Kap Pharm Cns Drugs 2

Front 1

What are the inhaled anesthetic drugs?

Back 1

nitrous oxide, halothane, isoflurane, and the "-fluranes"

Front 2

What is the MAC value of an anesthetic?

Back 2

the measure of anesthetic potency, is the minimal alveolar anesthetic concentration (% of inspired air) at which 50% of patients do not respond to a surgical stimulus.

Front 3

What are the MAC values for the main inhaled anesthetics?

Back 3

Halothane = 0.8
Isoflurane = 1.3
nitrous oxide = >100%

Front 4

Which a MAC of over 100% why is NO used?

Back 4

MAC values are additive

Front 5

What are the circumstances which lower the MAC value?

Back 5

lower in elderly and reduced by other drugs including opioids and sedative-hypnotics

Front 6

What is the mech of action of the inhaled anesthetics?

Back 6

mechanism of action may involve interaction with neuronal membrane lipids leading to inhibition of ion flux

Front 7

What determined the rate of onset and recovery of inhaled anesthetics?

Back 7

High blood solubility meas it takes longer to achieve a partial pressure that allows movement from the blood into the CNS.
Thus, high blood gas solubility ratio = slow onset

If the drug has a high solubility it will also take longer to get out of the blood once the anesthesia ends

Front 8

What inhaled anesthetics have been developed which have low blood gas solubility rations, affording both rapid onset of anesthesia and rapid recovery

Back 8

desflurane and sevoflurane

Front 9

What are the actions of inhaled anesthetics?

Back 9

-lower response to increased pCO2
-increased cerebral blood flow and relax uterine smooth muscle

-Vasodilation and some cardiodepression (hypotension) - although haloperidol may sensitize myocardium to catecholamines

-malignant hyperthermia (rare) with halogenated agents in combination with NM blockers

-Halothane associated hepatitis

Front 10

What is the use of thiopental?

Back 10

rapid-onset and short acting barbiturate used mainly for induction

Front 11

What are the actionso f theopental?

Back 11

decreased respiratory and cardiac function, but no increased cerebral blood flow

Front 12

How is thiopental metabolized?

Back 12

Rapid recovery via redistribution from CNS to peripheral tissues, but liver metabolism required for elimination

Front 13

What is midazolam and what is it used for?

Back 13

IV benzodiazepine for preop sedation and in anesthesia protocols

Front 14

What are the effects of midazolam?

Back 14

anterograde amnesia and decreased respiratory function

Front 15

What is a drug given to assist in the recovery from midazolam?

Back 15

flumazenil

Front 16

What is the action of Ketamine?

Back 16

rapid onset and short duration - "dissociative anesthesia" with amnesia, catatonia, and analgesia

Front 17

What is unique about ketamine?

Back 17

CV STIMULATION

Front 18

What are the adverse effects of ketamine?

Back 18

emergence reactions (bad dreams, hallucinations)

Front 19

What is one way of decreasing the effects of ketamine?

Back 19

give a benzodiazipine before hand.

Front 20

Which drug has a very rapid onset and recovery, plus antiemetic effects and is frequently used?

Back 20

Propofol

Front 21

What is propofol used for?

Back 21

induction and maintenance, especially outpatient surgury

Front 22

What is the main opioid analgesic?

Back 22

Fentanyl

Front 23

What is the main adverse effect of fentanyl?

Back 23

chest wall rigidity with IV use

Front 24

What is the action of fentanyl?

Back 24

short duration IV, oral and patch forms

Front 25

Which drugs in combination make upu Neurolept anesthesia?

Back 25

fentanyl+droperidol+nitrous oxide

Front 26

What are the intravenous Anesthetics?

Back 26

Thiopental, Midazolam, Propofol, Fentanyl, Ketamine

Front 27

What is a characteristic of local anesthetics and what are they used for?

Back 27

weak abaes for regional anesthesis via infiltration near nerve bundles, or by epidural and subarachnoid injection

Front 28

What are the two groups of drugs that make up the local anesthetics and that are the drugs in each group?

Back 28

Esters - procaine, cocaine, benzocaine

Amides - lidocaine, bupivacaine

Front 29

What are the esters metabolized by?

amides metabolized by?

Back 29

esters - plasma and tissue esterases

amides - liver

Front 30

What determines whether a locat anesthetic is able to cross membranes?

