Week 4--lecture slides Flashcards
1
Q
what should you discuss with patients before starting antidepressants
A
be realistic about benefits time to effect what if it doesnt work duration of treatment side effects discontinuation
2
Q
how do you measure response or remission for antidepressant treatment
A
HAM-D and other tools
expect 50-60% remission or response
3
Q
should you use antidepressants with mild depression
A
unlikely to be better than placebo
4
Q
which antidepressants are best
A
escitalopram
mirtazapine
sertraline
venlafaxine
(moderate superiority, level I evidence)
5
Q
when do you see improvement with antidepressants
A
“4-6 weeks” but those that are improving at the 204 week time mark is correlated with response and remission at 6-12 weeks
lack of early improvement is a predictor of non response and non remission
want to see some change within 2-4 weeks
6
Q
how long does it take for antidepressants take to treat anxiety
A
up to 12 weeks for full effect
2-8 weeks for symptom relief
start low and titrate up q1-2 weeks
follow up q2 weeks for the first 6 weeks then monthly
7
Q
what causes the side effects of anti depressants
A
related to in vivo affinity for/activity on neurotransmitters/receptors
usually higher incidence within first week
consider starting at lower dose for 5-7 days before increasing to ensure tolerance
unexpected side effects can affect adherence
8
Q
common side effects for:
buproprion
A
stimulation
9
Q
common side effects for:
sedation
A
mirtaz
fluvoxamine
10
Q
common side effects for:
sertraline
A
diarrhea
11
Q
common side effects for:
venlafaxine
A
nausea
12
Q
uncommon but serious antidepressant SEs
A
long Qtc suicidality serotonin syndrome falls and fractures (especially in first 6 weeks) hyponatremia possible bleeding
13
Q
what disorders are antidepressants used to treat
A
MDD anxiety disorders OCD PTSD social anxiety disorder panic disorder GAD bulemia nervosa bipolar depression binge eating disorder BPD fibromyalgia pain hot flashes smoking cessation
14
Q
what are the most commonly used antidepressants
A
SSRIs
SNRIs
NDRIs
NaSSAs (i.e mirtaz)
less common:
TCAs
MAOIs
15
Q
MOA of TCAs
A
non selective inhibition of 5HT and NA reuptake
block muscarinic, histamine and adrenergic receptor
16
Q
SEs of TCAs
A
anticholinergic
antihistaminic
risk of arrhythmias if OD
17
Q
should you use TCAs first line?
A
NO
not first line because of unfavorable SEs
primarily used for pain currently
consider consulting psychiatry before starting
18
Q
MOA of MAOIs
A
IRREVERSIBLE inhibition of MAO-A and MAO-B which increases levels of NA, DA, 5HT
19
Q
examples of MAOIs
A
phenelzine, tranylcypromine
20
Q
SEs of MAOIs
A
anticholinergic
decreased sleep efficiency (stimulant)
21
Q
should you use MAOIs first line?
