Diabetes Mellitus Definition
-chronic multisystem disease related to: Abnormal insulin production, Impaired insulin utilization, Or both
Diabetes Mellitus Statistics
- 20.8 million diabetics in the U.S.
- 41 million people with prediabetes
- 73% of adults with diabetes have hypertension
- 5th leading cause of death in the U.S.
Diabetes Mellitus Complications
Leading cause of:
- End-stage renal disease
- Adult blindness
- Nontraumatic lower limb amputations
Diabetes Mellitus Comorbidities
Major Contributing Cause for Heart Disease and Stroke. Diabetics are 2-4 times more likely to develop heart disease or stroke.
5 Common Types of Diabetes
1. Type 1
2. Type 2
3. Gestational
4. Prediabetes
5. Secondary Diabetes
Normal Insulin Metabolism
-hormone produced by the B cells in the islets of Langerhans of the pancreas
-average daily secretion 0.6 units/kg of body weight
Tight Glycemic Control
70-120 mg/dL
Normal Insulin Action
- Promotes glucose transport from bloodstream across cell membrane to cytoplasm of cell
- Decreases free floating glucose in the bloodstream
- ? Insulin after a meal
Average Daily Secretion of Insulin
0.6 units/kg of body weight
Insulin Action on the Body
- Stimulates storage of glucose as glycogen in liver and muscle
- Inhibits gluconeogenesis
- Enhances fat deposition
- ? Protein synthesis
Type 1 Diabetes Age Range
- Peak onset 11-13 yrs old
- most often ppl under 30 yrs old
Type 1 Diabetes Patho
- Progressive destruction of pancreatic B cells by body's own T cells
- Autoantibodies cause a reduction of 80- 90% of normal B cell fx before manifestations occur
Type 1 Causes
- genetic predisposition r/t human leukocyte antigens (HLAs)
-viral infection
Type 1 Onset
- long preclinical period
- manifestations develop when pancreas can no longer produce insulin then: rapid onset, present w/ ketoacidosis
Type 1 Signs
- weight loss
3 P's:
- polydipsia
-polyuria
- polyphagia
Diabetic Ketoacidosis
- Occurs in absence of insulin
- Life-threatening condition
- Results in METABOLIC ACIDOSIS
Prediabetes
- Known as:
-- impaired glucose tolerance (IGT) or
-- impaired fasting glucose (IFG)
Prediabetes Test Levels
- IFG: Fasting glucose levels higher than normal (>100 mg/dl, but <126 mg/dl)
- IGT: 2-hour plasma glucose higher than normal (between 140 and 199 mg/dl)
Prediabetes Significance
- If no preventive measure taken�usually develop diabetes within 10 yrs
- Long-term damage already occurring to:
-- Heart, blood vessels
Prediabetes Signs
- Usually present with NO symptoms
- Must watch for diabetes symptoms:
-- Polyuria
-- Polyphagia
-- Polydipsia
Type 2 Diabetes Risk Factors
Biggest Risk Factor- abdominal/visceral obesity
- 80-90% are overweight
- Age: over 35 yrs old, prevalence increases w/ age
- genetics
- race
Type 2 Culture
- ? rate in African Americans, Asian Americans, Hispanic Americans, and Native Americans
- Highest rate in the world: Native Americans & Alaskan Natives
Type 2 Patho
- Insulin produced is either insufficient or poorly utilized by tissues
Four Major Metabolic Abnormalities
1.) Insulin Resistance
2.) Pancreas ? ability to produce insulin
3.) Inappropriate glucose production from liver
4.) Alteration in production of hor
1.) Insulin Resistance
- Body tissues do not respond to insulin: receptors either unresponsive or insufficient in number
- Results in hyperglycemia
2.) Pancreas ? Ability to Produce Insulin
- ? cells fatigued from compensating
- ? -cell mass lost
3.) Inappropriate Glucose Production from Liver
- Liver's response of regulating release of glucose is haphazard
- Not considered a primary factor in development of type 2
4.) Alteration in Production of Hormones and Adipokines
- Play a role in glucose and fat metabolism
- Two main adipokines:
