* 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.
* A chronic disorder of impaired glucose metabolism, protein and fat metabolism
BASIC PATHOLOGY : Insulin problem (deficiency or impaired action)
* 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 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
* 4. Age of more than 45
* 5. Previously unidentified IFG/IGT
* 6. Hypertension
* 7. Hyperlipidemia
* 8. History of Gestational 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
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
Etiology:
1. Genetic susceptibility- HLA DR3 and DR4
2. Autoimmune response
3. Toxins, unidentified viruses and environmental factors
PATHOPHYSIOLOGY
* Destruction of BETA cells--> decreased insulin production --> uncontrolled glucose production by the liver--> hyperglycemia --> signs and symptoms
CLASSIC P’s
* Polyuria
* Polydipsia
* Polyphagia
TYPE 2- Diabetes Mellitus
* A type of DM characterized by insulin resistance and impaired insulin production
Etiology:
1. Unknown
2. Probably genetic and obesity
PATHOPHYSIOLOGY
* Decreased sensitivity of insulin receptor to insulin --> less uptake of glucose --> HYPERGLYCEMIA
* Decreased insulin production --> diminished insulin action --> hyperglycemia --> signs and symptoms
* 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
* 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
* 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
* 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)
* 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
* 3. RBS of equal to or greater than 200 mg/dL PLUS the 3 P’s
NURSING MANAGEMENT OF DM
* The main goal is to NORMALIZE insulin activity and blood glucose level by:
Nutritional modification
2. Regular Exercise
3. Regular Glucose Monitoring
4. Drug therapy
5. Client Education
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
* 1.Review the patient’s diet history to identify eating habits and lifestyle
* 2. Coordinate with the dietician in meal planning for weight loss
* 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
* 1. Teach that exercise can lower the blood glucose level
* 2. Diabetics must first control the glucose level before initiating exercise programs.
* 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.
* 5. Advise that exercise should be done at the same time every day, preferably when blood glucose levels are at their peak
* Regular exercise, not sporadic exercise, should be encouraged.
* 7. For most patient, WALKING is the safe and beneficial form of exercise
Glucose Self Monitoring
* Self-monitoring of blood glucose (SMBG) enables the patient to adjust the treatment regimen to obtain optimal glucose control
* 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
* 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.
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.
* Normal value is 4 to 6 %
* No patient preparation is needed for this testing
* Done to monitor therapy
Diabetes Mellitus
* 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.
* Because the patient with TYPE 1 DM cannot produce insulin, exogenous insulin must be administered for life.
* 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:
1. Source- Human, pig, or cow
2. Onset of action- Rapid-acting, short-acting, intermediate-acting, long-acting and very long acting
* This may be grouped into several categories according to:
3. Pure or mixed concentration
4. Manufacturer of drug
GENERALITIES
* 1. Human insulin preparations have a shorter duration of action than animal source
* 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
* 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
* 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
* ONSET- 2-4 hours
* PEAK- 4 to 6-12 hours
* DURATION- 16-20 hours
LONG- ACTING INSULIN
* “UltraLENTE”
* Referred to as “peakless” 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
* 2. Cloudy insulin should be thoroughly mixed by gently inverting the vial or ROLLING between the hands
* 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
* 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
1. LOCAL ALLERGIC REACTIONS
* Redness, swelling, tenderness and induration appearing 1-2 hours after injection
* Usually occurs in the beginning stage of 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.
2. SYSTEMIC ALLERGIC REACTIONS
* Very rare
* Generalized urticaria is the manifestation
* Treatment is desensitization
3. 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
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
5. 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!
* There are several agents:
* Sulfonylureas
* Biguanides
* Alpha-glucosidase inhibitors
* Thiazolidinediones
* Meglitinides
SULFONYLUREAS
* MOA- stimulates the beta cells of the pancreas to secrete insulin
* Classified as to generations- first and second generations
* FIRST GENERATION- Acetoheximide, Chlorpropamide, Tolazamide and Tolbutamide
* SECOND GENERATION- Glipizide, Glyburide, Glibenclamide, Glimepiride
* The most common side –effects of these medications are Gastro-intestinal upset and dermatologic reactions.
* HYPOGLYCEMIA is also a very important side-effect
* 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
BIGUANIDES- “ Formin”
* MOA- Facilitate the action of insulin on the peripheral receptors
* These can only be used in the presence of insulin
* They have no effect on the beta cells of the pancreas
* Metformin (Glucophage) and Phenformin are examples
* The most important side effect is LACTIC ACIDOSIS!
