Med Surg Exam 2

What are the 4 key structures of the renal system and their functions?

1. Nephron: Functional unit of the kidney; filters blood and makes urine.

2. Glomerulus: Tiny bundle of capillaries that filters blood using hydrostatic pressure.

   • Proteins and blood cells are NOT normally filtered.

3. Bowman's Capsule: Surrounds the glomerulus and collects the filtrate.

4. Tubules: Reabsorb needed substances back into the blood and secrete wastes into the urine.

What is the process of urine formation? (In order)

1. Filtration – The glomerulus filters water, electrolytes, glucose, and waste from the blood.

2. Reabsorption – Water, glucose, sodium, and other needed substances return to the bloodstream.

3. Secretion – Drugs, H⁺, K⁺, and other wastes move from the blood into the tubules.

4. Excretion – Urine leaves the body through the renal pelvis → ureter → bladder → urethra (KUBU).

What are 7 functions of the kidneys?

1. Maintain Acid-Base Balance – Removes excess H⁺ and conserves bicarbonate to maintain normal blood pH.

2. Regulate Blood Pressure – Releases renin, which activates the RAAS, causing vasoconstriction and increasing blood pressure.

3. Regulate Calcium Levels – Helps maintain calcium balance for bone, muscle, and nerve function.

4. Activate Vitamin D – Converts vitamin D into its active form so the intestines can absorb calcium.

5. Erythropoietin (EPO) Production – Stimulates red blood cell production in the bone marrow.

   • If kidney function decreases, EPO production decreases, leading to anemia.

6. Fluid & Electrolyte Balance – Regulates water, sodium, potassium, and other electrolytes.

7. Garbage Removal (waste) – Removes urea, creatinine, drugs, and toxins through urine.

What are the 5 key labs for kidney function and their meanings?

1. Creatinine: waste from muscle metabolism

   • Best indicator of kidney filtration

2. BUN: blood urea nitrogen (waste)

   • Elevated in decreased kidney function OR dehydration

3. eGFR: estimates filtration rate

   • Decreased eGFR indicates worse filtration/function

4. Electrolytes: K⁺, Na⁺, Ca²⁺, phosphate

   • kidneys regulate electrolytes; imbalances occur with dysfunction

5. UO: volume produced per day/hr

   • Normal: 800-2000mL/day or 30mL/hr

What are the normal urine output values, and what do oliguria and anuria indicate?

• Normal: 800–2000 mL/day or ≥30 mL/hr

• Oliguria: <400–500 mL/day or 20 mL/hr → concern for hypoperfusion, AKI, dehydration

• Anuria: Almost no output → severe kidney injury or obstruction → medical emergency

What is cystitis, what is its major complication, and 2 laboratory tests are used to diagnose it?

• Cystitis is an infection of the bladder (lower urinary tract infection).

• Major complication: Progression to pyelonephritis.

• Labs

  1. Urinalysis: WBCs, Bacteria, Leukocyte esterase, Nitrites

  2. Urine culture: Identifies the organism and guides antibiotic therapy.

What are 7 manifestations of a UTI?

1. Dysuria (burning with urination)

2. Frequency

3. Urgency

4. Suprapubic pain/discomfort

5. Cloudy or foul-smelling urine

6. No systemic signs of CVA tenderness

7. Older adults may present with AMS/falls/confusion rather than classic symptoms

What is pyelonephritis, and what are its major complications?

• Pyelonephritis is an infection of the kidney (upper urinary tract infection).

• Major complications: sepsis and AKI

What are 8 manifestations of pyelonephritis?

1. Fever (>102°F/38.9°C)

2. Chills

3. Flank pain

4. Costovertebral angle (CVA) tenderness

5. Nausea and vomiting

6. Malaise/fatigue

7. May also have dysuria, urgency, and frequency

8. Systemic infection: tachycardia, hypotension (sepsis)

What 5 laboratory tests are used to diagnose pyelonephritis?

1. Urinalysis (same findings as a UTI)

2. Urine culture

3. CBC with differential (↑ WBCs)

4. BUN, Creatinine, eGFR (kidney function)

5. Blood cultures (if sepsis is suspected)

What are 8 things to teach a patient to prevent a UTI?

1. Encourage fluids 2–3 L/day (if not contraindicated — HF, CKD)

2. Void regularly; void after sexual activity

3. Wipe front to back — prevents E. coli from anus to urethra

4. Showers rather than baths

5. Avoid bladder irritants: caffeine, alcohol, spicy foods

6. Manage constipation — full bowel can compress bladder

7. Take antibiotics as prescribed — do not stop early

8. Report fever, flank pain, urinary retention — may = pyelonephritis/obstruction

What are the key components of the CAUTI Prevention Bundle?

1. Use only when appropriate

   • Acute urinary retention or obstruction

   • Accurate urine output monitoring in a critically ill patient

   • Perioperative use (remove within 24 hours after surgery when appropriate)

   • Open sacral/perineal wounds in incontinent patients

   • End-of-life comfort care

2. Maintain safely: closed drainage, bag below bladder, no kinks, secure catheter, routine hygiene

3. Alternatives: toileting schedule, bladder scanner, external catheter, intermittent catheter

What is the pathophysiology of Urolithiasis (Kidney Stones)?

1. Minerals crystallize and form stones (calculi) within the urinary tract.

2. Stones obstruct urine flow.

3. Urine backs up, increasing pressure.

4. Severe colicky pain develops.

5. Hematuria occurs as stones scratch the urinary tract.

6. Prolonged obstruction may lead to infection, hydronephrosis, or acute kidney injury (AKI).

What are the 7 risk factors for urolithiasis?

