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Endocrinology > Digestive Endocrinology and Glucose Metabolism > Flashcards

Digestive Endocrinology and Glucose Metabolism Flashcards

1
Q

What do duct cells in the pancreas secrete?

What do acinar cells secrete in the pancreas?

What funtions are these a part of?

A

NaHCO2 solution

Digestive enzymes/pancreatic enzymes

Exocrine portion of the pancreas

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2
Q

Where is the location of the pancreas?

A

Location:

  1. retro-peritoneum*,
  2. 2nd lumbar vertebral level

Extends in an oblique, transverse position

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3
Q

What are the parts of the pancreas?

4

A

head
neck
body
tail

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4
Q

Embryology of pancreas:
Develops from the ventral and dorsal buds.

What does the ventral bud become?2

What does the dorsal bud become? 4

A

Ventral bud becomes the uncinate process and inferior head of pancreas

Dorsal bud becomes superior head, neck, body and tail

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5
Q

What happens when the ventral bud duct does not fuse with the dorsal bud duct?

A

Pancreas divisum when fails to fuse

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6
Q

Exocrine definition?

Endocrine definition?

A

Exocrine: secreting outwardly via a duct

Endocrine: secreting inwardly: applied to organs and structures whose function is to secrete into the blood or the lymph a hormone that has a specific effect on another organ or part

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7
Q

The head of the pancreas connects to the duodenum through what?

A

papilla/ampulla of vater

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8
Q

Islets of langerhan cells secrete hormones into where?

A

into the blood vessels

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9
Q

Alpha cells secrete what?
Beta cells secrete what?
Delta cells secrete what?
F cells (Gamma) secrete what?

A

– glucagon
– insulin
– somatostatin
– pancreatic polypeptide

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10
Q

What is the main action of alpha cells?

A

Release Glucagon; main action to produce an increase in blood glucose

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11
Q

Glucogon does what?
3

What do high levels activate?

A
  1. Breakdown of glycogen
  2. Stimulates gluconeogenesis (inhibits glycogenesis)
  3. Increases transport of AA into the liver and stimulates their conversion to glucose

High levels activate adipose cell lipase making fatty acids available for use as energy

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12
Q

Alpha cells release glucagon into what area of circulation?

This is in response to what?

Two things stimulate this. What are they?

A

portal circulation

low glucose levels in the blood

  1. high concentrations of AA
  2. strenuous exercise
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13
Q

Metabolic Effects of Glucagon:
Glucose levels?
Amino acid levels?
Ketoacids?

A

increase
decrease
increase

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14
Q

What causes stimulation of glucagon?

6

A
  1. Hypoglycemia
  2. Amino acids
  3. Gastrointestinal hormones
  4. Fasting
  5. Exercise
  6. Neural influences
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15
Q

What are the amino acids that stimulate glucagon?
2

What are the gastrointestinal hormones that stimulate glucagon?
2

What neural influences stimulate glucagon?
2

A

Arginine
Alanine

Cholecystokinin (CCK)
Gastrin

  1. Vagal activity-acetylcholine
  2. Sympathetic activity-
    β-adrenergic stimulation
    (norepinephrine, epinephrine)
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16
Q

What causes inhibition of the secretion of glucagon?

7

A
  1. Glucose
  2. Somatostatin

3, Insulin (direct effect)

  1. Gastrointestinal hormones
  2. Free fatty acids
  3. Ketoacids
  4. Neural influences
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17
Q

What gastrointestinal hormones inhibit glucagon?
2

Neural influences that inhibit secretion of glucagon? 1

A
  1. Secretin
  2. Glucagon-like peptide-1 (GLP-1)
  3. α-adrenergic stimulation
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18
Q

DPP-4 inhibitors cause lowering of blood glucose how?

2

A
  1. stimulates insulin release

2. inhibits glucagon release

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19
Q

Fuel Metabolism in Anabolic states:
Hormone changes? 2
Fuel Source?
Processes involved? 3

A

increased insulin
decrease glucagon

Diet

Glycogen synthesis
TG Synthesis
Protein synthesis

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20
Q

Fuel Metabolism in Catabolic States
Hormone changes? 2
Fuel Source?
Processes involved? 4

A

Decrease insulin
Increase glucagon

Storage deposits

Glycogenolysis
Lipolysis
Proteolysis
Ketogenesis

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21
Q

Metabolic Effects of Epinephrine:
Glucose?
Free fatty acids?
Ketoacids?

