Diabetes Mellitus - by Ibrahim Rawhi Ayasreh

7/30/2019 Diabetes Mellitus - by Ibrahim Rawhi Ayasreh

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Diabetes Mellitus

Ibrahim R. Ayasreh

RN, MSN

2011


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Definition

Diabetes mellitus is a group of metabolic diseases

characterized by elevated levels of glucose in the blood

(hyperglycemia) resulting from defects in insulin secretion,

insulin action, or both.


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Introduction

Sources of glucose in the blood are : absorption of ingestedfood in the gastrointestinal (GI) tract and formation of glucoseby the liver from food substances


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Pancreas


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Insulin

Insulin, a hormone produced by the pancreas, controls thelevel of glucose in the blood by regulating the production andstorage of glucose.

In the diabetic state, the cells may stop responding to insulin orthe pancreas may stop producing insulin entirely. This leads tohyperglycemia.

Another pancreatic hormone called glucagon (secreted by thealpha cells of the islets of Langerhans) is released when bloodglucose levels decrease and stimulate the liver to release storedglucose.


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Functions of insulin

Transports and metabolizes glucose for energy

Stimulates storage of glucose in the liver and muscle (in the form of glycogen).

Signals the liver to stop the release of glucose.

Enhances storage of dietary fat in adipose tissue.

Accelerates transport of amino acids (derived from dietary protein) into cells.

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


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Regulation of Glucose Level in Blood


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Risk factors of DM

Family history of diabetes (ie, parents or siblings withdiabetes).

Obesity ( BMI 27 kg/m2).

Race/ethnicity (eg, African Americans, Hispanic Americans,Native Americans, Asian Americans, Pacific Islanders).

Age 45 years.

Previously identified impaired fasting glucose or impairedglucose Tolerance.

Hypertension (140/90 mm Hg) HDL cholesterol level 35 mg/dL (0.90 mmol/L) and/or

triglyceride level 250 mg/dL (2.8 mmol/L)

History of gestational diabetes or delivery of babies over 9 lbs


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Classifications of insulin

Type 1 diabetes (previously referred to as insulin-dependent

diabetes mellitus)

Type 2 diabetes (previously referred to as noninsulin

dependent diabetes mellitus)

Gestational diabetes mellitus.

Diabetes mellitus associated with other conditions or syndrome


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Nowadays we dont use terms of dependent

or non-independent insulin DM.

Why

????????????????


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Type 1 Diabetes Mellitus

Type 1 diabetes is characterized by destruction of thepancreatic beta cells.

So that no or very little insulin is produced.

Require insulin injections to control their blood glucose levels.

5% to 10% of people with diabetes have type 1 diabetes.

Type 1 diabetes is characterized by an acute onset, usuallybefore age 30


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Causes of Type 1 Diabetes Mellitus

Viral Infections.

Genetics predisposition.

Autoimmune response.


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Pathophysiology of DM type 1


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Pathophysiology of DM type 1


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Type 2 Diabetes Mellitus

Results from decreased sensitivity to insulin (called insulinresistance) and impaired beta cell functioning resulting indecreased insulin production.

Approximately 90% to 95% of people with diabetes have type2 diabetes.

Type 2 diabetes occurs more among people who are older than

30 years and obese.

Type 2 diabetes is treated with diet and exercise and oralhypoglycemic agents.


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Insulin Resistance

Normally Insulin resistance


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Clinical Manifestations

Polyuria (increased urination).

Polydipsia (increased thirst).

Polyphagia (increased appetite).

fatigue and weakness.

Sudden vision changes.

Tingling or numbness in hands or feet,

Dry skin, skin lesions or wounds that are slow to heal.

Recurrent infections.

For type 1 patient is usually thin at diagnosis, whereas fortype2 patient is usually obese at diagnosis.


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Assessment & Diagnostic Findings


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Assessment & Diagnostic Findings

Hgb(A1C)

Is a blood test that reflects average blood glucose levels over aperiod of approximately 2 to 3 months.

When blood glucose levels are elevated, glucose moleculesattach to hemoglobin in the red blood cell. The longer theamount of glucose in the blood remains above normal, themore glucose binds to the red blood cell and the higher theglycosylated hemoglobin level.

The normal values differ slightly from test to test and fromlaboratory to laboratory and normally range from 4% to 6%.


