LAST!!! Flashcards Preview

Pharmacology 1 > LAST!!! > Flashcards

Flashcards in LAST!!! Deck (53)
Loading flashcards...
1
Q

Abnormal growth/tumor:

A

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
2
Q

What does a tissue with a high growth fraction mean?

A

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
3
Q

Chemo agents are most effective on what type of cancers?

A

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.

4
Q

What are the COMMON adverse effects of chemo agents?

A
  • 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
5
Q

What are the DRUG SPECIFIC adverse effects of chemo agents?

A
  • More for 3rd semester

Fetal
Sterility

6
Q

What are the DOSE LIMITING adverse effects?

A

“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)
7
Q

What are some reasons to use multiple types of chemo agents, vs one?

A
  1. Can use lower doses. Minimizes the adverse effects of each of the drugs.
  2. Lessens the chance of drug resistance. Cancer cells can develop resistance… but if hitting with 3 different one, higher chance of success.
  3. Mechanism of action: drugs coming at the cancer cells from different ways (attach cell wall or inhibits folic acid production, etc)
8
Q

What 3 factors to consider when figuring which chemo agents to combine:

A
  1. The drug must be effective by itself (DUH!?)
  2. We want an different mechanism of action than the other 2.
  3. Want to minimize overlapping toxicities.
9
Q

Unlike antimicrobial therapy where we are given a prescription of meds to take until gone… cancer chemo agents are given intermittently. Why?

A

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.

10
Q

What do we want to assess regarding a cancer patient?

A
  • 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
11
Q

What type of planning and/or implementation should be expected regarding chemotherapy treatment?

A
  • 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.
12
Q

What type of evaluation/monitoring may be needed regarding chemo agents?

A
  • 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).
13
Q

What type of teaching should we keep in mind with these patients?

A
  • 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.
14
Q

What are the 3 different ways to categorize anti-infectants?

A
  1. Classes of the drugs… Beta-lactam group (cell wall attack [penicillins, cephalosporins]), Aminoglycocides, Fluroquinolones, Sulfonamides, Tetracyclines, Erythromycins.
  2. Bacteriostatic vs Bactericidal:
    Static does not move. A drug that makes bacteria not multiply (doesn’t kill it).
    Cidal means death. Killing the bacteria.
  3. 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.
15
Q

Why do you select certain types of anti-infectants?

A

Depends on a lot of different things…

  1. What type of organism is it?
  2. 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).
  3. Allergies. Don’t want to give a drug they’re allergic to.
  4. 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.
16
Q

What are the prototype anti-infectants?

A

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.
17
Q

What is a “Superinfection”?

A

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

18
Q

What is selective toxicity?

A

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.

19
Q

Bacterial cells have high osmotic pressure inside, this is used against them in which way?

A

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.

20
Q

What are the 3 forms of Penicillin G?

A
  1. Benzathine: IM slow absorption and long effect
  2. Potassium *only one safe for IV
  3. Procaine: IM, slow absorption and long effect

Class is “natural” (original form, not synthetic)
Narrow spectrum

21
Q

What is the enzyme that some bacteria release that damage the beta lactam ring, rendering antibiotics useless?

A

Betalactamase

22
Q

This cell-wall antibiotic is a synthetic penicillin and is also known as an aminopenicillin:

A

ampicillin (Principen)

Similar to penicillin G but it is a Broad spectrum.

amoxicillin is chemically similar to ampicillin but more commonly seen.

23
Q

For what illnesses would we use ampicillin?

A
  • Strep infection
  • Pneumococcus
  • Bordetella pertussis
  • H. Influenza
  • Limited by resistance
24
Q

These are very powerful antibiotics that are given to those who are very ill. Its affect can be canceled out if mixed in the IV with penicillin:

A

Aminoglycosides.

Not good at getting inside the cell wall, so use penicillin to weaken the cell wall… but if mixed in the IV pen. will deactivate the aminoglycoside.

25
Q

What are some drug interactions to be concerned with regarding penicillin?

A
  1. Aminoglycoside inactivation if mixed in IV
  2. Bacteriostatic antibiotics: macrolides, tetracyclines, sulfonomides. The cell wall antibiotics will not work on cells not growing/dividing
  3. Probenecid is used to inhibit the excretion of penicillin to keep the drug in the body to fight the infection that much longer. Increases the risk of toxicity.
  4. Oral contraceptives may be inactivated by penicillin. Teaching: use other forms of BC during penicillin use.
26
Q

What are the adverse effects of antibiotics?

A
  • Diarrhea
  • GI upset
  • Anaphylaxis WATCH for 30 minutes after dose.
  • – Cross allergies: other beta lactam similar chemically, such as cephalosporin… if allergic reaction, don’t give penicillin.
  • Nerve damage with high doses of penicillin as well as possible seizures.
27
Q

This is a first generation cephalosporin and is a broad spectrum antibiotic used for respiratory, skin infections, and prophylactic before surgery:

A

cefazolin (ancef, keflex)

Effective on Gram Positive organisms

Binds to PBP’s - penicillin binding proteins

Sensitive to betalactamase … bacteria can develop a resistance

respiratory problems like pneumonia/sinus infection

taken closest to time of surgery to prevent infection

28
Q

What varies considerably regarding cephalosporins?

