Davidson's Principles and Practice of Medicine [with Student Consult Online Access] Quotes

“Alkaloids develop in potato tubers exposed to light, causing green discoloration. Ingestion induces acute vomiting and anticholinesterase-like activity.”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine

“Sepsis is defined and discussed on pages 188–190. It describes patients with signs of the systemic inflammatory response syndrome (SIRS: two of temperature > 38 °C or < 36 °C, pulse rate > 90 beats per minute, respiratory rate > 20 per minute or PCO2 < 4.3 kPa (32.5 mmHg), and white blood cell count > 12 or < 4 × 109/L—see Box 8.3, p. 184) and evidence of infection.”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine

“Endocarditis caused by Strep. bovis and infection caused by C. septicum are both associated with colonic carcinoma and their isolation is considered to be an indication for colonoscopy.”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine

“It is dangerous to give thyroid replacement to patients with adrenal insufficiency without first giving glucocorticoid therapy, since this may precipitate adrenal crisis.”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine

“Cortisol regulates cell function by binding to glucocorticoid receptors which regulate the transcription of many genes. It can also activate mineralocorticoid receptors, but it does not normally do so because most cells containing mineralocorticoid receptors also express an enzyme, 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which converts cortisol to its inactive metabolite, cortisone. Loss of the protection of mineralocorticoid receptors by inhibition of 11β-HSD2 (e.g. by liquorice or as a result of an inherited enzyme defect) results in cortisol acting like aldosterone as a potent sodium-retaining steroid (see Box 20.49, p. 777).”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine

“Primary hyperparathyroidism Primary hyperparathyroidism is caused by autonomous secretion of PTH, usually by a single parathyroid adenoma which can vary in diameter from a few millimetres to several centimetres. It should be distinguished from secondary hyperparathyroidism, in which there is a physiological increase in PTH secretion to compensate for prolonged hypocalcaemia (such as in vitamin D deficiency, p. 1121), and tertiary hyperparathyroidism, in which continuous stimulation of the parathyroids over a prolonged period of time results in adenoma formation and autonomous PTH secretion (Box 20.37). This is most commonly seen in individuals with advanced chronic kidney disease (p. 487).”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine

“Terminology and classification Leukaemias are traditionally classified into four main groups: • acute lymphoblastic leukaemia (ALL) • acute myeloid leukaemia (AML) • chronic lymphocytic leukaemia (CLL) • chronic myeloid leukaemia (CML). In acute leukaemia there is proliferation of primitive stem cells leading to an accumulation of blasts, predominantly in the bone marrow, which causes bone marrow failure. In chronic leukaemia the malignant clone is able to differentiate, resulting in an accumulation of more mature cells. Lymphocytic and lymphoblastic cells are those derived from the lymphoid stem cell (B cells and T cells). Myeloid refers to the other lineages, i.e. precursors of red cells, granulocytes, monocytes and platelets (see Fig. 24.2, p. 989). The diagnosis of leukaemia is usually suspected from an abnormal blood count, often a raised white count, and is confirmed by examination of the bone marrow. This includes the morphology of the abnormal cells, analysis of cell surface markers (immunophenotyping), clone-specific chromosome abnormalities and molecular changes. These results are incorporated in the World Health Organization (WHO) classification of tumours of haematopoietic and lymphoid tissues; the subclassification of acute leukaemias is shown in Box 24.47. The features in the bone marrow not only provide an accurate diagnosis but also give valuable prognostic information, allowing therapy to be tailored to the patient’s disease.”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine

“In general, haematological neoplasms are diseases of elderly patients, the exceptions being acute lymphoblastic leukaemia which predominantly affects children, and Hodgkin lymphoma which affects people aged 20–40 years.”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine

“LMWHs are nearly 100% bioavailable and therefore produce reliable dose-dependent anticoagulation. • LMWHs do not require monitoring of their anticoagulant effect (except possibly in patients with very low body weight and with GFR < 30 mL/min). • LMWHs have a half-life of around 4 hours when given subcutaneously, compared with 1 hour for UFH. This permits once-daily dosing by the subcutaneous route, rather than the therapeutic continuous intravenous infusion or prophylactic twice-daily subcutaneous administration required for UFH. • While rates of bleeding are similar between products, the risk of osteoporosis and heparin-induced thrombocytopenia is much lower for LMWH. • However, UFH is more completely reversed by protamine sulphate in the event of bleeding and at the end of cardiopulmonary bypass, for which UFH remains the drug of choice.”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine

“Broadly speaking, antiplatelet medications are of greater efficacy in the prevention of arterial thrombosis and of less value in the prevention of venous thromboembolism. Thus, anti-platelet agents such as aspirin and clopidogrel are the drugs of choice in acute coronary events, and in ischaemic cerebrovascular disease, while warfarin and other anticoagulants are favoured in venous thromboembolism.”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine

“Neutrophils Neutrophilia • Infection: bacterial, fungal • Trauma: surgery, burns • Infarction: myocardial infarct, pulmonary embolus, sickle-cell crisis • Inflammation: gout, rheumatoid arthritis, ulcerative colitis, Crohn’s disease • Malignancy: solid tumours, Hodgkin lymphoma • Myeloproliferative disease: polycythaemia, chronic myeloid leukaemia • Physiological: exercise, pregnancy Neutropenia • Infection: viral, bacterial (e.g. Salmonella), protozoal (e.g. malaria) • Drugs: see Box 24.11 • Autoimmune: connective tissue disease • Alcohol • Bone marrow infiltration: leukaemia, myelodysplasia • Congenital: Kostmann’s syndrome Eosinophils Eosinophilia • Allergy: hay fever, asthma, eczema • Infection: parasitic • Drug hypersensitivity: e.g. gold, sulphonamides • Skin disease • Connective tissue disease: polyarteritis nodosa • Malignancy: solid tumours, lymphomas • Primary bone marrow disorders: myeloproliferative disorders, hypereosinophilia syndrome (HES), acute myeloid leukaemia Basophils Basophilia • Myeloproliferative disease: polycythaemia, chronic myeloid leukaemia • Inflammation: acute hypersensitivity, ulcerative colitis, Crohn’s disease • Iron deficiency Monocytes Monocytosis • Infection: bacterial (e.g. tuberculosis) • Inflammation: connective tissue disease, ulcerative colitis, Crohn’s disease • Malignancy: solid tumours Lymphocytes Lymphocytosis • Infection: viral, bacterial (e.g. Bordetella pertussis) • Lymphoproliferative disease: chronic lymphocytic leukaemia, lymphoma • Post-splenectomy Lymphopenia • Inflammation: connective tissue disease • Lymphoma • Renal failure • Sarcoidosis • Drugs: corticosteroids, cytotoxics • Congenital: severe combined”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine

“There are two major patterns of bleeding: 1. Mucosal bleeding Reduced number or function of platelets (e.g. bone marrow failure or aspirin) or von Willebrand factor (e.g. von Willebrand disease) • Skin: petechiae, bruises, post-surgical bleeding • Gum and mucous membrane bleeding • Fundal haemorrhage 2. Coagulation factor deficiency (e.g. haemophilia or warfarin) • Bleeding into joints (haemarthrosis) or muscles • Bleeding into soft tissues • Intracranial haemorrhage • Post-surgical bleeding”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine

“Hyperbaric oxygen therapy is controversial. In theory, at 2.5 atmospheres, it reduces the half-life of carboxyhaemoglobin to 20 minutes and increases the amount of dissolved oxygen by a factor of 10. The logistical difficulties of transporting sick patients to hyperbaric chambers and managing them therein should not be underestimated and recent systematic reviews have shown no improvement in clinical outcomes.”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine

“The body’s initial response to a noxious local insult is to produce a local inflammatory response with sequestration and activation of white blood cells and the release of a variety of mediators to deal with the primary ‘insult’ and prevent further damage either locally or in distant organs. Normally, a delicate balance is achieved between pro- and anti-inflammatory mediators. However, if the inflammatory response is excessive, local control is lost and a large array of mediators, including prostaglandins, leukotrienes, free oxygen radicals and particularly pro-inflammatory cytokines (p. 72), are released into the circulation. The inflammatory and coagulation cascades are intimately related. The process of blood clotting not only involves platelet activation and fibrin deposition but also causes activation of leucocytes and endothelial cells. Conversely, leucocyte activation induces tissue factor expression and initiates coagulation. Control of the coagulation cascade is achieved through the natural anticoagulants, antithrombin (AT III), activated protein C (APC) and tissue factor pathway inhibitor (TFPI), which not only regulate the initiation and amplification of the coagulation cascade but also inhibit the pro-inflammatory cytokines. Deficiency of AT III and APC (features of disseminated intravascular coagulation (DIC)) facilitates thrombin generation and promotes further endothelial cell dysfunction. Systemic inflammation During a severe inflammatory response, systemic release of cytokines and other mediators triggers widespread interaction between the coagulation pathways, platelets, endothelial cells and white blood cells, particularly the polymorphonuclear cells (PMNs). These ‘activated’ PMNs express adhesion factors (selectins), causing them initially to adhere to and roll along the endothelium, then to adhere firmly and migrate through the damaged and disrupted endothelium into the extravascular, interstitial space together with fluid and proteins, resulting in tissue oedema and inflammation. A vicious circle of endothelial injury, intravascular coagulation, microvascular occlusion, tissue damage and further release of inflammatory mediators ensues. All organs may become involved. This manifests in the lungs as the acute respiratory distress syndrome (ARDS) and in the kidneys as acute tubular necrosis (ATN), while widespread disruption of the coagulation system results in the clinical picture of DIC. The endothelium itself produces mediators that control blood vessel tone locally: endothelin 1, a potent vasoconstrictor, and prostacyclin and nitric oxide (NO, p. 82), which are systemic vasodilators. NO (which is also generated outside the endothelium) is implicated in both the myocardial depression and the profound vasodilatation of both arterioles and venules that causes the relative hypovolaemia and systemic hypotension found in septic/systemic inflammatory response syndrome (SIRS) shock. A major component of the tissue damage in septic/SIRS shock is the inability to take up and use oxygen at mitochondrial level, even if global oxygen delivery is supranormal. This effective bypassing of the tissues results in a reduced arteriovenous oxygen difference, a low oxygen extraction ratio, a raised plasma lactate and a paradoxically high mixed venous oxygen saturation (SvO2). Role of splanchnic ischaemia In shock, splanchnic hypoperfusion plays a major role in initiating and amplifying the inflammatory response, ultimately resulting in multiple organ failure (MOF). The processes involved include: • increased gut mucosal permeability • translocation of organisms from the gastrointestinal tract lumen into portal venous and lymphatic circulation • Kupffer cell activation with production and release of inflammatory mediators.”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine

“Disseminated intravascular coagulation (DIC) Also known as consumptive coagulopathy, this is an acquired disorder of haemostasis (p. 1050); it is common in critically ill patients and often heralds the onset of MOF. It is characterised by an increase in prothrombin time, partial thromboplastin time and fibrin degradation products, and a fall in platelets and fibrinogen. The clinically dominant feature may be widespread bleeding from vascular access points, gastrointestinal tract, bronchial tree and surgical wound sites, or widespread microvascular and even macrovascular thrombosis. Management is supportive with infusions of fresh frozen plasma and platelets, while the underlying cause is treated.”
― Nicki R. Colledge, Davidson's Principles and Practice of Medicine