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Clin Med I Exam 3 Heme/ENT > Anemias > Flashcards

Anemias Flashcards

1
Q

what are the normal hemoglobin levels in males and females

normal MCV?

A

Hemoglobin <13 g/dl MEN

Hemoglobin <12 g/dl WOMEN

MCV 80-100

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2
Q

MCV characterizing microcytic anemia

A

<80 fl

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3
Q

Name examples of microcytic anemia

A

iron deficency anemia (most common)

anemia of chronic disease

sideroblastic

thalassemias

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4
Q

MCV for normocytic anemias

name some normocytic anemias

A

80-100 fl

hereditary spherocytosis

PNH

G6PD deficency

autoimmune hemolytic anemia

sickle cell

cold aggutinin

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5
Q

MCV for macrocytic anemia vs Megaloblastic anemia

A

macro - >100 fl

megalo - >115 fl

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6
Q

when we see a patient with a LOW reticulocyte count we should think ____?

A

macrocytic anemia - think PRODUCTION ISSUE

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7
Q

name some examples of macrocytic anemia

A

aplastic anemia

fanconi anemia

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8
Q

name some exaples of megaloblastic anemia

A

vit b12 deficency

pernicious anemia

folic acid deficency

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9
Q

explain the role of EPO

A

hormone produced by kidney and small amounts in the liver stimulates erythropoiesis

  • Kidney sense decreased O2 levels In blood à stimulating kidney to release EPO
  • EPO acts aa a messenger to bone marrow to enhance red cell production
  • Up regulation leads to increase in committed cells (proerythroblasts) and subsequentially reticulocytes
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10
Q

explain the role of Bilirubin

A

breakdown of heme portion of RBC porphyrin ring

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11
Q

explain how iron is absorbed in intestines

A
  • Transferrin – transports iron
  • Ferritin simple storage
  • Hemosiderin – complex iron stores in macrophages, helpful with insoluble ion

•

•Iron from RBC breakdown is stored and reused in erythropoiesis

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12
Q

You suspect anemia in a patient and order an iron study the results are as follows:

DECREASED - iron, transferrin, ferritin

INCREASED - TDIC

dx?

A

iron deficency anemia -

sideroblastic is OPPOSITE of these labs

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13
Q

what is the most common cause of anemia worldwide

A

iron deficency anemia

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14
Q

which anemia is associated with copper deficency and defect in ALA synthase

A

sideroblastic

Bone marrow defect – makes ringed sideroblasts (not normal RBCs)

Since marrow cannot use iron to make hemoglobin, iron accumulates in the mitochondria of RBCs –

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15
Q

name conditions where we would see hypochromic microcytic cells on a smear

A

ALL microcytic anemias

Iron deficency

sideroblastic

thalaseemias

NOT - anemia of chronic disease youw ould see NORMOchromic, microcytic

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16
Q

describe the stages of iron deficency anemia

A
  1. Depletion of iron stored w/o anemia
  2. Anemia with nl RBC size (nl MCV)
  3. Anemia with reduced RBC size (low MCV)
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17
Q

anemia of chronic disease is most likely caused by: (3 things)

A

chronic inflammation

endocrine disorders

infection

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18
Q

which anemia would present with an INC ferratin and a LOW iron?

along with LOW EPO and TIDC?

A

anemia of chronic disease - body protecting iron as ferritin

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19
Q

pt labs come back:

INC: iron, transferrin, ferritin

DEC: TIBC

Dx?

what would we see on peipheral smear

A

siderblastic anemia - iron def is opposite

basophilic stippling, target cells,

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20
Q

Iron deficeny anemia has a LOW/ HIGH EPO while anemia of chronic disease has a LOW / HIGH EPO.

A

iron def - HIGH

chronic disease - LOW EPO

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21
Q

anemia where bone marrow cannot use iron to make hemeoglobin so heme accumulates in mitochondria of RBCs

A

siderblastic

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22
Q

meds that can cause siderblastic

A

Chloramphenicol and linezolid

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23
Q

how would iron deficency anemia present

A
  • Pica – craving non-food
  • Phagophagia
  • Glossitis
  • Mouth soreness
  • Angular cheilitis
  • Koilonychia
  • Dysphagia
  • Fatigue
  • Conjunctival pallor
  • Tachycardia/palpitations
  • Dyspnea
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24
Q

how do we tx iron def anemia

A
  • Ferrous sulfate 325 mg TID – titrate to TID take w/ vit C
  • Cooking on iron skillet
  • Iron sucrose (Venofer) IV
  • Sodium ferric gluconate (Ferrlicit) IV

•

•Recheck labs in 2-3 wks

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25
Q

how do we tx anemia of chronic disease

A
  • Treat the underlying condition
  • Supplemental iron
  • EPO – educate on risks
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26
Q

how do we tx sideroblastic

A
  • Transfusion PRN
  • Chelation PRN – remove iron overload
  • B6 repletion
  • Copper repletion
  • Bone marrow transplant –severe cases
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27
Q

can we tx siderblastic w/ splenectomy

A

•Splenectomy CI – congenital issue

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28
Q

describe the differences in etiology in thalaseemia A vs B

A

A - DELETION

B- POINT MUTATION

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29
Q

asians are affected mostly by thalessemia A/ B

greeks / italians are mostly affected by thalsemia A/B

A

A - asians

B- greeks

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30
Q

young child less then 2 presents with irratibility and growth retardation?

