BIO 169 Spring 2019

Exam 4 Essays

Ms. Jones has smoked 1 pack/day for 25 years. Describe the implication of this for the layers of the
trachea. Why would chronic smoking create the cough associated with chronic bronchitis? Describe
the pathway of the smoke as it enters the respiratory center, through both functional zones! What are
the divisions of upper and lower respiratory tracts? You should also include the layers of the trachea.

Answer: The epithelium coating the upper respiratory tract acts as a first line of defense against invasive
agents (pollutants, allergens, microorganisms), and it can cause upper airway symptoms and diseases
when in contact with these agents. Inhaled cigarette smoke, both passively as well as actively, has been
associated with chronic irritation and discomfort on the eyes, nose and oropharynx. Since 1964, when a
report was published about smoking by the U.S. Department of Health, there already was evidence of
cigarette smoking as a factor that worsened and prolonged rhinosinusitis. Cigarette combustion
produces a smoke with more than 4000 noxious components, including gas and particulate substances -
among them we have acrolein, formaldehyde, carbon monoxide, nicotine, cotinine; acetaldehyde,
phenol and potassium cyanide, and many of these components are provenly toxic to the respiratory
epithelium. n developed countries, cigarette smoking is responsible for 85 to 90% of cases of chronic
bronchitis and COPD. Cigarette smoke is composed of a complex mixture of > 400 particles and gases;
the specific etiologic role of each of these constituents has not been established. Many studies have
confirmed the association of cigarette smoking, chronic cough, and low lung function. The incidence of
chronic bronchitis is directly proportional to the number of cigarettes smoked. Other risk factors for
chronic mucus hypersecretion that have been identified are increasing age, male gender, childhood
respiratory infections, frequent lower respiratory tract infections, occupational exposures, and asthma.
Pipe and cigar smoking are also risk factors for both complications even in the absence of former
cigarette smoking. Constituents of tobacco smoke cause damage throughout the respiratory tree from
the main airways (bronchi) to the peripheral airways (bronchioles), right down to the terminal alveoli
(air pockets), as well as to the immune system. Loss of cilia and mucous gland hypertrophy occur in the
upper airways; inflammation, epithelial changes, fibrosis and secretory congestion occur in the
peripheral airways, and alveoli are destroyed with loss of gas exchange surface area and airways
flexibility. There are vascular changes to the small arteries and capillaries of the bronchioles and the
alveoli. Smoke also causes inflammation of the cells of the bronchial tree leading to squamous
metaplasia (a precancerous condition), smooth muscle hypertrophy, and peribranchial fibrosis. Damage
is evident in the results of bronchoalveolar lavage (a fiberoptic scope is placed into the lung of a patient,
and sterile water is injected into the lung). The overall cell count in the lavage is increased with people
who smoke, with many more neutrophils and eosinophils but fewer lymphocytes. Concentrations of the
antibody’s immunoglobulin M and immunoglobulin E (markers of sensitization) are increased, showing
that allergic processes are involved.
Your patient in the NICU is a premature male infant born at 33 weeks gestation. He requires a CPAP
because, in part, he has low levels of surfactant. What are the implications of this condition? Describe,
in your response, surface tension, and other factors that influence respiration. Which cells are
involved?

Answer: Until your baby is born, her lungs are filled with a liquid that helps them grow and develop.
During labor and birth this fluid is absorbed so that after birth she can take in the surrounding air.
Premature babies are at high risk of developing breathing problems because their lungs are not yet
mature enough to make this switch without some extra help. The healthcare team will aim to use a
ventilation (breathing) strategy that is as gentle as possible, because in some cases artificial breathing
machines (ventilators) can cause lung problems such as bronchopulmonary dysplasia. My patient which
is a premature born baby requires Continuous positive airway pressure (CPAP). Short prongs or a mask
are positioned by the nostril or nose, and air or oxygen is blown in at a constant pressure. Your baby
does all of his own breathing, but the machine helps keep the lungs open in between breaths.
Respiratory distress syndrome of prematurity is a major cause of morbidity and mortality in preterm
infants. Primarily, respiratory distress syndrome is caused by deficiency of pulmonary surfactant.
Surfactant is a complex mixture of phospholipids and proteins that reduces alveolar surface tension and
maintains alveolar stability. As most alveolar surfactant is produced after about 30-32 weeks' gestation,
preterm infants born before then will probably develop respiratory distress syndrome. In addition to
short gestation, several other clinical risk factors have been identified. There are a variety of factors that
influence newborn respiratory functions; these factors include chemical, mechanical, thermal, and
sensory. Respirations begin when fetal aortic and carotid chemoreceptors are stimulated by the varying
concentrations of oxygen and carbon dioxide. The lungs are one of the last organs to undergo full
maturation in a baby's body. Children that are born very prematurely do not have fully developed lungs,
and are therefore more susceptible to associated complications. The most common of these is a chronic
lung disease known as bronchopulmonary dysplasia (BPD), which mainly occurs when the (immature)
newborns require mechanical ventilation or oxygen supplementation. The disease is characterized by a
lack of fully developed alveoli and small blood vessels that support them. This leads to an increase in
oxygen demand and makes breathing more difficult, effects which can be clinically measured. It revealed
that certain mutations in the gene for PDGFR-α (platelet-derived growth factor receptor alpha)
significantly increased the risk of developing the disease. That stands to reason, as the cells in the lung
tissue that produce PDGFR-α are involved in the formation of the alveoli and in the development of lung
structure. In further experiments, the researchers also demonstrated that the TGF-ß (transforming
growth factor beta) signaling molecule plays a role in the development of BPD by decreasing production
of PDGFR-α. The scientists presume that the messenger substance TGF-ß is released particularly
frequently due to injury to the lung caused during mechanical ventilation.

