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Patho > Hematology > Flashcards

Hematology Flashcards

1
Q

Plasma is __% water and __% solutes

A

90% and 10%

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2
Q

Composition of blood

A

Plasma, water, plasma proteins, electrolytes, gases, nutrients, waste, hormones

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3
Q

Main plasma proteins

A

1) Albumin (large, carrier molecules responsible for oncotic pressure)
2) Globulins
3) Clotting factors (fibrinogen)

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4
Q

Types of globulins

A

1) Alpha and Beta globulins (transport lipids and lipid soluble vitamins)
2) Gamma globulins (made by lymphocytes in the lymph node and are part of the immune response. Most significant of the gamma globulins are the immunoglobulins)

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5
Q

RBC description

A

Non-nucleated cytoplasmic disl of hemoglobin. It’s biconcavity allows for gas diffusion and reversible deformity so that it can squeeze through capillaries. RBCs have the longest average life-span of the blood cells at 120 days.

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6
Q

Examples of granular phagocytes

A

BENM

Basophils, eosinophils, neutrophils, mast cells

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7
Q

Examples of agranular phagocytes

A

Monocytes and macrophages

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8
Q

What is the diference between a leukocyte and a lymphocyte?

A

Leukocyte is a general term for a WBC

Lymphocyte refers to B, T, plasma cells, and NK cells

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9
Q

Are NK cells granulocytes?

A

Yes

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10
Q

What are granulocytes?

A

WBCs with membrane-bound granules that may contain digestive enzymes or biochemical mediators. These cells kill microorganisms, catabolize debris and have inflammatory / immune functions. They also exhibit diapedesis to pass through vessel walls.

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11
Q

Neutrophils

A 
PMN- polymorphonuclear neutrophil
First responder to injury! 
Acts as a phagocyte of cellular debris in early inflammation
55% of WBCs
Reaches maturity in the bone marrow
Lifespan of about 4 days
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12
Q

Eosinophils

A

Ingest antigen-antibody complexes
Involved in the recovery phase of the inflammatory process
1-4% of WBCs

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13
Q

Basophils

A

Least common of the WBCs (<1%)
Contain vasoactive amines (histamine and seratonin)
Contain anticoagulant (heparin)

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14
Q

Mast cells

A

Found in vascularized connective tissue
Involved in acute and chronic inflammation, fibrotic disorders, and wound healing
Releases histamine, chemotactic factors, and cytokines
Causes rapid BV permeability

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15
Q

Lymphocytes

A 
B, T, plasma cells, and NK cells
Mononuclear
25-33% of WBCs
Do NOT contain digestive vacuoles
NK cells, however, are granular
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16
Q

Monocytes and Macrophages

A

Agranulocytes

Are larger and have fewer digestive vacuoles than granulocytes

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17
Q

What cells make up the Mononuclear Phagocyte System (MPS)

A

Referring to MONOcytes (MONOcytes and MONOnuclear!)

From the bone marrow > monoblasts > promonocytes > monocytes (circulating)> macrophage (once in tissue)

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18
Q

What are the functions of the MPS?

A

1) Ingest and destroy microorganisms and foreign material, debris, and defective/dead cells
2) Cleanse the blood in the liver and spleen

Have a life-span of months to years!

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19
Q

Description of platelets

A 
They are not cells in the classical sense (they are disk-shaped fragments of megakaryocytes)
Contain secretory vesicles 
Responsible for blood coagulation
Reserves are located in the spleen
Lifespan around 10 days
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20
Q

Lymphoid system

A

Site for residence, proliferation, differentiation, or function of lymphocytes / MPS

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21
Q

Primary lymphoid organs

A

Thymus and BM

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22
Q

Secondary lymphoid organs

A

Spleen, tonsils, adenoids, Peyer’s patches, and lymph nodes

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23
Q

This is the largest secondary lymphoid organ

A

Spleen

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24
Q

Red splenic pulp

A

This is the main site of filtration. Results in filtration and phagocytosis of old, damaged, and dead blood cells (mostly RBCs). Also filters antigen, microorganisms, and other debris. Site of Hb catabolism (makes sense because it’s red!)

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25
Q

White splenic pulp

A

Masses of lymphoid tissue containing macrophages and lymphocytes. Here, the mononuclear phagocytes cleanse and filter the blood, while the lymphocytes initiate the immune response and convert lymphoid follicles into germinal centers.

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26
Q

What is the spleen?

