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MHD V: Renal > 11.5: Anemia II > Flashcards

11.5: Anemia II Flashcards

1
Q

3 broad types of anemia?

A
  1. Blood loss
  2. Hemolytic
  3. Diminished erythropoesis
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2
Q

What are thalassemias?

A
  • Group of genetic disorders characterized by lack / decreased production of alpha or beta globin chain of hemoglobin A
  • Hemoglobin A is 95% of hemoglobin in adults and is made of two alpha and two beta chains
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3
Q

What are alpha, beta plus, and beta zero thalassemia?

A
  1. Alpha: decrease alpha globin chain
  2. Beta zero: absent beta globin chain
  3. Beta plus: Deficient beta globin chain
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4
Q

Consequences of thalassemias?

A
  • Low intracellular hemoglobin: hypochromic: pale cells

- Relative excess of other chain = toxicity

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5
Q

How many alpha globin alleles?

A
  • 4
  • Varying degrees of thalassemia depending on how many missing
    1. Silent carrier
    2. Mild anemia: blacks and asians
    3. HbH disease: Sever anemia
    4. Hydrops fetalis: relatively fatal
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6
Q

What is HbH?

A
  • 3 of 4 alpha globin alleles missing

- relatively sever anemia

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7
Q

What is Hydrops fetalis?

A
  • Zero alpha alleles
  • Very deadly
  • Intrauterine transfusions necessary
  • HSC transplant can cure on birth
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8
Q

How many beta alleles?

A
  • 2

- Beta plus and zero thalassemia

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9
Q

What is thalassemia major?

A
  • Severe beta thalassemia w/ reliance on transfusions
  • Marrow expands to compensate = bone deformities
  • Hepatosplenomegaly
  • Transfusions lead to deposition of Fe, cardiac failure
  • Expansion of marrow skull: not normal
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10
Q

What is thalassemia minor?

A
  • Clinical term for patients with asymptomatic, mild, or absent microcytic anemia with some RBC abnormalities
  • Need to distinguish from Fe deficiency
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11
Q

Where are RCBs produced?

A
  • Long bones in adults
  • Live are spleen as well in KIDS
  • Marrow will expand in skull in thalassemia major to try to compensate
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12
Q

How to distinguish Diminished Fe from Thalassemia minor?

A

Hemoglobin electrophoresis: normal if Fe deficiency
Fe studies: abnormal in Fe deficiency
Increase in Hgb A2

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13
Q

When in increase in Hgb A2 seen?

A
  • Beta thalassemias

- Hgb A2 is alpha and delta chain, no beta

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14
Q

What is only acquired, intrinsic abnormality of RBCs?

A

PNH

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15
Q

What happens in PNH?

A
  • Mutation in GPI anchor preventing GPI-anchored proteins from attaching to RBC membrane
  • Stem cell disorder
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16
Q

What are GPI proteins involved in?

A
  • Inactivating the complement pathway
  • GP 55 and 59 are most important
  • Hemolysis occurs if you cannot inactivate complement pathway
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17
Q

Clinical findings in PNH?

A
  1. Intravascular hemolysis
  2. Paroxysmal and nocturnal in 25%
  3. Infections
  4. Portal vein thrombosis
  5. Occasional evolution to aplastic anemia or acute leukemia
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18
Q

What can cause extrinsic anemias?

A
  1. Antibody mediated
  2. Mechanical trauma
  3. Infections
  4. Chemical injuries
  5. Sequestration
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19
Q

2 most common examples of external trauma to RBCs?

A
  1. Anemia due to prosthetic valves
  2. Anemia due to small vessel narrowing and fibrin deposition
    - AKA microangiopathic hemolytic anemia
20
Q

What can cause microangiopathic hemolytic anemia?

A
  1. TTP: thrombotic thrombocytopenic purpura
  2. HUS: Hemolytic urea syndrome
  3. DIC
    * **Schistocytes in peripheral blood from fibrin deposition in vessels in all 3 cases
21
Q

What are Schistocytes in peripheral blood indicative of??

A

Microangiopathic hemolytic anemia

22
Q

What can cause Fe deficiency anemia?

