Nurse Licensure Examination Review

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Nurse Licensure Examination Review

• Diabetes Mellitus

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Diabetes Mellitus

• A group of metabolic diseases characterized by
  elevated levels of glucose in the blood
  resulting from defects in insulin secretion,
  insulin action, insulin receptors or any
  combination of conditions.

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Diabetes Mellitus

• A chronic disorder of impaired glucose
  metabolism, protein and fat metabolism

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Diabetes Mellitus

• BASIC PATHOLOGY Insulin problem (deficiency or
  impaired action)

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Diabetes Mellitus

• Insulin is a hormone secreted by the BETA cells
  of the pancreas
• Stimulus of insulin- HYPERGLYCEMIA

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Diabetes Mellitus

• Action of insulin it promotes entry of Glucose
  into the body cells by binding to the insulin
  receptor in the cell membrane

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INSULIN Physiology

• Insulin Metabolic Functions
• 1. Transports and metabolizes GLUCOSE
• 2. Promotes GLYCOGENESIS
• 3. Promotes GLYCOLYSIS
• 4. Enhances LIPOGENESIS
• 5. Accelerates PROTEIN SYNTHESIS

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Diabetes Mellitus

• RISK FACTORS for Diabetes Mellitus
• 1. Family History of diabetes
• 2. Obesity
• 3. Race/Ethnicity

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Diabetes Mellitus

• RISK FACTORS for Diabetes Mellitus
• 4. Age of more than 45
• 5. Previously unidentified IFG/IGT
• 6. Hypertension

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Diabetes Mellitus

• RISK FACTORS for Diabetes Mellitus
• 7. Hyperlipidemia
• 8. History of Gestational Diabetes Mellitus

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Diabetes Mellitus

• CLASSIFICATION OF DM
• 1. Type 1 DM
• Insulin dependent Diabetes Mellitus
• 2. Type 2 DM
• Non-insulin dependent Diabetes Mellitus
• 3. Gestational DM
• Diabetes Mellitus diagnosed during pregnancy
• 4. DM associated with other conditions or
  syndromes

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Diabetes Mellitus

• CLASSIFICATION OF DM
• 1. Type 1 DM
• Insulin dependent Diabetes Mellitus

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Diabetes Mellitus

• CLASSIFICATION OF DM
• 2. Type 2 DM
• Non-insulin dependent Diabetes Mellitus

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Diabetes Mellitus

• CLASSIFICATION OF DM
• 3. Gestational DM
• Diabetes Mellitus diagnosed during pregnancy

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Diabetes Mellitus

• CLASSIFICATION OF DM
• 4. DM associated with other conditions or
  syndromes

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Diabetes Mellitus

• Other types of DM
• 1. Impaired Glucose Tolerance
• 2. Impaired Fasting Glucose
• 3. Pre-diabetes

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TYPE 1- Diabetes Mellitus

• This type of DM is characterized by the
  destruction of the pancreatic beta cells

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TYPE 1- Diabetes Mellitus

• Etiology
• 1. Genetic susceptibility- HLA DR3 and DR4
• 2. Autoimmune response
• 3. Toxins, unidentified viruses and environmental
  factors

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TYPE 1- Diabetes Mellitus

• PATHOPHYSIOLOGY
• Destruction of BETA cells? decreased insulin
  production ? uncontrolled glucose production by
  the liver? hyperglycemia ? signs and symptoms

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TYPE 1- Diabetes Mellitus

• PATHOPHYSIOLOGY
• CLASSIC Ps
• Polyuria
• Polydipsia
• Polyphagia

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TYPE 2- Diabetes Mellitus

• A type of DM characterized by insulin resistance
  and impaired insulin production

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TYPE 2- Diabetes Mellitus

• Etiology
• 1. Unknown
• 2. Probably genetic and obesity

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TYPE 2- Diabetes Mellitus

• PATHOPHYSIOLOGY
• Decreased sensitivity of insulin receptor to
  insulin ? less uptake of glucose ? HYPERGLYCEMIA

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TYPE 2- Diabetes Mellitus

• PATHOPHYSIOLOGY
• Decreased insulin production ? diminished insulin
  action ? hyperglycemia ? signs and symptoms

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TYPE 2- Diabetes Mellitus

• PATHOPHYSIOLOGY
• BUT () insulin in small amount ? prevent
  breakdown of fats ? DKA is unusual

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GESTATIONAL Diabetes Mellitus

• Any degree of glucose intolerance with its onset
  during pregnancy
• Usually detected between 24-28th week gestation

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GESTATIONAL Diabetes Mellitus

• Blood glucose returns to normal after delivery of
  the infant
• NEVER administer ORAL HYPOGLYCEMIC AGENTS to
  PREGNANT MOTHERS!

