1.
Alkylating agent and platium compounds info:: mutagenic, teratogenic, and carcinogenic
toxicities to normal tissues (bone marrow, hair follicles, and GI mucosa)
drug resistance is common
2.
Alkylating agent and platium compounds MOA:: cross-links DNA during all phases of cell cycle (CCNS), disrupting DNA synthesis and leading to cell cycle arrest and apoptosis
3.
Antimetabolites MOA:: interferes with DNA and RNA synthesis by preventing folic acid production
cell-cycle specific (S-phase)
4.
Antitumor Antibiotics MOA:: block DNA synthesis, damage DNA during all phases of cell cycle (CCNS)
Used to treat cancer, not infections (too Toxic)
5.
Benign Prostatic Hyperplasia:: 5-Alpha-reductase inhibitors
Selective alpha-1blockers
6.
BPH monitor: rule out prostate cancer
7.
BPH patient teaching: annual prostate screenings
Elderly: risk for falls due to orthostatic hypotension
8.
Cancer cells: Growth, differentiation, proliferation, supervision:: uncontrolled growth
persistent proliferation
supervision is unchecked, unrepaired
9.
Cancer cells: Migration, apoptosis, normal function, outcome: invasive, metastases, migrates
no apoptosis = immortality
less or no normal function
outcome is compression, necrosis, malnutrition, abnormal hormone
10.
Cell growth rate impact each cell's responsiveness to chemo:: solid tumors (breast, lung, prostate, colon, and rectum) grow slowly and respond poorly to drugs
11.
chemo drugs are more toxic to the normal cells with rapid growth rate:: bone marrow, skin, hair follicles, sperm, and GI tract
12.
Chemo drugs only kill: cells that grow fast, does not do well when they start to grow slow in later stages. Rate of growth really effects treatment.
13.
Chemo MOA: Kills both normal & cancer cells:: skin, hair, brown, sperm, GI
14.
Combination OC health Risks:: Thromboembolic Disorders: pulmonary embolism, MI, Stroke
HTN
Cancer, cervical, breast
teratogenic effects
abnormal uterine bleeding
use in pg and lactation
benign hepatic adenoma
glucose intolerance
15.
Combination therapy:: attack at different stages:
increase killing effects
decrease drug resistance
decrease side effects
16.
ED drugs are also used in the treatment of: pulmonary arterial hypertension and COPD
17.
ED PDE5 contraindications:: MI, stroke, dysrhythmia, hypo/hypertension, HF, angina with nitroglycerin
18.
ED PDE5 DDI/DFI:: nitrates, alpha blockers, high-fat diet
19.
ED PDE5 SE/ADE: hypotension
20.
ED phosphodiesterase - 5 (PDE5) inhibitor MOA:: Sildenafil (Viagra)
Vaso dilate smooth muscle to increase penis blood flow by inhibiting the breakdown of cyclic guanosine monophosphate cGMP and block Ca++ entry into the cell
21.
ED phosphodiesterase - 5 inhibitor can be dangerous if used concurrently with certian: vasodilators (alpha-adrenergic blockers and nitrates)
22.
Erectile Dysfunction Drugs:: Phosphodiesterase - 5 (PDE5) inhibitor
23.
Estradiol produced by, function, uses, ADEs:: produced by ovaries
functions in bone mineralization and lipid metabolism
ADEs: endometrial, breast, ovarian CA, N/V, cardio events
24.
HRT Estrogen AE:: Endometrial Hyperplasia and cancer
Breast cancer, ovarian cancer
Cardio events
risk of gallbladder disease
CNS reactions (HA, dizzy, dementia, and depression)
25.
HRT Estrogen SE:: irregular menstrual flow and break-through menstrual bleeding
Premenstrual-like syndrome: HA GI upset, chloasma, photosensitivity, Urinary incontinence
26.
HRT Progestins contraindications:: thrombophlebitis
cerebral hemorrhage
breast or genital cancer
undiagnosed vaginal bleeding
missed abortion
27.
