HEMA LEC - Anemia Flashcards
1
Q
defined as a decrease in erythrocytes and hemoglobin, resulting in decreased oxygen delivery to the tissues.They can also be classified based on etiology/cause.
A
Anemia
2
Q
defined as a decrease in erythrocytes and hemoglobin, resulting in decreased oxygen delivery to the tissues.They can also be classified based on etiology/cause.
A
Anemia
3
Q
The anemias can be classified morphologically using
A
RBC indices (MCV, MCH, and MCHC).
4
Q
Anemia is suspected when the hemoglobin is [male and female]
A
5
Q
RBC mass is normal, but plasma volume is increased.
Secondary to an unrelated condition and can be transient in nature.
Reticulocyte count normal; normocytic/normochromic anemia.
A
Relative (pseudo) anemia
6
Q
Causes include conditions that result in hemodilution, such as pregnancy and volume overload.
A
Relative (pseudo) anemia
7
Q
causes of relative pseudo anemia include conditions ___
A
conditions which result in hemodilution
8
Q
RBC mass is decreased, but plasma volume is normal.
A
Absolute anemia
9
Q
indicative of a true decrease in erythrocytes and hemoglobin.
A
Absolute anemia
10
Q
mechanisms involved in absolute anema
A
Decreased delivery of red cells into circulation
Increased loss of red cells from the circulation
11
Q
a. Most common form of anemia in the United States
A
Iron-deficiency anemia
12
Q
Prevalent in infants and children, pregnancy, excessive menstrual flow, elderly with poor diets, malabsorption syndromes, chronic blood loss (GI blood loss, hookworm infection)
A
Iron-deficiency anemia
13
Q
Laboratory: Microcytic/hypochromic anemia; serum iron, ferritin, hemoglobin/hematocrit, RBC indices, and reticulocyte count low; RDW and total iron-binding capacity (TIBC) high; smear shows ovalocytes/ pencil forms.
A
Iron-deficiency anemia
14
Q
Clinical Symptoms: Fatigue, dizziness, pica, stomatisis (cracks in the corners of the mouth), glossitis (sore tongue), and koilonychias (spooning of the nails).
A
Iron-deficiency anemia
15
Q
Due to an inability to use available iron for hemoglobin production.
A
ACD
Anemia of Chronic Disease
16
Q
b. Impaired release of storage iron associated with increased hepcidin levels
A
ACD
Anemia of Chronic Disease
17
Q
is a liver hormone and a positive acute-phase reactant. It
A
Hepcidin
18
Q
plays a major role in body iron regulation by influencing intestinal iron absorption and release of storage iron from macrophages.
A
Hepcidin
19
Q
Inflammation and infection cause hepcidin levels to ___; this decreases release of iron from stores.
A
increase
20
Q
Laboratory: Normocytic/normochromic anemia, or slightly microcytic/hypochromic anemia; increased ESR; normal to increased ferritin; low serum iron and TIBC
a. Associated with persistent infections, chronic inflammatory disorders (SLE, rheumatoid arthritis, Hodgkin lymphoma, cancer)
A
ACD
21
Q
second only to iron deficiency as a common cause of anemia
A
ACD
22
Q
Caused by blocks in the protoporphyrin pathway resulting in defective hemoglobin synthesis and iron overload
A
Sideroblastic anemia
23
Q
Excess iron accumulates in the mitochondrial region of the immature erythrocyte in the bone marrow and encircles the nucleus; cells are called ringed sideroblasts.
A
Sideroblastic anemia
24
Q
Excess iron accumulates in the mitochondrial region of the mature erythrocyte in circulation; cells are called siderocytes; inclusions are siderotic granules (Pappenheimer bodies on Wright’s stained smears)
A
Sideroblastic anemia
25
Siderocytes are best demonstrated using ___
Perl’s Prussian blue stain.
26
Laboratory: Microcytic/hypochromic anemia with increased ferritin and serum iron; TIBC is decreased
Sideroblastic anemia
27
Two Types of sideroblastic anemia:
1. ) Primary – irreversible; cause of the blocks unknown
a. ) Two RBC populations (dimorphic) are seen.
b. ) This is one of the myelodysplastic syndromes – refractory anemia with ringed sideroblasts (RARS)
2. ) Secondary – reversible; causes include alcohol, anti-tuberculosis drugs, chloramphenicol
PRIMARY
| SECONDARY
28
type of sideroblastic anemia
| irreversible; cause of the blocks unknown
Primary
29
This is one of the myelodysplastic syndromes – refractory anemia with ringed sideroblasts (RARS)
primary sideroblastic anemia
30
Two RBC populations (dimorphic) are seen. [type of sideroblastic anemia
primary sideroblastic anemia
31
reversible; causes include alcohol, anti-tuberculosis drugs, chloramphenicol
secondary sideroblastic anemia
32
Multiple blocks in the protoporphyrin pathway affect heme synthesis.
