Question | Answer |
Pancreas A&P | Located behind stomach, between spleen and duodenum
Exocrine (Lipase, Amylase)
Endocrine (Insulin)
Alpha Cells (Glucagon, released when below 70)
Beta Cells (Insulin)
Delta Cells (Inhibit production of insulin, Maintains homeostasis) |
Fasting Blood Glucose (FBG or FBS) | 70-110 mg/dL
NPO 8 hours, water allowed
Series over 125 = diabetic
Can be altered to a false positive by corticosteroids and diuretics |
Oral Glucose Tolerance Test (OGTT) | 2hours
<139-normal
140-199:impaired
200-diabetes mellitus
30, 60, 120 min. (blood and urine)
May get dizzy or sick, may stop test |
Glycosylated Hemoglobin (HbA1C) | 4-5.9% normal
7% or < = well controlled diabetes
8% or > = poor control
Measures Hgb for past 3 months |
Pancreas MRI & CT Scan | Looking to tumors |
Age Related Changes in Pancreas | Decreased ability to metabolize glucose
Delayed release of insulin
Decreased sensitivity to circulating insulin |
Diabetes Mellitus Quick Facts | 6thleading cause of death in America
Leading cause of end stage renal disease (ESRD)
Most frequent cause of blindness and amputations
Affects ~23.6 million, 1.6 million new cases dx/year
Over $174 billion spent for care in 2002 |
4 Types of Diabetes | DM 1
DM 2
Gestational DM
Other (Drug induced and Infection) |
Diabetes Type 1 (Stats and Triggers) | 5-10% of diabetes
Children/adolescents (avg age 10-15)
Genetic predisposition
Environmental triggers: Viral infections (measles, mumps, coxsackievirus); Chemical Toxins (smoked and cured meats)
Acute illness: 80-90% of cells are destroyed.
> in infec |
Diabetes Type 1 Pathophysiology | Autoimmune/Idiopathic (no know cause)
Beta cells destroyed (insulin not produced to unlock cell door to accept glucose); Alpha cells produce excess glucagon (glucose can’t get in cell to be used, excess build up) |
Type 1 Diabetes Manifestations | Polyuria (> urine)
Polydipsia (> thirst)
Glycosuria (glucose in urine)
Polyphagia (> hunger)
Anorexia, malaise, fatigue
Blurred vision (lenses swell)
Diabetic ketoacidosis: Body thinks not enough glucose in blood, breaks down fats and muscle for ene |
Type 2 Diabetes | Most common age: middle-older adult
Insulin present but tissues resistant. (key to cell does not fit) (Obesity, inactivity, illnesses, meds, age)
Sufficient insulin to prevent DKA
Gradual onset; delayed diagnosis (1/2 dsagnosis already have complicatio |
Type 2 Diabetes Risk Factors | Family Hx
Obesity
Physical inactivity
Race/ethnicity: African-American, Hispanic, Native or Alaskan American/Asian
Female Hx
HTN (> 130/85)
HDL cholesterol (<35 mg/dL)
Triglyceride level (>250 mg/dL)
Metabolic syndrome
Anti-platelet + treat hyper |
Metabolic Syndrome | Places patient at risk for Coronary Artery Disease
Combination of factors noted: Abdominal obesity, Hyperlipidemia, HTN, Insulin resistance, Increased tendency toward clotting and inflammation (elevated C-reactive protein) |
Manifestations of Type 2 Diabetes | Hyperglycemia
Polyuria (excessive urination)
Polydipsia (excessive hunger)
Blurred vision
Fatigue
Paresthesias (numbness)
Skin infections
HTN
Recurrent Infections |
Why increased Diabetes in Elderly | Baby Boomers (> 50+; Type 1s living longer, medical advancement)
Normal physiologic changes with aging: Lost thirst mechanism, < hungar, tired, visual changes, excess sugar confusion blamed on delusion/dementia, polyuria
