| Normal response to strenuous exercise | Suggested by: fit healthy, unaccustomed exercise 1–2 days before. |
| Confirmed by: spontaneous resolution. | |
| Polymyalgia rheumatica | Suggested by: onset over weeks or months, stiff, painful, and tender proximal muscles. Fatigue, fever in elderly person. |
| Confirmed by: ↑↑ESR. Rheumatoid factor -ve, prompt response to prednisolone, no other cause (e.g. infection on follow-up). | |
| Management: OHCM p424. | |
| Rheumatoid arthritis | Suggested by: early morning stiffness. Fingers showing ‘swan neck’ or ‘boutonnière’ deformities. Thumbs show Z-deformities. MCP joints and wrists—sublux giving ulnar deviation. Knees—valgus or varus deformity and popliteal ‘Baker's’ cysts. Feet—subluxation of meta-tarsal heads with hallux valgus, clawed toes. |
| Confirmed by: rheumatoid factor +ve, ↑anti-IgG autoantibody. FBC: Normochromic anaemia, ↑ESR when active. | |
| Management: OHCM p414. | |
| Ankylosing spondylitis | Suggested by: onset over months or years. Stiffness and progressive loss of spinal movement. Kyphosis and spinal extension. |
| Confirmed by: ‘bamboo’ spine on back X-ray and loss of sacroileal joint space. Rheumatoid factor -ve, HLA-B27 +ve. | |
| Management: OHCM pp410, 418. | |
| Primary muscle disease | Suggested by: onset over weeks to years. Predominant weakness. |
| Confirmed by: CPK ↑, electromyography and muscle biopsy. | |
| Management: OHCM p420. | |
| Primary hypothyroidism | Suggested by: onset over weeks to months. Predominant fatigue. Also cold intolerance, depression. |
| Confirmed by: ↑TSH, ↓FT4. | |
| Management: OHCM p306. | |
| Early manifestation of occult malignancy | Suggested by: onset over weeks or months. Weight loss, anorexia. |
| Confirmed by: subsequent appearance of malignancy, especially spinal secondary deposits. | |
| ‘Fibromyalgia’ | Suggested by: variable onset—weeks to years. Diffuse pain and stiffness but no features of specific diagnosis. |
| Confirmed by: no ‘subsequent’ development of features of a specific diagnosis, normal ESR, Rheumatoid factor -ve, CPK normal, TSH & FT4 normal. |
Hypnagogia, or the hypnagogic state, is a brief period of altered consciousness that occurs between wakefulness and sleep, typically as people "doze off" on their way to normal sleep. During this period, thoughts can become loosely associated, whimsical, and even bizarre. Hallucinations are very common and may take the form of flashes of lights or colors, sounds, voices (hearing your own name being called is quite common), faces, or fully formed pictures. Mental imagery may become particularly vivid and fantastical, and some people may experience synaesthesia, in which experiences in one sense are experienced in anothersounds, for example, may be experienced as visual phenomena.
It is a normal stage of sleep and most people experience it to some degree, although it may go unnoticed or be very brief or quite subdued in some people. It is possible, however, to be more aware of the hypnagogic state as it occurs and to experience the effects of the brain's transition into sleep more fully.
HOW
Although there is no guaranteed technique to extend or intensify the hypnagogic state, sometimes it can be enough to simply make a conscious effort to be aware of any changes in consciousness as you relax and drop off, if practiced regularly. Trying to visualize or imagine moving objects and scenes, or passively noting any visual phenomena during this period might allow you to notice any changes that take place. Extended periods of light sleep seem more likely to produce noticeable hypnagogia, so being very tired may mean you enter deep sleep too quickly. For this reason, afternoon dozing works well for some.
Some experimenters have tried to extend or induce hypnagogia by using light arousal techniques to prevent a quick transition into deep sleep. A microphone and speaker were used in one study to feed the sound of breathing back to the sleeper. Another method is the use of "repeat alarm clocks" (like the snooze function on many modern alarm clocks)on entering sleep, subjects are required to try and maintain enough awareness to press a key every 5 minutes; otherwise, a soft alarm sounds and rouses them.
Try this yourself on public transport. Because of the low background noise and occasional external prompting, if you manage to fall asleep, dozing on buses and trains can often lead to striking hypnagogic states. In spite of this, this is not always the most practical technique, as you can sometimes end up having to explore more than your own consciousness if you miss your stop.
