Cardizem

General Information about Cardizem

Cardizem belongs to a category of medications often known as calcium channel blockers. These medicine work by blocking the motion of calcium into the muscle cells of the center, which helps to loosen up and widen the blood vessels. This leads to a lower in heart price and blood stress, thereby lowering the workload on the guts.

Cardizem, also called diltiazem, is a medication generally used in the remedy of supraventricular tachycardia (SVT). This rhythm disturbance of the center is characterized by a rapid coronary heart price that starts within the higher chambers of the center, or the atria. It may end up in symptoms such as palpitations, dizziness, shortness of breath, and chest pain.

In some circumstances, Cardizem could also be prescribed for off-label uses, such as in the remedy of migraine headaches or Raynaud's illness. While there is restricted evidence for its use in these situations, some sufferers might discover reduction from their signs with the usage of this medicine.

Cardizem is often well-tolerated, with the commonest aspect effect being a headache. Other potential unwanted effects include dizziness, lightheadedness, nausea, and constipation. It is important to tell your doctor of any current medical circumstances or drugs you take before beginning Cardizem, because it will not be appropriate for everybody.

Another frequent use of Cardizem is in the management of atrial fibrillation or atrial flutter. These are also forms of SVT that involve a chaotic and irregular coronary heart rhythm. Cardizem is usually used in mixture with other drugs, similar to beta blockers, to manage the guts fee and stop issues related to these situations.

One of the main uses of Cardizem is the remedy of paroxysmal supraventricular tachycardia (PSVT). This is a type of SVT that happens all of a sudden and resolves on its own without remedy. However, in some circumstances, the episodes may be extended and require intervention to revive a standard coronary heart rhythm. Cardizem could be administered intravenously in a hospital setting for this purpose, or taken orally to forestall future episodes.

In addition to its use in SVT, Cardizem has also been found to be effective in the therapy of angina, a situation characterized by chest ache because of lowered blood flow to the guts. It may help to alleviate signs and enhance exercise tolerance by lowering the workload on the guts.

In conclusion, Cardizem is a generally used medication in the remedy of supraventricular tachycardia and different heart situations. It works by blocking calcium channels and reducing the workload on the guts, leading to a lower in heart fee and blood strain. While typically safe and well-tolerated, it is very important discuss any current medical circumstances or drugs along with your doctor earlier than beginning Cardizem.

A transdermal preparation that delivers clonidine continuously over a 7-day interval is effective and causes milder side effects than does oral therapy (Giugliano et al. Clonidine has been reported to be useful in numerous conditions that may accompany hypertension, including Restless legs syndrome (Wagner et al. Because of severe postural hypotension, the use of guanethidine has virtually disappeared. Peripheral Adrenergic Inhibitors Reserpine First reported to be an effective antihypertensive in the 1940s (Bhatia, 1942), reserpine became a popular drug in the 1960s and 1970s but has been used less and less because, being an inexpensive generic, it has no constituency pushing for its use, and when used in high doses, it has caused depression, earning it a bad reputation. Reserpine, one of the many alkaloids of the Indian snakeroot Rauwolfia serpentina, is absorbed readily from the gut, is taken up rapidly by lipidcontaining tissue, and binds to sites involved with storage of biogenic amines. Catecholamines also are depleted in the brain, which may account for the sedative and depressant effects of the drug, and in the myocardium, which may decrease cardiac output and induce a slight bradycardia. Antihypertensive Efficacy -Adrenergic Receptor Blockers Selective 1-blockers have had a relatively small share of the overall market for antihypertensive drugs in the U. Mode of Action the nonselective -blockers phenoxybenzamine and phentolamine are used almost exclusively in the medical management of pheochromocytoma, because they are only minimally effective in primary hypertension (see Chapter 12). These agents block the activation of postsynaptic 1-receptors by circulating or neurally released catecholamines, reducing peripheral resistance without major changes in cardiac output. Presynaptic Postsynaptic By itself, reserpine has limited antihypertensive potency, resulting in an average decrease of only 3/5 mm Hg; when combined with a thiazide, the reduction averaged 14/11 mm Hg (Veterans Administration Cooperative Study, 1962). By blocking the 1-adrenergic receptor on the vascular smooth muscle, catecholamine-induced vasoconstriction is inhibited. Despite this selective blockade, neurally mediated responses to stress and exercise are unaffected, and the baroreceptor reflex remains active. Accompanying these desirable attributes may be other actions that lessen the usefulness of -adrenergic blockers: They relax the venous bed as well and, at least initially, may affect the visceral vascular bed more than the peripheral vascular bed. The subsequent pooling of blood in the viscera may explain the propensity to first-dose hypotension seen with the fastacting prazosin (Saxena & Bolt, 1986). Volume retention is common, perhaps because renin and aldosterone levels are less suppressed than they are with other adrenergic-inhibiting drugs. Prazosin is rapidly absorbed, reaches maximal blood levels at 2 hours, and has a plasma half-life of approximately 3 hours. Terazosin and doxazosin are less lipid soluble and have half, or less, of the affinity for 1-receptors as compared with prazosin. Side Effects Postural hypotension developing in 30 to 90 minutes may be seen particularly in volume-depleted patients given the shorter-acting prazosin. Urinary incontinence in women may be caused by -blockers (Marshall & Beevers, 1996). Although they are no more effective than other antihypertensive agents and may on occasion induce serious side effects, they offer the special advantage of relieving a number of concomitant diseases. To the contrary, -blockers have failed to reduce heart attacks better than other classes (Bangalore et al.

