is a group of metabolic diseases characterized by elevated of glucose in the blood (hypergltcemia) resulting from defects in insulin and insulin action. Major sources of this glucose are absorption of ingested food in gastrointestinal tract and formation of glucose by the liver from food substance.

Insulin a hormone produced by the pancreas, controls the level of glucose in the blood by regulating the production and storage of glucose

In diabetic state, the cells may stop responding to insulin or the pancreas may stop producing insulin intirely.

Leads to hyperglycemia, which may result in acute metabolic complication sush as: a. diabetic ketoacidosis (DKA) b. hyperglycemic hyperosmolar nonketotic syndrome (HHNS)

Long-term effects of hyperglycemic contribute to:



macro vascular complication (coronary artery disease, cerebrovascular disease and peripheral vascular disease) chronic macrivascular complication (kidney and eye disease) neuropathic complication (disease of the nerve)

Primary Goal of treatment for patients with diabetes  controlling blood glucose level  preventing acute  long term complication


Several different types of DM
a. b. c.

cause clinical course treatment

Major classifications of diabetes are a. type 1 diabetes (previously referred to as insulinindependent diabetes mellitus) IDDM


b. c.

type 2 diabetes (previously referred to as non-insulinindependent diabetes mellitus) NIDDM gestational diabetes mellitus DM with others conditions or syndrome


terms “insulin-dependent diabetes” and “non-insulindependent diabetes” are no longer used because they have resulted in classification of patients on the basis of the treatment of their diabetes rather than the underlying etiology.

Approximately 5% to 10% of people with diabetes have type 1 diabetes, which the insulinproducing pancreatic beta cells are destroyed by an autoimmune process.  type 1 diabetes is characterized by an acute onset, usually before age 30

approximately 90% to 95% of people with diabetes have type 2 diabetes, which result from decreased sensitivity to insulin (called insulin resistance) and impaired beta cell functioning resulting in decreased insulin production.

 type

2 diabetes occurs more among people who are older than 3o years and obese  type 2 diabetes is first treated with diet and exersice

borderline diabetes is classified as impaired glucose tolerance (IGT) or impaired fasting glucose (IFG) and refers to a condition in which blood glucose level fall between normal levels and levels considered diagnostic for diabetes.

Risk Factors for Diabetes Mellitus
1. 2. 3. 4.

Family history of diabetes Obesity Race/Ethnicity Age


2. 3. 4.

Previously independent impaired fasting glucose or impaired glucose tolerance Hypertension HDL cholesterol level or triglyceride level History of gestational diabetes or delivery of babies over 9 lbs.


insulin is secreted by beta cells, which are one of four types of cells in the islets of Langerhans in the pancreas. Insulin is an anabolic, or storage, hormone. Insulin secretion increases and moves glucose from the blood into muscle, liver, and fat cells, when the person eats a meal. In those cells, insulin:

1. 2. 3.

transports and metabolize glucose for energy stimulates storage of glucose in the liver and muscle signals the liver to stop the release of glucose

1. 2.

enhances storage of dietary fat in adipose tissue accelerates transport of animo acids into cells

insulin also inhibits the breakdown of stored glucose, protein, and fat.

Classification of Diabetes Mellitus and Related Glucose Intolerances
Current Classification Type 1 Previous Classification Juvenile diabetes Juvenile-onset diabetes Ketosis-prone diabetes Brittle diabetes Insulin-dependent Diabetes mellitus(IDDM) Characteristics and Implication
Onset any age, but usually young (<30yrs). Usually thin at diagnostic; with recent weight loss. Etiology includes genetics, immunologic, or environmental factors. Often have islet cell antibiotics. Little or no endogenous insulin. Need insulin to reserve life Ketosis-prone when insulin

Type 2

Adult-onset diabetes Maturity-onset diabetes Ketosis-resistant diabetes Stable diabetes Non-insulinindependent diabetes (NIDDM)

hyperglycemia:diabetic s ketoacidosis. Onset any age, usually over 30 years. Usually obese at diagnose Causes include obesity, heredity, or environmental factors. No islet cell antibodies Decrease in endogenous insulin, or increased with insulin resistance. Moat patients can control  blood glucose through weight loss if obese.

