Diabetes Flashcards
What is diabetes?
A chronic multi-system disease related to abnormal or impaired insulin utilization
Diabetes is characterized by
Hyperglycemia resulting from lack of insulin, lack of insulin effect, or both
Diabetes is a combination of causative factors
Genetic, hereditary
Autoimmune
Lifestyle
Pancreas
Exocrine function
Produces enzymes for digestion
Pancreas
Endocrine function
Islets of Langerhans
Hormones: insulin and glucagon
Liver
Stores and produces glucose
Insulin is made by the
Beta cells of the pancreas and is released in small amounts to the blood stream
Liver and muscle cells store
Excess glucose as glycogen
Skeletal muscle and adipose tissue are
Insulin dependent tissues
(Insulin is required to “unlock” receptor sites in cells, allowing transport of glucose into cells to be used for energy)
Glucagon is released from the
Alpha cells of the pancreas
Insulin
Facilitates transport
Insulin is a hormone that is produced by
The beta cells in the islet of langerhans
Insulin is normally released in
Small increments when food is ingested
Counterregulatory hormones
Cortisol
Growth hormone
Epinephrine
Glucagon
Insulin resistance
The body is making keys (insulin), BUT the keys don’t work very well at opening the locked doors of the cells in the body
Insulin insufficiency
The body is making insulin, but not enough
Hypoglycemia
Low blood sugar
Hypoglycemia occurs when
There is too much insulin in proportion to available glucose
Hypoglycemia ___________ _____________
Worsens rapidly and needs to be treated ASAP
What is released with hypoglycemia?
Counterregulatory hormones
What provides a defense against hypoglycemia?
Suppression of insulin secretion and production of glucagon & epinephrine
Hypoglycemia untreated
Loss of consciousness
Seizures
Coma
Death
Causes of hypoglycemia
Alcohol intake without food
Too little food
Too much diabetic meds (insulin, orals)
Too much exercise without adequate food intake
Weight loss without change in meds
Sendentary lifestyle with an unusually active day
S/S of hypoglycemia
Cold, clammy skin
Numbness of fingers, toes, mouth
Tachycardia, palpitations
Headache
Nervousness
Faintness, dizziness
Stupor
Slurred speech
Hunger
Changes in vision
Seizures, coma
Irritability
Epinephrine release causes
Shakiness
Palpitations
Nervousness
Diaphoresis
Anxiety
Hunger
Pallor
Hypoglycemia can affect
Mental functioning, because the brain needs a constant supply of glucose in sufficient quantities to function properly
Hypoglycemia can mimic
Alcohol intoxication
Neuroglycopenia manifestations
Difficulty speaking
Visual changes
Stupor
Confusion
Coma
Physiological consequences of hypoglycemia
Neurological symptoms
Hypoglycemia unawareness
Hypoglycemia treatment
Rule of 15
IV dextrose
Glucagon IM or sub Q
Bagsimi (glycagon) nasal
Factors affecting hypoglycemia
Hospitalization
-overuse of SSI
-lack of dosage changes when dietary intake is changed
-overly vigorous treatment of hyperglycemia
-delayed meal after fast acting insulin is used
Hyperglycemia
High blood sugar (>200 mg/dl)
Hyperglycemia occurs when
There is not enough insulin working, too much glucose in the blood
Hyperglycemia has a more
Gradual onset of
Hyperglycemia untreated can lead to
Diabetic ketoacidosis (DKA) or Hyperosmolar Hyperglycemia syndrome (HHS)
Coma and death
Causes of hyperglycemia
Illness, infection
Corticosteroids
Too much food
Not enough diabetic medication (insulin, oral)
Inactivity
Emotional, physical stress
Poor absorption of insulin
Hyperglycemia S/S:
Hot and dry
Polyuria
Polydipsia
Polyphagia
Weakness, fatigue
Blurred vision
Headache
Glycosuria
N/V, abdominal cramps
Mood swings
Slow healing wounds/infections
Treatment of hyperglycemia
Continue diabetic meds
Check blood glucose frequently
Check urine for ketones
Drink fluids at least on hourly basis
Exercise/stay active
factors affecting hyperglycemia
Hospitalization
-changes in treatment regimen
-meds
-IV dextrose
-overly vigorous treatment of hypoglycemia
Diagnostic studies for DM
HA1C
Fasting plasma glucose
Oral glucose tolerance test
Random blood glucose
C-Peptide test
Hemoglobin A1C (HA1C) is also known as
Glycosylated Hemoglobin A1C
Glycosylated hemoglobin (HA1C) s
The hemoglobin that glucose is bound
Hemoglobin A1C reflects
The average blood glucose levels over the past 2-3 months
Hemoglobin A1C levels
Normal: less than 5.7%
Pre-diabetes: 5.7-6.5%
Diabetes: 6.5% and higher
Fasting plasma glucose (FPG)
Checks fasting blood sugar levels
Blood is drawn at least 8 hours after the last meal eaten
Fasting plasma glucose levels
Normal: less than 100 mg/dL
Pre-diabetes: 100-125 mg/dL
Diabetes: 126 mg/dL or higher
Oral Glucose Tolerance Test (OGTT)
Two hour test that checks blood sugar before and two hours after a glucose drink is consumed
-tests how well your body processes sugar!
