Nursing Care of Endocrine System PDF

Summary

This document is a study guide for nursing students on the endocrine system. It covers the anatomy and physiology, discusses age-related changes, and mentions diagnostic exams related to endocrine disorders.

Full Transcript

LEARNING OBJECTIVES FOR NURS B43: Medical Surgical Nursing 2 Unit 9– Nursing Care of the Patient with Problems of the Endocrine System (Week 12): 1. Review anatomy and physiology of the endocrine system. Pituitary Two parts: Gland (right -Anterior -...

LEARNING OBJECTIVES FOR NURS B43: Medical Surgical Nursing 2 Unit 9– Nursing Care of the Patient with Problems of the Endocrine System (Week 12): 1. Review anatomy and physiology of the endocrine system. Pituitary Two parts: Gland (right -Anterior - releases growth hormone, prolactin, thyroid stimulating hormone, below adrenocorticotropic hormone (ACTH), gonadotropin hormone, follicle stimulating hypothalamus) hormone, luteinizing hormone -Posterior - releases antidiuretic hormone (ADH), oxytocin Pineal Gland Located on the back side of the brain stem -Releases melatonin which helps with Circadian rhythm (internal process that regulates the sleep-wake cycle and repeats roughly every 24 hours, responds to changes in light levels. Melatonin levels typically increase in the evening as it gets darker) Parathyroid -Releases parathyroid hormone which helps with calcium and phosphate Gland metabolism (PTH stimulates the release of calcium from the bones, where it is stored. PTH promotes the reabsorption of calcium in the kidneys, reducing the amount of calcium excreted in urine. PTH decreases the reabsorption of phosphorus in the kidneys, leading to increased excretion of phosphorus in urine. This helps to maintain an appropriate balance between calcium and phosphorus in the blood) Thyroid -Releases thyroid hormone which increases metabolism and calcitonin hormone which slows calcium releasing activity of Gland bone cells if serum level is excessive (essentially calcitonin is released to counteract this by inhibiting the activity of osteoclasts, which are cells that break down bone tissue and release calcium into the bloodstream) Thymus -Releases thymosin which controls t-lymphocyte activity (teaches them what to do which is important in immune system function) Adrenal Made up of: Gland -medulla - responsible for epinephrine (adrenaline) and norepinephrine -cortex - secretes corticosteroids (cortisol and cortisone which depresses inflammatory responses) and mineralocorticoids (aldosterone which promotes sodium and water retention- RAAS) Pancreas -Regulates carbohydrate metabolism -Production of glucagon and insulin Gonads Source of sex hormones: -Testes - mainly testosterone - Ovaries - estrogen and progesterone 2. Discuss age related changes and age-appropriate care. -Decrease in pancreas mass and enzyme reserves which results in reduced insulin secretion and increased insulin resistance 3. Identify diagnostic exams/lab data to assess problems of the endocrine system & Discuss nursing interventions before and after diagnostic exams. Cortisol Used to evaluate adrenal function: ↑ in Cushing’s Syndrome, and ↓ in Addison’s Disease - No food or drink 2 hours prior to test CT To assess adrenal gland for tumors -Consent needed if IV contrast, Allergies to iodine or shellfish, metformin can be nephrotoxic with the contrast ACTH Used for both Cushing’s and Addison’s Stimulation -decreased (negative) it’s an adrenal insufficiency - it’s primary insufficiency Test -increased (positive) it’s from the pituitary tumor - it’s secondary insufficiency (ACTH stimulates the adrenal glands to produce cortisol. If we give the patient ACTH, we should see their cortisol level increase, but if we don’t see cortisol increased, then that means there is adrenal gland issue; whereas, if it does increase that means the adrenal gland is acting fine/normal because it increased. So if it’s increased that means the pituitary gland (which produces ACTH) has an issue 4. Describe etiology, pathophysiology, clinical manifestations, complications, and collaborative care of the client with: ★ Disorders of the adrenal gland involve changes in the production of ACTH. -Can be caused through use of glucocorticosteroids “sone”: know SE -ACTH is produced by the pituitary gland that stimulates the adrenal glands to produce cortisol -Cortisol is a stress response hormone and increases BP & Glucose, causes potassium excretion and sodium retention Cushing’s Hypersecretion of ACTH or Cortisol Syndrome -Females, 30-50 years (excess ★ Etiology: cortisol) ○ Pituitary tumor- causes increase ACTH ○ Adrenal tumor- causes increase cortisol ○ ACTH secreting tumor (small cell CA- lungs) ○ Long term steroid use (Iatrogenic- side effect causing adrenal insufficiency of cortisol) ★ Manifestations: ○ Fat pads → Moon Face, Buffalo Hump, Thinning of Skin → Abdominal Striae, Hirsutism (excess hair growth), Poor Wound Healing, DM, Hypertension, Osteoporosis → reduces intestinal calcium absorption, and blocks it from entering the bone, also competes with aldosterone, Hypokalemia (loss of potassium), Hypernatremia, Hyperglycemia ★ Diagnostics: ○ Plasma cortisol - ↑ ○ Na- ↑, K- ↓ , Glucose- ↑ ○ 24 hr urine- free cortisol ○ Plasma ACTH (decreases if it’s r/t adrenal, increased if it’s r/t pituitary) ○ Metabolic alkalosis (increased sodium leads to H excretion (acidic), decrease K leads to HCO3 retention (basic), leading to more alkalotic state) ★ Management: ○ Hx (tumor, infections, changes in appearance - weight, bruising, weakness) ○ Physical (VS, Appearance, Hair, Fat Distribution, Muscle Strength + Strength ○ Diet: low sodium ★ Treatment: ○ Mitotane- kills adrenal cells which suppresses the activity of the adrenal cortex ○ Aminoglutethimide- inhibits cortisol synthesis ○ Pasireotide- synthetic hormone that suppresses corticotropin (ACTH) release by the pituitary gland ○ Somatostatin- suppresses ACTH secretion ★ Surgical: ○ Adrenalectomy for tumor ○ Removal of pituitary gland for disorder WHAT ARE PRIORITY PROBLEMS? -Fluid Volume Excess, RC of Electrolyte Imbalance (decreased CO/RC dysrhythmias), RC for Infection, RC for Injury, Disturbed Body Image, Knowledge Deficit Addison’s Adrenal hypofunction- Adrenal glands not producing sufficient amounts of hormones Disease -Females, 30-50 (little ★ Pathophysiology: Destruction of the adrenal cortex (outer layer of the adrenal glands) occurs, which causes cortisol) underproduction of glucocorticoids (like cortisol) and mineralocorticoids (like aldosterone)​ ★ Etiology: ○ Autoimmune reactions (70-80%) ○ Genetic link ○ Pituitary tumor or metastasis from lung CA ○ Abrupt Withdrawal from steroid therapy ★ Manifestations ○ Anorexia, Hyperpigmentation (r/t primary adrenal insufficiency. Pituitary stimulates production of ACTH which also produces MSH which causes increase of melanin production), Abdominal Pain, N/V, Salt Craving, Hypotension, Fatigue, Muscle Weakness, Osteoporosis → imbalance of sodium, but mostly SE of tx, Hyperkalemia, Hyponatremia, Hypoglycemia, Hypocalcemia ★ Diagnostics: ○ Plasma Cortisol- ↓ ○ ACTH- ↑ (indicates primary) ○ Aldosterone- ↓ (indicates primary) ○ Na- ↓, K- ↑, Glucose- ↓, Ca- ↓ ○ BUN- ↑ (r/t dehydration) ○ H&H- ↑ (r/t dehydration) ○ ACTH Stimulation Test- view cortisol levels to see adrenal function as ACTH stimulates the adrenal glands to produce cortisol. ★ Management: ○ History: Weight Loss, Skin Changes, SE​ ○ Physical Assessment: VS (BP), Height/Weight, Skin Color, Muscle Strength​ ○ Diet: Increase Sodium​ ★ Medication: ○ IVF (not hypotonic solutions)​ ○ Glucocorticoids- cortisone, dexamethasone, prednisone​ ○ Mineralocorticoids- florinef ​ WHAT ARE PRIORITY PROBLEMS? -Deficient Fluid Volume, RC of Electrolyte Imbalance, Knowledge Deficit, Disturbed Body Image, RC for Ineffective Therapeutic Regimen Management 5. Compare & contrast Cushing’s Syndrome and Addison’s Disease (*especially diagnostics above*) Unit 10– Nursing Care of the Patient with Problems of the Urinary System (Week 12): 1. Review anatomy and physiology of the urinary system: Kidneys Bean shaped organs located outside of the peritoneal cavity in the posterior abdomen on either side of the spinal column T12 to L3 region, At costovertebral angle – hiding under ribs -Supported 3 layers of connective tissue and three internal regions: -cortex- contain glomeruli - capillaries -medulla- contain collecting tubules and nephrons – 1 mill/kidney -pelvis- channels urine toward ureters Ureters Lead from the renal pelvis to the bladder Bladder -located in the pelvis anterior of the uterus and vagina behind the pubis symphysis in females -located between pubis symphysis and rectum in males Urethra leads from voluntary sphincters to the meatus -longer in males than in females ★ Function of the kidneys: ○ Form urine and to balance water and solute transport ○ Excrete metabolic waste ○ Regulate acid base balance ○ Secrete hormones to regulate BP ○ Erythrocyte production and calcium metabolism ★ Process of Urine Formation/Elimination: ○ Nephrons are the working units in the kidneys – each kidney contains 1 million nephrons. ○ Blood comes to the kidneys/nephrons via the renal arteries, the making of urine is started in the glomerulus → Very porous capillaries allow for absorption of much fluids into glomerular (Bowman’s) capsule → fluid is now called filtrate and it is channeled into proximal convoluted tubule → some reabsorption of water and active transport of substances happens here → Moves to Loop of Henle, descending loop is permeable to water, ascending not so much → to distal convoluted tubule → collecting ducts and ureters 2. Recall the physiologic changes related to age: Age Related Renal Changes Consequences -Size of reno-vascular bed decreases -Impaired tubular reabsorption -Renal blood flow decreases -Reduced ability to conserve and excrete sodium -Loss of cortical vasculature -Impaired concentration ability -Sclerosis of glomeruli -Inability to excrete an acid load -Loss of glomeruli -Increased risk for fluid and electrolyte imbalances -Tubular size and number decrease -Renal vasoconstrictive response to sympathetic stimulation is exaggerated Age Related Genitourinary Changes Consequences -Decline of bladder capacity and control -Incontinence of urine -Decline in urethral length and sphincter -strength -Increased risk of UTI -Prostate hypertrophy -Narrowing of urethral lumen with incomplete bladder -Pelvic floor muscle weakness emptying leading to incontinence 3. Identify diagnostic exams used for urinary problems & nursing interventions before/after exams: Values to Know BUN: 8-25 Creatinine: 0.5-1.5 GFR: 90-120 Sodium: 135-145 Potassium 3.5-5.5 Chloride: 97-107 Creatinine Clearance: 90-130 Hemoglobin: Male: 13.6-17.2, Female 12.1-15.1 Hct: Male: 40-50%, Female: 36-44% UA WBC, crystal fragments, pH which helps to identify the type of stone), RBC (hematuria) Serum Calcium, Phosphorus, Help identify factors contributing to stone formation uric acid levels -Urine Ca, uric acid, and oxalate levels in urine collected over 24 hrs helps find causes of lithiasis (stones) Chemical analysis of stones Can help in suggesting measures to prevent future stone formation KUB XR of kidneys, ureters and bladder – this also helps to identify stones Renal US Helps to detect stones and evaluate kidneys for hydronephrosis CT detects stones and ureteral obstructions IVP (intravenous Done if other tests fail to show clear evidence of calculi. pyelogram) -IV is started and contrast medium is injected, consent is needed -Caution in people with DM, multiple myeloma, and increased serum creatinine levels 4. Describe the etiology, pathophysiology, manifestations, complications and care of the client with: Renal Calculi Kidney stones (“Lithiasis”- stone formation) -Males, South-Midwest, Caucasians, African Americans ★ Etiology: ○ Supersaturation- precipitation of minerals, contributing to the formation of kidney stones ○ Nucleation - minerals begin to cluster and form the core of a stone. ○ Lack of Inhibitory substances- absence or insufficient presence of substances that normally inhibit the formation or growth of crystals. ★ Pathophysiology: ○ 75-80% Calcium stones ○ Remaining 20% Uric Acid, Struvite, Xanthine, Cystine stones ★ Risk Factors: ○ Industrialized country, family hx, dehydration, immobility ○ Ca, Oxalate, Protein, High Vitamin C. Intake ○ Gout, Urinary Stasis ○ Hyperparathyroidism (High serum calcium levels) ★ Diagnostics: discussed earlier, but includes UA, Serum Calcium, Phosphorus, Uric Acid levels, Chemical analysis of stones, KUB, Renal US, CT, and IVP ★ Complications: ○ UTI- Chills, fever, urgency, frequency, dysuria ○ Hydronephrosis- Back of urine in the kidneys Acute- Acute colicky pain that may radiate into groin and abdomen, hematuria, pyuria (pus in urine), fever, N/V Chronic- Dull, aching flank pain, hematuria, pyuria, fever, palpable flank mass ★ Management: ○ Limit foods that can contribute to stone formation (oxalate, vitamin C, protein, calcium) ○ Retrograde Ureteroscopy- stones are manually removed and a ureteroscope is passed backward through the urinary tract to visualize stones ○ Extracorporeal shock wave lithotripsy (ESWL)- sound shock wave to break stone into small fragments Under conscious sedation, strain urine to monitor the passage of the stone, bruising may occur on flank ○ Percutaneous ultrasonic lithotripsy- use of nephroscope that is inserted and stone fragmented using ultrasonic waves (Usually used for large stones (>2 cm, Staghorn Calculi if located in calyces & renal pelvis)) ○ Laser Lithotripsy- performed using either a nephroscope, which requires a small incision in the back to access the