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CM 1A: Heme/Onc/Endo > Lecture 4: Anemia II > Flashcards

Lecture 4: Anemia II Flashcards

1
Q

What is aplastic anemia?

A

Failure of hematopoietic bone marrow due to suppression of or injury to stem cells.

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2
Q

What is the MC of aplastic anemia?

A

Idiopathic autoimmune suppression of hematopoiesis.

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3
Q

What kind of diseases result in aplastic anemia?

A

PNH
SLE
Transfusion GVHD

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4
Q

What toxins can cause aplastic anemia?

A

BENZENE
toluene
insecticides
mercury

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5
Q

What medications can cause aplastic anemia?

A

CHEMO
anticonvulsants
chloramphenicol
cimetidine
sulfa

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6
Q

What infections can cause aplastic anemia?

A

HEPATITIS
EBV
Parvovirus B19
CMV

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7
Q

What other things can cause aplastic anemia?

A

Radiation exposure
Pregnancy
Congenital

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8
Q

Describe the pathology of aplastic anemia.

A

Hypoplasia of hematopoietic bone marrow leads to decrease in ALL hematopoietic cell lines.

Note:
This means platelets and WBC production are affected as well.

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9
Q

What does hypoplastic bone marrow look like?

A

Very white due to increased fat deposits and reduced hematopoeisis.

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10
Q

How does aplastic anemia present clinically?

A

Decreased WBCs leads to increased infections.
Decreased RBCs leads to pallor, fatigue, dyspnea, and palps.
Decreased platelets leads to bruising, bleeding from mucosa and skin.

Exam findings:
Pallor, purpura, petechiae.

Lack of hepatomegaly or splenomegaly.

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11
Q

How do I differentiate rashes from petechiae/purpura?

A

Rashes will blanch when pressure is applied.

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12
Q

How does aplastic anemia present on lab findings?

A

WBC: decreased
Platelets: decreased
Retic: Little to none
MCV: normal or increased
MCH: normal

Bone marrow biopsy would show hypocellular aspirate with little to no hematopoietic precursors.

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13
Q

What kind of anemia is aplastic anemia usually? (Morphologically)

A

Normocytic normochromic anemia.

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14
Q

What kind of supportive treatment can be given with aplastic anemia?

A

RBC transfusion
Platelet Transfusion
Antimicrobials

Note:
Do not transfuse WBCs, since risk of fever or autoimmune reaction is high.

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15
Q

What kind of growth factors can be given for aplastic anemia? Why?

A

Multilineage: Eltrombopag/Promacta. Helps boost RBC and WBC production.

Erythropoietic: Epoetin, Darbepoetin

Myeloid: Filgrastim, Sargramostim

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16
Q

What are the two major treatments for aplastic anemia?

A

Bone marrow transplants for pts under 40 yo with full HLA-matched sibling donors.

Immunosuppression for ineligible transplant candidates.
Equine ATG + cyclosporine + steroids +/- eltrombopag + bone marrow stimulating drug

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17
Q

Why are corticosteroids given with horse/equine ATG?

A

Preventing anaphylaxis.

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18
Q

What are epoetin and darbepoetin?

A

Human EPO made via recombinant DNA.

Darbepoetin alfa has 3x the halflife of epoetin alfa

They are also cytokines and growth factors.

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19
Q

What is the purpose of human EPO?

A

It stimulates division and differentiation of the erythroid precursors.

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20
Q

What are the other indications of human EPO?

A

Anemia due to CKD, chemotherapy, and myelodysplasia

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21
Q

What are the CIs for human EPO?

A

Allergy
Uncontrolled HTN
Pure red cell aplasia post tx

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22
Q

What is pure red cell aplasia?

A

RBC production suddenly stops, meaning the bone marrow is too dependent on EPO.

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23
Q

What are the main SE associated with human EPO?

A

HTN and thrombosis.

Most increased risks of death are due to an infarct or thrombosis.

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24
Q

What should be monitored in someone being given human EPO?

