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PMP > Week 1 and 2--Notes > Flashcards

Week 1 and 2--Notes Flashcards

1
Q

what are the components of whole blood

A

packed red cells

platelets

frozen plasma and cryoprecipitate
(FP can also be further separated into immunoglobulins, albumin, factor concentrates)

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2
Q

what is cryoprecipitate

A

plasma enriched in fibrinogen, vWF, but deficient in other factors

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3
Q

indications for pRBC transfusion

A
  1. symptomatic anemia
  2. severe acute anemia with signs and symptoms or ongoing bleeding
  3. significant obstetric or traumatic hemorrhage
  4. as per anesthesiologist comfort
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4
Q

contraindiations for pRBC transfusion

A

not generally used for:

  1. compensated patients with chronic anemia
  2. patients with iron deficiency anemia
  3. asymptomatic anemia
  4. mild anemia of any cause
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5
Q

indications for platelet transfusion

A

thrombocytopenia or dysfunctional platelets and bleeding (or bleeding risk)

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6
Q

contraindications for platelet transfusion

A

useless in ITP

dangerous in TTP, HUS, HITT, DIC/MAHA

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7
Q

indications for plasma transfusion

A
  1. factor replacement (i.e best for urgent multifactor replacement) i.e vitamin K deficiency, warfarin overdose, DIC, liver failure
  2. coagulopathy NYD in a preoperative patient
    (3. trauma)
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8
Q

contraindications for plasma transfusion

A

not generally used for single factor replacement

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9
Q

indications for cryoprecipitate transfusion

A

fibribogen replacement

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10
Q

contraindications for cryoprecipitate transfusion

A

should not be used for haemophilia A in Canada

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11
Q

when should patients with the following platelet count be transfused?
more than 100

A

never

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12
Q

when should patients with the following platelet count be transfused?
50-100

A

patients who are actively bleeding

neurosurgery patients preoperatively

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13
Q

when should patients with the following platelet count be transfused?
10-50

A

preoperative patients

other patients at high risk for bleeding

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14
Q

when should patients with the following platelet count be transfused?
less than 10

A

basically everyone

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15
Q

why should you NOT transfuse platelets in ITP

A

transfusion is USELESS because transfused platelets will be destroyed as fast as the patients own platelets are destroyed therefore no increase in platelet count

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16
Q

why should you NOT transfuse platelets in TTP, DIC etc

A

transfusion is DANGEROUS because platelets are pathologically activated in the circulation before being cleared by the spleen–> can cause pathological thrombosis–> adding more platelets increases this risk

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17
Q

what is the overarching theme for who needs transfusion

A

when you need higher oxygen capacity in the patient

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18
Q

when should you transfuse the patient with the following HgB value?
100 or above

A

no transfusions

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19
Q

when should you transfuse the patient with the following HgB value?
less than or equal to 80

A

consider for post surgical, the stable hospitalized patient with cardiac disease, and SYMPTOMS OF ANEMIA

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20
Q

when should you transfuse the patient with the following HgB value?
less than 70

A

consider for adult ICU patient who is stable

pediatric ICU patient who is stable

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21
Q

when is platelet transfusion dangerous

A

TTP
DIC
HUS
HITT

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22
Q

should you use plasma for fluid resuscitation

A

no

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23
Q

what are 3 indications for plasma replacement

A

liver failure with multifactor deficiency

DIC

trauma induced coagulopathy

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24
Q

is plasma the product of choice for urgent warfarin reversal

A

no

but can still be used if dont have access to prothrombin complex concentrate (“octoplex”)

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25
Q

which blood group is the universal donor

A

O

no A or B antigens on the RBCs

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26
Q

which blood group is the universal recipient

A

group AB

no antibodies to RBC antigens

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27
Q

what are the Rh antigens

A

D, C, c, E, c

Rh antibodies can be involved in hemolytic transfusion reactions (usually caused DELAYED HEMOLYTIC transfusion reactions)

patients only develop anti-D antibodies if they are without D and have been exposed to D+ cells ie through pregnancy or transfusion