Back 30

whether it is in it's ionized (protonated) or nonionized (nonprotonated) form

Front 31

Which form for the drugs bonds to the Na channel and where is the Na channel located?

Back 31

Ionized (NH3+)forms bind to a component of the Na ion channel located inside nerve membrane

For access to its "target" the local anesthetic must first cross the lipid bilayer and it does so in its non-ionized (NH2) form

Front 32

What is the response of vasculature to a local anesthetic?
and what is the remedy to this?

Back 32

vasodilation, except with cocaine
thus local anesthetic are often gives with alpha 1 receptor agonsits

Front 33

Which fibers are most sensitive to local anesthetic?
Which fiber type?

Back 33

smaller diameter and high firing rates (state-dependent)

Myelinated fibers are also more sensitive. But our only nonmyelinated fiber is Type C, which is small and highly firing, which makes it very vulmnerable

Front 34

What are type C fibers involved in?

Back 34

nociception (pain impulses)

Front 35

What is the order of fiber type sensitivity to Anesthetics?

Back 35

Type B and C > Type A Delty > type A beta and gamma > type A alpha

Front 36

What are the adverse effects of local anesthetics?

Back 36

neurotoxicity - dizziness, nystagmus, sensory impairment, SEIZURES (like lidocaine
-decrease CV parameters, except cocaine
-Allergies - esters via PABA formation

Front 37

What is the pufferfish toxin and what is it's mechanism?

Back 37

tetrodotoxin binds externally to the "ready state" of Na channels in both cardiac and nerve cell membranes and block the influx of Na, thus PREVENTING conduction

Front 38

What is the exotic fish, Moray eel toxin and what is it's mechanism

Back 38

Ciguatoxin binds in the Na channel, keeping it open to cause a persistent depolarization and channel inactivation

Front 39

What is the South American frogs toxin and what is it's mechanism?

Back 39

Batrachotoxin binds in the Na channel, keeping it open to cause a persistent depolarization and channel inactivation

Front 40

What is the red tide/shellfish toxin and what is it's mechanism?

Back 40

saxitoxin binds externally to the "ready state" of Na channels in both cardiac and nerve cell membranes and block the influx of Na, thus PREVENTING conduction

Front 41

What are the actions of nicotinic receptor antagonists?

reversed by?

Back 41

Non-depolarizing (competitive)

decrease frequency of Na channel opening at skeletal endplate causing progressive muscle paralysis

Reversed by ADhE inhibitors

Front 42

What is the action of D-tubocurarine?

Back 42

blocks ANS ganglia and releases histamine, thus decreasing BP

Front 43

What serious analgesic situation is tubocurarine associated with?

Back 43

malignant hyperthermia

Front 44

What are the nicoting receptor antagonist drugs?

Back 44

tubocurarine
Any drug that ends in "onium" or "curium"

Front 45

What is the Nicotinic receptor agonist and what is it's course?

Back 45

Succinylcholine
Depolarizing (noncompetitive) acting in 2 phases:
phase 1: brief stimulation = fasciculations
Phase 2: depolarization = flaccid paralysis, not reversed by AChE inhibitors

Front 46

What is significant about the metabolism of succinylcholine?

Back 46

short duration since rapidly inactivated by esterases....genotypic veriants with low enzyme activity can greatly increase the duration of succinylcholine action

Front 47

What are unique characteristics about succinylcholine?

Back 47

low dose = decreased HR (vegal)

High dose = increased HR (ganglionic stimulation)

Hyperkalemia = implicated in malignant hyperthermia

Front 48

What is the action of spasmolytics?

Back 48

reduce excessive muscle tone or spasm in acute muscle injury and CNS dysfunction

Front 49

What would spasmolytics be used?

Back 49

cerebral palsy, MS, stroke

Front 50

What are the drugs used as spasmolytics?

Back 50

Benzodiazepines, Baclofen, and Dantrolene

Front 51

What is the mechanism for benzodiazepine spasmolytics?

Back 51

facilitate BABA at BABAa receptor, thus decreasing tonic output of primary spinal motoneurons

Front 52

What is the mechanism of baclofen?

Back 52

direct agonist at GABAb receptors in spinal cord. Activation of GABAb receptors leads to increased efflux of K and thus hyperpolarization and inhibition

Front 53

What is the drug used to treat malignant hyperthermia?

Back 53

dantrolene

Front 54

Waht is the mechanism of Dantrolene?

Back 54

blocks release of Ca from SR

Thus it has direct action on the skeletal muscle