Hematology & Oncology - Anatomy & Physiology

sefomepu's version from 2015-06-19 17:54

Types of cells in the blood

Question Answer
Erythrocytosis =polycythemia = ↑ hematocrit
Anisocytosis =varying sizes
Poikilocytosis =Varying shapes
Reticulocyte =immature erythrocyte, marker of erythroid proliferation
Where are platelets derived from?megakaryocytes
Life span of RBCs120 days
Life span of platelets8-10 days
Dense granules of plateletsADP, calcium
alpha granules of plateletsvWF, fibrinogen
Thrombyocytopenia or platelet dysfn →petechiae
vWF receptorGlycoprotein Ib
Fibrinogen receptorGlycoprotein IIb/IIIa
Leukocytes are divided into 2 categoriesgranulocytes, mononuclear cells
Granulocytes includeneutrophil, eosinophil, basophil
Mononuclear cells includemonocytes, lymphocytes
Population of WBCs, in order from most to fewestNeutrophils (54-62%)
Lymphocytes (25-33%
Monocytes (3-7%)
Eosinophils (1-3%)
Basophils (0-0.75%)
NeutrophilAcute inflammatory response to bacterial infections
Contents of smaller, more numerous specific granules in PMNsalkaline phophatase, collagenase, lysozyme, lactoferrin
Contents of larger, less numerous azurophilic granules (lysosomes)acid phosphatase, myeloperoxidase, B-glucuronidase
PMNs and vitamin B12/folate deficiencyHypersegmented - 5 or more lobes
↑ band cells indicates what?immature neutrophils
indicates increased states of myeloid proliferation (bacterial infections, CML)
MonocyteDifferentiates into macrophages in tissues
MacrophageDifferentiates from monocyte
Activated by gamma-interferon
APC cell via MHC II
CD14 is a cell surface marker
EosinophilDefends agains helminthic infections
Bi-lobate nucleus
Phagocytizes antigen-antibody complexes
What does an eosinophil produce?Histaminase & MBP
Helps limit reaction following mast cell degranulation
Causes of eosinophiliaNAACP
Allergic processes
Collagen vascular diseases
Parasites (invasive)
BasophilMediates allergic reaction
Contents of basophilic granulesheparin - anticoagulant
histamine - vasodilator
leukotrienes - LTD4
Mast cellMediates allergic reaction in local tissues
bind to Fc portion of IgE to membrane
Type 1 hypersensitivity
Action of mast cellBinds the Fc portion of IgE to the membrane → antigen binds to IgE → IgE's cross-link → degranulation → histamine, heparin, and eosinophil chemotactic factos
What prevents mast cell degranulation?Cromolyn sodium
Dendritic cellshighly phagocytic APCs
Express MHC II and Fc receptor on surface
AKA Langerhans cells in the skin
LymphocyteDivided into T cells and B cells (adaptive immunity)
B lymphocyte developmentStem cells in BM → matures in BM &rarrl migrates to peripheral lymphoid tissue: follicles of LNs, white pulp of spleen, and unencapsulated lymphoid tissue
Can fn as an APC via MHC II/B7
CD19, CD20, CD21, CD40
Plasma cellDifferentiated from B cells to produce large amount of antibody specific to a particular antigen
Muliple myeloma
Off-center nucleus, clock-face chromatin dist., abundant RER, and well-developed Golgi
T lymphocyte activation requiresCD28 (costimulatory signal)
T cells expressTCR, CD3, CD28

Types of cells in the blood - Picture quiz

Question Answer
Mast cell
Dendritic cell
Plasma cell

Blood groups

Question Answer
AA antigen on RBC surface
anti-B antibody in plasma
BB antigen on RBC surface
anti-A antibody in plasma
ABA&B antigens on RBC surface
no antibodies in plasma
"universal recipient" of RBCs
"universal donor" of plasma
ONeither A nor B antigens on RBC surface
both antibodies in plasma
"universal donor" of RBCs
"universal recipient" of plasma
Blood antibodies and placentaanti-A/anti-B antibodies = IgM (do not cross placenta)
anti-Rh = IgG (does cross placenta)
Rhantigen on RBC surface
Rh-negative moms having an Rh-positive child must take Rho(D) immune globulin to prevent the production of anti-Rh IgG which will cause erythroblastosis fetalis in the next fetus that is Rh+

