Pharmacology Flashcards

(159 cards)

1
Q

catecholamines pass the blood brain barrier well? poorly?

A

very poorly

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2
Q

acetylcholine affects what 2 receptors

A

nicotinic
muscarinic

secreted by cholinergic fibers

after a threshold stimulus, liberation of Ach alters the cell membrane’s permeability

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3
Q

epinephrine is a direct acting catecholamine and adrenergic agonist or antagonist?

A

AGONIST

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4
Q

norepinephrine is a direct acting catecholamine that works through which receptors in the CNS?

A

a1, a2, b-adrenergics

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5
Q

dopamine (intropin) is an immediate precursor to?

acts through which 2 subtype receptors?

A

NE

D1 - activates adenylyl cyclase
D2 - inhibits adenylyl cyclase

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6
Q

serotonin (5-hydroxytryptamine) works through at least 14 subreceptors __ type neurons

A

tryptominergic

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7
Q

the major inhibitory neurotransmitter in the CNS is

A

GABA

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8
Q

opioid peptides include (3)

A

beta-endorphin
enkephalines
dynorphin

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9
Q

these 2 nts have EXCITATORY effects on neurons everywhere in the CNS

A

glutamate

aspartate

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10
Q

catecholamines are a group of

A

sympathomimetic compounds

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11
Q

these 2 catecholamines stimulate the myocardium

A

epi

NE

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12
Q

clinically, epi is for

A

anaphylaxis, glaucoma, asthma, vasoconstriction to prolong anesthesia

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13
Q

clinically, norepi causes

A

vasoconstriction in hypotension

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14
Q

CNS stimulants include

  1. analeptics
  2. xanthines
  3. sympathomimetic amines
A
  1. analeptics - can overcome drug-induced RESPIRATORY DEPRESSION and hypnosis [metrazol, coramine, dopram, picrotoxin, strychnine]
  2. xanthines - improve mental ALERTNESS, reduce urge to sleep, elevate MOOD [caffeine, theophylline, theobromine]
  3. sympathomimetic amines - to treat NARCOLEPSY, OBESITY, ADHD [amphetamines, methylphenidate, phenmetrazine]
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15
Q

__ is the only xanthine important in asthma tx, by stimulating medulla respiratory centers to cause bronchial dilation

A

theophylline

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16
Q

caffeinism occurs if you intake > __ mg caffeine per day

A

600-750 (10 cups)

> 1000 mg is TOXIC

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17
Q

caffeine stimulates the CNS unequally, with the __ being the most excited, and __ least excited

A

CORTEX most,

spinal cord least

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18
Q

the Autonomic Nervous System (ANS) is an efferent motor system that fxns independent of consciousness and controls __

A

automatic VISCERAL fxns required for life

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19
Q

drugs block or mimic ANS transmitters to clinically modify what functions?

A

autonomic fxns like: cardiac and smooth muscle, vascular endothelium, exocrine glands, presynaptic nerve terminals)

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20
Q

ANS consists of 2 parts

A

sympathetic nervous system - response to STRESS, fight or flight

parasympathetic - at REST, rest and digest

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21
Q

SYMPATHETIC NERVOUS SYSTEM FUNCTION

A
  • epi released from adrenal medulla
  • HR incr (tachycardia)
  • CO, Bp, blood flows from skin and internal organs into SKELETAL MUSCLE
  • energy stores are mobilized
  • pupils dilate (MYDRIASIS
  • bronchioles dilate
  • FEAR activates ANS sympathetics -> HYPERTENSION (a1 adrenergic receptors cause arteriolar vasoconstriction)
  • DECR. salivation
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22
Q

PARASYMPATHETIC NERVOUS SYSTEM FUNCTION

A
  • effectors are activated as needed, does not discharge as a complete system
  • Cranial nerves with PS activity = 3, 7, 9, 10
  • MIOSIS (pupils constrict)
  • bradycardia
  • incr. salivation
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23
Q

4 types of drug-receptor binding

A
  1. ionic - from electrostatic attraction btw ions of opp. charge
  2. H bonds - btw polar (water) molecules
  3. Van der Waals - weak interactions when atoms close
  4. Hydrophobic - btw drug, receptor and aqueous environment
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24
Q

covalent bonds

A

sharing e- by pair of atoms, for structural integrity of molecules, NOT involved in drug-receptor rxns

