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GI Pharm > GI Cancer Rx > Flashcards

GI Cancer Rx Flashcards

1
Q

Agents used in Rx of Anal Cancer? (3)

A

“Clears My Feces”

  1. Cisplatin
  2. Mitomycin
  3. Fluorouracil (5-FU)
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2
Q

Anal Cancer incidence and prognosis?

A

Incidence→Uncommon; 4% of lower alimentary tract tumors

Prognosis→Usually curable

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3
Q

Anal cancer treatment regimens? (2)

A

a. Radiation alone→5 yr survival is 70%

b. Radiation + Cisplatin, Mitomycin, 5-FU→this combo leads to improved outcomes

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4
Q

Agents used in Rx of Colorectal Cancer (CRC)? (7)

A

Fiery Colon Cancer BOIL

  1. Fluorouracil (5-FU)
  2. Capecitabine
  3. Cetuximab
  4. Bevacizumab
  5. Oxaliplatin
  6. Irinotecan
  7. Leucovorin
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5
Q

CRC incidence and prognosis?

A

Incidence: 3rd mc cancer; 2nd most deadly cancer
Prognosis: 20% have metastases at time of diagnosis

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6
Q

Standard treatment regimens for CRC? (2)

A
  1. FOLFOX→5-FU + Leucovorin + Oxaliplatin
  2. FOLFIRI→5-FU + Leucovorin + Irinotecan
    Capecitabine can be substituted for 5-FU.
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7
Q

What are the targeted agents (2) used for CRC? When are they not effective (1)?

A

Bevacizumab or Cetuximab

They appear to improve outcomes, except in pt;s with KRAS mutations

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8
Q

First line therapy for CRC?

A

Bevacizumab or Cetuximab + FOLFOX or FOLFIRI

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9
Q

Agents used in the Rx of Esophageal Cancer? (3)

A

esophageal “Cancer Frustrates Digestion” in my throat

  1. Cisplatin
  2. Fluorouracil (5-FU)
  3. Docetaxel
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10
Q

When esophageal cancer becomes symptomatic (dysphagia) what does that tell the physician?

A

Once symptomatic (usually dysphagia), the esophageal cancer has invaded into the muscularis propria (externa) and metastasized.

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11
Q

Rx Recommendations for Esophageal cancers?

A

a. Endoscopic stents for palliation of dysphagia

b. Radiation and Chemotherapy for metastatic disease

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12
Q

1st and 2nd line chemotherapy treatments in Rx of metastatic esophageal cancer?

A

a. 1st line = Cisplatin + 5-FU

b. 2nd line (for those whose ds progresses after 1st line Rx and can tolerate 2nd line) = Docetaxel (taxanes)

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13
Q

Agents used in Rx of Gastric Cancers? (7)

A

“Carl’s Irritated Gastric Tract Doesn’t Digest Food”

  1. Cisplatin
  2. Docetaxel
  3. Doxorubicin
  4. Fluorouracil (5-FU)
  5. Glutamic Acid
  6. Irinotecan
  7. Trastuzumab
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14
Q

Incidence and prognosis of gastric cancer?

A

4th most deadly cancer; 5-yr survival is 20%

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15
Q

Treatment regimen for gastric cancers? (2)

A

Test ALL gastric cancer pt’s HER2 Status→if positive add trastuzumab
1. HER2-Positive Regimen: (2→T+FC)
Trastuzumab + 5-FU and Cisplatin

  1. HER2-Negative Regimen: (FCDID)
    a. 5-FU/Cisplatin Combo
    b. +/- Doxorubicin
    c. + Irinotecan or Docetaxel
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16
Q

What is the use of Glutamic acid in the Rx of gastric cancers?

A

It is an ancillary agent employed as a GASTRIC ACIDIFIER to counterbalance deficiencies of HCl in the gastric juice.

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17
Q

Two Agents used in the Rx of GI carcinoid tumors?

A

“Car(cinoid)s Irk Octopi”

  1. Interferon-alpja
  2. Octreotide
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18
Q

What are GI carcinoid tumors and where do they originate from?

A

GI Carcinoids are rare malignancies arising from cells linking the endocrine and central nervous systems. They originate in cells responsible for the production of key neurosecretory hormones.

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19
Q

Octreotide MoA and effects (3) in Rx of GI carcinoids?

A

MoA: Somatostatin analog→activates somatostatin receptors→inhibition of the secretion of serotonin and other gastroentero-pancreatic peptides.
Effects: this results in:
1. Increased intestinal transit time
2. Increased intestinal absorption of water/electrolytes
3. Decreased gastric acid secretions

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20
Q

Duration of Octreotide treatment? Why?

