anemia and RBCs Flashcards

1
Q

What is anemia

A

Decreased circulating red cell mass
Leads to decreased Hemoglobin concentration of blood
leads to ddecreased O2 carrying capacity of blood
Leads to decreased O2 delivery to tissues (final physiologic consequence)

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2
Q

Compensatory mechanisms in anemia

A

increased red cell production

Increased 2,3 DPG, shunting of blood from non-vital to vital areas, increased CO, increased pulmonary Function

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3
Q

SIgns and symptoms of anemia

A

Tissue hypoxia–> weakness, malaise, easy fatigability

Increased RBC production–> marrow expansion with potential bony abnormalities

Shunting of blood to vital organs–> pallor

Increased CO–> tachycardia, cardiac ischemia in severity

Increased pulmonary function–> dyspnea on exertion

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4
Q

funtional classification of anemia

A

blood loss, decreased production, accelerated destruction

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5
Q

Morphologic classification of anemia

A

microcytic:
Normochromic- irond deficiecy early, thalesemia trait, anemia of chronic disease, some hemoglobinopathies
Hypochromic- iron deficiency, thalassemia trait, sideroblastic anemia, anemia of chronic disease

Normochromic/normocytic:
Anemia of chronic diseasea, anemia of renal failure, marrow infiltrative, aplastic anemoa, blood loss hemolysis

Macrocytic:
B12/folate deficiency, liver disease, myelodysplastic syndromes, blood loss, hemolysis, some drugs

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6
Q

investigation of anemia

A

clinical history, physical exam, CBC, Reticulocyte count, peripheral blood smeat diagnostic tests

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7
Q

CBC

A

Hb concentration (HB, g/dl, g/l): hemoglobin in a lysed sample with reagents, complexes are measured spectraphotometrically, MOST IMPORTANT PARAMETER FOR ASSESSMENT OF O2 CARRYING CAPACITY OF BLOOD

Hematocrit (Hct,%): packed cell colume (percentage of blood volume comprised of RBCs, centrifucation or calculated as MCV x RBC, USUALLY 3 TIMES HB DOES NOT ADD INDEPENDENT INFORMATION

RBC count: (direct number / volume, generally correlates well with Hb and Hct, adds little)

Mean cellular/coruscular voluem (MCV fL), measured directly based on either electricla impedence or light scatter, verry useful in differential of anemia (micor-normor, macro cytic anemia)

Mean corpuscular hemoglobin (MCH pg), calculated as Hb/RBC, measure of amount of hemoglobin/RBC, high correlation with MCV

Mean corpuscular hemoglobin concentration (MCHC)measure of chromacity of RBCs, Calculated as Hb/
(MCV x RBC), decreased in hypochromic anemias, increased ina few hyper chromic states- spherocyteosis, hemoglobin CC disease

Red cell distribution width- variation of red cell columes

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8
Q

Microcytic anemia differential diagnosis

A

Iron deficiency, thalassemia, anemia of chronic disease

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9
Q

Macrocytic anemia differential diagnosis

A

megaloblastic (impaired DNA dyntheis (B12 and folate deficiency, some drugs, myelodysplastic syndromes

Non megaloblastic- reticulocytosis, liver disease, hypothryoidism, some drugs

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10
Q

abnormal RBC shape

A
poikilocytosis
Sphericytes- balls
Target cells- targets
Ellipocyteis-ovalocyted
teardrop cells
Sickle cells
schistocyted- fragmented
Bite cells- bites of spleen
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11
Q

REd cell size variabily,

average red cell size

A

Abnormal variablity- anisocytosis

Small average cell- micro, large-macrocytodis

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12
Q

hemoglobinization

A

Hypochromia, normochromia look at central pallor

Polychromasia- reticulocytes- wierd color (blue)

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13
Q

Red cell inclusions

A

Howell jolly bodies (nuclear fragments)- splenectomy megalo- little blue dots
Pappenheimer- iron dots

Basophillic stippling- little blue dots all over rBC

HbC crysitals- large bars

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14
Q

red cell arrangements

A

rouleaux- chains of RBC

Agglutination- globs of RBC (IgM ntibodie)

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15
Q

anemia of blood loss- acute

A

initially no anemia by CBC parameters despite decrease in blood volume

Ademia develops as tissue fluid enters vascular space to restore blood volume, producing dilution of cellular elements

Reticulocyte count will increase after 2-3 days and peaks after 7-10 days

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16
Q

anemia of blood loss- chronic

A

no anemia initially because marrow is able to compensate
Slight reticulocytosis
Eventual development of iron deficiency with resultant iron deficiency anemia

17
Q

RBC production

A

Sites of RBC production- embryo (tolk sac) fetus (liver), bone marrow thru adults

Regulation: decreased o2–> kidney make more EPO, EPO causes prolifertion and differentiation of committed progenitor cells

18
Q

normoblastic maturation

A

normoblasts (nucleated RBC precursors) obtain iron from plasma transferrin for hemoglobin syntheis

Up to 16 retivulocytes produced from each pronormoblast (earliest morphologically recognizable erythroid precursor)

Roughly equal numbers of reticulocytes and normoblasts in marrow

blue- mRNA, red Hb

19
Q

Reticulocytes

A

earliest a nucleat erythroid form, a little larger than mature RBCs, contains residual TNA gives the cytoplasm a blue tinge on routinely stained blood smears (polychromasia)

Stai in marrow for a day or two making Hb, before being released into circulation

Normally continue as reticulocyte for a day in circulation before losing ribosomes, mitchondria, other organelles to become mature erythrocytes

1% of peripheral eirthorocytes
RNA stains, used as a measure of marrow RBC production (percent varies depending on total RBC) theres a corrected percentage and absolute RC

20
Q

Anemia due to decreased RBC production: Innefective erythropoiesis

A

decreased RBC production despite increased RBC precursors in marrow

Characterized by defects in maturation

iron deficiency (cytoplasmic maturation defect), megaloblastic anemia (nuclear maturation defect),
MDS.

Prominent morphologic abnormalities of erythrocytes due to disordered maturation, dysmaturation of of erythroid precursors in marrow, decreased reticulocyte count despite increased erythroid mass in marrow

21
Q

Decreased RBC production: decreased RBC precursors aka marrow failure

A

proliferaton defect

Absolute decrease in the marrow mass of erythroid precusors
(decreased erythroid progenitors available for RBC production, decreased proliferation capacity of numerically adequate erythroid progenitor)

Normochromic/normocytic, usually little anisopoikilocytosis , decreased reticulocyte counts

Stem cell defects with adequate erythropoietin
Marrow replacement, decreased erythropoeietin

22
Q

decreased RBC production due to anemia of chronic disease aka anemia of inflammation

A

inflammatory block in erythropoiesis, IL1 TNF alpha and IFN gamma mediated,

23
Q

Accelerated destruction anemia

A

biconcave RBC, durability , flexibily and tensile strength

spectrin bound by ankyrin

Hemolysis, should live for 120 days, increased destruction results in marrow production (8x normal if needed, with enough iron folate and health)

when destruction>BM compensation, anemia develops

intavascular, extravascular or in combination

24
Q

Extravascular hemolysis

A

most common form of hemolytic anemia

Final common pathway- decreased RBC deformability
Rigid cells cant get in narrow spaces between splenic cords and sinusoids, cells are damaged further with prolonged exposure to cordal envolvement, damaged cells phagocytized by cordal macrophages

25
Q

fate of hemoglobin

A

could go to free haptoglobin in the liver where its dead

or splenic macrophage breaks it up into lipid, protein and heme–metabolized to bilirubin