Diabetes Mellitus

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Diabetes Mellitus by Mind Map: Diabetes Mellitus

1. Report BG >300 x2

2. Non-diabetic patients may require insulin while taking the medication.

3. Usually appears 10-20 years after diagnosis

4. Fasting plasma glucose: blood draw after fasting

5. Pancreas Transplantation

5.1. For Type 1 diabetes with kidney transplant

5.2. Eliminates need for exogenous insulin, SMBG, and dietary restrictions

6. 1 drink/day for women, 2 for men

7. Eye problems.

8. Bed wetting.

9. Plasma Glucose Testing

9.1. Oral Glucose Tolerance Test (OGTT)

10. No insulin is produced.

10.1. Autoimmune disease.

11. If unable to swallow: glucagon 1mg IM or SQ

12. Insulin

13. Decreased weight.

14. Limit cholesterol to < 200 mg/day

15. Classification

15.1. Type 1

15.1.1. Juvenile Onset: DM 1 can occur at any stage of life but is most commonly found in young people

15.1.2. Often diagnosed before age 15.

15.1.3. Daily insulin required for life.

15.1.4. 5-10% of diabetes.

15.2. Sedentary Lifestyle

15.2.1. Insufficient insulin production or improper use of insulin..

15.3. Type 2

15.3.1. Most common in adults aged 35 or older.

15.3.2. Obesity

15.3.3. Risk Factors Age greater than 45 Positive family history (10x more likely) Ethnicity Hypertension

15.3.4. May need to supplement insulin.

15.3.5. Over 90% of diabetes.

15.3.6. Genetic link.

15.4. Diabetic Ketoacidosis (DKA)

15.4.1. Profound deficiency of insulin

15.4.2. Hyperglycemia (>250), ketosis, acidosis (<7.3), and dehydration

15.4.3. Normal pH range: 7.35-7.45

15.4.4. Most likely to occur in Type 1

15.4.5. Ensure patent airway, administer O2

15.4.6. Establish IV access; begin fluid resuscitation

15.4.7. Clinical Manifestations Dehydration: poor skin turgor, tachycardia, dry membranes Lethargy and weakness Eyes soft and sunken Fruity sweet breath odor Kussmaul respirations

15.4.8. Higher risk of maternal/neonatal complications

15.5. Goes away after pregnancy.

15.6. Impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT)

15.7. Occurs during pregnancy.

15.8. Gestational

15.8.1. May not reoccur.

15.8.2. May have a large baby.

15.8.3. Usually detected 24-28 weeks when OGTT is done.

15.8.4. Nutritional therapy is the first line of treatment!

15.9. Pre-Diabetes

15.9.1. Blood glucose levels are higher than normal but not high enough for a diagnosis of diabetes.

15.10. Secondary Diabetes

15.10.1. Diabetes caused by an outside factor. Stress increases blood glucose levels.

15.10.2. Drug or chemical induced. Dilantin Corticosteroids Antipsychotic meds

16. Signs and Symptoms

16.1. Type 1

16.1.1. Increased thirst.

16.1.2. Rapid onset.

16.2. Duration: 5-8 hours

16.3. Type 2

16.3.1. Increased weight.

16.3.2. Slow onset.

16.3.3. Recurrent infections

16.3.4. Prolonged wound healing

16.3.5. Nerve disruption

16.4. Type 1 and 2

16.4.1. 3-P's Polyphagia Polydipsia Primarily seen in Type 1 but can be seen in Type 2. Polyuria

16.4.2. Fatigue

17. Treatments and Interventions

17.1. Early Diagnosis

17.2. Monitor glucose before, during, after exercise

17.3. Reduces CV risk factors

17.4. Glucose Monitoring

17.5. Routine Exercise

17.5.1. Meal planning

17.5.2. Do not exercise if blood glucose level > 300 mg/dL and if ketones are in urine

17.5.3. Increases insulin sensitivity Saturated fats < 7% of total calories

17.6. Nutritional Therapy

17.6.1. Type 1 Consistency More flexibility with rapid acting insulin, multiple daily injections, or insulin pump

17.6.2. Type 2 Low fat and carbs

17.6.3. Carbohydrates Spacing meals May decrease need for DM meds for Type 2 Minimum of 130 g/day Nonnutritive and nutritive sweeteners can be used in moderation

