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Hematology-Immunology > Hematology IM > Flashcards

Hematology IM Flashcards

1
Q

are immature red blood cells (RBCs) produced in the bone marrow and released into the peripheral blood, where they mature into RBCs within 1 to 2 days

A

Reticulocytes

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2
Q

Is a laboratory value that measures the average size and volume of a red blood cell. Micoytosis is reflected by a lower than nORmal MCV (<80) whereas high values (>100) REFLECTS Macrocytosis.

A

MCV

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3
Q

is a calculation of the average amount of hemoglobin contained in each of a person’s red blood cells. Is the least useful of the INDECES; it tends to TRACK with the MCV

A

MCH

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4
Q

is a measurement of the average amount of hemoglobin in a single red blood cell (RBC) as it relates to the volume of the cell. MCHC reflects defects in hemoglobin synthesis (HYPOCHROMIA)

A

MCHC

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5
Q

Marrow Examination (Aspirate)

A

-M/E ratio
-Cell Morphology
-Iron stain

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6
Q

Marrow Examination (Biopsy)

A

-Cellularity
-Morphology

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7
Q

Increased M:E ratio may be seen in

A

infection, chronic myelogenous leukemia or erythroid hypoplasia

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8
Q

This procedure is particularly helpful when evaluating patients with anemia, iron overload, myelodysplasia, etc.

A

The iron staining procedure utilizes the Prussian Blue stain for ferric iron to assess bone marrow iron stores.

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9
Q

Functional classification of Anemia

A
  1. Marrow production defects hypoproliferation
  2. Red cell maturation defects ineffective erythropoiesis
  3. Decreased red cell survival blood loss/hemolysis
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10
Q

Index >2.5 Hemolysis/Hemorrhage

A

-Blood loss
-Intravascular hemolysis
-Metabolic defect
-Membrane Abnormality
-Hemoglobinopathy
-Immune destruction
-Fragmentation hemolysis

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11
Q

Index <2.5 Red cell morphology (Normocytic Normochromic)

A

Hypoproliferative
-Marrow Damage
1. Infiltration/Fibrosis
2. Aplasia
-Iron Deficiency
-Decrease Stimulation
1. Inflammation
2. Metabolic defect
3. Renal Disease

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12
Q

Index >2.5 (Micro-or Macrocytic)

A

Maturation Disorder
-Cytoplasmic defects
1. Iron deficiency
2. Thalassemia
3. Sideroblastic anemia
-Nuclear defects
1. Folate deficiency
2. Vitamin B12 deficiency
3. Drug toxicity
4. Myelodysplasia

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13
Q

Major components of the hemostatic system

A
  1. platelets and other formed elements of blood, such as monocytes and red cells
  2. plasma proteins (the coagulation and fibrinolytic factors and inhibitors)
  3. the vessel wall
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14
Q

are large blood cells whose principal function is the production of platelets

A

Megakaryocytes

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15
Q

Platelets are

A

anucleate, small (2–4µm), short-lived (7–10d) circulating cells in the blood

physiologically very active, but are anucleate, and thus have limited capacity to synthesize new proteins

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16
Q

are more numerous and contain compounds like P-selectin, GPIIb/IIIa, GPIb, von Willebrand factor (vWF), factors V, IX, and XIII, and others.

A

Alpha granules

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17
Q

Contain some of these compounds but are principally responsible for storing calcium, potassium, serotonin, and important nucleotides such as ATP and ADP

A

Dense granules

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18
Q

A large multimeric protein present in both plasma and the extracellular matrix of the subendothelial vessel wall

serves as the primary “molecular glue”

A

VWF

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19
Q

most abundant receptor on the platelet surface and convert this into an active receptor, enabling binding to fibrinogen and VWF

A

Gp IIb/IIIa receptor

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20
Q

STEPS In Stable Platelet Plug (INITIATION)

A

Occurs when moving platelets become tethered to exposed VWF/ collagen complexes and remain in place long enough to become activated by collagen. This step produces a platelet monolayer that supports the subsequent adhesion of activated platelets to each other

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21
Q

STEPS In Stable Platelet Plug (Extension)

A

• Occurs when additional platelets adhere to the initial monolayer and become activated.

• Thrombin, adenosine diphosphate (ADP) secreted by platelets, and thromboxan A, (TXA,) released by platelets play an important role in this step

• Subsequent intracellular activates allbß3 (also known as glycoprotein [GP] b-Illa) on the platelet surface, providing a molecular basis for cohesion between platelets.

• Activated platelets stick to each other via bridges formed by the binding of fibrinogen, fibrin, or VWF to activated allbß3

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22
Q

STEPS in Stable Platelet Plug (STABILIZATION)

A

• Refers to the subsequent events of platelet plug formation that help to consolidate the platelet plug and prevent premature disaggregation, in part by amplifying signaling within the platelet.

