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Post Midterm Patho > Anemia > Flashcards

Anemia Flashcards

1
Q

What is the most common blood disorder? What percentage of the global population are affected?

A

Anemia.

Around 30%.

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2
Q

Anemia is a deficiency in what?

A

RBC or Hb

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3
Q

What is the etiology of anemia? 3 things.

A
  1. Defective erythropoesis
  2. Increased hemolysis
  3. Blood loss
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4
Q

What is the pathophysiology of anemia?

A

Abnormal #, structure or function of RBC –> decreased 02 carrying capacity –> hypoxia

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5
Q

What is the underlying cause for all manifestations?

A

Systemic hypoxia

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6
Q

What are the moderate mnfts for anemia?

A

Chronic fatigue, palpitations, dyspnea

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7
Q

What are the severe mnfts for anemia?

A

Chronic exhaustion, ^^ palpitations, dyspnea, dizziness, headaches, sensitivity to the cold

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8
Q

What is one of the main complications that can be caused by anemia? Why?

A

Acidosis

The systemic hypoxia will cause anaerobic metabolism to occur, therefore lactic acid builds up, therefore acidosis

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9
Q

What are the 7 Types we discuss of anemia?

A
  1. Iron deficiency Anemia
  2. Vit B12 and Folic acid Deficiency
  3. Pernicious Anemia
  4. Aplastic Anemia
  5. Hemolytic Anemia
  6. Hemorrhagic Anemia
  7. Sickle Cell Anemia
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10
Q

Explain Iron deficient anemia:

  1. What is the importance of Fe?
  2. What causes it?
  3. Why is CBC not the blood test choice?
  4. Tx?
A
  1. 02 binds to iron
  2. inadequate intake or increased losses of Fe
  3. Because normal # of RBC and Hb, it is an abnormal structure of Hb
  4. treat underlying cause, PO Fe 4-6 months
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11
Q

What is the importance of Vit B12 & Folic acid?

A

Involved in cell division and DNA synthesis

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12
Q

If there is not adequate levels of Vit B12 or Folic acid, what occurs?

A

Impaired RBC, WBC, platelets

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13
Q

Vit B12 & Folic acid Deficiency causes anemia and what 2 other problems?

A
  1. Problems with Immune Response

2. Problems with coagulation

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14
Q

What is the treatment for Vit B12 & Folic acid Deficiency?

A
  1. Vit B12

2. Folic acid

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15
Q

Describe the process of Pernicious Anemia.

A

Damage gastric mucosa –> no intrinsic factor –> poor or no B12 absorption

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16
Q

What is the importance of intrinsic factor?

A

For B12 to absorbed.

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17
Q

What is the treatment for Pernicious anemia?

A

HIGH dose of B12, so that it can be passively absorbed without the intrinsic factor!
- Can be IM if neuro symptoms are present.

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18
Q

Aplastic anemia occurs when?

A

Bone marrow failure –> not producing enough cells

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19
Q

Do the cells in aplastic anemia have the required components?

A

Yes. The RBC would have heme, globin, and Fe. The problem is there is not enough of them.

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20
Q

What blood cells are affected in aplastic anemia?

A

All of them!

21
Q

What is the etiology of aplastic anemia?

A
  • 1/3 autoimmune, radiation, toxic chemicals

- 2/3 are idiopathic

22
Q

What is the treatment for aplastic anemia?

A
  1. Treat the underlying cause
  2. Transfusions? (ongoing basis)
  3. Marrow transplant in sever cases
23
Q

Define Hemolytic Anemia.

A

Premature or excessive hemolysis.

24
Q

What is the etiology of hemolytic anemia?

A
  1. Acquired (ex. autoimmunity, drugs)

2. Genetic (ex. thalassemia)

25
Q

What are the 3 Manifestations of Hemolytic Anemia?

A
  1. Jaundice
  2. Splenomegaly
  3. Heptaomegaly
26
Q

Why would jaundice occur in hemolytic anemia?

