Diabetes Flashcards
What is Diabetes?
*Chronic disorder of impaired carbohydrate, protein, and lipid metabolism caused by a deficiency of insulin
What are the functions of Insulin? (6)
*Transports and metabolizes GLUCOSE for energy
*Stimulates storage of glucose in the liver and muscle as GLYCOGEN
* Signals the liver to stop the release of glucose
*Enhances storage of FAT in adipose tissue
*Accelerates transport of AMINO ACIDS into cells (PROTEIN SYNTHESIS)
* Inhibits the breakdown of stored glucose, protein, and fat
*↑ fat, ↑ cholesterol
CLASSIFICATIONS OF DIABETES? (5)
Type 1 diabetes (Insulin dependent, onset early, autoimmune)
Type 2 diabetes (Insulin resistant)
Gestational diabetes (GDM)
Prediabetes
Diabetes associated with other conditions or syndromes (pancreas, corticosteroids)
-Insulin produced by islet of Langerhans and beta cells within the pancreas → damaged cells don’t produce enough insulin
-Corticostroids ↑ blood sugar → insulin resistance
How do you know if you’re Prediabetic?
What Tests? (3)
- Impaired glucose intolerance (IGT) [mostly during pregnancy]
- Two-hour oral glucose tolerance test (OGTT):
140 to 199 mg/dL
- Two-hour oral glucose tolerance test (OGTT):
*Impaired FASTING glucose (IFG) [Non-pregnancy]
* Fasting glucose level: 100 to 125 mg/d
Name 4 things about Type 1 Diabetes
Type 1 Diabetes (insulin-dependent) →
*autoimmune disorder → no insulin produced
*(requires insulin)
*Onset is ACUTE
*Usually BEFORE 30 years old
Type 1 diabetes is characterized by the destruction of pancreatic beta cells that require exogenous insulin
Risk Factors of type 1 Diabetes
(7/12)*
*Family history Obesity
Hx of gestational DM *HDL< 35
45 yrs + *Triglycerides > 250
*GENETICS Pre-hx IFG LEVELS HIGH
*Early Onset (CHILDHOOD)
*Possible IMMUNOLOGIC(AUTOIMMUNE) or
*ENVIRONMENTAL (viral or toxins) factors
Race (African, Hispanic, Asian, Native American, Pacific Islander/Native Hawaiian)
CLINICAL MANIFESTATIONS OF TYPE 1 DM (ASSESSMENT)
*Polyuria: increased urination
*Polydipsia: Increased thirst
*Polyphagia: Increased appetite
*Weight loss
*fatigue
Hyperglycemia
*Blurred vision/VISION CHANGES
Tingling/numbness in hands/feet (Parasteshia)
*Absent of minimal insulin production
*Islet cell antibodies-Present at onset
*INSULIN REQUIRED FOR ALL DM1
**Type 1 may have sudden weight loss, nausea, vomiting, and abdominal pain if DKA (diabetes ketoacidosis) has developed **
Diagnosis Criteria for Diabetes
*Fasting Blood Sugar → ≥ 126mg/dL
(no caloric intake for at least 8 hrs)
*Random Glucose → ≥ 200 w/symptoms of DM
*2hr Oral Glucose (OGTT) 2-hour postload (75 g)
→ ≥ 200 mg/dL [Normal 140-199]
*Hgb A1C →6.5 % or higher
- Glycosylated hemoglobin – reflects glucose level over *2-3mos although, hgb stays attached to glucose up to 120 days.
A1C LEVELS AND GOAL
Normal A1C is below 5.6% (GOAL)
PREDIABETES → 5.7-6.4%
DIABETES → 6.5% OR HIGHER
-A1C is used to diagnose, screen, and monitor treatment response
Diabetic goal is 1% below initial A1C
- Glycosylated hemoglobin – reflects glucose level over *2-3mos as a % of total Hgb although, Hgb stays attached to glucose up to 120 days.
-Anemic patients have ↓ HgbA1c d/t ↓Hgb –>
check fructosamine levels
KEY FACTORS (6/8) of Type 2 DM?
WHAT IS IT?
*Insulin resistance d/t impaired beta cell
function results in
*DECREASED INSULIN PRODUCTION
Islet cell antibodies= ABSENT
-onset over age 30 years,
*increasing in children, obesity
-Slow, progressive glucose intolerance: Many times discovered with routine testing and elderly pts.
