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Flashcards in Chapter 12 - Red Blood Cell Disorders Deck (219):
0

What is erythropoiesis?

Erythropoiesis: RBC production in bone marrow

1

Where is EPO synthesized?

EPO: synthesized in interstitial cells of peritubular capillary bed

2

What are the stimuli for EPO release?

EPO stimuli: ↓PaO2/↓SaO2, left-shifted OBC, high altitude

3

What suppresses EPO release?

↑O2 content ↓EPO

4

What are the other sources of EPO?

Other EPO sources: renal cell carcinoma, hepatocellular carcinoma

5

What is the reticulocyte count a measure of?

Reticulocyte count: measure effective erythropoiesis

6

What does effective erythropoiesis refer to?

Effective erythropoiesis: good bone marrow response to anemia; ↑reticulocyte synthesis/release

7

The initial percentage reticulocyte count must be corrected for what?

Reticulocyte count: must correct for degree of anemia

8

What is the equation for correction of the reticulocyte count?

Correction = Hct/45 × reticulocyte count

9

What is the correction if RBC polychromasia is present?

Polychromasia: original correction ÷ 2

10

What is the cutoff for effective erythropoiesis when calculating the corrected reticulocyte count?

Corrected reticulocyte count: <3% ineffective erythropoiesis; ≥3% effective erythropoiesis

11

What is extramedullary hematopoiesis?

EMH: erythropoiesis outside bone marrow

12

Where does EMH most often occur?

EMH: most often occurs in liver and spleen

13

What does EHM produce?

EMH: hepatosplenomegaly

14

Where does hematopoiesis begin in the fetus?

Fetus: hematopoiesis begins in yolk sac

15

How are the PaO2 and SaO2 affected in anemia?

Anemia: PaO2/SaO2 normal

16

How is the O2 content of blood affected in anemia?

Anemia: ↓O2 content

17

Anemia is a sign of _____ not a _____.

Anemia: sign of disease not a diagnosis

18

What are the signs of severe anemia?

Signs severe anemia: pallor of skin and conjunctivae; palmar creases

19

What is high-output cardiac failure due to?

High output failure: anemia ↓blood viscosity

20

What is frequently used to classify anemias?

MCV: classification of anemias

21

How are microcytic, normocytic and macrocytic anemia defined?

Microcytic MCV 100 µm3
Normocytic MCV 80–100 µm3
Macrocytic MCV >100 µm3

22

How is the MCHC affected I the microcytic anemias and hereditary sphrerocytosis?

MCHC: ↓microcytic anemias; ↑hereditary spherocytosis

23

What does RDW measure?

RDW: measure RBC size variation

24

How is the RDW affected in iron-deficiency anemia?

Iron deficiency: ↑RDW

25

What to mature RBCs lack?

Lack mitochondria and nucleus

26

Describe the metabolism of glucose in mature RBCs.

Anaerobic glycolysis; lactic acid end product

27

Describe the Cori cycle.

Cori cycle: lactic acid → glucose in liver → glucose to RBC

28

What does glutathione in mature RBCs do?

GSH: neutralizes H2O2/acetaminophen FRs

29

Describe the reaction catalyzed in the methemoglobin reductase pathway.

MetHb reductase: reduces Fe3+ to Fe2+

30

What does the Luebering-Rapoport pathway synthesize?

2,3-BPG: product of glycolytic cycle

31

What do mature RBCs lack on their membrane surface?

RBCs lack HLAs

32

What is UCB a end product of?

UCB: end product of heme degradation by macrophages

33

Describe how platelets are formed.

Platelets: pinch off megakaryocyte cytoplasm

34

What is ferritin and what does it do?

Ferritin: soluble iron-binding protein; keeps iron in non-toxic form

35

Where is ferritin synthesized?

Ferritin: synthesized in bone marrow macrophages/hepatocytes

36

How is serum ferritin levels affected in iron deficiency, ACD and iron overload disease?

