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Heme/Lymph 2 CP > 19b - Hypoproliferative Anemias > Flashcards

19b - Hypoproliferative Anemias Flashcards

1
Q

What is pernicious anemia?

A

A decificney in vitamin B12 secondary to intrinsic factor (IF) abnormalities.

Most frequent cause of vitamin B12 deficiency.

Autoantibodies against IF are requiredfor diagnosis.

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2
Q

What are four lab findings seen with vitamin B12 deficiency?

A
  • Low vitamin B12 levels
  • Low reticulocyte count
  • Auto-antibodies to IF or parietal cells (if pernicious anemia)
  • Elevated methylmalonic acid
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3
Q

What are four causes of folate deficiency?

A
  • Decreased intake (alcoholism, poverty)
  • Increased requirements (growth, pregnancy, staes or high cell turnover like leukemia)
  • Defective absorption (jejunal restriction or malabsorption)
  • Folic acid antagonists
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4
Q

What are sources of folate? How is it stored?

A

Sources: green veggies and fortified flour

Storage: can deplete in months

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5
Q

What are clinical symptoms of folate deficiency?

A

Megaloblasticanemia

Neural tube defects: 300,000 children/yr

  • spina bifida occulta causing anencephaly
  • Important of supplementation
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6
Q

What are three lab findings seen with folate deficiency?

A
  • Low serum folate levels
  • Low RBC folate levels
    • Marker of folate status at time of RBC production
    • May be decreased in VitB12 deficiency too
  • Normal methylmalonic acid levels (this helps rule out B12 deficiency in which methyllamonic acid levels would be high)
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7
Q

How do you treat B12 or folate deficiency?

A

VitB12 or folate supplementation (oral or IM)

Do NOT treat vitB12 deficiency with folate!

  • Anemia will reverse
  • Neurologial manifestations will not.
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8
Q

A 30yo previously heathy woman presents to Dr. Allie Cotter, primary care extraordinaire, and complains of fatigue. She has recently become shortness of breathe with strenuous exercise. She is pale in no acute distress. Her labs are as follows: What would you expect her peripheral blood smear to look like?

A

Her MCV is 61 so she is macrocytic.

Her MCHC is low so it will be hypochromic.

Her hemoglobin is low which also indicates that the RBCs will have hypochromicity.

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9
Q

What is the most common cause of iron deficiency in young women? What about in the elderly?

A

Young women: menstrual cycle

Elderly: GI bleeds

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10
Q

What are five compensatory mechanisms in anemia?

A
  1. Increased 2,3-DPG
  2. Shunting of blood from non-vital to vital areas
  3. Increased CO
  4. Increased RR
  5. Increased red cell production
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11
Q

What three things should be on your ddx with microcytic, hypochromic anemia?

A
  • Iron deficiency anemia
  • Thalassemia
  • Anemia of chronic disease
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12
Q

Where is the “functional” iron found in the body?

A

Component of heme (80%)

Component of myoglobin, cytochromes, and catalases (20%)

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13
Q

Where is the “storage” iron found in the body? What are the different forms that iron is stored in?

A

Stored iron is 15-20% of total iron

  • It’s found in the liver, spleen, and marrow.
  • Hemosiderin is the breakdown of ferritin
  • Ferritin

(There are differences in sexes)

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14
Q

How common is iron deficiency? Who gets it?

A

MOST COMMON world wide nutritional disorder (4-5 billion people worldwide).

Infants, children, and women most susceptible. Also elderly with occult GI bleeding.

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15
Q

What are the clinical features of iron deficiency?

A
  • Microcytic, hypochromic anemia
  • Impaired cognition, work capacity
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16
Q

What are four causes of iron deficiency?

A
  • Dietary (milk fed infants)
  • Impaired absorption (duodenum)
  • Increased requirement (pregnant)
  • Chronic blood loss (GI in <50yo or mentrual bleed)
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17
Q

How is non-heme vs heme iron absorbed?

A

Heme iron is absorbed by the heme transporter while non-heme iron is reduced by the duodenal cytochrome B (using VitC) and then taken up by

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18
Q

What happens once heme iron and non-heme iron are taken up by intestinal epithelial cells?

A

They are transported to mucosal ferritin and then transported out into the peripheral blood and hephaestin oxidizes Fe2+ it into Fe3+.

In the peripheral blood it is bound by plasma transferrin.

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19
Q

_______ from the liver regulates the activity of ferroportin 1.

A

Hepcidin

20
Q

What is seen on peripheral blood smear in iron deficiency anemia?

A
  1. Microcytic, hypochromic anemia with high RDW.
  2. Increased RBC pallor
  3. Significant anisopoikilocytosis
    • Pencil cells
    • Ovalocytes/elliptocytes
    • Target cells
    • Tear drop cells
  4. No reticulocytes
  5. Thrombocytosis (reactive)
21
Q

In iron deficiency anemia, it can be helpful to get an iron study. What are the components of an iron study?

A
  • Serum ferritin (most robust analysis for determining iron status)
  • Serum iron
  • Total iron binding capacity
  • % iron binding capacity
  • BM iron stores (gold standard for iron store assessment - but is NOT needed for diagnosis).
22
Q

What does serum ferritin tell us? What is it a surrogate for?

A

Most sensitive assay for iron deficiency anemia.

Surrogate for total body iron stores.

  • <12 microgram/L in females and <30 in males
23
Q

When do ferritin levels increase?

