Pathophysiology
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| One of the body's major fluid tissues. | Blood
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| Where does the blood circulate through after it is pumped by the heart? | The blood vessels
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| What are the components of the blood? | Liquid component: plasma. Cellular component: erythrocytes, leukocytes, and thrombocytes.
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| What does the plasma do? | Carries antibodies and nutrients to tissues and carries waste away.
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| This blood component has RBCs that carry oxygen to the tissues and removes carbon dioxide from them. | Erythrocytes
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| This blood component has WBCs that participate in the inflammatory and immune response. | Leukocytes
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| This blood component has platelets, along with coagulation factors in plasma that are essential for normal clotting. | Thrombocytes
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| Clear, straw-colored fluid that consists mainly of proteins, globulin, and fibrinogen. | Plasma
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| Characteristics of plasma. | Osmotic pressure, viscosity, suspension qualities. These all depend on protein content.
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| 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.
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| Viscosity | The ability or inability of a fluid solution to flow easily.
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| Other plasma components | Regulate acid-base balance, regulate immune response, carry nutrients to tissues, and help to mediate coagulation.
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| Glucose, lipids, amino acids, electrolytes, pigments, hormones, oxygen, and carbon dioxide. | Plasma components
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| What are the products of metabolism and where do they circulate? | Urea, uric acid, creatinine, lactic acid. They circulate in the plasma.
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| Where are RBCs usually produced? | In the bone marrow (erythropoesis). Liver and spleen also participate in production.
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| What do RBCs transport? | Oxygen to body tissues and carbon dioxide away from them.
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| What is hemoglobin? | An oxygen-carrying substance that gives RBCs the ability to transport oxygen.
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| What is RBC production regulated by? | Tissue's demand for oxygen and the blood cells' ability to deliver it.
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| Hypoxia | A lack of oxygen to the tissues.
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| What does hypoxia stimulate? | The formation and release of erythropoietin (hormone that activate bone marrow to produce RBCS).
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| What % of EPO is produced by the kidney? | 80-90%
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| Where is the remainder of EPO produced? | The liver
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| What enhances EPO production? | Androgens (any steroid hormone that increases male characteristics).
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| What is the life span for a typical RBC? | 120 days (about 4 months).
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| What formation begins as a stem cell which develops into a RBC? | Erythrocyte.
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| What does the development of RBCs require? | Vitamin B12, folic acid, minerals (copper, cobalt, and iron).
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| Iron | A component of hemoglobin and vital to the blood's oxygen-carrying capacity.
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| Where is iron found? | In food and, once consumed, is absorbed in the duodenum and upper jejunum.
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| What specifically are good food sources of iron? | Poultry, eggs (egg yolk), dried beans, dried fruit, and salmon.
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| 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.
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| What is unused iron temporarily stored as? | Ferritin.
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| Where is ferritin most commonly located? | In specialized cells called reticuloendothelial cells (in liver most commonly).
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| Small, colorless, disk-shaped cells that have a life span of 7-10 days. | Platelets
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| What are the platelet functions? | Help constrict damaged blood vessels, form hemostatic plugs in injured blood vessels, and provide substances that accelerate blood clotting.
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| How do platelets form hemostatic plugs? | By becoming swollen, spiky, sticky, and secretory.
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| What substances provided by platelets accelerate blood clotting? | Factors III and XIII and platelet factor 3.
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| How is homeostasis maintained? | Platelets, plasma, and coagulation factors interact to control bleeding.
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| What do blood vessels do when tissue injury occurs? | They constrict at the injury site and platelets mesh or clump to help prevent hemorrhage.
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| An abnormal or pathologic condition of the blood. | Dyscrasia.
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| What is primary blood dyscrasia? | A blood disorder within the blood itself.
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| What is secondary blood dyscrasia? | It results from a cause other than a defect in the blood (side effect of medication).
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| Name 2 RBC disorders. | Anemia and Polycythemia
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| What is anemia? | Too little RBCs. Decreased RBC production, increased RBC destruction. Results in blood loss.
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| What is polycythemia? | Too many RBCs. Results in hypoxia, tumors that secrete EPO, and genetic defects.
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| Name 2 WBC disorders. | Neutropenia and Lymphocytopenia.
