CARE OF CLIENTS WITH DIABETES MELLITUS

PPT4 || NCM332
DIABETES MELLITUS (DM) PATHOPHYSIOLOGY OF TYPE 1 DM – HYPERGLYCEMIA
• A group of metabolic disease characterized by
hyperglycemia.
• Hyperglycemia- elevated blood glucose level
• Normal blood glucose: 80-120 mg/dL
• A chronic, multisystem disease related to abnormal insulin
production, impaired insulin utilization, or both
• A disorder of glucose metabolism related to absence or
insufficient insulin supply and/or poor utilization of the insulin
GENERAL RISK FACTORS
• Family history
• Obesity
• Race/Ethnicity (i.e., African- Americans, Hispanics, Native
Americans, Asian American, Pacific Islander)
• Age ≥ 45 years old
• Previously identified impaired fasting glucose
• Hypertension (≥140/90)
• Decreased HDL, increased triglycerides
• History of gestational diabetes/ delivery of babies over 9lbs
TYPES OF DM
Type I Diabetes Mellitus
• Juvenile- onset diabetes
• Insulin- dependent diabetes mellitus (IDDM)
Type II Diabetes Mellitus
• Adult- onset diabetes
TYPE 2 DIABETES MELLITUS
• Non-Insulin- Dependent Diabetes Mellitus (NIDDM)
CHARACTERISTICS
NORMAL INSULIN PRODUCTION AND ACTION
• Most prevalent type
• Slow onset
• Usually after 30 years old
• Common among obese
Risk Factors:
• Overweight/Obesity
• Old age
• Family history of DM type 2
• African Americans, Asian Americans, Hispanics, Native
Hawaiians or other Pacific Islanders, and Native Americans
Etiology:
• Insulin resistance: decreased tissue sensitivity to
INSULIN RODUCTION DURING FASTING PERIODS insulin
• Unknown cause
• Impaired insulin secretion
PATHOPHYSIOLOGY OF TYPE 2 DM:

CLASSICAL SIGNS (4P’s)

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CARE OF CLIENTS WITH DIABETES MELLITUS
PPT4 || NCM332
Diagnostic Criteria INTERMEDIATE-ACTING INSULIN
• Symptoms of DM plus casual plasma glucose concentration AGENT ONSET PEAK DURATION NRSG RESP
NPH (Neutral
greater than or equal to 200 mg/dL; OR
Protamine
• Fasting plasma glucose greater than or equal to 126mg/dL; Hagedorn) 4-12 Usually taken after
2-4 hours 6-20 hours
OR Humulin N hours food
• Two- hour post load glucose greater than or equal to
“cloudy insulin”
200mg/dL during an oral glucose tolerance test; OR Insulin
• HbA1-C greater than or equal to 6.5% Lente/Humulin 3-4 hours Same Same Same
• Glycosylated hemoglobin L/Novolin L.
• Measures the percentage of hemoglobin that carries - VERY LONG ACTING INSULIN
glucose AGENT ONSET PEAK DURATION NRSG RESP
INSULIN
• Reflects glucose control for the past 3 months GLARGINE 1 hour No peak 24 hours For basal dose
TEST SPECIMEN PREPARATION (LANTUS/TOUJEO)
Fast Blood Sugar Blood Fastline 8-10 hours INSULIN REGIMEN
(FBS) REGIMEN TYPE OF INSULIN and IMPLICATION
FREQUENCY
HbA1-c Blood None ONCE A DAY (SINGLE Intermediate (NPH) at • One injection should
Capillary Blood Blood (Capillary) Usuallt taken AC DOSE) bedtime provide night-time
Sugar (CBS) meals coverage
Long-Acting (Lantus) in • One injection will last
MEDICAL MANAGEMENT AM or bedtime 24 hours with no peaks
Goal: Achieve euglycemia without episodes of hypoglycemia and less chance for
hypoglycemia.
while maintaining a high quality of life • Does not cover
Type 1 DM (I-DEMo) Type 2 DM (DEMOHI) postprandial blood
Insulin therapy Dietary modification glucose levels
Dietary modification Exercise TWICE A DAY (SPLIT-MIXED NPH and regular or • Two injections provide
Exercise Monitoring DOSE) rapid- acting ac coverage for 24 hours
Monitoring Oral Hypoglycemic Agents (OHA) breakfast and at dinner • Patient must adhere
Insulin, if unresponsive to noninsulin to a set meal plan.
treatment THREE TIMES A DAY NPH and regular or • Three injections
INSULIN THERAPHY rapid- acting ac provide coverage for
breakfast 24 hours, particularly
• Historically, insulin was derived from beef and pork pancreas + during early AM hours.
