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Books on the topic 'Hypertension Patient education'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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1

Association, American Diabetes, ed. American Diabetes Association guide to medical nutrition therapy for diabetes. 2nd ed. Alexandria, Va: American Diabetes Association, 2012.

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2

Kaplan, Norman, J. Willis Hurst MD, and Scott Grundy. Patient Education Booklets: What You Should Know About Cardiovascular Disorders: Hypertension (Patient Education Booklets). Mosby International, 1992.

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3

The effects of a selected health education intervention upon the compliance behavior of individuals diagnosed as having high blood pressure. 1988.

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4

The effects of a selected health education intervention upon the compliance behavior of individuals diagnosed as having high blood pressure. 1987.

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5

Kaplan, Norman, J. Willis Hurst MD, and Scott Grundy. Patient Education Booklets: What You Should Know About Cardiovascular Disorders: Coronary Artery Disease/hyperlipidemia/heart Failure/hypertension (Patient Education Booklets). Mosby International, 1992.

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6

(Editor), Jo Gulledge, and Shawn Beard (Editor), eds. Hypertension Management: Clinical Pathways, Guidelines, and Patient Education (Aspen Chronic Disease Management Series). Jones & Bartlett Publishers, 1999.

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7

National Heart, Lung, and Blood Institute, ed. Facts about how to prevent high blood pressure. [Bethesda, Md.?: National Heart, Lung, and Blood Institute, National Institutes of Health, 1994.

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8

Haymann, Jean-Philippe, and Francois Lionnet. The patient with sickle cell anaemia. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0167.

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In sickle cell anaemia (SCA) a single mutation in the haemoglobin beta-globin gene is responsible for a pleomorphic phenotype leading to acute and chronic life-threatening complications. Healthcare management programmes, patient and family education, infection prophylaxis (especially in childhood), and long-term treatment for some patients (such as hydroxyurea) have significantly improved survival, giving rise to some new long-term issues.Sickle cell-associated nephropathy (SCAN) leads in some cases to chronic renal failure with a significant impact on survival. SCAN is characterized by an increased effective plasma renal flow and glomerular filtration rate, glomerular hypertrophy, and damaged vasa recta system leading to albuminuria and impaired urinary concentration.Early onset of hyperfiltration occurs in 60% of SCA patients often associated with microalbuminuria. SCAN risk factors are still under investigation, but may be related to chronic haemolysis at an early time point. Other lesions in patients with sickle cell anaemia include papillary necrosis, and recurrent acute kidney injury in association with crises or infections.ACEI are recommended if there is proteinuria. There is no current agreement on whether angiotensin-converting enzyme inhibitors (ACEI) should be introduced earlier, but systematic screening for microalbuminuria and hypertension, and avoidance of nephrotoxic agents are strongly advised.Patients with sickle cell trait (carriers for sickle cell anaemia) are prone to microscopic haematuria and abnormalities of the vasa recta have been described. A very rare tumour, renal medullary carcinoma, is largely restricted to this group (in whom it is still extremely rare). Increased risk of other renal problems is still largely hypothetical rather than proven.The prevalence of nephropathies in other sickle cell diseases (in particular haemoglobin SC disease) is much lower.
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9

Korabelnikov, Daniil, and Andrey Strahov. Arterial hypertension: guide on diagnostics, treatment, examination. Moscow Medical - Social Institute named after Friedrich Haass, 2018. http://dx.doi.org/10.35571/mmsi.2018.1.001.

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The Guide is intended to systematize and update information on the diagnostics, treatment of arterial hypertension; examination of temporary disability, medical-social and military-medical examination of patients with arterial hypertension, for educational and practical assistance to students of medical universities in clinical residency, postgraduate and post-graduate programs, advanced training of specialist doctors; professors of medical universities in the process of their self-education and self-development, methodological and pedagogical activities.
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10

Abdur-Rahman, Veronica. A COMMUNITY-BASED EDUCATIONAL APPROACH TO ENHANCE LEARNING OUTCOMES IN BLACK HYPERTENSION PATIENTS (HYPERTENSION). 1991.

