Nose and upper airway
The nose heats, wets and filters every breath taken through it and carries about half the airway's resistance; the pharynx behind it has no bone or cartilage holding it open. Both block — the nose from swollen blood vessels, the pharynx from muscle tone that falls away in sleep.
What it normally does
The nose brings air close to body temperature (about 32-34 degrees Celsius by the nasopharynx, the last degrees added lower down) and close to full water saturation in roughly a quarter of a second. It manages that by breaking flow into turbulence over the scrolled shelves of the turbinates (conchae), which carry an unusually dense blood supply running just under a thin lining — including an anastomosis on the front of the septum where branches of both the internal and external carotid systems meet (Little area, or the Kiesselbach plexus).
The plumbing that heats the air sits millimetres from the surface, which is exactly why the nose bleeds so easily — epistaxis.
Goblet cells and glands lay down a two-layer blanket: a watery periciliary layer the cilia beat in, and a sticky gel layer on top that catches particles larger than about 10 micrometres. Cilia beat roughly 10 to 15 times a second and sweep most of the sheet backwards to the pharynx to be swallowed (mucociliary clearance); only the anterior few centimetres clear forwards. The sinuses drain into this system through ostia only 1 to 3 mm wide, and the maxillary ostium sits high on the medial sinus wall, so its mucus has to be moved uphill.
Anything that swells an ostium shut leaves a warm, closed, mucus-filled box — rhinosinusitis.
Most nasal blood is not in capillaries but in wide venous sinusoids (capacitance vessels) wrapped around the turbinates. Sympathetic nerves hold them partly constricted through alpha adrenoceptors. Let them fill and the turbinate swells and the airway closes; the two sides alternate over a few hours (the nasal cycle). Even a normal nose supplies about half the total resistance to breathing.
A blocked nose is mainly a vascular event, not a mucus event — that is what obstructs in allergic rhinitis, and why constricting those vessels opens it in minutes.
Between the soft palate and the epiglottis there is no bone and no cartilage holding the airway open. It stays open mainly because dilator muscles — genioglossus pulling the tongue forward, tensor veli palatini stiffening the palate — fire with every breath against the negative pressure that inspiration creates, helped by the tracheal traction of a larger lung volume. That drive falls at sleep onset and falls furthest in REM sleep.
Sleep withdraws most of what holds the pharynx open — obstructive sleep apnoea.
What goes wrong
- Allergic rhinitis← from “Most nasal blood is not in capillaries but in …”
Inhaled allergen cross-links IgE on mast cells sitting in the nasal mucosa. Within minutes they release histamine, tryptase, prostaglandin D2 and leukotrienes. Histamine on sensory nerve endings gives itch and triggers the sneeze reflex. Histamine and leukotrienes on the capacitance sinusoids let them fill, and the turbinate swells like a wet sponge — that is the block. A parasympathetic reflex plus direct glandular stimulation gives the watery discharge. Hours later eosinophils and T cells arrive and keep the mucosa swollen: the late phase, which is why the block outlasts the exposure by hours or days.
Roughly one in five Australians has allergic rhinitis — one of the higher national rates reported. Uncontrolled rhinitis worsens asthma control — the same airway, top and bottom — so ask about the nose in every asthmatic. The 2016 Melbourne thunderstorm asthma event killed 10 people, and the people hit hardest were those with rye grass hay fever, many of whom did not think of themselves as asthmatic.
You would find: Pale, boggy, swollen inferior turbinates and clear watery discharge — not the red mucosa and yellow discharge of infection. Itchy eyes and palate, sneezing in runs, a horizontal crease across the nose from rubbing upwards, dark 'allergic shiners' under the eyes. In children, mouth-breathing and snoring.
