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Hem/Onc > RBC and anemia 0503 > Flashcards

RBC and anemia 0503 Flashcards

1
Q

acanthocyte (spur cell)

A

liver disease

abetalipoproteinemia

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2
Q

basophilic stippling

A

Lead poisoning
Thalassemia
Anemia of Chronic Disease

“Love The Angry Crawfish of Drew”

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3
Q

bite cell

A

G6PD deficiency

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4
Q

elliptocyte

A

hereditary elliptocytosis

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5
Q

macro-ovalocyte

A 
megaloblastic anemia (w/ hypersegmented neutrophils)
marrow failure
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6
Q

ringed sideroblasts

A

sideroblastic anemia

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7
Q

schistocyte (helmet cell)

A

microangiopathic anemia: TTP, HUS
DIC
traumatic hemolysis

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8
Q

sickle cell

A

sickle cell anemia

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9
Q

spherocyte

A

hereditary spherocytosis

autoimmune hemolysis

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10
Q

tear drop cell

A

bone marrow infiltration - MYELOFIBROSIS

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11
Q

target cell

A

HbC disease
Asplenia
Liver disease
Thalassemia

“HALT, said the hunter to his target”

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12
Q

Heinz bodies

A

alpha thalassemia

G6PD deficiency

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13
Q

Heinz bodies pathogenesis

A

oxidation of iron from ferrous to ferric form leads to denatured Hb precipitation and damage to RBC membrane – leads to bite cells

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14
Q

Howell-Jolly bodies

A

functional hyposplenia

asplenia

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15
Q

Howell-Jolly bodies pathogenesis

A

basophilic nuclear remnants found in RBCs (one obvious darker spot)

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16
Q

anemia presentation

A 
signs of hypoxia:
weakness, fatigue, dyspnea
pale conjunctiva and skin*
HA, lightheaded
angina (esp w/ CAD)
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17
Q

cause of microcytic anemia

A

decreased production of Hb.
extra RBC division tries to maintain Hb conc.

  1. Fe deficiency anemia
  2. thalassemias
  3. lead poisoning
  4. sideroblastic anemia
  5. ACD
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18
Q

where does Fe absorption occur?

A

duodenum

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19
Q

ferroportin

A

allows Fe across enterocyte membrane into bld

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20
Q

transferrin

A

binds and transports Fe in bld, deliver to storage sites

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21
Q

ferritin

A

stores Fe in macrophages, liver, BM (prevent from free radical formation)

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22
Q

as ferritin decreases, what value increases?

A

TIBC - increased transferrin molecules in bld to find more Fe

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23
Q

presentation of Fe deficiency anemia

A

anemia
koilonychia (spoon nails)
pica

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24
Q

causes of Fe deficiency anemia

A

(decreased heme synth)
chronic bleeding- GI loss, menorrhagia
malnutrition/malabsorption
increased demand (preg)

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25
Q

Plummer Vinson syndrome

A
  1. Fe deficiency anemia
  2. esophageal webs (dysphagia)
  3. atrophic glossitis (beefy red tongue)
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26
Q

cause of alpha thal

A

alpha globin gene deletion
= decreased synth of alpha globin

(4 genes present at chromo 16)

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27
Q

alpha thal population

A

Asians

Africans

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28
Q

alpha thal 4 gene deletion

A

Hb Barts (gamma-4).
hydrops fetalis.
fatal in utero.

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29
Q

alpha thal 3 gene deletion

A 
HbH disease (beta-4).
tetramers damage RBCs.
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30
Q

alpha thal 1 or 2 gene deletion

A

no significant anemia

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31
Q

cause of beta thal

A

POINT mutation in splice sites and promoter regions of beta globin gene
= decreased synth of beta globin

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32
Q

beta thal population

A

Mediterranean

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33
Q

beta thal minor

A

heterozygote.
beta chain is UNDERPRODUCED.
mildest form.
usually asymptomatic.

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34
Q

beta thal minor DX

A

TARGET CELLS.

electrophoresis: increased HbA2 > 3.5% (alpha-2, delta-2).
increased HbF (alpha-2, gamma-2).
decreased HbA1 (alpha-2, beta-2).
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35
Q

beta thal major

A

homozygous.

beta chain is ABSENT.

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36
Q

beta thal major SX

A

severe anemia requiring TRANSFUSION (secondary hemochromatosis).

marrow expansion (erythroid hyperplasia). skel deformities.
crew cut on skull XR.
chipmunk facies.