Jim is in speech therapy because he has a recent history of aspirating his food. Which structures does
the food pass through? Where is it more likely to lodge? Describe the structures that normally prevent
this from happening, and how they do so.

Answer: Mechanical digestion is the physical act of breaking down the food by non-chemical means.
Mechanical digestion begins in the mouth by the physical act of mastication (chewing). The specialized
teeth break down the food as it is cut by the incisors, torn by the cuspids and ground by the molars. The
food is manipulated in the mouth by the tongue, and cheeks to mix and moisten the food forming a
bolus or ball which is pushed to the back of the tongue. Swallowing occurs when the tongue slides back
and locks the epiglottis over the larynx which allows the bolus to be pushed into the esophagus. The
bolus is then pushed by wave-like muscular contractions called peristalsis that moves the food to the
stomach. In the stomach the food is churned by peristalsis in order to mix with the gastric juices and
pushed to the pyloric sphincter at the base of the stomach. The food which is now a paste called chyme
is pushed through the pylorus into the duodenum the first loop of the small intestine. The chyme is
pushed through the small intestine by peristalsis allowing the absorption of food nutrients by the villi
lining the intestinal walls. This peristalsis and absorption continue through both the small (duodenum,
Jejunum, Ileum) and large intestine (Caecum, Ascending, transfers, depending, sigmoid colon). Osmosis
pulls most of the water out in the large intestine. The remaining waste called feces is gathered in the
sigmoid colon until a mass movement called defecation releases the waste through the rectum and
anus. When food enters the lungs instead of the esophagus, it affects breathing and can cause choking
and other problems. The structures inside the mouth and neck each have a distinct role in breathing,
speaking and swallowing. The swallowing mechanism is a complex process that, when it works properly,
moves food to the esophagus for transport to the stomach. Dozens of muscles and nerves work to move
food in the right direction. A piece of cartilage called the epiglottis plays a key role in ensuring that food
does not enter the windpipe or the lungs. The epiglottis moves back and forth to prevent the passage of
food and liquids into the lungs. The usual upright position of the epiglottis allows air to flow into the
lungs and the larynx. When you swallow, the epiglottis flattens backward to cover the entrance to your
larynx and prevent food from entering the lungs and windpipe. The epiglottis returns to its usual
position after swallowing.

Your patient presents with a temperature of 105⁰F. Predict the effect of a fever on unloading of
oxygen from hemoglobin. Describe other factors that would cause a shift in this same direction. In
your response, include the impact of the Bohr effect regarding the hemoglobin saturation curve.

Answer: Hemoglobin carries almost all the oxygen to our metabolizing tissues. This lesson discusses
physiological factors that stimulate hemoglobin to unload oxygen in our tissues. For example,
temperature, carbon dioxide, pH and metabolism all influence the affinity of hemoglobin for oxygen. As
you know, we breathe to get oxygen into our body. Specifically, our cells need the oxygen to make ATP,
which then provides energy for work: for example, muscular contraction. Our red blood cells contain
hemoglobin, which is a complex protein that carries the oxygen from our lungs to the metabolizing
tissues. As blood flows through the lungs, oxygen is loaded onto hemoglobin, and that forms what we
call oxyhemoglobin. Oxyhemoglobin is like a delivery truck that will transport the oxygen to the tissues.
As blood flows through the metabolizing tissues, oxygen is unloaded from the oxyhemoglobin, forming
what we call deoxyhemoglobin. Most people consider normal body temperature to be 37 degrees
Celsius. While this may be accurate, body temperature is not the same everywhere in our body. For
example, temperature can increase a few degrees in our metabolizing tissues as heat is released from
the cells when they work. As it turns out, temperature affects the affinity, or binding strength, of
hemoglobin for oxygen. Specifically, increased temperature decreases the affinity of hemoglobin for
oxygen. As oxyhemoglobin is exposed to higher temperatures in the metabolizing tissues, affinity
decreases and hemoglobin unloads oxygen. This is very important, as only free oxygen can enter the
cells. In other words, it has to be released from the hemoglobin before it can get into our cells. Cellular
metabolism produces carbon dioxide and lectic acid, which lowers pH to about 7.2, now that’s
compared with a pH of 7.4 in the lungs. While this may seem like a small decrease, it represents a
relatively large increase in acidity. When cells have a high metabolic rate, they produce an excess
amount of thermal energy as a waste by-product. This thermal energy is typically transferred into the
blood plasma of nearby capillaries via the process of heat. Once inside the blood, it increases the
average kinetic energy of the molecules and particles within the plasma, thereby increasing its
temperature. A higher temperature is correlated to the cells working harder and therefore means they
need a higher supply of oxygen to keep them going. Therefore, at higher blood plasma temperatures,
the hemoglobin becomes less likely to bind to oxygen and much more likely to unload to into the cells of
the tissue. Therefore, as temperature increases, this shifts the entire oxygen-hemoglobin dissociation
curve to the right. This ultimately means that the exercising cells will receive more oxygen.

