L1 Diabetes Flashcards
SOC
Standard of Care
Diabetes definition
means siphon, describes the large urinary volume excreted by sufferers of this disease
Exocrine component of pancreas
-most cells in pancreas
-produce enzymes to digest proteins, carbs, fats in small intestine
-Enzymes flow into ducts
Endocrine component of pancreas
only 1-2% of total pancreatic cells
hormones are released into blood
-islands of cells within exocrine that release insulin, glucagon, somatostatin
Diabetes mellitus is characterized by
Chronic hyperglycemia
Relative deficiency in insulin (b/c of reduced secretion or action)
Type 1 Diabetes
Autoimmune disease
characterized by a lack of insulin production
Type 2 Diabetes
Ineffective response to insulin or tissue insulin resistance
In the last 20 years, # of adults diagnosed with diabetes has _______
doubled
____ of adults worldwide has diabetes
9.3%
annual cost of diabetes
327 billion
Diabetes dramatically increases the risk of
End-stage renal disease
amputation
heart disease
blindness
pregnancy complications
Type 1 DM Etiology
-appears before age 20
-most common in caucasians
-accounts for 5-10% of diabetic population
-not always a genetic component
Onset/treatment of Type 1
Generally rapid onset
no prevention and no cure
treatment is exogenous insulin
Classic signs of Type 1 Diabetes
RAPID onset of:
Polydipsia
Polyuria
Polyphagia
Weight loss
Polyphagia
excessive eating
Polydipsia
excessive drinking
Type 2 DM Etiology
-Appears mostly in adult population
-Increasingly occurring in children
-accounts for 90-95% of total diabetic population
-older adults and non-caucasians are disproportionately affected
Type 2 DM Risk Factors
Increasing age (65+)
Ethnicity (American indians)
Genetics
Overweight/Obesity
Physical inactivity
Type 2 DM Onset/Treatment
Onset: SLOW, initial signs present in type 1 are subtle or absent
Tx: weight loss, exercise, diet (which can all delay onset)
What occurs with glucose in an individual with TYPE 2 DIABETES
- reduced sensitivity of target tissues to respond to insulin
- Beta cells secrete more insulin to overcome resistance
- Later in disease process, insulin production decreases as beta cells fatigue, signal transduction pathway breaks down
What are possible reasons for insulin resistance?
changes in insulin receptors
problems in the signal transduction pathway activated by insulin receptor binding
Insulin sensitivity definition
relatively small amount of insulin is needed to maintain normolglycemia and supply cells with glucose they need
Insulin Resistance
a lot more insulin is needed to get the same blood glucose lowering effect because insulin’s targets tissues are not as responsive to insulin
Impaired glucose tolerance
known as impaired fasting glucose
condition in which individuals have blood glucose levels higher than normal, but not high enough to be called diabetes
Tests used to in diagnosis
- Fasting plasma glucose (fasting for 8 hrs)
- Oral glucose tolerance test
- Random plasma glucose level (any time during 24 hr period)
- A1C
Fasting plasma glucose levels
Normal: 70-99
Prediabetes: 100-125
Diabetes: >126
Fasting Plasma Glucose
direct measurement of plasma glucose levels after overnight fast
Oral Glucose Tolerance Test
measurement of body’s ability to appropriately handle excess sugar after drinking very high glucose drink
Non-diabetic OGTT Results
Plasma glucose level rises after drinking a glucose drink. Peaks within one hour, then falls quickly back to normal level
this is a normal insulin reaction
Diabetic OGTT results
glucose level rises higher than normal after drinking glucose drink and comes down in normal levels much slower
occurs with insulin resistance
What occurs with Type 1 Diabetics?
