Antibiotics, antifungal, antivirals, and cancer Flashcards
Ibuprofen
NSAID
CV risk
Nephrotoxicity
Safest for GI risk
Advil
Motrin
naproxen (Aleve)
NSAID
Safest for CV risk
indomethacin
NSAIDs oral
Aspirin Ind,MOA,AE
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
celecoxib (Celebrex)
NSAID, COX-2 selective, use if GI risk but no CV risk
meloxicam (mobic)
NSAIDs oral
diclofenac (Voltaren gel, Flector patch)
Topical NSAID
Solution (Pennsaid)
Gel (voltaren)
Patch (Flector)
trolamine salicylate (aspercreme)
Topical NSAID
Aspercreme
codeine
Opioid
*Antitussive
hydrocodone
opioids
hydrocodone with acetaminophen ()
Opioid
*Vicodin
morphine ()
Opioid
*MS Cotin
Can accumulate after extended dosing
oxycodone ()
Opioid
- Oxycotin
- negligible levels of metabolites (OK for liver)
oxycodone with acetaminophen ()
Opioid
*Percocet
fentanyl ()
Opioid
*Duragesic
Dont apply heat to patch
hydromorphone ()
Opioid
- Dilaudid
- neuroexcitatory metabolite
meperidine ()
opioid
- Demerol
- neurotoxic metabolite esp with decrease liver function
- anxiety and seizures
tramadol
opioid
Risk of Sezure
methadone
Opioid
cortisone
corticosteroids
prednisone
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
methylprednisolone
corticosteroids
prednisolone
corticosteroids
triamcinolone
corticosteroids
betamethasone
corticosteroids
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
hydrochloroquine
Non-biologic DMARD
anti-malarial
MOA: impacts mediator of inflammatory response
AE: GI, renal toxicity
adalimumab (Humira)
Biologic TNF inhibitors
DMARDs
MOA: bind to TNF alfa
AE: headache, infection
etanercept (Enbrel)
Biologic TNF inhibitors
DMARDs
MOA: bind to TNF alfa
AE: headache, infection
rituximab (Rituxan)
Biologic Non-TNF DMARDs
MOA: impacts inflammation
lidocaine
anesthetics
adalimumab (Humira)
TNF inhibitor
DMARD
etanercept (Enbrel)
TNF inhibitor
DMARD
rituximab (Rituxan)
Non TNF inhibitor
DMARD
piperacillin/tazobactam (Zosyn)
antibiotic
azathromycin
macrolides
CYP450 inhibitor
lidocaine
Regional anesthetics
vancomycin
antibiotic
glycopeptide
hypotension
amoxicillin
penicillin antibiotic
amoxicillin/clavulanate (Augmentin)
penicillin antibiotic
piperacillin/tazobactam (Zosyn)
penicillin antibiotic
cephalexin (Keflex)
Cephalosporins Antibiotic
ceftriaxone (Rocephin)
cephalosporin antibiotic
cephalexin
Cephalosporins
Keflex
gentamicin
Aminoglycosides antibiotic
ototoxicity
Nephrotoxicity
Usage p. aeeruginosa
azithromycin (Z-pack)
macrolide antibiotic
doxycycline
tetracycline antibiotic
Photosensitivity
clindamycin
lincosamide antibiotic that can cause cdiff
ciprofloxacin
Fluoroquinolone Antibiotic
tendon rupture
phototoxicity
hypoglycemia
levofloxacin (Levaquin)
Fluoroquinolone Antibiotic
tendon rupture
phototoxicity
hypoglycemia
Treatment for pain cancer
Mild: NSAIDS, Acetaminophen, short acting opioid
Moderate: short acting opioid
Severe: strong opioid or long acting
cancer concerns
Increased fall risk fatigue pain emotional distress Chemo induced peripheral neuropathy decrease cognition decreased muscle strength (sarcopenia) cardiac and pulmonary damage
nystatin
antifungal
Treats FI
Route: PO, Topical
AE: PO- N/V/D, cramps, topical-rash, urticaria (hives/itching)
Pharmacotherapy: Immunotherapy
hormones and drugs that use the immune system to treat cancer
Pharmacotherapy: Targeted therapy
DAmage cancer cells by blocking specific genes or proteins
Pharmacotherapy: chemotherapy
Drugs that inhibit growth and replication of cancer cells
Radiation Considerations
FATIGUE!!!
