week 14

Question 1

What effect does PO2 have on ventilation?

Answer 1

PO2 indirectly effects ventilation by changing chemoreceptors sensitivity to PCO2 via the Hypoxic Drive: carotid bodies contain neuron-like gloms cells that sense a large drop in PO2. They depolarize and stimulate different afferent neurons of the carotid sinus nerve (part of glossopharyngeal nerve) which signals medulla to increase breathing as a Hypoxic Ventilatory Response. the carotid bodies respond to O2 dissolved in plasma, and the level of hypoxemia that would stimulate this response only occurs in extreme conditions like high altitude (normally PO2 has no direct effect on breathing!)

Question 2

*What are the three respiratory stimuli in normal conditions? Rank them from more important to least

Answer 2

1. pH: directly stimulates breathing
2. PCO2: main determiner of pH
3. PO2: weakest stimuli, under normal conditions has no effect

Question 3

*How is the control of breathing changed in a person with emphysema?

Answer 3

Emphysema causes chronically high CO2 that causes chemoreceptors to become blunted. Therefore the Hypoxic Drive becomes the main stimulus of breathing instead of pH. This is a problem when emphysemic patients are given an oxygen mask because the high oxygen will lower the hypoxic drive response and the person will cease breathing (respiratory arrest). You can use a bag-valve mask to manually ventilate the patient if needed.

Question 4

What is the structure of the molecule that contains most of the oxygen in blood?

Answer 4

Hemoglobin consists of four polypeptide chains (globins) and four iron-containing pigment molecules (hemes). The protein part is made of two alpha chains and two beta chains. The iron molecule is located at the center of the heme (which is in center of proteins) and can combine with oxygen.

Question 5

Describe four different types of hemoglobin depending on what it is bound too

Answer 5

Oxyhemoglobin: iron is bound to oxygen (tomato red color)
Deoxyhemoglobin/Reduced hemoglobin: iron is not bound to oxygen, but is still reduced (maroon color?)
Methemoglobin/Oxidized hemoglobin: iron is in oxidized state and cannot participate in oxygen transport
Carboxyhemoglobin: iron is bound to carbon monoxide instead of oxygen. CO is 210 times stronger bond than O2. (maroon cranberry juice color)

Question 6

What is measured to assess how well lungs have oxygenated the blood? What is a normal value and what is one condition that can lower this value?

Answer 6

Percent Oxyhemoglobin Saturation (percentage of oxyhemoglobin to total hemoglobin) is measured by a pulse oximeter or blood-gas machine. Normal value is 97% and is determined because each hemoglobin types has a unique color and absorbs light differently (oximeter measures light absorption). Oxyhemoglobin is bright red and carboxyhemoglobin is maroon.
Carbon Monoxide poisoning lowers the oxyhemoglobin saturation but is not detectable via pulse oximeter because the CO bound hemoglobin still measures the same result (?). CO poisoning causes bright red skin in its victims

Question 7

What factors increase or decrease oxygen carrying capacity?

Answer 7

Anemia (low hemoglobin) lowers oxygen content while polycythemia (high RBC count) increases oxygen content at high altitude. Production of hemoglobin and RBCs is controlled by Erythropoietin produced in the kidneys. Testosterone also promotes RBC production, which is why men have higher hemoglobin than women.

Question 8

What are the loading and unloading reactions and where do they occur? What factors affect the extent of each reaction?

Answer 8

Loading reaction is Deoxyhemoglobin + oxygen = oxyhemoglobin while unloading reaction is oxyhemoglobin = deoxyhemoglobin + oxygen. Loading occurs in lungs and unloading in capillaries/tissues. PO2 of the environment and the affinity of hemoglobin/oxygen affect the direction of the reaction. High PO2 drives loading in lung capillaries and low PO2 drives unloading in tissue capillaries. Strong affinity (bond strength) favors loading and weak affinity favors unloading, normally bonds are strong enough so 97% of hemoglobin is oxygen bound in lungs but weak enough to unload in tissues.

Question 9

Describe the graph that shows unloading percentages. How much oxygen is unloaded to tissues at rest and how long does the remaining oxygen last if breathing stops?