Oral antidiabetes agents may improve blood glucose levels if dietary modification and exercise are unsuccessful. May need insulin on a short- or longterm basis to prevent hyperglycemia. Ketosis rare,

Diabetes mellitus Secondary associated with diabetes other conditions or syndrome

hyperglycemic Hyperosmolar nonketonic syndrome. Accompanied by condition known or suspected to cause the disease: pancreatic diseases, hormonal abnormalities, medications such as corticosteroids and estrogen-containing preparation. Depending on the ability of the pancreas

Gestational diabetes

Gestational diabetes


produces insulin, the patient may require treatment with oral antidiabetes agents or insulin. Onset during pregnancy, usually in the second or third trimester Due to hormones secreted by the placenta, which inhibit the action of insulin. Above-normal risk for perinatal complication, especially macrosomia. Treatment with diet and if needed insulin to strictly maintain normal blood glucose level. Occurs in about 2%-5% of

Impaired glucose Intolerance

Borderline diabetes Latent diabetes Chemical diabetes Subclinical diabetes Asymptomatic diabetes

in subsequent pregnancies 30%-40% will develop overt diabetes within 10 years Risk factors include obesity, age older than 30years, family history of diabetes, previous large babies. Screening tests should be performed on all pregnant women between 24 and 28 wks gestation. Oral glucose tolerated test value between 140


Previous abnormality of glucose tolerated  

is defined as a fasting plasma glucose between 110 mg/dL and 126 mg/dL. 29% eventually develop diabetes Above-normal susceptibility to atherosclerosis disease. Renal and retinal complication usually not significant. May be obese or nonobese; obese should reduce weight.

Current normal glucose metabolism. Previous history of hyperglycemia Periodic blood glucose screening after age 40 if there is a family history of diabetes or if symptomatic. Encourage ideal body weight, because loss of 10-15 lbs may improve glycemic control. No history of glucose intolerance. Increased risk of diabetes if: positive family history obesity mother of babies over 9lbs at birth Screening and weight

1. 2. 3. 4. 5.

3P’s – polyuria, polydipsia and polyphagia Fatigue Weakness Sudden vision changes Tingling or numbness in hands or feet

1. 2. 3. 4.


Dry skin Skin lesions or wounds slowly to heal Recurrent infections Onset of type 1 diabetes – sudden weight loss, nausea, vomiting. Abdominal pain – if DKA developed.

Criteria for the Diagnostic of Diabetes Mellitus



Symptoms of diabetes plus casual plasma glucose concentration equal to or greater than 200 mg/dL. Casual is defined as any time of day without regard to time since last meal. The classic symptoms of diabetes include polyuria, polydipsia and unexplained weight loss. Fasting plasma glucose greater than or equal to 126 mg/dL. Fasting is defined as no caloric intake for at least 8 hours.

1. 2. 3. 4.

history physical examination laboratory examination need for referral 

 2. 3.

Goal to normalize insulin activity blood glucose levels to reduce the development of vascular and nauropathic complication


Nutritional Management  Goals b. Providing all the essential food constituents necessary for optimal nutrition. c. Meeting energy



Achieving wide daily fluctuations in blood glucose levels, with blood glucose levels as close to normal as is safe and practical to prevent or reduce the risk for complication. Decreasing serum lipid levels, if elevated, to reduce the risk for macrovascular disease.

Meal planning and related teaching  caloric requirements  caloric distribution  carbohydrates  fats  Fiber  food classification systems

exchanges lists  food guide pyramid  glycemic index  Other Dietary concerns  Alcohol consumption  Sweetness  Misleading food lebels

Exercise  Benefits  Exercise precaution  General Precautions for Exercise in Diabetes: b. Use proper foor wear and, if appropriate, other protective equipment.

Avoid exercise in extreme heat or cold Inspect feet daily after exercise Avoid exercise during after periods of poor metabolic control

Exercise recommendations

Monitoring Glucose levels and Ketones  blood glucose is monitoring is cornerstone of diabetes management and selfmonitoring of blood glucose (SMBG) level by patients has dramatically altered diabetes care.

Advantages and disadvantages of SMBG system common sources of error include: 1. Improper application of food 2. Improper meter cleaning and maintenance 3. Damage to the reagent strips

Candidates for SMBG  Unstable diabetes  A tendency for severe ketosis or hypoglycemia  Hypoglycemia without warning symptoms  Frequency of SMBG  Responding to SMBG results  Glycosylated hemoglobin

Glycosylated hemoglobin = (referred to as HgbA or A1C) is a blood test that reflects average blood glucose levels over a period of approximately 2 to 3 months.  Urine testing for glucose

Disadvantages of urine testing include the following:  Result does not accurately reflect the blood glucose level at the time of the rest.  The renal threshold foe glucose is 180-200 mg/dL, for above target blood glucose levels.

