What is a little round pill orange in color says Lurin on one side and 20 on the other side?


Did you mean lupin? There is a little, round orange pill that has Lupin on one side and 20 on the other and it is called Lisinopril 20 MG. Lisinopril is used in the treatment of high blood pressure; heart failure; heart attack and more.

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Key:JZUFKLXOESDKRF-UHFFFAOYSA-NYes  Hydrochlorothiazide, abbreviated HCTZ, HCT, or HZT, is a diuretic drug of the thiazide class that acts by inhibiting the kidneys' ability to retain water. This reduces the volume of the blood, decreasing blood return to the heart and thus cardiac output and, by other mechanisms, is believed to lower peripheral vascular resistance. Hydrochlorothiazide is frequently used for the treatment of hypertension, congestive heart failure, symptomatic edema, diabetes insipidus, renal tubular acidosis, and the prevention of kidney stones. It is also sometimes used for treatment of hypoparathyroidism, hypercalciuria, Dent's disease and Ménière's disease. For diabetes insipidus, the effect of thiazide diuretics is presumably mediated by a hypovolemia-induced increase in proximal sodium and water reabsorption, thereby diminishing water delivery to the ADH-sensitive sites in the collecting tubules and reducing the urine output. Thiazides are also used in the treatment of osteoporosis. Thiazides decrease mineral bone loss by promoting calcium retention in the kidney, and by directly stimulating osteoblast differentiation and bone mineral formation. It is frequently given together with other antihypertensive agents in fixed combination preparations, such as losartan (an angiotensin II receptor antagonist) as hydrochlorothiazide/losartan (Hyzaar in the US). Many prescribers mistakenly assume that allergy to a sulfa drug predisposes the patient to cross sensitivity to a thiazide diuretic. Hydrochlorothiazide belongs to thiazide class of diuretics. It reduces blood volume by acting on the kidneys to reduce sodium (Na) reabsorption in the distal convoluted tubule. The major site of action in the nephron appears on an electroneutral Na+-Cl- co-transporter by competing for the chloride site on the transporter. By impairing Na transport in the distal convoluted tubule, hydrochlorothiazide induces a natriuresis and concomitant water loss. Thiazides increase the reabsorption of calcium in this segment in a manner unrelated to sodium transport. Additionally, by other mechanisms, HCTZ is believed to lower peripheral vascular resistance. Hydrochlorothiazide is sold both as a generic drug and under a large number of brand names, including Apo-Hydro, Aquazide H,Dichlotride, Hydrodiuril, HydroSaluric, Hydrochlorot, Microzide, Esidrex, and Oretic. Hydrochlorothiazide is also used in combination with many popular drugs used to treat hypertension such as Diovan HCT, Zestoretic, Benicar HCT, Olmy-H, Atacand HCT, and Lotensin HCT, Temax-H and others. Hydrochlorothiazide was detected in the urine of the Russian cyclist Alexandr Kolobnev during the 2011 Tour de France. Kolobnev was the only cyclist to leave the 2011 race in connection with adverse findings at a doping control. While Hydrochlorothiazide is not itself a performance-enhancing drug, it may be used to mask the use of performance-enhancing drugs, and is classed by the World Anti-Doping Agency as a "specified substance". Kolobnev was subsequently cleared of all charges of intentional doping. M: VAS anat (a:h/u/t/a/l,v:h/u/t/a/l)/phys/devp/cell/prot noco/syva/cong/lyvd/tumr, sysi/epon, injr proc, drug (C2s+n/3/4/5/7/8/9)