1. Dehydration (most important)

2. Hypercalcemia (e.g., hyperparathyroidism)

3. Immobility (↑ calcium release from bones)

4. UTIs (struvite stones)

5. High-protein diet (uric acid stones)

6. High oxalate intake (spinach, nuts)

7. Family history

What are 6 clinical manifestations of urolithiasis (kidney stones)?

1. Severe colicky flank pain (comes in waves)

2. Pain radiating to the lower abdomen, groin, testicle, or labia

3. Nausea and vomiting (severe pain stimulates the GI tract)

4. Hematuria (stone scratches the urinary tract)

5. Dysuria, urgency, and frequency (if the stone is lower in the urinary tract)

6. Restlessness due to intense pain

What are 4 emergency cues of urolithiasis (kidney stones)?

1. Fever or chills (possible infection)

2. Anuria (complete urinary obstruction)

3. Hypotension or tachycardia (possible sepsis or shock)

4. Rising creatinine (possible acute kidney injury)

What are 6 nursing interventions for a patient with urolithiasis (kidney stones)?

1. Control pain and nausea.

2. Encourage fluids (if not contraindicated).

3. Monitor intake and output to evaluate hydration, kidney function, and worsening obstruction.

4. Strain the urine to catch the stone after it passes (for analysis and prevention of future stones)

5. Monitor for complications:

   • Fever

   • Anuria

   • Rising creatinine

   • Worsening pain

6. Prepare for procedures

What 4 procedures are used to treat urolithiasis (kidney stones)?

1. Lithotripsy: Uses shock waves to break the stone into smaller fragments so they can pass naturally.

2. Ureteroscopy: A scope is used to remove or break up stones that do not pass on their own.

3. Ureteral Stent Placement: A small tube is placed in the ureter to keep it open and allow urine to drain.

4. Percutaneous Nephrolithotomy (PCNL): Surgical removal of large or complex kidney stones through a small incision in the back; used for stones too large for lithotripsy or ureteroscopy.

What is the pathophysiology of Polycystic Kidney Disease (PKD)?

1. Genetic disorder causes fluid-filled cysts to develop from the renal tubules.

2. Cysts enlarge and compress healthy nephrons.

3. Functional kidney tissue is gradually replaced by cysts.

4. Kidney filtration decreases and the kidneys enlarge.

5. Waste products build up (uremia).

6. May progress to hypertension (HTN), chronic kidney disease (CKD), and end-stage renal disease (ESRD).

What are 7 clinical manifestations of Polycystic Kidney Disease (PKD)?

1. Flank or abdominal pain

2. Hypertension

3. Hematuria or cloudy urine

4. Recurrent UTIs

5. Kidney stones

6. Increased abdominal girth

7. Constipation

What are 7 nursing interventions for Polycystic Kidney Disease (PKD)?

1. Control blood pressure: high BP speeds up damage

2. Manage pain safely: patients have chronic flank pain from enlarged kidneys

3. Encourage prescribed hydration plan: reduce stone formation and help maintain kidney health

4. Monitor for infection: UTIs can worsen kidney damage

5. Prevent constipation:enlarged kidneys may already compress the intestines

   • Straining can increase discomfort

6. Avoid nephrotoxic medications unless prescribed: some drugs can further damage the kidneys

   • NSAIDs and contrast dyes

7. Teach follow-up and renal-protective lifestyle habits

   • Control BP, stay hydrated, avoid smoking, take medications, etc

What 3 dietary considerations should be taught to patients with Polycystic Kidney Disease (PKD)?

1. Encourage prescribed hydration to reduce kidney stone formation.

2. Follow renal-protective, low-sodium habits.

3. Prevent constipation with adequate fiber (as tolerated).

What is the pathophysiology of Hydronephrosis, Hydroureter, and Urethral Stricture?

1. Urine drainage becomes blocked (stone, stricture, clot, tumor, pregnancy, BPH, neurogenic bladder, etc.).

2. Urine backs up.

3. Pressure increases above the obstruction.

4. The kidney and/or ureter dilates.

5. Urinary stasis increases infection risk.

6. Prolonged obstruction impairs kidney function.

What are 9 clinical manifestations of Hydronephrosis, Hydroureter, and Urethral Stricture?

1. Flank, suprapubic, or pelvic pain

   • Flank pain: kidney involvement

   • Suprapubic pain: bladder involvement

2. Difficulty starting urine stream

3. Weak stream or dribbling

4. Feeling of incomplete bladder emptying

5. Decreased urine output or anuria

6. Bladder distention

7. Fever or chills

8. Hematuria

9. Elevated BUN and creatinine

What 3 imaging and diagnostic procedures are used to evaluate hydronephrosis and hydroureter?

1. Renal/Bladder Ultrasound – First-line imaging to detect hydronephrosis.

2. CT Scan – Used if a stone, tumor, or other obstruction is suspected.

3. Cystoscopy or Ureteroscopy – Allows direct visualization of the urinary tract and may also be used to treat the obstruction.

What 6 treatments are used to relieve hydronephrosis and hydroureter?

Goal: Relieve the obstruction and protect kidney function.

1. Catheterization – Drains the bladder in urinary retention or bladder outlet obstruction.

2. Ureteral Stent – Keeps the ureter open so urine can flow from the kidney to the bladder.

3. Nephrostomy Tube – Drains urine directly from the kidney when urine cannot pass through the ureter.

4. Stone Removal or Lithotripsy – Removes obstruction caused by kidney stones.

5. Dilation for Stricture – Widens a narrowed urethra or ureter.

6. Surgery – Used for tumors, severe strictures, or prostate obstruction.

What are 6 nursing interventions for Hydronephrosis, Hydroureter, and Urethral Stricture?

