Diabetes Mellitus
Ella’s Story (7 min 28 seconds) https://www.youtube.com/watch?v=jniek-5BRg4
ETIOLOGY
• Diabetes – ‘like a sieve or siphon’• Mellitus – ‘sweet or r/t honey’
• A systemic metabolic disorder that involves improper metabolism of CHO, fats and proteins
ETIOLOGY
• Chronic multisystem disease r/t:– 1. a decrease or absolute lack of insulin
production by the beta cells of the islets of Langerhans in the pancreas, or
– 2. by impaired insulin utilization, or – 3. Both
ETIOLOGY
• Exact cause: unknown• Contributing factors: – Genetic– Virus– Aging process– Diet, lifestyle , ethnicity
ETIOLOGY
• Other contributing factors:– Obesity– T-lymphocytes may play a role in the autoimmune
destruction of the pancreatic insulin-producing cells
TYPES OF DIABETES
• 2 main types: “Type 1” and “Type 2”• Type 1 was formerly called:– Juvenile or juvenile-onset – Insulin Dependent Diabetes Mellitus (IDDM)
• Type 2 was formerly called:– Adult-onset diabetes or Maturity-onset diabetes– Non-insulin dependent Diabetes Mellitus (NIDDM)
Type 1 Diabetes
• Absence of endogenous insulin • An autoimmune process, possibly triggered by a
viral infection, destroys beta cells in the pancreatic islets deficient insulin production– Pt. retains normal sensitivity to the action of insulin– Within 5 years of diagnosis, all of the pt.’s beta cells will
have been destroyed and no insulin is produced
• Affected people require exogenous insulin for the rest of their lives
TYPE 2 Diabetes
• MAIN PROBLEM: an abnormal resistance to insulin action
• Continuous high glucose level in the blood desensitizes the beta cells; they become less responsive to the elevated glucose chronically elevated blood glucose
• Controlled by diet and exercise; may require oral hypoglycemic agents or exogenous insulin
http://www.bing.com/videos/search?q=youttube+bach+music&FORM=VIRE3#view=detail&mid=C55B52AB9E21E0B2205EC55B52AB9E21E0B2205E (an hour of BACH study music)
Type 1/Type 2
Type 1 Diabetes• s/sx more rapid and acute• Usually appears before 30
years of age• Significant decrease or lack
of insulin production• Exogenous insulin needed
Type 2 Diabetes• More gradual onset• Usually occurs in 35+ years
old with most dx. >55 yr. old and overweight
• Decreased response to insulin = insulin resistant
• Oral hypoglycemics utilized• Diet change and weight loss
can often reverse this process
Youtube.com
Diabetes Type 1 https://www.youtube.com/watch?v=_OOWhuC_9Lw (2 minutes 14 sec)
Diabetes Type 2http://www.youtube.com/watch?v=OXAe3eOjqCk (8 minutes)
METABOLIC SYNDROME
• Metabolic syndrome – Thought to be a precursor to diabetes
• Includes:– Impaired glucose tolerance, high serum insulin,
hypertension, elevated triglycerides, low HDL cholesterol, altered size and density of LDL cholesterol
– Believed that metabolic syndrome is a chronic low-grade inflammatory process affecting endothelial tissue
METABOLIC SYNDROME
– Long-term effects: atherosclerosis, ischemic heart disease, left ventricular hypertrophy, type 2 DM
– Research directed at learning how to detect this syndrome early and what interventions might slow or arrest the progress
PATHOPHYSIOLOGY of DM
• In normal metabolism, the end products of digestion (glucose, fatty acids and glycerol, and amino acids) are absorbed into the venous circulation and carried to the liver where they can be used immediately or stored for later use.
• The liver can change glycerol and fatty acids into glucose which serves as fuel for muscles and as an energy source for the brain.– Insulin must be present for muscles and other body cells to
utilize glucose
Pathophysiology
• In the diabetic person, lack of proper amounts of insulin or it’s inadequate utilization, impairs the use of glucose in the body.
• The excess glucose accumulates in the bloodstream, and hyperglycemia results.– To get rid of this abnormal amount of glucose, the
kidneys excrete it in the urine (glycosuria). • Glycosuria necessitates an extra amount of water
intake to dilute the urine
Pathophysiology
• The patient then develops:– Polyuria – Polydipsia
• Even though excess glucose is available in the bloodstream, the body cannot utilize it without the help of insulin cells are not properly nourished polyphagia develops
Pathophysiology
• Ketone bodies: Fatty acids (normal metabolic products from which acetone may spontaneously arise) may also be changed by the liver into glucose and ketone bodies.
