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Diabetes

Prevalence, pathophysiology, risk factors, S/Sx, physical assessment, labs, pharmacological & non-pharmacological management, lifestyle changes, & nursing management of Diabetes, a disorder of carb, fat, & protein metabolism.
by

Kana Thompson

on 5 December 2014

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Transcript of Diabetes

Non-Pharmacological Management
Self-monitor blood glucose
Diet & exercise
Lowers body wt, BP, & blood glucose levels
Decreases CV risks
Decreases insulin and glucose resistance
Diet:
Carb 50-60%
Fat 20-30%
Protein 10-20%
Fiber 50 g
Limit alcohol intake
Labs: Managing Glucose
Labs: Diagnosis
Glucose, Plasma
Diagnosis based on FPG

Glucose Tolerance Test,
Diagnosis based on fasting and 2-hour (post 75g glucose loading) specimens (2-h OGTT)
2 Specimens (75g)
Diagnosis of gestational diabetes
Gestational, 4 Specimens (100g)
Disease Prevalence
Total:
29.1 million people (9.3%) of the U.S population have diabetes
Diagnosed:
21.0 million people
Undiagnosed:
8.1 million people
Prediabetes:
79 million people

→ 7th leading cause of death in the U.S ←

(CDC, 2012)
TYPE 1
1 million diagnosed
In Whites, Blacks, and Hispanics
Occurs early in life


TYPE 2
20 million diagnosed
In Hispanics, Native Americans, Blacks, Asians, and Pacific Islanders
Common by age 30
Prevalence increase with age


Disease Prevalence
(CDC, 2012)
Risk Factors
Type II
Age 45+
Ethnicity (Native American, Black, Hispanic)
Signs of Insulin Resistance
Hypertension
Dyslipidemia
PCOS
Family Hx of T2DM in an immediate relative
History of GDM
Obesity
Sedentary Lifestyle
History of Prediabetes
Physical Assessment - Type 1
History
3 Ps, fatigue, muscle cramps, vision changes, abd discomfort/nausea, skin infections/rashes
Autonomic neuropathy
Kussmaul respirations if DKA present
Retinopathy (hemorrhage or exudates)
Foot infections
Absence of dorsalis pedis and posterior tibialis pulses
Peripheral neuropathy
Skin and other infections
(ie: urinary tract, ears, nose, renal, blood)
Physical Assessment - Type 2
Hx of 3 Ps, wt loss, weakness, fatigue, frequent infections
Complications of hyperglycemia
Hypertension
Acanthosis nigricans
Muscle atrophy
Kussmaul respirations with DKA
Retinopathy (hemorrhage or exudates)
Weak dorsalis pedis and posterior tibialis pulses
Decreased sensation with foot ulcers
Type 1 Specific
3 P's
Fatigue
Increased frequency of infections
Usually < 30 years
Thin, with recent weight loss
Islet cell and insulin antibodies
Insulin dependent
Ketosis prone while insulin is absent
Acute complications of hyperglycemia: diabetic ketoacidosis

General Signs and Symptoms
Fatigue
Weakness
Sudden change in vision
Tingling or numbness in hands and feet
Dry skin
Lesions or wounds slow to heal
Recurring infections

Classic Signs: 3 P's
Pathophysiology
What to know about Insulin:

Hormone secreted by the beta cells in the pancreas
Moves glucose from blood, muscle, fat.
6 Functions
Transports & metabolizes glucose to energy
Stimulates storage of glucose in liver & muscle as glycogen
Signals liver to stop the release of glucose
Enhance storage of dietary fat in adipose tissue
Accelerate transport of amino acids into cells
Inhibits breakdown of glucose, protein, fat.
Risk Factors
Type I
Family History of any types of Diabetes
Environmental Trigger?
Virus triggering the Autoimmune Process
Retrovirus
Viruses that cause mumps, hepatitis and congenital rubella.





Type 2 Specific
Usually obese and inactive
Usually 30< years
No islet cell antibodies
Decrease in endogenous insulin or increase in endogenous insulin with insulin resistance
May need insulin, and possibly oral anti diabetics
Ketosis uncommon, except with stress or infection
Acute complication: hyperglycemic hyperosmolar syndrome

Pre-Diabetic Signs & Symptoms
Hx of hyperglycemia (such as GDM)
Current normal glucose metabolism
Impaired glucose tolerance or impaired fasting glucose
Screening at 40 years if patient has family Hx of Diabetes

GDM Specific
Usually presents 2nd and 3rd trimester
Screening tests (glucose challenge) performed between 24-28 weeks
Additional screening through pregnancy as needed
Similar S/Sx as type 1 and 2

GlycoMark®
Measures PPG excursions; Evaluate glycemic control as a way to monitor/prevent complications of diabetes.

