W10: Eye Pathology; NS Pathology; Neurology; Neurovasc.; Neurosurgery Flashcards

1
Q

principles behind investigations such as FFA, OCT, ERG, EOG and VEP.

A

FFA: normal fluorescence of optic nerve; Na fluorescein;

Optical Coherence Tomography (OCT): measures input waves (neurosensory img of retina); macular disease.

ERG: electroretinogram (ERG) is a diagnostic test that measures the electrical activity of the retina in response to a light stimulus. The ERG arises from currents generated directly by retinal neurons in combination with contributions from retinal glia

electroocoulogram (EOG) is an elecrophysiologic test that measures the existing resting electrical potential between the cornea and Vitreous membrane. Normal Retinal pigment epithelium is 6 millivolts (mV)

Visual Evoked Potentials (VEPs) testing measures the signals from your visual pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the retinal diseases that lead to sudden painless loss of vision

A

Central retinal arterial occlusion

Branch retinal art. occlusion

central vein occlusion
-retinal haemorr. | -swelling: macula + optic nerve
=> intravitreal anti-VEGF

Art. ischaemic optic neuropathy (AION)
-ARTERITIC: giant cell arteritis (temporal art.)
*headache, scalp tenderness, loss of appt., pain on chewing
=> systemic steroids
-NON-ARTERITIC: painless (NAION)
=> RF (aspirin e.g.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the retinal conditions that cause gradual painless loss of vision

A

CATARACTS: lens opcaficiation +dazzle/glare
=>sx; phacoemulsification w/ intraoc lens implant

DM RETINOPATHY: microaneurysms,retinal haemorr. etc. | fluorescein OCT
=> intravitreal antiVEGF; Laser panretinl photocoag., AIDS

GLAUCOMA: optic neuropathy w/ optic nerve dmg. peripheral vis loss. intraoc. pressure
*open/closed angle | chronic / acute
=>topical
=> Trabeculectomy

MACULAR DEGEN. (AGE-RELATED):calcification @ macula, progressive central vis. loss.
- octomography: oedema ID, fluoro ID leakage
*neovasc. @ choroid + pigment changes
*advanced: atrophy => loss of vis.
=>antiVEGF
=> low vision aids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Elaborate on the retinal appearance in central retinal artery or central retinal vein occlusion

A

CRAO:
It usually causes sudden loss of eyesight in one eye.
retinal whitening and a cherry red spot are due to opacification of the nerve fiber layer as it becomes edematous from ischemia. The fovea is cherry red because it has no overlying nerve fiber layer

A branch retinal vein occlusion occurs when part of this branch vein system is blocked. A blockage causes backpressure and leads to hemorrhaging, exudation, and/or decreased blood flow in the area of the retina drained by that particular branch retinal vein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Understand how optic neuritis and ischaemic optic neuropathy develop

A

optic neuritis: arises from auimm attack of myelin

ischaemic neuropathy: inflamm of vasc and RF HT, hyperglycaemia, DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give a differential diagnosis for conditions that cause a Red Eye

A

ALLERGIC CONJUNCTIVITIS:itchy mucoid discharge, lid swelling, CHEMOSIS (conj. swelling)
=> topical antihistamines

INFECTIVE CONJUNCTIVITIS: gritty discharge
=> topical abx

CORNEAL ABRASION: pain/watering
=> topical abx + analgesia

SCLERITIS: systemic AuIm. pain++ tender++, deep vessels.
*nodule
=> systemic steroids

ACUTE ANTERIOR UVEITIS: iris+cilliary body inflamm
*photophobia, floaters, pain
*HYPOPYON - wbc sedimentation
=> topical steroids
=> dilating drop (prevents posterior synechei complication - attachment to lens capsule + prevent dilatation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hallmarks of orbital cellulitis

A

orbital tissue infection. often visual +systemic illness/SEPSIS

=> IV abx / urgent CT drainage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Watershed cerebral infarctions

A

Watershed cerebral infarctions, also known as border zone infarcts, occur at the border between cerebral vascular territories where the tissue is furthest from arterial supply and thus most vulnerable to reductions in perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Causes of generalised interruption

A

HYPOXIA w/ intact circulation: CO2 poisoning, resp arrest

INABILITY TO USE O2: cyanide, CO

ISCHAEMIA: cardiac arrest (partial/complete cortical necrosis); brain swelling (trauma); HypoT + Shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Encephalitis

A

Viral ∴ slower pres.

