By F. Ketil. William Penn College.
Follow response: "I want to follow the treatment by assessing his pain (I will ask him about the degree of exercise he is able to perform without chest pain) purchase clindamycin cheap online, perfo rm a cardiac stress test order clindamycin 150mg online, and reassess him after the test is done cheap clindamycin 150 mg on-line. The next step depends upon the clinical state of the patient (if unstable, the next step is therapeutic), the potential severity of the disease (the next step may be staging), or the uncertainty of the diagnosis (the next step is diagnostic). This question goes further than making the diagnosis, but also requires the student to understand the underlying mechanism for the process. The student is advised to learn the mechanisms for each disease process, and not merely memorize a constellation of symptoms. The platelets-antibody complexes are then taken from the circulation in the spleen. Because the disease process is specific for platelets, the other 2 cell lines (erythrocytes and leukocytes) are normal. Also, because the thrombocytopenia is caused by excessive platelet peripheral destruction, the bone marrow will show increased megakaryocytes (platelet precursors). Understanding the risk factors helps the practitioner to establish a diagnosis and to determine how to interpret tests. For example, understanding the risk factor analysis may help manage a 45-year-old obese man with sudden onset of dyspnea and pleu ritic chest pain following an orthopedic surgery for a femur fracture. This patient has numerous risk factors for deep venous thrombosis and pulmonary embolism. The physician may want to pursue angiography even if the ventilation/perfsion scan result is low probability. Thus, the number of risk factors helps categorize the likelihood of a disease process. A clinician must understand the complications of a disease so that one may monitor the patient. Sometimes the student has to make the diagnosis from clinical clues and then apply his/her knowledge of the sequelae of the pathological process. For example, the student should know that chronic hypertension may afect various end organs, such as the brain (encephalopathy or stroke), the eyes (vascular changes), the kidneys, and the heart. Understanding the types of consequences also helps the clinician to be aware of the dangers to a patient. The clinician is acutely aware of the need to monitor for the end-organ involvement and undertakes the appropriate intervention when involvement is present. To answer this question, the clinician needs to reach the correct diagnosis, assess the severity of the condition, and weigh the situation to reach the appropriate inter vention. For the student, knowing exact dosages is not as important as understand ing the best medication, the route of delivery, mechanism of action, and possible complications. It is important for the student to be able to verbalize the diagnosis and the rationale for the therapy. A common error is for the student to "jump to a treatment," like a random guess, and therefore is given "right or wrong" feedback. Instead, the student should verbalize the steps so that feedback may be given at every reason ing point. For example, if the question is, "What is the best therapy for a 25-year-old man who complains of a cough, fever, and a 2-month history of 10 lb weight loss? Therefore, the best treatment for this man is either antimicrobial therapy such as with trim ethoprim/sulfa, or chemotherapy after confirmation of the diagnosis. Knowing the limitations of diagnostic tests and the manifestations of disease aid in this area. There are 4 steps to the clinical approach to the patient: making the diagnosis, assessing severity, treating based on severity, and following response. Assessment of pretest probability and knowledge of test characteristics are essential in the application of test results to the clinical situation. There are 7 questions that help bridge the gap between the textbook and the clinical arena. The focus of the infection is the urinary tract and that should determine the antibiotic choices. The presence of tachycardia, tachypnea, hypotension, hypoxemia, and low urine output combined with a decreased mental status are all responses to sepsis. To be familiar with the treatment strategies to correct abnormal vital signs and early goal-directed therapy. Co nsidertions The patient described in this scenario was about to be discharged from the hospital. The nurse called regarding abnormal vital signs, which were dramatically altered from normal. For instance, the oxygen saturation of 80% likely correlates to an oxygen partial pressure of 45 mm Hg, which is incompatible with life. This hospital has a rapid response team, which is a mul tidisciplinary team that assesses patients quickly when there are potential critical illnesses. A delay in assessment, recognition, or therapy could lead to adverse consequences, including death. The recently developed rapid response teams or medical emergency teams which consist of a group of clinicians and nurses, brings critical care expertise to the bedside. Their expertise has drastically reduced both the incidence of cardiac arrests and subsequent deaths. This has resulted in an increase in the number of patients who are discharged in a fnctional state. Scoring systems utilizing routine observations and vital signs taken by the nursing and ancillary stafare used to evaluate the possible deterioration ofpatients. This dete rioration is fequently preceded by a frther decline in physiological parameters. Fur thermore, a failure ofthe clinical stafto recognize this failure in respiratory or cerebral fnction will put patients at risk of cardiac arrest. Precautions to prevent aspiration such as elevation of the head of the bed to 30° to 45° should be instituted whenever there is a change in mental status, or increased risk of aspiration, provided the current blood pressure allows this. Cardiac arrest has been associated with the failure to correct physiological derangement in oxygenation (breathing), hypotension (blood pressure), and mental status (see Table 1-1). The respiratory rate varies with age, but the normal reference range for an adult is 12 to 20 breaths/minute. A narrow pulse pressure value is also caused by aortic stenosis and cardiac tamponade. When excessively elevated, these values are associated with an increased risk of stroke and heart disease. The pulse rate is usually measured at the wrist or at the ankle and is recorded as beats/minute. The pulse rate can also be measured by listening directly to the heartbeat using a stethoscope.
Nonetheless purchase on line clindamycin, the drug is suspected because (1) sudden hearing loss is unusual and (2) it developed when sildenafil was taken buy cheap clindamycin on-line. About 3% of patients experience mild transient visual disturbances (blue color tinge to vision clindamycin 150 mg on line, increased sensitivity to light, blurring). In addition, sildenafil may intensify symptoms of obstructive sleep apnea (perhaps by relaxing pharyngeal muscles or dilating pulmonary blood vessels). At least 24 hours should elapse between the last dose of sildenafil and giving a nitrate. P ro t o t y p e D r u g s Drugs for Erectile Dysfunction and Benign Prostatic Hyperplasia Drugs for Erectile Dysfunction Phosphodiesterase Type 5 Inhibitor Sildenafil Nonoral Drugs Papaverine/phentolamine Alprostadil Drugs for Benign Prostatic Hyperplasia 5-Alpha-Reductase Inhibitor Finasteride Alpha-Adrenergic Antagonist Tamsulosin Alpha Blockers. Alpha-adrenergic antagonists—including doxazosin [Cardura] and other alpha blockers used for prostatic hyperplasia (see later discussion)—dilate arterioles and can thereby lower blood pressure. However, there was a question as to what caused the adverse events: sildenafil or the sexual activity that sildenafil permitted. Accordingly, the drug should be used with caution by men with the following conditions: • Myocardial infarction, stroke, or life-threatening dysrhythmia within the last 6 months • Resting hypotension (blood pressure below 90/50 mm Hg) • Resting hypertension (blood pressure above 170/110 mm Hg) • Heart failure • Unstable angina In addition, sildenafil should not be used at all by men taking nitroglycerin or any other drug in the nitrate family. To reduce the risk for adverse events, candidates for sildenafil therapy should undergo a careful evaluation of cardiovascular function. Those with impaired function should be counseled about the risks posed by sexual activity and all other moderate to intense physical activity. Vardenafil, Tadalafil, and Avanafil Vardenafil, tadalafil, and avanafil are very similar to sildenafil. As with sildenafil, benefits derive from relaxing arterial and trabecular smooth muscle in the penis. There is no evidence that vardenafil works faster, longer, or better than sildenafil. Plasma levels peak about 1 hour after dosing, or after 2 hours if dosing is done with a high-fat meal. Vardenafil is contraindicated for use with alpha-adrenergic blockers and with nitroglycerin and other nitrates. On average, therapeutic levels of the drug are reached by 2 hours after dosing and persist about 36 hours —much longer than with sildenafil or vardenafil. The most common adverse effects are headache, dyspepsia, back pain, myalgia, limb pain, flushing, and nasal congestion. Because tadalafil has a long duration of action, adverse effects may persist for many hours. Tadalafil is contraindicated for use with nitrates or alpha blockers (except tamsulosin [Flomax]). The manufacturer does not identify a minimum time between dosing and sexual activity. However, because blood levels peak more slowly than with sildenafil or vardenafil, allowing at least 1 hour for absorption would seem reasonable. Daily dosing is recommended only for men who anticipate sexual activity at least twice a week. Plasma levels peak about 30 to 45 minutes after dosing in fasting patients, or after 1. It can increase the hypotensive effects of alcohol and antihypertensive drugs, especially alpha-adrenergic antagonists. A starting dose of 50 mg (the lowest strength available) is recommended if prescribed for patients taking antihypertensive drugs. Specifically, they are administered either by injection into the penis or by insertion into the urethra. Administration is accomplished by loading a pellet into a small plastic applicator, which is then inserted an inch and a half into the urethra. Erection develops 5 to 10 minutes after drug insertion and lasts 30 to 60 minutes. Relaxation of smooth muscle1 1 (arterial, venous, and trabecular), causing a rapid inflow of arterial blood. As explained when discussing physiology of erection, the blood fills the vascular sinusoidal spaces of the corpora cavernosa resulting in an erection. Pressure from the engorged penis helps block venous outflow to promote maintenance of the erect state. Adverse Effects The most common adverse effect, dull ache in the penis, occurs in 32% of users. Systemic symptoms are rare when taken as directed and approximate those of placebo