Prapared by maria carmela l. domocmat, rn, msn

MANAGEMENT OF DIABETES
Medical Management of DM

 No cure
 Goal: Euglycemia and prevention of
  complications
 Individualized treatment plans
      Appropriate goal setting
      Diet
      Exercise
      Self-monitoring of blood glucose (SMBG)
      Regular monitoring for complications
      Laboratory assessment
      Oral meds/insulin
Surgical management of DM

 pancreas transplant
   not usually done
 Islet cell transplants
Dietary management
Dietary management of DM
Foundation of Diabetic control
 Goals
   Maintain near-normal blood glucose levels
   Achieve optimal serum lipid levels
   Provide adequate calories for reasonable weight
   Prevent & treat acute complications of insulin-
    treated diabetes
   Improve overall health through optimal nutrition
Diet Composition
 Carbohydrates: 60 – 70% of daily diet
 Protein: 15 – 20% of daily diet
 Fats: No more than 10% of total calories from
  saturated fats
 Fiber: 20 to 35 grams/day; promotes intestinal
  motility and gives feeling of fullness
 Sodium: recommended intake 1000 mg per 1000
  kcal
 Sweeteners approved by FDA instead of refined
  sugars
 Limited use of alcohol: potential hypoglycemic
  effect of insulin and oral hypoglycemics
The exchange system

 Six categories
   Bread/starch
   Meat
   Milk
   Vegetable
   Fruit
   Fat
General guidelines of Dietary
Management
 Protein
   20%
 Fat
   20%
 Carbohydrates
   60%
 ADA: American
  Diabetic Association
Diabetic Meal Plan

 Small frequent meals
   CONSISTENCY!
       Amount of calories
       Amount of carbohydrates
       Time
       Snacks
Diabetic Meal Plan

 If the pt is obese, the key to treatment is…
   Weight los!
Sweeteners

 Nutritive sweeteners
   Not calorie free
   Cause less h in BS (than
    regular sugar)
   Sorbitol  laxative effect
 Non-nutritive sweeteners
   Minimal or no calories
   Do not h BS
Meal Plan considerations

 Food preferences
 Lifestyle
 Schedule
 Ethnic / Cultural
  background
Alcohol and Diabetes

 Increase risk of…
   Hypoglycemia
   Affects the liver
   Don’t take on empty
    stomach
   Esp. if on insulin or
    oral hypoglycemic
    meds
   Moderation
Exercise
Exercise and Diabetes

 i blood glucose levels
   h the uptake of glucose by body muscle
   Potentiates action of insulin
     i insulin requirement
   Effect lasts 24 hours
More Benefits of exercise

 Increases circulation
 Improve serum lipid
  levels
 Improves cardiovascular
  status
 Assist with wt control
 Decreases stress
Rules for the exercising
diabetic
 Talk to MD first
 Regular vs. sporadic
 Correlate exercise and glucose levels
 Don’t exercise when hypoglycemic
 Don’t exercise when hyperglycemic >250
Rules for the exercising
diabetic
 Do not exercise when insulin is peaking
 Carry a quick source of sugar
 Best time = 60-90 minutes after a meal
Rules for the exercising
diabetic
 Proper footwear
 May need a pre-exercise snack
 Consistency!
Self monitoring of blood glucose
(SMBG)
Monitoring Glucose

 SMBG
 Glucometers
 Urine testing for glucose
   2-4 times a day

 Continuous glucose monitoring system
Monitoring Ketone levels

 Dipstick method
 Perform when:
   Glucosuria
   Unexplained elevated glucose level
   Illness
   Pregnancy
Foot care
Regular monitoring for complications
Foot care
Foot Care

 Inspect feet daily
 Wash feet with warm water and mild soap
 Pat dry – do not rub
 Wash daily: wash feet in warm water every
  day, using a mild soap.
   Dry between toes
   Lubricate dry feet
 Inspect
   Mirror
   Family
   Between toes
 Do not soak feet.
 Dry feet well,
  especially between
  the toes.
 If the skin on feet is
  dry, keep it moist by
  applying lotion after
  washing and drying.
 Apply lotion on feet
  (not interdigital areas)
Foot care
  Check toenails once a
   week.
  Trim toenails with a nail
   clipper straight across.
  Do not round off the
   corners of toenails or cut
   down on the sides of the
   nails.
  After clipping, smooth
   the nails with an emery
   board.
Foot care

 Always wear socks or stockings with soft
  elastic, and that fit feet.
 Wear socks at night if feet get cold.
 Always wear closed-toed shoes or slippers.
 Do not wear sandals and do not walk
  barefoot, even around the house.
Foot care

 Wear comfortable properly fitted shoes
 Buy shoes made of canvas or leather and
  break them in slowly.
 Extra wide shoes are also available in
  specialty stores that will allow for more room
  for the foot for people with foot deformities.
 Break in new pair of shoes for 1 -2 hours only
  until it becomes comfortable
Foot care

 Maintain the blood flowing to feet
 Elevate feet up when sitting
 Do not wear knee high/ stay up stockings
Foot care

 wiggle toes and move ankles several times a
  day
 don't cross legs for long periods of time
 Avoid activities that icirculation
   Smoking
   Crossing legs
   Tight socks
 Good shoes             Prevent injuries
   Comfortable            Wear socks
   Closed toe               Cotton
   No bare feet             Light color
   New shoes                No wrinkles
     Break in slowly
                           Check inside of
                            shoe
 No temperature        See doctor
  extremes               regularly
   Check bath water      Podiatrist
   No water bottles      Trim straight across
   No heating pads       Do not cut calluses
                           or corns
                        Range of Motion
Foot care

 see podiatrist q2 to 3 months for check-ups,
    even if don't have any foot problems.
   include inspection of skin
   check for redness or warmth of the skin.
   check for pulses and temperature of feet
   Monofilament assessment of foot sensation
When to contact Dr?

