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Pharm 250 > Module 4 - immune system > Flashcards

Module 4 - immune system Flashcards

1
Q

Def:

Inflammation

A

A defence mechanism, with a purpose to contain the injury and destroy a foreign agent.
*good to a point but then becomes a hindrance to healing.

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2
Q

Mediators of inflammation

A 
Histamine*
Bradykinin
Leukotrienes
Cytokines
Interleukins
Prostaglandins*
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3
Q

Classes of medications for inflammation

A
  1. Non-Steroidal Anti-Inflammatories (NSAIDs)

2. Corticosteroids

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4
Q

MOA: NSAIDs

A

Inhibit cycle-oxygenase (COX)

reduce Prostaglandin synthesis leading to inhibition of inflammation

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5
Q

COX-1

A

In all tissues, stomach lining (mucosa), involved in platelet aggregation
- reason for most of the adverse effects associated with NSAIDs

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6
Q

Cox-2

A

More specific for inflammation

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7
Q

Common Adverse effects of NSAIDs

A 
Nausea
dyspepsia
ulcers (w/ longe-term use)
potential anti-platelet action
increases risk of cardiac event
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8
Q

indications for NSAIDs

A 
Mild to moderate inflammation
fever
mild to moderate pain 
dysmenorrhea 
musculoskeletal pain 
arthritis
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9
Q

cautions for NSAIDs

A

Take with food
Caution in kidney disease, CVD, and GI conditions
* use short term and as needed only

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10
Q

MOA: Corticosteroids

A

Anti-inflammatory and Immuno- suppressive

Mimic endogenous cortisol, attempt to bring body back to homeostasis after a Fight-or-flight response

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11
Q

indications: Corticosteroids

A

Severe inflammation (MS, Rheumatoid Arthritis, auto-immune diseases)

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12
Q

Nurse’s Role: Anti-inflammatories

A 
cause - remove and/or treat 
screen for containdications
Labs - CBC, Liver and Kidney function 
pt. response to treatment (monitor for adverse effects)
ensure taken with food
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13
Q

Adverse effects: Corticosteroids

A 
Hyperglycaemia
hypertension
nausea 
insomnia 
psychosis ( w/ increased dose)
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14
Q

Contraindications for Anti-infmmitories

A

Kidney or liver disease
GI disease
CVD
active infections (due to immune suppression)

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15
Q

Def: Fever

A

a defence mech. - increase in body temp in attempt to destroy harmful bacteria.

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16
Q

Drugs that reduce fever

A

Antipyretics

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17
Q

Fever medications: Classes

A
  1. Acetaminophen

2. NSAIDs

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18
Q

MOA: Acetaminophen

A

acts at hypothalamus to cause peripheral vasodilation, which enables sweating and allows body to rid excess heat.
* NO anti-inflammatory action

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19
Q

Adverse effects: Acetaminophen

*bonus - whats the max dose (the one on OTC bottles) and why is different than the max dose in clinical setting?

A

Very rare: liver tox.
avoid alcohol
interacts w/ warfarin
*Publicly - max dose is 3g/24hrs. clinically 4g/24hrs - due to the frequent addition of it to OTC products (eg: cold and flu meds) this lower max dose for public consumers is to make for safer use of OTC products.

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20
Q

indications: Acetaminophen

A

Fever
mild to moderate pain
osteoarthritis

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21
Q

MOA: NSAIDs (for fever)

*bonus - why is Acetaminophen the first-line for fever treatment and not NSAIDs? Why would we choose NSAIDs over Acetaminophen for fever?

A

acts at hypothalamus to cause peripheral vasodilation, which enables sweating and allows body to rid excess heat.

  • Acetaminophen has a very good safety record and fewer drug interactions and side-effects than NSAIDs.
    NSAIDs are chosen when Inflammation AND fever are present.
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22
Q

Nurse’s Role: Fever

A

cause of fever - determine if other treatment is needed
monitor pt. response - AE: GI upset, sudden change in urine output (kidney), signs of liver too.
vitals
warfarin levels

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23
Q

Signs of liver toxicity

A 
Jaundice
pale 
tired
sweating 
dark urine 
confusion 
coma
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24
Q

Antigen

A

Anything that the body identifies as foreign - causes allergy symptoms

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25
Q

allergy symptoms

A 
Tearing eyes 
sneezing 
nasal congestion
postnasal drip --> cough
itchy mucous membranes (inside nose, mouth, and eyes)
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26
Q

