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Holibobs Revision of all Semester 1 (yr 2) diseases > Neuro > Flashcards

Neuro Flashcards

To learn the very basics

1
Q

basic pathology of diabetic neuropathy

A

nerve damage caused by diabetes, because high triglycerides and high blood glucose damages the nerves.

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2
Q

basic pathology of stroke (2)

A

ischaemic = infarction/ischaemia due to disrupted blood supply
haemorrhagic = intracranial bleeding

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3
Q

Causes of ischaemic stroke i.e. due to disrupted blood supply- 4

A

Thrombosis, atherosclerosis, shock, vasculitis

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4
Q

what’s vasculitis

A

group of conditions that cause inflammation of the blood vessels such as autoimmune vasculitis

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5
Q

first-line treatment for vasculitis

A

no cure… Anti-inflammatory medications, notably glucocorticoids such as prednisone or methylprednisolone, are the most common first-line treatments.

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6
Q

does TIA have infarction?

A

no

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7
Q

TIA is temporary neurological dysfunction lasting what length of time

A

less than 24 hours

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8
Q

Presentation of stroke- fast

A

FAST
facial weakness
(arm) limb weakness
speech difficulties
(TIME)

other symptoms
visual field defects
sensory loss
ataxia/vertigo

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9
Q

the combined contraceptive pill carries a tiny increased risk of what

A

stroke

risk is higher in patients with migraines with aura

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10
Q

what tool/score gives a score for patients with stroke like symptoms

A

rosier

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11
Q

TIA treatment/management (3)

A

aspirin 300mg daily immediately
referral to specialist treatment within 24 hrs
MRI scan imaging

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12
Q

Immediate management for stroke (excludetwo things, then give this drug)

Obvs admittance as well

A

exclude hypoglycemia
immediate CT scan to exclude haemorrhage
aspirin 300 mg daily

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13
Q

when is thrombolysis with alteplase considered for management of stroke

A

when haemorrhage is excluded, within 4.5 hours of symptom onset

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14
Q

thrombolysis is used in ST elevation myocardial infarction, true or false

A

true

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15
Q

In which type of stroke is blood pressure usually treated

A

Blood pressure is treated aggressively in haemorrhagic stroke

But in ischaemic stroke, lowering blood pressure can worsen the ischaemia

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16
Q

We believe the stroke was related to the patient’s atrial fibrillation. What treatment do we give?

A

anticoagulation such as apixiban

after excluding haemorrhage, and finishing two weeks of aspirin

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17
Q

Following a stroke: what imaging do we do to assess for underlying causes? (2) -most common being atrial fibrillation, and carotid artery stenosis

A

carotid imaging like carotid ultrasound or CT/MRI angiogram

ECG

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18
Q

secondary prevention of stroke- 2 meds and 2 general health things

A

clopidogrel
atorvastatin (statin to lower cholesterol)

blood pressure/diabetes control
addressing other risk factors like obesity, smoking, exercise

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19
Q

what’s clopidogrel

A

an antiplatelet

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20
Q

presentation of parkinsons -triad

A

resting tremor
bradykinesia
rigidity-resisting passive movement

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21
Q

what disease does this gait describe- stooped, fascial masking, forward tilt, reduced arm swing, shuffling gait

A

parkinsons

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22
Q

pathophysiology of parkinson’s

A

progressive loss of dopaminergic neurons in pathway originating in the substantia nigra of the basal ganglia.

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23
Q

importance of dopamine in regulation of movement

A

it’s a key neurotransmitter.

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24
Q

no dopamine in parkinson’s leads specifically to what

A

Therefore no dopamine, = increase in antagonistic indirect pathway = bradykinesia and rigidity

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25
Q

formation of lewy bodies/ protein clumps in parkinsons- true or false

A

true

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26
Q

Is the tremour in parkinsons the same on both sides or unilaterally worse

A

asymmetrical and importantly, worse at rest

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27
Q

pill rolling tremor seen in what disease

A

parkinsons

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28
Q

initial symptoms of Parkinson’s, seen before the triad of resting tremor, rigidity, and bradykinesia? (5)