1. Monitor intake & output closely.

2. Assess pain and bladder distention.

3. Trend BUN, creatinine, and eGFR.

4. Maintain catheter, stent, or nephrostomy tube patency.

5. Monitor for fever and signs of sepsis.

6. Teach the patient to report:

   • Decreased urine output

   • Fever

   • Flank pain

   • Hematuria

What is the pathophysiology and 4 common causes of Glomerulonephritis (Nephritic Syndrome)?

1. Immune-mediated inflammation damages the glomeruli.

2. Antigen-antibody complexes deposit in the glomeruli.

3. The damaged filter allows blood to leak into the urine.

4. Glomerular filtration rate (GFR) decreases.

5. Fluid and waste are retained, causing edema and hypertension.

Common Causes:

• Acute: Post-streptococcal infection

• Chronic: Lupus, Diabetes Mellitus, Goodpasture syndrome

What are 5 clinical manifestations of Glomerulonephritis (Nephritic Syndrome)?

1. Hematuria (cola/tea-colored urine): hallmark sign

2. Oliguria

3. Periorbital edema

4. Hypertension

5. Mild to moderate proteinuria (foamy urine)

What 4 diagnostic tests are used for Glomerulonephritis (Nephritic Syndrome)?

1. Urinalysis (hematuria, RBC/protein casts)

2. BUN, Creatinine, eGFR

3. Serum albumin

4. Possible kidney biopsy

What are 4 treatments for Glomerulonephritis (Nephritic Syndrome)?

1. Restore fluid balance

2. Control blood pressure

3. Treat the underlying cause (e.g., antibiotics for post-strep)

4. Corticosteroids or immunosuppressants for immune-mediated disease

What are 7 nursing interventions for Glomerulonephritis (Nephritic Syndrome)?

1. Monitor BP

2. Monitor daily weight and I&O

3. Assess urine color and output

4. Monitor edema

5. Trend BUN, creatinine, eGFR

6. Monitor for fluid overload (pulmonary edema, heart failure)

7. Prepare for possible kidney biopsy: determines exact cause and severity of glomerular damage

What is the pathophysiology and 5 common causes of Nephrotic Syndrome?

1. The glomerulus becomes abnormally permeable ("leaky").

2. Large amounts of protein leak into the urine.

3. Serum albumin decreases (hypoalbuminemia).

4. Fluid moves into tissues, causing generalized edema.

5. The liver increases lipid production, causing hyperlipidemia.

Common Causes:

1. Diabetes Mellitus

2. Glomerulonephritis

3. Lupus

4. Certain drugs

5. Kidney damage

What are 6 clinical manifestations of Nephrotic Syndrome?

1. Massive proteinuria (>3.5 g/day): hallmark

2. Severe generalized edema

3. Hypoalbuminemia

4. Hyperlipidemia/lipiduria

5. Increased risk of blood clots

6. Increased risk of infection

What diagnostic tests 4 used for Nephrotic Syndrome?

1. Urinalysis (heavy proteinuria, lipiduria, fatty/protein casts)

2. Serum albumin (low)

3. Lipid panel (high)

4. BUN, Creatinine, eGFR

What are 6 treatments and nursing interventions for Nephrotic Syndrome?

1. Corticosteroids or immunosuppressants

2. ACE inhibitors/ARBs (decrease proteinuria and BP)

3. Diuretics for edema

4. Statins for hyperlipidemia

5. Anticoagulants if clot risk is high

6. Encourage a low-sodium diet

What are 5 characteristics of Acute Glomerulonephritis?

1. Onset: Sudden inflammation of the glomeruli, often after a streptococcal infection.

2. Pathophysiology: Antigen-antibody complexes deposit in the glomeruli, causing inflammation and decreased filtration.

3. Course: Presents suddenly and may improve significantly if treated early.

4. Goals of Treatment:

   • Control blood pressure.

   • Improve urine output.

   • Reduce edema.

   • Prevent fluid overload complications.

5. Prognosis: May fully resolve with appropriate treatment.

What are 5 characteristics of Chronic Glomerulonephritis?

1. Onset: Long-term, ongoing immune-mediated damage that gradually destroys kidney tissue.

2. Common Causes: Lupus, Diabetes Mellitus, Goodpasture syndrome.

3. Course: Healthy nephrons are progressively destroyed, leading to a gradual decline in kidney function.

4. Goals of Treatment:

   • Slow progression of kidney damage (cannot be cured)

   • Preserve remaining kidney function.

   • Control hypertension.

   • Prepare for chronic kidney disease (CKD) management if needed.

5. Prognosis: May progress to Chronic Kidney Disease (CKD) or End-Stage Renal Disease (ESRD).

What is the pathogenesis of thyroid disorders?

• Hypothyroidism (decrease in thyroid hormones)

  • Caused by hashimotos (autoimmune), iodine deficiency, thyroidectomy, pituitary failure

  • Decrease in T3/T4 → slower metabolism → increase in TSH due to loss of feedback

• Hyperthyroidism

  • Caused by graves disease (autoimmune), thyroid tumors, excess hormone intake

  • Increased T3/T4 → increased metabolism → less TSH due to negative feedback

What are the thyroid hormone lab patterns for primary, secondary, and tertiary hypothyroidism and hyperthyroidism?

1. Primary Hypothyroidism

   • Problem: Thyroid gland

   • TSH: ↑ High and Free T4/T3: ↓ Low

2. Secondary Hypothyroidism

   • Problem: Pituitary gland (can't make enough TSH)

   • TSH: ↓ Low or Normal and Free T4/T3: ↓ Low

3. Tertiary Hypothyroidism

   • Problem: Hypothalamus (can't make enough TRH)

   • TSH: ↓ Low and Free T4/T3: ↓ Low

4. Primary Hyperthyroidism

   • Problem: Thyroid gland makes too much hormone

   • TSH: ↓ Low and Free T4/T3: ↑ High

5. Secondary Hyperthyroidism

   • Problem: Pituitary gland makes too much TSH

   • TSH: ↑ High or Normal and Free T4/T3: ↑ High

What are 8 clinical manifestations of hypothyroidism?

