WVC IGGY chpt 67 to pg 1491 Flashcards

blood glucose
Terms Definitions
In the United States, diabetes mellitus (DM) is the leading cause of
new cases of blindness, end-stage kidney disease requiring dialysis or transplantation, and foot or leg amputations.
Studies show that __________ controls reduces complication of diabetes
glycemic
An essential part of preventing complications that occur with DM is
Treatment of hypertension and hyperlipidemia
The main feature of chronic DM is
hyperglycemia resulting from problems with insulin secretion, insulin action, or both.
DM is classified by
underlying problem causing a lack of insulin and the severity of the insulin deficiency.
The 2 types of islet cells that are responsible for insulin control
alpha and beta cells
Alpha cells produce ___________, beta cells produce _________ and ________
glucagon; insulin and amylin.
A major “counterregulatory” hormone that has actions opposite those of insulin
glucagon,
It causes the release of glucose from cell storage sites whenever blood glucose levels are low
glucagon
This allows body cells to use and store carbohydrate, fat, and protein
insulin
TYPE 1 DIABETES
• Beta-cell destruction leading to absolute insulin deficiency • Autoimmune • Idiopathic
TYPE 2 DIABETES
• Ranges from insulin resistance with relative insulin deficiency to secretory deficit with insulin resistance
Other conditions resulting from hyperglycemia
• Genetic defects of beta-cell function/ insulin action•pancreatitis, trauma, neoplasia, cystic fibrosis, hemochromatosis•acromegaly, Cushing's disease, glucagonoma, pheochromocytoma, hyperthyroidism, aldosteronism• congenital rubella, cytomegalovirus•
GESTATIONAL DIABETES MELLITUS (GDM)
• Glucose intolerance with onset or first recognition during pregnancy • Diagnosis is based on results of a 100-g oral glucose tolerance test during pregnancy
Proinsulin, secreted by and stored in the beta cells of the islets of Langerhans in the pancreas, is transformed by
the liver into activated insulin.
Insulin attaches to receptors on target cells, where it promotes
glucose transport into the cells through the cell membranes.
C-peptide levels are used to measure
the rate that beta cells secrete insulin.
Insulin is allows
glucose in the blood to move into cells to generate energy.
The liver is the first major organ to be reached by insulin in the blood. In the liver, insulin promotes
glycogenesis at the same time that it inhibits glycogenolysis, protein and lipid synthesis and inhibits ketogenesis & gluconeogenesis
In muscle, insulin promotes
protein and glycogen synthesis. Keeps blood glucose levels in the norm
In fat cells, insulin promotes
triglyceride storage. Keeps blood lipid levels in the norm.
The pancreas secretes about
40 to 50 units of insulin daily directly into liver circulation in a two-step manner (basal insulin secretion & prandial)
Glucose is the main fuel for central nervous system (CNS) cells.The brain needs a continuous supply from circulation to prevent
neuronal dysfunction and cell death.
______ _________can be used as fuel by some cells when glucose is not available.
fatty acids
Glucose and free fatty acids are stored inside cells as
glycogen in the liver and muscles
In the fat cells, glycogen is stored as
triglyceride
The most efficient means of storing energy is in the form of
triglyceride
During a prolonged fast or after illness or injury
proteins are broken down and some amino acids are converted into glucose.
During a fasting state, plasma glucose is maintained by
a balance between glucose uptake by cells and glucose production by the liver.
During a fasting state, liver processes are regulated by glucagon release from
pancreatic alpha cells that stimulate glucose production.
During fasting, insulin is released from
pancreatic beta cells to prevent excessive liver glucose output.
Glucose in the blood after a meal is controlled by
the emptying rate of the stomach and delivery of nutrients to the small intestine, where they are absorbed into circulation
In response to food in the stomach, Incretin hormones
increase secretion of insulin and slow the rate of gastric emptying, preventing hyperglycemia after meals
In type 2 diabetes, hyperglycemia results from
excessive liver glucose production and reduced glucose uptake in other cells due to a combination of INSULIN RESISTANCE and DEFICIENT INSULIN SECRETION.