A

Increase in all

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22
Q
  1. Glucocorticoids and GH stimulate 1 and inhibit 1 what?

2. Insulin stimulates 1 and inhibits 1 what?

A
    • Stimulate glucose produciton
    • Inhibit Glucose consumption
    • Inhibits glucose produciton
    • Stimulates Glucose consumption (muscle and adipose tissue)
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23
Q

Glucagon and Epinephrine stimulate what?

A

Glucose produciton in the liver

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24
Q

How does insulin lower blood glucose?

6

A
  1. Promoting uptake of glucose by target cells
  2. Provides for glucose storage as glycogen
  3. Prevents fat & glycogen breakdown
  4. Inhibits gluconeogenesis and increases protein synthesis
  5. Promotes fat storage by increasing transport of glucose into fat cells
  6. Increases triglyceride synthesis
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25
Q

Beta cells produce what?

A

pro-insulin

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26
Q

What is proinsulin formed by?

How does proinsulin become active insulin?

A

an A-chain and B-chain separated by inactive C-peptide chain

C-peptide chain is cleaved by enzymes in the beta cells and packaged in secretory granules

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27
Q

2/3 of glucose is stored as what in the liver?

When is insulin released back into the blood?

A

glycogen

Released back into the blood to keep blood glucose at steady state after intake

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28
Q

WHat is the main regulator of insulin?

What does glucokinase do?

What does the result of glucokinase result in?

A

glucose

In pancreatic beta cell glucose transporters allow influx of glucose

Results in closure of K+ channels and opening of Ca+ channels allowing secretion of insulin by exocytosis

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29
Q

What causes the stimulaiton of insulin?

8

A
  1. Glucose
  2. Amino acids
  3. Free fatty acids
  4. Keto acids
  5. Glucagon (direct and indirect effects)
  6. Gastro-intestinal hormones
  7. Neural influences
  8. Sulfonylurea drugs
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30
Q

Stimulation of insulin secretion:

  1. Types of glucose? 2
  2. Types of AA? 4
  3. Types of gastrointestinal hormones?
  4. Types of neural influences?
A
  1. Mannose
    Galactose
  2. Arginine
    Lysine
    Leucine
    Alanine
  3. Glucagon-like peptide 1 (GLP-1)
    Gastric inhibitory polypeptide (GIP)
  4. Vagal activity (acetylcholine)
    β-adrenergic stimulation
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31
Q

What causes the inhibition of insulin?

5

A
  1. Somatostatin
  2. Fasting
  3. Exercise
  4. Neural influences
  5. Leptin
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32
Q

What are the neural influences that inhibit the secretion of insulin?

A

Sympathetic activity-

α-adrenergic stimulation (norepinephrine, epinephrine)

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33
Q

Insulin affects on carbohydrates:

What do carbohydrates from a meal release?

What does this stimulate?

A

Carbohydrates from a meal release glucose

Stimulates secretion of insulin

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34
Q

The secretion of insulin cause what?

Once liver has stored all the glycogen it can, insulin promotes what?

A

The uptake and storage of glucose in all tissue

conversion of glucose to fatty acids

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35
Q 
Metabolic Effects of Insulin:
Glucose?
Free fatty acid?
Ketoacids?
AA?
A

All decrease

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36
Q

Insulin increases what in the muscle?

5

A
  1. ↑ GLUT4 transporters
  2. ↑ Glycogen
  3. ↑ Glycolysis (glucose –> pyruvate)
  4. ↑ Protein synthesis, protein degradation
  5. ↑ Triglycerides (FA’s from circulation)
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37
Q

What does insulin increase in the liver?

7

A
  1. ↑ Glucokinase
  2. –↑ Glycogen
  3. ↑ Glycolysis
  4. —↑ acetyl CoA, 5. ↑ FA synthesis
  5. ↑ Triglyceride storage and export (VLDLs)
  6. ↑ Protein synthesis, protein degradation
38
Q

What does insulin decrease in the liver?

2

A
  1. Glucose release

2. –G6Pase

39
Q

Insulin on Fat Metabolism:
First insulin ____ the utilization of glucose (uptake) by most of the body’s tissues, which decreases utilization of fat.

