Gastrointestinal Physiology - Theoretical Questions Flashcards

1
Q

What are the components of the Gastrointestinal Nervous system:

A

Intrinsic - Enteric Nervous system (Aka “Peripheral Brain”)

Extrinsic - Sympathetic and Parasympathetic (ANS)

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2
Q

What are the Gastrointestinal plexuses? Where are they located?

A

1) Myenteric Plexus (Auerbach’s) - Between Inner-Circular and Outer Longitudinal parts of Muscularis Externa
2) Meissner Plexus - in the Submucosa layer

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3
Q

How is the Autonomic nervous system acts on GI system - Generally?

A

Sympathetic - Inhibits Digestion

Parasympathetic - Activates Digestion

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4
Q

What are the Short Reflexes coming through the Meissner Plexus:

A

Meissner Plexus:

1) Stimulation of Glands and Enteroendocrine Cells
2) Dilation of Blood Vessels

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5
Q

What are the Short Reflexes coming through the Myenteric Plexus:

A

Myenteric Plexus:

-Motility reflexes for stomach and Peristaltic contractions of Intestinal tract

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6
Q

Long Reflexes Parasympathetic:

Passage of Stimulus, Border between paths

A

Long Reflexes Parasympathetic: (Vagovagal)
From Vagal or Pelvic Nerves to the Enteric Plexuses.
Cannon-Bohm point is the edge of Vagal stimulation and the Beginning of Pelvic nerve.

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7
Q
Long Reflexes Parasympathetic:
Neurotransmitter used (Postganglionic)
A

Substance P, VIP and Ach

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8
Q

Long Reflexes - Sympathetic:

Passage of Stimulus

A

Long Reflexes - Sympathetic:
Celiac, SM, IM and Hypogastric ganglions are carrying the fibers to Greater, Lesser and Lumbar splanchnic Nerves. These could stimulate directly the muscles of the GI tract with/Without Synapsing with Enteric Plexuses.

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9
Q
Long Reflexes - Sympathetic: 
Neurotransmitter used (Postganglionic)
A

Norepinephrine

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10
Q

Long Reflexes - Sympathetic:

Direct Innervation

A

Alpha-2 : NE - SMC relaxation

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11
Q

Long Reflexes - Sympathetic:

Indirect Innervation

A

Alpha-1 : NE - SMC contraction (Sphincters) and Vasoconstriction.
Beta-2 : NE - SMC relaxation

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12
Q

What are the Local Stimuli that start the Long and Short Reflexes?

A
GI Chemoreceptors (Epithelium) - pH, Food Content
GI Mechanoreceptors (Epithelium) - Sterch
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13
Q

What makes GI hormone unique?

What are the four ones fall to this specific category?

A

Released by GI Mucosa Endocrine cells travel into the portal circulation, enter the general circulation, and have physiologic actions on target cells.
Gastrin, Cholecystokinin (CCK), Secretin, Glucose Dependent Insulinotropic Peptide (GIP)

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14
Q

Gastrin:

Family type, Site of Secretion

A

Gastrin:
Gastrin-CCK Family
G-Cells of Stomach

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15
Q

Gastrin:

Stimuli, Actions

A

Stimuli of Gastrin:
Peptides and Amino acids, Stretch signal (GRP), Inhibited by H+ and SST.
Actions (Gq): Parietal Cells H+ Release, Histamine secretion from ECL cells.

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16
Q

CCK:

Family and Secretion sites

A

CCK:
Gastrin-CCK family
Secreted from I cells of Duodenum and Jejunum

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17
Q

CCK:

Stimulus

A

CCK Stimulus:

Peptides, Amino and Fatty acids.

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18
Q

CCK: Actions

A

CCK:

1) Contraction of gallbladder and Relaxation of sphincter of Oddi
2) Pancreatic Enzymes and Bicarbonate secretion↑
3) Growth of Exocrine Pancreas and Gallbladder ↑
4) Inhibits gastric emptying

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19
Q

Secretin:

Family and Secretion sites

A

Secretin-Glucagon Family

S cells of Duodenum

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20
Q

Secretin:

Stimulus and Actions

A

Stimulus - H+ and FA in Duodenum

Actions - Pancreatic bicarbonate secretion↑, Biliary bicarbonate secretion↑, Gastric H+ secretion↓

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21
Q

GIP:

Family and Secretion sites

A

GIP:
Secretin-Glucagon Family
Duodenum and Jejunum

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22
Q

GIP:

Stimulus and Actions

A

GIP:
Stimulus -FA and Amino acids, and Oral Glucose (an Incretin Function) .
Actions - ↑ Insulin secretion,
↓ Gastric H+ secretion

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23
Q

What are the Paracrine Hormones: Enterochromaffin (EC)

A

SST - D cells; Inhibition of H secretion and SMC contraction.
HIstamine - ECL cells; Acid Production
Serotonin - SMC Contraction

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24
Q

What are the “Candidate” Hormones?

