LOs Depression Headaches Flashcards
(28 cards)
Sumatripan Contraindications
Serotonin syndrome
Migraine Headache
High Blood Pressure
heart attack
Angina
coronary artery disease
Sumatrip MOA
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.
Sumatrip Indications
For the treatment of migraine attacks with or without aura.
Sumatrip Side Eff
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,
Sumatrip Metabolism
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.
Primary Headaches
o Tension-type headaches (TTH) o Migraine o Cluster Headaches • Primary cough headache • Primary stabbing headaches • Primary sexual headache • Hypnic headache
Tension Type Headache
Bilateral
Pressing
mild-to-moderate
no nausea
Migraine Headache
Unilateral
Throbbing
Nausea
Visual Symptoms (Aura)
CLuster Headache
Severe Unilateral Pain Trigeminal Distribution Common in Men, people who smoke May wake patient Ipsilateral eye watering, swelling, ptosis.
Migraine Definition
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.
Migraine Risk Factors
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
Migraine Diff Dx
Tension headache Cluster headache Subarachnoid haemorrhage Raised ICP/tumour Temporal arteritis Medication overuse headache Meningitis
Migraine Epid
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
Migraine CLinical Feat
Throbbing headache Nausea and vomiting Diarrhea Lightheadedness Dizziness Tinnitus Slurred speech Sensitivity to light and sound
Migraine Pathophys
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
Migraine Investigations
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
Migraine management
Remove triggers Lifestyle modification OTC ibuprofin NSAIDs Triptans
Preventative:
Beta Blockers
Amitryptaline
Antiepileptics
Amitryp Indications
Depression Eating disorders fibromyalgia IBS Tension Headaches Anxiety
Amitryp Contraindications
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.
Amitryp Side Eff
dizziness headache weight gain sleep disturbances sinus tachycardia impotence
Amitryp Interactions
MAO Cyp2D6 Inhibitors Anticholinergic Agents Analgesics Antipsychotics SSRIs Triptans
Amitryp MOA
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
Amitryp Metabolism
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
Headache red flags
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
