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Pathophysiology > Ch. 13 ANEMIA > Flashcards

Ch. 13 ANEMIA Flashcards

1
Q

What is the definition of anemia?

A

an abnormally low hemoglobin level, number of circulating red blood cells, or both, resulting in diminished oxygen-carrying capacity of the blood.

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2
Q

What are the causes of anemia?

A

Blood loss

Destruction of RBCs (hemolysis) faster than they can be replaced

Impaired RBC production

  • – lack of nutritional elements
  • – bone marrow failure
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3
Q

How is anemia classified?

A

Based of etiology (such as iron-deficient or hemolytic anemia)

Based morphology

    • MCV, MCH, and MCHC values
    • Size (macrocytic, microcytic, normocytic)
    • Hemoglobin content (normochromic and hypochromic)
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4
Q

What is anisocytosis?

A

Red cells are present in various sizes

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5
Q

What is poikilocytosis?

A

Red cells are present in various shapes

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6
Q

What does microcytic mean and what is it associated with?

A

Smaller than normal. (morphologic)

associated with abnormal hemoglobin production.

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7
Q

What does normocytic mean and what is it associated with?

A

normal size

associated with decreased RBC production or shortened RBC life span

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8
Q

What does macrocytic mean and what is it associated with?

A

Larger than normal.

associated with abnormal erythrocyte maturation (large number of immature “blast” cells)

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9
Q

Why would someone have microcytic cells?

A

Not enough building blocks or a bone marrow issue.

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10
Q

Why would someone have normocytic anemia?

A

renal failure (decreased EPO)

spleen issue destroying RBCs too early

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11
Q

What would the morphology and hemoglobin content be in iron-deficiency anemia? What color would they be?

A

They would be microcytic and hypochromic and pale red in color.

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12
Q

What would the morphology of megaloblastic anemia be? What about their shape?

A

They would be macrocytic and present with poikilocytosis.

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13
Q

What are the different clinical manifestations of anemia?

A

decreased RBC count - pallor and decreased O2 levels
Leads to:

Tissue hypoxia: Muscle weakness, fainting, angina

General adaptation syndrome (gas): vasoconstriction (pallor and sweating), tachycardia

Kidneys release erythropoietin: Bone marrow produces more RBCs: Bone marrow expands: Bone pain and sternal pain

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14
Q

What is hemolytic anemia?

A

This is anemia caused by the premmature destruction of RBCs

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15
Q

What does hemolytic anemia cause?

A

retention of iron and other products of hemoglobin (can lead to a buildup of bilirubin and cause jaundice)

Marked increase in erythropoiesis

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16
Q

What do the cells of hemolytic anemia look like?

A

normocytic and normochromic

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17
Q

What are the signs and symptoms of hemolytic anemia?

A

easy fatigability, dyspnea, and other signs of impaired O2 transport

Also may cause jaundice by a rise in serum bilirubin

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18
Q

What are some of the intrinsic and extrinsic causes of hemolytic anemia?

A

Intrinsic: defect of RBC membrane, various hemoglobinopathies, inherited enzyme defects

Extrinsic: drugs, bacteria, chemical toxins, antibodies, physical trauma

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19
Q

What are the different types of hemolytic anemias and their causes?

A

Membrane disorders: hereditary spherocytosis (no biconcavity), and the acquired hemolytic anemias and hemolytic disease of the newborn.

Hemoglobinopathies: Sickle cell disease, Thalassemia (alpha and beta)

G6PD deficiency

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20
Q

What is sickle cell disease?

A

A point mutation in the beta chains of the hemoglobin that, when is deoxygenated, makes them link together to form a long protein rod that gives the cell a sickle shape.

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21
Q

Why is a newborn protected from sickle cell disease?

A

Because fetal hemoglobin doesn’t have beta chains, they have gamma chains in their hemoglobin until their body makes adult hemoglobin. (usually have all adult hemoglobin after 120 days)

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22
Q

What does it mean that sickle cell disease is an autosomal recessive trait?

A

This means that if mom is a carrier and dad is a carrier then there is a 25% chance that the child will have no disease, 25% chance it will have the disease, and a 50% chance that it will be a carrier with no symptoms.

