Endocrine Lecture 1 Diabetes

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cmatthews
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Endocrine Lecture 1 Diabetes
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2013-09-09 21:48:18
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BC CRNA PV3 Endocrine Lecture
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Endocrine Lecture 1 Diabetes
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  1. __% of USA population has diabetes
    7
  2. Type 1 is the result of ______ and accounts for ______%  of cases of diabetes
    beta cell destruction; 5-10
  3. Which type of diabetes is more common in young people?
    Type 1
  4. What can cause the beta cell destruction seen in type 1 diabetes?
    Beta cell destruction itself can occur from some sort of viral syndrome or autoimmune process. Also a hereditary factor in terms of susceptibility (even in absence of autoimmune or viral disorder)
  5. What is the pathophysiology of type 1 diabetes?
    • Dehydration
    • ICF: 2° increased
    • ECF osmolarityECF: 2° osmotic diuresis

    • Glucose accumulates in IVF,↑osmoloarity, ↑ glucose in urine & blood.
    • Polyuria (osmotic diuresis)
    • Cells can’t utilize glucose,so starved, stimulates a hunger (polyphagia) , also stimulate lipolysis and proteolysis (breakdown of lipids and proteins) in order to get nutrition in place of glucose we can’t utilize. So FA levels will increase, AA levels will increase, exceeding livers ability to metabolite them. This is where we get the metabolic acidosis.
  6. S/S of DM type 1
    • Increased BS
    • Increased fat utilization
    • Protein depletion
    • Polydipsia, polyuria, polyphagia
  7. How is the diagonsis of DM type 1 made?
    • Fasting BS level (greater than 120mg/dL)
    • Or random BS more than 200mg/dL
    • Glycosuria (normal threshold is 180 mg/dl)
    • (Fasting level 100-125mg/dL is considered to be pre-diabetic)
  8. Long term DM causes tissue injury from chronically high BS levels. What types of tissue injuries are common?
    • Blood vessel abnormalities
    • ↑ risk of MI, CVA, ESRD, retinopathy, PVD
    • Neuropathy (Peripheral& Autonomic)
  9. What happens due to the increased fat utilization in Type 1 DM?
    • acidoisis
    • Ketoacids get released because of the shift to fat metabolism. Again, acetoacetic acid, beta-hydroxybutyric acid, get released into the plasma faster than can be oxidized by the tissues. And so as those acids accumulate the patient develops a metabolic acidosis. Couple the severe acidosis w/severe dehydration (because of osmotic diuresis) = diabetic coma and potential death if untreated.
  10. Why do we see tissue wasting in Type 1 DM?
    From depletion of body proteins
  11. 90-95% of all cases of DM are type 1 or 2?
    Type 2, MUCH MORE COMMON
  12. Which type of diabetes has a gradual onset, type 1 or type 2?
    Type 2

    Gradual onset after age 30 (“Adult Onset”)
  13. What is the MOST important risk factor for diabetes?
    obesity
  14. In a nut shell, what is the pathophysiology behind type 2 diabetes?
    • Insulin resistance
    • Increased insulin secretion
    • “Metabolic syndrome"
  15. Does Type 2 diabetes usually lead to ketoacidosis?
    No, patient develops hyperglycemia but rarely does it lead to ketoacidosis
  16. Syndrome X (or metabolic syndrome or insulin resistant syndrome) is characterized by...
    HTN, atherosclerosis, and central obesity
  17. Type 1 diabetes has beta cell destruction. what happens in type 2?
    • Inadequate response of beta cells to glucose. This causes an increase in beta cell mass and a decrease in responsiveness of the tissues to insulin.
    • Patients will frequently secrete normal amounts of insulin when fasting but just can’t respond to a glucose load or a meal (so they only secrete say 70% of normal in response to meal
  18. What is the etiology at cellular level of DM Type 2?
    • Abnormalities of glucose transport across the membrane, or abnormality of insulin synthesis of the beta cells.