 Hypoglycemia

cannot be detected because a “negative” urine glucose result may occur when the blood glucose leel ranges from 0-180 mg/dl or higher.  Patients may have a false of being in good control when results are always negative.

 Various

medications may interfere with the test result.  In elderly patients and patients with kidney disease, the renal threshold is raised, thus the false negative may occur at dangerously elevated glucose levels

Testing for ketones

1. 

   

Pharmacology therapy Insulin Therapy and Insulin Preparations Time course of action Species (source) Manufacturer Insulin Regimens

Conventional regimens  Intensive regimens  Complication of insulin therapy  Local allergic reactions  Systemic allergic reactions  Insulin resistance  Insulin lipodystrophy  Morning hyperglycemia

Alterative methods of insulin delivery  Insulin pens  Jet injections  Insulin pumps  Implantable and inhalant insulin delivery  Transplantation of pancreatic cells

First-Generation Sulfonylureas  acetohexamide (Dymelor)  chlorpropamide (Diabinese)  tolazamide (Tolinase)  talbutamide (Orinase)  Second-Genaration Sulfonylureas  glipizide (Glucatrol)

glipizide (Glucatrol XL)  glyburide (Micronase)  glimepiride (Amaryl)  Biguanides  metformin (Glucophage+GlucosephageXL)  metformin with glyburine (Glucovance)  Alpha Glucosidase Inhibitors

Acarbose (Precose)  Thiazolidinediones  Pioglitazone (actos)  Rosiglitazone (Avandia)  Meglitinides  Repaglinide (Prandin)  Nateglinide (Starix)  General Considerations for Oral Agents

1. 2.

Education Developing a Diabetes Teaching Plan

 

Organizing Information Teaching Survival Skills

Outline of survival information include: 1. Simple pathophysiology a. Basic definition of diabetes b. Normal blood glucose ranges and target blood glucose levels.

a. b.


Effects of insulin and exercise Effects of food and stress, including illness and infections Basic treatment approaches


Treatment modalities a. Administration of insulin and oral antidiabetes medications b. Diet information c. Monitoring of blood glucose and ketones


Recognition, treatment, and prevention of acutr complications
a. b.

Hypoglycemia Hyperglycemia


Recognition, treatment, and prevention of acutr complications a. Where to buy and store insulin, syringes and glucose monitoring supplies b. When and how to reach the physician

Planning in Depth and Continuing Education  Preventive measures include:  Foot care  Eye care  General hygiene  Risk factor management  Assessment Readiness to Learn  Determining Teaching Methods


Implementing The Plan  Teaching Experienced Diabetic Patients  Teaching Patients to SelfAdminister Insulin  Storing insulin  Selecting syringes  Preparing the injection: Mixing insulin


insulin Selecting and Rotating the injection site Preparing the skin Injecting the needle Promoting home and community-based care Teaching patients self-care

The following approaches by the nurse are help for promoting self-care management skills:  Address any underlying factors that may affect diabetic control.

Simply the treatment regimen if it is too difficult for the patient to follow  Adjust the treatment regimen to meet patient’s request.  Establish a specific plan or contract with the patients with simple, measurable goals.

 Provide

positive reinforcement of self-care behaviors performed instead of focusing on behaviors that were neglected.  Help the patients to identify personal motivating factors rather than focusing on wanting to please the doctors or nurse.

 Encourage

the patients to pursue life goals and interest: discourage an undue focus on diabetes.  Continuing Care


Hypoglycemia (insulin reactions)  hypoglycemia (abnormally low blood glucose level) occurs when the blood glucose falls to less than 50 to 60 mg/dL.

 It

caused by too much insulin or oral hypoglycemic agents, too little food, or excessive physical activity.  May occur at any time of the day or night and often occurs before meals; if meals are delayed or snacks are omitted.

Clinical Manifestations  Mild hypoglycemia  Blood glucose levels falls  Sympathetic nervous stystem is stimulated  Resulting in a surge of epinephrine and norepinephrine

 Causes

symptoms sush as sweating, tremor, tachycardia, palpitation, nervouaness and hunger  Moderate hypoglycemia  Fall in blood glucose level deprives the brain cells of needed for functioning.

