Electrolyte Movement, Osmolar Gradients, pH, and Edema Lecture Review

Flashcards covering electrolyte movement, osmolar gradients, pH regulation, acid-base balance, and the mechanisms and clinical relevance of edema, based on lecture notes.

pH

A measure of the acidity or alkalinity of a solution.

Acid-base balance

The physiological mechanisms that maintain the proper balance between acids and bases in the body fluids to keep the pH within a narrow, normal range.

Edema

Swelling caused by the expansion of interstitial fluid volume in tissues or an organ, resulting from increased fluid movement from intravascular to interstitial space or decreased water movement from interstitium into capillaries or lymphatic vessels.

Interstitial fluid volume

The fluid that surrounds the cells in tissues, outside the blood vessels and lymphatic vessels.

Plasma oncotic pressure

The component of osmotic pressure in a blood vessel that is exerted by plasma proteins (especially albumin); it tends to pull water into the capillaries.

Capillary permeability

The ease with which substances can pass through the walls of capillaries; increased permeability can lead to leakage of fluid and proteins into the interstitial space.

Lymphatic system obstruction

A blockage in the lymphatic vessels that impairs the return of interstitial fluid to the venous circulation, leading to fluid accumulation and edema.

Increased capillary hydrostatic pressure

An elevated pressure within the capillaries that pushes more fluid out into the interstitial space. Pathologically, it leads to edema, as seen in conditions like congestive heart failure.

Congestive heart failure

A condition in which the heart is unable to pump sufficient blood to meet the body's needs, often leading to increased capillary hydrostatic pressure and edema.

Venous obstruction

A blockage in a vein that impedes blood flow, increasing upstream pressure and contributing to increased capillary hydrostatic pressure and edema.

Right-sided heart failure

Failure of the right ventricle to pump blood effectively, leading to systemic vein congestion and peripheral edema.

Left-sided heart failure

Failure of the left ventricle to pump blood effectively, leading to increased pressure in the pulmonary circulation and pulmonary edema.

Pulmonary edema

Fluid accumulation in the lungs, typically due to increased pressure in the pulmonary arteries associated with left-sided heart failure.

Decreased capillary oncotic pressure

A reduction in the osmotic pressure exerted by plasma proteins, leading to less fluid being pulled back into the capillaries and contributing to edema.

Plasma proteins

Proteins dissolved in blood plasma, such as albumin, that are crucial for maintaining plasma oncotic pressure and fluid balance.

Albumin

The most abundant plasma protein, synthesized by the liver, which is the primary contributor to plasma oncotic pressure.

Hepatic disease

Liver disease that can impair the synthesis of plasma proteins like albumin, leading to decreased capillary oncotic pressure and edema.

Malnutrition or malabsorption

Conditions resulting in insufficient dietary protein or impaired nutrient absorption, which can lead to reduced plasma protein levels and edema.

Renal disease

Kidney disease, specifically conditions like nephrotic syndrome, that can cause significant loss of proteins (proteinuria) through urine, thereby decreasing plasma oncotic pressure and causing edema.

Proteinuria

The presence of excess protein in the urine, often indicative of renal disease, which can lead to decreased plasma oncotic pressure.

Cirrhosis

Chronic liver damage leading to scarring and impaired liver function, including decreased synthesis of plasma proteins, which can cause edema.

Nephrotic syndrome

A kidney disorder characterized by excessive protein loss in the urine (proteinuria), leading to decreased plasma oncotic pressure and widespread edema.

Vascular injury

Damage to blood vessels, which can compromise the integrity of the capillary endothelium and increase permeability, leading to protein leakage and edema.

Inflammation

A protective response of tissues to injury or infection, characterized by redness, swelling, heat, and pain, and involving the release of mediators that increase vascular permeability.

Histamine

A chemical mediator released during inflammation that causes vasodilation and increased capillary permeability, contributing to swelling.

Prostaglandins

Lipid compounds involved in inflammation, which can dilate arterioles and widen endothelial gaps, increasing vascular permeability.

Electrolyte

Any of various ions (e.g., sodium, potassium, chloride) required by cells to regulate electric charge, water flow across cell membranes, and maintain nerve, muscle, and acid-base balance.

Sodium (Na+)

A major extracellular electrolyte essential for fluid balance, nerve signaling, and muscle contraction.

Potassium (K+)

A major intracellular electrolyte essential for nerve signaling, muscle contraction, and maintaining cell membrane potential.

Chloride (Cl-)

A major extracellular electrolyte that helps maintain osmotic pressure and is involved in acid-base balance.

Magnesium (Mg2+)

An intracellular electrolyte involved in enzyme function, muscle and nerve function, and bone health.

Calcium (Ca2+)

An essential electrolyte for bone structure, muscle contraction, nerve impulse transmission, and blood clotting.

Phosphate (PO4 3-)

An intracellular electrolyte vital for energy metabolism (ATP), bone formation, and acid-base balance.

Optimum pH for protein structure

proteins, especially enzymes, require a narrow pH range to maintain their functional structure and activity; deviations can impair biological processes.

Body Fluid pH Normal Range

The physiological pH range of human body fluids, typically maintained between 7.36 and 7.44.

Weak acids

Acids that ionize less completely in solution and release fewer hydrogen ions (H+), such as H2CO3 or HAc.

Strong acids

Acids that ionize more completely in solution and release more hydrogen ions (H+), such as HCl or H2SO4.

Weak bases

Bases that ionize less completely in solution and release fewer hydroxyl ions (OH-), such as HCO3-.

Strong bases

Bases that ionize more completely in solution and release more hydroxyl ions (OH-), such as NaOH.

Volatile acids

Acids, like carbonic acid (H2CO3) derived from CO2 and H2O, that can be eliminated through the lungs as CO2.

Non-volatile (fixed) acids/bases

Acids and bases produced from the metabolism of proteins, lipids, and carbohydrates (e.g., sulfuric acid, phosphoric acid, ketone bodies, lactic acid) that cannot be eliminated by the lungs and must be handled by the kidneys.

Acid load

An increase in the amount of acid in the body, such as from CO2 accumulation, which can acidify body fluids.

Base load

An increase in the amount of base in the body, such as from excessive CO2 loss, which can alkalinize body fluids.

Buffers

Chemical systems that resist drastic changes in pH by readily accepting or donating hydrogen ions, providing instantaneous pH defense.

Respiratory system

The organ system responsible for gas exchange, which can rapidly adjust blood pH by altering the exhalation of CO2.

Kidneys

The organs responsible for long-term regulation of pH by conserving or excreting bicarbonate (HCO3-) and excreting excess hydrogen ions (H+) in urine.

Buffer system

A solution that resists changes in pH when small amounts of acid or base are added, typically consisting of a mixture of a weak acid and its conjugate base (or a weak base and its conjugate acid).

Bicarbonate/CO2 system

The most important extracellular buffer system in the body, involving carbonic acid (H2CO3) and bicarbonate ions (HCO3-), crucial for maintaining blood pH.

Hemoglobin (as a buffer)

The most important intracellular buffer in red blood cells, which can bind to hydrogen ions and CO2 to help regulate blood pH.

Phosphates (as buffers)

Buffer chemicals that supplement the bicarbonate/CO2 system, especially in the extracellular fluid (ECF) and intracellular fluid.

Proteins (as buffers)

Important supplementary buffers, particularly within cells, which can accept or donate hydrogen ions due to their amino and carboxyl groups.

Carbonate in bone

A buffering source activated in chronic states of acidosis, providing an extra source of bicarbonate.

Carbonic anhydrase (CA)

An enzyme that catalyzes the rapid interconversion between carbon dioxide and water and carbonic acid, facilitating the bicarbonate/CO2 buffer system.

Open system (pH regulation)

Refers to the bicarbonate/CO2 buffer system, which is regulated by both the kidneys (bicarbonate) and the lungs (CO2), allowing for dynamic adjustment of pH.

pKa value

The pH at which 50% of a buffer system is dissociated, representing the point where its buffering activity is most optimal.

Henderson-Hasselbach Equation

A mathematical equation that allows for the determination of pH from the concentrations of a buffer's acid and conjugate base (e.g., CO2 and HCO3-) and the known dissociation constant (pKa).

Chloride shift

A process where chloride ions move into red blood cells as bicarbonate ions move out, maintaining electrical neutrality during CO2 transport and buffering.

Rapid Chemical Buffering

The body's first line of defense against acid-base loads, instantaneously using buffer systems (like bicarbonate) to absorb excess hydrogen ions.

Fast Respiratory Component

The body's second line of defense against acid-base loads, involving rapid changes in alveolar ventilation to remove excess CO2 and adjust pH, also known as respiratory compensation.

Respiratory compensation

An physiological response where increased alveolar ventilation decreases pCO2 to help raise blood pH in response to acidosis, or decreased ventilation increases pCO2 in response to alkalosis.

Slow Renal Compensation

The body's third and long-term line of defense against acid-base loads, where the kidneys increase reabsorption of bicarbonate ions and secrete excess hydrogen ions, typically over a period of days.