NSG 322 - Exam 2 Study Guide.
ENDOCRINE SYSTEM
Glucose Regulation Key Players
● Insulin
○ When blood sugar is high
○ Produced by Beta Cells in pancreas (islets of Langerhans)
○ Function:
■ Move glucose into the cells/metabolism
■ Stimulates storage of glucose in liver/muscle
■ Stimulates storage of dietary fat in adipose tissue
■ Signals liver to stop releasing glucose
■ Inhibits breakdown of glycogen *(PREVENTS glycogenolysis)
■ *Signals to inhibit lipolysis = breakdown of fat
● Glucagon
○ When blood sugar is low
○ Produced by the Alpha Cells in pancreas (Islets of Langerhans) go to liver
○ Function:
■ Stimulates liver cells to convert glycogen into glucose = (STIMULATES glycogenolysis)
■ Stimulates production of glucose from non-carb substances =
(STIMULATES gluconeogenesis)
● Glycogen = stored form of glucose
● Incretins
○ Peptides produced in the GI tract
○ Functions:
■ Stimulate insulin release
■ Decrease glucagon release
■ Stimulate satiety center
■ Slow GI emptying
○ Example: Glucagon-like polypeptide 1 (GLP-1)
, ● Dipeptidyl peptidase 4 (DDP-4)
○ Enzyme that metabolizes GLP-1
● Adiponectin (hormones produced by fat cells) plays role in metabolism
○ Increase insulin sensitivity
○ Decrease glucose released from liver
○ Protect blood vessels from inflammatory changes
Biphasic Insulin Release
● Post Prandial Insulin Production
○ “After meals” – when there’s sudden high levels of glucose
● Basal Insulin Production
○ “Maintain steady state”
○ During ‘fasting period’
○ What else occurs –
■ Glycogenolysis occurs
● By glucagon
■ Gluconeogenesis occurs
Types of Diabetes Mellitus
● Type 1 Diabetes
○ Pathophysiology:
■ Beta cells in the pancreas are destroyed by an autoimmune process
● Beta cells produce what? insulin
■ Often common +autoantibodies to pancreatic Beta cells
■ Cause of autoimmune destruction:
● Genetic susceptibility
● Environmental trigger agents
■ Little to no endogenous insulin
● Will require insulin therapy
● Ketosis can occur
■ Common acute complication:
● Hyperglycemic diabetic ketoacidosis
○ Without insulin…
■ Glucose can’t enter tissues
■ Accumulates in the blood = hyperglycemia
○ Hyperglycemia causes intracellular dehydration…..how? pulls water from body
○ Dehydration stimulates hypothalamus polydipsia develops
○ Amount of glucose filtered by kidneys exceeds its limits
■ Results in glucose ‘spilling’ into the urine
■ ….What will follow high glucose? water
■ Result in fluid loss (large volumes that are dilute) polyuria (going to the
bathroom a lot)
○ 3 Things get activated (body attempts to create more glucose b/c cells aren’t getting the
glucose needed)
■ Glycogenolysis via glucagon
■ Gluconeogenesis
■ Ketosis (breakdown of fats & proteins ATP)
○ Result:
■ Polyphagia (hunger)
, ■ Fatigue (due to intracellular dehydration)
■ Weight loss
■ Ketosis Diabetic Ketoacidosis (ketones in the bloodstream)
Type 2 Diabetes
o Metabolic Abnormalities include: (failure of
tissues to) Insulin resistance
Increased glucose production by the liver
Impaired secretion of insulin by the beta cells
o Causes:
Complex interaction of many genes, environmental factors
Most common risk factor = obesity and decreased physical inactivity
Likely related to: increased fat= increase secretion adipokines inflammatory cytokines
increase tissue insulin resistance
o Onset: slow, progressive
o Treatment: lifestyle initially oral meds oral meds + insulin (if difficult to treat)
o Acute complications: Hyperosmolar hyperglycemic NON-ketotic syndrome
o Risk factors for developing Type 2
Diabetes: Age >45 years
Overweight (BMI > 25)
Habitual physical inactivity (sedentary lifestyle weight gain)
Race/Ethnicity (Asians, Hispanics, African Americans)
Previous impaired fasting glucose or impaired glucose
tolerance Hx gestational DM (when woman is pregnant &
develop diabetes) HTN (elevated blood pressures)
Metabolic Syndrome
PCOS = polycystic ovarian syndrome (they have some degree of insulin resistance)
