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Endocrine Physiology > CH 7 Endocrine Pancreas > Flashcards

CH 7 Endocrine Pancreas Flashcards

1
Q

What does EXOcrine pancreas do?

A

secrete alkaline fluid rich with digestive enzymes into small intestine

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2
Q

What is the functional unit of ENDOcrine pancreas?

A

islets of Langerhans

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3
Q

What cell types are in the islets of Langerhans? What do they secrete?

A

beta (insulin), alpha (glucagon), delta (somatostatin), other (pancreatic polypeptide)

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4
Q

How do endocrine pancreas hormones reach circulation? What is the major target organ?

A

hepatic portal vein. liver

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5
Q

What are the neurotransmitters of parasympathetic stimulation?

A

acetylcholine, vasoactive intestinal polypeptide, pituitary adenylate cyclase-activating polypeptide, & gastrin-releasing peptide

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6
Q

How does the Vagus N. (parasympathetics) effect the pancreas?

A

stimulate secretion of insulin, glucagon, somatostatin, and pancreatic polypeptide

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7
Q

What are the neurotransmitters of sympathetic stimulation?

A

norepinephrine, galanin, neuropeptide Y

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8
Q

How does Sympathetic Nerve Stimulation effect the pancreas?

A

inhibits basal and glucose-stimulated insulin secretion & somatostatin release; stimulates glucagon & pancreatic polypeptide secretion

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9
Q

What type of regulation is Insulin under?

A

Pancreatic B-cells respond to plasma levels of energy substrates (glucose/amino acid), hormones (insulin, glucagon-like peptide I, somatostatin, epinephrine), & neurotransmitters (norepinephrine/acetylcholine)

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10
Q

Track how glucose stimulates insulin secretion.

A

Glucose is transported into pancreatic B-cell by GLUT2. Glucose is phosphorylated & undergoes oxidative phosphorylation to make ATP. When conc. of ATP is high, it causes ATP-sensitive K+ channels (sulfonylurea receptor) to close (K+ was going out to hyperpolarize cell). Cell becomes depolarized, and Voltage-dependent Ca++ channels open and Ca++ rushes in. Ca++ lead to fusion of insulin-containing secretory granules to fuse with plasma membrane and release insulin.

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11
Q

What receptor regulates ATP sensitive K+ Channels?

A

sulfonylurea (used in treatment of diabetes)

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12
Q

What is a major characteristic of glucose-stimulated insulin secretion?

A

it is biphasic; release throughout the day is pulsatile and rhythmic

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13
Q

What type of physiologic effect does insulin have on metabolism?

A

anabolic

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14
Q

What is the IRS-PI3K Pathway?

A

insulin receptor substrates-phosphatidylinositol 3-kinase pathway: mediates insulin’s metabolic effects (glucose transport, glycolysios, glycogen synthesis, regulation of protein synthesis)

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15
Q

What is the MAPK pathway?

A

mitogen-activated protein kinase pathway: mediates proliferative and differentiation effects of insulin

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16
Q

What protein does insulin stimulate in muscle and adipose tissue for glucose uptake?

A

GLUT 4 (recall: GLUT 2 is in pancreas as glucose sensor). GLUT 4 is typically held within cell until stimulation by insulin translocates proteins to membrane

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17
Q

What is GLP 1? Where is it produced? When? What effects does it have?

A

product of proglucagon processing (aka Incretin); produced in intestine from proglucagon processing); occurs in response to a glucose load (e.g. after eating); amplifies insulin release from B-cells of pancreas

18
Q

What are the two products of proglucagon processing?

A

glucagon (alpha cells of pancreas) & GLP1 (intestine)

19
Q

How does somatostatin effect insulin & glucagon release?

A

inhibits both

20
Q

What kind of meal stimulates glucagon release?

A

high in amino acid levels

21
Q

How does epinephrine effect insulin and glucagon release?

A

inhibit insulin (alpha2-adrenergic receptors), stimulate glucagon (beta2-adrenergic receptors)

22
Q

What stimulates release of somatostatin from delta-cells of pancreas?

