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heme II > section 16 - anemias > Flashcards

section 16 - anemias Flashcards

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1
Q

what pH is necessary for iron reduction

A

<4

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2
Q

define anemia

A
  • less oxygen delivered to tissues
  • may result from increased RBC loss or decreased production of RBCs
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3
Q

when iron is entering the stomach, what form is it in and what is it reduced to

A

orignally in ferric form, reduced to ferrous form

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4
Q

what enxyme is responsible for initially reducing iron in the stomach

A

duodenal cytochrome B (DCYTB)

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5
Q

what cell does iron enter into after reduction in the stomach

A

enterocytes - absorptive stomach lining cells

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6
Q

how is ferrous iron transported into enterocytes (what transporter)

A

divalent metal transporter 1 (DMT1)

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7
Q

what are the two fates of iron w/in enterocytes

A
  • storage
  • transport to other cells
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8
Q

in iron storage, what is combined to form the iron storage unit

A

ferric iron and apoferritin

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9
Q

define ferritin

A

storage form of iron

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10
Q

in iron transport how does iron exit the enterocyte

A

vie ferroportin 1 (FPN1)

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11
Q

what is the transport from of iron and how is it formed

A

ferric iron combines with apotransferrin to form transferrin

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12
Q

what enzyme facilitates conversion of ferrous iron into ferric iron (useable) in the enterocyte

A

hephaestin, copper dependent enzyme

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13
Q

how is iron uptake by cells regulated

A

hepcidin
- binds ferroportin 1 to inactivate it
- keeps iron in cells

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14
Q

how is hepcidin regulated

A
  • erythroferrone: released from rubriblasts
  • hemochromatosis gene (HFE): allows hepcidin formation in high iron levels
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15
Q

how many molecules of iron can transferrin transport at a time and in what state

A

2 ferric irons

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16
Q

define and describe hemosiderin

A

breakdown product of ferritin for storage of iron (water insoluble)

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17
Q

how is iron moved into nRBCs

A

via transferrin receptor 1 (TfR1) on red cell surface

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18
Q

once transferrin iron is absorbed in nRBC endosome, what state must iron be converted to

A

ferrous

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19
Q

how is ferrous iron released into the nRBC

A

via Divalent metal transporter 1 (DMT1)

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20
Q

how is ferrous iron incorporated into the protoporphyrin ring

A

ferrochelatase

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21
Q

how does TfR1 level relate to iron stores

A

inner iron stores low, TfR1 increases to allow more iron to enter

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22
Q

true or false:
intracellular stored ferritin and serum ferritin are in equilibrium

A

true
- this allows for stored ferritin to be measured w/o BM exam

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23
Q

describe serum iron evaluation

A

measure of transferrin bound iron
- free iron is toxic = existing iron is protein bound

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24
Q

describe Total Iron Binding Capacity (TIBC)

A

total amount of iron that can be bound to transferrin in serum or plasma
- how many empty spaces in transferrin exist

