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PMP > Week 4--lecture slides > Flashcards

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
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2
Q

how do you measure response or remission for antidepressant treatment

A

HAM-D and other tools

expect 50-60% remission or response

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3
Q

should you use antidepressants with mild depression

A

unlikely to be better than placebo

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4
Q

which antidepressants are best

A

escitalopram
mirtazapine
sertraline
venlafaxine

(moderate superiority, level I evidence)

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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

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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

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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

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8
Q

common side effects for:

buproprion

A

stimulation

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9
Q

common side effects for:

sedation

A

mirtaz

fluvoxamine

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10
Q

common side effects for:

sertraline

A

diarrhea

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11
Q

common side effects for:

venlafaxine

A

nausea

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12
Q

uncommon but serious antidepressant SEs

A 
long Qtc
suicidality 
serotonin syndrome 
falls and fractures (especially in first 6 weeks)
hyponatremia 
possible bleeding
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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
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14
Q

what are the most commonly used antidepressants

A

SSRIs
SNRIs
NDRIs
NaSSAs (i.e mirtaz)

less common:
TCAs
MAOIs

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15
Q

MOA of TCAs

A

non selective inhibition of 5HT and NA reuptake

block muscarinic, histamine and adrenergic receptor

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16
Q

SEs of TCAs

A

anticholinergic
antihistaminic
risk of arrhythmias if OD

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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

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18
Q

MOA of MAOIs

A

IRREVERSIBLE inhibition of MAO-A and MAO-B which increases levels of NA, DA, 5HT

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19
Q

examples of MAOIs

A

phenelzine, tranylcypromine

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20
Q

SEs of MAOIs

A

anticholinergic

decreased sleep efficiency (stimulant)

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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

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22
Q

what is a RIMA

A

a reversible MAOI

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23
Q

name the RIMA

A

moclobemide

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24
Q

SEs of moclobemide

A

anticholinergic

insomnia

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25
Q

why would you use a RIMA/moclobemide

A

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

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26
Q

name some SSRIs

A 
citalopram
escitalopram
fluoxetine
sertraline
fluvoxamine
paroxetine
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27
Q

name some SNRIs

A

venlafaxine

duloxetine

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28
Q

name an NDRI

A

bupropion

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29
Q

name an NaSSA

A

mirtazapine

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30
Q

what guidelines to use for starting antidepressants

A

CANMAT guidelines

based on efficacy, tolerability and safety

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31
Q

what to consider before starting antidepressants

A

patient factors:

  • clinical features
  • comorbidities
  • response to prior trials
  • patient preference

medication factors:

  • comparative efficacy/tolerability
  • potential drug interactions
  • simplicity of use
  • cost/availability
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32
Q

common side effects for:

sertraline and paroxetine

A

sexual dysfunction

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33
Q

common side effects for:

mirtazapine, paroxetine

A

weight gain

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34
Q

common side effects for:

paroxetine, venlafaxine

A

more withdrawal

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35
Q

what antidepressants do we worry about long QTc with

A

citalopram and escitalopram

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36
Q

what are the recommended daily max doses of citalopram and escitalopram

A

citalopram 40 mg
escitalopram 20 mg
(half that is over 65)

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37
Q

what other medications other than antidepressants also increase QT

A 
antipsychotics
antibiotics (macrolides, ciprofloxacin)
antifungals (azoles)
methadone
anti-emetics
some chemotherapies
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38
Q

how does hyponatremia present

A 
headache
nausea
lethargy
weakness
muscle cramps
somnolence

more severe–
confusion
seizure
coma

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39
Q

who is at increased risk for hyponatremia

A 
elderly
female
low BMI
smokers
diuretic use
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40
Q

what is serotonin syndrome

A

toxicity

seen with therapeutic med use, drug interactions, poisoning

can range from benign to lethal

is clinical diagnosis

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41
Q

what is the classic triad that diagnoses serotonin syndrome?

A

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

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42
Q

name some common drugs that can increase the risk of serotonin syndrome

A 
amphetamines
cocaine
MDMA
levodopa/carbidopa
tramadol
st johns wort 
MAOIs
triptans
fentanyl
LSD
lithium
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43
Q

what lab tests may change in serotonin syndrome

A

increased WBC
increased CPK
decreased bicarb

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44
Q

what criteria should you use to diagnose serotonin syndrome

A

Hunter Toxicity criteria

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45
Q

what are some of the complications that can arise out of serotonin syndrome

A 
DIC
rhabdo
metabolic acidosis 
renal failure 
ARDS
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46
Q

when does serotonin syndrome usually present

A

6-24 hours after a dose change or initiation

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47
Q

what are some of the symptom criteria in the hunter criteria

A

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

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48
Q

how do you manage serotonin syndrome

A

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

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49
Q

what age group should you be particularly concerned about with regard to increased suicidality with anti-depressants

A

18-24 years old (especially in first few weeks after starting)

