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RBC Flashcards

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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
megablastic anemias
CBC shows pancytopenia vitamin B12 and folate def hypersegmented neutrophils BM-giant bands, nuclear-cytoplasmic asynchrony
26
symptoms of B12 and folate def
anemia atrophic glossitis gastric gland atrophy neuro (B12 only)-demyelination of dosolateral columns
27
B12 def causes
pernicious anemia GI surgery vegans-dietary insufficiency
28
states requiring increased B12
pregnancy disseminated cancer hyperthyroid
29
pernicious anemia
absent intrinsic factor type 1 blocks B12 binding to If type 2 blocks complex diagnose with Schilling test
30
causes of pernicious anemia
autoimmune-Hashimoto, adrenalitis, graves | chronic atrophic gastritis-lost parietal cells
31
folate def
``` dietary insufficiency depleted stores (liver) in 3-6 months ```
32
diagnosis megablastic anemia
autoantibodies in pernicious anemia high methylmalonic acid in B12 high homocysteine for both
33
treatment of megablastic anemia
B12-IM injections (reverse neuro if less than 6 months) folate-passively absorbed folate partially corrects for B12 def but not neuro deficits
34
aplastic anemia
stem cell injury/suppression pancytopenia with no reticulocytosis dry tap-no abnormal cells
35
clinical signs of aplastic anemia
anemia prone to infections-neutropenia bleeding-thrombocytopenia no splenomegaly
36
acquired aplastic anemia
benzene, alcohol, myelotoxic drugs, chloramphenicol, NSAIS radiotherapy/irradiation viral-Hep, EBV, HIV, parvo SLE
37
hereditary aplastic anemia
``` Fanconi anemia autosomal recessive defects in DNA repair mechanism congenital anomalies can progress to AML or CML or MDS ```
38
treatment of aplastic anemia
transfusion and antibiotics immunosuppression-ATG, cyclophosphamide bone marrow transplantation
39
pure red cell aplasia
only erythroid cell line affected severe anemia no reticulocytes bone marrow-few to absent erythroid precursors
40
causes of pure red cell aplasia
autoimmune mediated against T lymphs or IgG antibody SLE, CLL, lymphomas, thymomas chloramphenicol secondary-parvo B19, solid tumors, rheumatic diseases, phenytoin, azathioprine, isoniazid
41
Diamond-Blackfan snydrome
severe anemia first year of life with congenital anomalies | results in pure red cell aplasia
42
treatment of pure red cell aplasia
stop offending drugs thymoma resection IVIG (parvo) immunosuppression-ATG and cyclosporine
43
sideroblastic anemias
failure to incorporate heme into protoporphyrin to form hemoglobin dimorphic red cells, hypochromia, ineffective erythropoiesis
44
iron indices for sideroblastic
high serum iron high ferritin high transferrin saturation
45
hereditary sideroblastic
X linked | ALA synthase defect (rate limiting enzyme in heme synthesis)
46
acquired sideroblastic anemias
myelodysplasia drugs-alcohol, isoniazid, chloramphenicol toxins-lead, zinc nutrional-pyridoxine, copper
47
treatment of sideroblastic anemias
pyridoxine (B6) | treat underlying condition and remove exposure to toxins
48
hemolytic anemias lab findings
unconjugated bilirubin decreased haptoglobin (take up free Hb) increased LDH reticulocytosis
49
extravascular hemolysis
outside bloodstream in reticuloendothelial system defects in hemoglobins, RBC membrane, RBC enzyme spherocytes in peripheral blood
50
intravascular hemolysis
hemoglobinuria, hemsiderinuria decreased haptoglobin extrinsic causes-immune, microangiopathic anemias, infection, burns, hypersplenism
51
HbA
A2B2
52
HbA2
A2D2
53
HbF
A2G2
54
thalassemia
reduced production of one or more globin chains
55
beta thalassemia
decreased production of HbA | point mutations and partial deletions on chromosome 11
56
beta0
no beta globin at all (abnormal messenger RNA degraded)
57
beta+
reduced beta-globin gene
58
beta thalassemia major
onset 6-9 months after switch from HbF to HbA anemia compensation-abnormal bone growth, hepatosplenomegaly, damage to organs
59
treatment of beta thalassemia major
transfusion dependent for life | see increase in A2 and F on electrophoresis
60
beta thalassemia minor
one normal and one abnormal | iron makes beta thal worse (but PB looks like IDA)
61
alpha thalassemia
complete deletion of genes severity depends on number of genes lost PB shows basophilic stippling, target cells
62
loss of all 4 alpha
death in utero from hemoglobin bart
63
loss of 3 alpha
HbH are bitten off by splenic macrophages | Heinz bodies
64
loss of 2 alpha genes
alpha thalassemia trait
65
cis alpha thal 1
Hb bart | HbH inclusions during life
