Antibiotics, antifungal, antivirals, and cancer Flashcards

(226 cards)

1
Q

Ibuprofen

A

NSAID
CV risk
Nephrotoxicity
Safest for GI risk

Advil
Motrin

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2
Q

naproxen (Aleve)

A

NSAID

Safest for CV risk

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3
Q

indomethacin

A

NSAIDs oral

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4
Q

Aspirin Ind,MOA,AE

A

Indications: analgesia, antipyretic, anti-inflammatory, antithrombotic
MOA: irreversibly inhibits cox 1 and cox2 enzymes and forms prostaglandin derivative
decreases formation of prost. precursors
thromboxane= dec. platelet aggregation
Route:PO and rectal
AE: GI, bleeding/bruising, rash, photosensitivity, bronchospasm
*Avoid if Hx of GI bleed or under 12 or recent flu (reyes syndrome)
*low dose is selective for cox1- cardioprotection
*need increased doses for analgesia and inflammatory

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5
Q

celecoxib (Celebrex)

A

NSAID, COX-2 selective, use if GI risk but no CV risk

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6
Q

meloxicam (mobic)

A

NSAIDs oral

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7
Q

diclofenac (Voltaren gel, Flector patch)

A

Topical NSAID
Solution (Pennsaid)
Gel (voltaren)
Patch (Flector)

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8
Q

trolamine salicylate (aspercreme)

A

Topical NSAID

Aspercreme

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9
Q

codeine

A

Opioid

*Antitussive

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10
Q

hydrocodone

A

opioids

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11
Q

hydrocodone with acetaminophen ()

A

Opioid

*Vicodin

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12
Q

morphine ()

A

Opioid
*MS Cotin
Can accumulate after extended dosing

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13
Q

oxycodone ()

A

Opioid

  • Oxycotin
  • negligible levels of metabolites (OK for liver)
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14
Q

oxycodone with acetaminophen ()

A

Opioid

*Percocet

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15
Q

fentanyl ()

A

Opioid
*Duragesic
Dont apply heat to patch

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16
Q

hydromorphone ()

A

Opioid

  • Dilaudid
  • neuroexcitatory metabolite
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17
Q

meperidine ()

A

opioid

  • Demerol
  • neurotoxic metabolite esp with decrease liver function
  • anxiety and seizures
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18
Q

tramadol

A

opioid

Risk of Sezure

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19
Q

methadone

A

Opioid

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20
Q

cortisone

A

corticosteroids

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21
Q

prednisone

A

Corticosteroids
Synthetic version of corticosteroids to treat RA (and other diseases)
MOA: decreases inflammation and supresses immune system

Route: PO, IV, Intraarticular, Topical

Short term AE: inc blood glucose, mood changed, fluid retention

Long term AE: osteoporosis, inc fracture risk, thin skin, muscle wasting, poor wound healing, adrenal supression, cushing disease, inc infection risk

