35. Anemia Flashcards

1
Q

Immature RBCs are known as ___

A

reticulocytes

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2
Q

After ___ days, the reticulocytes mature into ___, which have a lifespan of about ___ days

A

1-2 days
erythrocytes
120 days

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3
Q

Erythrocytes are removed from circulation by macrophages, mainly in the ___

A

spleen

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4
Q

S/sx of anemia

A

Fatigue, weakness, SOB, exercise intolerance, HA, dizziness, anorexia and/or pallor

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5
Q

What symptoms can develop with iron deficiency anemia?

A

Glossitis (inflamed sore tongue)
Koilonychias (thin, concave, spoon-shaped nails)
Pica (craving and eating non-foods such as chalk or clay)

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6
Q

What can cause anemia?

A

Nutritional deficiencies (e.g. iron, folate, vit B12)
CKD
Malignancy

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7
Q

Patients with vit B12 (cobalamin) deficiency can present with ____ symptoms

A

neurologic symptoms (including peripheral neuropathies, visual disturbances, and/or psychiatric symptoms)

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8
Q

A low MCV means RBCs are (smaller/larger) than normal and high MCV means that RBCs are (smaller/larger) than normal

A

low MCV = smaller RBCs (microcytic)
high MCV = larger RBCs (macrocytic)

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9
Q

Likely cause of anemia if MCV <80

A

Microcrytic
likely cause: iron deficiency

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10
Q

Likely cause of anemia if MCV 80-100

A

Normocrytic
likely causes: acute blood loss, malignancy, CKD, bone marrow failure (Aplastic anemia), hemolysis

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11
Q

Likely cause of anemia if MCV >100

A

Macrocrytic
likely causes: vit B12 or folate deficiency

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12
Q

Reticulocyte count is low in untreated anemia d/t ____

A

iron, folate, B12 deficiency and with bone marrow suppression

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13
Q

Reticulocyte count is high in ___

A

acute blood loss or hemolysis

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14
Q

___ deficiency is the most common nutritional deficiency in the US

A

Iron

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15
Q

Common causes of iron deficiency

A

Low iron intake (vegetarian/vegan diet, malnutrition, disease-related (e.g. dementia, psychosis))
Blood loss
Decreased iron absorption (high gastric pH (e.g. PPIs), GI diseases (e.g. celiac, IBD, gastrectomy, gastric bypass)
Increased iron requirements (pregnancy, lactation, infants, rapid growth (e.g. adolescence))

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16
Q

Laboratory findings consistent with dx of iron deficiency anemia (IDA)

A

Low Hgb, MCV < 80, reticulocyte count, serum iron, ferritin, and TSAT
High TIBC

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17
Q

Common treatment dosing for iron deficiency anemia (IDA)

A

1 tab once daily or every other day (no superior oral formulation, typically 40-80mg per dose)
Take on empty stomach (1hr before or 2 hrs after meals) for best absoprtion

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18
Q

What meds should be avoided when taking oral iron therapy for IDA?

A

Avoid H2RAs and PPIs
Separate from antacids (2hrs before or 4 hrs after taking antacids)
Rationale: Decrease iron absorption by increasing gastric pH

Separate from iron:
Quinolone and tetracycline abx
Bisphosphonates
Levothyroxine
INSTIs
Rational: iron can decrease absorption of these drugs

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19
Q

T/F: Sustained-release or enteric-coated formulations of oral iron therapy are recommended d/t less GI irritation

A

False - they do cause less GI irritation but not recommended d/t poor absorption

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20
Q

Goals of treating iron deficiency anemia

A

Increased serum Hgb after 1-2 weeks
Continue treatment for 3-6 months or until iron stores return to normal

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21
Q

What is the difference between strength of ferrous sulfate vs ferrous sulfate, dried?

A

Ferrous sulfate (FeroSul, Fer-In-Sol): 325mg (65mg elemental iron)
Ferrous sulfate dried (Slow Fe, Slow Iron, ER formulation): 160mg (50mg elemental iron)

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22
Q

Boxed warning for oral iron

A

accidental overdose causing fatal poisoning in children
In case of accidental overdose, got o ED or call poison control immediately (even if asymptomatic)

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23
Q

Side effects for oral iron

A

Constipation (dose-related), dark and tarry stools

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24
Q

What is the antidote for iron overdose?

A

Deferoxamine (Desferal)

25
Q

IV iron administration is typically restricted to which patients?

A

CKD on HD and/or receiving ESAs
Unable to tolerate oral iron
Severe anemia or losing iron too fast for oral replacement (e.g. chronic blood loss)
As an alt when blood transfusions are not accepted by the patient (e.g. religious reasons)

26
Q

____ can increase absorption of iron (using together may enhance iron absorption to minimal extent)

A

Vit C (ascorbic acid)

27
Q

Why is IV iron administration typically restricted to certain patients?

A

Adverse reactions and cost

28
Q

Boxed warning for IV iron

A

serious and sometimes fatal anaphylactic reactions with iron dextran or ferumoxytol
All pts receiving iron dextran should be given a test dose prior to first full therapeutic dose (fatal reactions have occurred even in pts who tolerated test dose)

29
Q

All IV iron products carry a risk for ____

A

hypersensitivity reactions (including anaphylaxis)

30
Q

Common IV iron products used for iron deficiency anemia

A

Iron sucrose (Venofer)
Ferumoxytol (Feraheme)

31
Q

Macrocytic anemia is caused by ____ or ___ deficiency, or both

A

Vit B12 or folate

32
Q

_____ anemia, the most common cause of vit B12 deficiency, occurs due to a lack of ____ factor (required for adequate vit B12 absorption in the small intestine). This type of anemia requires lifelong parenteral vit B12 replacement.

A

Pernicious
Intrinsic

33
Q

Other causes of macrocytic anemia include ____

A

Alcoholism
Poor nutrition
GI disorders (e.g. Crohn’s disease, celiac disease)
Pregnancy

34
Q

Long term use (≥ __ years) of ____ can decrease absorption of vit B12, resulting in serious ______ (may be irreversible if undiagnosed)

A

≥2 yrs
Metformin, PPIs or H2RAs
neurologic dysfunction, including cognitive impairment and peripheral neuropathies

35
Q

Folic acid deficiency causes ____

A

Ulcerations of the tongue and oral mucosa and changes to skin, hair, and fingernail pigmentation

36
Q

Diagnosis of macrocytic anemia

A

Low Hgb and high MCV
Low reticulocyte counts and vit B12 and/or folate serum levels

37
Q

Treatment of macrocytic anemia

A

Vit b12 injections as first-line for severe deficiency or neurologic symptoms

38
Q

Treatment options for vit b12 deficiency

A

Cyanocobalamin (vit B12) - comes in IM, deep SC, PO/SL, and nasal
Nascobal - one nostril once weekly

39
Q

___ is a hormone produced by the kidneys that stimulates the bone marrow to produce RBCs

A

Erythropoietin (EPO)

40
Q

___ deficiency causes anemia of CKD

A

Erythropoietin (EPO)

41
Q

Treatments for anemia of CKD

A

Iron therapy and eryhtropoiesis-stimulating agents (ESA)

42
Q

What is the role of ESAs in anemia of CKD?

A

Maintain Hgb levels and reduce need for blood transfusions but ineffective if iron stores are low

43
Q

IV Iron is first line for ___ patients with anemia of CKD

A

HD

44
Q

Boxed warnings for ESAs

A

Increase risk of death, MI, stroke, VTE, thrombosis of vascular access
Use lowest effective dose to reduce need for blood transfusions

CKD: increase risk of death, serious CV events, and stroke when Hgb > 11

Cancer: not indicated when anticipated outcome is cure, shortened overall survival and/or increase risk of tumor progression or recurrence in clinical studies in some cancers

45
Q

Warnings for ESAs

A

HTN

Others: seizures, serious allergic reactions, serious skin reactions (SJS/TEN)
Epoetin alfa - contains albumin (remote risk for transmission of viral diseases)

46
Q

Monitoring for ESAs

A

Hgb, Hct, TSAT, serum ferritin, BP

47
Q

___ route is recommended for HD patients on ESAs

A

IV route

48
Q

Storage for ESAs

A

Refrigerator, protect from light, do NOT shake

49
Q

Darbepoetin half life vs epoetin alfa half-life

A

darbepoetin half-life is 3x longer than epoetin alfa

50
Q

Epoetin alfa (Epogen, Procrit) CKD dosing frequency

A

IV or SC 3x/week

51
Q

Epoetin alfa (Epogen, Procrit) should be initiated when Hgb _____ (both cancer + CKD pts)

A

Hgb <10

52
Q

At what point should Epotein alfa (Epogen, Procrit) dose be decreased or interrupted in a CKD HD patient?

A

When Hgb approaches or exceeds 11

53
Q

Side effects of ESAs

A

Arthralgia/bone pain
Others: fever, HA, pruritus/rash, N/V, cough, dyspnea, edema, injection site pain, dizziness

54
Q

What are the 2 most common mechanisms by which drug-induced hemolytic anemia occurs?

A

Immune-mediated (identified with + Coombs test)
G6PD deficiency

55
Q

The G6PD enzyme protects RBCs from ____; without sufficient levels of G6PD, RBCs hemolyze 24-72 hrs after exposure to oxidative stress.

A

oxidant injury

56
Q

What can increase risk of hemolytic anemia in pts with G6PD deficiency?

A

Select drugs
Certain foods (e.g. fava beans)
Severe stress

57
Q

What meds should be avoided in pts with G6PD deficiency d/t risk of hemolytic anemia?

A

Dapson
Methylene blue
Nitrofurantoin
Primaquine
Pegloticase
Rasburicase
Quinidine
Quinine
Sulfonamides

58
Q

What meds should be avoided in pts with + Coombs Test d/t risk of hemolytic anemia (immune mediated)?

A

PCNs
Cephalosporins
Isoniazid
Levodopa
Methyldopa
Rifampin
Quinidine
Quinine
Sulfonamides