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

Anemias Flashcards

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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
how do we tx anemia of chronic disease
* Treat the underlying condition * Supplemental iron * EPO – educate on risks
26
how do we tx sideroblastic
* Transfusion PRN * Chelation PRN – remove iron overload * B6 repletion * Copper repletion * Bone marrow transplant –severe cases
27
can we tx siderblastic w/ splenectomy
•Splenectomy CI – congenital issue
28
describe the differences in etiology in thalaseemia A vs B
A - DELETION B- POINT MUTATION
29
asians are affected mostly by thalessemia A/ B greeks / italians are mostly affected by thalsemia A/B
A - asians B- greeks
30
young child less then 2 presents with irratibility and growth retardation? Dx? what can we do to confirm?
Thalessemia B Major ## Footnote * Peripheral smear (target cells, dacrocytes, basophilic stippling) * Ferritin (normal) * Hgb electrophoresis – reduced or absent HbA and INC HbA2 and HbF
31
Thalassemia A presents with what on smear?
•target cells, Heinz bodies)
32
Thalassemia B presents with what on smear?
target cells, dacrocytes, basophilic stippling)
33
how do we tx thalassemias
* Transfusions PRN * Chelation if iron overload * Splenectomy * Stem cell transplant (SCT) * Supplemental folic acid * Genetic counseling
34
Hgb electrophoresis will show what in thal B? A/ HbH?
reduced or absent HbA and INC HbA2 and HbF when up to 30% HbH can be detected à HbH
35
what is HgB electropharesis used mostly to dx?
thalaseemias
36
name some hemolytic anemias
* Hereditary Spherocytosis * G6PD Deficiency * PNH * Autoimmune hemolytic Anemia * Sickle Cell Disease
37
Lab studies common to ALL hemolytic anemias
DEC haptoglobin INC serum LDH
38
explain difference b/w a direct and indirect coombs test
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
name anemia caused by ## Footnote Cell membrane defect due to abnormal spectrin & ankrin. what is th eresult of the abnormal spectrin and ankarin
herediatry spherocytosis DEC RBC flexibility that does not make it through the spleen - hemolysis
40
when you have a suspicion for hereditary sherocytosis what clinical manifestations are you looking for (3)
* Family hx * Splenomegaly * May or may not be anemic
41
PNH is caused by
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
anemia where the pt will have episodic hemoglobinuria – reddish brown urine (first urine in the morning) free hemoglobin
PNH
43
what is key in dx PNH
Flow cyometry ## Footnote •Flow cytometry KEY – deficient of CD55 and CD59 cells
44
how do we tx PNH
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
leading cause of death in PNH
•Thrombosis – leading cause of death (mesenteric, hepatic (Budd Chiari), CNS veins, skin vessels form painful nodules
46
PNH will have (+/-) Coombs test and an INC/DEC LDH
- INC
47
Hereditary enzyme defect (X-linked recessive) ® RBCs cannot sustain oxidative stress - hemoglobin denatures
G6PD deficency
48
what exacerbates or brings on aneia due to G6PD deficency?
Non-immune hemolytic anemia (ex. after drug exposure, fava bean consumption, a/w infection)
49
drugs to avoid w/ G6PD deficency
Dapsone Methylene blue Nitrofurantoin Sulfa drugs
50
•Peripheral smear shows “Bite cells” and Heinz bodies. Dx?
G6PD Def
51
G6PD is protective for
* Protective for malaria * Less coronary artery disease * Fewer cancers * Greater longevity
52
are reticulocytes and serum indirect billi ELEVATED or DECREASED in G6PD def?
Elevated
53
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 \_\_\_\_
Coombs auto + hereditary - (defective spleen not autoimmune)
54
IgG antibody mediated attack on RBCs that has a warm and cold phase
autoimmune hemolytic anemia
55
IgM medicated destruction of RBCs
cold agglutinin
56
what conditions is autoimmune hemolytic anemias seen with
SLE CLL Lymphomas
57
name si/sx of cold aggutinin dx
* Mottled or numb fingers, toes, ears * Acrocyanosis * Episodic lower back pain * Dark colored urine – when cold * Hemoglobinuria w/ cold exposure
58
Rituximab is used to tx
Cold agglutinin disease
59
in aplastic anemia we would expect lab findings to show
panycytopenia ## Footnote •Wont see abnormal cells – morphologically normal just FEWER
60
hwo would we tx sickle cell disease w/ supportive care
* 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
risks assoc w/ sickle cell
* 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
Si/sx of vaso-occlusive crisis in sicle cell
* MSK pain * Dactylitis * Chest pain * Stoke * Priapism * Pulmonary HTN
63
Si/Sx of Hematologic crises in sickle cell
* Splenic sequestration * Aplastic crisis * Hemolytic crisis
64
describe what causes sickle cell
Point mutation in β-globin chain (glutamate ® valine) hemoglobin S (HbS) auto recessive
65
in a pt w/ sickle cell what would we see on a smear
* Irreversibly sickled cells * Howell-jolly bodies * Target cells (hallmark of hyposplenism)
66
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.
aplastic anemia
67
name 2 congential aplastic anemias
* Fanconi anemia - defect in DNA repair pathway * Dyskeratosis congenita – defect in maintenance of hematopoietic stem cell telomere length maintenance
68
what are common si/sx in aplastic anemia
* Pallor petechia most common findings * Cardiopulmonary compromise – no red cells (unable to carry oxygen) walking up the stairs short of breath
69
what should we NOT see in aplastic anemia
* Hepatosplenomegaly * Lymphadenopathy * Bone tenderness – bone would be working overtime
70
Hydroxyurea is used to tx?
Sickle cell - induce fetal hemoglobin
71
moderate aplastic anemia is defined as
* Dec cell lines but NO neutropenia * BM ceelularity \<30% * Few or no symtpma * NO tx
72
very severe aplastic anemia is defined as
* Criteria SAA met * \<200microL
73
how would we tx mild aplastic anemia
yx underlying cause EPO growth factors (epoetin, darbepoetin) myeloid growth factors (•GSCF, sargramostim) transfusions abx/antifungals
74
how wouldwe tx severe aplastic anemia
•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
Equine ATG cyclosporin txs?
severe asplastic anemia
76
Most common cause of congenital inherited aplastic anemia
fanconi
77
si/sx of fancoi
* Several congenital anomalies * Short stature * Rudimentary thumbs * Hypoplastic radii * Renal dysfunction
78
tx fancoi
* Supportive modalities (ex. androgens, hematopoietic growth factors) – usually resistant * Allogenic hematopoietic stem cell transplant – only tx to restore normal hematopoiesis
79
what may we use metabolite testing to differentiate b/w?
vit b12 and folic acid def
80
in vit b12 def MMA, total homocysteine are ? in folic acid deficency they are?
BOTH elevated folic acid - ELEVATED homocysteine and normal MMA
81
what is required for absoprtion of B12
IF - produced by pareital cells
82
•Medications (ex. Methotrexate, Bactrim(Tri), phenytoin can all lead to )
folic acid def
83
when determinig b/w folic acid deficency and vit b12 deficincy what physical exam finding will differentiate the two
vit b12 •Neurologic syndrome (neurological lesions) – peripheral nerves affected first – distal/peripheral paresthesia folic acid - NO NUERO SX
84
what conditions present w/ hypersegmented nuetrophils
vit b12 and folic acid def
85
Methylcoabalamin is used to tx?
vit b 12 along w/ concurrent therapy for folic acid def
86

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

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