Quesmed wrong answers

Question 1

What is myotonic dystrophy? What causes it?

Answer 1

Myotonic dystrophy is a multi-system disorder that is part of a group of genetic diseases known as the trinucleotide repeat disorders. It is characterized by progressive muscle wasting and weakness, and affects specific chloride channels in the muscle.

This disorder predominantly presents in individuals during their 20s, although the onset can vary. The pattern of inheritance for myotonic dystrophy is autosomal dominant.

The aetiology of myotonic dystrophy is rooted in a genetic mutation leading to an abnormal expansion of trinucleotide repeats in the DMPK gene. The result is an abnormal protein that disrupts the function of certain muscle cells and other body systems.

Question 2

What are the clinical features of myotonic dystrophy?

Answer 2

Myotonic dystrophy exhibits a broad spectrum of clinical features which are best considered from head to toe:
1. Face: Frontal balding, myopathic facies (a long and thin face), bilateral ptosis, cataracts.
2. Speech: Dysarthria caused by a myotonic tongue and pharyngeal muscles.
3. Neck: Wasting of sternocleidomastoid muscles.
4. Hands: Distal muscle wasting and weakness, slow relaxing grip, and percussion myotonia (thumb flexion on percussion of the thenar eminence).
5. Internal features: Insulin resistance/metabolic syndrome, cardiomyopathy/arrhythmia, testicular atrophy.

Question 3

How is myotonic dystrophy investigated and managed?

Answer 3

The key investigation for myotonic dystrophy is genetic analysis, which is employed to identify the abnormal expansion of trinucleotide repeats within the DMPK gene.

Management
The management of myotonic dystrophy is primarily focused on symptomatic control and the prevention of complications. To date, there is no curative medical management available for the condition. This typically involves a multidisciplinary approach with the use of physical and occupational therapies, pharmacologic management of symptoms, and regular screening for associated complications such as heart disease and diabetes.

Question 4

How are carbon dioxide levels managed during raised ICP?

Answer 4

Cushing’s triad: Widening pulse pressure, bradycardia, Irregular breathing, which is suggestive of raised ICP.

Controlled hyperventilation aims to reduce ICP by reducing pCO2, which causes the vasoconstriction of cerebral arteries.
However this should be used with caution as this can cause hypoperfusion to already ischaemic areas of brain.

Question 5

What are the causes of meningitis?

Answer 5

Infective causes of meningitis include:
- Bacterial: Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Listeria monocytogenes, among others.
- Viral: Enteroviruses (Echoviruses, Coxsackie viruses A and B, poliovirus), herpes viruses (HSV2, HSV1), Paramyxovirus, measles and rubella viruses, Varicella Zoster Virus, Arboviruses, Rabies virus.
- Fungal: Particularly Cryptococcus neoformans, mainly affecting the immunosuppressed population.
- Parasitic: Amoeba (Acanthamoeba), Toxoplasma gondii.

Non-infective causes of meningitis encompass:
- Malignancies such as leukemia, lymphoma, and other tumors
- Chemical meningitis
- Certain drugs, including NSAIDs and trimethoprim
- Systemic inflammatory diseases such as sarcoidosis, Systemic Lupus Erythematosus, Behcet’s disease.

Question 6

What are the CSF features in meningitis?

Answer 6

CSF sample should be taken via lumbar puncture and the opening pressure should be measured.

1. CSF Features of bacterial meningitis
   - May be clear or turbid
   - 100-200 PMNs
   - Culture results positive (may be negative depending on how heavily infected the meninges are)
   - Protein raised due to bacterial protein contamination
   - Low glucose as bacteria use as an energy source
   Note that these features can also be consistent with a brain abscess
2. CSF Features of Aseptic meningitis
   Misnomer as usually due to viral infection (or treated bacterial meningitis)
   - Clear or slightly turbid, 15-500x109 lymphocytes
   - Negative culture results
   - 0.5-1g/l protein, glucose normal (viruses use cell machinery to replicate)
3. CSF Features of Tubercular meningitis
   - Clear or slightly turbid
   - Fibrin web may develop.
   - 30-500x109 lymphocytes plus PMNs, negative gram stain (need Auramine staining)
   - Protein 1-6g/L
   - Glucose 0-2.2.
4. CSF Features of Crytococcal meningitis
   - Classically the opening pressure is very high (poor prognostic sign)
   - May give any of the results above, so should consider as a differential in any HIV or immunocompromised patient.
   - Cryptococcal antigen testing or India Ink staining should be requested.

Question 7

How is meningitis managed?

Answer 7

Empirical antibiotic therapy for suspected bacterial meningitis typically includes 2g of IV ceftriaxone twice daily to ensure CNS penetration, with IV amoxicillin added in patients at age extremes for listeria coverage.

In cases of suspected viral encephalitis, IV aciclovir should also be administered. For patients allergic to penicillin, alternatives such as chloramphenicol may be used.

It’s important to note that any empirical antibiotic regimen should be adjusted based on culture results when available.

Question 8

What are the complications of meningitis?

Answer 8

• Septic shock
• Disseminated Intravascular Coagulation
• Coma
• Subdural effusions
• Syndrome of inappropriate antidiuretic hormone secretion
• Seizures
• Delayed complications: Hearing loss, cranial nerve dysfunction, hydrocephalus, intellectual deficits, ataxia, blindness
• Death

Question 9

What treatment can be used to reduce the risk of long term neurological symptoms in bacterial meningitis?

Answer 9

Dexamethasone IV

Dexamethasone reduces morbidity and mortality in bacterial meningitis, specifically Pneumococcal meningitis. This has been shown to improve outcomes if given within 4 hours of IV antibiotics. It has a modest reduction in mortality however significantly reduces hearing loss and neurological sequelae. If the patient is showing signs of meningism it is important to administer this quickly

Question 10

Which treatment is offered to contacts in meningitis?

Answer 10

Oral Ciprofloxacin is offered usually to household/close contacts

Question 11

What is MS and what causes it?

Answer 11

Multiple sclerosis is a chronic autoimmune disease, primarily involving the central nervous system, which is marked by the degeneration of the insulating covers of nerve cells in the brain and spinal cord, leading to demyelination and eventual axonal loss.

Aetiology
The exact cause of multiple sclerosis remains unknown. However, a combination of genetic and environmental factors, including potential viral pathogens, are believed to be contributing factors. Pathologically, CD4-mediated destruction of oligodendroglial cells and a humoral response to myelin binding protein are key features of the disease.

Question 12

What are the clinical features of MS and how is it classified?

Answer 12

1. Signs and Symptoms
   - Sensory disease, marked by patchy paraesthesia
   - Optic neuritis, characterised by loss of central vision and painful eye movements
   - Internuclear ophthalmoplegia, a lesion in the medial longitudinal fasciculus of the brainstem
   - Subacute cerebellar ataxia
   - Spastic paraparesis, as seen in transverse myelitis, including Lhermitte’s sign.

Classification
Multiple sclerosis may be divided into two groups:
1. Relapsing-remitting (which may become secondarily progressive)
2. Primary progressive.

Relapsing remitting MS makes up 80% of disease at presentation, compared with primary progressive which is <10%.

The remaining 10% fall into a difficult to classify intermediate group of progressive-relapsing disease.

Question 13

What are the differential diagnoses for MS?

Answer 13

1. Neuromyelitis optica (Devic’s disease): Characterised by optic neuritis and transverse myelitis.
2. Systemic lupus erythematosus (SLE): Presents with multisystem involvement, including the CNS. Symptoms may include fatigue, joint pain, rash, and fever.
3. Lyme Disease: Early signs and symptoms include fever, chills, headache, fatigue, muscle and joint aches, and swollen lymph nodes. Later signs and symptoms may involve the nervous system.
4. Neurosarcoidosis: Symptoms include seizures, hearing loss, facial palsy, and psychiatric symptoms.
5. Vitamin B12 Deficiency: Presents with weakness, tiredness, or lightheadedness, heart palpitations and shortness of breath, pale skin, constipation, loss of appetite, nerve problems like numbness or tingling, and mental problems like depression, memory loss, or behavioral changes.

Question 14

How is MS diagnosed?

Answer 14

The diagnosis of multiple sclerosis is based on at least two of:

1. Clinical history/examination
2. Imaging findings
   - Typically these are periventricular white matter lesions seen on MRI.
3. Oligoclonal bands in the CSF
   - These reflect various immunoglobulins seen on CSF electrophoresis and indicate the presence of an auto-immune process in the CNS. They are very sensitive for multiple sclerosis although they can also be found in other auto-immune and infectious conditions including Lyme disease, SLE and neurosarcoid.

Question 15

How is an acute attack of MS managed?

Answer 15

An acute attack of multiple sclerosis should be treated with glucocorticoids.

1g of intravenous methylprednisolone every 24 hours for 3 days is a typical regimen, however oral courses are probably equally as effective. Infections must first be excluded.

Severe acute attacks who do not respond to glucocorticoids should be covered with plasma exchange.

While these interventions does not appear to affect long term outcome, it does appear to reduce the duration and severity of individual attacks.

In practical terms, it is usually necessary to involve the local neurology team for guidance on when to start steroids for patients with an acute flare of multiple sclerosis.

Always ensure to check routine bloods and urine dip to rule out any intercurrent infection.

Question 16

How is MS managed in the long term?

Answer 16

There are two groups of drugs used in the long term management of relapsing remitting multiple sclerosis: disease modifying therapies (DMTs) and symptomatic therapies.

The former group may be divided into three:
- First-line injectables such as beta-interferon and glatiramer
- New oral agents such as dimethyl fumarate, teriflunomide and fingolimod
- Biologics such as natalizumab and alemtuzumab.
As a general rule, increasingly effective treatments are associated with increasingly significant side effects.

The extent to which long-term use of DMTs reduces risk of secondary progressive MS is not yet clearly established.

Symptomatic therapies include:
- Physiotherapy
- Baclofen and Botox for spasticity
- Modafinil and exercise therapy for fatigue
- Anticholinergics for bladder dysfunction
- SSRIs for depression
- Sildenafil for erectile dysfunction
- Clonazepam for tremor

Question 17

What are the risk factors for a worse prognosis of MS?

Answer 17

1. Age at onset: Onset of MS at an older age, typically over 40, is associated with a worse prognosis.
2. Male gender: Men with MS often experience a more severe and rapidly progressing form of the disease compared to women.
3. Primary Progressive MS: This form of MS is characterised by a steady and continuous worsening of symptoms without distinct relapses and remissions. It tends to have a worse prognosis compared to relapsing forms of the disease.
4. High relapse rate: Frequent relapses and a higher relapse rate can indicate a more aggressive form of the disease, which may lead to greater disability over time.
5. Rapid accumulation of disability: A quick accumulation of physical disability in the early stages of the disease is associated with a less favorable prognosis.
6. High lesion load: A higher burden of lesions (plaques) in the brain and spinal cord on MRI scans is associated with a worse prognosis.
7. Cognitive impairment: Cognitive dysfunction, such as memory problems and difficulties with thinking and processing information, can indicate a worse prognosis.
8. Comorbid conditions: The presence of other medical conditions, such as depression or cardiovascular disease, can complicate the management of MS and lead to a worse prognosis.
9. Smoking: Smoking has been associated with an increased risk of developing MS and may also contribute to a worse prognosis.

Question 18

What is idiopathic intracranial hypertension and what are the causes?

Answer 18

IIH is a disorder of unidentified cause which leads to increased intracranial pressure, typically with an opening pressure above 25 cmH2O on lumbar puncture.

It has been previously referred to as benign intracranial hypertension, though it is not benign, and pseudotumor cerebri, which can cause confusion.

This condition most frequently occurs in young and obese women, with a sex ratio of approximately 9:1 favoring women.

The aetiology of IIH remains uncertain. There are some reported associations with several drugs, including:
- Oral contraceptive pill
- Steroids
- Tetracycline
- Vitamin A
- Lithium

Question 19

What are the features of idiopathic intracranial hypertension?

Answer 19

Classic symptoms of IIH include:
- Non-pulsatile, bilateral headaches, typically worse in the morning or after bending forwards. Some patients may also experience morning vomiting.
- Visual disturbances, such as transient visual darkening or loss, likely due to optic nerve ischaemia.
- Bilateral papilloedema seen on fundoscopy, indicating increased intracranial pressure.

If untreated, permanent visual damage may result, with 1-3% of patients experiencing vision loss within a year of onset.

Question 20

How is idiopathic intracranial hypertension diagnosed?

