28340696 hypersensitivity
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This document discusses different types of hypersensitivity reactions. Type II hypersensitivity involves autoantibodies that stimulate host target cell receptors, causing issues like autoimmune hemolytic anemia or Graves' disease. Type III hypersensitivity involves immune complex deposition that can cause conditions like Raynaud's phenomenon or membranous glomerulonephritis. Type IV delayed hypersensitivity involves T cell-mediated responses to environmental antigens, commonly causing contact dermatitis.
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Leukopenia is an abnormal reduction in white blood cells. It can result from reduced white blood cell production or increased destruction. The main types of white blood cells are neutrophils, lymphocytes, basophils, monocytes, and eosinophils, which help fight different types of infections. Kostmann syndrome is a rare, congenital neutropenia disorder characterized by lack of mature neutrophils and recurrent bacterial infections. Growth factor therapy increases neutrophil production and aids the body's natural healing process.
Leukopenias
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This document defines and classifies haemolytic anaemia. It describes acquired haemolytic anaemia, which can be immune or non-immune. Immune haemolytic anaemia is further divided into autoimmune, alloimmune, and drug-induced types. Warm and cold autoimmune haemolytic anaemias are explained in detail, including their causes, clinical features, laboratory findings, and treatments. Other types of non-immune haemolytic anaemias such as paroxysmal nocturnal haemoglobinuria, red cell fragmentation syndromes, and traumatic cardiac haemolytic anaemia are also summarized.
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#reference: Shafer's book of oral pathology, Davidson's, A.k jain
#intro: preksha singh, BDS student
#E-mail: preksha.srajput@gmail.com
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Microangiopathic hemolytic anemia (MAHA) is caused by damage to red blood cells as they pass through abnormally narrowed small blood vessels. This leads to fragmentation of red blood cells seen on peripheral blood smears. MAHA is associated with thrombotic microangiopathy syndromes like thrombotic thrombocytopenic purpura and hemolytic uremic syndrome (HUS). HUS is primarily caused by endothelial injury from bacterial toxins like Shiga toxin from E. coli O157:H7, leading to platelet aggregation and blood clots in small vessels that obstruct blood flow and damage red cells. Classic HUS mostly affects children after intestinal infection and is clearly associated with Shiga-
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Leukopenia is an abnormal reduction in white blood cells. It can result from reduced white blood cell production or increased destruction. The main types of white blood cells are neutrophils, lymphocytes, basophils, monocytes, and eosinophils, which help fight different types of infections. Kostmann syndrome is a rare, congenital neutropenia disorder characterized by lack of mature neutrophils and recurrent bacterial infections. Growth factor therapy increases neutrophil production and aids the body's natural healing process.
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This document discusses leukopenia, which is a low white blood cell count. It defines leukopenia and outlines its various causes such as cancer, infections, medications, and nutritional deficiencies. Symptoms are related to an increased risk of infection. Diagnosis involves a complete blood count showing low white blood cell levels. Treatment focuses on addressing the underlying cause, using medications to stimulate white blood cell production, following an immunocompromised diet, and preventing infections.
Pathophysiology of leukopenia
This PPT covers the pathophysiology of leukopenia and includes causes of leukopenia, symptoms of leukopenia and diagnosis of leukopenia
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Paroxysmal nocturnal hemoglobinuria
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, acquired blood disorder characterized by complement-induced hemolytic anemia, red urine, and thrombosis. It results from a genetic mutation causing blood cells to be missing a protein that protects them from destruction. Thrombocytopenia, or low platelet count, occurs in 40% of PNH patients and is a major cause of complications and death. Testing for PNH includes flow cytometry to detect affected blood cells and treatments focus on supportive care, monoclonal antibodies, immunosuppressants, or bone marrow transplantation.
Hemolytic Anemia
Anemia- a decrease in total amount of RBC or hemoglobin in blood
can be caused due to blood loss, iron or vitanminB12 deficiency
thalassemia
hemolysis-destruction of red blood cell
hemolytic anemia- a disorder where RBBC are destroyed faster than they are made.
