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Case 16 Flashcards

1
Q

What are the general routes of bloodbourne infection ? (4)

A

Peripheral nerves, local from ears/sinuses, local injury (face/skull/spine), congenital

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2
Q

How do blood Bourne infections differ depending on their path of transfer ?

A

Across the blood brain barrier -> Encephalitis

Across the blood CSF barrier -> Meningitis

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3
Q

How do the BBB and blood CSF barrier differ in terms of structure ?

A

BBB - astrocyte footplates, thick BM, endothelium (no fenestrations)
Blood CSF barrier - choroid plexus, thin BM, endothelium (with fenestrations)

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4
Q

How can microbes traverse the barriers into the CNS?

A

Grow across (infect cells that comprise the bacteria) , Passive transport across in intracellular vacuoles, carried in via infected WBCs, invasion via peripheral nerves

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5
Q

How does Rabies track to the CNS ?

A

Bite site -> muscle -> peripheral nerves -> CNS glial cells/nerves where it multiplies

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6
Q

What are the common bacterial causes of meningitis ?

A

Streptococcus pneumoniae, Neisseria Meningitidis, Listeria monocytogenes

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7
Q

Which form of meningitis is more serious and why ?

A

Bacterial because it can develop into invasive sepsis -> multiple organ failure -> cognitive/limb dysfunction -> death

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8
Q

How do bacterial causes of meningitis vary with age ?

A

Listeria monocytogenes occurs in the extremes of age.

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9
Q

What are the risk fx for bacterial meningitis ? (3)

A

Newborn (weak immune system, passed on at birth), community setting (large groups ^spread), travel (sub Sahara, Mecca)

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10
Q

What are the common signs and sx for meningitis in a kid ?

A

Tense bulging fontanelle (soft spot), fever, cold, extremities , stiff neck, abnormal behaviour, blotchy skin/rash

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11
Q

What are the 3 key signs of meningitis for an adult ?

A

Fever, stiff neck, severe headache

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12
Q

When is CT indicated for meningitis ? (5)

A

GCS drops, new focal neurology, ^ICP, papilloedema, immunocompromised (^susceptible to infection)

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13
Q

LP is normally performed if meningitis is suspected. When is it CI? (4)

A

^ICP (GCS down) , extensive/spreading purpua, shock/convulsion/coag abnormalities, superficial infection at LP site.

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14
Q

How is bacterial meningitis indicated in LP results ?

A

Yellow/turgid, ^P, ^polymorphs, ^protein, glucose drops

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15
Q

How is viral meningitis indicated in LP ?

A

Clear fluid, ^lymphocytes, normal everything else

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16
Q

How are TB and fungal results similar and different on LP ?

A

Same; yellow/viscous fluid, ^/normal P, normal polymorphs, ^lymphocytes
Different; TB has ^protein , Glucose decrease in TB whereas normal/low in Fungal

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17
Q

How would you manage bacterial meningitis ?

A

abx and steroids ->Cefotaxine, Ceftriaxone +/- Vancomycin if in area of drug resistance.

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18
Q

When does mx of bacterial meningitis change ?

A

With newborns give Ampicillin/amoxicillin as it covers listeria
Can’t give Ceftriaxone with a Ca containing infusion.

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19
Q

What is significant about Meningitis ?

A

It’s a notifiable disease, consultant in communicable disease control needs to be alerted.

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20
Q

What medication is given close contacts of those infected with meningitis ?

A

Ciprofloxacin and rifampicin (chemoprophylaxis)

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21
Q

Viral meningitis is ^common but milder form. What are the main causes ? (4)

A

HSV, mumps (paramyxovirus), enteroviruses (Coxsackie, polio), HIV

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22
Q

What is encephalitis and what is major UK cause ?

A

Acute inflam/swelling of brain from infection/immune response. V rare, most common is HSV1.

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23
Q

How would you dx and tx Encephalitis ?

