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Endocrine 2 > Glucose Metab and Digestive Endocrinology > Flashcards

Glucose Metab and Digestive Endocrinology Flashcards

1
Q

What is the difference between the endocrine and exocrine functions of the pancreas?

A
  • Exocrine: secreting outwardly via a duct. (i.e- pancreatic duct)
  • Endocrine: secreting inwardly; applied to organs and structures who’s function is to secrete hormones into the blood or lymph that has a specific effect on another organ or part.
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2
Q

What are the cells of the pancreas?

What % of pancreas is endorcrine?

A

-acinar cells secrete enzymes into the pancreatic duct.

  • Islets of Langerhan cells secrete hormones into the blood vessels.
  • made up of alpha (glucagon), beta(insulin), gamma(secrete pancreatic peptide) and delta cells(somatostatin)
  • beta, alpha, delta = layers of islet of langerhan cells, innermost to outermost.
  • 2% of pancreatic mass.
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3
Q

Glucagon:

  • secreted by what cells?
  • function
  • what happens when there is low glucose in the blood?
A
  • alpha cells
    function: produce an increase in blood glucose by creating glucose from glycogen via gluconeogensis.

Low glucose:
-Glucagon is released into portal circulation stimulated by low blood glucose or during strenuous exercise to prevent low BS. Glucagon initiates glycogenolysis (break down of glycogen in the liver to glucose). Glucagon also increases transport of AA into the liver and stimulates their conversion into glucose(gluconeogenesis).

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4
Q

What are some factors that stimulate glucagon secretion? Inhibit?

A

Stimulate:

  • Hypoglycemia
  • AA (arginine & alanine)
  • GI Hormones (CCK & Gastrin)
  • Fasting
  • Exercise
  • Neural influences (vagal activity-ACH, sympathetic activity; beta adrenergic-E and NE)

Inhibit:

  • Glucose
  • Somatostatin
  • Insulin
  • GI Hormones (Secretin, Glucagon Like Peptide-1)
  • Free Fatty Acids
  • Ketoacids
  • Neural influences (alpha adrenergic)
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5
Q

What is DPP? What is it used for?

What is Incretin? What is it used for?

A

Dipeptidyl Peptidase; essential for glucose production

Incretin is a hormone, inhibits glucagon and stimulates insulin release.

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6
Q

What is occurring metabolically during anabolism and catabolism in regards to:

  • Hormones insulin and glucagon
  • Fuel source
  • Metabolic Process
A

Anabolism:

  • Hormones: Insulin increases and glucagon decreases.
  • Fuel Source: diet
  • Metabolic Process: Glycogen synthesis (insulin is pushing glucose into liver and producing glycogen). Triglyceride synthesis and Protein synthesis.

Catabolism:

  • Hormones: decreased insulin and increased glucagon
  • Fuel source: storage deposits
  • metabolic process: Glycogenolysis, lipolysis, proteolysis, ketogenesis
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7
Q

Metabolic Effects of Epinepherine

A

During periods of stress E is released from adrenal medulla causing glycogenolysis in the liver, thus causing large quantities of glucose to be released into the blood. It also inhibits insulin release from the beta cells and thereby decreases the movement of glucose into the muscle cells, while at the same time increasing the breakdown of muscle glycogen stores. Glucose released from muscle glycogen cannot be released into the blood, the mobilization of these stores for muscle use conserves blood glucose for use by other tissues such as brain and nervous system.

E also has effects on adipose tissue, increasing the mobilization of fatty acids for use as an energy source.

pg 1307 porth.

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8
Q

How does blood glucose affect growth hormone?

