diabetes- jurski

What does hyperglycemia cause?

- Glucose increases extracellular osmotic pressure leading to CELLULAR DEHYDRATION - glucose is lost in the urine -GLUCOSURIA causes osmotic diuresis depleting body fluids and electrolytes - it damages blood vessels- VASCULAR INJURY leads to heart attack, stroke, end-stage renal disease, and blindness

What risk factors for diabetes type II are inherited and what risk factors are acquired?

- Insulin resistance is an inherited component of type II diabetes - obesity and sedentary lifestyle are acquired and contributing factors

Describe signs and symptoms of diabetic peripheral neuropathy?

- It is distal symmetric diffuse sensory motor polyneuropathy - Loss of light touch and proprioception, muscle weakness, decreased perception of pain and temp have abnormal and neuropathic pain - ulcers - significant mortality from recurrent infection, fractures, and petitions

What effects does glucagon have on the liver and in the rest of the body?

- It causes breakdown of liver glycogen (each step amplifies the next step so that there is a millionfold amplification of the final response_ - It increases gluconeogenesis in the liver (glucagon causes the liver to take up amino acids and convert them to glucose) - It activates adipose cell lipase which increases fatty acids It's overall effect is that it INCREASES BLOOD GLUCOSE- it breaks down glycogen and increases gluconeogenesis and increases fatty acids is as an energy source

What are the components of metabolic syndrome? What is the major adverse event of metabolic syndrome?

-Obesity -insulin resistance (diminished sensitivity of tissues to insulin) -fasting hyperglycemia -lipid abnormalities -hypertension - the major adverse event of metabolic syndrome is cardiovascular disease

Describe the MOA of SULFONYLUREAS in treating diabetes type II?

-Their target organ is the pancreas -they increase insulin release -they lower hgbA1c by 1% - 2% -They block ATP sensitive K channels to increase secretion of insulin -they are taken with or without food - there are first, second, and third generation drugs with all different duration of action and potency (she said that we did not have to know specifics on each drug) 1ST GEN-orinase (tolbutamide), tolinase (tolazamide), diabinase (chlorpropamide) 2ND GEN- Glucotrol (glipizide), Glucotrol XL (ext release glipizide), Micronase/diabeta ( glyburide), gylnase (micronized glyburide) 3RD GEN- Amaryl (glimepride)

how is insulin made?

-preproinsulin is cleaved to proinsulin- proinsulin is cleaved in the golgi apparatus of the pancreatic beta cells to form connecting peptide (c peptide) (A,B, & C peptide chains) - A & B are connected by disulfide bonds to form insulin. -Insulin and C peptide are packaged together in granules and secreted together in equimolar amounts with a small amount of proinsulin -C peptide binds to membrane structure most likely a G protein

What medications are the first line of treatment for type II diabetes? What are the other medications for type II diabetes? *******

***** Secretagogues - they cause additional release of insulin by the pancreas (SULFONYLUREA-i.e. glipizide; AND MEGLITINIDES i.e. Brandon Others: BUGUANIDES (METFORMIN) - suppress liver glucose production THIAZOLIDIINEDIONES OR GLITAZONES- (AVANDIA, ACTOS) -IMPROVE INSULIN SENSITIVITY a-GLUCOSIDASE INHIBITORS (PRECOSE, GLYSET)- - delay G.I. glucose absorption

What are the six artificial sweeteners that have been tested and approved by the US FDA

Acesulfame potassium aspartame saccharine sucralose Neotame advantame (she has a slide that lists these as FDA approved, and then tells us on another slide that stevia is the only FDA approved artificial sweetener???)

Describe how insulin promotes glucose transport through the fat cells?

-It mostly forms large quantities of glycerol - glycerol combines with fatty acids to make triglycerides - triglycerides are the storage form of fat and adipose cells - a lack of insulin will block the storage

What are the main causes of diabetes type I? What is the most frequent cause?

- Autoimmune disorders (most frequent) - antibodies to beta cells are formed - viral infections - hereditary tendency for beta cell degeneration - it occurs over an extended period exact cause is unknown, triggers include enteral viruses, dietary proteins, drugs, chemicals in genetically susceptible hosts

What is an insulinoma?

- A rare benign tumor - adenoma of islets of Langerhans neckline - primary and metastatic cancers produce tremendous amounts of insulin - affects women in their 50s to 60s more - as is a MENS type I endocrine disorder(versus a MENS type to pheochromocytoma) - these people have a ton of insulin and require a ton of glucose until they can get the tumor resected - the books as they require 1000 g of sugar over 24 hours DX - symptoms of hypoglycemia with fasting - glucose <50 mg/dL with symptoms - relief of symptoms by administration of glucose - extremely high level of insulin while fasting confirms diagnosis GIVE DIAZOXIDE preop to inhibit insulin release TX-resection of the tumor is curative

What are some causes that lead to insulin resistance?

- Obesity/overweight (especially access visceral adiposity) - access glucocorticoids (Cushing's syndrome or steroid therapy) - excess growth hormone (acromegaly) - pregnancy, gestational diabetes - polycystic ovary disease - lipodystrophy (acquired or genetic associated with lipid accumulation in the liver) - autoantibodies to the insulin receptor - mutations of insulin receptor - mutations of the peroxisome proliferators activator receptor y (PARy) - mutations that cause genetic obesity (melanocortin receptor mutations) - hemochromatosis (a hereditary disease that causes tissue iron accumulation)

Describe the preop management of glycemic control?

