Pathophysiology Exam Three Study Guide Flashcards

A comprehensive collection of 160 traditional vocabulary flashcards covering gastrointestinal disorders, pain pathways, thyroid and adrenal endocrinopathies, pituitary fluid imbalances, renal failure syndromes, and musculoskeletal pathology based on the Exam Three study guide.

Cirrhosis of the liver

A chronic liver disease where healthy hepatocytes are replaced by diffuse fibrosis and nodular scar tissue, impairing hepatic blood flow and causing synthetic and metabolic liver failure.

MASLD (Metabolic dysfunction-associated steatotic liver disease)

A liver condition formerly known as NAFLD where excess fat accumulates within hepatocytes, which can progress to steatohepatitis, fibrosis, and cirrhosis; strongly linked to obesity, insulin resistance, and metabolic syndrome.

Portal hypertension

Abnormally elevated blood pressure within the hepatic portal venous system resulting from fibrotic resistance in the cirrhotic liver, leading to ascites, splenomegaly, and collateral vascular varices.

Esophageal varices

Dilated, thin-walled submucosal veins in the lower esophagus formed as collateral circulation due to portal hypertension, carrying a severe risk of rupture and life-threatening hematemesis.

Ascites

Accumulation of fluid in the peritoneal cavity seen in advanced liver disease, driven by portal hypertension, low oncotic pressure from hypoalbuminemia, and altered renal sodium and water handling.

Hepatic encephalopathy

A reversible neuropsychiatric abnormality in liver failure caused by the accumulation of gut-derived neurotoxins, such as ammonia, that bypass hepatic detoxification.

Hepatorenal syndrome

Progressive, functional renal failure developing in the setting of severe portal hypertension and advanced liver disease due to marked renal vasoconstriction.

AST and ALT in liver disease

Serum transaminases that serve as sensitive laboratory markers of active hepatocellular injury and necrosis.

Serum albumin and PT/INR in liver disease

Key laboratory parameters used to assess hepatic synthetic function; declining albumin and a prolonged PT/INR indicate impaired synthesis of serum proteins and clotting factors.

Alkaline phosphatase (ALP)

A hepatic enzyme commonly measured in blood that rises in response to biliary tract obstruction or cholestasis.

Crohn's disease (Anatomical distribution)

A chronic inflammatory bowel disease that can affect any segment of the gastrointestinal tract from the mouth to the anus, with a predilection for the terminal ileum.

Skip lesions

Discontinuous segments of inflamed bowel separated by intervening areas of normal mucosal tissue, pathognomonic for Crohn's disease.

Transmural inflammation

Inflammation extending across all histological layers of the intestinal wall, a defining feature of Crohn's disease that promotes sinus tracts, fistulas, and strictures.

Ulcerative colitis (Anatomical distribution)

An inflammatory bowel disease strictly localized to the colon and rectum, beginning in the rectum and extending proximally in an uninterrupted fashion.

Ulcerative colitis (Histologic depth)

Inflammation primarily confined to the mucosa and submucosa of the intestinal wall, presenting with mucosal ulcerations and friability.

Toxic megacolon

An acute, life-threatening complication of severe colitis (notably ulcerative colitis) characterized by rapid non-obstructive colonic dilation, systemic toxicity, and high risk of perforation.

Appendicitis

Acute inflammation of the vermiform appendix, usually initiated by luminal obstruction from a fecalith or lymphoid tissue hyperplasia.

Fecalith

A hard, calcified pellet of inspissated fecal material that frequently lodges in the appendiceal orifice, obstructing the lumen and triggering appendicitis.

McBurney's point tenderness

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

Peritonitis from appendiceal rupture

Widespread inflammation of the peritoneal cavity resulting from spillage of infected appendiceal contents, suggested clinically by sudden pain relief followed by worsening diffuse pain and rigidity.

Mechanical bowel obstruction causes

Physical blockages restricting gastrointestinal transit, commonly including postoperative fibrous adhesions, incarcerated hernias, neoplasms, volvulus, intussusception, and fecal impaction.

