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Abnormality in blood glucose regulation and nutrient storage related to an absolute deficeincy of insulin or resistance to that actions of insulin
Diabetes mellitus
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Glucose Metabolism
- Glucose breaks down to form Carbon Dioxide and Water...
- *the BRAIN and NERVOUS systems rely almost exclusively on glucose metabolism
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Glycogenolysis
*Glycogen is broken down into glucose when glucose levels fall belowe normal (as they do between meals)
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Gluconeogenesis
Liver syntehesis of glucose from amino acids, glycerol, and lactic acid
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Actions of Insulin:
- *Promote target cell glucose uptake
- *Promotes Glucose storage (glycogen)
- *Inhibits gluconeogenesis
- *Inhibits fat, protein, & glycogen breakdown
- *Increases protein synthesis
- *Transports glucose to fat cells
- *Facilitates K+ transport into cells
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How do you measure the insulin levels in the blood?
C-peptide levels (indicating Beta cell functioning)
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How is Insuling transported?
- *From beta cells travels to liver
- *50% used up or degraded
- *Half life of about 15 mins
- *Binds to & activates membrane receptor
- *Activated receptor acts on cell
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Actions of Glucagon:
-Produced by pancreatic alpha cells
-Fosters glycogenolysis
-Stimulates gluconeogenesis
-Stimulates lipolysis
-Maintains blood glucose between meals
-Maintains blood glucose in fasting
-Antagonistic to insulin
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Glucose Regulating Hormones and Effects:
- -Amylin
- -Somatostatin
- -Gut-derived hormones
- Effects:
- •Decreases gluconeogenesis
- •Decreases gastric emptying
- •Increases satiet
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Hormones that counteract the storage functions of insulin in regulatory blood glucose levels during periods of fasting, exercise and other situations that either limit glucose intake or deplete glucose stores
Counterregulatory Hormones
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Examples of Counterregulatory Hormones:
- EpinephrineGrowth HormoneGlucocorticoid Hormones
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What do blood glucose levels reflect?
*The difference between the amount of glucose released into the circulation by the liver and the amount of glucose removed from the blood by body tissues
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How does insulin work?
Insulin's blood glucose-lowering action results from its ability to increase the transport of glucose into body cells and decrease hepatic production and release of glucose into the bloodstream
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Counteregulatory Hormones that INCREASE blood glucose:
*Epinephrine *Growth Hormone *Cortisol
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Manifestations of Type 1 Diabetes:
- *Polyphagia
- *Polydipsia
- *Polyuria
- *Wt. loss, fatigue
- *Ketosis
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Manifestations of Type 2 Diabetes:
- *3 P’s possible
- *Pruritis
- *Visual changes
- *Fatigue
- *Recurrent infections, slow wound healing
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Pathophysiology of Type 2 Diabetes:
- Insulin resistance
- Beta cell dysfunction
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Risk Factors Increasing chances of Gestational Diabetes:
Family history
Ethnicity
Age > 25 yrs. old
Polycystic ovarian syndrome
Prior history
BMI > 25
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Diagnoses of Diabetes:
*Fasting Blood Glucose (BG) > 126 mg/dL on 2 checks
Normal <100 mg/dL
Impaired fasting glucose = BG 100 -126 mg/dL
*Random BG > 200 with symptoms
*Glucose Tolerance Test – Abnormal > 200 mg/dL at 2 hrs post 75Gm glucose load
*Glycosylated Hemoglobin (HgA1c or A1C)
Normal < 6%
Goal for DM < 7%
Only measures control of DM
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Hypoglycemia
*Excess blood insulin
*Below normal blood glucose level (<65 mg/dL)
*Common in insulin users
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Manifestations of Hypoglycemia:
- Headache
- Sweating
- Impaired Vision
- Dizziness
- Tachycardia
- Hunger
- Diaphoresis, Pallor, Tremors, Seizures, Shaking, Irritability Anxiety
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Precipitating Factors of Hypoglycemia:
- *Lack of food intake
- *Insulin dose error
- *Medication dose change
- *Increased exercise
- *Alcohol intake
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Treatment for Hypoglycemia:
*Provide quick source of sugar
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Somagyi Effect
- Hypoglycemia ---->
- compensatory stimulation of glucagon, catecholamines, cortisol, & GH ---->
- produce gluconeogenesis ---->
- rebound hyperglycemia
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Dawn Phenomenon
- *Increased fasting blood glucose &/or insulin requirements
- *Types 1 & 2 diabetes
- *Altered glucose tolerance & circadian rhythm
- *Nocturnal GH
- *Mild to profound hyperglycemia
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Acute Complications of Diabetes Mellitus
- *Somagyi Effect
- *Dawn Phenomenon
- *Diabetic Ketoacidosis
- *Hyperglycemic Hyperosmolar Non-ketotic Syndrome (HHNS)
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Diabeteic Ketoacidosis
- *Type 1 diabetes
- *No insulin to use glucose
- *Increased liver glucose production
- *Peripheral glucose use decreased
- *Fat breakdown ---> fatty acids ---> ketone production
- *First diagnosis of diabetes for many
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Hallmark of DKA (Diabetic Ketoacidosis)
- *Ketosis
- *Hyperglycemia
- *Metabolic acidosis
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Manifestations of Diabetic Ketoacidosis:
- -Polyuria
- -Polydipsia
- -Dehydration
- -Electrolyte imbalances
- -Nausea
- -Vomiting
- -Fatigue
- -Abdominal pain
- -Fruity breath
- -Low BP
- -Tachycardia
- -Kussmaul respiration
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HHNS
- -Type 2 DM
- -Hyperglycemia
- -Hyperosmolarity
- -Dehydration
- -Ketones absent
- -Depressed neurological state
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Precipitating Factors to HHNS (Hyperglycemic Hyperosmolar Non-ketonic Syndrome)
- -Severe infections
- -MI
- -Acute pancreatitis
- -Parenteral nutrition solutions
- -Increased resistance to insulin
- -Carbohydrate intake in excessive quantities
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Manifestations of HHNS
¢ Polyuria
¢ Polydipsia
¢ Excessive thirst
¢ Dehydration
¢ Seizures
¢ Hypotension
¢ Tachycardia
¢ Nystagmus
¢ Hallucinations
¢ Coma
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CHRONIC complications of Diabetes:
¢MICRO-VASCULAR
¢Retinopathy
¢Nephropathy
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Micro-vascular chronic complications of diabetes:
¢Coronary artery disease
¢Cerebrovascular disease
¢Peripheral vascular disease
¢Foot ulcers
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Neuropathy chronic complications of Diabetes:
Manifestations on body systems
¢Gastroparesis
¢Neurogenic bowel & bladder
¢Orthostatic hypotension
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Infections often occuring in people that have Diabetes:
¢ Urinary Tract Infection (UTI)
¢ Candida
¢ Soft tissue- extremities
¢ Tuberculosis (TB)
¢ Pyelonephritis
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