3.3a RBC: Anemia Flashcards
0
Q
Intravascular anemia
A
G6PD
PNHH
1
Q
What do you look for when you diagnose anemia? (Lab and PE)
A
Levels of hemoglobin and hematocrit
Pallor
2
Q
Megaloblastic anemia is a deficiency in what?
A
B12 and folic acid
3
Q
What is the only substance that will cause neurological effects?
A
Methlymalonic acid
4
Q
Does WBC contain DNA (nucleus)?
A
Yes!
5
Q
Expected reticulocyte in anemia
A
Increased because the body’s response (BM) is to proliferate more red cells
6
Q
Site of hematopoiesis (blood development) (3)
A
- Yolk sac
- Liver
- Bone marrow
7
Q
What is the sole source of all blood cells and lymphocyte precursors?
A
Bone marrow
8
Q
It maintains the red marrow and is the most hematopoeitically active
A
Central bones
9
Q
What is the normal adult hemoglobin?
A
HbA (alpha2, beta2)
10
Q
Which type of hemoglobin is significant in diabetic patients?
A
HbA1c
11
Q
Which type of hemoglobin is 2% in normal adults and is increased in smokers?
A
HbA2
12
Q
- It is the major fetal hemoglobin for 3-9 months and at birth
- Has increased oxygen transport from the placenta
A
HbF
13
Q
Type of hemoglobin that have the tendency to keep oxygen and not release it (2)
A
- HbH
2. Barts
14
Q
What is the main stem cell from which both myeloid and lymphoid cells originate?
A
Pluripotent stem cells
15
Q
It is the source of erythrocytes, platelets, macrophages, basophiles, eosinophiles, neutrophils
A
Myeloid progenitors
16
Q
It is the source of T-cells, B-cells, NK cells
A
Lymphoid progenitors
17
Q
What regulates the marrow response to short-term physiologic needs?
A
Hemapoietic growth factors
18
Q
What do hematopoietic growth factors stimulate?
A
Committed progenitor cells (colony forming unit)
19
Q
It is the largest and the youngest of all cells with prominent nucleoli
A
Pronormoblast
20
Q
When the nucleoli is abolished, it is no longer called a pronormoblast. What is it called?
A
Reticulocyte
21
Q
What are the first committed progenitor cells of RBCs?
A
Pronormoblasts
22
Q
- These are the first red cells seen in peripheral blood smear
- They are also known as polychromatic erythrocytes
A
Reticulocyte
23
Q
All nucleated red cells are termed as?
A
Normoblast
24
Changes seen when a red cell matures (3)
1. Smaller
2. Nucleus is lost
3. Cytoplasm becomes red
25
What stimulates the production of mature erythrocytes?
Erythropoietin
26
How long does it take to produce mature erythrocytes from pronormoblasts?
5 days
27
It is defined as the reduction below normal limits of total circulatinf RBCs --> decreased oxygen transport --> hypoxia
Anemia
28
T/F: Anemia is about the mineral, vitamins, or proteins that blood carries with it.
False. Anemia is about the capability of hemoglobin to carry oxygen
29
The ff are PE findings of which disease?
1. Pallor
2. Dizziness, headache
3. Angina
4. Anemic/Hemic murmur
5. Oliguria, Anuria
6. Koilonychias, brittle nails
Anemia
30
Laboratory diagnosis of anemia is based on? (2)
1. Hematocrit
| 2. Hemoglobin concentration
31
It is the ratio of packed red cell:total blood volume
Hematocrit
32
Laboratory tests used for anemia (6)
1. Hemoglobing
2. Hematocrit
3. Reticulocyte count
4. PBS
5. RBC distribution width
6. Red Cell Indices
33
This lab test is a measure of bone marrow activity
Reticulocyte count
(Should be high in anemia because the BM must actively compensate. If it is low, there may be a more serious problem like aplastic anemia)
34
This lab test indicates the morphology of anemia
PBS
1. Size
2. Color
4. RBS Distribution Width
35
Central pallor of the RBC should be how big?
