nervous system Flashcards

1
Q

Multiple sclerosis

A
  • 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

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2
Q

Meningitis

A

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

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3
Q

Bacterial Menginitis

A

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

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4
Q

Brain or Spinal cord Abscess

A

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

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5
Q

Encephalitis

A

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

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6
Q

Guillain-Barré Syndrome

A

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

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7
Q

Stroke Syndromes

A

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

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8
Q

Ischemic Strokes

A

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

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9
Q

Transient Ischemic Attacks

A

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__

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10
Q

Thrombotic Strokes (cerebral thromboses)

A

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)

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11
Q

Embolic Strokes

A

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

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12
Q

Lacunar Strokes

A

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

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13
Q

Hemodynamic

A

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

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14
Q

Clinical manifestations of ischemic strokes

A

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.

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15
Q

Hypoxic Brain Injury

A

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

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16
Q

Hemorrhagic stroke

A

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.

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17
Q

Parkinsons disease

A

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

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18
Q

Strabismus

A

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)

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19
Q

Nystagmus

A

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

20
Q

Amblyopia

A

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

21
Q

Cataract

A

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

22
Q

Glaucomas

A

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

23
Q

Age-related macular degeneration

A

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

24
Q

Myopia

A

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

25
Hyperopia
farsightedness Light rays are focused behind the retina when a person is looking at a near object.
26
Astigmatism
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
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photophobia
eye discomfort due to light
28
ptosis
drooping eye lid
29
reduced peripheral field
aka tunnel vision – loss of peripheral sight
30
Acute Confusional States and delirium
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
31
Dementia
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
32
Myasthenia gravis
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
33
Spondylolysis
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
34
Spodylolithesis
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
35
Spinal stenosis
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
36
Pulmonary Edema
Right side Peripheral edema jvd left side crackles sputum both SOB Cyanotic
37
Asthma
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
38
Emphysema
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
39
Pulmonary embolism
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
40
Respiratory distress syndrome of newborn
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.
41
Cystic fibrosis
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.
42
SIDS
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
43
Bronchiolitis
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
44
Epiglottis
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
45
Croup
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
46
Pneumonia
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