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23
Q

What is the Hb S (beta mutated hemoglobin) sensitive to?

A

the oxygen content of the RBC

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24
Q

What can the sickling of the cells cause?

A

clumping inside the vessels => obstruction of microcirculation=> tissue hypoxia

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25
Q

Is sickling reversible?

A

YES, it is initially reversible. BUT repeated sickling episodes can lead it to be permanent.

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26
Q

What are some of the precipitating factors of cell sickling?

A

Cold, stress, physical exertion, hypoxia, dehydration, infection, acidosis

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27
Q

What are the clinical manifestations of sickle cell disease?

A

Hemolytic anemia:

    • severe anemia
    • low Hct levels

Chronic hyperbilirubinemia: (sickled cells are more fragile and get destroyed easier)

    • jaundice
    • gallstones

Vaso-occlusion:

    • occlusion of microcurculation=> tissue hypoxia=> severe pain
    • infarction to liver, spleen, heart, kidneys, retina
    • acute chest syndrome
    • stroke (most serious)
    • splenic injury = immunodeficient
28
Q

What is acute chest syndrome?

A

This is an atypical pneumonia resulting from a pulmonary infarction

can cause fever, chest pain, cough

29
Q

What is so special about fetal hemoglobin and why does it pertain to sickle cell disease?

A

They don’t have beta chains, instead they have gamma chains that can’t sickle.

30
Q

Do some adults have some fetal hemoglobin?

A

Yes, and it can protect them from complications with sickle cell disease.

31
Q

What is thalassemia? (hemolytic anemia)

A

inherited disorder also called cooley anemia.

prevalent in mediterranean descent

32
Q

What does thalassemia cause?

A

decreased or defective synthesis of chains of hemoglobin. 2 TYPES, ALPHA AND BETA

33
Q

Describe alpha thalassemia.

A

defective synthesis of the alpha chain of hemoglobin

caused by a defective gene (may have 1-4 genes defective)

affects both fetal and adult Hb

In fetus: gamma4 Hb may form

In adult: beta4 Hb may form

Pretty mild symptoms usually

34
Q

Describe beta thalassemia.

A

defective synthesis of beta chain

caused by a defective gene. (may have 1-2 genes defective)

affects only adult Hb

Alpha4 Hb may form (Heinz Bodies)

often have a coagulation disorder that leads to thrombotic events like stroke or pulmonary emboli

MORE SERIOUS

35
Q

What happens if an infant has Rh+ blood and the mother has Rh- blood the first pregnancy.

A

The mother, once introduced to these Rh antigens, will begin produce antibodies against that antigen.

36
Q

What happens if a mother with Rh- blood has a second baby with Rh+ blood?

A

The antibodies that the mothers body produced during the first pregnancy will cross the placenta and begin attacking the second babies blood.

37
Q

What happens when the mothers Rh antibodies start attacking the fetal blood?

A

agglutination and hemolysis of fetal Rh+ erythrocytes.

38
Q

What are some symptoms in the baby that the mother antibodies began attacking the fetal Rh+ blood?

A

severe anemia

enlargement of the spleen and liver

impaired liver function: edema and jaundice

39
Q

When does the baby start showing symptoms of the mother Rh antibodies attacking its blood?

A

A lot of the time it happens after birth when the core blood starts to mix.

If severe it can also happen in the uterus because the mothers Rh antibodies can cross the placenta.

40
Q

Can the mothers Rh antibodies be prevented from attacking the babies cells?

A

YES, the mother can get a shot to prevent this.

41
Q

Does the mother get the shots that suppress her Rh antigens during her first pregnancy?

A

YES, because the mother could have had a very early miscarriage that was thought to have been a late period that could have caused exposure to the Rh antigens and the mother could have Rh antibodies already built up.

42
Q

What are some anemias of deficient RBC production?

A

Iron-deficiency anemia

megaloblastic anemias

aplastic anemia

chronic disease anemias

43
Q

decscribe iron-deficiency anemia.

