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AAClinical school conditions > MS, meningitis and coma > Flashcards

MS, meningitis and coma Flashcards

1
Q

MS incidence

A

1.2 per thousand

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2
Q

MS geography

A

More common away from the equator, and in white populations.

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3
Q

MS age

A

Initial presentation between 20 and 40 (patient I saw started in teens). Later if primary progressive.

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4
Q

MS sex

A

Women twice as likely, ratio widening.

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5
Q

MS likely presenting symptoms

A

Optical neuropathy
Brainstem demyelination symptoms
Spinal cord lesion symptoms

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6
Q

MS optical neuropathy

A

central loss of vision, can be foggy or dense

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7
Q

MS brainstem demyelination symptoms.

A

Diplopia, vertigo, facial weakness/numbness, dysarthria and dysphagia. Pyramidal signs in limbs can also occur.

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8
Q

MS spinal cord lesions symptoms

A

Paraparesis, tingling or numbness on walking. Tightness around chest.

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9
Q

MS clinical signs.

A

Lhermitte’s sign

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10
Q

MS clinical symptoms that are less often presenting.

A

Other visual changes, strange sensations on skin, clumsiness, unsteadiness, urinary symptoms, pain, fatigue, spasticity, depression and sexual dysfunction.
Rare but pathognomic: tonic spasms.

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11
Q

MS investigations.

A

MRI of brain and spinal cord - latter useful for specificity to inflammatory disorders e.g. MS.

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12
Q

MS diagnosis

A

Two attacks separated in time affecting different parts of CNS. Important to ask about any previous neurological symptoms. MRI imaging.

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13
Q

MS treatment

A

No cure. Treat individual symptoms.
Acute relapses treat with steroids.
Some immunomodulatory treatments are disease modifying. B-interferon and galtiramer.

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14
Q

MS pathology - overview

A

T cell mediated autoimmune inflammatory disorder leading to demyelination of brain and spinal cord.

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15
Q

MS pathology - plaque size

A

2 - 10 mm in size.

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16
Q

MS pathology - common places for plaques to form

A

Optic nerves, periventricular region, corpus callosum, brainstem and cervical cord.

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17
Q

MS disease progression overview.

A

Relapsing-remitting (common) most of which evolve into secondary progressive. A few start with primary progressive.

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18
Q

Indications for a CT head.

A

GCS is either less than 13, or 13/14 2h after injury. Focal neurological deficit, post traumatic seizure, suspected skull fracture and vomiting more than once.
Loss of consciousness AND > 65 yr, or coagulopathy, or dangerous mechanism of injury, or anterograde amnesia for greater than 30 minutes.

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19
Q

Common causes of predominantly motor peripheral neuropathies.

A

Guillain-Barré syndrome, Charcot-Marie-Tooth syndrome, porphyria, lead poisoning and diphtheria.

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20
Q

Common causes of peripheral painful neuropathy

A

alcoholic neuropathy, diabetic amyotrophy, porphyria, vitamin B1 deficiency or vitamin B12 deficiency and carcinoma

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21
Q

Common causes of peripheral neuropathy

A

Diabetic neuropathy.

Nutritional, including alcohol (with or without vitamin B1 deficiency), B12 deficiency

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22
Q

Clinical features of shingles

A

Tingling or pain preceding vesicular rash usually in dermatomal distribution.
Can be followed by post-herpetic neuralia, CNV and VII involvement and myelitis.

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23
Q

Treatment of shingles

A

Aciclovir 800mg 5 times/d, PO for 7 d

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24
Q

Clinical features of sagittal venous sinus thrombosis

A

Headache, vomiting, seizures, deteriorating vision, papilloedema.

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25
Q

Cinical features of transverse venous sinus thrombosis

A

headache +/- mastoid pain, focal CNS deficit, seizures, papilloedema.

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26
Q

Differential diagnosis with dural venous sinus thrombosis

A

SAH
meningitis
encephalitis

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27
Q

Investigations for dural venous sinus thrombosis

A

MRI T2 may visualise directly

CT after 1 wk can show delta sign: transversely cut sinus shows contrast filling defect.

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28
Q

Treatment of dural venous sinus thrombosis

A

Escalate to specialist
heparin
sometimes fibrinolytics

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29
Q

Prognosis for dural venous sinus thrombosis

A

Variable

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30
Q

Questions for blackout.