1. Fatigue and lethargy (cells produce less energy)

2. Cold intolerance (less body heat is produced)

3. Weight gain (slower metabolism burns fewer calories)

4. Dry skin, brittle nails, thinning hair

5. Constipation (slower GI motility)

6. Bradycardia

7. Depression, forgetfulness, slowed thinking

8. Heavy or irregular menstrual periods

What 3 laboratory tests are used to diagnose hypothyroidism?

1. TSH: ↑ High in primary hypothyroidism

2. Free T4: ↓ Low

3. Thyroid antibodies (Hashimoto thyroiditis):

   • TPOAb (Thyroid Peroxidase Antibodies)

   • TgAb (Thyroglobulin Antibodies)

What are 4 goals and nursing priorities for managing hypothyroidism?

1. Restore normal thyroid hormone levels.

2. Identify whether the disorder is:

   • Primary (thyroid)

   • Secondary (pituitary)

   • Tertiary (hypothalamus)

3. Monitor older adults closely because starting thyroid therapy may cause:

   • Angina

   • Dysrhythmias

4. Remember that improvement is gradual—response to therapy takes weeks.

What 6 teachings should be provided to a patient taking levothyroxine (hypothyroidism)?

1. Levothyroxine is synthetic T4 that replaces missing thyroid hormone.

2. Take on an empty stomach, 30–60 minutes before breakfast.

3. Separate from calcium, iron, antacids, and vitamins because they decrease absorption.

4. Usually requires lifelong therapy and takes weeks to improve

5. Take it at the same time every day and do not skip doses.

6. Report signs of over-replacement (hyperthyroidism):

   • Tachycardia

   • Palpitations

   • Weight loss

   • Heat intolerance

What is myxedema coma, what triggers it, and what are the priority interventions?

1. Definition: A severe, life-threatening complication of hypothyroidism.

2. Common Triggers:

   • Infection

   • Trauma

   • Surgery

   • Cold exposure

3. Clinical Manifestations (5 H's):

   • Hypothermia: hallmark

   • Heart rate low (bradycardia)

   • Hypotension

   • Hypoventilation

   • Head changes (altered mental status/coma)

4. Priority Actions:

   • Notify the provider immediately.

   • Maintain airway and breathing (ABCs first).

   • Administer IV thyroid hormone and supportive care as ordered.

What 7 laboratory tests and diagnostic studies are used to diagnose hyperthyroidism?

Labs:

1. TSH: ↓ Low

2. Free T4: ↑ High

3. T3: May be ↑ High

4. TRAb (TSH receptor antibodies): Positive in Graves disease

Other Diagnostics:

1. ECG (tachycardia, palpitations, atrial fibrillation)

2. Thyroid ultrasound (goiter or nodules)

3. Radioactive iodine uptake (RAIU) scan

What are 13 clinical manifestations of hyperthyroidism?

1. T = Tremor (nervous system overstimulation)

2. H = Heart rate up (tachycardia)

3. Y = Yawning/fatigue (body is working so hard that patients become fatigued)

4. R = Restlessness (overstimulated nervous system)

5. O = Oligomenorrhea (infrequent menstrual periods)

6. I = Intolerance to heat

7. D = Diarrhea (increased GI motility)

8. I = Irritability (brain overstimulation)

9. S = Sweating (increased heat production)

10. M = Muscle wasting (muscle breakdown from increased metabolism)

Graves Disease Findings:

• Goiter

• Exophthalmos (proptosis)

• Pretibial myxedema

What are 4 ways hyperthyroidism affects overall health?

1. Cardiovascular: Tachycardia, palpitations, atrial fibrillation (↑ stroke risk), heart failure risk

2. Metabolic: Weight loss, muscle weakness/wasting, heat intolerance, fatigue

3. Psychological: Anxiety, irritability, mood changes, insomnia

4. Pregnancy: Miscarriage, hypertensive complications, preterm birth, low birth weight

What are 6 nursing interventions for hyperthyroidism

1. Provide a calm, low-stimulation environment.

2. Monitor for dysrhythmias (especially AFib).

3. Administer antithyroid medications as prescribed.

4. Teach medication adherence (do not stop abruptly).

5. Encourage increased calorie and protein intake.

6. Provide eye care for Graves disease (lubrication, elevate HOB, report vision changes).

What 4 treatments are used for hyperthyroidism?

1. Antithyroid medications (Methimazole, PTU):

   • Decrease T3/T4 production.

   • PTU also blocks T4 → T3 conversion.

2. Beta blockers:

   • Reduce tachycardia, tremors, and anxiety.

   • Do NOT decrease thyroid hormone levels.

3. Radioactive iodine (RAI) ablation:

   • Destroys overactive thyroid tissue.

   • May result in hypothyroidism.

4. Thyroidectomy:

   • Surgical removal of the thyroid.

   • Used for large goiters, thyroid cancer, ineffective medications, or when RAI is not appropriate.

What 4 patient teachings are important for hyperthyroidism treatment?

1. Do not stop antithyroid medications abruptly.

2. Report fever or sore throat immediately (possible agranulocytosis).

3. Report palpitations, fever, or confusion (possible thyroid storm).

4. After radioactive iodine ablation or thyroidectomy, lifelong levothyroxine replacement may be needed.

What is thyroid storm, 4 triggers, and what are 6 clinical manifestations?

