Unit 2 - Blood Disorders (Midterm #1) Flashcards

1
Q

What is the disorder called when there is an excess of RBCs?

A

Polycythemia

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2
Q

What is the disorder called when there is a reduction in hemoglobin (Hb)?

A

Anemia

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3
Q

What is primary polycythemia due to?

A

Due to cancer of erythropoietic cells in the red bone marrow

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4
Q

If a patient has primary polycythemia, how high could you expect their hemoglobin to be?

A

80%

- RBC count as high as 11 million (instead of 4-6 million)

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5
Q

What is secondary polycythemia due to?

A

Dehydration, emphysema, high altitude, or physical conditioning

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6
Q

Why is polycythemia experienced if the patient exercises a lot?

A

The more we exercise, the higher the oxygen consumption, the more RBCs are produced to transport the needed oxygen

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7
Q

What are the dangers of polycythemia?

A
  • Increased blood volume, pressure and viscosity

- Could result in embolism, stroke, or heart failure

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8
Q

What are some clinical manifestations of polycythemia

A
  • Hypertension
  • Dark red or flushed face
  • Headaches, visual problems, neurologic symptoms
  • Splenomegaly
  • Hypercellular bone marrow
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9
Q

If a patient has polycythemia, why would they experience headaches, visual problems, or neurological symptoms?

A

There would be an increase in intracranial pressure

  • there could be hypo-perfusion
  • clotting is possible
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10
Q

If a patient has polycythemia, why would they experience splenomegaly? What is it?

A

An enlarged spleen

- spleen is overworked, breaking down old RBCs causing it to increase in size

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11
Q

At what levels is a patient defined as being anemic?

A
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12
Q

What are the three things that are associated with anemia?

A
  1. Presence of abnormal hemoglobin
  2. Reduced number of RBCs (low hemoglobin, low iron -> low oxygen)
  3. Structural abnormalities of RBCs (don’t have structure that accommodates oxygen binding)
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13
Q

What are the key causes of anemia?

A
  1. Inadequate vitamin B12 - critical for the synthesis of heme
  2. Inadequate folic acid - needed for synthesis of heme
  3. Iron deficiency
  4. Kidney failure (not enough EPO)
  5. Blood loss
  6. RBC destruction
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14
Q

What are the effects of anemia?

A
  • tissue hypoxia and necrosis
  • low blood osmolarity (tissue edema)
  • low blood viscosity (heart races and pressure drops)
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15
Q

What happens if we have low blood osmolarity?

A

If we do not have enough heme in the blood vessel, the water will NOT be drawn into the blood vessel, results in edema in the tissues

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16
Q

What are three etiological classifications of anemia?

A
  1. Decreased hematopoiesis
  2. Abnormal hematopoiesis
  3. Increased loss and destruction of RBCs
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17
Q

What does hematopoiesis mean?

A

To make new RBCs

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18
Q

What are the three causes for decreased hematopoiesis (anemia)?

A
  1. Bone marrow failure
  2. Deficiencies of nutrients
  3. Chronic diseases
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19
Q

What are the two kinds of bone marrow failure in decreased hematopoiesis?

A
  1. Aplastic anemia (deficient in all types of blood cells)

2. Myelophthisic anemia (RBCs retain nuclues, not good for O2 transport)

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20
Q

What are the different types of nutrient deficiencies that cause decreased hematopoiesis?

A
  1. Vitamin B12 and folic acid
  2. Protein deficiency
  3. Iron deficiency
21
Q

What is megaloblastic anemia?

A

Deficient in vitamin B12 and folic acid (decreased hematopoiesis)
- immature RBCs that are released into circulation

22
Q

Why is decreased hematopoiesis caused by a protein or iron deficiency?

A

Globin is a protein (part of hemoglobin) and iron are essential for the transport of O2

23
Q

What are the causes for decreased Fe+2 in the body?

A
  1. Increased loss of iron (chronic bleeding)
  2. Inadequate iron intake or absorption
  3. Increased iron requirements
24
Q

What happens to iron in the stomach?