Answer 9

Oxyhemoglobin dissociation curve shows % O2 saturation vs PO2 can predict unloading percentage given PO2 values (arterial and venous). At rest, there is only 22% of oxygen that is unloaded to tissues (arterial PO2 is 22% higher than venous PO2). The large amount of remaining oxyhemoglobin provides a reserve that will keep the brain and heart alive for 4-5 minutes without breathing (CPR can extend this time by circulating the oxygen reserve). Exercise can also tap this reserve

Question 10

What is the shape of the oxyhemoglobin dissociation curve and what does that indicate about the effect of PO2 changes?

Answer 10

It is sigmoidal (S shaped). When PO2 values are very high the graph is flat, so changes in PO2 have little effect on loading reaction. When PO2 values are very low the graph is steep, meaning that small changes in PO2 cause large changes in percent saturation. Note that it is Venous PO2 that decreases, not arterial which remains at 97%. For example, during exercise the venous PO2 drops as low as 20 mmHg or 17% saturation, so unloading percent is 97% - 17% = 80%

Question 11

*Describe the effects of pH and temperature on oxygen transport and the oxyhemoglobin dissociation curve

Answer 11

Affinity of hemoglobin for oxygen directly impacts the rate of loading vs unloading reaction in a tissue

1. Affinity increases when pH increases due to the Bohr effect. Active tissues metabolize = makes CO2 = lowers pH = lower hemoglobin affinity = more oxygen released. The curve shifts right when pH is lowered (acidic) meaning greater unloading, and left which pH is raised (alkaline) meaning less unloading
2. Affinity decreases as temp increases. Active tissues are warmer = lower hemoglobin affinity = more oxygen released. Curve shifts right with rising temperature meaning greater unloading and shifts left with lower temperature meaning less unloading.

Question 12

Sickle cell anemia is the most common monogenic disorder and is found in people of African descent. What is the cause of the disease and how is it treated?

Answer 12

It is a hemoglobinopathy where a single valine is substituted for a glutamic acid in the beta chains of hemoglobin, producing Hemoglobin S instead of the normal hemoglobin A. When hemoglobin S is deoxygenated it makes long fibrous (sickle) shapes that blocks vessels and reduces blood flow, leading to infarctions, severe pain/damage, and hemolysis/anemia. It is treated with Hydroxyurea which stimulates production of hemoglobin gamma chains instead of beta (Hemoglobin F). Bone marrow transplant or gene therapy are also sometimes used

Question 13

Name two hemoglobinopathies and who they effect

Answer 13

Sickle cell anemia in Africans

Thalassemia in Mediterraneans

Question 14

How is myoglobin different from hemoglobin?

Answer 14

Found only in striated muscles, it has one heme instead of four and so only bonds one oxygen molecule. It also has higher affinity for oxygen than hemoglobin (dissociation curve is to the left) and only releases oxygen when PO2 is very low (curve is rectangular, not sigmoidal). It acts as a go-between from blood to mitochondria (where PO2 is very low) and functions to store oxygen, particularly in the heart. Remember, myoglobin releases O2 while in systole. Carbon Monoxide has even higher affinity for myoglobin than hemoglobin, so CO easily causes myocardial depression

Question 15

What are the three forms that CO2 is transported in? Describe how the most common form is made

Answer 15

1. dissolved CO2 in plasma is about 1/10th of total CO2
2. carbaminohemoglobin (CO2 attached to an amino acid in hemoglobin) is about 1/5th of total CO2
3. bicarbonate ion in blood is the rest of CO2 (Vast majority!). CO2 combines with water and converts to carbonic acid via the enzyme *Carbonic Anhydrase, present *only in RBCs. The carbonic acid then quickly dissociates into H+ and bicarbonate, which diffuses into plasma

Question 16

*What is the chloride shift?

Answer 16

CO2 converts to carbonic acid (Carbonic Anhydrase) which dissociates to H+ and bicarbonate. Bicarbonate diffuses outward into the plasma more than H+ does, so the trapped H+ ions create a net positive charge in the RBC. This attracts chloride ions to move in the cell in exchange for bicarbonate moving out. This is the Chloride Shift and occurs in metabolically active Tissues!
The Bohr effect states that H+ increases unloading of oxygen from oxyhemoglobin, and deoxyhemoglobin bonds H+ more strongly than oxyhemoglobin meaning O2 stays unloaded in metabolically active tissues. As H+ is removed by binding hemoglobin, the law of mass action supports creation of carbonic acid and increases transport of CO2 away in blood.