Thyroid storm is a life-threatening emergency caused by severe, untreated or undertreated hyperthyroidism.

Common Triggers:

1. Infection or acute illness

2. Surgery or trauma

3. Postpartum state

4. Abrupt withdrawal of antithyroid medication (never stop abruptly)

Clinical Manifestations:

1. High fever: hallmark

2. Severe tachycardia or atrial fibrillation

3. Hypertension early → hypotension/shock later

4. Agitation, delirium, confusion

5. Nausea, vomiting, diarrhea

6. Heart failure

What is the emergency treatment for thyroid storm?

1. ABCs first – support airway, breathing, oxygenation, and cardiac stabilization.

2. Beta blocker – decreases heart rate and cardiac workload.

3. Antithyroid medication (Methimazole or PTU) – stops new thyroid hormone production.

4. Iodine (AFTER antithyroid medication) – prevents release of stored thyroid hormone.

   • Never give iodine first, because it provides the thyroid with more iodine to make hormone.

5. Glucocorticoids – decrease conversion of T4 → T3.

6. Cooling measures – cooling blanket, ice packs, antipyretics as appropriate.

7. Treat the underlying trigger (e.g., infection) and correct dehydration/electrolyte imbalances.

What are 3 preoperative priorities and medications before a thyroidectomy?

Goal: Make the patient euthyroid and prevent thyroid storm before surgery.

1. Antithyroid medications (Methimazole or PTU) – Given first to decrease T3/T4 production.

2. Iodine solution (SSKI or Lugol's solution) – Given after antithyroid medication to decrease thyroid size and vascularity, reducing bleeding during surgery.

3. Beta blockers (Propranolol or Metoprolol) – Reduce heart rate, tremors, and anxiety; do not lower thyroid hormone levels.

What are 4 major postoperative complications of a thyroidectomy, how are they recognized, and how are they treated?

1. Respiratory Distress (Highest Priority)

   • Recognition: Laryngeal edema, vocal cord paralysis (recurrent laryngeal nerve injury)

   • Treatment: Keep tracheostomy tray and suction at bedside; notify the provider immediately for airway compromise.

2. Hemorrhage

   • Recognition: Bleeding on the dressing, behind the neck, increased drain output, frequent swallowing.

   • Treatment: Notify the provider, monitor vital signs closely, prepare for possible return to surgery.

3. Hypocalcemia

   • Recognition: Tingling, tetany, positive Chvostek's and Trousseau's signs.

   • Treatment: Keep calcium gluconate available and administer as ordered.

4. Thyroid Storm

   • Recognition: Fever, tachycardia, hypertension, agitation.

   • Treatment: Beta blockers, antithyroid medications, and cooling measures.

What causes a goiter, what 2 complications can it cause, and how is it managed?

• Cause:

  1. Iodine deficiency

  2. Constant TSH overstimulation (e.g., hypothyroidism)

• Possible Complications:

  1. Dysphagia (difficulty swallowing)

  2. Dyspnea (difficulty breathing) from compression

• Nursing Care:

  1. Assess swallowing and breathing.

  2. Avoid tight clothing around the neck.

  3. Treat the underlying cause (iodine supplementation, antithyroid medications, or surgery).

What causes proptosis (exophthalmos) in Graves disease, and what nursing care is required?

• Cause: Autoimmune inflammation behind the eyes causes tissue swelling, pushing the eyes forward.

• Complications:

  1. Eyes may not close completely.

  2. Dryness and irritation.

  3. Vision changes.

• Nursing Care:

  1. Assess for vision changes (double vision, eye pain).

  2. Administer eye lubrication as prescribed.

  3. Elevate the head of the bed to reduce swelling.

  4. Teach the patient to report:

     • Eye pain

     • Diplopia (double vision)

     • Worsening vision

What are 13 risk factors for atherosclerosis?

Non-modifiable:

1. Age

2. Family history

3. Male sex

4. Postmenopausal women

Modifiable:

1. Diet high in saturated fats

2. Sedentary lifestyle

3. Obesity

4. Smoking

5. Hypertension

6. Diabetes mellitus

7. Elevated homocysteine/lipid levels

What are the clinical manifestations of atherosclerosis?

• Often asymptomatic until significant arterial narrowing occurs.

• Angina may develop:

  1. Tightness, fullness, or pressure in the midsternal chest

  2. Pain may radiate to the left arm, neck, jaw, or back (referred pain)

  3. Initially triggered by physical exertion or stress

What 5 medications are used to treat atherosclerosis and coronary artery disease?

1. Nitrates – Improve blood flow and relieve angina.

2. Beta blockers – Decrease heart rate and oxygen demand.

3. Calcium channel blockers – Relax blood vessels and reduce cardiac workload.

4. Aspirin/Antiplatelet agents – Prevent clot formation and future cardiac events.

5. Statins – Lower cholesterol and slow plaque progression.

What 2 revascularization procedures are used to treat significant coronary artery blockage?

1. PCI (Percutaneous Coronary Intervention) – Balloon angioplasty with stent placement to open the blocked artery.

2. CABG (Coronary Artery Bypass Graft) – Creates a new pathway around the blocked coronary artery using a graft.

What 7 patient teachings should be provided for atherosclerosis?

1. Stop smoking.

2. Control blood pressure.

3. Manage diabetes.

4. Stay physically active as tolerated.

5. Take medications as prescribed.

6. Nitroglycerin relieves angina but does NOT treat the underlying atherosclerosis.

7. Report chest pain that is worsening, occurs at rest, or is not relieved by nitroglycerin, as it may indicate acute coronary syndrome (ACS).

What are the 3 types of angina and how do they differ?

