Flashcards in Chapter 12 - Red Blood Cell Disorders Deck (219):
What is erythropoiesis?
Erythropoiesis: RBC production in bone marrow
Where is EPO synthesized?
EPO: synthesized in interstitial cells of peritubular capillary bed
What are the stimuli for EPO release?
EPO stimuli: ↓PaO2/↓SaO2, left-shifted OBC, high altitude
What suppresses EPO release?
↑O2 content ↓EPO
What are the other sources of EPO?
Other EPO sources: renal cell carcinoma, hepatocellular carcinoma
What is the reticulocyte count a measure of?
Reticulocyte count: measure effective erythropoiesis
What does effective erythropoiesis refer to?
Effective erythropoiesis: good bone marrow response to anemia; ↑reticulocyte synthesis/release
The initial percentage reticulocyte count must be corrected for what?
Reticulocyte count: must correct for degree of anemia
What is the equation for correction of the reticulocyte count?
Correction = Hct/45 × reticulocyte count
What is the correction if RBC polychromasia is present?
Polychromasia: original correction ÷ 2
What is the cutoff for effective erythropoiesis when calculating the corrected reticulocyte count?
Corrected reticulocyte count: <3% ineffective erythropoiesis; ≥3% effective erythropoiesis
What is extramedullary hematopoiesis?
EMH: erythropoiesis outside bone marrow
Where does EMH most often occur?
EMH: most often occurs in liver and spleen
What does EHM produce?
Where does hematopoiesis begin in the fetus?
Fetus: hematopoiesis begins in yolk sac
How are the PaO2 and SaO2 affected in anemia?
Anemia: PaO2/SaO2 normal
How is the O2 content of blood affected in anemia?
Anemia: ↓O2 content
Anemia is a sign of _____ not a _____.
Anemia: sign of disease not a diagnosis
What are the signs of severe anemia?
Signs severe anemia: pallor of skin and conjunctivae; palmar creases
What is high-output cardiac failure due to?
High output failure: anemia ↓blood viscosity
What is frequently used to classify anemias?
MCV: classification of anemias
How are microcytic, normocytic and macrocytic anemia defined?
Microcytic MCV 100 µm3
Normocytic MCV 80–100 µm3
Macrocytic MCV >100 µm3
How is the MCHC affected I the microcytic anemias and hereditary sphrerocytosis?
MCHC: ↓microcytic anemias; ↑hereditary spherocytosis
What does RDW measure?
RDW: measure RBC size variation
How is the RDW affected in iron-deficiency anemia?
Iron deficiency: ↑RDW
What to mature RBCs lack?
Lack mitochondria and nucleus
Describe the metabolism of glucose in mature RBCs.
Anaerobic glycolysis; lactic acid end product
Describe the Cori cycle.
Cori cycle: lactic acid → glucose in liver → glucose to RBC
What does glutathione in mature RBCs do?
GSH: neutralizes H2O2/acetaminophen FRs
Describe the reaction catalyzed in the methemoglobin reductase pathway.
MetHb reductase: reduces Fe3+ to Fe2+
What does the Luebering-Rapoport pathway synthesize?
2,3-BPG: product of glycolytic cycle
What do mature RBCs lack on their membrane surface?
RBCs lack HLAs
What is UCB a end product of?
UCB: end product of heme degradation by macrophages
Describe how platelets are formed.
Platelets: pinch off megakaryocyte cytoplasm
What is ferritin and what does it do?
Ferritin: soluble iron-binding protein; keeps iron in non-toxic form
Where is ferritin synthesized?
Ferritin: synthesized in bone marrow macrophages/hepatocytes
How is serum ferritin levels affected in iron deficiency, ACD and iron overload disease?
Serum ferritin: ↓iron deficiency; ↑ACD, iron overload disease
What is hemosiderin and how is it detected?
Hemosiderin: degradation product of ferritin; Prussian blue +
What is serum iron?
Serum iron: iron bound to transferrin
How serum iron affected in iron deficiency, ACD and iron overload?
Serum iron: ↓iron deficiency, ACD; ↑iron overload disease
Describe the relationship between TIBC and transferrin levels.
↓TIBC = ↓transferrin
↑TIBC = ↑transferrin
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
Where does transferrin iron come from?
Transferrin iron: from macrophages/duodenum
How is iron saturation affected in iron deficiency, ACD and iron overload?
↓Iron saturation: iron deficiency, ACD; ↑iron saturation: iron overload disease
Describe the structure of the different normal hemoglobins.
Describe the pathogenesis of the microcytic anemias.
