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Red blood cell destruction

Antimalarial dragp interfere with, or are active against, die life cycle of die plasmodium, primarily when it is present in the red blood cells. Destruction at this stage of die plasmodium life cycle prevents die development of die male and female forms of the plasmodium. This in turn keeps die mosquito (when die mosquito bites an infected individual) from ingesting the male and female forms of the plasmodium, thus effectively ending die plasmodium life cycle (Pig. 16-1). [Pg.143]

Effects reported in humans following dermal exposure to phenol include liver damage, diarrhea, dark urine, and red blood cell destruction. Skin exposure to a relatively small amount of concentrated phenol has resulted in the death of humans. Small amounts of phenol applied to the skin of animals for brief periods can produce blisters and burns on the exposed surface, and spilling dilute phenol solutions on large portions of the body (greater than 25% of the body surface) can result in death. [Pg.26]

Repeated inhalation exposure to rats and mice caused changes in white blood cell counts, anesthesia, and reduced weight gain. Chronic exposure of rats to 20 000 ppm (2%) caused liver weight reduction and alteration in enzymes associated with liver damage. In another study, observations included decreased red blood cell counts, spleen changes, and decreased survival of males at 10000 and 25 000 ppm. Hemolysis and red blood cell destruction occurred at 25 000 ppm. [Pg.861]

Several human diseases are associated with deficiencies in GSH metabolism. One of the most notable is GSH synthase deficiency (also known as 5-oxopro-linuria). GSH synthase deficiency is characterized by a severe acidosis, hemolysis (red blood cell destruction), and central nervous system damage. Because of the enzyme deficiency, the concentration of y-glutamylcystcinc increases. This molecule is then converted to 5-oxoproline and cysteine by y-glutamyl... [Pg.485]

In patients such as Will Sichel who have severe and recurrent episodes of increased red blood cell destruction (hemolytic anemia), greater than normal amounts of the red cell pigment heme must be processed by the liver and spleen. In these organs, heme (derived from hemoglobin) is degraded to bilirubin, which is excreted by the liver in the bile. [Pg.585]

CHRONIC HEALTH RISKS destruction of red blood cells destruction of erythrocytes hemorrhagic nephritis hepatitis yellow staining of skin and hair yellow tinted vision blood in urine sensitization dermatitis hematuria albuminuria allergic reactions. [Pg.851]

The first reports of vanadium poisoning in humans described rather widespread systemic effects consisting of polycythemia, followed by red blood cell destruction and anemia, loss of appetite, pallor and emaciation, albumin and blood in the urine, gastrointestinal disorders, nervous complaints and cough, sometimes severe enough to cause hemoptysis. More recent reports describe symptoms that are restricted to the conjunctivae and respiratory system. No evidence is found for disturbances of the gastrointestinal tract, kidneys, blood, or central nervous system. [Pg.653]

Administration of dapsone may result in hemolysis (destruction of red blood cells), nausea, vomiting, anorexia, and blurred vision. [Pg.117]

Anemia is a decrease in the number of red blood cells (RBCs), a decrease in die amount of hemoglobin in RBCs, or bodi a decrease in die number of RBCs and hemoglobin. When diere is an insufficient amount of hemoglobin to deliver oxygen to die tissues, anemia exists. There are various types and causes of anemia For example, anemia can be die result of blood loss, excessive destruction of RBCs, inadequate production of RBCs, and deficits in various nutrients, such as in iron deficiency anemia Once the type and cause have been identified, die primary health care provider selects a method of treatment. [Pg.433]

Hereditary spherocytosis is a genetic disease, transmitted as an autosomal dominant, that affects about 1 5000 North Americans. It is characterized by the presence of spherocytes (spherical red blood cells, with a low sur-face-to-volume ratio) in the peripheral blood, by a hemolytic anemia, and by splenomegaly. The spherocytes are not as deformable as are normal red blood cells, and they are subject to destruction in the spleen, thus greatly shortening their Ufe in the circulation. Hereditary spherocytosis is curable by splenectomy because the spherocytes can persist in the circulation if the spleen is absent. [Pg.617]

Intrinsic factor is produced by the parietal cells. Within the stomach, it combines with vitamin Bu to form a complex necessary for absorption of this vitamin in the ileum of the small intestine. Vitamin B12 is an essential factor in the formation of red blood cells. Individuals unable to produce intrinsic factor cannot absorb vitamin B12 and red blood cell production is impaired. This condition, referred to as Pernicious anemia, occurs as a result of an autoimmune disorder involving destruction of parietal cells. [Pg.293]