Oral glucose tolerance test levels
Normal: less than 140 mg/dL
Pre-diabetes: 140-199 mg/dL
Diabetes: 200 mg/dL or higher
Random blood glucose
Blood can be drawn at anytime
Seen on a BMP or CMP
Random blood glucose levels
Diabetes: 200 mg/dL or higher plus symptoms of diabetes
C-Peptide test
Measures the amount of C-peptide in the blood or urine
-can help determine which type of diabetes a patient has
-can reveal how well treatment is working
C-Peptide test levels
Low: Type 1 diabetes
Normal: 0.5 to 2.0 ng/mL
High: Type 2 diabetes
Blood glucose monitoring
Finger stick (most common)
Continuous glucose monitoring (CGM)
Provides timely feedback to patient
Advised before each meal and bedtime
Most common error in blood glucose monitoring
Blood sample size
Types of diabetes
Type 1
Type 2
Gestational
Type 1 diabetes
Autoimmune disease
Results from beta cell destruction in the pancreas
Autoantibodies present for months to years before clinical symptoms
Leads to absolute insulin deficiency
Insulin dependent
Type 1 risk factors
Autoimmune
Viral
Medically induced
S/S of type 1
Polyuria
Polydipsia
Polyphagia
Weight loss
Fatigue
^ frequency of infections
Rapid onset!!
Familial tendency
Type 1 diabetes diagnosis
HA1C
Fasting plasma glucose
Oral glucose tolerance test
Random blood glucose plus symptoms of diabetes
Type 1 diabetes treatment
Insulin dependent
-administration of subQ insulin multiple times a day
-external insulin pump
Tight glycemia control
Dietary modifications
Active lifestyle
Type 2 diabetes
Caused by insulin resistance or deficiency
More common in adults
Progressive disease, slower onset!!!
Types 2 causes
Insulin resistance or deficiency
Pre-diabetes
Metabolic syndrome
Type 2 modifiable risk factors
Obese/fat distribution
Physical inactivity/sedentary lifestyle
Hypertension/high cholesterol
Poor diet
Smoking/alcohol
Type 2 non-modifiable risk factors
Family history
Race/ethnic background
Age
Pre-diabetic & Gestational diabetes
PCOS
Chronic glucocorticoid exposure
Type 2 diabetes S/S
Genetic mutations (insulin resistance & familial tendency)
Polyuria, nocturia
Polydipsia
Polyphagia
Recurrent infections
Prolonged wound healing
Visual changes
Fatigue
Prediabetes
Metabolic syndrome
Type 2 diagnosis
HA1C
Fasting plasma glucose
Oral glucose tolerance test
Random blood glucose plus symptoms of diabetes
Type 2 treatment
Diabetic meds (insulin or oral)
Lifestyle changes
Tight glycemia control
Increase activity levels
Short term diabetic complications
Hypoglycemia
Hyperglycemia
Ketoacidosis
Long term diabetic complications
MICROVASCULAR
Retinopathy
Nephropathy
Neuropathy
Long term diabetic complications
MACROVASCULAR
Cerebrovascular
Cardiovascular
Peripheral vascular
Long term diabetic complications
OTHER
Foot ulcerations
Amputations
Sexual dysfunction
Preventing complications
Patient education
Assess barriers to learning
Teach in increments
Promote self care
Adjust regimen to meet needs
Barriers
Degree of life changes/complexity of management plan
Cost of care
Access to treatment
Cultural factors
Lack of family support
Lack f knowledge
Fears
Other stressors
Exercise is
An essential part of prediabetes and diabetes management
Exercise
Decreases insulin resistance and can have direct effect on lowering blood glucose levels
What can occur is a sedentary patient that has an unusually active day?
