Conditional Anemias Flashcards

1
Q
A
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1
Q

By definition, _____ is present when hematocrit is reduced

A

anemia

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2
Q

Anemia in Men vs. women

A

○ Men- Generally below about 39-40%
○ Women- Generally below about 35-36%

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3
Q

For the most part, anemias as either _____ or _____

A

conditional; inherited

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4
Q

We can also look at anemias according to pathophysiologic basis:

A

○ Decreased production: Lacking nutrient, bone marrow suppression, etc.
○ Accelerated blood loss: Hemolysis or hemorrhage
○ Red blood cell size (MCV)

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5
Q

Tests to help us differentiate between the types of anemia are the _____

A

reticulocyte count, the MCV, and the peripheral blood smear

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6
Q

S/S common to most types of anemia

A

○ Fatigue or weakness
○ Exercise intolerance
○ Tachycardia
○ Palpitations
○ Dyspnea on exertion
○ Pallor, pale palpebral conjunctiva
○ Headache, depression (less common)

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7
Q

_____ – destruction of the cell by physical ripping or bursting

A

Hemolysis

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8
Q

Hemolysis of RBCs is always occurring at
a slow, steady rate, taken out of
circulation after ~ 120 days. This is called ____

A

“physiologic hemolysis”

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9
Q

Hemolytic Anemia

A

pathologic conditions can result in an
accelerated hemolysis, where RBCs are being destroyed faster than the marrow normally produces them

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10
Q

_____ – A group of disorders in which RBC survival is reduced, either episodically or continuously

A

Hemolytic Anemias

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11
Q

Classifications of hemolytic anemias

A

○ Intrinsic Defect
■ Defect is within the RBC – problem with the membrane, enzyme systems, or Hgb creation
■ Typically hereditary

○ Extrinsic Defect
■ Defect from outside the RBC – immune mediated, microangiopathic, infection, burns, and hypersplenism

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12
Q

Anemia caused by IgG antibodies

A

Autoimmune Hemolytic Anemia

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13
Q

The Antiglobulin Coombs Test (Direct) is the basis of diagnosis for _____

A

Autoimmune Hemolytic Anemia

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14
Q

Treatment of autoimmune hemolytic anemia

A

Corticosteroids

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15
Q

Diagnostic studies that may suggest hemolytic anemia

A

○ Reticulocytosis – Bone marrow will respond to most hemolytic
disorders with an increased production of young RBCs
○ Lactate dehydrogenase (LDH) – Levels can be elevated
○ Bilirubin – Levels can be elevated
○ Peripheral blood smear – shows evidence of hemolysis

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16
Q

Look at the supplementary study material for the anemia slides

A

:)

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17
Q

Anemias from Nutritional
Deficiency

A

○ Iron deficiency anemia
○ Vitamin B12 deficiency
anemia
○ Folate deficiency anemia

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18
Q

Anemias from Chronic Disease

A

○ “Anemia of chronic disease”
○ Anemias associated with:
■ Chronic renal disease
■ Chronic liver disease

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19
Q

Other selected anemias

A

Aplastic anemia

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20
Q

Most common cause of anemia worldwide

A

Iron Deficiency Anemia

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21
Q

Iron Deficiency Anemia

A

In the developed world, it is caused by chronic, slow bleeding unless
proven otherwise

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22
Q

Iron deficiency anemia causes

A

Excessive menstruation, chronic GI blood loss, etc.
○ Pregnancy/Lactation – increased iron utilization/demand
○ Malabsorption – Celiac disease, intestinal worm, gastritis, etc.
○ Infants – most common cause of anemia in infants
○ Inadequate dietary intake – rare in US
○ Idiopathic (up to 5% of cases)

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23
Q

Iron Deficiency Anemia pathophysiology

A

○ If due to chronic, slow blood loss, an increase in the production of RBCs depletes iron stores slowly
○ Initially H&H remain normal while iron stores are being depleted (iron deficiency without anemia)
○ Once iron stores are depleted, RBCs form at a slower rate, and less Hgb can be made
■ Results in hypochromia, anisocytosis, poikilocytosis

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24
Q

Less Hgb means _____ cells (MCV decreases)

A

smaller

25
Q

Iron Deficiency Anemia unique S/S

A

○ Pica – craving for food (ice chips, etc.) or even dirt
○ Cheilosis – painful cracking at the corners of mouth
○ Glossitis – smooth tongue
○ Brittle nails
○ Koilonychia – spooning of nails
○ Heme-positive stool (if due to a GI bleed)

26
Q

Iron Deficiency Anemia Management

A

○ Treat underlying disorder if one is identified (celiac disease, colon cancer, menorrhagia, gastritis/bleeding ulcer, hookworms, etc.)
○ PO Ferrous Sulfate (325 mg 1-3 times daily; 100 mg of elemental iron) Take on an empty stomach to ensure absorption
○ Reticulocyte count should increase by 7 days of treatment and signifies appropriate response to therapy
○ Treatment should be continued for approximately 6 months following normalization of Hgb
○ If patient cannot tolerate PO Ferrous Sulfate, IM or IV Iron can be given, but beware of anaphylaxis.
○ Because IDA is rarely life-threatening, the most important part of treatment is identification and correction of blood loss

27
Q

Iron deficiency demands a search for ____

A

chronic blood loss, especially
if menorrhagia and frequent blood donations are not the cause

28
Q

The most common cause of B12 deficiency in the US is _____

A

Pernicious Anemia

29
Q

Those at risk for B12 deficiency due to inadequate dietary intake include the following groups:

A

○ Strict vegetarians and vegans
○ Those who have had a gastrectomy (low
production of intrinsic factor)
○ Those with disease of the ileum (as commonly
seen with Crohn’s disease)

