MedSurg I Diabetes Mellitus

olanjones's version from 2016-10-09 00:42

Etiology and Pathophysiology

Question Answer
Insulin is produced bybeta cells in islets of Langherans (in pancreas), it is continuously pumped out but increases when food is eaten
Normal insulin metabolismInsulin facilitates movement of glucose into cells - glucose is stored as glycogen; other hormones increase serum glucose by breaking glycogen into glucose
Insulin-dependent tissuesSkeletal muscle, Adipose tissue; have receptors that allow sugar to move into the cell
Non-insulin dependent tissuesBrian, Liver, Blood cells; only need glucose to be available in serum
Why is hypoglycemia so dangerousBrain REQUIRES glucose, it cannot use another energy source. No glucose = No brain function
What is the pattern of normal insulin metabolism1-2 hours after meal insulin rises rapidly peaking at about 1 hour, then declines back to preprandial levels; during the night insulin levels are usually low and constant, slightly increasing at dawn


Question Answer
Characteristics of typical patient< 30 years old (usually presents btwn 11-13 y.o.), Lean body type; May present as weak and fatigued
Etiology/PathologyGenetic predisposition, Auto-antibodies cause progressive destruction of beta cells, reducing 80-90% of normal function before manis appear
Onset (rapid)Preclinical period of 3-9+ months, Manis develop with rapid onset when insulin is no longer produced; Often 1st present at ER with DKA (or impending DKA)
Classic S/SWeight loss, Polyuria, Polydipsia, Polyphagia
What happens if they do not receive exogenous insulin?hyperglycemia which will lead to DKA which will lead to metabolic acidosis (LIFE-THREATENING)

Pre-Diabetes/Impaired Glucose Tolerance

Question Answer
Blood Glucose Levels> 100 but < 126
At risk for type 2 DM becauseThere is already a mild alteration in beta cell function
Preventative measuresWeight loss, Diet, Exercise (wt loss is most important)
Without preventative measuresType 2 DM follow ins approx 10 years
With preventive measuresDM may be avoided or delayed *** No guarantee of this***
Why is Pre-diabetes alone still harmful?Higher blood glucose levels have already begun to damage the body (esp. CV system)


Question Answer
What percentage of DM patients have type II?90% (most prevalent type)
Characteristics of typical patient> 35 years old (incidence increases with age), 80-90% are overweight, a family member with DM II
Etiology/PathologyGreater genetic predisposition than DM I, Ethnic predisposition (Black, Asian, Latino, Native - AK Natives highest)
Onset (gradual)Fatigue, recurrent infections, prolonged would healing, recurrent yeast infections, vision changes; Person blames increasing age or lack of sleep (may go years undetected)
Identifiable factorsInsulin resistance, Decreased insulin production, Inappropriate liver glucogenesis, Altered hormone production (adipokines)
Insulin resistanceTissues do not respond (receptors insufficient/non-responsive), Pancreas responds by secreting more insulin
Decreased insulin productionPancreatic beta cells “wear out” from compensatory overproduction
Inappropriate liver glucogenesisLiver no longer responds appropriately to serum glucose levels (Normal = high glucose triggers liver to store as glycogen, low glucose triggers liver to break down glycogen to produce glucose)
Altered hormone productionIncreased adipose tissue leads to increased levels of leptin (inhibits hunger - body downgrades response)/ decreased levels of adiponectin (glucose regulation)
Metabolic syndrome definition; RFCluster of abnormalities that act synergistically to increase the risk of cardiovascular disease; Central obesity, sedentary lifestyle, urban/western areas
What conditions are associated with Metabolic syndrome?↑ Insulin resistance, ↑ insulin levels, ↑ triglycerides, ↓ HDLs, ↑ LDLs, Hypertension
Gestational diabetes4% of pregnancies, Detected at 24-28 weeks & dx through OGGT. Higher risk of C-section, neonatal death, & neonatal complications; Increased risk of DM II in 5 – 10 years


Question Answer
FPG (fasting plasma glucose)Preferred method, > 126 mg/dl fasting (no sugar for 8 hours). If impaired, signals the intermediate stage of prediabetes
RPG (random (casual) plasma glucose)> 200 mg/dl + symptoms (taken anytime w/o regard to food)
OGTT (2 hour oral glucose tolerance test)> 200 mg/dl using a glucose load of 75 g. If impaired, signals the intermediate stage of prediabetes but Can have false lows/highs depend on other factors
HgA1C (glycosylated hemoglobin)Not used an initial dx test, shows effectiveness of serum glucose control over past 120 days.
FPG guidelinesNormal=<100, Pre=100-125, Diabetic=126 or above
OGTT guidelinesNormal=<140, Pre=140-199, Diabetic=200 or above
HgA1C guidelinesIdeal level is ≤ 7% (ADA) or ≤ 6.5% (American College of endocrinology)


