Hepatic Portal Venous System

Hepatic portal system

  • A special circulation system that transports venous blood from the digestive organs to the liver.
  • Transports blood from the stomach, spleen, pancreas, and small and large intestines to the liver. This distinct circulatory pathway exists to allow the liver to metabolize nutrients and toxins from blood that leaves the digestive organs.

Primary tributaries of the hepatic portal vein:

Superior mesenteric vein

Drains tissues of the right side of the abdomen.

  • Ileocolic vein drains blood from the distal small intestine and the proximal large intestine
  • Right colic vein courses from the right side of the abdomen to drain blood from the large intestine
  • Middle colic vein drains blood from the large intestine.
  • Intestinal veins drain the jejunum and ileum of the small intestine. These drain into the left side of the superior mesenteric vein.
  • Pancreatic and duodenal veins
  • Right gastro-omental vein, which runs along the inferior border of the stomach (aka, greater curvature), drains into the superior mesenteric vein.
  • The “omental” portion of the gastro-omental name is derived from the greater “omentum,” the apron-like fold of peritoneum that drapes over the intestines anteriorly.

Splenic vein

Drains structures on the left side of the abdomen.

  • Merges with superior mesenteric vein to form hepatic portal vein
  • Short gastric veins from stomach
  • Left gastro-omental vein, which courses along the inferior border of the stomach and meets the right gastro-omental vein.
  • Pancreatic veins
  • Inferior mesenteric vein

Inferior mesenteric vein

Drains tissues of the lower left side of the abdomen into the splenic vein.

  • Superior rectal vein
  • Multiple sigmoid veins, which drain the sigmoid colon
  • Left colic vein, which drains the descending and transverse colon segments.

Additional information:

  • Hepatic vein
    • Drains blood from liver to inferior vena cava
    • Helps secure liver in place
  • Smaller tributaries of the hepatic portal vein:
    • Cystic veins from gallbladder
    • Left and right gastric veins from stomach

Clinical Correlations:

  • Portal hypertension occurs when the hepatic portal vein becomes blocked.
  • Blood clots can cause obstruction of the hepatic portal vein, but, more commonly, portal hypertension is the result of cirrhosis, in which the liver tissue is replaced by scar tissue in response to damage from a variety of causes, including chronic alcohol intoxication or hepatitis C.
  • As blood flow is obstructed, blood pressure in the hepatic portal system increases, and venous engorgement occurs. These enlarged veins form thin-walled varices, which are susceptible to trauma.
  • Rupture of esophageal varices, which form at the junction of the stomach and esophagus, can cause fatal gastrointestinal hemorrhage.

Biliary and Pancreatic Ducts

Key organs of Biliary and Pancreatic Duct System:

  • Liver produces bile
  • Gallbladder stores and concentrates bile
  • Pancreas produces pancreatic juices
  • Duodenum receives bile and pancreatic juice, and mixes them with the contents of the GI tract

Key terms:

  • Duct is a small tube.
  • Ampulla is the dilated terminal end of the duct.
  • Sphincter is a circular muscle.
  • Papilla is a protuberance of target organ where the ampulla releases secretions.

Drainage Pathways:

  • Right, left, and common hepatic ducts drain bile from the liver; their function is reflected in their name, as “hepatic” refers to the liver.
  • Cystic duct carries bile to and from the gallbladder; it’s helpful to know that “cystic” refers to the gallbladder (recall the “cystic” artery).
  • Bile duct receives bile from the cystic and common hepatic ducts, and delivers it to the duodenum. Notice that its name simply reflects its contents (bile), not a specific organ.
  • Main pancreatic duct drains pancreatic juice from pancreas
  • Main pancreatic and common bile duct merge at hepatopancreatic ampulla (regulated by hepatopancreatic sphincter)
  • Pancreatic juice and bile is drained into duodenum via major duodenal papilla.
  • When present, accessory pancreatic duct drains pancreatic juice into duodenum via minor pancreatic papilla.

Embryologic Origins

Clinical correlations:

  • Post-hepatic jaundice (aka, obstructive jaundice) refers to the yellow staining of body tissues, including skin and mucous membranes; it is the result of accumulation of yellow bile pigments in the blood, and is a sign that bile is not exiting the gallbladder appropriately.
  • Gallstones, which are formed from crystalized bile, can become lodged within and obstruct the ducts of the biliary system, with serious health consequences.
    For example:
  • Cholecytitis (inflammation of the gallbladder) occurs when obstruction of the cycstic duct causes excessive bile accumulation in the gallbladder; subsequent swelling and irritation of the gallbladder can cause intense pain.
  • Pancreatitis (aka, pancreatic inflammation) can result from obstruction of the hepatopancreatic ampulla; instead of entering the small intestine, bile and pancreatic juices back up into the pancreas, causing inflammation.

