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Pathophysiology > Hematopathology > Flashcards

Hematopathology Flashcards

1
Q

blast

A

immature

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2
Q

cyt

A

cell

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3
Q

dys

A

bad, defective

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4
Q

emia

A

blood condition

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5
Q

erythro

A

red

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6
Q

heme

A

blood

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7
Q

leuko

A

white

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8
Q

lysis

A

destruction

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9
Q

macro

A

large

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10
Q

myelo

A

bone marrow

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11
Q

osis

A

disease or increase

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12
Q

penia

A

deficiency

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13
Q

thrombo

A

blood clotting

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14
Q

Total WBC…

A

the summation of the five types of WBCs

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15
Q

hematocrit is ____x the value of hemoglobin

A

3X

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16
Q

The actual count of the cells is the ____ count

A

absolute count

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17
Q

What are the “3 branches” of hematopoiesis?

A

thrombopoiesis, erythropoiesis, leukopoiesis

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18
Q

What are the two major stem cell lines of hematopoiesis?

A

myeloid stem cell, lymphoid stem cell

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19
Q

Thrombopoiesis takes place…

A

inside the bone marrow

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20
Q

Platelets have an average life span of…

A

8-9 days

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21
Q

Old platelets are destroyed in the…

A

spleen and the liver

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22
Q

Erythropoiesis takes place inside the…

A

bone marrow

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23
Q

An immature red blood cell is called a…

A

reticulocyte

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24
Q

What do reticulocytes require to become a mature erythrocyte?

A

Vitamin B12 and Vitamin B9 (folic acid)

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25
Q

What stimulates the production of red blood cells in the bone marrow?

A

erythropoietin

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26
Q

Where is erythropoietin produced?

A

in the kidneys and the liver

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27
Q

What is erythropoietin produced in response to?

A

low oxygen

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28
Q

True or False: WBCs are formed from both the myeloid stem cell line and the lymphoid stem cell line

A

true

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29
Q

Disruption of hematopoiesis can be _____ or _____

A

malignant or non-malignant

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30
Q

What are some disorders of non-malignant hematopoiesis?

A 
nutritional deficiencies 
autoimmune disorders 
infectious etiology 
DIC 
TTP 
Hypersplenism
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31
Q

What are some disorders of malignant hematopoiesis?

A 
leukemia 
lymphoma 
myeloma 
myelodysplastic syndrome 
aplastic anemia
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32
Q

What are some examples of myeloproliferative disorders? (malignant)

A 
acute myeloid leukemia 
chronic myeloid leukemia 
myeloma 
essential thrombocythemia 
polycythemia vera 
myelofibrosis
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33
Q

What are some examples of lymphoproliferative disorders? (malignant)

A

acute lymphoblastic leukemia
chronic lymphoblastic leukemia
multiple myeloma
lymphoma

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34
Q

Leukemia is neoplastic cells in the…

A

blood stream

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35
Q

lymphoma is neoplastic cells in the …

A

lymph system

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36
Q

myeloma is neoplastic cells in the…

A

plasma cells

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37
Q

True or False…there can be overlap between leukemia and lymphoma

A

True- this would be in a case of having blood involvement in lymphoma

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38
Q

What are the two major types of leukemia?

A

acute- composed of blast cells
chronic- composed of more mature precursor cells
(acute is more severe because it is in the original stem cells)

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39
Q

CLL

A

chronic lymphocytic leukemia

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40
Q

CML

A

chronic myeloid leukemia

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41
Q

ALL

A

acute lymphoblastic leukemia

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42
Q

AML

A

acute myeloid leukemia

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43
Q

What are some risk factors for leukemia?

A

radiation exposure
chemotherapy exposure
benzene exposure (second hand smoke, gasoline, in plastics, resins, synthetic fibers, rubber lubricants, dyes, detergents, pesticides)

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44
Q

What are the signs and symptoms of leukemia?

A

leukocytosis- monocytes and lymphocytes
pancytopenia- anemia (pallor, dyspnea, fatigue), neutropenia (infections), thrombocytopenia (excess bleeding or bruising)
hypogammaglobulinemia
bone pain (expansion of bone marrow)
lymphadenopathy
splenomegaly
onset varies…acute is sudden onset of a few months and chronic can be an incidental diagnosis

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45
Q

How is the diagnosis of leukemia made?

A

bone marrow bx

flow cytometry

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46
Q

What is the most common leukemia in adults?