ACE inhibitor
An ACE inhibitor (or angiotensin-converting-enzyme inhibitor) is a medication pharmaceutical drug used primarily for the treatment of hypertension and congestive heart failure. This group of drugs causes dilation of blood vessels which results in lower blood pressure. In treating heart disease ACE inhibitors are usually used with other medications. A typical treatment plan will often include an ACE inhibitor, beta blocker, a long acting nitrate and a calcium channel blocker in combinations that are adjusted to the individual patient's needs. ACE inhibitors inhibit angiotensin-converting enzyme (a component of the blood pressure-regulating renin-angiotensin system), thereby decreasing the tension of blood vessels and blood volume, thus lowering blood pressure. Frequently prescribed ACE inhibitors include perindopril, captopril, enalapril, lisinopril, and ramipril. ACE inhibitors are used primarily to treat hypertension, although they may also be prescribed for cardiac failure, diabetic nephropathy, chronic renal failure, renal involvement in systemic sclerosis (scleroderma renal crisis ), left ventricular systolic dysfunction, and acute myocardial infarction. Angiotensin-converting enzyme inhibitors reduce the activity of the renin-angiotensin-aldosterone system. One mechanism for maintaining the blood pressure is the release of a protein called renin from cells in the kidney (to be specific, the juxtaglomerular apparatus). This produces another protein, angiotensin, which signals the adrenal gland to produce a hormone called aldosterone. This system is activated in response to a fall in blood pressure (hypotension) and markers of problems with the salt-water balance of the body, such as decreased sodium concentration in the distal tubule of the kidney, decreased blood volume, and stimulation of the kidney by the sympathetic nervous system. In such situations, the kidneys release renin, which acts as an enzyme and cuts off all but the first 10 amino acid residues of angiotensinogen (a protein made in the liver, and which circulates in the blood). These 10 residues are then known as angiotensin I. Angiotensin converting enzyme (ACE) then removes a further two residues, converting angiotensin I into angiotensin II. Angiotensin II is found in the pulmonary circulation and in the endothelium of many blood vessels. The system increases blood pressure by increasing the amount of salt and water the body retains, although angiotensin is also very good at causing the blood vessels to tighten (a potent vasoconstrictor). ACE inhibitors block the conversion of angiotensin I to angiotensin II. They thereby: lower arteriolar resistance and increase venous capacity; decrease cardiac output, cardiac index, stroke work, and volume; lower resistance in blood vessels in the kidneys; and lead to increased natriuresis (excretion of sodium in the urine). Renin will increase in concentration in the blood as a result of negative feedback of conversion of AI to AII. Angiotensin I will increase for the same reason. Angiotensin II and Aldosterone will decrease. Bradykinin will increase because of less inactivation that is done by ACE. Under normal conditions, angiotensin II will have the following effects: With ACE inhibitor use, the production of angiotensin II is decreased, leading to decreased blood pressure. Epidemiological and clinical studies have shown ACE inhibitors reduce the progress of diabetic nephropathy independently from their blood pressure-lowering effect. This action of ACE inhibitors is used in the prevention of diabetic renal failure. ACE inhibitors have been shown to be effective for indications other than hypertension even in patients with normal blood pressure. The use of a maximum dose of ACE inhibitors in such patients (including for prevention of diabetic nephropathy, congestive heart failure, and prophylaxis of cardiovascular events) is justified,][ because it improves clinical outcomes independently of the blood pressure-lowering effect of ACE inhibitors. Such therapy, of course, requires careful and gradual titration of the dose to prevent the effects of rapidly decreasing blood pressure (dizziness, fainting, etc.). ACE inhibitors have also been shown to cause a central enhancement of parasympathetic nervous system activity in healthy volunteers and patients with heart failure. This action may reduce the prevalence of malignant cardiac arrhythmias, and the reduction in sudden death reported in large clinical trials. ACE Inhibitors also reduce plasma norepinephrine levels, and its resulting vasoconstriction effects, in heart failure patients, thus breaking the vicious circles of sympathetic and renin angiotensin system activation which sustains the downward spiral in cardiac function in congestive heart failure The ACE inhibitor enalapril has also been shown to reduce cardiac cachexia in patients with chronic heart failure. Cachexia is a poor prognostic sign in patients with chronic heart failure. ACE inhibitors are under early investigation for the treatment of frailty and muscle wasting (sarcopenia) in elderly patients without heart failure. Common adverse drug reactions include: hypotension, cough, hyperkalemia, headache, dizziness, fatigue, nausea, and renal impairment. Fein also suggests ACE inhibitors might increase inflammation-related pain, perhaps mediated by the buildup of bradykinin that accompanies ACE inhibition. A persistent dry cough is a relatively common adverse effect believed to be associated with the increases in bradykinin levels produced by ACE inhibitors, although the role of bradykinin in producing these symptoms has been disputed. Patients who experience this cough are often switched to angiotensin II receptor antagonists. Rash and taste disturbances, infrequent with most ACE inhibitors, are more prevalent in captopril, and this is attributed to its sulfhydryl moiety. This has led to decreased use of captopril in clinical setting, although it is still used in scintigraphy of the kidney. Renal impairment is a significant potential adverse effect of all ACE inhibitors, but the reason is still unknown. It may be associated with their effect on angiotensin II-mediated homeostatic functions, such as renal blood flow][. Renal blood flow may be affected by angiotensin II because it vasoconstricts the efferent arterioles of the glomeruli of the kidney, thereby increasing glomerular filtration rate (GFR). Hence, by reducing angiotensin II levels, ACE inhibitors may reduce GFR, a marker of renal function. To be specific, they can induce or exacerbate renal impairment in patients with renal artery stenosis. This is especially a problem if the patient is concomitantly taking an NSAID and a diuretic. When the three drugs are taken together, there is a significantly increased risk of developing renal failure. ACE inhibitors may cause hyperkalemia. Suppression of angiotensin II leads to a decrease in aldosterone levels. Since aldosterone is responsible for increasing the excretion of potassium, ACE inhibitors can cause retention of potassium. Some people, however, can continue to lose potassium while on an ACE inhibitor. A severe rare allergic reaction can affect the bowel wall and secondarily cause abdominal pain.][ Some patients develop angioedema due to increased bradykinin levels. There appears to be a genetic predisposition toward this adverse effect in patients who degrade bradykinin more slowly than average. In pregnant women, ACE inhibitors taken during the first trimester have been reported to cause major congenital malformations, stillbirths, and neonatal deaths. Commonly reported fetal abnormalities include hypotension, renal dysplasia, anuria/oliguria, oligohydramnios, intrauterine growth retardation, pulmonary hypoplasia, patent ductus arteriosus, and incomplete ossification of the skull. Overall, about half of newborns exposed to ACE inhibitors are adversely affected. The ACE inhibitors are contraindicated in patients with: ACE inhibitors should be used with caution in patients with: ACE inhibitors are ADEC