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Physiology II > GI Physiology (ALL) > Flashcards

GI Physiology (ALL) Flashcards

1
Q

What are the exocrine glands involved in delivering secretions into the tubular lumen?

A

Salivary glands

Pancreas

Liver

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2
Q

What is the GI system composed of?

A

Tubular tract from the lips to the anus including exocrine glands that deliver secretions to the lumen via ductular systems.

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3
Q

What are the functions of the GI tract?

A

Procure and process nutrients

Eliminate endogenous and exogenous wastes

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4
Q

Processing and elimination are made possible through control of _____ and _____.

A

Motility

Secretion

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5
Q

What are the components of the physical/chemical digestion of ingesta? How small do the ingesta breakdown products have to be?

A

Physical digestion is promoted by muscle movement and associated structures (e.g. teeth). Chemical digestion is promoted through secretions of the glands (enzymes).

Ingesta breakdown must be small enough to undergo absorption by epithelial cells in the tubular tract.

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6
Q

TRUE/FALSE.

It is said that the GI system serves a protective function because it is populated by a significant number of immunocytes.

A

TRUE.

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7
Q

TRUE/FALSE.

The GI tract always gets the same amount of blood during sympathetic and parasympathetic stimulation.

A

FALSE.

SNS decreases GI perfusion while PSNS increases it.

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8
Q

What is the main component of exocrine secretions?

A

Water. These secretions are aqueous solutions.

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9
Q

TRUE/FALSE.

Bile contains only enzymes for the breakdown of lipids.

A

FALSE.

The liver also puts waste in bile.

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10
Q

What is indirect vs. direct control of an organ?

A

Direct: the signal speaks directly to the organ to increase or decrease work.

Indirect: message is sent to the vasculature to increase or decrease its nutrients/O2; hormones/neurotransmitters alter the diameter of vasculature.

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11
Q

Why are changes seen in aldosterone, renin, and angiotensin II levels during digestion?

A

Water is secreted into the GI lumen. Aldosterone sends a signal to the kidney to increase water reabsorption.

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12
Q

What are local tissue factors?

A

Increased work at a cell causes increased metabolism and waste. These waste products (H+ and CO2) also act as vasodilators to increase their perfusion. The cell is doing more work and is demanding more blood.

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13
Q

What are the three types of messages that act on blood vessels? Give some examples.

A

Paracrine (Histamine), endocrine and neurocrine.

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14
Q

How would you indirectly decrease the secretion at salivary glands?

A

Constrict the blood vessels going to the salivary acinar cells.

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15
Q

Describe the actions of histamine at the GI tract.

A

Stimulate parietal cells to secrete more HCl

Vasodilator at blood vessels

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16
Q

TRUE/FALSE.

Prostaglandins are secreted constituitively.

A

TRUE.

(Also done at the kidney)

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17
Q

Why is it important to have an empty stomach prior to surgery?

A

During surgery, an animal is already bleeding and becoming hypotensive. By simply having food in the stomach, it will cause vasodilation to increase GI perfusion and further decrease the blood pressure.

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18
Q

TRUE/FALSE.

An animal can be dead and have alive cells.

A

TRUE.

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19
Q

In response to chemical/mechanical stimulation, EC cells produce ____. Describe the function of this product.

A

5-HT (serotonin). It is a paracrine vasodilator.

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20
Q

What are the different types of cells found in the GI tract?

A

Epithelial cells

Secretory -

absorptive - Electrolytes, organic substances

Stem Cells - In the crypts, to divide.

and goblet cells.

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21
Q

What are the different kinds of stimulation received in the gut?

A

Mechanical (stretch); chemical (glucose, amino acids, sodium).

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22
Q

Describe peristalsis.

A

It is an involuntary, repetitive motility pattern.

Stretch caused by the product in the lumen causes two reflexes:

1) Oral: contraction through an excitatory neurotransmitter (Ach). This increases pressure and flow.
2) Aboral: relaxation through inhibitory motor neuron cascade. Nitric oxide is released and relaxes the muslce. ATP/VIP may also releax the muscle. This decreases pressure/resistance/flow.

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23
Q

What is the cryptovilliary escalator?

A

Stem cells at the base of the crypts divide into two cells: one stem cell and one crypt cell.

Crypt cells are predominantly secretory and move up the villi. At a certain point (and as a result of unknown stimuli, possibly changes in pH), crypt cells turn into villis cells. These are mainly absorptive as they are in the most contact with the lumen.

At the very top of the escalator, the cells die. This is a continuous process that takes about 2-4 days.

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24
Q

Contraction of longitudinal muscles of the lumen _____ the diameter, while contraction of the circular muscle _____ diameter.

A

Increases

Decreases

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25
Q

How many reflexes are involved in peristalsis?

A

4 reflexes:

1) Contraction of oral muscle
2) Relaxation of aboral muscle
3) Contraction of lungitudinal muscle

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26
Q

What are the excitatory and inhibitory signals involved in peristalsis?

A

Excitatory (Contraction): Ach

Inhibitory (Relaxation): ATP, NO, VIP

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27
Q

Define an intramural reflex.

A

All components are found within the same organ that received the stimulus. e.g. peristalsis. It does not need input from the CNS.

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28
Q

TRUE/FALSE.

When giving a drug that influences ANS, you have control over its influence on GI.

A

FALSE.

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29
Q

What receptors are present in the GI vasculature? How are they affected bt AS activity ?

A

α1 and β2 are both present. When acted on by the SNS (NE) and adrenal medulla (Epinephrine), they cause vasocontriction & vasodilation, respectively.

Although these are contradictory actions, α1 > β2 to ensure that during increased sympathetic activity, the GI tract is not completely shut down.

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30
Q

Describe the vagovagal reflex.

A

The vagus nerve serves to transmit infomation to various parts of the GI tract. In this reflex, stretch in one part of the GI sends afferent information to the CNS, which sends efferent information to the subsequent portions of the GI tract. Both fibers run within the vagus nerve.

E.g., When food enters the esophagus a signal is sent to the CNS and subsequently the cardiac sphincter (Lower Esophageal Sphincter) to relax in order for it to be open upon arrival of the food.

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31
Q

Describe excitatory/inhibitory stimuli at the LES.

A

Excitatory: Ach - Close/contract as a result of gastric stimuli.

Inhibitory: Relax/open as a result of esophageal stimuli.

This is communicated through PSNS in the vagal/myenteric plexus.

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32
Q

What are the different types of cells that spontaneously depolarize and where are they located?

A

Pacemaker cells: SA node of the heart

Respiratory neurons in the medulla

Interstitial cells of Cajal (ICC) through the gut.

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33
Q

TRUE/FALSE.

ICC reach threshold during each spontaneous de/repolarization.

A

FALSE.

ICC do not generate action potentials but they rhythmically bring the cells closer to threshold.

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34
Q

How does the ANS affect the frequency of ICC membrane protential cyclicity?

A

SNS: ↓ frequency

PSNS: ↑ frequency

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35
Q

What happens to ICC when food is in the lumen of the intestine?

A

EC cells release 5-HT

This excites an afferent neuron to excite an efferent neuron and release excitatory neurotransmitter (Ach).

Since the ICC already spontenously depolarize, this means less Ach is needed to reach threshold and generate an action potential.

ICCs are priming the gut for peristalsis.

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36
Q

ICC frequency of de/repolarization in the duodenum is _____ ( >, <, = ) the stomach.

A

Less than.

This allows more contraction in the stomach to push the food aborally.

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37
Q

Describe a baseline secretory cell

A

1) Na/K ATPase - basolateral
2) Na/K/2Cl- Basolateral Symport
3) Cl- Lumenal ports
4) Na/Cl- Symport

*Water follows chloride secretion in the gut

*The number of ports can be altered to increase secretion

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38
Q

TRUE/FALSE.

Sodium and potassium move into the lumen transcellularly.

A

FALSE.

They move in a paracellular fashion. Only in gastric parietal cells, K+ also moves trasncellularly.

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39
Q

What is the fundamental gastric secretion?

A

H2O

Cl-

Na+

K+

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40
Q

How is the fundamental secretion altered by ductular cells? Parietal cells?