A

Half life… Some may a once a day where some others may be given 4 times a day.

29
Q

What are the adverse effects of cephalosporins?

A

RASH - may not be a allergic reaction… have to reassess the patient… could just be an adverse effect.

Diarrhea

RARE anaphylactic reaction

Painful injections (IV/IM). Administer more slowly to minimize. Also rotate sites of injection.

30
Q

What drug interactions should we be cognizant of regarding cephalosporins?

A
  • Probenecid keeping the cephalosporin in our system but may develop toxicity because of it.
  • Increased risk of nephrotoxicity. Primarily when used with OTHER nephrotoxic drugs… a double wammy.
31
Q

This antibiotic has a double action of cell wall destruction as well as RNA interference:

A

vancomycin (Vancocin)

Reserved for severe infections (MRSA, C-diff).

  • Red man syndrome: prevent by administering slowly. At lease over an hour, minimum. Also helps by being easier on the blood vessels.
32
Q

Adverse effects of vancomycin:

A
  • Nausea
  • Rash
  • Red man syndrome
  • Phlebitis / Necrosis
  • Ototoxicity / Nephrotoxicity
33
Q

This drug is in the tetracycline class, and is used on inhaled and cutaneous anthrax:

A

tetracycline (Sumycin)

Inhibits bacterial protein synthesis.

BacterioSTATIC

Has selective toxicity due to ability to enter bacterial cells but not mammalian.

34
Q

Adverse effects of tetracycline:

A

Stomach upset

Esophageal irritation

Teeth staining of infants deciduous or child’s adult.

Super-infection

Photosensitivity

35
Q

Which drug has many different types and therefore different half lives?

A

tetracyclines.

Some may have 1 dose, some may have 4/day.

36
Q

Tetracycline teaching:

A
  1. Sunscreen
  2. Best absorption on empty stomach
  3. Avoid foods with Ca Mg Fe Al (they bind with drug, decreasing absorption up to 50%!)
  4. Don’t take at bedtime… stay upright for 30 min, drink full glass of water with it.
  5. NOT pregnancy and NOT under 8 years old
37
Q

What do we call ringing in the ears?

A

Tinnitus

38
Q

What is onychomycosis?

A

Fungal infection of the nails.

39
Q

How do we treat superficial fungal infections?

A

Topical agents.

powder

swish and swallow/spit

nail polish

cream

40
Q

What agents do we use for the subcutaneous fungal infections?

A

Better-absorbing topical agents OR, more commonly, PO drugs.

41
Q

How do we treat systemic fungal infections?

A

PO or IV

Can be life threatening. Usually in those who are immune compromised.

burns
AIDS
cancer

42
Q

How are antifungals similar to antibiotics?

A

Cell wall interference
or
Disruption of replication

43
Q

These are chains of amino acids:

A

Proteins:

Provide stability for cell wall.

Provide “stickiness” for successful colonization.

May be toxic.

44
Q

Which RNA has been “read” off of the genetic material?

A

m RNA

45
Q

Which RNA reads the mRNA to build the amino acids?

A

t RNA

That’s how we get the polypeptide chain, and the protein.

If the peptide bond is inhibited, then the bonds cannot be made and the protein will not be made.

46
Q

Inflammation of the urethra:

A

Urethritis.

Often seen in addition to STI (STD).

Treatment is of the STI pathogen, not the normal UTI pathogen.

Will experience burning but not urgency because infection is distal to bladder.

47
Q

Inflammation of the bladder:

A

Cystitis.

Will experience urgency because of spasms. May have burning as well.

Treatment can b 1 time dose (fluroquinolones) or
Short course, 3 days
Conventional is 7 days

48
Q

Inflammation of the kidneys:

A

Pyelonephritis.

Most severe of UTI’s. Can damage kidneys.

Symptoms: may have burning, may have urgency, also flank pain. Fever, Nausea.

Treatment more aggressive. May be admitted and given IV. More long-term course of antibiotics.

49
Q

What do we call a UTI that has another issue at the same time, such as kidney stone?

A

Complicated UTI:

Kidney stones can make flushing of the kidney more difficult.

Structural problem with the kidney itself.

Prostate enlargement (BPH), makes treatment difficult.

Indwelling catheter = more pathogens and foreign body.

Chronic UTI’s

50
Q

80 - 90% of outpatient UTI’s are caused by which pathogen?

A

E. coli.

From our stool.

51
Q

Inpatient UTI’s are caused by which pathogen?

A

Tend to be caused by stronger, resistant bacteria due to their repeated exposure in the hospital.

Ex:
Pseudomonas enterococcus.
Group B strep

Less than 50% of inpatient UTI’s are caused by E.coli.

52
Q

What do we call the bilirubin-induced brain dysfunction?

A

Kernicterus.

Neuro damage due to the build up of bilirubin.

53
Q

Severe itching of the skin as a symptom of another ailment:

A

Pruritis.

Can be an adverse effect of Bactrim.