Palestinian Board Part I key terms

The proportion of people who truly have a disease and are correctly identified by a test as positive. It measures a test's ability to detect disease when present and is calculated as true positives divided by all diseased individuals.

The proportion of people without a disease who are correctly identified by a test as negative. It reflects how well a test rules out disease in healthy people and equals true negatives divided by all non-diseased individuals.

The probability that a person with a positive test result actually has the disease. Unlike sensitivity, it depends strongly on disease prevalence in the tested population and equals true positives divided by all positive results.

The proportion of a population that has a particular condition at a given point in time or during a specified period. It describes disease burden and directly influences predictive values of diagnostic tests.

The number of new cases of a disease arising in a defined population over a specified period, expressed as a rate or cumulative risk. It measures how quickly new disease develops and is used to study causation.

The ratio of disease incidence in an exposed group to incidence in an unexposed group. A value above one suggests exposure increases risk; it is the main effect measure in cohort studies and clinical trials.

The ratio of the odds of exposure among cases to the odds of exposure among controls. It approximates relative risk when disease is rare and is the standard effect measure in case-control studies.

Distortion of the true exposure-outcome relationship by a third variable that is associated with both the exposure and the outcome but is not on the causal pathway. It must be controlled by design or analysis.

A systematic error arising when the groups compared differ in ways related to both exposure and outcome because of how participants were chosen or retained. It threatens validity and cannot be fixed by statistical adjustment alone.

Allocating participants to treatment groups by chance so that known and unknown prognostic factors are distributed similarly between groups. It protects against confounding and supports causal interpretation of trial results.

Analyzing trial participants according to the group to which they were originally randomized, regardless of whether they completed or adhered to treatment. It preserves randomization benefits and gives a realistic estimate of effectiveness.

An observational design that follows a group of people over time, classifying them by exposure status and comparing subsequent disease occurrence. It can estimate incidence and relative risk but is inefficient for rare outcomes.

An observational design that selects people with a disease (cases) and comparable people without it (controls), then looks back at past exposures. It is efficient for rare diseases but yields odds ratios and is prone to recall bias.

A test applied to apparently healthy people to detect unrecognized disease early, when treatment may be more effective. It requires high sensitivity and a suitable confirmatory test, and the condition must have an accepted treatment.

Apparent improvement in survival after screening caused merely by earlier diagnosis rather than by delayed death. It makes screened patients seem to live longer even when the disease course is unchanged, so mortality is a better endpoint.

A membrane protein that opens in response to depolarization, allowing sodium ions to enter cells and generating the rapid upstroke of the action potential. It is the target of local anesthetics and some antiarrhythmic drugs.

A rapid, all-or-none change in membrane potential produced by sequential opening of ion channels, used for signaling in neurons and muscle. Its phases include depolarization, repolarization, and sometimes a hyperpolarized afterpotential.

The interval after an action potential during which a neuron or muscle fiber cannot fire another impulse, or needs a stronger stimulus. It limits maximum firing frequency and prevents backward conduction of impulses.

The volume of plasma filtered by the kidneys per unit time, normally about 125 mL per minute. It is estimated clinically from creatinine and is the key marker of kidney function and drug dosing.

The volume of plasma cleared of creatinine per minute, calculated from serum creatinine and urine creatinine excretion or estimated by formulas. It approximates glomerular filtration rate and guides renal drug dosing.

Increased urine output caused by non-reabsorbable solutes in the tubular fluid that hold water osmotically. It occurs in uncontrolled diabetes mellitus and after mannitol administration, and can cause volume depletion.

The physiological principle that increased ventricular filling (preload) stretches cardiac muscle and increases stroke volume within physiological limits. It explains how the heart matches output to venous return and why fluid loading can raise blood pressure.

The degree of ventricular stretch at the end of diastole, reflecting the volume of blood in the ventricle before contraction. It is a major determinant of stroke volume and is manipulated clinically with fluids and diuretics.

The volume of blood ejected by one ventricle per heartbeat, typically about 70 mL in adults. It depends on preload, afterload, and contractility and, multiplied by heart rate, gives cardiac output.

The volume of blood pumped by the heart per minute, equal to stroke volume multiplied by heart rate. It is a central determinant of tissue oxygen delivery and falls in shock states.

The average arterial pressure throughout the cardiac cycle, approximated as diastolic pressure plus one-third of the pulse pressure. It represents the perfusion pressure driving blood through organs and is a key resuscitation target.

Life-threatening organ dysfunction caused by a dysregulated host response to infection. It is identified clinically by a rise in the sequential organ failure score and requires prompt antibiotics, fluids, and source control.

Sepsis with persisting hypotension requiring vasopressors to maintain mean arterial pressure and with elevated serum lactate despite adequate fluid resuscitation. It carries high mortality and is managed with fluids, vasopressors, and antibiotics.

A product of anaerobic glucose metabolism that rises when tissue oxygen delivery is inadequate or when stress hormones increase glycolysis. An elevated level signals hypoperfusion and is used to guide resuscitation and risk assessment.

Acute hypoxemic respiratory failure with bilateral lung infiltrates and reduced lung compliance not fully explained by cardiac failure. It reflects inflammatory alveolar-capillary injury and is managed with lung-protective ventilation and treatment of the cause.

Use of a machine to support or replace spontaneous breathing by delivering gas to the lungs through an endotracheal tube or mask. Settings are chosen to protect the lungs and maintain adequate oxygenation and carbon dioxide clearance.

A ventilator setting that maintains positive airway pressure at the end of expiration, preventing alveolar collapse and improving oxygenation. It is central to managing acute respiratory distress syndrome but can reduce venous return.

A drug that reversibly blocks voltage-gated sodium channels in nerve membranes, preventing impulse conduction and producing loss of sensation. Examples include lidocaine and bupivacaine; systemic toxicity can cause seizures and arrhythmias.

Elimination of a drug during its passage through the gut wall and liver before it reaches the systemic circulation after oral dosing. It reduces oral bioavailability and explains why some drugs require higher oral than intravenous doses.

The fraction of an administered drug dose that reaches the systemic circulation unchanged. Intravenous dosing is by definition complete, while oral bioavailability is reduced by incomplete absorption and first-pass metabolism.

A theoretical volume relating the amount of drug in the body to its plasma concentration. A large value indicates extensive tissue uptake, while a small value suggests confinement to plasma, and it guides loading-dose calculation.

The time required for the plasma concentration of a drug to fall by half during elimination. It determines dosing interval and the time to reach steady state, which is about four to five half-lives.

Programmed cell death in which cells shrink, fragment, and are cleared without inflammation, controlled by caspases and mitochondrial signals. It is distinct from necrosis and is important in development and cancer biology.

Pathological cell death caused by injury, characterized by swelling, membrane rupture, and inflammation. Its patterns include coagulative, liquefactive, caseous, and fat necrosis, each suggesting particular causes.

Reversible replacement of one mature cell type by another, often as an adaptation to chronic irritation, such as squamous change in smoker airways. It is not cancer but may create a substrate for malignant transformation.

Criteria linking a microorganism to a disease: it must be found in all cases, be isolated and cultured, cause disease when inoculated into a host, and be recovered again. They remain a foundation of medical microbiology.

A patient's voluntary agreement to a medical intervention after receiving adequate information about its nature, risks, benefits, and alternatives, and after demonstrating capacity to decide. It protects autonomy and is a legal and ethical requirement.

A patient's ability to understand relevant information, appreciate the consequences of a decision, reason about options, and communicate a choice. It is decision-specific and assessed clinically rather than assumed from a diagnosis.

The ethical and legal duty to protect patient information from unauthorized disclosure. It may be overridden only in defined situations such as serious risk to others or legal obligation, ideally after informing the patient.