Week 13

Question 1

What symptoms are produced by immediate hypersensitivity and what cells/molecule signals cause them?

Answer 1

Allergic Rhinitis (runny/stuffy nose), Conjunctivitis (red eyes), allergic asthma, atopic dermatitis (hives), and food allergies. All result from humoral (B cell) immune response to the allergen. Normally, the allergen stimulates T helper 1 cells (secretes interferon gamma and interleukin-2) but if allergic, dendritic cells stimulate T helper 2 cells to secrete IL-4, IL-5, IL-9, IL-13 which recruit eosinophils, promote mucus production, and stimulates bronchiole constriction. The lymphokines also stimulate B cells to secrete IgE antibodies!
Short version: caused by humoral (B cell) mediated immunity which secretes IgE antibodies

Question 2

Describe how an allergy is created (first vs second exposure).

Answer 2

IgE antibodies are released in response to the allergen upon first exposure. IgE concentrates in mucosal membranes where Fc portion binds to receptor proteins on Mast cells and Basophils surface.

Second exposure causes allergen to bind to the IgE antibodies on the Mast and basophil cells which stimulates release of Histamine. Histamine causes allergy symptoms like bronchoconstriction, vasodilation, edema, inflammation, and anaphylaxis

Question 3

What is the molecule that causes primarily allergic reaction symptoms and what responses does it stimulate? How is it a drug target?

Answer 3

Histamine stimulates smooth muscle contraction in airways (bronchoconstriction) and smooth muscle relaxation in blood vessels (vasodilation). It also increases capillary permeability causing edema and releases inflammatory cytokines. Anaphylaxis occurs with widespread histamine release and can lead to Shock.

Hay Fever symptoms (itch, sneezing, tearing, runny nose) are also produced by histamine and can be treated by Antihistamine drugs that block the H1-histamine receptor.

Question 4

What causes asthma and what drugs are used to treat it?

Answer 4

Inflammation and smooth muscle constriction of the bronchioles due to Leukotrienes secreted by eosinophils. Treatments include epinephrine and other B2-adrenergic stimulating drugs to cause bronchodilation. Corticosteroids also help to inhibit inflammation and *leukotriene synthesis

Question 5

What is food allergy vs food intolerance? what would treatments include for allergy?

Answer 5

Intolerance is caused by NONimmune mechanisms, such as a lack of enzyme (lactase in lactose intolerance)

Allergy is caused by a food allergen that evokes IgE mediated responses that lead to gastrointestinal disorder, urticaria (hives), hypotension, and bronchiole inflammation. Can also be mediated by TH2 helper T cells. May be life threatening, so must avoid the food! No therapy exists, but antihistamines can help alleviate symptoms and epinephrine can control life-threatening systemic reactions

Question 6

How is immediate hypersensitivity tested for? What are two common allergies of this type and what is their allergen?

Answer 6

Flare and Wheal Reaction: antigens are injected in the skin and if a spreading flush (flare) from vasodilation with an elevated area (wheal) from edema occurs, they are allergic.
The most common allergy of this type is hay fever, provoked by ragweed (ambrosia) pollen grains. People with chronic allergic rhinitis and asthma due to dust allergy are allergic to a tiny dust mite (and its feces) which are constantly present in dust.

Question 7

What causes delayed hypersensitivity and how is it treated? What medical test uses delayed hypersensitivity??

Answer 7

Delayed hypersensitivity is cell-mediated (T cell) immune response. Symptoms are caused by lymphokine secretion instead of histamine, so antihistamines don't help. Corticosteroids are the only effective drugs as they suppress immune system.
Tuberculosis tests (tine test and Mantoux test) involve injecting or rubbing tubercle antigens on a person's skin and if the skin is hard after a few days, they have been exposed!

Question 8

*What is a common example of a delayed hypersensitivity reaction?

Answer 8

Allergic Contact Dermatitis is hypersensitivity caused by poison ivy, poison oak, poison sumac, and metals (nickel and chromium aka stainless steel). The person develops an inflammatory skin rash in response to jewelry or cosmetics as small molecules penetrate the skin and bond to self proteins, producing antigens in Haptenization. This activates T cell response and rash development.

Question 9

What 3 functions are included in respiration and what are the two types of respiration?

