Digestion & Absorption (mccabe) Flashcards

1
Q

which portion of the GI tract is responsible for absorbing majority of macronutrients?

A

proximal small intestine!!! (cuz the pancreatic enzymes enter here)

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2
Q

What are some key jobs of the duodenum/ early jejunum?

A

Secrete: CCK, secretin, disaccharidases (ie lactase)
Absorb: glucose (glucose transporters located here)

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3
Q

What are some key jobs of the ileum?

A

Re-absorb bile for re-cycling! (therefore Crohn’s have decrease bile absorption)

and

Absorb B12 attached to intrinsic factor

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4
Q

What are triglycerides?

A

a glycerol molecule w/ 3 attached fatty acids w/ varying number of carbons on them… if FA has > 12 carbons then it is defined as “long-chain”

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5
Q

How does long-chain fat digestion work?

A

in stomach: chief cells secrete gastric lipase which only removes one fatty acid chain resulting in diglycerides

in intestine:
*Acid in duodenum stimulates secretin (from S cells) from endocrine cell which 1) stimulates secretion of bicarb 2) moves pH in duodenum toward normal

Fatty acids in duodenum stimulate CCK (from I cells) which stimulates pancreatic enzymes, gallbladder contraction, causes relaxation of sphinter of oddi thus increase bile into the lumen!!!

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6
Q

How is pancreatic lipase different from gastric lipase?

A

It clips off 2 FA’s from the triglyceride!… free fatty acids and monoacylglycerides are readily absorbed

VS

gastric lipase which just clips off a single fatty acid (which is absorbed well) but the diacylglycerols are almost not absorbed at all

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7
Q

Explain bile synth and recycling

A

made in liver… excess is stored in gall bladder… used to help digest fatty acids… 95% is reabsorbed back into the ILEUM which sends it back to the liver

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8
Q

Explain fat absorption and the role of lipase, bile, and co-lipase

A

with fatty acid release lipase will bind the fat first, but then release of CCK will cause bile secretion… Bile has a much high affinity for fat than lipase, so it will bind fat and DISPLACE lipase… so co-lipase (not an ezyme just an anchor) stabilizes lipase on the fat so that lipase can bind to the bile salt-coated fat droplet –> “micelle” production which gets taken to the epithelial barrieri for FA’s can be absorbed… non of this would happen without bile!

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9
Q

How does bile help with absorption of fats?

A

Fats are lipids… which means they will be repelled by water… so when lipids approach intestinal epithelium they encounter an unstirred water layer which acts as a permeability layer… BUT when bile salts are bound around the fat (micelles)… it markedly increases the solubility of the lipids allowing them access to the epithelium

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10
Q

Explain chylomicron synthesis

A

absorbed fatty acids enter intestinal epithelial cells where they go to the golgi where they are packaged into vesicles that fuse with BM and get released into exrtracellular space (because too large to enter blood vesssels)… as a result they get absorbed into the lymphatics and THEN enter circulation… along the way they get modified with new apoproteins. As the chylomicron (fats w. apoproteins) get smaller and smaller it becomes a chylomicron remnant which is then absorbed by the liver and turned into LDL and VLDL

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11
Q

Name 6 ways medium chain fatty acids are different than long chain

A

1) more soluble
2) micelles are NOT needed
3) paracellular absorption is important
4) absorbed directly into portal blood (no need for chylomicron)
5) Taste way shittier than long-chain
6) # carbons = 6-12

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12
Q

What kind of diet should a patient with intestinal lymphatic problems be on/

A

one that avoids long-chain fats, and includes more medium chain fatty acids…

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13
Q

Why would a diet high in medium chain fatty acids be good for a patient with cystic fibrosis?

A

in CF you have reduced pancreatic bicarb secretion and reduced pancreatic enzyme secretion!!! Medium-chain fatty acids do not need pancreatic enzymes for absorption… vs long-chain which would stimulates CCK which would stimulate pancreatic enzymes to cleave off 2 fatty acids to allow for proper absorption…

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14
Q

How does pancreatitis cause steatorrhea?

A

If pt eats long-chain fatty acid foods then it will require pancreatic enzymes to be properly absorbed… but in the case of pancreatitis this will not happen… ONLY gastric lipase will be present creating very few FA’s and diacylglycerols which are must less readily absorbed so the excess “malabsorbed” fat goes out in the shit.

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15
Q

How would a bile problem/obstruction cause steatorrhea/malabsorption?

A

Recall that bile salts engulf the fat droplets to allow them to pass through the water barrier that sits over the epithelium… without it absorption will be significantly reduced!