With DM II, during a meal, the rate of gastric emptying is
faster than normal. Stomach contents reach the intestine & the rate of glucose entry into circulation increase →hyperglycemia. The ↑rate of gastric emptying is thought due to ↓secretions of amylin and GLP-1
Glucagon is the main
counterregulatory hormone. It increases blood glucose by actions opposite those of insulin when more energy is needed.
Other hormones that increase blood glucose levels are
epinephrine, norepinephrine, growth hormone, and cortisol
Insulin and counterregulatory hormones keep the level of blood glucose normally
70 to 100 mg/dL
Gluconeogenesis, is the
conversion of amino acids into glucose.
Lipolysis, is the
breakdown of fat
Proteolysis, is the breakdown of
proteins, provide fuel for energy
Levels of counterregulatory hormones increase in an
attempt to make glucose from other sources
Hyperglycemia causes fluid and electrolyte imbalances, leading to the classic symptoms of diabetes:
polyuria, polydipsia, and polyphagia.
Polyuria results in excess
sodium, chloride & potassium being excreted In the urine→dehydration →polydipsia→ cell breakdown → polyphagia
With insulin deficiency, fats break down, releasing free fatty acids. Conversion of fatty acids to
ketone bodies provides a backup energy source.
Ketones are
abnormal breakdown products of fatty acids,
Collection of ketones in the blood when insulin is not available, results in
metabolic acidosis.
The dehydration that occurs with diabetes leads to
hemoconcentration, hypovolemia, hyperviscosity, hypoperfusion & hypoxia.
Physiologic Response to Insufficient Insulin
• Decreased glycogenesis• Increased glycogenolysis • Increased gluconeogenesis • Increased lipolysis • Increased ketogenesis • Proteolysis
Kussmaul respiration
an increase in respirations due to diabetic metabolic acidosis. Acetone is exhaled, giving the breath a “fruity” odor.
Hyperkalemia or hypokalemia in DM is related to
patients response to treatment, severity of acidosis and level of hydration.
Three glucose-related emergencies can occur in patients with diabetes
•Diabetic ketoacidosis (DKA) caused by lack of insulin and ketosis•Hyperglycemic-hyperosmolar state (HHS) caused by insulin deficiency and profound dehydration•Hypoglycemia from too much insulin or too little glucose
DM can lead to health problems and early death due to
macrovascular and microvascular
Macrovascular complications are
coronary heart disease, cerebrovascular disease, and peripheral vascular disease, lead to increased early death among those with diabetes.
Microvascular complications of blood vessel structure and function lead to
nephropathy (kidney dysfunction), neuropathy (nerve dysfunction), and retinopathy (vision problems).
Chronic hyperglycemia causes
irreversible basement membrane thickening and organ damage.
Glucose toxicity directly or indirectly affects
functional cell integrity.
Chronic ischemia in small blood vessels causes
connective tissue hypoxia and microischemia
Complications in patients with type 2 diabetes seem more related to
hypertension, a sedentary lifestyle, high blood lipid levels, and smoking than to hyperglycemia, and obesity
Many older diabetic patients have no classic signs of high blood glucose levels, and the diagnosis is made
when the patient seeks treatment for another illness or for complications of diabetes, such as visual problems.
The most common complication of DM is
cardiovascular disease
The leading cause of death in patients with DM is
MI, coronary artery disease, diabetic cardiomyopathy, and abnormal blood clotting. Left ventricular dysfunction with cardiac failure and fatal cardiac dysrhythmias are more common in diabetic patients after MI.
Diabetic patients often have a higher incidence of traditional cardiovascular risk factors of
obesity, HTN, dyslipidemia, and sedentary lifestyle. Cigarette smoking / positive family history also increase risk for cardiovascular disease. Renal disease, indicated by albuminuria, increases the risk for coronary heart disease and mortality from MI.