* These are not given to patient with renal impairment
* These drugs are usually given with a sulfonylurea to enhance the glucose-lowering effect more than the use of each drug individually
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
* 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
* Side-effect if used with other drug is HYPOGLYCEMIA
* Note that sucrose absorption is impaired and IV glucose is the therapy for the hypoglycemia
THIAZOLIDINEDIONES
* MOA- Enhance insulin action at the receptor site
* They do not stimulate insulin secretion
* Examples- Rosiglitazone, Pioglitazone
* These drugs affect LIVER FUNCTION
* Can cause resumption of OVULATION in peri-menopausal anovulatory women
MEGLITINIDES
* MOA- Stimulate the secretion of insulin by the beta cells
* Examples- Repaglinide and Nateglinide
* They have a shorter duration and fast action
* Should be taken BEFORE meals to stimulate the release of insulin from the pancreas
* Principal side-effect of meglitinides- hypoglycemia
* Can be used alone or in combination
ACUTE COMPLICATIONS OF DM
* Hypoglycemia
* Diabetic ketoacidosis
* Hyperglycemic hyperosmolar non-ketotic syndrome (HHNS)
* Macrovascular complications- MI, Stroke, Atherosclerosis, CAD, and Peripheral vascular disease
* Microvascular complications- micro-angiopathy, retinopathy, nephropathy
* Peripheral neuropathy
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
ASSESSMENT FINDINGS
* 1. Sympathetic manifestations- sweating, tremors, palpitations, nervousness, tachycardia and hunger
* 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
* 2. For unconscious patients- glucagon injection 1 mg IM/SQ; or IV 25 to 50 mL of D50/50
* 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
* 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
* Hyperglycemia--> kidney attempts to excrete glucose --> increased osmotic load --> diuresis --> Dehydration
* No glucose in the cell--> fat is broken down for energy --> ketone bodies are produced--> Ketoacidosis
Risk factors
* 1. infection or illness- common
* 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
* 4. Nausea, vomiting and abdominal pain
* 5. Acetone (fruity) breath
* 6. Hyperventilation or KUSSMAUL’s breathing
LABORATORY FINDINGS
* 1. Blood glucose level of 300-800 mg/dL
* 2. Urinary ketones
* 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
* 2. Assist in restoring Electrolytes
* Kidney function is FIRST determined before giving potassium supplements!
* 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!
* A serious condition in which hyperosmolarity and extreme hyperglycemia predominate
* Ketosis is minimal
* Onset is slow and takes hours to days to develop
* Lack of insulin action or Insulin resistance --> hyperglycemia
* Hyperglycemia--> osmotic diuresis --> loss of water and electrolytes
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
Precipitating factors
* 1. Infection
* 2. Stress
* 3. Surgery
* 4. Medication like thiazides
* 5. Treatment like dialysis
ASSESSMENT FINDINGS
* 1. Profound dehydration
* 2. Hypotension
* 3. Tachycardia
* 4. Altered sensorium
* 5. Seizures and hemiparesis
DIAGNOSTIC TESTS
* 1. Blood glucose- 600 to 1,200 mg/dL
* 2. Blood osmolality- 350 mOsm/L
* 3. Electrolyte abnormalities
NURSING INTERVENTIONS
* Approach is similar to the DKA
* 1. Correction of Dehydration by IVF
* 2. Correction of electrolyte imbalance by replacement therapy
* 3. Administration of insulin injection and drips
* 4. Continuous monitoring of urine output
MACROVASCULAR CX
Nursing management
* 1. Diet modification
* 2. Exercise
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
* 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
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
ASSESSMENT findings for diabetic nephropathy
* 1. Albuminuria
* 2. Anemia
* 3. Acidosis
* 4. Fluid volume overload
* 5. Oliguria
* 6. Hypertension
* 7. UTI
NURSING MANAGEMENT
1. 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
4. Assist in dialysis
5. 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
* Two most common types of Diabetic Neuropathy are sensori-motor polyneuropathy and autonomic 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
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
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, recommend use of low-heeled shoes
* 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
INSULIN
Types of Insulin
1. Rapid Acting Insulin- Ex. Insulin Lispro ( Humalog)
2. Short Acting Insulin- Ex. Regular Insulin (Humulin R)
3. Intermediate Acting Insulin Ex. NPH Insulin ( Humulin N)
4. Long Acting Insulin- Ex. Insulin Glergene ( Lantus), InsulinDetermir
( Levemir)
5. Fixed Combination of N and R- Ex. 70/30%- 70% N, 30 % R
6. Fixed Combination- Ex. Humalog Mix 75/25, 75% lispro protamine,
25% lispro insulin
Insulin
> Enhances transmembrane passage of glucose across cell membrane.
> Promotes conversion of glucose to glycogen.
Common Uses
1. Oral hypopglycemic Agents- Type 2 DM
2. Insulin- Type 1 DM
Common adverse effects: hypoglycemia.
Types
1. Rapid- acting insulin
> Onset: within 15 minutes
> Peak: 30-90 minutes
> Duration: 3-4 hrs
2. Short- acting insulin
> Onset: 30-60 minutes
> Peak: 2-3 hrs
> Duration: 3-6 hrs
3. Intermediate –acting insulin
> Onset: 2-4 hrs
> Peak: 6-10 hrs
> Duration: 10-16 hrs
4. Long-acting insulin
> Onset: 2 hrs
> Peakless
> Duration: 24 hrs
5. Fixed Combination of N and R
> Onset: 30-60 minutes
> Peak: 6-10hrs
> Duration: 10-16 hrs
6. Fixed combination
> Onset: 15 minutes
> Peak: 1-6.5 hrs (average 2.5 hrs)
> Duration: 10-16 hrs
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