Question 17

*What is the reverse chloride shift

Answer 17

In Pulmonary capillaries, carbonic acid (formed because deoxyhemoglobin is converted to hemoglobin which has less H+ affinity, so free H+ combines with bicarbonate to make carbonic acid) is converted to water and CO2 gas (via Carbonic Anhydrase in low PCO2 conditions) which can be eliminated in breath (bicarbonate cannot be exhaled). Entrance of bicarbonate into the RBCs causes chloride to leave the cell, making a reverse chloride shift.

Question 18

What is the normal pH of blood and what is abnormal? What are the normal acids in blood and what buffers them?

Answer 18

Normal pH is 7.35 - 7.45, slightly alkaline. Below 7.35 is called acidosis and above 7.45 is alkalosis. There is volatile acid (carbonic acid) which can be exhaled and nonvolatile acids (lactic acid, ketone bodies, fatty acids) that cannot be exhaled. Usually, these nonvolatile acids don’t affect pH too much because H+ ions are bound to buffers, particularly Bicarbonate. The kidneys also serve to remove excess H+ and reabsorb bicarbonate to maintain acid-base balance of the blood.

Question 19

*describe the four types of acid-base imbalances and what causes them

Answer 19

1. Respiratory acidosis: inadequate ventilation (hypoventilation) rises CO2 and carbonic acid. Emphysema, asthma, and COPD may cause
2. Respiratory alkalosis: hyperventilation decreases CO2
3. Metabolic acidosis: excessive production of nonvolatile acids (ketone bodies in diabetes mellitus) that produce H+. Or loss of bicarbonate (which buffers H+) due to excessive diarrhea that eliminates bicarbonate in pancreatic juice
4. Metabolic alkalosis: excessive bicarbonate from intravenous infusion or inadequate nonvolatile acids due to vomiting that eliminates acid in gastric juice

Question 20

What organs maintain blood pH? How can they work together in response to imbalance and how long does it take to respond?

Answer 20

Lungs maintain the respiratory component (CO2 concentration) and kidneys maintain the metabolic component (bicarbonate concentration). Disturbances in one component may be compensated for by changes in the other component. If the primary disturbance is metabolic, changes in ventilation will adjust within hours. But if the disturbance is respiratory, the secondary metabolic response will take days.

Question 21

Describe the ventilation responses that occur with acid-base imbalances in blood. Also what other symptoms occur with hyperventilation?

Answer 21

Hypoventilation increases CO2, causing respiratory acidosis, while Hyperventilation decreases CO2, causing respiratory alkalosis. (Hyperventilation also causes dizziness by raising pH of CSF and inducing cerebral vasoconstriction, and Hypocalcemic Tetany by increasing the amount of calcium bound to albumin and lowering free calcium which makes nerves overexcitable.) Changing ventilation can also compensate for metabolic imbalances, e.g. metabolic acidosis (from diabetes!) causes hyperventilation and metabolic alkalosis causes hypoventilation

Question 22

Describe the mechanism responsible for ventilation during exercise

Answer 22

It is complex and I don’t need to know much about it! Just that blood PO2, PCO2, and pH remain very constant during exercise so it is NOT the increased CO2 that causes increased ventilation like you might think

Question 23

What occurs as part of acclimatization? What do people who have lived at high altitudes their whole lives have that others do not?