A

sleep disturbance like sleepiness, or shouting/kicking etc during REM

low mood

autonomic symptoms like: constipation, light headed, excessive sweating or salivation

Motor troubles with handwriting

cognitive impairment

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29
Q

one bedside investigation of Parkinson’s, as well as cognitive assessment, is checking the difference between lying and standing blood pressure

A

patient’s with PD have postural hypotension

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30
Q

Diagnosis of PD is based on what

A

By a specialist, based on history and neuro examination findings

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31
Q

management of PD (3)

A

levadopa = first line
and this is taken with:

COMT inhibitors to prolong levadopa action, and decreases dopamine action

MOA-B inhibitors inhibit breakdown of dopamine

response decreases with time

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32
Q

Anti-parkinsonian medications are ‘critical medications’ and are time-sensitive. Patients who miss doses or receive late doses could experience

A

freezing (akinesia).

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33
Q

Deep brain stimulation for PD is reserved for who

A

It is reserved for those with severe symptoms refractory to medical management yet still fit with few co-morbidities.

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34
Q

Huntington’s pathology

A

autosomal, genetic error on chromosome 4, causing loss of striatum.

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35
Q

when do symptoms of huntington’s begin

A

age 30-50

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36
Q

How does harry Huntington present?

A

insidious, progressive worsening of symptoms: BASICALLY personality and cognitive problems, and chorea.

Followed by movement disorders like: weird posture, rigidity, eye movement difficulties, swallowing and speech difficulties

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37
Q

Death in Huntington’s is often due to what:

A

aspiration pneumonia, and suicide.

NB often falls etc due to frailty

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38
Q

Management of Huntington’s (3)

A

No cure/treatment. But can include:

tetrabenazine for chorea

anti-depressants e.g. SSRI’s

Speech and language therapy and physiotherapy

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39
Q

Life expectancy of someone with Huntington’s after diagnosis

A

10-20 years after onset of symptoms

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40
Q

Pathology of epilepsy

A

recurrent epileptic seizures of abnormal electrical activity from a specific focus that spreads throughout the brain

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41
Q

how do epileptic seizures manifest

A

usually they manifest with motor and sensory symptoms, and often associated with reduced consciousness levels

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42
Q

Seizures can either be motor or non-motor. But they are either classified as:

A

focal, generalised, or unknown origin

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43
Q

Are you conscious during a focal/partial seizure?

A

maybe, maybe not

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44
Q

generalised/tonic clonic seizures often affect what parts of the brain

A

both cerebral hemispheres

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45
Q

which type of seizure can have an aura

A

focal - like a premonition that something is about to happen

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46
Q

an absence seizure is a type of generalised seizure. Is it more often seen in children or adults?

A

children

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47
Q

what is seen in a tonic clonic seizure?

A

stiffening followed by intermittent jerking movements

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48
Q

could tinnitus and vision loss ever be aura for seizure? or not

A

yes

also unusual emotions, strange smells/sensations etc, abnormal behaviours, deja vu.

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49
Q

what investigations for epilepsy

A

EEG (electrodes placed on patient’s head)
MRI brain to detect tumour

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50
Q

why would you look at Capillary blood glucose in epilepsy

A

To identify hypoglycaemia, an important reversible cause of seizures

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51
Q

what 4 investigations can be considered in epilepsy to exclude important pathology

A

ECG

serum electrolytes

blood glucose (for hypoglycaemia)

blood and urine culture and lumbar puncture if sepsis, encephalitis or meningitis suspected

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52
Q

First line therapies for epilepsies

A

Lamotrigine or Levetiracetam- if men/can’t have children AND it’s generalised, then sodium valproate.

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53
Q

what does sodium valproate do

A

calms the brain by increasing GABA.

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54
Q

what’s status epilepticus

A

medical emergency when:

seizure lasts more than 5 mins, or multiple seizures when consciousness isn’t regained.