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Diabetes Mellitus

• ASSESSMENT FINDINGS
• 1. Classic 3 Ps
• 2. Fatigue
• 3. Body weakness

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Diabetes Mellitus

• ASSESSMENT FINDINGS
• 4. Visual changes
• 5. Slow wound healing
• 6. Recurrent skin and mucus membrane infections

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Diabetes Mellitus

• DIAGNOSTIC TESTS
• 1. FBS- gt 126
• 2. RBS- gt200
• 3. OGTT- gt 200

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Diabetes Mellitus

• DIAGNOSTIC TESTS
• 4. HgbA1- for monitoring!!
• 5. Urine glucose
• 6. Urine ketones

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Diabetes Mellitus

• DIAGNOSTIC CRITERIA
• 1. FBS equal to or greater than 126 mg/dL
  (7.0mmol/L)
• (Normal 8 hour FBS- 80-109 mg/dL)

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Diabetes Mellitus

• DIAGNOSTIC CRITERIA
• 2. OGTT value 1 and 2 hours post-prandial equal
  to or greater than 200 mg/dL
• Normal OGTT 1 and 2 hours post-prandial- is
• 140 mg/dL

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Diabetes Mellitus

• DIAGNOSTIC CRITERIA
• 3. RBS of equal to or greater than 200 mg/dL PLUS
  the 3 Ps

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Diabetes Mellitus

• NURSING MANAGEMENT OF DM
• The main goal is to NORMALIZE insulin activity
  and blood glucose level by

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Diabetes Mellitus

• NURSING MANAGEMENT OF DM
• 1. Nutritional modification
• 2. Regular Exercise
• 3. Regular Glucose Monitoring
• 4. Drug therapy
• 5. Client Education

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Diabetes Mellitus

• The Patient with DM
• HISTORY
• Symptoms and characteristics
• PHYSICAL EXAMINATION
• VS, BMI, Fundoscopy, Neuro
• LABORATORY EXAMINATION
• FBS, RBS, HgbA1c, lipid profile, ECG, UA
• REFERRALS
• Ophthalmologist, Podiatrist, Dietician, etc..

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Diabetes Mellitus

• The Patient with DM
• HISTORY
• Symptoms and characteristics
• PHYSICAL EXAMINATION
• VS, BMI, Fundoscopy, and Neuro assessment

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Diabetes Mellitus

• The Patient with DM
• LABORATORY EXAMINATION
• FBS, RBS, HgbA1c, lipid profile, ECG, and
  Urinalysis
• REFERRALS
• Ophthalmologist, Podiatrist, Dietician, etc..

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DM Nutritional management
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Diabetes Mellitus

• NUTRITIONAL MANAGEMENT
• 1.Review the patients diet history to identify
  eating habits and lifestyle
• 2. Coordinate with the dietician in meal planning
  for weight loss

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Diabetes Mellitus

• NUTRITIONAL MANAGEMENT
• 3. Plan for the caloric intake distributed as
  follows- CHO 50-60 Fats 20-30 and Proteins
  10-20
• 4. Advise moderation in alcohol intake
• 5. Using artificial sweeteners is acceptable

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DM Exercise management
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Diabetes Mellitus

• EXERCISE Management
• 1. Teach that exercise can lower the blood
  glucose level
• 2. Diabetics must first control the glucose level
  before initiating exercise programs.

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Diabetes Mellitus

• EXERCISE Management
• 3. Offer extra food /calories before engaging in
  exercise
• 4. Offer snacks at the end of the exercise period
  if patient is on insulin treatment.

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Diabetes Mellitus

• EXERCISE Management
• 5. Advise that exercise should be done at the
  same time every day, preferably when blood
  glucose levels are at their peak

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Diabetes Mellitus

• EXERCISE Management
• 6. Regular exercise, not sporadic exercise,
  should be encouraged.
• 7. For most patient, WALKING is the safe and
  beneficial form of exercise

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Glucose Self Monitoring
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Diabetes Mellitus

• GLUCOSE MONITORING
• Self-monitoring of blood glucose (SMBG) enables
  the patient to adjust the treatment regimen to
  obtain optimal glucose control

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Diabetes Mellitus

• GLUCOSE MONITORING
• Most common method involves obtaining a drop of
  capillary blood applied to a test strip.
• The usual recommended frequency is TWO-FOUR times
  a day.

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Diabetes Mellitus

• When is it done?
• At the peak action time of the medication to
  evaluate the need for adjustments.
• To evaluate BASAL insulin ? test before meals

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Diabetes Mellitus

• When is it done?
• To titrate bolus or regular and lispro? test 2
  hours after meals.
• To evaluate the glucose level of those taking
  ORAL hypoglycemics ? test before and two hours
  after meals.

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Diabetes Mellitus Monitoring therapy

• Testing the glycosylated hemoglobin (HbA1c)
• This glycosylated hemoglobin refers to the blood
  test that reflects the average blood glucose over
  a period of TWO to THREE months.

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Diabetes Mellitus Monitoring therapy

• Normal value is 4 to 6
• No patient preparation is needed for this testing
• Done to monitor therapy

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Diabetes Mellitus

• Urine testing for glucose
• Benedicts test

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Diabetes Mellitus

• Urine testing for ketones
• Ketones are by-products of fat breakdown

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Diabetes Mellitus

• Urine testing for ketones
• This is performed whenever TYPE 1 DM have
  glucosuria or persistent elevation of blood
  glucose, during illness, and in gestational
  diabetes

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DM Drug therapy
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Diabetes Mellitus

• DRUG THERAPY and MANAGEMENT
• Usually, this type of management is employed if
  diet modification and exercise cannot control the
  blood glucose level.

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Diabetes Mellitus

• DRUG THERAPY and MANAGEMENT
• Because the patient with TYPE 1 DM cannot produce
  insulin, exogenous insulin must be administered
  for life.

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Diabetes Mellitus

• DRUG THERAPY and MANAGEMENT
• TYPE 2 DM may have decreased insulin production,
  ORAL agents that stimulate insulin production are
  usually employed.

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Diabetes Mellitus

• PHARMACOLOGIC INSULIN
• This may be grouped into several categories
  according to
• 1. Source- Human, pig, or cow
• 2. Onset of action- Rapid-acting, short-acting,
  intermediate-acting, long-acting and very long
  acting

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Diabetes Mellitus

• PHARMACOLOGIC INSULIN
• This may be grouped into several categories
  according to
• 3. Pure or mixed concentration
• 4. Manufacturer of drug

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Diabetes Mellitus

• GENERALITIES
• 1. Human insulin preparations have a shorter
  duration of action than animal source

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Diabetes Mellitus

• GENERALITIES
• 2. Animal sources of insulin have animal proteins
  that may trigger allergic reaction and they may
  stimulate antibody production that may bind the
  insulin, slowing the action

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Diabetes Mellitus

• 3. ONLY Regular insulin can be used INTRAVENOUSLY!

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Diabetes Mellitus

• 4. Insulin are measured in INTERNATIONAL UNITS or
  iu
• 5. There is a specified insulin injection
  calibrated in units

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Diabetes Mellitus

• RAPID ACTING INSULIN
• Lispro (Humalog) and Insulin Aspart (Novolog)
• Produces a more rapid effect and with a shorter
  duration than any other insulin preparation

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Diabetes Mellitus

• RAPID ACTING INSULIN
• ONSET- 5-15 minutes
• PEAK- 1 hour
• DURATION- 3 hours
• Instruct patient to eat within 5 to 15 minutes
  after injection

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Diabetes Mellitus

• REGULAR INSULIN
• Also called Short-acting insulin
• R
• Usually Clear solution administered 30 minutes
  before a meal