**Treated initially with DIET & EXERCISE
*Oral hypoglycemic agents initially- may need to convert to insulin or use both (METFORMIN)
CLINICAL MANIFESTATIONS OF
T2DM (7/12)*
*** “Three Ps”: Polyuria; Polydipsia;
Polyphagia
*Weight loss, fatigue, weakness,
*vision changes, tingling or numbness in hands
or feet, dry skin, skin lesions or
wounds that are slow to heal,
*recurrent vaginal yeast or
*candidal infection
RISK FACTORS FOR
METABOLIC SYNDROME? (3/6)
HOW MANY DO YOU NEED TO BE AT RISK TO BE POSITIVE?
- *Metabolic syndrome
-(3/5 risk)-
*FBS >100,
*abdominal obesity (waist)
((M) waist >40” ; (F)>35”
*BMI >30),
*hypertension (≥130/85),
*Low HDL (<40 (M); <50 (F) or
*High Triglycerides (>150)
*CAD,
-Previously identified (IFG) impaired
fasting glucose,
*hx of GDM
*babies > 9 pounds
-Prediabetic patients
* African Americans, Asian Americans, Hispanics, Native Hawaiians or other Pacific Islanders, and Native Americans
Five Components of DM management
[MENPE]
- Nutritional therapy
- Exercise
- Monitoring
- Pharmacologic therapy
- Education
The goals of diabetes management(= balance diet)
Reduce symptoms
Promote well-being
Prevent acute complications of hyperglycemia, and
Prevent or delay the onset and progression of long-term complications
Dietary Management Goals for DM
*Carbohydrates: 50%-60% of total calories;
*emphasize whole grains
*Fat: 20% to 30%, with <10% from
saturated fat and <300 mg cholesterol,
-Two or more servings of fish/week to provide polyunsaturated fatty acids
*Protein: 10% to 20% of total calories,
-Fiber: 25 -30g daily *
*Alcohol (inhibits gluconeogenesis): ↓BS
Limit to moderate amount
**(1-2 drinks/day [W=1 drink/M=1-2], drink w/ food,
do not omit regular meal
[12 oz= beer/15 oz= liquor/5 oz= wine]
EXERCISE PRECAUTIONS FOR DM
*Monitor glucose before, during, and after exercise
* *Exercise with elevated blood sugar levels (>250 mg/dL) &
*KETONES in urine should be AVOIDED (type 1 DM)
*↓ BS; Aids in weight loss; ↓ cardiovascular risk
-↓ insulin resistance and BG
-Insulin secretion normally decreases w/ exercise; it does not occur in patients on exogenous insulin
should eat a 15g carbohydrate snack before moderate exercise to prevent HYPOGLYCEMIA
* Glucose-lowering effect of exercise lasts up to 48 hours
* Effect of strenuous activity makes body perceive “stress” causing release of counter-regulatory hormones and temporary increased glucose; makes
condition worse
* Get medical clearance; start slowly and
progress to goal:
**Exercise stress test for patients > age 30 who have
2 or > risk factors is recommended
What are 4 ways to monitor Glucose/insulin Levels?
WHICH 2 ARE MAINLY FOR DM1 patients?
- Self-Monitoring Blood Glucose (SMBG) using at home device
- Continuous Glucose Monitoring System (CGMS) used by type 1 DM
- Urine Ketone Strips – Type 1 DM w/ Blood sugar ≥ 240 when under stress (illness/gestational DM) → [DKA]
- Hgb A1C – every 2-3 months (GOAL 5.6% or lower)
RAPID-ACTING INSULIN
GENERIC/TRADE (3)
ONSET, PEAK, DURATION
LISPRO (HUMALOG)
ASPART(NOVOLOG)
GLULISINE (APIDRA)
ONSET-10-30 MIN [INJECT within 15 min of meal]
PEAK: 30 MIN-3 HRS [1 HOUR]
DURATION: 3-5 HOURS [4-5 HOURS -PPT]
**Injected within 15 minutes of mealtime;
duration 4-5 hours
PREVENTS POST-MEAL HYPERGLYCEMIA
“15 minutes feels like an hour during 4 rapid responses”
SHORT-ACTING INSULINS (2)
ONSET, PEAK, DURATION
REGULAR (HUMULIN R, NOVOLIN R)
ONSET: 30 MIN-1 HOUR (Injected 30 to 45 min b4 meal)
PEAK: 2-5 Hours (2-4 hours PPT)
DURATION: 5-8 HOURS
Injected 30 to 45 minutes BEFORE meal; Peak 2-4 hrs
PREVENTS POST-MEAL HYPERGLYCEMIA
“Short-staffed nurses went from 30 patients to(2) 8 patients”
