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DT1 > RBC > Flashcards

RBC Flashcards

1
Q

characteristics of RBC

A

biconcave with central pallor
7-8 micrometers in diameter
deformable for capillaries and splenic fenestrations

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2
Q

anemia

A

reduction in circulating Hb, total number of RBCs, or circulating RBC mass

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3
Q

acute and chronic anemia compensation from bone marrow

A

acute-3x increase in 7-10 days

chronic-6 to 8x increase

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4
Q

signs of anemia

A 
due to tissue hypoxia
easy fatigue
dyspnea
pallor
syncope
postural hypotension
angina
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5
Q

cardiovascular compensation

A

heart murmurs
more forceful apical impulse, palpitations
tachycardia
CHF

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6
Q

blood volume

A

3L plasma and 2L blood cells

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7
Q

MCH

A

Hb/RBC count

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8
Q

MCHC

A

(Hb/Hct)x100

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9
Q

RDW

A

distribution of size (high=anisocytosis)

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10
Q

reticulocyte count

A

young RBC with residual rRNA

increases in patients with normal renal (epo) and bone marrow functions

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11
Q

microcytic

A

iron def

thalassemia

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12
Q

normocytic

A

acute blood loss

chronic disease

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13
Q

macrocytic

A

vitamin B12

folate def

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14
Q

iron def anemia

A

most common
babies-excessive milk intake
decrease MCV, MCH, MCHC, increased RDW

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15
Q

iron cycle

A

transferrin-delivered to duodenum
transferrin receptor
ferritin-storage in cells and circulation (acute phase reactant)

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16
Q

causes of def in iron

A

nutritional
malabsorptional-GI surgery, enteritis, celiac sprue
blood loss-menstural, occult GI bleeding, hookworm, aspirin, chronic hemolysis, traumatic hemolysis

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17
Q

states requiring increased iron intake

A

infancy
adolescence
pregnancy
lactation

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18
Q

clinical signs of IDA

A

pallor
koilonychia
esophageal webs
pagophagia, pica

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19
Q

iron studies for IDA

A

high TIBC

low serum Fe, low ferritin

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20
Q

anemia of chronic disease

A

second only to iron def anemia in incidence

most common anemia in hospitalized patients

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21
Q

RBC life span in chronic disease

A

increased phagocytosis
factors released by damaged tissues
physical damage during passage of red cells through tissues

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22
Q

bone marrow in chronic disease

A

suppression by TNF, IL1

defective reutilization of iron salvaged from old RBC-sequestered in phagocytes

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23
Q

anemia studies in chronic disease

A

low serum iron
low transferrin
high ferritin

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24
Q

diseases associated with anemia

A 
chronic renal failure
DM
inflammation
cancer
liver disease 
alcoholism
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25
Q

megablastic anemias

A

CBC shows pancytopenia
vitamin B12 and folate def
hypersegmented neutrophils
BM-giant bands, nuclear-cytoplasmic asynchrony

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26
Q

symptoms of B12 and folate def

A

anemia
atrophic glossitis
gastric gland atrophy
neuro (B12 only)-demyelination of dosolateral columns

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27
Q

B12 def causes

A

pernicious anemia
GI surgery
vegans-dietary insufficiency

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28
Q

states requiring increased B12

A

pregnancy
disseminated cancer
hyperthyroid

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29
Q

pernicious anemia

A

absent intrinsic factor
type 1 blocks B12 binding to If
type 2 blocks complex
diagnose with Schilling test

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30
Q

causes of pernicious anemia

A

autoimmune-Hashimoto, adrenalitis, graves

chronic atrophic gastritis-lost parietal cells

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31
Q

folate def

A 
dietary insufficiency
depleted stores (liver) in 3-6 months
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32
Q

diagnosis megablastic anemia

A

autoantibodies in pernicious anemia
high methylmalonic acid in B12
high homocysteine for both

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33
Q

treatment of megablastic anemia

A

B12-IM injections (reverse neuro if less than 6 months)
folate-passively absorbed
folate partially corrects for B12 def but not neuro deficits

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34
Q

aplastic anemia

A

stem cell injury/suppression
pancytopenia with no reticulocytosis
dry tap-no abnormal cells

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35
Q

clinical signs of aplastic anemia

A

anemia
prone to infections-neutropenia
bleeding-thrombocytopenia
no splenomegaly

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36
Q

acquired aplastic anemia

A

benzene, alcohol, myelotoxic drugs, chloramphenicol, NSAIS
radiotherapy/irradiation
viral-Hep, EBV, HIV, parvo
SLE

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37
Q

hereditary aplastic anemia

A 
Fanconi anemia
autosomal recessive
defects in DNA repair mechanism
congenital anomalies 
can progress to AML or CML or MDS
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38
Q

treatment of aplastic anemia

A

transfusion and antibiotics
immunosuppression-ATG, cyclophosphamide
bone marrow transplantation

