LAST!!! Flashcards
Abnormal growth/tumor:
Neoplasm
- Persistent proliferation (don’t stop multiplying)
- Invasive (invades other tissues)
- Formation of metastases (parts break off and travel to other parts of the body
- Cell immortality
What does a tissue with a high growth fraction mean?
Larger percentage of proliferating cells.
Cancer chemotherapy agents have a greater toxic affect on tissues that have a high growth fraction.
They can’t tell the difference between our cells and the cancer cells… so ours are killed as well.
Which tissues in our body have a high growth fraction:
- GI tract
- Hair follicles
- Bone marrow
- Lymph tissue
- Mouth / mucus membranes
- Testes/ Ovaries
Chemo agents are most effective on what type of cancers?
Disseminating cancers
Cells are spread around and multiplying… the bigger the tumor, the more cells in resting stage, so chemo agents wont attack as much.
What are the COMMON adverse effects of chemo agents?
- N / V (GI will be greatly affected due to the nature of the GI having proliferating cells)
- Stomatitis: inflammation and sores in mouth = difficulty eating
- Anorexia: lose weight to no appetite
- Alopecia: Hair loss
- Immunosuppression: attacking bone marrow and killing WBCs
- Fatigue: Anemia (bone marrow), depression
What are the DRUG SPECIFIC adverse effects of chemo agents?
- More for 3rd semester
Fetal
Sterility
What are the DOSE LIMITING adverse effects?
“Our treatment is causing more of a problem than the disease, so we need to stop”
- Bone marrow suppression (knocked out immune sys)
- Organ toxicity (severe liver toxicity, etc)
- Pulmonary fibrosis (can’t breath)
What are some reasons to use multiple types of chemo agents, vs one?
- Can use lower doses. Minimizes the adverse effects of each of the drugs.
- Lessens the chance of drug resistance. Cancer cells can develop resistance… but if hitting with 3 different one, higher chance of success.
- Mechanism of action: drugs coming at the cancer cells from different ways (attach cell wall or inhibits folic acid production, etc)
What 3 factors to consider when figuring which chemo agents to combine:
- The drug must be effective by itself (DUH!?)
- We want an different mechanism of action than the other 2.
- Want to minimize overlapping toxicities.
Unlike antimicrobial therapy where we are given a prescription of meds to take until gone… cancer chemo agents are given intermittently. Why?
Because the agents are also killing our healthy cells.
We give time for our body’s to repopulate our normal cells.
Our healthy cells repopulate quicker than the cancer cells so each time there are less and less cancer cells.
Also, if the patient is not tolerating treatment well, then treatment may cease all together for a couple of weeks for them to regain their strength for another round.
What do we want to assess regarding a cancer patient?
- What type of cancer do they have? Care will be determined on that… throat vs brain… what to anticipate will be different.
- Financial status: medications are expensive. No insurance? Need to find a way to pay.
- Family/social support: they’ll be wiped out, so will need care… possibly home care nursing? Nursing home?
- Nutritional status: What can we do to maintain their nutritional status. We let them eat what they want. Need them to keep their calorie intake up.
- chemotherapy may stop to allow healing
What type of planning and/or implementation should be expected regarding chemotherapy treatment?
- Only chemo trained nurses/providers administer these meds. (special training is involved)
- Consider adverse effects (don’t use drugs with overlapping effects) Be ready to treat for the adverse effects.
- Follow administration guidelines Some drugs are guaranteed to cause emesis so guidelines * May include premedication with anti-emetics (Zofran).
- Dispose of syringes/ drugs, body fluids appropriately. (May still be just as toxic as when they went in). Depends on the agent.
What type of evaluation/monitoring may be needed regarding chemo agents?
- Monitor for adverse effects
- Need anti-emetics? Skin care? Nutritional counseling? (this is about how to find foods they’d be interested in eating, NOT what a “proper” or “healthy” diet would be)
- CBCs (platelets, leukocytes) If counts are too low, may need protective isolation (where we protect THEM from possible microbes).
What type of teaching should we keep in mind with these patients?
