Basem Goueli's Heme Onc Flashcards
(219 cards)
1
Q
Erythrocytes
A
Live for 120 days; 100% of energy is from glucose (10% used for HMP shunt, 90% energy); membrane contains chloride/Bicarbonate antiporter;
2
Q
Platelets/Thrombocyte
A
Involved in primary hemostasis, derived from megakaryoctye, lives for 8 to 10 days, Contains dense granules (ADP and calcium) and alpha granules (vWF, fibrinogen). about 1/3 of platelet pool is stored in spleen
3
Q
what is the vWF receptor
A
GpIb
4
Q
what is the fibrinogen receptor
A
GpIIb/IIIa
5
Q
What are the granulocytes
A
neutrophils, eosinophils, basophils;
6
Q
What are the mononuclear cells
A
monocytes and lymphocytes
7
Q
What is the normal WBC differential %
A
Neutrophils (54 to 62), Lymphocytes (25-33), Monocytes (3-7), Eosinophils (1-3), Basophils (0-.75)
8
Q
Neutrophil
A
acute inflammatory response cell. Small Granules contain ALP, collagenase, lysozymes, lactoferrin; Larger granules (lysosomes) contain proteinases, acid phosphatase, myeloperoxidase, beta-glucuronidase
9
Q
Hypersegmented neutrophils (5 or more lobes) seen in
A
Vit b12/folate deficiency
10
Q
Increased neutrophil “band cells” seen in
A
immature neutrophils seen in states of increased myeloid proliferation (bacterial infections, CML)
11
Q
Monocyte
A
differentiates into macrophages in tissues; Large, kidney shaped nucleus, “frosted glass” cytoplasm
12
Q
macrophage: activated by? Functions?
A
activated by gamma interferon; can be a MHC class II antigen presenting cell; phagocytoses stuff; important in granuloma formation
13
Q
Eosinophils
A
defend against hemonthic infections (using major basic protein), Bilobate nucleus, highly phagocytic for antigen antibody complexes. Produces histamine and arylsulfastase (helps limit reaction following mast cell degranulation)
14
Q
Causes for eosinophilia
A
Always pronounce Eosinophilia like a stereotypically black person: NAACP! N=neoplasia, A=Asthma, A=Allergic processes, C=Connective tissue, P=Parasites
15
Q
Basophils
A
Mediates allergic responses, Densely basophilic granules, contain heparin, histamine, and leukotrienes
16
Q
Isolated Basophilia: what is going on
A
Super rare; can be sign of myeloproliferative state such as CML
17
Q
Mast cell
A
mediates allergic reaction in local tissues, Can bind the Fc portion of IgE to membrane. IgE cross links upon antigen binding, causing degranulation, which releases histamine, heparin, and eosinophil chemotactic factors; involved in Type I hypersensitivity reactions. Cromolyn sodium prevents mast cell degranulation.
18
Q
Dendritic cell
A
Highly phagocytic APC. Is a link between innate and adaptive immune system. Called langerhans cell in the skin, expresses MHC class II and Fc receptor on surface
19
Q
Lymphocytes
A
Divided into B cells, T cells, and NK cells. B cells and T cells mediate adaptive immunity. NK cells are part of the innate immune response. Round densely staining nucleus with small amounts of pale cytoplasm.
20
Q
B lymphocytes
A
part of humoral (antibody mediated) immune response; arises from stem cells in bone marrow; matures in marrow; migrates to peripheral lymphoid tissue (follicles of lymph nodes, white pulp of spleen, unencapsualted lymphoid tissue). When antigen is encountered, B cells differentiate into plasma cells that produce antibodies, and memory cells. Can function as an APC via MHC II
21
Q
T lymphocytes
A
Mediates cellular immune response, originates from stem cells in the bone marrow, but matures in thymus. T cells differentiate into Cytotoxic T cells (CD8, recognize MHC I), helper T cells (CD4 recognize MHC II), and regulatory T cells, CD28 (costimulatory signal) necessary for T cell activation. The majority of circulating lymphocytes are T cells (80%).
22
Q
Plasma cells
A
Produces large amounts of antibody specific to a particular antigen. Eccentric nucleus. Clock faced chromatin distribution, abundant RER, well developed Golgi.
23
Q
Multiple Myeloma is a caner of what cells
A
plasma cells
24
Q
Blood group A
A
A antigen on RBC surface and anti B antibody in plasma
25
Blood group B
B antigen on RBC surface and Anti A antibody in plasma
26
Blood group AB
A and B antigen on RBC surface; no antibodies in plasma; universal recipient of RBCs; universal donor of plasma
27
Blood group O
Neither A or B antigen on RBC surface; both anti A and anti B antibodies in plasma; universal donor of RBC, universal recipient of plasma.
28
Rh factor
Rh antigen on RBC surface. Rh- mothers exposed to fetal Rh + blood (often through delivery) may make anti-Rh IgG. In next pregnancies anti Rh IgG can cross placenta causing hemolytic disease of the newborn (erythroblastosis fetalis) in the next Rh+ fetus. treat with Rho(D) immune globulin
29
What does Rho(D) immune globulin do
For mother who is Rh-. Protects against initial sensitization of Rh- mom.
30
Hemophilia A is a deficiency in
Factor VIII
31
Hemophilia B is a deficiency in
Factor IX
32
Vitamin K deficiency
decreased synthesis of factors II, VII, IX, X, protein C, protein S.
33
vWF carries/protects what factor?
