This document discusses anemic syndrome, including its causes, signs and symptoms, classifications, and complications. Key points include:
- Anemic syndrome is defined as a decrease in circulating hemoglobin below normal values and can be caused by decreased red blood cell production or increased red blood cell destruction/loss.
- Causes of decreased production include bone marrow diseases/damage, low erythropoietin from kidney/liver disease, and deficiencies in iron, B12, or folic acid.
- Increased destruction can be from bleeding, hemolytic anemias due to physical/chemical/biological factors, or corpuscular issues like enzyme deficiencies.
- Complications arise from tissue hypoxia
This document provides an overview of nephritic and nephrotic syndrome, describing their pathophysiology and clinical features. Nephritic syndrome is characterized by inflammation of the glomeruli, resulting in hematuria, hypertension, and mild proteinuria. Glomerulonephritis causes include post-streptococcal and rapidly progressive crescentic glomerulonephritis. Nephrotic syndrome is caused by increased glomerular permeability, leading to massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Specific causes discussed include minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, and membranoproliferative glomerulone
1) Poststreptococcal glomerulonephritis (PSGN) is an acute inflammation of the renal glomeruli that occurs after infection with certain strains of Streptococcus.
2) It is characterized by hematuria, edema, hypertension, and oliguria.
3) The pathogenesis involves molecular mimicry between streptococcal antigens and renal antigens, resulting in the trapping of immune complexes in the glomeruli.
Edema is swelling caused by excess fluid trapped in your body's tissues. Although edema can affect any part of your body, you may notice it more in your hands, arms, feet, ankles and legs.
Edema can be the result of medication, pregnancy or an underlying disease — often congestive heart failure, kidney disease or cirrhosis of the liver.
Taking medication to remove excess fluid and reducing the amount of salt in your food often relieves edema. When edema is a sign of an underlying disease, the disease itself requires separate treatment.
Amyloidosis is characterized by the deposition of insoluble protein fibrils in tissues. There are different types based on the precursor protein, such as immunoglobulin light chain (AL), serum amyloid A (AA), and transthyretin (ATTR). In the kidney, amyloid deposits can involve the glomeruli, vessels, tubules, and interstitium. On microscopy, amyloid appears as an eosinophilic hyaline material that shows apple-green birefringence under polarized light after Congo red staining. Typing is important for management and involves immunohistochemistry for different precursor proteins. Treatment involves controlling the underlying condition driving amyloid formation and may include chemotherapy, transplantation, or controlling inflammation.
This document discusses glomerular disease and glomerulonephritis. It begins by defining glomerular disease and glomerulonephritis, noting that glomerulonephritis is a type of glomerular disease involving inflammation of the glomeruli. It then discusses the main clinical presentations of glomerular disease, including nephrotic syndrome, acute glomerulonephritis, and asymptomatic urinary abnormalities. The causes, symptoms, investigations, and management of various glomerular diseases are subsequently outlined. Throughout, examples are provided of specific diseases like post-streptococcal glomerulonephritis, membranous nephropathy, and crescentic glomerulone
This document provides an overview of cyanosis, including its definition, mechanisms, types (central, peripheral, differential), etiology, factors affecting detection, and treatment principles. Cyanosis is a bluish discoloration of the skin and mucous membranes that results from low oxygen saturation in the blood. It can be caused by issues in oxygen intake, diffusion, or circulation. The underlying etiology could be pulmonary (hypoventilation, diffusion impairment), cardiac (decreased or increased pulmonary blood flow), or a hemoglobinopathy. Detection is affected by hemoglobin level, fetal hemoglobin, and skin pigmentation. Treatment focuses on addressing the underlying condition rather than cyanosis itself, and may include oxygen therapy, warming, and intravenous
1) Microcytic hypochromic anemia is characterized by small, pale red blood cells and can be caused by iron deficiency, thalassemia, sideroblastic anemia, or other conditions.
2) Iron deficiency anemia is the most common cause and results from inadequate iron intake or absorption. It disrupts hemoglobin synthesis and cellular proliferation.
3) Thalassemia is an inherited disorder of hemoglobin production that can range from mild to severe. Thalassemia major requires regular blood transfusions and causes severe anemia from ineffective erythropoiesis and hemolysis.
This document provides an overview of nephritic and nephrotic syndrome, describing their pathophysiology and clinical features. Nephritic syndrome is characterized by inflammation of the glomeruli, resulting in hematuria, hypertension, and mild proteinuria. Glomerulonephritis causes include post-streptococcal and rapidly progressive crescentic glomerulonephritis. Nephrotic syndrome is caused by increased glomerular permeability, leading to massive proteinuria, hypoalbuminemia, edema, and hyperlipidemia. Specific causes discussed include minimal change disease, membranous nephropathy, focal segmental glomerulosclerosis, and membranoproliferative glomerulone
1) Poststreptococcal glomerulonephritis (PSGN) is an acute inflammation of the renal glomeruli that occurs after infection with certain strains of Streptococcus.
2) It is characterized by hematuria, edema, hypertension, and oliguria.
3) The pathogenesis involves molecular mimicry between streptococcal antigens and renal antigens, resulting in the trapping of immune complexes in the glomeruli.
Edema is swelling caused by excess fluid trapped in your body's tissues. Although edema can affect any part of your body, you may notice it more in your hands, arms, feet, ankles and legs.
Edema can be the result of medication, pregnancy or an underlying disease — often congestive heart failure, kidney disease or cirrhosis of the liver.
Taking medication to remove excess fluid and reducing the amount of salt in your food often relieves edema. When edema is a sign of an underlying disease, the disease itself requires separate treatment.
Amyloidosis is characterized by the deposition of insoluble protein fibrils in tissues. There are different types based on the precursor protein, such as immunoglobulin light chain (AL), serum amyloid A (AA), and transthyretin (ATTR). In the kidney, amyloid deposits can involve the glomeruli, vessels, tubules, and interstitium. On microscopy, amyloid appears as an eosinophilic hyaline material that shows apple-green birefringence under polarized light after Congo red staining. Typing is important for management and involves immunohistochemistry for different precursor proteins. Treatment involves controlling the underlying condition driving amyloid formation and may include chemotherapy, transplantation, or controlling inflammation.
This document discusses glomerular disease and glomerulonephritis. It begins by defining glomerular disease and glomerulonephritis, noting that glomerulonephritis is a type of glomerular disease involving inflammation of the glomeruli. It then discusses the main clinical presentations of glomerular disease, including nephrotic syndrome, acute glomerulonephritis, and asymptomatic urinary abnormalities. The causes, symptoms, investigations, and management of various glomerular diseases are subsequently outlined. Throughout, examples are provided of specific diseases like post-streptococcal glomerulonephritis, membranous nephropathy, and crescentic glomerulone
This document provides an overview of cyanosis, including its definition, mechanisms, types (central, peripheral, differential), etiology, factors affecting detection, and treatment principles. Cyanosis is a bluish discoloration of the skin and mucous membranes that results from low oxygen saturation in the blood. It can be caused by issues in oxygen intake, diffusion, or circulation. The underlying etiology could be pulmonary (hypoventilation, diffusion impairment), cardiac (decreased or increased pulmonary blood flow), or a hemoglobinopathy. Detection is affected by hemoglobin level, fetal hemoglobin, and skin pigmentation. Treatment focuses on addressing the underlying condition rather than cyanosis itself, and may include oxygen therapy, warming, and intravenous
1) Microcytic hypochromic anemia is characterized by small, pale red blood cells and can be caused by iron deficiency, thalassemia, sideroblastic anemia, or other conditions.
2) Iron deficiency anemia is the most common cause and results from inadequate iron intake or absorption. It disrupts hemoglobin synthesis and cellular proliferation.
3) Thalassemia is an inherited disorder of hemoglobin production that can range from mild to severe. Thalassemia major requires regular blood transfusions and causes severe anemia from ineffective erythropoiesis and hemolysis.