Coagulation/complement/kinin pathways

Question Answer
Order of coagulation cascade11a→9a→10a→2a (thrombin)→Fibrin
Intrinsic coagulation pathway12a→11
Extrinsic coagulation pathwaythromboplastin=tissue factor → activates factor 7 → activates factor 10
Factor 2 (thrombin)activates fibrinogen to fibrin
Activates factors 5, 8, 13
The actions of which factors require Ca?5, 7, 8, 9, 10, 11, 13
Factor 8Activated by 2a
Works with factor 7, 9, & Ca to activate factor 10
vWF carries/protects Factor 8
What actiavtes factor 12 (intrinsic coagulation pathway)?Collagen, basement membrane, activated plalets, HMWK
BradykininKinin cascade: ↑ vasodilation, ↑ permeability ↑ pain
Activated by Kallikrein
Inactivated by ACE
KallikreinActivated by factor 12 (intrinsic coagulation pathway)
Activates bradykinin and plasmin
PlasminActivated by Kallikrein and the fibrinolytic system
Activates C3 (complement cascade)
Hemophilia Adeficiency of factor 8 → ↑ PTT → hemarthroses, easy bruising
Hemophilia Bdeficiency of factor 9 → ↑ PTT → hemarthroses, easy bruising
Vitamin K deficiency↑ PT, ↑ PTT
↓ synthesis of factors 2, 7, 9, 10, protein C, protein S
PTtests fn of common and extrinsic pathways
Factors 1, 2, 5, 7, 10
PTTtests fn of common and intrinsic pathways
All factors except 7 & 13
Vitamin KActivates Factors 2, 7, 9, 10, C, S
Activated (reduced) by epoxide reductase
Warfarin inhibits epoxide reductase
Antithrombininhibits activated forms of factors 2, 7, 9, 10, 11, 12
activated by heparin
Protein CActivated by thrombomodulin (endothelial cells)
Works with Protein S to inactivate factors 5, 8
Factor V Leiden mutationproduces a factor 5 that's resistant to inhibition by activated protein C
tPAactivates plasmin from plasminogen → cleavage of fibrin mesh
Factor 5Works with factors 2 and 10 to activate factor 2
Inhibited by Protein C & protein S
vWFBinds/protects factor 8
Initiates platelet plug by binding to exposed collagen upon endothelial damage

Platelet plug formation

Question Answer
InjuryvWF binds to exposed collagen
AdhesionPlatelets bind vWF via GPIb receptor at the site of injury only
Platelets release ADP and Ca (necessary for coagulation cascade)
ADP helps platelets adhere to endothelium
ActivationADP binding to receptor induces GPIIb/IIIa expression at platelet surface
AggregationFibrinogen binds GPIIb/IIIa receptors and links platelets
Pro-aggregation factorsTXA2 - released by platelets
↓ blood flow
↑ platelet aggregation
Anti-aggregation factorsPGI2 and NO (released by endothelial cells)
↑ blood flow
↓ platelet aggregation
Aspirininhibits cyclooxygenase (inhibits TXA2 formation from arachidonic acid)
Ticlopidine and clopidogrelinhibit ADP-induced expression of GpIIb/IIIa → platelets can't attach to fibrinogen and aggregate
Abciximabinhibits GpIIb/IIIa directly → platelets can't attach to fibrinogen and aggregate
ESRmeasures RBC aggregation caused by acute-phase reactants in plasma (fibrinogen)
↑ ESR→ infections, autoimmune diseases (SLE, RA, temporal arteritis), malignant neoplasms, GI disease (ulcerative colitis), pregancy
↓ ESR→ polycythemia, sickle cell anemia, congestive heart failure, microcytosis, hypofibrinogenemia
Order of platelet plug formationInjury (vWF binds) → Adhesion (platelets bind to vWF and release ADP) &rarrl Activation (ADP binds to GpIIb/IIIa) → Aggregation (fibrinogen binds GpIIb/IIIa linking platelets to each other)

Pathologic RBC forms

Question Answer
Acanthocyte (spur cell)Liver disease, abetalipoproteinemia (states of cholesterol dysregulation)

Basophilic stipplingThalassemias
Anemia of chronic disease
Lead poisoning

Bite cellG6PD deficiency

ElliptocyteHereditary elliptocytosis

Macro-ovalocyteMegaloblastic anemia (also hypersegmented PMNs)
Marrow failure

Ringed sideroblastsSideroblastic anemia
Excess iron in mitochondria = pathologic

Helmet cell
DIC, TTP/HUS, traumatic hemolysis (metal heart valve)

Sickle cellSickle cell anemia

SpherocyteHereditary spherocytosis
drug and infection induced hemolysis

Teardrop cellBone marrow infiltration (i.e. myelofibrosis)"sheds a tear because it is being forced out of it's home in the BM"

Target cellHALT - the hunter said to his target
HbC disease
Liver disease

Heinz bodiesoxidation of Hb SH groups →
Seen in G6PD and (similar looking inclusion) in a-thalassemia

denatured Hb

Howell-Jolly bodiesBasophilic nuclear remnants in RBCs - Normally removed by splenic macrophages
Seen in functional hyposplenia or asplenia
Or after mothball ingestion (naphthalene)