Core conditions 3 Flashcards

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1
Q

Glycaemic index (GI)

A

The 2 hour blood glucose response to 50grams of food. A low glycaemic index diet is beneficial to diabetes.

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2
Q

Exercise recommendation

A

Recommendation of 30mins on at least 5 days of the week for moderate intensity. For example: walking groups or swimming.

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3
Q

T2D: BP target and review

A

Blood pressure target in diabetes: 140/90

Patients with T2D get an annual review

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4
Q

The 2 investigations to check for evidence of kidney disease

A

A blood test for u+es and an early morning urine sample to measure thealbumin:creatinineratio (ACR). Urine dipsticks are less accurate for proteinuria

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5
Q

Focal seizures

A
  • These start in a specific area, on one side of the brain
  • thelevel of awarenesscan vary in focal seizures. The termsfocal awarefocal impaired awarenessand awareness unknown are used to further describe focal seizures
  • further to this, focal seizures can be classified as being motor (e.g. Jacksonian march), non-motor (e.g. déjà vu, jamais vu; ) or having other features such as aura
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6
Q

Generalised seizures

A
  • these engage or involve networks on both sides of the brain at the onset
  • consciousness lost immediately. The level of awareness in the above classification is therefore not needed, as all patients lose consciousness
  • generalised seizures can be further subdivided into motor (e.g. tonic-clonic) and non-motor (e.g. absence)
  • specific types include: tonic-clonic (grand mal), tonic, clonic, typical absence (petit mal), atonic
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7
Q

Tonic clonic seizure

A

Tonic phase where patient becomes rigid followed by clonic phase where the limbs shake rhythmically and symmetrically. Have a post ictal phase with reduced GCS and muscle tone, risk of aspiration. Tonic phase is preceded by shouting as air is expelled from the lungs

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8
Q

Absence seizures and focal onset to tonic clonic

A
  • Absence: causes a brief (normally <10s) period of loss of awareness. May look upwards with fluttering eyelids. Patients unaware of what happened
  • Tonic-clonic seizures that have “warning” symptoms tend to represent a focal-onset seizure that progresses into a generalised tonic-clonic seizure i.e. smelling burnt toast
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9
Q

Status epilepticus is defined as

A
  • a single seizure lasting >5 minutes, or
  • > = 2 seizures within a 5-minute period without the person returning to normal between them
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10
Q

Management of status epilepticus <10min

A
  • ABC= airway adjunct, oxygen, check blood glucose
  • First-line drugs are benzodiazepines= in theprehospital setting PR diazepam or buccal midazolammay be given. in hospitalIV lorazepamis generally used. This may berepeated onceafter 5-10minutes
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11
Q

Management of status epilepticus >10 minutes

A
  • If ongoing (or ‘established’) status it is appropriate to start a second-line agent such aslevetiracetam, phenytoin or sodium valproate
  • If no response (‘refractory status’) within 45 minutes from onset, then the best way to achieve rapid control of seizure activity is induction of general anaesthesia or phenobarbital.
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12
Q

Medication for generalised tonic-clonic seizures

A
  • males:sodium valproate
  • females:lamotrigine or levetiracetam
  • girls aged under 10 years and who are unlikely to need treatment when they are old enough to have children or women who are unable to have children may be offered sodium valproate first-line
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13
Q

Treatment for epilepsy

A
  • Focal seizures: Lamotrigine or levetiracetam
  • Absence seizures (Petit mal): Ethosuximide
  • Myoclonic seizures: in males its sodium valproate and in females its Levetiracetman
  • Tonic or atonic seizures: in males its sodium valproate and in females its Lamotrigine
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14
Q

Provoked seizures

A
  • physical trauma (immediately after a head injury)
  • acute vascular injury (at onset of stroke for example)
  • metabolic disturbance (hypoglycaemia or hyponatraemia for example)
  • stimulant drugs (e.g. amphetamines or MDMA)
  • withdrawal from sedative drugs (e.g. alcohol or benzodiazepines).
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15
Q

Epilepsy

A

A disorder of the brain characterised by an enduring predisposition to epileptic seizures. In children its usually genetic or metabolic. In adults its triggered by a physical structural change i.e. tumour, stroke, traumatic brain injury and inflammatory brain condition i.e. MS

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16
Q

Diagnosis of epilepsy

A

The official diagnosis of epilepsy requires 2+ unprovoked seizures within 5 years, the seizures must be >24hours apart. If there are clinical features which suggest an enduring predisposition to seizures, then epilepsy is sometimes diagnosed after just 1 seizure. These cases may involve a structural cause or EEG changes.

