NURS 370 Final Exam Study Guide Renal & Fluid/Electrolytes, Endocrine, Neurological

Indicators of Fluid Imbalance in Chronic Kidney Disease (CKD): Key indicators

• Edema (hands, feet, face, periorbital): kidney failure leads to sodium and water retention.​ Severe CKD leads to ascites or anasarca; appears as pitting or nonpitting swelling.​

• Rapid weight gain (most sensitive indicator): 1 kg gain = 1 liter fluid retained.​

• Crackles/dyspnea/pulmonary edema: Overload leads to fluid in the lungs.​ Dyspnea, crackles, orthopnea, paroxysmal nocturnal dyspnea.​

• Hypertension/JVD: Fluid retention increases vascular volume and BP.​

• Low urinary output (oliguria/anuria): declining GFR leads to decreased excretion.​ Output falls as GFR drops; <400 mL/day = oliguria, possible anuria in late CKD.

• Skin and Mucous Membranes: Dry, itchy, uremic frost seen only in severe cases. Pallor, bruising due to anemia and platelet dysfunction.​

• Vital Signs: Hypertension most common (from fluid and sodium retention), may see tachycardia in advanced overload.

Indicators of Fluid Imbalance in Chronic Kidney Disease (CKD): Lab & Physical Exam Findings

• Serum Electrolytes:

  • Low/High sodium (dilutional or hypernatremic, varies by volume status)

  • High potassium (hyperkalemia) in advanced CKD

  • High phosphate, low calcium.

• High BUN and creatinine: Gradually rise as kidneys fail.

• Decreased GFR: eGFR used to stage CKD; declining trend is most critical.

• Serum osmolality and urine specific gravity

  • Urine Specific Gravity: Can be low in renal damage (loss of concentrating ability) or high if dehydrated/overloaded. High specific gravity in dehydration/chronic fluid loss

  • Serum/Urine Osmolality: Low in overhydration or kidney concentrating defects, high in dehydration/SIADH. Low with overhydration or impaired concentrating ability.

• Physical Exam: Skin changes (dry, itchy), pitting edema, pallor, bruising, uremic frost possible in advanced disease.​

• Strict daily weights and I/O monitoring are essential!​

Patient Symptoms:

• Fatigue (anemia, toxin buildup), restless legs, confusion (uremia or hyponatremia), muscle cramps (electrolyte shifts), SOB, decreased appetite.​

Acute Kidney Injury (AKI) Causes/Mechanisms

• Pre-renal AKI: Most common; results from decreased perfusion, e.g., ECV depletion (hemorrhage, dehydration, burns), hypotension/shock, sepsis, heart failure.​

• Intra-renal AKI: Direct injury to the nephron, e.g., acute tubular necrosis (ischemia/toxins), nephrotoxic drugs (NSAIDs, aminoglycosides, IV contrast), glomerulonephritis, vasculitis.​

• Post-renal AKI: Obstruction to urine outflow, e.g., stones, tumors, BPH, strictures, neurogenic bladder.​

Acute Kidney Injury (AKI) Presentations: Oliguric/Anuric Phase

• Output <400 mL/day, often near zero

• Fluid overload: progressive weight gain, edema, JVD, crackles, pulmonary congestion, hypertension

• Uremic symptoms: nausea, vomiting, pruritus, confusion, seizures, metallic taste​

• Electrolyte imbalance: rapid rises in K (hyperkalemia), metabolic acidosis (low bicarbonate), dilutional hyponatremia/hypervolemia

• Labs: BUN/Cr climb rapidly, Ca↓, PO₄↑, anemia develops (↓EPO)​

Acute Kidney Injury (AKI) Presentations: Diuretic Phase

• Massive urine loss (1–5+ L/day) but poor concentration: risk of dehydration, hypotension, loss of Na/K​

• K, Na fall—careful replacement required

• BUN/Cr begin to drop but remain high, output gradually normalizes​

Acute Kidney Injury (AKI) Presentations: Recovery Phase

Gradual restoration of output and normalization of acid/base/electrolyte balance over weeks to months; some may never fully recover​

High-Risk Electrolyte Disturbances in Renal Failure: Hyperkalemia (K>5.5)

• Most life-threatening! Results from inability to excrete K; seen in oliguria, ESRD, missed dialysis

• Symptoms: Muscle weakness, paresthesias, peaked T-waves, prolonged PR, wide QRS, risk for heart block and arrest

• Treatment: Restrict K intake; urgent medical management includes insulin/glucose, calcium gluconate, kayexalate, or dialysis.​

High-Risk Electrolyte Disturbances in Renal Failure: Hyperphosphatemia/Hypocalcemia

• CKD leads to phosphate retention, binding/free calcium reduction, and decreased vitamin D activation

• Manifestations: bone pain, fractures (renal osteodystrophy), pruritus, calcifications in soft tissues, muscle cramps, tetany, Chvostek/Trousseau signs​

• Management: phosphate binders, dietary avoidance, Ca supplements, activated vitamin D

High-Risk Electrolyte Disturbances in Renal Failure: Metabolic Acidosis

• HCO₃ is depleted; kidneys can’t excrete acid load or reabsorb bicarbonate

• Symptoms: confusion, Kussmaul respirations, fatigue, vomiting, arrhythmias

• Management: sodium bicarbonate if pH <7.2, treat underlying AKI/CKD​

High-Risk Electrolyte Disturbances in Renal Failure: Sodium

• Can be low (dilutional, SIADH, fluid excess) → seizures, coma

• Can be high (profound water loss, DI) → neurologic instability​

• Management: depends strictly on underlying pathology and fluid status, slow correction needed

SIADH (Syndrome of Inappropriate ADH)

Endocrine-Related Fluid/Electrolyte Disorders

• Patho: Excess ADH → water retention, dilutional hyponatremia, low serum osmolality, high urine osmolality

• Labs: Na <135, low serum osmolality, high urine specific gravity

• Presentation: confusion, seizures, muscle cramps, headache, weight gain, decreased urine output.​

• Management: fluid restriction, salt tabs, correct cause, slow Na correction to prevent central pontine myelinolysis.​

DI (Diabetes Insipidus, Central or Nephrogenic)

Endocrine-Related Fluid/Electrolyte Disorders

• Patho: ADH deficit (central) or renal resistance (nephrogenic) → massive polyuria, hypernatremia, dehydration

• Labs: Na >145, dilute urine (SG <1.005), high serum osmolality, low urine osmolality

• Presentation: thirst, dry mucosa, hypotension, tachycardia, confusion, fatigue

• Management: vasopressin/desmopressin for central DI, thiazide diuretics for nephrogenic, careful fluid replacement.

Common Risk Factors for Progression to Advanced Kidney Disease

Most significant factors (with mechanisms):

• Diabetes Mellitus: Persistent hyperglycemia causes glomerulosclerosis and vascular injury, leading to proteinuria and nephron death.​

• Hypertension: High pressure damages glomeruli and microvasculature; RAAS activation worsens retention and fibrosis.​

• Autoimmune/Glomerular disease: Lupus, IgA nephropathy, vasculitis trigger chronic inflammation and scarring.​

• Chronic obstruction: Stones, BPH, tumors cause pressure damage and repeated infection risk.​

• Nephrotoxins: NSAIDs, aminoglycosides, IV iodine contrast—direct tubular toxicity and necrosis.​

• Infections: Untreated pyelonephritis or urosepsis can destroy nephrons.​

• Genetic diseases: PKD—large cysts crowd functional tissue, leading to ischemia and failure.​

• Older age, family history, smoking, CVD: Accelerate decline by compounding vascular/nephron injury.​

• Non-adherence: Missing BP/glucose control, dialysis, or nephroprotective diet accelerates GFR loss.​

Hypothyroidism (‘everything slows down’): General Assessment Findings

Fatigue, lethargy, weight gain, cold intolerance, slow speech, depression, impaired memory, myxedema (puffy non-pitting edema esp. face/hands).​

Hypothyroidism (‘everything slows down’): Skin/Hair Assessment Findings

Dry, coarse, brittle hair, hair loss (esp. outer 1/3 eyebrow), pale cool skin, slow wound healing.

Hypothyroidism (‘everything slows down’): Cardiac Assessment Findings

Bradycardia, possible pericardial effusion, hypotension; risk ↑ if hypothyroidism is severe.​

Hypothyroidism (‘everything slows down’): Other Assessment Findings

Menstrual irregularities (menorrhagia or amenorrhea), infertility, muscle stiffness.​

Hypothyroidism (‘everything slows down’): Labs

↑TSH, ↓T3/T4 (primary), all low in secondary hypothyroidism; autoantibodies in Hashimoto’s.

Hypothyroidism (‘everything slows down’): Complications

Myxedema coma—coma, hypothermia, hypotension, hypoventilation, hyponatremia, hypoglycemia.

Hypothyroidism (‘everything slows down’): Nursing Actions

Monitor for cardiac compromise if starting/restarting levothyroxine in older/cardiac patients. Start low-dose, titrate by TSH.​

Hyperthyroidism (‘everything speeds up’): General Assessment Findings

Nervousness, anxiety, insomnia, weight loss despite increased appetite, heat intolerance.​

Hyperthyroidism (‘everything speeds up’): Eye Assessment Findings

Exophthalmos, lid lag (Graves’), periorbital edema.

Hyperthyroidism (‘everything speeds up’): Cardiac Assessment Findings

Tachycardia, palpitations, arrhythmias (esp. afib), hypertension, bounding pulses, ↑CO failure in elderly.​

Hyperthyroidism (‘everything speeds up’): GI Assessment Findings

Diarrhea, increased motility, weight loss.

Hyperthyroidism (‘everything speeds up’): Skin/Hair Assessment Findings

Warm, moist, fine hair, flushed skin, weakness, muscle wasting.​

Hyperthyroidism (‘everything speeds up’): Other Assessment Findings

Menstrual irregularities, decreased fertility, osteopenia (long term).​

Hyperthyroidism (‘everything speeds up’): Labs

↓TSH, ↑T3/T4; autoimmune antibodies (Graves’).

Hyperthyroidism (‘everything speeds up’): Complications

Thyroid storm—high fever, severe tachycardia, delirium, heart failure, shock, death.​

Hyperthyroidism (‘everything speeds up’): Nursing Actions

Avoid stimulant meds/foods; teach med adherence—abrupt withdrawal can precipitate storm.​

Thyroid Storm Precipitating factors

Infection, surgery, trauma, MI, iodine/contrast, abrupt withdrawal of antithyroid meds.​

Thyroid Storm Symptoms

Hyperpyrexia (104+), tachycardia (180+), arrhythmia, confusion, agitation, delirium, vomiting, diarrhea, shock, possible death.​

Thyroid Storm Treatment

High-dose thionamides, iodine to block hormone release, beta-blockers for cardiac, steroids, cooling, fluids, monitor for arrhythmias.​

Myxedema Coma Precipitating factors

Illness, infection, cold stress, anesthesia/surgery, abrupt withdrawal of thyroid meds.​

Myxedema Coma Symptoms

Hypothermia, bradycardia, hypoventilation, Areflexia, altered LOC/coma, hypoglycemia, hypotension, hyponatremia.

Myxedema Coma Treatment

IV thyroxine, IV corticosteroids, passive rewarming, treat underlying cause, airway/ventilation, correct fluids/electrolytes.​

Adrenal Crisis Precipitating

Stress, infection, trauma, abrupt steroid withdrawal, surgery.​

Adrenal Crisis Symptoms

Sudden hypotension/shock, severe weakness, confusion, abdominal/back pain, vomiting/diarrhea, dehydration, hyperkalemia, hyponatremia, hypoglycemia, lethargy.

Adrenal Crisis Treatment

IV hydrocortisone, large volumes NS/D5, treat hyperkalemia/hyponatremia, continuous cardiac monitoring, stress dosing and education.​

Pheochromocytoma Crisis Symptoms

Episodes of severe hypertension (crisis), tachycardia, palpitations, headache, sweating, hyperglycemia, weight loss, anxiety, tremors.​

Pheochromocytoma Crisis Precipitating

Trauma, surgery, emotional stress, certain foods (tyramine), some meds.​

Pheochromocytoma Crisis Treatment

Pre-op alpha-blockers then beta-blockers, surgical resection, avoid stimulants, monitor BP/HR, steroid replacement after bilateral adrenalectomy.​

DKA (Diabetic Ketoacidosis) Patho

Insulin deficiency leads to fat breakdown → ketones/acidosis, severe dehydration, electrolyte loss.

DKA (Diabetic Ketoacidosis) Symptoms

Polyuria, polydipsia, dehydration, tachypnea (Kussmaul), N/V, abdominal pain, acetone breath, confusion/coma.​

DKA (Diabetic Ketoacidosis) Labs

BG >250, pH <7.3, HCO₃ <18, positive ketones, high AG, variable K.​

DKA (Diabetic Ketoacidosis) Priorities

1. Rapid IV saline for ECV restoration

2. Check/correct K before insulin!

3. IV insulin (regular)

4. Correct acidosis, monitor K (risk for hypokalemia as acidosis resolves).​

Monitor: Mental status, signs of cerebral edema, hourly BG, frequent K and arterial blood gases.

HHS (Hyperosmolar Hyperglycemic State) Patho

Severe insulin resistance (type II)—no ketones, BG >600, severe dehydration, hyperosmolarity.​

HHS (Hyperosmolar Hyperglycemic State) Symptoms

Profound dehydration, altered mental status/neuro findings, seizures, higher rates of thrombosis.

HHS (Hyperosmolar Hyperglycemic State) Labs

BG >600, osmolality >350, negative ketones, normal pH/HCO₃, elevated BUN/Cr.​

HHS (Hyperosmolar Hyperglycemic State) Priorities

1. IV fluids (slower than DKA)

2. Careful electrolyte monitoring; insulin drip for glucose control (lower dose than DKA)

3. Monitor for thrombosis, seizure, aspiration.

HHS (Hyperosmolar Hyperglycemic State) Outcome

• Slow, steady correction minimizes risks of cerebral edema and vascular complications.​

Metformin Safe Medication Practices

• First-line type II DM; suppresses hepatic gluconeogenesis, increases sensitivity.​

• Safe unless eGFR <30 or risk for lactic acidosis.​

• Hold 48hr pre/post contrast dye—risk lactic acidosis.

• Pairs best with consistent meal timing; take with food, not if not eating; do not cause hypoglycemia alone.

Insulin Types

• Rapid (Lispro, Aspart), Short (Regular), Intermediate (NPH), Long-acting (Glargine, Detemir, Degludec).​

Insulin Timing

• Rapid: 15min before meals

• Short: 30min before meals

• NPH: 1-2x/day, never IV

• Long/Ultra-long: Basal, don’t mix.​

Insulin Mixing

Only mix Regular (clear) and NPH (cloudy), do “clear before cloudy” draw up.​

Insulin Safe Medication Practices

• Avoid sliding scale alone—use basal, prandial, correction doses, coordinated with meals/IV therapy.​

• Rotate sites; verify doses with another nurse; treat hypoglycemia following 15/15 protocol (15g carbs, wait 15 min, repeat).

Other Oral Meds (Key Principles) Safe Medication Practices DM Treatment

• Sulfonylureas (glipizide) before meals, risk hypoglycemia. Meglitinides with meals, skip if not eating.​

• Thiazolidinediones: avoid in CHF; risk fluid retention. DPP4s/SGLT2s: monitor for urinary/genital infection.

Long-Term Considerations for Addison’s Adrenal Condition

Lifelong steroid replacement; stress dosing during illness, surgery, trauma. Avoid abrupt withdrawal! Monitor for crisis; teach family/stress management, maintain EM kit.

Long-Term Considerations for Cushing’s Adrenal Condition

High infection risk, skin fragility, osteoporosis; monitor for glucose/BP extremes; gradual steroid tapering; post-surgical watch for adrenal insufficiency and crisis.

Long-Term Considerations for Conn’s (primary hyperaldosteronism) Adrenal Condition

Lifetime BP/K management, dietary adaptation (low sodium), monitor for hypokalemia, effects of spironolactone.​

Long-Term Considerations for Hypothyroid Conditions

Lifelong levothyroxine at same time daily; frequent TSH checks; increase slowly, esp. in CV disease.

Long-Term Considerations for Hyperthyroid Conditions

Lifelong med adherence; avoid sudden withdrawal; post-thyroidectomy risk for airway compromise/hypocalcemia—have IV calcium ready; regular labs and symptom monitoring.

Long-Term Considerations for General Thyroid Conditions

atch for secondary effects (osteopenia, cardiac, fertility issues); manage comorbidities; reinforce education, adherence.

Immediate Priorities in Unresponsive or Unstable Neurologic Patients: Airway, Breathing, Circulation (ABCs)

• Airway protection is critical: decreased LOC (change is most sensitive indicator) increases risk for aspiration, obstruction—prepare for intubation if any compromise.​

• Monitor breathing: RR, SpO₂, effort, need for O₂, prepare for suction, intubation, ventilation in deteriorating patients, especially with brainstem or high spinal injury.​

• Circulation: Maintain adequate cerebral perfusion pressure (CPP), monitor for hypotension (worsens outcomes in brain injury), correct shock or arrhythmia.​

Immediate Priorities in Unresponsive or Unstable Neurologic Patients: Rapid neuro checks

Use AVPU or Glasgow Coma Scale (GCS); any score drop or sudden confusion/agitation is a neurological emergency—report immediately.​

• AVPU: Alert, responds to Voice, responds to Pain, Unresponsive. GCS <8 is comatose.​

Immediate Priorities in Unresponsive or Unstable Neurologic Patients: Prevent secondary injury

Avoid hypotension, hypoxia, hypoglycemia, hyperthermia, electrolyte imbalances, fever, and infection to prevent worsening brain injury.

Immediate Priorities in Unresponsive or Unstable Neurologic Patients: Monitor and treat increased ICP

HOB at 30°, neutral neck, avoid clustering care, no coughing/suctioning unless necessary, watch for change in LOC (earliest sign!), late sign is Cushing’s triad (widened pulse pressure, bradycardia, bradypnea).

Immediate Priorities in Unresponsive or Unstable Neurologic Patients: Protect immobilized or unconscious patients

Frequent turning, passive ROM, fall precautions, skin care, eye/mouth care, avoid pulling on paralyzed limbs, prevent DVT.

BEFAST tool

• Balance—sudden loss/unsteady gait/dizziness,

• Eyes—sudden vision loss/double/blurring,

• Face—facial droop, uneven smile,

• Arms—weakness, numbness, arm drift,

• Speech—slurred, confusion, trouble finding words,

• Time—call 911, act immediately; note “last known well” time for tPA/treatment eligibility.​

Stroke symptoms

Sudden onset focal deficit (opposite side from brain lesion), speech/language problems (L hemisphere), or impulsive/visual-spatial issues (R hemisphere).

Stroke Key diagnostic steps 

Address ABCs, comprehensive neuro assessment including GCS, cranial nerve check.​

• Noncontrast CT/MRI before any treatment—must rule out hemorrhage before tPA.​

• Labs: BG (rule out hypoglycemia), O₂, CBC, coagulation, ECG, carotid dopplers for embolic etiology, swallow assessment before oral intake.​

• Document and report new weakness, confusion, visual changes; trend neuro status frequently.

Preventable Complications in Neurological Impairment: Aspiration

Due to dysphagia, cranial nerve deficits—screen swallowing daily x72h post-stroke; NPO until passed; position upright, suction, tube feed if needed.​

Preventable Complications in Neurological Impairment: Pneumonia

Due to impaired airway/immobility; frequent repositioning, O₂ monitoring, early out-of-bed activity, suction PRN, avoid prolonged supination.​

Preventable Complications in Neurological Impairment

Preventable Complications in Neurological Impairment: DVT

Immobility after stroke—early mobilization, SCDs, ROM exercises, avoid catheters >72h.​

Preventable Complications in Neurological Impairment: UTI

Avoid catheters if possible, early removal, monitor urine.​

Preventable Complications in Neurological Impairment: Skin breakdown

Regular turns, maintain position of function for paralytics, use lift sheets for flaccid limbs, frequent skin checks.

