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HMS Homeostasis II > Digestive Physiology and Malabsorption > Flashcards

Digestive Physiology and Malabsorption Flashcards

1
Q

Liver B12 storage

A

The liver stores ~1000x the daily intake/loss of B12

As such, unless stores are already depleted, or there is a deeper physiological problem with B12 transport, symptomatic B12 deficiency may not develop until months-years of insufficient intake and/or absorption have occurred.

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2
Q

Bile acid insufficiency malabsorption

A

This includes inadequate production or secretion, or premature intraluminal inactivation. Patients may have steatorrhea, and they will certainly have deficiency of fat-soluble vitamins such as E, D, A, and/or K

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3
Q

Control of bile secretion summary

A
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4
Q

Lingual lipases

A

Triacylglycerol lipases secreted by salivary glands, but of no use in the mouth! Their optimum pH is acidic (~4.5-5), which makes them perfect for the stomach. Like other human digestive lipases, they also require fat to be emulsified into micelles, so doubly useless in the mouth.

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5
Q

Vitamin D deficiency

A

Vitamin D deficiency can cause nutritional rickets and osteopenia

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6
Q

Peptidomimetic Drugs

A

It is well recognized that many drugs are absorbed successfully because of transport through PepT1.

This includes beta-lactam antibiotics, angiotensin-converting enzyme inhibitors, and sartans.

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7
Q

Inulin

A

Fiber found in many plants, and a common dietary supplement.

Contains many bonds between monomers that human enzymes do not recognize. Considered fermentable and water soluble.

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8
Q

Digestion of proteins diagram

A
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9
Q

Critical micellular concentration

A

Concentration above which bile salts are able to form tiny micelles.

Below this concentration, lamellar vesicle production remains largely intact, adequate absorption is only possible for molecules with some degree of water solubility, and so cholesterol, vitamin E, and other fat-soluble vitamins will remain locked within the lamellar body, inaccessible.

Triglyceride absorption, in this case, will only be moderately impeded due to the loss of surface area. Thus, even with biliary obstruction, 50-70% triglyceride absorption is possible in an otherwise normal intestinal tract.

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10
Q

Diagnosing exocrine pancreatic insufficiency

A
  • Symptoms of malabsorption
  • Fecal elastase test (effective b/c enzyme is resistant to degratation)
  • Direct sampling of pancreatic secretions (technically involved, expensive, invasive)
  • Upper endoscopy fluid sampling and biopsy
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11
Q

Celiac disease

A
  • Autoimmune enteropathy
  • Caused by the ingestion of gluten containing grains (wheat, rye, & barley)
  • Characterized by gastrointestinal complaints (diarrhea, constipation, abdominal pain), malabsorption, and a variety of symptoms outside of the intestine
  • GI symptoms worst in pediatric group, may cause failure to thrive
  • Commonly present with nutritional deficiency, including iron, B12, or vitamin D
  • Primarily affects the duodenum and proximal jejunum
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12
Q

Lactose breath hydrogen test

A

Used to diagnose lactose intolerance.

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13
Q

Gastric malabsorption

A

Surgical or inflammatory disease might cause malabsorption of iron, B12

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14
Q

Histopathology of Celiac’s (the Marsh criteria)

A
  1. Increase in intraepithelial lymphocytes (IEL) with normal villi
  2. Increase in IEL’s, crypt hyperplasia, and normal villi
  3. Increase in IEL’s, crypt hyperplasia, villous blunting
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15
Q

Lactulose-mannitol assay for barrier permeability

A
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16
Q

Collateral lymphatic drainage in the gut

A

Over time, when gut lymphatic drainage and fat absorption are poor, new collateral lymphatic vessels will form de novo in order to reconnect the gut to the systemic lymphatics.

This is part of what makes gut transplants feasible. Otherwise, those with gut transplants would have permanent long-chain fatty acid and fat-soluble vitamin malabsorption.

