This part of PHS 220 looks like three unrelated subjects (the nervous system, the special senses and the kidney) but they share one theme: every one of them is about moving charged particles across a membrane to create and control a signal. A neuron fires because sodium and potassium move; a photoreceptor and a hair cell respond because ion channels open and close; and the kidney works because sodium reabsorption drags water and solutes with it. Hold that idea and the whole block reads as variations on membrane transport rather than three separate mountains of detail. This page is a student-written study companion for the nervous system, special senses and renal blocks of PHS 220 Physiology, part of the compulsory second-semester course for ABUAD 200 Level Pharmacy students.
This guide brings the three blocks together in one place: how the nervous system is organised, neurons and the action potential, synapses and the brain and spinal cord, the autonomic nervous system, then vision, hearing, balance, smell and taste, and finally the kidney and nephron and how urine is formed and concentrated. The summaries below turn the syllabus into plain-English notes, with original practice questions and worked answers so you can check that each idea has stuck, and callout boxes for the high-yield mechanisms and clinical correlates examiners like to test. The full illustrated workbook, with every comparison table and labelled diagram, sits in the reader at the end of this page as a free bonus to the notes here.
- Course: PHS 220 – Physiology (Nervous, Special Senses & Renal blocks)
- College / Department: College of Medicine and Health Sciences – Department of Physiology
- Level / Semester: 200 Level, Second Semester
- Topics covered: Organisation of the nervous system, neurons, glia and the action potential, synapses, the brain and spinal cord, the autonomic nervous system and reflexes, vision, hearing, balance, smell and taste, renal anatomy and the nephron, and urine formation, concentration and clinical correlates
- Best for: Continuous assessment + second-semester exam revision
Topics Covered in the PHS 220 Nervous System, Senses & Renal Blocks
1. Organisation of the Nervous System
The nervous system is the body's fast communication network, and it is organised in two ways at once. Structurally it splits into the central nervous system (the brain and spinal cord, where integration and decision-making happen) and the peripheral nervous system (the cranial and spinal nerves that carry signals in and out). Functionally it splits by job: the somatic system handles voluntary movement and conscious sensation, the autonomic system runs the involuntary control of viscera, glands and smooth and cardiac muscle, and the enteric system acts as a semi-independent "brain in the gut" for digestion. A second organising axis is direction: afferent (sensory) fibres carry signals towards the CNS, while efferent (motor) fibres carry them out.
One structural detail is worth fixing early because it recurs throughout the block: somatic motor pathways run directly from the CNS to skeletal muscle in a single neuron, whereas autonomic pathways use a two-neuron chain, a preganglionic neuron that synapses in a ganglion onto a postganglionic neuron that reaches the target. Exam tip: keep the structural split (CNS versus PNS) separate from the functional split (somatic versus autonomic versus enteric), because a question can ask you to place the same nerve on both axes, and mixing the two classifications is a common error.
2. Neurons, Glia and the Action Potential
A neuron is built for signalling: dendrites receive and summate inputs as graded potentials, the cell body integrates them, the axon hillock is where an action potential is triggered because it has the highest density of voltage-gated sodium channels, and the axon carries the impulse to terminals that release neurotransmitter. Neurons are supported by glia, and each glial type has a clear job: astrocytes form the blood-brain barrier endfeet and mop up potassium and glutamate, oligodendrocytes myelinate CNS axons (and are the cells destroyed in multiple sclerosis), Schwann cells myelinate PNS axons and guide regeneration, microglia are the resident immune cells, and ependymal cells make and circulate cerebrospinal fluid. The blood-brain barrier itself, built from tight junctions reinforced by astrocytes, lets oxygen, carbon dioxide and lipid-soluble drugs through freely but forces glucose and amino acids to use transporters and keeps most large drugs out.
The action potential is the block's central mechanism. At rest the membrane sits near -70 mV, set mainly by potassium leaking out, with the sodium-potassium pump maintaining the gradients. When a stimulus reaches threshold (about -55 mV), voltage-gated sodium channels snap open and sodium rushes in to depolarise the cell towards +30 mV; those channels then inactivate while potassium channels open to repolarise it, briefly overshooting into after-hyperpolarisation. The inactivation of sodium channels creates the absolute refractory period, which forces the impulse to travel one way and caps the firing rate. In myelinated axons the impulse leaps from node to node (saltatory conduction), which is faster and more efficient. Exam tip: learn the action potential as a sequence of channel states, not just a graph, because questions about local anaesthetics (which block sodium channels) or refractory periods are really questions about which channels are open, closed or inactivated at each moment.