Microcytic anemias: defects in Hb synthesis; Hb = heme + globin chains
What are the types of iron?
Types of iron: reduced Fe2+ (heme iron in meat), oxidized Fe3+ (nonheme iron in plants)
Where is functional iron present?
Functional iron: Hb, enzymes, myoglobin
How is iron primarily stored?
Storage iron: ferritin in bone marrow macrophages
How does iron stores compare between men and women?
Iron storage in men > women
What is the effect of gastric acid on elemental iron?
Gastric acid: frees elemental iron from food
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
What regulates iron absorption?
Iron bound to transferrin regulates iron absorption
What differentiates sensor cells into enterocytes?
HFE protein product + transferrin receptors differentiate sensor cells to enterocytes
What is the master iron regulator?
Hepcidin: master iron regulator
What are the effects of a decrease in transferrin-bound iron?
↓Transferrin-bound iron → ↓hepcidin synthesis → ↑iron bound to transferrin → ↑iron released from macrophages
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)
What is the most common overall anemia?
Iron deficiency: MC overall anemia
What is the most common cause of iron deficiency?
Iron deficiency: MCC bleeding
What are the clinical findings of chronic iron deficiency?
Chronic iron deficiency: esophageal web, achlorhydria, glossitis/cheilosis, spoon nails
What are the lab findings of iron deficiency?
Iron deficiency: ↓iron, % saturation, ferritin; ↑TIBC, RDW
Describe the stages of iron deficiency.
Stages of iron deficiency: all lab studies abnormal before anemia is present
Name a finding in chronic iron deficiency.
Thrombocytosis: chronic iron deficiency
What is the treatment for iron deficiency?
Rx iron deficiency: ferrous sulfate
What is the most common anemia in hospitalized patients?
ACD: MC anemia in hospitalized patients
What is the most common anemia in malignancy and alcohol excess?
ACD: MC anemia in malignancy, alcohol excess
Describe the pathogenesis of ACD.
ACD: ↓synthesis heme, ↓EPO synthesis/response, ↑hepcidin
What are the lab findings of ACD?
ACD: ↓iron, TIBC, % saturation; ↑ferritin
What is the inheritance of thalassemia?
thal: autosomal recessive
Blacks can be affected by which types of thalassemia?
Blacks can have α- or β-thalassemia
Describe the pathogenesis of α-thal.
α-thal: α-globin chain gene deletions
Describe the pathogenesis of α-thal trait.
α-thal trait: 2 gene deletions
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
Describe the pathogenesis of α-thal trait in black individuals.
Black α-thal trait: trans α/− α/−
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
Describe the pathogenesis of HbH.
HbH: 3 gene deletions; 4 β-chains; severe hemolytic anemia
Describe the pathogenesis of Hb Bart.
Hb Bart: 4 γ-chains; incompatible with life
Describe the pathogenesis of β-thal.
β-thal: mild—DNA splicing defect; severe—stop codon
Describe β-globin chain synthesis in β-thal minor.
β-thal minor: β/β+
What are the lab findings of β-thal minor?
β-thal minor: ↓HbA; ↑RBC count, HbA2, HbF; normal RDW; target cells, tear drop cells
Describe β-globin chain synthesis in β-thal major.
β-thal major: β°/β° or βo/β+
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
Describe the epidemiology of sideroblastic anemia.
Sideroblastic anemia: chronic alcoholism MCC, ↓pyridoxine, Pb poisoning, XR
Describe the pathogenesis of sideroblastic anemia.
Sideroblastic anemia: defect in mitochondrial heme synthesis; ringed sideroblasts
What is the most common cause of pyridoxine deficiency?
Pyridoxine deficiency: INH MCC
What are the causes of lead poisoning?
Pb poisoning: paint, batteries, pottery glazes, radiator repair, moonshine
What does lead denature?
Pb denatures ferrochelatase, ALA dehydrase, ribonuclease
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
What is the treatment for lead poisoning?
Rx Pb poisoning: chelation therapy
What are the lab findings in sideroblastic anemia?
Sideroblastic anemia: ↑serum iron, iron saturation, ferritin; N/↓MCV, ↓TIBC
Vitamin B12 is only present in what?
Vitamin B12: only present in animal products
What do parietal cells synthesize?
Parietal cells: synthesize IF and HCI
What does vitamin B12 bind to?
Vitamin B12 binds to R-binder
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
Where is vitamin B12 absorbed and stored?
Vitamin B12: absorbed in terminal ileum; 6- to 9-year supply in liver
What is the most common cause of pernicious anemia?
Vitamin B12 deficiency: PA MCC
Describe folic acid metabolism.
Intestinal conjugase: polyglutamate → monoglutamate; inhibited by phenytoin
What is monoglutamate absorption inhibited by?
Monoglutamate absorption: inhibited by alcohol and OCPs
What is the most common cause of folic acid deficiency?
Folic acid deficiency: alcohol MCC
Describe the pathogenesis of macrocytic anemia in folic acid and vitamin B12 deficiency.
Vitamin B12/folic acid deficiency: delayed nuclear maturation; megaloblasts
What are folic acid derivatives important in?
Folic acid derivatives: important in single carbon transfer reactions
What is the effect on plasma homocysteine levels in folic acid and vitamin B12 deficiency?
↑Homocysteine: folic acid deficiency (MC) and vitamin B12 deficiency
What is the effect of 5-FU on thymidylate synthase?
Thymidylate synthase: irreversibly inhibited by 5-fluorouracil
What inhibits dihydrofolate reductase?
Dihydrofolate reductase: inhibited by methotrexate (reversible), trimethoprim
Vitamin B12 is involved in the metabolism of which type of FA?
Vitamin B12: odd-chain FA metabolism
What does propionyl CoA replace in demyelination?
Demyelination: propionyl CoA replaces acetyl CoA
Describe the HSR that occurs in PA.
PA: type II hypersensitivity reaction destroys parietal cells (↓acid, ↓IF)
Describe how gastrin levels are affected in PA.
PA: chronic atrophic gastritis → achlorhydria → ↑gastrin
PA increases the incidence of what type of cancer.
PA: ↑incidence gastric cancer
What areas of the spinal cord are demyelinated in vitamin B12 deficiency?
Spinal cord demyelination: posterior columns, lateral corticospinal tract, dorsal spinocerebellar tract
There is deficiency of what if there is macrocytic anemia with neurological disease?
Macrocytic anemia with neurologic disease: vitamin B12 deficiency
What is the most sensitive test for vitamin B12 deficiency?
↑Methylmalonic acid: most sensitive test for B12 deficiency
The hypersegmented neutrophil is a marker of what?
Hypersegmented neutrophil: marker for folic acid/vitamin B12 deficiency
What is the Schilling test used for?
Schilling test: cause of B12 deficiency
Decreased intake of maternal folic acid increases the risk of what?
↓Maternal intake folic acid: ↑risk open neural tube defect in newborn
RBC folic acid is the best indicator of what?
RBC folic acid: best indicator of folic acid stores
What are the lab findings in nonmegaloblastic macrocytosis?
Nonmegaloblastic macrocytosis: round macrocytes, no hypersegmented neutrophils
What are the hematologic findings in alcoholic liver disease?
Alcohol liver disease: round macrocytic target cells; no anemia
What are the two main categories of acute blood loss?
Acute blood loss: external, internal
What is the most common cause of hypovolemic shock?
Acute blood loss MCC hypovolemic shock
What are the initial CBC results in acute blood loss?
Hb, Hct, RBC count initially normal; anemia uncovered with IV saline
How long does it take before a reticulocyte response is seen in acute blood loss?
Reticulocyte response 5–7 days after blood loss
Describe the MCV in early iron deficiency and ACD.
Iron deficiency/ACD: anemia normocytic before becoming microcytic
Describe the causes of aplastic anemia.
Aplastic anemia: most cases idiopathic; drugs MC known cause
Describe the pathogenesis of aplastic anemia.
Immunologic destruction in myeloid stem cells; mutations in TERT, the gene for the RNA component of telomerase
What are the clinical findings in aplastic anemia?
Aplastic anemia: fever, bleeding, fatigue
What are the lab findings in aplastic anemia?
Aplastic anemia: pancytopenia, reticulocytopenia, hypocellular marrow
Complete recovery occurs in what percentage of cases of aplastic anemia?
Complete recovery <10%
What is RBC aplasia?
RBC aplasia: suppression/destruction erythroid colony-forming unit
What are the causes of RBC aplasia?
RBC aplasia: Diamond-Blackfan syndrome, thymomas, leukemia, drugs, parvovirus
What is the pathogenesis of anemia in CRF?
Anemia CRF: ↓EPO + ACD
What are the hematologic lab findings in CRF?
CRF: platelet dysfunction (reversible with dialysis), burr cells
What are the causes of anemia in malignancy?
Anemia malignancy: ACD (MC anemia), blood loss, metastasis to marrow, immunologic
What are the types of hemolytic anemia?
Types hemolytic anemia: intrinsic (defect in RBC), extrinsic (factors outside RBC)
What are the reasons for RBC phagocytosis?
