Acetate Diabetes

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APPENDIX B PATHOPHYSIOLOGY OF DM TYPE 2



Alpha glucosidase inhibitor: a category of oral

agents are used to treat type 2 diabetes that delay the

absorption of carbohydrate, resulting in lower

postprandial blood glucose level.

Continuous subcutaneous insulin infusion: a small

device that delivers insulin on a 24-hour basis as

basal insulin; it is also programmed by the patient to

deliver a bolus dose before eating a meal in attempt

to mimic normal pancreatic function.

Diabetes mellitus: a group of metabolic diseases

characterized by hyperglycemia resulting from defects

in insulin secretion,insulin action or both.

Diabetic ketoacidosis (DKA): a diabetic derangement

in type 1 diabetes that results from a deficiency of

insulin. Highly acidic ketone bodies are formed,

resulting in acidosis; usually requires hospitalization

for treatment and is usually caused by nonadherence

to the insulin regimen, concurrent illness, or infection.

Fasting plasma glucose (FPG): blood glucose

determination obtained in the laboratory after fasting

for more than 8 hours. Although plasma levels are

specified in diagnostic criteria, blood glucose levels,

which are slightly higher than plasma levels, are morecommonly used.



Glycosylated hemoglobin (hemoglobin A1c): a-long

term measure of glucose control that is the result of

glucose attaching to hemoglobin for the life of the red

blood cell (120 days). The goal of diabetes therapy isa normal to near-normal level of glycosylated

hemoglobin(referred to as HgbA1c or A1C), the same

as in nondiabetic population.

Hyperglycemia: elevated blood glucose level-fasting

level greater than 110mg/dL (6.1mmo/L); 2-hour

postprandial greater than 140mg/dL(7.8mmo/L)

Hyperglycemic hyperosmolar nonketotic

syndrome(HHNS): a metabolic disorder of type 2

diabetes resulting from a relative insulin difeciency

initiated by an intercurrent illness that raises thedemand for insulin; associated with polyuria and

severe dehydration.

Hypoglycemia: low blood glucose level (less than 60

mg/dL [less than 2.7mmo/L])

Insulin: a hormone secreted by the beta cells of the

islets of langerhans of the pancreas that is necessary

for th e metabolism of carbohydrates, proteins, and

fats; a deficiency of insulin results in d iabetes

mellitus.



Impaired fasting glucose(IFG), impaired glucose

tolerance(IGT): a metabolic stage intermediate

between normal glucose homeostasis and diabetes;

not clinical intities in their own right but risk factors forfuture diabetes and cardiovascular disease

Islet cell transplant: an investigational procedure in

which purified islet cells from cadaver donors are

injected into the portal vein of the liver, with the goal

of having these cells secrete insulin and cure type1diabetes.

Ketone: a highly acidic substance formed when the

liver breaks down free fatty acids in the absence of

insulin. The result is diabetic ketoacidosis.

Nephropathy: a long-term complication of diabetes in

which the kidney cells are damaged; characterized by

albuminoria in early stages progressing to end-stage

renal disease.

Neuropathy: a long- term complication of diabetes

resulting from damaged to nerve cell.

Retinopathy: a long-term complication of diabetes in

which the microvascular system of the eye is

damaged.



Self-monitoring of blood glucose (SMBG)2: a method

of capillary blood glucose testing in which the patient

pricks his/her finger and applies a drop of blood to a

test strip that is ready by a meter.

Sulfunyurea: a classifaction of oral antidaibetic

medication for treating type 2 diabetes; enhances

insulin secretion and insulin action.

Thiazolidinedione: a class of oral antidiabetic

medications that reduce insulin resistance in target

tissues, enhancing insulin action without directly

stimulating insulin secretion.

RISKS FACTORS

Family history of diabetes (ie. Parents or sibling withdiabetes)

Race/ethinicity (eg. African Americans,HispanicAmerican , Native Americans, Asian American)

Age > 45 y.o.

Previously identified impaired fasting glucose or

impaired glucose tolerance Hypertension (>140/90mm Hg)

HDL cholesterol level <35 mg/dl (0.90mmol/L)and / ortri-glyceride level>250 mg/dl (2.8mmol/L)

History of gestational diabetes or delivery over 9 lbs



ANATOMY AND PHYSIOLOGY of the endocrine

system

hypothalamus The hypothalamus is located in the brain, near theoptic chiasm. It secretes hormones that stimulate orsuppress the release of hormones in the pituitarygland, in addition to controlling water balance, sleep,temperature, appetite, and blood pressure.

pineal body

The pineal body is located below the corpus callosum,a part of the brain. It produces the hormonemelatonin.

pituitary The pituitary gland is located at the base of the brain.No larger than a pea, the gland controls manyfunctions of the other endocrine glands.

thyroid and parathyroids The thyroid gland and parathyroid glands are locatedin front of the neck, below the larynx (voice box). Thethyroid plays an important role in the body's



metabolism. Both the thyroid and parathyroid glandsalso play a role in the regulation of the body's calcium

balance.

thymus The thymus is located in the upper part of the chestand produces T-lymphocytes (white blood cells that

fight infections and destroy abnormal cells).