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| What is neutropenia? | Decreased number of neutrophils in the blood.
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| What is lymphocytopenia? | Decreased number of lymphocytes in the blood.
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| Name 3 platelet disorders. | Thrombocytopenia, Thrombocytosis, and Thromboctopathy.
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| What is thrombocytopenia? | Too few platelets.
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| What is thrombocytosis? | Too many platelets.
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| What is thromboctopathy? | Dysfunctional platelets.
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| A disorder of oxygen transport in which hemoglobin synthesis is deficient. | Iron-deficiency anemia.
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| How much iron can the body store before iron-deficiency anemia may be diagnosed? | 1/3 to 1/4 of the body's iron.
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| 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.
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| 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.
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| 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.
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| When does iron-deficiency anemia occur? | When the supply of iron is too low for optimal RBC formation.
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| What happens to the cells when iron-deficiency anemia occurs? | They are smaller (microcytic) and contain less color when seen under a microscope.
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| 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.
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| 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).
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| What is the definitive method to identify iron-deficiency anemia? | Bone marrow aspiration.
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| What happens after the iron stores are depleted? | Hemoglobin levels fall.
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| 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.
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| Patients have a low serum iron and an elevated TIBC when focused on what deficiency? | Iron-deficiency anemia.
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| What does the TIBC (total iron binding capactiy) measure? | The transport protein supplying the marrow with iron. Also known as transferrin.
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| What are the most reliable methods in evaluating iron-deficiency anemia? | Measuring the ferritin and hemoglobin levels. Know normal lab values.
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| 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).
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| Folic acid anemia. | A vitamin found in most body tissues and is essential for the formation and maturation of RBCs and synthesis of DNA.
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| What % of folic acid is taken in through diet but is excreted unabsorbed? | 20%
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| 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.
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| Where is folate found? | In green vegetables and in the liver.
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| Who is prone to folic acid anemia? | People who rarely eat uncooked vegetables and alcoholics.
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| Why is folic acid so easily destroyed? | Because it is water-soluble and heat-liable, thus being destroyed in the cooking process.
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| 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.
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| What are risk factors associated with folic acid anemia? | Alcohol abuse, poor diet, pregnancy and breast feeding, and malignant or intestinal disease.
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| Signs and symptoms of folic acid anemia. | Weakness, progressive fatigue, shortness of breath, palpitations, forgetfulness, glossitis, heachache, irritability, and pallor.
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| What is pernicious anemia characterized by? | Decreased production of HCL in the stomach acid. Also recognized as a deficiency of intinstic factor.
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| Intrinsic factor. | Normally secreted by the parietal cells of the gastric mucosa and is essential for vitamin B12 absorption in the ileum.
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| Anemia caued by malabsorption of vitamin B12. | Pernicious anemia.
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| 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.
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| Primarily a disorder of adults that tends to run in families. | Prenicious anemia.
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| 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.
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| Who is most prone to pernicious anemia? | Strict vegetarians who do not consume any meat or dairy products.
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| 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.
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| GI signs and symptoms of pernicious anemia. | Nausea, vomiting, anorexia, diarrhea, constipation, flatulence, gingival bleeding and tongue inflammation.
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| Cardiovascular signs and symptoms of pernicious anemia. | Low hemoglobin, palpitations, and tachycardia.
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| Respiratory signs and symptoms of pernicious anemia. | Dyspnea, orthopnea.
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| Sickle cell anemia/disease | Hemolytic anemia that results from inheritance of the sickle hemoglobin gene (HbS).
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| 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.
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| 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.
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| 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).
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| What is the most benign state of sickle cell disease? | The carrier state of sickle cell.
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| What % of the erythrocyte is hemoglobin? | 50%
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| 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.
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| 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).
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| 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
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| What are complications associated with sickle cell anemia? | Infection, stroke, renal failure, impotence, heart failure, pulmonary hypertension.
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| Results from tissue hypoxia and necrosis due to inadequate blood flow to a specific region of tissue or organ. | Sickle cell crisis; very painful.
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| Results from infection with the human parvovirus. | Aplastic crisis; hemoglobin falls rapidly and marrow can't compensate; absence of RBCs.
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| 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.
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