- High plasma glucose occurs because of reduced uptake of glucose to insulin’s target tissues
- Liver continues to produce glucose
- Accelerated lipolysis leads to high plasma levels of FFA and glycerol
- Liver produces excessive amounts of ketones
Diabetic Ketoacidosis
Major life-threatening complication mainly occurring in type 1
Processes of diabetic ketoacidosis
- Increased plasma glucose filtered by kidney cells overloads tubular reabsorption of glucose -> glucose and ketones are spilled into urine
- Increased nutrient concentration in kidney tubules leads to an osmotic diuresis and increased loss of water/sodium > causes decreased plasma volume and blood pressure
- Increased ketone production results in blood acidosis > causes coma and death
Insulin Therapy Goals
- Achieve optimal glycemic control
- minimize risk of severe hypo/hyper glycemia (acute)
- delay or prevent late vascular and neuropathic complications (chronic)
Hyperglycemia
patient not receiving enough insulin
greater than 250
S/s: polyuria, polydipsia, polyphagia, fatigue, nausea, blurred vision
Hypoglycemia
less than 50
S/S: weakness, hunger, profuse sweating, headaches, shaking confusion
Acute diabetic complications
- Hyperglycemia
- Hypoglycemia
- Ketoacidosis
- Surface infections and abscesses
Situations that increase diabetics’ risk of hypoglycemia
Fasting
delayed meals
alcohol consumption
intense physical activity
sleep
Insulin therapy and type 1 DM
insulin is required for life
Insulin therapy and type 2 DM
insulin use is reserved for those that are unable to control glucose levels with diet/exercise
most type 2 diabetics will eventually need insulin
Multiple daily insulin injections
has rapid, short, intermediate, long acting types
onset of action, peak response, duration of action determines what type of insulin you would need
Methods of insulin therapy
- Multiple daily insulin injections
- Continuous subcutaneous insulin infusion
- Inhaled insulin
Continuous subcutaneous insulin infusion
-driven by mechanical force and delivered via needle
-uses only rapid acting insulin
-programmable, helps to optimize glycemic control
-lowers HbA(1c) levels
Rapid-acting insulin
onset is in 5 min, with a peak at 30-90 min
Humalog
Intermediate acting insulin
onset is 1.5 hours, peak is at 4-12 hrs
Insulin NPH
Long-acting insulin
onset in 1 hr, with no peak
Insulin glargine
Insulin injection sites
- make sure to rotate sites
- areas with more subcutaneous fat may absorb insulin more slowly
- exercise/massage/heat will increase absorption rate
Insulin absorption rates vary in tissues…
abdomen > arm > leg and buttock
Common insulin ADRs
Hypoglycemia
weight gain
injection site bruising/lipodystrophy
How are blood glucose levels measured?
ACUTE: capillary pin prick and test with glucometer
instant and accurate snapshot
Capillary blood glucose (CBG)
measured with a glucometer
Glucometer and therapy
patients should bring their glucometer to therapy sessions
they should prick their own skin
Continuous Glucose Monitors
-inserted under skin that measures glucose levels in the INTERSTITIAL FLUID
does not replace daily CBGs
used to identify trends in glucose levels
Acute measurements of glucose levels
Glucometer
Continuous glucose monitors
Long term measurement of blood glucose
best measure of glycemic control
HbA(1c)
Glycemic Control
target goal of diabetes care
maintenance of stable blood glucose levels as close to normal as possible over time
helps to decrease the risk of chronic diabetic complications
What is the HbA(1c)?
also known as glycated hemoglobin
glucose sticks to hemoglobin, forming it. The more glucose in the blood, the more HbA(1c) will be in the blood
What does HbA(1c) measure?
estimates the mean blood glucose level over previous 4 weeks
A1C is tested at diagnosis and at least 2 times/year
What measurements are used to diagnose diabetes?
A1C > 6.5%
FBG >126
Prediabetes A1C
5.7% to 6.4%
Normal A1C levels
<5.7%
ADA’s goal for diabetics is to keep A1C…
<7%
A1C is correlated with…
estimated average glucose
using EAG is better with patients when talking about glucemic control
its not a percentage, its the same units as daily CBG values
Why should we care about A1C levels?
higher A1C indicates poor glycemic control, which is associated with a higher risk of chronic diabetic complications
Chronic diabetic complications fall into 2 main categories…
Neuropathies
Vascular diseases
Neuropathic complications
ALL nerves are affected, mechanisms unknown
S/S: numbness, insensitivity, muscle atrophy, altered thermoregulation, tachycardia, erectile dysfunction
Charcot joint disease
loss of sensation leading to joint dysfunction
most frequently affects the weightbearing joints, and occurs after minor injury
Muscle atrophy–> arch collapses –> weight bearing differently –> ulcer
What is optimal treatment for charcot foot?
subject of ongoing debate
options of conservative limb salvage, surgical conservation, CROW, amputation
Conservative limb salvage
involves offloading, casting, therapeutic footwear
goal is slow down and minimize degree of joint pathology
does not entail return normal jt structure
Disadvantages of conservative limb salvage
bones can heal in deformed positions
CROW device can limit activity
hard to be NWB
CROW
Charcot restrain orthotic walker
custom made rigid boot that completely immobilizes foot and ankle
worn for 6-12 months
Other off-loading devices
Traditional, roll-on, removable, CROW
don’t use wedge or post-op shoe
Diabetic Foot Exam
Vascular
Infection/Inflammation
Pressure
Sensation
Vascular (diabetic foot exam)
Vital signs
Foot pulses
ABI
Infection (diabetic foot exam)
For each ulceration note…
Location, size, depth, debride, probe to bone
Pressure
also look for deformity
look for toes, ankles, calluses
What is protective sensation?