--Adiponectin
--Leptin
Type 2 Onset
- Gradual onset
- Person may go many years with undetected hyperglycemia
- Osmotic fluid/electrolyte loss from hyperglycemia may become severe:
-- Hyperosmolar coma
Gestational Diabetes
- Detected at 24-28 weeks of gestation
- Usually normal glucose levels at
6 weeks postpartum
Gestational Diabetes Complications
- ? risk for cesarean delivery, perinatal death, and neonatal complications
- ? risk for developing Type 2 in
5-10 years
- Therapy: First nutritional, second insulin
Secondary Diabetes
- Results from another medical condition:
1. Cushing syndrome
2. Hyperthyroidism
3. Pancreatitis
4. Parenteral nutrition
5. Cystic fibrosis
6. Hematochromatosis
Type 1 Clinical Manifestations
Classic symptoms:
1. Polyuria (frequent urination)
2. Polydipsia (excessive thirst)
3. Polyphagia (excessive hunger)
Weight loss
Weakness
Fatigue
Type 2 Clinical Manifestations
- Nonspecific symptoms
- May have classic symptoms of Type 1: ( 3 P's)
- Fatigue
- Recurrent Infections
- Recurrent vaginal yeast or monilia infections
- Prolonged wound healing
- Visual changes
Diagnostic Studies
Three methods of diagnosis:
1.) Fasting plasma glucose level >126 mg/dl
2.) Random or casual plasma glucose measurement ? 200 mg/dl plus symptoms
3.) Two-hour OGTT level ? 200 mg/dl using a glucose load of 75 g
Hemoglobin A1C Test
- glycemic levels over time
- Not diagnostic but monitors success of treatment
- amount of glucose attached to hemoglobin molecules over RBC life span
- Ideal goal: ADA ?7.0%
Exogenous insulin
Insulin from an outside source
Rapid-Acting Examples
1.) Lispro (Humalog)
2.) Aspart (Novolog)
3.) Glulisine (Apidra)
4.) Exubera
Rapid-acting (bolus) Action
- Lispro, aspart, glulisine
- Injected 0 to 15 minutes before meal
- Onset of action 15 minutes
Short- Acting Examples
Regular
Short-Acting (bolus) Action
- Regular
- Injected 30 to 45 minutes before meal
- Onset of action 30 to 60 minutes
Long-Acting (basal) Examples
1.) Glargine (Lantus)
2.) detemir (Levemir)
Long-Acting (basal) Action
- Glargine (Lantus)
- detemir (Levemir)
- Injected once a day at bedtime or in the morning
- Released steadily and continuously
- No peak action
- Cannot be mixed with any other insulin or solution
Regimen that closely mimics endogenous insulin production
is basal-bolus.
- Long-acting (basal) once a day
- Rapid/short-acting (bolus) before meals
Storage of Insulin
- In-use vials may be left at room temperature up to 4 weeks
- Extra insulin should be refrigerated
Admn of Insulin
- SQ or IV
- Fastest absorption from Abdomen, followed by Arm, Thigh, Buttock
- Preferred site: Abdomen
- Rotate injections within one particular site
U100 (100 units)
0
Potential Complications with Insulin Therapy
- Hypoglycemia
- Allergic reactions
- Lipodystrophy
- Somogyi effect
- Dawn phenomenon
Somogyi Effect
- Rebound effect in which an overdose of insulin causes hypoglycemia
- Usually during hours of sleep
- Counterregulatory hormones released
- Rebound hyperglycemia and ketosis occur
Dawn Phenomenon
- Characterized by hyperglycemia present on awakening in the morning
- Due to release of counterregulatory hormones in predawn hours
- Growth hormone/cortisol possible factors
Oral Drug Agents Action
- Work on three defects of type 2 diabetes
-- Insulin resistance
-- Decreased insulin production
-- Increased hepatic glucose production
Oral Drug Agents Examples
1.) Sulfonylureas
2.) Meglitinides
3.) Biguanides
4.) ?-Glucosidase inhibitors
5.) Thiazolidinediones
Sulfonylureas
Examples:
1. Glipizide (Glucotrol)
2. Glimepiride (Amaryl)
- ? Insulin production from pancreas
- ? Chance of prolonged hypoglycemia
- 10% experience decreased effectiveness after prolonged use
Meglitinides
Examples