pregnancy category D, and should be avoided in women who are likely to become pregnant. In the U.S., ACE inhibitors must be labeled with a "black box" warning concerning the risk of birth defects when taken during the second and third trimester. Their use in the first trimester is also associated with a risk of major congenital malformations, particularly affecting the cardiovascular and central nervous systems. Potassium supplementation should be used with caution and under medical supervision owing to the hyperkalemic effect of ACE inhibitors. ACE inhibitors can be divided into three groups based on their molecular structure: This is the largest group, including: All ACE inhibitors have similar antihypertensive efficacy when equivalent doses are administered. The main differences lie with captopril, the first ACE inhibitor. Captopril has a shorter duration of action and an increased incidence of adverse effects. Captopril is also the only ACE inhibitor which is capable of passing through the blood–brain barrier, although the significance of this characteristic has not been shown to have any positive clinical effects. In a large clinical study, one of the agents in the ACE inhibitor class, ramipril (Altace), demonstrated an ability to reduce the mortality rates of patients who suffered a myocardial infarction, and to slow the subsequent development of heart failure. This finding was made after it was discovered that regular use of ramipril reduced mortality rates even in test subjects who did not suffer from hypertension. Some believe that ramipril's additional benefits may be shared by some or all drugs in the ACE inhibitor class. However, ramipril currently remains the only ACE inhibitor for which such effects are actually evidence-based. A meta-analysis confirmed that ACE inhibitors are pivotal and certainly the first-line choice in hypertension treatment. This meta-analysis was based on 20 trials and a cohort of 158 998 patients, of whom 91% were hypertensive. Angiotensin-converting enzyme (ACE) inhibitors were used as the active treatment in 7 trials (n=76 615) and angiotensin receptor blocker (ARB) in 13 trials (n=82 383). Results showed that ACE inhibitors were associated with a statistically significant 10% mortality reduction: (HR 0.90; 95% CI, 0.84-0.97; P=0.004). In contrast, no significant mortality reduction was observed with ARB treatment (HR 0.99; 95% CI, 0.94-1.04; P=0.683). Interestingly, analysis of mortality reduction by different ACE inhibitors showed that perindopril-based regimens were associated with a statistically significant 13% all-cause mortality reduction. Taking into account the broad spectrum of the hypertensive population, one might expect that an effective treatment with ACE inhibitors, in particular with perindopril, would result in an important gain of lives saved. The ACE inhibitors have different strengths with different starting dosages. Dosage should be adjusted according to the clinical response. ACE inhibitors possess many common characteristics with another class of cardiovascular drugs, angiotensin II receptor antagonists, which are often used when patients are intolerant of the adverse effects produced by ACE inhibitors. ACE inhibitors do not completely prevent the formation of angiotensin II, as blockage is dose-dependent, so angiotensin II receptor antagonists may be useful because they act to prevent the action of angiotensin II at the AT1 receptor, leaving AT2 receptor unblocked; the latter may have consequences needing further study. The combination therapy of angiotensin II receptor antagonists with ACE inhibitors may be superior to either agent alone. This combination may increase levels of bradykinin while blocking the generation of angiotensin II and its activity at the AT1 receptor. This 'dual blockade' may be more effective than using an ACE inhibitor alone, because angiotensin II can be generated via non-ACE-dependent pathways. Preliminary studies suggest this combination of pharmacologic agents may be advantageous in the treatment of essential hypertension, chronic heart failure, and nephropathy. However, the more recent ONTARGET study showed no benefit of combining the agents and more adverse events. While statistically significant results have been obtained for its role in treating hypertension, clinical significance may be lacking. Patients with heart failure may benefit from the combination in terms of reducing morbidity and ventricular remodeling. The most compelling evidence for the treatment of nephropathy has been found: This combination therapy partially reversed the proteinuria and also exhibited a renoprotective effect in patients afflicted with diabetic nephropathy, and pediatric IgA nephropathy. The first step in the development of ACE inhibitors was the discovery of ACE in plasma by Leonard T. Skeggs and his colleagues in 1956. Brazilian scientist Sergio Ferreira reported a bradykinin-potentiating factor (BPF) present in the venom of Bothrops jararaca, a South American pit viper, in 1965. Ferreira then went to John Vane's laboratory as a postdoctoral fellow with his already-isolated BPF. The conversion of the inactive angiotensin I to the potent angiotensin II was thought to take place in the plasma. However, in 1967, Kevin K. F. Ng and John R. Vane showed plasma ACE is too slow to account for the conversion of angiotensin I to angiotensin II in vivo. Subsequent investigation showed rapid conversion occurs during its passage through the pulmonary circulation. Bradykinin is rapidly inactivated in the circulating blood, and it disappears completely in a single pass through the pulmonary circulation. Angiotensin I also disappears in the pulmonary circulation because of its conversion to angiotensin II. Furthermore, angiotensin II passes through the lungs without any loss. The inactivation of bradykinin and the conversion of angiotensin I to angiotensin II in the lungs was thought to be caused by the same enzyme. In 1970, Ng and Vane, using BPF provided by Sérgio Henrique Ferreira, showed the conversion is inhibited during its passage through the pulmonary circulation. BPFs are members of a family of peptides whose potentiating action is linked to inhibition of bradykinin by ACE. Molecular analysis of BPF yielded a nonapeptide BPF teprotide (SQ 20,881), which showed the greatest ACE inhibition potency and hypotensive effect in vivo. Teprotide had limited clinical value as a result of its peptide nature and lack of activity when given orally. In the early 1970s, knowledge of the structure-activity relationship required for inhibition of ACE was growing. David Cushman, Miguel Ondetti and colleagues used peptide analogues to study the structure of ACE, using carboxypeptidase A as a model. Their discoveries led to the development of captopril, the first orally-active ACE inhibitor, in 1975. Captopril was approved by the United States Food and Drug Administration in 1981. The first nonsulfhydryl-containing ACE inhibitor, enalapril, was marketed two years later. At least twelve other ACE inhibitors have since been marketed. In 1991, Japanese scientists created the first milk-based ACE inhibitor, in the form of a fermented milk drink, using specific cultures to liberate the tripeptide isoleucine-proline-proline (IPP) from the dairy protein. Valine-proline-proline (VPP) is also liberated in this process—another milk tripeptide with a very similar chemical structure to IPP. Together, these peptides are now often referred to as lactotripeptides. In 1996, the first human study confirmed the blood pressure-lowering effect of IPP in fermented milk. Although twice the amount of VPP is needed to achieve the same ACE-inhibiting activity as the originally discovered IPP, VPP also is assumed to add to the total blood pressure lowering effect. Since the first lactotripeptides discovery, more than 20 human clinical trials have been conducted in many different countries. M: VAS anat (a:h/u/t/a/l,v:h/u/t/a/l)/phys/devp/cell/prot noco/syva/cong/lyvd/tumr, sysi/epon, injr proc, drug (C2s+n/3/4/5/7/8/9)

