Diabetes Cases.1 Ppt


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  • Hyperglycemia in type 2 diabetics can be viewed as a continuum of progressive insulin resistance; this pathophysiology underscores the gradual development of increasing insulin resistance (first in muscle cells then in liver cells) with resultant hyperinsulinemia and culminating in beta cell failure and decreasing insulin levels. The stages in Diabetes can be characterized as follows: Stage 1: Normal glucose tolerance; some degree of hyperinsulinism but no evidence of impaired glucose tolerance (HgA1c under 5.5)Stage 2: Impaired glucose tolerance develops when muscles have significant insulin resistance and the raised insulin levels are not enough to bring the glucose to normal after a meal. Since the liver is more sensitive to insulin than muscle, fasting hyperglycemia has not developed (HgA1c= 5.5-6.1).Stage 3: Both muscle and liver demonstrate insulin resistance; the hyperinsulinemia does not prevent the liver from generating glucose in the fasting state and this is reflected in an elevated fasting glucose level (HgA1c = 6.2-7.5).Stage 4: The pancreas is now failing and the insulin levels start to falter. There is both moderately severe fasting hyperglycemia as the liver increases its glucose output as well as poorly controlled Diabetes (HgA1c = 7.6 - 10).Stage 5: The pancreas has overtly failed. The patient has severe fasting as well as severe insulin resistance; oral agents on their own will not correct this hyperglycemia (HgA1c is more than 10).Understanding these stages is important in managing diabetics more effectively. Thus, in a patient who is in stage 4, providing monotherapy is unlikely to work effectively. In such cases, both an insulin secretagogue (to stimulate insulin secretion) as well as an insulin sensitizer (to minimize insulin resistance) is needed to meet the moderately severe hyperglycemia that develops.Approved oral diabetic agents by mechanism of action include: Insulin secretagogues: Sulfonylureas and meglitinidesInsulin sensitizers: Metformin and thiazolidinediones
  • Centralpontinemyelinolysis is a neurologic disease caused by severe damage of the myelin sheath of nerve cells in the brainstem, more precisely in the area termed the pons. It can also occur outside the pons. [1] The term \"osmotic demyelinization syndrome\" is similar to \"centralpontinemyelinolysis\", but also includes areas outside the pons. [2]
  • Diabetes Cases.1 Ppt

    1. 1. Jimmy Santana, MBA, P.A. - C 1 3/13/2009
    2. 2.  A 24-year-old, white female has recently being diagnosed with insulin-dependent diabetes. The disease is being managed on a split dose of 60/40 insulin suspension, which she injects herself at 8:00 a.m. and 5:00 p.m. She was told to call in if she experiences any strange symptoms, which she does this afternoon. At 2:45 p.m. she is not feeling well and notices that her skin is cool and damp. Her hands are shaking and she is very anxious. What do you tell her to do right away, before having somebody take her to your office?  A. Inject 4 IU of her insulin  B. Drink a can of diet soda  C. Drink six ounces of fruit juice  D. Eat a large candy bar  E. Eat a cube of sugar
    3. 3.  The above described symptoms are classical for hypoglycemia. An inexperienced patient needs to be monitored by medical personnel until the blood glucose level is stabilized again. The first priority though is to prevent the blood sugar to drop any further and send the patient into a coma.  A six-ounce drink of fruit juice should be sufficient. Since the symptoms suggest hypoglycemia, injecting insulin would worsen the situation. If in doubt if the patient is hypo- or hyperglycemic and there is no possibility for a test, always give sugar first and see if the patient improves. An increase of a blood glucose level of, for example, 350 is not going to hurt the patient, but lowering a level of 45 is going to send the diabetic into a coma.  Since diet soda contains only sugar substitutes it is not going to influence the blood glucose level. A large candy bar could be eaten too, but it may raise the glucose level higher than required, therefore the fruit juice is a better choice. One cube of sugar is an insufficient amount to raise blood sugar; it will take several cubes.