 Signs

of impaired function of the CNS may include inability to concentrate, headache, lightheadedness, confusion, memory lapses, numbness of the lips and tongue, slurred speech impaired coordination, emotional changes, irrational or combative behavior, double vision and drowsiness

 Severe

hypoglycemia  CNS function is so impaired that the patient needs the assistance of another person for treatment of hypoglycemia.  Symptoms may include disoriented behavior, seizures, difficulty arousing from sleep, or loss of consciousness

Assessment and Diagnostic Finding
 Symptoms

can occur suddenly and unexpectedly  Patients who have usually a Patients blood glucose level in the hyperglycemic range (eg. 200s or greater) may feel hypoglycemic symptoms when their blood glucose quickly drops to 120mg/dL or less.

Patients who frequently have a glucose level in the low range of normal be symptomatic when the blood glucose slowly falls to less than 50mg/dL  To altered hypoglycemic symptoms is a decreased hormonal response to hypoglycemia  Severe CNS impairment patients perform SMBG frequently.

Management  the usual recommended is for 15g of a fast-acting concentrated source of carbohydrate such as the following, given orally,

 three

or four commercially prepared glucose tablets  4 to 6oz of fruit or regular soda  6 to 10 life savers or other hand candies  2 to 3 teaspoons of sugar or honey

1. 2. 3.

Teaching Patients Initiating Emergency Measures Promoting Home and Community-Based Care

Teaching patients self care


Diabetic Ketoacidosis  caused by an absence or markedly inadequate amount of insulin  disorder in the metabolism of carbohydrate, protein and fat  3 main clinical features

 Hyperglycemia(300-800mg/dL)  Dehydration

(6.5 L water loss) and electrolyte loss (400500meq of  Na+,K+ and C1-24 hr period)  Acidosis (low serum HCO3=015meq/L; low pH=6.8-7.3)

3 main causes:  Decreased or missed dose of insulin  Illness or infection  Undiagnosed and untreated diabetes

Clinical Manifestation  hyperglycemia leads to polyuria, polydipsia, blurred vision, weakness, and headache  intravascular volume depletion-orthostatic hypotension

 volume volume

depletion leads to trank hypotension with a weak rapid pulse  ketosis and acidosis of DKA lead to GI symptoms such as anorexia, nausea, vomiting and abdominal pain.

 Acute Acute

levels  Hyperventilation

breath- elevated ketone

Assessment and Diagnostic Findings  blood glucose levels may vary blood from 300-800 mg/dl  severity of DKA is not severity necessarily related to the blood glucose level  patient have severe patient mat acidosis with modestly elevated blood glucose levels

 blood

glucose levels of 400500mg/dl have no evidence of DKA  Evidence Evidence of ketoacidosis is reflecting in low serum bicarbonate and low pH values.  Low Low PCO2 level reflect to respiratory compensation for the metabolic acidosis

 Sodium

and potassium levels may be low, normal or high depending on the amount of water loss  Elevated levels of creatinine, Elevated blood urea nitrogen (BUN), hemoglobin and hematocrit


rules”) take insulin or oral antidiabetes agents as usual test blood report glucose and test urine ketones every 3-4 hours report elevated glucose levels or urine ketones to the physician insulinrequiring patients may need supplemental doses of regular insulin q3 -4 hrs if usual meal plan cannot be fallowed, substitute soft foods(eg. 1/3 cup regular cola or orange juice, ½ cup broth, 1 cup Gatorade)q ½ 1 hr to prevent dehydration and to provide calories

patients must be taught “sick day” patients GUIDELINE TO FOLLOW DURING PERIODS OF ILLNESS (“sick day rules

Medical Management


important for maintaining important tissue perfusion fluid replacement fluid

 Patients

may need 6-10 liters of IVF initially  After the first few hours: 0.45% NS 200-500ml/hr  monitor V/S, I&O, electrolyte


Restoring Electrolytes  Potassium is a major electrolyte concern during treatment.  Factors related to treating DKA that reduce the serum potassium concentration include:

 Rehydration,

which leads to increased plasma volume and subsequent decreased in the concentration of serum potassium. Rehydration also leads to increased urinary excreation of potassium.  Insulin administration, which enhances the movement of potassium from the


Reserving Acidosis  ketones bodies accumulate as result of fat breakdown,  hourly blood glucose values must be measured  administered IV solution with concentration


Hyperglycemic Hyperosmolar Nonketotic Syndrome  Serious condition in which hyperosmolarity and hyperglycemia predominate, with alteration of the sensorium.

