Exam 2 II Flashcards
1
Q
aspirin
A
- cox inhibitor; more selective for cox 1
- anti-inflammatory
2
Q
acetaminophen
A
- cox 2 inhibitor
- more of analgesic than anti-inflammatory
- metabolized to cannabinoid
3
Q
ibuprofen
A
- non-specific cox inhibitor
- anti-inflammatory AND analgesic
4
Q
naproxen
A
- longer acting non-specific cox inhibitor
- anti-inflammatory
5
Q
examples of NSAIDs / antipyretics
A
- aspirin
- acetaminophen
- ibuprofen
- naproxen
- methyl salicylate
- camphor
- menthol
- trolamine
- capsacin
6
Q
methyl salicylate
A
- wintergreen oil
- counter irritant; cause low level stimulation of pain receptors so that pain is transmitted less
- metabolized to salicylic acid
7
Q
camphor
A
counter irritant
8
Q
menthol
A
counter irritant
9
Q
trolamine
A
metabolized to salicylic acid
10
Q
capsacin
A
- TRPV1 channels mediates sensation and pain
- TRPV1 agonist
- you become tolerant to the heat effect
- stimulating those channels keeps from pain mediation
11
Q
examples of steroidal anti-inflammatory drugs
A
- hydrocortisone
- triamcinolone
- beclomethasone
- fluticasone
- mometasone
12
Q
hydrocortisone
A
same as cortisol
13
Q
What are the synthetic analogues of hydrocortisone and what effect does it have on them?
A
- triamcinolone
- beclomethasone
- fluticasone
- mometasone
- much more active
14
Q
MOA of glucocorticoid /corticosteroid
A
decrease release and synthesis of cytokines and chemokines
15
Q
examples of antihistamines
A
- these are H1 blockers
- diphenhydramine
- doxylamime
- cetirizine
- loratadine
- fexofenadine
- ketotifen
- pheniramine
16
Q
With respect to antihistamines, what is the difference between sedating and non-sedating?
A
- sedation happens when you block H1 in the brain
- if it’s peripherally restricted -> no sedation
17
Q
Which one of the anti-histamines are (non-) sedating?
A
- sedating: diphenhydramine and doxylamime
- somewhat sedating: cetirizine
- non-sedating: fexofenadine
18
Q
example of mast cell stabilizer
A
cromolyn sodium
19
Q
cromolyn sodium
A
- has almost no side effects
- stabilize mast cells that release inflammatory mediators
- Rx ophthalmic drops
20
Q
What antitussive is available OTC?
A
dextromethorphan
21
Q
dextromethorphan
A
- opioid structure
- MOA: blocks medullary cough center
22
Q
levorphanol
A
- L- isomer of dextromethorphan
- potent opioid
23
Q
example of expectorant
A
guafenesin
24
Q
guafenesin
A
increases volume and decreases viscosity of bronchial /tracheal secretions
25
MOA of decongestants
alpha-1 adrenoceptor agonists
26
examples of decongestants
- phenylephrine
- pseudoephedrine
- naphazoline
- oxymetazoline
- tetrahydrozoline
27
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
28
examples of local anesthetics
- lidocaine
- xylocaine
- benzocaine
- dyclonine
29
MOA of local anesthetics
- block pain neurotransmission through fast voltage-gated sodium channels
- jams up sodium channel in skin; causes decrease in pain transmission
30
examples of topical anti-microbials
- cetylpyridium
- Neosporin
- carbamide peroxide
- phenol
- terbenafine
- clotrimazole
- miconazole
- zinc pyrithone
- Permethrin
31
cetylpyridium
4° NH4 antiseptic
32
Neosporin
- neomycin gram- (a little+)
- polymyxin B gram-
- bacitracin gram+
33
carbamide peroxide
- broad spectrum antimicrobial
| - oxidizing agen
34
phenol
local anesthetic and antimicrobial
35
terbenafine
- tinea pedis (foot fungus)
| - corporis (ring worm)
36
clotrimazole
- tinea pedis (foot fungus)
- corporis (ring worm)
- anti-yeast
37
miconazole
- tinea pedis (foot fungus)
- corporis (ring worm)
- vaginal yeast infections
38
zinc pyrithone
- very weak
| - used for dandruff
39
Permethrin
- fairly broad spectrum and weak
- insecticide from chrysanthemum
- lice treatment
40
What are the types of GI drugs?
- H2 blockers
- PPI
- Antacids
- Anti-gas
- Anti-diarrheals
- Laxatives
41
H2 blockers MOA and examples
- blocks H2 receptors in parietal cells -> decrease stomach acid
- ranitidine
- famotidine
42
PPI MOA
blocks H/K ATPase in parietal cells -> decrease stomach acid
43
Examples of antacids
- calcium carbonate
| - magnesium / aluminum hydroxide
44
Anti-gas MOA and examples
- decrease surface tension on gas bubbles
| - simethicone
45
examples of anti-diarrheals
- loperamide: µ opioid agonist → ↓ GI motility; actus on gut and low CNS activity
- bismuth subsalicylate: antibacterial / NSAID
46
examples of laxatives
- fiber
- PEG 3350
- bisacodyl
- senna
- docusate
47
fiber
draws water/ add bulk into stool
48
PEG 3350
draws water into stool
49
bisacodyl
stimulant (local irritant)
50
senna
stimulant (local irritant)
51
docusate
- stool softener
| - surfactant - makes stool easier to pass
52
examples of acne drugs
- benzoyl peroxide: peeling agent - ↑ skin turnover → ↓ bacterial count
- salicylic acid: peeling agent, antibacterial, lyses pimples
53
Where are fast action potentials found?
- atria
- ventricles
- Purkinje fibers
54
Where are slow action potentials found?
- SA node
| - AV node
55
What is responsible for automaticity of cardiac tissues?
pacemakers
56
Parasympathetic effect on SA and AV node
- ↓Ca++ channels
- ↑K+ channels
- ↓I-f currents
- ↓APs
- ↓HR
57
Sympathetic effect on SA and AV node
- ↑Ca++ currents
| - ↑HR
58
What does after-depolarization lead to?
- getting a second stimulation during refractory period
| - ineffective pumping throughout the body
59
conduction block
- abnormal conduction through AV node, bundle of His, bundle branch
- leads to stimulation of the tissue itself
60
What are the reasons for which conduction block can occur?
- Abnormal anatomy (Wolf-Parkinson White)
| - Damaged cardiac tissue
61
What is the therapeutic class of Vaughn-Williams Classification?
anti-arrhythmic
62
What are the Vaughn-Williams Classification?
- Type I: sodium blockers
- Type II: beta blockers
- Type III: potassium channel blockers
- Type IV: calcium channel blockers
63
Type I VWC
- affect conductive tissue
| - there are three types: IA, IB, IC
64
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
65
examples of drugs for Type IA VWC
- procainamide
- disopyramide
- quinidine
66
Type IB VWC
- binds loosely to sodium channels
- inhibits over-stimulation to heart
- selective for depolarized tissue
67
examples of drugs for Type IB VWC
lidocaine
68
Type IC VWC
- high affinity for Na channel
- slows conduction of heart
- also blocks potassium channels
- arrhythmogenic
69
Torsades de Pointes
QT interval prolongation
70
examples of drugs for Type IC VWC
- propafenone
| - flecainide
71
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
72
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
73
examples of drugs for Type III VWC
in order of decreasing activity:
- ibutilide
- dofetilide
- sotalol
- amiodarone
74
pacemaker conduction
SA -> AV -> bundle of His -> Perkinje
75
Type IV VWC
- block Ca channels in SA and AV nodes
- slows conduction
- prolonged refractory
- slows ventricular response to AFIB
76
adenosine
- ↑K+ channels in atria and SA/AV nodes
| - ↓automaticity
77
digoxin
- affects nodes
- ↓Ca channels
- ↑K+ channels
- parasymp. effects
78
angina definition and goals
- cardiac ischemia = decreased O2 to the heart
| - increase O2 to heart or decrease O2 demand
79
Define demand (equation) with respect to cardiac output
CO = HR x PVR
80
What are the consequences of cardiac ischemia?