The document discusses edema and fluid balance in the body. It describes the normal circulation of fluid between blood and tissues, mediated by hydrostatic and oncotic pressures. Edema occurs when there is increased hydrostatic pressure, decreased oncotic pressure, increased capillary permeability, or impaired lymphatic drainage. Specific types of edema discussed include cardiac, hepatic, pulmonary, cerebral, and lymphatic edema. Sites of common edema and clinical significance are also reviewed.
Pneumonia can be classified in several ways, including by anatomical location (lobar, bronchopneumonia, interstitial), etiology (bacterial, viral, fungal, mycobacterial, parasitic, non-infectious), and age of the patient. Common causative pathogens vary by age group. Hospitalization is often required for young children, immunocompromised patients, or those with severe symptoms. Recurrent pneumonia can be caused by hereditary disorders impacting immunity or airway function. Bacterial pneumonia results in different pathology depending on the invading organism. Viral pneumonia predisposes to secondary bacterial infection by disrupting host defenses.
Edema is an excessive accumulation of fluid in the interstitial spaces or body cavities. There are several types and causes of edema. Cardiac edema is caused by congestive heart failure which increases venous pressure and hydrostatic pressure, pulling fluid from blood vessels into tissues. Renal edema can be caused by nephritic syndrome which causes salt and water retention, or nephrotic syndrome which decreases plasma protein levels. Hepatic edema manifests as ascites and is caused by portal hypertension or low plasma proteins in conditions like liver cirrhosis. Pulmonary edema can result from left heart failure or inflammation while cerebral edema includes cytotoxic edema from cell injury or vesogenic edema from blood brain barrier disruption.
This document summarizes renal pathology and glomerular diseases. It discusses how diseases can affect the glomeruli, tubules, interstitium and vasculature. The glomeruli are described as a network of capillaries lined by endothelial cells, the glomerular basement membrane, and podocytes. Immunological and toxic mechanisms can cause glomerular injury. Membranous glomerulopathy is described as the most common cause of nephrotic syndrome in adults, characterized by thickening of the glomerular capillary wall.
The document provides details on evaluating a patient presenting with fever. It includes sections on taking a thorough history with perspectives on biomedical factors, the patient's experience, and contextual background. A review of systems explores all major organ systems for localizing symptoms. The physical exam findings note vital signs and examination of different body systems. Analyzing symptoms like fever patterns, associated issues, and past medical history are essential for determining the underlying cause.
Pleural effusion is an abnormal collection of fluid in the pleural space that can be caused by various conditions. It is classified as a transudate or exudate based on the characteristics of the fluid. Investigation of pleural effusion involves examination of blood, chest x-rays, and analysis of pleural fluid obtained via thoracentesis to determine the cause and appropriate treatment. Common causes include cardiac failure, pneumonia, tuberculosis, malignancy, and liver or kidney diseases.
This document discusses the pathology of the male genital tract, including structural anomalies, inflammatory conditions, neoplastic conditions of the penis, diseases of the prostate like benign prostatic hyperplasia and prostatic carcinoma, diseases of the testis including cryptorchidism, inflammatory conditions, vascular disturbances, and testicular tumors. It covers the staging and grading of prostatic carcinoma and testicular tumors, as well as common tumor markers.
This document provides information on bronchial asthma including its definition, classification, pathophysiology, and treatment approaches. It discusses the different types of asthma such as atopic, non-atopic, and drug-induced asthma. It describes the cells and mediators involved in asthma inflammation. It covers the mechanisms and classes of drugs used to treat asthma, including bronchodilators, leukotriene antagonists, mast cell stabilizers, corticosteroids, and anti-IgE antibody. It provides details on the mechanisms of action and side effects of various bronchodilators and corticosteroids. It also discusses inhalational drug delivery systems and the treatment of acute asthma attacks.
Megaloblastic anaemia is a red blood cell disorder due to the inhibition of DNA synthesis during erythropioesis.
Mitotically, the inhibition of the DNA synthesis impaires the progression of the cell cycle development from G2 to (M) stage.
This document provides an overview of the management of bronchial asthma. It discusses the pathophysiology of asthma including chronic airway inflammation and hyperresponsiveness. It describes the clinical presentation of asthma and drug treatments including bronchodilators, corticosteroids, leukotriene inhibitors, and cromones. The document highlights the roles of these drugs in controlling inflammation and reducing exacerbations to manage asthma symptoms.
1. Aplastic anemia is a condition characterized by pancytopenia (low red blood cells, white blood cells, and platelets) due to bone marrow failure.
2. It can be caused by exposure to toxins, radiation, viruses, or immune system attacks on the bone marrow. The bone marrow is hypocellular with fatty replacement of hematopoietic tissue.
3. Symptoms include anemia, increased risk of infection, bruising/bleeding due to low blood cell counts. Diagnosis involves blood tests showing pancytopenia and a bone marrow biopsy revealing a hypocellular marrow. Treatment options include supportive care, immunosuppressants, bone marrow transplant, or androgens
This document discusses megaloblastic anemia, its causes, symptoms, and treatments. It is characterized by abnormally large red blood cells due to a deficiency in vitamin B12 or folic acid, which is needed for DNA synthesis. The deficiencies can result from inadequate intake, malabsorption, or increased demand. Treatments include injections or supplements of vitamin B12, folic acid, or erythropoietin to stimulate red blood cell production. Adverse reactions are also discussed.
Pallor is a pale skin color caused by reduced oxyhemoglobin levels. It can be caused by anemia, leukemia, heart disease, shock, endocrine disorders, and more. Anemia itself is a reduction in red blood cells, hemoglobin, or red blood cell volume. The most common type is iron deficiency anemia from inadequate iron intake or absorption. Other types include megaloblastic anemia from B12 or folate deficiency, hemolytic anemia from red blood cell membrane issues or immune/non-immune causes, aplastic anemia from bone marrow failure, and anemia of chronic disease seen in infections, inflammation, or cancers.
This document discusses iron deficiency anemia, including its causes, stages, clinical features, diagnosis, and treatment. It notes that iron deficiency anemia is the most common type of anemia worldwide. The stages of iron deficiency progress from depletion of iron stores to latent deficiency to anemia when hemoglobin levels fall below normal. Causes include inadequate dietary iron intake, impaired absorption, and increased losses. Treatment involves dietary sources of iron as well as oral or parenteral iron supplements.
This document discusses the anatomy and diseases of the gastrointestinal (GI) tract. It covers the structure and function of the digestive system, as well as common diseases that can affect the esophagus, stomach, small intestine, and colon. Specific GI diseases mentioned include esophageal achalasia, peptic ulcers, celiac disease, inflammatory bowel disease, and colon cancers. The document provides an overview of evaluating and understanding diseases of the GI system.
Iron Deficiency Anemia occurs when iron levels are too low to support normal red blood cell production. It has various causes like bleeding, low dietary iron intake, or loss of iron in the urine. Symptoms include fatigue and pale skin. Investigations show low hemoglobin, ferritin and iron levels with microcytic red blood cells. Treatment involves oral or intravenous iron supplementation depending on severity. Complications can include impaired development in children or increased risk of falls in the elderly. Prevention focuses on consuming iron-rich foods and supplements. Differential diagnoses include thalassemia and anemia of chronic disease.
Chronic pyelonephritis is a chronic inflammation of the renal tubules and interstitium that occurs due to recurrent urinary tract infections and scarring. It most commonly affects children with congenital anomalies or spinal cord injuries and is the leading cause of end-stage renal disease. It is typically caused by either chronic obstructive pyelonephritis due to obstruction of urine outflow, or reflux nephropathy caused by vesicoureteral reflux allowing urine to flow back into the kidneys. Symptoms may include fever, flank pain, and symptoms of chronic renal failure like hypertension. The condition can lead to complications like proteinuria, focal glomerulosclerosis, and papillary necrosis.
