Diabetes Mellitus

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Diabetes Mellitus by Mind Map: Diabetes Mellitus

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

2. Report BG >300 x2

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

4. Used in sliding scale

5. Usually appears 10-20 years after diagnosis

6. Oral Hypoglycemics

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

8. Fasting plasma glucose: blood draw after fasting

9. Pancreas Transplantation

9.1. For Type 1 diabetes with kidney transplant

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

10. 1 drink/day for women, 2 for men

11. Eye problems.

12. Bed wetting.

13. Plasma Glucose Testing

13.1. Oral Glucose Tolerance Test (OGTT)

14. No insulin is produced.

14.1. Autoimmune disease.

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

16. Can be mixed with short or rapid acting insulins

17. Insulin

18. Decreased weight.

19. Limit cholesterol to < 200 mg/day

20. Classification

20.1. Type 1

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

20.1.2. Often diagnosed before age 15.

20.1.3. Daily insulin required for life.

20.1.4. 5-10% of diabetes.

20.2. Sedentary Lifestyle

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

20.3. Type 2

20.3.1. Most common in adults aged 35 or older.

20.3.2. Obesity

20.3.3. Risk Factors

20.3.3.1. Age greater than 45

20.3.3.2. Positive family history (10x more likely)

20.3.3.3. Ethnicity

20.3.3.4. Hypertension

20.3.4. May need to supplement insulin.

20.3.5. Over 90% of diabetes.

20.3.6. Genetic link.

20.4. Diabetic Ketoacidosis (DKA)

20.4.1. Profound deficiency of insulin

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

20.4.3. Normal pH range: 7.35-7.45

20.4.4. Most likely to occur in Type 1

20.4.5. Ensure patent airway, administer O2

20.4.6. Establish IV access; begin fluid resuscitation

20.4.7. Clinical Manifestations

20.4.7.1. Dehydration: poor skin turgor, tachycardia, dry membranes

20.4.7.2. Lethargy and weakness

20.4.7.3. Eyes soft and sunken

20.4.7.4. Fruity sweet breath odor

20.4.7.5. Kussmaul respirations

20.4.8. Higher risk of maternal/neonatal complications

20.5. Goes away after pregnancy.

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

20.7. Occurs during pregnancy.

20.8. Gestational

20.8.1. May not reoccur.

20.8.2. May have a large baby.

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

20.8.4. Nutritional therapy is the first line of treatment!

20.9. Pre-Diabetes

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

20.10. Secondary Diabetes

20.10.1. Diabetes caused by an outside factor.

20.10.1.1. Stress increases blood glucose levels.

20.10.2. Drug or chemical induced.

20.10.2.1. Dilantin

20.10.2.2. Corticosteroids

20.10.2.3. Antipsychotic meds

21. Signs and Symptoms

21.1. Type 1

21.1.1. Increased thirst.

21.1.2. Rapid onset.

21.2. Duration: 5-8 hours

21.3. Type 2

21.3.1. Increased weight.

21.3.2. Slow onset.

21.3.3. Recurrent infections

21.3.4. Prolonged wound healing

21.3.5. Nerve disruption

21.4. Type 1 and 2

21.4.1. 3-P's

21.4.1.1. Polyphagia

21.4.1.2. Polydipsia

21.4.1.3. Primarily seen in Type 1 but can be seen in Type 2.

21.4.1.4. Polyuria

21.4.2. Fatigue

22. Treatments and Interventions

22.1. Early Diagnosis

22.2. Monitor glucose before, during, after exercise

22.3. Reduces CV risk factors

22.4. Glucose Monitoring

22.5. Routine Exercise

22.5.1. Meal planning

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

22.5.3. Increases insulin sensitivity

22.5.3.1. Saturated fats < 7% of total calories

22.6. Nutritional Therapy

22.6.1. Type 1

22.6.1.1. Consistency

22.6.1.2. More flexibility with rapid acting insulin, multiple daily injections, or insulin pump

22.6.2. Type 2

22.6.2.1. Low fat and carbs

22.6.3. Carbohydrates

22.6.3.1. Spacing meals

22.6.3.2. May decrease need for DM meds for Type 2

22.6.3.3. Minimum of 130 g/day

22.6.3.4. Nonnutritive and nutritive sweeteners can be used in moderation

