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Boards High Yield > Hematology/Oncology > Flashcards

Hematology/Oncology Flashcards

1
Q

Lifespan of erythrocyte

A

120 days

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2
Q

Anisocytosis

A

Varying sizes

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3
Q

Poikilocytosis

A

Varying shapes

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4
Q

Erythrocytosis

A

Polycythemia = ↑ Hematocrit

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5
Q

Reticulocyte

A

Immature erythrocyte marker of erythroid proliferation

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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

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7
Q

Results of Thrombocytopenia or Platelet Dysfunction

A

Petechiae

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8
Q

vWF receptor

A

GpIb

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9
Q

Fibrinogen receptor

A

GpIIb/IIIa

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10
Q

Leukocyte

Subtypes

A

Granulocytes (Neutrophils, Eosinophils, Basophils)

Mononuclear cells (Monocytes, Lymphocytes)

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11
Q

what is leukocyte alkaline phosphatase (LAP) and when is it elevated or decreased

A

An enzyme found in mature leukocytes. A high LAP –> increased number of mature white blood cells (e.g., from leukemoid reaction or myeloproliferative disorders);
a low LAP –> increased number of immature white blood cells (e.g., from CML)

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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)

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13
Q

Hypersegmented polys
Histo
Seen in

A

5 or more lobes

VitB12/Folate Deficiency

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14
Q

Increased Band Cells
What are they?
What do they reflect?

A

Immature Neutrophils

Increased myeloid proliferation (bacterial infection or CML)

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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

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16
Q 
Macrophage 
Function 
Lifespan
What activates them?
Marker
A

Phagocytosis, APC via MHCII
Long life in tissues
Activated by γ-Interferon
CD14

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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

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18
Q

Causes of eosinophilia

A

“NAACP”

Neoplastic, Asthma, Allergy, Collagen vascular disease, Parasites

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19
Q

Basophil
Function
Histo with function

A

Mediates allergic reactions

Basophilic granules with heparin (anticoagulant), Histamine (vasodilator), and Leukotrienes (LTD4)

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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

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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

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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

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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

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24
Q

Plasma Cell
Function
Histo
Pathology

A

Ab production
Off center nucleus, clock face chromatin, RER, well developed Golgi
Multiple Myeloma

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25
Q 
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
A 
Cellular immune response 
Bone marrow
Thymus 
Tc cells (CD8), Th (CD4), Treg (CD28)
CD3
80%
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26
Q

Blood group A

A

A Ag and B Ab

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27
Q

Blood group B

A

B Ag and A Ab

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28
Q

Blood group AB

A

A and B Ag. No Abs
Universal Recipient of RBCs
Universal Donor of Plasma

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29
Q

Blood group O

A

No Ag. A and B Abs
Universal donor of RBCs
Universal Recipient of Plasma

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30
Q

Rh factor

A

Ag on RBC surface

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31
Q

Erythroblastosis Fetalis
PathoPhys
Treatment

A

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

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32
Q

Blood groups Re crossing placenta

A

anti A and anti B IgM does not cross placenta

anti Rh IgG does cross the placenta

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33
Q

Intrinsic Coagulation Pathway

A

Collagen, Basement membrane, Activated platelets, or HMWK –> XII –> XI –> IX
IX + VIII –> X
XII –> Kallikrein

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34
Q

Extrinsic Coagulation Pathway

A

Thromboplastin (tissue factor) –> VII –> X

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35
Q

Common Coagulation Pathway

A

X + V –> II (thrombin) –> Fibrin
XIII (fibrin stabilizing factor) helps stabilize fibrin mesh
Thrombin also activates V, VIII, XIII

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36
Q

Kinin Cascade

A

Kallikrein thurs HMWK into Bradykinin

Bradykinin ↑ Vasodilation, Permeability, and Pain

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37
Q

Fibrinolytic System

A

XII –> Kallikrein –> Plasmin –> Fibrin mesh degradation

Plasmin also activates C3

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38
Q

Which reactions of the coagulation cascade require Ca and Phospholipids

A

XIa –> IX
VII –> VIIa
VIIa and (IXa + VIIIa) activation of X
Xa + Va activation of II

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39
Q

Hemophilia A

A

Deficiency in VIII

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40
Q

Hemophilia B

A

Deficiency of IX

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41
Q

VitK Pathway

A

Oxidized VitK –> [epoxide reductase] –> Reduced VitK

Reduced VitK is a cofactor for the maturation of II, VII, IX, X, C, and S

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42
Q

Warfarin

MoA

A

Inhibits Epoxide Reductase

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43
Q

Why are neonates given VitK?

A

They lack enteric bacteria that produce VitK

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44
Q

What does vWF do?

A

Carries/protects VIII

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45
Q

Anticoagulation cascade

A

Thrombomodulin on endothelial cells –> Protein C

C + S cleaves and inactivates Va and VIIIa

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46
Q

What does antithrombin do?

A

Inhibits activated forms of II, VII, IX, X, XI, XII

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47
Q

Function of Heparin

A

Activates Antithrombin

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48
Q

Factor V Leiden mutation

Classical presentation

A

Factor V resistant to inhibition by protein C

DVT –> PE

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49
Q

tPA

A

Thrombolytic that activates plasmin

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50
Q

Platelet Plug Formation Schematic

A

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

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51
Q

How does ADP affect coagulation

A

Released by platelets.

Helps platelets adhere to endothelium and induces platelets to express GpIIb/IIIa at platelet surface

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52
Q

Platelet Aggregation Pathway

A

Fibrinogen binds GpIIb/IIIa and links platelets

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53
Q

Pro Platelet Aggregation Factors

A

TXA2 (released by platelets), ↓ blood flow, ↑ platelet aggregation

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54
Q

Anti Platelet Aggregation Factors

A

PGI2 and NO (released by endothelial cells)
↑ blood flow
↓ platelet aggregation

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55
Q

Ticlopidine

A

Inhibits ADP induced expression of GpIIb/IIIa

Causes Neutropenia, Oral Ulcers, Fever

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56
Q

Clopidogrel

A

Inhibits ADP induced expression of GpIIb/IIIa

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57
Q

Abciximab

A

Inhibits GpIIb/IIIa directly

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58
Q

ESR
What causes it to increase?
↑ ESR
↓ ESR

A

Acute phase reactants in plasma (Fibrinogen) cause RBC aggregation and ↑ ESR
↑: Infection, Autoimmune, Malignancy, Pregnancy
↓: “CHaMP”
Polycythemia, Sickle Cell Anemia, CHF, Microcytosis, Hypofibrinogenemia

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59
Q

Acanthocyte

A

Spur cell indicative of Liver disease or Abetalipoproteinemia (cholesterol dysregulation)

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60
Q

Basophilic Stippling

A

“BASte the ox TAiL”

Thalassemias, Anemia of chronic disease, Lead Poisoning

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61
Q

Bite Cell

A

G6PD deficiency

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62
Q

Eliptocyte

A

Hereditary Elliptocytosis

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63
Q

Macro-Ovalocyte

A

Megaloblastic anemia (w/ hypersegmented polys) and Marrow failure

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64
Q

Ringed Siderblasts

A

Sideroblastic anemia

Excess Fe in Mito

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65
Q

Schistocyte

A

Helmet Cell

DIC, TTP/HUS, Traumatic Hemolysis (metal heart valve prosthesis)

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66
Q

Sickle Cell

A

Sickle Cell Anemia

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67
Q

Spherocyte

A

Hereditary spherocytosis, Autoimmune hemolysis

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68
Q

Teardrop cell

A

“RBC sheds a tear because it has been forced out of its home”

Bone marrow infiltration (myelofibrosis)

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69
Q

Target Cell

A

“HALT said the hunter to his target”

HbC disease, Asplenia, Liver disease, Thalassemia

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70
Q

Heinz Bodies
Process
Associated pathology

A

Oxidation of sulfhydryl groups leads to denatured Hb precipitation and damage to RBC membrane –> formation of bite cells
G6PD deficiency and α-thalassemia

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71
Q

Howell-Jolly Bodies
What is it?
How are they normally dealt with?
Associated pathology

A

Basophilic nuclear remnants found in RBCs
Normally removed from RBCs by splenic macrophages
Functional hyposplenia, asplenia, mothball ingestion (naphthalene)

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72
Q

Microcytic Anemias

A

“Find Those Small Plump Cells”

Iron Deficiency, ACD, Thalassemia, Pb poisoning, Sideroblastic anemia

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73
Q

Nonhemolytic Normocytic Anemias

A

ACD, Aplastic, Chronic Kidney Disease

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74
Q

Hemolytic Normocytic Anemias

A

Intrinsic: “SHEEPS”
Spherocytosis, G6PD or PK deficiency, HbC, Sickle Cell Anemia, Paroxysmal Nocturnal Hemoglobinuria
Extrinsic: Autoimmune, Microangiopathic, Macroangiopathic, Infections

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75
Q

Megaloblastic Macrocytic Anemias

A

Folate deficiency, B12 deficiency, Orotic Aciduria

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76
Q

NonMegaloblastic Macrocytic Anemias

A

Liver disease, Alcoholism, Reticulocytosis

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77
Q 
Iron Deficiency Anemia
What kind of anemia 
What causes it?
PathoPhys
Labs
Histo
How may it manifest
A 
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
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78
Q 
α Thalassemia 
What kind of anemia 
PathoPhys
Epidemiology 
How # of gene mutations re disease
A

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

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79
Q

β Thalassemia
What kind of anemia
PathoPhys
Epidemiology

A

Microcytic, Hypochromatic
Point mutation in splice sites and promoter sequence –> ↓ β
Mediterranean populations

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80
Q

β Thalassemia minor
PathoPhys
Symptoms
Diagnosis

A

Heterozygote: β chain underproduced
Asymptomatic
Increased HbA2 on electrophoresis

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81
Q 
β Thalassemia major
PathoPhys
Symptoms 
Treatment
Complications 
Presentation  
Hb
A 
Homozygote: β chain absent 
Severe anemia 
Blood transfusions (--> hemochromatosis)
Marrow expansion (crew cut on skull XR) --> skeletal deformities. Chipmunk facies 
HbF (α2γ2)
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82
Q

Presentation of HbS/β-Thalassemia Heterozygote

A

Mild to moderate sickle cell disease depending on amount of β globin production

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83
Q 
Lead Poisoning 
What kind of anemia 
PathoPhys
Presentation 
Treatment
A

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

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84
Q 
Sideroblastic Anemia 
What kind of anemia 
PathoPhys
What causes it?
Histo
Labs
Treatment
A

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

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85
Q

Megaloblastic Anemia
Basic Pathology
Consequences

A

Impaired DNA synthesis –> maturation of nucleus delayed relative to cytoplasm
Ineffective erythropoiesis –> pancytopenia

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86
Q 
Folate Deficiency 
What kind of anemia 
Etiologies 
Presentation 
Histo 
Labs
A

Megaloblastic
Malnutrition (alcoholics), malabsorption, antifolates (methotrexate, trimethoprim, phenytoin), ↑ requirement (hemolytic anemia, pregnancy)
Glossitis
Hypersegmented neutrophils
↓ Folate, ↑ Homocysteine, normal Methylmalonic acid

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87
Q 
B12 Deficiency 
What kind of anemia 
Etiologies 
Presentation 
Histo
Labs
A

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

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88
Q 
Orotic Aciduria 
What kind of anemia?
PathoPhys
Presentation 
Histo
Labs
Treatment
A

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

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89
Q

NonMegaloblastic Macrocytic Anemia
Pathology
What causes it?

A

Macrocytic anemia in which DNA synthesis is unimpaired

Liver disease, Alcoholism, Retculocytosis, Drugs (5FU, AZT, Hydroxyurea)

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90
Q

Intrinsic Hemolytic Normocytic, Normochromic Anemias
Intravascular w/ examples and findings
Extravascular w/ examples and findings

A

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
Q 
Anemia of Chronic Disease 
What kind of anemia?
PathoPhys
Findings
What can it become?
A 
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
Q

Aplastic Anemia
What kind of anemia
What causes it?

A

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
Q

Aplastic Anemia
Labs/Histo
Presentation
Treatment

A

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
Q

How does chronic kidney disease lead to anemia?

What kind of anemia?

A

↓ erythropoietin –> ↓ hematopoiesis –> Normocytic, Normochromic NonHemolytic anemia

95
Q 
Hereditary Spherocytosis 
What kind of anemia?
PathoPhys
How do RBCs look?
What happens to RBCs
Presentation 
Findings 
Treatment
A

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
Q 
G6PD Deficiency 
What kind of anemia?
Inheritance 
PathoPhys
What happens to RBCs?
Presentation 
Histo
A

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
Q 
PK deficiency 
What kind of anemia 
Inheritance 
PathoPhys
Presentation
A

Extravascular Intrinsic Hemolytic Normocytic Anemia
AR
Defective PK –> ↓ ATP –> rigid RBCs
Hemolytic anemia in a newborn

98
Q

HbC defect
What kind of anemia
PathoPhys
HbSC vs HbSS

A

Extravascular Intrinsic Hemolytic Normocytic Anemia
Glutamic Acid –> Lysine mutation at reside 6 of β globin
HbSC less severe than HbSS

99
Q 
Paroxysmal Nocturnal Hemoglobinuria 
What kind of anemia 
PathoPhys
Genetics 
Presentation 
Labs 
Treatment
A

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
Q 
Sickle Cell Anemia 
What kind of anemia?
Genetics 
Pathogenesis  
Newborns  
Heterozygotes
A

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
Q

Sickle Cell Anemia
Histo
XR
Treatment

A

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
Q

Sickle Cell Anemia Complications

A

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
Q

Autoimmune Hemolytic Anemia
What kind of anemia?
2 kinds?
Labs

A

Extrinsic Hemolytic Normocytic Anemia
Warm and Cold Agglutinin
Coomb’s Positive

104
Q

Coomb’s Test

A

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
Q

Warm Agglutinin
Ab
Course
What causes it?

A

“Warm weather is Great”
IgG
Chronic
SLE, CLL, drugs (metyldopa)

106
Q

Cold Agglutinin
Ab
Course
What causes it?

A

“Cold ice cream is yuMMM”
IgM
Acute anemia triggered by cold
CLL, Mycoplasma pneumonia infections, infectious Mononucleosis

107
Q 
Microangiopathic Anemia 
What kind of Anemia?
Pathogenesis 
Seen in what conditions 
Histo
A

Extrinsic Hemolytic Normocytic Anemia
RBCs damaged when passing through obstructed or narrowed vessel lumina
DIC, TTP/HUS, SLE, Malignant HTN
Schistocytes

108
Q

Macroangiopathic Anemia
What kind of Anemia?
Pathogenesis
Histo

A

Extrinsic Hemolytic Normocytic Anemia
Prosthetic heart valve and aortic stenosis damage RBCs
Schistocytes

109
Q

Infectious anemia
What kind of anemia
Examples

A

Extrinsic Hemolytic Normocytic Anemia

Malaria, Babesia

110
Q 
Iron Deficiency 
Serum Fe
TIBC (transferrin)
Ferritin 
Transferrin Saturation (Serum Fe/TIBC)
A

↓ (primary)
↑
↓
↓↓

111
Q 
Chronic Disease 
Serum Fe
TIBC (transferrin)
Ferritin 
Transferrin Saturation (Serum Fe/TIBC)
A

↓
↓
↑ (primary)
No change

112
Q 
Hemochromatosis 
Serum Fe
TIBC (transferrin)
Ferritin 
Transferrin Saturation (Serum Fe/TIBC)
A

↑ (primary)
↓
↑
↑↑

113
Q 
Pregnancy or OCP use
Serum Fe
TIBC (transferrin)
Ferritin 
Transferrin Saturation (Serum Fe/TIBC)
A

No change
↑ (primary)
No change
↓

114
Q 
Pb Poisoning 
What enzymes are affected?
What builds up where?
General Presentation 
Adults vs Children re exposure and presentation
A

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
Q 
Acute Intermittent Porphyria 
Enzyme affected
What accumulates where?
Presentation 
Treatment
A

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
Q 
Porphyria Cutanea Tarda 
Enzyme affected
What accumulates where?
Presentation 
Frequency
A

Uroporphyrinogen decarboxylase
Uroporphyrin (tea colored urine)
Blistering cutaneous photosensitivity
Most common porphyria

117
Q

Heme Synthesis Pathway

A

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
Q

Rate limiting step of Heme synthesis with regulation

A

δALA synthase

Inhibited by Glucose and Heme

119
Q

PT

A

Extrinsic and Common pathways

I, II, V, VII, X

120
Q

PTT

A

Intrinsic and Common pathways

all factors except VII, XIII

121
Q 
Hemophilia A or B
PT
PTT
PathoPhys
Presentation
A 
No change in PT
↑ PTT
Intrinsic coagulation defect 
A: VIII
B: IX
Macrohemorrhage: Hemarthrosis, Easy bruising
122
Q

VitK deficiency
PT
PTT
PathoPhys

A

↑ PT
↑ PTT
↓ synthesis of II, VII, IX, X, C, S

123
Q

Presentation of platelet abnormalities

A

Microhemorrhage: Mucus membrane bleeding, Epistaxis, Petechiae, Purpura, ↑ bleeding time, possible ↓ platelet count

124
Q

Bernard-Soulier Syndrome
PC
BT
PathoPhys

A

↓ PC
↑ BT
↓ GpIb –> defect in platelet to vWF adhesion

125
Q 
Glanzmann's Thrombasthenia 
PC
BT
PathoPhys
Labs
A

No change in PC
↑ BT
↓ GpIIb/IIIa –> defect platelet-to-platelet aggregation
No platelet clotting on blood smear

126
Q 
Idiopathic Thrombocytopenic Purpura (ITP)
PC
BT
PathoPhys
Labs
A

↓ PC
↑ BT
Anti-GpIIb/IIIa Ab –> splenic macrophage consumption of platelet/Ab complex –> ↓ platelet survival
↑ megakaryocytes

127
Q 
Thrombic Thrombocytopenic Purpura (TTP)
PC
BT
PathoPhys
Histo
Labs 
Symptoms
A

↓ 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
Q 
von Willebrands Disease 
PC
BT
PT
PTT
A

No change in PC
↑ BT
No change in PT
No change or ↑ PTT

129
Q 
von Willebrands Disease 
PathoPhys
Frequency 
Severity 
Inheritance 
Diagnosis 
Treatment
A

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
Q 
DIC
PC
BT
PT
PTT
A

↓ PC
↑ BT
↑ PT
↑ PTT

131
Q 
DIC
PathoPhys
What causes it?
Histo
Labs
A

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
Q

Factor V Leiden
PathoPhys
Epidemiology

A

Mutant V resistant to degradation by C –> hypercoagulability
Most common cause of inherited hypercoagulability in whites

133
Q

Prothrombin Gene mutation

A

Mutation in 3’ UTR –> ↑ production of prothrombin –> ↑ plasma levels and venous clots –> hypercoagulability

134
Q

AntiThrombin Deficiency
PathoPhys
Treatment

A

Inherited deficiency of antithrombin –> hypercoagulability

↑ PTT is blunted after heparin administration

135
Q

Protein C or S deficiency
PathoPhys
Treatment

A

↓ ability to inactivate V and VIII –> hypercoagulability

↑ risk of thrombotic skin necrosis with hemorrhage following administration of warfarin

136
Q

Packed RBCs
Purpose
Use

A

↑ Hb and O2 carrying capacity

Acute blood loss, severe anemia

137
Q

Transfusion of platelets
Purpose
Use

A

Increase platelet count

Stop significant bleeding (Thrombocytopenia, Qualitative platelet dysfunction)

138
Q

Transfusion of fresh frozen plasma
Purpose
Use

A

↑ Coagulation factor levels

DIC, Cirrhosis, Warfarin OD

139
Q

Transfusion of Cryoprecipitate
Contains
Use

A

Contains Fibrinogen, VIII, XIII, vWF, and Fibronectin

Treats coagulation factor deficiencies involving fibrinogen and VIII

140
Q

Risks of Blood Transfusions

A

Infection, Transfusion reaction, Iron Overload, HypoCa (citrate is a Ca chelator), HyperK (RBC lysis)

141
Q

Leukemia
What is it?
Where are tumors found?

A

Lymphoid or Myeloid neoplasm with widespread involvement of bone marrow
Tumor cells are usually found in peripheral blood

142
Q

Lymphoma
What is it?
Presentation?

A

Discrete tumor masses arising form lymph nodes

Presentations blur definitions

143
Q

Leukemoid Reaction
What is it?
Labs
Contrast with CML

A

Acute inflammatory response to infection
↑ WBC count with ↑ neutrophils and bands
↑ Leukocyte ALP
In CML, ↓ Leukocyte ALP

144
Q 
Hodgkin's Lymphoma 
Distribution 
Stage re prognosis 
Histo
Epidemiology 
What is it associated with?
Presentation
A

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
Q 
Non-Hodgkin's Lymphoma 
Distribution 
Histo
Epidemiology 
What is it associated with?
Presentation
A

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
Q 
Reed-Sternberg Cells
Appearance 
What kind of cancer?
Markers
Origin
Re Diagnosis 
Re Prognosis
A

