bluuebunny/crossref_metadata_2025 huggingface dataset:
Horse Nations
Authors: Mitchell Peter
Published: November 2020

The Native American on a horse is an archetypal Hollywood image, but though such equestrian-focused societies were a relatively short-lived consequence of European expansion overseas, they were not restricted to North America's Plains. Horse Nations provides the first wide-ranging and up-to-date synthesis of the impact of the horse on the Indigenous societies of North and South America, southern Africa, and Australasia following its introduction as a result of European contact post-1492. Drawing on sources in a variety of languages and on the evidence of archaeology, anthropology, and history, the volume outlines the transformations that the acquisition of the horse wrought on a diverse range of groups within these four continents. It explores key topics such as changes in subsistence, technology, and belief systems, the horse's role in facilitating the emergence of more hierarchical social formations, and the interplay between ecology, climate, and human action in adopting the horse, as well as considering how far equestrian lifestyles were ultimately unsustainable.
Introducing Horse Nations
Authors: Mitchell Peter
Published: November 2020

Hidden by rocks near a waterhole in Australia’s desert interior an Aboriginal woman and her children catch their first sight of the shockingly large animal of which they have previously only heard: the newcomer’s kangaroo. Thousands of kilometres to the west and high in southern Africa’s mountains a shaman completes the painting of an animal that does not exist, horned at the front, bushy tail at the rear, a composite of two species, one long familiar, the other new. Across the Atlantic Ocean on the grasslands of Patagonia the burial of an Aónik’enk leader is in its final stages, four of his favourite possessions killed above the grave to ensure his swift passage to the afterlife. To the north in what Americans of European descent call New Mexico, Diné warriors chant the sacred songs that ensure their pursuers will not catch them and that they will return safely home. And on the wintry plains of what is not yet Alberta, Siksikáwa hunters charge into one of the last bison herds they will harvest before the snows bring this year’s hunting to an end. Two things unite these very different scenes. First, though we cannot be sure, the historical, ethnographic, and archaeological sources on which they are based allow for them all happening on precisely the same day, sometime in the 1860s. Second, all concern people’s relationship with one and the same animal—pindi nanto, karkan, kawoi, ∤íí’, ponokáómita·wa—the animal that English speakers know as ‘horse’. And that simple fact provides the basis for this book. For, before 1492, horses were confined to the Old World—Europe, Asia, and Africa north of the tropical rainforests and a line reaching east through South Sudan, Ethiopia, and Somalia to the sea. They were wholly unknown in Australasia, the Americas, or southern Africa. As a result, the relationships implied by the vignettes I have just sketched, as well as those involving Indigenous populations in Colombia, Venezuela, Brazil, Paraguay, Uruguay, Chile, Mexico, South Africa, and New Zealand, evolved quickly. And they were still evolving when these societies were finally overwhelmed by European colonization.
South America I: Caribbean Deserts and Tropical Savannahs
Authors: Mitchell Peter
Published: November 2020

These two quotations, dating to within almost a decade of each other, refer to very different parts of South America, the first the La Guajira Peninsula at its northern tip, the second the savannahs of the Gran Chaco at its very heart. The Wayúu, dwelling in the first, had no direct connection with the Mbayá of whom Dobrizhoffer wrote here (though he is more famous for his work on their cousins, the Abipones). Nevertheless, both regions shared aspects of their respective experiences of colonial intrusion and settlement: the frequent adoption not just of horses but also of other exotic species like cattle and sheep; Spanish use of missionaries to try and pacify their Indigenous inhabitants; and the fact that the latter could play off one European power, or Spanish province, against another, thereby maintaining their own freedom of action. Aiding the Native peoples in this was their geographically, politically, and economically marginal position with respect to the main foci of colonial power in the Andes and along the Atlantic. Spain began exploiting Venezuela’s pearl fisheries as early as 1508, even settling on the mainland from 1522, but the real impetus to conquest in South America came only with Francisco Pizarro’s invasion of the Inka Empire in 1533. The highlands of Peru, Bolivia, Ecuador, and Colombia (the latter never part of Inka domains), the lowlands between them and the Pacific Ocean, the northern half of Chile, and the northwestern corner of Argentina all passed quickly—if not always easily—under Spanish control. So too did parts of Paraguay, settled by following rivers inland from the Atlantic. Portugal, on the other hand, secured for herself the coast of Brazil, eventually expanding her reach across virtually the entire Amazon Basin. Horses were as much a part of the conquistadores’ repertoire in South America as in Mexico. They sowed panic when Pizarro first confronted Inka troops at Cajamarca in 1533, but Native American surprise and fear did not last. Inka armies quickly devised tactics to neutralize the effects of horses on the battlefield in vain efforts to expel the invader.
Putting Horse Nations in Context
Authors: Mitchell Peter
Published: November 2020