   Changes in skin color
   Changes in skin temperature
   Swelling in the foot or ankle
   Pain in the legs
   Open sores on the feet that are slow to heal or
    are draining
   Ingrown toenails or toenails infected with fungus
   Corns or calluses
   Dry cracks in the skin, especially around the heel
   Unusal and/or persistent foot odor
Risk for infection

 Frequent hand washing
 Early recognition of signs of infection and
  seeking treatment
 Meticulous skin care
 Regular dental examinations and consistent oral
  hygiene care
Sexual dysfunction

 Effects of high blood sugar on sexual
  functioning,
 Resources for treatment of impotence, sexual
  dysfunction
MANAGEMENT DM:
PHARMACOLOGIC MGMT
Oral Hypoglycemic Agents

 Oral hypoglycemic meds are NOT Insulin
 Oral hypoglycemic meds require some
  production of insulin
 Oral hypoglycemic agents are used in the
  treatment of type 2DM
 Oral hypoglycemic meds are meant to
  supplement diet and exercise, NOT replace them
Oral Hypoglycemic Agents

 Oral hypoglycemic meds cannot be used
  during pregnancy
 Oral hypoglycemic meds may need to be
  halted temporarily and insulin prescribed if
  BS levels rise due to infection, trauma, stress,
  surgery etc.
 Action vary so effect may be enhanced by use
  of multiple meds
Oral Medication

   Biguanides
   Sulfonylureas
   Meglitinide derivatives
   Alpha-glucosidase inhibitors
   Thiazolidinediones (TZDs)
   Glucagonlike peptide–1 (GLP-1) agonists
   Dipeptidyl peptidase IV (DPP-4) inhibitors
   Insulins
   Amylinomimetics
   Bile acid sequestrants
   Dopamine agonists
Biguanides

 Metformin (Glucophage)
 first choice for oral type 2 diabetes
  treatment.
 Action: decreases overproduction of
  glucose by liver and makes insulin more
  effective in peripheral tissues
Biguanides

 Major side effects : anorexia/ wt. Loss
 CI in patients with Renal impairment
 D/C temp of (+) illness that leads to
  dehydration or hypoperfusion --lactic
  acidosis.
Sulfonylureas

 Glyburide (Micronase, DiaBeta, Glynase)
 Glipizide (Glucotrol, Glucotrol XL)
 Glimepiride (Amaryl)
 Cholpropamide (Diabanese)
Sulfonylureas

 Action: Stimulates pancreatic cells to
  secrete more insulin and increases
  sensitivity of peripheral tissues to insulin
 (insulin secretagogues)
 indicated for use as adjuncts to diet and
  exercise in adult patients with type 2 DM
 Used: to treat non-obese Type 2 diabetics
Sulfonylureas

 taken with food
   except Glucotrol/Glipizide : taken 30 mins before
    meals
Sulfonylureas

 (esp. Diabinese) when      Side-effects
  taken with alcohol can      Hypoglycemia
  cause severe
  Disulfiram reactions        GI upset
 Disulfiram (antibus): a
  compound when used
  with alcohol produces
  distressing symptoms
 Symptoms: Flushed
  skin, N/V, palpitations,
  hyperventilation
Meglitinides

 Repaglinide (Prandin)
 Nateglinide (Starlix)
 Action: stimulates pancreatic cells to
  secret more insulin
 much shorter-acting insulin secretagogues
  than the sulfonylureas
 may be used in patients who have allergy to
  sulfonylurea medications.
Alpha-glucosidase inhibitors

 Acarbose (Precose)
 Miglitol (Glyset)
 Action: Slow carbohydrate digestion and
  delay glucose absorption
 S/E : diarrhea & flatulence
 Take immediately before meals
Thiazolidinediones (TZDs)

 Pioglitazone [Actos]
 Rosiglitazone [Avandia]
 Used for patients with type 2 DM who take
  insulin injections
   Acts by increasing insulin action at the receptor site
   reduce insulin resistance
   act as insulin sensitizers; thus, they require the
    presence of insulin to work.
 must be taken for 12-16 weeks to achieve
  maximal effect.
Thiazolidinediones (TZDs)

 Affects liver function  liver function tests
 Indications of altered liver function
   Yellow skin tone
   Nausea
   Abdominal pain
   Dark urine
Drug Interactions

Directly interact with   Sulfonamides
Sulfonylurea and         NSAIDS
increase risk of
hypoglycemia

Sulfonylurea+ * Med =
Hypoglycemia
Drug Interactions

h blood glucose levels   Potassium-losing diuretics
Regardless of what       Corticosteriods

med you might also be    Estrogen compounds
taking                   Phenytoin (Dilantin)

                         Salicylates (ASA)
Drug interactions

Meds that cause   Acetaminophen
Hypoglycemia      Alcohol

                  Monoamine oxidase
Without drug      inhibitors / MAO inhibitors
interaction
Drug interactions

Meds that can    Propranolol (Inderal)
                 
MASK signs and
symptoms of
Hypoglycemia
Oral Hypoglycemic Agents
 Client must also maintain prescribed diet and
  exercise program; monitor blood glucose levels
 Not used with pregnant or lactating women
 Specific drug interactions may affect the blood
  glucose levels
Insulin
 Instituted in 1923
   Beef
   Pork
 1979 – human insulin
 Can not be taken by mouth (digested)
Onset – Peak - Duration

 Onset
   The time period from injection to when it begins to
    take effect
 Peak
   When insulin is working its hardest and therefore
    blood glucose levels are at their lowest
 Duration
   Length of time the insulin works or lasts
Types

