Week 4--notes Flashcards
lifetime prevalence of back pain
70-85%
annual prevalence of back pain
15-45%
when is sciatic pain most common in the lifespan
between ages 40-45
usually from herniated disc
*herniation pain decreases with age because the disc dessicates
which gender has higher risk of back pain form herniation
men
which gender has higher overall risk of back pain from all causes
women
at what age do back pain complaints generally start to decrease
age 50
what are the types of back pain
- structural–i.e disc disease
- inflammatory–i.e ankylosing spondylitis
- infectious–i.e discitis
- neoplastic–i.e mets
- visceral–i.e aortic aneurysm
- idiopathic–i.e non specific
what patient factors can be associated with back pain
- age
- gender
- previous history of back injury
- relative strength
- smoking
- psychosocial factors–time off in past, understanding of cause, what patient expects will help
- “inheritance”
- occupational influences
what occupational influences can contribute to back pain
whole body vibration
forward bending and twisting
manual handling of materials
poor psychosocial conditions
frequent heavy lifting
what are some modifiable risk factors with regard to back pain
lack of fitness
poor health
obesity
smoking
drug dependence
what are some factors that have little to no association with back pain
height and weight
aerobic activity
absolute strength
define mechanical back pain
inflammation, irritation or injury to disc, facet joints, ligaments or muscles in the back
pain NEVER occurs below the knee
what is the most common cause of mechanical back pain
AGE related degeneration of discs, facet processes
muscle or ligament related injuries
define compressive back pain
occurs when nerve root leaving the spine is irritated or pinched
commonly due to herniated disc
what are waddells non-organic signs
- superficial tenderness
- non-anatomic tenderness
- axial loading
- simulated rotation
- distracted straight leg raise
- regional sensory changes
- regional weakness
- overreaction
* when these occur, look also for other causes of pain
describe a method of triaging low back pain
- simple back pain
- back pain with neuro involvement
- back pain with suspected serious spinal pathology (red flags)
what is simple back pain
lumbar or lumbosacral pain with no neuro involvement
“mechanical” pain, varying over time and with physical activity
patient’s general health is good
*xray/CT/MRI results are not associated with symptoms described by patient or perceived disability (many findings are common with asymptomatic patients and there is a poor association with pain)
how should you exclude serious spinal pathology in simple back pain
xray is sufficient
what is back pain with neurological involvement
patients must have one or more symptoms and signs indicating possible neuro involvement
i. e
- pain radiating below the knee which is as intense or more intense than the back pain
- pain often radiating to foot or toes
- numbness or paresthesias in the painful area
- positive for radicular irritation with straight leg raise
- motor/sensory or reflex signs supporting nerve root involvement
how should you manage back pain with neuro involvement
neuro signs and sx in the absence of red flags often resolve themselves without recourse to surgery
patients progress statistically twice as slowly as patients with simple back pain
referral for specialist consult should NOT be required until clinician has seen functional deficit persistent or deteriorating after 4 WEEKS
x ray sufficient to exclude spinal path
what are red flags for back pain (suggestive of serious spinal pathology)
- violent trauma (fall from height, auto accident)
- constant, progressive, non mechanical pain
- thoracic or abdo pain
- pain at night that is not eased by prone position
- hx or suspected cancer, HIV or other pathologies that can cause back pain
- chronic corticosteroid consumption
- unexplained fever, weight loss, chills
- significant and persistent limitation of lumbar flexion
- loss of feeling in the perineum (saddle anesthesia)
- recent onset urinary incontinence
if someone is off work 0-4 weeks, how likely are they to RTW
80-100% will RTW
if someone is off work more than 12 weeks how likely are they to RTW
less than 60%
how should you treat acute low back pain
i.e within 0-4 weeks
after 48 hours from acute injury, suggest NSAIDs
muscle relaxants
advise to remain active
how should you treat subacute low back pain
4-12 weeks
advise to remain active and do exercises
consider multidisciplinary rehab program
low evidence for massage, NSAIDs, other analgesics
how should you treat persistent low back pain
