Endocrine Refresh VOCABULARY Flashcards
Page 1
- Endocrine Refresh
- NR325
Page 2
- Endocrine System components listed
- Parathyroid Gland
- Adrenal Gland
- Kidney
- Stomach
- Brain
- Thyroid Gland
- Skin
- Hypothalamus
- Testicle
- Liver
- Pineal Gland
- Pituitary Gland
- Thymus
- Uterus
- Ovary
- Pancreas
Page 3
- Pituitary Gland Hormones (Anterior Pituitary Gland)
- Adrenocorticotropic hormone (ACTH)
- Follicle-stimulating hormone (FSH)
- Luteinizing hormone (LH)
- Growth hormone (GH), or somatotropin
- Melanocyte-stimulating hormone (MSH)
- Thyroid-stimulating hormone (TSH), or thyrotropin
- Target Tissues & Functions
- ACTH → Adrenal cortex
- FSH & LH (Gonadotropic hormones) → Reproductive organs
- GH → All body cells
- MSH → Melanocytes in the skin
- TSH → Thyroid gland
- Specific Functions
- Growth of the adrenal cortex; corticosteroid secretion
- Secretion of sex hormones resulting in reproductive organ growth; reproductive processes
- Promotes growth and tissue repair
- Increases melanin production in melanocytes making skin darker
- Stimulates milk production in lactating women; increases response of follicles to LH and FSH; stimulates synthesis and release of thyroid hormones
- Posterior Pituitary Gland Hormones
- Antidiuretic hormone (ADH)
- Oxytocin
- Target tissues/functions
- ADH → Renal tubules; promotes water reabsorption from renal tubules; vascular smooth muscle effects
- Oxytocin → Uterus; Mammary glands; stimulates uterine contractions and milk secretion
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- Thyroid Gland & Parathyroid Gland Hormones
- Hormones
- Calcitonin (thyroid) → Bone tissue; regulates serum calcium and phosphorus (lowers serum Ca)
- Thyroxine (T4) (thyroid) → All body tissues; precursor to T3
- Triiodothyronine (T3) (thyroid) → All body tissues; regulates metabolic rate
- Parathyroid hormone (PTH), or parathormone (parathyroid) → Bone; intestines; kidneys; regulates cell growth and tissue differentiation; increases serum Ca; promotes bone demineralization; increases intestinal absorption of Ca
- Note on relationship: Calcitonin lowers serum Ca; PTH raises serum Ca
Page 5
- Adrenal Gland Hormones and Tumors
- Hormones
- Epinephrine (adrenaline)
- Norepinephrine (noradrenaline)
- Androgens and estradiol
- Corticosteroids
- Mineralocorticoids
- Adrenal Gland Tumors (catecholamine-secreting or steroid-secreting tumors)
- Target Tissues & Functions (summary interpretation)
- Epinephrine → Reproductive organs (generalized SNS effect when stressed)
- Norepinephrine → All body tissues (SNS support)
- Androgens and estradiol → Kidney (androgenic effects) and secondary sexual characteristics (context from content)
- Corticosteroids (glucocorticoids) → Adrenal cortex functions: promote growth during adolescence; anti-inflammatory properties; regulate metabolism; respond to stress
- Mineralocorticoids (e.g., aldosterone) → Regulate sodium and potassium balance and water balance; influence blood volume and pressure
- Adrenal Gland Tumors
- Can cause excess catecholamines or steroids depending on tumor type
- General emphasis from the page
- Catecholamines increase in response to stress and enhance/prolong SNS effects
- Adrenal cortex hormones (corticosteroids) support stress, metabolism, growth, and immune modulation; mineralocorticoids regulate electrolyte/water balance
Page 6
- Pancreatic Hormones and their targets/functions
- Amylin (from beta cells) → Pancreas; targets Liver and Stomach
- Function: decreases gastric motility; decreases glucagon secretion; decreases endogenous glucose release from the liver; increases satiety
- Glucagon (from alpha cells) → General
- Function: stimulates glycogenolysis and gluconeogenesis
- Insulin (from beta cells) → General
- Function: promotes glucose transport from the blood into the cells
- Pancreatic polypeptide (from F cells) → General
