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Advanced Pathophysiology > Hematology > Flashcards

Hematology Flashcards

1
Q

Name the three types of cells that result from lymphopoiesis.

A
  1. NK cell
  2. Plasma (B) cell
  3. T cell
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2
Q

Name the types of cells that result from the myeloid stem cell:

A
  1. Erythrocytes
  2. Platelets
  3. Basophils
  4. Eosinophils
  5. Neutrophils
  6. Monocytes/Macrophages
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3
Q

From what does all hematopoietic and lymphopoietic stem cells originate?

A

The pluripotent stem cells (then myeloid and lymphoid)

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4
Q

Describe the components of blood.

A

Plasma (55%)
RBCs (45%)
Buffy Coat-WBCs and platelets (<1%)

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5
Q

What is the main function of the RBCs?

A

Gas transport. Delivery/transport of O2 and getting rid of CO2

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6
Q

Name the two different categories of leukocytes.

A

Granulocytes and Agranulocytes

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7
Q

Which leukocytes are granulocytes?

A

Phagocytes: Neutrophils, Eosinophils, Basophils, and Mast cells

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8
Q

Which leukocytes are agranulocytes?

A

Phagocytes: Monocytes(blood) and macrophages(tissue)

Immunocytes/lymphocytes (T and B): NK cells (granular-atypical)

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9
Q

Describe erythropoiesis.

A

Pluripotent stem cell is stimulated by erythropoietin which creates a nucleated committed proerythroblast. Next the nucleus shrinks and is reabsorbed creating a normoblast. This then becomes a non-nucleated reticulocyte which leaves the marrow and enters the blood stream. The cell then becomes an eyrthrocyte and Hb synthesis ceases.

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10
Q

What is the normal reticulocyte count and what is it an indication of? Which type of patient would have a higher reticulocyte count?

A

Less than 1%. It indicates the effectiveness of erythropoiesis. Anemic or sickle cell patients.

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11
Q

What role do the kidneys play in erythropoiesis?

A

The peritubular cells of the kidney release EPO which stimulates erythrocyte production. Released in hypoxic state.

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12
Q

What is the breakdown of iron in the body at any given time.

A
  • 67% is bound to heme
  • 30% stored bound to ferritin or hemosiderin (mononculear phagocytes or hepatic parenchymal cells)
  • 3% lost in the urine/sweat/gut/epithelial cells
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13
Q

Explain the iron cycle.

A

Iron is released by the liver and transported in the plasma as transferrin. The transferrin binds to receptors on the erythroblast membrane (in bone marrow) and transported to the erythroblast mitochondria binding to heme and forming hemoglobin and released into the blood stream. The iron is removed from the bloodstream by macrophages in the spleen and broken down. It is stored as ferrtin in the tissue or transferred as transferrin to bone marrow to begin process again.

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14
Q

Define anemia.

A

Decrease in the total number of erythrocytes in the circulating blood or in quality/quantity of Hb

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15
Q

Name three common causes of anemia.

A

1- Decreased erythrocyte production
2- Increased erythrocyte destruction
3- Acute/chronic blood loss

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16
Q

What are MCV, MCH, and MCHC values?

A

Mean corpuscular volume (cell size)
Mean corpuscular Hb (Hb amount per cell)
Mean corpuscular Hb concentration (Hb amount relative to cell size)

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17
Q

Macrocytic Normochromic anemias include(2):

A

Megaloblastic Anemia and Pernicious Anemia

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18
Q

Describe Megaloblastic Anemia

A

A macrocytic normochromic anemia. Unusually large stem cells. Defective DNA synthesis d/t deficiencies in B12 and folate.

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19
Q

Describe Pernicious Anemia

A

A macrocytic normochromic anemia. Lack of IF from gastric parietal cells=unable to absorb B12 which is necessary for nuclear maturation and DNA synthesis.

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20
Q

What roles do Vit B12 and folate play in Hb synthesis?