Cardizem Dosage and Price

Cardizem 180mg

• 30 pills - $54.33
• 60 pills - $69.54
• 90 pills - $84.76
• 120 pills - $99.97
• 180 pills - $130.39
• 270 pills - $176.03
• 360 pills - $221.67

Cardizem 120mg

• 30 pills - $34.11
• 60 pills - $51.47
• 90 pills - $68.84
• 120 pills - $86.20
• 180 pills - $120.93
• 270 pills - $173.02
• 360 pills - $225.12

Cardizem 60mg

• 60 pills - $36.00
• 90 pills - $44.50
• 120 pills - $52.99
• 180 pills - $69.98
• 270 pills - $95.47
• 360 pills - $120.96

Fetal dexamethasone exposure accelerates development of renal function: relationship to dose, cell differentiation and growth inhibition. Induction of terminal differentiation in epithelial cellsrequires polymerization of hensin by galectin-3. Renin-expressing cells are associated with branching of the developing kidney vasculature. Vascular development: from precursor cells to branched arterial and venous networks. Differentiation and vascularisation of the metanephric kidney grafted on the chorioallantoic membrane. Expression and potential role of angiopoietins and Tie-2 in early development of the mouse metanephros. Expression of vascular endothelial growth factor and its receptors in human renal ontogenesis and in adult kidney. Embryonic neurons as in vitro inducers of differentiation of nephrogenic mesenchyme. The emphasis in this chapter is on the pathologic evaluation of native kidney lesions in real biopsy specimens, and thus is most relevant to the medical renal diseases covered in Chapters 5 through 28. Renal developmental defects and cystic diseases are covered in Chapter 4, renal transplant pathology in Chapter 29, and renal neoplasms in Chapter 30. Beginning in the second half of the 19th century and extending into the 20th century, Ellis, Fahr, and Klebs made major advances in the pathologic classification of kidney disease using light microscopy on postmortem specimens. Pioneered by Alwall, Brun, Iverson, and Kark in the 1950s, the renal biopsy allowed access to the early stages of kidney diseases and provided an opportunity to make a pathologic diagnosis that could inform clinical care. These advances and those that have followed are chronicled in the seven editions to date of the textbook on pathology of the kidney first published by Robert Heptinstall in 1966 (2) and culminating, at least for now, with this seventh edition. This chapter serves as a guide to renal biopsy evaluation by focusing on each renal compartment and its pathology in turn, and it refers the reader to detailed discussions of the specific diseases in other chapters of the book. Several factors make evaluation of renal pathology challenging, especially in renal biopsy specimens. In other words, diverse pathogenetic mechanisms may produce a similar morphologic response. Even the venerable Kimmelstiel-Wilson lesion of diabetic glomerulosclerosis (see Chapter 21) and the fibrils of amyloid seen by electron microscopy (see Chapters 22 and 23) are now subject to differential diagnoses. The second major problem is the small size of the biopsy, although the amount of tissue that is sufficient for a specific diagnosis is influenced by the disease that is present. Small sample size also impairs the assessment of the overall severity, activity, and chronicity of the disease, which can be as important in prognostication and therapeutic decisions as is the specific disease diagnosis. Another problem is that it is not always easy to identify the primary lesion because more than one compartment may be involved by the primary process, secondary processes may intervene, and major findings may be subtle. Finally, progression of many forms of renal injury toward end-stage disease results in nonspecific chronic changes that obscure the nature of the original pathologic process.