Goff Study Questions Flashcards

1
Q

Cations added to the blood cause the blood pH to change- in which direction. If a dog is exhibiting acidosis and blood bicarbonate is higher than normal, what kind of acidosis would this suggest was occurring (metabolic or respiratory)? If the kidneys are putting out urine with a pH of 5.3 would that be contributing to the acidosis or a compensatory mechanism in this dog? What if blood potassium was 8 mEq/L?

A

A. Adding cations will cause the blood to become more alkaline.
B. Respiratory acidosis – if the body was compensating using the respiratory system, bicarb would be lowered to promote respiratory alkalosis.
C. The urine would be compensatory because it is removing anions, reducing pH of the blood.
D. If the potassium is 8 mEq/L it is compensatory for the acidotic state.

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2
Q

Which sections of the GI tract are innervated by pelvic parasympathetic neurons?

A

The second half of the colon, the rectum, and the bladder.

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3
Q

It’s been a wet year. A horse is exhibiting severe drooling. You notice its hay has some red clover in it and is a bit moldy. What is going on? Give mechanism!!

A

The horse is exhibiting Slaframine Slobbers from the mold, Rhizoctonia leguminicola. The mold has parasympathomimetic effects. The horse can drool up to 10 gallons per day.

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4
Q

Anesthetics tend to depress the heart rate of dogs. If I give a dog atropine or glycopyrolate prior to induction of anesthesia would I increase or decrease the risk of saliva being aspirated during anesthesia? Cows salivate a lot!! If I was doing standing surgery in a cow under local anesthesia with Rompun (xylazine) a sedative that causes drooling (don’t worry about how Rompun does this- this year!!), could I give her atropine for the same reasons? Any health risks??

A

Atropine blocks muscarinic receptors on target tissues (salivary glands) which inhibits Ach, produced by postganglionic parasympathetic neurons, from binding to these receptors. This would decrease the risk of saliva being aspirated during anesthesia. It also increases the heart rate (blocked vagus signals). Additionally, a potential health risk could be that the cow would be unable to eructate causing bloat and death. The whole reflex is removed.

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5
Q

What is the purpose of the intercalated duct of a salivary gland? What do the ductal cells secrete? When and what stimulates them to secrete?

A

A. They form the duct leading from the acinus to the striated duct. They form part of the intralobular duct.
B. They secrete electrolytes.
C. Beginnings of digestion cause them to secrete to begin starch and fat digestion along with reducing osmolarity.
D. Note: the striated ducts were more focused on and they produce and alkaline solution to put into the saliva and buffer the stomach acid.

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6
Q

A rabbit comes into your office with wet matted hair on its chest and has maggots in the area around its anus. What is a likely cause of this and why???

A

Malocclusion and resultant spurs make the rabbit too uncomfortable to groom and cause slobbers. As a result, the rabbit becomes unclean and has a wet chest. Flies will use this as an opportunity to lay eggs, and the condition is called Flystrike.

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7
Q

Why do old horses need their teeth floated? What are the repercussions of not having good teeth to the horse? Why do a horse’s molars stay sharp on the occlusal surface? How come your dog’s molars don’t?

A

Horse teeth are constantly erupting through the gum line and the equine upper arcade is more laterally extending than the lower arcade. This results in the development of labial and buccal sharp points, which cause the development of ulcers. If your horse does not have good teeth, they can lose weight drastically and may be unable to hold food in their mouth in addition to the painful ulcers. Behavior will also likely change, especially in response to a bit pressing against the ulcers. A dog will not experience this because of the difference in how the occlusal surfaces meet and how they chew – horses grind their food side to side while dogs only use their molars to break off chunks or crush food.

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8
Q

A cow spends 7-10 hrs a day chewing. How is it possible for the cow to accidentally ingest a piece of wire?? Why is the horse less likely to ingest a piece of wire?

A

Cows will eat as fast as possible, swallow, and regurgitate their food later. They’re not picky and will eat most anything. Horses spend all day browsing and will avoid toxic or inedible items in addition to chewing their food at the time of picking it up to eat.

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9
Q

Your client is having trouble pilling his cat. What does he need to do to ensure the cat swallows the pill? Explain the swallowing reflex! What could happen if I give oral liquids into the mouth (drench) of a cow with clinical hypocalcemia and weakness??