- PTS ARE TOLD TO TAKE 1/2 OF THEIR INTERMEDIATE ACTING INSULIN ON THE DAY OF SURGERY - ORAL AGENTS ARE HELD - USUALYDOSE OF LANTUS (LONG ACTING ) INSULIN GIVEN - PTS WITH INSULIN PUMP SHOULD BE CONTINUED ON BASAL RATE -check blood sugar - minimal prep for diabetic who has fair glycemic control (fasting 130 - 180 MG/DL) - diabetics with poor glycemic control (fasting >180) may require a BOLUS OF REGULAR insulin for SHORT procedures or a CONTINUOUS INFUSION for LONG procedures - schedule case as early as possible to REDUCE NPO PERIOD - Alice says you don't really need to treat glucose unless it's over 180 to 200

How do you diagnose diabetes type I?

- Random glucose level > 200mg/dL - hemoglobin A1c > 7% - glucosuria above 180 mg/100 ML (threshold) -dehydration causes classic symptoms of polyuria, intracellular and extracellular dehydration, increased thirst - other symptoms :include weight loss, lack of energy, polyphagia, wasting of muscle/ body tissues, blurred vision

Describe how you would give glucagon to a patient? What must you be aware of after you give glucagon?

- Reconstitute with one mL of sterile water Shake file gently until powder is completely dissolved inconsistency is clear - this gives the concentration of 1 mg per mL of glucagon neckline - use immediately after reconstitution - onset varies - usual dose for relaxation of the stomach, duodenal bulbl, duodenum, and small bowel is 0.2 mg - 0.5 mg IV or 1 mg IM - the usual dose to relax the colon is 0.5 mg - 0.75 mg IV and 1 mg - 2 mg IM - You must be aware that it can increase blood glucose level so check it blood sugar

Name some factors that affect glucose readings?

- Sample site - peripheral vasoconstriction - anemia - high or low PaO2 - interference from other sugars or meds - electrolyte abnormality - hyperbilirubinemia - hyperuricemia

How is blood glucose regulated in summary?

- The liver acts as a blood glucose buffer system - insulin and glucagon function as feedback control systems - epi can be released during stress to increase glucose - GH and cortisol increase use of fatty acids

In diabetes type II what are the theories that explain why there is insulin resistance?

- There are fewer receptors in obese versus lean subjects - abnormalities of signaling pathways i.e. receptor activation - impaired signaling may be related to toxic effects of lipid accumulation in tissues (they make insulin they just have insulin resistance for these reasons, not all patients with these issues get diabetes)

How do you generally diagnose diabetes?

- Urine glucose elevated - fasting glucose > 110 indicates diabetes or insulin resistance - plasma insulin - insulin low to nonexistent in type I diabetes, insulin higher than normal after glucose load in type 2 - acetone breath -keto acids in the urine - glucose tolerance test (one GM of glucose per KG of body weight given - if they have a normal pancreas, their glucose will come down in like 2 1/2 hours in their resting glucose is lower. The patient with diabetes, the resting glucose is higher and it takes doubletime for their glucose to come down) - hemoglobin A1c test

explain what happens within seconds of insulin binding to its alpha and beta receptors?

-80% of cells increase uptake, storage, and use of glucose (esp muscle, fat, and liver) (doesn't happen in most neurons in the brain) -vesicles with multiple glucose transport proteins move insulin to the cell membrane and facilitate glucose uptake into the cells -at the same time, the cell also becomes more permeable to entry of amino acids, K ions, and phosphate ions into cells -10-15 ins later, theres a change in activity level of intracellular metabolic enzymes - in hours to days, there is formation of proteins, DNA transcription

What are the goals of therapy for type II diabetes?

-HbA1c < 7% - LDL < 100 -HDL > 40 IN MEN, > 50 IN WOMEN - TIGLYCERIDES < 200 -BP <130/80

Under normal operating conditions (non-diabetic) list whether the following increase or decrease insulin secretion: 1. Fasting 2 .sulfonyurea drugs (glyburide, tolbutamide) 3. Somatostatin 4. Beta-adrenergic simulation 5. Insulin resistance/obesity 6. Alpha adrenergic activity 7. Leptin 8. Increase blood glucose 9. Increased blood free fatty acids (under normal conditions) 10. Gastrointestinal hormones (gastrin, cholecystokinin, secretin, gastric inhibitory peptide) 11. Decreased blood glucose 12. Glucagon, growth hormone, cortisol 13. Parasympathetic stimulation (ach)

1. Decrease 2. Increase 3. Decrease 4. Increase 5. Increase 6. Decrease 7. Decrease 8. Increase 9. Increase 10. Increase 11. Decrease 12. Increase 13. Increase

Describe three things that happen in relation to fat cells when there is insulin deficiency?

