Lung anatomy and spread
Two bags of alveoli divided into lobes and hung off a hilum — and much of what a lung tumour does to a patient is explained by what the lung is lying against, not by the lung itself.
What it normally does
The right lung has three lobes split by two fissures (oblique and horizontal); the left has two lobes, one oblique fissure, and a lingula (part of the left upper lobe) where a middle lobe would be. On the surface the oblique fissure runs from about the T3 spinous process posteriorly — the root of the spine of the scapula, and a little higher on the left — down and forward to the 6th costal cartilage; the horizontal fissure runs from the 4th costal cartilage backwards to meet it near the midaxillary line. So the upper lobe sits mostly in front and the lower lobe mostly behind.
disease that fills one lobe gives signs in one region rather than throughout the chest — and you listen for upper lobes on the front of the chest and lower lobes on the back, or you will miss it.
Everything entering or leaving a lung squeezes through the hilum: main bronchus, pulmonary artery, two pulmonary veins, bronchial vessels and a cuff of lymph nodes. On the right the artery is in front of the bronchus, on the left it arches over it (RALS). The phrenic nerve descends in front of the lung root on the pericardium (the vagus passes behind it), and the superior vena cava lies in the right paratracheal groove just anterior and medial to the right hilum.
a central mass sits within reach of the superior vena cava and the phrenic nerve as well as the airway — so a swollen face or a raised hemidiaphragm can be the first sign, sometimes before any wheeze, cough or lobar collapse.
Lung lymph flows one way and inwards: from alveoli to nodes along the airways, to hilar nodes, to mediastinal nodes, then up to the scalene and supraclavicular nodes at the root of the neck. Drainage can cross the midline — left lower lobe lymph often reaches right-sided mediastinal nodes.
spread is fairly predictable, the neck is where you can feel and biopsy it, and which node station is involved decides whether an operation is possible.
The lung apex pokes above the first rib into the neck. Lying directly on it are the sympathetic chain with the stellate (cervicothoracic) ganglion, the lower trunk of the brachial plexus (C8-T1) and the subclavian vessels. Lower down on the left only, the recurrent laryngeal nerve hooks under the aortic arch just above and medial to the hilum (the aortopulmonary window).
an apical tumour causes a drooping lid and small pupil with arm pain, and a left hilar one makes the voice hoarse — neither is a lung symptom at all.
What goes wrong
- Pancoast (superior sulcus) tumour with Horner syndrome← from “The lung apex pokes above the first rib into t…”
A tumour arising at the lung apex grows out of the lung and into the tissue resting on it. It damages the sympathetic chain at the stellate ganglion, so that side of the face loses its sympathetic supply: the small smooth muscle helping hold the eyelid up (superior tarsal, Müller's) fails, giving partial ptosis; the pupil dilator stops pulling so the pupil sits small (miosis); and sweat glands lose their drive (anhidrosis). Growing backwards and laterally it invades the C8-T1 lower trunk of the brachial plexus, and it erodes the first and second ribs and can reach the vertebral bodies.
Apex pain + Horner + T1 wasting = Pancoast until proven otherwise. It is still a lung cancer, but the damage is done outside the lung and the apex is poorly seen on a plain film, so an unremarkable-looking lung field does not exclude it. Sweating is lost over the face and often the neck and arm as well, because the break is preganglionic — proximal to the superior cervical ganglion, from which the sudomotor fibres for the face run on with the external carotid artery.
You would find: A long-term smoker with months of severe shoulder and inner-arm pain, usually treated as frozen shoulder or cervical spine disease first. Same-side droopy lid, small pupil and a dry face; wasting of the small muscles of the hand. On chest X-ray the apex hides under the clavicle and first ribs — this is the classic missed film, and CT or MRI is what actually shows the lesion.
- Left recurrent laryngeal nerve palsy (hoarseness)← from “The lung apex pokes above the first rib into t…”
The left recurrent laryngeal nerve loops under the aortic arch immediately above and medial to the left hilum. Tumour or enlarged nodes in that window stretch or invade it, and the vocal cord on that side is paralysed. The cords can no longer close properly, so the voice is breathy, the cough has no explosive start (bovine cough), and the larynx seals poorly during a swallow.
Hoarseness from lung cancer is nearly always left-sided disease, because the right nerve loops higher around the right subclavian artery and is out of reach of the hilum (a right apical tumour can occasionally catch it). It means mediastinal involvement — the tumour is at least locally advanced, and that usually moves the plan away from surgery towards concurrent chemoradiotherapy.
You would find: New hoarseness lasting more than three weeks in a smoker, with a bovine cough and coughing on thin fluids. Nasendoscopy shows one cord sitting motionless. Refer, do not treat as laryngitis.
- Lobar pneumonia and aspiration← from “The right lung has three lobes split by two fi…”
Inhaled organisms or gastric contents go where geometry and gravity send them. The right main bronchus is wider, shorter and more vertical, so aspirated material tends to go right — to the posterior segment of the upper lobe or the superior segment of the lower lobe if the patient was lying flat, to the basal segments of the lower lobe if upright. Alveoli of that lobe fill with fluid, neutrophils and fibrin (consolidation), and solid lung conducts sound far better than aerated lung does.
Signs sit inside a lobe rather than spread through both lungs — that is how consolidation is told from heart failure at the bedside. Pneumonia and bronchiectasis rates are several times higher in Aboriginal and Torres Strait Islander communities, particularly in remote central and northern Australia, where repeated childhood chest infection drives adult lung damage.
You would find: Fever, pleuritic pain, dull percussion over one zone, with bronchial breathing and increased vocal resonance concentrated in that zone. Right middle lobe disease is heard at the front near the right nipple; on X-ray it blurs the right heart border but leaves the diaphragm crisp (the silhouette sign).
- Superior vena cava obstruction← from “Everything entering or leaving a lung squeezes…”
A right hilar or right paratracheal mass presses on the superior vena cava — a valveless, thin-walled, low-pressure vein sitting right there. Return from head, neck and arms is obstructed, so pressure backs up and blood finds collateral routes through chest wall and azygos veins; how well those collaterals cope depends partly on whether the block is above or below where the azygos vein joins. Thrombus in the compressed segment often adds to the obstruction.
Fixed non-pulsatile distended neck veins + facial swelling + dilated chest wall veins = SVC obstruction; lung cancer (small cell in particular) and lymphoma are the usual causes. Endovascular stenting gives the fastest relief. Get tissue before steroids where the patient is stable, because steroids can wipe out a lymphoma diagnosis.
You would find: Puffy face and eyelids, worse in the morning and on bending forward, headache, and neck veins that are distended, non-pulsatile and do not fall on inspiration. Dilated veins visible over the upper chest. Stridor, confusion or laryngeal oedema makes it an emergency.
- Nodal and distant spread — why you feel the neck← from “Lung lymph flows one way and inwards: from alv…”
Tumour cells travel the same one-way route as the lymph: along the airways to hilar nodes, on to mediastinal nodes, then to the supraclavicular fossa. Reaching the opposite side of the mediastinum or the neck (N3) puts the disease beyond what a surgeon can resect. Tumour also seeds the pleura, giving an effusion, and goes by blood to brain, bone, liver and adrenal.
Feel both supraclavicular fossae in anyone with suspected lung cancer. Node station (N stage), not tumour size, usually decides operability, which is why PET-CT and EBUS sampling of mediastinal nodes come before any talk of surgery. Lung cancer kills more Australians than any other cancer (of the order of 8,700-9,000 deaths a year), and both incidence and mortality are roughly twice as high in Aboriginal and Torres Strait Islander peoples.
You would find: A firm fixed node in the supraclavicular fossa — often the easiest biopsy in the body. Often the presenting problem is not the chest at all: a first seizure, back pain from a vertebral deposit, or weight loss.
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
- The cytoplasmic glucocorticoid receptor
- Which does
- The drug-receptor complex moves into the nucleus, where it switches on anti-inflammatory genes such as annexin-1 (which restrains phospholipase A2, so fewer prostaglandins and leukotrienes are made) and represses NF-κB-driven transcription (so fewer cytokines are made). Capillary leak falls.
- So you see
- Oedema around the mass shrinks, the squeezed vein and airway get a little room back, and facial swelling and breathlessness may ease within a day — though the evidence for steroids in SVC obstruction is weak and stenting or radiotherapy is what actually relieves it.
- And the same mechanism causes
- The same receptor in liver and muscle drives gluconeogenesis and protein breakdown, so blood glucose climbs and proximal (thigh and shoulder) muscles waste — over a few weeks of continued dosing the patient may not be able to rise from a chair without using their arms.
