FINAL - MSK & Pain Flashcards
(200 cards)
1
Q
What is gout?
A
Derangement in metabolism resulting in hyperuricemia, urate crystal deposits in tissues (tophi) and synovium (microtophi).
2
Q
What is the most common type of inflammatory arthritis?
A
Gout
3
Q
Is gout more common in M or F?
A
Male (5.2 % of males, 2.4% females)
4
Q
What age group of men is gout most common in
A
30 -60
5
Q
T/F Women have increased suscepitbility to gout after menopause
A
True
6
Q
What are some non modifiable risk factors for gout?
A
Genetic mutations, male gender, and advanced age
Presence of medical conditions like renal failure, metabolic syndrome, DM (though I would argue how well you are managing these diseases is modifiable/ within your influence)
7
Q
What are some modifiable risk factors for gout?
A
Diet -alcohol, purine rich foods such as meats and seafoods, fructose/sugar sweetened foods
8
Q
What are some medications that are known to precipitate gout
A
Drugs are FACT
-Furosemide
-Aspirin, alcohol
-Cyclosporin
-Thiazide diuretics
9
Q
Briefly describe the patho of gout.
A
-Uric acid can be obtained from the diet or made endogenously by xanthine oxidase
-An excess of uric acid results in hyperuricemia
-Uric acid can deposit in the skin/subcutaneous tissues (tophi), synovium (microtophi), and kidney, where they can crystalize to form monosodium urate crystals
-Intense inflammatory reaction is triggered in response to crystals
10
Q
Differentiate primary and secondary gout.
A
Primary: high levels of uric acid from either increased production or decreased excretion
Secondary: Hyperuricemia from primary disease processes such as HTN, renal failure, kidney disorders, etc.
11
Q
True or false: In acute gout, the maximal severity of the flare is reached in 12-24 hours
A
True
12
Q
When will an acute gout attack subside?
A
Subsides spontaneously in 5-10 days
13
Q
What is chronic/ tophaceous gout
A
Inadequately treated gout results in urate crystal deposits in joins that cause deformity and disability of joint
14
Q
What joint is most commonly affected in gout?
A
First metatarsal phalangeal joint (base of great toe)
15
Q
What other joint is commonly affected in gout?
A
The knee
16
Q
T/F, 80% of initial gout flares involve a single joint
A
True
Most often the great toe or the knee
17
Q
T/F, onset of most gout flares occur at night
A
True
18
Q
What is the classic presentation of acute gout?
A
-Severe pain
-Erythema
-Joint swelling
-May have limited joint mobility
-Onset most commonly at night
-Great toe
19
Q
What are tophi?
A
Urate deposits found on cartilage, tendons, bursae, soft tissues, and synovial membranes.
20
Q
Where are common sites for tophi formation?
A
First MTP, ear helix, olecranon bursae, tendon insertions (common in Achilles tendon
21
Q
T/F Tophi are exquisitely tender
A
False- Tophi typically are not painful or tender, but can be accompanied by chronic inflammation and destructive changes to surrounding tissue.
22
Q
Name 2 renal complications of gout.
A
Gouty nephropathy
Uric acid nephrolithiasis
23
Q
What is the single most important differential to assess in gout?
A
Septic arthritis
24
Q
What are other important differentials in gout?
A
Pseudogout (CPP arthritis)
Bursitis
Cellulitis
Hyperparathyroidism
Trauma
25
Diagnosis of gout?
Joint aspiration!
From Up To Date:
In patients with a suspected gout flare in whom the diagnosis has not been previously established or in whom the cause of acute arthritis is uncertain should undergo arthrocentesis; testing of the synovial or bursal fluid should include cell counts and differential white count, Gram stain and culture, and examination for crystals under polarizing light microscopy,
26
"But that's not how my preceptor diagnoses gout"... Is there another way to diagnose gout?
In primary care, if unable to do aspiration/ synovial fluid analysis, can apply clinical criteria (IF no signs of infection, i.e., red/ hot/ swollen/ painful joint with fever or evidence of extraarticular infection).
From Up To Date
Use of a clinical diagnostic rule — A clinical diagnostic approach ("rule"), which can be used to estimate the likelihood of gout, has been shown to improve the accuracy of diagnosis of a gout flare made in primary care practice without joint fluid analysis (algorithm 1) [81]. The model uses seven variables (which were assigned weighted scores) that can be ascertained in primary care to distinguish three levels of risk for gout. It uses the following variables and scoring values:
●Male sex (2 points)
●Previous patient-reported arthritis flare (2 points)
●Onset within one day (0.5 points)
●Joint redness (1 point)
●First metatarsal phalangeal joint involvement (2.5 points)
●Hypertension or at least one cardiovascular disease (1.5 points)
●Serum urate level greater than 5.88 mg/dL (3.5 points)
Based upon the total score, patients can be identified as having low (≤4 points), intermediate (>4 to <8 points), or high (≥8 points) probability of gout
27
T/F Serum urate will be elevated in a gout flare
Not always- most accurate time for assessment is at least 2 weeks after a flare
28
What are characteristic XR findings of tophi?
Soft tissue swelling, bone/joints - punched-out lesions, erosion with “over-hanging” edge
29
T/F Initiation of gout treatment should be initiated only after 24 hours into an acute flare.
False- early treatment of a gout flare leads to more rapid and complete resolution of the flare.
30
T/F Septic arthritis should be excluded before using glucocorticoids
True
31
T/F Urate lowering medications should be stopped during a gout flare
False
During a gout flare, urate-lowering medication (i.e., allopurinol, probenicid) should be continued, without interruption. There is no benefit to temporary discontinuation of these medications. Moreover, subsequent reintroduction of urate-lowering therapies may precipitate another flare.
32
What is the first line treatment of an acute gout flare?
- Latest evidence suggests that if possible, intrarticular glucocorticoid injection is best (esp if first or infrequent episodes). This avoids complications of systemic therapy.
