GEP (Life control) Week 5 Flashcards
What is the lympic system
Limbic system; process and regulate emotion and memory.
Also related to sexual stimulation, learning, behaviour motivation, long-term memory and smell.
What is the role of the amygdala, Hippocampus, Cerebellum and prefrontal cortex
Amygdala; regulate emotions eg fear and aggression eg flight or fight. Also how memories are stored (influenced by stress hormones)
Hippocampus; declarative episodic and recognition memory. Also memory consolidation, eg new learning to long-term memory
Cerebellum; processing procedural memories eg playing piano. (as well as motor memory)
Prefrontal cortex; remembering semantic tasks. (and motor function)
Corpus callosum; primary commisural region of the brain, consisting of white matter and connecting the left and right cerebral hemispheres
Stria terminalis; connects amygdala and fornix
Fornix; means ‘arch’, and is the major out put tract from hippocampus
The anatomy of the lymbic system
What is primary headaches and secondary headaches
PRIMARY = no underlying cause; the headache itself is the main problem
eg tension headache, migraine, cluster
SECONDARY = headache caused by an underlying condition (of which there are many
eg head trauma, meningitis, sinusitis, otitis, stroke/TIA, giant cell arteritis, malignant hypertension, brain tumours, subarachnoid haemorrhage, drug side effect, closed angle glaucoma, carotid dissection… and many more
When is tension headaches and migranes classified as chronic
Tension headaches and migraines are classified as chronic if:
>15 days/month for +3 months
What are the clincal features, diagnosis and management of primary headaches (Tension headache)
**Clinical features: **
“Band-like” pain or pressure
Gradual onset
Featureless (ie no photophobia, throbbing, nausea/vomiting, etc)
Diagnosis: clinical (ie history of symptoms)
**Management: **
Reassure patient
Simple analgesia → paracetamol, ibuprofen
If frequent or chronic, consider amitriptyline
What are the clincal features, diagnosis and management of primary headaches (Cluster headache)
**Clinical features: **
Severe, unilateral headache
Often centred around one eye (red, swollen and teary)
Unilateral sweating, ptosis and miosis
Nasal discharge
Short- lived - last between 15 mins to 2 hours
Recurring (sometimes cyclical) - eg 3 or 4 episodes per day for months
Diagnosis: clinical
Management:
Avoid triggers (see below)
Acute attacks:
Subcut. or intranasal sumatriptan
100% high-flow oxygen for 15-20 mins
Prophylaxis:
Verapamil tablet (a calcium-channel blocker)
**Triggers: **alcohol, exercise, strong smells, stress
RFs: male, FHx of cluster headaches
Orbital/supraorbital pain
Miosis = pupillary constriction
Ptosis = eyelid droop
Verapamil = calcium channel blocker; MOA unclear
What triggers primary headaches (Migranes)
TRIGGERS:
Chocolate
Hangovers
Orgasms
Cheese + caffeine
Oral contraceptives
Lie-ins
Alcohol
Travel
Exercise
Stress
Menstruation
Odors
Worth remembering those circled on the right
Foods/smells: basically any stimulus can trigger migraines, so don’t consider this list to be exhaustive
Keeping a diary can be helpful in trigger identification
What are the Secondary headaches- Vascular disorder ( Exracranial)
Carotid dissection
Spontaneous or post-traumatic tear in the carotid artery, leading to separation of its layers. This can cause stenosis of the vessel and promotes thrombus formation
Most common cause of stroke in young patients
Giant cell arteritis (aka temporal arteritis - a type of vasculitis)
Clinical features: severe + unilateral headache around temple and forehead, visual disturbances, jaw & tongue claudication, scalp tenderness (combing hair in SBA vignettes); tender temporal artery on palpation
What are the Secondary headaches- Vascular disorder ( Intracranial)
Cerebral venous thrombosis
Leading to occlusion of cerebral sinuses and veins causing brain infarcts
Most often occurs in sagittal and transverse sinuses
Subarachnoid haemorrhage
Usually due to rupture of a Berry aneurysm
Clinical features: “thunderclap” headache, vomiting, seizures, meningism
