X

Loading



STUDENT DIGITAL NEWSLETTER ALAGAPPA INSTITUTIONS

Veena Venugopalan, PharmD

A B C D E Cardiac glycosides Calcium-channel blockers Angiotensin-converting enzyme inhibitors -Adrenergic antagonists Nitrites and nitrates Directions for questions 20­25: the questions and incomplete statements in this section can be correctly answered or completed by one or more of the suggested answers blood pressure over 180 order trandate 100mg. Her physician wants to increase the dose of the drug to 40 mg/d and asks you if this strategy will be successful heart attack lyrics sum 41 trandate 100 mg. The patient is becoming desensitized to the 20 mg dose so doubling it will not have any additional benefit hypertension organizations purchase 100 mg trandate overnight delivery. The patient must have increased her dietary intake of cholesterol and increasing the dose of drug will only cause her to eat more cholesterolcontaining foods pulse pressure under 20 order 100 mg trandate with mastercard. Bradycardia, hypotension, increased airway resistance, and congestive heart failure 27. Produce a vasodilation by reducing the influx of a cation necessary for contraction Directions for questions 31­34: Each statement in this group is most closely characterized by one of the following drugs. A B C D E Furosemide Hydrochlorothiazide Spironolactone Mannitol Acetazolamide 31. It interferes with collecting tubular aldosteronemediated sodium­potassium exchange and may cause hyperkalemia, gynecomastia, and menstrual irregularities. Freely filtered, this drug limits tubular reabsorption of water and is useful in reducing cerebral edema and intracranial pressure. The principal site of action of this drug is on the thick ascending limb of the loop of Henle; it is useful in treating pulmonary edema and ascites. Pharmacology and Medicinal Chemistry of Cardiovascular and Diuretic Drugs 223 Directions for questions 35­38: Each of the questions, statements, or incomplete statements in this section can be correctly answered or completed by one of the suggested answers or phrases. By blocking the influx of calcium into vascular smooth muscle (via L-type channels), these agents decrease rather than increase the contractile response of various arterial beds. Heparin is a highly acidic mucopolysaccharide, whereas protamine is a highly basic protein. When administered after heparin, protamine chemically combines with it (presumably by an acid­base interaction) and inactivates its anticoagulant effect. Caution must be employed when using protamine because an excess of protamine can cause an anticoagulant effect. Digoxin is composed of a steroid nucleus, unsaturated lactone ring, and three sugars attached via a glycosidic bond. Of all the drugs on the list, amiodarone is most likely to cause life-threatening pulmonary fibrosis. The structure is a benzothiadiazine (or thiazide) derivative and, more specifically, it is the diuretic hydrochlorothiazide. Only this class of diuretics contains the benzothiadiazine nucleus even though the sulfonamide moiety is common to others such as the loop diuretics and carbonic anhydrase inhibitors. Valsartan has no antiarrhythmic activity and would not be useful in supraventricular arrhythmias, but it is used to treat all the other listed conditions. Like all diuretics, hydrochlorothiazide increases Na loss in the renal filtrate, which osmotically draws water with it to cause a diuresis. Sildenafil is not associated with hepatotoxicity, although all the other adverse events have been reported with use. Warfarin competes with vitamin K epoxide for access to the reductase that converts the epoxide back to the reduced (active) form. This leads to elevation of the epoxide form and a reduction in the reduced form of vitamin K in hepatocytes. Direct thrombin inhibitors such as lepirudin can be used to control thrombin-induced coagulation without perpetuating the immune reaction. Thus, ventricular filling is reduced and this decreases the tension on the ventricular walls to reduce oxygen demand. Reduced wall tension, especially during diastole, also allows subendocardial arteries to remain patent for longer periods to increase blood flow to the heart muscle. Thus, bronchospasm, lowering of blood pressure, and reduced heart rate result from blockade of autonomic -adrenergic receptors. Digoxin would worsen angina symptoms by increasing cardiac contractility and thereby increasing myocardial oxygen demand. This allows verapamil to have