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Diabetes Mellitus

• REGULAR INSULIN
• ONSET- 30 minutes to 1 hour
• PEAK- 2 to 3 hours
• DURATION- 4 to 6 hours

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Diabetes Mellitus

• INTERMEDIATE ACTING INSULIN
• Called NPH or LENTE
• Appears white and cloudy

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Diabetes Mellitus

• INTERMEDIATE ACTING INSULIN
• ONSET- 2-4 hours
• PEAK- 4 to 6-12 hours
• DURATION- 16-20 hours

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Diabetes Mellitus

• LONG- ACTING INSULIN
• UltraLENTE
• Referred to as peakless insulin

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Diabetes Mellitus

• LONG- ACTING INSULIN
• ONSET- 6-8 hours
• PEAK- 12-16 hours
• DURATION- 20-30 hours

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Diabetes Mellitus

• HEALTH TEACHING
• Regarding Insulin SELF- Administration
• 1. Insulin is administered at home subcutaneously

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Diabetes Mellitus

• HEALTH TEACHING Regarding Insulin SELF-
  Administration
• 2. Cloudy insulin should be thoroughly mixed by
  gently inverting the vial or ROLLING between the
  hands

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Diabetes Mellitus

• HEALTH TEACHING Regarding Insulin SELF-
  Administration
• 3. Insulin NOT IN USE should be stored in the
  refrigerator, BUT avoid freezing/extreme
  temperature

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Diabetes Mellitus

• 4. Insulin IN USE should be kept at room
  temperature to reduce local irritation at the
  injection site

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Diabetes Mellitus

• 5. INSULIN may be kept at room temperature up to
  1 month

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Diabetes Mellitus

• 6. Select syringes that match the insulin
  concentration.
• U-100 means 100 units per mL

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Diabetes Mellitus

• 7. Instruct the client to draw up the REGULAR
  (clear) Insulin FIRST before drawing the
  intermediate acting (cloudy) insulin

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Diabetes Mellitus

• 8. Pre-filled syringes can be prepared and should
  be kept in the refrigerator with the needle in
  the UPRIGHT position to avoid clogging the needle

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Diabetes Mellitus

• 9. The four main areas for insulin injection are-
  ABDOMEN, UPPER ARMS, THIGHS and HIPS

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Diabetes Mellitus

• Insulin is absorbed fastest in the abdomen and
  slowest in the hips
• Instruct the client to rotate the areas of
  injection, but exhaust all available sites in one
  area first before moving into another area.

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Diabetes Mellitus

• 10. Alcohol may not be used to cleanse the skin
• 11. Utilize the subcutaneous injection technique-
  commonly, a 45-90 degree angle.

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Diabetes Mellitus

• 12. No need to instruct for aspirating the needle
• 13. Properly discard the syringe after use.

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Diabetes Mellitus

• T-I-E
• Test blood? Inject insulin ? Eat food

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Diabetes Mellitus

• COMPLICATIONS OF INSULIN THERAPY
• 1. Local allergic reactions
• Redness, swelling, tenderness and induration
  appearing 1-2 hours after injection
• Usually occurs in the beginning stage of therapy

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Diabetes Mellitus

• COMPLICATIONS OF INSULIN THERAPY
• 1. Local allergic reactions
• Disappears with continued use
• Antihistamine can be given 1 hour before
  injection time
• Porcine and bovine insulin preparations have a
  higher tendency to produce this reaction.

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Diabetes Mellitus

• 2. SYSTEMIC ALLERGIC REACTIONS
• Very rare
• Generalized urticaria is the manifestation
• Treatment is desensitization

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Diabetes Mellitus

• COMPLICATIONS OF INSULIN THERAPY
• 3. INSULIN DYSTROPHY
• A localized reaction in the form of lipoatrophy
  or lipohypertrophy

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Diabetes Mellitus

• Lipoatrophy- loss of subcutaneous fat usually
  caused by the utilization of animal insulin

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Diabetes Mellitus

• Lipohypertrophy- development of fibrofatty
  masses, usually caused by repeated use of
  injection site

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Diabetes Mellitus

• 4. INSULIN RESISTANCE
• Most commonly caused by OBESITY
• Defined as daily insulin requirement of more than
  200 units
• Management- Steroids and use of more concentrated
  insulin

