Module - Immune System Flashcards

1
Q
  • Inflammation is? With a purpose of?
  • Symptoms
  • Is it good or bad

-itis

A

Inflammation is a defence mechanism, with a purpose to contain the injury and destroy a foreign agent

Swelling, pain, redness, warmth

Good until it hinders healing

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2
Q

Inflammation Mediators 6

A
Histamine
Bradykinin
Leukotrienes
Cytokines
Interleukins
Prostaglandins
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3
Q

Classes of Inflammation System Drugs 2

A

Non-steroidal anti-inflammatories (NSAIDs)

Corticosteroids

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4
Q
Inflammation
NSAIDs
-What do they inhibit 
-What properties do they have
-What are they for

-Forms of things they inhibit
C1 & C@

A
  • Inhibit cyclo-oxygenase (COX), which reduces prostaglandin synthesis - >inhibiting inflammation
  • Also have analgesic and antipyretic properties
  • For mild to moderate inflammation

-COX-1 – In all tissues, stomach lining (mucosa), involved in platelet aggregation
(Responsible for most adverse effects of NSAIDs)
-COX-2 – more specific for inflammation

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5
Q
Inflammation
(NSAIDS)
Ibuprofen
-What are the primary uses
-What are the NSAID adverse effects 
-Take with?
-Caution when?
A

Primary use: mild to moderate inflammation, fever, mild to moderate pain, dysmenorrhea, musculoskeletal pain, arthritis

NSAID adverse effects: nausea, dyspepsia, ulcer with long-term use, potential anti-platelet action, hypertension, increased risk of cardiac event with long-term use

Take with food

Caution in kidney disease, cardiovascular disease, GI conditions

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6
Q

CV Risks of NSAIDS

  • What happened 15 years ago
  • Increase in CV events from?
  • What drug was safe
  • Further analysis showed?
A
  • 15 years ago – large influx of selective COX-2 inhibitors
  • increase in cardiovascular events in those patients using long term (for arthritis, chronic conditions)
  • [only drug left = celecoxib]
  • Further Analysis: celecoxib and non-selective show risks, only use short-term as needed
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7
Q
Inflammation
Corticosteroids
-Mimic what 
-Two forms
-Whats it for
-Adverse effects?
-How to give
A
  • Mimic endogenous cortisol, attempting to bring body back to homeostasis after a fight-or-flight response
  • Anti-inflammatory and immuno-suppressive

For severe inflammation

Serious systemic effects, limit use to emergencies and severe inflammation (multiple sclerosis, rheumatoid arthritis, auto-immune diseases)

Local administration, short-term use preferred whenever possible

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8
Q

Anti-inflammatories: Nurses Role

  • First job
  • Screen for?
  • What do you find in the labs
  • Find out what?
  • Monitor what adverse effects (NSAIDs, Corticosteroids)
  • Take with?
A

Cause of inflammation – remove or treat

Screen for contraindications (kidney or liver disease, GI disease, cardiovascular disease, active infection, etc.)

Labs – CBC, liver & kidney function

Response to treatment

Monitor adverse effects
[NSAIDs – GI upset, bleeding, cardiovascular risk?

Corticosteroids – hyperglycemia, hypertension, nausea, insomnia, psychosis (↑ doses)]

Take both with food

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9
Q

Fever

  • What mechanism is it
  • What can it cause in children
  • Fever is a indicator of? (can you solve it)
  • Treating fever is for
  • Drugs that reduce fever are for?
A

-Fever is a defence mechanism (many species of bacteria are destroyed by high temperature)

-Fever can cause febrile seizures in children (6mos to 5 years)
[Cannot prevent a febrile seizure besides avoiding infections]

  • Fever is a indicator of immune system functioning
  • Treating a fever is for comfort
  • Drugs that reduce fever = antipyretics
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10
Q

Classes of Fever Medications 2

A

Acetaminophen

NSAIDs

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11
Q
Fever
Acetaminophen
-What is the mechanism of action
-Primary use?
-Adverse effects (Liver toxicity dose? Avoid? interacts with what and how?)
A
  • Mechanism of action: acts at hypothalamus to cause peripheral vasodilation, which enables sweating and allows body to rid excess heat (No anti-inflammatory action)
  • Primary use: fever, mild to moderate pain, osteoarthritis
  • Adverse effects: very rare liver toxicity (max dose of 4g/24hours), avoid alcohol, interacts with warfarin (but doesn’t ↑ bleeding on its own)
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12
Q

Max dose of Acetaminophen

  • what is the max dose?
  • OTC contain? (says?)
  • Ingestion by unaware consumer has caused what?
A

3g / 24 hours

over-the-counter products contain acetaminophen as an additional ingredient
(“…..& Flu”)

inadvertent ingestion by unaware consumers, warnings for public have been reduced to allow for safer use

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13
Q
Fever
NSAIDs
-Mechanism of action?
-Why is it the first line for fever
-When is NSAID more appropriate?
-ASA is contraindicated in?
A
  • Same mechanism of action as acetaminophen (for fever)
  • Acetaminophen’s safety record (few drug interactions and side effects), it is first-line for fever
  • NSAID appropriate if inflammation is also present (ibuprofen > ASA)

ASA is contraindicated in children = Reye’s Syndrome (ASA + virus + fever in child)

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14
Q

Fever: Nurses Role

  • Find what?
  • Monitor?
  • Assess adverse effects:
  • Symptoms
A

-Cause of fever – if other treatment is needed such as antibiotics

  1. Monitor response to treatment – can use fever as indicator if safe to do so
  2. Vitals
  3. Watch warfarin levels (NSAIDs, acetaminophen)

Assess adverse effects: GI upset, sudden change in urine output (kidney!), signs of liver toxicity
-Jaundice, pale, tired, sweating, dark urine, confusion, coma

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15
Q

Allergies
Allergic Rhinitis (hay fever)
-symptoms similar to?
-Antigen labeled as what and causes?

