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A. REVISION FROM QBANKS > 27/10/2024 > Flashcards

27/10/2024 Flashcards

(68 cards)

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1
Q

What nerve roots are affected in erbs palsy?

A

C5 and C6

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2
Q

What causes erbs palsy?

A

Usually birthing related e.g. breech or shoulder dystocia

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3
Q

Sx of erb’s palsy?

A

Waiters tip appearance - as issues with abduction, external rotation, elbow flexion, supination and wrist extension
Winged scapula

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4
Q

Which nerve roots are affected in Klumpke’s paresis?

A

C8 and T1

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5
Q

What can cause klumpke’s paresis?

A

Birth trauma
Traction injuries e.g. pulling a child’s arm
Pancoast tumours
Cervical rib

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6
Q

Sx of klumpke’s paresis?

A

Claw hand and wasting of hand muscles - due to weak intrinsic hand muscles
Hand is typically held supinated
Sensory loss in medial forearm and arm - due to C8 and T1 dermatomes

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7
Q

prognosis of erbs palsy

A

Usually resolves completely & spontaneously in first year of life - recovery begins in first month of life

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8
Q

prognosis of klumpke paresis?

A

Usually resolves by 6 months
Usually requires some PT

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9
Q

Contraception considerations in a pt with hypertension?

A

Oestrogen can increase bp further
If hypertension is adequately controlled its 2 for progesterone injectable and 3 for CHC
If systolic is >140 or diastolic >90 its UKMEC 3 for CHC
If systolic is >=160 or diastolic >=100 its UKMEC 2 for progesterone injectable and 4 for CHC

IUD, IUS, implant or POP are good options!

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10
Q

When a pt has menopause symptoms how long should the woman use contraception?

A

12 months after the last period in women > 50 years
24 months after the last period in women < 50 years

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11
Q

When is a woman offered sequential combined HRT?

A

If you have menopause Sx but still have periods
E.g. monthly HRT where you take oestrogen every day and progesterone alongside it for the last 10-14 days of the menstrual cycle every month
(Oestrogen helps manage menopause Sx by replenishing that hormone level, the progesterone is meant to represent the luteak phase where the body naturally produces progesterone and this is important to protect the endometrium from thickening too much due to the continuous oestrogen exposure. Stopping the progesterone will then cause bleed.)

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12
Q

Outline motor response for GCS?

A
  1. Obeys commands
  2. Localises to pain
  3. Withdraws from pain
  4. Abnormal flexion to pain (decorticate posture)
  5. Extending to pain
  6. None

(You can remember it as In Out shake it all about… arm going in towards pain and then out away from pain. Arm then goes in as you flex and then out as you extend)

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13
Q

Sx of third nerve palsy?

A

Eye down and out
Ptosis
Mydriasis can occur

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14
Q

Causes of a third nerve palsy?

A

DM
Vasculitis e.g. temporal arthritis and SLE
It can be a false localising sign due to uncal herniation through the tentorium if raised ICP
Posterior communicating artery aneurysm
Cavernous sinus thrombosis
Webers syndrome
Amyloid and MS

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15
Q

How does a posterior communicating artery aneurysm present?

A

Third nerve palsy that is painful!
Severe headache
Visual acuity loss

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16
Q

What imaging should be done for a suspected posterior communicating artery aneurysm?

A

A CT angiography

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17
Q

Explain the term surgical and medical third nerve palsy?

A

A surgical third nerve palsy is one which causes ipsilateral pupil dilation. This is because the parasympathetic fibres are located superficially on CN3 so they are more suspectible to compression. E.g. posterior communicating artery aneurysm
Medical third nerve palsies are when there is no Mydriasis and are therefore more likely due to microvascular infarction within the nerve fibres e.g. DM, temporal arthritis, SLE

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18
Q

Features of neurogenic claudication versus vascular claudication?

A

Neurogenic claudication occurs with exercise but is not immediately relived by rest
Worsens with extension e.g. descending stairs
Typically manifests more proximally (thigh or buttock)
Occurs in the absence of vascular risk factors

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19
Q

Causes of raised ICP?

A

SOL
Hydrocephalus
Venous sinus thrombosis
Idiopathic intracranial hypertension

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20
Q

Causes of provoked seizures?