1. Decrease insulin activates adipose lipase causing hydrolysis of stored triglycerides - this releases large quantities of fatty acids and glycerol - this reaction occurs within minutes - the first main energy substrate for all tissues except for the brain would be free fatty acids -there would be a big increase in free fatty acids coming out of the fat cells to provide an energy source first - then blood glucose will increase next within 1 to 2 days (per the chart on slide 18 - then acetoacetic acid will increase from days 2-4 (So free fatty acids are used first for energy, then the blood glucose increases and is used, then acetoacetic acid increases and is used) 2. Decreased insulin promotes liver conversion of some fatty acids into phospholipids and cholesterol. They are carried in the blood stream by lipoproteins. High lipid concentrations especially cholesterol, promotes the development of atherosclerosis in diabetics and leads to to heart disease 3. Without insulin, excess fatty acids in the liver produce extreme amounts of acetyl CoA. It's condensed into acetoacetic acid and released into the bloodstream. Lack of insulin depresses utilization of acetoacetic acid in peripheral tissues. This causes a build-up of ketone bodies in the blood (acetoacetic acid plus B - hydroxybutyric acid). Ketosis may occur. Diabetics are at risk of acidosis and coma (fasting state leads to decreased insulin which leads to glucagon release from the pancreas and fatty acid release from fat cells. Both are converted to ketones in the liver via ketogenesis and deposited into the bloodstream putting the diabetic patient at risk for DKA)

In a diabetic coma, described the following are increased or decreased? What are the normal levels and elevated levels? 1. Glucose 2. Keto acid 3. Total cations 4. HCO3 5. Chloride 6. PH 7. Cholesterol

1. Increased - normal glucose 100, in diabetic coma glucose is >400mg/dL 2. Increased, normal is one meq, diabetic, is> 30meq 3. Decreased - normal is 155 Meq, diabetic coma < 130 Meq 4. Decreased - normal 27 mew, diabetic coma < 5 meq 5. Decreased - normal 103 meq, diabetic coma< 90meq 6. Decreased- normal 7.4, diabetic come 6.9 7. Increased - normal 180 mg/dL, diabetic com 360 mg/dL

What are the two key functions of the pancreas?

1. It aids in digestion - secretes enzymes into small intestine to help break down protein, carbohydrates, and fats 2. It regulates metabolism - secretes hormones insulin and glucagon into the bloodstream to maintain proper glucose levels.

Match the characteristic of diabetes with type I or type II or both ? 1. Age of onset usually > 30 years old 2. Body mass low to normal 3. Plasma insulin low or absent 4. Plasma glucagon high/resistant to suppression 5. Plasma glucose increased 6. Insulin sensitivity reduced 7. Therapy equals weight loss, Thiazolidnediones, Metformin, insulin, sufonylureas 8. Age of onset usually <20 years old 9. Body mass obese 10. Plasma insulin normal to high initially 11. Plasma glucagon high, can be suppressed 12. Insulin sensitivity normal 13. Therapy - insulin

1. TYPE II 2. TYPE I 3.TYPE I 4.TYPE II 5. Both 6. TYPE II 7. TYPE II 8.TYPE I 9.TYPE II 10. TYPE II 11.. TYPE I 12.TYPE I 13. TYPE I

how is insulin associated with energy abundance?

1. increased carbs causes increased insulin secretion 2.excess carbs are stored as glycogen in the liver and muscles 3. insulin stimulates additional carbs to be stored as fat in adipose tissue 4. insulin promotes amino acid uptake by cells and conversion of amino acids into protein 5. insulin inhibits the breakdown of proteins already in cells

Plasma glucose is approximately________% higher or lower than whole blood ?

11% higher

What is the average age of onset of diabetes type I?

14 years old

insulin increase the uptake of glucose into the muscle by ______?

15 fold

Glucose test strips disagree_____% of the time?

15% - it's acceptable if it's less than fine 20% variation

When does insulin secretion peak?

1st stage: preformed insulin is released within 3 - 5 minutes 2nd stage preformed insulin and newly synthesized insulin released in 15 minutes - There is an An increase in plasma insulin concentration after a sudden increase in blood glucose to 2 - 3X the normal range. The initial rapid surgeon insulin concentration happens, but then there is a delayed yet higher and continuing increase in concentration beginning with the 2nd stage 15 - 20 minutes later.

an insulin molecule is made up of ______?

2 amino acid chains with a molecular weight of 5808

The quality care of benchmark determined by the joint commission and centers for Medicare and Medicaid say that glucose levels should be <_______ for cardiac operations on postop days 1 and 2?

200

Stevia is __________ times sweeter than sugar?

200-400X (Several hundred times) sweeter than sugar

1 µg per kilogram of glucagon can increase blood glucose concentration by ________% in______ minutes? _

25%, and 20 minutes

During periods of insulin deficiency, what are ketone bodies made of?

Acetoacetic acid and B - hydroxybutyric acid - lack of insulin depresses utilization of acetoacetic acid in peripheral tissues and causes buildup of ketone bodies - ketosis may occur leading to diabetic ketoacidosis and coma

What is the molecular weight of glucagon?

3485 (larger molecular weight polypeptide just like insulin)

Diabetes type II is usually unrecognized and underdiagnosed for how many years?

4 - 7 years

What percentage of the population has type I diabetes?

5 - 10%

Why is it important that no insulin is secreted during the inter-digestive period?

Because if insulin was secreted during this time, the muscles and tissues would get the glucose instead of the brain - in between meals, glucose is used by the brain, see you don't want to have insulin release at this point because then the muscles in the tissues get the glucose and not the brain, retina, and germinal epithelium of the gonads

Agave and honey have ________ grams of carbohydrate per teaspoon and________ calories per teaspoon?

