Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
205 Cards in this Set
- Front
- Back
Generic of Avastin
|
bevacizumab
|
|
Generic of Erbitux
|
Cetuximab
|
|
Generic of Rituxan
|
rituximab
|
|
Generic of Gleevec
|
Imatinib
|
|
Generic of Herceptin
|
trastuzumab
|
|
Generic of Yervoy
|
ipilimumab
|
|
Generic of Tykerb
|
iapatinib
|
|
Pre treatment for monoclonal antibodies infusion:
|
APAP, Benadryl, corticosteroid, and meperidine(regrugs and chills)
|
|
MOA of Rituximab
|
Binds to CD20+ antigen on B-lymphocytes
Antibody dependent cytotoxicity |
|
Consideration of Rituximab infusion:
|
- First exposure is the worse
- it may take up to 8 hrs |
|
Toxicities of Rituximab
|
Infusion related reactions
Possible anaphylactic reactions (Pretreat APAP and diphenhydramine) - Tumor lysis syndrome (black box warning) Allopurinol and monitor electrolytes - Reactivation of Hep B, CMV, etc… (Must check for previous Hep B) |
|
MOA of Tositumomab
|
Binds to CD20+ cells
Linked to Iodine-131 |
|
Indication for Tositumomab
|
NHL refractory to rituximab
|
|
Toxicities of Tositumomab:
|
Premedicate with APAP and Benadryl
Give thyro-protective agent: Potassium iodide (SSKI) drops at least one day prior to giving Prolonged pancytopenia (nadir 4-7 WEEKS) - Pregnancy category X - High incidence of secondary malignancies |
|
MOA of ofatumumab
|
Bind to CD20+ antigen on B-cells
Causes B-cell lysis |
|
Indication for ofatumumab
|
CLL
Second line after rituximab |
|
Toxicities of ofatumumab
|
Severe infusion reactions (44%) although is a human antibody.
Prolonged thrombocytopenia and neutropenia Reactivation of Hepatitis B Severe infections (70%) (even being a fully human AB) Very long infusion administration ( 8-9 hrs) |
|
MOA of alemtuzumab
|
Binds to CD 52+ on malignant lymphocytes
|
|
Toxicities of alemtuzumab
|
- PROLONGED immunosuppression
- HSV and PCP prophylaxis (fungal?) - CMV reactivation (prophylaxis w/ ganciclovir) Infusion related reactions |
|
Cell surface cycloprotein monoclonal antibodies:
|
Rituximab
Ibritumomab tiuxetan Tositumomab Ofatumumab Alemtuzumab |
|
Anti-angiogenesis agents (VEGF):
|
Bevacizumab
|
|
MOA of Bevacizumab:
|
Binds to vascular endothelial cell growth factor in circulation
VEGF ligand binding antibody |
|
Toxicities of Bevacizumab
|
May cause DVTs or PEs
GI perforation Delayed wound healing Thrombotic events Hypertension Bleeding Proteinuria |
|
MOA of cetuximab
|
Binds to cell surface of epidermal growth factor receptor (EGFR)
Prevents EGFR binding and signal transduction |
|
Indication for cetuximab
|
Colon cancer (without KRAS mutation)
Head and neck |
|
EGFR should be avoided in the treatment of cancer with what specific mutation:
|
K-RAS
|
|
Toxicities of cetuximab
|
Acneiform skin rash
N/V Mucositis |
|
Characteristics of cetuximab rash:
|
starts within 1st week
No bacteria found Treatment: - Creams - Anti-inflammatory |
|
MOA of Panitumumab:
|
Binds to EGFR similar to cetuximab
Used after cetuximab |
|
toxicities of panitumumab
|
Acneiform skin rash
N/V Mucositis |
|
Indication for panitumumab
|
Colon cancer
|
|
MOA of trastuzumab
|
HER2/neu
Oncogene overexpressed in 25% breast Ca Herceptin binds and leads to antibody dependent cellular cytotoxicity |
|
Indication for trastuzumab
|
Breast Cancer that overexpress HER2/neu
|
|
Toxicities of trastuzumab:
|
DLT is cardiovascular
Not given in combination with Doxorubicin Infusion reactions: - Rash - Myelosuppression |
|
MOA of pertuzumab
|
HER dimerization inhibitor (HER2/neu receptor antagonist)
|
|
Toxicities of pertuzumab:
|
Left ventricular dysfunction (CHF) but it is still given in combination with trastuzumab
Rash Myelosuppression Pregnancy D: Fetal death and birth defects |
|
MOA of ipilimumab
|
Increase T-cell activation and response
|
|
Toxicity of ipilimumab:
|
Severe and fatal immune reactions due to T-cell activation/proliferation
- Enterocolitis/diarrhea/abdominal pain - High dose steroids for treatment |
|
How to recognized Tyrosine kinase inhibitors?