- If practitioner cannot do this in a timely manner/ IA glucocorticoids are not available, systemic (NSAIDs), colchicine, or glucocorticoids are alternatives. Patient factors, prior experience, and availability should guide the choice of therapy.
33
Can you treat with NSAIDs and colchicine at the same time?
Great question- if anyone knows the answer please tell me.
From my reading it seems to be just one or another?
Lexicomp says no interactions between the two drugs indicating it is safe. However, they both have adverse GI effects and are CI in renal impairment.
Up To Date has a great treatment algorithm for gout and says to choose ONE of the options (oral glucocorticoids, NSAIDs, colchicine)
34
How much colchicine would you give?
* Colchicine 1.2 mg at the first signs of attack, then 0.6mg 1 hour later and 0.6 mg BID on subsequent days until the attack has resolved
35
Describe conservative management of chronic gout.
o Avoid foods with high purine content (visceral meats, sardines, shellfish, beans, peas)
o Avoid drugs with hyperuricemic effects (pyrazinamide, ethambutol, thiazide, alcohol)
o Additional management of lifestyle factors: limiting alcohol intake, high fructose corn syrup, weight loss (if overweight)
36
Describe when medication is indicated for chronic gout.
>2 attacks/year, bone erosions/arthritis, high risk of severe gout
37
What kind of medication is used for chronic gout?
o Antihyperuricemic drugs – decrease uric acid production by inhibiting xanthine oxidase. Start low and titrate up.
38
What medication is first line for medical management of chronic gout?
Allopurinol
39
What is an important consideration when starting a patient on urate lowering therapy
Acute falls in urate levels can precipitate a gout attack.
Either start low and titrate up or use low doses of colchicine/ NSAID to prevent
40
Order these opioids from most to least potent
Tramadol, hydromorphone, codeine, morphine, hydrocodone, fentanyl, oxycodone
Fentanyl > hydromorphone > morphine > hydrocodone >oxycodone > codeine/ tramadol
41
T/F When starting opioids for chronic pain, clinicians should prescribe extended release/ long acting opioids (instead of immediate release) in order to better manage the patients pain/ avoid break throughs in pain.
False. Clinicians should prescribe IR opioids instead of ER when starting opioid therapy. Risk of OD with ER (patient keeps taking expecting instant effect) is what Sarah explained in class.
42
At what number of morphine miligram equivalents (MME) day should a clinician be mindful of reassessing evidence of individual benefits?
When increasing dosage to 50+ MME/ day
43
Clinicians should avoiding increasing dosage to ______MME/ day or carefully justify their decision to titrate doses above this level.
90
44
T/F When opioids are prescribed for acute pain, the prescriber should prescribe 1.25x the quantity needed for the expected duration of pain.
False. Prescribe no greater than quantity needed.
45
How many days of opioids are typically needed for acute pain?
3; more than 7 days will rarely be needed
46
When a clinician prescribes opioids for chronic pain, when should they reassess the patient?
Sarah's ppt: within 1-4 weeks of starting opioid therapy/ escalating dosage. Reassess harms/ benefits q3 months or more frequently.
47
What factors increase risk for opioid OD?
Hx of OD
Hx SUD
MME/ day 50+
Concurrent BZD use
48
When prescribing/ renewing a prescription for opioids, what should the clinician do every encounter?
Check pharmanet/ prescription drug monitoring program to determine whether the patient is receiving opioid dosages or dangerous combos that put them at higher risk for OD.
(Among other things, but this is something Sarah emphasized in exam review)
49
T/F When prescribing opioids for chronic pain, clinicians should use urine drug testing before therapy and annually
True per Sarah's ppt.
50
Why is it important to calculate total daily dosage of opioids?
-ID patients who may benefit from closer monitoring, reduction/ tapering of opioids, naloxone, or other measures to reduce risk of OD
51
How do we calculate the total daily dose of opioid?
1) Determine the daily amount of each opioid the patient takes.
2) Convert each to MMEs (multiply the dose for each opioid by its conversion factor- found in a table)
3) Add them together.
52
T/F You can use the calculated dose of MMEs to determine dosage for converting one opioid to another
False. The new opioid should be lower to avoid unintentional OD caused by incomplete cross tolerance and individual pharmacokinetic differences.
53
When considering opioid therapy for chronic pain, providers should take the following steps:
Assess risks to patient safety by conducting a physical examination, mental health screening, prescription drug monitoring program (PDMP) check, and urine drug tests
Set goals for improvements in pain and function with the patient
Check that non-opioid therapies are tried and optimized
Discuss risks and benefits with the patient
Establish criteria for stopping or discontinuing opioid therapy
54
You have a patient on hydromorphone 2 mg BID. How many MME per day?
Conversion factor for hydromorphone: 5
1) Calculate daily dosage of HM (2mg BID= 4mg)
2) Multiply total dosage of HM by conversion factor (4mgx 5)
Answer: 20MME
55
You have a patient on Codeine 30mg QID. How much is the MME per day?
Conversion factor for codeine: 0.15
1) Calculate daily dose of codeine (30mg x QID= 120mg)
2) Multiply by conversion factor: 120mg x 0.15
Answer= 18 MME daily
56
You have a patient on Codeine 30mg BID. How much is the MME per day?
1) Total daily dosage of codeine: 30mg x BID= 60 mg
2) Conversion factor: 0.15
9MME
57
T/F The relation between dosage and overdose risk is different for buprenorphine. The MME thresholds of 50 and 90 MME do not apply, and there isn't a calculation to identify equivalency.
True
58
Why is dosing methadone complicated?
Long and unpredictable t1/2
QTc prolongation
Potential for cardiac arrythmia
59
Name some medical conditions that can pose a life threatening risk with opioid use.
Sleep-disordered breathing such as sleep apnea
Pregnancy
Renal or hepatic insufficiency
Age >= 65
Certain mental health conditions
Substance use disorder
Previous nonfatal overdose
60
Reasonable tapering regiment for opioids?
Individualized. Reduction of 10% per week/ month
61
Which three bones compose the shoulder girdle?
