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Step 1 (Let's Do This)! > Heme Oncology > Flashcards

Heme Oncology Flashcards

1
Q

Hypersegmented neutrophils are seen in what disease? What is the defect/pathology?

A

Megaloblastic anemia: -impaired DNA synthesis (low B12 and/or folate) -cell cycle cannot G2–> Mitosis. Continued cell growth w/o division–> Macrocytes

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2
Q

What are causes of folate deficiency?

A

Malnutrition (alcoholics) Malabsorbtion Anti-folate Rx (methotrexate, trimethoprim, phenytoin, sulfonamides) Pregnancy, Hemolytic anemia (increased need) Cancer (use up for DNA..)

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3
Q

How does folate deficiency present?

A

Hyperseg neutrophils Glossitis Increased Homocysteine, but normal methylmalonic acid levels *no neuronal findings* Neural tube defects (fetus)

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4
Q

Risks for Homocystenemia?

A

…

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5
Q

Significance of Folate/Folic acid?

A

After conversion to THF, is is a coenzyme for 1-cabon transfer (methylation) rxns. Necessary for making nitrogenous bases in DNA & RNA.

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6
Q

What is vitamin designation for folic acid? Where is it found?

A

Vitamin B9 Natural source, Folate, found in lefy green veggies. Small reserve in liver. “FOLate from FOLiage”

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7
Q

What specific reaction is Folic acid used for DNA?

A

Pyrimidine base production dTMP

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8
Q

What does increase band cells indicate?

A

Increased myeloid proliferation. Ex:

  • bacterial infection
  • CML
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9
Q

Describe contents of Neutrophil large and small granules

A

Small: more numerous

  • Alkaline phosphatase
  • Collegenase
  • Lysozyme
  • Latoferin

Large Azurophilic (lysosome)

  • Acid phosphatase
  • Peroxidase
  • ß-glucoronidase
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10
Q

Describe appearance of monocytes. What is normal % in CBC?

A

Kidney-shaped nucleus with frosted glass cytoplasm.

3-7%

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11
Q

Function of Macrophages

A
  • Phagocytose
    • bacteria
    • cell debris
    • old RBCs
  • APC via MHC II
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12
Q

What activates macrophages?

What is surface marker of macrophage?

A

gamma-interferon activates.

Marker CD14.

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13
Q

Causes of eosinophilia?

A

“NAACP”

  • Neoplastic
  • Asthma
  • Allergic process
  • Collagen vascular diseases
  • Parasites (invasive, like helminths)
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14
Q

What enzymes eosinophils make?

What are eosinophils highly phagocytic to?

A

Make histaminase and arylsulfatase

target Ag-b complexes

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15
Q

Function of basophils?

A

Mediates allergic rxns

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16
Q

What are contents of basophil granules?

A
  • Histamine (vasodilation)
  • heparin (anticoagulant)
  • leukotriene (LTD4)
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17
Q

List WBCs from normal CBC in descending % (give %s)?

Normal WBC range?

A

“Neutrophil Like Making Everything Better”

  • Neutrophils (54-62%)
  • Lymphocytes (25-33%)
  • Monocytes (3-7%)
  • Eosinophils (1-3%)
  • Basophils (0-0.75%)
    ​

Normal WBC range: 4-10K cells/mm3

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18
Q

Platelet granules and contents?

A

Dense granules

  • ADP
  • calcium

Alpha-granules

  • vWF (receptor GpIb)
  • fibrinogen (receptor GpIIb/IIIa)
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19
Q

Where are PLTs stored? How much?

A

1/3 stored in spleen

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20
Q

What is receptor for vWF?

A

GpIb

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21
Q

What is receptor for Fibrinogen?

A

GpIIb/IIIa

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22
Q

What is the energy source of RBCs? What pathways are it used in and %distribution?

A

Glucose 90% in glycolysis 10% in HMP shunt (Pentose Phosphate Pathway)

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23
Q

What damage can free radicals cause?

A
  • Lipid membrane peroxidation
  • Protein modification
  • Breaking DNA
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24
Q

Where do free radicals come from?

A
  • Radiation
  • Drug metabolism; PHASE I
  • Redox rxns
  • Nitric Oxide
  • Transition metals (Iron, etc)
    • Iron must be found in body (prevent Fenton rxn)
  • Leukocyte oxidatie BURST
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25
Q

What role does glutathione have in RBCs?