Once liver glycogen is maxed all additional glucose forms ____?

Fatty acids in the liver form ______ which are released into the blood stream and are transported to adipose tissue

Once there, insulin activates ____ which splits the triglycerides into fatty acids again for them to be absorbed into the adipose cells

A

increases

fatty acids

triglycerides

lipoprotein lipase

40
Q

Insulin affects on Adipocytes?

What is increased 6 and what is decreased? 1

A
  1. ↑ GLUT4 transporters
  2. ↑ Glycolysis
  3. –↑ α-glycerol phosphate
  4. –↑ acetyl CoA, ↑ FA synthesis
  5. ↑ Triglycerides
  6. –decrease in Hormone sensitive lipase
  7. –↑ Lipoprotein lipase
41
Q

Insulin Effects on AAs?

What does it stimulate (1) and inhibit (2)?

A
  1. Stimulates transport of many AA into the cells
  2. Inhibits the catabolism of proteins especially in muscle cells
  3. In the liver depresses rate of gluconeogenesis
42
Q

Delta cells secrete what?

Which is turned into what? (2)

A

Secrete prosomatostatin that is processed to somatostatin-14 and somatostain-28

43
Q

What is the action of somatostatin? 4

What is its circulating half life?

A
  1. Inhibits secretion of growth hormone and thyro-tropin from pituitary
  2. Inhibits insulin and glucagon in the endocrine pancreas***
  3. Inhibits gastrin release and gastric acid secretion from parietal cells
  4. Inhibits exocrine secretion of pancreas***

3 minutes

44
Q

At what plasma glucose levels will the following occur:

  1. Decrease in insulin?
  2. Increase in glucagon?
  3. Increase in Epinephrine?
  4. Increase in cortisol and GH?
  5. Deccrease in brain glucose uptake?
  6. decreased cognition?
  7. Coma?
  8. Convulsions?
  9. Permanent brain damage?
A
  1. 80-85
  2. 65-70
  3. 65-70
  4. 65-70
  5. 65-70
  6. 45-50
  7. 30-35
  8. 20-25
  9. 10-15
45
Q

What is important to secrete bicarbonate for exocrine function of the pancreas?

A

carbonic anhydrase

46
Q

What are the two major components of the exocrine pancreas?

What is the funtional unit of the exocrine pancreas and what is it made of?

What is the second cell type in the acinus and what is it responsible for?

A

2 major components – acinar cells and ducts

20 to 40 acinar cells coalesce into a unit called the acinus

Centroacinar cell (2nd cell type in the acinus) is responsible for fluid and electrolyte secretion by the pancreas

47
Q

What is the ductular system?

Describe the path of exocrine secretions out of the pancreas. 4 steps.

What ducts and cells contribute the fluid and electrolyte secretion?
(2)

A

network of conduits that carry the exocrine secretions into the duodenum

Acinus → small intercalated ducts → interlobular duct → pancreatic duct

Interlobular ducts Centroacinar cells

48
Q

Digestive enzymes in that are secreted from the pancreatic acini are in what form?

In the intestinal lumen what form are these enzymes in?

What causes the conversion?

A

inactive form

active form

In the intestinal lumen glycoprotein peptidase***** activates trypsinogen then trypsin activates the other inactive proenzymes

49
Q

Trypsin and chymotrypsin split proteins into what?

Carboxypolypeptidase splits peptides into what?

Pancreatic amylase hydrolyzes glycogen and carbohydrates into what? 2

Lipase hydrolyzes fat into what? 2

Cholesterol esterase hydrolyzes what?

Phospholipase splits fatty acids from what?

A

peptides

some amino acids

disacharides and trisaccharides

fatty acids and monoglycerides

cholesterol esters

phospholipids

50
Q

What is secreted in large volumes by the small ductules leading frmo the acini?

What are these ductule cells stimulated by?

They then release large volumes of water and bicarb which makes the contents of the small intestine more what?

Why do we want this to happen?

A

Sodium bicarbonate

secretin released when acidic chyme enters the small inestine

Alkaline

so the pancreatic enzymes work better and more pancreatic enzymes flow out with the water and bicarb

51
Q

Combined enzymes and bicarb flow through _____ duct joins hepatic duct and empties into duodenum through papilla of Vater, surrounded by the Sphincter of Oddi.