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25
describe % saturation lab evaluation
% saturation is measured as max amt iron bound in plasma or serum
26
describe serum ferritin lab evaluation
serum ferritin is proportional to amount of iron stored - ferritin is an acute phase reactant
27
describe soluble transferrin receptor lab evaluation
sTfRs are shed from cells and can be measured in serum - inversely proportional to amt body iron - will increase when iron stores are depleted
28
describe hepcidin level lab evaluation
hepcidin is proportional to amount of iron in body - low iron = low hepcidin - high iron = high hepcidin
29
describe free erythrocyte protoporphyrin and zinc protoporphyrin
- FEP = heme w/o iron inserted - ZPP = heme w/ zinc instead of iron in heme (can't carry oxygen - inversely related to ferritin level
30
describe reticulocyte corpuscular hemoglobin (CHr)
how much hemoglobin is w/in retics - retic numbers decrease with diminished and ineffective erythropoiesis
31
list common causes of iron deficiency anemia
- increased demand - excess loss - decreased absorption - iron poor diet
32
list and describe the stages of IDA
- stage 1: normal serum iron, low storage iron - stage 2: iron deficient erythropoiesis (low serum iron, low red cells) - stage 3: classic IDA
33
describe lab findings of IDA
- low: serum iron/ferritin, % saturation, hepcidin, marrow iron (sideroblasts) - increased: TIBC, sTfRs, FEP/ZPP, retic hgb content (CHr) - erythroid hyperplasia - target and ovalocytes
34
define anemia of chronic inflammation (ACI)
appears secondary to another disease that that has an inflammatory and suppressive effect on hgb production
35
list proposed mechanisms of ACI
- iron stores trapped (increased hepcidin) - ineffective level of erythropoietin (low cytokines) - hemolysis (damage to rbc membranes) - response to pathogen
36
list ACI lab findings
- decrease: serum iron, sideroblasts, % saturation, TIBC - increase: serum ferritin, marrow iron, hepcidin, FEP/ZPP - hypocellular honemarrow - normal sTfRs
37
true or false: TIBC is an acute phase reactant
false - negative acute phase reactant
38
RPI equation
RPI= (corrected retic)/(# days to mature)
39
How to calculate increased # days to mature for retics
Days increase =((pt hct- normal hct)/2)*0.1 1+Days increase= total days to mature in blood
40
describe the main defect in sideroblastic anemia
defect in heme synthesis from inadequate iron utilization
41
describe the rwo main forms of sideroblastic anemia
- hereditary - X linked mutation causing disruption early in synthesis and back up of precursor substances (defective ALAS2) - acquired
42
describe acquired sideroblastic anemia
- primary - form myelodysplastic syndromes that damage stem cell line - secondary - from exposures (generally to lead) that inhibit ferrochelatase from inserting iron into heme ring (or two other inhibitory locations)
43
describe typical lab findings of sideroblastic anemia
- low H&H - dimorphic red cell population (increased RDW) - basophilic stippling and pappenheimer bodies - increase serum iron and ferritin - TIBC and sTfRs normal to decrease
44
define hemosiderosis
excessive accumulation of iron deposits (hemosiderin) in the tissues
45
define hemochromatosis
disorders of iron storage leading to excessive iron deposited in tissues via hemosiderin
46
state the cause of hereditary hemochromatosis
hepcidin deficiency causing excess iron absorption via HFE mutation
47
state the cause of secondary hemochromatosis
acquired secondary to anemia or treatment - increased iron intake causing deposition since there's no iron excretion mechanism
48
define porphyria and the general cause
usually a hereditary, rare disease that result in errors of heme synthesis each caused by specific enzymes
49
define megaloblastic anemia
anemias caused by (1) vitamin B12 deficiency (2) folate deficiency (3) drugs that interfere with DNA synthesis - large red blood cells
50
state the function of vitamin B12
required for degredation of certain fatty acids and metabolizing folate to useable form
51
discuss the role of intrinsic factor in DNA synthesis
IF is released from parietal cells in the stomach and is required for B12 absorption - anti IF antibodies lead to pernicious anemia
52
list possible causes of vitamin B12 deficiency
- B12 poor diet - increased requirments - disease of terminal ileum (bas absopriton) - competing organisms (diphyllobothrium latum) - gastric failure - pernicious anemia w/ anti IF antibodies
53
list possible causes of folate deificiency
- diet - increased requirements - chromic hemolysis - malabsorption
54
describe morphology of megaloblastic anemias (all 3 cell lines)
- megaloblastic red cells - oval macrocytes - high MCV and MCHC - basophilic stippling/HJ bodies - cabot rings - erythroid hyperplasia - increase bilirubin and LDH
55
describe white cell morphology in megaloblastic anemias
- decrease white cells - neutropenia - hypersegmented PMNs
56
clinical presentations of megaloblastic anemias
- stomatitis: inflammation of tongue and mouth w/ rapid cell turnover
57
what tests can be done for early detection of megaloblastic anemias and what can they indicate (besides anemia)
- MMA: B12 deficiency - homocysteine: B12/folate
58
how does B12 relate to folate and red cell production
- B12 necessary to reduce folate to useable form - breaks down fatty acids - red cell production in BM
59
discuss absorption, transport and storage of B12
- attached to IF (released by parietal cells in stomach) - transport across mucosal membrane - B12 splits from IF - B12 transported to destination by transcobalamin II
60
list the major causes of B12 deficiency
- vitamin poor diet - competing organisms - gastric failure - disease of terminal ileum
61
define aplastic anemia
anemia resulting from damage to hematopoietic stem cell causing damage to all cell lines
62
list general causes of aplastic anemia
- hereditary: fanconis,diamond black fan - aquired: exposure, viral infeciton (epstein-barr, HepC, parvo)
63
define and describe Fanconi's anemia
rare genetic defect causing unstable cell chromosomes leading to aplastic anemia and death by 20s
64
define and describe diamond-blackfan syndrome
a form of aplastic anemia of pure RBC lineage - stem cells unable to commit to red cell lineage
65
describe congenital dyserythropoietic anemia (CDA)
- alterations of red cell nuclear membrane - dyserythropoiesis and megaloblastoid characteristics
66
discuss the cause of anemia associated with marrow infiltration
infiltration of the bone marrow by malignant cells (leukemia) causing extramedullary hematopoiesis and leukoerythroblastosis
67
describe WBC characteristics in aplastic anemia
- neutropenia, monocytopenia and relative lymphocytosis - see increased in infections due to low white cells

heme II (11 decks)

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