A

Treatment duration is ~12 months b/c of TACHYPHYLAXIS (less frequent w/ long-acting formulations) and/or disease progression

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21
Q

Effects of IFN-alpha in Rx of GI carcinoids? (2)

A
  1. Inhibits disease progression
  2. Provides symptom relief
    Greater anti-tumor effect than octreotide, but it has substantial ADE’s
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22
Q

ADEs of IFN-alpha (5)

A

My AA Friend-likes Suicides

  1. Myelosuppression
  2. Alopecia
  3. Anorexia/weight loss
  4. Flu-like symptoms (fever, fatigue)
  5. Suicidal Ideation
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23
Q

Two agents used in the Rx of Gastrointestinal Stromal Tumors (GIST’s)?

A

gISt
1. Imatinib
2. Sunitinib
These are TKI’s

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24
Q

Incidence and Epidemiology of GIST’s?

A

Incidence: s 50-80 y.o.

b. Equally distributed across both sexes and all geographic/ethnic groups

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25
Q

4 Subgroups of GIST’s?

A

GIST’s can fall into one or more of the following groups:

  1. KIT-mutant (CD117-positive) (80%)
  2. KIT negative (5%)
  3. PDGFRA-mutant (5-8%)
  4. Wild-type (12-15%)
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26
Q

Is conventional chemotherapy useful in Rx of GIST?

A

No, conventional chemo is essentially futile, partly due to P-gp overexpression

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27
Q

What class of drugs has revolutionized the Rx of GIST’s?

A

Tyrosine Kinase Inhibitors (TKI’s)

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28
Q

1st line agent for Rx of unresectable, metastatic, or recurrent GIST?

A

Imatinib (TKI that targets KIT???)

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29
Q

Why do the majority of pt’s with GIST’s experience delayed resistance to Imatinib?

A

It is often due to the development of secondary mutations in a separate portion of the KIT-coding sequence.

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30
Q

What is the second line agent for GIST’s? When is it used?

A

Sunitinib is given to patients w/ unresectable disease who progress on higher-dose imatinib.

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31
Q

Agents used in the Rx of Pancreatic Cancers? (6)

A 
"OLE FIG" in the Pancreas
Oxaliplatin
Leucovorin
Erlotinib
Flurouracil (5-FU)
Irinotecan 
Gemcitabine
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32
Q

Incidence and Prognosis of Pancreatic Cancer?

A

Pancreatic cancer is a poorly understood cancer of increasing incidence.
Rarely Curable
<20% are organ-confined at diagnosis

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33
Q

What non-chemotherapeutic treatment can help in the Rx of pancreatic cancer? Why?

A

Pancreatic Enzyme Replacement:
Frequently, malabsorption caused by exocrine insufficiency leads to malnutrition. Pancreatic Enzyme Replacement can help alleviate this problem.

34
Q

Use of chemotherapeutic drugs in the Rx of pancreatic cancer?

A

As adjuvants to surgery and/or radiation, resulting in incremental rather dramatic increases in overall survival.

35
Q

Drug Regimens used to Rx pancreatic cancer? (2)

A

Gemcitabine or 5-FU based

a. Gemcitabine + Erlotinib
b. FOLFIRINOX: 5-FU + Leucovorin + Irinotecan + Oxaliplatin

36
Q

Three Agents used in the Rx of Liver Cancer?

A

the liver “Filters Drugs & Stuff”
Fluorouracil (5-FU)
Doxorubicin
Sorafenib

37
Q

Etiologic cause associated with the development of Hepatocellular (liver) cancer (HCC)? Mechanism?

A

`~80% associated w/ HBV or HCV infections:
HBV/HCV→interact w/ cell proliferation signaling pathways (ie p53 pathway)→frequent cell division→increased risk for genetic alterations

38
Q

What unique technique is used in the Rx of Liver cancer (HCC)?

A

TACE→Transcatheter Arterial Chemo-embolization

39
Q

Describe Transcatheter Arterial Chemoembolization (TACE) in the Rx of HCC?

A

Doxorubicin is injected while the hepatic arterial branch feeding the tumor is occluded with an embolic agent.

40
Q

What is the advantages of TACE? (2)

A

Super-selective catheterization of segmental arteries feeding the tumor:

  1. Spares normal tissue
  2. Minimizes dispersion of the drug away from the tumor site
41
Q

Which agent is the standard of care for patients with advanced HCC?