A
  • in reduced form, it is an antioxidant.
    • converts H2O2 to water
    • Reduced by NADPH
  • If not reduced, it will cause oxidative stress–> Hemolysis
    • G6PD deficiency
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26
Q

What prevets free radical injury?

A
  • Antoxidants
    • Vit A, C, E
    • Glutathione
    • Uric acid
    • Coenzyme Q
  • Enzymes
    • Catalase
    • Superoxide dismutase
    • Gluathione peroxidase
  • Spontaneous decay
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27
Q

Pathalogies of free radical injury?

A
  • iron overload (heochromatosis)
  • retinopathy of prematurity
  • bronchopulmonary dysplasia
  • carbon tetrachlorida –> liver necrosis (fatty change)
  • Acetaminophen overdose (fulminant hepatitis)
  • Repurfusion after anoxia (superoxide)
    • 3 hrs after stroke
    • after thrombolytic treatment
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28
Q

Repurfusion damage. How?

A
  • Superoxide O-
  • Mitochondrial damage
  • Inflammation (increased neutrophil)
  • Compliment activation
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29
Q

What is the purpose of HMP shunt (Pentose Phosphate Pathway)?

A
  • Alternative route for glucose oxidation w/o using ATP.
  • Generates NADPH .
  • Produces pentose sugars
    • Ribose 5-P (for DNA)
    • Glycolytic intermediates: G3P, F6P
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30
Q

Write out the Pentose Phosphate Pathway/ HMP shunt.

Differentiate oxidative and nonoxidative portion.

A

FA, pg 103

Lange card #8

Oxidative (irrev) makes Ribulose 5-P, CO2, & 2 NADPH

Nonoxidative makes Ribose 5P, G3P, F6P.

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31
Q

Where does HMP shunt located?

A

Cytoplasm of liver cells, adrenal cortex, and lactating mammary glands.

(site of FA or steroid synthesis)

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32
Q

Function of NADPH?

A

Reduce free radicals and peroxides. Keep glutathione in reduced state.

Used in FA and Chol synthesis.

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33
Q

Deficiency in B12 and/or Folic Acid has neurological Sx?

Explain path & Biochem of Neuro Sx.

A

B12 defciency (not folate)

B12 a cofactor for Methylmalonyl-CoA Mutase, for conversion of MM-CoA to Succinyl-CoA. If B12 deficiency, MM-CoA converted to Methylmalonic Acid, a myelin destabilizer. Excessive MMA will prevent normal fatty acid synthesis, or it will be incorporated into fatty acid itself rather than normal malonic acid. If abnormal FA incorporated into myelin, the resulting myelin will be too fragile, and demyelination will occur.

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34
Q

Beta-thalassemia minor Sx & in lab how is it confirmed?

A

No Sx!

Confirmed on electrophoresis with increased HbA2 (>3.5%).

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35
Q

Differentiate Beta-thalassemia minor, major, and HbS/Beta heterozygote regarding Hgb chains. Disease severity.

A
  • ß-thal minor (heteroz): ß chain underproduced-> no Sx. Decreased Hgb A, increased Hgb A2 (5%, normal 2.5%), and Hgb F (2%, normal 1%)
  • ß-thal major: ß chain absent → severe anemia, presents few months after birth (HgbF temporarily protective)
    • increase fetal Hgb, HbF (α2γ2). Little to no HgbA. Increased Hgb A2.
  • HbS/ß-thal (heteroz): varible ß-globin production. Mild to moderate sickle disease.
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36
Q

Desribe ß-thalassemia

A

Point mutation in splice site and promoter sequence–> decreased ß-globin made genetically

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37
Q

Which race/demo is ß-thalassemia common in?

A

Mediterranean & African

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38
Q

Describe Sx of ß-thalassemia major and causes

A

Skeletal deformities; Chipmunk facies

X-ray: “crew cut” skull appearance due to marrow expansion (like in sickle cell Xray), due to Massive erythroid hyperplasia.

Extramedullary hematopoiesis with hepatosplenomegaly

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39
Q

What enzymes do lead inhibit? what pathway are they from?

A

From Heme synthesis, enzymes inhibited by lead:

Ferrochelatase & ALA dehydratase

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40
Q

How does Lead cause basphilic stippling?

A

Lead inhibits rRNA degradation, causing RBCs to retain aggregates of rRNA

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41
Q

First line of Tx for Lead intoxication?

A

Dimercaprol & EDTA.

