Exam (elaborations)
Nu 545 Patho Study Guide Unit 5 Questions and Answers
- Course
- NU 545
- Institution
- University Of South Alabama
Nu 545 Patho Study Guide Unit 5 Questions and Answers
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Nu 545 Patho Study Guide Unit 5Questions and Answers
Know type I and Type II alveolar cells (pg 1229) - ANSWER The alveolar
septa consist of an epithelial layer in a thin, elastic basement membrane but no
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muscle layer. Two major types of epithelial cells appear in the alveolus. Type I
Alveolar cells provide structure, and type II Alvoelar cells secrete surfactant, a
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lipoprotein that coats the inner surface of the alveolus and facilitates its expansion
during inspiration, lowers alveolar surface tension at end-expiration, and prevents
lung collapse. Surfactant also contributes to control of lung inflammation and
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innate and adaptive immunity.
Role of surfactant in the lungs-infants and adults (Pg 1235, 1256, 1292) -
ANSWER • Alveolar ventilation, or distention, is made possible by surfactant,
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which lowers the surface tension by coating the air liquid interface in the alveoli.
Surfactant, a lipoprotein produced by type II alveolar cells, includes two groups of
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surfactant proteins. Surfactant lines at Alveolar side of the Alveolocapillary
membrane and in effect reverses Laplace's law (pg 1235).
• The decrease in surface tension caused by surfactant also is responsible for
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keeping the alveoli free of fluid. If surfactant production is disrupted or surfactant
is not produce in adequate qualities, alveolar surface tension increases, causing
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alveolar collapse, decreased lung expansion, increased work of breathing, and
severe gas exchange abnormalities.
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• In the absence of surfactant the surface tension tends to attract fluid into the
alveoli. Surfactant participates in host defense against respiratory pathogens.
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• Atelectasis-Is the collapse of lung tissue. There are three types of atelectasis:
Compression, absorption, and surfactant impairment.
o Surfactant impairment results from decreased production or inactivation of
surfactant, which is necessary to reduce surface tension in the alveoli and thus
prevent lung collapsed during expiration. Surfactant impairment can occur because
of premature birth, and acute respiratory distress syndrome, anesthesia, or
mechanical ventilation. (pg 1256)
,o Pediatrics: surfactant is critical for maintaining alveolar expansion thus allowing
normal gas exchange reduces surface tension, prevents alveolar collapse at the end
of each exhalation. Without surfactant the alveoli tend to stay closed, demanding
greater inspiratory force and work of breathing to re-expand on next breath.
Deficiency of surfactant is often seen in premature infants and causes respiratory
distress syndrome (RDS), also known as hyaline dis
Know Chronic Bronchitis-pathophysiology, etiology, prevention, clinical
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manifestations, treatment, complications (Pg 1267) - ANSWER • Chronic
bronchitis is defined as hypersecretion of mucus and chronic productive cough that
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continues for at least 3 months of the year (usually the winter months) for at least
two consecutive years. Inspired irritants result in airway inflammation with
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infiltration of neutrophils, macrophages, and lymphocytes into the bronchial wall.
Initially chronic bronchitis affects only the larger bronchi, but eventually all
airways are involved. The thick mucus and hypertrophied bronchial smooth muscle
narrow the airways and lead to obstruction, particularly during expiration when the
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airwaves are constricted. Obstruction leads to ventilation perfusion mismatch with
hypoxemia. The airways collapsed early an expiration trapping gas in the distal
portions of the lung. This leads to decreased title volume, hypoventilation, in
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hypercapnia.
• Clinical= Common symptoms include decreased exercise tolerance, wheezing,
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and shortness of breath. Individuals have a productive cough "Smokers cough", An
evidence of airway instruction is shown by spirometry. As disease progresses
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copious amounts of sputum or produced accompanied by frequent pulmonary
infections. Mark hypoxemia leads to polycythemia (overproduction of
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erythrocytes) and cyanosis. If not reversed hypoxemia leads to pulmonary
hypertension and eventually results in cor pulmonale and can lead to severe
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disability or death.
