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MPharm Y3S2 > Clinical CNS Pain > Flashcards

Clinical CNS Pain Flashcards

1
Q

What are the questions to ask patients how to measure pain?

A

How long have they felt the pain?
What could have caused it?
Where is the pain?
What makes it better/worse time of day?
Does it come or go?
Does it vary with position?
What does the pain feel like?
What have they tried to help?

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2
Q

What are there ways of measuring a patient’s pain?

A

VAS (visual analogue scale) 0-10
NRS (numerical rating scale):
0-10 123= mild, 456=moderate, 789=severe
For younger patients can use facial expressions

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3
Q

What are aspects to examine on a patient in terms of pain?

A

Colour changes
Swelling
Tenderness
Asymmetry
Any weakness
Range of movement
Sensation

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4
Q

How do we classify pain?

A

Duration- acute/chronic
Underlying mechanisms
Physical origin
Cause e.g cancer/ post op

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5
Q

What are the underlying mechanisms of pain?

A

Nociceptive
Neuropathic
Nociplastic

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6
Q

What is the physical origin of pain?

A

Visceral (internal organs)
Somatic (external- bone, muscle)
Referred pain (e.g MI pain in arm/jaw)

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7
Q

Describe acute pain:

A

Comes on suddenly
Treated by resolving the cause of the pain
Usually due to trauma, injury or surgery
Lasts less than 6 months
OTC treatments/ analgesic ladder
Best to rest area

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8
Q

Describe chronic pain?

A

Comes on gradually
Usually, the result of a condition that is difficult to treat/diagnose
Lasts more than 6 months
Difficult to find lasting relief
Better to mobilise the area
Musculoskeletal pain 50-80% of UK pop at a time

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9
Q

What are the factors contributing to pain?

A

Social
Psychological
Biological

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10
Q

What is nociceptive pain?

A

E.g reflex arc, hand near flame
Nociception- the ability to detect painful stimuli via nociceptors that respond to painful stimuli
Preventing or in repsonse to tissue damage

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11
Q

What is neuropathic pain?

A

Malfunction in the NS or damage to the nerves e.g diabetic neuropathy
Central pain, peripheral neuropathy, complex regional pain syndrome
Burning, electric shocks, shooting pain

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12
Q

What is nociplastic pain?

A

Altered nociception in the absence of tissue or nerve damage
Widespread intense pain e.g fibromyalgia
Exercise/psychological/accupuncture
Antidepressants off label

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13
Q

Describe the first step in the WHO analgesic ladder:

A

Non-opioid:
Paracetamol
NSAIDs
Topical treatments (NSAIDs, lidocaine, capsaicin)
± adjuvant

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14
Q

Describe the second step in the WHO analgesic ladder:

A

Mild opioid as an alternative or an addition:
Mild to moderate pain
Codeine/ dihydrocodeine/ tramadol
Limited potency at the MU receptor
± adjuvant

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15
Q

Describe the third step in the WHO analgesic ladder:

A

Strong opioid to replace the mild opioid:
Moderate to severe pain
Morphine/ diamorphine/ oxycodone
Fentanyl/buprenorophine/ alfentanil
Strong potency at the MU receptor
± adjuvant

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16
Q

Name and give examples of adjuvant therapies in the WHO ladder:

A

Anti-epileptics (neuropathic)- pregabalin, gabapentin, carbamazepine (TN)
Anti-depressants- TCA, SSRIs
Other- dexamethasone, bone pain in palliative
Non pharmaceutical- physio, exercise, psychological

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17
Q

What is the evidence for the use of opioids?

A

Acute pain in palliative care
Limited evidence of efficacy in long term pain:
-if don’t achieve useful pain relief in 2-4 weeks unlikely to gain long term benefit
No efficacy with high dose (>120mg/ day morphine/ equivalent) due to lack of trial data

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18
Q

What are the risk of treatment with weak opioids?

A

Metabolism of weak opioids
Cyp2D6 enzyme- converts codeine into morphine
Interpatient variability dependent on gene expression (if a supermetaboliser and breastfeeding can pass more morphine to baby)
Unpredictable variation in efficacy and toxicity

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19
Q

What are the SEs of opioids?

A

N&V- likely to reduce with time
Constipation, drowsiness, sedation, resp depression
-use stim and osmotic
Renal function- increase morphine in body
Dependence/ addiction

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20
Q

What are the signs of overdose of an opioid?