A

Motilin - SMC ↑
GLP - Epithelial Proliferation↑
Leptin (from Adipose) and Ghrelin (from Stomach)

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25
Q

What are the types of contraction of the gastrointestinal tract smooth muscle layers?

A

Tonic (Basal) contractions and Phasic Contractions

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26
Q

What is the neurogenic basis for the Tonic contractions?

A

The Tonic contractions are the result of general fluctuations of the potential levels of the SMCs. They originate from the Interstitial Cajal cells that are linked by Gap junctions to the SMCs. This keeps a Basal level of “Slow waves” of Repol. and Depol. thae allow for these weak contractions.

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27
Q

What type of SMCs are the ones that are found in the GI tract?

A

Single unit, they are connected via gap junctions meaning that they excite each other and contraction practically simultaneously.

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28
Q

What is the molecular basis for Slow wave production in the interstitial cajal cells?

A

Special Slow Na+ Channels are responsible for the Depolarization and Repolarization is caused simply by general K channels.

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29
Q

What is the molecular basis for the SMC contractions once depolarized by the Slow waves?

A

Ca2+ VDC

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30
Q

What are the rhythm of the contractions in the Stomach (Lowest) and in the Duodenum (Highest)?

A

Stomach - 3 per Min

Duodenum - 12 per Min

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31
Q

Where can we find the Interstitial Cajal Cells?

A

Myenteric Plexus, Part of the ENS (Intrinsic)

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32
Q

What is the cause of the Phasic contractions in the GI tract?

A

Phasic contractions or Peristalsis are caused by Gq mechanisms of Muscarinic Ach receptors (M1/3/5) that cause Ca2+ channels to open and form an AP on top of the Slow wave electrical amplitude. (Extrinsic NS)

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33
Q

What are the Phases of Swallowing?

A

Oral Phase
Pharyngeal Phase
Esophageal Phase

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34
Q

Chewing:

Muscles involved and Reflexes

A

Masseter, Medial Pterygoid and Temporalis are responsible for Opening mouth and Lateral Pterygoid for closing it. The Masseteric reflex (V3) coordinates and Senses the voluntary movement (proprioception)

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35
Q

What happens in the Oral phase of Swallowing?

A

Voluntary movement of the Tongue - Tip goes forwards and Base goes backwards. This pushes the Food bolus backwards to the Oropharynx.

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36
Q

What happens in the Sensory Part of Pharyngeal phase of Swallowing?

A

Esophageal, Palatal and Pharyngeal Mechano- and Thermo - and Taste receptors detect the bolus and send via V3+IX+X the information to Swallowing center in the Medulla oblongata .

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37
Q

What happens in the Motor Part of Pharyngeal phase of Swallowing?

A

This is a Involuntary directed by the Medulla Oblongata center - 3 muscle actions: 1) Soft palate elevation 2) Epiglottis depression 3) Upper esophageal sphincter relaxes.

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38
Q

What happens in the Esophageal phase of Swallowing?

A

The vagovagal reflexes cause of the tube distension cause release of VIP to the SMCs of the Esophagus guide the bolus way to the Lower Esophageal sphincter.

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39
Q

How long does it take for Solid and Liquid foods to reach the stomach?

A

Solid - 10 sec

Liquid - 1 Sec

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40
Q

What is the Receptive Relaxation ?

A

Vagovagal reflex allowing the relaxation of the Lower Esophageal Sphincter and Orad part of Stomach. Destination causes the reflex and VIP is the Neurotransmitter (Like in rest of esophagus)

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41
Q

What is the Intraesophageal pressure equal to?

A

It is Equal to the Intrathoracic pressure

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42
Q

What happens if the Primary peristaltic wave doesn’t push all the bolus to below?

A

Vagovagal Reflex cause Secondary Peristaltic reflex

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43
Q

What is the names of the Proximal and Distal parts of the stomach (Not Pyloric Antrum/Body/Fundus)

A

Proximal - Orad Part

Distal - Caudad Part

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44
Q

What is the name of the digested food that leaves the stomach?