17.6.4. Exercise 1 hour after meal

17.6.5. Fats Minimize trans fat

17.6.6. 15%-20% of calories

17.6.7. Protein High-protein diets are not recommended

17.6.8. Alcohol Inhibits glucogenesis by liver Can cause severe hypoglycemia

17.6.9. General Guidelines Raw/Whole Foods will lower a glycemic response Emphasis on achieving glucose, lipid, and BP goals

17.7. Fewer symptoms lead to higher glucose levels (>600)

17.8. Bariatric Surgery

17.8.1. For DM Type 2

17.8.2. Used when lifestyle/drug therapy management is difficult Combine carbs, protein, and fat to slow down absorption and decrease glycemic response

17.9. BMI >35

17.10. Monitor for Complications

17.10.1. Hyperosmolar Hyperglycemic Syndrome (HHS) Life-threatening syndrome in Type 2 DM Enough insulin to prevent DKA More severe neurologic manifestations Change in LOC? Check BG! High mortality rate Therapy IV insulin and NaCl infusions Monitor serum potassium, replace if needed Cardiac monitoring

18. Complications

18.1. Angiopathy

18.1.1. Damage to blood vessels secondary to chronic hyperglycemia

18.1.2. Leading cause of diabetes-related death

18.1.3. Macrovascular and microvascular Macrovascular Angiopathy Diseases of large and medium sized blood vessels Higher frequency and earlier onset in patients with DM Cerebrovascular Disease Cardiovascular Disease Peripheral Vascular Disease Decrease risk factors Screen for and treat hyperlipidemia Microvascular Angiopathy Thickening of vessel membranes in capillaries and arterioles Specific to diabetes Aspiration of blood, membrane, and fibers inside the eye

18.1.4. Tight glucose levels can help prevent/minimize risks

18.2. Peripheral Vascular Disease (PVD)

18.3. Retinopathy

18.4. Nephropathy

18.5. Neuropathy

18.6. Infections

18.7. Hypertension

18.8. Poorly Controlled Diabetes

18.8.1. Diabetic Ketoacidosis (Type 1)

18.8.2. Fluid and Electrolyte Imbalance

18.9. Nail care

18.10. Chronic Foot Complications

18.10.1. Sensory neuropathy leads to decrease of protective sensation, leading to unawareness injuries

18.10.2. Peripheral artery disease decrease blood flow and wound healing, while increasing the risk of infection

18.10.3. Teach frequent assessment of feet

18.10.4. Proper footwear

18.10.5. Diligent wound care for foot ulcers

18.10.6. Neuropathic arthropod (Charcot's foot) Ankle and foot changes that lead to joint dysfunction and footdrop Increases chance of foot ulcer

18.11. Chronic Skin Problems

18.11.1. Diabetic dermopathy Most common Red-brown, round or oval patches

18.11.2. Acanthosis nigricans Manifestation of insulin resistance Brown-black skin seen on flexures, axillae, and neck

18.11.3. Defect in mobilization of inflammatory cells and impaired phagocytosis

18.11.4. Necrobiosis lipoidica diabeticorum Red-yellow lesions

18.12. Infection

18.12.1. Recurring/persistent infections

18.12.2. Treat promptly and vigorously

18.12.3. Hand hygiene and flu/PNU vaccine

19. Diagnostic Studies

19.1. Hemoglobin A1C

19.1.1. Does not require fasting

19.1.2. Measure glycemic levels over the past 90-120 days

19.1.3. Normal A1C: 4.5%-6.5%

19.2. Fructosamine

19.2.1. Formed by a chemical reaction of glucose with plasma protein

19.2.2. Reflects glycemic in the previous 1-3 weeks.

19.2.3. May show a change in blood glucose levels before A1C does.

19.3. Autoantibodies

19.3.1. Helps distinguish between autoimmune Type 1 diabetes and diabetes due to other causes.

19.4. Urine Studies

19.4.1. Urine testing for glucose

19.4.2. Urine testing for ketone bodies

19.4.3. Tests for renal function Presence of protein such as albumin to detect early onset of nephropathy 24-hour urine test for creatinine clearance to evaluate renal function if albumin is present