Clinical findings of bowel obstruction

A symptom complex including episodic cramping abdominal pain, abdominal distention, emesis, and obstipation (inability to pass flatus or stool).

Auscultation pattern in early bowel obstruction

Hyperactive, high-pitched tinkling bowel sounds occurring as the bowel attempts to force contents past the luminal blockage, which later diminish or become silent.

Signs of bowel strangulation/ischemia

Clinical red flags during obstruction including severe unrelenting pain, involuntary abdominal guarding, fever, marked tachycardia, and hemodynamic instability indicating necrosis.

Autodigestion in pancreatitis

The premature intraparenchymal activation of zymogens (pancreatic proenzymes), resulting in enzymatic digestion of pancreatic tissue, fat necrosis, and acute local inflammation.

Most common causes of acute pancreatitis

The two primary etiologic factors are biliary tract stones (choledocholithiasis) and chronic alcohol misuse.

Serum lipase in acute pancreatitis

A diagnostic pancreatic biomarker typically elevated to at least three times ($3\times$) the upper limit of normal during acute pancreatitis, with greater specificity than amylase.

Systemic complications of severe pancreatitis

Severe systemic disturbances including hypocalcemia (from enzymatic fat saponification), hyperglycemia (from impaired insulin secretion), and multiorgan failure.

Hepatitis A virus (HAV)

A hepatotropic virus transmitted primarily through the fecal-oral route via contaminated food or water; typically produces self-limiting acute hepatitis without chronic carrier states and is preventable by vaccine.

Hepatitis B virus (HBV)

A parenterally and sexually transmitted hepatotropic virus (via blood, sexual exposure, or vertical transmission) that can lead to chronic hepatitis, cirrhosis, and hepatocellular carcinoma; preventable by vaccine.

Hepatitis C virus (HCV)

A bloodborne viral infection transmitted largely through percutaneous exposure (e.g., shared needles) that frequently establishes chronic infection; curable with direct-acting antivirals.

Hepatitis D virus (HDV)

A defective RNA virus that requires the presence of Hepatitis B surface antigen to assemble and replicate; effectively prevented by immunization against HBV.

Diverticulosis

The presence of acquired mucosal outpouchings (diverticula) herniating through weak muscular layers of the colon wall; usually asymptomatic but a frequent cause of painless lower GI bleeding.

Diverticulitis

Microperforation and acute inflammation or infection of one or more pre-existing colonic diverticula, classically causing left lower quadrant pain, low-grade fever, and leukocytosis.

Complications of diverticulitis

Pathological outcomes of complicated diverticular inflammation including pericolic abscesses, free peritonitis from perforation, colovesical fistulas, and bowel strictures.

Gastroesophageal reflux disease (GERD)

A chronic condition where acidic gastric contents reflux into the esophagus due to transient relaxations or incompetence of the lower esophageal sphincter (LES).

Clinical manifestations of GERD

Symptoms of esophageal acid exposure including postprandial retrosternal heartburn (pyrosis), regurgitation of sour fluid, globus sensation, dysphagia, chronic dry cough, and hoarseness.

Barrett's esophagus

Specialized intestinal metaplasia of the lower esophagus, where normal stratified squamous epithelium is replaced by columnar epithelium due to chronic acid irritation, increasing adenocarcinoma risk.

Internal hemorrhoids

Symptomatic, dilated vascular cushions located proximal to the dentate line in the anal canal, typically presenting with painless bright-red bleeding during defecation.

External hemorrhoids

Dilated, congested veins situated distal to the dentate line covered by somatic skin, which can cause significant pain, particularly when complicated by acute intravascular thrombosis.

Stomatitis

Inflammation and ulceration of the oral mucous membranes resulting from infections, nutritional deficiencies, cytotoxic chemotherapy, radiation, or mechanical irritation.

Mallory-Weiss syndrome

Non-transmural, longitudinal mucosal tears at the gastroesophageal junction typically caused by acute elevations in intragastric pressure from forceful retching or repeated vomiting.

