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  #1  
Old 06-19-2011
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Neuro Headache and a Skull radiograph case

Case 1
A 73-year-old man presents to the physician with a 1-year history of progressively worse headaches. A skull radiograph is shown. What is the most likely diagnosis?

Headache and a Skull radiograph case-skull.jpg

Answer Choices

A. Hairy-cell leukemia
B. Multiple myeloma
C. Paget disease
D. Scurvy
E. Thalassemia

Last edited by USMLE-Syndrome; 06-19-2011 at 01:27 PM.
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mmm .. i think it`s Paget disease
right
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crew cut appearance of skull is typical of thalassemia.
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in the first case my option is c paget..i think...

about the 2nd case i dont know...there are findings in the righ arm too,left, skull. metastasis?,paget? mri or psa i can t tell...
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Old 06-19-2011
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Answer E. Thalassemia
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Default E

Thalassemia - my vote
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thalassemia - hair on end appearance from the extramedullary hemopoesis in the diploic layer....
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Old 06-20-2011
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Paget disease.
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Paget disease ("cotton wool" appearance due to the disruption of normal bone architecture)

I don't think any qs will require us to diagnose thalassmia in a 73 year old
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pagets
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i would go wid Paget s disease....
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Option C (Paget disease) is correct. This radiograph demonstrates a thickened cortex and patchy new bone formation, giving a cotton wool appearance to the image. This type of radiograph is highly suggestive of Paget disease, which is a disease of abnormal bone resorption. Other classic radiographic findings include thickening of the iliopectineal line and prominent bony trabeculae.

Option A (Hairy-cell leukemia) is incorrect. Hairy-cell leukemia is so named because of the characteristic hairy cell appearance on light microscopy of affected B cells. The cells appear hairy as a result of cytoplasmic projections. There is no radiographic characteristic appearance.

Option B (Multiple myeloma) is incorrect. Multiple myeloma presents with multiple, well circumscribed lytic lesions in the skull.

Option D (Scurvy) is incorrect. Scurvy can present with crew-cut or hair-on-end skull radiographs where it appears as though a short haircut can be visualized on radiograph. However, there is no sclerosis as is evident on this radiograph.

Option E (Thalassemia) is incorrect. Beta-thalassemia can present with crew-cut or hair-on-end skull radiographs where it appears as though a short haircut can be visualized on radiograph. However, there is no sclerosis as is evident on this radiograph.

High-yield Hit 1
5. What are the three phases of Paget's disease of bone?
Paget's disease progresses through three distinct phases. The initial phase is the osteolytic phase where osteoclastic bone resorption predominates. About 1-2% of patients exhibit this purely lytic phase. The osteolytic phase evolves into one marked by both osteoclastic and osteoblastic overactivity. This mixed phase is followed by a less active period of bone remodeling and marked sclerosis. In the final phase, excessive osteoblastic bone deposition predominates. Most patients who come to medical attention will be in this final phase.

From Endocrine Secrets 4E by McDermott
High-yield Hit 2
6. Describe the radiographic findings during the osteolytic phase of the disease.
The characteristic radiographic finding found in patients in the initial osteolytic phase of Paget's disease of bone is an advancing wedge-shaped resorption front at either end of the long tubular bones. In the skull, this phase is manifested by large circumscribed osteolytic lesions (termed osteoporosis circumscripta).

From Endocrine Secrets 4E by McDermott
High-yield Hit 3
7. What are the radiographic findings most commonly found in the osteoblastic phase of the disease?
Evolution of osteolytic lesions into the osteoblastic phase may require years or even decades, during which the affected bone may become sclerotic and enlarged and demonstrate bowing deformities, incomplete transverse fractures (pseudofractures), and even complete fractures. When the skull is involved in the osteoblastic phase, thickening of the calvarium and a patchy increase in bone density may give the skull a "cotton-wool" appearance. In this sclerotic phase, the sclerotic bone changes may be so extensive that they may be confused with metastatic disease. Both metastatic cancer and Paget's disease are common in the elderly and may coexist in the same patient. Thus, the clinician caring for patients with Paget's disease must be alert for evidence of metastatic disease to bone.
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Quote:
Originally Posted by ibmsyd View Post
Paget disease ("cotton wool" appearance due to the disruption of normal bone architecture)

I don't think any qs will require us to diagnose thalassmia in a 73 year old
Yes well done! Patient's age counts!

