diabetes mellitus

Nurse Licensure Examination

Review

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

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-

Diabetes Mellitus



Action of insulin: it

promotes entry of Glucose

into the body cells by

binding to the insulin

receptor in the cell

INSULIN : Physiology

Insulin Metabolic Functions:

 1. Transports and metabolizes GLUCOSE  2. Promotes GLYCOGENESIS

 3. Promotes GLYCOLYSIS  4. Enhances LIPOGENESIS

Diabetes Mellitus

RISK FACTORS for Diabetes Mellitus

 1. Family History of diabetes

 2. Obesity

Diabetes Mellitus

RISK FACTORS for Diabetes Mellitus

 4. Age of more than 45

 5. Previously unidentified

IFG/IGT

Diabetes Mellitus

RISK FACTORS for

Diabetes Mellitus



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

Diabetes Mellitus

CLASSIFICATION OF DM 1. Type 1 DM

 Insulin dependent Diabetes

Diabetes Mellitus

CLASSIFICATION OF DM

2. Type 2 DM



Non-insulin dependent

Diabetes Mellitus

CLASSIFICATION OF DM

3. Gestational DM



Diabetes Mellitus diagnosed

Diabetes Mellitus

CLASSIFICATION OF DM

4. DM associated with other

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

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

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 

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

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

Diabetes Mellitus

ASSESSMENT FINDINGS



4. Visual changes



5. Slow wound healing



6. Recurrent skin and mucus

Diabetes Mellitus

DIAGNOSTIC TESTS



1. FBS- > 126

2. RBS- >200

Diabetes Mellitus

DIAGNOSTIC TESTS



4. HgbA1- for monitoring!!

5. Urine glucose

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

Diabetes Mellitus

DIAGNOSTIC CRITERIA



3. RBS of equal to or

greater than 200 mg/dL

Diabetes Mellitus

NURSING MANAGEMENT OF

DM



The main goal is to

NORMALIZE insulin activity

Diabetes Mellitus

NURSING MANAGEMENT OF DM 1. Nutritional modification

2. Regular Exercise

3. Regular Glucose Monitoring 4. Drug therapy

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

Diabetes Mellitus

The Patient with DM

 HISTORY

 Symptoms and characteristics

 PHYSICAL EXAMINATION

 VS, BMI, Fundoscopy, and

Diabetes Mellitus

The Patient with DM

 LABORATORY EXAMINATION

 FBS, RBS, HgbA1c, lipid profile,

ECG, and Urinalysis

 REFERRALS

 Ophthalmologist, Podiatrist,

Diabetes Mellitus

NUTRITIONAL MANAGEMENT

 1.Review the patient’s diet history

to identify eating habits and lifestyle

 2. Coordinate with the dietician in

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

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

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

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 

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

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

Diabetes Mellitus Monitoring therapy



Normal value is 4 to 6 %

No patient preparation is

needed for this testing

Diabetes Mellitus



Urine testing for glucose

Diabetes Mellitus



Urine testing for ketones



Ketones are by-products

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

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

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

Diabetes Mellitus



3. ONLY Regular insulin

can be used

Diabetes Mellitus

 4. Insulin are measured in

INTERNATIONAL UNITS or “iu”

 5. There is a specified insulin

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

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

Diabetes Mellitus

INTERMEDIATE ACTING

INSULIN



Called “NPH” or

“LENTE”

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”

Diabetes Mellitus

LONG- ACTING INSULIN



ONSET- 6-8 hours

PEAK- 12-16 hours

Diabetes Mellitus

HEALTH TEACHING

Regarding Insulin SELF-

Administration



1. Insulin is administered at

Diabetes Mellitus

HEALTH TEACHING Regarding Insulin SELF- Administration

 2. Cloudy insulin should be

thoroughly mixed by gently

inverting the vial or ROLLING

Diabetes Mellitus

HEALTH TEACHING Regarding Insulin SELF- Administration

 3. Insulin NOT IN USE should be

stored in the refrigerator, BUT

avoid freezing/extreme

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

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

Diabetes Mellitus

T-I-E

Test blood Inject insulin  Eat

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

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

2. SYSTEMIC ALLERGIC

REACTIONS



Very rare



Generalized urticaria is the

manifestation



Treatment is desensitization

COMPLICATIONS OF INSULIN THERAPY

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

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

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

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

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

Diabetes Mellitus

ORAL HYPOGLYCEMIC AGENTS

 These may be effective when

used in TYPE 2 DM that cannot be treated with diet and exercise

Diabetes Mellitus

ORAL HYPOGLYCEMIC AGENTS  There are several agents:

 Sulfonylureas  Biguanides

 Alpha-glucosidase inhibitors  Thiazolidinediones

Diabetes Mellitus

SULFONYLUREAS



MOA- stimulates the beta

cells of the pancreas to

secrete insulin

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

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

Diabetes Mellitus

BIGUANIDES



MOA- Facilitate the action of

insulin on the peripheral

receptors

Diabetes Mellitus

BIGUANIDES= “formin”



They have no effect on the

beta cells of the pancreas



Metformin (Glucophage) and

Diabetes Mellitus: Biguanides



The most important side effect

is LACTIC ACIDOSIS!



These are not given to patient

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!

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

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

Diabetes Mellitus

THIAZOLIDINEDIONES

 Examples- Rosiglitazone, Pioglitazone  These drugs affect LIVER

FUNCTION

 Can cause resumption of

Diabetes Mellitus

MEGLITINIDES



MOA- Stimulate the

secretion of insulin by the

beta cells



Examples- Repaglinide and

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

Diabetes Mellitus

ACUTE COMPLICATIONS OF DM

 Hypoglycemia

 Diabetic ketoacidosis

 Hyperglycemic hyperosmolar

Diabetes Mellitus

CHRONIC COMPLICATIONS OF DM

 Macrovascular complications- MI,

Stroke, Atherosclerosis, CAD, and Peripheral vascular disease

 Microvascular complications-

micro-angiopathy, retinopathy, nephropathy

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

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



DIAGNOSTIC FINDINGS

RBS- less than 50-60 mg/dL

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

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

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 

DKA

PATHOPHYSIOLOGY



Hyperglycemia kidney

attempts to excrete glucose 

increased osmotic load 

DKA

PATHOPHYSIOLOGY



No glucose in the cell fat is

broken down for energy 

ketone bodies are produced

DKA

Risk factors

 1. infection or illness- common  2. stress

 3. undiagnosed DM

 4. inadequate insulin, missed dose

DKA

ASSESSMENT FINDINGS

 1. 3 P’s

 2. Headache, blurred vision and

weakness

DKA

ASSESSMENT FINDINGS

 4. Nausea, vomiting and

abdominal pain

 5. Acetone (fruity) breath

 6. Hyperventilation or

DKA

LABORATORY FINDINGS



1. Blood glucose level of

300-800 mg/dL

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

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

HHNS

 A serious condition in which

hyperosmolarity and extreme hyperglycemia predominate

 Ketosis is minimal

 Onset is slow and takes hours to

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

HHNS

Precipitating factors

 1. Infection

 2. Stress

 3. Surgery

HHNS

HHNS

HHNS

NURSING INTERVENTIONS

 Approach is similar to the DKA

 1. Correction of Dehydration by

IVF

 2. Correction of electrolyte

HHNS

NURSING INTERVENTIONS

 3. Administration of insulin

injection and drips

 4. Continuous monitoring of

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

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

MICROVASCULAR CX

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

MICROVASCULAR CX

NURSING INTERVENTIONS

 1. Assist in diagnostic procedure

 2. Assist in the preparation for

MICROVASCULAR CX

NURSING INTERVENTIONS

 3. Health teaching regarding

prevention of retinopathy by

regular ophthalmic examinations, good glucose control and

self-management of eye care regimens

MICROVASCULAR CX

DIABETIC NEPHROPATHY

 Progressive deterioration of

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

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

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

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

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

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

MICROVASCULAR CX

MANAGEMENT of Foot Ulcers

 Teach patient proper care of the

foot

 Daily assessment of the foot

 Use of mirror to inspect the

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