Pneumonia is acute INFLAMMATION of the lung PARENCHYMA (Parenchyma is medicalese for the substance of an organ; in the lung, this means the very smallest bronchi and the alveoli – of which, more later).

I’ve previously mentioned ‘acute’ and ‘chronic’ which to a doctor mean something slightly different to lay people. Inflammation that is ‘acute’ means it comes on quickly and involves mainly NEUTROPHILS (aka neutrophil polymorphonuclocytes), a type of white blood cell. Pus is dead neutrophils. Inflammation that is ‘chronic’ lasts a long time and involves mainly LYMPHOCYTES (another type of white blood cell), which become (ie change into) plasma cells, and MACROPHAGES (which occur in the blood but are also omni-present in tissues). Acute inflammation may go away, especially if humans intervene, but it may also become ‘acute-on-chronic’ (a mixture of the 2 types) and eventually ‘chronic’. If the body walls off the acute infections (by the formation of a fibrous tissue wall around it), then it may became an abscess (with pus inside).

The term’CHEST INFECTION’ is a generic term for (not surprisingly) infection in the chest, This can include BRONCHITIS (acute or chronic, referring to the type of white blood cell) which is inflammation of the bronchi (pleural of bronchus) the tubes that transfer air to the ALVEOLI (pleural of alveolus – it’s all Latin!), which are the end-sacs where air meets the blood and oxygen is transferred.

When pneumonia occurs, infection gets down to the alveoli, and these fill up with neutrophils (pus cells) and fluid (OEDEMA or, if you’re from the US, EDEMA). Thus air and blood do not interact properly and oxygen cannot transfer from air to blood. It can be LOBAR PNEUMONIA (meaning that an entire lung lobe is infected throughout – the right lung has 3 lobes, the left has 2 to make room for the heart) or BRONCHOPNEUMONIA (meaning that there is patchy involvement throughout the lobes, most commonly the lower lobes. DOUBLE PNEUMONIA means both right and left lung are involved. When looked at with the naked eye, the affected lung tissue is no longer like an empty sponge, it is like a sponge that that has been dipped in diluted blood and pus; it is heavy and solid, hence the term CONSOLIDATION.

Pneumonia is usually caused by bacteria; which bacteria cause it depends on who you are and what pre-existing conditions you have. Pneumonia de novo (‘from new’ – Latin again) tends to occur in the young and the old. If you have chronic bronchits, you are prone of pneumonia. The term PNEUMONITIS is reserved for infection of the lung parenchyma by viruses.


We are made of cells – a lot of them. They cooperate to make tissues, and those tissue make up organs. The cells take on different characteristics (it’s called DIFFERENTIATION), according to what they’re required to do (eg they may become nerve cells, or gut lining cells, or bones, or skeletal muscles etc). Generally, they behave. Indeed, there is a theory that normal cells die unless they are constantly told not to.

All cells (except red blood cells) have a nucleus and in that nucleus is a complete copy of the individual’s GENOME – that is, about 30,000 genes – which can be found in the DNA (DEOXYRIBONUCLEIC ACID). Not all of them are turned on, however. The genes that are turned on determine what the cell does and what it looks like (ie how it differentiates); in other word, different genes are active in nerve cells to those active in muscle cells.

By ‘behave’ I mean they die when they are told to (programmed cell death or APOPTOSIS), or they divide when they are told to, or they do their everyday job. When a cell divides, it has to replicate its DNA.

Cancer cells have changes in their DNA so that they ignore the messages that all other cells obey. They divide when they’re not supposed to, and don’t die when they should. This behaviour leads to a lump. The cells that don’t do as their told gradually pick up more genetic abnormalites because when a cell divides it is at its most vulnerable to mistakes in DNA replication. Thus cancers get worse and worse as they age. Malignant lumps infiltrate the surrounding tissues., perhaps getting around nerves or into thin-walled vessels

Bits of the tumour may break off (METASTASISE) and grow elsewhere; cancers of the surface cells usually go to lymph nodes, but they make also go to the liver, to the lungs, to the bones or to the brain. In fact they may go anywhere. Cancers of the cells that make up muscles, fat, fibrous tissue etc tend not to head for lymph nodes; I don’t know why.

There are many different kinds of cancer because there are many different kinds of cell. In face, at a genetic level, each cancer is unique, hence in future, genetic analysis of the tumour may lead to optimisation of treatment. That’s the hope, anyway.