Kids can also get Succimer for chelation.

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42
Q

Sx of Lead poisoning

A

LEAD:

  • Lead lines on gingiva (Burton’s lines) and on metaphyses of long bones on x-ray
  • Encephalopathy & Erythrocyte basophilic stippling
  • Abdominal colic and sideroblastic Anemia
  • Drops- wrist nd foot drop. Dimercaprol & EDTA 1st line for Tx.
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43
Q

Causes of Sideroblastic anemia (genetic and acquired)

A
  • X-linked defect in δ-ALA synthase gene
  • EtOH, lead, & Isoniazid (inhibits cofactor Vit B6). Reversible.
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44
Q

Lab presentation of Sideroblastic anemia

A

Ringed sideroblasts (w/ iron-laden mitochondria)

↑ Iron, ↑ Ferritin. Normal to low TIBC, ↑%sat

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45
Q

How do you treat Sideroblastic anemia

A

Pyridoxine (B6, cofactor for δ-ALA synthase)

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46
Q

What does PTT test?

A

Common & intrinsic pathway (all factors except 7 & 13)

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47
Q

What does PT lab value test?

A

Comon & extrinsic pathway

(factors 1, 2, 5, 7, 10)

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48
Q

What are Sx of Hemophilia

A

Macrohemorrhaging:
hemarthroses (bleeding in joints), easy bruising, and elevated PTT

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49
Q

What factors effected in Vit. K deficiency?

A

Factors 2, 7, 9, 10, C, & S

50
Q

Defect in PLT plug formation for adhesion.
Decreased in GpIb. What is disease?

How does it present on blood smear?

A

Bernard- Soulier syndrome

Mild thrombocytopenia w/ enlarged PLTs“Big-Suckers”

51
Q

Defect in PT plug formation. Decreased GpIIb/IIIa–> defect in PLT-to-PLT aggregation. No cumping on labs. What is disease?

A

Glanzmann’s thrombasthenia

52
Q

What increase bleeding time? When does it increase?

A

> than Normal BT (2-7min). Defect in PLT plug formation, increases for all quantitative and qualitative PLT disorders.

53
Q

Clinical Sx of Primary Hemostasis disorders

A
  • Mucosal bleeding
    • epistaxis- most common Sx
    • hemoptysis
    • GI bleeding
    • hematuria
    • menorrhagia
    • intracranial bleeding (severe thrombocytopenia)
  • Skin bleeding
    • petechiae, purpura, ecchymoses
  • increase BT
  • possible decrease in PLT count
54
Q

What is Idiopathic thrompotic Purpura (ITP)?

A

Anti-GpIIb/IIIa Abs, causing splenic macrophage sonsumption of PLT-Ab complex –> reduced PLT count.

Auto-Abs from spleenic plasma cells.

55
Q

Differentiate lab presentation of ITP vs TTP

A

Both show

  • ↑megakaryocytes on BM biopsy
  • Thrombocytopenia
  • Normal PT/PTT

TTP: Anemia w/ schistocytes, ↑LDH

56
Q

What is TTP?

A

a Microangiopathic hemolytic anemia.

Deficiency in ADAMTS 13 (vWF metalloprotease)–>
↑vWF multimers –> Microthrombi.
Decrease ADAMTS13 due to auto-ABs.

Microthrombi rip RBCs –> Hemolyic anemia

57
Q

What are Sx of TTP & HUS?

A
  • Skin & mucosal bleeding
  • microangiopathic hemolyic anemia
  • Fever
  • Thrombocytopenia, increase BT
  • hemolytic anemia w/ schistocytes
  • Renal and/or CNS abnormalities
58
Q

What non-cancer clinical use is Methotrexate used for? Eplain MOA.

A

Rheumatoid arthritis & Psoriasis.

Cytotoxic to rapidly dividing immune cells due to
inhibition of dihydrofolate disorders hepatotoxicity,
reductase.

Also used for Hydatidiform mole, abortion & ectopic pregnancy

59
Q

What cancers are MTX used for?

A

Effective in choriocarcinoma, sarcomas,
acute leukemias, non-Hodgkin’s and primary CNS
lymphomas, and a number of solid tumors, including breast cancer, head and neck cancer, and bladder cancer.

60
Q

S/E of MTX? How drug can be given to manage?