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Other Assessment & Diagnostic Tests

Fasting lipid profile

Test for microalbuminuria Serum creatinine level

Urinalysis

Electrocardiogram


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Diabetes Management

The main goal of diabetes

treatment is to normalize

insulin activity and blood

glucose levels to reduce the

development of vascular and

neuropathic complications.


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Nutritional Management

50% to 60% of calories should be derived from carbohydrates,

20% to 30% from fat, and the remaining 10% to 20% from

protein.

Focus on starchy food rather than sugar (sucrose) foods.

The recommendations regarding fat content of the diabetic dietinclude both reducing the total percentage of calories from fat

sources to less than 30% of the total calories and limiting the

amount of saturated fats to 10% of total calories.


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The meal plan may include the use of some nonanimal sourcesof protein (eg, legumes and whole grains) to help reducesaturated fat and cholesterol intake

Increasing fiber in the diet may also improve blood glucoselevels and decrease the need for exogenous insulin, loweringtotal cholesterol and low-density lipoprotein cholesterol in theblood.

Soluble fiber - in foods such as legumes, oats, and some fruits- plays more of a role in lowering blood glucose and lipidlevels than does insoluble fiber,


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Soluble fiber is thought to be related to the formation of a gel

in the GI tract. This gel slows stomach emptying and the

movement of food through the upper digestive tract.

Insoluble fiber is found in whole-grain breads and cereals and

in some vegetables. This type of fiber plays more of a role in

increasing stool bulk and preventing constipation.

Both insoluble and soluble fibers increase satiety, which is

helpful for weight loss.


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Exercise

Exercise lowers the blood glucose level by increasing the

uptake of glucose by body muscles and by improving insulin

utilization. It also improves circulation and muscle tone.

Exercise also alters blood lipid levels, increasing levels of

high-density lipoproteins and decreasing total cholesterol and

triglyceride levels. This is especially important to the person

with diabetes because of the increased risk of cardiovascular

disease.


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Exercise Precautions

Patients who have blood glucose levels exceeding 250 mg/dL(14 mmol/L) and who have ketones in their urine should notbegin exercising until the urine tests negative for ketones andthe blood glucose level is closer to normal.

the patient who requires insulin should be taught to eat a 15-gcarbohydrate snack (a fruit exchange) or a snack of complexcarbohydrate with a protein before engaging in moderateexercise, to prevent unexpected hypoglycemia.

Patients participating in extended periods of exercise shouldtest their blood glucose levels before, during, and after theexercise period, and they should snack on carbohydrates asneeded to maintain blood glucose levels


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People with diabetes should exercise at the same time and inthe same amount each day.

Regular daily exercise, rather than sporadic exercise, should beencouraged.

A slow, gradual increase in the exercise period is encouraged.

For many patients, walking is a safe and beneficial form ofexercise.


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Self-Monitoring of Blood Glucose

(SMBG)

Frequent SMBG enables people with diabetes to :

1) Adjust the treatment regimen to obtain optimal bloodglucose control.

2) Allows for detection and prevention of hypoglycemia and

hyperglycemia

3) Reduce the risk of long-term diabetic complications


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Types of SMBG devices


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Candidates of SMBG

Diabetes patients who treated with intensive treatment therapy.

Patients with unstable diabetes.

Patients who suffer severe hypoglycemia without warning

signs.

Patients with diabetes type 2 , to examine the effect of diet,

exercise, and oral antidiabetic agents.


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Frequency of SMBG

For most patients who require insulin, SMBG is recommended

two to four times daily (usually before meals and at bedtime).

For patients not receiving insulin may be instructed to assess

their blood glucose levels at least two or three times per week.


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Sources of error in SMBG

Improper application of blood (eg, drop too small).

Improper meter cleaning and maintenance (eg,

allowing dust or blood to accumulate on the optic

window).

Damage to the reagent strips by heat or humidity; use

of outdated strips.


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Urine Testing for Glucose

The advantages of urine glucose testing are that it is less expensive than SMBGand it is not invasive.

Disadvantages of urine testing include the following:

- Results do not accurately reflect the blood glucose level at the time of the test.

- The renal threshold for glucose is 180 to 200 mg/dL (9.9 to 11.1 mmol/L), farabove target blood glucose levels.

- Hypoglycemia cannot be detected because a negative urine glucose result

may occur when the blood glucose level ranges from 0 to 180 mg/dL (9.9

mmol/L) or higher.

- Patients may have a false sense of being in good control when results are

always negative.

-Various medications (eg, aspirin, vitamin C, some antibiotics) may interfere

with test results.