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28
Q

which is the most common blood group

A

O

then A, then B, then AB is most rare

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29
Q

what do we get concerned about with transfusions in female patients

A

hemolytic disease of the newborn is more common than hemolytic transfusion reactions–> get concerned about giving Rh compatible cells to female patients

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30
Q

list some of the other antigen families

A 
duffy
kidd
kell
MNS
lutheran
lewis

all have antigens from these families on our RBCs, only develop antibodies if transfused or pregnant

in general these are less clinically significant than ABO or Rh

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31
Q

why do we do pretransfusion testing

A

ensures the right product for the right patient

prefer to give ABO and Rh matched RBCs whenever possible

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32
Q

what are the pretransfusion tests

A

group, screen, crossmatch

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33
Q

what is the screen pretransfusion test

A

AB screen
negative–> no antibodies against AB antigens
positive–> there are antibodies to antigens–> must do extended antibody panel to determine which

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34
Q

what is the group pretransfusion test

A

ABO/Rh group

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35
Q

what is the crossmatch pretransfusion test

A

checking the unit against the patient to ensure compatibility

trying to match any antigens on the unit’s RBCs with any anti-RBC antibodies in the patients serum

electronic crossmatch–> group compatibility check, performed if no clinically significant Ab in patient

full (“wet”) crossmatch–> mix patient serum unit RBCs to show there is no Ab-Ag reaction

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36
Q

how long does the group and screen take

A

30 min

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37
Q

how long does the electronic crosmatch take

A

15 min

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38
Q

how long does the antibody panel take

A

2-3 hours

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39
Q

how long does the wet crossmatch take

A

20-30 min

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40
Q

when do you order a group and screen

A

order for ANYONE who gets a transfusion or if patient MIGHT need a transfusion

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41
Q

what does ordering a crossmatch mean

A

asking for RBCs to be set aside specifically for this patient

need to specify number of unit of RBCs

units are set aside in separate fridge, labelled with patients name, would be immediately available if needed

order if patient will likely need transfusion in next couple days

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42
Q

what do you need to write when you order blood

A

component, volume, rate, other (consent, age, volume status, CV status, reasons for transfusion)

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43
Q

what are the standard durations for RBCs, platelets, plasma, cryo

A

RBC–3-4h per unit

platelets–1-2hours per dose

plasma 1-2h per unit

cryo–just run it in

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44
Q

max duration for any transfusion

A

4 hours

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45
Q

what should you do if you need blood in an emergency

A

communicate clinical urgency to transfusion medicine lab

allows TML staff to better prioritize testing

sometimes better to give blood NOW that is “probably safe” then wait and give “almost definitely safe” blood later

1st choice–group specific blood that has been crossmatched

2nd choice–group specific blood not crossmatched

3rd choice–O- blood not crossmatched (Rh negative especially important for women of childbearing age, can provide O+ for men and post menopausal women in emergencies)

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46
Q

what does ABO incompatibility cause in transfusion med

A

acute hemolytic transfusion reaction (AHTR)

one of two leading causes of death related to transfusion

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47
Q

in which patients do you need to be careful about volume overload with transfusion

A

older age

infants

hx CV disease

*consider PROPHYLACTIC DIURETIC

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48
Q

what is the risk of the following transfusion reaction?

any reaction to RBC transfusion

A

0.6%

severe is 0.04%

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49
Q

what is the risk of the following transfusion reaction?

overall reaction to platelet transfusion

A

11%

severe is 0.1%

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50
Q

what is the risk of the following transfusion reaction?

urticaria

A

1/100 transfusions

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51
Q

what is the risk of the following transfusion reaction?

anaphylaxis

A

1/1600 transfusions

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52
Q

what is the risk of the following transfusion reaction?

fever

A

1/300 transfusions (febrile non hemolytic transfusion reaction)

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53
Q

what is the risk of the following transfusion reaction?