Histamine

A

bodies response to antigen –> histamine release

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27
Q

H1

A

smooth muscle of vascular system, bronchial tree, digestive tract

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28
Q

H2

A

Lining of stomach, producing gastric acid

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29
Q

med Classes: allergies

A
  1. Antihistamines (1st gen and 2nd gen)
  2. Intranasal corticosteroids
  3. decongestants
  4. drugs for anaphylaxis
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30
Q

MOA: 1st Gen Antihistamines

A

anticholinergic effects
block H1 receptors

*shorter acting, cause more drowsiness and work faster than 2nd gen.

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31
Q

MOA: 2nd Gen Antihistamines

A

Block H1 receptors
SOME cholinergic activity, but less than 1st Gen.
longer acting, less sedation, and take longer to reach onset of action the 1st gen.

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32
Q

MOA: intranasal Corticosteroids

A

reduce inflammation in nasal mucous membranes, and. local immunosuppresion

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33
Q

Adverse Effects: Intranasal Corticosteroids

A

Nasal irritation, dryness and bleeding (epistaxis), bad taste, loss of smell.

*local administration prevents systemic side effects

can be taken up to 2wks - daily use to PREVENT symptoms of allergic rhinitis

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34
Q

MOA: decongestants

A

Sympathomimetics - stimulants - cause vasoconstriction and reduction of mucous production

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35
Q

Adverse effects: Decongestants
oral -
Intranasal-

A

Oral: hypertension, anxiety, insomnia
Intranasal: Nasal irritation, rebound congestion, rarely systemic effects

*short term use only - Rebound congestion if longer than 3-5days (intranasal)

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36
Q

Nurse’s Role: Allergies

A

hlth Hx - triggers/ antigens, previous therapy
correct product - prevention vs. treatment
monitor Anticholinergic effects: sedation, 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 Antihistamines as sleep aids - sleep hygiene

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37
Q

Def: Anaphylaxis & symptoms

A

Fatal, hyper-response to an allergen
symptoms ensue within second or minutes of exposure to antigen
symptoms:
itching, hives, tightness in throat or chest, difficulty breathing, facial swelling, non-productive cough and hoarse voice as larynx begins to close, rapid hypotension (w/ reflex tachycardia) and bronchoconstriction

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38
Q

MOA: epinephrine

A
  • Stimulated Alpha and Beta adrenergic receptors.
  • Alpha: counters vasodilation and higher vascular permeability that occurs during anaphylaxis that leads to loss of intravascular fluid hypotension
  • Beta: Causes bronchial smooth muscle relaxation and relieves bronchospasm, dyspnea, and wheezing

alleviate Pruritus (itching), Urticaria (hives), and angioedema (deep swelling of face and throat)

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39
Q

outpatient treatment of Anaphylaxis

A

epinephrine injection given at onset of symptoms - IM - vastus lateralus

*Given En-route to hospital - does NOT resolve situation just allows more time

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40
Q

Hospital treatment of Anaphylaxis

A

Oxygen
more epinephrine
bronchodilator (Salbutamol - Beta- agonist)
corticosteroids - due to anti inflammatory and immune suppressive effects

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41
Q

Contraindications for Epinephrine

A

Hypersensitivity to adrenergic amines (sympathomimetic drugs)

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42
Q

Monitoring: Anaphylaxis

  • family teaching
  • In hospital
A

Hlth Hx
Educate Family on S&S and what to do
Educate proper use of epinephrine
in hospital: response to treatment - vitals, hypertension, tachycardia, headache, dysrhythmias, edema, bronchoconstriction
support for traumatic experience

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43
Q

Mechanism by which bacteria can cause disease

A
  1. rapid growth

2. toxin production

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44
Q

Bacterial classification:

Gram positive

A

Have thick cell walls and retain purple gram-stain

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45
Q

Bacterial Classification:

Gram Negative

A

Have thin cell walls and lose purple gram-stain

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46
Q

Bacterial Classification:
Bacilli:
Cocci:
Spirilla:

A

Bacilli: rod shaped
Cocci: spherical
Spirilla: Spirals

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47
Q

Bactericidal antibiotics

A

Drugs that KILL the bacteria

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48
Q

Bacteriostatic antibiotics

A

Drugs that slow down the GROWTH of the bacteria, allowing the body’s immune system to kill the bacteria

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49
Q

Def: Antibiotic resistance

A

due to high rate of multiplication of bacteria there is an increased chance of mutations. some mutations give rise to bacteria that have antibiotic properties - if the bacteria is not destroyed it will replicate passing on the beneficial resistance traits.