A

Pinpoint pupils
Pale skin
Blue lips (cyanosis)
Unconscious
Shallow/slow breathing
Snoring/gasping for breath

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21
Q

Describe how pinpoint pupils are a sign of opioid overdose:

A

Stimulation of parasympathetic NS causes contraction pinpoint pupils
Less/no response to light or abnormal movements
Use eye examination and light test

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22
Q

Describe how pale skin and blue lips are a sign of opioid overdose:

A

Hypoxia- low blood oxygen, low blood circulation

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23
Q

Describe how unconsciousness and the breathing abnormalities are a sign of opioid overdose:

A

Resp depression
Activation of the µ-opioid receptors in the brain stem that co-ordinate respiratory rhythm

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24
Q

What are the aspects of the NEWS2 score that indicates an opioid overdose?

A

Resp rate <8bmp (normal= 12-20)
O2 sats can be <85% (96-99%)
HR= tachycardia
BP= high or low
Sedation score= VPU higher

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25
Q

What does VPU stand for in the NEWS2 score?

A

V= verbally
P= pain
U= unconscious/unresponsive

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26
Q

What is the non-pharmacological treatment for lower back pain (musculoskeletal)?

A

Exercise (aerobic) programmes and manual therapies- spinal manipulation, massage (as part)
Psychological therapies- CBT (as part)
Return to work programmes

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27
Q

What is the pharmacological treatment for lower back pain (musculoskeletal)?

A

NSAIDs- look at CI
Weak opioids for acute lower back pain if NSAIDs CI or ineffective
Do not offer paracetamol alone

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28
Q

What is sciatica?

A

Musculoskeletal pain
Leg pain 2º to lumbosacral nerve root pathology due to compression or irritation to the sciatic nerve- shooting pain

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29
Q

What is the pharmacological treatment for sciatica?

A

Do not offer gabapentinoids/antiepileptics/ benzodiazepines
If already prescribed, discuss problmes and withdrawal
Limited evidence of NSAID benefit
Do not offer opioids
Epidural injections (acute and severe sciatica)

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30
Q

What are the surgical treatments for sciatica?

A

Spinal decompression surgery
Other surgical intervention depending on cause

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31
Q

What are the symptoms of osteoarthritis?

A

Pain
Stiffness
Tenderness
Grating sensation
Swelling
Bone spurs

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32
Q

What is the non-pharmacological treatment for osteoarthritis?

A

Exercise/ physiotherapy
Weight loss if indicated to decrease pressure on joints
Manual therpaies

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33
Q

What are the pharmacological treatments for osteoarthritis?

A

Topical NSAID, if ineffective/ CI oral can be considered
Paracetamol and weak opioid may be considered
Intra-articular corticosteroid if others ineffective/unsuitable
Joint replacement

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34
Q

What are the main medications indicated for neuropathic pain?

A

Amitriptyline
Duloxetine
Gabapentin
Pregabalin

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35
Q

What should be the process of using medications for neuropathic pain?

A

Each indicated for things slightly different
If initial treatment ineffective/ not tolerated then try another

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36
Q

What are other medications that can be used for neuropathic pain?

A

Tramadol only if acute rescue therapy needed
Capsaicin cream for localised pain who with to avoid oral- normal for burning/stinging
Carbamazepine for trigeminal neuralgia

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37
Q

What is the initial pain relief in palliative care?

A

24 hour pain relief- simple analgesia or strong opioid, no max dose of opioid
Begin with anticipatory (PRN) injection

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38
Q

Name and state the doses of the anticipatory injection in palliative care:

A

Morphine SC 2.5-5mg 2-4 hrly (eGFR >60)
Oxycodone SC 1.25-2.5mg 2-4 hrly (eGFR 30-60)
Alfentanil SC 125-250mcg 2-4 hrly (eGFR <30)

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39
Q

When would a patient need a syringe driver in palliative care?

A

If needing 3 or more injections in a 24 hour period, may be less than 3 in certain situations

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40
Q

What is the treatment for breathlessness in palliative care?

A

Opioid/ midazolam- slows down breathing

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41
Q

What should be co-prescribed with opioids in palliative care?

A

Naloxone- toxicity

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42
Q

What are syringe drivers?

