Hematopathology Flashcards
0
Q
EPO
A
Erythropoietin
- Activates erythroid progenitor cells
- Released by KIDNEY interstitial peritubular cells in response to hypoxia
1
Q
What is the composition of bone marrow?
A
cellularity is the ratio of hematopoeitic cells to fat
varies w/ age
2
Q
Trilineage hematopoiesis
A
Bone marrow consists of:
granulocytic precursors
erythroid precursors
megakaryocytes
3
Q
TPO
A
Thrombopoietin
- facilitates production and maturation of MEGAKARYOCYTES
- produced by LIVER AND KIDNEY
4
Q
What does a left shift mean?
A
Leukoerythroblastic reaction (immature cells getting out too soon)
5
Q
Left shift
A
shift toward immature leukocytes
- significant number of bands and neutrophils
6
Q
How do we evaluate bone marrow?
A
iliac crest - needle core biopsy/aspiration
anterior tibia - source for infants
7
Q
Cytoskeleton of red blood cell - Horizontal
A
Spectrin heterodimers
Spectrin-actin-protein 4.1
8
Q
Hgb A
A
Adult hemoglobin
2 alpha, 2 beta globin chains
9
Q
Cytoskeleton of red blood cell - vertical
A
Spectrin-ankryn-band 3
Spectrin-protein 4.1 - glycophorin
10
Q
Hgb A2
A
2 alpha and 2 delta chains
11
Q
Hgb F
A
Fetal hemoglobin
2 alpha and 2 gamma globin chains
12
Q
Heme portion of hemoglobin
A
porphyrin ring and Fe2+
13
Q
Oxygen dissociation curve
A
relates percent Hgb saturation to partial pressure of oxygen
14
Q
Factors that influence oxygen binding
A
- temperature
- pH
- organic phosphates
15
Q
Anemia
A
a reduction in circulating erythrocyte mass
decreased:
hemoglobin
hematocrite
RBCs
*there will be decreased oxygen transport to tissues = tissue hypoxia
16
Q
Deoxygenated blood has a _______ oxygen affinity.
A
Low
17
Q
What might we see on examination of anemic patient?
A
- tachycardia
- SOB
- systolic murmur
- “severe signs” : syncope, signs of hypovolemia, tissue hypoxia, patient is very fatigued
18
Q
How does the body compensate for anemia
A
- increase cardiac output
- increased respiratory rate
- preferential blood flow to vital organs
- decreased oxygen affinity
- increased erythrocyte production
19
Q
Microcytic
A
small size RBC
20
Q
Normocytic
A
normal size RBC
21
Q
Normochromic
A
normal amount of hemoglobin
22
Q
Hypochromic
A
small amount of hemoglobin
23
Q
Macrocytic
A
large RBC
24
Anemia from acute blood loss
- Normocytic, normochromic anemia
- volume depletion
- decreased perfusion
- extravascular fluid mobilization
- recovery is slow as RBCs need to be manufactured for replacement
- cells may have polychromasia during the recovery phase
25
Iron-deficiency anemia
- interferes w/ normal Hgb
| - impairs erythropoiesis
26
Hyperchromic
large amount of hemoglobin
27
Etiologic factors of iron-deficiency anemia
- dietary deficiency (most common cause)
- pregnancy/lactation
- chronic blood loss
- gynecological blood loss
28
Most common cause of anemia worldwide
iron-deficiency anemia
29
Transferrin
Delivers iron to cells including erythroid precursors
| iron is transported in the plasma by transferrin
30
Total iron-binding capacity (TIBC)
indicates the maximum amount of iron needed to saturate plasma or serum transferrin
31
Ferritin
derived from the storage pool of iron and closely CORRELATES W/ TOTAL BODY IRON
32
If ferritin is high
lower binding capacity of iron
33
If ferritin is low
lots of capacity to bind iron
34
Iron-deficiency anemia (pathology)
- microcytic, hypochromic anemia
- anisopoiklocytosis (variation in erythrocyte size and shape)
- no reticulocytes
- serum iron decreased
- ferritin decreased
