Case 2: Toxicology Flashcards

(55 cards)

1
Q

What is the clinical presentation of a tension headache ?

A
  • Most common type of headache
  • Exacerbated by stress, fatigue, glare and noise.
    Symptoms:
  • Mild to moderate dull pain
  • Tightness or pressure across forehead or sides of head- band like pain
  • Doesn’t get worse with movement
    Duration:
  • 30 mins to several days
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2
Q

What is the clinical presentation of a cluster headache ?

A

Symptoms:
- Severe pain on one side
- Teary and or red eyes
- Congestion of same side as pain
- Restlessness
- Periorbital swelling
Duration:
- 15 mins to 3 hours
- Can occur several times a day

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3
Q

What is the clinical presentation of a migraine ?

A

Symptoms:
- Moderate to severe throbbing pain on one or both sides
- Nausea and vomiting
- Light, smell or sound sensitivity
- Gets worse with movement
Duration:
- 4 to 72 hours

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4
Q

What is the clinical presentation of MOH ?

A

Symptoms:
- Dull, constant headache, often worse in the morning
- Present on most days
- Can be very painful and disabling

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5
Q

Define toxicology

A

The study of adverse effect of chemicals on various biological systems, including humans

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6
Q

Define adverse drug reaction

A

A response to a drug that is noxious and unintended and occurs at doses normally used in humans for the prophylaxis, diagnosis, or therapy of disease or for modification of physiological function.
They can be dose-related or idiosyncratic.

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7
Q

Define idiosyncratic

A

Peculiar or individual

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8
Q

Define idiopathic

A

Disease of unknown cause

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9
Q

What do we know about preventable ADRs ?

A

They contribute to 5-8% of unplanned hospital admissions eg. Wrong dose or drug is given by staff
These cost the NHS £1-2.5 billion a year

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10
Q

How does the MHRA yellow card system work ?

A

It is a way to monitor the satety of all healthcare products.
It collects info on:
1. Side effects(ADRs)
2. Medical device adverse incidents
3. Defective medicines
4. Counterteit or fake medicines
5. Safety concerns for e-cigarettes
It is important for post marketing surveillance.

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11
Q

Define medication overuse headache (MOH)

A

A headache occuring on 15 or more days per month developing as a consequence of regular overuse of acute or symptamatic headache medication (on 10/15 or more days a month) for more than 3 months.

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12
Q

What is a primary headache ?

A

A disease themselves
Eg. Migraine, cluster, tension etc.

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13
Q

What is a secondary headache ?

A

Symptom of another condition
Eg. Brain tumour, neck trauma, infection

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14
Q

What are red flags that may suggest secondary headaches ?

A

• New/sudden onset (“thunder clap”)
• Change in pattern
• Effort-induced pain
• Positional pain
• Onset in middle age or later
• Recent head trauma
• Setting of chronic illness (eg, cancer, AIDS, fever)
• Any neck stiffness
• Change in personality or behavior
• Neurologic findings on examination

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15
Q

What are criteria for low risk headaches ?

A

• Age younger than 30 years
• Features typical of primary headache
• History of similar headache
• No concerning change in normal headache pattern
• No high-risk comorbid conditions (for example, HIV)
• No new concerning history/physical examination
findings
• No abnormal findings on neurologic exam

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16
Q

What is abortive treatment ?

A

To stop or reduce the severity of the condition once the symptoms have started

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17
Q

What is prophylactic treatment ?

A

Taken regularly to prevent to condition from occurring or reduce to severity of it

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18
Q

What is the first line abortive treatment of migraines ?

A

Ibuprofen, Aspirin or paracetamol

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19
Q

What is cyclooxygenase ?

A

COX

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20
Q

Nociception

A

The perception of pain

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21
Q

What is serotonin ?

A

5-HT

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22
Q

Describe the pathway of a migraine ?

A
  1. Migraine originates deep within the brain
  2. Electrical impulses spread to other regions of the brain
  3. Changes in nerve cell activity and blood flow and may result in symptoms such as visual disturbance, numbness and dizziness
  4. Chemicals in the brain cause blood vessel dilation and inflammation
  5. The inflammation spreads across nerve supplied by the trigeminal nerve causing pain
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23
Q

What is cortical spreading depression (CSD) ?

A

Slowly propagating wave of near-complete depolarisation of neurons/glial cells.
It is thought to contribute to the underlying pathophysiology of migraine aura, and an intrinsic brain activity causing migraine headache.

24
Q

If a migraine is resistant to NSAIDs what should you do ?

