Chapter 12 - Red Blood Cell Disorders Flashcards
(219 cards)
0
Q
Where is EPO synthesized?
A
EPO: synthesized in interstitial cells of peritubular capillary bed
1
Q
What is erythropoiesis?
A
Erythropoiesis: RBC production in bone marrow
2
Q
What are the stimuli for EPO release?
A
EPO stimuli: ↓PaO2/↓SaO2, left-shifted OBC, high altitude
3
Q
What suppresses EPO release?
A
↑O2 content ↓EPO
4
Q
What are the other sources of EPO?
A
Other EPO sources: renal cell carcinoma, hepatocellular carcinoma
5
Q
What is the reticulocyte count a measure of?
A
Reticulocyte count: measure effective erythropoiesis
6
Q
What does effective erythropoiesis refer to?
A
Effective erythropoiesis: good bone marrow response to anemia; ↑reticulocyte synthesis/release
7
Q
The initial percentage reticulocyte count must be corrected for what?
A
Reticulocyte count: must correct for degree of anemia
8
Q
What is the equation for correction of the reticulocyte count?
A
Correction = Hct/45 × reticulocyte count
9
Q
What is the correction if RBC polychromasia is present?
A
Polychromasia: original correction ÷ 2
10
Q
What is the cutoff for effective erythropoiesis when calculating the corrected reticulocyte count?
A
Corrected reticulocyte count: <3% ineffective erythropoiesis; ≥3% effective erythropoiesis
11
Q
What is extramedullary hematopoiesis?
A
EMH: erythropoiesis outside bone marrow
12
Q
Where does EMH most often occur?
A
EMH: most often occurs in liver and spleen
13
Q
What does EHM produce?
A
EMH: hepatosplenomegaly
14
Q
Where does hematopoiesis begin in the fetus?
A
Fetus: hematopoiesis begins in yolk sac
15
Q
How are the PaO2 and SaO2 affected in anemia?
A
Anemia: PaO2/SaO2 normal
16
Q
How is the O2 content of blood affected in anemia?
A
Anemia: ↓O2 content
17
Q
Anemia is a sign of _____ not a _____.
A
Anemia: sign of disease not a diagnosis
18
Q
What are the signs of severe anemia?
A
Signs severe anemia: pallor of skin and conjunctivae; palmar creases
19
Q
What is high-output cardiac failure due to?
A
High output failure: anemia ↓blood viscosity
20
Q
What is frequently used to classify anemias?
A
MCV: classification of anemias
21
Q
How are microcytic, normocytic and macrocytic anemia defined?
A
Microcytic MCV 100 µm3
Normocytic MCV 80–100 µm3
Macrocytic MCV >100 µm3
22
Q
How is the MCHC affected I the microcytic anemias and hereditary sphrerocytosis?
A
MCHC: ↓microcytic anemias; ↑hereditary spherocytosis
23
Q
What does RDW measure?
A
RDW: measure RBC size variation
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How is the RDW affected in iron-deficiency anemia?
Iron deficiency: ↑RDW
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What to mature RBCs lack?
Lack mitochondria and nucleus
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Describe the metabolism of glucose in mature RBCs.
Anaerobic glycolysis; lactic acid end product
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Describe the Cori cycle.
Cori cycle: lactic acid → glucose in liver → glucose to RBC
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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
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What is UCB a end product of?
UCB: end product of heme degradation by macrophages
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Describe how platelets are formed.
Platelets: pinch off megakaryocyte cytoplasm
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What is ferritin and what does it do?
Ferritin: soluble iron-binding protein; keeps iron in non-toxic form
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Where is ferritin synthesized?
Ferritin: synthesized in bone marrow macrophages/hepatocytes
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How is serum ferritin levels affected in iron deficiency, ACD and iron overload disease?
Serum ferritin: ↓iron deficiency; ↑ACD, iron overload disease
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What is hemosiderin and how is it detected?
Hemosiderin: degradation product of ferritin; Prussian blue +
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What is serum iron?
Serum iron: iron bound to transferrin
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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
```
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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
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Where does transferrin iron come from?
Transferrin iron: from macrophages/duodenum
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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
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Describe the pathogenesis of the microcytic anemias.
Microcytic anemias: defects in Hb synthesis; Hb = heme + globin chains
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What are the types of iron?
Types of iron: reduced Fe2+ (heme iron in meat), oxidized Fe3+ (nonheme iron in plants)
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Where is functional iron present?
Functional iron: Hb, enzymes, myoglobin
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How is iron primarily stored?
Storage iron: ferritin in bone marrow macrophages
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How does iron stores compare between men and women?
Iron storage in men > women
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What is the effect of gastric acid on elemental iron?
Gastric acid: frees elemental iron from food
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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
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What regulates iron absorption?
Iron bound to transferrin regulates iron absorption
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What differentiates sensor cells into enterocytes?
HFE protein product + transferrin receptors differentiate sensor cells to enterocytes
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What is the master iron regulator?
Hepcidin: master iron regulator
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What are the effects of a decrease in transferrin-bound iron?