Normal electrical pattern of a heart beat

Cardiac Arhythmias are also called cardiac DYSRHYTHMIAS and can cause an irregular heartbeat. The heart beats in a coordinated fashion because it has a CONDUCTION SYSTEM, although the myocytes (heart cells) beat on their own without it, and the heart will beat slowly (about half speed) anyway. The above diagram represents what is seen on an ECG during a normal heart beat. It should occur regularly in SINUS RHYTHM (there is slight variation with breathing). The P bit is the contraction of the atria, the Q-R-S bit is the contraction of the ventricles. and the T bit is the ventricles recovering. The U wave may not be seen. It is probably a bit like the T-wave (ie it is a repolarization).

A lot can be told from an ECG – entire books have been written on it – and not just different rhythms. If the blood supply to the heart is reduced, (ischaemia or ischemia), the flat line at the end of S and beginning of T is raised; if part of the heart muscle dies (INFARCTION, that is, a heart attack) then the T wave swings round and dips down. Because an ECG looks at the heart from multiple viewpoints (hence all the leads), these changes may occur in some views but not others; hence an ECG has multiple traces.

Cardiac arhythmias come in all sorts. The simplest is that the heart may speed up (TACHYCARDIA is the medicalese) or slow down (BRADYCARDIA). The atria and the ventricles may become electrically separated (HEART BLOCK) but the commonest is ATRIAL FIBRILLATION (AF).

The ECG in AF shows no P waves before the QRS complex. The atria ‘flutter’ rather than pump (hence the alternative name of ATRIAL FLUTTER). It doesn’t especially bother a normal heart as the ventricles fill and work relatively normally, but it’s important because blood may clot on the inside walls of the atria. This, in itself, does not matter. It only matters because bits of the clot (EMBOLI) may break off, go into the circulation, and lodge in the brain, where they cause a STROKE (of which more next week).


There are 4 common causes for a big heart – by which I mean a big LEFT heart. They are ISHCAEMIC (or if you’re not British, ISCHEMIC) HEART DISEASE, HYPERTENSION, CARDIAC VALVE DISEASE, CARDIOMYOPATHIES. Rarely, things like infection (‘MYOCARDITIS’) cause a big heart but these are the big 4.

ISCHAEMIC HEART DISEASE (IHD) is a term that is often written on certificates of the cause of death. It’s a catch-all term for what happens to the heart when ATHEROMA (that thing again) narrows the arteries that supply blood to the heart muscle (the CORONARY ARTERIES supplying blood to the MYOCARDIUM, as doctors put it). The heart muscle cells (the MYOCYTES) die and the heart muscle scars (FIBROSES). The surviving myocytes have to do more work and the heart becomes less efficient; moreover, the beat of the heart becomes more likely to be disrupted. People die suddenly and the pathologist finds only a big heart and coronary artery atheroma, and no other likely cause of death. The pathologist writes the cause of death as Ischaemic Heart Disease because that is the likeliest.

HYPERTENSION is high blood pressure. Most times, there is no known cause, when it’s called ESSENTIAL (medicalese again). To get the blood around the body, the heart has to work harder because it has to push blood out against a higher pressure. Like all muscles, the heart muscle over time becomes larger. Unfortunately, larger hearts require more blood to feed them via the coronary arteries. When the blood supply is insufficient, myocytes die and the heart muscle scars. Sudden death because of terminal arrhythmia may occur.

A big heart because of CARDIAC VALVE DISEASE is usually because of abnormalities of the MITRAL VALVE (between the left atrium and the left ventricle) or the AORTIC VALVE (where the left ventricle meets the aorta). As previously discussed, the abnormality may be regurgitation (also called INCOMPETENCE) when the valve allows blood to go backwards, or stenosis (when the valve becomes narrowed). Either way the heart has more work to do, and becomes larger, etc. etc..

CARDIOMYOPATHY is in intrinsic abnormality of the heart muscle itself – ie the myocardium is diseased. There are various types of cardiomyopathy, but the main ones are HYPERTROPHIC (aka HOCM, pronounced ‘hokum’) or CONGESTIVE (aka COCM, pronounced ‘cokum’). HOCM is usually an inherited disease; COCM is usually a result of lifestyle (‘ACQUIRED’ is the medicalese). Either way, the heart doesn’t behave normally when it comes to beating and terminal arrhythmia my occur. The pathologist can only diagnose it as a cause of death if there’s no other evidence of hypertension, IHD or cardiac valve disease.


There are 4 heart valves, 2 on the right side and 2 on the left. There is one between the two chambers on the right (the tricuspid valve), and one between the two chambers on the left (the mitral valve). There is one at the exit of the right heart (the pulmonary valve) and one at the exit of the left heart (the aortic valve).

Three of the valves (the tricuspid, the pulmonary and the aortic) have 3 leaflets, one (the mitral) has two. As with all valves, the role of the heart valves is to ensure that the blood goes in one direction and one direction only.

The valves may be INCOMPETENT (meaning that they leak, ie that they don’t seal properly) or STENOSED (which is medicalese for narrowed). Reasons for heart valve problems are most often due to infection (bugs in the blood), but can be congenital. The problem is that narrowing of the valve or leaking of the valve results in blood going the wrong way. Effectively, then, the bit of the heart behind the valve has to work harder. Eventually, that hard work causes the heart muscle to give up (or fail).

Valve replacements can be entirely artificial (ie metal, usually titanium because it’s hard and doesn’t tarnish) or biological (from another human being who, of course, is dead) or even from another animal (usually a pig because pigs and humans have a lot in common).


There are 3 common types of cancer, although there are many types of rare skin cancer. The 3 common types – BASAL CELL CARCINOMA (BCC), SQUAMOUS CELL CARCINOMA (SCC) and MALIGNANT MELANOMA (MM) – are all very different in behaviour and who they usually affect.

BCC and SCC usually affect older people. They are often associated with sun exposure, although BCCs may occur in areas of the skin where there is prolonged immune suppression, such as the lower legs when there is long-term venous eczema.

BCCs spread locally but very, very rarely do they spread beyond the point where they arise (they don’t METASTASISE as the medical jargon has it). That doesn’t mean they’re not dangerous, because they are inexorable. They grow and grow to incredible size if not treated, SO GET THEM SEEN EARLY. They may invade bone, and blood vessels, and eat away at the body. There are some shocking examples of what they can do in medical museums. There are different types of BCC – low risk types (superficial and nodular) and high risk types (because their edges are difficult to identify clinically – morphoeic and micronodular). Superficial BCCs can be treated by cream, other types by surgery or radiotherapy, both of which have both advantage and disadvantages.

SCCs can spread from the original site (but also invade locally as BCCs do) and so are more dangerous. They usually spread to local LYMPH GLANDS or NODES; in the case of the leg, those are in the groin, arm (armpit, aka AXILLA), head (neck). It is more common for people to die from SCC although it is still rare in the UK.

MM can affect the young as well as the old, and are much more worrying. They can be very difficult for pathologists to identify (the pathologists often say that MM can look like anything. They don’t have to be very advanced to spread; far-flung deposits can show up years after the original lesion has been treated and all-but-forgotten. They made spread to the liver, lungs or anywhere (another old saw of doctors is to ‘beware the patient with the false eye and the big liver) because an MM of the eye (yes, it can occur in the eye) treated by its removal may result in liver deposits years later.


Atheroma not only narrows the smaller arteries (such as the coronary arteries around the heart), it also weakens the walls. This means, that in larger arteries, there is no significant narrowing, but the wall is compromised. The biggest artery of them all is the AORTA. It carries all the blood that comes out of the heart, distributing it to the arms, the internal organs, and then to the legs; this last it does by splitting into 2 ILIAC arteries.

The weakening of the wall caused by atheroma and the pressure of the blood as it is pumped from the heart causes the aorta to expand. It expands either as a balloon to one side, or as generalised expansion of a segment. This expansion is the aneurysm. It usually affects the lower aorta and one or more iliac arteries, but may occur anywhere along the aorta, including the bit in the chest. Unfortunately, the laws of physics mean that the larger the aneurysm gets the easier it is to expand (think of blowing up a balloon).

When the aneurysm bursts, there is a catastrophic loss of blood, and is a frequent cause of death.

Atheroma is not the only cause of weakness in blood vessel walls, but it is the commonest, especially among the elderly. There is a screening programme for aortic aneurysm, and it can be treated surgically before rupture; this operation has a much lower mortality than operating on an aneurysm that has already burst.


The brain is covered by the MENINGES of which there are nominally 3 – the PIA MATER, the ARACHNOID MATER and the DURA MATER (‘mater’ means ‘mother’). The pia is practically non existent and we may consider it no more. The brain sits within the skull (as if you didn’t know) but the significance of this is that there is no room for anything else; if ‘something else’ arises within the skull, then the brain has to make room for it. This is why doctors talk about ‘space occupying lesions’ and why they are so important; they squash the brain and that does the brain no good at all.

Bleeds in the skull are one such example of space occupying lesions. They may be associated with skull fractures, which may let in infection, but if there’s a bleed in the skull, it matters.

Such bleeds may be extra-dural (ie outside the dura and just under the skull), sub-dural (ie between the dura and the arachnoid) or subarachnoid. Extra-dural haemorrhages occur in babies when they are abused. Subdural haemorrhages may be ‘acute’ (that is, occurring quickly) or ‘chronic’ (that it occurring over a long time); they are always associated with a head injury but the head injury that leads to a chronic subdural may be so long ago and very slight, so that the afflicted swears blind that it never happened.

