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AD pathophysiology
Amyloid plaques and neurofibrillary tangles that occurred from chronic inflammation and caused structural damage in brain.
Where in the brain does AD affect?
Hippocampus (memory and learning)
Symptoms of AD
Memory loss
Disorientation and confusion
Inability to recognise family and friends
Aggressive behaviour
Depression
Psychoses
Anxiety
Mood stabilizers
Citalopram, sertraline, fluoxetine
Anxiolytics
Buspirone or some benzodiazepines
Mild stage of AD
May function independently
Memory lapses
Moderate stage of AD
Longest stage, can last many years
Difficulty with ADLs
Memory loss
Disoriented to time and place
Wandering/pacing
Severe stage of AD
Pharmacotherapy is not effective at this stage
Loses ability to respond to their environment
Total dependence on caretaker
Dysphagia and dysphasia
Early onset AD
Symptoms appearing at 40 years old
Typical age of AD onset
Symptoms appearing at 65+ years old
Goals of AD pharmacological therapy
Slows and improve symptoms
No cure for AD
Cholinesterase Inhibitors
Prevents breakdown of Ach and slows progression of AD
donepezil (Aricept) Contraindications
Pts with bleeding and jaundice
donepezil (Aricept) OD treatment
Anticholinergics (e.g. Atropine)
donepezil (Aricept) Administration
Give prior to bedtime
Take with food or milk
Monitor pt for hypotension
Monitor for changes in mental status and mood
Monitor for dizziness, insomnia or anorexia
Assess baseline vitals
Can be given 1x daily due to long ½ life
S/S of AchEI OD
Severe N/V
Sweating
Salivation
Hypotension
Bradycardia
Convulsions
Increased muscle weakness
Parkinson’s disease pathophysiology
Progressive loss of dopamine due to death and destruction of dopamine-producing neurons
Affects (unconscious) muscle movement
Where in the brain does PD affect?
Corpus striatum & substantia nigra
Most common degenerative CNS disease
Parkinson’s disease
Symptoms of PD
tremors
muscle rigidity
bradykinesia
postural instability
Pill rolling motion
Antiparkinsonian agents
Dopaminergics and Anticholinergics
Restores balance of Dopamine and Ach in the brain
Constantly needs adjustment based on s/s
Goal of PD pharmacotherapy
Increase the ability of the pt. to perform ADLs
Dopaminergic/dopamine agonist
Increases dopamine in brain
levodopa-carbidopa (Sinemet) Class
Dopamine agonist
donepezil (Aricept) Class
Acetylcholinesterase inhibitor
levodopa-carbidopa (Sinemet) adverse effects
acute MI
shock
involuntary movements
narrow angle glaucoma
Neuroleptic Malignant Syndrome (NMS)
levodopa-carbidopa (Sinemet) interactions
Ca2+ antacids can decrease the drug’s effectiveness
levodopa-carbidopa (Sinemet) administration
Take on an empty stomach for better absorption
Abrupt withdrawal of drug can cause NMS
Increase fibre and fluids
May take several months for full effect
tolcapone (Tasmar)
Dopaminergic adjunct agent
Inhibits enzymes that break down dopamine
ropinirole (Requip)
Dopaminergic adjunct agent
Activates dopamine receptors
amantadine (Symmetrel)
Dopaminergic adjunct agent
Causes dopamine release from nerve terminals
Catechol-O-Methyl Transferase (COMT) inhibitors mechanism
Increases concentration of existing dopamine in nerve terminals
Catechol-O-Methyl Transferase (COMT) inhibitors side effects
mental confusion
nausea
vomiting
headache
diarrhea
possible liver damage
Anticholinergic agents primary use
Used in early stages of PD therapy
Centrally acting
Not as effective as dopaminergics
Benztropine (cogentin) class
Anticholinergic agent
Benzatropine (cogentin) mechanism
Blocks excess cholinergic stimulation of neurons in the corpus striatum
Inhibits overactivity in the brain
Benztropine (cogentin) adverse effects
sedation
paralytic ileus
cardiovascular collapse
loss of balance
hallucinations
treatment of Benztropine (cogentin) OD
Physostigmine 1-2 mg subQ or IV
Benzatropine (cogentin) administration
Take with food or milk to prevent GI upset
Avoid alcohol
Photosensitivity
Monitor HR as it can cause tachycardia
Avoid OTC cold medicine
Do not stop abruptly
Notify provider if eye twitches or tremors occur
Nursing actions for PD
Monitoring chewing/swallowing to prevent aspiration
Instruct pt to call for assistance prior to getting out of bed or attempting to walk alone
Be cautious with older adults → higher risk for hypotension
Teach pt to stand or sit up slowly to avoid dizziness or falls
If dizziness occurs, teach pts to lie down until the sensation passes
Psychological factors+
Can decrease or increase the perception of pain
Anxiety, depression or fatigue can increase pain perception
Acute pain
Intense
Defined period of time
Sudden onset
Chronic pain
lasts longer than 6 months
Interferes with daily activities
Nociceptive pain
Due to injury to tissues
Somatic pain
Type of nociceptive pain
sharp, localized sensation
visceral pain
Type of nociceptive pain
Dull, throbbing, aching sensation
Neuropathic pain
Due to injury to nerves
Burning, shooting, numbing pain
Common in diabetics
Treated with anti-seizure & antidepressants
Nonpharmacological techniques for pain management
can be used alone or in conjunction with pharmacotherapy
may allow for lower doses and possibly fewer side effects
Opioid agonist mechanism
stimulates mu and kappa receptor sites
Morphine class
opioid agonist
Morphine primary use
relieves moderate to severe pain.