A

CBC
Iron
BP
Hb (weekly)

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25
Q

What is sideroblastic anemia?

A

A mixed group of disorders sharing abnormalities in heme synthesis and mitochondrial function.

All of them result in ring sideroblasts when a bone marrow aspiration is performed.

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26
Q

What is the etiology of sideroblastic anemia?

A

Decreased Hb synthesis 2deg

Reduced ability to synthesize heme bc of impaired ability to incorporate iron into protoporphyrin IX. (precursor to heme)

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27
Q

What does a ring sideroblast look like?

A

Ring of blue

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28
Q

What are the causes of inherited/congenital sideroblastic anemia?

A

X-linked (MC inherited)
Autosomal recessive
Mitochondrial inheritance

AKA males are more likely.

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29
Q

What are the causes of acquired sideroblastic anemia?

A

Acquired is the most common type of sideroblastic anemia.

Often part of a general myelodysplastic syndrome.

Chronic alcoholism
Lead poisoning
Copper deficiency
Chronic infection/inflammation
Medications: mainly antimicrobials such as isoniazid, linezolid, and chloramphenicol.

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30
Q

Why does lead poisoning cause sideroblastic anemia?

A

Lead gets stored in the bones in excess.

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31
Q

How does sideroblastic anemia present clinically?

A

General anemia symptoms.

S/S of myelodysplastic syndrome are possible too.

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32
Q

What PE finding on the hand is suggestive of anemia?

A

Palmar creases.

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33
Q

What lab findings would I expect in sideroblastic anemia?

A

Hb/Hct: variable decreases, mainly in Hct.
MCV: can be decreased, but sometimes elevated in acquired.
RDW: increased
Retic: normal or decreased
TIBC: normal or minor decrease
Transferrin sat: increase since more iron is being carried.
Iron: increased
Ferritin: increased

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34
Q

Why does iron increase in sideroblastic anemia?

A

Iron increases because there is more available since the protoporphyrin IX can’t incorporate the iron into the heme.

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35
Q

How does sideroblastic anemia present on peripheral smear?

A

Basophilic stippling
Poikilocytosis
Anisocytosis
Polychromasia

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36
Q

What test must be done to confirm sideroblastic anemia?

A

Bone marrow aspiration with a prussian blue stain.

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37
Q

What exactly is a ring sideroblast?

A

Erythroid cells with iron deposits in mitochondria encircling the nucleus.

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38
Q

What does erythroid hyperplasia on a bone marrow aspirate indicate?

A

Ineffective erythropoiesis.

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39
Q

How do I treat congenital sideroblastic anemia?

A

Some forms will respond to B6 (pyridoxine) or B1 (thiamine).

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40
Q

How do I treat drug-induced sideroblastic anemia?

A

Stopping the med.

If it was due to isoniazid, B6/pyridoxine may help.

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41
Q

What is the MC of anemia worldwide?

A

Iron deficiency.

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42
Q

What is the MC of anemia in the US?

A

Folate deficiency.

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43
Q

What are the two types of iron, and which one is best absorbed?

A

Heme, 40% of meat, which is 10-20% absorbed.

Non-heme, 60% of meat, 100% of veggies, which is 1-5% absorbed.

10% overall absorption in an ACIDIC environment.

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44
Q

What is ferroportin?

A

Major iron transporter and the only exporter of iron from cells.

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45
Q

What is hepcidin?

A

Promotes the breakdown of ferroportin and thus inhibits iron release.

Note:
This is why chronic inflammation alters iron concentrations. Hepcidin is induced via IL-6.

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46
Q

Why do vegan diets and chronic antacid use impair iron absorption?

A

Veggies have non-heme iron, which is poorly absorbed.
Chronic antacids neutralize stomach acidity, but iron is best absorbed in an acidic environment.

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47
Q

When is increased iron needed?

A

Pregnancy
Lactation
Growth spurts

48
Q

What are the causes of iron deficiency?

A

Deficient diets
Increased usage of iron
Chronic blood loss
Decreased absorption
Iron Sequestration

49
Q

What can cause decreased iron absorption?