↓Transferrin-bound iron → ↓hepcidin synthesis → ↑iron bound to transferrin → ↑iron released from macrophages
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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)
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What is the most common overall anemia?
Iron deficiency: MC overall anemia
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What is the most common cause of iron deficiency?
Iron deficiency: MCC bleeding
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What are the clinical findings of chronic iron deficiency?
Chronic iron deficiency: esophageal web, achlorhydria, glossitis/cheilosis, spoon nails
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What are the lab findings of iron deficiency?
Iron deficiency: ↓iron, % saturation, ferritin; ↑TIBC, RDW
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Describe the stages of iron deficiency.
Stages of iron deficiency: all lab studies abnormal before anemia is present
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Name a finding in chronic iron deficiency.
Thrombocytosis: chronic iron deficiency
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What is the treatment for iron deficiency?
Rx iron deficiency: ferrous sulfate
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What is the most common anemia in hospitalized patients?
ACD: MC anemia in hospitalized patients
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What is the most common anemia in malignancy and alcohol excess?
ACD: MC anemia in malignancy, alcohol excess
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Describe the pathogenesis of ACD.
ACD: ↓synthesis heme, ↓EPO synthesis/response, ↑hepcidin
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What are the lab findings of ACD?
ACD: ↓iron, TIBC, % saturation; ↑ferritin
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What is the inheritance of thalassemia?
thal: autosomal recessive
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Blacks can be affected by which types of thalassemia?
Blacks can have α- or β-thalassemia
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Describe the pathogenesis of α-thal.
α-thal: α-globin chain gene deletions
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Describe the pathogenesis of α-thal trait.
α-thal trait: 2 gene deletions
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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
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Describe the pathogenesis of α-thal trait in black individuals.
Black α-thal trait: trans α/− α/−
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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
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Describe the pathogenesis of HbH.
HbH: 3 gene deletions; 4 β-chains; severe hemolytic anemia
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Describe the pathogenesis of Hb Bart.
Hb Bart: 4 γ-chains; incompatible with life
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Describe the pathogenesis of β-thal.
β-thal: mild—DNA splicing defect; severe—stop codon
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Describe β-globin chain synthesis in β-thal minor.
β-thal minor: β/β+
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What are the lab findings of β-thal minor?
β-thal minor: ↓HbA; ↑RBC count, HbA2, HbF; normal RDW; target cells, tear drop cells
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Describe β-globin chain synthesis in β-thal major.
β-thal major: β°/β° or βo/β+
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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
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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
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What does lead denature?
Pb denatures ferrochelatase, ALA dehydrase, ribonuclease
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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
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What is the treatment for lead poisoning?
Rx Pb poisoning: chelation therapy
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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
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What do parietal cells synthesize?
Parietal cells: synthesize IF and HCI
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What does vitamin B12 bind to?
Vitamin B12 binds to R-binder
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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
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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
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Vitamin B12 is involved in the metabolism of which type of FA?
Vitamin B12: odd-chain FA metabolism
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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
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What areas of the spinal cord are demyelinated in vitamin B12 deficiency?
Spinal cord demyelination: posterior columns, lateral corticospinal tract, dorsal spinocerebellar tract
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There is deficiency of what if there is macrocytic anemia with neurological disease?
Macrocytic anemia with neurologic disease: vitamin B12 deficiency
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What is the most sensitive test for vitamin B12 deficiency?
↑Methylmalonic acid: most sensitive test for B12 deficiency
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The hypersegmented neutrophil is a marker of what?
Hypersegmented neutrophil: marker for folic acid/vitamin B12 deficiency
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What is the Schilling test used for?
Schilling test: cause of B12 deficiency
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Decreased intake of maternal folic acid increases the risk of what?
↓Maternal intake folic acid: ↑risk open neural tube defect in newborn
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RBC folic acid is the best indicator of what?
RBC folic acid: best indicator of folic acid stores
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What are the lab findings in nonmegaloblastic macrocytosis?
Nonmegaloblastic macrocytosis: round macrocytes, no hypersegmented neutrophils
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What are the hematologic findings in alcoholic liver disease?
Alcohol liver disease: round macrocytic target cells; no anemia
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What are the two main categories of acute blood loss?
Acute blood loss: external, internal
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What is the most common cause of hypovolemic shock?
Acute blood loss MCC hypovolemic shock
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What are the initial CBC results in acute blood loss?
Hb, Hct, RBC count initially normal; anemia uncovered with IV saline
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How long does it take before a reticulocyte response is seen in acute blood loss?
Reticulocyte response 5–7 days after blood loss
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Describe the MCV in early iron deficiency and ACD.
Iron deficiency/ACD: anemia normocytic before becoming microcytic
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Describe the causes of aplastic anemia.
Aplastic anemia: most cases idiopathic; drugs MC known cause
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Describe the pathogenesis of aplastic anemia.
Immunologic destruction in myeloid stem cells; mutations in TERT, the gene for the RNA component of telomerase
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What are the clinical findings in aplastic anemia?
Aplastic anemia: fever, bleeding, fatigue
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What are the lab findings in aplastic anemia?