Hypoglycemia
ADA exercise recommendations
150 mins of exercise a week (30 mins, 5 days a week)
DM2 pts to perform resistance training 3 times a week
If taking diabetic medications, there is an increased risk for
Hypoglycemia
Alcohol
Moderation
Inhibits gluconeogenesis
Monitor blood glucose
Consume carbs
High in calories
Sick day rules
Maintain normal diet if able
Increase non-caloric fluids
Continue taking antidiabetic meds
If normal diet not possible, supplement with carb containing fluids while continuing meds
S (sick rules)
Sugar!
Check your blood glucose every 2-3 hours or as necessary
I (sick rules)
Insulin!
Always take your insulin! Not taking could lead to DKA
C (sick rules)
Carbs!
Drink lots of fluids!
If sugars high = drink sugar free liquids
If sugars low = drink carb containing drinks
K (sick rules)
Ketones!
Check your urine or blood ketones every 4 hours
Take rapid acting insulin if ketones are present
2 types of insulin
Endogenous insulin
Exogenous insulin
Exogenous insulin corrects
Hyperglycemia
Many associated metabolic imbalances
Exogenous insulin actions
Restores ability of cells to use glucose as an energy source
Lowers plasma potassium levels
Insulin preparations are HIGH ALERT agents
Exogenous insulin treats
Both type 1 and type 2 diabetes
Human insulin
Identical to insulin produced by the pancreas
Human insulin analogs
Modified forms of human insulin
Basal-Bolus Insulin therapy
Mimics physiological insulin secretion of a “normal” pancreas!
A little insulin is given all day and night (__________), and a burst of insulin with meals to cover the carbs eaten (_____________)
Basal
Bolus/mealtime
Correction dose
Sliding scale is given in ADDITION to schedules insulins (basal and mealtime) to bring an elevated blood glucose back into target range
Rapid acting insulin
Administered with meals (prandial)
-hold if NPO!
Rapid acting insulin levels
Fastest onset, shortest duration
Onset: 10-30 mins
Peak: 30 mins to 3 hours
Duration: 3-5 hours
Types of rapid acting insulin
Aspart (Novolog)
Lispro (humalog)
Glulisine (apidra)
Short acting insulin
Can be given subQ, IM or IV (only one that can be given IV)
For routine treatment to control postprandial hyperglycemia (subQ) and basal glycemia control (subQ infusion via insulin pump)
Short acting insulin levels
Onset: 30-60 mins
Peak: 2-5 hours
Duration: 5-8 hours
Types of short acting insulin
Regular insulin (humulin R, Novolin R)
Intermediate insulin
Onset is delayed, therefore can’t be used for postprandial control
Used 2-3 times per day to provide glycemia control between meals and during the night
intermediate insulin is
Cloudy!
Given subQ
The only one that can be mixed with rapid/short acting insulin
Intermediate insulin can cause
Allergic reactions
-local or systemic
Intermediate insulin levels
Onset: 1.5-4 hours
Peak: 4-12 hours
Duration: 12-18 hours
types of intermediate insulin
NPH (Humulin, Novolin N)
Long duration insulin
Dosing can be done at anytime, but at the same time everyday
Given subQ
Type 1 must have to prevent DKA
long duration insulin levels
Onset: 45 min to 4 hours
Peak: none
Duration: 16-24 hours
Types of long duration insulin
Glargine (lantus)
Determir (levemir)
Longer duration insulin
Injected once daily
Only comes in pre filled pens
Longer duration insulin levels
Onset: 30-90 mins
Peak: none
Duration: >24 hours
Types of longer duration insulin
Glargine U-300 (toujeo)
Degludec (tresiba)
Combination or pre-mixed insulin
Short or rapid acting insulin mixed with intermediate acting insulin
Allows for both mealtime and correction insulin in the same syringe
Offers convenience
Insulin appearance
Clear, colorless
NPH is only cloudy suspension
Inspect before use
Discard if abnormal
Insulin concentration
U-100 is 100 units/mL
U-200 is 200 units/mL
U-300 is 300 units/mL
U-500 is 500 units/mL
Mixing insulin
Draw up the clear before the cloudy
Insulin administration
All types can be given subQ
NPH must roll gently between hands to mix the suspension
Insulin injection sites
Upper arm
Abdomen
Upper thigh
Upper buttock
High dose steroids for prolonged period =
Kills pancreas
Steroids can
Increase blood sugar
What produces insulin
Pancreas
Insulin _______ blood sugar
Lowers
Glucagon ________ blood sugar
Raises
What makes glucose?