Meredith has been very ill and is brought to the ER for hypoventilation. What would you expect to
find in her lab results? Why? What is hypoventilation? Which centers within the CNS control this
mechanism, typically?

Answer: Meredith’s lab results will show hypercapnia that increased PaCO2 and decreased PO2, along
with lowering of the pH. Hypoventilation occurs when a patient's alveolar ventilation is inadequate to
sufficiently clear CO2 from the lungs, which also increases blood pCO2. This can be seen in obstructive
lung diseases, such as chronic obstructive lung disease or asthma, use of certain medications or illicit
drugs that can blunt the respiratory drive (i.e. morphine, heroin, propofol, or benzodiazepines), or
obesity hypoventilation syndrome. Hypoxia seen in hypoventilation can be identified by calculating an A-
a gradient, which takes into account the elevated CO2 and should be near normal in cases of hypoxia
caused by pure hypoventilation. Hypoventilation is a condition that arises when air entering the alveoli,
small air sacs in the lungs that are the site of respiratory gas exchange, is reduced. This causes levels of
oxygen to decrease and the levels of carbon dioxide to increase. Hypoventilation may occur when
breathing is too slow or shallow and is usually a consequence of other medical conditions, such as
obesity. The respiratory control system tightly regulates ventilation. Alveolar ventilation (VA) is under
the control of the central respiratory centers, which are located in the ventral aspects of the pons and
medulla. The control of ventilation has metabolic and voluntary neural components. The metabolic
component is spontaneous and receives chemical and neural stimuli from the chest wall and lung
parenchyma and receives chemical stimuli from the blood levels of carbon dioxide and oxygen.
Metabolism rapidly generates a large quantity of volatile acid (carbon dioxide) and nonvolatile acid in
the body. The metabolism of fats and carbohydrates leads to the formation of a large amount of carbon
dioxide, which combines with water to form carbonic acid (H2 CO3). The lungs excrete the volatile
fraction via ventilation. Therefore, acid accumulation does not occur. PaCO2 is tightly maintained in a
range of 39-41 mm Hg in normal states. Ventilation is influenced and regulated by chemoreceptors for
PaCO2, PaO2, and pH, located in the brainstem; by neural impulses from lung stretch receptors; and by
impulses from the cerebral cortex. Failure of any of these mechanisms results in a state of
hypoventilation and hypercapnia.

Your patient has carbon monoxide poisoning. Describe “affinity” and how this plays a role in this
condition. The same patient is placed in a hyperbaric oxygen chamber for treatment. This has an
increased partial pressure of oxygen. Describe the use of this chamber in treatment. Include the
pertinent “Laws” you have learned.

Answer: Carbon monoxide (CO) gas exposure is the most common human poisoning. Upward of 50,000
patients a year are poisoned with CO in the United States. The initial clinical presentation varies in
patients suffering from CO poisoning: it can take the form of a headache, altered mentation, or coma,
and carries a 1–3% mortality rate. Up to a third of moderate to severely CO poisoned patients will show
signs of cardiac dysfunction, which is associated with long-term mortality. Even with current therapy,
15–40% of patients will experience long-term neurocognitive sequelae. These neurologic and cardiac
deficits do not necessarily correlate with blood CO levels, but more likely result from the pleiotropic
effects of CO poisoning on oxygen delivery and cellular function. CO competes with oxygen by binding
directly to hemoglobin, thus reducing oxygen carrying capacity. CO also exerts an R-state stabilizing
effect that cooperatively increases ligand affinity, reducing hemoglobin P50 and oxygen delivery. Finally,
CO directly inhibits mitochondrial respiration via binding to a heme a3 of cytochrome c oxidase.