A
NO
risk of hypertensive crisis when combined with tyramine containing foods or with a sympathomimetic
WASHOUT PERIOD REQUIRED
22
Q
what is a RIMA
A
a reversible MAOI
23
Q
name the RIMA
A
moclobemide
24
Q
SEs of moclobemide
A
anticholinergic
insomnia
25
why would you use a RIMA/moclobemide
lower risk of hypertensive crisis than traditional MAOIs (need to eat 3 kgs of cheese to raise BP by 30 mmHg)
still need washout period when switching to or from MAOIs
there is LESS sexual dysfunction and weight gain than with SSRIs, MAOIs, TCAs
26
name some SSRIs
```
citalopram
escitalopram
fluoxetine
sertraline
fluvoxamine
paroxetine
```
27
name some SNRIs
venlafaxine
| duloxetine
28
name an NDRI
bupropion
29
name an NaSSA
mirtazapine
30
what guidelines to use for starting antidepressants
CANMAT guidelines
based on efficacy, tolerability and safety
31
what to consider before starting antidepressants
patient factors:
- clinical features
- comorbidities
- response to prior trials
- patient preference
medication factors:
- comparative efficacy/tolerability
- potential drug interactions
- simplicity of use
- cost/availability
32
common side effects for:
| sertraline and paroxetine
sexual dysfunction
33
common side effects for:
| mirtazapine, paroxetine
weight gain
34
common side effects for:
| paroxetine, venlafaxine
more withdrawal
35
what antidepressants do we worry about long QTc with
citalopram and escitalopram
36
what are the recommended daily max doses of citalopram and escitalopram
citalopram 40 mg
escitalopram 20 mg
(half that is over 65)
37
what other medications other than antidepressants also increase QT
```
antipsychotics
antibiotics (macrolides, ciprofloxacin)
antifungals (azoles)
methadone
anti-emetics
some chemotherapies
```
38
how does hyponatremia present
```
headache
nausea
lethargy
weakness
muscle cramps
somnolence
```
more severe--
confusion
seizure
coma
39
who is at increased risk for hyponatremia
```
elderly
female
low BMI
smokers
diuretic use
```
40
what is serotonin syndrome
toxicity
seen with therapeutic med use, drug interactions, poisoning
can range from benign to lethal
is clinical diagnosis
41
what is the classic triad that diagnoses serotonin syndrome?
CAN
Cognitive changes--> anxiety, agitated delirium, restlessness, disorientation, startles easily
Autonomic changes--> diaphoresis, tachycardia, HTN, hyperthermia, vomiting, diarrhea
Neuromuscular changes--> tremor, rigidity, myoclonus, hyper reflexia, bilateral babinsky
42
name some common drugs that can increase the risk of serotonin syndrome
```
amphetamines
cocaine
MDMA
levodopa/carbidopa
tramadol
st johns wort
MAOIs
triptans
fentanyl
LSD
lithium
```
43
what lab tests may change in serotonin syndrome
increased WBC
increased CPK
decreased bicarb
44
what criteria should you use to diagnose serotonin syndrome
Hunter Toxicity criteria
45
what are some of the complications that can arise out of serotonin syndrome
```
DIC
rhabdo
metabolic acidosis
renal failure
ARDS
```
46
when does serotonin syndrome usually present
6-24 hours after a dose change or initiation
47
what are some of the symptom criteria in the hunter criteria
spontaneous clonus
inducible clonus AND agitation OR diaphoresis
ocular clonus AND agitation OR diaphoresis
tremor AND hyperreflexia
hypertonia AND temperature above 38 degrees AND spontaneous or inducible ocular clonus
48
how do you manage serotonin syndrome
discontinuation of all serotonergic agents
supportive care aimed at normalization of vital signs
sedation with benzodiazepines
administration of serotonin antagonists
assessment of the need to resume the use of the causative serotonergic agents after resolution
49
what age group should you be particularly concerned about with regard to increased suicidality with anti-depressants
18-24 years old (especially in first few weeks after starting)
NO DIFFERENCE beteen antidepressant classes
50
how long should patients take anti depressants for
CANMAT guidelines suggest 6-9 months after achieving sx remission
if there are risk factors for recurrence, suggest 2 years or more
most common recurrence at 24 and 52 weeks
51
sx of anti depressant sudden discontinuation syndrome
FINISH
```
Flu like symptoms
Insomnia
Nausea
Imbalance
Sensory disturbances
Hyper arousal
```
52
which anti depressants have high potential for drug interactions
fluoxetine
fluvoxamine
moclobemide
paroxetine
(low risk is citalopram, desvenlafaxine, venlafaxine, escitalopram, mirtazapine)
53
what drugs do you need to be careful about mixing with paroxetine, fluoxetine and buproprion and why
