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GEN PATH > RBC DISORDER 3 > Flashcards

RBC DISORDER 3 Flashcards

1
Q

Diseases in Normocytic Normochromic RBC

A
  • Acute Blood Loss

- Hemolytic Anemia

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2
Q
  • LOW MCV
  • Low MCH
  • low MCHC
  • found in Iron Deficiency Anemia and Thalassemias
A

Microcytic Hypochromic

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3
Q
  • high MCV
  • high or normal MCH
  • normal MCHC
  • Found in megalosblastic anemia
A

Macrocytic Normochromic

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4
Q
  • low MCV
  • low MCH
  • normal MCHC
  • found in anemia of chronic inflammation
A

Microcytic Normochromic

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5
Q
  • defect in spectrin, ankyrin, protein 4.2
  • defect spectrin α and β chain, protein4.1
  • Spectrin deficiency
A

Hereditary Spherocytosis- defect in spectrin, ankyrin, protein 4.2
Hereditary Elliptocytosis-defect spectrin α and β chain, protein4.1
Hereditary Poikilocytosis- Spectrin deficiency

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6
Q
  1. CBC- red cell mass hematocrit
  2. Bone marrow
    • Normoblastic hyperplasia
  3. Peripheral blood smear
    • Normocytic and normochromic
    • Reticulocytes- usually after 7 days
    • Polychromatophilia
    • macrocytes
  4. Serum
    • increased Erythropoietin
A

Acute Blood Loss

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7
Q

»Anemia =
»Neutropenia = < 500 cells/cumm
»Thrombocytopenia = < 20,000/cumm
» Reticulocyte count = < 1 %

A

APLASTIC ANEMIA: Pancytopenia

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8
Q 
Bone Marrow
– hypocellular
– “dry tap”
– Iron stores decreased
• Serum iron concentration increased 
• LAP score increased
• Very high plasma and urine erythropoietin
• Normal RDW
A

Aplastic Anemia

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9
Q
  • Pancytopenia becomes obvious after infancy and usually significant by eight year
  • increased levels of fetal hemoglobin (HB F) and i Antigen
  • Congenital anomalies present:
    Hyperpigmentation. malformations of extremities
    Short stature microcephaly
    Hypogonadism malformations of other organs
    Heart and kidneys
A

Fanconi Anemia

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10
Q
  • Congenital red cell aplasia
  • 1 year to 6 year old
  • Laboratory:
    1. Severe normocytic and normochromic anemia (Sometimes slightly macrocytic)
    2. WBC – normal or slightly decreased
    3. Bone marrow – Red cell aplasia
    – Normal granulocytic and megakaryocytic cell line
    4. Hemoglobin F increased (5 to 25%)
    5. Increased red cell adenosine deaminase (ADA)
A

Diamond-Blackfan Anemia

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11
Q
  • low serum iron
  • high TIBC
  • low % sat
  • low ferritin
  • low bone marrow iron
A

Iron deficiency anemia

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12
Q
  • low serum iron
  • normal or TIBC
  • normal or low % sat
  • normal or high ferritin
  • normal or high bone marrow iron
A

Anemia of hronic Disease

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13
Q
  • high serum iron
  • low TIBC
  • high % sat
  • high ferritin
  • high bone marrow iron
A

Sideroblastic anemia

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14
Q
  • normal or low serum iron
  • normal or high TIBC
  • normal or high % sat
  • nromal or high ferritin
  • normal or high bone marrow iron
A

Thalassemia

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15
Q
  • Group of disorders characterized by iron loading and its accumulation in the mitochondria in the erythroid precursors due to a defect in heme synthesis
  • May occur as a result of decreased activity of the enzyme ALA synthetase
A

Sideroblastic Anemia

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16
Q

Sideroblastic Anemia Classification

  • Clinical Picture: X –linked recessive trait; Males
  • Iron Parameters: Marked increased in serum Iron; Increased transferrin% sat
  • Red Cells: Severe anemia: Normocytic, normpchromic or Microcytic, hypochromic
  • WBCs & Platelets: Normal count and morphology
  • BOne Marrow: Marked increased Iron;10 – 40% Ringed sideroblasts
A

Hereditary

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17
Q

Sideroblastic Anemia Classification

  • Clinical Picture: More common; Adults > 50yo
  • Red Cells: Moderate anemia; normocytic to slightly microcytic
  • WBCs & Platelets: Normal count and morphology
  • BOne Marrow: Increased ringed sideroblasts
A

Primary Idiopathic

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18
Q

Sideroblastic Anemia Classification

  • Clinical Picture: In association with other diseases
A

Secondary

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19
Q
  • accumulation of iron in the macrophages, with less parenchymal injury
  • accumulation of iron in the parenchymal cells, with tissue injury
A
  • Hemosiderosis

