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PMP > Week 4--notes > Flashcards

Week 4--notes Flashcards

1
Q

lifetime prevalence of back pain

A

70-85%

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2
Q

annual prevalence of back pain

A

15-45%

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3
Q

when is sciatic pain most common in the lifespan

A

between ages 40-45

usually from herniated disc

*herniation pain decreases with age because the disc dessicates

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4
Q

which gender has higher risk of back pain form herniation

A

men

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5
Q

which gender has higher overall risk of back pain from all causes

A

women

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6
Q

at what age do back pain complaints generally start to decrease

A

age 50

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7
Q

what are the types of back pain

A
  1. structural–i.e disc disease
  2. inflammatory–i.e ankylosing spondylitis
  3. infectious–i.e discitis
  4. neoplastic–i.e mets
  5. visceral–i.e aortic aneurysm
  6. idiopathic–i.e non specific
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8
Q

what patient factors can be associated with back pain

A
  1. age
  2. gender
  3. previous history of back injury
  4. relative strength
  5. smoking
  6. psychosocial factors–time off in past, understanding of cause, what patient expects will help
  7. “inheritance”
  8. occupational influences
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9
Q

what occupational influences can contribute to back pain

A

whole body vibration

forward bending and twisting

manual handling of materials

poor psychosocial conditions

frequent heavy lifting

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10
Q

what are some modifiable risk factors with regard to back pain

A

lack of fitness

poor health

obesity

smoking

drug dependence

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11
Q

what are some factors that have little to no association with back pain

A

height and weight

aerobic activity

absolute strength

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12
Q

define mechanical back pain

A

inflammation, irritation or injury to disc, facet joints, ligaments or muscles in the back

pain NEVER occurs below the knee

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13
Q

what is the most common cause of mechanical back pain

A

AGE related degeneration of discs, facet processes

muscle or ligament related injuries

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14
Q

define compressive back pain

A

occurs when nerve root leaving the spine is irritated or pinched

commonly due to herniated disc

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15
Q

what are waddells non-organic signs

A
  1. superficial tenderness
  2. non-anatomic tenderness
  3. axial loading
  4. simulated rotation
  5. distracted straight leg raise
  6. regional sensory changes
  7. regional weakness
  8. overreaction
    * when these occur, look also for other causes of pain
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16
Q

describe a method of triaging low back pain

A
  1. simple back pain
  2. back pain with neuro involvement
  3. back pain with suspected serious spinal pathology (red flags)
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17
Q

what is simple back pain

A

lumbar or lumbosacral pain with no neuro involvement

“mechanical” pain, varying over time and with physical activity

patient’s general health is good

*xray/CT/MRI results are not associated with symptoms described by patient or perceived disability (many findings are common with asymptomatic patients and there is a poor association with pain)

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18
Q

how should you exclude serious spinal pathology in simple back pain

A

xray is sufficient

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19
Q

what is back pain with neurological involvement

A

patients must have one or more symptoms and signs indicating possible neuro involvement

i. e
- pain radiating below the knee which is as intense or more intense than the back pain
- pain often radiating to foot or toes
- numbness or paresthesias in the painful area
- positive for radicular irritation with straight leg raise
- motor/sensory or reflex signs supporting nerve root involvement

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20
Q

how should you manage back pain with neuro involvement

A

neuro signs and sx in the absence of red flags often resolve themselves without recourse to surgery

patients progress statistically twice as slowly as patients with simple back pain

referral for specialist consult should NOT be required until clinician has seen functional deficit persistent or deteriorating after 4 WEEKS

x ray sufficient to exclude spinal path

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21
Q

what are red flags for back pain (suggestive of serious spinal pathology)

A
  1. violent trauma (fall from height, auto accident)
  2. constant, progressive, non mechanical pain
  3. thoracic or abdo pain
  4. pain at night that is not eased by prone position
  5. hx or suspected cancer, HIV or other pathologies that can cause back pain
  6. chronic corticosteroid consumption
  7. unexplained fever, weight loss, chills
  8. significant and persistent limitation of lumbar flexion
  9. loss of feeling in the perineum (saddle anesthesia)
  10. recent onset urinary incontinence
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22
Q