Clavicle, scapula and proximal humerus
62
When assessing the shoulder (and doing other MSK assessments), what are the three steps in the assessment?
Look, feel, move
63
When doing the inspection for MSK assessments, what are you looking for? There is an acronym for it..
SEADS
Swelling
Erythema
Atrophy
Deformity
Skin changes/scars/symmetry
64
When doing the palpation for MSK assessments, what are for feeling for? There is an acronym for that too!
TESTCAPS+
Tenderness
Effusion
Swelling
Temperature
Crepitus
Atrophy
Pulses
Sensation
+DTR
65
Susan is reporting a gradual onset of anterior and deep shoulder pain. On exam you find decrease in both active and passive motion of the shoulder. What might the source of this shoulder pain be?
Osteoarthritis
66
What are some risk factors you might expect to uncover in the history of a patient with shoulder osteoarthritis?
Older age
Trauma
Previous shoulder injuries
67
Which shoulder condition is associated with the connective tissue of the shoulder becoming inflamed and stiff?
Adhesive Capsulitis (frozen shoulder)
68
What is the time course of adhesive capsulitis?
9 months of disabling pain and increasing stiffness
Followed by up to 12 months of progressive ROM limitation to passive and active ROM to the point where the should can barely move. Pain is less pronounced in this stage
Finally the recovery phase occurs in which patients regain their mobility, can take up to 2 years!!!
69
Risk factors for adhesive capsulitis
Diabetes
Immobilizing disability (stoke, injury requiring a sling)
70
What are some shoulder injuries that may occur with trauma to the joint/limb?
Acromioclavicular dislocation
Glenohumeral dislocation
Clavicle fractures
Proximal humerus fractures
71
The Grinch undertakes a lot of overhead work preparing his sleigh and undecorating everyone's trees. What shoulder injury might he experience if he sustains these movements over time?
His symptoms would include anterolateral shoulder pain worsening with overhead movement and pain with external rotation
Degenerative rotator cuff injury - tendinopathy/impingement of supraspinatus tendon is the most common degenerative rotator cuff injury
72
What are some special tests for assessing the Grinch for rotator cuff impingement?
Empty can test
Full can test
Neers test
Hawkins Kennedy test
lots of others
73
In addition to rotator cuff impingement/tendinopathy, the rotator cuff can also tear. What is a special test for this?
Drop arm test
74
Findings with a torn rotator cuff
Pain and weakness with testing (whereas the impingement would mostly just show pain)
Most common is age > 40
75
What are some non-MSK sources of shoulder pain to keep in mind?
Referred from thoracic or abdo source
Cervical nerve root impingement - sharp pain radiating from neck into the posterior shoulder or arm
Splenic injury can present as shoulder pain in MVAs
Myocardial ischemia - especially if associated with diaphoresis or dyspnea
76
What physical exam findings would suggest a non-shoulder cause of pain?
Normal MSK assessment
77
UTD has a 4 step frame work to evaluate shoulder complaints
Step 1 - Determine if traumatic or atraumatic. Plain x-rays may be needed if traumatic
Step 2 - Determine if intrinsic (shoulder related) or extrinsic (from something else) - Extrinsic pain may be difficult to localize and vague or sharp with radiation if neurologic
Step 3 - Glenohumeral or extra-glenohumeral. For extra-glenohumeral source, patient often able to localize pain and passive ROM of glenohumeral joint should be normal. Extra glenohumeral disorders could include biceps tendinopathy and AC osteoarthritis.
Step 4 - Differentiate glenohumeral pathology if extra-glenohumeral ruled out. Use history and assessment to differentiate rotator cuff tendinopathy, rotator cuff tear, adhesive capsulitis, osteoarthritis.
78
For the hand and wrist, as with other MSK injuries, a good first question to ask is whether there was any trauma. What are the two common wrist fractures?
Colles fracture and Smith fracture
79
What do you remember about Colle's fracture?
Complete fracture of the distal radius bone with posterior displacement of the radius. Ulnar styloid ma also be fractured.
From FOOSH
Associated with "Dinner fork appearance"
80
What do you remember about Smith's fracture?
Fracture of the distal end of the radius from a fall on the back of the flexed hand
Results in volar displacement of the fractured fragment
81
What is the most common carpal fracture?
Scaphoid fracture
From FOOSH
Tenderness in the anatomical snuffbox
See peds cards for the full story!
82
Which nerve is implicated in Carpal tunnel syndrome?
The median nerve
83
What are risk factors for carpal tunnel syndrome
Pregnancy
Edema
Obesity
RA
Hypothyroidism
Diabetes
Acromegaly
Repetitive use of hands/wrist
84
How does carpal tunnel syndrome present? What are the names of the special tests?
Pain or paresthesia (numbness/tingling) along the median nerve territory - involvement of the first three digits and the radial half of the 4th
Typically worse at night
Phalen's
Tinel
85
T/F: Carpal tunnel is a clinical diagnosis and never requires diagnostic testing.
False - kind of
It is typically a clinical diagnosis, but if diagnosis is uncertain or severity is moderate-severe then electrodiagnostic testing is warranted.
86
T/F: The recommended treatment for carpal tunnel syndrome includes wrist splints, NSAIDS, glucocorticoid injections and surgery if needed
False, NSAIDS are not part of the recommended treatment.
87
What is the patho behind tenosynovitis?
What is a common type of this in the hand/wrist
Inflammation of the sheath around a tendon
de Quervain tenosynovitis - affects abductor pollicis longus and extensor pollicis brevis
88
How does de Quervains present? What is the special test?
Pain and tenderness at the radial side of the wrist/over radial styloid, pain when holding or gripping objects
Can be bilateral
Finkelstein test - pain at the radial styloid with active or passive stretch of the thumb tendons in thumb flexion
89
How is de Quervain's managed?
Thumb splint, NSAIDs, steroid injections if needed. Possible surgery
90
What causes neuropathic pain?
Damage or dysfunction to nerves leading to misfiring pain signals - analogy to software malfunction
91
How does neuropathic pain present?