WHY
Very little research has been done on brain function during the hypnagogic state, partly because conducting psychology experiments with semiconscious people is difficult at the best of times and partly because many of the neuroimaging technologies are not very soporific. fMRI scanning tends to be noisy and PET scanning often involves having a drip inserted into a vein to inject radioactive tracer into the bloodstreamhardly the most relaxing of experiences. As a result, most of the research has been done with EEG (electroencephalogram) readings that involve using small scalp electrodes to read electrical activity from the brain.
Hideki Tanaka and colleagues1 used EEG during sleep onset and discovered that the brain does not decrease its activity evenly across all areas when entering sleep. A form of alpha wave activity (electrical signals in the frequency range of 8-12 Hz that are linked to relaxed states) spreads from the front of the brain to the other areas before fading away. The frontal cortex is associated with attention (among other things), and it may be that the hypnagogic state results from the progressive defocusing of attention. This could cause a reduction in normal perception filtering, resulting in loosely connected thoughts and unusual experiences.
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Some scientists have argued that the hypnagogic state is not necessarily sleep-related and may be the result of a reduction in meaningful perceptual information, perhaps leading to defocused attention or other similar effects. A study published in 20022 aimed to test this by comparing hypnagogic states with a condition in which awake participants were fed unstructured sensory information in the form of white noise and diffuse white light. The researchers used EEG recordings and found that, although participants in both conditions reported unusual visual experiences, the pattern of brain activation were quite different, suggesting that hypnagogia is more than just the result of relaxation and lack of structured sensory input.
One problem with recording electrical activity from the scalp is that activity from structures that lie deep in the brain may not be detected. This means we could be missing important information when it comes to understanding what happens as we slip from consciousness into sleep, and even back again into wakefulness (known as the hypnopompic state)particularly as deep structures (such as the brain stem, pons, thalamus, and hypothalamus) are known to be crucial in initiating and regulating sleep.
An ingenious study published in Science did manage to investigate the role of some of the deeper brain structures in hypnagogia,3 specifically the medial temporal lobes, which are particularly linked to memory function. The researchers asked five patients who had suffered medial temporal lobe damage to play several hours of Tetris. Damage to this area of the brain often causes amnesia, and the patients in this study had little conscious memory for more than a few minutes at a time. On one evening, some hours after their last game, the players were woken up just as they started to doze and were asked for their experiences. Although they had no conscious memory of playing the game, all of the patients mentioned images of falling, rotating Tetris blocks. This has given us some strong evidence that the hypnagogic state may be due (at least in part) to unconscious memories appearing as unusual hypnagogic experiences.
The concept of priming runs all the way through explanations of how perception influences behavior. Subliminal perception of photographs can prime you to prefer those photos in the future , and simply spending time with someone who is, say, rubbing his face can infect you with his mannerism . It's not necessary to consciously perceive the photographs or the gestures for them to automatically alter our behavior.
Nowhere is this truer than in exemplar activation: being exposed to ideas of stereotypes of people (the exemplars), not even the people themselves, will prime the characteristic traits of those people, and you'll begin to act in that way. It's very odd, and very cool.
HOW
Here's what John Bargh, Mark Chen, and Lara Burrows did1: they gave 30 psychology undergraduates word puzzles to do (undergraduates are the raw material for most psychology studies). In half of the experiments, the puzzles included words associated with the elderly, like "careful," "wise," "ancient," and "retired." In the other half, all the puzzle words were neutral and not deliberately associated with any single concept. Immediately after individual students had completed the puzzle, they were free to go.
Bargh and team timed, using a hidden stopwatch, how long it took each undergraduate to walk down the corridor to the elevator. Students who had been given the puzzle featuring elderly related words took, on average, a whole second longer to make the walkan increase from 7.3 to 8.3 seconds. They had picked up one of the perceived traits of the elderly: slower walking speed.
WHY
The specifics of how exemplar activation works is still an open question, but the basic mechanism is the same as how we pick up mannerisms . It's a feature of the brain that perceiving something requires activating some kind of physical representation of the thing being perceived: simply making that representation primes that behavior, making us more likely to do what we see. Exemplar activation takes this a little further than we're used to, because it's the reading of wordsin an apparently unrelated task to walking along the corridorthat primes the concept of "the elderly," which then goes on to influence behavior. But the principle is the same.