Set against the millennia in which people have herded or hunted horses, the few centuries on which this book concentrates were short-lived. Only 350 years, or 14 human generations, passed between the Araucanians and Chichimecs first acquiring horses and the world-wide closure of colonial frontiers at the close of the nineteenth century. Yet in that time many different equestrian adaptations emerged. This chapter looks for patterning within them and sets out some of the directions in which future studies of Horse Nations might progress. It also draws parallels with the historical experience of equestrian nomads in Eurasia and the ethnically mixed cattle frontiers of Latin America, asks how far an equestrian way of life turned those who committed to it into pastoralists, and enquires into the circumstances—ecological and political—that favoured, or discouraged, the adoption of horses. Recognizing their agency, as well as that of people, it tries to gauge the importance of horses relative to other factors in the histories of the societies that adopted them, before asking where those Horse Nations are now. Having looked at four continents, four centuries, and well over forty Indigenous groups, what stands out is surely the diversity of Native societies that made horses their own. Employed to hunt deer to make European trousers in eighteenth-century Mississippi, on the North American Plains horses led to a wholesale reorganization of how people used bows and arrows to kill bison. In Patagonia, by contrast, where guanaco and rhea were the main prey, they encouraged that same technology to disappear, replaced by a much older weapons system, the bolas, while in southern Africa eland came to be killed with metal spears, not poisoned arrows. The variety of ways in which people hunted from horseback offer just one illustration of an unsurprising fact: not all Horse Nations were alike. Much the same can be said of the details of the equipment people employed to ride, or the variations in how they transported household possessions, and even houses: the travois, for example, was unique to the Plains and to nearby groups influenced by their inhabitants.
Principles of management of the badly broken down tooth
Authors: Banerjee Avijit , Watson Timothy F.
Published: November 2020

This textbook has covered the common causes of broken down teeth: dental caries, tooth wear, and trauma. In addition, long-term failure of parts, or all, of the existing tooth–restoration complex can be significant and may require further operative intervention for its successful management (see Chapter 9). Many intra-coronal defects can be repaired with direct adhesive restorations, as discussed in Chapters 5 and 9. However, the situation can be complicated by the loss of significant portions of existing restoration or tooth structure (e.g. cusps, buccal/lingual walls), which influence the restorative procedures used in an attempt to maintain the tooth longevity, as well as pulp viability, for as long as possible. For direct restorations to succeed clinically, they require healthy dental tissues to aid support, retention, and ideally provide an element of protection from excessive occlusal loads. With diminishing amounts of tooth structure to work with, greater thought and care are required to manage and prepare the remaining viable hard tissues to support and retain the larger restoration. The core restoration describes the often large direct plastic restoration used to build up the clinically broken down crown. It is retained and supported by remaining tooth structure wherever possible (sometimes including the pulp chamber and posts in root canals of endodontically treated teeth). These large restorations often benefit from further overlying protection to secure their clinical longevity, by means of indirect onlays, and partial or full coverage crowns. Before carrying out a detailed clinical examination of the individual tooth and the related oral cavity, it is always important to justify your clinical decisions, for both operative and non-operative preventive interventions. The five key reasons for minimally invasive (MI) operative intervention are:… • to repair hard tissue damage/cavitation caused by the active, progressing caries/tooth-wear process (where non-operative prevention has failed repeatedly) • to remove plaque stagnation areas within cavities/defects which will increase the risk of caries activity due to the lack of effective plaque removal by the patient • to help to manage acute pulpitic pain caused by active caries by removing the bacterial biomass and sealing the defect, thereby protecting the pulp • to restore the tooth to maintain structure and function in the dental arch • aesthetics.
Long-term management of direct restorations
Authors: Banerjee Avijit , Watson Timothy F.
Published: November 2020

As has been emphasized throughout this book, minimum intervention oral/dental care involves more than just the minimally invasive operative treatment of the consequences of dental disease. It involves identifying and predicting disease patterns, and concerns the control/ prevention of disease by modifying aetiological factors and reassessing the adherence to changes in patient behaviours, attitudes, and responsibility. Monitoring the oral cavity and restored dentition ensures that the treatment undertaken, and subsequently improved oral health, is maintained. This should be accomplished through individualized strategic recall regimes. Restorations need to be reviewed regularly and occasionally refurbished, resealed, repaired, or replaced (see Figures 9.1, 9.2, and 9.3, and Section 9.5). Therefore periodic recall appointments, once an episode of treatment has been completed, are just as important as the treatment itself. It is critical that the patient understands the importance of these recall consultations as part of the ongoing care that is being offered to help to maintain their oral health. Three aspects of dental care need to be assessed at recall visits:… • the overall state of the patient’s oral and dental health (review) • the individual patient’s longer-term response/adherence to previous preventive advice and/or treatment, in moderating any aetiological factors that could cause future dental disease (reassessment) • the status and quality of the restorations present (monitoring and maintenance)…. The potential causes of restoration failure have been identified and outlined in Table 9.1. It is important to appreciate that the causes of restoration and tooth failure (see Table 9.2) are often multifactorial in nature. Indeed, as the causes of both tooth and restoration failure are inextricably linked, it is wise to consider them together, as a tooth–restoration complex. The multifactorial aetiology of restoration failure is often due to manifestations of inherent long-term weaknesses in the mechanical properties of different restorative materials (e.g. poor edge strength, wear, compressive strength, water absorption, etc.) and/or problems with the technical application of the restorative material for the chosen clinical situation (i.e. incorrect choice of material and poor placement technique). The chemistry and physical properties of the different direct, plastic restorative dental materials at a dentist’s disposal have been discussed in Chapter 7.
Conclusion : What Future Should We Want?
Authors: Susskind Richard , Susskind Daniel
Published: November 2020