1/3 of the diameter
36
It is the coefficient of variation of red cell volume (variability of RBC size and shape)
RBC Distribution Width
37
Mean Cell Volume indicates what?
Size
38
Mean Cell Hemoglobin Concentration indcates what?
Color
39
What do you call the average content (mass) of hemoglobin per red cell?
Mean Cell Hemoglobin
40
What is the most common type of anemia?
Iron Deficiency Anemia
41
What time of RBCs are produced in Iron Deficiency Anemia (in terms of size and color)?
Microcytic
| Hypochromic
42
Most kinds of anemia produce what type of RBCs in terms of size and color?
Normochromatic
| Normocytic
43
If there is an abnormality in hemoglobin, what type of RBCs are produced?
Hyperchromic
| Microcytic
44
If there is a problem with DNA (ie. folic acid or B12 deficiency), what type of anemia is produced?
Macrocytic anemia
45
What are the classifications of anemia acc to morphology? (3)
1. Normochromatic, normocytic
2. Hypochromatic, microcytic
3. Macrocytic anemia
46
Hypochromatic microcytic anemia has a abnormality in what?
Hemoglobin
47
Macrocytic anemia has a deficiency in what?
B12 and folic acid
48
In acute blood loss, the bone marrow will produce what cell first?
WBC via stimulation of adrenaline. Reticulocytes are produced last
49
The effects of acute blood loss is mainly due to the loss of what?
intravascular volume
| -can lead to shock, CVS collapse, death (if massive)
50
In chronic blood loss: loss of iron --> loss of heme --> ______
What is the morphology of the red cell?
Hypochromic microcytic
51
Causes of Hemolytic anemia (2)
1. Intrinsic: Defect in the red cell (hereditary:G6PD, sickle cell, thalassemia)
2. Extrinsic: Alterations present (ie. infection, Ab-mediated causing RBC to lyse)
52
In impaired cell production, defects in DNA synthesis is due to deficiency of? (2)
1. B12
| 2. Folic acid
53
In impaired red cell production, defects in hemoglobin synthesis are due to? (2)
1. Iron deficiency (heme)
| 2. Thalassemia (globin)
54
In impaired red cell production, disturbances in stem cell proliferation are due to? (2)
1. Aplastic anemia
| 2. Anemia of renal failure
55
What causes impaired red cell production? (3)
1. Defective DNA synthesis
2. Defective hemoglobin synthesis
3. Disturbance of stem cell proliferation
56
What are the characteristics of Intravascular hemolysis? (5)
1. Presence of free hemoglobin
2. Methalbuminemia
3. Decreased serum haptoglobulin
4. Hemosiderinuria
5. Jaundice, anemia
57
Evidence of extravascular hemolysis (patient presents with?) (2)
1. Jaundice
| 2. Anemia
58
Presence of intravascular hemolysis refers to? (3)
1. Discoloration of urine
2. Decrease in carrier protein
3. Presence of methemoglobin
59
Hemoglobinuria is only present in intravascular or extravascular hemolysis?
Intravascular hemolysis, indicated by tea-colored urine. There is no presence of hemoglobinuria in extravascular hemolysis
60
What are the causes of Intravascular hemolysis? (4)
1. Mechanical injury: heart vavles, thrombi (DIC)
2. Antibody: transfusion mismatch
3. Infection: malaria
4. G6PD
61
What is the only cause of extravascular hemolysis that is related to an intrinsic defect?
G6PD
62
What are the characteristics of extravascular hemolysis? (4)
1. Anemia
2. Jaundice
3. Splenomegaly - where hemolysis occurs. Caused by hyperplasia of phagocytes due to persistent extravascular hemolysis
4. Hemosiderosis
63
What is the response of the bone marrow to anemia?
Increased erythropoiesis
64
What is the erythroid:myeloid ratio in normal bone marrow?
1:3-5
65
What is the erythroid:myeloid ratio in periphery?
