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How are does an endocrine organ communicate with it's target organ?
- -ductless, no direct anatomic connection between endocrine and target organs
- -secretes hormones into interstitial space, then to IVF
- -circulates to target organ
What is the major purpose of the endocrine system?
coordinates and organizes cellular activity and organ function to maintain a constant interval environment
What are characteristics of hormone receptors?
How do we know what organs a hormone will affect?
- -target organs have receptors
- -if there's no receptor, there will be no response
organ that shows a biological response when the hormone binds to a receptor on it
chemical released from a cell that exerts a biological effect
3 major classifications of hormones
- 1) proteins
- 2) steroids
- 3) amines
- -most hormones
- -made up of amino acids bound together
- ->100 AA = protein
- -<100 AA = peptide
- -GH, TSH, ACTH, ADH
- -derived from cholesterol
- -usually not stored
- -ex: cortisol and aldosterone
- -synthesized from AA tyrosine
- -ex: catecholamines, TSH, dopamine
types of chemical messenger systems: neurotransmitters
- -released by axons into synaptic junction
types of chemical messenger systems: endocrine (telecrine)
-hormone released into the circulation and travels to a distant target organ to have an effect
types of chemical messenger systems: neuroendocrine
- -hormone secreted by neurons into the circulation
- -circulation takes it to another part of the body to have its effect
- -a NT can have a local or distant effect
types of chemical messenger systems: paracrine
- -hormone released from 1 cell and its effect is produced in a neighboring cell
- -not travelling far
- -could be a different type of cell in the same organ
- -travels in the interstitium to get there
types of chemical messenger systems: autocrine
-hormone affects the same cell that released it
types of chemical messenger systems: cytokine
- -peptides secreted into ECF
- -ex: leptin and interleukin
Examples of immediate onset hormones
epi and NE
Examples of delayed onset hormones
GH and thyroxine
Hormone transport of peptides and catecholamines (water soluble)
- -dissolved in plasma
- -travel in circulation
- -once reach target organ, they diffuse out of the capillaries
- -to individual target cell
- -Fick's Law of diffusion applies here
Hormone transport of steroid and thyroid hormones
- -bound to plasma proteins
- -frequently < 10% is unbound and free
- -bound portion acts as a reservoir and slows clearance
Methods of hormone clearance
- -metabolic destruction by tissues (by an enzyme, ex: epi)
- -binding with tissues
- -excretion into bile by the liver
- -excretion into urine by the kidneys
- -decreased sensitivity and number of receptors
- -may be due to signaling mechanisms or inactivation of a receptor
- -increased sensitivity and number of receptors
- -may be due to a stimulating hormone
What receptors are located on the cell membrane surface?
-protein, peptide, catecholamines
What receptors are located in the cytoplasm?
What receptors are located in the cell nucleus?
3 mechanisms that control hormone release
- 1) neuro control (NT are often the mediators), neuroendocrine
- 2) hormonal control (+ or - feedback)
- 3) nutrient / ion regulation (glucose and insulin, PTH and Ca++ levels)
-hormone release may be by more than 1 of these mechanisms
- -1 hormone influences the release of another
- -ex: TSH secretion (from anterior pituitary) causes thyroxine to be secreted by the thyroid gland
example of negative feedback
- -TSH secretion (from anterior pituitary) causes thyroxine to be secreted by the thyroid gland
- -when thyroxine is present this inhibits the anterior pituitary from secreting more TSH
which is more common + or - feedback
example of positive feedback
- -surge of LH from the stimulation of estrogen, then LH acts on ovaries to stim add’l
- estrogen, this increases LH
- -when appropriate concentration of hormone is reached then negative feedback takes
pancreas major functions- exocrine or endocrine?
