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Systemic Conditions > CNS > Flashcards

CNS Flashcards

1
Q

Common S+S

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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2
Q

Disorders affecting olfactory nerve

A
  • The olfactory nerve is the first cranial nerve (CN I)
  • It is part of the autonomic nervous system, which regulates body functions
  • Nerve enables sense of smell
  • CN I is the shortest sensory nerve in your body – it starts in the brain and ends in the upper, inside part of the nose
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3
Q

Symptoms of impaired olfactory nerve function

A

Ansomia- complete loss of smell
Dysomia- aka phantosmia, unpleasant or strange odours that occurs spontaneously
Hyposmia- partial loss of smell
Parasmia- distorted sense of smell

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4
Q

Conditions that affect olfactory nerve

A
  • Sinus infection
  • Nasal polyps
  • Tobacco use
  • Poor dental hygiene
  • Environmental toxins and chemicals like insecticides
  • Severe head injuries, including concussions
  • Medications like antibiotics
  • Covid
  • Head and neck cancer
  • Diabetes
  • Alzheimer’s disease
  • Brain tumour
  • Parkinson’s disease
  • Epilepsy
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5
Q

Glaucoma

A
  • Group of eye conditions that damage the optic nerve
  • The optic nerve sends visual information from your eye to your brain and is vital for good vision
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6
Q

Causes of glaucoma

A

Develops after optic nerve damage
As nerve gradually deteriorates blind spots develop in vision
Related to inc pressure in eye- can happen as result of build up that flows through inside of eye
Fluid= aqueous humor

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7
Q

Open-angle glaucoma

A

o Most common form
o Drainage angle formed by the iris and cornea remains open
o But other parts of the drainage system don’t drain properly
o This may lead to a slow, gradual increase in eye pressure

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8
Q

Angle-closure glaucoma

A

o Occurs when the iris bulges
o The bulging iris partially or completely blocks the drainage angle
o The fluid cant circulate through the eye and pressure increases
o May occur suddenly or gradually

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9
Q

Glaucoma in children

A

o May be born with it
o Can also develop it within the first few years of life
o Blocked drainage, injury or an underlying medical condition may cause optic nerve damage

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10
Q

Pigmentary glaucoma

A

o Small pigment granules flake off from the iris and block or slow fluid drainage from the eye
o Leads to a deposit of pigment granules on tissue located at the angle where the iris and cornea meet
o Granule deposits cause an increase in pressure

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11
Q

Glaucoma population

A
  • People from black, Asian and Hispanic heritage over 40
  • All other people over 60
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12
Q

Glaucoma risks

A
  • High internal eye pressure, also known as intraocular pressure
  • Age over 55
  • Black, Asian or Hispanic heritage
  • Certain medical conditions
    o Diabetes
    o Migraines
    o High blood pressure
    o Sickle cell anaemia
  • Corneas that are thin at the centre
  • Extreme near-sightedness or farsightedness
  • Eye injury or certain types of eye surgery
  • Taking corticosteroid medications, especially eye drops, for a long time
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13
Q

Open angle glaucoma S+S

A

Defend on type and stage
o No symptoms in early stages
o Gradually, patchy blind spots in the peripheral vision
o In later stages, difficulty seeing things in your central vision

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14
Q

Acute angle-closure glaucoma S+S

A

o Severe headache
o Severe eye px
o Nausea or vomiting
o Blurred vision
o Halos or coloured rings around lights
o Eye redness
Chronic- symptoms would have been developing for prolonged period

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15
Q

Normal-tension glaucoma

A

o No symptoms in early stages
o Gradually blurred vision
o In later stages, loss of side vision

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16
Q

Glaucoma in children S+S

A

o Dull or cloudy eye (infants)
o Increased blinking (infants)
o Tears without crying (infants)
o Blurred vision
o Near sightedness that gets worse
o Headache

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17
Q

Pigmentary glaucoma S+S

A

o Halos around lights
o Blurred vision with exercise
o Gradual loss of peripheral vision