• Recent insulin preparations are genetically engineered Regular or rapid- acting • Decreased potential
human insulins derived from E. coli or yeast cells using ac dinner for 2-3 AM
+ hypoglycemia.
recombinant DNA technology NPH at bedtime
• Commonly given subcutaneously, but regular insulin may be BASAL-BOLUS Regular or rapid- acting • More flexibility is
given IV/SQ ac bf, lunch, and dinner allowed at mealtimes
+ and for amount of
• Dose is prepared in “units” Long-acting (glargine) food intake. Good
PREPARATION: OD postprandial control.
• Groups insulin according to onset (O), Regular or rapid- acting • Pre-prandial blood
ac bf, lunch, and dinner glucose checks and
peak (P), and duration (D) + establishing and
• Rapid- acting, Short- acting, Intermediate-acting, Very Long- NPH BID following individualized
acting algorithms are
necessary
- RAPID-ACTING INSULIN • Most physiologic
AGENT ONSET PEAK DURATION NRSG RESP approach, except for
INSULIN ASPART pump
(NovoRapid) Let patient eat
5-15 30-60
2 hours w/n 15 mins after COMBINATION OF INSULIN THERAPY
minutes minutes • A short- or rapid-acting insulin is mixed with intermediate-
INSULIN GLUSLINE administration
(APIDRA) acting insulin in the same syringe.
• This allows the patient to have both mealtime and basal
coverage without having to administer two separate
injections.
COMBINING INSULINS IN ONE SYRINGE
1. Wash hands.
2. Gently rotate NPH insulin bottle.
3. Wipe off tops of insulin vials with alcohol sponge.
4. Draw back amount of air into the syringe that equals total
dose. (Ex. 48 units of air for 36 units NPH and 12 units regular
PARTS OF A FLEX PEN
insulin)

- SHORT-ACTING INSULIN
AGENT ONSET PEAK DURATION NRSG RESP
REGULAR INSULIN
(HUMULIN R, Typically given 15
NOVOLIN R) 30-60 AC meals
2-3 hours 4-6 hours
minutes
Humulin R – May be given IV
“clear insulin”

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CARE OF CLIENTS WITH DIABETES MELLITUS
PPT4 || NCM332
• Small doses of insulin are given in increasing amounts
MIXING INSULIN LIPODYSTROPHY
Clear (clear and fast-acting) > before the cloudy (cloudy and • Lipoatrophy- loss of subcutaneous fat and appears as a
long-acting) > to prevent contaminating a SHORT-ACTING slight dimpling or more serious pitting of SQ.
INSULIN with a LONG-ACTING INSULIN • Lipohypertrophy- development of fibrofatty masses at the
STORAGE OF INSULIN injection site
• Heat and freezing alter insulin molecule
• In use insulin vials and pens
• ROOM temperature for up to 4 weeks
• Unopened insulin vials and pens
• Stored in the REFRIGERATOR
• Pre-filled insulin syringe
• Prefilled syringes with two different insulins
• Store in refrigerator for up to 1 week ONLY
• Prefilled syringes with only one type of insulin
• Store in refrigerator for up to 30 days ONLY
• Store in a vertical position with needle pointed up (to avoid
clumping of suspended insulin in the needle)
• Before injection, gently roll prefilled syringes between the • Cause: repeated use of an injection site
palms 10 to 20 times (to warm the insulin and resuspend the • Management: rotate injection sites
particles)
INSULIN ADMINISTRATION
• Route: • Subcutaneous
• Regular insulin can be given IV
• PO is contraindicated because insulin is inactivated by
gastric acid
Golden rule: Never assume that because the patient
already uses insulin, he or she knows and practices the correct
insulin injection technique.