a significant bradycardia effect by blocking these channel activities. Lidocaine also has little effect on atrial myocardial cell depolarization because its Na channels are only in the inactive state for very brief periods and so would not be effective against ectopic atrial arrhythmias. Overall, lidocaine is not effective in the management of supraventricular arrhythmias, unlike the other agents on the list. All the adverse events listed except for hypertension have been reported with heparin use. However, heparin needs to be used cautiously in uncontrolled hypertension in order to prevent the occurrence of strokes. It is not approved for decreasing clots after stent placement or in intermittent claudication. Alteplase is a recombinant form of tissue plasminogen activator that requires plasminogen to be bound to the fibrin of clots before it can cleave to plasmin. Urokinase is able to catalytically activate free plasminogen to plasmin, which can lead to generalized dissolving of clots and a systemic bleeding or lytic state. Dabigatran does not interact with platelets but rather inhibits thrombin directly to reduce clot formation. Visual disturbances (yellow or green vision) are peculiar to cardiac glycoside overdose. Calcium influx during arterial smooth muscle contraction is blocked by L-type channel blockers resulting in a rapid vasodilation. Spironolactone interferes with aldosterone-mediated sodium­potassium exchange, reducing the amount of potassium excreted and is often used with other diuretics that promote the excretion of potassium, such as the benzothiadiazines. Mannitol increases the osmolarity of the glomerular filtrate because it is reabsorbed poorly. By increasing the osmolarity of the glomerular filtrate, mannitol limits tubular reabsorption of water, thus promoting diuresis. Furosemide is a diuretic of choice for treating acute congestive heart failure and ascites because it promotes a significant, rapid excretion of water and sodium. This is accomplished by inhibiting the actions of the Na / K /2Cl transporter in the thick ascending loop of Henle. This is one of the few unique uses of carbonic anhydrase inhibitors such as acetazolamide. By covering the ionic carboxylic acid functional group with the more lipophilic ethyl ester, the oral bioavailability of enalapril is enhanced. Prodrugs can also be used to mask a foultasting drug, enhance water solubility, or increase the stability of a drug, but this is not the case with enalapril. Although the other choices are sometimes true statements, they do not address the question related to the side effects. Ethacrynic acid, an aryloxyacetic acid derivative, is the only loop diuretic that does not have a sulfonamide substituent. The thiazide and thiazide-like diuretics also have a sulfonamide, including hydrochlorothiazide, and also contain a sulfonamide substituent. This may be important in patients with a hypersensitivity to sulfonamides, although cross-reactivity with sulfonamide antibiotics is not always apparent. The reduced metabolic capacity of the variants can increase the likelihood of bleeding with usual doses. Specific polymorphisms in the vitamin K reductase gene can lead to altered hepatic levels of the enzyme such that patients with low expression can be more susceptible to anticoagulant effects of standard warfarin doses, again increasing the potential for bleeding. Autacoids, such as prostaglandins, leukotrienes, kallidin, bradykinin, serotonin, and histamine, have varied structures and physiological activities that are modulated by several different drugs. Although some autacoids (histamine and serotonin) function as neurotransmitters, their autacoid functions will be covered here. Currently, there are no agents that specifically modulate the function of bradykinin or kallidin; however, drugs or analogs that mimic, block, or modulate other autacoid functions and/or synthesis have important therapeutic roles. The only clinically relevant thromboxane currently identified is thromboxane A2 (TxA2), which causes platelet aggregation. Subscripts relate to the number and position of double bonds in the aliphatic chains (Figure 11-2). It is used as an abortifacient between the 13th and 20th week of gestation or for the treatment of postpartum uterine hemorrhage. Adverse effects of carboprost are usually related to its contraction of smooth muscle (vomiting, diarrhea, and bronchoconstriction); however, elevated body temperature has also been reported.

