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Heme > Anemia > Flashcards

Anemia Flashcards

0
Q

Iron Deficiency anemia (Pathogenesis, labs, morphology)

A
  • Most common form in the world,
  • Microcytic, Decreased hemoglobin synthesis
  • Decrease in serum ferratin, and decreased % saturation, Increase in TIBC, increased FEP
  • central pallor much lighter, wider range of cell size
  • iron absorbed in gut
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1
Q

Classifications of anemias (3)

A
  • microcytic (100): folate, B12 deficiency
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2
Q

Causes of iron deficiency anemia

A
  • infants: Breast Feeding
  • children: Nutrition
  • Adults: peptic ulcer disease/Menorrhagia
  • Elderly: colon polyps/carcinoma in the west, Undeveloped countries include Hookworm (ancyclostoma and necator)
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3
Q

Plummer-Vinson syndrome

A
  • Esophageal web
  • Atrophic glossitis
  • Dysphagia
  • Beefy red tongue
  • Anemia
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4
Q

Anemia of chronic disease

A
  • Hepcidin Sequester’s iron And suppresses EPO to inhibit bacterial development
  • ## Lab findings include increased ferratin, decreased TIBC, decreased serum iron, and decreased % saturation, Increased FEP
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5
Q

Sideroblastic anemia

A
  • Defective protoporphyrin synthesis
  • iron (and associated proteins) increase, Hb decrease
  • ALAS -> ALAD -> / (mitos) -> ferrochetalase
  • most commonly congenital lack of ALAS
    ~ alcoholism, Pb (ALAD) and B6 deficiency
  • ringed sideroblasts: iron builds up around the nucleus of primitive RBCs
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6
Q

Ringed sideroblasts

A
  • iron builds up around the nucleus of primitive RBCs
  • sideroblastic anemia
  • iron overloaded state
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7
Q

Thalassemia

A
  • mutating gene ends up producing inappropriately matched dimers
  • less protein + intact DNA replication = microcytic anemia (extra division)
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8
Q

Alpha thalassemia

A
  • 4 alpha genes on ch 16
  • number of deletions corresponds to severity
  • double cis more dangerous
  • HbH: beta tetramers
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9
Q

Beta thalassemia

A
  • B/B+ mildest
  • Bo/Bo most severe
  • crew cut/ chipmunk cheeks
  • a-tetramers cause ineffective erythropoisis and extra vascular hemolysis
  • target cells
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10
Q

Target cells

A
  • results from microcytic cells having excess cytoplasm due to decreased protein content
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11
Q

Parvovirus B19

A
  • initial viremic symptoms, followed by slapped rash

- increase RBC precursors: any condition that results in

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12
Q

Macrocytic anemia

A
  • MCV: > 100
  • decreased DNA synthesis -> less division
  • folate, B12 deficiency, drugs (5-FU, et al)
  • also shows hyper segmented nucleus
  • hyper segmented neutrophils
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13
Q

Folate deficiency (etiology (3), morphology, lab findings)

A
  • poor diet (EtOH), increased demand (preggers), drugs (methotrexate)
  • macrocytic RBCs, hyper seg nuetrophils, glossitis, increased serum homocysteine, normal methylmalonic acid (indicates B12 in normal)
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14
Q

B12 deficiency

A
  • Less common than folate deficiency because of larger B12 stores
  • Pernicious anemia most common cause
  • pancreatic insufficiency, and inflammatory causes
  • dietary is rare
  • macrocytic RBCs, glossitis, central demyelination
  • B12 deficiency -> increase in methylmalonic acid
  • will also show increase in serum homocysteine
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15
Q

Normocytic anemia

A
  • MCV ~ 80-10
  • Reticulocytes (RC) can increase to 3%
  • correct with Hb x (Hct/45)
  • 3+% -> good marrow response = increased destruction/loss
  • 3-% -> poor marrow response = decreased production
  • spherocytosis, HbS/C, PNH, G6PDHD, autoimmune, parvovirus, aplastic anemia,
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16
Q

Peripheral hemolysis (mechanism, effect)

A
  • globin, Iron and protoporphyrin are released (iron is scavanged, globin is broken into AAs, proph is conjugated as biliruben)
  • jaundice
  • hemoglobinurea
  • hemoglobinemia
  • hemosiderinurea
  • decreased haptoglobin
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17
Q

Heriditery spherocytosis (pathenogenesis, indicators, diagnosis, trt)

A
  • congenital mutation of actin anchoring system
  • loss of central pallor
  • increase in RWD and MCHC (mean corpuscular [Hb])
  • splenomegaly (killing all the unusual blood cells)
  • hypotonic fragility
  • splenectomy if anemia gets bad
18
Q

HbS (mutation, complications, trt)