A

acute myeloid leukemia (AML)

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47
Q

True or False…AML is a common form of cancer

A

False…while AML is the most common type of leukemia in adults, it is overall a rare disease accounting for 1% of all adult cancer deaths in the US

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48
Q

What finding is considered to be pathognomonic in AML?

A

**circulating blasts greater than 20%* (blasts are immature myeloid cells)
auer rods on pathology

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49
Q

What is the prognosis of AML?

A

technically a curable disease
60-80% of young healthy patients achieve a CR but only 1/3 are ultimately cured
rapidly lethal if left untreated

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50
Q

Why do patients with AML have anemia and what can be done for them?

A

it is a complication of low circulating oxygen, they can be given transfusions

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51
Q

Why do patients with AML get infections?

A

Low normally functioning WBCs

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52
Q

Why do patients with AML experience bleeding?

A

Low normally functioning platelets

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53
Q

What are the other names for a stem cell transplant?

A

Bone marrow transplant

hematopoietic cell transplantation (HCT)

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54
Q

What occurs during a stem cell transplant?

A

very high dose chemotherapy is administered, killing all normal cells in the bone marrow, including the stem cells. new stem cells are reintroduced and reestablish blood cell production in the bone marrow

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55
Q

What are the two types of stem cell transplant?

A

autologous vs allogenic stem cell transplant

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56
Q

What is the most common childhood malignancy? What is the peak incidence?

A

acute lymphoblastic leukemia (ALL)

peak incidence between 2-5 years of age

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57
Q

What syndrome is there an increased incidence of ALL?

A

down syndrome

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58
Q

Is there thought to be a genetic component to ALL?

A

yes

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59
Q

What does pathology of ALL confirm?

A

lymphoblasts (lymphoid lineage)

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60
Q

Is ALL considered to be a curable disease? What is the prognosis?

A

Yes, ALL is considered to be a curable disease, with lots of chemo and high risk for complications later in life
five year overall survival is 85%

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61
Q

What demographics have a good prognosis with ALL?

A

hyperdiploid (>50 chromosomes per cell)
2-10 years of age
CD10+ (mutation)
low WBC count

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62
Q

What demographics have a poor prognosis with ALL?

A 
hypodiploid (less chromosomes per cell) 
less than 2 years of age 
greater than 10 years of age 
male gender 
high WBC count (>100,000)
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63
Q

What is CAR-T therapy?

A

chimeric antigen receptor - T cells
individual’s own T lymphocytes are genetically modified with a gene that encodes a chimeric antigen receptor to direct the patient’s own T cells against the leukemic cells
modified ex vivo, infused back into patient, long term remission because t cells are trained

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64
Q

What is the downside to CAR-T therapy?

A

cytokine release syndrome occurs in a high percentage of the patients,

65
Q

What cells undergo uncontrolled proliferation in Chronic Myeloid Leukemia?

A

maturing granulocytes

66
Q

What is pathognomonic for CML?

A

Philadelphia chromosome

67
Q

What is the Philadelphia chromosome?

A

the fusion of 2 genes- BCR on chromosome 22 and ABL1 on chromosome 9 results in an abnormal chromosome 22

68
Q

What are the phases of CML?

A

CML….accelerated phase…blast crisis

without treatment it will progress to a terminal condition

69
Q

Outlook for CML

A

technically curable with a stem cell transplant but stem cell transplant poses significant risk and mortality, oral chemo can manage the disease but are not curative

70
Q

What is the epidemiology of CML?

A

male predominance

diagnosed 50 or later

71
Q

In CLL, what kind of cells progressively accumulate?

A

functionally incompetent lymphocytes

72
Q

What are the other names for CLL?

A

CLL= chronic lymphocytic leukemia
small lymphocytic lymphoma
non-Hodgkin lymphoma SLL

73
Q

What is the epidemiology of CLL?

A

male predominant

mostly diagnosed after age 70

74
Q

What is the cytology in CLL?

A

blood lymphocyte count >5,000
gingersnap appearance of cells
cells are fragile and break during processing- smudge cells (broken cells)

75
Q

Is CLL curable?

A

not considered curable but treatable

stem cell transplant is risky with increased mortality

76
Q

True or false…CLL frequently does not require treatment at the time of diagnosis

A

true

77
Q

What are the indications for treatment “active disease” in CLL?

