Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Hematology And Oncology > Anemias > Flashcards

Anemias Flashcards

1
Q

Macrocytic anemia is divided to

A
  1. Megaloblastic

2. Non-megaloblastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Megaloblastic macrocytic anemias - types

A
  1. B12 deficiency
  2. Folate deficiency
  3. Orotic aciduria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Non-Megaloblastic macrocytic anemias

A
  1. Hypothyroidism
  2. Liver disease
  3. Alcoholism
  4. Reticulocytosis
  5. Diamond-Blackdan anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Normocytic anemia is divided to

A
  1. Nonhemolytic (reticulocytes normal or decreased)

2. Hemolytic (reticulocyte increased)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Nonhemolytic normocytic anemias

A
  1. Anemia of chronic disease (early)
  2. Iron deficiency (early)
  3. Chronic kidney disease
  4. Aplastic anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hemolytic normocytic anemias are divided to

A
  1. Intrinsic

2. Extrinsic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Extrinsic Hemolytic normocytic anemias

A
  1. Autoimmune
  2. Macroangiopathic
  3. Microangiopathic
  4. Infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Causes of iron deficiency

A

Chronic bleeding (gi, menorrhagia)
Malnutrition
Malabsorption
Increased demand (pregnancy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Iron deficiency iron labs

A
  • Decreased iron
  • Decreased ferritin
  • Increase TIBC
  • microcytosis and hypochromasia (central pallor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Iron deficiency symptoms

A
  • Fatigue
  • Conjunctival pallor
  • Spoon nails (koilonychia)
  • Macrocytosis and hypochromia
  • pica (consumption of nonfood substance)
  • Plummer-Vinson syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Plummer-Vinson triad

A
  1. Iron deficiency anemia
  2. Esophageal web
  3. dysphagia
    (also atrophic glossitis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

a Thalassemia: cis vs trans thalassemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

4 allele a deltion

A 
Hb bart (4γ)
Hydrops fetalis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

3 allele a deletion

A

very little α

HbH (4β)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

β-thalassemia mechanism

A

Point mutation in splice sites and promoters–> decreased β-globin synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Β thalassemia minor (heterozygotes) - definition/ mechanism/presentation/diagnosis

A

heterozygote –> β chain is underproduced –> usually asymptomatic
HbA2>3,5% on electrophoresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

HbS/β-thalassemia heterozygote

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Microcytic anemias

A
  1. Iron deficiency (late)
  2. Thalassemias
  3. Anemia of chronic disease (late)
  4. Lead poisoning
  5. Sideroblastic anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Lead inhibits (causing)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Used for lead chelation in kids

A

Succimer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Lead poisoning-first line treatment

A

Dimercaprol, EDTA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Genetic causes of sideroblastic anemia

A

X-linked defect in δ-ALA synthase gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Causes of acquired sideroblastic anemia

A

Myelodysplastic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Causes of reversible sideroblastic anemia

A
  1. Alcohol (MC)
  2. Lead
  3. Vit B6 deficiency
  4. Isoniazid
  5. Copper deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

sideroblastic anemia - labs

A
  • Prussian blue-stained mitochondria (iron) seen in bone morrow (Ringed sideroblasts)
  • basophilic stippling of RBCs in peripheral smear
  • increased iron, normal/low TIBC, increased ferritin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Findings of megaloblastic anemia

A

mechanism: impaired DNA synthesis –> maturation of nucleus of precursor cells in bone marrow delayed relative to maturation of cytoplasm
findings: 1. RBC macrocytosis 2. Hypersegmented neutrophils 3. Glossitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Causes of folate defciency

A
  1. Malnutrition (alcohol)
  2. Malabsorption
  3. Drugs (trimethoprim, phenytoin, methotrexate)
  4. Requirement (hemolytic anemia, pregnancy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Causes of B12 (cobolamin) deficiency

A
  1. Insufficient intake (veganism)
  2. Malabsorption (crohn)
  3. Pernicious anemia
  4. Diphyllobothrium latum
  5. Gastrectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Orotic aciduria pathophysiology

A

Defect in UMP synthesis (orotic acid to UMP, de novo pyrimidine synthesis pathway)
AR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Orotic aciduria symptoms

A
  1. Failure to thrive
  2. Developmental delay
  3. Megaloblastic anemia refractory to folate and B12
    (NO HYPERAMMONIA)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Orotic aciduria treatment/diagnosis

