nervous system

Question 1

Multiple sclerosis

Answer 1

• A chronic inflammatory disease involving degeneration of CNS myelin, scarring, and loss of axons -

Cause: autoimmune response to self or microbial antigens in genetically susceptible individuals

Treatments: immunosuppressants, corticosteroids
No cure, but try to mitigate exacerbations and progressions

Risk factors:
Smoking
Vitamin D deficiency
Epstein-Barr virus infection

Cause:
Autoreactive T and B cells cross the BBB and recognize myelin and oligodendrocyte autoantigens, triggering inflammation and loss of oligodendrocytes (produce myelin)
Activation of microglia cells (brain macrophages) contributes to inflammation ad injury with plaque formation and axonal degeneration
Loss of myelin disrupts nerve conduction with subsequent death of neurons and brain atrophy

Clinical manifestations:
Paresthesias of the face, trunk, or limbs
Weakness
Impaired gait
Visual disturbances
Urinary incontinence
Nystagmus
Ataxia
Weakness with all four limbs
Intention tremor
Slurred speech

Question 2

Meningitis

Answer 2

Inflammation of the brain or spinal cord

Cause: bacteria, virus, fungi, parasites, toxins
Classified as: acute, subacute, or chronic

Fungal meningitis:
chronic and less common
Produces a granulomatous reaction
Can extend along perivascular sites in the subarachnoid space and into the brain tissue
Leads to arteritis with thrombosis, infarction, and communicating hydrocephalus

Clinical manifestations:
Dementia symptoms
Communicating hydrocephalus
Afebrile

Viral Meningitis:
AKA aseptic or nonpurulent meningitis
No identifiable bacterium
Usually enteroviral virus, arboviruses, and herpes simplex type 2
Virus enters the NS by:
Crossing the BBB
Direct spread along peripheral nerves
Through the choroid plexus epithelium
Virus activates inflammatory response
Similar symptoms to those of bacterial meningitis

Question 3

Bacterial Menginitis

Answer 3

An infection of the pia mater and arachnoid layers, the arachnoid space, the ventricular system, and the CSF

Bacteria: Meningococci & Pneumococci

Transmission: respiratory droplets or contact with droplets
Treatments: antibiotics and prophylactic vaccines

Most common

Common bacteria:
Meningococci (Neisseria meningitis), when the infection is caused by this bacteria it can be called meningococcemia
Pneumococi (Streptococcus penumoniae)
Most common in children
Can be carriers and spread the virus without symptoms
Bacteria enter bloodstream and cross the BBB to infect the meninges. Causing neutrophils to enter subarachnoid space and exhibit inflammatory response. This thickens CSF, interfering with normal CSF function causing hydrocephalus. Blood vessels also engorge.

CM:
Systemic infection symptoms
Severe throbbing HA
Severe photophobia
Nuchal rigidity
Positive Kernig and Brudzinski signs
Decrease in LOC
Cranial nerve palsies
Focal neurologic deficits
Seizures
Projectile vomiting
Specifically for meninogococcal meningitis you may have petechial or purpuric rash covering the skin and mucus membranes

Complication: purpura fulminans

Question 4

Brain or Spinal cord Abscess

Answer 4

Localized collections of pus form within the parenchyma of the brain or spinal cord

Very rare
Classifications: epidural, subdural, or intracerebral
Commonly found in drug abuser who share needles or immunosupressed
Treatment: antibiotics, aspiration/decompression

Epidural is associated with osteomyelitis in a cranial bone, but in the spine the osteomyelitis occurs in the vertebrae.

Subdural brain abscesses arise from a sinus infection or a vascular source.

Intracerebral brain abscesses arise from a vascular source.

Clinical manifestations of brain abscess:
low-grade fever
Headache
N/V
Neck pain and stiffness
Confusion
Drowsiness
Sensory deficits
Communication deficits
Decreased attention span
Memory deficits
Decreased visual acuity
Narrowed visual fields
Papilledema
Ocular palsy
Ataxia
Dementia
Seizures

Clinical manifestations of spinal abscess:
Spinal aching
Severe root pain, back spasms and stiffness
Weakness caused by progressive cord compression
Paralysis

Question 5

Encephalitis

Answer 5

An acute febrile illness, usually of viral origin, with nervous system involvement

Causes: mosquito, tick or fly bites, Herpes SImplex type 1, or complications of systemic viral diseases

Treatments: antiviral agents (acyclovir), steroids, sometimes antibiotics

Systemic viral diseases:
Poliomyeltitis
Rabies
Mononucleosis
Rubella
Varicella
Rubeola
Yellow fever

Can occur after vaccination with a live attenuated virus.