• Because CHO cannot be utilized properly, protein and
fats are broken down ketone bodies and used for heat and energy diabetic ketoacidosis/diabetic coma may develop
Role of Insulin
• Glucose – Insulin stimulates active transport of glucose into cells – If insulin absent, glucose remains in the bloodstream – Blood becomes thick, which increases its osmolality – Increased osmolality stimulates the thirst center– Increased fluid does not pass into body tissues; high
serum osmolality retains fluid in the bloodstream – As blood passes through the kidneys, some glucose
eliminated – Osmotic force created by glucose draws extra fluid and
electrolytes with it, causing abnormally increased urine volume
Role of Insulin
• Fatty acids– Without adequate insulin, fat stores break down and
increased triglycerides are stored in the liver – Increased fatty acids in the liver can triple the production
of lipoproteins; promotes atherosclerosis
Role of Insulin
• Protein– Without adequate insulin, protein storage halts; large
amounts of amino acids dumped into the bloodstream – High levels of plasma amino acids place people with
diabetes at risk for development of gout – Changes in protein metabolism lead to extreme
weakness and poor organ functioning
CLINICAL MANIFESTATIONS
• Type 1 – 3 classic “polys”:– Polyuria– Polydipsia– Polyphasia
As ketone bodies accumulate in the bloodstream, imbalances of Na+, K+, and bicarbonate result
CLINICAL MANIFESTATIONS
• Type 2– Asymptomatic in early disease– But later may c/o sx Type 1 DM– May not seek medical care until severe
complications such as: kidney involvement, retinopathy, impotence, neuropathy, or gangrene
ASSESSMENT
• Subjective Data:– Pt. c/o hunger, thirst, and nausea– Frequent and large amt. urination– Weakness and fatigue– Blurred vision– Decreased sensation to pain and temperature in
the feet; numbness and tingling of the LE– C/O his or her body and his/her ability to cope
with the illness
ASSESSMENT
• Objective Data:– Assess skin, wound healing, ulcerations, etc– Women: freq. UTI’s and vaginal infections;
bothersome vaginal discharge– Obesity– Legs and feet cold to touch; ↓ hair present on LE– Ability and compliance with glucose testing and
proper use of medication – oral and insulin s.q.
DIAGNOSTIC TESTS
• The patient with the following results should be further evaluated:– random blood glucose > 200mg/dL– a FBS >126 mg/dL– a 2 hr post prandial level > 200mg/dL
• See p. 512 Box 11-2 for Diagnostic Tests
DIAGNOSTIC TESTS
• ADA recommends self-monitor blood glucose instead of urine testing
• However, urine testing for ketonuria is valuable in determining the advent of DKA– Recommended for Type 1 diabetics experiencing
hyperglycemia and acute illness.
MEDICAL DIAGNOSIS
• For “Diabetes Mellitus”:– One or more of the following criteria needs to be
met on 2 separate occasions:• Polyuria, polydipsia, polyphagia, unexplained weight
loss + random glucose level = or > 200 mg/dL• FBS = or > 100mg/dL (after 8 hrs fast , minimum)• 2 hr Post Prandial blood sugar = or > 200mg/dL during
an oral glucose tolerance test (OGTT)
MEDICAL DIAGNOSIS
• For “Prediabetes”:– Impaired fasting glucose (IFG) and/or impaired
glucose tolerance (IGT)
– Individuals should receive education on weight reduction and increasing physical activity
MEDICAL MANAGEMENT
• SUMMARY:– Education– Monitoring– Meal Planning– Medication – Exercise
MEDICAL MANAGEMENT
• OVERALL GOAL– Assist people with diabetes in making changes in
nutrition and exercise habits leading to improved metabolic control
• Additional goals:– Maintenance of as near-normal blood glucose levels as
possible– Achievement of optimal serum lipid levels– Provision of optimal calories for maintaining or attaining
reasonable weight and normal growth and development rates for children and adolescents and pregnancy
MEDICAL MANAGEMENT
• ADDITIONAL GOALS cont.– Prevention and treatment of acute complications– Improvement of overall health through optimal
nutrition• IMPORTANCE OF THE NURSE AS A TEACHER
In supporting Diabetes Self Care:– Dietary information– Medication routine– SMBG– Exercise
DIET
• Nutritional Therapy– Aimed at achieving a normal glucose leves of <
126 mg/dL– Attaining a reasonable body weight– Ensuring proper growth and maintenance
• Reduce total fat –esp. saturated fat• Monitor Lab results: esp. HgbA1c, SMBG
results, and lipids
DIET
• DIETICIAN REFERRAL – inpatient and outpatient
• Diets based on ADA recommendations• Home Care Issues– Ability to choose, shop, and pay for groceries– Prepare food, store leftovers– Ability to follow dietary regimen
DIET
• Glycemic Index– Different CHO foods affect the blood glucose level
in different ways– This varying effect is termed the “glycemic index”– What is the glycemic index of the foods that are