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Diabetes Mellitus

• 5. MORNING HYPERGLYCEMIA
• Elevated blood sugar upon arising in the morning
• Caused by insufficient level of insulin
• DAWN phenomenon
• SOMOGYI effect
• INSULIN WANING

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Diabetes Mellitus

• DAWN PHENOMENON
• Relatively normal blood glucose until about 3 am,
  when the glucose level begins to RISE
• Results from the nightly surges of GROWTH HORMONE
  secretion
• Management Bedtime injection of NPH

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Diabetes Mellitus

• SOMOGYI EFFECT
• Normal or elevated blood glucose at bedtime,
  decrease blood glucose at 2-3 am due to
  hypoglycemic levels and a subsequent increase in
  blood glucose (rebound hypergycemia)

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Diabetes Mellitus

• SOMOGYI EFFECT
• Nocturnal hypoglycemia followed by rebound
  hyperglycemia

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Diabetes Mellitus

• SOMOGYI EFFECT
• Due to the production of counter regulatory
  hormones- glucagon. cortisol and epinephrine
• Management- decrease evening dose of NPH or
  increase bedtime snack

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Diabetes Mellitus

• INSULIN WANING
• Progressive rise in blood glucose from bedtime to
  morning
• Seen when the NPH evening dose is administered
  before dinner
• Management Move the insulin injection to bedtime

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Diabetes Mellitus

• ORAL HYPOGLYCEMIC AGENTS
• These may be effective when used in TYPE 2 DM
  that cannot be treated with diet and exercise
• These are NEVER used in pregnancy!

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Diabetes Mellitus

• ORAL HYPOGLYCEMIC AGENTS
• There are several agents
• Sulfonylureas
• Biguanides
• Alpha-glucosidase inhibitors
• Thiazolidinediones
• Meglitinides

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Diabetes Mellitus

• SULFONYLUREAS
• MOA- stimulates the beta cells of the pancreas to
  secrete insulin
• Classified as to generations- first and second
  generations

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Diabetes Mellitus

• SULFONYLUREAS
• FIRST GENERATION- Acetoheximide, Chlorpropamide,
  Tolazamide and Tolbutamide
• SECOND GENERATION- Glipizide, Glyburide,
  Glibenclamide, Glimepiride

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Diabetes Mellitus Sulfonylureas

• The most common side effects of these
  medications are Gastro-intestinal upset and
  dermatologic reactions.
• HYPOGLYCEMIA is also a very important side-effect

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Diabetes Mellitus Sulfonylureas

• Chlorpropamide has a very long duration of
  action. This also produces a disulfiram-like
  reaction when taken with alcohol
• Second generation drugs have shorter duration
  with metabolism in the kidney and liver and are
  the choice for elderly patients

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Diabetes Mellitus

• BIGUANIDES
• MOA- Facilitate the action of insulin on the
  peripheral receptors
• These can only be used in the presence of insulin

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Diabetes Mellitus

• BIGUANIDES formin
• They have no effect on the beta cells of the
  pancreas
• Metformin (Glucophage) and Phenformin are examples

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Diabetes Mellitus Biguanides

• The most important side effect is LACTIC
  ACIDOSIS!
• These are not given to patient with renal
  impairment

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Diabetes Mellitus Biguanides

• These drugs are usually given with a sulfonylurea
  to enhance the glucose-lowering effect more than
  the use of each drug individually

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Diabetes Mellitus

• ALPHA-GLUCOSIDASE INHIBITORS
• MOA- Delay the absorption of glucose in the GIT
• Result is a lower post-prandial blood glucose
  level
• They do not affect insulin secretion or action!
• Side-effect DIARRHEA and FLATULENCE

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Diabetes Mellitus

• Examples of AGI are Acarbose and Miglitol
• They are not absorbed systemically and are very
  safe
• They can be used alone or in combination with
  other OHA

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Diabetes Mellitus

• Side-effect if used with other drug is
  HYPOGLYCEMIA
• Note that sucrose absorption is impaired and IV
  glucose is the therapy for the hypoglycemia

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Diabetes Mellitus

• THIAZOLIDINEDIONES
• MOA- Enhance insulin action at the receptor site
• They do not stimulate insulin secretion