5.3 - 5.7 g of carbohydrate per teaspoon and 21 cal per teaspoon

____% Of patients with diabetes for______ years or longer yet peripheral neuropathy?

50% of patients with diabetes for >25 years or longer Peripheral neuropathy

How long is the pancreas?

6 inches (15 cm)

how long is the half life of insulin?

6 min- it's short

after you eat, what percent of the glucose you ate is stored in the liver?

60% is stored in the liver as glycogen

What is the normal fasting blood glucose? What does it increased to after a meal?

80 - 90 mg/100 mL - it increases to 120 - 140 mg/100 mL after a meal

In diabetes type I, Hyperglycemia occurs when ___________% of beta cell function is lost?

80 - 90% - so it goes unrecognized for a long time, you can't get it back, the beta cell function is gone forever

What percentage of patients with PCOD have diabetes?

80%

within seconds of insulin binding to its receptor (alpha and beta which then open the cells) ________% of cells increase their uptake, storage, and use of glucose, especially muscle , fat, and liver.Where doesn't this occur?

80%, this doesn't occur in most neurons in the brain

Type II diabetes affects______% of all cases of diabetes?

90 - 95% the number of cases is expected to double by 2025

What percentage of diabetics does autonomic neuropathy occur in?

<5% of diabetics

What purpose does losing weight serve in type II diabetics?

A decrease in adiposity or fat or losing weight improves hepatic and peripheral tissue insulin sensitivity, enhances post receptor insulin action, and may possibly increase insulin secretion

Match the cells of the pancreas of their function: A. Acini cells B. Islets of Langerhans cells C. Beta cells D. Alpha cells E. Delta cells F. PP cells G. Beta cells 1. Synthesized insulin 2. Synthesize glucagon 3. Synthesize somatostatin 4. Synthesize pancreatic polypeptide 5. Secrete hormones directly into the bloodstream 6. Secrete bicarb and enzymes that break down proteins (trypsin), carbohydrates (amylase), and fats (lipase, cholesterol esterase, phospholipase) 7. Synthesize Amylin (function unclear)

A. 6 B. 5 C. 1 D. 2 E. 3 F. 4 G. 7

What percentage of total cells to each of these cells make up in the pancreas? What hormones do they produce? A. Beta cells B. Alpha cells C. Delta cells

A. Beta cells 60% - insulin B. Alpha cells - 25% - glucagon C. Delta cells - 10% - somatostatin

When glucose - 6 - phosphate is oxidized to ATP, does the ATP inhibit or enhance ATP - sensitive K channels?

ATP inhibits ATP - sensitive K channels leading to K channels closing and voltage - gated calcium channels opening. This causes an influx of calcium which stimulates vesicles to fuse with the cell membrane leading to insulin being released into the bloodstream by exocytosis

True or false, distal asymmetric diffuse sensory motor polyneuropathy occurs in diabetic peripheral neuropathy?

False, it is distal symmetric diffuse sensorimotor polyneuropathy

All sweeteners except______________ are excreted unchanged in your body?

Aspartame -(it causes diarrhea)

What type of cells make up the majority of the cells in the pancreas? What percentage do they make up?

Beta cells - 60% this is why insulin has such an important role

Describe how insulin is secreted from the pancreas? (I COULD SEE THIS AS AN ESSAY)

Beta cells release insulin in proportion to blood concentrations of glucose - glucose transporters allow glucose into beta cells - glucose is converted to glucose - 6 - phosphate (this is a rate limiting step to slow down the process) - glucose - 6 - phosphate is oxidized to ATP - ATP inhibits ATP - sensitive K channels - K channels close and the voltage - gated calcium channels open - there is an influx of calcium - calcium stimulates vesicles to fuse with the cell membrane - insulin is released into the bloodstream by exocytosis (KNOW THAT CALCIUM CAUSES INSULIN TO BE RELEASED)

What specifically causes insulin to be released?

Calcium

Diabetes causes a shift from ______ metabolism to________ metabolism? What does this lead to?

Carb, fat - this leads to increased release of keto acids - it can cause severe metabolic acidosis - polyuria - may lead to diabetic coma and death - may see rapid, deep breathing to increase exhalation of CO2 - kidneys try to compensate by decreased urine excretion of bicarb and by formation of new bicarb

Describe other random mechanisms of insulin secretion?

Certain amino acids and hormones stimulate insulin secretion - some hormones (such as glucagon, glucose - dependent insulinotropic peptide) - ACH increases intracellular calcium and enhances the effect of glucose - somatostatin and norepinephrine hormones inhibit the release of insulin -sulfonyurea drugs block ATP - sensitive K channels and stimulate insulin secretion in type II diabetics

DKA versus HHS?