- thickening or tinning of heart muscle
- systolic hypotension
- contractility decrease
- myocardial damage
81
What are the factors that determine myocardial oxygen demand?
- heart rate
- preload
- after load
- contractility
82
What are the three major types of angina?
- fixed stenosis - stable occlusion
- coronary artery spasm
- unstable angina - dislodging -> thrombosis
83
MOA of nitrates
MOA cleaves nitrate → NO → ↑guanylate cyclase →↑ cGMP → vasorelaxation
84
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
85
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
86
coronary steal
- dilating vessels that are already dilated
| - these vessels are small and they don't really contribute to helping the heart itself
87
MOA of beta blockers
- ↓β1-adrenoceptors
- ↓HR & contractility
- ↓myocardial oxygen consumption
88
examples of Ca blockers
- verapamil
- amlodipine
- nifedipine
- nicardipine
- diltiazem
89
MOA of Ca blockers
- ↓ voltage-gated Ca++ channels
- ↓contractility
- ↓HR (slight)
- ↓myocardial oxygen consumption
- will also decrease preload
90
Drugs for angina
- beta blocker
- Ca blocker
- ranolazine
- ivabradine
91
ranolazine
- ↓ intracellular sodium level
- ↓ sodiumdependent calcium channels
- ↓myocardial contractility
- ↓myocardial oxygen demand
92
ivabradine
- ↓ If sodium current in the SA node
- ↓myocardial APs in SA node
- ↓HR
- ↓myocardial oxygen demand
- Little to no effect on BP, contractility and conductance
93
examples of inotropes
- Cardiac Glycosides
- Beta agonists
- Phosphodiesterase (PDE) inhibitors
94
Cardiac Glycosides
- digoxin
- blocks Na/K ATPase
- increases intracell. Ca and Na
- increase contractility and decreased heart rate
- parasymp. stimulation
- can lead to arrhythmias
95
What happens to digoxin in hypokalemia?
higher affinity for Na/K ATPase
96
examples of beta agonists
- dopamine
- dobutamine
- isoproterenol
97
dopamine
- dose dependent
- low dose: inotrophic effect, ↑ contractility
- high doses: ↑ contractility AND α adrenoceptor stimulation → vasoconstriction
- cut off is at 10 µg/kg/min
98
dobutamine
- favors β1 but also stimulates β2
| - ↑ inotropy
99
isoproterenol
- nonselective β agonist
- ↑ inotropy /chronotropy
- ↓ PVR, ↑HR
100
examples of PDE3 inhibitors
- inamrinone
| - milrinone
101
effect of PDE3 inhibitors
- ↑ cAMP
- ↑ myocardial contractility
- ↑ CO
- ↑ myocardial relaxation
- ↑ arteriole>venous dilation
- ↓ afterload> preload
102
lusitropy
- myocardial relaxation
| - how well the heart is going back to its resting state between beats
103
chronotropy
- heart rate
| - due to conduction system of heart
104
inotropy
- contractility of heart
| - due to contract of heart muscle
105
What innervates 60-80% of neurons?
- glutamate
- major excitatory neurotransmitter in the
CNS
106
What are the receptors for glutamate?
- NMDA
- AMPA
- they are ion channels
- when they are bound -> neurotransmission
107
What are the inhibitory neurotransmitters?
- GABA - released via CNS
- glycine - released via brainstem and spinal cord
- hyperpolarize neuron
108
What is responsible for the fine tuning of the brain?
Monoamine neurotransmitters:
- DA
- NE
- 5-HT (serotonin)
109
What does fine tuning mean?
can tweak considerably and still be alive
110
What are drugs that are not a benzodiazepine but have the same effects?