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39
Q

pure red cell aplasia

A

only erythroid cell line affected
severe anemia
no reticulocytes
bone marrow-few to absent erythroid precursors

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40
Q

causes of pure red cell aplasia

A

autoimmune mediated against T lymphs or IgG antibody
SLE, CLL, lymphomas, thymomas
chloramphenicol
secondary-parvo B19, solid tumors, rheumatic diseases, phenytoin, azathioprine, isoniazid

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41
Q

Diamond-Blackfan snydrome

A

severe anemia first year of life with congenital anomalies

results in pure red cell aplasia

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42
Q

treatment of pure red cell aplasia

A

stop offending drugs
thymoma resection
IVIG (parvo)
immunosuppression-ATG and cyclosporine

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43
Q

sideroblastic anemias

A

failure to incorporate heme into protoporphyrin to form hemoglobin
dimorphic red cells, hypochromia, ineffective erythropoiesis

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44
Q

iron indices for sideroblastic

A

high serum iron
high ferritin
high transferrin saturation

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45
Q

hereditary sideroblastic

A

X linked

ALA synthase defect (rate limiting enzyme in heme synthesis)

46
Q

acquired sideroblastic anemias

A

myelodysplasia
drugs-alcohol, isoniazid, chloramphenicol
toxins-lead, zinc
nutrional-pyridoxine, copper

47
Q

treatment of sideroblastic anemias

A

pyridoxine (B6)

treat underlying condition and remove exposure to toxins

48
Q

hemolytic anemias lab findings

A

unconjugated bilirubin
decreased haptoglobin (take up free Hb)
increased LDH
reticulocytosis

49
Q

extravascular hemolysis

A

outside bloodstream in reticuloendothelial system
defects in hemoglobins, RBC membrane, RBC enzyme
spherocytes in peripheral blood

50
Q

intravascular hemolysis

A

hemoglobinuria, hemsiderinuria
decreased haptoglobin
extrinsic causes-immune, microangiopathic anemias, infection, burns, hypersplenism

51
Q

HbA

A

A2B2

52
Q

HbA2

A

A2D2

53
Q

HbF

A

A2G2

54
Q

thalassemia

A

reduced production of one or more globin chains

55
Q

beta thalassemia

A

decreased production of HbA

point mutations and partial deletions on chromosome 11

56
Q

beta0

A

no beta globin at all (abnormal messenger RNA degraded)

57
Q

beta+

A

reduced beta-globin gene

58
Q

beta thalassemia major

A

onset 6-9 months after switch from HbF to HbA
anemia
compensation-abnormal bone growth, hepatosplenomegaly, damage to organs

59
Q

treatment of beta thalassemia major

A

transfusion dependent for life

see increase in A2 and F on electrophoresis

60
Q

beta thalassemia minor

A

one normal and one abnormal

iron makes beta thal worse (but PB looks like IDA)

61
Q

alpha thalassemia

A

complete deletion of genes
severity depends on number of genes lost
PB shows basophilic stippling, target cells

62
Q

loss of all 4 alpha

A

death in utero from hemoglobin bart

63
Q

loss of 3 alpha

A

HbH are bitten off by splenic macrophages

Heinz bodies

64
Q

loss of 2 alpha genes

A

alpha thalassemia trait

65
Q

cis alpha thal 1

A

Hb bart

HbH inclusions during life

66
Q

trans alpha thal 2

A

Hb bart

no HbH in life

67
Q

sickle cell reversible to irreversible

A

initially reversible

later irreversible with repeated sickling (spectrin dimers instead of tetramers)

68
Q

HbS

A

valine replaces glutamic acid in 6 of beta globin

69
Q

sickle cell anemia presentation

A 
expanded bone marrow
extramedullary hematopoiesis
autosplenectormy-salmonella osteomyelitis
chronic leg ulcers 
vaso-occlusive crises
dactylitis-swollen fingers
avascular necrosis of femoral head
70
Q

acute chest syndrome

A

dangerous microvascular occlusive crisis
CVA, fever cough and pulmonary infiltrates
infection from encapsulated-Strep and H. flu
prophylactic ABX
aplastic crises-parvo bone marrow suppression
splenic sequestration-splenomegaly and hypovolemia
priapism
organ infarction
gallstone formation from chronic extravascular hemolysis

71
Q

peripheral blood sickle cell

A

crescent shaped sickles, basophilic stippling, Howell-Jolly bodies

72
Q

diagnosis of sickle

A

sickling test with metabisulfate

73
Q

HbA

A

weak interaction, need severe hypoxia to sickle

74
Q

HbF

A

inhibits polymerization, can moderate severity

75
Q

HbC

A

lysine substituted for glutamic acid in position 6 of beta globin chain
clinically less severe than SS
forms crystals in PB