A diuretic is any substance that promotes the production of urine. This includes forced diuresis. There are several categories of diuretics. All diuretics increase the excretion of water from bodies, although each class does so in a distinct way. Alternatively, an antidiuretic such as vasopressin is an agent or drug which reduces the excretion of water in urine. In medicine, diuretics are used to treat heart failure, liver cirrhosis, hypertension and certain kidney diseases. Some diuretics, such as acetazolamide, help to make the urine more alkaline and are helpful in increasing excretion of substances such as aspirin in cases of overdose or poisoning. Diuretics are often abused by sufferers of eating disorders, especially bulimics, in attempts at weight loss. The antihypertensive actions of some diuretics (thiazides and loop diuretics in particular) are independent of their diuretic effect. That is, the reduction in blood pressure is not due to decreased blood volume resulting from increased urine production, but occurs through other mechanisms and at lower doses than that required to produce diuresis. Indapamide was specifically designed with this in mind, and has a larger therapeutic window for hypertension (without pronounced diuresis) than most other diuretics. High ceiling diuretics may cause a substantial diuresis – up to 20% of the filtered load of NaCl (salt) and water. This is huge when compared to normal renal sodium reabsorption which leaves only about 0.4% of filtered sodium in the urine. Loop diuretics have this ability, and are therefore often synonymous with high ceiling diuretics. Loop diuretics, such as furosemide, inhibit the body's ability to reabsorb sodium at the ascending loop in the nephron, which leads to an excretion of water in the urine, whereas water normally follows sodium back into the extracellular fluid. Other examples of high ceiling loop diuretics include ethacrynic acid, torsemide, furosemide and bumetanide. Thiazide-type diuretics such as hydrochlorothiazide act on the distal convoluted tubule and inhibit the sodium-chloride symporter leading to a retention of water in the urine, as water normally follows penetrating solutes. Frequent urination is due to the increased loss of water that has not been retained from the body as a result of a concomitant relationship with sodium loss from the convoluted tubule. The short-term anti-hypertensive action is based on the fact that thiazides decrease preload, decreasing blood pressure. On the other hand the long-term effect is due to an unknown vasodilator effect that decreases blood pressure by decreasing resistance. Carbonic anhydrase inhibitors inhibit the enzyme carbonic anhydrase which is found in the proximal convoluted tubule. This results in several effects including bicarbonate retention in the urine, potassium retention in urine and decreased sodium absorption. Drugs in this class include acetazolamide and methazolamide. These are diuretics which do not promote the secretion of potassium into the urine; thus, potassium is spared and not lost as much as in other diuretics. The term "potassium-sparing" refers to an effect rather than a mechanism or location; nonetheless, the term almost always refers to two specific classes that have their effect at similar locations: The term "calcium-sparing diuretic" is sometimes used to identify agents that result in a relatively low rate of excretion of calcium. The reduced concentration of calcium in the urine can lead to an increased rate of calcium in serum. The sparing effect on calcium can be beneficial in hypocalcemia, or unwanted in hypercalcemia. The thiazides and potassium-sparing diuretics are considered to be calcium-sparing diuretics. By contrast, loop diuretics promote a significant increase calcium excretion. This can increase risk of reduced bone density. Compounds such as mannitol are filtered in the glomerulus, but cannot be reabsorbed. Their presence leads to an increase in the osmolarity of the filtrate. To maintain osmotic balance, water is retained in the urine. Glucose, like mannitol, is a sugar that can behave as an osmotic diuretic. Unlike mannitol, glucose is commonly found in the blood. However, in certain conditions, such as diabetes mellitus, the concentration of glucose in the blood (hyperglycemia) exceeds the maximum reabsorption capacity of the kidney. When this happens, glucose remains in the filtrate, leading to the osmotic retention of water in the urine. Glucosuria causes a loss of hypotonic water and Na+, leading to a hypertonic state with signs of volume depletion, such as dry mucosa, hypotension, tachycardia, and decreased turgor of the skin. Use of some drugs, especially stimulants, may also increase blood glucose and thus increase urination. The term "low ceiling diuretic" is used to indicate a diuretic has a rapidly flattening dose effect curve (in contrast to "high ceiling", where the relationship is close to linear). It refers to a pharmacological profile, not a chemical structure. However, certain classes of diuretic usually fall into this category, such as the thiazides. Classification of common diuretics and their mechanisms of action: Chemically, diuretics are a diverse group of compounds that either stimulate or inhibit various hormones that naturally occur in the body to regulate urine production by the kidneys. As a diuretic is any substance that promotes the production of urine, aquaretics that cause the excretion of free water are a sub-class. This includes all the hypotonic aqueous preparations, including pure water, black and green teas, and teas prepared from Herbal medications. Any given herbal medication will include a vast range of plant-derived compounds, some of which will be active drugs that may also have independent diuretic action. The main adverse effects of diuretics are hypovolemia, hypokalemia, hyperkalemia, hyponatremia, metabolic alkalosis, metabolic acidosis and hyperuricemia. The most effective use would be before a doping test. Diuretics increase the urine volume and dilute doping agents and their metabolites. The other use would be to rapidly lose weight to meet a weight category in sports like boxing, wrestling and others. M: VAS anat (a:h/u/t/a/l,v:h/u/t/a/l)/phys/devp/cell/prot noco/syva/cong/lyvd/tumr, sysi/epon, injr proc, drug (C2s+n/3/4/5/7/8/9)