    4. 4.  A 61-year-old white male presents to your office for the first time. In reviewing his medical records, you note a history of diabetes type 2 onset 4 years ago. He is currently well controlled to normal blood sugars and hemoglobin A1Cs. You do note that his previous blood pressure readings were above normal on multiple visits. In addition to his usual diabetic care, you recommend initiation of drug therapy for his hypertension. Your drug of choice is  A. Calcium channel blocker  B. ACE inhibitor  C. Alpha blocker  D. Thiazide diuretic  E. Beta blocker
    5. 5.  ACE inhibitors have been shown to slow the progress of proteinuria in patients with diabetes. Control of their blood pressure is just as important. Your drug of choice should be an ACE inhibitor for any diabetic with hypertension as long as there are no contraindications to giving them this medicine.
    6. 6. A 55-year-old male is brought into the urgent care center of your hospital by paramedics. He is 3. obtunded, and today his wife could not get him out of bed. He has no significant past medical history. His wife states that he has not been well for the last week, with decreased energy and fatigue. In addition, he has had a productive cough, which has worsened during the last 3 days. Also, according to his wife, he appears to be drinking more water. Physical exam reveals a lethargic male who moves to deep pain but has no intelligible speech. Paramedics have given the patient Narcan with no change in his status but have withheld glucose bolus due to a high dextro stick reading. Vital signs are pulse 115; BP 90/50; respiration 18; Temp 38.2° C (100.7° F) HEENT shows dry mucous membranes. Lungs are clear. Cardiac exam is significant for tachycardia.  Abdominal exam is nonspecific. Neurologic exam shows the patient to be responsive only to pain, with withdrawal. No abnormal reflexes noted. Initial laboratory studies show: Na 118; K 4.2; Cl 97; HCO3 21; Glucose 1050. ABG reveals pH 7.34, pCO2  20; pO2 79; O2 saturation 90%. CBC shows a normal H/H with WBC count of 14K; the serum is reported as very lipemic. Chest X-ray shows an LLL consolidation. The most likely cause for the change in the patient's mental status is A. Acute diabetic ketoacidosis  B. Pseudohyponatremia  C. Pneumococcal pneumonia with hypoxia  D. Hyperglycemic hyperosmolar nonketotic coma  E. Central pontine myelinolysis 
    7. 7.  Hyperglycemic hyperosmolar nonketotic coma (HHNC) represents a syndrome characterized by marked hyperglycemia, hyperosmolarity, and dehydration. It is manifested by decreased mental functioning that may progress to frank coma. Ketosis and acidosis are generally minimal. DKA, acute diabetic ketoacidosis, will have similar electrolyte  abnormalities; however, there will be an associated metabolic acidosis and ketosis. The patient does show pseudohyponatremia, which is due to the presence  of hyperglycemia and hyperlipidemia. In the absence of marked lipemia, the true value for sodium can be approximated by adding 1.3 to 1.6 mEq/L to the sodium value for every 100 mg/dl glucose over the norm. But this is not the cause of this patient's altered sensorium. The patient most likely has pneumococcal pneumonia, which is a  common precipitating factor in the development of HHNC. He is mildly hypoxic, though this does not explain the degree of obtundation seen. Overly aggressive restoration of serum sodium levels in hyponatremic  patients can be associated with central pontine myelinolysis and circulatory overload.