Radiation fibrosis
Chemotherapy effects
myelosuppression NVD stomatitis reproductive dysfunction hair loss
**try Nadir after chemotherapy
Neoadjuvant therapy
treatment used before primary treatment
Adjuvant therapy
used after primary treatment in conjunction with other therapy
Cancer treatment goals
Cure, control, or palliation
cancer cure
chemotherapy, biotherapy, radiation, and/or surgery
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
What is cancer?
uncontrolled cell growth
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
Primary concern with antifungals
damage to liver and kidneys (fluid retention)
Fluconazole and Ketoconazole
Azoles that treat FI
AE: N/V, photophobia, cardiac arrhythmia, menstrual irregularities
Azoles
Broad Spectrum
PO: fluconazole and ketoconazole
Polyenes
Nystatin and Amphotericin B
Types of drugs for Fungal Infections
Polyenes and Azoles
Common CYP interactions
Drug target for fungal infections
Cell membrane
Types of fungal infections (2)
Superficial (ring worm or vaginal yeast infection) and systemic (meningitis)
Fungal Infections
aka mycoses
Risk for FI increased after antibacterial use, immunisuppression, pregnancy, diabetes, elderly
Rehab concerns: Antiviral
Exercise tolerance may be affected (malaise, fatigue, INFs may cause flu like symptoms, anemia)
Track vital signs and Rate of PE
Rehab concerns: HIV
Opportunistic infections: look out for long term antibiotics and wash hands
Neuromuscular: pain, dysfunction, myopathy, peripheral neuropathy
Biktarvy
Antiretroviral agents in combo
Treatment for naive patients
bictegravir/emtricitabine/tenofovir alafenamide
Triumeg
dolutegravir/abacavir/lamivudine
Antiretroviral agents in combo
Treatment for naive patients
Types of Antiretroviral agents
NRTI NNRTI Protease Inhibitor Entry Inhibitors Integrase inhibitor
HAART
treatment for HIV
HIV treatment
HAART= highly active antiretroviral treatment
Synergistic drug-drug interation
Direct-Acting Antivirals (DAAs)
AE: fatigue, weakness, and headache
Also when combined with amiodarone will see bradycardia
Chronic Hepatitis C
In the past treatments hardly tolerated, now there are 11 DAA products to cure
Hepatitis B Treatment
Interferon- (injection) but causes flu like symptoms
Nucleoside/nucleotide analogs- (PO) better tolerated
Hepatitis A
Pre and post exposure prophylaxis
Vaccine, immune globulin, rest and hydration, antiemetics (nausea), antipyretics (fever)
2-6 months of recovery
Hepatitis
inflammation of the liver caused by a virus
Treatments for the flu
Oseltamavir (Tamiflu)
Baloxavir (Xofluza)
Antiviral endings
- ovir
- ivir
- alfa
- ine
Life cycle of a virus
Attachment to host cell Entry Replication Assembly Release (budding or host cell lysis)
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
Macrolide
antibiotic that fights Atypical pathogens causing pneumonia- this is a CYP450 inhibitor (look out for DDIs)
Fluroquinolone
Used to treat community acquired pneumonia- look out for tendon rupture
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
MRSA (Methicillin resistant Staphylococcus aureus)
On skin
Spread via contact
Treatments: linezoid and quinupristin/dalfopristin
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
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
Two Main Treatment Goals: TB
Contain and cure infection
This process can last months to a year
Latent vs. Active TB
Latent TB: carries bacteria without symptoms
Active: individuals are infectious and can spread disease
TB symptoms
fever, night sweats, malaise, weight loss
How does tuberculosis take effect?
Myobacterium tuberculosis is inhaled into lungs, aveoli and surrounded by macrophages to set off an immune response
How is TB transmitted?
airborne particles
What contributes to drug resistance?
