Module 4 Pathophysiology: GI, Liver, Acid–Base, and Elimination

Comprehensive vocabulary flashcards covering the etiology, cellular adaptations, tissue pathology, diagnostic cues, and complications of gastrointestinal, hepatic, and acid-base disorders.

Metaplasia

A reversible cellular adaptation where one mature adult cell type is replaced by another mature cell type better equipped to withstand chronic environmental stress; in GERD, stratified squamous epithelial cells convert into tall gastric-type columnar cells.

GERD (Gastroesophageal Reflux Disease)

A condition characterized by the repeated backflow of acidic gastric contents into the esophagus, commonly caused by an incompetent or relaxed lower esophageal sphincter, subjecting the esophageal mucosa to recurrent chemical injury.

Gastric Mucosal Barrier

The protective defense system of the stomach wall consisting of a thick alkaline mucus layer, tight intercellular junctions, prostaglandin-mediated mucus stimulation, and a rich microvascular blood supply essential for continuous tissue repair.

Acute Gastritis

Sudden, short-lived, and reversible inflammation of the gastric mucosa provoked by chemical irritants such as NSAIDs, alcohol, ischemia, or microorganisms, progressing through mucosal erythema, superficial erosion, necrosis, and potential hemorrhage.

Chronic Gastritis (H. pylori Type)

A persistent inflammatory condition caused by the gram-negative bacterium Helicobacter pylori, characterized by mucosal and glandular atrophy with decreased gastric acid output over time, occurring in the absence of mucosal erosions.

Urease

A neutralizing enzyme synthesized by Helicobacter pylori that breaks down urea to produce ammonia, buffering the acidic microenvironment and permitting bacterial colonization of the gastric mucus layer and epithelium.

Autoimmune Gastritis

A form of chronic gastritis characterized by immune-mediated antibody destruction of gastric parietal cells and intrinsic factor, accompanied by mucosal T-cell infiltration, gastric mucosal atrophy, achlorhydria, and loss of vitamin $B_{12}$ absorption.

Intrinsic Factor (IF)

A glycoprotein synthesized and secreted by gastric parietal cells that binds dietary vitamin $B_{12}$ in the stomach, permitting its subsequent absorption across the mucosal lining of the terminal ileum.

Pernicious Anemia

A megaloblastic anemia resulting from autoimmune destruction of parietal cells or intrinsic factor, leading to severe vitamin $B_{12}$ deficiency and impaired erythrocyte DNA synthesis.

Zymogen Granules

Specialized intracellular storage vesicles within pancreatic acinar cells that package powerful digestive proenzymes in an inactive state to safeguard pancreatic tissue from premature enzymatic breakdown.

Autodigestion

The pathophysiologic hallmark of acute pancreatitis in which inactive proenzymes (including trypsinogen converting to active trypsin) activate prematurely within pancreatic tissue, causing enzymatic liquefaction, necrosis, and hemorrhage of the organ.

Acute Pancreatitis

An acute inflammatory disorder of the pancreas triggered by premature intrapancreatic enzyme activation and autodigestion, most commonly initiated by biliary duct obstruction from gallstones or excessive alcohol consumption.

Acute Edematous Pancreatitis

An early phase of acute pancreatic inflammation characterized by widespread infiltration of neutrophils, TNF, and interleukins, causing marked increases in capillary permeability and localized interstitial edema.

Chronic Pancreatitis

An irreversible, progressive inflammatory disease characterized by recurrent ductal protein plugging, ischemia, acinar cell atrophy, and dense fibrosis, culminating in permanent failure of both exocrine ($\approx 80\%$) and endocrine ($\approx 20\%$) functions.

Steatorrhea

The passage of pale, greasy, voluminous, and foul-smelling stools caused by pancreatic exocrine failure and the inability to hydrolyze and absorb dietary fats once approximately $90\%$ of pancreatic tissue is damaged.

Crohn Disease

A chronic inflammatory bowel disease capable of involving any gastrointestinal segment from mouth to anus (favoring the small intestine and ascending colon), characterized by transmural inflammation, patchy skip lesions, granulomas, and fistulas.

Skip Lesions

Discontinuous segments of inflamed, diseased bowel interspersed with normal, unaffected mucosa, serving as a classic diagnostic gross architectural hallmark of Crohn disease.

Transmural Inflammation

Inflammatory tissue damage that penetrates across the entire thickness of the intestinal wall—mucosa, submucosa, muscularis, and serosa—predisposing patients to structural strictures, abscesses, and fistula formation.

Fistula

An abnormal, epithelialized tract or tunnel extending through all bowel layers to connect two epithelial surfaces (such as bowel loops, the bladder, or the cutaneous skin), originating from deep ulcerations in Crohn disease.

