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Pharm II Exam 1 > Exam 1 General > Flashcards

Exam 1 General Flashcards

1
Q

What are the 3 steps in the neurophys of pain?

A

initiation
propagation
perception

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2
Q

What are the pain fibers?

A

C fibers and A delta fibers

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3
Q

What are second order neurons?

A

spinothalamic neurons

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4
Q

How do local anesthetics work?

A

by binding to and inhibiting voltage gated Na channels which inhibits depolarization of pain fibers and the stimulus never reaches somatosensory cortex

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5
Q

At the synapse what is the neurotransmitter that is being released by the A delta fibers?

A

glutamate which binds to glutamenergic NMDA receptors on neospinothalamic neurons and activates voltage gated ion channels allowing Ca to flow in and causes depolarization and propagation of pain fibers

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6
Q

What neurotransmitter do C fibers release at the neurotransmitter?

A

substance P which then binds to sub p receptors on termini which activated cation channels which leads to depolarization of paleo spinothalamic neurons

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7
Q

What causes edema in the injured area?

A

C fibers have bifurcation (axon reflex branches) that terminate at original site of injury and release substance P which acts as a chemotaxis factor for mast cells which release histamine which binds to receptor on vasculature and causes vasodilation

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8
Q

What causes sensitization (exacerbation) of pain stimulus?

A

sub p released by C fiber termination attracts prostaglandins which bind to receptors and causes sensitization

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9
Q

Which pain fibers are myelinated?

A

A delta fibers (transmit 15-80 m/s)

C fibers are unmyelinated and transmit (0.5-1m/s

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10
Q

What type of pain are fast confucting A delta fibers responsible for?

A

sharp, stinging, high intensity pain immediately after injury

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11
Q

What pain are slower conducting C fibers responsible for?

A

second pain, dull aching, lower intensity, chronic pain experienced after the injury

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12
Q

What do local anesthetics and NSAIDs block?

A

the first pain from fast conducting A delta fibers and the second pain from slower conducting C fibers

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13
Q

How do NSAIDs provide pain attenuation?

A

inhibiting COX 2 in inflammatory immune cells which prevents prostaglandin synthesis

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14
Q

When is the sodium channel in the resting state?

A

-70 mV (H gate open and M gate closed which prevents Na from depolarizing

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15
Q

When is the Na channel activated?

A

-50 opens M gate and allows sodium to enter and depolarize pain fibers

(inactivates in a few seconds & H gate closes then goes back into resting state)

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16
Q

Why do you wait 10-15 min after numbing to perform a procedure?

A

waiting for all Na channels to spontaneously activate allowing them to be blocked by the local anesthetic

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17
Q

What factors increase the lipophilicity of local anesthetics?

A
  1. the number of hydrocarbon chains connected to Nitrogen atom and the longer the length
  2. longer length of intermediate connecting chain
  3. greater number and length of hydrocarbon chains connected to the ring
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18
Q

What is the effect on the local anesthetic when lipophilicity is increased?

A

increased potency and earlier onset of action

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19
Q

If a patient has an allergic reaction to a local anesthetic what is it most often due to?

A

the esther linkage because it releases PABA which is immunogenic in some patients

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20
Q

How are the ester anesthetics metabolized?

A

by plasma and liver pseudocholinesterases

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21
Q

How are the amide anesthetics metabolized?

A

metabolized in the liver by cyp P450 enzymes

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22
Q

When you are applying local anesthetic to infected tissue (slightly acidic <7) what is the effect?

A

there is more protonated form and less uncharged form which is the kind that can cross the lipid bilayer so the potency decreases and onset of action takes longer

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23
Q

What for of LA crosses the membrane?

What form blocks the channel?

A

crosses-uncharged

blocks-charged

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24
Q

What fibers are blocked more easily by LA?

A

small diameter fibers

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25
Q

What fibers are blocked more readily by LA?

A

myelinated fibers (of the same diameter as unmyelinated fibers)

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26
Q

When a nerve fires more is it blocked more or less by LA?

A

MORE

27
Q

What position of fibers (interior or exterior) are blocked more readily blocked by LA?

A

exterior

28
Q

What is MAC?

A

minimum alveolar concentration

1 MAC is the concentration that renders 50% of subjects exposed to noxious stimuli immobile

29
Q

When does mild anesthesia begin?

Amnesia?

A

Mild anesthesia ~0.3 MAC

Amnesia ~ 0.5 MAC

at 1.3 MAC 99% are immobile (so we use this dose to be safe)

30
Q

What does of inhalation agents could potentially be lethal?

A

higher than 2.0 MAC

BUT 2.0 MAC is used for induction (and then reduced once induced)

31
Q

What dose of MAC is what you want as a maintenance dose for surgery?

