Acute Medicine Exam Flashcards

1
Q

Spinal Mets - Surgery vs Radiotherapy

A

The main indications for surgical decompression are uncertain cause with no histology, radioresistant tumour e.g. sarcoma/melanoma, unstable spine, previous RT, major structural compression, cervical cord lesion, solitary vertebral metastasis.

Indications for radiotherapy: radiosensitive tumour, several levels of compression, unfit for major surgery, patient choice.

The real extra benefit of surgical decompression would seem to be for the non-ambulant patient with a single site of cord compression and a prognosis of >3 months

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2
Q

Ilio-femoral DVT Rx options

A

Catheter-directed thrombolytic therapy should be considered in those patients who have symptomatic iliofemoral DVT if they have had symptoms for <14 days, have good functional status, >1 year to live, and low bleeding risk. An IVC filter would be considered if the patient was unable to be anticoagulated (e.g. recent intracranial bleed) or if they had recurrent VTEs despite adequate anticoagulation therapy.

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3
Q

HIV Associated Kaposi Rx

A

Kaposi’s sarcoma is caused by human herpesvirus-8. The majority of cases of Kaposi’s sarcoma associated with HIV infection respond to HAART. In the minority that does not respond to HAART, treatment with chemotherapy or radiotherapy can be offered. HIV-associated KS typically occurs in patients who have low CD4+ T-cell counts (10,000 copies/mL).

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4
Q

Biphosphanates

A

These drugs are pyrophosphate analogues that bind to hydroxyapatite crystals in bone matrix and inhibit osteoclastic bone resorption. They have no effect on parathyroid hormone or parathyroid-related protein.

Reference:

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5
Q

Demyelinating diseases

A

Inflammatory:
- Multiple sclerosis
- Acute-disseminated encephalomyelitis,
- Acute Haemorrhagic Leucoencephalitis

  • Progressive multifocal leucoencephalopathy
    (PML) and
  • Pontine Myelinolysis
  • Extrapontine myelinolysis.
  • Hypoxic-Ischemic Demeylination

Acute inflammatory demyelination in a patient &laquo_space;10 years of age is more likely to be due
to ADEM.

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6
Q

Multiple Sclerosis Presentation

A

Common presenting features include:
= weakness, paraesthesia or focal sensory loss, optic neuritis, diplopia,
ataxia and vertigo.
= Autonomic motor abnormalities of
bladder, bowel and sexual function are common.
Other manifestations can include
= painful muscle spasms,
= trigeminal neuralgia,
= fatigue and depression,
= subtle cognitive difficulties,
= psychiatric disturbances and seizures

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7
Q

MS Diagnostic Approach

A

A simple practical approach relies on a combination of a
= myelin stain (such as luxol fast blue/cresyl violet or solochrome
cyanin,
= a macrophage marker (eg, antibody to CD68)
and
= a stain for axons (eg, Palmgen silver impregnation or
immunohistochemistry for neurofilament proteins) to subdivide plaques into the following:
1. Active plaques
2. Inactive plaques
3. Chronic Active plaques
4. Shadow plaques

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8
Q

Leucodystrophies

A

The leucodystrophies are progressive,
usually inherited, disorders of myelin metabolism, and tend to be of onset in childhood and to produce symmetrical,
diffuse loss of myelin and degeneration of white matter, sometimes associated with accumulation of metachromatic material or multinucleated cells. The leucodystrophies most
likely to be confused with multiple sclerosis are adrenoleucodystrophy and adrenomyeloneuropathy, in both of which
there is inflammation and demyelination that can, particularly in the brain stem, appear plaque-like.
Patients with adrenoleucodystrophy and adrenomyeloneuropathy also have high levels of saturated, very long-chain fatty acids in
their brain and plasma.

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9
Q

Acute (Marburg-type) multiple sclerosis

A

a rare, fulminant variant of
multiple sclerosis. It is believed, based on anecdotal evidence, to affect children and young adults usually. Some patients diagnosed with this disease may have had aggressive forms of ADEM. This designation may also overlap acute inflammatory demyelination presenting as a space-occupying lesion.

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10
Q

Neuromyelitis optica (Devic’s disease)

A

This variant of MS is characterised by the development of optic neuritis and acute transverse myelitis within days, weeks or occasionally months of each other.

Most patients present with visual loss and subsequently develop paraplegia and
sensory loss, but the order may be reversed.

Neuromyelitis optica is pathogenetically distinct from most other types of multiple sclerosis in that the demyelination is antibody dependent and complement mediated.2

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11
Q

ADEM - Acute Disseminated Encephalomyelitis

A

The most prominent clinical features are usually ataxia, headache and weakness.
Other manifestations can include vomiting, slurring or impairment of speech, extraocular or other cranial nerve nerve palsies, agitation, seizures, lethargy, delirium and stupor.

Approximately 80% of patients
make a full recovery.

Although ADEM is classically a
monophasic disease, relapses have been reported in 5–10% of cases (multiphasic disseminated encephalomyelitis)

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12
Q

Central Pontine & Extra-Pontine Myelinolysis

A

The presentation is usually rapid onset of confusion, limb weakness (often progressing to spastic tetraparesis) and mutism. Other frequent manifestations include ataxia,
dysphagia and hypotension.
Movement disorders (dystonia,
choreoathetosis and parkinsonism) occur in some patients and are probably related to EPM

CPM is a monophasic demyelinating disease of the pons and lower midbrain. It most often occurs in association with alcoholic liver disease or correction of hyponatraemia, some times with Post Liver transplant High ciclosporin levels, Hypernatremia etc

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13
Q

Concentric sclerosis (Balo´’s sclerosis)

A

This rare and unmistakable variant of multiple sclerosis is characterised by lesions composed of alternate bands of demyelinated and myelinated white matter, forming concentric rings or irregular stripes.

Concentric sclerosis is often rapidly progressive. However, the distinctive lesions may be admixed with other, typical plaques and can occur in chronic multiple sclerosis.

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14
Q
A
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