A

Chyme

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45
Q

What are the cell kinds on the different positions of the Mucosa of the stomach?

A

Fundus - Parietal cells
Body - Chief cells
Pyloric Antrum - Mucus and G cells

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46
Q

What extra lamina are in the inner part of the Muscularis externa?

A

Oblique layer

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47
Q

What are the Particle size of chyme able to pass through the Pylorus? What happens if they are bigger?

A

1 mm particles can go through the Pylorus, if they are smaller they get pushed back (Repulsion) for further mechanical and chemical breakdown.

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48
Q

What is the muscular part responsible for the mechanical breakdown in the stomach? although the rhythm is pretty (constant 3 per min ) what elevates the contraction forces?

A

Cauded part is a strong contraction area which is further increased upon Gastrin stimulation (AP -f higher) when there is Amino acids or Peptides present, and is decreased by Secretin and GIP action.

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49
Q

What determines the length of stomach emptying time? Generally how long does it take?

A

1) Liquids travel faster
2) Volume of the food
3) Very Fatty or Acidic Chyme will empty more slowly.

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50
Q

How will Very Fatty or Acidic Chyme will empty more slowly?

A

High Fat will cause CCK release (Duodenum - I cells) that decreases Gastric Motility (SMC relaxation).
Acidic Chyme will cause Secretin (Duodenum - S cells) and Sympathetic action to also decrease Gastric Motility ( SMC relaxation)

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51
Q

Why is Acidic chyme slowing down stomach emptying?

A

More time for the Bicarbonate secretion of Pancreas to build up and neutralize the Acid later in the duodenum

52
Q

What are the two patterns of contractions that occur in the small intestine?

A

Segmental contractions - Pinching Chyme in the middle

Peristaltic contractions - Propelling the Chyme forward

53
Q

How are the Peristaltic Contractions propel the chyme forward? How are the contractions coordinated?

A

Steps:
1) Contraction behind chyme 2) Relaxation infront of chyme allow 3) Repetition - creates a wavy motion of chyme forward.
The Inner circular and Outer longitudinal layers contract RECIPROCALLY one layer at the time for this .
“Larger Hole” + “Shorter tube” and vice versa.

54
Q

What is the Paracrine mediator that causes the Peristalsis in the Small intestines? What are the other substances aiding here?

A

Enterochromaffin cells secrete Serotonin which activates the Peristaltic movements locally. Neuropeptide Y, Substance P and Ach are also released behind the chyme (Not Paracrine) for also stimulating contractions.

55
Q

What happens in Vomiting ?

A

Reverse Peristalsis

56
Q

What happens in Retching ?

A

Lower esophageal sphincter opens, Acidic reflux passes.

57
Q

What are the unique arrangement of contractions in the Colon?

A

Segmental contractions go according to the Haustra

58
Q

How many times a day there are mass movements in the colon?

A

1-3 times a day

59
Q

What happens in the Rectosphincteric Reflex?

A

When 25% of Rectum is Filled, SMC on wall contract, Inner Anal sphincter relaxes and Outer Anal sphincter relaxes on command (Skeletal Muscle).

60
Q

What process aids the Defecation?

A

Valsalva Maneuver: Increase in intrabdominal pressure thanks to respiratory muscle contractions and Epiglottis closing the air passage.

61
Q

What are MMCs?

A

Migrating motor complexes : while fasting Motilin is released and sets the contractions of colon to a rate of 1 per 90 minutes.

62
Q

Give examples for Local Peristaltic reflexes in the GI tract? What is common for all?

A

Gasrto-enteric, Gastro-Ileal, Gastro-colic, Dudenocolic, Enterogastric, Colocolic, Rectocolic.
First name senses the stimulus (Stretch/pH/Content) and later sends with AND/ENS/Hormone the signal to the second to Contract/Relax.

63
Q

Salivary glands - Daily production of Saliva? Sites of Production?

A

1 Liter from Parotid, Submandibular and Sublingual glands

64
Q

What is the contractile unit around the salivary glands acini?

A

Myoepithelial cells

65
Q

What are the components of human Saliva?

A

Lingual Lipase, Amylase, and Hypotonic/Isotonic solution similar to plasma (Depends on eating/fasting states).

66
Q

What is the First step of Sequential secretion ?

