Pathophysiology Exam Three Study Guide Flashcards

Comprehensive review flashcards covering gastrointestinal disorders, pain pathways, thyroid abnormalities, adrenal diseases, posterior pituitary dysfunction, renal pathophysiology, and musculoskeletal conditions.

Cirrhosis of the liver

A chronic liver disorder where healthy liver cells are replaced by fibrosis and nodular scar tissue, restricting blood flow and causing liver function to decline.

Causes of cirrhosis

Chronic alcohol use, hepatitis B or C, metabolic dysfunction-associated steatotic liver disease (MASLD), autoimmune disease, and inherited disorders.

Portal hypertension

Increased resistance to blood flow through the fibrotic liver, resulting in esophageal and gastric varices, ascites, splenomegaly, enlarged collateral veins, and rectal varices.

Esophageal and gastric varices

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

Ascites

Pathological accumulation of fluid in the peritoneal cavity driven by portal hypertension, low albumin synthesis, and altered sodium and water regulation.

Hepatic encephalopathy

A neuropsychiatric complication of advanced liver disease resulting from impaired detoxification, allowing neurotoxins such as ammonia to accumulate.

Hepatorenal syndrome

A severe, life-threatening complication of advanced cirrhosis characterized by renal failure secondary to severe renal vasoconstriction and impaired perfusion.

AST and ALT in liver disease

Serum aminotransferases that become elevated and directly reflect hepatocellular injury rather than liver synthetic capability.

Serum albumin in liver assessment

A key laboratory indicator synthesized by hepatocytes that falls in liver failure and reflects impaired hepatic synthetic function.

PT/INR in liver assessment

A coagulation lab measurement that prolongs as clotting factor synthesis declines, serving as an important marker of liver synthetic function.

Blood ammonia level

A byproduct of protein metabolism that may rise in liver failure but does not reliably correlate with or measure the clinical severity of hepatic encephalopathy.

Alkaline phosphatase (ALP)

A liver enzyme that typically rises in conditions characterized by cholestasis or bile duct obstruction.

Thrombocytopenia in cirrhosis

A decrease in circulating platelet counts often caused by splenomegaly and splenic pooling secondary to portal hypertension.

Metabolic dysfunction-associated steatotic liver disease (MASLD)

Accumulation of fat inside liver cells (formerly NAFLD) that can progress to inflammation, fibrosis, and cirrhosis; often asymptomatic in early stages.

Risk factors for MASLD

Obesity, abdominal adiposity, type 2 diabetes, insulin resistance, elevated triglycerides, hypertension, and metabolic syndrome.

Crohn's disease

An inflammatory bowel disease that can affect any segment from mouth to anus (often the terminal ileum), featuring skip lesions and transmural inflammation.

Ulcerative colitis

An inflammatory bowel disease limited to the colon and rectum, characterized by continuous mucosal and submucosal inflammation starting at the rectum.

Skip lesions

Discontinuous areas of inflammation separated by normal tissue along the gastrointestinal tract, characteristic of Crohn's disease.

Transmural inflammation

Inflammation extending across all histological layers of the bowel wall, predisposing to fistulas, strictures, and abscesses in Crohn's disease.

Toxic megacolon

A life-threatening acute dilation of the colon that represents a major emergency complication of ulcerative colitis.

Stool characteristics in ulcerative colitis

Frequent, urgent episodes of bloody diarrhea accompanied by rectal tenesmus due to diffuse mucosal ulceration in the colon and rectum.

Appendicitis

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

McBurney's point tenderness

Localized tenderness in the right lower quadrant of the abdomen that is a classic physical exam finding in acute appendicitis.

Appendicitis pain migration

Abdominal pain that characteristically begins as dull discomfort near the umbilicus and progressively shifts to localized pain in the right lower quadrant.

Appendiceal rupture

Perforation of the appendix leading to peritonitis, abscess, and sepsis; suggested clinically by sudden temporary pain relief followed by generalized worsening pain.

Bowel obstruction

Mechanical or functional blockage of intestinal flow caused by postoperative adhesions, hernias, tumors, volvulus, intussusception, or fecal impaction.