A

pancreatic

52
Q

Regulation of Pancreatic Secretion

  1. Describe what is secreted and what that is controlled by from the acini in the Gastric phase and Cephalic phase of regulation of pancreatic secretion.
  2. Describe what is secreted and what that is controlled by from the acini in the Intestinal phase of regulation of pancreatic secretion.
    - what does this stimulate?
  3. What is secreted from the duodenal and upper jejunal mucosa when food enters it?
  4. What prevents activation of trypsinogen?
A
  1. Acetylcholine—from vagal nerve—moderate amounts enzymes secreted in acini (20%)—Gastric phase and Cephalic phase
  2. Secretin—from upper intestinal mucosa—stimulates release of water and bicarb from ductules so gets the enzymes out of the acini—Intestinal phase (alkaline pH)‏
  3. Cholecystokinin—from duodenal and upper jejunal mucosa—secreted when food enters—cause greater release of enzymes (80%)‏
  4. Trypsin inhibitor in acini prevents activation of trypsinogen
53
Q

Since trypsin activates other enzymes this prevents what?

A

enzymes from being activated and digesting pancreas

54
Q

Acid from the stomach releases ____ from the wall of the duodenum.

What causes the release of cholecystokinin?

Where are both of these enzymes absorbed into?

A

secretin

Fats and AA

blood stream

55
Q

What happens if the pancreas becomes damaged or the duct is blocked?

A

then secretions back up and overwhelm trypsin inhibitor and pancreatic secretions become activated and “digest” pancreas causing acute pancreatitis a very serious conditions

56
Q

Signs and Symptoms of Hypoglycemia

A 
Sweating
Palpitations
Tremor
Nervousness
Irritability
Paresthesias
Hunger
Nausea/vomiting
Headache
Tired and drowsy
Dizzy and fainting
Blurred vision
Confusion
Abnormal behavior
Seizures
Coma
57
Q

Hypoglycemia:

Sympathoadrenal symptoms? 5

Neuroglycopenic?
5

A
  1. Sweating, and warmth
  2. nausea, hunger
  3. Tremor
  4. palpitations,
  5. tachycardia
  6. Fatigue, headache, drowsiness
  7. Dizziness, visual disturbances
  8. Difficulty speaking, inability to concentrate
  9. Abnormal behavior, loss of memory, confusion
  10. Loss of consciousness, seizures
58
Q

Whipple’s Triad

ITS AN EMERGENCY

A
  1. Grouping of symptoms consistent with hypoglycemia
  2. Low plasma glucose (glucose (less than 55 mg/dL)‏
  3. Relief of symptoms by raising plasma glucose
59
Q

What is reactive hypoglycemia?

2

A

External influences

  1. severe exercise
  2. medication use
60
Q

What medications cause reactive hypoglycemia?

6

A
  • -Insulin (timing and dose)
  • -B-blockers
  • -Bactrim
  • -Haloperidol
  • -MAO inhibitors
  • -Sulfonylureas
61
Q

Causes of functional hypoglycemia?

5

A
  1. Hepatic and renal dysfunction
  2. Malnutrition
  3. Endocrinopathies
  4. Pancreatic tumors
  5. Alcohol consumption (inhibits gluconeogenesis)
62
Q

What are the different endocrinopathies that cause functional hypoglycemia?
4

A
  1. Adrenal (glucocorticoid) insufficiency
  2. Growth hormone deficiency
  3. Glucagon deficiency
  4. Pituitary disease (decreased corticotropin/GH)
63
Q

Fasting hypoglycemia is associated with symptoms what?

whereas postprandial hypoglycemia is more likely to produce what?

A

neuroglycopenia

adrenergic responses

64
Q

What are neuroglycopenia manifestations the result of?

And what are the symptoms?
6

A

decreased glucose supply to the central and peripheral nervous systems, including

  1. headaches,
  2. confusion,
  3. slurred speech,
  4. neuromuscular symptoms,
  5. seizures,
  6. coma
65
Q

What are adrenergic responses the result of?

And what are the symtpoms? 4

A

caused by an abrupt decrease in the glucose level and counter-regulatory release of epinephrine,

resulting in sudden onset of 1. hunger,

  1. diaphoresis,
  2. weakness,
  3. palpitation
66
Q

What is a posthypoglycemic coma?

