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124 Cards in this Set

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DKA
Diabetic Ketoacidosis
Gestational Diabetes
Diabetes during pregnancy
HHNKS
Hyperosmolar hyperglycemic non-ketotic syndrome
HLA
Human leukocyte antigen
Hyperglycemia
High blood glucose
Hypoglycemia
Low blood glucose
ICA
Islet Cell Antibody
Ketonuria
Ketones present in urine
Lipodystrophy
Atrophy of SC tissue
Polydipsia
Excessive thirst
Polyphagia
Excessive hunger
Polyuria
Excessive urination
Introduction
*Lesson objectives: recall list given during orientation
*Vocabulary: see handout
*Historical Perspectives: clinical trials, ADA, Joslin clinic, & recall from video
Commonalities
*All diabetics (Type I and Type II)have high blood sugar
*All are at risk for developing complications
*All have the same diagnostic studies to dx. DM
Health Promotion
*Diabetes Mellitus: Definition
*Chronic disorder of altered fat, carbohydrate and protein metabolism caused either by a relative or absolute lack of insulin or inability of tissues to respond to insulin
Statistics
*18 million have DM in the U.S.
*210,000 deaths occur annually
*increase risk of CAD
*More than 65% have HTN as well
*5th leading cause of death in U.S.
*1/3 do not know have it (PreDiabetes)
Pathophysiology of Diabetes
*Production of insulin is the main issue in DM
*Known as endogenous insulin (within your body)
*Decreased or no insulin leads to hyperglycemia
*Chronic hyperglycemia leads to many complications
Pathophysiology of Normal Insulin Metabolism
*Usually insulin is constantly released into the blood
*Release of insulin is regulated by blood glucose
*Insulin facilitates glucose transport into skeletal muscles, adipose tissue and body cells
Normal Insulin Production
*Cells have insulin receptors where insulin attaches and transports the glucose across the cell membrane and into the cell
*When glucose enters the cell, blood glucose is decreased
Patho. of Type I DM
*Autoimmune disease triggered by environmental factors (i.e. virus)
*>90% Type I have islet cell antibodies, an indication of autoimmune response
*Many also have HLA's: human leukocyte antigens (indicative of autoimmune response)
Patho. of Type I DM
*As islets are destroyed, ICA's and insulin antibodies increase, which lowers circulating insulin, which increases blood glucose
Pre-Diabetes
*Blood glucose is higher than normal but not high enough to be dx. w/ diabetes
*More common Type II and gestational DM
*Can prevent getting Type II
*OGTT will be done to dx. this
*At least 20.1 million have this in U.S.
Gestational Diabetes
*Occurs only during pregnancy
*Caused by hormonal changes
*Disappears after delivery
Patho of Type II DM
*No autoimmune disease: no ICA's, HLA's
*90% have Type II
*Usually older than 30 body (1/2 older than 55)
*Obesity is a major factor
Type II
*May require insulin in times of stress
*Onset of symptoms is usually slow
*Highest prevalence in Native Americans
*Low incidence of diabetic ketoacidosis
Type II Patho. R/T Age
*BS increases w/ age
*Decline in release of glucose regulating hormones: insulin, glucagon, epinephrine
*Body mass decreases with age
Treatment Procedures/Modalities (Type I)
*Health promotion & maintenance is crucial
*Goal is prevent development of complications
*Insulin
*Diet
*Exercise
Treatment (Type II)
*Goal is reduce risk of developing it:
*Recall pre-diabetes
*Reduce and maintain ideal weight
*Adhere to nutritional plan
*Increase physical activity
Health Promotion of all clients
*Early detection: test everyone over 45
*Test younger when risk factors present
*Educate clients about early S&S to watch for and ways to reduce risk factors (obesity)
Collaborative Care
*Nutritional Therapy
*Drug therapy
*Exercise
*Monitoring blood glucose
Risk factors: Type I
*Genetic: HLA and ICA common
*Environmental (virus)
*Ethnic: more common among whites
Risk factors: Type II
*Genetic but no HLA's or ICA's