A

Masses of lymphoid tissue with red and white pulp. Has venous sinuses for blood storage (it acts as a reservoir for blood)

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27
Q

Lymph nodes

A

Provide filtration to the lymph during it’s journey through the lymphatics, towards the SVC. Lymph nodes are the primary site for the first encounter between antigen and lymphocytes. In the germinal centers, B cells respond to antigenic stimulation by undergoing proliferation and further differentiation, including class-switch, into memory cells and plasma cells. Results in antibody formation.

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28
Q

What is hematopoiesis?

A

The production of blood cells. Includes proliferation and differentiation.

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29
Q

Where does hematopoiesis occur?

A

Embryo: liver and spleen
Adults: bone marrow
Diseased states: extramedullary sites (outside the BM)

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30
Q

Marrow biopsy can tell you

A

How much hematopoiesis is occurring depending on the ratio of red:yellow marrow

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31
Q

What causes a higher rate of hematopoiesis, chronic disease or acute hemorrhage?

A

Chronic disease

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32
Q

What is the origin of all peripheral blood cells?

A

Pluripotent hematopoietic stem cells. Found primarily in BM. These cells are uncommitted and multiple possibly indefinitely.

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33
Q

Leukocytosis

A

WBC count above normal

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34
Q

Causes of cytosis and penia

A

Problems with bone marrow (over or underproduction) or premature destruction of cells

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35
Q

Is leukocytosis normal?

A

It is the normal protective physiologic response to physiologic stressors

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36
Q

What is infectious mononucleosis?

A

1) Acute, self-limiting infection of B cells.
2) Often caused by the Epstein-Barr virus.
- Cells have an EBV receptor site
3) Transmitted via saliva and personal contact
4) Symptoms: fever, sore throat, swollen cervical lymph nodes, increased lymphocyte count, atypical (activated lymphocytes). At least 10% atypical lymphocytes

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37
Q

Difference between leukemia and lymphoma

A

Leukemia: bloodstream
Lymphoma: lymph

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38
Q

What is anaplasia?

A

Lack of differentiation (reversal from further committed to less committed cells). Variable in size and shape, multiple atypical mitoses, lack of structure.

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39
Q

Difference between benign and malignant

A

Benign: Well differentiated cells. Features of parent cells are preserved (like hormone release). Tumor is usually well demarcated. No local invasion of distant metastases.

Malignant: Anaplasia (lack of differentiation). Invasive and metastatic.

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40
Q

Sites in the body where cell proliferation is normal

A

BM (myeloblasts), immune cells, epidermal cells, epithelial cells, and regenerating tissues

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41
Q

6 features of cancer cells

A

1) Self-sufficiency of growth hormones
2) Insensitivity to growth inhibition signals (loss of contact inhibition)
3) Sustained angiogenesis
4) Limitless replicative potential
5) Ability to invade and metastasize
6) Evasion of host immune response

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42
Q

Tumors are kind of like ______. They are complex tissues containing ______.

A

Unorganized organs.

Contain tumor cells, fibroblasts, immune cells (in there trying to get rid of it), blood vessels, and lymphatic vessels.

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43
Q

What causes cancer?

A

Direct damage to the DNA. Damage may be caused by diet, hormones, genotoxic carcinogens (cause DNA mutations and replication errors), non-genotoxic carcinogens (change the expression of genes involved in DNA repair, methylation, cell signaling, and proliferation), UV, and x-rays. The extent that these will cause damage often relies on the person’s heredity.

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44
Q

Genotoxic carcinogens

A

cause DNA mutations and replication errors

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45
Q

Non-genotoxic carcinogens

A

change the expression of genes involved in DNA repair, DNA methylation, cell signaling, and proliferation

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46
Q

Genomic instability and cancer

A

Related to dysfunction of p53. There is now no longer regulation of DNA replication. There are no more cell cycle checkpoints or DNA repair and the mutated cell avoids apoptosis.

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47
Q

Non-specific signs of cancer

A

Fatigue, fever, unexplained weight loss, pain, skin changes.

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48
Q

Difference between BM biopsy vs. BM aspiration

A

Biopsy removes bone and marrow.

Aspiration removes only marrow.

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49
Q

What is immunocytochemistry?

A

Detects tumor cells by using antibodies against tumor-specific antigens

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50
Q

Long-term effects of chemo

A

Infertility, secondary cancers, osteoporosis, and growth abnormalities

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51
Q

Cell deviations vary greatly

A

Between different types of cancers, between patients with the same type of cancer, and between subclones of cells within the same tumor

The genetic instability of cancer cells allows them to adapt to the new conditions, and may acquire drug resistance or develop into a more malignant phenotype. If one cell becomes resistant, the other cells die, but this one proliferates (and at a rapid rate cause that’s what cancer does!)

