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Hematology > Anemia2 > Flashcards

Anemia2 Flashcards

1
Q

ANEMIA OF ABNORMAL NUCLEAR DEVELOPMENT 5

A 
CONGENITAL DYSERYTHROPOIETIC ANEMIAS
MEGALOBLASTIC ANEMIAS
PERNICIOUS ANEMIA
FOLATE DEFICIENCY ANEMIA
CONGENITAL DYSERYTHROPOIETIC ANEMIAS
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2
Q

ANEMIA OF ABNORMAL IRON METABOLISM

A

IRON DEFICIENCY ANEMIA

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3
Q

ANEMIA OF CHRONIC DISEASES

A

SIDEROBLASTIC ANEMIAS

LEAD INTOXICATION

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4
Q

are a group of disorders in which cell maturation in the bone marrow is abnormal as a result of abnormal development of the nuclei.

A

anemias of abnormal nuclear development

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5
Q

MEGALOBLASTIC ANEMIA

Less common causes include:

A

Defects of DNA synthesis

Drug induced disorders of DNA synthesis

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6
Q

anemias of abnormal nuclear development are characteristically classified as 4

A

MACROCYTIC, NORMO to HYPERCHROMIC,
abnormal leukocytes (hypersegmented neutrophils),
erythrocytes (macrovalocytes), and
platelets (giant platelets)

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7
Q

abnormalities in erythrocytic cell precursors but are INHERITED and NOT ASSOCIATED with leukocyte and platelet disorders.

A

CONGENITAL DYSERYTHROPOIETIC ANEMIAS

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8
Q

Have a corrin ring (a ring composed of 4 pyrrole rings similar to hemoglobin) that contains cobalt

A

VITAMIN B12 CYANOCOBALAMIN

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9
Q

Coenzyme forms of B12
– represents 75% of cobalamin in the plasma
– represents 75% of cobalamin in the liver , rbcs, and the kidneys

A

Adenosylcobalamin

Methylcobalamin

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10
Q

Represents a family of compounds derived from folic acid (pteroylglutamic acid)

A

FOLATE

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11
Q

Participates in carbon transfers and is required in three reactions that lead to DNA synthesis : 2 for purine and 1 for pyrimidine synthesis

A

FOLATE

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12
Q

Folate is necessary for efficient _ synthesis and production of _.

A

thymidilate

DNA

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13
Q

is the most important transcobalamin is a b-globulin synthesized in the liver and transports B12 to the liver, tissues and some in the bone marrow; it is needed in the transport of B12 across membranes

A

TC II

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14
Q

are present in gastric fluid, plasma, amniotic fluid, milk, saliva, and granulocytes; called R (rapid) proteins or R-binders , since they migrate faster than intrinsic factor on zone electrophoresis

A

TC I and III

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15
Q

binds most of the B12 in plasma and this is not transported in the marrow; believed to be secreted by granulocytes

A

TCI

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16
Q

Deficiency in TC II causes _; TC I and III deficiencies are apparently harmless

A

megaloblastic anemias

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17
Q

Derived from green leafy vegetables, liver, kidney, and whole grain cereals, , yeast, and fruits(especially oranges)

A

FOLIC ACID

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18
Q

Folate uptake in rbcs require _ as a cofactor!

A

Vit B12

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19
Q

_ and _ are integral components in DNA synthesis

A

Vitamin B12 and Folate

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20
Q

MEGALOBLASTIC ANEMIAS

PATHOPHYSIOLOGY:

A

Vitamin B12 deficiency

“mehylfolate trap” hypothesis

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21
Q

When B12 is deficient, _ cannot be converted to methionine and folate

A

homocysteine

22
Q

. THE __ PROVIDES A SENSITIVE TEST FOR B12 DEFICIENCY THAT IS NOT AFFECTED BY FOLIC ACID DEFICIENCY.

A

methylmalonic acid MMA LEVEL

23
Q

MEGALOBLASTIC ANEMIA PERIPHERAL BLOOD FINDINGS

```
anemia
MCV
MCH
MCHC
WBC
+
RDW
~~~

A

Mild to moderate anemia
MCV increased
MCH is increased
MCHC is normal
WBC count is normal but declines
(+) Macroovalocytesn with little or no central pallor
Anisocytosis common [increased random distribution width (RDW)]

24
Q

is associated with Vitamin B12 deficiency that results from an acquired atrophy of the stomach lining

A

Pernicious anemia or PA

25
Q

Vitamin B12 deficiency is associated with _; Folate deficiencies DO NOT exhibit these findings.

A

NEUROLOGIC DEFICIENCIES

26
Q

OTHER CAUSES OF ACQUIRED VITAMIN B12 DEFICIENCY 7

A
  • Dietary deficiency
  • Castle’s Intrinsic Factor Deficiency
  • Intrinsic Factor Molecular Defect
  • Small Bowel Bacterial Overgrowth
  • Fish Tapeworm disease (Diphyllobothriasis)
  • Ileal Disease
  • Drugs ( neomycin and ethanol)
27
Q

A rare hereditary disorder that causes B12 malabsorption
Affects homozygous children in the first 2 years of life
Autosomal recessive inheritance
Vitamin cannot be absorbed with or without IF
Gastric secretion is normal

A

HEREDITARY VITAMIN B12 DEFICIENCY

IMMERSLUND SYNDROME

28
Q

Usually same with Vit B12 deficiency

No neurologic findings

Other causes:

Dietary deficiency
Alcoholic cirrhosis
Pregnancy
Infant malnutrition
Folate antagonists

