Pancreas plays a key role in...?

a. digestion

b. metabolism

c.utilization of energy substrates

d. storage of energy substrate

Pancreatic duct

Hepatic duct

Cystic duct

(Discuss later:  gallbladder, liver and common bile duct procedures)

1. Alpha cells secrete glucagon

2. Beta cells which account for the LARGEST number in the islets and secrete insulin

3. Delta cells secrete somatostatin

4. PP cells:  secrete Pancreatic Polypeptide_?what it does

Somatostatin

(actually 6 forms in humans with unique receptors they attach to; secreted in the stomach, intestine, brain, delta cells of pancreas)

What hormone plays a role in regulating GI function by restraining (or INHIBITING) the rate at which nutrients are digested and absorbed?

Active; preproinsulin (insulin is translated by the ribosome)

and

proinsulin (endoplasmic reticulum has cleaved insulin)

are physiologically INACTIVE forms of insulin

• Cells increase their uptake of glucose (especially in muscle and adipose tissue)-when transported into BUT not used, muscle stores glucose as glycogen.  Glucose is also stored as glycogen in the liver (glycogenesis)-DOES NOT OCCUR in BRAIN and neuron tissue!
• Cell membrane becomes more permeable to amino acids and potassium transport into the cell-
• Insulin inhibits catabolism of proteins-FAVORS the formation of new proteins and muscle growth
• INSUFFICIENT insulin causes lypolysis to occur where FAT becomes the primary source of energy-BREAKDOWN OF FATTY ACIDS produces acetoacetic acid (broken down into acetone and beta hydroxybutyric acid-FRUITY SMELL on breath during DKA) i.e. the KETONE bodies
• Impacts ion transport pumps (Na/K/ATPase pump increases its activity causing K+ to be pumped INTO the cell)
• Phosphorylation of many other enzyme reactions (metabolism)

• Increase in plasma glucose
• Increase in plasma amino acids
• GI hormones (gastrin, secretin, cholesystokinin and gastric inhibitory peptide)
• Other hormones (growth hormone, cortisol, estrogen, progesterone and glucagon)
• Sympathetic BETA 2 AGONISTS (epinephrine increases plasma glucose by stimulating BETA 2 AGONIST receptors on the liver and adipose tissue when SNS is excited-Inc BS levels on Epi gtts)

• Secreted by alpha cells
• OPPOSITE action of insulin
• Works in concert with epinephrine, cortisol and growth hormone
• Increases blood sugar concentration
• Causes glycogenolysis (breakdown of glycogen in liver) freeing glucose, freeing fatty acids and inhibiting the storage of triglycerides
• Increases blood flow through the kidneys
• Inhibits gastric acid secretion

Positive inotropic effects

• "Starvation in a sea of food"
• BS Fasting>125mg/dl or random>200mg/dl
• HbA1C-6.5% or greater (more exposure, more glucose attaches to hgb)
• incidence on the rise (elderly, obesity and sedentary lifestyle)

Diabetes Mellitus-impaired carbohydrate, fat and protein metabolism due to lack of insulin secretion or insulin resistance

• Juvenile onset
• Insulin dependent
• Lack of insulin secretion
• Viral or autoimmune-destroys beta cells of islet (can be familial)
• Rapid onset-age 14 yo
• S+S=fatigue, weight loss, polyuria, polydispia, intravascular dehydration, ketoacidosis (SEVERE insulin deficiency-SICK)

• 90% of all diabetic cases
• Non-insulin dependent
• Insulin resistance
• Often occuring gradually after age 30 yo (but obesity can cause earlier diagnosis)
• S+S=hyerinsulinemia, pancreas 'burns out', not enough insulin produced-transition from oral meds to insulin dependency

• Obesity (belly fat)
• Hyperglycemia
• Lipid abnormalities (inc. triglyc, LDL, dec HDL)
• HTN

• Polycystic ovarian syndrome
• Glucocorticoids (Cushing's)
• Steroid administration
• Growth Hormone (Acromegaly)

• Decrease glucose uptake into cells (high serum levels)
• Spilling of glucose in urine (tmax occurs at 180-200mg/dl in the PCT-proximal convuluted renal tubule)
• Glucosuria (hyperosmolar) produces water loss (polyuria) and dehydration and thrist (polydypsia)
• Cells switch to fat (atherosclerotic and angiopathic changes) and protein metabolism (muscle wasting and fatigue) to survive; extreme hunger (polyphagia) in an attempt to replace amino acids

• Thrombotic lesions (arterial thrombotic lesions distributed through extremeties, kidneys, eyes, muscle, myocardium, and nervous system):  MICROVASCULAR vs. MACROVASCULAR

• Heart disease (70% of diabetics have HTN; 2-4x greater risk for stroke)

• Vascular complications (Diabetics 17x more likely to suffer gangrene-VERY common in OR)

• Blindness (25x more likely in diabetics)

• ESRD

• Neuropathy (occurs in 50% of all diabetics; impacts PERIPHERAL and AUTONOMIC NERVOUS SYSTEM!)