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17
Q

Breathing test

A
  • Non-invasive way of assessing digestive function
  • The patient ingests a nutrient that should be absorbed completely in the small intestine, resulting in no change in the composition of exhaled gases.
  • However, if one malabsorbs the ingested nutrient, the nutrient can enter the colon and be fermented. Carbohydrate fermentation results in hydrogen gas production, with diffuses into the blood and is exhaled in the breath. The hydrogen can be detected quantitatively over time.
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18
Q

Bile salt reabsorption

A

The majority of bile salts are reabsorbed via sodium-coupled carrier-mediated uptake by ileal absorptive cells, and then return to the liver via the mesenteric-portal venous system.

A very small amount of bile salt (~700mg) enters the colon each day, some of which is deconjugated and absorbed passively (~200mg), while most (~500mg) is lost in the feces.

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19
Q

What happens when a banana ripens?

A

Starch in the banana is broken down into simpler sugars. This is why it tastes sweeter when ripe!

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20
Q

Adequate intake of dietary fiber is associated with reduced risk for. . .

A
  • Heart disease
  • stroke
  • certain GI conditions
  • obesity
  • constipation
  • type II diabetes
  • certain cancers
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21
Q

Intra-luminal lipases (reference only, not tested)

A
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22
Q

Pepsin’s cleavage

A

Fairly minimal. Pepsin cleaves at bulky, nonpolar residues, which tend to be relatively scarce in proteins. So it leaves behind lots of large peptides and undigested whole proteins.

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23
Q

Basic dietary carbohydrate terminology

A
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24
Q

Glucoamylase

A

α1,4 short glucose molecules ⇒ glucose monomers

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25
Q

Bile acid summary figure

A
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26
Q

Vitamin A deficiency

A

Vitamin A deficiency can cause night blindness, dry eye, and is a leading cause of preventable blindness worldwide.

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27
Q

Human enzymes cannot cleave ___, explaining ___.

A

Human enzymes cannot cleave β-glycosidic bonds, explaining the caloric unavailability of soluble fibers

28
Q

Multilamellar vesicles

A

Closed, layered spherical liposomes. In the gut these are produced by micelle digestion and contain the products of triacylglyceride digestion – largely fatty acids and monoglycerides, as well as cholesterol, lysolecithin and fat-soluble vitamins.

In the presence of bile salts at or above the CMC, these will further break down into smaller, unilamellar mixed micelles.

29
Q

Taurochenodeoxycholic acid

A

A ‘conjugated’ bile acid. Conjugated to taurine (2-aminoethanesulfonic acid). Notice that the sulfonic acid moity renders the molecule more polar at that end, and thus the molecule becomes amphipathic due to its hydrophobic sterol.

30
Q

Pancreatic lipase

A

Works at the surface of emulsified lipid droplets. Requires colipase to function when in a bile acid-rich environment. Bile acid would normally displace pancreatic lipase due to its higher affinity, but colipase helps anchor it even when bile acids are around.

31
Q

Peptide transport

A

Coupled to H+ for efficient uptake into enterocytes via specific transporters. The proton gradient is set up by apical sodium-hydrogen exchangers (NHEs), driven by the basolateral Na+/K+ ATPase.

Di- and tri-peptide absorption via this mechanism is difficult to saturate, making nutritional supplementation with peptides rather than whole proteins much more efficient (due to rate limitation).

Peptides are degraded in the cytosol to single AAs by various peptidases.

32
Q

Absorbing simple, digested lipids at the brush border

A

When the micelle comes close to the enterocyte apical membrane, these molecules can passively diffuse across the apical plasma membrane of the enterocyte.

Once inside the cell, monoacylglycerides and fatty acids are re-packaged into triacylglycerides, then those triacylglycerides are wrapped up by apolipoproteins in a chylomicron and sent off into the lacteals and the lymphatic system.

33
Q

Why do micelles form more easily in the duodenum than in the stomach?

A

Because of the pH! In the stomach, many fatty acids are relatively close to their pKa. But, once they reach the duodenum and the bicarbonate-rich pancreatic juices neutralize that acid, almost every monoacylglyceride will be deprotonated, making them nice and polar for micelle formation.