An acute subdural is caused by blood accumulating quickly and pressing on the brain. A chronic subdural starts out small and grows over weeks, months even years. It may grow so slowly that the brain is able to compensate, and may present after months or years with headaches. They occur in the elderly.

Subarachnoid haemorrhages are bad news. They may be associated with head trauma but they can occur spontaneously, when a tiny bubble on the wall of a basal artery (a ‘berry’ aneurysm) bursts. Because they are associated with arterial (ie high pressure) bleeds, they do a lot of damage.

Moles and Malignant Melanoma

MELANOCYTES are funny things. They sit in the bottom layer of the EPIDERMIS (which is the outer covering of the skin; the rest of the skin is the DERMIS) and their job is to make melanin, which they pass onto the cells on either side of them. Melanin protects cells from damage to their DNA by UV light. DNA damage can lead to cancer. People with pigmented skin do not have more melanocytes, just more melanin.

They make moles that are benign and evolve from purely intraepidermial (‘junctional’) to mix epidermal and dermal (‘compound’) and eventually purely (‘intradermal’). ie they move downwards. They may be disfiguring, or become inflamed, or be a nuisance, but they are BENIGN, although they may become malignant.

Dysplastic naevi are not entirely benign and may progress to cancer; therefore, they need to be excised completely and with a sufficient margin of normal tissue.

Melonoma (with or without the prefix ‘malignant’) is NEVER benign. Once diagnosed and excised, it is the job of the pathologist to tell the dermatologist all the technical factors which influence how it will behave and therefore what further treatment is required. The most important thing the pathological assesses is how thick the melanoma is: less than 1 millimetre (see how thin that is?) 1-2 millimetres thick, 2-3 millimetres thick, 3-4 millimetres thick or over 4 millimetres thick. The thicker they are, the worse it is.

Further treatment may include a wider local excision (WLE) of up to 3cm around the original melanoma to mop up any satellite deposits. That’s a lot, believe me.

Melanomas can spread, but they may spread in a funny way. The most usual is to the local lymph glands (or nodes). Sentinel node biopsy is a way of determining if the local nodes are involved or not. Melanoma may spread to the liver or lungs or anywhere, though. Also melanoma may occur in funny locations that never see the sun.

All cancers have abnormal genes. Some melanomas have BRAF mutations that may be used as a therapeutic target – ie if the mutation is present, certain drugs may be of help.

Lastly, people can occasionally live a long time with melanoma that has spread. Usually, though it is an aggressive cancer that kills quite quickly.

Heart Failure

Heart failure is a mode of death and not, in itself, a natural disease. As such, it must be followed on a Death Certificate by what disease caused it. It merely means that the heart can no longer fulfill its function as well as it should. If it causes death, the failure is obviously profound.

But what does ‘failure’ mean? It doesn’t usually mean the heart stops, although technically it could. It usually means that its pumping action is no longer efficient and the heart’s output is reduced. People can live with cardiac failure for a long time.

Since the heart is in fact 2 pumps, heart failure can affect just the right side, or just the left side, or most commonly both. Because the ventricle(s) is/are no long pushing out the blood as well as it/they should, it/they dilate(s) (because blood is left in them when the heart beats) and there is a rise in upstream pressure. This is why the lungs fill with water in left or biventricular failure (the atria don’t contribute a great deal to the act of pushing blood out of the heart), because the pressure in the veins of the lungs increases. The blood coming out of the lungs is slightly thicker because water has been pushed out of the blood vessel walls.

This is also why ankles swell in biventricular or right side heart failure. it also affects internal organs such as the liver and can be so severe that the liver scars (‘cardiac cirrhosis’) and may even fail itself.

The water causes breathlessness (aka DYSPNOEA). It’s worse if the patient lies flat, which is why people with cardiac failure sleep with multiple pillows propping them up.

And if the heart is not pushing out blood as it should, arteries constrict to keep up blood pressure, and the heart enlarges because blood is not being ejected but it is still coming in from the veins. The kidneys need blood pressure because they are essentially just high pressure filters; they have their own mechanisms for making sure that the pressure of blood remains reasonable.

But why? Why does it fail?

It might be for one or more of a variety of reasons. Intrinsic problems with the heart muscle (reduced blood supply causing death of myocytes and fibrosis of the heart muscle due to coronary atheroma), myocarditis (where the heart muscle is inflamed, perhaps due to an infection), cardiomyopathy (in which the heart muscle is not normal), etc; or extrinisic problems such as hypertension. If the heart has to push blood out against raised blood pressure, it has to do more work, and eventually that tells.