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!!!

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