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Anesthetics and Analgesics Flashcards

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1
Q

General CNS Pharmacology

A

 Drugs Act on Specific Receptors that Modulate Synaptic Transmission
 Mechanisms:
 Act Directly on Receptor
 2nd Messenger Coupling
 Affecting Ion Channels
 Agonists or Antagonists
 Either Excite or Inhibit Neural Function

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2
Q

Neurotransmitters of CNS

A

 Glutamate – Excitatory
 GABA/Glycine – Inhibitory
 Acetylcholine – Excitatory or Inhibitory –
Muscarinic Receptors mainly in CNS
 Dopamine – slow inhibitory action
 Norepinephrine – Excitatory
 Serotonin - Excitatory or Inhibitory

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3
Q

Blood brain barrier

A

 Unique to CNS & created by combination of
different tissues
 “Tight junctions” between endothelial cells
 astrocytes (CNS supporting cells)
 impermeable basement membrane in CNS

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4
Q

What is the only thing that can penetrate the blood brain barrier

A

lipid soluble chemicals and molecules transported by specific active transport systems
 most chemical enter brain by simple diffusion

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5
Q

What are anesthetics

A

implies loss of consciousness
 loss of memory of event or pain
 ideal for longer surgery/procedures
 local versus general (systemic)

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6
Q

What are analgesics

A

implies relief of pain
 conscious and aware
 no memory loss

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7
Q

An ideal anesthetic must:

A
  1. Produce LOC with rapid onset
  2. Amnesia (especially in orthopedic Sx)
  3. Skeletal muscle relaxation
  4. Inhibition of sensory & autonomic reflexes
  5. Minimum of toxic side effects
  6. Rapid onset of anesthesia, easy adjustment, and rapid recovery of consciousness
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8
Q

Stage I of anesthesia

A

Analgesia: Conscious, but with loss of somatic pain/sensation

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9
Q

Stage II of anesthesia

A

Excitement (Delirium): conscious & amnesiac, but agitated/restless

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10
Q

Stage III of anesthesia

A

Surgical anesthesia: begins with onset of regular, deep respiration, progresses to hypoventilation and bradynpea
** this is where they keep you during surgery

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11
Q

Stage IV of Anesthesia

A

Medullary paralysis: cessation of spontaneous breathing decreased ability to self regulate BP, HR, etc
** this real bad

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12
Q

In general, how are anesthetics administrated?

A

combination of inhaled and IV

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13
Q

Inhaled anesthetic Agents

A

 Halothane (Fluothane)
 Nitrous Oxide (laughing gas)

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14
Q

IV Anesthetics: Barbituates

A

fast acting, relatively safe
 Increase time Cl channels are open
 Thiopental (Pentothal), Methohexital

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15
Q

What are adverse effects of Barbiturates?

A

long 1/2 life = greater general sedation, potential for OD

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16
Q

IV Anesthetics: Benzodiazepines

A

 Suffixes commonly pam or lam
 Diazepam (Valium), Lorazepam, Midazolam
 adverse effects: similar to barbiturates, but milder due to being more selective
 Increases frequency of CL channel openings

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17
Q

IV Anesthetics: Propofol (Diprivan)

A

most used anesthesia drug in surgery and for drug induced comas
 Faster clearance that older drugs
 Less of a “hangover: effect

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18
Q

IV Anesthetics: Katamine (this is on test)

A

“dissociative anesthesia”- is a cardiovascular stimulant

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19
Q

IV Anesthetics: Etomidate

A

produces hypnotic anesthesia w/o CV adverse effects

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20
Q

IV Anesthetics: Opioids

A

Fentanyl & Morphine – Used more post-operatively for pain control

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21
Q

Pharmacokinestics of general anesthetics

A

These agents are lipid soluble & cross BBB
 and become widely distributed throughout
body
 stored in fat tissue and released slowly  prolonged recovery/hangover-like effect
 confusion, disorientation, lethargy, stage II anesthesia
 worse in patients with larger adipose stores

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22
Q

3 things that affect drug metabolism

A

age, pulmonary, and hepatic function

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23
Q

Preoperative medications

Study These Flashcards
A

 Barbiturates: anti-anxiety & amnesia
 Benzodiazepines: anti-anxiety, amnesia,
relaxation
 Antihistamines: sedation & inhibit vomiting
 Antacids: decrease risk of aspiration damage

24
Q

Neuromuscular Blockers pre op

Study These Flashcards
A

skeletal muscle paralysis
 anticholinergics at NMJ: Curare (Tubocurarine)
 depolarizing blockers: Succinylcholin