Serum ferritin: ↓iron deficiency; ↑ACD, iron overload disease

37

What is hemosiderin and how is it detected?

Hemosiderin: degradation product of ferritin; Prussian blue +

38

What is serum iron?

Serum iron: iron bound to transferrin

39

How serum iron affected in iron deficiency, ACD and iron overload?

Serum iron: ↓iron deficiency, ACD; ↑iron overload disease

40

Describe the relationship between TIBC and transferrin levels.

↓TIBC = ↓transferrin
↑TIBC = ↑transferrin

41

Describe the relationship between ferritin and TIBC. How are ferritin and TIBC affected in iron deficiency, ACD and iron overload?

↓Ferritin stores = ↑TIBC; iron deficiency
↑Ferritin stores = ↓TIBC; ACD, iron overload

42

Where does transferrin iron come from?

Transferrin iron: from macrophages/duodenum

43

How is iron saturation affected in iron deficiency, ACD and iron overload?

↓Iron saturation: iron deficiency, ACD; ↑iron saturation: iron overload disease

44

Describe the structure of the different normal hemoglobins.

HbA: 2α/2β
HbA2: 2α/2δ
HbF: 2α/2γ

45

Describe the pathogenesis of the microcytic anemias.

Microcytic anemias: defects in Hb synthesis; Hb = heme + globin chains

46

What are the types of iron?

Types of iron: reduced Fe2+ (heme iron in meat), oxidized Fe3+ (nonheme iron in plants)

47

Where is functional iron present?

Functional iron: Hb, enzymes, myoglobin

48

How is iron primarily stored?

Storage iron: ferritin in bone marrow macrophages

49

How does iron stores compare between men and women?

Iron storage in men > women

50

What is the effect of gastric acid on elemental iron?

Gastric acid: frees elemental iron from food

51

Describe the reabsorption of iron in the GI tract.

Oxidized Fe3+ must be reduced to Fe2+ for reabsorption in duodenum
Reduced Fe2+ directly reabsorbed in duodenum

52

What regulates iron absorption?

Iron bound to transferrin regulates iron absorption

53

What differentiates sensor cells into enterocytes?

HFE protein product + transferrin receptors differentiate sensor cells to enterocytes

54

What is the master iron regulator?

Hepcidin: master iron regulator

55

What are the effects of a decrease in transferrin-bound iron?

↓Transferrin-bound iron → ↓hepcidin synthesis → ↑iron bound to transferrin → ↑iron released from macrophages

56

What are the effects of an increase in transferrin-bound iron?

↑Transferrin bound iron → ↑hepcidin synthesis → ↓iron bound to transferrin → ↓iron released from macrophages (iron blockade)

57

What is the most common overall anemia?

Iron deficiency: MC overall anemia

58

What is the most common cause of iron deficiency?

Iron deficiency: MCC bleeding

59

What are the clinical findings of chronic iron deficiency?

Chronic iron deficiency: esophageal web, achlorhydria, glossitis/cheilosis, spoon nails

60

What are the lab findings of iron deficiency?

Iron deficiency: ↓iron, % saturation, ferritin; ↑TIBC, RDW

61

Describe the stages of iron deficiency.

Stages of iron deficiency: all lab studies abnormal before anemia is present

62

Name a finding in chronic iron deficiency.

Thrombocytosis: chronic iron deficiency

63

What is the treatment for iron deficiency?

Rx iron deficiency: ferrous sulfate

64

What is the most common anemia in hospitalized patients?

ACD: MC anemia in hospitalized patients

65

What is the most common anemia in malignancy and alcohol excess?

ACD: MC anemia in malignancy, alcohol excess

66

Describe the pathogenesis of ACD.

ACD: ↓synthesis heme, ↓EPO synthesis/response, ↑hepcidin

67

What are the lab findings of ACD?

ACD: ↓iron, TIBC, % saturation; ↑ferritin

68

What is the inheritance of thalassemia?

thal: autosomal recessive

69

Blacks can be affected by which types of thalassemia?

