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Hematology And Oncology > FA + MTB > Flashcards

FA + MTB Flashcards

1
Q

site of B cells in periphery

A
  1. follicles of Lymph node
  2. white pulp of spleen
  3. unencapsulated lymphoid tissue
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2
Q

fetal erythropoiesis

A
  1. yolk sac: 3-8 weeks
  2. liver: 6 weeks - birth
  3. spleen: 10-28 weeks
  4. Bone marrow: 18 weeks - adult
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3
Q

from fastests to slowest Hb (FROM (-) to (+))

A

A - F - S - C

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4
Q

extrinsic pathway (tissue factor pathway) - factors

A

7 –> 10

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5
Q

coagulation intrinsic pathway - factors (contact pathway)

A

12 –> 11 –> 9 (and then combined)

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6
Q

coagulation cascade - combined pathway

A

X –> Xa
Xa + Va –> prothrombin to thrombin
thrombin –> fibrinogen to fibrin and XIII to XIIIa
–> aggegation of fibrin + Ca2+ + XIIIa –> firin mesh stabilizes platelet plug

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7
Q

thrombin actions

A
  • fibrinogen to fibrin monomers
  • XIII –> XIIIa
  • V –> Va
  • VIII –> VIIIa
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8
Q

Coagulation steps that require calcium and phospholipids

A

Around activated 10

Around activated 7

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9
Q

Factor Xa inhibitors anticoagulants

A
  1. LMWH (greatest efficacy)
  2. Heparin
  3. Direct Xa inhibitors (apixaban, rivaroxaba)
  4. Fondaparinux
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10
Q

Thrombin inhibitors (anticoagulants)

A
  1. Heparin (greatest efficacy)
  2. LMWH (delteparin, enoxaparin)
  3. Direct thrombin inhibitors (argatroban, bivalirudin, dagigatran)
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11
Q

role of vitamin K in procoagulation

A

oxidized vit K –> reduced K (epoxide reductase)

–> act as a cofactor of γ-glutamyl trasnferase to 2, 7, 9, 10, C, S maturation

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12
Q

Pr C to activated Pr C (inactivates …)

A

Thrombin- trombomodulin complex (endothelial cells)

inactivates 5+8

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13
Q

Heparin enhances the activity of

A

Antithrombin

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14
Q

Principles targets of antithrombin

A

Thrombin and factor Xa

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15
Q

Ristocetin - mechanism of action

A

Activates vwf to bind GpIb

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16
Q

Basophilic stippling RBCs - seen in

A
  1. Lead poisoning
  2. sideroblastic anema
  3. Myelodisplastic syndromes
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17
Q

Acanthocytes RBCs - seen in

A
  1. liver disease

2. abetalipoproteinemia (states of cholesterol dysregulation)

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18
Q

Acanthocytes RBCs - also called

A

spur cell

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19
Q

Target RBCs - seen in

A
  1. HbC disease 2. asplenia

3. Liver disease 4. Thalassemia

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20
Q

Echinocytes - seen in

A
  1. end-stage renal disease
  2. liver disease
  3. pyruvate kinase
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21
Q

Echinocytes vs acanthocytes according to image

A

Echinocytes projection are more uniform and smaller

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22
Q

Heinz bodies - seen in

A
  1. G6PD deficiency

2. Heinz body - like inclusions in α-thalassemia

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23
Q

Heinz bodies - mechanism

A

Oxidation of HB-SH groups to S-S –> Hb precipitation (Heinz bodies) –> phagocytic damage to RBC membrane –> bite cells

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24
Q

Howell-Jolly bodies - seen in

A
  1. asplenia

2. functional hyposplenia

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25
Q

ringed sideroblasts cells vs basophilc cells regarding area

A

basoph: peripheral smear
siderob: BM

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26
Q

Non-Megaloblastic macrocytic anemias

A
  1. Hypothyroidism
  2. Liver disease
  3. Alcoholism
  4. Reticulocytosis
  5. Diamond-Blackdan anemia
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27
Q

Nonhemolytic normocytic anemias

A
  1. Anemia of chronic disease (early)
  2. Iron deficiency (early)
  3. Chronic kidney disease
  4. Aplastic anemia
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28
Q

Extrinsic Hemolytic normocytic anemias

A
  1. Autoimmune
  2. Macroangiopathic
  3. Microangiopathic
  4. Infections
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29
Q

Intrinsic Hemolytic normocytic anemias

A
  1. RBC membrane defects (hereditary spherocytosis)
  2. RBC enzymes deficiency (G6PD, pyruvate kinase)
  3. HBC defects
  4. Paroxysmal nocturnal hemlglobinuria
  5. Sickle cell anemia
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30
Q

another cause of megalobastic anemia

A

fanconi

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31
Q

Iron deficiency iron labs

A
  • Decreased iron
  • Decreased ferritin
  • Increase TIBC
  • microcytosis and hypochromasia (central pallor)
  • INCREASED ERYTHRO PROTOPORPHYRIN
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32
Q