Intracerebral haemorrhage = haemorrhagic stroke
Subarachnoid space = where CSF circulates
Other causes of SAH - encephalitis, tumours, vasculitis, idiopathic
Meningism = headache + stiff neck + photophobia
These will require CT head for diagnostics
What are the Secondary headaches- Other CNS causes
Meningitis
Bacterial, viral, fungal, TB
Meningism = headache + stiff neck + photophobia
Encephalitis
Causes: Viral (VZV, MMR, HSV, rabies), bacterial, fungal, autoimmune
S&S: Fever, fits + funny behaviour
Raised intracranial pressure (ICP) - not strictly a cause (more a complication)
Causes: tumours, hydrocephalus, brain haemorrhages, meningitis, haematomas - all can cause life-threatening mass effects in the CNS (esp. brainstem)
S&S: Headache, vomiting, altered mental state (assess GCS), papilloedema
Cushing’s triad = hypertension + bradycardia + apnoea
What are the other types of secondary headaches
Trigeminal neuralgia
Unilateral, stabbing pain in branches of the trigeminal nerve (CN V)
Medication overuse/side effect
Other infections
Flu, Covid, malaria + many more
CN V: from Latin for “three” and “twin” referring to the two nerves having three respective branches - ophthalmic (V1), maxillary (V2) and mandibular (V3)
All three branches have sensory function(, while the mandibular nerve has motor supply to our chewing muscles and provides taste sensation in the anterior 2/3rds of the tongue via one of its own branches, the lingual nerve)
Usually maxillary and mandibular branches
What are the red flags for headaches
As a rule of thumb, signs suggestive of a serious cause of secondary headache should be considered red flags. SNOOP mnemonic can be helpful:
What is pharmokenetic, pharmodynamic, Bioavaliability and relate this to the drug sumatriptan.
Pharmacodynamics; how a drug works on the body
Pharmacokinetics; how the body interacts with a drug
Bioavailability = ‘the proportion of a drug or other substance which enters the circulation when introduced into the body and so is able to have an active effect”
MoA: MAO inhibitor, increases synaptic cleft monoamine neurotransmitter levels (eg 5-HT, NA, dopamine)
**Indications: **migraine, cluster headache
Route of admin: oral tablet (migraine), subcutaneous injection (cluster headache), nasal spray
**Adverse effects: **asthenia, drowsiness, dyspnoea, flushing, epistaxis (NS), taste altered (NS), throat irritation (NS), haemorrhage (SC), swelling (SC)
Sumatriptan; Subcutaneous injection bioavailability is 96% compared to 16% for the oral tablet.
Oral tablet is metabolised before reaching systemic blood stream (1st pass metabolism)
Gastroparesis also occurs in migraine
Absorption and distribution are dependent on a drug’s mode of delivery.
Define somatisisation
DEFINE: the tendency to experience psychological distress in the form of somatic symptoms, vice versa and to seek medical help for these symptoms when there is no underlying tissue or organ damage
Approach to the patient displaying signs of somatisation:
1) Listen, empathise and take time to talk
2) Offer understandable explanations
3) Address specific fears
4) Reinforce benefits of a healthy lifestyle
5) Manage associated conditions (anxiety, depression)
6) Encourage mindfulness, meditation, and relaxation
Chronic disease/chronic pain can fuel depression/anxiety which can lead to somatisation: a vicious cycle
What are the risk factors of depression and the clincial features
What is the DDx for Depression
What are the conditions that are presenting with depression
Bipolar Disorder:
Type 1; manic and depressive episodes
Type 2; hypomania and depressive episodes
Mania = persistently elevated mood, expansive, erratic, irritable, >1 week
Hypomania = >4 days, not impairing social/ occupational function
Depressive = core and associated symptoms, >2 weeks. It is not required for diagnosis but most people can present with depressive episode.
**Generalised anxiety disorder: **fatigue, irritability, impaired concentration, nervousness, physical symptoms (pain, headaches etc)
Grief: transient depressive symptoms lasting up to 6-12 months is normal.