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25
4 families of physiologic receptors
1. receptors as enzymes (cell surface protein kinases) - kinases work by phosphorylating proteins 2. ion channels - drugs bind channels to cause opening or closing -> alters cell membrane potential 3. G-protein coupled receptors - second messengers like cyclic AMP are produced to cause an effect in the cell 4. Receptors in the cell nucleus - receptors for steroid hormones are soluble DNA-transcription factors in nucleus
26
alpha (a) receptors are primarily excitatory or inhibitory? located where?
EXCITATORY vascular smooth muscle, pre-synaptic nerve terminals, blood platelets, fat cells, CNS neurons *exception, some a-receptors relax GI smooth muscle
27
2 types of alpha receptors
1. post junctional a1 adrenergic (MORE COMMON) - radial smooth muscle in iris, arteries/arterioles/veins, GI tract - causes CONTRACTION and VASOCONSTRICTION - in arterioles of skin, mucosa, viscera, kidney 2. pre-junctional a2 adrenergic - INHIBITS release of NE - on presynaptic nerve endings to stop NE release - on post-synaptic endings in CNS to DECR. sympathetic tone
28
what nts combine with both types of alpha receptors
epi and norepi
29
beta receptors are mainly responsible for excitatory or inhibitory effects?
INHIBITORY, like vasodilation and relaxation of respiratory smooth muscle *exception: some mediate excitatory increases in heart's force and rate of contraction
30
2 types of beta receptors
1. post-junctional b1 adrenergic - in HEART myocardium cell, intestine smooth muscle, adipose tissue - NE and epi both bind to INCR. HR, CO, BP, force of contraction 2. post-junctional b2 adrenergic (MOST COMMON) - in BRONCHIOLAR and VASCULAR smooth muscle - cause VASODILATION in bronchial and uterine muscle to cause relaxation - incr. blood glucose - ONLY EPI (NE combines weakly or not at all to these)
31
epi combines with __ receptors to vasodilate bronchioles and tx asthma?
b-2 adrenergic receptors
32
pharmacologic agonist
binds to physiologic receptors to cause specific cellular effects, a full response
33
pharmacologic antagonist
binds receptor, does not trigger effect | -agonist can't reach receptor site
34
competitive antagonism is when? non-competitive antagonism is when?
- response CAN be achieved by increasing agonist dose | - NO response with increasing agonist
35
sympathomimetic agents (adrenergic AGONISTS) do what?
mimic effects of STIMULATION of organs/structures of the SYMPATHETIC nervous system
36
uses for adrenergic agonist therapy includes
1. control hemorrhage - a1 vasoconstriction 2. allergic shock (anaphylaxis) - a1 vasoconstriction, b2 airway dilation, b1 incr. cardiac output 3. nasal decongestant - a1 vasoconstriction 4. bronchial relxation/airway - b2 agonist 5. cardiac stimulation - b1 agonist
37
__ is the prototypical adrenergic agonist
epi
38
in anaphylaxis, epi works on what receptors, doing what?
a1 - vasoconstriction to incr. BP b1 - incr. cardiac output b2 - dilates bronchial tubes
39
bronchodilators (b2 agonists) to tx acute asthma include
epi albuterol salmeterol metaproterenol
40
amionphylline is a theophylline compound used for
bronchodilation for asthma or COPD, RELAX bronchial smooth muscle, a CNS stimulant that tx asthma
41
epi, penylephrine, albuterol, and isoproternol are all __ agonists
adrenergic; bind to adrenergic receptors
42
Direct acting Sympathomimetic agents - interact with a or b receptors, can be receptor selective or non-selective Include ->
phenylephrine - a1 selective agonist, nasal decongestant, mydriatic, tx chronic orthostatic hypotension, 100x less potent than epi clonidine - a2 selective agonist, anti-hypertensive dobutamine - b1 selective agonist terbutaline - b2 selective agonist, tx COPD, bronchopasm albuterol - b2 selective agonist, long term tx obstructive airway diseases, ER tx bronchospasm, delay premature delivery
43
epinephrine (adrenaline) is a vasoconstrictor and stimulates what receptors