  • HSV >CN V. (latent) =>ACICLOVIR
  • Arbovirus; travel hx (animal vector)

flu prodrome > progressive headache + fever
+meningism +!temporal/memory dysf.

  • lymphocytosis, normal glucose, (+) protein, mononuclear
  • transitory PLEDS EEGs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Meningitis

A

Nisseria men. (meningococcous)
Strep. pneumon. (pneumococcus) => peniccillin sens
Enteroviruses (faecooral) > non-paralytic men.

FEVER-STIFF NECK-ALTERED MENTAL. => confusion+delirium
+ etc. (photo, petichial rash, headache)

  • cultures, lumbar, CT
  • ↑pressure, neutropenia, hypoglycaemia, (++) protein

=>CEFTRIAXONE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

BRAIN ABSCESS + EMPYEMA

A

Polymicrobia, (bact. endocarditis!), trauma, infection spread (dental, sinus, ear)

IMAGING Dx +biopsy +culture

=> Penicillin / Ceftriaxone
=> Metronidazole
=> Sx drain

!HIV

  • toxoplasmosis
  • aseptic meningitis
  • 1º cerebral lymphoma
  • fungal (cryptococcal) men.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the use of passive and active immunisation to prevent neurological disease

A

RABIES: paraesthesia, ascending paralysis, animal bite
=> select vax. | HUMAN RABIES Ig (passive)

TETANUS: soil spore toxin release. blocks motor inhibition = rigid + spasm
=> TOXOID VAX. + Ag. | Penicillin + Ig.

BOTULISM: infantile, food borne, IVDU
irreversible binding = ACh block @ autonomic nerve junction
=> anti toxin / penicillin / wound debdridement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Post infective inflamm syndromes

A

Think: children

Acute Disseminated Encephalomyelitis (ADEM):
Post-infective. AuIm attack of myelin sheath.
•nausea and vomiting, headache, irritability and sleepiness, unsteadiness or inability to walk, problems with vision, weakness or tingling in certain areas of the body

Guillain-Barre Syndrome: AuIm attack on peripheral nerves => pins needles, weakness, numb., balance and co-ord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Creutzfeldt–Jakob disease

A

prion.
sporadic, familial acquired

  • rapid dementia, insidious
  • MYOCLONUS (sudden twitching jerking)
  • global decline
    ~6mos

•MRI

=> supportive tx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Discuss epidemiology and aetiology of head injury

A
SKULL FRACTURES
•contre-coup
• depressed fracture: men. risk
• linear > hinge fracture
•mosaic
•ring fracture

INTRACRANIAL INJURIES
• EDH: outer dura-skull. d/t skull fracture MMA tear
-fast. sport. young.

• SDH: tear of bridging veins nil fracture
slow venous.

• SAH: beneath arachnoid. natural disease - berry aneurysm.
-trauma: contusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

INTRINSIC BRAIN INJURIES

A

CEREBRAL CONTUSION: surface bruises
cerebral laceration

DIFFUSE AXONAL INJURY: microscopic dx, blobs. vasc injury.

Coup + Contracoup

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

List the clinical conditions that can cause raised intracranial pressure and the body’s physiological response to such an insult

A
  • morning headache + sickness (brainstem)
  • papilloedma (optic nerve)
  • pupillary dilatation (CN III)
  • ↓Glasgow (cortex+brainstem)
  • Brainsteam death (coning)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Understand how raised ICP can lead to subfalcine, tentorial and brainstem herniation

A

Increased pressure = shift of tissue
=> subfalcine herniation: herniation under falx cerebri, crushing lateral ventricles + midline shift
+ tentorial herniation + brainstem herniation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Classify brain tumours

A

1º Tumours & 2º Tumours (Mets)

1º: Brain cells: glial + embryonic neuronal cell tumours
1º cells surrounding CNS

Malignant gliomas:

  • medulloblastoma
  • meningioma: skull invasion common
  • nerve sheath: acoustic neuroma (CN VIII)

2º: commonly from *BREAST LUNG KIDNEY MELANOMA *

21
Q

Describe the features and histology of certain tumours

A
  • CNS lymphoma: diffuse large B cell lymphoma, deep central
22
Q

Understand the different presentations of multiple sclerosis

A

-OPTIC NEURITIS most common; vis loss. + pain eye moving +desaturation => optic disc swelling + relative afferent pupillary defect

  • Brainstem Relapse: +CN involvement
    • NYSTAGMUS (internucler opthalmoplegia @ PONS)
    • vertigo; ataxia (cerebellum)
    • UMN symptoms: weakness, reflexes+++, hypertonic, clonus, babinski

-Spinal Cord Lesion: partial/transverse myelitis +BLADDER/URINARY
• hyperaesthesia
• UMN signs below level of demyelination

23
Q

Understand the different courses of multiple sclerosis

A

d/t episodic demyelination or clinically isolated syndrome, greatly relapsing-remitting in nature.

