Porth's Pathophysiology, Concepts of Altered Health States 9th Edition by Sheila Grossman-Carol Mattson Porth
Porth's Pathophysiology, Concepts of Altered Health States 9th Edition by Sheila Grossman-Carol Mattson Porth
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Chapter 26- Disorders of Hemostasis
Complete Chapter Questions With Answers
Sample Questions Are Posted Below
| 1. | A hospital laboratory technologist is analyzing the complete blood count (CBC) of a patient. Which of the following statements best reflects an aspect of the platelets that would constitute part of the CBC? | |
| A) | Platelets originate with granulocyte colony–forming units (CFU). | |
| B) | The half-life of a platelet is typically around 8 to 12 days. | |
| C) | The a-granules of platelets contribute primarily to vasoconstriction. | |
| D) | New platelets are released from the bone marrow into circulation. | |
| Ans: | B | |
| Feedback: | ||
| Platelets’ half-life is typically around 8 to 12 days. They originate from megakaryocytes, and d-granules facilitate vasoconstriction. New platelets are released from the spleen into circulation. | ||
| 2. | A 71-year-old male patient with a history of myocardial infarction (MI) and peripheral vascular disease (PVD) has been advised by his family physician to begin taking 81 mg aspirin once daily. Which of the following statements best captures an aspect of the underlying rationale for the physician’s suggestion? | |
| A) | Platelet aggregation can be precluded through inhibition of prostaglandin production by aspirin. | |
| B) | Aspirin helps to inhibit ADP action and minimizes platelet plug formation. | |
| C) | Aspirin can reduce unwanted platelet adhesion by inhibiting TXA2 synthesis. | |
| D) | Aspirin inhibits the conversion of fibrinogen into fibrin and consequent platelet plug formation. | |
| Ans: | A | |
| Feedback: | ||
| Aspirin prevents platelet plug formation by inhibiting synthesis of prostaglandins that mediate clot formation. Aspirin does not influence ADP, TXA2 synthesis, or fibrinogen conversion. | ||
| 3. | A hospital client is receiving intravenous infusion of heparin for treatment of a pulmonary embolus. Which of the following phenomena is most likely to occur, resulting in the drug’s therapeutic effect? | |
| A) | Inhibition of vitamin K synthesis in the liver | |
| B) | Suppression of fibrin formation | |
| C) | Deactivation of the intrinsic clotting pathway | |
| D) | Inhibition of ADP-induced platelet aggregation | |
| Ans: | B | |
| Feedback: | ||
| Ultimately, heparin inhibits the clotting factors that mediate the formation of fibrin. It does not inhibit vitamin K synthesis, nor does it deactivate the intrinsic clotting pathway in particular. Heparin does not act on platelet plug formation. | ||
| 4. | When discussing the sequence of clot dissolution, the science instructor will talk about which item that begins the process? | |
| A) | Plasminogen | |
| B) | Dabigatran | |
| C) | Platelets | |
| D) | a2-plasmin inhibitor | |
| Ans: | A | |
| Feedback: | ||
| As with clot formation, clot dissolution requires a sequence of steps controlled by activators and inhibitors. Plasminogen, the proenzyme for the fibrinolytic process, normally is present in the blood in its inactive form. It is converted to its active form, plasmin, by plasminogen activators formed in the vascular endothelium, liver, and kidneys. Dabigatran is an anticoagulant. Platelets actually help cells stick together or adhere. | ||
| 5. | In which of the following patients, would diagnostic investigations least likely reveal increased thrombopoietin production? | |
| A) | An 81-year-old woman with diagnoses of rheumatoid arthritis and failure to thrive | |
| B) | A 55-year-old man with dehydration secondary to Crohn disease | |
| C) | A 66-year-old woman with a diagnosis of lung cancer with bone metastases | |
| D) | A 21-year-old woman awaiting bone marrow transplant for myelogenous leukemia | |
| Ans: | D | |
| Feedback: | ||
| Diseases such as myelogenous leukemia and other cases of primary thrombocytosis result in abnormalities in the thrombopoietin receptor and platelet binding. Cases of secondary thrombocytosis have an etiology rooted in increased thrombopoietin production. The common underlying causes of secondary thrombocytosis include tissue damage due to surgery, infection, cancer, and chronic inflammatory conditions such as rheumatoid arthritis and Crohn disease. | ||
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