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5 - Neuro > deck_3051775 > Flashcards

deck_3051775 Flashcards

1
Q

How can you get CNS infections?

A

Direct spread e.g. trauma, middles ear infectionBlood borne e.g. sepsis, infective endocarditisIatrogenic e.g. ventriculoperitoneal shunt, lumbar puncture

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2
Q

How can you get a temporal lobe abscess?

A

Untreated middle ear infection

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3
Q

Define meningitis

A

Inflammation of the meninges

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4
Q

Give the causative organism for meningitis in a neonate

A

E coli, L monocytogenes

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5
Q

Give the causative organism for meningitis in a 2-5 year old

A

Haemophilus influenzae type B

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6
Q

Give the causative organism for meningitis in a 5-30 year old

A

Neisseria meningitidis

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7
Q

Give the causative organism for meningitis in an over 30 year old

A

Streptococcus penumoniae

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8
Q

How does meningitis present?

A

HeadacheNon-blanching rashNeck stiffnessPhotophobia

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9
Q

Define chronic meningitis

A

Has a chronic clinical course.Presents with: sub-acute headaches, increasing confusion, neurological signs

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10
Q

Give the common cause of chronic meningitis

A

Mycobacterium tuberculosis, causing granulomatous inflammation and fibrosis of the meninges. This leads to entrapment of the cranial nerves.

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11
Q

Give some complications of meningitis

A

Death - swelling and increased ICPCerebral infarctionCerebral abscessSubdural empyema

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12
Q

What is a subdural empyema?

A

Infection between dura mater and arachnoid mater

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13
Q

Describe encephalitis

A

Infection of the brain tissue. Usually a viral causes. Brain cells become haemmorhagic

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14
Q

Give some causes of encephalitis

A

Herpes virus - temporal lobePolio = spinal cord Rabies = brain stemLymphocytic inflammation reaction- signs of perivascular cuffing w/ lymphocytes in spaces around vessels in the brainCytomegalovirusToxoplasmosis

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15
Q

Describe the process involved in cytomegalovirus infection

A

Viral replication takes over cell body machinery. Causes eventual cell body destruction and death. Have Owl’s Eye inclusions

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16
Q

Describe the process involved in toxoplasmosis

A

Have toxoplasms in cells bodiesDestruction of cell body and death of neurone.

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17
Q

What is the cause of toxoplasmosis?

A

Caused by intracellular protein parasite Toxoplasm Gondii. Lives in guts of cats and humans are infected via contaminated cats faeces.

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18
Q

Describe prion diseases

A

Acts like an infection but isnt an infection. Prion proteins are found normally in the synapses. Mutations in these bins to normal PrPs, and undergo a post translational conformational change, to create more mutated prion proteins. This causes aggregates to form, which leads to neuronal death and holes in the grey matter

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19
Q

Describe the process of infection with a prion disease

A

Bovine spongiform encephalopathies in cowsNew variant creutzfeld-Jacob disease- infects humans if they have ingested mutated PrP from cows with BSE

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20
Q

Give some different types of dementia

A

AlzheimersVascular dementiaLewy Body DementiaPick’s Disease

21
Q

Give some characteristics of alzheimers

A

Exaggerated ageing processLoss of cortical neurones- decreased brain weight and cortical atrophy- caused by neuronal damage- neurofibrillary tangles caused by twisted filaments of Tau proteins- senile plaques due to amyloid deposition

22
Q

How does the intracranial pressure stay stable?

A

Change in volume of one component must be accompanied by an equal and opposite change in the volume of the other two. - brain- CSF fluid- blood

23
Q

What is normal intracranial pressure?

A

0-10 mmHg- rise to 20 mmHg when coughing or straining

24
Q

What are the three areas involved in compression and herniation with raised ICP?

A

Cingulate gyrusUncusCerebellar tonsils

25
Q

What are Tau proteins?

A

Proteins that normally bind and stabilise microtubules. They become hyperphosphorylated in Alzheimer’s disease.

26
Q

Describe senile plaques

A

Are foci of enlarged axons, synaptic terminals and dendrites.