Answer 23

1. increased ventilation
2. increased hemoglobin affinity for oxygen
3. increased total hemoglobin concentration
4. decreased blood volume
   Genetic adaptations also occur in native highlanders
5. Large barrel chests so more air enters lungs
6. more capillaries develop
7. lower hemoglobin/RBC levels than adapted lowlanders
8. produce pulmonary nitric oxide to dilate pulmonary arteries and lower after load of right ventricle

Question 24

What changes in ventilation occur during acclimatization? What additional adaptation occurs in people who are native to a high altitude

Answer 24

Decreased PO2 stimulates carotid bodies to cause hyperventilation (hypoxic ventilatory response) that lowers PCO2 and produces respiratory alkalosis. Alkalosis blunts the hypoxic ventilatory response to decrease hyperventilation some. Over the next few days, the kidneys excrete bicarbonate to produce a compensatory metabolic acidosis to move pH toward normal and increase the hypoxic ventilator response. Carotid bodies also increase sensitivity to hypoxia to increase ventilation and activate sympathetic system to raise blood pressure. Note that while hyperventilation improves oxygenation, it cannot increase PO2 beyond that of the inspired air. Hypoxia also causes pulmonary vasoconstriction, but genetic adaptations have been seen to increased nitric oxide (vasodilator) to lower pulmonary artery pressure and decrease after load of right ventricle = higher cardiac output in native people.

Question 25

*What drug is used to prevent/treat mountain sickness and how does it work?

Answer 25

Acetazolamide (Diamox) is a Carbonic Anhydrase Inhibitor and a diuretic that treats mountain/altitude sickness by forcing kidneys to excrete bicarbonate and making blood more acidic. Blood acidity fools the body into thinking it has excess CO2 it eliminates CO2 by deeper and faster breathing which then increases the amount of oxygen in blood. It is not an immediate cure for altitude sickness, but speeds up acclimatization and relieves symptoms.

Question 26

What is the effect of high altitude on red blood cell production?

Answer 26

Hemoglobin concentration rises within a day or two (dehydration and reduced plasma volume) and then kidneys secrete erythropoietin to cause increased RBC and hemoglobin concentration over weeks (higher hematocrit). So, while percent oxyhemoglobin saturation is lower than at sea level, the total oxygen content is actually greater! However, polycythemia (high RBC) increases viscosity and vascular resistance and contributes to hypertension, edema, right ventricular hypertrophy, and heart failure. *Pregnant women with polycythemia have increased fetal mortality. Chronic Mountain sickness occurs with high hemoglobin concentration (21 to 23 g/dl) and native highlanders actually have lower hemoglobin/RBC levels than acclimatized lowlanders

Question 27

What do the kidneys regulate (4 things)

Answer 27

1. volume of blood (and therefore blood pressure)
2. concentration of waste products in plasma
3. concentration of electrolytes in plasma
4. pH of plasma
   Also secretes erythropoietin!

Question 28

Describe the structure of the kidneys, which lie on either side of the vertebral column below the diaphragm and liver, and the structures they flow into. How does male and female structure differ?

Answer 28

The kidney has an outer cortex (reddish brown and granular) and inner Medulla (striped) which is composed of conical Renal Pyramids separated by Renal Columns. Each pyramid projects into a Minor Calyx and those unite to form a Major Calyx which join to form the Renal Pelvis. Urine drains into the hollow cavity of the Renal Pelvis and then travels through two Ureters (ducts) to the Urinary Bladder (shape is pyramidal if empty and ovoid if full). This drains through a single urethra, in females it is short (prone to infection) and males it is long but encircled by the prostate gland (prostate enlargement impedes urination and causes UTIs)

Question 29

What causes pain when passing a kidney stone? Name the specific area that causes this action

Answer 29

The ureter undergoes peristalsis (wavelike contractions) that are controlled by pacemakers in the renal calyces and pelvis smooth muscle. These contribute to emptying of urine and also the intense pain of a kidney stone

Question 30

Describe the muscles involved in control of micturition. Which ones are important for potty training and causing incontinence?

Answer 30

The *Detrusor muscle is stimulated by parasympathetic axons (ACh) to cause emptying of the bladder. Two muscular sphincters surround the urethra: upper Internal Urethral Sphincter (smooth muscle under autonomic control) and lower External Urethral Sphincter (voluntary skeletal muscle control). Potty training (around age 2-3) targets the external urethral sphincter which is under voluntary control. Kegel exercises strengthen external urethral sphincter and pelvic floor (weak pelvic floor = cannot delay urination = incontinence). Spinal cord damage also causes incontinence by interrupting voluntary signals, a urinary (Foley) catheter is often inserted in such people.