A

Symptoms similar to common cold but no fever

Antigen – causes the symptoms – anything that the body has ‘labeled’ as foreign

  • Tearing eyes
  • Sneezing
  • Nasal congestion
  • Postnasal drip = cough
  • Itchy mucous membranes (inside of nose, mouth, eyes)
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16
Q

Histamine

  • When are they released
  • The two kinds and what do they affect
A

Body responds to antigen by releasing histamine = causes most annoying symptoms

H1 – smooth muscle of vascular system, bronchial tree, digestive tract

H2 – lining of stomach, producing gastric acid

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17
Q

Classes of Allergy Medications

4

A

Antihistamines

  • 1st-generation
  • 2nd-generation

Intranasal Corticosteroids

Decongestants

Drugs for Anaphylaxis

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18
Q
Allergies
1st-Generation Antihistamines
-What do they block
-Difference from 2nd generation
-Used to treat
-2 common types
-Have what kind of effects
-Significant?
A

Block H1 receptors

Shorter acting, cause more drowsiness, and work faster than 2nd Generation

Used mostly to treat allergic response

Diphenhydramine and chlorpheniramine most common

Have anticholinergic effects

Significant sedation – some use as a sleep aid

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19
Q
Allergies
2nd-Generation Antihistamines
-What do they block
-Difference from 1nd generation 
-How long for the effect
-Used to treat
-Have what kind of effects
-Take how often
- effectiveness ?
-4 common types

-Significant?

A

Block H1 receptors

Longer acting (12-24h), less sedating, and take longer to start working (onset of action) than 1st Gen.

Can take a few hours  days for full effect, but safe to use for years

Still some anticholinergic activity (much < than 1st Gen)

Take daily to prevent symptoms during troubling season

Trial-and-error for effectiveness

Cetirizine (Reactine®), loratidine (Claritin®), desloratidine (Aerius®), fexofenadine (Allegra®)

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20
Q
Allergies
Intranasal Corticosteroids
-What do they do
-used to prevent
-how long does it take
-Local administration does
-Adverse effects
A

To reduce inflammation in nasal mucous membranes, and local immunosuppression

Used daily to prevent symptoms

Can take up to 2 weeks for full effect

Local administration prevents systemic side effects

Adverse effects: nasal irritation, dryness and bleeding (epistaxis), bad taste, loss of smell

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21
Q

Allergies
Decongestants (Phenylephrine, pseudoephedrine)
-What are Sympathomimetics and what do they cause
-Immediate relief of?
-What is the length of used for and consequence if used otherwise
-Adverse effects

A

Sympathomimetics – stimulants – cause vasoconstriction and reduction of mucous production

For immediate relief of nasal congestion – oral or intranasal

Short term-use only – rebound congestion if longer than 3-5 days (intranasal)

Adverse effects: oral – hypertension, anxiety, insomnia; intranasal – nasal irritation, rebound congestion, rarely systemic effects

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22
Q

Allergies
Decongestants

Restrictions on selling

  • What is the main restriction on this drug
  • single ingredient products contain?
  • Where can they be found
A

Pseudoephedrine is used in manufacturing process of crystal meth – cant be sold as single ingredient in oral med
(difficult to isolate ephedrine if there is >1 ingredient)

Single-ingredient products now contain phenylephrine – not as potent

Pseudoephedrine is still available, but need to ask for it at the pharmacy (Schedule II)

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23
Q

Allergies: Nurses Role

  • Document
  • Correct product?
  • Monitor what
  • nasal dryness?
  • Educate
  • Assess?
A

Health history to identify triggers/antigens and previous therapy

Correct product = Prevention vs. treatment

Monitor anticholinergic effects, sedation, changes in vitals, urinary retention, effectiveness of product, stimulant adverse effects

Nasal dryness – humidifiers, saline drops, vaseline

Educate on short-term use of decongestants

Assess use of anti-histamines as sleep aids= sleep hygiene, etc.

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24
Q
Allergies
Anaphylaxis
-Response to what
-How fast do symptoms appear
-example
A

Fatal, hyper-response to an allergen (different from allergies/hay fever)

Symptoms within seconds or minutes

Itching, hives, tightness in throat or chest, difficulty breathing, facial swelling, non-productive cough and hoarse voice as larynx begins to close, rapid hypotension (with reflex tachycardia) and bronchoconstriction

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25
Q
Allergies
Anaphylaxis Drug
 Epinephrine
-Stimulate what
-Does so via what and how 2
-Alleviates?
A

Stimulates both α and β adrenergic receptors

Via α–receptors: counters the high vascular permeability that occurs during anaphylaxis that leads to loss of intravascular fluid and hypotension

Via β–receptors: causes bronchial smooth muscle relaxation and relieves bronchospasm, dyspnea, and wheezing

Also alleviates pruritus, urticaria, and angioedema

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26
Q
Allergies
Anaphylaxis: Outpatient Treatment
-What is a epi-pen
-Given when
-What route
A

Epi-Pen® - epinephrine injection given an onset of symptoms

To be given on way to hospital – won’t resolve situation, just gives them more time

IM – give in large muscle in leg through clothing

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27
Q
Allergies
Epinephrine Auto-Injectors
-How many brands
-Designed for
-Variations of
-Leave injector for how long
-Injected where
A

Many brands now available

All designed for ease of use and clarity

Variations of “Remove cap and jab into top of thigh”

Leave injector in place for 5-15 seconds

To be injected ON WAY TO HOSPITAL

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28
Q

Anaphylaxis: Treatment in Hospital 6

A

-Oxygen
-More epinephrine
-IM or IV diphenhydramine
-Bronchodilator – salbutamol (β-agonist)
-Corticosteroids – both anti-inflammatory and immuno-suppressive effects
+ Comfort measures (traumatic experience)

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29
Q

Anaphylaxis: Monitoring and Nurse’s Role

  • Document?
  • Educate
  • In hospital?
  • support?
A

Health history to identify triggers/antigens

  • Educate family on signs of anaphylaxis and what to do
  • Educate proper use of epinephrine (EpiPen® or other) and follow-up

In hospital: vitals in response to treatment (hypertension, tachycardia, headache, dysrhythmias, edema, bronchoconstriction)
-Fight-or-flight response

Support for traumatic experience

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30
Q

Antibiotics
Bacterial Disease
-Bacteria cause disease by two mechanisms

A

Bacteria grows rapidly and causes disease by sheer numbers

Bacteria produce toxins that cause disease
E.g. botulinum toxin

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31
Q

Classification of Bacteria
-2 kinds

different antibiotics usually target either gram + or -

A

Gram-positive: have thick cell walls and retain purple gram-stain

Gram-negative: have thin cell walls and lose purple gram-stain

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32
Q
Classification of Bacteria
Bacilli
Cocci
Spirilla
Aerobic
Anaerobic
A

Bacilli – rod-shaped
Cocci – spherical
Spirilla – spirals
Aerobic – bacteria that require oxygen to live and thrive
Anaerobic – bacteria that do not require oxygen to live and thrive
(some can live in both)

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33
Q
Antibiotics
-target bacteria depending on?
-Classified by?
Bactericidal?
Bacteriostatic?
A

Antibiotics target certain bacteria depending on if they are:

  • Gram positive or negative
  • Bacilli, cocci, or spirilla
  • Aerobic or anaerobic

Antibiotics are classified either by their structure or their mechanism of action

Bactericidal – drugs that KILL the bacteria

Bacteriostatic – drugs that slow down the growth of the bacteria, allowing the body’s immune system to dispose of the bacteria

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34
Q

Antibiotic Resistance
(Bacteria multiply increasing chance of mutation)
-Mutations give what
-if antibiotic doesn’t destroy mutated bacteria?

