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1
Q

Types of microcytic anemias

A
  1. Iron deficiency anemia
  2. Anemia of chronic disease (ACD)
  3. Thalassemia
  4. Sideroblastic anemia
  5. Lead poisoning
2
Q

Microscopic appearance of microcytic anemia

A
  1. Hypochromic
  2. Mirocytic (smaller than WBC nucleus) –> cells are smaller due to decreased Hb and increased cellular mitosis
3
Q

Hemoglobin is made of:

A
  1. Protoporphyrin
  2. Iron
  3. Globin
4
Q

Cause of anemia in ACD

A

Insufficient iron

5
Q

Cause of anemia in thalassemia

A

No globin for hemoglobin production

6
Q

Cause of anemia in sideroblastic anemia and read poisoning

A

No porphyrin

7
Q

Types of non-hemolytic normocytic anemia

A
  1. Anemia of chronic disease 2. Aplastic anemia 3. Kidney disease
8
Q

Types of intrinsic hemolytic anemia

A
  1. Hereditary Spehrocytosis 2. Enzyme deficiencies 3. Hemablogin C 4. Sickle Cell disease 5. Paroxysmal nocturnal hemoglobinuria
9
Q

Types of extrinsic hemolytic anemia

A
  1. Autoimmune 2. Microangiopathic hemolytic anemia (heart valve) 3. MIAHA 4. Disease or infection 5. Blood transfusion
10
Q

Types of macrocytic megaloblastic anemia

A
  1. Folate deficiency 2. B12 deficiency
11
Q

Types of macrocytic normoblastic anemia

A
  1. Metabolic 2. Liver disease 3. Alcoholism (Kendall…) 4. Reticulocytosis 5. Drugs (not the good kind)
12
Q

What does the corrected reticulocyte count tell you?

A

If bone marrow is compensating for anemia

13
Q

How many days does it take for reticulocytes to become elevated in anemia?

A

5-7 days

14
Q

How to correct reticulocyte count

A

(Hct/45)*retic count = Corrected retake count –> if cells are polychromic, divide by 2

15
Q

What corrected reticulocyte count indicates hemolytic anemia?

A

>3%

16
Q

How can you estimate Hct from Hb?

A

Hb x 3 = HCT

17
Q

What protein carries iron in the blood for Hb synthesis?

A

Transferin

18
Q

Clinical causes of iron deficiency anemia

A
  1. Malabsorption (duodenum) 2. GI bleeding (Meckel’s in neonates) 3. Hookworm 4. Blood donations 5. Picca
19
Q

Clinical presentation of iron deficiency anemia

A
  1. Green pallor 2. Dizziness 3. Breathlessness 4. Glossitis 5. Koilonychia
20
Q

Peripheral smear appearance for iron deficiency anemia

A

Microcytic and hypochromic

21
Q

Laboratory findings with iron deficiency anemia

A
  1. Low serum iron
  2. Low ferritin
  3. High total iron binding capacity/transferrin binding
  4. Low iron saturation
22
Q

Treatment for iron deficiency anemia

A
  1. Ferrous sulfate (oral)
  2. Iron dextran (IV)
23
Q

Iron overload treatment

A
  1. Deforoxamine (IV)
  2. Deferasirox (Oral + OJ)
24
Q

Etiology of anemia of chronic disease

A

No iron for heme synthesis –> IL-6 from chronic disease increases hepcidin –> decreased release of iron

Protective mechanism to sequester iron from bacteria

25
Q

Clinical presentation of anemia of chronic disease

A

Presents with concurrent disease (AIDS, TB, rheumatoid arthritis, cancer)

26
Q

Peripheral smear appearence of anemia of chronic disease

A

Bone marrow stained with prussian blue shows iron inside bone marrow macrophages, but otherwise normal

27
Q

Lab findings in anemia of chronic disease

A
  1. Low serum iron
  2. High ferritin
  3. Low TIBC/transferrin binding (Ferritin and TIBC are always inverses)
  4. Low % Fe saturation
28
Q

Causes of sideroblastic anemia

A

Defective porphyrin ring synthesis

  1. Alcoohlics (poisoned mitochondria)
  2. B6 deficiency (cofactor for ALA dehydrase)
  3. Lead (inhibits ferrocheletase)
29
Q

Clinical presentation of siderblastic anemia

A
  1. Alcoholic
  2. B6 deficient
  3. Lead poisoning
30
Q

Peripheral smear appearance of sideroblastic anemia

A

Ringed sideroblasts –> abnormal nucleated RBCs with iron granules accumulate din perinuclear mitochondria

31
Q

Lab findings in sideroblastic anemia

A
  1. Serum iron raised
  2. Ferritin raised (iron overload problem)
32
Q

Treatment for sideroblastic anemia

A

Treat underlying cause (Pyridoxine B6)