- transferrin and TIBC increased
- transferrin iron saturation is low
- RDW WILL ALWAYS BE LARGER, IN GENERAL
35
Iron deficiency anemia (appearance of cells)
area of pallor is bigger
36
Iron-deficiency anemia (treatment)
- correct blood loss
| - iron supplementation
37
Iron-deficiency anemia (clinical features)
- Atrophic glossitis (smooth glistening tongue)
- Angular stomatitis (inflammation at the corners of mouth)
- Koilonychia (spoon-shaped deformity of fingernails)
38
Anemia of Chronic Disease
- occurs w/ inflammatory or malignant conditions
- mild to moderate anemia
- normochromic, normocytic; can be microcytic
- IRON STORES CAN BE NORMAL OR EVEN INCREASED
- FUNCTIONAL IRON DEFICIENCY (body has enough iron, it's just not able to use it)
- decreased erythroid iron
- decreased EPO
- erythrocyte lifespan can be decreased
- INFLAMMATORY CYTOKINES MAY DECREASE IRON MOBILIZATION
39
Aplastic Anemia
Disorder of pluripotent stem cells that lead to BONE MARROW FAILURE
- ALL BLOOD ELEMENTS ARE DECREASED (PANCYTOPENIA)
40
Aplastic anemia - causes
insult to stem cells
- idopathic (2/3 of cases)
- drugs
- chemicals
- virsues
- hereditary
dose dependent - w/ drugs and chemicals
idiosyncratic - dose independent, immunologic injury as see in idiopathic cases or after viral infections
41
Aplastic anemia (Pathology)
- decreased bone marrow cellularity
(Anemia, thrombocytopenia, and leukopenia; granulocytopenia is most common)
Because of the precursors involved, they tend to have a DECENT AMOUNT OF LYMPHOCYTES
- increased fat
- EPO levels increase but there is no reticulocytosis
42
Anemia of Chronic Disease: TIBC, Ferritin, and Transferrin levels
Total iron binding capacity - DECREASES
Ferritin - normal, maybe a little increased
Transferrin - normal, sometimes decreased
43
Aplastic anemia (clinical presentation)
Pancytopenia effects including weakness, easily fatigued, bleeding, and infections
-Median survival 3-6 months
44
Pure Red Cell Aplasia (pathology)
- Absence of erythroid precursors (the rest of bone marrow cellularity is normal)
- EPO is decreased - NO RETICULOCYTES
45
Aplastic anemia (treatment)
- immunosuppressive therapy
| - bone marrow transplant
46
Pure Red Cell Aplasia
Selective suppression of committed red cell precursors in the bone marrow (white cells and platelets unaffected)
47
Parvovirus B19
Causes a relapsing form of Pure Red Cell Aplasia
- viral inclusions in proerythroblasts
- usually self limited
- aplastic crisis when there is underlying anemia
48
Anemia of Renal Disease
- Normocytic and normochromic
| - DECREASED EPO in proportion to disease severity
49
Burr Cells
ANEMIA OF RENAL DISEASE
50
Schistocytes
If there is malignant hypertension w/ ANEMIA OF RENAL DISEASE, cells may be fragmented
51
Diamond-Blackfan Syndrome
PURE RED CELL APLASIA
- seen in first 2 years of life
- short stature, cleft lip or palate, micrognathia, limb abnormalities
- defective erythroid precursors
- poor EPO response
52
Myelophthisic Anemia
```
Associated w/ BONE MARROW INFILTRATION
- myelofibrosis
- hematologic malignancies
- metastatic carcinomas
- granulomatous disease (competing for bone marrow space)
Normocytic Anemia
Leukoerythroblastosis
EXTRAMEDULLARY ERYTHROPOIESIS is a compensatory mechanism
```
53
Anemia of lead poisoning
Interferes w/ enzymes involved in heme synthesis
- alpha-amnolvulinic acid dehydratase
- Ferrochelatase
54
How do you expect cells to look on the peripheral smear for anemia of lead poisoning?
