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Books on the topic 'Dyslipidaemic'

Author: Grafiati

Published: 5 June 2025

Last updated: 2 August 2025

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1

J, Betteridge D., ed. Dyslipidaemia. Baillière Tindall, 1995.

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2

(Gabriele), Riccardi G., ed. Clinician's manual on diabetic dyslipidaemia. Science Press, 2004.

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3

(Editor), P. Durrington, M. I. Mackness (Editor), J. P. Miller (Editor), and J.A.E. Rees (Editor), eds. The Year in Dyslipidaemia 2004 (Year in Dyslipidaemia). Informa Healthcare, 2004.

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4

The Year in Dyslipidaemia 2002 (Year in Dyslipidaemia). Informa Healthcare, 2003.

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5

Reiner, Željko, Olov Wiklund, and John Betteridge. Lipids. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656653.003.0015.

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Dyslipidaemia, particularly elevated low-density lipoprotein (LDL) cholesterol, is one of the most important risk factors for cardiovascular disease (CVD). Low concentrations of high-density lipoprotein (HDL) cholesterol are independently associated with high CVD risk, while moderately elevated triglycerides are considered to be a marker of increased CVD risk. The presence of dyslipidaemias secondary to other conditions must be excluded before beginning treatment. All patients with familial hypercholesterolaemia are at high risk and should be treated by lipid-lowering therapy. Lifestyle change

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6

Thompson, Gilbert. Dyslipidaemia Clinical Practice. Taylor & Francis, 2001.

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7

Morrell, Jonathan, and Gilbert Thompson. Dyslipidaemia in Clinical Practice. Taylor & Francis Group, 2006.

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8

Thompson, Gilbert. Dyslipidaemia in Clinical Practice. Taylor & Francis Group, 2001.

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9

Staff, Durrington P. Year in Dyslipidaemia 2002. Taylor & Francis Group, 2003.

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10

Staff, Durrington P. Year in Dyslipidaemia 2003. Taylor & Francis Group, 2003.

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11

Miller, J. P., P. Durrington, M. I. Mackness, and J. A. E. Rees. Year in Dyslipidaemia 2004. Taylor & Francis Group, 2004.

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12

Thompson, G. R., Peter W. F. Wilson, and John Dean. Dyslipidaemia in Clinical Practice. Taylor & Francis Group, 2004.

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13

Morrell, Jonathan, and Gilbert Thompson. Dyslipidaemia in Clinical Practice. Taylor & Francis Group, 2006.

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14

Durrington, P. The Year in Dyslipidaemia 2004. CRC Press, 2004. http://dx.doi.org/10.1201/9780203500415.

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15

The Year in Dyslipidaemia 2003. Informa Healthcare, 2003.

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16

Betteridge Dyslipidaemia Bipr Em9: 4. Bailliere Tindall, 1995.

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17

Thompson, Gilbert, Jonathan Morrell, and Jonathan Morrell. Dyslipidaemia in Clinical Practice, Second Edition. CRC Press, 2006. http://dx.doi.org/10.1201/b13796.

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18

Dyslipidaemia in Clinical Practice, Second Edition. 2nd ed. Informa Healthcare, 2006.

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19

Grundy, Scott M., and Ole Faergeman. Rapid Reference to Dyslipidaemia (Rapid Reference Series). C.V. Mosby, 2003.

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20

Galton, David J. Churchill's In Clinical Practice Series: Dyslipidaemia (Churchill's In Clinical Practice). Churchill Livingstone, 2003.

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21

Jolly, Elaine, Andrew Fry, and Afzal Chaudhry, eds. Endocrine. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0007.

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Chapter 7 covers the basic science and clinical topics relating to the endocrine system which trainees are required to learn as part of their basic training and demonstrate in the MRCP. It covers endocrine physiology, acid-base balance, thyrotoxicosis, hypothyroidism, goitre and thyroid nodule, Cushing syndrome, acromegaly, hyperprolactinaemia, hypopituitarism, diabetes insipidus, adrenal incidentaloma, primary hyperaldosteronism, adrenal insufficiency, phaeochromocytoma and paraganglioma , male hypogonadism and Gynaecomastia, menstrual disorders and anovulation, hirsutism and the polycystic o

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22

Doumas, Michael, and Chrysoula Boutari. Erectile dysfunction: definition and size of the problem. Edited by Charalambos Vlachopoulos. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0243.

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Erectile dysfunction is currently considered a manifestation of vascular disease in the majority of cases. It is therefore of no surprise that erectile dysfunction is commonly found in patients with overt cardiovascular disease and/or cardiovascular risk factors. Indeed, more than 50% of patients with stable coronary artery disease or acute coronary syndromes suffer from erectile dysfunction, while the prevalence of erectile dysfunction in patients with heart failure is even higher. Likewise, erectile dysfunction is frequently encountered in patients with arterial hypertension, diabetes mellit

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23

Jardine, Alan G., and Rajan K. Patel. Lipid disorders of patients with chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0102.

