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Organ Systems Exam 4 > Chamberlin's Study Guide > Flashcards

Chamberlin's Study Guide Flashcards

0
Q

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

A

Blood glucose levels would rise. A new set point (higher one) will be established.

(Glucose Regulation - slide 4)

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1
Q

What is the relationship between glucagon and insulin?

A

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

(Glucose Regulation - slide 3)

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2
Q

How are decreased insulin levels and insulin resistance related?

A

End up doing the same thing (blood glucose levels rise)

Glucose Regulation - slide 4

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3
Q

What organ has both endocrine & exocrine function?

A

pancreas

Glucose Regulation - slide 6

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4
Q

Which cells produce insulin, which produce glucagon, which produce somatostatin?

A

Insulin - beta cells
Glucagon - alpha cells
Somatostatin - delta cells

(Glucose Regulation - slide 6)

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5
Q

What is the difference between D cells and delta cells?

A

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

(Glucose Regulation - slide 6)

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6
Q

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

A

Glycogenolysis & gluconeogenesis

Glucose Regulation - slide 8

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7
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

(Glucose Regulation - slide 15)

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8
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.

(Glucose Regulation - slide 15)

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9
Q

What is paracrine secretion?

A

Secretion into the local area only

Glucose Regulation - slide 15

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10
Q

Which pancreatic hormone utilizes paracrine secretion?

A

Somatostatin

Glucose Regulation - slide 15

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11
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

(Glucose Regulation - slide 15)

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12
Q

Why is calming things down important (in regards to somatostatin release)?

A

So you don’t exhaust nutrients too quickly

Glucose Regulation - slide 15

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13
Q

What stimulates somatostatin’s release?

A

Glucagon, insulin, & AA

Glucose Regulation - slide 15

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14
Q

What is the most effective most immediate treatment for hypoglycemia?

A

Glucagon

Glucose Regulation - slide 16

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15
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

(Glucose Regulation - slide 16)

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16
Q

What does insulin do?

A
  1. Glucose uptake into cells
  2. Protein, fat, & glycogen synthesis
  3. Growth & gene expression
  4. Satiety signal

(Glucose Regulation - slide 9)

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17
Q

What is the function of the IRS?

A

It’s the receptor that insulin binds to, and subsequently causes glucose channels to increase in number on the cell membrane thus increasing glucose uptake into the cell.

(Glucose Regulation - slide 10)

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18
Q

What does the insulin receptor trigger?

A

Translocation of GLUT-4 glucose transporter into cell membrane to facilitate glucose absorption

(Glucose Regulation - slide 10)

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19
Q

What are the old antiquated classifications of diabetes?

A

Insulin & non-insulin dependent

Glucose Regulation - slide 17

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20
Q

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

A

Eventually most non-insulin dependent diabetics will require insulin.

(Glucose Regulation - slide 17)

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21
Q

How do the autoimmune processes of type I & type II DM differ?

A

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

(Glucose Regulation - slide 17)

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22
Q

If the body chooses to store glucose, what are the 2 primary forms that it is stored as?

A

Glycogen & TG

Glucose Regulation - slide 11

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23
Q

Where is glycogen normally stored?

A

Liver & muscle

Glucose Regulation - slide 11

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24
Q

Where are TG normally stored?

A

adipose tissue

Glucose Regulation - slide 11

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25
Q

Do myocytes normally store fat for later use as energy?

A

No, they store glycogen

Glucose Regulation - slide 11

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26
Q

Does insulin cause lipogenesis or lipolysis?

A

Insulin promotes lipogenesis (TG formation & storage) in adipose tissue & liver (it inhibits lipolysis of TG).

(Glucose Regulation - slide 11)

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27
Q

Where are GLUT-2 receptors found?

A

Beta-cells in the pancreas

Glucose Regulation - slide 12

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28
Q

What is the effect of GLUT-2 receptors on beta cells becoming activated?

A

Insulin is released from the pancreas

Glucose Regulation - slide 12

29
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

(Glucose Regulation - slide 12)

30
Q

In what phase does parasympathetic activity stimulate beta cells?