TRALI (transfusion related acute lung injury) or bacterial sepsis

A

1/10 000 transfusions

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54
Q

what is the risk of the following transfusion reaction?

wrong blood transfused

A

1/14000

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55
Q

what is the risk of the following transfusion reaction?

fatal hemolytic reaction

A

1/600 000

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56
Q

HIV risk

A

1/21 million

“more likely to die of a lightening strike in Canada then get HIV from a transfusion

that means human error is more likely to cause problems than the actual blood product

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57
Q

what are the types of transfusion reactions

A

acute vs delayed

immune vs non immune

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58
Q

what are the acute transfusion reactions

A

anything within 24 hours

usually bacterial infections

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59
Q

what are the delayed transfusion reactions

A

after 24 hours

often viral

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60
Q

what should you think of or rule out in a patient who has received a transfusion and is showing the following symptom:
urticaria or itching

A

anaphylaxis or allergic

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61
Q

what should you think of or rule out in a patient who has received a transfusion and is showing the following symptom:
fever

A

febrile non hemolytic

acute hemolytic

TRALI (tho usually presents more with SOB than fever)

sepsis

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62
Q

what should you think of or rule out in a patient who has received a transfusion and is showing the following symptom:
hypotension

A

anaphylaxis

AHTR

septic shock

less likely is TRALI

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63
Q

what should you think of or rule out in a patient who has received a transfusion and is showing the following symptom:
anxiety, pain, red urine

A

AHTR

*there are historical accounts of patients saying “something feels wrong” while getting a transfusion and they end up having AHTR

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64
Q

what should you think of or rule out in a patient who has received a transfusion and is showing the following symptom:
SOB or hypoxia

A

transfusion associated circulatory overload

TRALI

transfusion associated dyspnea

*signs of common and non severe reactions overlap with life threatening ones so ASSUME THE WORST

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65
Q

what should you do if you suspect a transfusion reaction

A
  1. STOP the transfusion
  2. GO TO THE PATIENT–cannot manage a transfusion reaction over the phone–> dont transfuse in the middle of the night because then you wont have help if theres a problem
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66
Q

when should you suspect bacterial contamination or transfusion associated sepsis

A

fever above 39 + sx like hypotension, tachy, nausea, vomiting, dyspnea, temp unresponsive to Rx

more likely associated with PLATELETS than RBCs

do NOT restart transfusion

tell the lab to culture the bag but also do blood cx on patient and start broad spectrum abx

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67
Q

when should you suspect febrile nonhemolytic transfusion reaction

A

no clinical consequence but must rule out other causes

do NOT restart transfusion

(may also be fever unrelated to transfusion)

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68
Q

when should you suspect AHTR

A

fever + hypotension + hemoglobinuria/emia (from lysed RBCs) + vomiting + bleeding from puncture sites

sx–chills, feeling of apprehension etc

almost always due to ABO incompatibility and usually results from failure in patient ID or lab process

less likely due to mechanism or thermal injury to RBCs prior to or during transfusion

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69
Q

how do you manage AHTR

A
  1. STOP transfusion, REMOVE the bag
  2. assess vitals, give IV fluid support
  3. CALL SENIOR RESIDENT OR STAFF ASAP–do not manage this alone as a junior as patients often end up in ICU
  4. confirm patient identity
  5. send blood sample down ASAP
  6. treat hypotension and prevent ATN–crystalloid at 3L/m2 daily
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70
Q

when should you suspect TRALI

A

generally present with SOB but should also consider bronchospasm, TACO

71
Q

when should you suspect TACO

A

non productive cough, dyspnea, tachy, pulm edema, hypertension, raised JVP

must prevent in at risk patients

72
Q

What are the two different scales used for EBM

A
  1. levels A-D

2. Levels I-V

73
Q

what do each of the levels A-D represent for EBM

A

A–> consistent randomized, controlled trial, cohort, “all or none” trials; clinical decision rule validated in different populations

B–> consistent, retrospective cohort, exploratory cohort, ecological studies, outcomes research, case control studies or extrapolations of level A studies

C–> case series or extrapolations from level B studies

D–> expert opinion without explicit critical appraisal or based on physiology, bench research or first principles

74
Q

what do the levels I-V represent for looking at EBM

A

I–> evidence is based on RCTs or meta analyses of such trials of adequate size to ensure a low risk of incorporating false positive or false negative data