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11

Chiraseveenuprapund, Anuluck. OBSERVATION OF THE EFFECTS OF THERMAL BIOFEEDBACK ASSISTED BY AUTOGENIC RELAXATION IN PATIENTS WITH BORDERLINE OR MILD HYPERTENSION (BIOFEEDBACK). 1994.

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12

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 and seafood, beer, and fructose, contribute to development of hyperuricaemia and gout. Gout treatment includes: (1) management of the acute attack using non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or low-dose colchicine; (2) prophylaxis against gout attacks when commencing urate-lowering therapy (ULT), with NSAIDs or colchicine; and (3) long-term ULT to achieve a target serum urate of less than 0.36 mmol/litre. Interleukin (IL)-1β‎ is a central mediator of acute gouty inflammation and anti-IL-1β‎ therapies show promise for treatment of acute attacks and prophylaxis. The mainstay of ULT remains allopurinol. However, old ULT agents such as probenecid and benzbromarone and newer agents such as febuxostat and pegloticase are also effective, and should be considered in patients in whom allopurinol is ineffective or poorly tolerated. Management of gout should be considered in the context of medical conditions that frequently coexist with gout, including type 2 diabetes, hypertension, dyslipidaemia, and chronic kidney disease. Patient education is essential to ensure that acute gout attacks are promptly and safely managed, and long-term ULT is maintained.
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13

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 and seafood, beer, and fructose, contribute to development of hyperuricaemia and gout. Gout treatment includes: (1) management of the acute attack using non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or low-dose colchicine; (2) prophylaxis against gout attacks when commencing urate-lowering therapy (ULT), with NSAIDs or colchicine; and (3) long-term ULT to achieve a target serum urate of less than 0.36 mmol/litre. Interleukin (IL)-1β‎ is a central mediator of acute gouty inflammation and anti-IL-1β‎ therapies show promise for treatment of acute attacks and prophylaxis. The mainstay of ULT remains allopurinol. However, old ULT agents such as probenecid and benzbromarone and newer agents such as febuxostat and pegloticase are also effective, and should be considered in patients in whom allopurinol is ineffective or poorly tolerated. Management of gout should be considered in the context of medical conditions that frequently coexist with gout, including type 2 diabetes, hypertension, dyslipidaemia, and chronic kidney disease. Patient education is essential to ensure that acute gout attacks are promptly and safely managed, and long-term ULT is maintained.
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14

Association, American Diabetes. American Diabetes Association Guide to Medical Nutrition Therapy for Diabetes (Clinical Education Series). American Diabetes Association, 2003.

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15

Naess, Halvor. Long-term prognosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0016.

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Knowledge of prognosis is important for patients in the prime of life in order to make informed decisions about treatment, choice of education, and profession. Median first-year mortality after first-ever cerebral infarction among young adults is about 4% while median annual average mortality after the first year is about 1.7%. Likewise, median first-year recurrence rate of cerebral infarction is 2% and thereafter 1.5% per year. Risk factors for recurrent cerebral infarction include hypertension, diabetes mellitus, symptomatic atherosclerosis, and smoking. Recurrent cerebral infarction and mortality are associated with increasing number of traditional risk factors. About 10% of patients develop post-stroke seizures within 6 years of the acute stroke. Almost 90% of patients report good functional outcome (modified Rankin Scale score ≤2) on long-term follow-up, but up to 30–50% of patients do not resume employment. Many patients have cognitive impairment. Fatigue and depression are also common on long-term follow-up.
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16

J, Franz Marion, Bantle John P. 1947-, and American Diabetes Association, eds. American Diabetes Association guide to medical nutrition therapy for diabetes. Alexandria, Va: American Diabetes Association, 1999.

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