Nurse Licensure Examination Review

Diabetes Mellitus

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.

Diabetes Mellitus

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

Diabetes Mellitus
 BASIC

PATHOLOGY : Insulin problem (deficiency or impaired action)

Diabetes Mellitus

Insulin is a hormone secreted by the BETA cells of the pancreas  Stimulus of insulinHYPERGLYCEMIA

Diabetes Mellitus
 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

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

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

Diabetes Mellitus

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

Diabetes Mellitus
CLASSIFICATION OF DM 1. Type 1 DM

Insulin dependent Diabetes Mellitus Non-insulin dependent Diabetes Mellitus Diabetes Mellitus diagnosed during pregnancy

2. Type 2 DM

3. Gestational DM

4. DM associated with other conditions or syndromes

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

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

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

Diabetes Mellitus
CLASSIFICATION OF DM 4. DM associated with other conditions or syndromes

Diabetes Mellitus
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: 1. Genetic susceptibility- HLA DR3 and DR4 2. Autoimmune response 3. 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: 1. Unknown 2. 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 24th 28 week gestation

GESTATIONAL Diabetes Mellitus

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

Diabetes Mellitus

ASSESSMENT FINDINGS  1. Classic 3 P’s  2. Fatigue  3. Body weakness

Diabetes Mellitus

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

Diabetes Mellitus

DIAGNOSTIC TESTS  1. FBS- > 126  2. RBS- >200  3. OGTT- > 200

Diabetes Mellitus

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

Diabetes Mellitus

DIAGNOSTIC CRITERIA  1. FBS equal to or greater than 126 mg/dL (7.0mmol/L)  (Normal 8 hour FBS- 80109 mg/dL)

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

Diabetes Mellitus

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 by:

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

Diabetes Mellitus
The Patient with DM
   

HISTORY

Symptoms and characteristics VS, BMI, Fundoscopy, Neuro FBS, RBS, HgbA1c, lipid profile, ECG, UA Ophthalmologist, Podiatrist, Dietician, etc..

PHYSICAL EXAMINATION

LABORATORY EXAMINATION

REFERRALS

Diabetes Mellitus

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

Diabetes Mellitus

The Patient with DM 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

Diabetes Mellitus

DM Exercise management

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.

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.

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

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

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

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.

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

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.

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.

Diabetes Mellitus Monitoring therapy
 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

Diabetes Mellitus

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

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

DM Drug therapy

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

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

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

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

Diabetes Mellitus

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

Diabetes Mellitus
GENERALITIES  1. Human insulin preparations have a shorter duration of action than animal source

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

Diabetes Mellitus
 3.

ONLY Regular insulin can be used INTRAVENOUSLY!

Diabetes Mellitus

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

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

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

Diabetes Mellitus
REGULAR INSULIN  Also called Short-acting insulin  “R”  Usually Clear solution administered 30 minutes before a meal

Diabetes Mellitus

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

Diabetes Mellitus

INTERMEDIATE ACTING INSULIN  Called “NPH” or “LENTE”  Appears white and cloudy

Diabetes Mellitus

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

Diabetes Mellitus

LONG- ACTING INSULIN  “UltraLENTE”  Referred to as “peakless” insulin

Diabetes Mellitus

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

Diabetes Mellitus

HEALTH TEACHING Regarding Insulin SELFAdministration  1. Insulin is administered at home subcutaneously

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

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

Diabetes Mellitus

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

Diabetes Mellitus

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

Diabetes Mellitus

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

Diabetes Mellitus
 7.

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

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

Diabetes Mellitus

9. The four main areas for insulin injection areABDOMEN, UPPER ARMS, THIGHS and HIPS

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.

Diabetes Mellitus
10. Alcohol may not be used to cleanse the skin  11. Utilize the subcutaneous injection techniquecommonly, a 45-90 degree angle.

Diabetes Mellitus

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

Diabetes Mellitus
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

Diabetes Mellitus

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.

Diabetes Mellitus 2. SYSTEMIC ALLERGIC REACTIONS  Very rare  Generalized urticaria is the manifestation  Treatment is desensitization

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

Diabetes Mellitus

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

Diabetes Mellitus  Lipohypertrophydevelopment 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

Diabetes Mellitus

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

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

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)

Diabetes Mellitus

SOMOGYI EFFECT  Nocturnal hypoglycemia followed by rebound hyperglycemia

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

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

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!