Slow walking is only the half the story, though. Ap Dijskerhuis and Ad van Knippenberg2 performed similar experiments. Instead of influencing their subjects with an "elderly" stereotype, they set up an experiment in which participants had to spend 5 minutes describing either professors or secretaries. (The subjects, again, were undergraduates.)
This time the experiment measured general knowledge, so the next stage of the experiment had the subjects answering Trivial Pursuit questions. They weren't aware the two stages were connected.
What happened is almost unbelievable: subjects who had previously described professorsknown for their perceived intelligenceattained, on average, 60% correct answers, against 46% for the people who had to describe secretaries.
It could be that people who have been considering the professor stereotype are more likely to trust their own judgment; the particular attribute of this stereotype that is causing the response isn't really known. The people exposed to the secretary stereotype didn't do any worse than they should have done: compared to people who hadn't been primed at all, they got about the same number of questions correct and worked their way through the questionnaire in only 6 minutes (compared to an 8-minute average). So in this case it turns out that both stereotypes have good qualities going for them. Secretaries are efficient. But it isn't always the case that stereotypes are positive.
People who identify with groups commonly stereotyped to be poor at math tend to do worse at math tests when their membership in that group is made relevant immediately before the test, as with a checkbox at the top of the test that asks them to indicate their ethnic identity or gender.3
Fortunately, it is possible to counteract this kind of exemplar activation. If you were in this situation, the activation can be overridden by reasserting yourself against the stereotype. Women who have been explicitly told that the math test they are about to do shows no gender bias don't underperformit's the subtle, nonconscious stereotyping that has a real effect (like having to tick a box at the top of the page), causing people who identify with a commonly stereotyped group to take on the stereotype assumption, even if incorrect. Once thinking about the stereotype and the effects it might have is made conscious, the bias disappears.
These exemplar activation experiments are as challenging as any you'll find in psychology. Word puzzles about the elderly slow your walking speed (and actually your reaction time too); just focusing on the stereotype of a professor for 5 minutes makes you better at general knowledge. But it also reinforces the stereotype: people who already hold that identity are pushed into their pigeonholes. Our need to conform runs deep, even when it's against our best interests. But in those cases, concentrating on your individuality is all you need to push back.
Find yourself a pen, preferably a nontoxic, nonleaky one. We're going to use this little item to improve your quality of life and give you a little pleasure.
HOW??
Put the pen between your teeth, in far enough so that it's stretching the edges if your mouth back without being uncomfortable. Feeling weird? Just hold it there for a little, and appraise your level of mood. You should find that you end up feeling just a little happier.
If you want to go for the reverse effect, remove the pen (maybe give it a wipe), then trap it between your upper lip and nose like a mustache. If you're feeling anything, it's likely to be a touch of gloom, particularly in contrast to when you had the pen in your mouth.
Alternatively, if you're pen-averse, refer to the pictures in and scrutinize the smiling face for a while. You should find yourself perked upwhile the unhappy photo will likely send you downhill if you stare at it a little.
WHY
Emotional expressions are much more than just by-products of our affective system, the system that deals with emotions. Expressions serve as agents that transmit emotions to other individuals and are crucial in creating and maintaining our own emotional experience. And while aspects of this may be conscious and deliberatemy girlfriend may throw me a grin to let me know she's not mad that I've been glued to the computer all evening, and that reassurance will make me happythere is a deeply automatic component. This is termed primitive contagion and is characterized as a three-stage process: it begins with perception, which triggers mimicry, which itself produces emotion. deals with how we perceive emotions, so here we`ll unpack the other two stages: mimicry and resulting emotion.
What are you paying attention to? These words? In a minute it could switch to a friend or to making coffee or to the person on the bus who just stood up and you noticed out of the corner of your eye. We don't pay attention to everything we see or experience. Following two conversations at the same time is hard, even though we hear both perfectly well, and, likewise, it's simply not possible to read every word on the page of a book simultaneously, although they're all in plain view.
While your senses work overtime to provide as much input as possible, there's a bottleneck in the brain's limited capacity for attention. So we consciously decide which line of text to focus on and read across and down the page, line by line. And this happens at the expense of all the other stimuli we could have attended to, such as the color of the walls or the traffic noise from the road outside.
