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Organ systems Exam 4 > GI- hormonal regulation, Dr. Chamberlain > Flashcards

GI- hormonal regulation, Dr. Chamberlain Flashcards

1
Q

What is the relationship between glucagon and insulin?

A

When one goes up, the other one goes down, and a set point is reached between 70-110 mg/dl.

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2
Q

If there were a reduction in insulin levels across all levels of blood glucose levels, how would this change the glucose set point?

A

Blood glucose levels would rise. A new set point–a higher one will be established.

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3
Q

How are decreased insulin levels and insulin resistance related?

A

Either end up doing the same thing, blood glucose levels rise.

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4
Q

What organ has both endocrine and exocrine function?

A

Pancreas

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5
Q

What cells produce insulin?

A

insulin from beta cells

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6
Q

Which cells produce glucagon?

A

Glucagon from alpha cells

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7
Q

Which cells produce somatostatin?

A

Somatostatin from delta cells

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8
Q

What is the different between D cells and delta cells?

A

D cells are found in the stomach, delta cells are found in the pancreas, both secrete somatostatin into the blood stream.

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9
Q

What are the two mechanisms glucagon employs to increase blood glucose?

A

Glycogenolysis and gluconeogenesis

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10
Q

What stimulates glucagon secretion and what inhibits it?

A

Stimulated by: low glucose, amino acids, ACh, Epi, NE

Inhibited by: high glucose, insulin, fatty acids

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11
Q

Why does activation of the sympathetic nervous system stimulate glucagon release?

A

you need to put as much immediately usable fuel into the circulatory system to provide for the needs of the muscles that will be fleeing or fighting soon.

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12
Q

What is paracrine secretion?

A

secretion into a local area

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13
Q

What pancreatic hormone utilizes paracrine secretion?

A

somatostatin

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14
Q

What is the purpose of somatostatin?

A

To down regulate both insulin and glucagon secretion so that levels of both don’t get out of control.

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15
Q

Why is calming things down important? (re: somatostatin)

A

so you don’t exhaust nutrients quickly

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16
Q

What stimulates somatostatin release?

A

Glucagon, insulin, and AA.

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17
Q

What is the most effective most immediate treatment for hypoglycemia?

A

Glucagon

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18
Q

Why does glucagon reduce the uptake of glucose into adipose cells?

A

its action is to keep as much glucose as possible in the circulatory system

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19
Q

What does insulin do?

A
  • glucose uptake into cells
  • protein, fat, and glycogen synthesis
  • growth and gene expression
  • satiety signal
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20
Q

What is the function of the IRS (insulin receptor substrates)?

A

it is the receptor that insulin binds to, and subsequently causes glucose channels to increase in number on the cell membrane thus increasing glucose uptake into cells.

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21
Q

What does the insulin receptor trigger?

A

Insulin receptor triggers translocation of the GLUT-4 glucose transporter into cell membrane to facilitate glucose absorption.

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22
Q

What are the old antiquated classifications of diabetes?

A

Insulin and non-insulin dependent diabetes

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23
Q

Why was it important to change the old classification of diabetes?

A

Eventually most non-insulin dependent diabetics will require insulin, so then what could you even call those patients.

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24
Q

How do the autoimmune processes of Type I and Type II diabetes differ?

A

Type I involves the destruction of the beta cells in the pancreas
Type II: the alteration of IRS and/or GLUT-4 receptors in the target adipose tissue

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25
Q

If the body chooses to store glucose, what are the two primary forms that it is stored as?

A

Glycogen and Triglycerides

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26
Q

What is glycogen normally stored?

A

Liver and Muscle

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27
Q

Where are TG normally stored?

A

adipose tissue

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28
Q

Do myocytes normally store fat for later use as energy?

A

no, they store glycogen

29
Q

Does insulin cause lipogenesis or lypolysis?

A

In adipose tissue and liver, insulin promotes lipogenesis (TG formation and storage) and inhibits lipolysis of TG.