> comorbidities
Polypharmacy |
Recognizing Diabetes in Elderly | Indicators: Orthostatic hypotension, Periodontal disease, Infections, Stroke, Gastroparesis, Impotence, Neuropathy, Confusion, Glaucoma
Longer recovery periods after surgery, illness
Increases potential for complications from illness or treatment |
Diabetes Diagnostics | Manifestations + Random (or casual) plasma glucose >200 mg/dL
Fasting Plasma Glucose >126 mg/dL
OGTT: 2 hr. plasma glucose >200 mg/dL |
Who to test for Diabetes? | Age 45+
BMI >25
Clients with risk factors: HTN, Ethinsity, Over 50, Obesity, Problems with lipids (metabolic syndrom), Female reproduction |
Blood MGT Tests | Fasting Blood Glucose (normal 70-110)
Hemoglobin A1C
Can dx DM: >6.5%
Elevated if 7-9%
Poor control at >9%
Glycemic goals are age-related. |
Urine MGT Tests | Urine Testing: Glucose, Ketones (protein breakdown)
Urine albumin (U/A): possible nephropathy, need a creatine clearance for “albumin to creatine ratio”
Microalbumin; earliest indicator of nephropathy, usually followed by macroalbuminuria |
Lipid MGT Tests | Cholesterol Levels
LDL<100 mg/dL (ADA recommends <70)
HDL>45 mg/dL (Women: >50)
Triglycerides<150 mg/dL |
Self-Monitoring Blood Glucose Levels | Type 1: 3-4/day (on insulin only)
Type 2: enough to reach goals
> BGM when ill, pregnant, change meds
BGM affected by: Hematocrit (High=false low, Low=false high), Medications, Supplies (dry/cool, matching codes, exp), blood vol, Gout |
Goal of Diabetes Treatment | Maintain glycemic control
Prevent complications |
Diabetes Diet Treatment | Maintain as near normal glucose as possible
Optimum serum lipid levels
Low-fat diet
Attain or maintain optimum weight
Low-carb diet
Eat complex carb rather than simple |
Exercise Treatment of Diabetes | Increases uptake of glucose by cells
Decreases cholesterol/triglycerides
May need cardiac screening before beginning |
Rapid-acting Insulin | Humalog, Novolog
(SubQ)
Onset 10-15 min
Peak 1-1.5 hour
Duration 1-1.5 hour |
Short-acting Insulin | Regular “R”
(IM, SubQ, IV)
Onset ½-1hour
Peak 2-3 hours
Duration 4-6hours |
Intermediate Insulin | NPH, Lente, Levemir
Onset 1 ½-2 hours
Peak 6-8 hours
Duration 12-16 hours |
Long-acting Insulin | Lantus, (cannot mix)
Onset Not defined
Peak None
Duration 24+hours |
Combination Insulin | Humulinor Novolin 50/50, 70/30
Onset 30 min
Peak 4-8 hours
Duration 24 hours |
Factors influencing insulin absorption | Injection site: Abdomen is fastest, Deltoid, Thigh, Buttocks is slowest
Speed of absorption
Fastest: abdomen
Rotate to prevent lipohypertrophyand lipoatrophy
Rotate within ONE site |
Hypoglycemic Agents: Sulfonylureas | Glimepiride(Amaryl)
Glipizide(Glucotrol)
Glyburide(Diabeta)
Tolbutamide(Orinase)
Stimulate pancreas to secrete more insulin
Increase sensitivity in peripheral tissues
Side effects: Hypoglycemia, Weight gain, GI symptoms |
Hypoglycemic Agents: Biguanides | Metformin (Glucophage)
Reduces FBG and postprandial (after meals) hyperglycemia
< glucose production
Makes insulin more effective
Use with diet and lifestyle changes
Cannot take 2 days pre or post contrast testing |
Hypoglycemic Agents: Alpha-glucoside inhibitors | Acarbose (Precose)
Slows carb digestion and delay glucose absorption
Take immediately before a meal
SE: flatulence, diarrhea, abdominal discomfort.