- Acute rhinosinusitis← from “Goblet cells and glands lay down a two-layer b…”
A viral URTI, or allergic swelling, inflames the mucosa lining the sinus ostium. The ostium is only a few millimetres wide, so it shuts. The cilia inside keep pushing mucus towards an outlet that is now closed. Oxygen in the cavity falls, mucus thickens and stagnates, and cilia beat poorly in thick secretions — the escalator stalls. If bacteria are present (Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis) they are now growing in a warm, undrained box.
Almost all acute sinusitis is viral, and even in the bacterial minority antibiotics add little — most people are better within about two weeks either way, roughly one in eighteen treated gains a cure they would not have had, and adverse effects are common. The treatment that actually matters is symptomatic and aimed at reopening the ostium: analgesia, saline irrigation, a steroid spray, and if needed a few days of a topical decongestant. Red flags that infection has escaped the sinus: swelling or redness of the eyelid, proptosis, painful or restricted eye movements, double vision, altered consciousness. That is orbital or intracranial spread and it is an emergency.
You would find: Blocked nose plus facial pressure over the cheek or between the eyes, worse leaning forward, with discoloured discharge and loss of smell. Viral sinusitis peaks around day 2 to 3 and settles by about day 10. Suspect bacterial infection when it runs beyond 10 days without improving, or improves and then clearly worsens again ('double sickening'), or comes with fever above 39 degrees Celsius alongside frank purulent discharge and facial pain.
- Obstructive sleep apnoea← from “Between the soft palate and the epiglottis the…”
Sleep drops dilator muscle tone. Anything that narrows the tube means the tone that remains is no longer enough: fat in the parapharyngeal tissues and the tongue, big tonsils and adenoids, a set-back jaw, or a blocked nose forcing mouth breathing, which drops the jaw and slides the tongue base backwards. Inspiration generates negative pressure and the soft palate and tongue base suck shut. Airflow stops while the chest keeps trying, oxygen falls and carbon dioxide rises, the brain arouses briefly, tone returns and the airway snaps open with a snort. Then it happens again, often dozens of times an hour. Fragmented sleep gives the daytime sleepiness; each arousal fires a sympathetic surge, which gives the night-time and eventually daytime hypertension.
Around 5% of Australian adults have symptomatic OSA — more again if you count sleep-disordered breathing found on testing without daytime symptoms — and most are undiagnosed. It carries hard consequences, including motor vehicle crash risk and fitness-to-drive obligations that are stricter for commercial drivers. The burden falls disproportionately on Aboriginal and Torres Strait Islander people, who have higher rates of obesity and type 2 diabetes and, in children, a very high burden of chronic upper airway and middle ear disease — while access to sleep studies and CPAP is worst in remote communities. First-line treatment is mechanical, not pharmacological.
You would find: Loud snoring, apnoeas witnessed by a bed partner, choking or gasping arousals, unrefreshing sleep, morning headache and daytime sleepiness (score it with the Epworth scale). Examine for obesity, a crowded oropharynx, a large neck and a receding jaw. Suspect it behind resistant hypertension, atrial fibrillation and poorly controlled type 2 diabetes. Diagnosis is by sleep study — laboratory polysomnography or a validated home study — reported as the apnoea-hypopnoea index, events per hour of sleep. Children look different: big tonsils and adenoids, and hyperactivity and poor school performance rather than sleepiness.
The vessels that exist to heat inspired air run immediately under a thin mucosa on the front of the septum, where branches of the internal and external carotid systems anastomose (Little area, Kiesselbach plexus). Dry air, nose-picking, trauma, a steroid spray aimed at the septum, or inflamed mucosa cracks that surface and opens one of those vessels. Bleeding is then harder to stop, and more likely to recur, if the person is anticoagulated or thrombocytopenic. Hypertension is associated with more severe and recurrent bleeds and makes tamponade harder, but it is not established as a cause — do not stop looking for a local source because the blood pressure is high.
Repeated bleeding from one side with persistent blockage in an adult is a mass until proven otherwise, not a dry nose. In a teenage boy with unilateral obstruction and heavy bleeds, think juvenile nasopharyngeal angiofibroma — image it, do not biopsy it in clinic.
