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HEME II > Anemias of Diminished Erythroposeisis > Flashcards

Anemias of Diminished Erythroposeisis Flashcards

1
Q

most common and important anemias associated with RBC underproduction

A

nutritional deficiencies then renal failure then chronic inflammation

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2
Q

pernicious anemia cause

A

B12 (cobalamin) deficiency; autoimmune gastritis, failure of intrinsic factor production

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3
Q

what are B12 and folic acid required for

A

coenzymes for synthesis of thymidine (one of 4 bases found in DNA)

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4
Q

characteristics of megablastic anemias

A

macrocytic and oval; ample hemoglobin; lack central pallor, but MCHC not elevated; anisocytosis and poikilocytosis; reticulocyte count low; occasional nucleated RBC if severe in circulation; neutrophils larger than normal and hypersegmented; marrow hypercellular

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5
Q

what secretes intrinsic factor

A

parietal cells of fundic mucosa

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6
Q

what frees B12 from binding proteins in food

A

pepsin in stomch and binds to salivary proteins called cabalophilins or R-binders

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7
Q

what occurs to bound B12 in duodenum

A

released by pancreatic proteases and associates with intrinsic factor

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8
Q

where is the intrinsic factor/B12 absorbed

A

ilial enterocytes, where B12 associates eith transcobalamin II and secreted into plasma

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9
Q

2 rxns that require B12

A

1) methycobalamin serves as essential cofactor in conversion of homocysteine to methionine by methionine synthase (yields FH4) 2) isomerization of methylmalonyl coA to succinyl coA

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10
Q

what builds up in urine and plasma with B12 deficiency

A

methylmalonic acid and propionate

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11
Q

neural effects may be caused by what due to B12 deficiency

A

formation and incorporation of abnormal fatty acids into neuronal lipids = predisposes to myelin breakdown

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12
Q

What is FH4 crucial for

A

conversion of dUMP to dTMP (deoxyuridine monophosphate to deoxythymidine), immediate precursor of DNA

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13
Q

autoantibodies in pernicious anemia

A

75% type I-blocks binding of vit B12 to intrinsic factor; Type II-prevent binding og intrinsic factor-vit B12 complex to ileal receptor; Type III in 85-90%-recognize the alpha and beta subunits of the gastric proton pump

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14
Q

where is the gastric proton pump normally localized

A

microvilli of canalicular system of gastric parietal cell

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15
Q

primary cause of gastric pathology in pernicious anemia

A

NOT auto antibodies; autoreactive T-cell response initiates gastric mucosal injury and triggers formation of autoantibodies

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16
Q

achlorhydria and loss of pepsin secretion

A

B12 not readily released from proteins in food and can cause anemia

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17
Q

exocrine pancreas fxn and B12

A

with loss, can’t release B12 from R-binder-B12 complexes

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18
Q

anemia due to B12 with normal absorption causes

A

pregnancy, tapeworms, hyperthyroidism, disseminated cancer, chronic infection

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19
Q

atrophic glossitis

A

tongue shiny, glazed, and ‘beefy’; seen in B12 deficiency

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20
Q

CNS and B12 deficiency findings

A

demyelination of dorsal and lateral tracts, sometimes followed by loss of axons

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21
Q

diagnosis of pernicious anemia

A

1) moderate/severe megaloblastic anemia
2) leukopenia with hypersegmented granulocytes
3) low serum B12
4) elevated homocysteine and methylmalonic acid in serum

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22
Q

elevated homocysteine levels risk factors

A

increase artherosclerosis and thrombosis

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23
Q

FH4 fxn

A

serves as acceptor of 1-carbon fragments from cmpds such as serine and formimonoglutamic acid, then donates these 1-carbon units to various rxns

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24
Q

most important metabolic processes involving FH4

A

1) purine synthesis
2) conversion of homocysteine to methionine
3) deoxythmidylate monophosphate synthesis