A

Some mutations may give bacteria a benefit over others of the same species – antibiotic resistant properties

If the antibiotic doesn’t destroy these mutated bacteria, it will replicate, passing on the beneficial traits = resistant to the previous antibiotic

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35
Q

Activities that Promote Resistance 3

Examples: MRSA (methicillin-resistant staphylococcus aureus), VRE (vancomycin-resistant enterococcus)

A

Not completely finishing a course of antibiotics – some bacteria are left over even after symptoms disappear

Not a high enough dose of antibiotics – does not reach high enough of a concentration to get rid of all bacterial cells

Using an antibiotic when it is not indicated – every time an antibiotic is used, there is an increased chance of resistance due to exposure

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36
Q

Spectrum of Antibiotics 2

A

Broad-spectrum antibiotics: drugs that are effective against a wide variety of bacteria
(Prescribed empirically (according to experience) when we don’t know specific pathogen)

Narrow-spectrum antibiotics: drugs that are effective against very specific microorganism or restricted group
(Prescribed when pathogen is clear from a C & S, or symptoms, or type of infection)

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37
Q

Culture & Sensitivity (C & S)

Ideal situation and real life situation

A

Ideal situation:
-A patient comes in with an infection, we swab the infected area, grow it in a culture, and test it with classes of antibiotics to find out what it is sensitive to, then prescribe that agent in an appropriate way

Real life:

  • We prescribe an agent right away (usually broad-spectrum, empirically prescribed), order a C & S, then change the antibiotic or dose if needed according to results
  • Unfortunately, because it is done after the fact, there are instances where C & S results are not reviewed, therefore inappropriate and ineffective treatment can occur
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38
Q

Superinfections

  • What kind of infection
  • When does this happen and what antibiotic causes this
  • Normal flora does what
  • what creates an opportunity of super infection
A

A secondary infection

When an antibiotic also kills bacteria in the normal flora of our body (most commonly skin, lungs, GI and urinary tract)
(Broad spectrum antibiotics are more likely to do this than narrow spectrum)

Normal flora has useful purposes such as aiding in digestion and fighting pathogens through competition for nutrients

Absence of normal flora + tiny amount of remaining pathogen = opportunity for superinfection

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39
Q

Signs of Superinfections

  • what is the sign
  • Common SS
A

Another infection during or immediately after antibiotic therapy

  • May be a different site of infection (Yeast infection after treating an upper respiratory tract infection - URTI)
  • Common sites: GI tract, genitourinary tract

Common: diarrhea, blood or pus in stool, cramping, abdominal pain, bladder pain, painful and frequent urination, signs of vaginal infection (yeast or bacterial)

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40
Q

Probiotics

  • What antibiotics cause diarrhea
  • Do probiotics work
  • When do you give
  • What do susceptible pts use
A

Any/every antibiotic (especially given orally) has potential to cause diarrhea, due to disruption of normal flora = does not ALWAYS lead to superinfection

Maybe! (i.e. some products have shown evidence in preventing diarrhea)

Don’t give at exact same time as antibiotic dose – separate as much as possible

If patient is more susceptible (regularly gets diarrhea from antibiotics – assess with med history), can use probiotics to prevent diarrhea

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41
Q

Choosing an antibiotic

We consider? 8

A

-C & S
-Site of infection
Immune system status of patient (bactericidal or –static more appropriate?)
-Kidney and liver function
-Dosage forms available
-Variables affecting absorption, distribution, metabolism and elimination of antibiotic
-Patient allergies or intolerances
-Ease of administration and adherence issues

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42
Q

Classes of Antibiotics 9

A
Penicillins
Cephalosporins
Tetracyclines
Macrolides
Aminoglycosides
Fluoroquinolones
Sulfonamides
Carbapenems
Miscellaneous VIPs
43
Q
Antibiotics 
Penicillins (-cillin)
-Disrupt what
-how do they do it
-What do they contain
-How do they fight this antibiotic 
-Why is Clavulanic Acid essential (Amoxicillin + Clavulanic Acid (Amoxiclav))
A

Disrupt bacterial cell walls (Bactericidal)

Penicillin-binding protein: a protein only in bacterial cell walls that penicillin binds to = weakens the cell wall, allows fluid to enter and destroys the cell

Penicillins contain a beta-lactam ring in its structure necessary for activity

Many bacteria produce beta-lactamase (penicillinase) that is a natural defense to penicillin – it breaks the beta-lactam ring, leaving it ineffective = penicillin resistance

-Clavulanic acid inhibits β–lactamases (penicillinases) of some microorganisms to allow amoxicillin to be active against it (Synergistic relationship)

44
Q

I don’t think you need to memorize drugs but look

Narrow Spectrum

Broad Spectrum

Extended spectrum

A

Narrow Spectrum

  • Penicillin G
  • Penicillin V
  • Cloxacillin
  • Dicloxacillin

Broad Spectrum

  • Amoxicillin
  • Amoxicillin/clavulanate
  • Ampicillin

Extended Spectrum

  • Carbenicillin
  • Piperacillin
  • Piperacillin tazobactam
  • Ticarcillin
45
Q
Penicillins
Penicillin G Potassium (Pen G)
-Drug of choice for?
-Adverse effects
-Comparison to Pen V
A

Drug of choice against streptococci, pneumococci, staphylococci, gonorrhea and syphilis (given IV or IM)

Penicillin adverse effects: anaphylaxis, diarrhea, nausea, vomiting, pain at injection site, superinfections, some (minor) drug interactions

Comparison to Pen V: Pen V is given orally, slightly different spectrum of activity

46
Q

Allergy to Penicillins

  • What is its rarity
  • How many people are allergic
  • How often does a rash occur

(Question patient about the reaction and get as much information as possible)

A

The most common allergy listed

Very rarely an actual allergy (90% of patients who claim they’re allergic to penicillin actually aren’t)

  • 80% of those with a severe penicillin allergy will lose their sensitivity 10 years after a reaction
  • Usually is an intolerance (“….gave me diarrhea”, “….got a rash as a baby”)

Rash occurs ~2%

47
Q

Monitoring for Penicillins

4

A

Electrolyte levels (Na+, K+)

Response to therapy (infection clearing?↓ fever?)

