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Organ Systems II > Allison Siebecker Lecture > Flashcards

Allison Siebecker Lecture Flashcards

1
Q

IBS effects what % of Americans?

A

up to 20%; 50% visit gastroenterologist

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2
Q

What is IBS?

A

Irritable bowel syndrome
Sx: bloating, pain, constipation, diarrhea or mixture both
Thought to be caused by GI infection in most cases; results in SIBO (small intestinal bacterial overgrowth)

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3
Q

What are the underlying mechanism of SIBO?

A

carbohydrate malabsorption from SIBO

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4
Q

What is digestion?

A

breaking down food into smallest particles, mechanically by chewing, chemically by acids and enzymes

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5
Q

What are the acids & enzymes involved in digestion?

A
  • HCl and pepsin in stomach & bile from Liver & gallbladder in small intestine
  • enzymes from pancreas in small intestine
  • enzymes that sit on the small intestine BB
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6
Q

What is absorption?

A
  • movement of smallest particles of food across SI lining (1 cell thick)
  • food particles go through the cell via transporters & into blood/lymph circulation on the other side
  • transporters can get overwhelmed OR too few ‘doorways’
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7
Q

What is the order of the segments of the SI?

A
  1. duodenum
  2. jejunum
  3. ileum
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8
Q

What are the two types of ilieoecal valves?

A

papillary & labial

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9
Q

What are the three parts of the SI?

A

lumen, folds, villi

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10
Q

What makes up the villi of the stomach?

A

microvilli= brush border

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11
Q

What are the two cells of the pancreas which secrete substances?

A
  • acinar cell–> secrete digestive enzymes

- duct cells secrete water & bicarbinate (NaHCO3)

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12
Q

What does the pancreatic duct drain and into what structure?

A

enzymes, water & bicarb into the SI

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13
Q

What are the Islets of Langerhans for (what do they secrete & into where)?

A

secrete hormones (insulin & glucagon) into the blood

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14
Q

Digestion beings with what?

A

pancreas secretions

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15
Q

What are bicarb & H2O for in terms of digestion?

A

neutralize acid from stomach

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16
Q

What are the pancreatic enzymes for?

A

digest the food

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17
Q

What stimulates the release of pancreatic enzymes?

A

neuroendocrine system

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18
Q

What are the 3 pancreatic phases?

A
  1. cephalic
  2. gastric
    3.
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19
Q

What is the cephalic phase?

A
  • before food in mouth & once food in mouth

- vagus stimulates pancreatic secretions in response to reflexes

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20
Q

What are the reflexes which stimulate pancreatic secretions

A
  • smell
  • taste
  • chewing
  • swallowing
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21
Q

What is the gastric phase?

A
  • food in the stomach

- vagus stimulates pancreatic secretion in response to gastric distention

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22
Q

What is the intestinal phase?

A
  • most important phase!
  • digestive products trigger release of hormones that control secretion
  • CCK: released from I cells, stimulates enzyme & bile secretion for digestion
  • Secretin: released from S cells, stimulates water and bicarb secretion to neutralize acid
  • parasympathetic procsses (stress inhibits secretion)
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23
Q

What stimulates CCK secretion?

A

fat, protein (peptides/amino acids)

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24
Q

What stimulates secretin secretion?

A

H+ (acid), fat

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25
Q

SI CHO & Protein digestion occcurs in how many and what phases?

A
  • 2 phases
  • pancreatic enzymes (& bile from liver) in lumen break big into smal
  • brush border enzymes on membrane break small into single units for absorption
26
Q

What are the monosaccharides?

A
  • glucose, fructose, galactose

- 1 sugar

27
Q

What are the disaccharides?

A
  • sucrose: fructose, glucose
  • lactose: glucose, galactose
  • 2 sugars
28
Q

What are the oligosaccharides?

A
  • FOS, GOS, MOS

- few, 3-10 sugars

29
Q

What are polysaccharides?

A
  • starch, fiber

- many, 10+

30
Q

What dietary carbs can humans not digest?

A

fiber & oligosaccharides–> we don’t have the enzymes to break bonds between the sugars

31
Q

Humans can digest…

A
  • starch (amylose, amylopectin): rice, potato, corn, wheat, etc.
  • sucrose: table sugar
  • lactose: milk sugar
  • trehalose: mushrooms, honey, shrimp/lobster, algae, insects, rye
  • glucose: honey, fruit, veggies
  • fructose: HFCS, agave, honey, fruit, veggies
32
Q

What are the 6 major carbohydrases?

A

amylase, isomaltase, maltase, sucrase, lactase, trehalse

33
Q

Describe amylase

A
  • source: pancreas
  • site of action (SOA): duodenal lumen
  • substrate: starch
  • end product: dextins, maltotriose, maltose
34
Q

Describe isomaltase

A
  • source: BB
  • SOA: brush border
  • substrate: dextrin, maltotriose
  • end product: maltose
35
Q

Describe maltase

A
  • source: BB
  • SOA: BB
  • substrate: maltose
  • end product: glucose, glucose
36
Q

Describe sucrase

A
  • source: BB
  • SOA: BB
  • substrate: sucrose
  • end product: glucose, fructose
37
Q

Describe lactase

A
  • source: BB
  • SOA: BB
  • substrate: lactose
  • end product: glucose, galactose
38
Q

Describe trehalse

A
  • source: BB
  • SOA: BB
  • substrate: trehalose
  • end product: glucose, glucose
39
Q

What are the 3 carbohydrate transporters?