analgesia and anesthesia
Morphine adverse effects
Resp depression
Sedation
Nausea
Hypoactive bowel sounds
Constipation
Decreased peristalsis
Orthostatic hypotension → falls and injuries
Morphine contraindications
may mask pain of gallbladder disease due to biliary tract spasm
Morphine interactions
alcohol
other opioids
general anesthesia
MAOIs
sedatives → severe resp. depression → death
Treatment of Morphine OD
Naloxone (Narcan)
Activated charcoal
Laxatives
Opioid antagonists mechanism
blocks opioid activity
blocks mu and kappa receptors competitively
naloxone (Narcan) class
Opioid antagonist
naloxone (Narcan) administration
Administered parenterally: IV, IM, subQ
Administer for RR of <10 breaths/min
Monitor resp status
Have resuscitative equipment available
Should NOT be used for resp. depression caused by NONOPIOID MEDICATIONS (NSAIDs & acetaminophen)
Treatment for opioid dependence
switch from IV and inhalation forms to methadone PO
Methadone does not cure but avoids withdrawal symptoms
treatment may be needed for months or years
Buprenorphine
Mixed opioid agonist-antagonist
Sublingual or transdermal route
Non-opioid analgesics
Includes:
NSAIDs
Centrally-acting non-opioids
Non-opioid analgesics primary use
used for fever, inflammation and analgesia
Used for mild or moderate pain associated with inflammation
Signs of inflammation
Pain
Itching
Warmth
Redness
Aspirin class
Salicylates
Aspirin mechanism
anticoagulant, antipyretic, anti-inflammatory, analgesic
Aspirin adverse effects
High doses may cause GI distress and bleeding
May result in ulceration and bleeding (dark stools)
May increase action of oral hypoglycemic agents
Causes irreversible platelet aggregation inhibition
Should be discontinued 1 week prior to surgery
Aspirin contraindications
Should not be given to pts. receiving anticoagulant therapy such as warfarin and heparin
Aspirin interactions
GI ulcers when taken with NSAIDs, alcohol and steroids
Antacids, glucocorticoids and Phenobarbitals decreases effects
NSAIDs
Ibuprofen
Selective COX-2 Inhibitors
Ibuprofen (Motrin, Advil) class
NSAID
Ibuprofen (Motrin, Advil) mechanism
to inhibit cyclo-oxygenase and prevent formation of prostaglandins
Celecoxib mechanism
to inhibit cyclo-oxygenase and prevent formation of prostaglandins
Ibuprofen (Motrin, Advil) primary use
for mild - moderate pain and to reduce inflammation
Ibuprofen (Motrin, Advil) adverse effects
GI upset
Acute renal failure and nephrotoxicity
Ibuprofen (Motrin, Advil) administration
Take with food to prevent GI upset
Max dose in 24 hrs: 4000 mg
Older pts more prone to increased bleeding
Report bleeding and bruising to provider
Increase fluid intake to prevent nephrotoxicity
celecoxib (Celebrex) class
Selective COX-2 inhibitors
celecoxib (Celebrex) primary use
to relieve pain, fever and inflammation
celecoxib (Celebrex) adverse effects
Mild and related to GI system
acetaminophen (Tylenol) class
Centrally acting nonopioid analgesics
acetaminophen (Tylenol) mechanism
treats fever at the level of the hypothalamus
causes dilation of peripheral blood vessels, enabling sweating and dissipation of heat
acetaminophen (Tylenol) primary use
treatment of fever and to relieve pain
acetaminophen (Tylenol) adverse effects
uncommon with therapeutic doses
acetaminophen (Tylenol) administration
Hepatotoxic and may cause problems in clients who consume alcohol
inhibits the metabolism of warfarin → could result in a toxic accumulation of warfarin
Rheumatoid arthritis (RA) characteristics
systematic autoimmune inflammatory disorder
disfigurement and inflammation of multiple joints
joint stiffness and pain
pain more intense in the morning
tender and warm joints
Autoantibodies
a.k.a rheumatoid factor
activates inflammatory response in joints
S/s of RA
fever
weakness
fatigue
weight loss
scleritis
corneal ulcers
vasculitis
nodules under the skin
Diseases associated with RA
pulmonary disease & pericarditis
Non-pharmacological measures for RA
Physical therapy
Massage
Warm baths
heat to affected areas
exercise
surgery: joint replacement
Pharmacological treatment goals for RA
Relieve symptoms - reduce pain
maintain joint function
minimize systematic involvement/disability
delay progression of disease
Classes of non-arthritic drugs
NSAIDs
DMARDs
Glucocorticoids
Types of glucocorticoids
Prednisone/prednisolone
PO glucocorticoids (generalized symptoms)
Intra-articular injections (for 1 or 2 affected joints)
Methotrexate class
Non-biologic DMARD
Methotrexate adverse effects
Hepatic fibrosis
Bone marrow suppression
GI ulcerations
Pneumonitis
Methotrexate therapeutic effect
Most rapid acting DMARD
3-6 weeks
Sulfasalazine class
Non-biologic DMARD
Sulfasalazine primary use
Used to treat IBD and RA
Anti-inflammatory and immunomodulary actions
Can slow progression of joint deterioration
GI side effects may be intolerable
hydroxychloroquine sulfate (Plaquenil) class
Non-biologic DMARD
hydroxychloroquine sulfate (Plaquenil) primary use
relieves severe inflammation of arthritis and lupus for pts who have not responded well to other drugs
hydroxychloroquine sulfate (Plaquenil) mechanisms
not known
hydroxychloroquine sulfate (Plaquenil) adverse effects
anorexia
GI disturbances
hair loss
possible ocular effects
headaches
mood and mental changes