a1,2 b1,2 direct acting agonist actions: vasoconstriction, incr BP, bronchodilation (b2), decr. blood volume in nasal tissue, OPPOSITE effects of histamine
44
epi is contraindicated in pts with common epi side effects
ANGINA, cause of cardistimulatory effects headaches, agitation (anxiety), tachycardia
45
norepinephrine is a __ agonist
a1, 2 | b1
46
isoproterenol is a __ agonist
b1,2 MOST POTENT BRONCHODILATOR
47
Indirect acting Sympathomimetic agents - cause release of stored NE at post-ganglionic nerve endings, similar to STIMULATING the SYMPATHETIC nervous system includes these drugs:
``` tyramine amphetamine methamphetamine hydroxyamphetamine methoxamine ephadrine ```
48
DA, EPI, NE< isoproterenol and phenylephrine are used as pressor agents to?
maintain BP in vascular shock; bronchodilators for asthma attacks and anaphylactick shock
49
amphetamines
stimulate CNS and PND increase systolic and diastolic bp weak bronchodilator and respiratory stimulant pass readily in CNS and cause rapid release of NE in brain
50
ADHD drugs
``` methylphenidate (ritalin) - mild CNS stimulant focalin - new form of above concerta - long acting ritalin Adderal (mixed amphetamine salts) strattera (atemoxetine) - non-stimulant metadate CR - controlled delivery dextroamphetamine (dexedrine) ```
51
dextroamphetamine (dexedrine) is used to treat
narcolepsy
52
4 types of Sympatholytic agents (anti-adrenergic) that act in a way OPPOSITE to the sympathetic nervous system. 4 types that all treat hypertension are
1. beta-adrenergic receptor blockers (b blockers) 2. alpha-adrenergic receptor blockers (a blockers) 3. centrally-acting anti-hypertensive agents (a 2 selective agonists) 4. neuronal depleting agents
53
beta blockers treat? side effects?
hypertension, angina, cardiac arrhythmias, MI, glaucoma, prophylaxis of migraine weakness, drowsiness
54
propranolol, timolol, nadolol
block b1 and b2, so they are NON-selective beta blockers propranolol is the drug of choice for adrenergically induced arrythmias
55
non-selective b blockers are contraindicated in pts with
asthma or other chronic obstructive airway disease -> cause fatal bronchospasm
56
acebutolol (sectral) is a
b1 selective antagonist, tx HTN and arrhythmias
57
metoprolol is a
competitive b1 cardioselective antagonist tx HTN, acute angina pectoris, good after heart attack
58
atenolol (tenormin) is a
competitive b1 cardioselective antagonist tx HTN, chronic angina pectoris, after MI, LONG PLASMA 1/2 life excreted by kidneyes
59
___ and __ are longer acting and more predictable than propranolol, b1 selective so SAFER to use in pts with asthma or bronchitis
metoprolol | atenolol
60
a blockers can cause
tachycardia, lower BP, vasodilation, orthostatic hypotension any alpha antagonist can cause EPI reversal main effects - reduce BP, reflex tachycardia
61
a blockers act by? major adverse effect is?
competitively inhibiting catecholamines at the a receptor site -> blood vessels DILATE hypotension
62
after vasovagal syncope, __ is the 2nd most likely cause of transient unconsciousness in the dental office
orthostatic hypotension
63
factors that can cause orthostatic hypotension include
drugs, bad postural reflex, pregnancy, Addison's, CHRONIC ORTHOSTATIC HYPOTENSION (Shy-Drager Syndrome) increases with age also an adverse effect of NSAIDs
64
drugs that can cause orthostatic hypotension (5)
1. antihypertensives 2. phenothiazines 3. tricyclic antidepressants 4. narcotics 5. antiparkinson drugs
65
2 types of alpha blockers (selective and non-selective) a1 to treat? non-selectives do not treat what conditions?
1. Selective a1 blockers - tx cardiac conditions (HTN, benign prostatic hyperplasia (BPH)) 2. Non-Selective block a1 and a2, NOT for cardiac conditions cause it can cause tachycardia. Used for pre-surgery mgmt of PHEOCHROMOCYTOMA and RAYNAUD'S PHENOMENON
66
selective a1 blockers include (3)
1. Doxazosin (cardura) - tx HTN, long duration of action 2. Prazosin (minipress) - not used much 3. Terazosin (Hytrin) - mild to mod HTN, and BPH
67
non-selective a1 and a2 blockers include (2)
