Class 8: Endocrine Flashcards
Diabetes diagnostic studies (positive results)
-FBG ≥ 7 mmol/L
-Two-hour glucose level ≥11.1 mmol/L during 75 g oral glucose tolerance test (OGTT)
-Random glucose level ≥11.1 mmol/L
-A1C ≥ 6.5% (in adults)
Hemoglobin A1C test
-Useful in determining glycemic levels over time; amount of glucose attached to hemoglobin molecules over RBC life span (90-120 days)
-Regular assessments required
Ideal A1C test results
Ideal goal; Canadian Diabetes Association (CDA) ≤7.0%, normal range is <6.0%
Normal A1C does what
Reduces risks pathy’s: Retinopathy, nephropathy, and neuropathy
DM collaborative care
-Oral antihyperglycemic agents and noninsulin injectables
-ACEI or ARBs
-BP control; target is <130/80 mm Hg
-Drug therapy
DM collaborative care cont’d
-Exercise & nutritional therapy
-Teaching and follow-up programs
-Self monitoring of blood glucose (SMBG)
-Vascular protection
Drug therapy for DM
-Enteric-coated acetylsalicylic acid (ASA)
-Insulin
-Lipid-lowering drugs
Exogenous insulin
-MUST be used for Type 1 Diabetes; may be additional treatment for Type 2 Diabetes
-Always includes separate rapid/short acting + intermediate or long acting
Just bc a pt is on insulin…
Does not mean they have been diagnosed with type 1 diabetes
Preparations of rapid-acting (bolus) clear insulin
-Injected 0-15 minutes before meal
-Onset: 10-15 minutes, peak; 60- 90 min, duration; 3-5h
Preparations of short-acting (bolus) clear insulin
-Injected 30-45 minutes before meal
-Onset; 30-60 min, peak; 2-4h, duration; 5-8h
Preparations of intermediate-acting (basal) cloudy insulin
-BID; am & pm (not specific to meals)
-Onset; 1-3h, peak; 6-8h, duration; 12-16h
Preparations of long-acting (basal) insulin
-Injected OD at bedtime OR in the morning
-Onset; 1-2h, peak; none, duration; 24+h
-Released steadily and continuously, CANNOT be mixed with any other insulin or solution
Slide 9
Conflicts with slide 8…. Figure out which one is right
Rapid-acting (clear) insulins
-Novorapid, apidra & humalog
-NAH
Short acting (clear) insulins
-Humulin R, novolin GE, Toronto
Intermediate (cloudy) insulins
Humulin N, novolin GE NPH
Long acting (clear) insulin
Lantus
Long acting insulin
Levemir
Intermediate insulins are…
The only cloudy insulins
Insulin therapy regimens
-Basal-bolus; long-acting (basal) OD & rapid/short-acting (bolus) before meals
-Fixed combination insulins
-Sliding scale insulin dosing
Basal-bolus insulin…
Closely mimics endogenous insulin production
Premixed insulin (cloudy)
-Ratio of rapid/fast-acting to intermediate acting insulin: Humulin (rapid) 30/70 & novolin GE (fast acting) 30/70
-Not for Type 1 diabetes
Insulin therapy considerations
-Regimens should be adapted to tx goals, lifestyle, capacity and general health
Administration of insulin (routes)
-Cannot be taken PO
-SC injection for self-administration
-IV administration of Regular insulin ONLY
Administration of insulin (sites)
-Fastest absorption from abdomen, followed by arm, thigh, and buttock
-Abdomen is the preferred site
-Rotate injections within one particular site (think – checkerboard)
-Do not inject in site to be exercised
Administration of insulin (preparation)
No alcohol swab on site needed before injection (home therapy)
Slide 15 (checkerboard rotation)
Insulin syringe sizes
-1.0, 0.5 & 0.3 mL
-The 0.5mL size may be used for doses of 50 units or less, and the 0.3mL syringe can be used for doses of 30 units or less
-The 0.5mL & 0.3mL syringes are marked in 1-unit increments
Giving an insulin injection
-Wash hands with soap & water
-Do not recap needle
-45-90 degree angle (depending on fat)
Slide 18&19
Insulin pump
-Continuous SC infusion (basal rate)
-Potential for tight glucose control
PO hypoglycemic agents (OHA)