Key:XPCFTKFZXHTYIP-PMACEKPBSA-NYes  Benazepril, brand name Lotensin (Novartis), is a medication used to treat high blood pressure (hypertension), congestive heart failure, and chronic renal failure. Upon cleavage of its ester group by the liver, benazepril is converted into its active form benazeprilat, a non-sulfhydryl angiotensin-converting enzyme (ACE) inhibitor. Benazepril is available as oral tablets, in 5-, 10-, 20-, and 40-mg doses. Benazepril is also available in combination with hydrochlorothiazide, under the trade name Lotensin HCT, and with amlodipine (trade name Lotrel). Most commonly, headaches and cough can occur with its use. Anaphylaxis, angioedema and hyperkalemia, the elevation of potassium levels, can also occur. Benazepril may cause harm to the fetus during pregnancy. Benazepril should be discontinued during pregnancy. According to a 2006 article in the New England Journal of Medicine, patients with advanced renal insufficiency taking benazepril showed "substantial" kidney benefits. A long-term study of patients' kidney disease revealed patients who took benazepril had better kidney function and slower progressions of kidney disease than their peers who took a placebo drug. This is notable because this category of pharmaceuticals has long been thought to cause further kidney damage or increase the rate of progression for kidney disease. According to coverage of the study on WebMD: This study marks the first indication that benazepril, and perhaps other ACE inhibitors, may actually be beneficial in the treatment of hypertension in patients with kidney disease. Under the brand names Fortekor (Novartis) and VetACE (Jurox Animal Health), benazepril hydrochloride is used to treat congestive heart failure in dogs and chronic renal failure in dogs and cats. M: VAS anat (a:h/u/t/a/l,v:h/u/t/a/l)/phys/devp/cell/prot noco/syva/cong/lyvd/tumr, sysi/epon, injr proc, drug (C2s+n/3/4/5/7/8/9)