1. Tolazine (Priscoline) - direct peripheral vasodilation, treats persistent pulmonary HTN of newborn 2. PHentolamine HCl (Regiitine) and PHenoxybenzamine HCl (Dibenzylene) - manage pheochromocytoma (adrenal medulla tumor)
68
pheochromocytoma is a tumor of the?
adrenal medulla | releases excess EPI and NE -> causes HTN, tachycardia, arrhythmias
69
epi reversal is a predictable result of using epi with a pt who received what kind of drug?
alpha blocker without blockers, epi and NE will cause BP to increase after a blocker, the pressor effect of NE is reduced and EPi causes a fall in BP (because NE only stimulates a receptors and has no b2 effects) after blocking a receptors, only b can be stimulated
70
pressor response produces
increase in BP and is mediated by a receptors | -depressor response produces decr. bp, mediated by b2 receptors
71
centrally acting anti-HTN agents are a2 selective agonists that include (3)
reduce BP by reducing cardiac output, vascular resistance 1. Clonidine - a2 selective, in combo with thiazide and hydralazine, relaxes blood vessels 2. Guanfacine and Guanabenz - stimulate a2 to inhibit sympathetic outflow, reduce peripheral resistance 3. Methyldopa - combine with diuretic to produce FALSE transmitter tat replaces NE, good to tx HTN in pts with RENAL DAMAGE
72
adverse effects of methyldopa
orthostatic hypotension, bradycardia, sedation and fevere, GI colitis, hepatitis, cirrhosis
73
neuronal depleting agents deplete includes (2)
catecholamine (NE, EPI, serotonin) 1. Reserpine blocks uptake of NE, EPI, serotonin 2. Guanethidin - blocks release of NE
74
a and b adrenergic blockers act by
competitive inhibition of postjunctional adrenergic receptors
75
autonomic nervous system has __ fibers that secrete __, and __ fibers that secrete norepi, epi, or dopamine.
cholinergic fibers secrete acetylcholine adrenergic fibers secrete norepi, epi, dopamine (catecholamines)
76
cholinergic fibers (neurons) release/secrete __ 2 kinds
ACh -primary nt 1. Preganglionic sympathetic & parasympathetic 2. Postganglionic parasympathetic - a MUSCARINIC response
77
postganglionic SYMPathetic fibers are what kind?
adrenergic!! not cholinergic
78
postganglionic sympathetic fibers that innervate sweat glands secrete
acetylcholine
79
acetylcholine receptors are divided into 2 groups
1. Muscarinic - autonomic effector cells in CNS (heart, vascular endotheliu, smooth muscle, prseynaptic nerve terminals, exocrine glands) - respond to MUSCARINE and ACh 2. Nicotinic - in ganglia, skeletal muscle end plates, CNS - respond to NICOTINE and ACh - acts at neuromuscular jxn of skeletal muscle
80
2 major nicotinic receptors
1. at neuromuscular jxns at somatic nervous systems - where neuromuscular blockers work here 2. at autonomic ganglia in both sympathetic and parasympathetic systems - ganglionic blockers work here
81
ACh is the chemical mediator at:
all autonomic ganglia, parasympathetic postganglionic synapses, transmitter at neuromuscular junction in skeletal muscle and sweat glands
82
ACh causes alteration in cell membrane permeability to produce these actions:
cholinergic drug actions - slow hear, miosis, simtulate bronchi, GI tract, gallbladder, bile duct, bladder, ureters, stimulate sweat + salivary + tear + bronchial glands
83
cholinesterase inhibitors increase/decrease salivation?
increases cause it reduces acetylcholine metabolism
84
overdose of cholinergic drugs cause
sweating, urination, bradycardia, copieous saliva but NOT mydriasis (dilation)
85
all __ receptors are CHOLINERGIC
M receptors bind acetylcholine and are antagonized by ATROPINE
86
3 classes of cholinergic agonists
choline esters cholinergic alkaloids cholinesterase inhibitors -stimulate muscarinic sites by mimicking ACh, BUT if these are given before ACh, then the action of ACh is enhanced and prolonged
87
indirect acting cholinergic agonists (cholinesterase inhibitors) act by cause a __ effect inhibit at what sites?
increase the effects of ACh in the autonomic nervous system and at neuromuscular junctions cause a CHOLINERGIC EFFECT -> eventually causes muscle paralysis they inhibit acetylcholinesterase at BOTH muscarinic and nicotinic sites