*Major: obesity, aging, sedentary lifestyle
*Environmental
*Ethnic
*Gestational
Basic Care and Comfort
*Exercise: current regiment
*Nutrition: current diet
Pharmacological Therapies
*Current medication regimen
*1. Insulin
*2. Oral hypoglycemic agents
*Adverse effects
*Expected effects
Reduction of Risk Potential: Diagnostic Studies
*Complete H&P
*Fasting blood glucose >126mg/dl
*Sx & plasma glucose >200
*2 hour post-load >200 during OGTT
*Not one test to diagnose, look at whole picture
Diagnostic Studies/Lab Studies:
*Postprandial blood glucose
*Glycosylated hemoglobin (HgbA1X) last 120 days measurement of blood glucose
*Urinalysis
*Electrolytes, BUN, creatinine
System specific: clinical manifestations of Type I
*3 P's: polydypsia, polyphagia, polyuria
*Weight loss, ketonuria, weakness, fatigue, dizziness
*Blurred vision, pruritis, skin infection, vaginitis
Clinical manifest. of Type II
*Can be asymptomatic
*Recurrent blurred vision, pruritis, skin infection, vaginitis are common
*Cardinal sx: 3 P's, weakness, fatigue, dizziness
*NOT COMMON: weight loss, ketonuria
Part II
*Sequelae/Complications of DM
*Including Nursing Process
*Care of the diabetic patient in special situations
Acute Complications
*DKA: Diabetic Ketoacidosis
*HHNK: Hyperglycemic Hyperosmolar Nonketosis
*Hypoglycemia
DKA
*Caused by physical or emotional stress
*Often undiagnosed Type I diabetic
*Rare with type II
*Blood sugar high >300
Pathophysiology of DKA
*Cells are deprived of glucose because of lack of insulin
*Body responds by liver making glucose and breaking down protein and fat for energy (causes ketones to form)
*Ketones in blood cause acidosis in the body
*Rapid lowering of pH level causes DKA
Symptoms of DKA
*Anorexia, fatigue, headache, then 3 P's, blurred vision
*Increased HR & RR, fruity breath, flushed skin, abdominal pain, n/v
*Late Signs: lethargy, coma and Kussmaul's respirations (deep rapid breathing)--death
Treatment of DKA
*Correct:
*Hyperglycemia
*Fluid volume depletion (hypovolemic)
*Hyperosmolality
*Acidosis
*electrolyte imbalance
HHNKS
*Usually only Type II
*Caused by stress, acute illness, surgery
*Often symptoms missed, mortality rate high
*No acidosis with HHNKS
*Elderly and hospitalized patients at higher risk
HHNKS: pathophysiology
*Insulin not completely absent and fat breakdown does not occur (no ketones)
*Insulin needs are increased and body cannot compensate
*Major infection, kidney failure, shock can lead to HHNKS 600-1200 blood sugar
HHNKS: clinical manifestations
*Extremely high BS 600-1200mg/dL
*Neuro changes: confusion
*Often missed: 3 P's, dehydration, electrolyte loss, hypovolemia
Treatment of HHNKS
*IV regular insulin drip
*Fluid volume replacement based on age and cardiovascular Hx
*Electrolyte replacement
*Monitor mental status
*No n/v different from DKS
Hypoglycemia: Causes
*Action of insulin
*Decreased dietary intake
*Medications can decrease BS
*Onset of menses
*Change from and animal source to human insulin
*ETOH
Hypoglycemia: Pathophysiology
*Brain relies on glucose for energy and cannot use it from fats
*BS < 50-60mg/dL
*Severe if < 40mg/dL
Every patient is different
Symptoms of Hypoglycemia
*MILD: pallor, diaphoresis, tachycardia, palpitations, hunger, parestheisias, tremors, apprehension
*MODERATE: H/A, mood changes, inability to concentrate, confusion, slurred speech, blurred vision, impaired judgement, drowsiness, difficulty walking (appear to be drunk)
Symptoms of Hypoglycemia
*SEVERE: disorientation, seizures, unconscious, shallow respirations
*Symptoms can vary from client to client
Treatment for Hypoglycemia
*CONSCIOUS: simple carbohydrates
*UNCONSCIOUS: at home 1 mg of glucagon IM
*UNCONSCIOUS: hospital D50 IV push
Once they wake up give something to eat, drink and recheck BS
*15 grams carbohydrates, wait 15 minutes, recheck BS if not > 100 or they are still symptomatic give another 15 grams carbs. CALL MD
Symptoms of Hypoglycemia
MILD: pallor, diaphoresis, tachycardia, palpitations, hunger, paresthesias, tremors, apprehension