Duct/Artery associations:

  • Cystic duct travels with the cystic artery
  • Right and left hepatic ducts travel with the right and left hepatic arteries
  • Common hepatic duct arises near the hepatic artery proper.

Small and Large Intestine Histology

SMALL INTESTINE: GENERAL FEATURES

Includes the duodenum, jejunum, and ileum (which can be remembered with the mnemonic Don’t Jiggle It)

Wall Layers

  • Mucosa
    • Villi are finger-like extensions of mucosa
    • Covered in surface columnar epithelial cells, including absorptive enterocytes, from which microvilli extend into the lumen as a brush border.
    • Surface epithelium also secretes surface mucous for protection and lubrication.
    • Villi and microvilli increase surface area for absorption
  • Submucosa
    • Separated from mucosa by muscularis mucosae
  • Muscularis externa
    • Longitudinal and circular layers of smooth muscle
    • Innervated by enteric nervous system
  • Serosa

Circular folds, aka, plicae circulares, (aka, folds of Kerkring)

  • Provide increased surface area for digestion. Recall that continued digestion of foods and absorption of nutrients are key functions of the small intestine.
    • Are most prominent in the middle region of the small intestine (largely absent in colon).

Lacteals

  • Lacteals are the lymphatic structures of the small intestine that absorb lipids, and are in close association with the vasculature.
    Tubular intestinal glands/crypts
  • Further increase the surface area of the small intestine.
  • Paneth cells, which are not distinguishable here, reside at the base of the crypts; they secrete antimicrobial peptides that protect enterocytes from bacteria.
    Goblet cells
  • Secrete lubrication

SMALL INTESTINE: SPECIFICS

Brunner’s glands in submucosa of duodenum

Peyer’s patches

  • Aggregations of lymphoid tissues with a germinal center surrounded by a dome.
    Lymphoid tissues are present in all parts of the gastrointestinal tract (except the stomach), and are collectively referred to as GALT – gut-associated lymphoid tissue. Peyer’s patches are most prevalent in the distal section of the small intestine and the colon.

COLON

The large intestine includes the colon, which is subdivided per its direction of travel within the abdominopelvic cavity, and the rectum and anus.

Walls

  • Four layers, continuous with those of small intestine

Tubular glands in mucosa

  • Abundant goblet cells
    The large intestine is responsible for absorption of water, salt, vitamins and minerals; though not visible in our sample, the glands are deeper than in the small intestine.

Again, remember that the large intestine does not have circular folds.

Large Intestine

Key Features

  • Large intestine begins at the ileocecal valve and ends at the anus.
  • It frames the small intestine, with which it is continuous.
  • Compared to the small intestine, it is shorter in length, but larger in diameter.
  • Teniae coli
    • Three longitudinal ribbon-like bands of muscle fibers that travel the length of the large intestine. The teniae coli represent the muscularis tunic of the large intestine.
    • They act like an elastic band that pulls on the large intestine and causes it to bunch and form haustra.
  • Haustra
    • Pouch-like structures.
  • Epiploic appendages (aka, omental appendages)
    • Small fat-filled sacs, attach to the tenaie coli.

Key Functions:

  • Receives undigested materials from the small intestine.
  • Absorbs water and ions from the undigested materials, which converts the remaining materials to feces (the small intestine is the primary place of nutrient absorption).
  • Stores and expels feces.

Subdivisions:

  • Cecum (appendix attaches, here)
  • Ascending colon
  • Transverse colon
  • Descending colon
  • Sigmoid colon
  • Rectum
  • Anal canal, which opens to external environment via the anus.
    • External and internal anal sphincters regulate passage of feces.
    • External anal sphincter comprises voluntary skeletal muscle
    • Internal anal sphincter comprises involuntary smooth muscle

Key Landmarks:

  • Right colic flexure (aka, hepatic flexure)
    Indicates where the ascending becomes the transverse colon inferior to the liver.
  • Left colic flexure (aka, splenic flexure)
    Indicates where the transverse colon becomes the descending colon inferior to the spleen.
  • Distal sigmoid colon and rectum lie within the pelvis.
  • Anal canal lies within the perineum, external to the abdominopelvic cavity.