DKA - glucose level >300 - precipitated by infection or acute illness 9 comes on suddenly) - more common in type I diabetics - osmotic diuresis with marked hypovolemia - gluconeogenesis and ketogenesis = overproduction of KETO ACIDS - metabolic acidosis - water, K +, phosphorus deficits (values may appear normal) fluid deficit can be 3 - 6 leaders - hyponatremia (due to diuresis from hyperglycemia) -TX-FLUIDS, INSULIN, ELECTROLYTES- large amounts of normal saline, insulin, and electrolyte - loading dose of insulin than infusion -mortality is 5 - 10% HHS - hyperglycemic hyperosmolar syndrome - glucose level >600 (double DKA) - precipitated by an acute illness (same as DKA) - evolves over days to weeks with persistent glycosuric diuresis - polyuria, polydipsia, hypovolemia, hypotension, tachycardia, organ hypoperfusion - hyper osmolarity leads to obtundation /, neckline - metabolic acidosis without ketoacidosis - DIC may occur -TX- FLUIDS INSULIN ELECTROLYTES - fluid resuscitation depends on serum osmolarity (osmolarity >320 = hypOtonic saline, osmolarity <320 = isotonic saline) -insulin bolus than infusion - mortality rate is higher than DKA, it 10 - 15% - increased incidence in African-Americans, Hispanics, and Native Americans

True or false, DKA has a higher mortality rate than HHS?

False, the mortality rate of DKA is 5 - 10% - the mortality rate for HHS is 10 - 15%

What specifically is the issue with the kidneys and diabetic neuropathy? What are the signs and symptoms of this issue? What is the treatment?

Develop glomerulosclerosis, with glomerular basement membrane thickening, arteriosclerosis, and tubulointerstitial disease s/s-HTN, albuminuria, peripheral edema, progressive decrease in glomerular filtration rate tx-HD and maybe eventually transplant

What is the difference between diabetic coma, and hypoglycemic coma ?

Diabetic coma is when you don't have enough insulin and get acidotic (see with type I) Hypoglycemic coma is when there is excess insulin and you forget to eat

True or false, diabetics should not have any carbs in their diet?

False, they should have an almost normal carb diet - this decreases fat metabolism and depresses the high-level of blood glucose

True or false, patients should take all of their intermediate acting insulin on the day of surgery?

False, they should take half of their intermediate acting insulin on the day of surgery

What is the treatment for diabetes type II?

Early stages - - exercise, caloric restriction, weight reduction medications: 1ST LINE TREATMENT IS SECRETAGOGUES THAT CAUSE ADDITIONAL RELEASE OF INSULIN BY THE PANCREAS (SULFONYLUREAS LIKE GLYPIZIDE,; MEGLITINIDES LIKE PRANDIN) BIGUANIDES- (METFORMIN) - SUPPRESS GLUCOSE LIVER PRODUCTION' THIAZOLIDINEDIONES OR GLITAZONES (I,E, AVANDIA, ACTOS) - IMPROVE INSULIN SENSITIVITY A-GLUCOSIDASE INHIBITORS (PRECOSE, GLYSET) - DELAY GI GLUCOSE ABSORPTION LATER STAGES: INSULIN REQUIRED (30% OF TYPE 2 DIABETICS EVENTUALLY TREATED WITH INSULIN)

Describe the early and later stages of prolonged insulin resistance in type II diabetes?

Early stages - moderate hyperglycemia occurs after eating carbs Later stages - beta cells are exhausted or damaged and do not produce enough insulin - hyperglycemia occurs

Where is epi released from and how does it affect energy sources?

Epi is released from the adrenal medulla during periods of stress such as exercise, shock, or anxiety, it increases both plasma glucose and fatty acid concentrations in the blood - use the fatty acids is far greater

True or false, the patient should turn their insulin pump off when there N PO time begins for surgery?

False - insulin pumps should be kept on basal rate for surgery

True or false, HHS is similar to DKA and that they are both hypovolemic , however in DKA they get metabolic acidosis without ketoacidosis

False, and DKA they get metabolic acidosis WITH ketoacidosis

What are the hyperglycemia increasing hormones? Where are they released from?

GH (anterior pituitary) cortisol (adrenal cortex) epi (adrenal cortex) glucagon (alpha cells of the pancreas)

Where is growth hormone secreted from? What stimulates it?? Where is cortisol secreted from? What stimulates its release? How are these two related?

GH is secreted from the anterior pituitary. Cortisol is secreted from the adrenal cortex. Both GH and cortisol are secreted in hypoglycemia. They inhibit cellular use of glucose and promote fat utilization

Where is glucagon released from?

Glucagon is synthesized and released from the alpha cells of the pancreas

What is the only nutrient that can be used by the brain, retina, and germinal epithelium of the gonads for energy?

Glucose

What is the pathophysiological reason for diabetic autonomic neuropathy? What are the signs and symptoms of autonomic neuropathy?

Hyperglycemia affects the autonomic fibers leading to damaged vasoconstrictor fibers, impaired baroreceptor function, and ineffective CV reactivity neckline - these of the patients that have silent MIs and don't know that they are having chest pain - pathos is not completely understood S/S - tachycardia, loss of heart rate variability, heart rate that doesn't respond to exercise, dysrhythmias cause sudden death, silent MIs, orthostatic hypotension, gastroparesis, diarrhea, constipation, altered respiratory reflexes

Where is most of the glucose formed by gluconeogenesis during the inter-digestive period used?

In the brain

How do sulfonylurea drugs affect insulin release? (glyburide, tolbutamide)

In type II diabetics, sulfonyurea drugs block the ATP - K channel - this helps close the channel and leads to opening of the calcium channel which stimulates insulin release - Simply put sulfonylurea drugs stimulate insulin secretion in type II diabetics

What is the treatment for type I diabetes?