Question 31

Describe the mechanism (reflexes) that control micturition

Answer 31

As bladder is filling, stretch stimulates interneurons in S2 through S4 of spinal cord to cause Guarding Reflex, where parasympathetic nerves to the detrusor muscle are inhibited while external urethral sphincter is stimulated via Pudendal Nerve = prevents involuntary emptying of bladder.

Once bladder is really stretched, the Voiding Reflex passes sensory info up to the pons Micturition Center which activates parasympathetic nerve to detrusor muscle to cause contractions. Inhibition of sympathetic axons relaxes internal urethral sphincter. Person feels urgency, but still has voluntary control over external urethral sphincter via pudendal nerve. When decision to urinate is made, the micturition center (pons) activates and pudendal nerve is inhibited so external urethral sphincter relaxes.

Question 32

What contractions occur before birth actually starts? What other sign occurs just before parturition starts? review the signals/hormones that cause contraction

Answer 32

Uterus contracts throughout pregnancy, the Braxton Hicks (“false labor”) contractions serve to tone the uterus for labor. A “bloody show” occurs prior to stage one of partition as mucous plug is expelled. True contractions occur every 15-20 minutes and last 40 seconds or more. A positive feedback mechanism occurs: cervix stretches and causes oxytocin release which directly (and through Prostaglandins) stimulates uterine contraction, which pushes fetus down and stretches cervix more which causes more oxytocin, etc.

Question 33

Describe the events of Stage 1 of parturition

Answer 33

No movement occurs in this stage. First, effacement or “taking up the cervix” occurs where cervix slowly thins out and pulls up toward fetus head. Then the fetus’ head acts as a wedge to assist Cervical Dilation. The amniotic sac often ruptures now and leaks fluid out vagina (“breaking the bag of waters” or “bilateral shoe sign”). Sometime babies are born inside the amniotic sac, this is En-caul birth. Stage one ends with cervix completely dilated to 10 cm.

Question 34

Describe Stage 2 of parturition

Answer 34

Movement of fetus toward cervix and vaginal canal begins as contractions occur every 1-2 minutes. The desire to push (Valsalva’s maneuver) becomes greater as the fetus’ head descends to vagina. Squatting is a good and common stance taken to widen pelvic space and help mother use abdominal muscles to push, also reduces tearing of perineum. An Episiotomy may be performed if necessary to enlarge vaginal opening as baby’s head emerges. “Molding” of the baby’s head is normal and goes away soon. The umbilical cord is clamped and cut.

Question 35

What is the functional unit of the kidneys? name all of its tubules and track where fluid flows from start to finish

Answer 35

Nephrons, consisting of tubules. The Glomerular (Bowman’s) capsule is in the cortex and surrounds the glomerulus (the capsule + glomerulus = Renal Corpuscle). The capsule contains an inner visceral layer and outer parietal layer, the space between is continuous with the lumen of the tubule and it receives filtrate. Filtrate passes into the Proximal Convoluted Tubule, which has millions of microvilli, and reabsorption occurs. Fluid passes then to the Nephron Loop or Loop of Henle which carries to the renal medulla in the Descending Loop and returns to the cortex in the Ascending Loop. Back in the cortex, the Distal Convoluted Tubule empties into a collecting duct which drains from cortex to medulla through renal pyramids to form “urine” at the Minor Calyx (*only now is it called urine!)

Question 36

Name the two types of nephrons

Answer 36

Juxtamedullary nephrons: originate in inner one-third of the cortex and have longer nephron loops. These play a role in concentrating urine

Cortical nephrons: originate in the outer two-thirds of the cortex and are much more numerous.

Question 37

How does fluid get to the kidneys? name the vessels that feed into the kidney

Answer 37

Arterial blood enters the Renal Artery which divides into Interlobar Arteries that pass between pyramids. Arcuate Arteries branch from these at the boundary between cortex and medulla. Arcuate arteries then branch into Interlobular Arteries in the cortex and these divide into Afferent Arterioles, which deliver blood into Glomeruli to produce filtrate that enters urinary tubules. Remaining blood leaves the glomerulus through Efferent Arterioles which deliver blood to the Peritubular Capillaries. Blood drains via interlobular veins, arcuate veins, and interlobar veins to a renal vein

This is the only time in the body that a capillary bed (glomeruli) is drained by an arteriole rather than a venue and delivered to a second capillary bed (peritubular capillaries)!