    • Could involved the processing of insulin (storage and secretion).
    • All different areas along the pathway could be effected
  19. In type 2 DM, we see a delayed acute insulin response to glucose. What does this mean?
    • ↑ plasma glucose level.
    • There is a second phase hyperinsulinemia. Because of this, we get down regulation of insulin receptors, so there is a decreased sensitivity and insulin resistance.
    • The actual insulin resistance may precede the onset of diabetes by several years. Ultimately the beta cells then fail, an the combination of insulin resistance, impaired glucose tolerance, the fact the beta cells aren’t really functioning will characterize type 2 diabetes
  20. How is exercise a treatment for Type 2 diabetes?
    Exercise may decrease insulin resistance as a method of treatment
  21. Describe Metabolic syndrome
    • Obesity, insulin resistance, fasting hyperglycemia, hypertension, and increased triglycerides and LDL
    • CV disease is major adverse consequence
    • But the duration and severity of hyperglycemia leads to tissue damage of all types.
  22. What are the goals of therapy for treatment of DM type 2?
    • Glucose control
    • Prevention & assessment of end organ damage
  23. How is the HbA1C useful in monitoring?
    • Glycosylated Hb is hemoglobin in which glucose is bound.
    • Bound covalently, reflects the last 2-3M of control because the glucose will stay attached to Hb for the life of the RBC.
    • Gives idea of effectiveness of tx.
  24. The HbA1C levels for Non diabetic is <__, goal of therapy is <__,  and __% reflects poor control.
    Non diabetic is <6, goal of therapy is <7.5, and 9% reflects poor control.
  25. Name 3 types of oral hypoglycemics
    • Sulfonylureas
    • Biguanides
    • Glycoside inhibitors
  26. DKA is a life threatening acute complication! Name the S/S and Tx
    • Dyspnea, hyperventilation (to blow of CO2 to compensate for met. acidosis), abdominal pain, N/V, changes in sensorium (up to and including coma)
    • 1st order in tx: correct volume with 1-2L, followed by 200-500ml/hr of NS. Think in terms of type of crystalloid.
    • 2. Correct BS by giving insulin. If we’re giving insulin, we may need to give some K+.
    • You can give 10units of insulin/hr or 0.1units/kg/hr (for 70kg = 7 u/hr)
  27. Why don't we use LR in correcting DKA?
    Lactate can get converted to glucose, also has K+ in it. So want NS is the isotonic fluid to correct it
  28. For DKA, the goal is to
    Goal is to decrease BS by 75-100mg/dL/hr or by about 10%.
  29. What is Hyperosmolar non-ketotic coma?
    There is enough insulin available so ketone bodies aren’t formed but still get dehydration. The osmolarity is often greater than 360osm/L.
  30. Hyperosmolar non-ketotic coma, what are the S/S and treatment?
    • The dehydration alone can lead to renal failure, lactic acidosis, and will predispose to vascular thrombosis. Mental status changes and seizures can occur.
    • The other thing is that, each 100mg/dL of increasing glucose level will decrease serum sodium by 1.6mEq/L.
    • Tx for this is fluid resuscitation: small doses of insulin and K+ to along with it.
  31. What is hypoglycemia defined as?
    Defined as a BS <50mg/dL.
  32. Hypoglycemia: name the cause, S/S, and treatment
    • excess insulin relative to CHO intake
    • s/s: because of increase catecholamine release. Diaphoresis, tachycardia, HTN, anxiety, for us this is masked by general anesthesia.
    • Tx: D50 (50% dextrose) each ml will increase blood sugar of 70kg patient by about 2mg/dL.
  33. Neuropathy in diabetes can be peripheral or autonomic. What is our concern w/peripheral neuropathy in the OR?
    • Think about pt we’re putting in positions intraop be careful not to place pressure on anything.
