levels to 7. Bobryshev‚ Y.A.‚ and Lord‚ R.S.A. (1995). Ultrastructural recognition of cells with dendritic cell morphology in human aortic intima: contacting interactions 8. Boisvert‚ W.A.‚ Santiago‚ R‚ et al. (1998). A leukocyte homologue of the IL-8 receptor CXCR-2 mediates the accumulation of macrophages in 9. Boring‚ L.‚ Gosling‚ J.‚ Cleary‚ M.‚ and Charo‚ I.F. (1998). Decreased lesion formation in CCR2-/- mice reveals a role for chemokines in the initiation of 10. Bresalier‚ R.S.‚ Sandler‚ R.S.‚ Quan
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localized ischemia and possibly the formation of emboli or thrombi. The tonicity and shape of the endothelium are controlled by the release of several vasoconstrictor (endothelin and angiotensin II) and vasodilator (prostacyclin‚ bradykinin and nitric oxide) chemical mediators (Davignon & Ganz‚ 2004). Angiotensin II works to stimulate production of endothelin; these two work together to exert vasoconstricting properties and promote proliferation of the smooth muscle cells‚ which in turn contributes
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are hypertension‚ hyperlipidemia‚ anemia‚ electrolyte abnormalities‚ abnormal fluid balance‚ hyperkalaemia‚ metabolic acidosis‚ and bone and mineral disorders. Hypertension in kidney disease patients is treated with angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (Mayo Clinic Staff‚ 2015). Other high blood pressure medications can decrease function of the kidney as well as alter electrolyte levels. High cholesterol is treated with lipid-lowering agents such as statins
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Mary the Nursing Student Mary is 39 -year-old LPN and single mother who is attending a local community college to prepare for an A.S. degree in nursing so she can then become an RN. Mary has not been feeling well for several months. She has had bouts of nausea‚ a low fever‚ and has found that she no longer enjoys eating and smoking as much as she used to. She has also noticed that her urine is darker than usual and she has yellowing of her eyes. She has noted that she has a puffy appearance
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Congestive Heart Failure Olasumbo Dada Liberty University Abstract The prevalence of congestive heart failure is on the increase both in the United States and all over the world‚ and it is the leading cause of hospitalization in the elderly population. Congestive heart failure is a progressive disease generally seen in the elderly‚ which if not properly managed‚ can lead to repeated hospital admissions or death. Heart failure means that the heart muscle is weakened. A weakened heart muscle
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Beta Blockers In Case of Heart Failure Noor M. Al-Tarouti Beta Blockers in Case of Heart Failure Introduction : Beta-blockers‚ also known as beta antagonists‚ beta-adrenergic blocking agents‚ or beta-adrenergic antagonists‚ are drugs that are prescribed to treat several different types of conditions‚ including hypertension (high blood pressure)‚ angina‚ some abnormal heart rhythms‚ heart attack (myocardial infarction)‚ anxiety‚ migraine‚ glaucoma‚ and overactive thyroid symptoms. Beta-blockers
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Side Effects Nursing Implications Assessment to be done Morphine Page 822-824 Opioid analgesic Recommended Subcut/IM- 5-10mg q4hr PO- 10-30mg q4hr prn Depresses pain impulse transmission at the spinal cord level by interacting with opioid receptors Drowsiness Dizziness Confusion Head aches Seizures Bradycardia Nausea Vomiting Respiratory depression Respiratory arrest Apnea Pain- location‚ type‚ character‚ give dose before pain becomes severe Bowel status- constipation commonly
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What portions of the CNS modify the autonomic reflex? What neurotransmitter is used in all preganglionic fibers? What is the receptor in the ganglia? Why is the adrenal medulla included in the sympathetic nervous system? What does it release‚ and what effect does that have on the body? Which three cutaneous effectors receive innervation only from the SNS? What receptors are used by the SNS? The PSNS? What cranial nerves carry parasympathetic fibers? Which cranial nerve is the most important
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abnormalities are a frequent and potentially hazardous complication in patients with heart failure. This may be due to the pathophysiological alterations seen in the heart failure state leading to neurohumoral activation (stimulation of the renin-angiotensin-aldosterone system‚ sympathoadrenergic stimulation)‚ and due to the complications of therapy with diuretics‚ cardiac glycosides or ACE inhibitors. Patients with heart failure may exhibit hyponatremia due to a decrease in water excretion‚ which may
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increased mean arterial pressure‚ renal vascular resistance and vasomotor tone [29]. Losartan‚ an antagonist of angiotensin II receptor 1‚ decreased greater blood pressure in hyperglycemic than in euglycemic conditions [30]. Large randomized controlled trials including RALES‚ EPHESUS‚ and EMPHASIS have demonstrated that inhibition of aldosterone role through blocking its mineralocorticoid receptor decrease morbidity and mortality and in both mild and moderately severe heart failure [31]. Immune cells including
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