Question 38

*How do glomerular capillaries filter fluid and prevent cells/proteins from being excreted in urine?

Answer 38

three layers which fluid must pass through before entering interior of glomerular capsule (cells don’t fit through any fenestrations):

1. Capillary Fenestrae: large enough to allow proteins but has some charges to form barrier for plasma proteins
2. Glomerular Basement Membrane: collagen IV and proteoglycans offer some barrier to plasma proteins (Alport’s syndrome = defect in collagen IV = glomerulonephritis). Very thick and greatly restricts rate of fluid flow
3. Inner/Visceral Layer of the Glomerular Capsule: *Podocytes are unique cells with primary processes and foot processes interdigitating on the basement membrane, leaving narrow slits for proteins to pass through. *Slit Diaphragms link the foot processes and present the final filtration barrier

Question 39

What is the MAJOR barrier to proteins passing into filtrate and what would defect of this barrier cause?

Answer 39

The Slit Diaphragm. defects cause mass leakage of proteins into filtrate and Proteinuria. A small amount of albumin does normally enter filtrate, but almost none is excreted in urine. This is because it is reabsorbed (via endocytosis) or transported across the proximal tubule into blood. Proteinuria occurs when damage to the slit diaphragm causes more protein to enter the filtrate than can be reabsorbed by this mechanism.

Question 40

Filtrate (ultra filtrate) is made by what force? How does dehydration effect filtrate and what is the result on the body?

Answer 40

Hydrostatic pressure of blood (caused by left ventricular systole) contributes to Starling forces and formation of filtrate. Dehydration (diarrhea, blood loss, heart failure, no water) reduces blood pressure and increases time to transit waste from tissues to kidneys, increasing retention of wastes. Glomerular filtration rate also decreases so lest waste enters glomerular capsule for excretion. Result is acidosis, *uremia, impaired metabolism, and death.

Question 41

What is glomerular filtration rate and what forces contribute to it?

Answer 41

Volume of filtrate produced by both kidneys per minute (super high btw, total blood volume is filtered every 40 mins!), determined by the net filtration pressure. Fluid is pushed into the glomerular capsule by the hydrostatic force of blood pressure and it is pushed in the opposite direction by hydrostatic pressure of fluid in the glomerular capsule. Higher protein concentration in the plasma also promotes osmotic return of water. The difference between these forces is the net filtration pressure and is relatively low, but due to the large surface area of the glomerular capillaries the total volume of filtrate is large

Question 42

How is GFR regulated

Answer 42

Glomerular Filtration Rate is regulated by afferent arteriole constriction/dilation that affects rate of blood flow to the glomerulus. Changes occur from both extrinsic mechanisms (sympathetic innervation) and intrinsic mechanisms (renal autoregulation)
- Sympathetic activity (from fight-or-flight, or exercise) stimulates constriction of afferent arterioles to preserve blood volume and divert blood to heart/muscles. Cardiogenic shock produces a similar vasoconstriction effect where decreased GFR helps compensate for blood pressure dropping.

Question 43

What is the Obligatory Water Loss value and meaning? How does this value compare to the total amount of filtrate produced and what does that tell you about where most filtrate goes?

Answer 43

The minimum amount of urine needed to excrete the metabolic wastes of the body, about 400 ml per day. Excess of this amount makes more diluted urine. Since 108 L of filtrate are produced each day, most of it is reabsorbed. 85% of reabsorption happens by an unregulated fashion (osmosis) in the proximal tubules and descending limbs of the nephron loops, therefore a concentration gradient is necessary to promote osmosis and reabsorption

Question 44

Describe the main mechanism for reabsorption of water from filtrate

Answer 44

In the proximal tubule: filtrate is isosmotic with plasma because plasma solutes (except proteins) can freely enter filtrate. The proximal tubule cells are joined by tight junctions and their apical sides (closest to tubule lumen) has microvilli, basal side faces peritubular capillaries, and lateral sides face adjacent cells. Intracellular Na+ is low due to low permeability and Na+/K+ pumps on the basal and lateral sides only. This creates a gradient to favor diffusion of Na+ from tubule fluid to inside cells and then Na+ is pumped into tissue fluid. Na+ gradient also makes the lumen more negatively charged and the electrical gradient favors passive Cl- transport into interstitial fluid (where Na+ is high) mainly in late proximal tubule where junctions are leakiest (Paracellular Transport occurs). Result is high NaCl in tissue fluid around proximal tubule that promotes reabsorption of water through aquaporin channels

Question 45

Where is most fluid reabsorbed (2 locations) and what are some basic characteristics of this type of reabsorption?