Allodynia (pain from stimuli that does not normally provoke pain), numbness, tingling ,burning, radiating, electrical sensations
92
According to the PEER chronic pain guidelines, which drugs have clear evidence for use in neuropathic pain?
Gabapentinoids (gabapentin, pregabalin)
SNRIs (venlafaxine, duloxetine, milnacipran)
Rubefacients (things like topical capsaicin)
93
If the gabapentinoids/SNRIs/Rubefacients have already been considered, then these other drugs with unclear evidence could be considered
TCAs
Cannaboids
Topical nitrate spray
Note: No benefit seen with acupuncture, topical ketamine, topical amitriptyline
Harms likely exceed benefits with opioids, topiramate, oxcarbazepine
94
What are some examples of causes of neuropathic pain?
Peripheral neuropathies:
painful diabetic neuropathy, post-herpetic
neuralgia (after herpes zoster), trigeminal neuralgia, chemotherapy induced, post-surgical & radicular neuropathic pain
Central neuropathies:
Stroke, MS, spinal cord injury, complex regional pain syndrome
Drugs:
alcohol, chemo, isoniazid, antiretrovirals
95
Types of mechanical back pain
lumbar strain
degenerative disease
spondylolisthesis
herniated disc
spinal stenosis
spinal fractures
96
Acronym for red flags of back pain?
break it down!
NIFTI
Neurological
Infection
Fracture
Tumour
Inflammation
97
What neurologic symptoms are red flags for back pain?
diffuse motor/sensory loss
progressive neurological deficits
cauda equina syndrome
* Urgent MRI indicated
98
Under "infection" for the red flags of back pain, what do we need to consider?
fever, IV drug use, immune suppressed
May need X-ray and MRI
99
Under "Fracture" component of the red flags of back pain, what are we thinking about?
trauma, osteoporosis risk/ fragility fracture
100
Under "tumour" component of the red flags of back pain, what are we thinking about?
hx of cancer, unexplained weight loss, significant unexpected night pain, severe fatigue
*X-ray and MRI
101
1) Chronic low back pain > ___ months
2) Age of onset < ____
3) Morning stiffness > ____
These are 3 indicators of potential inflammatory back pain. Fill in the blanks
1) 3
2) <45 years
3) >30 mins
102
Does inflammatory back pain worsen with exercise?
No, improves
103
What time of day is inflammatory pain worst?
disproportionate night pain
104
What is the significance of the yellow flags in the CORE back pain tool?
Indicate the potential of psychosocial risk factors for developing chronic pain
A patient with a positive yellow flag will benefit from education and reassurance to reduce risk of chronicity
If significant, CBT or 1:1 psychoeducation counselling may be necessary for pain management
105
You ask your patient “Do you think your back pain will improve or become worse?”.
What answer is a yellow flag?
Worsen - Belief that back pain is harmful or potentially severely disabling.
106
You ask your patient with back pain: “Do you think you would benefit from activity, movement or exercise?”
What answer is a yellow flag?
Answer no - Fear and avoidance of activity or movement is yellow flag.
107
You ask your patient with back pain: “How are you emotionally coping with your back pain?”
What answer is a yellow flag?
Tendency to low mood and withdrawal from social interaction is a yellow flag
108
You ask your patient with back pain: “What treatments or activities do you think will help you recover?”
What answer is a yellow flag?
Expectation of passive treatment(s) rather than a belief that active participation will help is a yellow flag.
109
What are the symptoms of cauda equina syndrome?
Urinary retention followed by insensible urinary overflow
- Unrecognized fecal incontinence
- Distinct loss of saddle/perineal sensation
110
T/F Imaging tests like X- rays, CT scans and MRIs are not helpful
for recovery or management of acute or recurring low back
pain unless there are signs of serious pathology
True!
Straight from CORE tool
111
Your examination today does not demonstrate that
there are any red flags present to indicate serious
pathology, but if your symptoms persist for > ___ weeks,
schedule a follow-up appointment
> 6 weeks
112
Heel walking tests what spinal nerves?
L4-L5
113
Toe talking tests what spinal nerves?
S1
114
Repeated toe raises tests what nerve?
S1
115
Trendelenburg test is testing what spinal nerve?
What is this test?
The provider stands behind the patient at the hip level and places their hands on the iliac crests on either side of the pelvis observing to see if it stays level during the single-leg stance. Repeat the test on the opposite side. A positive Trendelenburg sign is when the pelvis drops on the unaffected side
116
Common mechanical/soft tissue causes of forefoot pain in adults?
Big list incoming...
Hallux valgus - bunions (most common problem of forefoot)
Hallux rigidus and hallux limitus HR is usually due to OA, HL is used to describe decreased ROM that is secondary to soft tissue causes or mild OA that hasn't caused significant degenerative changes.
Metatarsalgia - affects older patients and F>M. Pain arising from complete or partial collapse of the transverse arch formed by the metarsal heads.
Interdigital neuroma AKA Morton neuroma - collapse of transverse arch places pressure on interdigital nerve
Bunionette - bony prominence over lateral aspect of baby piggy.
Hammer toes, other toe deformities
Brachymetarsia - Abnormally shortened metatarsals
Cutaneous conditions - corns, callouses, plantar warts
Acute injuries/fractures
117
Some common medical causes of forefoot pain in adults?
Gout
RA
DM
118
What are some common mechanical causes of midfoot pain in adults?
Acute injuries/fractures
Arthritis
Tendinopathy
Cuboid subluxation/cuboid syndrome - most commonly seen in ballet and running
Neuropathic Charcot changes
Tarsal coalitions - abnormal fibrous, cartilaginous, or bony unions
119
What are some non-drug management points for neuropathic pain?
Establish cause and address - ex. glucose control in PDM
Multimodal approach - ex. physio, exercise, psychological support, massage
Other - radiofrequency ablation, spinal cord stimulation
120
T/F: There is no benefit of tylenol/NSAIDs in neuropathic pain
True-ish - generally not recommended but may be used during an acute exacerbation
121
What are some common medical causes of mid-foot pain?