-Used for patients with type 2 diabetes, NOT type 1
-Patients may be on both OHA’s and insulin, but they will still be classified as a patient with Type 2 Diabetes
Insulin drug classes
-Sulfonylurea
-Alpha glucosidase inhibitor
-Biguanide
-Megltinide
-SABM
Biguanide
-Reduces production & output of sugar by the liver, acts on the liver
-Metformin
Sulfonylurea
-Promotes insulin secretion, acts on the pancreas
-Gliclazide, Glyburide & Chlopromaide
Megltinide
-Promotes insulin secretion, acts on the pancreas
-Regaglinide & nateglinide
Alpha glucosidase inhibitor
-Prevents breakdown of carbs and delays carb digestion, acts on the small intestine
-Acarbose & sitagliptin
Biguanide (metformin) MOA
-Decreases glucose production
-Lowers glucose absorption & enhances insulin receptor uptake
Biguanide (metformin) AE
GI upset & lactic acid
Biguanide (metformin) contraindications
-Hepatic & renal failure
-Respiratory insufficiency & hypoxemic conditions
-Alcohol abuse
Biguanide (metformin) does…
-NOT cause hypoglycemia
-Take with food
Biguanide (metformin) dosing
-250-2500 mg/day
-May be divided doses dependent on the patient’s needs
Sulphonylurea (liclazide, glyburide & glimepiride) MOA
-Stimulates beta cell insulin release
-Increases peripheral glucose utilization & insulin receptor sensitivity
-Decreases hepatic glucose production
Sulphonylurea (liclazide, glyburide & glimepiride) AE
-Hypoglycemia, weight gain, hyperinsulemia
-Caution with renal/liver dysfunction (reduce dose)
Sulphonylurea (liclazide, glyburide & glimepiride) dosing
-Take 30min before meals
Meglitinides (repaglinide) MOA
-Short acting secretagogue
-Binds to beta cell to stimulate insulin release at a different site than sulfonylureas
Meglitinides (repaglinide) rule of thumb
No meal, no dose; extra meal, extra dose (take 15 minutes before meal)
Meglitinides (repaglinide) AE
Weight gain & hypoglycemia
Meglitinides (repaglinide) interactions
Interacts with CYP 3A4
Alpha-Glucosidase Inhibitor (acarbose) MOA
Inhibits intestinal amylase and alpha-glucosidase, therefore delaying breakdown of complex carbohydrates and slows glucose absorption
Alpha-Glucosidase Inhibitor (acarbose) AE & cautions
-Flatulence, diarrhea & cramps
-Caution in patient with GI disorders
Alpha-Glucosidase Inhibitor (acarbose) administration considerations
-Not absorbed, decreased hypoglycemia (except with sulfonylureas)
-Take with first bite of food, no food no dose
Thiazolidinediones (glitazones): (pioglitazone & rosiglitazone) MOA
Enhances insulin sensitivity at the cell level
Thiazolidinediones (glitazones): (pioglitazone & rosiglitazone) AE
Hypertensive effect, headache, upper respiratory infection, anemia, edema & weight gain
Dipeptidyl Peptidase 4 (DPP-4) inhibitors (sitagliptin) MOA & AKA
-Also known as ‘gliptins’
-Delays breakdown of incretin hormones by inhibiting the enzyme DPP-4
-Reduces postprandial and fasting glucose concentrations
Dipeptidyl Peptidase 4 (DPP-4) inhibitors (sitagliptin) AE
Respiratory tract infection, headache & diarrhea
Combination therapy options
-Glyburide & metformin
-Avandamet (avandia and metformin)
Combination therapy MOA
-Increases effectiveness of drugs by targeting different sites at the same time
-Minimizes side effects because lower doses are used
Combination therapy considerations
May add up to 3-4 OHA’s before placing patient on insulin with/without OHA (primarily metformin)
Diabetic medication drug interactions
-Alcohol & sulfonylureas
-Arcabose & sulfonylureas
-Antihypertensives
-Beta-blockers
-Digoxin & propranolol
Diabetic medications + alcohol & sulfonylureas
-Disulfiram-like reaction (flushing, nausea, dizzines & tachycardia)
Diabetic medications + antihypertensives
-(Thiazides, furosemide & CCBS)