76
Q

tendency to sickle

A

dehydration
thalassemia
low pH
increased temperature

77
Q

sickle cell therapy

A 
hydroxyurea to increase HbF
transfusions
pain management
folate
ABX
78
Q

hereditary spherocytosis

A

AD
RBC lose membrane as they pass thru spleen
mutation in ankyrin-anchor for lipid bilayer
leads to def of spectrin

79
Q

hereditary spherocytosis presentation

A 
hemolytic anemia
jaundice, splenomegaly
gallstones
anemic crisis
fever and infection induced crises
80
Q

diagnosis hereditary spherocytosis

A

osmotic fragility test
microcytosis with increased MCHC
negative DAT

81
Q

osmotic fragility test

A

put in sodium chloride and see if they lyse

82
Q

treatment of hereditary spherocytosis

A

folic acid supplements

splenectomy

83
Q

G6PD deficiency

A

may protect from falciparum malaria
episodic hemolysis with oxidant stress
not enough NADPH to maintain GSH

84
Q

presentation of G6PD def

A

intravascular hemolysis due to Heinz bodies

fever, chills, hemoglobinemia, hemoglobinuria

85
Q

G6PD infections

A

viral hep, typhoid, pneumonia

86
Q

G6PD drugs

A

oxidant drugs

antimalarials, sulfonamides, nitrofurantoin, chloramphenicol

87
Q

G6PD foods

A

fava beans

88
Q

immune hemolytic anemias

A

autoimmune hemolytic anemias

alloimmune hemoltyic anemias

89
Q

DAT

A

antiglobulin used to detect RBC coated with antibodies

used to diagnose autoantibodies in autoimmune hemolytic anemias

90
Q

WAHA

A

IgG autoantibodies
extravascular hemolysis
drug induced-L-dopa, penicillin, tetracyclines, cephalosporins, tolbutamide

91
Q

disorders with WAHA

A

lymphatic malignancies

SLE, RA, UC

92
Q

treatment of WAHA

A

corticosteroids
blood transfusions, gammaglobulins, plasmapheresis
splenectomy

93
Q

CAIHA

A 
monoclonal IgM at low temperatures
I-A,B,O
i
fix complement C3
extravascular hemolysis without splenomegaly
94
Q

acute CAIHA and chronic CAIHA

A

acute-mycoplasma pneumo (I) and mono (i)

chronic-lymphoid malignancy

95
Q

paroxysmal cold hemoglobinuria

A

IgG autoantibody in biphasic hemolysis

96
Q

causes of paroxysmal cold hemoglobinuria

A

mycoplasma pneumo
mono
syphilis
no jaundice or splenomegaly

97
Q

Donath-Landsteiner

A

differentiate PCH from CAIHA

98
Q

hemolytic transfusion reaction

A

ABO incompatible blood

intravascular hemolysis via complement fixation

99
Q

hemolytic disease of newborn

A

hemolysis of newborn RBCs

transplacental transmission of maternal antibodies against Rh positive fetal RBCs

100
Q

sources of maternal immunization in hemolytic disease of newborn

A

previous blood transfusion

previous pregnancy, delivery (due to fetal-maternal hemorrhage)

101
Q

nonimmune hemolytic anemias

A

microagniopathic HA
infections
acquired-alcoholic liver disease, paroxysmal nocturnal hemoglobinuria
mechanical and physical factors

102
Q

microangiopathic HA

A 
abnormalities in microcirculation-fibrin deposition
DIC
HUS
TTP
preeclampsia
103
Q

alcoholic liver disease peripheral blood

A

acanthocytes or spur cells

104
Q

paroxysmal nocturnal hemoglobinuria

A 
mutation in phosphatidyl inositol glycan class A (PIGA)
synthesis of GPI in cell membrane
defects in CD59/55
105
Q

CD55

A

DAF

106
Q

CD59

A

MIRL

107
Q

tests for paroxysmal nocturnal hemoglobinuria

A

sucrose lysis test
Ham’s test
flow cytometry

108
Q

progression of paroxysmal nocturnal hemoglobinuria

A

aplastic anemia
myelodysplasia
AML

109
Q

treatment of paroxysmal nocturnal hemoglobinuria

A

iron supplements
prednisone
bone marrow transplant

110
Q

prosthetic heart valves

A

artificial more than porcine valves

mild anemia to hemolytic anemia

111
Q

march hemoglobinuria

A

marching, marathon running
hemoglobinuria after exercise
normal PB smear, anemia is rare

112
Q

burn injury PB

A

microspherocytes, barbell shapes, rod shapes

DT1 (4 decks)

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