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Anesthesiology > 11. Pain management > Flashcards

11. Pain management Flashcards

1
Q

Algogenic (pain producing) substances

A
  • K+ from damaged cells
  • Serotonin from active platelets
  • Histamine from mast cells
  • Badikinin from tissue kallikrein
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2
Q

Sensitizing agents in pain

A
  • PGs, LTs from damaged cells

- Primary polymodal afferents: Substance P, Calcitonin Gene Related Peptide (CGRP)

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3
Q

Unimodal receptors

A

Mechanical

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4
Q

Bimodal receptors

A

Mechanical + thermal (> 45 degrees)

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5
Q

Polymodal receptors

A

Mechanical + thermal + chemical

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6
Q

Pain receptor fibres

A

1) Fiber Aδ - fast, sharp pain, easy to localize

2) Fiber C - slow, blunt/burning pain, harder to localize

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7
Q

CNS components of pain

A

Spinothalamic - spinoreticular - spinomesencephalic tracts

  • Complex association between many brain regions*
  • Somatosensory cortex (feeling, localization)
  • Hypothalamus (vegetative, humoral)
  • Limbic (mood, behaviour)
  • Frontal cortex (socialization)
  • Amygdala (cognitive reactions)
  • Hippocampus (pain memory)
  • Ant. Cingular cortex (emotional)
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8
Q

Gate-control theory of pain

A

Ascending inhibitory pathways of brain and ascending Abeta fibers can inhibit spread of incoming pain in SUbstantia Gelatinosa

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9
Q

Opioid and NMDA antagonists action

A

Inhibit inhibitory GABAerg cells which inhibit descending pathways (noradrenaline, serotonin)
Inhibition of inhibition reduces pain sensation

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10
Q

Endogenous opioids

A

Released by stimulation of periaqueductal grey stock (serotonin, noradrenaline)

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11
Q

Pain classifications

A

1) By duration
2) By etiology
3) By associated social/cognitive effects

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12
Q

Pain duration

A

Acute (< 6 weeks/3 months)
- No cognitive-emotional, socializing effects!

Chronic
- Often psychosomatic etc

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13
Q

Nociceptive pain

A

Released mediators activate pain receptors

  • Somatic
  • Visceral
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14
Q

Neuralgia

A

Direct irritation of nerves by mechanic or metabolic disturbance

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15
Q

Deafferentation pain

A

Hyperexcitability of spinal nerves after sensory deafferentation

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16
Q

Special pain syndrome

A

Migraine

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17
Q

Psychosomatic pain

A

Somatic symptoms caused by psychological stress

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18
Q

Afferentation of visceral pain

A
  • Thoracic / abdominal => sympathetic nerves
  • Pelvic viscera => parasympathetic nerves
  • Esophagus, trachea, pharynx => vagus + glossoph. nn
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19
Q

Visceral pain

A
  • Difficult to localize (C fiber)
  • Radiating pain
  • Accompanied by nausea and vegetative signs
  • Can be large pain
  • Reflex contraction of surrounding muscles
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20
Q

Etiology of abdominal pain + quadrants

A

Se internal

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21
Q

Pain radiation visceral pain

A

CNS cannot distinguish between somatic and visceral stimuli, so visceral pain radiates to skin (head zones)
- Dermatoma rule - to same emrbyonic dermatome

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22
Q

Radiation GERD

A

To the back

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23
Q

DDx chest pain that I don’t think of

A
  • Pleuritis sicca
  • Boerhaave SY
  • Tietze SY
  • Herpes zoster
24
Q

IPAT, BPI, McGill questionaire

A

Pain scales:

  • Initial pain assessment tool
  • Brief pain inventory
  • McGill questionaire
25
Q

Pain assessment in ICU

A
  • Behvioural pain scale (BPS) - face, upper limb, ventilation compliance
  • Critical-care observation tool (CPOT) - face, body, muscle tension, ventilation compliance
  • The most valid pain assessment tools*
26
Q

WHO guidelines for cancer pain

A
  • Mild pain: NOA (non-opoid analgetics)
  • Moderate: Low-potential opioids
  • Strong: High potential opioids
27
Q

Pain management in ICU

A
  • Routinely performed
  • BPS and CPOT pain assessment
  • Opioids as first line therapy
  • Gabapentine or carbamazepine in addition - for neuropathic pain
  • Thoracic epidural anesthesia in rib fractures
28
Q