How do we treat this?
3

A

Unconsciousness lasting more than 30 minutes after plasma glucose is corrected

  1. IV mannitol (40 g as a 20% solution over 20 minutes) or
  2. glucocorticoids (e.g., dexamethasone, 10 mg), or both can be used along with 3. maintenance of normal plasma glucose levels
67
Q

Hypoglycemia Unawareness.
1. Describe why this is a big problem?

  1. What is it usually associated with? 4
A
  1. 50% of type 1 patients undergo diminution in their epinephrine response to hypoglycemia
    Further patients lose the autonomic warning symptoms of hypoglycemia and may recognize (or even fail to recognize) the condition only when somatic neurologic function becomes impaired (neuroglycopenia)
  2. Usually associated with
    –duration of diabetes and
    –autonomic neuropathy
    May also occur when patients are switched to
    –intensive insulin regimens.
    –Beta blockers- can blunt cardiac response to hypoglycemia
68
Q

Hypoglycemia in insulin-treated diabetic patients is usually due to what? 3

What should we treat with? 2

If the pt cant ingest food?

In the hospital setting the standard treatment is what?

A
  1. omission of a meal while insulin was given,
  2. an error in medication, or 3. unpredictive absorption of food in a pt (gastroparesis)

responds well to

  1. oral glucose or
  2. carbohydrate-containing products.

glucagon given SC or IM may be given outside of the hospital setting.

  • IV glucose administration, which is followed by subsequent glucose infusion, feeding, or both.
  • 1 amp of D50 *****
69
Q

Fate of Absorbed Glucose
1st priority?
2nd priority?
3rd priority?

A

1st Priority: glycogen storage
Stored in muscle and liver

2nd Priority: provide energy
Oxidized to ATP

3rd Priority: stored as fat
Only excess glucose
Stored as triglycerides in adipose

70
Q

Glucose can be utilized how?

4

A

Adipose
Glycogen
Ribose-5-phosphate
Pyruvate

71
Q

Consequences of Insulin Deficiency-Diabetes Mellitus:

Metabolic consequences? 3

Fluid and Electrolyte? 7

A

Metabolic

  1. Increased blood glucose concentration
  2. Increased blood FFA and ketoacid concentration - fat depletion
  3. Increased blood amino acid concentration - protein depletion

Fluid and Electrolyte

  1. Metabolic acidosis - diabetic ketoacidosis
  2. Glycosuria and osmotic diuresis
  3. Increased osmolality
  4. Hyperphagia
  5. Polydipsea
  6. Hypovolemia and hypotension
  7. Coma and death
72
Q

For type 1 and 2 DM:

  1. Severity?
  2. Insulin dependancy?
  3. Oral hypoglycemics?
  4. Ketoacidosis?
  5. Onset of disease?
  6. Complications?
  7. Stability?
  8. Familly history?
  9. Insulin receptor defects?
A

Type 1:

  1. severe
  2. almost all
  3. few respond
  4. common
  5. rapid
  6. 90% in 20 yrs
  7. unstable
  8. common
  9. uncommon

Type 2:

  1. mild
  2. 25-30%
  3. 50% respond
  4. uncommon
  5. slow
  6. less common
  7. stable
  8. more common
  9. common
73
Q

Diabetic Ketoacidosis
is most commonly seen in what form of diabetes?

Describe the onset?

A

Most commonly seen in Type 1
Can happen with Type 2

Onset is hours to days

74
Q

Diabetic Ketoacidosis is
defined as being present with absolute or relative insulin deficiency when the following criteria are met:
3

A
  1. Blood glucose levels >250
  2. Ketosis – ketones in urine and blood
  3. Acidosis – pH
75
Q

Diabetic Ketoacidosis:
Associated metabolic and plasma abormalities?

6

A
  1. Dehydration
  2. Increased osmolality (15) – metabolic acidosis
  3. Increased serum amylase
  4. Elevated white count ( if infection is the culprit)
  5. Hypertriglyceridemia
76
Q

In ketoacidosis stress leads to what (2)?

A

increases in catecholamines and GH

77
Q

Increases in catecholamines and GH in ketoacidosis lead to what? 2

Which then causes what? 2

What three things can this cause?