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17
Q

Seizures related to brain lobes

A
  • Frontal: motor (tonic, clonic, posturing), rapid onset, motor/vocal agitation, emotional lability
  • Parietal: Somatosensory paraesthesia/illusion, dysphagia, visual (objects appear larger/smaller)
  • Temporal: Automatisms (lip smacking, chewing), Autonomic features (epigastric sensation, tachycardia, palpitations), auditory hallucinations, Deja vu, feeling of dread/fear, abnormal tastes or smells
  • Occipital lobe: visual hallucinations, eye movement
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18
Q

Seizures: frontal onset to generalised tonic clonic

A

More common in adults. Persistent area of damage acts as focus of abnormal electrical activity which spreads to the rest of the cortex

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19
Q

Epilepsy investigations

A
  • Bloods: FBC, U&E, LFT
  • ABG: raised lactate supports diagnosis
  • EEG: can tell if attack is caused by electrical disturbance
  • ECG
  • MRI head: use if focal onset, onset in adulthood or before age 2, epilepsy refractory to anti-epileptics. Looks for structural cause
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20
Q

Seizure: what increases risk of re-occurrence

A
  • Persistently abnormal neurological examination
  • Focal area of change on the MRI (e.g. previous stroke) acting as a focus to generate seizures. These would be termed “remote symptomatic seizures”.
  • Epileptiform abnormalities on EEG
  • A seizure that occurred during sleep
  • Two unprovoked seizure >48 hours apart
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21
Q

Epilepsy complications

A
  • Sudden unexplained Death in Epilepsy (SUDEP)
  • Status epileptics
  • Injuries sustained during the seizure or the post-ictal period
  • Mood disorder and anxiety
  • Cognitive impairement
  • Cardiovascular and respiratory disease are more common in patients with epilepsy
22
Q

Epilepsy: when to offer medication

A
  • Single seizure with adverse features for recurrence (history, exam, MRI or EEG suggest recurrence risk)
  • Two or more siezures
23
Q

Anticonvulsants: common side effects 1

A
  • Cognitive:Slowed cognition, memory problems, reduced concentration, fatigue and drowsiness
  • Psychological: Mood and behavioural changes. The risk of death due to suicide is reported to be greater on anticonvulsant drugs.
  • Balance:Unsteadiness, ataxia, reduced coordination and vertigo
24
Q

Anticonvulsants: common side effects 2

A
  • Dermatological:Skin reactions are common with anticonvulsant drugs. Severe reactions (E.g. Stevens Johnson Syndrome, Toxic Epidermal Necrolysis, and DRESS syndrome) are much less common but occur more frequently with carbamazepine, phenytoin and lamotrigine.
  • Gastrointestinal:problems such as diarrhoea, nausea or vomiting are commonly reported.
  • Hyponatraemia: common with older drugs (e.g. valproate, phenytoin, carbamazepine)
  • Osteoporosis: long term side effect
25
Q

Anticonvulsants: drug interactions

A
  • Hepatic CYP inducers:carbemazepine and phenytoin. Increase clearance of other drugs e.g. COCP, reducing their efficacy.
  • Drugs that increase clearance of AEDs (more seizure risk):doxycycline
  • Drugs that decrease clearance of AEDs (more side effect/toxicity):erythromycin and clarithromycin
26
Q

Epilepsy: surgery

A

Patients whose epilepsy remains poorly controlled over a period of 2 years or more despite two drugs, are less likely to gain control.

