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Neorologia > Pain > Flashcards

Pain Flashcards

(67 cards)

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1
Q

Two types of Pain

A

Nociceptive and Neuropathic

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2
Q

Nociceptive Pain Defined and Two types

A

transduction of noxious stimuli, irrespective of cognitive awareness.

1) Somatic: cutaneous or deep tissues
2) Visceral: internal organs

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3
Q

Neuropathic pain defined

A

Caused by a primary lesion or dysfunction in the nervous system

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4
Q

Itch vs pain

A

Both mediated by thin unmyelinated nerve fibers from skin

Mediated by different mechanisms

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5
Q

Itch definition and causes

A

-Unpleasant sensation with desire to scratch

Pruritogens: histamine, environmental chemicals, drugs

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6
Q

Chronic Pain common mediators

A

Inflammatory

-TNF alpha and IL-1beta

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7
Q

Where do neuroimmune mediators act? Effects?

A
  • peripheral nociceptive nerve terminals
  • causes hyperalgesia
  • Chronic pain causes synaptic sensitization
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8
Q

Which tract does pain follow? what is it?

A

Anterolateral Spinothalamic tract

  • Synapses in Dorsal horn
  • Crosses sides
  • next synapse isn’t until the thalamus
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9
Q

Dermatome

A

Area of skin whoses sensory nerves all come from a single spinal nerve root

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10
Q

Dermatome significance

A

Why pain associated with a visceral organ (heart) might be perceived as peripheral (arm).

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11
Q

Chemical modulators of pain

A

Bradykinin (sensory neurons)

  • 5HT (platelets)
  • Histamine (mast cells)
  • Neuropeptides
  • ATP, K+ (Injured cells)
  • Chemokines
  • Ion Channels: Na, Ca, NMDA, AMPA, Kainate, TRPV1, H+ sensing channels
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12
Q

Most important sensitizers of peripheral pain sites

A

Prostaglandins (PGE2)

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13
Q

Sex differences in Pain

A
  • Women have lower pain thresholds
  • Women respond better to Opiod kappa agonists
  • Red headed women have even lower threshold: polymorphism to melanocortin-1 receptor
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14
Q

How to trap salicylic acid in urine

A

increase pH higher percentage ionized, remains in urine

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15
Q

asa metabolism

A

Mosly 1st pass, some plasma esterase

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16
Q

types of eicosanois

A
  • prostaglandins
  • Thromboxanes
  • Leukotrienes
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17
Q

Prostanoids

A
  • prostaglandins

- Thromboxanes

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18
Q

Arachidonic Acid Metabolites by Cox:Actions

A

-Pain & Inflammation: PGE2

  • Vasodilation: Prostaglandins
  • Vasoconstriction: Thromboxane
  • Platelet aggregation: thromboxane
  • Platelet dis aggregation: prostacycline
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19
Q

PGE

A

Pain and inflammation,
inhibit acid secretion
stimulate Mucous secretion
Na and water excretion

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20
Q

Prostaglandins

A

Pain, Vasodilation, acid secretion, mucous secretion

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21
Q

Prostacyclin

A

Vasodilation, platelet disaggregation,
inhibit acid secretion
Stimulate Mucous secretion
Na and water excretion

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22
Q

Thromboxane

A

Vasoconstriction, platelet aggregation

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23
Q

Cox-2 binding site specificity

A

Val substituted for Ile

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24
Q

Cox2/Cox1 ratio

A

Relative selectivity

>1 Cox 1 selective

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25
Antipyretic is antifever, what is the difference between fever and hyperthermia?
Fever: elevated temp due to elevated set point Hyperthermia: Heat production > Heat dissipation
26
Which hypothalamic nucleus is heat sensitive?
Anterior
27
Which hypothalamic nucleus is cold sensitive?
Posterior
28
NSAID Antipyretic MOA
PGE2 increases cAMP production, increases heat generation and decreases heat loss 1) Inhibition of PGE2 prodution 2) Increase heat loss to vasodilation and sweating
29
COXIs GI Effects
- Gastric intolerance: Chemoreceptor trigger zone stimmmulation and direct irritant - Ulcer: gastric H+ increases, mucus secretion decreses, bicarbonate decreases, decreased mucosal blood flow (PGI2)
30
ASA risk Dose ore Duration? DDIs?
GI bleeding Dose Clopidogrel, warfarin, and other NSAIDs
31
Does enteric coated ASA cause GI Stomach problems?
Yes, still reaches stomach via blood stream. Duh.
32
Salicylate and URAT1
URAT1 resporbs uric acid in proximal tubule (is bidirectional)
33
Low salicylate
decrease urate excretion by competitive transport
34
High salicylate
increases urate excretion: somehow
35
ASA and pregers
Category C: no evidence | Avoid near-term as it can increase duration of labor, increase bleeding
36
Preeclampsia
Sudden spike in BP | Current cure: premature delivery of fetus
37
Salicylate intoxication
over 40 mg/dl after ingestion
38
Salicylate poisoning symptoms
``` Tinnitus N/V Lethargy/excitibility Increase temp Hyperventylation -> respiratory alkalosis ``` Severe: Metabolic acidosis, seqizures
39
>35 mg/dl
Stimulates medullary respiratory center -> hyperventilation -> respiratory alkalosis -> renal excretion of HCO3-, Na+, and K+ to compensate for respiratory alkalosis; reduced buffering capacity uncoupling of oxidative phosphorylation Now have compromized respiratory alkalosis
40
>50 mg/dl
hypoventilation -> increased CO2 retention, respiratory acidosis, Cannot compensate due to previous loss of HCO3-
41
Salicylate intoxication Tx
- Lavage or charcoal for large engestion - Whole body irrigation with PEG until shitting clear - Correct for dehydration - Alkaline diuresis (increase urine pH
42
Ketorolac MOA Time limit Admin
NSAID (COXI) 5 days IV,IM, Intranasal
43
Ibuprofen (Caldolor)
IV formulation | 400 - 800 mg over 30 min Q6H
44
NSAID BBW
Cardiovascular: may increase Thrombolic events GI: Increased GI bleeds, ulceration, perforation
45
Nephrotoxicity:
Na/K,Cl retention, Edema COX-1 mediated Risks: kidney function, CHF, diabetes, liver disease, ACEIs, ARBs
46
Renal Tox and NSAIDS
High NSAID dose increases risk
47
Indicators of Liver Damage
Serum aminotransferases - AST aspartate transaminase - ALT alanine transferase
48
NSAIDS and pregers
Do not use in 3rd trimester due to closure of ductus arteriosis
49
What is the only shown benefit of Cox2 selective?
Decreased GI issues
50
Is Cox2 inhibition cardioprotective in absence of Cox1 inhibition?
No, infact it increased risk of MI
51
APAP/paracetamol
COX2 selective Mildly anti inflammatory Brain selective
52
Paracetamol and bleeding
Low anti-platelet activity, but | May increase INR respons to warfarin? may inhibit 3A4
53
APAP toxicity
IMINE Conjugation to proteins | Hepatic enzymes
54
N-acetylcysteine
Given w/in 8-10h of OD Oral: mucomyst IV: Acetadote
55
How is Naltrexone used to treat ethanol dependence
Decreases ethanol-induced dopamine release in nucleus accumbens
56
Naloxegol | MOA and use
Opioid antagonist | Not orally absorbed, used to treate opioid induced constipation
57
Symptoms of Opioid overdose
``` Euphoria, drive depression CNS/Respiratory depression Miosis, Hyperthermia decreased bowel sounds ```
58
Opioid intoxication treatment
1. Maintain respiration | 2. Reverse OD with antagonist
59
Opioid tolerance to
Analgesia CNS depression Euphoria
60
No opioid tolerance to
pupillary constriction or increased smooth muscle tone
61
Opioid tolerance mechanism
increased adenylate cyclase, countering opioid induced decrease in cAMP
62
Opioid Withdrawal Symptoms
``` Piloerection Muscle contractions Anxiety restlessness diarrhea lacrimation ```
63
Which drugs have most severe withdrawal?
short acting with coadministered antagonist
64
Neuropathic pain
Hyperalgesia to mechanical and thermal stimuli Allodynia: pain to normally non-painful stimulus
65
Why is neuropathic pain not responsive to opioids?
damage to primary afferent neurons decreases expression of opioid receptors
66
What is most effective in neuropathic pain?
TCAs?
67
What antiepileptic drugs are approved for neuropathic pain?
Gabapentin and Pregabalin

Neorologia (12 decks)

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