> 2ºProgressive OR 1º Progressive from start: spinal + bladder

PROGRESSIVE PHASE d/t accumulating axonal loss
=> cerebral atrophy
• fatigue, temp/sensation, dysethesia paraesthesia
• stiffness spasms, etc
• bladder+bowel, swallowing
• vis problems

24
Q

Understand the criteria for diagnosis of multiple sclerosis

A
  • Clinical or MRI (new demyelination via T2)
  • Episodic evidence
  • Oligocloncal CSF
  • EEG (vis. or somatosens)
  • bloods: systemic
25
Understand when treatment of multiple sclerosis is appropriate.
ACUTE RELAPSE: => oral pred. | => rehab. DISEASE MOD: => B-interferon / Natalizumab (LT SFX! - progressive multifocal leukoencephalopathy) SYMPTOMATIC: => relaxants => amitriptyline/gabapentin (dysaesthesia) => urinary: anticholnergic / catherisation => Laxatives
26
Describe the classifications of muscle and nerve diseases
AUTOIMMUNE MUSCLE DISEASE: Polymyotisis; Dermatomyotisis | ↑CK, EMG Abn. *BIOPSY* PERIPHERAL NERVE DISEASE ANTERIOR HORN DISEASE
27
Define the aeitilogy, clinical features, investigations, management and complications of myasthenia gravis
neuromuscular junct. AuAb blocking ACh R. = prevent muscle contraction + cholinesterase breakdown of ACh • fatiguable weakness • OCULAR MG: ptosis + diplopia (Anti ACh Ab found) • GENERALISED MG: limbs, bulbar, breathing (Anti MUSK Ab; CT chest) > respiratory failure (myasthenic crisis) > aspiration pneumonia => symptomatic tx + Cholinesterase inhibitor => Disease mod: plasma exchange, Ig infusion, Imm suppr. =>Thymectomy
28
List the causes of a peripheral neuropathy
hereditary nature, metabolic syndrome, toxic: drugs, LYME, HIV, Leprosy >nerve root disease: moyotomal weakness >individual lesion periph. nerve: dermatome/myotome >generalised periph. neuropathy: distal disturbances. !postural hypoT. ACUTE DEMYELINATING: GUILLAINE BARRE SYNDROME (POST-INFECTIVE) CHRONIC DEMYELINATING: CHRONIC INFLAMM DEMYL. POLYNEUROPATHY (RELAPSE-REMISSION) => steroids
29
Lower Motor Neurone Damage
``` signs: fasiculations muscle wasting hypotonia weakness (-) loss of tendon reflex ```
30
Define the etiology, clinical features, investigations, management and complications of Guillain-Barre syndrome.
ACUTE DEMYELINATING: GUILLAINE BARRE SYNDROME (POST-INFECTIVE) paresthesia, weakness, pain, numbness, balance/coord dysfunction in limbs. > paralysis; breathing difficulty; diplopia; difficulty speaking; bladder/bowel; pain+++ *lumbar, LFT, spirometry, nerve conduction => IVIg => plasmapheresis + ventilator, feeding tube, analgesia, catheter, laxatives, TED stockings
31
Describe the clinical presentation and management of motor neurone disease
degeneration of anterior horn => spinal muscle atrophy MND: limb > bulbar spread / > resp spread +LMN signs: fasiculations; wasting; weakness; tongue atrophy +UMN signs: spasticity, brisk reflex, extensor plantar cognitive decline => supportive => TILUZOLE (glutamate antagonist => anticipatory planning
32
UMN Signs
Nil wasting, ↑Tone; reflexes; spasticity; extensor plantar *pyramidal pattern of weakness (strong flexors, weak extensors, pronation) => below level of any lesion; bilateral
33
Spinal Cord Lesion Features
Dorsal Column Lesions = loss of proprioception + vibration only Anterior Lesion: pain+temp loss below, intact proprio + temp +UMN signs
34
Spondylosis
Neck pain,
35
cauda equina syndrome
spinal stenosis = nerves in the lower back compressed d/t tumour (breast, prostate, lung); Lumbar disc herniation: most commonly L4/5, L5/S1 levels , trauma, infection *!sx emergency*; incomplete/complete CES (severity of incontinence/retention) * MRI spine bilateral: sciatica, weakness/numbness, urinary/bowel! + numbness genitals/anus (saddle anesthesia) + pain+++ => decompression by a lumbar laminectomy
36
Define myelopathy and radiculopathy