Preventable Complications in Neurological Impairment: Contractures and malnutrition

Early PT/OT, splints, nutrition consult; monitor swallowing, regular meal assistance, frequent ROM.​

Preventable Complications in Neurological Impairment: Falls/injury

Bed/chair alarms, reorient frequently, environmental safety, supervision; never leave confused or impulsive patients unsupervised.​

Preventable Complications in Neurological Impairment: Other

Bowel/bladder incontinence (neurogenic)—monitor, regulate, routine, scheduled toileting.​

Preventable Complications in Neurological Impairment: Medication errors

Supervision, education, check for cognitive/communication deficits.​

Communication and Safety Strategies for Cognitive or Speech Deficits

• Aphasia: One idea at a time, yes/no questions, gestures/pictures for basic needs

• Allow time: Don’t rush; process time is often slowed. Provide structured routines, minimize distractions.​

• Repetitive reorientation: Use clocks, calendars, familiar objects. Place needed items on intact side if hemianopsia.​

• Environmental safety: Clear pathways, call light within reach, bed low, approach from intact side for visual neglect, encourage scanning deficit side.​

• Caregiver/mental health support: Involve family, psych support, education re behaviors, wandering, supervision needs.​

• For cognitive impairment: Medication reconciliation, close supervision, watch judgment, maintain dignity, avoid confrontation; redirect as needed.​

Increased Intracranial Pressure (ICP) Signs: Earliest sign

Change in LOC (restlessness, confusion, slowed speech, delayed response, inability to follow commands).

Increased Intracranial Pressure (ICP) Signs: Progression

Headache, nausea, vomiting (often projectile), pupil changes (sluggish, unequal, fixed, dilated), vision changes, papilledema, decorticate/decerebrate posturing, Cheyne-Stokes respirations.​

Increased Intracranial Pressure (ICP) Signs: Classic late sign

Cushing’s triad—wide pulse pressure (high SBP, low DBP), bradycardia, bradypnea—impending herniation.

Increased Intracranial Pressure (ICP) Signs: Other

Seizures, abnormal motor responses, flaccidity, loss of brainstem reflexes (gag, cough, corneal).​

Increased Intracranial Pressure (ICP) Signs: Red flags

If ICP >20mmHg or CPP <50mmHg (will cause irreversible brain injury).​

Increased Intracranial Pressure (ICP) Signs: Care priorities

Report and intervene early; keep HOB 30°, prevent clustering care, avoid stimuli that raise ICP (coughing, suction, hip flexion, hypotonic fluids).​

Change in LOC (restlessness, confusion, slowed speech, delayed response, inability to follow commands): Key presentation

Hepatic encephalopathy (toxin buildup especially ammonia due to liver failure).

Change in LOC (restlessness, confusion, slowed speech, delayed response, inability to follow commands): Progression

Can advance to irreversible coma.

Change in LOC (restlessness, confusion, slowed speech, delayed response, inability to follow commands): Contributing factors

GI bleeding, infection, electrolyte imbalance, constipation, dehydration, high-protein diet, renal dysfunction, sedatives—must treat underlying cause.

Change in LOC (restlessness, confusion, slowed speech, delayed response, inability to follow commands): Symptoms

LOC changes (from mild confusion and personality changes to somnolence and coma), asterixis (flapping tremor with outstretched hands), disorientation, agitation, slurred speech, inappropriate behavior, altered sleep patterns.

Change in LOC (restlessness, confusion, slowed speech, delayed response, inability to follow commands): Focused assessment

Frequent LOC checks, psych changes, monitor ammonia, electrolytes.

Change in LOC (restlessness, confusion, slowed speech, delayed response, inability to follow commands): Management priorities

Reduce ammonia (lactulose, antibiotics), treat precipitating cause, safety (fall risk), maintain hydration/nutrition, protect airway in advanced encephalopathy.