42
Q

Bevacizumab MoA?

A

mAb against VEGF

43
Q

Bevacizumab ADEs? (3)

A

Triple H

  1. (Hemorrhage) Bleeding, GI perforation, Wound dehiscence (rupture)
  2. Hypertension
  3. Hypersensitivity
44
Q

Capecitabine MoA?

A

Oral pro-drug metabolized to 5-FU

45
Q

Issues (1), CIs (1), ADEs (4) of Capecitabine?

A 
Double Ranch Chicken Never Helps Clotting
1. Issue: Dihydropyrimidine Dehydrogenase (DPD) Deficiency (familial pyrimidinemia) prevents metabolic activation of Capecitabine
2. CI: Renal dysfunction
ADE's:
3. CV adverse effects
4. Neurologic toxicities
5. Hematologic toxicities
6. DDI w/ Coumarin (anticoagulant)
46
Q

Cetuximab MoA?

A

mAb against EGFR

47
Q

Cetuximab ADEs? (3)

A

AIR–>cetuximab
cardiac/respiratory Arrest and/or sudden death
Infusion reactions
acneiform Rash (common, can be severe)

48
Q

Cisplatin MoA?

A

Forms DNA intrastrand crosslinks and adducts

49
Q

Cisplatin ADEs? (4)

A

Cis-BROP

  1. Bone marrow suppression
  2. Renal toxicity/failure
  3. Ototoxicity (hearing impairment)
  4. platinum Hypersensitivity
50
Q

Docetaxel MoA?

A

Mictrotubule stabilizer inhibiting depolymerization

51
Q

Docetaxel ADEs? (4)

A

NELN: “Never Even Learned Nothing” about Docetaxel
1. increased tx-related mortality in NSCLC
2. Edema
3. Liver disease→CONTRAINDICATION
4, Neutropenia→Dose-limiting toxicity

52
Q

Doxorubicin MoA? (3) NOT ON TEST

A

a. Intercalator
b. Free radical generator
c. Topo-II inhibitor

53
Q

Doxorubicin ADEs? (5) NOT ON TEST

A

Heavy (liver) Bowel Movements (BM) Hurt (heart) External Sphincters

  1. BM suppression
  2. Heart Disease
  3. Hepatic Disease
  4. Secondary malignancies
  5. Extravasational necrosis
54
Q

Erlotinib MoA?

55
Q

Erlotinib ADEs? (5)

A

Earl GOBEL (Earl=Erlotinib)

  1. GI toxicity (N/V, diarrhea)
  2. Ocular tocxicity
  3. prolonged Bleeding
  4. Elevated LFTs
  5. Rare→interstitial Lung disease
56
Q

Fluorouracil (5-FU) MoA?

A

Pyrimidine antimetabolite that inhibits thimidylate synthase and interferes w/ RNA synthesis and function. Also has some effects on DNA.

57
Q

5-FU ADEs? (2)

A

“HD Neurotoxicity” w/ Fluorouracil

  1. severe Hematologic toxicity including BM suppression.
  2. DPD deficiency leads to enhanced Neurotoxicity (DPD needed for inactivation of 5-FU)
58
Q

Gemcitabine MoA?

A

DNA polymerase inhibitor via incorporation of triphosphate form during DNA synthesis

59
Q

Gemcitabine ADEs? (4)

A 
GemcitaBINE
B: Bone marrow/myelo-suppression
I: Infection
N: peripheral sensory Neuropathy
E: Everything else→Arthralgia, drowsiness, fatigue, N/V, diarrhea, anorexia are common place, resolve 2-3 days
60
Q

Glutamic Acid MoA? When is taken? NOT ON TEST

A

Nutritional supplement used to counterbalance deficiencies of HCl in the gastric juice.
It is taken orally before meals.

61
Q

Imatinib MoA and clinical use?

A

Oral TKI used as adjuvant treatment following complete resection of Kit (CD117)-positive GIST

62
Q

Imatinib ADEs? (3)

A

“I Gist (just) Can Not” (Imatinib→GI, neuro, CHF)

  1. GI toxicity (pain bloating, N/V, constipation, stomatitis, dyspepsia, etc) common
  2. CHF→edema/fluid retention
  3. Neurologic toxicity
63
Q

IFN-alpha MoA?