|
AKA ...nibs = oral agents
|
|
MOA of gefitinib and erlotinib
|
Tyrosine kinase inhibitors
- Inhibit phosphorylation of EGFR (EGFR-TK) |
|
Indication for erlotinib
|
NSCLC and pancreatic cancer (increase survival 12 days in combination with gemcitabine)
|
|
Toxicities of erlotinib
|
Diarrhea
Rash (acneiform) Interstitial lung disease (SOB or pneumonia type symptoms), rare but fatal CYP 3A4 - Increases INR |
|
Drugs that bind to CD20
|
Rituximab
Ibritumomab tiuxetan Tositumomab Ofatumumab |
|
What VEGF stands for?
|
Vascular endothelial growth factor
|
|
MOA of imatinib:
|
Inhibit bcr-abl tyrosine kinase
- Stops proliferation |
|
Toxicities of imatinib
|
Myalgias/Arthralgias (affects compliance)
Myelosuppression N/V Edema (CHF) |
|
BCR-ABL tyrosine kinase inhibitors
|
Imatinib
Dasatinib Nilotinib Bosutinib Ponatinib |
|
Toxicities of Dasatinib and Nilotinib:
|
- Toxicities and dosing similar to imatinib
- Don’t use with PPIS or H2 - QT prolongation black box warning |
|
Characteristic of Ponatinib
|
BCR-ABL tyrosine kinase inhibitors
- 3rd generation - Does target T3151 mutation (it can be used in CML resistant to the other TKIs |
|
MOA of Lapatinib
|
Inhibits Her2/Neu phosphorylation
|
|
Toxicity of Lapatinib
|
Hand Foot syndrome
|
|
MOA of Crizotinib
|
ALK (anaplastic lymphoma kinase) tyrosine kinase
|
|
Indication for Crizotinib
|
ALK+ NSCLC
- EML4–ALK fusion - Must have FDA approved test done to confirm ALK+ |
|
Toxicity of Crizotinib
|
Severe and fatal pneumonitis
Hepatotoxicity QT-prolongation |
|
MOA of Vemurafenib
|
Inhibits BRAF serine thireonine kinase
|
|
Indication for Vemurafenib
|
Malignant melanoma
- (V600E mutation of the BRAF gene) |
|
Drugs approved for renal cell
|
Sunitinib
Sorafenib Pazopanib Axitinib Temsirolius Everolimus Bevacizumab |
|
Toxicities of Sunitinib
|
GI
Skin discoloration (yellowish) CYP 3A4 Hypothyroidism (txt with levothyroxine) |
|
Toxicities of Pazopanib
|
Severe and fatal hepatotoxicity—black box warning
Prolonged QT-intervals Fatal hemorrhagic events Hypertension Hypothyroidism GI perforations |
|
Agents that inhibit numerous TK including VEGF, platelet derived GF
|
Sunitinib
Sorafenib |
|
MOA of Pazopanib and Axitinib
|
Binds to VEGF, PDGFR, c-KIT, etc…
|
|
Typical treatment for anticipatory N/V:
|
Benzo
(Ativan) Lorazepam |
|
Type of N/V produced by cisplatin:
|
Delayed N/V
The most emetic cancer medication |
|
High emetic drugs
|
Cisplatin