22.6.4. Exercise 1 hour after meal

22.6.5. Fats

22.6.5.1. Minimize trans fat

22.6.6. 15%-20% of calories

22.6.7. Protein

22.6.7.1. High-protein diets are not recommended

22.6.8. Alcohol

22.6.8.1. Inhibits glucogenesis by liver

22.6.8.2. Can cause severe hypoglycemia

22.6.9. General Guidelines

22.6.9.1. Raw/Whole Foods will lower a glycemic response

22.6.9.1.1. Emphasis on achieving glucose, lipid, and BP goals

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

22.8. Bariatric Surgery

22.8.1. For DM Type 2

22.8.2. Used when lifestyle/drug therapy management is difficult

22.8.2.1. Combine carbs, protein, and fat to slow down absorption and decrease glycemic response

22.9. BMI >35

22.10. Monitor for Complications

22.10.1. Hyperosmolar Hyperglycemic Syndrome (HHS)

22.10.1.1. Life-threatening syndrome in Type 2 DM

22.10.1.2. Enough insulin to prevent DKA

22.10.1.3. More severe neurologic manifestations

22.10.1.4. Change in LOC? Check BG!

22.10.1.5. High mortality rate

22.10.1.6. Therapy

22.10.1.6.1. IV insulin and NaCl infusions

22.10.1.6.2. Monitor serum potassium, replace if needed

22.10.1.6.3. Cardiac monitoring

23. Complications

23.1. Angiopathy

23.1.1. Damage to blood vessels secondary to chronic hyperglycemia

23.1.2. Leading cause of diabetes-related death

23.1.3. Macrovascular and microvascular

23.1.3.1. Macrovascular Angiopathy

23.1.3.1.1. Diseases of large and medium sized blood vessels

23.1.3.1.2. Higher frequency and earlier onset in patients with DM

23.1.3.1.3. Cerebrovascular Disease

23.1.3.1.4. Cardiovascular Disease

23.1.3.1.5. Peripheral Vascular Disease

23.1.3.1.6. Decrease risk factors

23.1.3.1.7. Screen for and treat hyperlipidemia

23.1.3.2. Microvascular Angiopathy

23.1.3.2.1. Thickening of vessel membranes in capillaries and arterioles

23.1.3.2.2. Specific to diabetes

23.1.3.3. Aspiration of blood, membrane, and fibers inside the eye

23.1.4. Tight glucose levels can help prevent/minimize risks

23.2. Peripheral Vascular Disease (PVD)

23.3. Retinopathy

23.4. Nephropathy

23.5. Neuropathy

23.6. Infections

23.7. Hypertension

23.8. Poorly Controlled Diabetes

23.8.1. Diabetic Ketoacidosis (Type 1)

23.8.2. Fluid and Electrolyte Imbalance

23.9. Nail care

23.10. Chronic Foot Complications

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

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

23.10.3. Teach frequent assessment of feet

23.10.4. Proper footwear

23.10.5. Diligent wound care for foot ulcers

23.10.6. Neuropathic arthropod (Charcot's foot)

23.10.6.1. Ankle and foot changes that lead to joint dysfunction and footdrop

23.10.6.2. Increases chance of foot ulcer

23.11. Chronic Skin Problems

23.11.1. Diabetic dermopathy

23.11.1.1. Most common

23.11.1.2. Red-brown, round or oval patches

23.11.2. Acanthosis nigricans

23.11.2.1. Manifestation of insulin resistance

23.11.2.2. Brown-black skin seen on flexures, axillae, and neck

23.11.3. Defect in mobilization of inflammatory cells and impaired phagocytosis

23.11.4. Necrobiosis lipoidica diabeticorum

23.11.4.1. Red-yellow lesions

23.12. Infection

23.12.1. Recurring/persistent infections

23.12.2. Treat promptly and vigorously

23.12.3. Hand hygiene and flu/PNU vaccine

24. Diagnostic Studies

24.1. Hemoglobin A1C

24.1.1. Does not require fasting

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

24.1.3. Normal A1C: 4.5%-6.5%

24.2. Fructosamine

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

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

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

24.3. Autoantibodies

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

24.4. Urine Studies

24.4.1. Urine testing for glucose

24.4.2. Urine testing for ketone bodies

24.4.3. Tests for renal function

24.4.3.1. Presence of protein such as albumin to detect early onset of nephropathy

24.4.3.2. 24-hour urine test for creatinine clearance to evaluate renal function if albumin is present