ENDOCRINE SYSTEM
Glucose Regulation Key Players
● Insulin
○ When blood sugar is high
○ Produced by Beta Cells in pancreas (islets of Langerhans)
○ Function:
■ Move glucose into the cells/metabolism
■ Stimulates storage of glucose in liver/muscle
■ Stimulates storage of dietary fat in adipose tissue
■ Signals liver to stop releasing glucose
■ Inhibits breakdown of glycogen *(PREVENTS glycogenolysis)
■ *Signals to inhibit lipolysis = breakdown of fat
● Glucagon
○ When blood sugar is low
○ Produced by the Alpha Cells in pancreas (Islets of Langerhans) go to liver
○ Function:
■ Stimulates liver cells to convert glycogen into glucose = (STIMULATES glycogenolysis)
■ Stimulates production of glucose from non-carb substances =
(STIMULATES gluconeogenesis)
● Glycogen = stored form of glucose
● Incretins
○ Peptides produced in the GI tract
○ Functions:
■ Stimulate insulin release
■ Decrease glucagon release
■ Stimulate satiety center
■ Slow GI emptying
○ Example: Glucagon-like polypeptide 1 (GLP-1)
, ● Dipeptidyl peptidase 4 (DDP-4)
○ Enzyme that metabolizes GLP-1
● Adiponectin (hormones produced by fat cells) plays role in metabolism
○ Increase insulin sensitivity
○ Decrease glucose released from liver
○ Protect blood vessels from inflammatory changes
Biphasic Insulin Release
● Post Prandial Insulin Production
○ “After meals” – when there’s sudden high levels of glucose
● Basal Insulin Production
○ “Maintain steady state”
○ During ‘fasting period’
○ What else occurs –
■ Glycogenolysis occurs
● By glucagon
■ Gluconeogenesis occurs
Types of Diabetes Mellitus
● Type 1 Diabetes
○ Pathophysiology:
■ Beta cells in the pancreas are destroyed by an autoimmune process
● Beta cells produce what? insulin
■ Often common +autoantibodies to pancreatic Beta cells
■ Cause of autoimmune destruction:
● Genetic susceptibility
● Environmental trigger agents
■ Little to no endogenous insulin
● Will require insulin therapy
● Ketosis can occur
■ Common acute complication:
● Hyperglycemic diabetic ketoacidosis
○ Without insulin…
■ Glucose can’t enter tissues
■ Accumulates in the blood = hyperglycemia
○ Hyperglycemia causes intracellular dehydration…..how? pulls water from body
○ Dehydration stimulates hypothalamus polydipsia develops
○ Amount of glucose filtered by kidneys exceeds its limits
■ Results in glucose ‘spilling’ into the urine
■ ….What will follow high glucose? water
■ Result in fluid loss (large volumes that are dilute) polyuria (going to the
bathroom a lot)
○ 3 Things get activated (body attempts to create more glucose b/c cells aren’t getting the
glucose needed)
■ Glycogenolysis via glucagon
■ Gluconeogenesis
■ Ketosis (breakdown of fats & proteins ATP)
○ Result:
■ Polyphagia (hunger)
, ■ Fatigue (due to intracellular dehydration)
■ Weight loss
■ Ketosis Diabetic Ketoacidosis (ketones in the bloodstream)
Type 2 Diabetes
o Metabolic Abnormalities include: (failure of
tissues to) Insulin resistance
Increased glucose production by the liver
Impaired secretion of insulin by the beta cells
o Causes:
Complex interaction of many genes, environmental factors
Most common risk factor = obesity and decreased physical inactivity
Likely related to: increased fat= increase secretion adipokines inflammatory cytokines
increase tissue insulin resistance
o Onset: slow, progressive
o Treatment: lifestyle initially oral meds oral meds + insulin (if difficult to treat)
o Acute complications: Hyperosmolar hyperglycemic NON-ketotic syndrome
o Risk factors for developing Type 2
Diabetes: Age >45 years
Overweight (BMI > 25)
Habitual physical inactivity (sedentary lifestyle weight gain)
Race/Ethnicity (Asians, Hispanics, African Americans)
Previous impaired fasting glucose or impaired glucose
tolerance Hx gestational DM (when woman is pregnant &
develop diabetes) HTN (elevated blood pressures)
Metabolic Syndrome
PCOS = polycystic ovarian syndrome (they have some degree of insulin resistance)