 Rapid-acting insulins or Ultra short-acting
 Short-Acting Insulins
 Intermediate-Acting Insulins
 Long-Acting Insulins
Rapid-acting insulins/
or Ultra short-acting
 have a short duration of action
 appropriate for use before meals or when
  blood glucose levels exceed target levels and
  correction doses are needed.
 These agents are associated with less
  hypoglycemia than regular insulin.
Rapid-Acting Insulins/
or Ultra short-acting
 Insulin aspart (NovoLog)
 Insulin glulisine (Apidra)
 Insulin lispro (Humalog)
Rapid-Acting Insulins

  Insulin aspart (NovoLog)
  Insulin glulisine (Apidra)
  Insulin lispro (Humalog)

Appearance      Onset           Peak       Duration

  Clear      5-15 minutes   30-90 (1hr)   3-5 hours
              (10 min)                     (4 hrs)

  Insulin pumps
  Rapid reduction of glucose level
Short-Acting Insulins

 Regular insulin (Humulin R, Novolin R)
 Preparations:
   mixture of 70% neutral protamine Hagedorn
    (NPH) and 30% regular human insulin
   (ie, Novolin 70/30, Humulin 70/30)
Short-Acting Insulins

 Humalog R; Novolin R; Iletin II Regular
Appearance       Onset       Peak     Duration
     Clear      ½ - 1 hr    2-4 hrs    4-6 hrs
                (1 hour)   (3 hour)   (5 hours)

   Administered 20-30 minutes before meals
   IV
   Usually given 4 x a day
   May to taken alone or in combination
Intermediate-Acting Insulins

 Insulin NPH (Humulin N,     onset of action: 3-4
  Novolin N)                     hours.
 have a slow onset of          Peak: 8-14 hours
  action and a longer           duration of action : 16-24
  duration of action.            hrs
 commonly combined             appears cloudy
  with faster-acting
  insulins to maximize the      must be gently mixed
  benefits of a single           and checked for
  injection                      clumping
                                if clumping occurs, the
                                 insulin should be
                                 discarded.
Intermediate-Acting Insulins

 Insulin NPH (Humulin N, Novolin N)
Appearance        Onset      Peak      Duration
  Cloudy          2-4 hrs   6-12 hrs   16-20 hrs
                  (2 hrs)   (12 hrs)    (24 hrs)



 Administer after meals
 Usually given 2x a day
 Eat at onset!
Long-Acting Insulins

 provide a longer            Insulin detemir
  duration of action, and,     (Levemir)
  when combined with          Insulin Glargine
  rapid- or short-acting       (Lantus)
  insulins, they provide
  better glucose control
Types of Insulin –
Long-acting
 Ultra Lente (UL)

 Appearance      Onset       Peak      Duration
   Cloudy       4-8hour    10-30 hrs   36+ hours
                 (6 hrs)    (24 hrs)    (36 hrs)


 To control fasting glucose levels
 Cannot be mixed!
Long-Acting Insulins

 Insulin detemir               Insulin glargine
   for once- or twice-daily      onset of action: 4-8
    dosing                         hours
   duration of action is up      Duration: 24 hours.
    to 24 hours                   Peak effects; 16-18 hrs
                                  FDA has advised of a
                                   possible association of
                                   insulin glargine with an
                                   increased risk of cancer
Rapid-Acting Insulins
Appearance      Onset          Peak         Duration

  Clear      5-15 minutes      30-90       3-5 hours
              (10 min)         (1hr)        (4 hrs)

 Short-Acting Insulins
   Appearance        Onset        Peak     Duration
     Clear          ½ - 1 hr     2-4 hrs    4-6 hrs
                    (1 hour)    (3 hour)   (5 hours)
Learning Tip: Even and Odd

 Short-acting think
  odd
   (1-3-5)
 Intermediate-acting
  think even
   (2-12-24)
Intermediate-Acting Insulins
Appearance   Onset        Peak       Duration
  Cloudy     2-4 hrs     6-12 hrs    16-20 hrs
             (2 hrs)     (12 hrs)     (24 hrs)

Long-acting insulin
Appearance   Onset        Peak      Duration
  Cloudy     4-8hour    10-30 hrs   36+ hours
              (6 hrs)    (24 hrs)    (36 hrs)
When should insulin be
administered
 Short-acting / regular
   30 minutes before meals
   Do not allow more than 30 minutes to pass by without
    eating
      hypoglycemia
 Intermediate acting
   After meals
 If mixed (regular & intermediate)
   30 minutes before meals
What route is insulin
administered
 Sub-cutaneous
 IV
   Regular
 Pump
Insulin Type   Onset       Peak        Duration

Ultra Short    15 mins   30-90 mins    2- 4 hrs

   Short       30 mins    2- 4 hrs      6-8 hrs

Intermediate   1-2 hrs    6-12 hrs    18-24 hrs

   Long        4-6 hrs   16-24 hrs    18-36 hrs

Combination  30-60        2- 4 hrs,   6-8hrs,then
70/30       mins then    then 6-12     18-24 hrs
               1-2 hrs       hrs
Insulin Type   Onset     Peak   Duration


  Insulin       30-60    None   24 hours
 glargine      minutes
Diabetes Mellitus
 Mixing insulin
Adverse effects of insulin
Adverse effects of insulin

    Local allergic reactions
    Insulin lipodystrophy
    Insulin resistance
    Dawn Phenomenon
    Somogyi phenomenon
    Insulin waning
Insulin lipodystrophy

 or lipoatrophy
 is primary idiopathic atrophy of adipose
  tissue
 can be a lump or small dent in the skin that
  forms when a person keeps performing
  injections in the same spot.
Insulin lipodystrophy   lipohypertrophy
Rotate site of injection
Nursing Responsibilities

 Route : Subcutaneous
 Steady absorption
 Less painful
 IV – in emergency cases ( DKA)
 Only regular insulin is given through the IV
  route
 Do not massage the site
 Fastest absorption site is the abdomen, then
  deltoids, thighs then buttocks
Nursing Responsibilities