    8. 8.  A 28-year-old type I diabetic on multiple daily insulin injections regimen presents to your office for a follow up visit. She complained to you about her early morning glucose level during her last visit and you recommended for her to chart the numbers and bring it for her next appointment. Her pre- breakfast glucose averaged 285mg/dL; dinnertime was 95mg/dL and 68mg/dL at 3 AM. How will you treat her diabetes?  A. Increase the evening dose of long acting insulin  B. Decrease the evening dose of long acting insulin  C. Decrease the evening dose of short acting insulin  D. Increase the evening dose of short acting insulin  E. Increased activity before bedtime
    9. 9.  Three mechanisms can account for early morning hyperglycemia in patients with diabetes on insulin: 1. Inadequate dose of long acting insulin at night 2. Somogyi effect or rebound hyperglycemia is a condition often seen in type I diabetes, in which there is nocturnal hypoglycemia. The hypoglycemia subsequently stimulates the release of counter regulatory hormones leading to increase of glucose level in the blood. Diagnosis can be made by several plasma glucose analyses done at 2.00 A.M, 3.00 A.M, and 7.00A.M. 3. In the dawn phenomenon, the hyperglycemia is secondary to increased need for insulin in the early morning due to the normal early morning surge of growth hormone, which antagonizes insulin action.  Checking the blood glucose level at 3 AM can help differentiate between Somogyi effect and dawn phenomenon: the level will be low in Somogyi phenomenon. The patient's early morning hyperglycemia is due to Somogyi effect since her 3 AM level was low. Treatment of this will be to decrease the evening dose of long-acting insulin or give bedtime snacks. The treatment of dawn phenomenon involves increasing the evening dose of long-acting insulin.  There is no nocturnal hypoglycemia if the night dose of insulin is inadequate.
    10. 10. A 62-year-old male with a history of diabetes for twenty-five years and hypertension for  ten years is referred to your office by a retired physician. He complains of worsening edema on the right lower extremity during the last two weeks. Vital signs show T 97.8 Pulse 78 RR 20 BP 165/93. Physical examination disclosed periorbital edema and left lower extremity edema 1+ below the knee and right lower extremity edema 3+ below the knee that is nontender to palpation. He denies any fever, chills, or malaise. He is currently on glipizide 20 mg twice a day and amlodipine 10-mg once daily. Laboratory result from two weeks ago shows Na 145, K 4.5, Cl 102, HCO3 25, BUN 14, Creat 1.2, CA 7.2, Glucose 287, HgA1C 8.6, and Albumin 2.5. The U/A test shows 3+ proteins with no WBC or RBC. Question: What is the most appropriate next step in management of his diabetes? A. Start the patient on glyburide  B. Start the patient on insulin therapy  C. There is no indication to change his diabetes therapy. His HgA1C shows that his  diabetes is under control D. Start the patient on metformin  E. Repeat the patient's HgbA1C; result is too old to reflect the current HgbA1C level 
    11. 11.  This patient's diabetes mellitus is poorly managed. Glycosylated hemoglobin (HbA1c) is the best indicator of glycemic control over the previous 3 months. Maintaining an HgA1C of 7 or less lowers the rate of complications of diabetes mellitus. Adding a second class of oral hypoglycemic agent would be the next best choice. Metformin is the drug from the biguanides class; therefore, it is the drug of choice.  Starting the patient on glyburide is incorrect because both glyburide and glipizide belong to the sulfonylurea class. Starting the patient on insulin therapy is incorrect because oral therapy should be maximized before starting on insulin. HgA1c of 8.6 indicates poorly controlled diabetes. There is a need to change his diabetes management. There is no need to repeat HgA1C. Glycosylated hemoglobin (HbA1C) is the best indicator of glycemic control over the previous 3 months. The result is not too old.
    12. 12.  A 38-year-old obese female with type 2 diabetes mellitus presents to your office for follow up visit. Her blood sugar has been well controlled on metformin. She wants to have a baby and wants to know if there is any special thing to do so that her diabetes will not affect her pregnancy. Which of the following is appropriate for her?  A. Switch her to insulin  B. Switch to glyburide  C. Tell her it is not advisable for her to be pregnant because her child will be diabetic  D. Increase the dose of her metformin to prevent worsening of her blood sugar during pregnancy  E. Continue her present treatment and dose
    13. 13.  Diabetic patients that are pregnant or attempting to get pregnant, irrespective of whether they are insulin requiring or not, should be switched to insulin therapy for their glucose control. Oral glucose lowering agents are contraindicated in pregnancy. Although a poor glucose control predisposes to increased maternal and fetal risks, it is not a contraindication to pregnancy. A good glucose control is however necessary prior to and during pregnancy.