Clinical Manifestation  hypotension  dehydration ( dry mucous membrane, poor skin turgor)  tachycardia  variable neurologic signs (eg. Alteration of sensorium, seizures, hemiparesis)

Assessment and Diagnostic Findings
laboratory Test  blood glucose  electrolytes  BUN  Complete blood count  Serum osmolality  And arterial blood gas analysis  mental status changes,

Medical Management  fluid replacement  correction of electrolyte imbalance  insulin administration 

Nursing Management  monitor vital sign, fluid status, and laboratory values  maintain safety  prevent injury  I&O monitor

Nursing Intervention 1. Maintaining Fluid and Electrolyte Balance a. Measured I&O b. Administered IV fluids and electrolyte as prescribed

a. b.

c. d.

Encourage oral fluid intake Monitor laboratory values of serum electrolytes(sodium & potassium) Monitor VS For sign of dehydration


Improving Nutritional Intake a. Diet is planned with control of glucose as the primary goal. b. Appropriate caloric intake allows the patient to achieve and maintain the desired body weight c. Encourage the patient to eat full meals and snacks as prescribed


Reducing Anxiety a. Provide emotional support b. Assisted to focus on learning self-care behaviors c. Encourage to perform the skills that are feared most. d. Positive reinforcement

1. 2.

Improving Self-Care

Patients teaching

Monitoring and Managing Potential Complication

Fluid Overload

Occur because of the administration of a large volume of fluid at a rapid rate is often required to treat the patient

Risk is increased in elderly patients and in those with preexsisting cardiac disease.  Nurse monitor fluid intake and keeps careful records of IV and other fluid intake, with urine output measurement



Low serum levels may result rehydration, Prevention include cautions replacement of potassium
a. b. c.

Hyperglycemia and Ketoacidosis Hypoglycemia Cerebral Edema


Monitoring Home and Community-based Care a. Teaching Patients self-care b. Continuing care

Long term complications  Are seen in both type 1 and type 2 diabetes but usually do not occur with in 1st 5-10 yrs. Of diagnosis  Renal disease is more prevalent among patient with type 1 diabetes  Cardiovascular complication is more prevalent among older patient with type 2 diabetes

MACROVASCULAR COMPLICATION  Result from changes in the medium to large blood vessels  Blood vessel wall thicken, sclerose and become occluded by plaque that adheres to the vessel wall

Three main types of macrovascular complication  CAD typical ischemic symptoms  CVA  Peripheral vascular disease.

Cerebral blood vessels are similarly affected by accelerated atherosclerosis, occlusive changes or the formation of an embolus.  vascular that lodges in a cerebral blood vessel can lead to transient ischemic attacks and stroke

Cerebrovascular disease is common among diabetic patient. Recovery from a stroke may be impaired in patient who have elevated blood glucose level at the time of or immediately after stroke  It is important to assess the blood glucose level

atherosclerosis changes increasing of occlusive peripheral arterial disease in patient with diabetes  Severe form of arterial occlusive disease due to lower ext. is largely responsible for the increased incidence of gangrene and subsequent amputation in diabetic patient.

Neuropathy and impairment in wound healing also play a role in diabetic signs and symptoms of peripheral vascular dse. a. diminished peripheral pulse b. intermittent claudication – pain in the buttocks, thigh, calf during walking

ROLE OF DIABETES IN MACROVASCULAR DISEASE  one of the main feature of diabetes in elevated blood glucose  Risk factor for macrovascular disease a. obesity b. inc. triglyceride level c. hypertension

Diabetes itself is seen as an independent risk factor for the development of accelerated atherosclerosis  Other potential factor that may play a role in diabetes related atherosclerosis include

a. b. c. d. e.

platelet clotting factor abnormalities dec. flexibility of RBC changes in the arterial wall related to hyperglycemia hyperinsulinemia

MANAGEMENT  Diet and exercise- for managing obesity, hypertension, hyperlipidemia  Use of medication- to control hypertension and hyperlipidemia  Smoking cessation

 Control

blood glucose- to reduce triglyceride\  Patient may require increase ed the amount of insulin  May need to switch from oral antidiabetic agents to insulin

MICROVASCULAR COMPLICATIONS AND DIABETIC RETINOPATHY 1. Diabetic microvascular dse. a. AKA microangiopathy b. Characterized by capillary basement membrane thickening




Basement membrane surrounds the endothelial cells of the capillary Increase blood glucose level reacts through a series of biochemical response to thicken the basement membrane to several times it’s normal thickness 2 areas are affected  Retina  Kidney


changes in microvasculature
   

microaneurysm intraretinal hemorrhage hard exudates focal capillary closure


Diabetic retinopathy- leading cause of blindness a. is caused by changes in small blood vessel in the retina the area of the eye that receive images and sends information to the brain


richly supplied with blood vessels of all kinds
   

small arteries veins arterioles venules capillaries


3 main stages of retinopathy
  

Non proliferative Preproliferative Proliferative

type 1 and type 2 diabetes- lead to visual distortion and loss of central vision  preproliferative retinopathy- is considered a precursor to the more serious proliferative retinopathy

proliferative retinopathy widespread vascular changes and loss of nerve fibers  if visual changes occur during preproliferative stage caused by macular edema

PROLIFERATIVE RETINOPATHY 1. characterized by proliferation of new blood vessel growing from the retina into the vitreous 2. Blood vessel are prone to bleeding 3. Vitreous hemorrhage caused visual losses associated with proliferative retinopathy.



NORMAL vitreous are clear allowing light to be transmitted to the retina If hemorrhage occur the vitreous becomes clouded and cannot transmit light resulting in loss of vision



Another consequence is that vitreous hemorrhage resorption of blood in the vitreous leads to the formation of fibrous scar tissue scar tissue place traction in the retina resulating in retinal detachment and subsequent visual loss


SIGNS AND SYMPTOMS  Blurry vision secondary to macular edema  Indicative of hemorrhaging 1. floaters 2. cobwebs in visual field 3. sudden visual changes – spotty hazy vision complete loss of vision

DIAGNOSTIC PROCEDURE 1. Flourescein angiography – where dye is injected into an arm vein is carried to various parts of the body SIDE EFFECTS of this procedure


during dye injection Yellowish fluorescent discoloration of the skin and urine


This side effects last for 1224 hours  Allergic reaction Hives and itching Opthalmoscope



intensive insulin therapydecreases development of retinopathy Argon laser Photocoagulationmain treatment of diabetic retinopathy. a. This is a laser treatment that destroys blood vessel and areas of neovascularization


panretinal photocoagulationpatient increase risk for hemorrhaging  reduces the rate of progression to blindness  this stops the widespread of new vessel and hemorrhaging of damaged blood vessel


Vitrectomy- removal of fluid with a special drill like instrument and replaced with saline

NURSING MANAGEMENT regular opthalmoligoc examination Blood glucose control Self management of eye care regimen


with type 1 diabetes frequently show initial signs of renal disease after 10-15 yrs Type 2 diabetesw develop renal disease within 10 yrs of the diagnosis


after the onset of diabetes and especially if the glucose levels are elevated, the kidney’s filtration mechanism is stressed, allowing blood protein to leak into the urine. Pressure in the blood vessels of the kidney increases


Albumin is the most important blood proteins that leaks into the urine 1. urine should be checked annually for microalbuminuria 2. Urine dipstick test for albumin, creatinine and BUN level are obtained


of hypertension – use of ACE inhibitors Prevention or treatment of UTI Avoidance of nephroroxic substances Adjustment of medication as renal Ffunction changes Low Sodium diet

if the patient has already developed microalbuminuria and level exceeds 30mg/24hours in 2 consecutive test. An ACE inhibitor should be prescribed

IN chronic endstage of renal failure 1. Hemodialysis 2. Peritoneal dialysis has major risk factor --- infection and peritonitis Laser or surgery may be performed

DIABETIC NEUROPATHIES Include the peripheral sensorimotor, autonomic and spinal nerve Elevated blood glucose level over a period of years have been implicated in the etiology of neuropathy


basement membrane thickening and demyelinization of the nerves related to hyperglycemia Nerve conduction is disrupted when there are aberration of the myelin sheaths

Most common type of diabetic neuropathy are 1. sensorimotos polyneuropathy commonly affects the distal portions of the nerves 2. Autonomic neuropathy 3. Cranial nerve also occurs in diabetes common among elderly