codeine and tamoxifen--these anti depressants are potent 2D6 inhibitors, and codeine is metabolized by this enzyme, while tamoxifen is a prodrug metabolized by 2D6
54
what anti depressant is known to cause CV malformations at higher rates
paroxetine
55
what anti depressants (2) are known to possibly cause septal heart defects
sertraline and citalopram
56
what anti depressant is relatively well documented as safe in lactation
sertraline (so consider this is pharmacotherapy is needed in lactation)
if need to use another agent, take a single dose prior to the infants longest sleep to avoid peak levels getting into the infant thru breastmilk
57
why do patients most often choose MAID
to maintain autonomy/control in the face of illness
to keep dignity
less likely due to pain/symptom control
58
who is involved in MAID
minimum 5 people
patient
2 independent witnesses (who know what the request is for, who are adults--cannot be anyone who will benefit from death of this patient i.e in the will, usually no family, no one who provides healthcare to the patient, no one who provides personal care to the patient, no one who owns a healthcare facility)
2 independent medical assessments to determine if eligible (+/- extra consultants if needed)
59
how do you access MAID
1. patient makes written request--must be witness properly by 2 independent witnesses (if patient cant write, form can be filled in by proxy)
2. 10 day waiting period after making the request (begins day after request made by patient)
3. medical assessments by 2 independent practitioners
60
who is eligible for MAID
Must meet all of these criteria
1. must be an ADULT (18 years and above)
2. must be eligible to receive Canadian healthcare
3. request must be made voluntarily (no external suggestions from spouse, children, etc)
- -therefore MUST MEET WITH PATIENT ALONE
4. patient must be suffering from a GRIEVOUS and IRREMEDIABLE condition (must meet all 5 below criteria)
- a serious disease or disability
- disease must be putting you in an advanced state of decline in capability (describes functional impairment)
- disease cannot be reversed (by any means acceptable to the patient)
- patient must be suffering unbearably (as defined by the patient themselves)
- patients natural death has become reasonably foreseeable, taking into account medical condition (no one really knows what it means) -->this is being challenged in the courts
5. patient must be capable of making the request at the time of making the request AND ALSO at the time of procedure (NO advanced directives)
61
what is the gist of the Meredith principles governing worksafeBC
employers bear direct cost of compensation but are in turn protected from lawsuits
fault is not taken into consideration with regard to compensation
62
rather than an approach based on volume status, what is another way to assess the cause of hypotonic hyponatremia
are the kidneys able to excrete free water?
if CONCENTRATED urine (urine osmolality > serum osmolality) --> then ADH is HIGH and kidneys cannot excrete free water
if DILUTE urine (urine osmolality is equal to or less than serum osmolality) --> then ADH is LOW and kidneys can excrete free water
63
in the case of hypotonic hyponatremia, with concentrated urine, and thus high ADH, what might be the causes
ADH may be high due to either physiologic or pathologic causes
physiologic:
- pain
- nausea
- vomiting
- anxiety
- decreased effective circulating volume (i.e from blood loss, diarrhea, vomiting or from edema states like CHF or cirrhosis)
pathologic:
- DRUGS--> may act by enhancing ADH release or potentiate its effect (i.e opioids, SSRIs, nicotine, anticonvulsants, amphetamines, NSAIDs)//ADH analogs
- endocrinopathies--> glucocorticoid deficiency, hypothyroid, SIADH
64
ddx for hypotonic hyponatremia with dilute urine
1. psychogenic polydipsia
2. malnourishment ("tea and toaster")
* water intake is overwhelming the excretory capacity of the kidneys
65
what is the maximum urine dilution
50 mOsm/kg
*cant excrete pure water
66
what should the body's normal response to hyponatremia be
suppress ADH release
with no ADH, should result in maximally dilute urine to get rid of water and return sodium balance (Uosm < 100 mOsm/kg)
values higher than 100 indicate ADH is inappropriately on and preventing the excretion of free water
67
what urine sodium concentration suggests a pre-renal problem
U [Na] < 20-30 mEq/L
*FENa is a better test because it corrects for urine concentration--> FENa < 1% suggests pre renal state
68
define acute hypotonic hyponatremia