- zolpidem
| - zaleplan
111
MOA of GABA(a) agonists
- Cl channel
- Cl goes into cell
- hyperpolarize cell
112
Effects of benzo's and GABA(a) agonists
- muscle relaxation
- sedation
- anti-anxiety
- hyponosis
113
ADR of benzo's / GABA(a) agonists
- sedation
- muscle relaxation
- stimulatory effects
- anterograde amnesia
- psychological dependence
114
melatonin
involved in circadian clock
115
suvorexant
- orexin antagonist
| - associated with "wake" part in the sleep/wake cycle
116
disease states of spasticity of muscle
- CP
- MS
- MG
- sroke
- spinal injury
117
mechanisms against spasticity
- ↓ activity of nerve fibers that excite motor neurons
| - ↑ activity of inhibitory interneurons (i.e., GABA)
118
baclofen
- GABA(b) agonist
- skeletal muscle relaxant
- mostly used for milder spasticity diseases
119
tizanidine
- central alpha-2 agonist
- skeletal muscle relaxant
- decrease NE
120
dantrolene
- calcium blockers via ryanodrine receptor
| - skeletal muscle relaxant
121
misc. skeletal muscle relaxants
- carisoprodol
- cyclobenzaprine
- chlorzoxazone
122
define depression
decreased of synaptic transmission of 5-HT, NE, and DA in brain
123
How can you treat depression to get clinical results quicker?
- NMDA receptor antagonist (ex. ketamine)
- stimulation of dopaminergic pathway
- keeping BDNF in the brain
124
iproniazid
- MAO inhibitor
| - used for depression
125
reserpine
used for BP but also depletes stores of NT -> depression
126
examples of tricyclic antidepressants
- amitripyline
| - imipramine
127
MOA of tricyclic antidepressants
- inhibit reuptake of NT
| - block specific 5-HT receptors
128
ADR of tricyclic antidepressants
- drowsiness
- CNS stimulation
- hypotension
- dry mouth, blurred vision
- increased suicide risk
129
examples of SSRI
- fluoxetine
- paroxetine
- citalopram
- escitalopram
- sertraline
130
MOA of SSRI
inhibit reuptake of 5-HT
131
ADR of SSRI
- decreased libido
- drowsiness
- insomnia
- dry mouth
- increase suicide risk
132
MOA of SNRI
- inhibit reuptake of 5-HT and NE
133
examples of SNRI
venlafaxine
134
ADR of SNRI
- drowsiness
- insomnia
- increased suicide risk
- FYI may work better than anxiety patients
135
examples of DNRI
bupropion
136
MOA of DNRI
inhibit reuptake of NE and DA
137
ADR of DNRI
- less change of weight gain
- decreased libido
- should not be used on patients with insomnia
138
lithium
- drug of choice for manic phase of bipolar disorder
139
MOA of lithium
decreases neuronal signaling proteins
140
ADR of lithium
- metallic taste
- lethargy
- cognition problems
- muscle spasms
- cleared by kidneys; if pt on diuretic, will decrease levels of this
141
MOA of anti-epileptics
- Na channel blocker/ inactivator
- Ca channel blocker/ inactivator
- Cl channel enhancers (via GABA)
- down-regulation of neuronal firing
- Glutamate antagonism
- K enchancement
142
anti-epileptics and metabolism
- highly lipophilic -> high protein binding
| - CYP450 inducer
143
phenytoin
- antiepileptic
- Na channel blocker
- Michaelis Menten metabolism
144
carbamazepine
- antiepileptic
| - Na blocker
145
ethosuximide
- antiepileptic
- Ca blocker
- drug of choice for absence seizures
- ADR: can make other types of seizures worst
146
gabapentin
- antiepileptic
- can also be used for: fibromyalgia, headache
- Ca blocker
147
lamotrigine
- antiepileptic
- Na and glutamate blockers
- also used for bipolar
148
valproate
- antiepileptic
- broad: affects Na, Ca, GABA, etc
- also used for: pain, bipoar
149
dopamine pathway: mesocortical
affect thoughts; cognition and processing information
150
dopamine pathway: nigrostriatal
affect movement
151
dopamine pathway: tuberoinfundibular
regulate prolactin level
152
L-DOPA
- enters CNS but broken down by DOPA decarboxylase, COMT, and MAO
153
carbidopa
