alpha -- glucogen

beta -- insulin

1) synthesized and released in response to low levels of blood glucose, protein ingestion, and exercise

2) increase blood glucose

3) works in a reciprocal manner with insulin to maintain normal blood glucose levels

1) principal regulator of metabolism and storage of ingested carbs, fats, and proteins

2) facilitates transport of glucose across cell membranes in most tissues

3) increase glucose level is major stimulus for insulin synthesis and secretion

What percentage of diabetes cases are Type 1?

What is the typical body type of someone with Type 1?

Is there a genetic predisposition to the disease?

5-10%

Lean

Yes

Rapid onset

Polydipsia (excessive thirst)

Polyuria (frequent urination)

Polyphagia (excessive hunger) w/ weight loss

Diabetic ketoacidosis

Weakness and fatigue

Continue insulin production by pancreas that is either 1) insufficient or 2) poorly utilized/absorbed by body

Presence of endogenous insulin is major difference b/t Type 1 and Type 2

Gradual onset

Insulin resistance and hyperglycemia

Decrease in pancreatic ability to produce insulin

Inappropriate insulin production by liver

Alteration in production of hormones and cytokines by adipose tissue

Obsesity (80-90% overweight, > 20% above BMI)

Ethnic facotors: AA, Native Amer, Eskimos

Family Hx

Age, 35+

Apple shape

Women w/ gestational diabetes

PCOS

Insulin resistance syndrome

High Triglycerides

High LDL

Low HDL

Hypertension

Sedentary lifestyle

Western culture

Frequently none, rarely those associated w/ Type 1

Fatigue

Recurrent infections, immune system compromised, yeast infections

Visual changes

Prolonged wound healing

Severe carbohydrate restrictions

Acute illness

Medications such as contraceptive or corticosteroids

Restricted activity such as bed rest

IFG - Impaired fasting glucose (100-126 mg/dl)

IGT - Impaired glucose tolerance (140-199)

Represent intermediate stage b/t normal glucose homeostasis and diabetes called prediabetes

Test shows the amount of glucose attached to hemoglobin molecules over their life span; when glucose is elevated over time, the amount of glucose attached to the hemoglobin molecule increases and remains attached to the RBC for its life span

A1C indicates glucose control over 90-120 days

What do patients with near normal AICs decrease their risk of ?

What level should the patient strive for?

Retinopathy

Nephropathy

Neuropathy

ADA - 7.0% or less

ACE - 6.5% or less

Insulin from an outside source (not from the body)

Type 1 - must be on for the rest of life

Type 2 - may be needed, given when diabetes is poorly controlled

How long does long acting insulin last?

When does it onset?

When does it peak?

What are some examples?

Onset: 1-2 hours

Never peaks (hallmark of basal insulin)

Last 24 hours

glargine (Lantus), clear

detemir (Levemir), clear

How long does intermediate acting insulin last?

When does it onset?

When does it peak?

What are some examples?

Lasts: 10-16 hours

Onset: 2-4 hours

Peaks: 4-10 hours

Examples: NPH (Humulin N, Novolin N, Relion N), cloudy

How long does short acting insulin last?

When does it onset?

When does it peak?

What are some examples?

Lasts: 3-6 hours

Onset: 30-60 minutes

Peaks: 2-3 hours

Examples: regular (Humulin R, Novolin R, ReliOn R), clear

ONLY insulin that can be give IV

How long does rapid acting insulin last?

When does it onset?

When does it peak?

What are some examples?

Lasts: 3-4 hours

Onset: 15 minutes

Peaks: 60-90 minutes

Examples: lispro (Humalog), clear

aspart (Novolog), clear

glulsine (Apidra), clear

U100

1 ml = 100 U insulin

ALWAYS use insulin syringe

What is inhaled insulin called?

What type of insulin is it?

What are the requirements for its use?

What are potential side effects?

What are potential pitfalls?

What type of testing is required?