1. Repaglinide (Prandin)
2. Nateglinide (Starlix)
- ? Insulin production from pancreas
- Taken 30 minutes before each meal up to time of meal
- Should not be taken if meal skipped
Biguanides
Example
1. Metformin (Glucophage)
- ? glucose production by liver
- Enhance insulin sensitivity at tissues
- Improve glucose transport into cells
- Do not promote weight gain
?-Glucosidase inhibitors
Example
1. Acarbose (Precose)
- "Starch blockers"
- Slow down absorption of carbohydrate in small intestine
Thiazolidinediones
Examples
1. Pioglitazone (Actos)
2. Rosiglitazone (Avandia)
- Most effective in those with insulin resistance
- Improves insulin sensitivity, transport, and utilization at target tissues
Drug Therapy Other Agent- Amylin analog
Example
1. Pramlintide (Symlin)
- Hormone secreted by B cells of pancreas
- Cosecreted with insulin
- Indicated for type 1 and type 2 diabetics
- Administered SQ: Thigh or Abdomen
- Slows gastric empyting, reduces postprandial glucagon secretion, increase
Type 1 Diabetes Nutrition
- Meal plan based on individual's usual food intake and is balanced with insulin and exercise patterns
- Insulin regimen managed day to day
Type 2 Diabetes Nutrition
- Emphasis based on achieving Glucose, Lipid, and BP goals
- Calorie reduction
Carbs
- Carbs and MonoUNsaturated fats should provide 45-65% of total energy intake
- ? Carbohydrate diets are not recommended for diabetics
Glycemic Index (GI)
- Term used to describe rise in blood glucose levels after consuming carb containing food
- Should be considered when formulating a meal plan
Ex: potato might have a high GI
Fats
- No more than 25-30% of meal plan's total calories
<7% from saturated fats
Protein
- Contribute <10% of total energy consumed
- Intake should be significantly less than general population
Alcohol
- High in calories
- No nutritional value
- Promotes hypertriglyceridemia
- Detrimental effects on liver
- Can cause severe hypoglycemia
Exercise
- ? Insulin receptor sites
- Lowers blood glucose levels
- Several small carb snacks can be taken every 30 min during exercise to prevent hypoglycemia
- Best done after meals
- Monitor blood glucose levels before, during, and after exercise
Stress of Illness & Surgery
- Ketone testing if glucose > 240 mg/dl
- Patients undergoing procedures requiring contrast medium should HOLD their METFORMIN day of surgery and 48 hours
Diabetic Ketoacidosis (DKA)
- Caused by profound deficiency of insulin
- most likely occurs in Type 1
- Glucose cannot be properly used for energy; Body breaks down fat
-- Ketones are by-products of fat metabolism they:
--- Alter pH balance, causing METABOLIC acidosis
--- are excret
Diabetic Ketoacidosis (DKA) Characteristics
- Hyperglycemia
- Ketosis
- Acidosis
- Dehydration
DKA Precipitating Factors
- Illness; Infection
- Inadequate insulin dosage
- Undiagnosed type 1
- Poor self-management
- Neglect
DKA S&S
- Early Sign: Lethargy/weakness
- Dehydration: poor skin turgor, tachycardia, orthostatic hypotension
- Abdominal Pain: N&V
- Kussmaul Respirations: rapid deep breathing, attempt to reverse metabolic acidosis
- Sweet, fruity odor
DKA Lab Findings
- Blood glucose > 300 mg/dl
- Arterial blood pH below 7.30
- Serum bicarbonate <15 mEq/L
- Ketones in blood and urine
DKA Interventions
- Admn Oxygen
Fluids:
1. IV infusion 0.45% or 0.9% NaCl
--restores urine output, ? BP
2. 5% dextrose if:
--blood glucose levels approach 250
--prevents hypoglycemia
3. K+ replacement
4. Sodium Bicarbonate if pH<7
5. When fluids restored, bolus followed by
Hypoglycemia Manifestations
- Confusion
- Irritability
- Diaphoresis
- Tremors
- Hunger
- Weakness
- Visual disturbances
- Can mimic alcohol intoxication
Untreated Hypoglycemia can lead to:
loss of consciousness, seizures, coma, and death
At first sign of Hypoglycemia
- check blood glucose
- If <70 mg/dl, begin treatment
Hypoglycemia Tx if alert enough to swallow
- 15-20g of a simple carb (4-6 oz fruit juice OR regular soft drink
- Recheck blood sugar 15 min after tx and again 45 min after
Hypoglycemia Tx if Not Alert enough to swallow OR 2-3 doses of simple carb hasn't worked
- Admn 1 mg of glucagon IM or SQ
-- S/e: Rebound hypoglycemia
- ingest a complex carb after recovery
- in acute care, 20-50 ml of 50% dextrose IV push
Angiopathy- Macrovascular
- Development promoted by altered lipid metabolism common to diabetes
- diabetics should be screened for dyslipidemia at dx
Angiopathy- Macrovascular Risk Factors
- Obesity
- Smoking
- Hypertension
- High-fat intake
- Sedentary lifestyle
Angiopathy- Microvascular
- SPECIFIC TO DIABETES unlike macrovascular
- thickening of vessel membranes in capillaries and arterioles, as a result of chronic hyperglycemia
Angiopathy- Microvascular Damage Affects:
- Eyes (retinopathy)
- Kidneys (nephropathy)
- Skin (dermopathy)
- manifestations usually appear after 10- 20 yrs of diabetes
Retinopathy
- #1 cause of new cases of blindness in people 20-74 yrs
Two Types:
-- Nonproliferative
-- Proliferative
Proliferative Retinopathy
- more SEVERE form
- body forms new blood vessels that are fragile and hemorrhage easily
- produce vitreous contraction
- retinal detachment can occur
Diabetes Mellitus Definition
-chronic multisystem disease related to: Abnormal insulin production, Impaired insulin utilization, Or both
Diabetes Mellitus Statistics
- 20.8 million diabetics in the U.S.
- 41 million people with prediabetes
- 73% of adults with diabetes have hypertension
- 5th leading cause of death in the U.S.
Diabetes Mellitus Complications
Leading cause of:
- End-stage renal disease
- Adult blindness
- Nontraumatic lower limb amputations
Diabetes Mellitus Comorbidities
Major Contributing Cause for Heart Disease and Stroke. Diabetics are 2-4 times more likely to develop heart disease or stroke.
5 Common Types of Diabetes
1. Type 1
2. Type 2
3. Gestational
4. Prediabetes
5. Secondary Diabetes
Normal Insulin Metabolism
-hormone produced by the B cells in the islets of Langerhans of the pancreas
-average daily secretion 0.6 units/kg of body weight
Tight Glycemic Control
70-120 mg/dL
Normal Insulin Action
- Promotes glucose transport from bloodstream across cell membrane to cytoplasm of cell
- Decreases free floating glucose in the bloodstream
- ? Insulin after a meal
Average Daily Secretion of Insulin
0.6 units/kg of body weight
Insulin Action on the Body
- Stimulates storage of glucose as glycogen in liver and muscle
- Inhibits gluconeogenesis
- Enhances fat deposition
- ? Protein synthesis
Type 1 Diabetes Age Range
- Peak onset 11-13 yrs old
- most often ppl under 30 yrs old
Type 1 Diabetes Patho
- Progressive destruction of pancreatic B cells by body's own T cells
- Autoantibodies cause a reduction of 80- 90% of normal B cell fx before manifestations occur
Type 1 Causes
- genetic predisposition r/t human leukocyte antigens (HLAs)
-viral infection
Type 1 Onset
- long preclinical period
- manifestations develop when pancreas can no longer produce insulin then: rapid onset, present w/ ketoacidosis
Type 1 Signs
- weight loss
3 P's:
- polydipsia
-polyuria
- polyphagia
Diabetic Ketoacidosis
- Occurs in absence of insulin
- Life-threatening condition
- Results in METABOLIC ACIDOSIS
Prediabetes
- Known as:
-- impaired glucose tolerance (IGT) or
-- impaired fasting glucose (IFG)
Prediabetes Test Levels
- IFG: Fasting glucose levels higher than normal (>100 mg/dl, but <126 mg/dl)
- IGT: 2-hour plasma glucose higher than normal (between 140 and 199 mg/dl)
Prediabetes Significance
