learning guide M6

Categoty

HCR240-Chapter25Diabetes.pptx

Home >Nursing homework help >learning guide M6

Chapter 25

Diabetes Mellitus and Metabolic Syndrome

Diabetes Mellitus (DM)

Disorder of carbohydrate metabolism

High levels of blood glucose

Body’s inability to produce or utilize insulin

Increased:

Morbidity and mortality

CVD, renal damage

Peripheral vascular disease, neurological disorders

Blindness

Amputation

Four Major Categories of DM

Type 1 (T1DM)

Type 2 (T2DM)

Gestational diabetes (GDM)

Develops only during pregnancy due to hormonal changes decreasing insulin sensitivity

Approximately 4% of U.S. pregnancies

Other specific types of diabetes

Pancreatitis, cystic fibrosis, neonatal

Epidemiology

In U.S., over 30 million people affected

~10% with T1DM and 90% T2DM

Increased DM has paralleled obesity increase

Sedentary lifestyle also a risk factor

Polygenic disorder

Environmental factors

Classic Signs DM

Polydipsia

High BG increases plasma osmolarity

Fluid shifts from ICF into ECF (cellular dehydration)

Increased thirst

Polyuria

Increased thirst and drinking (polydipsia)

Osmotic diuresis

Glucose appears in urine (transport maximum of kidney exceeded)

Water follows glucose, increasing urine output

Signs of DM

Blurred vision

Accumulation of glucose in aqueous fluid of eye

Changes refraction of light

Electrolyte imbalance

Fluid shifts

ICF to ECF may cause dilutional hyponatremia

K+ moves out of cells (IC depletion of K+)

“False hyperkalemia”

Serum levels of K+ are elevated, but total body K+ not increased

Signs of DM (continued)

Polyphagia

If body can not use glucose:

Fat and muscle breakdown occur

Weight loss with increased appetite

Ketone levels may elevate

Glycogenolysis and Gluconeogenesis

Increasing BG further, compounding problem

Low BG is not the problem, the inability to use BG is the issue

Etiology

T1DM

Autoimmune destruction of beta cells of pancreas

Antibodies present

No insulin

T2DM

More gradual onset

Insulin resistance

Insulin still produced

Sedentary behavior

Obesity

Pathological Mechanism T1DM

T-cell mediated attack of beta cells

Genetic influence

Presenting sign is often DKA

Polyuria, polydipsia, polyphagia

Pathological Mechanism T2DM

Insulin resistance with increased insulin levels

Polyuria, polyphagia, polydipsia

Metabolic syndrome

HTN, dyslipidemia, hyperinsulinism, centralized obesity

Hyperosmolar hyperglycemia syndrome (HHM)

DKA does not normally occur in T2DM, presence of some insulin prevents ketone formation

Long-Term Complications DM

Gestational Diabetes Mellitus

Fetal defects, premature delivery, hypoglycemia in newborn, and large-for-gestational-age infants (macrosomia)

Hormone levels increase insulin resistance

Women screened

2nd trimester OGTT (oral glucose tolerance test)

GDM normally resolves after pregnancy

Can increase risk for T2DM

Background Information on Next Few Slides – NOT Required

Basics of Carbohydrate Metabolism

Insulin-supported process of facilitated diffusion moves glucose from blood into cells

Insulin produced by beta cells of islets of Langerhans in pancreas

After eating:

Synchronous rise and fall of glucose and insulin

Insulin Facilitates Glucose Uptake

Carbohydrate Metabolism

Glucose

Used for energy, stored as glycogen, or converted to component of lipid molecules

Glycogenesis

Glycogen formation

Primarily in liver and muscle

Glycogenolysis

Glycogen breakdown

Occurs when blood glucose falls and body needs energy

Blood Glucose Maintenance: Starvation

Gluconeogenesis

Amino acids and glycerol of lipids (fats) converted to glucose

Fatty acids remains as lipids

Converted to acetoacetic acid, beta-hydroxybutyric acid, and acetone

Known as ketones or ketoacids

Fruity odor: breath, saliva, sweat

Accumulation of ketones may lead to diabetic ketoacidosis (DKA)

Diabetic Ketoacidosis (DKA)

Develops in those with no insulin reserves

High levels of ketone formation

1/3 of children with T1DM first present with DKA

DKA is a critical condition requiring immediate treatment

Starvation or Inability to Use Glucose

Blood Glucose Levels

Normal BG

70–100 mg/dL (fasting)

Hypoglycemia

BG less than 70 mg/dL

Brain functioning affected

Hyperglycemia

BG greater than 200 mg/dL

Fasting BG

100–125 mg/dL

Impaired glucose tolerance (IGT) = “prediabetes”

Greater than 126 mg/dL = diabetes

Postprandial BG

Glucose after eating

Greater than 200 mg/dL = diabetes

Role of Insulin

Facilitates glucose uptake by cells

Muscle, adipose, liver

Glycogenosis in liver and muscle

“Fat sparer”

Anabolic hormone

Hyperinsulinism

Increased insulin level to overcome insulin resistance

Hyperinsulinism hypoglycemia

Low blood glucose levels from too much insulin

Other Glucose-Regulating Hormones

Glucagon

Alpha cells of pancreas

Released when BG levels are low

Glycogenolysis and gluconeogenesis

Stimulates lipase

Injectable form in severe hypoglycemia

Somatostatin

Delta cells of pancreas

Diminishes secretion of insulin and glucagon

Decreases GI activity, slow absorption

Glucose-Regulating Signals from Pancreas

Other Glucose-Regulating Hormones (continued)

GI glucose-regulating hormones

Stimulate insulin secretion, may also suppress glucagon, slow GI motility

Called incretins (GIP, secretin, cholecystokinin)

Cortisol

From adrenal cortex, increases BG

Epinephrine

From adrenal medulla, increases BG

Fluid Shifts

Fuel Utilization

learning guide M6

image3.png

image2.png

image4.jpg

image5.jpeg

image6.jpeg

image7.jpeg

image8.jpeg

image9.jpeg

image10.jpeg

image11.jpeg

image12.jpeg

image1.png