27
Q

Living with epilepsy

A
  • Driving: stop driving and inform the DVLA once you’ve had seizure. If patient refuses clinician must inform. After one unprovoked seizure you have to stop driving for 6 months, after 2 or more unprovoked you stop for 12 months
  • Employment: need to inform if bus/lorry or taxi driver or for pilot license. Pilot must be seizure free for 10 years with no continuing predisposition
  • At home: no bath, swim with companion, keep pans on stove top away from them
28
Q

Epilepsy: Pregnancy

A
  • Increased risk of pre-eclampsia, premature delivery, haemorrhage, Fetal growth restriction, stillbirth, maternal mortality
  • Some have more seizures
  • Sodium valproate is teratogenic
  • Folate supplements reduce risk in all anti-convulsants
29
Q

Migraine symptoms

A
  • Severe throbbing headache
  • Usually unilateral
  • Sensitivity to light and noise
  • Nausea and vomiting
  • Aura

Lasts from 4 hours to 3 days

30
Q

Phases of a migraine

A
  • Prodrome- symptoms before the migraine i.e. stiff neck/ irritability/ tiredness/ food cravings
  • Aura- Perceptual disturbances. 90% are visual i.e. fortification spectra/ scotoma. Lasts up to an hour. Can also be sensory i.e. paraesthesia. Can have numbness and tingling, difficulty talking and balance problems
  • Headache
  • Postdrome
31
Q

Migraine diagnosis

A

At least 5 attacks lasting 4-72 hours with nausea/vomiting

  • Nausea/vomiting
  • Photo/phonophobia

And 2 of:
- Unilateral headache
- Pulsating character
- Worsening by daily activities

32
Q

Migraine: acute management

A
  • Analgesia e.g. paracetamol, NSAIDs and aspirin
  • Antiemetics i.e. Metoclopramide or Prochlorperazine- even in absence of nausea and vomiting. Metoclopramide shouldn’t be used regularly due to extra-pyramidal side effects
  • Triptans e.g. sumatriptan - take when the headache starts not during aura. Intranasal or subcutaneous preparations if vomiting. Use triptans alone or in combination with NSAID’s
33
Q

Migraine: Prophylactic management

A
  • Propranolol - CI asthma
  • Topiramate i.e. anti-epileptic drug (teratogenic)
  • Antidepressants e.g. amitriptyline
  • Use Botulinum A toxin injections if 3 prophylactic agents have failed
  • Other options: CBT, Mindfulness therapy, Acupuncture (10 sessions over 5-8 weeks), Riboflavin supplements (400mg OD)
34
Q

Headache follow up

A
  • Keep headache diary to track incidence and severity
  • Patients should be reviewed after 2-3 weeks for side effects, after stable every 6-12 months
  • Prophylaxis takes 4-8 weeks to work
  • If failure to respond to max tolerated dose of prophylaxis for 3 months then refer to neurology
35
Q

Cluster headache

A
  • Cluster headaches typically present with long episodes (months long) of recurrent daily headaches.
  • These headaches are unilateral, and are accompanied by autonomic symptoms around the eye on the same side. These symptoms include: drooping eyelid, constricted pupil, red watering eyes, runny/blocked nose, forehead sweating
36
Q

Tension type headache

A

The commonest form of headache. Episodic or chronic headaches, described as occurring in a band like distribution. Associated with stress, anxiety, and functional disorders. Not aggravated with physical activity.

37
Q

Trigeminal neuralgia

A

Paroxysms ofintensestabbing, burning or electrical shock type pain in the distribution of the trigeminal nerve. No symptoms are felt between attacks. Symptoms are provoked by movement of the face or touching of the skin

38
Q

Sinusitis

A
  • Inflammation of the mucosal lining of the sinuses. Sinusitis involving the ethmoid or frontal sinuses can produce migraine like headaches.
  • Typically present with facial discomfort or pain, nasal obstruction or discharge and post nasal drip. Other symptoms include: headache, halitosis, fatigue, cough
  • Migraine headaches don’t typically produce tenderness like sinusitis does.
39
Q

Medication overuse headache

A

These headaches are defined as:

