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NURS 4380 PATHOPHYSIOLOGY,PHARMACOLOGY & PHYSICAL ASSESSMENT FINAL EXAM STUDY GUIDE Latest 2021/2022 $17.49   Add to cart

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NURS 4380 PATHOPHYSIOLOGY,PHARMACOLOGY & PHYSICAL ASSESSMENT FINAL EXAM STUDY GUIDE Latest 2021/2022

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NURS 4380 PATHOPHYSIOLOGY,PHARMACOLOGY & PHYSICAL ASSESSMENT FINAL EXAM STUDY GUIDE / NURS 4380 PATHOPHYSIOLOGY,PHARMACOLOGY & PHYSICAL ASSESSMENT FINAL EXAM STUDY GUIDE Latest 2021/2022

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  • March 16, 2022
  • March 16, 2022
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  • 2021/2022
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NURS 4380 PATHOPHYSIOLOGY,PHARMACOLOGY &
PHYSICAL A S S E S S M EPatho
N T Pharm
FINALFinal
EXAM STUDY GUIDE Latest 2021/2022
Review
Basics of Antibiotics (13)
1. Define selective toxicity as it applies to the general mechanisms by which antibiotics
work against invading pathogens but not against host cells.
o Selective toxicity means that the drug interferes with necessary microbial
biochemical processes. The pathogen is a prokaryote, while the host (us) is
eukaryote, so their genetic makeup is different.
• Explain disruption of bacterial cell wall (Ex: Penicillin and cephalosporins)
➢ Prokaryotes (Bacteria) are encased in a rigid cell wall
➢ The protoplasm within this wall has a high concentration of
solutes, making osmotic pressure within high
➢ Without this cell wall, bacteria would absorb water, swell, and
then burst
Several drug families weaken the cell wall and thereby promote bacterial lysis
• Explain Inhibition of an enzyme unique to bacteria and provide example
➢ Sulfonamides: Inhibit enzyme PABA (para-aminobenzoic acid), a
precursor to folic acid, which is necessary for bacteria to
synthesis folic acid; without this enzyme they die
• Explain disruption of bacterial protein synthesis
➢ Disrupts ribosomal protein synthesis but not in us because we
have different ribosomes than bacteria
2. Give a working definition of narrow-spectrum and broad-spectrum antibiotics and state
when one or the other would be preferred as a therapeutic approach and why.
• Narrow spectrum: preferred to decrease chance of building resistance and
superinfections. Doesn’t attack our normal bacteria (flora). Has high specificity-
only attacks certain bacteria. This is what we want to use.
• Broad spectrum: Kill many/all bacteria. Even normal bacteria die when these are used.
Resistant bacteria flourish because nutrients help them thrive/multiply. Since
everything else dies off, the resistant bacteria can use up all of the nutrients available.
1.Superinfection can occur. Ex: yeast infection bc normal flora is disrupted.
3. State the main mechanisms by which microbes develop resistance to antimicrobial drugs.
Also, address the important issues of spontaneous mutations and R factors.
o Resistance:
• Selection pressure occurs- resistant microbes flourish as sensitive microbes
die off; Basically, on all humans there is a population of bacteria (Most are
susceptible strains, and some are antibiotic-resistant). These bacteria
compete with each other (for food and stuff) and your good normal flora fight
off bad bacteria that doesn’t normally live on you. So, when a person takes
antibiotics all of the susceptible strains are killed (which can be good or bad)
but the resistant strains of bacteria survive. Because of this the remaining
resistant strains do not have anyone to compete with, so they thrive because
they now have no one to compete with for food or anyone trying to fight
them off and if they are a bad microbe they can cause an infection on that
person.
• All antibiotics promote resistance

, • Overuse of antibiotics promote overgrowth of normal flora which promotes
a playground for more resistance through pressure selection.
• 4 basic actions of drug resistance:
1. Decrease concentration of a drug at its site of action:
▪ Bacteria ceases active uptake or increases active export.
2. Inactivate a drug:
▪ Produce a drug metabolizing enzyme that renders it, making the
drug inactive; Ex: PCNase (penicillinase) or beta-lactamase
3. Alter the structure of the drug target molecules:
▪ Most drugs must interact with target molecules (receptors)
to produce their effects
▪ Alter bacterial ribosomes- now the “receptor” has changed, and
drug cannot “select.”
4. Produce a drug antagonist:
▪ Rare, bacteria produces a compound that “antagonizes” drug; ex:
By acquiring the ability to synthesize increased quantities of PABA,
some bacteria have developed resistance to sulfonamides
a. Bacteria cannot “take up” folic acid from
environment-they NEED folic acid to create their
cell wall. They must synthesize it to make DNA,
RNA.
b. Folic acid is synthesized from PABA; PABA helps
bacteria grow, so you want to inhibit it to
inhibit bacterial growth.
o Spontaneous mutations:
• Produce random changes in microbe’s DNA; The result is a gradual increase in
resistance, low level resistance occurs first; with additional resistance
becomes greater
• As a rule, spontaneous mutations confer resistance to only one drug
o Conjugation:
• Two unique, extrachromosomal, DNA segments whose end result is an
“R” factor (resistant factor); this is transferred from one bacterium to
another)
• Can occur across the same species or different species; therefore, it is
possible for pathogenic bacteria to acquire R factors from the normal flora of
the body; this is a significant clinic concern because it is occurring more often
• RESULTS IN MULTIPLE DRUG RESISTANCE (this can be achieved by
transferring DNA that codes for several different drug metabolizing enzymes;
so, in a single event a drug sensitive bacterium can become highly resistant)
• Most are Gram negative bacteria (gram negative are bad; they are hard to
treat because of the extra envelope that they have)
• Basically, they’re mixed together and produce a resistant factor and it can
occur in one bacterium to another and across species.
4. Describe generally accepted indications for prophylactic antimicrobial therapy.
o Agents given to prevent infection rather than to treat an established infection
o Surgery: cardiac, peripheral vascular, orthopedic, hysterectomy, c-section, GI
tract, “dirty” surgeries, contaminated surgeries (aka GI perforations), animal
bites.
o Bacterial endocarditis: bacteria sit on heart valves (aka an infection in heart
valves); Who’s at risk? Pt with prosthetic heart valves, valvular heart disease.

