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GIGU test! > Endocrine Pancreas > Flashcards

Endocrine Pancreas Flashcards

1
Q

What are the cells located in the Islets of Langerhans and what all do these cells secrete?

A

B cells:

  • 60-65% of islet centrally located
  • secrete insulin and C peptide

A cells:

  • 20% of islet, peripherally located
  • secrete glucagon

Delta cells:

  • 5% of islet; interspread between alpha and beta cells
  • secrete somatostatin
  • Neuronal in apperance and send dendrite-like processes to B-cells

F Cells:

  • Secrete Pancreatic Polypeptide
  • Acts like satiety signal (neuropeptide Y, peptide YY family)
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2
Q

how do the cells in the islets communicate with each other?

A

gap junctions - rapid cell to cell communication

-between a-a and a-b

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3
Q

What is the blood supply for the cells of Islets of Langerhans?

A

-Recieve 10 percent of pacreatic blood flow
-Venous blood from one cell type bathes other cell types
-Venous blood from B-cells carries insulin to alpha and delta cells
(blood flow first to center for insulin then through periphery to inhibit release of glucagon from alpha cells)

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4
Q

what are the precursors and components to Insulin?

A

Insulin is a Peptide hormone that are 2 chains linked by disulfide bridges

Preproinsulin: Proinsulin: Insulin and C peptide

Preproindulin: signal peptide with A and B chains with connecting peptide (C peptide) no disulfide bonds

Proinsulin: no signal peptide

  • C peptide still attached in insulin
  • packaged into secretory granules
  • proteases here cleave proinsulin

C-Peptide:

  • packaged together with insulin in secretory vesicles
  • secreted in equimolar quantities into blood
  • can be used as a marker of endogenous insulin secretion
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5
Q

What are the 8 steps to insulin release?

A

1) glucose enters cell via GLUT-2
2) Glucose is phosphorylated by glucokinase
3) Glucose-6-phosphate is oxidized promoting ATP generation
4) ATP closes the inward rectifing K channel
5) PLasma membrane is depolarized
6) Activation of Voltage gated Ca channels
7) Ca enters the cell and
8) initiates mobilization of insulin (and C peptide) containing vesicles to plasma membrane and exocytosis

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6
Q

what are some key concepts with Insulin release?

A

-Rises in ATP closes the K+ channel (ATP dependent K+ channel)

Sulfonylurea receptor, associated with ATP dependant K+ channels increase insulin secretion

  • causes membrane depolarization to occur more easily
  • More Ca entry
  • used for treatment of type 2 DM
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7
Q

how is the insulin response?

A

Biphasic

First phase insulin secretion is lost in diabetic individuals

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8
Q

what are the characteristics of the Insulin receptor?

A

Insulin = insulin receptor

  • bound insulin receptor will autophosphorylates itsself and phosphorylates other proteins
  • insulin receptor complex is internalized by target cell
  • downregulation of receptor by insulin itself
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9
Q

what does insulin do when it binds to its receptor

A

Phosphorylation of insulin receptor substrate (IRS) and other proteins

Leads to downstream activation of pathways like:

  • PI3K/Akt/mTOR
  • MAP kinases
  • THese mediate metabolic and mitogenic responses

this all leads to translocation of vesicles containing GLUT4 to membrane
-GLucose enters via facilitate diffusion

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10
Q

what is the alternative intracellular pathway for glucose Uptake independant of insulin?

A

Activation of AMPK results in GLUT4 translocation to plasma membrane

Muscle contractions stimulate this process

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11
Q

Stimulatory factors of Insulin secretion?

A
  • Increased glucose concentration
  • increased amino acid concentration
  • increased fatty acid and ketoacid concentration
  • GLucagon
  • cortisol
  • Glucose dependant insulinotropic peptide (GIP)
  • Potassium
  • Vagal stimulation; acetylcholine
  • sulfonylurea dugs
  • Obesity
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12
Q

Inhibitory factors of insulin secretion

A

-Decreased blood glucose
-Fasting
-Exercise
-Somatostatin
-a adrenergic agonists; norepinephrine
Diazoxide (smooth muscle vasodilater to treat hypoglycemia)

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13
Q

how does ACh, CCK, and GLP-1 modulate insulin release?

A

activates and increases insulin release

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14
Q

how does somatostatin and glucagon affect insulin release

A

inhibits insulin release

glucagon is inhibited by insulin release but helps modulate insulin release

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15
Q

How does insulin affect the skeletal muscle?

A
  • Increases glucose uptake
  • Increased glycogen synthesis
  • Increased glycolysis and CHO oxidation
  • Increased protein synthesis
  • Decreased protein breakdown
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16
Q

How does insulin affect the liver?

A
  • Promotes glycogen synthesis
  • increases glycolysis and CHO oxidation
  • Decreases gluconeogenesis
  • Increases hexose monophosphate shunt
  • Increase pyruvate oxidation
  • Increase lipid storage and decreases lipid oxidation
  • Increases protein synthesis and decreases protein breakdown
17
Q

How does insulin affect Adipose tissues?

A
  • Increased glucose uptake
  • increased glycolysis
  • decreased lipolysis
  • promotes uptake of fatty acids
18
Q

what are the effects insulin has on blood level metabolites?

A
  • decreases glucose
  • decreases amino acids
  • decreases fatty acids
  • decreases keto acids
  • decreases K+
19
Q

Characteristics of glucagon and where is it made and stored?

A
  • Single straight-chain polypeptide with 29 AA
  • Membrane of same peptide family as secretin and GIP
  • Synthesized as preproglucagon
  • stored in dense granules of A cells
20
Q

what stimulates the secretion of GLucagon?

A

Stimulated by major decreased blood

also by:

  • increased AA (arginine and alanine)
  • Fasting
  • CCK
  • B adrenergic agonists
  • ACh
21
Q

what inhibits the secretion of glucagon?

A

Insulin inhibits glucagon production and secretion

other inhibitory factors

  • Somatostatin
  • Fatty acids
  • Keto acids
22
Q

what are major actions of glucagon on the liver?

A

Glucagon increases blood glucose
- substrates are directed toward glucose formation

  • increases gluconeogenesis (reduced productions of fructose 2,6-bisphosphate)
  • increased glucogenolysis
  • inhibits glycogen synthesis
23
Q

Glucagon actions throughout the body?

A

Stimulates lipolysis, both adipose tissue and skeletal muscle

Ketoacids produced from fatty acids

24
Q

what is the underlying cause of Type 1 diabetes mellitus? and some of the symptoms that come with it?

A

Inadequate insulin secretion:

  • destruction of B cells often from autoimmune disease
  • symptoms dont show until >80 percent b cells destroyed
  • increased glood glucose, fatty acids, ketoacids, and amino acids
  • decreased utilization of ketoacids results in diabetic ketoacidosis

Hyperkalemia: shift of K+ out of cells

  • intracellular concentration is thuus low
  • lack of insulin effect on Na+/K+ ATPase
  • plasma levels may be normal, total K+ usually low due to polyuria and dehydration

Osmotic diuresis/Glucosuria

  • increased blood glucose increases filtered load of glucose, exceeds reabsorptive capacity of proximal tubule
  • water and electrolyte reabsorption also blunted
  • Polyuria
  • polydipsia
25
Q

Treatment for Type 1 DM?

A 
insulin replacement
drawbacks:
-painful and time consuming
-lag between glucose measurements and insulin dosing
-delayed absorption
-poor blood glucose control

Transplantation of B cells

26
Q

underlying cause of type 2 diabetes mellitus

A

Insulin resistance

-progressive exhaustion of active B cells due to environmental factors

27
Q

Pathophysiology of the progression of insulin resistance and type 2 DM

A

Reactive hyperinsulinemia

Obesity induced insulin resistance:

  • decreased GLUT4 uptake of glucose in response in insulin
  • decreased abillity of insulin to repress hepatic glucose production
  • inabillity of insulin to repress adipose tissue uptake and lipolysis
  • ultimately results in decreased glucose transporter number and mobilization of GLUT4
28
Q

how does T2DM appear in non-obese patients

A

decreased insulin release by pancreas independant of peripheral insulin resistance, however both can and often do occur

29
Q

what are incretin hormones?

A

Intestine derived hormones

  • GLP-1, GIP
  • SHort half life
  • Secreted in response to GI glucose and fat

Stimulates insulin secretion
inhibits glucagon secretion
slow gastric emptying

30
Q

What is the Treatment of Type 2 DM?

A

Caloric restriction, weight reduction, physical activity/exercise

Insulin secretagogues

  • sulfonylurea drugs
  • incretin analog of GLP-1 (exenatide)

Slow absorption of CHO

  • alpha glucosidase inhibitors (acarbose, miglitol)
  • amylin analogs (pramlintide)

Insulin sensitizers
-Biguanide drugs (metformin) - better insulin receptor trafficking

Bariatric surgery

GIGU test! (40 decks)

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