- -digestion, metabolism, utilization and storage of energy substrates
- -both exocrine and endocrine
pancreas exocrine function
- -release of pancreatic digestive juices, sodium bicarb, and enzymes (amylase and lipase)
- -drains into pancreatic duct, then into duodenum
2 major tissue types of the pancreas
- -acini (lobules divided by CT), exocrine function
- -islets of langerhans (very vascular and embedded within the acini), endocrine function
pancreatic blood supply
arterial- splenic artery and superior and inferior pancreatic duodenal arteries
venous- portal vein
-SNS, PNS, and sensory
- -retroperitoneal, near the duodenum
- -above naval, slightly left
3 types of pancreatic endocrine cells
- 1) beta- majority (60%), secrete insulin
- 2) alpha- (25% of islet cells), secrete glucagon
- 3) delta- (10%), secrete somatostatin
- -stored form of glucose
- -facilitated by insulin
- -polypeptide hormone
- -increases rate of glucose transport into cells
- -promotes uptake, storage, and use of glucose by the liver
- -most important anabolic hormone
T or F, insulin is related to carb metabolism only?
F, it also plays a role in fat and protein metabolism
Primary target organ of insulin
skeletal muscle (glucose stored here as glycogen)
Insulin half life
Is most insulin protein bound or unbound?
unbound (remember it's a peptide hormone)
What is the brain's only energy source?
How does insulin effect carb metabolism?
- -resting muscle membrane is only slightly permeable to glucose in the absence of insulin
- -glucose is stored as glycogen in the muscle
- -in between meals, when BG falls, glycogen is split back into glucose and released into the blood
After a large meal, when BS is high, what happens?
- -large amounts of insulin are secreted
- -preferential use of glucose by muscle fibers
- -increased rate of glucose transport by 15X
- -excess glucose is stored as glycogen (a glucose polymer)
breakdown of glycogen back into glucose when BG gets too low
What happens when BG falls?
- -decreased insulin secretion by beta cells
- -glycogen synthesis stops
- -glycogen split into glucose (by phosphorylase)
- -glucose diffuses back into the blood
How is the liver involved in controlling BG?
-when glucose is in excess, the liver removes it from the circulation and stores it, then returns it to the blood when BG levels fall between meals
What happens to excess glucose in the liver?
- 1) used for hepatic metabolism
- 2) stored as glycogen
- 3) that beyond what can be used or stored is converted into fatty acids, packaged into triglycerides, and stored as fat
synthesis of glucose from non-carb sources
effects of excess glucose
- 1) converted to FA
- 2) gluconeogenesis is inhibited
Is insulin required for glucose uptake and utilization in the brain?
- No, brain cells are permeable to glucose and can use it without insulin acting as an intermediary
- -however the brain needs glucose and if BG falls too low (<50 mg / dl) CNS symptoms will develop
How does insulin affect fat metabolism?
- -It promotes fat synthesis and storage (inhibits lipase)
- -insulin increases glucose utilization so we don't have to use fat as an energy source
- -FA are synthesized via glycolysis (excess glucose is stored as FA)
Why do diabetics often have arteriosclerosis?
- Due of the effect of lack of insulin on fat metabolism
- -fat can't be stored so it's used for energy
- -FA get converted to cholesterol and triglycerides by the liver
- -enter circulation as lipoproteins
- -these high concentrations seen in DM are responsible for arteriosclerosis
effects of insulin deficiency on fat metabolism
- -fat can't be stored and so is used for energy
- -lipolysis of stored fat (triglycerides)
- -increased cholesterol and phospholipid conc.
- -ketosis and acidosis
effect of insulin on protein metabolism
- -protein synthesis and storage
- -inhibits protein breakdown
- -decreased gluconeogenesis
effect of insulin lack on protein metabolism
- -protein depletion and increased AA in the blood
- -catabolism of protein and increased urea excretion
average daily insulin secretion
50 u / day
when is insulin secretion at it's max?