- If no preventive measure taken�usually develop diabetes within 10 yrs
- Long-term damage already occurring to:
-- Heart, blood vessels
Prediabetes Signs
- Usually present with NO symptoms
- Must watch for diabetes symptoms:
-- Polyuria
-- Polyphagia
-- Polydipsia
Type 2 Diabetes Risk Factors
Biggest Risk Factor- abdominal/visceral obesity
- 80-90% are overweight
- Age: over 35 yrs old, prevalence increases w/ age
- genetics
- race
Type 2 Culture
- ? rate in African Americans, Asian Americans, Hispanic Americans, and Native Americans
- Highest rate in the world: Native Americans & Alaskan Natives
Type 2 Patho
- Insulin produced is either insufficient or poorly utilized by tissues
Four Major Metabolic Abnormalities
1.) Insulin Resistance
2.) Pancreas ? ability to produce insulin
3.) Inappropriate glucose production from liver
4.) Alteration in production of hor
1.) Insulin Resistance
- Body tissues do not respond to insulin: receptors either unresponsive or insufficient in number
- Results in hyperglycemia
2.) Pancreas ? Ability to Produce Insulin
- ? cells fatigued from compensating
- ? -cell mass lost
3.) Inappropriate Glucose Production from Liver
- Liver's response of regulating release of glucose is haphazard
- Not considered a primary factor in development of type 2
4.) Alteration in Production of Hormones and Adipokines
- Play a role in glucose and fat metabolism
- Two main adipokines:
--Adiponectin
--Leptin
Type 2 Onset
- Gradual onset
- Person may go many years with undetected hyperglycemia
- Osmotic fluid/electrolyte loss from hyperglycemia may become severe:
-- Hyperosmolar coma
Gestational Diabetes
- Detected at 24-28 weeks of gestation
- Usually normal glucose levels at
6 weeks postpartum
Gestational Diabetes Complications
- ? risk for cesarean delivery, perinatal death, and neonatal complications
- ? risk for developing Type 2 in
5-10 years
- Therapy: First nutritional, second insulin
Secondary Diabetes
- Results from another medical condition:
1. Cushing syndrome
2. Hyperthyroidism
3. Pancreatitis
4. Parenteral nutrition
5. Cystic fibrosis
6. Hematochromatosis
Type 1 Clinical Manifestations
Classic symptoms:
1. Polyuria (frequent urination)
2. Polydipsia (excessive thirst)
3. Polyphagia (excessive hunger)
Weight loss
Weakness
Fatigue
Type 2 Clinical Manifestations
- Nonspecific symptoms
- May have classic symptoms of Type 1: ( 3 P's)
- Fatigue
- Recurrent Infections
- Recurrent vaginal yeast or monilia infections
- Prolonged wound healing
- Visual changes
Diagnostic Studies
Three methods of diagnosis:
1.) Fasting plasma glucose level >126 mg/dl
2.) Random or casual plasma glucose measurement ? 200 mg/dl plus symptoms
3.) Two-hour OGTT level ? 200 mg/dl using a glucose load of 75 g
Hemoglobin A1C Test
- glycemic levels over time
- Not diagnostic but monitors success of treatment
- amount of glucose attached to hemoglobin molecules over RBC life span
- Ideal goal: ADA ?7.0%
Exogenous insulin
Insulin from an outside source
Rapid-Acting Examples
1.) Lispro (Humalog)
2.) Aspart (Novolog)
3.) Glulisine (Apidra)
4.) Exubera
Rapid-acting (bolus) Action
- Lispro, aspart, glulisine
- Injected 0 to 15 minutes before meal
- Onset of action 15 minutes
Short- Acting Examples
Regular
Short-Acting (bolus) Action
- Regular
- Injected 30 to 45 minutes before meal
- Onset of action 30 to 60 minutes
Long-Acting (basal) Examples
1.) Glargine (Lantus)
2.) detemir (Levemir)
Long-Acting (basal) Action
- Glargine (Lantus)
- detemir (Levemir)
- Injected once a day at bedtime or in the morning
- Released steadily and continuously
- No peak action
- Cannot be mixed with any other insulin or solution
Regimen that closely mimics endogenous insulin production
is basal-bolus.