A

BM suppression and toxic effects on the skin and gastrointestinal mucosa (mucositis). The toxic effects of MTX on normal cells may be reduced by administration of folinic acid (leucovorin); this strategy is called leucovorin rescue. Long-term
use of methotrexate has led to hepatotoxicity; fatty liver

61
Q

MOA of 5-Fluorouracil

A

Pyrimidine analog.

First bioactivated to 5F-dUMP, and covalently complexes to Folic acid. Complex inhibits thymidylate sythase–> decrease dTMP-> decrease DNA & protein made

62
Q

When is 5-FU used clinically?

Toxicity effects?

A

Colon cancer & Basal cell carcinoma (topical)

S/E: BM supression, and Photosensitivity. If OD, give thymidine.

63
Q

MOA of Cytarabine?

What diseases is drug used?

A

Inhibit DNA polymerase.

Used in Leukemias and Lymphomas.

64
Q

Alternate name for Cytarabine?

Toxicity of drug?

A

Arabinofuranosyl cytidine

Toxicity: Leukopenia, thrombocytopenia, & megaloblastic anemia.

65
Q

Which drugs are Purine analogs that decrease de novo Purine synthesis. Also, activated by HGPRT?

A

Azathioprine

6-mercaptopurine (6-MP)

6-thioguanin (6-TG)

66
Q

Drugs activated by HGPRT that decrease purine synthesis, what disease do they treat?

Toxicity S/E???? What drug increase this when used in combo?

A

Treat Leukemias.

BM, GI, & liver.
Metabolized by Xanthine oxidase. So enhanced by Allopurinol,

67
Q

What does Dactinomycin (actinomycin D) Tx?

Toxicity?

A

Wilm’s Tumor

Ewing’s sarcoma

Rhabdomyosarcoma

“Children act out”. Drug for childhood tumors.

68
Q

Name Antitumor antibiotics

A

Dactinomycin

Doxorubicin (Adriamycin), daunorubicin

Bleomycin

69
Q

MOA Dactinomycin

A

Intercalates in DNA

70
Q

MOA of Doxorubicin & Daunorubicin

What does it treat?

A

Generates free radicals. Noncovalently intercalate in DNA –> breaks in DNA –> decrease replication

Tx: Solid tumors, leukemias, lymphomas

71
Q

Toxicity of Doxorubicin & Daunorubicin. Which medication can prevent a specific S/E?

A
  • Cardiotoxicity
    • dilated cardiomyopaty
    • Prevent with Dexrazoxane (iron chelator)
  • Myelosuppression (BM)
  • Alopecia
  • toxic to tissues following extravasation- movement of WBCs from capillaries to surrounding tissue
72
Q

MAO of Bleomycin

A

Induces free radicals–> breaks in DNA strand

73
Q

Toxicity of Belomycin

A

Pulmonary fibrosis

skin changes

minimal BM suppresion

74
Q

What does Bleomycin treat?

A

Testicular cancer

Hodgkin’s lymphoma

75
Q

Acute vs Chronic ITP?

A

Acute: kids weeks after vial infection or imunization. Self-lmited, resolves in weeks.

Chronic: Adults, mostly women (child-bearing age). 1o or 2o (SLE); Lupus has Abs to blood cells (WBC, RBC, or PLT). Abs are IgG, can cross placenta and cause short-term thrombocytopenia in baby.

76
Q

What are steps of primary Hemostasis?

A
  1. Transient vasoconstriction of damaged cessel
  2. PLT adhesion to surface of disrupted vessel
  3. PLT degranulation
  4. PLT aggregation
77
Q

What causes vasoconstriction of a damaged vessel pior to PLT adhesion?

A

reflex neural stimulation and endothelin (from endothelial cells)

78
Q

What is source of vWF?

A

Weibel-Palade bodies of endothelial cells & alpha-granules of PLTS

79
Q

PLT adhesion vs aggregation?

A

Adhesion: PLT binding to exposed subendothelial collagen (via vWF & GpIb receptor on PLT)

Aggregation: PLTs binding to PLTs at injury site w/ their GpIIb/IIIa receptor with linker Fibrinogen.

80
Q

Desribe what happens to PLT following adhesion to exposed collagen.

A
  • PLT shape changes
  • PLT degranulation follows. releasing mediators:
    • ADP- binds to ADP-receptor, promotes expression of GpIIb/IIIa receptors on PLT
      • also helps PLT bind to endothelium
    • Ca release (for coagulation cascade)
    • TXA2- calls PLTs to aggregate & decreases blood flow
81
Q

What is soure of TXA2?

