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Panda Anemia Flashcards

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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
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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
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3
Q

Hemoglobin is made of:

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

Cause of anemia in ACD

A

Insufficient iron

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5
Q

Cause of anemia in thalassemia

A

No globin for hemoglobin production

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6
Q

Cause of anemia in sideroblastic anemia and read poisoning

A

No porphyrin

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7
Q

Types of non-hemolytic normocytic anemia

A
  1. Anemia of chronic disease 2. Aplastic anemia 3. Kidney disease
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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
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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
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10
Q

Types of macrocytic megaloblastic anemia

A
  1. Folate deficiency 2. B12 deficiency
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11
Q

Types of macrocytic normoblastic anemia

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

What does the corrected reticulocyte count tell you?

A

If bone marrow is compensating for anemia

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13
Q

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

A

5-7 days

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14
Q

How to correct reticulocyte count

A

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

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15
Q

What corrected reticulocyte count indicates hemolytic anemia?

A

>3%

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16
Q

How can you estimate Hct from Hb?

A

Hb x 3 = HCT

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17
Q

What protein carries iron in the blood for Hb synthesis?

A

Transferin

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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
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19
Q

Clinical presentation of iron deficiency anemia

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

Peripheral smear appearance for iron deficiency anemia

A

Microcytic and hypochromic

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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
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22
Q