Lead poisoning
33
Seen mostly in children exposed to lead-based paint
Lead poisoning
34
Clinical Symptoms: Abdominal pain, muscle weakness, and a gum lead line that forms from blue/black deposits of lead sulfate
Lead poisoning
35
Laboratory: Normocytic/ normochromic anemia with characteristic coarse basophilic stippling
Lead poisoning
36
These are a group of inherited disorders characterized by a block in the protoporphyrin pathway of heme synthesis. Heme precursors before the block accumulate in the tissues, and large amounts are excreted in urine and/ or feces.
Porphyrias
37
Clinical Symptoms: Photosensitivity, abdominal pain, CNS disorders
Porphyrias
38
Defective DNA Synthesis causes abnormal nuclear maturation; RNA synthesis is normal, so the cytoplasm is not affected. The nucleus matures slower than the cytoplasm (asynchronism). Megaloblastic maturation is see n
Megaloblastic anemias
39
Caused by either a vitamin B12 or folic acid deficiency.
Megaloblastic anemias
40
Laboratory: Pancytopenia, macrocytic/normochromic anemia with oval macrocytes and teardrops, hypersegmented neutrophils; inclusions include Howell-Jolly bodies, nucleated RBCs, basophilic stippling, Pappenheimer bodies and Cabot rings; elevated LD, bilirubin, and iron levels due to destruction of fragile, megaloblastic cells in the blood and bone narrow
Megaloblastic anemias
41
2.) Other causes of ___ deficiency include malabsorption syndromes, Diphyllobothrium latum tapeworm, total gastrectomy, intestinal blind loops, and a total vegetarian diet.
Vitamin B12 deficiency (cobalamin)
42
secreted by parietal cells and is needed to bind vitamin B12 for absorption into the intestine.
INTRINSIC FACTOR
43
Prevalent in older adults of English, Irish and Scandinavian descent
Pernicious anemia–
44
Caused by deficiency of intrinsic factor, antibodies to intrinsic factor, or antibodies to parietal cells
Pernicious anemia–
45
Characterized by achlorhydria and atrophy of gastric parietal cells
Pernicious anemia–
46
Clinical Symptoms: Jaundice, weakness, sore tongue (glossitis), and gastrointestinal (GI) disorder, numbness and other CNS problems
Vit B12 deficiency
47
takes 3-6 years to develop because of high body stores.
Vitamin B12 deficiency
48
causes a megaloblastic anemia with a blood picture and clinical symptoms similar to vitamin B12deficiency, except there is no CNS involvement.
folic acid deficiency
49
associated with poor diet, pregnancy, or chemotherapeutic anti-folic acid drugs such as methotrexate.
folic acid deficiency
50
low body stores
folic acid
51
anti-folic acid drugs
methotrexate
52
include alcoholism, liver disease, and conditions that cause accelerated erythropoiesis.
Non-megaloblastic macrocytic anemias
53
The erythrocrytes are round, not oval as is seen in the megaloblastic anemias
Non-megaloblastic macrocytic anemias
54
Bone marrow failure causes pancytopenia
Aplastic Anemia
55
Laboratory: Decrease in hemoglobin/ haematocrit and reticulocytes; normocytic/normochromic anemia; no response to erythropoietin
Aplastic Anemia
56
most commonly affects people around the age of 50 and above. It can occur in children.
Aplastic Anemia
57
Patients have poor prognosis with complications that include bleeding.
Treatment includes bone marrow or stem cell transplant and immunosuppression.
Aplastic Anemia
58
Can be genetic, acquired or idiopathic.
aplastic anemia
59
a. ) Autosomal recessive trait
| b. ) Dwarfism, renal disease, mental retardation
Genetic aplastic anemia (Fanconi anemia)
60
antibiotics that cause AA
Chloramphenicol and sulphonamides
61
Chemicals that cause AAA
Benzene and herbicides
62
About 30% of acquired aplastic anemias are due to
drug exposure
63
viruses that cause AAA
B19 parvovirus secondary to be hepatitis, measles, CMV, and Epstein-Barr Virus
64
50-70% of aplastic anemias are
idiopathic
65
1. ) True red cell aplasia (leukocytes and platelets normal in number)
2. ) Autosomal inheritance
Diamond-Blackfan anemia
66
Hypoproliferative anemia caused by replacement of bone marrow hematopoietic cells by malignant cells or fibrotic tissue
Myelophthisic (marrow replacement) anemia
67
c. Laboratory: Normocytic/normochromic anemia; leukoerythroblastic blood picture.
