• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/77

Click to flip

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;

77 Cards in this Set

  • Front
  • Back
Standard combo tx for ALL
Prednisone and Vincristine OR
POMP
-Predinisone
-Oncovin (aka Vincristine)
-Methotrexate
-Purimethol (6-MP)
MOA Prednisone
steroid that causes lymphocytopenia (is the condition of having an abnormally low level of lymphocytes in the blood)
MOA Vincristine
Binds tubulin and blocks the from forming microtubules
(inhibits mitosis)
SE Vincristine
Peripheral neuropathy
Phlebitis
Alopecia
Multiple GI problems
MOA Methotrexate
Inhibits dihydrofolate reductase (inhibits folate usage)
Purimethol aka
6-MP
SE Purimethaol (6-MP)
Stomatitis
SEVERE BM suppression
Alopecia
N/V
Renal & hepatic damage
Tx Wilm's tumor
(congenital kidney tumor 2-5 yo)
Dactinomycin & Vincristine
DOC combo for Hodgkin's disease
MOPP
-Mechlorethamine
-Oncovin
-Prednisone
-Procarbazine

ABVD
-Adriamycin
-Bleomycin
-Vinblastine
-Dacarbazine
MOA Bleomycin & adriamycin
Destroy DNA via ROS
MOA Dacarbazine
Alkylating agent
SE Dacarbazine
Highly emetogenic
Extreme BM suppression
MOA Mechlorethamine
Alkylates guanines in DNA --> cross-linking in pairs or removal
SE Mechlorethamine
Severe N/V
Extreme BM suppression
Herpes Zoster (if VZV provirus present)
Potential to cause 2nd CA
Extreme blisters if on skin or mucus membranes
MOA Procarbazine
Inhibits DNA & RNA synthesis
SE Procarbazine
BM suppression
Disulfiram rxn
Neurotoxicity
Cancer chemotherapeutics: MOA cyclophosphamide
Alkylating agent --> destroys DNA
(Requires biotransformation via P450 for activation)
Cancer chemotherapeutics: SE Cyclophosphamide
Alopecia
BM suppression
Leukocytosis
Amenorrhea
Sterility
HEMORRHAGIC CYSTITIS (bladder fibrosis)
Cancer chemotherapeutics: SE Bleomycin
Pulmonary fibrosis
Cancer chemotherapeutics: MOA Cisplatin
Platinum compound
Intra- & interstrand cross-linking b/t nucleotides --> ceasing all RNA & DNA synthesis
Cancer chemotherapeutics: Cisplatin used for
Solid tumors
(metastatic testicular CA, ovarian CA, bladder CA)
Cancer chemotherapeutics: SE Cisplatin
Persistent, intractable V
Nephrotoxicity
Ototoxicity
PERIPHERAL NEUROPATHY
Cancer chemotherapeutics: MOA L-asparaginase
Asparagine --> aspartic acid
(some Ca require asparagine, deprives them)
Cancer chemotherapeutics: L-asparaginase used to tx
ALL
Cancer chemotherapeutics: SE L-asparaginase
HYPERSENSITIVITIES
Decreased clotting factors
Liver problems
Pancreatitis
Seizures
Coma
6-MP DOC for
ALL
Bleomycin DOC for
testicular cancer
Vincristine DOC for
Hodgkin's lymphoma
Vinblastine used to tx
Testicular CA
Lymphoma
Mechlorethamine used to tx
Hematologic malignancy
(leukemia & lymphoma). Has the potential to induce secondary cancers, such as leukemia.
Cyclophosphamide used to tx
Lymphomas & Leukemias
Ovarian & breast CA
Childhood malignancies
Multiple myeloma
Cisplatin DOC and 2 drugs which are similar to Cisplatin
DOC: Testicular and bladder cancer
Carboplatin - less renal tox, more BM tox
Oxaliplatin - neurtoxic when exposed to cold
SE Chlorambucil (similar MOA Mechlorethamine)
Extremely BM tox
Potential 2nd CA

(Others - Melphalan, lomustine, busulfan)
Leuprolide & Flutamide used to tx
Prostate CA
MOA & SE Leuprolide
synthetic analog GnRH
Hot flashes
MOA & SE Flutamide
Antagonizes testosterone R
Gynecomastia
MOA Hydroxyurea
Inhibits ribonucleotide reductase
(req. for nucleotide synthesis in WBC)
Hydroxyurea used to tx
Leukemia
(Sickle cell pt - reduces # crises)
SE hydroxyurea
BM tox (managed via titration)
Causes synthesis fetal Hgb (useful in sickle cell pt)
MOA ATRA (all-trans-retinoic acid)
Binds to mutated form retinoic acid R
(causes blasts to differentiate --> mature myeloid cells) This induces remission.
ATRA used to tx
AML subtype 3 (15:17 translocation)
SE ATRA
Induces disseminated intravascular coagulation.
MOA Tamoxifen
Inhibits Estrogen R in breast. Use in treatment and in women who are at high risk for the development of breast cancer.
SE Tamoxifen
Hot flashes
Increased risk DVT & PE
Increased risk endometrial CA
Taxanes (2 drugs)
Paclitaxel
Doxetaxel
MOA taxanes
Inhibit microtubule disassembly --> apoptosis
Taxanes used to tx
Breast, Lung, Ovarian CA
SE Taxanes
Dose-limiting BM suppression
PGE2 responsible for
Sensitizing n. endings to other pain mediators
Fever
PGI2 responsible for
Inhibiting gastric secretions
PGE2 & PGF2 responsible for
Stimulate production protective mucus in stomach & small intestine
MOA Aspirin
IRREVERSIBLY acetylates cyclooxygenase
(central and peripheral tissue)
Effects of ASA
-decrease inflammation & fever
-decreases coaguation via platelets
-analgesic
How does ASA reduce coagulation
Decreases thromboxane (d/t COX inhibition)
Thromboxane - enhanses platelet aggregation
(takes 2 wks for reversal of this - new platelets formed)
Who is ASA contraindicated in
GOUT pt
(competes w/ uric acid at renal transporters)
Some uses of ASA
RA
HA, arthralgia, angina, PDA
Topically - corns & calluses
Prophylactically - Hx MI, stroke, A. fib
Overdose of ASA causes
Uncoupling Ox-Phos
Effect of ox-phos uncoupling resulting from OD ASA
Increase CO2 --> hyperventilation --> resp. alkalosis
Kidney response w/ metabolic acidosis
Immediate acid-base disturbance ASA
Metabolic acidosis (acidic nature ASA)
ASA toxic levels leads to
Central resp. paralysis --> hypoventilation --> increase CO2 --> Resp. acidosis
Other SE ASA
Tinnitus
(mild ASA intox)
Special about APAP
NO peripheral anti-inflammatory action
(CNS cyclooxygenase)
APAP used for
-reducing fever
(good antipyretic w/o risk reye's syndrome in kids)
-reducing pain perception
-Children w/ viral infection
Use of Indomethacin (Etodolac, Sulindac)
Acute gouty arthritis
Ankylosing spondylitis
OA of hip
Pain control for uveitis & post-op ophthalmic
Fever in Hodgkin's disease
SE Indomethacin
GI distrubances (ulceration)
RARE
-Pancreatitis
-Fatal hepatitis
-Aplastic anemia
Other non-selective NSAIDS
Ibuprofen
Ketorolac
Tolmetin
Naproxen
COX-2 inhibitor? Effect?
Celecoxib
(decreasing formation PG in inflammatory or injurious conditions)
GI SE w/ COX-2 inhibitors
Less
Who can you NOT use COX-2 inhibitor in?
Allergic to sulfa drug
SE of ALL NSAIDS (except APAP)
Increase risk of miscarriage
Exacerbate HF & HTN
Promote GI d/o (chronic use)
Inhibit platelet fnct --> increase bleeding
Aspirin overdose
Causes uncoupling of oxidative phosphorylation. This results in an increase in pre-respiratory processes in an attempt to overcome the ability to make as much ATP as usual. This results in an accumulation of carbon dioxide, which causes hyperventilation by the patient. Repsiratory alkalosis is established. As the level of aspriin increases to toxic levels, a central respiratory paralysis occurs, resulting in hypoventilation. CO2 ldevels rise, creating a respiratory acidosis. Generally also a metabolic acidosis.
Acetaminophen
No peripheral anti-inflammatory action, but it does inhibit cox.
Acetaminophen DOC
Children with viral infections, as it is as effective an antipyretic as asprin but without the risk of inducing Reye's syndrome.
Phenylbutazone
Used in animals. Tends to cause agranulocytosis and fatal aplastic anemia.
Indomethacin, etodolac and sulindac
Have anti-inflammatory, analgesic, and antipyretic activity. Indomethacin is mostly reserved for certain severe instances, such as acute gouty arthritis, ankylosing spondylitis, and osteoarthritis of the hip.
COX-2 Inhibitors
Selectively inhibit COX2. Ex. celecoxib, cannot e used in sulfa-allergic patients.
AE of all NSAIDS
Increase the risk of miscarriage if used around the time of conception. They can also exacerbate heart failure and hypertension. Chronic use can promot serious GI sidorders.