over 12 weeks
multidisciplinary program
behavioural therapy
exercises
what % of back pain will not have a precise diagnosis
85%
define radiculopathy
objective neurological deficit
define nociceptive pain
nociceptors sense and respond to tissue damage
pain usually localized, constant, throbbing, dull
i.e burns, bruises, sprains, fracture
define neuropathic pain
result of dysfunction or injury to PNS or CNS
nerves can be inflamed or compressed
pain usually burning, electric, tingling, sharp
i.e carpal tunnel syndrome, phantom limb, post shingles, RSD
LMN signs
weakness
decreased tone
decreased reflexes
decrease sensation
UMN signs
babinski
increased reflexes
usually increased tone
red flags on back pain physical exam
very decreased ROM
midline tenderness
new or progressive deformity
neuro deficit
lower extremity spasticity
abnormal gait
loss of balance
saddle anesthesia
how do you manage cauda equina syndrome
medical and surgical emergency
what signs would suggest inflammatory causes of back pain
morning stiffness lasting more than 1 hour
age of onset younger than 30 or over 60
worse earliest in am and with activity
*advil better than tylenol for the pain
symptoms suggestive of benign low back pain
dull and achy
diffuse aching with associated muscle tenderness
exacerbated with movement (“mechanical”)
relieved with rest in recumbent position
no radiation of paresthesias
no dermatomal pattern
able to find a position of comfort
DTRs normal
what are red flag low back pain conditions
tumours
infection
fracture
cauda equina
examples of inflammatory back pain
ankylosing spondylitis
PMR
what is the most common disease of the SPINAL CORD after middle life
cervical degenerative myelopathy
signs of cervical degenerative myelopathy
UMN signs
spasticity
loss of balance
signs of cervical or lumbar radiculopathy
objective signs of neuro deficit (sensory loss, motor loss or impaired reflexes) in segmental distribution (LMN findings)
caused my compression or compromise of spinal nerve or its root
how does acute radiculopathy present
abrupt onset
severe shooting, “electric” pain with radicular distribution
accompanied by motor or sensory deficits
most often due to herniated disc (“soft disc”)
how does chronic radiculopathy present
gradual
sensory symptoms predominate
wasting and decreased tone, might have weakness
usually due to osteophytic compression (“hard” disc)
which are more common, pharmacodynamic or pharmacokinetic drug interactions
pharmacodynamic are 75%
i.e additive CNS depression, serotonin syndrome etc
what are the 2 main pharmacokinetic systems that contribute to drug interactions
CYP P450 system
transport protein system
what is the CYP p450 system
super family of heme-containing mono-oxygenases
responsible for detoxing foreign compounds mostly in the liver
large variability between people–enviro and genetic
what drug should not be combined with the drug below, and why:
NSAIDs
ACEi–> causes inhibition of vasodilating renal prostaglandins, leading to renal impairment
what drug should not be combined with the drug below, and why:
clopidogrel
omeprazole –> inhibition of CYP metabolism to active metabolite leading to decreased clopidogrel effectiveness
major severity
what drug should not be combined with the drug below, and why:
warfarin
NSAIDs–> increased bleeding risk, delayed onset
what drug should not be combined with the drug below, and why:
ACEi
spironolactone–>
enhanced hyperkalemic effects
what drug should not be combined with the drug below, and why:
SSRIs
warfarin–> leads to enhanced anticoagulation/antiplatelet action leading to altered anticoagulation
what should you think of when syncope presents as:
slow onset, slow offset
hyperventilation or hypoglycemia
what should you think of when syncope presents as:
abrupt onset, slow offset
seizure disorder
what should you think of when syncope presents as:
abrupt onset, abrupt offset
usually cardiac
arrhythmic–> brady or tachy
obstructive–> aortic stenosis, HCM, myxoma
vascular–> vasovagal, orthostatic hypotension
prominent risk factors for long QT syndrome
congenital
elderly, female
heart failure
myocardial ischemia
hypokalemia
more than one QT prolonging drug
other risk factors for long QT syndrome
brady less than 50
electrolyte disturbances
altered nurtition
hypothyroid
hyperglycemia
hypertension
one QT prolonging drug
list 3 commonly used QT prolonging drugs
methadone –> risk as normal doses
fluoxetine–> risk at normal doses
trazodone
name the 4 dopamine pathways
- mesocortical pathway
- nigrostriatal pathway
- mesolimbic pathway
- tuberoinfundibular pathway
what does the mesocortical pathway do?