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22
Q

methylprednisolone

A

corticosteroids

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23
Q

prednisolone

A

corticosteroids

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24
Q

triamcinolone

A

corticosteroids

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25
betamethasone
corticosteroids
26
methotrexate
Non Biological Gold Standard for RA Also treats SLE MOA: unknown in RA Route: PO x1 week Give with folic acid to reduce GI, hepatic, and hematological toxicity Common AE: N/V/D, alopecia, malaise Less Common: hepatoxicity, nephrotoxicity, thrombocytopenia, bone marrow suppression
27
hydrochloroquine
Non-biologic DMARD anti-malarial MOA: impacts mediator of inflammatory response AE: GI, renal toxicity
28
adalimumab (Humira)
Biologic TNF inhibitors DMARDs MOA: bind to TNF alfa AE: headache, infection
29
etanercept (Enbrel)
Biologic TNF inhibitors DMARDs MOA: bind to TNF alfa AE: headache, infection
30
rituximab (Rituxan)
Biologic Non-TNF DMARDs MOA: impacts inflammation
31
lidocaine
anesthetics
32
adalimumab (Humira)
TNF inhibitor | DMARD
33
etanercept (Enbrel)
TNF inhibitor DMARD
34
rituximab (Rituxan)
Non TNF inhibitor | DMARD
35
piperacillin/tazobactam (Zosyn)
antibiotic
36
azathromycin
macrolides CYP450 inhibitor
37
lidocaine
Regional anesthetics
38
vancomycin
antibiotic glycopeptide hypotension
39
amoxicillin
penicillin antibiotic
40
amoxicillin/clavulanate (Augmentin)
penicillin antibiotic
41
piperacillin/tazobactam (Zosyn)
penicillin antibiotic
42
cephalexin (Keflex)
Cephalosporins Antibiotic
43
ceftriaxone (Rocephin)
cephalosporin antibiotic
44
cephalexin
Cephalosporins | Keflex
45
gentamicin
Aminoglycosides antibiotic ototoxicity Nephrotoxicity Usage p. aeeruginosa
46
azithromycin (Z-pack)
macrolide antibiotic
47
doxycycline
tetracycline antibiotic Photosensitivity
48
clindamycin
lincosamide antibiotic that can cause cdiff
49
ciprofloxacin
Fluoroquinolone Antibiotic tendon rupture phototoxicity hypoglycemia
50
levofloxacin (Levaquin)
Fluoroquinolone Antibiotic tendon rupture phototoxicity hypoglycemia
51
Treatment for pain cancer
Mild: NSAIDS, Acetaminophen, short acting opioid Moderate: short acting opioid Severe: strong opioid or long acting
52
cancer concerns
``` Increased fall risk fatigue pain emotional distress Chemo induced peripheral neuropathy decrease cognition decreased muscle strength (sarcopenia) cardiac and pulmonary damage ```
53
nystatin
antifungal Treats FI Route: PO, Topical AE: PO- N/V/D, cramps, topical-rash, urticaria (hives/itching)
54
Pharmacotherapy: Immunotherapy
hormones and drugs that use the immune system to treat cancer
55
Pharmacotherapy: Targeted therapy
DAmage cancer cells by blocking specific genes or proteins
56
Pharmacotherapy: chemotherapy
Drugs that inhibit growth and replication of cancer cells
57
Radiation Considerations
FATIGUE!!! | Radiation fibrosis
58
Chemotherapy effects
``` myelosuppression NVD stomatitis reproductive dysfunction hair loss ``` **try Nadir after chemotherapy
59
Neoadjuvant therapy
treatment used before primary treatment
60
Adjuvant therapy
used after primary treatment in conjunction with other therapy
61
Cancer treatment goals
Cure, control, or palliation
62
cancer cure
chemotherapy, biotherapy, radiation, and/or surgery
63
Cell life cycle and cancer
G0: rest stage- cells considered resistant to exposure from many chemotherapeutic agents G1: pre DNA: protein synthesis G2: premitosis: all cellular and structural compnents needed..checkpoint for cell sructures M: mitosis- cell division PMAT= 2 daughter cells
64
What is cancer?
uncontrolled cell growth
65
Types of vaccines
Inactivated (killed pathogen) Subunit or conjugated (piece of pathogen) Live attenuated (weakened pathogen)- avoid if immunocompromised Toxoid (pathogen toxin) **AE: injection site reaction, fever, headaches
66
Primary concern with antifungals
damage to liver and kidneys (fluid retention)
67
Fluconazole and Ketoconazole
Azoles that treat FI AE: N/V, photophobia, cardiac arrhythmia, menstrual irregularities
68
Azoles
Broad Spectrum | PO: fluconazole and ketoconazole
69
Polyenes
Nystatin and Amphotericin B
