Module 8: Diabetes Flashcards

Question

Insulin Administration

Answer 1

Given by subcutaneous injection * Avoid IM—risk of hypoglycemia  Regular insulin may be given IV  Cannot be taken orally—inactivated by gastric fluids Steps for insulin injection  Absorption is fastest from abdomen, followed by arm, thigh, and buttock  Abdomen is often preferred site  Do not inject in site that will be exercised  Rotate injections within and between sites U100 insulin—1 mL contains 100 U of insulin; must be used with U100-marked syringe  Syringes marked for units  0.3 and 0.5 mL syringes have 1 U increments  1 mL syringe has 2 U increments  Needle sizes vary in length and gauge  6 mm (½ in), 8 mm (5⁄16 in), and 12.7 mm (½ in)  Administer at 90 degrees  Extremely thin or muscular at 45 degrees Self-injection * Only user recaps syringe * No alcohol swab; wash with soap and water * In hospital, follow policy to cleanse site  Insulin pen * Portable, convenient, compact, discrete * Various lengths and gauges * Good option for patients with decreased vision * Patient education and printed instructions

Answer 2

Continuous subcutaneous infusion of rapid-acting insulin  Small device connected to a catheter inserted into subcutaneous tissue in abdominal wall  Some pumps are tubing-free  Change set and site every 2 to 3 days  Program basal and bolus doses that increase or decrease throughout the day based on carbohydrate intake, activity, or illness  Check glucose 4 to 8x/day or continuous monitoring Major advantage—keeps glucose in a tighter range; avoid highs and lows  Careful programming and constant monitoring makes it possible as delivery is similar to normal physiologic pattern  More flexibility with meals and activities Potential concerns of insulin pump  Infection at insertion site  Risk for DKA  Cost of pump and supplies  Attached to a device

Answer 3

 Hypoglycemia  Allergic reactions -Local or systemic (rare) -Other: preservative or latex or rubber stopper  Lipodystrophy—Changes in subcutaneous tissue -Atrophy—wasting of subcutaneous tissue; indentations -Hypertrophy—thickening of subcutaneous tissue -Overuse of site; alters absorption of insulin Somogyi effect  High dose of insulin causes decreased glucose during the night  Release of counterregulatory hormones causes rebound hyperglycemia * Danger of this effect: when glucose checked in the morning and increased insulin is given * Determine if Somogyi effect by checking glucose between 2 to 4 A.M.  Assess patient for headache, night sweats, or nightmares  Treatment is a bedtime snack, reducing the dose of insulin, or both Dawn phenomenon  Morning hyperglycemia present on awakening  May be due to release of counterregulatory hormones in predawn hours * Growth hormone and cortisol * More severe in adolescence and young adulthood—peak time for growth hormone  Treatment is increase in insulin or adjustment of administration time

Answer 4

Afrezza  Rapid-acting inhaled insulin  Administered at beginning of each meal or within 20 minutes after starting a meal  Used in combination with long-acting insulin for type 1 DM  Common adverse reactions: hypoglycemia, cough, throat pain or irritation  Not recommended for treatment of DKA, smokers; patients with asthma or COPD due to risk of bronchospasm

Answer 5

Work to improve the mechanisms by which the body makes and uses insulin and glucose  Work on 3 defects of type 2 DM -Insulin resistance -Decreased insulin production -Increased hepatic glucose production  Can be used in combination

Answer 6

Metformin (Glucophage)  Most effective 1st line treatment for type 2 * Available as immediate release, extended release, liquid forms  Action: reduces glucose production by liver  Enhances insulin sensitivity  Improves glucose transport  May cause weight loss  Used in prevention of type 2 diabetes Withhold if patient is undergoing surgery or radiologic procedure with contrast medium  24-48 hrs before and at least 48 hrs after when serum creatinine WNL Contraindications  Renal, liver, cardiac disease; lactic acidosis  Iodine based contrast medium can cause AKI  Excessive alcohol intake

Answer 7

Action: Increases insulin production from pancreas  Major side effect: hypoglycemia Examples:  Glipizide (Glucotrol)  Glyburide (Glynase)  Glimepiride (Amaryl)

