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Discuss the similarities and differences in the etiology and pathophysiology of types 1 and 2 DM.

o Diabetes in Generalo In healthy people, blood glucose ranges from 60-110mg/dL (%) in the fasting state

In the post-prandial state, blood glucose will rise to 140mg/dL for 2 hours,then fall back down to WNL

y Any random blood sugar > 200mg/dL is diagnostic for DM Anyfasting blood sugar > 126mg/dL x2 is diagnostic

An important point: in the absence ofglucose/glycogen, the body can biochemically

convert TG/FFAs into glucose and AAs into glucoseo In acute sickness, which is a physiological stressor, the diabetic should check sugars

multiple times during the day and adjust with R-insulin injections

o Ketones/ketosiso Adipose tissue is especially finicky about adequate and regular glucose levels

If the adipose tissue cannot utilize glucose as an energy source for lack ofinsulin, then it shifts its internal metabolism from carbohydrate to FFA

oxidation

FFAs are broken down converted into ketones in the liver and given offy Ketosis can be picked up in both urine and blood

o Clinical Manifestationso The polys- Both T1&T2

Polyuria with hyperglycemia, the blood is hypertonic, drawing water fromthe cells, when blood glucose >180mg/dL, the kidneys cannot reabsorb the

glucose from the renal tubules back into the vasculature, and sugar begins

to spill into the urine (glycosuria)- the kidneys attempt to deal with this

extra water in the tubules by frequent urination

Polydipsia excessive urination leads to fluid volume depletion andintracellular dehydration, which stimulates the thirst receptors, pt is thirsty

all the time

Polyphagia with the loss of intracellular glucose, cells semi-starve and thepatient is hungry all the time, is eating like a horse, and still losing weight

2. BS Normal Range:a. ICU patient: 140-180; non-ICU patient:

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o Diabetic Ketoacidosis (DKA)o Resulting from hyperglycemia in the type 1 diabetico Resulting in a metabolic acidosis

Kussmauls respirations in an attempt to correct the acidosis acetone breath Watch for hyperK+

o DKA also causes muscle protein breakdown, to convert AAs into glucose, to make thehyperglycemia worse

o Acidosis, hyperosmolarity, dehydration will lead to shock, coma, and death in untreatedDKA

o What brings DKA on: physiological stressors: infection, trauma, surgery, MI,interruptions in insulin administration, emotional stressorso Catecholamines, GH, cortisol (counter-regulatory hormones) get released and increase

glucose

o Tx: Insulin, IVF, watch e-lytes, prevention is the ultimate goalType 2 Diabetes

o Common characteristicso Beta cells are still functional, just enough insulin production to keep the patient out of

ketosis, but not enough insulin production to meet metabolic needs of the body

o Insulin resistance is keyo Results when the insulin produced is sufficient in units/day but the glucose receptor on

key cell lines becomes insensitive

o Hyperinsulinemia and insulin resistance correlates with obesityo Why the insulin resistance?

Production of an abnormal beta cell secretory product Circulating anti-insulin Abs, anti-insulin receptor Abs Receptor defects in the target tissues

o Generally, T2DM has an onset >40yoa, but big epidemic in obese children, youngadults pancreas is burning out early!

o Obesity is commono T2DM is generally not ketotic (but some are when your patient comes in with high FBS

(>400), get a urine for ketones

o HHNC (hyperosmotic hyperglycemic, nonketotoc coma) Hyperosmolar state, glucose >800mg/dl Severe dehydration from osmotic diuresis and elyte shifting

y Decreased GFR only concentrates plasma osmolarity morey Neurologic changes from hypovolemia and e-lyte shifting

o Clinical Manifestations The polys, as in T1DM Weakness, fatigue Blurred vision Impotence Peripheral neuropathy Proteinuria, hematuria Constipation Nocturia Recurrent infections Tachycardia, hypotension, dry mucous membranes from dehydration SOB, chest pains watch out for the MI!!

o Labs FBS UA

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Chem 7 Lipids HgbA1c (glycosylated hemoglobin)

o Tx Diet + exercise + medication Control lipids with statin, LDL 8%

o Measures hemoglobin A1c in the blood and provides long term index of ptsaverage blood glucose levels(over 3-4 months)

Pharmacokinetics

Insulin Generic Onset/Duration Appearance Route Compatibility Peak

rapid-acting LisproAspartGlulisine

15min/2-4hr Clear Sub Q 1-2hr

Short Acting Regular 30min/3-5 hr Clear Sub Q NPH 2-4hr

Intermediate NPHdetemir

~2hr/8-28hr Clear(exceptNPH is

cloudy)

Sub Q NPH Okwith short

acting

6-12hrs

Long Acting Glargine ~2hr/ 20-24+hr Sub Q None None

a) Intermediate- and short-acting available in combination: 70/30, 75/25b) Intermediate- and rapid-acting available in combination: 70/30, 50/50

3. Metformin should be held if pt is undergoing sx or radiologic procedures thatinvolve the use of a contrast medium and should not resume metformin until 48 hrs

after the sx or the procedure and after serum creatinine has been checked and is

normal.

4. Analyze the collaborative care and nursing management of the patient with DKA, HHS,hypoglycemia, infection, neuropathy, and integumentary, feet, and lower extremity complications.

DKA Relative or absolute insulin deficiency Counterregulatory hormone excess (glucagon, catecholamines, cortisol, and growth

hormone).

Symptoms: Nausea/vomiting

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Thirst/polyuria Abdominal pain Shortness of breath

Physical findings Tachycardia Dehydration

(Dry mucous membranes/reduced skin turgor) Hypotension from dehydration Tachypnea

(Kussmaul respirations/respiratory distress) Abdominal tenderness (may resemble acute pancreatitis)

Lethargy (obtundation, possibly coma)

Hyporeflexia (decreased reflexes r/t lowK)

Hypotonia (uncoordinated eye movements and fixed/dilated late sign poor prognosis)

y HHSo Pathophysiology- only T2DMo Hyperglycemia: BG > 600 mg/dLo Hyperosmolar: BG = an osmotic diuresis that leads to intravascular volume depletion,

which is exacerbated by inadequate fluid replacement

o Non-ketotic: Still producing insulin