In the long run, increasingly capable machines will transform the work of professionals, giving rise to new ways of sharing practical expertise in society. This is the central thesis of our book. We cannot commit to timeframes, in large part because the speed of change is not in our hands. But we are confident that the change will constitute an incremental transformation rather than an overnight revolution. In the language of the book, the shift itself can be characterized in many ways: as the industrialization and digitization of the professions; as the routinization and commoditization of professional work; as the disintermediation and demystification of professionals. Whatever terminology is preferred, we foresee that, in the end, the traditional professions will be dismantled, leaving most (but not all) professionals to be replaced by less expert people and high-performing systems. We expect new roles will arise, but we are unsure how long they will last, because these too, in due course, may be taken on by machines. In the post-professional society, we predict that practical expertise will be available online. Our strong inclination is to encourage the removal of current and future gatekeepers, and to provide people with as much access as is feasible to this collective knowledge and experience. The final step in our argument is to explain why we think that it is desirable to liberate practical expertise in this way. When we speak above and throughout about technology and its impact on the professions, we are conscious that it might sound as though we believe the future is already mapped out in detail and is somehow inevitable— that we are hardline ‘determinists’. Our analysis in Chapter 4, for example, makes it clear that we expect machines to become increasingly capable, that devices will be increasingly pervasive, and that human beings will be increasingly connected. And we certainly do anticipate an exponential growth in information technology. While we do not foresee these developments unfolding as a matter of necessity, we do regard them as extremely probable (barring asteroids, nuclear wars, pandemics, or the like). However—and this is where we part company with determinists—this does not mean that human beings have no control over future direction.
Headache
Authors: Farne Hugo , Norris-Cervetto Edward , Warbrick-Smith James
Published: November 2020

The sinister causes can be remembered using the mnemonic VIVID: . . . Vascular: subarachnoid haemorrhage (SAH), haematoma (subdural or extradural), cerebral venous sinus thrombosis, cerebellar infarct Infection: meningitis, encephalitis Vision-threatening: temporal arteritis, acute glaucoma, cavernous sinus thrombosis, pituitary apoplexy, posterior leucoencephalopathy Intracranial pressure (raised): space-occupying lesion (SOL; e.g. tumour, abscess, cyst), cerebral oedema (e.g. trauma, altitude), hydrocephalus, malignant hypertension, idiopathic intracranial hypertension Dissection: carotid dissection . . . The approach to headache is the same as that to pain anywhere in the body: you need to start by characterizing the pain. One useful way of doing this is by following another mnemonic, SOCRATES: . . . Site of pain, and has it moved since it began? Onset of pain—was it sudden or gradual, and did something trigger it? Character of pain—throbbing, dull ache, sharp stabbing? Radiation of pain—has the pain spread? . . . Attenuating factors—does anything make the pain better (e.g. position, medications)? Timing of pain—how long has it gone on for, has it been constant or coming and going? Is it worse at a particular time of the day? Exacerbating factors—does anything make the pain worse (e.g. lying down, standing up, coughing, fatigue)? Severity—on a scale of 0 to 10, where 10 is the worst pain ever (e.g. childbirth). In addition, you should enquire about the presence or absence of the following ‘red flags’: • Decreased level of consciousness. This is a worrying feature of any medical presentation. Combined with headache, SAH needs exclusion. If there is a history of head injury, it could suggest a subdural haematoma (fluctuating consciousness) or extradural haematoma (altered consciousness following a lucid interval). Meningitis and encephalitis can also affect consciousness. • Sudden onset, worst headache ever. Suggests SAH, with blood in the cerebrospinal fluid (CSF) irritating the meninges. It can be informative to ask the patient whether they remember the exact moment when the headache started—a very severe headache of almost instantaneous onset is characteristic of SAH. Patients describe it like, for example, ‘being hit on the back of the head with a bat’.
Dysphagia
Authors: Farne Hugo , Norris-Cervetto Edward , Warbrick-Smith James
Published: November 2020

When a patient says ‘swallowing difficulty’, they could mean: • Dysphagia: difficulty swallowing. If they really mean dysphagia, try to understand when/where exactly it feels as though the food ‘gets stuck’. Those with high dysphagia (oropharyngeal and upper oesophageal) describe difficulty initiating a swallow or immediately upon swallowing. Those with low dysphagia (lower oesophageal) feel the food getting stuck a few seconds after swallowing. • Odynophagia: painful swallowing. Odynophagia may be due to malignancy, but is more commonly a feature of infection such as candidiasis. • Globus: the common sensation of having a lump in the throat without true dysphagia. Globus is very common and its aetiology is poorly understood—however, only a small proportion of affected patients will seek medical help and it is an entirely benign condition. Broadly speaking, high dysphagia is more likely to be due to generalized/systemic neuromuscular disease, whereas low dysphagia is more likely to be due to a local obstructing lesion. New-onset dysphagia in middle-aged to elderly patients is carcinoma until proven otherwise. • What is the duration of the symptoms? This is a key question: a food bolus stuck in the oesophagus will typically appear immediately during a meal; cancer typically presents with a short history of days to weeks (not because the cancer has appeared in such a short space of time, but because it has reached a size where symptoms rapidly become apparent), whereas chronic motility disorders such as achalasia present with symptoms lasting months to years. • Is the dysphagia progressive or intermittent? Progressive dysphagia is highly suggestive of a stricture (benign or malignant), whereas intermittent symptoms are more characteristic of motility disorders. • Is the dysphagia to solids, fluids, or both? If the patient is able to swallow fluid as normal but has difficulty with solid food items (which feel as if they are sticking) this points towards a mechanical obstruction, i.e. a stricture (benign or malignant). Of course, as the stricture becomes more severe, then the dysphagia may start to involve fluids as well.
Haemoptysis
Authors: Farne Hugo , Norris-Cervetto Edward , Warbrick-Smith James
Published: November 2020

You need to ensure that you are not mistaking haemoptysis with: • Haematemesis: brownish-red blood that is vomited from the gastrointestinal (GI) tract. • Epistaxis (nosebleed): particularly a posterior nosebleed. • Bleeding gums: combined with a cough, this may be confused with true haemoptysis. To tell if it is really haemoptysis, you can ask the patient where they think the blood is coming from (they may say it initially dripped from their nose), its colour (darker, coffee-ground appearance suggests partially digested blood), any history of nosebleeds, nausea, vomiting, gastric disease, or alcoholism. For the latter, asking if he is an alcoholic is unlikely to yield a valid response. Instead, you can try the TACE questions to detect alcohol dependence: . . . Does it Take more than three drinks to make you feel high? Have you ever been Annoyed by people’s criticism of your drinking? Are you trying to Cut down on drinking? Have you ever used alcohol as an Eye-opener in the morning? A positive response to the first question scores 2 points and a positive response to each of the rest, scores 1 point each. A positive response to two of these four questions is considered to indicate possible alcohol abuse or dependence as does a total score of two or more points. Haemoptysis should always be investigated thoroughly for two reasons: 1 It may be the presenting symptom for life-threatening lung disease. 2 Massive haemoptysis, variably defined as anything from >100 mL to >1000 mL over 24 hours, may be life-threatening itself, usually through asphyxiation but potentially also shock. Haemoptysis is thus a ‘red flag’ symptom and any patient with haemoptysis requires a thorough diagnostic work-up. These can be grouped together under a ‘surgical sieve’—we have used INVITED MD: Infective: pulmonary tuberculosis (TB), bronchitis, pneumonia, lung abscess, mycetoma Neoplastic: primary lung cancer, metastatic lung cancer Vascular: pulmonary embolism, left ventricular failure, bleeding diathesis (i.e. a bleeding tendency e.g. coagulopathy, severe thrombocytopenia), arteriovenous malformation, vascular–bronchial fistula Inflammatory: granulomatosis with polyangiitis (formerly called Wegener’s granulomatosis), Goodpasture’s syndrome, systemic lupus erythematosus, hereditary haemorrhagic telangiectasia (Osler–Weber–Rendu syndrome), polyarteritis nodosa, microscopic polyangiitis
Breast lump
Authors: Farne Hugo , Norris-Cervetto Edward , Warbrick-Smith James
Published: November 2020

The four most common diagnoses for a breast lump are: • Benign cystic change (also known as fibrocystic change, fibroadenosis, or benign breast change) • Fibroadenoma • Cyst • Carcinoma If we consider women of all ages, there are a number of other potential diagnoses: • Fat necrosis • Periductal mastitis • Abscess • Galactocele • Phyllodes tumour • Sarcoma • Duct papilloma • ‘Non-breast’ lumps, e.g. lipoma, sebaceous cyst, prominent costal cartilage/rib. The age of the patient is one of the most useful pieces of information for narrowing the differential. As an approximate guide, the most common diagnoses in the following age groups are: • <30 years: physiologically normal lumpy breast; benign cystic change; fibroadenoma; abscess (if breast-feeding); galactocele (if breast-feeding) • 30–45 years: benign cystic change; cyst; abscess (especially smokers); carcinoma • 45–60 years: cyst; abscess (smokers); carcinoma • >60 years: carcinoma ▲ Note: It is worth emphasizing that breast cancer is possible in all ages, is common, and is potentially very serious. Therefore you must exclude it in any presentation of breast lump, regardless of how benign it seems. Failure to diagnose breast cancer is one of the most common malpractice claims in the USA. Galactoceles may occur during or shortly after the cessation of lactation. They may present as a firm mass (often subareolar) and are caused by the obstruction of a lactiferous duct. The duct gradually becomes more distended with milk and epithelial cells, and may rarely be complicated by a secondary infection leading to abscess formation. Clinically, a galactocele is very similar to a cyst on examination. In addition, lactating women are predisposed to mastitis (whether or not they have a galactocele). The causative organisms are usually skin commensals such as Staphylococcus aureus or Staphylococcus epidermidis—this is in contrast to the periductal mastitis and abscess formation seen in older women, in whom anaerobic bacteria may also be implicated. Two of the greatest risk factors for breast cancer are being female and increasing age. Otherwise, the following are recognized as important factors: • Previous breast cancer • Family history of breast cancer. Suspicions should be raised if: ■ Three close blood relatives (on the same side of the family) develop breast cancer at any age
Nausea and vomiting
Authors: Farne Hugo , Norris-Cervetto Edward , Warbrick-Smith James
Published: November 2020

The vomiting centre (mainly histamine and acetylcholine receptors) in the medulla oblongata can be activated by four main input systems shown in Figure 13.1: the vestibular system, the central nervous system, the chemoreceptor trigger zone (in the fourth ventricle of the brain), and cranial nerves IX and X. With these four inputs in mind, it becomes easier to understand some of the pathologies that can activate the vomiting centre and cause nausea and vomiting, as is shown in Figure 13.2. • Contents ■ Undigested: oesophageal disorders, e.g. achalasia, pharyngeal pouch ■ Partially digested: gastric outlet obstruction, gastroparesis (delayed stomach emptying, e.g. seen in diabetes mellitus) ■ Bile (green): small bowel obstruction (distal to the ampulla of Vater) ■ Faeculent: distal intestinal or colonic obstruction. Note: the only time you will see faecal (i.e. true faeces), as opposed to faeculent (i.e. foul looking), vomiting is in patients with a gastrocolonic fistula… or coprophagia ■ Blood/coffee-ground: haematemesis (see Chapter 5) ■ Large volume: less likely to be functional. • Timing ■ Early morning: classically in pregnancy and raised intracranial pressure. ■ Duration: this is useful in identifying the severity (patients with severe nausea and vomiting present early) and a longer time course makes acute pathologies such as bowel obstruction less likely, as untreated this will either deteriorate or resolve. • Association with eating? ■ Vomiting within an hour of eating suggests an obstruction high in the gastrointestinal (GI) tract proximal to the gastric outlet. If this is the case, you should ask about peptic ulcer disease (or a history of dyspepsia) as this can cause scarring and pyloric stenosis. ■ Vomiting after a longer postprandial delay is consistent with an obstruction lower in the GI tract, usually in the small bowel. ■ Early satiety, postprandial bloating, and abdominal discomfort together suggest gastroparesis or outlet obstruction. • Use the SOCRATES mnemonic to characterize the pain (see Chapter 12). • The site is indicative of certain pathologies (e.g. right upper quadrant suggests a hepatobiliary cause, epigastric suggests a pancreatic or gastroduodenal cause). However, localization of pain is far from accurate in abdominal pathology due to the neural wiring and embryology, and also anatomical variations.
Jaundice
Authors: Farne Hugo , Norris-Cervetto Edward , Warbrick-Smith James
Published: November 2020

The metabolism of bilirubin in humans is summarized in Figure 14.1 and can be divided into three sequential steps: 1 Production of unconjugated bilirubin. Red blood cells are broken down by macrophages (mainly in the spleen), which degrade haemoglobin into iron and unconjugated (water insoluble) bilirubin. The iron is stored inside transferrin proteins. Unconjugated bilirubin travels to the liver bound to albumin. In disease, unconjugated bilirubin can be produced by haemolysis of red cells intravascularly, rather than in the spleen. 2 Conjugation of bilirubin. Liver hepatocytes uptake unconjugated bilirubin and conjugate it to glucuronate, thus making water soluble, conjugated bilirubin. 3 Excretion of bilirubin. Once conjugated, bilirubin is secreted into the bile canaliculi. Conjugated bilirubin flows with bile down the bile ducts and into the duodenum. Inside the bowel, conjugated bilirubin is metabolized by bacteria into colourless products (urobilinogen, stercobilinogen). Some of these can be reabsorbed by the gut and excreted via the kidneys, but the vast majority are oxidized in the gut into coloured pigments (urobilin, stercobilin) which give faeces their brown colour. Consequently, if there is complete obstruction of the bile ducts there will be no flow of conjugated bilirubin into the gut, no conversion into urobilinogen, and therefore not even a trace of urobilinogen in the urine. The terminology is confusing because different people mean different things. If you are going to use this terminology, make sure that you and your colleagues agree on the definitions. Nonetheless, this is what people usually mean: • Prehepatic jaundice: this refers to jaundice caused by an excessive production of bilirubin. Remember that bilirubin is produced by the breakdown of haemoglobin in the blood vessels or the spleen, hence the term prehepatic. • Hepatic jaundice: for some people, this means any jaundice due to pathology in the liver (anatomically), such as points 3, 4, and 5 in Figure 14.1, and can thus include problems with hepatocytes (e.g. hepatitis) or with the bile canaliculi (e.g. primary sclerosing cholangitis, PSC).
Poor urinary output
Authors: Farne Hugo , Norris-Cervetto Edward , Warbrick-Smith James
Published: November 2020

You should ask the nurse: • What the trend is in urine output—has it been gradually decreasing, or suddenly stopped? If the latter, have they checked if the urinary catheter is blocked by flushing it? This is a rapidly reversible cause of poor urinary output. • What the observations are for the patient. Ask for the heart rate, blood pressure, respiratory rate, oxygen saturations, and temperature, so you can get an idea of how unwell the patient is. This will help you prioritize how soon you need to see the patient. Healthy adults have a urine output of about 1 mL/kg/hour. Oliguria refers to a reduced urine output and is defined variously as <400 mL/day, <0.5 mL/kg/hour, or <30 mL/hour. Anuria refers to the complete absence of urine output. Decreased urine output should be taken very seriously as it may be the first (and only) sign of impending acute renal failure. Untreated, patients may die from hyperkalaemia, profound acidosis, or pulmonary oedema due to the kidneys not performing their usual physiological role. Normal urine output requires: • adequate blood supply to the kidneys • functioning kidneys, and • flow of urine from the kidneys, down the ureters, into the bladder, and out via the urethra. Pathology affecting any of these requirements can result in poor urine output, which is why the differential diagnosis for poor urinary output is often classified as shown in Figure 22.1. In practice, as a junior doctor you want to diagnose and treat the prerenal and postrenal causes. If you come to the conclusion that it is a renal cause (by exclusion), call the renal physicians for an expert opinion. This is crucial in determining the diagnosis: • Adequate intake? Remember that an adult of average size will require about 3 L of fluid intake per 24 hours (30–50 mL/kg/day). Febrile patients will require an extra 500 mL for every 1 °C above 37.0 °C to compensate for increased loss of fluids from evaporation and increased respiratory rate.
Polyuria
Authors: Farne Hugo , Norris-Cervetto Edward , Warbrick-Smith James
Published: November 2020

In both polyuria and high urinary frequency the patient will be passing urine more often than before. But in polyuria, patients will pass abnormally large volumes of clear urine each time. In urinary frequency, the volume voided each time will be normal or reduced. The only way of knowing objectively whether this is the case is by collecting a 24-hour urine sample (>3 L = polyuria). As this is usually impractical outside of hospital, one must rely on the patient’s recall, with the caveat that many patients find it difficult to estimate urine output. In the history, then, ask them whether they feel they are passing a larger volume every time they go to the toilet. Remember that it is important to be as sure as you can that you are dealing with polyuria and not urinary frequency or nocturia, as the differential diagnoses are quite distinct. Chronic renal failure and hypercalcaemia (e.g. due to bone metastases) cause polyuria by inducing nephrogenic diabetes insipidus. Similarly, steroids and Cushing’s syndrome can cause polyuria by causing diabetes mellitus. • Temporal pattern of urine output (number of times in the day and at night), especially nocturia. At night, the kidneys concentrate urine in order to retain fluid (as intake is zero), removing the need to urinate during sleep. Thus nocturia (in the absence of other causes of nocturia, e.g. benign prostatic hyperplasia (BPH)) is often one of the earliest signs of a loss of concentrating ability. This symptom makes primary polydipsia less likely. • Fatigue, weight loss, recurrent infections. All can be features of diabetes mellitus. • Lower urinary tract symptoms (LUTS), e.g. frequency, urgency, hesitancy, terminal dribbling, incomplete voiding. These symptoms indicate pathology in the bladder or the outflow tract, e.g. prostatism in men, detrusor instability and prolapse in women. Not strictly speaking polyuria. • Pain, frequency, change in urine colour and smell. These are all symptoms suggestive of a urinary tract infection (UTI), which would cause increased frequency but not polyuria. • Past medical history. Look for any history of renal problems or conditions that may precipitate chronic renal failure (e.g. vasculitides, hypertension, chronic urinary retention).
Groin lump
Authors: Farne Hugo , Norris-Cervetto Edward , Warbrick-Smith James
Published: November 2020

Considering the anatomy and associated pathology in a systematic fashion, the lump may represent: • Psoas sheath → psoas abscess or psoas bursa • Femoral nerve → neuroma • Femoral artery → femoral aneurysm or pseudoaneurysm • Femoral vein/long saphenous vein → saphena varix (dilated great saphenous vein due to incompetence at the saphenofemoral junction) • Lymph nodes → lymphadenopathy (infectious or malignant) • Hernial orifices → inguinal hernia, femoral hernia • Testicular apparatus → ectopic testis, undescended testis, hydrocele of cord • Skin/subcutis → lipoma, infected abscess (e.g. from intravenous (IV) drug use), sebaceous cyst. In common with lumps anywhere on the body, you will need to establish: • How long has the lump been there? Many of the diagnoses listed in Figure 24.1 will develop rather insidiously, but there are some that may have a rather shorter history. For example, a patient may develop a femoral artery pseudoaneurysm (a collection of blood outside the vessel lumen) following angiography, a direct inguinal hernia may be precipitated by a period of heavy lifting, or inguinal lymphadenopathy may follow a lower limb infection. Ectopic or undescended testes would be present from birth, but it is extremely unlikely that a man would reach adulthood in the Western world without having had this defect corrected by orchidopexy (orchid = testis, -pexy = fixation in correct position) or orchidectomy (orchid = testis, -ectomy = removal). • Is the lump always there? Does it reduce when the patient lies down? This question relates to hernias and saphena varix. Increases in intra-abdominal pressure, for example during coughing or straining at stool, may cause hernias to increase in size. A saphena varix may increase in size if the patient stands for long periods of time as retrograde flow through incompetent venous valves will allow blood to pool. A saphena varix will disappear completely when the patient lies down. • Has the lump got bigger, smaller, or stayed the same size? Almost all of the pathologies on our differential (with the possible exception of ectopic/undescended testes) may change in size over time.
Swollen calf
Authors: Farne Hugo , Norris-Cervetto Edward , Warbrick-Smith James
Published: November 2020

