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8/2/2019 Acetate Diabetes
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APPENDIX B PATHOPHYSIOLOGY OF DM TYPE 2
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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.
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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.
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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.
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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
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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
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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
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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
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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
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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
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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.
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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.
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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.
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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.
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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
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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.
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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
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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)
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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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