NurseReview.Org Diabetes Mellitus

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 insulin- HYPERGLYCEMIA

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

4. Age of more than 45

5. Previously unidentified IFG/IGT

6. Hypertension

Diabetes Mellitus

7. Hyperlipidemia

8. History of Gestational Diabetes Mellitus

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

Diabetes Mellitus

1. Type 1 DM

Insulin dependent Diabetes Mellitus

Diabetes Mellitus

2. Type 2 DM

Non-insulin dependent Diabetes Mellitus

Diabetes Mellitus

3. Gestational DM

Diabetes Mellitus diagnosed during pregnancy

Diabetes Mellitus

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

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

PATHOPHYSIOLOGY

CLASSIC P’s

Polyuria

Polydipsia

Polyphagia

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

PATHOPHYSIOLOGY

Decreased insulin production  diminished insulin action  hyperglycemia  signs and symptoms

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 24-28 th 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- 80-109 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

PHYSICAL EXAMINATION

VS, BMI, Fundoscopy, Neuro

LABORATORY EXAMINATION

FBS, RBS, HgbA1c, lipid profile, ECG, UA

REFERRALS

Ophthalmologist, Podiatrist, Dietician, etc..

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

Diabetes Mellitus

NUTRITIONAL MANAGEMENT

3. Plan for the caloric intake distributed as follows- CHO 50-60%; Fats 20-30%; and Proteins 10-20%

4. Advise moderation in alcohol intake

5. Using artificial sweeteners is acceptable

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

Because the patient with TYPE 1 DM cannot produce insulin, exogenous insulin must be administered for life.

Diabetes Mellitus

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 SELF- Administration

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 are- ABDOMEN, 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 technique- commonly, 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

T est blood  I nject insulin  E at food

Diabetes Mellitus

COMPLICATIONS OF INSULIN THERAPY

1. Local allergic reactions

Redness, swelling, tenderness and induration appearing 1-2 hours after injection

Usually occurs in the beginning stage of therapy

Diabetes Mellitus

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

Diabetes Mellitus

3. INSULIN DYSTROPHY

A localized reaction in the form of lipo atrophy or lipo hypertrophy

Diabetes Mellitus

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

Diabetes Mellitus

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

Diabetes Mellitus

4. INSULIN RESISTANCE

Most commonly caused by OBESITY

Defined as daily insulin requirement of more than 200 units

Management- Steroids and use of more concentrated insulin

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 generations- first and second generations

Diabetes Mellitus

SULFONYLUREAS

FIRST GENERATION- Acetoheximide, Chlorpropamide, Tolazamide and Tolbutamide

SECOND GENERATION- Glipizide, Glyburide, Glibenclamide, Glimepiride

Diabetes Mellitus: Sulfonylureas

The most common side –effects of these medications are Gastro-intestinal upset and dermatologic reactions.

HYPOGLYCEMIA is also a very important side-effect

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 non-ketotic syndrome (HHNS)

Diabetes Mellitus

CHRONIC COMPLICATIONS OF DM

Macrovascular complications- MI, Stroke, Atherosclerosis, CAD, and Peripheral vascular disease

Microvascular complications- micro-angiopathy, 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 manifestations- sweating, 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

HYPOGLYCEMIA

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 sugar- glucose tablets, fruit juice, table sugar, honey or hard candies

HYPOGLYCEMIA

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

HYPOGLYCEMIA

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

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 300-800 mg/dL

2. Urinary ketones

DKA

LABORATORY FINDINGS

3. ABG result of metabolic acidosis- LOW pH, LOW pCO2 as a compensation, LOW bicarbonate

4. Electrolyte imbalances- potassium levels may be HIGH due to acidosis and dehydration

DKA

NURSING INTERVENTIONS

1. Assist in the correction of dehydration

Up to 6 liters of fluid may be ordered for infusion, initially NSS then D5W

Monitor hydration status

Monitor I and O

Monitor for volume overload

DKA

2. Assist in restoring Electrolytes

Kidney function is FIRST determined before giving potassium supplements!

DKA

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

Approach is similar to the DKA

1. Correction of Dehydration by IVF

2. Correction of electrolyte imbalance by replacement therapy

HHNS

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

1. Assist in diagnostic procedure

2. Assist in the preparation for surgery- laser photocoagulation

MICROVASCULAR CX

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

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 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

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

End of DM

NurseReview.Org Diabetes Mellitus

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