25. Criteria for Diabetes

25.1. A1C > 6.5%

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

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

25.4. 2 hour plasma glucose > 200 mg/dl during an OGTT

25.5. Pre-Diabetes

25.5.1. A1C of 5.7%-6.4%

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

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

26. Glucose Lowering Agents

26.1. Insulin

26.1.1. Categorized according to onset, peak action, and duration.

26.1.1.1. Rapid-Acting

26.1.1.1.1. The -logs: lispro (Humalog), aspart (NovoLog), glulisine (Apidra)

26.1.1.1.2. Onset: 10-30 mins.

26.1.1.1.3. Peak: 30 mins - 3 hours

26.1.1.1.4. Duration: 3-5 hours

26.1.1.2. Short-Acting

26.1.1.2.1. Regular (Humulin R, Novolin R)

26.1.1.2.2. Onset: 30 mins - 1 hour

26.1.1.2.3. Peak: 2-5 hours

26.1.1.3. Intermediate-Acting

26.1.1.3.1. NPH (Humulin N, Novolin N)

26.1.1.3.2. Onset: 1.5-4 hours

26.1.1.3.3. Peak: 4-12 hours

26.1.1.3.4. Duration: 12-18 hours

26.1.1.4. Long-Acting

26.1.1.4.1. glargine (Lantus), detemir (Levemir), degludec (Tresiba)

26.1.1.4.2. Onset: 0.8-4 hours

26.1.1.4.3. Peak: Less defined, or no pronounced peak

26.1.1.4.4. Duration: 16-24 hours

26.1.2. Basal-Bolus Regimen

26.1.2.1. Most closely mimics endogenous insulin production

26.1.2.2. Rapid or short acting (bolus) insulin before meals

26.1.2.2.1. Rapid Acting Insulin (Bolus)

26.1.2.2.2. Short Acting Insulin (Bolus)

26.1.2.3. Intermediate or long acting (basal) background insulin once or twice daily

26.1.2.3.1. Intermediate Acting Insulin (Basal)

26.1.2.3.2. No prolonged exposure to sunlight

26.1.2.3.3. Long Acting Insulin (Basal)

26.1.2.4. Combination Insulin (premixed)

26.1.2.4.1. Provides both mealtime and basal coverage but not as effective as basal-bolus regimen

26.1.2.4.2. Decreases the number of injections

26.1.2.4.3. NPH/regular 70/30

26.1.2.4.4. Good for patients unable to draw up two types of insulin

26.1.3. Administration

26.1.3.1. Subcutaneous injection

26.1.3.1.1. Allow no air bubble in the syringe

26.1.3.1.2. Don't mix insulin of different manufactures

26.1.3.1.3. Abdomen is the fastest absorption area

26.1.3.2. IV: Regular only

26.1.3.3. Never oral

26.1.3.4. Storage

26.1.3.4.1. Unopened: refrigerator

26.1.3.4.2. Opened: room-temperature

26.1.3.4.3. Pre-filled syringes: store upright for 1 week if mixed, 30 days if not

26.1.3.4.4. Open vials and pens can be stored at room-temp for 4 weeks

26.1.3.5. Insulin Pump

26.1.3.5.1. Continuous subcutaneous infusion

26.1.3.5.2. Program basal and bolus douses that can vary throughout the day

26.1.3.5.3. Keep glucose levels in a tighter range

26.1.3.6. Inhaled Insulin

26.1.3.6.1. Afrezza

26.1.3.6.2. Rapid-acting inhaled insulin

26.1.3.6.3. Administered at beginning of each meal or within 20 mins of starting

26.1.3.6.4. Not a substitute for long-acting insulin

26.1.4. Hyperglycemia in the morning

26.1.5. Adverse Effects

26.1.5.1. Hypoglycemia

26.1.5.2. Somogyi Effect

26.1.5.2.1. High evening dose of insulin causes low glucose in the night, body reacts causing hyperglycemia

26.1.5.2.2. Treatment: less insulin in the evening

26.1.5.3. Carry rapidly absorbed carbs with you!

26.1.5.3.1. Decreased insulin production

26.1.5.4. Dawn Phenomenon

26.1.5.4.1. Hyperglycemia on awakening

26.1.5.4.2. Growth hormones and cortisol are secreted by the body during the early morning, causing an increase in blood sugar