Microcytic
| *often confused w/ iron deficiency anemia
55
Megaloblastic Anemia (physical features)
- small nucleus
- increased erythrocyte precursor pool (but cells are not as easily distributed in the bone marrow)
- normal cytoplasm
- nuclear-to-cytoplasm asynchrony
- large precursor cells - MEGALOBLASTS
56
Megaloblastic Anemia
defective DNA synthesis secondary to B12 or folic acid (B9) deficiency
57
Megaloblastic anemia - from folate/folic acid deficiency
- deficiency is usually inadequate dietary intake
- alcoholics
- pregnancy/lactation
- inflammatory bowel disease (may interfere w/ absorption of folic acid)
58
Megaloblastic anemia - Pernicious anemia
- autoimmune disorder
- antibodies to parietal cells and intrinsic factor
- previous surgery could cause injury
- can decrease acid production (achlohydria)
- fish tapeworm (Diphyllobothrium)
59
Megaloblastic anemia (pathology)
- bone marrow shows increased hematopoietic activity w/ large precursors
- Large RBCs result; anisopoikylocytosis
- intermedullary cell death is increased
- fewer cells of larger size
- large bands form and hypersegmented neutrophills
60
B12 deficiency (clinical presentations)
- demyelinates the posterior and lateral columns
- sensory and motor deficits may occur
*this does not occur w/ folate deficiency
61
How long does it take to develop and B12 deficiency?
Years
62
Thalassemia
Congenital anemias that result from deficient synthesis of globin chain subunits of normal hemoglobins
- globin subunit of interest is reduced or absnent
- abnormal or unstable structures lead to RBC fragility and destruction
63
Thalassemia (epidemiology)
- common in Mediterranean areas
| - also seen in areas where malaria has been prevalent (possible malaria protection from heterozygous state)
64
How long does it take to develop and folate deficiency?
months
65
Cooley Anemia
HOMOZYGOUS B-THALASSEMIA
- moderate to sever microcytic and hypochromic anemia
- anisopoikylocytosis w/ basophilic stippling
- unstable a4 tetramers precipitate in the cytoplasm of developing erythroid precursors
- SOME A2 IS PRESENT IN ALL B-THALASSEMIA SINCE THE DELTA GENE IS UPREGULATED
66
B0 type in Cooley Anemia
Produces fetal hemoglobin and A2
67
A patient w/ Cooley anemia has an increased amount of Hgb F... what happens to O2 delivery?
O2 delivery will be DECREASED because of the anemia and because of the increased oxygen affinity of Hgb F
- this will lead to bone marrow hyperplasia (abnormal facial features)
68
B+ type in Cooley Anemia
produces some hemoglobin A and A2 is mildly increased
69
B-thalassemia
Transcription is entirely or partially suppressed due to a point mutation
B0 and B+ types
70
Heterozygous B-Thalasemia
- patients typically asymptomatic
- iron absorption is increased
- minimal anisocytosis
- target cells and basophilic stippling occurs
71
a-thalassemia
typically caused by gene deletions
72
Silent Carrier a-thalassemia
- 1 gene missing
- CAN MAKE HEMOGLOBIN NOMRALLY
- no clinical problems, blood count usually normal or has mild decreases in the RBC mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH)
73
a-thalassemia trait
2 genes missing
- can make Hgb A