A

Converted from Fe+3 to Fe+2.
- excessive sue of antacids can lead to inadequate iron absorption (decreasing pH of the stomach so that the conversion cannot occur)

25
Q

What are the two kinds of abnormal hematopoiesis?

A
  1. Sickle cell anemia

2. Thalassemia

26
Q

What is hemolytic anemia?

A

Increased loss and destruction of RBCs (associated with bleeding, intrasplenic sequestration, immune hemolysis, and infections)

27
Q

What in intrasplenic sequestration?

A

When the spleen store RBCs

28
Q

What is hemolytic anemia?

A
  • increased RBC destruction (intracellular or extracellular)
29
Q

What is immune hemolytic anemias?

A

Mediated by antibodies that destroy RBCs

  • mismatched blood transfusions
  • hemolytic disease of newborn
30
Q

What does to following mean?

  • Normocytic
  • Normochromic
  • Microcytic
  • hypochromic
  • macrocytic
A
  • Normocytic = normal size
  • Normochromic = normal colour
  • Microcytic = smaller cells
  • hypochromic = paler cells
  • macrocytic = larger cells
31
Q

Describe sickle-cell disease.

A

Hereditary Hb defect (HbS instead of HbA)

- caused by recessive allele, which modifies hemoglobin structure

32
Q

How does “sickling” occur in Sickle-cell disease?

A
  • beta chains link together when hemoglobin is deoxygenated
  • Forms long chains
  • Chains cause cells to sickle
33
Q

Why do sickle-cells clump together?

A

Sickle cells “poke” each other causing clumpting (aggluntination) that block small blood vessels

34
Q

Why is the cranium and the spleen enlarged for sickle-cell disease?

A

Cranium = constantly producing new RBCs, b/c of hypoxic conditions
Spleen is enlarged b/c it is working to destroy damaged RBCs

35
Q

What protection does sickle-cell disease provide?

A

Protection against malaria

- parasites cannot digest HbS (cannot digest abnormal hemoglobin)

36
Q

What is thalassemia?

A

Genetic defect in the synthesis of HbA that reduces the rate of globin chain synthesis

37
Q

What is the difference between thalassemia minor and major?

A
Minor = only 1 parent had the gene
Major = both parents have the gene
38
Q

What are clinical manifestations of thalassemia?

A
  • hypochromic anemia (paler RBCs)
  • splenomeglay (enlarged spleen b/c RBCs are dying easily)
  • Hemosiderosis = accumulation of iron in tissues
  • Hepatomegaly = enlarged liver b/c of iron storage
39
Q

What is ferritin?

A

Chief iron storage protein in tissues
- If there is a high level of Fe+2 in the blood, there will also be a high level of ferritin, b/c ferritin is needed to transport all that Fe+2

40
Q

What three things result in bleeding disorders?

A
  1. Vessel wall related
  2. Platelet related
  3. Clotting factor related
41
Q

What is the normal platelet count range?

A

130,000 - 400,000 platelets per microlitre

42
Q

What is the function of platelets?

A
  • Secrete clotting factors

- Form temporary platelet plugs

43
Q

What is hemostasis?

A

Stopping the flow of blood

44
Q

What are the two pathways through which normal hemostasis occurs?

A
  1. Extrinsic pathway

2. Intrinsic pathway

45
Q

What factor is part of the common pathway?

A

Factor X (ten)

46
Q

Describe the steps involved in the common pathway.

A

Factor X –> Prothrombinase - converts prothrombin to thrombin. Thrombin converts fibrinogen to fibrin. Fibrin creates strands that plug

47
Q

Why can leukemia cause a platelet disorder?

A

There is a demand for leukocytes, the red bone marrows won’t have space to create megloblastocytes (creates platelets)

48
Q

What does DIC stand for?

A

Disseminated intravascular coagulation

49
Q

What happens during DIC?

A

Infection, tumors, or shock create many small clots in the blood vessels. Prone to thrombi! Increased risk of bleeding b/c all the platelets are being used up in the small clots