Adverse effects & anaphylaxis (first or second dose)

Signs of superinfection – diarrhea that didn’t start until finished course, or did not go away when finished course; complaints of yeast or urinary infection, etc.

48
Q
Antibiotics
Cephalosporins ([C]ef/ph)-)
-how are they related to  penicillins
-Mechanism?
-Classified how?

4 general rules?

A

Related to penicillins (1st gen. also have beta-lactam ring)

Also inhibit cell wall synthesis
(Bactericidal)

Classified according to “generation” (1 - 4)

General Rules

  • 1st generation not effective against bacteria producing beta-lactamase
  • More potent as go up in generation
  • Fewer similarities with penicillins as go up in generation
  • Higher generations reserved for known resistant infections
49
Q

1st Gen. 3
2nd Gen 5
3rd Gen 4
4rth Gen 1

A

1st Gen

  • Cefadroxil
  • Cefazolin
  • Cephalexin

2nd Gen

  • Cefaclor
  • Cefotetan
  • Cefoxitin
  • Cefprozil
  • Cefuroxime

3rd Gen

  • Cefixime
  • Cefotaxime
  • Ceftazidime
  • Ceftriaxone

4rth Gen
-Cefepime

50
Q
Antibiotics 
Cephalosporins
Cefotaxime (3rd Gen.)
-What kind of spectrum and for what
-adverse effects
-given how?
A

Has broad-spectrum activity against gram-negative organisms; for serious infections of lower respiratory tract, CNS, genitourinary system, bones, blood, and joints

Adverse effects: hypersensitivity, rash, itching, anaphylaxis, diarrhea, vomiting, nausea, pain at injection site, some (minor) drug interactions

Must be given IV or IM (not orally)

51
Q

Cross-Sensitivity with Penicillins?

Cephalosporins are related to penicillins – so what if a patient is (truly) allergic to penicillin?

[Product mammograms (legal document) says cross-reaction rate between cephalosporins and penicillins is 10%, the generalized rate of reaction has been redefined to 1.1% )

  • Important to know what
  • Less chance of what
A

It is important to know what type of reaction a patient had to penicillins to base a decision (true allergy?)

Less of a chance of cross-sensitivity with higher generation cephalosporins (less similarities to penicillins)

52
Q
Antibiotics 
Tetracyclines [-cycline]
(doxycycline, minocycline, tetracycline)
-Inhibit what?
-What spectrum
-Given by what route 
-Should not be given with?
-Used for what bacteria
-Adverse effects?
-Interfere with?
-Higher chance of superinfections because
A

Inhibit bacterial protein synthesis (Bacteriostatic)

Broad-spectrum (both gram-positive and negative)

Usually given orally (PO)

Should not be given at the same time as iron, calcium, magnesium (ions bind to drug so it can’t absorb) – separate by 2h

Used for Rocky Mountain spotted fever, h.pylori infections, acne vulgaris, chlamydia

Adverse effects: diarrhea, yeast infections, nausea, vomiting, epi-gastric burning, yellow-brown teeth discolouration in young children (why we don’t use), photosensitivity

Can potentially interfere with oral contraceptives (recommend backup method)

Higher chance of superinfections because it is broad-spectrum

53
Q

Bacteria
Macrolides (-thromycin)
[azithromycin, clarithromycin, erythromycin, fidaxomicin]

  • Inhibit
  • What are the similarities to penicillin
  • First drug was? and newer versions had what
A

Inhibit bacterial protein synthesis
(Some are bactericidal, some bacteriostatic)

No structural similarities to penicillin – zero chance of cross-reactivity

First drug was erythromycin, others were developed later on with longer duration of action and are easier on the stomach

54
Q

Antibiotics
Macrolides (Erythromycin)

  • Whats it used for
  • Adverse effects?
  • Fidaxomicin used for?
A

Used for upper and lower respiratory tract infections, whooping cough, diphtheria, or for other infections in patients who cannot take penicillins

Adverse effects: significant nausea, vomiting, diarrhea (take with food), some important drug interactions (Warfarin, cyclosporine, anticonvulsants (all via CYP450 inhibition/induction) )

Fidaxomicin – new; for treatment of c. difficile; not absorbed, stays in GI tract = nausea, constipation, vomiting

55
Q
Antibiotics
Aminoglycosides (-m(y/i)cin)
(amikacin, gentimicin, streptomycin, tobramycin)
-Inhibit what?
-How well does it work
-Require what
-Route
-adverse effects
-Used when
A

Inhibit bacterial protein synthesis and cause abnormal protein synthesis
(Dose-dependent bactericidal)

Very effective, usually reserved for serious infections (like tuberculosis) or when other antibiotics have failed

Require therapeutic drug monitoring – levels must be in specific range to be effective, but not toxic

Injection or topical

nephrotoxicity and ototoxicity

Used for serious (life-threatening) infections or when other antibiotics have failed (also topically as eye drops and creams/ointments – this would not require therapeutic drug monitoring)

56
Q
Aminoglycosides
Ototoxicity
-what is it
-can you fix it
-Symptoms
-How is it solved
A

Damage to the inner ear and/or nerve damage

Often irreversible, but not guaranteed

Presentation: hearing loss, vertigo, tinnitus
-Remove drug immediately

57
Q

Aminoglycosides
Nephrotoxicity

  • Effect on?
  • Symptoms
  • How is it solved and is it reversible
A

A direct poisonous effect on the kidney

Different than toxicity of a drug that is eliminated by the kidneys (accumulation of a drug could be toxic to any organ or system)

Presentation: protein and/or blood in urine, elevated blood-urea nitrogen (BUN), ↑ serum creatinine (SCr), either no or excessive urine output, edema, confusion, delirium (due to toxins accumulating)

Stop administration of drug, may start hemodialysis

Usually reversible

58
Q

Antibiotics
Fluoroquinolones (-floxacin)
[besifloxacin, ciprofloxacin, gatifloxocin, levofloxacin, moxifloxacin, norfloxacin, ofloxacin]

  • Mechanism of action
  • Route?
  • Absorption effected by and separated from
  • not used for
  • New info on adverse effects
  • Commonly prescribed for
  • Nursing role
  • Used commonly for
  • Adverse effects
A

Affect bacterial DNA synthesis (Bactericidal)

Most often used orally (also ear, eye)

Absorption is affected by minerals (calcium, iron, magnesium) and need to be separated (-2h)

Generally not used in children – affects cartilage development

  • Tendinitis/tendon rupture, cardiac arrhythmias, CNS effects (Seizures, tremors, altered mental state), peripheral neuropathy
  • commonly prescribed for acute sinusitis, acute bronchitis, and uncomplicated urinary tract infections (risk > benefit for these indications now)
  • Nursing Implication: watch for inappropriate prescribing, monitor for these adverse effects, avoid in patients with seizures

Used commonly for respiratory, urinary, ophthalmic, gastrointestinal, and gynecological infections – high usage in community/out-patient

Adverse effects: nausea, diarrhea (can take with food), photosensitivity

59
Q

Antibiotics
Sulfonamides (Sulfa-)
(sulfacetamide, sulfamethoxazole, sulfapyridine)

  • How do they supress bacterial growth
  • What spectrum
  • Route
  • Common what?
  • Sulfamethoxazole-Trimethoprim (SMZ-TMP, Septra®, Bactrim®, -DS) does what together
  • Used to treat
  • Adverse effects
  • Take with
  • Monitor?
  • -DS, Error alert?
A

Suppress bacterial growth by inhibiting essential folic acid needed within the cell
(Bacteriostatic)

Broad spectrum, older class =more resistance seen

Orally and topically (acne)

“Sulfa” is also a common “allergy”
-Question type of reaction and get as much information as you can (document!) = check with pharmacy about sulfa drugs (can be difficult to identify – remember hydrochlorothiazide?)

Both drugs inhibit essential folic acid synthesis; work synergistically (a pharmacodynamic interaction)

Used to treat urinary tract infections

Adverse effects: nausea, vomiting, skin rashes, photosensitivity, anemia, crystalluria

Drink lots of water to prevent crystalluria

Monitor for: painful urination, abdominal pain, blood in urine, fever

DS = Double strength, can substitute but must use appropriate dosage and watch for errors
-Always have someone check your calculations – do the math every time

60
Q
Antibiotics 
Carbapenems (ertapenem, imipenem, meropenem)
-How old is this drug
-Contain?
-Spectrum
-Adverse effects
-If you take this drug how ill are you
A

Relatively new

Contain beta-lactam ring and inhibit cell wall synthesis (like penicillins)
-The beta-lactam ring is very resistant to destruction by penicillinase

Broad spectrum – and very effective; as a newer class, they are being reserved for resistant infections (like MRSA, etc.)

Adverse effects: skin reactions, inflammation at injection site, diarrhea, nausea, vomiting

Many patients receiving carbapenems are severely ill

61
Q

Antibiotics
Miscellaneous
-What does it stand for?

Clindamycin, mechanism

  • What route
  • Risk of superinfection?

Nitrofurantoin, mechanism

  • How does it travel and what is it used for
  • How does it change the body
  • Take with?

Metronidazole, mechanism

  • for what bacteria
  • Cant be used with
  • what is the Disulfiram reaction that happens and how often
A

‘Miscellanous’ label does NOT mean they are less used or are less effective

Clindamycin – protein synthesis inhibitor; bacteriostatic

  • Used topically (acne), oral or IV for serious systemic infections
  • High risk of superinfection (GI)

Nitrofurantoin – inhibits protein, RNA, DNA, and cell wall synthesis; bactericidal

  • Excreted unchanged through the kidney (no metabolism), therefore used only for urinary tract infections
  • Changes urine to orange colour
  • Must take with food

Metronidazole – destroys bacterial DNA; bactericidal

  • For anaerobic bacteria
  • NO ALCOHOL USE (even small amounts present in cough syrup or mouthwash)
  • Disulfiram reaction – flushing, tachycardia, shortness of breath, severe nausea & vomiting, throbbing headache, visual disturbance, confusion, dizziness
  • Occurs ~ 5-10 minutes after intake, lasts 30 mins to several hours
62
Q

Antibiotics
Miscellaneous

Vancomycin, mechanism

  • Reserved for when and where
  • Route and what happens if you use wrong route
  • Nursing Role
  • adverse effects

Linezolid, mechanism

  • used to treat?
  • Adverse effects
  • Major interaction with what drug
  • when was this interaction discovered
A

Vancomycin – inhibits cell wall synthesis; bactericidal (through different mechanism than aminoglycosides)

  • Reserved for severe infections that are resistant to anything else = usually only used in hospital (methicillin-resistant staph. aureus - MRSA)
  • Injection or oral
  • If IV given too quickly  Red Man Syndrome (flushing, red face, hypotension)  slow down infusion
  • Therapeutic drug monitoring required (like aminoglycosides)
  • Ototoxicity and nephrotoxicity (like aminoglycosides)

Linezolid – inhibits bacterial protein synthesis

  • Use to treat vancomycin-resistant enterococcus (VRE), pneumonia or skin infections caused by MRSA
    (i. e. Severe infections resistant to other antibiotics)
  • Adverse effects: lactic acidosis, myelosuppression (↓WBC and platelets), peripheral and optic neuropathy, serotonin syndrome, diarrhea,
  • Major drug interaction with any serotonergic drug, may need to discontinue until course of treatment finished
  • Was only discovered post-marketing, as linezolid also inhibits MAO
63
Q

Antibiotic Response

  • What is the expected response
  • What happens if there is none
A

-A patient should respond in some way (i.e. fever reduction, site of infection improving, generally feeling better) within 24-48 hours of initiating an antibiotic
(Not completely resolved, but some indicator of improvement)
-If not, investigation needs to occur as to WHY the patient has not responded

64
Q

Antibiotics & Oral Contraceptives

  • What happens when you mix them 2
  • What is the clinical impact
  • Bottom line?
A
  1. Reports ofcontraceptivefailure with concomitant ampicillin, amoxicillin, tetracycline, erythromycin, sulfamethoxazole/ trimethoprim or nitrofurantoin
  2. Antibacterials may destroy intestinal bacteria that provide hydrolytic enzymes essential for enterohepatic recirculation of ethinyl estradiol resulting in a lower plasma concentration of ethinyl estradiol = effectiveness of oral contraceptives may be decreased

Clinical impact is controversial

  • Initial reports were anecdotal
  • Thorough investigation has only shown clinical impact with rifampin and griseofulvin

Bottom line: These antibiotics may reduce effectiveness of oral contraceptives, and backup method should be recommended