if someone is off work 0-4 weeks, how likely are they to RTW

A

80-100% will RTW

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23
Q

if someone is off work more than 12 weeks how likely are they to RTW

A

less than 60%

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24
Q

how should you treat acute low back pain

A

i.e within 0-4 weeks

after 48 hours from acute injury, suggest NSAIDs

muscle relaxants

advise to remain active

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25
Q

how should you treat subacute low back pain

A

4-12 weeks

advise to remain active and do exercises

consider multidisciplinary rehab program

low evidence for massage, NSAIDs, other analgesics

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26
Q

how should you treat persistent low back pain

A

over 12 weeks

multidisciplinary program

behavioural therapy

exercises

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27
Q

what % of back pain will not have a precise diagnosis

A

85%

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28
Q

define radiculopathy

A

objective neurological deficit

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29
Q

define nociceptive pain

A

nociceptors sense and respond to tissue damage

pain usually localized, constant, throbbing, dull

i.e burns, bruises, sprains, fracture

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30
Q

define neuropathic pain

A

result of dysfunction or injury to PNS or CNS

nerves can be inflamed or compressed

pain usually burning, electric, tingling, sharp

i.e carpal tunnel syndrome, phantom limb, post shingles, RSD

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31
Q

LMN signs

A

weakness

decreased tone

decreased reflexes

decrease sensation

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32
Q

UMN signs

A

babinski

increased reflexes

usually increased tone

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33
Q

red flags on back pain physical exam

A

very decreased ROM

midline tenderness

new or progressive deformity

neuro deficit

lower extremity spasticity

abnormal gait

loss of balance

saddle anesthesia

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34
Q

how do you manage cauda equina syndrome

A

medical and surgical emergency

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35
Q

what signs would suggest inflammatory causes of back pain

A

morning stiffness lasting more than 1 hour

age of onset younger than 30 or over 60

worse earliest in am and with activity

*advil better than tylenol for the pain

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36
Q

symptoms suggestive of benign low back pain

A

dull and achy

diffuse aching with associated muscle tenderness

exacerbated with movement (“mechanical”)

relieved with rest in recumbent position

no radiation of paresthesias

no dermatomal pattern

able to find a position of comfort

DTRs normal

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37
Q

what are red flag low back pain conditions

A

tumours

infection

fracture

cauda equina

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38
Q

examples of inflammatory back pain

A

ankylosing spondylitis

PMR

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39
Q

what is the most common disease of the SPINAL CORD after middle life

A

cervical degenerative myelopathy

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40
Q

signs of cervical degenerative myelopathy

A

UMN signs

spasticity

loss of balance

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41
Q

signs of cervical or lumbar radiculopathy

A

objective signs of neuro deficit (sensory loss, motor loss or impaired reflexes) in segmental distribution (LMN findings)

caused my compression or compromise of spinal nerve or its root

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42
Q

how does acute radiculopathy present

A

abrupt onset

severe shooting, “electric” pain with radicular distribution

accompanied by motor or sensory deficits

most often due to herniated disc (“soft disc”)

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43
Q

how does chronic radiculopathy present

A

gradual

sensory symptoms predominate

wasting and decreased tone, might have weakness

usually due to osteophytic compression (“hard” disc)

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44
Q

which are more common, pharmacodynamic or pharmacokinetic drug interactions

A

pharmacodynamic are 75%

i.e additive CNS depression, serotonin syndrome etc

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45
Q

what are the 2 main pharmacokinetic systems that contribute to drug interactions

A

CYP P450 system

transport protein system

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46
Q

what is the CYP p450 system

A

super family of heme-containing mono-oxygenases

responsible for detoxing foreign compounds mostly in the liver

large variability between people–enviro and genetic

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47
Q

what drug should not be combined with the drug below, and why:
NSAIDs

A

ACEi–> causes inhibition of vasodilating renal prostaglandins, leading to renal impairment

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48
Q

what drug should not be combined with the drug below, and why:
clopidogrel

A

omeprazole –> inhibition of CYP metabolism to active metabolite leading to decreased clopidogrel effectiveness

major severity

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49
Q

what drug should not be combined with the drug below, and why:
warfarin

A

NSAIDs–> increased bleeding risk, delayed onset

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50
Q

what drug should not be combined with the drug below, and why:
ACEi

A

spironolactone–>

enhanced hyperkalemic effects

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51
Q

what drug should not be combined with the drug below, and why:
SSRIs

A

warfarin–> leads to enhanced anticoagulation/antiplatelet action leading to altered anticoagulation

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52
Q

what should you think of when syncope presents as:

slow onset, slow offset

A

hyperventilation or hypoglycemia

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53
Q

what should you think of when syncope presents as:

abrupt onset, slow offset

A

seizure disorder

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54
Q

what should you think of when syncope presents as:

abrupt onset, abrupt offset

A

usually cardiac

arrhythmic–> brady or tachy

obstructive–> aortic stenosis, HCM, myxoma

vascular–> vasovagal, orthostatic hypotension

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55
Q

prominent risk factors for long QT syndrome

A

congenital

elderly, female

heart failure

myocardial ischemia

hypokalemia

more than one QT prolonging drug

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56
Q

other risk factors for long QT syndrome

A

brady less than 50

electrolyte disturbances

altered nurtition

hypothyroid

hyperglycemia

hypertension

one QT prolonging drug

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57
Q

list 3 commonly used QT prolonging drugs

A

methadone –> risk as normal doses

fluoxetine–> risk at normal doses

trazodone

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58
Q

name the 4 dopamine pathways

A
  1. mesocortical pathway
  2. nigrostriatal pathway
  3. mesolimbic pathway
  4. tuberoinfundibular pathway
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59
Q

what does the mesocortical pathway do?

A

associated with cognition and motivation

associated with negative symptoms of schizophrenia/psychosis

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60
Q

what are the negative symptoms of psychosis/schizophrenia associated with the mesocortical dopamine pathway

A

5 As

alogia

anhedonia

affective flattening

avolition

asociality

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61
Q

what does the tuberoinfundibular dopamine pathway do

A

controls prolactin secretion

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62
Q

what does the nigrostriatal dopamine pathway do

A

controls motor functions

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63
Q

what does the mesolimbic dopamine pathway do

A

associated with memory and emotional behaviours

associated with positive symptoms of psychosis/schizophrenia

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64
Q

what are the positive symptoms of psychosis/schizophrenia associated with the mesolimbic pathway

A

delusions

hallucinations

disorganized speech/thinking

disorganized or catatonic behavior

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65
Q

which dopamine pathway is associated with:

mediation of antipsychotic efficacy, and the treatment of psychosis

A

mesolimbic

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66
Q

which dopamine pathway is associated with:

extrapyramidal symptoms

A

nigrostriatal

67
Q

which dopamine pathway is associated with:

increase in prolactin secretion with anti psychotic use

A

tuberoinfundibular

68
Q

which dopamine pathway is associated with:

neuroleptic induced deficit syndrome

A

mesocortical

69
Q

list some side effects of first gen antipsychotics and the receptors through which they are mediated

A

H1–> sedation, weight gain

alpha 1–> decreased BP, dizziness, drowsiness

M1–> dry mouth, urinary retention, blurred vision, constipation

70
Q

name a first gen antipsychotic with low affinity for D2 receptors

A

chlorpromazine

71
Q

side effects of chlorpromazine

A

related to H1, A1 and M1 receptor antagonism (because low affinity for D2)

sedation, weight gain, orthostatic hypotension, urinary retention etc

72
Q

name 3 first gen antipsychotics with high affinity for D2 receptors

A

haloperidol
pimozide
perphenazine

73
Q

side effects of haloperidol, pimozide, perphenazine

A

related to D2 receptor antagonism because high affinity–> EPS

74
Q

mechanism of action of 1st gen antipsychotics

A

D2 receptor antagonism

75
Q

how do first gen antipsychotics affect EPS, neuroleptic induced deficit syndrome, and prolactin compared to 2nd generation antipsychotics

A

2nd gen have LESS neuroleptic induced deficit syndrome, LESS EPS liability and REDUCED prolactin increases

76
Q

MOA of 2nd gen antipsychotics

A

D2 and possible 5HT2a receptor antagonism

77
Q

which of the commonly used antipsychotics cause the least weight gain? the most?

