Diabetes Mellitus

Prepared by: LORI R. LARA,R.N.

 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.
 Diabetes Mellitus

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

 BASIC PATHOLOGY : Insulin problem (deficiency or impaired action)
 Diabetes Mellitus
 Insulin is a hormone secreted by the BETA cells of the pancreas
 Stimulus of insulin- HYPERGLYCEMIA
 Action of insulin: it promotes entry of Glucose into the body cells by binding
to the insulin receptor in the cell membrane
 INSULIN : Physiology
 Insulin Metabolic Functions:
 1. Transports and metabolizes GLUCOSE
 2. Promotes GLYCOGENESIS
 3. Promotes GLYCOLYSIS
 4. Enhances LIPOGENESIS
 5. Accelerates PROTEIN SYNTHESIS

 RISK FACTORS for Diabetes Mellitus

 1. Family History of diabetes
 2. Obesity
 3. Race/Ethnicity
 RISK FACTORS for Diabetes Mellitus
 4. Age of more than 45
 5. Previously unidentified IFG/IGT
 6. Hypertension
 RISK FACTORS for Diabetes Mellitus
 7. Hyperlipidemia
 8. History of Gestational Diabetes Mellitus

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

 CLASSIFICATION OF DM
 Type 1 DM
 Insulin dependent Diabetes Mellitus

 CLASSIFICATION OF DM
 Type 2 DM
 Non-insulin dependent Diabetes Mellitus
 CLASSIFICATION OF DM
 Gestational DM
 Diabetes Mellitus diagnosed during pregnancy
 CLASSIFICATION OF DM
 DM associated with other conditions or syndromes

 Other types of DM
 1. Impaired Glucose Tolerance
 2. Impaired Fasting Glucose
 3. Pre-diabetes
 TYPE 1- Diabetes Mellitus
 This type of DM is characterized by the destruction of the pancreatic beta
cells
 TYPE 1- Diabetes Mellitus
 Etiology:
 Genetic susceptibility- HLA DR3 and DR4
 Autoimmune response
 Toxins, unidentified viruses and environmental factors
 TYPE 1- Diabetes Mellitus
 PATHOPHYSIOLOGY
 Destruction of BETA cells decreased insulin production  uncontrolled
glucose production by the liver hyperglycemia  signs and symptoms
 TYPE 1- Diabetes Mellitus
 PATHOPHYSIOLOGY
 CLASSIC P’s
 Polyuria
 Polydipsia
 Polyphagia
 TYPE 2- Diabetes Mellitus
 A type of DM characterized by insulin resistance and impaired insulin
production
 TYPE 2- Diabetes Mellitus
 Etiology:
 Unknown
 Probably genetic and obesity
 TYPE 2- Diabetes Mellitus
 PATHOPHYSIOLOGY
 Decreased sensitivity of insulin receptor to insulin  less uptake of glucose
 HYPERGLYCEMIA
 TYPE 2- Diabetes Mellitus
 PATHOPHYSIOLOGY
 Decreased insulin production  diminished insulin action  hyperglycemia
 signs and symptoms
 TYPE 2- Diabetes Mellitus
 PATHOPHYSIOLOGY
 BUT (+) insulin in small amount  prevent breakdown of fats  DKA is
unusual
 GESTATIONAL Diabetes Mellitus
 Any degree of glucose intolerance with its onset during pregnancy
 Usually detected between 24-28th week gestation
 GESTATIONAL Diabetes Mellitus
 Blood glucose returns to normal after delivery of the infant
 NEVER administer ORAL HYPOGLYCEMIC AGENTS to PREGNANT
MOTHERS!
 ASSESSMENT FINDINGS
 1. Classic 3 P’s
 2. Fatigue
 3. Body weakness
 ASSESSMENT FINDINGS
 4. Visual changes
 5. Slow wound healing
 6. Recurrent skin and mucus membrane infections
 DIAGNOSTIC TESTS
 1. FBS- > 126
 2. RBS- >200
 3. OGTT- > 200

 DIAGNOSTIC TESTS
 4. HgbA1- for monitoring!!
 5. Urine glucose
 6. Urine ketones
 DIAGNOSTIC CRITERIA
 1. FBS equal to or greater than 126 mg/dL (7.0mmol/L)
 (Normal 8 hour FBS- 80-109 mg/dL)
 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

 DIAGNOSTIC CRITERIA
 3. RBS of equal to or greater than 200 mg/dL PLUS the 3 P’s
 Diabetes Mellitus
 NURSING MANAGEMENT OF DM
 The main goal is to NORMALIZE insulin activity and blood glucose level
 NURSING MANAGEMENT OF DM
 Nutritional modification
 Regular Exercise
 Regular Glucose Monitoring
 Drug therapy
 Client Education

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..

 The Patient with DM

 HISTORY
 Symptoms and characteristics
 PHYSICAL EXAMINATION
 VS, BMI, Fundoscopy, and Neuro assessment
 LABORATORY EXAMINATION
 FBS, RBS, HgbA1c, lipid profile, ECG, and Urinalysis
 REFERRALS
 Ophthalmologist, Podiatrist, Dietician, etc..