Answer 9

1. Ventilation (breathing)
2. Gas exchange (between air and blood in lungs and between blood and other tissues)
3. Oxygen utilization (cell respiration in tissues)

Ventilation and exchange of cases between air and blood are External Respiration
Gas exchange between blood and tissues and oxygen utilization are Internal Respiration

Question 10

Describe how gas exchange occurs in lung tissue; what are the gases involved and in which direction do they each flow?

Answer 10

Gas exchange is entirely by diffusion, which occurs rapidly due to the large lung surface area and small diffusion distance between blood and air. We inhale 78% nitrogen, 21% oxygen, and 0.04% CO2 and exhale 16% oxygen, 3-5% CO2, and the rest is nitrogen. Therefore, oxygen flows from air to blood and CO2 flows from blood to air (down gradients!) and blood leaving lungs in pulmonary veins has higher oxygen than blood entering pulmonary arteries

Question 11

Where precisely does gas exchange occur? *What are the two types of cells involved?

Answer 11

Pulmonary alveoli are tiny air sacs where gas exchange occurs. They are super close to capillaries and have extremely thin cell layers separating air and blood.
Type I alveolar cells comprise most of the lung surface area and is where gas exchange primarily occurs
Type II alveolar cells secrete pulmonary surfactant and reabsorb Na+ and H2O, preventing fluid build up.

Question 12

Describe the structure of the lungs (like a tree).

Answer 12

Trachea/windpipe (trunk): sturdy tube supported by C-shaped rings of cartilage
Right and left primary bronchi (first branches): direct air between trachea and further bronchioles
Terminal bronchioles (next branches): narrowest airways with NO alveoli and NO gas exchange
Respiratory Bronchioles (final branches): thin air tubes that have alveoli clusters along them and at the ends
Alveolar Sacs (leaves on branches): clusters of air sacs that perform gas exchange

Question 13

What are the structures in the two functional zones?

Answer 13

Conducting Zone (dead air space) = mouth, pharynx, glottis (vocal cords and the opening between them), larynx/voice box (ventricular folds/false vocal cords and true vocal cords. Adams apple is formed by thyroid cartilage of the larynx), trachea, primary bronchi, and all successive bronchioles up to terminal bronchioles

Respiratory Zone = respiratory bronchioles and terminal alveolar sacs

Question 14

What are the functions of the conducting zone and how is the zone “cleared”

Answer 14

Conducts air to respiratory zone and performs warming, humidification, filtration, and cleaning of the air to ensure constant internal body temp and protect lung tissue. There are cilia located from terminal bronchioles to the top of the larynx (vocal chords do NOT have cilia) which move the mucus secreted by the conducting structures toward the pharynx by a Mucociliary Escalator. At the pharynx, it can be swallowed or expectorated to clear the mucous in a process called Mucociliary Clearance.

Question 15

What conditions damage the ability to filter out harmful molecules from entering the respiratory system?

Answer 15

Cystic Fibrosis causes mucociliary escalator to fail (reduced Cl- and low water content leads to mucus too thick to clear) and cigarette smoking damages cilia and reduces clearance ability. The result is lack of filtration to prevent harmful molecules from entering/damaging lungs.

Black Lung is a disease that occurred in miners who inhaled large amounts of carbon dust, which causes Pulmonary Fibrosis. Alveoli are normally kept clean by resident macrophages (Dust cells).

Question 16

Describe the anatomy of the thoracic cavity, two major cavities, the area between lungs, layers between lung and chest wall, etc

Answer 16

Diaphragm divides the cavity in two parts: Abdominopelvic cavity below diaphragm and thoracic cavity above diaphragm
Mediastinum or the central region is located between the lungs and is enveloped by pleural membranes: Parietal Pleura lines the inner thoracic wall and is joined to the Visceral Pleura lining the lung surface. The Intrapleural Space is a potential space that exists between the pleural layers, it becomes real if a lung collapses. It contains a thin layer of fluid that lubricates lungs to slide against chest. Lung collapse would cause the chest wall to budge out because the visceral pleura normally pulls the parietal pleura inward!

Question 17

Describe the pressure state of within lungs during inspiration and expiration. What causes lungs to stay against chest wall during both events?