 Administer at room temperature
   Cold insulin causes lipodystrophy
 Rotate site of injection
   To prevent lipodystrophy. Inhibits insulin
    absorption
 Store vial of insulin in current use at room
  temperature
   Other vials should be refrigerated
Nursing Responsibilities

 Gently roll vial in between the palms to
  redistribute insulin particles
   Do not shake. Bubbles make it difficult to
    redistribute insulin particles
Nursing Responsibilities

 Observe for side effects
   Localized
     Induration or redness
     Swelling
     Lesions at the site
     Lipodystrophy
   Edema
     Sudden resolution of hyperglycemia causes
      retention of water
   Hypoglycemia
Somogyi Effect

 Rebound hyperglycemia
 Normal or blood glucose levels are present
  at bedtime
 hypoglycemia : occurs at 2-3am
   This causes an increase in the production of
    counterregulatory hormones
 Hyperglycemia: by 7 am
   Resuts in response to the counterregulatory
    hormones
Somogyi Effect

 Treatment
   decreasing evening (predinner or bedtime) dose of
    intermediate acting insulin
   or increasing the bedtime snack
Dawn Phenomenon

 (6 AM – 8 AM) early AM increase in blood
  glucose levels associated with release of
  growth hormone at 12 MN to 3 AM
Dawn Phenomenon:TREATMENT

 Type 1 diabetes
   Intensify insulin therapy
   Avoid late night snacking, unless appropriate quick-
    acting insulin is given.
 Type 2 diabetes
   Adjust diet content (decrease carbohydrates) and
    timing of the evening meal so that the glucose level at
    bedtime is 70-110 mg/dl
   If dietary modification is not enough, consider an
    intermediate or long-acting sulfonylurea at evening
    meal.
   Basal insulin is indicated if the dawn phenomenon
    continues.
Insulin Waning

 Progressive rise in the blood glucose levels
  from bedtime to morning
 Treatment:
   Increase dose of evening intermediate acting or
    long acting insulin
Difference between dawn phen
  and insulin waning

                  10 PM     2 AM      4 AM     8 AM
  Dawn
                  100       110       135      250
  Phenomenon
  Waning of
                  100       160       220      270
  insulin
Dawn phenomenon shows an abrupt increase between
4 a.m. and 8 a.m., whereas waning of exogenous
insulin effect shows gradual rise between 2 a.m. and 8
a.m.
Other meds
Glucagonlike peptide–1 (GLP-1 )
agonists
 Exenatide injectable solution (Byetta)
 Exenatide injectable suspension (Bydureon)
 mimic the endogenous incretin GLP-1
 it enhances glucose-dependent insulin
  secretion by pancreatic beta cells, suppresses
  inappropriately elevated glucagon secretion,
  and slows gastric emptying.
Glucagonlike peptide–1 (GLP-1 )
agonists
 Liraglutide (Victoza)
   a once-daily injectable
   stimulates G-protein in pancreatic beta cells.
Dipeptidyl peptidase IV (DPP-4)
inhibitors
 prolong action of
  incretin hormones
 Sitagliptin (Januvia)
 Saxagliptin (Onglyza)
 Linagliptin (Tradjenta)
Amylinomimetics

 Pramlintide acetate
  (Symlin)
 amylin analog that
  mimics the effects of
  endogenous amylin,
  which is secreted by
  pancreatic beta cells.
 delays gastric emptying,
  decreases postprandial
  glucagon release, and
  modulates appetite.
Bile acid sequestrants

 bile acid sequestrant
  colesevelam
 lipid-lowering agents
  for the treatment of
  hypercholesterolemia
  but were subsequently
  found to have a
  glucose-lowering
  effect.
Antiparkinson Agents, Dopamine
Agonists
 Bromocriptine (Cycloset)        indicated as an adjunct to
 Quick-release                    diet and exercise to
  bromocriptine acts on            improve glycemic control.
  circadian neuronal
  activities within the
  hypothalamus to reset the
  abnormally elevated
  hypothalamic drive for
  increased plasma glucose,
  triglyceride, and free fatty
  acid levels in fasting and
  postprandial states in
  patients with insulin
  resistance.
Non-Insulin Injectables

 New drugs are available for people with type
  2 diabetes.
 Pramlintide (Symlin), exenatide (Byetta), and
  liraglutide (Victoza) are non-insulin injectable
  drugs.
 insulin pulls glucose into the cells
 these medications cause the body to release
  insulin to control blood sugar levels.
Other meds
Glucagonlike peptide–1 (GLP-1 )
agonists
 Exenatide injectable solution (Byetta)
 Exenatide injectable suspension (Bydureon)
 mimic the endogenous incretin GLP-1
 it enhances glucose-dependent insulin
  secretion by pancreatic beta cells, suppresses
  inappropriately elevated glucagon secretion,
  and slows gastric emptying.
Glucagonlike peptide–1 (GLP-1 )
agonists
 Liraglutide (Victoza)
   a once-daily injectable
   stimulates G-protein in pancreatic beta cells.
Dipeptidyl peptidase IV (DPP-4)
inhibitors
 prolong action of
  incretin hormones
 Sitagliptin (Januvia)
 Saxagliptin (Onglyza)
 Linagliptin (Tradjenta)
Amylinomimetics

 Pramlintide acetate
  (Symlin)
 amylin analog that
  mimics the effects of
  endogenous amylin,
  which is secreted by
  pancreatic beta cells.
 delays gastric emptying,
  decreases postprandial
  glucagon release, and
  modulates appetite.
Bile acid sequestrants

 bile acid sequestrant
  colesevelam
 lipid-lowering agents
  for the treatment of
  hypercholesterolemia
  but were subsequently
  found to have a
  glucose-lowering
  effect.
Antiparkinson Agents, Dopamine
Agonists
 Bromocriptine (Cycloset)        indicated as an adjunct to
 Quick-release                    diet and exercise to
  bromocriptine acts on            improve glycemic control.
  circadian neuronal
  activities within the
  hypothalamus to reset the
  abnormally elevated
  hypothalamic drive for
  increased plasma glucose,
  triglyceride, and free fatty
  acid levels in fasting and
  postprandial states in
  patients with insulin
  resistance.