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16
Q

Why would a person with Crohn’s be complaining of butt pee and parasthesias?

A

Recall that Crohn’s typically affects the ileum.. which is wear bile salts are re-absorbed and recycled back to the liver… so with either a ileal resection or chronic inflammation of the ileum… bile will be lost in the shit… the liver can make new bile but it is typically not enough to keep up with a fatty meal so again the fats would not be able to permeate the water barrier to reach the intestinal epithelium so they will be lost in the stool resulting in diarrhea….

Recall the ileum is also important for B12 absorption so without B12 some myelin starts to degenerate on sensory axons resulting in a feeling of numbness/tingling

17
Q

Why would a person wi crohn’s also maybe complain of back pain, night blindness, and bruising?

A

fat-soluble vitamins ADEK all require efficient absorption of fat to make it into the bloodstream… so again with ileal malfunction causing a decreased recycling of bile… there is less efficient fat absorption (liver cannot keep up with new bile synth)… so vitamins ADEK are lost in the shit
A def –> retinal rod malfunction (night blindness)
D def –> required for Calcium absorption in gut, without it it can cause secondary calcium deficiency leading to osteoporosis of lumbar vertebrae (so back pain)
K def –> required for synth of coag factors 9, 10, 7, 2… so without it, can cause easily bruising due to decreased clotting

18
Q

What is the diagnosis in a 30 year old woman w/ abdominal bloating, foul-smelling butt pee, and weight loss likely have?

A

Celiac sprue… immune reaction to gluten that causes chronic inflammation and blunting of villi in distal duodenum

19
Q

What are the breakdown products of lactose, maltose, sucrose?

A

lactose –> galactose + glucose (via lactase)
maltose –> glucose + glucose (via sucrase)
Sucrose –> fructose + glucose (via sucrase)

20
Q

How are monosaccharides absorbed? and what is the transporter?

A

Driving force for monosacc absorption is the Na+/K+ ATPase on the submucosa on enterocytes… it brings 2K+ in and pushes 3 Na+ out creating a concentration gradient for luminal Na+ to come in… and with it, it brings glucose or galactose via SGLT1 or fructose via GLUT 5 (both on luminal side)… once in cell, fructose, galactose, and glucose are transported via glut 2 on submucosal side to go into blood

21
Q

Why do you get butt pee & sharts with lactase deficiency?

A

being unable to breakdown lactose into galactose and glucose results in bacterial fermentation and gas distention and acts as an osmotic draw of water into the lumen –> butt pee + farts

22
Q

How does cholera cause rice water stools and how do you treat it?

A

enterotoxin that permanently activates Gs –> increased cAMP –> increased Cl- secretion so water follows it out…

Treatment = glucose with fluids because it co-transports with sodium

23
Q

How does amino acid transport differ from monosaccharide transport?

A

MANY different AA transporters vs just a few monosaccharide transporters

24
Q

What else is unique about AA transport?

A

That small peptides can also be transported!!! So it a kid with Hartnups disease (deficient neutral amino acid transporter) you can give them a high protein diet to force the peptides across!

25
Q

What happens to patients on total parenteral nutrition (TPN)?

A

1) gut hypotrophy
2) altered epithelial barrier function
3) altered microbiota
4) B12 deficient (no intrinsic factor so require parenteral B12 shots)

26
Q

Why would an elderly diabetic patient on omeprazole for GERD develop steatorrhea and macrocytic anemia w/ an intact ileum?

A

Despite an intact ileum… the patient still has B12 deficiency because both the diabetes and PPI make an environment for bacterial overgrowth which will use up the B12.

27
Q

What are the steps from dietary ingestion of B12 to absorption in ileum?

A

1) B12 is released from food by gastric pepsin
2) free cobalamin then binds gastric R to form a complex in the stomach
3) Parietal cells secrete intrinsic factor in stomach, but B12 stays bound to Gastric R
4) In the duodenum, pancreatic protease cleaves cobalamin free, THEN it binds to intrinsic factor which is resistant to pancreatic protease
5) the cobalamin-IF complex binds in the distal ileum for absorption
* note stored cobalamin in the liver can meet demands for several years prior to deficiency –> megaloblastic anemia

28
Q

What are some conditions that can cause B12 deficiency?

A

1) achlorhydria - due to pepsin deficiency or gastrectomy
2) pancreatic protease def - via chronic pancreatitis
3) intrinsic factor deficiency - antibodies against parietal cells in the stomach –> pernicious anemia
4) crohns –> ileum malabsorption
5) diabetes/PPIs –> bacterial overgrowth (use it up)