myocardial contractility
- inhibition of glucose uptake by muscle and adipose tissue
- permissive effect on angiotensin II
- decrease in vascular resistance
decrease in vascular resistance
regarding insulin
- it increases amino acid uptake
- it causes reduced K uptake in cells.
- its absorption is not affected by the site of injection
- it increases protein catabolism
- it is secreted by the α cells in the islets of Langerhan.
it increases amino acid uptake
Increases uptake of glucose, AA, and potassium
- it causes increased K uptake in cells
- its absorption is not affected by the site of injection
- Not specifically noted but almost certainly - different blood flows etc, IM vs SC
- it increases protein synthesis
- it is secreted by the beta cells in the islets of Langerhan
Which does not utilize the same type of receptor in its mechanism of action
- Insulin
- Glucagons
- PTH
- ACTH
- None of the above
Insulin.
Tyrosine kinase. Rest are GPCRs
Insulin secretion is stimulated by all of the following except
- Mannose
- Glucagons
- Noradrenaline.
- Leucine
- Acetylcholine
Noradrenaline.
and adrenaline
Net result is inhibition as the alpha effects overcome the beta effects.
Regarding insulin
- It increases protein catabolism in muscles
- Secretion is inhibited by somatostatin
- Secretion is stimulated by phenytoin
- It causes decreased K uptake into adipose tissue
- It causes decreased protein synthesis
Secretion is inhibited by somatostatin
- It increases protein synthesis in muscles
- Secretion is inhibited by phenytoin
- It causes increased K uptake into adipose tissue
- It causes increased protein synthesis
- Regarding glucagons
- a. It is secreted by the pancreatic B cells
- b. It increases glycogen formation
- c. It has a half life of 30 minutes
- d. Secretion is stimulated by glucose
- e. It stimulates insulin secretion
e. It stimulates insulin secretion
- a. It is secreted by the pancreatic alpha cells
- b. It increases glycogen breakdown
- c. It has a half life of 30 minutes
- probably more like 5-10min
- d. Secretion is inhibited by glucose
- Insulin secretion is stimulated by all of the following EXCEPT:
- a. Mannose
- b. Glucagons
- c. Noradrenaline
- d. Leucine
- e. Acetylcholine
c. Noradrenaline
As with adrenaline, the alpha effects (inhibition) outweigh the beta effects (secretion)
- Insulin
- a. Increases the number of glucose transporters on the cell surface
- b. Regulates intracellular glucose metabolism
a. Increases the number of glucose transporters on the cell surface
- GLUT 4 in skeletal muscle and adipose*
- GLUT 1 and 3 in brain, kidneys, placenta etc does not require insulin to take in glucose*
- GLUT 2 is in the beta cells -> helps regulate insulin secretion*
- Glucose reabsorption by the kidney
- a. Is independent of glucose load
- b. Occurs in the distal convoluted tubule
- c. Involves potassium reabsorption
- d. Occurs through passive diffusion
- e. Occurs through secondary active transport
e. Occurs through secondary active transport
- SGLT Sodium-Glucose co-transporter*
- Occurs in early PCT*
- Insulin
- a. Is synthesized in the Golgi apparatus of beta cells
- b. Is released mostly in its proinsulin form
- c. Has a half-life of 50 minutes
- d. Binds to intracellular receptors
- e. Is mostly degraded in the liver and kidneys
e. Is mostly degraded in the liver and kidneys
(40% kidneys, 60% liver; reversed in exogenous insulin administration)
- a. Is synthesized in the RER of beta cells
- b. Is released mostly in its pre-proinsulin form
- c. Has a half-life of 5 minutes
- d. Binds to cell-surface (tyrosine kinase) receptors
- Insulin secretion is increased by
- a. Thiazide diuretics
- b. Glucagon
- c. Potassium depletion
- d. Adrenaline
- e. Somatostatin
b. Glucagon
- Insulin release
- a. Is inhibited by raised cyclic AMP in pancreatic beta cells
- b. Is not stimulated by blood glucose levels below 6mmol/L
- c. Is increased by beta adrenergic stimulators
- d. Is inhibited by phosphodiesterase inhibitors
- e. Is increased by somatostatin
c. Is increased by beta adrenergic stimulators
with regard to thyroid physiology
- T3 and T4 are metabolized in the spleen and bone marrow.
- T3 and T4 bind and act at the same cell membrane receptor.
- T4 is synthesised from tyrosine held in thyroglobulin
- T3 is bound to a complex polysaccharide in the plasma
- T4 is more active than T3
T4 is synthesised from tyrosine held in thyroglobulin
- T3 and T4 are metabolized in the “Liver, kidneys and other tissues”
- T3 and T4 act at a n**uclear receptor
- T3 is bound to proteins (albumin and TBG) in the plasma.
- T4 is less active than T3
regarding the thyroid hormones in plasma
- glucocorticoids decrease free plasma T4
- concentration of binding proteins are increased in HTN
- oestrogens decrease total plasma T4
- free T3 levels are normal in hyperthyroidism
- plasma TSH is high in hypothyroidism
plasma TSH is high in hypothyroidism
TSH is high to try and stimulate T4 release (except in hypothalamic or pituitary failure)
- glucocorticoids increase free plasma T4
- free T3 levels are high in hyperthyroidism
Under physiological condition most circulating T4 is bound to
- Thyroxine binding prealbumin
- Tramothynetim
- Thyroxine binding globulin
- Α2 globulin
- Iodothyronine
Thyroxine binding globulin
T4: TBG >> TBPA > albumin
T3: Albumin >/= TBG >>> TBPA (1%)
With respect to the thyroid gland which is false
- Serum iodide is passively transported into the colloid
- MIT and DIT are not secreted
- The action of T4 on tissues is faster than T3
- Albumin has the largest capacity to bind T4
- Free T3 and T4 exert a negative feedback effect on both the anterior pituitary and the hypothalamus
The action of T4 on tissues is slower than T3
T3 is less bound, and thus has a shorter half-life, and a more rapid action on tissues
Serum iodide is actively transported into the thyrocytes, but passively diffuses into the colloid
Albumin binds the lowest proportion of T4 (13%), but its concentration is nearly 2000x that of TBG hence its capacity is higher
In the thyroid
- Passage of iodide from the thyroid cells into the colloid is an active process.
- RT3 is inert
- Most T4 is metabolized to T3.
- Thyroglobulin is formed in the colloid.
- Thyroxine binding globulin has the highest capacity to bind thyroid hormones in the plasma.
RT3 is inert
- Passage of iodide from the thyroid cells into the colloid is a passive process.
- Uptake into thyroid is active, but then to colloid is passive
- Most T4 is metabolized to RT3.
- 1/3 metabolised to T3, ½ metabolized to RT3
- Thyroglobulin is Synthesized in thyrocytes and then secreted into colloid
-
Albumin has the highest capacity to bind thyroid hormones in the plasma.
- Ganong states albumin has the highest capacity (as there is much more of it), whilst TBG has the highest affinity and carries the most T4