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hemodynamics
Stack #150433
| Question | Answer |
|---|---|
| active bleeding into extravascular tissues or spaces resulting from disruption of the integrity of vascular walls | hemorrhage |
| hemmorrhages into skin, mucous membrans or serosal surfaces, pinpoint | petechiae |
| hemorrhages into skin, mucous membranes or serosal surfaces greater less than 1.ocm | purpura |
| hemorrhages into skin, mucous membranes or ersoals surfaces greater than 1.0 cm | ecchymoses |
| Extravascular blood clots | hematomas |
| blood in stool, dark tary | melena |
| bright red blood in stool | hematochezia |
| Clinical significane is dependent on 3 things | amount, location and rate of loss |
| Body's intrinsic ability to slow down or stop hemorrhage | hemostatsis |
| intravascular blood coagulum | thrombus |
| When does vasoconstriction occur with hemmorrhage | immediately |
| Do all venules and veins contain muscles to constrict during hemorrhage | no, small veins do not. ex. paper cut |
| When does a platlet plug develop in relation to hemorrhage | with in minutes |
| Where do platelets adhere to in a hemorrhage | to site of injury on endothelium |
| Where is platelet formed | bonemarrow |
| When does coagulation occur in hemorrhage | with in several minutes |
| What interactions takes place to produce coagulation | platelets, calcium and protein factors |
| What is the end result of coagulation | formation of fibrin, an insoluble fiber like protein |
| Pathway activiated by contact of factor 7 with subendothelial matrix of damaged vessel wall | intrinsic pathway |
| What is intresic pathway activited by | cotact of factor 7 with the subendothelial matrix of damaged vessel wall |
| The time it takes for blood to coagulate by intrinsic pathway mechanism is measured in the lab by | Partial thromboplastin time |
| Partial thromboplastin tim | The time it takes for blood to coagulate by the intrinsic pathway mechanism |
| Pathway activated by chemicals that are relaesed from injured tissue and from platelets | extrinsic pathway |
| The time it takes for blood to coagulate by exrinsic pathway mechanism is measured in the lab by | prothrombin time |
| Mechanism when both the intrinsic and extrinsic pathways converge on inactove factor 10 to produce activated factor 19 | common pathway |
| What enzyme catalyzes the conversion of fibrinogen into fibrin | thrombin |
| the process that opposes and counteracts coagulation | fibrinolysis |
| What is the key player in fibrinolysis | plasminogen |
| Type of beeding disorder that is usually characterized by a single factor deficiency | congential |
| Factor 8 deficiency | hemophilla a |
| Patients with this disease have difficulty controlling bleeding after minor trauma, hemarthrosis, normal platlet, normal PT and increased PTT | hemophilla a |
| What lab value will be abnormal in hemophilla a | PTT |
| Factor 9 deficiency | hemophilia b |
| Coagulation abnormality, easy bleeding, but will not bleed into joints | vonwilebrand disease |
| Two bleeding disorders that are inherideted | hemophilia a and b |
| Bleeding disordrs that are characterized by multiple factor deficiences and clotting abnormalities | acquired |
| Many clotting factors made in teh liver are dependent on what vitamen | K |
| When would deficiencies in vit k occur | malnutrition, malabsorption, biliary obstruction or drug therapy |
| platelet abnormality that refers to a decrease in the number of platelets | thrombocytopenia |
| Platelet abnormalitiy that is characterized by petechcial bleeding from small vessels into the skin, GI tract, UT and brain | thrombocytopenia |
| What level of plateletes would impeded coagulation | 20,ooo/uL |
| DIC is an example of what type of platelet abnormality | thrombocytopenia |
| Platelet abnormality, ex. asprin interfers with the function of platelets | functional |
| Bleeding disorder manifested by petechial hemorrhages into the skin or mucous membranes and usually are not sefver, life threating situations | vessel abnormalities |
| 3 predisposing factors to thrombosis | alteration of vascular endotheliumblood flowblood componenets |
| What are the 3 predisposing factorws to throbosis referred to? | virchow's triad |
| Atherosclerosis, DM, HTN, bacterial toxins, chemical agents, immunologic reacts that could iniate thrombus formationh is an example of which component of virchow's triad | alteration of vascular endothelium |
| Stasis or turbulence decreases bloodflow and will do what to platelets | bring them in direct contact with the endothwlium |
| Examples of alteration of blood componenets | presence of precoagulants ( as seen in SLOE and neoplasms) causing hypercoaguloatibility |
| Form of thrombi frequently seen in areas of atherosclerotic damage | arterial thrombi |
| Form of thrombi seen in areas of blood stasis | venous thrombi |
| Form of thrombi, due to local endothelial damage, consist of platelets and are not grossly visable | capillary thrombi |
| a thrombus fragment that has detatched from its site of orgin and is moving through circulation | thromboembolus |
| process of tissue necrosis secondary to an abrupt reduction in tissue oxygenation | infarction |
| What tissues are more sensitive to the effects of hypoxia/anoxia | highly speacilized and very metabolically active |
| What organs have single blood supply, but rich anastomoses or dual blood supply | small bowel, liver, lung |
| Are organs with rich anastomes and dual blood supply protcted against hypoxia? Why? | yes, they arteries can re route. |
| In organs with richanastomesis or dual blood supply what type of infarct occurs | red hemorrhage infarct |
| infarct in which an alternate blood source may bleed into necrotic tissue | red hemorrhage/ one in which there is a dual lumen or anastomesis |
| Where do the majority of pulmonary emboli arise? | deep leg veins |
| What is the major cause of fat emboli? | after fracture of long bone |
| form of shock that occurs with loss of blood or fulid from circulation | hypovoemic |
| Type of shock resulting from hemorrhage, burns, vomiting, diarrhea & third spacing | hypovolemic |
| Type of shock that develops from the inability of the heart to maintain adequate output | cardiogenic |
| What is cardiogenic shock a result of | MI, cardiac tamponade, pulmonary emboli |
| Type of shock that results from hypersensitivity reactions | anaphylactic |
| Type of shock that may lead to widespread vasocilation and increased permaeability | anaphylatic |
| What type of shock doesn't result in a decreased cardiac output | septi |
| What produces oligouria in shock victims | decreased blood volume tells the kidneys to retain sodium and h2o |
| What develops as a result of the tissue hypoxia in shock | lactic acidosis |
| What are s&s of lactic acidosis | restlessness, mental obtundation and compensatory hyperventalation |
| form of shock that occurs with loss of blood or fulid from circulation | hypovoemic |
| Type of shock resulting from hemorrhage, burns, vomiting, diarrhea & third spacing | hypovolemic |
| Type of shock that develops from the inability of the heart to maintain adequate output | cardiogenic |
| What is cardiogenic shock a result of | MI, cardiac tamponade, pulmonary emboli |
| Type of shock that results from hypersensitivity reactions | anaphylactic |
| Type of shock that may lead to widespread vasocilation and increased permaeability | anaphylatic |
| What type of shock doesn't result in a decreased cardiac output | septi |
| What produces oligouria in shock victims | decreased blood volume tells the kidneys to retain sodium and h2o |
| What develops as a result of the tissue hypoxia in shock | lactic acidosis |
| What are s&s of lactic acidosis | restlessness, mental obtundation and compensatory hyperventalation |
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