A

least–> aripiprazole, haldol

most–> olanzapine, clozapine

78
Q

are second generation antipsychotics better than first gen for treating POSITIVE symptoms of depression

A

no clear and consistent difference (except for clozapine is better for treatment resistant)

SGA may be better for NEGATIVE symptoms

SGA agents have more metabolic SEs like weight gain, DM, dyslipidemia

79
Q

name 3 long acting injectable antipsychotics

A

aripiprazole
risperidone
paliperidone

80
Q

how to treat EPS acutely

A

with anticholinergic agents

benztropine 2-6 mg/day

81
Q

what is a framework that you can use to decide on an antipsychotic

A
  1. trial of a single SGA–assess over 2 weeks
  2. if partial/no response–> trial a different single SGA
  3. if partial/no response–> trial high dose olanzapine or FGA, or go straight to clozapine
  4. if no response to clozapine, augmentation of clozapine plus ECT
  5. if no response to that, no real evidence for it but can combine clozapine with SGA, or SGA + FGA
82
Q

what is the major risk associated with clozapine use

A

agranulocytosis

also myocarditis in first 4 weeks

83
Q

what should you monitor in patients on clozapine

A

weight

glucose

lipids

CRP and troponins first 4 weeks due to myocarditis risk

risk of seizures at doses over 500 mg

initiate at hospital or with daily home visits

84
Q

list some possible SEs of anti psychotic therapy

A

acute dystonia

pseudo-parkinsonism

akathisia

tardive dyskinesia

neuroleptic malignant syndrome

85
Q

describe onset and presentation of acute dystonia

A

may occur within hours (or minutes of IV) of starting anti psychotics

may involve neck, eyes, jaw, tongue and back–can be painful, frightening

patient may not be able to swallow

response to IV tx in approx 5 min, IM in 20 in

86
Q

treatment for acute dystonia

A

benztropine

diphenhydramine

87
Q

management of pseudo-parkinsonism

A

reduce anti psychotic dose

change anti psychotic

treat with oral anticholinergic –benztropine, trihexphenidyl

88
Q

describe onset and presentation of pseudoparkinsonism

A

can occur days to weeks after an antipsychotic is started or dose increased

tremor, rigidity, bradykinesia, bradyphrenia, salivation

89
Q

describe onset and presentation of akathisia

A

occurs within hours to weeks of starting antipsychotic or increasing dose

may be misinterpreted as psychotic agitation

internal dysphoric restlessness associated with need to move

90
Q

treatment of akathisia

A

beta blockers and benzos can be used in combo however may be better to trial a different antipsychotic

reduce antipsychotic dose

propanolol

benzo at low dose

91
Q

prevalence of akathisia with anti psychotic therapy

A

25%

92
Q

which antipsychotics cause more and less akathisia

A

aripiprazole high

clozapine low

93
Q

what is the risk of tardive dyskinesia with anti psychotic use

A

2-5% per year of anti psychotic exposure

more common with FGAs, elderly, mood disorders, acute EPS

94
Q

management of tardive dyskinesia

A

reduce anti psychotic dose

switch to atypical anti psychotic

switch to clozapine or quetiapine

neuro evaluation–botox?

can also try benzos, propanolol, vitamin E, tetrabenazine

95
Q

describe onset and presentation of tardive dyskinesia

A

occurs in months to years

approx 50% reversible

repetitive, purposeless movements–i.e lip smacking or chewing, tongue protrusion, choreiform hand movements, pelvic thrusting

movement worse under stress

stop anti cholinergic if prescribed

96
Q

describe onset and presentation of NMS

A

sx are muscle rigidity, confusion, fluctuating consciousness, diaphoresis, fever, hyperthermia, fluctuating BP, tachy

progression of sx is medical emergency requiring supporting medical interventions

97
Q

risk factors for NMS

A

young age

male

dehydration

neuro disabilities

exhaustion

agitation

rapid or parenteral dosing of anti psychotics

*reported with all antipsychotics

98
Q

management of NMS

A

stop anti psychotic

treat with BROMOCRIPTINE and DANTROLENE

amantidine

99
Q

what is NMS

A

sympathetic hyperactivity occurring as a result of dopaminergic antagonism in the context of psychological stressors and genetic predisposition

100
Q

how do you treat agitation/aggression associated with psychosis if MILD sedation is required

A

lorazepam +/- risperidone, olanzapine or quetiapine

101
Q

how do you treat agitation/aggression associated with psychosis when moderate to significant sedation is required

A
  1. lorazepam + loxapine or haldol
  2. haldol + antihistamine
  3. olanzapine IM
102
Q

why might you choose loxapine over haldol

A

works faster, may be more sedating

103
Q

why is it good to use lorazepam with haldol

A

reduces incidence of EPS

104
Q

should you admin olanzapine IM with haldol/ lorazepam /midaz

A

no–can result in hypotension, brady, respiratory/ CNS depression

105
Q

how do you treat agitation/aggression associated with psychosis if sedation required for extended period