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Haemolytic anemia
Anemia is a condition where blood lacks healthy red blood cells (RBC), decreasing the competence of blood to carry oxygen to tissues.
In clinical medicine, it refers to decrease in the normal concentration of Haemoglobin (Hb). Anemia is caused by either – 1. A decrease in the production of RBCs (decreased erythropoiesis) or haemoglobin.
2. An increase in loss of blood.
3. Destruction of red blood cells (haemolytic anaemia).
Hemolytic anemia is decreased level of Erythrocytes in circulating blood (anemia) caused because of their accelerated destruction (haemolysis) extravascularly or intravascularly either due to intrinsic or extrinsic factors.
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Hemolytic anemia extracorpuscular defects.
This document discusses hemolytic anemias caused by extracorpuscular defects. It describes immune and non-immune mechanisms that can destroy red blood cells, including autoimmune disorders, drug reactions, alloimmune responses to blood transfusions or pregnancy, infections, and membrane defects. The main types of immune hemolytic anemias are autoimmune (warm or cold antibody types), alloimmune (due to blood transfusions or pregnancy), and drug-induced. Workup may include blood tests to detect anemia, spherocytes, a positive direct Coombs test, and the thermal amplitude of any detected antibodies. Management depends on the underlying cause.
Hemolytic anemia
1. Hemolytic anemia results from the premature destruction of red blood cells, either intravascularly or extravascularly. It can be classified as acquired or hereditary.
2. Acquired hemolytic anemias are caused by extrinsic factors like antibodies, infections, toxins, or mechanical trauma. Hereditary hemolytic anemias result from intrinsic red blood cell defects.
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hemolytic anemia (cell membrane defect)
This document discusses various types of hemolytic anemia, including abnormalities of red blood cells, red blood cell membranes, and extrinsic factors. Red blood cell membrane disorders include hereditary spherocytosis, elliptocytosis, and stomatocytosis. Immune hemolytic anemia can be drug-related, alloimmune due to blood transfusions or hemolytic disease of the newborn, or autoimmune including warm or cold types. Other causes discussed include enzymopathies like glucose-6-phosphate dehydrogenase deficiency and paroxysmal nocturnal hemoglobinuria.
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On hemolytic anemia (sorry the spelling of hemolytic is wrong everywhere), its classification, and esp in the inherited forms where there is defect in membrane cytoskeleton
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Haemolytic anaemia is a disorder where red blood cells are destroyed faster than they can be replaced. It can be inherited or acquired. Inherited causes include defects in the red blood cell membrane like hereditary spherocytosis, defects in haemoglobin like sickle cell anaemia and thalassaemia, or metabolic defects. Acquired causes include immune haemolytic anaemia due to autoantibodies or drug reactions, or non-immune causes like paroxysmal nocturnal haemoglobinuria. Common symptoms include anaemia, jaundice, and enlargement of the spleen and liver.
Haemolytic anaemia
Red blood cells normally live for around 120 days before being destroyed. Destruction can occur either inside or outside blood vessels. Defects in red blood cells themselves or outside factors can lead to hemolysis. Hemolytic anemia results when red blood cell destruction outpaces bone marrow production of new cells. Causes include immune problems, infections, enzyme deficiencies affecting red blood cell metabolism, and genetic disorders impacting hemoglobin or the red blood cell membrane. Treatment focuses on managing anemia through blood transfusions, preventing iron overload, and addressing specific underlying defects when possible.
CLINICAL FEATURES AND COMPLICATIONS OF MALARIA
Major clinical manifestations of malaria include:
1. Cerebral malaria, which can cause coma, convulsions, and residual neurological deficits.
2. Severe malarial anemia.
3. Low birth weight in newborns whose mothers had malaria during pregnancy.
Complications include cerebral malaria, renal impairment, hypoglycemia, acidosis, and noncardiogenic pulmonary edema. Chronic complications include splenomegaly and nephropathy. Malaria can also increase risk of other infections.