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37
Q

beta thal major DX

A

TARGET CELLS.

electrophoresis: little or no HbA1 (alpha-2, beta-2).
increased HbF (alpha-2, gamma-2).
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38
Q

HbS/beta thal heterozygote

A

mild to moderate sickle cell dz depending on amt of beta globin production

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39
Q

enzymes inhibited by lead

A

ALA dehydratase

ferrochelatase

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40
Q

lead poisoning

A

lead inhibits enzymes leading to decreased heme synth.

also inhibits RNA degradation.

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41
Q

SX of lead poisoning

A

“LEAD”
Lead lines on gingiva (Burton’s lines) and on epiphyses of long bones on XR

Encephalopathy and Erythrocyte basophilic stippling

Abdominal colic and sideroblastic Anemia

Drops - wrist and foot

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42
Q

what is basophilic stippling?

A

aggregation of ribosomes in RBC

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43
Q

TX of lead poisoning

A

1st line: Dimercaprol and EDTA

for kids: succimer

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44
Q

sideroblastic anemia

A

defective protoporphyrin synth
= defective heme synth

*reminder: heme = proto + iron

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45
Q

ringed sideroblasts

A

erythroid precursor with IRON-laden mitochondria around nucleus

*heme is formed in mito. lack of proto leads to iron being trapped in mito.

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46
Q

hereditary sideroblastic anemia

A

X-linked defect in ALA synthase

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47
Q

acquired (reversible) sideroblastic anemia

A

alcohol

lead

48
Q

LABS in sideroblastic anemia

A

increase serum Fe
increase ferritin
normal (decrease) TIBC

49
Q

TX of sideroblastic anemia

A

pyridoxine (B6) - cofactor for ALA synthase

50
Q

megaloblastic anemia

A

impaired DNA synthesis: maturation of nucleus is delayed relative to cytoplasm (one less division than normal)

ineffective erythropoiesis: pancytopenia.

51
Q

megaloblastic anemia

FOLATE deficiency

A 
due to:
malnutrition (ALCOHOLICS)
malabsorption - jejunum
impaired metab (MTX, TMP)
increased requirement (preg, hemolytic anemia)
52
Q

findings in megaloblastic anemia

FOLATE deficiency

A 
hypersegmented neutrophils.
glossitis.
decreased serum folate.
increased serum homocysteine.
NORMAL METHYLMALONIC ACID.
53
Q

megaloblastic anemia

B12 deficiency

A 
due to:
pernicious anemia 
insufficient intake (strict vegans)
malabsorption (Crohns)
Diphyllobothrium latum (fish tapeworm)
54
Q

pernicious anemia

A

most common cause of B12 def.
autoimmune destruction of gastric parietal cells that make intrinsic factor.

intrinsic factor def = less B12 absorption in ileum.

55
Q

findings in megaloblastic anemia

B12 deficiency

A 
hypersegmented neutrophils.
glossitis.
NEURO SX.
decreased serum B12.
increased serum homocysteine.
INCREASED METHYLMALONIC ACID.
56
Q

NEURO problems in B12 deficiency

A

subacute combined degeneration (B12 is involved in fatty acid pathways - myelinization)

  1. peripheral neuropathy w/ sensorimotor dysfunction
  2. posterior columns (vibration, proprioception)
  3. lateral corticospinal (spasticity)
    4 dementia
57
Q

TX of B12 deficiency

A

parenteral B12

58
Q

nonmegaloblastic macrocytic anemia

A 
due to:
liver disease
alcoholism
reticulocytosis (increase MCV)
metab d/o: congenital deficiency in purine or pyrimidine synthesis
drugs: 5-FU, AZT, hydroxyurea
59
Q

nonhemolytic normocytic anemias

A
  1. anemia of chronic dz
  2. aplastic anemia
  3. kidney dz

UNDERPRODUCTION
corrected retic count < 3%.

60
Q

anemia of chronic disease

A

inflammation = increased HEPCIDIN from liver.

hepcidin binds ferroportin on enterocytes and macrophages - inhibit Fe transport. decreased Fe release from macrophages (more storage).

increase ferritin
decrease TIBC
decrease serum Fe

*can become microcytic, hypochromic over time

61
Q

aplastic anemia causes

A

due to failure or destruction of myeloid stem cells:

  1. radiation, drugs: benzene, chloramphenicol, alkylating agents, antimetabolites
  2. viral agents: parvo B19, EBV, HIV, HCV
  3. Fanconi anemia (DNA repair defect)
  4. idiopathic: autoimm? primary stem cell defect? may follow acute hepatitis
62
Q

aplastic anemia findings

A

PANCYTOPENIA- severe anemia, neutropenia, thrombocytopenia.

hypocellular BM with FATTY infiltration.

