Hematology/Oncology Flashcards
1
Q
Lifespan of erythrocyte
A
120 days
2
Q
Anisocytosis
A
Varying sizes
3
Q
Poikilocytosis
A
Varying shapes
4
Q
Erythrocytosis
A
Polycythemia = ↑ Hematocrit
5
Q
Reticulocyte
A
Immature erythrocyte marker of erythroid proliferation
6
Q
Platelet
Derived from…
What do they contain
Storage
A
Derived from Megakaryocytes
Dense granules (ADP, Ca) and α granules (vWF, fibrinogen)
1/3 stored in spleen
7
Q
Results of Thrombocytopenia or Platelet Dysfunction
A
Petechiae
8
Q
vWF receptor
A
GpIb
9
Q
Fibrinogen receptor
A
GpIIb/IIIa
10
Q
Leukocyte
Subtypes
Normal range
A
Granulocytes (Neutrophils, Eosinophils, Basophils)
Mononuclear cells (Monocytes, Lymphocytes)
4000-10000
11
Q
WBC differential
A
"Neutrophils Like Making Everything Better" Neutrophils (60%) Lymphocytes (30%) Monocytes (7%) Eosinophils (2%) Basophils (<1%)
12
Q
Neutrophil Increased in what state? Function Histo Granules
A
Bacterial infection
Phagocytic
Multilobed nucleus
Small numerous specific granules (ALP, Collagenase, Lysozyme, Lactoferrin)
Larger less numerous Azurophilic granules are lysosomes (Acid phosphatase, Peroxidase, β-glucuronidase)
13
Q
Hypersegmented polys
Histo
Seen in
A
5 or more lobes
VitB12/Folate Deficiency
14
Q
Increased Band Cells
What are they?
What do they reflect?
A
Immature Neutrophils
Increased myeloid proliferation (bacterial infection or CML)
15
Q
Monocyte
Where do they exist?
What does it differentiate into?
Histo
A
In blood
Macrophages in tissue
Large, kidney shaped nucleus with extensive frosted glass cyto
16
Q
Macrophage Function Lifespan What activates them? Marker
A
Phagocytosis, APC via MHCII
Long life in tissues
Activated by γ-Interferon
CD14
17
Q
Eosinophil
Function
Histo
What does it produce?
A
Defends again helminthic infections. Phagocytic for Ag-Ab complex
Bilobate nucleus. Large eosinophilic granules
Produce Histaminase and Arylsulfatase to limit reaction following mast cell degranulation
18
Q
Causes of eosinophilia
A
“NAACP”
Neoplastic, Asthma, Allergy, Collagen vascular disease, Parasites
19
Q
Basophil
Function
Histo with function
A
Mediates allergic reactions
Basophilic granules with heparin (anticoagulant), Histamine (vasodilator), and Leukotrienes (LTD4)
20
Q
Mast Cells Function Histo Physiology Molecules it releases What type of reaction is it involved with? Inhibition?
A
Allergic reactions in local tissue
Resemble basophils
Can bind Fc portion of IgE to membrane. IgE cross-links upon Ag binding –> degranulation
Releases Histamine, Heparin, Eosinophil chemotactic factors
Type I hypersensitivity reaction
Cromolyn prevents degranulation
21
Q
Dendritic cells Function Role Re Immune systems Expresses... In skin they are called
A
Phagocytic APC
Link between innate and adaptive immune systems
MHCII and Fc receptor
Langerhans cells in skin
22
Q
Lymphocyte
Mediates what kind of immunity
Subtypes
Histo
A
Adaptive immunity
B and T cells
Densely stained nucleus with small amount of cytoplasm
23
Q
B Lymphocyte What kind of immune response? Where does it arise from? Where does it mature? Where does it migrate to? What does it differentiate into? Function MHC Markers
A
Humoral response
Bone marrow
Bone marrow
Migrates to peripheral lymphoid tissues (follicles of lymph nodes, white pulp of spleen, unencapsulated lymphoid tissue)
When encounters Ag, differentiates into Ab producing plasma cell and memory cells
APC via MHCII
CD19 and CD20
24
Q
Plasma Cell
Function
Histo
Pathology
A
Ab production
Off center nucleus, clock face chromatin, RER, well developed Golgi
Multiple Myeloma
25
```
T Lymphocyte
What kind of immune response?
Where does it arise from?
Where does it mature?
What does it differentiate into?
Surface marker
Percentage of circulating lymphocytes
```
```
Cellular immune response
Bone marrow
Thymus
Tc cells (CD8), Th (CD4), Treg (CD28)
CD3
80%
```
26
Blood group A
A Ag and B Ab
27
Blood group B
B Ag and A Ab
28
Blood group AB
A and B Ag. No Abs
Universal Recipient of RBCs
Universal Donor of Plasma
29
Blood group O
No Ag. A and B Abs
Universal donor of RBCs
Universal Recipient of Plasma
30
Rh factor
Ag on RBC surface
31
Erythroblastosis Fetalis
PathoPhys
Treatment
Rh- mother exposed to fetal Rh+ blood. Mother makes anti-Rh IgG that crosses placenta and causes hemolytic disease in the next fetus
Rho (D) immune globulin for mother at first delivery to prevent initial sensitization of Rh- mother to Rh Ag
32
Blood groups Re crossing placenta
anti A and anti B IgM does not cross placenta
| anti Rh IgG does cross the placenta
33
Intrinsic Coagulation Pathway
Collagen, Basement membrane, Activated platelets, or HMWK --> XII --> XI --> IX
IX + VIII --> X
XII --> Kallikrein
34
Extrinsic Coagulation Pathway
Thromboplastin (tissue factor) --> VII --> X
35
Common Coagulation Pathway
X + V --> II (thrombin) --> Fibrin
XIII (fibrin stabilizing factor) helps stabilize fibrin mesh
Thrombin also activates V, VIII, XIII
36
Kinin Cascade
Kallikrein thurs HMWK into Bradykinin
| Bradykinin ↑ Vasodilation, Permeability, and Pain
37
Fibrinolytic System
XII --> Kallikrein --> Plasmin --> Fibrin mesh degradation
| Plasmin also activates C3
38
Which reactions of the coagulation cascade require Ca and Phospholipids
XIa --> IX
VII --> VIIa
VIIa and (IXa + VIIIa) activation of X
Xa + Va activation of II
39
Hemophilia A
Deficiency in VIII
40
Hemophilia B
Deficiency of IX
41
VitK Pathway
Oxidized VitK --> [epoxide reductase] --> Reduced VitK
| Reduced VitK is a cofactor for the maturation of II, VII, IX, X, C, and S
42
Warfarin
| MoA
Inhibits Epoxide Reductase
43
Why are neonates given VitK?