Key:RLAWWYSOJDYHDC-BZSNNMDCSA-NYes  Lisinopril ( ) is a drug of the angiotensin-converting enzyme (ACE) inhibitor class primarily used in treatment of hypertension, congestive heart failure, and heart attacks, and also in preventing renal and retinal complications of diabetes. Its indications, contraindications and side effects are as those for all ACE inhibitors. Historically, lisinopril was the third ACE inhibitor (after captopril and enalapril) and was introduced into therapy in the early 1990s. A number of properties distinguish it from other ACE inhibitors: It is hydrophilic, has a long half-life and tissue penetration, and is not metabolized by the liver. Lisinopril is typically used for the treatment of hypertension, congestive heart failure, acute myocardial infarction, and diabetic nephropathy. The dose needs to be adjusted in those with poor kidney function. Side effects, some or all of which are serious and require immediate medical attention, include: Lisinopril causes the kidneys to retain potassium, which may lead to hyperkalemia. From a study of more than 1,000 patients who have hyperkalemia when using it, the condition may happen more in older male users. A rare but severe allergic reaction can occur that affects the bowel wall and secondarily causes abdominal pain. This "anaphylactic" reaction is very rare and must be given immediate medical attention. Lisinopril has been assigned to pregnancy category D by the FDA for use during the second and third trimesters and to category C during the first trimester. Animal and human data have revealed evidence of embryolethality and teratogenicity associated with angiotensin converting enzyme (ACE) inhibitors. There are no controlled data in human pregnancy. Congenital malformations have been reported with the use of ACE inhibitors during the first trimester of pregnancy, while fetal and neonatal toxicity, death, and congenital anomalies have been reported with their use during the second and third trimesters of pregnancy. If the patient becomes pregnant, lisinopril should be discontinued as soon as possible; it is considered contraindicated during pregnancy. There are no data on the excretion of lisinopril into human milk. The manufacturer recommends, due to the potential for serious adverse reactions in nursing infants, a decision should be made to discontinue nursing or discontinue the drug, taking into account the importance of the drug to the mother. Lisinopril is the lysine-analog of enalapril. Unlike other ACE inhibitors, it is not a prodrug and is excreted unchanged in the urine. In cases of overdosage, it can be removed from circulation by dialysis. For adult patients, following oral administration of lisinopril, peak serum concentrations occur within about seven hours, although there was a trend to a small delay in time taken to reach peak serum concentrations in acute myocardial infarction patients. Declining serum concentrations exhibit a prolonged terminal phase which does not contribute to drug accumulation. This terminal phase probably represents saturable binding to ACE and is not proportional to dose. Lisinopril does not appear to be bound to other serum proteins. Lisinopril does not undergo metabolism and is excreted unchanged entirely in the urine. Based on urinary recovery, the mean extent of its absorption is approximately 25%, with large intersubject variability (6–60%) at all doses tested (5–80 mg). Lisinopril absorption is not influenced by the presence of food in the gastrointestinal tract. Its absolute bioavailability is reduced to about 16% in patients with stable NYHA Class II-IV congestive heart failure, and the volume of distribution appears to be slightly smaller than that in normal subjects. The oral bioavailability of lisinopril in patients with acute myocardial infarction is similar to that in healthy volunteers. Upon multiple dosing, it exhibits an effective half-life of accumulation of 12 hours. Impaired renal function decreases elimination of lisinopril, which is excreted principally through the kidneys, but this decrease becomes clinically important only when the glomerular filtration rate is below 30 ml/min. Above this rate, the elimination half-life is little changed. With greater impairment, however, peak and trough levels increase, time to peak concentration increases, and time to attain steady state is prolonged. Older patients, on average, have (approximately doubled) higher blood levels and area under the plasma concentration time curve (AUC) than younger patients. Lisinopril was developed by Merck & Co., and is marketed worldwide as Prinivil or Tensopril, and by AstraZeneca as Zestril. In India, it is marketed by Micro Labs as Hipril. In the United States, a generic version is available. Like other ACE inhibitors, it is a synthetic functional and structural analog of a peptide derived from the venom of the jararaca, a Brazilian pit viper (Bothrops jararaca). Lisinopril can also be used in conjunction with the diuretic hydrochlorothiazide and drugs which combine these two medications are available under the brand names Prinzide and Zestoretic. M: VAS anat (a:h/u/t/a/l,v:h/u/t/a/l)/phys/devp/cell/prot noco/syva/cong/lyvd/tumr, sysi/epon, injr proc, drug (C2s+n/3/4/5/7/8/9)