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52
Q

When is chemo strictly contraindicated?

A

Pregnancy. Remember that chemo targets rapidly dividing cells!

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53
Q

Is leukemia benign or malignant?

A

Malignant

54
Q

What is leukemia and what causes it?

A

Malignant disorder of the blood and blood-forming organs (bone marrow). Causes excessive accumulation of leukemic cells. Often due to philadelphia chromosome (translocation btw 9 and 22).

55
Q

Difference between acute and chronic leukemia

A

Acute- affects the undifferentiated, precursor cells.

Chronic- affects terminal / more differentiated cells. The cell is mature, but doesn’t function properly. Primary cells affected at B & T lymphocytes.

56
Q

Acute Lymphocytic Leukemia (ALL)

A

Most common in children

More than 30% of circulating cells are lymphoblasts (they are in the precursor form)

57
Q

Acute Myelogenous Leukemia (AML)

A

Abnormal proliferation of myeloid precursors.

58
Q

Chronic Myelogenous Leukemia (CML)

A

Myeloproliferative disorder. This is a RBC disorder and includes polycythemia vera (the bone marrow is making too many RBCs!!)

59
Q

Chronic lymphocytic leukemia

A

Accumulation of B lymphocytes but they fail to develop into plasma cells

60
Q

Malignant Lymphoma

A

Cancers that begin malignant transformation proliferation of lymphocytes in the lymphoid tissue. This is caused by damage to the DNA of a lymphocyte. The two major categories are hodgkin’s and non-hodgkin’s lymphoma

61
Q

Cells that must be present in lymph nodes for the diagnosis of Hodgkin’s Lymphoma

A

Reed-Sternberg cells. These are necessary for diagnosis, but they are not specific to Hodgkin’s lymphoma

62
Q

Patho of Hodgkin’s Lymphoma

A

Changes in proto-oncoogenes or tumor suppressor genes results in clonal expansion of lymphocytes (B, T, and NK cells). Linked to chromosome translocations, viral and bacterial infections, environmental agents, immunodeficiencies, and autoimmune disorders.

63
Q

Major difference between Hodgkin’s and non-Hodgkin’s

A

Hodgkin’s generally remains localized (Hodgkin likes to stay put! He’s comfy and warm)

Non-Hodgkin’s is more likely to travel to multiple peripheral nodes and often involves the mesenteric nodes.

64
Q

Virchow’s triad of thrombosis

A

Hypercoagulability, abnormal blood flow (turbulence), and endothelial injury

65
Q

What happens when a BV is damaged (when we need to form a clot)?

A

1) Vasoconstriction to minimize blood loss
2) Form a platelet plug to seal the injured epithelium (this is primary hemostasis!)
3) Coagulation cascade is activated, resulting in a protein meshwork (secondary hemostasis)
4) Clot dissolution via fibrinolysis (lysin fibrin). This is tertiary hemostasis.

66
Q

This is the main protein used to form clots

A

Fibrin

67
Q

Why do we form clots?

A

To minimize blood loss, and to repair the tissue below the clot. Once the repair is done, we don’t need the clot anymore.

68
Q

Process of primary hemostasis

A

Platelet plug formation!

1) Exposure to collagen (in the subendothelial matrix)
2) Platelets adhere
3) Platelets become activated and adhere to other platelets
4) Plug is now formed

69
Q

What happens when a platelet is activated?

A

It releases it’s granule contents (prothrombotic factors) and undergoes a conformational change

70
Q

Cascade from prothrombin.

A

Prothrombin is converted into thrombin by factor X. Thrombin then turns fibrinogen into fibrin. The fibrin meshwork is able to trap other cells.

71
Q

What is meant by the intrinsic and extrinsic pathways?

A

These are two cascade pathways that both lead to fibrin formation. Both pathways converge at factor X.

Intrinsic- the platelets themselves generate the pathway
Extrinsic- other cells release cytokines and chemokines that cause clotting

72
Q

Extrinsic pathway

A

Tissue factor (TF is released by damaged endothelial cells)

73
Q

What does factor X do?

A

Converts prothrombin into thrombin.

74
Q

What are the two prostaglandin derivatives and what is their role in clotting regulation?

A

Thromboxane (TXA2)
- Regulates platelets. TXA2 is released by platelets, causing vasoconstriction, activation of other platelets, and increases the number of fibrinogen receptors which allows circulating fibrinogen to bind to platelets and strengthen the clot.