RBCs coated with IgG and/or C3b; abnormal shape (spherocyte, sickle cell); inclusions (G6PD deficiency)
Describe the characteristics of extravascular hemolysis.
Extravascular hemolysis: macrophage phagocytosis; ↑UCB
What are the causes of intravascular hemolysis?
Intravascular hemolysis: enzyme deficiency, complement destruction, mechanical damage
What are the lab findings in intravascular hemolysis?
Intravascular hemolysis: ↓serum haptoglobin; hemoglobinuria, hemosiderinuria
Describe the epidemiology of HS.
HS: intrinsic defect, extravascular hemolysis; autosomal dominant
What is the most common defect in HS?
HS: mutation in spectrin in cell membrane
Describe spherocyte formation in HS.
HS: microvesicle formation/loss + loss K+ and H2O (dehydrate cell) → spherocyte formation
What are the clinical findings in HS?
HS: jaundice, calcium bilirubinate gallstones, splenomegaly, aplastic crisis (parvovirus-induced)
What are the lab findings in HS?
HS: ↑MCHC, ↑RBC osmotic fragility (↓surface to volume ratio), ↑RDW
What is the treatment for HS?
HS: Rx splenectomy
Describe the pathogenesis of hereditary elliptocytosis.
Elliptocytosis: AD disorder; mutation spectrin and band 4.1
What are the lab findings in hereditary elliptocytosis?
Hereditary elliptocytosis: >25% elliptocytes in peripheral blood
What is the epidemiology of PNH?
PNH: intrinsic defect with intravascular hemolysis
Which gene is affected in PNH?
PNH: mutation in PIG group A gene in myeloid stem cell clone
What is the effect of the mutation in PNH?
PNH: defect in anchoring inhibitors of complement (CD55 [decay accelerating factor], CD59)
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
What are the clinical findings in PNH?
PNH: episodic hemoglobinuria, ↑vessel thrombosis, acute myeloblastic leukemia
What are the lab findings in PNH?
PNH: pancytopenia; ↓LAP stain; hemoglobinuria
How is PNH diagnosed?
PNH Dx: flow cytometry best test; sucrose hemolysis test and acidified serum test outdated
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
What are the clinical findings in PCH?
PCH: pain, Raynaud, hepatosplenomegaly, jaundice, renal failure
Describe the type of defect and hemolysis that occurs in HbSS anemia.
HbSS anemia: intrinsic defect, predominantly extravascular hemolysis
Describe the type of mutation that occurs in HbSS anemia.
HbSS anemia: missense mutation; substitute valine for glutamic acid
Describe the offspring of two individuals with sickle cell trait.
Trait × trait: 25% normal, 50% trait, 25% disease
What do HbS molecules do when deoxygenated?
HbS molecules aggregate and polymerize when deoxygenated; O2 inhibits sickling
What are the factors that increase the risk for sickling?
Sickling: ↑HbS, ↑deoxyHb (acidosis, volume depletion, hypoxemia)
Describe the characteristics of irreversibly sickled cells.
Irreversibly sickled cells: dehydrated; correlate with degree of severity of hemolysis; extravascular removal
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
What prevents sickling in addition to oxygen? How is its synthesis increased?
HbF prevents sickling: hydroxyurea ↑HbF synthesis
What are the key pathologic processes in HbSS anemia?
HbSS anemia: severe hemolytic anemia; vasoocclusive crises
What is the most common presentation of HbSS anemia in infants?
Dactylitis: aseptic necrosis in metacarpal bones; MC presentation in infants
What is the most common cause of death in young people with HbSS anemia?
Acute chest syndrome: MCC death in young people
What process may affect the femoral head in HbSS anemia?
Aseptic necrosis of femoral head
What is a sign of splenic dysfunction?
Howell-Jolly bodies: sign of splenic dysfunction
What does autosplenectomy refer to?
Autosplenectomy: spleen fibrosed/smaller
There is increased susceptibility to which infections in HbSS anemia?
Pathogens: S. pneumoniae sepsis, Salmonella paratyphi osteomyelitis
What are the characteristics of an aplastic crisis?
Aplastic crisis due to parvovirus; no reticulocytes
How do sequestration and aplastic crisis differ?
Sequestration vs. aplastic crisis: reticulocytosis, reticulocytopenia, respectively
There is increased risk for which type of gallstones in HbSS anemia?
Calcium bilirubinate gallstones
What is a common cause of death in children with HbSS anemia?
Strokes common in children; common cause of death in children
Where are recurrent leg ulcers located in HbSS anemia?
Recurrent leg ulcers around malleoli
What commonly leads to blindness in HbSS anemia?