Management of Diabetes Mellitus

  • 1.
    Prapared by mariacarmela l. domocmat, rn, msn MANAGEMENT OF DIABETES
  • 2.
    Medical Management ofDM  No cure  Goal: Euglycemia and prevention of complications  Individualized treatment plans  Appropriate goal setting  Diet  Exercise  Self-monitoring of blood glucose (SMBG)  Regular monitoring for complications  Laboratory assessment  Oral meds/insulin
  • 3.
    Surgical management ofDM  pancreas transplant  not usually done  Islet cell transplants
  • 4.
  • 5.
    Dietary management ofDM Foundation of Diabetic control  Goals  Maintain near-normal blood glucose levels  Achieve optimal serum lipid levels  Provide adequate calories for reasonable weight  Prevent & treat acute complications of insulin- treated diabetes  Improve overall health through optimal nutrition
  • 8.
    Diet Composition  Carbohydrates:60 – 70% of daily diet  Protein: 15 – 20% of daily diet  Fats: No more than 10% of total calories from saturated fats  Fiber: 20 to 35 grams/day; promotes intestinal motility and gives feeling of fullness  Sodium: recommended intake 1000 mg per 1000 kcal  Sweeteners approved by FDA instead of refined sugars  Limited use of alcohol: potential hypoglycemic effect of insulin and oral hypoglycemics
  • 9.
    The exchange system Six categories  Bread/starch  Meat  Milk  Vegetable  Fruit  Fat
  • 10.
    General guidelines ofDietary Management  Protein  20%  Fat  20%  Carbohydrates  60%  ADA: American Diabetic Association
  • 11.
    Diabetic Meal Plan Small frequent meals  CONSISTENCY!  Amount of calories  Amount of carbohydrates  Time  Snacks
  • 12.
    Diabetic Meal Plan If the pt is obese, the key to treatment is…  Weight los!
  • 13.
    Sweeteners  Nutritive sweeteners  Not calorie free  Cause less h in BS (than regular sugar)  Sorbitol  laxative effect  Non-nutritive sweeteners  Minimal or no calories  Do not h BS
  • 14.
    Meal Plan considerations Food preferences  Lifestyle  Schedule  Ethnic / Cultural background
  • 15.
    Alcohol and Diabetes Increase risk of…  Hypoglycemia  Affects the liver  Don’t take on empty stomach  Esp. if on insulin or oral hypoglycemic meds  Moderation
  • 16.
  • 17.
    Exercise and Diabetes i blood glucose levels  h the uptake of glucose by body muscle  Potentiates action of insulin  i insulin requirement  Effect lasts 24 hours
  • 19.
    More Benefits ofexercise  Increases circulation  Improve serum lipid levels  Improves cardiovascular status  Assist with wt control  Decreases stress
  • 20.
    Rules for theexercising diabetic  Talk to MD first  Regular vs. sporadic  Correlate exercise and glucose levels  Don’t exercise when hypoglycemic  Don’t exercise when hyperglycemic >250
  • 21.
    Rules for theexercising diabetic  Do not exercise when insulin is peaking  Carry a quick source of sugar  Best time = 60-90 minutes after a meal
  • 22.
    Rules for theexercising diabetic  Proper footwear  May need a pre-exercise snack  Consistency!
  • 23.
    Self monitoring ofblood glucose (SMBG)
  • 25.
    Monitoring Glucose  SMBG Glucometers  Urine testing for glucose  2-4 times a day  Continuous glucose monitoring system
  • 26.
    Monitoring Ketone levels Dipstick method  Perform when:  Glucosuria  Unexplained elevated glucose level  Illness  Pregnancy
  • 27.
  • 28.
  • 29.
    Foot Care  Inspectfeet daily  Wash feet with warm water and mild soap  Pat dry – do not rub
  • 30.
     Wash daily:wash feet in warm water every day, using a mild soap.  Dry between toes  Lubricate dry feet  Inspect  Mirror  Family  Between toes
  • 31.
     Do notsoak feet.  Dry feet well, especially between the toes.  If the skin on feet is dry, keep it moist by applying lotion after washing and drying.  Apply lotion on feet (not interdigital areas)
  • 32.
    Foot care Check toenails once a week.  Trim toenails with a nail clipper straight across.  Do not round off the corners of toenails or cut down on the sides of the nails.  After clipping, smooth the nails with an emery board.
  • 33.
    Foot care  Alwayswear socks or stockings with soft elastic, and that fit feet.  Wear socks at night if feet get cold.  Always wear closed-toed shoes or slippers.  Do not wear sandals and do not walk barefoot, even around the house.
  • 34.
    Foot care  Wearcomfortable properly fitted shoes  Buy shoes made of canvas or leather and break them in slowly.  Extra wide shoes are also available in specialty stores that will allow for more room for the foot for people with foot deformities.  Break in new pair of shoes for 1 -2 hours only until it becomes comfortable
  • 35.
    Foot care  Maintainthe blood flowing to feet  Elevate feet up when sitting  Do not wear knee high/ stay up stockings
  • 36.
    Foot care  wiggletoes and move ankles several times a day  don't cross legs for long periods of time  Avoid activities that icirculation  Smoking  Crossing legs  Tight socks
  • 37.
     Good shoes  Prevent injuries  Comfortable  Wear socks  Closed toe  Cotton  No bare feet  Light color  New shoes  No wrinkles  Break in slowly  Check inside of shoe
  • 38.
     No temperature  See doctor extremes regularly  Check bath water  Podiatrist  No water bottles  Trim straight across  No heating pads  Do not cut calluses or corns  Range of Motion