33
Q

Alpha thalassemia etiology

A

Decreased alpha chain production –> excess beta globin

Whole gene deletion of chromosome 16 –> beta hemochromes cause membrane damage –> RBC intravascular hemolysis

34
Q

Alpha thalaseemia possible conditions

A

2 genes/chromosome 16 –> more genes affected, more serious condition

  1. Silent Alpha Thalassemia: one gene deletion –> asymptomatic
  2. Alpha Thalassemia Trait: two gene deletions –> mild anemia and increased RBC count
  3. HbH (beta tetramer): three gene deletions –> hypersplenism, gallstones, leg ulcers
  4. Hg Bart’s: four gene deletions –> hydrops fetalis at 30-40 weeks; 4 gamma chains damage RBC
  5. Hg Constant Spring: single base mutation in stop codon causing unstable mRNA –> no translation of alpha globin
35
Q

Clinical presentation of alpha thalassemia

A

Asian and African populations

Intravascular hemolysis

36
Q

Diagnostic techniques for alpha thalassemia

A

Hg electrophoresis and PCR

CBC: RBC count will be normal

Iron levels will be normal

37
Q

Peripheral smear appearance of alpha thalassemia

A

Target cells

38
Q

Treatment of alpha thalassemia

A
  1. Blood transfusions
  2. Cure with allogenic transplant

DO NOT TREAT WITH IRON

39
Q

Etiology of beta thalassemia

A

Decreased beta chain –> excess alpha globin

Point mutation chromosome 11

Alpha hemochromes cause RBC hemolysis in bone marrow –> ineffective erythropoeisis

40
Q

Possible conditions with beta thalassemia

A
  1. Beta thalassemia trait: 1 abnormal gene, underproduction of Beta

globin (B+) –> mild anemia –> Lots of HbA2

  1. Beta thalassemia major: both genes abnormal –> severe anemia
  2. Hg Lapore –> fused beta/delta gene underproduced beta –> relative increase in alpha –> Thalaseemia intermedia
  3. Hereditary Persistence of fetal hemoglobin –> co-deletion of beta/ delta –> all HbF
41
Q

Clinical presentation of beta thalassemia

A

Mediterranean and African populations

“Hair on end” and chipmunk face due to bone marrow expansion in skull

Hypercoagulation and endocrinopathies

42
Q

Peripheral smear appearance of beta thalassemia

A

Hypochromic, microcytic, target cells and basophilic stippling

43
Q

Diagnostics and lab finding in beta thalassemia

A

CBC/Iron: Normal CBC and ferritin

Diagnose with Hg electrophoresis –> HbA2 and HbF with little or no HbA

44
Q

Treatment of beta thalassemia

A

Blood transfusions –> risk iron overload

Bone marrow translpant to cure

45
Q

Etiology of lead poisoning anemia

A

Lead inhibts key enzymes in Hb production –> Lead inhibits ferrocheletase (inserts Fe into protoporphyrin), ALA dehydrase, and ribonuclease (RNA destruction) –> ringed sideroblasts and basophilic stippling

46
Q

Clinical presentation of lead poisoning anemia

A

Pt is automechanic, makes pottery, paint chipping, or moonshiner

47
Q

Peripheral smear appearance of lead poisoning anemia

A

Ringed sideroblasts and basophilic stippling

48
Q

Lab findings in lead poisoning anemia

A

Increased ferritin

49
Q

Clinical relevance of anemia of chronic disease

A

If RBCs are microcytic it is associated with malignancies

50
Q

Aplastic anemia causes

A

Idiopathic, chemicals (chloramphenicol), infection (Parvovirus), radiation

51
Q

Lab findings in aplastic anemia

A

Pancytopenia

52
Q

Peripheral smear/bone marrow appearance in aplastic anemia

A

Bone marrow has few hematopoietic elements –> largely acellular

53
Q

Mechanism of anemia of chronic renal failure

A

Decreased erythropoietin –> decreased hematopoiesis

54
Q

Peripheral smear appearance in anemia of chronic renal failure

A

Burr cells (echinocytes) –> RBCs

55
Q

Treatment for anemia of chronic renal failure

A
  1. Epoetin alfa
  2. Darbapoetin
  3. Methoxy-PEG-epoetin beta
56
Q

Mechanism of hereditary spherocytosis

A

Defect in RBC membrane protein band3, spectrin, ankryin –> TOO LITTLE MEMBRANE leads to osmotic fragility