A

Sumatriptan as an abortive treatment

25
What must you not give to someone with a migraine ?
Ergots Opioids As they are addictive
26
What are ergotamines ?
Serotonin 1D and Alpha adrenergic receptor agonist Causes prolonged vasoconstriction
27
What does Rx mean ?
Prescription
28
What is a migraine ? What occurs ?
A complex neurovascular disorder. A decrease in levels of 5-HT. An increase in levels of CGRP.
29
What gives Sumatriptan its activity ?
Sulphonamide functional group
30
What class of drugs are ‘triptans’ ?
5-HT 1B/1D receptor agonists
31
Does Sumitriptan cross the BBB ?
Not very well as it is hydrophilic, however evidence suggests that inflammatory pain can alter BBB permeability, allowing the drug to pass through
32
What are common side effects of ‘triptans’ ?
Chest pressure, malaise/fatigue, dizziness (vertigo), vomiting, paraesthesia (warm/cold sensations, tingling), sleep disturbance. MOH.
33
What are serious side effects of ‘triptans’ ?
Serotonin syndrome (symptoms include high body temperature, agitation, increased reflexes, tremor, sweating, dilated pupils, and diarrhea), heart attacks, strokes, and seizures (life-threatening!!). With excessive use medication overuse headaches may occur.
34
What are contradindications of ‘triptans’ ?
Coronary vasospasm; hypertension; peripheral vascular disease; previous cerebrovascular accident; previous myocardial infarction; previous transient ischaemic attack.
35
What is Sulfhaemoglobinaemia ?
Rare condition, where there’s excess sulfhaemoglobin (SulfHb) in the blood. SulfHb is a greenish derivative of haemoglobin (Hb), cannot be converted back to normal, functional Hb. Causes cyanosis -blue or green skin, lips, nails turn due to lack of blood oxygen Can be caused by taking medications that contain sulphonamides (eg. overdose of sumatriptan).
36
What is CGRP ?
Calcitonin gene-related peptide It is a neuropeptide that is a potent vasodilator and pain modulator
37
What type of drug is propranolol ?
A beta blocker Antagonist
38
What are the common side effects of propranolol ?
1. Brachycardia 2. Depression 3. Dizziness 4. Erectile dysfunction
39
What are the uncommon side effects of propranolol ?
1. AV block 2. Hallucinations 3. Bronchospasm
40
What are the contraindications of propranolol?
1. Asthma 2. Hypotension 3. Diabetes
41
What type of drugs are ‘mAb’ ?
Monoclonal antibodies They are CGRP mAb antagonists
42
What are the adverse effects of CGRP mAb antagonists ?
1. Injection site pain 2. Constipation 3. Cramps 4. Skin reactions
43
What are the contraindications of CGRP mAb antagonists ?
Hypersensitivity reactions
44
What type of drugs are ‘ditans’ ?
Selective 5-HT1F receptor agonists
45
What are the adverse effects of ditans ?
Do not need to learn as Lasmiditan is not licensed for use in the UK
46
What type of drugs are ‘gepants’ ?
Small molecule CGRP receptor antagonists
47
What are the common side effects of gepants ?
1. Drowsiness 2. Dizziness 3. Fatigue
48
What are the uncommon side effects of gepants ?
1. Serotonin syndrome ( fever, vomiting, agitation etc.) 2. Palpitations 3. Anxiety
49
What are the contraindications of gepants ?
Used with SSRI or SNRI antidepressants
50
Which drugs don’t lead to MOH and may even help it ?
Gepants CGRP mAb antagonists
51
Describe the side effects of rimegepant ?
Nausea and hypersensitivity
52
Describe the adverse effects of atogepant ?
1. Appetite decreased 2. Constipation 3. Weight loss Increased risk of drowsiness
53
Describe the mechanism that may underlie MOH ?
1. Central sensitisation- due to dysregulation in pain modulation pathways. 2. Changes in levels of NT in the brain that are involved in pain (serotonin and CGRP) 3. Up regulation of vaso-active and prop-inflammatory mediators 4. Increased susceptibility to cortical spreading depression
54
What are the treatment strategies for MOH ?
1. Reduce analgesic medication without additional treatment 2. Or to do so with migraine prophylaxis (eg. CGRP antagonists)
55
Compare the effect of triptans on the meninges and the heart
Triptans stimulate 5-HT1B receptors in the meninges (brain) more potently than those in the heart. This is because 5-HT1B receptors are more dense in meningeal than in coronary arteries.