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Pathoma > RBC Disorders > Flashcards

RBC Disorders Flashcards

1
Q

Basic principles of anemia

A

Reduction in circulating RBC mass
- Hgb < 13.5 g/dL in males and < 12.5 in females
Presents with signs and symptoms of hypoxia
- weakness, fatigue, dyspnea
- pale conjunctiva and skin
- headache and light headedness
- angina, especially with preexisting coronary artery disease

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2
Q

Basic principles of microcytic anemias

A

Anemia with MCV < 80
Due to decreased production of hemoglobin
- RBC progenitor cells in the bone marrow are large and normally divide multiple times to produce smaller mature cells
- microcytosis is due to an extra division which occurs to maintain hemoglobin concentration
Hgb is made of heme and globin; heme is composed or iron and protoporphyrin
- decrease in any of these components leads to microcytic anemia
Microcytic anemias =
- iron deficiency anemia
- anemia of chronic disease
- sideroblastic anemia
- thalassemia

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3
Q

Iron deficiency anemia

A

Due to decreased levels of iron = low heme = low hgb = microcytic anemia
Most common type of anemia - most common nutritional deficiency in the world
Iron is consumed in heme (meat derived) and non-heme (veggie derived) forms
- absorption occurs in the duodenum
- enterocytes have have heme and non-heme (DMT1) transporters - heme form is more readily absorbed
- enterocytes transport iron across the cell membrane into blood via ferroportin
- transferrin transports iron in the blood and delivers it to the liver and bone marrow macrophages for storage
- stored intracellular iron is bound to ferritin, which prevents iron from forming free radicals via the Fenton reaction

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4
Q

Lab measurements of iron status

A
  • Serum iron - measure of iron in the blood
  • Total iron binding capacity (TIBC) - measure of transferrin molecules in the blood
  • % saturation - percentage of transferrin molecules that are bound by iron; normal = 33%
  • serum ferritin - reflects iron stores in macrophages and the liver
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5
Q

Causes of iron deficiency

A

Usually caused by dietary lack or blood loss
- Infants - breast feeding (human milk is low in iron)
- children - poor diet
- adults - peptic ulcer disease in males and menorrhagia or pregnancy in females
- elderly - colon polyps/carcinoma in the western world; hookwork in the developing world
Other causes
- malnutrition
- malabsorption
- gastrectomy - acid aids iron absorption by maintaining the Fe2+ state, which is more readily absorbed than Fe3+

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6
Q

Stages of iron deficiency

A
  1. Storage iron is depleted = decreased ferritin + increased TIBC
  2. Serum iron is depleted = decreased serum iron + decreased % saturation
  3. Normocytic anemia - bone marrow makes fewer, but normal sized RBCs
  4. Microcytic, hypochromic anemia - bone marrow makes smaller and fewer RBCs
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7
Q

Clinical features of iron deficiency

A
  • anemia
  • koilonychia
  • pica
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8
Q

Laboratory findings in iron deficiency anemia

A
  • microcytic, hypochromic RBCs with increased RDW
  • decreased ferritin + increased TIBC
  • decreased serum iron + decreased % saturation
  • increased free erythrocyte protoporphyrin (FEP)
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9
Q

Treatment of iron deficiency anemia

A

Supplemental iron - ferrous sulfate

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10
Q

Plummer Vinson syndrome

A

Iron deficiency anemia with esophageal web and atrophic glossitis - presents as anemia, dysphagia and beefy red tongue

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11
Q

Anemia of chronic disease

A

Anemia associated with chronic inflammation or cancer; most common type of anemia in hospitalized patients
Chronic disease results in production of acute phase reactants from the liver, including hepcidin
- hepcidin - sequesters iron in storage sites by limiting iron transfer from macrophages to erythroid precursors and suppressing EPO production –> aim is to prevent bacteria from accessing iron
- decreased available iron = decreased heme = decreased hgb = microcytic anemia

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12
Q

Laboratory findings in anemia or chronic disease and treatment

A
  • increased ferritin + decreased TIBC
  • decreased serum iron + decreased % saturation
  • increased free erythrocyte protoporphyrin (FEP)
  • Tx: address underlying cause
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13
Q