Diseases

discount trandate 100mg on line

Inadequate treatment of comorbidities - Patients with PsA have a high risk of comorbidities heart attack telugu movie generic trandate 100mg mastercard, including hypertension understanding prehypertension order trandate 100 mg free shipping, cardiovascular diseases arrhythmia and alcohol buy cheap trandate 100 mg on-line, diabetes and gastrointestinal disorders blood pressure medications that start with l trandate 100mg online. Limited awareness - the awareness of comorbidities associated with PsA is low among non­rheumatologists 3 Lack of resources and networks - Clinicians at many centres face challenges with a lack of time and resources to adequately monitor PsA comorbidities - They may also have limited access to other specialties required to initiate the adequate therapy What can be done to address it? This includes running clinics for newly diagnosed patients with PsA which is supported by a telephone helpline Findings Case study 1 What are the key features of the clinic? Place in the pathway Patients are referred to a rheumatology nurse specialist when a diagnosis has been made by their consultant rheumatologist and their treatment has been agreed. At the start of the treatment, patients are seen once a month which becomes less frequent as their condition stabilises Dose escalation the advanced nurse practitioner at the centre is responsible for altering the dose to help patients reach the treatment outcome, i. During the clinic, she also provides patients with information before they start any drug therapy so they are fully informed and engaged in their treatment Telephone helpline Challenge What was the rationale behind the clinic? The clinic for newly diagnosed patients was established to support people with this new diagnosis and help them develop better coping strategies. This is especially important as the centre does not have a dedicated psychologist. In addition, the clinic was meant to improve their understanding of the disease, therapeutic options and treatment goals the clinic is supported by a telephone helpline service where patients can leave a message and the nurse will get back to them, typically within 24 hours. Findings Case study 1 Improved patient education: the clinic is key in providing patient education. The centre used to have problems with patients refusing to take dose increases or have their treatment changed. Within six years following the clinic set­up, the percentage of patients reluctant to dose increase dropped to 8% Better relationship with the patient: Nurses tend to be more empathetic than doctors and develop better relationships with patients which is important to ensure that the patients are fully engaged in their treatment. Most of these activities are carried out at a nurse­led clinic which was set up in 2013 Hospital Authority What are the key features of the clinic? Patients are typically referred to the nurse­led clinic by a rheumatologists or by dermatologists. Consultations normally last 30­45 minutes and the waiting time for an appointment is 12 weeks Specialism During the clinics, the rheumatology nurse supports the clinical team in a number of key activities along the patient pathway, including: - - - - Treatments: Administration of infusions and patient education on administering sub­cutaneous injections Disease activity assessment: Monitoring of the disease including skin assessment, joint count, X­ray scans Drug monitoring: Monitoring of compliance to the treatment and adverse effects Patient education and support: the nurse­led clinics are key in providing education and counselling to patients. During these clinics patients are educated on the disease, its treatment and its side effects, on how to administer self­injections, and pregnancy advice. In addition, patients are provided with details of support groups which they are encouraged to join Screening for comorbidities: Annual assessment of cardiovascular risk Challenge What was the rationale for setting up the clinic? Due to the limited number of rheumatologists, the waiting time to see a specialist can be relatively long (approximately six months). The nurse­ led clinic was set up to enable patients to talk to specialised healthcare professionals and obtain advice in between appointments with rheumatologists - the clinic is also supported by a nurse­led rheumatology hotline which is open during work hours on Monday to Friday. There is only one rheumatology nurse at the hospital, leading to a heavy workload and long waiting times for appointments. It usually takes approximately three months to schedule an appointment with the nurse but it can be longer for newly diagnosed PsA patients What are the next steps? Lack of systems to monitor patients - Limited use of electronic databases makes it challenging to identify patients with whom an appointment should be scheduled Limited awareness and stigmatisation - Patients may not be aware of the need for regular assessments and not report to their doctor. This can be further exacerbated by the difficulty that patients with psoriasis may have in describing the impact of their disease on their lives What can be done to address it? The cohort collects detailed information on psoriasis and PsA patients treated at the centre in order to: - Identify predictors of treatment failure and response, and to characterise treatment transitions - Determine predictors of PsA among patients presenting with psoriasis PsA Challenge Home - Characterise health services utilisation