A

clopixol–> zuclopenthixol acetate

106
Q

how do you treat insomnia related to psychosis

A

benzo prn or zopiclone prn or trazodone prn

107
Q

how do you treat persistent sx of aggression/hostility mania

A

mood stabilizer like lithium, valproate, carbamazepine

108
Q

why dont you want to use carbamazepine with clozapine

A

increases risk of bone marrow suppression

109
Q

why dont you want to use carbamazepine with quetiapine

A

carbamazepine reduces quetiapine bioavailability

110
Q

how do you treat depression, OCD associated with psychosis

A

SSRI, venlafaxine XR, bupripion SR, mirtaz

111
Q

risk factors for bipolar disorder

A
  1. age less than 25 years
  2. symptoms of hypomania, mania
  3. course of symptoms is abrupt onset and discontinuation
  4. family hx
  5. response to treatment–> anti depressant tx leads to mania/hypomania or fails 2 diff antidepressants
112
Q

suicide completion rates in bipolar I

A

5-10%

113
Q

suicidality in mixed mania

A

57%

114
Q

what 3 drugs are approved for bipolar depression

A

quetiapine

lurasidone

olanzapine/fluoxetine (symbax)

115
Q

first line for bipolar disorders maintenance

A

lithium

lamotrigine monotherapy

divalproex

olanzapine

quetiapine

risperidone long acting injection

abilify

116
Q

what should you check before starting lithium

A

renal function–> can cause diabetes insipidus

TSH–> thyrotoxic

get ECG–> can cause ST depression, QT prolongation and T wave depression

117
Q

why should you avoid NSAIDs with lithium

A

renal excretion

118
Q

what are therapeutic lithium levels in the serum

A

maintenance–> 0.6-1 mmol/L

acute–> 0.8-1.2 mmol/L

119
Q

when should you consider dialysis for lithium toxicity

A

if ataxia, delirium

toxic events usually only happen above 1.5

120
Q

what problems can lithium cause in pregnancy

A

can cause Ebstein’s anomaly in the fetus–> 1 in 20 000 at baseline, 1 in 1000 when on lithium

121
Q

what should you check before starting valproate

A

LFTs–> hepatotoxic

if woman of childbearing age, get pregnancy test and make sure using contraception

122
Q

why dont we use valproate in pregnant women

A

1 in 20 rate of neural tube defects

123
Q

what is the therapeutic blood level of valproate

A

544-693 umol/L maintenance

650-741 umol/L for acute mania

*inhibits CYP450

124
Q

what should you check before starting carbamazepine

A

LFTs–>hepatotoxic

CBC–> can cause fatal aplastic anemia

childbearing age–> pregnancy test and get contraception

125
Q

what should you monitor when treating with carbamazepine

A

BMP–> causes hyponatremia

can also cause stephen’s-johnson syndrome

126
Q

recommended length of benzo taper

A

6-12 months

high drop out rate if done faster

127
Q

what are the strongest predictors of benzo withdrawal severity

A

high baseline neuroticism

female sex

mild to moderate etoh use

128
Q

what is the amine hypothesis of depression

A

depression is due to decreased noradrenaline and 5HT in synapse as well as adrenoreceptor downregulation

129
Q

mnemonic to adjust mood meds

A

OSCAR

optimize

substitute

combine

augment

refractory/refer

130
Q

why is buproprion often preferred by patients

A

no sexual SEs

131
Q

for how much of their illness are people with bipolar symptomatic

A

about 50% of the time

bipolar depression is most frequently linked to completed suicide

132
Q

what is lithium effective for

A

manic and depressive states of bipolar

not as effective for rapid cycling and mixed states

133
Q

drug interactions of lithium

A

NSAIDs

diuretics

ACEI

caffeine

verapimil

134
Q

when is valproate used over lithium for bipolar?