Prostacyclin (PGI2)
- Produced by endothelial cells, and prevents clot formation.Does so by inhibiting the degranulation of platelets and promoting vasodilation.

75
Q

Nitric oxide

A

Released from endothelial cells and is antithrombotic. Causes vasodilation, and decreases the adhesion and aggregation of platelets.

76
Q

Antithrombin III

A

Protease inhibitor released by endothelial cells that inhibits thrombin. This system is downregulated by inflammation, because we WANT clots during inflammation!

This is how heparin sulfate works.

77
Q

Examples of antithrombotics

A

Prostacyclin, Antithrombin III, Tissue factor pathway inhibitor, protein C, and protein S

78
Q

Tissue factor pathway inhibitor

A

Released by endothelial cells. and inhibits factor Xa.

Remember that endothelial cells will release tissue factor as part of the extrinsic pathway.

79
Q

Protein C and Protein S

A

These are the “thrombomodulin system”

Activated protein C (APC) will degrade factors Va and VIIIa.

80
Q

Example of a fibrinolytic

A

tPa (tissue plasminogen activator)

81
Q

How does tPa work?

A

Think about the name. Tissue plasminogen ACTIVATOR!

tPa activates plasminogen to plasmin. Plasmin then cleaves fibrin and fibrinogen

82
Q

What is D-Dimer?

A

It is a product of the breakdown of fibrin and fibrinogen. It is a “fibrinogen/fibin degradation product”. The presence of D-dimer indicates that we are breaking up clots. So that means that there were a lot of clots in our body that are now being broken down.

83
Q

What is thrombocytopenia usually caused by?

A

Often secondary to congenital or acquired conditions that decrease platelets or platelet survival

84
Q

Two types of thrombocytopenia

A

1) Immune thrombocytopenia purpura
- Autoimmune
2) Thrombotic thrombocytopenia purpura
- We have active thrombosis. This thrombosis activates other platelets, decreasing the number of circulating platelets
- Von Willebrane Factor (vWF) is also present on the basement membrane. This tends to be activated during TTP, causing clotting
TTP can be chronic and relapsing, or acute and idiopathic

85
Q

DIC

A

In DIC, there is a shift out of balance between the body’s thrombins and antithrombins. Inappropriate formation of blood clots due to widespread activation of thrombin within the microcirculation as well as release of TF.

Causes many microinfarcts and hemolysis. Widespread damage to endothelial cells.

86
Q

Will D-dimer be increased or decreased in DIC?

A

Increased

87
Q

How to treat DIC?

A

Treat the underlying therapy, canticoagulants, and FFP to replace clotting factors.

88
Q

DIC is caused by widespread activation of

A

Thrombins

89
Q

Steps of DIC

A

1) Homeostasis out of balance between thrombins and antithrombins
2) TF released by endothelial cells
3) Fibrin clots
4) Fibrinolysis (diminished in DIC. We do not remove clots at the rate we form them)

90
Q

Hypercoagulable states are usually related to what?

A

Genetic predisposition

91
Q

Difference between ALL and AML

A

ALL is specific to lymphocytes

AML is all myeloid cells

92
Q

Who produces thromboxane?

A

Activated platelets

93
Q

Locate of heme synthesis

A

Mtochondria

94
Q

Erythropoiesis

A

Uncommitted pluripotential stem cell, proerythroblast, normoblast, reticulocyte, erythrocyte

95
Q

Most common form of hemoglobin

A

HgbA

96
Q

Iron in our bodies

A

67% bound to heme
30% as ferritin, homosiderin, mononuclear phagocytes, and hepatic parenchymal cells
3% lost in urine, sweat, epithelial cells, or gut
Iron gets recycled

97
Q

Anisocytosis

A

abnormal RBC size

98
Q

Poikilocytosis

A

Abnormal RBC shape

99
Q

This type of anemia results in demyelination and neurologic manifestations

A

Pernicious anemia (due to lack of B12 and folate)

100
Q

Diagnosis of pernicious anemia

A 
Look for antibiodies against IF/parietal cells
Gastric biopsy (total achlorhydria)
101
Q

Tx of pernicious anemia

A

B12/folate replacement

102
Q

This anemia results in cracked, brittle, spoon-shaped nails and a red, painful tongue

A

IDA

103
Q

This is the most common anemia in the world

A

IDA

104
Q

Sideroblastic anemia is due to altered

A

mitochondrial metabolism. The mitochondria have problems incorporating iron into heme, resulting in heme deposits around the nucleus of the cell. This results in iron overload in the RBCs and BM.