88
indirect acting cholinergic agonists (cholinesterase inhibitors) include (4)
1. edrophonium - good to dx myasthenia gravis 2. neostigmine and pyridostigmine - tx myasthenia gravis, can reverse blockade 3. malathion and parathion - insecticides 4. physostigmine
89
pralidoxime (protopam) is a cholinesterase reactivator used as an antidoe to reverse?
muscle paralysis due to organophosphate anticholinesterase pesticide poisoning
90
symptoms of organophosphate poisoning
excess salivation, bronchoconstriciton, diarrhea, skeletal muscle fasciculations (twitching)
91
organophosphates inhibit cholinesterase. 5 of them are
1. isoflurophate and echothiophate - tx glaucoma 2. malathion - insecticide 3. parathion - insecticide 4. tabun 5. metrifonate - anthelmintic
92
direct acting cholinergics are in 2 gruops
1. choline ESTERS - decrease BP due to general vasodilation, flushing of skin, slow HR [carbachol to produce miosis, bethanecol for post-op ab distension and urinary retention] 2. cholinergic ALKALOIDS - pilocarpine used as a MIOTIC and to tx open-angle glaucoma and xerostomia
93
xerostima is caused by
meds, cancer therapy, Sjogren's syndrome, head and neck trauma, bone marrow transplants, endocrine disorders, etc.
94
cholinergics tx dry mouth by inducing salivation. cholinergics used are (2)
1. pilocarpine (salagen) - cholinergic agonist and alkaloid, tx xerostomia caused by salivary gland hypofunction 2. cevimeline (evoxac) tx xerostomia in pts with Sjogren's
95
cholinergic crisis symptoms
bradycardia, lacrimation, extreme salivation, vasodilation, muscle weakness
96
typical cholinergic effects caused by stimulation of ACh (cholinergic) receptors are
salivation, miosis, excess sweating, flushing, incr. GI motility and bradycardia
97
mecamylamine (inversine) is a __ blocking drug
nicotinic ganglion
98
anti-cholinergic (anti-muscarinic) drugs produce opposite effects of cholinergics like
xerostomia (block postganglionic cholinergic fibers), mydriasis (dilation), anti-spasmodic, decr. GI motility, less gastric and salivary secretions, tachyardia
99
anti-cholinergics are contraindicated in __ patients
GLAUCOMA, cardio probs, GI obstruction, asthma
100
anticholinergics work by therapy for:
preventing ACh from occupying the same receptor Parkinson's, motion sickness, bladder syndrome, traveler's diarrhea
101
anticholinergic/antimuscarinic drugs include
``` glycopyrrolate - diarrhea, bladder propantheline bromide - diarrhea benzotropine - Parkinson's trihexyphenidyl HCl - Parkinson's atropine sulfate - causes mydriases, cycloplegia scopolamine - reduces motion sickness belladonna derivatives ```
102
nicotinic receptor antagonists (nicotinic blockers) divided into 1. Ganglionic blockers 2. Neuromuscular blockers
1. Ganglionic - not used cause of parasympathetic blockade that causes xerostomia, constipation, blurred vision, postuarl hypotension [mecamylamine, trimethaphan for HTN in emergency, cause fall in BP] 2. Neuromuscular - complete skeletal muscle relaxation and helps in endotracheal intubation, interact with nicotinic receptors, danger is it can lead to paralysis
103
2 classes of neuromuscular blockers include
1. non-depolarizing (competitive) - cause paralysis [Tubocurare (curare] is the prototype] * Neostigmine/Pyridostigmine used to REVERSE paralysis 2. depolarizing (non-competitive) - [Succinylcholine prototype], used in caution with pts with low pseudocholinesterase (can cause respiratory failure)
104
Skeletal muscle spasmolytics (relaxants) are used for some CNS diseases like? include (5)
multiple sclerosis, cerebral palsy, CVAs 1. baclofen - derivative of GABA 2. carisoprodol 3. cyclobenzaprine 4. methocarbamol 5. quinine - nocturnal leg cramps
105
bioavailability measures
rate and amount of therapeutically active drug that reaches systemic circulation amt of drug absorbed/amt of drug administered IV provides 100% bioavailability
106
drug's onset of action is primarily determined by rate of?
absorption major effect of a drug is determined by how much is FREE IN PLASMA