overuse/misuse
international OTC antibiotics
Antibiotics in livestock
Types of Resistance
Innate: organism isnt susceptible
Acquired: Inactivated drug, modify drug target, export drug from bacteria, or bypass antibiotic inhibition
Antimicrobial resistance
when bacteria or other microbes become resistant to the effects of a drug after being exposed to it
Sulfamethoxazole/trimethoprim (Bactrim)
Sulfonamides
Steven-Johnsons syndrome
Sulfonamides
Sulfamethoxazole/trimethoprim (Bactrim, SMX/TMP)
Broad coverage of Gram - and +
AE: can cause allergy or steven johnson syndrome
Metronidazole (Flagyl)
Nitroimidazole antibiotic
Metallic taste
neuropathy
Nitroimidazole
Metronidazole (Flagyl)
Use: Anaerobes
AE: GI, metallic taste,
Uncommon: peripheral neuropathy
Fluroquinolones
Ciprofloxacin
Levofloxacin (levaquin)
Gram -
AE: GI, Photosensitivity
Rare: tendon rupture, significant hypoglycemia
Lincosamides
Clindamycin
Gram +
GI and can Cause cdiff
Tetracyclines
Doxycycline
Broad coverage gram + and - and atypicals
AE: GI or photosensitivity
Macrolides
Azithromycin (Z-pak)
Some gram + and -
AE: GI issues, QT prolongation, CYP450 inhibitor (DDI)
Aminoglycosides
Gentamicin
Usage: Gram +, P. aeruginosa
AE: ototoxicity and nephrotoxicity
Glycopeptides
Vancomycin
MRSA, Cdiff Increasing resistance (VRE)
AE: Hypotension
Cephalosporins
Cephalexin (Keflex), ceftriaxone (Rocephin)
Nosocomial infections, surgical prophylaxis
GI and Hypersensitivity
Penicillins
Amoxicillin, Amoxicillin/clavulanate (Augmentin) and Piperacillin/tazobactam(Zosyn)
Broad coverage of Gram+ and Gram-
AE: GI and hypersensitivity
MOA for antibacterials
Cell wall cell membrane protein synth dna synth dna strand
Broad vs Narrow
effective against many or few types of infection
3 considerations for selecting treatment
Bacterial factors (identify and susceptibility) Host specific factors (allergies, renal function, ect) Drug specific factors (DDI, route, ect)
Bactericidal
kill bacteria
Bacteriostatic
inhibit bacterial growth, requires an immune host
Gram negative
Positively charged but favors negatively charged compounds
Thinner cell wall (5-7 strands)
Gram Positive
Is negatively charges but favors positvely charged compounds
Thick cell wall (20-30 strands)
Antibiotic
Drug that is only actively against bacteria
Antimicrobial
Drug that is active against bacteria, virus, fungi, or parasite
Propofol
general anesthetic
causes loss of consciousness
General Anesthesia rehab concerns
Neuromuscular Weakness
Impaired airway clearance
Immune function suppressed
In older adults pulmonary complications or reduced cough reflex
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
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
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
Where does inhaled general anesthetics create a hang over effect?
Adipose tissue
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
General Anesthetics- types of inhaled
Gas (nitrous oxide) Volatile Liquids (halothane)
How are general anesthesia goals achieved?
Balanced anesthesia: combo of IV and inhaled anesthetics, analgesics and neuromuscular blocking agents
Goal of general anesthesia
loss of consciousness, analgesia, amnesia, skeletal muscle relaxation, inhibition of sensory and autonomic reflexes
General Anesthesia- Medullary Paralysis
Can have respiratory or cardiovascular collapse
General Anesthesia- Surgical Anesthesia
Completely unconscious and respiration is more regular
General Anesthesia- Delirium/Disinhibition
Will lose consciousness and respirations may change
General Anesthesia- Analgesia/Induction
May or may not remember but generally still conscious
Anesthesia (3 categories)
General: Iv and inhaled
Regional: Intrathecal and epidural
Local: Injection and topical
Anesthesia (3 categories)
General: Iv and inhaled
Regional: Intrathecal and epidural
Local: Injection and topical
Patient-controlled analgesia (PCA) side effects
Pharmacological side effects (AE to meds)
Problems with delivery
PCA- types of anesthetics
Opioids (Morphine, fetanyl, hydromorphine)
Local anesthetics (epidural)
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
What does PCA do?