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55
Q

management of status epilepticus

A

ABCDE incl giving oxygen and inserting cannula, securing airway, and checking blood glucose

A benzodiazepine first-line, repeated after 5-10 minutes if the seizure continues

Second-line options (after two doses of benzodiazepine) are IV levetiracetam, phenytoin or sodium valproate

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56
Q

Options for benzodiazepines are:

A

Buccal midazolam (10mg)
Rectal diazepam (10mg)
Intravenous lorazepam (4mg)

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57
Q

Myasthenia Gravis is an autoimmune condition that consists of fatigable fatigue. What does it affect?

A

The neuromuscular junction, because of acetylcholine receptor antibodies

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58
Q

Myasthenia gravis affects men and women at different ages:

A

typically affecting women under 40 and men over 60.

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59
Q

Myasthenia gravis is strongly linked with what tumour

A

thymoma, a thymus gland tumour

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60
Q

what causes cell damage at the post synaptic membrane in myasthenia gravis, further worsening symptoms?

A

acetylcholine receptor antibodies

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61
Q

muscle weakness in the face causes what symptoms in myasthenia gravis?

A

difficulty swallowing, fatigue in jaw when chewing, slurred speech, double vision, droopy eyelids/ptosis.

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62
Q

if we want to elicit symptoms in clinic of myasthenia gravis, what would we ask to do.

A

repeated blinking, and prolonged upward gazing

and check for thymoma scar

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63
Q

investigations: what antibody tests for myasthenia gravis?

A

AChR antibodies

also CT and MRI to look for thymoma

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64
Q

what happens in the endrophonium chloride test

A

blocks the cholinesterase enzymes that break down acetylcholine. If little rise = positive test.

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65
Q

What treatment for myasthenia gravis? (3)

A

pyridostigmine = cholinesterase inhibitor

immunosuppression like prednisolone

thymectomy even when no thymoma

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66
Q

respiratory failure in myasthenia gravis = (2)

A

immunoglobulins and ventilation

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67
Q

pathophysiology of motor neuron disease

A

progressive degeneration of all motor neurons- upper and lower

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68
Q

Muscle wasting
Reduced tone
Fasciculations (twitches in the muscles)
Reduced reflexes

is this lower or upper neuron disease

A

lower

so basically reduced, + fasciculations

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69
Q

Increased tone or spasticity
Brisk reflexes
Upgoing plantar reflex

is this upper or lower

A

upper

increased everything incl. brisk reflexes

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70
Q

What can slow the progression of the disease and extend survival by several months in ALS? (ALS is the most common type of motor neuron disease).

A

Riluzole

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71
Q

breathlessness worsened by anxiety in motor neuron disease- what might we give?

A

benzodiazepine (depressant)

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72
Q

why would you give an anti-muscarinic for motor neuron disease

A

excessive saliva

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73
Q

what for muscle spasticity (upper) do you give, in motor neuron disease?

A

baclofen

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74
Q

how does baclofen work?

A

muscle relaxant by reducing nerve transmission

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75
Q

what is a subarachnoid haemorrhage?

A

haemorrhage between the arachnoid mater, and the pia mater.

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76
Q

Difference in clinical presentation of the haemorrhages?

extra-dural
sub-dural
sub-arachnoid

A

Extra-dural- lucid interval, then unconsciousness

Sub-dural- Gradual deterioration

Sub-arachnoid- Thunderclap headache/ sudden onset of symptoms

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77
Q

Pathology of different haemorrhages?

A

Extradural = middle meningeal artery

Sub-dural = rupture of bridging veins

Sub-arachnoid = rupture of berry aneurysm

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78
Q

Management for haemorrhages

A
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79
Q

cocaine use is associated with what type of haemorrhage

A

sub-dural

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80
Q

typical history of sub-arachnoid haemorrhage?

A

sudden onset occipital headache during strenuous activity like heavy lifting or sex

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81
Q

what additional symptoms for arachnoid haemorrhage? (4)

A

1) neck stiffness
2) photophobia
3) vomiting
4) neurological symptoms like visual changes, dysphasia, focal weakness, seizures etc).

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82
Q

First line investigations in haemorrhage

A

CT head (normal doesn’t exclude subarachnoid haemorrhage)

lumbar puncture to check for bilirubin (looks yellow)

then:
CT angiography to find exact source of bleeding

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83
Q

why use nimodipine after subarachnoid haemorrhage?

