Post Midterm Patho > Anemia > Flashcards

Anemia Flashcards

(48 cards)

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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?

21
Q

What is the etiology of aplastic anemia?

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A
  • 1/3 autoimmune, radiation, toxic chemicals

- 2/3 are idiopathic

22
Q

What is the treatment for aplastic anemia?

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

Define Hemolytic Anemia.

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A

Premature or excessive hemolysis.

24
Q

What is the etiology of hemolytic anemia?

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A
  1. Acquired (ex. autoimmunity, drugs)

2. Genetic (ex. thalassemia)

25
What are the 3 Manifestations of Hemolytic Anemia?
1. Jaundice 2. Splenomegaly 2. Heptaomegaly
26
Why would jaundice occur in hemolytic anemia?
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
Why would splenomegaly occur?
Enlarged spleen d/t overwhelmed by the excessive breakdown of RBC.
28
Why would Hepatomegaly occur?
Enlarged liver d/t overwhelmed
29
What is the treatment for hemolytic anemia? (6 things listed)
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
Hemorrhagic anemia can be classified as _____ or _____.
Acute or chronic.
31
Explain the acute hemorrhagic anemia. What is being lost? What does the severity of it depend on?
Rapid loss of whole blood (RBC & Hb) | Severity depends on... site, rate & volume lost
32
Explain the chronic hemorrhagic anemia.
Gradual ongoing blood loss | - usually minor but persistent
33
What is the etiology of hemorrhagic anemia? (4 things)
1. Prolonged or heavy menses 2. Peptic ulcer 3. Hemerrhoids 4. CA in GIT (malignancies)
34
What is the treatment for hemorrhagic anemia?
Treat the cause.
35
What is considered to be the most complex type of anemia?
Sickle cell anemia
36
What is the etiology of sickle cell anemia?
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
In sickle cell anemia, if only one allele has the defect, what does this mean?
- Heterozygous: sickle cell trait | - would be a carrier. May have no symptoms or very mild anemia.
38
The normal Hb in an adult is HbA. What is the Hb in sickle cell anemia?
HbS.
39
HbS is what type of acid?
valine.
40
HbA is what type of acid?
glutamic acid.
41
Sickle cell anemia is 1 amino acid change (valine instead of glutamic acid) in what ______
The Beta chain.
42
HbS crystalizes at dissociation at low P02...this causes the RBC to do what?
Deform and sickle.
43
The full patho sequence of sickle cell anemia....
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
What do the manifestations of sickle cell anemia relate to? 3 things.
1. Hemolysis 2. Thrombosis & Infarction 3. Increased Bilirubin.
45
State the 4 treatments for sickle cell anemia.
1. Supportive 2. Hypertranfusion in increased risk (ex. Sx, pregnancy ) 3. Hydroxyurea 4. Marrow / Stem transplant
46
Explain the supportive therapy for sickle cell anemia?
02, rest, analgesics for pain, IV fluids, electrolytes
47
Explain the hypertransfusion in sickle cell anemia?
Ongoing transfusion until circulating blood in pt. is 75% of donor blood.
48
Explain the Hydroxyurea. 2 Benefits: 2 Risks / SE:
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)
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