NO DIFFERENCE beteen antidepressant classes

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50
Q

how long should patients take anti depressants for

A

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

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51
Q

sx of anti depressant sudden discontinuation syndrome

A

FINISH

Flu like symptoms
Insomnia
Nausea
Imbalance 
Sensory disturbances
Hyper arousal
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52
Q

which anti depressants have high potential for drug interactions

A

fluoxetine
fluvoxamine
moclobemide
paroxetine

(low risk is citalopram, desvenlafaxine, venlafaxine, escitalopram, mirtazapine)

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53
Q

what drugs do you need to be careful about mixing with paroxetine, fluoxetine and buproprion and why

A

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

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54
Q

what anti depressant is known to cause CV malformations at higher rates

A

paroxetine

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55
Q

what anti depressants (2) are known to possibly cause septal heart defects

A

sertraline and citalopram

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56
Q

what anti depressant is relatively well documented as safe in lactation

A

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

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57
Q

why do patients most often choose MAID

A

to maintain autonomy/control in the face of illness

to keep dignity

less likely due to pain/symptom control

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58
Q

who is involved in MAID

A

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
Q

how do you access MAID

A
  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
Q

who is eligible for MAID

A

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
Q

what is the gist of the Meredith principles governing worksafeBC

A

employers bear direct cost of compensation but are in turn protected from lawsuits

fault is not taken into consideration with regard to compensation

62
Q

rather than an approach based on volume status, what is another way to assess the cause of hypotonic hyponatremia

A

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
Q

in the case of hypotonic hyponatremia, with concentrated urine, and thus high ADH, what might be the causes

A

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
Q

ddx for hypotonic hyponatremia with dilute urine

A
  1. psychogenic polydipsia
  2. malnourishment (“tea and toaster”)
    * water intake is overwhelming the excretory capacity of the kidneys
65
Q

what is the maximum urine dilution

A

50 mOsm/kg

*cant excrete pure water

66
Q

what should the body’s normal response to hyponatremia be

A

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
Q

what urine sodium concentration suggests a pre-renal problem

A

U [Na] < 20-30 mEq/L

*FENa is a better test because it corrects for urine concentration–> FENa < 1% suggests pre renal state

68
Q

define acute hypotonic hyponatremia

A

less than 24 - 48 hours

69
Q

why do we care about acute hypotonic hyponatremia

A

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
Q

sx of cerebral edema

A

GI and neuro–> lethargy, confusion, obtundations, seizures

neurogenic pulmonary edema

death

71
Q

how does the brain adapt to chronic hypotonic hyponatremia

A

brain cells extrude osmoles to help balance the osmotic gradient and normalize the brain water content

72
Q

how do you treat acute (documented less than 48 hours) hypotonic hyponatremia

A

*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
Q

how do you treat chronic hypotonic hyponatremia

A

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
Q

what are the general treatment principles with hyponatremia

A

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
Q

how do you calculate Na deficit

A

Na deficit in mEq = TBW x Na deficit per L

=

  1. 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
Q

when should you consider using hypertonic (3%) NS to treat hyponatremia

A

when severely symptomatic (i.e seizures, obtundation)

77
Q

symptoms of osmotic demyelination syndrome

A

often delayed by days

dysarthria
dysphagia
paresis
lethargy
coma
78
Q

risk factors for osmotic demyelination syndrome

A

chronic hyponatremia < 110 mEq/L

alcoholism

hepatic failure

liver transplant

malnutrition

hypokalemia

79
Q

why is hypovolemia + hyponatremia dangerous?

A

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
Q

what should you do if you realize you are correcting hyponatremia too rapidly

A

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
Q

in what etiology of hyponatremia should you beware of NS administration

A

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
Q

define integrative medicine

A

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
Q

lover’s fracture

A

fractures of the calcaneus after falling from height

associated with lower T spine fractures (don juan’s fracture)

84
Q

how do flexion vs. extension teardrop fractures differ

A

flexion–> very unstable, often associated with ligamentous injury

extension–> usually at base of C2, stable

85
Q

night-stick fracture

A

ulnar fracture and radial dislocation–> Montagia fracture

86
Q

what should you always look for when you see a pelvis #

A

there are usually two breaks

87
Q

when is a sign of a proximal tibial #

A

fat effusion secondary to the fracture (lipohemarthrosis)

88
Q

describe the spirit and style of motivational interviewing

A

collaborative

evocative (draw out rather than impose)

autonomy (choice and method of change is with patient)

89
Q

what are SMART goals

A

Stated in the positive, Specific

Measurable

Attainable

Realistic

Time specific

90
Q

if a patient rates their importance level for a behavioural change as less than 7, what are the chances of them making that change

A

low

91
Q

what % of spinal fractures are multiple fractures

A

20%

92
Q

what % of multiple spinal fractures are at multiple levels

A

5%

93
Q

what % of spinal cord injuries are at the time of trauma vs. which are a late complication

A

time of trauma–85%

late complications–15%

94
Q

what % of spine traumas are from MVCs? falls?

A

MVCs–50%

falls–20%

95
Q

where are the most common sites for c spine fracture

A

C1-C2

C5-C7

96
Q

name the type of flexion C spine injury–stable or unstable?