associated with cognition and motivation
associated with negative symptoms of schizophrenia/psychosis
what are the negative symptoms of psychosis/schizophrenia associated with the mesocortical dopamine pathway
5 As
alogia
anhedonia
affective flattening
avolition
asociality
what does the tuberoinfundibular dopamine pathway do
controls prolactin secretion
what does the nigrostriatal dopamine pathway do
controls motor functions
what does the mesolimbic dopamine pathway do
associated with memory and emotional behaviours
associated with positive symptoms of psychosis/schizophrenia
what are the positive symptoms of psychosis/schizophrenia associated with the mesolimbic pathway
delusions
hallucinations
disorganized speech/thinking
disorganized or catatonic behavior
which dopamine pathway is associated with:
mediation of antipsychotic efficacy, and the treatment of psychosis
mesolimbic
which dopamine pathway is associated with:
extrapyramidal symptoms
nigrostriatal
which dopamine pathway is associated with:
increase in prolactin secretion with anti psychotic use
tuberoinfundibular
which dopamine pathway is associated with:
neuroleptic induced deficit syndrome
mesocortical
list some side effects of first gen antipsychotics and the receptors through which they are mediated
H1–> sedation, weight gain
alpha 1–> decreased BP, dizziness, drowsiness
M1–> dry mouth, urinary retention, blurred vision, constipation
name a first gen antipsychotic with low affinity for D2 receptors
chlorpromazine
side effects of chlorpromazine
related to H1, A1 and M1 receptor antagonism (because low affinity for D2)
sedation, weight gain, orthostatic hypotension, urinary retention etc
name 3 first gen antipsychotics with high affinity for D2 receptors
haloperidol
pimozide
perphenazine
side effects of haloperidol, pimozide, perphenazine
related to D2 receptor antagonism because high affinity–> EPS
mechanism of action of 1st gen antipsychotics
D2 receptor antagonism
how do first gen antipsychotics affect EPS, neuroleptic induced deficit syndrome, and prolactin compared to 2nd generation antipsychotics
2nd gen have LESS neuroleptic induced deficit syndrome, LESS EPS liability and REDUCED prolactin increases
MOA of 2nd gen antipsychotics
D2 and possible 5HT2a receptor antagonism
which of the commonly used antipsychotics cause the least weight gain? the most?
least–> aripiprazole, haldol
most–> olanzapine, clozapine
are second generation antipsychotics better than first gen for treating POSITIVE symptoms of depression
no clear and consistent difference (except for clozapine is better for treatment resistant)
SGA may be better for NEGATIVE symptoms
SGA agents have more metabolic SEs like weight gain, DM, dyslipidemia
name 3 long acting injectable antipsychotics
aripiprazole
risperidone
paliperidone
how to treat EPS acutely
with anticholinergic agents
benztropine 2-6 mg/day
what is a framework that you can use to decide on an antipsychotic
- trial of a single SGA–assess over 2 weeks
- if partial/no response–> trial a different single SGA
- if partial/no response–> trial high dose olanzapine or FGA, or go straight to clozapine
- if no response to clozapine, augmentation of clozapine plus ECT
- if no response to that, no real evidence for it but can combine clozapine with SGA, or SGA + FGA
what is the major risk associated with clozapine use
agranulocytosis
also myocarditis in first 4 weeks
what should you monitor in patients on clozapine
weight
glucose
lipids
CRP and troponins first 4 weeks due to myocarditis risk
risk of seizures at doses over 500 mg
initiate at hospital or with daily home visits
list some possible SEs of anti psychotic therapy
acute dystonia
pseudo-parkinsonism
akathisia
tardive dyskinesia
neuroleptic malignant syndrome
describe onset and presentation of acute dystonia
may occur within hours (or minutes of IV) of starting anti psychotics
may involve neck, eyes, jaw, tongue and back–can be painful, frightening
patient may not be able to swallow
response to IV tx in approx 5 min, IM in 20 in
treatment for acute dystonia
benztropine
diphenhydramine
management of pseudo-parkinsonism
reduce anti psychotic dose
change anti psychotic
treat with oral anticholinergic –benztropine, trihexphenidyl
describe onset and presentation of pseudoparkinsonism
can occur days to weeks after an antipsychotic is started or dose increased
tremor, rigidity, bradykinesia, bradyphrenia, salivation
describe onset and presentation of akathisia
occurs within hours to weeks of starting antipsychotic or increasing dose
may be misinterpreted as psychotic agitation
internal dysphoric restlessness associated with need to move
treatment of akathisia
beta blockers and benzos can be used in combo however may be better to trial a different antipsychotic
reduce antipsychotic dose
propanolol
benzo at low dose
prevalence of akathisia with anti psychotic therapy
25%
which antipsychotics cause more and less akathisia
aripiprazole high
clozapine low
what is the risk of tardive dyskinesia with anti psychotic use
2-5% per year of anti psychotic exposure
more common with FGAs, elderly, mood disorders, acute EPS
management of tardive dyskinesia
reduce anti psychotic dose
switch to atypical anti psychotic
switch to clozapine or quetiapine
neuro evaluation–botox?