30
Q

Where are GLUT-2 receptors found?

A

beta cells in the pancreas

31
Q

What is the effect of GLUT-2 activation?

A

Insulin is released from the pancreas

32
Q

Does insulin travel through the pancreatic duct to the duodenum?

A

No, just the exocrine products (lipase, HCO- ) hormones are secreted in the vascular system

33
Q

In what phase does parasympathetic activity (ACh) stimulate beta cells?

A

Cephalic phase

34
Q

What is the ultimate function of the interaction between glucagon and insulin?

A

To keep blood glucose levels into a very narrow range during fasting.

35
Q

When a person gets hypoglycemia, why does then sympathetic nervous system activate?

A

To keep the person conscious as the brain relies on glucose alone for energy and on a second to second basis.

36
Q

If stress is causing continuous sympathetic activation, what will happen to the equilibrium point of glucose?

A

The ANS will cause constant glucagon release and the point will shift upward to result in a higher concentration of fasting glucose levels (stress can lead to diabetes in this way).

37
Q

Iron and B12 are both absorbed in specific locations, what are they?

A

Duodenum and terminal ileum

38
Q

Do fat soluble vitamins avoid the first pas effect?

A

yes

39
Q

What is the first pass effect?

A

This is when substances with a high fat content avoid being degraded by the liver by bypassing it and going to the peripheral tissue first.

40
Q

Where does intestinal absorption occur?

A

absorption occurs by enterocytes on the villi

41
Q

Where does intestinal secretion occur?

A

secretion by enterocytes within the crypts of Lieberkuhn

42
Q

Daily secretion and absorption of fluid are massive. About how much fluid is secreted a day by the stomach alone?

A

2L

43
Q

Daily secretion and absorption of fluid are massive. About how much fluid is secreted a day by the entire GI system?

A

about 9 L

44
Q

Both small and large intestine absorb water, but do entirely different things from K+, what are they?

A

The small intestine absorbs K+, the large intestine secretes it.

45
Q

Why does most NaCl and water absorption occur in the duodenum and jejunum and less absorbed in the ileum and colon?

A

Because the tight junctions in the duodenum and jejunum are more permeable to water and solutes than in the ileum and colon.

Na+ follows Cl- movement and water follow both

46
Q

If by controlling Cl- and thus controlling Na+, how does controlling just one molecule control all other things?

A

Mechanisms have developed so that every time a Na+ enters a cell it drags a glucose with it and at the same time expels a H+

47
Q

Describe chloride absorption in the duodenum & jejunum vs. ileum and colon

A

In the duodenum and jejunum, Cl- just diffuses into or around the cells and is absorbed.

In the ileum and colon, it has a special pump where Cl- is absorbed via an exchange with HCO3- (this is not the same as the CFTR pump)

48
Q

What is the difference between the way Cl- is absorbed and secreted?

A

It is absorbed by diffusion through gap junctions. When it needs to be secreted into lumen it has to use a CFTR. (cystic fibrosis transmembrane regulator)

49
Q

About how much water is secreted into the intestine and how much is reabsorbed in a 24 hour period?

A

secreted: 9000 ml
absorbed: 8900 ml

50
Q

About how much water is lost by the intestines in a day?

A

100 ml

51
Q

Why is secretory diarrhea so deadly?

A

it causes the CFTR to endlessly secrete Cl- ( and thus water) and it does so don low below the duodenum and jejunum where water could be normally reabsorbed. In this way you no longer loose 100 ml a day, but liters and liters.

52
Q

How does secretory diarrhea differ from osmotic diarrhea?

A

Osmotic diarrhea does not involve the CFTR but is rather a “water drag” situation” where the overall water losses are much much smaller.

53
Q

How can loosing just 2 BMI points lead to a vast change in health?

A

The visceral fat “dissolves” first lessening intrabdominal mass effects (causing hiatal hernia for instance), and may decrease the likelihood of an autoimmune reaction in the peripheral fat (decrease of metabolic risk factors)

54
Q

How does fat storage differ in men and women?