3. Synapses, the Brain and the Spinal Cord
At a chemical synapse the arriving action potential opens voltage-gated calcium channels, and calcium is the trigger that makes vesicles fuse (via SNARE proteins) and release neurotransmitter across the cleft. The transmitter binds receptors that are either ionotropic (fast, directly opening a channel) or metabotropic (slower, through a GPCR cascade), and is then cleared by reuptake, enzymes or diffusion. The main transmitters are worth knowing with one association each: glutamate is the major excitatory transmitter and is central to memory, GABA is the major inhibitory one and the site benzodiazepines act on, acetylcholine works at the neuromuscular junction and in memory circuits, dopamine handles reward and movement (and is depleted in Parkinson disease), serotonin governs mood and sleep, and noradrenaline drives alertness.
The brain is organised by region: the cerebrum for cognition, movement and sensation; the diencephalon (thalamus and hypothalamus) for relay and homeostasis; the brainstem for cranial nerves and vital centres; and the cerebellum for coordination. In the cortex, a handful of areas are high-yield because their lesions give named deficits: the primary motor and sensory strips are contralateral, Broca's area produces speech (its loss gives non-fluent aphasia) while Wernicke's area comprehends it (its loss gives fluent but meaningless speech). The basal ganglia refine movement through a direct pathway that facilitates it and an indirect pathway that suppresses it, and losing nigral dopamine tips this balance to cause Parkinson disease. In the spinal cord, three tracts are essential: the dorsal columns (fine touch and proprioception, crossing in the medulla), the spinothalamic tract (pain and temperature, crossing in the cord), and the corticospinal tract (voluntary movement, crossing in the medulla). Exam tip: memorise where each of the three tracts crosses, because that single fact explains Brown-Sequard syndrome, where a cord hemisection loses motor power and fine touch on the same side but pain and temperature on the opposite side.
4. Autonomic Nervous System and Reflexes
The autonomic nervous system runs the involuntary body through two opposing divisions. The sympathetic system ("fight or flight") leaves the cord in the thoracolumbar region, uses short preganglionic and long postganglionic neurons, and releases noradrenaline onto adrenergic receptors. The parasympathetic system ("rest and digest") leaves in the craniosacral region, uses long preganglionic and short postganglionic neurons, and releases acetylcholine onto muscarinic receptors. Their effects on each organ are mostly opposite: the sympathetic system speeds the heart, dilates the bronchi and pupils, and inhibits the gut and bladder, while the parasympathetic system slows the heart, constricts the bronchi and pupils, and drives digestion and urination. A couple of exceptions are examiner favourites: sweat glands are sympathetic but use acetylcholine, and the adrenal medulla is driven directly by a preganglionic fibre.
Reflexes are the nervous system's built-in automatic responses, each with a defined arc. The stretch (deep tendon) reflex is monosynaptic, running from a muscle-spindle afferent straight to a motor neuron, and it is absent in lower motor neuron lesions but brisk in upper motor neuron lesions. The withdrawal reflex is polysynaptic and protective, and the pupillary light reflex uses the optic nerve as its afferent and the oculomotor nerve as its efferent, testing both a direct and a consensual response. Exam tip: build one two-column table of sympathetic versus parasympathetic effects organ by organ, and learn the transmitter-receptor pairing for each division, because that framework answers both the "which division does what" questions and the pharmacology that builds on them.
5. Vision
The eye is essentially a camera that focuses light precisely onto the retina. The cornea supplies most of the fixed focusing power and the lens supplies the adjustable part, changing shape during accommodation to focus on near objects. Refractive errors are simply a mismatch between the eye's power and its length: in myopia the eye is too long so images focus in front of the retina (corrected with a diverging lens), in hypermetropia it is too short (corrected with a converging lens), and presbyopia is the age-related stiffening of the lens that blurs near vision. The retina does the actual sensing with two receptor types: rods are numerous, very sensitive and used in dim light but see no colour, while cones are concentrated at the fovea, need bright light, and give sharp colour vision.