A

The client must push the pill to the back the pharynx where swallowing becomes an involuntary reflex. The pharynx senses using nerves V, IX, and X then responds with efferent VII, IX, X, and XII to initiate the reflex. The back of the tongue and floor of the mouth will elevate to drive the bolus back, and then the dorsal soft palate will elevate to close the nasopharynx. The hyoid will elevate, the epiglottis will move downward, and the laryngeal muscles will close the glottis. The upper esophageal sphincter will relax to allow the bolus into the esophagus and the vacuum within the esophagus will draw food in.
The oral liquids would take too long to absorb which is why IV calcium is needed to treat milk fever cows.

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10
Q

Explain the difference between intrinsic and extrinsic control of gut functions. Diagram a local reflex response to stretching of a segment of gut contained entirely within the Enteric nervous system.

A

Extrinsic control of the gut is done by the vagus – afferent signals must travel all the way to the medulla and parasympathetic efferent response occurs.
Intrinsic control is specific to the enteric nervous system. Afferent signals from chemoreceptors and stretch mechanoreceptors send signals to the submucosal and myenteric plexi, which the send efferent responses back which control secretion, peristalsis, and mixing movements.

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11
Q

What is the path of the vagus nerve? Are there any other sources of parasympathetic innervation to the GI tract? Where are cell bodies of pre and post-ganglionic fibers of the sympathetic and parasympathetic system affecting the stomach and intestines located?

A

Sympathetic: Spinal cord nerve cell bodies are in the section of T2 – L3. Axons come out of the spinal cord, to the sympathetic chain and then to ganglia. At the ganglia, the pre-ganglionic meets the post-ganglionic and acetylcholine is released to the nicotinic receptor. The post-ganglionic releases acetylcholine to nicotinic receptors.
Parasympathetic: Nerve bodies are found in the sacral spinal cord and medulla. The vagus nerve parasympathetic will travel from the medulla, traveling with the vagus into the thoracic cavity and then into the abdominal cavity through the esophageal hiatus.

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12
Q
  1. Where is the myenteric nerve plexus? Where is the submucosal nerve plexus.. Diagram a reflex response to stretching of a segment of gut that involves the autonomic nervous system plus the Enteric nervous system
A

The myenteric plexus is found between the circular and longitudinal muscle layers while the submucosal nerve plexus is found between the mucosa and circular layer.

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13
Q

Where are muscarinic receptors located, and what do they respond to? Where are nicotinic receptors located, and what do they respond to? Name an antagonist of the nicotinic and an antagonist of muscarinic receptors.

A

Muscarinic receptors are located in the target cells of the parasympathetic system.
Nicotinic receptors are located on both sympathetic and parasympathetic post-ganglionic nerve cell bodies.
They all recognize acetylcholine. An antagonist of muscarinic receptors is atropine and an antagonist of nicotinic receptors is curare.

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14
Q
  1. What do you think you might see in a horse that has broken out of its fenced area and gotten into seed corn coated with an organophosphate poison? WHY?
A

The horse will exhibit excessive drooling, diarrhea, constricted pupils, and other symptoms. This is because of an inability to break down Acetylcholine, causing an increase in parasympathetic stimulation. There is technically an increase in both parasympathetic and sympathetic responses, but the parasympathetic response dominates.

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15
Q
  1. What are borborygmi? Where can I best listen for them in the horse and what should they sound like – what frequency? What do I hear if there is intestinal stasis? What should you hear when you put your stethoscope in the left paralumbar fossa of a cow? How often?? Where do I put the stethoscope to hear the reticulum?
A

A. Borborygmi are rumbling sounds made by gas passing through the small intestine or colon. They’re really useful to listen to in the equine large intestine.
B. You should listen for loud booming gurglings of the colon and cecum that reach peak intensity every 15-20 seconds. Listen to them on the right flank.
C. In early stages of spasmodic colic, they become more crackly and loud. In stasis, the sounds quit. With blockages, you might hear a trickling sound of fluid dropping out of the ileocecal valve through empty space into the cecum.
D. In a cow, you should hear three mixing contractions every two minutes. It’s a gurgling sound coinciding with a slight lift to your hand in the flank and then followed by a second more pronounced lift of the flank and a booming sound of gas moving.
E. To hear the reticulum, listen to the lower left ribs.

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16
Q

Which enzymes are present in saliva? What do they do?

A

Salivary amylase – Starch digestion
Salivary lipase – Fat digestion
There are also lysozymes, water, and alkaline buffers in saliva. The alkaline buffers come from the striated duct cells.

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17
Q

What is the difference between segmental and peristaltic contractions of GI tract? What is the difference between a short (inches) and a long (feet) peristaltic contraction -ie in terms of how this is controlled?