Dx?

what can we do to confirm?

A

Thalessemia B Major

  • Peripheral smear (target cells, dacrocytes, basophilic stippling)
  • Ferritin (normal)
  • Hgb electrophoresis – reduced or absent HbA and INC HbA2 and HbF
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31
Q

Thalassemia A presents with what on smear?

A

•target cells, Heinz bodies)

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32
Q

Thalassemia B presents with what on smear?

A

target cells, dacrocytes, basophilic stippling)

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33
Q

how do we tx thalassemias

A
  • Transfusions PRN
  • Chelation if iron overload
  • Splenectomy
  • Stem cell transplant (SCT)
  • Supplemental folic acid
  • Genetic counseling
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34
Q

Hgb electrophoresis will show what in thal B?

A/ HbH?

A

reduced or absent HbA and INC HbA2 and HbF

when up to 30% HbH can be detected à HbH

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35
Q

what is HgB electropharesis used mostly to dx?

A

thalaseemias

36
Q

name some hemolytic anemias

A
  • Hereditary Spherocytosis
  • G6PD Deficiency
  • PNH
  • Autoimmune hemolytic Anemia
  • Sickle Cell Disease
37
Q

Lab studies common to ALL hemolytic anemias

A

DEC haptoglobin

INC serum LDH

38
Q

explain difference b/w a direct and indirect coombs test

A

DIRECT COOBS –

  • looking for antibodies or complement proteins on surface of RBCs
  • Hemolytic anemia, CLL

INDIRECT COOMBS-

  • Detects antibodies that are in your serum/blood and could attack RBCs your body views as foreign
  • Auto-immune or drug induced hemolytic anemia
39
Q

name anemia caused by

Cell membrane defect due to abnormal spectrin & ankrin.

what is th eresult of the abnormal spectrin and ankarin

A

herediatry spherocytosis

DEC RBC flexibility that does not make it through the spleen - hemolysis

40
Q

when you have a suspicion for hereditary sherocytosis what clinical manifestations are you looking for (3)

A
  • Family hx
  • Splenomegaly
  • May or may not be anemic
41
Q

PNH is caused by

A

Abnormal sensitivity of RBC membranes to lysis by complement

RBC lysis bc of lack of protective membrane proteins (ex. CD55, CD59) ® attack by complement

42
Q

anemia where the pt will have episodic hemoglobinuria – reddish brown urine (first urine in the morning) free hemoglobin

43
Q

what is key in dx PNH

A

Flow cyometry

•Flow cytometry KEY – deficient of CD55 and CD59 cells

44
Q

how do we tx PNH

A

mild - none

severe

  • Transfusions PRN
  • Eculizumab – monocolonal against C5
  • Iron supplementation as needed
  • Corticosteroids – shut down immune system
  • Allogenic stem cell transplant – or in setting of aplastic anemia of myelodysplasia
45
Q

leading cause of death in PNH

A

•Thrombosis – leading cause of death (mesenteric, hepatic (Budd Chiari), CNS veins, skin vessels form painful nodules

46
Q

PNH will have (+/-) Coombs test and an INC/DEC LDH

47
Q

Hereditary enzyme defect (X-linked recessive) ® RBCs cannot sustain oxidative stress - hemoglobin denatures

A

G6PD deficency

48
Q

what exacerbates or brings on aneia due to G6PD deficency?

A

Non-immune hemolytic anemia (ex. after drug exposure, fava bean consumption, a/w infection)

49
Q

drugs to avoid w/ G6PD deficency

A

Dapsone

Methylene blue

Nitrofurantoin

Sulfa drugs

50
Q

•Peripheral smear shows “Bite cells” and Heinz bodies.

Dx?

51
Q

G6PD is protective for

A
  • Protective for malaria
  • Less coronary artery disease
  • Fewer cancers
  • Greater longevity
52
Q

are reticulocytes and serum indirect billi ELEVATED or DECREASED in G6PD def?

53
Q

spherocytes are found on smears of both autoimmune hemolytic anemia and heriditary spherocytosis. But the differentiating test is the _____ test.