A
  1. SLGT1= glucose, galatose; high affinity, active transport (ATP required)
  2. Glut 5= fructose; facilitated diffusion (easily saturated)
  3. Glut 2= glucose, galactose & fructose; backup= fructose when Glut 5 is overwhelmed; exiting= transports out of enterocyte to blood; facilitated diffusion
40
Q

What forms of carbs can be absorbed? What is carbohydrate malabsorption caused by?

A

monosaccharides only! dis and anything larger can’t transport across the BB (need BB enzymes to digest dis & larger to monos or they will become food for bac= carbohydrate malabsorption)

41
Q

What is carbohydrate malabsorption?

A

when CHOs are left in lumen of SI & LI, bac then ferment them= GAS, also CHOs sitting in lumen draw in water= DIARRHEA–> triggers bloating, constipation/diarrhea, pain, nausea, flatulence, belching, GERD, fatigue

42
Q

What do bacteria produce in relation to GI malaise?

A

-hydrogen, methane= gas & bloating-> abdominal pain, gas exiting via mouth or anus, altered motility

43
Q

What is the difference b/w primary and secondary lactose malabsorption?

A
  • primary= genetic, congenital, born w/o lactase

- secondary= damage, loss of lactase after wearing, due to DAMAGE, leaves lactose in the SI

44
Q

What is fructose malabsorption?

A
  • fructose transporter, Glut 5 gets easily saturated (facilitated diffusion has limited capacity)
  • 15 g absorbed in healthy ppl (5-50 g range)
  • well absorbed w/glucose in 1:1 ratio by Glut 2
  • seeing increase in occurence b/c of increased consumption of fructose
45
Q

Why could CHO malabsorption occur?

A
  • no enzyme to digest it (oligosaccharides)
  • decreased enzymes (genetic= primary= lactose & fructose intolerant OR damage= secondary= BB enzymes may be effected)
  • inefficient absorption by transporters
  • substance too large= polyols/sugar alcohols
  • too fast of transit
  • bacterial overgrowth/imbalance
46
Q

SI protein digestion occurs in how many phases & what are they?

A

2 phases

  1. pancreatic enzymes in SI lumen= trypsin, chymotrypsin, elastase (protein–> polypeptides, 2-6 a.a.s long) AND carboxypeptidase A & B (polypeptides–> amino acids)
  2. BB enzymes= aminopeptides (peptides (2-3 a.a.s long)–> amino acids
47
Q

What are the 5 major SI proteases and the one BB? And their proenzyme form?

A
  1. trypsin (trypsinogen)
  2. chymotrypsin (chymotrypsinogen)
  3. elastase (proelaste)
  4. carboxypeptidase A (procarboxypeptidase)
  5. carboxypeptidase B
  6. BB: aminopeptidase (simply activated by a.a.s, dis & tris)
48
Q

Pancreatic enzymes are secreted in what form & why?

A

zymogens (proenzymes) so as to not digest the pancreas itself

49
Q

What activates trypsin?

A

enteropeptidase/enterokinase (BB enzyme), released by detergent action of bil (fat helps protein digestion)

50
Q

What are the protein transporters? What absorbs?

A
  • numerous BB transporters for a.a.s

- a.as, dis & tris absorb BECAUSE of peptidases w/in the enterocytes

51
Q

What does protein malabsorption lead to?

A

leads to muscle wasting, immunodeficiency & edema in its severe form (not GI sx’s like with CHO malabsorption b/c bac can’t ferment protein)

52
Q

What are the 3 ‘parts’ of cell junctions?

A
  • zonula occludens
  • zonula adherens
  • macula adherens (desmosome)
53
Q

What is the tight junction structure?

A
  • caludins, occludens, JAM (junctional adhesion molecules)
  • attached to zonulin 1 & 2 anchors
  • attached to actomysin filaments
54
Q

What are the functions of tight junctions?

A
  1. gate: regulate passage of macro & micro molecules through paracellular space b/w cells
  2. fence: keeping microbiotia & large substances out for protection
    * *TJ permeability constantly changes
55
Q

What is increased intestional permeability? What happens?

A
  • when TJs b/w cells ope= allow unintended items through

- absorption of unintended items can also occur through cell itself

56
Q

Paracellular vs Transcellular

A

Paracellular: between two cells
Transcellular: through the cell to the other ‘side’

57
Q

What opens the TJs?

A

contraction of actin

58
Q

What is leaky gut? What can it lead to?

A
  • allows absorption of things that are not supposed to be getting in: partially digested food particles, baceria & bacterial toxins, viruses, yeast, metabolites & acids
  • leads to immune rxns & sxs anywhere inside the body
  • *intestinal permeability causes systemic symptoms & is the main cause of food rxns
  • *can have leaky gut w/o sx’s
59
Q

What are the seven broad categories that can lead to increased intestinal permeability?

A
  1. diet
  2. medications
  3. infections
  4. stress
  5. hormonal
  6. neurological
  7. metabolic
    bonus: NSAIDS!!!
60
Q

Take homes

A
  • digestion occurs by pancreatic & BB enzymes
  • absorption occurs through transporters
  • saccs need BB enz digestion into monos to be absorbed
  • peptides can absorb since they will be digested into a.a.s inside the enterocyte
  • pancreatic proteases need activation (so don’t digest pancreas) BUT amylases don’t
  • gluc absorbs efficiently via SGLT but fruc may nto due to saturability of GLUT5
  • stress inhibits digestion (HCl, bicarb, bile, enz) & increases intestinal permeability which leads to systemic sx’s from food/eating

Organ Systems II (2 decks)

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