Phototransduction has a counter-intuitive twist worth learning carefully: in the dark the photoreceptor is depolarised and releasing glutamate, and light turns it off. A photon changes the shape of retinal in rhodopsin, which activates transducin and then phosphodiesterase, cGMP falls, the cation channels close, and the cell hyperpolarises and releases less glutamate. The visual pathway then carries the signal so that each side of the brain sees the opposite visual field: at the optic chiasm the nasal fibres cross while the temporal fibres stay put, which is why the lesions are so predictable. An optic nerve lesion blinds one eye, a chiasm lesion (classically a pituitary tumour) causes bitemporal hemianopia, and an occipital lesion causes a contralateral hemianopia with macular sparing. Exam tip: the visual pathway lesions are guaranteed marks if you can draw the chiasm and remember that only the nasal (crossing) fibres are cut at the midline, so learn the diagram rather than a list of defects.
6. Hearing, Balance, Smell and Taste
Hearing depends on turning air vibration into a nerve signal. The external ear collects sound, the middle-ear ossicles match the impedance so energy is not lost passing into fluid, and the cochlea analyses frequency because its basilar membrane is tonotopic: the stiff base responds to high frequencies and the floppy apex to low ones. Movement of the membrane bends the hair cells' stereocilia, opens transduction channels, lets potassium-rich endolymph in, and triggers glutamate release onto the auditory nerve. Two clinical tests read hearing loss: comparing air and bone conduction (Rinne) and lateralisation (Weber) distinguishes conductive loss (a mechanical problem such as wax or otosclerosis) from sensorineural loss (a cochlear or nerve problem such as noise damage or presbycusis). Balance uses the same hair-cell trick in the vestibular apparatus, where the semicircular canals detect rotation and the utricle and saccule detect linear acceleration and gravity.
Smell and taste are the chemical senses. Olfactory receptor neurons in the roof of the nose each express one of about 400 receptor genes, and their axons form the olfactory nerve and synapse in the olfactory bulb. Smell is unique in projecting directly to the cortex and the limbic system without a thalamic relay, which is why smells trigger such strong emotion and memory, and why loss of smell can be an early sign of Parkinson or Alzheimer disease. Taste comes in five primary types (sweet, umami and bitter through GPCRs, sour through proton channels and salty through sodium channels), carried by three cranial nerves to the brainstem and on to the insula. Exam tip: learn the Rinne and Weber patterns as a small grid, because the two tests together are the classic "is this conductive or sensorineural" question, and remember that olfaction is the one sense that skips the thalamus.
7. Renal Physiology: The Kidney and Nephron
The kidneys keep the internal environment stable by filtering blood and forming urine, and they do far more than excretion: they balance water and electrolytes, control acid-base status, and act as endocrine organs, making renin, erythropoietin and the active form of vitamin D. The functional unit is the nephron, about 1.2 million per kidney, made of a filtering renal corpuscle and a long tubule. Filtrate passes from Bowman's space through the proximal convoluted tubule, the loop of Henle, the distal convoluted tubule and the collecting duct. The filtration barrier has three layers (fenestrated endothelium, a negatively charged basement membrane and podocyte slits) that let water and small solutes through but hold back blood cells and protein, so protein or blood in the urine signals damage to that barrier.
The kidney's blood supply is unusual and central to how it works. It receives about a quarter of the cardiac output, not for its own metabolism but to drive filtration, and blood passes through two capillary beds in series separated by the efferent arteriole. Filtration itself is governed by the net filtration pressure, the balance of the hydrostatic pressure pushing fluid out against the capsular and osmotic pressures holding it in, giving a normal GFR of about 125 mL/min. Because a stable GFR is vital, it is autoregulated by a myogenic response and by tubuloglomerular feedback from the macula densa, and it is further tuned by sympathetic tone and by the renin-angiotensin system. Exam tip: be able to write the net filtration pressure as one subtraction (hydrostatic pressure out minus capsular pressure minus colloid osmotic pressure), because it turns a wordy topic into a single calculable line and shows exactly how each pressure changes GFR.