- Long-acting (basal) once a day
- Rapid/short-acting (bolus) before meals
Storage of Insulin
- In-use vials may be left at room temperature up to 4 weeks
- Extra insulin should be refrigerated
Admn of Insulin
- SQ or IV
- Fastest absorption from Abdomen, followed by Arm, Thigh, Buttock
- Preferred site: Abdomen
- Rotate injections within one particular site
U100 (100 units)
0
Potential Complications with Insulin Therapy
- Hypoglycemia
- Allergic reactions
- Lipodystrophy
- Somogyi effect
- Dawn phenomenon
Somogyi Effect
- Rebound effect in which an overdose of insulin causes hypoglycemia
- Usually during hours of sleep
- Counterregulatory hormones released
- Rebound hyperglycemia and ketosis occur
Dawn Phenomenon
- Characterized by hyperglycemia present on awakening in the morning
- Due to release of counterregulatory hormones in predawn hours
- Growth hormone/cortisol possible factors
Oral Drug Agents Action
- Work on three defects of type 2 diabetes
-- Insulin resistance
-- Decreased insulin production
-- Increased hepatic glucose production
Oral Drug Agents Examples
1.) Sulfonylureas
2.) Meglitinides
3.) Biguanides
4.) ?-Glucosidase inhibitors
5.) Thiazolidinediones
Sulfonylureas
Examples:
1. Glipizide (Glucotrol)
2. Glimepiride (Amaryl)
- ? Insulin production from pancreas
- ? Chance of prolonged hypoglycemia
- 10% experience decreased effectiveness after prolonged use
Meglitinides
Examples
1. Repaglinide (Prandin)
2. Nateglinide (Starlix)
- ? Insulin production from pancreas
- Taken 30 minutes before each meal up to time of meal
- Should not be taken if meal skipped
Biguanides
Example
1. Metformin (Glucophage)
- ? glucose production by liver
- Enhance insulin sensitivity at tissues
- Improve glucose transport into cells
- Do not promote weight gain
?-Glucosidase inhibitors
Example
1. Acarbose (Precose)
- "Starch blockers"
- Slow down absorption of carbohydrate in small intestine
Thiazolidinediones
Examples
1. Pioglitazone (Actos)
2. Rosiglitazone (Avandia)
- Most effective in those with insulin resistance
- Improves insulin sensitivity, transport, and utilization at target tissues
Drug Therapy Other Agent- Amylin analog
Example
1. Pramlintide (Symlin)
- Hormone secreted by B cells of pancreas
- Cosecreted with insulin
- Indicated for type 1 and type 2 diabetics
- Administered SQ: Thigh or Abdomen
- Slows gastric empyting, reduces postprandial glucagon secretion, increase
Type 1 Diabetes Nutrition
- Meal plan based on individual's usual food intake and is balanced with insulin and exercise patterns
- Insulin regimen managed day to day
Type 2 Diabetes Nutrition
- Emphasis based on achieving Glucose, Lipid, and BP goals
- Calorie reduction
Carbs
- Carbs and MonoUNsaturated fats should provide 45-65% of total energy intake
- ? Carbohydrate diets are not recommended for diabetics
Glycemic Index (GI)
- Term used to describe rise in blood glucose levels after consuming carb containing food
- Should be considered when formulating a meal plan
Ex: potato might have a high GI
Fats
- No more than 25-30% of meal plan's total calories
<7% from saturated fats
Protein
- Contribute <10% of total energy consumed
- Intake should be significantly less than general population
Alcohol
- High in calories
- No nutritional value
- Promotes hypertriglyceridemia