Hemoglobin A1c
Determines long-term average blood glucose; expressed as % HbA1c
Available with testing with eAG:
Provides results as conventional blood glucose units for easier comparison to those familiar with SMBG values.
Available with testing with Reflex to GlycoMark®a,b:
Measures PPG excursions.

Self-Monitoring of Blood Glucose (SMBG)
Determines response to insulin therapy on a daily basis.
Labs: Managing Diabetic Complications
Creatinine
Includes estimated glomerular filtration rate (eGFR)
Monitor onset and progression of kidney disease

Microalbumin, Random Urine with Creatinine
Monitor onset and progression of kidney disease

Lipid Panel
Monitor dyslipidemia and thus risk of heart disease

Insulin Therapy
When do diabetics use insulin?

Type 1: “exogenous insulin must be administered for life because body losses ability to produce insulin”

Type 2: “long term basis to control glucose levels if meal planning and oral agents are ineffective or when insulin deficiency occurs”
Preparation
3 Main Characteristics
1 - Time course of action
2 - Species or source:
3 - Manufacturer
Time Course of Action
Rapid Acting Insulin (RA)
Short Acting Insulin (R)
Intermediate Acting Insulin (NPH)
Long Acting Insulin (Basal Insulin)
Complications
Local Allergic Reaction at injection site
Systemic Reactions:
Hives
Edema or anaphylaxis
Treat with desensitization with small doses of insulin and gradually increasing amounts
Insulin Lipodystrophy
Lipidatrophy: loss of subcutaneous fat, dimpling
Lipidhypertrophy: fibrofatty masses from repeated use of same site

Insulin Regimen
Conventional: (Simplified)
Aim of avoiding acute complications of diabetes (hypoglycemia and symptomatic hyperglycemia)
1 injection per day ( short and intermediate acting)
Patient does not change diet or activity patterns
Appropriate for terminally ill, elderly, or person with limited self-care unwilling or unable to participate in self-management activities
Linda Lam / Amos Patiag / Christina Bedolla-Reyes / Kana Thompson
NURS 420:
in USA human from recombinant DNA technology
Intermediate Acting - NPH
Neutral Protamine Hagedorn
Also called “lente insulin”
WHITE and CLOUDY
If taken alone, not critical to be taken 30 mins before meal
Should be taken with food around time of onset and peak insulin
Rapid Acting
Rapid effect, short duration, quick peak
Admin 5-15 mins before a meal
Important to educate patient on speediness of insulin
Because of it’s rapid nature, other insulins taken in conjunction
“Peakless” or Basal Insulin
Very long acting, given once daily
Given once a day, q24hr
Not to be mixed, has pH of 4, causes precipitation
Patient teaching to be taken at the same time
Pancreatic Cell Implants
Oral Antidiabetic Agents
Methods of Insulin Delivery
Pre-Filled Pens
Jet Injectors
Insulin Pump
Pancreatic Cell Transplants
Future Possibilities
Nursing Management
3. Monitor and Manage for Potential Complications
Hyperglycemic Hyperosmolar State (HHS)
Ketones are not produced
Enough insulin to prevent fat breakdown
Onset is slower
Patients seek treatment later
T2DM
Lifestyle Changes
What everyone hears:
Maintain a healthy body weight.
Make healthy food choices.
Exercise regularly.
Nursing Management
2. Monitor and Manage for Potential Complications
Diabetic Ketoacidosis
Resulting in
Hyperglycemia
Dehydration & Electrolyte Loss
Metabolic Acidosis
Nursing Management
1.Normalize Insulin Activity and Blood Glucose Levels
Hypoglycemia (<70)
S/Sx – Fatigue, Sweating, Polyphagia, Trembling
Hyperglycemia (180<)
S/Sx – Polyuria, Headache, Polydypsia, Fatigue
Nursing Management
Nursing Management
4. Developing a Diabetes Education Plan
Goals:
Nutrition
Meal Planning
Weight Control
Increasing Activity
Medications
Healthy Coping
References
American Diabetes Association. (2014). Retrieved from http://www.diabetes.org
Centers for Disease Control. (2014). Retrieved from http://www.cdc.gov/diabetes/home/index.html
Dumain, T. (2011, November 1). Retrieved from http://www.prevention.com/health/diabetes/diabetes-treatment-what-do-when-youre-diagnosed
Hinkle, J. L., Cheever, K. H. (2013, November 1). Hinkle & Cheever: Brunner & Suddarth's Textbook of Medical-Surgical Nursing, 13th Edition [VitalSource Bookshelf version]. Retrieved from http://online.vitalsource.com/books/9781469863801
Kelly, M. A., Rayner, M. L., Mijovic, C. H. et al. (2003). Molecular aspects of type 1 diabetes. Molecular Pathology, 56(1), 1–10.
Laboratory Testing for Diabetes Diagnosis and Management. (2012, December 1). Retrieved from http://www.questdiagnostics.com/testcenter/testguide.action?dc=TG_Diabetes
Porth, C. Essentials of Pathophysiology: Concepts of Altered Health States, 3rd Edition. Wolters Kluwer Health, (2010, October 1). VitalBook file.
The End!
Pathophysiology
Disorder of carbohydrate, fat, & protein metabolism.
Type 1
Beta cells lose function & are destroyed
= absolute insulin deficiency
Type 2
GDM
Diabetes associated with other conditions or syndromes
Pathophysiology
Type 1a. Autoimmune disorder with:
Genetics
Environmental Trigger
T-lymphocyte-mediated Hypersensitivity Reaction against B-cell antigen
Research evidence: genes in chromosomes 6 & 11
Lymphocytic infiltration & destruction of insulin-secreting cells in islets of langerhans occurs, causing:
Decreased level of absence of circulating insulin
Increased level of plasma glucagon
Failure for Pancreatic B-cells to respond to stimuli
Pathophysiology
Type 1b.
B-cell destruction w/ no evidence of autoimmunity
Smaller group of people (vs. type 1a)
Mostly of African & Asian descent
Have episodes of ketoacidosis.

