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Neorologia > Pain > Flashcards

Pain Flashcards

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
Q

Antipyretic is antifever, what is the difference between fever and hyperthermia?

A

Fever: elevated temp due to elevated set point

Hyperthermia: Heat production > Heat dissipation

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26
Q

Which hypothalamic nucleus is heat sensitive?

A

Anterior

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27
Q

Which hypothalamic nucleus is cold sensitive?

A

Posterior

28
Q

NSAID Antipyretic MOA

A

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
Q

COXIs GI Effects

A
  • Gastric intolerance: Chemoreceptor trigger zone stimmmulation and direct irritant
  • Ulcer: gastric H+ increases, mucus secretion decreses, bicarbonate decreases, decreased mucosal blood flow (PGI2)
30
Q

ASA risk
Dose ore Duration?
DDIs?

A

GI bleeding
Dose
Clopidogrel, warfarin, and other NSAIDs

31
Q

Does enteric coated ASA cause GI Stomach problems?

A

Yes, still reaches stomach via blood stream. Duh.

32
Q

Salicylate and URAT1

A

URAT1 resporbs uric acid in proximal tubule (is bidirectional)

33
Q

Low salicylate

A

decrease urate excretion by competitive transport

34
Q

High salicylate

A

increases urate excretion: somehow

35
Q

ASA and pregers

A

Category C: no evidence

Avoid near-term as it can increase duration of labor, increase bleeding

36
Q

Preeclampsia

A

Sudden spike in BP

Current cure: premature delivery of fetus

37
Q

Salicylate intoxication

A

over 40 mg/dl after ingestion

38
Q

Salicylate poisoning symptoms

A 
Tinnitus
N/V
Lethargy/excitibility
Increase temp
Hyperventylation -> respiratory alkalosis

Severe: Metabolic acidosis, seqizures

39
Q

> 35 mg/dl

A

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
Q

> 50 mg/dl

A

hypoventilation -> increased CO2 retention, respiratory acidosis,
Cannot compensate due to previous loss of HCO3-

41
Q

Salicylate intoxication Tx

A
  • Lavage or charcoal for large engestion
  • Whole body irrigation with PEG until shitting clear
  • Correct for dehydration
  • Alkaline diuresis (increase urine pH
42
Q

Ketorolac
MOA
Time limit
Admin

A

NSAID (COXI)
5 days
IV,IM, Intranasal

43
Q

Ibuprofen (Caldolor)

A

IV formulation

400 - 800 mg over 30 min Q6H

44
Q

NSAID BBW

A

Cardiovascular: may increase Thrombolic events
GI: Increased GI bleeds, ulceration, perforation

45
Q

Nephrotoxicity:

A

Na/K,Cl retention,
Edema
COX-1 mediated
Risks: kidney function, CHF, diabetes, liver disease, ACEIs, ARBs

46
Q

Renal Tox and NSAIDS

A

High NSAID dose increases risk

47
Q

Indicators of Liver Damage

A

Serum aminotransferases

  • AST aspartate transaminase
  • ALT alanine transferase
48
Q

NSAIDS and pregers

A

Do not use in 3rd trimester due to closure of ductus arteriosis

49
Q

What is the only shown benefit of Cox2 selective?

A

Decreased GI issues

50
Q

Is Cox2 inhibition cardioprotective in absence of Cox1 inhibition?

A

No, infact it increased risk of MI

51
Q

APAP/paracetamol

A

COX2 selective
Mildly anti inflammatory
Brain selective

52
Q

Paracetamol and bleeding

A

Low anti-platelet activity, but

May increase INR respons to warfarin? may inhibit 3A4

53
Q

APAP toxicity

A

IMINE Conjugation to proteins

Hepatic enzymes

54
Q

N-acetylcysteine

A

Given w/in 8-10h of OD
Oral: mucomyst
IV: Acetadote

55
Q

How is Naltrexone used to treat ethanol dependence

A

Decreases ethanol-induced dopamine release in nucleus accumbens

56
Q

Naloxegol

MOA and use

A

Opioid antagonist

Not orally absorbed, used to treate opioid induced constipation

57
Q

Symptoms of Opioid overdose

A 
Euphoria, drive depression
CNS/Respiratory depression
Miosis,
Hyperthermia
decreased bowel sounds
58
Q

Opioid intoxication treatment

A
  1. Maintain respiration

2. Reverse OD with antagonist

59
Q

Opioid tolerance to

A

Analgesia
CNS depression
Euphoria

60
Q

No opioid tolerance to

A

pupillary constriction or increased smooth muscle tone

61
Q

Opioid tolerance mechanism

A

increased adenylate cyclase, countering opioid induced decrease in cAMP

62
Q

Opioid Withdrawal Symptoms

A 
Piloerection
Muscle contractions
Anxiety
restlessness
diarrhea
lacrimation
63
Q

Which drugs have most severe withdrawal?

A

short acting with coadministered antagonist

64
Q

Neuropathic pain

A

Hyperalgesia to mechanical and thermal stimuli

Allodynia: pain to normally non-painful stimulus

65
Q

Why is neuropathic pain not responsive to opioids?

A

damage to primary afferent neurons decreases expression of opioid receptors

66
Q

What is most effective in neuropathic pain?

A

TCAs?

67
Q

What antiepileptic drugs are approved for neuropathic pain?

A

Gabapentin and Pregabalin

Neorologia (12 decks)

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