65
Q

Antibiotics: Nurse’s Role 11

A
  • Importance of culture & sensitivities (C&S) in choosing and continuing antibiotics
  • Baseline infection status to monitor effectiveness of drug – temperature, site of infection (redness, swelling, pus – describe)
  • Kidney and liver function – may alter choice of antibiotic, as well as serve as baseline for monitoring (some drugs nephrotoxic)
  • If IV, always check compatibilities before administering
  • Watch for anaphylaxis (esp. penicillins, sulfonamides)
  • Signs of superinfections – severe diarrhea that does not resolve after course of antibiotics is finished
  • Monitor ototoxicity and nephrotoxicity for aminoglycosides + vancomycin
  • Dose around the clock (if ordered) to maintain appropriate drug levels and avoid resistance
  • *[(Example: TID (3x/day) is not with each meal, it is q8h (every 8 hours)
  • *If serum levels fall below minimum effective concentrations, it gives the bacteria opportunity to grow)]
  • Watch for interactions with dosing (food, antacids, supplements) when appropriate
  • Encourage adherence and finishing the entire course of antibiotic even though infection appears gone
  • Educate about photosensitivity (if necessary)
66
Q

Preventative Antibiotics

A

We also use antibiotics when there is a high risk of infection during or after a procedure

Examples:

  • Amoxicillin 2 g PO (by mouth) 1 hour before dental appointment to prevent bacterial endocarditis
  • 3rd generation cephalosporin before & directly after surgery
67
Q

Tuberculosis (TB)

  • How contagious is it
  • What province has the highest
  • What stages
  • What route does it spread
  • what are the 2 stages
A

Highly contagious infection caused by mycobacterium tuberculosis

Saskatchewan has high rates of TB as compared to the rest of Canada and US

Exhibits both active and latent stages

Spread via respiratory route

  1. Initial/induction phase of treatment (~2 months) – kill actively dividing mycobacteria
  2. Continuation phase of treatment (~6 months or longer) – kill dormant mycobacteria
68
Q

Tuberculosis (TB)
-3 Characteristics of treatment
]

A
  1. Therapy must continue for 6-12 months (mycobacteria have a thick mycolic acid layer surrounding them, resisting treatment)
    - Patient may not have symptoms during this time, therefore adherence is a challenge
  2. A minimum of 2 and up to 7 drugs are administered concurrently due to large numbers of resistant mycobacteria
    - Regimens are complicated and difficult to follow
  3. Because of the high infectious nature of TB, prophylactic therapy is indicated for close contacts & family members of diagnosed patients
    - Prophylaxis is shorter term (2 months), but adherence still an issue

-Non-adherence is the most common cause of treatment failure in TB patients, therefore directly observed therapy (DOT) is necessary
(Nurses are essential with this!)

69
Q
Tuberculosis (TB)
Rifampin (RMP)
-How potent
-What does bactericidal activity
-Current doses are based  
-What does it do to the body
-What colour are the secretions
A

Most potent anti-TB drug available

Good bactericidal activity, prevents acquired drug resistance and is very important in preventing relapse

Current doses are based on studies performed in the 1960s, when the lowest effective dose was used because of the high cost of the drug; concerns now that dose is too low -> current trials -> dosing recommendations may change

Rashes, blood dyscrasias, GI disturbances, liver damage, nephrotoxicity

Secretions coloured a reddish-orange (sweat, urine, sputum, tears)

70
Q

Tuberculosis: Nurse’s Role 6

A
  • Awareness of guidelines (continuously changing) and importance of adherence
  • Community teaching and involvement
  • Recognizing important cultural aspects that influence effective treatment
  • Education regarding stigma of disease
  • Participation in directly observed therapy (DOT)
  • Advocate for patient
71
Q

Fungal Infections

  • What kind of infections can be treated easily
  • What kind of infections
  • How often do systemic fungal infections occur
  • Who do they commonly occur with who
A

Superficial infections (outer layers of skin, nails, hair) most common and can be treated easily

Thrush (oral candidiasis), vaginal yeast infection, nail infections, athlete’s foot, ringworm, seborrheic dermatitis

Systemic fungal infections (affecting internal organs) rarely occur in a healthy individual

More commonly occur in those with compromised immune system (HIV, or taking immuno-suppressants)

72
Q

Why do inhaled corticosteroids (for asthma) cause oral candidiasis?

A

Disrupts the normal flora

73
Q

Classes of Antifungals 3

A

Amphotericin B
Azole Antifungals
Miscellaneous

74
Q

Systemic Fungal Infections

  • What is a fungal infection
  • What causes suppressed immune system
  • How long is the therapy
  • Treated with what and which route
A

Fungal infection = mycoses

Suppressed immune system = caused by HIV or AIDS, prolonged corticosteroid therapy, other immunosuppressant therapy (transplant recipient), burns, chemotherapy

Antifungal therapy is long (several months)

Usually treated with amphotericin B – given IV

75
Q
Fungal Infections
Amphotericin B
-function 
-Given route
-adverse effects 
Monitor
A

Binds to fungal cell membranes, making them leaky

Given IV

Adverse effects: fever & chills during infusion, vomiting, headache, phlebitis, nephrotoxicity, hypokalemia, ototoxicity

Monitor and manage these adverse effects, but usually does not require therapeutic drug monitoring

76
Q

Fungal Infections

Amphotericin B Monitoring 7

A
  • Temperature
  • Nausea and vomiting – may benefit from antiemetic
  • Phlebitis – infuse slowly
  • Renal function – creatinine, urine output, electrolytes, BUN, blood in urine
  • Hypokalemia – electrolytes, dysrhythmias
  • Ototoxicity – hearing, balance, vertigo
  • Overall response to medication
77
Q
Fungal Infections
Azole Antifungals (fluconazole, itraconazole, ketoconazole, miconazole, voriconazole)
-Mechanism 
-Route
-How safe is it compared amphotericin B
-What infections does it treat
-What toxicity does it provide and what should you look for
-What is a common misconstrued
A

Alter fungal cell membranes by depleting ergosterol

Used orally, topically, injection; fluconazole available OTC

Safer than amphotericin B

Most often for vaginal candidiasis, athlete’s foot, or thrush

Rare hepatotoxicity – avoid alcohol, watch for jaundice, monitor liver enzymes

Note: metronidazole is NOT an azole antifungal

78
Q
Fungal Infections
Miscellaneous
-Ciclopirox
-Terbinafine
-Nystatin
-How to solve Oral thrush
A

Ciclopirox – topical med used for fungal nail or scalp infections (nail polish or shampoo)

Terbinafine – oral med for fungal nail infections

Nystatin – cream available without prescription for many topical fungal infections (ringworm, diaper rash)

Oral thrush – swish and swallow oral suspension four times daily (works topically) (needs Rx)

79
Q

Fungal Infections: Nurse’s Role
2
-How long does it take to treat fungal infections

A
  1. Baseline info regarding infection – immunosuppression?, previous therapy, comorbid condition management
  2. Baseline function to monitor – liver enzymes, WBC, fever, etc.

