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Peds Final > Peds Hematology -Junkins > Flashcards

Peds Hematology -Junkins Flashcards

1
Q

What will the Serum Iron, TIBC, Ferritin, % transferrin saturation, RDW and MCV look like for iron deficiency anemia?

A
  • Serum iron: dec
  • TIBC: inc
  • Ferritin: dec
  • % transferrin saturation: dec
  • RDW: inc
  • MCV: dec
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2
Q

What will the Serum Iron, TIBC, Ferritin, % transferrin saturation, and MCV look like for Anemia of chronic disease?

A
  • Serum iron: dec
  • TIBC: dec
  • Ferritin: Nl–> inc
  • % transferrin saturation: dec
  • MCV: Nl–> dec
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3
Q

What will the Serum Iron, TIBC, Ferritin, and % transferrin saturation look like for Hemolytic anemia?

A
  • Serum iron: inc
  • TIBC: Nl–> dec
  • Ferritin: inc
  • % transferrin saturation: inc
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4
Q

What will the Serum Iron, TIBC, Ferritin, % transferrin saturation, RDW and MCV look like for Sideroblastic anemia ?

A
  • Serum iron: Nl -> inc
  • TIBC: Nl–> inc
  • Ferritin: Inc
  • % transferrin saturation: Inc
  • RDW: Inc
  • MCV: Dec
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5
Q

A 12 month old infant is brought in by his mother for irritability and shortness of breath. He drinks > 30 oz of cow’s milk per day. PMHx The patient was born at 27 weeks EGA
PE is remarkable for fussiness, conjunctival pallor, and tachypnea
Lab: A hct = 17
Peripheral Blood Smear: Microcytic, hypochromic anemia
What’s the most likely diagnosis for this child?

A

Iron deficiency anemia

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6
Q 
A patient presents to the ER with head trauma. An x-ray of the skull reveals no fracture, but the skull appears to have a "crew cut" appearance. Which of the following conditions could result in this finding?
A. microangiopathic hemolytic anemia
B. hereditary spherocytosis
C. β-thalassemia
D. sickle cell anemia
E. iron deficiency
A

C. β-thalassemia

(due to extramedullary hematopoiesis)

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7
Q

A child is brought to the pediatrician because her parents are concerned about lead poisoning. A CBC reveals anemia. How does lead poisoning cause anemia?

(a) Disrupts heme synthesis by causing decreased iron absorption from the gut
(b) Disrupts heme synthesis by increasing the activity of aminolevulinate dehydratase
(c) Disrupts heme synthesis by inhibiting ferrochelatase
(d) Disrupts hemoglobin function by binding to hemoglobin with high affinity, preventing oxygen binding
(e) Disrupts RBC DNA synthesis, causing megaloblastic changes in RBCs

A

(c) Disrupts heme synthesis by inhibiting ferrochelatase (–> dec heme synthesis, inc RBC protoporphyrin)

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8
Q

What are Burton lines? What is this associated with?

A

Bluish lines on the gingiva

associated with Lead poisoning (late finding)

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9
Q

What is the management for BLL > 45? BLL>70?

A
  • BLL > 45 mcg/dL Succimer
  • BLL >70 mcg/dL calcium-disodium EDTA can be added
  • First dose always is succimer, followed 4 hours later by EDTA, because EDTA when given alone can worsen lead encephalopathy
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10
Q

What are the signs and symptoms of lead poisoning? What is the mnemonic?

A

LEADS

  • Lead lines on gingival (burton lines)
  • Encephalopathy and Erythrocyte basophilic stippling
  • Abdominal colic and sideroblastic Anemia
  • Drops –> wrist and foot. Dinercaprol and EDTA and 1st line reatment
  • Succimer for chelation in kids
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11
Q

What is Fanconi anemia?

A
  • Ages 2 to 10 years
  • Thrombocytopenia, leukopenia, pancytopenia, fatigue, spontaneous bruising, mucosal bleeding, fever and rigors
  • Other features: short stature, STRUCTURAL ABNORMALITIES OF THE LIMBS, eyes and ears, hyperpigmentation, café au lait spots, purpura or petechiae
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12
Q

What should be suspected if a black 2 year old male presents with hemolysis after eating fave beans?

A

G6PD deficiency

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13
Q 
A 9-year-old African-American boy is brought to the ED with sudden onset of chest pain and dyspnea. Last year, the patient was diagnoses with multiple radiopaque stones. There is a history of a “blood problem” that runs in the family. 
PE: Tachycardia and hypoxemia
CXR: Bilateral patchy infiltrates
Which of the following peripheral blood smear findings is most consistent with his clinical condition?
A. Heinz bodies
B. Howell-jolly bodies
C. Microcytes
D. Ringed sideroblasts
E. Spherocytes
A

B. Howell-jolly bodies

this is sickle cell disease

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14
Q

What is the defect in Sickle cell anemia? What does this cause?

A
  • change in codon 6 in the beta-globulin gene (replaces glutamic acid with valine)
  • Dehydration, hypoxemia and acidosis make the hemoglobin molecules glom into ropelike cables
  • Howell Jolly bodies
  • Target cells
  • RBC sickling causes microvascular occlusions and tissue ischemia
  • increased susceptibility to infection by encapsulated bacteria (prophylactic PCN up to 5 yo)
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15
Q

Which labs will be altered in VonWillebrand disease?

A

Bleeding time and PTT

platelet dysfunction and lack of factor VIII carrier

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16
Q

Which labs will be altered in Bernard-Soulier disease? What is the mechanism?

A

Bleeding time

defect in platelet adhesion due to decreased expression of glycoprotein Ib

17
Q

Which labs will be altered in Glanzmann thrombocytopenia? What is the mechanism?

A

bleeding time

platelets don’t have glycoprotein IIb/IIIa receptor that binds to fibrinogen

18
Q

Which labs will be altered in Hemophilia A? What is the mechanism?

A

increased PTT

19
Q

Which labs will be altered in vitamin K deficiency? What is the mechanism?

A

increased PT and PTT (can be normal)

impairs II, VII, IX, and X

20
Q

Which labs will be altered in VonWillebrand disease? What is the inheritance of this?

A

Bleeding time and PTT

platelet dysfunction and lack of factor VIII carrier

autosomal dominant –> present with easy bleeding and dental procedures that wouldn’t stop bleeding

21
Q

Which labs will be altered in Glanzmann thrombocytopenia? What is the mechanism?

A

bleeding time

platelets don’t have glycoprotein IIb/IIIa receptor that binds to fibrinogen

autosomal recessive

22
Q

Which labs will be altered in Hemophilia A? What is the mechanism?

A

increased PTT

X-linked

can present with bleeding into tissues and joints

23
Q

What is the treatment for Von Willebrand disease?

A

DDAVP

Peds Final (21 decks)

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