1. Vasospastic (Prinzmetal) Angina

   • Caused by sudden coronary artery spasm

   • Occurs at rest (not activity-related)

   • May cause transient ST-segment elevation

   • Relieved by nitrates and calcium channel blockers (CCBs)

2. Chronic Stable Angina

   • Predictable chest pain with moderate/prolonged exertion

   • Similar pattern over months

   • Relieved by rest or nitroglycerin

   • Causes only slight activity limitation

3. Unstable Angina

   • Occurs at rest or is becoming more frequent/severe

   • Lasts >15 minutes

   • Not relieved by rest or nitroglycerin

   • May have ECG changes

   • Warning sign of an impending MI (no heart muscle death yet)

How do STEMI and NSTEMI differ?

1. STEMI

   • Complete coronary artery occlusion

   • ST-segment elevation

   • Deep Q waves may develop

   • Extensive/full-thickness myocardial damage

2. NSTEMI

   • Partial coronary artery blockage

   • ST-segment depression

   • Some myocardial cell death, but not full-thickness

What 4 cardiac biomarkers are used to diagnose myocardial injury?

1. Troponin I – Highly specific for myocardial injury.

2. Troponin T – Highly specific for myocardial injury.

3. CK-MB – Indicates cardiac muscle damage.

4. Myoglobin – Earliest marker to rise after myocardial injury.

What are 5 initial treatments for a myocardial infarction (MI)?

MONA

1. Morphine

2. Oxygen

3. Nitrates

4. Aspirin

• STEMI: Eligible patients may receive tPA (thrombolytic therapy) within 4.5 hours of symptom onset.

What are 7 classic manifestations of a myocardial infarction (MI)?

1. Chest pain, pressure, tightness, or heaviness

2. Pain radiating to the left arm, neck, jaw, or back

3. Diaphoresis (profuse sweating)

4. Dizziness

5. Nausea and vomiting

6. Shortness of breath (dyspnea)

7. Sense of impending doom

Which 3 patients are more likely to have atypical MI symptoms, and what are those 3 symptoms?

Higher-risk groups:

1. Women

2. Older adults

3. Patients with diabetes mellitus

Atypical Symptoms:

1. Dyspnea (shortness of breath)

2. Fatigue

3. Nausea

These patients may have an MI WITHOUT chest pain due to nerve damage and altered pain perception (especially in diabetes).

What are 2 compensatory mechanisms in heart failure, and why do they occur?

1. Sympathetic Nervous System (SNS) Activation

   • Trigger: The body senses decreased cardiac output (↓ CO).

   • Response:

     • ↑ Heart rate

     • ↑ Contractility

     • Vasoconstriction

   • Purpose: Immediately improve blood pressure and tissue perfusion.

2. Renin-Angiotensin-Aldosterone System (RAAS) Activation

   • Trigger: The kidneys sense decreased blood flow.

   • Response:

     • Sodium retention

     • Water retention

     • ↑ Preload (more blood returning to the heart)

   • Purpose: Increase blood volume and improve cardiac output.

• Helpful initially but lead to cardiac remodeling (chamber enlargement, myocardial hypertrophy, fibrosis) → decompensated HF

How do the 5 types of heart failure differ?

1. HFpEF (Diastolic): Can't fill → preserved EF (>50%), stiff ventricle.

2. HFrEF (Systolic): Can't squeeze → reduced EF (<40–45%), weak ventricle.

3. Left-Sided HF: Blood backs up into the lungs → dyspnea, crackles, pulmonary edema.

4. Right-Sided HF: Blood backs up into the body → JVD, edema, ascites.

5. High-Output HF: Heart pumps normally, but the body's oxygen demand exceeds supply.

What are the assessment findings, causes, treatment, and patient teaching for Diastolic Dysfunction (HFpEF)?

1. Assessment: LVEF >50% (preserved EF), pulmonary congestion, normal contraction but poor filling.

2. Etiology/Risk Factors: Chronic HTN/LV hypertrophy, diabetes, obesity, atrial fibrillation, aging (stiff, noncompliant ventricle).

3. Treatment: Beta blockers, calcium channel blockers, diuretics for congestion, blood pressure control.

4. Patient Teaching: Control BP, monitor daily weight, take medications as prescribed, follow a low-sodium diet.

What are the assessment findings, causes, treatment, and patient teaching for Systolic Dysfunction (HFrEF)?

1. Assessment: LVEF <40–45%, volume overload, weak ventricular contraction.

2. Etiology/Risk Factors: CAD/MI, dilated cardiomyopathy, long-standing HTN, valvular disease.

3. Treatment: ACE inhibitors/ARBs, beta blockers, diuretics, inotropes if severe.

4. Patient Teaching: Monitor daily weight, take medications as prescribed, pace activities, report rapid weight gain.

What are the assessment findings, causes, treatment, and patient teaching for Left-Sided Heart Failure?

1. Assessment: Dyspnea, orthopnea, PND, crackles, pulmonary edema, cough.

2. Etiology/Risk Factors: Hypertension, CAD, valvular disease.

3. Treatment: Diuretics, ACE inhibitors/ARBs, beta blockers, oxygen.

4. Patient Teaching: Recognize worsening dyspnea/orthopnea, sleep with the head of the bed elevated, take medications as prescribed.

What are the assessment findings, causes, treatment, and patient teaching for Right-Sided Heart Failure?

1. Assessment: JVD, hepatomegaly, splenomegaly, peripheral edema, ascites, weight gain, early satiety.

2. Etiology/Risk Factors: Most commonly caused by left-sided HF; also RV MI and pulmonary hypertension.

3. Treatment: Diuretics, fluid and sodium restriction, treat the underlying left-sided HF.

4. Patient Teaching: Monitor daily weight (most reliable indicator of fluid status) and report increasing abdominal bloating or edema.