A
  • growth hormone is inhibited by insulin and increased levels of blood glucose. When insulin and glucose decrease GH increases.
  • Chronic hypersection of GH (acromegaly) can lead to glucose intolerance and the development of DM.
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9
Q

Insulin

-function

A

Function:

  • lowers blood glucose by:
  • -promoting uptake of glucose by target cells
  • -promotes glucose storage as glycogen
  • -prevents fat and glycogen breakdown
  • -inhibits gluconeogensis and increases protein synthesis.
  • -increases triglyceride synthesis
  • -promotes fat storage by increasing transport of glucose into fat cells.
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10
Q

Insulin synthesis

A

main steps of insulin synthesis and secretion is by the Beta cells in the islets of langerhands.

Preproinsulin is converted to proinsulin in the rough ER. It is released into cytoplasm and is then taken up into small vesicles. The gogli apparatus secretes granules that enable the conversion of proinsulin to insulin. Insulin is stored here until they are released into the capillary system(portal venous circulation).

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11
Q

What is the major regulator of insulin? How does this work?

A
  • glucose is the regulator of insulin.
  • Beta cell has GLUT 2 receptor allowing glucose to enter beta cell. This results in depolarization and excretion of insulin from beta cell.
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12
Q

Factors Affecting Insulin Secretion

  • stimulation
  • inhibition
A

Stimulation:

  • Glucose
  • AA (arginine, lysine, alanine, leucine)
  • Free FA
  • Keto Acids
  • Glucagon

Inhibition:

  • Somatostatin
  • fasting
  • exercise
  • Leptin
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13
Q

Insulin Effect on Carbs

A

-carbs from a meal release glucose and stimulate secretion of insulin leading to uptake and storage of glucose in all tissues.

In muscle if not used glycogen is stored.

In liver stored as glycogen, once liver stores max amount of glycogen, insulin promotes conversion of glucose to FA.

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14
Q

Insulin effects on skeletal muscle and adipose tissue?

A

-insulin binds to receptor on skeletal muscle or adipose cell causing intracellular signal and insertion of GLUT-4 receptor into cell membrane leading to transport of glucose into cell. Resulting in increased glycogen via glycolysis, increased protein synthesis and triglycerides

1307 porth

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15
Q

Insulin Effects on the Liver

A

–insulin binds to receptor on liver causing intracellular signal and insertion of GLUT-2 receptor into cell membrane leading to transport of glucose into cell. Resulting in increased glycogen via glycolysis, increased protein synthesis and triglycerides

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16
Q

Effects of Insulin on Fat Metabolism

A

First Insulin increases the uptake of glucose by most of the body tissues, thereby decreasing utilization of fat.

Once liver glycogen is maxed, additional glucose forms fatty acids. These FA form triglycerides that are released into the blood stream and transported via VLDLV to adipose tissue where it must be cleaved by lipoprotein lipase into FA’s so it can be absorbed into the adipose tissues.

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17
Q

What blood sugar levels correspond with:

  • normal
  • decreased cognition
  • coma
  • convulsions
  • permanent brain damage
A 
Normal- 100-70
Sx- 55-50
cognition- 45-50
Coma- 30-35
Convulsions- 20-25
Permanent brain damage- 10-15
18
Q

Action of Somatostatin

A
  • inhibits secretion of growth hormone and thyro-tropin from pituitary.
  • *inhibits insulin and glucagon
  • *inhibits exocrine pancreas
19
Q

What is the functional unit of the exocrine pancreas?

WHat cells make up this unit?

Compromises how much of
the pancreas?

A
  • acinus and its draining ductule make up the functional unit.
  • acinar cells(digestive enzymes) and centroacinar cells( fluid and electrolyte secretion) make the functional unit.
  • 80-90% of pancreatic mass.
20
Q

Describe the activation of the digestive enzymes in the pancreas.

A
  • all enzymes are inactive in the pancreas, if they were activated while still in the pancreas they would dissolve/eat the pancreas.
  • Trypsinogen is activated by glycoprotein peptidase creating trypsin. Typsin then activates all of the other inactive proenzymes.
21
Q

Describe secretion of pancreatic enzymes into the gut.