II–> evidence is based on RCTs that are too small to provide level I evidence –may show either positive trends that are not statistically significant or no trends and are associated with a high risk of false negative results

III–> evidence is based on non randomized controlled or cohort studies, case series, case control studies or cross sectional studies

IV–> evidence is based on the opinion of respected authorities or expert committees as indicated in published consensus conferences or guidelines

V–> evidence is based on the opinions of those who have written and reviewed the guidelines, based on their experience, knowledge of the relevant literature and discussion with their peers

75
Q

what are the two types of overall study design

A

experimental vs observational

76
Q

describe experimental study design

A

randomized controlled trials (randomization equalizes confounders) –> RCTs can have tests of significance (i.e p values)

offers cause and effect information

can also include meta analyses or systematic reviews–> can look at combined odds ratios and relative risk

77
Q

describe observational study design

A

observational studies do NOT answer questions based on cause and effect, they can show ASSOCIATIONS however

have increased biases relative to experimental designs

78
Q

what is bias in study design

A

any systematic error in the design, conduct or analysis of a study that results in a mistaken estimate of an exposure’s effect on the risk of disease

i.e selection bias, information bias, confounding

79
Q

how is a cohort study designed

A

looks at exposure–> disease (retrospective or prospective)

two or more groups are assembled that differ based on exposure

you then follow individuals and monitor outcomes –> i.e follow exposed and non exposed individuals and monitor outcomes

(vs ecological studies that look at group level exposure and outcomes)

80
Q

how is a case control study designed

A

looks at disease–> exposure

identify people with a disease and look back for the exposure

i.e do all individuals with cancer (case) have the same exposure as those without cancer (control)

81
Q

how are cross sectional studies designed

A

exposure and disease are measured together at one point in time in a group

informs prevalence

82
Q

how are case series studies designed

A

multiple cases

meant to inform regarding disease and exposure (i.e SARS)

83
Q

how do you evaluate new diagnostic tests

A

“new” diagnostic tests need to be assessed against an alternative/ “the gold standard”

multiple summary measures can be easily calculated by creating a 2x2 table of results from both the new and the gold standard test

i.e “gold standard” along the top, with + and - results and “new” test along the side with + and - results
AB
CD
where A is + for both tests, B is - gold standard, + new, C is + for gold and - new, and D is - for both

then calculate sensitivity and specificity

84
Q

what is sensitivity

A

of those with the disease (according to the gold standard test) how many tested positive in the new test

85
Q

what is specificity

A

of those without the disease in the gold standard test, how many tested negative in the new test

86
Q

how do you calculate prevalence

A

A+C/(A+B+C+D)

87
Q

how do you calculate sensitivity

A

true positive/(true positive + false negative)

A/A+C

88
Q

how do you calculate specificity

A

true negative/(true negative + false positive)

D/B+D

89
Q

what is a likelihood ratio and how do you calculate it

A

LR+ tells you how much the odds of the disease increase when a test is positive
= sensitivity/(1-specificity)

LR- tells you how much the odds of the disease decrease when a test is negative
= (1-sensitivity)/specificity

90
Q

how do you calculate pre test odds

A

prevalence/(1-prevalence)

91
Q

how do you calculate pre test probability

A

pre test odds / (pre test odds +1)

92
Q

what is another way to determine pre and post test odds

A

likelihood ratio normograms

93
Q

how do you evaluate a new treatment/therapy?

A

use relative risk reduction, absolute risk ratios and number needed to treat to discuss the measurement of a treatment effect

also use a 2x2 table for a therapeutic intervention

have outcome along the top, with + and -
have therapy along the side, with control and treatment

                \+        - control         a .     b treatment .   c .     d

outcome rate control = a/a+b
outcome rate tx = c/c+d

94
Q

what is relative risk reduction

A

the difference in outcomes between the treatment and control groups expressed as a proportion of the outcome rate in the control

calculate control event ratio and treatment event ratio then express as a proportion

