Pathophysiology Exam Three Study Guide Flashcards

Comprehensive vocabulary flashcards covering gastrointestinal disorders, pain pathways, thyroid and adrenal conditions, fluid balance disorders (DI and SIADH), renal pathophysiology, and musculoskeletal disorders and fracture classifications.

Cirrhosis of the liver

A chronic liver disease where healthy liver cells are replaced by fibrosis and nodular scar tissue, resulting in restricted hepatic blood flow and declining liver function.

Portal hypertension

Increased pressure within the portal venous system due to restricted blood flow through a cirrhotic liver, leading to ascites, splenomegaly, and collateral vein enlargement.

Esophageal and gastric varices

Enlarged collateral veins in the esophagus and stomach caused by portal hypertension in cirrhosis that carry a high risk of life-threatening bleeding.

Rectal varices (in cirrhosis)

Enlarged collateral veins in the rectum that can develop secondary to portal hypertension in patients with cirrhosis.

Ascites (in cirrhosis)

Accumulation of fluid in the peritoneal cavity driven by portal hypertension, decreased serum albumin, and altered renal sodium and water regulation.

Splenomegaly (in cirrhosis)

Enlargement of the spleen resulting from venous congestion and backpressure caused by portal hypertension, often contributing to low platelet counts.

Hepatic encephalopathy

A neurological disorder resulting from impaired hepatic detoxification of toxins such as ammonia in cirrhosis or liver failure.

Hepatorenal syndrome

Development of progressive renal failure occurring as a severe systemic complication of advanced liver cirrhosis and portal hypertension.

Jaundice and pruritus (in cirrhosis)

Yellowing of the skin and eyes accompanied by severe itching caused by impaired hepatic processing and excretion of bilirubin.

Coagulation impairment in cirrhosis

Increased bruising and bleeding caused by the cirrhotic liver's reduced capacity to synthesize essential clotting factors.

AST and ALT (in liver evaluation)

Serum transaminases (aspartate aminotransferase and alanine aminotransferase) that elevate during active hepatocyte injury.

Liver synthetic function markers

Laboratory tests, specifically serum albumin and $PT/INR$, that directly assess the liver's capacity to synthesize proteins and clotting factors.

Serum Ammonia (in liver disease)

A nitrogenous toxin that may rise in liver failure due to impaired detoxification, though it does not reliably correlate with hepatic encephalopathy severity.

Alkaline Phosphatase (ALP)

A liver enzyme that may rise in hepatobiliary disease as an indicator of cholestasis or impaired bile excretion.

Metabolic dysfunction-associated steatotic liver disease (MASLD)

Formerly termed NAFLD, a condition where fat accumulates in hepatocytes with the potential to progress to inflammation, fibrosis, and cirrhosis.

MASLD risk factors

Metabolic conditions increasing fatty liver risk, including obesity, abdominal adiposity, type 2 diabetes/insulin resistance, high triglycerides, hypertension, and metabolic syndrome.

Crohn's disease

An inflammatory bowel disease characterized by transmural inflammation and skip lesions that can affect any part of the GI tract from mouth to anus, commonly involving the terminal ileum.

Ulcerative colitis

An inflammatory bowel disease characterized by continuous mucosal and submucosal inflammation restricted to the colon and rectum, presenting with urgency and bloody diarrhea.

Skip lesions

Discontinuous segments of diseased bowel separated by areas of normal mucosa, a hallmark finding characteristic of Crohn's disease.

Transmural inflammation

Inflammation extending through all layers of the intestinal wall, characteristic of Crohn's disease and predisposing to fistulas, strictures, and abscesses.

Toxic megacolon

A life-threatening complication characterized by severe, acute non-obstructive dilation of the colon, seen as a major risk in ulcerative colitis.

Intestinal fistulas (in Crohn's disease)

Abnormal tracts connecting the bowel to other bowel loops, organs, or skin, arising from the transmural inflammation of Crohn's disease.

Intestinal strictures (in Crohn's disease)

Pathological narrowing of the intestinal lumen caused by transmural inflammation and fibrosis, a frequent complication of Crohn's disease.

Appendicitis

Acute inflammation of the appendix, most commonly caused by luminal obstruction from a fecalith or lymphoid swelling.

Fecalith

A hard, calcified stone of feces that commonly obstructs the opening of the appendix, triggering acute appendicitis.

McBurney's point tenderness

Focal tenderness in the right lower quadrant, approximately one-third of the distance from the anterior superior iliac spine to the umbilicus, classic for appendicitis.

Appendix rupture presentation

Perforation of the appendix manifested by sudden temporary relief of abdominal pain followed by generalized, worsening peritonitis and sepsis.

Bowel obstruction

Mechanical or functional blockage that impairs the normal transit of intestinal contents, presenting with cramping, distention, vomiting, and absent flatus or stool.

Postoperative adhesions

Fibrous bands of scar tissue forming after abdominal surgery that represent a leading cause of mechanical bowel obstruction.

Volvulus

Twisting of a bowel loop around itself and its supporting mesentery, causing mechanical intestinal obstruction and compromised blood flow.

Intussusception

The telescoping or invagination of one segment of the intestine into an adjacent downstream segment, causing bowel obstruction and ischemia.

Bowel obstruction bowel sounds

Auscultatory findings in bowel obstruction that are typically high-pitched early in the course and progressively decrease or disappear later.

Complications of bowel obstruction

Severe consequences of intestinal blockage including dehydration, electrolyte imbalance, reduced perfusion, bowel ischemia, necrosis, perforation, peritonitis, and sepsis.

Acute pancreatitis

Acute inflammation of the pancreas resulting from premature activation of digestive enzymes inside the parenchyma, causing autodigestion.

Autodigestion (in pancreatitis)

Pathological digestion of pancreatic and surrounding tissues by enzymes activated prematurely within the pancreas itself.

Common causes of acute pancreatitis

Gallstones and heavy alcohol use, which together account for the vast majority of acute pancreatitis cases.

Serum lipase (in acute pancreatitis)

A diagnostic pancreatic enzyme that characteristically rises to at least three times the upper limit of normal ($\ge 3\times \text{ULN}$) during acute pancreatitis.

Serum amylase (in acute pancreatitis)

A digestive enzyme produced by the pancreas that commonly rises in the serum alongside lipase during acute pancreatitis.

Hypocalcemia (in acute pancreatitis)

A reduction in serum calcium seen in severe acute pancreatitis as calcium precipitates into areas of fat necrosis and saponification.

Hyperglycemia (in acute pancreatitis)

Elevated blood glucose occurring in severe acute pancreatitis due to impaired endocrine insulin release from damaged islet cells.

Hepatitis A virus (HAV)

A viral infection transmitted via the fecal-oral route through contaminated food or water that causes acute hepatitis, does not cause chronic infection, and is vaccine-preventable.

Hepatitis B virus (HBV)

A viral liver infection transmitted via blood, sexual contact, or childbirth that can progress to chronic infection and is vaccine-preventable.

Hepatitis C virus (HCV)

A viral liver infection transmitted primarily through blood exposure (such as shared needles) that often becomes chronic and is treatable with curative antivirals.

Hepatitis D virus (HDV)

A defective virus transmitted via blood and body fluids that requires co-infection with HBV to replicate; prevented by the Hepatitis B vaccine.

Diverticulosis vs. diverticulitis

Diverticulosis refers to pouches in the colon wall that are often asymptomatic or cause painless bleeding; diverticulitis is inflammation or infection of those pouches causing LLQ pain, fever, and leukocytosis.

Gastroesophageal reflux disease (GERD)

A disorder where stomach contents reflux backward into the esophagus, often because the lower esophageal sphincter is weak or relaxes inappropriately.

Lower esophageal sphincter (LES) in GERD

The muscular barrier at the gastroesophageal junction whose weakness or inappropriate transient relaxation permits acidic gastric reflux.

Esophagitis

Inflammation and mucosal injury of the esophageal lining resulting from persistent acid exposure in chronic GERD.

Barrett's esophagus

A complication of chronic GERD characterized by metaplastic replacement of normal squamous epithelium with columnar mucosa, increasing cancer risk.

Internal vs. external hemorrhoids

Internal hemorrhoids are swollen vascular cushions above the dentate line causing painless bright-red bleeding; external hemorrhoids are located below the dentate line and may be painful, especially when thrombosed.

