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Patho. Hematology


One of the body's major fluid tissues. Blood
Where does the blood circulate through after it is pumped by the heart? The blood vessels
What are the components of the blood? Liquid component: plasma. Cellular component: erythrocytes, leukocytes, and thrombocytes.
What does the plasma do? Carries antibodies and nutrients to tissues and carries waste away.
This blood component has RBCs that carry oxygen to the tissues and removes carbon dioxide from them. Erythrocytes
This blood component has WBCs that participate in the inflammatory and immune response. Leukocytes
This blood component has platelets, along with coagulation factors in plasma that are essential for normal clotting. Thrombocytes
Clear, straw-colored fluid that consists mainly of proteins, globulin, and fibrinogen. Plasma
Characteristics of plasma. Osmotic pressure, viscosity, suspension qualities. These all depend on protein content.
Osmotic pressure The pressure exerted on a differentially permeable membrane separating a solution from a solvent, the membrane being impermeable to the solutes in the solution and permeable only to the solvent.
Viscosity The ability or inability of a fluid solution to flow easily.
Other plasma components Regulate acid-base balance, regulate immune response, carry nutrients to tissues, and help to mediate coagulation.
Glucose, lipids, amino acids, electrolytes, pigments, hormones, oxygen, and carbon dioxide. Plasma components
What are the products of metabolism and where do they circulate? Urea, uric acid, creatinine, lactic acid. They circulate in the plasma.
Where are RBCs usually produced? In the bone marrow (erythropoesis). Liver and spleen also participate in production.
What do RBCs transport? Oxygen to body tissues and carbon dioxide away from them.
What is hemoglobin? An oxygen-carrying substance that gives RBCs the ability to transport oxygen.
What is RBC production regulated by? Tissue's demand for oxygen and the blood cells' ability to deliver it.
Hypoxia A lack of oxygen to the tissues.
What does hypoxia stimulate? The formation and release of erythropoietin (hormone that activate bone marrow to produce RBCS).
What % of EPO is produced by the kidney? 80-90%
Where is the remainder of EPO produced? The liver
What enhances EPO production? Androgens (any steroid hormone that increases male characteristics).
What is the life span for a typical RBC? 120 days (about 4 months).
What formation begins as a stem cell which develops into a RBC? Erythrocyte.
What does the development of RBCs require? Vitamin B12, folic acid, minerals (copper, cobalt, and iron).
Iron A component of hemoglobin and vital to the blood's oxygen-carrying capacity.
Where is iron found? In food and, once consumed, is absorbed in the duodenum and upper jejunum.
What specifically are good food sources of iron? Poultry, eggs (egg yolk), dried beans, dried fruit, and salmon.
What happens to iron once it's absorbed? It may be transported to the bone marrow for hemoglobin synthesis or to tissues (muscle) for myoglobin synthesis.
What is unused iron temporarily stored as? Ferritin.
Where is ferritin most commonly located? In specialized cells called reticuloendothelial cells (in liver most commonly).
Small, colorless, disk-shaped cells that have a life span of 7-10 days. Platelets
What are the platelet functions? Help constrict damaged blood vessels, form hemostatic plugs in injured blood vessels, and provide substances that accelerate blood clotting.
How do platelets form hemostatic plugs? By becoming swollen, spiky, sticky, and secretory.
What substances provided by platelets accelerate blood clotting? Factors III and XIII and platelet factor 3.
How is homeostasis maintained? Platelets, plasma, and coagulation factors interact to control bleeding.
What do blood vessels do when tissue injury occurs? They constrict at the injury site and platelets mesh or clump to help prevent hemorrhage.
An abnormal or pathologic condition of the blood. Dyscrasia.
What is primary blood dyscrasia? A blood disorder within the blood itself.
What is secondary blood dyscrasia? It results from a cause other than a defect in the blood (side effect of medication).
Name 2 RBC disorders. Anemia and Polycythemia
What is anemia? Too little RBCs. Decreased RBC production, increased RBC destruction. Results in blood loss.
What is polycythemia? Too many RBCs. Results in hypoxia, tumors that secrete EPO, and genetic defects.
Name 2 WBC disorders. Neutropenia and Lymphocytopenia.
What is neutropenia? Decreased number of neutrophils in the blood.
What is lymphocytopenia? Decreased number of lymphocytes in the blood.
Name 3 platelet disorders. Thrombocytopenia, Thrombocytosis, and Thromboctopathy.
What is thrombocytopenia? Too few platelets.
What is thrombocytosis? Too many platelets.
What is thromboctopathy? Dysfunctional platelets.
A disorder of oxygen transport in which hemoglobin synthesis is deficient. Iron-deficiency anemia.
How much iron can the body store before iron-deficiency anemia may be diagnosed? 1/3 to 1/4 of the body's iron.
A common disease that affects 10-30% of the adult population, but particularly premenopausal women, infants (esp. premature and low birth rate infants), children, and adolescents. Iron-deficiency anemia.
What is typically the cause of iron-deficiency anemia in children, adolescents, and pregnant women? Inadequate iron in the diet to keep up with the increased growth.
What are risk factors associated with iron-deficiency anemia? Inadequate intake of iron, vegetarian diet, low intake of fish, meat, poultry, and iron-fortified foods, frequent dieting, substance abuse, malabsorption, pregnancy, and blood loss secondary to GI bleeds.
When does iron-deficiency anemia occur? When the supply of iron is too low for optimal RBC formation.
What happens to the cells when iron-deficiency anemia occurs? They are smaller (microcytic) and contain less color when seen under a microscope.
Name the signs and symptoms of iron-deficiency anemia. Generalized weakness or fatigue, inability to concentrate, dyspnea or exertion, pica (craving for nonnutritive substances), pallor, tachycardia, and increased cardiac output.
What occurs if the iron-deficiency anemia is prolonged? The patient may experience dry, brittle, ridged nails with frequent concave contours; smooth, sore, pale tongue; and angular chelosis (an ulceration of the corner of the mouth).
What is the definitive method to identify iron-deficiency anemia? Bone marrow aspiration.
What happens after the iron stores are depleted? Hemoglobin levels fall.
What do diminished iron stores cause? Small erythrocytes to be produced by the bone marrow, thus as anemia progresses, the MCV, which measures this size of the erythrocytes, also decreases.
Patients have a low serum iron and an elevated TIBC when focused on what deficiency? Iron-deficiency anemia.
What does the TIBC (total iron binding capactiy) measure? The transport protein supplying the marrow with iron. Also known as transferrin.
What are the most reliable methods in evaluating iron-deficiency anemia? Measuring the ferritin and hemoglobin levels. Know normal lab values.
Lab tests associated with iron-deficiency anemia. TIBC increased, serum iron levels decreased, low hemoglobin and hematocrit levels, small (microcytic) RBCs, hypochromic (less color than normal).
Folic acid anemia. A vitamin found in most body tissues and is essential for the formation and maturation of RBCs and synthesis of DNA.
What % of folic acid is taken in through diet but is excreted unabsorbed? 20%
What is considered insufficient daily intake of folic acid? Less than 50mcg/day. Usually induces folic acid deficiency within 4 months, as the liver supplies are depleted.
Where is folate found? In green vegetables and in the liver.
Who is prone to folic acid anemia? People who rarely eat uncooked vegetables and alcoholics.
Why is folic acid so easily destroyed? Because it is water-soluble and heat-liable, thus being destroyed in the cooking process.
What does folic acid deficiency inhibit? Cell growth, particularly RBCs, leading to production of few, deformed RBCs. Megaloblastic cells (enlarged red cells) havea shortened life span; weeks.
What are risk factors associated with folic acid anemia? Alcohol abuse, poor diet, pregnancy and breast feeding, and malignant or intestinal disease.
Signs and symptoms of folic acid anemia. Weakness, progressive fatigue, shortness of breath, palpitations, forgetfulness, glossitis, heachache, irritability, and pallor.
What is pernicious anemia characterized by? Decreased production of HCL in the stomach acid. Also recognized as a deficiency of intinstic factor.
Intrinsic factor. Normally secreted by the parietal cells of the gastric mucosa and is essential for vitamin B12 absorption in the ileum.
Anemia caued by malabsorption of vitamin B12. Pernicious anemia.
Even if adequate vitamin B12 and intrinsic are present, can a deficiency still occur? Why or why not? Yes, because the disease involving the pancreas or ileum impairs absorption.
Primarily a disorder of adults that tends to run in families. Prenicious anemia.
What does vitamin B12 deficiency inhibit? Cell growth, particularly RBCs, leading to produciton of few, deformed RBCs with poor oxygen-carrying capacity. It also causes neurologic damage by impairing myelin formation.
Who is most prone to pernicious anemia? Strict vegetarians who do not consume any meat or dairy products.
Neurologic signs and symptoms of pernicious anemia. Weakness on extremites, fatigue, peripheral numbness, disturbed positions sense, lack of coordination, altered vision, altered tase and smell, tinnitus, loss of bowel & bladder control, impotence in males, irritability, poor memory, headache.
GI signs and symptoms of pernicious anemia. Nausea, vomiting, anorexia, diarrhea, constipation, flatulence, gingival bleeding and tongue inflammation.
Cardiovascular signs and symptoms of pernicious anemia. Low hemoglobin, palpitations, and tachycardia.
Respiratory signs and symptoms of pernicious anemia. Dyspnea, orthopnea.
Sickle cell anemia/disease Hemolytic anemia that results from inheritance of the sickle hemoglobin gene (HbS).
What happens when cells are exposed to low oxygen levels? The erythrocytes will lose its round, pliable, biconcave disk shape and become rigid, deformed, and sickle-shaped. Effects are seen in larger blood vessels.
How does the sickling process work? It takes time, so if the sickled cell is again exposed to adequate amounts of oxygen, before the membrane becomes too rigid, it can revert to a normal shape. Sickling crisis are intermittent.
In what race is sickle cell anemia most prevelant? Inherited in people of African descent and to a lesser degree in people from the Middle East (Mediterranean).
What is the most benign state of sickle cell disease? The carrier state of sickle cell.
What % of the erythrocyte is hemoglobin? 50%
How many genes will a child birthed from 2 people with the trait have? 2 abnormal genes. These children will only produce hemoglobin and therefore will have sickle cells anemia.
Signs and symptoms of sickle cell anemia. Range from chronic hemolysis to thrombosis, erythrocytes have a shortened life span, anemia is always present and Hgb is 7-10g/dL, jaundice, bone marrow expansion, and chronic anemia (tachycardia, cardiac murmurs, and enlarged heart).
Which organ(s) can be affected by thrombosis (an abnormal condition where a clot develops in the blood vessel)? Any organ can be affected but primarily the sites with lower circulation: spleen, lungs, CNS
What are complications associated with sickle cell anemia? Infection, stroke, renal failure, impotence, heart failure, pulmonary hypertension.
Results from tissue hypoxia and necrosis due to inadequate blood flow to a specific region of tissue or organ. Sickle cell crisis; very painful.
Results from infection with the human parvovirus. Aplastic crisis; hemoglobin falls rapidly and marrow can't compensate; absence of RBCs.
Results when other organs pool the sickled cells. Sequestration crisis; most children by 10 years have a nonfunctioning spleen. The liver and lungs are affected in adults.
Created by: shanhaup on 2008-09-29

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