The main causes of an acutely swollen calf are shown in Figure 28.1. Note that it is possible for different pathologies to coexist: a patient may present with a deep vein thrombosis (DVT) and ruptured Baker’s cyst, for example. Also, many patients will get a swollen leg following surgery to that leg, but this shouldn’t present much of a diagnostic challenge (although you must obviously exclude DVT if the symptoms and signs warrant this) and therefore this is not included in the list in Figure 28.1. Yes, because most of the diseases listed in Figure 28.1 are local diseases and it would be highly unlikely for the patient to have two similar events in both legs at the same time. Instead, it would be more likely that the patient has either a systemic problem or a problem affecting central vessels. However, it is worth remembering that a DVT can arise in a patient with pre-existing bilateral leg oedema, so don’t rule out a DVT just because both legs are swollen. Figure 28.2 gives the main causes of bilateral swollen legs. • Are there any risk factors for venous thrombosis? Consider Virchow’s triad: ■ Hypercoagulable blood? Trauma, major surgery within the last 3 months, pregnancy and postpartum state (women are at increased risk of a venous clot for 6 weeks after birth and the risk is actually higher during the first few weeks after birth than during pregnancy itself), inflammatory bowel disease, active cancer, obesity (body mass index (BMI) >30 kg/m2), combined oral contraceptive pill or hormone replacement therapy (HRT), family history or past medical history of DVTs. ■ Stasis? Bed rest (>3 days) or long-haul travel (the actual length of flight that qualifies as ‘high risk’ is controversial). ■ Vessel injury? Trauma, surgery. • Has she felt breathless, had any chest pain, or coughed up any blood? If DVT is high on your differential list, it would be wise to enquire about symptoms of a possible pulmonary embolism (PE).
Leg ulcer
Authors: Farne Hugo , Norris-Cervetto Edward , Warbrick-Smith James
Published: November 2020

Venous ulcers account for by far the majority (about 70%), with mixed arterial/venous (about 10%) and arterial (about 10%) most of the remainder. Pressure ulcers have become increasingly common because of the increase in elderly, frail, and relatively immobile patients. The other causes are relatively rare with the exception of neuropathic ulcers in patients with diabetes mellitus. Note that many leg ulcers may have a multifactorial aetiology, i.e. they may involve more than one of the pathologies listed in Figure 29.1. The first thing is to ask about the ulcer. You should consider: • Is the ulcer painful? ■ Venous ulcers are caused by venous stasis in the leg and are thus less painful when elevated and drained of blood. However, only about 30% of venous ulcers are painful. ■ Arterial (atherosclerotic) ulcers are caused by ischaemia to the leg and are thus more painful when elevated and drained of blood. Patients often say the ulcers are painful enough to wake them up at night and that they obtain relief by lowering their leg over the side of the bed. ■ Neuropathic ulcers are caused by loss of sensation (which predisposes to constant trauma) and are thus not painful. ■ Pressure ulcers are caused by, as the name suggests, prolonged pressure on the affected site. They tend to be exquisitely tender but not necessarily painful if no pressure is being applied. • How long has the ulcer been there? ■ Venous ulcers are less painful and can therefore present late. They often have a long and recurring history. ■ Arterial ulcers tend to present relatively early because of pain. They often occur secondary to trivial trauma. ■ Neuropathic ulcers are associated with a loss of sensation and thus often present late. ■ Pressure ulcers can develop surprisingly rapidly (e.g. days in immobile patients if they are not turned regularly during their admission, even hours in patients who suffer a long lie following a fall), but can have a more indolent course depending on how much pressure is put on for how long. Thus the time course is not especially helpful. ■ A long history should arouse suspicion of a Marjolin ulcer, which only occurs in long-standing ulcers.
Student Power
Authors: Rose Jonathan
Published: November 2020