kidney, or a ureteroscope, which is introduced through the urinary tract without the need for an incision, to break down kidney stones using a laser. Pre-op for Lithotripsy: Assess knowledge, Informed Consent, Bowel Prep, NPO Post-op for Lithotripsy: Monitor VS frequently, Monitor UO, Strain Urine, Discharge Teaching, Dietary Changes, Increase Fluid Intake ★ Medication: ○ Analgesics ○ Prevention of further calculi - examples include thiazide diuretic (prevent calcium formation by reducing excretion in urine), potassium citrate (inhibit formation of calcium oxalate/phosphate stones), Allopurinol (decrease uric acid), calcium supplements, phosphate binders ○ Tamsulosin- alpha blocker which does lower blood pressure, but is also a smooth muscle relaxer which can helps facilitate the passage of kidney stones through the urinary tract and improve flow of urine ○ Abx- for infection ○ Oral/IVF- isotonic (lactated ringers, 0.9% NaCl), to increase urine volume to pass stone Nephrolithiasis- stone in kidney ★ Manifestations: often asymptomatic, dull aching flank pain, microscopic hematuria, UTI Urolithiasis- stone in any part of urinary tract (kidney, ureters, bladder, urethra) ★ Manifestations: may be asymptomatic, dull suprapubic pain, gross or microscopic hematuria, UTI Ureterolithiasis- stone in ureter (most severe) ★ Manifestations: renal colic (sudden pain), acute severe flank pain which radiates to suprapubic region, groin, and external genitals, N/V, pallor, cool clammy, UTI WHAT ARE THE PRIORITY PROBLEMS? -Impaired Urinary Elimination, Fluid Volume Deficit, RC for Infection, Acute Pain, Activity Intolerance, Knowledge Deficit Benign Enlargement of the prostate gland Prostatic -Hyperplasia (increase in number of cells) vs. Hypertrophy (increase size of cells) Hypertrophy -Non-malignant (BPH) -Age-Related, begins 40-45, affects mostly >60 ★ Risks: Age, Family Hx, Race (Black, Hispanic), Diet (red meat, fat) ★ Manifestations: Diminished force of urinary system, post-void dribble, sensation of incomplete emptying, urinary retention, nocturia, frequency, urgency/urge incontinence, dysuria ★ Diagnostics: ○ Physical Examination: Digital Rectal Examination, Post-void bladder scan, post-void catheterization ○ Tests: BMP (BUN, Cr, WBC), UA, Prostate Specific Antigen (increases with age), KUB/IVP (abdominal XR) ★ Complications: ○ Bladder distention - leads to damage ○ UTI - urinary stasis ○ Hydronephrosis - from urinary retention - kidney damage ○ Renal insufficiency ○ Does not increase risk of prostate CA ★ Medication: ○ Anti-androgen: 5-Alpha Reductase Inhibitors: finasteride (decrease testosterone in prostate) ○ Alpha-adrenergic antagonists: Alpha 1 adrenergic antagonists: tamsulosin, doxazosin, doxazosin, etc. (it decreases BP but relaxes smooth muscles) ○ Herbal: saw palmetto, african plum ○ Meds to Avoid: antihistamines, anticholinergics (due to SE retention) ★ Treatment/Surgical Tx: Criteria for Sx- Chronic Bladder Infection, Acute Urinary Retention, Hematuria, Hydronephrosis, Bladder Neck Obstruction Syndrome (frequency, urgency) ○ Transurethral microwave thermotherapy- using microwaves, aims to treat BPH by heating and shrinking prostate tissue without the need for surgical removal. ○ Transurethral resection of prostate (TURP)- a surgical procedure where excess prostate tissue is removed using a resectoscope inserted through the urethra ○ Transurethral needle ablation (TUNA)- involves inserting needles into the prostate and delivering radiofrequency energy to ablate excess tissue, reducing obstruction to urine flow ○ Transurethral incision of the prostate (TUIP or TIP)- involving small incisions in the prostate gland to alleviate urinary symptoms associated with BPH, particularly in cases with a smaller-sized prostate. ○ Prostatectomy- Open surgery of large prostate that can be retropublic (through abdominal wall incision), perineal (incision between scrotum/rectum) Pre-Op: Assess knowledge of procedure, explain procedure Post-Op: VS, I&O’s, Pain Management, Labs (CBC-assess for bleeding, infection, obstruction), SCDs, Encourage Fluid Intakes, Catheter Patency Continuous Bladder Irrigation- 3-way foley catheter (One lumen for irrigation of blood clots, One lumen for inflation, securing catheter within bladder, One lumen for drainage of urine). Make sure to assess urine, VS, I&O’s, Catheter q1-2 hours, labs: H&H, Na+ WHAT ARE THE PRIORITY PROBLEMS? -Urinary Retention, RC for Infection, RC for Imbalanced Fluid Volume, Acute Pain, Knowledge Deficit

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