Which of the following clinical manifestations of Disseminated intravascular coagulation (DIC)?
Decreased hematocrit, increased platelet counts, increased D-dimer
Decreased platelet counts, increased D-dimer, increased prothrombin time
Decreased Antithrombin III, increased platelet counts, increased fibrinogen
Decreased D-dimer, increased platelet counts, Increased hemoglobin
The Correct Answer is B
Disseminated Intravascular Coagulation (DIC) is a condition characterized by widespread activation of the coagulation system, leading to both excessive clot formation and consumption of clotting factors and platelets. This process can result in both bleeding and thrombosis.
The manifestations mentioned in option B are commonly seen in DIC:
Decreased platelet counts: DIC leads to platelet consumption and destruction, resulting in low platelet counts (thrombocytopenia).
Increased D-dimer: D-dimer is a fibrin degradation product, and its levels are increased DIC due to the breakdown of fibrin clots.
Increased prothrombin time (PT): DIC can lead to the depletion of clotting factors, resulting in prolonged prothrombin time, indicating impaired coagulation.
The other options mentioned do not represent the typical clinical manifestations of DIC:
A. Decreased hematocrit, increased platelet counts, and increased D-dimer in (option A) are incorrect because While platelet counts and D-dimer are increased in DIC, decreased hematocrit is not a characteristic finding.
C. Decreased Antithrombin III, increased platelet counts, and increased fibrinogen in (option C) is incorrect because: Decreased Antithrombin III can be seen in DIC, but increased platelet counts and fibrinogen levels are not specific to DIC.
D. Decreased D-dimer, increased platelet counts, and increased hemoglobin in (option D) is incorrect because Decreased D-dimer and increased hemoglobin are not typical findings in DIC, while increased platelet counts can be seen in some cases.
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Related Questions
Correct Answer is A,B,D,C
Explanation
A. Decreased blood volume: Burn injuries can lead to fluid loss, primarily through damaged skin. This fluid loss causes a decrease in blood volume, leading to hypovolemia. Hypovolemia contributes to decreased cardiac output and tissue perfusion.
B. Increased vascular permeability: Burn injuries cause an inflammatory response, leading to increased vascular permeability. This increased permeability allows fluid, electrolytes, and proteins to leak from the intravascular space into the interstitial space.
C. Development of edema: The increased vascular permeability and fluid leakage lead to the development of edema. Edema occurs as fluid accumulates in the interstitial spaces, further contributing to tissue swelling and compromised perfusion.
D. Increased peripheral resistance: In response to decreased blood volume and tissue hypoperfusion, the body activates compensatory mechanisms to maintain blood pressure and tissue perfusion. One of these mechanisms is increased peripheral resistance, which occurs as blood vessels constrict to maintain blood pressure. Increased peripheral resistance helps redirect blood flow to vital organs but also contributes to increased workload on the heart.
Therefore, the correct sequential order of events involved in burn shock following a patient's exposure to burns is:
A. Decreased blood volume B. Increased vascular permeability D. Development of edema C. Increased peripheral resistance
Correct Answer is D
Explanation
In the compensatory stage of shock, the body initiates various mechanisms to maintain perfusion to vital organs and restore homeostasis. Activation of the renin-angiotensin system is one of the compensatory responses. The decreased blood flow and oxygen delivery to the kidneys stimulate the release of renin from the kidneys. Renin acts on angiotensinogen, converting it into angiotensin I, which is further converted to angiotensin II by the action of angiotensin-converting enzyme (ACE). Angiotensin II is a potent vasoconstrictor and also stimulates the release of aldosterone, leading to sodium and water retention. These mechanisms aim to increase blood pressure and cardiac output and restore fluid balance.
A. The initial stage of shock in (option A) is incorrect because it is characterized by inadequate tissue perfusion and the activation of various compensatory mechanisms, including the release of stress hormones. However, the renin-angiotensin system is not specifically mentioned as activated in this stage.
B. The progressive stage of shock in (option B) is incorrect because it occurs when compensatory mechanisms fail to maintain adequate perfusion, leading to worsening hypoperfusion and organ dysfunction. The renin-angiotensin system continues to be activated during this stage, but it is primarily associated with the compensatory stage.
C. The refractory stage of shock in (option C) is incorrect because it is the stage of severe and prolonged hypoperfusion, where organ failure becomes irreversible. The renin-angiotensin system may still be activated, but it is not the primary focus of this stage.
Therefore, the activation of the renin-angiotensin system occurs during the compensatory stage of shock.
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