57
Q

Clinical presentation of hereditary spherocytosis

A

Splenomegaly due to premature removal of RBC from spleen

58
Q

Peripheral smear appearance of hereditary spherocytosis

A

Spehrocytes with Howell-Jolly bodies

59
Q

Diagnosis of hereditary spherocytosis

A

Positive osmotic fragility test

60
Q

Treatment for hereditary spherocytosis

A

Splenectomy

61
Q

Mechanism of G6PD deficiency anemia

A

No G6PD so no NADPH for preventing Hb –> Methemoglobin and for preventing spectrin cross linking

Oxidative stress precipitates Hb as Heinz bodies –> caused by drugs or fava beans

62
Q

Peripheral smear appearance in G6PD deficiency anemia

A

Heinz bodies, bite cells
*Heinz bodies result from Hb (ferrous) –> Mb (ferric) –> denatured Hb –> ppt in membrane

63
Q

Diagnosis of G6PD deficiency anemia

A

Check enzyme activity

64
Q

Mechanism of anemia in pyruvate kinase deficiency

A

Decreased ATP production causes:
1. No energy for RBC membrane maintenance –> RIGID RBC

  1. No Na/K pump –> H20 lyses cell
65
Q

Clinical presentation of pyruvate kinase deficiency anemia

A

Autosomal recessive

66
Q

Peripheral smear appearance in pyruvate kinase deficiency anemia

A

Polychromasia, general findings of anemia

67
Q

Mechanism for paroxysmal nocturnal hemoglobinuria

A

Defective pig-A gene –> defective GPI anchor for DAF/CD59 –>

increased complement lysis of RBC

Normal: DAF/CD59 are protective anti-complement mediators

68
Q

Peripheral smear appearance in Paroxysmal Nocturnal Hemoglobinuria

A

Normal

69
Q

Diagnosis of Paroxysmal Nocturnal Hemoglobinuria

A

Urine hemosiderin + flow cytometry

70
Q

Treatment for Paroxysmal Nocturnal Hemoglobinuria

A

Ecluzimab or allogeneic bone marrow transplant

71
Q

Mechanism of anemia in Sickle cell disease

A

Base change in AA#6: Glu–>Val (GAG-GTG) –> HbS/HbSS

IN DEOXYGENATED STATE: Hydrophobic valine cross-links/RBC polymerizes –> vaso-occlusion + hemolysis of RBC –> anemia + NO scavenger (free Hb) + reperfusion injury

instigated by hypoxia, anemia, cold, acidosis, and dehydration

72
Q

Clinical presentation of Sickle cell disease anemia

A

initially asymptomatic newborns because HbF is protective

Dactylitis (children), Pain, leg ulcers, asplenia (Howell-Jolly bodies)

73
Q

Peripheral smear appearance in Sickle cell disease

A

Sickle cells and target cells

74
Q

Diagnosis of sickle cell anemia

A

Hg Electrophoresis, Low Hg

75
Q

Treatment of sickle cell anemia

A

Hydroxea urea (increase HbF –> binds hydrophobic valine); bone marrow transplant

76
Q

Mechanism for Microangiopathic and Macroangiopathic Hemolytic Anemia

A

RBCs are damaged when passing through obstructed vessel lumen (micro) or via mechanical damage (macro)

77
Q

Clinical presentation for Microangiopathic and Macroangiopathic Hemolytic Anemia

A

dysfunctional calcified aortic valve/march, running (macro)

78
Q

Diseases associated with Microangiopathic and Macroangiopathic Hemolytic Anemia

A

Disseminated intravascular coagulation, thrombotic thrombocytopenic pupura, systemic lupus erythematosus

79
Q

Peripheral smear appearance for Microangiopathic and Macroangiopathic Hemolytic Anemia

A

Schistocytes and helmet cells

80
Q

Mechanism of Warm Autoimmune Hemolytic Anemia (IgG)

A

IgG targeted at RBC –> direct phagocytosis or complement-mediated –> Extravascular (RES in spleen) or intravascular (complement) lysis

Occurs in newborns due to RhD incompatibility

81
Q

Clinical presentation of Warm Autoimmune Hemolytic Anemia (IgG)

A

seen w/SLE or with Rx (methlydopa, penicillin, quinidine) –> patient will have mild icterus, jaundice symptoms

82
Q

Peripheral smear appearance in Warm Autoimmune Hemolytic Anemia (IgG)

A

Microspherocytes (partial phagocytosis from RES)

83
Q

Diagnosis of Warm Autoimmune Hemolytic Anemia (IgG)

A

Coomb’s + Direct Ab

84
Q

Treatment of Warm Autoimmune Hemolytic Anemia (IgG)

A

Steroids, rituximab, splenectomy, azathioprine, blood transf

85
Q

Mechanism of Cold Autoimmune Hemolytic Anemia (IgM)

