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pharmacology > cns (patho review for pharm) > Flashcards

cns (patho review for pharm) Flashcards

1
Q

cerebrum

A

thinking portion = perception, speech, memory, smell, voices

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2
Q

cerebellum
- damage to this = ?

A

muscle movement, posture, balance, tone, smooth gait
- damage: seizures, tremors, uncoordinated jerkiness

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3
Q

thalamus
- damage to this =?

A

relay center = sounds, sights, pain, touch, (NOT SMELL), control MOOD and MOTIVATION
- damage = bipolar disorder, anxiety, panic disorder, OCD

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4
Q

spinal cord
- damage to this = ?

A

transmits signals to and from brain
- damage: paresthesia, paralysis

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5
Q

limbic system
- not developed in what population?

A

hypothalamus, thalamus, hippocampus = mood, emotion, fear, anger, anxiety
- not developed in peds pts

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6
Q

basal ganglia

A

memory, learning, planning

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7
Q

reticular activating system (RAS)
- damage/inhibition of this = ?

A

heightened alertness, arousal
- damage/inhibited: drowsiness, sleepiness

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8
Q

blood brain barrier
- which population is it not developed in?
- protect from _____
- supplies ______

A

tight junctions to prevent toxins from vessels to cross over to brain and spinal cord
- not developed at birth (newborns)
- protect from pathogens and toxins
- supply: O2, glucose, nutrients

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9
Q

how can drugs cross over the BBB

A
  1. must be lipophilic (bc of double phospholipid membrane)
  2. can’t be protein bound or highly ionized
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10
Q

brainstem

A

connects spinal cord to brain; maintains VITAL BODY FXNS

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11
Q

aminobutyric acid (GABA)
- class of neurotransmitter ?
- job

A

AMINO ACID
INDUCES SLEEP
most abundant in brain, relaxes you

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12
Q

glutamate
- class of neurotransmitter ?
- job

A

AMINO ACID
STIMULATE BRAIN
produces excitation

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13
Q

what patients have imbalance of GABA and glutamate?

A

anxiety and seizure patients

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14
Q

what is the theory of different pain threshold

A

some ppl make more endogenous opioids peptides than others, making pain perception different

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15
Q

endorphins
- class of neurotransmitter?
- job

A

OPIOID PEPTIDE
RELEASE –> PLEASURE

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16
Q

“-erase” suffix meaning
- ex?

A

job of enzyme is to break down neurotransmitters
- acetylcholinerase

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17
Q

4 actions of drugs

A
  1. block reuptake of neurotransmitters (REUPTAKE INHIBITORS)
  2. block enzymes that break down neurotransmitters
  3. stimulating specific receptor sites when neurotransmitter is unavailable
  4. stimulating presynaptic nerve to release greater amounts of neurotransmitters
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18
Q

order of pain process

A
  1. transduction
  2. transmission
  3. modulation
  4. pain perception
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19
Q

transduction
- patho

A

trauma stimulates NOCICEPTORS

patho: injured tissue –> chemicals –> pain messages –> neurotransmitters

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20
Q

transmission
- patho

A

pain travels ALONG PERIPHERAL NERVES to spinal cord

patho: travels along A and C fibers –> pain stimuli enters spinal cord in dorsal horn –> SUBSTANCE P release in response to pain (neurotransmitter that interprets pain and regulates analgesic response)

21
Q

modulation
- patho

A

limbic system reacts to pain and releases new neurotransmitters

patho: send along descending spinal cord tracts –> new NTS that will impede pain (serotonin, norepinephrine, GABA, endogenous opioids) –> activate opioid receptors kappa and mu

22
Q

what is the response when mu is activated?

A

“ARSEPD”
analgesic
respiratory depression
sedation
euphoria
physical dependence
decreased GI motility

23
Q

what is the response when kappa is activated?

A

“SAD”
sedation
analgesic
decreased GI motility

24
Q

which opioid receptor is more dangerous

A

mu is more dangerous and potent

25
Q

pain perception
- patho

A

conscious awareness of pain

patho: pain impulse reaches brain –> conscious awareness of painful sensation –> limbic system = emotional response

26
Q

nociceptive pain
- 3 diff types?