- Hemochromatosis

20
Q
  • Rare autosomal recessive trait; caused by certain variants in the HFE gene
  • In middle aged men
  • Laboratory:
  • Iron derangement:
  • Increased serum iron
  • Slightly decreased transferring
  • Increased transferring saturation
  • Hemoglobin, Hematocrit and peripheral smear are normal
  • Bone marrow:
  • Macrophages with stainable iron particles
  • Absorption of iron is increased
A

Hereditary Hemochromatosis

21
Q 
• Impaired DNA synthesis
• Types
  1. Vitamin B12 deficiency
     * Pernicious Anemia
     * Imerslund’s Syndrome
  2. Folic acid deficiency
A

MEGALOBLASTIC ANEMIA

22
Q

Mechanisms:
I. Inadequate Intake
- Extremely rare
- Seen in persons who completely abstain from animal food, milk and eggs.
2. Defective Production of Intrinsic factor
- Most common cause
- PERNICIOUS ANEMIA

A

Cobalamin (Vitamin B12) Deficiency

23
Q
  1. Pathological lesions of the fundus and body of the stomach
    • gastric mucosal atrophy
    • selective loss of parietal and chief cells from the gastric mucosa
    • submucosal lymphocytic infiltrates.
  2. Autoantibodies are directed against the a- & b-subunit of the gastric H+/K+-
    ATPase, a hydrogen transporting enzyme, responsible for the acidification of the stomach lumen.
  3. Gastrectomy
A

Pernicious Anemia

24
Q

Pernicious Anemia

Clinical Features:

A
  • Equally common in males and females
  • Symptoms: Pallor, Jaundice, Glossitis
  • Gastrointestinal - diarrhea, constipation and episodic pain
  • Central nervous system - pains, numbness peripheral neuropathies, irritability etc.
25
Q
  • Inherited autosomal recessive trait
  • Mainfest during the first 2 years of life
  • Deficiency inreceptor site in the terminal ileum.
A

Imerslund’s Syndrome

26
Q

Other Causes of Vitamin B12 Deficiency
- affects the terminal ileum
- lodges in the ileum
• Zollinger Ellison syndrome

A 
Other Causes of Vitamin B12 Deficiency
• Crohn’s Disease
- affects the terminal ileum
• Diphyllobotrium latum infection
- lodges in the ileum
• Zollinger Ellison syndrome
- hypersecretion of gastric juice, results to low pH with 
interference in the binding og VitB12 to the intrinsic factor
27
Q 
– CBC- anemia, usually macrocytic and normochromic
– Indices
* MCV and RDW high
* MCH – Normal to high
* MCHC - Normal
A

Pancytopenia

28
Q

Therapeutic trial

  • Give parenteral physiologic dose of ____(10 ug/d) physiologic dose of ___ (50 to 200 ug/d)
  • Optimal hematologic response means deficiency
    i. ___ - Reticulocytosis starting 3rd and 4th day peaks on the 7th day
    ii. ___ - Erythropoiesis becomes normoblastic by 2 days
    • Leukopoiesis becomes normal by 12 to 14 days
    • WBC and platelet counts become normal in a week
A
  • cobalamin
  • folic acid
  • PBS
  • BM
29
Q
  • Measures ability of the marrow cells in vitro to utilize deoxyuridine for DNA synthesis
  • Sensitive, produces abnormal result before anemia or macrocytosis is observed
A

Deoxyuridine suppression test

30
Q

Folic acid coenzymes required for the conversion of FIGLU to glutamic acid in the
catabolism of histidine
- If oral histidine, FIGLU will appear in increased amount in urine

A

Urinary formiminoglutamic acid

31
Q

Red Blood Cell Destruction

  • Takes place in the reticulo-endothelial system - Liver, bone marrow, lymph nodes and circulating monocytes. Account for 90% of red cell destruction
  • Destruction of severely damaged blood cells normally occurs intravascularly. Account for 10% of RBC destruction
A
  • Extravascular

- Intravascular

32
Q

Those anemia which result from premature and excessive destruction of red cells either within the blood vessels or outside it.

A

Hemolytic Anemia

33
Q 
Classification of Hemolytic Anemia
ACUTE VS CHRONIC
- Rapid onset
- Isolated, episodic or paroxysmic
- Hemolysis either disappears or subsides between episodes
- Examples
    > Paroxysmal cold hemoglobinuria
    > Paroxysmal nocturnal hemoglobinuria
    > Hemolytic Transfusion reaction
A

Acute

34
Q 
Classification of Hemolytic Anemia
ACUTE VS CHRONIC
- RBC life span is chronically shortened
- Categories:
1. Bone Marrow maybe able to compensate -> anemia may not be evident.
2. Bone Marrow cannot generate RBC fast enough -> anemia
- Examples
    > Thalassemia
    > Hemoglobinopathies
    > Glucose 6-Phosphate Dehydrogenase
A