Suicidal ideation, persistent hopelessness, psychotic symptoms is not normal.
Good PPS lecture regarding this.
How do you diagnose depression
What are the key points in history taking for depression
Start with open questions:
-’how are you doing?’
-’how are you sleeping’?
Ask directly about 3 core symptoms (anhedonia, fatigue, low mood)
Medication and social history is very important
In depression/low mood history taking; always assess suicide risk:
Ask if they have had thoughts about harming themselves / taking their own life.
If yes, have to ask how and if they have the means; to determine risk and safety plan
What is the management for depression
Treatment goals: eradicate symptoms of depression, improve daily functioning and quality of life, improve workplace functioning, reduce suicidality, minimise treatment adverse effects, and prevent relapse.
Exclude underlying causes
Assess severity (severe, moderate, mild)
Severe: suicide risk management, pharmacotherapy, ECT, supportive care, psychotherapy
Moderate: pharmacotherapy, suicide risk, therapy (psychotherapy, CBT, IPT)
Mild: therapy (mainly CBT), supportive care (self help, exercise, yoga, music therapy etc), pharmacotherapy
It’s important to reassess and check in, pharmacotherapy takes time and can have side effects and therapies can have long waitlists.
What is serotonin
Serotonin (5-HT) is a key neurotransmitter that plays a role in many functions such as sleep/wakefulness, mood and appetite. Low levels of serotonin are associated with depression, so antidepressant medications are designed to increase its availability in synaptic clefts.
Serotonin at synapses:
Taken up at pre-synaptic 5-HT reuptake transporters (see right) → regulates serotonin levels in the synaptic cleft
Broken down by an enzyme called monoamine oxidase (MAO) → inactivates serotonin
What are the different types of antidepressent drug classes, some examples and mode of action, as well as some side effect.
Dry mouth - antimuscarinic effect in both SNRIs and TCAs
Food interactions - initiate MAOi under specialist guidance
TCAs a bit less common now - see them used more for treating neuropathic pain
How do you prescribe antidepressents
SSRIs are a preferred starting point as they carry fewer side effects
They can take up to 6 weeks to start working
Initially, they can increase anxiety → assess risk of self-harm + review at 1-2 weeks after starting treatment
Patients should continue taking antidepressants for up to 6 months after symptoms have resolved
Reduce dose over 4 weeks when stopping antidepressants to minimise withdrawal symptoms
No need to learn treatment of serotonin syndrome - just recognise that it can occur as a serious adverse effect
Adherence is crucial for 2nd, 4th and 5th bullet point
What is seretonin syndrome
Beware serotonin syndrome = autonomic hyperactivity + altered mental state + neuromuscular excitation (see above)
What is psychotherapy and consists of
Therapy that involves counselling individually and group
Cognitive therapy
Targets maladaptive thoughts - what you think
Interventions:
Self-monitoring
Socratic questioning
Behavioural therapy
Targets maladaptive behaviour - what you do
Interventions:
Cognitive restructuring
Exposure therapy
Relaxation techniques
CBT
Self-led, group or one-to-one sessions where an individual identifies and challenges maladaptive beliefs and behaviours.
Teaches positive strategies for coping with different problems. It focuses on empowering the individual by encouraging self-reflection and setting goals, thus preventing relapses
Strong evidence base for treating: depression, bipolar disorder, anxiety, phobias, eating problems, drug/alcohol problems, OCD, PTSD, schizophrenia, sleep problems, anger problems
Who is suitable for psychotherapy
**Suitable **
Awareness/recognition that they have a problem
Ownership and responsibility
Curiosity - ability to reflect and question
Motivation to change
Reliability
Capacity to relate
Ability to tolerate self discomfort
Less-suitable
Someone who is impulsive violent
Organic brain disease affecting cognitive function and memory
Currently abusing drugs and alcohol
Current / active psychotic symptoms (not suitable for psychodynamic psychotherapy, but CBT may help)