MODERATE: H/A, mood changes, inability to concentrate, confusion, slurred speech, blurred vision, impaired judgement, drowsiness, difficulty walking (appear to be drunk)
Symptoms of Hypoglycemia
SEVERE: disorientation, seizures, unconscious, shallow respirations
SYMPTOMS can vary from client to client
Treatment for Hypoglycemia
CONSCIOUS: simple carbohydrates (candy, juice, glucose tablets)
UNCONSCIOUS: at home 1 mg of glucagon IM
UNCONSCIOUS: hospital D50 IV push (once they wake up give something to eat, drink and recheck BS)
15 - 15 - 15 Rule
15g carbs, wait 15 minutes, recheck BS if not >100 or patient is still symptomatic give another 15grams card. CALL MD
Chronic/Long-Term Complications
*Major cause of morbidity & mortality in DM
*Common degenerative change that occur in the general population
*Much earlier in diabetics
Complications include
*Blindness
*Risk for MI or stroke
*Destruction of the kidneys
*Destruction of nerve cells
*Slower wound healing and infections
*Impotence
*Foot injuries/amputation
Classification of Complications
MACROANGIOPATHY: disease of the large and medium sized blood vessels (artherosclerosis)
MICROANGIOPATHY: disease of the small blood vessels (specific to diabetes)
Complications: MACROANGIOPATHY
MACROANGIOPATHY:
1. Cardiovascular
2. Cerebrovascular
3. PVD
Complications: MICROANGIOPATHY
MICROANGIOPATHY
1. Retinopathy
2. Nephropathy
3. Neuropathy
Retinopathy (Most common complication)
*Major cause of blindness in DM
*10 years = 50%, 15 years = 80%
*Microvascular damage & occlusion of retinal capillaries
2 classes of retinopathy
NONPROLIFERATIVE: most common, partial occlusion of sm. vessels causing microaneurysms, may not affect vision
PROLIFERATIVE: most severe, involves retina & vitreous, sees black or red spots, lines (w/out tx will become blind)
Nurse's Role
ASSESS: for blurred vision, Hx of cataract or glaucoma and what was done
*If no Hx, assess for changes in visual acuity
*Ophthalmologist consult (yearly)
*Educate patients regarding routine eye exams
Nurse's Role
DIAGNOSIS: Risk for injury r/t decreased vision secondary to diabetic retinopathy
PLAN: recognize the psychosocial impact of altered vision, address health promotion & maintainance issues
Nurse's Role
IMPLEMENTATION: normal blood glucose, eye exams, refer to agencies, teach visual S&S to watch for when they should notify MD
Nurse's Role: Evaluation
*pt. will describe S&S of diabetes related eye problems and what to do about them
*pt. will avoid activities that cause straining
*pt. will normalize blood glucose levels in an effort to clear blurred vision
*pt. will adapt to lifestyle with decreased vision
Nephropathy
*Most common cause of ESRD
*Test yearly for microalbuminuria (MAU)
*Proteinuria develops in 70% of pt.'s (indicative of kidney problems)
*Risk factors include HTN, genetic, smoking, and chronic hyperglycemia
*Controlling HTN affects renal status
*ACE inhibitors standard of care (Protective effect on kidneys, ex: Lisinopril)
Nephropathy
*Can progress to UREMIA=lower GFR (amount of blood that gets filtered) & high BUN & creatinine
*Protein restricted diet, dialysis, renal transplant
*Avoid nephrotoxic meds (ex: Gentamycin), caution IVP dyes, hydration is critical
Nurse's Role
*ASSESS for proteinuria, lab results, monitor diet, review medications
*DIAGNOSIS: Ridk for injury r/t renal damage secondary to DM
*PLAN: Maintain physiologic integrity, address health maintenance & promotion issues
Nurse's Role
*IMPLEMENTATION: educate, refer to PCP for HTN
*EVALUATION:
-pt. will not experience diabetic nephropathy
-pt. will follow prescribed diet
Neuropathy
*Most common complication of DM
*2 categories:
1. Sensory
2. Autonomic
Sensory
*Distal Symmetry Neuropathy: affect hands and/or feet bilaterally
*S&S: pain, parethesias (tingling, itching), loss of sensation (numbness)
*DM is responsible for 50% of lower limb amputations in U.S. *FOOT CARE IS KEY!
