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Pathophysiology > Hematopathology > Flashcards

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

A

duodenum

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
Q

Folate Deficiency

A

nutritional (alcoholics, pregnancy/lactation), intestinal diseases (inhibit folate uptake in GI tract): celiacs disease, inflammatory bowel disease

26
Q

How is B12 absorbed?

A

Intrinsic Factor (IF) is secreted by parietal cells in the stomach- required for absorption in the small intestine

27
Q

Vitamin B12 Deficiency

A
  • 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
Q

Anemia of Chronic Disease

A

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
Q

Anemia of Chronic Renal Disease/Renal Failure

A

kidneys produce erythropoietin (EPO)- decreased EPO in chronic kidney disease leads to decrease erythropoiesis, which is treated with recombinant EPO

30
Q

Hemolytic Anemia

A

sickle cell anemia, thalassemia

31
Q

Sickle Cell Anemia

A
  • 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
Q

Beta-Thalassemia

A

“cooley’s anemia”, microcytic/hypochromic, point mutations on beta globin gene: no normal beta globin protein, alpha4 globin forms instead = unstable precipitates

33
Q

What is the result of white blood cell overproduction?

A

infection, leukemias, lymphomas

34
Q

Polycythemia vera

A
  • 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
Q

Blood Coagulation Tests

A

prothrombin time (PT), activated partial thromboplastin time(aPTT), fibrinogen levels, D-dimer levels, platelet levels

36
Q

Prothrombin Time (PT)

A

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
Q

Activated Partial Thromboplastin Time (aPTT)

A

measure of the intrinsic pathway, screens function of factors (XII, XI, IX, VIII, X, V, II and fibrinogen)

38
Q

Platelet Disorder Symptoms

A

bruises easily, bleeding-petachiae (lower extremeties, buccal cavity, pressure points)

39
Q

Thrombocytopenia

A

low platelet count (<150,000/mcL)- risk of spontaneous hemorrhage if <10,000/mcL

40
Q

Acquired Platelet Disorders

A
  • 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
Q

Coagulopathies

A

due to deficient or abnormal/less functional coagulation factors- could be hereditary or acquired

42
Q

Hemophilia

A

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
Q

Hemophilia A

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
Q

Von Willebrand Disease

A

due to abnormal von willebrand factor- autosomal inheritance, which is responsible for platelet adherence after vascular endothelium injury and platelet aggregation

45
Q

How does severe liver disease lead to coagulation defects?

A

the liver produces most coagulation factors

46
Q

How does a vitamin K deficiency lead to coagulation defects?

A

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
Q

Hypercoagulability

A

inherited syndrome, acquired- venous stasis (prolonged immobility or congestive heart failure)

Pathophysiology (4 decks)

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