Patients with diabetes tend to have higher levels of C-reactive protein (CRP),
an acute-phase inflammatory marker associated with increased risk for future cardiovascular problems and death.
Cardiovascular disease complication rates can be reduced through
aggressive management of hyperglycemia, hypertension, and hyperlipidemia..
Considerations for stroke in pt with DM are
Hypertension, hyperlipidemia, nephropathy, peripheral vascular disease, and alcohol and tobacco abuse
The cause and progression of diabetic retinopathy are related to
problems that block retinal blood vessels and cause them to leak, leading to retinal hypoxia
Retinopathy is linked to fasting blood glucose levels
above 129 mg/dL
_______________ & ___________________increase the rate of retinopathy development in patients with type 1 diabetes
Hyperglycemia and hypertension
Vision loss also occurs from
macular degeneration, corneal scarring, and changes in lens shape or clarity
Hyperglycemia may cause
blurred vision even with glasses
Hypoglycemia may cause
double vision
Open-angle glaucoma and cataracts are
more common in patients with diabetes
The older patient with retinopathy may have
blurred vision, distorted central vision, fluctuating vision, loss of color perception, and mobility problems resulting from loss of depth perception.
It is especially important to assess the ability of the patient to
perform tasks such as measurement and injection of insulin and blood glucose monitoring to determine if adaptive devices are needed to assist in self-management activities.
It is a common complication of diabetes and often involves all parts of the body.
neuropathy
Damage to sensory nerve fibers results in
either pain or loss of sensation.
Damage to motor nerve fibers results in
muscle weakness.
Damage to nerve fibers in the autonomic nervous system can cause
dysfunction in every part of the body.
the most common neuropathies in diabetes and involve widespread nerve function loss
Diffuse neuropathies
They have a slow onset, affect both sides of the body, involve motor and sensory nerves, progress slowly, are permanent, and include autonomic nerve dysfunction.
Diffuse neuropathies
Late complications include foot ulcers and deformities
Diffuse neuropathies
They usually are caused by an acute ischemic event or by the physical trapping of a nerve and effect a single nerve or nerve group
Focal neuropathies
The symptoms begin suddenly, affect only one side of the body or body area, and are self-limiting
ischemic neuropathies
These stem from compression of a nerve in a body compartment or between tissues. Symptoms begin gradually and can occur anywhere. They may be bilateral, having a waxing and waning course without spontaneous recovery
Focal entrapment neuropathy (ie:CTS)
Autonomic nervous system neuropathy leads to problems in
cardiovascular, GI, and urinary function.
Hyperglycemia leads to neuropathy through
blood vessel changes that cause nerve hypoxia
Orthostatic hypotention and syncope
increase the risk for falls, especially among older adults
Common GI symptoms from diabetic neuropathy are
dysphagia N/V, and bowel elimination problems. Diarrhea often occuring at night. Constipation, Gastroparesis
The most common GI symptom of DM is
Constipation, intermittent and may alternate with bouts of diarrhea.
Gastroparesis a cause of
hypoglycemia
Loss of nerve input to the bladder results in
incomplete emptying, which leads to urinary infection and kidney problems
Diabetes is the leading cause of
end-stage kidney disease (ESKD) and kidney failure in the United States
Risk factors for nephropathy
a 10- to 15-year history of diabetes, diabetic retinopathy, poor blood glucose control, uncontrolled hypertension, and genetic predisposition.