Answer 17

inspiration: atmospheric pressure > intrapulmonary (intra-alveolar) pressure so air enters lungs. Because intrapulmonary pressure is below atmospheric, it is a Negative Pressure of -1 cmH2O.
expiration: atmospheric pressure < intrapulmonary (intra-alveolar) pressure to air leaves lungs. This is Positive Pressure of +1 cmH2O.

The Intrapleural Pressure (sub atmospheric pressure in intrapleural space as lungs pull in while thoracic wall pulls out) is lower than intrapulmonary pressure during BOTH inhale and exhale. The difference between those two pressures is the Transpulmonary (Transmural) Pressure and it keeps lungs against chest wall!

Question 18

*What is Boyle’s Law

Answer 18

Pressure of a given quantity of gas is INVERSELY proportional to its volume. So increased lung volume during inspiration decreases intrapulmonary pressure, causing air to go in. A decreased in lung volume then raises intrapulmonary pressure and expels air from the lungs.

Question 19

Describe the properties of lungs that are required for inspiration (3 things)

Answer 19

1. Compliance: must be distensible (stretchy) as given by change in lung volume per change in trans pulmonary pressure. Note that compliance is reduced by factors that resist distention, i.e. connective tissue in lungs = pulmonary fibrosis
2. Elasticity: tends to return to initial size after distended. Lungs have high elastic protein content and are stuck to chest wall in state of elastic tension, which increases while inhaling and reduces by exhaling
3. Surface Tension: resists distension via fluid in the alveoli. Fluid is osmotically absorbed by active Na+ transport and secreted by active Cl- transport. Water molecules create surface tension by attractive forces (H bonds) and collapse alveolus, increasing air pressure in the alveolus.

Question 20

What genetic disorder effects the fluid of the lungs and what is the specific defect causing the disease?

Answer 20

Cystic Fibrosis is caused by a defect in a Cl- carrier called the Cystic fibrosis transmembrane conductance regulator (CFTR). The result is improper fluid absorption and secretion so airway fluid becomes very viscous (low water) and difficult to clear

Question 21

*What is the Law of Laplace

Answer 21

Pressure is directly proportional to surface tension and inversely proportional to radius of the alveolus. So a smaller alveolus has greater pressure than a larger one, if surface tension is equal. However, this does NOT normally occur because as alveolus decrease in size, the surface tension is also decreased and this prevents alveoli from collapsing! Surfactant is the substance that reduces surface tension

Question 22

Describe the substance that reduces surface tension in the lungs. What secretes it, what is it made of, and how does it work? When does production begin and what does this mean for premature babies?

Answer 22

Surfactant (surface-active agent) is secreted by type II alveolar cells and consists of primarily Phosphatidylcholine and Phosphatidylglycerol. It intersperses between water molecules and reduces surface tension, thus *preventing alveoli from collapsing during expiration as predicted by the law of Laplace! What is left in the alveoli after expiration is a Residual Volume of air.
Surfactant is made in late fetal life, but a newborn has partially collapsed alveoli and the first breath of life must overcome great surface tension. Premature babies don’t have mature lungs/surfactant and every breath is a great effort.

Question 23

Describe the different muscles used in restful and intense breathing (both inspiration and expiration)

Answer 23

Diaphragm (innervated by phrenic nerves from C3-C5) is the primary muscle of all ventilation. It lowers/flattens when it contracts to cause inspiration and relaxes (rises) for expiration

• Restful inspiration = External intercostal muscles and Paarasternal intercostals (aka the Interchondral part of the internal intercostals b/c oriented similar to internal intercostals)
• Intense inspiration: Internal intercostal muscles, scalenes, pectoralis minor, sternocleidomastoid muscles.
• Restful expiration: passive process of thorax/lung elastic recoil and relaxation
• Intense expiration: intercostal muscles (depress rib cage) and abdominal muscles (force organs against diaphragm)

Question 24

Describe tests for assessing pulmonary function and what type of disorder each would diagnose

Answer 24

Spirometry: records how much air is inhaled/exhaled (spirogram). Can assess Vital Capacity which is the maximum amount of air that can be forcefully exhaled after max inhalation. If vital capacity is below normal, but rate is normal, a restrictive disorder (like pulmonary fibrosis) is diagnosed