INSULIN THERAPY

Morning Hyperglycemia
• An elevated blood glucose level on arising in the morning
• Causes: Dawn Phenomenon or Somogyi Effect
Dawn Phenomenon
• Normal glucose level until approximately 3AM when blood
glucose begins to rise
• The elevation is associated with the release of growth
hormone which decreases tissue sensitivity to insulin
DAWN = DOWN INSULIN
Somogyi Effect
• High dose evening/bedtime insulin produces a decline in
blood glucose during the night
• Hypoglycemia triggers release of counterregulatory
hormones (i.e., glucagon, epinephrine, growth hormone,
cortisol) which produces rebound hyperglycemia in the AM
SoMogyi = So MOch insulin
Morning Hyperglycemia Diagnostics
BEDTIME CBG 3AM CBG MORNING CBG CULPRIT
NORMAL NORMAL HIGH Dawn
Phenomenon
NORMAL HIGH HIGH Somogyi Effect
MANAGEMENT
DAWN PHENOMENON SOMOGYI EFFECT
• Give intermediate- acting • Decrease evening/bedtime
insulin at bedtime (10PM) dose of insulin and/or
Teach patients to rotate the injection within one anatomic site,
• Increase bedtime snack
such as the abdomen, for at least 1 week before using a
different site, such as the right thigh. (This allows for better ORAL HYPOGLYCEMIC AGENTS
insulin absorption) BIGUANIDES
• Metformin (Glucophage)
COMPLICATIONS OF INSULIN THERAPY
• MOA: reduces glucose production by the liver and
Local allergic reaction
enhances tissue sensitivity at the tissue level
• Appears at the injection site 1 to 2 hours after administration
• S/E: lactic acidosis, diarrhea
• S/Sx: redness, swelling, tenderness, and induration
• NRSG RESP: Needs to be held 1-2 days before IV contrast
• Usually resolves spontaneously, otherwise insulin type is
media given and for 48 hr after.
changed
Systemic allergic reaction
• Rare
• Begins immediately after injection and becomes generalized
urticaria
• Treatment is desensitization
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CARE OF CLIENTS WITH DIABETES MELLITUS
PPT4 || NCM332
insulin or insulin secretagogues.
• Moderate alcohol consumption has
no acute effect on glucose and insulin
concentrations, but carbohydrate
taken with the alcohol (mixed drink)
may raise blood glucose

SULFONYLUREAS
• Glipizide (Glucotrol), Glyburide (Glynase), Glimepiride
(Amaryl)
• MOA
• Stimulate beta cells to secrete insulin
• Decrease glycogenolysis and gluconeogenesis.
• Enhance cellular sensitivity to insulin.
• S/E: weight gain, hypoglycemia
MEGLITINIDES Diabetes Meal Planning
• Nateglinide (Starlix), Repaglinide (Prandin) - A non-specific guide for when, what, and how much food to
• MOA: stimulates a rapid but short- lived release of insulin from consume to receive adequate nutrition while maintaining
the pancreas blood glucose at the target range
• S/E: Weight gain, hypoglycemia - Must take into consideration a patient’s goals, preferences,
ALPHA GLUCOSIDASE INHIBITOR and lifestyle
• “Starch blocker” Characteristics of Diabetes Diet
• Acarbose (Precose), Miglitol (Glyset) • Includes more non-starchy vegetables
• MOA: slows down the absorption of CHO in the small • High- fiber, fewer added sugars and refined grains
intestine • Whole foods are preferred over highly processed foods
• S/E: Gas, abdominal pain, diarrhea • Total calories will be prescribed by physician
• NRSG RESP: Taken with the first bite of each main meal • Caloric distribution:
THIAZOLIDINEDIONES • CHO: 50% to 60%
• “Insulin sensitizers” • Fats: 20% to 30%
• Pioglitazone (Actos), Rosiglitazone (Avandia) • CHON: 10-15% to 20%
• MOA: increases insulin sensitivity, transport, and utilization at • The plate method is a
target tissues simple, visual way to
• S/E: make sure the patient
• Pioglitazone: increases risk for bladder cancer and gets enough non-
exacerbates heart failure starchy vegetables and
• Rosiglitazone: increases risk for cardiovascular events lean protein while
DIPEPTIDYL PEPTIDASE-4 (DPP-4) INHIBITOR limiting the amount of
• Linagliptin (Trajenta), Sitagliptin (Januvia) higher-carb foods
• MOA: stimulate release of insulin from beta cells, decrease eaten that have the
hepatic glucose production highest impact on
• S/E: pancreatitis, allergic reactions blood sugar levels.
