Glucose Regulation - prelecture talk
● Main Organs: Liver and Pancreas, kindeys *sometimes*
● Elimination- Diabetes patients experience polyuria/osmotic diuresis
○ Electrolyte impacted: potassium (high) —> metabolic acidosis
○ Breaking down a lot of ketones
● Nutrition- will help manage the glucose regulation, important component
● Treatment- insulin is always given , and iv fluids
● How insulin works- insulin is like a key, it opens up the cell so glucose can go in, we
need it for brain function cuz brain doesnt make/store its own insulin
Diabetes Mellitus
● A chronic multisystem disease characterized by hyperglycemia related to abnormal
insulin production, impaired insulin utilization, or both
● Etiology and patho: It can be genetic, autoimmune, and environmental; r/t
absent/insufficient and/or poor utilization of insulin.
✨Differentiating between Type 1 and Type 2 diabetes ✨
Type 1 Diabetes:
● Formerly known as juvenile onset or insulin dependent diabetes
● Accounts for only about 5-10% of people with diabetes
● Generally affects people under 40 years old (but it can occur at any age)
● Etiology
○ Autuoimmune disorder (body against insulin or pancreatic B cells)
○ Which results in not enough insulin to survive… absence of endogenous insulin
○ Has a Genetic component
○ Other kinds:
■ Idiopathic diabetes - not autoimmune
■ Latent Autoimmune diabetes in adults (LADA) - does not necessary need
insulin
● Onset
○ Auto-antibodies are present for months to years before symptoms occur
○ Manifestations develop when pancreas can no longer produce insulin - then rapid
onset with ketoacidosis
○ Necessitates insulin
○ Patient may have temporary remission after initial treatment
● Clinical Manifestations for TYPE 1
○ Classic symptoms are the three P’s
■ Polyuria (frequent urination)
■ Polydipsia (excessive thirst) ent
■ Polyphagia (excessive hunger)
sulin
Pen:
Look at the Number
Straight Up!
, ○ Weight loss
○ Weakness
○ Fatigue
Type 2 Diabetes
● Formerly known as adult-onset diabetes or non–insulin-dependent diabetes
● Most prevalent type (90% to 95%)
● Many risk factors: overweight, obesity (greatest risk factor), advanced age, family
history
● Increasing prevalence in children
● Greater prevalence in ethnic group (african americas, hisapnics, and american indians)
● Etiology
○ Pancreas is producing some endogenous insulin but NOT ENOUGH .. OR
○ Body does not use the insulin effectively
○ Genetic component increases insulin resistance with obseity
● Risk factors:
○ Metabolic syndrome
○ Things such as:
■ Elevated glucose levels
■ Abdominal obesity
■ Elevated BP
■ High levels of triglycerides
■ Decreased levels of HDLs
● Onset
○ Gradual onset
○ Hyperglycemia may go many years without being detected
○ Often discovered with routine laboratory testing
○ About 50-80% of B cells are no longer secreting insulin
● Clinical Manifestations for TYPE 2
○ Nonspecific symptoms
■ Classic symptoms of type 1 may manifest
○ Fatigue
○ Recurrent infection
○ Recurrent vaginal yeast or candida infection
○ Prolonged wound healing
○ Visual changes
Collaborative Care of Patient with Diabetes Mellitus
● Goals of diabetes managment
○ Decrease symptoms
○ Promote well-being
○ Prevent acute complications
○ Delay onset and progression of long-term complications
○ Maintain blood glucose levels as near to normal as possible
● Patient Teaching
■ Nutritional therapy (low calorie diet)
■ Drug therapy (insulin for type 1 always)
■ Exercise (physical weight loss. 150min/week)
■ Self-monitoring of blood glucose (tight control of blood glucose levels can
● Main Organs: Liver and Pancreas, kindeys *sometimes*
● Elimination- Diabetes patients experience polyuria/osmotic diuresis
○ Electrolyte impacted: potassium (high) —> metabolic acidosis
○ Breaking down a lot of ketones
● Nutrition- will help manage the glucose regulation, important component
● Treatment- insulin is always given , and iv fluids
● How insulin works- insulin is like a key, it opens up the cell so glucose can go in, we
need it for brain function cuz brain doesnt make/store its own insulin
Diabetes Mellitus
● A chronic multisystem disease characterized by hyperglycemia related to abnormal
insulin production, impaired insulin utilization, or both
● Etiology and patho: It can be genetic, autoimmune, and environmental; r/t
absent/insufficient and/or poor utilization of insulin.
✨Differentiating between Type 1 and Type 2 diabetes ✨
Type 1 Diabetes:
● Formerly known as juvenile onset or insulin dependent diabetes
● Accounts for only about 5-10% of people with diabetes
● Generally affects people under 40 years old (but it can occur at any age)
● Etiology
○ Autuoimmune disorder (body against insulin or pancreatic B cells)
○ Which results in not enough insulin to survive… absence of endogenous insulin
○ Has a Genetic component
○ Other kinds:
■ Idiopathic diabetes - not autoimmune
■ Latent Autoimmune diabetes in adults (LADA) - does not necessary need
insulin
● Onset
○ Auto-antibodies are present for months to years before symptoms occur
○ Manifestations develop when pancreas can no longer produce insulin - then rapid
onset with ketoacidosis
○ Necessitates insulin
○ Patient may have temporary remission after initial treatment
● Clinical Manifestations for TYPE 1
○ Classic symptoms are the three P’s
■ Polyuria (frequent urination)
■ Polydipsia (excessive thirst) ent
■ Polyphagia (excessive hunger)
sulin
Pen:
Look at the Number
Straight Up!
, ○ Weight loss
○ Weakness
○ Fatigue
Type 2 Diabetes
● Formerly known as adult-onset diabetes or non–insulin-dependent diabetes
● Most prevalent type (90% to 95%)
● Many risk factors: overweight, obesity (greatest risk factor), advanced age, family
history
● Increasing prevalence in children
● Greater prevalence in ethnic group (african americas, hisapnics, and american indians)
● Etiology
○ Pancreas is producing some endogenous insulin but NOT ENOUGH .. OR
○ Body does not use the insulin effectively
○ Genetic component increases insulin resistance with obseity
● Risk factors:
○ Metabolic syndrome
○ Things such as:
■ Elevated glucose levels
■ Abdominal obesity
■ Elevated BP
■ High levels of triglycerides
■ Decreased levels of HDLs
● Onset
○ Gradual onset
○ Hyperglycemia may go many years without being detected
○ Often discovered with routine laboratory testing
○ About 50-80% of B cells are no longer secreting insulin
● Clinical Manifestations for TYPE 2
○ Nonspecific symptoms
■ Classic symptoms of type 1 may manifest
○ Fatigue
○ Recurrent infection
○ Recurrent vaginal yeast or candida infection
○ Prolonged wound healing
○ Visual changes
Collaborative Care of Patient with Diabetes Mellitus
● Goals of diabetes managment
○ Decrease symptoms
○ Promote well-being
○ Prevent acute complications
○ Delay onset and progression of long-term complications
○ Maintain blood glucose levels as near to normal as possible
● Patient Teaching
■ Nutritional therapy (low calorie diet)
■ Drug therapy (insulin for type 1 always)
■ Exercise (physical weight loss. 150min/week)
■ Self-monitoring of blood glucose (tight control of blood glucose levels can