Gout
RA
OA
Dorsal foot ganglia
122
What are some causes of pain to the hind-foot?
Plantar fasciitis
Tarsal tunnel syndrome
Achilles tendon insertion deformity
Ankle impingement
Heel contusion
Calcaneal and talar stress fractures
Rheumatological diseases
Paget Disease
Osteomyelitis
Sickle cell disease
Gout
Mets
123
Key features of a foot exam include:
●Position of the calcaneus while standing. Is there a varus or valgus shift?
●Redness or other skin changes.
●Swelling along any portion of the hindfoot. Does swelling localize to the area anterior and inferior to the lateral malleolus?
●Appearance of the sinus tarsi.
●Longitudinal arch type: cavus (high arch), neutral, or planus (flatfoot).
●Notable thickening of the Achilles tendon or any bony abnormality. Comparing feet may be useful.
●Walking and running gait as appropriate.
124
Anatomical structures to palpate during a foot exam:
●Insertion of the plantar fascia particularly at the medial calcaneus.
●Calcaneal tuberosity on plantar surface.
●Calcaneus bony contour lateral, medial, and posterior.
●Achilles tendon and insertion onto calcaneus.
●Medial and lateral ankle tendons, particularly as they pass around respective malleoli.
125
In patients with hindfoot pain not associated with injury or overuse, clinicians should consider medical conditions as the source of pain. A good history is the key to assessing such medical conditions.
What are some historical "red flags" that hindfoot pain may relate to a medical condition?
Systemic symptoms such as fever or chills, weight loss, prolonged morning stiffness, swelling or pain in other joints, prior history of cancer, long-standing chronic disease, history of sickle cell anemia, and neuropathy.
126
Which controlled substances did Sarah identify as common, in her MSK powerpoint?
Codeine
Morphine
Hydromorphone
Methadone
Hyrdocodone
Buprenorphine
Fentanyl
127
You do not need to use your duplicate pad for Tylenol 3 or ketamine.
True/false?
True!
128
What MUST you do before you prescribe controlled drugs?
Check Pharmanet.
129
10 mg of which opioid is equivalent to 50 mg of morphine?
Hydromorphone
130
Matchy match the opioid doses for equivalent dosing to 50 mg of morphine
Tramadol 334 mg
Codeine 10 mg
Oxycodone 300 mg
Hydromorphone 33 mg
Tramadol 300 mg
Codeine 334 mg
Oxycodone 33 mg
Hydromorphone 10 mg
NOTE! This conversion was in Sarah's notes (one of the articles) but the Switching Opioids form stated that dose equivalents are unreliable for fentanyl and tramadol.
131
Switching from current opioid to morphine equivalent:
1. Morphine to morphine:
multiply by _________.
2. Oxycodone to morphine:
multiply by ___________.
3. Hydromorphone to morphine:
multiply by ___________.
1. Morphine to morphine:
multiply by 1.
2. Oxycodone to morphine:
multiply by 1.5
3. Hydromorphone to morphine:
multiply by 5.
132
Switching from morphine equivalent to a new opioid:
1. Morphine equivalent to morphine:
multiply by __________.
2. Morphine equivalent to oxycodone:
multiply by ___________.
3. Morphine equivalent to
hydromorphone: multiply by _______.
1. Morphine equivalent to morphine: multiply by 1
2. Morphine equivalent to oxycodone: multiply by 0.667
3. Morphine equivalent to hydromorphone: multiply by 0.2
133
When switching to a different opioid:
1. If current opioid dose is high, the suggested dose of the new opioid is ?
2. If the current opioid dose is low or moderate?
1. 50% or less of previous dose (converted to morphine equivalent)
2. 60-75% of previous dose (converted to MEQ)
134
When should you conduct a "tolerance check" to see how your patient is doing after switching opioids?
3 days - check for signs of over-sedation and to check pain management
135
Which patients are at highest risk of accidental opioid overdose?
Elderly, patients on benzos, those with renal or hepatic impairment, COPD, sleep apnea, sleep disorders and cognitive impaired.
136
Severe acute opioid withdrawal has been associated with which outcomes in pregnant people?
Premature labour and spontaneous abortion. Manage switching opioids carefully. Sarah recommends consulting.
137
What is the highest morphine equivalent dose that is recommended?
90 mg
138
When initiating opioid therapy for chronic pain, what is realistic goal for pain reduction?
30%.
As per Sarah
139
The hand that prescribes the opioids should also prescribe the ________.
Laxatives
140
What is a caution when prescribing methadone?
QTc prolongations nd potential cardiac arrhythmia.
141
In an opioid-naive patient, the best dose for a transdermal fentanyl patch is the lowest dose with careful monitoring.
True of false.
False, they will probably die.
Transdermal fentanyl is never an appropriate choice for an opioid-naive person.
142
What is a reasonable rate to taper someone to a lower dose of opioid?
For patients who agree to taper opioids to lower doses, collaborate with the patient on a tapering plan.
A reasonable starting regimen would be a reduction of 10% of the original dose/week or month. Some patients do better with slower tapers. The plan should be individualized.
Do not try to taper too quickly, even for someone who hasn't been on opioids for very long. Slower tapers can help minimize withdrawal symptoms.
Opioids may be stopped when taken less frequently than once a day.
143
What are some commonly used medications in palliative care, as per Sarah's pp?
Hydromorphone
Haldol
Acetaminophen
Midazolam - very end of life agitation
Scopolamine - very end of life upper airway secretions
144
Define spondyloarthropathy
Inflammatory joint disease of vertebral column
145
What are some inflammatory back pain characteristics?
Arranged in order of most predictive to least:
-Improvement with exercise
-Paint at night (with improvement getting up)
-Insidious onset
-Age at onset <40
-No improvement with rest
146
What types of arthritis can cause spondyloarthropathy?
-Ankylosing spondylitis
-Psoriatic arthritis
-Reactive arthritis
-Enteric arthritis
147
What is ankylosing spondylitis?
