Step 1 - Hemonc

Front 1

Erythrocyte

Back 1

Anucleate
Biconcave
Large surface area to volume ratio
Glucose for energy
120 day survival
Chloride-bicarbonate antiport in membrane for CO2

Front 2

Basophil

Back 2

Mediates allergic reaction
Bilobate nucleus
Granules contain heparin (anticoagulant), histamine (vasodilator), and leukotrienes

Front 3

Mast cell

Back 3

Mediates allergic reaction
Granules of histamine, heparin, and eosinophilic chemotactic factors
Type I hyperesensitivity (asthma)
Degranulation prevented by cromolyn sodium

Front 4

Eosinophil

Back 4

Bilobate nucleus
Defends against helminths and protozoans (major basic protein)
Produces histamine and arylsulfatase

Front 5

Causes of eosinophilia

Back 5

Neoplastic
Asthma
Allergic
Collagen vascular diseases
Parasites

Front 6

Neutrophil

Back 6

Acute inflammatory response cell
Phagocytic
Granules contain hydrolytic enzymes, lysozyme, lactoferrin, and myeloperoxidase

Front 7

Monocyte

Back 7

Kidney-shaped nucleus
Differentiates into macrophages in tissue

Front 8

Macrophage

Back 8

Phagocytoses bacteria, cell debris, and senescent RBCs
Scavenges damaged cells and tissues
Activated by gamma interferon
Function as APCs via MHC II

Front 9

Platelet

Back 9

Derived from megakaryocytes
Aggregates to form hemostatic plug with fibrinogen
Dense granules (ADP, calcium)
Alpha granules (vWF, fibrinogen)

Front 10

Dendritic cells

Back 10

APCs
Express MHC II and Fe receptor on surface
Induce primary antibody response

Front 11

B lymphocyte

Back 11

Humoral immune response
Arise from stem cells in bone marrow
Migrates to peripheral lymphoid tissue
Differentiate into plasma cells and form antibodies
CD19 and CD20 markers

Front 12

Plasma cell

Back 12

Clock-face chromatin
Abundant RER
Produce large amounts of specific antigen

Front 13

T lymphocyte

Back 13

Mediates cellular immune response
Matures in thymus
CD4 - helper T cell, MHC II
CD8 - cytotoxic T cell, MHC I
Majority of circulating lymphocytes

Front 14

Thrombomodulin

Back 14

Cleaves protein C to activated protein C
Surface of vascular endothelial cells

Front 15

Activated protein C

Back 15

Degrades factor Va and VIIIa

Front 16

Factor V Leiden

Back 16

Mutant factor V that can't be degraded by protein C
Bleeding
DVT
Cerebral vein thrombosis
Recurrent pregnancy loss

Front 17

Prothrombin gene mutation

Back 17

Increases prothrombin levels
Associated with venous clots

Front 18

ATIII deficiency

Back 18

Prevents inactivation of thrombin
Reduced increase in PTT after administration of heparin

Front 19

Protein C or protein S deficiency

Back 19

Inability to inactivate factors V and VIIIa
Risk of hemorrhagic skin necrosis after administration of warfarin

Front 20

Platelet plug formation

Back 20

Adhesion - vWF mediates linking of Gp1b receptor to subendothelial collagen
Aggregation - TxA2 from platelets is pro-aggregation, PGI2 and NO released by endothelial cells are anti-aggregation
Swelling - binding of ADP on platelet receptors causes GpIIb/IIIa insertion and platelet cohesion

Front 21

Vitamin K-dependent factors

Back 21

II
VII
IX
X
Proteins C and S
Inhibited by warfarin

Front 22

Antithrombin III effects

Back 22

Inactivates II, VII, IX, X, and XI

Front 23

Plasminogen

Back 23

Cleaves fibrin mesh
Used as a thrombolytic

Front 24

Bradykinin

Back 24

Kinin cascade
Increased vasodilation
Increased permeability
Increased pain

Front 25

Blood reactions in pregnancy

Back 25

AB antibodies are IgM - don't cross placenta
Rh antibodies are IgG - cross placenta
Rh negative mother exposed to Rh+ blood can cause hemolytic disease of newborn in subsequent pregnancies