What are the assessment findings, causes, treatment, and patient teaching for High-Output Heart Failure?

1. Assessment: Normal or increased cardiac output, but tissues remain hypoxic; heart failure symptoms despite adequate pumping.

2. Etiology/Risk Factors: Sepsis, high fever, anemia, hyperthyroidism.

3. Treatment: Treat the underlying cause (infection, anemia, thyroid disease).

4. Patient Teaching: Manage the underlying condition and report worsening shortness of breath or fatigue.

What 9 diagnostic tests are commonly used to evaluate heart failure?

Laboratory Tests

1. Serum Electrolytes – Detect sodium and potassium imbalances

2. Hemoglobin (Hgb) & Hematocrit (Hct) – Assess for anemia

3. BNP (B-type Natriuretic Peptide) – Released when the ventricles are stretched by excess fluid; an elevated BNP supports the diagnosis of heart failure.

4. ABGs (Arterial Blood Gases)

Imaging Studies
5. Chest X-ray (CXR) – Detects pulmonary congestion and cardiomegaly =
6. Echocardiogram
7. Radionuclide Study (MUGA Scan) – Measures how well the heart pumps by calculating the ejection fraction (EF).

Cardiac Catheterization
8. Right Heart Catheterization – Measures pressures inside the heart and pulmonary circulation.
9. Left Heart Catheterization – Evaluates the coronary arteries for coronary artery disease (CAD).

What are 4 common heart failure medications and how do they relate to HF?

1. ACE Inhibitors/ARBs: Block the RAAS → lower blood pressure and afterload → reduce cardiac workload and slow HF progression.

2. Beta Blockers: Block excessive SNS stimulation → decrease heart rate and myocardial oxygen demand.

3. Diuretics: Remove excess sodium and water retained from RAAS activation → reduce edema and improve breathing.

4. Hydralazine/Isosorbide Dinitrate: Cause vasodilation → decrease preload and afterload, reducing the heart's workload.

What are 7 Key Interventions for Heart Failure

1. LVS heart function assessment (echocardiogram) — determines EF and type of dysfunction

2. ACE-I/ARB at discharge for systolic dysfunction (LVEF <40%)

3. Anticoagulant at discharge for chronic/recurrent A-fib

4. Influenza immunization

5. Pneumococcal immunization

6. Smoking cessation counseling

7. Complete discharge instructions: activity level, diet, medications, follow-up, weight monitoring, what to do if symptoms worsen

What are 3 patient teaching and 2 follow-up techniques for a patient with HF?

1. Monitor daily weight and report:

   • Weight gain >2–3 lb in one day

   • Weight gain >5 lb in one week

2. Follow a low-sodium diet and fluid restriction if prescribed.

3. Take medications exactly as prescribed (do not stop abruptly)

4. Report worsening shortness of breath, edema, or fatigue promptly

5. Keep scheduled follow-up appointments to monitor symptoms, lab values, and heart function

What are the etiology, treatment, and surgery for Mitral Valve Prolapse (MVP)?

• Etiology: Mitral valve leaflets bulge into the left atrium during systole; most common valvular abnormality.

  • Located between the L atrium and L ventricle

• Treatment: Beta blockers for palpitations and anxiety if symptomatic.

• Surgery: May require mitral valve repair or replacement if severe mitral regurgitation develops.

What are 7 clinical manifestations of Mitral Valve Prolapse (MVP)?

1. Often asymptomatic

2. Chest discomfort

3. Palpitations

4. Exercise intolerance

5. Anxiety

6. Midsystolic click

7. Late systolic murmur at the apex

What are the etiology, treatment, and surgery for Mitral Valve Stenosis (MVS)?

• Etiology: Narrowed mitral valve obstructs blood flow from the left atrium to the left ventricle; most commonly caused by rheumatic fever.

• Treatment: Rate/rhythm control (AFib), anticoagulation, diuretics for pulmonary congestion.

• Surgery: Balloon valvuloplasty or valve repair/replacement for severe stenosis.

What are 7 clinical manifestations of Mitral Valve Stenosis (MVS)?

1. Dyspnea on exertion

2. Orthopnea

3. Paroxysmal nocturnal dyspnea (PND)

4. Palpitations (often due to atrial fibrillation)

5. Fatigue

6. Crackles

7. Low-pitched diastolic rumble at the apex

What are the etiology, treatment, and surgery for Aortic Regurgitation (AR)?

• Etiology: Aortic valve fails to close completely, allowing blood to leak back into the left ventricle during diastole.

• Treatment: Vasodilators and heart failure management.

• Surgery: Valve repair or replacement once symptoms or LV dysfunction develop.

What are 9 clinical manifestations of Aortic Regurgitation (AR)?

1. Exertional dyspnea

2. Orthopnea

3. Paroxysmal nocturnal dyspnea (PND)

4. Palpitations (severe disease)

5. Fatigue

6. Bounding pulses

7. Wide pulse pressure

8. Diastolic blowing murmur

9. Visible carotid pulsations

What are the etiology, treatment, and surgery for Aortic Stenosis (AS)?

• Etiology: Narrowing of the aortic valve, most commonly due to age-related calcification (also bicuspid valve or rheumatic disease).

• Treatment: Monitor for worsening dyspnea, syncope, and chest pain; manage symptoms medically.

• Surgery: Balloon valvuloplasty or surgical/transcatheter valve replacement (TAVR).

What are 6 clinical manifestations of Aortic Stenosis (AS)?

1. Exertional chest pain

2. Syncope with activity

3. Fatigue

4. Dyspnea on exertion

5. Harsh systolic murmur at the right sternal border

6. Diminished peripheral pulses

What are the 6 general medical management interventions for valvular heart disease?