Sideroblastic anemia

A

Anemia due to defective protoporphyrin synthesis
Protoporphoryn is synthesized via a series of reactions
- aminolevulinic acid synthetase (ALAS) - converts succinyl CoA to aminolevulinic acid (ALA) using bit B6 as a cofactor = rate limiting step
- aminolevulinic acid dehydrogenase (ALAD) converts ALA to porphobilinogen
- additional reactions convert porphobilinogen to protoporphyrin
- ferrochelatase - attaches protoporphyrin to iron to make heme = final reaction, occurs in mitochondria
- iron is transferred to erythroid precursors and enters the mitochondria to form heme - if protoporphyrin is deficient, iron remains trapped in mitochondria
- iron laden mitochondria form a ring around the nucleus of erythroid precursors = ringed sideroblasts

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14
Q

Causes of sideroblastic anemia

A

Can be congenital or acquired
Congenital defect - most commonly involves ALAS = rate limiting step
Acquired defects
- alcoholism - mitochondrial poison
- lead poisoning - inhibits ALAD and ferrochelatase
- vit B6 deficiency - required cofactor for ALAS; most commonly seen as a side effect of isoniazid treatment for TB

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15
Q

Laboratory findings in sideroblastic anemia

A
  • increased ferritin + decreased TIBC
  • increased serum iron + increased % saturation
  • iron overloaded state
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16
Q

Basic principles of macrocytic anemia

A

Anemia with MCV > 100 - most commonly due to folate or vit B12 deficiency = megaloblastic anemia
Folate and vit B12 are necessary for synthesis of DNA precursors
- folate circulates in the serum as methyl tetrahydrofolate - removal of the methyl group allows for participation in the synthesis of DNA precursors
- methyl group is transferred to vit B12 (cobalamin)
- vit B12 then transfers methyl group to homocysteine, producing methionine
Lack of folate or vit B12 impairs synthesis of DNA precursors
- impaired division and enlargement of RBC precursors leads to megaloblastic anemia
- impaired division of granulocytic precursors leads to hypersegmented neutrophils
- megaloblastic change is also seen in rapidly dividing epithelial cells (eg intestinal)
Other causes of marcocytic anemia without megaloblastic change:
- alcoholism
- liver disease
- drugs (5-FU)

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17
Q

Folate deficiency

A

Dietary folate is obtained from green veggies and some fruits
Absorbed in the jejunum
Folate deficiency develops within months - body stores are minimal
Causes:
- poor diet - alcoholics and the elderly
- increased demand - pregnancy, cancer, hemolytic anemia
- folate antagonists - methotrexate = inhibits dihydrofolate reductase

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18
Q

Clinical and laboratory findings of folate deficiency

A
  • macrocytic RBCs and hypersegmented neutrophils (> 5 lobes)
  • glossitis - decreased turnover of epithelial cells
  • decreased serum folate
  • increased serum homocysteine = increased risk for thrombosis
  • normal methylmalonic acid
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19
Q

Vit B12 deficiency

A

Dietary vit B12 is complexed to animal derived proteins
- salivary gland enzymes liberate B12, which is then bound by R binder and carried through the stomach
- pancreatic proteases in the duodenum detach vit B12 from R binder
- B12 binds intrinsic factor (produced by gastric parietal cells) in small bowel - IF-B12 complex is absorbed in the ileum
B12 deficiency is less common than folate deficiency and takes years to develop due to large hepatic stores of B12

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20
Q

Causes of B12 deficiency

A

Pernicious anemia = most common cause - autoimmune destruction of parietal cells leads to IF deficiency
Other causes of B12 deficiency
- pancreatic insufficiency
- damage to terminal ileum - crohn’s or diphyllobothrium latum (fish tapeworm)
- dietary deficiency is rare - only vegans