You would find: About 90% are anterior, and you can usually see the bleeding point on the front of the septum with a light. First aid is firm pressure on the soft cartilaginous part of the nose — not the bony bridge — for 10 to 15 minutes, sitting up and leaning forward. Blood running down the throat with nothing visible in front, in an older person on anticoagulants, points to a posterior bleed, typically from the sphenopalatine artery: heavy, and one for ENT.
What we give, and how it works
Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.
- Binds
- Cytoplasmic glucocorticoid receptors in the epithelial cells, mast cells, eosinophils and T cells of the nasal mucosa.
- Which does
- The drug-receptor complex moves into the nucleus. It switches on anti-inflammatory genes and, more importantly, represses NF-kB-driven transcription of cytokines. Over days the number of mast cells and eosinophils sitting in the mucosa falls.
- So you see
- Swelling, discharge, sneezing and itch all drop — including the late-phase blockage that antihistamines barely touch. Some effect appears within about 12 hours, but useful relief takes days and maximum effect one to two weeks, so it works best taken every day through the season rather than when symptoms flare.
- And the same mechanism causes
- The common adverse effects are local: dryness, crusting, irritation and epistaxis, in the order of 5-10% of users. The mechanism is mostly mechanical and vascular, not atrophic — the spray jet and the nozzle tip strike the anterior septum, exactly where Little area sits under a thin mucosa, and local vasoconstriction and drying crack that surface. Do not teach that the steroid thins the septum: biopsy studies of up to a year of modern intranasal steroid show no mucosal atrophy. Septal perforation is rare and is generally traced to repeated direct trauma from aiming at the septum. Technique is the fix — the bottle is held in the opposite hand and aimed outwards towards the same-side ear, away from the septum, without sniffing hard.
- Handling
- At recommended doses systemic effects are minimal, but 'zero' overstates it: a small reduction in growth velocity has been shown in children with some agents, so the lowest effective dose is used and the total corticosteroid burden counts in a child also on an inhaled steroid for asthma. When the spray 'does not work', the reason is usually technique or stopping after a couple of days.
Catches people out: Depot corticosteroid injections (the old 'hay fever shot') are not an appropriate treatment for allergic rhinitis and are advised against in Australia. Oral corticosteroids are rarely justified — at most a short course for severe refractory symptoms — and not as a repeated or routine seasonal treatment.
- Binds
- The histamine H1 receptor. They are inverse agonists — they stabilise the receptor in its inactive state rather than simply competing with histamine for it.
- Which does
- Damps Gq signalling, so the rise in intracellular calcium in endothelium and sensory neurons is blunted: less nitric-oxide-driven vasodilation, less endothelial gap formation and plasma leak, less firing of itch fibres.
- So you see
- Sneezing, itch and watery discharge settle within about an hour. The blocked nose barely improves, because congestion is sinusoid filling driven by leukotrienes and the late-phase cellular infiltrate as much as by histamine. This is why a patient whose main complaint is 'blocked' needs a steroid spray, not an antihistamine.
- And the same mechanism causes
- The brain's histaminergic neurons sit in the tuberomammillary nucleus of the posterior hypothalamus and project widely to cortex and thalamus, where H1 receptors carry one of the main wake signals. First-generation agents (promethazine, dexchlorpheniramine) are lipophilic, cross the blood-brain barrier and block those receptors — hence sedation, and impaired driving or schoolwork the next morning. They also block muscarinic receptors, so dry mouth, blurred vision and urinary hesitancy in an older man with a big prostate. Second-generation agents are more polar and (fexofenadine especially) are pumped back out by P-glycoprotein at the blood-brain barrier, so they largely stay out of the CNS; cetirizine is the one that still sedates a minority, and dose-dependently.
- Handling
- Sedating antihistamines are contraindicated in children under 2 years (respiratory depression and deaths reported with promethazine) and are avoided under 6. They are not an appropriate way to sedate a child, and sedation is not a reason to choose one in rhinitis.