Blacks can have α- or β-thalassemia

70

Describe the pathogenesis of α-thal.

α-thal: α-globin chain gene deletions

71

Describe the pathogenesis of α-thal trait.

α-thal trait: 2 gene deletions

72

What are the lab findings of α-thal trait?

α-thal trait: mild anemia; N/↑RBC count
α-thal trait: ↓HbA, HbA2, HbF (normal electrophoresis); ↑RBC count

73

Describe the pathogenesis of α-thal trait in black individuals.

Black α-thal trait: trans α/− α/−

74

Describe the pathogenesis of α-thal trait in Southeast Asian individuals. What is there danger of?

Southeast Asian α-thal trait: cis −/− α/α; danger severe types

75

Describe the pathogenesis of HbH.

HbH: 3 gene deletions; 4 β-chains; severe hemolytic anemia

76

Describe the pathogenesis of Hb Bart.

Hb Bart: 4 γ-chains; incompatible with life

77

Describe the pathogenesis of β-thal.

β-thal: mild—DNA splicing defect; severe—stop codon

78

Describe β-globin chain synthesis in β-thal minor.

β-thal minor: β/β+

79

What are the lab findings of β-thal minor?

β-thal minor: ↓HbA; ↑RBC count, HbA2, HbF; normal RDW; target cells, tear drop cells

80

Describe β-globin chain synthesis in β-thal major.

β-thal major: β°/β° or βo/β+

81

What are the findings in β-thal major?

β-thal major: severe hemolytic anemia; EMH; hair-on-end skull x-ray
β-thal major: no HbA; ↑HbA2, HbF, RDW, reticulocytes

82

Describe the epidemiology of sideroblastic anemia.

Sideroblastic anemia: chronic alcoholism MCC, ↓pyridoxine, Pb poisoning, XR

83

Describe the pathogenesis of sideroblastic anemia.

Sideroblastic anemia: defect in mitochondrial heme synthesis; ringed sideroblasts

84

What is the most common cause of pyridoxine deficiency?

Pyridoxine deficiency: INH MCC

85

What are the causes of lead poisoning?

Pb poisoning: paint, batteries, pottery glazes, radiator repair, moonshine

86

What does lead denature?

Pb denatures ferrochelatase, ALA dehydrase, ribonuclease

87

What are the findings in lead poisoning?

Pb poisoning: coarse basophilic stippling (persistent ribosomes)
Abdominal colic/constipation; encephalopathy (edema/demyelination)
Pb poisoning: Pb deposits in epiphyses; growth retardation
Peripheral neuropathy, nephrotoxic (proximal tubules), Pb line in gums


88

What is the treatment for lead poisoning?

Rx Pb poisoning: chelation therapy

89

What are the lab findings in sideroblastic anemia?

Sideroblastic anemia: ↑serum iron, iron saturation, ferritin; N/↓MCV, ↓TIBC

90

Vitamin B12 is only present in what?

Vitamin B12: only present in animal products

91

What do parietal cells synthesize?

Parietal cells: synthesize IF and HCI

92

What does vitamin B12 bind to?

Vitamin B12 binds to R-binder

93

What is the role of pancreatic enzymes in vitamin B12 metabolism? What does vitamin B12 then bind?

Pancreatic enzymes cleaves R-binder off; B12-IF complex

94

Where is vitamin B12 absorbed and stored?

Vitamin B12: absorbed in terminal ileum; 6- to 9-year supply in liver

95

What is the most common cause of pernicious anemia?

Vitamin B12 deficiency: PA MCC

96

Describe folic acid metabolism.

Intestinal conjugase: polyglutamate → monoglutamate; inhibited by phenytoin

97

What is monoglutamate absorption inhibited by?

Monoglutamate absorption: inhibited by alcohol and OCPs

98

What is the most common cause of folic acid deficiency?

Folic acid deficiency: alcohol MCC

99

Describe the pathogenesis of macrocytic anemia in folic acid and vitamin B12 deficiency.