VIII
34
Protein C pathway for anticoagulation
Protein C goes through Thrombin-thrombomodulin complex (endothelial cells) to become activated protein C. Protein S takes Activated C and cleaves and inactivates Va and VIIIa
35
Plasminogen pathway for anticoagulation
Plasminogen is activated to plasmin via tPA causing fibrinolysis (cleavage of fibrin mesh and destruction of coagulation factors)
36
Antithrombin inhibits what
inhibits active forms of factors II, VII, IX, X, XI, XII; antithrombin activity is enhanced several fold by heparin; Principal targets of antithrombin are thrombin and factor Xa
37
Go through primary hemostasis (platelet plug formation)
1) injury (vWF binds to exposed collagen upon endothelial damage); 2) Adhesion (platelets bind vWF via GpIb receptor at site of injury (specific), platelets release ADP and Ca, ADP helps platelets adhere to endothelium and ADP helps with activation; 3) ADP binding to receptor induces GpIIb/IIIa expression at platelet surface; 4) Aggregation (fibrinogen binds GpIIb/IIIa receptors and links platelets and this temporary plug stops bleeding but it is held by a balance of pro-aggregation factors and anti-aggregation factors)
38
Primary hemostasis: Pro-aggregation factors
TXA2 (released by platelets), Decreased blood flow, Increased platelet aggregation
39
Primary hemostasis: Anti-aggregation factors
PGI2 and NO (Released from endothelial cells), increased blood flow, decreased platelet aggregation
40
Aspirins effect on thrombogenesis
Inhibits cyclooxygenase (which stops TXA2, which is a pro-aggregation factor)
41
Ticlopidine
inhibit ADP induced expression of GpIIb/IIIa; can cause neutropenia (use clopidogrel instead); synergistic with aspirin
42
Clopidogrel
inhibits ADP induced expression of GpIIb/IIIa; synergistic with aspirin
43
Abciximab
inhibits GpIIb/IIIa directly
44
Ristocetin
Activates vWF to bind to GpIb. Useful for diagnosis: normal platelet aggregation response is not seen in willebrand disease
45
Erythrocyte sedimentation rate
Acute phase reactants in plasma (e.g. fibrinogen) can cause RBC aggregation, thereby increasing RBC sedimentation rate (RBC aggregates have a higher density than plasma).
46
Decreased ESR is a sign of
polycythemia, sickle cell anemia, CHF, microcytosis, hypofibrinogenemia
47
Increased ESR is a sign of
infection, autoimmune disease, malignant neoplasms, GI diseases, pregnancy
48
Acanthocyte
RBC pathology
AKA a spur cell;
Associated with liver disease, abetalipoproteinemia (cholesterol dysregulation);
Acantho means spiny, looks like red ball with spikes
49
Basophilic stippling
pathologic RBC, round dark RBC, spotted with dark granules;
Associated with Anemia of chronic disease, alcohol abuse, lead poisoning, Thalassemias (BASIClly, ACiD alcohol is LeThal)
50
Bite cell
pathologic RBC
| Associated with G6PD deficiency
51
Elliptocyte
pathologic RBC
| Associated with Hereditary elloptocytosis! Never would have guessed!
52
Macro-ovalocyte
pathologic RBC
Associated with megaloblastic anemia (also get hypersegmented PMNs), marrow failure;
Bot blueish circular RBC
53
Ringed sideroblast
pathologic RBC
Sideroblastic anemia, excess iron in mitochondria=pathologic;
Looks like normal RBC but with tons of dark dots around mitochondira
54
Schistocyte, Helmet cell
pathologic RBC, looks like evil characters from pac-man;
| Associated with DIC, TPP/HUS, traumatic hemolysis (like a mechanical heart valve)
55
Spherocyte
pathologic RBC;
Just a red ball with no central pallor;
Hereditary spherocytosis, autoimmune hemolysis
56
Teardrop cells
pathologic RBC;
look like fat sperm;
Associated with bone marrow infiltration (like myelofibrosis);
RBCs "shed a tear" because it's been forced out of its home in the bone marrow"
57
Target cell
pathologic RBC
Literally looks like the Target Store Logo;
Associated with HbC disease, Asplenia, Liver disease, Thalassemia;
"HALT, I have you targeted!"
58
Heinz bodies
pathologic RBC;
RBC with big spots of blue in it;
From the oxidation of hemoglobin sulfhydryl groups leading to denatured hemoglobin precipitation and phagocytic damage to RBC membrane causing bite cells;
Visualized with special stains like crystal violet;
Seen in G6PD deficiency;
59
Howell-Jolly Bodies
pathologic RBC;
Looks like RBC with 1 singular blue splotch;
Basophilic nuclear remnants found in RBCs. Normally Howell-Jolly bodies are removed by splenic macrophages;
See in patients with function hyposplenia or asplenia.
60
Differential Diagnosis for anemia with MCV being less than 80
Microcytic anemia; iron deficiency, Anemia of chronic disease, Thalassemias, Lead poisoning, sideroblastic anemia
61
Iron deficiency anemia
Decreased iron due to increased bleeding (GI loss or menorrhagia), malnutrition/absoprtion disorders or increased demand (e.g. pregnancy) causing decreased final step in heme synthesis;
Findings: increased TIBC, Decreased ferritin, fatigue, conjunctival pallor, microcytosis and hypochromia of RBCs. May present as plummer Vinson syndrome
62
What is the triad of plummer vinson syndrome
Iron deficiency anemia, esophageal webs, atrophic glossitis
63
Alpha thalassemia
Defect in alpha globin gene deletions causing decreased alpha globin synthesis;
Cis deletion prevalent in Asiain populations; trans deletion prevalent in african populations;
Get 4 allele deletion: no alpha globin, excess gamma globin froms gamma4 (Hb Barts). Will die (hydrops fatalis)
Get 3 allele deletion: HbH disease. Very little alpha globin, excess beta globin (beta 4 or HBH). Get heinz bodies;
Get 1-2 deletion; nothing significant (with 2 may get hypochromic microcytic anemia that shows some target cells, maybe)
64
Beta thalassemia
Point mutation in splice sites and promoter regions leading to decreased beta globin synthesis; prevalent in mediterranean populations.
65
Beta thalassemia minor
Heterozygote; beta chain is underproduced;
Usually asymptomatic;
Diagnosis confirmed by increased HbA2 (>3.5%) on electrophoresis
66
Beta Thalassemia major
homozygote;
Beta chain is absent causing severe anemia requiring blood transfusions (get secondary hemochromatosis);
Get Marrow expansion causing skeletal deformities (crew cut on skull x ray (also seen in sickle cell), chipmunk face)
Get extramedullary hematopoiesis: leads to hepatoosplenomegaly. Increased risk of parvovirus B19 induced aplastic crisis.
Increased HbF (alpha2gamma2) is protective in infant and disease becomes symptomatic after 6 months
67
Lead poisoning
Lead inhibits ferrochelatase and ALA dehydratase leading to decreased heme synthesis and increased RBC protoporhyrin;
Also inhibits rRNA degradation, causing RBCs to retaion aggregates of rRNA (basophilic stippling);
High risk in old houses with chipping paint
Treat: Dimercaprol and Succimer used for chelation in kids.
68
Lead poisoning: physical exam findings
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 of wrist and foot.
69
Sideroblastic anemia
```
Defect in heme synthesis;
Hereditary: X linked defect in delta ALA synthase gene;
Causes of it: genetic, acquired (myelodysplastic syndromes) and reversible (alcohol is most common, lead, vit b6 deficiency, copper deficiency, and isoniazid);
Ringer sideroblasts (iron in mitochondria) seen in bone marrow. Increased Iron, Normal TIBC, increased ferritin.
Treatment with pyridoxine (b6, cofactor for delta-ALA)
```
70
Folate deficiency
Macrocytic anemia
Caused by: malnutrition, malabsorption, anitfolates (methotrexate, trimethoprim, phenytoin), increased requirement (e.g. hemolytic anemia, pregnancy)
See: hypersegmented PMNs, glossitis, decreased folate, increased homocysteine but normal methylmalonic acid. No neurologic symptoms (distinguishes from B12 deficiency)
71
B12 Deficiency
Macrocytic anemia
Caused by: insufficient intake (strict vegans), malabsorption (e.g. crohns), pernicious anemia, Diphyllobothrium latum (fish tapeworm), PPI's
Get: hypersegmented PMNs, glossitis, decreased B12, increased homocysteine, increased methylmalonic acid
72
What are the neurologic symptoms of B12 deficiency
Subacute combined degeneration (due to involvement of B12 in fatty acid pathways and myelin synthesis: Peripheral neuropathy with sensorimotor dysfunction, Dorsal columns (vibration/proprioception), Lateral corticospinal (spasticity), Dementia
73
Orotic aciduria
Megaloblastic anemia;
Inability to convert orotic acid to UMP (de novo pyrimidine synthesis pathway) because of defect in UMP synthase. Autosomal recessive. Presents in children as megaloblastic anemia that cannot be cured by folate or B12 with failure to thrive. No hyperammonemia (vs. ornithine transcarbamylase deficiency which increases orotic acid with hyperammonemia)
See: hypersegmented PMNs, glossitis orotic acid in urine;
Treatment: Uridien monophophate to bypass mutated enzyme.
74
Nonmegaloblastic macrocytic anemias
Macrocytic anemia in which DNA synthesis is not impaired. Caused by: liver disease, alcoholism, reticulocytosis leading to increased MCV; drugs (5-FU, zidovudine, hydroxyurea)
Macryocytosis and bone marrow suppression can occur in the absence of folate/B12 deficiency.
75
Intravascular hemolysis
See normocytic, normochromic anemia;
Findings: decreased haptoglobin, increased LDH, schistocytes and increased reticulocytes on blood smear; and urobilinogen in urine; e.g. paroxysmal nocturnal hemoglobinurea, mechanical destruction, microangiopathic hemolytic anemias
76
Extravascular hemolysis
See normocytic, normochromic anemia;
Findings: macrophage in spleen clears RBC. Spherocytes in peripheral smear, increased LDH plus increased unconjugated bilirubin, which causes jaundice (e.g. hereditary spherocytosis)
77
Anemia of chronic disease
Non hemolytic, normoctyic anemia;
inflammation leads to increased hepcidin (released by liver, binds ferroportin on intestinal mucosal cells and macrophages, this inhibiting iron transport) leading to decreased release of iron from macrophages;
Labs Show: decreased iron, decreased TIBC, increased ferritin, can become microcytic, hypochromic with time
78
Aplastic anemia
Nonhemolytic, normocytic anemia;
Caused by failure or destruction of myeloid stem cells due to: Radiation or drugs (benzene, chloramphenicol, alkylating agents, antimetabolites), Viral agents (parvovirus B19, EBV, HIV, HCV), Fanconi anemia (DNA repair defect), Idiopathic (immune mediated, primary stem cell defect), may follow acute hepatitis;
See all bone cell lines decreased, fatty marrow, fatigue, easily bleeds/bruises
79
Hereditary spherocytosis
Extravascular anemia;
Defect in proteins interacting with RBC membrane skeleton and plasma membrane (e.g. ankyrin, band 3, protein 4.2, spectrin). Less membrane causes small and round RBCs with no central pallor (increased MCHC, increased RBC distribution width) causing premature RBC removal by spleen;
Splenomegaly, aplastic crisis with parvoB19 infection, gallstones made of black pigment;
Labs: osmotic fragility test +, Eosin-5-maleimide binding test useful for screening, normal to decreased MCV with abundance of cells, masks microcytia;
Treat: splenectomy
80
G6PD
intra and extravascular anemia;
most common enzymatic deficiency in RBCs;
X linked recessive;
Defect in G6PD leads to decreased glutathione causing increased RBC susceptibility to oxidant stress. Hemolytic anemia following oxidant stress (sulfa drugs, antimalarials, infections, fava beans);
Back pain and hemoglobinuria a few days after stressor;
Labs: blood smear shows RBCs with Heinz bodies and bite cells.
81
Pyruvate kinase Deficiency
Extravascular anemia;
Autosomal Recessive;
Defect in pyruvate kinase leading to decreased ATP causing rigid RBCs;
Get hemolytic anemia in a newborn
82
HbC defect
Extravascular anemia;
Glutamic acid to lysine mutation at residue 6 in beta globin;
Patients with HbSC (1 of each mutant gene have milder disease than have HbSS patients)
83
Paroxysmal nocturnal hemoglobinuria
Intravascular anemia and you urinate dark red/brown;
Increased complement mediated RBC lysis (impaired synthesis of GPI anchor for decay-accelerating factor that protects RBC membrane from complement-CD55/59). Acquired mutation in a hematopoietic stem cell. Increased incidence of acute leukemias.
Triad: Coombs negative hemolytic anemia, Pancytopenia, and venous thrombosis, increased chance of pigmented gall stones;
Labs: CD55/59 Negative RBCs on flow cytometry.
Treat: eculizumab
84
Sickle cell anemia
Extravascular anemia;
HbS point mutation (substitution of glutamic acid with valine) in beta chain at position 6;
Pathogenesis: Low O2, dehydration, or acidosis precipitates sickling (deoxygenated HbS polymerizes), which results in anemia and vasc-occulsive disease, Spleen will be enlarged in first decade then atrophy due to infarcts and become small, bone marrow expansion to increase RBC #;
Newborns usually have HbF so they don't show symptoms;
Heterozygotes resistant to malaria, 8% of blacks carry HbS trait
Diagnose: hemoglobin electrophoresis
Treat: hydroxyurea (increase HbF), and bone marrow transplant
85
Complications with Sickle Cell
Aplastic crisis (due to parvoB19);
Autosplenectomy (howell-jolly bodies) causing increased risk of infection by encapsulated organisms; early splenic dysfunction happens in childhood;
Splenic sequestration crisis;
Salmonella osteomyelitis;
Painful crisis: dactylitis, acute chest syndrome (most common cause of death in adults), avascular necrosis, stroke;
Renal papillary necrosis (Due to low O2 in papilla, also seen in heterozygotes) and microhematuria (medullary infarcts).