  • Present 15 or more days per month
  • Developed or worsened during medication overuse
  • Resolves or reverts to previous pattern within two months of discontinuing medication overuse
  • Regular use for 3 months or more of one of the following drugs for headache:
  • Triptans, opioids, ergots, or combinations of these on 10 or more days per month
  • Paracetamol, aspirin, NSAIDs or combinations of these on 15 days or more per month.
40
Q

Red flags in headache

A
  1. Symptoms of temporal arteritis (vision loss, jaw claudication, scalp tenderness)
  2. Worsening headache - suggests progressive mass lesion
  3. Red eyes and haloes around lights – angle closure glaucoma
  4. History of malignancy - metastasis
  5. History of Immunosuppression - increases likelihood of intracranial infection
  6. Meningism - CNS infection
  7. Focal neurology - various CNS pathology
  8. Thunderclap headache - subarachnoid haemorrhage
  9. Onset >50 years old
41
Q

Chronic migraine and status migrainosus

A

Chronic migraine: headaches that occur at least 15 days of the month, where 8 out of 15 are migrainous

Status migrainosus: migraines that are more severe and prolonged then normal i.e. >72 hours

42
Q

Migrainous infarction

A

rare complication where a migraine attack is associated with a neurological lesion. Features include:

  1. One or more features of migraine aura
  2. Migraine aura must be typical of previous attacks
  3. Ischaemic brain lesions demonstrated
  4. Focal neurological deficit(s) must persist longer than 60 minutes
  5. Episode must be associated with a pain crisis
43
Q

Interventional migraine treatment: secondary to medication

A
  • Transcutaneous electrical stimulation of the supra-orbital nerve: involves wearing a headband that firs small currents that stimulate the nerves in the forehead to reduce pain
  • Transcutaneous stimulation of the cervical branch of the vagus nerve: for cluster headaches and migraine
  • Transcranial magnetic stimulation: single or repeated magnetic pulses
  • Percutaneous closure of the foramen ovale: helps with recurrent migraines
  • Occipital nerve stimulation: delivers electrical impulses to the occipital nerve to mask migraine pain
44
Q

Migraine: conservative management

A
  • Nutrition: regular meals reduce attacks. Common trigger include caffeine, chocolate and alcohol
  • Specific diet: the ketogenic and Low glycaemic index diet help reduce migraines
  • Stress management
  • Improving sleep quality and hygiene: going to sleep and waking up at the same time each night
45
Q

Cataracts

A

A common eye condition where the lens of the eye gradually opacifies i.e. becomes cloudy. Makes it harder for light to reach the back of the eye (retina) causing reduced/blurred vision. Leading curable cause of blindness

46
Q

Cataracts risk factors

A
  • Smoking
  • Increased alcohol consumption
  • Trauma
  • Diabetes mellitus
  • Long-term corticosteroids
  • Radiation exposure
  • Myotonic dystrophy
  • Metabolic disorders: hypocalcaemia
  • Age
47
Q

Cataracts classification

A
  • Nuclear: change lens refractive index, common in old age
  • Polar: localized, commonly inherited, lie in the visual axis
  • Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis
  • Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy
48
Q

Cataracts: patients typically present with gradual onset of

A
  • Reduced vision especially near vision
  • Clouding of vision
  • Faded colour vision: making it more difficult to distinguish different colours
  • Glare: lights appear brighter than usual
  • Halos around lights
  • Change in refraction: causes short sightedness, if there is a big enough myopic shift the patient may no longer need reading glasses. Refractive index can change causing a hypermetropic shift. May have to keep changing glasses

Signs: A Defect in the red reflex.

49
Q

Cataracts investigations

A
  • Visual acuity: using a snellen chart
  • Ultrasound examination: used when the cataracts is so dense you cant determine whether there is any co-existing pathology so you use ultrasound instead of fundoscopy
  • Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
  • Slit-lamp examination: shows cataracts
50
Q

Cataracts management non-surgical

A

In the early stages, age-related cataracts can be managed conservatively by prescribing stronger glasses/contact lens, or by encouraging the use of brighter lighting. These options help optimise vision but do not actually slow down the progression of cataracts, therefore surgery will eventually be needed.