A

Ductular cells increase HCO3- by trading Cl- in order to protect enzymes from extreme pH decreases.

Parietal cells use lumenal H+/K+ ATPase to increase H+ secretion.

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41
Q

TRUE/FALSE.

Both the SNS and PSNS have generalized effects on the GI tract.

A

FALSE.

SNS does vasocontstrict everywhre.

PSNS is focal. E.g., food is in the mouth, fasodilate at the salivary glands.

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42
Q

What plays an important role in the focality of the PSNS on the GI tract?

A

Vago-vagal reflex. This allows the GI tract to speak to different areas.

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43
Q

How does the SNS communicate to the GI tract?

A

Mainly through controlling vasculature. It mostly speaks to the enteric NS and directly speaks to the musculature of the sphincters to contract to prevent food movement (cardiac, pyloric, ileocecal).

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44
Q

Who produces the most mucous? How? Why?

A

Duodenum through Brunner’s patches. This is done because the food entering the GI tract is extremely acidic. Increased mucuous secretion protects it from the “acid hit”.

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45
Q

TRUE/FALSE.

Cattle with faulty salivary glands will have damage to their teeth.

A

TRUE.

Due to the acid from vomiting their food.

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46
Q

TRUE/FALSE.

H+ secretion in parietal cells is obtained from plasma through CO2 reabsorption.

A
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47
Q

FALSE.

H+ does come from CO2 but only from the cell’s metabolism. Therefore, H+ is snthesized within the cell.

A
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48
Q

What part of the stomach initiates peristalsis?

A

Antrum

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49
Q

TRUE/FALSE.

Food is released into the intestine intermittently.

A

TRUE.

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50
Q

What cells in the stomach protect the epithelium from the low pH? How?

A

Mucous neck cells. They do so by releasing HCO3- in mucous and produce the gastric mucosal barrier.

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51
Q

What drugs compromise the gastric mucosal barrier and how?

A

Corticosteroids - they decrease prostaglandins. This would decrease the function, health and integrity of cells by decreasing perfusion, leading to ulceration (decrease mucus production by mucous neck cells).

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52
Q

List the agonists of the gastric parietal cells and the cells that secrete them.

A

Histamine (paracrine) - ECL

Ach (neurocrine) - Post-ganglionic Vagal PSNS neuron

Gastrin (endocrine) - G cells

**Vagovagal reflex acts on G cells and ECL cell to increase gastrin and histamine secretion, respectively.

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53
Q

List the antagonists of the gastric parietal cells and the cells that secrete them.

A

Somatostatin - G cell

Prostaglandin

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54
Q

Where are G cells located and what do they secrete?

A

Antrum of the stomach

Gastrin

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55
Q

TRUE/FALSE.

Striated muscle is present in the esophagus meaning that some esophageal motility is voluntary.

A

FALSE.

Striated muscle is present, but it is still involuntary.

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56
Q

TRUE/FALSE.

Secreted volumes into the GI lumen are lost forever.

A

FALSE.

They are put there on loan.

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57
Q

List the ports of a parietal cell (Basolateral vs. Lumenal).

A

Basolateral:

  • Na/K ATPase
  • Na/K/2Cl- Symport
  • HCO3-/Cl- Antiport

Lumenal:

  • Na+/H+ Antiport
  • Cl- Port
  • Cl/K Symport
  • Cl-/HCO3 Antiport (bicarb out.. Why?)
  • K+/H+ ATPase
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58
Q

List the receptors found basolaterally on gastric parietal cells.

A

Gastrin (+)

Histamine (+)

M3 Ach (+)

Prostaglandin (-)

Somatostatin (-)

(+) = Excitatory

(-) = Inhibitory

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59
Q

Explain why overadministration of corticosteroids and/or NSAIDs would result in stomach ucleration.

A

Corticosteroids and NSAIDs inhibit the production of prostaglandins, which provide constituitive inhibition to parietal cell acid secretion. The stomach itself is not at fault, it is the removal of inhibition that causes the excess acid production that is damaging to the epithelium.

