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Medical Genetics > Medications for EXAM #3 > Flashcards

Medications for EXAM #3 Flashcards

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Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

What is the difference between traditional chemotherapy and targeted therapy?

A

Traditional chemo targets ALL dividing cells, while targeted therapies bind antigens or receptors on tumor cells.
L19a #3

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2
Q

Name three monoclonal antibody cancer therapies

A

Bevacizumab, Rituximab, Trastuzumab.
BRT (bert)
L19a #5

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3
Q

Name three tyrosine kinase inhibitor cancer therapies

A

Gefitinib, Imatinib, Lapatinib.
GIL
L19a #5

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4
Q

What do the following suffixes for monoclonal antibody cancer treatments mean:

  1. ) -mab
  2. ) -umab
  3. ) -momab
  4. ) -ximab
  5. ) -zumab
A

1.) -mab = Monoclonal antibody.
2.) -umab = Human (only human protein).
3.) -momab = Mouse (murine).
4.) -ximab = Chimeric (mix of mouse and human; “x” indicates CROSSED).
5.) -zumab = Humanized (mix of human and mouse, less mouse compared to chimeric).
L19a #7

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5
Q

What are the consequences of:

  1. ) Caspase 3 activation (2)
  2. ) iPLA2 activation (3)
A

1.) Caspase 3 activation = Apoptotic tumor cell death = Tumor Shrinkage.
2.) iPLA2 activation = Release of PGE2 and AA = Accelerated tumor growth and repopulation = Tumor recurrence.
L19a #9

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6
Q

For the following monoclonal antibodies, list what their effect is and what they are specific for:

  1. ) Rituximab
  2. ) Trastuzumab
  3. ) Bevacizumab
  4. ) Nivolumab
A

1.) Direct cytotoxicity; specific for CD20 on B cells.
2.) Growth factor inhibitors; specific for HER2.
3.) Vascular endothelial growth factor inhibitors; inhibits angiogenesis (beV = Vascular).
4.) Program death-1 inhibitors; “Turns on” immune system.
L19a #10

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7
Q

What do the following CD molecules identify?
CD20
CD33
CD52

A

CD20: B cell
CD33: Myeloid cells
CD52: Lymphocytes
L19a #11

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8
Q

What is VEGF and what does it do?

A

Vascular endothelial growth factor – Promotes angiogenesis.

L19a #13

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9
Q

What is EGFR and what does it do?

A

Epidermal Growth Factor Receptor –Promotes cellular proliferation, invasion and metastasis.
L19a #13

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10
Q

What is HER2/neu, what does it regulate (4), and what cancer is it over-expressed in?

A

Human Epidermal Growth Factor Receptor 2: Regulates cell growth, differentiation, migration and adhesion.
Over-expressed in breast cancer
L19a #13

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11
Q

What does rituximab target and where, i.e. on which types of cancer cells (3)?

A

CD 20 found on B cell lymphomas, B cell chronic lymphocytic leukemia, and melanoma stem cells.
L19a #14

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12
Q
  1. ) What types of cancer is rituximab/rituxan for (2)?

2. ) What are its three possible mechanisms of action?

A

1.) B cell non-Hodgkin lymphoma, leukemias.
2.)
(a) ADCC (antibody-dependent cell mediated cytotoxicity) –via macrophage, monocyte, or NK cell.
(b) CDC (complement-mediated cytotoxicity) –complement activation followed by cell lysis.
(c) Apoptosis.
L19a #14

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13
Q

What are the drugs used for non-Hodgkin lymphoma treatment? (mnemonic)

A 
R-CHOP: 
Rituximab
Cyclophosphamide
Hydroxydaunorubicin (doxorubicin)
Oncovin (vincristine)
Prednisone
L19a #16
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14
Q

What is the action of Bevacizumab and what is cancers it used for (3)?

