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Z - M2 Heme/Onc > Heme/Onc - Week 1 Review - Part 2 > Flashcards

Heme/Onc - Week 1 Review - Part 2 Flashcards

1
Q

Four Major Chemotherapy Drug Classes

A

1) Alkylators
2) ANtimetabolities
3) DNA Repair Inhibitor
4) Anti-Tubulins

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2
Q

Cancers with a Chemotherapy as a Possible Cure (3)

A

1) Hodgkin
2) NHL
3) Testicular

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3
Q

Cancers with Chemotherapy Survival Benefit (6)

A

1) Breast
2) Ovarian
3) Endometrial
4) Cervical
5) Small Cell Lung
6) Colorectal

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4
Q

Alkylating Agents - Major Mechanism + Major Toxicities (4)

A

Mechanism - Trigger bifunctional moieties –> cause double strand breaks

Toxicity - GI Tract + Bone Marrow + Vesicant (infiltration) + Carcinogenic (Increased risk for of AML later in life)

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5
Q

CHOP Therapy for NHL and CLL

A

Cyclophosphamide (Alkylator) + Hydroxydaunorubicin (Doxorubicin) + Nocovorin (Vincristine - Microtubule Inhibitor) + Prednisone

Generics = CDVP

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6
Q

Capecitabine - Major Function + Toxicity

A

Function - Prodrug - Antimetabolite

Causes Foot and Hand Syndrome

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7
Q

Leucovorin - Mechanism + Toxicity

A

Mech - Methotrexate Rescue Drug

No Tox (Tricky)

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8
Q

6-MP - Key Toxicity

A

6-MP Deactivated by Xanthine Oxidase - XO is knocked out by allopurinol - must be careful for co-administration

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9
Q

Topoisomerase Inhibitors - Class + Name (3)

A

Topotecan - Top-1 Inhibitor = Single Strand DNA

Etoposide - Top-2 Inhibitor = Double Strand DNA

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10
Q

Vinblastine vs. Vincristine - Major Side Effect

A

Vinblastine - Vesicant (Infiltration)

Vincristine - Neurotoxicity

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11
Q

Lead Time Interval + Bias

A

Interval - Time from when you would detect disease on screening vs. when the patient would naturally present with s/sx

Bias - Because you see disease early patients who are screened may “live longer” but you may not be slowing the disease, you’re just seeing the course longer

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12
Q

Length Bias

A

Diseases caught on screening are more likely to be slower and less aggressive (rapid/aggressive will show symptoms fast)

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13
Q

Prevalence Impact on Screening

A

High Prevalence increases PPV of a test (more likely to get it right) - Over time screening reduces the prevalence of disease which reduces the effectiveness of the test

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14
Q

PSA Testing - Screening Basics

A

10/100 People Screened with PSA will be Postive

Of Those 10 who are positive 3 will have disease (30%)

Of The 90 who are negative 1 will have the disease (1/90)

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15
Q

Imantinib - Key Mechanism + Resistance Site

A

Mechanism - Blocks BCR-Abl fro t(9:22) in CML

Resistance Pathway - Change in the binding cleft of BCR-Abl

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16
Q

Trastuzumab - Mechanism + Key Toxicity

A

Alternative Name - (Herceptin)

Mechanism - HER2 Signaling

Toxicity - Cardiotoxic (with Doxorubicin)

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17
Q

Chronology of Hematopoesis Location During Development - 5 Sites Prior to Birth

A

1) Yolk Sac
2) Placenta
3-4) Spleen + Fetal Liver
5) Bone Marrow

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18
Q

Hematopoeisis Over A Life Time - Locations (After Birth)

A

High In tibia and femur at both - degenerate and central locations take over
Age 75 - Vertebrae still 75% cellular
Age 20 - Femur only 25% cellular

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19
Q

Embryological Origin of Bone Marrow

A

Mesoderm

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20
Q

HSC Niche - 5 Major Factors

A

1) Osteoblast Notch Pathway
2-4) Endothelial Cells - Kit + CXCL12 and 4
5) Thrombopoetin (Platlet stimulating factor)

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21
Q

Major HSC Markers (3)

A

1) CD34+ - N-Terminus binds ICAM and holds in the Niche
2) Thy1+
3) CD33(-)

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22
Q

Other Normal CD Markers (5)

A

1) CD2-10 - T-Cells
2) CD11-15 - Myeloid + Monocyte Markers
3) CD19-23 - B-Cells
4) CD33 - Immature Myeloid Marker - AML Sign
5) CD56+ - NK Cells

