Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

124 Cards in this Set

  • Front
  • Back
Diabetic Ketoacidosis
Gestational Diabetes
Diabetes during pregnancy
Hyperosmolar hyperglycemic non-ketotic syndrome
Human leukocyte antigen
High blood glucose
Low blood glucose
Islet Cell Antibody
Ketones present in urine
Atrophy of SC tissue
Excessive thirst
Excessive hunger
Excessive urination
*Lesson objectives: recall list given during orientation
*Vocabulary: see handout
*Historical Perspectives: clinical trials, ADA, Joslin clinic, & recall from video
*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
*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
*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
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
*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
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
*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
*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
*Fluid volume depletion (hypovolemic)
*electrolyte imbalance
*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
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
*Risk for MI or stroke
*Destruction of the kidneys
*Destruction of nerve cells
*Slower wound healing and infections
*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)
1. Cardiovascular
2. Cerebrovascular
3. PVD
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
*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)
*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
-pt. will not experience diabetic nephropathy
-pt. will follow prescribed diet
*Most common complication of DM
*2 categories:
1. Sensory
2. Autonomic
*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
*Might start w/ NSAIDS
*Tricyclic antidepressants: Elavil
*Antiseizure meds: Neurontin
*Topical creams: Zostrix
*Control blood glucose (improve neuropathy)
*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
*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
*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
*EVALUATION: client will inspect feet daily
*Client will be free of ulcers
Managing diabetes in special situations
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
Nursing Diagnosis: Risk
*Risk for ineffective management of therapeutic regimen
*Risk for noncompliance
*Risk for ineffective coping
*Risk for injury
Nursing Diagnosis: PC
*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
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
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
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
*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)
*Somogyi (rebound hyperglycemia)
*BG are low and high (too much insulin)
*Dawn (Hyperglycemia)
*BG are high and high
Pharmacological Therapies: Oral antidiabetic agents
*Alpha glucoidase inhibitors
Medications that affect BS
*Tricyclic antidepressants
Medications that affect BS
*Birth Control
*Thiazide Diuretics
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
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
1. Outcomes
2. Interventions
Critical Knowledge Application
Handout on critical thinking
Current Trends and Research
*Several national organizations (inside Living Your Life)
*See article
*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