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18
Q

Glaucoma prognosis

A
  • There are treatments for glaucoma but no cures as it’s a lifelong condition
  • Medications
    o Eye drops- serum to dry eyes
  • Laser therapy
  • Surgery
    o MIGS (minimally invasive glaucoma surgery)
    o Can help slow down vision loss but cant restore lost vision or cure glaucoma
  • Glaucoma is a chronic and progressive condition that causes some degree of vision loss overtime
  • Blindness is a rare complication so prognosis isn’t awful
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19
Q

Papilledema

A
  • Medical term for swelling of the optic disc
  • Almost always bilateral
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20
Q

Papilledema cause

A
  • High intracranial pressure causes papilledema
  • Other causes include
    o Hypertension
    o Tumours
    o Infection, bleeding or inflammation in the brain or the meninges
    o Cerebral venous sinus thrombosis (blood clot in a vein in your brain)
    o Iron-deficiency anaemia
    o Medication use
    o Idiopathic intracranial hypertension
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21
Q

Papilledema population

A

Overweight women
20-44

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22
Q

Papilledema risks

A

Those which raise intracranial pressure
Space occupying lesion- tumour, subarachnoid haemorrhage, dec absorption of CSF
Risk factors for idiopathic hypertension include- recent weight gain, underlying conditions- anaemia, thyroid disease, sleep apnoea

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23
Q

Papilldema S+S

A
  • Some people have no symptoms
  • Headaches
    o May be worse in the mornings or when lying down
  • Transient visual obscuration’s
    o Periods of about 5 to 15 seconds when vision gets blurry, goes grey or blacks out
    o Usually happen when you change posture
    o Can be unilateral or bilateral
  • Diplopia
  • Nausea
  • Vomiting
  • Neurological symptoms
    o May include problems with movement or thinking
  • Vision loss worsens as the condition progresses
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24
Q

Papilldema prognosis

A
  • If its due to idiopathic intracranial hypertension you may be prescribed a carbonic anhydrase inhibitor such as acetazolamide
  • If this doesn’t work surgical procedures are available
  • Maintaining a healthy weight is a long-term strategy
  • Should treat the underlying cause (if there is one)
  • If it is caught early the outlook is good
  • It needs to be treated because of the potential for blindness and other neurological effects
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25
Q

Optic neuritis

A
  • Occurs when inflammation damages the optic nerve
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26
Q

Optic neuritis cause

A
  • Exact cause is unknown
  • Believed to develop when the immune system mistakenly targets the substance covering the optic nerve, resulting in inflammation and damage to the myelin
  • The following autoimmune conditions are associated with optic neuritis
    o Multiple sclerosis
    o Neuromyelitis optica
    o Myelin oligodendrocyte glycoprotein (MOG) antibody disorder
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27
Q

Optic neuritis population

A

Females 20-40

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28
Q

Optic neuritis risks

A

20-40
Women
White people
Genetic mutations

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29
Q

Papilledema S+S

A

Unilateral
P worsened with eye movement, can feel like ache behind eye
Vision loss- develops over hours to days, improves over several weeks to months
Visual field loss
Loss of colour vision
Report of flashing lights

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30
Q

Optic neuritis prognosis

A

May spontaneously heal
Poor visual function- course of IV methylprednisolone (steroid medication) with a tapering course of oral steroids afterwards had been shown to speed recovery of visual function
Improves in about 80% of cases over few weeks
Some have continued worsening symptoms
Many people have complete resolution

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31
Q

Optic nerve atrophy

A
  • Optic atrophy is a condition that affects the cranial nerve
  • The cranial nerve carries impulses from the eye to the brain
  • Atrophy means to waste away or deteriorate
  • It is not a disease in itself but is a sign of a potentially more serious condition
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32
Q

Optic nerve atrophy cause

A
  • Where something interferes with the optic nerves ability to transmit impulses
  • The interference can be caused by numerous factors; including
    o Glaucoma
    o Stroke of the optic nerve
     Anterior ischemic optic neuropathy
    o A tumour that is pressing on the optic nerve
    o Optic neuritis
     An inflammation of the optic nerve caused by multiple sclerosis
    o A hereditary condition in which the person experiences loss of vision first in one eye, and then in the other
     Known as Leber’s hereditary optic neuropathy
    o Improper formation of the optic nerve
     Congenital problem
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33
Q