A

Acinus produces Isotonic secretion with plasma with NCCK, Na/K ATPase and CFTER pumps.

67
Q

What is the Second step of Sequential secretion ?

A

Ductal cells increase Potassium and Bicarbonate and Decrease Sodium and Chloride ion concentrations in Saliva turning it to Hyposmolar solution with Higher pH.

68
Q

What happens to the saliva during eating? and what happens while not eating?

A

Eating - Flow Rate ↑ - Ion exchange in the ductal cells↓ :
Saliva becomes Isosmotic
Not Eating - Flow Rate ↓ - Ion exchange in the ductal cells↑ :
Saliva becomes Hyposmotic

69
Q

What are the transmembrane proteins found on the ductal cells Apical surface?

A

Bicarbonate/Cl Exchanger, H/Na Exchanger and K/H Exchanger.

70
Q

What is the Unique feature of Salivary glands regulation? (Not like other GI parts)

A

Salivary glands regulation is purely neurogenic and Both Sym and Para INCREASE the saliva production.

71
Q

Salivary: What is the Ion secretion that is independent from the Flow rate effects on secretion? What regulates it?

A

Bicarbonate secretion is regulated selectively by Parasympathetic innervation

72
Q

What is the effect of Parasympathetic regulation on saliva ?

A

Smelling or tasting causes nerves to release :Ach - M3(Gq) - Calcium signal causes fluid and enzyme↑
and VIP - Gs - Vasodilation on Glands arterioles.
Ultimately Increasing secretion.

73
Q

What is the effect of Sympathetic regulation on saliva ?

A

Norepinephrine - Beta-2 receptors - PKA - Mucin↑

Ultimately Increasing secretion.

74
Q

What are the components of Gastric Juice? which are the cells secreting them?

A

Chief cells - Pepsinogen
Parietal cells -HCl, Intrinsic Factor
Mucus cells - Mucus.

75
Q

Mechanism of Parietal cells secretion:

Transmembrane proteins on the Apical surface

A

H-K PUMP , K and Cl channels

76
Q

Mechanism of Parietal cells secretion:
Transmembrane proteins on the Basal surface?
What is the enzyme needed here?

A

Na/K ATPase, Bicarbonate/Cl exchanger

Carbonic anhydrase allows for diffused CO2 and H2O to turn into Carbonic Acid and later form Bicarbonate and Proton.

77
Q

What happens to the Bicarbonate released back to blood Normally? and in Vomiting?

A

This Bicarbonate travels in blood to reach the pancreas and to be released to Small intestines, in vomiting since there is no stimulation of pancreas and no pH drop in Small intestine the Bicarbonate remains in blood - Metabolic alkalosis!

78
Q

Stimulators of HCl secretion in Parietal cells?

Drugs inhibiting?

A

Ach (Gq) - Atropine inhibits
Histamine (GS) - Cetamidine inhibits
Gastrin (Gq)

79
Q

What are the inhibitors of HCl secretion in Parietal cells?

Indirectly as well..

A

SST and Prostaglandins (both Gi)

SST also blocks G cells and ECL cells from secreting Gastrin and Histamine respectively

80
Q

What are the 3 stages of HCl secretion stimulation?

What are their relative proportions?

A

Cephalic (40%): Smell/Taste - Dorsal Vagal Nucleus - Ach
Gastric (50%): Destination/Protein - ENS/Vagovagal/Gastrin
Intestinal (10%)l: Gastrin

81
Q

What are the Pancreatic enzymes? What do they digest?

A

1) Carbohydrates - Amylase
2) Proteins - Trypsin, Chymotrypsin, Carboxypeptidase, Elastase
3) Lipids - Lipase and Colipase

82
Q

What is changing the amount of bicarbonate amount in the pancreatic secretion?

A

Bicarbonate/Cl exchanger

it is more active in high flow rate (to intercept stomach acid arrival to duodenum after eating)

83
Q

Phases of pancreatic secretion:

What happens in each stage?

A

Cephalic - Smell/Taste - Vagus - Ach - Acinar secretion
Gastric - Distention - Vagus - Ach - Acinar secretion
Intestinal phase (80%) - I cells sensing AA- CCK secretion + GI chemoreceptors - Vagus - Ach

84
Q

How is the Intestinal phase of the Pancreatic Secretion allows for an Increase in aqueous fluid and Bicarbonate secretion?

