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Migraine
is common, recurrent, primary headache of moderate to severe intensity that interferes with normal functioning and is associated with GI, neurologic and autonomic symptoms
Chocolate
Alcohol
Nitrate containing foods
Tyramine containing foods
Fermented and pickled foods
Caffeine/caffeine withdrawal
Monosodium glutamate
Food triggers of migraine
STW-GLH
Strong smells and fumes
Tobacco smokes
Weather changes
Glare/flickering lights
Loud noises
High altitude
Environmental triggers of migraine
Fatigue
Excess/insufficient sleep
Menstruation/menopause
Skipped meals
Stress and post-stress
Strenous physical activity
Behavioral physiologic triggers of migraine
Migraine
effect in the activity of neuronal calcium channels mediating neurotransmitter release in the brainstem areas that modulate cerebral vascular tone and nociception
It will lead to vasodilation of intercranial extracerebral blood vessels with activation of the trigeminovascular system
Ergot alkaloids
Triptan derivative
Acute antimigraine drugs such as _____ and _____ are agonist of vascular and neuronal 5HT1 receptor subtypes
Serotonin receptors
When these receptors are activated, they cause blood vessels in the brain to tighten (vasoconstriction) and stop the release of pain-causing neuropeptides.
This leads to reduced pain signal transmission, helping relieve migraine attacks.
5-HT₁
specific serotonin receptors called ___ receptors found on blood vessels and nerves.
Migraine
Recurring unilateral episodes of throbbing head pain
Associated with nausea, vomiting and sensitivity to light, sound and/ or movement
Migraine aura (classic migraine)
A recurring headache that strikes after or at the same time as sensory disturbances
Phonophobia
Photophobia
Hypersomnia
Difficulty in concentrating
Examples of Neurological premonitory symptoms of migraine
DEAD-RIH
Depression
Euphoria
Anxiety
Drowsiness
Restlessness
Irritability
Hyperactivity
Examples of Psychological premonitory symptoms of migraine
Polyuria
Diarrhea
Constipation
Examples of Autonomic premonitory symptoms of migraine
FASTY
Food cravings
Anorexia
Stiff neck
Thirst
Yawning
Examples of Constitutional premonitory symptoms of migraine
NC-HDG
Neuroimaging
Comprehensive headache history
Headache evaluation
Diagnostic and laboratory assessment
General medical and neurologic examination
Clinical assessments for migraine
Sleep (dark and quiet)
Application of ice in head
Behavioral intervention
Non-pharmacological interventions for migraine
PP-PENS
Prophylactic therapy
Preventive therapy
Pre-treatment with anti-emetics
Ergot alkaloids and derivatives
NSAIDs and simple analgesics
Serotonin receptor agonist
Pharmacological interventions for migraine
Simple analgesics and NSAIDs
First line treatment for mild to moderate migraine attacks
Prophylactic therapy
therapy for recurring migraine attacks
Preventive therapy
therapy for headache that occurs in a predictable pattern
Tension-Type Headache
It is the most common type of primary headache and more common in women than men
Pain is usually mild to moderate, bilateral, non-pulsatile
Episodic headaches may become chronic
Headache
It can originate from myofascial factors and peripheral sensitization of nociceptors
Involvement of central mechanism
Activation of supraspinal pain perception structures
Headache
Premonitory symptoms and aura are absent
Pain is usually mild to moderate, bilateral, non-pulsatile and in the frontal and temporal areas, but occipital and parietal areas can also be affected
Mild photophobia or phonophobia may occur
Pericranial or cervical muscles may have tender spots or localized nodules in some patients
Pain
An unpleasant, subjective, sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
Neuropathic pain
Functional pain
Two types of pain
Neuropathic pain
Resulted from nerve damage (e.g., Postherpetic neuralgia and Diabetic neuropathy)
Acute pain
is usually a nociceptive but can be neuropathic
Chronic pain
can be both neuropathic and functional pain, for example, a pain that persist after the healing of acute injury
Functional pain
Refers to the abnormal operation of the nervous System (e.g., Fibriomyalgia, Irritable bowel syndrome, Tension-type headache)
Nociceptors
are pain sensing nerve cells. It can be located in either somatic or visceral
Thalamus
acts as relay station and passes the impulses to the central structure
Pain
It will propagate the information to the spinal cord nearby
The action potential will trigger the release pain neurotransmitter
(substance P)
It will ascends to higher centers
Body will modulate the pain
Endogenous opiate system will be activated
Neurotransmitter such as enkephalins, dynorphins and Bendorphins will bind to the receptors mu, delta and kappa
Endogenous opioid system
The body activates this system to reduce pain.