Catches people out: It does not shrink a carcinoma. Lymphoid tissue is the exception — glucocorticoids are directly lymphotoxic, so if the cause turns out to be lymphoma the mass can melt away enough to destroy the diagnosis. Tissue first whenever the patient is stable enough to wait.
- Binds
- The N7 position of guanine in DNA
- Which does
- Platinum forms crosslinks within a strand and, less often, between the strands, so the helix cannot unwind; replication stalls at the damage and the cell triggers its own death (apoptosis).
- So you see
- Tumour and nodal masses shrink; in small cell lung cancer the response is fast and often dramatic, though usually not durable.
- And the same mechanism causes
- It cannot tell tumour from other fast-dividing tissue, so marrow fails (low counts, infection, bleeding) and the gut lining sheds (mucositis, diarrhoea); hair thins, more so with the taxanes platinum is often paired with. Cisplatin's severe acute vomiting is not simple mucosal damage — it releases serotonin from gut enterochromaffin cells onto vagal afferents and the chemoreceptor trigger zone, which is why highly emetogenic regimens are covered by combination antiemetic prophylaxis (a 5-HT3 antagonist, dexamethasone and an NK1 antagonist). Cisplatin is separately concentrated by transporters (OCT2, CTR1) into proximal tubular cells and cochlear hair cells, which accumulate it and are then killed by it even though they are not dividing — hence kidney injury and permanent high-frequency hearing loss with tinnitus.
Catches people out: Carboplatin is chosen when kidneys or hearing are already poor; the trade is more marrow suppression, thrombocytopenia in particular. Platinum is no longer given in isolation for most advanced non-small cell disease in Australia — molecular and PD-L1 testing come first, and the doublet is usually combined with, or replaced by, immunotherapy.
- Binds
- The ATP-binding pocket of the mutant epidermal growth factor receptor tyrosine kinase
- Which does
- It binds covalently and irreversibly at a cysteine (C797) in the pocket, so the receptor cannot phosphorylate itself, and the RAS-MAPK and PI3K signals that were telling the cell to grow and survive go quiet.
- So you see
- Tumour regresses within weeks on a tablet, and brain metastases respond too; resistance eventually emerges.
- And the same mechanism causes
- EGFR is also the growth signal for normal skin and gut lining, so blocking it produces an acne-like pustular rash over face and upper chest, painful split nail folds (paronychia) and diarrhoea. The rash is a sign the drug is engaging its target, not an allergy.
Catches people out: It works only if the tumour carries a sensitising mutation — the biopsy is tested first. Rarely it causes drug-induced lung inflammation (interstitial lung disease), so new breathlessness on treatment is not automatically progression; QT prolongation and a fall in ejection fraction are also monitored.
- Binds
- The α2δ subunit of voltage-gated calcium channels on presynaptic sensory nerve terminals
- Which does
- Binding reduces trafficking of new calcium channels into the terminal membrane, so less calcium enters when the sensitised fibre fires and less glutamate and substance P are released onto the second-order neuron.
- So you see
- The amplified pain signal is turned down; sleep often improves before the pain score does, and the benefit in cancer-related neuropathic pain is real but modest.
- And the same mechanism causes
- The same subunit is distributed widely on neurons through the brain, so the same dampening gives sedation, dizziness and unsteadiness — falls in older patients. Ankle swelling and weight gain also occur but come from a peripheral vascular effect rather than the dorsal horn action, so they are not predicted by the analgesic mechanism.
Catches people out: Despite the name, it has no meaningful action at GABA receptors. Cleared largely unchanged by the kidney, so it accumulates when renal function is poor, and sedation and respiratory depression compound with opioids. It is misused and diverted, and stopping it abruptly causes a withdrawal state. In Australia pregabalin is the gabapentinoid subsidised for neuropathic pain; gabapentin's PBS listing is for epilepsy, so its use here is off-label.
Hoarseness, Horner syndrome, a raised hemidiaphragm and fixed non-pulsatile neck veins are anatomy, not lung. Each one says the tumour has left the lung and touched a neighbour: the left recurrent laryngeal nerve under the aortic arch, the sympathetic chain over the apex, the phrenic nerve running down in front of the lung root on the pericardium, the superior vena cava in the right paratracheal groove beside the right hilum. In a stem they are not just symptoms — they are staging, and they are usually the line that rules out surgery.
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.