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USMLE 1 > Hematology and oncology- Anatomy and physioogy > Flashcards

Hematology and oncology- Anatomy and physioogy Flashcards

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USMLE® Step 1 flashcards
1
Q

Erythrocytes

  • Life span
  • Source of energy
  • Anisocytosis and poikilocytosis
  • Polychormasia
A

Life span of 120 days. Source of energy is glucose (90% used in glycolysis, 10% used in HMP shunt).

Membranes contain Cl−/HCO3 antiporter

Anisocytosis = varying sizes.
Poikilocytosis = varying shapes

Bluish color (polychromasia) on Wright-Giemsa stain of reticulocytes represents residual ribosomal RNA.

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2
Q

Thrombocytes (platelets)

  • Life span and amount stored in spleen
  • Dense and alfa granules
  • vWF and Fibrinogen receptors
A

Life span of 8–10 days. 1⁄3 of platelet pool is stored in the spleen.

Dense granules (ADP, Ca2+) and α granules (vWF, fibrinogen, fibronectin).

VWF receptor: GpIb.
Fibrinogen receptor: GpIIb/IIIa.

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3
Q

Leukocytes

- WBC differential count

A 
WBC differential count from highest to lowest
(normal ranges per USMLE):
Neutrophils (~ 60%)
Lymphocytes (~ 30%)
Monocytes (~ 6%)
Eosinophils (~ 3%)
Basophils (~ 1%)
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4
Q

Neutrophils

  • Hypersegmented
  • Band cells
  • Chemotactic agents
A 
Hypersegmented neutrophils (nucleus has 6+
lobes) are seen in vitamin B12/ folate deficiency.

band cells (immature neutrophils) reflect states of myeloid proliferation (bacterial infections, CML)

Important neutrophil chemotactic agents: C5a,
IL-8, LTB4, kallikrein, platelet-activating factor.

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5
Q

Monocytes

- Morphology

A

Large, kidney-shaped nucleus. Extensive “frosted glass” cytoplasm.

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6
Q

Macrophages

  • Activated by
  • Lipid A
A

γ-interferon. Can function as antigen-presenting cell via MHC II.

Lipid A from bacterial LPS binds CD14 on macrophages to initiate septic shock.

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7
Q

Eosinophils (*Bilobate nucleus)

- Causes of eosinophilia

A 
PACCMAN:
Parasites
Asthma
Churg-Strauss syndrome
Chronic adrenal insufficiency
Myeloproliferative disorders
Allergic processes
Neoplasia (eg, Hodgkin lymphoma)
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8
Q

Basophils

  • Basophilia
  • Cointainment
A

is uncommon, but can be a sign of myeloproliferative disease, particularly CML.

contain heparin (anticoagulant) and histamine (vasodilator). Leukotrienes.

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9
Q

Mast cells

  • Activated by
  • Cromolyn sodium
A

tissue trauma, C3a and C5a, surface IgE crosslinking by antigen.

prevents mast cell degranulation (used for asthma prophylaxis).

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10
Q

Dendritic cells

A

Function as link between innate and adaptive immune systems.

Express MHC class II and Fc receptors on surface. Called

Langerhans cell in the skin.

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11
Q

NK cells innate oder Adaptative inmmune response?

A

are part of the innate immune response

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12
Q

Plasma cells

  • Morphoology
  • Found in
A

“Clock-face” chromatin distribution and eccentric nucleus, abundant RER, and well-developed Golgi apparatus.

Found in bone marrow and normally do not circulate in peripheral blood.

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13
Q

Fetal erythropoiesis

A 
Fetal erythropoiesis occurs in:
ƒƒ Yolk sac (3–8 weeks)
ƒƒ Liver (6 weeks–birth)
ƒƒ Spleen (10–28 weeks)
ƒƒ Bone marrow (18 weeks to adult)
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14
Q

Hemoglobin development

  • Embryonic globins
  • Fetal hemoglobin (HbF)
  • Adult hemoglobin (HbA1)
  • HbA2
A

ζ and ε

α2γ2

α2β2

α2δ2

  • Alpha Always; Gamma Goes, Becomes Beta.
  • HbF has higher affinity for O2 due to less avid binding of 2,3-BPG.
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15
Q

Blood groups

A

Pag. 400

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16
Q

Rh hemolytic disease of the newborn

  • Interaction
  • Mechanism
  • Presentation
  • Treatment
A

Rh ⊝ mothers; Rh ⊕ fetus.

First pregnancy: mother exposed to fetal blood (often during delivery) Ž formation of maternal anti-D IgG.

Jaundice shortly after birth, kernicterus, hydrops fetalis

Prevent by administration of anti-D IgG to Rh ⊝ pregnant women during third trimester and early postpartum period.

17
Q

ABO hemolytic disease of the newborn

A

Type O mothers; type A or B fetus.

Pre-existing maternal anti-A and/or anti-B IgG antibodies cross placenta Ž HDN in the fetus.

Mild jaundice in the neonate within 24 hours of
birth. Usually less severe than Rh HDN.

Treat newborn with phototherapy or exchange
transfusion.

18
Q

Hemoglobin electrophoresis

A

HbA migrates the farthest, followed by HbF, HbS, and HbC. This is because the missense mutations in HbS and HbC replace glutamic acid ⊝ with valine (neutral) and lysine ⊕

19
Q

ANTICOAGULANTS: factor Xa

A
  • LMWH (greatest effcacy)
  • heparin
  • direct Xa inhibitors (apixaban, rivaroxaban)
  • fondaparinux
20
Q

ANTICOAGULANTS: IIa (thrombin)

A
  • heparin (greatest effcacy)
  • LMWH (dalteparin, enoxaparin)
  • direct thrombin inhibitors (argatroban, bivalirudin, dabigatran)
21
Q

THROMBOLYTICS:

A

alteplase, reteplase, streptokinase, tenecteplase

22
Q

Hemophilia A:
Hemophilia B:
Hemophilia C:

A

deficiency of factor VIII (XR)
deficiency of factor IX (XR)
deficiency of factor XI (AR)

23
Q

Vitamin K deficiency

  • Factors
  • Warfarin mechanism
  • Factors Life span
A

synthesis of factors II, VII, IX, X, protein C, protein S.

Warfarin inhibits vitamin K epoxide reductase.

Factor VII—Shortest half life.
Factor II—Longest half life

24
Q

Antithrombin

A

inhibits activated forms of factors II, VII, IX, X, XI, XII. Heparin enhances the activity of antithrombin.

Principal targets of antithrombin: thrombin and factor
Xa.

25
Q

Platelet plug formation (primary hemostasis)

A
  1. Injury
  2. Exposure
  3. Adhesion (vWF + GpIb)
  4. Activation (ADP + P2Y12 induces GpIIb/IIIa)
  5. Aggregation
26
Q

Clopidogrel, prasugrel, and ticlopidine

A

inhibit ADP-induced expression of GpIIb/IIIa by

irreversibly blocking P2Y12 receptor.

27
Q

Abciximab, eptifibatide, and tirofiban

A

inhibit GpIIb/IIIa directly.

28
Q

Ristocetin

A

activates vWF to bind GpIb. Failure of aggregation with ristocetin assay occurs in von Willebrand disease and Bernard-Soulier syndrome.

29
Q

Glanzmann thrombasthenia

Bernard- Soulier syndrome

A

GpIIb/IIIa

GpIb

USMLE 1 (73 decks)

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