    • The well meaning circulating nurse putting warm water by patients feet, for diabetic pt could be disastrous, this patient could get a burn and not even feel it
  34. Autonomic neuropathy presents in ____% of patients of DM
    • 20-40 (of type 1 diabetes?)
    • Dependent on severity and duration of hyperglycemia (could be poorly controlled type 2)
    • All systems innervated by autonomic NS effected (CV, GI, GU)
  35. Describe the complication of autonomic neuropathy on the CV system?
    • Resting tachycardia.
    • Orthostatic hypotension.
    • Either a decrease or absent beat to beat variability. (normal variability w/respiratory cycle would not happen)
    • In general will have decreased HR response to both BB and atropine.
    • Frequently they will have HTN. May have early satiety, a neurogenic bladder. May have hypoglycemic unawareness.
    • May have sudden death syndrome, sudden to profound bradycardia only responsive to epinephrine (serious lethal manifestation of CV autonomic neuropathy)
  36. The GI system is affected by autonomic neuropathy with gastroparesis. What % of patients are does this occur in? (at risk for aspiration)
    That kind of gastroparesis in these pt occurs in 20-30% of diabetic patients
  37. Diabetic complication associated with highest mortality
    Nephropathy (we think CV but not true!)
  38. Nephropathy occurs in __-__% of diabetic patients.
    40-50
  39. What causes micro or macro albuminuria in DM?
    Decreased GFR and end up w/end stage renal disease. Albuminuria is early finding and will precede the steady decline in renal function.
  40. What is the treatment of neuropathy?
    dialysis and transplant
  41. Vascular disease is a complication of DM. Name the macrovascular and microvascular events.
    • Macrovascular events: CAD, Cerebrovascular disease, & PVD
    • Microvascular disease:Retinopathy & Nephropathy
  42. Describe the retinopathy associated with DM
    • Development w/small micro aneurysms that tend to cluster near the macula (part of eye that focuses on central vision & visual acuity) retina can become ischemic and cause new vessels to proliferate.
    • Sometimes these patients will require some sort of photocoagulation of the leaking blood vessels to try and preserve vision.
  43. What is the incidences of Stiff Joint Syndrome in DM?
    • 30-40%
    • We really care about the antlantoccipital joint and the risk of difficult intubation
  44. What types of surgeries are a RED FLAG for DM?
    • Vascular surgery: Peripheral vascular → amputations, Aorta,  Carotid, & CABG
    • Dialysis access: HD & CAPD
    • Transplant:Renal & Pancreas
    • Retina surgery
  45. What kinds of things are we looking for in the pre-op eval for a patient w/DM?
    • Systems review (co-morbidities, end organ damage)
    • Laboratory data (esp if hx of renal dysfunction)
    • Physical exam
    • (Hx of vascular disease, want to know what systems have been effected and know the fact they may have silent ischemia. Chest pain may not be so helpful of a question.)
  46. Goal of anesthetic management is to maintain a normal BS. We'd like it to be...
    a target glucose of 120-180mg/dL.
  47. What are our concerns of pre-anesthetic management?
    • Hypoglycemia: look specifically at what meds the pt is on for lowering BS. If oral agent we’ll generally hold the oral agent. If insulin, as a rule we’ll have the pt bring insulin the morning of surgery. And frequently the patient (in general most clinicians likely to give ½ of morning dose and start an IV line w/some dextrose in it and monitor as necessary)
    • Sedation: These pt may be very sensitive to sedation. Not the patient we’d give heavy dose of pre-op sedation in holding area and walk away.
  48. Describe induction and airway management of the diabetic managment
    • Risk vs Benefit. Confounding things.
    • At risk for aspiration (gastroparesis) but also have stiff joint syndrome (potential difficult airway) want to check bag/mask but don’t. Thoughtfully weigh the risk benefit ratio for the individual patent
  49. Maintenance of anesthesia requires thought of fluid replacement & Positioning !!!! when should we use caution?
    Caution in renal dysfunction. Think of choice of crystalloid. Want NS as opposed to LR (LR converts in liver to glucose by gluconeogenesis) also K+ so renal function is consideration
  50. Autonomic neuropathy, HTN diabetic have __% likelihood of having it
    • 50%
    • And it ncreases w/age, diabetic for longer than 10 yr, CAD, or on betablockers.