Choosing what to give attention to is voluntary...mostly. But attention can also be captured.
After visual information leaves the eye, it doesn't just go to one place for processing; the signal divides. Our conscious appreciation of visual information is provided by processing done in the visual cortex. It sits at the back of the brain in the area called the occipital lobe and performs what we typically associate with the job of vision: figuring out exactly what shape the thing you're looking at is, what color, if it's moving, then in what direction and how fast, what it means, and so onproviding the raw information needed to put names to faces and avoid stepping in front of a car while crossing a road.
Attention capture, on the other hand, relies on processing done by a region of the brain called the superior colliculus. It gets a copy of the same visual information the visual cortex does from the retina, but processes it in a different way. This region is evolutionarily ancient, which means the basic structure was established and refined in brains far simpler than our own, through many species of animals. (Rather than relegating it to second place, fish and amphibians do most of their visual processing with their equivalent of the superior colliculus, called the optic lobe.) So as one might expect, it's not particularly sophisticated, compared to the visual cortex. And it doesn't use much of the information it receives; the superior colliculus looks at a black-and-white world through frosted glass. Then again, it doesn't need much. This processing is for rapid response, when it appears something potentially dangerous is happening and urgent action is needed quicker than the complex visual cortex can respond. It's just useful enough to guide reflex movements, tell the head and body to orient in a particular direction, and force attention to snap to important-seeming events.
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That's what's going on when attention is captured. There's a sudden movement and the rapid response bit of your brain says, "Hey, I don't know what that was, but pay it some attention and figure out what to do in case it attacks us." Looking at the crowd, your attention darts around automatically because this bit of your brain feels startled enough to interrupt consciousness every time somebody waves suddenly.
When you're sitting in a darkened theater, absorbed in the dialog on stage, think about what happens when a door opens at the side of the room. The sudden appearance of light grabs your attention. If it happens again, despite the fact that you know you're not interested, it still grabs your attention and demands a response. It's distracting. That's the automatic nature of attention capture coming into play.
On the upside, that bright light flashing in the corner of your eye could well be a ray of sunlight being revealed as a large dangerous something lumbering out of the shadows toward you. The automatic capture of attention serves to orient conscious perception in important directions.
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Events that capture attention include the two already mentioned: sudden light (actually, a sudden change in contrast) and sudden movement. In keeping with the purpose of facilitating rapid response, it's only new movement that captures attention. Ongoing motion, like a moving car or a walking person, doesn't trigger the automatic shift in attention.
Two other triggers provide hints as to what else our brains regard as so critical to survival that they deserve a rapid response. One is an object appearing abruptly. In general, our brains give special treatment to objectsas opposed to backgrounds and shadows, which are given less attention. This makes sense, as objects such as other people, animals or food usually require a response of some kind. There are even dedicated routines to object tracking. An extra person, rock, or car in the sceneespecially if it appears suddenlyis likely to be a big deal, so attentional capture is triggered.1
John Eastwood and his colleagues also suggest another trigger that is worth mentioning as it shows just how deep our social nature goes. The trigger here is facial expression.2 Eastwood's team made simple line-drawing faces, happy and sad ones, and asked people to count certain of the lines that made up the drawings. When the drawings were upside-down, so they were unrecognizable as faces, people did the counting exercise easily. But when the drawings were the right way up, counting took longer for drawings of faces that displayed negative emotions rather than for drawings of positive expressions. Why? The team's conclusion is that negative expressionssad or angry facesdistract you, in just the same way as light through a theater door grabs your attention away from the main action.
Injury or infection triggers a coordinated suite of physiological responses involving the brain, hormones, and immune system. The brain generates pain and fever, stress hormones mobilize energy from fat, and immune cells cause local swelling and redness. These processes are collectively known as the acute phase response because they occur rapidly and tend to subside after a few days. Medical assistance can help these unpleasant signs and symptoms to subside more quickly, even when that assistance is completely bogussuch as a witch doctor waving a rattle at you or a quack prescribing a sugar pill. This is known as the placebo effect.
