Current Treatments Targeting Raas And Its Effect On The Increase Of Blood Volume During Hf

While at the hospital, the patient, was having excessively slow AV nodal conduction rates that unfortunately haven’t been recognized. He started on the prescribed antihypertensive drug (s). As soon as blood levels climb towards the usual therapeutic range the patient goes into complete heart block. Which of the following drugs most likely provoked this further prolongation of the P-R interval, ultimately leading to the complete heart

M/A: This class of agents is indicated for the treatment of an irregular heart rhythm.

The use of strong cytochrome P450 3A4 inhibitors (e.g., ritonavir) with Symbicort may cause increased systemic corticosteroids. Formoterol, a component of Symbicort, can produce significant cardiovascular effects, such as flattening of the T-wave, prolongation of the QTc interval, and ST depression. In addition, because of the action of formoterol on the vascular system, taking with monoamine oxidase inhibitors and tricyclic antidepressants should be cautioned. Furthermore, beta-blockers, including eye drops may not only produce severe bronchospasm in patients with asthma, but may block the pulmonary effect of the beta-agonists, such as formoterol as well. Finally, caution is recommended when administered concomitantly with non-potassium-sparing

A seventy-five-year-old patient is ordered to take digoxin an anti-arrhythmic drug, coumadin an anticoagulant, lasix which is a loop diuretic, and a K-Dur which is a postassium chloride supplement. For each of these medications, I will explain the drug name and therapeutic category, the dosage size and schedule, the route and technique of administration, the expected therapeutic response and when it should develop, the non-drug measures to enhance the therapeutic responses if applicable, the probable duration of treatment, the method of drug storage, the signs and symptoms of major adverse effects, the major drug to drug and drug to food interactions, who to contact if there were any adverse reactions, and

Today, suggested treatments depend on patients’ health and type of ACS condition. Such treatments range from invasive surgery for high risk patients to prescribed medications for low risk patients. The medications vary in function and purpose. For example, thrombosis is the fast forming of an abnormal blood clot in an artery or vein. Therefore, it must be treated with a fast acting anticoagulant which could be Heparin or Fondaparinux (Hyers, 2005). Atrial fibrillation is an abnormal heartbeat and is frequently treated with another type of anticoagulant, Warfarin. Finally, unstable angina is a chest discomfort caused by the lack of blood flow through the heart and in most cases is treated with the most common antiplatelet medication, Aspirin.

Angina is a chronic condition characterised by pain or constructing discomfort which usually occurs in the front of the chest and then radiates to the neck, shoulders, jaws or arms. It is typically aggravated by exertion or emotional stress and only lasts for a few minutes (NICE, 2011). Along with chest pain, there are also atypical symptoms which can occur, such as breathlessness, nausea, feeling unusually tired, and dizziness (Sarembock et al., 2007). Stable angina results from the formation of atherosclerotic plaques in the coronary arteries, causing progressive narrowing of the arterial lumen and symptoms occur when the restricted blood flow does not provide adequate amounts of oxygen to the myocardium when there is increased oxygen demand

PJ’s symptoms including, a history of angina, mild hypertension which is controlled and chest pain that subsides with rest and or nitroglycerin tablets is consistent with the diagnosis of stable angina with underlying coronary artery disease. According to McCance and Huether (2014), stable angina is a condition that is the result of myocardial ischemia or the lack of oxygen needed related to the hardening of the arteries and their walls making them ineffectively dilate to increase the needed blood flow and oxygen to the myocardium for exertional efforts. The decrease in adequate blood flow and delivery of oxygen in turn creates an anaerobic metabolism by the cells

In this case pre-pregnancy counseling includes but not limited to evaluation of HTN control, discussion of increased risk of pre-eclampsia, and education about any drug alterations which would be needed to be made in the first trimester if she becomes pregnant. Research shows that angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) need to be stopped in the first trimester since it can increase risk of congenital abnormalities if these drugs taken during pregnancy (National Institute for Health and Care Excellence, 2010). So in this case ACE inhibitor should be stopped if she becomes pregnant most preferably offer alternative treatment. It is necessary to find out J.M.’s detail PMH if she had poor outcomes with previous pregnancies because of HTN then she needs to be counselled

When a patient’s heart is not preforming properly or a disease if affecting the blood volume, the heart will increase or decrease it’s contractility overall changing the systolic blood pressure. With congestive heart failure, the act of sodium, chloride, and water retention is detected. This is in result of the Renin-Angiotensin System. When there is a decrease in