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25
3 major causes of folic acid deficiency
1) decreased intake 2) increased requirement 3) impaired utilization
26
normal transport form of folate
5-methyltetrahydrofolate
27
how quickly can a defiency of folic acid appear
reserves modest; can arise within weeks-months if intake is inadequate
28
alcoholics and low folate
low intake (intestinal absorption), trapping within liver, excessive urinary loss, disordered metabolism
29
drugs that interfere with folate absorption
anticonvulsant phenytoin and oral contraceptives
30
folic acid antagonists
methotrexate-inhibit dihydrofolate reductase and lead to deficiency of FH4
31
diagnosis of folate deficiency
decreased folate levels in serum or red cells; serum homocysteine levels increased, but methylmalonate concentrations normal; neurologic changes do NOT occur
32
why should B12 deficiency be excluded b4 treating for folate deficiency
folate therapy with B12 deficiency doesn't effect or can exacerbate neurological deficits of B12 deficiency states
33
whom is iron deficiency common in the US
toddlers, adolescent girls, and women of childbearing age
34
heme iron vs nonheme iron absorption
20% heme and 1-2% nonheme
35
fxnal storage compartments for iron
80% in hemoglobin; myoglobin and iron-containing enzymes like catalase and cytochromes contain the rest
36
storage pool of iron
hemosiderin and ferritin=make up ~15-20% total body iron
37
transferrin
transports iron in plasma; synthesized in liver; usually 1/3 saturated with iron (120 ug/dL in men and 100 ug/dL in women)
38
ferritin
ubiquitous protein-iron complex that is found at highest concentrations in liver, spleen, bone marrow, and skeletal muscles
39
where is ferritin in liver
stored within parenchymal cells (from transferritin)
40
where is ferritin found in other tissues like spleen and bone marrow
mainly in macrophages (from breakdown of RBCs)
41
where is intracellular ferritin located
cytosol and lysosomes
42
basis of prussian blue stain to see hemosiderin
potassium ferrocyanide
43
what do blood ferritin levels correlate with
body iron stores since this is where it is derived; below 12 ul/L in iron deficiency, can be up to 5000 ug/L
44
where is iron absorbed
proximal duodenum; no regulated pathway for iron excretion (1-2 mg/day lost in shedding of skin and mucosal cells)
45
nonheme iron absorption
1) most in Fe3+/ferric state and must be reduced to Fe2+/ferrous by ferrireductases like cytochromes and STEAP3 in lumin 2) Fe2+ transported across apical membrane by divalent metal transporter 1 (DMT1)
46
2 pathways for iron that enters duodenal cells
1) transport to the blood | 2) storage as mucosal iron
47
how does Fe2+ enter circulation
1) transported from cytoplasm across the basolateral enterocyte membrane by ferriportin 2) newly absorbed Fe3+ binds rapidly to transferrin
48
what is ferriportin transport coupled to
oxidation of Fe2+ to Fe3+ via iron oxidases hephaestin and ceruloplasmin
49
what regulates iron absorption and how
hepcidin, made in liver; inhibits iron transfer from the enterocyte to plasma by binding to ferriportin and casuing it to be endocytosed and degraded; iron is then lost as cells are sloughed
50
what other fxn does hepcidin do
suppresses iron release from macrophages-important in anemia of chronic disease
51
TMPRSS6
hepatic transmembrane serine protease that normally suppresses hepcidin production when iron levels low; rare mutations cause microcytic anemia
52
hemochromatosis
systemic iron overload-low hepcidin
53
secondary hemochromatosis causes
diseases associated with ineffective erythropoiesis like B-thalassemia major and myelodysplastic syndromes
54
causes of iron deficiency
1) dietary lack 2) impaired absorption 3) increased requirement 4) chronic blood loss
55
daily iron requirement (accounting for absorption percentage)
~7-10 mg for men and 7-20 for women
56
what is absorption of inorganic iron enhanced by
asorbic acid, citric acid, aas, sugars in diet
57
what is absorption of inorganic iron inhibited by
tannates (in tea), carbonates, oxalates, and phosphates
58
impaired absorption causes