Proliferative retinopathy → blindness
What occurs after 40 years of age in HbSS anemia?
End-stage renal failure after 40 years old
What are the renal findings in sickle cell trait?
Sickle cell trait: no anemia; microhematuria; potential for renal papillary necrosis
What is the sickle cell screen?
Screen: sodium metabisulfite ↓O2 tension, induces sickling
What are the Hb electrophoresis findings in HbAS?
HbAS: HbA 55%–60%, HbS 40%–45%
What are the Hb electrophoresis findings in HbSS?
HbSS: HbS 90%–95%, HbF 5%–10%, no HbA
What causes the appearance of target cells? What are they a sign of?
Target cells: excess RBC membrane; sign hemoglobinopathy or alcohol excess
Describe the inheritance of G6PD deficiency. Where is it most common?
G6PD deficiency: XR; MC in tropical Africa
Describe the type of defect and hemolysis in G6PD deficiency.
G6PD def: intrinsic defect, predominantly intravascular hemolysis
What are the subtypes of G6PD?
Mediterranean and black variants
What is the most common enzyme deficiency causing hemolysis?
G6PD def: MC enzyme deficiency causing hemolysis
Describe the pathogenesis of G6PD deficiency.
G6PD def: ↓synthesis GSH; H2O2 cannot be neutralized
Describe the characteristics of the Mediterranean variant of G6PD.
Mediterranean variant: enzyme half-life markedly reduced in old RBCs (<10% activity)
Describe the characteristics of the black variant of G6PD.
Black variant: enzyme half-life moderately reduced in old RBCs (10% to 60% activity)
What system is dysfunctional in G6PD deficiency?
G6PD deficiency: O2 dependent MPO system dysfunctional; lack of NADPH cofactor
What are the drugs that may act as oxidant stressors in G6PD deficiency?
Drugs: primaquine, dapsone, sulfonamides
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
Describe the type of defect and hemolysis in PK deficiency.
PK deficiency: intrinsic defect, extravascular hemolysis
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
What does PK do?
PK converts PEP to pyruvate for net gain of 2 ATP
Describe the pathogenesis of PK deficiency?
PK def: loss ATP damages RBC membranes (echinocytes)
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
What are the immune hemolytic anemias?
Extrinsic hemolytic anemias with intravascular or extravascular hemolysis
What is the most common type of IHA?
AIHA: MC IHA
What are the types of AIHA?
AIHA: warm type (IgG; MC), cold type (IgM)
Describe the pathogenesis of IHA.
IgG-mediated: predominantly extravascular IHA; spherocytosis
Complement-mediated: intravascular or extravascular IHA
IgM-mediated: intravascular (MC) or extravascular hemolysis
What are the clinical findings of IHA?
Jaundice (extravascular), hepatosplenomegaly (warm type); Raynaud (cold type)
What does DAT detect?
DAT: detects IgG, C3b, C3d on surface of sensitized RBCs
What does the indirect Coombs test detect?
Indirect Coombs: detects IgG antibodies in serum (e.g., anti-D antibodies)
What are the lab findings in IHA?
Hemoglobinuria (intravascular), spherocytes, reticulocytosis, agglutination (cold type)
What types of hemolysis occur in MHA?
MHA: extrinsic, intravascular hemolysis
What are schistocytes a sign of?
Schistocytes: sign of MHA
What is the most common cause of MHA?
MHA: AV stenosis MCC
Describe the pathogenesis of microangiopathic hemolytic anemia.
Microangiopathic: small vessel fibrin or platelet thrombi; damage RBCs → schistocytes
What are the lab findings in MHA?
Normocytic/microcytic anemia, hemoglobinuria/hemosiderinuria, ↓serum haptoglobin, schistocytes
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
Describe the type of defect and hemolysis that occurs in malaria anemia.
Malaria anemia: extrinsic defect with intravascular hemolysis
Intravascular hemolysis correlates with what in malaria?
Malaria: intravascular hemolysis correlates with fever spikes
What is the most common cause of malaria worldwide? Describe the fever pattern.
P. vivax MC type; fever q48 hours (simple tertian)
What is the most lethal type of malaria? Describe the fever pattern.
P. falciparum most lethal type; fever quotidian (malignant tertian)
Which type of malaria is associated with nephrotic syndrome? Describe the fever pattern.
P. malariae fever q72 hours (quartan); association with nephrotic syndrome
What is the prophylactic treatment for malaria?
Malaria: chloroquine prevention
What is the treatment for malaria caused by P. vivax or P. ovale?
Malaria Rx P. vivax/ovale: chloroquine + primaquine