Pain/Fever Lecture Flashcards

1
Q

What is somatic pain?

A

Skin, bone, joint, muscle, connective tissue

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2
Q

What is visceral pain?

A

Internal organs–> pancrease, large intestine

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3
Q

Define nociceptive pain

A

acute pain

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4
Q

Define neuropathic pain

A

chronic pain

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5
Q

What is the gate control theory of pain?

A

Brain acts as a gate to increase/decrease flow of nerve impulses from peripheral fibers to CNS

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6
Q

What is the neuromatrix theory?

A

Each person has a unique genetically built in network of neurons called self body neuromatrix

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7
Q

What happens when there is stimulation of nociceptors?

A

Releases: luekotriens, serotonin, histamine, PGs, substance P, bradikinins
Receptor activation is transmitted along afferent nerve fibers to the spinal chord

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8
Q

What are nociceptors?

A

Found in somatic and viceral structures
Activated & sensitized by mechanical, thermal and chemical impulses
Distinguish between noxious and inncuous stimuli

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9
Q

How is nociceptive pain transmitted?

A

Large diameter and sparsely myelinated A fibers evoke sharp and well localized pain
Small diameter unmyelinated C fibers produce dull aching and poorly localized pain

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10
Q

What do afferenct nociceptive pain fibers release?

A

Neurotransmitters: glutamate, substance P and calcitonin gene-related peptide

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11
Q

What does the thalamus do?

A

Works as a relay station for transmission

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12
Q

What is pain influenced by?

A

Interactions between neuroreceptors and neurotransmittors in the synapse

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13
Q

What is pain perception?

A

Conscious experience takes place in higher cortical region in the brain
Brain can only accommodate limited number of pain signals
Cognitive and behavioral functions can modify pain by decrease pain signals
Relaxation, distraction, mediation, help in reduction

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14
Q

What is modulation of pain?

A

Endogenous opiate system
Neurotransmitters: endorphins, dynorphins, enkephalins
Recepts: mu, delta, kappa
Endogenous opioids bind to receptors- modulate pain impulse

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15
Q

NMDA activation leads to?

A

Decrease binding of opiates to receptors

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16
Q

What occurs in chronicn pain?

A

Disengaged from noxious stimuli
Nerve damage
Burning, tingling, shooting pain

17
Q

What is the location, nature, onset and duration of tension-type headaches?

A

Bilateral
Varies from diffuse ache to tight pressing constricting pain
Gradual
Minutes to days

18
Q

What is the location, nature, onset and duration of migraine headache?

A

Usually unilateral
Throbbing
Sudden
Hours to 2 days

19
Q

What is the location, nature, onset and duration of sinus headache?

A
Face, forehead, or periorbital area
Pressure behind eyes or face
> Dull, bilateral pain & worse in the morning
Simultaneous with sinus symptoms
Days
20
Q

What is the vascular hypothesis of migraine headaches?

A

Intracerebral aterial vasoconstriction followed by extracranial vasodilation

21
Q

What happens during a migraine headache?

A

Perivascular axons release calcitonin gene-related peptide, neurokinin A and substance P
Released peptides interact with dural blood vessels to promote vasodilation and neurogenic inflammation

22
Q

Migraine headache’s neurotransmitter is what?

A

Serotonin (5-HT)

23
Q

What is Devil’s Claw?

A

Inhibits lipoxygenase and COX-2
Helps in the production of TNF-alpha (anti-inflammatory)
- Lower back pain
50-100 mg harpagoside daily reduce low back pain
Cause hypoglycemic effects

24
Q

What is feverfew?

A
Leaves used for prevention of migraine headaches
- Reduce incidence of attacks
Less nausea and vomiting
Inhibits PG synthesis
Increases risk of photsensitivity
25
Q

What is comfrey?

A

Suppress degranulation of azurophil granules and superoxide generation in leucocytes
Reduces inflammation
Same effect as diclofenac in reducing pain and inflammation
Contains pyrrolizidine

26
Q

What is bromelain?

A

May inhibit the synthesis of PGs
Activates plasmin produciton from plasminogen
Reduces pain and inflammation after tooth extraction
May reduce pain while walking after episiotomy
Increase absorption of antibiotics
Inhibit platelet aggregation-risk of bleeding
Lowers bradykinin and kininogen

27
Q

What is a fever?

A
Rise in body temperature
Normal = 37 Fever - 37.8
Thermoregulation in response to pyrogens
Deregulation results in fever
Infections frequently cause this
28
Q

Define Hyperpyrexia

A

Temperature over 41.1 or 107

29
Q

What is the pathophysiology of fevers?

A

Microbial infection
Noninfectious: cancer, tissue damage, surgery, etc
Drug induced: anti-infective, anti-neoplastics, cardiovascular, CNS agents
Pyrogens: Exogenous (microbes, toxins) or endogenous (TNF)

30
Q

What are anti-infectives?

A

Isoniazid, sulfonamids

31
Q

What are anti-neoplastics?

A

Chlorambucil

Daunorubicin

32
Q

What are cardivascular?

A

Nifedipine

Procainamide

33
Q

What are CNS agents?

A

Barbiturates

Lithium

34
Q

How is the hypothalamus involved in fever pathophysiology?

A

Controls body temperature homeostasis by setting a target temp for the
Feedback: peripheral nerves sending cool/warm sensation to brain and tissue
Balances heat loss and production

35
Q

How could you increase the set temp?

A

Exposure to pyrogens results in release of arachidonic acid metabolites
These metabolites cross BBB, and increase the temp

36
Q

What do sympathetic signals cause?

A

Vasoconstriction and decreased heat loss through skin

37
Q

What drugs are used for pain/fever management

A

Acetaminophen (inhibit COX3)
Aspirin (inhibits cyclooxygenase –> decreases PGs; inhibit COX1)
Ibuprofen (inhibits cyclooxygenase –> decreases PGs; inhibit COX1)
Other NSAIDs