  • 39.
    Foot care  seepodiatrist q2 to 3 months for check-ups, even if don't have any foot problems.  include inspection of skin  check for redness or warmth of the skin.  check for pulses and temperature of feet  Monofilament assessment of foot sensation
  • 40.
    When to contactDr?  Changes in skin color  Changes in skin temperature  Swelling in the foot or ankle  Pain in the legs  Open sores on the feet that are slow to heal or are draining  Ingrown toenails or toenails infected with fungus  Corns or calluses  Dry cracks in the skin, especially around the heel  Unusal and/or persistent foot odor
  • 41.
    Risk for infection Frequent hand washing  Early recognition of signs of infection and seeking treatment  Meticulous skin care  Regular dental examinations and consistent oral hygiene care
  • 42.
    Sexual dysfunction  Effectsof high blood sugar on sexual functioning,  Resources for treatment of impotence, sexual dysfunction
  • 43.
  • 44.
    Oral Hypoglycemic Agents Oral hypoglycemic meds are NOT Insulin  Oral hypoglycemic meds require some production of insulin  Oral hypoglycemic agents are used in the treatment of type 2DM  Oral hypoglycemic meds are meant to supplement diet and exercise, NOT replace them
  • 45.
    Oral Hypoglycemic Agents Oral hypoglycemic meds cannot be used during pregnancy  Oral hypoglycemic meds may need to be halted temporarily and insulin prescribed if BS levels rise due to infection, trauma, stress, surgery etc.  Action vary so effect may be enhanced by use of multiple meds
  • 46.
    Oral Medication  Biguanides  Sulfonylureas  Meglitinide derivatives  Alpha-glucosidase inhibitors  Thiazolidinediones (TZDs)  Glucagonlike peptide–1 (GLP-1) agonists  Dipeptidyl peptidase IV (DPP-4) inhibitors  Insulins  Amylinomimetics  Bile acid sequestrants  Dopamine agonists
  • 47.
    Biguanides  Metformin (Glucophage) first choice for oral type 2 diabetes treatment.  Action: decreases overproduction of glucose by liver and makes insulin more effective in peripheral tissues
  • 48.
    Biguanides  Major sideeffects : anorexia/ wt. Loss  CI in patients with Renal impairment  D/C temp of (+) illness that leads to dehydration or hypoperfusion --lactic acidosis.
  • 49.
    Sulfonylureas  Glyburide (Micronase,DiaBeta, Glynase)  Glipizide (Glucotrol, Glucotrol XL)  Glimepiride (Amaryl)  Cholpropamide (Diabanese)
  • 50.
    Sulfonylureas  Action: Stimulatespancreatic cells to secrete more insulin and increases sensitivity of peripheral tissues to insulin  (insulin secretagogues)  indicated for use as adjuncts to diet and exercise in adult patients with type 2 DM  Used: to treat non-obese Type 2 diabetics
  • 51.
    Sulfonylureas  taken withfood  except Glucotrol/Glipizide : taken 30 mins before meals
  • 52.
    Sulfonylureas  (esp. Diabinese)when Side-effects taken with alcohol can  Hypoglycemia cause severe Disulfiram reactions  GI upset  Disulfiram (antibus): a compound when used with alcohol produces distressing symptoms  Symptoms: Flushed skin, N/V, palpitations, hyperventilation
  • 53.
    Meglitinides  Repaglinide (Prandin) Nateglinide (Starlix)  Action: stimulates pancreatic cells to secret more insulin  much shorter-acting insulin secretagogues than the sulfonylureas  may be used in patients who have allergy to sulfonylurea medications.
  • 54.
    Alpha-glucosidase inhibitors  Acarbose(Precose)  Miglitol (Glyset)  Action: Slow carbohydrate digestion and delay glucose absorption  S/E : diarrhea & flatulence  Take immediately before meals
  • 55.
    Thiazolidinediones (TZDs)  Pioglitazone[Actos]  Rosiglitazone [Avandia]  Used for patients with type 2 DM who take insulin injections  Acts by increasing insulin action at the receptor site  reduce insulin resistance  act as insulin sensitizers; thus, they require the presence of insulin to work.  must be taken for 12-16 weeks to achieve maximal effect.
  • 56.
    Thiazolidinediones (TZDs)  Affectsliver function  liver function tests  Indications of altered liver function  Yellow skin tone  Nausea  Abdominal pain  Dark urine
  • 57.
    Drug Interactions Directly interactwith Sulfonamides Sulfonylurea and NSAIDS increase risk of hypoglycemia Sulfonylurea+ * Med = Hypoglycemia
  • 58.
    Drug Interactions h bloodglucose levels Potassium-losing diuretics Regardless of what Corticosteriods med you might also be Estrogen compounds taking Phenytoin (Dilantin) Salicylates (ASA)
  • 59.
    Drug interactions Meds thatcause Acetaminophen Hypoglycemia Alcohol Monoamine oxidase Without drug inhibitors / MAO inhibitors interaction
  • 60.
    Drug interactions Meds thatcan Propranolol (Inderal)  MASK signs and symptoms of Hypoglycemia
  • 61.
    Oral Hypoglycemic Agents Client must also maintain prescribed diet and exercise program; monitor blood glucose levels  Not used with pregnant or lactating women  Specific drug interactions may affect the blood glucose levels
  • 62.
  • 64.
     Instituted in1923  Beef  Pork  1979 – human insulin  Can not be taken by mouth (digested)
  • 65.
    Onset – Peak- Duration  Onset  The time period from injection to when it begins to take effect  Peak  When insulin is working its hardest and therefore blood glucose levels are at their lowest  Duration  Length of time the insulin works or lasts