- peripheral DOPA decarboxylase inhibitor
| - given with L-DOPA to increase DA in CNS
154
tolcapone
COMT inhibitor
155
selegeline
MAO inhibitor
156
schizophrenia
- increased DA in CNS
| - psychosis
157
chlorpromazine
- class: phenothiazines
- used for psychosis
- non-specific D2 receptor blockers
- ADR: can also block ACh, H, NE; can cause pseudo-Parkinson
158
haloperidol
- used for psychosis
- increased D2 blocking activity
- ADR: non-selective so also blocks nigrostriatal
159
serotonin receptor antagonist
- used for psychosis
- clozapine
- risperidone
- aripiprazole
160
aripiprazole
- serotonin receptor antagonist
| - has dopaminergic activity and can help with Parkinsons
161
clozapine
- serotonin receptor antagonist
| - best agent but causes severe blood effects
162
What is the site of action of local anesthetics?
- bind to Na channels to block nerve conduction
| - decrease membrane permeability of Na
163
What happens with the administration of local anesthetics?
- nerve excitation threshold increases
- impulse conduction slows
- action potential declines
164
What are factors that affect a nerve's susceptibility to blockade by local anesthetics?
- myelination
- pH
- location of administration
- plasma protein binding
- metabolism
165
susceptibility to nerve blockade by LA: myelination
myelinated fibers more sensitive because they interact with nodes of ranvier
166
susceptibility to nerve blockade by LA: diameter
- smaller is more sensitive
| - 3 nodes must be exposed --> smaller diameter = more nodes exposed
167
loss of sensation in decreasing order
pain > cold > warmth > touch > deep pressure > motor
168
How can you create intracellular acidosis when administering LA?
administer solutions saturated with CO2
169
Why would you need to create intracellular acidosis with respect to LA?
- to make the drug into the cationic form
| - the cation form binds to Na channel
170
Onset of blockade is increased with addition of bicarbonate. Why is this?
- increases concentration of uncharged form of drug
| - more can pass through membrane
171
Percent of protein bound drug with respect to pH
decrease pH = decrease binding
172
What are the classes of anesthetics?
- esters
| - amide
173
What happens to esters in circulation?
- inactivated by hydrolysis
| - spinal fluid doesn't contain much esterases
174
How does amides get inactivated?
- metabolism by liver enzymes
| - but some metabolites are more active than their parent compound
175
What rx is a mixed structure between the two groups of LA?
- articaine
- classified as amide but ester required for binding
- hydrolysis of ester terminates action
- used for dental procedures
176
How does age affect plasma binding of LA?
- neonates and elders have fewer plasma binding proteins
| - elder have lower CO -> slow delivery to liver
177
How does lipid solubility affect LA rx?
- improve diffusion through neuronal membrane
| - reduce diffusion through extracellular fluids
178
What are examples of drugs with contain the vasoconstrictor enhancement effects?
- epi
- levonordefrin
- oxymetazoline
179
ADR of LA
- drowsiness
- CNS stimulation
- tongue numbness, metallic taste
- nystagmus / muscle twitching
- convulsions
180
What are the LA effects to the cardiovascular system?
- decrease pacemaker activity
| - hypotension
181
Which LA are antiarrythmic drugs?
- lidocaine
| - procainamide
182
Which LA is cardiotoxic?
bupivacaine
183
What are LA formulated with that can provoke allergic reactions?
- preservatives
| - anti-oxidants
184
methemoglobinemia
accumulation of hydrolytic metabolites
185
How can methemoglobinemia occur?
- administering > 400mg of prilocaine in adults
| - administering benzocaine to gums / mouth in children < 2 years
186
What symptoms does methemoglobinemia produce?