Clinical correlations:

  • In diverticulosis, multiple outpockets form within the mucosa of the large intestine, which can cause inflammation with or without infection (diverticulitis).
  • Inflammatory bowel disease (IBD) refers to chronic inflammation of the GI tract
    • Examples include:
      Ulcerative colitis, which causes continuous ulcers, specifically within the lining of the large intestine.
      Crohn’s disease, in which infection spreads deep into the walls of the GI tract; it more typically affects the small intestine than the colon.

Stomach

KEY FEATURES AND FUNCTIONS OF THE STOMACH:

Lesser curvature

  • Medial surface of the stomach
  • Attaches to the lesser omentum

Greater curvature

  • Lateral surface
  • Attaches to the greater omentum

4 MAJOR REGIONS OF THE STOMACH:

Cardiac region

  • Near the heart (“cardia” refers to the heart)
  • Cardiac orifice leads from esophagus to stomach
  • Cardiac sphincter regulates orifice

Fundus

  • Dome-shaped portion
  • Bulges superiorly and laterally to the cardiac region

Body

  • Middle portion of the stomach

Pyloric region

  • Final, distal portion.
  • Antrum and canal
  • Pyloric orifice leads to duodenum
  • Pyloric sphincter regulates orifice

TUNICS OF THE STOMACH

Serosa

  • Outer covering

Muscularis externa

  • Longitudinal layer
  • Circular layer
  • Oblique layer

Submucosa and mucosa

  • Wrinkle to form gastric folds
  • Mucosa comprises millions of gastric pits, which lead to gastric glands.
  • Gastric glands produce gastric juice, which is very acidic to chemically digest stomach contents.
  • Acidic secretions can be detrimental to body tissues, so specialized mucosal cells protect the stomach wall from degradation.

Clinical correlations:

  • Gastric ulcers are lesions in the mucosal lining of the stomach, which can cause pain and bleeding.
    Two common causes of gastric ulcers are:
  • Infection of H. pylori bacterium (Heliobacter pylori), which can be treated with antibiotics
  • Overuse of NSAIDs (non-steroidal anti-inflammatory drugs).

GI Tunics

4 TUNICS (LAYERS) OF THE GI TRACT

From deep to superficial:

Mucosa

  • Lines the lumen of the GI tract.
  • The mucosa subdivides into
  • Epithelia comes into contact with contents of GI tract.
  • Lamina propria comprises loose connective tissue; in stomach, houses gastric glands.
  • Muscularis mucosae comprises an inner circular and outer longitudinal layer (note that it is different than the muscularis externa).
  • Mucin-secreting cells for lubrication.

Submucosa

  • Lies under the mucosa.
  • Inner surface follows the contours of the mucosa.
  • Neurovascular, glandular and lymphatic structures travel within it.

Muscularis externa (aka, muscularis)

  • Comprises two or more layers of muscle to propel substance through the GI tract
  • Inner circular layer comprises muscle fibers that encircle the diameter of the GI tract
  • Outer longitudinal layer comprises muscle fibers that run lengthwise along the GI tract.
  • Oblique layer in stomach, facilitates twisting of stomach and churning of stomach contents.
  • Myenteric nerve plexus lies between the inner and outer layers of the muscularis externa.

Adventitia or serosa

  • Outer protective layer.
  • It is categorized as adventitia or serosa depending on its position in the abdominal cavity.
    — Serosa, which constitutes most of the GI tract, surrounds organs that are suspended in the abdomen by visceral peritoneum (such as the stomach).
    — Adventitia surrounds organs that adhere to the abdominal wall (such as the ascending colon).
    Otherwise, serosa is similar to adventitia.

GI Segments with Serosa

  • Stomach
  • Part of the duodenum
  • Jejunum and ileum
  • Cecum and appendix
  • Transverse colon
  • Sigmoid colon
    In general are organs that are “suspended” within the abdomen.

GI segments with Adventitia

  • Most of the duodenum
  • Pancreas
  • Ascending colon
  • Descending colon
  • Rectum
    In general, organs that adhere to the abdominal wall.

