Hematopathology Flashcards

Anemia

1
Q

Erythrocytosis/Polycthemia

A

increase in red blood cell count- HCT and Hb levels high, false/”pseudo”: due to reduction is plasma volume, dehydration, vomiting & diarrhea

  • primary: polycythemia
  • secondary: high altitude
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2
Q

Pancytopenia

A

decrease in all myeloid elements

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3
Q

Leukopenia

A

decrease in white blood cell count

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4
Q

Pancytosis

A

increase in all myeloid elements

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5
Q

Anemia

A

decrease in red blood cell count

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6
Q

Leukocytosis

A

increase in white blood cell count

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7
Q

Neutropenia

A

decrease in neutrophil count

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8
Q

Neutrophilia

A

increase in neutrophil count

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9
Q

Thrombcytopenia

A

decrease in platelet count

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10
Q

Thrombocytosis

A

increase in platelet count

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11
Q

Normocytic Anemia

A

normal size and appearance

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12
Q

Macrocytic Anemia

A

cells larger than normal, high mean corpusular volume(MVC)

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13
Q

Microcytic Anemia

A

cells smaller than normal, low mean corpusular volume(MCV)

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14
Q

Normochromic Anemia

A

Hemoglobin concentration is in normal range, RBCs appear deep red with small area of central pallor

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15
Q

Hypochromic Anemia

A

Hemoglobin concentration is reduced, RBCs have increased area of central pallor

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16
Q

Signs and Symptoms of Anemia

A

tired, easy fatigability, tachycardia, dyspnea, dyspnea on exertion, skin pallor, dizziness,

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17
Q

Pathological Mechanisms of Anemia

A

blood loss, decreased RBC production, increased RBC destruction (hemolysis)

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18
Q

Acute Blood Loss

A

could be: normochromic, normocytic- caused by accident, surgery, parturition/childbirth

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19
Q

Chronic Blood Loss

A

leads to iron deficiency anemia- caused by menstruation, bleeding ulcer, malignant colon cancer

20
Q

Iron Deficiency Anemia

A
  • most common type, could be: microcytic, hypochromic
  • caused by nutritional deficiency, susceptible populations include infants, children, pregnant/lactating women, and pre-menopausal, or chronic blood loss from heavy gynecological bleeding, or GI ulcer or malignancy
21
Q

Where is iron absorbed in the body

22
Q

Iron Laboratory Tests

A

serum ferritin, serum iron, total iron-binding capacity (TIBC), transferrin saturation (TSAT)

23
Q

Anemia Treatments

A

nutritional: supplements, diet recommendations; blood loss: gynecological( hormonal treatments), and GI cancer( surgery)

24
Q

Megalobastic Anemia

A

impaired DNA synthesis, caused by vitamin B12 or folic acid deficiency, macrocytic-normochromic anemia, pancytopenia

25
Folate Deficiency
nutritional (alcoholics, pregnancy/lactation), intestinal diseases (inhibit folate uptake in GI tract): celiacs disease, inflammatory bowel disease
26
How is B12 absorbed?
Intrinsic Factor (IF) is secreted by parietal cells in the stomach- required for absorption in the small intestine
27
Vitamin B12 Deficiency
- caused by autoimmune disorders, surgery such as gastrectomy and removal of terminal ileum - nutritional deficiency (vegans) - treated with cyanocobalamin injections intramuscularly (IM) monthly or large doses of B12 tablets
28
Anemia of Chronic Disease
associated with chronic diseases that produce systemic inflammation, impaired iron utilization, low iron serum volume, reduced total iron-binding capacity, normal ferritin, abundant stored iron in tissue macrophages
29
Anemia of Chronic Renal Disease/Renal Failure
kidneys produce erythropoietin (EPO)- decreased EPO in chronic kidney disease leads to decrease erythropoiesis, which is treated with recombinant EPO
30
Hemolytic Anemia
sickle cell anemia, thalassemia
31
Sickle Cell Anemia
- hereditary hemoglobinopathy - point mutation in beta-globin of hemoglobin, red blood cell distortion - hemolytic anemia- leads to vaso-occlusive crisis:microvascular obstruction- ischemic tissue damage
32
Beta-Thalassemia
"cooley's anemia", microcytic/hypochromic, point mutations on beta globin gene: no normal beta globin protein, alpha4 globin forms instead = unstable precipitates
33
What is the result of white blood cell overproduction?
infection, leukemias, lymphomas
34
Polycythemia vera
- increased marrow production of RBCs, granulocytes and platelets - associated with activating points on the tyrosine kinase JAK2 gene, elevated hematocrit, increased hemoglobin, low serum erythropoietin
35
Blood Coagulation Tests
prothrombin time (PT), activated partial thromboplastin time(aPTT), fibrinogen levels, D-dimer levels, platelet levels
36
Prothrombin Time (PT)
assesses the extrinsic pathway of coagulation - adds recombinant tissue factor to plasma, prolonged of the PT means the patient has functional deficiency in one or more clotting factor (II, V, VII, X, and fibrinogen)
37
Activated Partial Thromboplastin Time (aPTT)
measure of the intrinsic pathway, screens function of factors (XII, XI, IX, VIII, X, V, II and fibrinogen)
38
Platelet Disorder Symptoms
bruises easily, bleeding-petachiae (lower extremeties, buccal cavity, pressure points)
39
Thrombocytopenia
low platelet count (<150,000/mcL)- risk of spontaneous hemorrhage if <10,000/mcL
40
Acquired Platelet Disorders
- Aspirin: acetylates cycloocygenase cox-1, blocks production of platelet thromboxane A2 (necessary for platelet aggregation)- this last for the lifetime of the platelet (7-10 days)- no aspirin before surgery - NSAIDS- reversible inhibition of cyclooxygenase
41
Coagulopathies
due to deficient or abnormal/less functional coagulation factors- could be hereditary or acquired
42
Hemophilia
common types: A (factor VIII deficiency), B (factor IX deficiency)- X linked recessive disorder- symptoms include spontaneous bleeding into joints, muscles, and internal organs
43
Hemophilia A
most common sex-linked bleeding disorder, mutation of factor VIII gene on the X chromosome- bleeding could be mild, moderate, or severe- patients develop arthritis from repeated bleeding into joints- treated with human recombinant factor VIII
44
Von Willebrand Disease
due to abnormal von willebrand factor- autosomal inheritance, which is responsible for platelet adherence after vascular endothelium injury and platelet aggregation
45
How does severe liver disease lead to coagulation defects?
the liver produces most coagulation factors
46
How does a vitamin K deficiency lead to coagulation defects?
vitamin K is required for post-translational modification and functional factors II, VII, IX, and X- vitamin K is produced by gut bacteria so this mostly affects babies and adults with nutritional deficiencies, taking prolonged antibiotics, or colon resection
47
Hypercoagulability
inherited syndrome, acquired- venous stasis (prolonged immobility or congestive heart failure)