A

calcium channel blocker used to prevent vasospasm - narrowing of arteries causing brain ischaemia

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84
Q

treatment of hydrocephalus

A

lumbar puncture, external ventricular drain
ventriculoperitoneal shunt

85
Q

Myelin covers the axons of neurones and helps electrical impulses travel faster. Myelin is provided by cells that wrap themselves around the axons:

Oligodendrocytes vs Schwann cells, which for central vs peripheral nervous system

A

Oligodendrocytes in the central nervous system
Schwann cells in the peripheral nervous system

86
Q

Multiple sclerosis: does it affect oligodendrocytes, or Schwann cells

A

oligodendrocytes, because it affects the central nervous system.

87
Q

Recurring episodes of optic neuritis could be what condition

A

MS

88
Q

Lesions in MS are uniform, true or false

A

False
Lesions vary in location, and so affected sites and symptoms change over time

89
Q

optic neuritis- unilateral or bilateral reduced vision that develops over what time period?

A

hours or days- important to know- not like REALLY sudden, and it’s unilateral

90
Q

optic neuritis causes relative afferent pupillary defect, and a central blind spot called a scotoma. Is this painful or painless?

A

painfull

91
Q

how to treat optic neuritis

A

high dose steroids

92
Q

There is:
relaxing-remitting
primary progressive
secondary progressive.

What’s the difference between primary and secondary progressive?

A

secondary = used to be relaxing remitting, but now it’s simply progressing

93
Q

Diagnosis for MS is based on history of lesions changing location over time, where other causes are excluded. What are the two investigations that can support the diagnosis?

A

MRI scans to demonstrate typical lesions
Lumbar puncture can detect oligoclonal bands in CSF.

94
Q

Relapses of MS can be treated with what

A

steroids
500mg orally
or 1g intravenously daily for 3-5 days

95
Q

Urge incontinence in MS can be treated with

A

antimuscarinic medications

96
Q

What is the analgesic ladder?

A

non-opioid meds such as paracetamol vs NSAIDs

weak opioids such as codeine and tramadol

strong opioids such as morphine, oxycodone

97
Q

Guillain-Barre pathology?

A

neuropathy of the peripheral nervous system triggered by an infection

98
Q

Is Guillain barre symmetrical or asymmetrical, and is it sensory or motor?

A

symmetrical, ACUTE ascending weakness and sensory weakness… a tingle in my toes.

also reduced reflexes

99
Q

symptoms within how many weeks of infection (e.g. gastroenteritis) , and what recovery time

A

4 weeks
recovery period = months to years

100
Q

investigation of guillain barre

A

lumbar puncture - showing raised protein count normal cell count and normal glucose

nerve conduction studies showing reduced signal through the nerves

101
Q

management of guillain barre

A

supportive care

VTE prophylaxis - as pulmonary embolism is leading cause of death

IV immunoglobulins

102
Q

How long can recovery take for Guillain barre syndrome?

A

months to up to 5 years.

103
Q

Important characteristics of a cluster headache

A

sudden onset, severe, unbearable, UNILATERAL pain behind one eye

104
Q

How long do cluster headaches last?

A

15 mins-3 hours (pain peaks abt 15 mins)
3-4 a day

105
Q

(importantly) Visible signs of a cluster headache?

A

red, swollen, watering eye and nasal discharge

NB cluster headaches very much involve the eye, with miosis, ptosis, pupil constriction, facial swelling

106
Q

Acute management of cluster headache

A

triptans like sumatriptan and high flow oxygen

107
Q

Prophylaxis for cluster headache (suppress not eliminate factors causing a cluster headache)

A

prednisolone and verapamil

108
Q

Do tension headaches have any visual changes?

A

no

109
Q

Management for acute migraine? (zig zags)

A

sumatriptan and NSAIDs analgesics

110
Q

Prophylaxis for migraine?- first line and second line

A

1) propranolol (beta blocker that slows heart rate)

2) topiramate (espc. when propranolol is contraindicated e.g. in asthma)

111
Q

when propranolol is contraindicated as prophylaxis for migraine

A

asthma

112
Q

pathology of idiopathic intracranial hypertension

A

high pressure of unknown cause around the brain causing symptoms such as vision changes and headaches.