- Function: influences regulation of pancreatic function and metabolism of absorbed nutrients
- Somatostatin (from delta cells) → Pancreas
- Function: inhibits insulin and glucagon secretion
- Summary: Pancreas hormones regulate glucose and energy metabolism with insulin and glucagon as key regulators; amylin and pancreatic polypeptide modulate digestion and pancreatic function; somatostatin regulates the pancreatic endocrine/exocrine environment
Page 7
- Gonadal Hormones and Reproductive Characteristics
- Hormones
- Estrogen
- Progesterone
- Testosterone
- Target Tissues
- Estrogen & Progesterone → ovaries (and reproductive system, breast tissue)
- Testosterone → testes (gonads)
- Functions
- Estrogen: stimulates development of secondary sexual characteristics; maintains lining of the uterus for pregnancy
- Progesterone: prepares uterus for fertilization and fetal development; maintains uterine lining
- Testosterone: stimulates development of secondary sexual characteristics; spermatogenesis
Page 8
- Common Endocrine Disorders (overview)
- Hormones involved in disorders (examples)
- Adrenocorticotropic hormone or adrenal corticosteroids
- Growth hormone
- Antidiuretic hormone
- Thyroid-stimulating hormone
- Parathyroid hormone
- Over-Secretion (examples)
- Hypercortisolism (Cushing's disease)
- Acromegaly
- Syndrome of inappropriate antidiuretic hormone (SIADH)
- Hyperthyroidism
- Hyperparathyroidism
- Under-Secretion (examples)
- Adrenal insufficiency (Addison's disease)
- Dwarfism
- Diabetes insipidus
- Hypothyroidism
- Hypoparathyroidism
Page 9
- Antidiuretic Hormone Problems
- SIADH and Diabetes Insipidus (DI)
- Pathophysiology (summary)
- SIADH: excessive ADH → water retention, hyponatremia
- Central DI and nephrogenic DI: ADH deficiency or resistance → polyuria, hypernatremia
- Etiology (examples)
- Lung cancer, head trauma, some drugs (for SIADH/central DI)
- Head injury or nephrogenic causes for DI
- Symptoms/Diagnostic tests (summary)
- SIADH: hypervolemia, hyponatremia, low serum osmolality; urine osmolality high; low urine output
- DI: hypovolemia, hypernatremia, high serum osmolality; urine output high; urine specific gravity low
Page 10
- ADH imbalance: Nursing care and treatments
- SIADH treatment considerations
- Strict intake and output (I&O)
- Cardiovascular monitoring
- Daily weights
- Seizure precautions
- Diabetes Insipidus treatments
- Treat underlying cause
- Fluid restriction (for SIADH) vs hypertonic saline in severe hyponatremia (not for DI)
- Desmopressin (DDAVP) for DI
- Low sodium diet
- Diagnostic tests mentioned
- Water deprivation test
- General nursing notes
- Monitor electrolytes, fluid status, neuro status
Page 11
- Thyroid Problems (introductory header)
Page 12
- Thyroid Problems: Diagnostic Tests and Normal Values
- Tests and normal ranges (summarized)
- TSH: 0.3–4.2
- T4 (Total): 4.5–11.7; T4 (Free): 0.8–2.8
- T3: 80–200
- Calcitonin: Male < 14.3; Female < 7.6
- Anticipated findings by condition (summary)
- Abnormal TSH and T4/T3 indicate hypo- or hyperthyroidism
- Calcitonin is a tumor marker for medullary thyroid carcinoma
Page 13
- Thyroid Problems: Common Symptoms by Condition
- Hypothyroidism
- Dry hair; constipation; weight gain; cold intolerance; goiter; slow heart rate; fatigue; hair and skin changes
- Hyperthyroidism
- Hair loss; heat intolerance; goiter; weight loss; tachycardia; rapid heartbeat; diarrhea; infertility risks
- Menstrual changes
- Irregular cycles; possible infertility
Page 14
- Hyperthyroidism Causes & Feedback
- Graves' disease highlighted as a cause
- Mechanism concepts
- Primary hyperthyroidism (thyroid origin)
- Secondary hyperthyroidism (outside thyroid, e.g., pituitary)
- Hormonal feedback loops and potential heredity factors
- Other contributing factors listed: injury to thyroid gland, nerve shocks, infections, medications, thyroid dysfunction, etc.