- usually no clinical problems but often will have changes in their complete blood count including mild anemia, decreased RBC, MCV, and MCH
74
Hgb H disease (Heinz bodies) a-thalassemia
3 genes missing
- cannot make as much Hgb A
- increase in TETRAMERS OF BETA HEMOGLOBIN
- Hgb H has high binding capacity for oxygen
- patient has moderate to sever anemia, low MCH and MCV, high reticulocyte counts
- severity depends on how much hemoglobin A is made
75
Homozygous (Bart's hemoglobin) a-thalassemia
- 4 genes missing; a-thalassemia major
- CANNOT MAKE ANY HgB A AND PRODUCES BART'S HEMOGLOBIN TETRAMERS OF GAMMA HEMOGLOBIN CHAINS
- causes Hydrops Fetalis
76
Procoagulant complexes
- Prothrombinase complex
| - 2 X-ase complexes
77
Anticoagulant Complex
Protein C-ase complex
78
Hydrops Fetalis
Homozygous a-thalassemia w/ Bart hgb = incompatible w/ life
- heart failure develops due to profound tissue hypoxia and fluid accumulation in various compartments (at least 2 compartments)
- massive hepatosplenomegaly due to extramedullary hematopoiesis
79
Prothrombinase Complex
Xa/Va/PL complex cleaves factor II>IIa
* COMMON PATHWAY
- Ca is required
80
Protein C-ase complex
made of alpha-thrombin-thrombodulin in the endothelial membrane
Protein C w/ its cofactor protein S inactivate VIIa and Va
81
Purpura Simplex
- extravascular dysfunction
- transient occurence in the deep dermis
- enhanced by NSAIDs and other drugs
82
X-ase Complexes
TF/VIIa/PL complex initiates coagulation
IXa/VIIIa/PL complex activates X
83
Senile Purpura
- extravascular dysfunction
- older people; atrophy of supporting connective tissue
- sharply demarcated persistent purpuric spots on forearms and other sun exposed areas
84
Rendu-Osler-Weber Syndrome
- vascular dysfunction
- intrinsic genetic defects
- AD disorder of vneules and capillaries
- results from thinning of vessel wall due to inadequate elastic tissue and smooth muscle
85
Scurvy
- extravascular dysfunction
- decreased Vitamin C disturbs collagen synthesis
- perifollicular hemorrhages and purpura are seen
86
Telangectasias of mucous membranes and dermis
Rendu-Osler-Weber Syndrome
87
Arteriovenus malformations of solid organs
Rendu-Osler-Weber Syndrome
88
```
Mutation of TGF-Beta
also ENG (endoglin) and ALK1 (activin receptor-like kinase 1)
```
Rendu-Osler-Weber Syndrome
89
Henoch-Schonlein Purpura
- results from immunologic damage to the vessel wall
- leukocytoclastic VASCULITIS
- seen after viral illnesses in children
- abdominal pain, arthralgia
- renal involvement in 20-50% of cases
90
Rendu-Osler-Weber Syndrome (clinical features)
- begin as red colored punctate lesions
- easy to bleed, develop some anemia
- Recurrent epistaxis when younger (80%)
- various organs can be involved and having varying degrees of pathology (shunting of blood since there is no buffering from capillary)
91
PT
Prothrombin time
- evaluates factors of EXTRINSIC AND COMMON PATHWAY
- monitor COUMADIN
92
- Perivascular infiltration of neutrophils and eosinophils
- fibrinoid necrosis of vessel walls
- platelet plugs in the vasuclar lumen
- IgA-compelement complexes found circulating and some in vessel walls
Henoch-Schonlein Purpura
93
What does ITP stand for?