MYELOPATHY = d/t SC compression = whole SC RADICULOPATHY = individual nerve root
37
Identify the sinister features associated with back pain
TUNA FISH Trauma Unexplained wt loss Neuro symptoms Age >50 Fever IVDU Steroids Hx Cancer
38
Recognise red flags for secondary headache
* sudden onset + >50yo * ↑frequency/severity * new onset + underlying condition / SYSTEMIC * focal signs * papilledema + headache
39
1º Headaches
``` TENSION HEADACHE (most freq.) *BP, muscle tension bilateral => analgesia | => preventative: amitryptiline (antidepressants) ``` MIGRAINE *naussea, photo/sonophobia, anticipatory anxiety = medication overuse 1. premonitory features of migraine 2. aura: transient brainstem dysfunction (occipital) 3. early headache 4. severe headache 5. postdrome period > CHRONIC MIGRAINE: less severe more frequent headaches | anticipatory anxiety=overuse ACUTE MGMT => aspirin/NSAIDS; Triptans (5HT agonist) PROPHYLAXIS => propanolol, valporate (prego!), Antidepr., Botox
40
1º Headaches: Trigeminal Autonomic Cephalalgias
CLUSTER HEADACHES: unilateral orbital/temporal acute short duration +ipsilateral autonomic symptoms abortive => triptans (no overuse risk) transitional => prednisolone / greater occipital block preventative => verapamil (ECG!), Lithium, Melatonin PAROXYSMAL HEMICRANIA: sharp throbbing => INDOMETACIN RESPONSIVE (NSAID non COX2) > hemicrania continua: unilateral continuous headache +superimposed pain. +facial involvement
41
2º Headache
``` THUNDERCLAP CT, LP; ?SAH, aneurysm rupture+bleed => coiling/clipping =>Nimodipine -|Ca2+ spasms (vasospasms) => HHH Rx ``` GIANT CELL ARTERITIS: non-sepc +scalp tenderness; jaw claudication. *systemic unwell *↑ESR; CRP; Platelet => prednisolone + temporal artery biopsy LOW PRESSURE: postural headache, spontaneous d/t venous engorgement / subdural hygomas => rest, IV caffiene, epidural blood patch HIGH PRESSURE: *intracranial hypertension*; wakening, progressive headache + focal symptoms + papilloedema
42
TRIGEMINAL NEURALGIA
unilateral or mandibular/maxillary stabbing d/t phys. env. triggers = vascular compression of root nerve => CARBAMAZEPINE (ANTI-EPILEPTIC) pregbalin PHENYTOIN => Sx: glyceron ganglion injection
43
State the differential diagnosis of blackouts
Reflex Orthostatic: BP, dehydration, meds., endocrine Cardiogenic: arrythmia, AO stenosis, exertion trigger!
44
Describe the techniques used in the investigation of possible epilepsy
MRI or EEG | - rule out cardiac causes too
45
Identify the classification of seizures: generalised and focal
GENERALISED SEIZURE: quick spread of discharges - absence seizures(fleeting arrest) - generalised tonic-clonic: stiff-relax (lateral tongue bite! infective PMH) - myoclonic seizures FOCAL SEIZURE: +aura, can progress as 2º generalised - temporal lobe: deja vu; nil recollection - frontal lobe: unusual, bizarre motor, quick recovery exacerbating risks! - missed meds, fatigue, hormonal changes, drug/alcohol. stress/anxiety
46
Epilepsy Treatment
1ºGeneralised => Na Valporate - wt gain, ataxia, nausea !prego => Lamotrigine - skin rash, seep difficulty => Levetiracetam - depression Partial/2º Generalised => Lamotrigine => Carbamezapine (glutamate) - ataxia, drowsiness, nystagmus blurred vis. Absence: => Ethoosuximide -Drowsiness, dizziness, tiredness, headache, stomach upset,
47
Define the causes, presentation, investigation and management of status epilepticus
d/t nonadherence, alcoholism, refractory epilepsy, toxic cause, acute injury *generalised +/-convulsive seizure continuously w/ no intermittent recovery > permanent brain injury! => MIDALOZAM (buccal), LORAZEPAM (bolus) => Na valporate, Levetiracetam, phenytoin => Anaesthesia +propafol/thiopentone
48
Epilepsy DVLA regulation
seizure-free for 1yr | individual basis