Simvastatin, a member of the hydroxymethylglutaryl coenzyme A reductase or statin family has been shown to reduce the amount of inflammation in the arteries associated with atherosclerosis and other cardiovascular diseases presumably by lowering the LDL levels utilized for oxidative metabolism. It has also been proposed that statin therapy could help to decrease the production and circulation of the mediators that induce CRP production such as tumor-necrosis factor-α or IL-6.7 A cyclooxygenase inhibitor used in the treatment of cardiovascular problems, namely aspirin has also been found to reduce CRP levels by preventing the cell activation and proliferation of cells that trigger a CRP response in the

Attempts are made to eliminate the causative factor in secondary FSGS. In addition to treating the underlying condition, intraglomerular and systemic pressures are closely managed with agents such as inhibitors of the renin-angiotensin system. However, regardless of the etiology involved, all patients with nephrotic syndrome signs and symptoms and FSGS should be managed with diuretics, low-salt diets and inhibitors of the renin-angiotensin system. These assist in reducing the risk of cardiovascular disease and long-term damage to the kidney.

As a conclusion, blood vessels may relax and open up which makes it easier for blood to flow through the vessels so in this event it can reduce the blood pressure. Renin inhibitors contributes to another medication to balance hypertension. The side effects to Renin inhibitors is dizziness, headache, diarrhea, and stuffy nose. As a result of direct renin inhibitors which help the regulation of blood pressure, blood vessels relax and widen, making it easier for blood to flow through the vessels, which also lowers blood pressure. Direct renin inhibitors, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin II receptor blockers (ARBs) all help the same process that narrows blood vessels, but each type of medicine blocks a different part of the process. Calcium channel blockers is another medication treatment option. The side effects of this medication is lightheadedness, low blood pressure, slower heart rate, drowsiness, constipation, swelling of feet, ankles and legs, increased appetite, and gastroesophageal reflux disease (GERD). Calcium channel blockers dilate the blood vessels and this makes it easier for blood to flow through the vessels and balances blood

Mr Jones requires regular review and management of his Essential Hypertension which was first diagnosed 5 years ago. He has been well maintained on lower than recommendation (NICE, 2011) dose of angiotensin converting enzyme inhibitor Lisinopril dihydrate. He has no

JF is a 79-year-old retired female who was brought to our attention with chief complains of ongoing cramping in her legs since 3-4 months ago. She is about 160 cm tall and weighs ~68 Kg (BMI 26.6). The possibilities of a statin-induced myalgia will be discussed in her dyslipidemia PCP. JF’s current medical conditions include COPD, depression, dyslipidemia (secondary prevention of cardiovascular events), hypertension (pos-MI), and GERD. She currently takes the following medications: ramipril 5mg once daily (AM), HCTZ 25 mg once daily (AM), atorvastatin 40 mg once daily (AM), salbutamol 100 mcg 2 puffs QID, ipratropium 20 mcg 2 puffs TID, fluticasone/salmeterol 250/25 mcg 2 puffs BID, pantoprazole 40 mg once daily (AM), escitalopram 10 mg once daily (AM), ASA 81 mg once daily (AM), diltiazem CD 120 mg once daily (AM), and calcium carbonate/vitamin D (500 mg/800 IU BID PC). Please see the attachments for her latest lab results. JF was diagnosed with stage 1 HTN, GERD, and dyslipidemia ~13 years ago for which she took HCTZ 25 mg, ranitidine 300 mg, and atorvastatin 10 mg. Her past medical history include lung cancer (surgically removed a lobe from her left lung, treated with chemotherapy in 2004), heart attack (NSTEMI, MRP thought associated with chemotherapy, treated with

Renovascular hypertension is most commonly caused by prerenal factors, which are conditions that result in a decrease in blood flow to the kidney, which is also known as hypoperfusion. In many cases, the prerenal factor that causes renovascular hypertension is renal artery stenosis. Renal artery stenosis is defined as the narrowing of the renal artery that produces a decrease in blood flow into the kidneys (3). Renal artery stenosis is most often caused by atherosclerosis (1). Atherosclerosis occurs when there is a buildup of fatty substances within the walls of the arteries, which is what causes the narrowing. The fatty substances, like cholesterol and triglycerides, harden over time and become plaque, which increases the resistance of the arteries by decreasing the circumference, but also by making the arteries less elastic (5). When arteries are less elastic, they are unable to expand and recoil properly, which causes stiffening. Factors that can lead to atherosclerosis include a poor diet that is high in fat, physical inactivity, and cigarette smoking (1).