23
Q

HSC Develops into Two Lineages (IL Markers)

A

1) Common Myeloid Progenitor (CD33+) - IL-3

2) Common Lymphoid Progenitor (TdT+) - IL-7

24
Q

Major Small Lymphocyte IL Molecules - 2 Lineages

A

T-Lymphocyte (CD2-10) - IL 7 and IL-2

B-Lymphocyte (CD19-23) - IL-4

25
Q

Major IL Molecules for Myeloblast Development (3) + 4 Major Cell Types Produced

A

1) GM-CSF
2) IL-3
3) IL-5

1) Basophil
2) Eosinophil
3) Neutrophil
4) Monocyte/Macrophage

26
Q

JAK/STAT Pathway - 4 Key Steps

A

1) Receptor Binding
2) Triggers JAK Activation (Tyrosine Kinase)
3) Phosphorylates STAT
4) STAT Turn on Nuclear Signals

27
Q

Major Interlukins (IL1-8)

A

Hot T-Bone stEAK
IL-1 - Fever + Acute Inflammation
IL-2 - T-Cell Activation
IL-3 - Bone - Marrow Activation (Common Myeloid Progintor)
IL-4 - IgE + IgG Class Switching + Th2 Differentiation + B-Cell Growth (Think Hemoatopoesis)
IL-5 - IgA Class Switching + Eosinophilia
IL-6 - K - Acute Phase Protein Production (Fever + Protein Synthesis)
IL-7 - T-Cell Stimulation
IL-8 - Clean-Up on Aisle 8 - Neutrophil Chemotraction

28
Q

EPO Stimulation of RBC Production - 4 Effects

A

1) Cells Get Small (Microcytic)
2) Cytoplasm Changes - Blue to Pink (More chromatic)
3) Nucleus/Cytoplasm Ratio Falls
4) Nucleus extruded prior to the reticulocyte being kicked out

29
Q

EPO Mechanism of Stimulation

A

JAK/STAT-5 Pathway

30
Q

Polycythemia Vera - Mechanism (Genetics)

A

Acquired Jak2 Mutation - Valine to Phenylalaine - Continuous activation of JAX2/STAT5 leads to hypervisciousity

31
Q

Signs of T-Cell Deficiencies (3)

A

1-2) Fungal Infections - Pneumocystis + Cryptococcus) - Thrush!
3) Herpes

32
Q

Signs of B-Cell Deficiencies (5)

A

1) Bacterial Pneumonia + Streptococcus
2) Bacterial GI Infection
3) Parasitic Infections (Giardia)
4) Endovirus Infection
5) Encapsulated Bacterial Infection

33
Q

Signs of Granulomatous Phagocyte Deficiencies (4)

A

1) Recurrent Skin Infection
2) Staph
3) Nocardia (Pneumonia)
4) Aspergillus - Respiratory)

34
Q

Signs of Complement Deficiencies (2)

A

1) Straight to Sepsis

2) Neisseria

35
Q

Major T-Cell Deficiencies (4)

A

1) SCID
2) DiGeorge
3) Ataxia Telangiectasia
4) Wiskott-Aldrich

36
Q

SCID - Genetics + Cause

A

Genetics - X-Linked

Cause - Complete failure of immune T-Cell Function

37
Q

DiGeorge - Cause + Key Facts (5)

A

Cause - Defects om 3rd + 4th Pharygeal Arch End Organs

Key - Facts - CATCH
C - Cardiac Abnormality (Tetrology of Fallot)
A - Abnormal Facies
T - Thymic Aplasia (No T-Cells)
C - Cleft Palate
H - Hypercalciema due to hypo-parathyroid

38
Q

Ataxia Telangiectasia - Genetics + Cause + Key Facts

A

Genetics - Variable T-Cell (CD3/4) Deficit

Cause - Variable T-Cell (CD3/4) Deficit

Key - Facts - 3A’s

1) Ataxia
2) Spider Angiomas
3) IgA Deficiency

39
Q

Wiskott Aldrich - Genetics + Key Facts

A

Genetics - X-Linked (Male)

Key - Facts - WATER - Wiscott Aldrich Leads to Thrombocytopenic Purpura + Eczema + Recurrent Infection
Low IgG/IgM - High IgE

40
Q

Major B-Cell Deficiencies (3)

