Nutritional Anemias Flashcards

1
Q

What is normal WBC count?

A

4000-10000/uL

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2
Q

What is normal hgb?

A

12.6-17.7

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3
Q

What is normal hematocrit?

A

37.5-51.0 %

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4
Q

What is normal platelet count?

A

140,000-415,000/uL

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5
Q

What is normal MCV?

A

79-97 fL

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6
Q

What are the two causes of macrocytic anemias?

A

vitamin B12 and folate deficiency

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7
Q

What happens as a result of macrocytic anemia?

A

Megaloblastic cells. Effects development of RBCs in bone marrow and slows the synthesis of DNA but not RNA. The RBC increases in size before dividing resulting in macrocytic RBCs

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8
Q

sources of B12 for humans

A

Meat & dairy products

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9
Q

Adequate absorption of B12 depends on:

A

Dietary intake. Acid-pepsin in the stomach to liberate Cbl. Pancreatic proteases to free Cbl from binding to R factor. Secretion of intrinsic factor (IF) by the parietal cells to bind Cbl. An intact ileum with functional Cbl-IF receptors

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10
Q

Pernicious anemia:

A

Usually seen in older adults, African Americans & Caucasians. Autoimmune attack on gastric IF. One type of anti-IF antibodies blocks the attachment of Cbl to IF. Other type blocks attachment of the Cbl-IF complex to ileal receptors

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11
Q

Chronic Atrophic Gastritis:

A

Leads to a decline in IF production. Associated w/ autoantibodies directed against gastric parietal cells
Resulting in less acidic pH in the stomach. Also associated with increase risk of gastric cancer and gastric carcinoid tumor

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12
Q

Macrocytic anemia clinical presentation

A

MCV > 100 fL. elevated iron levels, indirect bilirubin & LDH: indicating increased RBC breakdown due to both peripheral destruction & ineffective erythropoiesis. Peripheral smear—megaoblasts, hypersegmented neutrophils & macrocytosis. When the anemia is severe there may be thrombocytopenia & neutropenia (?) pancytopenia

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13
Q

Hyperhomcysteinemia clinical presentation

A

Both Cbl & folate required for the metabolism of homocysteine to methionine. Deficiencies in these vitamins can result in elevations of homocysteine levels. Elevated homocysteine levels are a risk factor for atherosclerosis and venous thromboembolism

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14
Q

Neurologic changes (only seen in B12 deficiency) clinical presentation

A

Due to a defect in myelin formation. parasthesia, numbness, decreased strength. ataxia, spasticity, clonus & incontinence , memory loss, irritability & dementia

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15
Q

Why is there an increased risk of osteoporosis w/B12 deficiency?

A

Due to suppression of osteoblast activity-Increased risk of hip & spine fractures

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16
Q

Folate deficiency–Etiologies

A

Poor nutrition*—folate is found in meats, green leafy vegetables, nuts and fruit
Alcoholism** - common folate deficiency
Infant’s who are primarily fed goat’s milk

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17
Q

When there are increased folate requirements:

A

Pregnancy (Folate prevents ?) neural tube defects

Patients w/ chronic hemolytic anemia

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18
Q

Drugs that interfere w/ folate metabolism

A

Trimethoprim, methotrexate, phenytoin

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19
Q

Folate Deficiency–Presentation

A

Macrocytic anemia and hyperhomocysteinemia
NO neurologic findings
Folate deficiency can occur within 4-5 months intake is diminished
B12 deficiency occurs after YEARS of inadequate intake because B12 stores in the body are so high
Stored in the liver

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20
Q

Measure serum B12 level:

A

> 300 pg/mL = normal
200 – 300 pg/mL = borderline
< 200 pg/mL = low (consistent w/ deficiency)

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21
Q

Measure serum folate level:

A

> 4 ng/mL = normal
< 2 ng/mL = deficiency
RBC folate levels**

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22
Q

Metabolite testing —for those w/ borderline vitamin values:

A

Measure the metabolic intermediates: methymalonic acid and homocysteine
If these are ELEVATED then true B12 deficiency exists. If MMA is normal and homocysteine is increased folate deficiency is present

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23
Q

Diagnosing pernicious anemia:

A

Measure antibodies to IF—specificity of 100%. Elevated gastrin/low pepsinogen—highly sensitive if antibodies negative

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24
Q

Treatment of folate deficiency

A

Folic acid 1-5 mg po daily for 1-4 months or until complete hematologic recovery. Usually 1 mg/day is sufficient.

25
Q

Treatment for B12 deficiency

A

Usually treated w/ IM or deep SQ injections of Cbl

1000 mcg every day for 1 week, 1 mg every week for 4 weeks, and if the underlying disorder persists—1 mg every month

26
Q

Additional Treatment for B12 deficiency

A

Oral Cbl available—1-2 mg a day (200 x higher then the minimum daily requirement! Relies on patient compliance. Also sublingual** and nasal spray preparations

27
Q

What is one caveat when treating suspected folate deficiency?

A

Taking folic acid can partially reverse some of the neurologic effects of B12 deficiency. Important to rule out B12 deficiency BEFORE administering folic acid. If treatment w/ folic acid is urgent—draw blood prior to treatment to test for B12 deficiency and then threat with BOTH folic acid and B12 until test results are known

28
Q

Why is hypokalemia common during the early stages of B12 treatment?