A

high fat, high carbohydrate, high protein meals

23
Q

What inhibits release of somatostatin from delta-cells of pancreas?

A

insulin

24
Q

Where does pancreatic polypeptide come from? What role does it play?

A

endocrine type F cells of pancreas; inhibits pancreatic exocrine secretion (alkaline secretion), gallbladder contraction, modulation of gastric acid secretion, and gastrointestinal motility. Regulates feeding behavior (appetite suppression).

25
Q

What is Amylin? What does it do? Why is it important?

A

peptide released with Insulin by pancreatic B-cells that suppresses glucagon secretion and gastric emptying. Deposition of amyloid in pancreas leads to B-cell destruction (seen in type II non-insulin-dependent diabetes). In type I diabetes, almost no amylin present with no secretion after meals. In type II diabetes, normal amyline levels, but no increase following meals)

26
Q

How does an insulinoma present?

A

hypoglycemia, confusion, aggressiveness, palpitations, sweating, convulsions, unconsciousness. (observed before breakfast and after exercise)

27
Q

How do glucagonomas present?

A

symptoms of diabetes, severe weight loss, anorexia

28
Q

define polyuria

A

excess loss of water and sodium

29
Q

define polydipsia

A

thirst via dehydration

30
Q

define polyphagia

A

hunger

31
Q

What is type 1 diabetes mellitus

A

insulin-dependent diabetes mellitus (Beta-cell destruction), less common aka “juvenile-onset diabetes”

32
Q

adolescent presents with ketoacidosis. What is the likely diagnosis?

A

type 1 diabetes mellitus

33
Q

What is type 2 diabetes mellitus

A

insulin-independent diabetes mellitus (loss of normal regulation of insulin secretion), decreased responsiveness of peripheral tissues to insulin & inadequate responsiveness of B-cells to glucose

34
Q

What disease is often associated with type 2 diabetes mellitus? How does it present?

A

syndrome X aka “insulin-resistance syndrome”; hypertension, atherosclerosis, central obesity

35
Q

How does diabetes progress?

A

Accumulation of glucose in blood (hyperglycemia) –> increased plasma osmolarity –> polyuria along with urinary loss of glucose –> polydipsia. Patient also experiences polyphagia –> lipolysis / proteolysis –> diabetic ketoacidosis

36
Q

How does diabetes type 2 insulin secretion work?

A

patients secrete a regular amount of insulin during fasting and after a meal, not enough insulin is secreted and it is secreted in smaller, sluggish, and erratic pulses. this results in higher levels of fasting glucose after a meal.

37
Q

What is the earliest sign of type 2 diabetes?

A

B-cell dysfunction: delay in acute insulin response to glucose –> hyperglycemia –> hyperinsulinemic response –> downregulation of insulin receptors (in response to sustained insulin) –> decreased tissue sensitivity to insulin

38
Q

What level of fasting glucose must be hit for a diagnosis of diabetes?

A

126mg/dL

39
Q

What level of random glucose must be met for a diagnosis of diabetes?

A

200 mg/dL in association with symptoms of diabetes (polyuria, polydipsia, polyphagia)

40
Q

How does hypoglycemia present?

A

Excess Insulin –> hypoglycemia. Stress response to try to restore normal glucose levels. SNS –> catecholamines. HPA –> cortisol.

glucagon release (via cortisol to pancreas), GH release; tachycardia, palpitations, sweating, tremors, irritability, confusion, blurred vision, tiredness, headache, difficulty speaking, loss of consciousness or seizures if severe

41
Q

What is Diabetic Ketoacidosis? What causes it?

A

Type I Diabetes - no insulin. hyperglycemia. Ketoacidosis is precipitated by stress (infection, hospitalization, trauma, surgery) - stress increases catecholamines (epi/norepi) + cortisol –> lipolysis and ketone bodies

42
Q

What is a Hyperglycemia Hyperosmolar Coma?

A

type II Diabetes - lack of insulin. hyperglycemia –> hyperosmolar dehydration –> coma

Endocrine Physiology (15 decks)

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