Heme/Onc - Week 2 Review - Part 2 Flashcards

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
Q

Cryopercipitatie - Keys (3)

A

1) Thawed FFP
2) Fibrinogen + Factor VIII + vWF
3) Used for DIC

26
Q

Complications of Transfusion (6)

A

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
Q

Febrile Transfusion Reaction - Key Point

A

Reaction to donor HLA - Mild Fever

28
Q

Allergic Transfusion Reaction - Key Points (3)

A

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
Q

Acute Immune Mediated Hemolytic Reaction - Key Points (2)

A

1 Cause = Clerical Error - Also Cross and Type

Un-matached ABO Donor/Recipient

30
Q

Transfusion Associated Circulatory Overload - Key Point

A

TACO

Transfusion alters hemodynamic state - HTN + Pulm Edema

31
Q

Transfusion Related Acute Lung Injury (TRALI) - Key Points (4)

A

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