Page 15
- Graves' Disease Symptoms (key features)
- Sweating; exophthalmos; goiter; weight loss; nervousness; tremor; tachycardia; nausea/diarrhea; irritability; menstrual changes; muscle weakness; headaches
Page 16
- Hyperthyroidism Manifestations by System
- Nervous system: hyperreflexia, anxiety, rapid speech, irritability, tremors, insomnia, sleep pattern changes
- Reproductive system: decreased libido; menstrual irregularities; infertility
- Cardiovascular: hypertension, tachycardia, bounding pulses, systolic murmurs; angina
- GI: increased hunger/thirst, diarrhea, hyperactive bowel sounds
- Integumentary: warm moist skin; hair/nail changes; diaphoresis; skin fragility
- Other: heat intolerance; exercise intolerance; risk for falls; osteoporosis; thyroid storm; impaired thermoregulation
- Respiratory: tachypnea
- Skin integrity and overall risk considerations
Page 17
- More Hyperthyroidism Systemic Effects
- Nervous, reproductive, respiratory, integumentary systems effects continue
- Other effects: impaired skin integrity, risk for ineffective thermoregulation, thyroid storm (acute) and possible delirium
Page 18
- Acute Thyrotoxicosis: Thyroid Storm
- Treatment principles
- Antithyroid medications
- Rest, fluid/electrolyte replacement
- Oxygenation management
- Cardiac dysrhythmia management
- Cooling
- Pain/anxiety relief
- ABCs (Airway, Breathing, Circulation) monitoring
Page 19
- Hyperthyroidism: Treatments listed
- Antithyroid medications: Propylthiouracil and methimazole
- Iodine therapy
- Beta-adrenergic blockers
- Radioactive iodine therapy
- Surgical therapy
- Nutritional therapy: high-calorie, high-protein, high-carbohydrate diet; vitamins/minerals; low-fiber; avoid caffeine
Page 20
- Hyperthyroidism: Nursing Care
- Environment: Calm, quiet room; frequent linen changes due to diaphoresis
- Emotional support for anxiety/irritability
- Calorie/protein intake increase
- Do not palpate thyroid (stimulates hormone release)
- Exophthalmos care: sodium restriction; raise HOB; artificial tears; sunglasses
Page 21
- Post-Op Care: Thyroidectomy
- Preop: Antithyroid meds, iodine, beta-blockers as indicated
- Postop monitoring: risk of hypothyroidism, hypoparathyroidism, hypocalcemia, hemorrhage, infection, thyrotoxicosis, airway patency
- Positioning: Semi-Fowler's; support head/neck with pillows; avoid neck flexion; pain control
Page 22
- Hypothyroidism: Pathways & Causes
- Pituitary dysfunction vs Thyroid dysfunction
- Negative feedback loop: ↓ T4/T3 reduces TSH (depending on origin)
- Causes of hypothyroidism
- Iodine deficiency; thyroid inflammation/injury; drug therapies that suppress thyroid function; partial/complete thyroid gland destruction; use of radioactive iodine; congenital anomalies; environmental factors
- Primary vs Secondary hypothyroidism definitions
- Primary: thyroid-origin (TSH elevation with low T4/T3)
- Secondary: pituitary/hypothalamic origin (low TSH or inappropriate TSH response with low T4/T3)
Page 23
- Hashimoto's Thyroiditis (autoimmune)
- Symptoms: dry/thinning hair; enlarged/inflamed thyroid; joint/muscle pain; heavy/irregular menstrual periods; feeling cold; autoantibodies present
Page 24
- Hypothyroidism: Body System Manifestations (Summary)
- Cardiovascular: hypotension, bradycardia; decreased cardiac output; cholesterol elevation
- GI: decreased appetite, constipation; hypoactive bowel sounds
- Musculoskeletal: fatigue, muscle aches; joint pain; slow movements
- Nervous: slowed mental processes; hyporeflexia; depression; memory issues; hoarseness
- Complications: cardiac hypertrophy, heart failure, anemia, atherosclerosis; weight gain; risk for falls
- Nursing Diagnoses (examples): risk for unstable blood pressure; ineffective peripheral tissue perfusion; dysmotility; nutrition imbalance; fall risk; immune/skin concerns
Page 25
- Hypothyroidism: Reproductive, Respiratory, Integumentary, and Other System Effects
- Reproductive: menstrual irregularities, infertility
- Respiratory: bradypnea; reduced breathing capacity; dyspnea with exertion
- Integumentary: dry, thick, cold skin; dry hair; poor turgor; generalized edema; dry mucosa
- Other: decreased sweating; goiter; cold intolerance; infection risk; hearing changes; constipation; myxedema coma risk; thermoregulation issues
Page 26
