DIABETES MELLITUS

Majuvy L. Sulse MSN, RN, CCRN

Lola Oyedele MSN, RN, CTN

DIABETES MELLITUS

• DEFINE– CHRONIC SYSTEMIC DISEASE

CHARACTERIZED BY EITHER

– A DEFICIENCY OF INSULIN

– OR A DECREASED ABILITY OF THE BODY TO USE INSULIN (insulin resistant)

PANCREAS• CELL TYPES AND FUNCTION

– BETA - INSULIN• HYPOGLYCEMIC FACTOR

– ALPHA - GLUCAGON• HYPERGLYCEMIC FACTOR

– DELTA - SOMASTATIN• INHIBITS SECRETION OF BOTH INSULIN

AND GLUCAGON

ROLE OF INSULIN

• SKELETAL MUSCLE – INCREASE UPTAKE OF GLUCOSE, CONVERT

TO GLYCOGEN

• Liver– Increase uptake of glucose from blood and convert

to glycogen – Inhibits production of glycogenolysis – Inhibits gluconeogenesis

• CARBOHYDRATES– BREAKS DOWN TO GLUCOSE, INSULIN

TRANSPORTS ACROSS CELL MEMBRANE

– ENZYMES BREAKS DOWN FOR ENERGY OR STORED AS GLYCOGEN

• PROTEIN– INSULIN ENHANCES AMINO ACIDS TO

PROTEIN

• FATS– FREE FATTY ACIDS TO ADIPOSE

Critical thinking

• The process of breaking down material without insulin during metabolism is know as:

• A. Ketogenesis• B. Lipolysis• C. Glycogenesis• D. Catabolism

REGULATION• INSULIN

BLOOD SUGAR = INSULIN SECRETED FOR TRANSPORT INTO CELLS

• GLUCAGON BLOOD SUGAR = GLUCAGON SECRETED – STIMULATES LIVER TO BREAKDOWN

GLYCOGEN TO GLUCOSE & RELEASE ( GLYCOGENESIS)

– METABOLISE AMINO ACIDS TO GLUCOSE– LIPOLYSIS TO GLYCEROL

( GLUCONEOGENESIS)

PITUITARY

• GROWTH HORMONE

• ACTH

• CORTISOL GLUCONEOGENESIS LIPOLYSIS USE OF GLUCOSE BY CELLS – = BLOOD SUGAR

RISK FACTORS

• FAMILY HISTORY

• HISTORY OF GLUCOSE INTOLERANCE

• OBESITY

• HIGH FAT DIET

• SEDENTARY LIFE STYLE

• ELDERLY

• ETHNECITY

TYPES• TYPE 1

– IDDM ( 5-10%)

• TYPE 2– NIDDM ( 90%)

• GLUCOSE INTOLERANCE– FBS 110 BUT 126

• SECONDARY DIABETES– 2ND TO DISEASE OR DISORDER

• GESTATIONAL DIABETES– DURING PREGNANCY

TYPE 1 (IDDM)• DEFINE

– BETA CELL DESTRUCTION – ( AUTOIMMUNE, VIRAL, GENETIC)– INSULIN INSUFFICIENT TO SUSTAIN LIFE– REQUIRES EXOGENOUS INSULIN– REVERTS TO LIPOLYSIS &

GLUCONEOGENESIS

• ETIOLOGY 30 YEARS, THIN, ABRUPT ONSET

• S&S– POLYURIA, POLYDIPSIA, POLY PHASIA

TYPE 2 (NIDDM)• DEFINE

– DEFECIENT INSULIN TO MEET BODY DEMANDS

– INSULIN RESISTENCE– DOES NOT REVERT TO LIPOLYSIS OR

GLUCONEOGENESIS

• ETIOLOGY 30 YEARS, OBESE, GRADUAL ONSET

• S&S– VAGUE, FATIGUE, IRRITABILITY, GRADUAL

POLYURIA, POLYDIPSIA, POLYPHASIA

Critical Thinking

• Which of the following is true regarding Diabetes?

• Diabetes is an acute disorder that responds only to insulin

• Diabetes is curable• Diabetes is characterized by an abnormality

of carbohydrate metabolism• Diabetes is not a significant cause of death.