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60
Q

What are the different ways to block gastric HCl secretion? (Theoretical and actual)

A

-Block basolateral agonists - H2, gastrin, Ach, Ca2+
*Ca2+ is out of the question because it is very important.

  • Increase basolateral antagonist production (somatostatin/prostaglandin). These work all over and so there would be other issues associated with blocking them.
  • Block H/K ATPase at the lumenal membrane - this is good except now the secretion is neutral and allows bacterial overgrowth (Cl, K, Na, H2O would be the secretion)
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61
Q

What are some drugs involved in the decrease of gastric secretions?

A

Atropine - inhibits M3 (Ach). Also has CV implications given as a pre-surgery drug because it blocks PSNS at the heart.

Cimetidine - blocks H2 receptors (histamine)

Omeprazole - blocks H/K ATPase

Cimetidine < Omeprazole because other basolateral agonists can still work.

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62
Q

TRUE/FALSE.

Without the enzymes in the stomach, proper digestion cannot occur.

A

FALSE.

Their absence is unnoticeable.

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63
Q

What organs are important in the hydrolysis of food?

A

Pancreas & Small intestine. Their secretions contain hydrolytic enzymes.

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64
Q

TRUE/FALSE.

Liver secretions contains enzymes for the digestion of lipids.

A

TRUE.

It DOES NOT contain hydrolytic enzymes. Emulsification is its major digestive role.

65
Q

Where is peristalsis seen?

A

Anywhere in the tubular gut, including the antrum (it is also considered tubular gut).

66
Q

What is gastrin’s main purpose and what other cells does it act on?

A

Increased acid secretion.

It acts on visceral smooth muscle to increase motility of the stomach and close the LES/pyloric sphincters.

It is also stimulates blood vessels.

67
Q

TRUE/FALSE.

Antiperistalsis is a normal occurrence.

A

TRUE.

It occurs in the antrum if chunks are too pig.

Also at the pelvic flexure of equine large intestine.

It is a kind of size QC. It sends food back for further digestion.

68
Q

What is the small intestine’s first secretion to mechanical/chemical stimulus that food is there?

A

The low pH is not an ideal environment for digestive enzymes and so secretin is released in order to increase pH.

69
Q

Describe the strength of tight junctions throughout the intestin. That is, where is it tightest? Where is it leakiest?

A

Tight junctions in the intestine are similar to that of the kidney it that it goes from the leakiest at the beginning to tightest at the end. Therefore, the leakiest tight junctions are at the duodenum, while the tightest are at the large intestine.

70
Q

Where in the intestine is glucose absorbed? How is it absorbed?

A

Small intestine - duodenum (also similar to kidney in that it is the first segment).

Glucose gets absorbed through Na/glucose symports.

71
Q

Where in the intestine are lipids absorbed and why?

A

Jejunum/Ileum - it takes longer to digest them because they must be emulsified first to keep them apart.

72
Q

Where do symbiotic microbes exist in the ruminant vs. equine GI tracts? What is their significance?

A

Ruminants: Rumen

Equine: Large intestine

These microbe populations possess the enzymes necessary to breakdown cellulose to monomer.

73
Q

TRUE/FALSE.

There is anticipatory secretion of pancreatic and biliary exocrine products so that there are digestivce enzymes present when food arrives.

A

TRUE.

74
Q

What is the purpose of anticipatory insulin secretion?

A

To preven vast fluctuations in blood glucose levels.

75
Q

What cells are responseble for the HCO3-/Cl- exchange in order to alkalinize secretions?

A

Ductular cells (pancreatic and biliary)

76
Q

What are the main components in bile?

A

Waste - used as a detox route

Bile Acids/emulsifers in order to breakdown lipid.

77
Q

TRUE/FALSE.

The small intestine does not produce the hydrolytic enzymes found in its lumen.

A

TRUE.

78
Q

The small intestine ______ (increases/decreases) gastric emptying. Why?

A

Decreases.

Stimulation of the small intestine causes feedback inhibition. The pylorus closes, gastric motility decreases. This is because the intestine now needs time to do its job and digest the food.

79
Q

TRUE/FALSE.