Key differences in the tunics of the segments of the GI tract

Esophagus

  • Mucosa comprises stratified squamous epithelia, which protects against abrasions from swallowed foods; distal segments’ mucosal tunics comprise simple columnar epithelia
  • Submucosa is rich in elastic fibers, to accommodate foods and liquids.
    Stomach
  • Mucosa comprises mucosal cells and gastric pits
  • Muscularis externa layer comprises a third sublayer of muscle fibers, called the oblique layer, which wraps obliquely around the stomach to enhance mixing and churning of foods.
    Small Intestine
  • Mucosa forms circular folds (aka, plicae circulares, aka, valves of Kerckring), which are covered with villi; this arrangement increases the surface area of the small intestine, and, therefore, the amount of nutrient absorption.
  • There are additional histological differences among the segments of the small intestine.
    Large Intestine
  • Mucosa of the large intestine houses goblet cells, intestinal glands, and lymphatic structures.

Peritoneal Membranes

PERITONEUM

  • The continuous double-layered membrane that lines the abdominopelvic body walls and the viscera within.
  • The two layers of the peritoneum arise from embryonic mesoderm, and their complex arrangement reflects the developmental rotation of the gut.

Parietal peritoneum

Lines the internal surface of the body wall; it comprises the outer layer of the peritoneum.

Visceral peritoneum

Adheres to the organs; thus, it comprises the outermost covering of some organs in the abdominopelvic cavity and contributes to the serosa of the GI tract.

Peritoneal cavity

The (potential) space between the parietal and visceral layers.

Mesenteries

Folds of peritoneum that suspend organs in the abdominal cavity and provide protected neurovascular and lymphatic pathways.

  • The greater omentum is an apron-like fold that overlies the small intestine; it attaches to the greater curvature of the stomach and transverse colon.
  • The lesser omentum spans from the liver to the stomach and duodenum of the small intestine;
  • The mesocolon anchors the colon to the posterior body wall;
  • The mesentery proper (aka, mesentery) anchors the small intestine to the posterior body wall.

Intraperitonal vs Retroperitoneal:

Intraperitoneal organs

Enveloped in visceral peritoneum:

  • Liver, stomach, jejunum and ileum (of the small intestine), and the transverse colon (of the large intestine)

Retroperitoneal organs

Lie between the body wall and the parietal peritoneum.

  • Most of the pancreas and duodenum, the rectum, urinary bladder, uterus, and kidneys (not shown) (some of these are technically secondarily retro-peritoneal, which refers to their embryological origins).

Clinical correlation:

  • Retroperitoneal hemorrhage refers to bleeding in the retroperitoneal space and commonly occurs from trauma.
  • Peritonitis, aka, inflammation of the peritoneum, occurs when the GI tract is ruptured and gas, fecal matter, and bacteria enter the peritoneal cavity. Widespread infection can be fatal.
  • Adhesions, aka, scar tissue, form if the peritoneum itself is damaged. Adhesions can inhibit movement of the viscera and cause chronic pain.

Alkalosis and Acidosis

4 SIMPLE ACID-BASE DISORDERS

  • Metabolic acid-base disorder presents as an imbalance between bicarbonate, the primary extracellular buffer, and fixed, aka, non-volatile, acids.
  • Respiratory acid-base disorder presents as an imbalance between bicarbonate and carbon dioxide, the volatile acid.
  • Acid-base Disorders are distinguishable by their arterial blood profiles, compensatory respiratory and renal mechanisms, and common causes.

ACIDEMIA

pH < 7.35

Metabolic acidosis

  • Bicarbonate < 20 mEq/L
  • Caused by either a gain in hydrogen ions and/or a loss of bicarbonate, which lowers pH.
  • Consequently, the arterial blood profile shows reduced bicarbonate concentration and elevated hydrogen ion concentration.
  • In response to a drop in pH, the respiratory systemcompensates with hyperventilation:
    • Excess carbon dioxide is “blown off,” which lowers the partial pressure of carbon dioxide in the blood; the arterial blood profile reflects this.
  • Though slower to respond, renal bicarbonate conservation and acid excretion produce a more effective and longer-lasting pH elevation.

Anion Gap

Causes of metabolic acidosis into at least two categories: those associated with a normal anion gap (AG), and those associated with an elevated anion gap.