Viruses gain access to the CNS through:
Bloodstream
Olfactory bulb
Choroid plexus
Intraneuronal route from peripheral nerves

Viruses cause widespread nerve cell degeneration leading to edema, necrosis and increased ICP.

Mild symptoms:
Malaise
HA
Body aches
N/V

Severe symptoms:
Fever
Delirium
Confusion/unconsciousness
Difficulty finding words
Seizure activity
Cranial nerve palsies
Paresis & paralysis
Involuntary movement and abnormal reflexes

Question 6

Guillain-Barré Syndrome

Answer 6

Rare demyelinating disorder caused by a humoral and cell-mediated immunologic reaction directed at the peripheral nerves

Cause: complication of respiratory tract or GI viral infection

Treatment: IV immunoglobulin or plasmapheresis and aggressive rehab
Recovery can take weeks to 2 years

Manifestations:
Ascending motor paralysis
Paresis of legs to complete quadriplegia
Paralysis of eye muscles
Respiratory insufficiency
Autonomic NS instability
Sensory symptoms (pain, numbness, paresthesias)
Respiratory arrest or cardiovascular collapse

Question 7

Stroke Syndromes

Answer 7

Ischemic Strokes
Transient Ischemic Attacks
Thrombotic strokes
Embolic stroke
Lacunar strokes
Hemodynamic stroke
Hemorrhagic stroke
Intracranial aneurysm
Subarachnoid hemorrhage

Risk factors:
HTN
Type 2 diabetes mellitus
High cholesterol
Smoking
Polycythemia and thrombocythemia
CHF
Peripheral vascular disease
Atrial fibrillation

Question 8

Ischemic Strokes

Answer 8

Occurs due to an obstruction in arterial blood flow to the brain

Causes: thrombus formation, an embolus, or hypoperfusion related to decreased blood volume or heart failure

Result; ischemia of brain tissue which can lead to infarction of brain tissue

Types: TIAs, Thrombotic strokes. Embolic strokes. Lacunar strokes, Hypoperfusion stroke

Cerebral infarction occurs when an area of the brain loses its blood supply because of vascular occlusion.

When occlusion occurs the necrotic tissue become infiltrated with macrophages and the tissue becomes phagocytized. It heals but you still have a cavity present and glial scarring

Question 9

Transient Ischemic Attacks

Answer 9

Episodes of neurologic dysfunction lasting no more than 1 hour and resulting from focal cerebral ischemia

Clinical manifestations:
Weakness
Numbness
Sudden confusion
Loss of balance
Sudden severe headache

__At risk of a stroke in the near future__

Question 10

Thrombotic Strokes (cerebral thromboses)

Answer 10

Stroke that arise from arterial occlusions caused by thrombi formation in arteries supplying the brain or intracranial vessels

Caused by conditions that increase coagulation or cause inadequate cerebral perfusion
Dehydration, hypotension, prolonged vasoconstriction from
malignant hypertension

Usually occur at branches or curvature in cerebral circulation

Can grow for many years (artherosclerosis)

Question 11

Embolic Strokes

Answer 11

Strokes that are caused by fragments that break from a thrombus formed outside the brain
Also can be fat, air, tumor, bacterial clumps, and foreign
bodies
Involve small brain vessels and obstruct at bifurcations or other points of narrowing….Usually occurs in the branches of the middle cerebral artery

Middle cerebral artery is the largest cerebral artery.