Stomatitis

Inflammation of the oral mucosa caused by infection, irritation, nutritional deficiency, medications, chemotherapy, or radiation, causing redness, ulcers, and painful eating.

Mallory-Weiss syndrome

A mucosal tear near the gastroesophageal junction caused by forceful retching or vomiting, frequently associated with heavy alcohol use and presenting with hematemesis.

Hematemesis

The vomiting of bright red blood or coffee-ground material, a classic sign of upper gastrointestinal bleeding seen in Mallory-Weiss tears and bleeding ulcers.

Peptic ulcer disease (PUD)

Erosions or ulcers in the gastric or duodenal mucosa, most commonly caused by Helicobacter pylori infection or nonsteroidal anti-inflammatory drugs (NSAIDs).

Helicobacter pylori (H. pylori)

A bacterium that colonizes the stomach lining and disrupts mucosal defenses, serving as one of the two primary causes of peptic ulcer disease.

NSAID-induced peptic ulcers

Ulcerations in the stomach or duodenum resulting from nonsteroidal anti-inflammatory drugs (e.g., ibuprofen, naproxen) inhibiting protective mucosal prostaglandins.

Gastric vs. duodenal ulcer pain patterns

Gastric ulcer pain typically worsens with food intake; duodenal ulcer pain often improves temporarily after eating and recurs $2\text{--}3\text{ hours}$ later.

Biliary colic (Gallbladder attack)

Severe right upper quadrant or epigastric pain radiating to the right shoulder or back following a fatty meal, caused by a gallstone temporarily lodging in the cystic duct.

Murphy's sign

A physical exam finding where deep palpation of the right upper quadrant during inspiration causes sharp pain and inspiratory arrest, indicating acute cholecystitis.

Acute cholecystitis

Inflammation of the gallbladder wall, typically following sustained cystic duct obstruction by a gallstone, presenting with persistent RUQ pain, fever, and a positive Murphy's sign.

Referred pain

Pain perceived in an anatomical location distant from its original pathological source, such as jaw or arm pain during a myocardial infarction.

Cutaneous pain

Superficial, well-localized pain arising from the skin or subcutaneous tissues, such as from a cut or minor burn.

Neuropathic pain

Pain initiated or caused by nerve injury or nervous system dysfunction, characteristically presenting as burning, tingling, or electric sensations like diabetic neuropathy.

Chronic pain

Persistent or recurrent pain lasting beyond the normal tissue healing timeframe, commonly defined clinically as persisting for greater than 3 months ($>3\text{ months}$).

Deep somatic pain

Dull, aching pain originating from deeper somatic structures including muscles, bones, joints, tendons, and connective tissues, as seen in fractures or arthritis.

Gate Control Theory

A theory of pain describing how non-painful sensory input and dorsal horn interneurons can inhibit pain transmission signals before they reach conscious perception.

Gate Control Phase 1: Stimulus

The phase where tissue injury activates peripheral nociceptors, initiating afferent electrical signals that travel toward the spinal cord.

Gate Control Phase 2: Transmission

The phase where afferent pain impulses reach the dorsal horn of the spinal cord, where signal intensity can be amplified or inhibited.

Gate Control Phase 3: Gate modulation

The phase where touch fibers and inhibitory interneurons close the gate and reduce pain transmission, while small pain fibers tend to facilitate it.

Gate Control Phase 4: Perception

The phase where the brain interprets pain signals, which can be modified by attention, emotion, previous experience, and descending pathways.

Nociceptors

Specialized sensory nerve endings in peripheral tissues that detect noxious mechanical, thermal, or chemical stimuli and initiate pain signals.

Dorsal horn (Gate Control Theory)

The spinal cord region where incoming peripheral sensory signals synapse and where transmission can be gated or modulated before ascending.

Graves' disease

An autoimmune hyperthyroid condition where autoantibodies stimulate TSH receptors, causing excess T3/T4 secretion, goiter, and exophthalmos.

TSH receptor antibodies

Autoimmune antibodies present in Graves' disease that continuously stimulate thyroid TSH receptors, driving autonomous hyperthyroidism.

Exophthalmos

Abnormal protrusion or bulging of the eyes, an autoimmune ocular manifestation specifically associated with Graves' hyperthyroidism.

