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Test 2 Flashcards

(68 cards)

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1
Q

Where is iron stored from normal breakdown?

A

Reticuloendothelial organs like the liver and spleen

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2
Q

What is the transport protein for iron?

A

Transferrin

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3
Q

What is the main storage of iron?

A

Ferritin

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4
Q

What is an iron containing brown pigment derived from hemoglobin when red blood cells disintegrate?

A

Hemosiderin

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5
Q

What percentage of iron is absorbed through diet?

A

5 to 10%

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6
Q

Because ferric iron in foods is not absorbed What does our stomach acid produce this iron to?

A

Ferrous state

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7
Q

What would you see in the pre-latent stage of iron loss?

A

No anemia, however there is iron deficiency. Ferritin level is low, total iron binding capacity is high. Normal peripheral blood smear

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8
Q

What would you see in the latent stage of iron deficiency anemia?

A

Iron stores are exhausted so iron deficient Aretha paresis takes place. Serum iron falls, iron binding capacity increases, transfer and decreases, peripheral smear will see slight microcytic/hypochromic blood

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9
Q

What would you see in Frank anemia?

A

Total iron binding capacity is high everything else MCV MCHC hemoglobin and hematocrit transferin and MCH are low

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10
Q

What are some specific symptoms of iron deficiency anemia?

A

Pica, chelitis, developmental delays in infants, increase in preterm delivery in pregnant woman

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11
Q

Is the reticulocyte count helpful in identifying iron deficiency?

A

No because it’s a measurement of production

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12
Q

What inclusion can be observed after I am deficiency treatment has started?

A

Basophilic stippling

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13
Q

What are the two groups of chronic disease anemia?

A

Chronic renal disease, other chronic illnesses

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14
Q

Would you see an increase in reticulocytes in chronic renal disease?

A

No

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15
Q

What are possible ways of blood loss with anemia of chronic renal disease?

A

Uremia

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16
Q

What are the two causes of chronic renal disease anemia?

A

Failure of renal excretory or endocrine function

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17
Q

What happens in failure of renal excretory function?

A

A buildup of intermediate metabolic products causes red blood cell distortion and shorter lifespan

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18
Q

What happens in failure of renal endocrine function?

A

The kidney fails to produce Erythropoietin

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19
Q

What is the most common source of anemia in hospitalized patients?

A

Anemia of inflammation

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20
Q

When would you see anemia of inflammation?

A

In cases of chronic infection, chronic inflammatory diseases, and malignancies

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21
Q

If there are abundant iron stores in patients with anemia of inflammation, why do they have anemia?

A

Marrow is unable to use iron for hemoglobin synthesis because macrophages are secreting a substance that inhibits the use of stored iron

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22
Q

What would the laboratory results for anemia of inflammatory disease look like?

A

Low hemoglobin and hematocrit transferrin in total iron binding capacity. Platelets and white blood cell count would be high because of the infection. Ferritin would also be high because your body is unable to access stored iron peripheral blood smear would appear microcytic hypochromic

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23
Q

What causes megaloblastic anemia?

A

Defective nuclear maturation

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24
Q

What is asynchronous cell maturation a characteristic of?