A
  1. Chronic blood loss: Most common, usually in GI
  2. Malabsorption
  3. High iron demand in pregnancy
  4. Low dietary intake
23
Q

What happens in Fe anemia/

A
  1. Stored Fe depleted
  2. Marrow Fe depleted
  3. Serum Fe decreases
  4. INCREASED total Fe binding capacity (TIBC)
24
Q

Why is TIBC high in Fe anemia?

A
  • Measuring proteins ability to transport Fe

- Since Fe is low, there are lots of proteins willing to move Fe and lots of spare capacity

25
Q

Presentation of Fe anemia?

A
  • Low serum Fe
  • Hgb decreases
  • RBCs become small
  • Spoon shaped nails
  • Smooth tongue
  • Intestinal malabsorption
26
Q

What is expensed central pallor of RBC indicative of?

A

Fe deficient anemia: normally only middle is white

27
Q

What are megaloblastic anemias?

A
  • B12 or folate deficiency
  • Deficient DNA synthesis disturbing proliferation of Erythroblasts leading to their enlargement
  • Enlargement due to abnormal division
  • Nuclei are immature and cytoplasm is mature
28
Q

What are erythroblasts?

A

RBC precursors

29
Q

What are megaloblasts? Macrocytes?

A

Megaloblasts: Enlarged RBC precursors
Macrocytes: Enlarged RBCs
**Seen in megaloblastic anemia

30
Q

When is B12 deficiency seen?

A
  1. Decreased intake: vegetarians

2. Low absorption: IF deficiency, fish tapeworm

31
Q

What is IF important in?

A

“Intrinsic factor”

- B12 absorption

32
Q

What is pernicious anemia?

A
  • B12 deficiency secondary to gastritis with failure to produce IF
33
Q

Where is IF produced?

A
  • Parietal cells in the stomach
  • Necessary for B12 absorption in ileum
  • Mal Production of IF is autoimmune disorder
34
Q

What is B12 important in?

A
  • Essential cofactor for methionine synthase
  • Deficiency decreases THF availability
  • THF donates carbon unit for DNA synthesis
  • **This leads to anemia
35
Q

Clinical findings in B12 deficiency?

A
  1. Megaloblastic anemia
  2. Leukopenia with hypersegmented granulocytes
  3. Thrombocytopenia
  4. Atrophic glossitis
  5. Chronic gastritis
  6. Subate combined degeneration in CNS
    * **Affects areas where DNA synth. is important as cells are always being produced such as marrow and GI
36
Q

What is subacute combined degeneration?

A
  1. Spastic paraparesis
  2. Sensory ataxia
  3. Lower limb paresthesias
37
Q

Difference between folate and B12 deficiencies?

A

Folate does not show CNS abnormalities

38
Q

Can folate admin treat B12 deficiency?

A
  • Yes but it WILL NOT treat CNS abnormalities
39
Q

Most common anemia in hospital patients?

A
  • Anemia of chronic disease

- Hepcidin is seen at high levels in all these ptns.

40
Q

What is hepcidin?

A
  • Key protein in anemia of chronic disease
  • High levels block transfer of Fe from macs to erythroid precursors
  • In marrow macs give Fe to RBC precursors, hepcidin stops this at high levels
41
Q

Findings in anemia of chronic disease?

A

. High ferritin

  • Microcytic anemia with low serum Fe
  • Decreased TIBC
  • Increased marrow Fe stores
42
Q

What causes aplastic anemia?

A
  • Failure of suppression of stem cells
  • Leads to anemia
  • Granulocytopenia
  • Thrombocytopenia
  • Pancytopenia
43
Q

What is pancytopenia?

A

Decrease in RBC, WBC, and platelets

44
Q

Causes of aplastic anemia?

A
  1. Idiopathic
  2. Irradiation
  3. Drugs
  4. Virus
  5. Defect in marrow cells
  6. Suppression of marrow cells by T cells
45
Q

Appearance of marrow in aplastic anemia?

A

Hypocellular with increased fat and small foci of lymphocytes and plasma cells

46
Q

How can you treat aplastic anemia?

A
  • HSC implant

MHD V: Renal (28 decks)

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