70
Types of drugs for Fungal Infections
Polyenes and Azoles Common CYP interactions
71
Drug target for fungal infections
Cell membrane
72
Types of fungal infections (2)
Superficial (ring worm or vaginal yeast infection) and systemic (meningitis)
73
Fungal Infections
aka mycoses Risk for FI increased after antibacterial use, immunisuppression, pregnancy, diabetes, elderly
74
Rehab concerns: Antiviral
Exercise tolerance may be affected (malaise, fatigue, INFs may cause flu like symptoms, anemia) Track vital signs and Rate of PE
75
Rehab concerns: HIV
Opportunistic infections: look out for long term antibiotics and wash hands Neuromuscular: pain, dysfunction, myopathy, peripheral neuropathy
76
Biktarvy
Antiretroviral agents in combo Treatment for naive patients bictegravir/emtricitabine/tenofovir alafenamide
77
Triumeg
dolutegravir/abacavir/lamivudine Antiretroviral agents in combo Treatment for naive patients
78
Types of Antiretroviral agents
``` NRTI NNRTI Protease Inhibitor Entry Inhibitors Integrase inhibitor ```
79
HAART
treatment for HIV
80
HIV treatment
HAART= highly active antiretroviral treatment Synergistic drug-drug interation
81
Direct-Acting Antivirals (DAAs)
AE: fatigue, weakness, and headache Also when combined with amiodarone will see bradycardia
82
Chronic Hepatitis C
In the past treatments hardly tolerated, now there are 11 DAA products to cure
83
Hepatitis B Treatment
Interferon- (injection) but causes flu like symptoms Nucleoside/nucleotide analogs- (PO) better tolerated
84
Hepatitis A
Pre and post exposure prophylaxis Vaccine, immune globulin, rest and hydration, antiemetics (nausea), antipyretics (fever) 2-6 months of recovery
85
Hepatitis
inflammation of the liver caused by a virus
86
Treatments for the flu
Oseltamavir (Tamiflu) | Baloxavir (Xofluza)
87
Antiviral endings
- ovir - ivir - alfa - ine
88
Life cycle of a virus
``` Attachment to host cell Entry Replication Assembly Release (budding or host cell lysis) ```
89
What is a virus
A very small invader that can only replicate in a host cell and enters the body via skin, mucous membranes, GI or respiratory tract. 3 components: envelope, capsid, nucleic acid core
90
Macrolide
antibiotic that fights Atypical pathogens causing pneumonia- this is a CYP450 inhibitor (look out for DDIs)
91
Fluroquinolone
Used to treat community acquired pneumonia- look out for tendon rupture
92
Pneumonia
Leading cause of death Causes: bacteria, virus, or mycoplasmas Inflammation affecting parenchyma of the lungs Transmission: airborne pathogens, circulation, sinus or contiguous infection, aspiration May be nosocomial (hospital acquired) which is more deadly
93
MRSA (Methicillin resistant Staphylococcus aureus)
On skin Spread via contact Treatments: linezoid and quinupristin/dalfopristin
94
Clostridium Difficile (Cdiff)
Gram + Transmission: contact or fecal to oral Symptoms: diarrhea, cramping, fever Occurs when normal GI flora interrupted **can survive up to 5 months DOC: metronidazole (IV) vancomycin
95
TB therapeutic concerns
Liver and kidney issues visual disturbances CN VIII damage neurological symptoms Beware of resistance due to resistant strain of TB infection or noncompliance with medications
96
Two Main Treatment Goals: TB
Contain and cure infection This process can last months to a year
97
Latent vs. Active TB
Latent TB: carries bacteria without symptoms Active: individuals are infectious and can spread disease
98
TB symptoms
fever, night sweats, malaise, weight loss
99
How does tuberculosis take effect?
Myobacterium tuberculosis is inhaled into lungs, aveoli and surrounded by macrophages to set off an immune response
100
How is TB transmitted?
airborne particles
101
What contributes to drug resistance?
overuse/misuse international OTC antibiotics Antibiotics in livestock
102
Types of Resistance
Innate: organism isnt susceptible Acquired: Inactivated drug, modify drug target, export drug from bacteria, or bypass antibiotic inhibition
103
Antimicrobial resistance
when bacteria or other microbes become resistant to the effects of a drug after being exposed to it
104
Sulfamethoxazole/trimethoprim (Bactrim)
Sulfonamides Steven-Johnsons syndrome