There will be increased iron deposits in the tissues, resulting in hepatosplenomegaly.

105
Q

Treatment for sideroblastic anemia

A

Pyridoxine therapy (B6). Pyridoxine is involved in the heme synthesis pathway. The mitochondria are fucking up heme, so give them B6 to help them out.

106
Q

This is larger than a macrophage

A

Your mom.

107
Q

Thalassemia is _______-______

A

Microcytic-hypochromic

108
Q

Main patho of thalassemia

A

A mutant gene suppresses the rate of globulin synthesis. This can be a problem with either the alpha or beta chain. This abnormal globulin results in increased RBC hemolysis.

109
Q

Thalassemia treatment

A

Remember that you have lots of hemolysis, resulting in iron overload. Treatment is aimed at

1) Providing normal cells (transfusions and BM transplant)
2) Decreasing hemolysis (splenectomy)
3) Treating the iron overload (chelation therapy)
4) Genetic counseling

110
Q

This type of thalassemia results in erythroblastic hyperplasia

A

Beta thalassemia

There is increased hemolysis, and our BM is trying to keep up as much as possible by pumping out new RBCs.

Also in Beta thalassemia, there is an excess of alpha globulin, which will precipitate in the cell and cause hemolysis. The excess alpha globulin also causes abnormal hemoglobin synthesis, which decreases erythropoiesis and leads to anemia.
So overall in BT, you have anemia from destruction and decreased erythropoiesis.

The kidneys will respond to the anemia by releasing EPO, compounding the problem and further increasing iron absorption from the gut.

111
Q

Sickle cell anemia is _____-_____

A

microcytic?/hypochromic

112
Q

Main patho of sickle cell anemia

A

Genetic defect in hemoglobin synthesis. This defect causes hemoglobin instability and insolubility.

Sickle shape results in hemolysis and prehepatic jaundice, vascular occlusion, activation of other cells and inflammatory response, and recurrent painful episodes.

113
Q

Sickle cell anemia treatment

A

Cured via stem cell transplant. Will result in death otherwise.

114
Q

Fanconi anemia

A

Type of aplastic anemia due to a genetic defect in DNA repair. Most will end up with cancer (AML)

115
Q

Main causes of aplastic anemia

A

1) BM lesion (biopsy will show more yellow than red marrow)

2) Autoimmune reaction against HSCs

116
Q

Aplastic anemia treatment

A

Treat the cause

1) If bone marrow lesion, give bone marrow transplant
2) If autoimmune, give immunosuppresive drugs

117
Q

Pure red cell aplasia

A

Type of aplastic anemia only affecting RBC precursors

118
Q

Causes of hemolytic anemia

A

Accelerated destruction of RBCs due to:

1) Inherited/acquired conditions
2) Issues with BVs/lymphatic tissues
3) Autoimmune hemolytic anemias (AIHAs)

119
Q

Hemolytic anemia treatment

A

“Various”

Too many causes to name discrete treatment modalities

120
Q

Anemias of chronic diseases are ______-______

A

Normocytic-normochromic

121
Q

Patho of anemia of chronic disease

A

The chronic disease state causes a decreased BM response to EPO and altered iron metabolism. These result in a decreased erythrocyte life-span

122
Q

Patho for polycythemia

A

Primary- Abnormality of stem cells in the BM (polycythemia vera). These stem cells may have an increased sensitivity to growth factors.
Seconday - Most common and caused by an increase in EPO due to chronic hypoxia or tumor secretion

123
Q

Treatment for polycythemia

A

Minimize risk for thrombosis
Prevent progression to myelofibrosis and acute leukemia
Phlebotomy

124
Q

Nutritional requirements for hemoglobin synthesis

A

1) Proteins
2) Vitamins (B2, 6, 12, E, C, folic acid, niacin, and pantothenic acid)
3) Minerals (iron and copper)

125
Q

How is Fe stored in the blood?

A

Ferritin/hemosiderin

126
Q

What is the signal for EPO release?

A

Hypoxia

127
Q

This hormone stimulates platelet formation

A

TPO

128
Q

Most important factor in Virchow’s triad

A

Endothelial injury

129
Q

Bone marrow aspiration can not determine _____

A

efficiency of bone marrow activity

130
Q

Bone marrow biopsy is more _______ than aspiration

A

specific and reliable, but also more painful

Patho (14 decks)

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