Endocrine:
Diabetes Mellitus:
o Impaired glucose regulation
o Hyperglycemia form abnormal insulin production or impaired
insulin use
o 7th leading cause of death in US
o Affects function of all cells and tissues
o Managed by – diet, exercise, medication
o Either not producing insulin well, or you have an inability to use
insulin properly
o Affects every part of the body and body system
Pathophysiology:
o Beta and Alpha cells are made by the Islet of Langerhans’s
o Beta cells
Insulin and amylin
Insulin
allows the uptake of glucose into the cells – give
insulin for treatment, cells will no longer be starving
and will have energy
hormone made by the beta cells in the pancreas
key to let glucose get into the cell
Liver and brain – do not use insulin to import glucose
Two phase release of insulin
Basal rate – normally released into the blood in small
amounts
With meals – pancreas increased release when food
is ingested
Normal levels – 70-100
o Alpha cells
Release glucagon
Glucagon – release of glucose from the liver and
skeletal muscle
o Opposite of insulin, it increases blood sugar
o Work against insulin
o Increase blood glucose by stimulating glucose
production and release and decreasing
movement of glucose into the cell
, Glucose – broken down for energy inside the cell
Excess is stored in the liver and muscle cells as glycogen
Classifications:
o Pre-Diabetes:
Can lead to Diabetes if lifestyle changes do not occur
2 hour GTT of 140-199mg/dL
FBS of 100-125mg/dL
A1C of 5.7% - 6.4%
Monitor and educate S/S that they are now diabetic
Usually asymptomatic
May/may not require medications
Treatment:
Lose 5-10% of body weight
Exercise 30 mins a day
Diet – low fat protein, lots of veggies, plenty of fiber
o Limit portion size, calories, sugar and carbs
o Carb counting
o Eat Omega 3 fatty acids
Medications:
o Metformin – does not increase insulin
production
Decreases liver glucose production
Decrease intestinal production
Decreases intestinal absorption of
glucose
Improve insulin sensitivity
Why it needs to be withheld for surgical
patients and those receiving contrast dye
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o Type 1 DM:
Idiopathic
Beta cell destruction – no insulin at all
Autoimmune – body develops antibodies against beta cells
Destruction of beta cells
Often diagnosed when in ketoacidosis
S/S
Polyuria – increase urination
o Since there is excess sugar in the blood, the
body is trying to compensate by peeing it out
Osmotic diuresis
, Large amounts of dilute urine are voided
Polydipsia – increase thirst
o Patient is very dehydrated from peeing so often
that the body tries to compensate by
increasing thirst to help get fluid back into the
body
Polyphagia – increase hunger
o Cells are starving because glucose cannot get
into them, body compensates by eating more
to try to get more energy
*Hallmark* - Weight loss, fatigue, increase in
frequency of infections (sugary blood attracts
bacteria and bugs), slow healing wounds
o More prone to UTI, yeast infections, etc.
Peak incidence is 10-15 years, familial tendency, rapid
onset
Will require lifelong insulin therapy – needed to sustain life
3-12 months after diagnosis – honeymoon period occurs
Nutrition
Carb counting to determine insulin – pump
o *hallmark* 1 unit of rapid acting insulin for
15g of a carb
o Take glucose before meals and 2 hours after
Exercise
Need insulin for physical activity
o if no insulin, body will use fats for energy and
go into ketosis
o glucose levels need to be >100mg/dL
best time to exercise – 30 mins to 1 hour after meals
drugs:
insulin replacement therapy – check sugar levels at
peak
o types
Lispro – 15-30 min
Peaks in 30 mins to 2.5 hours
Check at 1-1.5 hours
Regular – 30-60 min
Peak in 1-5 hours
NPH – 60-120 min
Peak in 6-14 hours