INTERMEDIATE-ACTING INSULIN (2)
ONSET, PEAK, DURATION
NPH (HUMULIN N, NOVOLIN N)
-NPH is cloudy and can be mixed w/ REGULAR OR SHORT → given at BEDTIME to control fasting AM BS
DONT SKIP LUNCH-INSULIN IS PEAKING
ONSET: 1.5-4 HOURS [2]
PEAK: 4-12 HOURS [8]
DURATION: 12-18 HOURS [16]
“Nurses Play Hero TO(2) EIGHT 16 year olds”
Long Acting Insulin (3)
ONSET, PEAK, DURATION
GLARGINE (LANTUS) [BASAL, “PEAKLESS”]
DETEMIR (LEVEMIR)
DEGLUDEC (TRESIBA)
DO NOT MIX LONG ACTING INSULINS
Onset 1&1/2 hrs [ppt]
*CLOSEST TO BODYS NATURAL INSULIN d/t peakless”
ONSET: 0.8-4 HOURS [2]
PEAK: BASAL, “PEAKLESS”, rarely to none peak
DURATION: 16-24 hours [24]
“The TWO LONG nursing shifts NEVER PEAKED but lasted 24 HOURS”
INHALED INSULIN (1)
ONSET, PEAK, DURATION
AFREZZA
RAPID ACTING, no COPD, $$$
ONSET:12-15 MIN RAPID ACTING
PEAK: 60 MIN [1 HOUR]
DURATION: 2.5-3 HOURS
INSULIN PUMP USE & TEACHING
Insulin pump use: continuous subQ insulin (rapid or regular) infusion at a basal rate and bolus before meal/ Change set and site every 2 to 3 days
Storage of insulin/rotating sites
In-use vials/pens may be left at room
temperature up to 4 weeks (28 days)
*Extra insulin/pens should be REFRIGERATED *
-Avoid exposure to direct sunlight, extreme heat or cold/
-No freezer
-Abdomen is preferred site
-Do not inject in site to be exercised *
-Systemic rotation within one
anatomical area –not to use the same
site more than once in a 2-3 week
period (to prevent lipodystrophy) *
-Inject 1 to 1.5” apart within the anatomical area
-Best place to inject is ABD → Arms → Thighs → Butt
Oral Antidiabetic Agents:
Manifestation/SE/Nursing Interventions/Education
Used for type 2 DM who require more than diet & exercise
- Major side effect: hypoglycemia
- Nursing interventions: monitor blood glucose for →hypoglycemia and other potential side effects
- Patient Education
- Combinations of oral drugs may be used
ORAL MEDICATIONS GIVEN FOR T2DM
[2 CLASSES, 4 MEDICATIONS]
*2nd - Gen Sulfonylureas → (MOA) stimulate beta cells to secrete insulin→ taken w/ meals, will ↓BS → HYPOGLYCEMIA
-Glipizide (Glucotrol)
-Glyburide (Micronase)
-Glimepiride (Amaryl)
*Biguanides → inhibits the production of glucose by the liver/ increase body tissue sensitivity to insulin
-Metformin (Glucophage)
2ND GEN SULFONYLUREAS
MOA/EDUCATION/SE
*2nd - Gen Sulfonylureas → (MOA) stimulate beta cells to secrete insulin→ taken w/ meals, will ↓BS → HYPOGLYCEMIA
*Glipizide (Glucotrol) → Beta-blockers (-olol) will mask hypoglycemic symptoms (double check BS)
*Glyburide (Micronase) → If mixed with alcohol → Disulfiram (Antabuse) effect → will make you sick
*Glimepiride (Amaryl) → Sulfa Allergy → Do not use
Biguanides -
Metformin (Glucophage):
[MOA/EDUCATION/SE]
*Biguanides → (MOA) inhibits production of glucose by liver/ increase body tissue sensitivity to insulin
*Produces GI issues → upset stomach w/diarrhea
*Lactic acidosis → metabolism changes from aerobic
to anaerobic producing lactic acid
*Monitor Kidney function d/t acute kidney failure from
metformin
- SE: GI disturbances (tests with iodine =
increase in LACTIC ACIDOSIS)
-Metformin and Iodinated contrast dyes leads →
lactic acidosis OR acute kidney failure [MONITOR KIDNEY]
Must STOP 48 hrs before/after PROCEDURES/SURGERIES until renal function returns to normal
-Iodine is naturally toxic → requires NPO → will cause diuretic effect + nephrotoxic agent
*Dehydration + iodine = kidney unable to filter lactic → Lactic Acidosis
Acute Complications of Diabetes (3)
o Hypoglycemia
o DKA
o Hyperglycemic hyperosmolar syndrome (HHS)
What is Morning Hyperglycemia (Insulin Waning)
and its treatment?