- In elderly patients and patients with kidney disease, the renal threshold (the

level of blood glucose at which glucose starts to appear in the urine) is raised;

thus, false-negative readings may occur at dangerously elevated glucose levels.


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Pharmacologic Therapy

Insulin therapy.

Oral hypoglycemic drugs.


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Insulin Therapy

Insulin therapy is necessary for:

- Type 1 diabetes patients.

- Type 2 diabetes patients in which diet and oral agentsfail to control blood glucose.

- Temporarily for type 2 diabetes who is usuallycontrolled by diet alone or by diet and an oral agentmay require insulin during illness, infection,pregnancy, surgery, or some other stressful even


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Categories of Insulin


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Insulin Species

Animal insulins were obtained from beef

(cow) and pork (pig) pancreases.

Human insulins are now widely available.


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Insulin Regimens

(Conventional Approach)

One approach is to simplify the insulin regimen as much as

possible, with the aim of avoiding the acute complications ofdiabetes (hypoglycemia and symptomatic hyperglycemia).

With this type of simplified regimen (eg, one or moreinjections of a mixture of short- and intermediate-actinginsulins per day), patients may frequently have blood glucoselevels well above normal.

This approach would be appropriate for the terminally ill, thefrail elderly with limited self-care abilities, or any patient whois completely unwilling or unable to engage in the self-management activities.


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Insulin Regimens(Intensive Approach)

Intensive treatment (three or four injections of insulin

per day) reduced the risk of complications.

Another reason for using a more complex insulinregimen is to allow patients more flexibility to changetheir insulin doses from day to day in accordance

with changes in their eating and activity patterns, withstress and illness, and as needed for variations in theprevailing glucose level.


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Complications of insulin therapy

(Local allergic reactions)

A local allergic reaction (redness, swelling, tenderness, and

induration or a 2- to 4-cm wheal) may appear at the injection

site 1 to 2 hours after the insulin administration.

These reactions, which usually occur during the beginning

stages of therapy and disappear with continued use of insulin.

The physician may prescribe an antihistamine to be taken 1

hour before the injection if such a local reaction occurs.


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(Systemic allergic reactions)

An immediate local skin reaction that gradually spreads into

generalized urticaria (hives).

The treatment is desensitization, with small doses of insulin

administered in gradually increasing amounts.

These rare reactions are occasionally associated with

generalized edema or anaphylaxis.


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(Lipodystrophy)

Lipoatrophy is loss of subcutaneous fat and appears as slight

dimpling or more serious pitting of subcutaneous fat.

Lipohypertrophy, the development of fibrofatty masses at theinjection site, is caused by the repeated use of an injection site.

Rotation of injection sites is soimportant


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Lipoatrophy


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Lipohypertrophy


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Rotation is the solution


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(Insulin Resistance)

Clinical insulin resistance has been defined as a daily insulin

requirement of 200 units or more.

This may occur for various reasons, the most common being

obesity, which can be overcome by weight loss.

It may be related to formation of autoantibodies againstinsulin, but it is rarely occur.


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(Morning Hyperglycemia)


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Oral Antidiabetic Agents

Oral antidiabetic agents may be effective for patients who havetype 2 diabetes that cannot be treated by diet and exercisealone.

They cannot be used during pregnancy.

Oral antidiabetic agents include the sulfonylureas, biguanides,

alpha glucosidase inhibitors, thiazolidinediones, andmeglitinides


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Sulfonylureas

Directly stimulating the pancreas to secrete insulin. Therefore,a functioning pancreas is necessary for these agents to beeffective.

They cannot be used in patients with type 1 diabetes.

The sulfonylureas can be divided into first- and second-generation categories.

The most common side effects of these medications are GIsymptoms and dermatologic reactions. Hypoglycemia mayoccur when an excessive dose of a sulfonylurea is used orwhen the patient omits or delays meals, reduces food intake, orincreases activity.


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Biguanides

Metformin (Glucophage) produces its antidiabetic effects byfacilitating insulins action on peripheral receptor sites.

It can be used only in the presence of insulin. Biguanides have

no effect on pancreatic beta cells.

Lactic acidosis is a potential and serious complication ofbiguanide therapy

Metformin is contraindicated in patients with renal impairment(serum creatinine level more than 1.4) or those at risk for renaldysfunction (eg, those with acute myocardial infarction).