And headache-will thalassemia present with headache? I don't think so.
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Old 06-21-2011
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Thanks MissP... good question - is this from Consult or Rx? Age is very imp...
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Quote:
Originally Posted by ashishkabir View Post
Thanks MissP... good question - is this from Consult or Rx? Age is very imp...
u welcome
from usmleconsult q bank
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Default thalassemia case xray

A 44-year-old woman presents to the clinic for followup of her fractured jaw that she sustained in a motor vehicle accident. The radiographer accidentally takes a lateral image of the superior skull instead. The results of the radiograph are shown. What finding would be most likely to be detected on laboratory investigation?
http://usmlesteps123.examweb.com/ass.../Sxt0281f1.jpg

Answer Choices
A. Elevated monoclonal spike
B. Hypercalcemia
C. Positive Ham test
D. Reduced hemoglobin A1 (HbA1)
E. Reduced serum ferritin
Explanation
Option D (Reduced hemoglobin A1 [HbA1]) is correct. The X-ray demonstrates a classic hair-on-end appearance that is consistent with thalassemia. Therefore, reduced hemoglobin A1 (2 alpha, 2 beta globin chains) would be expected on hemoglobin electrophoresis. The hair-on-end appearance is the result of overactivity of the marrow in the skull in response to the anemia.

Option A (Elevated monoclonal spike) is incorrect. An elevated monoclonal spike would be expected in multiple myeloma where the skull X-ray shows multiple punched-out lesions.

Option B (Hypercalcemia) is incorrect. Hypercalcemia can be seen in multiple myeloma. There is no particular reason to suspect it in this case.

Option C (Positive Ham test) is incorrect. A positive Ham test is diagnostic for the rare hemolytic condition, paroxysmal nocturnal hemoglobinuria.

Option E (Reduced serum ferritin) is incorrect. Reduced serum ferritin is seen in iron-deficiency anemia.

High-yield Hit 1
β-Thalassemia.
Over 100 mutations have been described that lead to β-thalassemia, in which mutations decrease or eliminate expression from the β globin locus. The decreased expression of β globin can be caused by structural mutations in the coding region of the gene, resulting in nonsense mutations, truncated mRNA, and no expression of intact globin from the affected allele (β0-thalassemia). However, a large number of mutations that result in decreased transcription or translation or altered splicing of the β globin mRNA may result in reduction, but not elimination, of globin chain expression from the affected allele (β+-thalassemia).

From Cecil Essentials of Medicine 6E by Andreoli et al
High-yield Hit 2
Defective globin chain synthesis in β-thalassemia causes both decreased normal Hb production and the production of a relative excess of α chains. The decrease in normal Hb synthesis results in a hypochromic anemia, and the excess α chains form insoluble α chain tetramers and cause hemolysis. In mild thalassemic syndromes, the excess α chains are insufficient to cause significant hemolysis, and the primary presenting finding is a microcytic anemia. In severe forms of thalassemia, hemolysis occurs both in the periphery and in the marrow, with intense secondary expansion of the marrow production of red cells. The expansion of the marrow space causes severe skeletal abnormalities, and the ineffective erythropoiesis also provides a powerful stimulus to iron absorption.

From Cecil Essentials of Medicine 6E by Andreoli et al
High-yield Hit 3
The clinical spectrum of β-thalassemia reflects the heterogeneity of the molecular lesions causing the disease (Table 48-7). β-Thalassemia major results from homozygous β0-thalassemia, leading to severe hemolytic anemia; such patients are diagnosed in infancy and are transfusion dependent from birth. β-Thalassemia intermedia patients also have two β-thalassemia alleles, but at least one of them is a mild β+ mutation. These patients have severe chronic hemolytic anemia, but do not require transfusions. Because of ineffective erythropoiesis, these patients chronically hyperabsorb iron, and may develop iron overload in the absence of transfusions. β-Thalassemia minor is usually due to heterozygous β-thalassemia, although it may reflect the inheritance of two mild thalassemic mutations. These are the patients in whom iron deficiency is often misdiagnosed. Iron studies will show normal to increased iron with a normal iron saturation. Diagnosis can be confirmed by documenting a compensatory increase in HbA2 and HbF.
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