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50
Q

Activities that promote the development of Bacteria resistance and the reason

A
  • Not completely finishing a course of antibiotics - some bacteria remain even once symptoms have stopped
  • not high enough dose of antibiotics - concentration is does not get high enough to get rid of the bacteria cells
  • Using an antibiotic when it is not indicated - every time an antibiotic is used chance of resistance is increased
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51
Q

Antibiotic spectrums

A

Broad spectrum

Narrow spectrum

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52
Q

Broad spectrum antibiotics

A

drugs that are effective against a WIDE VARIETY of bacteria (prescribed when the specific pathogen is unknown)

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53
Q

Narrow spectrum antibiotics

A

drugs that are effective agains SPECIFIC microorganisms or a restricted group. (prescribed when pathogen is clearly identified from a C&s or symptoms)

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54
Q

Def: Culture and Sensitivity

A

a swab is taken from a pt w/ s&s of infection. culture is grown and then tested with classes of antibiotics to find out what it is sensitive to.

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55
Q

Def: Superinfection

A

A secondary infection
when an antibiotic also kills bacteria in the normal flora of our body - more common with broad spectrum use than narrow. because the normal bacterial flora of the body is no longer competing with the pathogen for nutrients the pathogen there is opportunity for superinfection to occure.

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56
Q

Signs of a superinfection

A

another infection during or immediately after antibiotic therapy (may be a different infection site - GI tract, GU tract))
symptoms: diarrhea, bld or pus in stool, cramping, abd pain, bladder pain, painful and frequent urination, signs of vaginal infection (yeast or bacterial)

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57
Q

Do probiotics work?

A

some evidence suggests YES. but should be taken at a different time than the antibiotic.

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58
Q

considerations when choosing an antibiotic

A 
C&S
site of infection 
immune system status of pt.
kidney and liver function 
dosage forms available 
variables affecting absorption, distribution, metabolism, and elimination of antibiotic
pt allergies or intolerances 
ease of administration and adherence issues
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59
Q

Antibiotic classes (9)

A
  1. Penicillins
  2. Cephalosporins
  3. Tetracyclines
  4. Macrolides
  5. Aminogycosides
  6. Fluoroquinolones
  7. Sulfonamides
  8. Carbapenems
  9. Miscellaneous
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60
Q

MOA: Penicillins

*what is the necessary component of their activity

A

Bactericidal. disrupt bacterial cell walls. Penicillin binding protein is only found in bacterial cell walls, penicillin binds to this protein which weakens the cell wall allowing fluid to enter and destroy the cell.

  • Beta-lactam ring is necessary for their activity.
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61
Q

Penecillin resistant bacteria characteristics

A

penecillin resistant bacteria produce Beta-lactamase which breaks the beta-lactam ring of penicillin making it ineffective.

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62
Q

what is the rationale for prescribing a combination of Clavulanic Acid and a penicillin class antibiotic together?

A

Clavulanic Acid inhibits Beta-lactamases of SOME microorganisms to allow the penicillin to be active against it.

*synergistic relationship

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63
Q

Some Narrow spectrum Antibiotics

A

Penicillin G
Penicillin V
Cloxacillin
Dicloxacillin

64
Q

some broad spectrum Antibiotics

A

Amoxicillin
Amoxicillin/Clavulanate
Ampicillin

65
Q

Adverse Effects: Penicillins

A 
Anaphylaxis
diarrhea
nausea and vomiting 
pain at injection site 
superinfection 
some (minor) drug interactions
66
Q

Monitoring: Penicillins

A

Electrolyte levels (Na+, K+)
Response to therapy (infection clearing? reduced fever?)
Adverse effects and anaphylaxis
signs of super infection (diarrhea that doesn’t start until course of antibiotics is finished, or did not go away once course was done, complaints of yeast or UTI.