86
Where in the Kidneys is a sickle cell anemia likely to infarct
Vasa recta has increased osmolarity (cells sickle with increased osmolarity); the renal medullar shows patchy papillary necrosis causing proteinuria, renal scarring.
87
Autoimmune Hemolytic anemia: Warm agglutination
IgG, chronic anemia seen in SLE, CLL, and drugs (like alpha methlydopa), Warm Weather is GGGreat;
Coombs +
88
Autoimmune hemolytic anemia: cold agglutination
acute anemia triggered by cold; seen in CLL, mycoplasma pneumonia infections, or infectious mono
89
Microangiopathic anemia
pathogenesis: RBCs are damaged when passing through obstructed or narrowed vessel lumina. Seen in DIC, TPP-HUS, SLE an malignant HTN.
Find: schistocytes (helmet cells) seen on blood smear due to mechanical damage to RBCs
90
Macroangiopathic anemia
Prosthetic heart valves and aortic stenosis may also cause hemolytic anemia secondary to mechanical destruction.
Schistocytes on peripheral blood smear.
91
Labs in iron deficiency anemia
Decreased serum iron, Increased TIBC (indirectly measures transferrin), decreased Ferritin, Decreased % transferrin saturation
92
Labs in anemia of chronic disease
Decreased serum iron, increased ferritin, decreased TIBC (measures transferrin indirectly)
93
Labs in anemia due to hemochromatosis
Increased serum iron, Decreased TIBC, increased ferritin, increased %transferrin saturated
94
Labs in anemia due to pregnancy or OCPs
increased transferrin/TIBC, decreased % transferrin saturation.
95
Neutropenia: what is it, cause
Neutrophil count
96
Lymphopenia: what is it, cause
Lymphocyte count
97
Eosinopenia: causes
Cushing syndrome, corticosteroids
98
Lead poisoning: enzymes and effects
Effects the ferrochelatase and ALA dehyratase enzymes;
Accumulation of protoporphyrin delta-ALA (blood);
Presents as Microcytic anemia, GI and kidney disease. Children get exposure and have mental issues, Adults get headache, memory loss, demylination
99
Acute intermittent porphyria: enzymes and effects
Effects the Porphobilinogen deaminase enzyme;
Accumulation of Porphobilinogen, delta ALA, coporphobilinogen (in urine);
Symptoms are the 5 Ps: Painful abdomen, Port wine colored urine, Polyneuropathy, Psychological disturbances, Precipitated by drugs, EtOH, starvation
Treat: Glucose and heme, which inhibit ALA synthase
100
Porphyria cutanea tardia: enzymes and effects
effects Uroporphyrinogen decarboxylase enzyme;
leads to accumulation of uroporhyrin (tea-colored urine);
Blistering cutaneous photosensitivity. Most common porphyria
101
PT test does what
Tests function of common and extrinsic pathway (I, II, V, VII, and X). Defect leads to increased PT
102
PTT test does what
Tests function of common and intrinsic pathways (tests everything BUT VII and XIII)
103
Hemophilia A and B lead to what changes in PT and PTT
```
No change in PT (extrinsic pathway is fine)
Increased PTT (intrinsic is not okay);
Hemophilia A is defect in VIII;
Hemophilia B is defect in IX;
Why you get easy to bruise and bleeding into joints
```
104
Vit K deficiency leads to what changes in PT and PTT
Increased PT and PTT;
General coagulation defect, but bleeding time is normal. Decreased synthesis of factors II, VII, IX, X, protein C and S;
Just like a patient on Warfarin
105
Defects in platelet plug formation lead to an increase in
bleeding time
106
Bernard-Soulier Syndrome
Decreased Platelet count, increased Bleeding time;
| Defect in platelet plug formation; decreased GpIb causing defect in platelet to vWF adhesion
107
Glanzmann thrombastenia
no change in platelet count, increased bleeding time;
Defect in platelet plug formation, decreased GpIIb/IIIa causing defect in platelet to platelet aggregation;
Labs: blood smear shows no platelet clumping
108
Idiopathic (immune) thrombocytopenia purpura
Decreased platelet count and increased Bleeding time;
Defect: anti-GpIIb/IIIa antibodies causing splenic macrophage consumption of platelet/antibody complex. May be triggered by viral illness (acute version). Decreased platelet survival;
Labs: increased megakaryoctyes on bone marrow biopsy
109
Thrombotic Thrombocytopenic purpura
Decreased Platelet count, increased bleeding time;
Inhibition or deficiency in ADAMTS13 (vWF metalloprotease) causing decreased degradation of vWF multimers.
Pathogenesis: Increased large vWF multimers cause increased platelet adhesion causing increased platelet aggregation and thrombosis. Decreased platelet survival.
Symptoms: pentad of neuro and renal symptoms, fever, thrombocytopenia, and microangiopathic hemolytic anemia.
Treat: exchange transfusion and steroids
110
von Willebrand Disease
Intrinsic pathway coagulation defect: decreased vWF causing normal to increased PTT(because it carries factor 8); Defect in platelet plug formation (decreased vWF causes decreased vWF to platelet adhesion);
Autosomal dominant, most common inherited bleeding dysorder;
Labs: normal platelet count, increased bleeding time, normal PT, increased or normal PTT
Diagnosed by ristocetin cofactor assay (see decreased agglutination)
Treat: DDAVP, which releases vWF stored in endothelium
111
DIC
Widespread activation of coagulation cascade leading to deficiency in clotting factors, which creates a bleeding state.
Causes: sepsis (gram -), Trauma (cytokine release), Obstetric complication, acute Pancreatitis, Nephrotic syndrome, Transfusion
Labs: Schistocytes, increased fibrin split products (D-dimers), decreased fibrinogen, decreased factors V and VIII.
See: decreased platelet count, increased bleeding time, increased PT, increased PTT.
112
Factor V Leiden Disease
Production of mutant Factor V that is resistant to degradation by activated protein C. Most common cause of inherited hypercoagulability in whites.