A

CSF for viral PCR + microscopy, culture/sensitivies, blood culture.
Tx; Aciclovir (antiviral)

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24
Q

What is cerebral abscess ?

A

Infection of brain ^mass of pus in or around skull (sinuses, otitis media, dental abscess)

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25
Q

What are the sx of expanding intracranial mass ?

A

4 F’s; fever, fits, focal, fatal

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26
Q

What happens when infections spread intracranially from the ‘danger triangle of the face’?

A

Septic cavernous sinus thrombosis

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27
Q

What is furious rabies ?

A

80% of infections. dysfunction/invasion of limbic system decreases inhibition so aggression ^. ^saliva and aversion to H2O

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28
Q

Where does rabies go once px bitten ?

A

replicated in skeletal muscle, binds to Ach receptors at neuromuscular junction travels within axons in peripheral nerves via retrograde fast ch. Replictes in motor neurone of spinal cord and DRG ^to brain.

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29
Q

What are the common CNS infections in immunocompromised px ?

A

CMV, mycobacterium TB, crytococcus neoformans (fungal meningitis)

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30
Q

How is the cortex differentiated?

A

Rim of grey matter (cell bodies) that surround white (connections)

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31
Q

What are the signs of an UMN lesion ?

A

No wasting. Spastic tone , pyramidal decrease power, brisk reflexes, planter response, fasciculations.

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32
Q

What is the classical presentation of extradural haemorrhage ?

A

Brief LOC -> Lucid interval -> sudden drop of headache, vomit, LOC, pupil problems

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33
Q

What is the cause of subdural haemotomas ?

A

Ruptured bridging veins, common in OAPs and alcoholics. Venous blood, worse outcome

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34
Q

Why would you give Nimodipine for subarachnoid haemorrhage ?

A

CCB so reduces vessel spasm risk. refer to neuro to clip aneurysm

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35
Q

What is the flow of CSF ?

A

Ependymal cells in choroid plexus -> lat ventricle -> foramen of monro -> 3rd -> aqueduct of slyvius -> 4th -> foramen of Lushcka (2 lat) and Forman of magendie (midline) -> midbrain -> sup sagittal sinus.

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36
Q

What are the causes of obstructive hydrocephalus ? (4)

A

tumour, abscess, cyst, congenital aquaduct stenosis

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37
Q

What are the causes of non obstructive/communication hydrocephalus ? (4).

A

intracranial haemorrhage (SAH, IVH), infection, meningitis, post trauma

38
Q

What is the tx for communicating hydrocephalus ?

A

Ventroperitoneal shunt, tube in lat ventricle down skin into peritoneum that absorbs CSF, goes past the obstruction.

39
Q

What are the causes of cauda equina syndrome ?

A

herniated lumbar disc, generative spinal stenosis, tumour, trauma

40
Q

What is the RAS ?

A

Reticular activating system, network processes info of brainstem hypothalamus cerebral cortex before cerebrum

41
Q

What are the indicators of GCS and how many is each category out of ?

A

14/15 - mild, 9-13 - moderate, <8 severe/coma

E/4 , V/5, M/6

42
Q

How is the verbal score broken down for GCS ?

A 
5 = normal response 
4 = confused/incorrect 
3 = random words 
2 = random noises 
1 = no response
43
Q

How is the motor score broken down on GCS ?

A 
6 = obeys commands 
5 = localise to pain
4 = withdraw from pain 
3 = Abnormal flex response 
2 = Abnormal ext response 
1 = No response
44
Q

What are the common non-neuro causes of coma

A

hypoglycaemia, hyponatremia, drugs, alcohol. (generalised brain tissue failure)

45
Q

What is the normal ICP and what are the contents of the cranial vault ?

A

5-15 mmHg

Vol = tissue (1400ml) , CSF (150ml), blood (150ml)

46
Q

What is the compensation mechanism as ICP ^ ?

A

blood and CSF move into spinal canal and extra cranial vasculature.