This system releases natural pain-relieving
B-endorphins
Enkephalins
Dynorphins
These substances bind to opioid receptors and help decrease the perception of pain
Pain
Patient can have a distress from trauma or appear to have no noticeable suffering
Acute pain
Chronic pain
Acute pain
Sharp or dull, burning, shock-like tingling, shooting radiating, fluctuating intensity, varying location and occur in a timely relationship with an obvious noxious stimulus
can cause HTN, tachycardia, diaphoresis, mydriasis and palor
there is no relation with comorbid conditions
Chronic pain
occurs without a timely relationship with a noxious stimulus
PPP-BM
Patient medical history
Pain scale
PQRST characteristic
Blood chemistry
Medications
Clinical assessment for Pain
INOM
Intrathecal and Epidural opioids
Non-opioid agents
Opioid agents
Morphine
Clinical intervention for Pain
Non-opioid agents
Given for mild to moderate pain
Fewer side effects (GI problems)
Opioid agents
Given for severe pain at high dose
Partial agonist and antagonist- selectivity with the pain receptor site
Might exhibit allergic reaction
Intrathecal and Epidural opioids
are often administered with patient controlled analgesia
Safe and effective (lesser side effect)
Morphine
is the first line agent for moderate to severe pain
Cause respiratory depression that why it’s given with Naloxone
Motor deficits
Mental deterioration
Parkinson’s disease has highly characteristic neuropathologic findings and clinical presentation. This includes what?
Loss of neurons
Presence of lewy bodies
Two known hallmarks in the substantia nigra pars compacta
Alpha-synuclein
The major component of lewy bodies
nigrostriatal dopamine
The degree of ___ loss has good correlation with loss and severity of motor function
thalamus
The inhibition of __ is resulted from inactivation of dopamine-1 and dopamine-2
nigrostriatal dopamine neurons
The tremor exhibited by the patients with Parkinson’s disease is due to degeneration of ___
Bladder problems and constipation
Thinking difficulties
Swallowing problems
Chewing and eating problems
Depression and emotional changes
Sleep problems and sleep disorders
Complications of Parkinsons
dementia (Thinking difficulties)
Cognitive problems such as ___ occurs in the later stage of Parkinson’s disease
depression and emotional changes
In the very early stage, it is usually developed
Receiving treatment for this can make it easier to handle the challenges of Parkinson’s disease
Swallowing problems
Saliva may accumulate in your mouth due to slowed swallowing, leading to drooling
Chewing and eating problems
Late-stage of PD affects the muscle in the mouth which makes chewing difficult
It can lead to choking and poor nutrition
Sleep problems and sleep disorders
People with PD often frequently waking up throughout the night, waking early or falling asleep during the day
MR-BIP
Muscle Rigidity
Resting tremor
Bradykinesia
Intellectual deterioration
Postural instability
Clinical manifestations of Parkinson's Disease
Resting tremor
Tremor is present mostly in the hands and sometimes characterize as pin- rolling
Muscle rigidity
Increase muscle resistance to passive range of motion
DNM
Deep Brain Stimulation (DBS)
Neuroimaging
Medical history
Clinical assessment for PD
Medical history
Medication that maybe a drug-induced parkinsonism
Neuroimaging
SPECT scan aka Dopamine transporter (DAT Scan)
Deep Brain Stimulation (DBS)
Placing electrodes that are surgically implanted in the brain
implant electrodes into specific part of the brain
The electric pulses from the heart is send to the brain to reduce Parkinson’s disease symptoms
Dopamine Transporter (DAT Scan)
SPECT scan is also known as?
