Renal and Neurological Pathophysiology: Clinical Essentials

Renal System Functions (GI-A-W-E-T-B-E-D)

• G: Acid-base balance
• I: Water balance
• A: Electrolyte balance
• W: Toxin removal
• E: Blood pressure (RAAS)
• T: Erythropoietin
• B: Vitamin D activation

Urine Formation

• Glomerular filtration: Filters water and small solutes.
• Tubular reabsorption: Returns substances to the blood.
• Tubular secretion: Adds wastes to tubules.
• Excretion: 1–2 L/day; ≥30 mL/hr minimum.

Key Renal Hormones

• ADH: Water reabsorption.
• Aldosterone: Increases Na⁺ reabsorption.
• ANP: Decreases Na⁺ and water reabsorption.

Urolithiasis (Kidney Stones)

Types: Calcium (alkaline urine), Uric acid (acidic urine; gout), Struvite, and Cystine.

Signs/Symptoms: Renal colic, sudden flank to groin pain, nausea/vomiting, sweating, tachycardia, and hematuria.

Treatment: Increased fluids, ESWL, surgery, and adjusting urine pH.

Hydronephrosis

Blocked urine flow leads to dilation of the renal pelvis and renal atrophy.

Causes: Stones, tumors, scar tissue, and BPH. Can progress to chronic renal failure.

Benign Prostatic Hyperplasia (BPH)

Prostate hyperplasia causes urethral compression and urinary obstruction.

Signs/Symptoms: Weak stream, hesitancy, dribbling, incomplete emptying, and nocturia.

Treatment: Tamsulosin (Flomax), Dutasteride/Finasteride, and surgery.

Acute Kidney Injury (AKI)

Causes: Nephrotoxins, shock/low perfusion, pyelonephritis, and obstruction.

Signs/Symptoms: Increased BUN, increased creatinine, metabolic acidosis, and hyperkalemia.

Treatment: Treat the underlying cause and use dialysis to stabilize.

Nervous System: Pain Physiology

Nociceptors: A-delta (sharp pain), C-fibers (dull pain).

Steps: Transduction → Transmission → Perception → Modulation.

Modulators:

• Excitatory: Substance P, glutamate.
• Inhibitory: GABA, glycine, serotonin.

Acute vs. Chronic Pain

• Acute: Short-term, protective.
• Chronic: >3–6 months, psychological effects, few physical signs.
• Neuropathic: Burning, shooting pain (nerve injury).

Acute Delirium

Sudden, fluctuating disturbance in consciousness due to RAS disruption. Hyperactive form may show agitation, increased heart rate, increased temperature, and dilated pupils.

Signs/Symptoms: Inattention, disorganized thinking, hallucinations, restlessness, or lethargy.

Treatment: Identify the cause (infection, drugs, metabolic) and assess with CAM-ICU.

Head Injuries

Focal Injuries: Coup/contrecoup contusions; Hematomas (Epidural, Subdural, Intracerebral).

Diffuse Axonal Injury (DAI): Shearing of axons due to rotational forces; ranges from mild to severe.

Concussion:

• Mild: Brief confusion ± amnesia.
• Classic: Loss of consciousness <6 hours; amnesia.
• Complications: Post-concussion syndrome (PCS), seizures, CTE.