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PAS 522 Clinical Pathophysiology 1 > Hematology > Flashcards

Hematology Flashcards

1
Q

erythrocytes

A

bio-concave disk shape: thicker portion is red, thinner is pale
no nuclei at maturity
function for about 120 days before degradation by spleen
heme is oxygen binding compound with iron as import atom

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2
Q

major hormone stimulating production of erythrocytes

A

erythropoietin (released by kidney)

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3
Q

presence of nuclei in peripheral blood suggests

A

disease

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4
Q

cytoplasm is filled with granules

A

granulocytes

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5
Q

granulocytes

A

most common white blood cells

neutrophils, eosinophils, basophils

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6
Q

most prevalent granulocytes

A

neutrophils

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7
Q

most important granulocyte in inducing inflammation

A

neutrophils

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8
Q

myelopoiesis

A

granulocyte production which is affected by many cytokines at different stages of development

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9
Q

granules in granulocytes contain

A

enzymes, prostaglandins and mediators of inflammation

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10
Q

basophils

A

very dark blue or purple granules when stained and associated with hypersensitivity reactions

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11
Q

eosinophils

A

red stained granules with bi-lobed nuclei and are part of inflammatory response to parasites

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12
Q

neutrophils

A

major function is in tissue

granules contain highly active enzymes that kill bacteria ingested by the neutrophil

first line of defense against bacterial pathogens

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13
Q

platelets

A

fragment of large multi-nucleated cells-megakaryocytes

crucial to normal blood clotting

stimulated by multiple cytokines (especially thrombopoietin)

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14
Q

maturation of RBCs

A

proerythroblast –> basophil erythroblast –> polychromatophil erythroblast –> orthochromatic erythroblast –> reticulocyte –> erythrocytes

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15
Q

proerythroblast

A

formed from the CFU-E cells

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16
Q

basophil erythroblast

A

very little hemoglobin, stain with basic dyes

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17
Q

polychromatophil and orthochromatic erythroblasts stages

A

cells become filled with hemoglobin

nucleus condenses to a small size and is reabsorbed or extruded from cell

ER is also reabsorbed-at this stage called reticulocyte

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18
Q

reticulocyte

A

contains a small amount of basophilic material (golgi, mitochondria, cellular organelles)

pass from marrow into blood (squeezing through pores in capillary membrane)

remaining basophilic material disappears within 24-48 hrs and cell is considered mature

19
Q

regulation of red blood cell production

A

total mass of RBC tightly regulated within the circulation

adequate number of RBC to transport oxygen

limit production so that cells do not impede blood flow

tissue oxygenation (most important regulator)

20
Q

erythropoietin stimulated RBC production

A

formed mainly in kidneys (90%) and liver (10%)

21
Q

renal tissue hypoxia leads to increased levels of

A

hypoxia-inducible factor-1 (HIF-1)

22
Q

HIF-1

A

binds to erythropoietin gene and increases synthesis of the hormone

23
Q

erythropoietin stimulates production of

A

proerythroblasts from hematopoietic stem cells

24
Q

sickle cell diseases

A

hemoglobinopathy caused by point mutation in beta-globin

hemolytic anemia

microvascular obstruction

ischemic tissue damage

25
Q

hemoglobinopathy caused by point mutation in beta-globin

A

promotes the polymerization of deoxygenated hemoglobin, red blood cell distortion

26
Q

sickle cell trait

A

heterozygous for HbS

asymptomatic

27
Q

sickle cell disease

A

homozygous for HbS

sympotomatic

28
Q

sickle cell diseases pathogenesis

A

interaction of HbS with other types of hemoglobin in the cell

intracellular dehydration increased MCHC and facilitates sickling

intracellular pH reduces oxygen affinity of hemoglobin leading to deoxygenation and sickling

transit time of red cells through microvasculature

29
Q

interaction of HbS with other types of hemoglobin in the cell

A

HbA interferes with HbS polymerization

HbF > HbA in inhibiting polymerization

30
Q

beta thalassemias

A

mutation that diminishes the synthesis of the beta-globin chains

31
Q

beta thalassemias molecular pathogenesis

A

B0 mutation associated with absent beta-globin synthesis

B+ reduced but detectable beta-globin synthesis

32
Q

impaired synthesis of beta-globin results in

A

under-hemoglobinized, hyperchromic, microcytic red cells

subnormal oxygen transport capacity

diminished survival of RBCs and their precursors

33
Q

diminished survival of RBCs and their precursors

A

unpaired alpha-globin chains precipitate

membrane damage occurs

ineffective erythropoiesis

splenic sequestration and hemolysis

34
Q

hereditary spherocytosis pathogenesis

A

caused by diverse mutations

insufficiency of membrane skeletal components (lifespan decreased to 10-20 days)

RBCs take on spheroidal shape and exhibit reduced deformability

spheroidal RBCs are trapped in spleen and subject to macrophage digestion

35
Q

mutations that cause hereditary spherocytosis most commonly affects

A

ankyrin, band 3, spectrin, band 4.2 (tethering interactions that stabilize lipid bilayer)

36
Q

glucose-6-phosphate dehydrogenase (G6PD) deficiency

A

hereditary-recessive x-linked trait

37
Q

G6PD sequence of normal enzyme reactions

A

G6PD reduces NADP to NADPH

NADPH facilitates oxidation or glutathione

glutathione protects against oxidant injury by neutralizing H2O2

38
Q

G6PD deficiency pathogenesis

A

hemolysis of RBC is caused by exposures that generate oxidant stress

oxidants in G6PD-deficient RBCs cause precipitates or inclusions in the RBC called Heinz bodies

as RBCs with these inclusions pass through the spleen, macrophages pluck out the inclusions

39
Q

anemias of diminished erythropoiesis

A

megaloblastic anemias

pernicious anemia: vitamin B12 deficiency

iron deficiency anemia

aplastic anemia

40
Q

peripheral blood findings shared by all megaloblastic anemias

A

RBCs are macrocytic and oval shaped

variation in size and shape (anisocytosis and poikilocytosis)

nucleated RBCs can appear in the blood

neutrophils show nuclear hypersegmentation

marrow is hypercellular

impaired DNA synthesis causes most cell precursors to undergo apoptosis in the marrow

41
Q

pernicious anemia: vitamin B12 deficiency

A

absorption of vitamin B12 requires intrinsic factor secreted by parietal cells of the fundic mucosa

42
Q

pernicious anemia: vitamin B12 deficiency pathogenesis

A

results from autoimmune attack on the gastric mucosa

chronic atrophic gastritis marked by loss of parietal cells and prevention of binding vitamin B12 and intrinsic factor

43
Q

iron deficiency anemia

A

hypochromic, microcytic anemia

disappearance of stainable iron from macrophages (bone marrow)

zone of pallor in RBCs is enlarged and observed only in a narrow peripheral rim of the RBC (peripheral blood smear)

deficiency can result from dietary lack, impaired absorption, increased requirement, chronic blood loss

44
Q

aplastic anemia major etiologies

A

extrinsic: immune-mediated suppression of marrow progenitors
intrinsic: abnormality of stem cells

PAS 522 Clinical Pathophysiology 1 (1 decks)

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