47
Q

What is Cushing’s triad and what does it indicate ?

A

Hypertension, bradycardia, irreg (normally decrease RR)

Indicates brainstem compression

48
Q

Why does the pupil become fixed and dilated in intracranial hypertension ?

A

Descending P on CN3 (autonomic constrictor) so paralysis -> dilation.

49
Q

What is indicated by P1, P2, P3 on the ICP waveform ?

A

P1, heart contraction
P2, tidal wave through brain tissue
P3, aortic valve closes small lift in pressure

50
Q

What is the indication if P2>P1 ?

A

Suggests high pressure/non compliant brain

51
Q

How would you open the airway in an unconscious px ?

A

Jaw thrust, thumbs behind jaw angle bring forward. Lifts tongue out of post pharynx

52
Q

What type of O2 would you give to a px to help with breathing ?

A

Mask with reservoir bag delivers high conc O2 and 15L/min. Target PO2 >94.

53
Q

What type of fracture is indicated by CSF leakage from the ear and nose ?

A

Basal skull fracture, compromising MMA

54
Q

When is Mannitol used ?

A

When bleeding has stopped assuming bbb is intact to decrease ICP. Draws out fluid from nerve tissue.

55
Q

What medication would be used to decrease ICP in a non trauma setting ?

A

Dexamathasone. Tissue swelling or inflammation.

56
Q

What is the MOA of Midazolam ?

A

Benzodiazepine ^GABA suppression of nerve activity. ^Cl ions in neurons which hyper polarises them to decrease AP.

57
Q

What is the name of an oral drug that is indicated for long term decrease in epileptic seizures ?

A

Carbamazepine. Inhibits aberrant CNS Na ch as GABA agonist.

58
Q

Px has 2 seizures in the space of 5 mins with no return to normal, what drug is first line ?

A

Midazolam (a benzodiazapine)

Life threatening status epileptics.

59
Q

What changes would be seen in a parietal lobe lesion ?

A

Attention deficits eg. contralat hemispatial neglect syndrome -> px doesn’t pay attention to side of body opposite lesion.

60
Q

What is the difference between agnosia and prosopagnosia and which area of the brain is affected ?

A

Agnosia - auditory px can’t recognise basic sounds
Prosopagnosia - can’t recognise faces
Temporal lobe

61
Q

What is the function of the angular gyrus ?

A

Relates language info. Located in the parietal lobe near the other brain areas.

62
Q

What area connects Broca’s and Wernicke’s and what action will the px be unable to perform if damage occurs ?

A

Arcuate fasciculus. Px can’t repeat auditory info.

63
Q

What are the 3 canals in the cochlea and what ions do they contain ?

A

Scala tympani and vestibuli contain ^Na ‘perilymph’

Scala media ^K ‘endolymph’

64
Q

Nerves cause organ of court and tectorial membrane to bounce disturbing the stercocilia (inner hair cells). what next ?

A

Mechanically gated K ch open on stercocilia, K from endolymph ^ membrane potential. Ca ch open , Ca -> release NT -> activates auditory nerves -> signal to brain.

65
Q

What is the difference between the medial and anterior temporal lobes ?

A

Medial creates LTM, role in episodic declarative involves hippocampus
Lateral creates semantic memory

66
Q

What is the action of the cerebellum and basal ganglia. How do they relate to temporal/limbic lesions ?

A

Non declarative (procedural) memory. Lesions to temporal preserve px ability to perform motor skill but they’ll lack the ability to remember having performed said skill

67
Q

What are the parts of the basal ganglia ? (4)

A 
Caudate nucleus (eye move)
Putamen (proceed/anticipate movement)
Globus pallidus (reg muscle tone for action)
Substantia nigra (reg sub conc activity in muscles)
68
Q

Why do the different presentations of Lewy body dementia and Parkinsons arise ?

A

LDB , cortex then basal ganglia so cognitive goes before movement
Parkinsons, mostly basal ganglia so cognitive 2nd

69
Q

What is the function of the ant cingulate cortex ?