Chronic glomerulonephritis is a kidney disorder caused by slow, cumulative damage and scarring of the glomeruli, or tiny blood filters in the kidneys, usually due to inflammation. This results in reduced kidney function over time and can lead to chronic kidney disease, end-stage renal disease, cardiovascular disease, renal failure, and death if left untreated. Treatment focuses on slowing disease progression, managing symptoms like high blood pressure and fluid retention, and renal replacement therapy with dialysis or kidney transplantation for kidney failure.
Pathology of Pneumonia:
Broncho- pneumonia,
Lobar Pneumonia,
Lung Abscess,
Lung Fungal Absces,
Normal Lung
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11.Hematopoietic.system.disorders in pharmacology.pdfalishmaart
This document provides an overview of hematopoietic system diseases and classifications of anemia. It discusses several types of anemia in detail, including their causes, characteristics, and impact on organs and tissues. The types covered include posthemorrhagic anemia, iron-deficiency anemia, megaloblastic anemia, hemolytic anemia, and sickle-cell anemia. It also briefly discusses hypo-aplastic anemia, leukemia, and lymphoma as hematopoietic system diseases.
This document provides an overview of anemia, including its classification and causes. It discusses:
1) The etiological classification of anemia into impaired red blood cell production, excessive destruction, and blood loss.
2) The morphologic classification into macrocytic, microcytic hypochromic, and normocytic normochromic anemia.
3) Causes of impaired red blood cell production such as bone marrow abnormalities and deficiencies in essential factors like iron, vitamin B12, and folate.
4) Causes of excessive red blood cell destruction including hereditary and acquired hemolytic anemias.
5) Different types of blood loss as a cause of anemia like acute
The document discusses edema and fluid balance in the body. It describes the normal circulation of fluid between blood and tissues, mediated by hydrostatic and oncotic pressures. Edema occurs when there is increased hydrostatic pressure, decreased oncotic pressure, increased capillary permeability, or impaired lymphatic drainage. Specific types of edema discussed include cardiac, hepatic, pulmonary, cerebral, and lymphatic edema. Sites of common edema and clinical significance are also reviewed.
Pneumonia can be classified in several ways, including by anatomical location (lobar, bronchopneumonia, interstitial), etiology (bacterial, viral, fungal, mycobacterial, parasitic, non-infectious), and age of the patient. Common causative pathogens vary by age group. Hospitalization is often required for young children, immunocompromised patients, or those with severe symptoms. Recurrent pneumonia can be caused by hereditary disorders impacting immunity or airway function. Bacterial pneumonia results in different pathology depending on the invading organism. Viral pneumonia predisposes to secondary bacterial infection by disrupting host defenses.
Edema is an excessive accumulation of fluid in the interstitial spaces or body cavities. There are several types and causes of edema. Cardiac edema is caused by congestive heart failure which increases venous pressure and hydrostatic pressure, pulling fluid from blood vessels into tissues. Renal edema can be caused by nephritic syndrome which causes salt and water retention, or nephrotic syndrome which decreases plasma protein levels. Hepatic edema manifests as ascites and is caused by portal hypertension or low plasma proteins in conditions like liver cirrhosis. Pulmonary edema can result from left heart failure or inflammation while cerebral edema includes cytotoxic edema from cell injury or vesogenic edema from blood brain barrier disruption.
This document summarizes renal pathology and glomerular diseases. It discusses how diseases can affect the glomeruli, tubules, interstitium and vasculature. The glomeruli are described as a network of capillaries lined by endothelial cells, the glomerular basement membrane, and podocytes. Immunological and toxic mechanisms can cause glomerular injury. Membranous glomerulopathy is described as the most common cause of nephrotic syndrome in adults, characterized by thickening of the glomerular capillary wall.
The document provides details on evaluating a patient presenting with fever. It includes sections on taking a thorough history with perspectives on biomedical factors, the patient's experience, and contextual background. A review of systems explores all major organ systems for localizing symptoms. The physical exam findings note vital signs and examination of different body systems. Analyzing symptoms like fever patterns, associated issues, and past medical history are essential for determining the underlying cause.
Pleural effusion is an abnormal collection of fluid in the pleural space that can be caused by various conditions. It is classified as a transudate or exudate based on the characteristics of the fluid. Investigation of pleural effusion involves examination of blood, chest x-rays, and analysis of pleural fluid obtained via thoracentesis to determine the cause and appropriate treatment. Common causes include cardiac failure, pneumonia, tuberculosis, malignancy, and liver or kidney diseases.
This document discusses the pathology of the male genital tract, including structural anomalies, inflammatory conditions, neoplastic conditions of the penis, diseases of the prostate like benign prostatic hyperplasia and prostatic carcinoma, diseases of the testis including cryptorchidism, inflammatory conditions, vascular disturbances, and testicular tumors. It covers the staging and grading of prostatic carcinoma and testicular tumors, as well as common tumor markers.
This document provides information on bronchial asthma including its definition, classification, pathophysiology, and treatment approaches. It discusses the different types of asthma such as atopic, non-atopic, and drug-induced asthma. It describes the cells and mediators involved in asthma inflammation. It covers the mechanisms and classes of drugs used to treat asthma, including bronchodilators, leukotriene antagonists, mast cell stabilizers, corticosteroids, and anti-IgE antibody. It provides details on the mechanisms of action and side effects of various bronchodilators and corticosteroids. It also discusses inhalational drug delivery systems and the treatment of acute asthma attacks.
Megaloblastic anaemia is a red blood cell disorder due to the inhibition of DNA synthesis during erythropioesis.
Mitotically, the inhibition of the DNA synthesis impaires the progression of the cell cycle development from G2 to (M) stage.
This document provides an overview of the management of bronchial asthma. It discusses the pathophysiology of asthma including chronic airway inflammation and hyperresponsiveness. It describes the clinical presentation of asthma and drug treatments including bronchodilators, corticosteroids, leukotriene inhibitors, and cromones. The document highlights the roles of these drugs in controlling inflammation and reducing exacerbations to manage asthma symptoms.
1. Aplastic anemia is a condition characterized by pancytopenia (low red blood cells, white blood cells, and platelets) due to bone marrow failure.
2. It can be caused by exposure to toxins, radiation, viruses, or immune system attacks on the bone marrow. The bone marrow is hypocellular with fatty replacement of hematopoietic tissue.
3. Symptoms include anemia, increased risk of infection, bruising/bleeding due to low blood cell counts. Diagnosis involves blood tests showing pancytopenia and a bone marrow biopsy revealing a hypocellular marrow. Treatment options include supportive care, immunosuppressants, bone marrow transplant, or androgens
This document discusses megaloblastic anemia, its causes, symptoms, and treatments. It is characterized by abnormally large red blood cells due to a deficiency in vitamin B12 or folic acid, which is needed for DNA synthesis. The deficiencies can result from inadequate intake, malabsorption, or increased demand. Treatments include injections or supplements of vitamin B12, folic acid, or erythropoietin to stimulate red blood cell production. Adverse reactions are also discussed.
Pallor is a pale skin color caused by reduced oxyhemoglobin levels. It can be caused by anemia, leukemia, heart disease, shock, endocrine disorders, and more. Anemia itself is a reduction in red blood cells, hemoglobin, or red blood cell volume. The most common type is iron deficiency anemia from inadequate iron intake or absorption. Other types include megaloblastic anemia from B12 or folate deficiency, hemolytic anemia from red blood cell membrane issues or immune/non-immune causes, aplastic anemia from bone marrow failure, and anemia of chronic disease seen in infections, inflammation, or cancers.