3-5:1
66
RBC life span
120 days
67
WBC life span
5-7 days. This is the reason why erythroids are higher in the periphery even though myeloid predominate in the BM. WBC have a shorter lifespan than RBC
68
What lab test is used to check for hemolytic anemia?
Reticulocyte count - it is a measure of BM activity
1. Fragmented reticulum indicates reticulocytes
2. Wright stain is NOT a good indicator for hemolytic anemia
69
In acute blood loss, what is the earliest change seen in peripheral blood due to the mobilization of granulocytes?
Leukocytosis
Note: Leukocytosis > reticulocytosis > thrombocytosis
70
What are the characteristics of Hemolytic anemia? (4)
1. Accumulation of production of Hb catabolism
- Hb breakdown --> heme --> hemosiderin --> bilirubin --> Jaundice
- increased siderocytes/blasts
- presence of pigment stones
2. Increased erythropoiesis
- Hypercellular marrow (increased normoblasts and reticulocyte count)
- Extramedullary hematopoiesis
3. Premature destruction of RBC
4. Elevated LDH
- LDH is s chemical that is high in RBC
71
What are examples of hemolytic anemia? (7)
1. Hereditary spherocytosis
2. G6PD Deficiency
3. Sickle cell anemia
4. Thalassemia
5. Paroxysmal Nocturnal Hemoglubinuria (PNH)
6. Immuno hemolytic anemia
7. Microangiopathic hemolytic anemia
72
Describe the PBS in Hereditary spherocytosis
RBC is small, dark-staining, spheroid, hypochromic (loss of central pallor)
73
What is the pathogenesis in Hereditary spherocytosis?
Abnormality of contractile membrane proteins (spectrin, actin, ankyrin) - intrinsic defects in red cell membrane skeleton
74
It is the ONLY red cell disorder wherein the red cell indices will go into opposite poles: Hyperchromatic BUT microcytic
Hereditary spherocytosis
75
The ff describes the pathogenesis of which type of hemolytic anemia?
1. Abnormalities in hexose monophosphate shunt or glutathione metabolism (due to deficient or impaired enzyme function) --> RBCs can't protect themselves from oxidative injuries --> hemolysis
G6PD
76
What happens to glutathione in the absence of G6PD?
Glutathione becomes elevated and gets converted to hydrogen peroxide leading to hemolysis (intravascular)
77
In G6PD deficiency, there is increased Hb+3 which produces?
Heinz bodies (denatured globin chains; membrane bound precipitates), which will be eaten up by the spleen (extravascular)
Explanation: G6PD functions
1. Utilizes glucose
2. Converts Hb+3 (oxidized Hb) to Hb+2 (Oxygen-carrying hemoglobin)
78
What is seen in PBS of G6PD? (4)
1. Normochromic, normocytic anemia
2. Increased reticulocyte
3. Heinz bodies
4. Bite cells
79
Episodic hemolysis is characteristic of which type of hemolytic anemia?
G6PD
80
What is the most common trigger of hemolytic anemia?
Infections (oxygen-derived free radicals are produced by active leukocytes)
81
What are the variants of G6PD? (2)
1. G6PD- : only mature RBCs lack G6PD
| 2. G6PD Mediterranean: ALL RBCs lack G6PD
82
What is the recovery phase of G6PD?
Reticulocytosis
83
What is the pathogenesis of Sickle Cell Anemia?
Substitution of GLUTAMINE for valine at the 6th position of the beta chain
84
In sickle cell anemia, there is chronic hemolysis in which organ?
Spleen
85
What are the factors that affect sickling? (4)
1. Amount and interaction of HbS
2. Increased MHCH and intracellular dehydration
3. Decreased pH (acidosis occurs)
4. Transit time in microvasculature
86
____ is a stimulus to sickle cell production
Deoxygenation
87
Where is sickling confined? (structure)
Microvasculature with slow transit time
88
What are the main manifestations of sickle cell anemia? (2)
1. Infarction
2. Pain
*capillary statis and thrombosis
89
Which process is being described?