66
trans alpha thal 2
Hb bart | no HbH in life
67
sickle cell reversible to irreversible
initially reversible | later irreversible with repeated sickling (spectrin dimers instead of tetramers)
68
HbS
valine replaces glutamic acid in 6 of beta globin
69
sickle cell anemia presentation
``` expanded bone marrow extramedullary hematopoiesis autosplenectormy-salmonella osteomyelitis chronic leg ulcers vaso-occlusive crises dactylitis-swollen fingers avascular necrosis of femoral head ```
70
acute chest syndrome
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
peripheral blood sickle cell
crescent shaped sickles, basophilic stippling, Howell-Jolly bodies
72
diagnosis of sickle
sickling test with metabisulfate
73
HbA
weak interaction, need severe hypoxia to sickle
74
HbF
inhibits polymerization, can moderate severity
75
HbC
lysine substituted for glutamic acid in position 6 of beta globin chain clinically less severe than SS forms crystals in PB
76
tendency to sickle
dehydration thalassemia low pH increased temperature
77
sickle cell therapy
``` hydroxyurea to increase HbF transfusions pain management folate ABX ```
78
hereditary spherocytosis
AD RBC lose membrane as they pass thru spleen mutation in ankyrin-anchor for lipid bilayer leads to def of spectrin
79
hereditary spherocytosis presentation
``` hemolytic anemia jaundice, splenomegaly gallstones anemic crisis fever and infection induced crises ```
80
diagnosis hereditary spherocytosis
osmotic fragility test microcytosis with increased MCHC negative DAT
81
osmotic fragility test
put in sodium chloride and see if they lyse
82
treatment of hereditary spherocytosis
folic acid supplements | splenectomy
83
G6PD deficiency
may protect from falciparum malaria episodic hemolysis with oxidant stress not enough NADPH to maintain GSH
84
presentation of G6PD def
intravascular hemolysis due to Heinz bodies | fever, chills, hemoglobinemia, hemoglobinuria
85
G6PD infections
viral hep, typhoid, pneumonia
86
G6PD drugs
oxidant drugs | antimalarials, sulfonamides, nitrofurantoin, chloramphenicol
87
G6PD foods
fava beans
88
immune hemolytic anemias
autoimmune hemolytic anemias | alloimmune hemoltyic anemias
89
DAT
antiglobulin used to detect RBC coated with antibodies | used to diagnose autoantibodies in autoimmune hemolytic anemias
90
WAHA
IgG autoantibodies extravascular hemolysis drug induced-L-dopa, penicillin, tetracyclines, cephalosporins, tolbutamide
91
disorders with WAHA
lymphatic malignancies | SLE, RA, UC
92
treatment of WAHA
corticosteroids blood transfusions, gammaglobulins, plasmapheresis splenectomy
93
CAIHA
``` monoclonal IgM at low temperatures I-A,B,O i fix complement C3 extravascular hemolysis without splenomegaly ```
94
acute CAIHA and chronic CAIHA
acute-mycoplasma pneumo (I) and mono (i) | chronic-lymphoid malignancy
95
paroxysmal cold hemoglobinuria
IgG autoantibody in biphasic hemolysis
96
causes of paroxysmal cold hemoglobinuria
mycoplasma pneumo mono syphilis no jaundice or splenomegaly
97
Donath-Landsteiner
differentiate PCH from CAIHA
98
hemolytic transfusion reaction
ABO incompatible blood | intravascular hemolysis via complement fixation
99
hemolytic disease of newborn
hemolysis of newborn RBCs | transplacental transmission of maternal antibodies against Rh positive fetal RBCs
100
sources of maternal immunization in hemolytic disease of newborn
previous blood transfusion | previous pregnancy, delivery (due to fetal-maternal hemorrhage)
101
nonimmune hemolytic anemias
microagniopathic HA infections acquired-alcoholic liver disease, paroxysmal nocturnal hemoglobinuria mechanical and physical factors
102
microangiopathic HA
``` abnormalities in microcirculation-fibrin deposition DIC HUS TTP preeclampsia ```
103
alcoholic liver disease peripheral blood
acanthocytes or spur cells
104
paroxysmal nocturnal hemoglobinuria
``` mutation in phosphatidyl inositol glycan class A (PIGA) synthesis of GPI in cell membrane defects in CD59/55 ```
105
CD55
DAF
106
CD59
MIRL
107
tests for paroxysmal nocturnal hemoglobinuria
sucrose lysis test Ham's test flow cytometry
108
progression of paroxysmal nocturnal hemoglobinuria
aplastic anemia myelodysplasia AML
109
treatment of paroxysmal nocturnal hemoglobinuria
iron supplements prednisone bone marrow transplant
110
prosthetic heart valves
artificial more than porcine valves | mild anemia to hemolytic anemia
111
march hemoglobinuria
marching, marathon running hemoglobinuria after exercise normal PB smear, anemia is rare
112
burn injury PB
microspherocytes, barbell shapes, rod shapes

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