Hematemesis

The vomiting of bright red blood or dark coffee-ground material, signifying acute upper gastrointestinal hemorrhage from lesions proximal to the ligament of Treitz.

Peptic ulcer disease (PUD)

A circumscribed mucosal breach extending into the muscularis mucosae of the stomach or duodenum, predominantly caused by Helicobacter pylori colonization or NSAID usage.

Gastric ulcer pain pattern

Epigastric burning or gnawing pain that is typically exacerbated immediately following the ingestion of meals as gastric acid secretion is stimulated.

Duodenal ulcer pain pattern

Epigastric pain that characteristically improves temporarily after eating or taking antacids, but recurs $2\text{--}3\text{ hours}$ postprandially or awakens the patient at night.

Biliary colic

Episodic right upper quadrant or epigastric pain provoked by transient impaction of a gallstone in the cystic duct during postprandial cholecystokinin-induced gallbladder contraction.

Referred pain patterns in biliary disease

Somatic pain radiation to the right subscapular area or the tip of the right shoulder, mediated by irritation of the adjacent diaphragm and phrenic nerve afferents ($C3\text{--}C5$).

Murphy's sign

A clinical maneuver where the examiner palpates the right upper quadrant below the costal margin while the patient inspires deeply; sudden arrest in inspiration due to sharp pain suggests acute cholecystitis.

Referred pain

Pain perceived at an anatomical site distant from the actual noxious visceral stimulus, resulting from convergence of visceral and somatic afferent fibers in the spinal cord dorsal horn.

Cutaneous pain

Superficial pain originating from somatic receptors in the skin and subcutaneous tissues, typically described as sharp, localized, and well-demarcated (e.g., superficial cuts or minor burns).

Neuropathic pain

Pain initiated or caused by a primary lesion or dysfunction in the peripheral or central nervous system, frequently characterized by burning, electric shocks, hyperalgesia, or allodynia.

Chronic pain

Pain that persists or recurs beyond the expected time course of normal tissue healing, commonly defined clinically as lasting longer than $3\text{ months}$.

Deep somatic pain

Dull, aching, poorly localized pain originating from deeper musculoskeletal structures including periosteum, cancellous bone, skeletal muscle, joints, ligaments, and tendons.

Stimulus phase (Gate Control Theory)

The first phase where noxious mechanical, thermal, or chemical stimuli activate peripheral primary nociceptive neurons (A-delta and C fibers) to fire action potentials toward the spinal cord.

Transmission phase (Gate Control Theory)

The second phase where incoming nociceptive afferent impulses enter the substantia gelatinosa in the spinal dorsal horn, where synaptic relay to projection neurons is either amplified or dampened.

Gate modulation phase (Gate Control Theory)

The third phase where concurrent activation of large myelinated A-beta tactile fibers excites inhibitory interneurons, 'closing the gate' to incoming small nociceptive afferents.

Perception phase (Gate Control Theory)

The fourth phase where modulated ascending sensory signals reach cerebral cortical and limbic structures to generate the conscious awareness, cognitive evaluation, and emotional response to pain.

Mechanism of rubbing an injury

Tactile stimulation of non-nociceptive A-beta fibers activates spinal dorsal horn inhibitory interneurons, dampening nociceptive transmission and decreasing the conscious perception of pain.

Graves' disease

An autoimmune thyroid disorder characterized by thyroid-stimulating immunoglobulin (TSI) autoantibodies that bind to and activate TSH receptors, resulting in diffuse toxic goiter and hyperthyroidism.

Exophthalmos

Proptosis (forward displacement of the globes) seen in Graves' disease caused by autoimmune retro-orbital adipogenesis, connective tissue inflammation, and glycosaminoglycan accumulation.

Graves' disease clinical symptoms

A hypermetabolic symptom complex characterized by weight loss with increased appetite, heat intolerance, diaphoresis, resting tachycardia, fine tremors, diarrhea, and emotional lability.