A

cephalic phase

Glucose Regulation - slide 20

31
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

(Glucose Regulation - slide 22)

32
Q

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

A

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

(Glucose Regulation - slide 22)

33
Q

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

A

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).

(Glucose Regulation - slide 21)

34
Q

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

A

Iron - duodenum
B12 - terminal ileum

(Intestinal Secretion - Slide 4)

35
Q

Where are other nutrients absorbed?

A

Water Soluble Vitamins (except B12) = Mainly Jejunum (Slide 6)
Fat Soluble Vitamins w/dietary fats = most of small intestine (Slide 7)
Electrolytes/Water = small & large intestine (Slide 8)

For list of specific nutrients and their order of absorption look at: Intestinal Secretion - Slide 4

36
Q

Do fat soluble vitamins avoid the first pass effect? And what is the first pass effect?

A

Yes, this is when substances with a high fat content avoid being degraded by the liver by bypassing it & going to the peripheral tissues first.

(Intestinal Secretion - Slide 7)

37
Q

Where does intestinal absorption occur?

Where does intestinal secretion occur?

A

Absorption - enterocytes
Secretion - crypts of Lieberkuhn

(Intestinal Secretion - Slide 8)

38
Q

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

A

stomach - 2L
GI system - 9L

(Intestinal Secretion - Slide 9)

39
Q

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

A

Sml intestine - absorbs K+
Lrg intestine - secretes K+

(Intestinal Secretion - Slide 9)

40
Q

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

A

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

(Intestinal Secretion - Slide 10)

41
Q

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

A

Na follows Cl movement and water follows both.
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+.

(Intestinal Secretion - Slide 11)

42
Q

In the jejunum, what is co-transported with glucose?

A

Na+
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+

(Intestinal Secretion - Slide 11)

43
Q

In the ileum and large intestine what is absorbed Na exchanged for and what buffers this system in the lumen?

A

Absorbed Na is exchanged for secreted H. In the lumen H is buffered by HCO3-

(Intestinal Secretion - Slide 11)

44
Q

In the duodenum & jejunum, how is Cl- absorbed?

A

Cl- just diffuses into or around the cells & is absorbed.

Intestinal Secretion - Slide 12

45
Q

In the ileum & colon how is Cl- absorbed?

A

Cl- has a special pump, where it is absorbed via an exchange with HCO3-.

(Intestinal Secretion - Slide 12)

46
Q

True/False. The pump that absorbs Cl- in the ileum & colon via an exchange with HCO3- is the same as the CFTR pump.

A

FALSE!

(HE WROTE THIS IN ALL CAPS, AND SO WILL I)

(Intestinal Secretion - Slide 12)

47
Q

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

A

Absorbed - diffusion through gap junctions
Secreted into a lumen - has to use CFTR

(Intestinal Secretion - Slide 17)

48
Q

What is does CFTR mean?

A

cystic fibrosis transmembrane regulator

Intestinal Secretion - Slide 17

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/day
reabsorbed - 8900 ml/day

(Intestinal Secretion - Slide 15)

50
Q

How much water is lost a day?

A

100 ml

Intestinal Secretion - Slide 15

51
Q

Why is secretory diarrhea so deadly?

A

It causes the CFTR to endlessly secrete Cl- (& water) and it does so down low below the duodenum & jejunum where water could be normally reabsorbed.
You would lose liters & liters of water/day versus 100 ml.

(Intestinal Secretion - Slide 18)

52
Q

How does secretory diarrhea differ from osmotic diarrhea?

A

Osmotic diarrhea does not involved the CFTR, but is a water drag situation where the overall water loss is much smaller.

(Intestinal Secretion - Slide 18)

53
Q

How can losing just 2 BMI points lead to a vast change in heath?

A

Visceral fat ‘dissolves’ first, lessening intra-abdominal mass effects (i.e. hiatal hernia), and may decrease the likelihood of an autoimmune reaction in the peripheral fat.

(Adiposity - Slide 4)

54
Q

How does fat storage differ in men & women?

A

Men tend to store visceral fat first, women peripheral fat first

(Adiposity - Slide 4)

55
Q

One of two theories about the development of type II DM involves inflammatory cytokines damaging peripheral fat cell receptors.
Which cytokines are thought to cause this damage?