SODIUM-GLUCOSE CO-TRANSPORTER 2 (SGLT2) INHIBITOR • The appropriate plate
• Canagliflozin (Invokana); Empagliflozin (Glyxambi) size is a 9- inch dinner plate
• MOA: blocks the reabsorption of glucose by the kidney, Diabetes Plate Method
increasing glucose excretion, and lowering blood glucose • Fill half with non-starchy vegetables
levels • Non-starchy vegetables are lower in carbohydrate, so they
DIETARY MODIFICATIONS do not raise blood sugar very much.
COMPONENT RECOMMENDATIONS • Examples: asparagus, cabbage, carrots, cauliflower,
TOTAL CARBOHYDRATES • Minimum of 130 g/day. cucumber, eggplant, okra, green beans, tomatoes
• Include carbohydrate from fruits,
vegetables, grains, legumes, and low-
• Fill one quarter with a lean
fat milk. protein
• Monitor by carbohydrate counting, • Animal- based:
exchange lists, or use of appropriate
proportions
• Chicken, eggs
• Glycemic index may provide • Fish
additional benefit. • Shellfish
• Sucrose-containing food can be
substituted for other carbohydrates in
• Lean beef, pork
the meal plan. • Cheese
• Fiber intake at 25-30 g/day. • Plant- based:
• Nonnutritive sweeteners are safe
when consumed within FDA daily intake
• Beans
levels. • Nuts
PROTEIN • 15%-20% of total calories. • Tofu
• High-protein diets are not • Fill one quarter with carb foods.
recommended for weight loss.
FAT • Limit saturated fat to <7% of total • Examples:
calories. • Whole grains
• Trans fat should be minimized. • Starchy vegetables (squash, potato, kamote)
• Dietary cholesterol <200 mg/day.
• ≥2 servings of fish per week to provide • Dairy products (milk, yogurt, soy milk)
polyunsaturated fatty acids. • Water is the best choice because it contains no calories or
ALCOHOL • Limit to moderate amount (maximum carbohydrates and has no effect on blood sugar. Other zero-
1 drink per day for women and 2 drinks
per day for men). or low-calorie drink options include:
• Alcohol should be consumed with • Unsweetened tea (hot or iced)
food toreduce risk of nocturnal • Unsweetened coffee (hot or iced)
hypoglycemia in those using

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CARE OF CLIENTS WITH DIABETES MELLITUS
PPT4 || NCM332
• Sparkling water/club soda MILD HYPOGLYCEMIA MODERATE HYPOGLYCEMIA
• Sweating • Confusion
• Flavored water or sparkling water without added sugar • Tremor • Double vision
• Diet soda or other diet drinks • Tachycardia • Drowsiness
EXERCISE • Palpitation • Irrational or combative behavior
• Nervousness • Headache
• Lowers blood glucose levels by increasing the uptake of • Hunger • Slurred speech
glucose by body muscles and by improving insulin utilization • Impaired coordination
Guidelines: MANAGEMENT OF HYPOGLYCEMIA
• Exercise 3x per week with no more than 2 consecutive days • “Rule of 15”
without exercise • Give 15 grams of fast- acting carbohydrate by mouth (e.g.,
• Perform resistance training 2x a week if with type 2 DM 4-6 oz of soda, 8-10 lifesavers, 4-6 oz orange juice, or tbsp
• Exercise at the same time of the day and for the same honey)
duration each session • Wait 15 minutes then recheck blood glucose.