  • 66.
    Types  Rapid-acting insulinsor Ultra short-acting  Short-Acting Insulins  Intermediate-Acting Insulins  Long-Acting Insulins
  • 67.
    Rapid-acting insulins/ or Ultrashort-acting  have a short duration of action  appropriate for use before meals or when blood glucose levels exceed target levels and correction doses are needed.  These agents are associated with less hypoglycemia than regular insulin.
  • 68.
    Rapid-Acting Insulins/ or Ultrashort-acting  Insulin aspart (NovoLog)  Insulin glulisine (Apidra)  Insulin lispro (Humalog)
  • 69.
    Rapid-Acting Insulins Insulin aspart (NovoLog)  Insulin glulisine (Apidra)  Insulin lispro (Humalog) Appearance Onset Peak Duration Clear 5-15 minutes 30-90 (1hr) 3-5 hours (10 min) (4 hrs)  Insulin pumps  Rapid reduction of glucose level
  • 70.
    Short-Acting Insulins  Regularinsulin (Humulin R, Novolin R)  Preparations:  mixture of 70% neutral protamine Hagedorn (NPH) and 30% regular human insulin  (ie, Novolin 70/30, Humulin 70/30)
  • 71.
    Short-Acting Insulins  HumalogR; Novolin R; Iletin II Regular Appearance Onset Peak Duration Clear ½ - 1 hr 2-4 hrs 4-6 hrs (1 hour) (3 hour) (5 hours)  Administered 20-30 minutes before meals  IV  Usually given 4 x a day  May to taken alone or in combination
  • 72.
    Intermediate-Acting Insulins  InsulinNPH (Humulin N,  onset of action: 3-4 Novolin N) hours.  have a slow onset of  Peak: 8-14 hours action and a longer  duration of action : 16-24 duration of action. hrs  commonly combined  appears cloudy with faster-acting insulins to maximize the  must be gently mixed benefits of a single and checked for injection clumping  if clumping occurs, the insulin should be discarded.
  • 73.
    Intermediate-Acting Insulins  InsulinNPH (Humulin N, Novolin N) Appearance Onset Peak Duration Cloudy 2-4 hrs 6-12 hrs 16-20 hrs (2 hrs) (12 hrs) (24 hrs)  Administer after meals  Usually given 2x a day  Eat at onset!
  • 74.
    Long-Acting Insulins  providea longer  Insulin detemir duration of action, and, (Levemir) when combined with  Insulin Glargine rapid- or short-acting (Lantus) insulins, they provide better glucose control
  • 75.
    Types of Insulin– Long-acting  Ultra Lente (UL) Appearance Onset Peak Duration Cloudy 4-8hour 10-30 hrs 36+ hours (6 hrs) (24 hrs) (36 hrs)  To control fasting glucose levels  Cannot be mixed!
  • 76.
    Long-Acting Insulins  Insulindetemir  Insulin glargine  for once- or twice-daily  onset of action: 4-8 dosing hours  duration of action is up  Duration: 24 hours. to 24 hours  Peak effects; 16-18 hrs  FDA has advised of a possible association of insulin glargine with an increased risk of cancer
  • 77.
    Rapid-Acting Insulins Appearance Onset Peak Duration Clear 5-15 minutes 30-90 3-5 hours (10 min) (1hr) (4 hrs) Short-Acting Insulins Appearance Onset Peak Duration Clear ½ - 1 hr 2-4 hrs 4-6 hrs (1 hour) (3 hour) (5 hours)
  • 78.
    Learning Tip: Evenand Odd  Short-acting think odd  (1-3-5)  Intermediate-acting think even  (2-12-24)
  • 79.
    Intermediate-Acting Insulins Appearance Onset Peak Duration Cloudy 2-4 hrs 6-12 hrs 16-20 hrs (2 hrs) (12 hrs) (24 hrs) Long-acting insulin Appearance Onset Peak Duration Cloudy 4-8hour 10-30 hrs 36+ hours (6 hrs) (24 hrs) (36 hrs)
  • 80.
    When should insulinbe administered  Short-acting / regular  30 minutes before meals  Do not allow more than 30 minutes to pass by without eating   hypoglycemia  Intermediate acting  After meals  If mixed (regular & intermediate)  30 minutes before meals
  • 81.
    What route isinsulin administered  Sub-cutaneous  IV  Regular  Pump
  • 82.
    Insulin Type Onset Peak Duration Ultra Short 15 mins 30-90 mins 2- 4 hrs Short 30 mins 2- 4 hrs 6-8 hrs Intermediate 1-2 hrs 6-12 hrs 18-24 hrs Long 4-6 hrs 16-24 hrs 18-36 hrs Combination 30-60 2- 4 hrs, 6-8hrs,then 70/30 mins then then 6-12 18-24 hrs 1-2 hrs hrs
  • 83.
    Insulin Type Onset Peak Duration Insulin 30-60 None 24 hours glargine minutes
  • 84.
  • 86.
  • 87.
    Adverse effects ofinsulin  Local allergic reactions  Insulin lipodystrophy  Insulin resistance  Dawn Phenomenon  Somogyi phenomenon  Insulin waning
  • 88.
    Insulin lipodystrophy  orlipoatrophy  is primary idiopathic atrophy of adipose tissue  can be a lump or small dent in the skin that forms when a person keeps performing injections in the same spot.
  • 89.
    Insulin lipodystrophy lipohypertrophy
  • 90.
    Rotate site ofinjection
  • 91.
    Nursing Responsibilities  Route: Subcutaneous  Steady absorption  Less painful  IV – in emergency cases ( DKA)  Only regular insulin is given through the IV route  Do not massage the site  Fastest absorption site is the abdomen, then deltoids, thighs then buttocks
  • 92.
    Nursing Responsibilities  Administerat room temperature  Cold insulin causes lipodystrophy  Rotate site of injection  To prevent lipodystrophy. Inhibits insulin absorption  Store vial of insulin in current use at room temperature  Other vials should be refrigerated
  • 93.
    Nursing Responsibilities  Gentlyroll vial in between the palms to redistribute insulin particles  Do not shake. Bubbles make it difficult to redistribute insulin particles