Summary Thalassemias as a group are the most common genetic diseases in the world. Beta thalassemia is an inherited blood disorder in which the body produces an abnormal form of hemoglobin. The disorder results in excessive destruction of red blood cells, which in a severe form manifests as life-shortening anemia shortly after birth. Short-chain fatty acids had previously been shown to be useful in the... [Pg.366]

Neurotoxin obtained from the larva of leaf-cutting beetles (Diamphidia nigro-ornata pupae) that is used by bushmen of Southern Africa as an arrow poison. It blocks neuromuscular function and also attacks the heart muscles (cardiotoxic) and is destructive to red blood cells (hemolytic). Dried poison is stable for over a year. [Pg.473]

Besides the odor, there may be no other immediate sign that a person is breathing arsine. Its main effect is to destroy red blood cells, causing anemia (destruction of red blood cells) and kidney damage (from red blood cell debris). Within hours after a serious exposure, the victim may develop dark red or brown urine, back pain or belly pain, weakness, or shortness of breath. The skin or eyes may become yellow or bronze in color. Although arsine is related to arsenic, it does not produce the usual signs of arsenic poisoning. [Pg.224]

Hemolysis Alteration, dissolution, or destruction or red blood cells in such a manner that hemoglobin is liberated into a medium in which the cells are suspended (e.g., by specific complement-fixing antibodies, toxins, various chemical agents, tonicity, alteration of temperature. [Pg.316]

Consequently, proteins with this GPI anchor are diminished or absent, two of which are crucial in protecting blood cells from inappropriate complement destruction. Without these two protective proteins, PNH red blood cells, in particular, are easily burst by complement, resulting in low red blood cell count (anemia), fatigue, bouts of dark colored urine, and various other complications. [Pg.263]

The red blood cell has no mitochondria and is totally dependent on anaerobic glycolysis for ATP. In pyruvate kinase deficiency, the decrease in ATP causes the erythrocyte to lose its characteristic biconcave shape and signals its destruction in the spleen. In addition, decreased ion pumping by Na /K -ATPase results in loss of ion balance and causes osmotic fragility, leading to swelling and lysis. [Pg.168]

Another example of a delivery system based on microbubbles and ultrasound is the delivery of circulating microparticles (polymer latex beads) or fluorescent red blood cells outside of the capillaries into the surrounding tissues by the action of ultrasound on the co-injected Optison microbubbles [79]. Interestingly, polymer beads and red blood cells could be detected tens of micrometers away from the capillaries where the bubble destruction took place. This may imply that during rapid destruction of a microbubble in a very strong ultrasound field, adjacent microsphere beads in the bloodstream can be propelled deep into the surrounding tissues. [Pg.97]

This scenario can be prevented by administration of anti-Rh (usually anti-D) antibodies to Rh-negative mothers immediately upon the birth of a Rh-positive baby. The administered antibodies bind the fetal Rh-positive erythrocytes, marking them for destruction before a maternal immunological reaction is triggered. Usually a dose of 200-300/ig of antibody is administered immediately post-delivery. This would be sufficient to suppress an immune response for up to 10 ml of Rh-positive red blood cells. [Pg.407]


See other pages where Red blood cell destruction is mentioned: [Pg.15]    [Pg.230]    [Pg.416]    [Pg.86]    [Pg.77]    [Pg.1417]    [Pg.1539]    [Pg.1550]    [Pg.23]    [Pg.24]    [Pg.196]    [Pg.73]    [Pg.539]    [Pg.282]    [Pg.221]    [Pg.15]    [Pg.230]    [Pg.416]    [Pg.86]    [Pg.77]    [Pg.1417]    [Pg.1539]    [Pg.1550]    [Pg.23]    [Pg.24]    [Pg.196]    [Pg.73]    [Pg.539]    [Pg.282]    [Pg.221]    [Pg.316]    [Pg.10]    [Pg.653]    [Pg.975]    [Pg.175]    [Pg.246]    [Pg.247]    [Pg.255]    [Pg.300]    [Pg.119]    [Pg.263]    [Pg.144]    [Pg.638]    [Pg.714]    [Pg.77]    [Pg.30]   
See also in sourсe #XX -- [ Pg.1808 , Pg.1808 ]




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