CER = a/a+b
EER = c/c+d

RRR = CER-EER/CER

or–> relative risk = EER/CER
and RRR = 1-relative risk

95
Q

what is absolute risk reduction and how do you calculate it

A

absolute risk reduction is the arithmetic difference in. outcome rates

CER-EER

96
Q

what is the number needed to treat and how do you calculate it

A

useful way to quantify the effects of an intervention

= 1/ARR

97
Q

define epidemiology

A

the study of patterns of health and illness and associated factors at the population level

98
Q

define clinical epidemiology

A

patient level research, examines intervention effect on individual patient outcome

99
Q

define incidence

A

rate of occurrences of new cases–> measure of RISK of developing some new condition within a specified time frame

100
Q

define prevalence

A

measure of the total number of cases of disease in a population –> how widespread is the disease?

101
Q

define pain

A

unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

102
Q

define nociceptive pain

A

initiated by stimulation of nociceptors which are peripheral nerve fibres (A delta and C fibres) that respond only to stimuli approaching or exceeding harmful intensity

103
Q

define central sensitization

A

increased response to stimulation that is mediated by amplification of signaling in the CNS

104
Q

examples of conditions causing:

acute nociceptive pain

A

fracture, burns, surgery

105
Q

examples of conditions causing:

acute neuropathic pain

A

lacerated nerve, herpes zoster

106
Q

examples of conditions causing:

chronic nociceptive pain

A

arthritis, headaches, back pain

107
Q

examples of conditions causing:

chronic neuropathic pain

A

amputation, post herpetic neuralgia, stroke/SCI

108
Q

how do you test for allodynia

A

cotton swab against skin

109
Q

how do people usually describe:

somatic nociceptive pain

A 
throbbing
aching
sharp
gnawing
constant

(i.e burn, sprained ankle)

110
Q

how do people usually describe:

visceral nociceptive pain

A 
dull
cramping
squeezing
deep
aching

i.e bowel obstruction

111
Q

how do people usually describe:

neuropathic pain

A

burning, shooting, tingling, electric, decreased sensation

i.e GBS, diabetic neuralgia

112
Q

describe the process of peripheral sensitization

A

injury–> release of proinflammatory mediators (bradykinin, substance P, prostaglandins, serotonin etc) and site of injury –> reduces threshold for activation of nociceptors

nociceptors are thus stimulated to fire–> activates immune cells and sympathetic terminals to release further pain generating substances–> positive feedback to increase nociceptive input to spinal cord

113
Q

how does peripheral pain sensitization manifest

A

wheal and flare response–> erythema, swelling, warmth

114
Q

what is primary hyperalgesia

A

pain and sensitivity of normal tissue surrounding injury and injury site itself

115
Q

what is the purpose of primary hyperalgesia

A

to protect and heal

is adaptive

decreases as injury heals

116
Q

describe the process of central sensitization

A

describes the increased response to stimulation that is mediated by amplification of signalling in the CNS

alterations in the excitability of spinal cord neurons to a variety of normal inputs following peripheral tissue damage or irradiation

mediators include chemicals released from central terminals of primary afferents like substance P, NMDA receptors etc

facilitates pain transmission, prolong stimulus, widens field of pain

117
Q

how does central pain sensitization manifest

A

secondary hyperalgesia–> increased response to a painful stimulus

signalling is via sensitized A delta and C fibres

118
Q

list physical agents that can be used to treat pain

A 
thermotherapy 
hydrotherapy
electrotherapy
light therapy 
manipulation and mobilization 
traction 
massage 
acupuncture
119
Q