113
Prothrombin gene mutation
Mutation in 3' untranslated regions causing increased production of prothrombin leading to increased plasma levels and venous clots
114
Antithrombin deficiency
Inherited deficiency of antithrombin: has no direct effect on PT or PTT or thrombin time, but diminishes the increase in PTT following heparin administration.
Can also be acquired: renal failure/nephrotic syndrome causes antithrombin loss in urine causing increased factors II and X
115
Protein C and S deficiency
Decreased ability to inactivate factors V and VIII. increased risk of thrombotic skin necrosis with hemorrhage following administration of Warfarin. Skin and subcutaneous tissue necrosis after warfarin administration, think protein C deficiency.
116
Packed RBCs
Increases Hb and O2 carrying capacity;
| Used for acute blood loss, severe anemia
117
Platelets given IV
Increases platelet counts (~5000 per unit given);
| stop significant bleeding
118
Fresh frozen plasma
Increase coagulation factor levels;
| Used for DIC, cirrhosis, Warfarin overdose, exchange transfusion in TPP/HUS
119
Cryoprecipitate
Contains Fibrinogen, factor VIII, factor XIII, vWF, and fibronectin:
Treats: coagulation factor deficiencies involving fibrinogen and factor VIII
120
Leukemia Vs. Lymphoma
Leukemia is Lymphoid or myeloid neoplasms with widespread involvement of bone marrow. Tumor cells are usually found in peripheral blood;
Lymphoma is discrete tumor masses arising form lymph nodes. Presentations often blur definitions
121
Leukemoid reaction
Acute inflammatory response to infection. Increased WBC count with increased neutrophils and neutrophil precursors such as band cells (left shift); increased leukocyte ALP. contrast with CML (also increase WBC count with left shift, but decrease leukocyte ALP)
122
Hodgkin Lymphoma
Localized, single group of nodules; extranodal rare; contiguous spread (stage is strongest predictor of prognosis). Prognosis is much better than non-hodgkin.
Characterized by Reed-Sternberg cells;
Bimodal distribution with young adulthood and >55 years; more common in men except for nodular sclerosing type;
50% of cases associated with EBV;
Constitutional ("B") symptoms: low grade fever, night sweats, weight loss
123
Non-Hodgkin lymphoma
Multiple peripheral nodes; extranodal involvement common; noncontiguous spread;
Majority involve B cells (some are lymphoblastic T cell type);
Peak incidence for many subtypes is 20-40 years old;
May be associated with HIV and immunosuppression;
Fewer constitutional signs and symptoms
124
Reed-sternberg cells
Distinctive tumor giant cell seen in Hodgkin disease; binucleate or bilobed with 2 halves as mirror images ("owl eyes"). RS cells are CD 15+ and CD 30+ B cell origin. Necessary but not sufficient for Hodgkin disease diagnoses. Better prognosis with strong stromal or lymphocytic reaction against RS cells. Nodular sclerosing form most common (affects genders equally). Lymphocyte rich form has best prognosis. Lymphocyte mixed or depleted forms have poor prognosis. "2 owl eyes x 15=30"
125
Burkitt Lymphoma
Non hodgkin lymphoma: B cell origin
Occurs in: adolescents or young adults;
Genetics: (8;14) translocation of c-myc (8) (activation of c-myc) and heavy chain Ig (14);
"Starry sky appearance," sheet of lymphocytes with interspersed macrophages and white clearings between;
Associated with EBV;
Jaw lesion in endemic form in Africa, and lesion on pelvis or abdomen (ovaries, bowel, retroperitoneum) in sporadic form
126
Diffuse Large B cell Lymphoma
Non-hodgkin lymphoma: B cell origin
Usually older adults, but 20% are kids;
Genetics: t(14;18);
Most common type of non-hodgkin lymphoma in adults
127
Mantle cell lymphoma
Non hodgkin lymphoma; B cell origin
Older males get this;
Genetics: t(11;14) translocation of cyclin D1 (11) and heavy chain Ig (14);
CD5+
128
Follicular lymphoma
Non-hodgkin lymphoma; B cell origin
Adults get this;
Genetics: t(14;18) translocation of heavy chain Ig (14) and bcl-2 (18);
Indolent course; bcl-2 inhibits apoptosis. Presents with painless "waxing and waning" lymphadenopathy; Palpable spleen and liver, See CD10, CD19, CD29
129
Adult T cell lymphoma
Non Hodgkin lymphoma; T cell origin;
Usually in adults;
Caused by HTLC-1 (associated with IV drug use);
Adults present with cutaneous lesions; especially affects populations in Japan, West africa, and the Caribbean;
Lytic bone lesions, hypercalcemia
130
Mycosis fungiodes/Sezary syndrome
Non-hodgkin lymphoma; CD4+ T cell origin;
Usually in Adults;
Adults present with cutaneous patches/plaques/tumors with potential to spread lymph nodes and viscera. Circulating malignant cells seen in Sezary syndrome. Indolent.
131
Multiple Myeloma: what is it, who gets it
Monoclonal plasma cell cancer that arises in the marrow and produce large amount of IgG (55%) or IgA (25%). Most common primary tumor arising within bone of the elderly (. 40-50 years old).
132
Multiple myeloma: Associated with
Increased susceptibility to infection; Primary amyloidosis (AL); Punched out lytic bone lesions on x rays; M spike on serum protein electrophoresis; Ig light chains (most likely IgG light chains) in urine (Bence Jones protein); Rouleaux formation (RBCs stacked like poker chips in blood smear); Russel bodies in cytoplasm of plasma cells (white circular lesions made up of Ig)
133
Multiple Myeloma: CRAB
hyperCalcemia, Renal insufficiency, Anemia, Bone lytic lesions/back pain;
Also Multiple Myeloma: monoclonal M protein spike
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Waldenstrom macroglobulinemia
It has an M spike like Multiple Myeloma but it is IgM; You get hyperviscosity symptoms, no lytic bone lesions
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Monoclonal gammopathy of undetermined significance (MGUS)
Monoclonal expansion of plasma cells with serum monoclonal protein
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Myelodysplastic Syndrome
Stem cell disorders involving ineffective hematopoiesis leading to defects in cell maturation of all non-lymphoid lineages. Caused by de novo mutations of environmental exposure (e.g. radiation, benzene, chemotherapy). Risk of transformation to AML.
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Pseudo-Pelger-Huet anomaly
neutrophils with bilobed nuclei (two nuclear masses connected with a thin filament of chromatin). Typically seen after chemotherapy.