A

progressive marrow failure
progressive or massive splenomegaly
progressive or symptomatic lymphadenopathy
progressive lymphocytosis
constitutional symptoms- fatigue, night sweats, unintentional weight loss, fevers

78
Q

Generally, what are considered “B symptoms” or “constitutional symptoms”?

A

fever
night sweats
unintentional weight loss
fatigue

79
Q

What are the signs and symptoms of lymphoma?

A 
constitutional symptoms 
lymphadenopathy 
splenomegaly 
anemia, thrombocytopenia, neutropenia
hypercalcemia 
hyperuricemia 
elevated LDH 
monoclonal immunoglobulin (M spike) on SPEP
80
Q

What is the difference hodgkin lymphoma and nonhodgkin lymphoma?

A

hodgkin- presence of Reed Sternberg cells
nonhodgkin- absence of Reed Sternberg cells
***

81
Q

What are the two types of non-hodgkin lymphomas?

A

indolent and aggressive lymphomas

82
Q

Follicular lymphoma- indolent or aggressive?

A

indolent

83
Q

Diffuse Large B cell lymphoma (DLBCL) - indolent or aggressive?

A

aggressive

84
Q

marginal zone lymphoma (MALT)- indolent or aggressive?

A

indolent

85
Q

Burkitt lymphoma- indolent or aggressive?

A

aggressive

86
Q

lymphoplasmocytic lymphoma-indolent or aggressive?

A

indolent

87
Q

mantle cell lymphoma- indolent or aggressive?

A

aggressive

88
Q

small lymphocytic lymphoma- indolent or aggressive?

A

indolent

89
Q

peripheral t cell lymphomas - indolent or aggressive?

A

aggressive

90
Q

Male or female predominance/peak incidence for Hodgkin lymphoma?

A

male
(female predominance for nodular sclerosis Hodgkin lymphoma)
peak incidence 20-50

91
Q

What are the signs and symptoms of Hodgkin lymphoma?

A

painless cervical adenopathy- most common presenting symptom
1/3 of patients have constitutional symptoms
generalized pruritus in the nodular sclerosis type
pain in lymph nodes with alcohol consumption (classic description)

92
Q

Describe the lymph node involvement in Hodgkin lymphoma

A

contiguous groups of lymph nodes- amenable to surgical excision
extranodal involvement is rare
mediastinal and neck nodes are most commonly involved

93
Q

What is the neoplastic cell in Hodgkin lymphoma?

A

Reed Sternberg cell

94
Q

What factors affect prognosis in Hodgkin lymphoma?

A

worse with mixed cell types
male gender
age over 40

95
Q

What is most common type of lymphoma worldwide?

A

diffuse large B cell lymphoma

96
Q

What is the epidemiology of DLBCL?

A

male predominance

median age and presentation-64

97
Q

What are the sxs of DLBCL?

A 
rapidly enlarging symptomatic mass (neck or abdomen most common) 
extranodal involvement is common 
constitutional symptoms in 30% 
elevated LDH in over half 
somme associated with EBV infection
98
Q

What is the prognosis of DLBCL?

A

60% present in the advanced stage of the disease

curable in approx. half of cases with current therapy

99
Q

What is the second most common type of non-hodgkin lymphoma?

A

follicular lymphoma

100
Q

what are the sxs of follicular lymphoma?

A

painless peripheral adenopathy (cervical, axillary, inguinal, femoral regions-waxes and wanes but never completely goes away)
involvement of organs other than the lymphatic organs or bone marrow is uncommon
constitutional symptoms and elevated LDH are uncommon
presentation is sometimes related to organ dysfunction secondary to large tumor growth

101
Q

what is the prognosis for follicular lymphoma?

A

may have waxing and waning symptoms for 5 years before diagnosis
can progress to diffuse large b cell or burkitt lymphoma

102
Q

Which lymphoma is a highly aggressive B cell neoplasm?

A

burkitt lymphoma

103
Q

burkitt lymphoma comprises ___% of pediatric lymphomas in the US

A

30%

104
Q

an endemic form of burkitt lymphoma seen in Africa presents with….

A

jaw or facial bone tumor

105
Q

the immunodeficiency-associated form of burkitt lymphoma is seen in which patient population?

A

HIV positive patients

106
Q

burkitt lymphoma typically presents as…

A

an abdominal or retroperitoneal mass

107
Q

What is tumor lysis syndrome?