Risk factors:
Atrial fibrillation
Left ventricular aneurysm or thrombus
Left atrial thrombus
Recent MI
Endocarditis
Rheumatic valve disease
Mechanical valvular protheses
Atrioseptal defects
Patent foramen ovale
Primary cardiac tumors

Question 12

Lacunar Strokes

Answer 12

Strokes caused by occlusion of a single, deep perforating artery that supplies small penetrating subcortical vessels

Cause ischemic lesions predominantly in basal ganglia, internal capsules, and pons

Very rare

Symptoms: pure motor or sensory deficits

Question 13

Hemodynamic

Answer 13

Associated with systemic hypoperfusion caused by cardiac failure, pulmonary embolism, or bleeding that results in inadequate blood supply to the brain

Symptoms: bilateral and perfuse

Question 14

Clinical manifestations of ischemic strokes

Answer 14

Carotid artery occlusion:
Dysphasia
Contralateral motor and sensory deficits

Middle cerebral artery occlusion:
Conjugate ipsilateral eye deviation
Contralateral sensory deficits

Vertebrobasilar system syndromes:
Dizziness
Ataxia
Quadriplegia
Coma

Reason for contralateral deficits – motor tracts originate in the cortex and cross over at the medulla.

Question 15

Hypoxic Brain Injury

Answer 15

Caused by: stroke, cardiac arrest, strangulation, severe anemia, hypotension, smoke inhalation, shock

All of the causes lead to inadequate amounts of oxygen to meet the metabolic demands of the brain

Usually starts after 4 minutes of anoxia

Question 16

Hemorrhagic stroke

Answer 16

Occur in the intraparenchyma or subarachnoid or subdural spaces

Primary cause: HYPERTENSION

Characterized by: massive, small, slit or petechial

Subarachnoid hemorrhage is associated with ruptured aneurysms or arteriovenous malformations or brain trauma.

Subdural hemorrhage is usually associated with brain trauma.

Hypertensive hemorrhagic strokes involve smaller arteries and arterioles:
putamen of the basal ganglia
Thalamus
Cortex and subcortex
Pons
Caudate nucelus
Cerebellar hemispheres

Massive = centimeters
Small = 1-2 cm
Slit = subcortical area
Petechial = pinhead bleed

Typically, cerebral hemorrhages resolves through reabsorption by macrophages and astrocytes and usual leave a glial scar.

Question 17

Parkinsons disease

Answer 17

Complex motor disorder accompanied by systemic nonmotor and neurologic symptoms.

Cause: degeneration of basal ganglia with dysfunctional or misfolded alpha-synuclein protein and loss of dopamine-producing neurons in the substantia nigra and dorsal striatum. This results in depletion of cholinergic (excitatory) activity in the feedback circuit are manifested by hypertonia and akinesia. Dementia can also occur.

Clinical manifestations:
- resting tremor
Rigidity
Bradykinesia – slowness of voluntary movements
Akinesia – decrease in voluntary and associated movements
Postural disturbances
Dysarthria
Dysphagia
Typically bilateral presentation of symptoms
Sleep disorders

Meds:
Levodopa
Deep brain stimulation

Question 18

Strabismus

Answer 18

one eye deviates from the other when the person is looking at an object

Due to weak or hypertonic muscle in one eye
Deviate up, down, in, out
Biggest symptom is diplopia(double vision)

Question 19

Nystagmus

Answer 19

involuntary unilateral or bilateral rhythmic motion of the eyes

Can be caused by imbalanced reflex activity of the inner ear, vestibular nuclei, cerebellum, medial longitudinal fascicle, or nuclei of the oculomotor, trochlear, and abducens cranial nerves

Question 20

Amblyopia

Answer 20

reduced vision in the affected eye caused by cerebral blockage of the visual stimuli

Question 21

Cataract

Answer 21

cloudy or opaque area in the ocular lens and leads to visual loss when located on the visual axis

Worsens with age as lens enlarges
Caused by alterations of metabolism and transport of nutrients within the lens
Signs/symptoms:
Decrease visual acuity
Blurred vision
Glare
Decreased color perception

Question 22

Glaucomas

Answer 22

condition leading to blindness characterized by increased intraocular pressures (>12-20mmHg) and cause death of the retinal ganglion

Question 23

Age-related macular degeneration

Answer 23

severe and irreversible loss of vision due to degeneration of macula of the eye
Atrophic and neovascular

Increased choroidal blood vessel growth
Limited night vision
Eventually complete vision loss (especially central vision)
Risk factors:
HTN
Cigarette smoking
Diabetes
Family hx

Question 24

Myopia

Answer 24

nearsightedness
Light rays are focused in front of the retina when the person is looking at a distant object.