 DM Nutritional management
 Diabetes Mellitus
 NUTRITIONAL MANAGEMENT
 1.Review the patient’s diet history to identify eating habits and lifestyle
 2. Coordinate with the dietician in meal planning for weight loss
 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
 DM Exercise management

 EXERCISE Management
 1. Teach that exercise can lower the blood glucose level
 2. Diabetics must first control the glucose level before initiating exercise
programs.
 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.
 EXERCISE Management
 5. Advise that exercise should be done at the same time every day, preferably
when blood glucose levels are at their peak
 EXERCISE Management
 6. Regular exercise, not sporadic exercise, should be encouraged.
 7. For most patient, WALKING is the safe and beneficial form of exercise
 Glucose Self Monitoring
 Diabetes Mellitus
 GLUCOSE MONITORING
 Self-monitoring of blood glucose (SMBG) enables the patient to adjust the
treatment regimen to obtain optimal glucose control
 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.

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
 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.
 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.
 Normal value is 4 to 6 %
 No patient preparation is needed for this testing
 Done to monitor therapy
 Urine testing for glucose
 Benedict’s test
 Urine testing for ketones
 Ketones are by-products of fat breakdown
 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
 DM Drug therapy
 DRUG THERAPY and MANAGEMENT
 Usually, this type of management is employed if diet modification and
exercise cannot control the blood glucose level.
 DRUG THERAPY and MANAGEMENT
 Because the patient with TYPE 1 DM cannot produce insulin, exogenous
insulin must be administered for life.
 DRUG THERAPY and MANAGEMENT
 TYPE 2 DM may have decreased insulin production, ORAL agents that
stimulate insulin production are usually employed.

PHARMACOLOGIC INSULIN
 This may be grouped into several categories according to:
 Source- Human, pig, or cow
 Onset of action- Rapid-acting, short-acting, intermediate-acting, long-acting
and very long acting
 PHARMACOLOGIC INSULIN
 This may be grouped into several categories according to:
 Pure or mixed concentration
 Manufacturer of drug
 GENERALITIES
 1. Human insulin preparations have a shorter duration of action than animal
source
 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
 3. ONLY Regular insulin can be used INTRAVENOUSLY!
 4. Insulin are measured in INTERNATIONAL UNITS or “iu”
 5. There is a specified insulin injection calibrated in units
 RAPID ACTING INSULIN
 Lispro (Humalog) and Insulin Aspart (Novolog)
 Produces a more rapid effect and with a shorter duration than any other
insulin preparation
 RAPID ACTING INSULIN
 ONSET- 5-15 minutes
 PEAK- 1 hour
 DURATION- 3 hours
 Instruct patient to eat within 5 to 15 minutes after injection

 REGULAR INSULIN
 Also called Short-acting insulin
 “R”
 Usually Clear solution administered 30 minutes before a meal
 REGULAR INSULIN
 ONSET- 30 minutes to 1 hour
 PEAK- 2 to 3 hours
 DURATION- 4 to 6 hours
 INTERMEDIATE ACTING INSULIN
 Called “NPH” or “LENTE”
 Appears white and cloudy
 INTERMEDIATE ACTING INSULIN
 ONSET- 2-4 hours
 PEAK- 6-12 hours
 DURATION- 16-20 hours
 LONG- ACTING INSULIN
 “UltraLENTE”
 Referred to as “peakless” insulin
 LONG- ACTING INSULIN
 ONSET- 6-8 hours
 PEAK- 12-16 hours
 DURATION- 20-30 hours
 HEALTH TEACHING
 Regarding Insulin SELF- Administration
 1. Insulin is administered at home subcutaneously
 HEALTH TEACHING Regarding Insulin SELF- Administration
 2. Cloudy insulin should be thoroughly mixed by gently inverting the vial or
ROLLING between the hands
 HEALTH TEACHING Regarding Insulin SELF- Administration
 3. Insulin NOT IN USE should be stored in the refrigerator, BUT avoid
freezing/extreme temperature
 4. Insulin IN USE should be kept at room temperature to reduce local
irritation at the injection site
 5. INSULIN may be kept at room temperature up to 1 month
 6. Select syringes that match the insulin concentration.
 U-100 means 100 units per mL
 7. Instruct the client to draw up the REGULAR (clear) Insulin FIRST before
drawing the intermediate acting (cloudy) insulin
  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
 9. The four main areas for insulin injection are- ABDOMEN, UPPER
ARMS, THIGHS and HIPS

 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.
 10. Alcohol may not be used to cleanse the skin
 11. Utilize the subcutaneous injection technique- commonly, a 45-90 degree
angle.
 12. No need to instruct for aspirating the needle
 13. Properly discard the syringe after use.
T-I-E
 Test blood Inject insulin  Eat food

 COMPLICATIONS OF INSULIN THERAPY

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

SYSTEMIC ALLERGIC REACTIONS

 Very rare
 Generalized urticaria is the manifestation
 Treatment is desensitization
 Diabetes Mellitus

