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By: V. Uruk, M.B. B.CH. B.A.O., M.B.B.Ch., Ph.D.

Clinical Director, Wayne State University School of Medicine

One explanation of how an antiarrhythmic agent may abolish reentry is by converting unidirectional block to bidirectional block symptoms tonsillitis order discount isoniazid. Thus symptoms 3 days before period discount isoniazid 300 mg with mastercard, although the grouping of antiarrhythmic agents into four classes is convenient medications ending in pam purchase isoniazid 300mg on-line, such a classification falls short of explaining the underlying mechanisms by which many drugs ultimately exert their therapeutic antiarrhythmic effect. Also, certain agents do not fall neatly into the four classes; these are discussed at the end of the chapter. Although many class I antiarrhythmic drugs possess local anesthetic actions and can depress myocardial contractile force, these effects are usually observed only at higher plasma concentrations. The antiarrhythmic drugs in class I suppress both normal Purkinje fiber and His bundle automaticity in addition to abnormal automaticity resulting from myocardial damage. Suppression of abnormal automaticity permits the sinoatrial node again to assume the role of the dominant pacemaker. The antiarrhythmic agents that belong to class I are divided into three subgroups (Table 16. Members of this class impair the function of the membrane sodium channel, thereby decreasing the number of channels available for membrane depolarization. Members of this class directly decrease the slope of phase 4 depolarization in pacemaker cells, especially those that arise outside of the sinoatrial node. Members of this class have a minimal effect on conduction velocity in ventricular myocardium and are without apparent effect on refractoriness. Class I Drugs Class I antiarrhythmic drugs are characterized by their ability to block the voltage-gated sodium channel. The class I agents may block the channel when it is in either the open or the inactivated state. Inhibition of the sodium channel results in a decrease in the rate of rise of phase 0 of the cardiac membrane action potential and a slowing of the conduction velocity. Minimally change Vmax of phase 0, decrease cardiac action potential duration, decrease inward sodium current in ventricular muscle, increase outward potassium current. The most pronounced electrophysiological effects are exerted on cardiac cells that depend on the Ca channel for initiating the action potential, such as those found in the sinoatrial and A-V nodes. This action may terminate supraventricular tachycardias and can slow conduction during atrial flutter or fibrillation. Because of the high incidence of ventricular proarrhythmia associated with its use and numerous other equally efficacious agents, quinidine is now used sparingly. Quinidine shares all of the pharmacological properties of quinine, including antimalarial, antipyretic, oxytocic, and skeletal muscle relaxant actions. The anticholinergic actions of quinidine predominate at lower plasma concentrations. Higher concentrations of quinidine have a direct effect of depressing the rate of spontaneous diastolic depolarization. Quinidine administration results in a dose-dependent depression of membrane responsiveness in atrial muscle fibers. The maximum rate of phase 0 depolarization and the amplitude of phase 0 are depressed equally at all membrane potentials. Quinidine also decreases atrial muscle excitability in such a way that a larger current stimulus is needed for initiation of an active response. These actions of quinidine often are referred to as its local anesthetic properties. A-V Node Both the direct and indirect actions of quinidine are important in determining its ultimate effect on A-V conduction. The indirect (anticholinergic) properties of quinidine prevent both vagally mediated prolongation of the A-V node refractory period and depression of conduction velocity; these effects lead to enhancement of A-V transmission. His-Purkinje System and Ventricular Muscle Quinidine can depress the automaticity of ventricular pacemakers by depressing the slope of phase 4 depolarization. Depression of pacemakers in the HisPurkinje system is more pronounced than depression of sinoatrial node pacemaker cells. Quinidine also prolongs repolarization in Purkinje fibers and ventricular muscle, increasing the duration of the action potential. As in atrial muscle, quinidine administration results in postrepolarization refractoriness, that is, an extension of refractoriness beyond the recovery of the resting membrane potential.

