Nokea
Non thrombocytopenic purpura is seen in all except:
- A. vasculitis
- B. uraemia
- C. hereditary haemorrhagic telangiectasia
- D. SLE
Correct Answer: D
Rationale: The correct answer is D: SLE. Non-thrombocytopenic purpura refers to purpura without low platelet count. In SLE, thrombocytopenia is common, leading to purpura. A: Vasculitis can cause non-thrombocytopenic purpura due to vessel inflammation. B: Uraemia can lead to non-thrombocytopenic purpura due to vascular damage. C: Hereditary haemorrhagic telangiectasia presents with telangiectasias and recurrent epistaxis, not purpura.
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Which of the following is a cause of secondary neutropaenia in adults?
- A. Congenital
- B. Anti-hypertensive drugs
- C. Part of general pancytopaenia
- D. Familial
Correct Answer: C
Rationale: The correct answer is C: Part of general pancytopenia. Secondary neutropenia in adults can occur as part of general pancytopenia, where there is a decrease in all blood cell types. This can be caused by various conditions such as infections, medications, autoimmune disorders, and bone marrow disorders.
Rationale:
A: Congenital is incorrect because congenital neutropenia refers to a condition present at birth, not secondary neutropenia.
B: Anti-hypertensive drugs may cause drug-induced neutropenia, but it is not the primary cause of secondary neutropenia in adults.
D: Familial neutropenia is a genetic disorder that runs in families and is not a common cause of secondary neutropenia in adults.
A patient receiving blood begins complaining of severe chest pain and a feeling of warmth. What should the nurse do first?
- A. Call the physician.
- B. Administer diuretics as ordered.
- C. Discontinue the blood transfusion.
- D. Assess vital signs and cardiovascular status.
Correct Answer: C
Rationale: The correct first action is to discontinue the blood transfusion (Choice C). This is because the patient's symptoms of severe chest pain and warmth suggest a possible transfusion reaction, which can be life-threatening. By stopping the transfusion, the nurse can prevent further harm to the patient. Calling the physician (Choice A) can be done after stopping the transfusion. Administering diuretics (Choice B) without knowing the cause of symptoms can exacerbate the situation. Assessing vital signs and cardiovascular status (Choice D) is important but should come after stopping the transfusion to prioritize patient safety.
A 4-year-old girl with a history of relapsed pre-B-cell acute lymphoblastic leukemia is being admitted for unrelated donor bone marrow transplantation with cyclophosphamide and total body irradiation conditioning. Pretransplant workup shows the following: Recipient: CMV IgG: negative, CMV IgM: negative, HSV I/II antibody: negative, Varicella IgG: positive (vaccinated), Hepatitis B surface antigen: negative, Hepatitis B surface antibody: positive (vaccinated), Hepatitis B core antibody: negative, Hepatitis C antibody: negative. Donor: CMV IgG: negative, CMV IgM: negative, HSV I/II antibody: positive, Varicella IgG: positive, Hepatitis B surface antigen: negative, Hepatitis B core antibody: negative, Hepatitis C antibody: negative. How should the patient be managed during the admission with respect to infection prophylaxis?
- A. Acyclovir IV for herpes simplex virus (HSV) suppression
- B. Weekly screening by polymerase chain reaction (PCR) for cytomegalovirus (CMV) in blood
- C. Antifungal prophylaxis
- D. Valganciclovir PO for CMV suppression
Correct Answer: C
Rationale: The correct answer is C: Antifungal prophylaxis. This patient is at high risk for fungal infections post-bone marrow transplantation due to the conditioning regimen with cyclophosphamide and total body irradiation. CMV and HSV prophylaxis are not indicated as the patient and donor are negative for CMV IgG and IgM and the donor is positive for HSV antibodies. Weekly CMV PCR screening is not necessary in the absence of CMV seropositivity. Valganciclovir for CMV suppression is also not required in this case. Fungal prophylaxis is essential to prevent invasive fungal infections in high-risk patients like this 4-year-old with leukemia.
A patient is presented with fever, vomiting, hypotension and facial edema after his business trip back from Africa. Viral hemorrhagic fever is suspected in this patient. Which of the following family does the suspected virus belong to?
- A. Filovirus
- B. Togavirus
- C. Adenovirus
- D. Bunyavirus
Correct Answer: A
Rationale: The correct answer is A: Filovirus. Viral hemorrhagic fevers are caused by viruses within the Filovirus family, which includes Ebola and Marburg viruses. Symptoms such as fever, vomiting, hypotension, and facial edema are characteristic of these infections. Togavirus (choice B) does not typically cause hemorrhagic fevers. Adenovirus (choice C) and Bunyavirus (choice D) are not commonly associated with viral hemorrhagic fevers. Therefore, the suspected virus in this patient most likely belongs to the Filovirus family.
A newborn infant develops jaundice on day of life 2. Labs are drawn, and she has a hemoglobin of 7.4 g/dL with a reticulocyte count of 8%. Upon peripheral blood smear review, she is found to have bizarre red cell forms with significant polkilocytosis. Although her parents have normal blood counts, on review of their peripheral blood smears, they both have a moderate number of ovalocytes. Which of the following is the most likely cause of the infant's red cell findings?
- A. She has an autosomal dominant ankyrin mutation from one of her parents causing hereditary spherocytosis.
- B. She has inherited band 3 variants from each parent and will likely need a splenectomy after she turns 5 years old.
- C. She has inherited an alpha-spectrin mutation from both of her parents and may experience an improvement in her anemia over time.
- D. She has inherited a PKLR variant from each parent, and enzyme testing will be consistent with her diagnosis of pyruvate kinase deficiency.
Correct Answer: C
Rationale: The correct answer is C because the infant's red cell findings of ovalocytes and polikilocytosis are consistent with hereditary elliptocytosis, which is caused by mutations in genes encoding spectrin. In this scenario, the inheritance pattern aligns with the infant receiving an alpha-spectrin mutation from both parents, leading to the observed erythrocyte abnormalities. This condition may improve over time due to compensatory mechanisms.
Choice A (autosomal dominant ankyrin mutation causing hereditary spherocytosis) is incorrect because the clinical presentation and red cell morphology do not support a diagnosis of hereditary spherocytosis.
Choice B (inherited band 3 variants and need for splenectomy) is incorrect as the infant's condition does not match the characteristics of hereditary spherocytosis requiring splenectomy.
Choice D (PKLR variant and pyruvate kinase deficiency) is incorrect as the infant's red cell morphology is not indicative