Lupinus andersonii
Lupinus andersonii is a species of lupine known by the common name Anderson's lupine. It is native to California and adjacent sections of Oregon and Nevada, where it grows in dry mountain habitat of various types. This lupine is similar to Lupinus albicaulis in appearance. It is a hairy, erect perennial herb growing 20 to 90 centimeters in height. Each palmate leaf is made up of 6 to 9 leaflets each up to 6 centimeters long. The inflorescence is up to 23 centimeters long, bearing whorls of flowers each roughly a centimeter long. The flower is purple to yellowish or whitish in color. The fruit is a silky-hairy legume pod up to 4.5 centimeters long containing several seeds.

Lupinus guadalupensis
Lupinus guadalupensis is a rare species of lupine known by the common name Guadalupe Island lupine. It is known only from San Clemente Island, one of the Channel Islands of California, and Guadalupe Island off the coast of Baja California. It is a member of the coastal scrub growing alongside other island endemics and more common plants. This is an annual herb growing 20 to 60 centimeters high. Each palmate leaf is made up of 7 to 9 narrow leaflets up to 5 centimeters long and just a few millimeters wide, sometimes linear in shape. The inflorescence bears whorls of flowers each about a centimeter long and blue in color with a white banner patch which may fade pink. The fruit is a very hairy legume pod up to 6 centimeters long and about one wide. It contains 6 to 8 seeds.
heart failure

Heart failure (HF), often called congestive heart failure (CHF) or congestive cardiac failure (CCF), occurs when the heart is unable to provide sufficient pump action to maintain blood flow to meet the needs of the body. Heart failure can cause a number of symptoms including shortness of breath, leg swelling, and exercise intolerance. The condition is diagnosed by patient physical examination and confirmed with echocardiography. Blood tests help to determine the cause. Treatment depends on severity and cause of heart failure. In a chronic patient already in a stable situation, treatment commonly consists of lifestyle measures such as smoking cessation, light exercise, dietary changes, and medications. Sometimes, depending on etiology, it is treated with implanted devices (pacemakers or ventricular assist devices) and occasionally a heart transplant is required.

