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

27/10/2024 Flashcards

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
Q

Where does blood accumulate in an extradural Haematoma?

A

Between the skull and periosteal layer of the dura mater

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26
Q

Why are extradural haematomas often in the temporal region?

A

since the thin skull at the pterion overlies the middle meningeal artery and is therefore vulnerable to injury.

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27
Q

Imaging findings in an extradural haematoma?

A

Biconvex hyperdense collection around the surface of the brain surface by the suture lines

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28
Q

Classical presentation of an extradural haematoma?

A

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
Q

Outline why extradural haematomas cause a lucid interval?

A

The brief regain in consciousness is termed the ‘lucid interval’ and is lost eventually due to the expanding haematoma and brain herniation.

30
Q

Outline why extradural haematomas cause a 3rd nerve palsy?

A

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
Q

What is the monro-kellie doctrine?

A

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
Q

Where does a subdural haemorrhage occur?

A

Between the dura and arachnoid mater

33
Q

Pathophysiology of subdural haemorrhage?

A

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
Q

Clinical presentation of subdural haemorrhage?

A

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
Q

CT appearance of a subdural haemorrhage?

A

Crescent-shaped collection of blood that crosses suture lines
Hyperdense if acute and hypodense (dark) if chronic

36
Q

Where does a subarachnoid haemorrhage occur?

A

Between arachnoid and pia mater

37
Q

Causes of a subarachnoid haemorrhage?

A

Most commonly traumatic

Spontaneous SAH causes:
85% caused by intracranial berry aneurysms
Other causes include AVMs, pituitary aploplexy or arterial dissection

38
Q

CT appearance of subarachnoid haemorrhage?

A

Hyperdense blood is typically distributed in basal cisterns, sulci and in severe cases the ventricular system

39
Q

What must be done if a SAH is suspected by CT head is normal?

A

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
Q

What imaging is done for a SAH?

A

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
Q

What is the general rule for where spinal nerves exit the spine?

A

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
Q

Dermatomes of the head?

A

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
Q

Upper limb dermatomes?

A

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
Q

Lower limb dermatomes?

A

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
Q

Myotome for C4?

A

Shoulder shrugs

46
Q

Myotome for C5?

A

Shoulder abduction
External rotation of shoulder
Elbow flexion

47
Q

Myotome for C6?

A

Wrist extension

48
Q

Myotome for C7?

A

Elbow extension and wrist flexion

49
Q

Myotome for C8?

A

Thumb extension and finger flexion

(C8 is great thumbs up)

50
Q

Myotome for T1?

A

Finger abduction

51
Q

Myotome for L2?

A

Hip flexion

52
Q

Myotome for L3?

A

Knee extension

53
Q

Myotome for L4?

A

Ankle dorsiflexion

54
Q

Myotome for L5?

A

Big toe extension

55
Q

Myotome for S1?

A

Ankle plantarflexion

56
Q

Sciatic nerve roots?

A

L4-S3

57
Q

Outline the genetics of huntingtons?

A

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
Q

Features of huntingtons?

A

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
Q

Prognosis of huntingtons?

A

Progressive
Life expectancy is 10-20 years after onset of Sx
Death is often due to aspiration pneumonia

60
Q

Management of huntingtons?

A

No treatment can slow the course of disease
Chorea - haloperidol, tetrabenazine, chlorpromazine, olanzapine
Manage depression
OT, SALT, PT are involved

61
Q

Where can a lesion be in a left homonymous hemianopia?

A

Either:
- lesion/pressure the right optic tract e.g. middle cerebral artery oclusion
- lesion of right occipital lobe

62
Q

What is a syingomyelia?

A

A collection of CSF within the spinal cord

63
Q

Causes of a syringomyelia?

A

Can be congenital but is more commonly acquired…
Chiari malformation - cerebellum bulges through into the spinal canal
Trauma
Tumours of the spinal cord

64
Q

Features of a syringomyelia?

A

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
Q

Symptoms of Bell’s palsy?

A

lower motor neuron facial nerve palsy → forehead affected

Others:
post-auricular pain (may precede paralysis)
altered taste
dry eyes
hyperacusis

66
Q

Management of Bell’s palsy?

A

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
Q

Neurological deficits that can occur as a result of a parietal lobe lesion?

A

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
Q

What should non-HDL cholesterol level be?

A

<4

A. REVISION FROM QBANKS (11 decks)

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