105
Sulfonamides
Sulfamethoxazole/trimethoprim (Bactrim, SMX/TMP) Broad coverage of Gram - and + AE: can cause allergy or steven johnson syndrome
106
Metronidazole (Flagyl)
Nitroimidazole antibiotic Metallic taste neuropathy
107
Nitroimidazole
Metronidazole (Flagyl) Use: Anaerobes AE: GI, metallic taste, Uncommon: peripheral neuropathy
108
Fluroquinolones
Ciprofloxacin Levofloxacin (levaquin) Gram - AE: GI, Photosensitivity Rare: tendon rupture, significant hypoglycemia
109
Lincosamides
Clindamycin Gram + GI and can Cause cdiff
110
Tetracyclines
Doxycycline Broad coverage gram + and - and atypicals AE: GI or photosensitivity
111
Macrolides
Azithromycin (Z-pak) Some gram + and - AE: GI issues, QT prolongation, CYP450 inhibitor (DDI)
112
Aminoglycosides
Gentamicin Usage: Gram +, P. aeruginosa AE: ototoxicity and nephrotoxicity
113
Glycopeptides
Vancomycin ``` MRSA, Cdiff Increasing resistance (VRE) ``` AE: Hypotension
114
Cephalosporins
Cephalexin (Keflex), ceftriaxone (Rocephin) Nosocomial infections, surgical prophylaxis GI and Hypersensitivity
115
Penicillins
Amoxicillin, Amoxicillin/clavulanate (Augmentin) and Piperacillin/tazobactam(Zosyn) Broad coverage of Gram+ and Gram- AE: GI and hypersensitivity
116
MOA for antibacterials
``` Cell wall cell membrane protein synth dna synth dna strand ```
117
Broad vs Narrow
effective against many or few types of infection
118
3 considerations for selecting treatment
``` Bacterial factors (identify and susceptibility) Host specific factors (allergies, renal function, ect) Drug specific factors (DDI, route, ect) ```
119
Bactericidal
kill bacteria
120
Bacteriostatic
inhibit bacterial growth, requires an immune host
121
Gram negative
Positively charged but favors negatively charged compounds Thinner cell wall (5-7 strands)
122
Gram Positive
Is negatively charges but favors positvely charged compounds Thick cell wall (20-30 strands)
123
Antibiotic
Drug that is only actively against bacteria
124
Antimicrobial
Drug that is active against bacteria, virus, fungi, or parasite
125
Propofol
general anesthetic | causes loss of consciousness
126
General Anesthesia rehab concerns
Neuromuscular Weakness Impaired airway clearance Immune function suppressed In older adults pulmonary complications or reduced cough reflex
127
Local Anesthetics (AE and duration)
AE: rare but possible: CNS stimulation progressing to depression, CV issues, respiratory depression Duration: 20 min up to 6 hours
128
Local Anesthetics (MOA, Advantages, diadvantages)
MOA: reversibly bind a receptor site within the pore of the Na+ channels in nerves ->block ion movement through the pore ->blocks action potential for nerve conduction, especially at small myelinated axons that carry nociceptive input Advantages: quick recovery, low systemic toxicity, confined to nerve tissue Disadvantages: incomplete analgesia, longer time to anesthesia
129
Regional Anesthetics (route and categories)
Route: topical, infiltration anesthesia, peripheral nerve block, IV regional block, epidural or spinal administration Categories: central neuraxial block: epidural or intrathecal space peripheral nerve block: near a nerve or the plexus innervating the are undergoing surgery field block: adjoining tissues so the drug will diffuse to the surgical area for minor hand or foot procedures Can be used in combo w/ decrease general anesthesia dose
130
Where does inhaled general anesthetics create a hang over effect?
Adipose tissue
131
General anesthetics- Intravenous types
``` Barbiturates (thiopental) Dissociative (ketamine) Misc (etomidate, propofol) Opioids (fentanyl) Benzodiazepines (midazolam) ``` Quick onset and quick recovery May be used with inhaled too
132
General Anesthetics- types of inhaled
``` Gas (nitrous oxide) Volatile Liquids (halothane) ```
133
How are general anesthesia goals achieved?
Balanced anesthesia: combo of IV and inhaled anesthetics, analgesics and neuromuscular blocking agents
134
Goal of general anesthesia
loss of consciousness, analgesia, amnesia, skeletal muscle relaxation, inhibition of sensory and autonomic reflexes
135
General Anesthesia- Medullary Paralysis
Can have respiratory or cardiovascular collapse