In autoimmune test is ___

in hereditary test is ____

A

Coombs

auto +

hereditary - (defective spleen not autoimmune)

54
Q

IgG antibody mediated attack on RBCs that has a warm and cold phase

A

autoimmune hemolytic anemia

55
Q

IgM medicated destruction of RBCs

A

cold agglutinin

56
Q

what conditions is autoimmune hemolytic anemias seen with

A

SLE

CLL

Lymphomas

57
Q

name si/sx of cold aggutinin dx

A
  • Mottled or numb fingers, toes, ears
  • Acrocyanosis
  • Episodic lower back pain
  • Dark colored urine – when cold
  • Hemoglobinuria w/ cold exposure
58
Q

Rituximab is used to tx

A

Cold agglutinin disease

59
Q

in aplastic anemia we would expect lab findings to show

A

panycytopenia

•Wont see abnormal cells – morphologically normal just FEWER

60
Q

hwo would we tx sickle cell disease w/ supportive care

A
  • Folic acid 1 mg PO QD
  • Pneumococcal vaccine – early
  • Avoid precipitating factors
  • Long term transfusion care
  • Hydroxyurea – induce fetal hemoglobin
  • Omega-3 FA supps
  • Allogenic hematopoietic stem cell transplant
61
Q

risks assoc w/ sickle cell

A
  • Sudden cardiac death and rhabdomyolysis w/ vigorous exercise especially at high altitudes
  • Increased risk of VTE
  • Microscopic and gross hematuria, hyposthenuria and possible CKD
62
Q

Si/sx of vaso-occlusive crisis in sicle cell

A
  • MSK pain
  • Dactylitis
  • Chest pain
  • Stoke
  • Priapism
  • Pulmonary HTN
63
Q

Si/Sx of Hematologic crises in sickle cell

A
  • Splenic sequestration
  • Aplastic crisis
  • Hemolytic crisis
64
Q

describe what causes sickle cell

A

Point mutation in β-globin chain (glutamate ® valine) hemoglobin S (HbS)

auto recessive

65
Q

in a pt w/ sickle cell what would we see on a smear

A
  • Irreversibly sickled cells
  • Howell-jolly bodies
  • Target cells (hallmark of hyposplenism)
66
Q

Injury to myeloid progenitor cells BM is not able to make any PLTs, RBCs, WBCs, due to something causing Injury / depletion of pluripotent stem cell. NO CELLS BEING MADE.

A

aplastic anemia

67
Q

name 2 congential aplastic anemias

A
  • Fanconi anemia - defect in DNA repair pathway
  • Dyskeratosis congenita – defect in maintenance of hematopoietic stem cell telomere length maintenance
68
Q

what are common si/sx in aplastic anemia

A
  • Pallor petechia most common findings
  • Cardiopulmonary compromise – no red cells (unable to carry oxygen) walking up the stairs short of breath
69
Q

what should we NOT see in aplastic anemia

A
  • Hepatosplenomegaly
  • Lymphadenopathy
  • Bone tenderness – bone would be working overtime
70
Q

Hydroxyurea is used to tx?

A

Sickle cell - induce fetal hemoglobin

71
Q

moderate aplastic anemia is defined as

A
  • Dec cell lines but NO neutropenia
  • BM ceelularity <30%
  • Few or no symtpma
  • NO tx
72
Q

very severe aplastic anemia is defined as

A
  • Criteria SAA met
  • <200microL
73
Q

how would we tx mild aplastic anemia

A

yx underlying cause

EPO growth factors (epoetin, darbepoetin)

myeloid growth factors (•GSCF, sargramostim)

transfusions

abx/antifungals

74
Q

how wouldwe tx severe aplastic anemia

A

•Allogenic hematopoietic stem cell transplant (HCT)

  • children <20 yo w/ HLA matched donor
  • adults (20-50) w/ HLA matched donor

•Immunosuppressive therapy (ex. Horse antithymocyte –-> Equine ATG cyclosporin ) (IST)- lower immune response

  • Adults over 50 or no HLA matched donor
  • Consider in adults w/ severe comorbidities
75
Q

Equine ATG cyclosporin txs?

A

severe asplastic anemia

76
Q

Most common cause of congenital inherited aplastic anemia

77
Q

si/sx of fancoi

A
  • Several congenital anomalies
  • Short stature
  • Rudimentary thumbs
  • Hypoplastic radii
  • Renal dysfunction
78
Q

tx fancoi

A
  • Supportive modalities (ex. androgens, hematopoietic growth factors) – usually resistant
  • Allogenic hematopoietic stem cell transplant – only tx to restore normal hematopoiesis
79
Q

what may we use metabolite testing to differentiate b/w?

A

vit b12 and folic acid def

80
Q

in vit b12 def MMA, total homocysteine are ?

in folic acid deficency they are?

A

BOTH elevated

folic acid - ELEVATED homocysteine and normal MMA

81
Q

what is required for absoprtion of B12

A

IF - produced by pareital cells

82
Q

•Medications (ex. Methotrexate, Bactrim(Tri), phenytoin can all lead to )

A

folic acid def

83
Q

when determinig b/w folic acid deficency and vit b12 deficincy what physical exam finding will differentiate the two

A

vit b12 •Neurologic syndrome (neurological lesions) – peripheral nerves affected first – distal/peripheral paresthesia

folic acid - NO NUERO SX

84
Q

what conditions present w/ hypersegmented nuetrophils

A

vit b12 and folic acid def

85
Q

Methylcoabalamin is used to tx?

A

vit b 12 along w/ concurrent therapy for folic acid def

Clin Med I Exam 3 Heme/ENT (3 decks)

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