A

increase in glucagon and decrease in insulin

Hyperglycemia and ketosis

Osmotic diuresis Dehydration Metabolic acidosis

78
Q

Diabetic Ketoacidosis
precipitating factors?
4

A
  1. Infection
  2. New onset of diabetes
  3. Insulin administration
  4. Stress
79
Q

Diabetic Ketoacidosis
symptoms?
7

A
  1. Nausea, vomiting
  2. Thirst, polydypsia
  3. Polyuria
  4. Abdominal pain
  5. Weakness
  6. Fatigue
  7. anorexia
80
Q

Diabetic Ketoacidosis
signs?
8

A
  1. Tachycardia
  2. Orthostatic hyptotension
  3. Poor skin turgor
  4. Dry skin and mucous membranes
  5. Kussmaul’s respirations
  6. Hypothermia
  7. Fruity breath (ketones)
  8. Altered mental status or coma
81
Q

What levels of ketones cause the pt to be:
Obtunded?
Stuperous?
Comatose?

A

321
343
369

82
Q

Diabetic Ketoacidosis
increases what?
2

Decreases what?

A
  1. Increased counter-regulatory hormones cause hyperglycemia
  2. Increased insulin deficiency
  3. Decreased peripheral glucose utilization
83
Q

Diabetic Ketoacidosis
Increased counter-regulatory hormones cause hyperglycemia. What are they?
4

A

Cortisol
Growth hormone
Glucogon
Epinephrine

84
Q

Does DKA cause hyper or hypo osmolality and what is this due to?

Osmotic diuresis leads to what?

How is potassium affected?
Serum Na?
Serum K?
Serum Bicarb? (why)

A

Hyperosmolality due to increased blood glucose levels.

Osmotic diuresis leads to dehydration.

Hyper osmol state leads to water shift and K+ from intracelluar to extracellular.

Serum Na+ is low to normal despite diuresis.

Serum K+ is normal or elevated (d/t intracellular fluid shift).

Metabolic acidosis from ketone production leads to marked decrease in serum bicarb.

85
Q

Diabetic Ketoacidosis
pathology?

Increased breakdown of fatty acid also leads what?

Whats the anion gap?

A

Body breaks down free fatty acids to try to utilize as energy, leading to production of ketones.

hyperTG

Anion gap = Na – (Cl + HCO3)

86
Q

What are the goals of therapy for DKA?

A

Restore circulatory volume

  • -NS or 1/2NS -depending on Na+ level
  • -10U IV bolus of regular insulin (then continuous drip at 6) must do it slowly
  • -Have to replace K because dilution of plasma with fluid administration will lower the K+
    • Bi carb replacement (only consider if a pH of 7)
87
Q

Hyperglycemic Hyperosmolar Nonketotic Syndrome occurs almost exclusively in what pts?
3

How is it distinguished from DKA?
3

A
  1. Occurs almost exclusively in Type 2
  2. Elderly and physically impaired
  3. Limited access to free water
  4. High hyperglycemia - >600
  5. Relative absence of acidosis and ketones
  6. Greater degree of dehydration
88
Q

Signs and symptoms leading to Hyperglycemic Hyperosmolar Nonketotic Syndrome:

Severe dehydration?
2

Neuro signs?
4

A

Severe dehydration

  1. Dry skin and mucous membranes
  2. Extreme thirst
Neuro signs:
1. Lethargy to coma
2. Sensory impairment
3. Seizures
4. Hyperthermia
(could be mistaken for a stroke)
89
Q

Hyperglycemic Hyperosmolar Nonketotic Syndrome lab findings?

7

A
  1. Blood glucose > 600
  2. Serum osmolality >320
  3. Serum Na+ - normal to high (135-145)
  4. Serum K+ - normal (4-5)
  5. Serum Bicarb - >15
  6. pH > 7.3
  7. Ketones – negative
90
Q

Treatment of Hyperglycemic Hyperosmolar Nonketotic Syndrome?

3

A

Treatment:

  1. IV fluid replacement
  2. Insulin replacement starts after rehydration is in progress
  3. Heparin 5000U SQ BID
    - -Prophylaxis d/t predisposition to vascular thrombosis from hyperosmol state.
91
Q

Whats different about the volume replacement needed in HHNS than DKA?

A
  1. Slower rate than DKA
  2. Greater volume needed
    –Rehydrate over 36 – 72hrs
    Patients are usually older and have co morbidities

More sensitive to insulin so may need lower doses

Endocrinology (23 decks)

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