A

1) Selective IgA Deficiency
2) X-Link Agammaglobulinemia - Burtons
3) CVID

41
Q

Selective IgA Deficiency - Cause + Key Facts

A

Cause - Only IgA Low

Key Facts - Transfusion is key - body thinks IgA is foreign (first time builds Abs - second transfusion body attacks)

42
Q

X-Linked Agammaglobulinemia - Genetics + Cause + Key Facts

A

Genetics - X-Linked

Cause - Defect in Burton tyrosine kinase - No B-Cell Maturation

Key Facts - High level of infection after 6-months (maternal IgG gone) - Enterovirus common

43
Q

Common Variable Immunodeficiency - Cause + Key Facts

A

Cause - Low levels of serum Ig with normal B-Cell Levels - don’t mature + produce Ig

Key Facts - Late Onset (10-30 y/o)

44
Q

Autosomal Dominant Heme/Onc Disorders (7) - With explanations

A

1) Familial Adenomatous Polyposis - APC Defect predisposes for Colon Cancer
2) Hereditary Spherocytosis - Normocytic Extravascular Anemia - Spheriod erythrocytes from defect in spectrin or ankyrin - Increased MCHC (Red) + RDW (Cell size variety)
3) Li-Fraumeni Syndrome - p53 abnormalities - massive increased risk for cancer
4) Von Hipple Lindaue
5) Retinoblastoma Mutation
6) Job’s Syndrome - Overactivation of JAK/STAT3 - Eosinophila + Hyper IgE
7) Diamond Blackfan Anemia - Snub Nose + Short + Pure RBC Aplasia

45
Q

Autosomal Recessive Heme/Onc Disorders (4)

A

1) Sickle Cell Anemia
2) Thalessemia
3) Leukocyte Adhesion Deficiency Type I
4) Fanconi Anemia

46
Q

X-Linked Recessive Heme/Onc Disorders (8)

A

1) Burton (X-Linked) Agammaglobulinemia) - B-Cell Disorder
2) Wiskott-Aldrich (T-Cell Disorder)
3) GP6D Deficiency - Low Glutatione = Low tolerance for oxidative stress (fava beans etc.)
4) Hemophilia A
5) Hemophilia B
6) SCID
7) Hyper IgM Syndrome
8) Dyskeratosis Congenita (DKC)

47
Q

Major Granulomatous/Phagocytosis Disease (3)

A

1) Chronic Granulomatous Disease
2) Chediak-Higashi Syndrome
3) Leukocyte Adhesion Deficiency Type 1

48
Q

Chronic Granulomatous Disease - Pathophysiology + Common Infections (6) + Key Facts (3)

A

Pathophysiology - Defect in NADPH Oxidase - No respiratory burst and superoxide formation

Infections - Catalatse Postive PLACES
Pseudomonas
Listeria
Aspirgilius
Candida
E. Coli
S. Aureus

Key Facts - Suceptible to Catalase + Organisms (because they avoid the alternative superoxide pathway)
Nitroblue Terazolium Test Postive
Major Treatment = PEG-Interferon

49
Q

Chediak-Higashi Syndrome - Pathophysiology + Key Facts

A

Pathophysiology - Defect in transport to the lysomome

Key Facts - Albanism + giant granules in the neutrophils

50
Q

Leukocyte Adhesion Deficiency Type 1 - Genetics + Pathophysiology + Key Facts

A

Genetics - Autosomal Recessive CD18 Defect

Pathophysiology - CD18 Defect

Key Facts - Delayed separation of umbilical cord + increased circulating neutrophils

51
Q

Chronic Granulomatous Disease - Key Test + Major Treatment Option

A

Nitroblue Tetrazolium Test - No NADPH Burst = Negative Test (Doesn’t Turn Blue)

Positive Test (Functional Burst/No Disease) - NTT Turns Blue

Treatment - PEG-Interferon Gamma

52
Q

Think T-Cell vs. Think B-Cell

A

T-Cell - Infant + Thursh

B-Cell - Otitis Media

53
Q

Myeloperoxidase Defeciency - Key Facts (3)

A

Loss of Conversion of H2O2 to HOCl

Increased Candida Infection

Normal Nitro Blue Test

54
Q

Job’s Syndrome - Key Fact (4) - Big For Exam

A

1) Hyper IgE Syndrome (B-Cell) - Eosinophilia
2) Triad - Eosinophilia + Eczema + Recurrent Sinopulmonary Infactions
3) Autosomal Dominant
4) JAK/STAT3 Over-activation

Z - M2 Heme/Onc (10 decks)

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