Front 26

Spherocytes

Back 26

Hereditary spherocytosis
Autoimmune hemolysis

Front 27

Macrocytic RBCs

Back 27

Megaloblastic anemia
Marrow failure

Front 28

Hemte cells and schistocytes

Back 28

DIC
TTP/HUS
Traumatic hemolysis

Front 29

Bite cells

Back 29

G6PD deficiency

Front 30

Acanthocytes

Back 30

Liver disease
Abetalipoproteinemia

Front 31

Target cells

Back 31

HbC disease
Asplenia
Liver disease
Thalassemia

Front 32

Heinz bodies

Back 32

Due to oxidation of iron from ferrous to ferric form
Alpha-thalassemia
G6PD deficiency

Front 33

Howell-Jolly bodies

Back 33

Functional hyposplenia or asplenia

Front 34

Microcytic hypochromic anemia

Back 34

Iron deficiency - low serum iron, low ferritin, high TIBC
Thalassemia - target cells
Lead poisoning - basophilic stippling
Anemia of chronic disease - low TIBC, high ferritin, low serum iron

Front 35

Macrocytic anemia

Back 35

Megaloblastic - B12 and folate deficiency (B12 has neurologic symptoms), hypersegmented PMNs
Drugs that block DNA synthesis (sulfa, phenytoin, AZT)

Front 36

Normochromic normocytic

Back 36

Acute hemorrhage
G6PD deficiency (X-linked)
Hereditary spherocytosis
Aplastic anemia/leukemia
Hemoglobinopathies
Autoimmune hemolytic anemia

Front 37

Indicators of RBC hemolysis

Back 37

Serum LDH
Low serum haptoglobin

Front 38

Porphyria

Back 38

Symptoms: painful abdomen, pink urine, polyneuropathy, psychologic disturbances, precipitated by drugs
Pathogenesis: lead poisoning (ferrochelatase and ALA dehydratase -> coproporphyrin and ALA), acute intermittent porphyria (uroporphyrinogen I synthase -> porphobilinogen and d-ALA), porphyria cutanea tarda (uroporphyrinogen decarboxylase -> uroporphyrin)

Front 39

Aplastic anemia

Back 39

Symptoms: pancytopenia, fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infection, hypocellular fatty bone marrow
Pathogenesis: failure or destruction of myeloid stem cells, radiation, benzene, chloramphenicol, alkylating agents, antimetabolites, virus, Fanconi's anemia (deficiency in DNA repair), after acute hepatitis
Treatment: withdraw offending agent, immunosuppression, allogeneic BMT, transfusion, G-CSF

Front 40

Sickle cell anemia

Back 40

Symptoms: crescent-shaped RBCs, aplastic crisis (parvovirus B19 infection), autosplenectomy, risk of encapsulated organism infection, painful crisis, renal papillary necrosis
Pathogenesis: HbS mutation in beta chain of Hb, low O2 or dehydration precipitates sickling
Treatment: hydroxyurea (increases HbF), BMT

Front 41

Alpha thalassemia

Back 41

Symptoms: Asian and African populations, microcytic hypochromic anemia
Pathogenesis: underproduction of alpha globin genes, HbH (lacks 3 alpha globin genes), Hb Barts (lacks 4 genes -> intrauterine fetal death)

Front 42

Beta thalassemia

Back 42

Symptoms: severe anemia, cardiac failure secondary to hemochromatosis, marrow expansion
Pathogenesis: underproduction or absence of beta chain of Hb

Front 43

General signs of hemolytic anemias

Back 43

Increased serum bilirubin (jaundice, pigment gallstones)
Increased reticulocytes
Hemoglobinuria (intravascular hemolysis)
Jaundice (extravascular hemolysis)

Front 44

Autoimmune anemia

Back 44

Warm agglutinin - chronic anemia seen in SLE, CLL, or certain drugs, mostly extravascular, IgG
Cold agglutinin - acute anemia triggered by cold, seen with infectious mono or mycoplasma pneumo, IgM
Erythroblastosis fetalis - Rh antigen incompatibility between mother and fetus

Front 45

Hereditary spherocytosis

Back 45

Symptoms: small round RBCs with no central pallor, Howell-Jolly bodies after splenectomy, splenomegaly, aplastic crisis, lyse on osmotic fragility test
Pathogenesis: ankyrin or spectrin defect

Front 46

Paroxysmal nocturnal hemoglobinuria

Back 46

Symptoms: intravascular hemolysis, increased urine hemosiderin
Pathogenesis: PIG-A mutation leads to loss of GPI anchor for CD55 an CD59, membrane defect causing increased sensitivity to complement-mediated lysis

