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SHF 204 Systemic conditions > CNS disorders > Flashcards

CNS disorders Flashcards

1
Q

MS

A
  • Potentially disabling disease of CNS
  • Immune system attacks myelin sheath that covers nerve fibres
  • Causes communication problems between brain and rest of body
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2
Q

MS cause

A
  • Unknown
  • Considered to be autoimmune
  • Reduced myelin exposes nerve fibres, interfering with speed and efficiency of message delivery
  • Combination of genetic and environmental factors
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3
Q

MS population

A
  • White women aged between 20-40
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4
Q

MS risks

A
  • Age- 20-40
  • Women 2-3x more likely
  • Family Hx
  • Certain infections- Epstein-Barr
  • Race- white people
  • Low vitamin D
  • Chromosome 6p21 defect
  • Smoking
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5
Q

MS presentation

A
  • Variable- depend on location and severity of nerve fibre damage
  • Numbness or weakness to one or more limbs, typically occurs unilaterally
  • Lack of coordination
  • Unsteady gait or inability to walk
  • Partial or complete loss of vision
  • Prolonged double/blurry vision
  • Vertigo
  • Slurred speech
  • Cognitive problems
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6
Q

MS prognosis

A
  • Can eventually cause permanent damage or deterioration of nerve fibres
  • No cure however there are treatments to help speed up recovery from attacks, modify course of disease and manage symptoms
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7
Q

Temporal arteritis

A
  • Inflammation of lining of arteries
  • Aka giant cell arteritis
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8
Q

Temporal arteritis cause

A
  • Caused by inflammation of blood vessels
  • This narrows blood vessels reducing amount of blood and oxygen to reach body tissue
  • Almost any artery can be affected, most common in temples
  • Cause unknown
  • Believed to be due to abnormal attacks on artery walls by immune system
  • Certain genes and enviro factors might be involved
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9
Q

Temporal arteritis risk

A
  • 70-80
  • Women 2x
  • White people
  • PMR
  • Family Hx
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10
Q

Temporal arteritis presentation

A
  • Head P and tenderness
  • Scalp tenderness
  • Jaw P when chewing or opening mouth wide
  • Fever
  • Fatigue
  • Vision loss/double vision
  • Sudden permanent loss of vision
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11
Q

Temporal arteritis prognosis

A
  • Prompt treatment with corticosteroid medication usually relives symptoms and might prevent vision loss
  • Relapse common even with treatment
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12
Q

Subarachnoid haemorrhage

A
  • Bleeding between space in brain and surrounding membrane (subarachnoid space)
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13
Q

Subarachnoid haemorrhage cause

A
  • Usually happens when aneurysm bursts in brain
  • Can be caused by trauma, tangle of blood vessels in brain or other health problems
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14
Q

Subarachnoid haemorrhage population

A
  • Most common in people aged between 45-70
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15
Q

Subarachnoid haemorrhage risks

A
  • Smoking
  • Excessive alcohol consumption
  • High blood pressure
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16
Q

Subarachnoid haemorrhage presentation

A
  • Described as worst headache ever felt
  • Nausea
  • Vomiting
  • Stiff neck
  • Problems with vision
  • Brief loss of consciousness
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17
Q

Subarachnoid haemorrhage prognosis

A
  • 1/3 survive with good recovery
  • 1/3 survive with disability or stroke
  • 1/3 will die
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18
Q

Dizziness/vertigo cause

A
  • Inner ear problems- house sensors that help detect gravity and back and fourth motion
  • Eyes- help determine where body is in space
  • Sensory nerves- sends messages to brain about body movements and positions
  • Circulation problems that cause dizziness- drop in blood pressure, poor blood circulation
  • Neurological conditions- e.g., Parkinson’s
  • Medication
  • Anxiety disorders
  • Anaemia
  • Damage to CN8
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19
Q

Vertigo population

A
  • Can happen at any age, more common in people over 65
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20
Q

Vertigo risks

A
  • Older adults
  • Past episodes of dizziness
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21
Q