A

-Ductule cells of the pancrease are stimulated by secretin released when acidic chyme enters the small intestine, they release large volumes of water and bicarb* to make the contents of the small intestine more alkaline. This allows the pancreatic enzymes to work better, these enzymes flow through the pancreatic duct, which joins with the hepatic hepatic duct and empties into the duodenum through teh ampulla of vater surrounded by the sphincter of Oddi.

22
Q

WHat hormones regulate pancreatic secretion?

A
  • Ach: from vagal nerve–gastric and cephalic phase
  • Secretin: stimulates release of water and bicarb (alkaline pH)–intestinal phase
  • Cholecystokinin: duodenal and upper jejunal cells; secreted when food enters leading to increased release of enzymes
  • Trypsin inhibitor: in acini prevents activation of trypsinogen(which activates other enzymes enzymes) and prevents enzymes from beign activated and digesting pancreas.
23
Q

Explain the pathophysiology of pancreatitis?

A

pancreas may become damaged or duct blocked, the secretions back up and overwhelm typsin inhibitor and pancreatic secretions become ACTIVATED and “digest” the pancreas causing acute pancreatitis!

24
Q

signs and sx of hypoglycemia

what are the two types of hypoglycemia?

A 
Sympathoadrenal: 
-sweating
-palpitations
-tremor
-nervousness
-irritability
-paresthesias
-hunger
-n/v
-tachycardia** (usually first sx)
Neuroglycopenic: 
-HA
-Blurred vision 
-confusion
-seizures
-coma 
-fatigue
-diff speaking
-loss of memory
-LOC
  • Fasting hypoglycemia (sx of neuroglycopenia d/t decreased glucose supply to the central and peripheral nervous system)
  • Postprandial hypoglycemia (d/t adrenergic response w/ abrupt decrease in glucose levels leading to increased Epinephrine release.
25
Q

What is whipples triad?

A
  • hypoglycemia sx
  • low plasma glucose less than 55mg/dL
  • relief of sx by raising plasma glucose (eating carbs)
26
Q

Hypglycemia may be reactive and/or functional, list potential causes of each.

A
  • Reactive:
  • severe exercise
  • medications :
  • -insulin
  • -B-blocker
  • -Bactrim
  • -Haloperidol
  • -MOA inhibitors
  • -Sulfonylureas
  • Functional:
  • -Hepatic and renal dysfunction
  • -malnutrition
  • -endocrinopathies: adrenal insufficiency, GH deficiency, glucagon deficiency
  • -Pancreatic tumors
  • -Alcohol consumption
27
Q

How to treat hypoglycemic coma?

A
  • IV mannitol (40g as a 20% solution over 20mins) OR glucocorticoids (dexamethasone 10mg).
  • increases the osmotic pressure, draws out the edema in the brain (mannitol)
28
Q

50% of type 1 patients under go diminished responses to epinephrine d/t hypoglycemia, True or false?

A

True, patients lose the autonomic warning sx of hypoglycemia and may recognize or fail to recognize the condition only when somatic neurologic function becomes impaired.

*beta blockers blunt cardiac response to hypoglycemia.

29
Q

Management of Hypoglycemic Disorders

A

Hypoglycemia in insulin-treated patient is usually due to omission of a meal while insuline was given, an error in medication, or unpredictive absorption of food.

  • give patient food
  • IM or SC glucagon
  • in hopsital: IV glucose administration (1amp D50)
30
Q

What are the fates of absorbed glucose?