-Cause hyperglycemia
Diabetic medications + beta-blockers
-Mask hypoglycemia
Diabetic medications + beta-blockers
-Mask hypoglycemia
Diabetic medications + fibrates & cholestyramine
Cause hypoglycemia
Diabetic medications + digoxin or propanolol
-Decrease absorption of digoxin or propranolol
Diabetic medications + sulfonylureas & acarbose
-Causes hypoglycemia (treat with honey, dextrose tabs or milk)
General diabetes management
Diet, exercise & glucose monitoring
Type 1 DM nutritional therapy (total calories)
Increase in caloric intake possibly necessary to achieve desirable body weight and restore body tissues
Type 1 DM nutritional therapy (effect of diet)
Diet & insulin necessary for glucose control
Type 1 DM nutritional therapy (distribution of calories)
Equal distribution of carbohydrates through meals or adjustment of carbohydrates for insulin activity
Type 1 DM nutritional therapy (consistency of daily intake)
Necessary for glucose control
Type 1 DM nutritional therapy (uniform timing of meals)
Crucial for NPH insulin programs; flexibility with multidose rapid-acting insulin
Type 1 DM nutritional therapy (intermeal & bedtime snacks)
Frequently necessary
Type 1 DM nutritional therapy (nutritional supplement for exercise programs)
Carbohydrates 20 g/hr for moderate physical activities
Type 2 DM nutritional therapy (total calories)
Reduction in caloric intake desirable for overweight or obese patient
Type 2 DM nutritional therapy (effect of diet)
Diet alone possibly sufficient for glucose control
Type 2 DM nutritional therapy (distribution of calories)
Equal distribution recommended; low-fat diet desirable; consistency of carbohydrate at meals desirable
Type 2 DM nutritional therapy (consistency in daily intake)
Desirable for weight reduction and moderation of blood glucose levels
Type 2 DM nutritional therapy (uniform timing of meals)
Desirable but not essential, unless using insulin or sulphonylureas
Type 2 DM nutritional therapy (intermeal & bedtime snacks)
Based on patient’s eating habits and preferences; may be necessary if using insulin or sulphonylureas
Type 2 DM nutritional therapy (nutritional supplement for exercise programs)
May be necessary if patient’s blood glucose levels are controlled on sulphonylureas or insulin
Slide 36
Food composition
-Protein; 15-20% of energy
-Fat: <35% of energy
-Fibre
-Carbohydrates: 45-60% of energy
Diabetic neuropathy + protein
Limit intake to 15% of energy & closely monitor
Saturated & trans-fatty acids
Should be reduced to less than 7% of energy intake
Polyunsaturated fat
Should be limited to 10% of energy intake
Fibre intake
25-50g/day
Carbohydrates
-Pts should try to consume high fibre carbohydrates
-<10% of energy intake should come from sucrose
-Low carbohydrate diets are not recommended for DM management
Glycemic index (slide 38)
-Low GI (55 or less); great
-Medium GI (56-69); okay
-High GI (70 or more); not great
Basic carb counting
-Make healthy choices, focus on the carbohydrate, set carbohydrate goals
-Determine carbohydrate content
-Monitor effect on BG
Slide 40 & 41
Continuous glucose monitoring
Updates every 1-5 minutes, helps identify patterns
Slide 45
Nursing care of DM
-Foot care, BP & cholesterol monitoring
Hypoglycemia
<4mmol/L
Manifestations of hypoglycemia
-Confusion, irritability, diaphoresis, tremors
-Hunger, weakness & visual disturbances
Untreated hypoglycemia can…
Progress to loss of consciousness, seizures, coma, and death
Hypoglycemia unawareness
-Person does not experience usual warning signs
-R/t autonomic neuropathy
-Unsafe for patients with risk factors for hypoglycemic unawareness to aim for tight blood glucose control because a major drawback of intensive treatment is hypoglycemia