- Causes of Goiters and Thyroiditis
- Drugs: Amiodarone, Lithium
- Foods: cruciferous vegetables (broccoli, Brussels sprouts, cabbage, cauliflower, kale, mustard greens, turnips), peanuts, strawberries; salicylates; sulfonamides
Page 27
- Myxedema Coma
- Medical emergency! Often due to infection, medications (opioids, barbiturates), cold exposure, trauma
- Manifestations: subnormal temperatures, extreme hypotension, hypothermia, severe bradycardia, hypoventilation
- Nursing care: aspiration precautions, airway support, measures to prevent cardiovascular collapse
Page 28
- Levothyroxine Review
- Dosage: start low, titrate every 4–5 weeks based on TSH
- Full effect up to ~8 weeks
- Avoid abrupt cessation
- Watch for hyperthyroid signs (overmedication)
- Interactions: ↑ effect with anticoagulants; ↓ effect with digoxin
- Diabetics may need more insulin while on levothyroxine
- Administration: take on an empty stomach 30–60 minutes before breakfast
Page 29
- Hypothyroidism: Nursing Care
- Safety: fall prevention; DVT prophylaxis; warm environment
- Diet: low-calorie, high-fiber, low-fat, low-cholesterol; stool softeners as needed
- Medication administration cautions: slowed metabolism/excretion; monitor for interactions
Page 30
- Adrenal Disorders (Introductory heading)
Page 31
- Cushing's Disease/Syndrome
- Symptoms of Cushing's syndrome
- Red, round face; CNS irritability; emotional disturbances; hypertension; obesity (central); cardiac hypertrophy; hyperplasia/tumor; purple striae; osteoporosis; muscle wasting; skin ulcers
- In females: amenorrhea, hirsutism; in males: erectile dysfunction
Page 32
- Cushing's: Glucocorticoid Excess – Clinical Manifestations
- Insulin resistance; glycosuria; hypercalciuria; muscle wasting; osteoporosis; thin skin; purplish abdominal striae; immunosuppression; dyslipidemia; labile emotions; weight gain (truncal obesity, moon face, buffalo hump)
- Complications: hyperglycemia, renal stones, risk for falls, osteoporosis, poor wound healing, cardiovascular disease, depression/anxiety
- Nursing Diagnoses: risk for infection, overweight, disturbed body image, impaired tissue integrity, risk for injury
Page 33
- Cushing's: Mineralocorticoid Excess
- Clinical manifestations and complications: hypokalemia; fluid/sodium retention; hypertension; peripheral edema; hypernatremia
- Nursing diagnoses: risk for electrolyte imbalance, risk for imbalanced fluid volume
Page 34
- Cushing's: Androgen Excess
- Clinical manifestations (females): menstrual irregularities, infertility, hirsutism; (males): erectile dysfunction, reduced self-esteem; acne; gynecomastia
- Nursing Diagnoses: risk for chronic low self-esteem, disturbed body image, risk for infertility
Page 35
- Cushing’s Disease: Diagnostic Testing
- Salivary cortisol levels
- Dexamethasone suppression test
- Urinary cortisol level
- Adrenocorticotropic hormone (ACTH)
Page 36
- Cushing's Disease: Treatment (three main steps)
- Treat the underlying cause
- Drug therapy
- Taper long-term steroids when appropriate
Page 37
- Cushing’s Disease: Nursing Care
- Monitor vital signs, daily weights, glucose, infection risk, thromboembolic risk, emotional support, corticosteroid education
Page 38
- Addison’s Disease: Acute Adrenal Insufficiency
- Life-threatening; triggers include stress, abrupt withdrawal of corticosteroids, adrenal surgery, sudden pituitary destruction
- Treatment: corticosteroids
Page 39
- Diabetes Mellitus (Introductory page for DM section)
Page 40
- Pancreas Hormones (revisited with targets)
- Amylin (from beta cells) → Pancreas; Liver; Stomach
- Decreases gastric motility; decreases glucagon secretion; decreases endogenous glucose release from the liver; increases satiety
- Glucagon (from alpha cells) → General
- Stimulates glycogenolysis and gluconeogenesis
- Insulin (from beta cells) → General
- Promotes glucose transport from the blood into the cells
- Pancreatic polypeptide (from F cells) → General
- Influences regulation of pancreatic function and metabolism of absorbed nutrients
- Somatostatin (from delta cells) → Pancreas
- Inhibits insulin and glucagon secretion
Page 41
- Metabolic pathways: Gluconeogenesis, Glycogenolysis, Lipolysis, and Ketogenesis (diagrammatic outline)
- Key components:
- Gluconeogenesis from lactate, alanine, glycerol, etc.