Ulcerative Colitis (UC)

A chronic inflammatory bowel disease confined exclusively to the colon and rectum, beginning in the distal rectum and extending proximally in an uninterrupted, continuous fashion through the mucosal and submucosal layers only.

Friable Mucosa

Fragile, hyperemic, and easily injured mucosal tissue that bleeds easily upon minor mechanical contact, recognized as a primary cue and source of recurrent bloody diarrhea in ulcerative colitis.

Pseudopolyps

Projecting tongues of surviving, regenerating, or inflamed mucosal tissue surrounded by areas of widespread ulceration and tissue loss, commonly observed on the luminal surface in ulcerative colitis.

Kupffer Cells

Specialized resident mononuclear phagocytes lining hepatic sinusoids that phagocytose foreign debris and degrade aged erythrocytes, releasing heme for processing into bilirubin.

Jaundice (Icterus)

Yellow staining of the skin and sclera resulting from hyperbilirubinemia, which develops when injured hepatocytes or obstructed biliary channels fail to process and excrete bilirubin into the intestinal tract.

Acute Viral Hepatitis: Prodrome Phase

The initial phase of acute viral hepatitis lasting approximately $2\,\text{weeks}$, characterized by non-specific, constitutional cues including profound fatigue, anorexia, malaise, headache, and low-grade fever.

Acute Viral Hepatitis: Icterus Phase

The second clinical phase of acute viral hepatitis lasting $2\text{--}6\,\text{weeks}$, characterized by clinical jaundice (appearing about $2\,\text{weeks}$ post-exposure), dark hyperbilirubinemic urine, clay-colored stools, and a tender, enlarged liver.

Acute Viral Hepatitis: Recovery Phase

The convalescent phase of acute viral hepatitis lasting approximately $8\,\text{weeks}$, during which jaundice and systemic cues resolve, though tender hepatomegaly often persists for an additional $1\text{--}4\,\text{weeks}$.

Fulminant Hepatitis

Severe acute hepatitis featuring extensive hepatic necrosis, sinusoidal vascular compromise, tissue hypoxia, and abrupt clinical onset of complete acute liver failure.

Protein Buffer System

The body's largest chemical buffering system, composed of intracellular proteins, serum albumin, and plasma globulins, which utilize their amphoteric properties to bind or release hydrogen ions for moment-to-moment pH stabilization.

Potassium–Hydrogen ($K^+/H^+$) Exchange

A transcellular ion exchange mechanism that maintains electrical neutrality; during metabolic acidosis, excess extracellular $H^+$ enters cells to be buffered, displacing intracellular $K^+$ into systemic circulation and precipitating hyperkalemia.

Bicarbonate-to-Carbonic Acid Ratio

The critical $20:1$ chemical equilibrium maintained between extracellular bicarbonate ($HCO_3^-$) and carbonic acid ($H_2CO_3$) necessary to preserve arterial blood pH within the physiological target of $7.35\text{--}7.45$.

Metabolic Acidosis

A systemic acid–base disturbance defined by arterial $\text{pH} < 7.35$ and subnormal plasma bicarbonate ($HCO_3^-$), provoked by excessive metabolic acid production, renal retention of fixed acids, gastrointestinal bicarbonate loss, or hyperchloremia.

Anion Gap

A calculation used to categorize metabolic acidosis, where an increased gap signifies the abnormal accumulation of unmeasured organic fixed acids (e.g., ketoacidosis, lactic acidosis), whereas a normal gap implicates excessive chloride.

Metabolic Alkalosis

A systemic acid–base disorder characterized by arterial $\text{pH} > 7.45$ and elevated plasma bicarbonate ($HCO_3^- > 31\,\text{mEq/L}$), caused by hydrogen ion loss, excessive base accumulation, or chloride and volume depletion that impairs renal bicarbonate clearance.

Diverticulosis

The asymptomatic presence of small, acquired outpouchings (diverticula) of the mucosa and submucosa herniating through focal weaknesses in the muscular wall of the colon, commonly associated with prolonged intraluminal pressure from chronic constipation.

Diverticulitis

Acute localized inflammation and microperforation occurring when inspissated fecal matter becomes trapped within a colonic diverticulum, characteristically presenting with acute left lower quadrant pain corresponding to the sigmoid colon.

Functional Fecal Incontinence

The recurrent passage of feces into inappropriate places by a neurologically intact child aged $\ge 4\,\text{years}$ in the complete absence of any underlying structural, anatomic, or physiologic abnormality.

Retentive Fecal Incontinence

A self-reinforcing behavioral subtype of functional incontinence where voluntary withholding of stool due to stress or painful defecation leads to fecal impaction, rectal dilation, desensitization, and eventual overflow soiling.