Disease Paths - Diabetes - Exam 4

Diabetes Mellitus

-Is common/ prevalent

-T2DM accounts for vast majority

-increased morbidity and mortality

-poor glucose control = affects nearly every system

What is diabetes

-is a disorder of carbohydrate metabolism

-characterized by high blood glucose = inadequate insulin production, impairs insulin action, both

-chronic hyperglycemia = tissue / blood vessel dmg over time

-glucose = in blood = body cant use it well

normal glucose metabolism

dietary carbohydrates = broken down into monosaccharides

-glucose is absorbed from GI tract = blood stream

-rising blood glucose = stimulate pancreas

-pancreatic beta cells = release insulin

-insulin helps move glucose from blood into cells for energy

-excess glucose may be stored as glycogen or converted to fat

role of insulin

-promotes glucose into cells

-lowers blood glucose after meals

-promotes glycogen formation in liver/ muscle

-promotes protein synthesis and fat storage

-inhibits breakdown of fat/ protein

-suppresses excessive fat and protein

-insulin is the body’s major glucose-lowering hormone

what happens during fasting

-when blood glucose falls, insulin secretion decreases

-liver releases stored glucose by glycogenolysis

-liver can make new glucose by gluconeogenesis

-fat / protein may be broken down to support energy needs

-insulin is absent = process becomes excessive / harmful

counterregulatory hormones

-hormones that raise blood glucose = glucagon, epinephrine, cortisol, growth hormone

-what they do = stimulate glycogen breakdown, promote gluconeogenesis, reduce glucose use by some tissues, help prevent hypoglycemia

glucose homeostasis summary

normal balance

-after eating → insulin rises, glucose enters cells

-during fasting → insulin falls, glucagon rises

-body works to keep glucose within narrow range

*diabetes is a breakdown of this normal balance

diagnostic overview

how diabetes identified = fating plasma glucose, random plasma glucose with symptoms, oral glucose tolerance testing, hemoglobin A1c

important concept = A1c reflects average glucose control over 3 months, prediabetes reflects abnormal glucose regulation before full diabetes develops

prefiabetes

-blood glucose above normal (not diabetes range)

-important warning sign for future T2DM / cardiovascular risk

-associated with sedentary lifestyle

-major prevention window

Type 1 diabetes

-autoimmune destruction of pancreatic beta cells → absolute insulin deficiency → glucose cant enter many body cells → blood glucose rises while cells are functionally starving

Common features: often younger onset (can occur at any age though), requires insulin therapy

Type 1 diabetes - without insulin

-glucose remain in bloodstream → cells cant access glucose well → liver keeps producing glucose → fat breakdown increases → ketone production increases

Type 1 diabetes - clinical manifestations

• Polyuria: Hyperglycemia pulls water into urine

• Polydipsia

• Polyphagia: Calorie loss and lack of cellular fuel cause hunger

• Weight loss

• Fatigue

• Blurred vision: fluid shifts affect lens shape and vision

Type 2 diabetes

insulin resistance → pancreas initially produces insulin → overtime, beta cells cant keep up → relative insulin deficiency develops later

Common features = obesity, more common in adults

Type 1 vs. Type 2 Diabetes

Type 1

• Autoimmune

• Absolute insulin deficiency

• Usually rapid onset

• More likely to develop DKA

• Requires insulin
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Type 2

• Insulin resistance with progressive beta-cell failure

• Relative insulin deficiency early, may worsen over time

• Usually gradual onset

• More likely to develop HHS than DKA

• Management may include lifestyle, oral agents, non-insulin injectables, and/or insulin

Insulin deficiency vs. insulin resistance

Insulin deficiency

• Too little insulin available

• Cells cannot take in glucose efficiently

• Blood glucose rises

• Fat breakdown and ketone formation increase

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insulin resistance
• Insulin is present, but tissues do not respond well

• Pancreas works harder to compensate

• Blood glucose gradually rises as compensation fails

acute complication = hypoglycemia

low blood glucose

-occur from too much insulin / glucose lowering med, missed meals, increased exercise, alcohol use, illness (can become a emergency)

-S/S = sweating, tremor, hunger, tachycardia, anxiety, irritability, confusion, weakness, seizures, loss of consciousness is severe

acute complications = diabetic ketoacidosis (DKA)

-most associated with type 1 DM = severe insulin deficiency prevents normal glucose use, lipolysis increases, liver converts fatty acids to ketones, ketones cause metabolic acidosis, hyperglycemia and osmotic diuresis cause dehydration, pt may developed electrolyte abnormalities

-typical findings = hyperglycemia, ketosis, acidosis, dehydration

-clinical features = polyuria, polydipsia, dehydration, nausea/ V, abdominal pain, fruity breath, weakens, altered mental status, Kussmaul respirations

acute complication: hyperomolar hyperglycemic state (HHS)

-associated type 2 DM = severe hyperglycemia, dehydration, increased serum osmolality, little or no ketosis, insulin may still be present (can suppress major ketone formation), HHS can be life-threatening, presents with severe neurologic symptoms

Metabolic syndrome

-cluster of metabolic abnormalities that increase risk for cardiovascular disease and T2DM

-central obesity, low HDL cholesterol, elevated BP and blood glucose,

-This is not a single disease, its a dangerous pattern of interrelated risk factors

Metabolic syndrome and CV disease

-promotes endothelial injury and atherosclerosis’

-associated with chronic inflammation and abnormal lipid metabolism

-raises risk for coronary artery disease, stoke, and vascular disease

-closely linked with insulin resistance

-metabolic syndrome is one of the clearest links between endocrine dysfunction and cardiovascular disease

Gestational diabetes

-glucose intolerance 1st recognized during pregnancy

-related to pregnancy hormones that create insulin resistance

-increases risk for maternal and fetal complications

-raises future risk for T2DM for mother

Chronic complications

-Retinopathy =

• Microvascular damage affects retinal vessels

• Can lead to vision changes and blindness

-nephropathy =

• Chronic hyperglycemia damages glomerular structures

• Leads to progressive renal dysfunction

• May advance to chronic kidney disease or kidney failure

-neuropathy =

• Sensory neuropathy

• Motor neuropathy

• Autonomic neuropathy

• Numbness, tingling, burning pain

• Loss of protective sensation

• GI, bladder, CV autonomic symptoms

• Diabetic Foot

Wrap up

• T1DM and T2DM both case hyperglycemia, but by different mechanisms

• Insulin deficiency means too little insulin

• Insulin resistance means the body is not responding well to insulin

• Metabolic syndrome is a major risk pattern tied to CV disease and T2DM

• Chronic hyperglycemia damages blood vessels, nerves, kidneys, and the CV system

• Good glucose control helps reduce complications