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
Q

Nodular Sclerosing Hodgkin’s Lymphoma
Frequency
Epidemiology

A

Most common

Affects women and men equally

148
Q

Hodgkin’s Lymphoma with worst prognosis

A

Lymphocyte mixed or depleted forms

149
Q 
Burkitt's Lymphoma 
What kind of cancer?
Neoplasm of what?
Epidemiology 
Genetics 
Histo
Associated with what?
Endemic vs sporadic
A 
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
Q 
Diffuse Large B cell Lymphoma 
What kind of cancer?
Neoplasm of what?
Epidemiology  
Frequency 
Origin
A 
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
Q 
Mantle Cell Lymphoma 
What kind of cancer?
Neoplasm of what?
Epidemiology 
Genetics 
Prognosis
Markers
A 
Non-Hodgkin's Lymphoma 
Neoplasm of mature B cells
Older males 
t[11 (cyclin D1), 14 (heavy-chain Ig)]
Poor
CD5
152
Q 
Follicular Lymphoma 
What kind of cancer?
Neoplasm of what?
Epidemiology 
Genetics 
Course 
PathoPhys
A 
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
Q 
Adult T cell Lymphoma 
What kind of cancer?
Neoplasm of what?
Epidemiology 
Genetics 
Presentation 
Population affected 
Course
A 
Non-Hodgkin's Lymphoma 
Neoplasm of mature T cells
Adults 
Caused by HTLV1
Cutaneous lesions 
Japan, West Africa, Caribbean 
Aggressive
154
Q 
Mycosis Fungoides 
AKA
What kind of cancer?
Neoplasm of what?
Epidemiology 
Presentation 
Markers
Course
A 
Sezary Syndrome 
Non-Hodgkin's Lymphoma 
Neoplasm of mature T cells
Adults 
Cutaneous patches/nodules 
CD4
Indolent course
155
Q 
Multiple Myeloma 
Histo
Where does it arise from
Frequency 
What does it produce?
A

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
Q 
Multiple Myeloma 
Associations 
XR
Electrophoresis 
UA
Blood smear 
Presentation
A

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
Q

How to distinguish Waldenstrom’s Macroglobinemia from Multiple Myeloma

A

Both have an M spike but WM doesn’t have lytic bone lesions

158
Q

What is the M spike?

A

Spike in γ on protein electrophoresis

Multiple Myeloma, Waldenstrom’s Macroglobulinemia, MGUS

159
Q 
MGUS
What does it stand for?
What is it?
Electrophoresis
Symptoms 
What is it a precursor to
A 
Monoclonal Gammopathy of Undetermined Significance 
Monoclonal expansion of plasma cells
M spike 
Asymptomatic 
Precursor to multiple myeloma
160
Q

Leukemia
What is it basically?
Pathway of Presentation
Infiltrates?

A

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
Q 
Acute Lymphoblastic Leukemia/Lymphoma 
Kind of cancer?
Epidemiology 
Presentation 
Markers 
Response?
Metastasis 
Genetics with prognosis
A

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
Q 
Small Lymphocytic Lymphoma (SLL)/Chronic Lymphocytic Leukemia (CLL)
Kind of cancer?
Epidemiology 
Presentation 
Difference between them
A

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
Q 
Hairy Cell Leukemia 
What kind of cancer 
Epidemiology 
In elderly?
Histo
Treatment
A

Lymphoid neoplasm
Adults
Mature B cell tumor in the elderly
Filamentous hair like projections. Stains TRAP+
Cladribine (adenosine analog resistant to ADA)

164
Q 
Acute Myelogenous Leukemia (AML)
What kind of cancer?
Epidemiology 
Histo 
Smear
Genetics Re Treatment 
Common presentation
A

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
Q 
Chronic Myelogenous Leukemia (CML)
What kind of cancer?
Epidemiology 
Genetics 
Origin
Presentation 
Course 
Labs
Treatment
A

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
Q

Auer Bodies (rods)
What are they?
Where are they commonly seen
What can they cause?

A

Peroxidase+ Cytoplasmic inclusions in granulocytes and myeloblasts
Acute polymyelocytic Leukemia (M3)
Treatment of M3 AML can release Auer rods and produce DIC

167
Q

Philadelphia Chromosome
Translocation
Associated disorder

A

t(9;22) bcr-abl hybrid

CML

168
Q

t(8;14)

A

Burkitt’s Lymphoma (c-myc activation)

169
Q

t(11;14)

A

Mantle Cell Lymphoma (cyclin D1 activation)

170
Q

t(14;18)

A

Folliclar Lymphoma (bcl2 activation)

171
Q

t(15;17)

A

M3 AML

Responsive to all trans retinoic acid

172
Q 
Langerhans Cell Histocytosis 
What is it?
Presentation 
Description of cells 
Markers 
EM
A

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
Q 
Polycythemia Vera 
What kind of disorder 
RBCs
WBCs
Platelets 
Philadelphia Chromosome 
JAK2 mutation
A 
Chronic Myeloproliferative Disorder 
↑
↑
↑
-
\+
174
Q 
Essential Thrombocytosis  
What kind of disorder 
RBCs
WBCs
Platelets 
Philadelphia Chromosome 
JAK2 mutation
A 
Chronic Myeloproliferative Disorder 
No change
No change
↑
-
\+ (30-50%)
175
Q 
Myelofibrosis   
What kind of disorder 
RBCs
WBCs
Platelets 
Philadelphia Chromosome 
JAK2 mutation
A 
Chronic Myeloproliferative Disorder 
↓
Variable
Variable
-
\+ (30-50%)
176
Q 
CML   
What kind of disorder 
RBCs
WBCs
Platelets 
Philadelphia Chromosome 
JAK2 mutation
A 
Chronic Myeloproliferative Disorder 
↓
↑
↑
\+
-
177
Q