A

flexion teardrop–unstable

97
Q

name the two types of extension c spine injuries–stable or unstable?

A

hangman’s–unstable

extension teardrop–stable

98
Q

name the two types of axial compression c spine injuries–stable or unstable?

A

jeffersons–unstable

burst fracture–stable

99
Q

name the two types of complex c spine injuries–stable or unstable?

A

odontoid fracture–unstable

atlantooccipital disassoc.–unstable

100
Q

in the setting of a c spine injury, when do you order flexion extension films?

A

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
Q

in the setting of a c spine injury, when should you get an MRI

A

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
Q

in the assessment of c spine films, what are the 4 parallel lines

A
  1. anterovertebral line
  2. posterovertebral line
  3. spinolaminar line
  4. posterospinous line
103
Q

what is a normal atlanto-dental interval in adults–what if this is widened on imaging?

A

less than 3 mm (less than 5 mm in kids)

*widening of this interval suggests disruption of the transverse ligament

104
Q

in the setting of a c spine injury, what signs on an AP film usually indicate injury

A

loss of alignment of the spinous processes or widening of the space between them

105
Q

what are radiographic indications of an unstable c spine injury

A
  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
Q

where is a hangman’s fracture

A

C2 vertebra

107
Q

what is the mechanism of a hangman’s fracture

A

hyperextension and traction of C2

best seen on lateral film

108
Q

how many types of odontoid process # are there

A

3

109
Q

type I odontoid process fracture

A

upper part of odontoid (potentially unstable )

110
Q

type II odontoid process fracture

A

base of odontoid (unstable)

111
Q

type III odontoid process fracture

A

base of odontoid into the body of the axis (unstable)

112
Q

what is a jefferson’s fracture

A

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
Q

what is a flexion teardrop fracture

A

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
Q

what might you expect to see on x ray in degenerative c spine disease

A

joint space narrowing

subchondral cysts

osteophytes

cartilage loss/disk space narrowing

sunchondral sclerosis

115
Q

when should you do a bone scan?

A

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
Q

what is the “ring phenomenon” in evaluating bone fractures

A

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
Q

how do you describe fractures

A
  1. fracture pattern
  2. anatomic site
  3. alignment
  4. associated soft tissue injuries
118
Q

what are the two clinical categories of fracture pattern

A

simple–> closed, skin intact

compound–> open, skin not intact

(complete vs. incomplete, depending on whether fracture traverses the complete width of the bone)

119
Q

communited fracture

A

more than 2 fragments of bone

120
Q

how do you describe fracture angulation?

A

described by the direction the DISTAL fragment deviates (varus or valgus)

121
Q

what is the most common type of shoulder fracture

A

clavicle–scapular fractures are rare

122
Q

hill sachs fracture

A

occurs when shoulder is dislocated anteriorly and the posterior humeral head makes contact with the anterior inferior glenoid rim

123
Q

bankart fracture

A

avulsion fracture of the anterior labrum (around the glenoid fossa)

124
Q

what fracture commonly results from FOOSH

A

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
Q

what fracture is associated with a sail sign

A

radial head fracture

findings otherwise are often subtle

126
Q

colles fracture

A

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
Q

what is the most common type of carpal bone fracture

A

scaphoid–from FOOSH

*suspect if snuffbox tenderness

128
Q

why must you always make sure not to miss a scaphoid fracture

A

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
Q

management of scaphoid #

A

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
Q

where do femoral fractures occur

A
  1. subcapital–intracapsular
  2. transcervical–intracapsular
  3. intertrochanteric–extracapsular
  4. subtrochanteric–extracapsular
    * no risk of AVN if extracapsular #
131
Q

how do people sustain tibial plateau fractures?

A

motor vehicles striking pedestrians

132
Q

why do we care so much about the lis franc fracture dislocation in the foot

A

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
Q

define: arthritis

A

inflammation of joints

134
Q

define: arthropathy

A

abnormality (non specific) of a joint

135
Q

define: erosion

A

focal bony defect of subchondral bone usually located at the site of synovial and capsular attachment to the bone

136
Q

define: osteophyte

A

bony spur arising at the margin of a joint

137
Q

define: sclerosis

A

focal increased density adjacent to a normal joint producing increased “whiteness” on the radiograph

138
Q

define: geode

A

fluid filled cyst within the subarticular aspect of the bone

139
Q

describe an approach to abnormal joint radiography

A

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
Q

in patients with a primary cancer tumour who have pain but negative x rays, what % have bone mets on bone scan

A

30%

141
Q

define: osteoarthritis

A

degenerative arthritis characterized by deterioration of the articular cartilage and formation of new bone (osteophytes) at joint surfaces and edges

142
Q

radiographic features of OA

A

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
Q

define: rheumatoid arthritis

A

inflammatory arthritis that originated in the synovium, typically symmetric and polyarticular

144
Q

radiographic features of rheumatoid

A

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

PMP (9 decks)

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