What drug can impair it’s production?

A

Made by PLT Cyclooxygenase (COX)

Aspirin irreversibly inactivates COX–> impaired PLT aggregation.

82
Q

What are disorders of Primary Hemostasis?

A
  • Quantitative
    • ITP (Acute vs Chronic)
    • Microangiopathic Hemolytic Anemia
      • TTP
      • HUS
  • Qualitative
    • Bernard-Soulier
    • Glanzmann thrombasthenia
    • Aspirin
    • Uremia
83
Q

ITP Tx?

A

Corticosteoirds-Effective in kids, short-term in adults but they relapse.

IVIG- raises PLT count in symtomatic bleeding, but temporary (gives spleen macrophages alternate target)

Splenectomy removes soure of Abs & PLT descruction

84
Q

What differs in TTP vs HUS for affected body site?

A

TTP more CNS vessel presence.

HUS more of renal vessel presence.

85
Q

Tx for TTP & HUS

A

Plasmapheresis (removes AutoAbs) & corticosteroids (decreases AutoAb production, used in TTP).

86
Q

What causes HUS?

A

Infection in chilren by E. coli O157:H7 dysentery from undercooked beef. Verotoxin from E. coli damages endothelium.

Drugs can also cause HUS.

87
Q

What is ESR test, ad what does it measure?

A

Measures how quickly RBCs will sererate and settle to bottom of test tube. Assesment of Acute Phase reactants in plasma that can cause RBC aggregation.

A measure of disease process, like inflammation or anything that damages cells (make cells heavier, clump and settle faster).

88
Q

When does ESR elevate?

A

Goes up: infections, autoimmune diseases (SLE, RA, temporal arthritis), malignant neoplasms, GI disease (UC), pregnancy.

Auto-Abs increase RBC clumping.

89
Q

When does ESR levels drop?

A

Polycythemia, sickle cell anemia, CHF, microcytosis, hypofibrinogenemia

90
Q

Where does PGI2 & NO come from and what role they have in Thrombosis?

A

From endothelial cells.
They are anti-aggregate factors for PLTs, and increase blood flow.

91
Q

What drug prevents expression of GpIIb/IIIa receptors indirectly? What is MOA?

A

Clopidogrel & Ticlopidine

Irreversibly block ADP-receptor

92
Q

What drug directly targets GpIIb/IIIa?

A

Abciximab

93
Q

Describe components of Iron studies

A
  • Seru iron- Total iron in serum
  • TIBC- total serum Transferrin molecules (bound or unbound)
  • % Saturation- % of transferrin bound to Iron
  • Ferritin- how much iron stored in BM & Liver macrophage
94
Q

Define Anemia.

What are Sx?

A

Reduced RBC mass. Cannot be measured directl,y use Hgb. Hgb <13.5g/dL (men) & <12.5g/dL (women)

  • Weakness, dyspnea
  • headache, lightheaded
  • Paleness
  • Angina (more in CAD)
95
Q

Name Microcytic anemias. What are cells small?

A

Microcytic anemias, cells have extra division to maintain [Hgb]. RBCs lack enough Hgb, so dviide again to paintain “pinkness”

  1. IDA
  2. ACD
  3. Sideroblastic anemia
  4. Thalassemia
96
Q

Where and how is iron absorbed and brought to liver, BM (specifics!). Significance of how Iron stored?

A

Iron abosrbed in duodenum via DMTI transporters.

Enterocytes trasport Iron across cell membrance into blood w/ ferroportin.

Delivered to liver & BM macrophages by Transferrin. Stored itracellularly, bound to ferritin, preventing iron to form free radicals (Fenton rxn).

97
Q

Why can infants and children have low iron?

A

babies: breast-milk low in iron.
children: malabsorbtion

98
Q

What causes low iron in adults (men/women) & elderly (poor and rich), other than malnutrition?

A
  • Adults (20-50yo):
    • men: Pepic ulcer disease
    • women: Menorrhagia
  • Elderly
    • western world: colon polyps, carcinoma
    • poor nations: Ancylostoma duodenale & Nector americanus hookworms
  • ​Gastrectomy
99
Q

Role of stomach acid in Iron absorbtion? What happens to patients with gastrectomy?

A

Keeps iron in Fe2+ state, easier to absorb.