Those at risk for hypoglycemia unawareness
Elderly patients and patients who use β-adrenergic blockers
Causes of acute hypoglycemia
Mismatch in timing of meals and peak action of medications
At the first sign of acute hypoglycemia
-Check BG
-If <4 mmol/L, begin treatment
-If >4 mmol/L, investigate further for cause of S&S
-If monitoring equipment not available, treatment should be initiated
Acute hypoglycemia tx
-15-20g of a simple carbohydrate, 175 mL of fruit juice, or a soft drink
-Check BG 15 min after & again in 45 min
-Repeat until BG >4mmol/L
Acute hypoglycemia tx considerations
-Avoid foods with fat as they decrease absorption of sugar
-Patient should eat regularly scheduled meal/snack to prevent rebound hypoglycemia
Acute hypoglycemia tx if pt cannot swallow
-1 mg of glucagon IM or SC; side effect: rebound hypoglycemia
-Have patient ingest a complex carbohydrate after recovery
-20-50 mL of 50% dextrose IV push in acute care settings
Pediatric considerations of hypoglycemia
-Children are often able to detect the onset of hypoglycemia; some are too young to implement treatment
-Parents should be able to recognize the onset of symptoms
-Give children 10-15mg simple carbs
-Illness can alter diabetes management; insulin requirements may increase or decrease
DKA
-Caused by profound deficiency of insulin
-Most likely to occur in Type 1 DM
Precipitating factors of DKA
-Illness, infection, inadequate insulin dosage, undiagnosed type 1, poor self-management or neglect
DKA pathophysiology
-Insufficient insulin prevents glucose from being used for energy
-Body breaks down fat & ketones are a by-product of fat metabolism
Ketones
-Alter pH balance, causing metabolic acidosis
-Ketone bodies are excreted in urine
-Electrolytes become depleted
DKA manifestations
-Lethargy/weakness (early symptoms)
-Dehydration (tachycardia)
-Abdominal pain (anorexia & vomiting)
-Kussmaul respirations (rapid deep breathing to reverse metabolic acidosis, sweet fruity odor)
Management of DKA
-Airway; O2
-Correct fluid & electrolytes; NaCl restores urine output & raises BP
-When BG levels approach 14 mmol/L (downward); 5% dextrose
-K+ replacement & Na+ bicarbonate
Acute management of DKA + insulin therapy
-Witheld until fluid resuscitation has begun
-Bolus followed by regular insulin drip
Pediatric considerations of DKA
-Children should be admitted to PICU
-Priorities = IV access
-Aim to decrease BG by 2.8-5 mmol/L per hour, keep BG 6.7-13.3mmol/l
-Cardiac and neuro monitoring: Risk of cerebral edema; caution with rehydration & risk of hypokalemia; watch for ecg changes
Pediatric considerations of DKA cont’d
-After acute period of DKA is over, goal is regulating insulin dosage in relation to diet and activity
-In children, often presentation with DKA is the first diagnosis of diabetes
Hyperosmolar hyperglycemic syndrome (HHS)
-Life-threatening syndrome, less common than DKA
-Often occurs in patients older than 60 years with type 2 DM
-Pt has enough circulating insulin that ketoacidosis does not occur, fewer symptoms in earlier stages
-Neurological manifestations occur because of ↑ serum osmolality
HHS common etiology’s/hx
-Inadequate fluid intake
-Increasing mental depression
-Polyuria
HHS lab values
-BG >34 mmol/L
-Increase in serum osmolality
-Absent/minimal ketone bodies
HHS is a…
-Medical emergency with a high mortality rate
HHS therapy
-Similar to DKA except HHS requires greater fluid replacement
Nursing management of DKA/HHS (administration)
-IV fluids, insulin & electrolytes
Nursing management of DKA/HHS (assessment)
-Renal & cardiopulmonary status
-Cardiac & VS monitoring
-LOC, signs of potassium imbalance
Incretin
-A group of metabolic hormones that augment the secretion of insulin
