OMSB Physician Exam key terms

A spectrum of myocardial ischemia from unstable angina through non-ST-elevation and ST-elevation myocardial infarction, usually caused by plaque rupture with thrombus. Diagnosis rests on symptoms, serial troponin, and ECG changes requiring urgent reperfusion or antithrombotic therapy.

Convex ST elevation in contiguous leads meeting voltage criteria, indicating transmural injury and usually an occluded epicardial artery. It triggers emergency reperfusion by primary percutaneous coronary intervention or fibrinolysis within guideline time windows.

Cardiac-specific contractile protein released into blood after myocyte necrosis. High-sensitivity assays detect small elevations; serial measurement showing a rise or fall distinguishes acute infarction from chronic elevation in renal failure or stable structural disease.

A clinical syndrome of congestion or low output with left ventricular ejection fraction of 40 percent or less. Guideline-directed therapy combines renin-angiotensin system inhibition, beta blockade, mineralocorticoid antagonism, and SGLT2 inhibition to reduce mortality.

Disorganized atrial electrical activity producing an irregularly irregular ventricular rhythm without discrete P waves. Management addresses stroke risk scoring, anticoagulation, rate or rhythm control, and correction of reversible triggers such as thyrotoxicosis or sepsis.

Anesthetic induction technique that minimizes aspiration risk by preoxygenation, prompt loss of consciousness, and immediate intubation without interposed positive-pressure ventilation, typically with a neuromuscular blocker such as succinylcholine or rocuronium.

A structured sequence of escalating rescue steps when ventilation or intubation fails, including repositioning, supraglottic rescue devices, and finally surgical cricothyrotomy. Early recognition and declaration of failure prevent hypoxic brain injury.

An autosomal dominant pharmacogenetic reaction to volatile anesthetics or succinylcholine causing uncontrolled muscle hypermetabolism, hypercarbia, rigidity, and hyperthermia. Immediate dantrolene, cooling, and supportive care are life-saving.

A model of enzyme velocity that rises hyperbolically with substrate concentration toward a maximum, described by Km and Vmax. Km equals the substrate concentration at half-maximal velocity and inversely reflects enzyme affinity.

A reversible inhibitor binds the enzyme active site, competing with substrate. It raises apparent Km without changing Vmax, and inhibition is overcome by increasing substrate concentration.

A protein catalyst that lowers activation energy and accelerates biochemical reactions without being consumed. Activity depends on pH, temperature, cofactors, and post-translational regulation, and enzymes are common targets of drugs and poisons.

A multifactorial, biofilm-mediated destruction of tooth mineral driven by fermentable carbohydrate and acid production. Prevention targets plaque control, fluoride, dietary sugar reduction, and sealants; treatment ranges from remineralization to restoration or extraction.

Inflammatory destruction of tooth-supporting tissues initiated by subgingival biofilm, causing attachment loss, pocket formation, and alveolar bone resorption. It is a major cause of tooth loss and is associated with diabetes and smoking.

Inflammation of the dental pulp, usually from caries or trauma, presenting as toothache that may be reversible or irreversible. Irreversible pulpitis requires root canal treatment or extraction; abscess formation warrants urgent drainage.

A chronic immune-mediated disorder with well-demarcated erythematous plaques bearing silvery scale, typically on extensor surfaces and scalp, with nail pitting and arthritis in some patients. Treatment escalates from topical agents to phototherapy and biologics.

An eczematous eruption caused by irritant exposure or type IV delayed hypersensitivity to an allergen. Distribution follows contact patterns, and patch testing identifies the responsible allergen; management avoids the trigger and uses topical corticosteroids.

A malignant neoplasm of melanocytes with asymmetry, irregular border, color variation, and diameter over six millimeters as warning features. Breslow thickness and ulceration guide staging; early excision offers the best prognosis.

The most common skin cancer, arising from basal keratinocytes and typically appearing as a pearly papule with telangiectasia or an ulcerated lesion on sun-exposed skin. It rarely metastasizes but causes local destruction if untreated.