This document discusses iron deficiency anemia, including its causes, stages, clinical features, diagnosis, and treatment. It notes that iron deficiency anemia is the most common type of anemia worldwide. The stages of iron deficiency progress from depletion of iron stores to latent deficiency to anemia when hemoglobin levels fall below normal. Causes include inadequate dietary iron intake, impaired absorption, and increased losses. Treatment involves dietary sources of iron as well as oral or parenteral iron supplements.
This document discusses the anatomy and diseases of the gastrointestinal (GI) tract. It covers the structure and function of the digestive system, as well as common diseases that can affect the esophagus, stomach, small intestine, and colon. Specific GI diseases mentioned include esophageal achalasia, peptic ulcers, celiac disease, inflammatory bowel disease, and colon cancers. The document provides an overview of evaluating and understanding diseases of the GI system.
Iron Deficiency Anemia occurs when iron levels are too low to support normal red blood cell production. It has various causes like bleeding, low dietary iron intake, or loss of iron in the urine. Symptoms include fatigue and pale skin. Investigations show low hemoglobin, ferritin and iron levels with microcytic red blood cells. Treatment involves oral or intravenous iron supplementation depending on severity. Complications can include impaired development in children or increased risk of falls in the elderly. Prevention focuses on consuming iron-rich foods and supplements. Differential diagnoses include thalassemia and anemia of chronic disease.
Chronic pyelonephritis is a chronic inflammation of the renal tubules and interstitium that occurs due to recurrent urinary tract infections and scarring. It most commonly affects children with congenital anomalies or spinal cord injuries and is the leading cause of end-stage renal disease. It is typically caused by either chronic obstructive pyelonephritis due to obstruction of urine outflow, or reflux nephropathy caused by vesicoureteral reflux allowing urine to flow back into the kidneys. Symptoms may include fever, flank pain, and symptoms of chronic renal failure like hypertension. The condition can lead to complications like proteinuria, focal glomerulosclerosis, and papillary necrosis.
Chronic glomerulonephritis is a kidney disorder caused by slow, cumulative damage and scarring of the glomeruli, or tiny blood filters in the kidneys, usually due to inflammation. This results in reduced kidney function over time and can lead to chronic kidney disease, end-stage renal disease, cardiovascular disease, renal failure, and death if left untreated. Treatment focuses on slowing disease progression, managing symptoms like high blood pressure and fluid retention, and renal replacement therapy with dialysis or kidney transplantation for kidney failure.
Pathology of Pneumonia:
Broncho- pneumonia,
Lobar Pneumonia,
Lung Abscess,
Lung Fungal Absces,
Normal Lung
Please leave a comment after downloading.
THANK YOU ^^
11.Hematopoietic.system.disorders in pharmacology.pdfalishmaart
This document provides an overview of hematopoietic system diseases and classifications of anemia. It discusses several types of anemia in detail, including their causes, characteristics, and impact on organs and tissues. The types covered include posthemorrhagic anemia, iron-deficiency anemia, megaloblastic anemia, hemolytic anemia, and sickle-cell anemia. It also briefly discusses hypo-aplastic anemia, leukemia, and lymphoma as hematopoietic system diseases.
This document provides an overview of anemia, including its classification and causes. It discusses:
1) The etiological classification of anemia into impaired red blood cell production, excessive destruction, and blood loss.
2) The morphologic classification into macrocytic, microcytic hypochromic, and normocytic normochromic anemia.
3) Causes of impaired red blood cell production such as bone marrow abnormalities and deficiencies in essential factors like iron, vitamin B12, and folate.
4) Causes of excessive red blood cell destruction including hereditary and acquired hemolytic anemias.
5) Different types of blood loss as a cause of anemia like acute
This document provides an overview of anemia, including its classification and causes. It discusses:
1) The etiological classification of anemia into impaired red blood cell production, excessive destruction, and blood loss.
2) The morphologic classification into macrocytic, microcytic hypochromic, and normocytic normochromic anemia.
3) Causes of impaired red blood cell production such as bone marrow abnormalities and deficiencies in essential factors.
4) Causes of excessive red blood cell destruction including hereditary and acquired hemolytic anemias.
5) Causes of blood loss such as acute or chronic bleeding.
1. The document discusses hematologic disorders including hematopoiesis, anemia, polycythemia, and hematologic malignancy.
2. It provides details on the pathophysiology of hematopoiesis, the definition and classification of anemia, the general approach to evaluating anemic patients, and discussions of common anemia types and their treatments.
3. Key anemia types covered include iron deficiency anemia, megaloblastic anemia due to vitamin B12 and folate deficiencies, and the morphological features seen in peripheral blood and bone marrow in these conditions.
The document discusses various blood disorders including changes in blood volume, anemias, and other conditions that affect the cellular components of blood. It describes how hypovolemia, hypervolemia, and normovolemia impact blood volume. Specific types of anemia are outlined such as iron-deficiency anemia, megaloblastic anemias, and aplastic anemia. Abnormal red blood cell morphologies associated with different anemias are also reviewed. Other conditions examined include polycythemia, leukopenia, leukocytosis, neutrophil shift, leukemia, and lymphoma.
The document discusses drug treatment for various blood disorders including anemias. It covers hematopoiesis and factors involved like iron, vitamin B12, folic acid, and hematopoietic growth factors. It then classifies and describes treatments for different types of anemia including iron deficiency anemia treated with oral or parental iron preparations, vitamin B12 deficiency anemia, folic acid deficiency anemia. It also discusses hematopoietic growth factors erythropoietin and colony stimulating factors used to treat chemotherapy-induced neutropenia. Overall, the document provides an overview of drug therapies for common blood disorders focused on different anemias.
Hemolytic anemia occurs when the bone marrow is unable to increase production to make up for the premature destruction of red blood cells and the abnormal breakdown of red blood cells either in the blood vessels (intravascular hemolysis) or elsewhere in the body (extravascular). It has numerous possible causes, ranging from relatively harmless to life-threatening. The general classification of hemolytic anemia is either inherited or acquired. Treatment depends on the cause and nature of the breakdown.Symptoms of hemolytic anemia are similar to other forms of anemia (fatigue and shortness of breath), but in addition the breakdown of red cells leads to jaundice and increases the risk of particular long-term complications such as gallstones and pulmonary hypertension.
Iron deficiency anemia is the most common type of anemia globally. It results from inadequate iron intake or absorption to meet physiological needs. Common symptoms include pallor, weakness, and fatigue. Diagnosis involves blood tests showing microcytic hypochromic anemia, low serum iron and ferritin levels, and high total iron binding capacity. Treatment consists of oral iron supplementation in the form of ferrous salts to replenish iron stores.
This document provides an overview of blood disorders and their classification. It discusses red blood cell disorders such as polycythemia vera, iron deficiency anemia, sickle cell anemia, and thalassemia. It also covers white blood cell disorders, platelet disorders, coagulation disorders, and disease-related coagulopathies. The document defines each disorder, describes their signs and symptoms, laboratory findings, treatment considerations, and oral health implications.
This document provides an overview of blood disorders, focusing on disorders of red blood cells, white blood cells, platelets, and coagulation. It begins with an introduction to blood and then covers specific disorders such as polycythemia vera, iron deficiency anemia, sickle cell anemia, and coagulation disorders. For each disorder, it discusses causes, clinical manifestations, oral manifestations, laboratory findings, and treatment considerations. The document aims to give healthcare practitioners a comprehensive review of various blood disorders and their impacts.
This document provides an overview of blood disorders and summarizes key information about red blood cells and related disorders. It discusses the structure and function of red blood cells, variations in red blood cell count, and disorders involving too many or too few red blood cells such as polycythemia, anemia, sickle cell anemia, thalassemia, and erythroblastosis fetalis. Specific conditions are defined and their signs, symptoms, causes, and treatments are outlined.
This document provides an overview of blood disorders and summarizes key information about red blood cells and related disorders. It discusses the structure and function of red blood cells, variations in red blood cell count, and disorders involving too many or too few red blood cells such as polycythemia, anemia, sickle cell anemia, thalassemia, and erythroblastosis fetalis. Specific conditions are defined and their signs, symptoms, causes, and treatments are outlined.