Exubera

Regular, short acting insulin

Pt needs healthy lungs (contra for smokers)

Side: SOB, cough, sore throat

Pitfalls: problems with absorption, dosing, potential for additional lung problems

Regular pulmonay function tests required

Heat/freezing can alter the insulin molecule, avoid direct exposure to sunlight

Vials may be left at room temp for up to 4 weeks, unless higher than 86 degrees

Otherwise, refrigerate

Keeping blood glucose level as normal as possible

May prevent complications/secondary effects of DM

Provides flexibility with eating and exercise

Individualized dosage, depends on pt needs

In hospital, used bc stress cortisol often increases blood glucose level

Used w/ pts at home whose diabetes is not well controlled or who are hypoglycemic

0-150, no insulin

150-200, 2 units given

Sub Q site -- rotate b/c of lipohypertrophy or lipotrophy

Not given at heat or cold

IV -- Regular only

Fastest absorption in abdomen, then arm, thigh, and buttock

Scar tissue can delay absorption

Continuous infusion

worn externally

connected to subQ tisue in abdomen

Site should be rotated every 2-3 days to avoid infection and promote good absorption

blood sugar check 4-6x/day

Invasive: blood glucose monitors (finger stick), subQ sensor under skin w/ updated glucose values every 5 minutes (help identify trends and track patterns which is useful for managment of insulin therapy)

Noninvasive: Watch which pulls glucose from skin

Carbs: 45-65% of total energy intake

Fat: 25-30%, no more than 7% saturated fat

Protein: <10%

Alcohol: moderate use may be safe if blood glucose levels are well controlled and if pt is not on medications that will cause adverse effects

Essential part of diabetes managment

Exercise increase insulin receptor sites in the tissue and can have a direct effect on lowering the blood glucose levels

Contribute to weight loss which also decreases insulin resistance

May also help reduce triglyceride and LDL cholesterol levels, increase HDL, reduce BP and improve circulation

Glucose lowering effects of exercise can last up to 48 hours after activity, so hypoglycemia can occur that long after the activity.

Stimulate beta cells to produce insulin

Enhances sesitivity of receptor sites on the cell for interaction with insulin

Metformin

Glucophage

insulin sensitizers

Avandia

Actos

improves insulin sensitivity in skeletel muscles and fat tissue

inhibits glucogenesis

can be used in combo or mono therapy

Januvia

Galvus

too much insulin

too little food

exercise excess

before meals, especially if meals are delayed or snacks omitted

when action of insulin is peaking

infection

illness

missed dose of insulin

undiagnosed DM

pt becomes severly dehydrated and suffer electrolyte loss (K, NA, CL) due to polyuria from hyperglycemia

fats are broken down as energy, resulting in increased amounts of ketones (acids which upset the acid-base balance of blood)

There is not enough insulin to prevent hyperglycemia but there is sufficient insulin to prevent breakdown of fat. 

Hyperglycemia leads to renal insufficiency causing hyperosmolality.

More often seen in Type 2 diabetes.

Ketosis and acidosis do NOT occur

Dehydration and electrolyte imbalance do occur

acute illness

thiazide diuretics

elderly

seizures

loss of consciousness

Blood Glucose >250 (kids), 300 (adults)

Polyuria

Polydipsia

Weakness

Headache

Dehydration

Acetone breathe (fruity odor)

Nausea, vomiting

Kussmaul's respirations

Abdominal pain

polydipsia

polyuria

nuerological changes

confusion

seizures

very high blood sugar

sever dehydration

hypotension

1) Immediately give 10-15 grams of fast acting sugar and repeat in 10-15 minutes if symptoms persist (4-6 oz fruit juice, 6-8 lifesavers, 1-1.5 tsps honey or sugar or 8 oz lowfat milk)

2) When symptoms decrease, give a snack with protein and CHO

3) Teach patient to follow regular pattern of eating, insulin, and exercise

4) Wear ID bracelet

5) For sever hypoglycemia, give Glucogon 1 mg subQ or IM or 25-50 ml of 50% dextrose IV

1) Treat dehydration, electrolyte loss, and acidosis.  For dehydration: IV fluid replacement, asses VS, and look for orthostatic hypotension

2) I&Os

3) Watch for fluid overload in elderly

4) K+ is major concern and will decrease with rehydration due to excretion in urine and explansion of plasma volume, with insulin K+ will move into cells with glucose

5) K+ added to IV fluids unless patient is not voiding

6) Assess for S&S of hypo or hyper glycemia

7) Frequent labs

8) For acidosis: Insulin is given IV

Similiar to DKA: fluids, electrolytes, and insulin

Treatment continues until metabolic abnormalities and neurological symptoms clear

take meds/insulin as usual

take SMBG and urine ketons every 3-4 hours

attempt to consume small portions of CHO

drink fluids every hour including broth

contact MD if unable to take fluids, BG>300, ketones present in urine

-major cause of death

-CAD is 3-4 times higher in Type 1 and 2-4 times higher in Type 2

-increased incidence of MI and more extensive CAD

- increase L ventricular dysfunction after MI, leading to diabetic cardiomyopathy, increase incidence of pump failure, and fatal dysrhythmias