    14. 14.  A 24-year old white male present to the flight physician assistant’s office for a routine physical. He has been taking flying lessons and is applying for a pilot’s license. Regulations state that he must have a physical examination.  Examination discloses a thin male, 74 inches, 140 pounds. Generally, the exam is unremarkable. Routine screening includes a urinalysis, which demonstrates 4+ glycouria. 16 3/13/2009
    15. 15. There is insufficient information to establish a diagnosis.  There are other reasons to spill glucose in the urine. You must ask additional questions. You find out that even though he denies any history of  diabetes, he admits to: Having incessant thirst 1. Increase hunger 2. Increase urination 3. He has lost 15 pounds over the last three months 4. 17 3/13/2009
    16. 16.  A glucometer reading revealed a glucose of 490 mg/dl  A blood glucose revealed a glucose level of 496 mg/dl. With normal electrolytes and anion gap  Does this patient have diabetes? 18 3/13/2009
    17. 17.  Three ways to diagnose diabetes mellitus:  Fasting glucose of > 126 mg/dl  Oral glucose tolerance test with a 2 hr value of > 200 and one other value in-between of > 200  Grossly elevated serum glucose with classic signs and 19 3/13/2009
    18. 18.  New onset Type I diabetics should be admitted because:  He needs to start on insulin  He requires a lot of patient education 20 3/13/2009
    19. 19.  32-year old woman who has type I diabetes calls you over the weekend. She has been having some nausea and vomiting for the last 24 hours and can not keep solids down. She has been able to keep liquids down. Her last glucometer reading was 261 mg/dl.  She is on a split dose of NPH and regular insulin twice daily. She did not take her morning insulin because a physician had told her never to take her insulin when she is not eating. She ask you for instructions? 21 3/13/2009
    20. 20.  Many patients do not take their insulin if they are not eating; this is wrong.  It is important for IDDM patients and their providers to learn how to manage “sick days”.  Note that one of the most common reasons for patient to go into DKA is poor management of their diabetes when they are sick.  Insulin should be taken regardless of whether or not they are eating  Adequate carbohyrates should be taken (15 – 20g q2h) 22 3/13/2009
    21. 21.  The patient can consume regular coke, Sprite, juices @ 4 – 6 oz q2hrs. They can also have gelatin, crackers, soup  Patients that are sick require more insulin  NOT less The intermediate or long acting insulin should  be given Regular insulin should be given q4h as per a  ‘sliding scale’ 23 3/13/2009
    22. 22.  69-year old white female was in good health until 3 weeks ago, when she suddenly developed severe polyuria, polydipsia and polyphagia. She has lost 20 pounds ( going from 120 to 100) during that period and feels extremely weak. When her daughter brings her to you, in the ED, she is somewhat lethargic. Past medical history reveals HTN(Tx with a small dose of enalapril). There is no history of cardiac disease. 24 3/13/2009
    23. 23.  Physical Exam reveals a pale, lethargic, confused woman, breathing rapidly.  B/P is 102/72 P 110 Resp 32  Her skin is very dry, bowel sounds are weakly positive  Blood test revealed Na+ 130 (135 – 145)  K+ 5.1 (3.5 – 5.1)  Glucose 794 ( 70 – 110)  Cl- 104 (95 – 105)  HCO3 3mEq/L (21 – 30)  pH 6.92 (7.35 – 7.45)  pO2 92 mm (80 – 105)  25 3/13/2009
    24. 24.  A 37 year old white female has a 20 year history of diabetes mellitus. She has been having difficulty with hypoglycemia in the early morning. She used to be on beef-pork insulin and did not have any problems.  She takes:  Human NPH 16U am; 8 U pm  Human Regular 8 U am; 3 U pm 26 3/13/2009
    25. 25.  Blood glucose monitoring reveal: 3am 7am 12pm 5pm 41 66 109 72 47 132 82 100 35 182 134 142  Why is she developing early-morning hypoglycemia? 27 3/13/2009
    26. 26.  Insulin have different peaks and duration of action.  In this case you must note that animal insulin has a slower peak than human insulin  In this case this lady was advised to move the NPH evening dose to qhs --- which allowed the NPH peak to occur later  To cover the evening problem one should also increase the bedtime regular insulin --- in this case it was increased by 2 U 28 3/13/2009