 COMPLICATIONS OF INSULIN THERAPY

 INSULIN DYSTROPHY
 A localized reaction in the form of lipoatrophy or lipohypertrophy
 Lipoatrophy- loss of subcutaneous fat usually caused by the utilization of
animal insulin
 Lipohypertrophy- development of fibrofatty masses, usually caused by
repeated use of injection site
 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
 MORNING HYPERGLYCEMIA
 Elevated blood sugar upon arising in the morning
 Caused by insufficient level of insulin
 DAWN phenomenon
 SOMOGYI effect
 INSULIN WANING
 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
 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)
 Nocturnal hypoglycemia followed by rebound hyperglycemia
 Due to the production of counter regulatory hormones- glucagon. cortisol
and epinephrine
 Management- decrease evening dose of NPH or increase bedtime snack
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
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!
 ORAL HYPOGLYCEMIC AGENTS
 There are several agents:
 Sulfonylureas
 Biguanides
 Alpha-glucosidase inhibitors
 Thiazolidinediones
 Meglitinides
 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

 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
 HYPOGLYCEMIA


ASSESSMENT FINDINGS
 1. Sympathetic manifestations- sweating, tremors, palpitations, nervousness,
tachycardia and hunger
ASSESSMENT FINDINGS
 2. CNS manifestations- inability to concentrate, headache, lightheadedness,
confusion, memory lapses, slurred speech, impaired coordination, behavioral
changes, double vision and drowsiness
DIAGNOSTIC FINDINGS
 RBS- less than 50-60 mg/dL level
 Nursing Interventions
 1. Immediate treatment with the use of foods with simple sugar- glucose
tablets, fruit juice, table sugar, honey or hard candies
 Nursing Interventions
 2. For unconscious patients- glucagon injection 1 mg IM/SQ; or IV 25 to 50
mL of D50/50
 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
 Nursing Interventions
 5. Advise in-between snacks, especially when physical activity is increased
 6. Teach the importance of compliance to medications
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
 PATHOPHYSIOLOGY
 No insulin reduced glucose breakdown and increased liver glucose
production  Hyperglycemia
 PATHOPHYSIOLOGY
 Hyperglycemia kidney attempts to excrete glucose  increased osmotic
load  diuresis  Dehydration
 PATHOPHYSIOLOGY
 No glucose in the cell fat is broken down for energy  ketone bodies are
produced Ketoacidosis
 Risk factors
 1. infection or illness
  2. stress
 3. undiagnosed DM
 4. inadequate insulin, missed dose of insulin

 ASSESSMENT FINDINGS
 1. 3 P’s
 2. Headache, blurred vision and weakness
 3. Orthostatic hypotension
 ASSESSMENT FINDINGS
 4. Nausea, vomiting and abdominal pain
 5. Acetone (fruity) breath
 6. Hyperventilation or KUSSMAUL’s breathing
 HYPERGLYCEMIA
 LABORATORY FINDINGS
 1. Blood glucose level of 300-800 mg/dL
 2. Urinary ketones
 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
 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
 NURSING INTERVENTIONS
 2. Assist in restoring Electrolytes
 Kidney function is FIRST determined before giving potassium supplements!
 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!

 Nursing management
 1. Diet modification
 2. Exercise
3. Prevention and treatment of underlying conditions such as MI, CAD and
stroke
 4. Administration of prescribed medications for hypertension,
hyperlipidemia and obesity
  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
 Retinopathy-ASSESSMENT FINDINGS
 Blurry vision
 Spotty vision
 Asymptomatic
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
NURSING INTERVENTIONS
 1. Assist in diagnostic procedure
 2. Assist in the preparation for surgery- laser photocoagulation
 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
 DIABETIC NEPHROPATHY
 Progressive deterioration of kidney function
 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
 ASSESSMENT findings for diabetic nephropathy
 1. Albuminuria
 2. Anemia
 3. Acidosis
ASSESSMENT findings for diabetic nephropathy
 4. Fluid volume overload
 5. Oliguria
 6. Hypertension
 7. UTI
 NURSING MANAGEMENT
1. Assist in the control of hypertension- use of ACE inhibitor
 Provide a low sodium and low protein diet
 Administer prescribed medication for UTI
NURSING MANAGEMENT
 Assist in dialysis
 Prepare patient for renal transplantation, if indicated
 Diabetic Neuropathy
 A group of disorders that affect all type of nerves including the peripheral,
autonomic and spinal nerves

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

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
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
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
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
 3. Provide LOW-fat, small frequent feedings
 4. Administer bulk-forming laxatives for diabetic diarrhea
 5. Provide HIGH-fiber diet for diabetic constipation
MANAGEMENT OF FOOT AND LEG PROBLEM
 Soft tissue injury in the foot/leg formation of fissures and callus  poor
wound healing  foot/leg ulcer
 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
MANAGEMENT of Foot Ulcers
 Teach patient proper care of the foot
 Daily assessment of the foot
 Use of mirror to inspect the bottom
 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

 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 for foot
problems