A

IgM targeted RBC –> COMPLEMENT MAC ONLY –> Intravascular hemolysis –> Hemoglobinuria

86
Q

Clinical presentation of Cold Autoimmune Hemolytic Anemia (IgM)

A

Occurs at low temperatures, common in patients with mycoplasma, EBV, cytomegalovirus

87
Q

Appearance of peripheral blood smear in Cold Autoimmune Hemolytic Anemia (IgM)

A

Aggregates of RBC

88
Q

Lab findings and diagnosis in Cold Autoimmune Hemolytic Anemia (IgM)

A

Hemoglobinuria, low haptoglobin

Direct Ab test, Coomb’s + for Ab

89
Q

Mechanism of Thrombotic Thrombocytopenic Purpura (TTP)

A

AutoAb at AdamTS13 an enzyme cleaving vWF –> long vWF –> cleaves RBC –> schistocytes

90
Q

Clinical presentation of Thrombotic Thrombocytopenic Purpura (TTP)

A

Thrombosis, hemorrhaging, bruising

91
Q

Peripheral smear appearance in Thrombotic Thrombocytopenic Purpura (TTP)

A

Schistocytes/helmet cells

92
Q

Lab findings in Thrombotic Thrombocytopenic Purpura (TTP)

A

Thrombocytopenia, microangiopathic hemolytic anemia

93
Q

Treatment of Thrombotic Thrombocytopenia Purpura (TTP)

A

Plasmapheresis to remove anti-AdamTS13 antibodies

94
Q

Mechanism of anemia in malaria

A

Mosquito vector infects RBC w/ protozoal species

Plasmodium falciparum is most lethal

95
Q

Clinical presentation of malaria

A

Traveler to third world country, tropical/subtropical, symtompatic

96
Q

Peripheral smear appearance in malaria

A

Merozoites and gametocytes

97
Q

Mechanism of anemia in babesia

A

Infected w/intracellular protozoal parasite from tick bite

98
Q

Clinical presentation of babesia

A

Traveler to US northeast, tick bite

99
Q

Peripheral smear appearance of babesia

A

Intracellular parasite

100
Q

Mechanism of bartonella bacilliformis

A

Sand flies transmit intracellular parasites

101
Q

Clinical presentation of bartonella bacilliformis

A
  1. Traveler to north andes, peru
  2. Acute presentation -> anemia
  3. Chronic presentation -> peruvian warts
  4. Splenomegaly
102
Q

Peripheral smear appearance of bartonella bacilliformis

A

Basophilic intracellular parasite

103
Q

Treatment for bartonella bacilliformis

A

Antibiotics

104
Q

Mechanism of C. perfringens

A

Normal component of skin flora causes sepsis and gas gangrene

105
Q

Clinical presentation of C. perfringens

A

Complications fo cholecystitis, septic abortion, trauma

106
Q

Peripheral smear apearance in C. perfringens

A

accumulation of microspherocytes; no Hg in cells –> Hg Shadow

107
Q

Mechanism of anemia in folate deficiency

A

Folate is required in reduction of homocysteine –> methionine; 1 carbon transfer reaction needed to (eventually) convert dUMP– >dTMP in DNA synthesis

Ingested as polyglutamate; absorbed/functions as monoglutumate

108
Q

Clinical presentation of folate deficiency

A

Pregnant women, the elderly, the poor, or alcoholics

109
Q

Lab findings in folate deficiency

A

Test for serum folate

Increased homocysteine –> causes MI and thrombosis

110
Q

Peripheral smear appearance in folate deficiency

A

Megaloblasts (mature cytoplasm, immature large nucleus) + hypersegmented polys

111
Q

Treatment for folate deficiency

A

Folic acid, leucovorin, levomofolate

*Methotrexate, trimethoprim, pyrimethamine, phenoytin cause folate deficiency

112
Q

Mechanism for anemia in B12 deficiency

A

B12 is required for homocysteine –> methionine (dUMP–>dTMP) Odd chain fatty acid

Absorption: distal ileum; binds to R-binder, then IF

Caused by decreased intake, malabsorption, pancreatic insufficiency

113
Q

Clinical presentation of B12 deficiency

A

Elderly, pernicious anemia
*PA is gastirc atrophy (loss of IF) due to CD4+ recognition of ATPase, anti-IF Ab, or anti-parietal cell antibodies

114
Q

Appearance of peripheral smear in B12 deficiency

A

Megaloblasts, hypersegmented polys

115
Q

diagnostic tests for B12 deficiency

A
  1. Serum B12
  2. Methylmalonic acid levels
  3. N5-met-THF levels
116
Q

Treatment for B12 deficiency

A

Cyanocobalamin, hydroxocobalamin