Normocytic Anemia Flashcards

1
Q

What is the second most common anemia?

A

ANEMIA OF CHRONIC DISEASE/ INFLAMMATION
–>2nd most common anemia after iron deficiency anemia

–>It is the most common anemia among inpatients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Indicate the relative change in the following values for iron deficient anemia (IDA):

  • Ferritin
  • Transferrin/ TIBC
  • T Saturation
  • Iron
  • Marrow Iron Stores
  • RPI
  • Sed rate (inflammatory markers)
A

Values for iron deficient anemia (IDA):

  • Ferritin: decreased
  • Transferrin/ TIBC: increased
  • T Saturation: decreased
  • Iron: decreased
  • Marrow Iron Stores: decreased
  • RPI: decreased
  • Sed rate (inflammatory markeres): normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Indicate the relative change in the following values for anemia of chronic disease (ACD):

  • Ferritin
  • Transferrin/ TIBC
  • T Saturation
  • Iron
  • Marrow Iron Stores
  • RPI
  • Sed rate (inflammatory markers)
A

Indicate the relative change in the following values for ACD:

  • Ferritin: normal to increased
  • Transferrin/ TIBC: decreased or normal
  • T Saturation: low normal
  • Iron: decreased
  • Marrow Iron Stores: increased
  • RPI: decreased
  • Sed rate (inflammatory markers): increased
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ID: 68 yo man with normocytic anemia

History of present symptoms:
“Progressive midepigastric pain over 6 months and a 30 lb weight loss.”

Past Medical History
Asthma
Normal colonoscopy 2 years ago

Social History
Retired teacher. Married. Three grown children
No history of tobacco, drug or alcohol use

Family medical history
Mother died of complications from diabetes
Father alive and well
No other family medical issues

Medications
Inhalers

Physical exam:
Stable vitals
Cachectic appearing man with tenderness to palpation in midepigastric area and RUQ,

Reticulocyte count: 1% (RPI = 0.48)
Iron studies:
↓Fe = 30 µg/dL (40-160 µg/dL)
↓TIBC = 190 µg/dL (205-395 µg/dL)
↓TS = 15 % (25-45 %)
↑Ferritin = 500 ng/mL (20-300 ng/mL)

What could be a potential diagnosis?

A

Pancreatic Adenocarcinoma

Inflammatory state
–>Anemia of a chronic disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the treatment for ACD (anemia of chronic disease)?

A

Ideally treatment of the underlying disease/disorder

Supportive care:
Transfusions if severe anemia present

Erythropoietin in some instances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is aplastic anemia?

A

“Aplastic anemia” is a misnomer because the disorder is defined as pancytopenia with an empty bone marrow

Anemia is often less of a clinical problem than the leukopenia (low WBCs) and thrombocytopenia (low platelets) which are also present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the causes of primary aplastic anemia?

A

–> Idiopathic (most common)

–> Fanconi Anemia: most often inherited in an autosomal recessive pattern,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the causes of secondary aplastic anemia?

A
SECONDARY ANEMIA
--> Radiation
--> Chemotherapy (alkylating agents)
--> Other drugs: chloramphenicol
	antiepileptic drugs
--> Benzene
--> Viruses: parvovirus, Epstein-Barr
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do you treat aplastic anemia?

A

Aplastic anemia can be treated effectively by :

–>bone marrow transplantation.

[target] LYMPHOCYTES

  • -> Cyclosporine
  • -> Cyclophosphamide
  • ->Anti-thymocyte globulin (ATG) may also reverse it when due to immune suppression.

[target] PLURIPOTENT HSC
–>Growth factors (erythropoietin, G-CSF may also be used).

[target] LEUKOCYTES/ GRANULOCYTES
–> blood transfusions, increase leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the etiology of anemia of chronic kidney disease

A
  • Decreased erythropoietin due to decreased renal cortical cells
  • ->Typically when kidney function Frequent phlebotomy
  • ->Blood loss in the dialysis circuit
  • ->Uremic platelet dysfunction: bad kidney
  • Shortened RBC survival
  • -> Uremic RBCs less deformable and more prone to mechanical destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the treatment for anemia of chronic kidney disease?

A

Treatment= erythropoietin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the possible etiologies of hypo proliferative normocytic anemias?

A

Drugs
–>E.g., chemotherapy

Infiltration of the bone marrow by
–>Malignancy or infection

Endocrine
-->Hypothyroidism
-->Panhypopituitarism
-->Low testosterone 
(generally mild)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens to the heme ring when rbcs are broken down.

A

Heme ring is metabolized to bilirubin and transported to liver where it is excreted into bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Provide an example of an inherited anemia

A

–> Sickle cell anemia

–>G6PD deficiency:X-linked recessive pattern.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Provide an example of an acquired anemia

A

Autoimmune hemolytic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Provide an example of an anemia with intravascular hemolysis

A

Paroxysmal nocturnal hemoglobinuria

17
Q

Provide an example an anemia with extravascular hemolysis

A

Hereditary spherocytosis

18
Q

Provide an example of an anemia with an intrinsic origin of RBC damage

A

G6PD deficiency

19
Q

Provide an example of an anemia with an extrinsic origin of RBC damage

A

TTP: thrombin thromobocytopenic purpura

20
Q

Describe the pathophysiology of intravascular hemolysis

A

–>Release of hgb and enzymes into the circulation

–>Haptoglobin (Hp) binds the Hgb

–>The haptoglobin-Hgb complexis removed by theRES

–>Prevents iron-utilizing bacteria from benefitting from hemolysis.

–>Not absolutely distinct from extravascular hemolysis

21
Q

What are the clinical manifestations of intravascular hemolysis>

A

Pallor, fatigue, tachycardia
Jaundice
Blood-tinged plasma
Blood-tinged urine