Free Biology 30 Exam Flashcards

About -70 mV (inside negative relative to outside). Maintained by the sodium-potassium pump (3 Na+ out, 2 K+ in) plus selective K+ permeability. A polarized neuron is 'at rest' but ready to fire.

Depolarization = Na+ rushes IN through voltage-gated Na+ channels (rises toward +35 mV). Repolarization = K+ moves OUT, restoring negativity. Knowing which gate opens tells you which phase you're in.

Once threshold (~-55 mV) is reached, an action potential fires fully at a fixed size; below threshold, nothing fires. Stimulus STRENGTH is coded by firing FREQUENCY, not by larger spikes.

Myelin insulates the axon; the action potential 'jumps' between gaps called nodes of Ranvier, where Na+ channels are concentrated. Result: much faster impulse conduction than in unmyelinated axons.

Brief interval after a spike when Na+ channels are inactivated, so no new action potential can fire regardless of stimulus. This forces one-way impulse travel and limits maximum firing rate.

Receptor to sensory (afferent) neuron to interneuron in the spinal cord to motor (efferent) neuron to effector. The brain isn't required, which is why reflexes are fast and protective.

Sympathetic = 'fight-or-flight' (raises heart rate, dilates pupils, diverts blood to muscles). Parasympathetic = 'rest-and-digest' (the opposite). Both are autonomic and act antagonistically.

Cones detect colour and work in bright light (densest at the fovea). Rods are highly light-sensitive for dim-light and motion vision but give no colour. Dark adaptation shifts vision from cones to rods.

Ciliary muscles change lens SHAPE to focus on near vs. far objects (lens rounds for near). Don't confuse with refraction (light bending) or dilation (pupil-size change by the iris).

Cerebellum coordinates voluntary movement, balance, and posture. Medulla oblongata (brainstem) controls involuntary vitals: heart rate, breathing, blood pressure. Damage to the medulla is often fatal.

Endocrine glands are DUCTLESS and secrete hormones directly into the bloodstream to reach distant target cells. Exocrine glands (sweat, salivary) release secretions through DUCTS to a surface or cavity.

Steroid hormones (e.g., estrogen) are lipid-soluble, pass through the membrane, and bind intracellular receptors, often altering gene transcription. Protein hormones (e.g., insulin) bind SURFACE receptors and act via second messengers.

Insulin (beta cells) LOWERS blood glucose: promotes cell uptake and glycogen storage. Glucagon (alpha cells) RAISES blood glucose: triggers liver glycogen breakdown. Antagonistic pair from the pancreatic islets.

A deviation triggers a response that REVERSES it back to a set point (e.g., high glucose to insulin to lower glucose). Contrast positive feedback, which AMPLIFIES a change (e.g., childbirth, LH surge).

When dehydrated, ADH rises, making kidney collecting ducts more permeable so MORE water is reabsorbed into blood and less is lost in urine. This conserves body water and restores blood volume.

Thyroxine (T4) sets metabolic rate and REQUIRES iodine; deficiency causes goitre. High thyroxine inhibits TSH (pituitary) and TRH (hypothalamus) by negative feedback to keep levels in range.

Adrenaline (epinephrine), from the adrenal MEDULLA, drives the rapid SHORT-term stress response (heart rate up, airways open). Cortisol, from the adrenal CORTEX, handles LONG-term stress and raises blood glucose.

Sperm are PRODUCED in the seminiferous tubules of the testes (spermatogenesis), then MATURE and are stored in the epididymis before traveling through the vas deferens. Don't confuse production with storage.

FSH stimulates Sertoli cells to support sperm production. LH stimulates interstitial (Leydig) cells to make testosterone. Both come from the anterior pituitary under hypothalamic GnRH.

In the oviduct (Fallopian tube), not the ovary or uterus. The ovary RELEASES the egg; the uterus is where the resulting zygote later IMPLANTS and develops.

A sharp surge in LH (around day 14) directly triggers ovulation, releasing the secondary oocyte. That LH surge is itself caused by rising estrogen, so estrogen triggers indirectly, LH directly.

After ovulation the ruptured follicle becomes the corpus luteum, secreting progesterone to MAINTAIN the endometrium. If no fertilization, it degenerates, progesterone drops, and menstruation follows.

Human chorionic gonadotropin, from the embryo/placenta, MAINTAINS the corpus luteum so progesterone keeps supporting early pregnancy. Its presence in urine is what home pregnancy tests detect.

Spermatogenesis: one diploid cell to FOUR functional haploid sperm. Oogenesis: one functional egg PLUS polar bodies that disintegrate. The unequal split concentrates cytoplasm/nutrients in the single egg.

Rapid mitotic divisions of the zygote with NO overall growth, producing many smaller cells (forming the morula). Comes before gastrulation (germ layers) and implantation of the blastocyst.