A

Hypoxia
Hypoglycaemia
Alcohol withdrawal
Uraemia and hepatic failure
Drugs - TCAs, macrolides, Tramadol
Raised ICP
Encephalitis
Acute stroke

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21
Q

How to test for an S1 nerve palsy?

A

Test for power of foot eversion and ankle plantarflexion

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22
Q

Features of cavernous sinus thrombosis?

A

Periorbital swelling
Exophthalmos
Conjunctival chemosis
Sharp severe pain in eye and forehead - ophthalmic division of V
Cranial nerve palsies - III, IV, VI
Diplopia
Fevers

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23
Q

Outline layers of scalp?

A

Skin
Dense connective tissue
Epicranial apnoeurosis
Loose areolar connective tissue
Periosteum

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24
Q

Outline layers of meninges?

A

Dura
Arachnoid
Pia

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25
Where does blood accumulate in an extradural Haematoma?
Between the skull and periosteal layer of the dura mater
26
Why are extradural haematomas often in the temporal region?
since the thin skull at the pterion overlies the middle meningeal artery and is therefore vulnerable to injury.
27
Imaging findings in an extradural haematoma?
Biconvex hyperdense collection around the surface of the brain surface by the suture lines
28
Classical presentation of an extradural haematoma?
a patient who initially loses, briefly regains “lucid interval” and then loses again consciousness after a low-impact head injury. fixed and dilated pupil Headache of increasing severity Vomiting Drowsiness Confusion Seizures May be sigs of hemispheric dysfunction e.g. dysphasia or hemiparesis
29
Outline why extradural haematomas cause a lucid interval?
The brief regain in consciousness is termed the 'lucid interval' and is lost eventually due to the expanding haematoma and brain herniation.
30
Outline why extradural haematomas cause a 3rd nerve palsy?
As the haematoma expands the uncus of the temporal lobe herniates around the tentorium cerebelli and the patient develops a fixed and dilated pupil due to the compression of the parasympathetic fibers of the third cranial nerve.
31
What is the monro-kellie doctrine?
The hypothesis that the sum of volumes of brain, CSF and intracranial blood is constant so an increase in 1 should cause a decrease in the others = this is compliance Once the compensatory compliance mechanism is overwhelmed, any small increases in the volume of any 1 of the 3 substances will lead to dramatic increases in ICP
32
Where does a subdural haemorrhage occur?
Between the dura and arachnoid mater
33
Pathophysiology of subdural haemorrhage?
Rupture of bridging cranial veins (the vessels that connect the venous blood from the cerebral cortex to the dural venous sinuses) More common in older pts, alcoholics, or pts on anticoagulants
34
Clinical presentation of subdural haemorrhage?
Altered mental status - fluctuations in levels of consciousness are common Focal neurological deficits Headache worsening overtime Seizures U/L dilated pupil Hemiparesis or hemiplegia N&V Signs of raised ICP - bradycardia, hypertension, respiratory irregularities Memory loss or personality changes if chronic
35
CT appearance of a subdural haemorrhage?
Crescent-shaped collection of blood that crosses suture lines Hyperdense if acute and hypodense (dark) if chronic
36
Where does a subarachnoid haemorrhage occur?
Between arachnoid and pia mater
37
Causes of a subarachnoid haemorrhage?
Most commonly traumatic Spontaneous SAH causes: 85% caused by intracranial berry aneurysms Other causes include AVMs, pituitary aploplexy or arterial dissection
38
CT appearance of subarachnoid haemorrhage?
Hyperdense blood is typically distributed in basal cisterns, sulci and in severe cases the ventricular system
39
What must be done if a SAH is suspected by CT head is normal?
An LP only if CT head was done >6 hours after onset of Sx It mist be performed at least 12 hours following the onset of Sx to allow development of xanthochromia
40
What imaging is done for a SAH?
Non contrast CT head is done first (+/- LP depending on result) CT intracranial angiogram to identify a vascular lesion cause such as an aneurysm or AVM May also do a catheter angiogram
41
What is the general rule for where spinal nerves exit the spine?