Diseases involving white blood cells in oral pathology
This document discusses various conditions related to abnormalities in white blood cell counts, including leukopenia (low white blood cell count) and leukocytosis (high white blood cell count). It provides details on specific types of leukopenia such as agranulocytosis and cyclic neutropenia. It also covers causes and clinical manifestations of these conditions as they relate to the oral cavity. Additionally, it discusses leukocytosis and associated diseases like infectious mononucleosis and various forms of leukemia.
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Hemolytic anemia (1)
Hemolytic anemia is a condition where red blood cells are destroyed and removed from circulation prematurely. There are many causes of hemolytic anemia including inherited disorders like sickle cell anemia and enzyme deficiencies, immune mediated destruction of red blood cells, infections, toxins and mechanical trauma. Hemolytic anemias can be classified based on location of hemolysis (intravascular or extravascular), source of defect (intracorpuscular or extracorpuscular), and mode of onset (hereditary or acquired). Common symptoms include paleness, fatigue, fever and signs of hemoglobin in urine, blood or stool.
Hemolytic anemia I
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polycythemia
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TOXIC RESPONSES OF VASCULAR SYSTEM
The document outlines several major toxic responses of the vascular system:
1. Hypertension can result from substances that cause excessive constriction of arteries or increased resistance of the microcirculation, raising blood pressure. Toxicants can directly or indirectly affect the nervous system to alter blood pressure.
2. Hypotension is decreased blood pressure caused by substances like nitrates that release nitric oxide, a potent vasodilator.
3. Atherosclerosis is hardening and loss of elasticity in the arteries over time due to injury from oxidized LDL, increased physical stress, infection, and risk factors like high cholesterol, smoking, age and diabetes.
Glomerulonephropathy PGY 1.pptx
1) Glomerular diseases involve either nephrotic syndrome characterized by massive proteinuria or nephritic syndrome characterized by hematuria and inflammation.
2) Workup includes labs, urinalysis, protein quantification, serologies, and often kidney biopsy.
3) Common causes discussed include minimal change disease, focal segmental glomerulosclerosis, membranous nephropathy, acute poststreptococcal glomerulonephritis, and membranoproliferative glomerulonephritis.
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Hemolytic Anemia
Anemia- a decrease in total amount of RBC or hemoglobin in blood
can be caused due to blood loss, iron or vitanminB12 deficiency
thalassemia
hemolysis-destruction of red blood cell
hemolytic anemia- a disorder where RBBC are destroyed faster than they are made.
1st year MBBS
Polycythemia
Relative polycythemia, also called hemoconcentration, is caused by a decrease in plasma volume rather than an increase in red blood cells. It can result from losses of body fluids due to diarrhea, vomiting, diuretic use, or adrenal insufficiency. Absolute polycythemia is caused by an increased production of red blood cells and can be primary, such as polycythemia vera, or secondary to tissue hypoxia due to conditions like heart or lung disease. Polycythemia vera is a chronic myeloproliferative disorder characterized by increased red blood cell volume and hyperviscosity syndrome. Treatment focuses on phlebotomy, medications to suppress bone marrow, and managing symptoms like
Haemolytic anemia
Anemia is a condition where blood lacks healthy red blood cells (RBC), decreasing the competence of blood to carry oxygen to tissues.
In clinical medicine, it refers to decrease in the normal concentration of Haemoglobin (Hb). Anemia is caused by either – 1. A decrease in the production of RBCs (decreased erythropoiesis) or haemoglobin.
2. An increase in loss of blood.
3. Destruction of red blood cells (haemolytic anaemia).
Hemolytic anemia is decreased level of Erythrocytes in circulating blood (anemia) caused because of their accelerated destruction (haemolysis) extravascularly or intravascularly either due to intrinsic or extrinsic factors.
Glomerular diseases
This document summarizes different types of glomerular diseases that affect the glomeruli in the kidneys. It describes major categories like glomerulonephritis which is inflammation of the kidney filter membrane, and glomerulosclerosis which is scarring of the tiny blood vessels in the kidneys. It also discusses nephrotic syndrome, which causes excessive protein in urine, edema, and other health risks. The document provides details on hematuria, treatments for nephrotic syndrome, and ICD-10 codes for classifying various glomerular diseases.
