Anatomy Test #4 Essays
6. A) For each of the 3 primary macromolecules (carbohydrate, lipid, protein) tell 2 enzymes/chemicals that digest each one. B) State the location of release for each enzyme/chemical above and where its site of action is. C) Then for the stomach, small intestines, and large intestines describe the major digestive and absorptive processes occuring in each one (be brief). No need to write in paragraphs but be complete with your answers. (12 pts)
A) Carbs-Pancreatic amylase and salivary amylase Lipid-pancreatic lipase and bile Protein-gastric pepsin and trypsin B) Pancreatic amylase is released from the pancreas. It site of action is primarily the small intestine. Add in salivary amylase. Salivary amylase released from the salivary glands in the mouth and its site of action is the mouth. Lipase is released from pancreas (most of it) and stomach (little of it). Its site of action is in the SI. Bile is released from liver and the gallbladder (made in liver). Its site of action is in the SI. Pepsin is released from the stomach. Its site of action is in the stomach. Trypsin is released from the pancreas. Its site of action is in the SI (duodenum). C) Stomach- mechanical digestion is completed in the stomach, denaturation of proteins, enzymatic digestion of protein by pepsin, secretes intrinsic factor needed for B12 absorption Small intestines- Brunner's glands secrete alkaline mucus to neutralize acidic chyme, peristalsis moves meal remains, bacteria, and debris to large intestines, segmentation moves the chyme through the SI to come into contact with the microvilli and villi to be absorbed small intestine first and primary place of nutrient absorption. Large intestines- minimal absorption of nutrients and maximum water, vitamins, and electrolytes, pushes feces towards anus through gastrocolic reflex
5. Describe the neural and hormonal mechanisms that stimulate and inhibit the release of gastric juice. You can divide your discussion into A) The control at the cephalic phase B) The control at the gastric phase C) The control at the intestinal phase. (11 pts)
A) Directed by CNS. Neural mechanisms of the cephalic phase are parasympathetic stimulation by vagus nerve due to sight, smell, taste, or thought of food. Hormonal mechanisms of the cephalic phase are when CNS stimulates the submucosal plexus through sensing food. The activation of submucosal plexus stimulates mucous cells (secrete mucus), chief cells (secrete pepsinogen), parietal cells (secrete HCl), and G cells (secrete gastrin). Increases gastric juice secretion up to 500 mL/hr. B) Neural mechanisms are when distension and swelling of the stomach occurs after eating which stimulates stretch receptors and elevated pH stimulates chemoreceptors. Both receptors activate the myenteric plexus. The submucosal plexus is stimulated by the CNS due to sensing of food. Myenteric plexus stimulates mixing waves (peristalsis) to help turn the bolus into chyme. Submucosal plexus stimulates mucous cells (secrete mucus), chief cells (secrete pepsinogen), parietal cells (secrete HCl), and G cells (break down partially digested peptides). Hormonal mechanisms are when gastrin secretes hormones that travel in the bloodstream to help stimulate the mixing waves and chief and parietal cells. C) Neural mechanisms involve the enterogastric reflex, which is a feedback loop from the small intestine to the stomach decreases gastrin production and contractions and closes the pyloric sphincter to slow the release of chyme into the duodenum. This occurs by the duodenal stretch and chemoreceptors inhibiting myenteric plexus. Hormonal mechanisms involve the presence of lipids and carbs in the chyme stimulating the release of CCK and GIP. The decreased pH also stimulates the release of secretin. All of these hormones travel through the bloodstream and inhibit chief cells and parietal cells from releasing gastric juices and inhibit peristalsis.
4. A) Name the parts of the glomerular filtration barrier. B) Discuss how each part participates in the filtration of solutes and what each part retains. (6 pts)
A) Fenestrated endothelium (tunica intima) of glomerular capillaries, fused basal laminae (basement membrane), visceral membrane capsule (filtration slits between the pedicles of the podocytes). B) Fenestrated endothelium-least selective part of filtration barrier, filters glucose, amino acids, electrolytes, gases, ions, but retains RBCs or WBCs Fused basal laminae- "mediumly" selective, filters small proteins, but retains large proteins negatively charged which is why it repells proteins from passing through Filtration slits- most selective, retains small proteins because of the smaller pores.. size barrier
3. A) Name and define the three processes involved in the production of urine. B) Give the major nephron structures involved in each process. (6 pts)
A) Filtration-everything gets filtered except for WBCs, RBCs, and large protein molecules, Filtering of the blood. Reabsorption- what we want to keep gets put back into bloodstream through peritubular capillaries Secretion- addition of materials to filtrate that didn't get filtered, metabolites, drugs, wastes, hydrogen and bicarbonate B) Filtration- glomerulus in renal corpuscle Reabsorption-proximal convoluted tubule Secretion-distal convoluted tubule
8. Ellen, a 47 year old woman has had high blood pressure for many years. Recently she has been diagnosed with proteinuria. A) Explain how high blood pressure can cause proteinuria. Now her hands and feet have begun swelling. B) How could release of protein out of the glomerular capillaries be linked to swelling (edema) in the limbs? C) To explain this answer be sure to explain the four Starling forces and use them in your explanation. (10 pts)
A) If someone has hypertension (high blood pressure), then their HPg will increase to 60 mmHg which will make filtration barrier more permeable to large proteins are able to pass through thus allowing protein into the urine causing proteinuria. OPc has a value of 10 mmHg now due to presence of more proteins in capsular space and less in the corpuscle so HPc decreases down to 15 mmHg. So NFP can increase up to +40 (compared to normal +10) (NFP= (60 + 10) - (15 + 15) = +40). B) Because the NFP ultimately increased, the glomerulus capillaries are more leaky than usual due to release of large proteins. This will cause fluid to build up in the surrounding tissues and lead to swelling (edema). Starling forces Chapter 21 C) Glomerular hydrostatic pressure is the chief pressure; it's a pushing pressure that pushes water and solute molecules out of glomerulus into the filtrate in the capsular space (filtration). Normal GHP is 50 mmHg; its higher than the other Starling forces because the efferent arteriole is smaller in diameter than the afferent arteriole. Osmotic pressure of the capsular space-pulling force but usually there is no pulling force since there are usually no proteins in the capsular space due to their large size, involved in filtration. Normal OPcap is 0 mmHg Colloid osmotic pressure of glomerular blood- pulling force due to presence of plasma proteins inside glomerulus. Involved in reabsorption; normal OPglom is 25 mmHg Capsular hydrostatic pressure- pushing pressure due to filtrate backpressure in a small space with only one exit (the PCT); involved in reabsorption; normal HPcap is 15 mmHg.
7. A) Explain myogenic autoregulation including all appropriate structures. B) Explain tubuloglomerular feedback autoregulation including all appropriate structures. C) If blood pressure decreased, explain how either myogenic or TGF would bring it back to normal. (9 pts)
A) Myogenic autoregulation maintains a constant renal blood flow and glomerular filtration rate at varying arterial pressure through the constriction and dilation of the smooth muscles of the afferent arteriole to the glomerulus. if bp increases, constrict afferent arteriole. if bp decreases, dilate afferent arteriole. B) Tubuloglomerular feedback autoregulation is a flow-dependent mechanism directed by the macula densa cells (how fast filtrate moves through nephron) and senses changes in the juxtaglomerular apparatus. C) If BP decreased, the myogenic autoregulation will stimulate dilation of the afferent arteriole. Lack of stretch due to low BP will cause reflexive dilation of the arteriole. This will cause the hydrostatic pressure of the glomerulus to increase so net filtration pressure increases. All of this helps to maintain glomerular filtration rate even when BP decreases.
9. Your patient has just had surgery and lost a lot of blood. A) Briefly describe the renin-angiotensin system (RAS) and its role in blood pressure homeostasis. B) What are all the ways angiotensin II can increase blood pressure? C) Your patient is taking an ACE inhibitor, how would taking this medication affect the ability of their RAS to respond to the drop in bp? (7 pts)
A) RAS begins when there is a decrease in BP, which stimulates the granular cells of the juxtaglomerular apparatus of the kidney to release renin. And renin combines with angiotensinogen to create angiotensin I. Angiotensin converting enzyme converts angiotensin I into angiotensin II. RAS is the hormonal mechanism to maintain BP homeostasis. B) Angiotensin II stimulates the adrenal cortex to secrete aldosterone, which targets the kidney tubules and increases sodium and water reabsorption in the kidneys. This reabsorption increases blood volume. Angiotensin II stimulates increased ADH release from posterior pituitary, and this increases water reabsorption by the kidneys. This water absorption increases blood volume which increases BP. Angiotensin II also stimulates the thirst center in the hypothalamus, which makes people increase their water intake which again increases blood volume and BP. Angiotensin II causes arterial vasoconstriction which increases peripheral resistance and BP. C) If the patient took an ACE inhibitor, then angiotensin I wouldn't be converted to angiotensin II in RAS. Therefore, no vasoconstriction of the arteries, water or sodium reabsorption in the kidneys, or water intake would occur which mean no increase or effect on BP. Other ways person can increase blood pressure. Sympathetic nervous system short term controllers.
1. A) Name two reasons why it is necessary for the stomach to be so acidic. B) What hormone primarily regulates the production of acid? C) Name the three ways the stomach protects itself from digestion by the acid? (6 pts)
A) To break down and denature the proteins so they are easier to digest and absorb in the small intestines. The acidity also helps to kill bacteria and other microorganisms so they do not get into the intestines. B) Gastrin primarily regulates the production of HCl. C) 1. Layer of bicarbonate rich mucus that helps to neutralize the acid 2. Tight junctions between epithelial cells 3. Quick division of stem cells to replace epithelial cells damaged by the acid
2. Discuss bile including where it is produced, concentrated, what it is made of, it's recycling, and the stimulus for its release. (6 pts)
Bile is produced in the liver. Bile is concentrated in the gallbladder. Bile is made of bile salts (cholesterol derivatives that function in fat emulsification and absorption), bilirubin (byproduct of hemoglobin breakdown), and cholesterol, neutral fats, phospholipids, and electrolytes. Bile is recycled through the enterohepatic circulation (Bile salts -> duodenum -> reabsorbed from ileum -> hepatic portal blood -> liver -> secreted into bile). Its release is stimulated by cholecystokinin (CCK) from intestinal cells exposed to proteins and fat in chyme, and vagal stimulation (minor stimulus).
10. Describe how cortical and juxtamedullary nephrons are different. (You should have 1 structural and 1 functional difference). (4 pts)
Cortical nephrons Superficial have a short loop of Henle that barely penetrates renal medulla and juxtamedullary nephrons deep have a long loop of Henle that extends to the deepest region of renal medulla. Cortical nephrons function in most of the absorptive and secretory functions of the kidneys. Juxtamedullary nephrons function in producing concentrated urine.
11. Describe the structures and functions of the enteric nervous system. (4 pts)
Submucosal plexus-within the submucosa of GI lining and mainly controls glandular secretions (chief cells, parietal, mucous cells, etc.) Myenteric plexus-within the muscular external in the GI and controls the motility in the GI tract.