A

UMP (to bypass)

diagnosis: Orotic acid in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Orotic aciduria vs ornithine trancarbamylase

A

Orotic aciduria has no hyperammonemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Anemia of chronic disease pathophysiology

A

Inflammation–> increases hepsidin –> binds ferroportin (on intestinal mucosal and macrophages) inhibiting iron trnasport–> decreases the releasing of iron from macrophages and decrease absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Anemia of chronic disease - associated conditions/treatment

A
  1. RA 2. SLE 3. Neoplasia 4. Chronic kidney disease
    treatment: EPO in chronic kidney
42
Q

Anemia of chronic disease iron status / type of anemia

A

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

43
Q

Aplastic anemia is caused by

A

Failure or destruction of myeloid stem cells

44
Q

Causes of aplastic anemia

A
  1. Radiation 2. Drugs (benzene, chloramphenicol, alkylating agents) 3. Viral agents (parvovirus B19, EBV, HIV, HCV)
  2. Fanconi anemia (DNA repair defect) 5. Idiopathic (immune mediate, 1ry stem cell defect)-may follow acute hepatitis
45
Q

Aplastic anemia-bone marrow appearance

A 
Hypocellular
Fatty infiltration  (Dry bone marrow tap)
46
Q

Aplastic anemia symptoms and findings

A

Fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infections
Pancytopenia (severe anemia, leukopenia, thrombocytopenia) –> but normal cell morphology

47
Q

Aplastic anemia treatment

A
  1. Withdrawal of offending agent
  2. Immunosuppressive regimens (antithymocyte globulin, cyclosporine)
  3. Bone marrow allograft
  4. RBC/platelets transfusion
  5. Bone marrow stimulation (eg. GM-CSF)
48
Q

Hereditary spherocytosis - due to defect in

A

proteins interacting iwth RBC membrane skeleton and plasma membrane

  1. Ankyrin
  2. Band 3
  3. Protein 4.2
  4. Spectrin
49
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
50
Q

Hereditary spherocytosis treatment/intravascular vs extravascular/susceptible for

A
  • Splenectomy (causes splenomegaly)
  • extravascular hemolysis
  • susceptible for B19
51
Q

Most common enzymatic deficiency of RBCs

52
Q

G6PD location of hemolysis / mechanism

A

Intravascular AND extravascular

defect in G6PD –> low glutathione –> high RBCs susceptibility to oxidant stress

53
Q

G6PD deficiency - hemolytic anemia following

A
  1. Sulfa drugs
  2. Antimalarias
  3. Infections
  4. Fava beans
54
Q

G6PD deficiency symptoms, beside anemia

A

BACK PAIN

HEMOGLOBINURIA (few days after oxidant stress)

55
Q

Pyruvate deficiency anemia - presentation

A

Hemolytic anemia in a newborn

56
Q

Pyruvate deficiency anemia pathophysiology

A

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

57
Q

HBC pathophysiology

A

Lysine instead of glutamic acid in β globin

58
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

59
Q

paroxysmal nocturnal hemoglobinuria increases the incidence of

A

ACUTE LEUKEMIAS

60
Q

paroxysmal nocturnal hemoglobinuria triad

A
  1. Coombs hemolytic anemia
  2. Pancytopenia
  3. Venous thrombosis
61
Q

paroxysmal nocturnal hemoglobinuria flow cytometry

A

CD 55/59 ( - )RBCs

62
Q

paroxysmal nocturnal hemoglobinuria treatment

A

Eculizumab (terminal complement inhibitor)

63
Q

Sickle cell anemia mutation / intravascular vs extravascular hemolysis

A

Valine instead of Glutamic acid

intravascular + extravascular

64
Q

Sickle cell x ray

A

Crew cut on skull (marrow expansion)

65
Q

Sickle cell complications

A
  1. Aplastic crisis (parvovirus B19)
  2. Autosplenectomy (howell-jolly bodies)
  3. Splenic infract/sequestration
  4. Salmonella osteomyelitis
  5. Renal papillary necrosis (low PO2 in papilla) –> microhematuria (medullary infracts)
  6. Painful crisis (vaso-occlusive): dactylitis (painful swelling of hands/feets), acute chest syndrome, avascular necrosis, stroke. priapism
66
Q