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Lymphoma
Unregulated growth of leukocyte in bone marrow leading to increase or decreased number of circulating leukocyte in blood and marrow failure leading to anemia (decreased RBC), infections (decreased mature WBCs), and hemorrhage (decreased platelets); leukemic cell infiltrates in liver, spleen, and lymph nodes are possible
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Acute Lymphoblastic leukemia/lymphoma (ALL)
Lymphoid neoplasm
| Age:
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Small lymphoblastic lymphoma (SLL)/ Chronic Lymphocytic Leukemia (CLL)
Age: >60 years old. CD20+, CD5+ B cell neoplasm. Often asymptomatic, progresses slowly, smudge cells in blood smear (leukocytes that are smashed open);
Autoimmune hemolytic anemia.
SLL same as CLL except CLL has increased peripheral blood lymphocytosis or bone marrow involvement.
Can progress to B cell lymphoma (Richter transformation)
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Hairy cell leukemia
Age: adults. Mature B cell tumor in the elderly. Cells have filamentous hair like prjections.
Get recurrent infections due to decreased WBC count; splenomegaly;
Neoplastic cells have positive B cell markers of CD19, 20, IgG surface molecules, kappa and lamda light chains and monocyte surface proteins of CD11c and CD25;
Stains TRAP (tartrate-resistant acid phosphate +). TRAP stain largely replaced by flow cytometry. Causes marrow fibrosis leading to dry tap on aspiration.
Treat: cladribine (2-CDA), and adenosine analog (inhibits adenosine deaminase)
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Acute Myelogenous Leukemia (AML)
Age: median onset 65 years;
See Auer rods, peroxidase + cytoplasmic inclusions seen mostly in M3 AML; Increased circulating myeloblasts on blood smear.
Risk factors: Exposure to alkylating chemo, radiation, myeloproliferative disorders, Down syndrome.
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AML with t(12;17)
M3 AML; Responds to all-trans retinoic acid (vitamin A) by inducing differentiation of myeloblasts. DIC is a common presentation in M3 and can be induced by chemotherapy due to release of Auer Rods.
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Chronic Myelogenous Leukemia (CML)
Age: peak incidence 45-85 years old. Median age is 64;
Defined by philadelphia chromosome (t(9;22), bcr-abl);
Myeloid stem cell proliferation;
presents with increased neutrophils, metamyelocytes (immature neutrophils), basophils; hepatosplenomegaly; may accelerate and transform to AML or ALL ("blast crisis").
Very low leukocyte alkaline phosphatase (LAP) as a result of low activity in mature granulocytes (vs. leukemoid reaction, in which LAP is increased).
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t(9;22)
Philadelphia chromosome;
get CML;
bcr-abl hybrid
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t(8;14)
Burkitt lymphoma; (c-myc activation)
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t(11;14)
Mantle cell lymphoma (cyclin D1 activation)
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t(14;18)
Follicular lymphoma (bcl-2 activation)
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t(15;17)
M3 type of AML (responsive to all-trans retinoic acid)
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langerhans cell histiocytosis
Proliferative disorders of dendritic (langerhans) cells from moncyte lineage. Presents in a child as lytic bone lesions and skin rash or as recurrent otitis media with a mass involving the mastiod bone. Cells functionally immature and do not efficiently stimulate primary T lymphocytes via antigen presentation. Cells express S-100 (mesodermal origin) and CD1a. Birbeck granules ("tennis rackets" on EM) are characteristic.
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Chronic myeloproliferative disorders
represent an often-overlapping spectrum, but there are classic findings. JAK2 is involved in hematopoietic growth factor signaling. Mutations are implicated in myeloproliferative disorders other than CML.
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Polycythemia vera
chronic myeloproliferative disorder;
Hematocrit >55%, somatic (non-hereditary) mutation in JAK2 gene. Often presents as intense itching after hot shower. Rare but classic symptom is erythomegalia (severe burning pain and reddish or bluish coloration) due to episodic blood clots in vessels of the extremities. Secondary polycythemia is via natural or artificial increase in EPO levels.
In primary polycthemia vera there is a decreased EPO.
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Essential thrombocytosis
chronic myeloproliferative disorder;
similar to polycythemia vera, but specific for overproduction of abnormal platelets leading to bleeding thrombosis. Bone marrow contains enlarged megakaryocytes.
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Myelofibrosis
chronic myleoproliferative disorder;
Fibrotic obliteration of bone marrow. Teardrop RBCs and immature forms at the myeloid line. "bone marrow is crying because it's fibrosed"
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Labs and genetics in polycythemia vera
increased RBCs; increased WBCs; Increased platelets; JAK2 mutation
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Labs and genetics in Essential thrombocytosis
Normal RBCs, Normal WBCs, Increased Platelets, increased JAK2 mutations (30-50%)
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Labs and genetics in Myelofibrosis
Decreased RBCs, Variable WBCs, Variable platelets, JAK2 mutations (30-50%)
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Labs and genetics in CML
decreased RBCs, Increased WBCs, Increased platelets, + philadelphia chromosome mutation.
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Heparin
cofactor for the activation of antithrombin, decreased thrombin, and decreased factor Xa, Short half life;
Used for immediate anticoagulation for PE, acute coronary syndrome, MI, DVT. Used during pregnancy (does not cross placenta. Follow aPTT.
Toxicity: bleeding, thrombocytopenia;
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Low molecular weight heparin
Enoxaparin, Dalteparin;
Act more on Factor Xa;
Better bioavailability and 2-4 times longer half life;
can be giving subcutaneously and without lab monitoring;
not easily reversed
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Heparin induced thrombocytopenia (HIT)
Development of IgG antibodies against heparin bound to platelet factor 4 (PF4). Antibody-heparin-PF4 complex activates platelets leading to thrombosis and thrombocytopenia. Give bivalirudin or argatroban after stopping heparin. May take a couple days to show up, but will look like purpuric non blanching lesions.
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Argatroban and bivalirudin
Derivatives of hirudin, the anticoagulant used by leeches;
inhibits thrombin directly;
Used instead of heparin for anticoagulating patients with HIT
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Mechanism of Warfarin
Interferes with norma synthesis of gamma carboxylation of vitamin K dependent clotting factors II, VI, IX, and X and proteins C and S (at therapeutic levels inhibits 7 (increased PT)
Metabolized by CYP450;
Has effect on Extrinsic pathway and increases PT
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Clinical use of Warfarin
Chronic anticoagulation after STEMI, venous thromboembolism prophylaxis, and prevention of stroke in A Fib.