Optic nerve atrophy population

A

White people
10-50

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34
Q

Optic nerve atrophy risks

A
  • High cholesterol
  • High blood pressure
  • Sudden drop in blood pressure or blood loss
  • Swollen arteries in the head
  • Clogged arteries
  • Heart disease
  • Diabetes
  • Sleep apnoea
  • Smoking
  • Migraines
  • Glaucoma
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35
Q

Optic nerve atrophy S+S

A
  • Symptoms relate to a change in vision
  • Specifically
    o Blurred vision
    o Difficulties with peripheral vision
    o Difficulties with colour vision
    o Reduction in sharpness of vision
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36
Q

Optic nerve atrophy prognosis

A
  • No real cure or treatment
  • Important to have regular eye exams
  • Prognosis depends on what is causing the problem
    o E.g. if the problem is optic neuritis, the pt can usually count on getting their vision back when the inflammation goes away
    o If the cause is something else, the pt vision might not improve
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37
Q

Optic nerve neuropathy

A
  • Sudden loss of vision due to an interruption of blood flow to the anterior of the optic nerve
  • 2 types
    o Arteritic AION
     Caused by inflammation of arteries supplying blood to the optic nerve
    o Nonarteritic AION
     Caused by reasons other than inflammation of the arteries
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38
Q

Optic nerve neuropathy cause- arthritic AION

A

o Dangerous condition
o Caused by inflammation of arteries supplying blood to the optic nerve
o Inflammation is due to a condition called giant cell arteritis (GCA) or temporal arteritis, which caused inflammation of medium and large sized arteries
o 3x more common in women
o Most often affects people over the age of 55

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39
Q

Optic nerve neuropathy- non-arteritic AION

A

o Most common form of AION
o Majority of people affected are over 50
o Both men and women affected equally
o Caused by one of the following
 A drop in blood pressure to such a degree that blood supply to the optic nerve is devreased
 Increased pressure inside the eyeball
 Narrowed arteries
 Increased blood viscosity
 Decreased blood flow to the optic nerve where it leaves the back of the eye

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40
Q

Optic nerve neuropathy population

A
  • Adults over 50
  • A-AION – women more than men
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41
Q

Optic nerve neuropathy risks

A
  • High blood pressure
  • Biabetes mellitus
  • High cholesterol
  • Smoking
  • Sleep apnoea
  • Heart disease
  • Blocked arteries
  • Anaemia or sudden blood loss
  • Sudden drop in blood pressure
  • Sickle cell trait
  • Vasculitis
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42
Q

Optic nerve neuropathy S+S- NA-AION

A

o Sudden, painless loss or blurring of vision in one eye
 Usually noticed upon waking from a nights sleep or a nap
o Decreased visual activity
o Dyschromatopsia
o A RAPD
 Relative afferent pupillary defect
o Swollen optic nerve with splinter haemorrhages
o Visual field defect

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43
Q

Optic nerve neuropathy S+S- A-AION

A

o Px in the temples
o Px when chewing
o Scalp px or tingling
o Neck px
o Muscle aches and pains
 Esp in upper legs or arms
o General fatigue
o Loss of appetite
o Unexplained loss of weight
o Fever

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44
Q

Optic nerve neuropathy prognosis

A

A-AION usually causes greater degree of vision loss
Degree of loss depends on location and amount of optic nerve that is damaged

In NA-AION about 40% show some amount of improvement in central vision in months after loss of vision or visual fields

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45
Q

Optic nerve neuropathy treatment

A

o A-AION = basically the same treatment as giant cell arteritis (corticosteroid therapy)
o NA-AION = treatment is for the underlying cardiovascular disease or the risk factors that help trigger and aggravate NA-AION

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46
Q

Macular degeneration

A
  • Also known as age-related macular degeneration
  • An eye disease that affects central vision
  • Top cause of vision loss in people over 50
  • 2 types
    o Dry (atrophic)
     Up to 90% have the dry form
    o Wet (exudative)
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47
Q

