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D&T - E1 > Anemia Lecture > Flashcards

Anemia Lecture Flashcards

1
Q

Acute anemia increase in RBC production

A

3x within 7-10 days

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2
Q

Chronic anemia increase in RBC production

A

6x - 8x

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3
Q

Average adult blood volume

A

5 L total = 3 L plasma + 2 L blood cells

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4
Q

Hb

A

Hemoglobin concentration (g/L)

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5
Q

Hematocrit

A

Packed red cell volume (%)

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6
Q

MCV

A
  • Mean corpuscular volume

- Average size of a RBC

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7
Q

MCH

A
  • Mean corpuscular hemoglobin
  • Average amount/mass of Hb in a RBC
  • = Hb/RBC count
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8
Q

RDW

A
  • Red cell distribution width

- Coefficient of variation of RBC volume, variation in cell size

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9
Q

MCHC

A
  • Mean corpuscular hemoglobin concentration

- Proportion of each red cell taken up by Hb (%)

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10
Q

Microcytic anemia

A

Decreased MCV, MCH, MCHC

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11
Q

Normocytic anemia

A

Normal MCV, MCH, MCHC

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12
Q

Macrocytic anemia

A
  • Increased MCV

- Variable MCH and MCHC

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13
Q

Transferrin saturation

A

TRF = Concentration Fe / TIBC

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14
Q

Megaloblastic anemia and folate

A

Folate treatment partially corrects B12 deficiency but does NOT affect neurologic defecits

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15
Q

Production deficit anemias include

A
  • Aplastic anemia

- Pure red cell aplasia → Diamond - Blackfan syndrome

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16
Q

Aplastic anemia

A

Acquired causes:

  • Viral infections: hepatitis, EBV, HIV, parvovirus
  • MOST COMMON CAUSES: autoimmune suppression by a T cell mediated mechanism

Hereditary causes - FANCONI’S ANEMIA:

  • AR
  • Defects in DNA REPAIR MECHANISM = chromosomal instability
  • Congenital anomalies (hypoplastic radii, thumbs and organs)
  • May be pre-malignant: evolves into myelodysplasia, AML, CML
17
Q

Pure red cell aplasia

A
  • Autoimmune disease mediated by T lymphocytes of IgG antibody VS red cell precursors
  • Associated with: SLE, CLL, lymphomas, THYMOMAS
  • Diamond-Blackfan syndrome
  • Drugs: phenytoin, azathioprine, isoniazid
18
Q

Sideroblastic anemia - nutritional deficiency

A

Pyridoxine (B6) and copper

19
Q

Hemolytic anemia

A

ACUTE SYMPTOMS: fatigue, fever, pallor, jaundice, LOW BACK PAIN, splenomegaly, CONGESTIVE HEART FAILURE

CHRONIC SYMPTOMS: acute + gallstones, abnormal bone growth, fractures

LAB FINDINGS:

  • ↑ unconjugated bilirubin
  • ↓ serum haptoglobin concentration (which take up free Hb)
  • ↑ serum LDH (RBC enzyme release
  • Reticulocytosis

INTRAVASCULAR HEMOLYSIS:
- Free hemoglobin released → haptoglobin released: excessive free Hb = hemoglobinuria and hemoglobinsiderinuria; EXPECT ↓ SERUM HAPTOGLOBIN CONCENTRATION

20
Q

Beta thalassemia VS Iron deficiency anemia

A
  • Iron therapy improves iron deficiency anemia, worsens beta thalassemia
  • Increased or normal serum iron and bone marrow iron in thalassemia
21
Q

Hereditary spherocytosis treatment

A

Treat with FOLIC acid supplements or SPLENECTOMY

22
Q

G6PD deficiency smears between attacks

A

Between attacks peripheral smears are normal

23
Q

WAHA and disease

A

WAHA may antedate the onset of disease by months or years

24
Q

CAD causes

A

ACUTE: associated with atypical pneumonia (against big I) and infectious mononucleosis (against little i)

CHRONIC: due to lymphoid malignancy or idiopathic, may be unremitting

25
Q

Paroxysmal cold hemoglobinuria

A
  • IgG autoantibody (Donath-Landsteiner Ab) = biphasic hemolysis
  • AT LOW TEMPS binds to cells without causing hemolysis
  • WARMING binds complement → intravascular hemolysis, hemoglobinuria
  • No jaundice or splenomegaly

Test for Donath-Landsteiner Ab → differentiates PCH from CAD

  • Mix patients serum (with antibody) with test RBCs
  • First chill them then warm them to 38C
  • Lysis of RBCs indicates PCH
26
Q

Test for hemolytic transfusion reaction

A

Coombs test

27
Q

Microangiopathic hemolytic anemias

A

Due to abrnomalities in microcirculation → fibrin deposition and vessel narrowing

  • DIC
  • HUS
  • Thrombotic-thrombocytopenia purpura (TTP)
  • Preeclampsia, HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets)
28
Q

Paroxysal nocturnal hemoglobinuria

A
  • CD59 (MIRL, membrane inhibitor of reactive lysis) and CD55 (DAF) need GPI membrane
  • Can evolve into: aplastic anemia, myelodysplasia, AML
  • TREATMENT: iron supplement, prednisone, BM transplant
29
Q

Mechanical and physical factors that cause nonimmune hemolytic anemia

A
  • Prosthetic heart valces
  • BURN INJURY: microspherocytes, barbell shapes, rod shapes
  • MARCH HEMOGLOBINURIA: marching, marathon running, drum beating; hemoglobinuria after exercise; normal peripheral blood smear; anemia is rare in these individuals

D&T - E1 (11 decks)

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