and quality of life of patients with PsA and psoriasis - Assess relevant subgroups of patients with specific phenotypes, including non­plaque disease. The PsA database was started in 1978 by Dr Gladman with the aim of monitoring and tracking changes to the disease over time 1 Findings Case study 2 What was the rationale behind their set­up? Dr Gladman realised that PsA was presenting in a noticeably different way than outlined in her training. There are challenges associated with patient retention for the psoriasis database due to psoriasis patients not considering their disease a problem in the same way that PsA patients do. The number of patients on the psoriasis database is now less than half that of the PsA database (650 versus 1,400 respectively) What are the next steps for the databases? The database fields have evolved over the years to divest those where the validity could not always be assured, or where technical difficulties associated with collecting data outweighed the insight that was being gained. The PsoBest registry is a German nationwide registry set up to gather information about psoriasis and PsA patients the aim of the registry is to evaluate the long­term efficacy and safety effects, and patient­reported outcomes in moderate to severe psoriasis and PsA patients treated with conventional systemic therapy or biologics the registry was commissioned by the German Society of Dermatology and the Professional Association of German Dermatologists Findings Case study 3 What are the key features of the registry? This national registry is intended to collect data useful for better planning and regulation of healthcare delivery at a national level. The registry is expected to have a number of benefits for patients and participating centres: - It will further the understanding of psoriasis and PsA by gathering data on comorbidities, risk factors, and disease progression - It will enable clinicians to compare the real­world efficacy and safety effects of multiple therapies Findings Case study 3 ­ It will help participating centres record disease characteristics and treatment outcomes, and track the disease progression, allowing clinicians to make better and more informed clinical decisions for individual patients Challenge What are the challenges associated with setting up a national registry? Motivating centres to participate and controlling data completeness are the two major challenges associated with creating a nation­wide registry. In a recent publication the centre was able to use a cohort of patients to demonstrate the relationship between PsA and cardiovascular disease PsA Research tool: It can be used as a strong research tool to gather data for existing clinical trials as well as to build a case for new trials. It may also be challenging to engage older doctors or patients who are less comfortable with technology. The database allows the centre to collect data on patients with inflammatory diseases (including PsA), their treatments and clinical outcomes. Collection and analysis of the clinical data was enabled by the employment of a data manager by the centre Findings Case study 5 What is the rationale behind the database? The centre has therefore set up its own database which allows clinicians to collect clinical data on patients suffering from inflammatory diseases What are the key features of the database? Better clinical decisions and research tool the database allows the centre to capture Findings Case study 5 What are the challenges associated with maintaining and using the database? Burden on clinicians: the database has to be updated by clinicians during each patient visit which can be challenging due to the short appointment times Amount of data collected: It can be challenging to analyse all the data that is collected; however, having a dedicated person to maintain the database and conduct the analysis helps with this issue detailed patient data, including the comorbidities associated with PsA, and use these to better understand PsA patients and make better­informed decisions. The centre has done a lot of analysis on rheumatoid arthritis patients to help demonstrate the effectiveness of their care at the centre; however, this has not yet been done for PsA patients. It allows us to learn from the patients we are treating and enables to determine whether we are following treatment recommendations. It is also easier to follow a treat­to­target approach if one collects the items in a standard way and prospectively" Rheumatologist, Toronto Western Hospital Pre­diagnosis Referral and diagnosis Treatment initiation and management Follow­up Challenge Home "Improve PsA diagnosis rate by sharing information on the key steps to making the correct diagnosis" Rheumatologist, Groote Schuur Hospital, Cape Town "Continue to increase collaboration between dermatology and rheumatology to improve care of PsA patients" Rheumatologist, Groote Schuur Hospital, Cape Town "If one can have combined clinics it is very helpful. Overview Detailed site specifications 2 Elements of care the centre offers a unique model of PsA care where patients are seen by both a dermatology and rheumatology specialist who work synchronously to evaluate their patients together Why is this a strength? This model enables improved collaboration to: - Improve the rate and consistency of PsA diagnosis - Improve treatment by addressing both skin and joint symptoms Multidisciplinary - Improve patient satisfaction with a one­stop clinic approach/ - Provide unique training