A

Frontal section of cingulate gyrus for attention and distraction. activated in pain, modulated in chronic pain to decrease suffering .

70
Q

What is delirium ?

A

Mental confusion from being medically unwell eg. surgery, meds. acute onset, self aware, daily live varies, STM impaired, disturbed sleep.

71
Q

Which inflammatory markers are produced during delirium ?

A

CRP, IL-1, IL-6, TNF-a

72
Q

How can stress cause delirium?

A

^sympa tone and decreases para -> impairs cholinergic function -> delirium.

73
Q

Which artery is occluded in lateral medullary syndrome ?

A

Post inferior Cerebellar artery

74
Q

What signs are shown during lateral medullary syndrome ? (6)

A

Spinothalamic (contra loss pain and temp body) , trigeminal tract (ipsilat loss of pain and temp face), dysphagia (nucleus ambiguous), ispilat Horner’s (DLF), vertigo (vestibular nuclei), ipsilat ataxia (spinocerebellar tract)

75
Q

What cells do brain tumours contain ?

A

Glial cells (gliomas) which can divide throughout life. Or meningeal coverings of brain (meningiomas)

76
Q

What is a neuroma ?

A

Peripheral nerve damage -> sprouting of axons that can’t find location -> lump on nerve V sensitive.

77
Q

How are Glial cells different in the CNS and PNS ?

A

CNS - oligodendrocytes (block regrowth) form myelin sheath.

PNS - Schwann cells (allow axonal regrowth)

78
Q

What structure controls extracellular K conc, removes and deactivates some NTs (particularly glutamate)

A

Astrocytes

79
Q

What are microglia ?

A

small glial cells, ‘WBCs’ of the brain. attack diseased organisms and phagocytose damaged cells

80
Q

What is the trigger of Apoptosis ?

A

Loss of trophic fx needed for cell to survive (BDNF), NGF or triggered by extracellular fluids (TNF)

81
Q

Apoptosis is orchestrated by proteolytic enzymes (capsases) and DNAses. What happens to the resulting apoptotic bodies ?

A

Phagocytose in CNS by microglia. No inflam response.

82
Q

How does necrosis occur ?

A

cell injury reduces integrity -> contents break down -> necrosis. Cell ruptures inflammation in tissue. Cells aren’t replaced so damage to bbb -> infiltration of peripheral phagocytic cells

83
Q

What factor to invading macrophages secrete to encourage axonal regrowth ?

A

Galectin 1. ^schwann cell migration and axon growth.

84
Q

Which cytokines are involved in the formation of a glial scar ?

A

IL-6, TGF-b, FGF-2. Released from microglia, neurons and astrocytes.

85
Q

Which inhibitory molecules block the growth of adult axons -> embryonic axons ?

A

NogoA (produced by oligodendrocytes), Tenascin, Versican

86
Q

What is the cause of LOC in concussion ?

A

functional disturbance of RAS of brainstem , high twisting force during sagittal rotation

87
Q

Which haemorrhage is most likely after a contrecoup injury?

A

Subdural, rebound hits opposite side of skull and bridging veins rupture between brain surface and dural sinuses.

88
Q

What are petechial haemorrhages ?

A

small source of blood leakage at interface of grey and white matter -> severe brain injury +/- midline shift

89
Q

Which NT is involved in excitotoxicty ? what are it’s normal and patho levels ?

A

Glutamate, toxic at 2-5 umol/L (normally 0.6). Stroke can ^>10.

90
Q

How can levels of Glutamate be decreased to avoid excitotoxicity ?

A

Converted to glutamine using glutaminase enzyme. This isn’t an NT so conc drops.

91
Q

What are the action of Ca dependant enzymes in necrosis ? (4)

A

Caplains degrade neuronal cytoskeleton
Proteases digest structural proteins
Phospholipases digest cell membranes
Endonucleases cause DNA fragmentation

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