Biochem: Digestion/Absorption Flashcards Preview

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Flashcards in Biochem: Digestion/Absorption Deck (44)
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1
Q

What is the major type of digestion in the mouth?

A

Physical by chewing.

2
Q

What are chemical components of digestion in the mouth?

A

Lingual liapse: digests short/medium chained fatty acids; newborns + milk
Alpha-amylase: carbs

3
Q

Is there protein digestion in the mouth?

A

Nope

4
Q

Digestion in the Stomach

A

Short/medium FAs by gastric lipase
No digestion of carbs
Proteins: pepsin activated by HCl

5
Q

Mucus Cells

A

Produce protective enzymes and mucins.

6
Q

Parietal Cells

A

Secrete HCl & intrinsic factor.

Also secrete bicarb into the blood via Cl/HCO3 exhanger.

7
Q

Chief Cells

A

Produce inactive pepsinogen.

8
Q

Pancreatic Enzymes

A

Trypsin (activated by enteropeptidase) activates Chymptrypsin, elastase, carboxypeptidase.
Pancreatic lipase, which can’t work without colipase.
Pancreatic amylase to break down chains in carbs.

9
Q

CCK

A

Produced in the I cells of the duodenum causes contraction of smooth muscle cells of the gallbladder and secretion of pancreatic enzymes.

10
Q

Gastrin

A

Produced by the G cells in the stomach to stimulate the secretion of HCl and intrinsic factor from the parietal cells via IP3.
Also stimulates Histamine secretion from ETC’s.

11
Q

Secretin

A

Secretion of H20, bicarb, insulin.

Inhibits G cell production of gastrin.

12
Q

Digestion of Carbs in the Mouth

A

Salivary amylase breaks alpha 1,4 bonds between glucose residues.
Has NO activity towards other sugar polmers or 1,6 bonds/branches.
It is inactivated by low pH in the stomach.

13
Q

Digestion of Carbs in the Intestine

A

Remember, no carbohydrate digestion occurs in the stomach.
Glucoamylase: specific for alpha 1,4 bonds b/t glucose residues.
Sucrase-isomaltase complex: hydrolyzes alpha 1,6 bonds/branches.
Trehalase: hydrolyzes glycosidic bond of trehalose
B-glycosidase (Lactase): cleaves beta bond between glucose and galactase.

14
Q

Absorption of Carbs in the Intestine

A

Absorbed in the duodenum mainly via Na+ dependent co-transporters. Na+ moves along its concentration gradient while the sugars move against theirs. Exit to blood via facilitated diffusion.
Exception is fructose, which is transported into and out of the intestinal cells via facilitated diffusion.

15
Q

GLUT 5 deficiency

A

Fructose transporter.
Common fructose allergy in kids. If they drink a lot of juice, they can’t absorb the fructose and bacteria in the GI use it as fuel. Leads to diarrhea.

16
Q

Protein Digestion in the Stomach

A

Low pH of the stomach begins the digestion process. No digestion would occur without it.
Pepsinogen is converted to pepsin at low pH due to gastric HCl from parietal cells.
Pepsin cleaves the peptide bonds in denatured proteins.

17
Q

Protein Digestion in Intestine

A

Pancreas secretes hormones into the duodenum due to food there: trypsin, chymotrypson, elastase, carboxypeptidase.
Bicarb is also secreted to raise pH.
Peptides are subject to brush border enzymes.
Aminopeptidases cleave one amino acid at a time to make single AAs.

18
Q

Other Pancreatic Secretions (not enzymes)

A

Inhibitors are secreted to prevent self-digestion of the pancreas by enzymes.

19
Q

Trypsin

A

Pancreatic enzyme activated by enteropeptidase.

Activates Chymotrypsin, proelastase, and procarboxypeptidase to active forms.

20
Q

Absorption of Proteins in the Intestine

A

Brush border enzymes finish digestion.
Multiple amino acid transporters are Na+ dependent and transport multiple AAs based on similar charge and size.
Hartnup disease: deficient amino acid transporters leads to deficiency of certain AAs.
Small peptides are endocytosed and other are transported via small PepT (di/tri) into the intestinal cells.

