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process of detecting and signalling potential tissue damage
protects body from harm
includes relfexes
sensory receptors - found in skin, viscera, muscles, joints and meninges
stimulated by chemical, heat, pressure, touch, temperature
emit signals to CNS
nociception
only achieved when the superthreshold for nociceptors are reach and induce a pain pathway
acute pain is protective
pain
slow and dull
autonomic relfexes
pain memory and discomfort
paleospinathalamic tract
chronic pain
C fibers of pain
rapid and sharp
pain localisation with withdrawal reflexes
neospinothalmatic tract
somatic pain
A delta fibers
can be acute or chronic
somatic and visceral pain - skin, muscle, joins
treated with analgesic and inflammatory medications
all parts of body
nociceptors - send signals to autonomic ganglion and conduction of spinal cord, transmission to brain and perception of pain
nociceptive pain
due to injury to a nerve
alteration in the process and modulation of pain
persistent and chronic pain - worsens by psychological factors - stress, anxiety
peripheral or central
treatment - antidepressants, opiods, NSAIDs
diabetic peripheral neuropathy
neuropathic pain
Increased excitability and sensitivity to pain, leading to heightened responses to a stimulus that is normally painful
Hyperalgesia
Painful responses triggered by a stimulus that is not normally painful
Allodynia
Vivid perception that a limb that has been removed
feel that the phantom limb is distorted or shorter than the original limb
Tickling, irritation, Cramps, Shooting, piercing, or stabbing pain, numb
even for people who are born without, not just limbs
Phantom limb pain
mechanism to alert individual of potential harmful tissue damage
Sudden onset, relief when stimulus removed
seconds to days, up to 3 months - short duration
causes stimulation of autonomic NS - increased heart rate and BP, anxiety - somatic, visceral pain
acute pain
persistent - more than 3-6months
no purpose - suffering
ongoing
absence of autonomic response
persistent inflammation and pain - linked to neuropathic pain
significant psychological responses
chronic pain
internal organs
pain and pressure
dull, aching
visceral pain
superifical pain - from skin
deep arises - bones, joints, tissues, tendons, blood vessels
touch, pressure, temperature, pain
sharp, burning, sharp radiating pain
somatic pain
perceived at a site which is different from the site of injury or origin of pain as innervated by same spinal segment - converge at same dorsal horn projection in spinal cord
referred pain
subjective
threshold - lowest intensity of pain recognised by individual
tolerance - duration or intensity individual can endure - can decrease with repeated exposure
increase with alcohol consumption and prolonged opioid medications
pain threshold
nociceptive nerve endings
dendron - pre-nerve ending before cell body in the autonomic ganglion
transduction - impulse along dendron
conduction - impulse along axon
sensory neurons
Nociceptors carry out transduction along the dendron, followed by further conduction along the axon.
the spinal cord, mediators are released until the signal threshold is reached. This leads to electrical impulse transmission along the spinothalamic tract to the brain, which leads to the integration and perception of pain.
signal relay occurs in the thalamus.
processing and conscious awareness take place in the cerebral cortex.
descending inhibitory pathways lead to the modulation of pain.
the dorsal horn in the spinal cord, mechanisms allow for gate control of pain.
pain pathway
When an injury happens, pain receptors send an excitatory signal up through the spinal cord toward the brain
The brain responds by sending a signal back down the spinal cord through a "descending inhibitory pathway"
this descending signal triggers the release of natural pain-relieving chemicals called endorphins - thus feeling less pain
cause of pain going away
Pathways traveling down from the brain release noradrenaline (NA) and serotonin (5-HT) to inhibit the transmission neuron going to the brain.
Local interneurons release enkephalin to suppress the signal directly at the primary nociceptive nerve.