A

Segmental type contractions of the GI tract result from the constriction of circular muscle close to the lumen, which divides the gut into dilated segments containing ingesta. The dilated and constricted segments swap, mixing and circulating the ingesta. This is largely stimulated by stretch.
Peristaltic contractions are a moving ring of luminal constriction preceded by areas of luminal distension. The area of constriction is created by contractions of circular muscle and areas of dilation are created by contraction of longitudinal muscle. Net action propels ingesta.
Long peristaltic contraction requires parasympathetic input from the vagus nerve while short contractions are a local reflex involving the enteric nervous system. Dogs and cats can evacuate their colon in one single constriction using the parasympathetic long peristaltic contraction.

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18
Q

Why and how does my stomach grumble when I am hungry? Where does contraction of the stomach begin? What factors determine speed and strengthen stomach contractions? What factors diminish them? What determines the fastest rate at which the stomach can contract?

A

A. Your stomach is grumbling because it is constantly contracting and mixing the contents in it. It is louder when you are hungry because it is less muffled by contents. Additionally, higher centers in the brain in response to sight, smell, or taste of food can initiate vagal parasympathetic stimulation of stomach contractility.
B. Contraction of the stomach begins mid-fundus. Distension of the fundus activate the stretch receptors, causing the activation of peristaltic contractions beginning mid-fundus and moving toward the pylorus. As peristaltic waves reach the pylorus, a small amount of chime is expelled into the duodenum.
C. Gastrin stimulates stomach motility along with vagal parasympathetic stimulation. Emptying is spurred by increased vagal tone in response to increased distension pressure in the stomach. Emptying is slowed by decreased vagal tone, Cholecystokinin (fat enters duodenum), and Secretin (pH drops in duodenum).
D. Contraction and relaxation of the pyloric sphincter determines the rate of emptying of the stomach

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19
Q

You get a call one evening just as you open a beer after supper. “My dog just ate a bottle of grape flavored children’s Tylenol!” Its 30 min to your clinic and this appears to be a lethal dose of Tylenol. What would you advise?

A

Give the dog a dose of hydrogen peroxide or salt to induce vomiting.

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20
Q

Why can’t a rat vomit? Why can’t a horse vomit? Can a goat “vomit” and what is a likely cause?

A

A rat can’t vomit because it doesn’t have a vomiting center in the medulla. It can’t coordinate diaphragm muscles and contraction of the stomach to develop pressure to overcome the lower esophageal sphincter. Horses can’t vomit either because the lower esophageal sphincter is too tight or because the esophagus is in a position where it is kinked shut when the horse stomach bloats.
No, technically goats cannot vomit because vomit must come from the glandular part of the stomach. Rarely, goats can move material from their abomasum to their omasum, but it is not considered a true vomit.

21
Q

Would dry kibbles or canned wet diet be best for a dog with mega-esophagus? What about a dog with a cleft palate??

A

For a dog with mega-esophagus, a diet of moist food would be best because it has to slide down the esophagus due to a lack of coordinated peristalsis. For a dog with a cleft palate, they should be feed dry kibble as it is less likely to get into the opening.

22
Q

Why do high fat diets hang out in the pig’s stomach longer than high starch diets? Is this true for ruminants too?

A

High fat diets must be aided in absorption through emulsification and then breakdown by bile salts, co-lipase, and lipase into mono and di-glycerides. They are then packaged into micelles and from there, are able to be absorbed by the stomach as the attached bile salts have both hydrophilic and hydrophobic ends. This takes longer than starches to break down.
This is not true for ruminants? Unsure of this answer, but from the next lecture, it looks like they efficiently take up fat to form adipose and milk fat and cannot exceed diets of 7% fat, especially in unsaturated forms, because of danger to CHO degrading bacteria and possibility of bio-hydrogenation of fat into toxic compounds.

23
Q

What factors stimulate upper small intestine motility? What inhibits it?

A

Stimulate: Gastrin, CCK, enteric nervous system(segmental), vagal coordination (peristaltic)
- Inhibit: Secretin, severe distension, glucagon, and epinephrine

24
Q

It’s late September in Iowa as you look out over an alfalfa field about knee high with six dead beef cows in it. They had been out there grazing less than a week. The survivors all seem to be in good flesh, but you notice another 5-6 that are breathing hard and look a little funny – puffed out on one side-from behind. Which side is likely puffed out?? What could be the cause and why can’t they perform this normal function?? What could you do??