Question 25

Hyperopia

Answer 25

farsightedness
Light rays are focused behind the retina when a person is looking at a near object.

Question 26

Astigmatism

Answer 26

unequal curvature of the cornea
Light rays are bent unevenly and do not come to a single focus on the retina
Coexist with myopia, hyperopia, or presbyopia

Question 27

photophobia

Answer 27

eye discomfort due to light

Question 28

ptosis

Answer 28

drooping eye lid

Question 29

reduced peripheral field

Answer 29

aka tunnel vision – loss of peripheral sight

Question 30

Acute Confusional States and delirium

Answer 30

Acute confusional states - transient disorders of awareness and may have either a sudden or gradual onset
Synonymous with delirium but also is a type of acute confusional
state

Types: excited delirium syndrome & hypoactive delirium

NOT the same as dementia

These states may occur due to disruptions in parts of the CNS such as:
Reticular activating system of the upper brainstem
Projections into the thalamus
Basal ganglion
Specific association areas of the cortex and limbic system

Delirium
It is a hyperactive confusional state
Associated with right-upper middle-temporal gyrus or left temporal-occipital junction disruption and several NTs (acetylcholine and dopamine) are involved

Excited delirium
Aka agitated delirium
Type of hyperkinetic delirium that can lead to sudden death
Cardiac death due to electrolyte imbalances and rhabdo
Treatment by police

Clinical manifestations:
Altered LOA
Combativeness
Aggressiveness
Tolerance to significant pain
Rapid breathing
Sweating
Severe agitation
Elevated temperature

Question 31

Dementia

Answer 31

An acquired deterioration and a progressive failure of many cerebral functions that includes impairment of intellectual process with a decrease in orienting, memory, language, judgment, and decision making

Usually due to environmental causes, genetic predispositions and sometimes CNS infections

No cures

Question 32

Myasthenia gravis

Answer 32

Neuromuscular junction disorder

An acquired chronic automimmune disease mediated by antibodies against the acetylcholine receptor at the postsynaptic membrane of the neuromuscular junction

Complications: myasthenic crisis and cholinergic crisis

Treatments: anticholinesterase drugs, steroids, and immunosuppressant drugs, thymectomy

Patho:
The post-synaptic acetylcholine receptors on the muscle cell’s plasma membrane are no longer recognized as “self” and elicit T-cell-dependent formation of IgG autoantibodies.
These block binding of acetylcholine and cause destruction of the sites. Not allowing nerve impulses to cross.

Clinical manifestations:
Muscles of the eyes, face, mouth, throat, and neck usually affected first
Drooling, difficulty chewing and swallowing
Aspiration risk
Muscles of the neck, shoulder girdle, and hip flexors can occur after exercise and become progressively weak
Respiratory muscles can become weak and impair ventilation

Myasthenic crisis
Severe muscle weakness cause:
Extreme quadriparesis or quadriplegia
Respiratory insufficiency with SOB could progress to respiratory arrest
Extreme dysphagia

Cholinergic crisis
S/S mneumonic – DUMBELLS
Diarrhea, urination, miosis, bradycardia, emesis, lacrimation, lethargy, salivation

Question 33

Spondylolysis

Answer 33

A response to continuous vertical compression of the spine (axial loading) that includes disruption of normal building and maintenance of the lumbar disk cartilage

Usually due to a genetic component and environmental interactions

structural defect in the pars interarticularis of the vertebral arch
L5 is most affected
can lead to spondylolisthesis
Lower back and lower limb pain

Question 34

Spodylolithesis

Answer 34

A response to continuous vertical compression of the spine (axial loading) that includes disruption of normal building and maintenance of the lumbar disk cartilage

Usually due to a genetic component and environmental interactions

An osseous defect of the pars iinterarticularis that allows a vertebra to slide anteriorly in relation to the vertebra below
Commonly L5-S1
Can cause pain to lower back, legs, and buttocks

Question 35

Spinal stenosis

Answer 35

A response to continuous vertical compression of the spine (axial loading) that includes disruption of normal building and maintenance of the lumbar disk cartilage