    • Instead of small roller coaster w/induction & laryngoscopy we see big roller coaster ride for these patients can’t compensate for the changes and get post induction hypotension.
  51. American College of Endocrinology recommends what for glycemic control?
    • ICU: Close to 100mg/dl (<180)
    • Intraop: <150mg/dl
    • Periop: non-critically ill 90-130mg/dl
  52. ICU glycemic control from the american diabetic association?
    <110mg/dl
  53. AHA/ACC ICU glycemic control recommendations
    110-180mg/dl
  54. what can cause insulin resistance in the periop period?
    • Insulin secretions can be decreased by the direct effect of anesthesia and insulin resistance can develop post-op.
    • The inflammatory mediators that can occur peri-op will increase catabolic hormones and contribute to insulin resistance.
    • The degree of insulin resistance is directly related to surgical trauma. Will be different for cataract surgery vs AAA repair.
  55. Why are we worried about hyperglycemia? What can it cause?
    • Will impair the ability to fight infection.
    • Also a decrease in NO formation, so impaired vasodilation
  56. Barash says to keep the blood glucose less than..
    180mg/dl
  57. Describe the bolus technique for insulin management of the DM patient
    • Preop: 5% dextrose in water at 1.5 ml/kg/hr + ½ usual am NPH dose
    • Intraop: Regular insulin prn (1 unit of regular insulin given to an adult usually lowers the plasma glucose by 25-30 mg/dl)
    • Postop: same as intraop (?balance of NPH dose depending on ability to eat)
  58. Describe the continuous infusion technique for insulin management of the DM patient
    • Preop/intraop/postop: 5% dextrose in water at 1 ml/kg/hr + regular insulin in units/hour = plasma glucose/150
    • 10-15 units of regular insulin can be added to 1L 5% dextrose in water & infused at a rate of 1 unit/hour/70 kg or can infuse 50 units of regular insulin in 250 NaCl via separate lines for greater flexibility adjusting to above formula.
    • Supplemental potassium may be needed
  59. What does Barash say the standard glucose dose for adult is?
    5-10g/hr, 100-200ml of D5W/hr.
  60. What should we be concerned about regarding NPH?
    • NPH: more at risk for protamine reactions because of protamine.
    • Give test dose of protamine sulfate (1-5mg over 5-10min) before we do the full reversal of Heparin
  61. What is the test dose of Protamine for the DM patient taking NPH?
    1-5mg over 5-10min
  62. What is insulinoma?
    Adenoma of an islet of Langerhans
  63. What % of insulinomas are malignant?
    10 – 15% malignant
  64. What is the major problem with the patient who has insulinoma?
    hyper insulin secretion. Hypoglycemia and insulin shock is the risk
  65. With insulinoma, what happens at the different BS levels?
    • BS 50 – 70 mg/dl – excites the CNS (hallucinations/anxiety)
    • BS 20 – 50 mg/dl – clonic seizures, LOC
  66. What is the treatment for insulinoma?
    IV glucose. Can take a large amount continuously. Particularly in those who have metastases, it can take a lot to control the blood glucose levelGoals for anesthetic management: control BS, maintain normal
  67. What is the anesthetic management for insulinoma?
    • Maintain normal BS?
    • Artificial pancreas
    • Glucometer for q 15 minute BS (administer insulin or glucose as necessary)
    • Glucose in IV solutions
  68. Minimum glucose requirement for glucose transport across blood-brain barrier varies, what does this mean in insulinoma?
    Some people w/insulinoma will adapt to BS of 40, and their CNS will function to ok. Others if drop from 300 to 40 they won’t do as well w/it.

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