- -after a meal
- -increases 5-10x after food intake
- -beta cells act as a fuel sensor
insulin metabolism and excretion
- -metabolized in the liver
- -excreted by the kidneys
- -pts with liver and kidney failure may have prolonged effect of insulin and may be at risk for hypoglycemia
normal fasting BG
80-90 mg/ dl
factors that increase insulin secretion
- -an increase in: blood glucose, free fatty acids, blood AA, GI hormones (gastrin, secretin, CCK), glucagon, GH, cortisol
- -activation of: PNS, beta adrenergic
- -insulin rx caused by obesity
- -sulfonyurea drugs
factors that decrease insulin secretion
- -decreased blood glucose
- -alpha adrenergic activity
With a glucose challenge, how is insulin secreted?
- 2 fold
- 1) within 3-5 mins it increases 10 fold, this is from the immediate dumping of preformed insulin from the beta cells of the islets of langerhans. This is not maintained as after 10 mins insulin concentration decreases halfway towards normal
- 2) after 15 mins, insulin concentration rises a second time, reaches a new plateau in 2-3 hours with a greater rate of secretion than the initial phase. Increased secretion results from add'l release of preformed insulin and new insulin production
what happens when BG levels decrease back to normal?
insulin secretion rapidly decreases as well (within 3-5 mins)
where is glucagon secreted from?
what kind of hormone is glucagon
what effects does glucagon have?
- -opposite insulin's effects
- -release is stimulated by hypoglycemia and inhibited by hyperglycemia
- -increases BG concentration by glycogenolysis and gluconeogenesis
where is somatostatin secreted from?
delta cells of islets of langerhans
what kind of hormone is somatostatin?
polypeptide made up of 14 AA
what stimulates secretion of somatostatin?
- -increased BG
- -increased AA
- -increased FA
- -increased GI hormones
main role of somatostatin
increases the length of time that food is in the GI tract and prevents rapid exhaustion of food nutrients
what organ acts as a buffer for glucose control?
- the liver
- -after a meal excess glucose is stored in the liver as glycogen
- -breaks down glycogen into glucose with hypoglycemia
- -reduces BG fluctuations by 1/3 and helps to maintain tight control
what effect does epi have on carb and fat metabolism?
It will cause glycogenolysis (increase BG levels) and lipolysis (increased levels of FA), leading to both an increase in glucose and FA utilization
what happens if there is a high level of glucose in the ECF?
- -cellular dehydration as glucose exerts a high osmotic pressure, water is drawn out of the cells into ECF by osmosis to try to normalize
- -osmotic diuresis
- -organ damage (DM pts)
type 1 DM
- -lack of insulin secretion due to beta cell destruction (viral or autoimmune)
- -5-10% of DM cases
- -juvenile onset
- -abrupt onset
type 1 DM patho
- -glucose can't enter the cell due to lack of insulin secretion
- -glucose accumulates in IVF, causing increased osmolarity, increased glucose level in urine and blood
- -polyuria (osmotic diuresis)
- -cells can't use glucose so proteolysis and lipolysis are stimulated
- -AA and FA levels increase exceeding the liver's ability to metabolize them
- -result is metabolic acidosis
type 1 DM s/sx
- increased BG
- increased fat utilization
- protein depletion
type 1 DM diagnosis
- FBS> 120 mg /dl
- random BG > 200 mg /dl
- glycosuria (> 180 mg/ dl)
what does a FBS of 100-125 mg/ dl indicate?
T or F, the duration and degree of abnormal BG levels correlate with tissue injury associated with DM?
T! Exact mechanism unknown.
What type of tissue injury can result from chronically high BG levels?