Fungal infections generally take longer to treat
-Nail infection via oral treatment is often ~ 6 months

80
Q

Antiviral Medications
-How specific are these drugs
3

A

Antiviral meds are very specific to a disease

HIV
Herpes Infections
Influenza

81
Q
Antiviral Medications
HIV
-Antiviral Medications let HIV pts do what  
-Mechanism
-What is HAART
-What is the goal of this
-What is the pt of using different classes
-Does each class do
A

Because of antiretroviral drugs, HIV patients are able to live symptom-free for much longer with very low counts of the retrovirus

Antiretroviral drugs block the HIV replication cycle

HAART – highly active antiretroviral therapy

  • Goal is to reduce plasma HIV to its lowest possible level - HIV still remains in the lymph nodes
  • Use different classes of antiretrovirals at same time to reduce resistance
  • Each class ‘attacks’ different step of replication cycle
82
Q

Antiretroviral Monitoring 7

A
  • Regarding immunodeficiency – watch for (and be vigilant!) signs of infection, educate on proper handwashing, avoiding infected persons, mouth ulcers
  • Blood pressure – many cause hypotension
  • Many labs – blood (effectiveness of drug; ‘counts’), liver and kidney function (side effects of drug)
  • Pancreatitis – abdominal pain & distension, nausea, vomiting
  • Blood glucose – many cause hyperglycemia
  • Peripheral neuropathy – numbing or tingling of extremities
  • Skin rashes common
83
Q

Antiretrovirals: Nurse’s Role

4

A

Many drug interactions including OTCs and herbals – educate and be a resource for patient

Educate supporting immune system with sleep, healthy diet, exercise

Reducing transmission – can still transmit with low viral load, protection during sex, avoid sharing needles, do not donate blood

Recognize cultural barriers to treatment, stigma, privacy

84
Q
Antiviral Medications
Herpes (simplex and zoster) 
-What does this family viruses cause (3 kinds of herpes)
-How long can is stay 
-Exacerbations are brought on by 
-Frequent lesions require?
A

An entire family of viruses causing blisters on skin, genitals and mucosa

  • HSV1: oral cold sores
  • HSV2: genital ulcerations
  • Zoster: shingles

Virus can stay dormant for years – stored in nerve ganglia

Exacerbations brought on by stress, physical changes (weather), immunosuppression

Frequent lesions may require prophylaxis

85
Q

Antiviral Medications
Herpes (simplex and zoster)
[Acyclovir, famciclovir, valacyclovir]

  • How are they controlled, when are they taken, and for how long
  • Mechanism
  • how well tolerated, taken with?
  • Where cant it be found
A

Acyclovir, famciclovir, valacyclovir

Mostly controlled by oral therapy of antivirals – taken at first sign of outbreak, continued for short term

These antivirals prevent viral DNA synthesis

Very well tolerated – take with food

Can be prescribed by pharmacist in Saskatchewan (for cold sores only) – considered a minor ailment

86
Q
Antiviral Medications
Herpes (simplex and zoster) 
OTC
-Lipactin - Made up of what and mechanisms 
-Abreva - made up with and mechanism, 
-Other products: do what for pt
A

Lipactin® - heparin + zinc = can reduce pain, may speed healing

Abreva® - docosanol = prevents viral entry into cells, stops spread if caught early (can reduce duration of cold sore by ~1 day)

Other products: based on keeping area moist to prevent cracking and bleeding

87
Q
Antiviral Medications
Influenza
-What is the best protection
-What do they do if taken properly
-Name the drugs for influenza
-Used for which patients
-When do you adjust doses
A

BEST PROTECTION = VACCINATION

Antiviral drugs may decrease severity of symptoms of influenza and may shorten symptom time by a couple days IF taken within first 48 hours

Amantadine, and neuraminidase inhibitors (oseltamivir and zanamivir)

Generally used only in patients at high risk of complications from influenza

Elderly = adjust dose for renal function

88
Q

Antiviral Medications
Influenza
High risk Patients 5

A
  • Pregnant women
  • Children (6-59 months)
  • Elderly (> 65) (esp. those in chronic care facilities)
  • Adults and children with chronic health conditions (cardiovascular disease, respiratory disease, neurological conditions, or renal disease, diabetes, cancer, severe obesity)

-……and caregivers and contacts of any of the above

89
Q

Antiviral Medications

Influenza Nurses Role 5

A
  • Reduce transmission rates by getting vaccinated and washing hands – and encouraging this behaviour in others
  • Administration of vaccines
  • Supportive management includes rehydration, encouraging eating, antipyretics
  • May see preventative antivirals in very high-risk individuals (HIV) who cannot be vaccinated
  • Monitor for signs of complications (worsening of heart failure, signs of pneumonia, edema, or flu symptoms not beginning to resolve within ~1 week)
90
Q

Why Use Immuno-suppressants?

What are Autoimmune diseases
-3 diseases needed for
2 situations where it is needed

A

Autoimmune diseases – a category of diseases where the body’s immune system has identified something that it shouldn’t as foreign  = therefore, the immune system attacks it and attempts destruction

  • Multiple sclerosis (MS) – attacks the myelin sheath surrounding the axon of a neuron
  • Hashimoto’s – attacks the thyroid gland/hormones
  • Rheumatoid arthritis – attacks the joints
  • Transplants – immune system would attack and destroy foreign object
  • Exacerbations of conditions (such as asthma or rheumatoid arthritis) to regain control
91
Q

Classes of Immunosuppressants

4

A

Calcineurin Inhibitors
Corticosteroids
Biologics
Chemotherapy

92
Q

Immunosuppressants
Calcineurin Inhibitors (Cyclosporine, tacrolimus, pimecrolimus (topical))
-What are classic immuno-suppressants for
-Mechanism
-Are they specific to how they treat system
-What is the monitoring

A

“Classic” immuno-suppressants used for transplants (or topically for psoriasis)

Disrupt T-cell function by binding to calcineurin

They are not specific – suppress the ENTIRE immune system  patient is very susceptible to any other infection

Extensive monitoring for detailed WBC counts and signs of infection (see slide on monitoring)

93
Q

Classic Immuno-suppressant Common Adverse Effects 10

A

-Increased risk of infections
-Increased risk of cancers such as lymphomas, cysts, and polyps
(Frequency increases with intensity and duration of treatment)
-Kidney impairment, hepatic impairment
-Hypertension, hyperlipidemia
-CNS: tremor, headache, skin prickling sensation
-GI: nausea, vomiting, abdominal pain, diarrhea, gingival hyperplasia
-MSK: Muscle cramps, myalgia
-Endocrine: Menstrual disturbances, gynecomastia
-Hypertrichosis (abnormal amount of hair growth over body)
-Fatigue

94
Q
Immuno-suppressant
Corticosteroids
-What kind of activity
-Used to control
-What kind of therapy
-How many side effects
A

Anti-inflammatory and immunosuppressant activity

Often used to control exacerbations of condition such as asthma, rheumatoid arthritis, MS, etc.