21
Q

Digestion of Lipids in the Intestine

A

Fats aren’t soluble. Need bile salts from gallbladder to become soluble. Fatty acids, 2-monoacylglycerols, are packaged into micelles by bile salts.
Can’t be digested by pancreatic lipase without colipase, which frees up surface area for lipase to break triacylglycerol into 2-MAG and fatty acids.

22
Q

Absoprtion of Lipids

A

Micelles float to intestinal cells and drop off their contents.
Once absorbed, lipids reform to triacylglyerolds by activation of 2 ATP and coenzyme A.

23
Q

Transport of Lipids

A

Not water soluble, so lipoproteins (Chylomicrons and VLDL) transport them.
Protein part: apoproteins (B-48 in chylomicrons and B-100 in VLDL).
Chylomicrons are mostly triglycerols.

24
Q

Chylomicrons

A

FAs re-esterfied to triglycerol in smooth ER.
Apoprotein B-48 is made in RER.
Both go to golgi for assembly into nascent (immature) chylomicrons 1-2 hours after a meal.

25
Q

Nascent Chylomicrons

A

Secreted into the blood to mature and accepted proteins from HDL in lymph and blood.
ApoE: recognized b the liver and allows digestion b lysosomes
ApoCII: activates lipoprotein lipase and allows for TG digestion in muscle and adipose

26
Q

Vitamin B12

A

Requires binding partners to prevent degradation; can be dietary protein or R binders. This protects it until a protease digests the protein and instrinct factor binds to B12 to allow for absorption in the terminal ileum.

27
Q

Fat Soluble Vitamins

A

ADEK

Absorbed with micelles and packaged into chylomicrons

28
Q

E & K deficiency

A

Bleeding disorders

29
Q

Vitamin A deficiency

A

Night blindness

30
Q

Vitamin D deficiency

A

Bone issues

31
Q

Iron Absorption

A

Only small amounts absorbed daily in heme or non-heme form bound to specific proteins.
Transferrin - transport
Ferritin- storage

32
Q

How is the majority of sodium absorbed?

A

As co-transport with glucose, amino acid, hydrogen in the jejunum.

33
Q

What causes hypokalemia?

A

Diarrhea.

34
Q

What is the purpose of bicarbonate?

A

Neutralizes H+ in intestine.

Forms CO2 and CO2. CO2 is absorbed and can form more bicarb.

35
Q

Cl-/HCO2- exchanger

A

Neutralizes acids produced by bacteria.

36
Q

Lactose Intolerance

A

Deficiency in lactase.
Extra lactose broken down by bacteria in gut, leading to diarrhea via an osmotic effect.
Methane and H2 production causes flatulence.

37
Q

Congenital Lactose Intolerance

A

Babies can’t digest milk.

38
Q

What causes damage to intestinal mucosa and lactase deficiency?

A

Chronic alcoholism.

39
Q

Cystic Fibrosis

A

Deficiency in CFTR Cl- channel and leads to blocked pancreatic duct.
Lack of pancreatic enzymes leads to impaired protein absorption.
Trx: pancreatic enzymes.

40
Q

What is the pathology of gall stones?

A

Block the common bile duct due to large amount of non-soluble bilirubin.
Bile salts can’t reach the small intestine, so fats aren’t absorbed properly.
Leads to seatorrhea and vitamin ADEK deficiency.

41
Q

Abetalipoproteinemia

A

Microsomal triglyceride transfer protein is required to assemble chylomicrons and enhance triglyceride transport across membranes by binding to ApoB.
This disease is caused by lack of MTP activity.
Leads to limited lipid absorption/steatorrhea and deficiency of vitamins ADEK.

42
Q

Hartnup’s Disease

A

Absence of neutral amino acid transporter leads to deficient amino acid absorption.
However, endocytosis and smal PepT (Di/Tri) transporters can compensate for nutritional needs.

43
Q

Celiac Sprue

A

Gluten diet destroys enterocytes and leads to mucosal inflammation and malabsorption.
Dx by Iga Transglutamase measurement

44
Q

Tropical Sprue

A

Likely due to a bacterial infection and involves the distal small bowel and required travel.
Sx: steatorrhea, malasorption, weight loss, lethargy.