20. Criteria for Diabetes

20.1. A1C > 6.5%

20.2. Fasting Plasma Glucose (FPG) > 126 mg/dl

20.3. Symptoms of hyperglycemia and random plasma glucose > 200 mg/dl

20.4. 2 hour plasma glucose > 200 mg/dl during an OGTT

20.5. Pre-Diabetes

20.5.1. A1C of 5.7%-6.4%

20.5.2. Impaired Fasting Glucose: 100-125 mg/dl after an overnight fast

20.5.3. Impaired Glucose Tolerance: 2 hour post-OGTT of 140-199 mg/dl

21. Self-Monitoring of Blood Glucose (SMBG)

21.1. Enables decisions regarding diet, exercise, and medication

21.2. Helps identify hypo/hyperglycemia

21.3. A must for insulin users

21.4. Never share meters!

21.5. Inaccurate BG Readings

21.5.1. Expired test strips

21.5.2. Squeezing the finger

21.5.3. Unclean hands with food/sugar

21.5.4. Not checking control solution regularly

21.5.5. Obtaining sample from alternate sites

21.5.6. Dehydration, elevated hematocrit

21.5.7. Always recheck!

22. Hypoglycemia

22.1. Rapid onset of symptoms

22.1.1. Confusion

22.1.2. Irritability

22.1.3. Diaphoresis - cold and clammy!

22.1.4. Tremors

22.1.5. Hunger

22.2. Symptoms can also occur when high glucose level falls too rapidly

22.3. Quickly reversible

22.4. At the first sign of hypoglycemia, BG should be checked

22.5. Hypoglycemic unawareness: person doesn't experience S/S, dangerous

22.5.1. Related to autonomic neuropathy and lack of counter regulatory hormones

22.5.2. Patients at risk should be BG levels a little higher

22.6. Treatment

22.6.1. Rule of 15 Consume 15g os simple carbs Recheck BG in 15 mins Repeat if BG remains <70

22.6.2. Actue Care Setting 50% dextrose, 20-50mL IVP

23. Sick Day Care

23.1. Take meds as prescribed

23.1.1. Get annual flu shot!

23.2. Test BG q. 4 hours

23.3. Eat sick day foods hourly (15 gm carbs)

23.4. Test ketones q. 4 hrs if BG >240

23.5. Report moderate ketones to HCP

24. Intraoperative Management

24.1. Observe clients for S/S of hypoglycemia

24.1.1. Type 2: d/c oral diabetics 48 hours before surgery, treat with insulin during surgery

25. Heat > 86F and freezing temperatures alter the insulin, making it less effective

26. Used in sliding scale

27. Oral Hypoglycemics

28. NPH (cloudy) - must agitate gently to mix

29. Can be mixed with short or rapid acting insulins

30. Glucose Lowering Agents

30.1. Insulin

30.1.1. Categorized according to onset, peak action, and duration. Rapid-Acting The -logs: lispro (Humalog), aspart (NovoLog), glulisine (Apidra) Onset: 10-30 mins. Peak: 30 mins - 3 hours Duration: 3-5 hours Short-Acting Regular (Humulin R, Novolin R) Onset: 30 mins - 1 hour Peak: 2-5 hours Intermediate-Acting NPH (Humulin N, Novolin N) Onset: 1.5-4 hours Peak: 4-12 hours Duration: 12-18 hours Long-Acting glargine (Lantus), detemir (Levemir), degludec (Tresiba) Onset: 0.8-4 hours Peak: Less defined, or no pronounced peak Duration: 16-24 hours