A

Enzyme activation following cell surface receptor binding and tyrosine kinase activation:
Binds IFN-alpha surface Receptor→TK activation→activation of enzymes

64
Q

IFN-alpha ADEs? (5)

A

My AA Friend-likes Neuropsych & Suicides
M: Myelosuppression
A: Alopecia
A: Anorexia (wt loss)
F: Flu-like symptoms→fever/chills, fatigue, malaise, myalgia, arthralgia, headache)
N&S: NEUROPSYCHIATRIC EVENTS→agression, depression, Suicide

65
Q

Irinotecan MoA? NOT ON TEST

A

Topo I inhibitor

66
Q

Irinotecan ADEs? (3) NOT ON TEST

A

BAD

  1. BM suppression
  2. Diarrhea
  3. Asthenia, fever, pain, weight loss
67
Q

Leucovorin MoA? NOT ON TEST

A

Reduced folate; modulates the effects of 5-FU

68
Q

Leucovorin ADEs? (2) NOT ON TEST

A

Luke is the Designated Driver (DD)

  1. Diarrhea
  2. Dehydration
69
Q

Methysergide MoA? Effect? Use? NOT ON TEST

A

a. Serotonin inhibitor in GI tract.
b. Vasoconstrictor of large and small arteries
c. Used for migraines

70
Q

Mitomycin MoA?

A

Mono- or bifunctional alkylating agent

71
Q

Mitomycin ADEs? (2)

A

Mighty BUS

  1. BM suppression→thrombocytopenia, leukopenia
  2. Hemolytic Uremic Syndrome (HUS)→microangiopathic hemolytic anemia + thrombocytopenia + renal failure (uremia)
72
Q

Octreotide MoA and effects (4)?

A

Somatostatin Analog→activation of Somatostatin Receptors→inhibition of secretion of serotonin and other gastro-entero-pancreatic peptides→ increased intestinal transit time, increased intestinal absorption of water/electrolytes, and decreased gastric acid secretions.

Effects:

  1. Reduces duodenal bicarb and amylase
  2. Reduces gastric acidity
  3. Inhibits Gb contractility and bile secretion
  4. Inhbits meal-induced increases in SMA and portal venous blood flow
73
Q

ADEs of Octreotide? (2)

A

“God Damn” Glucose Diarrhea w/ Octreotide

  1. monitor blood Glucose→it inhibits insulin and glucagon
  2. Dose-related Diarrhea
74
Q

How does Oxaliplatin compare to Cisplatin? Why?

OXALIPLATIN NOT ON TEST

A

More potent that cisplatin.
Has 1,2-diaminocyclohexane carrier that leads to:
1. Enhanced cytotoxicity
2. Lack of cross-resistance b/t oxaliplatin and cisplatin

75
Q

ADEs of Oxaliplatin? (3) NOT ON TEST

A
  1. Neurotoxicity→Dose-limiting
  2. Thrombocytopenia→if used w/ 5-FU+Leucovorin
  3. GI→Diarrhea, N/V, stomatitis
76
Q

Sorafenib MoA? What does it target specifically (5)? NOT ON TEST

A

a. Oral multi-kinase inhibitor→targets Ser/Thr kinases and RTK’s in both tumor and vasculature
b. Targeted kinases include: RAF, VEGFR-2 and 3, PDGFR-B, KIT, FLT-3, RET

77
Q

ADE of Sorafenib? (1) NOT ON TEST

A

Hand-Foot Skin Reaction (red, pain, swelling, or blisters on palms/soles) that generally apppears in first 6 weeks of treatment

78
Q

Sunitinib MoA?

A

Inhibits >80 Receptor Tyrosine Kinases (RTKs) (→PDGFRa/B, VEGFR-1,2,3, cKIT, FLT3, CSF-1R, RET)

79
Q

ADE of Sunitinib? (3)

A

“QuesTionable Performance This-Bloody SUN(itinib)day”

  1. Thrombocytopenia + Bleeding
  2. QT prolongation (sometimes fatal)
  3. GI perforation (rare)
80
Q

Trastuzumab MoA? (2)

A

mAb against HER2/neu:

  1. Downregulates HER2→p27 (cyclin-dependent kinase inhibitor) accumulates→cell cycle arrest
  2. Inhibits constitutive metalloprotease-mediated cleavage/shedding of HER2 (may correlate with clinical activity)
81
Q

Trastuzumab ADEs? (2)

A

“LC & SI Robertson Always Answer Pulitely” w/ Trastuzumab
1. Cardiac: LVEF dysfunction and Cardiomyopathy
2. Severe Infusion rxns→anaphylaxis, angioedema, pulmonary toxicity
Pulmonary toxicity→worse in pt’s w/ intrinsic lung ds (COPD, asthma, respiratory insufficiency)

GI Pharm (7 decks)

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