A

Vit B12 aids in DNA synthesis and maturation of RBCs. Folate aids in DNA/RNA synthesis and cell maturation.

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21
Q

Normocytic Normochromic Anemias include(4):

A

Sickle Cell Anemia
Hemolytic Anemia
Aplastic Anemia
Anemia of Chronic Disease

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22
Q

Describe Sickle Cell Anemia

A

Normocytic Normochromic Anemia. Genetic defect that causes cells to sickle in the absence of O2. Cells are more stiff, tend to cluster and could thrombose. Tx: bone marrow transplant.

23
Q

Describe Hemolytic Anemia

A

Normocytic Normochromic Anemia. Premature/accelerated destruction of RBCs, inappropriate bone marrow compensation, destroy but do not replace fast enough. Could be inherited/acquired, autoimmune, or drug induced. S/s: Jaundice d/t inability to excrete all the bili produced by hemolysis/iron

24
Q

Describe Aplastic Anemia

A

Normocytic Normochromic Anemia. Characterized by pancytopenia. Bone marrow failure or suppression of production. D/t excess hypocellular/fatty bone marrow or autoimmune disease that attacks hematopoietic stem cells.

25
Q

Describe Anemia of Chronic Disease

A

Normocytic Normochromic Anemia. Mild to moderate anemia (AIDS, RA, lupus, hepatitis, renal failure, malignancies). Decreased erythrocyte life span, ineffective bone marrow response to EPO, altered irone metabolism. Example-renal disease: peritubular cells do not detect hypoxia and do not release EPO.

26
Q

Microcytic Normochromic Anemias include (3):

A

Iron Deficiency Anemia
Sideroblastic Anemia
Thalessemia

27
Q

Describe Iron Deficiency Anemia.

A

Microcytic Normochromic Anemia R/t chronic blood loss, inadequate intake, or metabolic/functional deficiency. Iron not available for use in the bone marrow

28
Q

Describe Sideroblastic Anemia

A

Microcytic Normochromic Anemia Abnormal mitochondrial metabolism=unable to take iron up into mitochondria to make Hb Characterized by Fe overload in the blood and ringed sideroblasts

29
Q

Describe Thalassemia

A

Microcytic Normochromic Anemia Imbalance of beta and alpha d/t to mutant gene that suppresses rate of globin chain synthesis causing increased hemolysis resulting in decreased RBC survival rates. Example in beta thalassemia there is an alpha excess d/t a deficit in beta function. May have iron overload requiring chelation.

30
Q

Myeloproliferative Disorders include (1):

A

Polycythemia

31
Q

Describe Polycythemia

A

Overproduction of RBCs.

Relative: Dehydration, fluid loss results in relative increase in red cell counts and Hb/Hct values

Absolute:
Primary: Abnormality in bone marrow/stem cells leading to overproduction (polycythemia vera= increase in all blood cells, splenomegaly, and increased sensitivity to GF. Goal=prevent leukemia)

Secondary: Increase in EPO in response to chronic hypoxia/tumores. ie-lung cancer, high altitudes.

32
Q

Name the three components of a blood clot.

A

Localized vasoconstriction
Platelet activation
Coagulation cascade

33
Q

Describe the hemostasis sequence.

A
  • Localized vasoconstriction
  • Primary Hemostasis: Platelet Activation
  • Secondary Hemostasis: Coagulation cascade
  • Tertiary Hemostasis- Clot Dissolution
34
Q

______ are complex cell fragments containing numerous chemical mediators that are released when activated. They display a variety of cell surface proteins that mediate both adhesion to exposed endothelium and aggregation.

A

Platelets

35
Q

Describe the intrinsic pathway of the coagulation cascade.

A

Activated when blood is exposed to surface factors resulting in the activation of Factor XII initiating a cascade that ultimately activated Factor X, the first step in the final common pathway that leads fibrinogen polymerization(by thrombin) to fibrin.
**Workhorse

Activated factor Xa is the site at which the intrinsic and extrinsic coagulation cascades converge. The extrinsic pathway is initiated at the site of injury in response to the release of tissue factor (factor III) and thus, is also known as the tissue factor pathway

36
Q

Describe the extrinsic pathway of the coagulation cascade.

A

Activated when blood is exposed to tissue factors during tissue injury. Subsequent activation of Factor VII leads to the final common pathway.
**Spark by activating thrombin

–The mechanism that produces fibrin following tissue injury, beginning with formation of an activated complex between tissue factor and activated factor VII and leading to activation of factor X, which induces the reactions of the common pathway of coagulation

37
Q

What is required for hepatic synthesis of several coagulation factors?

A

Vitamin K

38
Q

Fibrin + activated platelet=_______

A

CLOT

39
Q

What does fibrinogen need to be activated to fibrin?

A

Fibrinogen must be ‘cleaved’ by thrombin.

40
Q

Homeostasis is a balance of______ and_______

A

Coagulation and Fibrinolysis

41
Q

What part does thrombin play in fibrinolysis?

A

The release of thrombin causes the plasminogen to become its activated form, plasmin which helps to break up fibrin clots by digesting fibrinogen and fibrin. Thrombin also produces antithrombin. Both produce negative feedback for the clotting cascade and help to maintain a balance or homeostasis.

42
Q

Describe DIC.

A

An acquired hemorrhagic syndrome in which clotting and bleeding happen simultaneously. Widespread clotting in small vessels leads to consumption of clotting factors and platelets causing bleeding. Ie- incompatible transfusion, abruptio placentae

43
Q

Von Willebrand factor is released by:

A

endothelial cells and platelets.

44
Q

What is leukemia?

A

Leukemia is a collection of cancers which create a large amount of immature blood cells. These immature blood cells take up space in the bone marrow, preventing the bone marrow from making healthy blood cells such as platelets, red blood cells, and white blood cells

45
Q

What is the distinguishing factor of Acute Leukemia?

A

Acute leukemias affect the cells early in the maturation process. They are characterized by the presence of undifferentiated/immature, usually blast cells. The onset is also acute/quick.

46
Q

What is the distinguishing factor of Chronic Leukemia?

A

Chronic leukemias affect the cells later in the maturation process. The cells mature but do not function normal. The onset is chronic or slow.

47
Q

Describe Acute Lymphocytic Leukemia

A

ALL is characterized by >30% lymphoblasts in BM/blood and is most common in children.

48
Q

Describe Acute Myelogenous Leukemia

A

AML is an abnormal proliferation of myeloid precursors; immature blast replacement of normal cells.

49
Q

Describe Chronic Myelogenous Leukemia

A

CML is a myeloproliferative disorder. Polycythemia vera is an exemple. Associated with the Philadelphia chromosome.

50
Q

Describe Chronic Lymphocytic Leukemia

A

CLL is an accumulation of B lymphocytes in the immature phase, which are unable to activate into plasma cells.

51
Q

Define Malignant Lymphoma

A

Cancers that begin malignant transformation of a lymphocytes and proliferation of lymphocytes, histiocytes, their precursors and derivatives in lymphoid tissues. An injury to the DNA of a lymphocyte.

52
Q

Describe Hodgkin Lymphoma

A
  • Localized to single center group of lymph nodes (cervical, mediastinal)
  • Mesenteric nodes rarely involved
  • Orderly spread and contiguity
  • Extranodal involvement is rare
  • Disease is often localized
  • Presence of Reed-Sternberg cells (large multinucleated cells, not specific to Hodgkin lymphoma but are necessary for diagnosis)
53
Q

Describe Non-Hodgkin Lymphoma

A
  • Multiple periphery nodes involved.
  • Mesenteric nodes often involved.
  • Noncontiguous
  • Exranodal involvement is common
  • Rarely localized, usually spreads
54
Q

Fibrinolysis occurs in response to:

A

Plasmin

Advanced Pathophysiology (12 decks)

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