A

The cows developed frothy bloat, the most common type in ruminants, from consumption of the legume hay (saponins caused thick froth development). In order to eructate, the lower esophageal sphincter must open but when froth is present, it will not open. As a result, the cows could not remove gas from the rumen through eructation and the diaphragm could not contract against the pressure of the rumen. The left side would be distended. You could pass a tube, give antifoaming agents, or place a trochar or cannula. You should probably take the cattle off of the pasture.

25
Q

What factors affect movement of ingesta from ileum to cecum or colon??

A

Distension of the ileum and gastrin relax the ileococlic sphincter to move ingesta forward while distension of the colon or cecum causes the sphincter to constrict and slow motility.

26
Q

Why are rabbit feces pelleted and cow feces are not??

A

Rabbits, like horses, are hindgut fermenters and have haustrations in their descending colon to hold fecal material longer to extract more water. As a result, a dry fecal ball is produced instead of the loose, wet feces of the cow, which has a less developed hindgut.

27
Q

A horse gets into a sack of corn and has eaten half. Now it is sweating and rolling on the ground. Explain the symptoms and unique aspect of a horse that contributes to the cause and what you can do about it. What if you do nothing?

A

The horse is experiencing colic because its stomach is not able to expand as a carnivore’s could. To treat this, you can tube the horse and it will likely reflux (they can’t vomit on their own, but this overcomes the physiologic barrier of the LES). If you leave it, the horse may rupture its stomach using abdominal contractions.

28
Q

A horse with sharp points to its molars is at increased risk of colic. Why? Where would the problems occur? Can you treat any of them from the back end of the horse (rectally)?

A

When a horse has sharp points on its molars, it will not want to chew as much and will swallow larger chunks. You would see problems in the pelvic flexure, transverse colon, and cecocolic junction. In cases of impaction closer to the rectum I think you could provide some relief with an enema, but further up issues wouldn’t be treatable rectally.

29
Q

What are the consequences of prolonged vomiting in a cat?

A

Prolonged vomiting in any animal can cause a depletion of chloride, dehydration, and a loss in nutrients. This is especially problematic in cats, as they tend to be more dehydrated as it is and could cause significant problems in tom cats, who are predisposed to urethral blockages.

30
Q

A H.B.C. cat whose pelvis was repaired by you now seems to go many days without a bowel movement. What might you see on x-ray? Why in physiological detail might the cat be in this predicament? Could an HBC cat have continuous bowel movement (or inability to control when it defecated?). What is affected in this situation.

A

The cat likely has disruption of the sacral spinal nerves, resulting in megacolon. As a result, you would see a buildup of feces in the colon and the cat would not be able to control its defection.

31
Q

When I put a stethoscope onto the right paralumbar fossa of a cow and listen, which kinds of contractions am I hearing (mostly) and how often should I hear them?

A

You can hear intestinal and cecal contractions but it’s hard to distinguish them. If you listen on the left instead, you can hear mixing contractions 3 times per 2 minutes. 1 time per minute you likely can hear eructation contractions.

32
Q

Why doesn’t milk go into the rumen in a young lamb that is suckling?

A

The lamb (and calf) have a rumenoreticular (gastric) groove that allows milk to bypass the rumen and go into the abomasum. Esophagus –> reticulo-omasal orifice –> abomasum

33
Q

What should I offer the neonatal ruminant to eat if I wish to stimulate rumen papillae development?

A

You should offer starter grain, as rumen development is dependent upon butyrate from the fermentation of grains.

34
Q

I feed my dog mashed potatoes (no butter). What is the fate of this foodstuff (bulk of it) ie how is it digested ? Would it have been different in my horse? What about my goat? What form (biochem) is the potato starch in when it is absorbed? What is the fate of this material when it reaches the portal vein? How is the energy stored? Where is it stored? How is this controlled (endocrinology!!)?

A

Salivary amylase will begin the breakdown of the starch and pancreatic amylase will occur during the luminal phase of digestion. As a result, the starch will be broken down into disaccharide maltose and trisaccharides along with 1-6 linked branch points. The reduced forms will then be absorbed at the brush border. Horses function the same as monogastrics do with starch digestion, but ruminants have amylolytic bacteria that produce amylase and convert starch to glucose.
When the digested forms of the starch reach the liver, they are converted there under the control of insulin (released by the pancreas) and become glycogen to be stored in adipose tissue and muscle.

35
Q

I feed my dog a piece of lean soy hamburger. What is the fate of this foodstuff? How is it digested? Would it have been different in my horse? What about my goat?