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Diabetes Mellitus

• THIAZOLIDINEDIONES
• Examples- Rosiglitazone, Pioglitazone
• These drugs affect LIVER FUNCTION
• Can cause resumption of OVULATION in
  peri-menopausal anovulatory women

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Diabetes Mellitus

• MEGLITINIDES
• MOA- Stimulate the secretion of insulin by the
  beta cells
• Examples- Repaglinide and Nateglinide

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Diabetes Mellitus

• MEGLITINIDES
• They have a shorter duration and fast action
• Should be taken BEFORE meals to stimulate the
  release of insulin from the pancreas

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Diabetes Mellitus

• MEGLITINIDES
• Principal side-effect of meglitinides-
  hypoglycemia
• Can be used alone or in combination

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Diabetes Mellitus

• ACUTE COMPLICATIONS OF DM
• Hypoglycemia
• Diabetic ketoacidosis
• Hyperglycemic hyperosmolar non-ketotic syndrome
  (HHNS)

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Diabetes Mellitus

• CHRONIC COMPLICATIONS OF DM
• Macrovascular complications- MI, Stroke,
  Atherosclerosis, CAD, and Peripheral vascular
  disease
• Microvascular complications- micro-angiopathy,
  retinopathy, nephropathy
• Peripheral neuropathy

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Diabetes Mellitus

• HYPOGLYCEMIA
• Blood glucose level less than 50 to 60 mg/dL
• Causes Too much insulin/OHA, too little food and
  excessive physical activity
• Mild- 40-60
• Moderate- 20-40
• Severe- less than 20

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HYPOGLYCEMIA

• ASSESSMENT FINDINGS
• 1. Sympathetic manifestations- sweating, tremors,
  palpitations, nervousness, tachycardia and hunger

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HYPOGLYCEMIA

• ASSESSMENT FINDINGS
• 2. CNS manifestations- inability to concentrate,
  headache, lightheadedness, confusion, memory
  lapses, slurred speech, impaired coordination,
  behavioral changes, double vision and drowsiness

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HYPOGLYCEMIA
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HYPERGLYCEMIA
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HYPOGLYCEMIA

• DIAGNOSTIC FINDINGS
• RBS- less than 50-60 mg/dL level

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HYPOGLYCEMIA

• Nursing Interventions
• 1. Immediate treatment with the use of foods with
  simple sugar- glucose tablets, fruit juice, table
  sugar, honey or hard candies

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HYPOGLYCEMIA

• Nursing Interventions
• 2. For unconscious patients- glucagon injection 1
  mg IM/SQ or IV 25 to 50 mL of D50/50

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HYPOGLYCEMIA

• Nursing Interventions
• 3. re-test glucose level in 15 minutes and
  re-treat if less than 75 mg/dL
• 4. Teach patient to refrain from eating
  high-calorie, high-fat desserts

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HYPOGLYCEMIA

• Nursing Interventions
• 5. Advise in-between snacks, especially when
  physical activity is increased
• 6. Teach the importance of compliance to
  medications

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Diabetic Ketoacidosis

• This is cause by the absence of insulin leading
  to fat breakdown and production of ketone bodies
• Three main clinical features
• 1. HYPERGLYCEMIA
• 2. DEHYDRATION electrolyte loss
• 3. ACIDOSIS

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DKA

• PATHOPHYSIOLOGY
• No insulin? reduced glucose breakdown and
  increased liver glucose production ? Hyperglycemia

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DKA

• PATHOPHYSIOLOGY
• Hyperglycemia? kidney attempts to excrete glucose
  ? increased osmotic load ? diuresis ? Dehydration

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DKA

• PATHOPHYSIOLOGY
• No glucose in the cell? fat is broken down for
  energy ? ketone bodies are produced? Ketoacidosis

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DKA

• Risk factors
• 1. infection or illness- common
• 2. stress
• 3. undiagnosed DM
• 4. inadequate insulin, missed dose of insulin

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DKA

• ASSESSMENT FINDINGS
• 1. 3 Ps
• 2. Headache, blurred vision and weakness
• 3. Orthostatic hypotension