All hormones produced by the stomach are polypeptides.

A

TRUE.

80
Q

What is the major stimulus for CCK release?

A

Fatty acid

81
Q

Where and why are osmoreceptors found in the GI tract?

A

They are found in the small intestine. This is because a lot of polymer is being broken down into monomer, which drastically increases the osmolarity. These osmoreceptors tell the small intestine to add H2O during these changes. (Maintains the integrity of epithelial cells?)

82
Q

What are incretins?

A

Hormones that greatly increase insulin and decrease glucagon. They are produced by the small intestine.

83
Q

TRUE/FALSE.

Protein hormones can be taken per os (orally).

A

FALSE.

They must be injected. This is because, they will be broken down into individual amino acid by hydrolytic enzymes and lose their function.

84
Q

TRUE/FALSE.

Steroid hormones can be taken per os.

A

TRUE.

These hormones can diffuse through the membranes of epithelial cells.

85
Q

What is the most important absorptive organ?

A

Small intestine

86
Q

Describe the organs in the aborption/digestion of carbohydrate, protein and lipid.

A

Carbohydrate & Protein:

Digestion: small intestine & Pancreas

Absorption: small intestine

Protein:

Digestion: bile + pancreas (NO SMALL INTESTINE)

Absorption: Small intestine

87
Q

For carbohydrate and lipid digestion, what enzymes start the work and which ones finish it?

A

Pancreatic enzymes start the work. They break down digested food to smaller pieces but NOT monomer.

Small intestine enzymes that are attached tot he villi finish the work and break down everything to monomer.

88
Q

Lipids are primarily consumed as ______.

A

Triacylglycerol

89
Q

TRUE/FALSE.

G cells are only found in the antrum of the stomach.

A

FALSE.

They are also found in the duodenal mucosa.

90
Q

What are the phases that result in changes in agonist/antagonist of the GI?

A

Cephalic phase

Gastric Phase

Intestinal phase

*Named based on where the stimuli is coming from.

91
Q

Once food has reached the lumen of the small intestine it is known as _____.

A

Chyme

92
Q

TRUE/FALSE.

The membrane of the lumen of the small intestine is lined with a brush border membrane.

A

TRUE.

This is to increase surface area and allow more enzymes to be in contact with the chyme.

93
Q

Carbohydrate is consumed as ______.
Give examples.

This is digested through enzymes called ______.

A

α-polymer

Glycogen (animals), Starch (plants)

α-amylase

94
Q

Carnivores lack the enzymes to break down ______, such as cellulose.

A

β-polymer

95
Q

Describe how α-amylase attackes α-polymer.

A

α-amylose cannot attack terminal bonds - it can only recognize a bond where there are glucoses on either side.

Therefore, you end up with dimers and trimers.

96
Q

TRUE/FALSE.

Once monomer of glucose is obtained, it can be absorbed through a glucose port.

A

FALSE.

Glucose will NOT get absorbed without SODIUM! Glucose is absorbed through a sodium/glucose symport.

97
Q

How did sodium get into the lumen of the small intestine?

A

It followd chloride paracellularly.

98
Q

TRUE/FALSE.

Galactose is so similar to glucose that it can get carried through Na/Glucose symporters.

A

TRUE.

99
Q

TRUE/FALSE.

Fructose is so similar to glucose that it can be carried through Na/Glucose symport.

A

FALSE.

Fructose has a separate carrier.

100
Q

What kinds of molecules do the enzymes in the small intestine membrane attack?

A

Oligosaccharides

For this reason, they are called oligosaccharidases.

101
Q

Amylase is in the bloodstream. How did it get there?
What can it be indicative of?

A

Amylase gets in the bloodstream when pancreatic cells die. Before it used by used an indicator for pancreatic damage but it may also be indicative of kidney disease.

102
Q

What is used to diagnose pancreatic damage?

A

Proteases and Lipases

103
Q

TRUE/FALSE.

There is a separate enzymes for each protein that is ingested.

A

FALSE.

There variety is too much.

104
Q

Describe the digestive attack on proteins.

