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heme II > section 16 - anemias > Flashcards

section 16 - anemias Flashcards

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
Q

describe % saturation lab evaluation

A

% saturation is measured as max amt iron bound in plasma or serum

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26
Q

describe serum ferritin lab evaluation

A

serum ferritin is proportional to amount of iron stored
- ferritin is an acute phase reactant

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27
Q

describe soluble transferrin receptor lab evaluation

A

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
Q

describe hepcidin level lab evaluation

A

hepcidin is proportional to amount of iron in body
- low iron = low hepcidin
- high iron = high hepcidin

29
Q

describe free erythrocyte protoporphyrin and zinc protoporphyrin

A
  • 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
Q

describe reticulocyte corpuscular hemoglobin (CHr)

A

how much hemoglobin is w/in retics
- retic numbers decrease with diminished and ineffective erythropoiesis

31
Q

list common causes of iron deficiency anemia

A
  • increased demand
  • excess loss
  • decreased absorption
  • iron poor diet
32
Q

list and describe the stages of IDA

A
  • stage 1: normal serum iron, low storage iron
  • stage 2: iron deficient erythropoiesis (low serum iron, low red cells)
  • stage 3: classic IDA
33
Q

describe lab findings of IDA

A
  • low: serum iron/ferritin, % saturation, hepcidin, marrow iron (sideroblasts)
  • increased: TIBC, sTfRs, FEP/ZPP, retic hgb content (CHr)
  • erythroid hyperplasia
  • target and ovalocytes
34
Q

define anemia of chronic inflammation (ACI)

A

appears secondary to another disease that that has an inflammatory and suppressive effect on hgb production

35
Q

list proposed mechanisms of ACI

A
  • iron stores trapped (increased hepcidin)
  • ineffective level of erythropoietin (low cytokines)
  • hemolysis (damage to rbc membranes)
  • response to pathogen
36
Q

list ACI lab findings

A
  • decrease: serum iron, sideroblasts, % saturation, TIBC
  • increase: serum ferritin, marrow iron, hepcidin, FEP/ZPP
  • hypocellular honemarrow
  • normal sTfRs
37
Q

true or false:
TIBC is an acute phase reactant

A

false
- negative acute phase reactant

38
Q

RPI equation

A

RPI= (corrected retic)/(# days to mature)

39
Q

How to calculate increased # days to mature for retics

A

Days increase =((pt hct- normal hct)/2)*0.1
1+Days increase= total days to mature in blood

40
Q

describe the main defect in sideroblastic anemia

A

defect in heme synthesis from inadequate iron utilization

41
Q

describe the rwo main forms of sideroblastic anemia

A
  • hereditary - X linked mutation causing disruption early in synthesis and back up of precursor substances (defective ALAS2)
  • acquired
42
Q

describe acquired sideroblastic anemia

A
  • 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
Q

describe typical lab findings of sideroblastic anemia

A
  • 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
Q

define hemosiderosis

A

excessive accumulation of iron deposits (hemosiderin) in the tissues

45
Q

define hemochromatosis

A

disorders of iron storage leading to excessive iron deposited in tissues via hemosiderin

46
Q

state the cause of hereditary hemochromatosis

A

hepcidin deficiency causing excess iron absorption via HFE mutation

47
Q

state the cause of secondary hemochromatosis

A

acquired secondary to anemia or treatment
- increased iron intake causing deposition since there’s no iron excretion mechanism

48
Q

define porphyria and the general cause

A

usually a hereditary, rare disease that result in errors of heme synthesis each caused by specific enzymes

49
Q

define megaloblastic anemia

A

anemias caused by (1) vitamin B12 deficiency (2) folate deficiency (3) drugs that interfere with DNA synthesis
- large red blood cells

50
Q

state the function of vitamin B12

A

required for degredation of certain fatty acids and metabolizing folate to useable form

51
Q

discuss the role of intrinsic factor in DNA synthesis

A

IF is released from parietal cells in the stomach and is required for B12 absorption
- anti IF antibodies lead to pernicious anemia

52
Q

list possible causes of vitamin B12 deficiency

A
  • B12 poor diet
  • increased requirments
  • disease of terminal ileum (bas absopriton)
  • competing organisms (diphyllobothrium latum)
  • gastric failure
  • pernicious anemia w/ anti IF antibodies
53
Q

list possible causes of folate deificiency

A
  • diet
  • increased requirements
  • chromic hemolysis
  • malabsorption
54
Q

describe morphology of megaloblastic anemias (all 3 cell lines)

A
  • megaloblastic red cells
  • oval macrocytes
  • high MCV and MCHC
  • basophilic stippling/HJ bodies
  • cabot rings
  • erythroid hyperplasia
  • increase bilirubin and LDH
55
Q

describe white cell morphology in megaloblastic anemias

A
  • decrease white cells
  • neutropenia
  • hypersegmented PMNs
56
Q

clinical presentations of megaloblastic anemias

A
  • stomatitis: inflammation of tongue and mouth w/ rapid cell turnover
57
Q

what tests can be done for early detection of megaloblastic anemias and what can they indicate (besides anemia)

A
  • MMA: B12 deficiency
  • homocysteine: B12/folate
58
Q

how does B12 relate to folate and red cell production

A
  • B12 necessary to reduce folate to useable form
  • breaks down fatty acids
  • red cell production in BM
59
Q

discuss absorption, transport and storage of B12

A
  • 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
Q

list the major causes of B12 deficiency

A
  • vitamin poor diet
  • competing organisms
  • gastric failure
  • disease of terminal ileum
61
Q

define aplastic anemia

A

anemia resulting from damage to hematopoietic stem cell causing damage to all cell lines

62
Q

list general causes of aplastic anemia

A
  • hereditary: fanconis,diamond black fan
  • aquired: exposure, viral infeciton (epstein-barr, HepC, parvo)
63
Q

define and describe Fanconi’s anemia

A

rare genetic defect causing unstable cell chromosomes leading to aplastic anemia and death by 20s

64
Q

define and describe diamond-blackfan syndrome

A

a form of aplastic anemia of pure RBC lineage
- stem cells unable to commit to red cell lineage

65
Q

describe congenital dyserythropoietic anemia (CDA)

A
  • alterations of red cell nuclear membrane
  • dyserythropoiesis and megaloblastoid characteristics
66
Q

discuss the cause of anemia associated with marrow infiltration

A

infiltration of the bone marrow by malignant cells (leukemia) causing extramedullary hematopoiesis and leukoerythroblastosis

67
Q

describe WBC characteristics in aplastic anemia

A
  • neutropenia, monocytopenia and relative lymphocytosis
  • see increased in infections due to low white cells

heme II (11 decks)

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