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An in-depth analysis of various types of anemia, including iron deficiency anemia and vitamin b12 deficiency anemia. It covers the causes, symptoms, and treatments of these conditions, as well as the role of compensatory mechanisms and underlying causes. The document also discusses normal erythropoiesis and other related blood disorders.
Typology: Lab Reports
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Bio 375
Pathophysiology
The anemias: Cause a reduction in oxygen transport in the blood due to: Decrease in hemoglobin production Decrease in erythrocytes Combination of these two Oxygen deficit results: Less energy is produced in cells Cell metabolism is decreased Cell reproduction is decreased
Compensatory mechanisms include tachycardia and peripheral vasoconstriction This leads to fatigue, pallor, dyspnea and tachycardia Decreased regeneration of epithelial cells causes the digestive tract to become inflamed and ulcerated; cracked lips; dysphagia; hair and skin may show degenerative changes
Severe anemia may lead to angina during stressful situations if oxygen supply to the heart is sufficiently reduced
Chronic severe anemia may cause congestive heart failure
Anemia may occur when: There is a deficiency of a nutrient When bone marrow function is impaired When blood loss is excessive When there is excessive destruction of RBC’s
Very common Ranges from mild to severe Occurs in all age groups Lack of iron impedes synthesis of Hb Produces microcytic, hypochromic RBC’s Decrease in stored iron with: Decreased serum ferritin Decreased hemosiderin Decreased iron containing histiocytes in bone marrow
Iron deficit can occur for several reasons: Inadequate iron containing vegetables or meat in diet Chronic blood loss from ulcers, hemorrhoids, cancer or excessive menstrual flow Malabsorption syndromes, e.g. achlorhydria Severe liver disease In some infections and cancer, iron is absorbed but not well utilized; leads to low hemoglobin counts but high iron storage levels
Characterized by very large, immature, nucleated erythrocytes (megaloblastic anemia)
Usually results from deficits of either folic acid (vitamin B 9 ) or vitamin B (^12) Folic acid deficits usually diet related B 12 deficit may have multiple causes
Often caused by the malabsorption of B 12 due to a lack of intrinsic factor (IF) from the gastric glands of the stomach
Lack of IF usually due to:
Formation of autoantibodies against IF or the parietal cells that produce it; results in atrophy of the gastric mucosa Any condition that reduces the gastric mucosa
The gastric mucosa atrophy not only causes IF deficiency but also achlorhydria which interferes with: Early protein digestion Absorption of iron Iron deficiency may coexist with pernicious anemia
Vitamin B 12 must bind to IF to enable absorption of the vitamin in the lower ileum.
Deficiency of vitamin B leads to impaired maturation of erythrocytes (it interferes with DNA synthesis) The RBC’s are very large and many have nuclei They are destroyed prematurely leading to low hemoglobin count or anemia Often granulocytes are also affected with hypersegmented nuclei
Thrombocyte (platelet) levels may be low Lack of B 12 is also a direct cause of demyelination of nerve fibers of peripheral nerves and eventually the spinal cord; first sensory nerves are affected and later motor nerves are involved Demyelination interferes with nerve conduction
Dietary deficiency not typically a cause Most common cause is malabsorption: Autoimmune reaction Chronic gastritis Inflammatory conditions like regional ileitis Oral supplements for pregnant women and vegetarians B 12 injections for people with pernicious anemia
Anemia (pallor, weakness and dyspnea
Leukopenia with recurrent or multiple infections
Thrombocytopenia with small pinpoint hemorrhages and a tendancy to bleed excessively especially in the mouth
About half the cases are middle aged and cause is unknown or ideopathic
In others, damage may be caused by myelotoxins, such as: Radiation Industrial chemicals (e.g. benzene) Drugs (e.g. chloramphenicol, gold salts, phenylbutazone, phenytoin, antineoplastic drugs)
Also viruses, particularly hepatitis C may cause aplastic anemia
If the risk is from cancer treatment, a patients stems cells may be harvested prior to drug treatment and then transfused later when needed
Hemolytic anemias Sickle cell anemia Thalassemia
Polycythemia vera Blood clotting disorders Hemophilia A Disseminated Intravascular Coagulation
These are malignant neoplasms involving lymphocyte proliferation in the lymph nodes
Two types are distinguished on the basis of lymph node biopsy: Hodgkin’s Lymphoma Non- Hodgkin’s Lymphoma
No specific etiology is known
Primarily occurs in adults 20-40 years old Initially involves a single lymph node but progresses to adjacent lymph nodes and finally to other organs via the lymphatic system
T lymphocytes appear to be defective Lymphocyte count is depressed Reed-Sternberg cell, found in lymph nodes, is used as marker in diagnosis
Typical spread of Hodgkin’s lymphoma
Staging is based on number of nodes and organs involved and whether they are located on one or both sides of the diaphragm Treatment involves: Radiation Chemotherapy Surgery Prognosis in early stages is excellent