what are the goals of physical agents to treat pain

A

resolve inflammation

activate temporary analgesia

change nerve conduction

provide counter-irritant

modify muscle tone and collagen extensibility

modify CNS

120
Q

what are two interventions that can be used for sympathetically mediated pain

A

i.e complex regional pain syndrome

can use sympathetic nerve blocks or bier blocks

can use IV infusions of lidocaine or ketamine

121
Q

where should the ETT be placed on CXR

A

at least 3 cm above the carina

122
Q

when should you use CT with contrast

A

inflammation
neoplastic
vascular
traumatic pathology

123
Q

what are you seeing when you describe “ground glass opacity” on CXR

A

increased density that does NOT obscure vessels

can also be seen in CT

124
Q

what does ground glass opacity on CXR or CT indicate

A

active disease–interstitial and alveolar process

i.e PE, PCP, ARDS, hypersensitivity pneumonitis, drug induced, pulmonary edema

125
Q

what are you seeing when you describe consolidation on CXR

A

increased density that DOES obscure vessels

usually pneumonia

if at R heart border, likely a right middle lobe process

if at LV border, likely a L lingular process

126
Q

when should you use MRI

A

superior to CT for soft tissue characterization

primarily a staging modality in the chest

127
Q

what is the first line imaging for the heart

A

U/S

can also localize pleural effusions

128
Q

what heart structure sits against the sternum in CXR lateral view

A

R ventricle

129
Q

how do you assess the following aspect of a CXR:

technique and quality

A

rotation–> spinous processes should be equidistant between the medial heads of the clavicles

inspiration–> dome of the right hemidiaphragm below or at the R 10th interspace

exposure–> lower thoracic disc spaces should be seen behind the heart

130
Q

how do you assess the following aspect of a CXR:

chest wall and soft tissues

A

cervical ribs can be associated with thoracic outlet

131
Q

how do you assess the following aspect of a CXR:

abdo

A

look for free air

132
Q

how do you assess the following aspect of a CXR:

diaphragm

A

look for clear edges/effusion

133
Q

what do you see on CXR in:

subcutaneous emphysema

A

see muscle fibrils of pec major because the air is between them

lucent axilla

134
Q

what do you see on CXR in:

hydropneumothorax

A

gas and effusion in pleural space

135
Q

what do you see on CXR in:

cavitating lesion

A

fissure is moved superiorly because of loss of volume

ddx TB, lung malignancy

136
Q

what do you see on CXR in:

reactivation of TB

A

fibronodularity in apices of the lung

137
Q

how do you diagnose tension pneumo

A

clinically

elevated JVP
decreased breath sounds
hyperresonance
trachea toward opposite side

138
Q

treatment of tension pneumo

A

emergency decompression with angiocatheter into the 2nd intercostal space at the MCL

can also do tube thoracostomy at 5th or 6th rib along midaxillary line

139
Q

what is the mainstay of cardiac imaging

A

TTE

provides anatomic and functional info

can measure degree of regurg, volume of compartments, wall motion, motion of heart valves, congenital defects, ejection fraction etc

140
Q

when do you use nuclear medicine in cardiac imaging

A

for functional assessment

MIBI scans–> asses myocardial viability/ischemia

141
Q

what is the best non-invasive test to exclude or detect CAD

A

CT angio

if high probability of CAD then go straight to coronary angio in the cath lab

142
Q

how does cardiac MRI compare to TTE and nuclear med scans

A

better than U/S for motion and EF

better than MIBI for ischemia /viability

143
Q

what conditions are associated with pectus excavatum

A

marfans

mitral valve prolapse

ehlers danlos

144
Q

what conditions are associated with pectus carinatum

A

congenital abnormalities like VSD, downs

145
Q

what do you see on CXR in: pulmonary edema

A

cephalization of blood flow

kerley B lines

airspace edema

pleural effusion

146
Q

when should you consider a trach for someone who is intubated

A

if need airway support or ventilation for over 1-3 weeks

147
Q

what are thoracostomy tubes

A

placed into pleural space to drain fluid (pus, blood) or air (pneumothorax)

all about patient position–> if the patient is supine, the air will be anterior and fluid posterior

148
Q

where do you place an NG for decompression? for feeding?