    27. 27.  A 56-year male has a history of type II diabetes for 10 years. He is currently on glipizde 20 mg BID and monitors his glucose twice a day. Over the last 2 weeks his fasting glucose were 157 – 278 (average 199); supper values were 145 – 292 (average 212). 29 3/13/2009
    28. 28.  Yesterday his fasting glucose was 234 and HgA1c was 14.8%  P.E.: B/P 142/90 P 72 Resp. 12 height:72 inches weight: 212  The rest of the physical was normal with no evidence of retinopathy or neuropathy  What is the best option for this patient? 30 3/13/2009
    29. 29.  Though this patient may not want to go on insulin …. We have no choice.  He has unacceptably high glucose values  HgA1C confirms the fact that insulin is needed  What do we start him on? 31 3/13/2009
    30. 30.  Many clinicians start their type II that now require insulin on NPH or ultralente and add regular insulin later as needed to tune – up treatment.  After knowing what it would take to treat this patient --- you may then decide to use pre- mixed insulin.  Should this patient be hospitalized?  No 32 3/13/2009
    31. 31.  A 30-year female has no prior medical problems. As part of a routine obstetric care, she has a glucose screen at 24 weeks. She is given 50-g glucose to drink and a glucose level is obtained 1 hour later. Her results revealed a level of 156 mg (<140)  She is 64 inches tall and weighs 220  What do you do know? 33 3/13/2009
    32. 32.  You should now order a 3 hr GTT, which they give 100 g of glucose  Her results were  Fasting: 112mg  1hour: 183mg  2hour: 172mg  3hour: 147mg  What is your opinion? 34 3/13/2009
    33. 33.  This patient has Gestational Diabetes. According to the National Diabetes Data Group – Dx is made if two or more values exceed the norm.  You should start this patient on a ADA 2000 calorie diet, give her a glucometer(she to take readings four times daily) and see her in a week. 35 3/13/2009
    34. 34.  You see her back in a week and her glucose log reveal: Fasting LunchSupper Bedtime 97 93 115 104 112 101 107 99 101 101 89 122 93 105 102 111 115 112 121 118 99 107 113 105 96 101 117 109 36 3/13/2009
    35. 35.  What should you do now?  This patient should be started on insulin. Though these level appear good; in pregnancy glucose levels are significantly lower.  Target glucose goals are: Fasting: 60 – 90  Non-fasting (before breakfast) 60 – 105  After meals: < 120  2am – 6am: >60  37 3/13/2009
    36. 36.  Since most of these patients seem to be insulin resistant it is recommended to start with 0.6U/kg/day. In this patient we would give 30 – 32 U NPH (or Longer acting) BID. She returns in four days with the following readings: Fasting LunchSupper Bedtime 93 99 97 122 86 100 98 113 74 78 99 107 68 90 79 112 38 3/13/2009
    37. 37.  How is our patient doing?  These reading show that we still have a problem at bedtime. Therefore, we should add 2U of regular insulin in the evenings 39 3/13/2009
    38. 38. 40 3/13/2009
    39. 39. A 58 year-old man with a 12 year history of type 2 diabetes comes to your office because of an ulcer in his right foot. Physical exam reveals a 1-cm irregular ulceration over the right metatarsal head, surrounded by an area of black gangrenous skin. The patient is admitted and undergoes amputation of the right forefoot. Which of the following would have been most effective in preventing this complication? Appropriate instructions on self-care of the feet A. B. Doppler exam of the lower extremities C. Nuerophysiologic and electromyographic studies D. Local application of platelet-derived growth factor E. Prophylactic treatment with cholesterol-lowering agents 41
    40. 40. Screening 1. Current guidelines 2. Use of oral agents 3. Insulin regimens 4. Gestational diabetes 5. 42
    41. 41. 45 years old; repeat q 3 years  Overweight (BMI 25 kg/m2*)  Physically inactive  Have a first-degree relative with diabetes  High-risk ethnic population  h/o GDM or baby >9 lbs  HTN  Hyperlipidemia  PCOS  Other sx of insulin resistance (acanthosis)  h/o vascular disease  43