Chronic inflammatory arthritis involving the sacroiliac joints and vertebrae
148
Describe the patho of ankylosing spondylitis (briefly)
-Seronegative rheumatic disease
-Prototypical spondyloarthropathy (spondyloarthropathy= inflammatory joint disease of vertebral column)
-Inflammation > osteopenia >erosion > ossification > osteoproliferation (syndesmophytes)
149
Describe the epidemiology of ankylosing spondylitis
M>F (3:1); F have milder disease (may be underdiagnosed), more peripheral arthritis, upper spine spondylitis
-90-95% of patients are HLA B27 positive (9% of the general population is HLA B27 positive)
150
Clinical presentation of ankylosing spondylitis?
Axial
-Inflammation often begins in SI joints
-Mid and lower back stiffness
-Morning stiffness >1 hour
-Night pain
-Alternating buttocks pain
-Painful SI joint (+ FABER test)
-Spinal restriction (decreased ROM): lumbar (decreased Schober), thoracic (decreased chest wall expansion, normal >5cm at T4), cervical (global decrease, often extension first)
-Postural changes: decreased lumbar lordosis + increased thoracic kyphosis + increased cervical flexion= increased occiput to wall distance (>5cm)
Peripheral
-Asymmetric large joint arthritis, most often involving lower limb
-Enthesitis is a major feature (i.e., Achilles tendinitis, plantar fasciitis)- tenderness over tibial tuberosity, Achilles tendon, or plantar fascia insertion into calcaneus
-Dactylitis: toes or fingers
151
Again, repeat the key features of ankylosing spondylitis.
Axial
-Inflammation often begins in SI joints (painful SI joint, + FABER)
-Mid and lower back stiffness (morning >1 hour, night pain, alternating buttock pain
-Spinal restriction (decreased ROM) affecting all parts of the spine
-Postural changes- loss of lumbar lordosis, increased thoracic kyphosis, increased cervical flexion > increased wall to occiput distance (>5cm)
Peripheral
-Asymmetric large joint arthritis (lower lumbs)
-ENTHESITIS (achilles, plantar)
-Dactylitis (sausage fingers)
152
What are some extra- articular features of ankylosing spondylitis?
-Opthalmic- acute anterior uveitis common (25-30% of patients)
-Renal- IgA nephropathy, amyloidosis (late and rare)
-GI- IBD
-Cardic- aortitis, aortic regurg, pericarditis, conduction disturbances, HF (rare)
-Resp- apical fibrosis (rare)
-Neuro- cauda equina syndrome (rare)
-Skin- psoriasis
153
How to diagnose ankylosing spondylitis?
XR SI joint and spine first line:
- SI joint: “pseudo widening” of joint due to erosion with joint sclerosis > bony fusion (late) > symmetric sacroiliitis
-Spine: “squaring of edges” from erosion and sclerosis on corners of vertebral bodies (“shiny corner sign”) leading to ossification of outer fibers of annulus fibrosis (bridging syndesmophytes)> bamboo spine
Labs: CBC, elevated ESR/ CRP, ALP, Ca2+, serum protein electrophoresis, BMD, HLA- B27
** Autoimmune serology (ANA, RF, anti CCP) NOT recommended in work up
MRI of spine- assess activity in early disease, detection of cartilage changes, bone marrow edema, bone erosions, and subchondral bone changes
-Note- if advanced imaging (CT, MRI) are being considered, it is reasonable to involve a rheumatologist for facilitation of the tests and interpretation of the findings in the clinical context
154
Non pharm treatment of ankylosing spondylitis?
-Prevent fusion from poor posture and disability through: exercise (i.e., swimming), postural and deep breathing exercises, outpatient PT, smoking cessation
155
Pharmacologic treatment for ankylosing spondylitis?
NSAIDs (first line for peripheral and axial disease)
-Initiation recommended if inflammatory back pain is clinically suspected while awaiting work up
-Full dose, consistent use for 2-4 weeks to determine if there is response
-80% of patients with AS who are treated with NSAIDS report good improvement in their symptoms (as opposed to only 15% with mechanical LBP)
Glucocorticoids (topical eye drops, local injections, occasionally requires systemic steroids prior to other effective rx)
DMARDS (i.e., methotrexate) for peripheral disease only
If inadequate response to two NSAIDs (or DMARD), consider anti-TNF agents or anti- IL17 for axial and peripheral involvement
156
Surgical treatment for ankylosing spondylitis?
Hip replacement, vertebral osteotomy may be required for marked deformity
157
Switching types of arthritis!
Clinical features of psoriatic arthritis?
Key: Pain, swelling, stiffness in joints (with morning stiffness, improvement with activity) in patient with psoriasis (esp. those with nail changes). + Enthesitis, dactylitis.
Full list:
Dermatologic
-Psoriasis = itchy and scaly
-well-demarcated erythematous plaques with silvery scale
-nail involvement: pitting, transverse or longitudinal ridging, discolouration, subungual hyperkeratosis, onycholysis, and oil drops
Musculoskeletal
5 general patterns
-asymmetric oligoarthritis (<5 small and/or large joints afected in asymmetric distribution; most common – 70%)
-arthritis of DIPs with nail changes
-symmetric polyarthritis (similar to RA)
-sacroiliitis and spondylitis (usually older, male patients)
-arthritis mutilans (destructive and deforming small joint polyarthritis
Other findings:
-Dactylitis (sausage fingers)
-Enthesopathy (problem with the attachment of tendons, ligaments, or components of a joint onto the bone)
-morning stiffness >30 min (50%)
ophthalmic- Conjunctivitis, iritis (anterior uveitis)
cardiac and respiratory (late fndings)- aortic insufficiency, apical lung fibrosis
neurologic- cauda equina syndrome
radiologic -floating syndesmophytes, pencil-in-cup appearance at IPs, osteolysis, periostitis
158
Who diagnoses psoriatic arthritis?