Macular degeneration cause- dry

A
  • Inherited eye disease
  • Occurs when the macula at the back of the eye starts to deteriorate for an unknown reason

o Develops when tiny yellow protein deposits called drusen form under the macula
o The build-up deposits dry and thin the macula
o Vision loss tends to occur gradually
o Most people don’t completely lose central vision

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48
Q

Causes macular degeneration- wet

A

o Occurs when abnormal blood vessels develop under the retina and macula
o The blood vessels leak blood and fluid
o Because of the fluid build-up a bulge forms in the macula
o May see dark spots in centre of vision
o Can quickly lead to total loss of central vision loss

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49
Q

Macular degeneration population

A

White people over 50

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50
Q

Macular degeneration risks

A
  • Older age
    o Over 50
  • Family hx
  • Being overweight
  • Smoking
  • Hypertension
  • Diet high in saturated fats
  • Being of European descent
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51
Q

Macular degeneration S+S

A
  • Many people don’t have symptoms until the disease progresses
  • Blurred vision
  • Blank or dark spots in field of vision
  • The appearance of waves or curves in straight lines
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52
Q

Macular degeneration prognosis

A
  • No cure
  • Prognosis depends on degree of vision loss
  • Not everyone will experience significant vision loss
    Vision rehab programme
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53
Q

Macular degeneration treatment

A

o Nutritional supplements- A, C, + E
o Antivascular endothelial growth factor (anti-VEGF)
o Photodynamic therapy (PDT)

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54
Q

Macular degeneration precautions you can take

A

o Quit smoking
o Lose weight
o Stay physically active
o Maintain healthy blood pressure and cholesterol levels
o Eat a healthy diet

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55
Q

Macular degeneration things that help day to day

A

o Wear eyeglasses or contact lenses
o Use brighter lights at home or at work
o Read with a magnifying device

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56
Q

Occulomotor palsy

A
  • The oculomotor nerve is the 3rd of 12 cranial nerves (CN III)
  • It is part of the autonomic nervous system
  • It allows movement of the eye muscles, constriction of the pupil, focusing the eyes and the position of the upper eyelid
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57
Q

Function of oculomotor

A
  • Controls 4 of the 6 muscles that enable eye movement
  • Elevate the upper eyelid
  • Focus the eyes
  • Respond to light by making the pupil smaller
  • Move your eyes inward, outward, up and down and control torsion
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58
Q

Cause of oculomotor palsy

A

Cause
- Oculomotor palsy is a group of disorders affecting the CN III
- They occur when the third cranial nerve becomes paralyzed
- Can be present at birth
- May occur later in life due to
o Inadequate blood flow – causes a lack of oxygen that nerves need to function properly
o Nerve compression – abnormal pressure on a nerve

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59
Q

Conditions which may cause oculomotor palsy

A

o Brain aneurysm
o Brain tumour
o Head injuries
o Demyelinating disease
 Multiple sclerosis
o Microvascular disease
 Diabetes
 High blood pressure
o Infections
 HIV
 Lyme disease
o Migraine

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60
Q

Trochlear nerve plays

A
  • The trochlear nerve is the 4th of 12 cranial nerves (CN IV)
  • It is part of the autonomic nervous system
  • It innervates many of the organs, including the eyes
  • It is a motor nerve that sends signals from the brain to the muscles
  • CN IV works with the oculomotor nerve and other eye muscles to control eye movement
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61
Q

Trochlear nerve palsy

A
  • A palsy occurs when illness or injury paralyzes nerves that control muscle movements
    Congenital
    Trauma
    More fragile- long and thin
    Can occur after minor injuries
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62
Q

Treatment of trochlear nerve

A
  • Treatment depends on what is causing symptoms
  • Vision injuries causes by minor injuries often go away on their own
  • For more severe palsy, treatments may include
    o Eye patch to help the eye rest
    o Special glasses to correct double vision
    o Surgery to repair cranial nerve 4
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63
Q

Trigeminal neuralgia

A
  • Causes painful sensations like an electric shock on side of face
  • Chronic P affects trigeminal nerve, which carries sensations from face to brain
  • Variety of treatment, effectively manage it- medications, injections or surgery
64
Q