less than 24 - 48 hours
69
why do we care about acute hypotonic hyponatremia
there is no time for brain adaptation
the reduction in plasma effective osmolality causes water to move out of ECF and into cells causing cerebral edema
70
sx of cerebral edema
GI and neuro--> lethargy, confusion, obtundations, seizures
neurogenic pulmonary edema
death
71
how does the brain adapt to chronic hypotonic hyponatremia
brain cells extrude osmoles to help balance the osmotic gradient and normalize the brain water content
72
how do you treat acute (documented less than 48 hours) hypotonic hyponatremia
*symptomatic acute hyponatremia is associated with high mortality
since the brain has not had a chance to adapt, rapid increases in plasma [Na] are SAFE to reverse cerebral edema
73
how do you treat chronic hypotonic hyponatremia
must be careful and do it SLOWLY as the brain HAS had a chance to adapt and extrude osmoles
if corrected too quickly, patients are at risk of OSMOTIC DEMYELINATING SYNDROME
correct sodium at rate of 8 mEq max per 24 hours
if patient is seizing in the ER, give 4 mEq now then aim for 8 mEq total over 24 hours
74
what are the general treatment principles with hyponatremia
treat the underlying cause!!
fluid restriction to less than 1.2-1.5 L per day
high sodium diet
IV fluid containing sodium
ADH antagonists possible but not routine practice
*giving Na not always best i.e in CHF
75
how do you calculate Na deficit
Na deficit in mEq = TBW x Na deficit per L
=
0. 5 x lean body wt (kg) x (desired[Na] - current[Na])
* desired[Na] is 8 mEq above current as you want to do 8 mEq in first 24 hours
this will give the Na deficit you need to over come
76
when should you consider using hypertonic (3%) NS to treat hyponatremia
when severely symptomatic (i.e seizures, obtundation)
77
symptoms of osmotic demyelination syndrome
often delayed by days
```
dysarthria
dysphagia
paresis
lethargy
coma
```
78
risk factors for osmotic demyelination syndrome
chronic hyponatremia < 110 mEq/L
alcoholism
hepatic failure
liver transplant
malnutrition
hypokalemia
79
why is hypovolemia + hyponatremia dangerous?
normally the main stimulus for ADH secretion is increase in serum osmolality, but if hypovolemia gets too bad then will turn on despite low serum osmolality (from low Na)--> as you try to correct the hypovolemia, you can cause the ADH to turn off which can actually correct the Na too rapidly
80
what should you do if you realize you are correcting hyponatremia too rapidly
stop sodium containing IV fluids
drink water of give IV D5W (rate matching urine output)
give ddAVP 4 mcg SQ every 6-8 hours which will stop free water excretion
81
in what etiology of hyponatremia should you beware of NS administration
SIADH type states where they are euvolemic or hypervolemic and Na and K excretion is high--> NS can actually make it worse by causing the patient to retain more water (due to ADH being on etc)
treat with fluid restriction plus high salt diet
82
define integrative medicine
healing oriented medicine that takes into account the whole person, including all aspects of lifestyle
it emphasizes the therapeutic relationship between practitioner and patient, is informed by evidence, and makes use of all appropriate therapies
83
lover's fracture
fractures of the calcaneus after falling from height
associated with lower T spine fractures (don juan's fracture)
84
how do flexion vs. extension teardrop fractures differ
flexion--> very unstable, often associated with ligamentous injury
extension--> usually at base of C2, stable
85
night-stick fracture
ulnar fracture and radial dislocation--> Montagia fracture
86
what should you always look for when you see a pelvis #
there are usually two breaks
87
when is a sign of a proximal tibial #
fat effusion secondary to the fracture (lipohemarthrosis)
88
describe the spirit and style of motivational interviewing
collaborative
evocative (draw out rather than impose)
autonomy (choice and method of change is with patient)
89
what are SMART goals
Stated in the positive, Specific
Measurable
Attainable
Realistic
Time specific
90
if a patient rates their importance level for a behavioural change as less than 7, what are the chances of them making that change
low
91
what % of spinal fractures are multiple fractures
20%
92
what % of multiple spinal fractures are at multiple levels
5%
93
what % of spinal cord injuries are at the time of trauma vs. which are a late complication
time of trauma--85%
late complications--15%
94
what % of spine traumas are from MVCs? falls?