Aplastic anemia: pancytopenia, reticulocytopenia, hypocellular marrow
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Complete recovery occurs in what percentage of cases of aplastic anemia?
Complete recovery <10%
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What is RBC aplasia?
RBC aplasia: suppression/destruction erythroid colony-forming unit
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What are the causes of RBC aplasia?
RBC aplasia: Diamond-Blackfan syndrome, thymomas, leukemia, drugs, parvovirus
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What is the pathogenesis of anemia in CRF?
Anemia CRF: ↓EPO + ACD
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What are the hematologic lab findings in CRF?
CRF: platelet dysfunction (reversible with dialysis), burr cells
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What are the causes of anemia in malignancy?
Anemia malignancy: ACD (MC anemia), blood loss, metastasis to marrow, immunologic
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What are the types of hemolytic anemia?
Types hemolytic anemia: intrinsic (defect in RBC), extrinsic (factors outside RBC)
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What are the reasons for RBC phagocytosis?
RBCs coated with IgG and/or C3b; abnormal shape (spherocyte, sickle cell); inclusions (G6PD deficiency)
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Describe the characteristics of extravascular hemolysis.
Extravascular hemolysis: macrophage phagocytosis; ↑UCB
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What are the causes of intravascular hemolysis?
Intravascular hemolysis: enzyme deficiency, complement destruction, mechanical damage
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What are the lab findings in intravascular hemolysis?
Intravascular hemolysis: ↓serum haptoglobin; hemoglobinuria, hemosiderinuria
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Describe the epidemiology of HS.
HS: intrinsic defect, extravascular hemolysis; autosomal dominant
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What is the most common defect in HS?
HS: mutation in spectrin in cell membrane
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Describe spherocyte formation in HS.
HS: microvesicle formation/loss + loss K+ and H2O (dehydrate cell) → spherocyte formation
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What are the clinical findings in HS?
HS: jaundice, calcium bilirubinate gallstones, splenomegaly, aplastic crisis (parvovirus-induced)
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What are the lab findings in HS?
HS: ↑MCHC, ↑RBC osmotic fragility (↓surface to volume ratio), ↑RDW
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What is the treatment for HS?
HS: Rx splenectomy
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Describe the pathogenesis of hereditary elliptocytosis.
Elliptocytosis: AD disorder; mutation spectrin and band 4.1
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What are the lab findings in hereditary elliptocytosis?
Hereditary elliptocytosis: >25% elliptocytes in peripheral blood
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What is the epidemiology of PNH?
PNH: intrinsic defect with intravascular hemolysis
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Which gene is affected in PNH?
PNH: mutation in PIG group A gene in myeloid stem cell clone
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What is the effect of the mutation in PNH?
PNH: defect in anchoring inhibitors of complement (CD55 [decay accelerating factor], CD59)
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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
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What are the clinical findings in PNH?
PNH: episodic hemoglobinuria, ↑vessel thrombosis, acute myeloblastic leukemia
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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
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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
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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)
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Describe the characteristics of irreversibly sickled cells.
Irreversibly sickled cells: dehydrated; correlate with degree of severity of hemolysis; extravascular removal
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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
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What prevents sickling in addition to oxygen? How is its synthesis increased?
HbF prevents sickling: hydroxyurea ↑HbF synthesis
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What are the key pathologic processes in HbSS anemia?
HbSS anemia: severe hemolytic anemia; vasoocclusive crises
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What is the most common presentation of HbSS anemia in infants?
Dactylitis: aseptic necrosis in metacarpal bones; MC presentation in infants
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What is the most common cause of death in young people with HbSS anemia?
Acute chest syndrome: MCC death in young people
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What process may affect the femoral head in HbSS anemia?
Aseptic necrosis of femoral head
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What is a sign of splenic dysfunction?
Howell-Jolly bodies: sign of splenic dysfunction
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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
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There is increased risk for which type of gallstones in HbSS anemia?
Calcium bilirubinate gallstones
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What is a common cause of death in children with HbSS anemia?
Strokes common in children; common cause of death in children
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Where are recurrent leg ulcers located in HbSS anemia?
Recurrent leg ulcers around malleoli
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What commonly leads to blindness in HbSS anemia?
Proliferative retinopathy → blindness
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What occurs after 40 years of age in HbSS anemia?
End-stage renal failure after 40 years old
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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%
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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
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Describe the inheritance of G6PD deficiency. Where is it most common?
G6PD deficiency: XR; MC in tropical Africa
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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
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What is the most common enzyme deficiency causing hemolysis?
G6PD def: MC enzyme deficiency causing hemolysis
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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
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What is the most common cause of malaria worldwide? Describe the fever pattern.
P. vivax MC type; fever q48 hours (simple tertian)
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What is the most lethal type of malaria? Describe the fever pattern.
P. falciparum most lethal type; fever quotidian (malignant tertian)
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Which type of malaria is associated with nephrotic syndrome? Describe the fever pattern.
P. malariae fever q72 hours (quartan); association with nephrotic syndrome
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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