- Glycogenolysis and glycogenesis in liver
- Lipolysis in adipose tissue yielding NEFAs and glycerol
- Utilization of glucose in tissues; interplay with liver and adipose tissue
- Pyruvate, alanine, glutamine as amino-acid sources feeding gluconeogenesis
- Note: This page provides a schematic view of how glucose is generated and utilized
Page 42
- Insulin Effects: When food is consumed
- Process: Food is converted to glucose; pancreas produces insulin; glucose is stored as glycogen in liver; insulin helps glucose uptake by muscles and other tissues; muscle tissue uses glucose for energy during activity
- Summary: Insulin shuttles glucose from blood into cells and promotes storage as glycogen; maintains euglycemia after meals
Page 43
- Regulation of Blood Glucose: Insulin and Glucagon interplay
- Insulin pathway (high blood glucose):
- Insulin triggers glucose uptake by cells; Liver stores glucose as glycogen (glycogenesis)
- Pancreas releases insulin; Glucose is stored; Blood glucose level drops toward normal
- Glucagon pathway (low blood glucose):
- Glucagon stimulates glycogenolysis and gluconeogenesis in liver; Blood glucose rises
- Visual mnemonic: High BG → insulin; Low BG → glucagon
Page 44
- Diabetes Mellitus: Diagnostic Testing – Key Values and Ranges (Overview)
- Glycosylated hemoglobin (A1C)
- Reference: < 5.6% (nondiabetic); 5.7–6.4% (prediabetes); ≥ 6.5% (diabetes)
- Fasting blood glucose (FBG)
- Reference: < 110 mg/dL (nondiabetic) [some sources vary here]
- 2-hour postprandial glucose (2-hour PPG) after 75 g load
- < 140 mg/dL (nondiabetic); 126 mg/dL or higher diagnostic for diabetes
- 1-hour postprandial and casual glucose values and thresholds provided
- Glucose tolerance test (GTT)
- Additional notes on testing timing (fasting 8 hours) and testing conditions
Page 45
- Diabetes Mellitus: Diagnostic Testing (Detailed Lab Values)
- Hemoglobin A1C: 4%-5.9% (normal); 6.5% or higher (diabetes)
- Fasting blood glucose (FBG): < 110 mg/dL (nondiabetic); 126 mg/dL or higher (diabetes)
- 2-hour postprandial plasma glucose (2-hour PPG): < 140 mg/dL (nondiabetic); 200 mg/dL or higher (diabetes)
- Random plasma glucose: < 200 mg/dL (nondiabetic); 200 mg/dL or higher with symptoms
- Special notes: 2-hour PPG values are age-dependent in some guidelines
Page 46
- Types of Diabetes Mellitus (DM)
- DM Type I (DM I): Autoimmune destruction of beta cells; produce no insulin; require insulin injections; more common in children
- DM Type II (DM II): Insulin resistance with some insulin production; may require oral agents; more common in adults
- Gestational Diabetes: Occurs during pregnancy; usually resolves after pregnancy but increases future DM II risk
Page 47
- Monitoring Blood Glucose
- Frequency depends on goals, type, meds, access to supplies, etc.