GABA, Enkephalins, Noradrenaline (NA), Serotonin (5-HT), and Glycine.
pain blockers
Tissue injury releases chemicals like Bradykinin, 5-HT, and prostaglandins, which excite the primary nociceptive neuron.
spinal cord synapse, Substance P (SP), Glutamate, and Nitric Oxide (NO) are released to transmit the excitatory signal onward to the brain
pain promotors
Block peripheral generation of the nociceptive impulses
inhibit prostaglandin synthesis
reduce sensitivity of sensory nociceptive nerve ending to spinal cord
NSAIDs
Act on spinal cord & limbic system
Stimulate descending inhibitory pathways
inhibit transmission to dorsal horn
minimal peripheral action
opioids
Semi rigid and slightly flexible structure which acts as a surface for articulating ends of skeletal joints
cartilage
attach bone to muscle
tendons
attach bone to bone
ligament
pain
limitation on mobility
decrease Qol
pyschological effect
disadvantages of muscoskeletal pain
Muscle strain or overuse
Stress fractures
Degenerative disc disease
Arthritis
Spondylitis
Lower back injury - due to hyperextension of lumbar spine
lower back pain causes
Worsening pain over several days
Pain radiating down into the leg(s)
Severe shooting pains into the leg(s) accompanied by loss of function or weakness in the leg(s)
Urinary or bowel incontinence
referral for lower back pain
local muscle damage due to mechanical overloading
sports related or trauma related
sudden, forced motion - stretch beyond normal capacity
strain
no muscle deformities
minimal strain
pain and brusing - for some muscle tearing
partial tearing strain
minimal pain, complete tear
muscle deformity
complete tear
Injury to ligaments surrounding the joint
pain, rapid swelling, heat, loss of function
pain and swelling subside more slowly
abnormal or excessive joint movement
sprain
ankle
knee
elbow
wrist
site of sprain injury
Severe pain, immediate swelling, loss of function, marked deformity and abnormal mobility
fracture
Very obvious, joint appears deformed. Displaced bone end often causes an abnormal lump or ridge or depression
dislocation
Suspected fracture
Bone abnormalities
Accompanying head injury
Severe pain at rest
Pain & wt bearing not better within 5-7 days.
Associated injury to skin (may require tetanus prophylaxis)
Suspected arthritis or other diseases
referral for pains
painful menstruation
Dysmenorrhoea
pain on sexual intercourse
Dyspareunia
1st period
12 years
day 1
menarche
FSH stimulates follicle development, leading to increased oestrogen and endometrial proliferation
Occurs at around Day 14 when a mature egg is released from the ovary - ovulation
period - 4 to 7 days - 30-40ml
21-35 days
optimal fertility - 18-31
menstrual cycle
FSH causes around 20 tiny sacs (follicles), each containing an egg (ovum), to start growing.
One follicle grows faster than the rest and becomes the dominant follicle.
The dominant follicle produces and releases oestrogen.
High oestrogen levels signal the body to lower FSH levels (negative feedback). Without enough FSH, the other competing follicles stop growing and break down.
The main winning follicle matures into a fully developed structure called the Graafian follicle (GF), which is ready to release the egg.
follicle growth
main hormone that stimulates oestrogen release
controls the proliferative phase of endometrium, which causes the endometrium to regenerate (thickens and increases vascularity, occurs days 5 to mid cycle)
High oestrogen level in mid cycle leads to surge of LH secretion
Follicle stimulating hormone
main hormone controlling subsequent progesterone secretion from the corpus luteum
Surge of LH stimulates ovulation mid cycle
Graafian follicle swells and ruptures releasing the ovum
Luteinising hormone
pain associated with menstruation in the absence of pathology
significant pain associated with menstruation
Recurrent, significant pain associated with menstruation
just before and during menstruation
primary dysmenorrhea
endometrial cells release prostaglandins - causing uterine contractions causing high pressure vasoconstriction, ischameia causes accumulation of anaerobic metabolites and nerve sensitsation
activation of stretch receptors
prostaglandins relaxes the bowel muscles - period poo
increase in progesterone - constipation
pathophysiology of mensturation
Early menarche
Younger age
Stress
Heavy/long duration of menstrual flow
Family history
Nulliparity
smoking
obesity
risk of primary dsymenorrhea
cramping
suprapubic pain
lower back and thigh pain
several hours before menstruation
diarrhoea, nausea, vomiting
altered pain sensitivity
hours before period
peak pain - max blood flow
symptoms of primary dysmenorrhea
constant pain
comes in goes within the cycle
pain during sex or passing motion
progression of symptom severity
bladder pain
symptoms after 25
how disabled they feel
maybe screen for STIs and rule out secondary dsymenorrhea
referral for period pain