Polycythemia Vera
PathoPhys
Presentation

A

Abnormal clone of hematopoietic stem cell with constitutively active JAK2 receptor that proliferate w/o EPO
Itching after a hot shower

178
Q

Essential Thrombocytosis

A

Similar to Polycythemia Vera but specific for megakaryocytes

179
Q

Myelofibrosis
What is it?
Histo

A

Fibrotic obliteration of bone marrow
Teardrop cell
“bone marrow is crying because it is fibrosed”

180
Q

Relative Polycythemia
Plasma Vol
RBC mass
O2 Sat

A

↓
No change
No change

181
Q 
Appropriate Absolute Polycythemia 
Plasma Vol
RBC mass
O2 Sat
Associated diseases
A

No change
↑
↓
Lung disease, Congenital Heart Disease, High Altitude

182
Q 
Inappropriate Absolute Polycythemia 
Plasma Vol
RBC mass
O2 Sat
Associated diseases 
What causes it?
A 
No change 
↑
No change
Renal Cell Carcinoma, Wilm's Tumor, Cyst, Hepatocellular Carcinoma, Hydronephrosis,  
Ectopic EPO
183
Q

Polycythemia Vera
Plasma Vol
RBC mass
O2 Sat

A

↑
↑↑
No change

184
Q 
Heparin 
MoA
Half-life 
Use
Can it be used during pregnancy 
Monitoring 
Tox
Antidote
A

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
Q

Low Molecular Wt Heparin

A

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
Q

Heparin-Induced Thrombocytopenia (HIT)

A

Development of IgG Abs against heparin bound to platelet factor 4
Ab-Heparin-PF4 –> platelets –> thrombosis –> thrombocytopenia

187
Q 
Lepirudin, Bivalirudin, Argatroban 
What kind of molecule 
Used by what animals 
MoA
Use
A

Derivative of Hirudin
Leeches
Anticoagulant that inhibits thrombin
Alternative to heparin in pts with HIT

188
Q 
Warfarin 
AKA
MoA
What molecules are affected?
Metabolism 
What happens in lab assay?
Half life
A 
"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
Q 
Warfarin 
Use
Pregnancy 
Monitoring 
Tox
Treatment for OD
A

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
Q 
Heparin 
Structure 
Route of Administration 
Site of action
Onset
Duration
A 
Large, anionic acid polymer 
Parenteral 
Blood
Rapid
Hours
191
Q

Do Heparin or Warfarin inhibit coagulation in vitro?

A

Only Heparin does

192
Q 
Warfarin 
Structure 
Route of Administration 
Site of action
Onset
Duration
A 
Small lipid soluble molecule 
Oral
Liver
Slow
Days
193
Q 
Thrombolytics 
Names
MoA
Labs
Use
A

Alteplase (tPA), Reteplase (rPA), Tenecteplase (TNK-tPA)
–> Plasmin
↑ PT, ↑ PTT, No change in platelet count
Early MI, Early Stroke, PE

194
Q

Thrombolytics
Tox
Contraindications
OD treatment

A

Bleeding, Reperfusion arrhythmias
Active bleeding, Intracranial bleeding, Recent surgery, known bleeding diatheses, HTN
Aminocaproic acid

195
Q 
ADP receptor inhibitors 
Names
MoA
Use
Usually combined w/...
Tox
A

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
Q

Cilostazol, Dipyridamole
MoA
Use
Tox

A

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
Q 
GP IIb/IIIa Inhibitors 
Names
Structure 
MoA
Use
Tox
A

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
Q 
Methotrexate 
Class of drug 
MoA
Use
Tox
A

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
Q 
5-Fluorouracil  
Class of drug 
MoA
Use
Tox
OD treatment
A

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
Q 
Cytarabine 
Name
Class of drug
MoA
Use
Tox
A 
Arabinofuranosyl Cytidine 
Antimetabolite 
Pyrimidine analog inhibits DNA pol
Leukemias, Lymphomas 
Leukopenia, Thrombocytopenia, Megaloblastic Anemia
201
Q 
Azathioprine, 6MP, 6-Thioguanine 
Class of drug
MoA
Use
Tox
Metabolism
A 
Antimetabolite 
Purine analog --/ de novo purine synthesis 
Activated by HGPRT
Leukemias 
Bone Marrow, GI, Liver
Metabolized by Xanthine Oxidase
202
Q 
Dactinomycin 
AKA
Class of drug
MoA
Use
Tox
A 
Actinomycin D
Antitumor antibiotic 
Intercalates DNA
Wilms Tumor, Ewing Sarcoma, Rhabdomyosarcoma, (Childhood tumors: "Children ACT out")
Myelosuppression
203
Q 
Doxorubicin (Adriamycin), Daunorubicin 
Class of drug
MoA
Use
Tox
How to prevent certain toxicity
A