• The net result is a hemostatic plug comprised of activated platelets embedded within a cross-linked fibrin mesh, a structure stable enough to withstand the forces generated by flowing blood in the arterial circulation

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23
Q

The Extrinsic Pathway consist of

A

-Tissue Factor
-Plasma Factor VII/VIIa (FVII/FVIIa)

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24
Q

The Intrinsic Pathway consist of

A

-FXI
-FIX
-FVIII

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25
converts prothrombin to thrombin, the pivotal protease of the coagulation system.
Factor Xa
26
Factor I
Fibrinogen
27
Factor II
Prothrombin
28
Factor III
Tissue factor (Extrinsic)
29
Factor IV
Ca2+ (Is usually not referred to as a coagulation factor)
30
Factor V
-Proaccelerin -Labile factor -Accelerator (Ac-) globulimn
31
Factor VII
-Proconvertin -Serum prothrombin conversion accelerator (SPCA) -Cothromboplastin
32
Factor VII
-Proconvertin -Serum prothrombin conversion accelerator (SPCA) -Cothromboplastin
33
Factor VIII
-Antihemophilic factor A -Antihemophilic globulin (AHG)
34
Factor IX
-Antihemophilic factor B -Christmas factor -Plasma thromboplastin component (PTC)
35
Factor X
Stuart-Prower factor
36
Factor XI
Plasma thromboplastin antecedent (PTA)
37
Factor XII
Hageman factor
38
Factor XIII
-Fibrin stabilizing factor (FSF) -Fibrinoligase
39
is a multifunctional enzyme that converts soluble plasma fibrinogen to an insoluble fibrin matrix. also activates factor XIII (fibrinstabilizing factor) to factor XIIIa, which covalently cross-links and thereby stabilizes the fibrin clot
Thrombin
40
are a hallmark of moderate and severe factor VIII and IX deficiency and, in rare circumstances, of other clotting factor deficiencies
Spontaneous Hemarthroses
41
are more suggestive of underlying platelet disorders or Von Willebrand disease (VWD), termed disorders of primary hemostasis or platelet plug formation
Mucosal bleeding symptoms
42
can also be a sign of medical conditions in which there is no identifiable coagulopathy; instead, the conditions are caused by an abnormality of blood vessels or their supporting tissues.
Easy Bruising
43
Menorrhagia
defined quantitatively as a loss of >80 mL of blood per cycle, based on the quantity of blood loss required to produce irondeficiency anemia.
44
is a common symptom in women with underlying bleeding disorders (VWD and symptomatic carriers of hemophilia
Postpartum hemmorhage
45
Life-threatening sites of bleeding
bleeding into the oropharynx, where bleeding can obstruct the airway, into the central nervous system, and into the retroperitoneum.
46
is the major cause of bleeding-related deaths in patients with severe congenital factor deficiencies
CNS bleeding
47
Most commonly used antiplatelet drug Irreversibly acetylates and thus inhibits the platelet cyclooxygenase (COX-1) involved in formation of TxA2 -a potent aggregator of platelets and also a vasoconstrictor
Aspirin
48
inhibitors of the P2Y12 receptor for ADP
-Clopidogrel -Prasugrel -Ticagrelor
49
antagonists of ligand binding to GPIIb-IIIa that interfere with fibrinogen and von Willebrand factor binding and thus platelet aggregation
-Abciximab -Eptifibatide -Tirofiban
50
Most procedures can be performed in patients with a platelet count
50,000 The level needed for major surgery will depend on the type of surgery and the patient’s underlying medical state, although a count of approximately 80,000/μL is likely sufficient.
51
Platelet count <150,000/uL Normal RBC morphology, platelets normal or Increase in size consider
Drug-induced thrombocytopenia Infection-induced thrombocytopenia Idiopathic immune thrombocytopenia Congenital thromboctyopenia
52
Most commonly seen in patients with systemic infections with gram-negative bacteria. Infections can affect both platelet production and platelet survival.
DIC
53
Heparin-Induced Thrombocytopenia
HIT is not associated with bleeding and, in fact, markedly increases the risk of thrombosis HIT can occur after exposure to low-molecularweight heparin (LMWH) as well as unfractionated heparin (UFH), (more common with the latter) Most patients develop HIT after exposure to heparin for 5–14 days
54
4T
-Thrombocytopenia -Timing of platelet count drop -Thrombosis and other sequelae such as localized skin reactions -oTher causes of thrombocytopenia not evident
55
Immune Thrombocytopenic Purpura (ITP)
Also termed idiopathic thrombocytopenic purpura) An acquired disorder in which there is immunemediated destruction of platelets and possibly inhibition of platelet release from the megakaryocyte. Characterized by mucocutaneous bleeding and a low, often very low, platelet count, with an otherwise normal peripheral blood cells and smear Patients usually present either with ecchymoses and petechiae, or with thrombocytopenia incidentally found on a routine CBC.
56
ITP Is termed secondary if it is associated with underlying disorder such as
Autoimmune disorders, particularly systemic lupus erythematosus (SLE), and infections, such as HIV and hepatitis C, are common causes.