Clinical findings of bowel obstruction

Abdominal cramping pain, abdominal distention, vomiting, obstipation, and bowel sounds that are high-pitched early and diminish or disappear later.

Complications of bowel obstruction

Dehydration, electrolyte imbalance, compromised bowel wall perfusion, bowel ischemia, necrosis, perforation, peritonitis, and septic shock.

Volvulus

Twisting of a loop of intestine around its mesentery, causing mechanical bowel obstruction and risking strangulation and bowel ischemia.

Intussusception

Telescoping of one segment of bowel into an adjacent segment, producing mechanical obstruction and potential vascular compromise.

Postoperative adhesions

Fibrous bands of scar tissue forming between abdominal tissues and organs after surgery; a leading cause of mechanical bowel obstruction.

Acute pancreatitis

Inflammation of the pancreas caused by premature intra-acinar activation of pancreatic enzymes leading to tissue autodigestion.

Primary etiologies of acute pancreatitis

Biliary tract disease (gallstones) and heavy alcohol consumption.

Clinical findings of pancreatitis

Severe, boring epigastric pain that characteristically radiates straight through to the back, associated with nausea, vomiting, and abdominal tenderness.

Serum lipase in acute pancreatitis

A pancreatic enzyme that is commonly elevated to at least $3\times$ the upper limit of normal during acute pancreatitis, offering greater specificity than amylase.

Metabolic complications of severe pancreatitis

Hypocalcemia (from fat saponification) and hyperglycemia (from impaired insulin secretion by injured islet cells).

Hepatitis A virus (HAV)

A liver virus transmitted via the fecal-oral route through contaminated food or water; typically causes acute self-limiting disease, does not cause chronic infection, and has a preventive vaccine.

Hepatitis B virus (HBV)

A liver virus transmitted through blood, sexual contact, and perinatal exposure from childbirth; can progress to chronic hepatitis and has an effective preventive vaccine.

Hepatitis C virus (HCV)

A bloodborne virus primarily transmitted through blood exposure (such as shared needles); often establishes chronic infection and is curable with direct-acting antivirals.

Hepatitis D virus (HDV)

An incomplete virus transmitted by blood and body fluids that requires co-existing HBV infection for replication; prevented by the hepatitis B vaccine.

Diverticulosis

The presence of outpouchings (diverticula) in the colonic muscular wall, which are usually asymptomatic but may cause painless lower gastrointestinal bleeding.

Diverticulitis

Inflammation and microperforation of colonic diverticula presenting with left lower quadrant pain, fever, nausea, altered bowel habits, and leukocytosis.

Complications of diverticulitis

Pericolonic abscess, bowel perforation, fistulas (e.g., colovesical), mechanical bowel obstruction, and generalized peritonitis.

Gastroesophageal reflux disease (GERD)

A condition in which gastric contents reflux retrograde into the esophagus, primarily due to transient relaxations or weakness of the lower esophageal sphincter (LES).

Barrett's esophagus

Premalignant metaplastic transformation of normal esophageal squamous mucosa into specialized intestinal columnar epithelium due to chronic GERD.

Clinical symptoms of GERD

Postprandial heartburn (pyrosis) exacerbated by recumbency, sour acid regurgitation, dysphagia, chronic cough, and hoarseness.

Internal hemorrhoids

Enlarged vascular cushions located above the dentate line in the anal canal, typically presenting with painless bright-red rectal bleeding during defecation.

External hemorrhoids

Dilated vascular cushions situated below the dentate line covered by somatic skin, which can become acutely painful when thrombosed.

Stomatitis

Inflammation and ulceration of the oral mucosa caused by infections, chemotherapy, radiation, malnutrition, or dry mouth, presenting with oral pain and dysphagia.

Mallory-Weiss syndrome

A longitudinal mucosal tear near the gastroesophageal junction caused by forceful retching or recurrent vomiting, classically presenting as bright-red hematemesis.

Peptic ulcer disease (PUD)

Erosive mucosal defect in the stomach or duodenum, most commonly resulting from Helicobacter pylori infection or chronic NSAID use.