  • In a routine blood test, only some cations and anions are measured; the anions that are not measured constitute the “anion gap.”
    • Because the total concentration of anions must be equal to the total concentration of cations, we know that the anion gap, the unmeasured anions, must be equal to:
      The measured cations (usually sodium) minus the measured anions (usually bicarbonate and chloride).
    • A normal average anion gap value is 12 mEq/L (typical range = 8 – 16 mEq/L).
  • Thus, an increased anion gap indicates that bicarbonate, a measured anion, has been lost and replaced by the unmeasured ions
  • A normal anion gap indicates that chloride is the ion that replaced the lost bicarbonate, which makes sense given that it is the other measured anion in the anion gap equation.
  • Common causes of a normal anion gap include:
    • Diarrhea
    • Renal tubular acidosis
    • Renal failure
    • Hyperchloremia
    • Addison disease
    • Acetazolamide
    • Spironolactone
    • Saline infusion
  • Common causes of an increased anion gap include MUDPILES:
    • Methanol intoxication (methanol is also called “wood alcohol,” commonly found in antifreeze and industrial settings)
    • Uremia
    • Diabetic ketoacidosis
    • Paraldehyde (which is sometimes used to treat alcoholism and certain convulsive and mental disorders)
    • Iron overdose
    • Lactic acid
    • Ethylene glycol poisoning (ethylene glycol is a compound commonly found in antifreeze)
    • Salicylate ingestion (key ingredient in aspirin, poisoning is common in children)

Respiratory acidosis

  • Pco2 > 44 mmHg
  • Caused by a gain in carbon dioxide and bicarbonate.
  • The degree of change in pH depends on the duration of the disorder:
    • The pH is more reduced in acute acidosis than in chronic because, in chronic acidosis, sufficient time has elapsed for renal mechanisms to have some effect.
  • There is no respiratory compensation when the respiratory system is itself the source of the imbalance.
    • To raise pH, the nephrons conserve bicarbonate and excrete hydrogen ions; notice that this is similar to the renal response to metabolic acidosis.

Caused by:

  • Hypoventilation
    • Inhibition of the medullary respiratory center, which can be induced by sedatives or brainstem lesions
    • Neuromuscular defects that inhibit the anatomical structures responsible for ventilation
    • Gas exchange defects, such as COPD.

ALKALEMIA

pH > 7.45

Respiratory alkalosis

  • Pco2 < 36 mmHg
  • pH is increased in proportion to the duration of the disorder.
  • There is no respiratory compensation for respiratory-induced acid-base disturbances.
  • Nephrons excrete excess bicarbonate and reduce titratable acid and ammonium ion secretion to conserve hydrogen ions; this is similar to the renal response to metabolic alkalosis.

Caused by:

  • Hyperventilation, which “blows off” too much carbon dioxide and lowers its arterial partial pressure.
    • Stimulation of the medullary respiratory center, hypoxemia (low blood oxygen), and physical or mental distress.

Metabolic alkalosis

  • Bicarbonate > 28 mEq/L
  • Caused by a loss of hydrogen ions and/or a gain in bicarbonate, which raises pH.
  • Consequently, the arterial blood profile shows elevated bicarbonate concentration, and decreased hydrogen concentration.
  • In response to elevated pH, hypoventilation retains carbon dioxide, which increases its arterial partial pressure; this is reflected in the arterial blood profile.
  • The nephrons increase bicarbonate excretion, and, by reducing secretion of titratable acids and ammonium, conserve hydrogen ions; these actions lower pH.

Most commonly caused by

  • Vomiting (HCL is lost from the body)
  • Loop and thiazide diuretics, which increase bicarbonate excretion in the urine.
    • Vomiting and diuretics cause extracellular fluid volume contraction, which, as we’ve learned elsewhere, triggers hormonal responses that increase bicarbonate reabsorption and maintain the metabolic alkalosis.
  • Hyperaldosteronism (excessive aldosterone secretion) causes over-excretion of hydrogen ions.

Acid Buffering and Regulation

KEY PRINCIPLES:

Volatile acid is the product of aerobic cellular respiration, which releases carbon dioxide. As we’ve learned elsewhere, when carbon dioxide interacts with water in the body fluids, carbonic acid forms.

  • “Volatile” refers to the fact that carbon dioxide is expired by the lungs

Non-volatile acids are the products of protein and phospholipid metabolism

  • They include sulfuric acid and phosphoric acid
  • They are excreted in the urine as titratable acids

Because enzymes and other proteins only function at particular pH values, the body must regulate the acidity of the intra- and extracellular fluids.

  • Three lines of defense against acid-base imbalance:
    • In the body, fluids (chemical mixtures), called buffers, minimize pH changes until hydrogen balance can be regained.
    • The respiratory system expires carbon dioxide, the source of volatile acid.
    • The urinary system excretes the non-volatile, aka, fixed, acids.
    • These systems operate interdependently to maintain an arterial blood plasma pH of 7.4.