This document provides an overview of blood disorders and summarizes key information about red blood cells, white blood cells, platelets, and coagulation disorders. It discusses specific disorders such as polycythemia vera, anemia including iron deficiency anemia and sickle cell anemia, thalassemia, and erythroblastosis fetalis. For each disorder, it describes characteristics, causes, clinical manifestations, oral manifestations, laboratory findings, and treatment considerations.
Iron, vitamin B12, and folic acid are important haematinic agents used to treat different types of anaemia. There are two main types of anaemia - iron deficiency anaemia, which occurs due to blood loss or malabsorption of iron, and megaloblastic anaemia, which can be caused by deficiencies in vitamin B12 or folic acid due to problems with absorption or diet. Haematinic agents work to treat the underlying cause of anaemia and help increase red blood cell production by providing the necessary nutrients.
Rhabdomyolysis is the breakdown of skeletal muscle fibers that results in the release of muscle contents into the bloodstream. This can lead to acute kidney injury through deposition of myoglobin casts in the renal tubules. Treatment involves aggressive fluid resuscitation to prevent renal failure, treatment of hyperkalemia, and alkalinization of urine to prevent tubular obstruction. While bicarbonate and mannitol are commonly used, evidence does not clearly support their benefit over fluid resuscitation alone. Oxygen therapy and antioxidants may help reduce muscle injury. Dialysis may be needed for severe cases with refractory acidosis or hyperkalemia.
This document provides an overview of hematopathology, focusing on red blood cell disorders including anemia and polycythemia. It defines anemia and classifies it based on underlying mechanisms such as blood loss, diminished erythropoiesis, and hemolytic anemias. Megaloblastic anemias caused by vitamin B12 and folate deficiencies are described in detail. Pernicious anemia, a specific form of vitamin B12 deficiency, is also summarized, covering its pathogenesis, morphology, clinical features and diagnosis.
This document discusses hematinics, which are agents used to treat anemia and increase red blood cell counts or hemoglobin levels. It provides details on normal red blood cell production, the indications and adverse effects of oral and parenteral iron therapy, iron absorption and transport, and iron poisoning. It also covers folic acid sources and roles, causes of folate deficiency, and indications for folic acid supplementation. Finally, it discusses vitamin B12 structure and sources, pharmacokinetics, and nutritional deficiency.
This document provides an overview of anemia, including its classification and causes. It discusses impaired red blood cell production, excessive destruction of RBCs, and blood loss as the main etiologic classifications. The morphologic classifications are macrocytic, microcytic hypochromic, and normochromic normocytic anemia. Causes of impaired RBC production include bone marrow abnormalities and deficiencies in essential factors or stimulation factors. Excessive destruction can be due to intracorpuscular or extracorpuscular defects. Blood loss can be acute or chronic. Specific causes are discussed under each classification.
- Anemia is caused by decreased oxygen carrying capacity leading to tissue hypoxia. The body attempts to compensate through various mechanisms but these eventually fail as hypoxia worsens.
- Symptoms of anemia are due to tissue hypoxia and the body's compensatory responses, and include pallor, weakness, breathlessness, palpitations, headaches, and gastrointestinal issues.
- Iron deficiency anemia is the most common type of anemia globally. It results from inadequate iron intake, increased losses, or poor absorption and leads to microcytic hypochromic anemia.
Pathological urine refers to urine that contains abnormal constituents that are not normally present or are present in abnormal amounts. The presence of these abnormal constituents can provide important clues to underlying diseases or conditions affecting the kidneys or other organs.
This is a concise presentation on the pathology of endometrial cancer based on the latest WHO female genital tumors latest edition, 5th edition
prepared on April 2022
- Hydatidiform mole is a benign tumor of the placenta that has malignant potential. It is more common in Asian women and those over 35.
- Complete moles are diploid and paternal in origin, while partial moles are triploid with both paternal and maternal chromosomes. Complete moles have no fetus while partial moles may have an abnormal fetus.
- Diagnosis is made through ultrasound showing cystic spaces and very high HCG levels. Management involves surgical evacuation followed by monitoring of HCG levels to detect malignant changes, as 20% of complete moles may develop into gestational trophoblastic neoplasia.
This document summarizes the key mediators involved in the inflammatory response. It discusses how chemical mediators called cytokines, chemokines, lipids like prostaglandins and leukotrienes, amines such as histamine, peptides, complement proteins, and nitric oxide are released from cells to coordinate and regulate inflammation. These mediators act through receptors on target cells to produce effects like increased vascular permeability, leukocyte migration, pain, and fever responses. The document also outlines the innate and acquired immune responses mediated by cells like phagocytes, natural killer cells, and antibodies.
1. Psoriasis is a chronic, inflammatory skin disease characterized by well-defined, red, scaly plaques located over extensor surfaces and scalp.
2. It has a genetic predisposition and can be triggered by environmental factors such as trauma, infection, drugs, and stress.
3. Treatment involves topical therapies for mild disease and systemic therapies such as phototherapy, retinoids, methotrexate, and biological agents for more severe disease.
This document discusses hypertensive disorders in pregnancy, specifically pre-eclampsia. It defines pre-eclampsia and lists risk factors. Diagnosis involves high blood pressure and proteinuria. Classification ranges from mild to severe. Complications for the mother include seizures, stroke, liver or kidney damage. Management involves controlling blood pressure, preventing seizures with magnesium sulfate, and delivering the baby to resolve symptoms. Close monitoring of the mother and baby postpartum is important.
This document summarizes various parasitic infestations and their clinical features. It discusses papular urticaria caused by sensitivity to insect antigens, scabies caused by the mite Sarcoptes scabiei, and different types of pediculosis caused by head lice, body lice, and crab lice. It also mentions other conditions like myiasis, pulicosis, tungiasis, cimicosis, blister beetle dermatitis, spider bites, demodicidosis, larva migrans, leishmaniasis, and lymphatic filariasis. For each condition, it provides details on the causative organism, clinical manifestations, distribution of lesions
This document summarizes several neurocutaneous disorders including neurofibromatosis type 1 and 2, tuberous sclerosis, and Sturge-Weber syndrome. It describes the neurological, cutaneous, and other system involvement for each disorder including common symptoms such as seizures, tumors, and skin lesions. Diagnostic criteria involving clinical findings are provided. The summary focuses on the key features and manifestations across body systems involved in these genetic neurocutaneous conditions.
This document discusses Mullerian anomalies/defects, which range from agenesis to duplication of the tubes, uterus, cervix and upper vagina. It covers the classification system used (AFS), incidence, etiology, genetics, embryogenesis, clinical features, diagnosis using imaging modalies like HSG, USG and MRI, and management of various anomalies like unicornuate uterus, didelphys, bicornuate, septate and arcuate uterus. Complications in reproduction from each anomaly and outcomes of treatments like metroplasty are also summarized. Diethylstilbestrol exposure related abnormalities are briefly discussed.
Toxoplasma gondii is a coccidian parasite transmitted through contact with infected cat feces or consumption of undercooked meat. It typically causes mild or asymptomatic infections but can cause severe brain and eye damage in fetuses, infants, and immunocompromised individuals. Strongyloides stercoralis is a nematode transmitted through skin contact with soil. It resides in the small intestine and can cause chronic diarrhea but also disseminate and cause potentially fatal infections in malnourished or immunosuppressed individuals. Both parasites are diagnosed through examination of infected tissues and confirmed with serological tests.
The jugular venous pulse reflects right atrial pressure and is best examined in the right internal jugular vein. It normally displays three positive waves and two negative troughs related to atrial filling and emptying. Abnormalities can indicate conditions that elevate or lower right atrial pressure such as heart failure, tamponade, constriction. Specific wave changes suggest problems like tricuspid regurgitation or stenosis. The jugular venous pulse is a useful physical exam finding for cardiovascular assessment.
Heart murmurs can be produced by turbulence in blood flow caused by abnormalities in heart valves or structures. A murmur is described by its timing in the cardiac cycle, location, intensity, quality, and radiation pattern.
A mid-systolic murmur is the most common murmur and can be caused by ventricular outflow obstructions like aortic stenosis, dilation of the aorta/pulmonary trunk, accelerated flow, or innocent murmurs from normal anatomical variations. Diastolic murmurs include early diastolic murmurs like aortic regurgitation and high-pressure pulmonary regurgitation, and mid-diastolic murmurs caused by stenosis of the mitral or tricuspid valves. Flow murmurs
The document describes the development of the male and female reproductive systems from the indifferent stage through sexual differentiation. It covers the development of the gonads (testes and ovaries), genital ducts, and external genitalia. Some key points include:
- The gonads initially develop as indifferent gonads before differentiating into testes or ovaries depending on the presence of the SRY gene on the Y chromosome.
- The genital ducts also initially develop in an indifferent stage before the mesonephric ducts develop into male structures like the epididymis and vas deferens, while the paramesonephric ducts develop into female structures like the uterus and fallopian tubes.
- External
This document discusses chronic osteomyelitis, including its causes, pathology, presentations, examinations, investigations, differential diagnoses, and treatments. It can develop following acute osteomyelitis or be caused by tuberculosis or fungi. Pathology involves spread of pus within bone leading to bone death and cavities. Presentations include discharging sinuses and bone fragments. Investigations include x-rays showing bone changes and cultures of pus. Surgical treatments aim to remove dead bone and tissue. Complications include exacerbations, growth abnormalities, and fractures. It also discusses Garre's osteomyelitis and Brodie's abscess as specific types.
Forceps delivery is an operative vaginal delivery procedure that uses obstetric forceps to assist in the extraction of the fetal head. Forceps have curved blades that fit around the fetal head to allow the operator to apply gentle traction. Forceps delivery is indicated when there are signs of fetal distress, prolonged second stage of labor, or maternal medical complications. Risks include laceration, hemorrhage, and injuries to the mother or baby. Proper technique and only performing the procedure when fully trained can help minimize risks.
This document provides information on face presentation during childbirth. It defines face presentation as a cephalic presentation with the fetus in a complete extended attitude and the presenting part being the face. The two types of face presentation are primary (presenting before labor) and secondary (caused by extension during labor). The main positions are left and right mentoanterior and mentoposterior. Face presentation has a higher risk of complications compared to vertex presentation such as prolonged labor and increased need for operative delivery. The management involves allowing labor to progress for mentoanterior positions but cesarean section is usually needed for persistent mentoposterior.
E. coli is a normal flora in the gut but can cause several infections. It is the most common cause of urinary tract infections and can lead to different types of gastroenteritis depending on the strain. Some strains like EHEC O157:H7 can cause hemorrhagic colitis and potentially fatal hemolytic uremic syndrome in young children and the elderly. E. coli is also known to cause neonatal meningitis, wound infections after surgeries, and sepsis.
The brain receives a high blood supply to meet its metabolic demands. Arterial blood reaches the brain through the internal carotid and vertebral arteries, forming the circle of Willis at the base of the brain before branching into smaller vessels. Venous blood drains from the brain into internal jugular veins. Disruption of blood flow to the brain through cerebrovascular accidents like stroke can cause rapid loss of consciousness or permanent brain damage. Cerebrospinal fluid produced by choroid plexuses circulates within ventricles and around the brain and spinal cord, carrying nutrients and waste products.
This document discusses genetic diseases and abnormal fetal development. It begins with definitions of genetic terms like genetic code, chromosomes, genes, and cell division. It then discusses abnormal fetal development including malformations, deformations, and disruptions caused by chromosomal abnormalities, genetic defects, and environmental factors. The document ends by covering perinatal pathology including birth defects and metabolic disorders.
This document provides information on thalassemia, a group of genetic disorders that result in reduced hemoglobin production and anemia. It discusses the different types of thalassemia including alpha and beta thalassemia. Alpha thalassemia is caused by genetic deletions of the alpha globin genes and has varying severity from silent carrier to Hemoglobin H Disease to Bart's Hydrops Fetalis Syndrome. Beta thalassemia results from mutations in the beta globin genes and includes forms ranging from silent carrier to beta thalassemia minor to intermedia to major. Laboratory tests outlined can help diagnose and differentiate types of thalassemia based on red blood cell morphology, hemoglobin analysis and iron studies.
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
2. Hematopoiesis
• Hematopoiesis is the process by which mature blood cells are generated
and functional, assuming the existence of cells of origin who have a long
series of transformations and hematopoetic microenvironment
(composed of stromal cells and stimulating factors).
• Bone marrow (BM) is the central component generating blood cells: red
cells, granulocytes, monocytes, lymphocytes, platelets and hematopoietic
functions are proliferation, differentiation and cell release into circulation.
• BM consists of:
– reticulovascular stroma (with supporting role, nutrition and
movement of hematopoietic cells);
– medullar parenchyma - composed of active cells forming islands of
hematopoiesis, usually arranged around a trophic cell - "nurse cell."
Nurse cells are involved in erythropoiesis (iron stores) in myelopoesis
and megacaryopoesis (liberate stimulating factors - e.g.. IL-3).
4. Anemic syndrome
• Definition
– Anemic syndrome is defined as a poly-etiologic syndrome
characterized by decrease in circulating hemoglobin (Hb) below the
normal values.
5. Anemic syndrome
Adults (>15 years)
Hb (g/dl) Hb (mmol/l)
Women 12.0 7.4
Men 13.0 8.1
Children
Hb (g/dl) Hb (mmol/l)
Children < 5 years 11.0 7,1
Children < 15 years 12.0 7.4
6. Signs and symptoms
• Presence of a history of bleeding (not in all cases)
• Dyspnea (initial effort)
• Pallor
• Dizziness
• Low grade fever
• Compensatory hemodynamic syndrome
– Tachycardia
– Murmurs
– Palpitations
– Low blood pressure
7. Signs and symptoms
• Ventilatory changes
– Polipnea
• Changes in the peripheral nervous system's activity caused by neuronal
hypoxia:
– Paresthesia
– Neurovegetative dystonia
– Changes of reflexes
– Positive Babinski sign
– Ataxia
– Sphincter incontinence
– Changes of the senses
9. Signs and symptoms
• Trophic disorders of the mucous membranes
– Glossitis
– Esophagitis
– Gastritis
– Dyspepsia
• Trophic disorders of the skin and appendages
– Brittle hair
– Digital hypocratism (hippocratic fingers)
– Pigmentation of the skin
– Leg ulcers
• Bone pain
10. Classification
• A. Anemia caused by decreased production of red blood cells
• B. Anemia caused by lost of red blood cells
• C. Anemia caused by combined mechanisms
11. A. Anemia caused by decreased production of red
blood cells
• 1. Involvement of hematogenous bone marrow (BM):
– a. Destructive processes:
• Physical factors: ionizing radiation
• Chemical factors: drugs (cytostatics, anti-inflammatory -
phenylbutazone, chloramphenicol, phenytoin), industrial -
benzene, insecticides;
• Biological factors: some viruses (Epstein - Barr virus, hepatitis C,
parvovirus infection, human immunodeficiency virus);
• Immune diseases: timom, graft versus host reaction, eosinophilic
fasciitis;
• Unknown etiology
12. A. Anemia caused by decreased production of red
blood cells
• 1. Involvement of hematogenous bone marrow (BM):
– b. Bone marrow infiltrative processes:
• Tumours of the bone marrow (BM): leukemia, lymphoma, multiple
myeloma (MM)
• Metastases in BM
• Sarcoidosis
• Bone marrow fibrosis
• Storage diseases (glicogenoze, lipidosis - Gaucher disease)
• Bone marrow necrosis
• Bone marrow infections: sepsis, miliary tuberculosis, fungal
infections
13. A. Anemia caused by decreased production of red
blood cells
• 1. Involvement of hematogenous bone marrow (BM):
– c. Low production of erythropoietin:
• Anemia of chronic disease (chronic inflammation, chronic
infections, cancers) - inflammatory cytokines (IL1, IL 6, TNF-α) - suppresses the
synthesis of erythropoietin and erythropoietin increases resistance to the action;
• Kidney disease - chronic renal insufficiency - insufficient production of
erythropoietin due to renal lesions;
• Liver disease - by parenchymal liver failure (cirrhosis, hepa-tice,
toxic hepatitis, chronic aggressive hepatitis, etc.) - It reduces the
synthesis of erythropoietin and hemoglobin precursors;
• Poliglandular hypofunction - production of erythrocytes is
influenced by thyroid hormones, testosterone, glucocorticoids.
14. A. Anemia caused by decreased production of red
blood cells
• 2. Deficiency of forming factors:
– a. Protein deficiency:
• Low protein intake
– Malnutrition - starvation, low protein in food;
– Maldigestion - exocrine pancreatic insufficiency, bile salt
deficiency, gastrectomy;
– Malabsorption - intestinal resection, bacterial diarrheal
diseases, viral (excluding the time of contact of food with
intestinal mucosa), intestinal parasites;
• The reduced synthesis of proteins - parenchymal liver
insufficiency;
• The additional consumption of protein - "trap" of protein in end-
stage of cancer;
• Increased protein loss - diarrheal diseases, burns, nephrotic
syndrome;
15. A. Anemia caused by decreased production of red
blood cells
• 2. Deficiency of forming factors:
– b. Lack of synthesis of purine and pyrimidine derivatives (nucleic acids,
macroergic phosphates)
• Lack of vitamin B12
• Lack of folic acid (B9)
• Other vitamin deficiencies - deficiency of fat soluble vitamins (A, D,
K, E, F), lack of water-soluble vitamins - B thiamine (B1), riboflavin
(B2), niacin (B3), pirodoxina (B6), pantothenic acid (B5), biotin
(B7);
– c. Caused by iron deficiency anemia (iron deficiency anemia)
• Loss of blood
• Low intake
• Increased needs
• Iron metabolism disorders
16. B. Anemia caused by lost of red blood cell mass
• 1. Bleeding or iatrogenic emissions of blood
• 2. Increased destruction of erythrocytes - hemolytic syndrome (prehepatic
jaundice)
– a. Extracorpusculare causes:
• Physical factors
– Mechanical
» Mechanical cardiac causes hemolytic anemia (acquired or
congenital) - aortic stenosis, coarctation of the aorta,
mitral insufficiency, aortic aneurysm, heart valves;
– Thermal – heat
– Ultrasound
– Radiation - ultraviolet (photodermatosis), high-energy ionizing
radiation;
17. B. Anemia caused by lost of red blood cell mass
• 2. Increased destruction of erythrocytes - hemolytic syndrome (prehepatic
jaundice)
– a. Extracorpusculare causes:
• Chemical factors
– Exogenous - arsenic, copper, lead, etc..
– Endogenous - hemolytic anemia in nitrogen retention (renal
failure);
• Biological factors
– Parasites - Malaria (Plasmodium falciparum), babesiosis
(Babesia genus)
– Bacteria - bacterial toxins (Clostridium, E. Coli, Streptococci)
– Viruses (Epstein Bar, herpes encephalitis virus);
– Toxic - venoms (snake, scorpion, spider)
18. B. Anemia caused by lost of red blood cell mass
• 2. Increased destruction of erythrocytes - hemolytic syndrome (prehepatic
jaundice)
– a. Extracorpusculare causes:
• Autoimmune hemolytic anemia
• Hypersplenism
– Removal of damaged erythrocytes
– Response to bacterial, viral, parasitic
– Autoimmune diseases
– Metabolic diseases
– Tumors
• Hemolytic anemia with combined mechanisms - vascular
coagulation (DIC)
– DIC is a clinical syndrome (infections, cancers, venoms, autoimmune diseases,
trauma, burns, etc. obsterticale cases.) characterized by intravascular
coagulation, with the formation of thrombosis and necrosis, accompanied by
secondary fibrinolysis and consumption of coagulation factors, with bleeding.
19. B. Anemia caused by lost of red blood cell mass
• 2. Increased destruction of erythrocytes - hemolytic syndrome (prehepatic
jaundice)
– b. Corpuscular causes:
• Metabolic - enzyme deficiency:
– At the level of glycolysis - glucose 6-phosphate dehydrogenase
(G6PDH) deficiency, pyruvate kinase deficiency, etc.
– In the cycle of glutathione - glutathione synthetase deficiency,
glutathione reductase deficiency;
– Lack of heme synthesis (porphyrias)
– Lack of globin synthesis (globinopathies)
– Lack of hemoglobin synthesis (hemoglobinopathies)
20. Complications of anemic syndrome
• Decreased Hb reduces oxygen to tissues with consequent hypoxia.
• The effct of hypoxia depends on cells needs (neurons and muscle cells
have greater needs) and on cell proliferation rate.
21. Complications of anemic syndrome
• Biochemical changes:
– Krebs cycle activity is reduced due to low oxygen. Following, the
synthesis of macroergic phosphates (plastic and energetic role) is
reduced.
– Reduced Warburg respiratory chain activity with reduced heat
production.
– Increased glycolitic activity with accumulation of non-volatile organic
acids (lactic acid, pyruvic acid) flattens the hemoglobin dissociation
curve (oxygen is released more easily to the tissue).
– Reduced liver metabolism.
22. Complications of anemic syndrome
• Hemodynamic changes:
– Preferential redistribution of blood flow to vital organs
(catecholamines causes vasoconstriction in the splanhnic and skin
territory) - skin blood flow reduction causes - pallor, decreased skin
temperature, feeling cold, shivering, trophic skin changes. Onset of
symptoms depends on the magnitude and duration of the anemic
syndrome.
– Hemodynamic compensatory hyperkinesia evidenced by: tachycardia,
increased blood flow, increased blood speed, murmurs, increased
circulatory flow.
– Hyperkinetic compensation increases oxygen consumption which, in
time, will lead to cardiac decompensation (dyspnea, swelling,
transudates, etc.)
• If there is a preexiting coronary obstruction, anemia and
compensatory tachycardia, may lead to angina or increased
frequency of its manifestation, instable angina or even myocardial
infarction.
23. Complications of anemic syndrome
• Respiratory changes
– Compensatory polipnea
• Renal changes
– Hypoxia stimulates production of erythropoietin
• Through hypoxia - induced transcription factor 1 * (HIF -1).
– Hypoxia stimulates renal renin → activates the renin - angiotensin -
aldosterone system → retention of sodium (electrolyte imbalance).
24. Complications of anemic syndrome
• Alteration of tissue perfusion:
– Vasomotor activity and angiogenesis are modiffied.
• Promotion of angiogenesis is through vascular - endothelial
growth factor - (VEGF).
– Changes in skin and mucous membranes (tissues with increased cell
turn-over):
• Glossitis, esophagitis, gastritis, bronchitis, vulvovaginitis
• Leg ulcers
• Pigmentation
– Changes to appendages
• Brittle hair, digital hipocratism
25. Complications of anemic syndrome
• Increased production of red blood cells
– Stimulation of erythropoietin encoding gene via hypoxia-induced
transcription factor (HIF-1), results in increased synthesis of
erythropoietin.
