Exam 2 II Flashcards
aspirin
- cox inhibitor; more selective for cox 1
- anti-inflammatory
acetaminophen
- cox 2 inhibitor
- more of analgesic than anti-inflammatory
- metabolized to cannabinoid
ibuprofen
- non-specific cox inhibitor
- anti-inflammatory AND analgesic
naproxen
- longer acting non-specific cox inhibitor
- anti-inflammatory
examples of NSAIDs / antipyretics
- aspirin
- acetaminophen
- ibuprofen
- naproxen
- methyl salicylate
- camphor
- menthol
- trolamine
- capsacin
methyl salicylate
- wintergreen oil
- counter irritant; cause low level stimulation of pain receptors so that pain is transmitted less
- metabolized to salicylic acid
camphor
counter irritant
menthol
counter irritant
trolamine
metabolized to salicylic acid
capsacin
- TRPV1 channels mediates sensation and pain
- TRPV1 agonist
- you become tolerant to the heat effect
- stimulating those channels keeps from pain mediation
examples of steroidal anti-inflammatory drugs
- hydrocortisone
- triamcinolone
- beclomethasone
- fluticasone
- mometasone
hydrocortisone
same as cortisol
What are the synthetic analogues of hydrocortisone and what effect does it have on them?
- triamcinolone
- beclomethasone
- fluticasone
- mometasone
- much more active
MOA of glucocorticoid /corticosteroid
decrease release and synthesis of cytokines and chemokines
examples of antihistamines
- these are H1 blockers
- diphenhydramine
- doxylamime
- cetirizine
- loratadine
- fexofenadine
- ketotifen
- pheniramine
With respect to antihistamines, what is the difference between sedating and non-sedating?
- sedation happens when you block H1 in the brain
- if it’s peripherally restricted -> no sedation
Which one of the anti-histamines are (non-) sedating?
- sedating: diphenhydramine and doxylamime
- somewhat sedating: cetirizine
- non-sedating: fexofenadine
example of mast cell stabilizer
cromolyn sodium
cromolyn sodium
- has almost no side effects
- stabilize mast cells that release inflammatory mediators
- Rx ophthalmic drops
What antitussive is available OTC?
dextromethorphan
dextromethorphan
- opioid structure
- MOA: blocks medullary cough center
levorphanol
- L- isomer of dextromethorphan
- potent opioid
example of expectorant
guafenesin
guafenesin
increases volume and decreases viscosity of bronchial /tracheal secretions
MOA of decongestants
alpha-1 adrenoceptor agonists
examples of decongestants
- phenylephrine
- pseudoephedrine
- naphazoline
- oxymetazoline
- tetrahydrozoline
What counseling point is important when dispensing nasal decongestants?
- take it for a few days
- if doesn’t work, then stop
- if you don’t stop, you’ll get rebound congestion and it’ll get worst
examples of local anesthetics
- lidocaine
- xylocaine
- benzocaine
- dyclonine
MOA of local anesthetics
- block pain neurotransmission through fast voltage-gated sodium channels
- jams up sodium channel in skin; causes decrease in pain transmission
examples of topical anti-microbials
- cetylpyridium
- Neosporin
- carbamide peroxide
- phenol
- terbenafine
- clotrimazole
- miconazole
- zinc pyrithone
- Permethrin
cetylpyridium
4° NH4 antiseptic
Neosporin
- neomycin gram- (a little+)
- polymyxin B gram-
- bacitracin gram+
carbamide peroxide
- broad spectrum antimicrobial
- oxidizing agen
phenol
local anesthetic and antimicrobial
terbenafine
- tinea pedis (foot fungus)
- corporis (ring worm)
clotrimazole
- tinea pedis (foot fungus)
- corporis (ring worm)
- anti-yeast
miconazole
- tinea pedis (foot fungus)
- corporis (ring worm)
- vaginal yeast infections
zinc pyrithone
- very weak
- used for dandruff
Permethrin
- fairly broad spectrum and weak
- insecticide from chrysanthemum
- lice treatment
What are the types of GI drugs?
- H2 blockers
- PPI
- Antacids
- Anti-gas
- Anti-diarrheals
- Laxatives
H2 blockers MOA and examples
- blocks H2 receptors in parietal cells -> decrease stomach acid
- ranitidine
- famotidine
PPI MOA
blocks H/K ATPase in parietal cells -> decrease stomach acid
Examples of antacids
- calcium carbonate
- magnesium / aluminum hydroxide
Anti-gas MOA and examples
- decrease surface tension on gas bubbles
- simethicone
examples of anti-diarrheals
- loperamide: µ opioid agonist → ↓ GI motility; actus on gut and low CNS activity
- bismuth subsalicylate: antibacterial / NSAID
examples of laxatives
- fiber
- PEG 3350
- bisacodyl
- senna
- docusate
fiber
draws water/ add bulk into stool
PEG 3350
draws water into stool
bisacodyl
stimulant (local irritant)
senna
stimulant (local irritant)
docusate
- stool softener
- surfactant - makes stool easier to pass
examples of acne drugs
- benzoyl peroxide: peeling agent - ↑ skin turnover → ↓ bacterial count
- salicylic acid: peeling agent, antibacterial, lyses pimples
Where are fast action potentials found?