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DKA

• ASSESSMENT FINDINGS
• 4. Nausea, vomiting and abdominal pain
• 5. Acetone (fruity) breath
• 6. Hyperventilation or KUSSMAULs breathing

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HYPERGLYCEMIA
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Hyperglycemia
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DKA

• LABORATORY FINDINGS
• 1. Blood glucose level of 300-800 mg/dL
• 2. Urinary ketones

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DKA

• LABORATORY FINDINGS
• 3. ABG result of metabolic acidosis- LOW pH, LOW
  pCO2 as a compensation, LOW bicarbonate
• 4. Electrolyte imbalances- potassium levels may
  be HIGH due to acidosis and dehydration

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DKA

• NURSING INTERVENTIONS
• 1. Assist in the correction of dehydration
• Up to 6 liters of fluid may be ordered for
  infusion, initially NSS then D5W
• Monitor hydration status
• Monitor I and O
• Monitor for volume overload

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DKA

• NURSING INTERVENTIONS
• 2. Assist in restoring Electrolytes
• Kidney function is FIRST determined before giving
  potassium supplements!

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DKA

• NURSING INTERVENTIONS
• 3. Reverse the Acidosis
• REGULAR insulin injection is ordered IV bolus
  5-10 units
• The insulin is followed by drip infusion in units
  per hour
• BICARBONATE is not used!

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HHNS

• A serious condition in which hyperosmolarity and
  extreme hyperglycemia predominate
• Ketosis is minimal
• Onset is slow and takes hours to days to develop

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HHNS

• PATHOPHYSIOLOGY
• Lack of insulin action or Insulin resistance ?
  hyperglycemia
• Hyperglycemia? osmotic diuresis ? loss of water
  and electrolytes

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HHNS

• PATHOPHYSIOLOGY
• Insulin is too low to prevent hyperglycemia but
  enough to prevent fat breakdown
• Occurs most commonly in type 2 DM, ages 50-70

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HHNS

• Precipitating factors
• 1. Infection
• 2. Stress
• 3. Surgery
• 4. Medication like thiazides
• 5. Treatment like dialysis

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HHNS

• ASSESSMENT FINDINGS
• 1. Profound dehydration
• 2. Hypotension
• 3. Tachycardia
• 4. Altered sensorium
• 5. Seizures and hemiparesis

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HHNS

• DIAGNOSTIC TESTS
• 1. Blood glucose- 600 to 1,200 mg/dL
• 2. Blood osmolality- 350 mOsm/L
• 3. Electrolyte abnormalities

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HHNS

• NURSING INTERVENTIONS
• Approach is similar to the DKA
• 1. Correction of Dehydration by IVF
• 2. Correction of electrolyte imbalance by
  replacement therapy

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HHNS

• NURSING INTERVENTIONS
• 3. Administration of insulin injection and drips
• 4. Continuous monitoring of urine output

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MACROVASCULAR CX

• Nursing management
• 1. Diet modification
• 2. Exercise

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MACROVASCULAR CX

• Nursing management
• 3. Prevention and treatment of underlying
  conditions such as MI, CAD and stroke
• 4. Administration of prescribed medications for
  hypertension, hyperlipidemia and obesity

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MICROVASCULAR CX

• Retinopathy- a painless deterioration of the
  small blood vessels in the retina, may be
  classified as to background retinopathy,
  pre-proliferative and proliferative retinopathy
• Permanent vision changes and blindness can occur

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MICROVASCULAR CX

• Retinopathy-ASSESSMENT FINDINGS
• Blurry vision
• Spotty vision
• Asymptomatic

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MICROVASCULAR CX

• Retinopathy Diagnostic findings
• 1. Fundoscopy
• 2. Fluorescein angiography
• Painless procedure
• Side-effects- discoloration of the skin and urine
  for 12 hours, some allergic reactions, nausea
• Flash of camera may be slightly uncomfortable

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MICROVASCULAR CX

• NURSING INTERVENTIONS
• 1. Assist in diagnostic procedure
• 2. Assist in the preparation for surgery- laser
  photocoagulation

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MICROVASCULAR CX

• NURSING INTERVENTIONS
• 3. Health teaching regarding prevention of
  retinopathy by regular ophthalmic examinations,
  good glucose control and self-management of eye
  care regimens
• 4. Maintain client safety

