Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endo/Repro Exam 1 > Endocrine Pancreas > Flashcards

Endocrine Pancreas Flashcards

1
Q
  • Endocrine cells of the pancreas are arranged into clusters called _
  • These are innervated by _,_ and _ neurons
  • What is the most predominant cell type and where in the cluster is it located + what does it secrete?
  • What other cells are present and what do they secrete
A
  • Islet’s of Langerhans
  • Adrenergic (sympathetics), Cholinergic (parasympathetics), and Peptidergic neurons
  • Beta cells-located in the center, secrete insulin
  • Alpha cells-around periphery, secrete glucagon
  • Delta cells-interspersed-secrete somatostain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
  • Gap junctions allow for rapid cell-cell communication between what cell types?
A
  • Alpha-alpha
  • Beta-beta
  • Alpha-beta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Insulin and C Peptide are secreted in a _ to _ fashion

A
  • 1 to 1
  • C peptide can be used as a long term marker for insulin secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is insulin secreted?

What is the most important factor regulating glucose secretion?

A
  • STEPS:
    • Glucose binds GLUT 2 on beta cells
    • Glucose goes thru TCA cycle and produces ATP
    • ATP closes ATP dependent K+ channel
    • Depolarization occurs
    • Ca2+ influx into cell
    • Increased Ca2+ stimulates exocytosis of insulin and C peptide
  • Most important regulator of insulin secretion: Glucose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
  • _ drugs promote closing of ATP dependent K+ channel (helps with insulin secretion and used to treat T2 Diabetes)
  • _ is secreted in equimolar amounts with insulin and excreted unchanged in the urine (used to monitor endogenous B cell function)
A
  • Sulfonylurea
  • C peptide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  • Glucose stimulates the secretion of insulin in a _ manner
  • _ is absent in a diabetic individual
A
  • Biphasic
  • Phase 1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
  • Besides glucose, what other factors stimulate insulin release?
  • What inhibits insulin release?
  • Through which types of G protein coupled receptors do these molecules work?
A
  • Stimulates:
    • Glucagon-Gs
    • GLP-1: Gs
    • CCK-Gq
    • ACh-Gq
  • Inhibits:
    • Somatostatin-Gi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  • Before insulin enters the systemic circulation, it bypasses in bursts through the _
  • What is significant about this?
A
  • Liver
  • Almost 80% of insulin that enters the liver stays in the liver
  • The rest is sent in pulsations to the systemic circulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  • How does insulin receptor signaling work?
A
  • Insulin receptor is an RTK
  • Insulin binding to receptor triggers autophosphorylation of the receptor and phosphorylation of IRS and substrate proteins
  • Substrate proteins activate downstream signaling cascades that lead to growth and metabolic effects
  • GLUT4 translocation to PM in Muscle Cells and Adipocytes
  • GLUT 2 translocation to PM in Liver Cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  • What are the actions of insulin in muscle cells
A
  • Increase glucose uptake (GLUT4)
  • Increase in glycogen synthesis (Activates glycogen synthase)
  • Increases glycolysis and carb oxidation (Increased activity of hexokinase, phosphofructokinase and pyruvate dehydrogenase)
  • Decreased gluconeogenesis
  • Increase protein synthesis and decrease in protein breakdown
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  • Alternative intracellular pathways for glucose uptake independent of insulin
  • What is significant about this finding?
A
  • Muscle contractions stimulate AMPK
  • Results in translocation of GLUT4 to PM
  • Exercise management can be used as part of treatment for patients with insulin resistance/diabetes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  • Insulin effects on triglyceride and fatty acid metabolisms in adipose tissue
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  • How does an increase in insulin affect the following nutrients’ concentration in the blood?
    • Glucose
    • Fatty acids
    • Ketoacids
      Amino Acids
A
  • ALL ARE DECREASED
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q
  • Summary of insulin actions and the effect on blood levels
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  • Summary of factors affecting insulin secretion
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  • Type I Diabetes Mellitus
  • What happens?
  • What causes it?
  • What are some key characteristics of the disease?
A
  • Destruction of beta cells (usually d/t AID); does not show sx until 80% of cells are destroyed
  • Increase in blood glucose
    • ​Decreased uptake of glucose
    • Decreased glucose utilization
    • Increase in gluconeogenesis in the liver
  • Increase in Blood FA and Ketoacids
    • ​Decreased fatty acid synthesis
    • Decreased triglyceride synthesis
    • Increased triglyceride breakdown
    • Increased conversion of FA to ketoacids and decreased ketoacid utilization by tissues (DKA-metabolic acidosis)
  • Increase in blood AAs
    • ​Increased protein breakdown
    • Decreased protein synthesis
    • Increased catabolism of aa’s (loss of lean body mass)
    • Increased ureagenesis
  • Hyperkalemia
    • ​Shift of K+ out of cell
    • Even though K+ is high in plasma, is low total K+ b/c of polyuria and dehydration
    • OSMOTIC DIURESIS
      ​      Increased BGL results in increased filtered load of glucose
    • Water and electrolyte absorption prevented (glucose reabsorption is prevented)
    • Polyuria-leads to excess excretion of Na+ and K+
    • Polydipsia
17
Q
  • The goal of insulin replacement therapy for T1 DM is to recreate normal physiology using _
  • Drawbacks of insulin replacement therapy?
A
  • Basal and bolus insulin
  • Drawbacks
    • Painful
    • Time consuming
    • Lag between glucose measurement and insulin dosing
    • Delayed absorption of insulin following subcutaneous injections
    • Poor BG control
      • Periods of hyperglycemia
18
Q
  • T2 DM
    • ​Progressive exhaustion of _ cells d/t environmental factors (sedentary lifestyle, malnutrition, obesity)
    • Patients can make insulin, but not enough to overcome _
    • Initially, insulin levels are _
    • As the disease progresses, insulin levels are _
A
  • Beta Cells
  • Insulin resistance
  • Normal or elevated
  • Deficient
    • Reactive hyperinsulinemia followed by relative hypoinsulinemia
19
Q
  • What are the three causes for obesity-induced insulin resistance?
A
  1. Decreased GLUT 4 uptake of glucose
  2. Decreased ability of insulin to repress hepatic glucose production
  3. Inability of insulin to repress HSL or increase LPL in adipose tissue
20
Q
  • Type II diabetics are not as prone to _ because the presence of some insulin secretion serves as protection
  • In non-obese patients, type II diabetes can occur d/t _ in insulin release by the _ (varying degrees of insulin resistance can also occur)
A
  • Ketoacidosis
  • Decrease in insulin release by the pancreas
21
Q
  • Treatment for Type II Diabetes
A
  • Caloric restriction and weight reduction
  • Insulin secretagogues:
    • sulfonylurea drugs
    • Incretin analog of GLP-1 (injection)
    • alpha glucosidase inhibitors
    • Amylin analogs
    • Insulin sensitizers
    • Biguanide drugs (EX: metformin): upregulate insulin receptors on target tissues
22
Q
  • Incretin hormones
  • Diabetic patients have a _ incretin effect
A
  • Intestine derived hormones (EX: GLP-1, GIP, Short T1/2)
  • Secreted in response to glucose and fat
  • Stimulate insulin secretion (glucose dependent)
  • Inhibit glucagon secretion
  • Slow gastric emptying
  • Diabetics have a reduced incretin effect
23
Q
  • Summary of Type I versus Type II Diabetes
A
24
Q
  • Glucagon is a 29 aa straight chain polypeptide and is members of the peptide family including _ and _ GI hormones
  • Synthesized as _
  • Undergoes processing in _ cells of the pancreas and _ cells of the intestine
  • Stored in _ until alpha cells are stimulated (what is the major stimulus?)
A
  • Secretin, GIP
  • Proglucagon
  • Alpha cells of pancreas and L cells of the intestine
  • Dense granules (main stimulus is decrease in BGL)
25
Q
  • Besides low BGL, what else has stimulatory effects on glucagon secretion?
  • What has inhibitory effects on glucagon secretion?
A
  • Stimulatory:
    • Low BGL
    • Increase in AAs (arginine and alanine)
    • Fasting
    • CCK
    • Beta adrenergic agonists
    • ACh
  • Inhibitors:
    • Insulin (also inhibits synthesis)
    • Somatostatin
    • Increased fatty acid and ketoacid concentration
26
Q
  • The major actions of glucagon are in the _
  • What happens?
A
  • Liver
  • Increase in gluconeogenesis (by decreasing production of fructose 2,6 phosphate)
  • Increase in glycogenolysis (inhibits glycogen formation from glucose)
  • Increases lipolysis and inhibits fatty acid synthesis
  • Ketoacids are produced from fatty acids
27
Q
  • Glucagon has what effect on the concentration of the following nutrients in the blood?
    • Glucose
    • Fatty Acids
    • Ketoacids
A
  • INCREASES CONCENTRATION IN BLOOD FOR ALL OF THESE
28
Q
  • Summary of factors regulating glucagon secretion
A
29
Q
  • Summary of overall effects of glucagon secretion
A

Endo/Repro Exam 1 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions