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By X. Gambal. The McGregor School of Antioch University.
Antimalarial Action: Chloroquine is a highly effective blood schizonticide and is most widely used in chemoprophylaxis and in treatment of attacks of vivax 45mg midamor mastercard arteria century 21, ovale discount midamor 45mg fast delivery heart attack bpm, malariae, or sensitive falciparum malaria. Chloroquine is not active against the preerythrocytic plasmodium and does not effect radical cure. Selective toxicity for malarial parasites depends on a chloroquine-concentrating mechanism in parasitized cells. Clinical uses: Acute Malaria Attacks (it clears the parasitemia of acute attacks of P vivax, P ovale, and P malariae and of malaria due to nonresistant strains of P falciparum), and chemoprophylaxis (It is the preferred drug for prophylaxis against all forms of malaria except in regions where P falciparum is resistant to 4-aminoquinolines). Adverse Effects: Gastrointestinal symptoms, mild headache, pruritus, anorexia, malaise, blurring of vision, and urticaria are uncommon. A total cumulative dose of 100 g (base) may, contribute to the development of irreversible retinopathy, ototoxicity, and myopathy. Contraindications: It is contraindicated in patients with a history of liver damage, alcoholism, or neurologic or hematologic disorders, psoriasis or porphyria, in whom it may precipitate acute attacks of these diseases. After oral administration, the drug is usually well absorbed, completely metabolized, and excreted in the urine. Primaquine is active against the late hepatic stages (hypnozoites and schizonts) of P vivax and P ovale and thus effects radical cure of these infections. Primaquine is also highly active against the primary exoerythrocytic stages of P falciparum. When used in prophylaxis with chloroquine, it protects against P vivax and P ovale. Pneumocystis carinii pneumonia Adverse Effects: Primaquine is generally well tolerated. Quinine Quinine is rapidly absorbed, reaches peak plasma levels in 1-3 hours, and is widely distributed in body tissues. The elimination half-life of quinine is 7-12 hours in normal persons but 8-21 hours in malaria-infected persons in proportion to the severity of the disease. Bulk of the drug is metabolized in the liver and excreted for the most part in the urine. Quinine is a rapidly acting, highly effective blood schizonticide against the four malaria parasites. The drug is gametocidal for P vivax and P ovale but not very effective against P falciparum gametocytes. Cinchonism; a less common effect and manifested by headache, nausea, slight visual disturbances, dizziness, and mild tinnitus and may subside as treatment continues. Severe toxicity like fever, skin eruptions, gastrointestinal symptoms, deafness, visual abnormalities, central nervous system effects (syncope, confusion), and quinidine-like effects occurs rarely. Proguanil and Pyrimethamine Pyrimethamine and proguanil are dihydrofolate reductase inhibitors. Pyrimethamine and proguanil are slow acting blood schizonticides against susceptible strains of all four malarial species. Proguanil (but not pyrimethamine) has a marked effect on the primary tissue stages of susceptible P falciparum and therefore may have causal prophylactic action. Resistance to pyrimethamine and proguanil is found worldwide for P falciparum and somewhat less ubiquitously for P vivax. Toxoplasmosis treatment Adverse Effects: In malaria treatment, pyrimethamine and proguanil are well tolerated. In the high doses pyrimethamine causes megaloblastic anemia, agranulocytosis and thrombocytopenia (leucovorin calcium is given concurrently). Sulfones and Sulfonamides Sulfonamides and sulfones have blood schizonticidal action against P falciparum by inhibition of dihydrofolic acid synthesis. But, the drugs have weak effects against the blood schizonts of P vivax, and they are not active against the gametocytes or liver stages of P falciparum or P vivax. When a sulfonamide or sulfone is combined with an antifol, synergistic blockade of folic acid synthesis occurs in susceptible plasmodia. Sulfadoxine with pyrimethamine (Fansidar) and dapsone with pyrimethamine (Maloprim) are the most used combination. Pyrimethamine-Sulfadoxine (Fansidar) Pyrimethamine-Sulfadoxine (Fansidar) is well absorbed. Its components display peak plasma levels within 2-8 hours and are excreted mainly by the kidneys.
The issue is complicated further because different allelic mutations in the same gene can produce different phenotypes buy generic midamor 45 mg online arteria zygomatica. For example buy midamor 45 mg free shipping blood pressure vertigo, different mutations in the alpha subunit can produce Tay-Sachs disease, a late infantile variant, a juvenile variant that clinically mimics spino-cerebellar degeneration, and an adult variant that looks like a motor neuron disease. Mucopolysaccharidoses: These are caused by mutations in enzymes that catabolize mucopolysaccharides, large molecules that are components of many organs. Thus, the clinical and pathological manifestations of these diseases are far more widespread than those of the gangliosidoses. Typical manifestations include hepato- and splenomegaly, joint and bone deformities, opacities of the lens and cornea, connective tissue abnormalities, and storage of mucopolysaccharides in neurons. Hydrocephalus is also common, due to mucopolysaccharide deposition in the meninges with resultant deficits in the circulation and resorption of cerebrospinal fluid. Three typical variants: infantile (chromosome 1) late infantile, and juvenile (chromosome 16) and an adult form are known. As in many of the storage diseases, the infantile form is the most severe and rapidly progressive. The diagnosis rests on clinical patterns and genetic testing, although the demonstration of typical intracellular inclusions by fluorescence and electron microscopy in neurons, skin, muscle, or white cells can be helpful in narrowing down the diagnosis. Leukodystrophies: As the name indicates, these are disorders that preferentially affect white matter and may be included under Diseases of Myelin. Since oligodendrocytes or myelin sheaths are affected, patients display a loss of myelin or abnormal myelination. Typically, they show neurological signs referable to white matter destruction, such as spasticity. Very long chain fatty acids, normally degraded in peroxisomes, are elevated or "stored" in brain and other organs, particularly the adrenal cortex. This disease was most commonly related to hemolysis from Rh incompatibilities but any source of hemolysis results in the presentation of excessive bilirubin to immature hepatic cells lacking sufficient glucuronyltransferase activity for conjugation. Therefore, large amounts of indirect or unconjugated bilirubin accumulate in blood. The incidence of kernicterus has been greatly reduced due to the decrease in hemolytic jaundice of the newborn. These infants also have superimposed anemic and oligemic hypoxia due to hemolysis and problems with cardiac function. Consequently, the lesions are thought to result from both unconjugated hyperbilirubinemia and hypoxic/ischemic damage to "old" neuronal groups, which are active metabolically at birth. Children who survive the kernicteric episode develop the classical triad of opisthotonus, sensorineural deafness and defective ocular supraversion. Episodic attacks (often following the use of barbiturates or sulfonamides) of emotional instability, sleeplessness, severe pains of abdomen, back, and limbs and vomiting commence in the postpubertal period. All, except the chromatolytic lesions, are believed to be hypoxic-ischemic in origin. Chromatolysis of anterior horn motor and dorsal root ganglion neurons is secondary to a distal axonopathy of peripheral nerve. This is a disease in which copper levels are elevated in organs, particularly liver and brain. Serum ceruloplasmin (a copper binding protein) and serum copper are low, while tissue copper is elevated. Neuropathologic lesions are concentrated in the basal ganglia where one finds subtotal rarefaction with neuronal loss to complete necrosis with astrocytosis and eventual atrophy. Excessive copper has been identified in the basal ganglia, probably within glial cells. These enzyme deficiencies lead to neuronal degeneration and mental retardation, abnormal hair, hypopigmentation, and vascular disease due to abnormal collagen formation. Tremors and profound alterations in consciousness are poorly reflected by the paucity of neutropathologic lesions. This change should not be confused with the Alzheimer changes of neuritic plaques and neurofibrillary degeneration.
The net effect is tachycardia purchase midamor 45 mg mastercard blood pressure guidelines chart, peripheral vasoconstriction cheap midamor 45mg with amex blood pressure chart emt, and renal conservation of fluid. Progressive stage This is characterized by tissue hypoperfusion and onset of worsening circulatory and metabolic imbalances. Unless the progressive stage is intervened, the process eventually enters an irreversible stage. A rule of the thumb is to consider the blood pressure as normal if it is less than 100 + Age in years) mmHg. However, many specialists have evidence to believe that rise in blood pressure with age is a price we have to pay for our lifestyle, specially the high salt content of our diet. Some experts assert that if no 213 additional salt is added to our food throughout life, the blood pressure will stay constant throughout our life. Since this hypothesis cannot be widely tested on human beings at present stage of our civilization, we have to accept some rise in blood pressure as a part of the aging process. Although the change is gradual, and there is no sharp dividing line between the normal and high blood pressure, an arbitrary dividing line is required for clinical use. The arbitrary upper limits are 140 and 90 mmHg for systolic and diastolic blood pressure respectively. A mean arterial pressure greater than 110 mmHg under resting conditions usually is considered to be hypertensive. Adverse effects of hypertension The lethal effects of hypertension are caused mainly in three ways: (1) Excess workload on the heart leads to early development of congestive heart disease, coronary heart disease, or both, often causing death as a result of heart attack. It is known, however, that a number of factors interact in producing long-term elevations in blood pressure; these factors include: 214 Hemodynamic Neural Humoral Renal Arterial hypertension occurs when the relationship between blood volume and total peripheral resistance is altered. For many of the secondary forms of hypertension, these factors are reasonably well understood. For example, in renovascular hypertension, renal artery stenosis causes decreased glomerular flow and decreased pressure in the afferent arteriole of the glomerulus. Secondary hypertension Only 5% to 10% of hypertensive cases are currently classified as secondary hypertension- that is, hypertension due to another disease condition. The disease states that most frequently give rise to secondary hypertension are: 216 (1) Renal disease (2) Vascular disorders (3) Endocrine disorders (4) Acute brain lesion. Discuss the regulation of erythropoiesis Discribe the functions of different types of leukocytes Discuss leucopoiesis What are physiological responses in hemostasis? Discuss the balance of clotting and anti-clotting mechanism Describe conduction tissue of the heart and origin and spread of cardiac impulse Describe the events of cardiac cycle Discuss cardiac cycle:- Factors influencing cardiac output ; venous return; Factors influencing heart rate, myocardial contractility and stroke volume. Discuss the regulation of arterial blood pressure: Short term control; long term control; role of hormones. Acetylcholine esterase: enzyme present in motor end plate membrane of skeletal muscle that inactivates acetylcholine. Albumin: the smallest and most abundant plasma protein, which binds and transports water, insoluble substances in the blood and contributes predominantly to plasma colloidal osmotic pressure. Antibody: An immunoglobulin produced by a specific activated B-lymphocyte against particular antigen. Antigen: A large complex molecule that triggers a specific immune response against itself when it gains entry in to the body. Aortic Valve: A one-way value that permits flow of blood from the left ventricle in to the aorta during ventricular emptying but/prevents the back flow into the ventricle during ventricular diastole. Arterioles: the highly muscular high-resistance vessels the caliber of which can be altered to control blood flow to each of the various tissues. Atherosclerosis: A progressive degenerative arterial disease that leads to gradual blockage of affected vessel, there by reducing blood flow through them. Atrioventricular valve: Value that permits the flow of blood from the atria to the ventricle during filling of the heart but prevents back flow from the ventricles to the atria during the emptying of the heart. Atrium (Atria, plural): an upper chamber of the heart that receives blood from the veins and transfers it to the ventricle. Autonomic Nervous system: the portion of the different division of the peripheral nervous system that innervates smooth muscles and cardiac muscle and exocrine glands; composed of two divisions: the sympathetic and parasympathetic nervous system. Axon hillock: the first portion of a neuronal axon, the site of action potential in most neurons. Baroreceptor reflex: an autonomically mediated reflex response that influence the heart and blood vessels to oppose change in mean arterial blood pressure. Bundle of His: a tract of specialized cardiac cells that rapidly transmits an action potential down the interventricular septum of the heart.