Trigeminal neuralgia cause

A
  • Trigeminal nerve function disrupted
  • Contact between blood vessel and nerve at base of brain
  • Contact puts pressure on nerve and causes it to malfunction
  • Sometimes related to MS
  • Tumour compressing nerve
65
Q

Trigeminal neuralgia population

A

50+
More common in women

66
Q

Trigeminal neuralgia risk

A
  • Hypertension
  • Arteriosclerotic changes
  • Aging
  • Family Hx
67
Q

Trigeminal neuralgia S+S

A
  • Episodes of severe, shotting or jabbing P that may feel like and electric shock
  • Spontaneous attacks triggered by things such as touching your face
  • Attacks of P lasting a few seconds to several mins
  • P occurs with facial spasms
  • P in areas supplied by trigeminal- jaw, cheek, teeth, gums, lips or forehead
  • P rarely occurs at night while sleeping
68
Q

Trigeminal neuralgia prognosis

A
  • Episodes can occur daily or weekly or months
  • 50% of people experience remission of at least 6 months
69
Q

Abducens palsy

A
  • Most common ocular motor paralysis in adults and second-most common in children
  • Causes problems with eye movements
70
Q

Abducens palsy risks

A
  • Inflammatory and microvascular conditions
  • MS
  • Meningitis
71
Q

Abducens palsy S+S

A

Headache, P around eyes, nausea, vomiting, pulse synchronous tinnitus

72
Q

Abducens palsy prognosis

A

Usual recovery between 3-6 months
Treatment- prisms, occlusion, botulinum toxin or surgery

73
Q

Facial nerve palsy

A
  • Causes sudden weakness in muscle of one side of face
74
Q

Facial nerve palsy cause

A
  • Not clear
  • Often related to viral infection
  • Viruses sought to be linked:
    1. Cold sores and genital herpes
    2. Herpes zoster
    3. Influenza
    4. Hand-foot-and-mouth disease
75
Q

Facial nerve palsy population

A
  • Pregnant, diabetic, influenza
76
Q

Facial nerve palsy risks

A
  • Pregnancy- especially third trimester
  • Have upper respiratory infection- such as flu or cold
  • Have diabetes
  • Have high blood pressure
  • Obesity
77
Q

Facial nerve palsy S+S

A
  • Rapid onset of mild weakness to total paralysis of one side of face
  • Facial droop and difficulty making facial expressions
  • Drooling
  • P around jaw or behind ear
  • Inc sensitivity to sound on affected side
  • Headache
78
Q

Facial nerve palsy prognosis

A

Full recovery usually 6 months

79
Q

Vestibular disorders- acoustic neuroma

A
  • Noncancerous, slow-growing tumour that develops on vestibular nerve leading from inner ear to brain
  • Branches directly influence balance and hearing
80
Q

Acoustic neuroma cause

A
  • Linked with defect of gene on chromosome 22
  • Normally this gene produces tumour suppressor protein that helps control growth of Schwan cells covering nerves
  • Most cases, no known cause
81
Q

Acoustic neuroma risks

A
  • Neurofibromatosis type 2- parent with rare genetic disorder neurofibromatosis type 2
82
Q

Acoustic neuroma clinical presentation

A
  • Easy to miss and may take years to develop
  • Hearing loss- usually gradually worsening over months to years
  • Tinnitus
  • Unsteadiness/loss of balance
  • Vertigo
  • Facial numbness/loss of muscle movement
83
Q

Acoustic neuroma prognosis

A
  • Treatment includes regular monitoring, radiation and surgical removal
84
Q

Vestibular disorder- Benign paroxysmal positional vertigo (BPPV)

A
  • Most common cause of vertigo
85
Q

BPPV causes

A
  • Idiopathic
  • Associated with minor to severe blow to head
  • Less common causes include disorders that damage inner ear
86
Q

BPPV risks

A
  • 50+
  • Women
  • Head injury
87
Q

BPPV S+S

A
  • Dizziness
  • Vertigo
  • Loss of balance/unsteadiness
  • Nausea/vomiting
  • Come and go, commonly last less than one minute
88
Q