A

Battery powered pump delivering a 24hr continuous SC infusion of medication
Usually matches PRN injections
Need a diluent to provide volume- WFI/NaCl
Compatibility- can put other drugs in there as well

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43
Q

Which surgeries would NSAIDs not be used for pain and why?

A

Not in fracture of hip or pelvis as affects bone recovery
IV paracetamol is used

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44
Q

When would you use oral opioids for post-operative pain?

A

Moderate/severe pain expected- larger/complex procedure
Not with PCA or opiate epidural
Aids in recovery- get coughing relax back and mobilise pt quicker

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45
Q

When would gabapentin be used for post-operative pain?

A

If neuropathic post op pain- orthopaedic/ thoracic chest drain insertion (temporary treatment)

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46
Q

What is PCA?

A

Patient controlled analgesia
Pts determine when and how much analgesia they receive (presses button)
IV admin
Opiates most common
Loading dose in recovery then PCA

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47
Q

What are the monitoring requirements for patients on PCA?

A

BP/pulse/RR/sedation/pain score/nausea (opioid effects)
First 8 hours= hourly
8-24 hours= 2 hourly
48 hours- end= 4 hourly

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48
Q

What is the typical PCA admin?

A

100mg morphine in 100ml NaCl 0.9% (1mg/1ml)
-administers 1mg at a time
-lockout 5 mins

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49
Q

What are the benefits of PCA?

A

Patient ownership and independence
Faster alleviation of pain
Decrease distress in waiting for nursing staff
Less time consuming for nurse
Easy to titrate accoring to response
Fewer peaks/ troughs than bolus

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50
Q

What are the disadvantages of PCA?

A

Patient may to be responsive or dextrous enough
Patient may lack understanding or be scared to use
Decrease mobility
Liable to abuse (comes with lockout)
SEs- normal opioids

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51
Q

What should be administered for N&V in PCA?

A

Cyclizine (oral/IM prn)
Ondansetron (oral/IV/IM)
Can have protocols so nurse can give without prescribing

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52
Q

What should be administered for pruritis in PCA?

A

Chlorphenamine 4mg TDS

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53
Q

What should be administered for respiratory depression in PCA?

A

Oxygen and monitor sats
Stop PCA
Consider naloxone 200-400mcg- may need repeated admin as short t1/2

54
Q

What should be administered for excessive sedation in PCA?

A

Remove PCA
Oxygen sats, pain, sedation
Ensure adequate non-opioid analgesia presented

55
Q

What is an epidural?

A

Numb nerves that carry pain impulses from birth canal to brain
Injection into spinal column into epidural space
Can be used post-op

56
Q

What is the subarachnoid space?

A

Consists of the CSF for lumbar puncture

57
Q

Describe an epidural infusion:

A

Does not induce paralysis- just uncoordinated when walking
There will still be sensation and movement both above and below
Bathing the nerve fibres- block transmission of sensory impulses from afferent nerves to the spinal nerve, and ongoing transmission to the efferent
Target a particular nerve root and to dampen the nociceptive transmission
Block groups of 3 to block out one dermatome

58
Q

Describe the different dermatomes:

A

Cervical region- C1-C8
Thoracic region- T1-T11
Lumbar region- L1-L5
Sacral region S1-S5
Common injection sites are low thoracic/ high lumbar T10-L3

59
Q

Describe the order of central nerve blockade and where an epidural works:

A

Small unmyelinated fibres
Autonomic pre ganglionic fibre (response to temp)
Pain
(Touch)- target of block
Deep pressure
Vibration and proprioception
During birth mother can’t feel pain but can feel pressure of baby

60
Q

Name the two classes of drugs in an epidural bag:

A

Opioid analgesic
Anaesthetic

61
Q

Describe opioid analgesics in an epidural bag:

A

E.g morphine
Diffuses into CSF
Inhibits pain transmission in spinal cord
Spinal opioid receptors-main site of action
No effect on motor or sensory functions
Reversible (naloxone)
Doesn’t migrate

62
Q

Describe the anaesthetic in an epidural bag:

A

E.g bupivacaine
Diffuses across myelin sheath into nerve cell
Inhibits Na+ channels, preventing depolarisation of the membrane, nerve impulse conduction and conduction
Reversible
Doesn’t migrate

63
Q

What doesn’t an epidural migrate and why is this good?

