Download Selected Neurological and Respiratory Disorders

Selected Neurological and
Respiratory Disorders
Neurological Disorders
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Muscle Paralysis
Neural Tube Disorders
Cerebrovascular Accidents (Stroke)
Transient Ischemia Attack
Aneurysm
Muscle Paralysis
• Flaccid paralysis
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Destruction of motor neurons by disease
Interruption of reflex arc responsible for muscle tone
Muscle deprived of innervation
Low muscle tone
Peripheral nerve destruction
• Spastic paralysis
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Reflex arc not disturbed
Injury to cortical neurons stops voluntary control
Muscle retains innervation
Increased muscle tone
Neural Tube Defects
• Anencephaly
– Failure of normal development of brain and cranial
cavity
– Multifactorial inheritance
• Spina bifida
– Diagnosis: amniocentesis and alpha-fetoprotein levels
– Alpha-fetoprotein leaks from fetal blood into amnionic
fluid through open neural tube defect; high levels
found in amnionic fluid
• Occult
• Meningocele
• Meningomyelocele
Characteristic appearance of anencephalic infant
Various types of spina bifida.
Neural Tube Defects
A. Thoracic meningomyelocele covered by thin membrane
B. Large meningomyelocele associated with neurologic deficit
Stroke: Cerebrovascular Accident (1
of 5)
• Any injury to brain tissue from disturbance of blood
supply to brain
• Types of stroke
– Cerebral thrombosis: most common; thrombosis of
cerebral artery narrowed by arteriosclerosis
– Cerebral embolus: occurs less frequently; blockage of
cerebral artery by fragment of blood clot from an
arteriosclerotic plaque or from heart
– Cerebral hemorrhage: most serious type of stroke; usually
from rupture of a cerebral artery in person with
hypertension
Stroke: Cerebrovascular Accident
(2 of 5)
• Predisposing Factors
– 1. Mural thrombus formed on wall of left ventricle
adjacent to a healing myocardial infarction
– 2. Thrombus formed on rough surface of diseased
mitral or aortic valve
– 3. Small thrombus in left atrium of person with
atrial fibrillation
Stroke: Cerebrovascular Accident (3
of 5)
• Ischemic infarct: no blood leaks into brain
• Hemorrhagic infarct: blood leaks into damaged
brain tissue
• Arteriosclerosis of extracranial arteries
– Sclerosis of a major artery from aorta that supply
brain
– Common affected site: carotid artery in neck;
arteriosclerotic plaque may narrow lumen and
reduce cerebral blood flow
Stroke: Cerebrovascular Accident (4
of 5)
• Diagnosis
– Cerebral angiogram
– Carotid endarterectomy
– Less invasive methods: similar to balloon
angioplasty and stent insertion procedures used to
treat coronary artery plaques
Stroke: Cerebrovascular Accident (5
of 5)
• CT scan: can distinguish a cerebral infarct from
cerebral hemorrhage
• Magnetic resonance imaging (MRI): provides
similar information and is equally effective
Effects of atherosclerosis of carotid
artery
A. Narrowing of lumen
B. Thrombus formation
C. Thrombus dislodged & forms
emboli
D. Complete occlusion of artery by
thrombus
Coronal section of brain illustrating large cerebral hemorrhage that has compressed
and displaced the cerebral ventricles.
Transient Ischemic Attack, TIA
• Brief episodes of neurologic disfunction
– From embolization of material from plaque in
carotid artery
– One-third of patients eventually suffer major
stroke
• Treatment: endarterectomy or medical therapy
Cerebral Aneurysm
• Congenital aneurysm of circle of Willis
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Congenital weakness in arterial wall allows lining to protrude
Weakness is congenital but aneurysm develops in adult life
Rupture causes subarachnoid hemorrhage
Hypertension predisposes
Treatment: aneurysm occluded surgically
• Arteriosclerotic aneurysm
– Cerebral artery dilates and compresses adjacent tissue
– Rupture uncommon
Dissection of vessels from the brain of a person with large congenital cerebral
aneurysm.
A cerebral aneurysm (arrow) demonstrated
by an angiogram.
Undersurface of brain, illustrating subarachnoid
hemorrhage secondary to ruptured cerebral aneurysm.