A

Previous episodes?
What was pt doing? (situational syncope)
Symptoms preceding blackout? Chest pain/palpitations (cardiac)? Aura (epilepsy)?
Witness history

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31
Q

Things to remember about elderly epilepsy

A

New epilepsy can occur e.g. 20% stroke pts withing a year.
Elderly are more susceptible to pharma causes.
Pallor suggests cardiac
Drowsiness suggests epilepsy.
Don’t forget to do an EEG if indicated, and check hypoglycaemia.

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32
Q

Investigations in blackout.

A

FBC, U&Es, glucose, TFTs, Ca++
ECG
24 hr ECG if indicated
EEG and/or CT scan.

33
Q

Cardiac causes of blackout in elderly

A

Arrhythmias
MI (can be pain free)
Aortic stenosis (w SOBOE, syncope OE, angina)
Hypertrophic cardiomyopathy
Postural hypotension
Carotid sinus syndrome
VV syncope ( c. 2 mins, urinary incontinence uncommon but possible. Brief clonic jerking).

34
Q

How is the Glasgow Coma Scale divided up?

A

E4, V5, M6

35
Q

Key symptoms of meningitis

A

Fever, neck stiffness, photophobia, petechial rash.

36
Q

A rare meningitis to keep in mind due to significant mortality

A

Listeria monocytogenes meningitis - more common in extremes of age, immunosuppressed, cancer, alcoholics, diabetics and liver/renal failure. Not treatable by cephalosporins, so use amoxicillin.

37
Q

Meningitis caused by inhaled pigeon droppings.

A

Cryptococcus neoformans infection. Causes pneumonia, cutaneous infections and meningitis.
Diagnose using CT/MRI, india ink or CrAg.

38
Q

Common causes of viral meningitis

A

Enterovirus (self-limiting)
HSV2 (IV aciclovir)
VZV and other herpes viruses (aciclovir)

39
Q

Uncommon causes of viral meningitis

A

Mumps
Measles
LCMV (v. rare)

40
Q

Presentation, diagnosis and treatment of viral meningitis caused by enteroviruses

A

Most original infections asymptomatic but may be associated with rash, pharyngitis, pericarditis and cardiomyopathy.
Neurovirulent strains EV70 and 71 may cause paralytic manifestations.

Use PCR on CSF

Often self-limiting

41
Q

Presentation, diagnosis and treatment of viral meningitis caused by HSV2 (3% of viral meningitides)

A

Generally primary genital infection, someties reactivation from sensory nerve.
May have not peripheral skin lesions
Diagnosis is realtime PCR on CSF
Treat with IV aciclovir

42
Q

RARE: meningitis caused by mumps - presentation and management.

A

Mild and selflimiting in 20% of cases of mumps, 0.1% develop severe encephalitis
Supportive management

43
Q

RARE: meningitis caused by measles - presentation and management.

A

Acute encephalitis in 0.1% of cases, mortality 15%.
SSPE leads to CNS degeneration 8-10 years later.
Supportive management

44
Q

People at risk of LCMV meningitis

A

Lab workers, pet owners and people living in unsalubrious places

45
Q

CSF: normal appearance, polymorphs, bacteria, protein and glucose

A

clear, 50% of blood glucose.

46
Q

CSF in acute bacterial infection

A

turbid, usually 500-10000 polymorphs, bacteria identifiable on gram stain unless treated, usually raised protein, low glucose.

47
Q

CSF in viral infection

A

Usually clear, sometimes turbid, usually 50-1000 polymorphs, no bacteria, protein sometimes raised, normal glucose.

48
Q

CSF in TB

A

often slightly turbid, occasionally with spider web clot. 50-1000 polymorphs, bacteria found with careful searching of auramine stained CSF, usually raised protein, low glucose.

49
Q

presentation of brain abscess

A

Intracranial mass effects

Raised intracranial pressure

50
Q

Causes of brain abscesses

A

Recent neurosurgery; commonly staph or throat/sinus flora.
Local parameningeal infections; abscesses occure in adjacent areas of brain from infected area. Mucosal anaerobes, oral strep, coliforms.
Distant infection with haematogenous spread; lung abscess, empyema, neglected appendicitis and endocarditis etc (anaerobes, strep)
Cranial trauma: skin or mucosal flora commonly.

51
Q

What increases risk of brain abscesses

A

Right to left congenital heart shunt.
Recent neurosurgery
Local parameningeal infections.

52
Q

What is the TB stain?

A

Rapid: auramine stain
Confirmation: Z-N stain
PCR if smear positive.

53
Q

Presentation of herpes encephalopathy

A

Altered consciousness, confusion, seizures, possible fever, usuallly in the elderly. Fatal untreated.

54
Q

Major cause of herpes encephalopathy

A

HSV1

55
Q

Arbovirus encephalopathies

A

Often self-limiting. Diagnosis by CSF and blood ELISA and PCR.

56
Q

Rabies encephalopathy

A

Tingling at wound site, fever, headache and malaise. Progresses to hallucinations, hydrophobia, maniacal behaviour, paralysis, coma and death.

57
Q

Causes of hypoglycaemic coma

A

Plasma glucose typically lower than 3.0 mmol/L
Caused by insulin, or rarely liver disease, glycogen storage disease, addison’s, post gastric surgery, insulinoma. Patients with DM1/2 who have taken alcohol.

58
Q

Presentation of hypoglycaemic coma

A

Sweating, anxiety, hunger, coma, fits, focal neurology.

59
Q

Causes of diabetic ketoacidosis

A

Decompensated DM1. Omission of insulin or undiagnosised.

Insulinopenic state → hyperglycaemia, acidosis, ketone presence in plasma/urine

60
Q

Cause of Wernicke’s encephalopathy

A

Thiamine deficiency - alcoholism or complication of bariatric surgery.
Treatment is thiamine.

61
Q

Signs and symptoms of Wernicke’s encephalopathy.

A

Confusion, dementia, ataxia, nystagmus, opthalmalplegia and coma.
Petechial haemorrhages in mammillary bodies, dorsal brain stem structures affected.

62
Q

Investigations for Wernicke’s encephalopathy

A

FBC: low platelets, high mean corpuscular volume (chronic ethanol ingestion)
slightly low phosphate (malnutrition)
slightly high bilirubin
High serum ethanol

63
Q

Hepatic encephalopathy - cause.

A

Hepatic dysfunction

64
Q

Hepatic encephalopathy - signs and symptoms

A

Confusion, reduced consciousness.
Stigmata of chronic liver disease
Investigations show reduced hepatic synthetic function and elevated plasma ammonia.

65
Q

Ethanol toxicity

A

Disinhibition, ataxia, and reduction in consciousness.

66
Q

Methanol toxicity - signs and symtoms

A

Metabolic acidosis, optic nerve toxicity.

Clinical suspicion, osmolar gap and plasma methanol.

67
Q

What are the causes and results of ethylene glycol toxicity?

A

Ethylene glycol toxicity is caused by ingesting anti-freeze.

Initially similar to ethanol toxicity, leading to metabolic acidosis, cardiovascular issues and acute renal failure.

68
Q

What do urea cycle defects lead to?

A

High ammonia.

69
Q

Anion gap calculation

A

[cations] - [anions]

70
Q

Normal anion gap acidosis is caused by

A

Bicarbonate loss or H+ ingestion as ammonium chloride.

71
Q

Increased anion gap acidosis causes

A

Uraemia, ketoacidosis, lactate acidosis and salycylate poisoning.

72
Q

Which spinal tracts carry pain sensation?

A

Lateral thalamic tracts to somatosensory cortex.

73
Q

If disturbed sleep is associated with pain, what does this mean?

A

If there is peripheral pathology, this is a red flag. If it is central, sleep is always disturbed.

74
Q

What are the red flags for any peripheral pain?

A

Disturbed sleep, Systemic upset, weight loss, night sweats, inflammatory pain.

75
Q

35-50% of all blackouts in the elderly are caused by…?

A

Vascular disease

76
Q

Causes of bacterial meningitis in young babies

A

Group B Streptococcus (most common cause in neonates)
E. coli
Listeria monocytogenes

77
Q

Causes of bacterial meningitis in 3 months - 6 years

A

Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenzae

78
Q

Causes of bacterial meningitis in 6 years to 60 years

A

Neisseria meningitidis

Streptococcus pneumoniae

79
Q

Causes of bacterial meningitis in over 60s

A

Streptococcus pneumoniae
Neisseria meningitidis
Listeria monocytogenes

AAClinical school conditions (32 decks)

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