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Patho Final (part 1)
Nightingale Pathophysiology Final Review Part 1 of 3
| Question | Answer |
|---|---|
| Plasma, Gases, Nutrients, Waste and Cells Cells suspended in protein and inorganic materials. 91% water and 9% Solutes | Composition of Blood |
| Water, electrolytes and Protiens (albumin, globulin, fibrogen, transferrin, ferritin) Gases - Co2, o2, n2 Nutrients - glucose, carbs, amino acids, colesterol, vitamins, elements, iron Waste - Urea, creatinine, uric acid, bilirubin, hormones | Plasma |
| Erythrocytes, leukocytes, neutrophils, eosinophils basophils, monocytes, macrophages, lymphocytes, NK cells, Platelets | The cells in Blood |
| When the demand for circulating mature neutrophils exceeds the supply immature neutrophils and leukocytes are released from the bone marrow. This leads to a lukemoid reaction and a high number of immature leukocytes in the blood - this is called .... | Shift Left |
| If infection and inflammation diminish and granulopoiesis is able to replenish the granulocytes the leukemoid reaction ... | Shifts Right or Back to Normal |
| A reduction in the total number of erythrocytes in the blood supply or a decrease in the quality and quantity of hemoglobin | Anemia |
| Erythrocytes are | Red Blood Cells |
| A protein in red blood cells that carries oxygen to the body and carbon dioxide back to the lungs | Hemoglobin |
| Impaired erythrocyte production, Blood Loss, increased erythrocyte destruction or a combination of these factors are causes of -- | Anemia |
| Anemia is classified by | Cause or change that affects shape, size and substance of RBC |
| Anemia type that causes large odd shaped erythrocytes and normal hemoglobin concentrations | Macrocytic |
| A macrocytic anemia that is caused by lack of B12, abnormal DNA and premature cell death and is a congenital or acquired deficiency of intrinsic factor | Pernicious Anemia |
| A Macrocytic anemia caused by lack of folate and premature cell death due to a dietary folate deficiency | Folate Deficiency Anemia |
| Anemia type that causes small abnormally shaped erythrocytes and reduced hemoglobin concentration | Microcytic |
| A microcytic anemia caused by lack of Iron and/or insufficient hemoglobin. Resulting from chronic blood loss, iron deficiency or a disrupted Iron cycle | Iron Deficiency Anemia |
| A microcytic anemia caused by a dysfunctional iron uptake resulting from a congenital or acquired conditon | Sideroblastic Anemia |
| A microcytic anemia caused by impaired synthesis of hemoglobin chains and phagocytossis of erthroblasts in bone marrow resulting from a congenital defect | Thalassemia |
| Anemia type that causes normal size of erythrocytes and a normal hemoglobin concentration | Normocytic |
| A normocytic anemia that is due to insuffiient erythropoiesis from depressed stem cell profliferation | Aplastic Anemia |
| A normocythic anemia causes by blood loss, increased erythropoiesis and or iron depletion | Post Hemorrhagic Anemia |
| A normocythic anemia caused by premature destruction of erythrocytes due to their fragility | Hemolytic Anemia |
| A normocytic anemia caused by abnormal hemoglobin synthesis, abnormal cell shape and susceptability due to a congenital defect | Sickle Cell Anemia |
| A normocytic anemia Caused by abnormally high demand for new erythrocytes because of chronic infection, inflammation or malignancy | Anemia of Chronic Inflammation |
| When bone marrow makes too many RBC's causing increased blood volume, vescocity and hyercoagulation | Polycythemia Vera |
| Plethora, engorgement of retinal and cerebral veins, headaches, drowsiness, delirium, mania, psychotic depression, chorea, visual disturbances, enlarged spleen, abdominal pain, abdominal discomfort, Intense painful itching made worse by heat and water | Clinical Manifestations of Polycythemia Vera |
| Platelet count less than 150000 resulting from decreased platelet production, consumption or both. | Thrombocytopenia |
| Venous or arterial thrombosis, DVT, pulmonary emboli, limb ischemia, cerebrovascular accidents can all be causes by | Thrombocytopenia |
| Excessive bruising, superficial bleeding, prolonged bleeding, bleeding from gums or teeth and blood in urine or stool | Clinical manifestations of Thrombocytopenia |
| Platelet count greater than 450000 causes by excessive platelet production. Patients are usually asymptomatic until count exceeds 1 million | Thrombocythemia |