- cyanosis
- SOB
- faituge
- increased heart rate
- headache, lightheadedness, confusion
187
ADR of EPI
- decrease peripheral resistance
- increase heart rate
- increase stroke volume
- in higher doses: heart palpitations, increase BP, CP
188
ADR of phenylephrine
- increase BP
| - increase HR
189
ADR of nordefrin
- increase BP
| - increase HR
190
properties of lidocaine
- amide
- potent
- rapid onset
- ADR: drowziness, heart block, arrythmia, hypotension
191
properties of mepivacaine
3% solution has its own vasoconstriction and doesn't need to be formulated with EPI
192
Which LA will give paresthesia (numbness / tingling) with a 4% solution?
articaine
193
Which LA is metabolized into PABA?
- Procaine
- Tetracaine
- PABA inhibits sulfonamide drugs
194
What is the LA that can be used intra-nasally?
Tetracaine + Oxymetazoline
195
With respect to the physical state of the skin, when is the potential for toxicity greater than normal?
when skin or mucous membrane is abraded and/or if applied to large surface area
196
Characteristics of ideal anesthetic
- rapid onset of action
- wide safety margin
- permit rapid recovery
- devoid adverse effects
197
Examples of inhaled anesthetics
- fluranes: volatile liquids
| - NO
198
If we can't measure how much drug gets into the brain, how do we measure how much medication reach CNS via inhalation route?
- assume equilibrium and measure how much gets into the lung
- Palv is used for substitute for Pcns
199
How do you compare potencies of gases?
- MAC: median alveolar concentration
| - concentration that produces immobility of 50% of patients
200
Factors that affect potency of therapeutic gas
- lipid solubility
- age
- body temp
- hematocrit
- PaO2, PaCO2
- current CNS being used
201
Factors that affect rate of induction of general anesthesia
- solubility (in different compartments)
- pulmonary ventilation
- pulmonary blood flow
202
Rate of induction consequences
- ↑ delivery of gas by ↑ ventilation
→ ↑ Palv
- ↑ Rate of uptake into blood by ↓ cardiac output (↓ pulmonary blood flow)
203
respiratory anesthetics
- resp. depressant
- ↓ response to CO2
- ↑ resp. rate
- ↓ tidal volume
- ↓ musociliary function
204
propofol
- GABAa and Glycine-R activator
- rapid recovery
- less N/V
- no histamine release
- no analgesic properties
205
etomidate
- enhance GABA but not glycine
- maintain CV stability
- induce nausea and vomiting
206
ketamine
- analgesia, amnesia, catalepsy
- NMDA agonist
- ADR: floating sensation, hallucinations, HTN, ↑ CO, tremor
207
dexmedetomidine MOA
α2A-AR agonist approved for sedation in intubated and pre- and perioperative nonintubated patients
208
dexmedetomidine advantages
- Analgesic and anxiolytic w/no respiratory
- ↓ MAC of inhaled anesthetics
- Sedation is short acting; pts easily aroused
- Shorter half-life than clonidine
209
dexmedetomidine disadvantages
no reversal agent yet
210
dexmedetomidine ADR
- hypotension
- bradycardia
- xerostomia
- large doses: OD, vasoconstriction, bradycardia, ↓ CO
211
For anesthesia, what would barbiturates be used for?
induce / maintain anesthesia
212
How does barbiturates help in anesthesia?
- increase duration of GABAa-receptor mediated Cl channel opening
- not GABA dependent
- inhibits excitatory AMPA/kainate receptors
- increases capacity of glycine receptor activation
213
For anesthesia, what would benzodiazepines be used for?
sedate and reduce anxiety
214
examples of benzodiazepines
- midazolam
| - versed
215
benzodiazepines MOA
- promote binding of GABA to its receptor
| - requires GABA for activity
216
What is the difference between benzodiazepines and barbiturates?
- benzodiazepines: do not produce true general anesthesia; antidote is flumazenil
- barbiturates: do produce true general anesthesia; no antidote