The earliest clinical sign of nephropathy is
microalbuminuria
Diffuse neuropathies
Distal symmetric polyneuropathy, Autonomic neuropathy
Sensory alterations of distal symmetric polyneuropathy
Paresthesias: burning/tingling sensations, starting in toes and moving up legs. Dysesthesias: burning, stinging, or stabbing pain. Anesthesia: loss of sensation
Motor alterations in intrinsic muscles of foot in distal symmetric polyneuropathy
Foot deformities: high arch, claw toes, hammertoes; shift of weight-bearing to metatarsal heads and tips of toes
Focal ischemia manifests as
Thoracolumbar radiculopathy w/sensory&reflex loss: Pain across back/side/front of chest/abdomen. Cranial nerve palsies, third/sixth nerves: Sudden diplopia/ptosis; eye pain. Amyotrophy Pain; asymmetric weakness; wasting of iliopsoas, quads/adductors
Autonomic neuropathy manifestations
:Gastroparesis/constipation, nausea/anorexia. Diabetic diarrhea; Diarrhea/bowel incontinence, bladder/urinary ret. Impotence, ED, Orthohypotension, resting tachycardia, Defective counterregulation, Loss of warning signs of hypoglycemia
Entrapment neuropathies
Carpal tunnel syndrome. Popliteal nerve/knee; Footdrop; Posterior tibial nerve at tarsal tunnel; Tarsal tunnel syndrome: sensory impairment in sole of foot; weakness of intrinsic muscles of foot; burning pain and paresthesias at ankle and plantar surface
Chronic high blood glucose levels cause
hypertension in kidney blood vessels and excess kidney perfusion
Increased pressure from hypertension in the kidney have what effect on the system
leaky blood vessels,→filtration of lg particles→ deposits in kidney tissue/blood vessels→vessels narrow ↓kidney oxy→kidney cell hypoxia/cell death. Time→ scarring in blood vessels in the glomerulus → unable to filter urine from the blood, →renal failure.
What items are included in the filtration of larger particles resulting from damage of kidney hypertension
albumin and other proteins
What disease process speeds the process of diabetic nephropathy
cardiac disease, both systolic and diastolic hypertension greatly speed the progression of diabetic nephropathy
What is an autoimmune disorder in which beta cells are destroyed in a genetically susceptible person
DM I
Describe the autoimmune disease process in type 1 diabetes
immune system cells, mediators, and antibodies attack and destroy insulin-secreting cells in the islets.
Antigen pattern for DM 1 and viral considerations
HLA-DR or HLA-DQ, mumps, congenital rubella, and coxsackievirus infection, appear to trigger autoimmune destruction of pancreatic beta cells
Development of the DM 1 is an interactive effect of
genetic predisposition and exposure to certain environmental factors.
Most patients with type 1-diabetes have what antibodies/markers
islet cell antibodies (ICAs), insulin autoantibodies (IAAs), autoantibodies to glutamic acid decarboxylase (GAD), or autoantibodies to tyrosine phosphates. Circulating ICA and IAA may be present before manifestations of DM1 develop. (key feature)
DM 1, average age at onset
Usually younger than 30 yr, occurs at any age
DM II average age at onset
Peaks in 50s; may occur earlier
Main symptoms of DM 1
Abrupt onset, thirst, weight loss
Main symptoms of DM II
Frequently none; thirst, fatigue, visual blurring, vascular or neural complications
Etiology of DM 1
Viral infection
Etiology of DM II
unknown
Basic pathology of DM II
Insulin resistance & Dysfunctional pancreatic beta cell
What antigen patterns/antibodies are present in DM II
none
Endogenous insulin and C-peptide in DM 1 and DMII
DM 1-none; DMII-Low, normal, or high
Is inheritance in DM1 recessive or dominant
recessive
Is inheritance in DMII recessive or dominant
dominant and multifactorial
How does nutritional status affect the onset of DM1
non-factorial, usually non-obese
What percentage of DMII patients are insulin dependent
20-30%
Sulfonylurea therapy is used in what type of DM
DMII
A progressive disorder in which the pancreas makes less insulin over time
DMII
A reduced ability of most cells to respond to insulin, poor control of liver glucose output, and decreased beta-cell function, eventually leading to beta-cell failure
insulin resistance
The simultaneous presence of metabolic factors known to increase risk for developing type 2 diabetes and cardiovascular disease
metabolic syndrome (syndrome X)
Features of metabolic syndrome are
Abdominal obesity: waist men >40” ; women >35” •Hyperglycemia: FBS> 100 mg/dL •HTN: systolic BP > 130, diastolic BP > 85 •Dyslipidemia: triglyceride > 150, HDL< 40 (men) or < 50 (women)
Any the features of metabolic syndrome can cause
atherosclerosis and the risk for stroke, coronary heart disease, and early death
What would you teach a client with DM
lifestyle changes: ↓wt to 20% of ideal BMI; modifying diet and exercising more will reduce cardiovascular risk. Drug therapy may be required to achieve desired lipid and blood pressure outcomes.