Pathophysiology
Type 2.
Tissues incapable of insulin use to full potential
AKA insulin resistance
B-cell dysfunction
Not enough insulin in the body OR
Impaired amount of insulin compared to blood glucose levels
(Bowden, 2013. Hinkle & Cheever, 2013)
(Kelly et al., 2003)
Short Acting
Called “regular insulin”
Marked R on the bottle
CLEAR solution
Admin 20-30 mins before a meal
Alone or with a longer acting
Only insulin approved for IV use
Pathophysiology
One step further:
Ignore the horror stories.
Walk a little more.
Get your pressure and cholesterol numbers.
Make one diet change.
Do daily foot checks.
Ask for support.
(Bowden, 2013. Hinkle & Cheever, 2013)
(Bowden, 2013. Hinkle & Cheever, 2013)
(Bowden, 2013. Hinkle & Cheever, 2013)

Pharmacological Management
Goal:
Normalize insulin activity and blood glucose levels to reduce the development of vascular & neuropathic complications
Intensive:
Aim to achieve as much control over blood glucose to match day to day levels
3-4 injections per day
Reduces risk to complications
Risk of severe hypoglycemia is increased by 3x
Kidney transplant patients use this to preserve new kidney
Not a regimen for many patients, requires commitment


(Bowden, 2013. Hinkle & Cheever, 2013)
Nursing Management
Clinical Manifestations
Kussmaul Respirations
Low HCO3 and low pH
Increased Creat, BUN, H/H
Rapid Onset
T1DM
http://whoisdiabetes.blogspot.com
(CDC, 2012)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(ADA 2014. Hinkle & Cheever, 2014)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Dumain, 2011)
(Quest Diagnostics, 2012)
(Porth, 2010)
(Porth, 2010)
(Porth, 2010)
(Porth, 2010)
(Porth, 2010)
(Porth, 2010)
(Quest Diagnostics, 2012)
(Quest Diagnostics, 2012)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
Pre-Filled Pens
Alternative to insulin and needle syringe administration
150-300 units pre-filled insulin cartridges in a pen like holder
Attach a disposable needle
Useful for patients who inject 1 insulin at a time
Convenient for travel, impaired dexterity, impaired vision, and cognitive function
Jet Injectors
Alternative to needle injections
Delivers insulin by sending a pressurized fine stream through the skin
Requires thorough training and supervision
Associated with bruising
Patient Education: when changing to a jet injector, you have faster absorption rates
Insulin Pump
Continuous sub-Q insulin infusion
Mimics function of a normal pancreas
Syringe attached to a long, thin, narrow lumen tube with needle or teflon catheter
Patient inserts the needle with catheter into sub-Q tissue and secures with tape, changed q3days
Insulin administered at a basal rate
Enter number of carbs eaten at a meal and pump will administer required dose of insulin
Allows for flexible meal timing and content

Problems:
Tubing becomes occluded
Supply of insulin runs out
Battery can deplete
Potential for infection
Inconvenient (can remove for shower, sex, and exercise)
Requires collaboration of a Medical Team
Requires constant monitoring
Risk for ketoacidosis
Only rapid acting insulin is used


Good for patients with Type 2 Diabetes with a hectic lifestyle that require insulin and have decreased beta cell function.

Transplant insulin producing pancreatic islet cells
Limitation, only 2 years of active functioning
Pancreas transplant is usually done as a kidney and pancreas transplant
Required to take anti-rejection medication
These alternatives are not as common, however showing promising results

Future Possibilities
Implantable pumps
Insulin patches
Insulin filled capsules or oral sprays
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
(Hinkle & Cheever, 2013)
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