A

1.3

32
Q

What is the effect of low solubility anesthetics vs high solubility anesthetics?

A

Low will act quicker for induction as well as emergence while high will take longer to be induced and longer to get off of

33
Q

What blood: gas partition coeff is fastest?

What fat:blood partition coeff is the fastest?

A

Low partition coeff are fast to be induced and eliminated but higher numbers will take longer to be induced and eliminated

34
Q

What is malignant hyperthermia?

A

genetic disorder triggered by volatile anesthetics and by some neuromuscular blockers.
Caused by an inability of the sarcoplasmic reticulum to sequester Ca2+. The triggering agents cause a sustained and prolonged release of Ca2+ and massive muscle contraction, lactate production and increased body temperature

35
Q

How do you treat malignant hyperthermia?

A

Dantrolene (reverses release of calcium from SR)

36
Q

How long does it take for vessel rich group to equilibrate?

A

4-8 min

37
Q

How long does it take for muscle group to equilibrate?

A

~1-2 hr

38
Q

How long does it take for fat group to equilibrate?

A

~10-20 hrs

39
Q

What do you need to be cautious with in trauma victims, elderly and cardiorespiratory disease pts when giving anesthetics?

A

hypotensive effects from anesthetics

40
Q

What happens when acetaldehyde is left in the bloodstream?

A

N/V HA, hypotension

41
Q

What does 1% BAC mean?

A

1g/100 ml

42
Q

What is volume of distribution for males of EtOH?

Females?

A
  1. 7 L/kg

0. 63 L/kg

43
Q

How many grams of ethanol are in 1 drink?

A

about 15 g

44
Q

What enzyme is primarily responsible for metabolizing ethanol at a BAC <0.1%

A

Alcohol dehydrogenase (ADH)

at a rate of 7-10 grams/hr

metabolizes 1 drink in 1.5-2 hrs

45
Q

What BAC causes Sedation, subjective high, slowing of reaction times

A

.05-.1 %

46
Q

What BAC causes Excitement, decreased inhibitions, impaired motor function, slurred speech, ataxia

A

.1-.2%

47
Q

What BAC causes Disorientation, confusion, poor coordination

A

.2-.3%

48
Q

What BAC causes Stupor, apathy, vomiting, incontinence

A

.3-.4%

49
Q

What BAC causes Abolished reflexes, coma

A

.4-.5%

50
Q

What BAC causes Respiratory depression, death

A

> .5%

51
Q

What is the MC neurological problem in alcoholics?

A

peripheral neuropathies

52
Q

Development of brain is particularly sensitive to teratogenic effects of ethanol during what trimesters?

Physical development of face particularly sensitive during what trimester?

A

Brain- 1st and 3rd

Face- 2nd

53
Q

What is tx for acute alcohol intoxication?

A

maintain vital signs, prevent aspiration of vomit

Administer IV dextrose and IV thiamine if Wernicke-Korsakoff syndrome is suspected

54
Q

How do you treat mild alcohol withdrawal symptoms (anxiety, insomnia, tremors, agitation, muscle aches, sweating, cramping, nausea, vomiting, diarrhea and arrhythmias)?

A

centrally-acting clonidine or peripherally-acting propranolol

55
Q

How does ethanol activate the reward pthwy?

A

by increasing synaptic concentrations of dopamine in NA and increasing synaptic levels of Beta endorphin in ventral tegmental area

56
Q

What is the reason why recovering alcoholics relapse?

A

the levels of beta endorphins can persist for years even without consuming ethanol which is what drives the craving and eventually leads to relapse

(can prevent with anti-craving drugs)

57
Q

What are the beneficial effects of moderate alcohol consumption?

A

More in men >65

↓ risk of heart disease, ↓ risk of diabetes

(red wine best bc contains antioxidant resveratrol)

58
Q

What is Sustained Virologic Response (SVR)?

A

Undetectable RNA after 12 weeks of treatmeant

AKA CURE

59
Q

What is the goal in treatment of Peptic Acid Disease?

A

Reduce gastric acid secretion
Neutralize gastric acid
Enhance mucosal defenses Agents that coat the mucosa
Eradicate H. pylori

60
Q

How do you eradicate H. Pylori?

A

usually a PPI plus several antibiotics (clarithromycin with metronidazole or amoxicillin

61
Q

What are laxative MOA?

A

Bulk-forming: ↑volume ↑ evacuation (psyllium/methylcellulose)

Stool surfactants: ↓surface tension/lubricate (mineral oil)

Stimulants: stimulate electrolyte/water secretion and
peristaltic activity (bisacodyl/senna)
62
Q

Laxation

A

evacuation of soft stool (rectum)

63
Q

Cathartic

A

intense/increased intestinal activity and watery stool – e.g. for a colonoscopy prep

Pharm II Exam 1 (7 decks)

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