Vitamin B12/folic acid deficiency: delayed nuclear maturation; megaloblasts

100

What are folic acid derivatives important in?

Folic acid derivatives: important in single carbon transfer reactions

101

What is the effect on plasma homocysteine levels in folic acid and vitamin B12 deficiency?

↑Homocysteine: folic acid deficiency (MC) and vitamin B12 deficiency

102

What is the effect of 5-FU on thymidylate synthase?

Thymidylate synthase: irreversibly inhibited by 5-fluorouracil

103

What inhibits dihydrofolate reductase?

Dihydrofolate reductase: inhibited by methotrexate (reversible), trimethoprim

104

Vitamin B12 is involved in the metabolism of which type of FA?

Vitamin B12: odd-chain FA metabolism

105

What does propionyl CoA replace in demyelination?

Demyelination: propionyl CoA replaces acetyl CoA

106

Describe the HSR that occurs in PA.

PA: type II hypersensitivity reaction destroys parietal cells (↓acid, ↓IF)

107

Describe how gastrin levels are affected in PA.

PA: chronic atrophic gastritis → achlorhydria → ↑gastrin

108

PA increases the incidence of what type of cancer.

PA: ↑incidence gastric cancer

109

What areas of the spinal cord are demyelinated in vitamin B12 deficiency?

Spinal cord demyelination: posterior columns, lateral corticospinal tract, dorsal spinocerebellar tract

110

There is deficiency of what if there is macrocytic anemia with neurological disease?

Macrocytic anemia with neurologic disease: vitamin B12 deficiency

111

What is the most sensitive test for vitamin B12 deficiency?

↑Methylmalonic acid: most sensitive test for B12 deficiency

112

The hypersegmented neutrophil is a marker of what?

Hypersegmented neutrophil: marker for folic acid/vitamin B12 deficiency

113

What is the Schilling test used for?

Schilling test: cause of B12 deficiency

114

Decreased intake of maternal folic acid increases the risk of what?

↓Maternal intake folic acid: ↑risk open neural tube defect in newborn

115

RBC folic acid is the best indicator of what?

RBC folic acid: best indicator of folic acid stores

116

What are the lab findings in nonmegaloblastic macrocytosis?

Nonmegaloblastic macrocytosis: round macrocytes, no hypersegmented neutrophils

117

What are the hematologic findings in alcoholic liver disease?

Alcohol liver disease: round macrocytic target cells; no anemia

118

What are the two main categories of acute blood loss?

Acute blood loss: external, internal

119

What is the most common cause of hypovolemic shock?

Acute blood loss MCC hypovolemic shock

120

What are the initial CBC results in acute blood loss?

Hb, Hct, RBC count initially normal; anemia uncovered with IV saline

121

How long does it take before a reticulocyte response is seen in acute blood loss?

Reticulocyte response 5–7 days after blood loss

122

Describe the MCV in early iron deficiency and ACD.

Iron deficiency/ACD: anemia normocytic before becoming microcytic

123

Describe the causes of aplastic anemia.

Aplastic anemia: most cases idiopathic; drugs MC known cause

124

Describe the pathogenesis of aplastic anemia.

Immunologic destruction in myeloid stem cells; mutations in TERT, the gene for the RNA component of telomerase

125

What are the clinical findings in aplastic anemia?

Aplastic anemia: fever, bleeding, fatigue

126

What are the lab findings in aplastic anemia?

Aplastic anemia: pancytopenia, reticulocytopenia, hypocellular marrow

127

Complete recovery occurs in what percentage of cases of aplastic anemia?

Complete recovery <10%

128

What is RBC aplasia?

RBC aplasia: suppression/destruction erythroid colony-forming unit

129

What are the causes of RBC aplasia?

RBC aplasia: Diamond-Blackfan syndrome, thymomas, leukemia, drugs, parvovirus

130

What is the pathogenesis of anemia in CRF?