Rheumatologist
159
What are the key features (CASPAR criteria) for psoriatic arthritis?
Inflammatory articular disease (joint, spine, or entheseal) with 3+ points:
1. Evidence of psoriasis (current, past, fhx)
2. Psoriatic nail dystrophy (onycholysis, pitting, hyperkeratosis)
3. Negative results for RF (preferrably by ELISA)
4. Dactylitis (current or past history)
5. Radiologic evidence (juxta-articular bone formation on hand or foot XR)
160
Ddx for psoriatic arthritis?
Rheumatoid arthritis (RA)
Ankylosing spondylitis (AS)
Osteoarthritis (OA)
Gout
Reactive arthritis.
161
Non pharm tx for psoriatic arthritis?
Early ID key to prevent irreversible joint damage!
Non-pharm:
Exercise on most days of the week. ROM exercises are encouraged for joint stiffness.
Heat application for stiffness and ice to affected joint for swelling may be used
For extended joint stiffness/pain, recommend physical therapy for assessment and treatment.
162
Pharm tx for psoriatic arthritis?
Treat skin lesions: steroid cream, salicylic and/or retinoic acid, tar, moderate sunlight exposure.
NSAIDs for swelling/pain and/or steroids (prednisone), benefit should be seen within a few wk., should not be the sole therapy >3 mo.
Some benefit from cortisone injections into joints
DMARDs to minimize erosive disease (use early in peripheral joint involvement)
Methotrexate used most commonly – treats both psoriasis and arthritis symptoms
Anit-TNF Biologics and small molecules are highly effective for those who don’t respond adequate to aforementioned treatments
163
What is the most common inflammatory arthritis?
Rheumatoid arthritis
164
What is rheumatoid arthritis?
Chronic, symmetric, erosive synovitis of peripheral joints (wrists, MCPs, MTPs)
165
Describe epidemiology of rheumatoid arthritis.
-Most common inflammatory arthritis
-1% of population
-F>M (3:1)
-Age of onset 20-40y
166
Describe patho of rheumatoid arthritis.
-Erosive synovitis of peripheral joints
-Inflammatory disease +/- extra-articular features
- Autoimmune disorder
-Complex genetic and environment interactions lead to disruption of immune tolerance, ultimately resulting in synovial inflammation
-Genetic predisposition: HLA DR4/DR1
-Environmental predisposition (i.e., cigarette smoking)
-Inflammatory process causes transformation of synovium leading to degraded cartilage and bone with absence of repair. Elevated TNF level increases osteoclasts and decreases osteoblasts at site of inflammation > peri articular osteopenia.
Up regulation of RANK ligand increases osteoclast mediated destruction
167
Describe time course of RA and factors contributing to poor prognosis.
Chronic
Variable course of exacerbations and remissions
Poor prognosis: young age at onset, RF+/ high RF titre, elevated ESR, activity of >20 joints, presence of extra articular features `
168
Describe the clinical presentation of RA.
Common presentation:
-Morning stiffness >1h, improves with use, worsens with rest
-Constitutional symptoms (profound fatigue, depression, myalgia, weight loss)
***Symmetric joint involvement
***Initially involves small joints of hands and feet (MCP, PIP, MTP)
Complications of chronic synovitis
-Mechanical joint damage- loss of motion, instability, deformity, crepitus, joint deformities
-Swan neck deformity, boutonniere deformity, ulnar deviation and subluxation of MCP, radial deviation of wrist joint, hammer toe, mallet tow, claw toe, flexion contractures
-Axial subluxation- c-spine instability (neurologic impairment, difficult/ dangerous intubation due to risk to SC)
-Limited shoulder mobility and tears of rotator cuff
-Tenosynovitis may cause tendon rupture
-Carpal tunnel
-Ruptured Baker cyst (outpouching of synovium behind knee)- presentation similar to DVT
169
T/F RA has extra articular features.
True
Skin- periungal infarction, cutaneous ulcers, palpable purpura
Ocular- episcleritis, scelritis
Head and neck- Hashimoto's thyroiditis, xerostomia
Cardiac- peri/ myocarditis, valvular disease, conduction defects
Pulmonary- pulmonary fibrosis, pleural effusion, pleuritis, pulmonary nodules
Neurologic- peripheral neurpathy, mononeuritis
Hematologic-splenomegaly, neutropenia
Renal- amyloidosis
170
T/F RA is a clinical diagnosis
True
171
Labs for suspected RA? Describe why we do each test.
RF is 80% sensitive but nonspecific, and may not be present at onset of disease. Levels do not correlate with disease activity. RF+ can be associated with more erosions, more extra articular manifestations, and worse function.
Anti-CCP: 80% sensitive, 94-98% specific; may precede onset of symptoms (actually considered a better test than RF for RA)
CBC- increased disease activity associated with decreased Hb (anemia of chronic disease) and increased platelets
ESR, CRP (elevated with increased disease activity)
172
What imaging for suspected RA?
XR: Bilateral hands/ wrists, ankles/ feet
C-spine XR (may be normal at onset)
US- changes of synovitis/ erosions noted before XR picks up
MRI- hands- to detect early synovitis and erosions
173
Goals of RA treatment?
Remission or lowest possible disease activity
Key is early diagnosis and intervention with DMARDs- window of opportunity (first 3 mo of disease may allow better control/ remission)
Clinical reassessment every month initially, then 3-6mo if still ongoing activity, then 6-12 mo after inflammation suppressed
174
Non pharm tx of RA?
-Exercise (active gentle ROM and isometric exercise during flares; aquatic/ aerobic. Strengthening exercise between flares)
-PT, OT
-Job modification, assistive devices as necessary
-Interventions to reduce CVD (smoking cessation, lipid control); screen for CVD
-Note: RA is an independent risk factor for atherosclerosis and CVD. It is associated with an increased overall mortality/ morbidity from all causes: CVD, neoplasm (esp. lymphoma), infection)
175
T/F Pharmacologic treatment of RA with NSAIDs can help alter disease progression
FALSE. NSAIDs cannot alter disease course, but they are helpful in reducing inflammation and pain.