Question Answer
Exogenous insulinRequired by type 1 (4-5 x daily); Type 2 may need temporarily (stress of illness/surgery) or may require it if their disease progresses (usually less frequently)
Rapid-acting: lispro, aspart, glulisineOnset 15 min, Peak 60-90 min, Duration 3-4 hours
Short-acting: regularOnset 30-60 min, Peak 2-3 hours, Duration 3-6 hours
Intermediate acting: NPH, LenteOnset 2-4 hours, Peak 4-10 hours, Durations10-16 hours
Long-acting: glargine, detemirOnset 1-2 hours, Peak None, Duration 24+ hours
Mealtime insulin (bolus)Rapid (preferred, most like normal-body insulin response to food), Short (need to take 30-45 mins before food)
Background insulin (basal)Covers insulin needs btwn meals & at night; steadily released (less hypoglycemic risk), 24-hour control decreases DKA risk (DO NOT MIX with other insulin)
Combo therapyintermediate (NPH) mixed with a short-acting, control is not as precise so not used much anymore
Mixing insulin1. Inject air into NPH vial equal to dose, remove syringe. 2. Inject air into regular vial equal to dose and withdraw insulin. 3. Without adding more air to NPH vial, withdraw NPH insulin dose.
Vial StorageVial in use can be kept at room temp x 4 weeks, Store extra vials in fridge (heat/freeze make it unusable), Avoid sunlight exposure to vial, May keep in a cooler when traveling (DO NOT FREEZE)
Pre-filled syringe/Pen storageGood for 30 days in fridge, NPH should be stored upright with needle up, Roll in hands to warm prior to use
Sub-q insulin injection sites (fastest to slowest absorption)Abdomen (preferred), Arm, Thigh, Buttocks (admin at 45 or 90 degree angle, depending on adipose tissue present)
Important teaching points for insulin injectionDo not inject into site that will be exercised, Rotate injection site to avoid lipodystrophy (now recommended rotate within one site), Use smallest syringe for dose (improves accuracy), If using a pen must change needles between uses (if not dose may be inaccurate - possible remnants in old needle)
Nurses clean site w/ alcohol at hospital & Do not recap needles, differs for pt how?If self-admin insulin, pt may clean site w/ soap & water, and may recap needle
How do insulin pumps work?Delivers rapid or short-acting insulin 24/7, at a basal rate by continuous subQ infusion (bolus doses can be programmed by user for meals/exercise)
Insulin pump teachingChange site every 2 – 3 days (refilled & reprogram), Check insertion site for redness, Monitor glucose levels 4 to 6 times daily
Somogyi effectblood glucose drops at night due to maintenance insluin, body reacts with glucogenesis, producing rebound hyperglycemia. S/S HA, Night sweats, Nightmares. To dx: Check glucose btwn 0200-0400
Dawn effectcounter-reg hormones work to increase glucose levels in AM, those with DM may not have enough insulin present causing morning hyperglycemia

Oral Agents

Question Answer
Work in 3 waysReduce insulin resistance, Increase insulin production, Reduce hepatic glucose production
5 ClassesSulfonylureas, Meglitinides, Biguanides, alpha-Glucosidase inhibitors, Thiazolidinediones
SulfonylureasAction -> enhance pancreatic production of insulin (less chance of hypoglycemia & work best early on): Glyburide, Glucotrol, Micronase
Meglitinide Action -> enhance pancreatic production of insulin (even less chance of hypoglycemia. Take 30 to right before a meal, do not take if skipping meal): Prandin, Starlix
BiguanidesAction -> ↓ glucose production by the liver, increases insulin sensitivity. (Most common oral anti-hypoglycemic, often used in combo-tx) Glucophage (metformin)
alpha-Glucosidase inhibitorsAction -> ↓ absorption of carbohydrates by small intestine (Ineffective on hyperglycemia outside of meals, Take with 1st bite of meal): Precose, Glyset
ThiazolidinedionesAction -> Improve insulin sensitivity, transport, & utilization at target tissues (No hypoglycemic risk if used alone but increased risk if in combo tx; CAN CAUSE EDEMA - NO for CHF): Avandia


Question Answer
Topics to teachNutrition, Drug therapy, Exercise, Glucose self-monitoring

Endocrine Overview

common characteristics and functions of hormones
locations of the endocrine glands
functions of hormones secreted by the pituitary, thyroid, parathyroid, and adrenal glands and the pancreas
locations and roles of hormone receptors
significant subjective and objective assessment data related to the endocrine system that should be obtained from a patient
Link age-related changes in the endocrine system to differences in assessment findings
Differentiate normal from common abnormal findings of a physical assessment of the endocrine system
purpose, significance of results, and nursing responsibilities related to diagnostic studies of the endocrine system

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