A

normal way we process pain, receptors working properly
- somatic, visceral, referred

27
Q

somatic pain
- s/s

A

pain from skin, muscles, deep or superficial tissue
- WELL LOCALIZED

s/s: constant, aching, gnawing, burning, cramping pain

28
Q

visceral pain
- ex?

A

pain much deeper, inflammation so severe that its pressing on organs
- gallbladder/gall stones

29
Q

referred pain
- ex?
- s/s?

A

pain felt is NOT where what is actually causing the pain
- POORLY LOCALIZED
- chest pain/earache = MI

s/s: squeezing, cramping pain

30
Q

acute pain
- s/s?

A

sudden onset of pain, we know what causes it, can –> chronic pain

s/s: hypoxia, hypercapnia (CO2 retention), HTN, tachy, emotional

31
Q

neuropathic pain
- s/s?

A

non nociceptive pain process bc nerves themselves are damaged

s/s: tingling, shooting, burning, radiating pain

32
Q

vascular pain
- ex?

A

spasming in vessel
- migraine

33
Q

psychogenic pain

A

brain is not interpreting pain correctly, no reason for pain
- HARD TO DETERMINE
- usually due to chemical imabalance

34
Q

chronic pain

A

pain that has been going on for long periods of time, very hard to treat

35
Q

4 subtypes of chronic pain

A
  1. pain past normal healing time
  2. pain with chronic disease
  3. pain w/o ID cause
  4. pain w/ both chronic and acute effects of cancer
36
Q

consequences of chronic unrelieved pain

A
  1. chronic stress
  2. impaired muscle movement
  3. quality of life changes
  4. decreased sleep, social relations
  5. anger, hopelessness, depression
37
Q

job of endorphins

A

endogenous opioid that binds with opioid receptors on dorsal horn = prevent further transmission of pain

38
Q

what should a nurse do before pulling pain med for pt?

A

pain assessment: numerical or FACES
- see if non pharmacological treatments are available and effective for situation

39
Q

transcutaneous electrical nerve stimulation (TENS)

A

electrodes placed around nerves causing pain –> electrical impulse –> brain can’t interpret pain so much (varies between pt)

40
Q

example of an off label drug (non opioid) used as analgesic

A

gabapentin (seizure drugs)

41
Q

tolerance

A

body becomes used to effects of a substance, pt has to use more to achieve desired effect

42
Q

dependence

A

PHYSIOLOGIC no psychologic, withdrawal symptoms when drug is discontinued bc body in need

43
Q

addiction

A

PSYCHOLOGIC not physiologic , compulsive use of a drug for secondary gain, NOT for pain control

44
Q

signs of inflammation

A

heat, redness, swelling, pain, loss of function

45
Q

prostaglandins
- patho

A

regulate inflammation, body temp, pain transmission, platelet aggregation, GI protection

patho: sits on nerve receptor to increase pain and regulate inflammatory response

46
Q

how to create a prostaglandin?

A

need ACID to convert cyclooxygenase (COX) enzyme to create prostaglandin

47
Q

what are some effects of prostaglandins

A

increase:
body temp
smooth muscle contraction
platelet agg
renal vasodilation
inflammation and capillary permeability
mucus production

decrease:
BP
gastric acid secretion

48
Q

COX1
- purpose
- jobs
- inhibition results

A

COX1

purpose: good cox; produce prostaglandins involved in REG CELL ACTIVITY

jobs: normal cell activity, protect GI, regulate smooth muscle, normal renal function, promote plt aggregation

inhibition =
- bad: GI ulcers, increased bleeding, renal impairment, bronchoconstriction and HTN
- good: MI/stroke protection bc decrease plt agg

49
Q

COX2
- purpose
- jobs
- inhibition results

A

COX2

purpose: bad cox; produces prostaglandins at sites of inflammation –> increased amounts of inflammation

jobs: sensitizes pain, increase fever, inflammation, increase capillary permeability, contribute to colon cancer

inhibition =
- good: decreased inflammation, pain, fever, and protection against colon cancer
- bad: increased vasoconstriction, risk of MI/stroke

pharmacology (15 decks)

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