Insulin - insulin pumps can deliver a continuous basal rate or a bolus dose at mealtime - dose delivered via a catheter taped into the fatty tissue neckline - the pump is not an artificial pancreas because you still have to monitor your blood sugar, but it helps achieve better control and replaces injections - bolus dosing through a insulin pump most closely mimics the body's normal response of insulin release two meals

What are the different types of insulin? What other treatments are there?

Insulin comes from animal pancreata or human insulin from recombinant DNA REGULAR INSULIN- 3 - 8 hours LONG ACTING INSULIN- contains zinc or protein derivatives, 10 - 48 hours COMBINATION PRODUCTS Almost normal carb diet - this decreases that metabolism and depresses the high level of blood cholesterol lipid-lowering drugs

What happens to protein metabolism during times of insulin deficiency?

Insulin deficiency causes catabolism of proteins, lack of protein synthesis, and a large amount of amino acids in the plasma - amino acids are used for energy or as substrate for gluconeogenesis - degradation of amino acids increases urea excretion

What causes increase in urea excretion in diabetics?

Insulin deficiency causes catabolism of proteins, lack of protein synthesis, and the large amount of amino acids in the plasma. The amino acids are used as energy. Degradation of amino acids leads to increased urea excretion.

What effect does insulin have on adipose cells?

Insulin helps store fat -after a meal you use up what you need, store glycogen in the liver, and then you also store extra glucose in the fat cells -first, extra liver glucose becomes pyruvate then acetyl CoA -excess ions are formed in the citric acid cycle - fatty acids are synthesized and then form triglycerides -they are transported throughout your body by lipoproteins - insulin helps activate an enzyme in adipose tissue that splits triglycerides back into fatty acids - fatty acids are then absorbed by adipose tissue - then they are converted back to triglycerides and stored Long story short is that insulin helps build up the triglycerides to use as energy stores

Does insulin inhibit or encourage the breakdown of that energy?

Insulin inhibits the breakdown of that energy - insulin inhibits lipase from converting triglycerides into fatty acids -So it helps store and at the same time, not use it hopefully when insulin is released, it's using the fresh glucose that you have ingested and not pulling from your fat cells

How does insulin affect protein metabolism?

Insulin promotes protein synthesis - amino acids are transported into tissue cells - this increases translation of mRNA - this increases the rate of transcription of DNA -INSULIN INHIBITS CATABOLISM OF PROTEINS - it depresses gluconeogenesis in the liver thereby conserving amino acids in the protein stores (so it prevents more glycogen from being formed and helps conserve those amino acids from protein)

What is insulin shock?

Insulin shock occurs when blood glucose drops to 50 - 70 mg /100ML - the CNS becomes excited - nervousness, troubles, sweating, hallucinations - if blood glucose 20 - 50 MG/100ML - see clonic seizures and LOC - if blood glucose <20 MG / 100ML- COMA TX-large amounts of glucose, glucagon, epi

Describe in detail microvascular complications associated with diabetes how to slow progression?

Intensive glycemic control delays the onset and slows progression of microvascular complications NEPHROPATHY- - kidneys develop glomerulosclerosis with glomerular basement membrane thickening, arteriosclerosis, and tubulointerstitial disease - characterized by hypertension, albuminuria, peripheral edema, progressive decreasing glomerular filtration rate (eventually need HD AV transplant) - GFR <15 - 20 ML/min leads to hyperkalemia in metabolic acidosis - GFR decreased by hypertension, hyperglycemia, hypercholesterolemia, and microalbuminuria -TX-dialysis or transplant - improved long-term survival with transplant versus dialysis especially if kidney - pancreas transplant done PERIPHERAL NEUROPATHY - 50% of patients with DM >25 years or longer get this (LIKE IN LONGSTANDING TYPE I) -DISTAL SYMMETRIC DIFFUSE SENSORIMOTOR POLYNEUROPATHY - especially sensory deficits (usually distally and hands or feet in symmetric loss of sensation) (called stocking and glove distribution) - loss of light touch proprioception, muscle weakness, Preception of pain - have abnormal sensations, paresthesia, and neuropathic pain - foot ulcers - can get a CHARCOT foot (neuropathy in foot or ankle with loss of sensation which can increase risk of foot injury and deformity) - significant mortality from recurrent infection, fractures, and amputation RETINOPATHY - impairment can range from changes in color vision to blindness - strict glycemic control and blood pressure control can reduce the risk AUTONOMIC NEUROPATHY - damaged visa constrictive fibers (elevated glucose affects the autonomic fibers question Mylan destruction) ,IMPAIRED BARORECEPTOR FXN, and ineffective CV reactivity - these people are at risk for silent MI, they don't know they had chest pain, don't feel it - <5% of diabetics - patho not completely understood - S/S - resting tachycardia, loss of heart rate variability, heart rate that doesn't respond to exercise, dysrhythmias cause sudden death, silent MIs, orthostatic hypotension, gastroparesis (25% of these patients have n/v, early satiety, bloating, epigastric pain), diarrhea, constipation, and altered respiratory reflexes

What is the problem related to fat utilization in diabetes?