8. Urine Formation, Concentration and Clinical Correlates
Of the roughly 180 litres filtered each day, about 99% is reabsorbed, leaving only 1 to 2 litres of urine, and three processes do the work: filtration at the corpuscle, reabsorption from tubule to blood, and secretion from blood into tubule. Sodium is the master solute: its reabsorption in the proximal tubule (where about two-thirds of the filtrate is reclaimed, along with all the glucose and amino acids) creates the gradients that pull water and other solutes with it. The distal nephron is where hormones fine-tune the final urine: aldosterone increases sodium reabsorption and potassium secretion, ADH inserts water channels (aquaporins) to concentrate the urine, ANP promotes salt and water loss when blood pressure is high, and PTH adjusts calcium and phosphate. Secretion, meanwhile, clears wastes and many drugs and helps regulate acid-base balance by secreting hydrogen ions.
The kidney's ability to concentrate urine rests on the countercurrent mechanism. The thick ascending limb of the loop pumps out sodium chloride but is impermeable to water, which makes the medulla progressively saltier, while the water-permeable descending limb loses water and concentrates its contents; the vasa recta preserve this gradient. ADH then decides how much of that gradient is used: when the body is dehydrated, ADH rises, aquaporins are inserted, and small volumes of highly concentrated urine are made, whereas overhydration switches ADH off and produces large volumes of dilute urine. This framework explains the classic clinical correlates: glycosuria when blood glucose overwhelms the reabsorption transporters, diabetes insipidus when ADH is missing or ineffective (huge volumes of dilute urine with no glucose), proteinuria and haematuria when the filtration barrier is damaged, and azotemia when output falls and wastes accumulate. Exam tip: pair each clinical correlate with the single mechanism it breaks, because questions here almost always give a urine pattern and ask which step of filtration, reabsorption, secretion or concentration has failed.
Sample Practice Questions (With Answers)
Here are a few representative questions across the three blocks, written in our own words, with the reasoning explained so you understand the why, not just the result:
Q1. A local anaesthetic is injected around a mixed nerve. The patient loses pain first and muscle power last, then recovers in the reverse order. Explain why.
Answer: Local anaesthetics block voltage-gated sodium channels, and they affect the smallest fibres first. Pain and autonomic fibres are the thinnest (C and A-delta), so they are silenced first, then the touch and pressure fibres, and finally the large, heavily myelinated A-alpha motor and proprioceptive fibres. Because the largest fibres are blocked last, motor power goes last, and as the drug wears off the large fibres recover first, giving the reverse order. It is fibre size, working through the same sodium channel, that sets the sequence.
Q2. A spinal cord is hemisected on the left. Below the injury, where would you expect loss of motor power, and where loss of pain sensation?
Answer: This is Brown-Sequard syndrome, and it is explained entirely by where each tract crosses. The corticospinal tract has already crossed in the medulla, so below a left-sided lesion motor power is lost on the same (left) side. The dorsal columns also cross high up, so fine touch and proprioception are lost on the left too. But the spinothalamic tract crosses within the cord soon after entering, so pain and temperature fibres in the left tract come from the right side of the body, meaning pain sensation is lost on the opposite (right) side below the lesion.
Q3. A patient with a pituitary tumour develops loss of the outer (temporal) half of vision in both eyes. Why this specific pattern?
Answer: The pattern is bitemporal hemianopia, and it comes from where the tumour sits. At the optic chiasm the nasal retinal fibres cross to the other side, and it is these crossing fibres that carry the temporal (outer) visual fields. A pituitary tumour grows up into the centre of the chiasm and compresses exactly those crossing nasal fibres, so both temporal fields are lost while the uncrossed temporal fibres, carrying the nasal fields, are spared. Knowing that only the crossing nasal fibres are hit at the midline gives the answer directly.
Q4. In phototransduction, light causes the photoreceptor to release less neurotransmitter. How can switching a cell off carry visual information?