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Alpha glucosidase inhibitors

Acarbose (Precose) and miglitol (Glyset) are oral alphaglucosidase inhibitors used in type 2 diabetes management.

They work by delaying the absorption of glucose in theintestinal system, resulting in a lower postprandial bloodglucose level. As a consequence of plasma glucose reduction,hemoglobin A1C levels drop.

Their side effects are diarrhea and flatulence. These effectsmay be minimized by starting at a very low dose andincreasing the dose gradually.


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Thiazolidinediones.

Rosiglitizone (Avandia) and pioglitozone (Actos) are oral

diabetes medications categorized as thiazolidinediones.

Thiazolidinediones enhance insulin action at the receptor site

without increasing insulin secretion from the beta cells of the

pancreas.

These medications may affect liver function; therefore, liver

function studies must be performed at baseline and at frequent

intervals(monthly for the first 12 months of treatment).


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Meglitinides

Repaglinide (Prandin), an oral glucose-lowering agent of theclass of oral agents called meglitinides, lowers the bloodglucose level by stimulating insulin release from the pancreaticbeta cells.

Its effectiveness depends on the presence of functioning betacells. Therefore, repaglinide is contraindicated in patients withtype 1 diabetes.

The principal side effect of repaglinide is hypoglycemia;however, this side effect is less severe and frequent than for asulfonylurea because repaglinide has a short half-life(approximately 1 hour).


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Self-administration of insulin

Storing Insulin:

- Cloudy insulins should be thoroughly mixed by gently

inverting the vial or rolling it between the hands before

drawing the solution into a syringe.

- Whether insulin is the short- or long-acting preparation, the

vials not in use should be refrigerated and extremes of

temperature should be avoided; insulin should not beallowed to freeze and should not be kept in direct sunlight

or in a hot car.


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The insulin vial in use should be kept at room temperature to

reduce local irritation at the injection site, which may occur

when cold insulin is injected.

Patients should be instructed to always have a spare vial of the

type or types of insulin they use.


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Selecting Syringes:


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Mixing Insulins:

When rapid- or short-acting insulins are to be given simultaneously

with longer-acting insulins, they are usually mixed together in thesame syringe.

the longer-acting insulins must be mixed thoroughly before useWhile there are varying opinions regarding which type of insulin(short- or longer-acting) should be drawn up into the syringe first

when they are going to be mixed, the ADA recommends that theregular insulin be drawn up first.

The most important issue isthat patients not inject one type ofinsulin into the bottle containing a different type of insulin.


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The ratio of 70/30 (70% NPH and 30% regular insulin in one

bottle) is the most common.

Most (if not all) of the printed materials available on insulin

dose preparation instruct patients to inject air into the bottle of

insulin equivalent to the number of units of insulin to be

withdrawn.


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Selecting and rotating injection site:

- The four main areas for injection are the abdomen, arms (posterior surface),thighs (anterior surface), and hips.

- The speed of absorption is greatest in the abdomen and decreasesprogressively in the arm, thigh, and hip.

- Systematic rotation of injection sites within an anatomic area isrecommended to prevent localized changes in fatty tissue (lipodystrophy).

- Patients should try not to use the same site more than once in 2 to 3 weeks. I

- if the patient is planning to exercise, insulin should not be injected into thelimb that will be exercised


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Sites of insulin injections


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Preparing the skin:

- Use of alcohol to cleanse the skin is not recommended, butpatients who have learned this technique often continue to use

it.

- If alcohol is used to cleanse the injection area, patients should

be cautioned to allow the skin to dry after cleansing with

alcohol. If the skin is not allowed to dry before the injection.


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Pinching is preferable


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Acute complications of DM

Hypoglycemia.

Diabetic Ketoacidosis (DKA).

Hyperglycemic Hyperosmolar Nonketotic Syndrome

(HHNS).


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Hypoglycemia

Hypoglycemia (abnormally low blood glucose level) occurs

when the blood glucose falls to less than 50 to 60 mg/dL (2.7

to 3.3 mmol/L).


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Causes of hypoglycemia

Too much insulin.

Too much oral hypoglycemic agents.

Too little food.

Excessive physical activity


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Clinical manifestations of hypoglycemia

They can be categorized into:

- Adrenergic symptoms.

- Central nervous system (CNS) symptoms.


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Mild hypoglycemia

In mild hypoglycemia, as the blood glucose level falls, the

sympathetic nervous system is stimulated, resulting in anincrease of epinephrine and norepinephrine.