Nobody knows for sure yet how the placebo effect works, but one theory is that the brain is very sensitive to the presence of social support during the process of recovery from injury and infection. The various components of the acute phase response are all designed to promote recovery and prevent further injury while recovery is taking place. Pain, for example, makes you guard the wounded area. But these measures also have costs; high levels of pain, for example, can actually lengthen the healing process. The brain makes a trade-off between the risks of further damage to the injured area and the delay to the healing process. The presence of social support during recovery shifts the balance between these competing risks because some of the burden of preventing further damage is transferred from the sick person to those around them. The sick person can therefore reduce his own costly self-protective measures, such as pain, and allow the healing process to progress more rapidly.
Another suggestion is that the placebo effect works by means of conditioning Conditioning is a very general kind of learning process in which one stimulus is substituted for another. The classic example is Pavlov's dogs, which learned to salivate on hearing a bell after Pavlov had trained them to associate the sound of the bell with the arrival of food. In technical terms, an unconditioned stimulus (the sight of the meat), which leads naturally to a certain unconditioned response (salivating at the sight of the meat), is repeatedly paired with a conditioned stimulus (the sound of the bell). Eventually, the dogs learn the conditioned response of salivating at the sound of the bell. Pavlov's students showed that immune responses can also be conditioned, and others have gone on to suggest that this is what lies behind the placebo response. The unconditioned stimulus is a real drug or some other medical treatment that works even if you have never tried it before and don't believe in it. The unconditioned response is the improvement you feel after receiving the treatment. The conditioned stimuli are all the things that are repeatedly paired with the treatmentthe size, shape, and color of the pill, for example. If you then take a pill that has the same size, shape, and color as the real one, but which lacks the active ingredient, you may still experience some improvement because your immune system has been conditioned to respond to such stimuli.
Placebos won't cure the vast majority of medical conditions. It is much easier and quicker to list the things that placebos can influencepain, swelling, stomach ulcers, some skin conditions, low mood, and anxietythan the things they don't. Everything else is probably not placebo-responsive. That said, placebos are able to help in the management of nearly all illnesses because nearly all illnesses involve pain, low mood, and/or anxiety.
| Drug induced due to excessive dose of hypotensive agent, L-dopa, carbidopa, phenothiazines, antidepressants | Suggested by: drug history. |
| Confirmed by: by resolution or improvement after stopping or reducing drug. | |
| Autonomic neuropathy due to diabetes mellitus or tabes dorsalis (rarely) | Suggested by: history of long standing diabetes (common) or tabes dorsalis (rare). Also, diarrhoea, abdominal distension and vomiting (gastroparesis), impotence, urine frequency. |
| Confirmed by: ECG monitor of beat to beat variation: <10> | |
| Management: OHCM p298. | |
| Idiopathic orthostatic hypotension | Suggested by: no other features except elderly. |
| Confirmed by: isolated phenomenon. |
| Atrial fibrillation caused by ischaemic heart disease, thyrotoxicosis, etc. | Suggested by: irregularly irregular pulse. |
| Confirmed by: ECG showing no P waves, and irregularly irregular normal QRS complexes. | |
| Management: OHCM p130. | |
| Atrial flutter with variable heart block caused by ischaemic heart disease, etc. | Suggested by: irregularly irregular pulse. |
| Confirmed by: ECG showing ‘saw tooth’ F waves, and irregularly irregular normal QRS complexes. | |
| Management: OHCM p130. | |
| Atrial or ventricular ectopics caused by ischaemic heart disease, etc. | Suggested by: regular rate with irregular dropped beat. |
| Confirmed by: ECG showing normal sinus rhythm with irregular QRS complexes not preceded by P wave, and then compensatory absence of subsequent QRS. | |
