B-lactam antibiotics
- penicillins, cephalosporins, clavulanic acid, tazobactam, meropenem, ertapenem
-
MOA
: irreversibly inhibit transpeptidases (which normally link layers of peptidoglycan to make cell wall strong)
penicillins
B-LACTAM ANTIBIOTIC
- bactericides
- time dependent
- selectively toxic (inhibit transpeptidase)
benzathine penicillin
- Natural Penicillin
-
SOA
: primarily gram (+) & also gram (-) cocci
- Susceptible to beta lactamase
-
Administration
: IM, slowly absorbed
amoxicillin
- Amino PCNs
-
SOA
: improved activity against gram (+) & gram (-) relative to natural PCNs
- Susceptible to beta lactamase
piperacillin
- Extended spectrum PCN
-
SOA
: same as amino PCN + most gram (-)
cefazolin
- 1st gen. cephalosporin
-
SOA
: most gram (+)
- often used for surgical prophylaxis (good tissue penetration)
cefuroxime
- 2nd gen. cephalosporin
-
SOA
: extended gram (-) activity relative to 1st gen., but less gram (+)
CefurOXime=oxygen
"respiratory cephalosporins"
- resistant to beta-lactamase
ceftriaxone
- 3rd gen. cephalosporin
-
SOA
: extended gram (-) activity relative to 2nd gen.
- resistant to beta-lactamase
- effective in penetrating the BBB
cefTRIaxone (TRI=3rd generation-->penetrates BBB)
cefepime
- 4th gen. cephalosporin
-
SOA
: extended spectrum agents with similar activity against gram (+) as 1st gen.
- greater resistance to beta-lactamase than 3rd gen.
- many cross BBB (effective against meningitis)
cefePIME=PRIME cephalosporin=4th generation=E
ceftaroline
- 5th gen. cephalosporin
-
SOA
: good resistance to beta-lactamase
- effective against multi-drug resistant bacteria (S. aureus & S. pneumonia)
Ceftaroline=Cephalosporin named after CAROLINE=5th generation=effective against STAPH
clavulanic acid, tazobactam
B-lactamase inhibitor ANTIBIOTIC
meropenem, ertapenem
- CARBAPENEM ANTIBIOTICS
-
broad SOA
: both gram (+) & (-)
- not effective against multi-drug resistant bacterial strains
vancomycin
- GLYCOPEPTIDE ANTIBIOTIC
-
MOA
: binds to peptidoglycan polymer, disrupting cell wall synthesis
-
SOA
: gram (+)
-
Adverse Rxns
: hypersensitivity, tachycardia & hypotension, "Red Man" syndrome, ototoxicity
- concentration dependent drug (ability to kill
Protein Synthesis Inhibitor Antibiotics
azithromycin, clindamycin, doxycycline
azithromycin
- MACROLIDE (2nd gen.) ANTIBIOTIC (protein synthesis inhibitor) azrithoMycin=Macrolide
- improved oral bioavailability
- extended half life compared to 1st gen. (can take orally)
-
SOA
: broad spectrum
-
MOA
: prevents translocation of tRNA from A site --
clindamycin
- LINCOSAMIDE ANTIBIOTIC (protein synthesis inhibitor)
cLindamycin=Lincosamide
-
SOA
: broad spectrum
-
MOA
: prevents translocation of tRNA from A site --> P site
doxycycline
- TETRACYCLINE ANTIBIOTIC (protein synthesis inhibitor)
-
SOA
: broad spectrum
-
MOA
: bind to 30S subunit & directly block the binding of tRNA to A site (bacteriostatic)
doxy=Tetracycline=binds to Tetrasubsunit (protein synthesis inhibitor)=STATIC=it is
metronidazole
- DNA DAMAGING ANTIBIOTIC
**Metro ppl are RADICAL AND DAMAGE DNA, especially anaerobic=PARASITEs (parasitic infections)
- nitroimidazole
-
SOA
: broad spectrum, some parasites
-
MOA
: reduction of drug creates cytotoxic free radicals --> DNA strand breaka
levofloxacin
- DNA DAMAGING ANTIBIOTIC
- 2nd gen. fluoroquinolone
-
SOA
: less effective against gram (+)
-
MOA
: bind to DNA gyrase --> produces double stranded breaks in DNA (bactericidal)
-
Selective Toxicity
: only works for bacterial enzyme
ciprofloxacin
- DNA DAMAGING ANTIBIOTIC
- 3rd / 4th gen. fluoroquinolone
-
SOA
: broad spectrum, anaerobic bacteria
-
MOA
: bind to DNA gyrase --> produces double stranded breaks in DNA (bactericidal)