- -BV abnormalities, increased risk of MI, PVD, CVA, ESRD, retinopathy
- -neuropathy (peripheral or autonomic)
- -increased fat utilization leading to metabolic acidosis
- -depletion of body proteins leading to tissue wasting
type 2 DM
- -insulin rx
- -increased insulin secretion
- -inadequate response of beta cells in response to glucose and decreased responsiveness of tissues to insulin
- -90-95% of cases
- -gradual onset
- -obesity is an important risk factor
- -associated with metabolic syndrome
in type 2 DM is the up or down regulation of insulin receptors?
down regulation, the receptors are less sensitive to insulin
DM goals of therapy
- -glucose control
- -prevent end organ damage
- -tight glycemic control delays onset of complications (esp microvascular)
What does Ha1C tell us
- -reflects past 2-3 months of glucose control
- -evaluates effectiveness current treatment
- -glycosylated Hgb, glucose binds covalently to Hgb and stays attached for the life of the RBC which is about 120 days
- non diabetic < 6%
- goal of therapy < 7.5%
- poor control 9%
- -elevated BG
- -more common in DM1
- -+ ketones in urine or blood
- -hyperventilation, (respiratory compensation for metabolic acidosis- try to blow off excess CO2)
- -abd pain
- -altered MS
- -replace volume with 1-2L, then 200-500 ml / hr of NS
- -correct BG with insulin
- -pt will likely need K+
Why do we want to avoid LR in DKA? What type of solution should be use
- -Avoid LR because lactate can be converted to glucose
- -Choose isotonic solutions
With DKA how quickly do we want to decrease the BG? How much insulin do we give to do this?
- -Goal is to decrease BG by 75-100 mg/dl / hr or by 10%
- -Usually give insulin 10 u / hr or 0.1 u/ kg
What is hyperosmolar nonketotic coma
- -AKA hyperglycemia hyperosmolar state (HHS)
- -there's enough insulin that ketone bodies aren't formed, but still get a hyperosmolar situation (dehydration)
- -can cause RF, lactic acidosis, and vascular thrombosis
- -osm > 360 mosm/L
- -MS changes and possible seizures
- -no ketosis
- BG often >600 mg/ dl
What BG level is considered hypoglycemia?
<50 mg /dl
- -due to increased catecholamine release
- -some s/sx may be masked by GA
Each ml of D50 increased BG by ___ mg / dl (for a 70 kg pt)
- -can occur in DM 1 or 2
- -affects CV, GI, and GU systems as all are innervated by the ANS
- -present in 20-40% of all pts with DM1
- -will see large fluctuations in BP as they can't compensate for changes in IV volume
autonomic neuropathy- CV effects
-CV effects include resting tachycardia, orthostatic hypotension, decreased HR response to both BB and atropine, HTN
autonomic neuropathy- GI effects
- -gastroparesis (aspiration risk)
- -occurs in 20-30% of all DM pts
autonomic neuropathy- GU effects
- -nephropathy is the complication associated with highest mortality (40-50% of diabetics)
- -micro or macro albuminuria may preceed steady decline in renal function
macrovascular complications of DM
microvascular complications of DM
Stiff joint syndrome- anesthesia implications
- -limited atlantooccipital ROM
- -30-40% of diabetics
What types of surgical procedures would alert us that the pt is likely a diabetic?
- -vascular procedures (amputations, aorta, carotid, CABG)
- -need for HD access
- -renal or pancreas transplant
- -retina surgery
Anesthesia goal BG
120-180 mg/ dl
T or F, inflammatory mediators occurring peri-op can contribute to insulin rx and the
degree of insulin rx is directly r/t degree of surgical trauma
anesthesia implications of DM pre-op
- -how long has pt been diabetic
- -degree of control
- -end organ damage
- -tumor on the islet of langerhans causes increased insulin secretion
- -some may be malignant (10-15%) and metastasize
- -pts may require huge amounts of IV glucose
Insulinoma: effects of hypoglycemia BG= 50-70 mg /dl?
20-50 mg / dl
- 50-70 mg/ dl= CNS excitation
- 20-50 mg/ dl= clonic seizures and LOC
Anesthesia management of insulinoma
- -maintain normal BG
- -q15 min BG
- -IV solutions with glucose
- -minimum glucose requirement for transport across BBB varies (some pts may adapt to BG level of 40 mg/dl and be able to maintain CNS function)
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