Primary hypothyroidism laboratory profile

A serum diagnostic pattern characterized by an elevated thyroid-stimulating hormone ($\text{TSH}$) concentration and a subnormal free thyroxine ($\text{free } T_4$) level.

Primary hypothyroidism clinical manifestations

A hypometabolic state manifesting as lethargy, fatigue, unintended weight gain, cold intolerance, constipation, bradycardia, dry coarse skin, and delayed tendon reflexes.

Primary hyperthyroidism laboratory profile

A diagnostic hormone profile demonstrating a suppressed or undetectable serum $\text{TSH}$ along with elevated concentrations of $\text{free } T_4$ and/or $\text{total } T_3$.

Negative feedback regulation of thyroid hormones

The reciprocal physiological mechanism wherein elevated circulating free $T_4$ and $T_3$ suppress anterior pituitary TSH release, whereas deficient thyroid hormones stimulate increased TSH release.

Systemic effects of glucocorticoid excess

Pathological sequelae including muscle protein catabolism, central visceral adiposity, glucose intolerance/hyperglycemia, immunosuppression, bone demineralization, and purple skin striae.

Systemic effects of glucocorticoid deficiency

Clinical deficits including profound weakness, fatigue, poor stress tolerance, anorexia, gastrointestinal distress, hypotension, and impaired gluconeogenesis resulting in hypoglycemia.

Systemic effects of mineralocorticoid excess

Increased renal epithelial sodium channel activity leading to excessive vascular sodium and water reabsorption, expanded extracellular fluid volume, systemic hypertension, and hypokalemia.

Systemic effects of mineralocorticoid deficiency

Failure of renal distal tubule sodium reabsorption resulting in urinary sodium wasting, hypovolemia, postural hypotension, prerenal azotemia, and impaired potassium excretion (hyperkalemia).

Adrenal androgen alterations

Adrenal hormonal shifts where overproduction induces virilization, acne, and hirsutism, while deficient production in women may cause thinning of pubic/axillary hair and reduced libido.

Catecholamine hypersecretion

Excess release of epinephrine and norepinephrine from the adrenal medulla (e.g., pheochromocytoma) provoking paroxysmal hypertension, severe headaches, diaphoresis, and palpitations.

Cushing syndrome

A clinical constellation resulting from chronic supraphysiologic levels of circulating glucocorticoids, commonly due to exogenous corticosteroid therapy, adrenal adenomas, or ACTH hypersecretion.

Cushing disease

A specific form of endogenous Cushing syndrome caused by an ACTH-secreting pituitary microadenoma leading to bilateral adrenal cortical hyperplasia.

Cushingoid habitus

Characteristic body composition changes including facial rounding (moon facies), interscapular fat deposition (buffalo hump), truncal obesity, and proximal limb muscle atrophy.

Diagnostic screening tests for hypercortisolemia

First-line screening modalities including a 24-hour urinary free cortisol excretion, late-night salivary cortisol assay, or an overnight low-dose ($1\,mg$) dexamethasone suppression test.

Addison disease

Primary chronic adrenal insufficiency caused by destruction of all three zones of the adrenal cortex, commonly from autoimmune adrenalitis, leading to deficient cortisol and aldosterone.

Cutaneous hyperpigmentation in primary adrenal insufficiency

Generalized bronzing of skin folds, scars, and buccal mucosa caused by elevated pro-opiomelanocortin (POMC) transcription, producing both ACTH and melanocyte-stimulating hormone (MSH).

Primary Addison disease laboratory profile

A distinct endocrine panel demonstrating low serum cortisol, markedly high plasma ACTH, hyponatremia, hyperkalemia, elevated plasma renin, and prone to fasting hypoglycemia.

Mechanisms of hypovolemia in Addison disease

Lack of aldosterone prevents sodium conservation in the distal nephron; unabsorbed sodium is lost in urine with obligate water, depleting extracellular fluid volume.

Adrenal crisis

An acute, life-threatening decompensation of adrenal insufficiency precipitated by infection, trauma, or stress, manifesting as refractory hypotensive shock, vomiting, and severe hyperkalemia.