Liver
What needs adequate glucose to function?
Brain, liver, blood cells
Insulin is a _________ hormone
Natural
Anabolic (storage hormone)
What is the normal insulin level?
40-50 units a day in normal adult with functioning pancreas (0.6 units/kg)
Insulin promotes
Glucose transport
Epinephrine
Adrenaline
Counterregulatory hormones helps
Naturally increase blood sugar
Growth hormone
Part of the brain, released from pituitary
Alcohol inhibits
Livers ability to release glucose
Conditions that may cause diabetes
Cushing syndrome
Hyperthyroidism
Recurrent pancreatitis
Cystic fibrosis
Hemochromatosis
Use of parental nutrition
How does the use of parenteral nutrition cause diabetes
Glucose enters the peripheral circulation, reaching high serum levels and producing hyperglycemia and hyperinsulinemia
Meds that can induce diabetes
Corticosteroids (prednisone)
Thiazides (hydrochlorothiazide)
Phenytoin
Atypical antipsychotics (clozapine)
Corticosteroids
Induce hyperglycemia
Long term use = insulin resistance
Thiazides
Reduce insulin release
Increase resistance to the action of insulin
Phenytoin
Can induce hyperglycemia, inhibits insulin release
Atypical antipsychotics (clozapine)
Inhibits insulin secretion or promotes insulin resistance
Diabetes caused by medical conditions or medications
Can resolve when the condition is treated or the medication is discontinued
Endocrine
5% endocrine cells called islets of langerhans
Look like grapes and produce hormones that regulate blood sugar and regulate pancreatic secretions
Insulin facilitates glucose metabolism by
Binding to insulin receptors on the cell wall, signaling glucose transporter molecules that facilitate glucose entry into the cell
Insulin suppresses _________ secretion and facilitates _________ storage
Glucagon
Glycogen
Counterregulatory hormones increase BG levels by
Stimulating glucose production and release by the liver
Decreasing the movement of glucose in cells
Counterregulatory hormones all lead to
Utilization of glycogen stores
Counterregulatory hormones are increased with
Stress related conditions, both physical (pain, illness, injury) and emotional
Often referred to as stress hormones
Epinephrine is released from
Nerve endings and adrenals
Acts directly on liver to promote sugar production (via glycogenolysis)
Promotes breakdown and release of fat nutrients that travel to liver and are converted into sugar and ketones
Cortisol
Steroid hormone secreted from adrenal glands
Makes fat and muscle cells resistant to action of insulin and enhances production of glucose
Normal circumstances, cortisol
Counterbalances the action of insulin
Under stress or if a synthetic cortisol is given as a medication (prednisone or cortisone injection)
Cortisol levels become elevated, and you become insulin resistant
High levels of Growth hormones
Cause resistance to the action of insulin
Brain depends on
Glucose as its only source for fuel
Hypoglycemia can progress from mild symptoms to
Neurological changes, seizures, LOC, death
Recurrent hypoglycemia can
Lower the glucose level that typically stimulates Counterregulatory hormones, thus symptoms do not occur until levels are dangerously low
Chronic hypoglycemia leads to
Hypoglycemia unawareness
Hypoglycemia unawareness
Condition in which a patient does not have the warning s/s of hypoglycemia until glucose levels reach a critical point
Patients risk for hypoglycemia unawareness
Repeated hypoglycemic episodes
Older adults
Use of beta blockers
Hypoglycemia occurs 2-3 more times in
DM1
Rule of 15
15g of simple carb (fruit juice or soda)
Glucose gels or tablets
Recheck BS in 15 mins, if still low repeat the process
Avoid carbs with fat (candy, cookies, milk) fat will slow down absorption of glucose
IV dextrose
In hospital pt can get 25-50 mls of 50% dextrose IV (if pt not alert and has IV)
Glucagon IM or SQ injection
Turn pt on side to prevent aspiration
Stimulates a strong hepatic response to convert glucagon to glucose
27 gauge needle
Can take up to 15 mins
Buttock, upper arm and thigh
Feed pt as soon as they wake (fast-juice/coke; long acting-crackers w cheese or PB)
Bagsimi
Dry nasal spray
Can be used if congested
Can be used before pt is unconscious and after
Turn pt on side
Feed pt as soon as they wake up
HA1C could be inaccurate in some pts with conditions:
Pregnancy
Chronic kidney
Liver disease
Recent severe bleeding/blood transfusions
Blood disorders (thalassemia, iron deficiency anemia, vit b 12 anemia)
Hemoglobin A1C levels should be less than
7%
What test is used when diabetes is suspected but can’t be definitively diagnosed by FPG or HA1C?
