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monster
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rocket
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thief
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What will the lab findings be for a patient with vWF disease and why: Bleeding time, PT, aPTT
Bleeding time- prolonged (impaired platelet plug formation; PT: normal (extrinsic fine); aPTT: prolonged (reduced VII->impaired intrinsic)
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thief
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fairy
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fairy
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thief
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trap
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rocket
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gift
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baam
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10
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why do we treat sickle cell disease with Hydroxyurea?
increases fetal hemoglobin to retard gelation and sickling of RBCs
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10
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Describe the pathophysiology of FH
Elevated LDL at birth due to lack of LDL clearance from plasma (absent/disorder LDL receptors)
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Describe the general appearance of cutaneous melanoma with the ABCDE criteria
A: Assymetrical; B: blurry border; C: more than 1 color; D: diameter>6mm; E: evolution of mole sudden change in shape/size/color
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Why is there an increase in serum lactate acid in infants with Von Gierk's disease
glucose-6-phosphate is also the substrate for glycolysis and produces lactate
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heart
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seesaw
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rocket
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lifesaver
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What is the pathophysiology of hereditary spherocytosis?
Primary membrane defect (akryin gene-> spectrin protein)-> membrane loss-> spherocyte forms-> splenic trap->erythrostasis = phagocytosis extravascular hemolysis
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Describe typical characteristics of a peripheral blood smear in a CML patient
leukocytosis, thrombocytosis, myleocytes, neutrophils
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Rationalize the vital signs in a child with Sickle Cell disease: Fever + Tachypnea + Tachycardia + Pain + Hypotensive
Fever (chest infection) + Tachypnea (RR, low o2 stat); Tachycardia (HR, low o2 stat) + Pain (bone infarction) + hypotensive (hypovolemia, pulmonary edema)
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Explain the main 3 factors in the pathophysiology behind Normocytic Anemia (where does TTP, HS, SCD fit within a factor)
1. Defects in RBC environment (TTP); 2. Defects in RBC membrane (HS); 3. Defects in RBC internal contents (SCD)
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Pertinent physical exam findings in progeria
alopecia, prominent scalp pain, skin discoloration, reduced subcutaneous adipose tissue, abnormal dentition, beaked nose,
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Discuss the role of specific mutations in cell signaling genes in the development of cutaneous melanoma: BRAF, RAS, C-KIT
BRAF-V600E mutation=proliferation; RAS-cell cycle kinetics (proliferative/survival); C-KIT-tyrosine kinase receptor=growth factor bind site-turn on cascade
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What are foamy macrophages and their role in FH?
Lipoproteins sequestered -> pro inflammatory -> phagocytes -> cholesterol -> foamy = LDL filled macrophage
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