Respiratory Disorders
Pneumothorax
Atelectasis
Pneumonia
Tuberculosis
Bronchitis
Chronic Obstructive Pulmonary Disease (COPD)
Emphysema
Bronchial Asthma
Pneumothorax
Pathogenesis/Manifestations
Pathogenesis
• Lung injury or pulmonary disease that allows air to
escape into the pleural space
• Stab wound or penetrating injury to the chest wall
• Spontaneous – generally in young healthy persons
Manifestations
• Chest pain
• Shortness of breath
• Air in pleural cavity
• Tension pneumothorax
Tension Pneumothorax
• Development of a higher than atmospheric pressure
in the pleural cavity – creating a tension
• Can accompany any type of pneumothorax
• Upon inhalation air enters pleural space – due to
drop in intrapleural pressure
• On exhalation – air gets trapped due to the edges of
the tear compressing as a result of the increased
intrapleural pressure – thus the pressure in the
intrapleural space is getting greater and greater
• Heart and Mediastinal structures shifted away from
pneumothorax
Atelectasis
An incomplete expansion of the lung, a collapse of a
part of the lung
There are two types
1. Obstructive atelectasis: complete bronchial
obstruction by
• Mucous secretions, tumor, foreign object
• Resulting in collapse of the part of the lung
supplied by the blocked bronchus
• Can also develop as a postoperative
complication, where because of the pain, the
patient does not cough or breathe deeply,
accumulating mucous secretions
Atelectasis
2. Compression atelectasis
– External compression on the lung
• Fluid, air, or blood in the pleural cavity,
reducing its volume and preventing lung
expansion
Pneumonia
An inflammation of the lung
• The exudate spreads unimpeded through the lung
• Filling the alveoli
• The affected portions of the lung become relatively
solid (consolidation)
• At times, the exudate reaches the pleural surface
Pneumonia
Classification
Classification
1. Etiology: most important because it serves as a
guide for treatment
– Bacteria, chlamydia, mycoplasmas, rickettsiae,
viruses, fungi
2. Anatomic distribution of the inflammatory processdescribes what part of the lung is involved
– Lobar: entire lung (bacteria, neutrophil
infiltration)
– Bronchopneumonia (bacteria, neutrophil
infiltration): parts of one or more lobes adjacent
to the bronchi – bronchopulmonary segments
Pneumonia
Classification
– Interstitial pneumonia or primary atypical
pneumonia (virus or mycoplasma; lymphocyte,
monocyte, and plasma cell infiltration): alveolar
septa affected
3. Predisposing factors that lead to its development
• Any condition associated with poor lung ventilation
and retention of bronchial secretions
– Postoperative – atelectasis and secondary
bacterial infection
– Aspiration
– Obstruction
– Clinical features of pneumonia
• Manifestations of systemic infection
– Feeling ill
– Elevated temperature
– Increased white blood cell count
• Manifestations of lung inflammation
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Cough
Purulent sputum
Pain on respiration if involves pleura
Shortness of breath
Tuberculosis
• It is a special type of pneumonia caused by
Mycobacterium tuberculosis – an acid – fast bacteria
• Because the tubercle bacillus has a capsule composed
of waxes and fatty substances, it is more resistant to
destruction than others – thick cell wall
• As a result of this organism’s resistance – monocytes
accumulate around the bacteria – many fuse with the
bacteria attempting phagocytosis – but the fusion
produces a large multinucleated “giant cell”.
Lymphocytes and plasma cells surround the area –
followed by fibrous tissue proliferation. The central
portion becomes necrotic – thus a granuloma is
formed. TB is termed a granulomatous disease.
– Manifestations
• Course of infection
– Acquired from organisms inhaled in airborne droplets
– Organisms lodge within pulmonary alveoli where they proceed to
multiply
– Initially the organisms do not elicit a marked inflammatory reaction
because they do not produce any toxins or destructive enzymes
– Macrophage phagocytose the bacteria but are unable to destroy them –
they may even carry the organisms to other parts of the lung and into
regional lymph nodes.
– After several weeks cell-mediated immunity develops
– Sensitized T- cytotoxic lymphocytes attract and activate macrophages –
the activated macrophages attack and destroy many of the organisms
forming the characteristic granulomas formed
– In the majority of cases the person is unaware they have been infected –
no symptoms
– Infection arrested in majority of cases
• Outcome depends
– Number of organisms inhaled
– State of body’s defenses
– May heal by scarring or progress to cavitation
• Sometimes the granuloma is large enough to be seen on X-ray
but most of the times it is too small
• The positive skin test reveals the infection
• Cell-mediated immunity generally controls the infection
• The healed granuloma may contain small numbers of viable
organisms and the infection may become reactivated when
the immune system drops
• In some individuals the primary infection does not respond
favorably to the immune system fight
• The granuloma may extend into a nearby bronchus and
necrotic inflammatory tissue is discharged into it
• A cavity may form
• If the person gets reactivation of the bacteria (becomes
active) and they have cavitation (into bronchus) their sputum
can be infectious to others
• Most cases of active TB do not result from the
initial infection – but rather by a reactivation –
however some are due to a reinfection (new
case)
• How does reactivation occur- it is due to a
drop in the immune system action as a result
of AIDS, other debilitating diseases, treatment
with corticosteroids, treatment with
immunosuppressive therapy
• Extrapulmonary tuberculosis
– Result of hematogenous spread of tubercle bacilli –
thus a secondary infection
– Sites
» Kidneys
» Bone
» Uterus
» Fallopian tubes
Sometimes the secondary infection may progress even
though the pulmonary infection has healed leading to an
active extrapulmonary TB without clinically apparent
pulmonary TB
Tuberculosis
Diagnosis
– Skin test (Mantoux): a positive test reveals recent
infection
– chest x-ray: when the granuloma is large enough
to be detected – or see pulmonary infiltrates
– sputum culture – acid fast bacteria
• The tuberculosis skin test (also known as the tuberculin test
or PPD test) is a test used to determine if someone has
developed an immune response to the bacterium that causes
tuberculosis (TB). This response can occur if someone
currently has TB, if they were exposed to it in the past, or if
they received the BCG vaccine against TB (which is not
performed in the U.S.).