Plummer-Vinson triad

A
  1. Iron deficiency anemia
  2. Esophageal web
  3. dysphagia
    (also atrophic glossitis)
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33
Q

a Thalassemia: cis vs trans thalassemia

A

Cis: Asia, -/- a/a (same chromosome)
Trans: Africa, a/- a/- (separate chormosomes)

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34
Q

3 allele a deletion

A

very little α

HbH (4β)

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35
Q

4 allele a deltion

A 
Hb bart (4γ)
Hydrops fetalis
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36
Q

Major β-thalassemia major - presentation (besides anemia) and mechanism (when starts)

A
  1. marrow expansion –> skeleta deformities (Crew cut on skull x ray) + chipmunk facies
  2. extramedullary hematopoiesis –> hepatosplenomegaly
    Until 6 months is asymptomatic (HbF)
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37
Q

Major β-thalassemia major - definition/lab/treatment

A

homozygote –> β chain is absent
severe microcytic, hypochromic anemia with target cells and increased anisopoikilocytosis, high HbF
treatment: blood transfusion (2ry hemochromatosis)

38
Q

HbS/β-thalassemia heterozygote

A

Mild to moderate sickle cell anemia depending on amount of β-globin production

39
Q

Microcytic anemias

A
  1. Iron deficiency (late)
  2. Thalassemias
  3. Anemia of chronic disease (late)
  4. Lead poisoning
  5. Sideroblastic anemia
40
Q

Lead inhibits (causing)

A

Ferrochelatase and ALA dehydratase –> decreases heme and increase protoporphyrin
rRNA degradation –> rRNA aggregation –> basophilic stippling

41
Q

Lead poisoning symptoms and signs

A
  1. Burton lines
  2. Metaphysis lines on x ray
  3. Encephalopathy
  4. Erythrocyte basophilic stippling
  5. Siderblastic anemia
  6. ABDOMINAL COLIC
  7. Drops of wrist and foot
  8. KIDNEY DISEASE
42
Q

Lead poisoning-first line treatment

A

Sideroblastic anemia types of causes (and causes)

43
Q

Sideroblastic anemia types of causes (and causes)

A
  1. Genetic –> X-linked defect in δ-ALA synthase gene
  2. acquired –> Myelodysplastic syndrome
  3. reversible –> Alcohol (MC), Lead, Vit B6 deficiency, Isoniazid, Copper deficiency, chloramphenicol)
44
Q

sideroblastic anemia - treatment

A

B6, cofactor for δ-ALA synthase

45
Q

Findings of megaloblastic anemia

A
  1. RBC macrocytosis 2. Hypersegmented neutrophils 3. Glossitis
46
Q

Folate deficiency vs b12 deficiency according to methylmalonic acid, homocystein, and neurologic symptoms

A
  1. Methylmalonic acid (increased only in B12)
  2. Neurologic symptoms (only in B12)
  3. Homocysteine (increased in Both)
47
Q

Neurologic symptoms of B12 deficiency (and why)

A

Sabacute combined degeneration due to its involvement in fatty acid pathays and myelin synthesis:

  1. Spinocerebellar tract
  2. Lateral corticospinal tract
  3. Dorsal column dysfunction
48
Q

Orotic aciduria symptoms

A
  1. Failure to thrive
  2. Developmental delay
  3. Megaloblastic anemia refractory to folate and B12
    (NO HYPERAMMONIA)
49
Q

Orotic aciduria treatment/diagnosis

A

UMP (to bypass)

diagnosis: Orotic acid in urine

50
Q

Anemia of chronic disease iron status / type of anemia

A

Decreased iron
Decreased TIBC
Increased ferritin
–> Normocytic, but can become microcytic

51
Q

Hereditary spherocytosis - due to defect in

A

proteins interacting with RBC membrane skeleton and plasma membrane

  1. Ankyrin
  2. Band 3
  3. Protein 4.2
  4. Spectrin
52
Q

Hereditary spherocytosis labs

A
  1. Osmotic fragility test (+)
  2. Normal to decreased MCV with abudance of cells
  3. Increased RDW
  4. Increased MCHC (no central pallor)
  5. round RBCs with less surface area
53
Q

Hereditary spherocytosis treatment/intravascular vs extravascular/susceptible for

A
  • Splenectomy (causes splenomegaly)
  • extravascular hemolysis
  • susceptible for B19
54
Q

G6PD deficiency - hemolytic anemia following

A
  1. Sulfa drugs
  2. Antimalarias
  3. Infections
  4. Fava beans
55
Q

Pyruvate deficiency anemia pathophysiology

A

AR. Decreased ATP–> rigid RBCs –> extravascular hemolysis

56
Q

HBC pathophysiology

A

Lysine instead of glutamic acid in β globin

57
Q

Starting event of paroxysmal nocturnal hemoglobinuria / mechanism

A

Acquired mutation in hematopoietic stem cell –> impaired synsthesis of for GPI anchor for decay-accelerating factor that protects RBCs from complement –> increased C-mediated intravascular RBCs lysis