What are hormones?

Hormones are chemical substances created by the

body that control numerous body functions. Theyactually act as "messengers" to coordinate functionsof various body parts. Most hormones are proteinsconsisting of amino acid chains. Some hormones aresteroids, fatty cholesterol-produced substances.

Functions controlled by hormones include activities ofentire organs; growth and development; reproduction;

sexual characteristics; usage and storage of energy;and levels of fluid, salt, and sugar in the blood.

adrenal gland The pair of adrenal glands are located on top of bothkidneys. Adrenal glands work hand-in-hand with thehypothalamus and pituitary gland.

kidney

The pair of kidneys are located near the middle of theback, just below the rib cage. The kidneys processthe blood to sift out waste products and extra water.This waste and extra water becomes urine, which isstored in the bladder.

pancreas The pancreas is located across the back of the

abdomen, behind the stomach. The pancreas plays arole in digestion, as well as hormone production.

ovary A female's ovaries are located on both sides of the



uterus, below the opening of the fallopian tubes(tubes that extend from the uterus to the ovaries). In

addition to containing the egg cells necessary for

reproduction, the ovaries also produce estrogen andprogesterone.

testis A male's testes are located in a pouch that hangssuspended outside his body. The testes produce

testosterone and sperm.

Figure 2. Pathophysiology

http://nursingcrib.com/wp-content/uploads/patho-diabetes.png



Disease Process

Type 2 diabetes is characterized by the combination of

peripheral insulin resistance and inadequate insulinsecretion by pancreatic beta cells. Insulin resistance,

which has been attributed to elevated levels of free fatty

acids in plasma leads to decreased glucose transport into

muscle cells, elevated hepatic glucose production, and

increased breakdown of fat.

For type 2 diabetes mellitus to occur, both defects

must exist. For example, all overweight individuals

have insulin resistance, but diabetes develops only in

those who cannot increase insulin secretion

sufficiently to compensate for their insulin resistance.

Their insulin concentrations may be high, yet

inappropriately low for the level of glycemia.

Beta cell dysfunction is a major factor across the

spectrum of pre-diabetes to diabetes. A study of

obese adolescents by Bacha et al confirms what is

increasingly being stressed in adults as well: Beta cellfunction happens early in the pathological process

and does not necessarily follow stage of insulin

resistance. Singular focus on insulin resistance as the

"be all and end all" is gradually shifting, and hopefully

better treatment options that focus on the beta cell

pathology will emerge to treat the disorder early.

In the progression from normal glucose tolerance to

abnormal glucose tolerance, postprandial blood

glucose levels increase first; eventually, fasting



hyperglycemia develops as suppression of hepatic

gluconeogenesis fails.

During the induction of insulin resistance, such as is

seen after high-calorie diet, steroid administration, or

physical inactivity, increased glucagon levels and

increased glucose-dependent insulinotropic

polypeptide (GIP) levels accompany glucose

intolerance; however, postprandial glucagonlike

peptide-1 (GLP-1) response is unaltered. This has

physiologic implications; for example, if the GLP-1

level is unaltered, GLP-1 may be a target of therapy in

the states mentioned above.

The high mobility group A1 (HMGA1) protein is a keyregulator of the insulin receptor gene

(INSR ). Functional variants of the HMGA1 gene are

associated with an increased risk of diabetes. These

variants were shown to lead to reduction in protein

content of both HMGA1 and INSR .

Although the pathophysiology of the disease differs

between the types of diabetes, most of the

complications, including microvascular,

macrovascular, and neuropathic, are similar

regardless of the type of diabetes.

Hyperglycemia appears to be the determinant of

microvascular and metabolic complications.

Macrovascular disease, however, is much less related



to glycemia. Insulin resistance with concomitant lipid

abnormalities (ie, elevated levels of small dense low-

density lipoprotein cholesterol [LDL-C] particles, low

levels of high-density lipoprotein cholesterol [HDL-C],elevated levels of triglyceride-rich remnant

lipoproteins) and thrombotic abnormalities (ie,

elevated type-1 plasminogen activator inhibitor [PAI-

1], elevated fibrinogen), as well as conventional

atherosclerotic risk factors (eg, family history,

smoking, hypertension, elevated LDL-C, low HDL-C),determine cardiovascular risk. Unlike liver and smooth

muscle, insulin resistance is not associated with

increased myocardial lipid accumulation.