- Detrimental effects on liver
- Can cause severe hypoglycemia
Exercise
- ? Insulin receptor sites
- Lowers blood glucose levels
- Several small carb snacks can be taken every 30 min during exercise to prevent hypoglycemia
- Best done after meals
- Monitor blood glucose levels before, during, and after exercise
Stress of Illness & Surgery
- Ketone testing if glucose > 240 mg/dl
- Patients undergoing procedures requiring contrast medium should HOLD their METFORMIN day of surgery and 48 hours
Diabetic Ketoacidosis (DKA)
- Caused by profound deficiency of insulin
- most likely occurs in Type 1
- Glucose cannot be properly used for energy; Body breaks down fat
-- Ketones are by-products of fat metabolism they:
--- Alter pH balance, causing METABOLIC acidosis
--- are excret
Diabetic Ketoacidosis (DKA) Characteristics
- Hyperglycemia
- Ketosis
- Acidosis
- Dehydration
DKA Precipitating Factors
- Illness; Infection
- Inadequate insulin dosage
- Undiagnosed type 1
- Poor self-management
- Neglect
DKA S&S
- Early Sign: Lethargy/weakness
- Dehydration: poor skin turgor, tachycardia, orthostatic hypotension
- Abdominal Pain: N&V
- Kussmaul Respirations: rapid deep breathing, attempt to reverse metabolic acidosis
- Sweet, fruity odor
DKA Lab Findings
- Blood glucose > 300 mg/dl
- Arterial blood pH below 7.30
- Serum bicarbonate <15 mEq/L
- Ketones in blood and urine
DKA Interventions
- Admn Oxygen
Fluids:
1. IV infusion 0.45% or 0.9% NaCl
--restores urine output, ? BP
2. 5% dextrose if:
--blood glucose levels approach 250
--prevents hypoglycemia
3. K+ replacement
4. Sodium Bicarbonate if pH<7
5. When fluids restored, bolus followed by
Hypoglycemia Manifestations
- Confusion
- Irritability
- Diaphoresis
- Tremors
- Hunger
- Weakness
- Visual disturbances
- Can mimic alcohol intoxication
Untreated Hypoglycemia can lead to:
loss of consciousness, seizures, coma, and death
At first sign of Hypoglycemia
- check blood glucose
- If <70 mg/dl, begin treatment
Hypoglycemia Tx if alert enough to swallow
- 15-20g of a simple carb (4-6 oz fruit juice OR regular soft drink
- Recheck blood sugar 15 min after tx and again 45 min after
Hypoglycemia Tx if Not Alert enough to swallow OR 2-3 doses of simple carb hasn't worked
- Admn 1 mg of glucagon IM or SQ
-- S/e: Rebound hypoglycemia
- ingest a complex carb after recovery
- in acute care, 20-50 ml of 50% dextrose IV push
Angiopathy- Macrovascular
- Development promoted by altered lipid metabolism common to diabetes
- diabetics should be screened for dyslipidemia at dx
Angiopathy- Macrovascular Risk Factors
- Obesity
- Smoking
- Hypertension
- High-fat intake
- Sedentary lifestyle
Angiopathy- Microvascular
- SPECIFIC TO DIABETES unlike macrovascular
- thickening of vessel membranes in capillaries and arterioles, as a result of chronic hyperglycemia
Angiopathy- Microvascular Damage Affects:
- Eyes (retinopathy)
- Kidneys (nephropathy)
- Skin (dermopathy)
- manifestations usually appear after 10- 20 yrs of diabetes
Retinopathy
- #1 cause of new cases of blindness in people 20-74 yrs
Two Types:
-- Nonproliferative
-- Proliferative
Proliferative Retinopathy
- more SEVERE form
- body forms new blood vessels that are fragile and hemorrhage easily
- produce vitreous contraction
- retinal detachment can occur