(Start: Childhood) Spleen is enlarged due to the trapping of sickled red cells in the cords and sinuses --> chronic erythrostasis leads to splenic infarction, fibrosis, progressive shrinkage --> by the time you reach adulthood, only a small amount of fibrous splenic tissue is left
Autosplenectomy
90
Evidences of chronic hemolysis (2)
1. Increased RBC destruction
- Anemia, bilirubin, hemosiderin, iron overload
2. Increased erythropoiesis
- Extramedullary hematopoiesis
- Skull xray: crew haircut, cheeks
- Hyperplastic BM
- Increased reticulocyte and normoblasts
91
Critical episodes that can complicate the clinical picture of sickle cell anemia (3)
1. Vaso occlusive crisis
(multiple simultaneous painful thrombi in different organs)
2. Aplastic crisis
(Sudden failure of BM to increase RBC production despite anemia; sudden severe anemia)
3. Sequestration crisis
(Massive detruction of RBC passing through spleen --> sudden splenomegaly --> hypovolemia --> shock)
92
This test is used to determine the susceptibility of the RBC to rupture
Osmotic Fragility Test
93
What is the main determining factor in osmotic fragility test?
SHAPE of the RBC
94
In osmotic fragility test, which do you expect to hemolyse earlier, sickle cell or spherocyte? Explain.
Spherocyte will hemolyse earlier because there is more fluid to put in (recall the shapes! sickle cells lack hemoglobin, spherocytes are small and rounded)
Expect spHerocytes to rupture at High concentrations
Expect sickLe cells to rupture at Low concentrations
95
These are a heterogenous group of disorders caused by inherited mutations that decrease the synthesis of adult hemoglobin
Thalassemia
96
Pathogenesis of thalassemia
Defective globin SYNTHESIS
97
Clinical syndromes in thalassemia are determined and classified by?
Number of ALPHA globin genes deleted
98
Major classifications of thalassemia (2)
1. Beta Thalassemia
| 2. Alpha Thalassemia
99
Types of B-Thalassemia (3)
1. B-Thalassemia minor (Cooleys Trait): Mild anemia
2. B-Thalassemia intermedia
3. B-Thalassemia major (Cooley's Anemia): Severe anemia
100
Types of A-Thalassemia (4)
1. Silent carrier
- deletion of a single globin gene
- no RBC abnormality
- slight microcytosis
2. A-Thalassemia triat
- mild anemia
- similar with B-talassemia
- deletion of 2 globin genes from a single chromosomes
3. HbH
- deletion of 3 globin genes
- extremely high affinity for oxygen :. not useful for O2 delivery --> hypoxia
4. Hydrops fetalis (Barts Hb)
- deletion of all 4 alpha globin genes
- severely hypoxic
- most severe form
101
Pathogenesis of Anemia in Thalassemia (2)
1. Decreased rate of globin synthesis
| 2. Aggregation and precipitation of unpaired globin
102
S/Sx of Thalassemia (4)
1. Massive erythroid hyperplasia
- crew cut appearance on xray
- chipmunk face (enlargement of face, small jaw)
2. Hemosiderosis/Hemochromatosis
3. Massive hepatosplenomegaly
4. Jaundice
103
Lab diagnosis for Thalassemia (3)
1. Hb electrophoresis
2. PBS
(hypochromic, microcytic)
3. Fe overload
(marked increase siderocytes and sideroblasts, hemochromatosis)
104
Evidences of BM Hyperplasia (2)
increased
1. reticulocyte
2. normoblasts
105
This type of hemolytic anemia results from acquired mutations in the phosphatidylinositol glycan complementation group A gene (PIGA)
Paroxysmal Nocturnal Hemoglobinuria (PNH)
106
it is an enzyme essential for the synthesis of certain cell surface receptors
HINT: important in PNH
PIGA
107
Pathogenesis in PIGA
Deficiency of phospathidylinositol-linked glycoproteins (abnormal PIGA gene)
108
In the pathogenesis of PNH, there is an abnormal PIGA gene leading to the deficiency which GPI-linked proteins that regulate complement activity? (3)
1. CD59 (lysis inhibitor)
- Most important! it inhibits C3 convertase that prevents the spontaneous activation of the alternative pathway
2. CD55 (Decay Accelerating Factor; DAF)
3. C8 binding protein
109
S/Sx of PNH (3)
1. Mild hemoglobinuria, IDA
2. Increased risk for AML
3. Episodic venous thrombosis
110
Defined as hemolysis due to the appearance of antibody against RBC
Immuno Hemolytic Anemia
111
What is the major diagnostic criterion for immuno hemolytic anemia?