A

Inhibits the action of VEGF (vascular endothelial growth factor) by binding directly to VEGF receptors on endothelial cells.
-Used for colon cancer (with 5-FU), non-small cell lung cancer, and breast cancer.
L19a #19

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15
Q
  1. ) What is the action of Trastuzumab and for what cancer?
  2. ) What are its two mechanisms?
  3. ) What are the risks and precautions with trastuzumab?
A

1.) Anti-HER2 for breast cancer (can feature uncontrolled HER2 activity).
HER-‘T’wo = ‘T’rastuzumab
2.) Block receptor signaling (PI3K/Akt signaling), and receptor internalization (dephosphorylation and downregulation).
3.) 2-7% incidence of cardiotoxicity during therapy (arrhythmias, heart failure, MI). Must have frequent screening for cardiomyopathy (baseline echocardiograms needed) due to increased risk for cardiac death.
L19a #22

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16
Q

What chemo drugs must be used with caution due to risk of causing arrhythmias and heart failure?

A

ADD
Anthracyclines —> Doxorubicin, Daunorubicin.
L19a #23

17
Q
  1. ) What roles do tyrosine kinases play in the cell cycle (6)?
  2. ) What is the result of constitutive phosphorylation (3)?
A

1.) Growth, differentiation, metabolism, adhesion, motility, and death.
2.) Oncogene over-expression, hyperactive kinase activity, and non-regulated growth of cancer cells.
L19a #25

18
Q

What tyrosine kinase is involved in CML? How?

A

Chronic myelogenous leukemia: Bcr-Abl kinase.
-Chromosomes 9 translocates to Ch22 to make the oncoprotein Bcr-Abl (forms the Philadelphia chromosome).
L19a #27

19
Q
  1. ) How does Bcr-Abl directly affect genetic expression (3), and
  2. ) What is the result (3)?
  3. ) What drug(s) blocks the effects of Bcr-Abl?
A

1.) Enhanced expression and/or function of RNA binding proteins increases (1) mRNA translation, (2) mRNA export/translation, and (3) transcription/translation.
2.) Growth advantage, enhanced survival, and differentiation arrest.
3.) Imatinib
L19a #28

20
Q
  1. ) What does Imatinib target and how does it work (2)?

2. ) What is the result (2)?

A

1.) Targets Bcr-Abl —> Inhibits c-kit and induces apoptosis.
2.) Decreases rate of cell division and enhances DNA repair.
L19a #30

21
Q
  1. ) What is Lapatinib used for?
  2. ) When is it used?
  3. ) What is one of its main advantages?
A

1.) Tyrosine kinase inhibitor that inhibits EGFr and HER2/neu in HER2-amplified, trastuzumab refractory breast cancer (i.e. used in patients with HER2 positive breast cancer that has progressed after treatment with trastuzumab).
Used in conjunction with Capecitabine
2.) Used to prolong life of patients with breast cancer after Trastuzumab fails to work well (hence, Trastuzumab-refractory breast cancer).
3.) It crosses the BBB.
L19a #32

22
Q

How does lapatinib work on the receptor level?

A

Lapatinib binds on the tyrosine kinase (TK) domain, prevents dimerization and phosphorylation; thereby inhibiting the downstream cascade of events.
L19a #33

23
Q
  1. ) List four types of epidermal growth factor receptors.
  2. ) What is the result of mutation or dysregulation?
  3. ) What cancers are they associated with (4)?
A

1.) EGFr (HER1), HER2/neu, HER3, and HER4.
2.) Uncontrolled cell division and cancer.
3.) Lung, epithelial, colon, and breast cancer.
L19a #34

24
Q
  1. ) What is the action of Gefitinib?
  2. ) What is its mechanism?
  3. ) What type of cancer is it mostly used for? Why?
A

Gef = EGFr
1.) EGF tyrosine kinase receptor (EGFr) inhibitor.
2.) Binds to the ATP-binding site and inhibits protein phosphorylation.
3.) Used for non-small cell lung carcinoma (and breast cancer) because EGFr (also HER1) is over-expressed in lung and breast cancer.
L19a #35

25
Q
  1. ) Give an example of cofactor/coenzyme supplementation in manipulation of metabolism and what it’s for.
  2. ) It’s efficacy is conditional of what?
A

1.) Sapropterin dihydrochloride (KUVAN) – BH4 cofactor effective in some PKU patients.
2.) Requires at least 12.5% residual enzyme activity.
L26 #10

26
Q

Name three medications that treat OTC deficiency through the mechanism of metabolic diversion.

