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D1 Spring - Physiology Exam 2 > 2/20: Insulin and Glucagon > Flashcards

2/20: Insulin and Glucagon Flashcards

1
Q

What kind of cells does the pancreas contain?

A

Islet of langerhans

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2
Q

What do alpha cells secrete?

A

Glucagon

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3
Q

What do beta cells secrete?

A

Insulin

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4
Q

What do delta cells secrete?

A

Somatostatin

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5
Q

What is somatostatin?

A

Inhibits glucagon and insulin

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6
Q

What constitutes a majority of the cells in the islets?

A

Alpha and beta cells

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7
Q

What majority of the pancreas is composed of acinar cells which produce _____________

A

Digestive enzymes (exocrine portion)

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8
Q

What is insulin secretion associated with?

A

Energy abundance

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9
Q

What is insulin composed of?

A

Two amino acid chains, conected by disulfide linkages

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10
Q

What happens when A and B chains split?

A

Functional activity of insulin molecule is lost

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11
Q

What kind of activity do proinsulin and C peptide have?

A

Virtually no activity

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12
Q

How does insulin circulate?

A

Entirely unbound (doesn’t need to bind to function)

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13
Q

What is insulin first made as?

A

Proinsulin

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14
Q

What is proinsulin cleaved into in the golgi?

A

Cleaved to form C peptide and insulin

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15
Q

What are incretins?

A

Hormones produced by the digestive system that work to stimulate insulin secretion BEFORE plasma glucose is elevated

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16
Q

What are examples of incretins?

A

Glucagon-like peptide-1 (GLP1) and glucose-dependent insulinotropic polypeptide (GIP)

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17
Q

What is the sulfonyluera receptor?

A

The closing of this channel causes insulin release

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18
Q

What is the key regulator of insulin secretion?

A

Glucose
- Amino acids, ketones, various nutrients, gastrointestinal peptides, and neurotransmitters also influence insulin secretion

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19
Q

What are the mechanisms of insulin secretion?

A
  1. Glucose enters beta cell via GLUT transporter down it’s concentration gradient (high-> low)
  2. Inside the beta cell, glucose is metabolized and ATP is produced
  3. ATP sensitive K+ channel is stimulated; SUR channel closes when ATP levels are elevated
  4. Closing of the SUR channel causes depol. moving away from K equilibrium; opening Ca2+ channels
  5. Ca2+ channel opening causes exocytosis
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20
Q

What does an increase in blood glucose cause?

A

An increase in insulin release

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21
Q

What is an antagonist of insulin?

A

Glucagon
- glucagon levels decrease as blood glucose levels increase

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22
Q

What kind of receptor is the insulin receptor?

A

Tyrosine kinase linked receptor

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23
Q

How do target cells respond quickly (seconds)?

A

Increased glucose uptake, especially by muscle cells and adipocytes due to translocation of vesicles containing GLUT-4 to the membrane

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24
Q

How do target cells respond slower (10-15min)?

A

Change in enzyme activity leading to changes in metabolism

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25
Q

How do target cells respond slowest (hours-days?

A

Changes in gene expression and growth

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26
Q

What are the effects of insulin on muscle?

A

Promote muscle glucose uptake and metabolism-anabolic effect via GLUT4

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27
Q

What is the resting muscle membrane permeable to?

A

Slightly to glucose

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28
Q

What does insulin stimulation increase?

A

Glucose transport

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29
Q

What are anabolic effects of insulin on muscle?

A
  • increases glycogen storage in skeletal muscle
  • increases protein synthesis and inhibits protein degradation
30
Q

What are effects of insulin on protein metabolism and growth?

A
  • promtoes protein synthesis and storage
  • inhibits protein degradation
31
Q

What does insulin interact synergistically with?

A

Growth hormone to promote growth

32
Q

What does a lack of insulin cause?

A

Protein depletion and increased plasma amino acids

33
Q

What are the effects of insulin on the liver?

A

Promotes the uptake and storage of glucose (as glycogen) by the liver

34
Q

What are the mechanisms for the effects insulin has on the liver?

A
  • increases glucose uptake (glucokinase)
  • increase glycogen synthase -> increase glycogen synthesis
  • decrease breakdown of glycogen by inhibiting liver phosphorylase
35
Q

What does insulin promote the conversion of in the liver?

A

Conversion of excess glucose into fatty acids

36
Q

What does insulin inhibit in the liver?

A

Gluconeogenesis

37
Q

What are the effects of insulin on fat metabolism?

A

Promotes fat synthesis and storage

38
Q

What does insulin enhance in fat metabolism?

A

glucose transport into adipocytes

38
Q

What does insulin inhibit in fat metabolism?

A

hormone-sensitive lipase (how fatty acids are released into blood)

38
Q

What does insulin activate in fat metabolism?

A

lipoprotein lipase to help fatty acids enter the adipose cell (absorption of fat into fat cells)

39
Q

What does lack of insulin in fat metabolism cause?

A

causes lipolysis and release of FFA (diabetic ketoacidosis) and inc plasma cholesterol and phospholipids

40
Q

What are the target tissues of insulin?

A

Muscle, liver, and adipose

41
Q

How does glucose enter adipose and muscle cells?

A

Via increased GLUT4 receptors

42
Q

What are the net effects of insulin in plasma levels?

A

Decrease glucose
Decrease free fatty acids
Decrease ketoacids
Decrease amino acids

43
Q

What are things that increase insulin secretion?

A
  • Increased blood glucose, increased blood free fatty acids, increased blood amino acids
  • Incretins, activate beta cell to secrete insulin (gastrointestinal hormones like GIP and GLP)
  • Glucagon, growth hormone, cortisol (cause inc in blood glucose -> insulin secretion)
  • Parasympathetic stimulation via acetylcholine
  • Sulfonylurea drugs (close K/ATP channel in beta cell)
  • Insulin resistance (if target cells are resistant to glucose, then more insulin would have to be produced to lower blood glucose)
44
Q

What are things that decrease insulin secretion?

A
  • Decreased blood glucose, fasting
  • Somatostatin/GHIH
  • a-Adrenergic activity Leptin
45
Q

What is the hormone of starvation?

A

Glucagon

46
Q

What is glucagon secretion stimulated by?

A

Hypoglycemia, epinephrine (B2) and the vagus nerve

47
Q

What is the primary target of glucagon?

A

Liver, to increase blood glucose

48
Q

How does glucagon increase blood glucagon?

A
  1. Stimulated glycogenolysis and inhibiting glycogen synthesis
  2. Increasing gluconeogenesis
  3. Increases blood fatty acid and ketoacid levels to provide more substrates for gluconeogenesis
49
Q

What are ketoacids?

A

(acetone, acetoacetate, beta-hydroxybutyrate) short chain fats that are substrates to make glucose and are energy substrates

50
Q

What is diabetes mellitus?

A

metabolic disorder characterized by hyperglycemia due to insufficient insulin or cellular resistance to insulin

51
Q

What are the two types of diabetes mellitus?

A

Type I: hypoinsulinemia (10%) – not making enough
Type II: hyperinsulinemia (90%) – resistance to insulin

52
Q

What are symptoms of diabetes mellitus?

A

Urinating often (Polyuria)
Feeling thirsty (Polydipsia)
Feeling hungry (Polyphagia)
3 P’s

53
Q

What are the diagnosis types for diabetes mellitus?

A

o Normal levels:
FFG (fasting plasma glucose, 8-hour fast): <100 mg/dL
2-h-PG: 2 hours post prandial glucose
A1C (hemoglobin, long term measurement): <5.6%
o Prediabetic levels: elevated from normal levels
o Diabetic levels: elevated (FPG >126 and A1C of >6.5%)

54
Q

What is the pathophysiology of diebetes mellitus type 1?

A

o Accounts for 5-10% of diabetes cases
o Formerly called juvenile onset diabetes or insulin dependent diabetes (IDDM)
o Approximately 25% present in diabetic ketoacidosis (hyperglycemia >250 mg/dl)

55
Q

What are risk factors for diabetes melltius type 1?

A

o Genetic predisposition - increased susceptibility
o Environmental triggers stimulate autoimmune response
- Viral infections (mumps, rubella)
- Chemical toxins
o Usually develops < age 40, non-obese younger patients

56
Q

What are manifestations of DM type I?

A

o Beta cell destruction occurs slowly
o Hyperglycemia occurs when 80 – 90% of beta cells destroyed
o Often triggered by stressor or illness

57
Q

What does hyperglycemia from DM type 1 lead to?

A
  • Polyuria (hyperglycemia acts as osmotic diuretic)
  • Polydipsia (thirst from dehydration from polyuria)
  • Polyphagia (hunger and eats more since cell cannot utilize glucose)
  • Glycosuria (presence of glucose in urine, renal threshold for glucose exceeded)
  • Weight loss (body breaking down fat and protein to restore energy source
  • Malaise and fatigue (due to muscle & electrolyte loss)
  • Hyperkalemia (due to lack of insulin, normally activates Na/K pump)
  • Insulin enhances action of Na/K, without insulin there is less activity so more K remains inside the cell (can cause changes in nerve excitability)
58
Q

What is diabetic ketoacidosis due to?

A

Increased lypolysis of fatty acids to produce ketoacids

59
Q

What is diabetic ketoacidosis?

A

response to cellular starvation brought on by relative insulin deficiency and counterregulatory or catabolic hormone excess (glucagon, catecholamines, cortisone and growth hormone) to increase blood glucose

60
Q

What is the pathophysiologyo of diabetic ketoacidosis?

A

smotic diuresis and dehydration (hyperglycemia), metabolic acidosis (accumulation of ketones), fluid and electrolyte imbalances

61
Q

What are signs and symptoms of diabetic ketoacidosis?

A
  • Fruity breath (due to acetone)
  • Nausea/abdominal pain
  • Dehydration
  • Tachycardia
  • Lethargy, Coma (because acidosis depresses neuronal function since it blocks inward current of Na and Ca)
  • Polydipsia, Polyuria, Polyphagia
  • Kussmaul respirations (deep, labored breathing)
62
Q

What are causes of diabetic ketoacidosis?

A

anything that increases stress causes increase of cortisol (antagonist to insulin)
I.e. surgery, trauma, infection, decrease or omission of insulin injection

63
Q

What is diabetes mellitus type II?

A

Insulin resistance
* Fasting hyperglycemia despite availability of insulin
* Was called non-insulin dependent diabetes or adult-onset diabetes. Both misnomers, type II DM may require insulin and can occur in children
* Can be genetic

64
Q

What is the pathophysiology of diabetes mellitus type II?

A

hyperinsulinemia due to insulin resistance (target cells)
Due to downregulation of insulin receptors in target tissue and insulin resistance

Early: target cells don’t respond to insulin like they should, so it doesn’t lower blood glucose. In response, beta cell produces more insulin
Late: can lead to beta cell dysfunctio

65
Q

DM Type II is part of this cascade of disorders that lead to Metabolic syndrome. What disorders?

A

Obesity, insulin resistance, fasting hyperglycemia, lipid abnormalities (high TG and low HDL), hypertension

66
Q

What are chronic complications of DM I and II?

A
  • Retinopathy: leading cause of blindness in the United States
  • Nephropathy: progressive renal dysfunction that can lead to end-stage renal disease
  • Neuropathy: peripheral loss of sensation and dysesthesias
  • Vascular disease: accelerated atherosclerotic cerebrovascular and peripheral vascular diseases, may occur due to abnormal lipid metabolism
  • Myopathies: progressive weakness and diminished exercise tolerance
67
Q

What are oral manifestations of DM?

A

o Periodontal Disease
o Salivary and taste dysfunction
o Oral bacterial and fungal infections (ex. candidiasis)
o Diminished salivary flow and burning mouth syndrome
o Delayed mucosal wound healing
o Xerostomia

68
Q

How are diabetes linked to periodontal disease?

A

o Periodontal disease exacerbates diabetic complications
- Poor glycemic control
- Cardiovascular complications (stroke, ischemia, infarction)
o Control of periodontal infection may improve glycemic control

D1 Spring - Physiology Exam 2 (7 decks)

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