Acid Production by Body Tissues

  • Body tissues produce acids, including carbon dioxide, sulfuric acid, and phosphoric acid
    • Each of these acids releases hydrogen ions that must be buffered in the body fluid compartments.

Buffering in Fluid Compartments

  • Intracellular compartment of body tissues = proteins and organic phosphates
  • Intracellular compartment of red blood cells = hemoglobin
  • Extracellular fluid = bicarbonate, which is the most important extracellular buffer, and, phosphate and proteins.

Acid Removal

  • In the Lungs
    • When carbonic acid reaches the lungs, it dissociates to form carbon dioxide, which is expired in ventilation.
    • When pH falls, increased ventilation triggers to release excess carbon dioxide.
      Rapidly, the partial pressure of carbon dioxide drops, and the acidity of the blood is reduced.
  • In the Kidneys
    • Nephrons reabsorb bicarbonate from the filtrate, and excrete hydrogen ions as tritratable acids and ammonium in the urine.
    • Nearly all of the filtered bicarbonate is reabsorbed from the proximal tubule.
    • Some hydrogen ions attach to ammonia and are secreted into the filtrate as ammonium; some of this ammonium is then reabsorbed from the thick ascending limb (where it participates in countercurrent multiplication in the renal interstitial fluid).
    • In the alpha-intercalated cells of the distal nephron, ammonium is again secreted into the tubular fluid, along with phosphoric acid. Phosphoric acid forms when hydrogen ions attach to phosphate, and is often referred to as “titratable acid”
    • Ammonium and phosphoric acid formation and secretion involve bicarbonate synthesis and reabsorption; this new bicarbonate contributes to the extracellular buffers.
    • Both mechanisms are responsive to aldosterone, which is a hormone secreted by the adrenal cortex secreted in response to low pH.

Clinical correlations

  • Aldosterone deficiency inhibits ammonium excretion, and causes type 4 renal tubular acidosis. Because potassium excretion is also inhibited by aldosterone deficiency, this type of acidosis is characterized by hyperkalemia.
  • Alkalosis is a consequence of excessive removal of hydrogen ions from the body fluids; as a result, the blood becomes more alkaline).
  • Acidosis is the opposite: excessive hydrogen ions are added to the blood or retained; the blood becomes more acidic. Retention of acids can be a sign of renal failure.

Introduction to Acids and Bases

Key Principles of Acids and Bases:

Acids and bases are defined by their ability to donate or accept hydrogen ions

  • Acids are chemical substances that can donate/release, hydrogen ions in water.
  • Bases, aka, alkalines, are chemical substances that can accept hydrogen ions.

pH

  • pH is a measure of the concentration of hydrogen ions in solution
  • pH scale displays the concentration of hydrogen ions from 0 – 14.
    • An acidic solution has a pH less than 7; it has a high concentration of hydrogen ions.
    • A neutral solution has a pH of 7
    • A basic solution has a pH of greater than 7; it has a lower concentration of hydrogen ions.
  • Calculation of pH:
    • Negative logarithmic function.

pH values for human bodily fluids:

  • Gastric juice, which is secreted by organs of the digestive system, has a pH value around 2; its acidity aids in food digestion.
  • Saliva is slightly acidic, but much closer to neutral than are the gastric juices.
  • For comparison, pure water has a neutral pH, 7.
  • Arterial blood has a pH of approximately 7.4

Homeostasis

Biological organisms are constantly adding acids to their bodily fluids during metabolism, but our blood is slightly basic.

  • Intra- and extra-cellular buffers operate to maintain homeostasis.
    • Buffers minimize changes of pH in solutions; they reversibly donate or accept hydrogen ions.
  • Example: Bicarbonate buffer system:
    When hydrogen ions are added to the extracellular fluid, they combine with bicarbonate to produce carbonic acid, which is a weaker acid.
    • If the extracellular fluid becomes too basic, the reaction can be reversed:
      Carbonic acid can dissociate to form hydrogen ions and bicarbonate; when pH increases (becomes more alkaline), carbonic acid dissociates to form bicarbonate, which is a base, and hydrogen ions.

Clinical Consequences

  • If the body cannot maintain homeostasis due to pathology, disturbances in bodily fluid pH inhibit enzymatic reactions.
    -Thus, failure to regulate pH causes a range of clinical symptoms associated with acidosis (too high blood acid content) or alkalosis (too low blood acid content); elsewhere, we discuss how the kidneys and lungs work to maintain homeostatic pH levels.