A

It is an acute phase reactant, and it can increase in inflammatory states.

  • Majority of pts with concomitant IDA and an inflammatory process or acute liver disease will have ferritins in the low normal range.
  • Elevated levels can also be seen in iron overload states and hemophagocytic syndromes.
24
Q

Is serum iron a sensitive or specific marker for iron deficiency? What does it vary with? What are the levels seen in IDA?

A

Not sensitive or specific.

Physiologic variations and pathology (inflammation, malignancy) affect levels.

Low to normal in IDA, unless taking supplements.

25
Q

What is total iron binding capacity (TIBC)? Normally how much is saturated with iron? How do levels change in IDA?

A

Essentially equivalent to a transferrin concentration (reflects the iron that can be bound by protein).

Normally 30% of transferrin is saturated with iron.

Increased in IDA.

26
Q

What is % iron saturation?

A

% iron saturation is serum iron/TIBC

27
Q

Is serum soluble transferrin receptor (sTfR) a good test for iron deficiency anemia?

A

It’s a sensitive but not specific marker (it’s seen in many states causing increased erythropoiesis).

28
Q

In bone marrow iron studies, what are the 2 sites of evaluation?

A

Storage iron: macrophages within particles

Sideroblastic iron: within erythroid precursors

29
Q

How does IDA impact storade and sideroblastic iron?

A

It’s depleted and there’s decreased storage and sideroblastic iron.

30
Q

How would you treat iron deficiency anemia?

A

Iron supplementation (oral or IV)

31
Q

Your patients information is listed below. What would you expect her serum ferritin, serum iron, TIBC, and % iron saturation to be?

A
32
Q

What are clinical associatiosn of anemia of chronic disease/inflamamtion (ie what can cause it)? What is the mechanism by which these things cause anemia?

A
  • Chronic infections
  • Immune dysfunction
  • Neoplastic disorders

Block in transport of iron from macrophages into erythroid precursors mediated by hepcidin (acute phase reactant).

33
Q

Anemia of chronic disease/Inflammation is the most common anemia in ________ _______. How severe is it?

A

Hospitalized pts.

Mild to moderate anemia (not severe).

34
Q

How would you diagnose anemia of chronic disease/inflammation?

A
  • Mild normocytic (80%) or microcytic (20%) anemia
  • Without significant anisopoikilocytosis
  • Iron studies
35
Q

How do you treat anemia of chronic disease/inflammation?

A
  • Treat underlying disorder
  • Erythropoietin vs iron therapy

Keep in mindm they have iron, they just can’t utilize it properly because they are sequestering it. To fix this issue we don’t need to give them more iron, we need to stop their body from sequestering it so their body can access the iron.

36
Q

What happens to the following values during Iron deficiency anemia?
Reticulocyte count:
Arrow storage iron:
Sideroblastic iron:
serum ferritin:
serum iron:
TIBC:
% iron saturation:

A

Reticulocyte count: decrease
Arrow storage iron: decrease
Sideroblastic iron: decrease
serum ferritin: decrease
serum iron: decrease
TIBC: increase
% iron saturation: decrease

37
Q

What happens to the following values during Anemia of chronic disease/inflammation?

Reticulocyte count:
Arrow storage iron:
Sideroblastic iron:
serum ferritin:
serum iron:
TIBC:
% iron saturation:

A

Reticulocyte count: decrease
Arrow storage iron: increase
Sideroblastic iron: decrease
serum ferritin: increase
serum iron: decrease
TIBC: normal or decrease
% iron saturation: normal or increase

38
Q

What is decreased in anemia of renal failure? What is the treatment?

A
  • Decreased EPO production due to kidney damage
    • hypoplastic erythroids in BM
  • Hemodialysis contribuets to blood loss
  • Treatment includes EPO
39
Q

What are two stem cell defects with adequate EPO? How do these occur?

A

Red cell aplasia (pure) vs. pan-aplasia (aplastic anemia)

Most ofetn acquired but can be congenital.

Most have no identifiable etiology.

40
Q

What are two mechanisms for pan-aplasia in hypoproliferative anemias?

A
  • Immune-mediated suppression of marrow progenitors
  • Intrinsic stem cell abnormality
41
Q

What arew the 5 causes of acquired aplastic anemia?

A
  1. Idiopathic (65%)
  2. Drugs and toxins (chemo, radiation, chloramphenicol)
  3. Autoimmune
  4. Infections (EBV, CMV, hepatitis)
  5. Paraneoplastic
42
Q

What are the two causes of congenital aplastic anemia?

A

Fanconi anemia - aut recessive DNA repair defect

Dyskeratosis congenita - short telomere syndrome

43
Q

What are three treatments for aplastic anemia?

A

Anti-thymocyte globulin (ATG)

Thronbopoietin (TPO)

Stem cell transplantation

44
Q

What is pure red cell aplasia? What 5 conditions can it be associated with?

A

Selective absence of marrow erythroid precursors.

  • Thymic hyperplasia or thymomas (excision may be curative)
  • Parvovirus (devastating hemolytic anemia)
  • Autoimmune disorders
  • Drugs
  • Large granular lymphocytic leukima (LGLL)
45
Q

What is myelophthisic anemia?

A

Anemia secondary to marrow infiltration by metastatic carcinoma, storage disorders, etc.

Leukoerythroblastic reaction with tear drop cells.

Heme/Lymph 2 CP (16 decks)

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