Forced Expiratory Volume (FEV): measures percentage of the vital capacity that can be exhaled in the first second (FEV1). FEV1 less than 80% diagnoses Obstructive disorder (like asthma or emphysema/COPD) where vital capacity is normal but expiration takes longer = slow rate

Question 25

What are the symptoms of asthma and what produces them? What is the most common type of asthma

Answer 25

Dyspnea, wheezing, and other obstructions to air flow. Caused by inflammation, mucus secretion, and bronchoconstriction provoked by allergic reactions (IgE), exercise, cold dry air, and aspirin. Atopic (allergic) asthma is most common and is caused by hyper-responsiveness to inhaled allergens which stimulate TH2 helper cells, B cells secrete IgE, mucus secretes, airway contracts, eosinophils and mast cells increase. These cells promote inflammation via histamine, leukotrienes, and prostaglandins.

Treatments: bronchodilator (albuterol) reverses bronchoconstriction, but advanced asthma may not be reversible b/c airway remodeling

Question 26

Why is asthma increasing in the population?

Answer 26

Early exposure to microbes protects children against later asthma, and as more kids grow up in sterile urban environments the incidence of asthma increases. Increased exposure to air pollutants may also increase asthma.

Question 27

What is Emphysema and what causes it?

Answer 27

Alveolar tissue is destroyed so there are fewer but larger alveoli, which reduces surface area for gas exchange and makes bronchioles collapse and lungs compress during expiration. This produces air trapping which decreases gas exchange further. Smoking is the most common cause. It causes inflammation and secretion of proteinases (Matrix Metalloproteinases from alveolar macrophages and Elastase from neutrophils) that cause destruction of ECM and loss of elasticity.

Question 28

Describe the symptoms and causes of COPD

Answer 28

Chronic Obstructive Pulmonary Disease is chronic inflammation and narrowing of airways and destruction of alveolar walls (barrel chest occurs!). COPD is a category that includes chronic obstructive bronchiolitis and emphysema. Unlike asthma, COPD inflammation is produced by cytotoxic lymphocytes and neutrophils (asthma = helper T lymphocytes and eosinophils). Smoking is the main cause of COPD and also causes lung cancer. Once COPD starts, stopping smoking will not stop the disease progression and pneumonia, pulmonary emboli, and heart failure may follow. Cor Pulmonale, pulmonary hypertension with hypertrophy and failure of right ventricle, also occur.

Question 29

What is pulmonary fibrosis caused by?

Answer 29

A restrictive disorder, the normal structure of the lungs is disrupted by accumulation of fibrous connective tissue proteins. Causes are poorly understood, but inhalation of particles <6 µm that accumulate in the lungs is one cause. This includes anthracosis or black lung, seen in coal miners who inhale coal (anthracite) dust

Question 30

*What is Dalton’s Law

Answer 30

Total pressure of a gas mixture is equal to the sum of the partial pressures of the constituent gases. One atmosphere is 760 mmHg (total pressure) which is the sum of the partial pressure of oxygen, nitrogen, and carbon dioxide. Note that increasing altitude results in decreasing total pressure, although the ratio of each partial pressure is the same!

Question 31

*What is Henry’s Law

Answer 31

The amount of gas dissolved in a fluid reaches a max value determined by solubility, temperature, and partial pressure. In alveoli, solubility and temperature are kept constant, so ONLY partial pressure of the gas determines the concentration of gas dissolved in the blood! (especially important for oxygen gas)

Question 32

How are blood gas measurements calibrated? What is a typical blood O2 measurement and where specifically is the oxygen located that is being measured?

Answer 32

Henry’s law tells us that the fluid has the same PO2 (partial pressure of O2) as the air around it. An oxygen specific electrode can be calibrated to match a known partial pressure of oxygen in the air (152 mmHg). Now when we place the electrode in blood we will see the PO2 of the sample, which should normally be around 100-105 mmHg (alveolar air has a PO2 of 105 mmHg and blood is almost in complete equilibrium). Note that the oxygen electrode response only to oxygen DISSOLVED in water/plasma, not in RBCs!! most oxygen is on RBCs, and is not read by PO2 measurement.