Answer 45

Through the proximal loop. Constant reabsorption takes place regardless of hydration levels via active and passive transport of Na+ and Cl- respectively. These are not subject to hormonal regulation and are very costly in terms of energy (the Na+/K+ pumps). Fluid is isosmotic with blood in this entire tubule, which accounts for 65% of reabsorption. An additional 20% occurs in the descending limb of the nephron loop and is also constant and not hormonally regulated. The Loops of Henle are not isotonic environments, they bend sharply so the ascending and descending limbs can interact and it creates a hypertonic interstitial fluid which promotes osmosis and reabsorption of water.

Question 46

What is Obstructive sleep apnea? cause, risk factors, dangers, and treatment

Answer 46

periodic hypopnea (reduction in breathing) and apnea (cessation of breathing) during sleep due to a partial or complete collapse of the upper airway. It is more common in men than women, and obesity is a significant risk factor. Oropharynx air passage narrows during sleep to cause apnea, and arterial PO2 and oxyhemoglobin saturation fall as arterial PCO2 rises = chemoreceptor reflex ends the apnea with a gasp and jerk. Snoring, sleepiness and fatigue during the day and a morning headache caused by cerebral vasodilation, are some of the other symptoms. Dangers include pulmonary hypertension that results in right ventricle hypertrophy. Treatment is CPAP (continuous positive airway pressure) devices keep the oropharynx air passage open while sleeping.

Question 47

What amount of carboxyhemoglobin is considered poisoning? What usually causes carbon monoxide poisoning, what are symptoms, and what is treatment?

Answer 47

Carbon monoxide poisoning occurs when the blood carboxyhemoglobin is greater than 10% in smokers and 3% in nonsmokers. Carbon monoxide poisoning is usually caused by the burning of fossil fuels by faulty appliances or vehicles within an enclosed space. Symptoms may include headache, weakness, dizziness, nausea, and confusion. More severe symptoms include neurological disturbances such as memory loss, psychiatric conditions, and cardiac injury. People may be treated for carbon monoxide poisoning by breathing 100% oxygen at 1 atmosphere pressure, or by breathing 100% oxygen at greater than 1.4 atmospheres pressure within a hyperbaric chamber.

Question 48

What is Physiological jaundice of the newborn and what causes it? Name specific molecules that cause jaundice and why they are built up in newborns. Treatment?

Answer 48

Physiological jaundice of the newborn is a yellowing of the skin, sclera, and mucous membranes that commonly occurs in newborns, caused by the pigment bilirubin produced from heme in destroyed red blood cells. Bilirubin is elevated in the newborn because fetal red blood cells containing hemoglobin F have shorter life spans than adult red blood cells containing hemoglobin A, and are rapidly destroyed after birth. In a fetus, bilirubin passes through the placenta because it is lipid soluble, but after birth it must be converted by the liver into a water-soluble form (conjugated bilirubin) to be excreted in the bile. it takes time for the newborn’s liver to produce conjugating enzyme. jaundice is not usually dangerous, but if bilirubin concentrations are great, the baby may undergo phototherapy (blue lights) which converts the unconjugated bilirubin into water-soluble derivatives that can be excreted.

Question 49

What are the symptoms/cause of acute mountain sickness? How can you treat it? What further complications can occur if left untreated?