Sweating.

Tremor.

Tachycardia.

Palpitation. Nervousness.

hunger


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Moderate hypoglycemia

In moderate hypoglycemia, the fall in blood glucose leveldeprives the brain cells of needed fuel for functioning. Signs ofimpaired 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.

- drowsiness.


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Severe hypoglycemia

In severe hypoglycemia, CNS function is so impaired that thepatient needs the assistance of another person for treatment of

hypoglycemia.

Symptoms may include:

- Disoriented behavior.

- Seizures.- Difficulty arousing from sleep.

- Loss of consciousness


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Management of hypoglycemia

For patients who are unconscious and cannot swallow, an

injection of glucagon 1 mg can be administered either

subcutaneously or intramuscularly.

A concentrated source of carbohydrate followed by a snack

should be given to the patient on awakening to prevent

recurrence of hypoglycemia.

In the hospital or emergency department, patients who are

unconscious or cannot swallow may be treated with 25 to 50

mL 50% dextrose in water (D50W) administered

intravenously. The effect is usually seen within minutes.


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Glucagon injection


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Prevention of hypoglycemia

DM patients must carry some form of simple sugar

with them at all times.

Patients are advised to refrain from eating high-calorie, high fat dessert foods (eg, cookies, cakes,

doughnuts, ice cream) to treat hypoglycemia. The

high fat content of these foods may slow the

absorption of the glucose.


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Diabetic Ketoacidosis

DKA is caused by an absence or markedly inadequate amountof insulin. This deficit in available insulin results in disorders

in the metabolism of carbohydrate, protein, and fat.

The three main clinical features of DKA are:

- Hyperglycemia

- Dehydration and electrolyte loss

- Acidosis.


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Clinical manifestations

Polyuria and polydipsia.

Blurred vision,

Weakness, and headache.

Orthostatic hypotension.

GI symptoms such as anorexia, nausea, vomiting, and

abdominal pain.

Patients may have acetone breath (a fruity odor), which occurs

with elevated ketone levels.

Hyperventilation.

Patients may be alert, lethargic, or comatose.


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Kussmaul respirations


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Assessment and Diagnostic Findings

Blood glucose levels may vary from 300 to 800 mg/dL (16.6to 44.4 mmol/L).

low serum bicarbonate (0 to 15 mEq/L) and low pH (6.8 to

7.3).

low PCO2 level (10 to 30 mm Hg).

Elevated levels of creatinine, blood urea nitrogen (BUN),hemoglobin, and hematocrit may also be seen withdehydration.

Medical management


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Medical management

(Rehydration)

Patients may need up to 6 to 10 liters of IV fluid to replace

fluid losses caused by polyuria, hyperventilation, diarrhea, andvomiting.

Initially, 0.9% sodium chloride (normal saline) solution isadministered at a rapid rate, followed by 0.45% sodiumchlorise solution.

When the blood glucose level reaches 300 mg/dL (16.6mmol/L) or less, the IV fluid may be changed to dextrose 5%in water (D5W) to prevent a precipitous decline in the bloodglucose level.

Medical management


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Medical management

(Restoring electrolytes)

The major electrolyte of concern during treatment of DKA is

Potassium. Why ???????????

Cautious but timely potassium replacement is vital to avoid

dysrhythmias that may occur with hypokalemia. Up to 40 mEqper hour may be needed for several hours.

Frequent (every 2 to 4 hours initially) electrocardiograms and

laboratory measurements of potassium are necessary duringthe first 8 hours of treatment.

Potassium replacement is withheld only if hyperkalemia ispresent or if the patient is not urinating

Medical management


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Medical management

(Reversing acidosis)

The acidosis that occurs in DKA is reversed with insulin,

which inhibits fat breakdown, thereby stopping acid buildup.

Insulin is usually infused intravenously at a slow, continuousrate.

Dextrose water such as (D5NS or D50.45NS), are

administered when blood glucose levels reach 250 to 300mg/dL (13.8 to 16.6 mmol/L) to avoid too rapid a drop in theblood glucose level


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Hyperglycemic Nonketotic Syndrome

(HHNS)

Hyperosmolar

L li i f DM


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Long-term complications of DM

Macrovascular complications.

Microvascular complications.

M l li i


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Macrovascualr complications

Coronary artery disease, cerebrovascular disease, and peripheral

vascular disease are the three main types of macrovascularcomplications.