MVCs--50%
falls--20%
95
where are the most common sites for c spine fracture
C1-C2
C5-C7
96
name the type of flexion C spine injury--stable or unstable?
flexion teardrop--unstable
97
name the two types of extension c spine injuries--stable or unstable?
hangman's--unstable
extension teardrop--stable
98
name the two types of axial compression c spine injuries--stable or unstable?
jeffersons--unstable
burst fracture--stable
99
name the two types of complex c spine injuries--stable or unstable?
odontoid fracture--unstable
atlantooccipital disassoc.--unstable
100
in the setting of a c spine injury, when do you order flexion extension films?
when no fractures are seen on the initial (later, AP, open mouth odontoid) films, and you want to exclude a soft tissue or ligamentous injury
101
in the setting of a c spine injury, when should you get an MRI
for assessment of the integrity of the spinal cord
can evaluate for cord edema/cord hemorrhage--> these are bad prognotic factors for recovery of function
can look for epidural hematoma or traumatic disc herniation
assess integrity of the anterior and posterior ligaments
102
in the assessment of c spine films, what are the 4 parallel lines
1. anterovertebral line
2. posterovertebral line
3. spinolaminar line
4. posterospinous line
103
what is a normal atlanto-dental interval in adults--what if this is widened on imaging?
less than 3 mm (less than 5 mm in kids)
*widening of this interval suggests disruption of the transverse ligament
104
in the setting of a c spine injury, what signs on an AP film usually indicate injury
loss of alignment of the spinous processes or widening of the space between them
105
what are radiographic indications of an unstable c spine injury
1. changes in the normal disc space--> widening or narrowing (widening disc space indicates serious hyperextension injury)
2. widening of the interspinous distance--> hyperflexion injuries may rupture the interspinous and supraspinous ligaments giving a widened intraspinous space
3. associated compression # of more than 25% of the affected vertebral body
4. anterosublixation of more than 3 mm of one vertebral body relative to the other
5. involvement of two columns
106
where is a hangman's fracture
C2 vertebra
107
what is the mechanism of a hangman's fracture
hyperextension and traction of C2
best seen on lateral film
108
how many types of odontoid process # are there
3
109
type I odontoid process fracture
upper part of odontoid (potentially unstable )
110
type II odontoid process fracture
base of odontoid (unstable)
111
type III odontoid process fracture
base of odontoid into the body of the axis (unstable)
112
what is a jefferson's fracture
compression force to C1, usually from a blow to the vertex of the head
uni or bilateral fracture of both anterior and posterior arches of C1
113
what is a flexion teardrop fracture
very severe fracture of the c spine--> often causes anterior cervical cord syndrome or quadriplegia
typically from flexion and compression i.e in an MVC
usually at C5/6
114
what might you expect to see on x ray in degenerative c spine disease
joint space narrowing
subchondral cysts
osteophytes
cartilage loss/disk space narrowing
sunchondral sclerosis
115
when should you do a bone scan?