• Use proper footwear and, if appropriate, other protective • If blood glucose is still < 70mg/dL, give another 15-g fast
equipment acting carbohydrate
• Avoid trauma to lower extremities • Once blood sugar is stable and next meal is more than 1
• Inspect feet daily after exercise hour away, give additional food of longer- acting combination
• Avoid exercise in extreme heat or cold plus protein or fat once symptoms subside.
• Avoid exercise during periods of poor metabolic control • Crackers with peanut butter
• Stretch for 10 to 15 minutes before exercising • 2 slices of white bread plus skimmed milk
Precaution: • Notify physician if symptoms do not subside after two to
• Patients with blood glucose greater than 250 mg/Dl and who three administrations of fast- acting carbohydrates
have ketones in the urine should not exercise until urine test SEVERE HYPOGLYCEMIA
results are negative for ketones and the blood glucose level is • CBG <40mg/dL
closer to normal. • Clinical Manifestations:
• Exercising with elevated blood glucose increases secretion • Unconsciousness or difficulty arousing from sleep
of glucagon, growth hormone, and catecholamines. • Seizures
• Patients who are on insulin therapy should be taught to eat a • Disoriented behavior
15- g CHO snack (a fruit exchange) or a snack of complex MANAGEMENT OF SEVERE HYPOGLYCEMIA
carbohydrate with a protein to prevent hypoglycemia. • Glucagon 1mg SQ/IM
MONITORING • Return of consciousness may take up to 20 minutes after
Self- monitoring of Blood Glucose (SMBG) administration
• Enables the patient to make decisions regarding food intake, • Provide snack on awakening to prevent recurrence of
activity patterns, and medication dosages. hypoglycemia, except if with nausea
• Produces accurate records of daily glucose fluctuations and • If nauseous, position to side lying
trends, and it alerts the patient to acute episodes of • D50W (50% dextrose in water)
hyperglycemia and hypoglycemia. • 25 to 50 mL of D50W IV Push
• Provides patients with a tool for achieving and maintaining • Used in hospital settings
specific glycemic goals. • Ensure IV-line patency
• Recommended for all insulin- treated patients with DM DIABETIC KETOACIDOSIS (DKA)
• A life- threatening complication of type 1 DM
Causes:
• Decreased or missed dose of insulin
• Illness or infection
• Undiagnosed or untreated DM
CLINICAL MANIFESTATIONS
HYPERGLYCEMIA DEHYDRATION and KETOSIS and ACIDOSIS
ELECTROLYTE LOSS
• Blood glucose levels • Orthostatic • Anorexia, nausea and
between 300 and 800 Hypotension vomiting, abdominal
mg/dL • Weak, rapid pulse pain
• Polyuria • Elevated creatinine, • Acetone breath
• Polydipsia BUN, and hematocrit • Kussmaul respirations:
deep, but unlabored
breathing pattern
• Changes in mental
status
• Hyperkalemia
MANAGEMENT OF DKA
Fluid Replacement
• PNSS (0.9% NaCl) at 0.5 to 1L per hour for 2 to 3 hours
• Half-strength NSS (0.45% NaCl) if hypertensive or
hypernatremic
CONTINUOUS GLUCOSE MONITORING (CGM)
• WOF: fluid overload (bounding pulse, crackles, headache)
• HbA1-c (Glycosylated Hgb) is also monitored to review
Restoring Electrolytes
glucose control over the past 3 months.