A

When the dog eats the burger, it reaches the stomach and HCl begins to partially hydrolyze some of the peptide bonds. It also cleaves inactive pepsinogen secreted by chief cells to make pepsin, which cleaves peptide bonds that are next to hydrophobic amino acids with aromatic side chains. Rennin, produced by chief cells as well, will cleave between phenylalanine and methionine. After, the protein will enter the small intestine for the lumenal phase of protein digestion where enteroendocrine cells are activated to secrete CCK into the blood which will increase pancreatic enzyme secretion and release of enteropeptidase by nearby epithelial cells (paracrine action). The enteropeptidase cleaves trypsinogen from the pancreas into trypsin which will activate other proteolytic enzymes.
To cross the apical membrane, the protein (primarily Lysine) will follow the basic amino acid pathway which uses secondary active transport via facilitated carriers that harness the energy from sodium moving down its gradient to move the amino acids into the cytosol. At the basal membrane, a protein aids in facilitated diffusion of the amino acid into the portal blood stream. The horse is similar, but there is evidence that they do also get some amino acids from their hindgut bacteria.
In ruminants, a great deal of the protein would be broken down and used by the bacteria that exist in it, but they eventually die and are used by the ruminant as a protein source. Some protein will not be digested by bacteria and is called Rumen Undegradable Protein (RUP). Both microbial protein and RUP are utilized by the ruminant in the small intestine.

36
Q

The stomach makes a very strong acid and very potent proteolytic enzymes. What prevents the stomach acid from burning holes (ulcers) thru the stomach wall?

A

The stomach contains goblet cells which secrete protective mucous; and prostaglandins E1 & 2 and I2 increase mucous porudction in addition to decreasing histamine mediated acid secretion and gastrin secretion. It also increases blood flow to renew and repair cells. Duodenal hormones like Secretin also function to increase alkaline secretions from the salivary glands, pancreas, and Brunner’s glands (the last two serve to protect the small intestine more).

37
Q

A farmer baled up a piece of barbed wire fence with his hay. Within weeks of feeding this hay to the cows, several cows are “off-feed” and have a fever. What could have happened? What could you learn with your stethoscope?

A

The cows may have consumed the wire, leading to “hardware” disease which could result in piercing through the reticulum and peritonitis (the density of the wire will push it forward into the reticulum). If it pierces through the diaphragm, it could cause pleuritis or further on it could cause pericarditis. You could auscultate on the left side and there would be less reticular and ruminal contractions. There should be 3 contractions every two minutes.

38
Q

Displacement of the abomasum rarely occurs in mid-late lactation cows. Why?

A

Anatomical: Pregnancy pushes the abomasum into one location and there is less free space. When they calve, they suddenly have a great deal of open space to shift around. The fundic area of the abomasum had been pushed out of place. LDA are more common.
Physiological: there are less issues with hypocalcemia and loss of the ruminal raft. Feeding high grain diets around the time of calving also increases the likelihood of a displaced abomasum. Abomasal atony prevents gas expulsion leading to distension and displacement during during DA. Lack of contracting abilities from the hypocalcemia! The ruminal raft provides scratch factor which stimulates rumen motility and then the abomasum. If the rumen doesn’t contract, then the abomasum doesn’t contract either and it fills with gas.

39
Q

I add soy oil (triglycerides – about 50% saturated and 50% unsaturated) to my dog’s diet. What is the fate of the soy oil? Would it have been different in my horse? What about my goat?

A

Monogastrics: Emulsification and then breakdown by bile salts, co-lipase, and lipase into mono and di-glycerides. They are then packaged into micelles and from there, are able to be absorbed by the stomach as the attached bile salts have both hydrophilic and hydrophobic ends and the smaller fats are able to diffuse into the apical cell membrane. At the basal membrane, a Chylomicron will be formed and move to lacteals, then move to general circulation via the thoracic duct. During circulation, they bump into High Density Lipoproteins which trade Apolipoprotein C and E for triglycerides. The APO C can be used to find receptors in the body for fasts and APO E is used by the liver receptor to take up the chylomicron and repackage the cholesterol.
Horses function the same.
Ruminants must have less than 7% fat in their diet, especially unsaturated fat. Fats can be toxic to bacteria that degrade structural CHO and they will respond by bio-hydrogenating unsaturated fatty acids which will creat 10-trans and 12-cis conjugated linoleic acid, depressing milk fat and causing other health problems.

