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
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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
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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
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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
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Rehydration
Replace electrolytes
Insulin
Vital signs hourly
Blood sugar hourly
Urine output hourly
Cardiac monitor
Complications
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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)
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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 = intraretinal 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
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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
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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 LEUKOCYTES
• RESISTANCE 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
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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