A

release of large amounts of potassium, phosphate, and nucleic acids into the systemic circulation, causing hyperuricemia

108
Q

Which lymphoma has a high propensity for tumor lysis syndrome?

A

burkitt lymphoma

109
Q

Mantle cell lymphoma can involve….

occasionally presenting as….

A

any region of the GI tract, occasionally presenting as lymphomatous intestinal polyposis

110
Q

In mantle cell lymphoma, nuclear staining for _____ is present in 95% of cases

A

cyclin D1

111
Q

What is the median overall survival in modern trials incorporating intensive therapy for mantle cell lymphoma?

A

8-10 years

112
Q

What is the full name for MALT lymphoma?

A

extranodal marginal zone lymphoma of mucosa associated lymphoid tissue

113
Q

Marginal zone lymphoma is frequently due to what kind of infections?

A

chronic gastritis from H. pylori infections

114
Q

what epithelial tissues does MALT lymphoma arise in?

A 
stomach*
salivary gland 
lung 
small bowel 
thyroid 
ocular adnexa 
skin 
(bx can be done during upper endoscopy)
115
Q

what are other types of marginal zone lymphoma other than MALT?

A

nodal marginal zone lymphoma

splenic marginal zone lymphoma

116
Q

lymphoplasmacytic lymphoma is also called…

A

waldenstrom macroglobulinemia

117
Q

which lymphoma is associated with an IgM monoclonal gammopathy, over-producing immunoglobulin?

A

lymphoplasmacytic lymphoma

118
Q

At what stage is lymphoplasmacytic lymphoma most often diagnosed?

A

more than 70% of patients have stage IV disease by virtue of bone marrow involvement at the time of diagnosis

119
Q

in lymphoplasmacytic lymphoma, cryoglobulins produce…

A

raynaud phenomenon

120
Q

What type of cells are present in lymphoplasmacytic lymphoma?

A

smudge cells

121
Q

non-hodgkin lymphoma

A

discontinuous groups of lymph nodes- not amenable to surgical excision for cure
extranodal involvement is possible
spleen is often involved
often disseminated at time of dx
painless lymphadenopathy- neck, inguinal and axillary regions MC
constitutional symptoms in 20%

122
Q

multiple myeloma is the neoplastic proliferation of…

A

plasma cells producing a monoclonal immunoglobulin

123
Q

in MM, proliferation of plasma cells causes…

A

skeletal destruction with osteolytic lesions, osteopenia, and/or pathologic fracture

124
Q

what is the epidemiology in MM

A

older age

mean age 66

125
Q

sxs of MM

A

anemia
hypercalcemia
renal dysfunction
increased total serum protein concentration
M-spike (monoclonal protein) on SPEP
Bence-jones protein (light chains from M-protein) in urine *
lytic lesions on skeletal imaging (punched out lesions)
bone pain
pathologic fractures
fatigue
weight loss

126
Q

What are the variations of MM

A

MGUS- monoclonal gammopathy of unknown significance
smoldering myeloma
myeloma with amyloidosis

127
Q

MM diagnosis

A

clonal bone marrow plasma cells greater than 10 percent or biopsy-proven bony or soft tissue plasmacytoma
+
presence of related organ or tissue impairment (anemia, hypercalcemia, renal insufficiency, bone lesions, or greater than 60% of plasma cells)

128
Q

What are the lab findings in MM

A 
SPEP shows M-spike (monoclonal gammopathy) 
elevated immunoglobulin (IgM, IgA, IgG), kappa or lambda, heavy or light chains
129
Q

What is the prognosis for MM

A

without effective therapy, symptomatic patients die within a median of 6 months
non-curable malignancy
stem cell transplant is a treatment option to prolong event free and overall survival

130
Q

myelodysplastic syndrome

A

heterogenous group of malignant hematopoietic stem cell dysplastic and ineffective blood cell production
reduction in the production of cells or reduction in function of existing cells (anemia, thrombocytopenia, leukopenia)
risk progression to AML increased male prevalence, median age at diagnosis is above 65
prognosis is based on risk- 6-54 month survival from the time of diagnosis

131
Q

describe the process of hemostasis

A
  1. endothelial injury and formation of the platelet plug
    2, propagation of the clothing process by the coagulation cascade
  2. termination of clotting by antithrombotic control mechanisms
  3. removal of the clot by fibrinolysis
132
Q

What are the disorders of hemostasis?

