LOs Depression Headaches Flashcards

1
Q

Sumatripan Contraindications

A

Serotonin syndrome

Migraine Headache

High Blood Pressure

heart attack

Angina

coronary artery disease

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2
Q

Sumatrip MOA

A

The 5-HT1B and 5-HT1D receptors function as autoreceptors, which inhibit the firing of serotonin neurons and a reduction in the synthesis and release of serotonin upon activation. After sumatriptan binds to these receptors, adenylate cyclase activity is inhibited via regulatory G proteins, incrases intracellular calcium, and affects other intracellular events. This results in vasoconstriction and inhibtion of sensory nociceptive (trigeminal) nerve firing and vasoactive neuropeptide release.

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3
Q

Sumatrip Indications

A

For the treatment of migraine attacks with or without aura.

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4
Q

Sumatrip Side Eff

A
mild headache (not a migraine),
pain or chest tightness,
pressure or heavy feeling in any part of your body,
weakness,
feeling hot or cold,
dizziness,
spinning sensation,
drowsiness,
nausea,
vomiting,
drooling,
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5
Q

Sumatrip Metabolism

A

In vitro studies with human microsomes suggest that sumatriptan is metabolized by monoamine oxidase (MAO), predominantly the A isoenzyme. Only 3% of the dose is excreted in the urine as unchanged sumatriptan; 42% of the dose is excreted as the major metabolite, the indole acetic acid analogue of sumatriptan.

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6
Q

Primary Headaches

A
o	Tension-type headaches (TTH)
o	Migraine 
o	Cluster Headaches 
•	Primary cough headache 
•	Primary stabbing headaches 
•	Primary sexual headache 
•	Hypnic headache
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7
Q

Tension Type Headache

A

Bilateral
Pressing
mild-to-moderate
no nausea

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8
Q

Migraine Headache

A

Unilateral
Throbbing
Nausea
Visual Symptoms (Aura)

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9
Q

CLuster Headache

A
Severe Unilateral Pain
Trigeminal Distribution
Common in Men, people who smoke
May wake patient
Ipsilateral eye watering, swelling, ptosis.
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10
Q

Migraine Definition

A

A headache typified by pulsation of pain, may be unilateral, often associated with gastrointestinal symptoms, lasting up to 3 days. Occur in attacks, with no symptoms between attacks.

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11
Q

Migraine Risk Factors

A
Family history
Female
Stress
Depression
Smoking
Inactivity
Head trauma
Raised CRP
Overweight
Hypertension
Hypercholesterolaemia
Impaired insulin sensitivity
Stroke
Coronary heart disease
Hormonal changes, including pregnancy and menopause
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12
Q

Migraine Diff Dx

A
Tension headache
Cluster headache
Subarachnoid haemorrhage
Raised ICP/tumour
Temporal arteritis
Medication overuse headache
Meningitis
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13
Q

Migraine Epid

A
More common in women, 2:1
Global incidence of around 15%
Chronic migraine affects 2%
Often begins in adolescence
80% have migraine without aura
15-20% have migraine with typical aura
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14
Q

Migraine CLinical Feat

A
Throbbing headache
Nausea and vomiting
Diarrhea
Lightheadedness
Dizziness
Tinnitus
Slurred speech
Sensitivity to light and sound
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15
Q

Migraine Pathophys

A

Best current theory is ‘Neurovascular theory’
Migraine initiated by complex series of neural and vascular events
Primarily neural, with vascular changes secondary
Extracranial vessels expand and become pulsatile during attack.

Cortical spreading depression (CSD) is a leading theory of migraine with aura
Wave of neuronal excitation spreading from origin that is associated with aura
Causes glutamate release (excitatory neurotransmitter)
CSD activates trigeminovascular system, which leads to increased pain perception through production of certain chemokines such as substance P and NO
This produces vasodilation, and further pain

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16
Q

Migraine Investigations

A

Visual field testing
ESR + CRP
Neuroimaging in cases where tumour/brain pathology is suspected, or temporal arteritis
Investigations are to rule out other causes of symptoms

17
Q

Migraine management

A
Remove triggers
Lifestyle modification
OTC ibuprofin
NSAIDs
Triptans

Preventative:
Beta Blockers
Amitryptaline
Antiepileptics

18
Q

Amitryp Indications

A
Depression
Eating disorders
fibromyalgia
IBS
Tension Headaches
Anxiety
19
Q

Amitryp Contraindications

A

Hypersensitivity to TCAs or to any of its excipients
History of myocardial infarction
History of arrhythmias, particularly heart block to any degree
Congestive heart failure
Coronary artery insufficiency
Mania
Severe liver disease
Being under 7 years of age
Breast feeding
Patients who are taking monoamine oxidase inhibitors (MAOIs) or have taken them within the last 14 days.

20
Q

Amitryp Side Eff

A
dizziness
headache
weight gain
sleep disturbances
sinus tachycardia
impotence
21
Q

Amitryp Interactions

A
MAO
Cyp2D6 Inhibitors
Anticholinergic Agents
Analgesics
Antipsychotics
SSRIs
Triptans
22
Q

Amitryp MOA

A

Amitriptyline has anticholinergic and sedative properties. It is metabolized to nortriptyline which inhibits the reuptake of norepinephrine and serotonin almost equally. Amitriptyline inhibits the membrane pump mechanism responsible for uptake of norepinephrine and serotonin in adrenergic and serotonergic neurons

23
Q

Amitryp Metabolism

A

Amitriptyline undergoes hepatic metabolism that mainly involves demethylation. Demethylation leads to the formation of its primary active metabolite, nortriptyline. This secondary amine retains a pharmacological activity. It can further undergo hydroxylation

24
Q

Headache red flags

A

The first or worst headache of the patient’s life, especially if rapid in onset
A change in frequency, severity, or clinical features of the attack
New progressive headache that persists for days
Precipitation of headache with Valsalva maneuvers (ie, coughing, sneezing, bearing down)
The presence of associated neurologic signs or symptoms (eg, diplopia, loss of sensation, weakness, ataxia)
Onset of headaches after the age of 55 years
Headache developing after head injury or major trauma
Persistent, 1-sided throbbing headaches
Headache accompanied by stiff neck or fever
Atypical history or unusual character that does not fulfill the criteria for migraine
Inadequate response to optimal therapy

25
Q

Space Occupying Lesions

A

Malignancy but it can be caused by other pathology such as an abscess or a haematoma.

A new headache with features suggestive of raised intracranial pressure, including papilloedema, vomiting, posture-related headache, or headache waking the patient from sleep.

A new headache with focal neurological symptoms, or non-focal neurological symptoms such as blackout, and change in personality or memory.

An unexplained headache that becomes progressively severe.

26
Q

Trigeminal Neuralgia

A

Severe, sharp stabbing pain
Unilateral
Abrupt onset
Can increase in intensity over time

Caused by neurovascular compression (superior cerebellar artery)
Compression can be due to malignancy

27
Q

Treatment of Trigemincal Neuralgia

A

Decompression Surgery
Na Channel Blocker
Ca channel blocker

28
Q

Secondary Headaches

A

Acute sinusitis

Arterial tears (carotid or vertebral dissections)

Blood clot (venous thrombosis)

Brain aneurysm

Brain tumor

Carbon monoxide poisoning

Concussion

Dehydration

Ear infection (middle ear)

Encephalitis (brain inflammation)

Giant cell arteritis (inflammation of the lining of the arteries)

Hangovers

hypertension

Influenza (flu) and other febrile (fever) illnesses

Intracranial hematoma

Medications

Meningitis

Overuse of pain medication