Common causes of heart failure include myocardial infarction and other forms of ischemic heart disease, hypertension, valvular heart disease, and cardiomyopathy. The term heart failure is sometimes incorrectly used for other cardiac-related illnesses, such as myocardial infarction (heart attack) or cardiac arrest, which can cause heart failure but are not equivalent to heart failure.

heart attack

Myocardial infarction (from Latin: Infarctus myocardii, MI) or acute myocardial infarction (AMI) is the medical term for an event commonly known as a heart attack. It happens when blood stops flowing properly to part of the heart and the heart muscle is injured due to not enough oxygen. Usually this is because one of the coronary arteries that supplies blood to the heart develops a blockage due to an unstable buildup of white blood cells, cholesterol and fat. The event is called "acute" if it is sudden and serious.

A person having an acute myocardial infarction usually has sudden chest pain that is felt behind the breast bone and sometimes travels to the left arm or the left side of the neck. Additionally, the person may have shortness of breath, sweating, nausea, vomiting, abnormal heartbeats, and anxiety. Women experience fewer of these symptoms than men, but usually have shortness of breath, weakness, a feeling of indigestion, and fatigue. In many cases, in some estimates as high as 64 percent, the person does not have chest pain or other symptoms. These are called "silent" myocardial infarctions.

high blood pressure

Hypertension (HTN) or high blood pressure, sometimes called arterial hypertension, is a chronic medical condition in which the blood pressure in the arteries is elevated. This requires the heart to work harder than normal to circulate blood through the blood vessels. Blood pressure is summarised by two measurements, systolic and diastolic, which depend on whether the heart muscle is contracting (systole) or relaxed between beats (diastole) and equate to a maximum and minimum pressure, respectively. Normal blood pressure at rest is within the range of 100-140mmHg systolic (top reading) and 60-90mmHg diastolic (bottom reading). High blood pressure is said to be present if it is persistently at or above 140/90 mmHg.

Hypertension is classified as either primary (essential) hypertension or secondary hypertension; about 90–95% of cases are categorized as "primary hypertension" which means high blood pressure with no obvious underlying medical cause. The remaining 5–10% of cases (secondary hypertension) are caused by other conditions that affect the kidneys, arteries, heart or endocrine system.

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Heart failure

Heart failure (HF), often called congestive heart failure (CHF) or congestive cardiac failure (CCF), occurs when the heart is unable to provide sufficient pump action to maintain blood flow to meet the needs of the body. Heart failure can cause a number of symptoms including shortness of breath, leg swelling, and exercise intolerance. The condition is diagnosed by patient physical examination and confirmed with echocardiography. Blood tests help to determine the cause. Treatment depends on severity and cause of heart failure. In a chronic patient already in a stable situation, treatment commonly consists of lifestyle measures such as smoking cessation, light exercise, dietary changes, and medications. Sometimes, depending on etiology, it is treated with implanted devices (pacemakers or ventricular assist devices) and occasionally a heart transplant is required.

Common causes of heart failure include myocardial infarction and other forms of ischemic heart disease, hypertension, valvular heart disease, and cardiomyopathy. The term heart failure is sometimes incorrectly used for other cardiac-related illnesses, such as myocardial infarction (heart attack) or cardiac arrest, which can cause heart failure but are not equivalent to heart failure.

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Organic chemistry

Organic chemistry is a chemistry subdiscipline involving the scientific study of the structure, properties, and reactions of organic compounds and organic materials, i.e., matter in its various forms that contain carbon atoms. Study of structure includes using spectroscopy and other physical and chemical methods to determine the chemical composition and constitution of organic compounds and materials. Study of properties includes both physical properties and chemical properties, and uses similar methods as well as methods to evaluate chemical reactivity, with the aim to understand the behavior of the organic matter in its pure form (when possible), but also in solutions, mixtures, and fabricated forms. The study of organic reactions includes both their preparation—by synthesis or by other means—as well as their subsequent reactivities, both in the laboratory and via theoretical (in silico) study.

The range of chemicals studied in organic chemistry include hydrocarbons, compounds containing only carbon and hydrogen, as well as compositions based on carbon but containing other elements. Organic chemistry overlaps with many areas including medicinal chemistry, biochemistry, organometallic chemistry, and polymer chemistry, as well as many aspects of materials science.

ACE inhibitors

An ACE inhibitor (or angiotensin-converting-enzyme inhibitor) is a pharmaceutical drug used primarily for the treatment of hypertension and congestive heart failure.

This group of drugs causes dilation of blood vessels, which results in lower blood pressure. In treating heart disease ACE inhibitors are usually used with other medications. A typical treatment plan will often include an ACE inhibitor, beta blocker, a long-acting nitrate and a calcium channel blocker in combinations that are adjusted to the individual patient's needs.

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