What would you teach for healthcare promotion in a patient with DM1
control of blood glucose levels, regularly follow-up with their HCP; regular yearly eye/urine microalbumin tested; Early diagnosis of changes allows adjustments in treatment regimens to be made that slow progression of eye and kidney problems
The major focus for healthcare promotion of DM1 is
Control of diabetes and its complications
The major focus for healthcare promotion of DMII is
prevention
What would you teach for healthcare promotion in DMII
maintain appropriate weight, reduce cardiovascular risk factors of tobacco use, hypertension, and high blood lipid levels reduce onset of DMII & and its long-term complications.
What is the percentage of heredity incidents of DMII
15%
In assessing the history of a patient, what are important questions to ask
about risk factors and symptoms related to diabetes (age, how large their children were at birth or if they were glucose intolerant); Asses for fatigue, polyuria, and polydipsia; vision/touch changes, infections (yeast too), ↑time to heal
The preferred test for DM in non-pregnant adults is
Fasting plasma glucose (FPG) NPO 8hrs; A diagnosis of diabetes is made with THREE separate test results > 126 mg/dL even with older adults
The classic symptoms of diabetes include
polyuria, polydipsia, and unexplained weight loss.
How is DMII diagnosed
Symptoms of diabetes plus casual blood glucose concentration > 200 mg/dL OR FPG OR 2-hr plasma glucose > 200 mg/dL (oral glucose tolerance test of 75 g glucose dissolved in water)
Normal ranges for FBG
100 mg/dL (older adults rise 1 mg/dL per decade)
Impaired fasting glucose(IFG) is defined as
>100 mg/dL but <126 mg/dL
Normal ranges for (GTT) Glucose tolerance test (2-hr post-load result)
<140 mg/dL
Impaired glucose tolerance test (IGT) are
>140 mg/dL but <200 mg/dL
IGT provisional diagnosis leves
200 mg/dL
Normal values for Glycosylated hemoglobin (hemoglobin A1c [HbA1c]) test
<7%
Levels >8% of glycosylated hemoglobin indicate
poor diabetic control and need for adherence to regimen or changes in therapy.
What instructions do you give your clients prior to undergoing an oral glucose tolerance test
good 3 day diet of at least 150 carbs and reg exercise, fast for 10-12 hrs prior to test, carb restriction, bedrest, acute illness, Phenytoin (Dilantin), anovulatory drugs, diuretics, nicotinic acid, and glucocorticoids adversely affect results
How will you explain an oral glucose test to your clients
after fasting for 10-12 hours, initial blood drawn, within 5 mins consume 300mL of glucose, then blood samples are drawn q 30mins for 2 hrs. During the test, you rest, no smoking/drinking
What are the indications for DMII testing
>45 yrs old, BMI >25%, 1st relative w/DM, inactive,↑risk ethnic pop, baby wt >9 lbs/GDM, HTN, HDL<35, trigl >250, polycystic ovarian syndrome, IGF/IGT previously, Hx of vascular disease
The most sensitive test for DM is
oral glucose tolerance testing (OGTT)
How is GDM tested
OGTT, with hourly tests. Two or more of the venous plasma levels must be met or exceeded for a positive diagnosis
Screening for diabetes is done with either
fasting plasma glucose test or 2-hour OGTT
Glycosylated hemoglobin assays are useful because
blood glucose permanently attaches to hemoglobin
What shows the average blood glucose level during the previous 120 days—the life span of red blood cells. to evaluate the treatment plan
glycosylated hemoglobin assays (HbA1c ) LONG TERM
What test is used to assess long-term glycemic control, as well as to predict the risk for complications
HbA1c. Unlike the fasting blood glucose test, HbA1c test results are not altered by eating habits the day before the test.