| Management: OHCM p132. | |
| Wenkenbach heart block caused by ischaemic heart disease, etc. | Suggested by: regular rate with regular dropped beat. |
| Confirmed by: ECG showing progressive prolongation of P-R interval with normal QRS complex followed by an absent QRS complex. | |
| Athletic heart | Suggested by: young/fit, asymptomatic. |
| Confirmed by: above clinical findings. | |
| Drugs | Suggested by: history e.g. beta blockers. |
| Confirmed by: improvement when drug withdrawn. | |
| Sinoatrial disease | Suggested by: elderly, ischaemic heart disease. |
| Confirmed by: ECG: abnormal P wave or P-R interval. | |
| Management: OHCM p127. | |
| Ventricular or supraventricular begemini | Suggested by: known ischaemic heart disease. |
| Confirmed by: ECG: premature ectopics with compensatory pause. | |
| Management: OHCM p126. | |
| Myocardial infarction | Suggested by: central, crushing chest pain (can be atypical pain). |
| Confirmed by: ECG: Q waves, raised ST segments, and inverted T waves. ↑CPK and troponin. | |
| Management: OHCM pp120–124. | |
| Hypothyroid | Suggested by: constipation, weight gain, dry skin, dry hair, slow relaxing reflexes. |
| Confirmed by: ↑TSH, ↓T4. | |
| Management: OHCM p306. | |
| Hypothermia | Suggested by: history of exposure to cold temperature and immobility. |
| Confirmed by: Core temperature <35(c. | |
| Management: OHCM p836. |
| Spontaneous sub-conjunctival haemorrhage | Suggested by: painless bright red area on conjunctiva (oxygenated blood) and no light sensitivity. |
| Confirmed by: clinical appearance and resolution over days. No Fl staining of cornea (not done often). | |
| Management: OHCS p432. | |
| Conjunctivitis due to bacterial infection | Suggested by: red eyes, dilated blood vessels on the eyeball and the tarsal (lid) conjunctiva with a purulent discharge ± bilateral ± gritty pain. |
| Confirmed by: above clinical appearance. Not light sensitive and no Fl stain of cornea. | |
| Management: OHCS p432. | |
| Conjunctivitis due to viral infection | Suggested by: red eyes with dilated vessels on the eyeball only, sometimes in one quadrant around the cornea with a watery ‘tap running’ discharge. Gritty pain ± impaired vision. |
| Confirmed by: Fl stain showing dendritic (branching) pattern and resolution with topical antiviral. | |
| Management: OHCS p432. | |
| Conjunctivitis due to allergy | Suggested by: red eyes with pink swollen conjunctiva and white stringy mucoid discharge. |
| Confirmed by: no Fl stain and no visual loss and resolution with chromoglycate (over six weeks) or steroid eye drops. | |
| Management: OHCS p432. | |
| Corneal ulcer (ulcerative keratitis) due to abrasion or Herpes simplex, Pseudomonas, Candida, Aspergillus, protozoa | Suggested by: painful, light-sensitive, deeply red eye with yellowish abscess in the cornea. Purulent discharge. |
| Confirmed by: slit lamp examination after fluorescein instillation showing hypopyon (pus in the eye). | |
| Management: OHCS p432. | |
| Episcleritis | Suggested by: localised red eye with superficial vessel dilatation. Mild pain. No visual loss or light sensitivity. |
| Confirmed by: Instillation of one drop of phenylephrine 2.5% causing a blanching of the lesion. | |
| Management: OHCS p432. | |
| Scleritis | Suggested by: localised area of dark red dilated superficial and deep vessel on the sclera with aching pain and tenderness. |
| Confirmed by: failure to blanche with one drop of 2.5% phenylephrine. | |
| Management: OHCS p432. | |
| Acute closed-angle glaucoma (emergency) | Suggested by: severely painful red eyeball with marked visual loss, accompanied by nausea and vomiting ± history of haloes around lights and severe headache with blurred vision. |
| Confirmed by: dull grey cornea, non reacting and irregular pupil with raised ocular pressures. | |
| Management: OHCS p430. | |
| Iritis or uveitis (see page 264) | Suggested by: redness around cornea and haze in front of iris and severe light sensitivity (photophobia). |
| Confirmed by: small non-reacting and irregular pupil. Slit lamp examination showing flare, cells and hypopyon (pus in eye). | |
| Management: OHCS p430. |
| Immature testis | Suggested by: adolescence and no testicular lump. |
| Confirmed by: normal testosterone, estrogen and LH levels normal ultrasound scan of testis. | |