A
  • 1st priority: glycogen storage; muscle and liver
  • 2nd priority: provide energy; ATP
  • 3rd priority: stored as fat (excess glucose, stored as triglycerides in adipose)
31
Q

Consequences of Insulin Deficiency Diabetes Mellitus

A

Metabolic:

  • increased blood glucose concentration
  • increased blood FFA and ketoacid concentration (fat depletion)
  • increased blood amino acid concentration (protein depletion)

Fluid and electrolyte:

  • metabolic acidosis (DKA)
  • glycosuria and osmotic diuresis(increased urination rate, the excretion of glucose enters the kidney tubules and cannot be reabsorbed, water follows sugar)
  • hyperphagia
  • polydipsea
  • hypovolemia and hypotension
  • coma and death
32
Q

Pathophysiology of DM 1 & 2

A
  • TYPE 1: autoimmune destruction of beta cells leading to insulinopenia and ketonemia.
  • *Dependent on insuline to sustain life and prevent ketoacidosis

TYPE II:

  • insulin resistance, normal or elevated insulin initially
  • increased hepatic glucose production
  • patients obese
  • may require insulin to control hyperglycemia.
33
Q

When do most develop T1D? Whats the progression like?

A
  • kids, teens, or 20’s before it starts to manifest itself.
  • 15yo age at onset

Progression is gradual and Beta cell mass gradually declines over the years.

34
Q

Describe the progression to T2D, age at onset?

A
  • obesity and insulin concentration are directly related, so the fatter we become the more insulin we secrete. THe body develops resistance to this insulin leading to elevated glucose in the body.
  • age at onset: 40+
35
Q

DKA

  • most commonly seen in which type of DM?
  • what is this?
  • associated metabolic and plasma abnormalitis
A

-Most common in Type 1 DM but can happen with T2D just not as likely.

  • defined as being present with absolute or relative insulin deficiency when the following criteria are met:
  • -blood glucose levels >250
  • -Ketosis: ketones in urine and blood
  • -Acidosis: pH less than 7.34 and/or serum bicarb is less than 15.

Associated with:

  • dehydration
  • increased osmolality
  • increased anion gap ( greater than 15) (metabolic acidosis)
  • increased serum amylase
  • elevated white count (if infection is culprit which triggers ketoacidosis)
  • hypertriglyceridemia
36
Q

pathophysiology of DKA

-what are some triggers causing hyperglycemia

A

Stress, infection, new onset DM, or insulin administration forgetting leads to increased catecholamine and GH release causing increased glucagon and decreased insulin release. This glucagon is converted to/and triggers production of glucose from the liver leading to increased glucose in the blood. Since we do not have insulin this glucose cannot get into the cells leading to hyperglycemia and Ketosis (from Protein and Fat depletion). Osmotic diuresis, dehydration, and metabolic acidosis result.

*IDDM has the first manifestation of diabetes as DKA.

  • Hyperglycemia:
  • -cortisol
  • -
37
Q

Signs and symptoms of DKA

A

Symptoms:

  • N/v
  • thirst
  • polyuria
  • abd pain
  • weakness, fatigue
  • anorexia

Signs:

  • tachycardia
  • orthostatic hypotension
  • poor skin turgor
  • dry skin
  • Kussmauls respirations
  • Hypothermia
  • Fruity Breath
  • AMS
38
Q

DKA:
-increased blood glucose results in____.

  • ____ leads to dehydration?
  • _____-osmol state leads to water shift and K+ from ___cellular to ___cellular.
  • Serum Na high or low?
  • Serum K+ high or low?
  • Metabolic acidosis from ____ production leads to marked ____ effects on serum bicarb??
A
  • results in hyperosmolality
  • Osmotic diuresis leads to dehydration
  • Hyperosmol state leads to water shift and K+ from intracellular to extracellular
  • Na is low to normal
  • K+ is normal to elevated
  • Metabolic acidosis from ketone production leads to marked decrease in serum bicarb
39
Q

Treatment of DKA

A
  • give fluids to drop blood glucose, check K+, if greater than 3.3 may give insulin, 10U bolus of regular insulin.
  • dont worry about bicarb replacement unless the pH is less than 7, as you correct everything else the bicarb will correct itself.
40
Q

who gets HHS? (Hyperglycemic Hyperosmolar Syndrome)

A

occurs excusively in Type 2, elderly and physically impaired. Limited access to free water.

Endocrine 2 (10 decks)

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