25
Goal of local anesthetic
block afferent neurotransmission  peripheral nerve (nerve block)  spinal cord (spinal block)
26
advantages of local anesthetics
 rapid recovery  absence of cognitive problems after surgery (no amnesia)  minimal effects on CV, respiratory or renal function
27
disadvantages of local anesthetics
not as complete loss of sensation
28
suffix of local anesthetics
"caine"
29
Common Local Anesthetic:
- Lidocaine - Onset: slow - Duration: short - Uses: Infiltration, peripheral nerve block, spinal
30
Mechanisms of action of local anesthetics
- Inhibit Na+ channel opening
31
Clinical uses of local anesthetics:
 Topical: applied to skin & mucous membranes  Transdermal: drive in w/ iontophoresis or phonophoresis  Infiltrate: applied to broken skin or sub-q  Peripheral nerve block: inject close to nerve trunk  Central nerve block (epidural or spinal): inject into (epidural) space surrounding the spinal cord or within the subarachnoid (intrathecal) space  Usually L3-4 or L4-5, indwelling catheter  Ganglionic block: inject sympathetic ganglion
32
What is ganglion block commonly used for?
chronic regional pain syndrome
33
"Differential" Nerve block
 Smaller diameter (C-fibers) and unmyelinated fibers are more sensitive to the anesthetic  Peripheral pain is carried by C-fibers --> good pain relief can be achieved at doses that do not causes paralysis  Sympathetic nervous system carried by C-fibers --> affecting vasomotor tone (vasoconstriction/ dilation)  But, depends on the dose (high concentration, larger fibers affected)
34
Systemic Effects of Local Anesthetics
anesthetic diffuses throughout body
35
CNS Effects of Local Anesthetics
 initial excitation (agitation, confusion, seizures)  latent effects: CNS depression (somnolence)
36
Cardiovascular Effects of Local Anesthetics
cardiovascular depression: decreased HR, BP
37
Local anesthetics may be useful when...
applied transdermally with ionto or phonophoresis
38
Patients with complex regional pain syndrome:
 schedule PT after pt receives ganglionic or nerve block, when maximally effective  maximize use of the involved extremity
39
Patients w/ indwelling cath for severe/chronic pain
Caution: possible loss of sensation/temperature
40
What does the term opiod refer to?
all compounds mimicking the effect of morphine (an opium derivative)
41
How to Opioids work?
 All utilize the endogenous neurotransmitters pathways involved in descending pain modulation  Receptors for opioids are primarily in periaqueductal gray and raphe magnus, but also in the SC and periphery  Descending fibers carry pain modulating signals through the lateral fasciculus to the SC, where it modulates pain through interneurons  Both central and peripheral effects of opioids
42
Endogenous opioids
 Enkephalins  Dynorphins  Endorphins (-endorphin: most potent for analgesia)
43
Endogenous opioid receptors
Primarily mu, but also kappa R’s are most important for analgesia
44
opiod receptors and their strength
- Mu: most potent for pain relief and in highest concentration in the periaqueductal gray (also the most side effects) - Gamma: brainstem and other locations in CNS - Kappa: Widely distributed, importance unknown
45
Strong (binding with Mu) Opioids
- Meperidine: given oral, IM, IV, SQ (2-4hr) - Morphine: Given IM, IV, SQ, Epi (4-5 hr)
46
Mild to moderate (bind with kappa and/or delta) Opioids
- Codine: Oral, IM, SQ (4 hr) - Oxycodone: Oral (3-4 hr)
47
Mixed (both agonist and antagonist effects) Opioids
Butorphanol: IM, IV (3-4 hr)
48
Effects of strong opioids
 Binds primarily at mu Rs  greatest analgesia, but greatest potential for OD  administration: oral, IM, SQ, IV or intrathecal (pump)
49
Effects of mild-moderate opioids
 tend to bind kappa and delta more than mu Rs
50
Effects of Mixed opioids
 antagonists at mu, but agonists at kappa & delta R  adequate analgesia, but less euphoria & sedation
51
Opioid Antagonist
- Naloxone - Block all opioid R - Reverse analgesia, euphoria, and respiratory depression
52
Mechanism of Opioid Analgesia
- 1st order afferents for peripheral pain reception move in - Endogenous or exogenous opioids inhibit transmission of substance P or other pain neurotransmitter from getting to descending pain modulators
53
Other effects of opioids
 Acting at central brain areas, opioids also produce central pain inhibition and euphoria  Thalamus, hypothalamus, limbic system  Alters “perception of pain” (pain doesn’t hurt)  Addiction  Tolerance  Respiratory and CV depression  Acting on peripheral receptors (such as in skin and joints), may cause local analgesia
54
adverse/side effects of opioids
 Sedation, drowsiness & mental slowing  Euphoria and confusion  Respiratory depression  rate and depth of respiration both decrease  Orthostatic hypotension  Nausea and vomiting  Constipation  Addiction: drug seeking behavior  Dependence: withdrawal in absence of drug  Tolerance: increased dose to achieve same effect
55
Opioid Withdrawal symptoms
 Body aches  Shivering  Diarrhea  Stomach cramps  Fever  Sweating  Gooseflesh  Tachycardia  Insomnia  Uncontrollable yawning  Irritability  Weakness/fatigue  Loss of appetite  Nausea & vomiting

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