↑ BS from bedtime to morning
Tx: increase evening NPH/long-acting insulin or add a
dose of NPH before dinner
WHAT IS Somogyi Effects and its tx?
*Hypoglycemia around 2-3 am d/t a sudden drop in BS causes body to think it is stressed → cortisol, catecholamines released →
*Rebound morning hyperglycemia (7am)around 3 am a sudden drop in BS causes body to think it is stressed → cortisol, catecholamines released → by morning 7am, → sugar is really high (usually caused by too much NPH at bedtime)
*Tx: ↓ evening bedtime NPH dose or add a bedtime snack –
-Ask pt to wake up and record 2 or 3am blood sugar levels
Dawn Phenomenon
- Pre-breakfast hyperglycemia (5-8 AM) d/t nocturnal
growth hormone (*common in young adolescents);
*Treatment- change dinnertime NPH → bedtime,
↑ (NPH) the current dosage
Hypoglycemia MANIFESTATIONS
blood sugar lower than 70 → too much insulin, medication, exercise, or not enough food
*Adrenergic symptoms (mild <60) → sweating, tremors, tachycardia palpitations, nervousness, hunger
*Central nervous system (moderate <40) → inability to concentrate, headache, confusion, memory lapses,
slurred speech, drowsiness (all involve the head)
*Severe Hypoglycemia (severe <20) → disorientation, seizures, loss of consciousness, death
Hypoglycemic Unawareness
No warning signs/symptoms [ASYMPTOMATIC] until glucose level critically low
* R/T autonomic neuropathy and lack of counterregulatory hormones
Beta-adrenergic blocking agents
* Patients at risk→ elderly should keep blood glucose levels somewhat higher
Management of Hypoglycemia (ALERT PT.)
(15/15 RULE)
Give 15 g of fast-acting, concentrated carbohydrate
* Three or four glucose tablets/ 8 oz of low-fat milk
* 4 oz of juice or regular soda (not diet soda) =1/2 cup
* 6 saltine crackers/ 3 graham crackers *
Retest blood glucose in 15 minutes; retreat if < 70 mg/dL; (repeat 2 times if <70)
* If glucose remains low after 2 to 3 times; call HCP or EMS
*
*Treat with 25–50 mL 50% dextrose IV or glucagon 1 mg subQ or IM *
**Provide a snack with PROTEINS AND CARBS unless the patient plans to eat a meal within 30 to 60 minutes
Management of Hypoglycemia
(UNCONSCIOUS AND HOSPITAL/ER)
(15/15 RULE)
-If the patient cannot swallow or is unconscious:
* SubQ or intramuscular glucagon 1 mg
*May repeat in 10 min if pt remains unconscious
* If regain consciousness-
**Provide a snack with PROTEINS AND CARBS unless the patient plans to eat a meal within 30 to 60 minutes
- Hospital or emergency room: 25–50 mL *50% dextrose *(D50W) *solution IV
- Ensure IV patency (very irritating to vein)
CLINICAL S/S & MANIFESTATIONS OF
Diabetic Ketoacidosis (DKA)
*MOSTLY Type 1 DM PATIENTS *
**Hyperglycemia/Dehydration/Acidosis (Ketosis) **
↑BS ↑Ketones ↑Acidosis (with dehydration)= DKA
Manifestations include
polyuria, polydipsia, blurred vision, weakness,headache, anorexia,
abdominal pain (cramps), nausea, vomiting, diarrhea, acetone breath, hyperventilation with Kussmaul respirations and mental status changes, dry & warm skin (dehydration), sunken eyes.