Anemia CRF: ↓EPO + ACD

131

What are the hematologic lab findings in CRF?

CRF: platelet dysfunction (reversible with dialysis), burr cells

132

What are the causes of anemia in malignancy?

Anemia malignancy: ACD (MC anemia), blood loss, metastasis to marrow, immunologic

133

What are the types of hemolytic anemia?

Types hemolytic anemia: intrinsic (defect in RBC), extrinsic (factors outside RBC)

134

What are the reasons for RBC phagocytosis?

RBCs coated with IgG and/or C3b; abnormal shape (spherocyte, sickle cell); inclusions (G6PD deficiency)

135

Describe the characteristics of extravascular hemolysis.

Extravascular hemolysis: macrophage phagocytosis; ↑UCB

136

What are the causes of intravascular hemolysis?

Intravascular hemolysis: enzyme deficiency, complement destruction, mechanical damage

137

What are the lab findings in intravascular hemolysis?

Intravascular hemolysis: ↓serum haptoglobin; hemoglobinuria, hemosiderinuria

138

Describe the epidemiology of HS.

HS: intrinsic defect, extravascular hemolysis; autosomal dominant

139

What is the most common defect in HS?

HS: mutation in spectrin in cell membrane

140

Describe spherocyte formation in HS.

HS: microvesicle formation/loss + loss K+ and H2O (dehydrate cell) → spherocyte formation

141

What are the clinical findings in HS?

HS: jaundice, calcium bilirubinate gallstones, splenomegaly, aplastic crisis (parvovirus-induced)

142

What are the lab findings in HS?

HS: ↑MCHC, ↑RBC osmotic fragility (↓surface to volume ratio), ↑RDW

143

What is the treatment for HS?

HS: Rx splenectomy

144

Describe the pathogenesis of hereditary elliptocytosis.

Elliptocytosis: AD disorder; mutation spectrin and band 4.1

145

What are the lab findings in hereditary elliptocytosis?

Hereditary elliptocytosis: >25% elliptocytes in peripheral blood

146

What is the epidemiology of PNH?

PNH: intrinsic defect with intravascular hemolysis

147

Which gene is affected in PNH?

PNH: mutation in PIG group A gene in myeloid stem cell clone

148

What is the effect of the mutation in PNH?

PNH: defect in anchoring inhibitors of complement (CD55 [decay accelerating factor], CD59)

149

What do the anchoring inhibitors affected in PNH normally do?

Inhibitors normally degrade C3/C5 convertase to prevent MAC activation; prevent lysis in RBCs, neutrophils, platelets

150

What are the clinical findings in PNH?

PNH: episodic hemoglobinuria, ↑vessel thrombosis, acute myeloblastic leukemia

151

What are the lab findings in PNH?

PNH: pancytopenia; ↓LAP stain; hemoglobinuria

152

How is PNH diagnosed?

PNH Dx: flow cytometry best test; sucrose hemolysis test and acidified serum test outdated

153

Describe the pathogenesis of PCH.

PCH: IgG cold antibody with bithermal activity; intravascular hemolysis
PCH: antibody binds to P antigen on RBCs
PCH: in cold temperatures antibody binds to RBCs and fixes complement
PCH: in warm temperatures antibody detaches, activates complement → intravascular hemolysis

154

What are the clinical findings in PCH?

PCH: pain, Raynaud, hepatosplenomegaly, jaundice, renal failure

155

Describe the type of defect and hemolysis that occurs in HbSS anemia.

HbSS anemia: intrinsic defect, predominantly extravascular hemolysis

156

Describe the type of mutation that occurs in HbSS anemia.

HbSS anemia: missense mutation; substitute valine for glutamic acid

157

Describe the offspring of two individuals with sickle cell trait.

Trait × trait: 25% normal, 50% trait, 25% disease

158

What do HbS molecules do when deoxygenated?

HbS molecules aggregate and polymerize when deoxygenated; O2 inhibits sickling

159

What are the factors that increase the risk for sickling?