Answer 49

Symptoms of headache, malaise, anorexia, nausea, dizziness, and fragmented sleep. The low arterial PO2 stimulates vasodilation in the pia mater, increasing blood flow and pressure within the skull (headache). This is reduced by normal hyperventilation that accompanies acclimatization (low arterial PCO2 stimulates vasoconstriction). Pulmonary arterioles respond in an opposite way—they constrict, raising pulmonary vascular resistance and pressure, increasing the afterload of the right ventricle. Acute mountain sickness can be treated by rest and nonsteroidal anti-inflammatory drugs (NSAIDs), or descending altitude. High-altitude pulmonary edema may occur after a couple of days at altitudes and produce shortness of breath, cough, and cyanosis. Dangerous high-altitude cerebral edema may cause coma and death. A hemoglobin concentration of 21 g/dL or greater is chronic mountain sickness (neurological disturbances and pulmonary hypertension leading to right heart failure)

Question 50

What are kidney stones and what are they commonly made of (3 types)? How to treat?

Answer 50

Nephrolithiasis (kidney stones) are hard objects formed in the kidneys containing crystallized minerals or waste products. Most are calcium stones (calcium phosphate or calcium oxalate). Struvite stones (magnesium ammonium phosphate) may result from certain UTIs. If a person has too much uric acid (the final metabolite of purines), due to a genetic defect, uric acid can precipitate in the joints (gout) and in the renal tubules (uric acid stones). Stones form when mineral concentrations exceed solubility and so form more if a person is dehydrated, but hydration with soft drinks increases risk of kidney stones. Large stones in the calyces or pelvis obstruct urine flow, and smaller stones that pass into a ureter produce intense pain. Medications are available to help pass kidney stones, but patient may need lithotripsy (lithotripter device produces shock waves that focus on the kidney stone and shatter it)

Question 51

Urinary incontinence (uncontrolled urination due to loss of bladder control) has many possible causes. Describe 3 causes

Answer 51

Stress urinary incontinence: due to increased abdominal pressure, as during sneezing, coughing, and laughing. This happens in women when the pelvic floor no longer provides adequate support to the urethra due to childbirth or aging. often treated by sling surgery where inserted mesh provides additional support for the urethra.
In men, urinary incontinence frequently occurs as a result of treatments for prostate cancer.
Urgency incontinence: uncontrolled contractions of the detrusor muscle produce a great urge to urinate and the leakage of a large volume of urine. Hallmark of an overactive bladder (also experiences frequent urinations and other symptoms)

Question 52

How is urinary incontinence diagnosed? names of tests

Answer 52

Urinary incontinence can be diagnosed by urodynamic testing. This includes cystometric tests, in which bladder pressure and compliance (dispensability) are measured as the bladder is filled with warm water and the subject is asked to say when the urge to urinate appears.

Question 53

What causes PKD (2 types)? Where is the specific gene responsible and what does it effect in the cell?

Answer 53

Polycystic kidney disease (PKD) is a congenital disorder in which the kidneys are enlarged by hundreds to thousands of fluid-filled cysts that form in all segments of the nephron and eventually separate from the tubules. Autosomal dominant(!) polycystic kidney disease (ADPKD) accounts for most cases. The disease may less commonly be inherited as an autosomal recessive(!) trait. The gene responsible for 85% of ADPKD is located on chromosome 16 and codes for polycystin-1, whereas a gene located on chromosome 4 that codes for polycystin-2 is responsible for the other cases. Polycystin-1 and polycystin-2 are important for the sensory function of the *primary cilium (serves as a mechanosensor, where the flow of filtrate bends the cilium and results in the movement of Ca2+ into the cell).

Question 54

What are the two types of diabetes insipidus and what causes them? How can they be distinguished and treated?

Answer 54

Diabetes insipidus is characterized by polyuria (a large urine volume), thirst, and polydipsia (drinking a lot of fluids). The urine is dilute, with a hypotonic concentration. Two major types: (1) central diabetes insipidus, caused by inadequate secretion of ADH (arginine vasopressin). Treat by taking desmopressin when needed. (2) nephrogenic diabetes insipidus, caused by the inability of the kidneys to respond to ADH due to genetic defects in either the aquaporin channels or the ADH receptors, or, more commonly, caused by drug therapy (lithium given to treat bipolar disorder, and certain antibiotics). No treatment, must drink a lot of water to prevent dehydration.
The types can be distinguished by measuring plasma arginine vasopressin, and by challenging the kidneys with desmopressin (synthetic ADH).