Pulse therapy (very high doses, gradual taper) to minimize side effects

Many, many side effects

95
Q

Immuno-suppressant
Biologics

What is a Biologic
How are the ingredients made
made up of
Revolutionized the treatment of
Three forms
A

Biologic = medications produced using biological processes in living organisms such as yeast and bacteria

Have active pharmaceutical ingredients that cannot reasonably be synthesized by chemical means (too complicated)

Are complex, large molecules derived from living sources and produced through a number of intricate steps

Have revolutionized the treatment of many conditions:
Diabetes, anemia, MS, cancer….

Biologics can be immunosuppressant or immunostimulant (very specifically) or replace a substance that is missing (insulin)….

96
Q

Immuno-suppressant
Biologics
Meds 6

A
Vaccines
Blood products 
Hormones &amp; growth factors
Enzymes
Gene therapy
Cancer treatment
97
Q

Immuno-suppressant
Biologics
-What are monoclonal antibodies
-What is conventional chemo
-What can we do by attaching drugs to antibodys
-How often are they used
-How do they work when they target specific factors in the immune system
-How are they similar to other immuno-suppressants

A

Monoclonal antibodies use the ability of antibodies to target specific receptors or pathogens
Example: HER-2 gene expressed on some breast cancer cells

Conventional chemotherapy targets all cells in the body  adverse effects of chemo such as hair loss, nausea & vomiting, etc.

We can attach a drug to an antibody, which then only targets and destroys those specific cancer cells, making therapy more effective (we can use higher doses) with fewer adverse effects (yay!)

Biologics are used across many therapeutic categories

It is extremely common for biologics to target specific factors in the immune system (such as inflammatory mediators) to delay progression of auto-immune diseases (like rheumatoid arthritis)
E.g. infliximab inhibits human TNF-alpha

In this way, biologics often carry similar risks and monitoring needs as other immuno-suppressants

98
Q
Immuno-suppressant 
Biologics
Infusion reactions
-What are they
-SS
-when are they given, what kind of drug 3 and theyre objective
-When is monitoring key
A

Common adverse effect during administration of biologics

Red, swollen, could be itchy at injection site

Often, patients are given ~5 mins before injection:

  1. Prednisone (corticosteroid)
  2. Diphenhydramine (antihistamine)
  3. And sometimes naproxen (NSAID)
  • All 3 to attempt to prevent reaction
  • Can also slow down infusion rate to reduce symptoms

Monitoring during infusion important

99
Q

Immunosuppressants: Monitoring

  • Needs monitoring for what signs 5
  • assess for
  • watch for signs
  • what are extra precautions
A

Any immunosuppressant therapy requires extensive monitoring for any sign of infection:

  • Fever
  • Vital signs (BP, heart rate, respirations, temp)
  • Electrolytes
  • Liver and kidney function
  • Sore throat or slight cough

Assess skin integrity, mouth sores

Watch for signs of organ rejection (depending on organ)

Extra precautions may be required to prevent infection (masks) – and don’t go to work if sick

100
Q

Chemotherapy Summary

Cytotoxic drugs - how how old mechanism

Hormonal therapy - are they cytotoxic, mediated through, doing what

Immunotherapy - what forms 2, and how do they work immune system

Targeted agents - 2 forms, what do they mean to chemotherapy and what do they target

A

Cytotoxic drugs – traditional; interfere with or damage DNA, causing apoptosis (programmed cell death)

Hormonal therapy – not cytotoxic; effects mediated through hormonal receptors (deprivation) – for hormone-responsive cancer (breast, prostate, etc.)

Immunotherapy – monoclonal antibodies, vaccines; non-specifically boost immune system to help eradicate cancer (interferon alfa)

Targeted agents – monoclonal antibodies, tyrosine-kinase inhibitors (TKIs); the future of treatment – to target cancer cells only

101
Q

Used for

How many challenges

What do they target

-What is the connection between killing cancer/health cells

A

Used for disseminated/metastasized cancers, micrometastatic diseases

Many drugs, many challenges

Target stages of the cell replication cycle – multiple drugs will target different stages

A balance of killing cancer cells and killing health cells (toxicity)

  • Killing healthy cells leads to most adverse effects of chemo
  • Target cells that rapidly multiply – bone marrow, GI epithelium, hair follicles, nail beds
102
Q

Adverse Effects of Chemotherapy

Short term 12
Long term 10

A

Short term

  • Nausea/vomiting
  • Diarrhea or constipation
  • Mucositis/stomatitis
  • Myelosuppression
  • Hair growth alterations
  • Weight gain / weight loss
  • Taste alterations
  • Fatigue
  • Hepatic and renal changes
  • Cardiac function changes
  • Rash / skin changes / nail changes
  • High blood pressure

Long term

  • Infertility
  • Secondary malignancies
  • Heart failure
  • Osteoporosis
  • Pulmonary fibrosis
  • Cataracts
  • Peripheral neuropathy
  • Hearing loss
  • Fatigue
  • Endocrine abnormalities
103
Q

Adverse Effect Management 7

A
  • Mouth sores – prevention is key; salt water rinses
  • Heartburn – PPIs and H2RAs (see Module 5)
  • Diarrhea – loperamide, diphenoxylate; risk of dehydration – can be life-threatening
  • Myalgia & arthralgia – acetaminophen, opioids, corticosteroids, gabapentin
  • Fatigue – up to 96% of patients – manage in any way possible
  • Skin – adequate moisture, minimize sun exposure, avoid harsh compounds (no acne products)
  • Nausea and vomiting – see Module 5
104
Q

Chemotherapy: Nurse’s Role
What must a RN to administer chemo
4

A

An RN must be certified in Saskatchewan in order to administer chemotherapy

There are guidelines for safe handling, administering, storage, and disposal of cytotoxic drugs
Be especially careful if female of child-bearing age – some drugs can be absorbed through skin or mucous membranes
Be aware of adverse effects and management
Be aware of supportive therapy available in community