Enables continuous pain control and lowers incidence side effects
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
Other rehab concerns with SLE drugs
Viral infections
Fungal infections
Photosensitivity
Rehab Concerns w/ SLE drugs (Bacterial Infections)
80 % of infections
soft tissue infection can lead to sepsis
Rehab concerns w/ SLE drugs (immunosupression)
Pts w/ SLE already risk for infection
Increased risk with DMARDS and steroids
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
SLE treatment (severe)
High Dose steroids
Immunosuppressants
SLE treatment (mild/moderate)
NSAIDS
Steroids
Antimalarials
Immunosupressants
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
Corticosteroids
Short term RA treatment
NSAIDS can help
Opioids for pain
Janus Kinase Inhibitors
Biological DMARD RA Route:PO Common AE: infection, nasopharyngitis Boxed warning: infections Tofacitinib (Xeljanz) Baricitinib (Olumiant)
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)
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)
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)
RA Treatment
Nonbiological DMARD
Biological DMARD (TNF inhibitors, NonTNF inhibitors and Janus Kinase inhibitors)
MOA: inflammation usually
rheumatoid arthritis (RA)
A chronic, progressive, systemic, inflammatory autoimmune disease
Often swollen and inflamed
Glucosamine- Chondroitin
Not recommended
But possibly help with OA
Antithrombotic effect
Intraarticular Steroids
OA treatment
Injections
Trimacincolone (Kenalog)
Methylprednisolone (Depo-Medrol)
Intraarticular hyaluronate
For hip or knee OA
MOA: visoelastic solution to provide joint lubrication
AE: injection site pain, swelling, rash
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)
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
Capsaicin cream
Neuropathic Treatment
AE: burning sensation and erythema
Gabapentin (Neurontin)
Neuropathic
GABA analog and anticonvulsant
AE: dizziness and drowsiness
INEXPENSIVE
Stimulus Independent- paroxysms
shooting or shock like
Stimulus Independent- paresthesia
numbness or tingling
Stimulus Independent- mechanical allodynia
normal stimulus that shouldnt cause pain but does
Stimulus Independent- Hyperalgesia
experiencing more pain than we would expect
Stimulus Independent
results from mechanical, thermal, or chemical stimuli
Stimulus Dependent
Shooting, shock-like, aching, crushing, burning
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
Diclofenac (Voltaren)
NSAID (topical)
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
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
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
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
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
Strong vs mild mu agonist
Strong: all but codeine and tramadol
Substantia Gelatinosa
gate keeper
rich in opioid receptors
Categories of Pain
Nocioceptive: injury, stabbing, aching
Neuropathic: burining, tingling sensation
Psychogenic: origin to psych
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
A fibers
myelinated and are localized pain
C fibers
unmyelinated and diffuse pain
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
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
DDI-Antagonistic
Effect
DDI- Synergistic
Response> sum of response to both
positive: HIV cocktail viral load suppression
negative: CNS depression with opioid and benzo
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.
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)
Receptor Change antagonism
Desensitization due to long term exposure to agonist
Pharmacokinetic antagonism
One drug induces or inhibits the metabolism of another
Physiologic antagonism
2 drugs with opposite effects
Chemical antagonism
2 substances that diminish the effect
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
Selectivity
Only bind to Beta 1 or Beta 2
Specificity
only bind to alpha or beta
Antagonist
Occupy receptors but do not activate
Agonist
Drugs occupy receptors= activate
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
Non-competitive antagonist
Greatly diminishes effect, increasing agonist will not overcome antagonist
Competitive Antagonist
Antagonist and agonist compete for receptor, higher concentration wins
ED50
Effective dose to get 50 % of expected response
Lower ED50= more potent drug b/c less drug is needed for greater effect
Emax
maximal response, receptors filled
Other drug targets
Enzymes and Non-human cells (penicillin-bacteria cell wall and oseltamauir-infected cells)
Boxed Warning
Calls attention to serious risks associated with medicine
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)
Therapeutic Index
Ratio of TD50 to ED50
Lower the TI= more likely AE/toxicity
Lipid soluble meds…
Cross BBB quicker
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
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
Distribution Vd?
Vd=total conc of drug in body/plasma
higher Vd= more drug in tissue
highly protein bound= less active drug in tissue
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)
Pharmacokinetics
What the body does to the drug (ADME)
Pharmacodynamics
How the drug affects the body (MOA, Potency, Efficacy)
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
Schedule V
Medical use and little to no abuse (ex: antidiarrheal, antitussive, analgesia)
Schedule IV
Medical use and low abuse (ex: tramadol, xanax, ambien)
Schedule III
Medical use and mid abuse (ex:codeine & anabolic steroids)
Schedule II
Medical Use and High abuse (ex: cocaine, meth, fetanyl, addy, oxy, hydros)
Schedule I
No medical use and high abuse ex:heroin, LSD, MaryJ
Brand
owned by manufacturer & uppercase
Generic
official name & lowercase
off-label
Using drugs for something not approved by the FDA (ex:different ages, diseases, or doses)
Off Patent
~20 years later other companies can make the drug without permission from the original manufacturers