Question 33

Describe molecule exchange across the placenta. What delivers blood to/from the fetus? How is gas exchanged? what other molecules are exchanged that may be harmful?

Answer 33

Mom blood volume increases by 40% to supply fetus. Two umbilical arteries deliver fetal blood to to vessels within chorionic villi and one umbilical vein drains blood back to from villi to the fetus (vein blood is oxygenated red!). The placenta serves as the gas (and other molecules) exchange site because it is where maternal blood is separated by fetal blood by only two cell layers. Placenta also has a very high metabolic rate and synthesis more protein than the liver! These proteins often serve to prevent dangerous molecules from harming the fetus, but some molecules like alcohol or other drugs can pass the barrier and cause problems (fetal alcohol syndrome)

Question 34

What pituitary-like hormones does the placenta secrete and what do they do?

Answer 34

Chorionic Gonadotropin: LH-like effects that maintain corpus luteum. May also prevent immunological rejection of embryo.
Growth Hormone variant (hGH-V) or Placental Growth Hormone (PGH): works like growth hormone and supplants maternal GH. Stimulates protein synthesis, gluconeogenesis, lipolysis, and provides nutrients to fetus
Chorionic Somatomammotropin (hCS) or Placental Lactogen (hPL): similar structure to prolactin, but lactation effects not shown.

Question 35

What causes and prevents gestational diabetes

Answer 35

Chorionic somatomammotropin and growth hormone from the mother’s pituitary produce a diabetic-like effect by promoting lipolysis, glucose sparing in tissues (increased blood glucose), and polyuria (increased urination, producing dehydration/thirst). This helps supply glucose for fetus and placenta. Meanwhile, mothers pancreatic beta cells are proliferating to supply more insulin and prevent gestational diabetes from occurring.

Question 36

What steroid hormones does the placenta produce and what do they cause? How does it synthesize these hormones?

Answer 36

Estrogen and Progesterone which relaxes smooth muscle of the myometrium to reduce contractility. Placenta is an incomplete endocrine gland, however, because it relies on maternal and fetal precursors to make estrogen and progesterone. This cooperation is termed the Fetal-Placental Unit. Cholesterol is supplied by mother, and androgens (like androstenedione) are supplied by the fetus. Placenta converts androstenedione to estriol, and placental health can be assessed by measuring urinary estriol.

Question 37

What hormones stimulate labor and what else do they do? What hormone stimulates animal parturition and what other function does it have in humans?

Answer 37

Oxytocin and prostaglandins (PGF2a and PGE2) produced by uterus or hypothalamus (oxytocin only). Artificial oxytocin (Pitocin) injections or prostaglandin vaginal suppositories induce labor as well. Note that oxytocin is also important to maintain myometrium muscle tone and reduce hemorrhaging after birth! It also promotes involution (size reduction) of uterus.
In animals, Relaxin causes softening of pubic symphysis and cervix relaxation, but in humans it is important for the decimal reaction during the first trimester! It also promotes growth of blood vessels into decidua basalis and nourishment of embryo.

Question 38

What is blood PO2 a good measurement of?

Answer 38

It only measures plasma O2, not oxygen in RBCs so its not good for measuring total oxygen content. It is good for measuring lung function, for example if arterial PO2 is low this could mean gas exchange in the lungs is impaired. Properly functioning lungs produce arterial blood PO2 of only 5 mmHg less than PO2 of alveolar air

Question 39

What is the effect of breathing 100% oxygen from a tank?

Answer 39

It does not significantly increase the amount of oxygen in RBCs because Oxyhemoglobin Saturation is already achieved at normal PO2 (100 mmHg). It does increase oxygen in the plasma, but since most oxygen is in hemoglobin the total blood oxygen only increases slightly! However, increased plasma oxygen would increase the rate of oxygen diffusion to tissues (not blood, only tissues!) There is no evidence that supplemental oxygen improves athletic performance or speeds removal of lactic acid in healthy individuals.

Question 40

What is the most clinically useful blood gas measurement?

Answer 40

PO2 and PCO2 in arterial blood, which is constant (veinous blood is variable). These values reflect lung function. Remember that the electrodes used to take these measurements only account for Plasma gas, not any gas in cells!