Front 47

Microangiopathic anemia

Back 47

Symptoms: schistocytes (mechanical destruction)
Pathogenesis: DIC, TTP/HUS, SLE, malignant HTN

Front 48

DIC

Back 48

Symptoms: activation of coagulation cascade, microthrombi, consumption of platelets, fibrin, and coagulation factors, increased PT and PTT, increased fibrin split products, helmet and schistocytes
Pathogenesis: gram negative sepsis, trauma, OB complications, acute pancreatitis, malignancy, nephrotic syndrome, transfusion

Front 49

Platelet abnormalities

Back 49

Symptoms: microhemorrhage (petechiae, purpura), increased bleeding time, epistaxis, mucous membrane bleeding
Pathogenesis: ITP (anti-GPIIb/IIIa antibodies, increased megakaryocytes), TTP (deficiency of vWF cleaving metalloproteinase, increased LDH, neuro and renal symptoms), DIC (schistocytes, fibrin split products), aplastic anemia, drugs

Front 50

Coagulopathies

Back 50

Symptoms: macrohemorrhage (hemarthroses, easy bruising, increased PT/PTT
Pathogenesis: hemophilia A (factor VIII deficiency), hemophilia B (factor IX deficiency), vWD (vWF deficiency, decreased platelet adhesion and factor VIII survival)

Front 51

PT

Back 51

Tests extrinsic pathway
Factors I,II, V, VII, X

Front 52

PTT

Back 52

Tests intrinsic pathway
All factors but VII and XIII

Front 53

Thrombocytopenia/DIC

Back 53

Decreased platelets
Increased bleeding time

Front 54

Hemophilia A and B

Back 54

Increased PTT

Front 55

von Willebrand's disease

Back 55

Increased bleeding time
Increased PTT
Decreased platelet to collagen adhesion
Diagnose with ristocetin test
Treat with DDAVP - releases vWF from endothelium

Front 56

Vitamin K deficiency

Back 56

Increased PT and PTT
Decreased synthesis of factors II, VII, IX, X, protein C and protein S

Front 57

Bernard-Soulier disease

Back 57

Decreased Gp1b -> defect in platelet to collagen adhesion
Decreased platelet count
Increased bleeding time

Front 58

Glanzmann's thrombasthenia

Back 58

Decreased GpIIb/IIIa -> defect in platelet aggregation
Increased bleeding time

Front 59

Reed-sternberg cell

Back 59

Giant tumor cell seen in Hodgkin's disease
Binucleate and bilobed
CD30 and CD15 positive

Front 60

Hodgkin's lymphoma characteristics

Back 60

Presence of Reed-Sternberg cells
Localized single group of nodes
B symptoms - low-grade fever, night sweats, weight loss
Mediastinal lymphadenopathy
50% of cases associated with EBV
Bimodal distribution

Front 61

Non-Hodgkin's lymphoma characteristics

Back 61

Associated with HIV or immunosuppression
Multiple peripheral nodes with extranodal involvement and non-contiguous spread
Mostly involve B cells
Few constitutional signs
Peak incidence at 20-40

Front 62

Types of Hodgkin's lymphoma

Back 62

Nodular sclerosing - collagen banding, lacunar cells
Mixed cellularity - numerous RS cells
Lymphocyte predominant - young males
Lymphocyte depleted - older males with disseminated disease

Front 63

Small lymphocytic lymphoma

Back 63

Adult B cell NHL
Focal mass, low grade

Front 64

Follicular lymphoma

Back 64

Adult B cell NHL
t(14,18)
bcl-2 expression - inhibits apoptosis

Front 65

Diffuse large cell lymphoma

Back 65

Mostly adult B cell NHL
Aggressive

Front 66

Mantle cell lymphoma

Back 66

Adult B cell NHL
t(11,14) - cyclin D1 activation
CD5 positive

Front 67

Lymphoblastic lymphoma

Back 67

Childhood T cell NHL
Presents with ALL and mediastinal mass

Front 68

Burkitt's lymphoma

Back 68

Childhood B cell NHL
t(8,14)
c-myc translocation
Starry sky appearance
Associated with EBV in endemic form
Pelvic or abdominal mass in sporadic form