A

Bilirubin is a byproduct of the breakdown of RBC, excessive hemolysis = ^^ bilirubin, overwhelms the liver so accumulates, produced the yellow colouring to skin, sclera, and even inside the body.

27
Q

Why would splenomegaly occur?

A

Enlarged spleen d/t overwhelmed by the excessive breakdown of RBC.

28
Q

Why would Hepatomegaly occur?

A

Enlarged liver d/t overwhelmed

29
Q

What is the treatment for hemolytic anemia? (6 things listed)

A
  1. Underlying cause?
  2. 02 (excessive breakdown would cause decreased 02)
  3. Transfusion ( ^ normal RBC)
  4. Steroids ( Damper hemolysis although not sure why)
  5. Renal Fx (precipitation in renal tubule d/t hemolysis)
  6. Splenectomy (remove the spleen)
30
Q

Hemorrhagic anemia can be classified as _____ or _____.

A

Acute or chronic.

31
Q

Explain the acute hemorrhagic anemia. What is being lost?

What does the severity of it depend on?

A

Rapid loss of whole blood (RBC & Hb)

Severity depends on… site, rate & volume lost

32
Q

Explain the chronic hemorrhagic anemia.

A

Gradual ongoing blood loss

- usually minor but persistent

33
Q

What is the etiology of hemorrhagic anemia? (4 things)

A
  1. Prolonged or heavy menses
  2. Peptic ulcer
  3. Hemerrhoids
  4. CA in GIT (malignancies)
34
Q

What is the treatment for hemorrhagic anemia?

A

Treat the cause.

35
Q

What is considered to be the most complex type of anemia?

A

Sickle cell anemia

36
Q

What is the etiology of sickle cell anemia?

A

It is genetic.

It is a recessive homozygous trait. (both alleles need to be affected in order for the offspring to have the defect)

37
Q

In sickle cell anemia, if only one allele has the defect, what does this mean?

A
  • Heterozygous: sickle cell trait

- would be a carrier. May have no symptoms or very mild anemia.

38
Q

The normal Hb in an adult is HbA. What is the Hb in sickle cell anemia?

A

HbS.

39
Q

HbS is what type of acid?

A

valine.

40
Q

HbA is what type of acid?

A

glutamic acid.

41
Q

Sickle cell anemia is 1 amino acid change (valine instead of glutamic acid) in what ______

A

The Beta chain.

42
Q

HbS crystalizes at dissociation at low P02…this causes the RBC to do what?

A

Deform and sickle.

43
Q

The full patho sequence of sickle cell anemia….

A

HbS crystalizes at dissociation at low P02 –> RBC deforms and sickles –> chronic hemolysis (in vessel and capillaries) –> vessel occlusion –> ischemia –> infarction

This then causes…
Obstructed capillaries –> hypoxia –> more sickling

This then causes….
Increased viscosity –> impairs circulation – Occlusion & Further hypoxia –> more RBCS sickle –> VISCOUS CYCLE!

44
Q

What do the manifestations of sickle cell anemia relate to? 3 things.

A
  1. Hemolysis
  2. Thrombosis & Infarction
  3. Increased Bilirubin.
45
Q

State the 4 treatments for sickle cell anemia.

A
  1. Supportive
  2. Hypertranfusion in increased risk (ex. Sx, pregnancy )
  3. Hydroxyurea
  4. Marrow / Stem transplant
46
Q

Explain the supportive therapy for sickle cell anemia?

A

02, rest, analgesics for pain, IV fluids, electrolytes

47
Q

Explain the hypertransfusion in sickle cell anemia?

A

Ongoing transfusion until circulating blood in pt. is 75% of donor blood.

48
Q

Explain the Hydroxyurea.
2 Benefits:
2 Risks / SE:

A

Benefits:

  1. Brings upon production of fetal hemoglobin (HbF) (wont crystalize, high affinity for 02.
  2. Prevents cells from sickling.

SE/ Risks:

  1. Hepatotoxic (can’t use longterm)
  2. Antineoplastic (known to cause risk for leukemia, toxic to the bone marrow)

Post Midterm Patho (16 decks)

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