A

This is caused by low iron in the diet or chronic or acute blood loss.

typically hypochromic and microcytic and presents with poikilocytosis as well as ansiocytosis (pale in color)

IN EARLY STAGE THEY CAN BE NORMOCYTIC AND NORMOCHROMIC

low hematocrit or hemoglobin

44
Q

describe megaloblastic anemia.

A

can be caused by a cobalamin (B12) deficiency (can be called pernicious anemia)

can also be cause by a folic acid deficiency.

45
Q

describe aplastic anemia.

A

caused by bone marrow depression

can be treated by stem cell transplantation

The body is secreting enough erythropoietin but the bone marrow has an issue with the precursor cells associated with erythrocyte production

46
Q

describe chronic disease anemias.

A

can be cause by chronic renal failure (erythropoietin issues)

chronic inflammation

47
Q

What are some symptoms of iron deficiency anemia?

A

fatigability

palpitations

dyspnea

angina

tachycardia

48
Q

What helps the body absorb iron?

A

vitamin C

49
Q

describe vitamin B12 (pernicious) anemia.

A

a type of megaloblastic anemia

macrocytic with oval or teardrop shapes (poikilocytosis)

neutrophils are hypersegmented.

THIS IS SLOW TO DEVELOP AND USUALLY IS COMPENSATED

CAN BE CAUSED BY DECREASED DIETARY (alcoholic or elderly) INTAKE OR AUTOIMMUNE ATOPIC GASTRITIS

50
Q

What is B12 used for in our bodies?

A

synthesis of DNA

preventing abnormal fatty acids from being incorporated into the neuronal lipids.

51
Q

What can a B12 deficiency cause neurologic symptoms?

A

it predisposes myelin the breakdown and results in neurologic symptoms associated with B12 deficiency.

52
Q

What are the neurologic symptoms associated with a B12 deficiency?

A

symmetric parethesias of the feet and fingers

loss of vibratory and position sense

spastic ataxia (lack of voluntary coordination)

53
Q

How does pernicious anemia cause a B12 deficiency?

A

Our parietal cells in our stomach can’t secrete intrinsic factor to bind to the B12 in the foods we eat so it cant get absorbed.

54
Q

How is pernicious anemia related to autoimmune atopic gastritis?

A

there are anti-parietal antibodies that interfere with the production of intrinsic factor.

55
Q

What is the treatment for pernicious anemia?

A

lifelong IM injections of B12.

56
Q

What does our body use folic acid for?

A

DNA synthesis and RBC maturation.

57
Q

What does a folic acid deficiency often induce?

A

megaloblastic anemia

58
Q

What are the only ways we can tell a B12 and folic acid deficiency anemia apart?

A

folic acid deficiency doesn’t produce any neurologic symptoms or gastric atrophy if it is pernicious anemia.

59
Q

What are some etiologies of folic acid deficiency anemia?

A

inadequate intake (alcoholics, elderly, indigent)

increased demand (pregnancy, infancy, cancer)

folate antagonist chemotherapy (methotrexate)

malabsorption syndromes (usually coupled with many anemias)

60
Q

describe aplastic anemia.

A

primarily a condition of the bone marrow stem cells that results in a reduction of all three hematopoietic cell lines (RBCS, WBCs, and platelets) PANCYTOPENIA

onset can be slow or very acute and severe

61
Q

What are the initial symptoms of aplastic anemia?

A

weakness

fatigability

pallor

petechia (small red or purple dots on the skin caused by small bleeds) LOW PLATELETS

bruises (low platelets)

bleeding (low platelets)

62
Q

Are people with aplastic anemia at a higher risk for infection?

A

YES, because of their decreased white count they have less neutrophils

63
Q

How can aplastic anemia be treated?

A

Stem cell or bone marrow transplants

64
Q

What causes aplastic anemia?

A

exposure to high doses or radiation, chemicals, and toxins (pesticides, chemotherapy, fertilizers) that suppress hematopoiesis

also some immune mechanisms associated with infectious processes like viral hepatits, mononucleosis, AIDS

65
Q

How does sickle cell disease present?

A

they can be in a lot of pain because of ischemia.

Pathophysiology (13 decks)

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