Central (neurogenic) diabetes insipidus

A condition characterized by insufficient synthesis or release of antidiuretic hormone ($\text{ADH}$) by the hypothalamus and posterior pituitary gland.

Clinical presentation of diabetes insipidus

A triad of profound hypotonic polyuria, intense compensatory polydipsia, and nocturia, which may rapidly advance to severe hypernatremic dehydration if access to free water is impaired.

Central DI diagnostic urinalysis

Laboratory confirmation marked by inappropriately dilute urine with low urine specific gravity ($< 1.005$) and urine osmolality below plasma osmolality despite elevated serum sodium.

SIADH (Syndrome of inappropriate antidiuretic hormone)

Non-physiological autonomous oversecretion of antidiuretic hormone leading to excessive renal free water reabsorption, dilutional hyponatremia, and extracellular volume expansion.

Common etiologies of SIADH

Diverse clinical triggers including paraneoplastic ectopic production (small-cell lung carcinoma), CNS infections or traumatic brain injury, pulmonary pathology, and SSRI or carbamazepine use.

SIADH diagnostic laboratory criteria

A metabolic state consisting of hypo-osmolal hyponatremia ($< 135\,mEq/L$) accompanied by inappropriately elevated urine osmolality and continuous urinary sodium excretion.

Cerebral edema in SIADH

The most feared complication of severe or rapid dilutional hyponatremia, wherein osmotic gradients force water into astrocytes, resulting in brain swelling, seizures, herniation, and coma.

Cardiovascular risk of Diabetes Insipidus

Severe vascular depletion and hypovolemic shock resulting from unreplaced renal water losses during profound, uninterrupted polyuria.

Memory trick: SIADH vs. DI

SIADH = 'Saving water' (concentrated urine, low serum sodium, fluid retention); DI = 'Dumping water' (dilute urine, elevated serum sodium risk, hypovolemia).

Prerenal acute kidney injury

A sudden reduction in renal clearance caused by systemic conditions that reduce renal arterial perfusion pressure without structural parenchymal damage (e.g., severe hemorrhage, dehydration, heart failure).

Intrarenal (intrinsic) acute kidney injury

Kidney failure arising from primary, direct parenchymal injury to the glomeruli, tubules, interstitium, or renal microvasculature (e.g., acute tubular necrosis, glomerulonephritis, nephrotoxic drugs).

Postrenal acute kidney injury

Acute kidney dysfunction secondary to mechanical obstruction of urinary outflow anywhere from the renal pelvis down to the urethral meatus (e.g., benign prostatic hyperplasia, bilateral calculi).

Extrarenal azotemia

A conceptual term denoting renal dysfunction driven by pathology outside the intrinsic renal parenchyma, such as systemic shock, massive fluid loss, or distal urinary tract obstruction.

Fundamental distinction: Prerenal vs. Intrinsic vs. Postrenal

Prerenal represents a hemodynamic perfusion deficit; intrinsic represents cellular tissue damage within the kidney; postrenal represents downstream outflow obstruction.

Erythropoietin deficiency in chronic kidney disease

The progressive loss of peritubular interstitial fibroblasts in diseased kidneys, halting the secretion of erythropoietin ($\text{EPO}$) and leading to defective erythropoiesis.

Morphology of anemia of CKD

Anemia characteristically exhibiting normocytic, normochromic RBC indices on peripheral blood smear, primarily driven by absolute erythropoietin deficiency.

Nephrolithiasis

The formation of macroscopic mineralized crystal concretions (calculi) within the renal calyces or pelvicalyceal system due to urinary supersaturation.

Calcium oxalate calculi

The most prevalent crystalline subtype of nephrolithiasis, primarily precipitated by low urinary volume, hypercalciuria, and hyperoxaluria.

Struvite calculi

Magnesium ammonium phosphate stones that precipitate exclusively in alkaline urine formed by urease-producing bacteria (e.g., Proteus mirabilis), frequently forming staghorn calculi.