67
Q

MOA: Cephalosporins

A

R/t penicillins
inhibit cell wall synthesis - bactericidal
generational classification (gen 1-4)

68
Q

classification of Cephalosporins

A

Generations 1-4. potency increases with increase in generation.
1st gen not effective against beta-lactamase producing bacteria
increase in generation = fewer similarities w/ penicillins
higher gen used for known resistant bacteria

69
Q

Adverse Effects: cephalosporins

A

Hypersensitivity, rash, itching, anaphylaxis, diarrhea, vomiting, nausea, pain at injection site, some (minor) drug interaction

CANNOT be given orally. must be IV or IM only.

70
Q

Will a pt who is allergic to Penicillins have an allergic reaction to Cephalosporins?

A

most likely not. BUT it depends on whether the pt is TRULY allergic to penecillins - important to know what kind of reaction they had (ie Diarrhea vs anaphylaxis)

risk for cross-sensitivity decreases with higher Cephalosporin Generation

71
Q

MOA: tetracyclines

A

Inhibit bacterial protein synthesis
bacteriostatic
broad-spectrum (both gram pos and neg)

72
Q

cautions w/ tetracyclines - why?

A

should not be given at the same time as Iron, Calcium, or Magnesium - Ions bind to drug and it cannot be absorbed.

must separate by 2h

73
Q

Indications: Tetracyclines

A

Rocky Mountain Spotted Fever (tick borne disease) H. Pylori infections, acne vulgarisms, chlamydia

74
Q

Adverse effects: Tetracyclines

A 
Diarrhea, 
yeast infections, 
nausea and vomiting
epi-pastric burning
yellow-brown teeth discolouration in young children (why it is not used)
photosensitivity  
unplanned preganacy - interferes with some contraceptives advise back up method
superinfections
75
Q

MOA: Macrolides

A

-THROMYCIN

Inhibit Bacterial Protein synthesis. some bactericidal and some bacteriostatic.
No structural similarities to penicillins = ZERO chance of cross sensitivity

76
Q

Indications: Macrolides

A

Upper and lower respiratory tact infections
whooping cough
diphtheria
or for patients who cannot take penicillins

77
Q

Adverse Effects: macrolides

A

significant nausea
vomiting
diarrhea (take w/ food)
some IMPORTANT drug interaction

78
Q

Drug interactions: Macrolides

A

Warfarin, cyclosporine, anticonvulsants (all via CYP450 inhibition/induction

79
Q

MOA: Aminoglysides

A

-MY(i)CIN

Inhibit bacterial protein synthesis AND cause abnormal protein synthesis. DOSE DEPENDANT bactericidal.

80
Q

Adverse Effects: Aminoglysides

A

nephrotoxicity (direct poisonous effect on kidney.)
ototoxicity (damage to inner ear and/or nerve damage) often irreversible

*require therapeutic drug monitoring - narrow therapeutic window

81
Q

indications: Aminoglysides

A

Serious (life threatening) infections (eg TB) OR when other antibiotics have failed.

82
Q

When would Aminoglysides NOT require therapeutic drug monitoring?

A

When used topically as eye drops and creams/ointments

83
Q

S&S of Nephrotoxicity

A

Protein and/or bld in urine, elevated blood urea nitrogen (BUN), increased serum creatinine (SCr), may be no OR excessive urine output, edema, confusion, delirium

84
Q

S&S of Ototoxicity

A

Hearing loss, vertigo, tinnitus

85
Q

MOA: Fluoroquinolones

A
  • FLOXACIN

Affect bacterial DNA synthesis. Bactericidal. absorption affected by minerals (Ca, Fe, Mg) - separate by 2h

86
Q

Adverse effects: Fluroquinolones

A 
GI adverse effects, photosensitivity. 
RARE:
tendonitis or tendon rupture
cardiac arrhythmia 
CNS - seizures, tremors, altered mental status
peripheral neuropathy

*generally not used in children as it affects cartilage development

87
Q

Indications: Fluoroquinolones

A

Respiratory, urinary, ophthalmic, GI, and gynaecological infection

88
Q

MOA: Sulfonamides

A
  • SULFA
    Suppress bacterial growth by inhibiting essential folic acid needed within the cell.
    Bacteriostatic
    broad spectrum. older classes with more resistance seen
89
Q

indications: Sulfonamides

A

Used to treat UTI, orally and topically (acne)

90
Q

Adverse Effects: Sulfonamides

A 
Allergic reaction
nausea 
vomiting 
skin rashes 
photosensitivity 
anemia 
crystalluria - prevent by drinking lots of water.
91
Q