It causes large amounts of cholesterol to be released into circulation and cholesterol deposits in arterial walls - untreated diabetes depletes storage of proteins and fats - rapid weight loss - asthenia (abnormal weakness/loss of energy) - polyphagia (excessive hunger or increased appetite ) - wasting of body tissues - death

How is IV glucagon beneficial during a colonoscopy?

It decreases peristalsis

What is the total daily amount and hourly rate of insulin for a 70 kg patient?

KG x 0.3 / 24 70 X 0.3 = 21 UNITS (TOTAL DAILY BASAL DOSE) 21 /24 = 0.875 UNITS PER HOUR

Does insulin deficiency lead to more or less triglycerides being stored in adipose cells?

Less - a lack of insulin will block storage of triglycerides in adipose cells - insulin promotes glucose transport through the fat cell membrane in which it then forms large quantities of glycerol. Glycerol combines with fatty acids to make triglycerides. Triglycerides are the storage form of fat in adipose cells. - When there is decreased insulin the first source used for energy is fatty acids

What is the treatment for type II diabetes?

Lifestyle changes, exercise and caloric restriction/Weight loss, Metformin, sulfonylurea drugs, thiazolidinediones - 30% of patients with type II diabetes are treated with insulin eventually

Describe the tissue injury associated with type I diabetes?

Long-standing type I diabetics are at risk for TISSUE INJURIES due to inadequate blood supply - heart attack, stroke, ESRD, blindness, ischemia, and gangrene of limbs PERIPHERAL NEUROPATHY AUTONOMIC NERVE DYSFUNCTION - elevated BS causes myelin sheath to break down so they get autonomic and peripheral neuropathies IMPAIRED CV REFLEXES, bladder control, decreased sensation in extremities, other peripheral nerve damage HTN secondary to renal injury (basement membrane has issues) ATHEROSCLEROSIS secondary to abnormal lipid metabolism

Describe the characteristics and risks of diabetes type II?

More common - usually occurs after age 30 - disease gradually develops - steady increase in the number of younger individuals today - most important risk factor is obesity (number of obese children age 3 to 5 has increased) - insulin resistance and metabolic syndrome usually precedes development of type II diabetes -DIMINISHED SENSITIVITY OF TISSUE TO INSULIN - impairs carb utilization in storage - increase blood glucose occurs followed by a compensatory increase in insulin secretion (hyperinsulinemia)

What type of sugar has the least amount of carbohydrates and calories?

Powdered sugar - it has 2.5 g of carbohydrate and 10 cal per teaspoon

Describe anesthesia management of a patient with diabetes?

Preop: - check for myocardial ischemia and infarction (stress test if multiple risk factors and poor exercise tolerance) - control hypertension - maintain renal blood flow - avoid nephrotoxins - watch for dysrhythmias and hypotension - may have limited joint mobility (trouble intubating) - check for SCLERODERMA OF DIABETES (firm, Woody, non-pitting edema in shoulders, neck, and upper back at also correlates to joint mobility so they may be a risk for difficult intubation) - check prayer sign (unable to straighten 4th and 5th fingers, incomplete palm print - sign of difficult airway due to joint IMmobility) INTRAOP: - monitor blood sugar closely - TARGET GOAL - KEEP BLOOD SUGAR 150 MG/DL - TREAT BS > 180 MG/DL - one unit of insulin IV lowers blood sugar 25 - 30 MG/DL - insulin infusion rates are higher end CABG surgery, patients on steroids, patients with severe infections, patients on hyper alimentation or vasopressor infusions - if they are on an insulin infusion you're supposed to give carbohydrates to them so add D5 1/2 normal with 20 of KCl at 100 - 150 ML's per hour -it blood sugar is high in the need insulin, give Regular Insulin IV intrAop POSTOP: - target level postop is 110 - 140 (this is what the PowerPoint says, however, Alice said that they are" loosening the blood sugar guideline to <200, so maybe about 150?"

Does the release of insulin turn on and off quickly or slowly?

Quickly (peaks when blood glucose reaches 400 - 600 mg/100ml) - insulin provides a quick transport of glucose into the cells thereby reducing serum glucose levels

Is stevia considered safe as a food additive and tabletop sweetener by the FDA?

REB-A or stevia is generally considered safe as a food additive and tabletop sweetener, this means it is recognized as safe by the FDA and experts have agreed that it is safe for use by the public inappropriate amounts

What stimulates the release of somatostatin and what effect does it have on insulin and blood sugar?

Somatostatin is stimulated by the ingestion of food -IT SUPRESSES SECRETION OF INUSLIN AND GLUCAGON - it decreases the motility of the stomach - it decreases secretion and absorption of the G.I. tract not sure the role of somatostatin but: - it is thought to extend the time during which food nutrients are assimilated into the blood (it keeps the chyme in the stomach longer) - it prevents rapid exhaustion of the food

The somatostatin inhibit or enhance insulin secretion?

Somatostatin inhibits secretion

Do all obese people develop type II diabetes?

Some obese people never developed diabetes because the pancreas produces enough insulin. Other obese people have full-blown diabetes from pancreas being exhausted or damaged by lipid accumulation - they believe that genetic factors play a role in whether or not you got it

Diabetic retinopathy causes changes in color vision and can lead to blindness. How can this be prevented?

Strict glycemic control and blood pressure control reduces the risk

How many grams of carbohydrates per teaspoon and how many calories do sugar and maple syrup have?