Myelophthisic (marrow replacement) anemia
68
b. Associated with cancers (breast, prostate, lung, melanoma) with bone metastasis
Myelophthisic (marrow replacement) anemia
69
The anemias can be classified morphologically using
RBC indices (MCV, MCH, and MCHC).
70
Anemia is suspected when the hemoglobin is [male and female]
71
RBC mass is normal, but plasma volume is increased.
Secondary to an unrelated condition and can be transient in nature.
Reticulocyte count normal; normocytic/normochromic anemia.
Relative (pseudo) anemia
72
Causes include conditions that result in hemodilution, such as pregnancy and volume overload.
Relative (pseudo) anemia
73
causes of relative pseudo anemia include conditions ___
conditions which result in hemodilution
74
RBC mass is decreased, but plasma volume is normal.
Absolute anemia
75
indicative of a true decrease in erythrocytes and hemoglobin.
Absolute anemia
76
mechanisms involved in absolute anema
Decreased delivery of red cells into circulation
| Increased loss of red cells from the circulation
77
a. Most common form of anemia in the United States
Iron-deficiency anemia
78
Prevalent in infants and children, pregnancy, excessive menstrual flow, elderly with poor diets, malabsorption syndromes, chronic blood loss (GI blood loss, hookworm infection)
Iron-deficiency anemia
79
Laboratory: Microcytic/hypochromic anemia; serum iron, ferritin, hemoglobin/hematocrit, RBC indices, and reticulocyte count low; RDW and total iron-binding capacity (TIBC) high; smear shows ovalocytes/ pencil forms.
Iron-deficiency anemia
80
Clinical Symptoms: Fatigue, dizziness, pica, stomatisis (cracks in the corners of the mouth), glossitis (sore tongue), and koilonychias (spooning of the nails).
Iron-deficiency anemia
81
Due to an inability to use available iron for hemoglobin production.
ACD
| Anemia of Chronic Disease
82
b. Impaired release of storage iron associated with increased hepcidin levels
ACD
| Anemia of Chronic Disease
83
is a liver hormone and a positive acute-phase reactant. It
Hepcidin
84
plays a major role in body iron regulation by influencing intestinal iron absorption and release of storage iron from macrophages.
Hepcidin
85
Inflammation and infection cause hepcidin levels to ___; this decreases release of iron from stores.
increase
86
Laboratory: Normocytic/normochromic anemia, or slightly microcytic/hypochromic anemia; increased ESR; normal to increased ferritin; low serum iron and TIBC
a. Associated with persistent infections, chronic inflammatory disorders (SLE, rheumatoid arthritis, Hodgkin lymphoma, cancer)
ACD
87
second only to iron deficiency as a common cause of anemia
ACD
88
Caused by blocks in the protoporphyrin pathway resulting in defective hemoglobin synthesis and iron overload
Sideroblastic anemia
89
Excess iron accumulates in the mitochondrial region of the immature erythrocyte in the bone marrow and encircles the nucleus; cells are called ringed sideroblasts.
Sideroblastic anemia
90
Excess iron accumulates in the mitochondrial region of the mature erythrocyte in circulation; cells are called siderocytes; inclusions are siderotic granules (Pappenheimer bodies on Wright’s stained smears)
Sideroblastic anemia
91
Siderocytes are best demonstrated using ___
Perl’s Prussian blue stain.
92
Laboratory: Microcytic/hypochromic anemia with increased ferritin and serum iron; TIBC is decreased
Sideroblastic anemia
93
Two Types of sideroblastic anemia:
1. ) Primary – irreversible; cause of the blocks unknown
a. ) Two RBC populations (dimorphic) are seen.
b. ) This is one of the myelodysplastic syndromes – refractory anemia with ringed sideroblasts (RARS)
2. ) Secondary – reversible; causes include alcohol, anti-tuberculosis drugs, chloramphenicol
PRIMARY
| SECONDARY
94
type of sideroblastic anemia
| irreversible; cause of the blocks unknown
Primary
95
This is one of the myelodysplastic syndromes – refractory anemia with ringed sideroblasts (RARS)
primary sideroblastic anemia
96
Two RBC populations (dimorphic) are seen. [type of sideroblastic anemia
primary sideroblastic anemia
97
reversible; causes include alcohol, anti-tuberculosis drugs, chloramphenicol
secondary sideroblastic anemia
98
Multiple blocks in the protoporphyrin pathway affect heme synthesis.