Answer 8

Action: Increases insulin production from pancreas  Rapid onset: Decreases risk of hypoglycemia Examples:  Repaglinide (Prandin)  Nateglinide (Starlix)

Answer 9

“Starch blockers”  Slow down absorption of carbohydrate in small intestine  Take with first bite of each meal  Check 2-hour postprandial glucose to determine effectiveness Examples:  Acarbose (Precose)  Miglitol (Glyset)

Answer 10

“Insulin sensitizers”  Most effective in those with insulin resistance  Improve insulin sensitivity, transport, and utilization at target tissues Examples:  Pioglitazone (Actos)  Rosiglitazone (Avandia)  Rarely used because of adverse effects

Answer 11

Incretin hormones  Increases insulin synthesis and release from pancreas and decreases hepatic glucose production  Levels increase after a meal  Action: DDP-4 inhibitors block action of DDP-4- inactivates incretin hormones  Examples (“gliptins”) * Alogliptin (Nesina) * Sitagliptin (Januvia) * Saxagliptin (Onglyza) * Sitagliptin (Januvia)

Answer 12

Action: block reabsorption of glucose by kidney  Increase urinary glucose excretion Examples:  Canagliflozin (Invokana)  Dapagliflozin (Farxiga)  Empagliflozin (Jardiance)

Answer 13

Bromocriptine (Cycloset)—improves glucose levels  Mechanism of action unknown; the thought is that patients with type 2 diabetes have low levels of dopamine that may interfere with the body’s ability to control glucose  Action: increases dopamine receptor activity  Alone or in combination with other type 2 DM treatments

Answer 14

Combine 2 different classes of DM medications in one pill  Advantage- fewer pills for patient to take

Answer 15

Action: simulate glucagon-like peptide–1 (GLP-1); one of the incretin hormones  Increase insulin synthesis and release  Inhibit glucagon secretion  Slow gastric emptying  Increases satiety, reduces food intake  Monotherapy or adjunct therapy for type 2 who don’t achieve optimal glucose levels on OAs (oral agents) Administered by subcutaneous injection in prefilled pen; frequency varies by medication Examples:  Albiglutide (Tanzeum)  Dulaglutide (Trulicity)  Exenatide (Byetta)  Exenatide ER (Bydureon)  Liraglutide (Victoza)  Lixisenatide (Adlyxin)  Semaglutide (Ozempic)

Answer 16

Incretin hormones are a group of metabolic hormones that significantly decrease blood glucose levels by augmenting the secretion of insulin from the pancreas after eating, even before blood glucose levels become elevated. They also slow the rate of absorption of nutrients into the blood stream by reducing gastric emptying and may directly reduce food intake. The two most well-known incretins are Glucagon-like peptide-1 (GLP-1) and Gastric inhibitory polypeptide (GIP), also known as glucose-dependent insulinotropic polypeptide. Functions of Incretin Hormones Stimulate Insulin Secretion: Incretins enhance the secretion of insulin by the pancreas in a glucose-dependent manner, meaning the stimulation of insulin release is more pronounced when glucose levels in the blood are high. This helps to prevent the overproduction of insulin and reduces the risk of hypoglycemia (low blood sugar levels). Inhibit Glucagon Secretion: In addition to promoting insulin release, incretins help regulate blood glucose levels by inhibiting the secretion of glucagon, a hormone that increases blood glucose levels by stimulating glucose production in the liver. Slow Gastric Emptying: Incretins slow down the rate at which the stomach empties its contents into the small intestine, leading to a slower absorption of glucose into the bloodstream. This helps prevent spikes in blood glucose levels following meals. Reduce Appetite: Some incretins, particularly GLP-1, can decrease appetite and promote satiety, contributing to weight management in individuals with obesity or type 2 diabetes. GLP-1 Receptor Agonists: These are synthetic versions of GLP-1 or compounds that mimic the action of GLP-1, enhancing insulin secretion, suppressing glucagon release, and often leading to weight loss. They are administered via injection. Dipeptidyl Peptidase-4 (DPP-4) Inhibitors: These oral medications work by inhibiting the enzyme DPP-4, which breaks down incretin hormones. By preventing the breakdown of GLP-1 and GIP, DPP-4 inhibitors extend the action of these endogenous incretins.