Syndromes

• Infection
• Damage to the teeth
• Washing of the skin (irrigation) -- perhaps every few hours for several days
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Clinical Symptoms Pertussis symptoms kidney failure order isoniazid in united states online, or whooping cough treatment 5th disease discount 300 mg isoniazid with visa, is characterized by four stages with relatively distinct clinical features symptoms when pregnant isoniazid 300mg with mastercard. Despite its nonspecific symptoms, this stage harbors the period of maximum infectivity. Patients have periodic paroxysms consisting of repetitive nonproductive coughing followed by an inspiratory "whoop"; this then cycles and is often terminated only by posttussive emesis or exhaustion. Finally, the convalescent stage lasts for approximately 1 month and is characterized by the gradual reduction in intensity and frequency of paroxysms. Treatment Macrolide antibiotic therapy is effective only when given during the incubation or catarrhal stages of the disease. Household contacts of patients with pertussis undergo chemoprophylaxis with 14 days of erythromycin. Legionella pneumophila Characteristics Legionella pneumophila is a motile, pleomorphic, gram-negative rod that is facultatively intracellular. The organism is poorly visualized on Gram stain; therefore, silver or fluorescent antibodies are used. Once engulfed, the organism multiplies inside the phagosomes of alveolar macrophages following phagocytosis, specifically inhibiting lysosome fusion so that it is not destroyed. Clinical Symptoms the mild form of legionellosis is an influenza-like illness called Pontiac fever. It is characterized by epidemic outbreaks with a high attack rate, as well as a clinical syndrome of fever, chills, and myalgias with resolution in about 1 week without treatment. Legionnaires disease is a severe community-acquired pneumonia that generally affects elderly persons with underlying lung disease. Clinical presentation includes a nonproductive cough, high fevers, headache, confusion, and watery diarrhea, with a rapid deterioration often leading to death if antibiotic therapy is not promptly started. Treatment the mainstay of treatment is fluoroquinolones; penicillins are not effective because of the presence of -lactamase. Pathogenic enteric microbes infect the lumen of the lower alimentary canal and can produce syndromes along two clinical spectra: diarrheal disease and systemic disease. Enterobacteriaceae: A large family consisting of organisms such as Shigella dysenteriae, E coli, Salmonella enterica, and K pneumoniae. Other notable members of the family include Yersinia enterocolitica, Proteus mirabilis, Enterobacter cloacae, and S marcescens. Vibrionaceae: Notable organisms are Vibrio cholerae, Campylobacter jejuni, and Helicobacter pylori. Bacteroidaceae: Bacteroides fragilis, an anaerobe that can cause gastrointestinal infections. The heat-labile K antigen refers to the polysaccharide capsule if present, and the heat-labile H antigen is a flagellar protein that may be present. Nonmotile, gram-negative rod-shaped organisms that do not ferment lactose but are able to produce H2S gas. Humans are the only host of Shigella; in contrast to many other Enterobacteriaceae, there is no animal reservoir. Pathogenesis Transmission is from person to person via the fecal-oral route, and as few as 10 organisms may cause symptomatic infection. Shigella species cause invasive gastroenteritis by attaching to and invading immune cells located in Peyer patches. Shiga toxin is a typical A-B toxin in which the B subunit binds to enterocytes, allowing the A unit to penetrate the cells and cause cell death. S dysenteriae specifically produces the Shiga toxin and can cause a more severe form of the disease termed bacterial dysentery; this species is also occasionally associated with the hemolytic-uremic syndrome. Salmonella species are motile, gram-negative rods that, like Shigella, produce H2S gas, and do not ferment lactose. Like Shigella, the main route of Salmonella invasion is via the M cells of the Peyer patches of the intestine, which may result in hematogenous spread. S typhi can reside in macrophage vesicles, allowing it to be carried to extraintestinal sites to cause typhoid fever.

Lymph nodes are encapsulated secondary lymphoid organs that receive lymph from multiple afferent vessels medications for ptsd discount 300mg isoniazid with mastercard, providing the opportunity for interaction between the stored immune cells and the lymphatic fluid medicine and science in sports and exercise cheap 300mg isoniazid otc. Primary medications varicose veins buy isoniazid online now, or inactive, follicles are dense with stored lymphocytes awaiting antigen presentation. For this reason, the thymus is underdeveloped and causes the classic finding of an absent thymic shadow on chest x-ray. From there, chemokines will guide T cells to the paracortex and B cells to lymphoid follicles. The medullary sinus drains cells and fluid in the medulla into the efferent lymphatic duct. Lymphatic System Lymphatic vessels drain fluid from the body, filter it through lymph nodes, and return it to the circulatory system. The right lymphatic duct drains the right arm and right half of the head and neck, whereas the thoracic duct drains all other body parts. The fluid from the thoracic duct drains into the left subclavian vein, and that from the right lymphatic duct drains into the junction of the right subclavian and internal jugular veins. Peripheral Lymphoid Tissue Collections of lymphocytes outside the spleen and lymph nodes that are at prime locations for antigen interaction are termed peripheral lymphoid tissue. Thoracic duct drains everything else into junction of left subclavian and internal jugular veins. Engulfed microbes trigger an oxidative burst that creates reactive oxygen species that are lethal to pathogens. Before antigen exposure, they can be identified by long, fingerlike processes of cytoplasm. After taking up antigen and becoming activated, they travel to lymph nodes where they present antigen to T cells. These hypersegmented neutrophils can be a sign of vitamin deficiencies, specifically B12 and folate. The classic pathway is activated when C1 recognizes and binds the constant fragment of either IgG or IgM in an antigen-antibody complex. The alternative pathway is triggered when activated C3 or IgA antibodies recognize antigens on microbial surfaces. The three activation pathways converge on the generation of C3 convertase, an enzyme that remains associated with the pathogen surface to trigger cleavage of other complement proteins. C3 convertase breaks down C3 molecules to the enzymatically active C3b and the anaphylatoxin C3a, which mediates a local inflammatory response. Binding of C3b to C3 convertase creates C5 convertase, which cleaves C5 into C5a (another anaphylatoxin) and C5b, which is inserted into the cell membrane of the pathogen. As with the coagulation system, the formation of a few active enzymes can lead to rapid activation and amplification of the complement cascade. Therefore, regulatory proteins are important in maintaining control of the cascade. Adaptive Immunity Adaptive immunity can be divided into cell-mediated immunity and humoral immunity. They are involved in cell-mediated immunity and have two major responsibilities (Table 3-6). Helper T cells (Th): "Help" B cells produce antibodies and secrete cytokines that "help" other cells perform their functions. Their main function is to recognize extracellular pathogens and differentiate into plasma cells that produce antibodies to target pathogens for elimination from the body. Antibodies Antibodies are proteins composed of two heavy (H) chains and two light (L) chains. Antibodies are composed of two antigen-binding fragments (Fab) and one constant fragment (Fc).

Although vasodilators would appear to be ideal drugs for the treatment of hypertension symptoms kidney failure dogs purchase generic isoniazid on-line, their effectiveness symptoms 9dp5dt order isoniazid paypal, particularly when they are used chronically medicine 6mp medication discount isoniazid 300mg without prescription, is severely limited by neuroendocrine and autonomic reflexes that tend to counteract the fall in blood pressure. How these reflexes compromise the fall in blood pressure produced by the vasodilators is shown in. The diagram does not show all of the possible interrelationships but rather is meant to draw attention to the most prominent reflex changes. Initially, diuretics produce a mild degree of Na depletion, which leads to a decrease in extracellular fluid volume and cardiac output. The effectiveness of diuretic therapy in mild hypertension may also involve either interference with or blunting of cardiovascular reflexes. High salt intake or low rates or glomerular filtration will eliminate the antihypertensive effects of the drugs. The value of diuretics lies in their ability to reverse the Na retention commonly associated with many antihypertensive drugs that probably induce Na retention and fluid volume expansion as a compensatory response to blood pressure reduction. When diuretic therapy is indicated for the treatment of primary hypertension, the thiazide-type compounds. Approximately 30% of patients with mild hypertension may be treated effectively with thiazide therapy alone. These pathways lead ultimately to an increase in blood pressure and thus compromise the effectiveness of the vasodilators. The effectiveness can be preserved by coadminstration of propranolol (P) and a diuretic (D). Large increases in cardiac output occurring as a result of vasodilator therapy will substantially counter the druginduced reduction of blood pressure. Increased reflex sympathetic input to the heart also augments myocardial oxygen demand; this is especially serious in patients with coronary insufficiency and little cardiac reserve. The hyperreninemia appears to be due in part to enhanced sympathetic nervous activity. Elevated renin levels lead to an increase in the concentration of circulating angiotensin, a potent vasoconstrictor (see Chapter 18) and thus an increase in peripheral vascular resistance. Thus, it seems that the lack of sympathetic nervous system inhibition produced by the vasodilators, which is advantageous in some ways, can also be a disadvantage in that reflex increases in sympathetic nerve activity will lead to hemodynamic changes that reduce the effectiveness of the drugs. Therefore, the vasodilators are generally inadequate as the sole therapy for hypertension. However, many of the factors that limit the usefulness of the vasodilators can be obviated when they are administered in combination with a -adrenoceptor antagonist, such as propranolol, and a diuretic. Propranolol reduces the cardiac stimulation that occurs in response to increases in sympathetic nervous activity, and the large increase in cardiac output caused by the vasodilators will be reduced. The reduction in Na excretion and the increase in plasma volume that occurs with vasodilator therapy can be reduced by concomitant treatment with a diuretic. Mechanism of Action Available evidence suggests that a single unifying mechanism does not exist but rather that various vasodilators may act at different places in the series of processes that couple excitation of vascular smooth muscle cells with contraction. For example, the vasodilators known as calcium channel antagonists block or limit the entry of calcium through voltage-dependent channels in the membrane of vascular smooth muscle cells. In this way, the calcium channel blockers limit the amount of free intracellular calcium available to interact with smooth muscle contractile proteins (see Chapter 14). Other vasodilators, such as diazoxide and minoxidil, cause dilation of blood vessels by activating potassium channels in vascular smooth muscle. An increase in potassium conductance results in hyperpolarization of the cell membrane, which will cause relaxation of vascular smooth muscle. The action of the nitrovasodilators appears to be quite similar to that of the endogenous vasodilator released by a variety of stimuli from endothelial cells of blood vessels. The knowledge that the nitrovasodilators generate nitric oxide in vivo suggests that this substance may be the final common mediator of a number of vascular smooth muscle relaxants. Two of these agents, hydralazine and minoxidil, are effective orally and are used for the chronic treatment of primary hypertension. The other two drugs, diazoxide and sodium nitroprusside, are effective only when administered intravenously. They are generally used in the treatment of hypertensive emergencies or during surgery. Interestingly, the half-life of the antihypertensive effect is somewhat longer than the plasma half-life.

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