A

Gastritis
Chronic diseases like celiac sprue or Crohn’s
Gastric surgery
Zinc deficiencies
Hereditary iron-deficiency anemia

50
Q

How does iron deficiency anemia present?

A

General anemia symptoms

Key:
Plummer-vinson syndrome on EGD.
Koilonychia
Smooth tongue
Brittle nails
Cheilosis

Pica

Restless leg syndrome, neurodevelopmental delay

51
Q

What is pica?

A

Craving for substances not rich in iron, like ice, clay, and dirt.

52
Q

How does iron deficiency progress?

A

Low iron with no anemia => Normocytic anemia => Microcytic anemia

53
Q

What lab findings would I expect in iron deficiency anemia?

A

Hb/Hct: variable decreases
MCV: normal early, decreased later.
MCH: decreased
Retic: normal or decreased
TIBC: increased (want iron but have none)
Transferrin sat: decreased (don’t actually have iron)
Iron: decreased
Ferritin: decreased

54
Q

How does iron deficiency anemia present on peripheral smear?

A

Hypochromic, microcytic cells
Target cells
Poikilocytosis
Anisocytosis
Increased platelets (different from thalassemia)

55
Q

What is the main treatment for iron deficiency anemia?

A

Oral Iron supplementation.

Ferrous sulfate 325mg PO TID on an empty stomach.

56
Q

What should improve CBC lab-wise with iron supplement?

A

Hct should go to halfway normal in 3 weeks.
Baseline in 2 months.

Retic should rise in a week and peak in 1.5 weeks.

57
Q

What are the main SE of iron supplementation?

A

Nausea, vomiting, and constipation in 15-20% of pts.

58
Q

What can you do to improve iron supplementation?

A

Gradually escalating dosage.
Taking with food if SE are too strong.
Ascorbic acid
QOD frequency

Make sure you take it for 6 months even after anemia resolves.

59
Q

How does pH affect iron absorption?

A

Acidic = better absorption.

60
Q

What is a common second-line iron supplement?

A

Ferrous gluconate, if people have severe GI upsets.

61
Q

What kind of anemia should never be given iron supplements?

A

Extravascular hemolytic anemias.

62
Q

What are the CI of iron supplementation?

A

Allergies
Hemochromatosis
Hemolytic anemias

63
Q

What lab finding responds very quickly to iron supplementation?

A

Retic count

64
Q

What is the alternative to oral iron supplementation?

A

Parenteral iron replacement therapy.

IV infusion for a few minutes.

65
Q

What is normally added to parenteral iron supplementation?

A

EPO, which will increase bone marrow response to iron.

66
Q

Why was parenteral iron supplementation not preferred before?

A

Iron dextran was the older form that took hours and had anaphylaxis risk.

IM forms had iron staining (cutaneous siderosis)

67
Q

How is anemia caused by inflammation/infection?

A

Proinflammatory cytokines => increased hepcidin => decreased iron absorption and availability.

68
Q

How does anemia of chronic inflammation present clinically?

A

Similar to iron deficiency anemia.

Mainly normocytic (75%) but sometimes microcytic (25%)
Decreased iron levels.

Increased/normal ferritin w/ hx of inflammation or infection separates it from iron deficiency anemia.

69
Q

How is anemia caused by CKD?

A

Failure to secrete adequate EPO by the kidneys.

CKD severity correlates with anemia severity.

70
Q

How does anemia of CKD present clinically?

A

Normocytic, normochromic anemia.

Normal iron studies.

Pts on dialysis can develop secondary iron/folate defiencies.

71
Q

What are the anemias of hypometabolic states?

A

Anemia of endocrine disorders
Anemia of chronic liver disease
Anemia of starvation

72
Q

What is anemia of endocrine disorders?

A

Decreased EPO secretion, which results in normocytic, normochromic anemia.

Mainly seen in decreased hormone secretion, such as decreased thyroid, testosterone, and/or cortisol.

73
Q

What is anemia of chronic liver disease?