| Digoxin, Spironolactone | Suggested by: taking of drug and no testicular lump. |
| Confirmed by: improvement when drug stopped. | |
| High alcohol intake | Suggested by: high alcohol intake and no testicular lump. |
| Confirmed by: improvement when alcohol stopped. | |
| Hepatic cirrhosis | Suggested by: long history of high alcohol intake (usually), spider naevi, abnormal liver size (large or small) and consistency (fatty or hard). |
| Confirmed by: very abnormal biochemical liver function tests, ↓LH, ↑oestrogens, ↓testosterone. | |
| Management: OHCM p232. | |
| Testicular tumours | Suggested by: scrotal mass ± pain, tenderness if haemorrhage occurs. (Sometimes arising in undescended testis). |
| Confirmed by: testicular ultrasound, inguinal exploration, ↑α-fetoprotein, ↑β-hCG. | |
| Management: OHCM 512. | |
| Hypogonadism (primary to testicular disease, or secondary to low LH from pituitary defect or tumour) | Suggested by: sparse pubic hair, no drug or alcohol history, poor libido. |
| Confirmed by: Testosterone↓, LH↑ (in primary testicular disease), LH↓ or normal (when secondary to pituitary diseases). | |
| Management: OHCM pp316, 318. | |
| Bronchial carcinoma | Suggested by: smoking history, haemoptysis, weight loss, clubbing. |
| Confirmed by: CXR, bronchoscopy with biopsy. | |
| Management: OHCM p182. | |
| Klinefelter's syndrome | Suggested by: poor sexual development, infertility, eunuchoid. |
| Confirmed by: 47, XXY karyotype. | |
| Obesity | Suggested by: no breast tissue, only mammary fat. |
| Confirmed by: improvement with weight loss. | |
| Management: OHCM p208. |
| Chronic bronchitis | Suggested by: grey sputum, slow progression over years and a smoker (nearly always). |
| Confirmed by: grey sputum >3 months over two consecutive years. | |
| Management: OHCM p188. | |
| Acute viral bronchitis | Suggested by: onset over hours or days. Fever, white/yellow sputum. |
| Confirmed by: no consolidation on CXR, quick spontaneous resolution. | |
| Acute bacterial bronchitis | Suggested by: onset over hours or days. Fever, mucopurulent sputum, dyspnoea. |
| Confirmed by: sputum culture and sensitivities, response to appropriate antibiotics. | |
| Management: OHCM p188. | |
| Pneumonia | Suggested by: onset over hours or days. Rusty brown sputum (i.e. purulent sputum tinged with blood). Sharp chest pain worse on inspiration, pleural rub, fever, cough, consolidation etc. |
| Confirmed by: patchy shadowing on CXR and sputum/blood culture. | |
| Management: OHCM pp173–6. | |
| Bronchiectasis | Suggested by: progression over months or years. Finger clubbing, cupful(s) of pus-like sputum per day. Coarse late inspiratory crepitations. |
| Confirmed by: CXR: cystic shadowing; high resolution CT chest: honeycombing and thickened dilated bronchi. | |
| Management: OHCM pp178, 179. | |
| Lung abscess | Suggested by: copious amount of foul smelling pus/brown sputum, haemoptysis, high swinging fever, chest pain over weeks, usually preceded by a prior significant respiratory infection (e.g. pneumonia). |
| Confirmed by: fluid level in cavity on CXR, CT chest, response to physiotherapy, antibiotics and aspiration. | |
| Management: OHCM pp176, 618. |
| Acute pulmonary oedema | Suggested by: onset over minutes or hours of shortness of breath, orthopnoea, displaced apex, loud 3rd heart sound, fine crackles at lung base. |
| Confirmed by: CXR appearance (see 640) poor LV function on echocardiogram. | |
| Management: OHCM pp136–8, 786. | |
| Mitral stenosis | Suggested by: months or years of orthopnoea, mitral facies, tapping, displaced apex, loud 1st heart sound, diastolic murmur, fine crackles at lung base. Enlarged left atrial shadow (behind heart) and splayed carina on CXR. |
| Confirmed by: large left atrium and mitral stenosis on echocardiogram. | |
| Management: OHCM p146. |
Eye opening
Spontaneous 4
To speech 3
To pain 2
No response 1
Verbal response
Orientated 5
Confused: talks in sentences but disorientated 4
Verbalizes: words not sentences 3
Vocalizes: sounds (groans or grunts) not words 2
No vocalization 1
Motor response
Obeys commands 6
Localizes to pain: e.g. brings hand up beyond chin to supraorbital pain 5
Flexion withdrawal to pain: no localization to supraorbital pain but flexes elbow to nail bed pressure 4
Abnormal flexion to pain 3
Extension to pain: extends elbow to nail bed pressure 2
No response 1