Answer 17

Amylin—hormone secreted by beta-cells in response to food intake  slows gastric emptying, reduces postprandial glucagon secretion, and increases satiety Example  Pramlintide (Symlin) * Used concurrently with mealtime insulin but can’t mix together in same syringe; decreased bolus insulin dose  Administer before meals with at least 250 cal  Watch for severe hypoglycemia ~ 3 hours after injection; have fast-acting glucose available

Answer 18

Drug interactions can potentiate hypoglycemia and hyperglycemia effects  Examples: * beta-adrenergic * Thiazide and loop diuretics

Answer 19

Registered dietitian with expertise in diabetes management  Others: nurses, CDEs, CNS, social worker, HCPs ADA guidelines  Person with DM can eat the same foods as without DM  Overall goal: Achieve and maintain safe and healthy glucose levels  Prevent or reduce the risk of complications  Achieve lipid profiles and BP that reduce risk for CVD  Prevent or slow development of chronic complications  Individual needs; personal, cultural preferences  Maintain pleasure of eating with healthy choices To have flexibility - rapid-acting insulin, multiple daily injections, insulin pump (for Type 1) -Moderate weight loss improves insulin sensitivity; appropriate serving sizes, reduced trans/saturated fats, regular exercise; monitor A1C, lipids, BP (type 2) -Fiber helps control glucose levels -20-35% total calories from fat *Healthy fats come from plants (nuts, seeds, avocado) Alcohol -inhibits gluconeogenesis from liver, can cause severe hypoglycemia -eat carbs when drinking

Answer 20

-Carb counting, track # of carbs per meal -Serving size, typically 15g CHO, 45-60g per meal -Insulin dose based on number of g; example: 1 unit per 15 g CHO *teach patient to read labels and serving sizes -My Plate guidelines; 1/2 non starchy veggies, 1/4 starch, 1/4 protein

Answer 21

At least 150 min/week moderate intensity Strength 3x week Decreases insulin resistance and glucose levels Weight loss Reduce need for DM drugs (type 2)  Reduce triglycerides and LDL , ↑ HDL  Decrease BP and improve circulation Be careful that physical activity can cause hypoglycemia **exercise 1 hour after a meal or have a 10-15g CHO snack first **carby snack every 30 min to prevent hypoglycemia **Effects of glucose lowering can last up to 48 hours after exercise **Carry fast acting source of carbs -If you're frequently hypoglycemic after exercise, talk to provider about decreasing meds **Strenuous exercise is perceived as stress by the body, temporarily increases glucose levels **For type 1 - delay activity if glucose is over 250mg/dl and ketones are present in urine, will make it worse

Answer 22

Before meals 2 hours after first bite suspected hypoglycemia q 4 hours during illness before and after exercise