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21
Q

Clinical and laboratory findings of B12 deficiency

A
  • macrocytic RBCs with hypersegmented neutrophils
  • glossitis
  • subacute combined degeneration of the spinal cord due to increased levels of methylmalonic acid - impairs spinal cord myelinization –> damage results in poor proprioception and vibratory sensation (posterior column) and spastic paresis (lateral corticospinal tract)
  • decreased serum B12
  • increased serum homocysteine = increased risk for thrombosis
  • increased methylmalonic acid
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22
Q

Thalassemia

A

Anemia due to decreased synthesis of the globin chains of hemoglobin
- inherited mutation - carriers are protected against plasmodium falciparum malaria
- divided into alpha and beta thalassemia based on decreased production of alpha or beta globin chains
Normal types of hemoglobin:
- HbF = alpha2 gamma2
- HbA = alpha2 beta2
- HbA2 = alpha2 delta2

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23
Q

Alpha thalassemia

A

Usually due to gene deletion - normally, 4 alpha genes are present on chromosome 16

  • one gene deleted = asymptomatic
  • two genes deleted = mild anemia with increased RBC count
  • -> cis deletion (when both deletions occur on the same chromosome; seen in asians) associated with an increased risk of severe thalassemia in offspring
  • -> trans deletion (when one deletion occurs on each chromosome, seen in Africans)
  • three genes deleted = severe anemia - beta chains form tetramers (HbH) that damage RBCs –> HbH is seen on electrophoresis
  • four genes deleted = lethal in utero - hydrops fetalis - gamma chains form tetramers (Hb Barts) that damage RBCs –> Hb Barts is seen on electrophoresis
24
Q

Beta thalassemia

A

Usually due to gene mutations - point mutations in promoter or splicing site - seen in individuals of African and mediterranean descent

  • 2 beta genes are present on chromosome 11 - mutations result in absent or diminished production of the beta globin chain
  • divided into beta thalassemia minor and major
25
Q

Beta thalassemia minor

A

Mildest form of disease and is usually asymptomatic with an increased RBC count

  • one normal copy of beta gene and one with diminished activity
  • microcytic, hypochromic RBCs and target cells are seen on blood smear
  • hgb electrophoresis shows slightly decreased HbA with increased HbA2 and HbF
26
Q

Beta thalassemia major

A

Most severe form of disease and presents with severe anemia a few months after birth - high HbF at birth is temporarily protective

  • two copies of defective gene with absent beta globin production
  • alpha tetramers aggregate and damage RBCs, resulting in ineffective erythropoiesis and extravascular hemolysis (removal or circulating RBCs by the spleen)
  • massive erythroid hyperplasia ensues resuting in
    1. expansion of hematopoeisis into the skull (reactive bone formation leads to crewcut appearance of x ray) and facial bones (chipmunk facies)
    2. extramedullary hematopoiesis with hepatosplenomegaly
    3. risk of aplastic crisis parvovirus B19 infection of erythroid precursos
  • chronic transfusions are often necessary; leads to risk for secondary hemochromatosis
  • smear shows microcytic, hypochromic RBCs with target cells and nucleated RBCs
  • electrophoresis shows HbA2 and HbF with little or no HbA
27
Q

Basic principles of normocytic anemia

A
  • anemia with normal sized RBCs (MCV + 80-100)
  • due to increased peripheral destruction or underproduction –> reticulocyte count helps to distinguish between these two etiologies
28
Q

Reticulocytes

A

Young RBCs released from the bone marrow - identified on blood smear as larger cells with bluish cytoplasm due to residual RNA

  • normal reticulocyte count is 1-2%
  • RBC lifespan is 120 days - each day roughly 1-2% of RBCs are removed from circulation and replaced by reticulocytes
  • a properly functioning marrow responds to anemia by increased the RB to >3%

RC is falsely elevated in anemia –> RC is measured as a percentage of total RBCs, so a decrease in total RBCs falsely elevated percentage of reticulocytes

  • RC is corrected by multiplying reticulocyte count by Hct/45
  • corrected count >3% = good marrow response - suggests peripheral destruction
  • corrected count <3% = poor marrow response - suggests underproduction
29
Q

Peripheral RBC destruction = hemolysis

A

Divided into extravascular and intravascular hemolysis - both result in anemia with a good marrow response