Hypertension

Hyperinsulinemia

Hyperlipidemia

Clotting abnormalities

Blood vessel problems

Albuminuria is associated with greater cardiovascular disease in both Type 1 and Type 2 diabetes

hyperlipidemia

hypertension

CAD

nephropathy

peripheral vascular disease

alcohol and tabacco use

elevated blood glucose levels at the time of CVA are associated with greater brain injury

proliferative diabetic retinopathy

nonproliferative diabetic retinopathy

microaneurysms

venous bleeding

changes in the small blood vessels of the retina

most diabetics develope some degree of retinopathy with 5-15 years of dx

varying degrees of vision impairment to total blindness

Pathologic changes in the kidney that reduce kidney function and may lead to renal failure (DM is leading cause of end stage renal disease)

Maintaining glucose levels in the normal range can delay onset on nephropathy

Microalbuminuria

Regularly

nepropathy

vascular disease

psychological factors

vascular changes

Progressive deterioration of nerves that result in loss of nerve function

Common in diabetics and can affect all parts of the body

Can be focal or diffuse

Insulin deficiency and hyperglycemia are thought to lead to neuropathy through blood vessel changes, cause by hypoxia to nerves. Both the axon and myelin sheath are damaged by reduced blood flow, resulting in blocked nerve impulse transmission.

Excessive glucose is converted to sorbitol, which accumulates in nerves and slows motor conduction.

appropriate weight and height -- stay on growth scale

age appropriate lifestyle

acheiving near normal A1C

preventing acute complications (hypoglycemia, hyperglycemia)

Nondiabetic: 70-110 mg/dl

Children w Type 1: 80-180 mg/dl

Infants/Toddlers w Type 1: 80-200 mg/dl

before meals

before bedtime snack

prolonged exercise

during illness

nighttime if hypoglycemia is suspected

3 dose/day

Combo (intermediate and rapid) breakfast

Rapid dinner

Intermediate dinner

reduction in B-cell function

decreased insulin sensitivity

altered carbohydrate metabolism

elderly more likely to be treated with medications that impair insulin action

adverse consequences from undeteced hyperglycemia

delayed psychomotor function that could interfer with ability to treat hypoglycemia

pt own desire for treatment

coexisiting medical problems such as cognitive impairment, and difficulty achieving strict glycemic control

diet

exercise

insulin if oral agents are not effective

based on individual needs

slower pace w/ simple printed or audio materials

family or support person in teaching

keep in mind: vision, mobility, mental status, function ability, financial and social situations, effects of multiple medications, eating habits, potential for undetected hypoglycemia, and quality of life issues

increased insulin release

significant hypoglycemia may occur, especially in women who experienced N/V and anorexia that often occur in early pregnancy

accumulation of fat prepares the mother for the rise in energy use by the growing fetus during the 2nd half of pregnancy

fetal growth accerlates, levels of placental hormones rise sharply

insulin resistance increases in mother to provide abundent glucose to baby

onset of glucose intolerance during pregnancy

account for 90% of all DM during pregnancy

affects 2-5% of all pregnancies

high rate of type 2 DM dx after delivery, and 20 years out

more likely to occur in subsequent pregnancies

more likely to occur in multifetal pregnancy

altered insulin requirements

difficulty with BG control

vascular disease progression

goal: maintain BG b/t 70 and 120

PIH: uknown etiology, risk increased even w/o renal or vascular impairment

UTI: increased bacterial growth in nutrient rich urine

ketoacidosis: uncontrolled hyperglycemia or infection, more common in women with Type 1

labor dystocia, c-sec, uterine atony w/ hemorrage as a result of hydranmnios 2nd to fetal osmotic diuresis cause by hyperglycemia, uterus overstretched

birth injury to maternal tissues: fetal macrosomia

women, multiparous women, people over 40, people w/ sedentary lifestyle, familial tendancy, obesity

whites

Native Americans

acute infection of gallbladder (stores biles and is released via common bile duct)

cholelithiasis: gallstones obstruct duct, can't drain into duodenum, inflammation occurs