• Target parameters: • Important: rehydration and insulin cause a drop in potassium
• Pre- prandial CBG: 80-130 mg/dL level
• Post- prandial CBG (1-2 hours PC): < 180mg/dL • Rehydration increases potassium excretion via urine
• Insulin transports potassium from the extracellular into the
• HbA1c: < 7%
• Non-diabetics: 4%- 5.6% intracellular compartment
• Potassium chloride IV infusion
ACUTE COMPLICATIONS OF DM
• INCORPORATE KCl into IV bottle. DO NOT GIVE KCl VIA IV
HYPOGLYCEMIA
PUSH SINCE IT CAUSES CARDIAC ARREST
• Means low blood sugar
• Use infusion pump for accurate delivery
• Occurs when blood glucose falls to less than 80 mg/dL
• Apply cold compress on IV site
• Severe hypoglycemia is when glucose levels are less than
• Hold if patient is not urinating
40mg/Dl
• Reversing acidosis and hyperglycemia
Causes:
• Regular insulin
• Too much medication
• Given via intravenous route at a slow, continuous rate
• Too little food
• Excessive physical activity
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CARE OF CLIENTS WITH DIABETES MELLITUS
PPT4 || NCM332
• Infuse D5NSS or D5 0.45%NSS when blood glucose levels Preventive Management:
reach 250 to 300 mg/dL to avoid rapid drop in the blood • Dilated eye exam within 5 years after
glucose level during treatment onset of DM type 1 and annually thereafter
HYPERGLYCEMIC HYPEROSMOLAR NON-KETOTIC SYNDROME • Maintain good glycemic control
(HHNKS) • Manage BP
• A metabolic disorder of type 2 DM Proliferative Diabetic Retinopathy
•Characterized by severe hyperglycemia and hyperosmolarity • Most severe form
• Occurs most often in older adults (50 to 70 years old) • Occurs in late stage of diabetic retinopathy
Causes: • Neovascularization sec. to complete occlusion of retinal
• Infection vessel
• Illness (e.g., stroke, MI) • Patient sees black or red spots or lines; blindness if left
• Medications that exacerbate hyperglycemia (thiazides) untreated
• Treatment/Procedures (dialysis or surgery)
Clinical Manifestations:
• Blood glucose levels from 600 to 2000mg/dL
• Hypotension
• Profound dehydration (dry mucous membranes, poor skin
turgor)
• Tachycardia
• Variable neurologic signs (ALOC, seizures, hemiparesis)
Management:
• Same as DKA Management:
• Monitor closely for fluid overload • Laser photocoagulation therapy
CHRONIC COMPLICATIONS OF DM • Reduces risk of vision loss
ANGIOPATHY • Destroys the ischemic areas of the retina that produce
• Damage to blood vessels secondary to chronic growth factors that encourage neovascularization.
hyperglycemia • Laser Photocoagulation
Etiology:
• Accumulation of damaging by-products of glucose
metabolism, such as sorbitol, which is associated with damage
to nerve cells;
• Formation of abnormal glucose molecules in the basement
membrane of small blood vessels such as those that circulate
to the eye and kidney;
• A derangement in red blood cell function that leads to a
decrease in oxygenation to the tissues.

DIABETIC NEUROPATHY
• A microvascular complication associated with damage to
MACROVASCULAR COMPLICATIONS the small blood vessels that supply the glomeruli of the kidney.
• Diseases of the large and medium-size blood vessels that • Results to end-stage kidney disease
occur with greater frequency and with an earlier onset in • Hypertension accelerates its progression
people with diabetes TEST SPECIMEN NORMAL DIABETIC IMPLICATION
Preventive Management: NEUROPATHY
Urine Urine (1st F: <3.5 Microalbuminuria: Re-checked
• Risk reduction: Albumin- morning mg/mmol F: 3.5-35 mg/mmol for 2
• Weight reduction Creatinine void M: <2.5 M: 2.5-25 more times.
• Smoking cessation Ratio sample) mg/mmol mg/mmol Confirmed if
(uACR) Re-check (+) in
• Control of BP annually 2/3 tests
• Dietary modification (Low salt, low fat) Macroalbuminuria A 24- hour
• Exercise (aka Proteinuria): urine
F: >35mg/mmol sample is
MICROVASCULAR COMLICATIONS M:>25mg/mmol done to
• Result from thickening of the vessel membranes in the quantify
capillaries and arterioles in response to conditions of chronic amount of
protein
hyperglycemia.
Creatinine Blood 0.6-1.2 >1.2 mg/dL Kidney
• Specific to diabetes (serum) mg/dL damage
DIABETIC RETINOPATHY
• Process of microvascular damage to the retina as a result of
chronic hyperglycemia, nephropathy, and hypertension in
patients with diabetes.
Non- proliferative Diabetic Retinopathy
• Most common form
• Occurs in early stage of diabetic retinopathy
• Microaneurysm sec. to partial occlusion of retinal vessel
• Asymptomatic, but vision may be affected if macula is
involved

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