Predominantly extravascular hemolysis:

  1. hereditary spherocytosis
  2. sickle cell anemia
  3. hemoglobin C

Predominantly intravascular hemolysis:

  1. paroxysmal nocturnal hemoglobinuria
  2. G6PD deficiency
  3. immune hemolytic anemia
  4. microangiopathic hemolytic anemia
  5. malaria
30
Q

Extravascular hemolysis

A

Involves RBC destruction by the reticuloendothelial system = macrophages of the spleen, liver and lymph nodes

  • macrophages consume RBCs and break down hemoglobin
  • globin –> broken down into amino acids
  • heme –> broken down into iron + protoporphorin
  • iron –> recycled
  • protoporphorin –> broken down into unconjugated bilirubin - bound to serum albumin and delivered to the liver for conjugation and excretion into bile

Clinical and lab findings:

  • anemia with splenomegaly
  • jaundice due to unconjugated bilirubin
  • increased risk for bilirubin gallstones
  • marrow hyperplasia with corrected reticulocyte count >3%
31
Q

Intravascular hemolysis

A

Involves destruction of RBCs within vessels

Clinical and lab findings:

  • hemoglobinemia
  • hemoglobinuria
  • hemosiderinuria –> renal tubular cells pick up some of the hemoglobin that is filtered into the urine and break it down into iron, which accumulates as hemosiderin –> tubular cells are eventually shed resulting in hemosiderinuria
  • decreased serum haptoglobin
32
Q

Hereditary spherocytosis

A

Inherited defect of RBC cytoskeleteon-membrane tethering proteins

  • most commonly involves ankyrin, spectrin, or band 3
  • membrane blebs are formed and lost over time
  • loss of membrane renders cells round (spherocytes) instead of disc shaped
  • spherocytes are less able to maneuver through splenic sinusouds and are consumed by splenic macrophages –> results in anemia
33
Q

Clinical and lab findings in hereditary spherocytosis

A
  • spherocytes with loss of central pallor
  • increased RDW and MCHC
  • splenomegaly
  • jaundice with unconjugated bilirubin
  • increased risk for bilirubing gallstones due to extravascular hemolysis
  • increased risk for aplastic crisis with parvovirus B19 infection of erythroid precursors
34
Q

Diagnosis and treatment of hereditary spherocytosis

A

Diagnosis: Osmotic fragility test –> reveals increased spherocyte fragility in hypotonic solution because RBCs don’t have extra membrane in which they can expand

Treatment: Splenectomy –> anemia resolves but spherocytes persist
- Howell-Jolly bodies (fragments of nuclear material in RBCs normally removed by spleen) emerge on blood smear

35
Q

Sickle cell anemia

A

Autosomal recessive mutation in beta chain of hemoglobin = a single amino acid change replaces normal glutamic acid (hydrophillic) with valine (hydrophobic)

  • gene is carried by 10% of African individuals likely due to protective role against falciparum malaria
  • sickle cell disease arises when two abnormal beta genes are present; results in > 90% HbS in RBCs

HbS polymerizes when deozygenated - polymers aggregate into needle like structures, resulting in sickle cells

  • increased risk of sickling occurs with hypoxemia, dehydration and acidosis
  • HbF protects against sickling –> high HbF at birth is protective for the first few months of life
  • Treatment with hydroxyurea increases levels of HbF
36
Q

Pathogenesis of sickle cell disease

A

Cells continuously sickle and de-sickle while passing through the microcirculation - results in complications related to RBC membrane damage

  • extravascular hemolysis –> reticuloendothelial system removes RBCs with damaged membranes, leading to anemia, jaundice with unconjugated hyperbilirubinemia and increased risk for bilirubing gallstones
  • intravascular hemolysis –> RBCs with damaged membranes dehydrate, leading to hemolysis with decreased haptoglobin and target cells on blood smear
  • massive erythroid hyperplasia ensues =
  • -> expansion of hematopoiesis into skull and facial bones
  • -> extramedullary hematopoeisis with hepatomegaly
  • -> risk of aplastic crisis with parvovirus B19 infection of erythroid precursors
37
Q