Answer 23

a serious complication of diabetes mellitus, most commonly type 2 diabetes. It is characterized by extremely high blood glucose levels, significant dehydration, and an increased serum osmolality, without the significant ketoacidosis typically seen in diabetic ketoacidosis (DKA), which is more common in type 1 diabetes. Key Features of HHS Severe Hyperglycemia: Blood glucose levels in HHS can exceed 600 mg/dL (33.3 mmol/L), and in extreme cases, can reach 1000 mg/dL (55.5 mmol/L) or even higher. Dehydration: Patients with HHS experience profound dehydration due to osmotic diuresis caused by high blood glucose levels, leading to increased urination and loss of fluids and electrolytes. Increased Serum Osmolality: Osmolality, a measure of the solute concentration in the blood, is significantly increased in HHS, often exceeding 320 mOsm/kg. This hyperosmolarity leads to the movement of water out of cells, exacerbating dehydration. Absence of Significant Ketoacidosis: Unlike DKA, HHS patients have minimal or no ketonemia and acidosis. This is because even the small amount of insulin present in most type 2 diabetes patients is enough to prevent ketone body production but not enough to control blood glucose levels. Symptoms and Signs Symptoms of HHS develop over days to weeks and may include: Extreme thirst and dry mouth Increased urination Weakness Confusion or altered consciousness, possibly progressing to coma Seizures (in severe cases due to extreme hyperosmolarity) Risk Factors HHS is often precipitated by a stressor in individuals with compromised fluid intake or increased fluid loss. Common precipitating factors include: Infections (e.g., pneumonia, urinary tract infections) Acute illness Medications that impair glucose tolerance (e.g., corticosteroids) Inadequate fluid intake Poorly managed or undiagnosed diabetes Treatment The management of HHS involves: Rapid Rehydration: Administration of intravenous fluids to correct dehydration and reduce blood glucose levels. Insulin Therapy: Low-dose insulin to gradually reduce blood glucose levels, avoiding rapid shifts in osmolality that can lead to cerebral edema. Electrolyte Replacement: Particularly potassium, as levels may drop rapidly once insulin therapy is initiated and osmotic diuresis decreases. Treatment of Precipitating Causes: Such as antibiotics for infections. Monitoring: Close monitoring of vital signs, fluid balance, blood glucose levels, electrolytes, and mental status. Management similar to DKA  IV insulin and NaCl infusions * Add dextrose when glucose levels ~ 250 mg/dL  More fluid replacement needed * Hemodynamic monitoring to avoid overload  Monitor: fluid and electrolytes (*K+), serum osmolality, VS, I &O, skin turgor, neuro, renal, and cardiac status  Correct underlying precipitating cause

Answer 24

-Caused by huge insulin deficiency Characterized by  Hyperglycemia  Ketosis  Acidosis  Dehydration  Most likely to occur in type 1 DM  May occur in people with type 2 DM with severe illness or stress Precipitating factors:  Illness  Infection  Inadequate insulin dosage  Undiagnosed type 1 DM  Lack of education, understanding, or resources  Neglect Insulin deficiency  Body burns fat as fuel source  By-product of fat metabolism—acidic ketones alter pH (metabolic acidosis)  Ketones excreted in urine along with electrolytes (cations)  Impairs protein synthesis, causes protein degradation resulting in nitrogen loss from tissues Insulin deficiency  Stimulates glucose production from amino acids in liver leading to further hyperglycemia  Hyperglycemia may cause osmotic diuresis Without treatment:  Severe depletion of sodium, potassium, chloride, magnesium, and phosphate  Acidosis  vomiting and further fluid and electrolyte losses Hypovolemia followed by shock may cause renal failure, causing retention of ketones and glucose and further acidosis  Dehydration, electrolyte imbalance, and acidosis causes coma and if not treated, death

Answer 25

Dehydration  Dry mucous membranes  Tachycardia  Orthostatic hypotension Early: Lethargy and weakness As progresses:  Skin dry and loose; eyes soft and sunken  Abdominal pain, anorexia, nausea/vomiting  Kussmaul respirations  Sweet, fruity breath odor (acetone)  Glucose level of greater than or equal to 250 mg/dL  Blood pH lower than 7.30  Serum bicarbonate level less than 16 mEq/L  Moderate to high ketone levels in urine or serum

Answer 26

-Less severe - outpatient -Hospitalization: Severe fluid and electrolyte imbalance, fever, nausea/vomiting, diarrhea, altered mental state, cause of DKA  Ability to communicate with health care provider every few hours Emergency management  Ensure patent airway; administer O2  Establish IV access; begin fluid resuscitation to replace extracellular and intercellular fluid and correct electrolyte balance * NaCl 0.45% or 0.9%; add 5% to 10% dextrose when glucose level approaches 250 mg/dL * Restore urine output to 30 to 60 mL/hr  Protect from cerebral edema; monitor for fluid overload, renal or cardiac compromise Monitor and replace potassium before starting insulin therapy; drives K+ into cells leading to hypokalemia; potentially life-threatening  IV regular insulin drip 0.1 U/kg/hr to correct hyperglycemia and ketosis * 36 to 54 mg/dL/hr drop in serum glucose will avoid complications