being consumed?• Check labels for “low glycemic index”
DIET
• Other diets: Quantitative and Qualitative– Quantitative Diet: follow the food choices and
number of servings recommended by the MyPyramid food planning tool• 45-50% of total kilocalories from CHO• 10-20% of total kilocalories from protein• 30% of total kilocalories from fats
– Qualitative Diet: unmeasured and unrestricted; stressing moderation when selecting foods from My Pyramid food planning tool• Reduce use of simple CHO, saturated fat, and alcohol
DIET
• Insulin-dependent diabetics– Snacks midafternoon and bedtime– Evenly distribute food intake throughout the day
EXERCISEhttp://www.webmd.com/diabetes/video/kahn-does-exercise-affect-diabetes
• Yes! Exercise regularly• Promotes proper utilization of glucose• Important for overall functioning of C-V
system• Increases sense of well-being• Can reduce insulin-resistance and increase
glucose uptake; reduces BP and lipid levels
Stress of Acute Illness and Surgery
• Emotional and physical stress can ↑ blood glucose level and hyperglycemia
• Acute Illness– May require extra insulin during times of stress– ↑ blood glucose monitoring during this time –
even every 1-2 hrs– Diet modifications (solids to liquids for a period of
time)– Monitor urinary output and degree of ketonuria
Stress of Acute Illness and Surgery
– Increase fluid intake to prevent dehydration (minimum 4oz per hour for adult)
– Call MD when CBG > 250mg/dL• Surgery– Preplan adjustments in diabetic regimen– IV fluids and insulin before, during, and after
surgery when no oral intake– The type2 pt. who usually takes oral hypoglycemics
will be on insulin during the surgical period
MEDICATIONS
• INSULIN AND ORAL HYPOGLYCEMICS are the drugs of choice
• INSULIN– Needed for all patients with Type 1 AND Type 2
diabetes whose condition cannot be controlled by diet, exercise or hypoglycemic meds alone
MEDICATIONS
• INSULIN cont.– Today, only Biosynthetic insulin– A hormone– Given subcutaneously• IV administration when immediate action needed
– Differ in regard to:• Onset• Peak• Action• Duration
MEDICATION
• INSULIN cont.– By adding zinc, protamine, and acetate buffers to
insulin in various ways, the onset of activity, peak, and duration times can be manipulated availability of rapid-, short-, intermediate-, and long-acting insulins
– Different combinations/premixed may be used– REVIEW Table 11-5 ppgs. 515 and 516 (((check book for
accuracy of page numbers)))
MEDICATION
• A human insulin formula: Insulin Lispro– Begins to take effect in less than half the time of
regular, fast-acting insulin– May be administered 15 min before a meal• This timing mimics more closely the body’s own
hormone activity
MEDICATION
• When giving insulin:– Inject into the subcutaneous tissue (fat)• The Space between the skin and muscle layers
– Requires the appropriate syringe• U-100 = 100u insulin per ml.• The concentration on the insulin bottle should match
the syringe indication - a U-100 syringe should be used with an insulin that has printed on the label “U-100”• Other syringes available for those taking a smaller
dosage: U-25, U-30, U-50
MEDICATION
– Appropriate syringe cont.• NOTE: ONE IMPORTANT DISTINCTION
– The U-100 syringe is marked in 2-unit increments, whereas– The 30 and 50 unit syringes are marked in 1-unit
increments
• The Joint Commission recommends using “units” instead of the abbreviation “U” on med orders and med administration records (MAR)• Needles: very fine: 25-30g
– Other options:• Insulin Pens
MEDICATION
• Insulin Injection sites– Abdomen (except for 2 inches around the navel)– Upper arms– Anterior or lateral aspects of the thighs– Hips and buttocks
• Because of differing anatomical absorption rates of insulin, injections should be given in all the available sites in one area before moving to another site
MEDICATION
• External Infusion Pump– P. 519 Figure 11-17– A continuous, or basal rate of rapid- or short-
acting regular insulin with bolus doses available• Basal rate is designed to keep the blood glucose level
steady between meals and during sleep• Pump is programmed –at the touch of a button- to
deliver a larger quantity to cover CHO at meals
– Mimics the pancreas
MEDICATION
• Refrigeration of Insulin– An open bottle of insulin in current use DOES NOT
have to be refrigerated– Current thought: administer at room temp (not
straight from the fridge) to help prevent insulin lipodystrophy (loss of local fat deposits)
– Extra bottles: store in refrigerator
MEDICATION
• Best Practice: Nurses administering insulin injections MUST ALWAYS have another licensed person check and document the dose drawn up in the syringe to prevent med errors
• Be alert for s/sx hypoglycemia at the peak of action for whatever type of insulin is given– Educate the pt. and cgrs re: s/sx hypoglycemia and
appropriate tx.