    42. 42. Symptoms of diabetes and a casual plasma glucose 200 mg/dl or.. 1. FPG 126 mg/dl ( no caloric intake for at least 8 hr) or… 2. BS 200 mg/dl after OGTT (2 hr after 75 gm glucose). 3. In the absence of unequivocal hyperglycemia, these  criteria should be confirmed by repeat testing on a different day. OGTT is not recommended for routine clinical  use, but may be required in the evaluation of patients with IFG or when diabetes is still suspected despite a normal FPG as with the postpartum evaluation of women with GDM. 44
    43. 43. A1C<7.0% (q 3 mo if uncontrolled; twice yr if at goal)  Preprandial BS 80-110 mg/dl (60-90 if pregnant)  Postprandial BS<140 mg/dl (<120 if pregnant)  Blood pressure<130/80 mmHg  LDL<100 mg/dl  Triglycerides <150 mg/dl  HDL>40 mg/dl  Annual influenza vaccine  Pneumococcal vaccine for adults with diabetes  Revaccination is for individuals >64 if vaccine was  administered >5 years ago. Other indications for repeat vaccination include nephrotic syndrome, chronic renal disease, and other immunocompromised states, such as after transplantation. 45
    44. 44.  SMBG TID w/ DM1 and GDM  BP each visit  Annual urinary microalbumin (<30ug/mg)  Annual lipids  Annual optho exam starting 3-5 yrs after onset w/ DM1, and upon diagnosis in DM 2  Visual foot exam each visit. Comprehensive exam yearly (sensation, biomechanics, foot structure, vascular status and skin integrity) 46
    45. 45. 47
    46. 46.  Risk assessment at first prenatal visit  Low-risk status requires no glucose testing  Age <25 years  Weight normal before pregnancy  Member of an ethnic group with low prevalence  No known diabetes in first-degree relatives  No history of abnormal glucose tolerance  No history of poor obstetric outcome  High risk features (obesity, h/o GDM, glycosuria, or FH) should undergo glucose testing as soon as possible 48
    47. 47.  FPG 126 mg/dl or a casual plasma glucose 200 mg/dl meets the threshold for the diagnosis of diabetes (confirm on subsequent day)  High-risk women not found to have GDM at initial screening and average- risk women should be tested between 24 and 28 weeks of gestation. Testing should follow one of two approaches: One-step approach: 100-g OGTT   95 mg/dl fasting  180 mg/dl at 1 h  155 mg/dl at 2 h and 140 mg/dl at 3 h. *Two or more of the plasma glucose values must be met or exceeded for a positive diagnosis  Two-step approach: perform an initial screening by measuring the plasma or serum glucose concentration 1 h after a 50-g oral glucose load and perform a diagnostic 100-g OGTT on that subset of women exceeding 140 mg/dl 49
    48. 48. Drug Class Mechanism of Action Side Effects ↑insulin secretion Sulfonylureas/ secretagogues weight gain, hypoglycemia ↓hepatic glucose output Metformin GI upset, lactic acidosis, TZD’s ↑ peripheral glucose fluid retention, weight gain disposal ↓ intestinal Alpha-glucosidase inhibitors flatulence, diarrhea carbohydrate absorption *Each will lower A1c by 1-2% compared to placebo. When combined, efficacy typically is additive 50
    49. 49. Sulfonylurea + Metformin Sulfonylurea + α-glucosidase inhibitors Sulfonylurea + TZD Metformin + Secretagogues Metformin + TZD Insulin + Sulfonylurea Insulin + Metformin Insulin + TZD 51
    50. 50.  Know the types of insulin and onset  Know how to adjust insulin  All regimens include basal and bolus 52
    51. 51. •Make changes slowly, taking into account diet, activity, stress •Asses the effectiveness of insulin at its peak time of action •Increase short/rapid insulin based on post-prandial readings •Increase long-acting when BG high fasting or throughout day •Inject into subcutaneous abdomen and rotate sites 53
    52. 52.  To ↓ pre-dinner BG…….↑AM intermediate-acting (e.g., NPH)  To ↓ fasting BG……….. ↑PM long/intermediate-acting insulin (e.g., glargine, NPH)  To ↓ pre-lunch BG……..↑AM short/rapid-acting insulin (e.g., regular, lispro, aspart)  To ↓ bedtime BG…...….↑PM short/rapid-acting insulin (regular, lispro, aspart) 54 3/13/2009
    53. 53.  Onset within 24 hours  Diabetic ketoacidosis DKA  usually seen with Type 1  Liver cannot metabolize and kidneys cannot excrete  Hyperglycemia (>250)  Ketosis (positive urine dipstick)  Metabolic acidosis (HCO3 < 15; pH <7.3)  May mimic “flu” Polyuria, polydipsia, nausea, vomiting, abdominal pain, breath smells like booze.