34
Q

Isomaltase

A

oligo-glucose with α 1,4 and 1,6 bonding ⇒ glucose monomers

35
Q

Types of small intestine malabsorption

A
  • Dysmotility
  • Anatomical anomaly
  • Inflammation
  • Ischemia
  • Infiltration
  • Enterocyte structural problem
36
Q

Terminal carbohydrate digestion

A
37
Q

Vitamin E deficiency

A

Vitamin E deficiency may present with muscle weakness and absent reflexes, hemolytic anemia, and visual impairment

38
Q

Pancreatic amylase cannot split ___, which results in ___.

A

Pancreatic amylase cannot split 1,6 glycosidic linkages, which results in the production of alpha-limit dextrins

39
Q

Amino acid transport

A

Utilizes a variety of apical transporters, specialized for the wide variety of amino acid structures. This system is also highly redundant – most amino acids can be transited by more than one transporter. All of these utilize either Na+ or H+ cotransport to provide the energy required for absorption.

Many of these transporters are also expressed in the proximal convoluted tubule of the nephron.

40
Q

SGLT1

A

Apical membrane Na+ coupled glucose transporter.

Uses secondary active transport to drive the uphill transport of glucose and galactose from lumen into the cytosol.

High affinity and low capacity transporter (high transporter binding relative to concentration, relatively lower rate of transport across the epithelium).

41
Q

Cholic acid

A

An ‘unconjugated’ bile acid

42
Q

Pancreatic and salivary amylases cleave. . .

A

α1,4 glucoside linkages except at either end of the chain, thereby digesting starch into maltotriose and maltose molecules.

43
Q

GLUT2

A

Basolateral membrane transporter of fructose, glucose, and galactose.

Uses facilitated diffusion

44
Q

Pancreatic malabsorption

A

Exocrine pancreatic insufficiency results in maldigestion, or, suboptimal action of pancreatic enzymes on food. Almost always there is steatorrhea, and fat soluble vitamin deficiency is common

45
Q

Proteases secreted by the pancreas include. . .

A
  • Trypsinogen
  • Chymotrypsinogen
  • Proelastase
  • Procarboxypeptidase A and B
46
Q

What kinds of fats do we see in our diet?

A
  • Mostly long, even-chain triacylglycerides (>14 carbons/branch, so palmitate or longer)
  • Cholesterol and cholesteryl esters
  • Fat-soluble vitamins (A, E, K, D)
  • Phospholipids
  • Plant sterols (seen in diet, but poorly absorbed)
47
Q

Gastric lipolysis

A

A combined effort of gastric lipases, lingual lipases, and the churning of the gastric antrum.

Accounts for ~30% of fat digestion, however this phase is especially important because it frees the more polar monoacylglycerides, which make the fat emulsify better by the time it reaches the duodenum (they contribute to the critical micellular concentration). This also frees up monoacylglycerides to stimulate CCK release, a prerequisite for pancreatic lipase activity.

Gastric and lingual lipases are denatured once they reach the neutral pH duodenal environment.

48
Q

Absorption of medium-chain fatty acids

A

Rely less on the micellular absorption mechanism than long-chain fatty acids do, and are more rapidly cleaved free by gastric and lingual lipases. Once freed, they will readily be taken up by the intestinal mucosa, and some are even absorbed in the gastric mucosa.

So, when pancreatic activity is low or when bile salts are below the CMC, medium-chain fatty acids will be preferrentially absorbed over long-chain.

Also, rather than being packed into apolipoproteins, medium-chain fatty acids will traverse the epithelium paracellularly and go directly to the portal system where they bind to albumin.

49
Q

Diagnosing malabsorption

A

Blood tests, stool analysis, and biopsies are the pillars.

Usually the first step is to send fecal elastase, as a marker for pancreatic enzyme secretion and function. An imaging study or ultrasound may be performed to assess for an anatomical issue. Then, an endoscopy may be performed to evaluate the mucosal structure, possibly with a biopsy.

From here more specialized tests may be performed.

50
Q

Lymphatic malabsorption

A

Imagine if intestinal lymph did not have a normal pathway out of the intestinal lymph channels? Proteins, fat, fat-soluble vitamins would be lost into the stool, resulting in hypoalbuminema and hypoproteinemia, and vitamin deficiencies.

This can occur when lymphatics get obstructed by cancers, or one is born with or develops malformations of mucosal lymphatics, as with a condition called intestinal lymphangiectasia

51
Q

Micelle to enterocyte

A
52
Q

What’s absorbed where?