A

due to the marked increase in K+ utilization in the production of new hematopoetic cells, so patients should be monitored

29
Q

What is absolute iron deficiency?

A

Iron stores in the bone marrow & in the liver/spleen are ABSENT. Serum ferritin is LOW. MCV < 80

30
Q

What is functional iron deficiency?

A

Insufficient availability of iron in the face of normal or increased iron stores

31
Q

What is iron anemia of inflammation?

A

Hepcidin-induced block in the release of iron from the macrophage back into circulation. This makes iron less available for red cell production. Seen in patients w/ infection, inflammation, or malignancy

32
Q

How can iron deficiency anemia be caused by treatment w/erythropoisis stimulating agents?

A

Available body iron stores may be unable to release iron rapidly enough to satisfy the increase brought about by the stimulating agent

33
Q

What are the clinical manifestations of iron deficiency anemia?

A

weakness, fatigue, HA, irritability, excercise intolerance, glossal pain/dry mouth, pica, RLS, exacerabtion of comorbidity (angina)

34
Q

What are the differential diagnoses of iron deficiency anemia?

A

thalassemia, anemia of chronic inflammation, siderblastic anemia

35
Q

What is the treatment of iron deficiency anemia?

A

Oral iron first best absorbed w/vitamin C. Should not be given with food, antacids, H2 blockers, PPIs, or Ca+ containing foods. 150-200mg elemental FE daily.

36
Q

What are SE of iron treatment?

A

nausea, constipation, diarrhea, epigastric pain, vomiting, black stools

37
Q

Describe parenteral iron therapy?

A

IV iron is effective for those unresponsive or intolerant to oral iron or when the amount blood loss exceeds the capacity of the GI tract to absorb oral iron.

38
Q

What are SE of parenteral iron therapy?

A

Life-threatening (primarily seen w/ HMW preparation). Patients multiple drug allergies have increased risk of anaphylactic reactions. fever, arthralgias, myalgias. Flare of arthritis

39
Q

How do you prevent an arthritis flare when treating with parenteral iron?

A

premedication w/ IV methylprednisone before infusion. 4 days of prednisone orally after infusion

40
Q

Serum Iron (Fe) Normal Values

A

mcg/dL: 60 – 170

41
Q

Ferritin Normal Values

A

ng/mL: 12 – 150 (females)/12 – 300 (males)

42
Q

Transferrin/Total iron binding capacity (TIBC) Normal Values

A

microgm/dL: 240 – 360*

43
Q

Transferrin saturation (Fe/TIBC) Normal Values

A

%: 15– 50

44
Q

Thalassemia expected lab results

A

May be + family hx
Serum Fe are normal to high
Hgb A2 level increased
RBC count is high

45
Q

Anemia of chronic inflammation expected lab results

A

Serum Fe and TIBC are low
Normal or increased Ferritin
Critical to look at the clinical setting and do thorough evaluation for chronic inflammation**

46
Q

Sideroblastic Anemias:

A

ringed sideroblasts on Prussian Blue stain of the bone marrow. Most commonly drug induced or due to a myelodysplastic disorder

47
Q

When is oral iron therapy is poorly tolerated or ineffective?

A

poor compliance due to GI SE, Malabsorptive states (celiac dz, Whipple’s dz, bacterial overgrowth syndromes). patients w/ inflammatory bowel dz, oral iron can worsen the underlying dz. heavy uterine bleeding, gastric bypass, or other causes of heavy blood loss. Dialysis patients

48
Q

Iron salts should not be given with:

A

Food, Antacids, H2 blockers, PPIs, Calcium containing foods, cereals, dietary fiber, coffee, tea and milk. Certain anitbiotics (e.g. quinalones, tetracyclines)

49
Q

When should iron be given if pt is taking antacids?

A

2 hours before or 4 hours after antacids

50
Q

Ferrous Sulfate

A

Most commonly used of elemental iron.

Recommended treatment is 150 – 200 mg of ELEMENTAL Fe daily

51
Q

SE oral iron

A

(50%) nausea, constipation, diarrhea, epigastric pain, vomiting (black stools)

52
Q

Iron Treatment options to reduce side effects:

A

Switch to a preparation w/ lower dose of elemental iron. Slowly increase from 1 pill a day to 3. Iron may be taken with meals. Use a liquid preparation. Try IV iron

53
Q

Maximum amount of ELEMENTAL iron absorbed orally and parenterally?

A

25 mg/day orally; w/ parenteral infusion the maximum is as high as 1000 mg

54
Q

Describe use of IV iron

A

effective for those unresponsive or intolerant to oral iron. IV iron is required when the amount of iron loss through daily blood loss exceeds the capacity of the GI tract to absorb oral iron

55
Q

Who gets a blood transfusion?

A

HEMODYNAMICALLY unstable because of active bleeding

56
Q

SE of IV Iron

A

fever, arthralgias, myalgias. Flare of arthritis in patients w/ inflammatory arthritis

57
Q

When are Life-threatening adverse drug effects seen with IV iron?

A

primarily seen w/ HMW preparation

58
Q

How do you prevent an arthritis flare when giving IV iron?

A

This can usually be prevented by premedication w/ IV methylprednisone before infusion and 4 days of prednisone orally after infusion