Cyclophosphamide (> 1500mg/m2) AC combination (doxorubicin/cyclophosphamide) Dacarbazine/Nitrogen mustards |
|
Moderate emetic drugs
|
Carboplatin
Most anthracyclines alone |
|
Low emetic drugs
|
Taxanes
5-FU Topoisomerase inhibitors |
|
5-HT3 antagonist agents used for N/V:
|
Dolasetron
Granisetron Ondansetron Palonosetron |
|
Role of 5-HT3 antag. agents in the txt of N/V:
|
Effective for prevention of ACUTE (first 24hrs) CINV
Prevention of post-op nausea and vomiting (PONV) and radiation induced N/V |
|
Palonosetron used:
|
IV
prevention of acute and delayed in moderately emetogenic chemo |
|
Trade name for Dolasetron
|
Anzemet
|
|
Trade name for Granisetron
|
Kytril
|
|
Trade name for Ondansetron
|
Zofran
|
|
Trade name for Palonosetron
|
Aloxi
|
|
Preferred route of admin for 5-HT3 antag.
|
Oral
|
|
Dose of ondasetron
|
Ondansetron 16 to 24 mg orally or 8 to 16 mg IV daily
|
|
Dose of Dolasetron
|
Dolasetron 100 mg PO QD
|
|
Dose of Granisetron
|
Granisetron 2 mg QD or 1mg BID
|
|
Dose of Palonsetron
|
Palonsetron 0.25mg IV x 1 dose
|
|
Adverse effects of 5-HT antag.
|
QT-prolongation
Constipation (pregnancy) Diarrhea (chemo txt) |
|
Patient education on 5-HT3 antag.
|
Take 30 minutes prior to chemo and on a scheduled basis after that OR 1x during surgery
PRN basis not recommended |
|
Used on corticosteroids in the txt of n/v
|
Prevention of Chemotherapy induced N/V (not FDA-approved)
Synergistic with 5HT-3 and metoclopramide |
|
Doses of corticosteriods when adding to a 5HT-3 or alone:
|
Highly emetogenic: 12-20 mg x 1 dose 30 min prior to chemo
Moderately emetogenic: 8-10 mg 1 dose 30 min prior to chemo Continue 4-8 mg BID x ~3 days after chemo |
|
rare corticosteriod AE:
|
Anal burning
(txt: slow infusion rate) |
|
Neurokinin-1 Receptor Antagonists agents:
|
Aprepitant and Fosaprepitant (Emend)
|
|
Uses of NK-1 antag.
|
Used in combination with steroids and 5HT-3 for prevention of acute and delayed N/V associated with highly and moderately emetogenic chemotherapy (3 drug regimen for cisplatin)
|
|
What kind of medications are affected by the use of NK-1 antag.?
|
Oral contraceptives
Warfarin: it may derease INR |
|
Dose of Aprepitant
|
125mg PO day 1
80mg PO day 2 80mg PO day 3 |
|
Dose of Fosaprepitant
|
150mg IV once
|
|
Dose of dexamethasone for high emetic chemotherapy:
|
12mg IV day 1
8mg IV/PO day 2 8mg IV/PO on days 3 and 4 (if fosaprepitant is used then BID) |
|
When does aprepitant should be given to patients?