MOA: Carbapenems

A

Contain Beta-lactam ring and inhibit cell wall synthesis (like penicillins) - beta-lactam ring is very resistant to destruction by penicillinase
broad spectrum
newer class

92
Q

Indications: Carbapenems

A

Reserved for resistant infection (like MRSA)

93
Q

Adverse effects: Carbapenems

A

Skin reactions, inflammation at injection site, diarrhea, nausea, vomiting

94
Q

MOA: Clindamycin

A

Protein synthesis inhibitor

bacteriostatic

95
Q

Indications: Clindamycin

A

topically for acne, orally or IV for serious systemic infections

96
Q

Adverse effects: Clindamycin

A

High risk for super infections (GI)

97
Q

MOA: Nitrofurantion

A

Inhibits protein, RNA, DNA, and cell wall synthesis.

Bactericidal

98
Q

Indications: Nitrofurantion

A

Used only for UTI because it is excreted unchanged by the kidney (no metabolism)

99
Q

Adverse Effects: Nitrofurantoin

A

Changes in urine colour (urine turns orange)

must be taken with food.

100
Q

MOA: Metronidazole

A

Destroys bacterial DNA
Bactericidal
for anaerobic bacteria

101
Q

indications: Metronidazole

A

C&S indicates precence of anaerobic bacteria

102
Q

Adverse effects: Metronidazole

A

NO ALCOHOL: even small amounts results in: Disulfiram reaction: flushing, tachycardia, SOB, severe nausea & vomiting, throbbing headache, visual disturbance, confusion, dizziness.

103
Q

MOA: vancomycin

A

Inhibits cell wall synthesis

bactericidal

104
Q

Indications: Vancomycin

A

reserved for severe infections that are resistant to anything else.

105
Q

Adverse effects: Vancomycin

A

if IV given too quickly results in Red Man Syndrome (flushing, red face, hypotension)
ototoxicity
nephrotoxicity
requires therapeutic drug monitoring

106
Q

By what MOA do antibiotic interfere with Oral Contraceptives.

A

By destroying intestinal bacteria that provide hydrolytic enzymes essential for enterohepatic recirculation of ethinyl estradiol, resulting in lower plasma levels of ethinyl estradiol. decreed ethinyl estradiol level may result in decreased effectiveness of oral contraceptives.
* recommendation of a back up method when taking antibiotics is always suggested.

107
Q

Tuberculosis (TB)

A

Highly contagious infection caused by Mycobacterium Tuberculosis. exhibits both active and latent stages. spread via respiratory route.

108
Q

Initial/ induction phase of TB treatment

A

~ 2 months - kill actively dividing mycobacteria

109
Q

Continuation phase of TB treatment

A

~ months or longer - kill dormant mycobacteria

110
Q

3 important Characteristics of TB treatment

A
  1. Therapy MUST continue for 6-12 months. (mycobacteria have thick mycelia acid layer surrounding them, resisting treatment) - adherence can be challenging because pt may not have any symptoms during treatment period.
  2. A minimum of 2 and up to 7 drugs are adminstered 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 is still an issue.
111
Q

What is Directly Observed Therapy (DOT) and why is it Necessary for TB treatment?

A

Non-adherence is the MOST common cause of TB treatment failure, therefor requiring DOT.

112
Q

What is Isoniazid (INH) used for and what are some important considerations?

A

Cornerstone of TB therapy
Very powerful bactericidal activity, highly effective in rapid killing of bacteria in the first few days.
also effective in preventing the emergence of resistance.
Important consideration: Pyridoxine (Vit B6) should routinely be added for patients with diabetes, renal failure, malnutrition, substance abuse or seizure disorders or for women who are pregnant or breastfeeding.

113
Q

what is Rifampin (RMP) used for and what are some important considerations?

A

most potent anti-TB drug available. good bactericidal activity, prevents acquired drug resistance and is very important in preventing relapse.
important considerations:
rashes, blood dycrasias, GI disturbances, liver damage, and nephrotoxicity are some adverse effects. also, secretions (sweat, urine, sputum and tears) would be coloured a reddish-orange

114
Q

Nurse’s role in TB

A

Awareness of guidelines and importance of adherence
community teaching and involvement
recognizing important cultural aspects that influence effective treatment
education regarding disease stigma
participation in directly observed therapy (DOT)
Advocate for Pt.

115
Q

Def: Fungal Infections

A

Systemic fungal infections very rarely occur in a healthy individual.

116
Q

Superficial Fungal infections

A

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

117
Q

Systemic fungal infections

A

affecting internal organs. are more are and very serious.

long anti fungal therapy required. usually treated with Amphotericin B (via IV)

118
Q

Classes of Antifungals

A
  1. Amphotericin B
  2. Azole Antifungals
  3. Miscellaneous
119
Q

Mycoses

A

Fungal infection

120
Q

causes for suppressed immune system

A 
HIV or AIDS
prolonged corticosteroid therapy 
Other immunosuppressant therapy (transplant recipient)
burns 
chemotherapy
121
Q

MOA: Amphotericin B

A

Binds to fungal cell membranes, making them leaking

given IV

122
Q

Adverse effects: Amphotericin B

A

Fever and Chills during infusion, vomiting, headache, phlebitis, nephrotoxicity, hypokalemia, ototoxicity
- usually does not require therapeutic drug monitoring.

123
Q

MOA: Azole Antifungals

A

Alter fungal cell membranes by depleting ergosterol. used orally, topically, injection. some forms available OTC.
safer than amphotericin B

124
Q

Indications: Azole Antifungals

A

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

125
Q

Adverse Effects: Azole Antifungals

A

Rare Hepatoxicity - avoid alcohol, watch for jaundice, motor liver enzymes

126
Q

Miscellaneous antifungals

A

Ciclopirox - topical med for fungal nail infections
Terinafine - oral med for fungal nail infections
Nystatin - cream available w/o prescription for many TOPICAL fungal infections (Ringworm, diaper rash) oral thrush (Swish and swallow oral suspension 4x daily - need Rx)

127
Q

Nurse’s role: Fungal infections

A

Baseline info regarding infection (immunosuppression? Previous therapy, comorbid condition management)
Baseline function to monitor - liver enzymes, WBC, fever, etc
Fungal infections generally take longer to treat (~6 months)

128
Q

HIV Antiviral therapy

A

Antiretoviral drugs block HIV replication cycle

129
Q

HAART

A

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 the same time to reduce resistance
  • Each class ‘Attacks’ different step of replication cycle
130
Q

Antiretroviral monitoring

A

Immunodeficiency - watch for signs of infection, educate pt on proper hand washing, avoiding infected persons, mouth ulcers
BP - many cause hypertension
MANY labs - blood, liver and kidney function (side effects of drug)
Pancreatitis - abdominal pain and distension, nausea, vomiting
Blood Glucose - many cause hyperglycaemia
Peripheral neurophathy - numbing or tingling of extremities
Skin rashes common

131
Q

Nurse’s role: Antiretrovirals

A

Drug interactions - provide education on OTC and herbal interactions
Educate - importance of sleep, healthy diet, and exercise
Reducing transmission - CAN still transmit with low viral load.
Recognize cultural barriers to treatment

132
Q

Herpes (simplex and zoster)

A

An entire family of viruses causing blisters on skin, genitals and mucosa
Virus cans tay dormant for years - stored in nerve ganglia
Exacerbations brought on by stress, physical changes (weather), immunosuppression

133
Q

Control of Herpes

A

Mostly controlled by oral therapy of antivirals - taken at FIRST sign of outbreak, continued for short term.
antivirals Prevent viral DNA synthesis. well tolerated - take w/ food. can be prescribed by pharmacist in Saskatoon (for cold sores only)

134
Q

drug therapy for Influenza

A

Best protection is Vaccination
Antiviral drugs MAY decrease severity of symptoms of influenza and MAY shorten symptom time by a couple days.
- Amantadine, and neuraminidase inhibitors
generally only used in its at high risk for complications from the flu.

135
Q

High risk Patients: influenza

A

Pregnant women
Children (6months - 5yrs)
Elderly (>65)
Patients with compromised immune systems
Adults and children with chronic health conditions
Aboriginal peoples

136
Q

Nurse’s role: Influenza

A

Reduce transmission rates by getting vaccinated and washing hands
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 ~1wk

137
Q

reasons for Immuno-suppressant use

A

Autoimmune diseases. (MS, Hashimoto’s, Rheumatoid arthritis)
Transplants
Exacerbation of conditions (such as asthma of rheumatoid arthritis) to regain control

138
Q

Immune suppressants medication classes

A
  1. Calcineurin Inhibitors
  2. Corticosteroids
  3. Biologics
  4. Chemotherapy
139
Q

MOA: Cacineurin Inhibitors

A

“classic” immune-suppressants used for transplants (or topically for psoriasis)
Disrupt T-cell function by binding to calcineurin
non specific - suppress the ENTIRE immune system
- require extensive monitoring

140
Q

Adverse Effects: Cacineurin Inhibitors

A

Increased risk of infection
Increased risk of cancers such as lymphomas, cysts and polyps
Kidney impairment, hepatic impairment
Hypertension, hyperlipidemia
CNS: tremors Headache, skin prickling sensation
GI: Nausea, vomiting, abdominal pain, diarrhea, gingival hyperplasia
MSK: Muscle cramps, myalgia
Endocrine: Mestrual disturbances, gynecomastia
Hypertrichosis (abnormal amount of hair growth over body)
Fatigue

141
Q

Biologics

A

Medications produced using biological processes in living organisms such as yeast and bacteria

  • done this way b/c the pharmaceutical compounds cannot be reasonably synthesized by chemical means

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

  • can be immune suppressant or immunostimulant - VERY specific (insulin is an example of a biologic)
142
Q

Biologics includes what types of therapies

A 
Vaccines 
blood products 
hormones and growth factors 
enzymes 
gene therapy 
cancer treatment
143
Q

biologics and cancer therapy

A

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

144
Q

Monitoring considerations for Biologics

A

Biologics often carry similar risk and monitoring needs as other immune-suppressants.
- signs of infection
- assess skin integrity
- watch for signs of organ rejection (in case of organ transplant)
Extra precautions may be required to prevent infection (PPE)

145
Q

Adverse Effects: Biologics

A

Infusion reactions:
Red, swollen, could be itchy ad injection site. prevent with prophalactic doses corticosteroid, antihistamine, and sometimes an NSAID to prevent the reaction. can slow down the infusion rate to reduce symptoms
- MUST monitor during infusion

146
Q

classes of Chemotherapy drugs

A
  1. Cytotoxic drugs
  2. hormonal therapy
  3. immune therapy
  4. targeted agents
147
Q

MOA: Cytotoxic drugs

A

Interfere with or damage DNA, causing apoptosis (programmed cell death)

148
Q

MOA: Hormonal therapies

A

Effects mediated through hormonal receptors (deprivation) - for hormone responsive cancers (breast, prostate, etc) *Traditional

149
Q

MOA: immunotherapy

A

Non-specifically boost immune system to help eradicate cancer (interferon alfa) *Monoclonal antibodies, vaccines

150
Q

MOA: Targeted agents

A

Target cancer cells only - FUTURE of cancer treatment. *monoclonal antibodies, tyrosine-kinase inhibitors (TKIs)

151
Q

what lead to the majority of chemotherapy treatment Adverse effects?

A

The killing of not only cancer cells, but also healthy cells.

152
Q

what do chemotherapy treatments target?

A

Target stages of the cell replication cycle - different drugs target different stages.

153
Q

Short-term Adverse effect of Chemotherapy

A 
Nausea/ vomiting 
Diarrhea or constipation 
mucositis/ stomatitis 
myelosuppression 
hair growth alterations 
weight gain/ loss 
taste alterations 
fatigue 
hepatic and renal changes 
cardiac function changes 
rash/ skin changes / nail changes 
high blood pressure
154
Q

Long-term Adverse effect os Chemotherapy

A 
Infertility 
secondary malignancies 
heart failure 
osteoporosis 
pulmonary fibrosis 
cataracts 
peripheral neuropathy 
hearing loss 
fatigue 
endocrine abnormalities
155
Q

Medications to help Managing Chemo-induced nausea / vomiting?

A

Dopamine blockers
Denzodiazepines (prevent anticipatory emesis
Corticosteroids
Serotonin antagonists
NK-1 antagonists
Cannabinoids
Dimehydrinate - useful if traveling after chemo. only effective for motion sickness

156
Q

Nurse’s role: Chemotherapy

A

follow guidelines for safe handling, administering, storage, and disposal of cytotoxic drugs - some drugs can be absorbed through skin!
Be aware of adverse effects and management
Be aware of supportive therapy available in community

Pharm 250 (5 decks)

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