Idiopathic Thrombocytopenic Purpura
94
PTT
Partial thromboplastin time
- evaluates factors in the INTRINSIC AND COMMON PATHWAYS
- monitor HEPARIN
95
ITP
- decreased platelets in the blood due to antibodies to platelet or megakaryocyte antigens (autoimmune)
96
Peripheral smears show large platelets and bone marrow has increased megakaryocytes
ITP
97
Acute ITP
- usually in children
- follows viral illness
- platelet antigens attacked by autoantibodies
- complement is bound
- platelets are destroyed in the circulation (MAC attack) or phagocytized in the spleen or liver by macrophages
98
IgG is detected on platelets in 80%; C3 is present on some
ITP
99
Chronic ITP
- usually in adults
- more women affected
- associated w/ collagen diseases, lymphoproliferative disease, and HIV
100
Acute ITP (clinical features)
- petechiae, purpura, epistaxis
- intracranial hemorrhage
- 80% spontaneously resolve within 6 months
- glucocorticoids decrease antiplatelet antibody production and down-regulate Fc receptors on macs
- gamma-globulin prevents clearing of IgG coated platelets
101
Chronic ITP (clinical features)
- bleeding episodes such as epistaxis, menorrhagia, or ecchymosis
- treatment w/ glucocorticoids, Danazol, or gamma-globulin
- if no response over time, splenectomy helps
102
What does TTP stand for?
Thrombotic Thrombopenic Purpura
103
TTP
```
- Thrombotic microangiopathy
Pentad
- fever
- thrombocytopenia
- microangiopathic hemolytic anemia
- transient neurologic deficits
- renal failure
```
104
What is TTP due to?
excessive activation of platelets; there is deposition as thrombi in microcirculatory beds
105
ADAMTS13 or VWF metalloprotease is deficient
- decreased vWF cleavage of large multimers
- greater chance of binding platlets
TTP
106
PAS-positive hyaline microthrombin arterioles - diffusely located but especially seen in the brain, heart, and kidneys
TTP
107
How is TTP different than vasculitis?
NO INFLAMMATION IN TTP
108
What does HUS stand for?
Hemolytic uremic syndrome
109
TTP clinical features
- women during 4 or 5th decade of life
- chronic and recurrent
- weakness, seizures, aphasia, altered consciousness (stroke-like symptoms)
- purpuric lesions
- hemolytic anemia w/ decreased Hgb/Hct
- Jaundice
- Renal insufficiency may develop
- PT and PTT are normal
110
Follows gastroenteritis caused by E.coli 0157:H7 or Shigella dysenteriae
Kidney failure main clinical feature
HUS
111
Kasabach-Merritt Syndrome
- a cause of thrombocytopenia (tumors sequester platelets)
| - baby pictures
112
TTP pathology
- Schistocytes (fragmented erythrocytes) are seen on peripheral blood smears due to shear force of microthrombi
- Bilirubin would be elevated because we're breaking down RBCs
113
Bernard-Soulier Syndrome
- AR platelet disorder
- GIANT PLATELETS
- GpIb does not attach to vWF
- patients present w/ petechiae, ecchymosis, epistaxis, bleeding gingiva; often in children
- can present as GI bleeding or menorrhagia as adults
114
Hemophlia A (clinical features)
mild to severe bleeding tendencies
- 1/2 have virtually no activity (spontaneously bleed)
- may bleed into joints and have secondary degeneration
- intracranial bleed
- hematuria, intestinal obstruction and respiratory obstruction can occur due to bleeding in these organs
115
Hemophilia B
X linked disorder of deficient Factor IX (9)
- Factor IX made in the liver and is vitamin K dependent
- variety of mutations are causative
- manifestations are similar to Hemophilia A
116
Hemophilia A
Most common X-linked inherited bleeding disorder
Factor VIII (8) on Xq28 can have deletions, insertions, point mutations, and inversions
117
Hemophilia A (treatment)
replacement of the factor
118
von Willebrand Disease
- deficiency or abnormality of vWF
| - most common INHERITED bleeding disorder of humans
119
Hemophilia B (treatment)
replacement of factor IX
120
vWF is produced by...
endothelial cells and megakaryocytes
121
vWF gene is located on chromosome...
