cns (patho review for pharm) Flashcards
cerebrum
thinking portion = perception, speech, memory, smell, voices
cerebellum
- damage to this = ?
muscle movement, posture, balance, tone, smooth gait
- damage: seizures, tremors, uncoordinated jerkiness
thalamus
- damage to this =?
relay center = sounds, sights, pain, touch, (NOT SMELL), control MOOD and MOTIVATION
- damage = bipolar disorder, anxiety, panic disorder, OCD
spinal cord
- damage to this = ?
transmits signals to and from brain
- damage: paresthesia, paralysis
limbic system
- not developed in what population?
hypothalamus, thalamus, hippocampus = mood, emotion, fear, anger, anxiety
- not developed in peds pts
basal ganglia
memory, learning, planning
reticular activating system (RAS)
- damage/inhibition of this = ?
heightened alertness, arousal
- damage/inhibited: drowsiness, sleepiness
blood brain barrier
- which population is it not developed in?
- protect from _____
- supplies ______
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
how can drugs cross over the BBB
- must be lipophilic (bc of double phospholipid membrane)
- can’t be protein bound or highly ionized
brainstem
connects spinal cord to brain; maintains VITAL BODY FXNS
aminobutyric acid (GABA)
- class of neurotransmitter ?
- job
AMINO ACID
INDUCES SLEEP
most abundant in brain, relaxes you
glutamate
- class of neurotransmitter ?
- job
AMINO ACID
STIMULATE BRAIN
produces excitation
what patients have imbalance of GABA and glutamate?
anxiety and seizure patients
what is the theory of different pain threshold
some ppl make more endogenous opioids peptides than others, making pain perception different
endorphins
- class of neurotransmitter?
- job
OPIOID PEPTIDE
RELEASE –> PLEASURE
“-erase” suffix meaning
- ex?
job of enzyme is to break down neurotransmitters
- acetylcholinerase
4 actions of drugs
- block reuptake of neurotransmitters (REUPTAKE INHIBITORS)
- block enzymes that break down neurotransmitters
- stimulating specific receptor sites when neurotransmitter is unavailable
- stimulating presynaptic nerve to release greater amounts of neurotransmitters
order of pain process
- transduction
- transmission
- modulation
- pain perception
transduction
- patho
trauma stimulates NOCICEPTORS
patho: injured tissue –> chemicals –> pain messages –> neurotransmitters
transmission
- patho
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)
modulation
- patho
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
what is the response when mu is activated?
“ARSEPD”
analgesic
respiratory depression
sedation
euphoria
physical dependence
decreased GI motility
what is the response when kappa is activated?
“SAD”
sedation
analgesic
decreased GI motility
which opioid receptor is more dangerous
mu is more dangerous and potent
pain perception
- patho
conscious awareness of pain
patho: pain impulse reaches brain –> conscious awareness of painful sensation –> limbic system = emotional response
nociceptive pain
- 3 diff types?
normal way we process pain, receptors working properly
- somatic, visceral, referred
somatic pain
- s/s
pain from skin, muscles, deep or superficial tissue
- WELL LOCALIZED
s/s: constant, aching, gnawing, burning, cramping pain
visceral pain
- ex?
pain much deeper, inflammation so severe that its pressing on organs
- gallbladder/gall stones
referred pain
- ex?
- s/s?
pain felt is NOT where what is actually causing the pain
- POORLY LOCALIZED
- chest pain/earache = MI
s/s: squeezing, cramping pain
acute pain
- s/s?
sudden onset of pain, we know what causes it, can –> chronic pain
s/s: hypoxia, hypercapnia (CO2 retention), HTN, tachy, emotional
neuropathic pain
- s/s?
non nociceptive pain process bc nerves themselves are damaged
s/s: tingling, shooting, burning, radiating pain
vascular pain
- ex?
spasming in vessel
- migraine
psychogenic pain
brain is not interpreting pain correctly, no reason for pain
- HARD TO DETERMINE
- usually due to chemical imabalance
chronic pain
pain that has been going on for long periods of time, very hard to treat
4 subtypes of chronic pain
- pain past normal healing time
- pain with chronic disease
- pain w/o ID cause
- pain w/ both chronic and acute effects of cancer
consequences of chronic unrelieved pain
- chronic stress
- impaired muscle movement
- quality of life changes
- decreased sleep, social relations
- anger, hopelessness, depression
job of endorphins
endogenous opioid that binds with opioid receptors on dorsal horn = prevent further transmission of pain
what should a nurse do before pulling pain med for pt?
pain assessment: numerical or FACES
- see if non pharmacological treatments are available and effective for situation
transcutaneous electrical nerve stimulation (TENS)
electrodes placed around nerves causing pain –> electrical impulse –> brain can’t interpret pain so much (varies between pt)
example of an off label drug (non opioid) used as analgesic
gabapentin (seizure drugs)
tolerance
body becomes used to effects of a substance, pt has to use more to achieve desired effect
dependence
PHYSIOLOGIC no psychologic, withdrawal symptoms when drug is discontinued bc body in need
addiction
PSYCHOLOGIC not physiologic , compulsive use of a drug for secondary gain, NOT for pain control
signs of inflammation
heat, redness, swelling, pain, loss of function
prostaglandins
- patho
regulate inflammation, body temp, pain transmission, platelet aggregation, GI protection
patho: sits on nerve receptor to increase pain and regulate inflammatory response
how to create a prostaglandin?
need ACID to convert cyclooxygenase (COX) enzyme to create prostaglandin
what are some effects of prostaglandins
increase:
body temp
smooth muscle contraction
platelet agg
renal vasodilation
inflammation and capillary permeability
mucus production
decrease:
BP
gastric acid secretion
COX1
- purpose
- jobs
- inhibition results
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
COX2
- purpose
- jobs
- inhibition results
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