, o Neutropenia: have low WBC so at risk for infection
o Recurrent UTI’s, antivirals (influenza), rheumatic endocarditis, exposure to STD’s

5. Discuss the misuse of antibiotics, its general prevalence, why misuse persists as a major
health problem, and the consequences. Give some examples of common situations in which
iatrogenic antibiotic misuse occurs.

o Misuses of Antimicrobial Drugs:

• Attempted treatment of untreatable infections

• Treatment of fever of unknown origin (try to figure out what is wrong first)

• Improper dosage

• Treatment in the absence of adequate bacteriologic information (MUST
figure out the cause/what’s wrong first!)

• Omission of surgical drainage (antibiotics may have limited efficacy in the
presence of foreign material, necrotic tissue, or exudate; hence, when
appropriate, surgical drainage and cleansing should be performed to
promote antimicrobial effects

• Use of antibiotics to produce growth in livestock; this has made bacteria
build resistance; Contamination can occur between livestock & humans.

o Antibiotic must be present:
• At the site of infection
• For a sufficient length of time
o Antibiotics must not be discontinued prematurely (recurrent infection -> can lead
to resistance)
o Teach patients to complete full prescription (most important info to provide to
your client about taking antibiotics); why?
• Early discontinuation is a common cause of recurrent infection, and the
organisms responsible for relapse are likely to be more drug resistant than
those present when treatment began
6. Describe the basic mechanism of action of the penicillins.

o Drug that weakens the bacterial cell wall, causing bacteria to take up excessive
water and rupture (cell lysis)

o Active ONLY against bacteria that are undergoing growth and division (bactericidal)

o WONT work with bacteriostatic because those just slows the growth (they prevent
the bacteria from undergoing growth and division)

7. Compare and contrast gram-positive and gram-negative bacteria
o Gram negative:

, • Cell envelope has THREE layers; Thin cell wall and an additional outer
membrane that is hard to penetrate (do not stain)
o Gram positive:
• Cell envelope only two layers; Relatively thick cell wall that is easily
penetrated by bacteria (stain purple)
8. Describe the beta-lactam ring. Also, explain why penicillins are part of the family of
antibiotics called the beta-lactam antibiotics and state how that relates to the vulnerability of
these antibiotic classes to inactivation by certain bacteria.
o Beta-lactam ring:
• It is a core part of the penicillin family structure
• A bacterium can produce an enzyme (beta-lactamase = penicillinases) that
destroys it and becomes resistant; can produce a large variety of these
enzymes specific for penicillins (and other beta-lactam antibiotics)
• If you’re allergic to penicillin, you might also be allergic to others in the
beta- lactam family (cephalosporins, monobactam, carbapenems,
ertapenem, imipenem, meropenem); Nearly all of these antibiotics work by
inhibiting bacterial cell wall synthesis
9. Recognize penicillins as a main cause of drug-induced allergic req22actions. Also, compare
and contrast immediate, accelerated, and delayed hypersensitivity reactions in terms of time
of onset and main signs and symptoms.
o Penicillin principal adverse effect: allergic reaction (If a person is going to have an
allergic reaction it will most likely be on these)
o If history of mild reaction, consider cephalosporin
o If history of anaphylaxis (worst kind of reaction), avoid administration of penicillin
or cephalosporin
o Immediate: reaction in 2-30 minutes
o Accelerated: reaction in 1-72 hours
o Late: reaction takes days or weeks to develop. Type IV – T Cell mediated
o Anaphylaxis s/s: laryngeal edema, bronchoconstriction/spasms, severe
hypotension, severe vascular collapse due to release of histamine, SOB, dyspnea,
edema of throat/epiglottis, urticaria (rashes), hypotension, shock, pruritis (itching),
death.
• Type I – IgE mediated; Antigen stimulated mast cell activation resulting
on massive histamine release.
o Stop the drip FIRST if any allergic reactions occur; treatment: Epi, Benadryl, steroids
stat IVP, prepare for intubation (must intubate before throat swells shut).
10. Given a patient’s history of severe hypersensitivity reactions to penicillin, state at least
one other group of antibiotics that should not be administered because of the risk of
cross- reactivity.

o If they have a history of anaphylaxis, AVOID cephalosporins

o If history of mild reaction, consider cephalosporins.

11. Recognize “mycin” antibiotics can cause ototoxicity and Nephrotoxicity.

o Ex: vancomycin, which is only given for severe infections (Given after Flagyl was
tried and found ineffective)

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