MEDICATION
• Oral Hypoglycemics– Treat Type II DM• For pts. whose insulin production or utilization is
inadequate
– This is NOT oral insulin or a substitute for insulin
MEDICATIONhttp://www.webmd.com/diabetes/video/kahn-whats-future-treating-diabetes
– 5 types:• Sulfonylureas: stimulate the pancreas to release insulin
– E.g. Glypizides (Glucotrol), Glyburide (Micronase)
• Meglitinides : stimulates increased insulin release from the pancreas– E.g. repalinide (Prandin)
• Alpha-Glucosidase Inhibitors: inhibits delay of CHO absorption from the small intestine– E.g. Miglitol (Glycet)
MEDICATION
– Thiazolidinediones : increases insulin sensitivity at the insulin receptor sites on the cells• E.g Rosiglitazone (Avandia)
– Biguanide: reduces hepatic glucose production and lowers FBS levels; enhances tissue response to insulin• E.g. Metformin
Nursing Interventions
• Main focus: on the primary diagnosis without losing sight of the diabetes
• Daily routine:– Accurate monitoring of blood glucose levels– Dietary monitoring and considerations– Good skin care
Nursing Interventions
– Good foot care – neuropathy concerns• Routine podiatry care• Daily inspection• Physicians written order for toenail trimming by nurse• No hot water bottles or heating pads on feet• Properly fitting shoes – DON’T GO BAREFOOT!
– Emotional aspects – denial, depression• Provide support and active listening• http://www.webmd.com/diabetes/video/kahn-diabetes-
patients-must-check-feet
Nursing Interventions
• Sick Days– Consult the MD or primary provider– Do not withhold insulin on a Type I diabetic• Without insulin, the body must seek an alternative
source for energy fats and proteins are used– When these cells breakdown, ketones are formed– Accumulation of ketones results in ketosis or acidosis– If situation is not corrected DKA
PATIENT TEACHING
• Proper administration of insulin and oral hypoglycemics
• Side effects of the above meds• Method(s) of blood sugar testing • Method of urine testing• Dietary instruction• Skin and foot care
PATIENT TEACHING
• f/u yearly with dentist and opthamologist• Traveling • Med alert jewelry
• Assess pt. willingness and ability to take responsibility for self-care
NURSING ASSESSMENT
• HEALTH HISTORY– Description of general health– Changes in skin and turgor– Visual changes– Abdominal Symptoms– GU symptoms– Leg pain– Numbness/tingling/ burning in the extremities– Changes in mental alertness or s/sx seizure activity
NURSING ASSESSMENT
• HEALTH HISTORY cont.– Functional Assessment: Explore factors that can
affect patient’s ability to perform self-care, including literacy, financial resources, and family support.