107
oral route of administration
safest and easiest hepatic FIRST PASS metabolism, not for emergencies drugs are absorbed best from the DUODENUM
108
intramuscular injection
- 5 min rapid onset - good for solutions too irritating to be subcutaneous - aqueous soln absorbs fast, and oily ones are slow - anterior thigh for kids - 1 inch deep for adults, 1/4 inch for kids
109
subcutaneous injection intra-arterial injection concern
- 15 min onset, less rapid | - can burn
110
intravenous injection
- most RAPID onset | - 100% bioavailability, allows TITRATION
111
inhalation
- 5 min | - most frequent in pediatric pts
112
patch delivery
- in blood over 12-24 hrs | - SYSTEMIC effect
113
distribution of a drug into tissue mainly depends on _
rate of blood flow to the tissue -also gastric emptying time and degree of plasma protein binding (albumin) matters but not as much
114
most drugs travel through blood by binding to __
albumin
115
physiochemical properties of drugs that influence their passage across membranes are
lipid solubility, degree of ionization, molecular size, molecular shape
116
most drugs are absorbed by what kind of transport
facilitated diffusion driving force is concentration difference
117
biotransformation of drugs in the liver in 2 phases
Phase I - P450 system | Phase II - conjugation
118
DEA Schedule I drugs
not for medical use, can't be prescribed
119
DEA Schedule II drugs
strong potential for ABUSE or ADDICTION, but have legitimate medical use amphetamines, morphine, cocaine, pentoarbital, oxycodone, methadone, codein need rx, can be prescribed but not refilled, can't be called in
120
DEA Schedule III
written rx signed, can call in, can have refills analgesic combos
121
DEA Schedule IV
diazepam (valium), lorazepam, triazolam, xanax
122
who determines which drugs can be sold by rx?
FDA
123
allergic rxns to anesthetics is more common with what kind? __ is the component of local anesthetics that causes allergy
esters (not amides) bisulfites
124
mechanism of local anesthetics
decrease Na+ uptake through sodium channels, decreases nerve's excitability and impulses fail to propagate NO effect on K+
125
when tissues are normal (pH = 7.4), what % of the local anesthetic is in free base form? (non-ionized)
10-20% enough to penetrate nerve to cause anesthesia
126
the lower the drug's pKa, and higher the pH of the solution or injected tissue, the MORE or LESS free base avail?
MORE
127
potential action of locals depends on the ability of
the SALT to liberate the FREE BASE (active form)
128
esters are metabolized in the __ | amides in the __
plasma | liver
129
esters mainly avail as
topicals PROCAINE (novocaine) one of the originals
130
the only local anesthetic that increases the pressor activity of EPI and NE is
cocaine - ester - causes definite vasoconstriction
131
amides
used with caution or not at all in pts with compromised liver -metabolized by P450 enzymes
132
the only amid local anesthetic metabolized int he bloodstream is
articaine (septocaine) contraindicated in pts sensitive to amides or sodium bisulfite max dose 7 mg/ kg
133
prilocaine (citanest)
- causes less vasodilation than lido - less potent than lido not for pts with liver disease, hypoxic conditions metabolized into orthotoluidine -> can produce methemoglobinemia
134
bupivacaine (marcaine)
longest duration of action of any local anesthetic
135
lidocaine (xylocaine)
anti-arrhythmic agent in the ventricle -decreases cardiac excitability lido + mepi most likely to show cross-allergy
136
mepivacaine (carbocaine)
equal to lido in efficacy and used without EPI TOXIC to neonates short lasting
137
max. lido dose in kids | max. in adults
in kids, by weight, 4.4 mg/kg in adults, 300 mg
138
chloral hydrate
only non-barbiturate sedative-hypnotic indicated in dentistry - used orally for anxious kids - kids will get excited and irritable before sedation - DOES NOT RELIEVE PAIN
139
nitrous oxide must be coupled with __ % oxygen
20
140
nitrous is contraindicated for