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
Q 
Bleomycin 
Class of drug
MoA
Use
Tox
A

Antitumor antibiotic
Induces free radical formation which causes breaks in DNA strand
Testicular cancer, Hodgkin’s Lymphoma
Pulmonary Fibrosis, Skin Changes, Minimal Myelosuppression

205
Q 
Cyclophosphamide, Ifosfamide 
Class of drug
MoA
Bioactivation 
Use
Tox
How to prevent toxicity?
A 
Alkylating Agent 
Covalently links DNA @ guanine N7
Bioactivation in liver 
Solid tumors, Leukemia, Lymphoma, Brain Cancers
Myelosuppression, Hemorrhagic cystitis
Mesna prevents toxicity
206
Q 
Nitrosoureas 
Names
Class of drug
MoA
Bioactivation?
Use
Tox
A 
Carmustine, Lomustine, Semustine, Streptozocin
Alkylating Agents 
Alkylates DNA
Requires bioactivation 
Brain tumors 
CNS toxicity
207
Q 
Vincristine, Vinblastine 
Class of drugs
MoA
Use
Tox
A

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
Q 
Paclitaxel 
Class of drug
MoA
Use
Tox
A 
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
Q 
Cisplatin, Carboplatin 
MoA
Use
Tox
How to prevent toxicity
A

Cross-links DNA
Testicular, Bladder, Ovary, Lung Carcinoma
Nephrotoxicity, Acoustic nerve damage
Amifostine (free radical scavenger) and Chloride Diuresis

210
Q

Etoposide, Teniposide
MoA
Use
Tox

A

–/ topoisomerase II –> ↑ DNA degradation
Solid tumors, Leukemias, Lymphomas
Myelosuppression, GI irritation, Alopecia

211
Q

Hydroxyurea
MoA
Use
Tox

A

–/ Ribonucleotide Reducatse –/ ↓ DNA synthesis
Melanoma, CML, Sicle Cell Disease (↑ HbF)
Bone marrow suppression, GI upset

212
Q

Prednisone as a cancer drug?

Tox

A

CLL, Non-Hodgkin’s Lymphoma

Cushing’s, Immunosuppression, Cataracts, Acne, Osteoporosis, Peptic ulcers, Hyperglycemia, Psychosis

213
Q

Tamoxifen, Raloxifene
MoA
Use
Tox

A

SERM: Receptor antagonist in breast and agonist in bone
Breast cancer. Prevents osteoporosis
T: Partial agonist at endometrium –> ↑ endometrial cancer; Hot flashes

214
Q 
Trastuzumab 
AKA
MoA
Use
Tox
A

Herceptin
Monoclonal Ab against HER-2 (c-erbB2), a Tyrosine Kinase
HER2+ breast cancer
Cardiotoxicity

215
Q 
Imatinib 
AKA
MoA
Use
Tox
A

Gleevec
Philadelphia chromosome bcr-abl tyrosine kinase inhibitor
CML, GI stroma tumors
Fluid retention

216
Q

Rituximab
MoA
Use

A

Ab against CD20 (found in most B cell lymphomas)

Non-Hodgkin’s Lymphoma, RA (w/ MTX)

217
Q

Vemurafenib
MoA
Use

A

–/ B-Raf Kinase with V600E mutation

Metastatic melanoma

218
Q

Bevacizumab
MoA
Use

A

Ab against VEGF inhibits angiogenesis

Solid Tumors

219
Q

Common Chemotoxicities

A 
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
Q

Busulfan
MoA
Uses
Tox

A

Alkylates DNA
Alkylates DNA
CML, Ablates bone marrow before transplantation
Pulmonary Fibrosis, Hyperpigmentation

221
Q

Heme degeneration

A

Heme –> [Heme oxygenase] –> Biliverdin –> Bilirubin

222
Q

Black man on TMP/SMX with anemia and dark urine

A

G6PD deficiency

223
Q

Dysphagia + Spoon nails

A 
Iron deficiency 
Plummer Vinson (esophageal webs)

Boards High Yield (28 decks)

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