Lead poisoning
99
Seen mostly in children exposed to lead-based paint
Lead poisoning
100
Clinical Symptoms: Abdominal pain, muscle weakness, and a gum lead line that forms from blue/black deposits of lead sulfate
Lead poisoning
101
Laboratory: Normocytic/ normochromic anemia with characteristic coarse basophilic stippling
Lead poisoning
102
These are a group of inherited disorders characterized by a block in the protoporphyrin pathway of heme synthesis. Heme precursors before the block accumulate in the tissues, and large amounts are excreted in urine and/ or feces.
Porphyrias
103
Clinical Symptoms: Photosensitivity, abdominal pain, CNS disorders
Porphyrias
104
Defective DNA Synthesis causes abnormal nuclear maturation; RNA synthesis is normal, so the cytoplasm is not affected. The nucleus matures slower than the cytoplasm (asynchronism). Megaloblastic maturation is see n
Megaloblastic anemias
105
Caused by either a vitamin B12 or folic acid deficiency.
Megaloblastic anemias
106
Laboratory: Pancytopenia, macrocytic/normochromic anemia with oval macrocytes and teardrops, hypersegmented neutrophils; inclusions include Howell-Jolly bodies, nucleated RBCs, basophilic stippling, Pappenheimer bodies and Cabot rings; elevated LD, bilirubin, and iron levels due to destruction of fragile, megaloblastic cells in the blood and bone narrow
Megaloblastic anemias
107
2.) Other causes of ___ deficiency include malabsorption syndromes, Diphyllobothrium latum tapeworm, total gastrectomy, intestinal blind loops, and a total vegetarian diet.
Vitamin B12 deficiency (cobalamin)
108
secreted by parietal cells and is needed to bind vitamin B12 for absorption into the intestine.
INTRINSIC FACTOR
109
Prevalent in older adults of English, Irish and Scandinavian descent
Pernicious anemia–
110
Caused by deficiency of intrinsic factor, antibodies to intrinsic factor, or antibodies to parietal cells
Pernicious anemia–
111
Characterized by achlorhydria and atrophy of gastric parietal cells
Pernicious anemia–
112
Clinical Symptoms: Jaundice, weakness, sore tongue (glossitis), and gastrointestinal (GI) disorder, numbness and other CNS problems
Vit B12 deficiency
113
takes 3-6 years to develop because of high body stores.
Vitamin B12 deficiency
114
causes a megaloblastic anemia with a blood picture and clinical symptoms similar to vitamin B12deficiency, except there is no CNS involvement.
folic acid deficiency
115
associated with poor diet, pregnancy, or chemotherapeutic anti-folic acid drugs such as methotrexate.
folic acid deficiency
116
low body stores
folic acid
117
anti-folic acid drugs
methotrexate
118
include alcoholism, liver disease, and conditions that cause accelerated erythropoiesis.
Non-megaloblastic macrocytic anemias
119
The erythrocrytes are round, not oval as is seen in the megaloblastic anemias
Non-megaloblastic macrocytic anemias
120
Bone marrow failure causes pancytopenia
Aplastic Anemia
121
Laboratory: Decrease in hemoglobin/ haematocrit and reticulocytes; normocytic/normochromic anemia; no response to erythropoietin
Aplastic Anemia
122
most commonly affects people around the age of 50 and above. It can occur in children.
Aplastic Anemia
123
Patients have poor prognosis with complications that include bleeding.
Treatment includes bone marrow or stem cell transplant and immunosuppression.
Aplastic Anemia
124
Can be genetic, acquired or idiopathic.
aplastic anemia
125
a. ) Autosomal recessive trait
| b. ) Dwarfism, renal disease, mental retardation
Genetic aplastic anemia (Fanconi anemia)
126
antibiotics that cause AA
Chloramphenicol and sulphonamides
127
Chemicals that cause AAA
Benzene and herbicides
128
About 30% of acquired aplastic anemias are due to
drug exposure
129
viruses that cause AAA
B19 parvovirus secondary to be hepatitis, measles, CMV, and Epstein-Barr Virus
130
50-70% of aplastic anemias are
idiopathic
131
1. ) True red cell aplasia (leukocytes and platelets normal in number)
2. ) Autosomal inheritance
Diamond-Blackfan anemia
132
Hypoproliferative anemia caused by replacement of bone marrow hematopoietic cells by malignant cells or fibrotic tissue
Myelophthisic (marrow replacement) anemia
133
c. Laboratory: Normocytic/normochromic anemia; leukoerythroblastic blood picture.
Myelophthisic (marrow replacement) anemia
134
b. Associated with cancers (breast, prostate, lung, melanoma) with bone metastasis
Myelophthisic (marrow replacement) anemia