A

for treatment of mixed episodes and rapid cycling bipolar

135
Q

when might you use lamotrigine for bipolar

A

for bipolar depression

136
Q

when might you use carbamazepine for bipolar

A

effective in pure and mixed mania, and rapid cycling

137
Q

side effects of risperidone

A

EPS

TD

prolactin increase

138
Q

side effects associated with all atypical antipsychotics

A

anti-HAM (histaminic, adrenergic, muscarinic)

Histaminic–> sedation

adrenergic–> orthostatic hypo, cardiac abnormalities, sexual dysfunction

muscarinic–> dry mouth, tachy, urinary retention, blurry vision, constipation

also glucose intolerance so monitor HbA1c

also monitor lipids yearly and weight at every visit

139
Q

how do benzos work

A

modulates Cl- ion channel opening by GABA and potentiates GABA effects

rapid onset

addictive

140
Q

why is xanax not recommended

A

most addictive

141
Q

what is used to treat ADHD

A
  1. methylphenidate (ritalin)–> displaces dopamine from reuptake into presynaptic terminal leading to increased dopamine in the brain
  2. dextroamphetamine (dexedrin)–> inhibits uptake of dopamine > NA
  3. adderal–> inhibits reuptake of dopamine and NA equally
  4. atomoxetine (strattera)–> NA reuptake inhibitor–less abuse potential because less dopaminergic
142
Q

how do you calculate serum osmolality

A

2[Na] + urea + glucose

143
Q

how does hyperglycemia affect sodium balance

A

glucose in the blood is an effective osmole–> draws water out of cells–> dilutional hyponatremia

*in this case, brain cells are shrinking because of the glucose drawing water out (serum osmolality is high)–> as glucose is corrected, water will move back into cells and Na will come back to normal (or it should)

example of hyperosmolar hyponatremia

144
Q

how do you correct Na values when patient is hyperglycemic

A

for every 10 mmol/L blood glucose is increased, add 3 mmol/L to the [Na]

145
Q

how can you tell a lab value indicates pseudohyponatremia

A

caused by hyperlipidemia or paraproteinemia–> [Na] measured on diluted specimen

know its “not real” because serum osmolality will be normal

can confirm by measuring [Na] directly thru ABG

146
Q

why do we care about hypotonic hyponatremia

A

risk of cerebral edema if correct too fast

occurs with low Na and low serum osmolality

147
Q

ddx for hypotonic hyponatremia

A

based on volume status

  1. hypovolemic–> total body sodium low
  2. euvolemic–> total body sodium normal
  3. hypervolemic–> total body sodium high
    * problem is the clinical volume assessment is often incorrect
148
Q

where is codeine metabolized

A

liver

metabolized to morphine

149
Q

define type A adverse drug event (ADE)

A

dose dependent, predictable (follows pathophys)

most common

150
Q

define type B ADE

A

hypersensitivity and idiosyncratic reactions

less common, not dose dependent, less predictable

151
Q

what body changes make ADEs more likely in older adults

A

decreased total body water–> lower Vd for hydrophilic meds

increased body fat–> higher Vd for hydrophobic/lipophilic meds (i.e diazepam)

increased gastric pH

152
Q

how does sensitivity to beta blockers change with age

A

reduced sensitivity as you get older to beta blockers due to down regulation of beta receptors

if BP control inadequate, consider switching to another anti HTN

153
Q

what result would you expect from the following drug combo:

amitriptyline + digoxin

A

delirium

154
Q

what result would you expect from the following drug combo:

amitriptyline + codeine

A

constipation

155
Q

what result would you expect from the following drug combo:

naproxen + ibuprofen

A

increased bleeding risk

156
Q

what result would you expect from the following drug combo:

naproxen/ibuprofen + digoxin

A

renal toxicity and decreased digoxin clearance

157
Q

what result would you expect from the following drug combo:

acetaminophen + amitriptyline

A

liver toxicity and reduced amitriptyline clearance

158
Q

what is the primary cause of delirium

A

drugs

159
Q

in the setting of alzheimer’s disease, what would the use of the following med put your patient as risk for:
CNS acting drugs

A

delirium

lorazepam on an injured brain = delirium + suppressed resp

160
Q

in the setting of alzheimer’s disease, what would the use of the following med put your patient as risk for:
H2 blockers

A

delirium

161
Q

in the setting of alzheimer’s disease, what would the use of the following med put your patient as risk for:
risperidone

A

EPS

162
Q

in the setting of the following disease/med combo, what would your patient as risk for:
COPD + lorazepam/trazodone

A

respiratory depression

163
Q

in the setting of alzheimer’s disease, what would the use of the following med put your patient as risk for:
PUD + aspirin

A

GI bleed

PMP (9 decks)

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