Sickling: ↑HbS, ↑deoxyHb (acidosis, volume depletion, hypoxemia)

160

Describe the characteristics of irreversibly sickled cells.

Irreversibly sickled cells: dehydrated; correlate with degree of severity of hemolysis; extravascular removal

161

What is overexpressed on the surface of sickle cells? What is the effect?

Sickle cells: ↑expression of adhesion molecules; stick to and damage endothelial cells in microvasculature

162

What prevents sickling in addition to oxygen? How is its synthesis increased?

HbF prevents sickling: hydroxyurea ↑HbF synthesis

163

What are the key pathologic processes in HbSS anemia?

HbSS anemia: severe hemolytic anemia; vasoocclusive crises

164

What is the most common presentation of HbSS anemia in infants?

Dactylitis: aseptic necrosis in metacarpal bones; MC presentation in infants

165

What is the most common cause of death in young people with HbSS anemia?

Acute chest syndrome: MCC death in young people

166

What process may affect the femoral head in HbSS anemia?

Aseptic necrosis of femoral head

167

What is a sign of splenic dysfunction?

Howell-Jolly bodies: sign of splenic dysfunction

168

What does autosplenectomy refer to?

Autosplenectomy: spleen fibrosed/smaller

169

There is increased susceptibility to which infections in HbSS anemia?

Pathogens: S. pneumoniae sepsis, Salmonella paratyphi osteomyelitis

170

What are the characteristics of an aplastic crisis?

Aplastic crisis due to parvovirus; no reticulocytes

171

How do sequestration and aplastic crisis differ?

Sequestration vs. aplastic crisis: reticulocytosis, reticulocytopenia, respectively

172

There is increased risk for which type of gallstones in HbSS anemia?

Calcium bilirubinate gallstones

173

What is a common cause of death in children with HbSS anemia?

Strokes common in children; common cause of death in children

174

Where are recurrent leg ulcers located in HbSS anemia?

Recurrent leg ulcers around malleoli

175

What commonly leads to blindness in HbSS anemia?

Proliferative retinopathy → blindness

176

What occurs after 40 years of age in HbSS anemia?

End-stage renal failure after 40 years old

177

What are the renal findings in sickle cell trait?

Sickle cell trait: no anemia; microhematuria; potential for renal papillary necrosis

178

What is the sickle cell screen?

Screen: sodium metabisulfite ↓O2 tension, induces sickling

178

What are the Hb electrophoresis findings in HbAS?

HbAS: HbA 55%–60%, HbS 40%–45%

178

What are the Hb electrophoresis findings in HbSS?

HbSS: HbS 90%–95%, HbF 5%–10%, no HbA

178

What causes the appearance of target cells? What are they a sign of?

Target cells: excess RBC membrane; sign hemoglobinopathy or alcohol excess

179

Describe the inheritance of G6PD deficiency. Where is it most common?

G6PD deficiency: XR; MC in tropical Africa

180

Describe the type of defect and hemolysis in G6PD deficiency.

G6PD def: intrinsic defect, predominantly intravascular hemolysis

181

What are the subtypes of G6PD?

Mediterranean and black variants

182

What is the most common enzyme deficiency causing hemolysis?

G6PD def: MC enzyme deficiency causing hemolysis

183

Describe the pathogenesis of G6PD deficiency.

G6PD def: ↓synthesis GSH; H2O2 cannot be neutralized

184

Describe the characteristics of the Mediterranean variant of G6PD.

Mediterranean variant: enzyme half-life markedly reduced in old RBCs (<10% activity)

185

Describe the characteristics of the black variant of G6PD.

Black variant: enzyme half-life moderately reduced in old RBCs (10% to 60% activity)

186

What system is dysfunctional in G6PD deficiency?

G6PD deficiency: O2 dependent MPO system dysfunctional; lack of NADPH cofactor

187

What are the drugs that may act as oxidant stressors in G6PD deficiency?

Drugs: primaquine, dapsone, sulfonamides

188

What are the lab findings in G6PD deficiency?