    54. 54. Decreased insulin, high counterregulatory hormones (catecholamines, glucagon, GH, cortisol), leading to hyperglycemia, proteolysis, lipolysis & ketone production Diagnostic Criteria hyperglycemia: glucose>250 mg/dl  acidosis: pH <7.35; HCO3 < 18  ketosis (blood &/or urine)  Therapeutic Goals Improve circulating volume & tissue perfusion  Identify precipitating factors  FLUIDS restores intravascular volume, decreases  counterregulatory hormones and lowers glucose levels Reduce Gluc. & serum osmolarity: lytes q2, glucose q1  Clear ketones, fix electrolytes  56
    55. 55.  HHNK - Hyperglycemic, hyperosmolar, non- ketotic coma. Onset 2 days to 2 weeks.  Osmolarity > 310  Glucose > 600  Usually seen with Type 2  exhibiting increasing insulin resistance, esp. after gorging on CHO.  Presents with marked dehydration and CNS SSx often mimicking a stroke.  Must correct S-L-O-W-L-Y to prevent cerebral edema. Watch K+ levels.
    56. 56.  Hypoglycemia  Glucose < 50  Causes:  Not enough to eat (or forgot)  Too much insulin (or pills)  Did not allow for exercise  CNS- confusion, delirium, coma  Autonomic - hunger, anxiety, SWEATING, tachycardia.  If patient is conscious - give OJ. Otherwise injection of glucagon, glucose gel in mouth, or 50% glucose by IV push.
    57. 57.  Neuropathies - peripheral  Obstruction of vessels that supply nerves  Demyelination  Sensory  Paresthesias  Decreased sensitivity to pain, temperature and light touch.  Decreased proprioception and vibration sense.  Motor  Weakness  Atrophy
    58. 58.  Neuropathies - central and autonomic  orthostatic hypotension  gastrointestinal atony  atonic urinary bladder  impotence  impairment of special senses
    59. 59.  Nephropathy Glomerulosclerosis (arteriolonephrosclerosis)  Thickened basement membrane in glomerulus  Causes microalbuminuria (300 mg / day)  Nodular scarring and destruction of glomerulus.  Kimmelstiel - Wilson lesion. Pathognomonic for diabetes mellitus.
    60. 60.  Retinopathy  Leading cause of blindness. DM has increased risk for cataracts and glaucoma  Pathogenesis:  new vessels, fragile vessels, microaneurysms, hemorrhage. Followed by scarring and retinal detachment. Takes 20 years to develop. 100% of Type 1; 60% Type 2. Need to evaluate yearly. Retinal photos excellent.
    61. 61.  Foot ulcers  Most common reason for hospitalization  Due to impaired circulation (PVD)  Abnormal glycoprotein thickens vessel wall  Chronic hypoxia (glycohgb has > affinity for O2)  Due to neuropathy  Cannot feel pain to prevent injury  Prevention: Wear good closed-toe shoes, white cotton socks, keep feet clean and dry, clip toenails straight across, inspect feet daily.
    62. 62.  Infections  Skin: boils and abscesses  Urinary tract infections - quickly spread to kidneys  Osteomyelitis  Infected cuts of extremities  Peridontal disease  Finger and toenail fungus