BPPV prognosis

A
  • Bothersome but rarely serious except when it inc chance of falls
  • Can receive treatment during doctor visits
    Epley manoeuvre
89
Q

Vestibular disorder- labrynthitis

A
  • Inflammation of labyrinth- part of inner ear
  • Inner ear infection- responsible for hearing and balance
90
Q

Labrynthitis cause

A
  • Mostly caused by virus, sometimes bacteria
  • Bronchitis or other respiratory illness
  • Viral infection of ear
  • Herpes virus
  • Stomach viruses
  • Bacterial infections
  • Measles, mumps, rubella, polio
91
Q

Labrynthitis S+S

A
  • Loss of balance
  • Dizziness
  • Vertigo
  • Nausea/vomiting
  • Blurry vision
  • Hearing loss
  • Tinnitus
92
Q

Labrynthitis prognosis

A
  • Most people completely better within 2-3 months
  • Symptoms usually go away within a week
93
Q

Vestibular disorders- Menderes disease

A
  • Inner ear problem that can cause vertigo and hearing loss
94
Q

Menieres disease cause

A
  • Unknown
  • May be due to extra fluid in inner ear called endolymph
  • Isn’t clear what causes liquid build up
95
Q

Menieres disease population

A
  • Can happen at any age
  • Usually starts between 40-60
96
Q

Menieres disease risks

A
  • Family Hx
  • Pressure changes
  • Stress
  • Changes hormones
  • Problems sleeping
97
Q

Menieres disease S+S

A
  • Regular dizzy spells
  • Hearing loss
  • Ringing in ear
  • Feeling of fullness in ear
98
Q

Menieres disease prognosis

A
  • No cure
  • Progressive disease which worsens over time
99
Q

Vestibular migraine

A
  • Nervous system problem that causes vertigo in people who have a Hx of migraine symptoms
100
Q

Vestibular migraine cause

A
  • Unsure
  • Potential misfires between nerve cells in brain
101
Q

Vestibular migraines population

A
  • More common in women
  • Symptoms tend to strike around 40
102
Q

Vestibular migraine risks

A
  • Mood- stress/anxiety
  • Poor sleep
  • Dehydration/hunger
  • Dietary triggers- e.g., caffeine
  • Hormonal changes
103
Q

Vestibular migraine S+S

A
  • Headaches and dizziness which comes and goes
  • Nausea and vomiting
  • Balance problems
  • Sensitivity to sound
104
Q

Vestibular migraine prognosis

A
  • No cure, management of triggers can lead to normal life
105
Q

MS

A
  • Potentially disabling disease of CNS
  • Immune system attacks myelin sheath that covers nerve fibres and axons
  • Causes communication problems between brain and rest of body
    Causes physical disability for 20-25 years in 30% of Px
106
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
    Infections- e.g. virus
107
Q

MS population

A
  • White women aged between 20-40
108
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
109
Q

MS S+S

A

First
Blurry vision
Diplopia
Red-green colour distortion
Optic neuritis- P and loss of vision
Trouble walking
Paresthesia

Other- muscle weakness in appendices, trouble w concentration, spasticity, fatigue, loss of sensation, speech problems, tremor, dizziness

About 50% have have cognitive problems- concentration, attention, memory

110
Q

MS Primary, secondary, tertiary

A

Primary- occur as a result of myelin destruction
Weakness
Numbness
Tremors
Loss of vision
P, paralysis
Loss of balance
Bladder problems

Secondary- as a result of primary
Paralysis–> bedsores
Bladder problems- repeated UTIs
Inactivity- poor posture, decreased bone density

Tertiary- external factors which are affected
Unable to to work- may lose livelihood
Strain of chronic illness may disrupt relationships

111
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
112
Q

Temporal arteritis

A
  • Inflammation of lining of arteries
  • Aka giant cell arteritis
113
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
114
Q

Temporal arteritis risks

A
  • 70-80
  • Women 2x
  • White people
  • PMR
  • Family Hx
115
Q

Temporal arteritis S+S

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
116
Q

Temporal arteritis prognosis

A
  • Prompt treatment with corticosteroid medication usually relives symptoms and might prevent vision loss
  • Relapse common even with treatment
117
Q