• The tuberculin skin test is based on the fact that infection
with M. tuberculosis produces a delayed-type hypersensitivity
skin reaction to certain components of the bacterium.
Tuberculosis
Treatment
• Cell-mediated immunity generally controls the
infection
• The healed granulomas, however, may contain small
numbers of viable organisms, and the infection may
become reactivated
• Not all primary infections respond as favorably
– If a large number of organisms are inhaled or if
the host is compromised (body’s defenses are
inadequate), the inflammation will progress,
causing more destruction of lung tissue
Tuberculosis
– People who have active progressive tuberculosis with a
tuberculous cavity can infect others because they can
discharge large numbers of tubercle bacilli in the sputum
– Treatment
• Antibiotics and Chemotherapeutic agents
• Drug-resistant tuberculosis treatment
– More prolonged
– Results less satisfactory
• Drugs recommended
– Following conversion of a negative into positive skin test
reaction
– Patients with inactive tuberculosis who have increased risk
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Bronchitis
An inflammation of the tracheobronchial mucosa
• Acute bronchitis
– Common and self-limiting
• Chronic bronchitis – often associated with
emphysema in COPD
– Secondary to chronic irritation by smoking or
atmospheric pollution
• Bronchiectasis
– Walls weakened by inflammation and dilate
– Distended bronchi retain secretions
» Chronic cough
» Production of large amounts of purulent sputum
– Diagnosed with bronchogram
– A specialized X-ray which consists of taking films after instilling
a radiopaque oil into the trachea and bronchi. The oil covers
the mucosa of the bronchi, and the abnormal bronchi can be
recognized as dilated
– Only effective treatment is surgical resection of affected
segments of lung
• Upper Respiratory System – From nose and
mouth down to Lungs – (includes nose,
mouth, pharynx, larynx, and trachea
• Lower Respiratory System – Mainstem
bronchus to Alveoli
• Upper Airway – From nose and mouth to and
inclusive of larynx (voice box)
• Lower Airway – Trachea down to alveoli
Chronic Obstructive Pulmonary Disease
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Emphysema and chronic bronchitis occur together so frequently
that they are usually considered a single entity, designated
COPD
Emphysema is characterized by loss of elasticity (increased
pulmonary compliance) of the lung tissue caused by
destruction of structures feeding the alveoli
• Chronic bronchitis – Secondary to chronic irritation
by smoking or atmospheric pollution
Clinical manifestations
• Dyspnea
• Cyanosis
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Emphysema
The air spaces distal to the terminal
bronchioles are enlarged and their walls are
destroyed
The normally fine alveolar structure of the
lung is destroyed
The large cystic air spaces form throughout
the lung
The destructive process usually begins in the
upper lobes but eventually may affect all lobes
Once emphysema has developed, the damaged
lungs cannot be restored to normal
Bronchial Asthma
• Spasmodic contraction of smooth muscles in the walls
of the smaller bronchi and bronchioles
• It causes shortness of breath and wheezing respiration
• Exerts a greater effect on expiration than on inspiration
• Attacks are precipitated by allergens: inhalation of
dust, pollens, animal dander, or other allergens
• Treated with drugs such as epinephrine or theophylline
that relax bronchospasms and block the release of
mediators from mast cells
• Bronchial Asthma
– Pathogenesis
• Spasmodic contraction of smooth muscles in walls of
smaller bronchi and bronchioles
• Associated with increased secretions from bronchial
mucous glands
– Clinical manifestations
• Shortness of breath
• Wheezing respirations
• Air flow impeded more on expiration than on
inspiration
– Air trapped in lungs
– Lungs become overinflated
– Attacks precipitated by allergens
• Interact with mast cells coated with IgE antibody
• Release chemical mediators that induce bronchospasm
– Treatment
• Drugs that relax bronchospasm
– Epinephrine
– Theophylline
• Drugs that block release of mediators from mast cells