Helicobacter pylori

A spiral-shaped bacterium that colonizes gastric mucosa, breaks down the protective mucosal barrier, and acts as a primary cause of peptic ulcers.

NSAID gastropathy mechanism

Inhibition of cyclooxygenase enzymes leading to reduced prostaglandin synthesis, diminishing gastric bicarbonate and mucosal blood flow.

Gastric ulcer pain pattern

Epigastric burning or gnawing pain that is typically exacerbated immediately by food ingestion.

Duodenal ulcer pain pattern

Epigastric gnawing discomfort that characteristically improves temporarily after meals, only to recur $2\text{--}3\text{ hours}$ later or awaken the patient at night.

Melena

Black, tarry, foul-smelling stools resulting from the bacterial degradation of hemoglobin during upper gastrointestinal bleeding.

Biliary colic

Episodic, intense right upper quadrant or epigastric pain that occurs when a gallstone temporarily blocks the cystic duct during gallbladder contraction.

Murphy's sign

Inspiratory arrest elicited by palpation of the right upper quadrant beneath the liver margin during deep inhalation, suggestive of acute cholecystitis.

Referred pain

Pain perceived at a clinical site distant from its actual visceral origin, such as jaw or arm pain during myocardial infarction, due to shared sensory pathways.

Cutaneous pain

Superficial somatic discomfort originating from the skin or subcutaneous tissues, exemplified by minor lacerations or superficial burns.

Neuropathic pain

Pain directly generated by a primary lesion or disease affecting the somatosensory nervous system, frequently characterized by burning, shooting, or tingling sensations.

Chronic pain

Pain that persists or recurs beyond the anticipated normal healing time frame, commonly operationalized as lasting longer than $3\text{ months}$.

Deep somatic pain

Pain originating within bones, joints, skeletal muscles, tendons, or deep connective tissue, exemplified by bone fractures and osteoarthritis.

Nociceptors

High-threshold sensory receptors located throughout peripheral tissues specialized to detect noxious thermal, mechanical, or chemical stimuli.

Gate Control Theory: Phase 1 (Stimulus)

The phase where tissue injury activates primary peripheral nociceptors, initiating afferent nerve impulses directed toward the spinal cord.

Gate Control Theory: Phase 2 (Transmission)

The passage of nociceptive signals into the dorsal horn of the spinal cord, where neural transmission can be amplified or inhibited.

Gate Control Theory: Phase 3 (Gate modulation)

Modulation of nociceptive input within the substantia gelatinosa, where activation of large touch fibers closes the gate via inhibitory interneurons.

Gate Control Theory: Phase 4 (Perception)

The conscious appreciation, emotional interpretation, and cognitive evaluation of pain within higher cortical centers of the brain.

Large-diameter touch fibers ($A\beta$)

Myelinated cutaneous mechanoreceptive fibers whose activation stimulates inhibitory spinal interneurons to close the pain gate.

Small-diameter pain fibers ($A\text{-delta}$ and $C$)

Afferent nerve fibers transmitting noxious inputs that facilitate nociception and open the spinal gate to allow signal transmission.

Rubbing an injured area

A mechanical intervention that activates tactile sensory fibers to diminish pain transmission at the dorsal horn without eliminating tissue injury.

Graves' disease

An autoimmune disorder in which thyroid-stimulating immunoglobulin (TSI) autoantibodies bind and stimulate TSH receptors, producing hyperthyroidism.

Exophthalmos

Proptosis or abnormal forward bulging of the eyes caused by retro-orbital fat deposition and autoimmune inflammation, characteristic of Graves' disease.

Clinical manifestations of hyperthyroidism

Unexplained weight loss with increased appetite, heat intolerance, diaphoresis, resting tachycardia, tremor, anxiety, insomnia, and hyperdefecation.

Laboratory findings in primary hyperthyroidism

Markedly suppressed or undetectable serum TSH with elevated concentrations of free $T_4$ and/or free $T_3$.

Clinical manifestations of hypothyroidism

Fatigue, unexplained weight gain, cold intolerance, persistent constipation, sinus bradycardia, coarse dry skin, and generalized mental slowing.