opportunities for staff to work across dermatology and rheumatology specialties combined clinic How does it work? The centre also trains medical students from both specialties as well as numerous residents and joint fellows Why is this a strength? The peer education is achieved by focusing on collaboration and dialogue between rheumatologists and dermatologists. All team members share the same office which further facilitates discussion between the two specialties. In addition, the centre offers a quicker transition to systemic disease­modifying therapies Why is this a strength? Although some symptoms of PsA can be managed with anti­inflammatory and topical medications, some patients may benefit from systemic treatment. There is some evidence that suggests that in many clinics PsA patients are undertreated 1 Availability of the latest therapies How does it work? Because of the multidisciplinary experience and expertise at the centre, the clinicians are familiar and comfortable with using the latest treatments Overview the centre has a clinical trials unit that provides novel therapies to PsA patients who have failed other treatment modalities Why is this a strength? There are many effective treatment options available for PsA but not all patients respond to the treatment, while others may lose their initial response over time. This awareness tool is being validated as a possible screening tool for PsA Why is this a strength? To increase awareness, referrals and diagnosis of PsA patients Development of How does it work? In 2012, the centre published a retrospective chart review that assessed whether the creation of combined rheumatology­dermatology clinics had resulted in changes in diagnosis and treatment decisions. Patients seen during the combined clinic had their diagnosis revised in 46% of cases and were more likely to be treated with a systemic and biologic therapy than before (25% vs 15% and 37% vs 16%, respectively) 1 "This clinic is exceptional for diagnosis and treatment. Although the centre does not routinely measure clinical outcomes, these have improved (anecdotally and through observations). The key outcomes in PsA include: - Objective measures such as: ­ ­ ­ - Skin measures.

buy trandate 100 mg overnight delivery

The drowning victim rescued from the water within a few minutes of submersion is likely to exhibit abnormal (agonal) breathing blood pressure diet discount trandate 100mg without a prescription. However it often takes more time to insuflate air than under normal conditions due to reduced compliance and high airway resistance cardiac arrhythmia 4279 generic trandate 100 mg free shipping. The higher inflation pressure may precipitate inflation of the stomach with regurgitation and also reduce cardiac output heart attack zippy cheap trandate 100mg fast delivery. Expert opinion suggests that cricoid pressure applied by trained and skilled personnel in casualties without a secured airway may reduce gastric inflation and enhance ventilation in drowning heart attack 4 stents buy cheap trandate 100 mg on line. If the victim has not responded to initial ventilations, they should be placed on a firm surface before starting chest compressions, as compressions are ineffective in the water. In some situations, massive amounts of foam caused by admixing moving air with water are seen coming out of the mouth of the victim. Regurgitation of stomach contents and swallowed water is common during resuscitation from drowning. During the initial assessment of the spontaneously breathing drowning victim, give high-flow oxygen (10­15 L min-1), ideally through an oxygen mask with reservoir bag. Reduced pulmonary compliance requiring high inflation pressures may limit the use of a supraglottic airway device. Pulmonary oedema fluid may pour from the airway and may need continuous suctioning to enable a view of the larynx. After the position of the tracheal tube is confirmed, titrate the inspired oxygen concentration to achieve a SpO2 of 94­98%. Palpation of the pulse as the sole indicator of the presence or absence of cardiac arrest is not always reliable. If the victim is hypothermic, modify the approach in accordance with the guidance for treatment of hypothermia (see hypo-/hyperthermia). After prolonged immersion, most victims will have become hypovolaemic due to the cessation of the hydrostatic pressure of water on the body. Discontinuing resuscitation efforts Making a decision to discontinue resuscitation efforts on a victim of drowning is notoriously difficult. Neurologically intact survival has been reported in several victims submerged for longer than 25 min, however these rare case reports almost invariably occur in children submerged in ice-cold water, when immersion hypothermia has preceeded hypoxia or in submersion of car occupants. Small differences in electrolyte disturbance are rarely of any clinical relevance and do not usually require treatment. The predominant pathophysiological process in the lungs is driven by surfactant wash-out and dysfunction, alveolar collapse, atelectasis, and intrapulmonary shunting. The severity of lung injury varies from a mild self-limiting illness to refractory hypoxaemia. Prophylactic antibiotics have not been shown to be of benefit584 but they may be considered after submersion in grossly contaminated water such as sewage. Neurological outcome, notably severe permanent neurological damage, is primarily determined by the duration of hypoxia. Compared to urban areas some terrains will be more difficult to access