30.1.2. Basal-Bolus Regimen Most closely mimics endogenous insulin production Rapid or short acting (bolus) insulin before meals Rapid Acting Insulin (Bolus) Short Acting Insulin (Bolus) Intermediate or long acting (basal) background insulin once or twice daily Intermediate Acting Insulin (Basal) No prolonged exposure to sunlight Long Acting Insulin (Basal) Combination Insulin (premixed) Provides both mealtime and basal coverage but not as effective as basal-bolus regimen Decreases the number of injections NPH/regular 70/30 Good for patients unable to draw up two types of insulin

30.1.3. Administration Subcutaneous injection Allow no air bubble in the syringe Don't mix insulin of different manufactures Abdomen is the fastest absorption area IV: Regular only Never oral Storage Unopened: refrigerator Opened: room-temperature Pre-filled syringes: store upright for 1 week if mixed, 30 days if not Open vials and pens can be stored at room-temp for 4 weeks Insulin Pump Continuous subcutaneous infusion Program basal and bolus douses that can vary throughout the day Keep glucose levels in a tighter range Inhaled Insulin Afrezza Rapid-acting inhaled insulin Administered at beginning of each meal or within 20 mins of starting Not a substitute for long-acting insulin

30.1.4. Hyperglycemia in the morning

30.1.5. Adverse Effects Hypoglycemia Somogyi Effect High evening dose of insulin causes low glucose in the night, body reacts causing hyperglycemia Treatment: less insulin in the evening Carry rapidly absorbed carbs with you! Decreased insulin production Dawn Phenomenon Hyperglycemia on awakening Growth hormones and cortisol are secreted by the body during the early morning, causing an increase in blood sugar More common in children Treatment: increase insulin or adjust insulin administration time Allergic Reaction Systemic Response Lipodystrophy

30.2. Oral Agents

30.2.1. Work on three defects of Type 2 diabetes Insulin resistance Increased hepatic glucose production

30.3. Connected to a catheter inserted into abdominal tissue

30.4. Non-insulin Drug Therapy

30.4.1. Biguanides metformin (Glucophage) Reduces glucose production by liver Withhold if patient is undergoing surgery or radiologic procedure with contrast medium (dyes) Increase insulin production from pancreas Does not increase insulin production Does not cause hypoglycemia Used in prevention of Type 2 diabetes BIGuanides = BIGgest oral antidiabetic Monitor serum creatinine SE: diarrhea, flatuelence

30.4.2. Sulfonylureas Increases insulin production from pancreas Major SE: hypoglycemia, weight gain Contraindications: renal, liver, or cardiac disease Not for patients with sulfa allergy

30.4.3. Increases insulin, lowers glucagon

30.4.4. Meglitinides

30.4.5. Alpha-glucosidase inhibitors "Starch blockers" SE: gas, abdominal pain, diarrhea

30.4.6. Can be used in combination with agents from other classes or insulin

30.4.7. Thiazolidinediones Rarely used because of adverse effects Discontinued Doubled risk of bone fractures in women with DM Type 2

30.4.8. Depeptidyl Peptidase-4 (DDP-4) Inhibitor SE: pancreatitis, lowered potential for hypoglycemia

30.4.9. Sodium-Glucose Co-Transporter 2 (SGLT2) Inhibitors Increases glucose excretion SE: increased genital tract infections and UTI's, hypoglycemia

30.4.10. Dopamine Receptor Agonist Increases dopamine receptor activity SE: orthostatic hypotension

30.4.11. Glucagonlike Peptide-1 Receptor Agonists non-insulin injection Not usually used for Type 1 DM SE: N/V, hypoglycemia, diarrhea, headache, acute pancreatitis, and kidney problems

30.4.12. Amylin Analog Injection used in addition to mealtime insulin Type 1 or 2 DM Not a replacement for insulin Combination Therapy Blend two different drug classes together Less pills for a patient to take Patient and HCP must be aware of drug interactions that could cause hypo/hyperglycemia SE: hypoglycemia

30.5. SE: hypoglycemia, weight gain