Laboratory findings in primary hypothyroidism

Elevated serum TSH accompanied by a subnormal concentration of circulating free $T_4$.

Primary thyroid disorder hormone relationship

An inverse relationship between serum TSH and circulating thyroid hormones caused by negative feedback on the anterior pituitary gland.

Goiter

An abnormal macroscopic enlargement of the thyroid gland, which can occur in hyperthyroid, euthyroid, or hypothyroid states.

Glucocorticoid excess (Cortisol)

Hypercortisolemia leading to central obesity, dorsocervical adiposity, facial rounding, purple abdominal striae, thin fragile skin, and hyperglycemia.

Glucocorticoid deficiency (Cortisol)

Adrenocortical insufficiency characterized by fatigue, generalized muscle weakness, hypoglycemia, anorexia, and impaired physiological stress tolerance.

Mineralocorticoid excess (Aldosterone)

Excessive adrenal aldosterone release that promotes renal sodium and water retention and potassium excretion, causing hypertension and hypokalemia.

Mineralocorticoid deficiency (Aldosterone)

Diminished adrenal aldosterone release leading to excessive renal sodium and water excretion, hypovolemic hypotension, dehydration, and hyperkalemia.

Adrenal androgen excess

Hypersecretion of adrenal sex steroids resulting in clinical hirsutism, oily skin, cystic acne, and virilization depending on the patient.

Catecholamine hypersecretion

Excessive paroxysmal secretion of epinephrine and norepinephrine causing episodic headaches, profuse diaphoresis, palpitations, and severe hypertension.

Cushing syndrome

The clinical constellation of signs and symptoms resulting from chronic, excessive tissue exposure to high glucocorticoid levels.

Cushing disease

A specific subtype of Cushing syndrome caused by an ACTH-secreting anterior pituitary adenoma stimulating bilateral adrenocortical hyperplasia.

Dorsocervical fat pad

An abnormal localized accumulation of adipose tissue at the posterior base of the neck, commonly referred to as a buffalo hump in Cushing syndrome.

Purple striae

Wide, violaceous cutaneous stretch marks typically observed over the abdomen and thighs in Cushing syndrome, caused by cortisol-induced collagen breakdown.

Screening tests for Cushing syndrome

Late-night salivary cortisol, 24-hour urinary free cortisol excretion, and the low-dose dexamethasone suppression test.

Addison disease

Primary chronic adrenocortical insufficiency typically caused by autoimmune destruction of the adrenal cortex, leading to deficient cortisol and aldosterone.

Cutaneous hyperpigmentation in Addison disease

Darkening of palmar creases and mucosal membranes due to high ACTH levels containing melanocyte-stimulating hormone (MSH) activity from lack of cortisol feedback.

Laboratory pattern in primary Addison disease

Low serum cortisol, high plasma ACTH, low serum sodium (hyponatremia), elevated serum potassium (hyperkalemia), and elevated plasma renin.

Renal mechanism of aldosterone in electrolyte balance

Stimulates apical sodium reabsorption and coupled potassium secretion within the principal cells of the late distal convoluted tubule and collecting duct.

Adrenal crisis

An acute, life-threatening exacerbation of adrenal insufficiency characterized by profound hypotension, refractory shock, intractable vomiting, and hypoglycemia.

Neurogenic (central) diabetes insipidus

A disorder resulting from inadequate synthesis or release of antidiuretic hormone (ADH) by the hypothalamus and posterior pituitary gland.

Pathophysiology of diabetes insipidus

Absence of ADH prevents aquaporin insertion in collecting ducts, impairing water reabsorption and producing large volumes of dilute urine.

Clinical presentation of diabetes insipidus

Marked polyuria, compensatory polydipsia, nocturia, dry mucous membranes, tachycardia, and potential hypovolemic hypotension.

Urinary labs in diabetes insipidus

Hypoosmolar, excessively dilute urine characterized by subnormal urine osmolality and low urine specific gravity.

Serum labs in unreplaced diabetes insipidus

Hypernatremia and elevated serum osmolality resulting from uncompensated free water loss through excessive renal excretion.