Meningitis

A
  • Infection and inflammation of the fluid membranes surrounding the brain and spinal cord
  • These membranes are called meninges
118
Q

Meningitis causes

A
  • Viral infections are most common cause of meningitis
  • Followed by bacterial infections and rarely fungal and parasitic infections
119
Q

Meningitis bacterial

A

o Bacteria that enters the bloodstream and travels to the brain and spinal cord
o Can also occur when bacteria directly invades the meninges
o May be caused by an ear or sinus infection or a skull fracture

120
Q

Common bacterial meningitis strains

A

Streptococcus pneumoniae- most common in infants, young children, adults. Vaccine helps prevent

Neisseria meningitidis- Commonly causes upper respiratory infection but can cause meningococcal meningitis when they enter the bloodstream

Haemophilus influenzae- Was once the leading cause in young children, vaccines have greatly reduced the number of cases

Listeria monocytogenes- Pregnant people, new-borns, older adults and people with weakened immune systems are most susceptible

121
Q

Viral meningitis

A

o Usually mild and often clears on its own
o Most cases are due to a group of viruses called enteroviruses
o Most common in late summer and early fall

122
Q

Chronic meningitis

A

o Long lasting
o Can be caused by slow growing organisms such as fungi and Mycobacterium tuberculosis
o Invade the membranes and fluid surrounding the brain
o Develops over 2 weeks or more
o Symptoms are similar to acute meningitis

123
Q

Fungal meningitis

A

o Isn’t common in western countries
o May mimic acute bacterial meningitis
o Often contracted by breathing in fungal spores that may be found in soil, decaying wood and bird droppings
o Isn’t spread from person to person
o Affects people with a weakened immune system
o Can come back even after treatment

124
Q

Parasitic meningitis

A

o Causes a rare type of meningitis called eosinophilic meningitis
o Can be caused by a tape worm infection in the brain or cerebral malaria
o Isn’t spread between people

125
Q

Meningitis population

A
  • Viral – children under 5
  • Bacterial – people under 20
126
Q

Meningitis risks

A
  • Skipping vaccinations
  • Age
    o Most cases of viral meningitis occur in children under 5
    o Bacterial meningitis is common in those under 20
  • Living in a community setting
    o College students living in dorms
    o Personnel on military bases
    o Children in boarding school or care facilities
  • Pregnancy
    o Increases the risk of an infection caused by listeria bacteria
    o Increased the risk of miscarriage, still birth and premature delivery
  • Weakened immune system
    o AIDS
    o Alcohol use disorder
    o Diabetes
    o Use of immunosuppressant drugs
    o Having spleen removed
127
Q

Meningitis S+S

A
  • Early meningitis symptoms may be similar to the flu
  • Symptoms may develop over several hours or over a few days
  • Possible symptoms in anyone older than 2 years include
    o Sudden high fever
    o Stiff neck
    o Severe headache
    o Nausea or vomiting
    o Confusion
    o Trouble concentrating
    o Seizures
    o Sleepiness or trouble waking
    o Sensitivity to light
    o No appetite or thirst
    o Skin rash in some cases, such as in meningococcal meningitis
128
Q

Signs of meningitis in new borns

A

o Nigh fever
o Constant crying
o Being very sleepy or irritable
o Trouble waking from sleep
o Being inactive or sluggish
o Not waking to eat
o Poor feeding
o Vomiting
o A bulge in the soft spot on top of the baby’s head
o Stiffness in the body and neck

129
Q

Meningitis prognosis

A
  • Viral meningitis can go away on its own within about a week
  • You can survive most forms of meningitis, though it is a very serious illness that requires immediate treatment
  • Treatment depends on the cause
  • You should start to feel better within a few days to a week after starting treatment for meningitis
  • Full recovery can take weeks to months
130
Q

Meningitis treatment

A

o Antibiotics for bacterial meningitis
o Antifungal for fungal meningitis
o Antivirals for certain cases of viral meningitis, like herpesvirus and influenza
o Corticosteroids, like dexamethasone or prednisone, to reduce inflammation
o Pain relievers
o IV fluids to keep hydrated