Not used in pregnant women, crosses placenta;
Follow PT/INR values
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Toxicity of Warfarin
Bleeding, teratogenic, skin/tissue necrosis;
To reverse give Vitamin K, unless it is real bad then you give fresh frozen plasma.
At toxic levels it increases not only PT but also PTT,
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Direct Factor Xa inhibitor
Apixaban, Rivaroxaban;
Mechanism: bind and directly inhibit the activity of factor Xa;
Uses: Treat and prophylaxis of DVT and PE(rivaroxaban), stroke prophylaxis in patients with atrial fib. Do not need lab monitoring;
Toxicity would be bleeding and there are no reversal agents
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Thrombolytics
Alteplase (tPA), reteplase (rPA), tenecteplase (TNK-tPA);
Mechanism: directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increased PT, Increased PTT, no change in platelet counts;
Used for: Early MI, early ischemic strokes, Direct thrombolysis of PE;
Toxicity: bleeding
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Thrombolytics are causing bleeding, how are you going to do to reverse it
aminocaproic acid which is an inhibitor of fibrinolysis;
| Fresh frozen plasma and cryoprecipitate can also help.
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Aspirin
Irreversibly inhibits COX 1 and 2 by covalent acetylation;
increase bleeding time, decrease TXA2 and prostaglandins. No effect on PT or PTT;
Antipyretic, analgesic, anti inflammatory, antiplatelet (decreases aggregation);
Toxicity: GI ulceration, tinnitus (CN VIII), chronic use leading to acute renal failure, interstitial nephritis, upper GI bleed
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Reye syndrome
Give a kid aspirin when they have a viral infection;
| Kids gets respiratory alkalosis early then a superimposed metabolic acidosis takes over.
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ADP receptor inhibitors
Clopidegrel, ticlopidine, prasurgrel, ticagrelor;
Mechanism: inhibit platelet aggregation by irreversibly inhibiting ADP receptors, inhibits fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen ;
Uses: acute coronary syndrome, coronary stenting. Decreased incidence or recurrence of thrombotic stroke.
Toxicity: Neutropenia (ticlopidine). TTP/HUS may be seen
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Cilostazol, dipyridamole
Phosphodiesterase III inhibitors; increase cAMP in platelets, thus inhibiting platelet aggregation; vasodilators.
Use: intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (combined with aspirin), angina prophylaxis.
Toxicity: Nausea, headache, facial flushing, hypotension, ab pain
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GPIIb/IIIa inhibitors
Abciximab, eptifibatide, tirofiban;
Mechanism: bind to the glycoprotein receptor GP IIb/IIIa on activated platelets, preventing aggregation. Abciximab is made from monoclonal antibody Fab fragments.
Use: unstable angina, percutaneous transluminal coronary angioplasty;
Toxicity: Bleeding and thrombocytopenia
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What are the M phase cancer drugs
Vinca alkaloids and taxols
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What are the S phase cancer drugs
Etoposides and antimetabolites
176
What are the G2 phase cancer drugs
Bleomycin and etoposides
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Methotrexate: mechanism
Antimetabolite (S phase)
Folic acid analog that inhibits dihydrofolate reductase leading to decreased dTMP causing decreased DNA and decreased Protein synthesis
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Methotrexate: clinical uses
Cancers: leukemias, lymphomas, choriocarcinomas, sarcomas
| Non-neoplastic: abortion, ectopic pregnancy, rheumatoid arthritis, psoriasis, IBD
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Methotrexate: toxicity
Myelosuppresion, which is reversible with leucovorin (folinic acid);
Macrovesicular fatty change in liver;
Mucositis;
Teratogenic
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5-fluorouracil (5-FU): mechanism
Antimetabolite (S phase)
Pyrimidine analog bioactivated to 5F-dUMP which covalently complexes folic acid.
This complex inhibits thymidylate synthase leading to an increase in dTMP causing decreased DNA and protein synthesis
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5-fluorouracil: uses
Colon cancer, pancreatic cancer, basal cell carcinoma (topical)
182
5-fluorouracil: toxicity
Myelosuppression, which is not reversible with leucorvin.
Overdose treated with uridine;
photosensitivity
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Cytarabine (arabinofuranosyl cytidine): mechanism
Antimetabolite (S phase)
| Pyrimidine analog causes inhibition of DNA polymerase
184
Cytarabine (arabinofuranosyl cytidine): Uses
Leukemias, lymphomas
185
Cytarabine (arabinofuranosyl cytidine): Toxicity
Leukopenia, thrombocytopenia, megaloblastic anemia
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Azathiprine, 6-MP, 6-thioguanine (6-TG): Mechanism
Antimetabolite (S phase);
| Purine (thiol) analog leading to decreased de novo purine synthesis. Activated by HGPRT.
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Azathiprine, 6-MP, 6-thioguanine (6-TG): Uses
Prevents organ rejection, RA, SLE (azathioprine). Leukemia IBD (6-MP and 6-TG)
188
Azathiprine, 6-MP, 6-thioguanine (6-TG): Toxicity
Bone marrow, GI, liver for all;
| Azathiprine and 6-MP are metabolized by xanthine oxidase so both have increased toxicity when given with allopurinol.
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Dactinomycin
Antitimumor antibiotics, actinomycin D;
Mechanism: intercalates in DNA;
Uses: wilms tumor, Ewing sarcoma, rhabdomyosarcoma, Used for childhood tumors;
Toxicity: myelosuppression
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Doxorubicin, adriamycin, daunorubicin
Antitumor antibiotics;
Mechanism: generates free radicals and intercalates into DNA leading to DNA breaks and decreases replication;
Uses: Solid tumors, leukemias, lymphomas
Toxicity: Cardiotoxicity (dilated cardiomyopathy), myelosuppression, alopecia, toxic to tissues following extravasation (CHF, S3 heart sounds). Dexrazoxane (iron chelating agent) used to prevent cardiotoxicity
191
Bleomycin
Antitumor antibiotic;
Induces free radical formation, which causes breaks in DNA strands.
Uses: testicular cancer, hodgkins lymphoma
Toxicity: pulmonary fibrosis, skin changes, minimal myelosuppression
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Cyclophosphamide, ifosfamide
Alkylating agent
Covalently X-linked (interstrand) DNA at guanine N-7. Require bio activation by liver.
Uses: Solid tumors, lymphomas, leukemias, and some brain cancers.