Diabetes Mellitus
ORAL HYPOGLYCEMIC AGENTS  There are several agents:  Sulfonylureas  Biguanides  Alpha-glucosidase inhibitors  Thiazolidinediones  Meglitinides

Diabetes Mellitus

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

Diabetes Mellitus
SULFONYLUREAS  FIRST GENERATIONAcetoheximide, Chlorpropamide, Tolazamide and Tolbutamide  SECOND GENERATION- Glipizide, Glyburide, Glibenclamide, Glimepiride

Diabetes Mellitus: Sulfonylureas

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

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

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

Diabetes Mellitus
BIGUANIDES= “formin”  They have no effect on the beta cells of the pancreas  Metformin (Glucophage) and Phenformin are examples

Diabetes Mellitus: Biguanides

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

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

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

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

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

Diabetes Mellitus

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

Diabetes Mellitus
 

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

Diabetes Mellitus

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

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

Diabetes Mellitus

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

Diabetes Mellitus
ACUTE COMPLICATIONS OF DM  Hypoglycemia  Diabetic ketoacidosis  Hyperglycemic hyperosmolar nonketotic syndrome (HHNS)

Diabetes Mellitus

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

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

HYPOGLYCEMIA

ASSESSMENT FINDINGS 1. Sympathetic manifestationssweating, tremors, palpitations, nervousness, tachycardia and hunger

HYPOGLYCEMIA

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

HYPERGLYCEMIA

HYPOGLYCEMIA

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

HYPOGLYCEMIA
Nursing Interventions  1. Immediate treatment with the use of foods with simple sugarglucose tablets, fruit juice, table sugar, honey or hard candies

HYPOGLYCEMIA
Nursing Interventions  2. For uncons cio us patient s- glucagon injection 1 mg IM/SQ; or IV 25 to 50 mL of D50/50

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

HYPOGLYCEMIA
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

DKA

PATHOPHYSIOLOGY  No insulin reduced glucose breakdown and increased liver glucose production  Hyperglycemia

DKA

PATHOPHYSIOLOGY  Hyperglycemia kidney attempts to excrete glucose  increased osmotic load  diuresis  Dehydration

DKA

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

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

DKA
ASSESSMENT FINDINGS  1. 3 P’s  2. Headache, blurred vision and weakness  3. Orthostatic hypotension

DKA
ASSESSMENT FINDINGS  4. Nausea, vomiting and abdominal pain  5. Acetone (fruity) breath  6. Hyperventilation or KUSSMAUL’s breathing

HYPERGLYCEMIA

Hyperglycemia

DKA

LABORATORY FINDINGS  1. Blood glucose level of 300800 mg/dL  2. Urinary ketones

DKA
LABORATORY FINDINGS  3. ABG result of metabolic acidosisLOW 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

DKA

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

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!

HHNS

 

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

HHNS
PATHOPHYSIOLOGY  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

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

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

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

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

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

MACROVASCULAR CX

Nursing management  1. Diet modification  2. Exercise

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

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

MICROVASCULAR CX
Retinopathy-ASSESSMENT FINDINGS  Blurry vision  Spotty vision  Asymptomatic

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

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

MICROVASCULAR CX
NURSING INTERVENTIONS  3. Health teaching regarding prevention of retinopathy by regular ophthalmic examinations, good glucose control and selfmanagement of eye care regimens  4. Maintain client safety

MICROVASCULAR CX
DIABETIC NEPHROPATHY  Progressive deterioration of kidney function

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

MICROVASCULAR CX
ASSESSMENT findings for diabetic nephropathy  1. Albuminuria  2. Anemia  3. Acidosis

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

MICROVASCULAR CX
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

MICROVASCULAR CX

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

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

MICROVASCULAR CX Diabetic Neuropathy  Two most common types of Diabetic Neuropathy are sensori-motor polyneuropathy and autonomic neuropathy

MICROVASCULAR CX
Peripheral neuropathyASSESSMENT findings  1. paresthesias- prickling, tingling or heightened sensation  2. decreased proprioception  3. decreased sensation of light touch  4. unsteady gait  5. decreased tendon reflexes

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

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

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

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

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

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

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

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

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

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