Hypoglycemia is NOT a side effect! |
Hypoglycemic Agents: D-Phenylalanine | Nateglinide (Starlix)
Stimulate insulin secretion after meals
Take shortly before meals
Side effects: Hypoglycemia, Weight gain |
Hypoglycemic Agents: IncretinMimetics | Exematide(Byetta)
Sub Q
Signals pancreas to make right amount of insulin after meals
< rate of glucose entering blood
< conversion of glycogen to glucose
Injected 30 min-2hrs before meals with 30+ Carbs
Don’t take after meals or more often than 12 h |
Hypoglycemic Agents: DPP-4 Inhibitors | Sitagliptin (Januvia)
Decrease liver release of glucose
Increase insulin secretion
Side effects: Headache, Nasopharyngitis, UTI
Diet and exercise modifications |
Medication Considerations | Monitor close, 7 days
Diet/exercise
Avoid when lactating or pregnant
Increase stress(trauma, surgery, etc) may discontinue and use insulin
Avoid ETOH
Interferes with birth control
ASA therapy (aspirin) is wanted in CAD
SE: GI bleed, ulcers, liver d |
Diabetic Diet | Consistent Carbohydrate Diabetes Meal Plan
ADA Diabetic Exchange List (Divides foods into carbs, fats, protein, etc.)
Diet Plan for T1 Diabetes: Based on insulin regiment
Diet Plan for T2 Diabetes: Balance meals and snacks
“No Concentrated Sweets” |
Dietary Considerations | No Alcohol
Non-nutritive sweeteners: Sweet & Low, Nutrasweet, Sunnette, Splenda
Nutritive sweeteners: sorbitol, fructose, xylitol
“sugar-free” and “dietetic” on labels |
Diabetic Sick Day Rules | Increase BG monitoring to every 4 hours
Test urine for ketones when BG >240
Continue insulin and oral meds
Hydrate
Call PCP: Persistent N/V, diarrhea; Moderate or large ketones; Persistent hyperglycemia; Fever for >24 hours |
Diabetic Exercise/Footwear/Inspection | Neuropathy, file/no clip/cut straight, buy afternoon, leather/canvas, no tight/loose
Toes, mirror, no barefoot, no cross legs, WHITE cloth.
No temp extremes or exercise during poor BGM
T1 (> risk for hypo/hyperglycemia)
T2 (may < meds, < cadiac risks) |
Special considerations for young | Continue sports with precautions
May require diet/insulin modifications
Start slow, extend activity over prolonged time
May need carbohydrate drink one hour into activity
Monitor BGL
Snack available after exercise
May need to adjust insulin prior to |
Complications of Diabetes | Hypo/hyperglycemia
Diabetic Ketoacidosis (DKA)
Hyperosmolic Hyperglycemic State (HHS)
Multiple Chronic Complications |
Manifestation of Hyperglycemia | Polydipsia
Polyuria
Polyphagia
Decreased energy
Malaise and fatigue
Blurred vision
Dry, itchy skin
Headache
HTN |
Hyperglycemia Symptoms | Major complications: DKA and HHS
Dawn Phenomenon (4-8 am)
SomogyiPhenomenon (Low at time, then high later, with no known reason; Can become insulin resistant for 2-24 hrs) |
Diabetic Ketoacidosis (DKA) | Breakdown of fats and proteins
Liver produces ketones (metabolic acidosis)
Bicarbs (buffering mechanism shot)
Fluid/electrolyte imbalance
Occurs with increased energy needs
Increased exercise
Emotional stress
Forgot to take insulin, sick, infection |
Manifestations of DKA | Dehydration
Warm/dry skin, poor turgor
Soft eyeballs, Dry mucous membranes
Weak, Malaise
Rapid, weak pulse
Hypotension
K+ and Glucoseare reciprocal
N/V, Ketonebreath “fruity”, Lethargy, Coma, Abd pain
Kussmaul's respirations (deep rapid hyperventi |
DKA Diagnostics | Blood glucose (250 or ^)
Blood pH (below 7.35)
Bicarb (low)
Ketones present in blood
Ketones and glucose present in urine
Electrolyte abnormalities (massive fluid loss)
Na+, K+, Cl- (low) |
DKA Treatment | Immediate medical attention
Frequent Blood Glucose monitoring
Insulin (more than likely it’s R, IV)
Restore fluid and electrolyte balance
Monitor cardiac rhythm (Low potassium, sodium, etc.)