light touch perception that corresponds to the ability to sense trauma to the foot and cease weightbearing
How do you test protective sensation?
with semmes-weinstein 5.07 monofilament
calibrated to apply 10 grams of force
Don’ts of diabetic foot care
Smoke
Wash in very hot or cold water
use heating pads
razors/scissors to cut corns
cross legs
wear girdles/garters
walk barefoot
Do’s of diabetic foot care
heave regular exams
inspect feet daily
wash feet daily
dry feet carefully
apply cream to dry areas
cut nails straight across
wear wide toe-box shoes
inspect shoes before putting them on
Macrovascular complications
affects large vessels of heart and peripheral arterial vessels
leads to CAD, MI, CVA, PVD
Microvascular Complications
smaller blood vessels of retina, kidneys, peripheral nerves
leads to blindness, renal failure, neuropathy
Why is long-term hyperglycemia toxic to blood vessels?
Endothelial cell dysfunction
Lipoprotein dysfunction
Thickening of basement membrane
Thrombogenesis
Arterial wall calcification
Endothelial cell dysfunction
normal/healthy endothelial cells modulates vascular tone, permeability, coagulation
leads to atherosclerosis
What factors contribute to hyperglycemia?
- Exogenous systemic glucocorticoids
- Stress
- Onset of new illness/infection
- Meals
Exogenous systemic glucocorticoids and hyperglycemia
induce a state of insulin resistance
Stress and hyperglycemia
hormones released during stress induce hyperglycemia
Meals and hyperglycemia
POSTPRANDIAL HYPERGLYCEMIA is a predominant feature in patients with type 2 DM and is a risk factor for development of CV complications
Recommendations for diabetes
Increasing PA
Nutritional management
Weight loss
Intense glycemic control
blood pressure
control dyslipidemia
Antiplatelet therapy
daily foot care, smoking cessation
Children and Adolescent exercise recommendations
should engage in 60 min/day of moderate to vigorous activity, strengthening 3 days a week, for either diabetes type
Adult exercise recommendations
- Exercise more than 150 minutes of aerobic activity
- No more than 2 consecutive days missed
- 2-3 sessions of resistance exercise
- Reduce daily sedentary time. Prolonged sitting should be interrupted every 30 min
How does exercise improve glycemic control?
Muscle contraction moves glut4 to the surface of muscle fibers and insulin is not needed for this
trained muscle can act like a sponge to suck up some of the glucose from the blood, decreasing blood glucose
the insulin sensitivity created can last 24 hours after the exercise
glut4 expression is enhanced with training only in those fibers recruited during exercise training
slow twitch fibers do better at this
more muscle mass, bigger sponges to suck up more glucose
Cornerstone treatment for Type 2 DM
- Weight loss
- Exercise
- Glucose-lowering meds
- Insulin
Weight loss benefits for diabetics
clinical benefits begin with 3-5% body weight loss
Lifestyle vs med treatments
Lifestyle intervention reduced the incidence of diabetes more than metaformin
Less sitting =
less risk of Type 2 DM
every hour spent watching TV there was a 3.4% increased risk of diabetes
General exercise prescription guidelines for diabetic
Warm up fro 5-10 min
30 min of continuous moderate intensity
Cool-down for 5-10 min
use RPE as a predictor of exercise intensity (12-14)
Postprandial hyperglycemia and exercise
aerobic exercise works better after a meal
Exercise contraindications and precautions
NEED to assess before: VS, vision, balance, foot exam, shoes
Monitor CBG pre and post exercise
Adjust insulin/food intake as needed
Hypoglycemia may occur during or after exercise
Evening exercise increases risk of nocturnal hypoglycemia
Neuropathy may lead to hyperthermia, ischemia, painless trauma
Don’t exercise during peak insulin
CBG and exercise
No exercise if CBG >300 mg/dl
No exercise if CBG > 240 mg/dl w/ketones
Metformin
MOA: decrease liver gluconeogenesis
ADRS: nausea, vomiting, diarrhea, flatulence, abdominal discomfort, asthenia
individuals with abnormal kidney/liver function: lactic acidosis may occur
5 Regulators of Insulin Secretion
Food intake
Increased amino acids
GLP1 and GIP (ff regulation)
Exercise (inhibits)
Parasympathetic Activity (ff regulation)
Stress management of diabetes
approaches to reduce stress are key components of diabetes management
psychological intervention can help to lower A1C levels