CONSEQUENCE OF INSULIN DEFECIENCY

• LIVER– CANNOT STORE GLUCOSE AS GLYCOGEN– FREE FATTY ACIDS BREAK DOWN = KETONE

BODIES– HYPERTRIGLYCERIDEMIA

• SKELETAL MUSCLE– NO GLUCOSE FOR ENERGY, METABOLISE

PROTEINS

• ADIPOSE TISSUE– LIPOLYSIS = FREE FATTY ACIDS

• KIDNEY– KIDNEY CAN EXCRET 180 MG/DL– (GLUSOSURIA)– = OSMOTIC DIURESIS= (POLYURIA)– = FLUID VOLUME & ELECTROLYTE

DEPLEATION – = HYPOVOLEMIA = THIRST (POLYDISPIA) GLUCOSE TO CELLS = STARVATION

(POLYPHAGIA)

Critical thinking• A diagnosis of diabetes suggests that a

client’s symptom of polyuria is most likely caused by :

• A. Increased insulin levels promote a diuretic effect

• B. Glucose acting as a hypertonic agent, draws water from the intracellular fluid into the renal tubules

• C. Electrolyte changes lead to the retention of sodium and potassium

• D. Microvascular changes alter the effectiveness of the kidney

DIAGNOSTIC STUDIES

• FASTING BLOOD SUGAR 126

• RANDOM BLOOD SUGAR 200

• POST PRANDIAL BLOOD SUGAR 200

• GLYCOSYLATED HgB. (HgA1c) 7%– (life of RBC – 120 days)

• GLYCOSYLATED ALBUMIN 1.5–2.7nmol/L

MANAGEMENT OUTCOMES

• PROMOTE PROPER NUTRITION

• PROMOTE EXERCISE

• ADMINISTER MEDICATION

ORAL ANTIDIABETIC MEDICATIONS

SULFONYLURES

INCREASE RELEASE OF INSULIN

ORINASE, TOLINASE

GLUTROL, DIABETA

WEIGHT GAIN, HYPOGLYCEMIA• MEGLITINIDES

– INCREASE RELEASE OF INSULIN• PRANDIN, STARLIX• WEIGHT GAIN, HYPOGLYCEMIA

ORAL ANTIDIABETIC MEDICATIONS

• BIGUANIDES– REDUCE GLUCOSE BY LIVER, INCREASED INSULIN

SENSATIVITY.• GLUCOPHAGE

– DIRRHEA, LACTIC ACIDOSIS • A-GLUCOSIDASE INHIBITORS

– DECREASE ABSORPTION OF CARBOHYDRATES• ACARBOSE,

– DIRRHEA, ABD PAIN• THIAZOLIDINEDIONES

– INCREASE GLUCOSE UPTAKE• ACTOSE, AVANDIA

– WEIGHT GAIN, EDEMA

ALTERED HEALTH MAINTENANCE

• R/T LACK OF KNOWLEDGE OF DIETARY MANAGEMENT DIABETES

• OUTCOME – CLIENT WILL STATE RELATIONSHIP OF

DIETARY MANAGEMENT TO BLOOD GLUCOSE CONTROL

– CLIENT WILL CHOOSE FOODS THAT MEET CALORC NEEDS AND OFFER A WELL BALANCED DIET

Dietary Proportions

• Carbohydrates 50-60%

• Fats 30%– 10% saturated ( animal fats)– 10% polysaturated ( fish)– 10% monounsaturated ( olive oil)

• Protein 10-20%

• Fiber 40 gms daily

Acute Complications of Diabetes Mellitus

• Hypoglycemia = BS below 60

• Causes– Insufficient food

• Missed meal, nausea/vomiting, interrupted enteral feeding

– Increased insulin dose, NPO exam, peak action of insulin

• Categories– Adrenergic– Neuroglycopenic

Hyperglycemia• Causes

• Undiagnosed type 1

• Know type 1– Omission of insulin– Illness/infection/ trauma/ surgery

• None DM– Cushing's syndrome/ hyperthyroid/

pregnancy– Medications ( Dilantin)

Diabetic Ketoacidosis• Criteria = Blood sugar greater than 250

– Arterial Ph less than 7.30– HCO3 less than 18

• Pathology cellular glucose = gluconeogenesis &

glycogenolysis

• Free fatty acids metabolized = ketone bodies

• Ketones release hydrogen ions

• Hydrogen ions exchanged for K at cell wall

= K

Diabetic Ketoacidosis

• Kidney regulates = K blood glucose = osmotic pressure

• Kidney regulates = diuresis = Na

• Glucosuria, dehydration & electrolyte imbalance

• S&S– Polyuria, polydipsia, polyphagia

– Headache with blurred vision

– Nausea/vomiting r/t peristalsis

respirations/ fruity breath

– Kussmaul's pattern

• Labs– Blood sugar = 300-800

– Na ( reflect level of dehydration)

– K first (hydrogen ions exchanged for K at cell wall

– then (kidney regulates)

Bun & Creatinine

– ABG’s = metabolic acidosis

Critical Thinking

• Which terms would best describe the condition of a ketoacidotic client on admission?