HRT Progestins SE/AE:: Teratogenic Effects- not for 1st 4 months of pg
can cause break-through bleeding, spotting and amenorrhea
breast tenderness
breast cancer-increase the risk of breast cancer from estrogens
28.
HRT types:: for post-hysterectomy, use estrogen alone, w/uterine, use estrogen plus progestin
29.
HRT used for how long?: short term
30.
Infertility vs. Sterility: Infertility-decreased ability to reproduce
Sterility-absence of reproductive ability
31.
Intermittent therapy (no drugs during G0 phase):: while its resting it will not be killed
32.
Lymphocytic leukemia, hodgkin's disease, and certain testicular cancers:: grow rapidly and respond well to drugs
33.
Major Tox of cancer chemo: Cardiotox
Anemia
Neurophathy
Cognitive impairment
Ear damage
Renal damage
34.
Major tox of cancer chemo: Bone marrow suppression
Alopecia
Diarrhea N/V
Anorexia/Anxiety
Cancer/candida
Hyperuricemia (gout)--hepatotox
Extravasation
Stomatitis/spermacide
35.
Major Toxicities of Cancer Chemo:: Bone marrow suppression
--neutropenia (white)
--thromobcytopenia (purple)
--anemia (red)
Alopecia
hyperuricemia
reproductive tox
local injury from extrasasation of vesicants
36.
Menotropins and Human Chorionic Gonadotropin AE: most serious-ovarian hyperstimulation syndrome: causes sudden enlargement of ovaries; severe cases have ascites, pleural effusion and pain
37.
Menotropins, Cloniphene and Human Chorionic Gonadotropin MOA: follicular maturation and ovulation in anovulatory patients
38.
Normal cells: Growth, differentiation, Proliferation and supervision: Growth is controlled
Highly differentiated
regulated proliferation
supervision, yes! repaired and killed
39.
Normal cells: migration, apoptosis, normal function, outcome: no migration
yes to apoptosis
normal function
outcome is to maintain health
40.
Oral Contraceptives (OC) Combo of estrogen and progestin: Monophasic: dose is constant
Biphasic: Estrogen constant; progestin increases 2nd 1/2
Triphasic: 3 phases; progestin changes in each phase
41.
Progesterone and estradiol both cause:: breast cancer
42.
Progesterone produced by, function, uses, ADEs:: produced by ovaries and placenta
functions to promote and sustain pg
Used to treat HRT, uterine bleeding, amenorrhea, endometrial CA and hyperplasia
ADEs: teratogenic, breast cancers, depression
43.
Progestin is to:: counterbalance estrogen mediated stimulation of endometrium
44.
Prostaglandins Contraindicated:: previous uterine scar and pelvic post surgery
45.
Prostaglandins uses:: cervical ripening, soften and dilate for delivery
46.
Targeted therapy is: BEST
47.
Use estrogen and progestin to:: prevent uterine cancer
48.
Uterine relaxants (tocolytics) used to suppress: preterm labor (before 37 wks gestation)
49.
Uterine relaxants, Tocos, MOA: relax uterine muscle contraction by stimulate B-2 adrenergic receptor, blocking oxytocin, prostaglandins and calcium channel blockers
NOT USED PRIOR TO 20 WKS GESTATION
GIVE CORTICOSTEROIDS TO HELP FETAL LUNGS MATURE
50.
Uterine Stimulants (Oxytocics) Oxytocin (Pitocin) ADH: MOA: Increases the uterine contractions
51.
Uterine Stimulants ADEs: water retention
CAN HAVE LONG PERIOD OF CONTRACTIONS-SO NOT TO INDUCE LABOR!
MUST MONITOR BLOOD PRESSURE, PULSE AND UTERINE CONTRACTABILITY- CAN HAVE SEVERE HYPERTENSION
52.
Why so hard to treat cancer?: nonselective toxicity
cure requires 100% kill
host defenses contribute little to cell kill
when to stop?
absence of truly early detection
solid tumors respond poorly
drug resistance
heterogeneity of tumor cells
limited drug access to tumor cell