sulfamethoxazole, trimethoprim
- DNA SYNTHESIS INHIBITOR ANTIBIOTIC
- sulfonamide
-
SOA
: broad spectrum
-
Selective Toxicity
: bacteria must synthesize folic acid (host cell lacks dihydropteroate synthase)
morphine
- OPIOID ANALGESIC
-
MOA
: full mu receptor
agonist
(analgesia, sedation, euphoria, constipation, respiratory depression)
fentanyl
- OPIOID ANALGESIC
-
MOA
: full mu receptor
agonist
- no analgesic relative to morphine (
greater toxicity
)
- more lipophilic than morphine (
faster acting
)
- transdermal application for chronic pain
tramadol
- OPIOID ANALGESIC
-
MOA
: full mu receptor
agonist
- efficacy similar to codeine + acetaminophen
- racemic mixture (+ is prodrug of weak opioid; - inc. synaptic NE & 5HT levels)
- analgesia not fully reversed by naltrexone
- increased incidence of seizur
codeine & tramadol
drugs that require enzyme CYP2D6 to be fully activated
naloxone
- OPIOID ANTAGONIST
-
MOA
: mu receptor antagonist
- reverse adverse effects of full agonists (respiratory depression)
- diagnose physical dependence to opioids
aspirin
- NSAID (salicylate)
-
MOA
: covalently modifies COX 1 & 2 -->
irreversible inhibition of COX activity
- duration of effects depends on rate of COX turnover
- more selective for
COX 1
- analgesia, antipyresis, anti-inflammatory (COX 2-mediated)
- prophyla
ibuprofen
- NSAID (propionic acid derivative)
- 400 mg ibuprofen = greater relief than (aspirin 650 mg + codeine 60 mg)
- less likely produce GI side effects compared to aspirin
-
MOST commonly used NSAID
naproxen
- NSAID (propionic acid derivative)
- antipyretic
acetaminophen
- NSAID (para-aminopherols)
-
MOA
: inhibition of
central COX
(does not inhibit peripheral inflammation or platelet aggregation)
- antipyretic analgesic
- adverse effect = hepatotoxicity (depletion of glutathione & accumulation of NAPQ1)
fluconazole
- ANTIFUNGAL
-
MOA
: inhibit 14a-sterol demethylase --> halt synthesis of ergosterol (NOTE: cytP450 absent in most host cells)
- high bioavailability, good BBB permeability
terbinafine
- ANTIFUNGAL
-
MOA
: inhibits squalene epoxidase --> halt synthesis of ergosterol
atorvastatin, rosuvastatin
- CHOLESTEROL MEDICATION
-
MOA
: HMG-CoA reductase inhibitors --> inhibit cholesterol synthesis in liver (LDL receptors up-regulated & increased removal of LDL from blood)
- myopathy with risk for rhabdomyolysis
- interaction with grapefruit juice
enoxaparin
- HEPARIN ANTICOAGULANT
-
MOA
: indirectly inhibit thrombin via
anti-thrombin III
(parenteral; must be given IV or SC)
- low molecular weight heparin
- less activity
unfractionated heparin
- HEPARIN ANTICOAGULANT
-
MOA
: indirectly inhibit thrombin via
anti-thrombin III
(parenteral; must be given IV or SC)
- combination of low & high molecular weight
- more activity
warfarin****
- ORAL ANTICOAGULANT
-
MOA
: inhibit vitamin K epoxide reductase --> prevent vitamin K reactivation
- CYP2C9 reduces metabolism --> inc. bleeding risk
- VKORC1 reduces sensitivity --> inc. clotting risk
- antidote = vitamin K
- outpatient Tx of DVT
dabigatran etexilate
- ANTICOAGULANT
- ORAL DTI
-
MOA
: directly inhibit thrombin activation
- less bleeding risk compared to warfarin
- antidote antibody available
rivaroxaban
- ANTICOAGULANT
- Factor Xa INHIBITOR
-
MOA
: prevents prothrombin activation to thrombin
- reduced bleeding risk compared to warfarin
amlodipine
- CALCIUM CHANNEL BLOCKER (for Tx of Coronary Heart Disease & HTN / angina)
-
non-cardioactive
-
MOA
: block L-type voltage-dependent calcium channels on cardiac & vascular smooth muscle
- vasodilator used to treat
stable angina pectoris
aspirin, clopidogrel, prasugrel