Front 69

Multiple myeloma

Back 69

Symptoms: hypercalcemia, anemia, renal insufficiency, bone and back pain, fried egg plasma cells, lots of IgG/IgA, destructive bone lesions, increased susceptibility to infection, M spike and Bence Jones protein
Pathogenesis: monoclonal IgG or IgA production, primary AL amyloidosis

Front 70

Waldenstrom's macroglobulinemia

Back 70

Symptoms: M spike, hyperviscosity, no lytic bone lesions
Pathogenesis: monoclonal IgM

Front 71

t(9,22)

Back 71

Philadelphia chromosome
bcr-abl
CML

Front 72

t(8,14)

Back 72

Burkitt's lymphoma
c-myc activation

Front 73

t(14,18)

Back 73

Follicular lymphoma
bcl-2

Front 74

t(15,17)

Back 74

M3 type of AML
Responsive to ATRA

Front 75

t(11,22)

Back 75

Ewing's sarcoma

Front 76

t(11,14)

Back 76

Mantle cell lymphoma

Front 77

Leukemoid reaction

Back 77

Increased WBC count with left shift to band forms
Increased leukocyte alkaline phosphatase

Front 78

General signs of leukemias

Back 78

Increased number of circulating leukocytes in blood
Bone marrow infiltrates of leukemic cells
Marrow failure can cause anemia
Infections (decreased WBCs)
Hemorrhage (decreased platelets)
Infiltrates in liver, spleen, and lymph nodes

Front 79

ALL

Back 79

Symptoms: bone marrow replacement by lymphoblasts, TdT positive, can spread to CNS and testes
Pathogenesis: children

Front 80

AML

Back 80

Symptoms: Auer rods, circulating myeloblasts, M3 responds to vit A (ATRA, induces myeloblsat differentiation)
Pathogenesis: older adults

Front 81

CLL

Back 81

Symptoms: lymphadenopathy, hepatosplenomegaly, smudge cells
Pathogenesis: over 60

Front 82

CML

Back 82

Symptoms: myeloid stem cell proliferation, neutrophil, metamyelocyte, and basophil, splenomegaly, transformation to AML/ALL (blast crisis), left shift, very low alkaline phosphatase
Pathogenesis: bcr-abl translocation t(9,22)

Front 83

Hairy cell leukemia

Back 83

Symptoms: filamentous hair like projections in cells, TRAP positive
Pathogenesis: mature B cell tumor in elderly

Front 84

Langerhans cell histiocytosis

Back 84

Symptoms: S-100 and CD1a, Birbeck granules
Pathogenesis: proliferation of Langerhans cells from monocyte lineage

Front 85

Polycythemia vera

Back 85

Symptoms: increased RBCs, WBCs, and platelets, JAK2 positive (hematopoietic growth factor signaling), decreased erythropoietin
Pathogenesis: abnormal clone of hematopoietic stem cells increasingly sensitive to growth factors

Front 86

Essential thrombocytosis

Back 86

Symptoms: increased platelets, 50% JAK2 positive
Pathogenesis: specific abnormal clone of megakaryocytes

Front 87

Myelofibrosis

Back 87

Symptoms: decreased RBCs, 50% JAK2 positive
Pathogenesis: fibrotic obliteration of bone marrow

Front 88

CML

Back 88

Symptoms: decreased RBCs, increased WBCs, increased platelets, bcr-abl positive
Pathogenesis: bcr-abl transformation causes increased cell division and inhibition of apopsosis

Front 89

Heparin

Back 89

Mechanism: catalizes activation of antithrombin III -> decreases thrombin and Xa
Use: anticoagulant, doesn't cross placenta, follow PTT
Toxicity: bleeding, heparin-induced thrombocytopenia (binds to platelets and induces autoantibodies), osteoporosis
Antidote: protamine sulfate (binds heparin)

Front 90

Warfarin

Back 90

Mechanism: interferes with gamma-carboxylation of vit K dependent clotting factors II, VII, IX, X, proteins C and S, metabolized by P450, effect on extrinsic pathway (increases PT)
Clinical use: not in pregnancy, follow PT/INR
Toxiicty: bleeding, teratogenic, skin/tissue necrosis

Front 91

Hemolytic uremic syndrome

Back 91

Symptoms: microangiopathic hemolytic anemia, helmet cells, normal coagulation, fever, renal failure, thrombocytopenia
Pathogenesis: endothelial cell injury forms microthrombi, which damage RBCs