. In vivo, Bowman’s capsule - Altius Test Prep · Bowman’s capsule and the descending limb of...

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1. See labeled diagram: FIGURE 1 2. See labeled diagrams. In vivo, Bowman’s capsule is in contact with a portion of the distal tubule rather than directed away from it as shown. The juxtaglomerular apparatus is made up of a patch of cells on the distal tubule (macula densa) and a patch of cells on the afferent arteriole (juxtaglomerular cells)—where the two structures meet. Together, these two patches of cells constitute the juxtaglomerular apparatus. In Figure 2 the distal tubule is labeled C. The macula densa are magenta and labeled #7. The juxtaglomerular cells are green and labeled #6. Flow through the afferent arteriole is demonstrated by #9. FIGURE 2

Transcript of . In vivo, Bowman’s capsule - Altius Test Prep · Bowman’s capsule and the descending limb of...

Page 1: . In vivo, Bowman’s capsule - Altius Test Prep · Bowman’s capsule and the descending limb of the Loop of Henle. Along the PCT sodium is reabsorbed via active transport, and glucose

1. See labeled diagram:

FIGURE 1

2. See labeled diagrams. In vivo, Bowman’s capsule is in contact with a portion of the distal tubule

rather than directed away from it as shown. The juxtaglomerular apparatus is made up of a patch of cells on the distal tubule (macula densa) and a patch of cells on the afferent arteriole (juxtaglomerular cells)—where the two structures meet. Together, these two patches of cells constitute the juxtaglomerular apparatus. In Figure 2 the distal tubule is labeled C. The macula densa are magenta and labeled #7. The juxtaglomerular cells are green and labeled #6. Flow through the afferent arteriole is demonstrated by #9.

FIGURE 2

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3. The glomerulus is a fenestrated capillary bed that strains the blood—allowing fluids, ions, and molecules the approximate size of glucose or smaller to pass through into Bowman’s capsule. Blood cells and larger blood components remain within the capillaries and exit via the efferent arteriole which eventually empties into the renal vein. Bowman’s capsule is a spherical enclosure around the glomerulus that catches the filtrate as it is formed and funnels it into the proximal tubule. The proximal convoluted tubule (PCT) is the section of the nephron between Bowman’s capsule and the descending limb of the Loop of Henle. Along the PCT sodium is reabsorbed via active transport, and glucose is reabsorbed via secondary active transport through a symporter identical to the one used to absorb glucose from the small intestine. Water follows the solutes via facilitated diffusion. However, because water and solutes are reabsorbed in the same ratio, the filtrate remains isotonic (i.e., the volume of filtrate decreases, but its concentration remains constant). The descending Loop of Henle travels into the very hypertonic medulla. This section of the nephron is impermeable to salts, but very permeable to water. Water therefore flows out of the filtrate and into the medulla, concentrating the urine. The ascending Loop of Henle carries the filtrate out of the medulla and back into the cortex. This portion of the loop is impermeable to water and actively transports ions out of the filtrate and into the medulla. This continuous “dumping” of salts into the medulla accounts for its hypertonicity. At the top of the ascending loop the filtrate is actually less concentrated due to the removal of these ions. The distal convoluted tubule (DCT) is the section of the nephron between the top of the ascending loop of Henle and the collecting duct. Recall that this segment passes directly by the opening to Bowman’s capsule where the juxtaglomerular apparatus is located. The distal convoluted tubule regulates calcium, sodium and hydrogen concentrations—although for the MCAT we suggest you focus only on its sodium reabsorption function as regulated by the hormone Aldosterone. Recall that aldosterone stimulates increased sodium reabsorption at the DCT and the collecting duct. Less important, but worth remembering, is the fact that the DCT also reabsorbs calcium in response to parathyroid hormone (PTH). When the juxtaglomerular apparatus detects decreased blood pressure in the afferent arteriole, it secretes Renin, setting into motion the renin-angiotensin pathway whose ultimate result is increased blood volume and blood pressure (this increased blood pressure would provide negative feedback inhibition to the juxtaglomerular apparatus). A number of DCTs from a number of different nephrons dump into a shared collecting duct. The collecting duct carries the filtrate through the medulla toward the renal pelvis. The collecting duct becomes very permeable to water in the presence of ADH from the posterior pituitary. If ADH is present the filtrate will be further concentrated as water flows out into the very salty medulla. Note to Tutors: Students should be intimately familiar with the above description of the anatomy and function of the nephron. A good goal would be for them to be able to recount all of the above information to you as a “story” told in their own words.

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4. The diagram below outlines the renin-angiotensin pathway in sufficient detail for the MCAT. We do NOT believe the MCAT will require memorized knowledge of this pathway, but it has appeared in passages before, and knowledge of this pathway will make some questions easier.

FIGURE 3

5. The tidal volume (TV) is the volume of air that enters and exits the lungs during an average, unforced respiration. There are two reserve volumes, an inspiratory reserve volume (IRV) and an expiratory reserve volume (ERV). This is the volume of additional air that can be exhaled or inhaled after a normal, unforced expiration or inhalation. The residual volume (RV) is the amount of air left in the lungs after a forced, maximal exhalation. Vital capacity (VC) is the total volume of air the lungs can hold at maximum inflation, minus the residual volume.

FIGURE 4

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6. If we assume—as seems to be implied—that this home remedy works because coating the vocal cords with honey hydrates and soothes these structures, then the remedy is entirely debunked by the anatomy of the respiratory system. At the back of the throat, near the base of the tongue, the pharynx essentially ends at a fork. The more posterior fork is the esophagus, which leads to the stomach. The more anterior fork is the larynx, which houses the vocal cords, and then continues on to the trachea, bronchi and lungs. The epiglottis is an upward-oriented cartilaginous flap that folds down over the opening to the larynx creating a one-way only route down the esophagus during swallowing. Thus, if honey or some honey concoction is consumed, it would coat the pharynx, epiglottis and esophagus, but be entirely separated from the vocal cords. To coat the vocal cords the honey would have to be inhaled—which would be very painful. At best, if any remedy does exist it would have to be the result of vapors given off by the honey in the throat reaching the vocal cords.

7. Each hemoglobin molecule has four subunits, each with one heme. Each heme can hold one O2 molecule. Therefore, at 100% saturation a hemoglobin molecule can hold 8 oxygen atoms.

8. The MCAT has demonstrated that they clearly expect prior knowledge of this curve as demonstrated by their asking stand-alone questions that cover these concepts without presenting an example of the curve or discussing it in a passage. It would be logical to expect future questions on all aspects of this curve, especially trends related to pH, carbon dioxide concentration, and temperature. One question asked previously about BPG, but some helpful information was given in the stem.

FIGURE 5

9. The two equations whose net equation is given in the outline are: CO2 + H2O ↔ H2CO3 H2CO3 ↔ HCO3

- + H+

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10. See the diagram below. You do not need to memorize the heart valves for the MCAT (but they are pretty easy to remember and you’ll need to learn them in medical school anyway). Think of Traveling to Bolivia, abbreviated: TRV BLV = Tricuspid Right Ventricle, Bicuspid Left Ventricle. The other two are named after what they lead to: pulmonary valve and aortic valve.

FIGURE 6

11. The pulmonary artery carries deoxygenated blood from the right ventricle to the lungs. The

veins of the systemic circulation all carry deoxygenated blood from the capillaries back to the right atrium. The pulmonary veins carry oxygenated blood from the lungs back to the left atrium. The arteries of the systemic circulation all carry oxygenated blood from the left ventricle to the capillaries.

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12. The electrical signal originates at the SA node, then spreads across both atria to the AV node. There is a slight delay, then the signal travels from the AV node down the bundle of His and through the Purkinje fibers. At the end of the Purkinje fibers the signal travels cell to cell through gap junctions.

FIGURE 7

13. On the arterial side of the capillary bed the hydrostatic pressure is at its maximum. At this same point, the osmolarity of the blood is greater than that of the interstitial fluid, creating an osmotic pressure that would drive fluid into the capillary. These two influences oppose one another, but the hydrostatic pressure is greater than the osmotic pressure, yielding a net filtration pressure (13 mmHg, driving fluid out of the capillary and into the interstitial fluid). On the venous side of the capillary bed the differences in osmolarity are about the same, but the hydrostatic pressure has decreased significantly. This makes the net filtration pressure negative and fluid flows out of the interstitial fluid and into the capillary (-7 mmHg). Note, however, that the net pressure on the arterial side is slightly greater than the net pressure on the venous side. As a result, about 10 percent of the fluid that exits on the arterial side does NOT re-enter the capillary on the venous side. What happens to that 10%? That is one of the primary functions of the lymphatic system—to pick up extra interstitial fluid from the capillary beds and return it to the venous system. (Net filtration data from McGraw-Hill Anatomy & Physiology, 2006).

