Heme/Onc - Week 2 Review - Part 2 Flashcards

(31 cards)

1
Q

LDH - Lab Value Meaning

A

Indicates Tumor or Hemolysis

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2
Q

Acute Leukemia Differentiation

A

AML - Auer Rods + MPO + CD33

ALL - TdT + Lymph (B=CD19/20/23 vs. T=2/7)

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3
Q

AML-M3 - Alternative Name + Genetics + Treatment + Associated Disease

A

Acute Promyelocytic Leukemia

t(17:15) - RAR Activated - Treatment = ARTA, vitamin will activate the receptor and force differentiation

Associated with DIC

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4
Q

Multiple Myeloma Labs (7)

A

1) Leukopenia
2) Thrombocytopenia
3) Low Hb
4) Low Hct
5) Elevated Total Protein with Low Albumin
6) High Creatine
7) Hypercalcemia

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5
Q

Multiple Myeloma Finds + Causes (6)

A

All due to Monoclonal Plasma Cells

1) Bone Break Down with Lytic Lesions - Osteoclast Activating Factor
2) Hypercalcemia - Osteoclast Activating Factor
3) Monoclonal Spike - Increased Ig
4) Infection - Monoclonal Ig
5) Proteinuria (with kidney damage) - Bence Jones Proteins - Light Chain
6) Roulox Formation on Smear - Spherocyte RBC Linking

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6
Q

Nodular Sclerosisng HL - Classic Case + Histology

A

Young Female with Medistinal/Cervical Mass

Reed Sternberg Cells - CD 15/30+

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7
Q

Nodular Sclerosing HL - ABVD Treatment

A

1) Adriamycin (Doxorubicin - Cardiotoxicity)
2) Belomycin (Anti-Tumor Abs - Pulm. Fibrosis
3) Vinblastine (Microtubule Inhibitor - Peripheral Neuropathy
4) Dacarbazine (Alkylating Agent)

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8
Q

Mechanisms of Drug Resistance (7)

A

1) Mutation
2) Gene Amplifaction (Overproduction of the drug’s target)
3) Efflux Pumps
4) Lack of Transport into cancer
5) DNA Repair - Cancer can learn DNA Repair
6) Drug Inactivation - Oxidation of the rug
7) Presence of Cancer Stem Cells (Hide)

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9
Q

Imatinib - Mechanism + Use (2) + Resistance Method (2)

A

Inhibits BCR-Abl and C-Kit

Use - CML (BCR) + Gastrointestinal Stromal Tumor (GIST) - C-Kit

Resistance - BCR-Amplication + Mutation in the drug binding site

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10
Q

hENT1-2 - Role In Resistance

A

Normally at the blood brain barrier to remove unwanted substance

Development elsewhere - Become drug efflux pumps

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11
Q

BRCA2 - Resistance Mechanism

A

BCRA2 - Mutation in DNA Repair Enzyme

Give drugs - it will mutate back and it can repair the DNA Again

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12
Q

Alkylating Agent Resistance (Platinums)

A

Gutathion S-Transferase Metabolizes Platinums and triggers their efflux

Increasing the GST System increases the efflux of the platinums

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13
Q

Atripimod - Mechanism + Resistance

A

JAK2 Inhibitor (works great in vivo)

In the body the cancer cells (SET2) are protected via the stromal cells

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14
Q

ABO Blood Groups - Sugars + Chromosome

A

Chromosome 9

A Antigen - N-Acetyl-Galactosamine
B Antigen - Galactose
O Antigen - None

Type O = Least vWF = Most Bleeding
Type AB = Most vWF = Least Bleading

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15
Q

Anti-ABO Antibodies - Key Points (3)

A

IgM - Warm Agglutanin - React at Normal Body Temperatures (key for transfusion)

IgM - Triggers Compliment Cascade - Rapid Intravascular Hemolysis - Why Matching Is Key

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16
Q

Anti-Rh Antibodies - Key Points (3)

A

IgG - Made in response to exposure

To small for compliment - bind and trigger splenic macrophage destruction (extravascular hemolysis)

Hemolytic Disease of Newborn (Small enough to cross placenta)

17
Q

Hemolytic Disease of the Newborn

A

IgG for Rh+ Crosses from baby #1 to mom (Rh(-)) - Not an issue for the first child

During second pregnancy mom has built anti Rh+ IgG which goes into the new Rh+ baby and attacks - Worse with each pregnancy

18
Q

Transfusion Implications of ABO (2)

A

Type O - Universal Donor - Won’t be attacked by any antibodies the person may have (E.g. Type A with Anti-B antibodies won’t get the Type O)

Type AB - Universal Recipient - No antibodies - can receive any type

19
Q

Rh-Immune Globulin - Mechanism + Use

A

Prevents hemolytic disease of the newborn

Give IgG Ab’s to the RhD Antibody - and newborn blood that escapes in the mom is knocked out before it has time to trigger mom’s Ab response

20
Q

Mycoplasma Pneumonia - Impact on Blood (3)

A

I Antigen - Triggers IgM and IgG after infection

IgM - Agglutinante in Cold Temps
IgG - Compliment Activation - Donath-Landstiener Anemia

21
Q

Blood Transfusion Components (4)

A

1) Packed RBCs
2) Platelets (HLA)
3) FFP
4) Cryopercipitate

22
Q

Packed RBCs - Key Points (3)

A

1) ABO Compitability
2) Expiration 3-6 Weeks (fridge)
3) Stored to long - low pH = hemolysis + 2,3 BPG drop (left shift)

23
Q

Platelets - Key Points (2)

A

1) HLA Matching if Possible

2) Expiration = 5 Days (then bacterial infection

24
Q

FFP - Uses (3) + Keys (2)

A

1) DIC
2) TTP
3) Warfarin Overdose

1) Stored Frozen (Expiration after 24 Hours)
2) Storage Factors V and VIII lost first

25
Cryopercipitatie - Keys (3)
1) Thawed FFP 2) Fibrinogen + Factor VIII + vWF 3) Used for DIC
26
Complications of Transfusion (6)
1) Infection 2) Febrile Reactions 3) Allergic Reaction 4) Acute Immune Mediated Hemolytic Reaction 5) Transfusion Associated Circulatory Overload (TACO) 6) Transfusion Related Acute Lung Injury (TRALI)
27
Febrile Transfusion Reaction - Key Point
Reaction to donor HLA - Mild Fever
28
Allergic Transfusion Reaction - Key Points (3)
1-3% of Transfusions - Circulating Ab's Against Donor Proteins KEY FOR EXAM IgA Deficient Recipient - Receives Blood with IgA - Recipient Anti-IgA Ab's attack the IgA from the donor causing sever anaphalxis Classic Presentation - Family Hx. of anaphlaxis with a "matched" patient (e.g. anaphalaxis not due to clerical error)
29
Acute Immune Mediated Hemolytic Reaction - Key Points (2)
Un-matached ABO Donor/Recipient #1 Cause = Clerical Error - Also Cross and Type
30
Transfusion Associated Circulatory Overload - Key Point
TACO Transfusion alters hemodynamic state - HTN + Pulm Edema
31
Transfusion Related Acute Lung Injury (TRALI) - Key Points (4)
1) 1-2 Hours After Transfusion 2) Severe Hypotension + Pulmonary Edema 3) Antibodies against donor HLA - Antibodies cause massive immune reaction with endothelial damage and fluid leak (pulm. edema) 4) #1 Cause of Transfusion Death