Types of anemias
The document discusses different types of anemias including their causes, mechanisms, and characteristics. It covers iron deficiency anemia, the most common type caused by lack of iron intake or increased loss. It also discusses megaloblastic anemias caused by vitamin B12 or folate deficiencies which result in large immature red blood cells. Thalassemia syndromes are genetic disorders that cause decreased hemoglobin production. The document also examines normocytic anemias and anemias associated with chronic diseases and infections.
Hemolytic anemia extracorpuscular defects.
This document discusses hemolytic anemias caused by extracorpuscular defects. It describes immune and non-immune mechanisms that can destroy red blood cells, including autoimmune disorders, drug reactions, alloimmune responses to blood transfusions or pregnancy, infections, and membrane defects. The main types of immune hemolytic anemias are autoimmune (warm or cold antibody types), alloimmune (due to blood transfusions or pregnancy), and drug-induced. Workup may include blood tests to detect anemia, spherocytes, a positive direct Coombs test, and the thermal amplitude of any detected antibodies. Management depends on the underlying cause.
Hemolytic anemia
1. Hemolytic anemia results from the premature destruction of red blood cells, either intravascularly or extravascularly. It can be classified as acquired or hereditary.
2. Acquired hemolytic anemias are caused by extrinsic factors like antibodies, infections, toxins, or mechanical trauma. Hereditary hemolytic anemias result from intrinsic red blood cell defects.
3. Common causes of acquired hemolytic anemia include autoimmune hemolytic anemia, microangiopathic hemolysis, paroxysmal nocturnal hemoglobinuria, and isoimmune hemolytic anemia from blood transfusions. Hereditary forms often involve defects in the red blood cell membrane or interior
Autoimmunity
This document discusses autoimmunity and autoimmune diseases. It begins by explaining how the immune system can mistakenly attack self-antigens, leading to autoimmunity. Several organ-specific and systemic autoimmune diseases are described in detail, including how they are mediated by direct cellular damage, stimulating or blocking autoantibodies. Current treatments aim to suppress the immune system generally but do not cure the underlying condition. Experimental therapies discussed include T-cell vaccination, peptide blockade of MHC molecules, and monoclonal antibodies.
hemolytic anemia (cell membrane defect)
This document discusses various types of hemolytic anemia, including abnormalities of red blood cells, red blood cell membranes, and extrinsic factors. Red blood cell membrane disorders include hereditary spherocytosis, elliptocytosis, and stomatocytosis. Immune hemolytic anemia can be drug-related, alloimmune due to blood transfusions or hemolytic disease of the newborn, or autoimmune including warm or cold types. Other causes discussed include enzymopathies like glucose-6-phosphate dehydrogenase deficiency and paroxysmal nocturnal hemoglobinuria.
Heamolytic anaemia
On hemolytic anemia (sorry the spelling of hemolytic is wrong everywhere), its classification, and esp in the inherited forms where there is defect in membrane cytoskeleton
Haemolytic anaemia
Haemolytic anaemia is a disorder where red blood cells are destroyed faster than they can be replaced. It can be inherited or acquired. Inherited causes include defects in the red blood cell membrane like hereditary spherocytosis, defects in haemoglobin like sickle cell anaemia and thalassaemia, or metabolic defects. Acquired causes include immune haemolytic anaemia due to autoantibodies or drug reactions, or non-immune causes like paroxysmal nocturnal haemoglobinuria. Common symptoms include anaemia, jaundice, and enlargement of the spleen and liver.
Haemolytic anaemia
Red blood cells normally live for around 120 days before being destroyed. Destruction can occur either inside or outside blood vessels. Defects in red blood cells themselves or outside factors can lead to hemolysis. Hemolytic anemia results when red blood cell destruction outpaces bone marrow production of new cells. Causes include immune problems, infections, enzyme deficiencies affecting red blood cell metabolism, and genetic disorders impacting hemoglobin or the red blood cell membrane. Treatment focuses on managing anemia through blood transfusions, preventing iron overload, and addressing specific underlying defects when possible.