In 1916 Columbia University dropped its Latin requirement for admissions, effectively opening its doors to the striving sons of immigrants. Thus (in a word) it became the first Ivy League school to deal with the issue of diversity. In the same year, Professor John Erskine proposed what became the General Honors course, Columbia’s celebrated core curriculum of Great Books. Much later that program would come under fire for not including enough female and non-Western authors—but measured against the standards of its time, it was strikingly democratic, inclusive, and anti-authoritarian. The students who were now entering, educated at public schools, lacked the common classical training of prep-school boys, so Erskine aimed to teach them a shared body of literature that was far more broad and accessible. It took the Classics Department a year to get through Herodotus in the original: General Honors covered him (in translation) in a week. And Erskine’s definition of “Great Book” was clearly flexible: he envisioned that the reading list would be revised from year to year, and at first it was. The aim was not to follow a rigid canon, but to create the basis for a common conversation. And so it did: the early cohort of students included young men who would go on to shape intellectual discourse in mid-century America: Lionel Trilling, Jacques Barzun, Clifton Fadiman, Whittaker Chambers, Joseph Mankiewicz (future screenwriter and director), and Leon Keyserling (later Harry Truman’s top economic advisor), with Mark Van Doren and Mortimer Adler serving as instructors. Early in his teaching career, Erksine explained his liberation pedagogy: . . . A college course in literature should provide for two things—the direct contact of the student’s mind with as many books as possible, and the filling in of any gaps in his sympathy with what he reads. Almost all the great books were intended for the average man, and the author contemplated an immediate relation with his audience. There is room for the annotator or teacher only when time has made the subject remote or strange, or when the reader’s imagination is unable to grasp the recorded experience . . . If the student’s task is to read great books constantly, the teacher’s part [is] to connect the reading with the pupil’s experience . . . . . .
Fire, Flowers, and Dinosaurs
Authors: Scott Andrew C.
Published: November 2020

The Mesozoic Era is the geological interval comprising the Triassic, Jurassic, and Cretaceous Periods, and it is best known for the rise and fall of the dinosaurs. The Mesozoic began around 250 million years ago and continued to around 66 million years ago—a not inconsiderable chunk of geological time, and framed by mass extinctions at its beginning and end. Fifty years ago there were very few published papers on fire in deep time, but the most important one, which I’ve touched on before, was ‘Forest fire in the Mesozoic’, by Tom Harris of the University of Reading. Tom was an important scientist, one of the leading palaeobotanists in the world. Energetic and passionate about his fossil plants, he was a scientist with broad interests, and given to experimentation and lateral thinking. The evidence that Tom used in his paper on fires in the Mesozoic was limited to only a couple of charcoal occurrences in these rocks. The Permian Period ended with the biggest known mass extinction in Earth history, when life was almost wiped out. Whole ecosystems collapsed. So what would the world have looked like at the start of the Triassic? Among whole groups of plants that had become extinct were the giant club mosses that had been the major coal-forming plants of the late Paleozoic, and the glossopterids that had dominated southern continental vegetation. In the first few million years after the extinctions, plant diversity appears to have been low, but some new plants became prominent, including the pole-like spore-bearing lycopod called Pleuromeia, and the scrambling seedplant called Dicroidium, which had fern-like foliage. The first 10 million years of the Triassic are thought to have been a time of ecosystem recovery. According to Berner’s model, the Triassic started with very low levels of oxygen in the atmosphere. Researchers had noticed that there were no coals found at the beginning of the Triassic, and this interval was called the ‘coal gap’. The problem, therefore, was that charcoal in coal could not be used as a proxy for atmospheric oxygen for this time interval.
The Kentucky Mummy: Encountering the American Past
Authors: Snead James E.
Published: November 2020

In September 1816 a notice appeared in the National Aegis of Worcester, Massachusetts: . . . Great Natural Curiosity TO BE SEEN AT COL. SIKE’S HALL A FEMALE MUMMY . . . Supposed to be more than 1,000 years old. She was recently discovered in a Saltpetre Cave, in Kentucky. At the time, she was shrouded in cloth made from the bark of the willow, and ornamented with beads and feathers, having her instruments for working and musick lying by her; as was also a very curious wooden bowl, containing burnt bones, the relics of some of her friends, and the preserved skin of a Rattle Snake— all of which are preserved, and now presented to the view of the curious. She appears to have been about 5 feet 8 inches in height, and of the most delicate and elegant symmetry. The hair is still on her head; some of her teeth yet remain, and the nails on her fingers and toes are still perfect. It is presumed that she, together with the articles found with her, is one of the greatest curiosities ever exhibited to the American public. Great conjectures are formed as to the period of her existence; but we presume it is no exaggeration to say that, in all probability she is as ancient as the immense Mounds of the western Country, which have so astonished the philosophical world. The arrival of the Kentucky Mummy—on view for only two weeks, at a visitor’s price of 25 cents—was the culmination of a summer of antiquarian excitement along the eastern seaboard of the United States. Journalists, poets, and impresarios were moved by the sight. Scholars schemed to acquire the mummy for their cabinets and scrutinized the withered remains for clues as to her origins and associations. But it was the interest of the general audience that made her progress particularly noteworthy. “All you gentlemen and ladies,” announced a Philadelphia newspaper, “have the opportunity to gratify yourselves and behold this rare curiosity.” The history of Euro-American encounters with the indigenous antiquities of the Americas is remarkably incomplete.