SX: fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infx.

63
Q

aplastic anemia TX

A

withdraw offending agent.

IMMUNOSUPPRESSION (antithymocyte globulin, cyclosporine)

allogeneic BMT.
RBC and plt transfusion.
G-CSF or GM-CSF.

64
Q

anemia due to kidney disease

A

decreased EPO production =

decreased hematopoiesis

65
Q

intravascular hemolysis findings

A

destruction of RBCs within vessels.

decrease haptoglobin (bind all the free Hb for reprocessing).
increase LDH.

SX: hemoglobinemia, hemoglobinuria

66
Q

extravascular hemolysis findings

A

splenic macrophages destroy RBC.

increase LDH
increase unconj. bilirubin (from proto)

SX: marrow hyperplasia
splenomegaly
jaundice

67
Q

hemolytic normocytic anemia

A

PERIPHERAL RBC DESTRUCTION.

corrected retic count > 3%.

68
Q

hereditary spherocytosis

A

intrinsic hemolytic anemia.
extravascular hemolysis.

defect in proteins that interact with RBC memb skeleton and plasma memb - ankyrin, spectrin, band 3, protein 4.2

69
Q

spherocytes

A

in HS: less membrane causes small and round RBCs with no central pallor.

prematurely removed by spleen.

70
Q

hereditary spherocytosis LAB

A

increase MCHC**
increase RDW

DX: osmotic fragility test

71
Q

hereditary spherocytosis SX

A

splenomegaly
jaundice
aplastic crisis (B19 infx)

72
Q

hereditary spherocytosis TX

A

splenectomy:

HOWELL-JOLLY BODIES present after splenectomy

73
Q

G6PD deficiency

A

intrinsic hemolytic anemia.
both extra and intravascular hemolysis.

X-linked defect in G6PD.

74
Q

normal G6PD function

A

G6PD generates NADPH which is needed to reduce GLUTATHIONE for antioxidant activity.

RBCs become susceptible to oxidant stress when glutathione can’t be reduced.

75
Q

causes of hemolytic episodes in G6PD def

A 
oxidant stress: 
sulfa drugs
primaquine
dapsone
infection
fava beans
76
Q

G6PD def SX

A

back pain

hemoglobinuria a few days later

77
Q

G6PD LAB

A 
RBCs with Heinz bodies.
BITE CELLS (created as splenic macros remove Heinz bodies).
78
Q

pyruvate kinase deficiency

A

intrinsic hemolytic anemia.
extravasc hemolysis.

auto rec defect in pyruvate kinase.
decreased ATP = rigid RBCs.

*hemolytic anemia in newborn

79
Q

HbC defect

A

intrinsic hemolytic anemia.
extravasc hemolysis.

Hb beta chain defect.
missense mutation (chain mutation): glutamic acid replaced by lysine at pos 6.
80
Q

HbSC

A

possess one of each mutant gene. milder disease than HbSS (sickle cell dz).

81
Q

HbC defect LAB

A

lysine is more positive…
HbC is more positive.
moves more slowly on gel electrophoresis.

82
Q

paroxysmal nocturnal hemoglobinuria

A

intrinsic hemolytic anemia.
intravasc hemolysis.

myeloid stem cell defect.
complement-mediatd RBC lysis.
impaired synth. of GPI anchor/decay accelerating factor (DAF) in RBC memb.

83
Q

normal DAF (CD55)

A

binds to RBC via GPI.

inhibits C3 convertase.

84
Q

PNH LAB

A

increased urine hemosiderin.

deficient in CD55 (and CD59).

85
Q

PNH SX

A

episodes occur at night - dark urine in the morning.

86
Q

PNH complications

A

thrombosis - PLATELETS are also destroyed. activate coag cascade and induce thrombosis.

87
Q

sickle cell anemia

A

intrinsic hemolytic anemia.
both extra and intravasc hemolysis.

AR HbS point mutation causes single AA replacement in beta chain - glutamic acid replaced by valine at pos6.

88
Q

sickle cell pathogenesis

A

low O2, dehydration (low bld vol), or low pH precipitate sickling - deoxy HbS POLYMERIZES and causes sickle shape.

RBCs with damaged memo are removed/destroyed. results in anemia, vaso-occlusive dz.

89
Q

sickle cell in newborns

A

newborns ASYMPTOMATIC in first few months - HbF is protective against sickling. newborns have more HbF, less HbS.