- Binds
- Alpha-1 and alpha-2 adrenoceptors on the vascular smooth muscle of the nasal sinusoids.
- Which does
- Alpha-1 is Gq coupled: phospholipase C, IP3, calcium release, smooth muscle contraction. Alpha-2 is Gi coupled — it lowers cyclic AMP and, on vascular smooth muscle, still ends in contraction through calcium entry. Either way the sinusoids empty and the turbinate physically shrinks.
- So you see
- The nose opens within minutes — faster than any other available treatment. It does nothing to the inflammation underneath.
- And the same mechanism causes
- Keep flogging those receptors and they desensitise and downregulate, and the vessels refill harder each time the drug wears off. After about five days of continuous use the patient needs the spray simply to breathe, and the nose is worse without it — rebound congestion (rhinitis medicamentosa). Oral pseudoephedrine's systemic effects follow its indirect mechanism rather than alpha receptors alone: alpha-1 on systemic arterioles raises blood pressure, and alpha-1A at the bladder neck and prostate gives urinary hesitancy in men; but the palpitations and tachycardia come from beta-1 stimulation by the noradrenaline it releases, and the insomnia and agitation from central sympathomimetic action.
- Handling
- Topical sprays are limited to about five days of continuous use, and the packet often does not make that clear. Oral pseudoephedrine is used with caution in uncontrolled hypertension, coronary disease, hyperthyroidism, closed-angle glaucoma and bladder outlet obstruction, and is avoided with MAO inhibitors. In Australia it is Pharmacist Only (Schedule 3) and each sale is logged in Project STOP with photo ID, because it is a methamphetamine precursor.
Catches people out: Rebound congestion is the exam point, and it is the reason a patient turns up with a nose blocked for six months and a bottle in their pocket.
- Binds
- The dopamine transporter (DAT). Its full mechanism is still not settled, but binding at DAT is required for the wake-promoting effect.
- Which does
- Weak reuptake inhibition leaves more dopamine in striatal and hypothalamic synapses, which keeps downstream orexin and histamine wake-promoting pathways firing.
- So you see
- The patient feels less sleepy. The apnoeas are untouched — the apnoea-hypopnoea index, the overnight oxygen dips and the cardiovascular risk are unchanged.
- And the same mechanism causes
- Driving that same dopaminergic and sympathetic arousal beyond the wake circuits gives headache (the commonest), anxiety, insomnia, palpitations and a small rise in blood pressure. And because it removes the symptom without fixing the obstruction, a patient can abandon CPAP, feel fine, and go on desaturating all night. Two adverse effects are not mechanism-derived but matter more than the rest: serious rash including Stevens-Johnson syndrome (it is stopped at any rash), and an increased risk of major congenital malformations with use in pregnancy.
- Handling
- Modafinil induces CYP3A4 and reduces the effectiveness of combined oral contraceptives — an additional or alternative method is needed during treatment and for at least a month after stopping, since enzyme induction takes weeks to wear off. It is not used in pregnancy, and effective contraception is expected to be in place before it is started in a woman of childbearing potential.
Catches people out: Sedatives, opioids and alcohol work the other way: they suppress pharyngeal dilator drive and deepen the obstruction. Each of them deserves a second look before it is added for a snorer.
A nose blocked by swelling needs a steroid spray, not an antihistamine — antihistamines fix the itch, sneeze and run, not the block. The drugs that unblock a nose in minutes, the topical decongestants such as oxymetazoline, are the ones limited to about five days before rebound congestion sets in. And in obstructive sleep apnoea no drug in routine use treats the obstruction itself: the pharynx is a floppy tube with no scaffolding, so it is held open with pressure, a splint, or less weight around it — a wakefulness agent only paints over the sleepiness in someone already on CPAP.
Now test whether it stuck
Reading this through is not the same as being able to reconstruct it. Every question in the bank is free, with a full debrief on each option.