NURSING ASSESSMENT
• PHYSICAL EXAM– LOC, posture and gait, and apparent well-being– Pt. record of blood sugar testing results– VS, height and weight– Skin: color, warmth, turgor, and lesions– Eye inspection for s/sx diabetic retinopathy or
cataracts– Presence of sweet, fruity odor to the breath– Feet
NURSING DIAGNOSIS
• Knowledge deficit• Ineffective Health Maintenance• Risk for deficient fluid volume• Risk for infection • Disturbed sensory perception• Impaired skin• Sexual Dysfunction• Imbalanced nutrition• Activity Intolerance• Sensory and Perceptual alteration: visual• Risk for situational low self-esteem
ACUTE COMPLICATIONS
ACUTE COMPLICATIONS
• COMA• 3 different causes:– During DKA• Inadequate insulin or inadequate insulin utilization
– Hyperglycemic hyperosmolar nonketotic Coma (HHNC)• Excess glucose, diuresis, and dehydration without
adequate fluid replacement
– During hypoglycemic reaction• Excess insulin; inadequate amt. of glucose present
ACUTE COMPLICATIONS
• Development of Infections– Hyperglycemia and ketonemia hinder the
phagocytic action of leukocytes– Poor wound healing– May be hospitalized
ACUTE COMPLICATIONS
• Diabetic Ketoacidosis (DKA)– Life-threatening– Caused by deficiency of insulin– Acidosis results with an accumulation of ketones
in the blood (fat metabolized for energy because carbs not available)
ACUTE COMPLICATIONS
• DKA cont.– Early signs/symptoms: anorexia, heachache,
fatigue; polydipsia, polyuria, polyphagia– If untreated dehydration, weakness, lethargy
with abdominal pain, n/v, fruity breath, increased respiratory and heart rates, blurred vision, hypothermia
ACUTE COMPLICATIONS
• DKA cont.– Late Signs: Air hunger (Kussmal Respirations),
coma, and shock– Death can result without prompt medical care
• Treatment– Aimed at correction of 3 main problems:• Dehydration• Electrolyte imbalance• Acidosis
ACUTE COMPLICATIONS
• Acute Hypoglycemia– Blood glucose level < 45-50mg/dL– 1. Glucose level falls rapidly epinephrine,
cortisol, glucagon and GH to be secreted in an attempt to ↑ glucose levels
– Symptoms: weakness, hunger, diaphoresis, tremors, anxiety, irritability, headache, pallor, and tachycardia
ACUTE COMPLICATIONS
• Acute Hypoglycemia cont.– 2. Blood sugar level that falls over several hours:– Due to lack of essential glucose to the brain tissue– Symptoms: confusion, weakness, dizziness,
blurred or double vision, seizure, and in some cases: coma
• Symptoms occur at different blood levels according to individual tolerances and how rapidly the level falls.
ACUTE COMPLICATIONS
• Functional Hypoglycemia– from a variety of causes:• Gastric surgery• Fasting• Malnutrition• Dumping syndrome
ACUTE COMPLICATIONS
• Exogenous hypoglycemia– d/t outside factors acting
on the body ↓ bld sugar
– Includes: insulin, oral hypoglycemic meds, alcohol, or exercise
• Endogenous hypoglycemia– d/t internal factors →an
excessive secretion of insulin or ↑in glucose metabolism
– May be r/t tumors or genetics
ACUTE COMPLICATIONS
• Acute Hypoglycemia cont.– Treatment: • 10 – 15 g of quick-acting CHO followed by complex CHO
and protein• Re-check Bld Sugar q 15 – 30 min until > 70mg/dL for
adults; 80-100mg/dL for older adults and children• If pt. is unable to swallow, an IM or SQ injection of 1mg
glucagon or and IV dose of 50ml of 50% D5W should be given as ordered or per protocol
CHRONIC COMPLICATIONS
CHRONIC COMPLICATIONS
• Related to “end organ disease” – results from damage to blood vessels– Blindness, cardiovascular problems, renal failure
• Diabetic Retinopathy– Progressive changes in microcirculation of the
retina hemorrhage, scar tissue, and retinal detachment
• Nephropathy– Capillary changes in the kidneys renal sclerosis
CHRONIC COMPLICATIONS
• Accelerated atherosclerotic changes MI, stroke, and gangrene in lower extremities amputations 2⁰ ischemia
• Pain and parasthesis– Pain: burning, cramping, itching, crushing– Loss of sensitivity and temperature
• Men: impotence d/t damage to the sacral parasympathetic nerves
• Orthostatic Hypotension• Bowel and/or Bladder dysfunction
Long-Term Complications: Prevention
• ADA recommends – Blood pressure: <130 systolic, <80 diastolic – Total cholesterol: <200 mg/dL – LDL: <100 mg/dL – HDL: >45 mg/dL for men (>55 mg/dL for women) – Triglyceride: <150 mg/dL– Daytime BG 80-120, Nightime 100-140
PROGNOSIS
• Early diagnosis and prompt accurate treatment promote longevity
• Life expectancy and quality of life are directly related to glycemic control
THE END!!!
Study Diligently! You are almost there!!!
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