Vertigo presentation

A
  • False sense of motion or spinning (vertigo)
  • Light-headedness of feeling faint
  • Unsteadiness or loss of balance
  • Feeling of floating, wooziness or heavy headedness
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22
Q

Vertigo prognosis

A
  • Most people get better without treatment
  • Treatment will depend on cause
  • ABs may be prescribed if caused by infection
  • Exercises to improve balance
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23
Q

Myasthenia gravis

A
  • Characterised by weakness and rapid fatigue of any muscle under voluntary control
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24
Q

Myasthenia gravis

A
  • Antibodies
    o Immune system produces antibodies that blocks or destroys muscle receptor sites for neurotransmitter acetylcholine
    o With fewer receptor sites available, muscle receives fewer signals, resulting in weakness
    o Can also impair function of protein called muscle-specific receptor tyrosine kinase (MuSK)
    o This protein is involved in forming nerve-muscle junction
  • Thymus gland
    o Believed that thymus gland can trigger or maintain production pf antibodies which block Ach
    o Common to have tumour in thymus gland, usually aren’t cancerous
  • Mother to child- if treated promptly child usually recovers within two months after birth
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25
Q

Myasthenia gravis population

A
  • Can affect anyone
  • Women more likely under 40
  • Men over 60
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26
Q

Myasthenia gravis risk

A
  • Women between 20-30
  • Men 60-70
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27
Q

Myasthenia gravis presentation

A
  • Muscle weakness worsens as affected muscle is used
  • Usually improves with rest
  • Muscle weakness can come and go
  • Eye muscles
    o Usually first sign
    o Drooping of one or both eyelids
    o Double vision
  • Facial and throat muscles
    o 15% of peoples symptoms involve throat/face
    o Impaired speaking
    o Difficulty swallowing
    o Affects chewing
    o Changes facial expressions
  • Neck and limb muscles
    o General weakness
    o Can affect walking
    o Weak neck muscles make it hard to hold head up
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28
Q

Myasthenia gravis prognosis

A
  • No cure but treatment can help relive signs and symptoms
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29
Q

Common S+S of cranial nerve injury

A
  • Specific S&S depend on the cranial nerve that is affected
  • Intermittent attacks of excruciating facial px
  • Vertigo
  • Hearing loss
  • Weakness
  • Paralysis
  • Facial twitch
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30
Q

Olfactory nerve

A

Smell
CN1

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31
Q

Symptoms of olfactory dysfunction

A
  • Ansomia
    o Complete loss of smell
  • Dysomia
    o Also called phantosmia
    o Unpleasant or strange odours that occur spontaneously
  • Hyposmia
    o Partial loss of smell
  • Parosmia
    o Distorted sense of smell
    o E.g. familiar foods that may smell like chemicals or mould
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32
Q

Conditions that affect olfactory nerve

A

Sinus infection
Covid
PD
Epilepsy
Diabetes
Alzheimers

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33
Q

Optic nerve

A

Visual info from eyes to brain

34
Q

Glaucoma

A

Damage of optic nerve

35
Q

Glaucoma cause

A

Damage to optic nerve, gradual deterioration- blind spots
Related to inc pressure in eye
Elevated pressure happens as result of build up of fluid in eye- aqueous humor

36
Q

Glaucoma population

A

Black, Asian and hispanic heritage over 40
Others 60+

37
Q

Glaucoma risks

A

High int eye pressure, aka intraocular pressure
55+
Black, Asian, Hispanic
Diabetes, migraines, high blood pressure
Extreme near/far sightedness

38
Q

Glaucoma S+S

A

Depend on stage of condition
No symptoms in early stage, gradual patchy blind spots in peripheral vision
In later stages, difficulty seeing things in central vision
Headaches, blurry/cloudy vision

39
Q

Glaucoma prognosis

A

Lifelong, treatments available
Meds- eye drops
Laser therapy
Surgery- minimally invasive glaucoma surgery
Chronic + progressive that cause some degree of vision loss
blindness is rare complication