Answer 20

Several investigations are used to diagnose IIH and rule out other causes of raised intracranial pressure:
- Ophthalmoscopy, which typically shows bilateral papilloedema. A referral to ophthalmology for a detailed visual field assessment may be warranted.
- Imaging studies such as CT and MRI of the head may show signs of increased intracranial pressure. An MRI Venogram may be performed to rule out secondary causes, particularly venous sinus thrombosis.
- Lumbar puncture is a key diagnostic tool, typically revealing an opening pressure above 20 cmH2O. An abnormal CSF profile may suggest a different diagnosis.

Question 21

How is idiopathic intracranial hypertension managed?

Answer 21

Managing IIH effectively includes:
- Encouraging weight loss as the first-line and best-supported intervention for managing IIH.
- Carbonic anhydrase inhibitors such as acetazolamide can be used, but are often poorly tolerated due to side effects like peripheral paraesthesia.
- Topiramate and candesartan are also commonly used alternatives.
- More invasive procedures such as therapeutic lumbar punctures, surgical CSF shunting or optic nerve sheath fenestration may be necessary for resistant cases with progressive visual loss.

Question 22

What is Ramsay-Hunt syndrome?

Answer 22

Ramsay Hunt syndrome is reactivation of the herpes zoster virus which was dormant within the CN7 root ganglion. Reactivation can cause facial nerve palsy (unilateral inability to bear teeth, smile and raise the eyebrow against resistance) as well the tell-tale vesicles, which clinches the diagnosis. May be accompanied by vertigo

Question 23

What is pseudobulbar palsy?

Answer 23

Pseudobulbar palsy is a condition caused by bilateral lesions affecting the corticobulbar tracts, which run from the motor cortex to the motor nuclei of cranial nerves 9, 10, and 12 in the medulla. As the cranial nerve motor nuclei have bilateral cortical representation (with the exception of the motor nuclei of the lower half of cranial nerve 7), a bilateral lesion is necessary. It is conceptualised as an ‘upper motor neurone’ lesion affecting speech and swallowing mechanisms.

Question 24

What are the causes and features of pseudobulbar palsy?

Answer 24

Pseudobulbar palsy may result from various causes, including:
- Vascular causes such as bilateral internal capsule stroke
- Degenerative causes such as motor neurone disease and progressive supranuclear palsy
- Neoplastic causes such as upper brainstem tumours
- Autoimmune causes such as multiple sclerosis
- Traumatic causes

Signs and Symptoms
The primary clinical features of pseudobulbar palsy include:
- Spastic tongue
- Slow, thick (“hot-potato”) speech
- Brisk jaw jerk reflex
- Emotional lability
Additional upper motor neurone signs may also present, such as:
- Spastic hypertonia
- Pyramidal weakness
- Hyper-reflexia

Question 25

What are the differentials of pseudobulbar palsy?

Answer 25

When evaluating a patient with suspected pseudobulbar palsy, other conditions with overlapping signs and symptoms should be considered: - Bulbar Palsy: Unlike pseudobulbar palsy, bulbar palsy is due to lower motor neuron lesions and can present with flaccid dysarthria, fasciculations, and hypotonia alongside difficulty with speech and swallowing. - Brainstem Stroke: This can cause similar symptoms due to the close anatomical proximity but is usually accompanied by other long tract signs or cranial nerve deficits. - Amyotrophic Lateral Sclerosis (ALS): ALS can also present with speech and swallowing difficulties but is typically accompanied by both upper and lower motor neurone signs in the limbs.

Question 26

How is pseudobulbar palsy diagnosed?

Answer 26

The diagnosis of pseudobulbar palsy is largely clinical and involves thorough history-taking and neurological examination. In addition: - Neuroimaging (MRI or CT scan) is often used to identify potential lesions in the brain that might cause symptoms. - Electrophysiological tests, such as EMG and nerve conduction studies, might be indicated in certain cases. - Additional investigations might be guided by the suspected underlying cause (e.g., CSF analysis in suspected multiple sclerosis).

Question 27

How is pseudobulbar palsy managed?

Answer 27

The management of pseudobulbar palsy is typically symptom-oriented and multidisciplinary. It may include: - Speech and language therapy for difficulties with speech and swallowing - Physiotherapy for management of hypertonia and weakness - Medications such as selective serotonin reuptake inhibitors (SSRIs) or tricyclic antidepressants to manage emotional lability - Regular follow-up and adjustments to the management plan

Question 28

What is optic neuritis? How does it occur?

Answer 28

Optic Neuritis (ON) is characterised by inflammation of the optic nerve, often resulting in visual impairment and ocular discomfort. Optic Neuritis predominantly affects adult women. The pathogenesis of Optic Neuritis is largely based on inflammatory processes triggering activation of T-cells. These activated cells can traverse the blood-brain barrier, leading to a hypersensitivity reaction against neuronal structures. Causes: - Demyelinating lesions: Multiple sclerosis (MS) is the most common cause of demyelinating Optic Neuritis. - Autoimmune disorders: Certain autoimmune disorders can also incite the inflammation of the optic nerve. - Infectious conditions: Infections, particularly those affecting the central nervous system, may contribute to the development of Optic Neuritis.

Question 29

What is the clinical triad of optic neuritis?

Answer 29

1. Visual loss: This is often the most prominent symptom. It can vary from slight visual impairment to severe vision loss. 2. Periocular pain: This may manifest as pain around the eye, often aggravated by eye movement. 3. Dyschromatopsia: Patients experience impaired color discrimination, particularly involving the red-green spectrum.

Question 30

What are the differentials of optic neuritis?

Answer 30

- Glaucoma: Characterised by gradual visual field loss, ocular pain, and potentially elevated intraocular pressure. - Optic neuropathy: Can manifest with similar symptoms to Optic Neuritis, but often lacks the inflammatory component. - Retinal disorders: These can present with visual disturbances but typically do not cause ocular pain. - CNS infections or tumours: These conditions can lead to similar symptoms, especially if they involve the optic nerve or optic tract.

Question 31

How is optic neuritis diagnosed and managed?

Answer 31

Key investigations in Optic Neuritis involve: 1. Visual function tests: These assess visual acuity, colour vision, and visual field. Despite improvement in visual acuity following treatment, contrast sensitivity, colour vision, and visual field deficits may persist. 2. MRI Head and Spine: This can reveal demyelinating lesions, especially in cases associated with multiple sclerosis. Management The Optic Neuritis Treatment Trial (ONTT) recommends intravenous methylprednisolone as the first-line treatment for Optic Neuritis. Oral prednisolone was shown in this trial to be associated with an increased risk of recurrent episodes, but this has not been replicated in other studies since. Therefore, although intravenous methylprednisolone is preferred, there is no absolute contra-indication to the use of oral steroids for optic neuritis.