Treatment for iron deficiency anemia

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

Iron overload treatment

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

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25
Clinical presentation of anemia of chronic disease
Presents with concurrent disease (AIDS, TB, rheumatoid arthritis, cancer)
26
Peripheral smear appearence of anemia of chronic disease
Bone marrow stained with prussian blue shows iron inside bone marrow macrophages, but otherwise normal
27
Lab findings in anemia of chronic disease
1. Low serum iron 2. High ferritin 3. Low TIBC/transferrin binding (Ferritin and TIBC are always inverses) 4. Low % Fe saturation
28
Causes of sideroblastic anemia
Defective porphyrin ring synthesis 1. Alcoohlics (poisoned mitochondria) 2. B6 deficiency (cofactor for ALA dehydrase) 3. Lead (inhibits ferrocheletase)
29
Clinical presentation of siderblastic anemia
1. Alcoholic 2. B6 deficient 3. Lead poisoning
30
Peripheral smear appearance of sideroblastic anemia
Ringed sideroblasts --\> abnormal nucleated RBCs with iron granules accumulate din perinuclear mitochondria
31
Lab findings in sideroblastic anemia
1. Serum iron raised 2. Ferritin raised (iron overload problem)
32
Treatment for sideroblastic anemia
Treat underlying cause (Pyridoxine B6)
33
Alpha thalassemia etiology
Decreased alpha chain production --\> excess beta globin Whole gene deletion of chromosome 16 --\> beta hemochromes cause membrane damage --\> RBC intravascular hemolysis
34
Alpha thalaseemia possible conditions
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
Clinical presentation of alpha thalassemia
Asian and African populations Intravascular hemolysis
36
Diagnostic techniques for alpha thalassemia
Hg electrophoresis and PCR CBC: RBC count will be normal Iron levels will be normal
37
Peripheral smear appearance of alpha thalassemia
Target cells
38
Treatment of alpha thalassemia
1. Blood transfusions 2. Cure with allogenic transplant DO NOT TREAT WITH IRON
39
Etiology of beta thalassemia
Decreased beta chain --\> excess alpha globin Point mutation **chromosome 11** Alpha hemochromes cause RBC hemolysis in bone marrow --\> ineffective erythropoeisis
40
Possible conditions with beta thalassemia
1. Beta thalassemia trait: 1 abnormal gene, underproduction of Beta globin (B+) --\> mild anemia --\> Lots of HbA2 2. Beta thalassemia major: both genes abnormal --\> severe anemia 3. Hg Lapore --\> fused beta/delta gene underproduced beta --\> relative increase in alpha --\> Thalaseemia intermedia 4. Hereditary Persistence of fetal hemoglobin --\> co-deletion of beta/ delta --\> all HbF
41
Clinical presentation of beta thalassemia
Mediterranean and African populations "Hair on end" and chipmunk face due to bone marrow expansion in skull Hypercoagulation and endocrinopathies
42
Peripheral smear appearance of beta thalassemia
Hypochromic, microcytic, target cells and basophilic stippling
43
Diagnostics and lab finding in beta thalassemia
CBC/Iron: Normal CBC and ferritin Diagnose with Hg electrophoresis --\> HbA2 and HbF with little or no HbA
44
Treatment of beta thalassemia
Blood transfusions --\> risk iron overload Bone marrow translpant to cure
45
Etiology of lead poisoning anemia
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
Clinical presentation of lead poisoning anemia
Pt is automechanic, makes pottery, paint chipping, or moonshiner
47
Peripheral smear appearance of lead poisoning anemia
Ringed sideroblasts and basophilic stippling
48
Lab findings in lead poisoning anemia
Increased ferritin
49
Clinical relevance of anemia of chronic disease
If RBCs are microcytic it is associated with malignancies
50
Aplastic anemia causes
Idiopathic, chemicals (chloramphenicol), infection (Parvovirus), radiation
51
Lab findings in aplastic anemia
Pancytopenia
52
Peripheral smear/bone marrow appearance in aplastic anemia
Bone marrow has few hematopoietic elements --\> largely acellular
53
Mechanism of anemia of chronic renal failure
Decreased erythropoietin --\> decreased hematopoiesis
54
Peripheral smear appearance in anemia of chronic renal failure
Burr cells (echinocytes) --\> RBCs
55
Treatment for anemia of chronic renal failure
1. Epoetin alfa 2. Darbapoetin 3. Methoxy-PEG-epoetin beta
56
Mechanism of hereditary spherocytosis
Defect in RBC membrane protein band3, spectrin, ankryin --\> TOO LITTLE MEMBRANE leads to osmotic fragility
57
Clinical presentation of hereditary spherocytosis
Splenomegaly due to premature removal of RBC from spleen
58
Peripheral smear appearance of hereditary spherocytosis
Spehrocytes with Howell-Jolly bodies
59
Diagnosis of hereditary spherocytosis
Positive osmotic fragility test
60
Treatment for hereditary spherocytosis
Splenectomy
61
Mechanism of G6PD deficiency anemia
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
Peripheral smear appearance in G6PD deficiency anemia
Heinz bodies, bite cells \*Heinz bodies result from Hb (ferrous) --\> Mb (ferric) --\> denatured Hb --\> ppt in membrane
63
Diagnosis of G6PD deficiency anemia
Check enzyme activity
64
Mechanism of anemia in pyruvate kinase deficiency
Decreased ATP production causes: 1. No energy for RBC membrane maintenance --\> RIGID RBC 2. No Na/K pump --\> H20 lyses cell
65
Clinical presentation of pyruvate kinase deficiency anemia
Autosomal recessive
66
Peripheral smear appearance in pyruvate kinase deficiency anemia
Polychromasia, general findings of anemia
67
Mechanism for paroxysmal nocturnal hemoglobinuria