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14. See diagram below. This diagram is intended to show general theoretical trends and is not drawn to scale. Q = AV explains the inverse relationship between the red and green lines.

FIGURE 8

15. Blood is a connective tissue.

16. Erythrocytes do NOT undergo mitosis because they lack nearly all of the cellular machinery to do so. Recall that red blood cells do not have nuclei or organelles. They are essentially membrane-bound sacks of hemoglobin.

17. Blood type is an example of co-dominance because both alleles are expressed equally in a heterozygote. A person with the AB genotype, for example, has both A and B antigens. In other words, both the A and B phenotypes are expressed simultaneously.

18. See diagram below.

FIGURE 9

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19. A dendrite is a finger-like projection from the cell body that receives signal information from an upstream neuron with which it forms a synapse. The signal will be received from the previous neuron via binding of a neurotransmitter on the dendrite portion of the membrane (i.e., postsynaptic membrane). The cell body is the main part of the neuron where the nucleus is located. The axon hillock is the area where the axon joins the cell body. This region has a very high concentration of voltage-gated sodium channels. This makes it both sensitive to action potentials and capable of regenerating a strong action potential for transmission down the axon. The terminal button (a.k.a., axon terminal) is a projection at the end of the axon that synapses with the dendrite of another neuron or with the effector. The axon is the long, narrow, tube-like extension between the cell body and the terminal button. Human axons can be up to 1.5 meters long! Along the axon are specialized neural support cells called Schwann cells. These cells contain high levels of fat and wrap themselves around the axon multiple times creating an insulating myelin sheath. There are small gaps between Schwann cells, called the nodes of Ranvier. A signal is able to “Jump” from one node to another without progressing along the entire length of the axon—dramatically increasing transmission speed.

20. The absolute refractory period is a portion of time during which an action potential cannot be initiated regardless of the strength of the stimulus. This time period occurs during the progression of a previous action potential. The progression of an action potential involves the depolarization of the membrane and a second stimulus cannot be initiated until the membrane is repolarized. The relative refractory period is a portion of time during which the membrane is hyperpolarized (i.e., is more negative than at normal resting potential). During this time, a second action potential can be initiated, but a stronger-than-normal stimulus will be required. This makes sense because the firing of an action potential is an all-or-nothing event dependent on the polarity of the membrane reaching the threshold potential.

21. See the labeled diagram below. The potassium channels open at some positive potential, before

the sodium channels close. The sodium channels close at the peak of depolarization. Note that some stimuli fail to result in an action potential because they fall short of the threshold stimulus. In this diagram it is also easy to see why a greater-than normal stimulus would be necessary to reach the threshold during the hyperpolarization phase (i.e., relative refractory period).

FIGURE 10

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22. When an action potential arrives at the presynaptic membrane it triggers voltage-gated calcium channels to open, allowing calcium ions to flow into the cell. Inside of the terminal button are numerous neurotransmitter bundles—vesicles filled with neurotransmitter. The presence of calcium initiates a cascade that results in an exocytosis process wherein these bundles fuse with the presynaptic membrane, and dump their contents into the synaptic cleft. These neurotransmitter molecules diffuse across the gap and bind to protein receptors on the postsynaptic membrane. These receptors are usually associated with sodium channels so that the binding of neurotransmitter opens the sodium channel allowing sodium ions to flow into the cell. If enough sodium ions flow into the cell the voltage will reach the threshold stimulus and an action potential will be generated in the second neuron.

23. An acetylcholinesterase antagonist would impede the normal activity of this enzyme, which breaks down acetylcholine. Decreased breakdown of the neurotransmitter would allow more of it to be present in the synaptic cleft, and to be present for a longer period of time—causing hyperstimulation of the subsequent neuron. Hyperstimulation of neurons could cause any number of problems depending on the effector with which a neuron is communicating. Muscle rigor, cramping, ticks, and pain would be logical possibilities. The drug effect would not necessarily be negative. An increase in the concentration of certain neurotransmitters in the brain has been shown to combat depression and therefore many antidepressants are actually acetylcholinesterase inhibitors (i.e., fluoxetine [Prozac], sertraline [Zoloft] and amitriptyline [Elavil]). If the drug were an agonist it would have the opposite effect, resulting in increased breakdown of acetylcholine and therefore decreased stimulation of neurons.