27
Q

What can lead to a raised intracranial pressure?

A

Expanding foalc lesions- tumours, haematoma, abscess, infarction with oedemaGlobal increase in brain mass- oedema, inflammation, trauma

28
Q

Give the characteristics that will be seen with an expanding lesion

A

Deformation/destruction of brain around lesionSulci flattened against the skullDisplacement of midline structuresBrain shift, due to internal herniation

29
Q

Define hernia

A

A protrusion of an organ or part of an organ through the wall that normally contains it

30
Q

Describe a subfalcine/cingulate herniation

A

Occurs when ICP pushes cingulate gyruns under the free edge of the falx cerebri - ischaemia of middle parts of frontal and parietal lobe and corpus callosum- compression of anterior cerebral artery

31
Q

Describe a tentorial/uncal herniation

A

Uncus is pushed through the tentorial notch

32
Q

What is damaged in an uncal/tentorial herniation?

A

Damage to occulomotor nerve on same side- compression of cerebral peduncles- occlusion of blood flow in post. cerebral and sup. cerebellar arteriesCommonly is fatal due to secondary haemmorhage into the brainstem (midbrain or pons)

33
Q

Describe a tonsillar herniation

A

Cerebellar tonsils are pushed down into the foramen magnum and compress the brainstem

34
Q

Describe a central herniation

A

Dienchepalon and temporal lobes are pushed down through the tentorial notch.

35
Q

Give the clinical signs for RICP

A

HeadacheVomitingPapilloedemaAcute phase- occulomotor nerve compression (dilation of pupil)- brainstem compression (coma)Compression of the cerebral peduncles leads to hemiparesis

36
Q

What is the name of a benign brain tumour?

A

Meningioma

37
Q

Give the name of a malignant brain tumour

A

Astrocytoma- Grade 1 to grade 4(grade 4 is the most aggressive, few months to live)- Spreads along the nerve tracts and through the sub-arachnoid space - Commonly presents with spinal secondaries- Never metastasise outside the CNS

38
Q

What are the two phases of head injury?

A

Primary damage- due to force causing the injurySecondary damage- reaction to the primary damage causes further damage

39
Q

Describe primary damage

A

Due to movement of brain inside the skullFocal damage- bruising of brain as it hits the inner surface of the skullDiffuse damage- direct tearing to axons (Diffuse Axonal Injury)- tearing of nerves and small vessels, as well as to the pituitary stalk- heals by gliotic scarring

40
Q

What are the bones that make up the pterion?

A

Frontal ParietalSphenoidalTemporal

41
Q

Give the characteristics that you will see on imaging for a subdural haematoma

A

Midline shiftCompressed ventricleFlattened gyriCrescent shaped bright lesion

42
Q

Why do subdural haematomas occur?

A

Head trauma leads to tearing of bridging vessels as they pass from the cerebral hemispheres to the dura. Causes venous bleeds. Blood accumulate slowly, leading to a gradual rise in the ICP.

43
Q

Which type of people are particularly vulnerable to subdural haematomas?

A

Elderly and alcoholics- due to shrinking of the brain

44
Q

What are the three main patterns of MS?

A

Relapsing-remitting MSSecondary Progressive MSPrimary Progressive MS

45
Q

What is the main type of MS?

A

Relapsin-remitting- symptoms occur in attackts- onset over day, recovery in weeks- average of one relapse a year

46
Q

Describe secondary progressive MS

A

Late stage of MS- gradually worsening disability- slowly progresses over the years- relapsing-remitting will lead to this in 75% of cases

47
Q

Describe primary progressive MS

A

Last common form- gradually worsening disability with no relapses- typically presents later- associated with fewer inflammatory changes on MRI

48
Q

What are the common symptoms in MS?

A

Visual changesSensory symtpoms- water trickling down skin- reduced vibration sensationAtaxiaBladder hyper-reflexiaNeuropathic painFatigueSpasticityTemperature sensitivity- worsening of symptoms with increasing temperature

49
Q

What can occur with HIV that affects the CNS?

A

EncephalopathyNeuropathy

5 - Neuro (17 decks)

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