A
  1. Proteases are secreted as their inactive form (if not, they will start digestion of the cell).
  2. Proteases cut similar proteins, produce oligopeptides (NOT ABSORBABLE).
  3. Oligopeptidases in the brush border membrane produce di/tripeptdies (ABSORBABLE)
  4. Absorption through Na/di-tripeptide symporters (individual Na/AA symporters also exist)
  5. When di/tri peptides are absorbed, there are intracellular enzymes (peptidases) to break them down into amino acids.
  6. Individual amino acids are placed into the blood stream
105
Q

The inactive form of a protease is known as a _______.

A

Zymogen

e.g. trypsin - derived from trypsinogen (inactive)

106
Q

Describe the cephalic phase.

A

This is when the Stimuli from the head (eyes, smell, taste, distension of the esophagus) & hypoglycemia, increase vagal efferent post-PSNS neurons to fire Ach.

Stimulate:

  • Parietal, peptic & mucus neck cells
  • Histamine-secreting cells

Inhibit:

Somatostatin δ cells - decreases somatostatin release

*Some neurons also secrete GRP, which acts on G cells to increase gastrin secretion.

107
Q

Describe the Gastric phase.

A

The most important stimuli in this phase is distension of the stomach. This causes initiation of the vagovagal reflex (stimulates the same thigs noted in the cephalic phase.

  • Amino acids & peptides in the lumen stimulate G cell secretion of gastrin
  • Low lumenal pH –> Increases somatostatin release by δ cells. This is feedback inhibitor of acid in the stomach to decrease HCl and Gastrin secretions.
108
Q

Describe the Intestinal phase.

A

This is mostly inhibitory.

  • The low pH that enters the intestinal lumen causes secretin secretion, which lowers the acid production in the stomach.
  • Fat digestion products, peptides and amino acids illicit the release of CCK from I cells, which decreases acid production and gastric emptying.
  • Gastrin release (from G cells in the duodenum) are stimulated by amino acids and peptides.
109
Q

What are the two major hormones that act on the liver to control its metabolism?

A

Insulin

Cortisol

110
Q

What is the major organ that stores glycogen? Who does it store it for?

A

Liver = ~7% of non-water weight

For other cells. Everyone synthesizes glycogen, the liver is the only organ to store it for others.

111
Q

Lipids are transported in the form of _____.

What are the different kinds?

A

lipoproteins

two kinds: chylomicrons and VLDL

112
Q

TRUE/FALSE.

Neurons perform glycogenesis.

A

FALSE.

Astrocytes do.

113
Q

What are the liver’s metabolic functions in regards to carbohydrate?

A
  1. Glycogenesis and glycogenolysis - intesnely regulated by insulin (genesis) and cortisol (lysis)
  2. Gluconeogensis - performs about 90% of it.
114
Q

What are the liver’s metabolic functions regarding lipid?

A
  1. β-oxidation of fatty acids - use it for energy. Obtain Acetyl Co-A and use it for gluconeogenesis.
  2. Fatty acid and triacylglycerol synthesis - will export it for storage.
  3. Lipoprotein synthesis and export - used for fatty acid export in order to safely mix with water.
  4. Ketone synthesis and export - ketones are valuable source (two acetyl Co-As stuck together). Longer fasting periods = ↑ ketone synthesis. Ketoacidosis? Feed the animal to get rid of it.
  5. Cholesterol synthesis and export - used as a precursor for steroid hormone synthesis. Therefore, a lot of cells need it and they depend on the liver to make it. Exported in lipoprotein.
  6. Conversion of carbohydrate and amino acid to triacylglycerol
115
Q

What are the metabolic functions of the liver in regards to protein?

A
  1. Deamination (especially when using a.a. to make glucose) and transamination
  2. Plasma protein synthesis (albumin, α, β globulins, coagulation factors, complement proteins, plasma antiproteases)
  3. NH3 uptake, urea synthesis and glutamine synthesis
116
Q

What substances, other than glycogen, does the liver store?

A

Vitamins: A, D, B12

Iron

117
Q

Describe the biotransformative function of the liver.