Increased cardiovascular risk appears to begin prior

to the development of frank hyperglycemia,

presumably because of the effects of insulinresistance. Stern in 1996

and Haffner and D'Agostino

in 1999

developed the "ticking clock" hypothesis of

complications, asserting that the clock starts ticking

for microvascular risk at the onset of hyperglycemia,

while the clock starts ticking for macrovascular risk at

some antecedent point, presumably with the onset ofinsulin resistance.

Gestational diabetes mellitus (GDM) is defined as any

degree of glucose intolerance with onset or first

recognition during pregnancy. Gestational diabetes

mellitus is a complication of approximately 4% of all

pregnancies in the United States.



See appendix B

Clinical manifestation

the “ three P’s” ;POLYURIA, POLYDIPSIA, POLYPHAGIA

Polyuria

Polyphagia

Fatigue & weakness

sudden vision changes

tingling or numbness in hands or feet

dry skin, skin lesions, or wounds that are slow to heal

recurrent infections.

The onset of type 1 diabetes may also be associated withsudden weight or nausea , vomiting or abdominal pains ,ifDKA has developed.

DIAGNOSTIC PROCEDURES

LABORATORY ASSESSMENT BLOOD TESTS

The nurse, the client or a family member monitors theongoing status of the disease by performing capillaryblood glucose testing using a blood glucose meter.

FASTING BLOOD GLUCOSE TEST

Fasting blood glucose test are most accuratewhen the blood is obtained by venipuncture.The client should fast for at least 8hours (wateris permitted). Draw the blood before insulin ororal antidiabetic agents have been taken.Diabetes is diagnosed when two separate test

Untreated gestational diabetes mellitus can lead to

fetal macrosomia, hypoglycemia, hypocalcemia, and

hyperbilirubinemia. In addition, mothers with

gestational diabetes mellitus have increased rates ofcesarean delivery and chronic hypertension.



results exceed 126 mg/dL. (7 mmol/L)(ADA,2003a).

ORAL GLUCOSE TOLERANCE TEST

The oral glucose tolerance test (OGTT) is themost sensitive test for diagnosing diabetes,although it is not routinely used except ingestational diabetes. The test is inconvenientto clients, costly, and time consumingcompared with the fasting blood glucosemeasure. Carbohydrate restriction or bedrest

before the test alters glucose tolerance. Theclient drinks a beverage containing a glucoseload of 75 g, and blood samples are collectedat 30-minute intervals for 2 hours. A diagnosisof diabetes is made if the blood glucose isgreater than 200mg/dL (11.1 mmol/L) at120mins.

GLYCOSYLATED HEMOGLOBIN ASSAYS

> Blood glucose permanently attaches to

hemoglobin. The higher the blood glucose level is

over time, the more glycosyted hemoglobin becomes.

Thus glycosylated hemoglobin (HbA1c) is a good

indicator of the average blood glucose level

B. pharmacology

The goal of medical treatment is to return the patient to asnear a euglycemic state as possible and correct any

related metabolic disorders.



DIET These will help to improve glycemic (blood sugar) controland prevent or minimize complications of diabetes.

Diet: A healthy diet is key to controlling blood sugar levelsand preventing diabetes complications.

He or she can be recommend a dietitian or a weightmodification program to help the patient reach a goal.

Oral Hypoglycemic Action

Sulfonylureas (SUF’s) Orinase

(Tolbutamide) Tolinase

(Tolazamide) Diabinese

(Chlorpropamide)

These medications act on thepancreatic tissue to produce

insulin.

Biguanides Glucophage

(Metformin)

These medications act bylowering the cells resistanceto insulin and they decreaseexcess sugar production fromthe liver by making the bodymore sensitive to naturalinsulin.

Alpha-glucosidase

inhibitors Precose

(Acarbose) Glyset (Miglitol)

These medications delay the

absorption of glucose from theintestine by slowing thebody’s digestion of carbohydrates.

ThiazolidinedionesRezulin

(Troglitazone)Avandia

(Rosiglitazone

These medications assist thebody by sensitizing body

tissues to insulin.



Eat a consistent, well-balanced diet that is high in fiber,low in saturated fat, and low in concentrated sweets.

It will also help to keep blood sugar at a relatively even

level and avoid excessively low or high blood sugarlevels, which can be dangerous and even life-threatening.

SPECIAL CONSIDERATIONS FOR TYPE 2 DIABETES.

A moderate caloric restriction (250 to 500 calories less

than average daily intake) and an increase in physicalactivity improves diabetic control and weight control.

Decrease of more than 10% of body weight can result in

significant improvement in glycosylated

hemologbin(hemoglobin A1c).