pain -- epigastric and RUQ pain, may radiate to back

tenderness

rididity

N&V

repeated bouts of gallbladder disease

fibrotic

deficiency of absorption

1) stones are stationary or mobile

2) size and location

3) degree of obstruction

4) prescence/extent of inflammation

indigestion

moderate to sever pain

fever

tenderness

epigastric pain

RUQ pain, often referred to back

N/V

restlessness

diaphoresis

stools may be clay colored, amber, or fatty (styatoria)

hx of fat intolerance

dyspepsia

heartburn

flatulance

increased WBC

fever

gangrenous cholecystitis (can become septic and perforate)

subphrenic abscess (develops on or near surface of diaphragm)

pacreaititis

cholangitis (bile duct inflammation)

biliary cirrhosis (flow of bile through ductules of liver is obstructed)

fistulas

rupture

peritonitis

older pts

diabetic pts

pts who delay seeking health care

90-95% accurate in dx gallstones

useful for pts with jaundice as does not depend on liver function

useful for pts allergic to contrast dye

rapid, non invasive, can be used for pregnant women

diagnostic procedure of choice

- Endoscopic retrograde cholangiopancreatography

 - Endoscope inserted through oral cavity into descending duodenum, then common bile and pancreatic ducts are cannculated to deliver medication or drain fluid

- Contrast medium injected into ducts, allows for visualization of structures (gallbladder, cystic duct, common hepatic duct, common bile duct)

retreive gallstone from distal common bile duct

dilate structures

obtain biopsy of tumors

diagnose pseudocysts

culture bile to ID possible infectious organisms

explain procedure

patient NPO for 8 hours

consent for signed

administer sedation immediatley before and during procedure

administer antibiotics, if order

check vital signs

check for signs of perforation or infection

be aware that pancreatitis is most common complication

check for gag reflex - NPO until returns

percutaneous tanshepatic cholangiography

after local anesthesia, liver is entered with long needle, bile duct is entered, bile withdrawn, and radiopaque contrast medium is injected

fluroscopy is used to determine filing of hepatic and biliary ducts

used to diagnose obstructive jaundice

used to locate stones within the bile duct

check for signs of hemorrhage or bile leakage

assess pts meds for possible contraindications, precautions, or complications with the use of contrast medium

increased WBC

elevation of direct and indirect bilirubin levels may indicate obstructive process is present

increased levels of alkalin phosphatase

increased serum amylase

X-ray film of gallbladder made after ingestino or injection of a radipaque substance, usually a contrast material containing iodine

Provides visualization of stones and of gallbladder functino

NPO 10-12 hours before procedure

contraindicated in pts who have allergies to iodine or shellfish

contraindicated in jaundice or hepatitis pts

control pain

control possible infection with antibiotics

maintain fluid and electrolytes

treat symptoms -- pain meds and antiemetics

gastric decompression w/ NG tube

especially effective at removing bile duct stones

endoscope passed through duodenum, spincter of Oddi is widened

basket is used to retreive stone

if stone is too large, endoscopist can crust the stone

limitation is ERCP induced pancreatitis

ERCP

Cholesterol solvents

ESWL

MTBE (methyl tertiary terbutyl ether) is instilled in gallbladder via percutaneous catheter, dissolve stones within hours (may reappear)

oral bile acids, work similiarly to MTBE

high energy shock waves used to disintegrate stones

ultrasound is first used to locate stones and determine where to direct shock waves

normal gallbladder function

mild symptoms

small stones

less effective in obese pts

used only in selected pts

removal of gallbladder through right subcostal incision

T-tube inserted into common bile duct during surgery, when a common bile duct exploration is part of surgical procedure

gallbladder is removed through one of four small punctures in abdoment

closed circuit monitors used to view abdominal cavity, surgeon retracts and dissects gallbladder and removes with grasping forceps

safe procedure with minimal morbidity

monitor for bleeding

pain managment (should be minimal and relieved with NSAIDS or codeine)

common to have referred pain in should bc of trapped CO2, place pt in Sim's position to help move gas away

CDB, splint incision

incentive spirometry

clear liquids, ambulate to bathroom, may even go home same day

adequate ventilation and prevention of respiratory complications

Low Fowler's

T-tube: maintain drainage, observe

antiemetics may need to be administered

pt should be taught diet progression as well as diet upon discharge