A

Megaloblastic anemia

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25
What were the laboratory results of megaloblastic anemia include?
Pancytopenia, reticulocytes, an increase of lactate dehydrogenase, increased Billy Rubin, macrocytic red cells, marked poikilocytosis including oval macrocytes teardrops, how will jolly bodies, target cells, hypochromia, polychromasia, nucleated red blood cells
26
Will the myeloid erythroid ratio be increased or decreased in lab results from megaloblastic anemia?
Decreased
27
A deficiency of Folic acid leads to what?
Impaired DNA synthesis in erythroid cells causing megaloblastic erythropoiesis
28
What are common causes of a folic acid deficiency?
Severe alcoholism and poor diet’s. This is because alcohol blocks to folate metabolism
29
What laboratory results would you look for to identify a folic acid deficiency?
Decreased folate assay
30
What is the most common cause of a megaloblastic anemia due to vitamin B 12 deficiency?
Pernicious anemia
31
In a patient with pernicious anemia the parietal cells of the gastric mucosal are unable to secrete what?
Intrinsic factor
32
What are the lab results in pernicious anemia?
Lack of free HCL, decreased B12, serum iron, indirect Billy Rubin, and folic acid or all normal to increased along with LDH Peripheral smear will be that of a megaloblastic anemia
33
What do patients have a pernicious anemia develop an antibody to?
An antibody to intrinsic factor or parietal cells
34
What are the test for a pernicious anemia?
They test for antibodies to intrinsic factor is the ELISA a test for antibodies to parietal cells is the ANA
35
How would you go about differentiating megaloblastic anemia’s?
Look at results for vitamin B12 and folate levels, methylmalonic acid and homocysteine will be increased in vitamin B 12 deficiency
36
What are other causes for macrocytes? Other than megaloblastic anemia’s
Hypothyroidism, chronic liver disease, alcoholism, newborns
37
What is the cause of hemolytic anemia is?
Hemolysis
38
What characteristic shapes can be seen in a peripheral spiel of a hemolytic anemia patient?
Spherocytes and polychromasia
39
What are two types of homolysis?
Intravascular hemolysis which is the fragmentation of red blood cells in extravascular hemolysis which is macro phages mediated
40
Red blood cells lysing in the circulating blood is an example of what kind of hemolysis?
Intravascular
41
What can cause intravascular hemolysis?
Complement destruction of red blood cell, mechanical damage, damage by toxins
42
What would you expect to see in an intravascular hemolysis laboratory results?
Hemoglobin and hematocrit along with red blood cells and haptoglobin will be decreased Billy Rubin lactose dehydrogenase retics will be increased
43
What are some anemias with intravascular hemolysis?
Glucose six phosphate dehydrogenase deficiency and peroxisomal nocturnal hemoglobinuria
44
Red blood cells getting destroyed by organs in the reticuloendothelial system is characteristic of what homolysis?
Extravascular
45
What will you see in the laboratory results for someone with extravascular homolysis?
Hematocrit and hemoglobin along with red blood cells and haptoglobin will be decreased Reticulocytes Billy Rubin and lactate dehydrogenase will be increased
46
What are some anemias associated with extravascular homolysis?
Pyruvate kinase deficiency, glucose six phosphate dehydrogenase deficiency, hereditary spherocytosis, hereditary elliptocytosis
47
What are the two types of hemolytic anemia’s?
Intrinsic and extrinsic
48
Intrinsic hemolytic anemia’s are due to a defect in what?
The individual red blood cell
49
What are causes of intrinsic defects?
Abnormal hemoglobin’s, defective glycolysis, membrane abnormalities
50
Pyruvate kinase deficiency causes what in red blood cells?
Red cells are unable to generate ATP this leads to a build up of two, 2,3-DPG and results in rigid inflexible cells
51
What would you expect the lab results of pyruvate kinase deficiency to be?
Fairly normal, normacytic/normochromic with Hines bodies and Mark polychromasia
52
What triggers G6 PD anemia?
Exposure to certain oxidative drugs
53
What causes the red cells to suffer oxidative damage in G6PD deficiency?
Reduced NADPH is not produced
54
What would the laboratory findings of G6PD deficiency be?
Hemoglobin and hematocrit, red blood cells, and have to globe and would be decreased reticulocytes LDH, Billy Rubin, white blood cells, plasma hemoglobin would be increased. The peripheral smear would appear normacytic/normochromic with marked polychromasia and bite cells may be present
55
What is used to test for G6PD deficiency?
Quantitative spectophotometric assay
56
What are some intrinsic hemolytic anemia is due to red blood cell membranes abnormalities?
Hereditary Spherocytes, hereditary elliptocytes and proximal nocturnal hemoglobinuria
57
What causes hereditary spherocytosis?
A deficiency of the key membrane protein Ankynn or Spectrin
58
What would the laboratory results of hereditary spherocytosis look like?
An increase in reticulocytes,RDW (important for diagnosis), and Bilirubin. MCHC, and MCV would be decreased The peripheral speaker would have spherocytes, polychromasia, and possibly nucleated red blood cells
59
What’s a confirmatory test for hereditary spherocytosis?
Osmotic fragility
60
What causes paroxysmal nocturnal hemoglobinuria?
Chronic, continuous intravascular hemolysis caused by mutation in the hematopoietic stem cell gene PIG-A which results in missing surface proteins cd55,CD 59, and CD 487, which prevents activation of compliments
61
What are the laboratory findings in proximal nocturnal hemoglobinuria?
Pancytopenia, hemoglobin and hematocrit are decreased, if severe anemia coffee colored urine and hemosiderin in urine
62
What are test used to diagnose paroxysmal nocturnal hemoglobinuria?
Flow cytometry, sugar water test, hams test
63
What causes hereditary elliptocytosis?
Gene mutations disrupt linkages and caused effective or deficient spectrin
64
Laboratory results of hereditary elliptocytosis would involve what?
Pretty normal however 25% or more of the population of red blood cells would be elliptocytes
65
Peroxisomal cold hemoglobinuria is caused by what?
Auto anti-P anti-body it attaches to red cells at lower temperatures and activate complement at warmer temperatures causing lysis.
66
What are the laboratory results of paroxysmal cold hemoglobinuria?
Increased reticulocytes and Bilirubin, hemoglobinuria, hemoglobinemia peripheral smear will have polychromasia spherocytes, schistocytes, nucleated red blood cells, anisocytosis, erythrophagocytosis
67
How is peroxisomal cold hemoglobinuria detected?
Donate- Landsteiner test Blood is split into two parts when is inoculated at 37° for one hour the other is inoculated at 4° for 30 minutes the second tube is checked for homolysis
68
What are the four causes of extrinsic hemolytic anemia’s?
Destruction due to antibodies, mechanical damage like a prosthetic heart, alterations in plasma lipids as seen in instances of liver disease, and infectious agents and toxins like malaria or snake venom

Hemo 2 (7 decks)

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