113
Q

3 main symptoms of intracranial hypertension

A

headache
blind spot
peripheral vision loss

can also get double vision

114
Q

Chief sign of intracranial hypertension

A

bilateral papilledema

115
Q

What exacerbates the symptoms of intracranial hypertension?

A

worse in the morning
worse leaning forward
worse when coughing/sneezing

116
Q

If intracranial hypertension is caused by an increase CSF, what is the management?

A

acetazolamide = this reduces CSF production, and also helps with the headaches

also diuretic = excrete more fluid

117
Q

what tumour causes bitemporal hemianopia

A

pituitary adenoma causing optic chiasm compression

118
Q

lesions affecting the flocculondular lobe =

A

vertigo and nystagmus

119
Q

raised intra-ocular pressure causes what affect on the optic disc

A

cupping

120
Q

High protein vs high glucose in lumbar puncture meaning?

A

high protein = viral
high glucose = bacterial

121
Q

fever, altered mental status, seizures, focal neurological deficits, vomiting, neck stiffness.

We know neck stiffness is often meningitis, but what two other things could it be?

A

encephalitis and brain abscess

espc after infection or brain injury

122
Q

Encephalitis pathology-

A

It means inflammation of the brain. Could be viral most commonly, or autoimmune next commonly.

123
Q

Most common viral causes of encephalitis

A

herpes simplex virus HSV

also VZV associated with chicken pox.

124
Q

Why do we ask about vaccinations with encephalitis

A

measles, mumps, rubella, polio viruses can cause

125
Q

Presentation of encephalitis (4)

(Knowing it starts with flu like symptoms)

A

Altered mental status and behaviour
Fever
Focal seizures
Focal neurological symptoms

126
Q

3 Investigations to help diagnose encephalitis?

A

1) lumbar puncture if GCS above 9- send CSF for viral PCR testing
2) MRI scan after lumbar puncture to visualise brain

HIV testing is recommended in all patients with encephalitis

127
Q

Management of encephalitis (1 and support)

A

aciclovir treats HSV and VZV. IT IS STARTED EMPIRACALLY in suspected encephalitis until results are available.

ganciclovir treats CMV (cytomegalovirus)

Then just supporting them recover.

128
Q

Acute management of MS? (2)

A

glucocorticosteroids like prednisolone
or
IV methylprednisolone

129
Q

What benefit/when do you use natalizumab in MS?

A

It’s a disease modifying therapy (DMT) that blocks leukicytes in the brain therefore decrease in inflammation. For relaxing and remitting, given by injection by nurse.

130
Q

Triad of signs of Horner’s

A

1) Decreased sweating
2) Drooping eyelids
3) Decreased pupil size

131
Q

Horner’s: lesion is on the parasympathetic or sympathetic?

A

sympathetic

132
Q

what do we use to diagnose Horner’s?

A

eyedrops
apraclonidine: to reverse pupillary constriction, because it has agonistic effect on alpha-2-receptors

133
Q

what tumour commonly causes Horner’s? With what symptoms?

A

Pancoast tumour- with cough and weight loss

so do CXR

134
Q

What’s a Pancoast tumour?

A

cancer starting in apex of the lung

135
Q

Is there a cure for Horner’s?

A

no
just treat underlying condition e.g. cancer

136
Q

lesion for Horner’s is on what side of the sympathetic system?

A

ipsilateral side to the symptom

137
Q

What is giant cell arteritis?

A

inflammation of arteries in the temples

138
Q

Key complication of giant cell arteritis?

A

Vision loss, which is often irreversible. Therefore emergency.

139
Q

Symptoms of giant cell arteritis? incl headache, (3)

A

UNILATERAL HEADACHE

scalp tenderness
jaw claudication
blurred/double vision

140
Q

Management of giant cell arteritis?

A

prednisolone 40-60mg daily

141
Q

Management of giant cell arteritis WITH jaw claudication?

A

500-1000mg daily methylprednisolone

142
Q

Over what length of time would you wean a patient off steroids in giant cell arteritis?