Chromosome 12
122
Weibel-Palade bodies
where vWF is stored (vWF is adhesive)
123
Type I vWD
75% of disease
```
AD inheritance, variable penetrance
quantitative deficiency (levels of all multimers are reduced)
```
124
Type II vWD
- 20% of disease
- AD inheritance
- activities of vWF and factor VIII are decreased
125
Type IIa VWD
ABSENCE of large multimers
126
Type IIb vWD
abnormally high PLATELET AFFINITY
127
vWD (clinical features)
- mild bleeding that goes unnoticed until there is some type of hemostatic stress such as a medical/dental procedure (type III is the exception)
128
Type III vWD
- AR inheritance; compound heterozygotes (mutant alleles on each chromosome)
- Most severe and least common
- vWF is ABSENT and Factor VIII is less than 10% of normal
129
vWD (treatment for I and II)
DDAVP, causes endothelial release of vWF
130
vWD (treatment for III)
vWF and/or cryoprecipitate
131
What factors does the liver produce?
2, 5, 7, 9, 10
132
What can be prolonged as a result of liver disease and coagulopathies?
PT and PTT; PT more severely affected since factor 7 is the workhorse
133
Which factor is not vitamin K dependent?
5
134
Decrease in Vitamin K
process of y-carboxylation in factors 2, 7, 9, and 10 is decreased
135
DIC
- A thrombohemorrhagic disorder characterized by excessive activation of coagulation that leads to thrombi formation in the microvasculature (arterioles, venules, capillaries)
- can be widespread
- coagulation factors are consumed
- NOT A PRIMARY DISEASE, caused by a variety of clinical disorders
- ischemia ensues
136
What does DIC stand for?
Disseminated Intravascular Coagulation
137
Treatment of DIC
heparin
platelets
clotting factors
treating the underlying disease
138
Most likely associations w/ DIC
malignant neoplasms
sepsis
obstretric complications
major trauma or burns
139
Neutrophilia
ANC > 7000
- caused by mobilization from the bone marrow
- enhanced release from the peripheral blood marginal pool
- increased granulopoiesis
140
Agranulocytosis
virtual absence of neutrophils
141
Neutropenia
Absolute neutrophil count (ANC) < 1500
142
Eosinophilia
- eosinophils differentiate in the bone marrow
- migrate to skin, lungs, and GI tract
- respond to chemotactic substances produced by mast cells or Ag-Ab complexes
143
Leukemoid reaction
- occurs in neutrophilia (cells are segmented neutrophils)
- WBC < 50,000
- Dohle bodies and toxic granulation
144
Idopathic Hypereosinophilic Syndrome
- eosinophils above 1500 for 6 months
| - diagnosis also requires organ involvement and know identifiable cause for the eosinophilia
145
Endomyocardial fibrosis
Idiopathic Hypereosinophilic Syndrome
146
Idiopathic Hypereosinophilic Syndrome (clinical features)
- Tissue necrosis (especially in heart)
- Neurologic dysfunction
- high mortality
147
Loeffler's endocarditis
Idiopathic Hypereosinophilic Syndrome
148
Basophilia is typically due to...
- immediate-type hypersensitivity reactions
| - chronic myeloproliferative neoplasms
149
Monocytosis
- Monocyte count > 800
- Due to infection, hematologic malignancies, solid cancers, immunologic conditions
- monocytosis in a neutropenic state is likely compensatory
150
Basophilia
- least abundant leukocyte
- differentiates in bone marrow
- contains inflammatory mediators
151
Myeloproliferative neoplasms
clonal hematopoietic stem cell disorders that cause PROLIFERATION OF ONE OR MORE MYELOID LINES
152
Myelodysplastic syndromes
MARROW FAILURE, DYSPLASTIC CHANGES OF ONE OR MORE CELL LINES, and PERIPHERAL CYTOPENIA
153
Reactive Mast Cell Hyperplasia
- Not malignant
- seen in lymph nodes that drain sites of malignant tumors
- seen in immediate and delayed-type hypersensitivities
154
Chronic Phase of CML
- increased neutrophils in ALL stages of development
- basophilia and eosinophilia
- hypercellular marrow w/ abnormal precursors
155
Most common myeloproliferative disease
CML
156
What does CML stand for?