osteomyelitis
stress fractures
occult fractures
mets
staging for tumours
AVN
*tracer gets taken up more with increase in blood flow and/or osseous remodelling
116
what is the "ring phenomenon" in evaluating bone fractures
if there is a break at one location in the ring (i.e pelvis) there is a good chance there is a second break in the ring somewhere else
117
how do you describe fractures
1. fracture pattern
2. anatomic site
3. alignment
4. associated soft tissue injuries
118
what are the two clinical categories of fracture pattern
simple--> closed, skin intact
compound--> open, skin not intact
(complete vs. incomplete, depending on whether fracture traverses the complete width of the bone)
119
communited fracture
more than 2 fragments of bone
120
how do you describe fracture angulation?
described by the direction the DISTAL fragment deviates (varus or valgus)
121
what is the most common type of shoulder fracture
clavicle--scapular fractures are rare
122
hill sachs fracture
occurs when shoulder is dislocated anteriorly and the posterior humeral head makes contact with the anterior inferior glenoid rim
123
bankart fracture
avulsion fracture of the anterior labrum (around the glenoid fossa)
124
what fracture commonly results from FOOSH
radial head fracture
*suspect it in a patient with elbow joint effusion and displacement of the fat pads--> SAIL SIGN
can also get a colles fracture, scaphoid fracture
125
what fracture is associated with a sail sign
radial head fracture
| findings otherwise are often subtle
126
colles fracture
from FOOSH
"dinner fork" deformity
fracture occurs through the distal metaphysis and epiphysis of the radius and will often extend to the joint surface
127
what is the most common type of carpal bone fracture
scaphoid--from FOOSH
*suspect if snuffbox tenderness
128
why must you always make sure not to miss a scaphoid fracture
blood vessels enter the scaphoid at the distal pole, thus a complete fracture can cause the proximal pole to lose its blood supple resulting in avascular necrosis
129
management of scaphoid #
if has snuffbox tenderness but radiograph negative, immobilize and follow up imaging in 10-14 days or immediate 3 phase bone scan, CT or MRI
130
where do femoral fractures occur
1. subcapital--intracapsular
2. transcervical--intracapsular
3. intertrochanteric--extracapsular
4. subtrochanteric--extracapsular
* no risk of AVN if extracapsular #
131
how do people sustain tibial plateau fractures?
motor vehicles striking pedestrians
132
why do we care so much about the lis franc fracture dislocation in the foot
forefoot is dislocated laterally and dorsally
there is extensive disruption of the ligaments, especially with the ligament extending from the second metatarsal to the medial cuneiform, which can cause severe disability
133
define: arthritis
inflammation of joints
134
define: arthropathy
abnormality (non specific) of a joint
135
define: erosion
focal bony defect of subchondral bone usually located at the site of synovial and capsular attachment to the bone
136
define: osteophyte
bony spur arising at the margin of a joint
137
define: sclerosis
focal increased density adjacent to a normal joint producing increased "whiteness" on the radiograph
138
define: geode
fluid filled cyst within the subarticular aspect of the bone
139
describe an approach to abnormal joint radiography
ABCDE'S
Alignment--subluxations
Bone proliferation--periosteal reaction
Cartilage--joint space narrowing
Density--bone mineral increased or decreased
Erosions--punched out defects
Soft tissue changes--masses, inflammation
140
in patients with a primary cancer tumour who have pain but negative x rays, what % have bone mets on bone scan
30%
141
define: osteoarthritis
degenerative arthritis characterized by deterioration of the articular cartilage and formation of new bone (osteophytes) at joint surfaces and edges
142
radiographic features of OA
narrowing of joint space
sunchondral sclerosis
osteophyte formation
subchondral cysts
*may also have heberdens, bouchards nodes in hands, deformity and malalignment, subchondral bony collapse
143
define: rheumatoid arthritis
inflammatory arthritis that originated in the synovium, typically symmetric and polyarticular
144
radiographic features of rheumatoid
periarticular soft tissue swelling
symmetric periarticular osteoporosis
marginal erosions
```
late findings:
boutonniere deformite
swan neck deformity
subluxation of affected joints with ulnar deviation
diffuse uniform joint space narrowing
```