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MICROVASCULAR CX

• DIABETIC NEPHROPATHY
• Progressive deterioration of kidney function

164
MICROVASCULAR CX

• DIABETIC NEPHROPATHY
• HYPERGLYCEMIA? causes the kidney filtration
  mechanism to be stressed ? blood proteins leak
  into the urine
• Pressure in the kidney blood vessels increases?
  stimulate the development of nephropathy

165
MICROVASCULAR CX

• ASSESSMENT findings for diabetic nephropathy
• 1. Albuminuria
• 2. Anemia
• 3. Acidosis

166
MICROVASCULAR CX

• ASSESSMENT findings for diabetic nephropathy
• 4. Fluid volume overload
• 5. Oliguria
• 6. Hypertension
• 7. UTI

167
MICROVASCULAR CX

• NURSING MANAGEMENT1. Assist in the control of
  hypertension- use of ACE inhibitor
• 2. Provide a low sodium and low protein diet
• 3. Administer prescribed medication for UTI

168
MICROVASCULAR CX

• NURSING MANAGEMENT
• 4. Assist in dialysis
• 5. Prepare patient for renal transplantation, if
  indicated

169
MICROVASCULAR CX

• Diabetic Neuropathy
• A group of disorders that affect all type of
  nerves including the peripheral, autonomic and
  spinal nerves

170
MICROVASCULAR CX

• Diabetic Neuropathy
• Two most common types of Diabetic Neuropathy are
  sensori-motor polyneuropathy and autonomic
  neuropathy

171
MICROVASCULAR CX

• Peripheral neuropathy- ASSESSMENT findings
• 1. paresthesias- prickling, tingling or
  heightened sensation
• 2. decreased proprioception
• 3. decreased sensation of light touch
• 4. unsteady gait
• 5. decreased tendon reflexes

172
MICROVASCULAR CX

• Peripheral neuropathy- Nursing Management
• 1. Provide teaching that good glucose control is
  very important to prevent its development
• 2. Manage the pain by analgesics, antidepressants
  and nerve stimulation

173
MICROVASCULAR CX

• Autonomic Neuropathy- ASSESSMENT findings
• 1. Silent, painless ischemia
• 2. delayed gastric emptying
• 3. orthostatic hypotension
• 4. N/V and bloating sensation
• 5. urinary retention
• 6. sexual dysfunction

174
MICROVASCULAR CX

• Autonomic Neuropathy-Nursing management
• 1. Educate about the avoidance of strenuous
  physical activity
• 2. Stress the importance of good glucose control
  to delay the development

175
MICROVASCULAR CX

• Autonomic Neuropathy-Nursing management
• 3. Provide LOW-fat, small frequent feedings
• 4. Administer bulk-forming laxatives for diabetic
  diarrhea
• 5. Provide HIGH-fiber diet for diabetic
  constipation

176
MICROVASCULAR CX

• MANAGEMENT OF FOOT AND LEG PROBLEMS
• Soft tissue injury in the foot/leg? formation of
  fissures and callus ? poor wound healing ?
  foot/leg ulcer

177
MICROVASCULAR CX

• RISK FACTORS for the development of foot and leg
  ulcers
• 1. More than 10 years diabetic
• 2. Age of more than 40
• 3. Smoking
• 4. Anatomic deformities
• 5. History of previous leg ulcers or amputation

178
MICROVASCULAR CX

• MANAGEMENT of Foot Ulcers
• Teach patient proper care of the foot
• Daily assessment of the foot
• Use of mirror to inspect the bottom

179
MICROVASCULAR CX

• MANAGEMENT of Foot Ulcers
• Inspect the surface of shoes for any rough spots
  or foreign objects
• Properly dry the feet
• Instruct to wear closed-toe shoes that fit well,
  recommend use of low-heeled shoes

180
MICROVASCULAR CX

• MANAGEMENT
• Instruct patient NEVER to walk barefoot, never to
  use heating pads, open-toed shoes and soaking
  feet
• Trim toenails STRAIGHT ACROSS and file sharp
  corners
• Instruct to avoid smoking and over-the counter
  medications and home remedies for foot problems

181
End of DM