• A. warm, flushed, dry• B. Cool and clammy• C. cool and dry• D. Warm, pale and clammy

Management

• Rehydration

• Replace electrolytes

• Insulin

• Vital signs hourly

• Blood sugar hourly

• Urine output hourly

• Cardiac monitor

Complications

• Hypovolemic shock

• Dysrhythmias

• Myocardial infarction

• Seizures

• Coma

• Acute renal failure

Hyperglycemic Hyperosmolar Nonketotic Syndrome

• Hyperglycemia, & Dehydration

• W/O acidosis ( enough insulin)

• Insidious onset

• ( tolerate polyuria, polydipsia, polyphagia headache & weakness)

HHNS• Dehydration R/T osmotic diuresis

• Hypovolemia = glomerular filtration rate

= glucose retained

Na retained

osmolarity.

• At risk– Elderly, type 2 or mild type 1– Burns, infection, renal & heart disease– Acute illness– Dialysis, hyperalimentation

• S&S– Profound dehydration– Blood sugar = 600-2000 BUN Creatinine– glycosuria

Management

• Rehydrate– Normal saline X 2 hours ( Isotonic)– .45 normal saline (hypotonic)

• Electrolyte replacement

• Insulin

• Hourly vital signs, output,

• Cardiac monitor

Chronic Complications

• Infections– monilia

• Skin r/t glucose & moisture• Vaginal R/T glucose & altered Ph

Vascular Complications

• Macrovascular– Atherosclerotic changes earlier & greater

frequency– Coronary artery disease– Cerebral vascular disease – peripheral vascular disease

• Microvascular

• Unique to diabetics

• Thickening of basement membrane of capillaries

• Retinopathy -

• Cataracts

• Neuropathy

• Nephropathy

Retinopathy

• R/t vascular fragility

• Stages– Early - capillary permeability = intra-

retinal hemorrhage– Moderate- macular edema, micro

hemorrhage– Progressive retinal ishemia, exudate,

cotton-wool patches– Advanced - neo-vascularization, retinal

detachment, blind

Cataracts

• Accumulation of sorbitol in the lens

• Opacity gradual onset

• Similar to senile cataracts

Neuropathy• Most commonly affects peripheral nervous system• Most common complication sensation motor function• Parasthesia ( tingle- burn, numbness)• Mononephropathy

– Sporadic, single focal area

• Symmetrical polyneuropathy– Distal symmetrical pattern ( stocking, glove)

• Autonomic nephropathy– Cardiac, GI ( gastroparesis) , GU ( neurogenic bladder)

NEPHROPATHY

• Most common cause of end-stage renal disease

• Type 1 = 45%, Type 2 = 20%

• Damage to capillaries of glomeruli

• Concomitant hypertension

• Dx glycosylated albumin

• Rx hypertension, maintain even blood sugar

SICK DAY MANAGEMENT

• TEST BLOOD SUGAR Q 2-4 HRS

• TEST URINE FOR KETONES Q 2-4 HRS

• TAKE INSULIN EVEN IF N/V

• 10-15 GMS CARBOHYDRATES Q 1-2 HRS.– EX. 1 POPSICLE, 1/2 CUP JELLO

• FLUIDS Q 30 MINS– EX. ICE CHIPS, GATORADE

FOOT PROBLEMS• 75% OF ALL LOWER EXTREMITY

AMPUTATIONS

• 3 FOLD PROBLEM– NEUROPATHY

SENSATION (INJURY)

– PERIPHERAL VASCULAR DISEASE CIRCULATION ( POOR WOUND

HEALING)

– IMMUNOCOMPROMISED ABILITY OF LEUKOCYTESRESISTANCE TO INFECTION

Critical thinking

• The goals of management of diabetes are based entirely on the patient's ability for self care. The general focus of short term goals then is:

• A. cure of the disease• B. Control of the disease• C. prevention of the disease• D. Recognition of complications

CARE OF THE ELDERLY

• TEACH AT SIMPELEST LEVEL• BARRIERS TO LEARNING

HEARING EYESIGHT MEMORY EYE HAND COORDINATION

RESOURCES COORDINATION

THE FUTURE HOPE

• PANCREAS TRANSPLANT

• ISLET CELL TRANSPLANTS

Islet cell transplant• Edmonton procedure• Utilizes cadaver donors• Requires 1 million cells• 80% success rate• Cells injected into liver• Pt carefully monitored while cells attach

themselves to blood vessels and begin insulin production

• Requires Immunosuppression drugs for life