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The risk of developing cardiovascular (CV) disease is increased in patients with chronic kidney disease (CKD) and although dyslipidaemia is a major contributory factor to the development of premature CV disease, the relationship is complex. Changes in lipid fractions are related to glomerular filtration rate and the presence and severity of proteinuria, diabetes, and other confounding factors. The spectrum of CV disease changes from lipid-dependent, atheromatous coronary disease in early CKD to lipid-independent, non-coronary disease, manifesting as heart failure, and sudden cardiac death in a

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24

Levy, Jerrold H., and David Faraoni. Pathophysiology and causes of severe hypertension. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0162.

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Hypertension affects multiple groups of patients characterized by different clinical presentations and a spectrum of potential causes. The pathophysiology is complex and multifactorial. Although most patients are labelled ‘essential hypertension’, multiple mechanisms are involved in blood pressure regulation. Factors that influence blood pressure homeostasis include endothelial function, the renin-angiotensin system, and the sympathetic nervous system. In elderly patients, hypertension is common as the vascular system and arterial stiffness also contribute. Other important factors include infl

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25

Barthel, Andreas, and Michael Bauer. Psychotropic drugs and metabolic risk. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0011.

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Increased appetite and weight gain represent a significant problem related with particular antipsychotic drugs, antidepressants, mood stabilizers, and—to a lesser extent—anxiolytic drugs. Psychotropic drug-induced weight gain may contribute to obesity-related metabolic changes and pathological conditions such as dyslipidaemia, type-2-diabetes and hypertension—summarized as the metabolic syndrome—with an increased risk for cardiovascular morbidity and mortality. Interestingly, psychotropic drugs are also used for the treatment of diabetes-related complications. For example, antidepressants are

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26

Levy, David. Adolescence and emerging adulthood. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198766452.003.0009.

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Adolescence and emerging childhood forms an increasing proportion of the lifespan of urbanized individuals. Glycaemic control worsens during adolescence; physiology and psychology contribute. A1C levels peak around 9% (75 mmol/mol) before declining from late teens onwards. However, unchanging glycaemia (tracking) is common. Glycaemia has generally improved in the past 10–15 years, but significant differences between and within countries persist. Microvascular complications are prevalent at this stage, but have probably also decreased with time. During this important period, the stage can be se

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27

Gissey, Lidia Castagneto, James R. Casella Mariolo, Geltrude Mingrone, and Francesco Rubino. Metabolic surgery and depression. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0012.

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The incidence of obesity is rising worldwide and so are its comorbidities: type-2 diabetes mellitus (T2DM), dyslipidaemia, hypertension, cardiovascular disease, sleep apnoea, and depression. Bariatric/metabolic surgery has established itself over the past several years as an effective treatment not only for morbid obesity but also for its associated morbidities. The effects of bariatric/metabolic surgery on depression are controversial, with some studies showing improvement and others demonstrating a worsening. However, a major drawback of these studies is that they do not compare patients wit

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28

Porst, Hartmut. Erectile dysfunction. Edited by David John Ralph. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0103.

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Erectile dysfunction (ED) can be improved by changing certain lifestyle factors such as sedentary lifestyle, unhealthy food, nicotine and alcohol abuse, or optimal management of risk factors/concomitant diseases causing or aggravating ED such as dyslipidaemia, hypertension, diabetes mellitus, depression, BPH/LUTS, or hypogonadism.First choice in the medical therapy of ED are PDE-5 inhibitors such as sildenafil, vardenafil, and tadalafil used p.r.n, or on a daily low-dose regimen regarding tadalafil, especially in patients suffering from ED and BPH/LUTS. Yohimbine and L-arginine may be consider

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29

Dalbeth, Nicola. Gout. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0141.

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Gout is a common and treatable disorder of purine metabolism. Gout typically presents as recurrent self-limiting episodes of severe inflammatory arthritis affecting the foot. In the presence of persistent hyperuricaemia, tophi, chronic synovitis, and joint damage may develop. Diagnosis of gout is confirmed by identification of monosodium urate (MSU) crystals using polarizing light microscopy. Hyperuricaemia is the central biochemical cause of gout. Genetic variants in certain renal tubular urate transporters including SLC2A9 and ABCG2, and dietary factors including intake of high-purine meats

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30

Dalbeth, Nicola. Gout. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0141_update_003.

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Gout is a common and treatable disorder of purine metabolism. Gout typically presents as recurrent self-limiting episodes of severe inflammatory arthritis affecting the foot. In the presence of persistent hyperuricaemia, tophi, chronic synovitis, and joint damage may develop. Diagnosis of gout is confirmed by identification of monosodium urate (MSU) crystals using polarizing light microscopy. Hyperuricaemia is the central biochemical cause of gout. Genetic variants in certain renal tubular urate transporters including SLC2A9 and ABCG2, and dietary factors including intake of high-purine meats

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