Sickle cell anemia diagnosis and treatment

A

Diagnosis: Hb electrophoresis
Treatment: hydroxyurea, hydration

67
Q

Hemolytic anemia-infections (mechanism)

A

Malaria and Babesia

increased destruction of RBCs

68
Q

Causes of Macroangiopathic anemia

A

Prosthetic heart valce and Aortic stenosis –> mechanical destruction

69
Q

Causes of microangiopathic anemia

A

DIC, SLE, MALIGNANT HYPERTENSION, TTP/HUS

70
Q

Pregnancy (ocp use) - iron status

A

Increases the Transferin/TIBC

Decrease the transferin saturation

71
Q

Autoimmune hemolytic anemia types

A

Warm (IgG)

Cold (IgM and complement)

72
Q

Causes of Warm agglutinin

A
  1. SLE
  2. CLL
  3. Drugs (methyldopa)
  4. Idiopathic
    - -> chronic anemia
73
Q

Causes of Cold agglutinin

A
  1. CLL
  2. Mycoplasma pneumonia
  3. Infectious mononucleosis
  4. Idiopathic
    - -> acute anemia
74
Q

Megaloblastic anemia mechanism

A

Impaired DNA synthesis –> maturation of nucleus of precursor cells i. Bone marrow delayed relative to maturation in cytoplasm

75
Q

B12 deficiency –> mechanism of neurological symptoms

A

Involvement of B12 in fatty acid pathway and myelin synthesis

76
Q

thalassemia-a - 2 allele vs 1 allele deletion

A

2 –> less clinically severe anemia

1 –> no anemia (clinically silent)

77
Q

β-thalassemia - prevalent in

A

Mediterranean populations

78
Q

risk of Lead exposure is increased in

A

old houses with chipped paint

79
Q

sideroblastic anemia - treatment

A

B6, cofactor for δ-ALA synthase

80
Q

how to predict simple the type of anemia (macro vs micro vs normocytic)

A

on peripheral blood smear, a lymphocyte nucleus is approximately the same size as a normocytic RBC:
if RBC larger than lymphocyte nucleus, consider macrocytosis. If smaller, microcytosis

81
Q

B12 deficiency - historically is diagnosed with (explain)

A

Schilling test, a 4-stage test that determines if the cause is dietary insufficiency vs malabsorption
(WITH RADIOLABELED B12)

82
Q

Non-Megaloblastic macrocytic anemias - mechanism / neutrophils

A
  • DNA synthesis is unimpaired

- not hypersegmented

83
Q

Diamond-Blackfan anemia - description

A

Rapid-onset anemia within 1st year of life due to intrinsic defect in erythroid progenitor cells

84
Q

Diamond-Blackfan anemia - lab

A

increased % of HbF (but low total Hb)

85
Q

Diamond-Blackfan anemia - presentation

A
  1. short stature
  2. craniofacial abnormalities
  3. upper extremity malformations (triphalangeal thumbs) in up to 50% of cases
86
Q

drugs that causes aplastic anemia

A
  1. benzene
  2. chloramphenicol
  3. alkylating agents
87
Q

aplastic anemia - EPO?

88
Q

HbSC - presentation

A

milder thatn HbSS patients

89
Q

HbC - homozygotes - blood smear

A

hemoglobin crystals within RBCs and target cells

90
Q

Heterozygoges of SC anemia - advantage

A

resistance to malaria

91
Q

prevelance of sickle cell in African american

A

8% carry an HbS allele

92
Q

RBC agglutination with cold exposure - presentation

A

acute anemia

painful, blue fingers and toes with cold exposure

93
Q

Autoimmune anemia are usually Coombs ..?

94
Q

Direct Coombs test - mechanism

A

anti-Ig antibody (Coombs reagent added to patient’s blood –> RBCs agglutinate if are coated with Ig

95
Q

Indirect Coombs test - mechanism

A

normal RBCs added to patient serum –> if serum has anti RBC surface Ig, RBCs agglutinate whtn Coombs reagent added

96
Q

The hemolytic anemias are divided according to

A
  1. the cause of hemolysis (intrinsic vs extrinsic to the RBC)
  2. the location of the hemolysis (intra vs extravascular)
97
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
98
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
99
Q

Fanconi anemia - mechanism of action

A

DNA repair defect causing bone marrow failure

100
Q

Fanconi anemia - presentation

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

Hematology And Oncology (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions