Module 4 - immune system Flashcards
(156 cards)
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.
2
Q
Mediators of inflammation
A
Histamine* Bradykinin Leukotrienes Cytokines Interleukins Prostaglandins*
3
Q
Classes of medications for inflammation
A
- Non-Steroidal Anti-Inflammatories (NSAIDs)
2. Corticosteroids
4
Q
MOA: NSAIDs
A
Inhibit cycle-oxygenase (COX)
reduce Prostaglandin synthesis leading to inhibition of inflammation
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
6
Q
Cox-2
A
More specific for inflammation
7
Q
Common Adverse effects of NSAIDs
A
Nausea dyspepsia ulcers (w/ longe-term use) potential anti-platelet action increases risk of cardiac event
8
Q
indications for NSAIDs
A
Mild to moderate inflammation fever mild to moderate pain dysmenorrhea musculoskeletal pain arthritis
9
Q
cautions for NSAIDs
A
Take with food
Caution in kidney disease, CVD, and GI conditions
* use short term and as needed only
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
11
Q
indications: Corticosteroids
A
Severe inflammation (MS, Rheumatoid Arthritis, auto-immune diseases)
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
13
Q
Adverse effects: Corticosteroids
A
Hyperglycaemia hypertension nausea insomnia psychosis ( w/ increased dose)
14
Q
Contraindications for Anti-infmmitories
A
Kidney or liver disease
GI disease
CVD
active infections (due to immune suppression)
15
Q
Def: Fever
A
a defence mech. - increase in body temp in attempt to destroy harmful bacteria.
16
Q
Drugs that reduce fever
A
Antipyretics
17
Q
Fever medications: Classes
A
- Acetaminophen
2. NSAIDs
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
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.
20
Q
indications: Acetaminophen
A
Fever
mild to moderate pain
osteoarthritis
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.
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
23
Q
Signs of liver toxicity
A
Jaundice pale tired sweating dark urine confusion coma
24
Q
Antigen
A
Anything that the body identifies as foreign - causes allergy symptoms
25
allergy symptoms
```
Tearing eyes
sneezing
nasal congestion
postnasal drip --> cough
itchy mucous membranes (inside nose, mouth, and eyes)
```
26
Histamine
bodies response to antigen --> histamine release
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H1
smooth muscle of vascular system, bronchial tree, digestive tract
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H2
Lining of stomach, producing gastric acid
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med Classes: allergies
1. Antihistamines (1st gen and 2nd gen)
2. Intranasal corticosteroids
3. decongestants
4. drugs for anaphylaxis
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MOA: 1st Gen Antihistamines
anticholinergic effects
block H1 receptors
*shorter acting, cause more drowsiness and work faster than 2nd gen.
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MOA: 2nd Gen Antihistamines
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.
32
MOA: intranasal Corticosteroids
reduce inflammation in nasal mucous membranes, and. local immunosuppresion
33
Adverse Effects: Intranasal Corticosteroids
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
34
MOA: decongestants
Sympathomimetics - stimulants - cause vasoconstriction and reduction of mucous production
35
Adverse effects: Decongestants
oral -
Intranasal-
Oral: hypertension, anxiety, insomnia
Intranasal: Nasal irritation, rebound congestion, rarely systemic effects
*short term use only - Rebound congestion if longer than 3-5days (intranasal)
36
Nurse's Role: Allergies
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
37
Def: Anaphylaxis & symptoms
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
38
MOA: epinephrine
- 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)
39
outpatient treatment of Anaphylaxis
epinephrine injection given at onset of symptoms - IM - vastus lateralus
*Given En-route to hospital - does NOT resolve situation just allows more time
40
Hospital treatment of Anaphylaxis
Oxygen
more epinephrine
bronchodilator (Salbutamol - Beta- agonist)
corticosteroids - due to anti inflammatory and immune suppressive effects
41
Contraindications for Epinephrine
Hypersensitivity to adrenergic amines (sympathomimetic drugs)
42
Monitoring: Anaphylaxis
- family teaching
- In hospital
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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Mechanism by which bacteria can cause disease
1. rapid growth
| 2. toxin production
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Bacterial classification:
| Gram positive
Have thick cell walls and retain purple gram-stain
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Bacterial Classification:
| Gram Negative
Have thin cell walls and lose purple gram-stain
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Bacterial Classification:
Bacilli:
Cocci:
Spirilla:
Bacilli: rod shaped
Cocci: spherical
Spirilla: Spirals
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Bactericidal antibiotics
Drugs that KILL the bacteria
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Bacteriostatic antibiotics
Drugs that slow down the GROWTH of the bacteria, allowing the body's immune system to kill the bacteria
49
Def: Antibiotic resistance
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.
50
Activities that promote the development of Bacteria resistance and the reason
- 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
51
Antibiotic spectrums
Broad spectrum
| Narrow spectrum
52
Broad spectrum antibiotics
drugs that are effective against a WIDE VARIETY of bacteria (prescribed when the specific pathogen is unknown)
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Narrow spectrum antibiotics
drugs that are effective agains SPECIFIC microorganisms or a restricted group. (prescribed when pathogen is clearly identified from a C&s or symptoms)
54
Def: Culture and Sensitivity
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.
55
Def: Superinfection
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.
56
Signs of a superinfection
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)
57
Do probiotics work?
some evidence suggests YES. but should be taken at a different time than the antibiotic.
58
considerations when choosing an antibiotic
```
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
```
59
Antibiotic classes (9)
1. Penicillins
2. Cephalosporins
3. Tetracyclines
4. Macrolides
5. Aminogycosides
6. Fluoroquinolones
7. Sulfonamides
8. Carbapenems
9. Miscellaneous
60
MOA: Penicillins
*what is the necessary component of their activity
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.
61
Penecillin resistant bacteria characteristics
penecillin resistant bacteria produce Beta-lactamase which breaks the beta-lactam ring of penicillin making it ineffective.
62
what is the rationale for prescribing a combination of Clavulanic Acid and a penicillin class antibiotic together?
Clavulanic Acid inhibits Beta-lactamases of SOME microorganisms to allow the penicillin to be active against it.
*synergistic relationship
63
Some Narrow spectrum Antibiotics
Penicillin G
Penicillin V
Cloxacillin
Dicloxacillin
64
some broad spectrum Antibiotics
Amoxicillin
Amoxicillin/Clavulanate
Ampicillin
65
Adverse Effects: Penicillins
```
Anaphylaxis
diarrhea
nausea and vomiting
pain at injection site
superinfection
some (minor) drug interactions
```
66
Monitoring: Penicillins
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
MOA: Cephalosporins
R/t penicillins
inhibit cell wall synthesis - bactericidal
generational classification (gen 1-4)
68
classification of Cephalosporins
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
Adverse Effects: cephalosporins
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
Will a pt who is allergic to Penicillins have an allergic reaction to Cephalosporins?
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
MOA: tetracyclines
Inhibit bacterial protein synthesis
bacteriostatic
broad-spectrum (both gram pos and neg)
72
cautions w/ tetracyclines - why?
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
Indications: Tetracyclines
Rocky Mountain Spotted Fever (tick borne disease) H. Pylori infections, acne vulgarisms, chlamydia
74
Adverse effects: Tetracyclines
```
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
MOA: Macrolides
-THROMYCIN
Inhibit Bacterial Protein synthesis. some bactericidal and some bacteriostatic.
No structural similarities to penicillins = ZERO chance of cross sensitivity
76
Indications: Macrolides
Upper and lower respiratory tact infections
whooping cough
diphtheria
or for patients who cannot take penicillins
77
Adverse Effects: macrolides
significant nausea
vomiting
diarrhea (take w/ food)
some IMPORTANT drug interaction
78
Drug interactions: Macrolides
Warfarin, cyclosporine, anticonvulsants (all via CYP450 inhibition/induction
79
MOA: Aminoglysides
-MY(i)CIN
Inhibit bacterial protein synthesis AND cause abnormal protein synthesis. DOSE DEPENDANT bactericidal.
80
Adverse Effects: Aminoglysides
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
indications: Aminoglysides
Serious (life threatening) infections (eg TB) OR when other antibiotics have failed.
82
When would Aminoglysides NOT require therapeutic drug monitoring?
When used topically as eye drops and creams/ointments
83
S&S of Nephrotoxicity
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
S&S of Ototoxicity
Hearing loss, vertigo, tinnitus
85
MOA: Fluoroquinolones
- FLOXACIN
Affect bacterial DNA synthesis. Bactericidal. absorption affected by minerals (Ca, Fe, Mg) - separate by 2h
86
Adverse effects: Fluroquinolones
```
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
Indications: Fluoroquinolones
Respiratory, urinary, ophthalmic, GI, and gynaecological infection
88
MOA: Sulfonamides
- SULFA
Suppress bacterial growth by inhibiting essential folic acid needed within the cell.
Bacteriostatic
broad spectrum. older classes with more resistance seen
89
indications: Sulfonamides
Used to treat UTI, orally and topically (acne)
90
Adverse Effects: Sulfonamides
```
Allergic reaction
nausea
vomiting
skin rashes
photosensitivity
anemia
crystalluria - prevent by drinking lots of water.
```
91
MOA: Carbapenems
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
Indications: Carbapenems
Reserved for resistant infection (like MRSA)
93
Adverse effects: Carbapenems
Skin reactions, inflammation at injection site, diarrhea, nausea, vomiting
94
MOA: Clindamycin
Protein synthesis inhibitor
| bacteriostatic
95
Indications: Clindamycin
topically for acne, orally or IV for serious systemic infections
96
Adverse effects: Clindamycin
High risk for super infections (GI)
97
MOA: Nitrofurantion
Inhibits protein, RNA, DNA, and cell wall synthesis.
| Bactericidal
98
Indications: Nitrofurantion
Used only for UTI because it is excreted unchanged by the kidney (no metabolism)
99
Adverse Effects: Nitrofurantoin
Changes in urine colour (urine turns orange)
| must be taken with food.
100
MOA: Metronidazole
Destroys bacterial DNA
Bactericidal
for anaerobic bacteria
101
indications: Metronidazole
C&S indicates precence of anaerobic bacteria
102
Adverse effects: Metronidazole
NO ALCOHOL: even small amounts results in: Disulfiram reaction: flushing, tachycardia, SOB, severe nausea & vomiting, throbbing headache, visual disturbance, confusion, dizziness.
103
MOA: vancomycin
Inhibits cell wall synthesis
| bactericidal
104
Indications: Vancomycin
reserved for severe infections that are resistant to anything else.
105
Adverse effects: Vancomycin
if IV given too quickly results in Red Man Syndrome (flushing, red face, hypotension)
ototoxicity
nephrotoxicity
requires therapeutic drug monitoring
106
By what MOA do antibiotic interfere with Oral Contraceptives.
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
Tuberculosis (TB)
Highly contagious infection caused by Mycobacterium Tuberculosis. exhibits both active and latent stages. spread via respiratory route.
108
Initial/ induction phase of TB treatment
~ 2 months - kill actively dividing mycobacteria
109
Continuation phase of TB treatment
~ months or longer - kill dormant mycobacteria
110
3 important Characteristics of TB treatment
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
What is Directly Observed Therapy (DOT) and why is it Necessary for TB treatment?
Non-adherence is the MOST common cause of TB treatment failure, therefor requiring DOT.
112
What is Isoniazid (INH) used for and what are some important considerations?
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
what is Rifampin (RMP) used for and what are some important considerations?
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
Nurse's role in TB
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
Def: Fungal Infections
Systemic fungal infections very rarely occur in a healthy individual.
116
Superficial Fungal infections
Infections (outer layers of skin, nails, hair) most common and can be treated easily.
117
Systemic fungal infections
affecting internal organs. are more are and very serious.
long anti fungal therapy required. usually treated with Amphotericin B (via IV)
118
Classes of Antifungals
1. Amphotericin B
2. Azole Antifungals
3. Miscellaneous
119
Mycoses
Fungal infection
120
causes for suppressed immune system
```
HIV or AIDS
prolonged corticosteroid therapy
Other immunosuppressant therapy (transplant recipient)
burns
chemotherapy
```
121
MOA: Amphotericin B
Binds to fungal cell membranes, making them leaking
| given IV
122
Adverse effects: Amphotericin B
Fever and Chills during infusion, vomiting, headache, phlebitis, nephrotoxicity, hypokalemia, ototoxicity
- usually does not require therapeutic drug monitoring.
123
MOA: Azole Antifungals
Alter fungal cell membranes by depleting ergosterol. used orally, topically, injection. some forms available OTC.
safer than amphotericin B
124
Indications: Azole Antifungals
Most often for vaginal candidiasis, athlete's foot , or thrush
125
Adverse Effects: Azole Antifungals
Rare Hepatoxicity - avoid alcohol, watch for jaundice, motor liver enzymes
126
Miscellaneous antifungals
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
Nurse's role: Fungal infections
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
HIV Antiviral therapy
Antiretoviral drugs block HIV replication cycle
129
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 the same time to reduce resistance
- Each class 'Attacks' different step of replication cycle
130
Antiretroviral monitoring
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
Nurse's role: Antiretrovirals
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
Herpes (simplex and zoster)
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
Control of Herpes
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
drug therapy for Influenza
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
High risk Patients: influenza
Pregnant women
Children (6months - 5yrs)
Elderly (>65)
Patients with compromised immune systems
Adults and children with chronic health conditions
Aboriginal peoples
136
Nurse's role: Influenza
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
reasons for Immuno-suppressant use
Autoimmune diseases. (MS, Hashimoto's, Rheumatoid arthritis)
Transplants
Exacerbation of conditions (such as asthma of rheumatoid arthritis) to regain control
138
Immune suppressants medication classes
1. Calcineurin Inhibitors
2. Corticosteroids
3. Biologics
4. Chemotherapy
139
MOA: Cacineurin Inhibitors
"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
Adverse Effects: Cacineurin Inhibitors
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
Biologics
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
Biologics includes what types of therapies
```
Vaccines
blood products
hormones and growth factors
enzymes
gene therapy
cancer treatment
```
143
biologics and cancer therapy
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
Monitoring considerations for Biologics
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
Adverse Effects: Biologics
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
classes of Chemotherapy drugs
1. Cytotoxic drugs
2. hormonal therapy
3. immune therapy
4. targeted agents
147
MOA: Cytotoxic drugs
Interfere with or damage DNA, causing apoptosis (programmed cell death)
148
MOA: Hormonal therapies
Effects mediated through hormonal receptors (deprivation) - for hormone responsive cancers (breast, prostate, etc) *Traditional
149
MOA: immunotherapy
Non-specifically boost immune system to help eradicate cancer (interferon alfa) *Monoclonal antibodies, vaccines
150
MOA: Targeted agents
Target cancer cells only - FUTURE of cancer treatment. *monoclonal antibodies, tyrosine-kinase inhibitors (TKIs)
151
what lead to the majority of chemotherapy treatment Adverse effects?
The killing of not only cancer cells, but also healthy cells.
152
what do chemotherapy treatments target?
Target stages of the cell replication cycle - different drugs target different stages.
153
Short-term Adverse effect of Chemotherapy
```
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
Long-term Adverse effect os Chemotherapy
```
Infertility
secondary malignancies
heart failure
osteoporosis
pulmonary fibrosis
cataracts
peripheral neuropathy
hearing loss
fatigue
endocrine abnormalities
```
155
Medications to help Managing Chemo-induced nausea / vomiting?
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
Nurse's role: Chemotherapy
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