A

men tend to store visceral fat first, women peripheral fat first.

55
Q

One of two theories about the development of type II diabetes involves inflammatory cytokines damaging peripheral fat cell receptors.

Which cytokines are thought to cause the damage?

and which receptors are the cytokines damaging?

A

Tumor Necrosis factor (TNF)
Interleukin-6 (IL-6)
….also excess free fatty acids (FFAs)

damage to insulin receptor (IRS)

56
Q

What is the consequence of damaging the IRS?

A

GLUT-4 receptors cannot translocate to the cell wall and thus the adipocyte cannot uptake glucose.

57
Q

Why are these IRS damaging cytokines thought to be released?

A

because of an immune reaction occurring between visceral fat (bacteria, LPS) and bacterial agents in the GI system. (generate local release of TNF)

58
Q

A similar mechanism can be responsible for atherosclerosis and has nothing to do with type II diabetes. What is this mechanism?

A

In a similar way cytokines (adipokines) attack the coronary arteries instead of the IRS and cause atherosclerosis.

59
Q

How is the amount of fat a person has normally determined?

A

Body weight (adiposity) is normally stabilized by balancing energy intake and energy expenditure (homeostasis).

60
Q

How does this homeostasis occur?

A

Neural and endocrine afferent pathways provide feedback for regulating neural behavioral aspects of eating.

61
Q

What is the difference between homeostatic and non-homeostatic regulation of energy uptake?

A

Non-homeostatic regulation of energy involves recognition, motivation, drive, stress, i.e. the limbic system’s processing of environment, early life events, predispostions, etc.

-eating is not based on how low glucose levels (energy deficit) but on appetite/hunger. Meals are based on habit, time of day, stress, i.e. factors unrelated to energy needs.

62
Q

How does the ileal brake work?

A

GLP-1 (glucagon like peptide) is released from the ileum (and colon), and acts on the anorexigenic hypothalamic pathway to stimulate insulin release (PS) and inhibit glucagon release, GI motility and secretion (ileal brake).

Peptide YY (PYY) also released from ileum and colon can reduce GI motility (ileal brake)

63
Q

How can the ileal brake be used clinically for weight loss?

A

Slower eating permits activation of satiety signals to reduce meal size.

64
Q

What are the basic gastric cell types and their functions?

A

There are two types of glands, oxyntic and pyloric, located in the stomach, each with a different complement of cells listed below.

Oxyntic gland in the body and fundus.

  • mucus cells/goblet cells
  • parietal cells–> HCl
  • peptic (chief) cells–> pepsin(ogen)
  • enterochromaffi n-like cell (a type of enteroendocrine cell)–> secrete histamine–> acid

Plyoric gland:

  • mucus cell/goblet cells
  • G-cells–> gastrin –> acid
65
Q

What stimulates the production of HCl?

A

peptides stimulate gastric release, which stimulate acid secretion. Vagus nerve stimulates acid secretion and inhibits somatostatin release.

66
Q

What inhibits HCl production?

A

Acid stimulates somatostatin (SS) release which inhibits gastrin release.

67
Q

Where is vitamin B12 absorbed?

A

depends on the secretion of intrinsic factor from gastric parietal cells and uptake by ilieal cells.

Normally: Ileum

if decreased parietal activity then decreased absorption of B12 via Intrinsic factor (IF) and diminished release of acid.

68
Q

What is the function of gastric mucus?

A

All areas of the stomach secrete mucus because all areas of the stomach need protection from HCl.

Ach–> G-cells –> gastrin –> parietal cells –> HCl –>Goblet cells –> mucus –> HCO3

69
Q

Why is an acid environment necessary to begin the digestion of proteins?

A

Acid initiates protein digestion in the stomach by converting pepsinogen to pepsin, a protease.

Organ systems Exam 4 (1 decks)

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