A

It transforms endogenous and exogenous substances into water-soluble derivatives, that are delivered to plasma for urinary excretion or to bile for fecal excretion.

Transforms things such as drugs, hormones, neurotransmitters because the message needs to get degraded.

118
Q

What are the two sources of blood supply to the liver?

A

Hepatic artery

Portal vein

119
Q

What orgains is the portal vein mainly draining?

A

Stomach, spleen, pancreas, small intestine, colon

120
Q

Why is it especially important that blood from the stomach goes straight to the liver in ruminant animals?

A

The ruminal epithelium is highly absorptive.

Microbes also have easy access to the bloodstream. For this reason, the liver is full of WBCs (kupffer cells)

121
Q

Who gets the highest concentration of glucagon and insulin?

A

LIVER

122
Q

What is the main reason that spleen venous drainage goes to the liver? Pancreas?

A

Due to the presence of bilirubin as a result of RBC breakdown.

Pancreas wants to tightly regulate liver metabolism. Insulin and glucagon can go straight there.

123
Q

Where do you expect to see the highest amount of ammonia?

A

Portal vein - it is a poison and the CNS depends on the liver to get rid of it.

124
Q

What is a portosystem shunt? Describe the two types.

A

When blood is able to to make it to bypass the liver and enter the caudal vena cava.

Extrahepatic shunt: outside the liver

Intrahepatic shunt: through the liver. e.g. ductus venosus you don’t want nutrients from the mother going to the liver. You want it going to the brain. If this does not close upon birth, then you have an intrahepatic shunt. You can also have blockage and you can inject with radioactive material to determine where.

125
Q

Describe the process of fat digestion and absorption.

A

Stomach: Warming and mixing results in liquid fat globules

Duodenum: bile causes emulsifed fat droplets

Jejunum: lipase, co-lipase and bile components lead to micelle formation. Diffusion into enterocytes.

Ileum: reabsorption of emulsifier molecules through Na/bie acid symports. 99% are reabsored.

126
Q

What are bile acids synthesized from?

A

Cholesterol - hydrocarbon and OH group make it optimal to begin the synthesis of a molecule that interacts with both hydrocarbons and water.

127
Q

What is the product of pancreatic enzyme attack on triacylglycerol?

A

2 fatty acids and a monoacylglycerol.

128
Q

What are the components of a mixed micelle?

A

phospholipids surround it

In the center are free fatty acids, fat soluble vitamins (A, D, E, K), cholesterol, monoacyl glycerol.

Sourrounded by bile acids (like a belt)

129
Q

How are bile acids absorbed once it has put into circulation?

A

Albumin binds to it and takes it to the liver.

The liver can’t take up everything on first pass so some are expected to be seen in circulation. However, if it there is liver damage, you expect to see more.

130
Q

What is the function of the large intestine?

A

Water and electrolyte reabsorption.

Only equine absorb organic material in the large intestine.

131
Q

The absorption of mixed micelles takes place in the _____. What process takes place?

A

Ileum and jejunum

Diffusion (at rates depending on the identity of the molecule; e.g. fatty acids are quick, cholesterol takes a little long).

132
Q

What occurs after lipid digestion products are reabsorbed?

A

Mostly in the jejunum, they are recombined with FFAs into the ingested form through ligases present in the smooth ER.

2 monoglycerol + FFA = Triacylglycerol

Lyso-phosopholipid + fatty acid = Phosopholipid

Cholesterol + FFA = Cholesterol ester.

Once they are reassembled, they are reassempled into lipoproteins (chylomicrons) and exocytosed into the interstitium.

133
Q

What happens to a chylomicron once it is exocytosed?

A

Since it cannot enter capillaries, it enters lymphatic vessels then travels to the heart, pulmonary arteries, and eventually to circulation. This is distinct from other molecules such as glucose, in that once glucose is absorbed, it goes to the liver. Chylomicrons bypass the liver.

134
Q

If chylomicrons are traveling in a form that cannot enter/exit capillaries or cell membranes, how does it get consumed? What control are they under?

A

There are enzymes found in capillary endothelium that attack the lipoprein in order to free lipid for further attack, until it can diffuse into cells.

