Anemia Flashcards by Megan Carnahan

normal total circulating blood volume

6-8 liters

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flow rate of blood

5L/ min

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What is in plasma?

water
proteins
carbohydrates
electrolytes
enzymes AST and ALT
Bilirubin
BUN, creatine

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what do high levels of BUN and creatine indicate?

impaired kidney function

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which enzymes indicate impaired liver functions?

AST and ALT

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what are the formed elements in blood?

Red blood cells
platelets
white blood cells

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What accounts for 45% of packed cell volume in blood?

Red Blood Cells

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Where are all cells in the blood made?

bone marrow
primarily flat bones: skull, sternum, pelvis

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hematopoietic stem cells

cells that are committed to become blood cells

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erythropoiesis

process by which red blood cells are produced
takes 5-14 days to complete
3-4 mitotic cell divisions
each stem cell can make 8-16 cells

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Reticulocyte

precursor to erythrocytes

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Red blood cell differentiation

degeneration of nucleus and organelles
reduction in size
accumulation of hemoglobin

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RBC physical characteristics

bionconcave disc to increase surface area
7um in diameter, 2 um thick
one of the smallest cells in the body

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Density of erythrocytes in blood

4-6 x 10^6 /mm^3

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How long does a new RBC stay in circulation?

100-120 days

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as an RBC ages what does the membrane do?

becomes rigid

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Functions of erythrocytes

pick up oxygen from the lungs and deliver it to tissues elsewhere
oxygen binds to iron atom at the center of heme
each erythrocyte contains 280 million molecules of hemoglobin

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Density of hemoglobin

12-16g/dL

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What determines the rate of RBC production?

Tissue oxygenation

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Hypoxia

lower than normal oxygen levels detected by the cells kidneys
decr blood flow
pulmonary diseases
decr RBC density and or decrease hemoglobin concentration
kidneys release erythropoietin

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Erythropoietin

a glycoprotein
hematopoietic growth factor
90% in kidneys; 10% in liver
constantly being produced
accelerates erythropoiesis when this is increased

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Which organs filter blood?

spleen and liver

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Monocytic-phagocytic system

network of cells residing in tissues that trap and digest aged RBC
recovers iron and amino acids
released from destroyed RBCs

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Why must 1% of RBC must be replaced each day?

to maintain homeostasis

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anemia

rate of RBC removed from circulation > rate of their replacement

Examples of anemia that result in decreased production of erythrocytes

Iron, B12, Folic Acid, Aplastic Anemia

Examples of anemia that results in increased destruction or loss of erthrocytes

acute blood loss hemolytic anemia

Clinical symptoms of anemia

pallor tiredness dyspnea, shortness of breath palpitations intermittent claudication decreased cognitive function

Hematocrit

RBC volume expressed as a fraction of total blood volume (37-47%)

Hemoglobin Level

concentration of oxygen carrying protein indicative of O2 carrying capacity (12-16 g/dL)

Reticulocyte counts

immediate precursor of RBC normal range 0.5-1.5% in blood reflects bone marrow activity low-> depressed erythropoiesis high-> stressed erythropoiesis

Polychromasia

variation in color (Hb-heme iron content) normochromic hyperchromic hypochromic

Mean corpuscular hemoglobin

average color of red blood cells

Ansiocytosis

variation in size normcytic microcytic macrocytic

mean corpuscular volume

average size of RBC

Poikilocytosis

variation in shape of RBC

Divalent metal transporter

absorbs elemental iron in the lumen

Transferrin

iron transport in blood circulation

ferritin

iron storage in tissues

iron absorption rate from diet

5mg/day

Iron distribution in body

4g total 2-3g hemoglobin <100mg myoglobin/enzyme/cytochromes

Iron demand

20-30 mg/day

Iron storage

ferritin 1 g

iron loss and typical intake

1-2 mg/day

How much iron is stored in the liver?

30 times daily needs

iron deficiency anemia becomes evident when hemoglobin concentration falls below?

10 g/ dL

symptoms of iron deficiency anemia

tired pale skin papillary atrophy and erythema of the tongue pearly white sclerae in eyes slight cardiomegaly tachycardia

Diagnosis of Iron deficiency anemia can be made based on

decreased Hb and Hct decreased MCV and MCH decreased ferritin increased transferrin

What does TIBC stand for?

total iron binding capacity

How should iron deficiency anemia be treated?

cannot be corrected by increasing dietary intake alone 2 months Hb is normal after iron therapy iron supplements should be used for another 6-12 months

Iron content in OTC products

ferrous fumarate > ferrous sulfate > ferrous gluconate

Folic acid deficiency

nutritional and megaloblastic anemia required for proliferation and differentiation of cells found in all food especially greens, yeast and liver treat with continual dietary supplement

How much folic acid is stored in the liver?

5-10 mg

Etiology of folic acid deficiency

pregnancy malabsorption syndromes inadequate dietary intake liver diseases some medications interfere with the absorption of folic acid

Vitamin B12 is important for?

DNA synthesis

Causes of Vitamin B12 deficiency

diet chronic alcoholism crohn’s disease abdominal or intestinal surgery that eliminates the site of intrinsic factor production/absorption

Pernicious Anemia

type of anemia due to inability to absorb B12 in the digestive tract autoimmune incr MCV decr MCH IF-antibodies

What do parietal cells secrete?

intrinsic factor

Schilling Test

used to determine if B12 can be absorbed orally

Megaloblasts

describe both folic and B12 deficiencies poorly differentiated, immature red cells

What does RDW stand for?

red cell distribution width

Clinical features common to both B12 and folate

megaloblastic anemia fatigue weight loss diarrhea loss of appetite fever sore tongue jaundice fundal hemorrhages in severe cases

Clinical features of Vitamin B12 deficiency

paraesthesiae dementia neuropathy demyelination of spinal cord

Clinical features of pernicious anemia

family and personal history of vitiligo autoimmune thyroid disease itself

What can mask the long term effects of B12 deficiency? How does it do it?

High dose folate temporarily reverses anemia without correcting the neurological damage

What are the types of increased destruction anemia?

Hemolytic Anemia- Glucose-6-Phosphate dehydrogenase deficiency hereditary cell defects drug induced

Sickle Cell Anemia

Hct that are about half the normal value production of RBCs in the bone marrow increases dramatically, but is unable to keep up with the destruction RBC production increases 5-10 fold half life of RBCs can be as low as 4 days recessive genetic disorder Point mutation Hydrophilic Glu -> hydrophobic Val HbA-> HbS aggregate to bury Val