40
Q

Papilledema

A

Medical term for swelling of optic disc
Almsot always bilateral

41
Q

Papilledema cause

A

High intracranial pressure causes it
Other causes- hypertension, diabetes, infection, amaemia

42
Q

Papilledema population

A

Overweight women

43
Q

Papilledema risks

A

Those that raise intracranial pressure
Space occupying lesions- tumours, subarachromial haemorrhage, dec absorption of CSF

Idiopathic risks- recent weight gain, thyroid disease, anaemia

44
Q

Papilledema S+S

A

Some have no symptoms
Headaches- worse in mornings/lying down
Diplopia
Nausea/vom
Problems moving/thinking

45
Q

Papilledema prognosis

A

If idiopathic- may be prescribed carbonic anhydrase inhibitor, if this doesn’t work surgery is option
Maintaining healthy weight is long term Strat
Treatment of underlying condition
If caught early prognosis is usually good
Treatment needed to avoid blindness

46
Q

Optic neuritis

A

Inflame of optic nerve

47
Q

Optic neuritis cause

A

Unknown
Thought to be autoimmune, whereby immune system attacks myelin around optic nerve
Associated autoimmune diseases- MS, neuromyelitis optics, myelin oligodendrocyte glycoprotein antibody disorder

48
Q

Optic neuritis population

A

Females 20-40

49
Q

Optic neuritis risks

A

20-40
Females
White people
Genetic mutations

50
Q

Optic neuritis S+S

A

Usually unilateral
P often worsened with eye movement
P sometimes felt behind eye
Vision loss in one eye- develops over months, sometimes permanent
Loss of colour perception
Flashing light like sensation reported with eye movements

51
Q

Optic neuritis prognosis

A

May resolve spontaneously without treatment
Steroid medication can speed up recovery
Improves in about 80% of Pt over few weeks
Some have impaired vision- reduced colour vision, inc difficulty with night-time vision
Most people have complete resolution of symptoms

52
Q

Optic nerve atrophy

A

Not a disease in itself but is a sign of potentially more serious condition

53
Q

Optic nerve atrophy cause

A

Interference with optic nerves ability to transmit impulses
Interference can be due to- glaucoma, stroke of optic nerve, tumour pressing on optic nerve, improper formation of optic nerve (congenital)

54
Q

Optic nerve atrophy population

A

White people
10-50

55
Q

Optic nerve atrophy risks

A

High cholesterol
High blood pressure
Sudden drop in blood pressure
Arteroscleortosis
Smoking
Migraines
Glaucoma

56
Q

Optic nerve atrophy S+S

A

Symptoms relate to change in vision
Specifically- blurred vision, difficulty with peripheral vision, difficulty with colour vision, reduction in sharp vision

57
Q

Optic nerve atrophy prognosis

A

No real cure or treatment
Important to have regular eye exams
Prognosis depends on what’s causing the problem- e.g., if optic neuritis the vision should amend once inflammation is reduced

58
Q

Optic nerve neuropathy

A

Sudden loss of vision due to interruption of blood flow to ant of optic nerve
Arteritic AION- caused by inflammation of arteries supplying blood to optic nerve
Nonarteritic AION- other reasons of inflammation of arteries

59
Q

Optic neuropathy cause arteritic

A

Dangerous condition
Inflame can be due to giant cell arteritis, causing inflammation to medium and large sized arteries
3x more common in women
55+

60
Q

Nonarteritic optic neuropathy cause

A

Most common form
50+
Men and women affected equally
Caused by- drop in blood pressure to such degree optic nerve supply is dec, inc pressure in eyeball, narrowed arteries, dec blood flow to back of eye

61
Q

Optic nerve neuropathy population

A

50+
A-AION more common in women

62
Q

Optic nerve neuropathy risks

A

High blood pressure
Diabetes
Smoking
High cholesterol
Heart disease
Anaemia or sudden blood loss
Vasculitits

63
Q

Optic nerve neuropathy S+S nonarteritic

A

Sudden, painless loss or blurring of vision unilaterally
Dec visual activity
Relative afferent pupillary defect
Swollen optic nerve with spinner haemorrhages
Visual field defect

