Patho 3 - Diabetes

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Cause of Development of T1 Diabetes

Genetic/Immune, 1million people

Cause of Development of T2 Diabetes

Lifestyle, 21 million people

Energy stored in liver

Glycogen

Energy stored in adipose tissue

Triglycerides

What type: Insulin not enough for body needs

T2

FPG Blood glucose level: Prediabetes

100-125

FPG Blood glucose level: Diabetes

Greater than or equal to 126

What type: Insulin Resistance

T2

T1 subtypes

A. Immune modulated B. Idiopathic

What type: Weight loss

T1

What type: Weight gain

T2

Glycated Hg or A1C

Hg into which glucose has been incorporated, useful in looking at long term (previous 6-12 weeks) control. Less than 7% desired.

Diabetic ketoacidosis

Decrease in ketones (using muscle mass for energy, FFAs), Metabolic acidosis (Low Bicarb), T1

Hyperosmolar Hyperglycemic state (HHS)

No ketoacidosis, Really high blood glucose, T2

Long-term complications of diabetes mellitus

Retinopathy, cataracts, glaucoma, dizziness, syncope, cerebral infarct, hemorrhage, ischemic heart disease, MI, hypertension, diarrhea, constipation, bladder stasis and infection, ED, glomerulosclerosis, chronic kidney disease, peripheral vascular disease, gangrene, infections, abnormal sensory and motor function, foot ulcers, cellulitis

Function of Pancreatic Acini

Secrete digestive juices into the duodenum

Function of Islets of Langerhans

Secrete hormones into the blood, composed of alpha, beta, and delta cells

Function of Pancreatic Alpha cells

Secrete glucagon

Function of Pancreatic Beta Cells

Secrete Insulin

Function of Pancreatic delta cells

Secrete Somatostatin

Function of Insulin

Glucose transport into skeletal muscle/adipose tissue, increase glycogen synthesis, Decrease gluconeogenesis

Function of Glucagon

Promotes glycogen breakdown, Increases gluconeogenesis

Catecholamines and affect on blood glucose

Epi, NE, Help to maintain blood glucose levels during stress periods

GH affects on blood glucose

Increase protein synth in all cells, breakdown of FAs from adipose tissue, antagonizes effects of insulin

Glucocorticoid effects on blood glucose

Critical to survival during periods of fasting and starvation, stimulate gluconeogenesis by liver

What type: Loss of Beta Cell Function

T1

What type: Absolute insulin deficiency

T!

What type: Impaired ability of tissue to use insulin

T2

What type: Relative lack of insulin or impaired release of insulin in relation to blood glucose

T2

Factors involved in dev of T1a

Genetic predisposition, hypothetical trigger event - environmental agent incites immune response, Immunologically mediated beta cell destruction

Type 1b diabetes

Idiopathic, small number of people most African or Asian, strongly inherited, episodic ketoacidosis with absolute insulin deficiency periods intermittently

Type 2 diabetes metabolic abnormalities

Impaired beta cell function and insulin secretion, peripheral insulin resistance, increased hepatic glucose production

Metabolic Syndrome

T2, Elevated triglycerides, low HDL, Increased BMI, increased waist circumference, increased BP, insulin resistance

Causes of Beta cell dysfunction in diabetes

Initial decrease in the beta cell mass, increased beta cell apoptosis/decreased regeneration, chronic hyperglycemia leading to beta cell desensitization (glucotoxicity), chronic elevation of FFAs causing beta cell toxicity (lipotoxicity), Amyloid deposition in beta cell can cause dysfunction

Three P's of diabetes

Polyuria (urination), Polydipsia (thirst), Polyphagia (hunger)

Characteristics of diabetic ketoacidosis

Hyperglycemia (>250 mg/dL), Low bicarb <15 mEq/L), Low pH <7.3, Ketonemia positive at 1:2 dilution, Moderate ketonuria

Characteristics of Hyperosmolar hyperglycemis state (HHS)

Hyperglycemia >600, Hyperosmolarity >310 mOsm/L, Dehydration, Absence of ketoacidosis, Sensorium depression

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