Treat underlying condition (Infection? Forgot insulin?) |
Hyperosmolar Hyperglycemic State (HHS) | T2 diabetes potential complication
Life-threatening—High mortality rate
Slow onset (over about 1-14 days) |
Hyperosmolar Hyperglycemic State (HHS) Triggers | Infection
therapeutic agent
acute/chronic illness |
Hyperosmolar Hyperglycemic State (HHS) Manifestations | Plasma osmolarity(>340mOsm/L.)
Stealing the fluid from everyone else
Blood glucose severely (>600-2000)
Normal <110
Neurological
Dehydration
No acidosis (difference in HHS and DKA) |
Hyperosmolar Hyperglycemic State (HHS) Treatment | May require: artificial ventilation and nasogastricsuction
Correct fluid and electrolyte imbalances (isotonic fluids, K+replacement)
Regular insulin until glucose decreases below 250 mg/dL
Treat underlying condition |
Hypoglycemia | AKA “low blood sugar” or “insulin shock”
Blood Glucose: <45-60mg/dL
Mismatch between insulin intake/needs
Can result in death
Causes: Alcohol, Drugs, Physical Activity, Lack of Carbohydrates |
Hypoglycemia Manifestations | Hunger
Nausea
Anxiety
Pale, cool skin
Sweating
Shakiness
Irritability
Tachycardia
Hypotension
Headache
Difficulty thinking/concentrating
Change in emotions
Slurred speech
Blurred vision
Decreased LOC
Seizures/Coma |
Treatment of Mild Hypoglycemia | 15g CHO: 3 glucose tabs, ½ cup fruit juice or regular soda, 5 lifesaver candies, 3 tsp of honey, 3 large marshmallows
DO NOT add sugar to fruit juice
15/15 rule
Wait 15 and repeat if necessary
Hypoglycemic episodes >2-3x/wk need diabetes MGT plan adju |
Treatment of Severe Hypoglycemia | Hospitalization if: Blood glucose < 50, Coma, seizures, altered behavior, no one to remain with client for 12 hours after treatment, caused by sulfonylurea drug
If alert administer 15 g CHO
If altered LOC, Parenteralglucose or glucagon |
Macrocirculation of Diabetes | Atherosclerosis
CAD
HTN
Stroke |
Microcirculation of Diabetes | Perpherial Vascular Disease
Intermittent claudication (pain with activity, goes away with rests)
Occlusions/Thrombosis
Ulcerations (Infection, Gangrene = amputation)
Diabetic Retinopathy
Cataracts
Diabetic Nephropathy (loves the heart and kidneys) |
Peripheral Neuropathies | Bilateral sensory disorders (Paresthesias, numbness/tingling, Pain-burning, shooting, aching, cold feet, Impaired sensations)
Single nerve (Palsy of 3rdCranial nerve, Radiculopathy, Femoral neuropathy, Entrapment or compression of nerve) |
Visceral Neuropathies | Sweating dysfunction
Abnormal pupillary function
Cardiovascular dysfunction
Gastroparesis
Genitourinary dysfunction (Bladder, Sexual function) |
Diabetes increases susceptibility to infection | Bladder/kidney infections
Skin, nails, and mucous membranes prone to tuberculosis
Osteomyelitis (bone infection, feet)
Risk factors (Sensory deficits lead to unknown trauma, vascular/neurological impairments, hyperglycemia altered neutrophil function) |
Diabetes Periodontal Disease | If occurs progresses more rapidly
Microangiopathy (gingivitis and periodonitis)
Diabetes doesn’t cause it, but can increase progression |
Diabetic Foot Complications | Angiopathy, neuropathy, infection
High risk for amputations
Unrecognized foot trauma
Daily foot care
Use proper fitting shoes
Have professional foot/nail care
Clean with white washcloth!
Buying and wearing shoes
Care of toenails |