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USMLE 1 > Hematology and oncology- Phatology > Flashcards

Hematology and oncology- Phatology Flashcards

1
Q

Acanthocytes (“spur cells”)

A

Liver disease, abetalipoproteinemia (states of cholesterol dysregulation).

Acantho = spiny

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2
Q

Basophilic stippling

A

Sideroblastic anemias (eg, lead poisoning, myelodysplastic syndromes), thalassemias.

*Seen primarily in peripheral smear, vs ringed sideroblasts seen in bone marrow.

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3
Q

Dacrocytes (“teardrop cells”)

A

Bone marrow infiltration (eg, myelofibrosis), thalassemias.

RBC “sheds a tear” because it’s mechanically squeezed out of its home in the bone marrow.

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4
Q

Degmacytes (“bite cells”)

A

G6PD deficiency.

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5
Q

Echinocytes (“burr cells”)

A

End-stage renal disease, liver disease, pyruvate kinase

deficiency.

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6
Q

Elliptocytes

A

Hereditary elliptocytosis (espectrin), usually asymptomatic

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7
Q

Macro-ovalocytes

A

Megaloblastic anemia (also hypersegmented PMNs)

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8
Q

Ringed sideroblasts

A

Sideroblastic anemia. Excess iron in mitochondria.

Seen in bone marrow with special staining (Prussian blue),

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9
Q

Schistocytes

A

Microangiopathic hemolytic anemias, including DIC, TTP/HUS, HELLP syndrome, mechanical hemolysis

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10
Q

Sickle cells

A

Sickle cell anemia.

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11
Q

Spherocytes

A

Hereditary spherocytosis, drug- and infection-induced hemolytic anemia.

Small, spherical cells without central pallor.

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12
Q

Target cells

A

“HALT,”

HbC disease, Asplenia, Liver disease, Thalassemia.

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13
Q

Heinz bodies

A

Seen in G6PD deficiency.

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14
Q

Howell-Jolly bodies

A

Seen in patients with functional hyposplenia or asplenia.

Basophilic nuclear remnants found in RBCs

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15
Q

Anemias Algorithm

A

Pag. 406

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16
Q

Iron deficiency anemia

  • Labs
  • Symptoms
A

Labs: Low iron, HighTIBC, Low ferritin, High free erythrocyte protoporphyrin, High RDW. Microcytosis and hypochromasia (central pallor).

Symptoms: fatigue, conjunctival pallor, pica, spoon nails
(koilonychia). May manifest as glossitis, cheilosis.

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17
Q

α-thalassemia

  • α-thalassemia minima
  • α-thalassemia minor
A

(α α/α –). No anemia (silent carrier)

(α –/α –; trans) or (α α/– –; cis). Mild microcytic, hypochromic anemia

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18
Q

α-thalassemia

  • Hemoglobin H disease (HbH); β4
  • Hemoglobin Barts disease (Hb Barts); γ4
A

(– –/– α). Moderate to severe microcytic hypochromic anemia.

(– –/– –). Hydrops fetalis; incompatible with life

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19
Q

β-thalassemia

  • β-thalassemia minor (heterozygote)
  • HbS/β-thalassemia heterozygote
A

β chain is underproduced. Usually asymptomatic. Diagnosis confirmed by HbA2 (> 3.5%) on electrophoresis.

mild to moderate sickle cell disease depending on amount of β-globin production.

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20
Q

β-thalassemia

- β-thalassemia major (homozygote)

A

severe microcytic, hypochromic ,anemia with target cells and increased anisopoikilocytosis requiring blood transfusion (2° hemochromatosis).

skeletal deformities. “Chipmunk” facies. hepatosplenomegaly. risk of parvovirus B19–induced aplastic crisis. 

HbF (α2γ2), HbA2 (α2δ2).

21
Q

Lead poisoning

  • Mechanism
  • Clinical features
  • Treatment
A

Lead inhibits ferrochelatase and ALA dehydratase.