A

Over 1-2 years

143
Q

How to diagnose giant cell arteritis? (3)

A

Based on:
1) clinical presentation
2) Raised inflammatory markers, particularly ESR
3) Temporal artery biopsy showing multinucleated giant cells

144
Q

What’s ESR?

A

a blood test

145
Q

Narcolepsy pathology?

A

Loss of orexin signalling cells in the hypothalamus. So low levels of orexin in CSF.

146
Q

Most cases of narcolepsy are due to

A

Autoimmunity.

147
Q

Cataplexy is often seen in narcolepsy. (as well as excessive daytime sleepiness, hallucinations when emerging from REM, and sleep paralysis).

What is cataplexy?

A

sudden muscle weakness triggered by strong emotions like laughter or surprise.

head falls forward, jaw drops, knees buckle. lasts 30 secs to 2 mins

148
Q

Manage narcolepsy?

A

1) anti-depressants or sodium oxybate for cataplexy
2) modafinil (central nervous system stimulant) first line for excessive stimulants

149
Q

Investigate narcolepsy how? 1)

A

CSF orexin levels

Best: multiple sleep latency test

150
Q

Theory of sleep: what builds up throughout the day, at and threshold leads to sleepiness?

A

adenosine

151
Q

Caffeine is an antagonist to what receptors?

A

adenosine receptors

152
Q

melatonin comes from where

A

pineal gland

153
Q

cauda equina is neuropathy of what

A

nerve roots

meaning numbness, peeing problems and sexual dysfunction

154
Q

is cauda equina syndrome bilateral or ipsilateral

A

bilateral

155
Q

is cauda equina an acute emergency, or chronic

A

emergency because if left untreated, = permanent paralysis

156
Q

how quickly do you need to do surgery for cauda equina

A

8 hours

157
Q

investigate cauda equina =

A

MRI to check for compression

158
Q

treat cauda equina how

A

lumbar decompression surgery and analgesia

159
Q

fever, neck stiffness and altered mental state = what

A

triad of symptoms for meningitis

also rash

160
Q

investigate/diagnose meningitis how?

A

Lumbar puncture for CSF findings, and blood culture for infection

161
Q

why photophobia in meningitis

A

irritation of the meninges around the diaphragma sellae

162
Q

when does meningitis become encephalitis

A

when the irritation of the brain occurs, because limited bacteria can get through the blood brain barrier

irritation of brain = focal neurological signs, and seizures, vomiting etc.

163
Q

management of meningitis

A

dexamethasone, IV

164
Q

meningitis vs encephalitis- which is more likely to have aphasia, behaviour change, visual disturbance

A

encephalitis

165
Q

management of encephalitis (3)

A

antibiotics
anti-convulsant
corticosteroids

166
Q

what condition does riluzole treat

A

motor neuron disease

167
Q

pathology of cavernous sinus thrombosis

A

infection spreads from nearby areas such as nose (sinusitis) to the cavernous sinus- the space behind the eyes and underneath the brain. A blood clot develops to stop the infection from spreading. Retrograde flow of venous blood leads to an increase in pressure.

168
Q

what nerve is compressed in cavernous sinus thrombosis?

A

oculomotor nerve

169
Q

why could the brain be damaged in cavernous sinus thrombosis

A

because blood to the brain is disrupted

170
Q

treat cavernous sinus thrombosis how?

A

antibiotics immediately
and
anticoagulants like heparin
and
corticosteroids for swelling/inflammation

171
Q

Korsakoff syndrome is a complication of what, and is characterised by what

A

Wernicke’s encephalopathy- where is becomes dementia, so it’s characterised by irreversible deficits in anterograde and retrograde memory

172
Q

Wernicke’s encephalopathy pathology

A

alcohol blocks thiamine- B12

173
Q

manage wernicke’s encephalopathy how

A

replace thiamine via IV very quickly

174
Q

triad for wernickes encephalopathy

A

ataxia
nystagmus
confusion

so eyes, gait, confused

175
Q

thiamine deficiency can impair processes like

A

the utilisation of carbs for energy therefore affects all organs

affects synthesis of neurotransmitters, and myelination etc.