Question 32

What are the types of brachial nerve injuries?

Answer 32

Brachial plexus injuries refer to damage sustained by the brachial plexus, a network of interlacing nerves, comprising roots from the anterior rami of the cervical nerves C5-C8 and the thoracic nerve T1. These injuries are typically classified into: 1. Erb's palsy: Involving damage to the C5-C6 nerve roots. 2. Klumpke's palsy: Involving damage to the C8-T1 nerve roots.

Question 33

What are the causes of brachial plexus injury?

Answer 33

Brachial plexus injuries predominantly occur due to trauma, often during childbirth or high-impact collisions such as road traffic accidents or sports injuries. Erb's palsy is more commonly associated with traumatic childbirth, while Klumpke's palsy can occur due to a variety of reasons, including axillary radiotherapy, often for breast cancer. Major causes of brachial plexus injuries include: 1. Trauma, especially during childbirth (more associated with Erb's palsy) 2. High-impact accidents 3. Axillary radiotherapy (commonly for breast cancer)

Question 34

What are the clinical features of Erb's palsy?

Answer 34

- Dermatomal sensory loss in the C5-6 distribution - "Waiter's tip" sign: Characterized by shoulder adduction, elbow extension, forearm pronation, and wrist flexion.

Question 35

What are the clinical features of Klumpke's palsy?

Answer 35

- Dermatomal sensory loss in the C8-T1 distribution - Weakness of the intrinsic muscles of the hand - Potential ipsilateral Horner's syndrome if T1 involvement occurs (partial ptosis, miosis and facial anhidrosis due to disruption in the sympathetic nerve supply)

Question 36

What is a malignant cause for Horner's syndrome?

Answer 36

Pancoast tumour (a type of squamous cell lung cancer that begins in the top parts of the lung) 50% of people with a pancoast tumour are affected by Horner's syndrome. The condition occurs when the tumour invades the sympathetic nervous system.

Question 37

How is a brachial plexus injury investigated?

Answer 37

1. Electrodiagnostic studies: EMG and nerve conduction studies can help confirm the diagnosis and provide information on the severity of the injury. 2. Imaging studies: MRI or high-resolution ultrasound can be useful for visualizing traumatic neuromas, nerve root avulsions, and other structural abnormalities.

Question 38

How are brachial plexus injuries managed?

Answer 38

- Physiotherapy: This forms the cornerstone of management, focusing on maintaining range of motion and preventing joint stiffness. - Medication: Analgesics, typically nonsteroidal anti-inflammatory drugs (NSAIDs), can help manage pain. - Surgery: If there's no improvement or if the injury is severe (like complete avulsion), surgical interventions, such as nerve grafts or nerve transfers, may be required. This is usually considered after a period of watchful waiting. - Occupational therapy: To help adapt daily activities and enhance functional recovery. - Regular follow-ups: To monitor recovery and adjust management strategies as needed.

Question 39

What are the three features of normal pressure hydrocephalus?

Answer 39

Gait instability, urinary incontinence, and mild dementia

Question 40

What are the two types of hydrocephalus?

Answer 40

1. Obstructive (or non-communicating) hydrocephalus: This occurs when the flow of CSF is blocked along one or more of the narrow passages connecting the ventricles. Common sites of obstruction include the foramen of Monro (e.g. due to colloid cysts), cerebral aqueduct (e.g. due to aqueduct stenosis), or fourth ventricle (e.g. due to posterior fossa tumour). 2. Communicating hydrocephalus: In this type, CSF can exit the ventricular system, but absorption into the bloodstream is impeded. This is commonly due to problems in the subarachnoid space, often stemming from complications like subarachnoid haemorrhage and infective meningitis.

Question 41

What are the features of hydrocephalus?

Answer 41

Patients with hydrocephalus often present with symptoms related to raised intracranial pressure. These include: - Early morning headaches - Nausea and vomiting - Lethargy - Vision disturbances - Balance problems - Cognitive difficulties

Question 42

What are the possible differentials for hydrocephalus?

Answer 42

The diagnosis of hydrocephalus can be complex, as its symptoms can mimic several other neurological conditions. Key differentials include: - Brain tumour: Presents with headache, seizures, cognitive changes, and focal neurological signs. - Subdural hematoma: History of trauma, fluctuating consciousness, headache, and weakness on one side of the body. - Benign intracranial hypertension (pseudotumor cerebri): Symptoms similar to a brain tumour without any mass lesion, more common in obese women of child-bearing age. - Normal pressure hydrocephalus: Triad of cognitive impairment, gait disturbance, and urinary incontinence, often seen in older adults.

Question 43

How is hydrocephalus diagnosed and managed?

Answer 43

The diagnosis of hydrocephalus is typically confirmed through imaging studies such as: 1. Computed Tomography (CT) scan: This can reveal ventricular enlargement and is generally the initial imaging modality. 2. Magnetic Resonance Imaging (MRI): This provides a more detailed view of the brain and can help determine the cause of hydrocephalus. Management The primary treatment for hydrocephalus is surgical insertion of a shunt, a flexible tube that is used to redirect the excess CSF from the brain to another part of the body, typically the heart or peritoneal cavity, where it can be more easily absorbed. This is called a ventriculoperitoneal or ventriculoatrial shunt. Regular follow-up is required to monitor for complications such as shunt malfunction or infection. In some cases, endoscopic third ventriculostomy (ETV) may be performed. This involves creating a hole in the bottom of one of the ventricles or between ventricles to allow the CSF to flow out of the brain.

Question 44

What are the differentials for vertigo?

Answer 44

The differential diagnosis for vertigo includes: 1. BPPV: Characterized by vertigo with positional change and fatiguable nystagmus. 2. Acute Labyrinthitis: Presents with severe, acute vertigo, associated with nausea and vomiting. Hearing loss and tinnitus may be present. 3. Ménière's Disease: Features recurrent episodes of vertigo, sensorineural hearing loss, tinnitus, and a feeling of fullness in the ear. 4. Acoustic Neuroma: Usually presents with unilateral hearing loss and cranial nerve dysfunction. 5. Ramsay Hunt Syndrome: Characterized by facial nerve palsy, which may be accompanied by vertigo, tinnitus, and hearing loss. 6. Ototoxicity: Presents with hearing loss or vertigo following exposure to ototoxic drugs.

Question 45

What is Huntington's disease and what is the cause?

Answer 45

Huntington's disease is a genetic disorder that causes progressive breakdown of nerve cells in the brain. It is characterized by motor, cognitive, and psychiatric abnormalities. As the most common hereditary neurodegenerative disorder. The disease is caused by an autosomal dominant mutation involving an excessive repetition of the CAG trinucleotide (>38 repeats) in the huntingtin gene, which encodes the huntingtin protein.

Question 46

What are the features of Huntington's disease?

Answer 46

Huntington's disease presents with a characteristic triad of symptoms: 1. Choreoathetosis: Unpredictable, flowing, and writhing movements 2. Cognitive impairment: Dementia, often marked by problems with judgment, memory, and other cognitive functions 3. Psychiatric abnormalities: Depression, irritability, apathy, and sometimes psychosis

Question 47

How is Huntington's disease investigated?

Answer 47

1. Neuroimaging: MRI and CT scans may show loss of striatal volume (striatum is biggest nucleus in basal ganglia - includes caudate nucleus and putamen) and an enlarged frontal horn of the lateral ventricles in moderate to severe disease stages 2. Genetic testing: Confirmatory, and also allows for predictive testing in at-risk family members with pre-test genetic counseling

Question 48

How is Huntington's disease managed?

Answer 48

Although no treatments can halt disease progression, management strategies aim at symptomatic relief and supporting the patient and their family: - Chorea management: Medications such as tetrabenazine are commonly used, with the most evidence base - Depression management: Selective serotonin reuptake inhibitors (SSRIs) are typically the first-line treatment - Psychosis management: Antipsychotics, preferably newer atypical agents, are used due to lower rates of extrapyramidal side effects - Supportive care: This includes a significant amount of physical and emotional support from a multidisciplinary team

Question 49

What is the prognosis for Huntington's disease?

Answer 49

The prognosis for Huntington's disease is poor, with an invariable decline in physical and cognitive abilities. Death usually occurs due to complications related to physical decline such as pneumonia, while suicide is the second most common cause of death.

Question 50

What are the causes of facial nerve palsy?

Answer 50

The causes of facial nerve palsy can be broadly classified into four groups: central nervous system involvement, peripheral nerve disease, neuromuscular issues, and muscular issues. Some specific causes include: 1. Central nervous system involvement, distinguished primarily on the basis of forehead-sparing weakness due to the bilateral cortical representation of the upper part of the face (an 'Upper Motor Neuron' lesion). 2. Physical lesions of the cerebellopontine angle, such as acoustic neuroma. 3. Basal meningitis, which is often bilateral and may be due to infections or inflammation, including Lyme disease and sarcoidosis. 4. Ramsay Hunt syndrome, a condition caused by herpes zoster affecting the facial nerve. 5. Trauma. 6. Diseases of the middle or inner ear. 7. Mononeuritis multiplex, a condition involving the simultaneous inflammation of multiple peripheral nerves. Neuromuscular and muscular mimics are typically distinguishable as they often present with bilateral symptoms and are associated with weakness elsewhere in the body.

Question 51

What are the features of facial nerve palsy?

Answer 51

Patients with facial nerve palsy may present with: - Unilateral or sometimes bilateral facial weakness or paralysis - Difficulty closing the eye on the affected side - Altered sense of taste - Hypersensitivity to sound in one ear - Decreased tearing and salivation - Loss of the nasolabial fold - Drooping of the mouth on one side

Question 52

How is facial nerve palsy investigated?

Answer 52

Diagnostic investigations may include: - Clinical examination - Neurological assessment - Imaging (MRI or CT scan) if a central cause is suspected or to rule out structural lesions. - Serologic tests for Lyme disease and other relevant infectious agents. - Nerve conduction studies and electromyography (EMG) in the case of neuromuscular differentials.

Question 53

How is facial nerve palsy managed?

Answer 53

- Corticosteroids for Bell's Palsy - Antiviral agents for Ramsay Hunt syndrome. - Antibiotics for Lyme disease and basal meningitis. - Surgical intervention for acoustic neuroma and trauma. - Physical therapy and rehabilitation to help restore facial muscle function. - Addressing underlying conditions in the case of diabetes or other systemic diseases.

Question 54

What is Lyme disease?

Answer 54

Lyme disease is an infectious disease caused by Borrelia Spirochetes bacteria that infects a person via a tick bite, commonly in hikers. Initial symptoms occur within a few days to a month following infection, and include constitutional illness (fever, rigors, myalgia, migratory polyarthritis) and a characteristic erythema migrans rash with central clearing. Often the rash is missed by the patient, which delays antibiotic treatment. If allowed to progress, later possible complications include large joint monoarthritis, unilateral or bilateral facial nerve palsy, neuropathic pain and palpitations

Question 55

What is guillain barre syndrome? what causes it?

Answer 55

GBS is an ascending inflammatory demyelinating polyneuropathy, typified by an acute onset of bilateral and roughly symmetric limb weakness. GBS typically occurs 1-3 weeks following an infection, with common culprits being Campylobacter, mycoplasma, and EBV. 40% of cases, however, are idiopathic. Other potential triggers include infections such as CMV, HIV, Hepatitis A, or following certain vaccinations such as for tetanus, rabies, or swine flu.

Question 56

What are the features of guillain barre syndrome?

Answer 56

Neurological decline often progresses over days to weeks. Clinical features of GBS include: - Progressive ascending symmetrical limb weakness (usually starting with the lower limbs) - Lower back pain due to radiculopathy - Paraesthesia, often preceding motor symptoms - Potential respiratory muscle involvement in severe cases - Potential cranial nerve involvement leading to diplopia, facial droop - Lower motor neurone signs in the lower limbs: hypotonia, flaccid paralysis, areflexia - Cranial nerve signs: ophthalmoplegia, lower motor neurone facial nerve palsy, bulbar palsy - Potential autonomic dysfunction (e.g., arrhythmia, labile blood pressure)

Question 57

How is Guillain barre syndrome investigated?

Answer 57

- Monitoring of forced vital capacity (FVC) for respiratory muscle involvement - Cardiac monitoring for autonomic instability - Blood tests, including arterial blood gas (ABG) - Serological tests: Anti-ganglioside antibodies - Lumbar puncture: may show albuminocytological dissociation (high protein without high white cells) - Nerve conduction studies: may show prolongation or loss of the F wave - Identification of the underlying cause: stool cultures, serology, CSF virology

Question 58

How is Guillain barre syndrome managed?

Answer 58

Management of GBS is primarily supportive and includes: - Regular monitoring of FVC - Venous thromboembolism (VTE) prophylaxis: TEDS + LMWH - Analgesia: NSAIDs or opiates for radiculopathy-related back pain - Management of cardiac arrhythmias as per ALS guidelines - Careful use of antihypertensives due to potential autonomic dysfunction - Consideration of enteral feeding in those with unsafe swallow Specific medical management for those with significant disability (e.g., inability to walk) include: - Intravenous immunoglobulin (IVIG) over a 5-day course - Plasmapheresis, which has similar efficacy to IVIG but is associated with more side effects.

Question 59

What are the main features of Wernicke's encephalopathy?

Answer 59

nystagmus/opthalmoplegia, confusion and ataxia

Question 60

What is a surgical nerve palsy? What is the most common cause?

Answer 60

The third (oculomotor) cranial nerve provides motor supply to the levator palpebrae superioris and extra-ocular muscles (except lateral rectus - supplied by the abducens VI nerve, and superior oblique - supplied by the trochlear IV nerve). It also provides parasympathetic supply to the sphincter pupillae muscles to mediate pupil constriction. A third nerve palsy causes: ptosis (due to impaired innervation to levator palpebrae superioris) and a 'down and out' pupil (due to unopposed activation of lateral rectus and superior oblique). In a 'surgical' third nerve palsy there is pupil involvement. This is because the parasympathetic (constrictive) fibres run on the outside of the nerve. External compression will impair function of these fibres, causing pupil dilation. The most common cause of a surgical third nerve palsy is a posterior communicating artery aneurysm. Other causes include cavernous sinus lesions (infection, thrombosis, tumour infiltration).

Question 61

What are the 5 syndromes of lacunar infarcts?

Answer 61

A lacunar infarct (LACI) is defined by: 1. a pure motor stroke, 2. pure sensory stroke, 3. sensorimotor stroke, 4. ataxic hemiparesis or 5. dysarthria-clumsy hand syndrome. A LACI affects small deep perforating arteries, typically supplying internal capsule or thalamus.

Question 62

What is beta-interferon?

Answer 62

A disease-modifying therapy used to treat multiple sclerosis

Question 63

What is the only medication licensed for the treatment of motor neuron disease?

Answer 63

Riluzole Extends life expectancy by around three months

Question 64

What is the cause of MND?

Answer 64

In most cases it is associated with misfolding of the TDP-43 protein

Question 65

What are the features of motor neuron disease?

Answer 65

Motor neuron diseases typically manifest as a combination of upper and lower motor neuron signs: 1. Upper motor neuron signs include: - Spasticity - Hyperreflexia - Upgoing plantars (although they are often downgoing in MND). 2. Lower motor neuron signs include: - Fasciculations - Muscle atrophy. Eye and sphincter muscles are generally spared until late in the disease course. Absence of sensory disturbance is typical, and if present, should prompt consideration of an alternative diagnosis.

Question 66

How is MND investigated?

Answer 66

Investigations for MND primarily aim to rule out treatable differential diagnoses. Key tests include: - Thyroid function tests (TFTs): To exclude thyrotoxicosis syndrome. - Protein electrophoresis: To rule out paraproteinaemias. - MRI of the brain and spinal cord: To assess for brainstem lesions mimicking MND or cervical spondylopathy. - EMG & nerve conduction studies: Important for looking for a myasthenicsyndrome, chronic inflammatory demyelinating polyneuropathy, or multifocal mononeuropathy.

Question 67

How is MND managed?

Answer 67

Currently, treatment for MND is primarily supportive, as the only disease-modifying treatment, Riluzole, only extends life expectancy by an average of 3 months. Non-invasive ventilation can prolong survival in patients with type 2 respiratory failure. Key management strategies include: - Coordinating treatment via a multidisciplinary team approach. - Providing pain relief with simple analgesia and treating spasticity and contractures with baclofen and botox injections. - Using anticholinergics to manage drooling. - Supporting feeding via an NG or PEG tube as bulbar disease progresses. - Discussing advanced care planning early in disease progression to minimise distress and complications.

Question 68

How are strokes classified?

Answer 68

1. A total anterior circulation infarct (TACI) is defined by: - Contralateral hemiplegia or hemiparesis, AND - Contralateral homonymous hemianopia, AND - Higher cerebral dysfunction (e.g. aphasia, neglect) A TACI involves the anterior AND middle cerebral arteries on the affected side. 2. A partial anterior circulation infarct (PACI) is defined by: - 2 of the above, OR - Higher cerebral dysfunction alone. A PACI involves the anterior OR middle cerebral artery on the affected side. 3. A lacunar infarct (LACI) is defined by: A pure motor stroke, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis or dysarthria-clumsy hand syndrome. A LACI affects small deep perforating arteries, typically supplying internal capsule or thalamus. 3. A posterior circulation infarct (POCI) is defined by: - Cerebellar dysfunction, OR - Conjugate eye movement disorder, OR - Bilateral motor/sensory deficit, OR - Ipsilateral cranial nerve palsy with contralateral motor/sensory deficit, OR - Cortical blindness/isolated hemianopia. A POCI involves the vertebrobasilar arteries and associated branches (supplying the cerebellum, brainstem, and occipital lobe).

Question 69

What are the posterior stroke syndromes?

Answer 69

1. Basilar artery occlusion is more likely to present with locked in syndrome (quadriparesis with preserved consciousness and ocular movements), loss of consciousness, or sudden death. 2. Anterior inferior cerebellar artery results in lateral pontine syndrome, a condition similar to the lateral medullary syndrome but with additional involvement of pontine cranial nerve nuclei. 3. Wallenberg's syndrome (lateral medullary syndrome) causes ipsilateral Horner's syndrome, ipsilateral loss of pain and temperature sensation on the face, and contralateral loss of pain and temperature sensation over the contralateral body. 4. Weber's syndrome/medial midbrain syndrome (paramedian branches of the upper basilar and proximal posterior cerebral arteries): causes an ipsilateral oculomotor nerve palsy and contralateral hemiparesis.

Question 70

What is hereditary spastic paraparesis?

Answer 70

Hereditary Spastic Paraparesis (HSP), also known as familial spastic paraplegia, comprises a group of inherited disorders that primarily affect the lower extremities. The main clinical features involve progressive spasticity and weakness of the legs due to degeneration of the axonal tracts of the corticospinal pathway in the spinal cord. The disorder can be inherited in autosomal dominant, autosomal recessive, or X-linked patterns, leading to varied presentations and onset across patients. The aetiology of HSP involves genetic mutations leading to axonal degeneration, primarily of the corticospinal tracts, but also potentially of the dorsal column pathways. These changes are most pronounced in corticospinal tracts leading to the lower limbs and the fasciculus gracilis fibres (part of the dorsal column) from the lower limbs. As a result, the lower limbs are usually more affected than the upper limbs.

Question 71

What are the features of hereditary spastic paraparesis?

Answer 71

Key diagnostic criteria for HSP include: - A family history of the condition - Progressive gait disturbance - Spasticity of lower limbs - Hyper-reflexia of lower limbs - Extensor plantar responses - Typically, the power in lower limb muscles is normal or only mildly reduced.

Question 72

How is hereditary spastic paraparesis managed?

Answer 72

Currently, there is no curative treatment available for HSP. The management strategy primarily focuses on symptomatic relief, which can include: - Medications such as baclofen for managing spasticity - Botulinum toxin injections for severe spasticity - Regular physiotherapy to maintain mobility and strength The prognosis of the HSP is variable, but most patients have a normal life expectancy.

Question 73

What is the most common cause of extradural haematoma?

Answer 73

An Extradural haematoma (EDH) is a pathological condition where blood collects between the dura mater, the outermost meningeal layer, and the inner surface of the skull. This condition is commonly arterial in origin, with the middle meningeal artery often implicated. EDH predominantly affects young patients who have experienced a head injury, such as during sports or road traffic accidents. Although it is a relatively rare condition, prompt recognition and treatment are crucial due to its potential for rapid progression and life-threatening consequences. The aetiology of EDH is almost always trauma-related, specifically severe head trauma that results in a tear of the middle meningeal artery. Unlike subdural haematomas, the cause of EDH is typically identifiable and tends to be a result of a well-defined traumatic event.

Question 74

What are the features of extradural haematoma?

Answer 74

Patients with EDH often present with a characteristic clinical course: - Initial brief loss of consciousness following the trauma - A period of regained consciousness and apparent recovery (the lucid interval) - Subsequent deterioration of consciousness and the onset of a headache

Question 75

How does an extradural haematoma present on imaging?

Answer 75

- CT scan: This is the investigation of choice for EDH. The typical finding is a lentiform or biconvex hyperdense extra-axial collection, most often unilateral and supratentorial. - Secondary features such as midline shift or subfalcine/uncal herniation should be assessed as they may necessitate urgent neurosurgical intervention.

Question 76

How is haemorrhagic stroke generally be managed?

Answer 76

The management of haemorrhagic stroke should include reversal of any anticoagulation (using beriplex/octaplex +/- vitamin K) and aggressive BP control. The systolic BP should be kept <140mmHg within an hour of admission and ideally kept above 120mmHg. This can be done with Glyceryl Trinitrate (GTN) or labetalol.

Question 77

What is internuclear opthalmoplegia? What are the features?

Answer 77

Internuclear ophthalmoplegia results from a lesion within the medial longitudinal fasciculus. The MLF is a white matter tract located close to the midline and running through the brainstem. It plays a crucial role in coordinating various eye movements by transmitting necessary information from the ocular motor nuclei. The lesion blocks the connection between the contralateral sixth nerve nucleus and the ipsilateral third nerve nucleus, leading to impaired horizontal gaze. Internuclear ophthalmoplegia typically presents with: 1. Impaired adduction in the ipsilateral eye during horizontal gaze. 2. Nystagmus in the abducting eye. 3. Some patients may retain the ability to converge to a near target, helping to distinguish MLF lesions from other causes of medial rectus weakness.

Question 78

What are the features of cluster headaches and how are they managed?

Answer 78

- Recurrent unilateral periorbital pain of sudden onset - Associated symptoms: watery and bloodshot eye, lacrimation, rhinorrhoea, miosis, ptosis, lid swelling, and facial flushing - Headache duration of 15 minutes to 3 hours, occurring once or twice daily over 4-12 weeks, followed by a pain-free period of several months Management strategies involve avoiding triggers, prophylaxis with Verapamil, and treating acute attacks with 100% oxygen via a non-rebreathable mask (contraindicated in COPD) and a subcutaneous or nasal Triptan (contraindicated in ischaemic heart disease).

Question 79

What is Brown-Sequard syndrome? What are the causes?

Answer 79

Brown-Séquard syndrome is characterized by anatomical disruption of nerve fibre tracts in one half of the spinal cord. Common causes of BSS include: - Cord trauma (penetrating injuries being the most common) - Neoplasms - Disk herniation - Demyelination - Infective/ inflammatory lesions - Epidural hematomas

Question 80

What are the features of Brown Sequard syndrome?

Answer 80

Disruption of descending lateral corticospinal tracts, ascending dorsal column and ascending spinothalamic tracts leads to the following findings below the level of the injury: - Ipsilateral hemiplegia - Ipsilateral loss of proprioception and vibration - Contralateral loss of pain and temperature sensation

Question 81

What is Todd's palsy?

Answer 81

Todd's paralysis is a neurological condition experienced by individuals with epilepsy, in which a seizure is followed by a brief period of temporary paralysis. The paralysis may be partial or complete but usually occurs on just one side of the body.

Question 82

What is the Jacksonian march?

Answer 82

Jacksonian seizures are also known as a Jacksonian march. This is because the tingling or twitching begins in a small area and then "marches" or spreads to a larger area of the body.

Question 83

What are the features of myasthenia gravis?

Answer 83

Patients with myasthenia gravis commonly present with: - Limb muscle weakness - Extra-ocular muscle involvement leading to drooping eyelids, diplopia - Facial muscle involvement causing difficulty in smiling or chewing - Bulbar muscle involvement causing a change in speech or difficulty swallowing - Fatigable muscle weakness, bilateral ptosis, a myasthenic snarl, head droop, and bulbar features on examination

Question 84

Which drugs can exacerbate myasthenia gravis?

Answer 84

Beta blockers Lithium Penicillamine Gentamicin Quinolones Phenytoin

Question 85

Which important side effect should patients be counselled to look out for when starting lamotrigine?

Answer 85

Look out for a large blistering rash throughout the body Lamotrigine is a well tolerated anti-epileptic drug, primarily acting as a Sodium channel blocker. It is associated with Stevens-Johnson syndrome, Toxic Epidermal Necrolysis or Hypersensitivity syndrome in 1:4000 patients. It is more common in children that adults, more common with co-administration of Valproate, higher doses and rapid titration

Question 86

How should haemorrhagic stroke be managed when the patient is taking warfarin?

Answer 86

Start labetalol (The aim is to maintain blood pressure at <140/80 mm Hg, as poor control in the acute phase is associated with worse long-term outcomes), stop warfarin and give IV vitamin K and prothrombin complex concentrate

Question 87

What are the 4 parkinson-plus syndromes?

Answer 87

There are four main Parkinson-plus syndromes, which present as Parkinsonism (triad of resting tremor, hypertonia, and bradykinesia) with additional clinical features described below. 1. Progressive supranuclear palsy Parkinisonism and vertical gaze palsy. 2. Multiple system atrophy Parkinisonism and early autonomic clinical features such as: postural hypotension, incontinence, and impotence. 3. Cortico-basal degeneration Parkinisonism and involves spontaneous activity by an affected limb, or akinetic rigidity of that limb. 4. Lewy body dementia Parkinisonism and fluctuations in cognitive impairment and visual hallucinations, often before Parkinsonian features occur.

Question 88

What are the long-term disease-modifying therapies for relapsing-remitting multiple sclerosis?

Answer 88

- First-line injectables such as beta-interferon and glatiramer - New oral agents such as dimethyl fumarate, teriflunomide and fingolimod - Biologics such as natalizumab and alemtuzumab. As a general rule, increasingly effective treatments are associated with increasingly significant side effects. The extent to which long-term use of DMTs reduces risk of secondary progressive MS is not yet clearly established.

Question 89

What are the symptomatic therapies for MS?

Answer 89

Physiotherapy Baclofen and Botox for spasticity Modafinil and exercise therapy for fatigue Anticholinergics for bladder dysfunction SSRIs for depression Sildenafil for erectile dysfunction Clonazepam for tremor

Question 90

What are the causes of foot drop?

Answer 90

1. Neurological lesions: The most common cause of foot drop is disease or trauma affecting the common peroneal nerve, particularly where it loops over the fibula's head on the knee joint's lateral aspect. 2. L5 root lesion (radiculopathy): Foot drop can be a symptom of this condition, characterized by loss of inversion and sensory loss over the L5 dermatome. Lumbosacral disc herniation is the most common cause of this type of foot drop. 3. Distal motor neuropathy: This condition is often associated with foot drop, accompanied by glove and stocking sensory disturbance and loss of all movements of the foot. 4. Small cortical lesions: Foot drop can be associated with small cortical lesions, often presenting with other upper motor neuron features. 5. Other causes: Intrinsic cord disease, partial sciatic nerve disease, and myopathy may also mimic foot drop, although these are less common.

Question 91

What are the findings in foot drop?

Answer 91

Key motor findings in foot drop include: - Weakness or paralysis of dorsiflexion and eversion of the foot - Difficulty in lifting the front part of the foot - A high-stepping gait or foot dragging In specific aetiologies, additional symptoms may be present: - In L5 root lesions, loss of inversion (a tibial nerve function not lost in common peroneal nerve lesions), sensory loss over the L5 dermatome, and sciatica-type shooting leg pain. - In distal motor neuropathy, glove and stocking sensory disturbance, and loss of all foot movements.

Question 92

What MMSE score suggests dementia?

Answer 92

A score of 24 or less

Question 93

What blood tests are done to rule out reversible causes when dementia is suspected?

Answer 93

FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12 and folate levels

Question 94

Which condition may be significantly worsened if Haloperidol is prescribed for delirium

Answer 94

Parkinson's - careful reduction of the Parkinson medication may be helpful - if symptoms require urgent treatment then the atypical antipsychotics quetiapine and clozapine are preferred

Question 95

What are the symptoms of acute digoxin toxicity?

Answer 95

gastrointestinal disturbance (nausea, vomiting, abdominal pain), dizziness, confusion, blurry or yellow vision, and arrhythmias

Question 96

What are the factors that predispose patients to pressure ulcers?

Answer 96

Pressure ulcers develop in patients who are unable to move parts of their body due to illness, paralysis or advancing age. They typically develop over bony prominences such as the sacrum or heel. The following factors predispose to the development of pressure ulcers: - malnourishment - incontinence - lack of mobility - pain (leads to a reduction in mobility)

Question 97

Which score is used to screen for patients at risk of developing pressure sores?

Answer 97

The Waterlow score is widely used to screen for patients who are at risk of developing pressure areas. It includes a number of factors including body mass index, nutritional status, skin type, mobility and continence.

Question 98

How are pressure ulcers graded?

Answer 98

Grade 1 - Non-blanchable erythema of intact skin. Discolouration of the skin, warmth, oedema, induration or hardness may also be used as indicators, particularly on individuals with darker skin Grade 2 - Partial thickness skin loss involving epidermis or dermis, or both. The ulcer is superficial and presents clinically as an abrasion or blister Grade 3 - Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia. Grade 4 - Extensive destruction, tissue necrosis, or damage to muscle, bone or supporting structures with or without full thickness skin loss

Question 99

How are pressure ulcers managed?

Answer 99

- A moist wound environment encourages ulcer healing. Hydrocolloid dressings and hydrogels may help facilitate this. The use of soap should be discouraged to avoid drying the wound - Wound swabs should not be done routinely as the vast majority of pressure ulcers are colonised with bacteria. The decision to use systemic antibiotics should be taken on a clinical basis (e.g. Evidence of surrounding cellulitis) consider referral to the tissue viability nurse - Surgical debridement may be beneficial for selected wounds

Question 100

How is a grade 2 pressure ulcer generally managed when there are no signs of infection?

Answer 100

Wound dressing, analgesia, nutritional assessment

Question 101

What investigation should be done when giving donepezil?

Answer 101

An ECG as it should not be used in bradycardia or heart block

Question 102

Which tool is used to identify medications where the risk outweighs the benefits in certain conditions?

Answer 102

The Screening Tool of Older Person's Prescriptions (STOPP) aims to improve the appropriateness of prescriptions, reduce the occurrence of adverse events and reduce drug costs. It looks at which drugs are potentially inappropriate in a patient who is 65 years or older.