reduce prostaglandin synthesis
decrease pain, nausea, diarrhoea
may require loading dose
can be trialled for 3 months
NSAIDS for period pain
reduced endometrium - reduced PG - reduced pain
less evidence
need continous use
trial for 3 months
pill, vaginal ring, IUD
Contraceptive pill
Low fat vegetarian diet
Increased dairy intake
Vitamin E for 5 days starting 2 days before menses - 500units daily OR 200units BD
Vitamin B1 100mg daily
Vitamin B6 100mg daily
Fish Oil Supplement
Ginger powder - days 1-3 of cycle
complementary medications for dysmenorrhea
Aerobic exercise
High frequency transcutaneous electrical nerve stimulation (TENS)
Acupuncture
Heat packs (may be as effective as ibuprofen)
Behavioural interventions
non-pharmacological for dysmenorrhea
Prolonged direct heat exposure, at a threshold below causing a thermal burn
heat packs, hot bottles
painless
rash will fade
temporary in early stages - fixed and darker of exposure continues
retinoids - reduce discolouration
Erythema Ig Abne
involves cyclically recurring mood, physical, and cognitive symptoms during the luteal phase, starting 4–10 days before a period and resolving a few days after menses begin.
can worsen other chronic conditions such as epilepsy, migraine, asthma, and Premenstrual Exacerbation (PME).
potential factors include progesterone or prostaglandin (PG) fluctuations, hormonal interactions (such as allopregnanolone) with central neurotransmitters (especially serotonin), and genetic or family history.
pre-menustral syndrome
irritability
anxiety/ nervous tension
lower coping ability
difficulty concentrating
wanting to be alone
lower libido
emotional PMS symptoms
fluid retention (swollen fingers or ankles)
bloating around the abdomen
breast swelling and tenderness
skin problems such as acne
headaches and/or migraines
poor coordination or clumsiness
physical PMS symptoms
limited to luteal phase
impact daily life
present for 2 consecutive cycles
not explained by other diagnosis
diagnosis of PMS
daily symptoms for 2-3months
if symptoms are not cyclial or not in luteal phase - alternate diagnosis
symptoms dont interfere with daily living
tried anything, other medical conditions, changes in period
assessment for PMS
Stress reduction strategies
patient education and symptom diary
better sleep practises
avoid minimise alcohol
exercise
diet - reduce caffeine and sodium if needed
non pharm management PMS
Chasteberry - 20-40mg
Vitamin B6 - 50mg
Magnesium 900mg daily
Calcium 600mg bd
complementary medicines for PMS
Recommended first-line treatment when mood is the primary symptom.
Any SSRI can be used, with fluoxetine studied most in clinical trials.
Intermittent dosing (taken 2 weeks before menses through day 1–3 of the period) is just as effective as continuous daily dosing.
Switch to continuous dosing if intermittent treatment is ineffective or causes withdrawal symptoms.
Remains the drug of choice for PMDD.
SSRIs for PMS
Suppress the hypothalamic-pituitary-ovarian axis and prevent ovulation.
Address both mood and physical symptoms, though trial results are mixed: 50% report no change, 25% improve, and 25% worsen.
Recommended for continuous use (no pill-free interval to prevent bleeding), supported by evidence for a 168-day cycle.
Formulations with an anti-androgen progestogen can be considered if fluid retention is a prominent symptom.
Contraceptive oral pill for PMS
25-100mg/day during luteal phase
Most helpful for fluid retention, bloating, breast tenderness (not emotional symptoms)
Diuretics – spironolactone - PMS
Naproxen, mefenamic acid - for physical symptoms
NSAIDs for PMS
Symptoms – mood and physical
Comparison to start of therapy
Side effects
Additional therapies
Non-pharmacological
Support from friends/family
Try one agent for 2-4 cycles before switching to alternate therapy
monitoring PMS
Repetitive stress on lower back including frequent bending, lifting heavy object
Long period of sitting down e.g. truck driver
Acute injury from excessive twisting
Long period of sitting down e.g. truck driver Acute injury from excessive twisting
localised or diffuse
stiff, aching
quick onset of pain
movement - restricted
low long symptoms have been present
acute low back pain
Worsening pain over several days
Pain that radiates to the leg(s)
Severe shooting pains into the leg(s) with loss of function/weakness in your leg(s) - sciatica
Urinary or bowel incontinence
Need for analgesic for > 7 days
Persistent pain after 4 weeks
acute lower back pain referral
topical NSAID
ibuprofen, ketoprofen, diclofenac, benzydamine, piroxicam, naproxen sodium
massage gently 2-4 times a day
caution with asthmatics
avoid preg
safe in breastfeeding
anticoagulant, lithium interactions
diarrhoea, heart burn, hypertension
take soon or after food
treatment of acute lower back pain - NSAIDs
Cause vasodilation, producing warmth that distracts the patient from underlying pain.
