Endocrine Module 2- Section 1-Pancreas Flashcards

1
Q

pancreas

A

endocrine and exocrine fxn
endocrine fxn consists of islets cells-alpha, beta, delta

alpha-glucagon
beta-insulin
delta-somatostatin

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2
Q

Glucagon Function

A

prevents hypoglycemia, increases blood glucose levels

catabolic and mobilizes fuel

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3
Q

Glucagon Target Cells

A

liver-glycogenolysis (break down glycogen), glucogenesis (glucose formation)

Fat tissue- lypolysis

Muscle-proteolysis (for amino acid release)

In response to hyporglycemia-glucagon trying to make fuel

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4
Q

Factors that stimulate glucagon secretion

A

hypoglycemia, exercise, stress, fasting

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5
Q

Factors that inhibit glucagon secretions

A

hyperglycemia

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6
Q

Amylin

A

co-secreated with insulin during feeding. Supress glucagon

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7
Q

Insulin-Function

A

prevents hyperglycemia, promotes “metabolic fuel” storage
decrease blood glucose levels, decrease blood levels if amino acid concentrations and FFA/ketons, decrease serum potassium uptake into cells

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8
Q

Insulin target-Liver

A

increased glucose uptake, formation of glycogen, lipid/protein synthesis

decreased ketogenesis, glycogenolysis

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9
Q

Insulin target- muscle

A

increased glucose uptake, formation of glycogen, amino acid uptake, protein synth

decreased glycogenolysis

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10
Q

Insulin Target- adipose tissue

A

Increased- glucose uptake, glucose to form glycerol phosphate, fat storage

Decreased-lypolysis

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11
Q

Factors that stimulate nsulin secretions

A

hyperglycemia
increased serum levels of FFA, amino acids
GI/digestive hormones
parasympathetic stimulation of pancreatic beta cells

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12
Q

Factors that inhibit insulin secretion

A

hypoglycemia, negative feedback loop (increased insulin levels)
sympathetic simulation of pancreatic beta cells
prostaglandins (PGE2)

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13
Q

Insulin Sensitivity

A

body can down or up regulate insulin receptors

excessive insulin will decrease number of insulin receptors

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14
Q

DM Type 1

A

insulin insufficiency d/t result of pancreatic destruction of beta cells islets of langerhans

Hyperglycemia–cells unable to take up glucose from blood

Hyperlipidemia–lack of insulin is inhibitory to fat storage, athersclerotic changes in BV

Increased Ketone Bodies/ketoacidosis- ketones formed from increased FFA metabolism in liver

Catabolic Affect on muscle mass (attempt to mobilize amino acids for fuel)

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15
Q

Insulin Shock

A

hypoglycemia
excessive insulin administration, increased physcial activity, poor glucose monitoring

will see hunger, sweating, irritability

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16
Q

DM Type 2

A

increased insulin resistance (ineffecient clearance of glucose from blood stream results in more insulin being secreted)
sets up perpetuating cycle of increased insulin resistance