Consequences of irreversible sickling in sickle cell disease

A

Leads to complications of vaso-occlusion

  1. dactylitis = swollen hands and feet due to vaso-occlusive infarcts in bones - common presenting sign in infants
  2. autosplenectomy = shrunken, fibrotic spleen
    - -> increased risk of infection with encapsulated organisms such as strep pneumo and h. flu = most common cause of death in children
    - -> increased risk of salmonella paratyphi osteomyelitis
    - -> Howell-jolly bodies on blood smear
  3. acute chest syndrome = vaso-occlusion in pulmonary microcirculation
    - -> presents with chest pain, shortness of breath, and lung infiltrates
    - -> often precipitated by pneumonia
    - -> most common cause of death in adult patients
  4. pain crisis
  5. renal papillary necrosis –> results in gross hematuria and proteinuria
38
Q

Sickle cell trait

A

The presence of one mutated and one normal beta chain –> results in results in microinfarctions leading to microscopic hematuria, and eventually decreased ability to concentrate urine

39
Q

Lab findings in sickle cell disease

A
  • sickle cells and target cells are seen on blood smear in sickle cell disease, but not in sickle cell trait
  • metabisulfite screen causes cells with any amount of HbS to sickle –> positive in both disease and trait
  • Hb electrophoresis confirms the presence and amount of HbS
  • disease = 90% HbS, 8% HbF, 2% HbA2 (no HbA)
  • trait = 55% HbA, 43% HbS, 2% HbA2
40
Q

Hemoglobin C

A

Autosomal recessive mutation in beta chain of hemoglobin

  • normal glutamic acid is replaced by lysine
  • less common than sickle cell disease
  • presents with mild anemia due to extravascular hemolysis
  • characteristic HbC crystals are seen in RBCs on blood smear
41
Q

Paroxysmal nocturnal hemoglobinuria

A

Acquired defect in myeloid stem cells resulting in absent GPI –> renders cells susceptible to destruction by complement

  • blood cells coexist with complement
  • decay accelerating factor (DAF) on the surface of blood cells protects against complement mediated damage by inhibiting C3 convertase
  • DAF is secured to the cell membrane by GPI
  • absence of GPI = absence of DAF –> renders cells susceptible to complement mediated damage

Intravascular hemolysis occurs episodically, often at night during sleep

  • mild respiratory acidosis develops with shallow breathing during sleep and activates complement
  • RBCs, WBCs, and platelets are lysed
  • intravascular hemolysis leads to hemoglobineamia and hemoglobinuria (especially in the morning)
  • hemosiderinuria is seen days after hemolysis

Main cause of death is thrombosis of the hepatic, portal or cerebral veins –> destroyed platelets release cytoplasmic contents into circulation, inducing thrombosis

Complications

  • iron deficiency anemia due to chronic loss of hemoglobin in the urine
  • AML develops in 10% of patients
42
Q

Testing for PNH

A
  • sucrose test is used to screen for disease

- confirmatory test is the acidifed serum test or flow cytometry to detect lack of CD55 (DAF) on RBCs

43
Q

G6PD deficiency

A

X linked recessive disorder resulting in reduced half life of G6PD –> renders cells susceptible to cell stress

  • RBCs are normally exposed to oxidative stress, particularly H2O2
  • glutathione (antioxidant) –> neutralizes H2O2 but becomes oxidized in the process
  • NADPH = a byproduct of G6PD –> needed to regenerate reduced glutathione
  • decreased G6PD = decreased NADPH = reduced glutathione = oxidative injury by H2O2 = intravascular hemolysis
44
Q

Variants of G6PD deficiency

A
  1. African variant = mildly reduced half life of G6PD –> mild intravascular hemolysis with oxidative stress
  2. Mediteranean variant = markedly reduced half life of G6PD –> marked intravascular hemolysis with oxidative stress

High carrier frequency in both populations is likely due to protective role against falciparum malaria

45
Q

Consequences of oxidative stress in G6PD deficiency

A

Oxidative stress precipitates Hb as Heinz bodies

  • causes of oxidative stress include infection, drugs (primaquine, sulfa drugs, dapsone) and fava beans
  • heinz bodies are removed from RBCs by splenic macrophages –> results in bite cells
  • leads to predominantly intravascular hemolysis

Presents with hemoglobinuria and back pain hours after exposure to oxidative stress

46
Q

Screening for G6PD deficiency

A

Heinz preparation - precipitated hemoglobin can only be seen with a special Heinz stain
- enzyme studies confirm deficiency –> performed weeks after hemolytic episode resolves

47
Q

Immune hemolytic anemia

A

Antibody mediated destruction of RBCs (IgG or IgM)

  • IgG mediated disease usually involves extravascular hemolysis
  • IgM mediated disease usually involves intravascular hemolysis
48
Q

IgG mediated immune hemolytic anemia

A

IgG binds RBCs in the relatively warm temperature of the central body = warm agglutinin –> membrane of antibody coated RBC is consumed by splenic macrophages –> results in spherocytes

  • associated with SLE (most common cause), CLL and certain drugs (penicillin and cephalosporin)
  • drugs may attach to RBC membrane with subsequent binding of antibody to drug membrane complex
  • drug may induce production of autoantibodies that bind self antigens on RBCs

Treatment:

  • cessation of drugs
  • steroids
  • IVIG
  • splenectomy
49
Q

IgM mediated immune hemolytic anemia

A

IgM binds RBCs and fixes complement in the relatively cold temperature of the extremities = cold agglutinin
- associated with mycoplasma pneumoniae and infectious mononucleosis

50
Q

Diagnosis of immune hemolytic anemia

A

Coombs test

  1. Direct Coombs test = confirms the presence of antibody coated RBCs
    - -> Anti-IgG is added to patient RBCs - agglutination occurs if RBCs are already coated with antibody
    - -> most important test for IHA
  2. Indirect Coombs test = confirms presence of antibodies in patient serum
    - -> Anti-IgG and test RBCs are mixed with the patient serum
    - -> agglutination occurs if serum antibodies are present
51
Q

Microangiopathic hemolytic anemia

A

Intravascular hemolysis that results from vascular pathology –> RBCs are destroyed as they pass through the circulation

  • iron deficiency anemia occurs with chronic hemolysis
  • occurs with microthrombi (TTP-HUS, DIC, HELLP), prosthetic heart valves and aortic stenosis
  • produce schistocytes on blood smear
52
Q

Malaria

A

Infection of RBCs and liver with plasmodium –> transmitted by female anopheles mosquito

  • RBCs rupture as a part of the plasmodium life cycle, resulting in intravascular hemolysis and cyclical fever
  • p. falciparum = daily fever
  • p vivax and ovale = every other day fever
  • spleen also consumes some infected RBCs –> results in mild extravascular hemolysis with splenomegaly
53
Q

Anemia due to underproduction

A

Decreased production of RBCs by bone marrow –> characterized by low corrected reticulocyte count

Etiologies:

  • causes of microcytic and macrocytic anemia
  • renal failure –> decreased production of EPO by peritubular interstitial cells
  • damage to bone marrow precursor cells –> may result in anemia or pancytopenia
54
Q

Parvovirus B19

A
  • infects progenitor red cells and temporarily halts erythropoiesis –> leads to significant anemia in the setting of preexisting marrow stress (eg sickle cell)
  • treatment is supportive
55
Q

Aplastic anemia

A

Damage to hematopoietic stem cells –> results in pancytopenia with low reticulocyte count

Etiologies

  • drugs/chemicals
  • viral infections
  • autoimmune damage

Biopsy reveals an empty, fatty marrow

Treatment:

  • cessation of any causative drugs
  • supportive care with transfusions and marrow stimulating factors = EPO, GM-CSF, G-CSF
  • immunosuppression may be helpful as some idiopathic cases are due to abnormal T cell activation with release of cytokines
  • bone marrow transplant is a last resort
56
Q

Myelophthisic process

A

Pathologic process that replaces bone marrow –> eg. metastatic cancer
- hematopoiesis is impaired –> results in pancytopenia

Pathoma (16 decks)

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