A
53
Q

Chylothorax

A

Occurs when there is trauma to the cisterna chyli which spills chyle into the thorax, resulting in an effective pleural effusion.

54
Q

Categorization of fibers

A

Fibers are meaningfully categorized by their viscosity and fermentability.

Viscosity impacts or reflects the fiber’s impact on stool bulk and compaction. However, it depends on many features, such as the milieu the fiber is in and the position and hydration status within the GI tract.

Fermentability indicates the property of a fiber to be transformed by colonic bacteria into short-chain fatty acids (SCFAs), which may be utilized by colonocytes as fuel or otherwise metabolized. However, of course, this depends upon the patient’s specific microbiome.

55
Q

Exocrine pancreas insufficiency

A

May have a wide array of causes. Manifestations include weight loss from inability to absorb adequate calories, steatorrhea from malabsorbed fat, abdominal discomfort from fermentation of undigested nutrients causing gas production and bloating, and symptoms or signs of fat soluble vitamin deficiencies

56
Q

Forms of complex carbohydrate

A
57
Q

Treating pancreatic enzyme insufficiency

A
  • Pancreatic enzyme replacement therapy (PERT!)
  • And vitamin supplementation
  • PERT enzymes are extracted and purified from porcine pancreas, put into a acid-resistant, base-labile pill capsule
  • In pediatrics, enzyme capsules can be opened into a small amount of pureed food and given on a spoon since infants and small children can’t swallow capsules
    *
58
Q

Diagnosing Celiac disease

A
  • History
  • IgA anti-tissue transglutaminase titer in serum has sensitivity of 90-100% and specificity of 95-100%
  • Intestinal biopsy is gold standard
59
Q

Wheat dextrin

A

Type of fiber. A commercial byproduct of wheat starch processing, contains high quantities of bonds not recognized by human enzymes. Considered fermentable and water soluble. In fiber supplements like Benefiber.

60
Q

Vitamin K deficiency

A

Vitamin K deficiency can present with bleeding and elevated INR (inability to synthesize clotting factors)

61
Q

Sacrosidase

A

Commercially available yeast-derived enzyme with sucrase activity.

It has been marketed to help the rare infant with a disorder called congenital sucrase-isomaltase deficiency (CSID), which presents with diarrhea, dehydration, and bad diaper rashes in infants when weaned from formula/breast milk to table foods

62
Q

GLUT 5

A

Apical membrane fructose transporter.

Uses facilitated diffusion. Transport capacity limited by lower affinity, lower expression in children, and by reliance on concentration gradient only. Thought to explain why fructose can cause diarrhea in infants, and sometimes in adults, when consumed in excess.

63
Q

Fiber

A

Carbohydrate that is not completely digested or absorbed in the small intestine but that may be fermented in the large intestine.

Common examples are non-digestable polysaccharides like cellulose and pectin, as well as lignins (polymers that gives plants physical strength). Both groups here are primarily found in plant matter.

64
Q

Treating chylothorax

A
  • Important to note that chyle only accumulates when the patient eats foods that promote chylomicron production
  • So, changing diet to favor medium-chain TAGs over long-chain will bypass this, as medium-chain TAGs are absorbed paracellularly and utilize blood albumin as a transporter rather than chylomicrons
  • Diagnosed by thoracentesis and measurement of TAG and cholesterol. TAG>110 in fluid is diagnostic
  • Another important note for treatment: Essential fatty acids (linoleic acid and linolenic acid) are long-chain, so there is high risk for development of essentially fatty acid deficiency on a medium-chain diet.
65
Q

Long-chain vs medium-chain fatty acid absorption

A
66
Q

Signs of malabsorption

A

Two major clusters of signs which may or may not occur together.

Gassy, burning, liquid stool suggests fermentation of malabsorbed carbohydrate

Frothy, pale, greasy, oily, difficult to flush stool suggests lack of fat absorption (aka steatorrhea)

67
Q

Disaccharidases

A

sucrase (sucrose ⇒ glucose + fructose), lactase (lactose ⇒ glucose + galactose)

HMS Homeostasis II (35 decks)

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