Patent’s who have gastrectomy can have IDA

100
Q

Explain drop in ferritin and effect on TIBC

A

When storage iron depletes, Ferritin, liver responds with increased production in Transferring (TIBC goes up)

101
Q

What are stages for Iron Deficiency Anemia?

A
  1. Ferritin ↓, TIBC ↑
  2. Serum Fe2+ , ↓%sat
  3. Normocytic anemia
  4. Microcytic anemia
102
Q

Blood smear early in IDA vs late IDA

A

Early: Normal RBCs, but less #

Later: Microcytes, hypochromic

103
Q

Clinical symptoms of IDA?

A

Anemia

Koilonychia- spoon nails

Pica- chewing on ice, dirt (trying to get iron)

other anemia Sx: weakness, palor, angina, etc

104
Q

Lab presnetation of IDA?

A
  • ↑RDW (measures spectrum of RBCs. IDA, small and normal cells)
  • ↓Ferritin, ↑TIBC, ↓Serum iron, ↓%sat
  • ↑FEP = free protoporphyrin
105
Q

How do you Tx IDA?

A

First, treat underlying IDA cause (i.e. malnutrition, hookworm, colon polyps,…)

Give Ferrous sulfate supplement

106
Q

Patient has IDA and difficulty swallowing. What do they have? What are other Sx you expect?

A

Plummer-Vinson syndrome

IDA w/ esophageal web & atrophic glossitis. Dysphagia anf beefy-red tongue.

107
Q

MC anemia in hospitalzied patients?

A

Anemia of chronic disease.

associated w/ chronic inflammation (autoimmune, endocarditis, etc), or cancer

108
Q

What causes ACD in body?

A

Chronic disease → APRs from liver

Hepcidin sequesters iron in storage sites by

  1. limiting iron transfer from macrophages to RBC precursors
  2. inhibit EPO

Body thinks inflammation from bacteria, so trying to preent bug access to Iron.

109
Q

What is formula for % saturation?

A

Serum Iron / TIBC

110
Q

Lab presentation of Anemia of Chronic Disease?

How do you treat?

A
  • ↑FEP
  • ↑ferritin, ↓TIBC, ↓serum iron, ↓%sat
  • Tx: fix underlying cause 1st. Then give exogenous EPO in some pts (especially cancer)
111
Q

Location of iron adition to form Heme. Explain serum iron levels in sideroblastic anemia.

A

Iron added to Protoporphyrin in Mitochondria. Lack of this heme precrsor leads to iron buildup in Mitchondria (once there, it remains in mitochondria). W/ time, cells can rupture and iron will increase in serum.

112
Q

What malaria are thalassemia patients protected from?

A

Plasmodium falciparum

113
Q

Describe two gene deletion for alpha-thalassemia

A

mild anemia w/ ↑RBC COUNT

Cis deletion: more severe for inheritance in next gen. More common in Asians.

Trans deletion: Africans, African-Americans

114
Q

Describe 3 gene alpha-thalassemia

A

Mirocytic anemia. Globin defect.

Severe anemia. Beta chains form tatramers, HgbH, which damage RBCs. Also seen on electrophoresis.

115
Q

Are genes mutated, deleted, or both in Alpha and beta Thalassemia? Give details.

A

Alpha: Deletion (4 alpha genes on Ch 16)

Beta: Mutated (point mutation in promoter or splicing sites)

116
Q

Describe 4 gene defect for Alpha-thalassemia

A

Lethal in utero: Hydrops fetalis

gamma chains form tertramer: Hgb Barts, which damage RBCs. Seen on electrophoresis.

117
Q

What infection are beta-thalassemia patients at risk for?

A

Parvovirus B19 infection of RBC precursors

Normal pts have enough precursors that B19 resovles wo major. beta thal precursors limited, and infection can lead to an aplastic crisis.

118
Q

How to treat Beta Thal pts? What are S/E

A

Chronic transfusions. Can cause secondary Hemochromatosis

119
Q

Blood smear in beta-thalassemia patients

A
  • Microcytes, hypochromic
  • Target cells- reduced Hgb → membrane blebbing (think basketball w/ air removed)
  • nRBCs- due to RBC production in abnormal sites..extramedullary hematopoiesis (skull, spleen)
120
Q

Hemolysis cause in Beta Thalassemia

A

Alpha tetramers build up and damage RBCs. Ineffective erythropoiesis & extravascualr hemolysis (spleen remvoes damaged RBCs)

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