Answer 27

Too much insulin in proportion to glucose in the blood  Glucose level < 70 mg/dL  Neuroendocrine hormones released  Autonomic nervous system activated  Epinephrine released Common manifestations  Shakiness  Palpitations  Nervousness  Diaphoresis  Anxiety  Hunger  Pallor Altered mental function—“neuroglycopenia”  Difficulty speaking  Visual disturbances  Stupor  Confusion  Coma  Mimics alcohol intoxication  Untreated hypoglycemia can progress to loss of consciousness, seizures, coma, and death Hypoglycemia unawareness  No warning signs/symptoms until glucose level critically low * Incoherent, combative, loss of consciousness  Related to diabetes-related autonomic neuropathy and secretion of counterregulatory hormones  Patients at risk should keep glucose levels somewhat higher Causes  Too much insulin or oral hypoglycemic agents  Too little food  Delaying time of eating  Too much exercise  Usually occurs at peak time for meds or with disruption in daily routine  Symptoms can also occur when high glucose level falls too rapidly

Answer 28

Check glucose level  If less than 70 mg/dL, begin treatment  If greater than 70 mg/dL, investigate further for cause of signs/symptoms  If monitoring equipment not available, treatment should be initiated Treatment: Rule of 15  Consume 15 g of a simple carbohydrate * Fruit juice or regular soft drink, 4 to 6 oz * Commercial products; gels or tablets  Recheck glucose level in 15 minutes * Repeat if still < 70 g/dL; if remains low after 2 to 3x, contact HCP * If glucose stable; give carb and protein  Avoid foods with fat; slows glucose absorption  Avoid overtreatment Treatment in Acute Care Settings Treatment in acute care settings * 50% dextrose 20 to 50 mL IV push  Patient not alert enough to swallow or no IV access; also teach family/caregiver * Glucagon 1 mg IM or subcutaneously  Watch for nausea; prevent aspiration  May not be effective with alcohol-related liver disease, starvation or adrenal insufficiency  Explore reason why occurred

Answer 29

-chronic disease of blood vessels, generic -caused by chronic hyperglycemia Leading cause of diabetes-related death  68% CVD and 16% stroke age 65 and older  2 categories  Macrovascular  Microvascular complications Theories of how chronic hyperglycemia damages cells and tissues:  Accumulation of damaging by-products of glucose metabolism (e.g. sorbitol) is associated with damage to nerve cells  Formation of abnormal glucose molecules in the basement membrane of small blood vessels that circulate to the eyes and kidneys  Derangement in RBC function results in decreased tissue oxygenation

Answer 30

Diseases of large and medium-sized blood vessels  Cerebrovascular disease  Cardiovascular disease  Peripheral vascular disease Greater frequency and earlier onset in patients with diabetes  Women 4 to 6x risk for CVD  Men 2 to 3x risk for CVD those without DM Thickening of vessel membranes in capillaries and arterioles from chronic hyperglycemia Areas most affected  Eyes—retinopathy  Kidneys—nephropathy  Nerves—neuropathy

Answer 31

Decrease and treat CVD risk factors  Obesity—nutrition and exercise  Smoking—blood vessel disease, stroke and lower extremity amputation; cessation  Hypertension—optimize BP; decrease CV and renal disease  High fat intake/dyslipidemia; statin and lifestyle interventions  Sedentary lifestyle—exercise

Answer 32

Microvascular damage to retina due to chronic hyperglycemia, nephropathy, and HTN  Most common cause of new cases of adult blindness Two classifications  Nonproliferative- more common  Proliferative- more severe Nonproliferative  Partial occlusion of small blood vessels in retina causes microaneurysms  Weakened walls cause fluid leaks resulting in edema and eventually hard exudates or hemorrhages  Mild to severe loss of vision * Retina (macula) involvement—severe Proliferative  Involves retina and vitreous  Retinal capillary occlusion results in compensation with new blood vessels formed (neovascularization)very fragile and bleed easily * Patient see black or red spots or lines  Can cause retinal detachment * Macula involvement causes vision loss  Glaucoma and cataracts can also occur Initially no changes in vision  Annual eye exam with dilation to monitor  Maintain healthy glucose levels and manage hypertension Treatments  Laser photocoagulation * Most common * Laser destroys ischemic areas of retina  Vitrectomy * Aspiration of blood, membrane, and fibers inside the eye  Iluvien * injectable micro-insert that delivers corticosteroids flucinolone acetonide for 36 months  Vascular endothelial growth factor (VEGF) blocking drugs—reduce inflammation