Coomb's antiglobulin test
112
Classification of IHA (3)
1. Warm Ab IHA
2. Cold Agglutinin IHA
3. Cold Hemolysin IHA
113
Which classification of IHA is being described?
1. IgG active at 37C
2. Does NOT fix complement
3. IgG-coated RBC binds to monocytes and splenic macrophage --> splenomegaly
4. Idiopathic
5. its secondary causes include: drugs, lymphomas, leukemias/neoplasias, autoimmune disorders (ie. SLE)
Warm Ab IHA
114
Which classification of IHA is being described?
1. IgM Ab binds to RBC at 0-4C --> ACTIVATES complement at a slightly higher temp --> dissociates at 30C
2. Its most common causes include: Mycoplasma pneumonia, Infectious mononucleosis
Cold Agglutinin IHA
115
Which classification of IHA is being described?
1. Paroxysmal cold hemogluninuria
2. IgG binds to RBC and complement at low temp --> as temp rises, activation and hemolysis start
3. Characterized by acute massive IV hemolysis following exposure to cold
4. Common causes: mycoplasma pneumonia, measles, mumps, other viral flu-like syndrome
Cold Hemolysin IHA
116
It is defined as hemolytic anemia resulting from trauma to RBC from narrowing/obstruction in the microvasculature
Microangiopathic Hemolytic Anemia
117
What is the common pathogenic feature in microangiopathic hemolytic anemia?
Microvasculature lesion that resutls in luminal narrowing, often due to the deposition of fibrin and platelets
-->vascular changes produce sheer stresses that mechanically injure passing red cells
118
What is seen in the PBS of microangiopathic hemolytic anemia?
Shistocytes (red cell fragments)
Burr cells
Helmet cells
Triangle cells
119
Types of Anemia due to diminished erythropoiesis (4)
1. Megaloblastic anemia
2. Pernicious anemia
3. IDA
4. Anemia of chronic disease
120
This general group of anemia is mostly caused by NUTRITIONAL DEFICIENCIES
Anemia due to decreased erythropoiesis
121
What are the 3 basic components responsible for nutritional anemias?
1. Vitamin B12
2. Folic Acid
3. Iron
122
This type of anemia develops due to B12 and Folic Acid deficiency
Megaloblastic Anemia
123
What is the distinct morphological change seen in megaloblastic anemia?
Macro-ovalocytes
| abnormally large and oval-shaped erythroid precursors and red cells
124
What is the pathology seen in megaloblastic anemia?
Loss of substances need for nuclear maturation and division, leading to asynchronism between the nucleus and cytoplasm (abnormally large nucleus aka immature)
Note: In megaloblatic anemia, maturation of nucleus is deficient but that of cytoplasm is intact
125
What term is used to describe the abnormal ratio of nucleus to cytoplasm?
nucleo-cytoplasmic dissociation
126
B12 is freed from food through the action of which enzyme?
Pepsin (in the stomach)
127
B12 binds to which salivary protein?
Cobalophilins/R-binders
128
Absorption of Vitamin B12 requires what?
Intrinsic factor
129
What is an essential factor in the conversion of homocysteine to methionine?
Methylcobalamine
130
What is needed in the conversion of dUMP to dTMP?