A

1.) Glycerol phenylbutyrate (Ravicti)
2.) Sodium phenylbutyrate (Buphenyl)
1 and 2 are metabolized to phenylacetate, which conjugates with glutamine, which then mobilizes nitrogen excretion
3.) Sodium benzoate, Sodium phenylacetate (Ammonul) –Benzoate combines with glycine to form HIPPURATE, which is excreted in the urine.
L26 #11

27
Q

What medication is an example of enzyme inhibition in the context of metabolic manipulation? Describe (what does it do, what is it for).

A

Allopurinol: A xanthine oxidase inhibitor used to decrease uric acid production.
-Used in Lesch-Nyhan syndrome, which is an HGPRT deficiency in which the body is unable to salvage hypoxanthine or guanine, which results in excessive production of uric acid.
L26 #12, p.40 njp

28
Q
  1. ) What class of medications are an example of enzyme inhibition (metabolic inhibitors) in the context of metabolic manipulation.
  2. ) What are they used for?
  3. ) How do they work?
A

1.) Statins –Structural analogs of HMG-CoA.
2.) Used for patients with familial hypercholesterolemia (heterozygous) —> Deficiency in functioning LDL receptors, which results in elevated LDL-cholesterol.
3.) Statins are competitive inhibitors of HMG-CoA reductase.
L26 #13

29
Q

What type of drug is often used with statins in order to reduce circulating LDL and increase LDL receptors? Give two examples.

A

Bile acid sequestrants —> Cholestyramine, Colestipol.

L26 #14

30
Q
  1. ) What drug utilizes the receptor antagonism mode of metabolism manipulation to exert its effect?
  2. ) What is it used for?
  3. ) How does it work?
A

1.) Losartan, an AT II receptor antagonist.
2.) Used to prevent dilatation of the ascending aorta in Marfan syndrome.
3.) Losartan inhibits AT II signaling, which decreases TGF-β (transforming growth factor) activity. Decreased TGF-β activity decreases rate of dilatation of the aorta in individuals with Marfan syndrome.
L26 #15, p.41 njp

31
Q
  1. ) What is the drug Ataluren most effective at?

2. ) What two disorders is this drug used for (describe the nature of these disorders)?

A

1.) Most effective in allowing UGA read-through (i.e. allows skipping over nonsense codons).
2.) (i) Cystic fibrosis: Nonsense mutation of the ∆F508 in the CFTR protein (Arg553). Shows significant improvement in lung function with Ataluren.
(ii) Duchenne Muscular Dystrophy (DMD): Helps patients walk an average of 47 meters farther.
L26 #20

32
Q
  1. ) What is the most common mutation that causes CF and how?
  2. ) Besides Ataluren, which other small molecular therapy drug treats Cystic Fibrosis and how? What else does it need?
A

1.) ∆F508 mutation in CFTR protein (most common of all CF mutations).
-Mutant protein trapped in ER and degraded by proteasome (trafficking defect).
2.) Lumacaftor: Drug serves as a pharmaceutical chaperone; it interacts directly with the mutant CFTR and stabilizes the 3D structure.
Not sufficient on its own —> needs to be combined with another drug —> Ivacaftor (serves as a potentiator for Lumacaftor)
L26 #21, p.42 njp

33
Q

A drug is of clinical benefit to cystic fibrosis if it increases ________________ of the cell by 20-25%.

A

Increases CFTR channels in the apical surface of the cell by 20-25%.
L26 #21

34
Q

What is the role of Ivacaftor?

A

Drug serves as a potentiator for Lumacaftor —> Improves Cl- transport of some mutant CFTR proteins.
FDA approved for 9 CFTR missense mutations
L26 #23

35
Q

Concerning protein/amino acid replacement, what treats hemophilia A and B (2)?

A

Hemophilia A: Clotting factor VIII.
Hemophilia B: Clotting factor IX.
L26 #23

36
Q

Concerning enzyme replacement therapy, how do you treat the following:

  1. ) Gaucher disease
  2. ) Pompe disease
  3. ) Fabry disease
  4. ) ADA deficient SCID
  5. ) Hurler syndrome, MPS I
  6. ) Hunter syndrome, MPS II
A

1.) Beta glucocerebrosidase
2.) Alpha glucosidase
3.) Alpha galactosidase
4.) Adenosine deaminase
5.) Alpha-L-iduronidase (Laronidase; aldurazyme)
6.) Iduronate-2-sulfatase (Idursulfase; elaprase)
L26 #23, p.43 njp

Medical Genetics (6 decks)

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