58
Q

paroxysmal nocturnal hemoglobinuria increases the incidence of

A

ACUTE LEUKEMIAS

59
Q

paroxysmal nocturnal hemoglobinuria triad

A
  1. Coombs hemolytic anemia
  2. Pancytopenia
  3. Venous thrombosis
60
Q

paroxysmal nocturnal hemoglobinuria flow cytometry

A

CD 55/59 ( - )RBCs

61
Q

paroxysmal nocturnal hemoglobinuria treatment

A

Eculizumab (terminal complement inhibitor)

62
Q

Sickle cell anemia mutation / intravascular vs extravascular hemolysis

A

Valine instead of Glutamic acid

intravascular + extravascular

63
Q

Sickle cell anemia diagnosis and treatment

A

Diagnosis: Hb electrophoresis
Treatment: hydroxyurea, hydration

64
Q

Pregnancy (ocp use) - iron status

A

Increases the Transferin/TIBC

Decrease the transferin saturation

65
Q

Autoimmune hemolytic anemia types

A

Warm (IgG)

Cold (IgM and complement)

66
Q

Causes of Warm agglutinin

A
  1. SLE
  2. CLL
  3. Drugs (methyldopa)
  4. Idiopathic
    - -> chronic anemia
67
Q

Causes of Cold agglutinin

A
  1. CLL
  2. Mycoplasma pneumonia
  3. Infectious mononucleosis
  4. Idiopathic
    - -> acute anemia
68
Q

Diamond-Blackfan anemia - description

A

Rapid-onset anemia within 1st year of life due to intrinsic defect in erythroid progenitor cells
increased % of HbF (but low total Hb)

69
Q

Diamond-Blackfan anemia - presentation

A
  1. short stature
  2. craniofacial abnormalities
  3. upper extremity malformations (triphalangeal thumbs) in up to 50% of cases
70
Q

HbC - homozygotes - blood smear

A

hemoglobin crystals within RBCs and target cells

71
Q

RBC agglutination with cold exposure - presentation

A

acute anemia

painful, blue fingers and toes with cold exposure

72
Q

extravascular hemolytic anemia - findings

A
  1. Spherocytes in peripheral smear
  2. high LDH
  3. no hemoglobinuria/hemosiderinuria
  4. increased UCB (–> jaundice)
  5. urobilinogen in urine
73
Q

intravascular hemolytic anemia - findings

A
  1. low haptoglobin
  2. high LDH
  3. schistocytes
  4. high reticulocytes
  5. hemoglobinuria
  6. hemosiderinuria
  7. urobilinogen in urine
  8. increased UCB
74
Q

Fanconi anemia - mechanism of action

A

DNA repair defect causing bone marrow failure

75
Q

Fanconi anemia - presentation

A
  1. Aplastic anemia
  2. Increased incidence of tumor/leukemia
  3. Cafe au lait spots
  4. Thumb/radial defects
76
Q

iron studies in iron deficiency anemia

A
  • serum iron: low
  • TIBC: high
  • Ferritin: low
  • iron/TIBC sat: low
77
Q

iron studies in hemochromatosis

A
  • serum iron: high
  • TIBC: low
  • Ferritin: high
  • iron/TIBC sat: high
78
Q

iron studies in Chronic disease

A
  • serum iron: low
  • TIBC: low
  • Ferritin: high
  • iron/TIBC sat: normal
79
Q

iron studies in pregnancy/OCP

A
  • serum iron: normal
  • TIBC: increased
  • Ferritin: normal
  • iron/TIBC sat: decreased
80
Q

neutropenia - cell count

A

less than 1500 cells/mm3

81
Q

lymphopenia - cell count

A

lymphocytes less than 1500 (3000 in children)

82
Q

eosinopenia - cell count / causes

A

less than 30 cells/mm3
Cushing syndrome
corticosteroinds

83
Q

Lead poisoning - enzyme affected (and where)

A
  1. Ferrochelatase (mit)

2. ALA dehydratase (cytoplasm)

84
Q

Lead poisoning - way of exposure and neurological symptoms (children and adults)

A

Children –> exposure to lead paint –> mental deterioration
Adults –> environmental exposure (batteries ammunition) –> headache, memory loss, demyelination

85
Q

Acute intermittent porhyria symptoms

A

mnemonic - 5 Ps

  1. Painful abdomen
  2. Port wine - colored urine
  3. Polyneuropathy
  4. Psychological disturbances
  5. Precipitated by drugs (P450 inducers) Alcohol, starvation
86
Q

Acute intermittent porhyria affected enzyme

A

Porphobilinogen deaminase

87
Q

Acute intermittent porhyria is precipitated by

A
  1. Drugs (cytochromic P-450 inducers)
  2. Alcohol
  3. Starvation
88
Q

Acute intermittent porhyria treatment

A

Glucose and heme (inhibit ALA synthase)

89
Q

Porphyria cutanea tarda affected enzyme

A

Uroporphyrinogen decarboxylase

90
Q

Porphyria cutanea tarda - presenting symptoms / assocaited with

A

Blistering cutaneous photosensitivity
HCV
exacerbated with alcohol

91
Q

MC porphyria

A

Porphyria cutanea tarda

Hematology And Oncology (21 decks)

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