Toxicity: Myelosuppression, hemorrhagic cystitis, partially prevented with mesna (thiol group of mesna binds toxic metabolites)
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Nitrosoureas
Carmustine, lomustine, semustine, streptozocin;
Alkylating agents;
Require bioactivation, crosses BBB, Cross links DNA;
Uses: Brain tumors (including glioblastoma multiforme);
CNS toxicity (convulsions, dizziness, ataxia)
194
Busulfan
Alkylating agent;
Cross links DNA;
Uses: CML, also used to ablate patient's bone marrow before bone marrow transplant;
Toxicity: severe myelosuppression (in every case), pulmonary fibrosis, hyperpigmentation
195
Name all the alkylating agents
Cyclophosphamide, Ifosfamide, carmustine, lomustine, semustine, streptozocin, busulfan
196
Vincristine, Vinblastine
Microtubule inhibitors;
Vinca alkaloids (M phase) that bind Beta tubulin, inhibits its polymerization into microtubules, thereby preventing mitotic spindle formation (M phase arrest);
Uses: solid tumors, leukemias, and lymphomas
Toxicity: vincristine neurotoxicity (areflexia, peripheral neuritis), paralytic ileus. Vinblastine blasts bones marrow (suppression)
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paclitaxel, -taxols
Microtubule inhibitors;
M phase, Hyperstabilizes microtubules so that mitotic spindle cannot break down (anapahse cannot occur). "it is taxing to stay polymerized"
Uses: Ovarian and breast carcinomas;
Toxicity: Myelosuppression, alopecia, hypersensitivity
198
Cisplatin, Carboplatin
Mechanism: Cross-links DNA;
Uses: Testicular, bladder, ovary, and lung carcinomas;
Toxicity: Nephrotoxicity and acoustic damage. Prevent nephrotoxicity with amifostine (free radical scavenger) and chloride diuresis.
199
Etoposide, Teniposide
Mechanism: inhibits TOPOisomerase II leads to increased DNA degradation;
Uses: Solid tumors (particularly testicular and small cell lung cancer), Leukemias, Lymphomas
Toxicity: Myelosuppression, GI irritation, alopecia
200
Irinotecan, topotecan, -tecan
Inhibit topoisomerase I and prevent DNA unwinding and replication;
Uses: colon cancer (irinotecan); ovarian and small cell lung cancers (topotecan);
Toxicity: severe myelosuppression, diarrhea
201
Hydroxyurea
Mechanism: Inhibits ribonucleotide reductase leading to decreased DNA synthesis (S phase);
Uses: Melanoma, CML, Sickle cell disease (increases HbF);
Toxicity: Bone marrow suppression, GI upset
202
Prednisone, prednisilone
Mechanism: may trigger apoptosis, may even work on non-dividing cells;
Uses: Most commonly used glucocorticoids in cancer chemo. Used in CLL, non-hodgkin lymphomas (part of combination chemotherapy regiment). Also used as immunosuppressant;
Toxicity: Cushings like symptoms, weight gain, central obesity, muscle breakdown, cataracts, acne, osteoporosis, HTN, peptic ulcers, hyperglycemia, psychosis.
203
Tamoxifen, Raloxifene, -oxifen
Selective estrogen receptor modulators (SERMs)- receptor antagonists in breast and agonists in bone. Block the binding of estrogen to ER + cells;
Used for breast cancer treatment (tamoxifen) and prevention. Ralozifene also used to prevent osteoporosis;
Toxicity: tamoxifen is partila agonist in endometrium leading to increase risk of endometrial cancer and hot flashes, Raloxifene is endometrial antagonist
204
Trastuzumab (herceptin)
Monoclonal antibody against HER-2 (c-erbB2), a tyrosine kinase receptor. Kills breast cancer cells that over express HER2 through inhibiting HER2 initiated cellular signaling and antibody dependent cytotoxicity;
Uses: HER2 + breast cancer and gastric cancer;
Toxicity: Cardiotoxicity
Remember tras2zumab (gastric and breast)
205
Imatinib (gleevac)
Tyrosine kinase inhibitor of bcr-abl (philadelphia chromosome fusion gene in CML) and c-KIT (common in GI stromal tumors);
Uses: CML, GI stromal tumors;
Toxicity: fluid retention
206
Rituximab
Monoclonal antibody against CD20, which is found on most B cell neoplasms;
Uses: Non-Hodgkin lymphoma, rheumatoid arthritis (with MTX), ITP;
Toxicity: Increased risk of progressive mutlifocal leukoencephalopathy
207
Vemurafenib
Small molecule inhibitor of forms of the B-Raf Kinase with the V600E mutation.
Used for metastatic melanoma
208
Bevacizumab
Monoclonal antibody against VEGF. inhibits angiogenesis;
Uses: Solid tumors (colorectal, renal cell carcinoma);
Toxicity: Hemorrhage and impaired wound healing
209
Labs show what in DIC
Decreased fibrinogen, elevated fibrin degradation products, D-Dimers, and prolonged bleeding
210
elevated D-Dimers mean what?
That clotting is taking place, or has taken place recently (clotting factors are being used)
211
Difference between D dimer and Fibrin degradation products
D Dimer can only come from the degradation of fibrin clots, where as FDPs can come from fibrin clots or from the normal breakdown of fibrinogen
212
Drugs that interfere with Warfarin
Drugs that also use CYP2C9 (so it increases Warfarin's effect): Azoles, Cimetidine, cotrimoxazole, fluoxitine, Fluoroquinolones, marolides (but not azithromycine), metronidazole, sulfinpyrazone
213
What is the name for "red dots in the cytoplasm of RBCs" and what does it mean
Probably Schuffner cells, means malaria
214
When you treat a patient with chemotherapy that has M3 leukemia, what is a possible side effect you are worried about
They get DIC. You give all trans retinoic acid and that probably won't happen (that is why we give ATRA)
215
Serum Lactate Dehydrogenase will be increased when
It is the enzyme in glycolysis that will be elevated when you have cell lysis (mostly elevated when RBCs lyse, but lots of cells have this)
216
Haptoglobin
Binds to hemoglobin when a RBC lyses its hemoglobin out. The serum haptoglobin will be decreased in cases of hemolytic anemia.
217
Microspherocytes are what
they are small RBCs that have antibody coated portions of the RBC clipped off by macrophages.
218
Direct coombs looks for
whether there are antibodies bound to RBCs
219
What does an aPTT measure
measures the intrinsic and common pathway. Factors I, II, V, VIII, IX, X, XI, XII;
Used to monitor Heparin