Chronic

35
Q 
Classification of Hemolytic Anemia
INHERITED VS ACQUIRED
- Develop in individuals who were previously hematologically normal but acquired condition that lyses RBCs
- Examples
    > Infectious disease (Malaria)
    > PNH
A

ACQUIRED

36
Q 
Classification of Hemolytic Anemia
INHERITED VS ACQUIRED
- Passed of to offspring by mutant genes from parents
- Examples
    > Thalassemias
    > Hemoglobinopathies
A

INHERITED

37
Q 
Classification of Hemolytic Anemia
EXTRINSIC (Extracorpuscular) vs INTRINSIC (Intracorposcular)
- Develop in individuals who were previously hematologically normal but acquired condition that lyses RBCs
1. Membrane defect
    > Hereditary Spherocytosis 
    > Hereditary Elliptocytosis
    > Hereditary Poikilocytosis
2. Enzyme deficiency
    > Glucsoe-6-Phosphate Dehydrogenase (Hexose Monophosphate Shunt)
    > Pyruvate Kinase (Embden Myerhof)
3. Globin Abnormalities 
    > Hemoglobinopathies -
4. Acquired Membrane Abnormality 
    > PNH
A

EXTRINSIC (Extracorpuscular)

38
Q 
Classification of Hemolytic Anemia
EXTRINSIC (Extracorpuscular) vs INTRINSIC (Intracorposcular)
- Conditions that arise from outside the RBCs 
- substances in the plasma
ex. Infectious agents – Malarial, sepsis
      Chemical agents – Toxins & Drugs
      Circulating antibodies
- conditions affecting the anatomy of the vascular system
ex. Mechanical 
   - Microangiopathic 
   - Traumatic uremic syndrome
   - Prosthetic valves
Physical agents - Burns
Blood loss
A

EXTRINSIC (Extracorpuscular)

39
Q

Classification of Hemolytic Anemia
EXTRAVASCULAR VS INTRAVASCULAR
- RBCs are engulfed by the macrophage and lyzed by their digestive system

A

EXTRAVASCULAR

40
Q 
Classification of Hemolytic Anemia
EXTRAVASCULAR VS INTRAVASCULAR
- Destruction of severely damaged blood cell occurs in the blood stream 
and can Lyze by fragmentation in the spleen and bone marrow
1. Inherited:
    > Membrane abnormalities
    > Enzyme deficiencies
    > Globin abnormalities
2. Acquired Membrane 
    > Abnormality – PNH
A

INTRAVASCULAR

41
Q
  • acquired clonal stem cell disorder
    -characterized by production of abnormal erythrocytes, granulocytes and megakaryocytes
    -Red cell defect render them more susceptible to complement-mediated chronic intravascular hemolysis
  • Bout of hemolysis could be initiated by
    > Infection
    > surgery
    > Whole blood transfusion
    > injection of contrast dyes
    > severe exercise
A

Paroxysmal Nocturnal Hemoglobinuria (Marchiafava-Micheli Syndrome)

42
Q 
Paroxysmal Nocturnal Hemoglobinuria (Marchiafava-Micheli Syndrome)
Laboratory:
- hemoglobinuria
- Hemosidinuria 
- Blood: Pancytopenia 
    > Normocytic anemia
    > Neutropenia (3/5ths of cases)
    > Thrombocytopenia (2/3rds of cases)
A
  • With or without
  • always present
  • is common
43
Q

Detects deficiencies in the pentose phosphate pathway: Glucose-6-Phosphate
Dehydrogenase deficiency
> Glutathione reductase
> Glutathione peroxidase

A

Ascorbate Cyanide Screening Test

44
Q

• Result from RBC destruction due to RBC autoantibodies: Ig G, M,
E, A
• Most commonly-idiopathic
• Classification
– Warm Autoimmune haemolysis:Ab binds at 37degree Celsius
– Cold Autoimmune haemolysis: Ab binds at 4 degree Celsius

A

Autoimmune Hemolytic Anemia

45
Q
  • Usually IgG
  • Idiopathic
  • Secondary causes
  • SLE, CLL,lymphomas,Drugs(e.g.Methyldopa)

INVESTIGATION
– Hemolysis, MCV
– P Smear: Microspherocytosis, n-RBC
– Confirmation: Coomb’s Test / Antiglobulin test

A

Warm Autoimmune hemolysis

46
Q

• Usually IgM
• Infections
Mycoplasm pneumonia,infectiousmononucleosis lymphoma
proxysmal cold haemoglobinuria

INVESTIGATION
• Periphral Smear:
- Microspherocytosis
- Ig M with specificity to I or I Ag

A

Cold Autoimmune Hemolysis

47
Q
  • Induced by red cell antigens
  • Haemolytic transfusion reactions
  • haemolytic disease of the new born
  • post stem cell grafts
  • Drug induced
  • Drug-red cell membrane complex
  • immune complex
A

Alloimmune

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