FH4
131
What are the two pathways known to require B12?
1. Conversion of homocysteine to methionine
(enzyme: methionine synthase)
2. Isomerization of methylmalonyl CoA to Succinyl CoA
(enzyme: methylmalonyl CoA Mutase)
132
Which of the 2 pathways known to require B12 can be improved by folic acid alone?
The conversion of homocysteine to methionine via methionine synthase
133
In megaloblastic anemia, deficiency in Folic Acid results to elevated levels of?
Homocystein ONLY
134
In megaloblastic anemia, deficiency in B12 results to elevated levels of?
BOTH homocysteine and methylmalonic acid
135
In megaloblastic anemia, the absence of B12 results to increased levels ____ in plasma and urine.
HINT: it is toxic to neurons, thus neurologic manifestations
Methylmalonic acid
136
What are the causes of megaloblastic anemia? (6)
1. Decreased intake
- vegetarian diet (deficient B12)
- alcoholics (deficient folic acid)
2. Impaired absorption
3. Fish tapeworm
- competitive parasitic uptake of B12
4. Increased requirement
- ie. pregnancy, thyrotoxicosis, disseminated CA, infancy
5. Folic acid antagonist (impaired utilization)
- ie. methotrexate
6. Increased losses
- ie. hemodialysis (folic acid deficieny)
137
What are seen in PBS of megaloblastic anemia? (3)
1. Macrocytic, hyperchromic RBCs
2. Leukopenia with macropolys (hypersegmented neutrophils)
3. Decreased platelets
Note: PBS of megaloblastic anemia affects RBC, WBC, platelets because they all require B12
138
Reticulocyte count in megaloblastic anemia
decreased. BM doesn't proliferate in nutritional anemias (only in hemolytic anemia)
139
What neurologic manifestation is very specific for B12 deficieny?
Dorsolateral demyelinization
140
It is the major form of B12 deficiency
Pernicious anemia
141
What is the main difference between megaloblast anemia and pernicious anemia?
HINT: it lies in the etiology
Pernicious anemia is AUTOIMMUNE
142
What features are seen in pernicious anemia that are NOT present in megaloblastic anemia? (2)
1. Presence of antibodies
| 2. Atrophy of stomach, achlorhydria - changes due to attack of Ab on the stomach
143
1. Major form of vit. B12 deficiency anemia
2. A specific form megaloblastic anemia
3. Caused by AUTOIMMUNE gastritis and failure of intrinsic factor production --> B12 deficiency
4. B12 CANNOT be absorbed d/t autoimmune destruction of gastric mucosa --> loss of parietal cells and IF
Pernicious anemia
144
Pathologies seen in pernicious anemia (2)
1. Ab vs. IF
| 2. Ab vs. gastric parietal cells
145
Effects of Ab vs. gastric parietal cells (pernicious anemia) (3)
1. Decline in number of parietal cells and IF
2. Chronic atrophic gastritis
3. Gastric atrophy
146
Term for losing HCl due to atrophy of stomach
Achlorhydria
147
What is the morphology of GIT in pernicious anemia? (2)
1. Atrophic glossitis
| 2. Atrophic gastritis
148
What is the most characteristic alteration seen in Pernicious anemia?
Atrophy of fundic glands
149
What is intestinalization?
Note: this is seen in pernicious anemia
A form of metaplasia wherein glandular lining of the epithelium is replaced by goblet cells that resemble those lining the large intestine
150
Gastric atrophy and metaplastic changes seen in pernicious anemia are due to?
Autoimmunity, NOT B12 deficiency
151
What is the most common nutritional disorder in developing countries?
IDA
152
Causes of IDA (4)
1. Low dietary intake
2. Poor absorption
3. Increased demand
4. Chronic blood loss
153
What is the transport form of iron?