and are remote from organised medical care. The chances of a good outcome from cardiac arrest may be reduced because of delayed access and prolonged transport. There are no epidemiological data on the causes of cardiac arrest at high altitude. However, it is conceivable that primary cardiac arrest is the major (60­70%) cause of sudden cardiac arrest. Continuous monitoring and treatment may be difficult during transport because the patient will be insulated from the harsh environment within a rescue bag, being well wrapped and secured on a stretcher. The pO2 falls with increasing altitude and this oxygen deficiency may lead to acute manifestations of mountain sickness. These recommendations should be interpreted in the context of local conditions and legislation. Prognostic factors are severity of injury, duration of complete burial, airway patency, core temperature and serum potassium. The highest recorded potassium in an avalanche victim who was successfully resuscitated is 6. Avalanche victims are not likely to survive when they are: · buried > 60 min (or if the initial core temperature is <30 C) and in cardiac arrest with an obstructed airway on extrication; · buried and in cardiac arrest on extrication with an initial serum potassium > 8 mmol L-1. Full resuscitative measures, including extracorporeal rewarming, are indicated for all other avalanche victims without evidence of an unsurvivable injury. Avalanches occur in areas that are difficult to access by rescuers in a timely manner, and burials frequently involve multiple victims. The decision to initiate full resuscitative measures should be determined by the number of victims and the resources available, and should be informed by the likelihood of survival. The admitting hospital must be capable of advanced active external or core internal rewarming. If potassium exceeds > 8 mmol L-1, consider terminating resuscitation (after excluding crush injuries and considering if depolarizing muscle relaxants were used). Electrical injury is a relatively infrequent but potentially devastating multisystem injury with high morbidity and mortality, causing 0. In adults, electrical injuries are common in the workplace and are generally associated with high voltage, whereas children are at risk primarily at home, where the voltage is lower (220 V in Europe, Australia and Asia; 110 V in the United States and Canada). Skin resistance is decreased by moisture, which increases the likelihood of injury. Electric current follows the path of least resistance; conductive neurovascular bundles within limbs are particularly prone to damage. Myocardial or respiratory failure may cause immediate death: · Respiratory arrest may be caused by paralysis of the central respiratory control system or the respiratory muscles. A transthoracic (hand-to-hand) pathway is more likely to be fatal than a vertical (hand-to-foot) or straddle (foot-to-foot) pathway. Blast (hyperbaric) injuries, injuries from being thrown from the point of contact and tetanic contraction causing limb fractures have all been reported. Both industrial shocks and lightning strikes cause deep burns at the point of contact. For industrial shocks the points of contact are usually on the upper limbs, hands and wrists, whereas for lightning they are mostly on the head, neck and shoulders. Injury may also occur indirectly through ground current or current splashing from a tree or other object that is hit by lightning. Lightning can also cause central and peripheral nerve damage; brain haemorrhage and oedema, and peripheral nerve injury are common. Mortality from lightning injuries is as high as 30%, with up to 70% of survivors sustaining significant morbidity. Unique pattern of skin lesions called feathering or Lichtenberg figure is a pathognomonic symptom that is seen only in patients struck by lightning. Ensure that any power source is switched off and do not approach the casualty until it is safe. High-voltage (above domestic mains) electricity can arc and conduct through the ground for up to a few metres around the casualty. It is safe to approach and handle casualties after lightning strike, although it would be wise to move to a safer environment, particularly if lightning has been seen within 30 min. Patients struck by lightning are most likely to die if they sustain immediate cardiac or respiratory arrest and are not treated rapidly. When multiple victims are struck simultaneously by lightning, rescuers should give highest priority to patients in respiratory or cardiac arrest. Victims with respiratory arrest may require only ventilation to avoid secondary hypoxic cardiac arrest. Resuscitative attempts may have higher success rates in lightning victims than in patients with cardiac arrest from other causes, and efforts may be effective even when the interval before the resuscitative attempt is prolonged. Early tracheal intubation is needed in these cases, as extensive soft-tissue oedema may develop causing airway obstruction. Maintain a good urine output to enhance the excretion of myoglobin, potassium and other products of tissue damage. There are conflicting reports on the vulnerability of the fetus to electric shock. The clinical spectrum of electrical injury ranges from a transient unpleasant sensation for the mother with no effect on her fetus, to placental abruption, fetal burn or intrauterine fetal death either immediately or a few days later. Several factors, such as the magnitude of the current and the duration of contact, are thought to affect outcome.