CLINICAL FEATURES AND COMPLICATIONS OF MALARIA
Major clinical manifestations of malaria include:
1. Cerebral malaria, which can cause coma, convulsions, and residual neurological deficits.
2. Severe malarial anemia.
3. Low birth weight in newborns whose mothers had malaria during pregnancy.
Complications include cerebral malaria, renal impairment, hypoglycemia, acidosis, and noncardiogenic pulmonary edema. Chronic complications include splenomegaly and nephropathy. Malaria can also increase risk of other infections.
Diseases involving white blood cells in oral pathology
This document discusses various conditions related to abnormalities in white blood cell counts, including leukopenia (low white blood cell count) and leukocytosis (high white blood cell count). It provides details on specific types of leukopenia such as agranulocytosis and cyclic neutropenia. It also covers causes and clinical manifestations of these conditions as they relate to the oral cavity. Additionally, it discusses leukocytosis and associated diseases like infectious mononucleosis and various forms of leukemia.
medicine.Renal 2.(dr.kawa)
Nephrotic syndrome is characterized by proteinuria (>3.5g/24hr), hypoalbuminemia, edema, and other issues. The proteinuria is caused by damage to the glomerular filtration barrier, and the other symptoms are secondary effects of protein loss in the urine. Nephrotic syndrome has potential complications including edema, hyperlipidemia, hypercoagulability, and infection risk. Management involves identifying the underlying cause, treating that cause if possible, controlling proteinuria with ACE inhibitors, and managing complications like edema and hyperlipidemia. Steroids are often used but renal biopsy is usually needed first in adults to guide treatment.
Hemolytic anemia (1)
Hemolytic anemia is a condition where red blood cells are destroyed and removed from circulation prematurely. There are many causes of hemolytic anemia including inherited disorders like sickle cell anemia and enzyme deficiencies, immune mediated destruction of red blood cells, infections, toxins and mechanical trauma. Hemolytic anemias can be classified based on location of hemolysis (intravascular or extravascular), source of defect (intracorpuscular or extracorpuscular), and mode of onset (hereditary or acquired). Common symptoms include paleness, fatigue, fever and signs of hemoglobin in urine, blood or stool.
Hemolytic anemia I
Hemolytic anemia is caused by the abnormal breakdown of red blood cells. It can be due to defects in the red blood cell membrane structure or permeability that cause cells to break down prematurely, or due to enzymatic defects that compromise the cell's energy production. The most common membrane defect is hereditary spherocytosis, while glucose-6-phosphate dehydrogenase deficiency is the most common enzymatic defect. Signs and symptoms of hemolysis include jaundice, gallstones, splenomegaly, and fatigue. Laboratory findings provide evidence of increased red blood cell breakdown and bone marrow compensation.
polycythemia
This document discusses polycythemia, which is characterized by an increased red blood cell mass. It can be absolute, due to increased red cell volume, or relative, due to decreased plasma volume. Causes of absolute polycythemia include primary polycythemia vera, which results from a clonal stem cell mutation, and secondary polycythemia, which is usually appropriate and resolves when the underlying cause is treated. Clinical findings of polycythemia vera include reddening of the skin and risk of blood clots. Treatment aims to maintain a normal blood count through phlebotomy, medications, or splenectomy.
TOXIC RESPONSES OF VASCULAR SYSTEM
The document outlines several major toxic responses of the vascular system:
1. Hypertension can result from substances that cause excessive constriction of arteries or increased resistance of the microcirculation, raising blood pressure. Toxicants can directly or indirectly affect the nervous system to alter blood pressure.
2. Hypotension is decreased blood pressure caused by substances like nitrates that release nitric oxide, a potent vasodilator.
3. Atherosclerosis is hardening and loss of elasticity in the arteries over time due to injury from oxidized LDL, increased physical stress, infection, and risk factors like high cholesterol, smoking, age and diabetes.