- atria
- ventricles
- Purkinje fibers
Where are slow action potentials found?
- SA node
- AV node
What is responsible for automaticity of cardiac tissues?
pacemakers
Parasympathetic effect on SA and AV node
- ↓Ca++ channels
- ↑K+ channels
- ↓I-f currents
- ↓APs
- ↓HR
Sympathetic effect on SA and AV node
- ↑Ca++ currents
- ↑HR
What does after-depolarization lead to?
- getting a second stimulation during refractory period
- ineffective pumping throughout the body
conduction block
- abnormal conduction through AV node, bundle of His, bundle branch
- leads to stimulation of the tissue itself
What are the reasons for which conduction block can occur?
- Abnormal anatomy (Wolf-Parkinson White)
- Damaged cardiac tissue
What is the therapeutic class of Vaughn-Williams Classification?
anti-arrhythmic
What are the Vaughn-Williams Classification?
- Type I: sodium blockers
- Type II: beta blockers
- Type III: potassium channel blockers
- Type IV: calcium channel blockers
Type I VWC
- affect conductive tissue
- there are three types: IA, IB, IC
Type IA VWC
- medium affinity for Na+ channels
- bind inactivated version of sodium channels and keep them in their inactivated form
- ↓ conduction velocity
- ↑ refractoriness (will take longer for cell to recover)
- ↓ automaticity through sodium channels
- also blocks potassium channels -> increase repolarization time -> arrhythmia
examples of drugs for Type IA VWC
- procainamide
- disopyramide
- quinidine
Type IB VWC
- binds loosely to sodium channels
- inhibits over-stimulation to heart
- selective for depolarized tissue
examples of drugs for Type IB VWC
lidocaine
Type IC VWC
- high affinity for Na channel
- slows conduction of heart
- also blocks potassium channels
- arrhythmogenic
Torsades de Pointes
QT interval prolongation
examples of drugs for Type IC VWC
- propafenone
- flecainide
Type II VWC
- block beta receptors
- affect mostly SA node
- indirectly affect Ca channels; ↓sympathetic effects on Ca channels
- slows ventricular response to AFIB via AV node
Type III VWC
- block K channels but not completely
- leads to delayed repolarization
- lengthen refractory period
- also affect slow potassium channels in pacemakers
- increased QT prolongation
- can be arrhythmogenic - not for chronic use
examples of drugs for Type III VWC
in order of decreasing activity:
- ibutilide
- dofetilide
- sotalol
- amiodarone
pacemaker conduction
SA -> AV -> bundle of His -> Perkinje
Type IV VWC
- block Ca channels in SA and AV nodes
- slows conduction
- prolonged refractory
- slows ventricular response to AFIB
adenosine
- ↑K+ channels in atria and SA/AV nodes
- ↓automaticity
digoxin
- affects nodes
- ↓Ca channels
- ↑K+ channels
- parasymp. effects
angina definition and goals
- cardiac ischemia = decreased O2 to the heart
- increase O2 to heart or decrease O2 demand
Define demand (equation) with respect to cardiac output
CO = HR x PVR
What are the consequences of cardiac ischemia?
- thickening or tinning of heart muscle
- systolic hypotension
- contractility decrease
- myocardial damage
What are the factors that determine myocardial oxygen demand?
- heart rate
- preload
- after load
- contractility
What are the three major types of angina?
- fixed stenosis - stable occlusion
- coronary artery spasm
- unstable angina - dislodging -> thrombosis
MOA of nitrates
MOA cleaves nitrate → NO → ↑guanylate cyclase →↑ cGMP → vasorelaxation
In nitrates, what happens with quantity of dose?
- low doses: favor venous dilation; decrease preload, decrease O2 consumption -> less stress on the heart
- high doses: arterial AND venous dilation -> decrease both pre and after load
An example of drug-drug interaction with nitrate (that we discussed in class)
PDE5 inhibitor (denafils) -> both increase cGMP which would decrease the blood pressure way too much
coronary steal
- dilating vessels that are already dilated
- these vessels are small and they don’t really contribute to helping the heart itself