136
General Anesthesia- Surgical Anesthesia
Completely unconscious and respiration is more regular
137
General Anesthesia- Delirium/Disinhibition
Will lose consciousness and respirations may change
138
General Anesthesia- Analgesia/Induction
May or may not remember but generally still conscious
139
Anesthesia (3 categories)
General: Iv and inhaled Regional: Intrathecal and epidural Local: Injection and topical
140
Anesthesia (3 categories)
General: Iv and inhaled Regional: Intrathecal and epidural Local: Injection and topical
141
Patient-controlled analgesia (PCA) side effects
Pharmacological side effects (AE to meds) Problems with delivery
142
PCA- types of anesthetics
Opioids (Morphine, fetanyl, hydromorphine) Local anesthetics (epidural)
143
Patient Controlled Anaglesia (PCA) dosing strategies
Load Dosing, Demand Dosing, Lockout interbal, 1 and 4 hour limits, background infusion rate Measures successful vs. total demand
144
What does PCA do?
Enables continuous pain control and lowers incidence side effects
145
What is patient-controlled analgesia (PCA)?
Patient self administers analgesic via small pumps worn, implanted devices, or pumps on a pole Route: Catheters, IV, Intrathecal, epidural space
146
Other rehab concerns with SLE drugs
Viral infections Fungal infections Photosensitivity
147
Rehab Concerns w/ SLE drugs (Bacterial Infections)
80 % of infections | soft tissue infection can lead to sepsis
148
Rehab concerns w/ SLE drugs (immunosupression)
Pts w/ SLE already risk for infection | Increased risk with DMARDS and steroids
149
Immunosuppressants for SLE
Methotrexate and azathioprine are most common MOA: Decrease the immune response so body does not attack itself AE: N/V Boxed warning: serious infection, secondary malignancy
150
SLE treatment (severe)
High Dose steroids | Immunosuppressants
151
SLE treatment (mild/moderate)
NSAIDS Steroids Antimalarials Immunosupressants
152
systemic lupus erythematosus (SLE)
chronic inflammatory autoimmune disease affecting variety of organs Direct infiltration of immune complexes into organs and joints -> destruction of tissue -> clinical symptoms
153
Corticosteroids
Short term RA treatment NSAIDS can help Opioids for pain
154
Janus Kinase Inhibitors
``` Biological DMARD RA Route:PO Common AE: infection, nasopharyngitis Boxed warning: infections Tofacitinib (Xeljanz) Baricitinib (Olumiant) ```
155
Non TNF inhibitors
``` Biological DMARD RA Route: IV or subcut Common AE: injection reactions, increased LFTs, antibody devlopment Boxed Warning: serious infections Rituximab (Rituxan) Abatacept (Orencia) Tocilizumab (Actemra) Sarilumab (Kevzara) Anakinra (Kineret) ```
156
TNF inhibitors
Biological DMARD RA Route: IV or subcut Common AE: headache, infection, antibody development, infusion reactions ``` Boxed warnings: serious infections ◦Adalimumab (Humira) ◦Golimumab (Simponi) ◦Infliximab (Remicaide) ◦Certolizumab pegol (Cimzia) ◦Etanercept (Enbrel) ```
157
Hydroxychloroquine
Non-biologic DMARD RA Treats Lupus too (reduces disease progression and prolongs survival) ◦MOA: impacts mediators of inflammatory response ◦Route: PO ◦Common AE: GI and skin reactions ◦Rare AE: retinal toxicity (regular ophthalmologic exams) ◦Addresses symptoms but not progression ◦Used for other disease states too (lupus, malaria, etc)
158
RA Treatment
Nonbiological DMARD Biological DMARD (TNF inhibitors, NonTNF inhibitors and Janus Kinase inhibitors) MOA: inflammation usually
159
rheumatoid arthritis (RA)
A chronic, progressive, systemic, inflammatory autoimmune disease Often swollen and inflamed
160
Glucosamine- Chondroitin
Not recommended But possibly help with OA Antithrombotic effect
161
Intraarticular Steroids
OA treatment Injections Trimacincolone (Kenalog) Methylprednisolone (Depo-Medrol)
162
Intraarticular hyaluronate
For hip or knee OA MOA: visoelastic solution to provide joint lubrication AE: injection site pain, swelling, rash
163
Treatment for OA
Tylenol, if not topical NSAID, corticosteroids, tramadol, or oral NSAID Second line: opioids, surgery, intraarticular hyaluronate If over 75 Topical NSAID or Capsaicin or tramadol (avoid oral NSAIDs)
164
Osteoarthritis (OA)