They lack enteric bacteria that produce VitK
44
What does vWF do?
Carries/protects VIII
45
Anticoagulation cascade
Thrombomodulin on endothelial cells --> Protein C
| C + S cleaves and inactivates Va and VIIIa
46
What does antithrombin do?
Inhibits activated forms of II, VII, IX, X, XI, XII
47
Function of Heparin
Activates Antithrombin
48
Factor V Leiden mutation
| Classical presentation
Factor V resistant to inhibition by protein C
| DVT --> PE
49
tPA
Thrombolytic that activates plasmin
50
Platelet Plug Formation Schematic
Injury: vWF binds exposed collagen upon endothelial damage
Adhesion: Platelets bind vWF via Gp1b and release Ca and ADP.
Activation: ADP binding induces GpIIb/ IIIa expression on platelet surface --> aggregation
51
How does ADP affect coagulation
Released by platelets.
| Helps platelets adhere to endothelium and induces platelets to express GpIIb/IIIa at platelet surface
52
Platelet Aggregation Pathway
Fibrinogen binds GpIIb/IIIa and links platelets
53
Pro Platelet Aggregation Factors
TXA2 (released by platelets), ↓ blood flow, ↑ platelet aggregation
54
Anti Platelet Aggregation Factors
PGI2 and NO (released by endothelial cells)
↑ blood flow
↓ platelet aggregation
55
Ticlopidine
Inhibits ADP induced expression of GpIIb/IIIa
| Causes Neutropenia, Oral Ulcers, Fever
56
Clopidogrel
Inhibits ADP induced expression of GpIIb/IIIa
57
Abciximab
Inhibits GpIIb/IIIa directly
58
ESR
What causes it to increase?
↑ ESR
↓ ESR
Acute phase reactants in plasma (Fibrinogen) cause RBC aggregation and ↑ ESR
↑: Infection, Autoimmune, Malignancy, Pregnancy
↓: "CHaMP"
Polycythemia, Sickle Cell Anemia, CHF, Microcytosis, Hypofibrinogenemia
59
Acanthocyte
Spur cell indicative of Liver disease or Abetalipoproteinemia (cholesterol dysregulation)
60
Basophilic Stippling
"BASte the ox TAiL"
| Thalassemias, Anemia of chronic disease, Lead Poisoning
61
Bite Cell
G6PD deficiency
62
Eliptocyte
Hereditary Elliptocytosis
63
Macro-Ovalocyte
Megaloblastic anemia (w/ hypersegmented polys) and Marrow failure
64
Ringed Siderblasts
Sideroblastic anemia
| Excess Fe in Mito
65
Schistocyte
Helmet Cell
| DIC, TTP/HUS, Traumatic Hemolysis (metal heart valve prosthesis)
66
Sickle Cell
Sickle Cell Anemia
67
Spherocyte
Hereditary spherocytosis, Autoimmune hemolysis
68
Teardrop cell
"RBC sheds a tear because it has been forced out of its home"
Bone marrow infiltration (myelofibrosis)
69
Target Cell
"HALT said the hunter to his target"
| HbC disease, Asplenia, Liver disease, Thalassemia
70
Heinz Bodies
Process
Associated pathology
Oxidation of sulfhydryl groups leads to denatured Hb precipitation and damage to RBC membrane --> formation of bite cells
G6PD deficiency and α-thalassemia
71
Howell-Jolly Bodies
What is it?
How are they normally dealt with?
Associated pathology
Basophilic nuclear remnants found in RBCs
Normally removed from RBCs by splenic macrophages
Functional hyposplenia, asplenia, mothball ingestion (naphthalene)
72
Microcytic Anemias
"Find Those Small Plump Cells"
| Iron Deficiency, ACD, Thalassemia, Pb poisoning, Sideroblastic anemia
73
Nonhemolytic Normocytic Anemias
ACD, Aplastic, Chronic Kidney Disease
74
Hemolytic Normocytic Anemias
Intrinsic: "SHEEPS"
Spherocytosis, G6PD or PK deficiency, HbC, Sickle Cell Anemia, Paroxysmal Nocturnal Hemoglobinuria
Extrinsic: Autoimmune, Microangiopathic, Macroangiopathic, Infections
75
Megaloblastic Macrocytic Anemias
Folate deficiency, B12 deficiency, Orotic Aciduria
76
NonMegaloblastic Macrocytic Anemias
Liver disease, Alcoholism, Reticulocytosis
77
```
Iron Deficiency Anemia
What kind of anemia
What causes it?
PathoPhys
Labs
Histo
How may it manifest
```
```
Microcytic, Hypochromatic
↓ Fe due to chronic bleeding, malnutrition, or pregnancy
Impaired final step in heme synthesis
↓ Fe and Ferritin, ↑ TIBC
Microcytosis (MCV<80) and hypochromia
Plummer Vinson Syndrome
```
78
```
α Thalassemia
What kind of anemia
PathoPhys
Epidemiology
How # of gene mutations re disease
```
Microcytic, Hypochromatic
α globin gene mutation
cis deletion in Asians, trans deletions in Africans
4 deletions: No α, excess γ forms γ4 (Hb Barts), Incompatible with life (Hydrops Fetalis)
3 deletions: HbH disease. Very little α, excess β forms β4 (HbH)
1-2 gene deletions: no clinical significance
79
β Thalassemia
What kind of anemia
PathoPhys
Epidemiology
Microcytic, Hypochromatic
Point mutation in splice sites and promoter sequence --> ↓ β
Mediterranean populations
80
β Thalassemia minor
PathoPhys
Symptoms
Diagnosis
Heterozygote: β chain underproduced
Asymptomatic
Increased HbA2 on electrophoresis
81
```
β Thalassemia major
PathoPhys
Symptoms
Treatment
Complications
Presentation
Hb
```
```
Homozygote: β chain absent
Severe anemia
Blood transfusions (--> hemochromatosis)
Marrow expansion (crew cut on skull XR) --> skeletal deformities. Chipmunk facies
HbF (α2γ2)
```
82
Presentation of HbS/β-Thalassemia Heterozygote
Mild to moderate sickle cell disease depending on amount of β globin production
83
```
Lead Poisoning
What kind of anemia
PathoPhys
Presentation
Treatment
```
Microcytic, Hypochromatic
Pb --/ ferrochelatase and ALA dehydratase which leads to ↓ heme synthesis
Pb --/ rRNA degradation causing RBCs to retain rRNA aggregates (Basophilic Stipling)
"LEAD"
Lead lines on Gingivae (Burton's Lines) and on metaphysis of long bones
Encephalopathy and Erythrocyte basophilic stippling
Abdominal colic and sideroblastic Anemia
Drops (wrist and foot)
Treat with Dimercaprol and EDTA
Succimer in children
84
```
Sideroblastic Anemia
What kind of anemia
PathoPhys
What causes it?
Histo
Labs
Treatment
```
Microcytic, Hypochromatic
Defect in Heme synthesis
X linked defect in δALA synthase, EtOH, Lead, Isoniazid
Ringed sideroblasts (with iron laden mito)
↑ Fe and ferritin, Normal TIBC
Treat with VitB6
85
Megaloblastic Anemia
Basic Pathology
Consequences
Impaired DNA synthesis --> maturation of nucleus delayed relative to cytoplasm
Ineffective erythropoiesis --> pancytopenia
86
```
Folate Deficiency
What kind of anemia
Etiologies
Presentation
Histo
Labs
```
Megaloblastic
Malnutrition (alcoholics), malabsorption, antifolates (methotrexate, trimethoprim, phenytoin), ↑ requirement (hemolytic anemia, pregnancy)
Glossitis
Hypersegmented neutrophils
↓ Folate, ↑ Homocysteine, normal Methylmalonic acid
87
```
B12 Deficiency
What kind of anemia
Etiologies
Presentation
Histo
Labs
```
Megaloblastic
Insufficient intake, Malabsorption, Pernicious anemia, Diphyllobothrium latum (fish tapeworm), PPI
Glossitis, B12 invovled with FA and myelin synthesis leading to Peripheral neuropathy w/ sensorimotor dysfunction, Posterior column (vibration/propioception), Lateral CST (spasticity), and Dementia
Hypersegmented neutrophils
↓ B12, ↑ Homocysteine, ↑ Methylmalonic acid
88
```
Orotic Aciduria
What kind of anemia?
PathoPhys
Presentation
Histo
Labs
Treatment
```
Megaloblastic
Enzyme deficiency impairs conversion of uridine from orotic acid
Children with glossitis and megaloblastic anemia that cannot be cured by folate or B12
Hypersegmented neutrophils
Orotic acid in urine
Uridine monophopshate to bypass mutated enzyme
89
NonMegaloblastic Macrocytic Anemia
Pathology
What causes it?
Macrocytic anemia in which DNA synthesis is unimpaired
| Liver disease, Alcoholism, Retculocytosis, Drugs (5FU, AZT, Hydroxyurea)
90
Intrinsic Hemolytic Normocytic, Normochromic Anemias
Intravascular w/ examples and findings
Extravascular w/ examples and findings
Intra: Paroxysmal nocturnal hemoglobinuria or mechanical destruction
↓ haptoglobin, ↑ LDH, hemoglobin in urine
Extra: Hereditary spherocytosis
Macs in spleen clears RBCs. ↑ LDH + ↑ UCB causes jaundice
91
```
Anemia of Chronic Disease
What kind of anemia?
PathoPhys
Findings
What can it become?
```
```
Normocytic, Normochromic NonHemolytic
Inflammation --> ↑ hepcidin
Hepcidin is released by liver binds ferroportin on intestinal mucosal cells and macs thus inhibiting iron transport
↓ release of iron from macs
↓ Fe, ↓ TIBC, ↑ Ferritin
Can become microcytic, hypochromic
```
92
Aplastic Anemia
What kind of anemia
What causes it?
Normocytic, Normochromic NonHemolytic
Caused by failure or destruction of myeloid stem cells due to: Radiation and drugs (benzene, chloramphenicol, alkylating agents, antimetabolites), Viral agents (parvovirus B19, EBV, HIV, HCV), Fanconi's Anemia, Idiopathic (immune mediated, stem cell defect, may follow acute hepatitis)
93
Aplastic Anemia
Labs/Histo
Presentation
Treatment
Pancytopenia, severe anemia, Leukopenia, Thrombocytopenia, Normal cell morphology, Hypocellular bone marrow with fatty infiltration (dry bone marrow tap)
Fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infection
Withdrawal of offending agent, Immunosuppressive regimens (antithymocyte globulin, cyclosporine), allogeneic bone marrow transplantation, RBC and platelet transfusion, G-CSF or GM-CSF
94
How does chronic kidney disease lead to anemia?
| What kind of anemia?
↓ erythropoietin --> ↓ hematopoiesis --> Normocytic, Normochromic NonHemolytic anemia
95
```
Hereditary Spherocytosis
What kind of anemia?
PathoPhys
How do RBCs look?
What happens to RBCs
Presentation
Findings
Treatment
```
Extravascular Intrinsic Hemolytic Normocytic Anemia
Defects in proteins interacting with RBC membrane (Ankryn, Band3, Protein4.2, Spectrin)
Less membrane causes small and round RBCs with no central pallor (↑ MCHC, ↑ red cell distribution width)
Premature removal of RBC by spleen
Splenomegaly, Aplastic crisis (Parvovirus B19 infection)
+ osmotic fragility test, normal or ↓ MCV with abundance of cells; Masks microcytia
Splenectomy
96
```
G6PD Deficiency
What kind of anemia?
Inheritance
PathoPhys
What happens to RBCs?
Presentation
Histo
```
Intra/Extra-vascular Intrinsic Hemolytic Normocytic Anemia
X linked
Defective G6PD --> ↓ Glutathione --> ↑ RBC susceptibility to oxidant stress (sulfa drugs, infections, fava beans)
RBCs destroyed extravascularly
Back pain followed a few days later by hemoglobinuria
Heinz bodies and bite cells
97
```
PK deficiency
What kind of anemia
Inheritance
PathoPhys
Presentation
```
Extravascular Intrinsic Hemolytic Normocytic Anemia
AR
Defective PK --> ↓ ATP --> rigid RBCs
Hemolytic anemia in a newborn
98
HbC defect
What kind of anemia
PathoPhys
HbSC vs HbSS
Extravascular Intrinsic Hemolytic Normocytic Anemia
Glutamic Acid --> Lysine mutation at reside 6 of β globin
HbSC less severe than HbSS
99
```
Paroxysmal Nocturnal Hemoglobinuria
What kind of anemia
PathoPhys
Genetics
Presentation
Labs
Treatment
```
Intravascular Intrinsic Hemolytic Normocytic Anemia
↑ complement mediated RBC lysis (impaired synthesis of GPI anchor or decay-accelerating factor that protects RBC membrane from complement
Acquired mutation in hematopoietic stem cell
Hemolytic anemia, Pancytopenia, Venous Thrombosis
CD55/59 negative RBCs on flow cytometry
Eculizumab
100
```
Sickle Cell Anemia
What kind of anemia?
Genetics
Pathogenesis
Newborns
Heterozygotes
```
Extravascular Intrinsic Hemolytic Normocytic Anemia
HbS point mutation in β globin at 6th residue (glutamic acid --> val)
Low O2 or dehydration precipitates sickling (deoxidized HbS polymerizes) --> anemia and vaso-occlusive disease
Newborns are initially asymptomatic b/c of ↑HbF and ↓HbS
Hets resistant to malaria
101
Sickle Cell Anemia
Histo
XR
Treatment
Sickled cells are crescent shaped RBCs
Crew cut on skull XR due to marrow expansion from erythropoiesis (also in thalassemias)
Hydroxyurea (↑ HbF) and bone marrow transplant
102
Sickle Cell Anemia Complications
Aplastic crisis (due to parvovirus B19)
Autosplenectomy (Howell-Jolly Bodies) --> ↑ risk of infections with encapsulated organisms; Functional splenic dysfunction in early childhood
Splenic sequestration crisis
Salmonella Osteomyelitis
Painful crisis (vaso-occlusive): Dactylitis, actue chest syndrome, avascular necrosis
Renal Papillary Necrosis (due to low O2 in papilla)
Microhematuria (medullary infarcts)
103
Autoimmune Hemolytic Anemia
What kind of anemia?
2 kinds?
Labs
Extrinsic Hemolytic Normocytic Anemia
Warm and Cold Agglutinin
Coomb's Positive
104
Coomb's Test
Direct: anti-Ig Ab added to pt's serum --> RBCs agglutinate if coated with Ig
Indirect: Normal RBCs added to pt's serum agglutinate if serum has anti-RBC surface Ig
105
Warm Agglutinin
Ab
Course
What causes it?
"Warm weather is Great"
IgG
Chronic
SLE, CLL, drugs (metyldopa)
106
Cold Agglutinin
Ab
Course
What causes it?
"Cold ice cream is yuMMM"
IgM
Acute anemia triggered by cold
CLL, Mycoplasma pneumonia infections, infectious Mononucleosis
107
```
Microangiopathic Anemia
What kind of Anemia?
Pathogenesis
Seen in what conditions
Histo
```
Extrinsic Hemolytic Normocytic Anemia
RBCs damaged when passing through obstructed or narrowed vessel lumina
DIC, TTP/HUS, SLE, Malignant HTN
Schistocytes
108
Macroangiopathic Anemia
What kind of Anemia?
Pathogenesis
Histo
Extrinsic Hemolytic Normocytic Anemia
Prosthetic heart valve and aortic stenosis damage RBCs
Schistocytes
109
Infectious anemia
What kind of anemia
Examples
Extrinsic Hemolytic Normocytic Anemia
| Malaria, Babesia
110
```
Iron Deficiency
Serum Fe
TIBC (transferrin)
Ferritin
Transferrin Saturation (Serum Fe/TIBC)
```
↓ (primary)
↑
↓
↓↓
111
```
Chronic Disease
Serum Fe
TIBC (transferrin)
Ferritin
Transferrin Saturation (Serum Fe/TIBC)
```
↓
↓
↑ (primary)
No change
112
```
Hemochromatosis
Serum Fe
TIBC (transferrin)
Ferritin
Transferrin Saturation (Serum Fe/TIBC)
```
↑ (primary)
↓
↑
↑↑
113
```
Pregnancy or OCP use
Serum Fe
TIBC (transferrin)
Ferritin
Transferrin Saturation (Serum Fe/TIBC)
```
No change
↑ (primary)
No change
↓
114
```
Pb Poisoning
What enzymes are affected?
What builds up where?
General Presentation
Adults vs Children re exposure and presentation
```
Ferrochelatats and ALA Dehydratase
Protoporphyrin and δALA in blood
Microcytic anemia, GI and Kidney disease
Children: lead paint --> mental retardation
Adults: battery, ammunition, radiator factory --> Headache, Memory loss, Demyelination
115
```
Acute Intermittent Porphyria
Enzyme affected
What accumulates where?
Presentation
Treatment
```
Porphobilinogen daminase
Porphobilinogen, δALA, uroporphyrin (urine)
Painful abdomen, Port wine colored urine, Polyneuropathy, Psychological disturbances, Precipitated by drugs
Glucose and heme inhibit ALA synthase
116
```
Porphyria Cutanea Tarda
Enzyme affected
What accumulates where?
Presentation
Frequency
```
Uroporphyrinogen decarboxylase
Uroporphyrin (tea colored urine)
Blistering cutaneous photosensitivity
Most common porphyria
117
Heme Synthesis Pathway
Mito:
Glycine + Succinyl-CoA --> [δALA synthase + B6] --> δALA
Cyto:
δALA --> [δALA dehydratase] --> Porphobilinogen --> [Porphobilinogen deaminase] --> Hydroxymetylbilane --> Uroporphyrinogen III --> [Uroporphyrinogen decarboxylase] --> Coproporphyrinogen III
Mito:
Coproporphyrinogen III --> Protoporphyrin
Protoporphyrin + Fe --> [Ferrochelatase] --> Heme
118
Rate limiting step of Heme synthesis with regulation
δALA synthase
| Inhibited by Glucose and Heme
119
PT
Extrinsic and Common pathways
| I, II, V, VII, X
120
PTT
Intrinsic and Common pathways
| all factors except VII, XIII
121
```
Hemophilia A or B
PT
PTT
PathoPhys
Presentation
```
```
No change in PT
↑ PTT
Intrinsic coagulation defect
A: VIII
B: IX
Macrohemorrhage: Hemarthrosis, Easy bruising
```
122
VitK deficiency
PT
PTT
PathoPhys
↑ PT
↑ PTT
↓ synthesis of II, VII, IX, X, C, S
123
Presentation of platelet abnormalities
Microhemorrhage: Mucus membrane bleeding, Epistaxis, Petechiae, Purpura, ↑ bleeding time, possible ↓ platelet count
124
Bernard-Soulier Syndrome
PC
BT
PathoPhys
↓ PC
↑ BT
↓ GpIb --> defect in platelet to vWF adhesion
125
```
Glanzmann's Thrombasthenia
PC
BT
PathoPhys
Labs
```
No change in PC
↑ BT
↓ GpIIb/IIIa --> defect platelet-to-platelet aggregation
No platelet clotting on blood smear
126
```
Idiopathic Thrombocytopenic Purpura (ITP)
PC
BT
PathoPhys
Labs
```
↓ PC
↑ BT
Anti-GpIIb/IIIa Ab --> splenic macrophage consumption of platelet/Ab complex --> ↓ platelet survival
↑ megakaryocytes
127
```
Thrombic Thrombocytopenic Purpura (TTP)
PC
BT
PathoPhys
Histo
Labs
Symptoms
```
↓ PC
↑ BT
Deficiency in ADAMTS13 (vWF metalloprotease) --> ↓ degradation of vWF multimers
↑ vWF multimers --> ↑ platelet aggregation and thrombosis
↓ platelet survival
Schistiocytes, ↑ LDH
Neurologic and renal symptoms, Fever, Thrombocytopenia, and Microangiopathic hemolytic anemia
128
```
von Willebrands Disease
PC
BT
PT
PTT
```
No change in PC
↑ BT
No change in PT
No change or ↑ PTT
129
```
von Willebrands Disease
PathoPhys
Frequency
Severity
Inheritance
Diagnosis
Treatment
```
Intrinsic pathway defect: ↓ vWF --> normal or ↑ PTT because vWF protects VIII
↓ vWF --> defect in platelet-to-vWF adhesion
Most common inherited bleeding disorder
Mild
AD
Ristocetin cofactor assay
Desmopressin releases vWF from endothelium
130
```
DIC
PC
BT
PT
PTT
```
↓ PC
↑ BT
↑ PT
↑ PTT
131
```
DIC
PathoPhys
What causes it?
Histo
Labs
```
Widespread activation of clotting leds to deficiency in clotting factors leading to bleeding
"STOP Making New Thrombi"
Sepsis (gram neg), Trauma, Obstetric complication, acute Pancreatitis, Malignancy, Nephrotic syndrome, Transfusion
Schistocytes, ↑ Fibrin split products (D-dimer), ↓ fibrinogen, ↓ factor V and VIII
132
Factor V Leiden
PathoPhys
Epidemiology
Mutant V resistant to degradation by C --> hypercoagulability
Most common cause of inherited hypercoagulability in whites
133
Prothrombin Gene mutation
Mutation in 3' UTR --> ↑ production of prothrombin --> ↑ plasma levels and venous clots --> hypercoagulability
134
AntiThrombin Deficiency
PathoPhys
Treatment
Inherited deficiency of antithrombin --> hypercoagulability
| ↑ PTT is blunted after heparin administration
135
Protein C or S deficiency
PathoPhys
Treatment
↓ ability to inactivate V and VIII --> hypercoagulability
| ↑ risk of thrombotic skin necrosis with hemorrhage following administration of warfarin
136
Packed RBCs
Purpose
Use
↑ Hb and O2 carrying capacity
| Acute blood loss, severe anemia
137
Transfusion of platelets
Purpose
Use
Increase platelet count
| Stop significant bleeding (Thrombocytopenia, Qualitative platelet dysfunction)
138
Transfusion of fresh frozen plasma
Purpose
Use
↑ Coagulation factor levels
| DIC, Cirrhosis, Warfarin OD
139
Transfusion of Cryoprecipitate
Contains
Use
Contains Fibrinogen, VIII, XIII, vWF, and Fibronectin
| Treats coagulation factor deficiencies involving fibrinogen and VIII
140
Risks of Blood Transfusions
Infection, Transfusion reaction, Iron Overload, HypoCa (citrate is a Ca chelator), HyperK (RBC lysis)
141
Leukemia
What is it?
Where are tumors found?
Lymphoid or Myeloid neoplasm with widespread involvement of bone marrow
Tumor cells are usually found in peripheral blood
142
Lymphoma
What is it?
Presentation?
Discrete tumor masses arising form lymph nodes
| Presentations blur definitions
143
Leukemoid Reaction
What is it?
Labs
Contrast with CML
Acute inflammatory response to infection
↑ WBC count with ↑ neutrophils and bands
↑ Leukocyte ALP
In CML, ↓ Leukocyte ALP
144
```
Hodgkin's Lymphoma
Distribution
Stage re prognosis
Histo
Epidemiology
What is it associated with?
Presentation
```
Localized, single group of nodes; extra nodal involvement rare. Contiguous spread
Stage is strongest predictor of prognosis
Reed-Sternberg cells
Bimodal distribution: young adulthood and over 55. More common in men except for nodular sclerosing type
EBV
Fever, night sweats, wt loss
145
```
Non-Hodgkin's Lymphoma
Distribution
Histo
Epidemiology
What is it associated with?
Presentation
```
Multiple, peripheral nodes. Extra nodal involvement common. Noncontiguous spread
Majority involve B cells (except for lymphoblastic T cell origin)
20-40
HIV and immunosuppression
Few constitutional signs/symptoms
146
```
Reed-Sternberg Cells
Appearance
What kind of cancer?
Markers
Origin
Re Diagnosis
Re Prognosis
```
Giant cell. Binucleate, bilobed w/ 2 halves as mirror images (owl eyes)
Hodgkin's Lymphoma
CD30, CD15
B cell origin
Necessary but not sufficient for diagnosis
Best prognosis with strong stromal or lymphocytic reaction against RS cells
RS rich has best prognosis
147
Nodular Sclerosing Hodgkin's Lymphoma
Frequency
Epidemiology
Most common
| Affects women and men equally
148
Hodgkin's Lymphoma with worst prognosis
Lymphocyte mixed or depleted forms
149
```
Burkitt's Lymphoma
What kind of cancer?
Neoplasm of what?
Epidemiology
Genetics
Histo
Associated with what?
Endemic vs sporadic
```
```
Non-Hodgkin's Lymphoma
Neoplasm of mature B cells
Adolescents or young adults
t[8 (cmyc), 14 (heavy-chain Ig)]
Starry sky appearance: sheets of lymphocytes with interspersed macs
EBV
Jaw lesion in endemic forms in Africa
Pelvis or abdominal in sporadic form
```
150
```
Diffuse Large B cell Lymphoma
What kind of cancer?
Neoplasm of what?
Epidemiology
Frequency
Origin
```
```
Non-Hodgkin's Lymphoma
Neoplasm of mature B cells
Older adults but 20% in children
Most common adult NHL
20% mature T cell origin
```
151
```
Mantle Cell Lymphoma
What kind of cancer?
Neoplasm of what?
Epidemiology
Genetics
Prognosis
Markers
```
```
Non-Hodgkin's Lymphoma
Neoplasm of mature B cells
Older males
t[11 (cyclin D1), 14 (heavy-chain Ig)]
Poor
CD5
```
152
```
Follicular Lymphoma
What kind of cancer?
Neoplasm of what?
Epidemiology
Genetics
Course
PathoPhys
```
```
Non-Hodgkin's Lymphoma
Neoplasm of mature B cells
Adults
t[14 (heavy-chain Ig), 18 (bcl2)]
Difficult to cure, indolent course
bcl2 inhibits apoptosis
```
153
```
Adult T cell Lymphoma
What kind of cancer?
Neoplasm of what?
Epidemiology
Genetics
Presentation
Population affected
Course
```
```
Non-Hodgkin's Lymphoma
Neoplasm of mature T cells
Adults
Caused by HTLV1
Cutaneous lesions
Japan, West Africa, Caribbean
Aggressive
```
154
```
Mycosis Fungoides
AKA
What kind of cancer?
Neoplasm of what?
Epidemiology
Presentation
Markers
Course
```
```
Sezary Syndrome
Non-Hodgkin's Lymphoma
Neoplasm of mature T cells
Adults
Cutaneous patches/nodules
CD4
Indolent course
```
155
```
Multiple Myeloma
Histo
Where does it arise from
Frequency
What does it produce?
```
Monoclonal Plasma Cell cancer (fried egg appearance). Clock face chromatin and intracytoplasmic inclusions w/ immunoglobulins
Arises in the marrow
Most common primary tumor of bone in those over 50
IgG (55%) and IgA (25%)
156
```
Multiple Myeloma
Associations
XR
Electrophoresis
UA
Blood smear
Presentation
```
Susceptibility to infection, Amyloidosis
Punched out lytic bone lesions
M spike on protein electrophoresis
Ig Light Chains in urine (Bence Jones Protein)
Rouleaux formation (RBCs staked like poker chips)
"CRAB"
hyperCa, Renal insufficiency, Anemia, Bone lytic lesions/Back pain
157
How to distinguish Waldenstrom's Macroglobinemia from Multiple Myeloma
Both have an M spike but WM doesn't have lytic bone lesions
158
What is the M spike?
Spike in γ on protein electrophoresis
| Multiple Myeloma, Waldenstrom's Macroglobulinemia, MGUS
159
```
MGUS
What does it stand for?
What is it?
Electrophoresis
Symptoms
What is it a precursor to
```
```
Monoclonal Gammopathy of Undetermined Significance
Monoclonal expansion of plasma cells
M spike
Asymptomatic
Precursor to multiple myeloma
```
160
Leukemia
What is it basically?
Pathway of Presentation
Infiltrates?
Unregulated growth of leukocytes in bone marrow
↑ or ↓ # of circulating leukocytes in blood and marrow --> anemia (↓RBCs), infections (↓ mature WBCs), and hemorrhage (↓ platelets)
Leukemic cells infiltrate liver, spleen, and lymph nodes
161
```
Acute Lymphoblastic Leukemia/Lymphoma
Kind of cancer?
Epidemiology
Presentation
Markers
Response?
Metastasis
Genetics with prognosis
```
Lymphoid Neoplasm
Under 15
T cell ALL presents with mediastinal mass (leukemic infiltration of the thymus). Peripheral blood and bone marrow have ↑ lymphoblasts
TdT+ (marker for pre-T and pre-B cells), CALLA
Most response to therapy
CNS and testes
t(12;21) --> best prognosis
162
```
Small Lymphocytic Lymphoma (SLL)/Chronic Lymphocytic Leukemia (CLL)
Kind of cancer?
Epidemiology
Presentation
Difference between them
```
Lymphoid neoplasm
Over 60
Often asymptomatic. Smudge cells in peripheral blood smear. Autoimmune hemolytic anemia
CLL has ↑ peripheral blood lymphocytosis or bone marrow involvement
163
```
Hairy Cell Leukemia
What kind of cancer
Epidemiology
In elderly?
Histo
Treatment
```
Lymphoid neoplasm
Adults
Mature B cell tumor in the elderly
Filamentous hair like projections. Stains TRAP+
Cladribine (adenosine analog resistant to ADA)
164
```
Acute Myelogenous Leukemia (AML)
What kind of cancer?
Epidemiology
Histo
Smear
Genetics Re Treatment
Common presentation
```
Myeloid Neoplasm
Median age of onset is 65
Auer Rods
↑↑↑ circulating myeloblasts on peripheral smear
t(15;17) --> M3 AML subtype which responds to all trans Retinoic acid inducing differentiation of myeloblasts
DIC is a common presentation in M3 AML
165
```
Chronic Myelogenous Leukemia (CML)
What kind of cancer?
Epidemiology
Genetics
Origin
Presentation
Course
Labs
Treatment
```
Myeloid Neoplasm
30-60
Philadelphia chromosome t(9;22) bcr-abl
Myeloid stem cell proliferation
↑ Neutrophils, Metamyelocytes, Basophils, Splenomegaly
May accelerate and transform into AML or ALL (blast crisis)
Low Leukocyte ALP from immature granulocytes (vs leukemoid reaction - mature cells)
Imatinib
166
Auer Bodies (rods)
What are they?
Where are they commonly seen
What can they cause?
Peroxidase+ Cytoplasmic inclusions in granulocytes and myeloblasts
Acute polymyelocytic Leukemia (M3)
Treatment of M3 AML can release Auer rods and produce DIC
167
Philadelphia Chromosome
Translocation
Associated disorder
t(9;22) bcr-abl hybrid
| CML
168
t(8;14)
Burkitt's Lymphoma (c-myc activation)
169
t(11;14)
Mantle Cell Lymphoma (cyclin D1 activation)
170
t(14;18)
Folliclar Lymphoma (bcl2 activation)
171
t(15;17)
M3 AML
| Responsive to all trans retinoic acid
172
```
Langerhans Cell Histocytosis
What is it?