ANTI-PLATELET DRUGS - prevent white thrombi
(for Tx of Coronary Heart Disease)
clopidogrel
- ANTI-PLATELET DRUG
-
MOA
: ADP receptor blocker (disrupting aggregation)
-
prodrug
metabolized by CYP2C19
- lots of drug interactions
prasugrel
- ANTI-PLATELET DRUG
-
MOA
: ADP receptor blocker (disrupting aggregation)
-
prodrug
with more consistent effects
omeprazole
-
MOA
: proton pump inhibitor (irreversible inhibition of acid release by forming covalent bonds with H+/K+ ATPase)
-
first line
Tx for PUD / GERD
- suppress active pumps only
- selectively inhibits CYP450 (diazepam)
famotidine
-
MOA
: histamine (H2) receptor antagonist
- Tx for PUD / GERD
- less effective than PPI
ondansetron
-
MOA
: serotonin receptor antagonist (block 5HT3 receptors in small bowel, vagus n. & chemoreceptor trigger zone)
- Tx for
visceral nausea
promethazine, chlorpromazine
-
MOA
: dopamine D2 receptor antagonist (block D2-like dopamine receptors, limiting emetic input to medullary vomiting center)
- Tx for
visceral nausea
- extensive side effect profile
hydrochlorothiazide
- THIAZIDE DIURETIC
-
MOA
: inhibit sodium reabsorption from distal tubule (side effect of hypokalemia)
- long-term Tx of HTN
diltiazem
- CCB (Tx of HTN)
-
cardioactive
CCB
-
MOA
: block voltage-dependent calcium channels on vascular smooth muscle (reduce CO)
lisinopril
- ACE INHIBITOR (Tx of HTN)
-
MOA
: inhibit conversion of ang I --> ang II (block effects of RAAS)
- hyperkalemia & teratogenic
losartan
- ANGIOTENSIN RECEPTOR BLOCKER (ARB)
- Tx of HTN
-
MOA
: competitive antagonist at AT1 angiotensin receptors
- hyperkalemia & teratogenic
ethinyl estradiol
- ORAL CONTRACEPTIVE
- estrogen alone inc. risk of endometrial cancer (when given in combination with a
progestin
, reduced risk)
- estrogen HRT (used w/progestin)
levonorgestrel
- ORAL CONTRACEPTIVE
- Plan B = high dose (morning after pill)
- synthetic progestin
Leveon PLays PRO=got her pregnant=buy plan B
drospirenone
- ORAL CONTRACEPTIVE
- progestin component of many combination hormonal contraceptives
-
MOA
: blocks mineralocorticoid & androgen receptors
-
USE
: reduced acne, hirtuism, weight gain & fluid retention
tamsulosin
- BPH Tx
-
MOA
: alpha 1a selective antagonist --> relax prostate & urethral smooth muscle to relieve LUTS
- does NOT slow progression of the disease, just relieves symptoms
sildenafil, tadalafil
- ED Tx
-
MOA
: inhibit PDE-5 (prevent breakdown of cyclic GMP, increased blood flow)
-
INTERACTION
: never use with nitrates (which increase cyclic GMP production --> severe hypotension)
-aFIL=inhibit 5, NO BREAKDOWN=INCREASED FIL, INCREASE FLOW=NEVER us
albuterol
- SHORT ACTING B2-adrenergic agonist
-
MOA
: relax bronchial / arterial smooth m., glucose mobilization
- bronchodilation
-
USE
: asthma short acting reliever (rescue relief)
salmeterol
- LONG ACTING B2-adrenergic agonist
-
MOA
: relax bronchial / skeletal m., glucose mobilization
- bronchodilation
-
USE
: asthma controller, not as monotherapy
fluticasone, budesonide
- INHALED GLUCOCORTICOID CONTROLLER (asthma)
-
MOA
: targets bronchoconstriction (B2 agonist) & targets inflammation (inhibit leukotriene synthesis & regulate NE & histamine)
atropine
-
MOA
: muscarinic receptor
antagonist
-
DECREASE SALIVATION
pilocarpine
-
MOA
: muscarinic receptor
agonist
-
INCREASE SALIVATION
Glucocorticoid Steroid Medications
-ones" = anti-inflammatory effects
-
MOA
: promote exchange of sodium & potassium in kidneys --> sodium & water retention / potassium excretion
- avoid administering >2 weeks at a time
prednisone, prednisolone
SHORT ACTING glucocorticoids
triamcinolone
INTERMEDIATE ACTING glucocorticoid
betamethasone, dexamethasone
LONG ACTING glucocorticoid