Life-threatening organ dysfunction from dysregulated host response to infection with persistent hypotension requiring vasopressors despite fluid resuscitation and elevated lactate. Early antibiotics, source control, and balanced fluids are priorities.

A severe systemic hypersensitivity reaction with rapidly developing airway, breathing, or circulatory compromise, often with skin and gastrointestinal features. Intramuscular epinephrine is first-line and must not be delayed for antihistamines or steroids.

Systematic testing of average-risk adults to detect adenomas and early cancer, using stool-based tests such as fecal immunochemical testing or structural examinations such as colonoscopy. Screening reduces mortality and begins around age 45 to 50 depending on local guidance.

A microcytic hypochromic anemia from inadequate iron stores, most often from blood loss, with low ferritin and elevated total iron-binding capacity. Identifying the source, especially gastrointestinal bleeding, is essential in adults.

Acute inflammation of the vermiform appendix, typically causing periumbilical pain migrating to the right lower quadrant with fever and leukocytosis. Early appendectomy or antibiotics prevents perforation and peritonitis.

Mechanical or functional impairment of intestinal transit causing colicky pain, vomiting, distension, and cessation of flatus. Small bowel obstruction commonly follows adhesions; management includes decompression, fluids, and surgery for strangulation.

A macrocytic anemia from inadequate cobalamin, causing megaloblastic marrow and neurological deficits such as paresthesia and subacute combined degeneration. Causes include pernicious anemia, ileal disease, and metformin; treatment replaces cobalamin.

A consumptive coagulopathy triggered by sepsis, trauma, or malignancy, causing microvascular thrombosis with depletion of platelets and clotting factors. Labs show prolonged prothrombin time, low fibrinogen, and elevated D-dimer; treatment targets the underlying cause.

A compact aggregate of activated macrophages, often with multinucleated giant cells, formed in response to persistent antigens such as mycobacteria or foreign material. Histologic pattern narrows the differential but rarely identifies the organism alone.

A form of necrosis with a cheese-like macroscopic appearance and amorphous eosinophilic debris microscopically, classically seen in tuberculosis and some fungal infections. It contrasts with coagulative and liquefactive necrosis in ischemic and pyogenic injury.

Reversible replacement of one mature cell type by another better adapted to stress, such as squamous change in smoker airways. It is not cancer but may predispose to dysplasia and malignancy.

A hyperglycemic emergency with ketosis and high anion gap metabolic acidosis, typically in type 1 diabetes with infection or insulin omission. Treatment requires fluids, insulin infusion, potassium replacement, and treatment of the precipitant.

Elevated serum potassium that destabilizes cardiac membranes, causing peaked T waves, widened QRS, and arrhythmia. Emergency treatment uses intravenous calcium, insulin with glucose, and beta agonists, then removes potassium from the body.

An abrupt decline in glomerular filtration with rising creatinine or reduced urine output, classified as prerenal, intrinsic, or postrenal. Management corrects hypovolemia, stops nephrotoxins, relieves obstruction, and treats complications.

A gram-positive coccus resistant to beta-lactam antibiotics through altered penicillin-binding protein. It causes skin, wound, bloodstream, and device infections; treatment uses vancomycin or other agents guided by susceptibility testing.

Life-threatening organ dysfunction resulting from a dysregulated host response to infection, identified by clinical deterioration and elevated lactate. Prompt cultures, broad-spectrum antibiotics, fluids, and source control improve survival.

A chronic infection by Mycobacterium tuberculosis, typically affecting lungs with cough, fever, night sweats, and weight loss. Diagnosis uses sputum microscopy, culture, and nucleic acid testing; treatment requires multidrug regimens to prevent resistance.

Coordinated efforts to optimize antibiotic selection, dose, and duration to improve outcomes while limiting resistance and adverse effects. Core strategies include de-escalation based on culture results and avoiding unnecessary broad-spectrum therapy.