SAMPLE MENU

Exchanges (2-starch, 3-meat, 1-vegetable, 1-fat, 1-fruit…

“Free”items (optional))

SAMPLE LUNCH #1

2 slices bread , 2 oz sliced turkey and 1 oz low fat cheese,

lettuce,tomato,onion, 1tsp mayonnaise, 1 medium apple,

Unswetened iced tea, mustard, pickled, hot pepper

SAMPLE LUNCH #2

Hamburger bun, 3 oz lean beef patty, green salad, 1tbsp

salad dressing, 1/4cup watermelons, diet soda, 1tbsp

catsup,pickle,onions

SAMPLE LUNCH #3

1 cup cooked pasta 3 oz boiled shrimp, ½ cup plum

tomatoes, 1tsp olive oil, 1 ¼ cup fresh strawberries, ice

water with lemon, garlic and basil



EXERCISE THERAPY

Regular exercise is an essential part of a diabetic

treatment plan.

Reduce the risk for atherosclerosis.

1. Exercise in the client with uncontrolled diabetes

results in further hyperglycemia and the formation of

ketone bodies. Diabetic clients may have prolonged

elevated blood glucose levels after vigorous exercise.

2. Exercise in the person with the diabetes can cause

hypoglycemia because of increased muscle glucose

uptake and inhibited glucose release from the liver.

Benefits of exercise.

Improves control by increasing insulin sensitivity,

enhancing cell uptake of glucose, and promoting

weight loss.

Regular exercise decreases risk factors for

cardiovascular disease. Exercise decreases blood

pressure and improves cardiovascular function.

Regular vigorous physical activity prevents or delaystype 2 diabetes by reducing body weight, insulinresistance, and glucose intolerance.

Risk related to exercise

prolonged hypoglycemia or hyperglycemia can

occur, particularly after sustained high-intensive

exercise.



Several complications of diabetes can be made

worse by exercise: 1. Proliferative retinopathy is advised to avoid the

Valsalva maneuver(breathe-holding while bearing

down ) and

2. Activities that increase blood pressure. Heavy lifting, rapid head motion, or jarring activities can causeeye hemorrhage or retinal detachment.

3. Exercise may increase proteinuria in clients with

diabetic nephropathy.

4. The for foot and joint injury rises for clients with

peripheral neuropathy.

Client education: exercise promotion.

1. Instruct the client to wear shoes with good traction

and cushioning and to examine

The feet daily and after exercise.2. Discourage exercise in the extreme heat or cold or

during periods of poor blood glucose control.

3. Advise the client to stay hydration specially during

and after exercise in a warm environment.

4. Exercise can increase absorption of insulin from the

injection site.

5. The risk for hypoglycemia increases when insulin is

injected into an area that is exercised.

NURSING MANAGEMENT

ASSESSMENTObtain a history of current problems, family history, andgeneral health history.

o Has the patient experienced polyuria, polydipsia,polyphagia, and any other symptoms?

o Number of years since diagnosis of diabeteso Family members diagnosed with diabetes, their

subsequent treatment, and complications



Perform a review of systems and physical examination toassess for signs and symptoms of diabetes, general

health of patient, and presence of complications.o

General: recent weight loss or gain, increased fatigue,tiredness, anxietyo Skin: skin lesions, infections, dehydration, evidence of

poor wound healingo Eyes: changes in vision”floaters, halos, blurred vision, dry

or burning eyes, cataracts, glaucomao Mouth: gingivitis, periodontal diseaseo Cardiovascular: orthostatic hypotension, cold extremities,

weak pedal pulses, leg claudicationo GI: diarrhea, constipation, early satiety, bloating,

increased flatulence, hunger or thirsto Genitourinary (GU): increased urination, nocturia,

impotence, vaginal dischargeo Neurologic: numbness and tingling of the extremities,

decreased pain and temperature perception, changes in

gait and balance

Nursing Diagnosis:

Alteration in Nutrition (hypo/hyperglycemia)

Alteration in Cardiac Output (atherosclerosis) Knowledge Deficit (treatment regimen)

Ineffective Coping Individual (denial, lifetimealteration)

Ineffective Coping Family (care giver strain) Potential for Fluid Volume Excess

(cardiovascular/renal complications) Potential for Fluid Volume Deficit (polyuria)

Potential for Social Isolation (BBQ’s, cocktail parties,work potlucks)



PLANNING

The patient must have a good understanding of both hypo

and hyperglycemia and be able to verbalize treatment for

both.

The patient should be provided support informationsuch as groups and organizations that can assist with

the necessary life style changes associated with adiagnosis of Diabetes Type II.

Dietician referral may be necessary.

The patient needs to be aware that periodic lab

testing will be required (usually life long). Originallyevery 3 months and when stable usually every 6

months.INTERVENTION

Monitoring blood glucose

Administering antidiabetics/insulin

Full body assessment, special attention made tocirculatory and skin

Prevention of ulcer formation

Monitoring VS

Monitoring for hyper/hypoglycemia

Offering snacks at bedtime if permitted.

E- Patients is able to avoid further complication in

relevance to disease



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