Usually due to a genetic component and environmental interactions

Narrowing of the spinal canal that causes pressure on the spinal nerves or cord and can be congenital or acquired and associated with trauma or arthritis
Can affect: cervical thoracic, or lumbar

Caused by:
Bulging disk
Facet hypertrophy
Thick ossified posterior longitudinal ligament

Symptoms:
Numbness or tingling in the neck, hands, arms, legs with weakness and difficulty walking

Question 36

Pulmonary Edema

Answer 36

Right side
Peripheral edema
jvd

left side
crackles
sputum

both
SOB
Cyanotic

Question 37

Asthma

Answer 37

Defined as: chronic inflammatory disorder of the bronchial mucosa that causes bronchial hyperresponsiveness, constriction of the airways and variable airflow obstruction that is reversible

Risk factors? Genetics play a heavy role & hygiene hypothesis

Other risk factors:
Age of onset of disease
Levels of allergen exposure
Urban residence
Exposure to indoor and outdoor air pollution
Tobacco smoke
Recurrent respiratory tract viral infections
GERD
Obesity

Combination of innate and adaptive immunity responding to a allergen or irritant.

Early stage:
Exposure causes activation of dendritic cells causing release of inflammatory cytokines and interleukins that activate B cells (plasma cells) and eosinophils
Plasma cells produce IgE and bind to mast cells which causes degranulation of mast cells causing a couple of responses (look at the chart), generally releasing inflammatory mediators
Histamine, ILs, prostaglandins, etc.

**eosinophils cause direct damage to tissue and contribute to increased bronchial hyperresponsiveness, this also causes airway scarring. Once the damage is irreversible this is known as AIRWAY REMODELING.

Late asthmatic response begins 4-8 hrs after the early response.
The early immune response causes a delayed release of inflammatory mediators

Causing more bronchospasm, edema and mucus secretion with obstruction to airflow

During an attack:
Chest constriction
Expiratory wheezes
Dyspnea
Nonproductive coughing
Prolonged expiration
Tachycardia
Tachypnea

During SEVERE attack:
Accessory muscles use increases
Inspiratory and expiratory wheezes
Pulsus paradoxus
Decreases oxygen saturation

Complication:
STATUS ASTHMATICUS – may have silent chest at this point

Showing respiratory failure = mechanical ventilation
Acute attack -> oxygen + inhaled beta-agonists + oral corticosteroids
Avoiding allergens and irritants

FOR PARAMEDICS – bronchoconstriction directive

Question 38

Emphysema

Answer 38

S/S
dyspnea
minimal cough
tachypnea
decreased breath sounds
pink skin and pursed lip breathing
cachexia
Hyperinflation / barrel chest
skinny due to work of breathing
pneumo due to bullae

Defined as: the abnormal permanent enlargement of gas-exchange airways (acini) accompanied by destruction of alveolar walls without obvious fibrosis

Cause: changes in lung tissues, specifically the elastic recoil of lung tissue, from damage from inflammation and mucous presence from exposure to cigarette smoking or pollution

Patho: inherited alpha1-antitrypsin deficiency and infiltration of inflammatory cells and release of cytokines can cause increased protease activity with breakdown of elastin in connective tissue of lungs which destroys alveolar septa and loss of elastic recoil of bronchial walls leading to clinical presentations

Question 39

Pulmonary embolism

Answer 39

risk factors:
smoking
age
blood clotting disorder
cardiovascular diseases like heart failure, a fib
obesity
cancer
hormonal factors
surgery
dvt hx
prolonged immobility

CM:
SOB
Chest pain localized
rapid or ireg HR
cyanosis
Cough
Peripheral Edema
Fainting or lightheadedness
anxiety / insomnia

Question 40

Respiratory distress syndrome of newborn

Answer 40

Typically presents in premature infants and is a significant cause of neonatal morbidity and mortality (29-30 weeks)

Death rates have declined due to antenatal steroid therapy and postnatal surfactant therapy

Cause: surfactant deficiency, leading to atelectasis

Clinically presents with: tachypnea (>60), expiratory grunting, intercostal and subcostal retractions, nasal flaring, and cyanosis

Preventative: corticosteroids

Treatments after birth: mechanical ventilation, nebulized or CPAPed with exogenous surfactant

Risk factors:
Premature birth/low birth weight (30weeks)
Male gender
Cesarean delivery without labor
Diabetic mother
Perinatal asphyxia

Increased pulmonary vascular resistance can cause a right-to-left shunt of blood through the ductus arteriosus and foramen ovale.

Metabolic acidosis can result from the hypoxia and hypoxemia.

Question 41

Cystic fibrosis

Answer 41

Autosomal recessive inherited disease (CF gene is on chromosome 7) that results from defective epithelial chloride transport

Affects the lungs, digestive tract and reproductive organs

Treatment: promotion of mucus clearance – chest therapy, mechanical devices, bronchodilators, aerosolized dornase alfa and hypertonic saline to liquefy mucus, antibiotics if needed, lung transplantation

Bacterio: staphylococcus aureus, haemophilus influenzae

Clinical manifestations:
Persistent cough or wheeze
Excessive sputum production
Recurrent or severe pneumonia
Chronic sinusitis
Barrel chest
Digital clubbing
Nasal polyps

Could be at risk for bronchial artery erosion, pulmonary hypertension and cor pulmonale.

Question 42

SIDS

Answer 42

Sudden death of an infant under 1 year of age which remains unexplained.

Most frequent at 2-4 months old

Risk factors:
prone and side-lying sleeping positions,
sleeping on soft bedding,
overheated sleeping environment,
lower socioeconomic status,
mothers younger than 20,
lower birth weight or growth restricted infants,
male infants,
preterm delivery,
multiple gestations,
sibling who died of SIDS,
smoking during pregnancy,
exposure to tobacco smoke,
lack of prenatal care,
illicit drug use or binge-drinking,
larger family size

Question 43

Bronchiolitis

Answer 43

Common viral respiratory tract infection (RSV – respiratory syncytial virus)

Infants and young toddlers

Patho:
Virus causes necrosis of bronchial epithelium and destruction
of ciliated epithelial cells, leading to a inflammatory response
Inflammation in the bronchioles causes air trapping,
hyperinflation and increased FRC —> hypercapnia and
increased WOB

Prognosis: typically, the affected will make a full recovery but premature or those with bronchopulmonary dysplasia or heart disease struggle to recover

Complications: increased risk for asthma

Treatment: palivizumab(antibiotic) and other supportive treatments

Clinical manifestations:
Rhinorrhea
Tight cough
Decreased appetite
Lethargy
Fever
Tachypnea
Respiratory distress
Wheezing, rales, ronchi
Severe apnea
Conjunctivitis
Otitis media

Question 44

Epiglottis

Answer 44

Cause: Haemophilus influenzae Type B

More common in adults now, but was very common in children 2-7 years

Patho: inflammation in the posterior tongue base, covering the laryngeal inlet during swallowing and can cause life threatening upper airway obstruction

Clinically: high fever, irritability, sore throat, inspiratory stridor, severe respiratory distress, drooling, absence of cough, preference to sit (sniffing position), dysphagia, high fever; toxic appearance; muffled voice; drooling; dyspnea; sits erect & quietly

Complications: pneumonia, cervical lymph node inflammation, otitis, meningitis, septic arthritis

DO NOT AGITATE, avoid laryngospasms

Question 45

Croup

Answer 45

age 6months 12 years
Types: acute laryngotracheobronchitis vs. acute tracheitis

Typically caused by parainfluenza (virus)a

Characterized as an infection causing obstruction of the upper airways
Subglottic inflammation and edema from infection, leading
to upper airway obstruction, increased resistance to airflow,
increased intrathoracic negative pressure and then collapse
of upper airway leading to respiratory failure

Most common in winter months

Clinically: rhinorrhea, sore throat, fever, hoarse voice, barking cough, inspiratory stridor

SEVERE WHEN ++WOB

As we know for treatment
Dexamethasone and Epi
Oxygen

Question 46

Pneumonia

Answer 46

Cause by: a virus, otherwise sometimes bacteria

Spread: direct contact, droplet transmission, or aerosol exposure

Treatment: supplemental oxygen, assisted ventilations, antibiotics (if bacterial), preventatively children should be receiving vaccines against influenza and pneumococcus