Hemeonc 4 Flashcards

1
Q

If you have an anemia with normocytic MCV, what is the next test you should order? Why?

A

Reticulocyte count, to see if there is a production problem (organ dysfunction, chronic disease, HIV, myelosuppression) or bleeding problem (GI bleed, acute blood loss, hemolytic anemia)

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2
Q

What type of anemia is persistent for greater than 1 to 2 months in patients with the associated conditions:

Infection
Malignancy
Endocrine disorders
Immune disorders (SLE, RA)
Others: 
HIV, DM, Heart failure
A

Anemia of Inflammation

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3
Q

What signals the production of RBC’s? And where is it produced?

A

The hormone erythropoietin, produced in the kidneys

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4
Q

Causes of anemia of inflammation (2)

A
suppressed erythropoiesis (renal issue)
inflammation (cytokines) results in poor iron metabolism/absorption
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5
Q

Do you expect ferritin to be low in an anemia of chronic disease? Why?

A

No, because ferritin is an acute phase reaction and it is often normal in chronic disease

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6
Q

What is the treatment for anemia of inflammation?

A

Treat the underlying cause

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7
Q

What type of anemia results in Bone Marrow Failure: (Global decrease in your stem cells and consequently there is a deficiency in all blood cells.)
PANCYTOPENIA

A

Aplastic Anemia

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8
Q

What is the major cause of aplastic anemia?

Other causes?

A
>50% AUTOIMMUNE (IDIOPATHIC)
Also caused by drug reaction (sulfa, chloramphenicol, chemo)
radiation
genetic
infection,
pregnancy
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9
Q

What are common clinical features of aplastic anemia?

A

bleeding (thrombocytopenia)
infection (neutropenia)
fatigue/pallor (anemia)

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10
Q

For aplastic anemia,what would you expect to see on a PBS? BMbx?

A

pancytopenia

Hypocellular marrow with excess fat (normal cytology, just too few)

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11
Q

What is the treatment for aplastic anemia (after RFL to Hematologist)?

A

Immunosuppression

Allogenic BM transplant if 40 years

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12
Q

Temporary shutdown of erythropoiesis due to acute infection, commonly associated with Parvo/5ths Disease?

A

Aplastic Crisis

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13
Q

What changes lead to the aged (120 days) RBC being trapped and removed by the RE (reticuloendothelial) system (3)

A

1) Decrease in lipids in membrane
2) Less pliability
3) Shape becomes more spherocytic

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14
Q

Premature or accelerated destruction of RBCs (<100 days) beyond the ability of the bone marrow to fully compensate

A

Hemolytic Anemia

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15
Q

Clinical presentation of hemolytic anemia includes:

A

Jaundice, scleral ichterus, splenomegaly, gallstones, hypotension, hemoglobinuria

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16
Q

In hemolytic anemia, Would you expect an increase in indirect bilirubin? Why?

A

Yes, because bilirubin is the byproduct of lysed RBC’s

17
Q

In hemolytic anemia, what would you expect to see on a PBS?

A

Nucleated red cells, high retic count, spherocytes, schistocytes

18
Q

What test specifically looks at hemolysis?

A

Coombs test (Cross and screen is indirect Coombs test)

19
Q

What genetic assay is associated with impaired metabolic pathways of RBC’s in hemolytic anemia?

A

G6PD assay (most common in males, blacks, Mediterraneans)

**Most common metabolic cause of hemolytic anemia, treat by avoiding oxidating drugs

20
Q

Reason for hemolysis is due to the RBC itself

A

intrinsic factors (issue with membrane, metabolic, hemoglobin type)

21
Q

Why would splenectomy often be effective tx for gallstones caused by hereditary spherocytes

A

because the spleen is breaking down the spherocytes rapidly and creating excess bilirubin that accumulates in the gallbladder

22
Q

What are 3 pathways that the rbc’s utilize in order to create ATP and break down glucose?

A

1) Glycolysis (Embden-Meyerhof) Pathway produces majority of ATP
2) Hexose Monophosphate Shunt produces 10%
3) Nucleotide Salvage Pathway (very little)

23
Q

Reason for hemolysis has nothing to do with properties of RBC itself:

A

Extrinsic factors (immune system, infection, mechanical destruction of RBC’s)

24
Q

development of antibodies that target the RBC membrane

A

Autoimmune hemolytic anemia

25
Q

When you think WARM autoimmune hemolytic anemia, think:

A

IgG, Fix complement weakly. Treat w/ steroids, splenectomy, immunosuppressants

26
Q

When you think COLD autoimmune hemolytic anemia, think:

A

IgM, Fix complement strongly. (Underlying lymphoma common). Treat w/ avoidance of cold, cytotoxic meds, plasmapheresis