30
Q

_____ – autoimmune destruction of gastric parietal cells
resulting in insufficient intrinsic factor

A

Atrophic Gastritis

31
Q

The impairment of DNA synthesis by B12 deficiency slows _____, but not
_____

A

nuclear maturation; cytoplasmic maturation

32
Q

B12 deficiency anemia results in _____

A

Megaloblastic anemia
Macro-ovalocytes (megaloblastic RBCs,
macrocytic), and may show characteristic
Hypersegmented Neutrophils

33
Q

Vit B12 Deficiency Anemia Unique S/S

A

○ Glossitis
○ Paresthesias – in the extremities (characteristic)
○ In severe disease, the posterior columns of the spinal cord become impaired, and cerebellar function may be altered as well
■ Diminished vibratory or position sense
■ Positive Romberg Test
■ Irreversible ataxia

34
Q

____ is very characteristic of a B12 deficiency

A

Paresthesias

35
Q

Clinical Management for vitamin B12 deficiency anemia

A

○ Parenteral administration of Vitamin B12, IM or SC injections of 100 mcg per dose
○ PO Vitamin B12 may be administered after repletion, but not always successful

36
Q

it is recommended that you also prescribe
simultaneous folic acid replacement (1 mg daily) with _____ because ____

A

Vit B12 Deficiency Anemia; Some patients are concurrently folic acid deficient from intestinal mucosal atrophy

37
Q

Highest risk populations for folate deficiency anemia

A

alcoholics, anorexic patients, those who do not eat fresh fruits and vegetables or overcook their food

38
Q

Medications that interfere with folate absorption

A

Phenytoin, methotrexate, TMP/SMX, etc.

39
Q

Sometimes seen in scenarios of increased requirement

A

Pregnancy, hyperthyroidism, or malignancy

40
Q

Folic acid (B9) is present in _____

A

fruits and vegetables, especially citrus fruits
and green leafy vegetables

41
Q

Folate Deficiency Anemia pathophysiology

A

○ Like Vitamin B12, Folate is necessary for adequate DNA synthesis
(affects all bone marrow precursors)
■ The impairment of DNA synthesis slows nuclear maturation, but
not cytoplasmic maturation
● Cells do not progress from the G2 growth stage into mitosis,
so they do not divide (stay large/flimsy)
● Megaloblastic anemia (sound familiar?)

42
Q

Folic Acid deficiency in pregnancy can result in ____

A

neural tube defects!
Prenatal folic acid is important

43
Q

Basically, folate deficiency anemia is clinically identical to _____

A

Vitamin B12 deficiency anemia

44
Q

If there is isolated folate deficiency, deficiency, the patient does not
develop the _____

A

neurologic symptoms

45
Q

Important lab findings of folate deficiency anemia

A

Hypersegmented neutrophils. Just like with Vitamin B12 deficiency. Decreased serum folate level. Decreased RBC folate level

46
Q

Clinical management of folate deficiency anemia

A

○ Folate replacement is the key to treatment
○ Monitor response to therapy by watching for increased reticulocyte count after 5-7 days
○ Do not treat without confirming Vitamin B12 levels are normal!

47
Q

Common causes of anemia of chronic inflammation:

A

Rheumatoid arthritis, HIV/AIDS, TB, lupus, inflammatory bowel disease, malignancy

48
Q

Pathophysiology of Anemia of Chronic Disease

A

○ Chronic inflammatory diseases seem to trigger increased storage and protection of iron stores (saving for later?)
○ Hepcidin is a protein hormone that normally impairs release of iron from storage
■ In chronic disease states, inflammatory cytokines trigger increased production of hepcidin, which results in iron being locked away in storage
■ Referred to as “iron-restricted erythropoiesis”

49
Q

Chronic kidney disease and anemia

A

Erythropoietin levels are
decreased, resulting in anemia

50
Q

Chronic liver disease and anemia

A

Portal hypertension leads to hypersplenism (increased RBC phagocytosis), resulting in anemia

51
Q

Signs and Symptoms of Anemia of Chronic Disease

A

Clinical presentation is generally consistent with the underlying condition

52
Q

Anemia of Chronic Disease clinical management

A

Treat the underlying disease process
■ The anemia often improves when the underlying condition is
adequately treated (if possible)

53
Q

A condition of bone marrow failure that arises from suppression or
injury to the hematopoietic stem cell

A

Aplastic Anemia

54
Q

Aplastic anemia is considered idiopathic about ___% of the time

A

50

55
Q

Pathophysiology of aplastic anemia

A

○ Most cell lines are affected, so it usually includes low WBC and platelet
counts in addition to anemia
■ The hallmark of aplastic anemia is pancytopenia due to bone marrow
hypocellularity
○ That being said, early in the evolution of aplastic anemia, only one or two
cell lines may be reduced

56
Q

Thrombocytopenia can result in

A

Gingival bleeding, epistaxis, other bleeding, and maybe bruising

57
Q

can cause vulnerability to bacterial and fungal infections

A

Neutropenia

58
Q

Clinical Management of Aplastic Anemia - Mild cases

A

■ Supportive care, including erythro or myeloid growth factors
■ Transfusions and antibiotics are often needed

59
Q

Clinical Management of Aplastic Anemia - Severe cases

A

■ Isolation precautions and bone marrow transplantation (BMT)
● If BMT is not possible due to lack of a donor match, immunosuppression with certain strong medications is attempted
○ Severe cases are fatal without treatment
■ Prognosis is better for those who get a BMT

60
Q

All cases of Aplastic Anemia need to be referred to and managed by a ____

A

Hematologist, usually urgently