- Patients on insulin often check 4–8 times daily (before meals and at bedtime)
- Check BG if symptoms of hypoglycemia occur
- Practical note: skill video on Checking Blood Glucose
Page 48
- Complications of Diabetes Mellitus
- EYES: Retinopathy, Glaucoma
- BRAIN: Stroke
- NERVES: Diabetic neuropathy
- KIDNEYS: Diabetic nephropathy
- HEART: Diabetic cardiomyopathy
- TEETH: Periodontal disease
- Circulatory system: Reduced blood flow
- SKIN: Diabetic foot
Page 49
- Diabetes Mellitus: Nutrition
- Carbohydrates: Healthy forms (whole grains, fruits, vegetables, low-fat dairy); Complex carbs promote stable glucose; avoid processed sugars
- Dietary fats: Limit saturated fat, cholesterol, and trans fats; promote healthy fats (plants, olives, nuts, avocados)
- Protein: Lean sources; essential for function
- Alcohol: Can inhibit gluconeogenesis; risk of hypoglycemia; moderate intake with carbohydrate planning
Page 50
- Glycemic Index (GI) Examples (selected list)
- High GI range (~70–100): white bread, donuts, white rice, potatoes, some fruits
- Medium GI (~50–70): rye/wholegrain bread, muesli, brown rice, pasta, lentils, yams, popcorn
- Low GI (~0–50): barley bread, apples, berries, citrus, milk, yogurt, oats, beans, leafy vegetables
- Practical use: choose lower GI foods to improve glycemic control
Page 51
- Symptoms of Hyperglycemia (polyuria, polydipsia, polyphagia, weight loss) and other signs
- Polyuria: Excessive urine production
- Polydipsia: Excessive thirst
- Polyphagia: Excessive hunger
- Weight loss with hyperglycemia
- Fatigue, blurry vision, nausea/vomiting
Page 52
- Types of Insulin: Onset, Peak, Duration (summary)
- Rapid-acting: Lispro, Aspart, Glulisine
- Onset: ~10–30 min; Peak: ~0.5–3 hours; Duration: ~3–5 hours
- Short-acting (Regular): Onset ~0.5–1 hour; Peak ~2–5 hours; Duration ~5–8 hours
- Intermediate-acting (NPH): Onset ~1.5–4 hours; Peak ~4–12 hours; Duration ~12–18 hours
- Long-acting (Glargine, Detemir, Degludec): Onset ~1–4 hours; Peak: less defined or no peak; Duration ~16–24 hours (Degludec can be longer)
- Important notes
- Rapid-acting must be given with meals; risk of hypoglycemia high
- Short-acting should be given 30 min before meals
- NPH is cloudy; mix by rolling (not shaking)
- Glargine/Detemir should not be mixed with other insulins
Page 53
- Insulin Types: Quick reference by class
- Rapid-acting: peaks 30 minutes to 3 hours
- Short-acting: peak 2–5 hours
- Intermediate-acting: peak 4–12 hours
- Long-acting: peak less defined or none
Page 54
- Insulin Regimens: Basal-Bolus vs Combination/Hybrid
- Basal-Bolus structure shown with meals and bedtime injections
- Glucose control pattern across 24 hours
Page 55
- Insulin Effect Schedule (example)
- 6 AM: Basal (long-acting) and/or fast-acting with breakfast
- Breakfast/Lunch/Dinner/Bedtime: corresponding rapid-acting or short-acting with meals
- Total insulin effect and stacking concepts
Page 56
- Insulin Storage & Administration Guidelines
- Unopened vials: refrigerate until use; opened vials: room temp up to 4 weeks
- Administration: subcutaneous (SQ) at 45–90 degree angle or IV in some cases
- Tools: insulin syringe, pen, or pump
- Pump/infusion set: change every 2–3 days
- Site rotation; insulin should be clear (except NPH), roll to mix (do not shake)
- Home hygiene: wash with soap and water
Page 57
- Somogyi Effect vs. Dawn Phenomenon
- Somogyi effect: nocturnal hypoglycemia triggers counterregulatory hormones → morning hyperglycemia
- Symptoms: headaches, night sweats, nightmares
- Management: bedtime snack, reduce evening insulin dose, test 2–4 AM to differentiate
- Dawn phenomenon: early morning hyperglycemia due to increased counterregulatory hormones (growth hormone, cortisol)
- Management: adjust insulin dose/time; consider earlier supper or bedtime snack adjustments
- Monitoring strategy: test between 2–4 AM to differentiate causes; if predawn levels elevated, increase insulin; if low, decrease dose
Page 58
- Hypoglycemia: Emergency treatment
- If conscious: 15 g fast-acting carbohydrate (e.g., 4 oz juice, 8 oz milk) or glucose gel/tabs
- Recheck in 15 minutes; repeat if needed; follow with protein and complex carbohydrate
- If unconscious: 25–50% Dextrose IV; or Glucagon 1 mg IM
Page 59
- Hypoglycemia vs Hyperglycemia Symptoms (quick reference)
- Hypoglycemia: sweating, pallor, dry mouth, confusion, shakiness, irritability, tremor, paleness, hunger
- Hyperglycemia: thirst, polyuria, fatigue, dry mouth, blurred vision, weight loss, nausea
Page 60
- Diabetes Patient Education & Self-care
- Regular exercise; hypoglycemia possible after exercise
- If BG < 100 mg/dL before exercise, eat a 15–30 g carbohydrate snack
- Vaccines: annual flu and COVID-19 recommended
- Report to provider if BG > 250 mg/dL on two consecutive days or if moderate ketonuria
- Regular dental/foot care; wear medical alert bracelet; follow sick-day rules
Page 61
- Sick Day Rules (S-I-C-K mnemonic)
- Sugar: Check blood glucose every 4 hours (2–3 hours ideal)
- Insulin: Always take; do not skip; could lead to DKA
- Carbohydrates: Drink fluids with carbohydrates if BG high; drink sugar-free fluids if BG low
- Ketones: Check urine or blood ketones every 4 hours if BG > 240 mg/dL; take rapid-acting insulin if ketones present
Page 62
- Diabetic Ketoacidosis (DKA)
- What is DKA?
