BackBIO 169 Exam #5 Study Guide: The Urinary System and Fluid, Electrolyte, & Acid-Base Balance
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Ch. 25: The Urinary System
Overview of Kidney Functions
Excretion of metabolic wastes (e.g., urea, creatinine, uric acid).
Regulation of blood volume and pressure by adjusting water output.
Regulation of electrolyte balance (Na+, K+, Ca2+, etc.).
Acid-base balance by excreting H+ and reabsorbing HCO3-.
Hormone production (e.g., erythropoietin, renin).
Anatomy of the Kidneys
Supportive layers:
Renal fascia: Anchors kidney to surrounding structures.
Perirenal fat capsule: Cushions and protects the kidney.
Fibrous capsule: Prevents infection spread to the kidney.
Three regions:
Renal cortex: Outer region; contains glomeruli and most of the nephron tubules.
Renal medulla: Contains renal (medullary) pyramids; site of nephron loops and collecting ducts.
Renal pelvis: Funnel-shaped; collects urine from major and minor calyces.
Renal hilum: Entry/exit for ureters, blood vessels, lymphatics, and nerves.
The Nephron: Structure and Types
Nephron: Structural and functional unit of the kidney; responsible for urine formation.
Types of nephrons:
Cortical nephrons: Located mostly in the cortex; short nephron loops.
Juxtamedullary nephrons: Long nephron loops extend deep into the medulla; important for concentrating urine.
Parts of the nephron:
Renal corpuscle: Includes the glomerulus (capillary tuft) and glomerular (Bowman's) capsule.
Renal tubule: Proximal convoluted tubule (PCT), nephron loop (loop of Henle), distal convoluted tubule (DCT).
Glomerulus and Filtration Membrane
Glomerulus: High-pressure capillary bed; site of filtration.
Glomerular capsule: Double-walled; visceral layer (podocytes) forms part of the filtration membrane.
Filtration membrane layers:
Fenestrated endothelium of glomerular capillaries
Basement membrane
Visceral layer of capsule (podocytes with filtration slits)
Filtrate normally lacks blood proteins and cells.
Capillary Beds: Glomerulus vs. Peritubular Capillaries
Glomerulus: High-pressure; filtration.
Peritubular capillaries: Low-pressure; reabsorption and secretion.
Vasa recta: Specialized capillaries in juxtamedullary nephrons; maintain medullary osmotic gradient (countercurrent exchanger).
Juxtaglomerular Complex (JGC)
Granular (juxtaglomerular) cells: Secrete renin; sense blood pressure.
Macula densa cells: Monitor NaCl content in filtrate.
Mesangial cells: Communicate signals between macula densa and granular cells; regulate glomerular filtration.
Filtration Pressures and Glomerular Filtration Rate (GFR)
Outward pressure: Hydrostatic pressure in glomerular capillaries (pushes fluid out).
Inward pressures: Osmotic pressure of blood (pulls fluid in) + hydrostatic pressure in capsular space.
Net Filtration Pressure (NFP):
Equation:
Where = glomerular capillary hydrostatic pressure, = glomerular capillary oncotic pressure, = capsular space hydrostatic pressure.
GFR is directly proportional to NFP.
High GFR: Increases urine output, decreases blood volume/pressure.
Regulation of GFR
Intrinsic (renal autoregulation):
Myogenic mechanism: Afferent arteriole constricts/dilates in response to pressure changes.
Tubuloglomerular feedback: Macula densa senses NaCl; adjusts afferent arteriole diameter.
Extrinsic mechanisms:
Sympathetic nervous system: Constricts afferent arterioles during stress.
Renin-angiotensin-aldosterone system (RAAS): Increases blood pressure/volume.
Other hormones: Nitric oxide (vasodilation), endothelin (vasoconstriction).
Renin-Angiotensin-Aldosterone Mechanism
Activated by low blood pressure/volume.
Renin converts angiotensinogen to angiotensin I; ACE converts it to angiotensin II (vasoconstrictor).
Angiotensin II stimulates aldosterone release, increasing Na+ (and water) reabsorption in DCT and collecting ducts.
Tubular Reabsorption and Secretion
PCT: Main site of reabsorption (glucose, amino acids, ions, water).
Transcellular route: Through cells; Paracellular route: Between cells.
Sodium: Key cation; drives reabsorption of other solutes via electrochemical gradient.
Nephron loop:
Descending limb: Water reabsorption.
Ascending limb: Na+, K+, Cl- reabsorption (impermeable to water).
DCT and collecting ducts: Reabsorption regulated by hormones:
Aldosterone (Na+ reabsorption), ADH (water reabsorption), ANP (inhibits Na+ reabsorption), PTH (Ca2+ reabsorption).
Countercurrent Mechanism
Purpose: Maintains medullary osmotic gradient (300–1200 mOsm) for urine concentration.
Countercurrent multiplier: Nephron loop; creates gradient.
Countercurrent exchanger: Vasa recta; preserves gradient.
Filtrate osmolality highest at loop bend.
Water Balance: Dehydration vs. Overhydration
Dehydration: Increased ADH, more aquaporins, concentrated urine.
Overhydration: Decreased ADH, fewer aquaporins, dilute urine.
Renal Clearance
Definition: Volume of plasma cleared of a substance per minute.
Interpretation:
C = 0: Complete reabsorption (e.g., glucose).
C < 125: Some reabsorption.
C = 125: No net reabsorption/secretion (e.g., inulin).
C > 125: Secretion into filtrate.
Physical Characteristics of Urine
Color: Yellow (urochrome pigment).
pH: 4.5–8.0 (average ~6).
Specific gravity: 1.001–1.035.
Normal components: Water, urea, ions.
Abnormal components: Glucose, proteins, blood cells, ketones (indicate pathology).
Urinary Tract: Ureters, Bladder, Urethra
Ureters: Transport urine from kidneys to bladder.
Bladder: Temporary urine storage.
Urethra: Conducts urine out of the body.
Control of Micturition (Urination)
Parasympathetic activity: Stimulates bladder contraction and sphincter relaxation.
Three events:
Bladder distends (fills with urine).
Internal urethral sphincter opens (involuntary).
External urethral sphincter opens (voluntary control).
Ch. 26: Fluid, Electrolyte, & Acid-Base Balance
Body Water Content and Distribution
Infants: ~73% water
Adult males: ~60% water
Adult females: ~50% water
Elderly: ~45% water
Total body water: ~40 L
Compartments:
Intracellular fluid (ICF): 25 L
Extracellular fluid (ECF): 15 L (Plasma: 3 L, Interstitial fluid: 12 L)
Electrolytes vs. Nonelectrolytes
Nonelectrolytes: Do not dissociate in water (e.g., glucose, lipids).
Electrolytes: Dissociate into ions in water (e.g., NaCl → Na+ + Cl-).
Major Electrolytes of ECF and ICF
Compartment | Major Cation | Major Anion |
|---|---|---|
ECF | Na+ | Cl- |
ICF | K+ | HPO42- |
Fluid Movement Between Compartments
Plasma ↔ Interstitial Fluid: Across capillary walls (hydrostatic and osmotic pressures).
Interstitial Fluid ↔ ICF: Across cell membranes (selective permeability).
Water Intake and Output
Intake: ~60% from beverages, rest from food and metabolism.
Output: ~60% via urine, rest via sweat, feces, and insensible loss.
Thirst Mechanism
Stimulated by:
1–2% increase in ECF osmolality
5–10% drop in blood pressure
Regulated by hypothalamic thirst center.
Role of ADH
Increases water reabsorption in kidneys.
Decreases urine output, increases blood volume/pressure, lowers ECF osmolality.
Disorders of Water Balance
Dehydration: Water loss exceeds intake; cells shrink.
Hypotonic hydration (water intoxication): Excess water; cells swell.
Edema: Accumulation of fluid in interstitial space.
Electrolyte Balance: Sodium, Potassium, Calcium
Sodium (Na+):
Major ECF cation; determines ECF osmolality and volume.
Regulated by ADH (concentration) and aldosterone/ANP (total content).
High Na+ increases blood volume/pressure; low Na+ decreases them.
Potassium (K+):
Major ICF cation; affects membrane potential.
Regulated by aldosterone (increases K+ secretion).
Hyperkalemia: High K+; can cause cardiac arrhythmias.
Hypokalemia: Low K+; can cause muscle weakness.
Calcium (Ca2+):
Regulated by parathyroid hormone (PTH): increases Ca2+ reabsorption, enhances phosphate excretion.
Hypercalcemia: High Ca2+; can cause muscle weakness, kidney stones.
Hypocalcemia: Low Ca2+; can cause tetany, convulsions.
Hormonal Regulation of Sodium and Water
Aldosterone: Increases Na+ reabsorption (and K+ secretion).
ANP (Atrial Natriuretic Peptide): Inhibits Na+ reabsorption, suppresses aldosterone, dilates vessels, lowers blood volume.
Estrogen/Glucocorticoids: Increase Na+ reabsorption.
Progesterone: Decreases Na+ reabsorption.
Renin Release Mechanisms
Sympathetic stimulation
Decreased NaCl in filtrate (sensed by macula densa)
Decreased stretch of granular cells (low blood pressure)
Acid-Base Balance
Normal arterial pH: 7.35–7.45
Alkalosis: pH > 7.45
Acidosis: pH < 7.35
Sources of H+:
Protein breakdown (phosphoric acid)
Lactic acid (anaerobic metabolism)
Fat metabolism (fatty acids, ketones)
CO2 (forms carbonic acid in blood)
Regulation of H+ (Acid-Base Homeostasis)
Chemical buffers: Bicarbonate, phosphate, protein systems
Fastest, but cannot remove H+ from body.
Bicarbonate buffer system:
Bicarbonate (HCO3-): Weak base; accepts H+.
Carbonic acid (H2CO3): Weak acid; donates H+.
Equation:
Respiratory centers: Regulate CO2 (bicarbonate-carbonic acid system)
Hyperventilation: Blows off CO2, raises pH (respiratory alkalosis).
Hypoventilation: Retains CO2, lowers pH (respiratory acidosis).
Renal mechanisms: Regulate HCO3- and H+ excretion/reabsorption
Increased HCO3- reabsorption: Metabolic alkalosis.
Increased H+ reabsorption: Metabolic acidosis.
New HCO3- generated by phosphate buffer or NH4+ excretion.
Compensation Mechanisms
Respiratory system compensates for renal (metabolic) disturbances by adjusting CO2 exhalation.
Kidneys compensate for respiratory disturbances by adjusting HCO3- reabsorption/secretion.
Summary Table: Major Electrolytes and Disorders
Electrolyte | Hyper- Condition | Hypo- Condition | Main Effects |
|---|---|---|---|
Na+ | Hypernatremia | Hyponatremia | Neural/muscle excitability, ECF osmolality |
K+ | Hyperkalemia | Hypokalemia | Cardiac/muscle function |
Ca2+ | Hypercalcemia | Hypocalcemia | Muscle contraction, nerve function |
Additional info: For more details on abnormal urine components and specific lab values, refer to Table 25.2 and Table 26.1 in your textbook or lab handouts.