A

S cells in the Duodenum senses Protons from gastric chyme. These will release Secretin a GI hormone that will stimulate the Ductal cells to release the Bicarbonate and Aqueous solution.

85
Q

What stops the pancreatic secretion?

A

Ileum and Colon release (when getting chyme) the Neuropeptide Y

86
Q

What is the gallbladder functions?

A

Stores, Concentrates and Releases Bile

87
Q

How is Bile being concentrated in the gallbladder?

A

Standing gradient osmotic mechanism:

NaCl reabsorption to blood that causes osmosis and remaining lipid molecules are now able to form Micelles.

88
Q

What is the composition of Bile?

A

Bile salts, Phospholipids, Cholesterol and Bilirubin (Pigmentation)

89
Q

Where is bile formed? How does it get to the gallbladder?

A

Cholesterol filtered from discontinuous capillaries into the hepatic spaces of Disse. Then in the hepatocytes Primary Bile acids from and NTCP and BSEP move them out of the hepatocytes canaliculi to the common hepatic and cystic duct to GB.

90
Q

What are the primary bile acids? what are the secondary bile acids and where do they form?

A

Primary - Cholic Acid and Chenodeoxycholic acid
Secondary - Deoxycholic acid and Lithocholic acid.
Secondary Bile acids are formed from the primary ones by Bacteria in the gut (7-dehydroxylases)

91
Q

What is the hormone responsible for the contraction of the Gallbladder? What is the trigger for its release?
What is another important target for it? in this regard?

A

CCK - I cells in Duodenum detect Chyme

relaxation of the sphincter of Oddi

92
Q

What are the special cells of the bile duct? what do they release?

A

Cholangiocytes - Release Bicarbonate

93
Q

What is the chemical nature of Bile salts? what does this allow them to do?

A

They have an Amphipathic structure allowing them to self assemble into Micelles that have an Hydrophobic (Lipophilic) interior that can store Fats- Emulsification.

94
Q

What is the importance of emulsification?

A

Increasing the surface area (Large to small particles of fat) thus allowing pancreatic lipase to effectively form Glycerol and FAs from it

95
Q

What happens when the gallbladder is impaired?

A

Steatorrhea - oily feces. Bile will be secreted more quickly then they are emulsifying

96
Q

How much of the bile salts are circulated back? how?

A

Through enterohepatic circulation 95% of Bile salts are being circulated back. Na cotransport carries them back to blood.

97
Q

What is the point from which bile secretion is sufficient for bile activity to be useful?

A

CMC - Critical micelle concentration

98
Q

What is the neural regulation of Bile secretion?

A

Vagus - Ach - GB contraction and Bile secretion
Vagus - VIP and No Sphincter relaxation
Sympathetic - GB relaxation

99
Q

What are 4 locations of Natrium reabsorption in the GI? How?

A

Duodenum - Na/H exchanger
Jejunum - SGLT, AA/Na cotransporter and Na/H excha.
Ileum - SGLT, AA/Na cotransporter and Na/H excha.
Colon - ENaC (Aldosterone) and Na/H exchanger

100
Q

How is Calcium reabsorption in the GI regulated?

A

PTH - allows for 1,25 HydroxyVitD formation in the Kidney and thus allowing for the Calbindin protein, NIS and Ca channels to form in the enterocytes.

101
Q

What are the water Absorption fragments? What are the divisions in the GI? How are they absorbed?

A

9L in total = 1L from Intake and 8L from Digestion.
8.5L in the small intestine and 0.5L in colon (Liquid state).
Paracellularly or with Aquaporins.

102
Q

What are the transporters allowing for Monosaccharide absorption in enterocytes?

A

SGLT1 for Cotransport of Glucose/Galactose with Na
GLUT5 for Fructose
GLUT2 (basal surface)

103
Q

What are the proteins allowing absorption of Iron in enterocytes?

A

DMT-1 is the Apical membrane transporter, Apoferritin is the intracellular binding protein and Transferrin is the Basal membrane transporter. Storage in Liver.
(Also Heme transporter and Heme oxygenase if bound)

104
Q

What is the process of Vit B12 (Cobalamin) protection from degredation until it reaches the Enterocytes?

A

1) Cobalamin is bound to Proteins
2) Cobalamin is released from digested proteins and bind Haptocorrin from Gastric Glands
3) Cobalamin is released from digested Haptocorrin and binds Intrinsic factor in the duodenum (From Parietal)
4) Intrinsic factor receptor on enterocytes binds the IF-CBL complex.