176
Describe pharmacologic treatment of RA.
DMARDS and biologics and prednisone (NOT analgesics/ NSAIDS) can alter disease course
-DMARDS
-Tx should be started as soon as RA dx made, and should be aimed at reaching sustained remission
-Methotrexate is the gold standard and is first line unless CI. Baseline CBC, liver enzymes (ALT), Cr, hepatitis B and C, CXR. Monitor and if inadequate response (3-6mo)> combine or switch. Consider combo therapy if poor prognostic factors or high disease activity
Biologics (bDMARDS)
-Use if inadequate response to DMARDS; should be combined with DMARD therapy
-First line options are anti-TNF (i.e., infliximab)
-Reassess q3-6mo and monitor disease activity
Supportive therpaies to reduce inflammation and pain
-NSAIDS, acetaminophen
-Corticosteroids- injection to control symptoms in specific joint; systemic or oral (low doses useful short term is NSAIDs are ineffective and to bridge gap until DMARDs take effect.
177
Some considerations if using oral corticosteroids in RA?
Do baseline DEXA bone density and consider supportive pharmacologic therapy (i.e., bisphosphonates) if using >3 mo.
Caution/ CI with active infection, TB, OP, HTN, gastric ulcer, DM.
AE include weight gain, OP, AVN , cataracts, glaucoma, PUD, susceptibility to infection, easy bruising, acne, HTN, hyperlipidemia, hypokalemia, hyperglycemia, mood swings.
178
When is surgery indicated for RA?
Surgical
-Indicated for structural joint damage
-Synovectomy, joint replacement, joint fusions, reconstruction/ tendon repair
179
What spinal nerve is responsible for the ankle (achilles) reflex?
S1
180
What spinal nerve is responsible for the patellar reflex?
L3-4
181
What nerve roots are responsible for quadriceps power?
L3-4
182
Nerve roots responsible for great toe extension and flexion power?
Great toe extension power (L5)
Great toe flexion power (S1)
183
What are the first line medications for disc and facet joint pain?
NSAID and tylenol
(as per core back tool)
184
Pain meds used for symptomatic spinal stenosis?
NSAIDS & tylenol
185
According to the CORE back tool, which pattern of back pain may require opioids if 1st line meds not sufficient?
Compressed nerve pain
Says for management in this category: "Patient is not usually suitable
for self management due to
high pain levels and possible
surgical intervention"
Also says "Short acting opioid medication may be used for intense pain such as leg dominant constant symptoms related to nerve radiculopathy"
186
As per CORE tool:
"You may need pain medication to help you return to your daily activities and initiate exercise more comfortably. It is _____, however, and not the medication that
will help you recover more quickly"
Activity
187
Criteria of back pain for sending to rehab referral (4-12 treatments)
Absence of red flags
Pain is managed well so that patient can tolerate treatment
Pain has mechanical directional preference – varies with movement, position or activity
Patient is ready to be an active partner in goal setting and self management
188
Criteria for surgical referral for back pain
Failure to respond to evidence based compliant conservative care of at least 12 weeks
Unbearable constant leg dominant pain
Worsening nerve irritation tests (SLR or femoral nerve stretch)
Expanding motor, sensory or reflex deficits
Recurrent disabling sciatica
Disabling neurogenic claudication
189
What is neurogenic claudication?
Usually caused by spinal stenosis (narrowing of spinal canal)
Compression of nerves in lower spine causing pain & weakness in the legs
190
What is the straight leg raise?
What nerves are being tested here?
commonly used to identify disc pathology or nerve root irritation, as it mechanically stresses lumbosacral nerve roots. It also has specific importance in detecting disc herniation and neural compression
This test places tensile stresses on the sciatic nerve and of traction at the lumbosacral nerve roots primarily from L4 to S2
191
A positive straight leg test creates radicular leg pain when the hip is flexed at what angle?
(according to physiopedia)
30 and 60 or 70 degrees from horizontal.
Pain at greater than 70 degrees of hip flexion might indicate tightness of the hamstrings, gluteus maximus, or hip capsule, or pathology of the hip or sacroiliac joints
192
How to do the SLR?
the patient is positioned in supine without a pillow under their head, the clinician stands at the tested side with their distal hand around the patient's heel and proximal hand on patient's distal thigh(anterior) to maintain knee extension. The clinician lifts the patient's leg by the posterior ankle while keeping the knee in a fully extended position. The clinician continues to lift the patient's leg slowly through flexing at the hip, until the patient's symptoms are replicated, or they experience tightness in the back or posterior thigh
193
What must NPs do before they can prescribe controlled drugs and substances?
Must first register for PharmNet access appropriate to the practice sites where they are prescribing controlled drugs & substances
(highlighted in class PPT)
- Must also complete one of the controlled drugs courses listed (4 to choose from)
- Complete the BCCNM CDS prescribing modules
- Must meet the BCCNM competencies for NP prescribing of controlled drugs and substances
194
Does a T3 need to be written on a duplicate pad? What about T4? What about codeine alone?
Tylenol #3 does not need to be written on a duplicate pad. However, Tylenol 4 or Codeine tabs alone does. See below:
“Codeine when prescribed as a single entity, when included in a preparation containing 60 mg or more per dosage unit , or when included in a liquid preparation containing 1.6 mg or more per mL
T4 has 60mg codeine.
T3 has 30mg of codeine (along with acetaminophen).
195
T/F You prescribe 15mg codeine. Does this require a duplicate?
Yes, because is codeine alone (doesn't matter what dose!)
196
Does ketamine require a duplicate?
No
197
Does nabilone require a duplicate?
No
198
Does phenobarbital require a duplicate?
No
199
Does methylphenidate require a duplicate?
No
200
Which drugs DO require a duplicate?
- Buprenorphine
- Codeine alone or if in combo with 60mg or more
- fentanyl
- hydrocodone
- hydromorph
- demerol
- methadone
- morphine
- oxycodone
etc