40
Q

A cow or horse is exhibiting melena, appears very dull, and has a PCV of 18. (Normal 30-35). Give me some “rule outs” that would explain the symptoms. What would you advise?

A

*Melena: black, tarry stool with a glistening sheet resulting from degradation of blood in the GI tract.
*Normal equine PCV: 32-52%
Patient is anorexic, usually my first thought is gastric ulcers especially with the presence of melena, indicating a problem that is higher up in the gastrointestinal tract (stomach or small intestine, often).
R/O: hepatic disease, gastric ulcers, internal abdominal abscess, cholangitis, granulomatous enteritis, internal parasites
Advise: Dx like CBC/Chem, fecal, gastroscopy

41
Q

A 9 year old Great Dane has been on a high dose of Rimadyl (carprofen) for 2 years for joint pain. Now he is anorexic, has melena, and is depressed. What could be going on?

A

More ulcers! NSAIDs block prostaglandin E2, leukotrienes, and pro-inflammatory thromboxanes but also block PGE1 and Prostaglandin I2, resulting in a drop of mucous production and an increase in stomach acid. Ulcers appear!

42
Q

How are fat soluble vitamins absorbed?

A

They join the micelle formed by bile salts. See above for answers on how micelles are formed and how fat is broken down.

43
Q

How are colostral antibodies absorbed across the gut of the newborn pig?

A

Specialized gut epithelium in the newborn pig will allow transfer of IgG through receptor-mediated endocytosis. Within 16 hours or shortly after the piglet’s first meal, the gut epithelium will shed and become “closed”.

44
Q

What is secretory IgA? How does it get to the gut lumen??

A

The secretory component of IgA gives it resistance to proteolysis. The secretory portion attaches to the J chain, they are taken up by the epithelium through endocytosis, and then part of it is cleaved so the sIgA is released into the lumen.

45
Q

Some pancreatic enzymes are secreted in an inactive form. Why and how are they activated? Why is a patent pancreatic duct important? What happens if it is blocked? Give me the whole biochemical mechanism!!

A

Enteroendocrine cells of the duodenum are activated to secrete CCK into the blood which will increase pancreatic enzyme secretion and release of enteropeptidase by nearby epithelial cells (paracrine action). The enteropeptidase cleaves trypsinogen from the pancreas into trypsin which will activate chymotrypsin, elastase, carboxypeptidase, RNAse, DNAse, and Active CoLipase to aid in digestion. Pancreatic hormones must stay inactivated until they reach duodenum or they’ll cause pancreatitis. Pancreatitis will result from activation of Pro-Phospholipase A within ducts because of blockage will result in the activation of Trypsinogen –> Trypsin in the pancreas and its own digestion.

46
Q

What are bile salts and how do they function? Do they end up in the feces?

A

Bile salts are a detergent that has both a hydrophobic and hydrophilic end. They function in degradation and transport of fats, fat soluble vitamins, and cholesterol from the lumen to the brush border. 5% of bile salts are excreted in feces while 95% reach the ileum and through active transport (via enterohepatic circulation to the portal system), are recycled back to the liver.

47
Q

How are glucose or amino acids absorbed across the brush border apical membrane? How are they absorbed across the basal membrane of small intestine cells so they can get into the blood? Can they be absorbed across the rumen wall? Can they be absorbed across the colon wall?

A

A. They are absorbed using proteins that utilize a sodium symporter as energy for secondary active transport into the epithelial cytosol.
B. Facilitated diffusion using a protein the basal membrane.
C. No? They’re absorbed across the small intestine, even in ruminants.
D. In hindgut fermenters there are bacteria which supply amino acids and there is evidence of amino acid transporters in the colon, but it’s unclear exactly how they function.

48
Q

What are the 2 phases of liver detoxification (elimination) of substances? Why does the hepatocyte often add sulfate or a glucuronic acid to the molecule it is trying to eliminate from the body?

A

Phase 1: Oxidation of the compound
Phase 2: Glucuronidation or sulfation to improve water solubility. Adding glucuronic acid or sulfate to the compound creates a more water-soluble molecule, which is excreted into canaliculi and converted to stercobilin by colon bacteria (or into urobilinogen by the kidney) to be excreted.

49
Q

Why would a bacterial infection of the gall bladder cause choleliths?

A

Hepatocytes conjugate bilirubin with glucoronic acid to form a more water soluble complex. Bacteria break glucuronide off of the bilirubin causing it to become unconjugated, which allows the formation of bilirubin stones. The bilirubin stones form when unconjugated bilirubin combines with cholesterol.