|
1 hour prior to chemo with the 5-HT3 antag. and the corticosteriod
|
|
Aprepitant AE:
|
Diarrhea / constipation
Hiccups (may use a dopamine antagonist for txt) Bradycardia |
|
Most commonly used dopamine antagonists:
|
Prochlorperazine (Compazine)
Promethazine (Phenergan) Metoclopramide (Reglan) |
|
Dose of Prochlorperazine
|
10mg IV/PO Q6H scheduled or PRN
IV/PO/PR |
|
Dose of Promethazine
|
12.5-25 mg Q4-6 H scheduled or PRN
Iv/PO/PR |
|
Dose of Haloperidol
|
Haldol: 1-3mg IV/PO q 2-4 H prn
|
|
Dose of metoclopramide
|
10-40mg IV/PO Q6H With higher doses consider diphenhydramine 25-50mg to prevent EPS
|
|
SE of metoclopramide
|
EPS and excessive sedation
Irreversible tardive dyskinesias |
|
SE of droperidol
|
black box warning for QT prolongation
|
|
SE of promethazine
|
Severe extravasation can occur
Must dilute with 10 ml NS if giving IV Try to use oral if possible |
|
Dose of lorazepam
|
Lorazepam 1-2mg IV/PO/SL q4-6 H prn OR 1 dose prior to chemo
|
|
Prevention of CINV with highly emetogenic drugs:
|
Aprepitant + 5-HT3 antagonist + dexamethasone
|
|
Prevention of CINV with moderately emetogenic drugs:
|
5-HT3 antagonist + dexamethasone +/- aprepitant
|
|
Prevention of CINV with low emetogenic drugs:
|
Dexamethasone or prochlorperazine or metoclopramide
|
|
Prevention of CINV with minimal emetogenic drugs:
|
None
|
|
Options for breakthrough N/V:
|
Dopaminergic agents
Haloperidol Dronabinol (Scheduled medications) |
|
How 5-HT3 antag. should be used in multiple day chemo regimens?
|
Every day chemo is given a 5-HT3 antagonist should be given
(for moderate to highly emetic drugs) |
|
Agents used on pregnancy induced N/V
|
Histamine antagonists and Phenothiazines are effective and equal to 5HT-3 in efficacy
|
|
What is the name of the cells used to identify HL?
|
Reed-Sternberg cells
(Multi-nucleated giant cells) |
|
Signs and Symptoms of HL:
|
Painless adenopathy usually in lymph nodes above the diaphragm (cervical)
Orderly spread from one node to contiguous node |
|
What are B-symptoms?
|
Fever
Unexplained weight loss Night sweats |
|
Stage I HL:
|
Single node or site
|
|
Stage II HL:
|
Two or more lymph node or sites on same side of diaphragm
|
|
Stage III HL:
|
Lymph node involvement on both sides of diaphragm
|
|
Stage IV HL:
|
Diffuse or disseminated involvement of organs/tissues
|
|
What is the meaning of A, B, and X in HL?
|
A = No fever (asymptomatic)
B = B-symptoms X = Bulky disease (nodal mass >10 cm) |
|
Prognosis factors in HL:
|
Serum albumin (< 4 g/dL)
Hemoglobin (< 10.5 g/dL) Male Stage IV disease Age (> 45 yo) Leukocytosis (WBC >15,000/mm3) Lymphocytopenia (< 600/mm3) |
|
ABVD regimen:
|
Doxorubicin (Adriamycin)
Bleomycin (pulmonary toxicity) Vinblastine (myelosuppression) Dacarbazine (N/V) |
|
Treatment of relapsing HL:
|
ABVD if relapse is more than 12 months later
Brentuximab (CD30+ antibody-conjugate used if two chemo regimens failed or failed stem cell transplant) |
|
Short term Effects of treatment for HL:
|
Infection
Tumor Lysis Syndrome (hydration and electrolytes) Pulmonary function Cardiac function Mycositis Neurotoxicities |
|
Overall survival of HD:
|
Good prognosis:
Stage I: 90-95% Stage II: 90-95% Stage III: 80-85% Stage IV: 60-70% |
|
Incidence for NHL:
|
Age: average 66yo
Males > females Whites > blacks |
|
Risk factors for NHL:
|
H. pylori, HIV, EBV, HHV-8
Chemicals exposures Immune dysregulation Chromosomal abnormalities |
|
What are the most common types of NHL:
|
Diffuse Large B cell Lymphoma
Follicular lymphoma |
|
What type of lymphoma is caused by H. pylori?