• Evaluation and treatment= Diagnosis is based on history of symptoms, physical
examination, chest x-ray, PFTs and blood gas analysis; tests reflect progressive
nature of the disease. Prevention of chronic bronchitis is the best treatment because
pathologic changes are not reversible. By the time an individual seeks medical care
for symptoms, considerable airway damages are present. If the individual stops
smoking, disease progression can be halted.
o Bronchodila
,Know gas exchange in the lungs (pg 1229) - ANSWER • The bronchioles
terminate in gas exchange airways, where oxygen enters the blood and carbon
dioxide is removed from it. The gas exchange airways consist of respiratory
bronchioles, alveolar ducts, and alveoli.These structures together or sometimes
called the acinus, and all of them participate in gas exchange.
o The alveoli are the primary gas exchange units of the lungs, where oxygen enters
the blood and CO2 is removed. Tiny passages called pores of Kohn permit some
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air to pass through the septa from alveolus to alveolus, promoting collateral
ventilation and even distribution of air among the alveoli. The lungs contain
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approximately 50 million alveoli at birth and about 480 million by adulthood.
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How is the patient's alveolar ventilation measured? (pg 1232) - ANSWER •
The adequacy of alveolar ventilation cannot be accurately determined by
observation of ventilatory rate, pattern, or effort. An arterial blood gas analysis
must be performed to measure Paco2 (arterial CO2).
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Know asthma (adult and childhood)- pathophysiology, etiology, prevention,
inflammatory mediators, clinical manifestations, treatment (acute and chronic),
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complications (Pg 1263 & 1308) - ANSWER • Asthma in Children is the most
prevalent chronic disease in childhood affecting about 10% of US children between
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age 5 and 17 years old, with boys more often affected than girls. Prevalence is
increasing among non-Hispanic blacks, obese children, and children from urban
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and low income populations. Environmental factors and genetic susceptibility play
a role.
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• Patho: Asthma is initiated by a type I hypersensitivity reaction primarily
mediated by IgE, which is same for adults. Inflammation, bronchial spasm, and
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mucus production in the airways lead to ventilation and perfusion mismatch with
hypoxemia and expiratory airway obstruction with air trapping and increase work
of breathing. In young children, airway obstruction can be more severe because of
smaller diameter of their airways.
• Clinical: In a typical acute asthma attack and children, the major complaints of
coughing, wheezing, and shortness of breath. About 70 to 80% of acute wheezing
episodes are associated with viral respiratory tract infections. There may be signs
of preceding URI, such as rhinorrhea or low-grade fever. In infants and toddlers
, younger than 2 years old, the most common of these is RSV. In older children and
adults the major viral trigger is rhinovirus.
o Expiratory wheezing is often described as high-pitched and musical, along with
prolongation of the expiratory phase of the respiratory cycle. Breath sounds may
become faint when air movement is poor. Sometimes barrel chest is visible,
respiratory and heart rates are elevated, Nasal flaring and accessory muscles use
are evident with retractions. Infants may be seen "head bobbing" because of
sternocleidomastoid muscle use. The child may appear anxious or diaphoretic,
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important signs of respiratory compromise. The child may speak in clip sentences
or not at all because of dyspnea. Findings of a
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Asthma in Adult - ANSWER • Asthma in Adults is a chronic inflammatory this
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disorder of the bronchial mucosa that causes bronchial hyperresponsiveness,
constriction of the airways, and variable air flow obstruction that is reversible.
Asthma occurs in all ages, half of cases developing during childhood and another
third before age 40. Estimated 24.6 million people have asthma, highest for adult
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female, black persons and adults older than 65. Asthma is most commonly if the
Milio disorder and milk more often hundred jeans have been identified that may
play a role in the susceptibility and pathogenesis of asthma, including those that
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influence the production of IL-4, IL-5, and IL-13; IgE; eosinophils, and others (pg
1263). Exposure to high levels of certain allergens during childhood increases the
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risk for asthma. Furthermore, decreased exposure to certain infectious organisms
appears to create immunologic imbalance that favors the development of allergy
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and asthma in some individuals. This complex relationship has been called the
hygiene hypothesis.
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• Patho: During early asthmatic response, antigen exposure to the bronchial
mucosa activates dendritic cells (antigen presenting cells) to present the antigen
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CD4+T cells, which differentiate into Th2 cells. These Th2 cells released
numerous cytokines. Together these mediators cause vasodilation, increased
capillary permeability, mucosal edema, brochial smooth muscle contraction
(Bronchial spasm), and tenacious mucus secretion from mucosal goblet cells with
narrowing of the airways and obstruction to airflow. The late asthmatic response
usually begins 4-8 hours after the early response. Eosinophil mediators cause direct
tissue injury with fibroblast proliferation and airway scarring. Airway obstruction
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