Physiology, immunity, ecology and evolution
Organismal Structure and Function (Anatomy and Physiology)
Physiology
Items test how organ systems maintain internal stability, how exchange surfaces are built, and how structure at each level serves function.
Homeostasis and control
Negative feedback reverses a deviation: a sensor detects change, an integrating center compares it with a set point, and an effector counters it (insulin lowers glucose; sweating lowers temperature). Positive feedback amplifies a change and must terminate (oxytocin in labor, clotting cascade). Levels of organization run from cells to tissues (epithelial, connective, muscle, nervous) to organs to systems.
Systems
- Circulation: mammals have a four-chambered heart and double circulation; arteries carry blood away from the heart, and pulmonary arteries carry deoxygenated blood.
- Gas exchange: alveoli and gill lamellae maximize surface area and minimize diffusion distance; countercurrent flow in fish gills maintains a gradient along the whole lamella.
- Digestion: enzymes act at specific pH (pepsin acid; pancreatic amylase and lipase alkaline); villi and microvilli increase absorptive area.
- Excretion: the nephron filters at the glomerulus, reabsorbs glucose, water, and ions, and secretes wastes; the loop of Henle builds a concentration gradient.
- Nervous and endocrine: fast neuronal action potentials involve sodium and potassium channel currents; the sodium-potassium pump maintains gradients over time rather than directly causing rapid repolarization; hormones act on target cells bearing receptors.
- Plants: xylem moves water and minerals upward under transpiration pull (cohesion–tension); phloem translocates sugars by pressure flow; guard cells open stomata when turgid.
Worked example
After a carbohydrate-rich meal, blood glucose rises. Pancreatic beta cells detect it and secrete insulin; insulin promotes glucose uptake in responsive muscle and adipose tissue, promotes glycogen storage and suppresses hepatic glucose production, so glucose falls toward the set point. When glucose drops below the set point, alpha cells release glucagon, triggering glycogen breakdown and gluconeogenesis in the liver. Both arms are negative feedback: the response opposes the original deviation. In diabetes mellitus, insulin secretion and/or action is impaired and hyperglycemia can result; this model is not a clinical diagnosis.
Traps
Labeling a loop positive because the outcome is "good"; forgetting that pulmonary arteries carry deoxygenated blood; confusing xylem and phloem direction; assuming diffusion suffices in large animals; mixing the roles of the loop of Henle and the collecting duct; assuming all hormones are lipid-soluble.
Microbiología, inmunología y biotecnología: virus, bacterias, respuesta inmunitaria, aplicaciones biotecnológicas
Esta revisión relaciona estructura microbiana, defensa inmunitaria y métodos de análisis de ADN. Se interpretan modelos celulares y datos suministrados; no se ofrecen diagnósticos, dosis, decisiones de tratamiento ni normas sanitarias extranjeras.
Virus y bacterias
Los virus son entidades acelulares con genoma de ADN o ARN, cápside y, en algunos casos, envuelta. Los ciclos lítico y lisogénico describen determinados bacteriófagos, no todos los virus. Los retrovirus utilizan transcripción inversa y pueden integrar ADN viral. Muchas bacterias poseen pared de peptidoglicano, pero existen bacterias sin pared; plásmidos, flagelos y endosporas no son universales. La estructura de una bacteria concreta debe leerse en los datos. Conjugación, transformación y transducción son mecanismos distintos de transferencia genética horizontal.
Inmunidad
Innata: barreras, pH, complemento, fagocitos, células NK e inflamación; reconoce patrones mediante receptores y no utiliza la memoria clonal clásica de linfocitos B y T; la inmunidad entrenada evita reducirla a una ausencia absoluta de memoria. Adaptativa: linfocitos B → células plasmáticas → anticuerpos (IgG, IgM, IgA, IgE, IgD); los linfocitos T auxiliares CD4 reconocen antígeno en MHC II y activan a B y a CD8; los T citotóxicos CD8 destruyen células infectadas presentadas por MHC I. Selección clonal, memoria y respuesta secundaria más rápida y con mayor título, sobre todo de IgG.
Biotecnología
Las enzimas de restricción reconocen secuencias determinadas y pueden producir extremos cohesivos o romos; no todas las enzimas reconocen el mismo tipo de secuencia. Las ligasas unen enlaces del esqueleto del ADN. Los vectores permiten estudiar secuencias introducidas en sistemas adecuados. PCR, electroforesis y secuenciación responden preguntas diferentes: amplificación de una región, comparación de fragmentos y orden de bases. En una comparación convencional de ADN lineal en el mismo gel, los fragmentos pequeños suelen migrar más lejos; la conformación y el sistema importan. Una banda no demuestra por sí sola identidad de secuencia ni expresión funcional. La ingeniería genética requiere comprobar tanto el cambio previsto como su efecto en el modelo estudiado.
Ejemplo resuelto
Partimos de una sola molécula de ADN y aplicamos PCR. En el modelo ideal de duplicación perfecta, tras 5 ciclos el número sería 2^5 = 32 y tras 20 ciclos aproximadamente 1,05 millones. El razonamiento es multiplicativo porque cada ciclo duplica cada molécula, hasta que la fase exponencial se satura al agotarse cebadores o dNTP. Si la muestra inicial tuviera 10 moléculas, tras 5 ciclos habría 320 copias.
Errores que cuestan puntos
Afirmar que los antibióticos matan virus, olvidar que los virus solo se replican dentro de una célula, tratar IgM e IgG como un diagnóstico binario de fase: una respuesta secundaria sistémica suele mostrar aumento de anticuerpos de alta afinidad, pero el isotipo depende del contexto y creer que los linfocitos T producen anticuerpos.
Ecology and Environmental Science
Ecology
This domain tests population dynamics, species interactions, energy and nutrient flow, succession, and human effects on ecosystems.
Populations and communities
- Exponential growth (r) is unlimited; logistic growth adds carrying capacity K, producing an S-curve with density-dependent limits (food, disease, space). Density-independent factors include weather and fire.
- Survivorship curves: Type I (late loss, humans), Type II (constant, birds), Type III (early loss, many fish and plants).
- Interactions: competition (competitive exclusion; resource partitioning allows coexistence), predation (including keystone effects), mutualism (+/+), commensalism (+/0), parasitism (+/−).
- Age structure informs growth potential: a broad base can indicate many future reproductive individuals, but survival, fertility and migration determine actual change.
Ecosystems
Energy flows one way and is lost as heat; a simplified example may assume 10 percent transfer, but actual efficiencies and food-web lengths vary. Gross primary productivity minus respiration equals net primary productivity. Biogeochemical cycles: carbon (photosynthesis, respiration, combustion, dissolution), nitrogen (fixation, nitrification, assimilation, denitrification - atmospheric N₂ is unusable to most organisms), phosphorus (mainly sedimentary, without a major atmospheric reservoir in the standard school model, and sometimes limiting). Primary succession begins on bare substrate (lichens, mosses); secondary succession follows disturbance with soil intact.
Worked example
A lake is sampled by mark–recapture: 50 fish are captured, marked, released, and mixed. A second sample of 120 contains 15 marked fish. Estimated population N = (marked in first sample × total in second sample) ÷ marked in second sample = (50 × 120) ÷ 15 = 400. The estimate assumes a closed population, no mark loss or mortality, thorough mixing, and equal catchability; if marked fish become trap-shy, the estimate is biased upward.
Traps
Confusing exponential with logistic growth; calling a density-dependent factor density-independent; reversing the 10% rule (energy is lost, not gained); assuming nitrogen gas is directly usable; mixing up primary and secondary succession; forgetting that habitat loss and invasive species, not pollution alone, are leading causes of biodiversity decline; treating a population estimate as a census.
Evolutionary Biology and Diversity of Life
Evolution
Items test the mechanisms that change allele frequencies, the evidence for common descent, speciation, and how organisms are classified and related.
Mechanisms of evolution
- Natural selection acts on heritable phenotypic variation that affects fitness; it is not goal-directed and does not create new variation.
- Mutation is the ultimate source of new alleles. Gene flow and genetic drift (bottleneck, founder effect) also change frequencies; drift is strongest in small populations and is random with respect to fitness.
- Directional, stabilizing, and disruptive selection shift, narrow, or split a trait distribution.
- Hardy–Weinberg equilibrium (p² + 2pq + q² = 1) holds only with no mutation, no migration, random mating, infinite population size, and no selection - a null model, not a description of most real populations.
- Speciation: allopatric speciation can follow geographic isolation; sympatric speciation can occur via polyploidy or habitat/behavioral divergence. Prezygotic barriers (temporal, habitat, behavioral, mechanical, gametic) prevent fertilization; postzygotic barriers (hybrid inviability, hybrid sterility) act afterward.
Evidence and classification
Homologous structures share ancestry (forelimb bones); analogous structures share function only (bird and insect wings) and indicate convergence. Fossils, biogeography, embryology, and molecular sequence comparisons support common descent. Cladistics groups organisms by shared derived characters (synapomorphies); monophyletic groups contain an ancestor and all its descendants. A common three-domain teaching model distinguishes Bacteria, Archaea and Eukarya; mitochondria and chloroplasts descend from endosymbiotic bacteria.
Worked example
In a supplied two-allele autosomal model with complete recessivity and penetrance, 16% show the recessive phenotype. Assuming Hardy-Weinberg equilibrium, aa = q² = 0.16, so q = 0.4 and p = 1 − 0.4 = 0.6. Heterozygote frequency is 2pq = 2(0.6)(0.4) = 0.48, and homozygous dominants are p² = 0.36; the three sum to 1.00. Note the reasoning step: the recessive phenotype frequency equals q² only when the trait is recessive and the population is in equilibrium.
Traps
Equating dominant with frequent; assuming a population at Hardy–Weinberg is evolving; confusing allele frequency with genotype frequency; calling drift "selection"; treating analogous structures as evidence of close relatedness; applying reproductive isolation as a universal species definition even to asexual organisms, rather than recognizing the limits of the biological species concept; using a phenotype frequency as q without squaring it.