A

primary and secondary

133
Q

primary disorders of hemostasis

A
  • primary= initial steps in clot formation, which mostly rely on vessel wall and platelet function
  • disorders of primary hemostasis often present with mucocutaneous bleeding or petechiae
134
Q

secondary disorders of hemostasis

A

secondary= the subsequent formation of the fibrin-based clot, which mostly relies on coagulation factors
disorders of secondary hemostasis present with deep tissue hematoma or joint bleeding

135
Q

what are the disorders of primary hemostasis

A

increased destruction of platelets
decreased production of platelets
platelet dysfunction

136
Q

which disorders of increased destruction of platelets are immune mediated?

A

immune thrombocytopenic purpura (ITP)

heparin induced thrombocytopenia (HIT)

137
Q

which disorders of increased destruction of platelets are thrombotic microangiopathy (TMA)

A

thrombotic thrombocytopenia purpura (TTP)

hemolytic uremic syndrome (HUS)

138
Q

what is DIC

A

disseminated intravascular coagulation (increased destruction of platelets)

139
Q

What is immune thrombocytopenic purpura?

A

antibody mediated destruction of platelets
aka idiopathic thrombocytopenic purpura ITP
can be primary or secondary (autoimmune or infectious)

140
Q

what is the timeline of immune thrombocytopenic purpura?

A

new diagnosed <3 months
persistent 3-12 months
chronic >12 months

141
Q

sxs of immune thrombocytopenic purpura

A

petechia, purpura, bleeding

142
Q

What is heparin induced thrombocytopenia

A

antibody mediated destruction of platelets
acquired with the use of heparin
antibody platelet factor 4 and heparin which triggers thrombosis

143
Q

what are the complications of heparin induced thrombocytopenia

A

stroke
MI
limb ischemia
DVT

144
Q

what is thrombotic thrombocytopenic purpura

A

when abnormalities in the vessel wall of arterioles and capillaries lead to microvascular thrombosis
promote platelet adherence and activation without exposing the blood to large amounts of procoagulant substances
pentad- fever, thrombocytopenia, renal failure, neurologic changes, and micoangiopathic anemia (hemolytic)

145
Q

what is hemolytic uremic syndrome?

A

abnormalities in the vessel wall of arterioles and capillaries that lead to microvascular thrombosis- similar to TTP
complement induced damage to the endothelium from shiga toxin produced by shigella dysenteriae and some kinds of e coli
renal dysfunction is more common than with TTP

146
Q

what is DIC

A

disseminated intravascular coagulation
dysfunction of platelets and coagulation cascade
activation of clotting and fibrinolytic system
thrombin contain fibrin and platelets
release of tissue factor resulting in damage to endothelial cells

147
Q

what are some causes of DIC

A

placental abruption, retained fetus, septic abortion, amniotic fluid embolism
sepsis, meningiococcemia and histoplasmosis
carcinomas of pancreas, prostate, and lung
massive trauma

148
Q

what are the secondary disorders of hemostasis

A

von willebrand disease
hemophilia A
hemophilia B

149
Q

what is the most common inherited bleeding disorder ?

A

von willebrand disease

150
Q

what is the deficiency in von willebrand disease?

A

deficiency of von willebrand factor (carrier for factor VIII)

151
Q

most cases of von willebrand disease are autosomal…

A

dominant

152
Q

sxs of von willebrand disease

A 
bleeding in mucous membranes 
epistaxis 
increased bleeding after trauma 
increased bleeding with menorrhagia 
elevated bleeding time and PTT
PT is normal
153
Q

Which factor has a deficiency in Hemophilia A?

A

factor VIII

154
Q

what kind of genetic disorder is hemophilia A

A

X linked recessive

155
Q

sxs of Hemophilia A

A

hemorrhage after trauma or surgery
hemorrhage into points and soft tissue
intracranial bleeding is MC cause of death
elevated PTT with normal PT and bleeding time

156
Q

what is the deficiency in hemophilia B

A

deficiency of Factor IX

157
Q

what is a hypercoagulable state?

A

increased risk of thromboembolism

158
Q

what are some inherited disorders that cause hypercoagulable states?

A 
Factor V Leiden mutation 
Prothrombin gene mutation 
Protein S deficiency 
Protein C deficiency 
Antithrombin deficiency

Pathophysiology (5 decks)

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