Slow, progressive degeneration of joint surfaces (cartilage all the way to bone) Inc thickness of subchondral bone reduces ability to absorb energy= more strain on articular cartilage-> cartilage erodes and bones directly contact each other
165
Capsaicin cream
Neuropathic Treatment | AE: burning sensation and erythema
166
Gabapentin (Neurontin)
Neuropathic GABA analog and anticonvulsant AE: dizziness and drowsiness INEXPENSIVE
167
Stimulus Independent- paroxysms
shooting or shock like
168
Stimulus Independent- paresthesia
numbness or tingling
169
Stimulus Independent- mechanical allodynia
normal stimulus that shouldnt cause pain but does
170
Stimulus Independent- Hyperalgesia
experiencing more pain than we would expect
171
Stimulus Independent
results from mechanical, thermal, or chemical stimuli
172
Stimulus Dependent
Shooting, shock-like, aching, crushing, burning
173
Neuropathic Pain
associated with disease or injury to PNS or CNS Causes: Diabetes, immune deficiencies, shingles, trauma, MS, ischemic issues, cancer, drugs, ect. Due to damage nocioreceptors are highly sensitive to stimuli or produce pain signals w/o a stimulus
174
Diclofenac (Voltaren)
NSAID (topical)
175
NSAIDs
Indications: analgesia, antipyretic, anti-inflammatory MOA: reversibly inhibits COX1 and 2 (decrease prostiglandins precursors) AE: GI, inc BP, nephrotoxicity, CV risk (variable) Look out for GI Bleed, elderly, and renal issues May impact muscle repair
176
NSAID mechanism of action
Stimulus signals arachidonic acid Which inc. inflammation, cytokines, and activates COX1 and COX2 COX2 does vasodilation, vascular perm, cytokine release, leukocyte migration, and pain COX1 does fever and neurotransmission- always present When NSAID blocks these enzymes anti-inflammatory, analgesia and antipyretic happen
177
Acetaminophen
not an NSAID Tylenol Indications: analgesia and antipyretic MOA: inhibits prostaglandin synthesis in CNS Route: PO,IV, Rectal AE: Hepatoxicity *SIP enzymes break it into metabolites that are toxic to the liver
178
Opioids
Codeine, Hydrocodone, Vicodin, Morphine, Oxycodone, Percocet, Fetanyl, Hydromorphone, Meperdine - Binds to receptors in CNS to inhibit asc pain pathway - Dont develop tolerance to constipation and miosos * anaglesia, antitissive - PO, rectal, IM, IV, topical, subcut, epidural, intrathecal, transmucosal
179
Opioid Antagonists
naltrexone (vivitrol)- PO- 4 maintenance of abstinence- not acute overdose naloxone (evizio/narcan)- IV,IM,Subcut, Intranasal- acute overdose or respiratory depression *reverses respiratory depression and euphoria
180
Strong vs mild mu agonist
Strong: all but codeine and tramadol
181
Substantia Gelatinosa
gate keeper | rich in opioid receptors
182
Categories of Pain
Nocioceptive: injury, stabbing, aching Neuropathic: burining, tingling sensation Psychogenic: origin to psych
183
Pain Pathway
Pain signal to brain via ascending pathway to brain stem to spinal cord Injury: produce cytokines which release prostaglandins Sensory nerve fibers (afferent) respond to prostaglandins (1st order) 2nd order goes up spinothalamic tract to brain to thalmus 3rd order relays yo somatosensory cortec on opposite sides of the brain Dorsal horn of SC- substance P activates next cell, so no sub P= inhibit
184
A fibers
myelinated and are localized pain
185
C fibers
unmyelinated and diffuse pain
186
Mechanism of pain
Descending Pathway: Neurons in gray matter signals to silence 2nd order and travels down dorsal horn to inhibit Substantia gelatinosa: gate keeper 2 regulate transmission of nocioceptive fibers This blocks release of substance p and inhibits pain
187
Opiod mechanism of action
Drug passes BBB Lipid soluble passes quicker Opioids bind to opioid receptors (G-coupled) Cause presynaptic and postsynaptic inhibition Blocks pain by stopping desc and thus stopping the pain loop with ascending pathway
188
DDI-Antagonistic
Effect
189
DDI- Synergistic
Response> sum of response to both positive: HIV cocktail viral load suppression negative: CNS depression with opioid and benzo
190
Drug-Drug Interactions (DDI) definition
The effect will be altered or modified when more than one drug is given because one drug changes another drug's action.
191
Statins
Lower blood cholesterol Block HMG-CoA to prevent liver from making chol Can be used for leukemia, dementia, lung cancer, OP Can induce myopathy (muscular weakness)
192
Receptor Change antagonism
Desensitization due to long term exposure to agonist
193
Pharmacokinetic antagonism
One drug induces or inhibits the metabolism of another
194
Physiologic antagonism
2 drugs with opposite effects
195
Chemical antagonism
2 substances that diminish the effect
196
Response and Drug Dose Graph
Smallest curve is most potent Shortest curve is also probably the partial agonist b/c there was not a high response Most effective curve is the quickest one to reach 100 percent response
197
Selectivity
Only bind to Beta 1 or Beta 2
198
Specificity
only bind to alpha or beta
199
Antagonist
Occupy receptors but do not activate
200
Agonist
Drugs occupy receptors= activate
201
Partial Agonist
Does not fit receptor exactly Lower dose= agonist effect Higher does= less response b/c it blocks receptors where agonists would usually bind
202
Non-competitive antagonist
Greatly diminishes effect, increasing agonist will not overcome antagonist
203
Competitive Antagonist
Antagonist and agonist compete for receptor, higher concentration wins
204
ED50
Effective dose to get 50 % of expected response | Lower ED50= more potent drug b/c less drug is needed for greater effect
205
Emax
maximal response, receptors filled
206
Other drug targets
Enzymes and Non-human cells (penicillin-bacteria cell wall and oseltamauir-infected cells)
207
Boxed Warning
Calls attention to serious risks associated with medicine
208
Receptor Types (Name and describe all 4)
Ligand- quick, ligand binds, voltage gated channels open to transmembrane protein to allow ion flow G- Protein- quick- transmembrane receptors cross 7 times- intracellular effects Kinase- hours- ligand binds and makes receptors pair up (ex:insulin, GLU4, uptake glucose) DNA- hours- intracellular with lipophilic ligand, receptor binds ligand and DNA to activate or depress gene expression (ex levothyroxine)
209
Therapeutic Index
Ratio of TD50 to ED50 | Lower the TI= more likely AE/toxicity
210
Lipid soluble meds...
Cross BBB quicker
211
Elimination/Excretion
- removal of a drug from the body - Kidneys and liver - First order (most common- proportional to concentration- 1/2 life) and second order (not proportional to conc- steady downward slope) - 1/2 life= how long it takes to eliminate half the drug - A drug is cleared after 5 (1/2) lives
212
Metabolism
CYP enzymes: break down molecule into active or inactive products **Some drugs inhibit CYP which inc. drug concentration and may inc. likelihood of AE
213
Distribution Vd?
Vd=total conc of drug in body/plasma higher Vd= more drug in tissue highly protein bound= less active drug in tissue
214
Absorption (Entheral, Parentheral, Diffusion-3, Bioavailability, First Pass)
Enteral (GI) vs. Parentheral (not GI) Passive Diffusion via lipid memebrane or aqueous channel or carrier mediated Bio-availability: % of drug in systemic circulation (varies with pH, gut motility, and food) First Pass: In liver, liver takes out most of the drug (PO)
215
Pharmacokinetics
What the body does to the drug (ADME)
216
Pharmacodynamics
How the drug affects the body (MOA, Potency, Efficacy)
217
FDA Clinical Trails 1-4
One: small, healthy, for safety Two: Small, diseased, for efficacy Three: Large, long, and randomized Four: After approval and post marketing
218
Schedule V
Medical use and little to no abuse (ex: antidiarrheal, antitussive, analgesia)
219
Schedule IV
Medical use and low abuse (ex: tramadol, xanax, ambien)
220
Schedule III
Medical use and mid abuse (ex:codeine & anabolic steroids)
221
Schedule II
Medical Use and High abuse (ex: cocaine, meth, fetanyl, addy, oxy, hydros)
222
Schedule I
No medical use and high abuse ex:heroin, LSD, MaryJ
223
Brand
owned by manufacturer & uppercase
224
Generic
official name & lowercase
225
off-label
Using drugs for something not approved by the FDA (ex:different ages, diseases, or doses)
226
Off Patent
~20 years later other companies can make the drug without permission from the original manufacturers