131
Q

Epilepsy

A
  • A CNS (neurological) disorder in which brain activity becomes abnormal, causing seizures or periods of unusual behaviour, sensations and sometimes loss of awareness
132
Q

Epilepsy causes

A
  • No identifiable cause in about half of people with the condition
    Contributing factors- brain abnormalities (e.g., tumours, stroke in 35+), infections (meningitis, HIV), prenatal injury (poor nutrition, O2 deficit), developmental disorders (autism)
133
Q

Epilepsy population

A
  • Anyone
  • Can affect people of all genders, races, ethnic backgrounds and ages
134
Q

Epilepsy risks

A

Age- children and older adults
Family Hx
Head injury
Stroke
Dementia
Brain infection (meningitis)
Seizures in childhood

135
Q

Epilepsy clinical presentation

A

o Temporary confusion
o Staring spell
o Stiff muscles
o Uncontrollable jerking movements of the arms and legs
o Loss of consciousness or awareness
o Psychological symptoms such as fear, anxiety or déjà vu

136
Q

Focal seizure S+S

A

 Can occur with consciousness or with impaired awareness
 Confusion
 Migraine
 Narcolepsy
 Mental illness

137
Q

Generalised seizures

A

Absence- staring into space
Tonic- stiff muscles and may affect consciousness
Atonic- drop seizures, loss of muscle control
Clonic- repeated or rhythmic, jerking muscle movement
Myoclonic- usually appear as sudden or brief jerks or twitches
Tonic-clonic- abrupt loss of consciousness and body stiffening, twitching and shaking- most dramatic

138
Q

Epilepsy prognosis

A

No cure but lots of treatment
Anti seizure meds- controls 60-70%
Diet therapy- high in fat, moderate protein and low carbs
Surgery- severance of corpus colosseum

139
Q

PD

A
  • A progressive disorder that affects the nervous system and the parts of the body controlled by the nerves
140
Q

PD cause

A
  • Certain nerve cells (neurons) in the brain gradually break down or die
  • Many of the symptoms are due to a loss of neurons that produce a chemical messenger in your brain – dopamine
  • When dopamine levels decrease, it causes atypical brain activity, leading to impaired movement and other symptoms of Parkinson’s disease
  • Exact cause is unknown but several factors appear to play a role
    o Genes
    o Environmental triggers
     Certain toxins or environmental factors
141
Q

PD population

A
  • Men at middle to late age
142
Q

PD risk factors

A

Age- middle-later life
Family Hx
Sex- men
Exposure to toxins- herbicides/pesticides

143
Q

PD clinical presentation

A

Variable
Early signs are mild and may go unnoticed
Often begins unilaterally

Tremor- starts in hand
Bradykinesia- slow movement
Rigid muscles
Stoop posture
Speech changes- monotone

144
Q

PD prognosis

A

No cure, manageable
Meds- levodopa
Deep brain stimulation
Experimental treatment- stem cell transplant, neuron-repair treatment

145
Q

Dizziness and 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
146
Q

Dizziness and vertigo population

A

65+

147
Q

Dizziness/vertigo risks

A
  • Older adults
  • Past episodes of dizziness
148
Q

Dizziness/vertigo S+S

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
149
Q

Dizziness/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
150
Q

Myasthenia gravis

A
  • Characterised by weakness and rapid fatigue of any muscle under voluntary control
    Most commonly affects eye/eye lid muscles
151
Q

Myasthenia gravis cause- antibodies

A

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

152
Q

Myasthenia gravis cause- thymus gland

A

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

153
Q

Myasthenia gravis other cause

A
  • Mother to child- if treated promptly child usually recovers within two months after birth
154
Q

Myasthenia gravis population

A
  • Can affect anyone
  • Women more likely under 40
  • Men over 60
155
Q

Myasthenia gravis risks

A
  • Women between 20-30
  • Men 60-70
156
Q

Myasthenia gravis S+S

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
157
Q

Myasthenia gravis prognosis

A
  • No cure but treatment can help relieve signs and symptoms

Systemic Conditions (8 decks)

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