Chronic Myelogenous Leukemia
157
What is necessary for the diagnosis of CML?
Philadelphia chromosome or bcr/abl fusion genes
| - Tyrosine kinase activity of fusion protein p210 can induce proliferation, differentiation, and overall survival
158
Association/cause of CML
radiation and benzene exposure - slight male predominance
159
CML is derived from...
an abnormal bone marrow stem cell and results in prominent neutrophilic leukocytosis
160
Accelerated phase of CML
- increasing WBC
- increasing splenomegaly
- 10-20% blasts in the marrow or peripheral blood
- thrombocytopenia/thrombocytosis
- additional chromosomal abnormalities
161
CML treatment
- Imatnib competes for ATP-binding site on bcr/abl (tyrosine kinase won't be able to be made)
- bone marrow transplant can be used
162
Polycythemia Vera (Major Criteria)
Hbg > 18.5 g/dL in men
Hbg > 16.5 g/dl in women
JAK 2 mutation
163
Blast phase of CML
- true CML
| - 20% blasts in blood and/or marrow w/ EXTRAMEDULLARY PROLIFERATION OF THE BLASTS
164
Polycythemia Vera (clinical features)
- 60 years
- insidious onset
- splenomegaly is typical and found early
- Circulatory problems/sluggish flow (blood is very thick)
- hypoxia to various organs; angina, claudication
- headache, dizziness, visual disturbances
165
Polycythemia Vera minor critieria
- NO EPO ELEVATION
- Hypercellular marrow w/ panmyelosis
- Erythroid colony formation in vitor w/o growth factor stimulation
166
Polycythemia Vera
- Myeloproliferative neoplasm arising from a clonal hematopoietic stem cell
- Autonomous RBC production NOT UNDER THE CONTROL OF EPO
167
Prepolycythemic phase
Borderline or mild erythrocytosis
168
Polycythemic phase
defining erythrocytosis
169
What occurs to patients w/ polycythemia vera perhaps due to chemotherapeutic agents used for treatment?
AML
170
Postpolycythemic phase/spent phase
- excessive proliferation stops
- can become anemic
- myelofibrosis develops
(bone marrow has been spent)
171
What does AML stand for?
Acute Myeloid Leukemia
172
Myelodysplastic Syndromes
- cytopenia of the peripheral blood
- bone marrow failure
- dysplastic morphology of 1 or more cell lines
discrepancy between amount of peripheral blood elements and marked hyperplasia seen in the bone marrow
173
Essential Thrombocythemia
- uncommon neoplastic disorder of hematopoietic stem cells
- uncontrolled proliferation of megakaryocytes (increased number of thrombocytes)
- Platelets > 600,000
- Thrombosis and hemorrhage can be recurrent
174
What is a major difference between Myelodysplastic syndromes and Myelodysplastic neoplasms?
In Myelodysplastic syndromes, there is not erythrocytosis, leukocytosis, or thrombocytosis as seen in the MPN diseases
175
Why are myelodysplastic syndromes paradoxical
Bone marrow remains hypercellular but there is hematopoeisis and apoptosis
176
What is the major problem w/ AML?
Accumulation of immature and undifferentiated myeloid cells in the bone marrow
177
Auer rods
AML
178
Acute suppurative lymphadenitis - posterior auricular
rubella
179
Acute suppurative lymphadenitis - occipital nodes
scalp infections
180
AML
- clonal proliferation of myeloblasts in the bone marrow followed by appearance in the blood and possible in tissues
- diagnosis requires MORE THAN 20% MYELOBLASTS IN THE PERIPHERAL BLOOD OR BONE MARROW
- bone marrow is infiltrated and displaced w/ malignant cells
181
Acute suppurative lymphadenitis - axillary
infection of upper extremity
182
Acute suppurative lymphadenitis - posterior cervical
toxoplasmosis
183
Acute suppurative lymphadenitis - generalized
systemic infections