A

Don’t want migration as don’t want it to travel to other areas of the spine and cause loss of pain sensation in other areas
Also if they do migrate there will be a decreased conc at the site they need to be, so lower efficacy
Balance between density:
-more dense than medium injection= sink down to spinal column
-less dense float to brain

64
Q

What are the properties of fentanyl in an epidural?

A

Stable in CSF
Penetrates neurones
Doesn’t migrate
Onset 4-10 mins
Duration 2.5-4 hours

65
Q

What are the properties of bupivacaine in an epidural?

A

Block sensory fibres, maintain motor function
Migration limited by slow infusion rate
Onset 15-20 mins
Duration 2-3 hours

66
Q

What are epidurals co-administered with and why?

A

Both emergency only
Naloxone
Ephedrine- combat any hypotension due to epidural

67
Q

What are the advantages of epidurals?

A

High quality pain relief and smaller opioid doses than systemic
Reduced incidence of DVT
Less sedation
Post-op lower over 24 hours if infusion
Improved pulmonary function
Decreases cardiac morbidity and sepsis
Faster re-establishment of oral intake

68
Q

What are the disadvantages of epidurals?

A

Accidental injection into the spinal cord (total spinal block)
Risk of permanent spinal damage
Accidental IV admin
Dural puncture headache (within 72 hours)
Epidural bleed/haematoma
Migration of drug can lead to resp paralysis
Infection risk

69
Q

What are the SEs of epidurals?

A

Resp arrest (opioid)- migration to C3-C5 blocking phrenic nerves
Resp depression
Hypotension/ hypothermia due to vasodilation
Decreased CO if T1-T4 affected
Reflex tachycardia
Overdose or IV given- depression of myocardial excitability
Reduced hepatic/ renal perusion
More common:
Tinnitus/ headache/ N&V/ pruritis/ sedation

70
Q

What is the rescue therapy for administering IV bupivacain?

A

Intralipid 20% to reverse cardiac arrest risk of life threatening toxicity

71
Q

What is the rescue therapy for a dural puncture headache?

A

Blood patch
Injected with own blood in hope of creating a seal around hole

72
Q

What is a dural puncture headache?

A

The hole has been made by the spinal needle, sometimes can cause leakage of CSF and can cause pressure in rest of fluid e.g in CNS to be decreased so can lead to severe headache- late onset

73
Q

What are the CI of epidurals?

A

Pt refusal
Infection at the site
Clotting abnormalities
Severe resp impairment
Uncorrected hypovolemia
Raised intracranial pressure
Neurological disease
Difficult anatomy
Tattoos

74
Q

Why are tattoos CI in epidurals?

A

Some say yes, some say no
Due to risk of ink bleeding into epidural space- ink toxicity
If tattoo is old/ healed some anaesthetists would say no risk

75
Q

Name the different classifications of primary headaches:

A

Tension-type
Cluster headache
Migraine
Miscellaneous

76
Q

What is a tension headache?

A

Most common cause
Thought to be due to muscle spasm in neck/scalp
Can be caused by emotional stress (tension, anxiety, fatigue, dehydration)

77
Q

What is the pain like in a tension headache?

A

Mild to moderate
Non-throbbing, vice like, a feeling of ‘tightness or squeezing’, weight pressing down on head
Usually affects both sides of the head- mainly front of head
May worsen throughout the day

78
Q

What is a cluster headache?

A

Rare but is 6-9x more common in men

79
Q

What is the pain like in cluster headaches?

A

Excruciating unilateral headache
Accompanied by red eye, lacrimation, nasal congestion, rhiborrhoea (runny nose), facial sweating, miosis (pupil constriction), droopy eye lid and eye lid oedema
May be mistaken for an eye injury

80
Q

What is the duration of a cluster headache like?

A

Sudden onset- may wake them up from sleep
Intermittent onset- can occur up to 8x a day
Lasts between 10mins- 3 hrs

81
Q

What is the differential diagnosis in cluster headaches?

A

Meningitis
Head bleed (arachnoid haemorrhage)- back of head
Cranial arteritis- inflammation, joint sitffness, go up side of head near jaw
Temporal arteries- scalp painful to touch, older patients

82
Q

What is the first line treatment for headaches if they don’t impact the patients life?

A

Paracetamol

83
Q

What is the second line treatment for a headache if it does impact a patients life?