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The document summarizes a chapter about autoimmunity and autoimmune diseases from three perspectives:
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3) It examines current therapeutic approaches that aim to suppress autoimmune responses through drugs or removal of target organs, and potential alternative strategies like inducing tolerance to self-antigens.
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Causes of Leukocytosis, Leokopenia, Lymphocytosis and Leukemoid reactions..pptx
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28340696 hypersensitivity
- 15. Autoimmune Hemolytic Anemia • Antibodies are formed to red blood cell antigens • Often occurs in association with other diseases such as lymphoma, or can occur in response to administration of certain drugs such as penicillin • Hemolysis of red blood cells results in anemia characterized by fatigue, dyspnea on exertion, and pallor. • Diagnosis is made by the findings of decreased hematocrit (and hemoglobin), destroyed red blood cells on blood smear, and a positive Coombs antiglobulin test which detects the autoantibodies. • Treatment is directed at the underlying problem or removal of the drug and may also include steroids
- 17. NK Host Target cell Perforin and enzymes Fc receptor Autoantibody Type II Hypersensitivity – Antibody-dependent cell mediated toxicity with activation of cytotoxic cells (natural killer or NK cells)
- 18. HOST TARGET CELL ACTIVATION OF CELL WITH RELEASE OF CELLULAR PRODUCTS Type II Hypersensitivity – autoantibodies stimulate host target cell receptors and alter function
- 19. Graves Disease • Autoantibodies (called thyroid stimulating immunoglobulins) bind to receptors in the thyroid gland. • Stimulate the gland to grow and produce more thyroid hormone, but are not subject to the normal TSH/T4 negative feedback loop. • Hyperthyroidism results with the clinical manifestations of weight loss, tremor, heat intolerance, muscle weakness, and menstrual irregularity. • Autoantibodies also cause infiltrative changes that swell the front of the lower leg (pretibial myxedema) and behind the eyeball causing it to protrude from the socket (exophthalmus) due to T cell- mediated stimulation of fibroblasts. • Diagnosis is confirmed by measuring increased thyroid hormone and thyroid stimulating immunoglobulins • Treatment consists of thyroid ablation – monoclonal AB are being studied GRAVES DISEASE BEFORE AND AFTER RX
- 20. Type III Hypersensitivity • Disorders are characterized clinical courses that tends to wax and wane over time. Exacerbations and remissions are common, although tissue damage may eventually result in organ failure. • Raynaud’s phenomenon is characterized by a constellation of symptoms that may be the only sequelae of the disorder, or they may be the first manifestations of several other diseases including systemic lupus erythematosus, scleroderma, and thromboangiitis obliterans. Immune complex deposition and resultant activation of complement and neutrophils causes inflammation of the blood vessels, joints and kidneys. The most common complaint is of severe pain, numbness, and progressive ischemic discoloration of the digits (white to blue to red) especially upon cold exposure or stress. Individuals with this syndrome may also complain of arthralgias, lymphadenopathy, fevers, and decreased urine output (renal dysfunction). • Membranous Glomerulonephritis is a slowly progressive disease that can occur in association with other disorders such as infections, cancers, collagen vascular diseases, drugs, and toxins, but is most commonly idiopathic. Immune complexes deposit along the glomerular basement membrane and activate complement and neutrophils. Gradually progressive proteinuria is followed by complete renal failure in approximately 40% of individuals with this disorder. Diagnosis is made by renal biopsy with staining for these immune complexes
- 24. A Closer look at Type III Mechanism
- 38. TYPE IV DELAYED HYPERSENSITIVITY
- 47. Type IV Hypersensitivity • Contact dermatitis results from the alteration of host skin cell antigens due to contact with an environmental antigen such as the catechols from the poison ivy plant. One to two days after contact with the plant, sensitized individuals will develop vesicles on the skin with erythema and itching, followed by scaling. Contact dermatitis is also common after contact with other substances including metals such as nickel (often found in inexpensive jewelry), cosmetics, topical medicines, and rubber products.