generic trandate 100 mg

Epinephrine is a catecholamine that binds to adrenergic receptors to increase heart rate and conduction velocity heart attack 720p kickass generic trandate 100 mg overnight delivery. As a sympathomimetic drug hypertensive urgency generic trandate 100mg line, epinephrine was one of the first medications developed and used in the clinical setting for management of bradycardia blood pressure ear order trandate 100mg visa, however mrf-008 hypertension trandate 100mg on-line, in cases of symptomatic bradycardia, epinephrine is administered after atropine where atropine has been ineffective. It may also be administered through an endotracheal tube, or through intramuscular, subcutaneous, or intracardiac methods, although at different concentrations and dosages than when administered intravenously. When a cardiac cell depolarizes, it then initiates depolarization in the surrounding cells as well. This occurs as response to the transfer of sodium ions across the cardiac cell membranes. In this manner, surrounding cells respond to the initial depolarization event and the process spreads from cell to cell, which is how the impulse is conducted along the electrical pathway. The electrical activity of the heart occurs with the transfer of certain ions, specifically sodium, potassium, calcium, and chloride ions across the cell membranes. The transmembrane potential describes the slight difference in voltage between the intracellular and extracellular compartments. A cardiac cell is considered to be excitable when it has the ability to be depolarized and to stimulate action potential. The excitability of the cell membrane is further dependent on the exchange of ions and a change in the transmembrane potential. If the cardiac cells are too excitable and depolarize beyond the normal channels of the electrical impulse, the heart may beat abnormally, resulting in tachyarrythmias that can be dangerous for the patient. Re-entry is another mechanism of cardiac arrhythmia associated with altered cardiac cell excitability, which is further described below. Each cardiac impulse passes through the normal pathway in the manner of a continuous loop, with each cell depolarizing and then repolarizing after the impulse is complete. This repolarization is what sets the cells up for the next impulse to pass through the heart and the cycle continues. Re-entry describes a situation in which the electrical signal does not complete a normal circuit but instead develops its own different circuit where it loops back on itself. Re-entry can occur in one area of the heart, such as only within the ventricles, or it may affect most of the electrical conduction pathway of the entire heart. Ventricular tachycardia is an example of an arrhythmia that may develop as a result of re-entry that impacts the ventricles. Because cardiac excitability is affected by the passage of ions through the cell membrane, drugs that alter this transfer are typically those administered for treatment of arrhythmias associated with alterations in cardiac excitability. Potassium channel blockers also affect the transfer of ions across cell membranes. Potassium channel blockers slow the movement of potassium ions during a certain phase of the action potential, which slows repolarization of cells. Because of the effects of altered levels of potassium on cardiac tissue, potassium channel blockers should be used with caution to avoid inducing potentially life-threatening arrhythmias. When the sodium channels are dampened, the cells are less excitable, and the cells will be less likely to create their own abnormal pathways for electrical impulses to pass. Quinidine, as previously mentioned, is one of the more common sodium channel blockers used to control cardiac excitability. It is typically administered as an oral agent in regular or immediate-release tablets. With immediaterelease formulations, the dose is given every 6 hours, and with extended release forms, the dose is given every 12 hours. However, it is also available in intravenous form and should be initiated in the hospital environment when used for the first time. Disopyramide is often initially administered when a patient is having a potentially life-threatening cardiac arrhythmia, such as ventricular tachycardia. The drug can be initiated for treatment of the arrhythmia while the patient is in the hospital, and the patient can continue to receive the oral form of the drug as an ongoing preventive measure. Consequently, the heart begins to beat abnormally and typically experiences premature contractions. Before depolarization begins at the start of the electrical impulse, ions transfer across the cell membrane so that a difference develops between the voltage inside the cell and the voltage outside of the cell. This is known as the transmembrane potential, which was described in the previous section. Spontaneous depolarization occurs once the