can also try benzos, propanolol, vitamin E, tetrabenazine
describe onset and presentation of tardive dyskinesia
occurs in months to years
approx 50% reversible
repetitive, purposeless movements–i.e lip smacking or chewing, tongue protrusion, choreiform hand movements, pelvic thrusting
movement worse under stress
stop anti cholinergic if prescribed
describe onset and presentation of NMS
sx are muscle rigidity, confusion, fluctuating consciousness, diaphoresis, fever, hyperthermia, fluctuating BP, tachy
progression of sx is medical emergency requiring supporting medical interventions
risk factors for NMS
young age
male
dehydration
neuro disabilities
exhaustion
agitation
rapid or parenteral dosing of anti psychotics
*reported with all antipsychotics
management of NMS
stop anti psychotic
treat with BROMOCRIPTINE and DANTROLENE
amantidine
what is NMS
sympathetic hyperactivity occurring as a result of dopaminergic antagonism in the context of psychological stressors and genetic predisposition
how do you treat agitation/aggression associated with psychosis if MILD sedation is required
lorazepam +/- risperidone, olanzapine or quetiapine
how do you treat agitation/aggression associated with psychosis when moderate to significant sedation is required
- lorazepam + loxapine or haldol
- haldol + antihistamine
- olanzapine IM
why might you choose loxapine over haldol
works faster, may be more sedating
why is it good to use lorazepam with haldol
reduces incidence of EPS
should you admin olanzapine IM with haldol/ lorazepam /midaz
no–can result in hypotension, brady, respiratory/ CNS depression
how do you treat agitation/aggression associated with psychosis if sedation required for extended period
clopixol–> zuclopenthixol acetate
how do you treat insomnia related to psychosis
benzo prn or zopiclone prn or trazodone prn
how do you treat persistent sx of aggression/hostility mania
mood stabilizer like lithium, valproate, carbamazepine
why dont you want to use carbamazepine with clozapine
increases risk of bone marrow suppression
why dont you want to use carbamazepine with quetiapine
carbamazepine reduces quetiapine bioavailability
how do you treat depression, OCD associated with psychosis
SSRI, venlafaxine XR, bupripion SR, mirtaz
risk factors for bipolar disorder
- age less than 25 years
- symptoms of hypomania, mania
- course of symptoms is abrupt onset and discontinuation
- family hx
- response to treatment–> anti depressant tx leads to mania/hypomania or fails 2 diff antidepressants
suicide completion rates in bipolar I
5-10%
suicidality in mixed mania
57%
what 3 drugs are approved for bipolar depression
quetiapine
lurasidone
olanzapine/fluoxetine (symbax)
first line for bipolar disorders maintenance
lithium
lamotrigine monotherapy
divalproex
olanzapine
quetiapine
risperidone long acting injection
abilify
what should you check before starting lithium
renal function–> can cause diabetes insipidus
TSH–> thyrotoxic
get ECG–> can cause ST depression, QT prolongation and T wave depression
why should you avoid NSAIDs with lithium
renal excretion
what are therapeutic lithium levels in the serum
maintenance–> 0.6-1 mmol/L
acute–> 0.8-1.2 mmol/L
when should you consider dialysis for lithium toxicity
if ataxia, delirium
toxic events usually only happen above 1.5
what problems can lithium cause in pregnancy
can cause Ebstein’s anomaly in the fetus–> 1 in 20 000 at baseline, 1 in 1000 when on lithium
what should you check before starting valproate
LFTs–> hepatotoxic
if woman of childbearing age, get pregnancy test and make sure using contraception
why dont we use valproate in pregnant women
1 in 20 rate of neural tube defects
what is the therapeutic blood level of valproate
544-693 umol/L maintenance
650-741 umol/L for acute mania
*inhibits CYP450
what should you check before starting carbamazepine
LFTs–>hepatotoxic
CBC–> can cause fatal aplastic anemia
childbearing age–> pregnancy test and get contraception
what should you monitor when treating with carbamazepine
BMP–> causes hyponatremia
can also cause stephen’s-johnson syndrome
recommended length of benzo taper
6-12 months
high drop out rate if done faster
what are the strongest predictors of benzo withdrawal severity
high baseline neuroticism
female sex
mild to moderate etoh use
what is the amine hypothesis of depression
depression is due to decreased noradrenaline and 5HT in synapse as well as adrenoreceptor downregulation
mnemonic to adjust mood meds
OSCAR
optimize
substitute
combine
augment
refractory/refer
why is buproprion often preferred by patients
no sexual SEs
for how much of their illness are people with bipolar symptomatic
about 50% of the time
bipolar depression is most frequently linked to completed suicide
what is lithium effective for
manic and depressive states of bipolar
not as effective for rapid cycling and mixed states
drug interactions of lithium
NSAIDs
diuretics
ACEI
caffeine
verapimil
when is valproate used over lithium for bipolar?