Transferrin
154
Functional pool of iron (3)
Blood
Muscle
Enzymes
155
Storage sites of iron (HINT: in reticuloendothelial system) (2)
Liver
| BM
156
It is the only way to remove iron from the body
Chelation
157
Protein that inhibits iron absorption in the gut
Hepcidin
158
PBS of IDA
Hypochromic, microcytic
159
What can be seen in the BM of those with IDA?
Decreased
1. Sideroblasts
Normal
1. Platelet
2. WBC
3. Reticulocyte
4. Normoblasts
160
Storage form of Iron
Ferritin
161
What stain is used to determine the amount of iron in the tissues?
Prussian blue (for IDA!!!)
162
Pathogenenesis of Anemia of Chronic Disease (3)
1. Impaired iron absortion
2. Reduced erythrocyte progenitors
3. Impaired iron utilization
163
Conditions seen in Anemia of Chronic Disease (3)
1. Chronic microbial infection
2. Chronic immune disease
3. Neoplasms
164
Morphology of red cells in chronic anemia
Normochromic, normocytic
165
An inflammatory mediator that can stimulate an increase in the hepatic production of hepcidin
Interleukin-6
166
It inhibits ferroportin function in macrophages and reduces the transfer of iron from the storage pool to developing erythroid precursors in BM
Hepcidin
167
Types of Anemia of Marrow Failure (7)
1. Aplastic anemia
2. Myelopthisic anemia
3. Chronic renal failure
4. Diffuse liver disease
5. Neoplasia
6. Hypothyroid disease
7. Polycythemia vera
168
It refers to a syndrome of chronic primary hematopoietic failure and attendant pancytopenia
Aplastic anemia
169
Pathogenesis of Aplastic anemia
Marrow failure due to suppression of hematopoiesis
170
BM in aplastic anemia
Hypocellular with no response to anemia
171
PBS in aplastic anemia
Pancytopenia
172
Reticulocyte count in aplastic anemia
Decreased, it's not responsive to BM
173
Treatment of Aplastic anemia
transplant
| immunosuppressive treatment
174
Causes of aplastic anemia (3)
1. Hereditary (Fanconi's anemia)
- Rare autosomal recessive disorder caused by defects in a multiprotein complex required for DNA repair
2. Idiopathic (stem cell defect)
- most common cause
3. Acquired
- drugs (chloramphenicol, carbamezipine, phenytoin)
- chemicals (benzene compounds, alkylating agents like insecticides)
- infections (CMV, parvovirus, viral hepatitis, EBV)
175
The pathogenesis of this type of anemia includes space-occupying lesions that destroy significant amounts of marrow
HINT: Anemia of Marrow failure
Myelophthisic anemia
176
Teardrop RBCs are seen in in the PBS of?
Myelophthisic anemia
177
What is the dominant cause of anemia in renal failure?
Diminished synthesis of erythropoietin by damaged kidneys --> inadequate RBC production
178
What is the most common cause of anemia in neoplasms?
Metastatic CA (breast, lung, prostate)
179
Type of anemia of marrow failure wherein there is:
1. increased red cell mass
2. increased production of MYELOID progenitors
Polycythemia vera
180
Endocrine disorders, particularly hypothyroidism, may be associated with what RBC morphology?
Normocytic, normchromic
181
Types of polycythemia vera (3)
1. Relative - dehydration
2. Absolute
3. Stress polycythemia (Gaisbock syndrome)
182
Pathogenesis of polycythemia vera
Mutation of tyrosine kinase JAK2
| -No control. JAK pathway is stimulated even without GFs
183
What is seen in the PBS of polycythemia vera?
Panmyelosis
184
Complications of polycythemia vera (2)
1. Bleeding/Thrombotic episodes
| 2. Hyperuricemia
185
Prognosis of polycythemia vera
May develop:
1. Myelofibrosis
2. AML
Note: Regular phlebotomy can save life
186
What is the most common cause of polycythemia?
Polycythemia vera
187
It refers to a myeloproliferative disorder associated with mutations that lead to erythropoietin-independent growth of red cell progenitors
Polycythemia vera