These enzymes are controlled by insulin.

135
Q

What is going to be the primary source of energy during the absorptive state?

Post-absorptive state?

A

Glucose and amino acids

Lipids (used between meals) - except for the heart. The heart uses it all the time. Cardiac capillaries have the enzyme to breakdown chylomicron.

136
Q

How much energy can be obtained from lipid vs. glucose?

A

Lipid has 2-2.5x ATP/gram than glucose or amino acids.

137
Q

How does slentrol combat obesity?

A

It inhibits the production and export of chylomicrons.

138
Q

What would happen to lipid metabolism if the lymphatic system was obstructed?

A

Chylomicrons would not be reaching circulation. Eventually they would get backed up enough that lipid would not even be reassembled in mucosal cells. Accumulation in the lumen of the intestine will eventually lead to fatty feces.

Dilation of the lymphatic vessels may also be seen and fluid may leak into the lumen of the small intestine.

139
Q

What is the importance of anabolism?

A

Storage of molecules for later use. No animal is eating 24/7 and so you bring in all the nutrients you need over a 24 hour time period in 3 meals. You don’t consume all of it at that point, you save some for later. While fasting, the energy being consumed was what was stored.

140
Q

How much energy is obtained from protein in relation to carbohydrate?

A

The same

141
Q

What is done with excess carbohydrate?

Protein?

A

It is converted to fat for storage.

Protein IS NOT stored. If there is left over amino acid it will be converted to energy (few exceptions such as seeds). It is very energetically expensive to make protein and so excess amino acid is not converted to anything (also why protein is not typically broken down to amino acids for fuel.

142
Q

TRUE/FALSE.

Nucleic acids are catabolized for energy.

A

FALSE.

143
Q

What is fat?

A

Glycerol + 3 fatty acids.

144
Q

TRUE/FALSE.

An animal is NEVER just performing anabolism or catabolism.

A

TRUE.

145
Q

In the absorptive state, an animal is net ______, while in the post-absorptive state an animal is net ______.

A

Anabolic

Catabolic

146
Q

What happens to excess amino acid?

A

It is used for energy - demination needs to occur (ammonia) - liver gets rid of it.

147
Q

Where does excess carbohydrate get converted to lipid?

A

Liver

148
Q

What 6 things should you NEVER forget about insulin?

A

Insulin is anabolic AND anticatabolic for

Carbohydrate

Protein

Lipid

149
Q

TRUE/FALSE.

Insulin promotes oxidation of glucose and lipid. It also promotes the storage of excess protein.

A

FALSE.

It promotes the oxidation of glucose and amino acids. It stores excess carbohydrate and lipid.

150
Q

What is insulin’s philosophy?

A

Lower plasma glucose.

151
Q

Describe insulin and glucagon concentrations before and after a meal.

A

Before: glucagon is at its highest; insulin is at its lowest.

After: insulin is at its highest; glucagon is at its lowest.

152
Q

How do glucagon/insulin concentrations differ in a high protein diet?

A

Gluconeogenesis needs to occur

Increase glucagon, decreased insulin.

153
Q

TRUE/FALSE.

Protein does not stimulate the release of insulin.

A

TRUE.

Amino acids in the blood stream do.

154
Q

What is insulin’s response to increased amino acids in the bloodstream?

A

Increase Amino acid ports

Increase protein synthesis - promotes polymerization - NOT FOR STORAGE

155
Q

During a meal excess potassium is absorbed (because potassium is the highest intracellular electrolyte). What message does insulin send to maintain potassium homeostasis?

A

It tells skeletal muscle to take up excess potassium. Once insulin levels decrease, it may be released.

156
Q

SNS promotes the convertion of amino acids to ______.

A

Glucose.

157
Q

TRUE/FALSE.

Glucagon promotes the secretion of insulin. Insulin inhibits glucagon secretion.

A

TRUE.

158
Q

What are the most important organs/tissues from a metabolic standpoint?

A

Liver

Skeletal muscle

Adipose Tissue

159
Q

What cells put glucose into the bloodstream?

A

Hepatocytes

PCT

Small intestine

Physiology II (8 decks)

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