MAD-DACCC
MAO-B inhibitors
Amantadine
Dopamine agonists
Deep Brain Stimulation (Surgical procedure)
Anticholinergics
COMT inhibitors
Carbidopa-Levodopa
Carbidopa-Levodopa infusion
Pharmacological interventions for PD
Levodopa
protects the conversion of dopamine outside the brain
Carbidopa-Levodopa infusion
It is administered through the feeding tube
Dopamine agonists
Mimics the dopamine in the brain
MAO-B inhibitors
Help prevents the breakdown of brain dopamine by inhibiting the enzyme MAO-B
COMT inhibitors
It prolongs the effect of levodopa therapy by blocking an enzyme that breaks down dopamine
Anticholinergics
This medication help control the tremor associated with Parkinson’s disease
Amantadine
Provide short-term relief of symptoms of mild, early-stage Parkinson’s disease
DES
Diet
Exercise
Speech-language pathologist
Non-pharmacological intervention for PD
Diet
Food high in fiber and drinking an adequate amount of fluids can help prevent constipation
Exercise
Increase muscle strength, flexibility and balance
Improve well-being and reduce depression or anxiety
TAMMY-P
Tai Chi
Alexander Technique
Massage
Meditation
Yoga
Pet Therapy
Alternative interventions for PD
Massage
Reduce muscle tension and promote relaxation
Tai Chi
It is an ancient form of Chinese exercise, tai chi employs slow, flowing motions that may improve flexibility, balance and muscle strength
Yoga
It can increase flexibility and balance
Alexander Technique
It focuses on the muscle posture, balance and thinking about how you use muscles and reduce muscle tension
Meditation
It can reflect and focus your mind on an idea or image
It may reduce stress and pain and improve your sense of wellbeing
Pet Therapy
Increase the flexibility and movement and improve your emotional health
Alzheimer’s Disease
It is a progressive disorder that causes brain cells to waste away or degenerate
It is the common cause of dementia
The early signs of the disease will develop severe memory impairment and lose ability to carry out everyday task
Current medications may temporarily improve symptoms or slow down the rate of decline
There is no treatment that cures this disease
U.I.
Uncharacteristic choices
Ineffective response
Symptoms of Alzheimer’s Disease
Making judgements and Decisions
IW-MAD-DAD
Irritability
Wandering
Mood swings
Apathy
Delusions
Distrusts in other
Aggressiveness
Depression
Symptoms of Alzheimer’s Disease
Changes in personality and behavior
Swallowing
Malnutrition
Balance Control
Bowel Control
Bladder Control
Bedsores
Symptoms of Alzheimer’s Disease
Disease Progression Symptoms
Genetic
Lifestyle
Environmental factors
Proteins
Plaque
Tangles
Causes of Alzheimer’s Disease
Genetic
Appears in middle ages
Lifestyle
Drug misuse
Environmental factors
Stress
Proteins (Plaque)
beta amyloid, a large protein leftover fragment which disrupts the cell to cell communications
Proteins (Tangles)
tau proteins, that initiates the neuron’s transport system of nutrients and essential materials are being deformed and cause “Neurofibrillary tangles” that causes disrupts the transport system
Down syndrome
Age
Poor sleep patterns
Sex
Family history and genetics
Lifestyle and heart health
Past head trauma
Mild cognitive impairment
Risk factors for Alzheimer’s Disease
Can’t communicate the pain experiencing
Can’t report symptoms of another illness
Can’t follow prescribed treatment plan
Can’t notice side effects
Complications of Alzheimer’s disease
Q-FEE
Quit smoking
Follow prescribed guidelines
Exercise regularly
Eat healthy
Preventions for Alzheimer’s disease
SLP-M
Self-reporting
Laboratory and imaging test
Thyroid hormone levels and vitamin deficiencies
MRI
CT
Physical and Neurological exam
Motor skills and cognitive function
Diagnosis for Alzheimer’s disease
MRI
may show possible brain shrinkage
CT
rule out strokes, tumors and head injuries
Memantine (Namenda)
Antidepressants
Cholinesterase inhibitors
Pharmacological intervention for Alzheimer’s disease
Cholinesterase inhibitors
Boost Cell to cell communication
Memantine (Namenda)
Slows the progression