12: Hematopoeisis Conditions Flashcards

1
Q

Most common nutritional disorder in the world

A

Iron deficiency anemia

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2
Q

S/S iron deficiency anemia

A

Fatigue, weakness, HA, dizziness, pale skin, arrhythmias, SOA, CP, cold hands and feet

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3
Q

Five steps in lab evaluation of anemia

A
  1. CBC and reticulocyte index
  2. Categorize as microcytic, macrocytic, or normocytic based on MCV
  3. Examine peripheral smear
  4. Examine serum Fe, Fe-binding capacity, serum ferritin levels
  5. Erythrocytes size-distribution width
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4
Q

What happens in peripheral blood + BM in anemia s caused by RBC loss/hemolysis?

A

Blood: elevated reticulocytes
BM: erythroid hyperplasia

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5
Q

Two things that can cause nucleated RBCs to be found in peripheral blood

A
  1. Compensatory erythropoeisis (due to severe anemia or chronic hypoxemia)
  2. Hypsplenism (due to sickle cell, traumatic splenectomy, etc.)
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6
Q

Extramedullary hematopoeisis can occur in response to these four things

A
  1. Severe chronic anemia, thallasemia, or sickle cell
  2. SC failure
  3. Infection
  4. Malignant transformation and replacement of BM in bone
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7
Q

What is acute neutrophilia with left shift associated with?

A

Acute bacterial infection

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8
Q

Left shift

A

Increased immature leukocytes

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9
Q

Toxic granulation

A

Dark coarse granules in neutrophils often seen with left shift

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10
Q

Leukemoid reaction

A

WBC count of >50,000 with increased neutrophils without leukemia

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11
Q

What can cause leukemoid reaction?

A

Infection, drugs, carcinomas

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12
Q

Three phases of CML

A
  1. Chronic phase
  2. Accelerated phase: 10-19% blasts in blood/BM
  3. Blast phase: >20% blasts in blood/BM
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13
Q

Causes of eosinophilic vs basophilic leukocytosis vs monocytosis

A
  1. Eosinophilic leukocytosis: allergies, parasites
  2. Basophilic leukocytosis: rare but can be seen in leukemia
  3. Monocytosis: atypical bacterial infections, autoimmune dz
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14
Q

Five overview steps of primary hemostasis

A
  1. Primary plug formation to seal vasculature
  2. Platelets bind GP1B to vWF on collagen
  3. Platelets change shape -> release ADP and thromboxane A2
  4. ADP and TXA2 cause additional platelet activation
  5. Fibrinogen binds GPIIB-IIIA receptor -> aggregation
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