90
Q

sickle cell and malaria

A

HETEROZYGOTES (sickle cell trait) have resistance to malaria.

8% of Af Am carry HbS trait

91
Q

sickle cell presentation

A

anemia
fatigue
splenomegaly
CREW CUT on skull XR, chipmunk facies (marrow expansion to compensate)

92
Q

complications w/ sickle cell dz

A
  1. aplastic crisis (B19)
  2. autosplenectomy
  3. splenic sequestration crisis
  4. salmonella osteomyelitis
  5. painful vaso-occlusive crisis
  6. renal papillary necrosis
93
Q

autosplenectomy in sickle cell

A

shrunken, fibrotic spleen.
functional splenic dysfunction occurs in early childhood.

leads to:
increased infx with encapsulated orgs.
Howell-Jolly bodies.

94
Q

vaso-occlusive crises in sickle cell

A

DACTYLITIS: painful hand and feet swelling.

ACUTE CHEST SYNDROME: chest pain, SOB, lung infiltrates.

95
Q

renal papillary necrosis in sickle cell

A

due to low O2 in papilla.

medullary infarcts - MICROSCOPIC HEMATURIA.

96
Q

sickle cell DX

A

Hb electrophoresis - HbS is more hydrophobic (POLAR). moves more slowly to anode than HbA does.

97
Q

sickle cell TX

A
  1. hydroxyurea: increased HbF

2. BM transplant

98
Q

autoimmune hemolytic anemia (AIHA)

A

extrinsic hemolytic anemia.
Ab-mediated destruction of RBCs.

many are idiopathic.
Coombs positive.
present w/ erythroblastosis fetalis.

99
Q

erythroblastosis fetalis

A

seen in newborns due to Rh or other bld Ag incompatibility - mom’s Abs attack fetal RBCs.

100
Q

direct Coombs test

A

asks: are there RBCs already bound by Ig?

add anti-Ig to pt’s RBCs. agglutination occurs if RBCs are already coated with Ig.

101
Q

indirect Coombs test

A

asks: is there Ig in the pt’s serum?

add anti-Ig with test RBCs to pt serum. agglutination occurs if serum Ig is present.

102
Q

AIHA: warm agglutinin

A

IgG

chronic anemia seen in SLE, CLL, certain drugs (alpha methyldopa)

103
Q

AIHA: cold agglutinin

A

IgM (Cold ice cream, Mmmm)

acute anemia triggered by cold.
seen in CLL, mycoplasma pneumonia infxs, infectious mononucleosis.

104
Q

microangiopathic anemia

A

extrinsic hemolytic anemia.
intravasc hemolysis.

RBCs are damaged when passing through obstructed or narrowed vessel lumen.

105
Q

diseases assoc. with microangiopathic anemia

A 
DIC
TTP
HUS
SLE
malignant HTN
106
Q

RBCs in microangiopathic anemia

A

SCHISTOCYTES (helmet cells) due to mechanical destruction

107
Q

macroangiopathic anemia

A

extrinsic hemolytic anemia.
secondary to mech destruction with prosthetic heart valves and aortic stenosis.

SCHISTOCYTES.

108
Q

anemia in infections

A

extrinsic hemolytic anemia.
increased destruction of RBCs.

ex: malaria, Babesia

109
Q

porphyrias

A

defective heme synthesis leading to accumulation of heme precursors

*most common: PCT

110
Q

lead poisoning

A

enz: ALA dehydratase, ferrochelatase

accumulated substrate: protoporphyrin (in bld)

sx: microcytic anemia, GI/kidney dz. abd pain, blue pigment (gingiva).

kids: mental deterioration.
adults: HA, memory loss, demyelination.

111
Q

source of lead poisoning

A

kids: exposure to lead paint
adults: environmental exposure (battery, ammunition, radiator factory)

112
Q

acute intermittent porphyria

A

enz: porphobilinogen deaminase

accumulated substrate: porphobilinogen, ALA, uroporphyrin (porphobilinogen in urine)

113
Q

AIP SX

A 
Painful abd
Pink urine (red wine) - darkens upon standing
Polyneuropathy
Psychological disturbances
Precipitated by drugs
114
Q

AIP TX

A

glucose and heme, which inhibit ALA synthase upstream

115
Q

porphyria cutanea tarda

A

enz: uroporphyrinogen decarboxylase

accumulated substrate: uroporphyrin - tea colored urine

other sx: blistering cutaneous photosensitivity.

*most common porphyria

Hem/Onc (9 decks)

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