transmembrane potential reaches a specific point. The transmembrane potential must reach its critical threshold at a specific time in order for the process of creating the impulse to go smoothly. An ectopic beat is described as any heartbeat that originates from another area outside of the sinus node. When ectopic beats occur continuously, the affected individual is experiencing an arrhythmia. This results in arrhythmias that are slower than the normal pace of the heart, including bradycardia. Abnormal automaticity may also involve a tachycardic state where the heart beats at a pace that is too fast. Arrhythmias may therefore develop when the normal system of automaticity is enhanced or when it is suppressed. Some of the more common causes that lead to abnormal automaticity include electrolyte imbalances and cardiac ischemia. Quinidine is used to restore normal sinus rhythm and may be administered to suppress ventricular tachycardia. It is classified as such because it has a moderate effect on sodium channels to prolong repolarization and action potential. Quinidine may be used to treat different forms of arrhythmias, including atrial fibrillation or supraventricular tachycardia. It is typically administered as a loading dose followed by maintenance doses of the drug; the amount and the rate of infusion also depend on the urgency of the situation. For patients with moderate cardiac impairment, a loading dose of 15 to 18 mg/kg administered as a slow infusion over 30 minutes, followed by a maintenance dose of 1 to 4 mg/kg by continuous infusion is a standard form of administration. It should be used with caution, particularly among patients who have had previous myocardial infarction or among patients with potassium imbalances. It is most often used to treat tachyarrhythmias, such as ventricular tachycardia or cardiac arrest as a result of ventricular fibrillation. Lidocaine has been shown to slow depolarization and to decrease automaticity without affecting cell excitability. If the arrhythmia does not initially respond to the dose, it may be repeated at 0. A patient with stable arrhythmia, such as significant premature ventricular contractions or ventricular tachycardia that has not caused cardiac arrest can receive 0. In contrast, maintaining normal blood pressure levels decreases the risk of and prevents intravascular and cardiac damage to the nursece4less. Because of the changes that it can cause within the cardiovascular system, hypertension is associated with a greater risk of complications such as stroke, ischemic heart disease, vision loss, kidney damage, and heart failure. The danger associated with hypertension is that many people who suffer from the condition are unaware of it until they develop symptoms of its associated complications. The American Heart Association has defined normal blood pressure readings and levels of hypertensive readings as follows:13 Normal blood pressure: Less than 120/80 mmHg Prehypertension: 120-139 mmHg (systolic) and 80-89 mmHg (diastolic) Stage 1 hypertension: 140-159 mmHg (systolic) and 90-99 mmHg (diastolic) Stage 2 hypertension: 160 mmHg or greater (systolic) and 100 mmHg or greater (diastolic) Hypertensive crisis: 180 mmHg or greater (systolic) and 110 mmHg or greater (diastolic) Unfortunately, hypertension is prevalent in society, affecting 1 out of 3 Americans over age 18. Instead, a range of normal values must be given to patients that would prevent cardiac complications and that is based on individual factors, including age and weight, as well as the presence of chronic medical conditions, such as diabetes or metabolic disorder. Hypertension is generally divided into two main types: primary hypertension and secondary hypertension. Primary hypertension develops under circumstances where there is no obvious cause of the condition, although the affected patient may have risk factors. Secondary hypertension describes high blood pressure that has developed as a result of a medical condition or some other reason that provides a specific cause for the hypertension. Primary hypertension is more commonly seen among those who have certain factors in common, and it is thought to have a genetic component. Risk factors associated with primary hypertension include advancing age, elevated dietary sodium intake, obesity, sedentary lifestyle, excess alcohol intake, and increased stress or anxiety. However, several mechanisms play a role in the development of the condition, such as increased vasomotor tone due to an elevated sympathetic drive, alterations in the renin-angiotensin-aldosterone system, and increased blood volume. Management of these conditions through pharmacologic interventions may successfully control the underlying circumstances that contribute to high blood pressure and may also satisfactorily control primary hypertension.

Purchase trandate 100 mg without a prescription. C-Reactive Protein (CRP) Positive Test.

References