Presentation
Description of cells
Markers
EM
```
Proliferative disorder of dendiritic cells from monocyte lineage
Child w/ lytic bone lesions and skin rash
Functionally immature and do not efficiently stimulate T lymphocytes via Ag presentation
S100 (neural crest cell origin) and CD1a
Birbeck granules (tennis rackets) on EM
173
```
Polycythemia Vera
What kind of disorder
RBCs
WBCs
Platelets
Philadelphia Chromosome
JAK2 mutation
```
```
Chronic Myeloproliferative Disorder
↑
↑
↑
-
+
```
174
```
Essential Thrombocytosis
What kind of disorder
RBCs
WBCs
Platelets
Philadelphia Chromosome
JAK2 mutation
```
```
Chronic Myeloproliferative Disorder
No change
No change
↑
-
+ (30-50%)
```
175
```
Myelofibrosis
What kind of disorder
RBCs
WBCs
Platelets
Philadelphia Chromosome
JAK2 mutation
```
```
Chronic Myeloproliferative Disorder
↓
Variable
Variable
-
+ (30-50%)
```
176
```
CML
What kind of disorder
RBCs
WBCs
Platelets
Philadelphia Chromosome
JAK2 mutation
```
```
Chronic Myeloproliferative Disorder
↓
↑
↑
+
-
```
177
Polycythemia Vera
PathoPhys
Presentation
Abnormal clone of hematopoietic stem cell with constitutively active JAK2 receptor that proliferate w/o EPO
Itching after a hot shower
178
Essential Thrombocytosis
Similar to Polycythemia Vera but specific for megakaryocytes
179
Myelofibrosis
What is it?
Histo
Fibrotic obliteration of bone marrow
Teardrop cell
"bone marrow is crying because it is fibrosed"
180
Relative Polycythemia
Plasma Vol
RBC mass
O2 Sat
↓
No change
No change
181
```
Appropriate Absolute Polycythemia
Plasma Vol
RBC mass
O2 Sat
Associated diseases
```
No change
↑
↓
Lung disease, Congenital Heart Disease, High Altitude
182
```
Inappropriate Absolute Polycythemia
Plasma Vol
RBC mass
O2 Sat
Associated diseases
What causes it?
```
```
No change
↑
No change
Renal Cell Carcinoma, Wilm's Tumor, Cyst, Hepatocellular Carcinoma, Hydronephrosis,
Ectopic EPO
```
183
Polycythemia Vera
Plasma Vol
RBC mass
O2 Sat
↑
↑↑
No change
184
```
Heparin
MoA
Half-life
Use
Can it be used during pregnancy
Monitoring
Tox
Antidote
```
Activates antithrombin leading to ↓ thrombin and ↓ X
Short half-life
PE, Acute Coronary Syndrome, MI, DVT
Can be used during pregnancy: does not cross placenta
Follow PTT
Bleeding, Thrombocytopenia (HIT), Osteoporosis, Drug-drug interactions
Protamine sulfate
185
Low Molecular Wt Heparin
Acts more on X, better bioavailability, and 2-4 times longer half-life
Can be administered subcutaneously and without laboratory monitoring
Not easily reversible
186
Heparin-Induced Thrombocytopenia (HIT)
Development of IgG Abs against heparin bound to platelet factor 4
Ab-Heparin-PF4 --> platelets --> thrombosis --> thrombocytopenia
187
```
Lepirudin, Bivalirudin, Argatroban
What kind of molecule
Used by what animals
MoA
Use
```
Derivative of Hirudin
Leeches
Anticoagulant that inhibits thrombin
Alternative to heparin in pts with HIT
188
```
Warfarin
AKA
MoA
What molecules are affected?
Metabolism
What happens in lab assay?
Half life
```
```
"The EX-PresidenT went to WARfarin"
Coumadin
Interferes with γ-carboxylation of VitK dependent clotting factors II, VII, IX, X, C, and S
CytP450
Affects extrinsic pathway and ↑ PT
Long half life
```
189
```
Warfarin
Use
Pregnancy
Monitoring
Tox
Treatment for OD
```
Chronic anticoagulant (after STEMI, Venous Thromboembolism, Stroke prevention after Afib)
Do not use in pregnant women (crosses placenta)
Follow PT/INR
Bleeding, Teratogenic, Skin/Tissue necrosis, Drug-drug interactions
VitK. For rapid reversal fresh frozen plasma
190
```
Heparin
Structure
Route of Administration
Site of action
Onset
Duration
```
```
Large, anionic acid polymer
Parenteral
Blood
Rapid
Hours
```
191
Do Heparin or Warfarin inhibit coagulation in vitro?
Only Heparin does
192
```
Warfarin
Structure
Route of Administration
Site of action
Onset
Duration
```
```
Small lipid soluble molecule
Oral
Liver
Slow
Days
```
193
```
Thrombolytics
Names
MoA
Labs
Use
```
Alteplase (tPA), Reteplase (rPA), Tenecteplase (TNK-tPA)
--> Plasmin
↑ PT, ↑ PTT, No change in platelet count
Early MI, Early Stroke, PE
194
Thrombolytics
Tox
Contraindications
OD treatment
Bleeding, Reperfusion arrhythmias
Active bleeding, Intracranial bleeding, Recent surgery, known bleeding diatheses, HTN
Aminocaproic acid
195
```
ADP receptor inhibitors
Names
MoA
Use
Usually combined w/...
Tox
```
Clopidogrel, Ticlopidine, Prasugrel, Ticagrelor
Irreversibly blocks ADP receptor. Inhibits fibrinogen binding by preventing glycoprotein IIb/IIIa from bind fibrinogen
Acute Coronary Syndrome; Coronary Stenting; ↓incidence or recurrence of thrombotic stroke
Aspirin
Ticlopidine: Neutropenia, oral ulcers, fever
196
Cilostazol, Dipyridamole
MoA
Use
Tox
Phosphodiesterase III inhibitor. ↑cAMP in platelets thus inhibiting platelet aggregation; Vasodilator
Claudication, Coronary Vasodilation, Prevention of stroke or TIA, Angina Prophylaxis
Nausea, Headache, Facial Flushing, Hypotension, Abdominal Pain
197
```
GP IIb/IIIa Inhibitors
Names
Structure
MoA
Use
Tox
```
Abciximab, Eptifibatide, Tirofiban
A is made from monoclonal Ab Fab fragment
Inhibits platelet aggregation by binding GP IIb/IIIa receptor on activated platelets
Acute coronary Syndromes, Percutaneous Transluminal Coronary Angioplasty
Bleeding, Thrombocytopenia
198
```
Methotrexate
Class of drug
MoA
Use
Tox
```
Antimetabolite
Folic Acid analog that inhibits DHF Reductase
↓ dTMP --> ↓ DNA and ↓ Protein synthesis
Leukemias, Lymphomas, Choriocarcinoma, Sarcomas, Abortion, Ectopic Pregnancy, RA, Psoriasis
Myelosuppression (reversible w/ leucovorin), Macrovesicular fatty change in liver, Mucositis, Teratogenic
199
```
5-Fluorouracil
Class of drug
MoA
Use
Tox
OD treatment
```
Antimetabolite
Pyrimidine analog. Bioactivated to 5F-dUMP, which covalentaly complexes folic acid. The complex inhibits Thymidylate synthase leading to ↓ dTMP --> ↓ DNA and ↓ Protein synthesis
Colon cancer, Basal cell carcinoma (topical)
Myelosuppression (irreversible w/ leucovorin), Photosensitivity
OD treat with Thymidine
200
```
Cytarabine
Name
Class of drug
MoA
Use
Tox
```
```
Arabinofuranosyl Cytidine
Antimetabolite
Pyrimidine analog inhibits DNA pol
Leukemias, Lymphomas
Leukopenia, Thrombocytopenia, Megaloblastic Anemia
```
201
```
Azathioprine, 6MP, 6-Thioguanine
Class of drug
MoA
Use
Tox
Metabolism
```
```
Antimetabolite
Purine analog --/ de novo purine synthesis
Activated by HGPRT
Leukemias
Bone Marrow, GI, Liver
Metabolized by Xanthine Oxidase
```
202
```
Dactinomycin
AKA
Class of drug
MoA
Use
Tox
```
```
Actinomycin D
Antitumor antibiotic
Intercalates DNA
Wilms Tumor, Ewing Sarcoma, Rhabdomyosarcoma, (Childhood tumors: "Children ACT out")
Myelosuppression
```
203
```
Doxorubicin (Adriamycin), Daunorubicin
Class of drug
MoA
Use
Tox
How to prevent certain toxicity
```
Antitumor antibiotic
Generates free radicals. Noncovalently intercalate in DNA --> breaks in DNA --> ↓ replication
Solid tumors, Leukemias, Lymphomas
Cardiotoxicity (dilated cardiomyopathy), Myelosuppression, Alopecia
Dexrazoxane (Fe chelator) used to prevent cardiotoxicity
204
```
Bleomycin
Class of drug
MoA
Use
Tox
```
Antitumor antibiotic
Induces free radical formation which causes breaks in DNA strand
Testicular cancer, Hodgkin's Lymphoma
Pulmonary Fibrosis, Skin Changes, Minimal Myelosuppression
205
```
Cyclophosphamide, Ifosfamide
Class of drug
MoA
Bioactivation
Use
Tox
How to prevent toxicity?
```
```
Alkylating Agent
Covalently links DNA @ guanine N7
Bioactivation in liver
Solid tumors, Leukemia, Lymphoma, Brain Cancers
Myelosuppression, Hemorrhagic cystitis
Mesna prevents toxicity
```
206
```
Nitrosoureas
Names
Class of drug
MoA
Bioactivation?
Use
Tox
```
```
Carmustine, Lomustine, Semustine, Streptozocin
Alkylating Agents
Alkylates DNA
Requires bioactivation
Brain tumors
CNS toxicity
```
207
```
Vincristine, Vinblastine
Class of drugs
MoA
Use
Tox
```
Alkaloids that bind to tubulin in M phase and blocks polymerization of MT. Mitotic spindle cannot form
Solid tumors, Leukemias, Lymphomas
Vincristine: Neurotoxicity (Areflexia, Peripheral Neuritis, Paralytic Ileus)
VinBLASTine: Blasts Bone marrow (suppression)
208
```
Paclitaxel
Class of drug
MoA
Use
Tox
```
```
Taxol, MT inhibitor
"It's TAXing to stay polymerized"
Hyperstabilizes polymerized MT in M phase so that anaphase cannot occur
Ovarian and breast carcinoma
Myelosuppression and hypersensitivity
```
209
```
Cisplatin, Carboplatin
MoA
Use
Tox
How to prevent toxicity
```
Cross-links DNA
Testicular, Bladder, Ovary, Lung Carcinoma
Nephrotoxicity, Acoustic nerve damage
Amifostine (free radical scavenger) and Chloride Diuresis
210
Etoposide, Teniposide
MoA
Use
Tox
--/ topoisomerase II --> ↑ DNA degradation
Solid tumors, Leukemias, Lymphomas
Myelosuppression, GI irritation, Alopecia
211
Hydroxyurea
MoA
Use
Tox
--/ Ribonucleotide Reducatse --/ ↓ DNA synthesis
Melanoma, CML, Sicle Cell Disease (↑ HbF)
Bone marrow suppression, GI upset
212
Prednisone as a cancer drug?
| Tox
CLL, Non-Hodgkin's Lymphoma
| Cushing's, Immunosuppression, Cataracts, Acne, Osteoporosis, Peptic ulcers, Hyperglycemia, Psychosis
213
Tamoxifen, Raloxifene
MoA
Use
Tox
SERM: Receptor antagonist in breast and agonist in bone
Breast cancer. Prevents osteoporosis
T: Partial agonist at endometrium --> ↑ endometrial cancer; Hot flashes
214
```
Trastuzumab
AKA
MoA
Use
Tox
```
Herceptin
Monoclonal Ab against HER-2 (c-erbB2), a Tyrosine Kinase
HER2+ breast cancer
Cardiotoxicity
215
```
Imatinib
AKA
MoA
Use
Tox
```
Gleevec
Philadelphia chromosome bcr-abl tyrosine kinase inhibitor
CML, GI stroma tumors
Fluid retention
216
Rituximab
MoA
Use
Ab against CD20 (found in most B cell lymphomas)
| Non-Hodgkin's Lymphoma, RA (w/ MTX)
217
Vemurafenib
MoA
Use
--/ B-Raf Kinase with V600E mutation
| Metastatic melanoma
218
Bevacizumab
MoA
Use
Ab against VEGF inhibits angiogenesis
| Solid Tumors
219
Common Chemotoxicities
```
Cisplatin/Carboplatin: C looks like like ears and kidney
Vincrisine: V like arms and legs
Bleomycin, Busulfan: B like lungs
Doxorubicin: D like heart
Trastuzumab: a T in the heart
CYclophosphamide: CY looks like bladder
5FU, 6MP, Methotrexate: Myelosuppression
```
220
Busulfan
MoA
Uses
Tox
Alkylates DNA
Alkylates DNA
CML, Ablates bone marrow before transplantation
Pulmonary Fibrosis, Hyperpigmentation
221
Heme degeneration
Heme --> [Heme oxygenase] --> Biliverdin --> Bilirubin
222
Black man on TMP/SMX with anemia and dark urine
G6PD deficiency
223
Dysphagia + Spoon nails
```
Iron deficiency
Plummer Vinson (esophageal webs)
```