Answer: The photoreceptor works in reverse of most sensory cells. In the dark, cGMP keeps cation channels open, the cell is depolarised, and it releases glutamate steadily. Light activates the cascade (rhodopsin, transducin, phosphodiesterase) that breaks down cGMP, the channels close, and the cell hyperpolarises and releases less glutamate. The reduction in glutamate is itself the signal: the downstream bipolar and ganglion cells are tuned to read a fall in transmitter as "light detected," so an off-response encodes information just as effectively as an on-response would.
Q5. A patient passes very large volumes of dilute urine that contains no glucose. Contrast this with the polyuria of uncontrolled diabetes mellitus.
Answer: Both cause polyuria but by different mechanisms, and the urine glucose separates them. In diabetes insipidus, ADH is either deficient (central) or ineffective (nephrogenic), so the collecting duct cannot insert aquaporins and reabsorb water; large volumes of dilute urine result, but glucose handling is normal, so there is no glucose in the urine. In diabetes mellitus, high blood glucose exceeds the renal threshold and saturates the SGLT transporters, so glucose spills into the tubule and holds water with it by osmotic diuresis; the polyuria therefore comes with glycosuria. Glucose in the urine points to mellitus, its absence to insipidus.
How to Study the Nervous System, Senses & Renal Blocks Effectively
- Learn the action potential as a sequence of channel states rather than a graph, because refractory periods, local anaesthetics and saltatory conduction are all really questions about which channels are open or inactivated.
- Memorise where the three spinal tracts cross (dorsal columns and corticospinal in the medulla, spinothalamic in the cord), because that one fact unlocks Brown-Sequard syndrome.
- Draw the optic chiasm and mark only the nasal fibres crossing, then read off each visual field defect from the diagram instead of memorising a list.
- Build a sympathetic-versus-parasympathetic table organ by organ, with the transmitter and receptor for each division, and note the exceptions (sweat glands, adrenal medulla).
- For the kidney, write the net filtration pressure as one subtraction and pair each clinical correlate (glycosuria, diabetes insipidus, proteinuria, azotemia) with the single step it breaks.
- Read the topic summaries here to build the framework, then work through the full illustrated workbook in the reader below and attempt the practice questions from memory before your class test.
Download the Full PHS 220 Nervous System, Senses & Renal Study Guide
The notes above stand on their own, but if you want all three blocks in one place, the full PHS 220 Nervous System, Special Senses and Renal Physiology illustrated study guide is loaded in the reader just below, with the fibre-classification and neurotransmitter tables, the labelled visual and auditory pathways, the sympathetic-versus-parasympathetic comparison, the nephron segment by segment, and the labelled callout boxes for the key mechanisms and clinical correlates. Read it right here on the page, or save a copy so you can keep drilling the pathways, tables and clinical patterns offline in the days before your test.
Frequently Asked Questions
Is this PHS 220 material free?
Yes, completely. There is no fee, sign-up, or paywall anywhere on this page. The nervous system, special senses and renal notes, the practice questions, and the downloadable study guide are open to any student who needs a hand with this part of physiology.
Why are the nervous system, senses and kidney combined into one guide?
Because they share the same underlying theme of membrane transport and signalling, and grouping them makes the connections easier to see. This single guide covers the nervous system, the special senses, and renal physiology in one place, which is why it replaces several shorter topic pages that used to be separate.
What is the fastest way to revise these blocks before a test?
Work from the diagrams and small tables. Sketch the action potential channel states, the optic chiasm, and the nephron from memory, reproduce the autonomic comparison table, and rehearse where the spinal tracts cross. Then attempt the practice questions above from memory, because active recall is close to how the course is examined.
Will these exact questions appear in my exam?
No. This is an original revision set written from scratch to rehearse the reasoning and the phrasing, not a forecast of what your lecturer will set. Use it to practise, then sit your test on the specimens, diagrams and outline your own course actually covers.
About this resource: All summaries, explanations, study tips, and practice questions on this page were written, paraphrased, and adapted by the EverythingABUAD student team to support exam revision. This is an original study aid, not an official ABUAD document, and it is not a prediction of any future exam. Always cross-check with your lecturer's current course outline.
Written by the Everything ABUAD Team
Current students at Afe Babalola University, Ado-Ekiti. Guides are checked against the official ABUAD portal and campus notices, and confirmed with department and course reps before publishing.