A

Cholesterol deposits in the RBC membranes shorten their survival + the body is secreting insuffficient EPO.

Typically, it is in alcoholics, who also have other nutritional deficiencies.

Macrocytic anemia! (cholesterol deposits increase RBC size)

74
Q

What is anemia of starvation?

A

Decreased protein intake leads to decreased metabolism which leads to decreased EPO.

Commonly seen in people starving themselves, eating disorders, and elderly pts.

75
Q

What is anemia of the elderly?

A

Occurs in 20% of pts >85 yo.

Caused by resistance to EPO, decreased EPO secretion, and a chronic low-level inflammation.

Presents with anemic s/s but has a negative work-up for anemia etiology.

Treated sometimes with EPO, but it may require a lot if resistant.

76
Q

What kind of anemia is a B12 deficiency?

A

Megaloblastic anemia.

77
Q

What is the role of B12?

A

Conversion of MMA to Succinyl-CoA
Conversion of homocysteine to methionine.

These are both part of DNA synthesis in erythroid precursors.

78
Q

Where does B12 come from?

A

Animal-based foods, fortified foods.

79
Q

What kind of vitamin is B12?

A

Water-soluble, so it is mainly stored in the liver.

80
Q

What is required to absorb B12?

A

Intrinsic factor from the stomach, which binds to B12 so it can be absorbed in the ileum.

81
Q

What causes a B12 deficiency?

A

Dietary deficiencies (vegan, alcohol, elderly)

Decreased intrinsic factor (pernicious anemia or gastric surgery)

Pancreatic insufficiency

Transcobalamin II deficiency (inherited disorder. Transcobalamin is similar to transferritin)

Medications: Metformin, PPIs, colchicine.

Competition of B12 (blind loop syndrome or a fish tapeworm)

Decreased B12 absorption (Surgical small bowel resection or Crohn’s)

82
Q

How does B12 deficiency present clinically?

A

Insidious onset of general S/S of anemia, along with decreased WBC and platelets.

Unique:
Gradual onset neuropathy, starting with peripheral paresthesia.

83
Q

What kind of anemia is a B12 deficiency?

A

Macrocytic hyperchromic anemia.

84
Q

What lab findings do I expect in a B12 deficiency?

A

Hb/Hct: variably decreased
MCV: increased
MCH: increased
MCHC: normal
Serum B12: decreased
Homocysteine & MMA: increased
Retic: normal or decreased
WBC & platelets: normal or decreased
LDH and bilirubin: increased (intramedullary destruction of abnormal RBCs)

85
Q

How does B12 deficiency anemia present on peripheral smear?

A

Hypersegmented neutrophils
Macro-ovalocytes
Bizarre RBC shapes (poikilocytosis due to DNA synthesis errors)
Basophilic stippling

86
Q

What are the main tests to check for pernicious anemia?

A

Anti-intrinsic factor antibodies: elevated in 50% of pts. specific but non-sensitive.

Anti-parietal cell antibodies: elevated in 85% of pts, non-specific
Gastrin levels: elevated in 80-90% of pts, non-specific

Gastric biopsy on EGD

Schilling Test (OLD TEST) w/ B12 IM.

87
Q

How is B12 deficiency treated?

A

B12 injection therapy. 1mg IM.

Oral B12 therapy once correction is fixed at 1mg/day.
Folic acid 1mg/day also.

Transfusions PRN
Dietary counseling

88
Q

Why can pernicious anemia not be treated by oral B12?

A

Impaired absorption since it is related to intrinsic factor.

89
Q

How quickly is the response to Oral B12 tx?

A

Reticulocytosis in 1 week.

Normal CBC in 2 months.

90
Q

What is cyanocobalamin?

A

Synthetic B12 to replace cobalamin in the body.

Only CI is allergy.

SE include HA, paresthesia, GI upset, and glossitis.

91
Q

What is the role of folate in the body?

A

Conversion of homocysteine to methionine.

92
Q

Where does folate come from?

A

Fruits and veggies, specifically citrus and leafy greens.

93
Q

How much folate do we use daily and eat/absorb?

A

We use up 50-100 mcg/day.

We eat 250 mcg/day and absorb about 125 mcg/day.

94
Q

How much folate do we store and where?

A

5-10mg stored in the liver.

95
Q

Where is folate absorbed?

A

Upper SI.
Jejunum

96
Q

What is the main cause of a folate deficiency?

A

Not eating enough folate.

Alcoholism, lack of fruits/veggies, overcooking, or anorexia.

97
Q

What other conditions can cause folate deficiencies?

A

Pregnancy
Chronic hemolytic anemia
Exfoliative skin disease
Methotrexate
Hemodialysis
Tropical sprue w/ concurrent B12 deficiency
Phenytoin, sulfasalazine, and trimethoprim-sulfamethoxazole.

98
Q

What is the metabolite absorption mnemonic?

A

DI
JF
IB
Dude Is Just Feeling Ill Bro

Duodenum-Iron
Jejunum-Folate
Ileum-B12

99
Q

How does folate deficiency present clinically?

A

S/S of anemia, insidious onset.

Similar to B12 EXCEPT no neuropathy!!!!!!

100
Q

What lab findings would I expect in folate deficiency?

A

Hb/Hct: variable decrease
MCV: increased
MCH: increased
MCHC: nrormal
B12: normal
Homocysteine: Increased
MMA: normal
Retic: Normal/decreased
WBC/platelets: normal/decreased
RBC folate/folic acid: decreased

Serum folic acid is preferred over RBC folate bc it checks more recent folic acid intake and is cheaper.

101
Q

How does folate deficiency present on peripheral smear?

A

Hypersegmented neutrophils
Macro-ovalocytes

102
Q

How is folate deficiency treated?

A

Folic acid PO 1-5 mg/daily for 4+ months.
RULE OUT B12 DEFICIENCY

L-methyfolate is the active form.

Transfusions are rare.

Note:
Malabsorption doesn’t affect the entire jejunum so malabsorption is rarely an issue.

103
Q

How quickly is the response to folate deficiency treatment?

A

Reticulocytosis in 1 week.
CBC normalization in 2 months.

104
Q

Why is folic acid used in pregnancy?

A

To prevent neural tube defects.

105
Q

What is a myeloproliferative disorder?

A

Any disorder that is categorized by excessive growth of 1+ hematopoietic stem cell lines.

106
Q

What are the myeloproliferative disorders?

A

Polycythemia vera: excessive production of all hematopoietic cells, esp. RBCs.

Essential thrombocytosis: Excessive platelet production

Myelofibrosis: excessive production of collagen or fibrous tissue in the marrow.

Chronic myelogenous leukemia (CML): excessive production of granulocytes

107
Q

How do myeloproliferative disorders generally present?

A

General: fatigue, anorexia, weight loss, night sweats

GI: Hepatosplenomegaly, abdominal discomfort, early satiety.

Skin: pallor, easy bruising, petechiae, bleeding, superficial vein thrombosis.

108
Q

Which myeloproliferative disorder causes flushing and plethora instead of pallor?

A

Polycythemia vera.

109
Q

How do myeloproliferative disorders cause anemia?

A

Abnormal cell growth competes with erythroid precursors for space.

110
Q

How are myeloproliferative disorders worked up lab-wise?

A

CBC and bone marrow biopsy.

111
Q

How is polycythemia vera treated?

A

Regular phlebotomies and myelosuppression.

112
Q

How is essential thrombocytosis treated?

A

Myelosuppression if symptomatic, otherwise observe.

113
Q

How is myelofibrosis treated?

A

Myelosuppression if symptomatic or bone marrow transplant. Observe if asymptomatic.

114
Q

How is CML treated?

A

Chemotherapy, myelosuppression, bone marrow transplant.

115
Q

Why does bone marrow suppression work on myeloproliferative disorders?

A

Bone marrow suppression targets the most metabolically active cells first.

CM 1A: Heme/Onc/Endo (28 decks)

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