| Clotting, Thrombosis, hemorrhage, abnormal clotting, leukocytosis, splenomegaly, bleeding, itching, and leukemic or bone marrow fibrotic transformation can all be caused by | Thrombocythemia |
| Ischemia in the fingers and toes, headache, parathesia and erythromelagia (warm red hands and feet that are painful and burning) are -- | Clinical manifestations of Thrombocythemia |
| Thickening and hardening of vessel walls caused by an accumulation of lipid heavy macrophages in the arterial walls leading to a plaque lesion | Atherosclerosis |
| Inadequate perfusion of tissue, transient ischemic attacks, tissue infarction, pain, disability, coronary artery disease and stroke | Clinical manifestations of atherosclerosis |
| Rudor or redness | Erythema |
| a reactive erythema associated with rheumatic fever | Erythema marginatum |
| A (rare) skin rash on the trunk and limbs. Appears round with a pink pale center and surrounded by a raised outline. | Erythema Marginatum |
| Often the first noticed symptom of leukemia is | Anemia |
| Anemia, bleeding, infection, weight loss, bone pain, liver enlargement, spleen enlargement, lymph node enlargement and elevated uric acid levels are all symptoms of | Acute Leukemia |
| The pathophysiology of _________________ is when B cells produce antibodies and cytotoxic T cells to activate and proliferate against the virus. The immune response leads to cell proliferation in the lymph tissue ( lymph nodes, spleen, tonsils and liver) | Infectious Mononucleosis |
| The epestine barr virus is the most common cause of this lympho proliferative viral infection of B lymphocytes. | Infectious Mononucleosis |
| Venous Stasis, Endothilelial damage and hypercoagulation are all legs of the __________________ | The Virchow Triad |
| Orthopedic trauma, surgery, spinal injury, obstetric and gynocological condtions can all lead to a ___________ | Deep vein Thrombosis |
| Early ambulation, pneumatic devices and prophlactic anticoagulants can all help prevent____________ | Deep vein Thrombosis |
| Immobility, Age and Heart Failure all contribute to improper vein function or _____________ | Venous Stasis |
| Trauma, Surgery and IV medications contribute to impaired function of the lining of blood vessels or _________________ | endothilelial damage. |
| Inherited conditions, malignancies, pregnancy, oral contraceptives and hormone therapy can lead to | hypercoagulation |
| Progressive occlusion of the superior vena cava that leads to venous distention of the upper extremities and head -- | Superior Vena Cava Syndrome |
| The most common cause of ____________ is bronchogenic cancers, lymphomas, and metastatic cancers. ________ can also be caused by TB, mdeiastinal fibrosis, cystic fibrosis, pacemaker wires, central vein catheters and pulmonary catheters | Superior Vena Cava Syndrome (SVCS) |
| A sustained increase in peripheral vascular resistance and/or a increase in circlating blood volume is the pathophysiology of | Hypertension |
| In people with hypertension - a given blood pressure means they tend to secrete less salt in the urine. Increased vascular volume = decreased salt excretion. In other words renal sodium retention leads to a | Shift in the Pressure Naturessis Curve |
| Increased SNS activity increases heart rate & vasoconstriction. this increases cardiac output and peripheral vascular resistance raising the BP. This leads to a thickening of blood vessels called | Vascular Remodeling |
| Over activity of the Renin Angiotensin System leads to high levels of Renin, Angiotensin II and aldosterone. This contributes to endothileal dysfunction, insulin resistance, platelet aggregation and permenant increase in PVR leading to____ | Arteriolar Remodeling |
| When the placement of temp dependent immune complexes in the capillary beds activate below normal body temperatures they are called | Cryoglobulins |
| When cryoglobulins in the fingers, toes or nose cause blanching, numbness followed by cyanosis and possible gangrene - this is called | Raynaud Phenomenon |
| Dyspnea, Couging, abnormal sputum, hemoptysis, altered breathing pattern, hypoventilation, hyperventilation, cyanosis, clubbing and chest pain are all clinical manifestations of | Pulmonary alterations |
| Coughing up blood | Hemoptysis |
| abnormally round shape to the nail bed | Clubbing |
Created by:
Jslatter
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