64
Q

S+S of arthritic optic neuropathy

A

P in temples
P when chewing
Scalp P or tingling
Neck P
Muscle aches and pains, esp upper legs and arms
General fatigue

65
Q

Optic nerve neuropathy prognosis

A

Depends on type
A- usually greater degree of vision loss
Degree of vision loss depends on location and amount of optic nerve damage
N- 40% show improvement in central vision in months after initial vision loss
25% of A develop bilaterally within 3 years

66
Q

Treatment of neuropathic optic nerve

A

A- corticosteroids
N- treatment for underlying CV disease or risk factors trigger and aggravate NA-AION

67
Q

Macular degeneration

A

Eye disease that affects central vision
Top cause of vision loss in over 50s
Dry (atrophic)- up to 90% have this form
Wet (exudative)

68
Q

Macular degeneration cause

A

Inherited eye disease
Occurs when macula at back of eye starts to deteriorate for unknown reason

Dry- develops when tiny yellow protein deposits called druses form under macula, build-up dries and thins macula, vision loss is gradual, unusual to lose it all
Wet- abnormal blood vessels develop under retina and macula, blood vessels leak blood and fluid, fluid build-up bulge forms macula, may see dark spots in centre vision, can quickly lead to central vision loss

69
Q

Macular degeneration population

A

White people 50+

70
Q

Macular degeneration risks

A

Older ages 50+
Family Hx
Overweight
Smoking
Hypertension
Diet high in saturated fats

71
Q

Macular degeneration S+S

A

Many don’t have symptoms until disease progresses
Blurred vision
Blank or dark spots in field of Vision
Appearance of waves or curves in straight lines

72
Q

Macular degeneration prognosis

A

No cure
Depends on degree of vision loss
Nutritional supplements, anti vascular endothelial growth
Quit smoking, lose weight, eat healthy diet
Wear glasses or contacts, use brighter lights at home/work, read with magnifying device

73
Q

Diabetes and eye conditions

A

Can damage eyes over time and cause vision loss, even blindness
Diabetic retinopathy, macular oedema, cataracts, glaucoma
Early diagnosis and treatment can protect eyesight
Managing diabetes and getting regular eye tests can prevent these conditions

74
Q

MS and eye conditions

A

First symptom in many people
Optic neuritis, nystagmus, diplopia
Prognosis is good

75
Q

Hypertension and eye conditions

A

High blood pressure can alter blood vessels which supply eyes
Can cause- retinopathy (damage to vessels in retina), choroidopathy (fluid build-up under retina), optic neuropathy (nerve damage)
Treatment can lifestyle changes can help control high blood pressure and reduce risk of developing eye disease

76
Q

B12 deficiency and eye conditions

A

Plays important role in protecting RBC
Helps create and regulate DNA and aids further function of brain
Can cause- disturbed or blurred vision, optic neuropathy
Happens when deficiency causes damage to optic nerve that leads to your eyes

77
Q

Occulomotor nerve palsy

A

3rd cranial nerve
Elevates upper eyelid
Focuses eye
Respond to light by making pupil smaller
Moves eye inward, outward, up and down and controls torsion

78
Q

Occulamotor nerve plays cause

A

Occurs when CN£ becomes paralysed
Can be present at birth
May occur later due to
- inadequate blood flow- causes lack of of oxygen that nerves need to function
Nerve compression

Conditions which may cause- infections (HIV), head injuries, brain aneurysm/tumour

79
Q

Trochlear nerve

A

CN4
Part of autonomic system
Innervates eyes
Sends signals from brain to muscles
Controls eye movement

80
Q

Trochlear nerve palsy cause

A

When illness or injury paralyses nerve that control muscle movement
Can be congenital
Trauma (RTA)
More fragile than other nerves as its long and thin- minor trauma can cause damage

81
Q

Treatment for trochlear nerve palsy

A

Depends on causing symptoms
Minor trauma- improves on its own
For more severe palsy- treatment can be eye patch for rest, special glasses to correct double vision, surgery to repair

SHF 204 Systemic conditions (6 decks)

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