A

decompression–antrum

feeding–proximal small bowel (post pyloric)

149
Q

what is the reason for inserting a CVC

A

measure central venous pressure, administer large volumes of fluid, or admin medications

150
Q

where is the ideal position for a CVC

A

distal SVC–> in the proximal RA

*arrhythmias can be triggered if in RA/RV

151
Q

what is a swan ganz catheter

A

measures PCWP –allows differentiation of causes of edema

152
Q

where is the ideal location of a swan ganz catheter

A

R or L pulmonary artery “within the mediastinal shadow”

*going too far can cause infarction or vessel rupture

153
Q

where are cannabinoids found

A

in the resins produced by the marijuana plant

154
Q

what are cannabinoids

A

a family of complex molecules (both synthetic and natural) that bind to cannabinoid receptors in the brain and on immune cells

155
Q

name the exogenous cannabinoids

A
  1. THC
  2. cannabidiol (CBD)
  3. nabilone–synthetic cannabinoid
156
Q

what is THC

A

main PSYCHOACTIVE compound derived from marijuana

percentage of THC depends on the strain of the plant and growing conditions

157
Q

what is CBD

A

NOT psychoactive

thought to have other medicinal properties like anti-cancer, anti-inflammatory etc

158
Q

name the endogenous cannabinoids

A
  1. anandamide (AEA)
  2. 2-arachnidonyl glycerol (2-AG)
  3. palmitoyl ethanolamide (PEA)

AEA and 2-AG are the most common endogenous forms and are found throughout the brain

they are synthesized from membrane phospholipids and act locally at the synaptic junction then are degraded

159
Q

name the 3 cannabinoid receptors

A
  1. CB1
  2. CB2
  3. ?CB3
160
Q

what does CB1 do

A

found widely in the CNS and also in parts of the PNS

NOT found around the respiratory centres of the CNS

161
Q

what does CB2 do

A

found mostly on immune cells like mast cells, macrophages, microglia and astrocytes

162
Q

what do cannabinoids do?

A

act on the presynaptic terminal to decrease the excitability of the presynaptic neuron–> “synaptic circuit breaker”

modulate neuronal activity at multiple points;

  • spinal cord level
  • subcortical brain level
  • cortical brain level
  • peripheral nerve level
163
Q

how quickly are smoked cannabinoids absorbed

A

rapidly diffuse into the blood stream and enter the CNS within minutes

ingested are much less bioavailable (25-30%) due to first pass metabolism by liver –> need 0.5-2 hours longer for onset of effect with ingested

once in the bloodstream, are widely distributed as they are very lipid soluble

164
Q

what is nabilone

A

synthetic cannabinoid that comes in a PO capsule

very potent CB1 agonist

currently approved for chemo induced nausea and vomiting

also shown positive results in studies on pain control in fibromyalgia

NOT detected in UDS

poor street value

expensive to buy but covered by MSP

165
Q

what is dronabinol

A

rx cannabinoid

synthetic THC

PO capsule

approved for chemo related nausea and vomiting and HIV/AIDS anorexia

166
Q

what is sativex

A

THC/CBD oral mucosal spray

formulated to improve mucosal absorption but can still take 1 hour to onset

dosing highly variable between patients and thus must self titrate dose

approved for MS neuropathic pain and cancer related pain

have shown some benefit in improving sleep and RA pain

very expensive

167
Q

other than N/V and pain, what are some other conditions that are being researched as benefitting from cannabinoids?

A

epilepsy

chronic non cancer pain (arthritis, fibromyalgia)

neuro disorders (ALS, MS, dystonia)

asthma

anxiety, PTSD, depression

168
Q

how effective is smoked marijuana in the treatment of HIV related peripheral neuropathy

A

NNT 3.6 for 30% reduction in pain

169
Q

what dose is recommended of cannabis for chronic non cancer pain

A

1g/day

170
Q

cardiac SEs of cannabis

A

tachy (?related to vasodilation)

postural hypotension

palpitations

vasodilation (red eyes, flushing)

increased risk of MI within 1 hour of use

171
Q

respiratory SEs of cannabis

A

COPD/bronchitis

lung infections

upper airway CA

172
Q

contraindications for cannabinoids

A

personal history of psychosis

unstable cardiac disease

schizophrenia

relative contraindication–> family hx of psychosis

173
Q

why do we advice youth to avoid cannabis

A

can cause functional and structural changes in the developing brain leading to damage

174
Q

what is the position of the CMA on cannabis use

A

“insufficient scientific evidence available to support the use of marijuana for clinical purposes”

i.e not enough info on dosing, interactions, overall risk and benefits

CMA encourages further rigorous research into clinical use of marijuana

PMP (9 decks)

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