A
  • Glu-> Val: hypoxia conditions = polymerization to crisis
  • homozygous mutant - 90% HbS
  • HbF is protective (hydroxyurea)
  • expansion of hematopoiesis (crew cut, chipmunk)
  • increased risk of Parvovirus due to increased RCs
19
Q

HbS sickling presentation and risks

A
  • autosplenectomy
  • dactylitis
  • increased risk of encapsulated bacteria (most common cause of death in kids)
  • increased risk of salmonella osteomyelitis
  • evidenced by Howell-Jolly bodies
20
Q

Acute chest syndrome

A
  • typically follows pneumonia -> crisis in pulmonary microcirculation
  • most common cause of death in adult patients
21
Q

Renal considerations in HbS

A
  • hypertonicity and hypoxic conditions of medulla lead to microinfarcts and eventual decreased ability to concentrate urine
22
Q

HbC

A
  • LyCine Crystals
  • mild anemia
  • HbC crystals are seen on smear
23
Q

Paroxysmal nocturnal hemoglobinurea (etiology, pathenogenesis, complication, diagnosis)

A
  • GPI anchor deficit (CD55, CD59, C8)
  • nighttime acidotic condition (or exercise) -> compliment activation not avoided by DAF and MIRL (gpi anchored CD55)
  • main cause of death is thrombosis
  • diagnosed by ID lack of CD55
24
Q

G6PDH deficiency (etiology, types, indicator)

A
  • reduced ability to respond to oxidative stress
  • drugs (sulfa et al)
  • African: longer 1/2life
  • Mediterranean: markedly decreased 1/2Life
  • Heinz bodies
25
Q

Heinz bodies

A
  • G6PDH deficiency
26
Q

Autoimmune hemolytic anemia (Abs, etiology, pathenogenesis)

A
  • IgG or IgM
  • macs pick off Igs -> spherocytosis
  • SLE, ALL and drugs (penicillin, quinidine, aldomet, cephalosporins, procainamide)
  • IgM: cold agglutination (assoc with reyneauds)
    ~ IgM assoc with Mycoplasma and Mononucleosis
  • direct (most important for IHA) and indirect Coombs test
27
Q

Microangiopathic hemolytic anemia

A
  • typically caused by TTP, HUS, DIC

- production of schistocytes

28
Q

Anemia due to underproduction

A 
- Parvovirus B19: Infects progenitor cells and halts erythropoiesis
    ~ supportive trt
- aplastic anemia: 
    ~ damage to HPSC: pancytopenia 
    ~ biopsy reveals empty fatty marrow
    ~ cessation of drugs, CFU-GM/G
29
Q

Iron overload in anemia

A
  • extra vascular only
30
Q

DIC in anemia

A
  • intravascular only
31
Q

Haptoglobin

A
  • Hemoglobin scavanger
  • decreases in anemia due to release of Hb
  • Hb Eq of ferritin
32
Q

Pyruvate kinase deficiency

A
  • anemia

- decreased ATP -> accumulates 2,3 BPG -> causes right shift thus tolerates greater of oxygen dissociation

33
Q

Warm autoimmune anemia

A
  • 37c, IgG
  • No complement activation
  • Predominantly extravascular
  • associated with SLE
34
Q

Cold autoimmune anemia (2)

A
  • 32c, IgM

- Cold agglutinin syndrome and Paroxysmal cold hemoglobinuria

35
Q

Cold agglutinin syndrome and associated conditions/infxns

A
  • IgM, extravascular
  • associated with raynauds ph.
  • associated with mycoplasma and mono/HIV, influenza infxns
36
Q

Paroxysmal cold hemoglobinuria

A
  • very rare
  • intermittent massive hemolysis following exposure to cold
  • compliment fixed by IgG-> rewarding leads to intravascular hemolysis
  • Donath-Landsteiner Ab (+)
  • idiopathic, can follow syphillis infxn
37
Q

Aplastic anemia

A
  • hypo proliferation at HPSC (anemia, neutropenia, thrombocytopenia)
  • etiologies:
    ~ loss of stem cells
    ~ suppression of stem cells by macs and T lymphs
    ~ Ab mediated inhibition
    ~ Unfavorable microenvironment
  • drugs: chloramphenicol, benzene et al
  • hepatitis C D and E
38
Q

Blackfan-Diamond syndrome

A

Pure red cell aplasia

- congenital

39
Q

Lack of CD 55

A

PNH diagnosis

40
Q

Ribonucleotide reductase inhibitor

A

Hydroxyurea:cml

41
Q

Donath-Landsteiner Abs and post syphilitic infxn

A
  • associated with paroxysmal cold anemia
42
Q

HbA2

A

Present in thalassemia minor

43
Q

Duodenum, jejunum, Ilium,

A

Iron, folate, B12

Heme (7 decks)

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