Question 41

How much does atmospheric pressure increase as you descend below sea level? What can this cause (3 conditions)?

Answer 41

One atm every 10 m (33 ft). Increased nitrogen and oxygen in blood plasma under these conditions have serious effects:

1. Oxygen Toxicity: as PO2 rises above 2.5 atm, enzymes are oxidized and damage to nervous system can cause death. This is why divers use gas mixtures and not pure oxygen
2. Nitrogen Narcosis: high nitrogen in plasma membranes while at high pressure depth resembles alcohol intoxication (dizziness and drowsiness). “rapture of the deep”
3. Decompression Sickness (the bends): while ascending too fast, bubbles of nitrogen gas form in tissue fluids and create Gas Emboli (like carbonated soda!). Bubbles block blood channels = muscle/ joint pain.

Question 42

In what TWO scenarios can decompression sickness occur and how is it prevented? how can it be treated?

Answer 42

Diving and airplanes. Divers who ascend too fast cause nitrogen bubbles to form in tissue fluids and create gas emboli that block blood channels and cause muscle/joint pain. Airplanes must have pressurized cabins so to not experience the low pressure of altitude. If the cabin rapidly depressurizes, people will experience decompression sickness (Aloha Flight airlines #243 in 1988). A Hyperbaric Oxygen Chamber can be used to place the person back in high pressure atmosphere and slowly return pressure to normal to allow nitrogen to be eliminated in the breath and avoid bubbles

Question 43

Describe the brain control centers for breathing and how they innervate their targets (what neurons they act through)

Answer 43

Respiratory muscles are stimulated by somatic motor neurons (cell bodies in Gray Matter of spinal cord). The Phrenic Nerve (cell body in cervical layer) stimulates diaphragm and other neurons (cell bodies in thoracolumbar region) stimulate rib cage/abdomen. These are regulated by the Rhythmicity center in the Ventrolateral region of the medulla oblongata. This is in turn influenced by the pons (Apneustic center promotes inspiration and Pneumotaxic center inhibits inspiration). note: role of pons in humans is unclear

Question 44

What senses changes in blood/interstitial fluid and signals the control of breathing in response? What do they stimulate?

Answer 44

Chemoreceptors sense pH of brain interstitial fluid and cerebrospinal fluid and PO2, pH, PCO2 of blood. The Central chemoreceptors are in the medulla and the Peripheral chemoreceptors are within the aortic arch (Aortic Bodies) and carotid arteries (Carotid Bodies). ((NOTE these are not the aortic/carotid sinuses, that’s where baroreceptors are!)). Aortic bodies send info to medulla via vagus nerve (X) and carotid bodies send info via glossopharyngeal nerve (IX)

Question 45

What molecule do chemoreceptors maintain at a constant level? Describe the response that occurs during hypoventilation and hyperventilation and why this supports maintaining this particular molecule

Answer 45

CO2 is maintained constant, and proper oxygenation is a side product! During hypoventilation, PCO2 rises and pH falls (CO2 and water make carbonic acid which releases H+ into solution via enzyme Carbonic Anhydrase) and oxygen falls slowly due to the large reservoir in hemoglobin. During hyperventilation, PCO2 falls and pH rises while oxygen is not significantly increased because blood is already 97% saturated normally. Because CO2 changes much more rapidly, this is what chemoreceptors respond to!

Question 46

How do babies breath uniquely? What stimulates them to take a first breath?

Answer 46

When a baby is born, the umbilical cord is cut and CO2 builds up and pH falls, stimulating the peripheral chemoreceptors to cause them to take a breath. You don’t need to hang them upside down and slap their bottom! They also breath mainly with their diaphragm because intercostal muscles are not developed yet, this means they get longer with each breath instead of rising/falling chest. Also they are nose breathers (diaphragmatic nose breathers)

Question 47

What condition is caused by hypoventilation and hyperventilation

Answer 47

Hypoventilation = hypercapnia (high CO2)
Hyperventilation = hypocapnia (low CO2). Also leads to Shallow Water Blackout where swimmer hyperventilates so they can reduce CO2 and raise pH to produce Respiratory Alkalosis and reduce the stimulus for breathing (chemoreceptors stimulated by CO2 and H+). Now they don't feel the need to breath so can swim longer, but oxygen falls during metabolism and eventually ATP drops, unconsciousness occurs, and they drown.