Myocardial infarction is twice as common in diabetic men and threetimes as common in diabetic women,

cerebrovascular disease includes transient ischemic attacks andstrokes.

Signs and symptoms of peripheral vascular disease includediminished peripheral pulses and intermittent claudication (pain inthe buttock, thigh, or calf during walking). The severe form ofarterial occlusive disease in the lower extremities is largelyresponsible for the increased incidence of gangrene leading to

diabetic foot.

Mi l li i


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Microvascualr complications

Diabetic microvascular disease (or microangiopathy) is

characterized by capillary basement membrane thickening.

The basement membrane surrounds the endothelial cells of the

capillary.

Two areas affected by these changes are the retina and the

kidneys.

N l R ti


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Normal Retina

Background Retinopathy


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Background Retinopathy

Early stage, asymptomatic retinopathy. Blood vessels within the retinadevelop microaneurysms that leak fluid, causing swelling and formingdeposits (exudates).

P lif ti R ti th


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Preproliferative Retinopathy

Represents increased destruction of retinal blood vessels

P lif ti R ti th


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Proliferative Retinopathy

Abnormal growth of new blood vessels on the retina. New vessels rupture,bleeding into the vitreous and blocking light. Ruptured blood vessels in thevitreous form scar tissue, which can pull on and detach the retina.

N h th


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Nephropathy

The earliest detectable change in the course of

diabetic nephropathy is a thickening in the

glomerulus. At this stage, the kidney may startallowing moreserum albumin ( plasma protein) than

normal in theurine ( albuminuria ), and this can be

detected by sensitivemedical testsfor albumin. This

stage is called " microalbuminuria "

Di b ti N th


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Diabetic Neuropathy

Refers to a group of diseases that affect all types of nerves,

including peripheral (sensorimotor), autonomic, and spinal

nerves.

P i h l N th


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Peripheral Neuropathy

Initial symptoms include paresthesias and burning sensations(especially at night).

As the neuropathy progresses, the feet become numb.

In addition, a decrease in proprioception (awareness of postureand movement of the body and of position and weight ofobjects in relation to the body).

Decreased sensation of light touch may lead to an unsteadygait.

Decreased sensations of pain and temperature place patientswith neuropathy at increased risk for injury and undetected foot

infections.

A t i N thi


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Autonomic Neuropathies

Neuropathy of the autonomic nervous system results in a broadrange of dysfunctions affecting almost every organ system of the

body.

Three manifestations of autonomic neuropathy are related to the

cardiac, GI, and renal systems.

Cardiovascular symptoms range from fixed, slightly tachycardic

heart rate; orthostatic hypotension; and silent, or painless,

myocardial ischemia and infarction.

GI symptoms include: Delayed gastric emptying may occur with the

typical symptoms of early satiety, bloating, nausea.

Urinary retention, a decreased sensation of bladder fullness, and

other urinary symptoms of neurogenic bladder result from

autonomic neuropathy.

Sudomotor Neuropathy


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Sudomotor Neuropathy

This neuropathic condition refers to a decrease or absence of

sweating (anhidrosis) of the extremities.

Foot and Leg ulcers


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Foot and Leg ulcers

From 50% to 75% of lower extremity amputations are performed on people withdiabetes.

Complications of diabetes that contribute to the increased risk of foot infectionsinclude:

- Neuropathy: Sensory neuropathy leads to loss of pain and pressure sensation, and

autonomic neuropathy leads to increased dryness and fissuring of the

skin (secondary to decreased sweating). Motor neuropathy results in

muscular atrophy, which may lead to changes in the shape of the

foot.

- Peripheral vascular disease: Poor circulation of the lower extremities contributes

to poor wound healing and the development

of gangrene.- Immunocompromise: Hyperglycemia impairs the ability of specialized leukocytes

to destroy bacteria. Thus, in poorly controlled diabetes,

there is a lowered resistance to certain infections.

Foot and Leg ulcers


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Foot and Leg ulcers

Foot and Leg ulcers


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Foot and Leg ulcers

High-risk characteristics include:

- Duration of diabetes more than 10 years

- Age older than 40 years

- History of smoking

- Decreased peripheral pulses

- Decreased sensation

- Anatomic deformities or pressure areas (eg, bunions,calluses, hammer toes)

- History of previous foot ulcers or amputation

Diabetes Mellitus - by Ibrahim Rawhi Ayasreh

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Transcript of Diabetes Mellitus - by Ibrahim Rawhi Ayasreh