DM Flashcards
The most common endocrine disorder of childhood
Type 2 is increasing in children due to obesity and sedentary lifestyles
Type 1
The most common endocrine disorder of childhood
Type 2 is increasing in children due to obesity and sedentary lifestyles
Type 1
The most common endocrine disorder of childhood
Type 2 is increasing in children due to obesity and sedentary lifestyles
Type 1
The most common endocrine disorder of childhood
Type 2 is increasing in children due to obesity and sedentary lifestyles
Type 1
Type 2
Things to note
More common in kids
Not genetic but child can be predisposed if parent has it esp father - autoimmune - viral infection then see sx of T1DM
Characterized by destruction of beta cells, usually leading to absolute insulin deficiency
Onset typically in childhood and adolescence but can occur at any age (peaks 10-15 years)
Most childhood cases of diabetes mellitus are type 1
More prominent in Caucasians
About 10% of world population
Type 1
Arises because of insulin resistance - because unhealthy and sedentary lifestyles
Onset usually after age 45
Increased incidence in Native American, Hispanic, and African-American children
Affected people may require insulin injections
Type 2
Not have insulin: glucose not go into cells = stay in blood - cannot use energy - too much in blood - pee it out or breathe it out - pee out water follows glucose - get polyuria - peeing a lot drinking a lot - T1DM: 1st sx - peeing and drinking a lot
Body starving from nutrients - also going to eat - polyphagia
With a deficiency of insulin, glucose is unable to enter the cell and remains in blood, causing hyperglycemia.
When serum glucose exceeds renal threshold, glucose spills into urine (glycosuria).
Cells break down protein for conversion to glucose by the liver (glucogenesis).
Insulin stimulates protein synthesis and free fatty acid storage in adipose tissues.
Deficiency of insulin or insulin resistance compromise the body tissues’ access to essential nutrients for fuel and storage.
Patho of DM
T1DM - quick onset - often show up in DKA; beta pancreatic cells not working so no insulin produced
T2DM - longer before notice it - infections more often - tired and not feel good - longer before diagnosed
Treatment with T1DM and T2DM - insulin: T1 - need insulin; T2 - give oral meds like metformin
Polyuria
Polydipsia
Polyphagia
Glycosuria
Weakness/fatigue
Enuresis/Nocturia
Dehydration
Weight loss
Vision changes
Frequent skin and UTI infections
Skin changes (cool temps and dry itchy skin)
Headaches
Hyperglycemia
Diabetic ketosis
DKA
CM
Glucose >250 mg/dL
Gradual onset
lethargic/weak
Confusion
Thirsty
N/V
Flushed
Deep/rapid breathing
Fruity breath (acetone)
Diminished reflexes
Acidosis
Coma
Hot and dry, sugar high
Hyperglycemia
Often with T1DM - decide not want eat after given insulin = complete life change - lots education
If this:
Glucose <60 mg/dL
Rapid onset
Irritable
Headaches
Pallor
Shallow breathing
Shaky
Tachycardia
Palpations
Sweating
Confusion
Shock
Coma
Cold and clammy, need some candy
Hypoglycemia
Give 10-15 g simple carb
Follow simple sugar with more complex carb or something more substance - protein/fiber/fat - PB&J sandwich
No conscious - D50 and glucagon
If this: - Hypoglycemia
Failure to grow at a normal rate
Delayed maturation - smaller
Recurrent infections
Neuropathy
Cardiovascular disease
Retinal disease
Renal disease
Long-term effects - Assessment
Hypoglycemia
Hyperglycemia
DKA
Hypokalemia
Hyperkalemia
Microvascular changes
Cardiovascular changes
Complications - Assessment
When no sugar, break down fat - get ketons - acidic - get rid it - breathe it out - sweet breath - kussmal respirations - deep and fast
Triggered by stress/illness: cortisol - releases this: not eating much food - glucose spikes because cortisol - fight/flight - body dumps sugar into blood so can sprint away - same with anxiety - glucose rises quickly since already resistant to insulin
Monitor heart: K - often high - treatment and K back into cells - K low so monitor closely
First thing start on them: fluids - want get them rehydrated then do continuous insulin infusion
Glucose around 250 then D10 and give sugar so not bottom numbers out - pay attention to electrolytes to see if need K - never bolus K: very slow infusion
Worry about cerebral edema - reperfusion injury - fluids in them - reperfuse too quickly and can cause edema - all side effects ICP - get all in them slowly
When glucose is unavailable for cellular metabolism, the body breaks down alternative sources of energy; ketones are released, and excess ketones are eliminated in urine (ketonuria) or by the lungs (acetone breath)
Ketones in the blood are strong acids that lower serum pH and produce ketoacidosis
Pediatric emergency
Results from progressive deterioration with dehydration, electrolyte imbalance, acidosis, coma; may cause death
Therapy: Should be instituted in an intensive care unit setting
Undiagnosed Type 1 diabetics typically present in DKA
Also triggered by stress/illness. Why? cortisol
Diabetic ketoacidosis
Check risk factors - recently been sick; hx
Glycosuria with or without ketonuria
Four different tests to confirm DM
8-hour fasting blood glucose of 126 mg/dL
Random blood glucose 200 mg/dL or more
Oral glucose tolerance test of 200 mg/dL or more in 2-hour sample
Hemoglobin A1C of 6.5% or more - goal: 7 or below with kids
Diagnostic evaluation
Lot more people involved - not care for self if kids - parents, school nurse, teacher, IUPs, diabetic nurse education, PCP, doc, lot appts esp after diagnosed
Insulin therapy
Insulin preparations
Monitoring
Multidisciplinary approach - Therapeutic management of DM
First diagnosed: regimen insulin 4 times/day - meals and snacks - checking BG also - checking BG after insulin and meals after - not easier as days go on
Have a dexcomp - continuous glucose monitor; insulin pumps - insulin continuously - glucose and insulin talk to each other - often on apps - lot edu on how properly wear them and how replace them - need have insulin
Insulin therapy
Dosage
Methods of administration
Insulin preparations
