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;
100 Cards in this Set
- Front
- Back
Cancer is a disease characterized by
|
a shift in the control mechanisms that govern cell survival, proliferation, and differentiation.
|
|
Cells that have undergone neoplastic transformation usually express
|
cell surface antigens that may be of normal fetal type or may display other signs of apparent immaturity
|
|
Describe chromosomal and gene sequence changes
|
qualitative or quantitative chromosomal abnormalities, including various translocations and the appearance of amplified gene sequences
|
|
describe tumor formation
|
Such cells proliferate excessively and form local tumors that can compress or invade adjacent normal structures
|
|
A small subpopulation of cells within the tumor can be described as
|
tumor stem cells.
|
|
in the process called metastasis,
|
cells retain the ability to undergo repeated cycles of proliferation as well as to migrate to distant sites in the body to colonize various organs
|
|
Tumor cells are derived from
|
normal cells in which proliferation is poorly controlled.
|
|
Most anticancer agents inhibit act by
|
inhibiting cell proliferation.
|
|
how is cell proliferation inhibited?
|
damaging DNA or preventing DNA repair
|
|
Newer agents selectively target cancer cells by using what kind of technology?
|
monoclonal antibody technology.
|
|
Neoplastic and normal cells differ primarily with regard to
|
the number of cells undergoing cell division,
|
|
The drugs kill dividing cells by these two specific mechanisms
|
interfering with DNA, RNA, or protein synthesis or by inhibiting the formation of microtubules in mitosis.
|
|
cell specific agents
|
exert their actions during distinct phases of the cell cycle.
|
|
Agents that interfere with DNA synthesis are specific to what phase?
|
S-phase
|
|
Agents that interfere with microtubules disrupt what process?
|
mitosis
|
|
Agents that interfere with microtubules are specific to what phase?
|
M-phase
|
|
DNA alkylating agents do what?
|
damage tumor cells regardless of whether the cell is actively dividing
|
|
DNA alkylating agents are also called
|
“cell cycle-nonspecific” drugs
|
|
Alkylating agents (3)
|
NITROGEN MUSTARDS, ALKL SULFONATES, NITROSOUREAS
|
|
Alkylating agents mechanism of action
|
Miscode DNA information or open purine ring with damage to the DNA molecule, depending on cell division not cycle specific.
|
|
what type of resistance do alkylating agents cause?
|
Acquired resistance
|
|
general side effects of alkylating agents
|
Bone marrow suppression, N/V, alopecia,pneuminitis, pulmonary fibrosis,seizures,
|
|
important side effect of alkylating agents related to anesthesia
|
decrease plasma cholinesterase (prolong succinylcholine)
|
|
describe the duration of the G1 phase of the cell cycle
|
varies markedly
|
|
G1 phase
|
synthesis of cellular components needed for DNA synthesis
|
|
S phase
|
replication of DNA genome
|
|
G2 phase
|
synthesis of cellular components needed for mitosis
|
|
M phase
|
mitosis
|
|
CCS drugs kill what type of cells?
|
actively dividing
|
|
CCNS drugs kill what type of cells?
|
non-dividing and actively dividing
|
|
Antimetabolite Agents (analogues)
|
FOLIC ACID ANALOGUES, PYRIMIDINE ANALOGUES, AND PURINE ANALOGUES
|
|
Describe Antimetabolite Agents
|
structural analogues of normal metabolites required for cell function and replication
|
|
Antimetabolite Agents react with
|
specific enzymes
|
|
Antimetabolite Agents reaction with enzymes leads to
|
inhibition of that enzyme and subsequent synthesis of an aberrant molecule that can not function normally.
|
|
what type of resistance do Antimetabolite agents cause?
|
acquired resistance
|
|
METHOTREXATE type of analogue
|
folic acid
|
|
Side effects of Methotrexate
|
ulcerative stomatitis, diarrhea, bone marrow depression, hemorrhagic enteritis, and death from perforation, pulmonary toxicity, renal and hepatic toxicity.
|
|
florouracil type of analogue
|
Pyrimidine
|
|
Florouracil can cause what life-threatening event?