• * HIF-1 functions as a regulator of adaptive responses induced by
hypoxia. Under conditions of hypoxia it activates transcription of
over 40 genes, including those responsible for synthesis
erythropoietin, glucose transporters, glycolitic enzymes, vascular -
endothelial growth factor (VEGF) and other proteins that facilitate
metabolic adaptation to hypoxia.
– Increasing production of red blood cells is mediated by erythropoietin.
Rates of synthesis of erythropoietin is in inverse relationship with Hb
concentration. Erythropoietin concentration can increase 1000 times
in severe anemia.
– It enhances erythropoiesis, with expandation of erythropoietic tissue,
possibly with sternal pain or diffuse bone pain.
26. Complications of anemic syndrome
• Immune system abnormalities:
– Hipoxia lowers the defense capacity of the immune system, especially
related to protection of mucosas;
– Anemic patient is prone to infections;
• Endocrine changes:
– Pituitary hypofunction
– Thyroid hypofunction
– Gonadal hypofunction
• Changes in menstrual cycle
• Amenorrhoea
• Impotence
27. Particular form of anemia - Iron deficiency anemia
• Iron deficiency is the most common cause of anemia.
• 20% of women (50% of pregnant women) and 3% of men do not have
enough iron in the body.
• Disruption of iron metabolism causes anemia and disturb cytochromes
activity (cell respiration).
• Iron is obtained through dietary intake (muscle, liver) and iron absorption
requires the presence of HCl and transferrin.
28. Iron deficiency anemia - causes
• Loss of blood:
– Bleeding
• Menstrual loss
– Frequent blood emission
• Polycythemia vera (PV) –
therapy
• Blood donors
– Neoplasms
• Inadequate intake:
– Vegetarian diet
– Global malabsorption / selective
for iron
• Aclorhydria
• Resected stomach
• Celiac disease
• Parasitosis
• Iron metabolism disorders
– Lack of transferrin
• Congenital
• Hepatic
• Nephrotic syndrome
– Defective / deficient transferrin
receptors
• Increased needs: pregnancy,
lactation, gemelarity, prematurity,
sports performance
30. Laboratory data
• Low Hb
• Normal or low number of reticulocytes
• Low sideremia
• Increased total iron binding capacity
• Elevated transferrin
• Low ferritin
• Absent iron reserves in the bone marrow (Perls staining)
• Blood smear
– Microcytosis
– Hypochromia
– Pokylocitosis
• CBC
– Low Hb, MCV ↓, MCH ↓, MCHC ↓
– WBC count normal or slightly decreased
– Frequently thrombocytosis
• Bone marrow
• Red series hyperplasia with iron deficiency erythroblasts
33. Anemia of chronic disease
• It is a normochromic, normocytic or hypochromic, microcytic anemia,
which develops through multiple mechanisms.
• Newest name, inflammation associated anemia, is more representative
because it reflects pathophysiological mechanisms.
• It secondary appears in:
– Chronic inflammation (infections, tuberculosis, endocarditis,
abscesses);
– Collagen diseases (SLE, RA, SS);
– Malignancy (carcinoma, multiple myeloma, lymphoma)
– Elderly anemia.
34. Pathogenesis
• This type of anemia is characterized by the inability of the body to increase red
cell production, to compensate for red cell destructions more or less
increased.
• Sustained stimulation of monocytic-macrophage system because of chronic
inflammation, autoimmune diseases or tumors, decrease life of erythrocytes
by increasing phagocytosis.
• During inflammation, iron releasing from macrophages and liver deposits is
significantly inhibited.
– Interleukin 6 (IL-6) produced during inflammation induces the synthesis of
hepcidine (iron regulating hormone), which in turn inhibits iron release from
macrophages and hepatocytes, with consequent decreasing sideremia.
• Hepcidine binds the feroportin molecules from the membrane, molecules
responsible for iron export, leading to their internalization and intracellular
degradation. In this way iron stuck in macrophages and can not be used for Hb
synthesis.
– It is known that iron is incorporated into protoporphyrin IX and zinc may substitute
iron for its synthesis.
35. Pathogenesis
• Another mechanism mediated through inflammation mediators (IL-1,
interferon alpha) is low compensation capacity through erythropoietin by
decreasing its synthesis.
• Finally there is a decreased iron in serum and erythrocyte precursors, with
increased reserves of iron. The lifespan of red blood cells decreases
without adequate compensation.
• Inflammatory cytokines promote the production of white blood cells.
36. Other anemia with low erythropoietin
• Kidney disease - chronic renal insufficiency - insufficient production of
erythropoietin due to renal lesions;
• Liver disease - by parenchymal liver failure (cirrhosis, toxic hepatitis,
chronic aggressive hepatitis, etc.) - It reduces the synthesis of
erythropoietin and hemoglobin precursors;
• Poliglandular hypofunction - production of erythrocytes is influenced by
thyroid hormones, testosterone, glucocorticoids.
37. Laboratory data
• Low Hb;
• Low number of reticulocytes;
• Low sideremia;
• Low total iron binding capacity;
• Increased ferritin;
• Perls staining of bone marrow shows reduced number of syderoblast and a
high amount of hemosiderine in the macrophages.
38. Megaloblastic anemia
• Anemia is normochromic, macrocytic defined by increasing MCV over 100
fl.
• Macrocytosis is typical in:
– Megaloblastic anemia
– Alcoholism
– Liver disease
• Megaloblastic anemia is characterized by nucleo-cytoplasmic asincronism
due to deficiency in DNA synthesis with normal RNA and protein synthesis
(immature nuclei and mature cytoplasm).
• The most common cause is vitamin B12 deficiency and / or folic acid
deficiency.
• A common cause of B12 deficiency is Biermer anemia. It is believed that
the mechanism is immune, mediated by antibodies to intrinsic factor (IF)
or / and anti gastric parietal cells. Thus vitamin B12 absorption disorder is
secondary to lack of IF.
39. Megaloblastic anemia
• Folic acid:
– It is found in fresh vegetable products, liver;
– The daily necessary amount is about 100 mg, normal diet providing
much more than this amount;
– The total reserve is up to 5 mg, enough for 3-4 months;
– Normal serum level is - 5 to 20 ng / ml;
– It is absorbed in the proximal jejunum;
• Vitamin B12:
– Food sources are animal products;
– B12 absorption occurs in the terminal ileum;
– The daily necessary is 1μg;
– B12 liver reserves are sufficient for 3-5 years;
– Serum B12 level is 200-600 pg / ml;
– Absorption is only in the presence of intrinsic factor (IF), glycoprotein
produced by gastric parietal cells.
40. Causes of B12 deficiency
• Deficient intake (malnutrition, vegetarian);
• Malabsorption:
– Inadequate production of IF (pernicious anemia), gastrectomy,
congenital deficiency;
– A disease of the terminal ileum: celiakie, Crohn's disease, intestinal
resection, intestinal neoplasms, selective malabsorption of B12;
– An intestinal consumption of B12: parasites, bacteria
– Drugs that interfere with B12 absorption: neomycin
• Deficiency in transportation and use of B12 : congenital deficiency of
transcobalamin II (TC), excess of I and III TC, enzyme deficiency.
43. Laboratory data
• Low Hb
• Low / normal number of reticulocytes
• CBC
– MCV > 100 fl
– Leucopenia
– Moderate thrombocytopenia
• Blood smear
– Macrocytosis (macrocytic anemia) , macro-ovalocytes, megalocytes
– Hypersegmented neutrophils (from 5 lobes)
• Bone marrow
– Hyperplasia, predominantly in red blood cells with asincronism in
maturation of the hematopoetic precursors
44. Laboratory data
• Biochemistry:
– Low serum cobalamin <100 pg / ml
– Increased level of intrinsic factor antibodies and anti-parietal cells
– Increased lactate dehydrogenase
– Increased or normal serum iron
– Schilling test positive - no excretion of radiolabelled B12
– Atrophy of gastric mucosa at endoscopy