sprue, fat malabsorption (steatorrhea), chronic diarrhea
59
most common cause of iron deficiency anemia in Western world
chronic blood loss
60
what type of anemia does iron deficiency cause
hypochromatic microcytic anemia
61
progressive loss of iron
first lowers serum iron and transferrin saturation levels without producing anemia
62
best way to see depletion of iron in bone marrow macrophages
Prussian blue stains on smears of aspirated marrow
63
central pallor of RBCs
normally 1/3 of RBC diameter
64
Plummer-Vinson syndrome
esophageal webs along with microcytic hypochromatic anemia and atrophic glossitis
65
CBC specs in iron deficiency
serum iron and ferritic low, TIBC high (elevated transferrin); transferrin saturation below 15%; low hepcidin levels; hgb and HCT low
66
3 groups of chronic diseases that cause iron deficiency
1) chronic microbial infections (osteomyelitis, bacterial endocarditis, lung abscess) 2) chronic immune diseases (RA, regional enteritis) 3) neoplasms (carcinomas of breast and lung, Hodgkin lymphoma)
67
CBC specs in chronic disease iron deficiency
low serum iron, reduced TIBC, abundant stored iron in macrophages; (also low erythropoietin)
68
IL-6
stimulates increase in hepatic production of hepcidin in chronic inflammation; inflammatory mediator
69
red cells in chronic iron deficiency anemia
normo or hypochromatic; and microcytic
70
what can rule out iron deficiency as cause of anemia
increased iron in marrow macrophages, high serum ferritin, reduced TIBC
71
most cases of known etiology of aplastic anemia
follow exposure to chemicals and drugs
72
Fanconi anemia
rare autosomal recessive disorder caused by defects in multiprotein complex that is required for DNA repair; marrow hypofunction early in lifealong with multiple congenital anomalies (hypoplasia of kidney and spleen, bone anomalies of thumbs or radii)
73
inherited defects in telomerase
found in 5-10% of adult-onset aplastic anemia; either short telomeres (more common) or telomerase mutations
74
65% aplastic anemias
idiopathic-no known cause
75
two major etiologies of aplastic anemias
1) extrinsic, immune-mediated suppression of marrow progenitors (T-cells) 2) intrinsic abnormality of stem cells
76
expression analysis of remaining marrow stem cells in aplastic anemia reveal
apotosis and death pathway genes up-regulated
77
what finding should seriously question diagnosis of aplastic anemia
spenomegaly
78
RBCs in aplastic anemia
usually slightly macrocytic and normochromatic; reticulocytopenia is the rule
79
marrow in aplastic anemia
hypocellular
80
myeloid neoplam marrow
hypercellular marrows filled with neoplastic progenitors
81
what is pure RBC aplasia associated with
neoplasms (thymoma, large grandular lymphocytic leukemia), drug exposures, autoimmune disorders, parvovirus infection
82
parvovirus B19
preferentially infects and destroys RBC progenitors; normally cleared 1-2 weeks and aplasia is transient; crisis in moderate/severe hemolytic anemias
83
myelophthisic anemia
marrow failure in which space-occupying lesions replace normal marrow elements (metastatic cancer, granulomatous disease, myeloproliferative diseases-spent phase)
84
fibrotic marrow causes appearance of what in peripheral smear
nucleated erythroid precursors, immature granulocytic forms (leukoerythroblastosis), teardrop-shaped RBCs (due to tortuous escape)
85
chronic renal failure anemia is proportional to
severity of uremia
86
kidney failure anemia causes
reduced erythropoietin, reduced RBC lifespan, iron deficiency due to platelet dysfxn, and increased bleeding
87
hepatocellular liver disease anemia cause
decreased marrow fxn; slightly macrocytic due to lipid abnormalities
88
hypothyroid anemia
mild normochromatic, normocytic anemia
89
relative polycythemia results from
dehydration; stress polycythemia or Gaisbock syndrome
90
seconary polycythemia
reponse to increased erythropoietin
91
polycythemia vera
myeloproliferative disorder associated with mutations that lead to erythropoietin-independent growth of RBC progenitors
92
HIF-1alpha
hypoxia-induced factor that stimulates transcription of erythropoietin gene

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