105
Q

How is VitB12(Cobalamin) absorbed once it is in contact with enterocytes?

A

Intrinsic factor receptor on enterocytes binds the IF-CBL complex. The endosome formed releases IF and the receptor for degredation or recycling. Transcobalamin II will form a complex with CBL and through the circulation go for storage in Liver.

106
Q

How are vitamins A, D, E and K absorbed?

A

Lipid soluble: by passive with lipids

107
Q

How are vitamins Bs, C, Niacin, Biotin absorbed?

A

Water soluble: By cotransport with Na

108
Q

How are Tri- and Dipeptides differ in absorption from Amino acids?

A

Tri- and Dipeptides - Proton cotransporter from Na/H exchanger formed gradient.
Amino acids simply cotranslocate with Na concentration gradient.

109
Q

What will happen for lactose intolerant people eating lactose? why?

A

Osmotic diarrhea: Impaired Lactase function on brush border causes accumulation of Lactose that osmotically attracts water from Enterocytes. Loss of water and Gut bacteria overdigestion.

110
Q

Where do Nicotine and Ethanol are able to be absorbed?

A

Oral cavity (and ethanol in stomach as well)

111
Q

After fatty acids and MAGs are formed in the micelles what are the 3 steps of Absorption of Lipids in the Intestine?

A
1)Diffusion of fatty acids,
monoglycerides, and cholesterol
into cell
2)Re-esterification in cell to
triglycerides and phospholipids
3) Chylomicrons form in cell (requires
apoprotein) and are transferred
to lymph
112
Q

What is the Respiratory Quotient? How is it calculated?

A

It is a unitless value signifying the food consumption properties - Higher RQ means well fed. for Carbohydrates it is 1, Proteins 0.8 and Fats 0.7 . It is calculated as Vco2/Vo2.

113
Q

How much does one calorie worth in KJ?

A

1 Calorie = 4.23 KJ/g

114
Q

What is the rule of Isodynamics?

A

Different kinds of foods can replace each other function through biochemical processes in the body.

115
Q

What are the specific food quality requirement that are crucial for ones well being?

A

Essential FAs and AAs

Vitamins

116
Q

What does our food content equal to in means of metabolism?

A

TEE - Total Energy Expenditure

117
Q

Resting state and no External work is done:
What will the TEE be equal to?
How can we calculate it?

A

TEE will be equal to Heat production
Direct calorimetry - Ice melting is proportional to Heat produced.
Indirect calorimetry - Oxygen consumption: 1 O2L = 21KJ.

118
Q

Active state and External Work is done:

What will the TEE be equal to?

A

TEE=BMR + DIT + EE
DIT - Diet Induced Thermogenesis
BMR - Basal metabolic Rate
EE - Energy Expenditure for Physical Activity

119
Q

BMR:

Requirements for measurement (Heat production)?

A
  • 12 hr after a meal
  • no physical activity
  • At rest no drugs
  • 20 degree thermoneutral environment
120
Q

BMR:

What will cause changes in it?

A

Age↓, Body Temp ↑, T3,T4, catecholamines↑ , Pregnancy↑, Inflammation or Surgery↑

121
Q

DIT:

Cause? Percentage of TEE?

A

After a meal there is increased motility in the GI that leads to Heat.
15% of TEE

122
Q

EE:

Cause? Percentage of TEE?

A

30% of TEE

Heat and External Work

123
Q

What happens in Positive Energy balance?

and in Negative?

A

Positive - Energy of Body>TEE, supports weight gain.

Negative -Energy of Body

124
Q

When does loss of weight is dangerous? What could be a reason?

A

40% loss - Immune and Cardiovascular Dysfunction

Anorexia - Psychiatric disorder

125
Q

What are Beige Adipocytes?

A

Induced by cold and Adrenergic Gs stimulus.

Forms in adults and allow heat production (UCP)

126
Q

What element of central nervous system allow for the changes in feeding? how?

A

Hypothalamus:
Satiety center and Feeding center. These receive input from integrator Arcuate nucleus: Orexinergic Neurons (Pro-feed) and Anorexigenic Neurons (Anti-Feed) which release POMC and Neuropeptide Y respectively.

127
Q

What biological signals does the Arcuate Nucleus receives?

A

Anorexigenic Neuron stimulus : Leptin, Insulin, GLP, Peptide YY, CCK, CART
Orexinergic Neuron Stimulus: Orexin and Ghrelin