- May need to teach about possible adverse effects, how to deal with them, perhaps anticipate them.
- Diet : what kind of foods to eat to keep up weight
- Dehydration : NEED to stay hydrated and teach signs of dehydration and ways to prevent
- Advise on support groups for client and family : often it’s one and the same.
What are the 3 different ways to categorize anti-infectants?
- Classes of the drugs… Beta-lactam group (cell wall attack [penicillins, cephalosporins]), Aminoglycocides, Fluroquinolones, Sulfonamides, Tetracyclines, Erythromycins.
- Bacteriostatic vs Bactericidal:
Static does not move. A drug that makes bacteria not multiply (doesn’t kill it).
Cidal means death. Killing the bacteria. - Broad vs Narrow spectrum:
Broad: kills a lot of bacteria but is hard on body. Will also kill good bacteria. Another downside = not as efficient killer for specific bacteria and increases risk for it to become resistant. Used when we aren’t sure which kinds of microbe infecting until we get lab results.
Narrow: easier on the body. Cater to the exact microbe that we’re trying to kill. Less likely to develop resistance.
Why do you select certain types of anti-infectants?
Depends on a lot of different things…
- What type of organism is it?
- What is the clinical picture?
- WHERE is the infection? UTI? Eye? Pneumonia?
- Regional differences/ resistance… Ohio resistance may be different than here in Colorado.
- Local tissue conditions… if in brain, will need different drug than antibiotic (wont cross bbb). Pus formation - IND (incision and drainage) will be performed in order to get antibiotic to the wound site (access to the bacteria). - Allergies. Don’t want to give a drug they’re allergic to.
- Culture and Sensitivity (C and S): 2 step process…
Culture - what’s growing there.
Sensitivity - what kills this organism.
Takes a couple of days… so broad spectrum is used in the mean time. MUST get CandS FIRST before any antibiotics are given because can skew results.
What are the prototype anti-infectants?
Mechanism of action, Primary indications, Drug interactions,
General adverse effects for antimicrobial therapy:
- Allergy [rash, respiratory decline] **Penicillin
- Organ toxicity [don’t give drug that’s hard on their diseased organ]
- GI distress [MOST common. D/N/V]
- Superinfection [supermembranous colitis (C.diff), yeast]
- Expensive - may need alternative. The newer the drug, the more expensive… most effective. If the person can’t afford to fill it, they’re not going to take it.
What is a “Superinfection”?
An infection on top of another one. Example, patient with pneumonia takes antibiotic which kills the flora in their mouth leaving a weakened state and getting a yeast infection. Very common super infection.
Anti - biotic = Anti - life
What is selective toxicity?
Unique biochemical pathways and enzymes:
Ex: Development of certain proteins that the bacteria need to make (but our body doesn’t) so the antibiotic will only affect those bacterial cells. Another ex: some bacterial cells produce their own folic acid so some drugs focus on preventing the synthesis of this = killing bacteria but not our cells because we get our folic acid from our food.
Cell wall:
Differences (several) rely on these differences… drug targets certain receptors? found only on the bacterial cell walls, leaving our cells alone.
Bacterial cells have high osmotic pressure inside, this is used against them in which way?
By damaging the cell wall, creating a weak spot, the bacterial cells lyse. Penicillin targets the penicillin binding proteins (PBPs) on the cell wall.
Only active during growth and division… So if patient on bacterial-static drug, will prevent growth and division so penicillin will not work.
Mechanism of action:
Penicillin binds to binding proteins on cell wall, they inhibit the enzyme transpeptidase in the cell wall. These help build the crossbridges that provide strength to the cell wall. By inhibiting this enzyme, weakens the cell wall.
What are the 3 forms of Penicillin G?
- Benzathine: IM slow absorption and long effect
- Potassium *only one safe for IV
- Procaine: IM, slow absorption and long effect
Class is “natural” (original form, not synthetic)
Narrow spectrum
What is the enzyme that some bacteria release that damage the beta lactam ring, rendering antibiotics useless?
Betalactamase