for treatment of mixed episodes and rapid cycling bipolar
when might you use lamotrigine for bipolar
for bipolar depression
when might you use carbamazepine for bipolar
effective in pure and mixed mania, and rapid cycling
side effects of risperidone
EPS
TD
prolactin increase
side effects associated with all atypical antipsychotics
anti-HAM (histaminic, adrenergic, muscarinic)
Histaminic–> sedation
adrenergic–> orthostatic hypo, cardiac abnormalities, sexual dysfunction
muscarinic–> dry mouth, tachy, urinary retention, blurry vision, constipation
also glucose intolerance so monitor HbA1c
also monitor lipids yearly and weight at every visit
how do benzos work
modulates Cl- ion channel opening by GABA and potentiates GABA effects
rapid onset
addictive
why is xanax not recommended
most addictive
what is used to treat ADHD
- methylphenidate (ritalin)–> displaces dopamine from reuptake into presynaptic terminal leading to increased dopamine in the brain
- dextroamphetamine (dexedrin)–> inhibits uptake of dopamine > NA
- adderal–> inhibits reuptake of dopamine and NA equally
- atomoxetine (strattera)–> NA reuptake inhibitor–less abuse potential because less dopaminergic
how do you calculate serum osmolality
2[Na] + urea + glucose
how does hyperglycemia affect sodium balance
glucose in the blood is an effective osmole–> draws water out of cells–> dilutional hyponatremia
*in this case, brain cells are shrinking because of the glucose drawing water out (serum osmolality is high)–> as glucose is corrected, water will move back into cells and Na will come back to normal (or it should)
example of hyperosmolar hyponatremia
how do you correct Na values when patient is hyperglycemic
for every 10 mmol/L blood glucose is increased, add 3 mmol/L to the [Na]
how can you tell a lab value indicates pseudohyponatremia
caused by hyperlipidemia or paraproteinemia–> [Na] measured on diluted specimen
know its “not real” because serum osmolality will be normal
can confirm by measuring [Na] directly thru ABG
why do we care about hypotonic hyponatremia
risk of cerebral edema if correct too fast
occurs with low Na and low serum osmolality
ddx for hypotonic hyponatremia
based on volume status
- hypovolemic–> total body sodium low
- euvolemic–> total body sodium normal
- hypervolemic–> total body sodium high
* problem is the clinical volume assessment is often incorrect
where is codeine metabolized
liver
metabolized to morphine
define type A adverse drug event (ADE)
dose dependent, predictable (follows pathophys)
most common
define type B ADE
hypersensitivity and idiosyncratic reactions
less common, not dose dependent, less predictable
what body changes make ADEs more likely in older adults
decreased total body water–> lower Vd for hydrophilic meds
increased body fat–> higher Vd for hydrophobic/lipophilic meds (i.e diazepam)
increased gastric pH
how does sensitivity to beta blockers change with age
reduced sensitivity as you get older to beta blockers due to down regulation of beta receptors
if BP control inadequate, consider switching to another anti HTN
what result would you expect from the following drug combo:
amitriptyline + digoxin
delirium
what result would you expect from the following drug combo:
amitriptyline + codeine
constipation
what result would you expect from the following drug combo:
naproxen + ibuprofen
increased bleeding risk
what result would you expect from the following drug combo:
naproxen/ibuprofen + digoxin
renal toxicity and decreased digoxin clearance
what result would you expect from the following drug combo:
acetaminophen + amitriptyline
liver toxicity and reduced amitriptyline clearance
what is the primary cause of delirium
drugs
in the setting of alzheimer’s disease, what would the use of the following med put your patient as risk for:
CNS acting drugs
delirium
lorazepam on an injured brain = delirium + suppressed resp
in the setting of alzheimer’s disease, what would the use of the following med put your patient as risk for:
H2 blockers
delirium
in the setting of alzheimer’s disease, what would the use of the following med put your patient as risk for:
risperidone
EPS
in the setting of the following disease/med combo, what would your patient as risk for:
COPD + lorazepam/trazodone
respiratory depression
in the setting of alzheimer’s disease, what would the use of the following med put your patient as risk for:
PUD + aspirin
GI bleed