“LEAD”

  • Lead Lines on gingivae (Burton lines) and on metaphyses of long bones on x-ray.
  • Encephalopathy and Erythrocyte basophilic stippling.
  • Abdominal colic and sideroblastic Anemia.
  • Drops—wrist and foot drop.

Dimercaprol and EDTA are 1st line of treatment. Succimer used for chelation for kids

22
Q

Sideroblastic anemia

  • Etiology
  • Labs
  • Treatment
A

Genetic (eg, X-linked defect in ALA synthase gene), acquired (myelodysplastic syndromes), and reversible (alcohol is most common).

High iron, normal/Low TIBC, High ferritin. Ringed sideroblasts. basophilic stippling.

Treatment: pyridoxine (B6, cofactor for ALA synthase).

23
Q

Megaloblastic anemia

  • Mechanism
  • Cell morphology
  • Etiology
A

Impaired DNA synthesis. delayed relative to maturation of cytoplasm.

RBC macrocytosis, hypersegmented neutrophils, glossitis.

  • Folate deficiency, Vitamin B12 (cobalamin) deficiency, Orotic aciduria
24
Q

Folate deficiency

  • Etiology
  • Labs
A

Causes: malnutrition, malabsorption, drugs (eg, methotrexate, trimethoprim, phenytoin),  requirement (eg, hemolytic anemia, pregnancy).

High homocysteine, normal methylmalonic acid.

*No neurologic symptoms

25
Q

Vitamin B12 (cobalamin) deficiency

A

Causes: pernicious anemia, malabsorption, gastrectomy, insufficient intake, Diphyllobothrium latum (fish tapeworm).

High homocysteine, Highmethylmalonic acid.

*Neurologic symptoms. Historically diagnosed with the Schilling test.

26
Q

Orotic aciduria

  • Phatogeny
  • Diagnosis
A

Inability to convert orotic acid to UMP (de novo pyrimidine synthesis pathway) because of defect in UMP synthase. AR

Orotic acid in urine.

27
Q

Orotic aciduria

  • Clinical presentation
  • Treatment
A

Presents in children as failure to thrive, developmental delay, and megaloblastic anemia refractory to folate
and B12.

Treatment: uridine monophosphate or uridine
triacetate to bypass mutated enzyme.

28
Q

Diamond-Blackfan anemia

  • Etiology
  • Labs
  • Clinical features
A

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

High% HbF (but total Hb).

Short stature, craniofacial abnormalities, and upper extremity malformations (triphalangeal thumbs) in up to 50% of cases.

29
Q

Intravascular hemolysis

  • Findings
  • Etiology
A

Low haptoglobin, schistocytes on blood smear. Characteristic hemoglobinuria, hemosiderinuria, and urobilinogen in urine.

Notable causes are mechanical hemolysis (eg, prosthetic valve), paroxysmal nocturnal hemoglobinuria,
microangiopathic hemolytic anemias.

30
Q

Extravascular hemolysis

- Findings

A

Findings: macrophages in spleen clear RBCs. Spherocytes in peripheral smear, no hemoglobinuria/
hemosiderinuria. Can present with urobilinogen in urine

31
Q

Anemia of chronic disease

  • Etiophatogeny
  • Labs
  • RBC morphology
A

Inflammation, high hepcidin.

Low iron, Low TIBC, High ferritin.

Normocytic, but can become microcytic.

32
Q

Aplastic anemia

- Etiologies

A
  • Radiation and drugs (eg, benzene, chloramphenicol, alkylating agents, antimetabolites).
  • Viral agents (EBV, HIV, hepatitis viruses)
  • Fanconi anemia; also short stature, incidence of
    tumors/leukemia, café-au-lait spots, thumb/radial defects.
  • Idiopathic (immune mediated, 1° stem cell defect); may follow acute hepatitis
33
Q

Aplastic anemia

  • Labs
  • Morphology
A

Pancytopenia characterized by anemia, leukopenia, and thrombocytopenia.

Normal cell morphology, but hypocellular bone marrow with fatty infiltration

34
Q

Hereditary spherocytosis

  • Etiology
  • Clinical features
  • Labs
  • Treatment
A

Defects RBC membrane (eg, ankyrin, band 3, protein 4.2, spectrin). AD

Splenomegaly, aplastic crisis (parvovirus B19 infection).