*PAIN = burning sensation worse at night
*5 C's of foot care in handout p. 10
Treatment
*Might start w/ NSAIDS
*Tricyclic antidepressants: Elavil
*Antiseizure meds: Neurontin
*Topical creams: Zostrix
*Control blood glucose (improve neuropathy)
Autonomic
*Orthostatic BP, resting tachycardia
*GI: gastroparesis (delayed gastric emptying causes abd. distention Treatment = Reglan
*Urinary retention
*Bowel incontinence
*Impotence, decreased libido
*Monilial & nonspecific vaginitis common
Nurse's Role
*ASSESS
*Clinical manifestations
*foot inspection
*blood glucose
*postural vital signs
Nursing Diagnosis
*Chronic pain r/t diabetic neuropathy
*Impaired skin integrity
*Knowledge deficit
*Sexual dysfunction
*Risk for Injury
Nurse's Role
*IMPLEMENTATION: teach patient to assess feet daily (5C's of foot care)
*maintain blood glucose levels, teach patient to get up slowly from sitting/lying positions
*medication teaching
*EVALUATE: client will have minimal Sx
*client will remain free of skin breakdown
PVD
*Common with diabetic clients
*complications: gangrene, infection & amputation
*Sx: claudication, absent pulses, pain at rest, cool, no hair, delayed capillary refill, dependent rubor (tan, red color)
Nurse's Role
*ASSESS: LE's for open areas, pulses, pain, skin color, temperature
*Dx: Altered peripheral perfusion
*Impaired skin integrity
*PLAN: Maintain physiological integrity
Nurse's Role
*IMPLEMENT: Teach FOOT CARE!
*EVALUATION: client will inspect feet daily
*Client will be free of ulcers
Managing diabetes in special situations
*Illness
*Surgery
*Travel
Care of the diabetic with an illness (Flu)
*Should continue to take insulin or Oral Agents (OA)
*Drink plenty of fluids
*Test urine for ketones & BS q 4 hours
*Call doctor if BS >250, fever, ketonuria, N/V
*High risk for developing DKA
*Stay away from caffeine - diuretic
*Replace carbs w/liquids Gatoraid, soups, jello
Care of the diabetic having surgery
*IV fluids
*hold insulin and OA's day of surgery
*may need to stop OA's 48 hours pre and post surgery Ex: Glucaphage
*Type II: usually receive insulin during hospitalization
*Monitor BS q 2 hours, u.o., ketones
*Increased risk of developing DKA
*Type I: 1/2 dose of insulin (long acting) Ex: 20 units NPH
Care of Diabetic client traveling
*Always wear medical bracelet
*Bring extra supplies (insulin etc.)
*Always carry snack (carry on)
*Stick with dietary regimen
*Keep watch on “home” time if w/in 1 to 2 hours
*Check with MD if big difference in time zones (Example: 6 hour difference)
Assessment: Safe, effective care environment
*Manage care
1. Case management
*Safety and infection control
Assessment: Psychosocial Integrity
1. Coping mechanisms
2. Religious + spiritual influences on health
3. Situational role changes
4. Support Systems
5. Stress management
Assessment: Promotion of wellness
1. Health and wellness
2. Aging process
3. Health screening
4. Lifestyle choices
Nursing Diagnosis: Actual
*Imbalanced nutrition: more than body requirements
*Powerlessness
Nursing Diagnosis: Risk
*Risk for ineffective management of therapeutic regimen
*Risk for noncompliance
*Risk for ineffective coping
*Risk for injury
Nursing Diagnosis: PC
*Ketoacidosis
*HHNKS
*Hypoglycemia
*Infection
*CAD
*PVD
*Retinopathy
*Neuropathy
*Nephropathy
Plan
*Maintain physiological integrity
*Provide a safe, effective care environment
*Recognize the psychosocial impact (get them involved in groups)
*Address health maintenance issues
*Establish outcomes
*
Implementation: Physiological Integrity
*BASIC CARE AND COMFORT
1. Foot care (recall)
*Nutrition and oral hydration: education
*Pharmacological therapies
Pharmacological Therapy
*2 Types of GLA's
1. Insulin: Intravenous or subcutaneous
2. Oral hypoglycemic agents
Types of Insulin
1. RAPID ACTING: Lispro, Aspart, Glulisine
2. SHORT ACTING: Regular SC, Exubera
3. INTERMEDIATE ACTING: NPH, Levemir
4. LONG ACTING: Glargine
5. COMBINATION THERAPY: 70/30, 50/50
**Regular insulin is only type of insulin that can be given IV**
Rapid Acting:
*Lispro (Humalog)
*Aspart (Novalog)
*Glulisine (Aprida)
*See handout
Short Acting: Regular
*Natural (unmodified)
*Clear solution
*Only type than can be given IV or IM
*Can also be given SC
*Used for sliding scale coverage
Intermediate: NPH, Levemir
*Onset delayed & duration longer
*NPH: allergic reaction possible due to protamine (rare)
*NPH: Cloudy in appearance
Long acting: Lantus
*Glargine (Lantus): does not have peak
*Given once a day usually at bedtime
*Not compatible with any other insulin
Administering Insulin
*Most common: SC
*IV *only regular insulin*
*Recommended injection sites (know these)
*Rotate sites within an area
*Abdomen is fastest absorption
Administering Insulin
*Standard syringe U-100 (US)
*Patients may use more than once (not a practice in the hospital) not more than 2-3 times
*Pen & Jet Injectors
*SC Insulin Pumps (portable and implanted)rapid or short acting only
*Inhalation http://www.exubera.com
Insulin Pump
An insulin pump administers insulin through a catheter in the abdominal fat to help control a person's blood sugar levels
Mixing Insulins
*Mix in one syringe *one injection*
*“Clear to cloudy”
Mixing Insulins
*Benefits client, only one shot
*NPH: can be mixed with regular, lispro, aspart & glulisine
*Call pharmacy for any recent updates (don't assume)
*Many premixed combinations available (see Lehne)
Storing Insulin
*Unopened bottles s/be kept in refrigerator
*Okay at room temperature for 1 month
*Mixed syringes need to be in fridge, good for 1 week, keep vertical
*Check expiration date on bottle
Complications of Insulin Therapy
*Allergic reactions
*Hypoglycemia
*Lipodystrophy
*Somogyi
*Dawn phenomenon
Somogyi (rebound hyperglycemia)
*Called “Rebound Hyperglycemia”
*More common with Type I (IDDM)
*HYPOGLYCEMIA while asleep, then body reacts by releasing glucose from muscle, liver & fat causing rebound HYPERGLYCEMIA
*CAUSE is too much insulin
*Symptoms: H/A, restless sleep, night sweats, nightmares, N/V
*Check BS between 2-3 AM
Somogyi (rebound hyperglycemia)
*Need to check BS between 2-3 am, then recheck when wake up (7-8am)
*If low at 2-3am and high when wake up then Somogyi has occurred
*Tx: decrease P.M. insulin and/or eat more carbs & fat with dinner or bedtime snack to prevent low BS while asleep
Dawn Phenomenon (Acute Complication)
Wake up w/ very high BS
*Cause counter-regulatory hormones are released in all people while sleeping which causes BS to rise
*Check BS at 2-3am. If HIGH at this time then HIGH at 7-8am then Dawn P. has occurred
*Tx: delay intermediate insulin until 10P.M. or increase dose of pills, limit carbs at night and eat bedtime snack of fat & protein, exercise in the P.M. (exercise before bed)
Summary
*Somogyi (rebound hyperglycemia)
*BG are low and high (too much insulin)
*Dawn (Hyperglycemia)
*BG are high and high
Pharmacological Therapies: Oral antidiabetic agents
*Sulfonyureas
*Meglitinides
*Biguanides
*Alpha glucoidase inhibitors
*Thiazokidinediones
KNOW ACTIONS
Medications that affect BS
DECREASE
*ETOH
*MAO's
*Tricyclic antidepressants
*Tylenol
*Allopurinol
Medications that affect BS
INCREASE
*Birth Control
*Corticosteroids
*Morphine
*Lasix
*Thiazide Diuretics
*Dilantin
Reduction of Risk Potential: Exercise
*Weight loss
*Decreases cholesterol
*Improves circulation
*Timing of exercise is important for all diabetics
-Snack before exercise good idea to take BS prior to exercising
Reduction of Risk Potential: Monitoring blood glucose
*Capillary sample
*Self or by nurse/nursing assistant
*Patient teaching
*Easy way to frequently monitor BS
*Now have monitors for the visually impaired
Physiological Adaptation
*Illness management
*Medical emergencies (recall)
1. Hypoglycemic reaction
2. DKA
3. HHNKS
Implementation: safe, effective care environment
*Management of care
1. Collaboration with the multidisciplinary team (includes family)
2. Case management (discharge planning)
3. Referrals
*Safety and infection control
1. Injury prevention
2. Home safety
Implementation: Psychosocial
*Coping mechanisms
*Religious + spiritual influences on health
*Situational Role Changes
*Support systems
*Stress management
Implementation: Promotion of wellness
1. Educate: disease prevention, early detection
2. Health screening
3. Self care: foot care
Evaluation
1. Outcomes
2. Interventions
Critical Knowledge Application
Handout on critical thinking
Current Trends and Research
*Several national organizations (inside Living Your Life)
*www.joslin.harvard.edu
*www.diabetes.org
*See article
Summary
*Nurse plays a major role in the Health promotion, maintenance and restoration of DM
*Assessing, Dx, planning, implementing(collaborative & independent) & evaluation
*Early prevention, education and treatment are the key components of DM