|
MALT lymphoma
(Mucos Assoc Lymphoid Tissue ) |
|
Type of indolent lymphoma:
|
Follicular
(hard to cure) |
|
Type of Highly aggressive lymphoma:
|
Burkitt's lymphoma
(curable but tumor may double in size in 48 hrs) |
|
What type of regimen can be used for a indolent lymphoma advance disease (stage III and IV):
|
No standard therapy
Rituximab based therapy |
|
Regimen for DLBC lymphoma:
|
R-CHOP
|
|
What does R-CHOP stands for?
|
Rituximab - (reactivation of HepB)
Cyclophosphamide (renal function) doxorubicin (hydroxydanorubicin) (liver function) vincristine (neuropathies) prednisone (blood sugar) |
|
additional therapy when using R-CHOP:
|
Rituximab as maintenance
CNS prophylaxis with methotrexate |
|
Length of therapy using R-CHOP
|
6 cycles
|
|
Characteristics of Tumor Lysis syndrome:
|
High potassium
High phosphate High uric acid Low calcium |
|
Treatment of high uric acid:
|
Allopurinol:
- affects only new production - takes days to have effect Rasburicase: - affects new and existent production - Takes just hours to work |
|
Difference in treatment between Acute and chronic leukemias:
|
Acute are a medical emergency while chronic may or may not require immediate treatment.
|
|
What type of leukemia is most common in childhood?
|
ALL
|
|
Prognostic risk factors for ALL:
|
Age (less than 1 and more than 10= high risk)
WBC (more than 50K = high risk) Philadelphia chromosome (high risk) Male |
|
Treatment of ALL:
|
Remmision induction (4 weeks)
Consolidation (4weeks) Delayed intensificacion (3-9 mo) Maintenance (2-3 yrs) CNS prophylaxis given in all phases |
|
REmission induction in ALL txt:
|
Vincristine IV
Dexamethasone PO L-asparaginase (pegaspargase) If High risk add to standard: Daunorubicin or doxorubicin IV |
|
What are the drugs for CNS prophylaxis in ALL:
|
Intrathecal cytarabine, hydrocortisone and/or methotrexate
|
|
What phase of treatment is important in ALL but it is not used in AML?
|
Maintenance phase (2-3 yrs)
|
|
Drugs used in maintenance therapy for ALL:
|
Mercaptopurine po q evening
Methotrexate po or IM q week Dexamethasone 5 days/month Vincristine IV q month Intrathecal meds q 3 months |
|
What is the AML that has a better prognosis?
|
M3 acute promyelocytic leukemia
|
|
Treatment phases for AML:
|
Remission induction
Consolidation (2-4) (No maintenance phase) |
|
Standard induction of AML:
|
7 + 3
7 days of continuous infusion cytarabine (low dose) 3 days of Idarubicin or Daunorubicin SE: prolonged neutropenia |
|
Consolidation treatment for AML:
|
High dose cytarabine
SE: Conjuctivitis (steroid eye drops) and Cerebral toxicity (test before every dose) 3-4 cycles |
|
AML M3 treatment:
|
All-trans retinoic acid (ATRA) (PO)
- differentiation syndrome Arsenic trioxide (IV) - QT prolongation - Differentiation syndrome |
|
Role of SCT in leukemia treatment:
|
For relapse disease especially for ALL in young patients
|
|
What causes CML:
|
Philadelphia Chromosome Abnormality
|
|
What is the translocation related to philadelphia chromosome:
|
BCR-ABL that encodes for a tyrosine kinase that has 100x more actiivty than the normal.