Contain salicylates and menthol (e.g., Metsal®, Dencorub® cream).
Apply to the affected area 2 to 3 times daily.
Salicylate-containing products require caution in patients with an aspirin allergy.
Common side effects include rash and skin irritation.
Herbal remedies (devil’s claw, white willow bark, cayenne)
Acupuncture
Massage
topical rubefacient
500 mg to 1 g qid; max of 4 g daily (Immediate release tablet)
1.33 g tds ; max of 3.99 g daily (Controlled release tablet)
safe in preg and breastfeeding
paracetamol - back pain
300 mg to 900 mg qid (max dose of 3.6 g daily)
Commonly associated with GI bleed especially in elderly
Avoid in patients with asthma, past history of GI bleed, children under age of 16
Avoid concurrent administration with warfarin
Avoid in pregnancy and breastfeeding
aspirin
product has 8-15mg of codeine
doses are too low to have significant effect
compounds with codeine
good posture
excerise at a moderate level for at least 30 minutes
proper lifting technique
wear low heeled shoes
take breaks
bed mattress
acute back pain self care
Suspected Fracture: More common in children under 12 years old and the elderly.
Bone Abnormalities: Deformed-looking joints.
Head Injury: Any accompanying trauma to the head.
Severe Pain at Rest: High pain levels even without movement.
Lack of Improvement: Pain and ability to bear weight do not improve within 5–7 days.
Associated Skin Injury: Open wounds or skin damage that may require tetanus prophylaxis.
Underlying Conditions: Suspected arthritis or other underlying diseases
referral for sprains and strains
heat, alcohol, running, massage
management for strain and sprains
Sprain and strain related injury can take 1 up to 6 weeks to recover depending on severity of injury
gradually increase movement after pain and swelling
prevent injury by wearing suitable footwear and protective clothing when playing sport
Warm up before sport
Run on even surface
Allow adequate recovery time in between training session
management for strain and sprains self care
Tension-type headache (episodic or chronic)
Migraine (with or without aura)
Cluster headache
primary headache
Headache that is caused by associated condition or disease (minor or serious and life threatening)
secondary headache
systemic symptoms
neurological symptoms
severe
older age
positional headache
sneezing, coughing
pregnancy
painful eye
pain killer overuse
referral for headache
Proton pump inhibitors (PPIs) and H2 antagonists.
Selective serotonin reuptake inhibitors (SSRIs).
Amphetamine and dexamphetamine.
Glyceryl trinitrate, long-acting nitrates, dipyridamole, and dihydropyridine calcium channel blockers.
Sildenafil, tadalafil, and vardenafil.
medications that cause headache
more common in men than women
acute - less than 15 days
chronic - more than 15 days
in the front of the head or neck
triggered by Mental and physical stress, Poor posture, High caffeine intake or caffeine withdrawal, Getting too much or too little sleep, Menstrual cycle-related problems.
tension type headache
Bilateral pain that is non-throbbing (dull, aching), feels like pressure or tightness around the head, and may extend into the back of the neck and shoulders.
Lasts anywhere from 30 minutes to 7 days, often occurring in the late afternoon or evening.
Mild to moderate in intensity and not aggravated by routine physical activity; symptoms generally do not stop a person from carrying out day-to-day activities.
treated with aspirin, paracetamol or other NSAIDs
tension type headache symptoms
Use heat packs or cold packs.
Perform massage therapy on target areas.
Stretch tight neck and scalp muscles.
Focus on posture correction.