C1–C7 spinal nerves: Originate above their corresponding vertebrae. C8 spinal nerve: Originates between C7 and T1 (no C8 vertebra). From T1 downwards: Spinal nerves exit below their corresponding vertebrae.
42
Dermatomes of the head?
Trigeminal nerve branches: V1 - ophthalmic branch - lateral aspect of forehead V2 - maxillary branch - cheek V3 - mandibular branch - lower jaw (although angle of mandible is C2/C3) C2 - top back of head C3 - upper neck, small area of jaw under each ear and back of head
43
Upper limb dermatomes?
C4 - AC joint C5 - regimental badge C6 - palmar side of thumb C7 - palmar side of middle finger C8 - palmar side of little finger T1 - medial aspect of antecubital fossa
44
Lower limb dermatomes?
L1 - inguinal region and very top of medial thigh L2 - middle & lateral anterior thigh L3 - medial epicondyle of femur L4 - medial malleolus L5 - dorsum of foot at third metatarsophalangeal joint S1 - lateral aspect of calcaneus S2 - midpoint of popliteal fossa S3 - horizontal gluteal crease S4/5 - perianal area
45
Myotome for C4?
Shoulder shrugs
46
Myotome for C5?
Shoulder abduction External rotation of shoulder Elbow flexion
47
Myotome for C6?
Wrist extension
48
Myotome for C7?
Elbow extension and wrist flexion
49
Myotome for C8?
Thumb extension and finger flexion (C8 is great thumbs up)
50
Myotome for T1?
Finger abduction
51
Myotome for L2?
Hip flexion
52
Myotome for L3?
Knee extension
53
Myotome for L4?
Ankle dorsiflexion
54
Myotome for L5?
Big toe extension
55
Myotome for S1?
Ankle plantarflexion
56
Sciatic nerve roots?
L4-S3
57
Outline the genetics of huntingtons?
Autosomal dominant A trinucleotide repeat disorder: repeat expansion of CAG Phenomenon of anticipation can be seen - presents at an earlier age & increased severity of disease in successive generations (Due to a defect in the Huntington gene in chromosome 4 = degeneration of cholinergic and GABAergic neurons in striatum of basal ganglia)
58
Features of huntingtons?
Around age 30-50 chorea personality changes (e.g. irritability, apathy, depression) and intellectual impairment dystonia Rigidity Dysarthria Dysphagia Eyes: Fixational instability, saccadic pursuit, difficulty initiating saccades, slow saccades
59
Prognosis of huntingtons?
Progressive Life expectancy is 10-20 years after onset of Sx Death is often due to aspiration pneumonia
60
Management of huntingtons?
No treatment can slow the course of disease Chorea - haloperidol, tetrabenazine, chlorpromazine, olanzapine Manage depression OT, SALT, PT are involved
61
Where can a lesion be in a left homonymous hemianopia?
Either: - lesion/pressure the right optic tract e.g. middle cerebral artery oclusion - lesion of right occipital lobe
62
What is a syingomyelia?
A collection of CSF within the spinal cord
63
Causes of a syringomyelia?
Can be congenital but is more commonly acquired… Chiari malformation - cerebellum bulges through into the spinal canal Trauma Tumours of the spinal cord
64
Features of a syringomyelia?
B/L cape-like pain, loss of sensation to temperature and crude touch (spinothalamic tract affected but DCML is preserved as lesion is at the central canal) - often pts present with burn-marks to finger tips! Corticospinal tract can be affected: can cause spastic weakness mostly lower limbs & Upgoing plantars Neuropathic pain Autonomic features e.g. Horners, bladder and bowel dysfunction Can lead to scoliosis over years
65
Symptoms of Bell’s palsy?
lower motor neuron facial nerve palsy → forehead affected Others: post-auricular pain (may precede paralysis) altered taste dry eyes hyperacusis
66
Management of Bell’s palsy?
Oral prednisolone within 72 hours of the onset Eye care to prevent exposure keratopathy - artificial tears and eye lubricants can be considered & tape eye shut at night
67
Neurological deficits that can occur as a result of a parietal lobe lesion?
Hemispatial neglect Amorphosynthesis Sensory inattention Optic ataxia (lack of coordination between visual input and movement i.e. can’t do visually guided movements such as reaching for an object) Astereognosis (tactile agnosia) - the inability to recognize objects by touch. Agnosia (inability to recognise things) - if dominant hemisphere Apraxia (inability to perform tasks or movements) - if dominant hemisphere C/L inferior homonymous quadrantonopia (PITS)
68
What should non-HDL cholesterol level be?
<4

A. REVISION FROM QBANKS (13 decks)

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