|
|
Effects of BCR-ABL translocation:
|
Increases proliferation
Affects differentiation Blocks apoptosis |
|
What Hematologic response indicates?
|
Normalization of peripheral blood count
WBC < 10 x 10^9/L Platelets <450 X 10^9/L No immature cells |
|
What Cytogenetic response inidicates?
|
Complete: elimination of Ph+ cells
|
|
What Molecular response indicates?
|
Absence of bcr-abl by RT-PCR
|
|
What is hydroxyurea used for in CML?
|
Used to reduce high circulating WBC and all cell lines
(for short term therapy) |
|
First line therapy drugs for CML
|
Imatinib mesylate (STI 571; Gleevec)
Dasatinib (Sprycel) Nilotinib (Tasigna) |
|
Dosage of gleevec:
|
400mg/day with food and water
CHR: 3 mo CCR: 9-12 mo Few achieve molecular remission |
|
SE for Gleevec:
|
Myelosuppression
Rash GI side effects Edema Arthralgias and myalgias Headaches Rare cardiotoxicity/CHF |
|
What TKI are used in patient that developed mutations or resistance to gleevec?
|
Dasatinib and Nilotinib
2nd generation tyrosine-kinase inhibitors Indicated first-line for chronic phase, accelerated and blast crisis |
|
SE of dasatinib:
|
Pleura effusions and bleeding
Avoid PPI and H2 blockers |
|
SE of nilotinib:
|
QT prolongation
take on empty stomach |
|
Bosutinib indication:
|
2nd generation bcr-abl TKI
Indications: CML that failed 1 TKI |
|
Ponatinib indication:
|
BCR-ABL tyrosine kinase inhibitors
3rd generation Does target T3151 mutation Indications: CML that failed 1 TKI |
|
What is the only option for cure for CML?
|
Allogeneic stem cell transplant
|
|
Characteristics of CLL:
|
Indolent disease
Elderly patients Many times patient forgo treatment |
|
When to treat CLL:
|
Treatment would be very aggressive if it is diagnosed in younger patients and/or it presents molecular markers
|
|
What drug to use in the treatment of CLL if patient has deletion of p17?
|
alemtuzumab
|
|
If a CLL patient is younger than 70 what is the treatment:
|
FCR:
- Fludarabine - cyclophosphamide - rituximab |
|
Risk factors for colon cancer:
|
Age
Family hx Personal hx of breast, ovarian, or endometrial cancer Colon polyps IBD (especially Ulcerative colitis) Genetic predisposition |
|
Prevention of colon cancer:
|
High-fiber; low-fat diet
Chemoprevention: - Calcium - Folate - COX-2 - NSAIDS |
|
Screening for Colon Cancer
|
Start at 50 yo
- FOBT = once a year - Digital rectal exam = once a year - Flexible sigmoidoscopy = q 5 yeats - Colonoscopy = q10yrs |
|
Common S/S of advance colon cancer:
|
Change in bowel habits
Rectal bleeding Abdominal pain Weight loss |
|
How many node are biopsied in the diagnosis of colon cancer?
|
All 12 nodes
|
|
What mutation has to be tested for in colon cancer?
|
K-RAS (Unresponsive to EGFR-inhibitors: Cetuximab or panitumumab)
|
|
Stage I colon cancer txt:
|
Superficial lession
Surgery and nothing else |
|
Stage II colon cancer txt:
|
Surgery and nothing else
|
|
Stage III colon cancer txt:
|
Lymph node involvement
Surgery AND chemo right after FOLFOX or CapeOX |
|
What adjuvant therapy mean:
|
Therapy given after surgery with the intention to cure the patient. No place in metastatic disease.
|
|
What does FOLFOX stands for?
|
Oxaliplatin IV over 2 hours on Day 1 (PN - cold)
Leucovorin IV over 2 hours on Days 1 and 2 5-FU IV bolus and continuous infusion (48 hours) Repeat every two weeks |
|
what does CapeOX stands for?
|
Capacitabine (PO) (hand foot symdrome)
Oxaliplatin (PN) |
|
What drugs should not be used for adjuvant colon cancer therapy?
|
irinotecan
cetuximab bevacizumab |
|
Why is Bevacizumab never given right after surgery? One more time - what's the trade name?
|
Bevacizumab delays wound healing (give 6 weeks later). Avastin is the Trade name.
|
|
Stage IV colon cancer txt:
|
incurable (Unless resectable liver mets)
Chemotherapy is mainstay: FOLFOX FOLFIRI CapeOX Infusional 5FU/LV FOLFOXIRI always add biologics bevacizumab, cetuximab or panitumumab |
|
Treat of isolated hepatic mets in colon cancer:
|
Single lesions resected
Hepatic artery infusion of 5-FU or FUDR Chemoembolization (mixed in Gelfoam) Mitomycin C Doxorubicin Cisplatin |
|
Important signs for skin cancer:
|
A sore that does not heal
Obvious change in wart or mole |
|
ABCDE of melanoma:
|
A: Asymmetric
B: Irregular Borders C: Color of lesion (not uniform) D: Diameter > 6mm or size of pencil eraser E: Evolving characteristics of lesion |
|
Guidelines for surgery in melanoma patients:
|
<1 mm in thickness, require 1 cm margin
2 mm in thickness, require 2 cm margin |
|
Role of chemotherapy in melanoma:
|
Not recommended
|
|
Treatment options for metastatic melanoma:
|
Clinical trial
Ipilimumab Vemurafenib (BRAF mutation) Aldesleukin (IL-2) chemo is 2nd or 3rd option |
|
MOA of ipilimumab
|
Increase T-cell activation and response to stimulate immune reaction
|
|
SE of ipilimumab
|
Severe enterocholitis (txt high dose steroids)
Immune AE |
|
What is the common mutation in melanoma:
|
BRAF (involve in cell growth) 45%
|
|
MOA of Vemurafenib
|
Inhibits BRAF serine threonine kinase
- mutation has to be confirmed by an FDA approved test |
|
How many doses of IL-2 are recommended for the txt of metastatic melanoma?
|
14 doses
(but most patients cannot tolerate more than 10-12) |
|
Survival rates with melanoma:
|
Localized dz: 98% (5yr)
Regional spread: 60% Metastatic spread: 16% |
|
How to calculate SPF:
|
# of min normally burn x (spf) = min of protection from the sun
|
|
How much UVB is blocked by SPF 15?
|
93%
|
|
How much UVB is blocked by SPF 30?
|
97%
|
|
Indication for Vismodegib:
|
Basal cell carcinoma; after failing other options
|
|
What is the type of skin cancer that is serious and fatal?
|
Melanoma
(non-melanoma rarely mets) |
|
Define pharmacogenomics:
|
differences in MULTIPLE genes influence variability in drug response (i.e., efficacy and toxicity)
|
|
CYP 2D6:
|
-Metabolizes 25-50% of drugs
- Substrates: Antidepressants Antiarrhythmics B-adrenergic antagonists Prodrugs such as codeine, tramadol and tamoxifen |
|
CYP 2C19:
|
Poor metabolizers common in Chinese and Japanese
Drugs involved include: Omeprazole Voriconazole Phenytoin Clopidogrel |
|
CYP 2C9:
|
2-10% are homozygous for low-activity
Drugs metabolized: - Warfarin - Losartan |
|
VLOR and Warfarin pharmacogenomic relationship:
|
Polymorphisms of VKOR account for 25-30% of dose variability
Some patients may require >100mg/week or never achieve anticoagulation |
|
What two drugs can be used for medullary thyroid cancer?
|
Vandetinib and Cabozantinib.
|