SICK DAY RULES
- Physical and emotional stress causes increased glucose secondary to counterregulatory hormones
*Do not eliminate insulin doses when nausea and vomiting occur *
Frequent self-monitoring blood glucose - If glucose is greater than 240 mg/dL, check urine for ketones every 3 to 4 hours * Two consecutive glucose levels greater than 300 mg/dL or moderate to high urine
ketone levels should be reported to HCP
PT. EDUCATION ON SICK DAY RULE
ASSESSMENT OF DKA (LAB VALUES)
- Blood glucose levels *>300 *to 1,000
- Severity of DKA is not only due to blood glucose level
Ketoacidosis is reflected in low serum bicarbonate, low pH;
low PCO2 reflects respiratory compensation (Kussmaul’s respirations) * Ketone bodies in blood and urine++
↑BUN/Cr –↑due to dehydration [BUN 10-20]
↑ K+ = Acidosis (H+ ↑) – K+ leaves cell to exchange with H+ - hyperkalemia
-Electrolytes vary according to water loss and level of hydration
treatment for DKA
& what do you monitor for ?
Ensure patent airway; administer O2
Rehydration with IV fluid: VAD (Vascular Access Device) –0.9 NS (or 0.45 % saline) and when glucose level reaches 250 mg/dL, 5% to 10% dextrose is added to the fluid regimen to prevent hypoglycemia, as well as a
sudden drop in glucose that can be associated with cerebral edema.
Reverse acidosis
-IV continuous infusion (0.1 U/kg/hr) of regular insulin after bolus (10 Units)
Restoring electrolytes: hypokalemia is the major concern
-Note: rehydration leads to increased plasma volume and decreased K+,
insulin enhances the movement of K+ from extracellular fluid into the cells
Monitor
* Blood glucose and renal function/UO: restore urine output to 30 to 60 mL/hr
* EKG and electrolyte levels—K+–> cardiac monitoring
* VS, lung assessments, signs of fluid overload
Hyperglycemic Hyperosmolar Syndrome
HHS Caused by a *lack of sufficient insulin; ketosis
is minimal or absent *
* It often occurs in patients older than 60 years w/
type 2 diabetes
High mortality rate: often occurs in elderly with no known history of DM or
type 2 DM
Precipitating factors: UTIs, pneumonia, sepsis, acute illness, Newly diagnosed type 2 diabetes
Hyperglycemia (> 800 mg/dL) causes osmotic diuresis with loss of water and electrolytes; hypernatremia, and increased osmolarity occur with dehydration
and glycosuria
MANIFESTATIONS OF HHS
hypotension, profound dehydration, tachycardia,
and variable neurologic signs D/T cerebral dehydration
TREATMENT OF HHS (5)
same as DKA (insulin is not as critical)
Rehydration,
Insulin administration –less critical role in the treatment
*Monitor fluid volume and electrolyte status *
Correct underlying precipitating cause
Long-Term Complications of Diabetes
Tight glucose control can prevent/minimize complications
Macrovascular complications
* Accelerated atherosclerotic changes
CAD, CVA, PVD (peripheral vascular disease)
disease
* Microvascular complications: kidney and eyes
Diabetic retinopathy: Most common cause of new cases of
adult blindness -needs annual exam
Nephropathy: Leading cause of end-stage kidney disease-
B assess for microalbuminuria – if present, use ACE-I or ARB
Neuropathic changes- Tingling and numbness in extremities
* Peripheral neuropathy- Major risk for amputation
* Autonomic neuropathies - hypoglycemic unawareness, sexual dysfunction,
Gastroparesis (delayed gastric emptying), painless myocardial infarction, Neurogenic bladder (→ urinary retention)
Foot Complications
*Sensory neuropathy and PAD are major risk factors for amputation *
* Smoking increases risk
Sensory neuropathy → loss of protective sensation → unawareness of injury
* Monofilament screening (Pg. 1496- Figure 51-10) * Peripheral artery disease
* ↓ Blood flow, ↓ wound healing, ↑ risk for infection
Patient teaching to prevent foot ulcers
(***Chart 51-10-Foot Care)
* Proper footwear
* Avoidance of foot injury
* Skin and nail care
*Daily inspection of feet
* Prompt treatment of small problems
EDUCATION ON FOOT (10)
- control DM
- DAILY INSPECTION → use mirror to see bottom
- wash/ dry feet daily → dry between toes, warm water
- cream on bottom of feet → not between toes
- smooth corns/callus with pumice stone softly
- trim nails → straight across
- wear shoes/socks always → white socks, protect your feet (cotton socks) can see if its bleeding
- protect your feet from temp changes
- elevate your feet, do not cross your legs, wiggle toes, move your ankles
- report any injuries
Buy shoes in the afternoon when feet are more swollen, break in shoes slowly 2 or 3 hrs at a time to reduce the r/o blisters
Peripheral artery disease (PAD) Nursing Interventions (3)
- ↓ Blood flow, ↓ wound healing, ↑ risk for infection
EDUCATION ON Foot care