(pyrimethamine [antimalarial] and

methotrexate [chemotherapeutic drug])

A

FOLATE DEFICIENCY ANEMIA

29
Q

affects the ENTIRE small intestine and causes both B12 and folate deficiency; appears to be caused by infectious agents and responds to folate therapy and antibiotics

A

TROPICAL SPRUE

30
Q

Usually affects the PROXIMAL small intestine
Two forms:
– seen in childhood
– seen in adults

A

GLUTEN SENSITIVE ENTEROPATHY–

Celiac Disease
Non-tropical Sprue

31
Q

– a rare hereditary autosomal recessive disorder of pyrimidine metabolism resulting in abnormal DNA synthesis, excessive urinary excretion of orotic acid, and megaloblastic anemia

A

OROTIC ACIDURIA

32
Q

– Is a rare X-linked disorder of purine metabolism caused by the lack of the enzyme xanthine-guanine phosphoribosyl transferase.

A

LESCH-NYHAN SYNDROME

33
Q

Characterized by refractory anemia that varies in severity, and abnormalities in rbc bone marrow precursors, including nuclear abnormalities, multinuclearity and other bizarre changes

WBC AND Platelets ARE NOT AFFECTED

A

CONGENITAL DYSERYTHROPOIETIC ANEMIAS

34
Q

Causes neonatal jaundice but patients have a normal lifespan; Bone marrow shows binucleated cells; Autosomal recessive

A

Type I CDA

35
Q

– Referred to as hereditary erythroblast multinuclearity; Most common of the three; positive HEMPAS antigen which makes these cells resistant to the sugar water test to screen PNH; Autosomal recessive

A

Type II CDA

36
Q

– characterized by pronounced multinuclearity (up to 12 nuclei per cell) – called gigantoblasts; Autosomal dominant

A

Type III cda

37
Q

___ are negative to acidified serum test; only _ is positive to this test!

A

CDA Type I and III

Type II

38
Q

ANEMIA OF ABNORMAL IRON METABOLISM
Three general etiologic mechanisms appear to be involved:
Deficiency in raw material
Defective release in of stored iron from macrophages
Defective utilization of iron within the erythroblasts

A

(iron deficiency anemia)
(anemia of chronic disorders)
(sideroblastic anemia and anemia of lead intoxication)

39
Q

– reflects the body tissue iron stores and thus a good indicator of iron storage status; first laboratory test to become abnormal; decreased ONLY IN IRON DEFICIENCY ANEMIA

Reference range:
Men:_
Women:_

A

SERUM FERRITIN
15-200ug/L
12-150ug/L

40
Q

CHEMICAL LABORATORY TESTS USEFUL IN DIFFERENTIATING DISORDERS OF IRON DEFICIENCY

A
  • -FREE ERYTHROCYTE PROTOPORPHYRIN
  • -TOTAL IRON BINDING CAPACITY (TIBC)
  • -TRANSFERRIN SATURATION
  • -SERUM IRON
41
Q

PICA

A

IRON DEFICIENCY ANEMIA

42
Q

IRON DEFICIENCY ANEMIA 6

cracks in the corners of the mouth
(soreness of the tongue)
(flattening and spooning of the nails)

A

Physical Findings:

Angular stomatitis  
Glossitis  
Gastritis
Koilonychia
Splenomegaly – rare
Neuropathies – not present
43
Q

Decreased Hgb, Hct and RBC]

Decreased Indices

Microcytic, hypochromic

Elevated RDW

Variable platelet count

WBC and Reticulocyte count normal

A

IRON DEFICIENCY ANEMIA

(+) marrow sideroblasts

44
Q

Are a diverse group identified by a common feature of abnormal iron kinetics that produces excess accumulation of iron, which is deposited in the mitochondria of normoblasts

A

SIDEROBLASTIC ANEMIAS

45
Q

Three types of Sideroblasts:
Type I – iron in the form of ferritin aggregates and at least _aggregates can be identified in approximately 50% of normoblasts
Type II – contains _ aggregates
Type III – __; shows larger granules situated in a ring or collar around the nucleus of a normoblast; are representatives of iron-laden mitochondria

A

4
6
pathologic ringed sideroblast

46
Q

For a diagnosis of Sideroblastic anemia, at least _ of normoblasts must be __ ringed sideroblasts.

A

15%

Type III

47
Q

CLASSIFICATION AND CAUSES OF SIDEROBLASTIC ANEMIA

HEREDITARY (rare)

ACQUIRED (common)
Primary (idiopathic)
Secondary

A

HEREDITARY (rare)
–ALA synthase deficiency

ACQUIRED (common)
Primary (idiopathic)
--Acute myeloid leukemia
--Myelodysplastic syndromes
--Myeloma
  • -Alcoholism
  • -Lead poisoning
  • -Chloramphenicol
    • Drugs used in the treatment of tuberculosis
48
Q

Lead poisoning causes increased levels of _ and normal _ _.

THIS CONFORMATION DISTINGUISH LEAD POISONING FROM ACUTE INTERMITTENT PORPHYRIA in which BOTH d-ALA and PBG are elevated.

A

d-ALA

porphobilinogen levels

49
Q

Injury to red cell membrane, possibly by inhibiting ATPase

Defects in a and b globin chain synthesis

A

LEAD INTOXICATION

50
Q

LEAD INTOX
Free erythrocyte protoporphyrin is _ in erythrocytes to A MUCH GREATER EXTENT than in iron deficiency.

Urinary ALA is _ and PBG is __. Urinary coproporphyrins are also __

A

increased

elevated
normal
increased

Hematology (5 decks)

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