- Insulin deficiency → cells cannot use glucose; fat/protein breakdown → metabolic acidosis, weight loss, fatigue
- Blood glucose > 200 ext{ mg/dL}; ketones present; glycosuria; ketonuria
- Signs: dehydration, dry mucous membranes, tachycardia, orthostatic hypotension; Kussmaul respirations; fruity breath
- Risk factors: Type 1 DM, illness, infection, poor insulin dosing; inadequate self-care
Page 63
- DKA Treatment Protocol
- IV fluids: start with 0.9% saline; aim for adequate BP and urine output (~30 mL/hr)
- When glucose approaches ~250 ext{ mg/dL}, add 5% dextrose to prevent hypoglycemia
- Insulin: Regular insulin IV infusion at 0.1 ext{ U/kg/hr} until metabolic goals reached
- Potassium: monitor and replace as needed (often follows insulin therapy and fluid resuscitation)
- Monitoring: continuous cardiac monitoring in ICU; hourly I&O and BG; monitor electrolytes
Page 64
- DM Type II: Pharmacologic Treatments (Class, Example, Mechanism, Special Considerations)
- Alpha-glucosidase inhibitors: Acarbose, Miglitol
- Delay GI carbohydrate absorption; take with first bite; monitor 2-hour postprandial glucose
- Biguanides: Metformin (most common)
- Increase insulin sensitivity; decrease hepatic glucose production; improve tissue glucose use; may cause weight loss; hold 48 hours before/after IV contrast to reduce lactic acidosis risk
- DPP-4 inhibitors: Alogliptin, Sitagliptin
- Prolong incretin effect; generally weight-neutral; potential pancreatitis risk
- Meglitinides: Nateglinide
- Stimulate pancreatic insulin release
- SGLT2 inhibitors: Canagliflozin
- Increase urinary glucose excretion by lowering renal glucose reabsorption
- Sulfonylureas: Glipizide, Glyburide
- Increase insulin secretion; take up to 30 minutes before meals; hypoglycemia risk; avoid if meals skipped
- Thiazolidinediones: Pioglitazone
- Increase insulin sensitivity; may not be used in sulfa allergy; risk of fluid retention and cardiovascular events
Page 65
- DM Type II: Non-insulin Injectables
- GLP-1 receptor agonists (e.g., albiglutide, exenatide): increase insulin synthesis/release, inhibit glucagon, slow gastric emptying, increase satiety; some weekly dosing; pancreatitis risk; avoid absorption interactions; take oral meds at least 1 hour before GLP-1 agonists when given concomitantly
- Amylin analogs (pramlintide): slows gastric emptying, reduces glucagon, increases satiety; used with insulin; cannot be mixed in the same syringe; may cause hypoglycemia; meals should be at least ~250 calories; carry fast-acting carbohydrate
Page 66
Hyperosmolar Hyperglycemic Syndrome (HHS)
Life-threatening complication of DM Type II
Similar to DKA but with some insulin presence; absent or low ketones
Symptoms: somnolence, seizures, hemiparesis, aphasia
Treatment: Regular insulin IV; initial 0.9% saline, then switch to dextrose-containing solution when BG < 250 mg/dL; monitor electrolytes; continuous cardiopulmonary monitoring in ICU
Monitoring: hourly I&O and BG; monitor mental status; close electrolyte management (especially potassium)
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