Ectoderm to nervous system + skin epidermis. Mesoderm to muscle, bone, blood/circulatory, kidneys. Endoderm to digestive and respiratory linings. Gastrulation creates these layers.

Exchanges nutrients, O2, CO2, and wastes between maternal and fetal blood WITHOUT the two bloodstreams mixing. It also secretes progesterone and estrogen to maintain pregnancy.

Enzyme-filled cap on the sperm head; releases enzymes that DIGEST through the egg's protective layers (e.g., zona pellucida) at fertilization. Energy comes from midpiece mitochondria, not the acrosome.

Mitosis: 2 identical diploid daughter cells (growth/repair). Meiosis: 4 genetically varied haploid gametes (chromosome number halved, e.g., 46 to 23 in humans). Fertilization restores the diploid number.

Sister chromatids split at the centromere and move to opposite poles as spindle fibres shorten, ensuring each daughter cell gets a complete, identical chromosome set.

(1) Crossing over in prophase I (homologues swap segments). (2) Independent assortment in metaphase I (random orientation of homologous pairs). Both reshuffle alleles into unique gametes.

Failure of chromosomes/chromatids to separate in meiosis produces gametes with extra or missing chromosomes. An extra chromosome 21 (trisomy) causes Down syndrome. Monosomy = one missing copy.

Genotype ratio 1 AA : 2 Aa : 1 aa. Phenotype ratio 3 dominant : 1 recessive (complete dominance). The 1:2:1 genotypes underlie the 3:1 phenotypes, a classic numerical-response setup.

Independent assortment gives a 9:3:3:1 phenotypic ratio. A dihybrid TESTCROSS (RrYy x rryy) instead gives 1:1:1:1. Recognizing which ratio appears tells you the parents' genotypes.

Incomplete dominance: heterozygote is a BLEND (red x white to pink snapdragons). Codominance: BOTH alleles fully and separately expressed (I^A I^B to type AB blood). Blend vs. both-shown is the distinction.

Appears in every generation, affects sexes equally, and affected children always have an affected parent. Autosomal RECESSIVE instead skips generations and can appear from two unaffected parents.

Sons get their single X from mom, so a carrier mother (X^H X^h) gives 50% of SONS the disorder (e.g., hemophilia, colour blindness). Affected males more common; trait can skip generations through carrier females.

Genes close together on the SAME chromosome are linked and tend to be inherited together, distorting expected ratios. Genes on different chromosomes (or far apart) assort independently.

A-T (2 H-bonds), C-G (3 H-bonds). Replication is semiconservative: each new double helix keeps ONE original strand as a template plus one new strand. Helicase unwinds; DNA polymerase builds.

Transcription (nucleus): DNA template to mRNA via RNA polymerase. Translation (ribosome): mRNA codons read by tRNA anticodons to assemble a polypeptide. A codon = 3 mRNA bases coding one amino acid.

Missense = base change gives a DIFFERENT amino acid (e.g., sickle cell). Silent = same amino acid despite the change. Frameshift = insertion/deletion shifts the whole reading frame, usually most damaging.

Restriction enzymes CUT DNA at specific recognition sequences; DNA ligase JOINS fragments. Gel electrophoresis separates fragments by SIZE (smaller fragments travel farther toward the + electrode).

p + q = 1 (alleles); p^2 + 2pq + q^2 = 1 (genotypes: dominant homozygote, heterozygote, recessive homozygote). Equilibrium needs: no mutation, random mating, no gene flow, very large population, no selection.

Exponential = J-shaped curve, unlimited resources, maximum rate. Logistic = S-shaped curve that levels off at carrying capacity (K) as limiting factors slow growth. The curve shape tells you which model applies.

Genetic drift = random allele-frequency change, strongest in SMALL populations. Founder effect = small group starts a new population. Bottleneck = sudden crash shrinks an existing one. Both reduce diversity by chance.

Resistance alleles already exist by random mutation. Antibiotics kill susceptible bacteria; resistant ones survive and reproduce, raising the resistance frequency. Bacteria do NOT mutate on demand, and the drug doesn't create the gene.

Primary succession starts where NO soil exists (bare rock); pioneer species like lichens build soil. Secondary succession starts where soil REMAINS (after fire or abandoned farmland), so it proceeds faster.

A geographic barrier splits a population, blocks gene flow, and the isolated groups diverge into separate species. Contrast sympatric speciation, which occurs WITHOUT physical separation, within one area.

60 machine-scored questions (48 multiple-choice + 12 numerical-response, equal value). The diploma is worth 30% of the final course mark; the school-awarded mark is the other 70%.

Designed for 3 hours (up to 6 allowed), closed-book, English only. Acceptable standard 50%, standard of excellence 80%. An approved calculator is permitted, useful for Hardy-Weinberg and genetics numerical-response items.