A

TNF, IL-6, FFAs (free fatty acids)

Adiposity - Slide 10

56
Q

What receptors are the inflammatory cytokines damaging on the peripheral fat cells in type II DM?

A

IRS

Adiposity - Slide 11

57
Q

What is the consequence of damaging the IRS?

A

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

(Adiposity - Slide 11)

58
Q

Why are these IRS damaging cytokines thought to be released?

A

Because of an immune reaction occurring between visceral fat and bacterial agents in the GI system.

(Adiposity - Slide 11)

59
Q

Describe the process of TNF (tumor necrosis factor) causing insulin resistance in other tissues (i.e. subcutaneous fat & muscle).

A

TNF is secreted from visceral fat. It interferes with IRS protein in cell signaling of GLUT-4 translocation. This reduces the release of adiponectin (usually secreted w/subcutaneous fat), which normally inhibits insulin resistance & inflammation.

(Adiposity - Slide 13)

60
Q

What is the mechanism responsible for atherosclerosis that is similar to the one for type II DM, but has nothing to do with it?

A

Cytokines (adipokines) attack the coronary arteries instead of the IRS and cause atherosclerosis.

(Adiposity - Slide 14)

61
Q

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

A

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

(Appetite Regulation - Slide 15)

62
Q

How does this homeostasis (balancing of energy intake & expenditure) occur?

A

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

(Appetite Regulation - Slide 15)

63
Q

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

A

Homeostatic - result of feedback regulation from the internal milieu (adipose, intestines, pancreas, etc) on hypothalamic/brain stem actions on eating.

Non-homeostatic - involves cognition, motivation, drive, stress (i.e. limbic’s system’s processing of environment, early life events, predispositions, etc).

(Appetite Regulation - Slide 16)

64
Q

How does the ileal brake work?

A

Ileal brake is the reduction of GI motility. It happens by a satiety peptide acting on the anorexigenic hypothalmic pathway to stimulate insulin release (parasympathetic) and inhibit glucagon release/GI motility/Secretion.

(Appetite Regulation - Slide 30)

65
Q

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

A

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

(Appetite Regulation - Slide 30)

66
Q

What are the basic gastric cells types and what are their functions?

A

Mucus Cells: secrete mucus & bicarb
Parietal Cells: secrete HCl, intrinsic factor (IF)
Peptic (Chief) Cells: secrete pepsinogen, gastric lipase
Enterochromatffin-like Cell: secretes histamine
G cells: secretes gastrin
D cells: secretes somatostatin

(Salivary & Gastric Secretion - Slide 18, 19)

67
Q

What stimulates the production of HCl?

A

Peptides stimulate gastrin release, which stimulates acid secretion. Vagus nerve stimulates acid secretion and inhibits somatostatin release

(Salivary & Gastric Secretion - Slide 22)

68
Q

What inhibits HCl production?

A

Acid stimulates somatostatin (SS) release which inhibits gastrin release

(Salivary & Gastric Secretion - Slide 22)

69
Q

Where is vitamin B12 absorbed and what are the steps required to absorb it?

A 
Terminal ileum (from later lecture), but it depends on secretion of IF from gastric parietal cells & uptake by ileal cells. 
Steps Required: dissociation from R-proteins by pepsin, binding with IF, and absorption by ileal cells & transport into portal vein.

(Salivary & Gastric Secretion - Slide 23)
(Intestinal Secretion - Slide 4)

70
Q

What is the function of mucus? And what is its pathway of secretion chemically?

A

Protection from HCl
Ach -> G cells -> Gastrin -> Parietal cells -> HCl -> Goblet cells -> mucus -> HCO3

(Salivary & Gastric Secretion - Slide 31)

71
Q

Why is an acidic environment necessary to begin the digestion of proteins? What is the overall chemical pathway to stimulate protein digestion?

A

Because acid secreted into the stomach converts pepsinogen to pepsin (protease), which is the main enzyme that breaks down proteins.
Ach -> G cells -> Gastrin -> Parietal cells -> HCl - > Pepsinogen -> Pepsin -> Protein

(Salivary & Gastric Secretion - Slide 28, 32)

Organ Systems Exam 4 (2 decks)

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