Answer 33

Damage to small blood vessels that supply the glomeruli of the kidney  Leading cause of end-stage renal disease in U.S.  20% to 40% of people with diabetes have it Risk factors  Hypertension  Genetics  Smoking  Chronic hyperglycemia Annual screening for albuminuria and albumin-to-creatinine ratio  If albuminuria present, drugs to delay progression * ACE inhibitors or angiotensin II receptor blockers  Control of hypertension and glucose levels in a healthy range is imperative

Answer 34

Nerve damage due to metabolic imbalances of diabetes  60% to 70% of patients with diabetes have some degree of neuropathy  Sensory neuropathy—most common * Loss of protective sensation in lower extremities, results in increased risk of amputation * 60% of nontraumatic amputation is related to diabetes  Screen * Type 2— time of diagnosis * Type 1— 5 years after diagnosis Theory: persistent hyperglycemia causes accumulation of sorbitol and fructose that damages nerves  Reduced nerve conduction and demyelination  Ischemic damage to peripheral nerves  May precede, accompany, or follow diagnosis Classifications  Sensory or autonomic

Answer 35

Distal symmetric polyneuropathy  Most common form  Affects hands and/or feet bilaterally; “stocking-glove neuropathy”  Loss of sensation, abnormal sensations, pain, and paresthesias * Pain—burning, cramping, crushing, tearing; worse or only occurs at night Paresthesias— tingling, burning, itching; “walking on pillows or numb feet;”  Hyperesthesia  Complete or partial loss of sensitivity to touch or temperature is common  Foot injury and ulcerations may occur without patient ever having pain  Small muscles of hands and feet may be affected causing deformity and limited fine movement Treatment  Managing glucose levels  Drug therapy * Topical creams * Tricyclic antidepressants * Selective serotonin and norepinephrine reuptake inhibitors * Antiseizure medications * Pregabalin

Answer 36

Can affect nearly all body systems and lead to * Hypoglycemic unawareness, bowel incontinence and diarrhea, and urinary retention  Gastroparesis can cause: * Delayed gastric emptying resulting in anorexia, nausea, vomiting, GERD, feeling full, hypoglycemia  Cardiovascular abnormalities * Postural hypotension/falls, resting tachycardia, painless myocardial infarction Sexual function * Erectile dysfunction—often first manifestation * Decreased libido * Vaginal infections  Neurogenic bladder can cause urinary retention * Empty frequently, use Credé’s maneuver * Cholinergic agonist drugs * Self-catheterization

Answer 37

Microvascular and macrovascular diseases increases risk for injury and infection  Sensory neuropathy and PAD are major risk factors.  Other factors clotting abnormalities, impaired immune function, autonomic neuropathy  Smoking increases risk Sensory neuropathy may cause loss of protective sensation (LOPS) prevents awareness of injury; major risk factor for amputation  Peripheral artery disease (PAD)  Decreased blood flow = decreased O2, WBCs, and nutrients causes longer wound healing, increased risk for infection Patient teaching: Foot care  Proper footwear  Avoidance of foot injury  Skin and nail care  Daily inspection of feet  Prompt treatment of small problems  Diligent wound care for foot ulcers  Neuropathic arthropathy (Charcot’s foot) -Joint dysfunction and footdrop may cause ulcers

Answer 38

Diabetic dermopathy—most common * Red-brown, round or oval patches * Scaly then flat and indented; shins  Acanthosis nigricans—manifestation of insulin resistance * Velvety light brown to black skin thickening; flexures, axillae, and neck  Necrobiosis lipoidica diabeticorum * Red-yellow lesions; atrophic skin, shiny and transparent

Answer 39

Defect in mobilization of inflammatory cells and impaired phagocytosis  Recurring or persistent infections * C. albicans, boils, and furuncles; cystitis  Antibiotics—prompt and vigorous  Patient teaching to prevent infection  Hand hygiene, avoid exposure  Flu and pneumococcal vaccine