A

Paracetamol
Codeine (30-60mg 4-6 hourly)- OTC doesn’t reach evidence based dosages
±ibuprofen

84
Q

What is the third line treatment for a headache if it means a patient can’t carry on with every day activities?

A

Paracetamol
Opioid e.g morphine, fentanyl, oxycodone
±Ibuprofen

85
Q

What should be used for breakthrough pain with a headache?

A

If ongoing daily pain relief not helping- give 1/6 amount of main opioid getting in a day

86
Q

What are the symptoms of a migraine?

A

Episodic- patients are well between attack
Prodrome
Aura
Headache
Postdrome- washout feeling

87
Q

Describe the symptoms of the headache in a migraine?

A

Lateralised (one side of head) and pulsating
Associated with N&V, phono/photophobia

88
Q

What is the epidemiology of migraines?

A

Common (15% population)
3x women greater, possible hormonal link
190,000 each day in UK
Underdiagnosed and under treated

89
Q

What is the onset of age of migraines?

A

Peaks at young children- 5 years
Peaks at early 20s then drop off
Very rare to get around 50-55 and above so red flag

90
Q

Name the divisions of migraines:

A

Classical migraine
Common migraine
Abdominal migraine
Migraine associated with childhood travel sickness

91
Q

Describe a classical migraine:

A

Migraine with aura (15%)
Focal neurological disturbance

92
Q

Describe a common migraine:

A

Migraine without aura (85%)

93
Q

Describe an abdominal migraine:

A

Migraine in children (3-10%)
50% remission after puberty
Often GI symptoms- stomach cramps, withdrawing from play, not like loud noises, nausea

94
Q

Describe the pathophysiology of migraines:

A

Genetic link, from familiar hemiplegic migraine (FHM)
Chromosome 19 and 1
10 potential polymorphism of Ca2+ channels which involve 5HT release
Brain hypothesis
Sensory nerve hypothesis
5HT implicated

95
Q

Describe the brain hypothesis in the pathophysiology of migraines:

A

Increased extracellular [K+] so decreased blood flow
Wave of neuronal inhibition

96
Q

Describe the sensory nerve hypothesis in the pathophysiology of migraines:

A

AKA inflammatory hypothesis
Activation of trigeminal nerve- feeds up side of head- meninges
Inflammatory mediators released- cytokines, PG, CGRP

97
Q

How is 5HT implicated in migraines?

A

Sharp increase in serotonin main metabolites during attack
If inject serotonin, can relieve migraine
Blood serotonin decrease
Can stimulate migraines which cause 5HT depletion

98
Q

Name and describe the trigger factors for a migraine:

A

Foods- alcohol, caffeine, choc, dairy
Hormonal changes- HRT, pill, pregnancy (stops during)
Environmental- emotion, weather
Points system- every trigger is a point until reach trigger threshold, keep a diary

99
Q

Describe the prodrome phase in a migraine:

A

Heightened sensations e.g craving
Foreboding- know its not gonna be a good day

100
Q

Describe the aura phase in a migraine:

A

Fortification spectra (visual field affected)
Flashing lights
Scotoma (black/blind spot on visual field)
Paraethesiae- pins and needles, can be prodrome

101
Q

Describe the symptoms of meningitis syndrome:

A

Headache, N&V, dislike of bright light, noises
Different symptoms for meningitis:
-rash (late onset), neck movement- can’t put chin on chest

102
Q

Describe the diagnosis points to be classed as a migraineur:

A

At least 5 repeated attacks of headaches lasting 4-72 hours which have these features:
At least 2 of:
-unilateral pain
-throbbing pain
-aggravated by movement
-moderate/severe intensity
At least 1 of:
-N&V
-phono/photophobia

103
Q

When should a patient be referred to the GP with a migraine/ headache?

A

Lasting more than 24 hours
Worse in morning (eases as day progresses)- effortless vomiting in morning (indicate growth)
Headache with unsteadiness/ clumsiness- esp in children
Children under 12
Suspected ADRs e.g nitrates/ CCBs

104
Q

What is the acute simple analgesic for migraines?