|
can cause myocardial ischemia up to 1 week after treatment. The incidence is low in patients without pre-exisisting heart disease but increases to 4.5% in patients CAD.
|
|
Plant Alkaloids examples (3)
|
VINBLASTINE, VINCHRISTINE (periwinkle plant), PACLITAXEL (bark of the pacific yew)
|
|
Vinblastine and Vincristine mechanisms of action
|
block mitosis in rapidly dividing cells
|
|
Most of the chemotherapeutic activity of Vinblastine and Vincristine is due to
|
their ability to bind to microtubules which arrest cell division during metaphase.
|
|
side effects of Vinblastine and Vincristine
|
Leukopenia, thrombocytopenia, anemia, neuropathy, parathesia of hands and feet, hyponatremia, tachycardia, autonomic NS involvement).
|
|
side effects of Paclitaxel
|
Bradycardia, MI, Atrial dysrhythmias, VTachy
|
|
Antibiotics are usually natural products of
|
soil fungi
|
|
Daunorubicin and Doxorubicin class
|
antibiotics
|
|
Doxorubicin used for treating
|
metasatic adenocarcinoma of breast, carcinoma of bladder, bronchogenic carcinoma, metasatic carcinoma of thyroid, oat cell, and osteogenic carcinoma.
|
|
side effects of Daunorubicin and Doxorubicin
|
Causes Cardiomyopathy wide range of cardiac problems from nonspecific ST-T changes to PVC, SVT, decreased QRS voltage.
|
|
describe onset of Daunorubicin and Doxorubicin induced cardiomyopathy
|
Onset is insidious with dry cough to heart failure that is unresponsive to inotropic drugs or mechanical ventricular devices.
|
|
acute left ventricular failure has been reported how long after cessation of treatment with doxorubiicin during general anesthesia
|
2 months
|
|
While receiving bleomycin, patients with lymphomas may develop
|
hyperthermia, hypotension, and hypoventilation.
|
|
Serious side effect of bleomycin
|
pulmonary toxicity and Interstitial fibrosis develops and may progress to the entire lung.
|
|
describe the pulmonary toxicity process of bleomycin
|
produces pulmonary endothelial damage and necrosis of type 1 and proliferation of type 2 alveolar cells.
|
|
Common cause of fibrosis-related postoperative respiratory failure in bleomycin-treated patients
|
arterial hyperoxia or excessive crystalloid administration
|
|
FiO2 for patients treated with bleomycin or mitomycin
|
30% or below
|
|
Patients on Bleomycin should receive this type of fluid administration
|
Replace fluids with colloids instead of crystalloids
|
|
Plicamycin (mithramycin) side effects
|
Highly toxic To GI and bone marrow.
|
|
Plicamycin (mithramycin) effect on calcium
|
Lowers calcium for metastatic bone tumors, tumors that produce parathyroid hormone and Paget’s disease. (hypocalcemia)
|
|
Plicamycin (mithramycin) effect on coagulation
|
Hemorrhagic diathesis occurs in 1-5%, prolong PT and fibrinolytic activity
|
|
Asparaginase effects on bone marrow, GI or hair follicles.
|
minimal
|
|
side effects of enzymes
|
Severe toxicity-liver, kidneys, pancreas, CNS, and inhibits clotting, hypofibrinogenemia.
|
|
side effects of Cisplatin
|
renal toxicity, ototoxicity,neuropathy, hyperurecemia, seizures, cardiac dysrhythmias.
|
|
side effect of Estrogen and Androgens
|
hypercalcemia
|
|
side effect of Flutamide (antiandrogen)
|
methemoglobinemia
|
|
Antiestrogens examples
|
Tamoxifen,anastrozole
|
|
anesthestic consideration of stomatitis
|
makes placement of pharyngeal airways, LMAs, esophageal catheters questionable.
|
|
anesthestic consideration of inhaled and injected drugs
|
response may be altered by drug-induced cardiac, hepatic, or renal dysfunction (including nondeplorizing muscle relaxants).
|
|
anesthestic consideration of nmb
|
May have decreased plasma cholinesterase and succinylcholine may be prolonged
|
|
Chemotherapeutic have high incidence of what for female personnel who handle the drugs.
|
spontaneous abortion in first trimester
|
|
anesthestic consideration of coagulation status
|
Patients may be anticoagulated, check labs.
|
|
CNS Stimulants
|
-- Armodafinil
– Caffeine – Dextroamphetamine – Dextroamphetamine and Amphetamine – Doxapram – Ergotamine and Caffeine – Lisdexamfetamine – Methamphetamine – Modafinil |
|
Doxapram
|
centrally acting analeptic (CNS stimulant) that selectively increases minute ventilation by activating the carotid bodies.
|
|
The stimulation produced by administration of doxapram, 1mg/kg IV, is similar to that produced by
|
a Pa02 of 38mmHg acting on the carotid bodies.
|
|
Doxapram has what type of margin of safety as reflected by?
|
large margin of safety as reflected by a 20-40-fold difference in the dose that stimulates ventilation and the dose that produces seizures.
|
|
Doxapram side effects
|
CNS stimulation-hypertension, tachycardia, cardiac dysrhythmias, vomiting, increased body temperature.
|
|
Doxapram use
|
temporary measure to maintain ventilation during administration of O2 to patients with COPD who are dependent on the hypoxic drive.
|
|
Arousal from the residual effects of inhaled anesthetics follows the administration of doxapram but the effects are
|
transient, nonselective, and not recommended.
|
|
Dantrolene produces skeletal muscle relaxation by
|
decreasing the amount of calcium released from the sarcoplasmic reticulum.
|
|
Dantrolene does or does not not work at the neuromuscular junction as do standard neuromuscular blocking drugs?
|
does not
|
|
describe dantrolene muscle relaxation
|
Does not render the muscle totally flaccid and without tone, but it may cause significant muscle weakness and respiratory insufficiency.
|
|
dantrolene pH; side effects of pH
|
Alkaline (pH 9.5) and can cause phlebitis, extravasation can cause tissue necrosis.
|
|
what drug is added to dantrolene to make it isotonic?
|
mannitol
|
|
describe dantrolene metabolism
|
Metabolized in the liver
|
|
dantrolene metabolite and activity
|
hydoxydantrolene, which is 30-50% as effective in depressing the twitch response.
|
|
dantrolene elimination half time
|
5-8 hours
|
|
Oral Dantrolene Prophylaxis for MH
|
oral 5mg/kg in 3-4 divided doses every 6 hours, with the last dose 4 hours preoperatively
|
|
IV Dantrolene Prophylaxis for MH
|
2.4mg/kg IV, 10-30 mins preinduction and ½ dose in 6 hours.
|
|
Dantrolene treating and max dose
|
2.5MG/KG IV,UNTIL SYMPTOMS SUBSIDE OR A CUMULATIVE DOSE OF 10MG/KGIV IS REACHED.
|
|
Dantrolene Side effects
|
skeletal muscle weakness, nausea, vomiting, diarrhea, blurred vision, uterine atony. Short term is not associated with hepatotoxicity.
|
|
Amphetamine and methamphetamine are powerful CNS
|
stimulants.
|
|
Amphetamines act as what type of agents and where?
|
indirect sympathomimetics, peripherally (similar to ephedrine)
|
|
amphetamines effect on opioids
|
Can enhance the effects of opioids
|
|
amphetamines mechanism of action and where
|
they release dopamine and other biogenic amines in the brain
|
|
amphetamines action on MAO
|
inhibit
|
|
amphetamines with
|
amine transporters in the plasma membrane
|
|
Methylphenanidate (Ritalin).
|
Less motor effect than amphetamines, mainly used in attention deficit disorder.
|
|
Caffeine
|
Causes cortical arousal and delay of fatigue.
|
|
caffeine use
|
One of the principal uses in anesthesia is the treatment of PDPH
|
|
caffeine in low doses can cause
|
nervousness and insomnia
|
|
caffeine in high doses it can cause
|
adrenal medullary stimulation and seizures.
|