  • 94.
    Nursing Responsibilities  Observefor side effects  Localized  Induration or redness  Swelling  Lesions at the site  Lipodystrophy  Edema  Sudden resolution of hyperglycemia causes retention of water  Hypoglycemia
  • 95.
    Somogyi Effect  Reboundhyperglycemia  Normal or blood glucose levels are present at bedtime  hypoglycemia : occurs at 2-3am  This causes an increase in the production of counterregulatory hormones  Hyperglycemia: by 7 am  Resuts in response to the counterregulatory hormones
  • 96.
    Somogyi Effect  Treatment  decreasing evening (predinner or bedtime) dose of intermediate acting insulin  or increasing the bedtime snack
  • 97.
    Dawn Phenomenon  (6AM – 8 AM) early AM increase in blood glucose levels associated with release of growth hormone at 12 MN to 3 AM
  • 98.
    Dawn Phenomenon:TREATMENT  Type1 diabetes  Intensify insulin therapy  Avoid late night snacking, unless appropriate quick- acting insulin is given.  Type 2 diabetes  Adjust diet content (decrease carbohydrates) and timing of the evening meal so that the glucose level at bedtime is 70-110 mg/dl  If dietary modification is not enough, consider an intermediate or long-acting sulfonylurea at evening meal.  Basal insulin is indicated if the dawn phenomenon continues.
  • 99.
    Insulin Waning  Progressiverise in the blood glucose levels from bedtime to morning  Treatment:  Increase dose of evening intermediate acting or long acting insulin
  • 100.
    Difference between dawnphen and insulin waning 10 PM 2 AM 4 AM 8 AM Dawn 100 110 135 250 Phenomenon Waning of 100 160 220 270 insulin Dawn phenomenon shows an abrupt increase between 4 a.m. and 8 a.m., whereas waning of exogenous insulin effect shows gradual rise between 2 a.m. and 8 a.m.
  • 101.
  • 102.
    Glucagonlike peptide–1 (GLP-1) agonists  Exenatide injectable solution (Byetta)  Exenatide injectable suspension (Bydureon)  mimic the endogenous incretin GLP-1  it enhances glucose-dependent insulin secretion by pancreatic beta cells, suppresses inappropriately elevated glucagon secretion, and slows gastric emptying.
  • 104.
    Glucagonlike peptide–1 (GLP-1) agonists  Liraglutide (Victoza)  a once-daily injectable  stimulates G-protein in pancreatic beta cells.
  • 105.
    Dipeptidyl peptidase IV(DPP-4) inhibitors  prolong action of incretin hormones  Sitagliptin (Januvia)  Saxagliptin (Onglyza)  Linagliptin (Tradjenta)
  • 106.
    Amylinomimetics  Pramlintide acetate (Symlin)  amylin analog that mimics the effects of endogenous amylin, which is secreted by pancreatic beta cells.  delays gastric emptying, decreases postprandial glucagon release, and modulates appetite.
  • 107.
    Bile acid sequestrants bile acid sequestrant colesevelam  lipid-lowering agents for the treatment of hypercholesterolemia but were subsequently found to have a glucose-lowering effect.
  • 108.
    Antiparkinson Agents, Dopamine Agonists Bromocriptine (Cycloset)  indicated as an adjunct to  Quick-release diet and exercise to bromocriptine acts on improve glycemic control. circadian neuronal activities within the hypothalamus to reset the abnormally elevated hypothalamic drive for increased plasma glucose, triglyceride, and free fatty acid levels in fasting and postprandial states in patients with insulin resistance.
  • 109.
    Non-Insulin Injectables  Newdrugs are available for people with type 2 diabetes.  Pramlintide (Symlin), exenatide (Byetta), and liraglutide (Victoza) are non-insulin injectable drugs.  insulin pulls glucose into the cells  these medications cause the body to release insulin to control blood sugar levels.
  • 110.
  • 111.
    Glucagonlike peptide–1 (GLP-1) agonists  Exenatide injectable solution (Byetta)  Exenatide injectable suspension (Bydureon)  mimic the endogenous incretin GLP-1  it enhances glucose-dependent insulin secretion by pancreatic beta cells, suppresses inappropriately elevated glucagon secretion, and slows gastric emptying.
  • 113.
    Glucagonlike peptide–1 (GLP-1) agonists  Liraglutide (Victoza)  a once-daily injectable  stimulates G-protein in pancreatic beta cells.
  • 114.
    Dipeptidyl peptidase IV(DPP-4) inhibitors  prolong action of incretin hormones  Sitagliptin (Januvia)  Saxagliptin (Onglyza)  Linagliptin (Tradjenta)
  • 115.
    Amylinomimetics  Pramlintide acetate (Symlin)  amylin analog that mimics the effects of endogenous amylin, which is secreted by pancreatic beta cells.  delays gastric emptying, decreases postprandial glucagon release, and modulates appetite.
  • 116.
    Bile acid sequestrants bile acid sequestrant colesevelam  lipid-lowering agents for the treatment of hypercholesterolemia but were subsequently found to have a glucose-lowering effect.
  • 117.
    Antiparkinson Agents, Dopamine Agonists Bromocriptine (Cycloset)  indicated as an adjunct to  Quick-release diet and exercise to bromocriptine acts on improve glycemic control. circadian neuronal activities within the hypothalamus to reset the abnormally elevated hypothalamic drive for increased plasma glucose, triglyceride, and free fatty acid levels in fasting and postprandial states in patients with insulin resistance.