1. Prophylactic antibiotics (when indicated) to reduce the risk of infective endocarditis.

2. Cardioversion and/or anticoagulants for dysrhythmias (e.g., atrial fibrillation).

3. Activity restriction to reduce myocardial oxygen demand.

4. Monitor cardiac status and hemodynamics.

5. Monitor anticoagulation therapy and laboratory values.

6. Monitor for postoperative complications after valve repair or replacement.

What are the 4 types of cardiomyopathy?

1. Dilated Cardiomyopathy (DCM) = Doesn't Contract

   • Dilated ventricles

   • Weak contraction

   • Systolic dysfunction (↓ EF)

2. Hypertrophic Cardiomyopathy (HCM) = Hard to Fill

   • Thickened left ventricle/septum

   • Small ventricular chamber

   • Diastolic dysfunction (preserved EF)

   • High risk of sudden cardiac death

3. Restrictive Cardiomyopathy (RCM) = Restricted Filling

   • Stiff, rigid ventricles

   • Poor ventricular filling

   • Diastolic dysfunction

   • Enlarged atria

4. Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) = Arrhythmias in the Right Ventricle

   • RV muscle replaced by fat/scar tissue

   • Dangerous ventricular arrhythmias

   • Right-sided heart failure

   • High risk of sudden cardiac death

What is Infective Endocarditis (IE), and what is its pathophysiology?

• Definition: Infection of the endocardium, usually involving the heart valves.

• Pathophysiology:

  1. Bacteremia occurs.

  2. Bacteria attach to damaged or abnormal heart valves.

  3. Vegetations (bacteria + platelets + fibrin) form.

  4. Valves become damaged.

  5. Vegetations may break off, causing emboli.

What are 10 clinical manifestations of Infective Endocarditis (IE)?

1. Fever and chills

2. Weight loss

3. New or changing heart murmur

4. Signs of heart failure

5. Petechiae

6. Splinter hemorrhages

7. Osler nodes (on palms of hands and soles of feet): painful red nodules

8. Janeway lesions (flat, reddened maculae on hands and feet)

9. Roth spots: red spots in the eye

10. Positive blood cultures

What are 5 nursing interventions, and 3 patient teaching for Infective Endocarditis (IE)?

Treatment/Nursing

1. Obtain blood cultures before antibiotics.

2. Administer IV antibiotics for 4–6 weeks.

3. Monitor temperature and cardiac status.

4. Assess for embolic complications.

5. Surgery if severe valve damage, HF, persistent infection, or large vegetations.

Patient Teaching

1. Complete the full antibiotic course.

2. Take prophylactic antibiotics before certain procedures if prescribed.

3. Report fever or signs of embolization immediately.

What is Pericarditis, and what is its pathophysiology?

• Definition: Inflammation of the pericardial sac surrounding the heart.

• Pathophysiology:

  1. Inflammation develops (viral most common; also post-MI, malignancy, uremia, autoimmune disease).

  2. Inflamed pericardial layers rub together, causing pain and a friction rub.

  3. Fluid may accumulate (pericardial effusion).

  4. Severe effusion may lead to cardiac tamponade.

What are 7 clinical manifestations of Pericarditis?

1. Sharp pleuritic chest pain

2. Pain worsens with coughing, inspiration, or lying flat

3. Pain improves when sitting forward

4. Pericardial friction rub

5. Tachycardia

6. Fever

7. Elevated WBC, CRP, and ESR

What are 6 nursing interventions and 2 patient teaching for Pericarditis?

Treatment/Nursing

1. NSAIDs

2. Colchicine

3. Corticosteroids (if indicated)

4. Antibiotics if bacterial

5. Monitor for cardiac tamponade (Beck's triad, pulsus paradoxus).

6. Pericardiocentesis if tamponade develops.

Patient Teaching

1. Restrict activity during the acute phase.

2. Report worsening chest pain, shortness of breath, or dizziness.

What is Rheumatic Carditis, and what is its pathophysiology?

• Definition: An inflammatory heart disease that develops as a complication of untreated streptococcal pharyngitis.

• Pathophysiology:

  1. Untreated strep throat

  2. Rheumatic fever develops.

  3. Autoimmune attack affects all three heart layers.

  4. Aschoff bodies form.

  5. Scar tissue develops, especially affecting the mitral valve.

What are 8 clinical manifestations of Rheumatic Carditis?

1. Precordial chest pain

2. New or changing murmur

3. Tachycardia or dysrhythmias

4. Pericardial friction rub

5. Heart failure

6. Cardiomegaly

7. Prolonged PR interval on ECG

8. Long-term: Mitral and/or aortic stenosis

What are the 4 nursing interventions and 2 patient teaching for Rheumatic Carditis?

Treatment/Nursing

1. Antibiotics for streptococcal infection.

2. NSAIDs or corticosteroids.

3. Bed rest during the acute phase.

4. Treat heart failure if present.

Patient Teaching

1. Complete the full antibiotic course.

2. Monitor for cardiac symptoms.

3. Keep follow-up ECG and echocardiogram appointments.

What is Myocarditis, and what is its pathophysiology?

• Definition: Inflammation of the myocardium (heart muscle), most commonly caused by a viral infection.

• Pathophysiology:

  1. Inflammation damages the myocardium.

  2. Contractility decreases.

  3. Cardiac output decreases.

  4. Risk of heart failure and dysrhythmias increases.

What are 8 clinical manifestations of Myocarditis?

1. Fatigue

2. Fever

3. Flu-like symptoms

4. Chest pain

5. Palpitations

6. Dyspnea

7. Severe cases: Heart failure, cardiogenic shock, dysrhythmias

8. Labs: ↑ WBC, ↑ ESR/CRP, ↑ Troponin