Defective pig-A gene --\> defective GPI anchor for DAF/CD59 --\> increased complement lysis of RBC Normal: DAF/CD59 are protective anti-complement mediators
68
Peripheral smear appearance in Paroxysmal Nocturnal Hemoglobinuria
Normal
69
Diagnosis of Paroxysmal Nocturnal Hemoglobinuria
Urine hemosiderin + flow cytometry
70
Treatment for Paroxysmal Nocturnal Hemoglobinuria
Ecluzimab or allogeneic bone marrow transplant
71
Mechanism of anemia in Sickle cell disease
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
Clinical presentation of Sickle cell disease anemia
initially asymptomatic newborns because HbF is protective Dactylitis (children), Pain, leg ulcers, asplenia (Howell-Jolly bodies)
73
Peripheral smear appearance in Sickle cell disease
Sickle cells and target cells
74
Diagnosis of sickle cell anemia
Hg Electrophoresis, Low Hg
75
Treatment of sickle cell anemia
Hydroxea urea (increase HbF --\> binds hydrophobic valine); bone marrow transplant
76
Mechanism for Microangiopathic and Macroangiopathic Hemolytic Anemia
RBCs are damaged when passing through obstructed vessel lumen (micro) or via mechanical damage (macro)
77
Clinical presentation for Microangiopathic and Macroangiopathic Hemolytic Anemia
dysfunctional calcified aortic valve/march, running (macro)
78
Diseases associated with Microangiopathic and Macroangiopathic Hemolytic Anemia
Disseminated intravascular coagulation, thrombotic thrombocytopenic pupura, systemic lupus erythematosus
79
Peripheral smear appearance for Microangiopathic and Macroangiopathic Hemolytic Anemia
Schistocytes and helmet cells
80
Mechanism of Warm Autoimmune Hemolytic Anemia (IgG)
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
Clinical presentation of Warm Autoimmune Hemolytic Anemia (IgG)
seen w/SLE or with Rx (methlydopa, penicillin, quinidine) --\> patient will have mild icterus, jaundice symptoms
82
Peripheral smear appearance in Warm Autoimmune Hemolytic Anemia (IgG)
Microspherocytes (partial phagocytosis from RES)
83
Diagnosis of Warm Autoimmune Hemolytic Anemia (IgG)
Coomb’s + Direct Ab
84
Treatment of Warm Autoimmune Hemolytic Anemia (IgG)
Steroids, rituximab, splenectomy, azathioprine, blood transf
85
Mechanism of Cold Autoimmune Hemolytic Anemia (IgM)
IgM targeted RBC --\> COMPLEMENT MAC ONLY --\> Intravascular hemolysis --\> Hemoglobinuria
86
Clinical presentation of Cold Autoimmune Hemolytic Anemia (IgM)
Occurs at low temperatures, common in patients with mycoplasma, EBV, cytomegalovirus
87
Appearance of peripheral blood smear in Cold Autoimmune Hemolytic Anemia (IgM)
Aggregates of RBC
88
Lab findings and diagnosis in Cold Autoimmune Hemolytic Anemia (IgM)
Hemoglobinuria, low haptoglobin Direct Ab test, Coomb's + for Ab
89
Mechanism of Thrombotic Thrombocytopenic Purpura (TTP)
AutoAb at AdamTS13 an enzyme cleaving vWF --\> long vWF --\> cleaves RBC --\> schistocytes
90
Clinical presentation of Thrombotic Thrombocytopenic Purpura (TTP)
Thrombosis, hemorrhaging, bruising
91
Peripheral smear appearance in Thrombotic Thrombocytopenic Purpura (TTP)
Schistocytes/helmet cells
92
Lab findings in Thrombotic Thrombocytopenic Purpura (TTP)
Thrombocytopenia, microangiopathic hemolytic anemia
93
Treatment of Thrombotic Thrombocytopenia Purpura (TTP)
Plasmapheresis to remove anti-AdamTS13 antibodies
94
Mechanism of anemia in malaria
Mosquito vector infects RBC w/ protozoal species Plasmodium falciparum is most lethal
95
Clinical presentation of malaria
Traveler to third world country, tropical/subtropical, symtompatic
96
Peripheral smear appearance in malaria
Merozoites and gametocytes
97
Mechanism of anemia in babesia
Infected w/intracellular protozoal parasite from tick bite
98
Clinical presentation of babesia
Traveler to US northeast, tick bite
99
Peripheral smear appearance of babesia
Intracellular parasite
100
Mechanism of bartonella bacilliformis
Sand flies transmit intracellular parasites
101
Clinical presentation of bartonella bacilliformis
1. Traveler to north andes, peru 2. Acute presentation -\> anemia 3. Chronic presentation -\> peruvian warts 4. Splenomegaly
102
Peripheral smear appearance of bartonella bacilliformis
Basophilic intracellular parasite
103
Treatment for bartonella bacilliformis
Antibiotics
104
Mechanism of C. perfringens
Normal component of skin flora causes sepsis and gas gangrene
105
Clinical presentation of C. perfringens
Complications fo cholecystitis, septic abortion, trauma
106
Peripheral smear apearance in C. perfringens
accumulation of microspherocytes; no Hg in cells --\> Hg Shadow
107
Mechanism of anemia in folate deficiency
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
Clinical presentation of folate deficiency
Pregnant women, the elderly, the poor, or alcoholics
109
Lab findings in folate deficiency
Test for serum folate Increased homocysteine --\> causes MI and thrombosis
110
Peripheral smear appearance in folate deficiency
Megaloblasts (mature cytoplasm, immature large nucleus) + hypersegmented polys
111
Treatment for folate deficiency
Folic acid, leucovorin, levomofolate \*Methotrexate, trimethoprim, pyrimethamine, phenoytin cause folate deficiency
112
Mechanism for anemia in B12 deficiency
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
Clinical presentation of B12 deficiency
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
Appearance of peripheral smear in B12 deficiency
Megaloblasts, hypersegmented polys
115
diagnostic tests for B12 deficiency
1. Serum B12 2. Methylmalonic acid levels 3. N5-met-THF levels
116
Treatment for B12 deficiency
Cyanocobalamin, hydroxocobalamin

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