Effects of NOA drugs

A

COX-1

  • Kidney function, gastric mucosa
  • ASA, Indomethacine, Piroxicam

COX-2
- Inflammatory augmentation, fever

29
Q

Current first-line NOA drugs

A
  • Ibuprophen, naproxen?
  • Acetaminophen (paracetamol)
  • Litterature: diclophenac (MOA)
30
Q

NOA drugs with the best analgetic potential

A

High - low:

1) ASA, oxicam, acetic acid derivatives
2) Ibuprophen ++
3) Paracetamol

31
Q

Most immportant SEs of mainetance of opoids

A
  • Obstipation
  • Sedation
  • Xerostomia
  • Pruritus
32
Q

Cannabinoid effects and indications

A

Effects: antiemetic, analgesic, appetite up, anti-tumorgenetic

Indications: Tumor, AIDS, Multiple Sclerosis

33
Q

Peripheral nerve block types + some advantages/disadvantages

A

Brachial plexus blockade and Femoral blockade

Advantages

  • Less cardiovascular effect
  • Enhanced bowel motility
  • No sedation

Disadvantages

  • Needs post-op observation
  • Needs intra-op supervision
34
Q

Neuroaxial blocks types + some advantages and disadvantages

A

SPA (spinal) and EDA (epidural)

Advantages
- Pain stimulus does not enter CNS - no sympathetic stimulation

Disadvantages

  • Parasympathetic tone enhancement
  • Circulatory and respiratory effects
  • Delayed mobilization
35
Q

Types of blockade in EDA

A
  • Sensory
  • Motoric
  • Vegetative
36
Q

Indications os EDA

A
  • Efficient anesthesia per se (abdominal, special ind: COPD)
  • Combined anesthesia
  • Obstetric anesthesia
  • Permanent anesthesia (acute pancreatitis, cancer?)
37
Q

Absolute CI of EDA

A
  • Hemophilias and/or coagulation disturbances

- Inflammation/wound on skin

38
Q

Relative CI of EDA

A
  • Hypovolemia/shock
  • Severe cardiovascular disease
  • Lack of informed consent
39
Q

EDA techniques

A

1) LOR: Loss of resistance technique
- CI: Narrow dura-myelon distance

2) Hanging Drop (hypobaric pressure of epidural space)
- Indication: Narrow epidural space

40
Q

Complications of EDA

A
  • Dural punction and Headache (lying position)
  • Dural punction and myelon punction
  • Epidural hematome
  • CNS infection
  • Cannule disruption
  • Intrathecal drug misadministration
41
Q

Where to put SPA in adults?

A

Under L2

42
Q

Effects SPA

A
  • Sensory
  • Motoric
  • Vegetative (hypotension, urinary stop)
43
Q

Solution used in SPA

A

2-4 ml (hyperbaric) bupivacaine 0,5 % solution

44
Q

Complications SPA

A
  • Headache (posture irrelevant)
  • Infection (sterility)
  • Backache
  • Epidural hematome (hemophilias, anticoag, TAG)
45
Q

Local anesthetics

A
  • Weak bases (pH 8-9)

- Less effective in inflammatory environment! (pH decreases)

46
Q

LA - esters

A
  • Cocaine
  • Benzocaine
  • Procaine
  • Chlorprocaine
  • Tetracaine
47
Q

LA - Amides

A
  • Lidocaine
  • Mepivacaine
  • Bupivacaine
  • Ropivacaine
  • Articaine
48
Q

Cocaine effects

A
  • Less psychostimulating than amphetamine
  • Sympathetic effects (vasoconstr, HT, tachyc, mydriasis)
  • Lethal dose per os 1 g, subcut 0,2-0,4 g
49
Q

Benzocaine

A

Powder and ointment for painful wounds

50
Q

Procaine

A

Infiltration anesthesia

- Rapid elimination in liver and by serum esterase

51
Q

Chlorprocaine

A

Infiltration and regional anesthesia

Twice as effective and less toxic than procaine

52
Q

Tetracaine

A

Topical anesthesia
Ten times more effective, but also more toxic than procaine
Accumulates easily in brain (lipid-soluble)

53
Q

Lidocaine

A

Topical anesthesia
Sudden onset and prolonged effect (Dur: 1,5-2 hours)
Hypersensitivity common
Single max dose ca. 500 mg

54
Q

Mepivacaine

A

Faster and last longer than lidocaine

55
Q

Bupivacaine

A

Very effective, but some cardiotoxic - cannot be used i.v!

56
Q

Ropivacaine (S-isomer)

A

Dissociative anesthesia

57
Q

Articaine

A

Short-acting, fast metabolism
Used in dentistry
Used in many ways (iv, spinal, epidural, ocular etc)

Anesthesiology (13 decks)

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