Labs: fragility in osmotic fragility test. Normal to MCV with abundance of cells.

Treatment: splenectomy.

35
Q

G6PD deficiency

  • Etiology
  • Findings
A

Most common enzymatic disorder of RBCs. XR

Hemolytic anemia following oxidant stress (eg, sulfa drugs, antimalarials, infections, fava beans).

Back pain, hemoglobinuria a few days after oxidant stress.

36
Q

Pyruvate kinase deficiency

  • Hereditance
  • Clinical presentation
A

AR.

Increases levels of 2,3-BPG. Hemolytic anemia in a newborn

37
Q

Paroxysmal nocturnal hemoglobinuria

  • Etiology
  • Clinical presentation
  • Labs
  • Treatment
A

intravascular RBC lysis. acquired mutation in PIGA gene, with impaired GPI and decay of CD55 and CD59.

Triad: Coombs ⊝ hemolytic anemia, pancytopenia, venous thrombosis. Patients may report red or pink urine.

Labs: CD55/59 ⊝ RBCs on flow cytometry.

Treatment: eculizumab (inhibits terminal complement formation).

38
Q

Sickle cell anemia

  • Etiology
  • Presipitants
A

HbS point mutation causes a single amino acid replacement in β chain (substitution of glutamic acid with valine).

low O2, high altitude, or acidosis precipitates sickling anemia, vaso-occlusive disease. “Crew cut” on skull x-ray due to marrow expansion from  erythropoiesis (also seen in thalassemias).

8% of African Americans carry an HbS allele.

39
Q

Sickle cell anemia

- Complications

A
  • Aplastic crisis (due to parvovirus B19).
  • Autosplenectomy
  • Splenic infarct/sequestration crisis.
  • Salmonella osteomyelitis.
  • Painful crises (vaso-occlusive): dactylitis, priapism, acute chest syndrome, avascular necrosis, stroke.
  • Sickling in renal medulla (low Po2), renal papillary necrosis, microhematuria.
40
Q

Sickle cell anemia

  • Diagnosis
  • Treatment
A

hemoglobin electrophoresis.

hydroxyurea ( HbF), hydration.

41
Q

HbC disease

  • Etiology
  • Cells morphology
A

Glutamic acid–to-lyCine (lysine) mutation in β-globin. Causes extravascular hemolysis.

Blood smear in homozygotes: hemoglobin Crystals inside RBCs, target cells.

42
Q

Autoimmune hemolytic anemia

- Types

A

Warm (IgG)—chronic anemia seen in SLE and CLL and with certain drugs (eg, α-methyldopa).

Cold (IgM and complement)—acute anemia triggered by cold; seen in CLL, Mycoplasma pneumoniae infections, and infectious Mononucleosis.

43
Q

Autoimmune hemolytic anemia

- Diagnosis

A

Autoimmune hemolytic anemias are usually Coombs ⊕.

Direct Coombs test—anti-Ig antibody (Coombs reagent) added to patient’s RBCs.

Indirect Coombs test—normal RBCs added to patient’s serum.

44
Q

Microangiopathic anemia

- Etiologies

A

DIC, TTP/HUS, SLE, HELLP syndrome, hypertensive emergency.

45
Q

Neutropenia

A

Absolute neutrophil count < 1500 cells/mm3

Severe infections typical when < 500 cells/mm3

46
Q

Lymphopenia

A

Absolute lymphocyte count < 1500 cells/mm3 (

47
Q

Eosinopenia

A

Absolute eosinophil count < 30 cells/mm3

48
Q

Anormalities on Lymphoid cells caused by Corticosteroids

A

Corticosteroids cause neutrophilia, despite causing eosinopenia and lymphopenia.

49
Q

Left shift

A

Increase neutrophil precursors.

Called leukoerythroblastic reaction when left shift is
seen with immature RBCs. Occurs with severe anemia or marrow response.

USMLE 1 (73 decks)

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