176
Q

we know alzheimer’s is associated with amyloidosis (build up of amyloid plaques and tau proteins. It’s also seen with the loss of what

A

cholinergic neurons

177
Q

manage Alzheimer’s how

A

cholinesterase inhibitors (because reduced acetylcholine causes some symptoms).

178
Q

Give three examples of cholinesterase inhibitors

A

donepezil, rivastigmine, galatamine

179
Q

Biggest presenting complaint of glaucoma

A

peripheral vision loss

180
Q

All symptoms of glaucoma (5)

A

headache
blurry vision
halo’s around lights
fluctuating pain

181
Q

does the pupil cup in open angle or acute angle closure glaucoma?

A

acute angle closure

182
Q

In glaucoma, what’s causing damage to the optic nerve?

A

raised-intraocular pressure

183
Q

How to surgically treat glaucoma?

A

laser trabeculoplasty
or
trabeculectomy surgery

184
Q

Which eye drops treat inflammation in glaucoma?

A

prostaglandin eye drops

185
Q

Why use beta blockers in glaucoma?

A

Inhibits production of aqueous humour

186
Q

Do you treat guillain barre or myasthenia gravis with cholinesterase inhibitor like pyridostigmine?

A

MG

187
Q

Normal pressure hydrocephalus: what does ‘wet, wacky, wobbly’ mean?

A

dementia
urine problems
difficulty walking

188
Q

pathology behind normal pressure hydrocephalus?

A

Increased CSF, leading to increased ICP (NB- the CSF looks normal, but ventricles are enlarged).

189
Q

4 examples of things that would block flow/absorption of CSF, thus leading to normal pressure hydrocephalus

A

subarachnoid haemorrhage

meningitis

head injury

surgical complications

190
Q

Treat normal pressure hydrocephalus how? (2)

A

1) therapeutic lumbar puncture
2) shunt CSF from brain to abdomen

191
Q

which type of dementia has hallucinations, is rapidly progressive, and has parkinsonian symptoms?

A

Lewy body dementia

192
Q

lewy body protiens in parkinsons vs lewy body dementia?

A

dementia = throughout brain,
vs
parkinsons = just deposited in the substantia nigra

(if physical symptoms before cognitive decline, then it’s Parkinson’s!)

193
Q

Which type of dementia has loads of hallucinations? (also mainly affecting motor skills and judgement).

A

vascular

NB stepwise with lots of cerebrovascular infarcts

194
Q

lumbar spinal stenosis is narrowing therefore compression of spinal nerves in the lumbar region. What symptoms?

A

pain, discomfort especially during physical activity. Claudication in thigh and buttock.

195
Q

When lumbar spinal stenosis (which would cause claudication) is caused by a tumour, what symptoms also?

A

weight loss, night sweats and other systemic symptoms

196
Q

When lumbar spinal stenosis (which would cause claudication) is caused by a herniated lumbar disc, what is it:

exacerbated by?
relieved by?

A

exacerbated by flexion
relieved by extension

197
Q

what usually causes coma?

A

toxic metabolic state

198
Q

depressed respiration during coma is usually caused by what

A

drug over dose

199
Q

Cushing’s triad

A

increased intracranial pressure = decrease in heart rate, increase in blood pressure, irregular breathing

200
Q

how would we correct clotting issues in a haemorrhage of the brain

A

platelet transfusions
vitamin k if warfarin previously used

201
Q

why would you give tetrabenazine to someone with Huntington’s

A

it inhibits dopamine uptake

202
Q

where do you place the tuning fork in rinne test, and what does it test?

A

bone conduction
anterior and posterior

203
Q

where do you place the tuning fork in weber’s test, and what does it test?

A

Sensio neural hearing loss, middle of forehead

204
Q

negative Rinne means whats

A

means bone conduction is greater than air conduction

205
Q

would a positive or negative Rinne mean that sound is greater in the bad ear?

A

negative

206
Q

What’s the meaning of the acronym, FOSSIT?

A

feeling of something stuck in throat

207
Q

What’s the meaning of the acronym, FOSSIT?

A

feeling of something stuck in throat

208
Q
A

Holibobs Revision of all Semester 1 (yr 2) diseases (5 decks)

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