57
VWF serves two roles
1. as the major adhesion molecule that tethers the platelet to the exposed subendothelium 2. as the binding protein for factor VIII (FVIII), resulting in significant prolongation of the FVIII half-life in circulation By far the most common type of VWD is type 1 disease- accounting for at least 80% of cases - with a parallel decrease in VWF protein, VWF function, and FVIII levels,
58
Mainstay of treatment for type 1 VWD
DDAVP -Results in release of VWF and FVIII from endothelial stores -DDAVP can be given intravenously or by a high-concentration intranasal spray (1.5 mg/mL). -is a synthetic vasopressin analog that causes a transient rise in FVIII and von Willebrand factor (VWF), but not FIX, through a mechanism involving release from endothelial cells
59
Bleeding in the gums, gastrointestinal tract, and during oral surgery requires the use of
Oral antifibrinolytic drugs such as ε-amino caproic acid (EACA) or tranexamic acid to control local hemostasis.
60
is a relatively common finding in patients with liver disease due to impaired fibrin polymerization
Dysfibrinogenemia
61
Because FV is only synthesized in the hepatocyte and is not a vitamin K–dependent protein, reduced levels of FV may be an indicator of
Hepatocyte failure
62
Normal levels of FV and low levels of FVII suggest
Vit K deficiency
63
Vitamin K levels may be reduced in patients with
Liver failure due to - Compromised storage in hepatocellular disease - Change in bile acids - Cholestasis that can diminsh the absorption of Vit K
64
Platelets concentrates are indicated
when platelet counts are <10,000–20,000/μL to control an ongoing bleed or immediately before an invasive procedure if counts are <50,000/μL
65
Platelets concentrates are indicated
when platelet counts are <10,000–20,000/μL to control an ongoing bleed or immediately before an invasive procedure if counts are <50,000/μL
66
is the most effective to correct hemostasis in patients with liver failure
Treatment with FFP
67
Cryoprecipitate is indicated only
When fibrinogen levels are less than 100 mg/mL; dosing is six bags for a 70-kg patient daily.
68
the obstruction of blood flow due to the formation of clot, may result in tissue anoxia and damage
Thrombosis
69
the obstruction of blood flow due to the formation of clot, may result in tissue anoxia and damage
Thrombosis
70
is the most common cause of acute myocardial infarction (MI), ischemic stroke, and limb gangrene.
Arterial trhombosis
71
is the most common cause of acute myocardial infarction (MI), ischemic stroke, and limb gangrene.
Arterial trhombosis
72
encompasses deep vein thrombosis (DVT), which can lead to postthrombotic syndrome, and pulmonary embolism (PE), which can be fatal or can result in chronic thromboembolic pulmonary hypertension.
Venous thromboembolism
73
encompasses deep vein thrombosis (DVT), which can lead to postthrombotic syndrome, and pulmonary embolism (PE), which can be fatal or can result in chronic thromboembolic pulmonary hypertension.
Venous thromboembolism
74
is the process by which thrombin is activated and soluble plasma fibrinogen is converted into insoluble fibrin
Coagulation
75
Acquired causes of Venous thrombosis
-Surgery -Malignancy -Antiphospholipid syndrome -Other (Trauma, Pregnancy,Long-haul travel, Obesity, Oral contraceptives/ Hormones replacement, Myeloproliferative disorders, Polycythemia vera)
76
mechanism for enhanced thrombosis appears to be due both to altered platelet function and to a procoagulant and hypofibrinolytic state
Metabolic syndrome
77
Genetics of Venous Thrombosis
- Heterozygous antithrombin deficiency - Homozygosity of the factor V Leiden mutation - Homozygous protein C or protein S deficiencies
78
Binding is mediated by:
Arg-Gly-Asp (RGD) sequence found on the α chains of fibrinogen and on VWF Lys-Gly-Asp (KGD) sequence located within a unique domain on fibrinogen
79
Heparin therapy can be monitored using
- Activated partial thromboplastin time (aPTT) or anti-factor Xa level - therapeutic heparin levels are achieved with a two- to threefold prolongation of the aPTT
80
Heparin therapy can be monitored using
- Activated partial thromboplastin time (aPTT) or anti-factor Xa level - therapeutic heparin levels are achieved with a two- to threefold prolongation of the aPTT
81
Heparin MOA
Heparin binds to antithrombin via its pentasaccharide sequence. This induces a conformational change in the reactive center loop of antithrombin that accelerates its interaction with factor Xa. To potentiate thrombin inhibition, heparin must simultaneously bind to antithrombin and thrombin
82
Heparin MOA
Heparin binds to antithrombin via its pentasaccharide sequence. This induces a conformational change in the reactive center loop of antithrombin that accelerates its interaction with factor Xa. To potentiate thrombin inhibition, heparin must simultaneously bind to antithrombin and thrombin

Hematology-Immunology (6 decks)

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