OGTT
OGTT is more
Expensive/time consuming
Not used routinely
Glucose drink contains
75 grams of sugar
C peptide test can determine diagnosis of
Pancreatic cancer, kidney failure, Cushing syndrome or Addison disease
C-peptide is a
Byproduct the pancreas releases into the body when it makes insulin
-when ppl take insulin, body doesn’t make or release c pep
The frequency of BG monitoring is individualized based on
Frequency of injections
Hypoglycemic reactions
Level of control (pt holds all the control!)
To adjust therapy
Need to increase BG frequency when
Therapy is being initiated or changed
There is acute or ongoing illness
There is hypoglycemia unawareness
Fasting or postprandial BG levels are consistent with HA1C
Continuous glucose monitoring
Assess interstitial glucose, which lags behind BG 5-10 mins
Gestational diabetes
Manifests during pregnancy, precursor for DM2 (35-60% chance of developing DM2 within 10years; or giving birth to 10+ lb baby)
Tight glycemia control
BS before meals 80-130
BS 1-2 hours after the start of meal <180
Exercise can worsen conditions in
DM1 who has hyperglycemia with ketones
Seeing more type 2 in
Children due to obesity
What ethnic groups are more likely to have DM2
African American, Latino, Native American, Asian American, Pacific Islander
Micro
Result from thickening of the vessel membranes in the capillaries and arterioles (small vessels) in response to chronic hyperglycemia
Macro
Are diseases of the large and medium sized blood vessels that occur with greater frequency and earlier onset
Retinopathy
Process of Microvascular damage to retina bc of hyperglycemia, Nephropathy and HTN
-nonproliferative: most common
-proliferative: most severe
Neuropathy
Nerve damage that occurs bc of metabolic imbalances that occur in DM
Sensory neuropathy
Affects hands/feet
Can lead to loss of sensation in lower extremities
Nephropathy
Damage to small blood vessels in glomeruli of kidney
-tight glycemic control!!
Cerebrovascular
Disease of blood vessels supplying brain
-stroke due to vessels narrowing (STENOSIS), clot formation (THROMBOSIS), artery blockage (EMBOLISM) or blood vessel rupture (HEMORRHAGE)
Cardiovascular
Disease of blood vessels supplying the heart muscle
-Coronary artery disease
-MI
Peripheral vascular
Disease of blood vessels supplying arms and legs
Tight glycemic control can reduce risk of
Eye, kidney, and nerve damage
Hormone regulation
Significant influence hormones have on regulation of glucose
Nutrition/mobility
Needed for optimal regulation of glucose concentration and management
Moderate alcohol consumption
1 drink per day women
2 drinks per day men
Gluconeogenesis
Breakdown of glycogen to glucose
Basal insulin
Long acting insulin that covers the BG the liver makes naturally, 24 hrs a day
-SHOULD be given if NPO, may need to be reduced
-overnight/between meals
Bolus insulin
Fast acing insulin given for rise in BG postprandial.
Never give until meal is in room and pt is ready to eat
Should be HELD if NPO
If rapid acting insulin dose is missed
Wait until next meal to give
U-500 is
Reserved for pts with extreme insulin resistance who take more than 200 units/day
Never give IV due to high concentration
Missed dose of short acting insulin
Take ASAP unless close to next scheduled dose
Missed dose of intermediate insulin
Take ASAP unless close to next scheduled dose
Basal (long duration) insulin should be given if
Patient is NPO
Dose may need to be adjusted
Missed dose of long duration insulin
Call HCP for instructions, no more than one dose in 24 hrs
Mixing insulin
Fastest acting first
Longer acting last
Rate of absorption
Abdomen- fastest
Arm- little slower
Leg- even slower
Butt- slowest