Question 48

What molecules actually stimulate the central and peripheral chemoreceptors? What is the speed of each response?

Answer 48

Central chemoreceptors (ventrolateral surface of medulla oblongata, near IX and X nerve exits) are only stimulated by CO2 which can cross the blood brain barrier, H+ cannot! CO2 crosses and lowers pH by becoming carbonic acid via Carbonic Anhydrase. Central chemoreceptors cause most of the ventilation response, but it takes a few minutes.
Peripheral chemoreceptors (aortic and carotid bodies) are directly stimulated by a rise in H+ concentration (low pH), which occurs when CO2/carbonic acid rises. Peripheral chemoreceptor response is immediate!

Question 49

What is a tracheotomy? What is the result of the procedure called?

Answer 49

A tracheotomy is the surgical procedure of creating a hole in the trachea, which is then called a tracheostomy and into which various types of tubes are often inserted. Tracheostomies are usually done in a hospital to allow the patient to breathe with the aid of a mechanical ventilator, but they may be performed by a surgeon in an emergency to allow a person to breathe when the trachea becomes occluded by aspiration of a foreign object, trauma, or inflammation.

Question 50

What is a pneumothorax and how can it be caused (two types)

Answer 50

A pneumothorax occurs when air enters the pleural space, raising the intrapleural pressure so that the pressure difference keeping the lung against the chest wall is abolished. The lung then collapses due to its elastic recoil. A spontaneous pneumothorax may occur without disease or trauma, but it can also be caused by air leaking from the lung due to puncture from a broken rib or to lung disorders such as COPD, cystic fibrosis, or rupture of a lung blister. An open chest wound can also allow air to enter the pleural space, and if air continues to enter and not leave, it produces a serious tension pneumothorax. Because each lung is in a separate pleural compartment, a pneumothorax usually occurs in only one lung.

Question 51

What is RDS? how is it treated?

Answer 51

Respiratory distress syndrome (RDS): alveoli are collapsed in a neonate due to lack of surfactant, occurs commonly in premature babies. Most can be saved by the use of mechanical ventilators and by exogenous surfactant delivered into the baby’s lungs by an endotracheal tube. When the baby’s lungs are sufficiently mature, they manufacture their own surfactant.

Question 52

What condition can develop in people with lung injuries? Describe the changes in the lungs are characteristic of this condition

Answer 52

People with lung injury caused by sepsis or pneumonia may develop acute respiratory distress syndrome (ARDS). Inflammation causes increased capillary and alveolar permeability, producing a protein-rich fluid in the lungs. This reduces lung compliance and surfactant production, and the decreased surfactant further reduces compliance. This produces hypoxemia (low blood oxygen) of the blood leaving the lungs. Severe hypoxemia can be fatal, but survival has improved in recent years due to improvements in medical interventions.

Question 53

What factors reduce FEV1 significantly?

Answer 53

Cigarette smoking has been found to promote obstructive lung disorders as measured by a reduced FEV1. FEV1 normally declines with age, but the age-related decline is accelerated in smokers. The rate of decline is reduced in people who quit smoking compared to those who continue to smoke. Also, the rate of decline in smokers with mild COPD who quit was found to be less than in those who continued to smoke. Air pollution has also been found to significantly affect the FEV1 of children with asthma, and other studies have suggested that it may be unhealthy to exercise on very smoggy days

Question 54

What are the categories of asthma medication

Answer 54

Quick-acting beta agonists (such as albuterol), which stimulate the β2-adrenergic receptors in the pulmonary smooth muscle to dilate the bronchioles, are used for rescue during an asthma attack. Long-acting beta agonists also stimulate the β2-adrenergic receptors, but their effects last for 12 or more hours. These are generally combined with a glucocorticoid to inhibit inflammation, and are used more for asthma control over a period of weeks rather than for rescue from an attack. Inhaled or even intravenous corticosteroids are sometimes given for serious asthma attacks. Leukotriene receptor antagonists, including montelukast (Singulair), are pills now often used for long-term alleviation of asthma symptoms.

Question 55

How does a pulse oximeter work?

Answer 55

A pulse oximeter is a device that clips on a fingertip or pinna and noninvasively measures the oxyhemoglobin saturation. The pulse oximeter has two light-emitting diodes (LEDs): one emits red light, and the other emits infrared light. Oxyhemoglobin absorbs more infrared light, allowing more of the red light to pass through the tissue to a sensor, whereas deoxyhemoglobin absorbs more of the red and passes more of the infrared light. From this information, the device determines the percent oxyhemoglobin saturation. This value can be abnormally low if gas exchange has been compromised by impaired lung or heart function.

Question 56

What is HBOT and what can it treat?

Answer 56

Hyperbaric oxygen therapy (HBOT), patient breathes 100% oxygen at 2 to 3 atm pressure, does not increase the amount of oxygen carried by hemoglobin, because this is already nearly maximum when breathing sea level air. But it does significantly increase the oxygen carried by plasma. This treats decompression sickness from scuba diving that results when air bubbles form in the tissues and travel in the blood as air emboli because (from Boyle’s law) raising the pressure decreases the size of the bubbles. HBOT also helps kill anaerobic bacteria and treat gas gangrene, caused by bacteria that produce gas and tissue necrosis. hyperbaric oxygen helps to treat carbon monoxide poisoning, severe traumatic injuries (such as crush injuries), certain inflammations, diabetic sores, and other conditions.

Question 57

*What is the condition that causes dysfunctional breathing while sleeping? What causes this condition?

Answer 57

Ondine’s curse, from a German folktale, is fatal apnea during sleep due to brainstem dysfunction. Voluntary regulation of breathing is not affected because it involves descending corticospinal tracts from the cerebral cortex. So patients breathe adequately when awake, but during sleep the compromised automatic control of breathing causes apnea. This may result from trauma to the brainstem, but more commonly it is congenital. Called congenital central hypoventilation syndrome (CCHS), the defective gene has been identified and shown to influence the *Retrotrapezoid Nucleus of the medulla oblongata. This area responds to a rise in PCO2 and to input from the carotid bodies. Patients with CCHS require a tracheostomy and a mechanical ventilator throughout their lives.

Question 58

What causes hypocapnia and what is the result? How can you treat it?

Answer 58

Hypocapnia (low plasma PCO2) due to hyperventilation causes cerebral vasoconstriction, which results in inadequate brain perfusion and hypoxia that can produce dizziness. The hypocapnia of hyperventilation also raises the blood pH (produces a respiratory alkalosis), which lowers plasma Ca2+. This can result in neuromuscular irritability and muscle spasms (tetany) in the legs, feet, and hands. People can raise their plasma PCO2 and alleviate these symptoms by breathing into a paper bag, but this could be dangerous for people hyperventilating because of asthma or because they have angina and myocardial infarction.

Question 59

What is SIDS and what causes it?

Answer 59

Sudden infant death syndrome (SIDS) is the sudden death of an infant under one year old that cannot be otherwise explained. Sometimes called crib death, it most often strikes infants between the ages of two and four months. The cause of SIDS is unknown, but evidence suggests it may be due to a failure of the central or peripheral chemoreceptors to detect a rise in carbon dioxide. The incidence of SIDS has been falling significantly since it is recommended that infants sleep on their backs and on a firm surface. SIDS still remains the leading cause of death in infants younger than one year

Question 60

What is cord blood banking and why would it be needed?

Answer 60

Cord blood banking is something that parents may elect to do when their baby is born. Blood from the umbilical cord contains stem cells that can be saved for later in life, when the child might need them to reconstitute a hematopoietic system if the bone marrow has been destroyed—for example, by chemotherapy for leukemia. Cord blood banking is a risk-free procedure, but it is an expensive one with a low probability that it will someday be needed.

Question 61

What required procedure is done on newborns between 24-48 hours old? What does it test for?

Answer 61

Genetic screening of neonates (newborns) is done on blood obtained by a heel prick when the baby is 24 to 48 hours old. This is a required procedure, and different states specify that 20 to more than 30 tests be performed on this blood. These include genetic tests for phenylketonuria (PKU), cystic fibrosis, lysosomal storage diseases, and many others, as well as tests for endocrine disorders (such as hypothyroidism) and hemoglobin disorders (such as sickle-cell anemia).