upper respiratory infxns, emphysema, bronchitis, 1st trimester of pregnancy, autistic pts (communication difficult), NEVER on pts with contagious disease
141
drug of choice against syncope is
inhaled ammonia | -irritates trigem nerve sensory endings
142
inhalation agents
1. isoflurane - for old ppl, safe for heart disease 2. halothane, enflurance - decreases cardiac output, halothane sensitizes heart to catecholamines (risk of ventricular arrhytmia); enflurane is CNS irritant so avoid in pts with seizures lipophilic moleculres
143
IV agents, classes
1. Barbiturates 2. Benzodiazepines 3. Neuroleptanalgesics 4. Others
144
Barbitruates (2)
1. thiopental (pentothal) - MOST COMMON, ultrashort acting | 2. methohexital (brevital) - outpatient, rapid recovery, short acting
145
Benzodiazepines do not provide anesthesia, provide anterograde amnesia, and include
1. midazolam (versed) - pt groggy, preferred to diazpema because more water soluble 2. diazepam (valium) and lorazepam (ativan) - ANTI ANXIETY, contraindicated in pts with narrow angle glaucoma. diazepam for cerebral palsy and status epilepticus 3. flumazenil -benzodiazepine antagonist for recovery 4. alprazolam (xanax) - anxioloytic effects in pts with agoraphobia
146
__ and __ are benzodiazepines that provide preop sedation but are more irritating
lorazepam (ativan) and diazepam (valim)
147
__ are the most effective oral sedative drugs in dentistry
benzodiazepines - used for anxiety and sleep disorders - dont' use during pregnancy
148
Neuroleptanalgesics are neruoleptic-opiod combos that combine __ and __
Fentanyl and Droperidol Fentanyl - opioid used as premed or adjunct to inhalation agents, used with droperidal and NO.
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opioid adverse effects are reversed and recovery hastened by admin of
Naloxone (Narcan) | -opioid antagonist
150
Propofol (Diprivan)
IV anesthetic, metabolized in liver - respiratory depressant - doesn't increase intracranial pressure - safer for pregnant women, less likely to cause bronchospasms - contraindicated in kids, caution if pt has hypotension
151
etimodate (amidate) andvantage is
minimal respiratory and cardiovascular depressant effects - no alnalgesic effects - no hypotension or significant HR effects
152
ketamine
for DISSOCIATIVE ANESTHESIA - cause catatonia, amnesia, analgesia without loss of consciousness - antagonist at NMDA receptor to block excitatory effects - not good for adults, better in kids
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only anesthetic that acts as a cardiovascular stimulant is
KETAMINE
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benzodiazepines, barbiturates and narcotic analgesics all produces
SEDATION and can cause physiologic dependence -FLUMAZENIL is a benzodiazepine antagonist used to REVERSE benzo overdose
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tranquilizer is a drug that promotes tranquility by
calming, soothing, quieting, or pacifying WITHOUT sedation or depressant effects major ones = anti-psychotics minor ones = anti-anxiety (benzos)
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Benzodiazepines (minor tranquilizers) how does it work? what nt? bad effects are?
anti-anxiety, induce sleep (sedative-hypnotic), anti-convulsant, skeletal muscle relaxant work by DEPRESSING LIMBIC SYSTEM and RETICULAR FORMATION through potentiation of GABA adverse effects - CNS depression, GI disturbances, hypotension, ataxia, muscle relaxation, NEVER take with alcohol
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benzodiazepines taken orally are
chlordiaepoxide (librium) lorazepam (ativan) alprazolam (xanax) diazepam (valium)
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benzodiazepines rx as HYPNOTICS for insomnia include
1. Flurazepam (Dalmane) 2. Temazepam 3. Triazolam (Halcion) - metab by liver by P450 isoform CYP 3A4 (avoid in pts taking inhibitors for that); antifungals can also elevate triazolam levels
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Midazolam (versed)
a benzodiazepine in liquid form for pre-op sedation of kids, and injectable for IV.