Engagement in regular exercise.
Practice relaxation exercises.
Utilization of a supporting neck pillow.
Reduction in caffeine intake.
tension type headache non-pharmacological treatment
for amitriptyline or noradrenaline 10 ot 75 mg daily
for 3-6 months and reduce dose
tension type headache - referral
common in women
family tendency
peak in adolscence
35-39 years
can cause aura - visual issues - can be positive or negative
cause by accumulation of factors
assess monthly frequency and medication tolerance after 8-12 weeks
migraine headache
Unilateral pain that is moderate to severe in intensity and described as pulsating.
Can be significantly disabling both physically and psychologically, and is aggravated by physical exercise.
Photophobia (sensitivity to light)
Phonophobia (sensitivity to sound)
Nausea (and vomiting)
Fatigue
Altered cognition
headache phase of migraine
fatigue, mood, difficulty concentrating
postdromal phase of migraine
fluctuating hormones
too much or little sleep
fasting
stress
change in weather
scents
glare
migrane triggers
Rest or sleep in a quiet, dark room.
Practice mental and physical inactivity, including meditation and relaxation techniques.
Apply hot and cold therapies.
Maintain fluid hydration if possible.
Keep a headache/migraine diary.
non-pharmacological treatment of migraines
Soluble aspirin: 900–1000 mg every 4 to 6 hours as needed (Maximum 4 g in 24 hours). prevent gastric statis
Ibuprofen: 400–600 mg every 4 to 6 hours as needed (Maximum 2.4 g in 24 hours).
Naproxen sodium: 550–825 mg every 4 to 6 hours as needed (Maximum 1.25 g in 24 hours).
Diclofenac sodium: 50 mg every 4 to 6 hours as needed (Maximum 200 mg in 24 hours).
Soluble paracetamol: 1000 mg every 4 to 6 hours as needed (Maximum 4 g in 24 hours).
take early stage
1st line for headaches
failure after 3 consecutive occasions
Eletriptan: 40mg
Naratriptan: 2.5mg
Rizatriptan: 5mg
Sumatriptan: 50mg
Zolmitriptan: 2.5mg
contains 2 tablets
can affect mental coordination
only used if migraine is diagnosed
2nd line headache
Constrict cranial vessels by acting selectively at 5HT 1B/1D receptors.
Thought to inhibit the abnormal activation of trigeminal nociceptors.
5HT antagonist
Cardiovascular conditions (e.g., uncontrolled hypertension, peripheral vascular disease, history of myocardial infarction, ischaemic heart disease, stroke).
Concomitant use with SSRIs and SNRIs.
Oral efficacy is not established in patients aged 12–17 years; intranasal products are preferred.
Sensations of tingling, flushing, dizziness, drowsiness, dry mouth, transient increase in blood pressure, and heaviness or tightness in any part of the body (including chest and throat).
Dependence may occur with overuse, leading to recurrent/rebound headaches and withdrawal.
precautions and contraindications for triptans and NSAIDs
work to block dopamine
Metoclopramide 10-20 mg
Prochlorperazine 5-10 mg
Domperidone 20 mg
Anti-Emetics
4 days of migraine symptoms per month
Individual attacks are difficult to manage with acute treatment
reduce frequency and decrease disability from attack
treatment of migraine is only for
Avoid identified trigger factors.
Reduce caffeine intake.
Utilize relaxation techniques.
Employs a "problem-focused" approach.
Employs an "action-oriented" approach.
prevention of migraine - non pharmacological
Adverse effects
Comorbidities and other medicines
Patient preference and symptoms
start slow and work up
trial for 8-12 weeks
choice of migraine drug depends on
Topiramate 25 –
Sodium Valproate
Propranolol
Botox - chronic migraines
CGRP peptide
complementary - Magnesium, Riboflavin
best drugs for migraine prevention
Migraine occurs due to the withdrawal of oestrogen between Day –2 and +3 of the menstrual cycle.
Start 1 to 2 days prior to the onset of menses and continue for 5 to 7 days, or as needed.
Ibuprofen: 400 mg three times daily (tds), OR
Naproxen SR: 750–1000 mg once daily, OR
Naratriptan: 1.25–2.5 mg twice daily
menstrual migraine