26.1.5.4.3. More common in children

26.1.5.4.4. Treatment: increase insulin or adjust insulin administration time

26.1.5.5. Allergic Reaction

26.1.5.6. Systemic Response

26.1.5.7. Lipodystrophy

26.2. Oral Agents

26.2.1. Work on three defects of Type 2 diabetes

26.2.1.1. Insulin resistance

26.2.1.2. Increased hepatic glucose production

26.3. Connected to a catheter inserted into abdominal tissue

26.4. Non-insulin Drug Therapy

26.4.1. Biguanides

26.4.1.1. metformin (Glucophage)

26.4.1.2. Reduces glucose production by liver

26.4.1.3. Withhold if patient is undergoing surgery or radiologic procedure with contrast medium (dyes)

26.4.1.3.1. Increase insulin production from pancreas

26.4.1.4. Does not increase insulin production

26.4.1.5. Does not cause hypoglycemia

26.4.1.6. Used in prevention of Type 2 diabetes

26.4.1.7. BIGuanides = BIGgest oral antidiabetic

26.4.1.8. Monitor serum creatinine

26.4.1.9. SE: diarrhea, flatuelence

26.4.2. Sulfonylureas

26.4.2.1. Increases insulin production from pancreas

26.4.2.2. Major SE: hypoglycemia, weight gain

26.4.2.3. Contraindications: renal, liver, or cardiac disease

26.4.2.4. Not for patients with sulfa allergy

26.4.3. Increases insulin, lowers glucagon

26.4.4. Meglitinides

26.4.5. Alpha-glucosidase inhibitors

26.4.5.1. "Starch blockers"

26.4.5.2. SE: gas, abdominal pain, diarrhea

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

26.4.7. Thiazolidinediones

26.4.7.1. Rarely used because of adverse effects

26.4.7.2. Discontinued

26.4.7.3. Doubled risk of bone fractures in women with DM Type 2

26.4.8. Depeptidyl Peptidase-4 (DDP-4) Inhibitor

26.4.8.1. SE: pancreatitis, lowered potential for hypoglycemia

26.4.9. Sodium-Glucose Co-Transporter 2 (SGLT2) Inhibitors

26.4.9.1. Increases glucose excretion

26.4.9.2. SE: increased genital tract infections and UTI's, hypoglycemia

26.4.10. Dopamine Receptor Agonist

26.4.10.1. Increases dopamine receptor activity

26.4.10.2. SE: orthostatic hypotension

26.4.11. Glucagonlike Peptide-1 Receptor Agonists

26.4.11.1. non-insulin injection

26.4.11.2. Not usually used for Type 1 DM

26.4.11.3. SE: N/V, hypoglycemia, diarrhea, headache, acute pancreatitis, and kidney problems

26.4.12. Amylin Analog

26.4.12.1. Injection used in addition to mealtime insulin

26.4.12.2. Type 1 or 2 DM

26.4.12.3. Not a replacement for insulin

26.4.12.4. Combination Therapy

26.4.12.4.1. Blend two different drug classes together

26.4.12.4.2. Less pills for a patient to take

26.4.12.4.3. Patient and HCP must be aware of drug interactions that could cause hypo/hyperglycemia

26.4.12.5. SE: hypoglycemia

26.5. SE: hypoglycemia, weight gain

27. Self-Monitoring of Blood Glucose (SMBG)

27.1. Enables decisions regarding diet, exercise, and medication

27.2. Helps identify hypo/hyperglycemia

27.3. A must for insulin users

27.4. Never share meters!

27.5. Inaccurate BG Readings

27.5.1. Expired test strips

27.5.2. Squeezing the finger

27.5.3. Unclean hands with food/sugar

27.5.4. Not checking control solution regularly

27.5.5. Obtaining sample from alternate sites

27.5.6. Dehydration, elevated hematocrit

27.5.7. Always recheck!

28. Hypoglycemia

28.1. Rapid onset of symptoms

28.1.1. Confusion

28.1.2. Irritability

28.1.3. Diaphoresis - cold and clammy!

28.1.4. Tremors

28.1.5. Hunger

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

28.3. Quickly reversible

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

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

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

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

28.6. Treatment

28.6.1. Rule of 15

28.6.1.1. Consume 15g os simple carbs

28.6.1.2. Recheck BG in 15 mins

28.6.1.3. Repeat if BG remains <70

28.6.2. Actue Care Setting

28.6.2.1. 50% dextrose, 20-50mL IVP

29. Sick Day Care

29.1. Take meds as prescribed

29.1.1. Get annual flu shot!

29.2. Test BG q. 4 hours

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

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

29.5. Report moderate ketones to HCP

30. Intraoperative Management

30.1. Observe clients for S/S of hypoglycemia

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