Peripheral Neuropathy  Signs and symptoms 1. paresthesia 2. burning sensation 3. feet become numb 4. decreased sensation of light touch which can lead to an unsteady gait




decreased sensation to pain and temperature place patient with neuropathy at high risk for foot injury Chariot joint – neuropathy related to joint. Abnormal distribution on joint due to lack of propioception On physical examination the there is a decreased in deep tendon reflex

 intensive

insulin therapy and control of blood glucose level that delays the progression of neuropathy  for some patients neuropathic pain spontaneously resolve within 6 mos.  Nonopiod analgesic  Triclylic antidepressant  Transcutaneous electric nerve stimulation


THERE ARE THREE MANIFESTATIONS 1. cardia 2. GI 3. renal system


symptoms range from fixed, slightly tachycardic heart rate, orthostatic hypertension, silent or painless myocardial ischemia and infarction Delayed gastric emptying bloating, nausea and vomiting


addition there is unexplained absorption of glucose from ingested food secondary to the inconsistent gastric emptying Urinary retention a decreased sensation of bladder, fullness and other urinary symptoms of neurologic bladder result

HYPOGLYCEMIC UNAWARENESS 1. autonomic neuropathy of the adrenal medulla is responsible for diminished or absent adrenergic symptoms of hypoglycemia.


Patient may report that they no longer feel the shakiness, sweating, nervousness and palpitations associated to hypoglycemia



Sudomotor neuropathy refers to a decrease or absence of sweating (adhidrosis) of the extremities Sexual dysfunction
  

impotence in men and decreased libido, reduced vaginal secretions in women if there is vaginal infection there is vaginal itching, decreased lubrication and tenderness


strenuous activities High sodium diet in orthostatic hypotension The discontinuation of medication that impede autonomic response and use of sympathomometics and other agents


stimulate an autonomic response and the use of lower body elastic garments that minimize venous return and prevent pooling of blob in the extremities


delayed gastric emptying includes low fat diet, small frequent meals, close blood glucose control and the use of other agents that increases gastric motility


of diarrhea bulk forming laxative or antidiarrheal agents Treatment for constipation use laxative and enemas


Complications of diabetes that contribute to the increased risk of foot infection 1. Neuropath: sensory neuropathy leads to loss of pain and pressure sensation and autonomic neuropathy leads to dryness and fissuring of the skin(secondary to sweating decrease

Peripheral vascular dse. Poor circulation of the lower ext,. contributing to poor wound healing and development of gangrene immunocompromise hyperglycemia impairs the ability of specialized leukocytes to destroy bacteria.

 typical

sequence of events in the development of diabertic foot ulcer begins with a soft tissue injury of the foot. Formation of a fissure between the toes or in an area pf dry skin or formation of callus.


patient with peripheral vascular dse. Ulcers of the foot may not heal because there is decrease oxygen Amputation may be necessary to prevent infection


swelling redness from cellulitis of the leg or gangrene may be the 1st sign of foot problems Treatment of foot ulcer involves bedrest, antibiotics and debridement

1. 2. 3. 4. 5. 6. 7.

Duration of diabetes more than 10n years age older than 40 yrs. history of smoking decreased peripheral pulse decreased sensation anatomic deformities history of foot ulcer or amputation


the feet must be inspected daily for redness, blisters, fissures, calluses, ulceration, changes in skin temperature and development of deformities

Aspect of preventive foot care
 proper

bathing, drying, and lubricating the feet  wearing closed toe shoe that fit well
 trimming

of toenails  reducing risk factors such as smoking, elevated lipids  avoiding home remedies to treat foot problems


Factors that may contribute to hyperglycemia
1. 2. 3. 4.

changes in the usual treatment regimen medications IV dextrose mismatched timing of meals and insulin


acting insulin is usually needed to avoid postprandial hyperglycemia IV antibiotics should be mixed in normal saline to avoid excess infusion of dextrose


Factors that may contribute to hypoglycemia 1. Overuse of regular insulin 2. lack of dosage change when dietary intake is changed 3. overuse medications for hyperglycemia


does of subcutaneous regular insulin should be administered no more frequently that every 34 hours Should have snacks

Common alteration in Diets

2. 3. 4. 5.

NPO- if the patient has procedure usual insulin dosage should be changed Clear fluid Diet- patient may take juice and gelatin desserts Enteral tube feeding Parenteral nutrition hygiene- foot should be clean and dried, use lubricating lotion to

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