use. Intracavernous Alprostadil [Caverject, Caverject Impulse, Edex] is also available in a form for direct injection into the corpus cavernosum. A training video demonstrating how to inject the medication plus a link to access written instructions is available online at http://www. The dosing end point is an erection that is sufficient for intercourse but that does not last for more than 1 hour. Injectable alprostadil should be used no more than 3 times a week and not more than once in 24 hours. Papaverine Plus Phentolamine The combination of papaverine (a vasodilator) plus phentolamine (an alpha- adrenergic blocking agent) can provide tumescence when injected directly into the corpus cavernosum. Arterial inflow is augmented by alpha-adrenergic blockade (causing arterial dilation) and by the direct relaxant action of papaverine on arterial smooth muscle. Adverse Effects Priapism (persistent erection lasting more than 6 hours) occurs in about 10% of patients. Other adverse effects include orthostatic hypotension with dizziness, transient paresthesias, ecchymosis (extravasation of blood into subcutaneous tissue), and difficulty in achieving orgasm or ejaculation. In 2015 the Canadian Urologic Association developed and published updated clinical guidelines for treatment of erectile dysfunction. Pathophysiology and Overview of Treatment Pathophysiology The prostate is a heart-shaped gland that surrounds the male urethra. Overgrowth of epithelial cells causes mechanical obstruction of the urethra, whereas overgrowth of smooth muscle causes dynamic obstruction of the urethra. Therefore some men with only moderate enlargement may be highly symptomatic, whereas others with substantial enlargement may have no symptoms. These procedures are most appropriate for men with severe symptoms or complications. Watchful waiting, which consists of annual reevaluation with reconsideration of management based on results, is appropriate for men with minimal symptoms. The 5-alpha- reductase inhibitors are most appropriate for men with very large prostates (mechanical obstruction), whereas alpha blockers are preferred for men with relatively small prostates (dynamic obstruction). Teratogenic to the Finasteride Proscar which reduces mechanical obstruction of male fetus. Swallow [Avodart] capsules whole Finasteride Tablets: 5 mg 5 mg once a day May take with or without food.
This is a product of ventilation/perfusion mismatch and intrapulmonary shunt due to alveolar ﬂooding and atelectasis generic clindamycin 150mg with mastercard. Pulmonary compliance is reduced due to atelectasis purchase clindamycin 150mg overnight delivery, alveolar oedema buy clindamycin 150mg with mastercard, and ﬁbroproliferation. This is due to hypoxic pulmonary vasoconstriction and the effect of inﬂammatory mediators (e. Death is usually as a result of multiorgan failure related to systemic inﬂammation, rather than as a result of hypoxaemic respiratory failure. During the ﬁrst 12–24h bilateral, hazy opacities develop, often described as ‘ground glass’. Consolidation is predominantly seen in the dependent areas, progressing through ground glass to normally aerated lung above, see Fig. Lung function Conventional pulmonary function testing cannot be performed on mechanically ventilated patients. Major complications (including bleeding, pneumothorax, and persistent air leak) are seen in 7% of patients, with minor complica- tions in 40%. Anti-inﬂammatory drugs Corticosteroids Steroids reduce levels of pro-inﬂammatory cytokines (e. Steroids cause hyperglycemia and exacerbate critical illness poly(myo)neuropathy, and concern exists surrounding the potential increased risk of infection. They were able to demonstrate an improvement in oxygenation and lung compliance but also an increase in the rate of neuromuscular weakness and hyperglycemia. It is associated with a number of side-effects, including hypotension, hypoxia, and dysrhythmias. Ketoconazole Ketoconazole is an antifungal drug that inhibits production of thrombox- anes and leukotrienes by pulmonary endothelial cells. Thromboxanes cause vasoconstriction and platelet aggregation, while leukotrienes cause bronchoconstriction and are important neutrophil chemokines. Pentoxifylline and lisofylline Pentoxifylline and its metabolite lisofylline are phosphodiesterase inhibitors that exhibit an anti-inﬂammatory action by reducing circulating levels of free fatty acids and inhibiting free radical formation. Inhaled vasodilators Vasodilatation within ventilated lung units should improve oxygenation by improving ventilation/perfusion matching. Sildenaﬁl Sildenaﬁl is a selective inhibitor of phosphodiesterase-5 that leads to relaxation of vascular smooth muscle, predominantly leading to pulmo- nary vasodilatation. Almitrine Almitrine causes pulmonary vasoconstriction by stimulating peripheral chemoreceptors. By augmenting hypoxic pulmonary vasoconstriction, almitrine is thought to improve hypoxaemia. Surfactant Surfactant prevents alveolar collapse by attenuating surface tension in the alveoli. Surfactant is a mix of four different proteins (10%) and lipid (90%) that is produced by type 2 pneumocytes. Exogenous surfactant may be nebulized or directly distilled into the airway via a bronchoscope. Multiple applications are often required as surfactant is dispersed by alveolar oedema. A meta-analysis of human trials showed a non-signiﬁcant improvement in oxygenation and no effect on mortality. Fluid balance Alveolar oedema forms as a result of increased vascular permeability and raised hydrostatic pressure. By reducing hydrostatic pressure less ﬂuid should leak into the alveolar air spaces. Institution of the study protocol did not occur until approximately 48h to allow appropriate ﬂuid resuscitation in the acute phase. Nutrition Appropriate nutritional support is required to look after all critically ill patients. A reduction in the ratio of carbohydrate in feed (‘pulmonary’ feed) has been advocated as a technique to reduce carbon dioxide pro- duction. This practice is not recommended as it increases the risk of mal- nutrition and is not supported by an evidence base. The use of sedation also reduces the respiratory muscles’ (and therefore the total) oxygen demand. In extreme circumstances there may be a need to add neuromuscular blocking drugs to heavy sedation. The effect of paralysis is unpredictable as gas exchange may be improved by reducing ventilator dyssynchrony or increasing chest wall compliance, or potentially worsened by increasing atelectasis resulting from abolishing any spontaneous breaths. The effects of the medication are difﬁcult to disentangle from the effects of mechanical ventilation (which has been shown to cause signiﬁ- cant and rapid atrophy of the diaphragm8). Daily breaks (‘holds’) in sedation, or sedation scoring and very regular adjustment of sedation to maintain patients as lightly sedated as safely possible, should be used to reduce the time to waking and decrease the risk of neuromuscular complications. Cardiovascular manipulation Increasing O2 delivery by addressing cardiac output and Hb concentration will increase the mixed venous oxygen saturation, and reduce the impact of intrapulmonary shunting on arterial oxygenation. By using small tidal volumes it was hoped that the progressive lung injury caused by mechanical ventilation could be minimized. Some criticism has been levelled at this trial for the relatively high tidal volumes used in the control arm, which may be injurious and are higher than are commonly used. Permissive hypercapnia A low tidal volume ventilation strategy will cause alveolar hypoventilation with resulting hypercapnia. This can be offset to a degree by increasing the respiratory rate (although the reduced inspiratory and expiratory times may cause a further fall in tidal volume). Permissive hypercapnia means that, as long as the ventilation strategy has been optimized with low tidal volumes and high respiratory rate, hypercapnia is tolerated. By preventing cyclical opening and closing of these units, the damaging effects of atelectrauma can be prevented. It may exacerbate ventila- tion perfusion mismatching by increasing the physiological dead space. It differs between patients and will change in the same patient with disease progression, ﬂuid status, patient position etc. Mechanical ventilation allows delivery of high concentrations of oxygen and has the added advantage of resting the respiratory muscles and therefore reducing oxygen demand. Oxygen concentrations should be reduced as quickly as possible in order to reduce the potentially toxic effects of reactive oxygen species and to help limit absorption atelectasis. Pressure- vs volume-controlled modes of ventilation There are no trials directly comparing pressure- with volume-limited ventilation. There are physiological differences between the modes that are more fully discussed in b Pressure control ventilation, p 135.
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