Vagal denervation occurs early and manifests as tachycardia, dysrhythmias, and loss of heart rate variability seen with DB. 

Orothostatic hypotension is d/t autonomic neuropathy as a result of the SNS loss of vasoconstrictive capability; pt.'s have postural syncope, dizziness, and lightheadedness

MI

(WANT A 12 LEAD ASAP)

1. Lethargy and seizures (brain not getting enough glucose
2. Ketone bodies in urine (fat breakdown=acetoacetate and B-hydroxybutyricate
3. Tachypnea (to correct metabolic acidosis)
4. N/V and SEVERE dehydration
5. May present with very high serum K+; as corrected...significant hypokalemia!

Anion

Metabolic

? cancel case

or

possibility of DKA occuring in the OR (treatment:  fluids, IV insulin, tx anion gap)

• Routine tests (HgbA1C, CXR, 12 lead, lytes, BUN/Cr, etc.) RISK FOR SILENT MI
• Significance of autonomic neuropathy and anesthesia (Diabetics with HTN have 50% chance of having diabetic autonomic neuropathy-INTRAOPERATIVE, post induction HYPOtension especially if on ACE inhibitors)
• Gastroparesis-risk for aspiration
• Renal dysfunction-Renal profile
• Immobilization of joints (Prayer sign)-Glycosylation of tissue proteins produces stiff joints.  IMPLICATIONS:  Limited temporomandibular joint and cervical spine movement=difficult intubation
• Oral antihyperglycemic meds (Gl- names have LONG 1/2 lives and are discontinued 24-48 hours before surgery
• Insulin therapy during their hospitalization

HYPOVOLEMIA (Also, consider: 

glucophage+NPO+IV contrast dye=RF)

Want to HYDRATE and monitor Renal profiles

Vagal denervation leads to:

• Tachycardia
• Arrhythmias
• Loss of heart:lung variability
• Delayed gastric emptying

• Orthostatic hypotension
• Dizziness
• Lightheadedness

• Goal BS<180mg/dl
• Specialty case considerations (neuro and ischemic heart cases-glucose extends the pnumbra which is the area of tissue that is in trouble but still salvageable)
• Pregnancy must have good sugar control to improve fetal outcome
• Poor insulin SQ uptake in the OR (hypothermia); GIVE IV INSULIN
• 1/2 dose patient regimen

KNOW:  1 unit of REGULAR insulin will decrease the plasma glucose by 25-30 mg/dl

Continuous Infusion:  1 unit/ml (100ml bag contains 100 units); Start infusion at 0.1units/kg/h

Quick & Dirty:  Units per Hour=Plasma Glucose (mg/dl)

                                          150

Onset, Peak Action, Duration

• Lispro (10-20min, 30-90min, 4-6hrs)
• Regular (15-30min, 1-3hrs, 5-7hrs)
• Semilente, Semitard (30-60min, 4-6hrs, 12-16hrs)

Intermediate-Acting Insulins

Lente, Lentard, NPH

Onset-2 to 4 h

Peak Action (TIME TO RECHECK in OR)-8 to 10h

Duration-18 to 24h

Ultralente, Glargine, Insulatard

Onset-4 to 5 h

Peak Action (TIME TO RECHECK in OR)-8 to 14h

Duration-25 to 36h

1. Peak action of insulin administered
2. Amount of insulin administered

Protamine

HAVE backup meds ready to treat anaphylaxis (Epi, benadryl, pepcid, steroids, etc...)

(Small test dose should be administered-1mg slowly and close monitoring of blood pressure as well as other signs of anaphylaxis)

Diabetic patients are at such high risk of suffering from autonomic neuropathy (or the anesthetist is HIGHLY suspicious)...ALWAYS monitor (3 vs. 5) lead? (choose one)

• Some practitioners determine "risk of aspiration" based on:

1. How long diabetic condition has existed
2. Insulin vs. non-insulin dependence
3. Other autonomic neuropathy symptoms

Bicitra-nonparticulate antacid

Reglan-prokinetic; increase GI motility

Why is ESRD a complicating factor when considering RSI?

Diaphoresis with tachycardia

(A vigilant provider should be suspicious and check blood sugar to rule out hypoglycemia as the cause)