Sugar(brown, powdered, raw, and white) and maple syrup have 2.5 - 4.6 g of carbohydrate per teaspoon and 10 - 18 cal

Describe type I and type II diabetes? Which is juvenile diabetes?

TYPE I- too thin - don't make enough insulin, LACK OF INSULIN - insulin-dependent - juvenile diabetes TYPE II- too fat- adult onset they make enough insulin but it doesn't couple with the insulin receptors correctly, there is some reason, genetic or otherwise, that they don't recognize the insulin - a.k.a. decreased sensitivity of target tissue to insulin - INSULIN RESISTANCE Both types: - metabolism of food is altered - increased blood glucose concentration - cell utilization of glucose falls - utilization of fats and proteins increases

In absence of glucose, what do most tissues utilize for energy?

The shift utilization of fats and proteins for energy use and absence of glucose

Describe the relationship between insulin and glucagon?

They work opposite of each other

Do insulin and growth hormone work independently or synergistically?

They work synergistically to promote growth - each is thought to promote cellular uptake of different amino acids - without one or the other insulin and growth hormone do not increase growth (they work synergistically) - when given together they increase growth dramatically

True or false, POC devices measure whole blood but are calibrated to report plasma glucose?

True

True or false, beta cell destruction occurs faster in children than it does in adults ?

True

True or false, oral glycemic agents are held the day of surgery?

True

True or false, treatment for DKA and HHS is similar - give fluids, insulin, and electrolyte?

True

Which type of diabetes is more common?

Type II diabetes

At what glucose level does insulin peak?

When blood glucose concentration reaches 400 - 600 MG/100 ML

When does secretion of glucagon increase? When is glucagon at its highest

When blood glucose is low - after a high protein meal (high concentration of amino acids) neckline - with exhaustive exercise Glucagon is at its highest when blood glucose is at its lowest

Is it better to use whole blood or a fingerstick to check a blood glucose?

Whole blood

What is usually responsible for death in diabetics?

abnormalities of fat metabolism- they die from acidosis of poor arteriosclerosis from impaired fat metabolism

after a meal, how do muscles get their energy?

after a meal, muscle cells preferentially use glucose over fatty acids. a muscle stores 2-3 % concentration of glycogen (good in case of anaerobic crisis)

what causes insulin to be released from the cell?

calcium

what type of metabolism does insulin effect?

carb, fat, and protein metabolism

In diabetics, having a rocker bottomed foot with neuropathy in the foot or ankle is known as______?

charcot foot

between meals is there an increase or a decrease in insulin secretion from the pancreas?

decreased blood glucose causes decreased insulin secretion from the pancreas

resting muscles get their energy from ______?

fatty acids

what happens to insulin and the liver in between meals?

insulin secretion is decreased due to decreased blood glucose levels -liver stops storing glycogen and no further glucose is taken up by the liver -decreased insulin and increased glucagon activates phosphorylates which cleave glycogen (forms glucose phosphate) -glucose phosphatase cleaves glucose phosphate -free glucose enters the blood stream basically btw meals your blood glucose levels fall, insulin secretion should stop, and at that point glucagon is released this causes the breakdown of glycogen in the liver so that (stored from of glucose) is the energy source between meals.

How does insulin attach to its cell receptor? (cell receptors for insulin)

it attaches to the membrane receptor that has 4 subunits. First insulin binds to 2 alpha receptors that are outside the cell . Insulin binding to alpha receptors causes autophosphorylation of beta subunits. Then it binds to 2 beta receptors. This opens the glucose channels and then glucose can go into the cells.

hormones causes changes to cells. what changes does insulin cause?

it facilitates uptake of glucose, K, amino acids, and phosphate into the cell, leads to a change in activity level of intracellular metabolic enzymes, and forms new proteins (DNA transcription)

What does insulin do in the liver?

it increase and decrease several enzymes -it inactivates liver phosphorylase preventing the breakdown of glycogen - it increases the activity of glucokinase whcih temporarily traps glucose in liver cells -itincrease the activity of glycogen synthase which promotes glycogen synthesis the net effect of insulin in the liver is an increase in glycogen, representing 5-6 % of liver mass

how is insulin broken down?

it is degraded by insulinase in the liver, kidneys, and muscle ( she stressed in the liver)

pancreas anatomy

know alice's picture but this is close

Is insulin secreted in bound or unbound form?

unbound

What areas don't require insulin for uptake of glucose into the cells?

most areas in your brain are permeable to glucose and don't require insulin (its the one exception)

during moderate to heavy exercise, how do muscles get their energy?

muscles cells vasodilate because they build up end products of metabolism, and can use glucose without insulin (normally the use it with insulin but with heavy exercise, they don't)

In the absence of insulin, the intracellular glucose concentration remains _________?

near zero, despite high extracellular glucose concentration.

does promote the build up of glycogen stores?

yes

describe what happens after you eat in relation to glucose and insulin ?

you eat-insulin is secreted- carbs are broken down in your gut- excess carbs spread throughout your body to be used as energy- extra carbs are stored as glycogen in the liver- if there are more carbs above that, they are to be stored as fat

What is the primary organ for glucose control in the body?

the liver

how are excess carbs stored?

they are stored as glycogen in the liver, if there are even more, then they are stored as fat