24. The pupils dilate in response to sympathetic stimulation and constrict in response to parasympathetic stimulation; heart rate is increased by sympathetic stimulation and decreased by parasympathetic stimulation; blood pressure is increased by sympathetic stimulation and decreased by parasympathetic stimulation; blood flow to the skeletal muscles is increased by sympathetic stimulation and decreased by parasympathetic stimulation; blood flow to the digestive organs is decreased by sympathetic stimulation and increased by parasympathetic stimulation; blood flow to the brain is increased by sympathetic stimulation and decreased by parasympathetic stimulation; blood flow to the skin is decreased by sympathetic stimulation and increased by parasympathetic stimulation.

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25. See diagram below.

FIGURE 11

26. In a G-protein cascade, a hormone or signal first binds to an integral protein on one of its

extracellular domains—this protein is called a G-protein-coupled receptor or GPCR. This causes a

conformational change that activates a cytosolic domain of that same integral protein. Near the

GPCR, or at least along the cytosolic face of the membrane, is a G protein made up of an alpha,

beta and gamma subunit. The alpha subunit binds both GTP and GDP. When GDP is bound the

protein is “off” and when GTP is bound it is “on.” Usually, but not always, the activated receptor

protein acts as a catalyst for the replacement of GDP by GTP, activating the alpha subunit of the

G protein. Usually, the activated alpha subunit then separates from the beta and gamma

subunits. The activated alpha subunit acts as an agonist for another enzyme, often adenylyl

cyclase. Adenylyl cyclase is an enzyme that catalyzes the conversion of ATP to cAMP and 2Pi.

Cyclic AMP just happens to be an agonist for Protein Kinase A, which phosphorylates proteins—

usually enzymes. Many enzymes are turned on or off through being phosphorylated or

dephosphorylated. The cascade can be shut down in various ways. Often the beta and gamma

subunits rebind with the alpha subunit deactivating it. In other cases GPCR is phosphorylated

one or more times which deactivates it. DO NOT MEMORIZE THIS. The MCAT will not test you on

names or other specifics. However, it does illustrate how cascades work and having a general

familiarity with G protein signaling pathways will be a tremendous help on any passages or

questions about G proteins—which have been fairly common.

27. Patient A has high blood glucose. The body’s hormonal reaction to this condition will be to attempt to re-establish homeostasis. High blood glucose levels stimulate the cells of the pancreas to secrete insulin. Insulin stimulates cells to import glucose, decreasing blood glucose levels. This would return the blood toward homeostasis and therefore insulin is expected in high levels. (Note: Some students resist this logic by claiming that high blood glucose is a potential indication of diabetes—a disease resulting from a lack of insulin or insulin resistance. However,

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there is nothing in this question that would lead you to suspect that a disease condition is present. The MCAT does not test you on disease symptoms. On the MCAT you should always assume normal physiology unless specifically told otherwise.) Patient B has low blood glucose levels. Glucagon—also secreted by the pancreas—stimulates the liver to breakdown glycogen to release glucose into the blood. In this case, more glucose would be necessary to reach homeostasis and therefore high glucagon levels would be expected.

28. Using the same logic as described for the previous question, Patient A is expected to have high levels of the hormone calcitonin because this hormone decreases calcium blood levels. Patient B has low blood calcium, so we expect him to have high levels of parathyroid hormone because its effect is to breakdown bone and release calcium into the blood.

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FIGURE CREDITS

1. Adapted by Altius from http://en.wikipedia.org/wiki/Kidney. Labels added. 2. http://www.tokresource.org/tok_classes/biobiobio/biomenu/kidney/index.htm

and http://en.wikipedia.org/wiki/Juxtaglomerular_apparatus

3. http://upload.wikimedia.org/wikipedia/commons/thumb/3/37/Renin-angiotensin-aldosterone_system-de.png/640px-Renin-

angiotensin-aldosterone_system-de.png

4. Adapted from http://en.wikipedia.org/wiki/Lung_volumes

5. Altius image.

6. http://www.texasheartinstitute.org/hic/anatomy/anatomy2.cfm

7. Altius image. 8. Altius image. 9. Adapted from http://en.wikipedia.org/wiki/Neuron 10. Source: Adapted from http://en.wikipedia.org/wiki/Action_potential 11. Altius image. 12. Source: http://en.wikipedia.org/wiki/Eye 13. Source: http://commons.wikimedia.org/wiki/File:Anatomy_of_the_Human_Ear.svg