Heinz bodies with supravital stain; bite cells in peripheral blood
G6PD def: active hemolysis screen with Heinz body prep
Confirmatory test: enzyme analysis

189

Describe the type of defect and hemolysis in PK deficiency.

PK deficiency: intrinsic defect, extravascular hemolysis

190

What is the most common enzyme deficiency producing hemolysis in glycolysis? What is its inheritance?

PK deficiency: AR disease; MC enzyme deficiency producing hemolysis in glycolysis pathway

191

What does PK do?

PK converts PEP to pyruvate for net gain of 2 ATP

192

Describe the pathogenesis of PK deficiency?

PK def: loss ATP damages RBC membranes (echinocytes)

193

How are the clinical effects of anemia offset in PK deficiency?

PK deficiency: ↑2,3-BPG shifts OBC to right; offsets clinical effects of anemia

194

What are the immune hemolytic anemias?

Extrinsic hemolytic anemias with intravascular or extravascular hemolysis

195

What is the most common type of IHA?

AIHA: MC IHA

196

What are the types of AIHA?

AIHA: warm type (IgG; MC), cold type (IgM)

197

Describe the pathogenesis of IHA.

IgG-mediated: predominantly extravascular IHA; spherocytosis
Complement-mediated: intravascular or extravascular IHA
IgM-mediated: intravascular (MC) or extravascular hemolysis

198

What are the clinical findings of IHA?

Jaundice (extravascular), hepatosplenomegaly (warm type); Raynaud (cold type)

199

What does DAT detect?

DAT: detects IgG, C3b, C3d on surface of sensitized RBCs

200

What does the indirect Coombs test detect?

Indirect Coombs: detects IgG antibodies in serum (e.g., anti-D antibodies)

201

What are the lab findings in IHA?

Hemoglobinuria (intravascular), spherocytes, reticulocytosis, agglutination (cold type)

202

What types of hemolysis occur in MHA?

MHA: extrinsic, intravascular hemolysis

203

What are schistocytes a sign of?

Schistocytes: sign of MHA

204

What is the most common cause of MHA?

MHA: AV stenosis MCC

205

Describe the pathogenesis of microangiopathic hemolytic anemia.

Microangiopathic: small vessel fibrin or platelet thrombi; damage RBCs → schistocytes

206

What are the lab findings in MHA?

Normocytic/microcytic anemia, hemoglobinuria/hemosiderinuria, ↓serum haptoglobin, schistocytes

207

Describe the malaria life cycle.

Female Anopheles mosquito transmits Plasmodia to humans; release sporozoites
Sporozoites enter liver → develop into merozoites → released into blood and infect RBCs
RBC phase: ring form → trophozoite → schizont; rupture RBCs with release of more merozoites (fever)
Male/female gametocytes ingested by mosquito; sexual reproduction → sporozoites

208

Describe the type of defect and hemolysis that occurs in malaria anemia.

Malaria anemia: extrinsic defect with intravascular hemolysis

209

Intravascular hemolysis correlates with what in malaria?

Malaria: intravascular hemolysis correlates with fever spikes

210

What is the most common cause of malaria worldwide? Describe the fever pattern.

P. vivax MC type; fever q48 hours (simple tertian)

211

What is the most lethal type of malaria? Describe the fever pattern.

P. falciparum most lethal type; fever quotidian (malignant tertian)

212

Which type of malaria is associated with nephrotic syndrome? Describe the fever pattern.

P. malariae fever q72 hours (quartan); association with nephrotic syndrome

213

What is the prophylactic treatment for malaria?

Malaria: chloroquine prevention

214

What is the treatment for malaria caused by P. vivax or P. ovale?

Malaria Rx P. vivax/ovale: chloroquine + primaquine

215

What is the treatment for malaria caused by P. falciparum?

Malaria Rx P. falciparum: chloroquine sensitive—chloroquine alone; resistant—quinine sulfate + doxycycline