A

Dispersible/ effervescent preps preferred
-aspirin 900mg
-ibuprofen 400mg
-paracetamol 1000mg

105
Q

Describe the use of OTC caffeine and codeine for migraines:

A

Caffeine can increase absorption but can be a trigger factor
Codeine not evidence based dosage
Chronic daily headache- analgesic induced
Dependence

106
Q

Name the OTC treatments for migraines:

A

Migraleve
Buccastem M
Triptans

107
Q

Describe Migraleve as an acute treatment for migraines:

A

Do not suggest
Pink tabs (onset of attack):
-buclizine- doesn’t work at right part of brain, antihistamine to cause drowsiness, paracetamol, codeine
Yellow tabs (during)
-paracetamol, codeine
BNF says less suitable for prescribing

108
Q

Describe Buccastem M as an acute treatment for migraines:

A

3mg Buccal prochlorperazine- works on the CTZ

109
Q

Describe how the triptans work for treating acute migraines:

A

5HT1 agonists
Specifically working on 5HT1B and 5HT1D
Constrict blood vessels back to normal

110
Q

What are the CI of the triptans?

A

IHD- 5HT subtypes in coronary area
Uncontrolled hypertension
Over 65

111
Q

What are the SEs of the triptans?

A

Tiredness and dizziness (common)
Heaviness on chest and throat

112
Q

Name some triptans:

A

Sumatriptan
Zolmitriptan
Naratriptan

113
Q

Describe the +/-ve of sumatriptan:

A

+ve:
SC: very fast acting
Nasal: fast acting+ can use on under 18
-ve:
Poorly absorbed by mouth

114
Q

Describe the +ve of zolmitriptan:

A

Melt: orange flavour so decreased taste disturbances

115
Q

Describe the +/-ve of naratriptan:

A

+ve:
long t1/2 for prolonged and recurrent migraines
-ve:
Less effective at 2 hours

116
Q

What should be the counselling points with the triptans?

A

If the migraine disappears but then reappears can take a second dose after 2 hours have passed
If doesn’t disappear originally then not effective to take a second dose

117
Q

What are medication overuse headaches?

A

Taking meds too often for headaches
1 in 50 people affected at some point (more common in women)
Pain oppressive, worse in morning as body used to chemical

118
Q

What is the treatment for medication overuse headaches?

A

Stop current therapy
Pain gets worse before it gets better

119
Q

Which are the patients at risk of getting a medication overuse headache?

A

Using analgesics/ triptans >15 days per month
Refer requests for ≥4 sumatriptan/ month

120
Q

How would you prevent medication overuse headache?

A

<15 days/month
3-4 doses over 1-2 days is okay
Don’t take consecutively for more than 2 days
Avoid codeine containing products

121
Q

When would it be ideal to use migraine prophylaxis?

A

Functional impairment- how much every day life affected
Headache more than 2x per week
Amount of acute med used
Will patient comply
Success or failure of previous therpay

122
Q

Describe counselling points for patients for migraine prophylaxis:

A

50% of patients have 50% relief
Will not provide migraine free living
Still need acute break through treatment

123
Q

What are the SEs of migraine prophylaxis?

A

Diminish with time (e.g valproate + nausea)
Weight gain/contraceptionn

124
Q

What should be the treatment time for migraine prophylaxis?

A

6-12 months effective therapy, if not withdraw
Need without time period to see if can not have anymore

125
Q

Name drugs that can be used for migraine prophylaxis:

A

B blockers- propranolol
Pizotifen (rare)
Methysergide
TCA- amitriptyline
Anticonvulsants (valproate/topiramate)
OTC feverfew- limited evidence

126
Q

Describe the SEs of BBs:

A

Fatigue, bronchoconstriction
Cold extremities

127
Q

Describe how pizotifen works and its SEs:

A

5HT2 antagonist- antihistamine
Weight gain, sedation

128
Q

Describe how methysergide works and its SEs:

A

5HT2 antagonist
N&V
Rare- fibrotic conditions

129
Q

Why are anticonvulsants used for migraine prophylaxis?

A

Prolonged or atypical migraine aura (no headache)

130
Q

Name and describe an injection for the prophylaxis of migraines:

A

Botulinum toxin type A (botox)- liscensed
Non systemic medication- mechanism is unknown
Relaxes muscles- blocks pain feedback
Repeated injections to head and neck

131
Q

Name potential future migraine prophylaxis:

A

CGRP antagonist- no vasoconstriction effects but liver toxicity
Serotonin receptor agonists (5HT1D/1F only)
Nitric oxide antagonists- vasodilator, no evidence

MPharm Y3S2 (23 decks)

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