Goiter

Enlargement of the thyroid gland that can develop in both hyperthyroidism (such as Graves' disease) and hypothyroidism due to continuous trophic stimulation.

Primary hyperthyroidism labs

A laboratory pattern characterized by suppressed (low) $TSH$ and elevated levels of $\text{free T4}$ and/or $T3$.

Primary hypothyroidism labs

A laboratory pattern characterized by elevated $TSH$ and reduced circulating $\text{free T4}$ due to primary thyroid gland failure.

Thermal intolerance in thyroid disease

Heat intolerance with diaphoresis occurs in hyperthyroidism due to high metabolism; cold intolerance occurs in hypothyroidism due to metabolic slowing.

TSH and thyroid hormone inverse relationship

The physiological negative feedback mechanism where high circulating thyroid hormones suppress pituitary TSH and low thyroid hormones stimulate TSH release.

Cortisol excess vs. deficiency

Excess cortisol produces Cushing syndrome features (central obesity, hyperglycemia); cortisol deficiency produces fatigue, weakness, hypoglycemia, and impaired stress response.

Aldosterone excess vs. deficiency

Excess aldosterone causes hypertension and hypokalemia; aldosterone deficiency causes renal sodium and water loss, dehydration, hypotension, and hyperkalemia.

Adrenal androgen alterations

Adrenal androgen excess leads to acne and hirsutism; androgen deficiency can cause reduction in body hair or libido.

Catecholamine excess

Hypersecretion of epinephrine and norepinephrine causing paroxysmal symptoms of episodic headache, profuse sweating, palpitations, and hypertension.

Cushing syndrome

A condition of prolonged cortisol excess caused by glucocorticoid medication, pituitary ACTH adenomas, adrenal tumors, or ectopic ACTH secretion.

Cushing disease

A specific etiology of Cushing syndrome resulting from an ACTH-secreting pituitary tumor.

Dorsocervical fat pad

An abnormal deposition of adipose tissue on the upper back and base of the neck, commonly seen in hypercortisolism (Cushing syndrome).

Moon face

Round, full facial appearance resulting from characteristic adipose redistribution in patients with Cushing syndrome.

Purple striae

Wide, purplish cutaneous stretch marks occurring in Cushing syndrome due to cortisol-induced protein catabolism and collagen breakdown.

24-hour urinary free cortisol test

A diagnostic screening test for Cushing syndrome that quantifies unbound cortisol excreted into the urine over an entire day.

Late-night salivary cortisol test

A diagnostic screening test evaluating loss of normal evening circadian nadir in cortisol levels, indicative of Cushing syndrome.

Low-dose dexamethasone suppression test

A screening test where failure of synthetic dexamethasone to suppress morning cortisol secretion suggests endogenous hypercortisolism.

Addison disease

Primary adrenal insufficiency caused by autoimmune destruction of the adrenal cortex, resulting in deficient cortisol and aldosterone.

Hyperpigmentation (in Addison disease)

Bronzing of the skin and mucous membranes caused by high levels of ACTH and melanocyte-stimulating hormone fragments produced during primary adrenal failure.

Salt craving (in Addison disease)

An intense physiological desire to consume salt resulting from renal sodium wasting caused by aldosterone deficiency.

Aldosterone deficiency mechanism (in Addison disease)

Loss of distal nephron sodium reabsorption and potassium excretion, causing urinary sodium and water wasting, hypotension, volume depletion, and hyperkalemia.

Adrenal crisis

A life-threatening exacerbation of adrenal insufficiency causing severe hypotension/shock, vomiting, abdominal pain, hypoglycemia, and critical electrolyte abnormalities.

Addison disease lab pattern

Characteristic laboratory findings in primary Addison disease showing low cortisol, elevated ACTH, low sodium, high potassium, and high renin.

Neurogenic (central) diabetes insipidus

A disorder where head trauma, surgery, or tumors cause the hypothalamus/posterior pituitary to secrete insufficient ADH, producing large volumes of dilute urine.

Antidiuretic hormone (ADH)

A posterior pituitary hormone that promotes water reabsorption in renal collecting ducts, concentrating urine and preventing volume loss.