What 2 conditions interfere with HbA1c
Hemolysis, blood loss, and pregnancy all increase red blood cell turnover and reduce HbA1c levels. Triglycerides and bilirubin interfere with the assay, leading to overestimation of HbA1c levels in patients with hypertriglyceridemia.
Glycosylated serum proteins and albumin
these proteins can indicate blood glucose control over a shorter period than HbA1c.
Glycosylated serum proteins and albumin measures are useful when
tight control of blood glucose is necessary (e.g., pregnancy) or in short-term follow-up of treatment changes.
What are the available tests for glycosylated serum proteins & albumin
glycosylated serum albumin (GSA), glycosylated serum protein (GSP), and fructosamine.
The presence of moderate to high urine ketones (hyperketonuria) indicates a
severe lack of insulin.
Hyperketonuria in the presence of hyperglycemia is a
medical emergency that, when detected early, can be treated with insulin and careful monitoring.
When should urine testing be performed
acute illness, stress, when blood glucose levels consistently exceed 300 mg/dL, during pregnancy, or when any symptoms of ketoacidosis are present. Ketone testing also is recommended for diabetic patients participating in a weight-loss program
Hyperketonuria without hyperglycemia suggests that
weight loss is occurring without disrupting blood glucose control
Tests for kidney function are important because the presence
of urine protein without kidney symptoms may indicate microvascular changes in the kidney
Urine albumin excretion rates of 20 to 200 g/min (30 to 300 mg/hr) indicate
microalbuminuria. Even minor elevations of albumin are associated with increased mortality.
Once clinical proteinuria has been detected, kidney function (e.g., glomerular filtration rate) is assessed by
creatinine clearance tests . In patients with nephropathy, a rise in serum creatinine level is related to both poor blood glucose control and hypertension
This test may be appropriate for a quick screening but should not be used for monitoring diabetes management.
Urine glucose testing is an indirect measurement of blood glucose and is much less precise than blood glucose testing. Fluid intake, urine elimination patterns, and certain drugs affect the results.
The long-term value is the
HbA1c Normal range 7% or below, correlate to an glucose level >135 mg/dL
The short-term values are the
FPG and the postmeal levels
Norman short-term value ranges
FPG: > 100 mg/dL even with older adults and post-meal >150
The management of diabetes mellitus is complicated and involves considerable
patient involvement and education.
Nonsurgical management of diabetes mellitus involves
nutritional interventions, blood glucose monitoring, a planned exercise program, and in some instances, drugs to lower blood glucose levels.
Who plans, coordinates, and delivers care to the diabetic
The nurse, together with the patient, physician, nutritionist, pharmacist, case manager, and in some cases, physical therapist
Sulfonylurea agents are classified as
insulin secretagogues and are used for patients with some remaining pancreatic beta-cell function.
The action of sulfonylurea agents are
stimulate insulin secretion from pancreatic beta cells and increase the number or sensitivity of cell receptor sites for interaction with insulin. The overall effect of sulfonylurea therapy is lowering of fasting plasma glucose levels.
Side effects of sulfonylurea agents include
weight gain and hypoglycemia. Hypoglycemic episodes are more likely to occur with chlorpropamide (Diabinese, Novo-Propamide) because of its long duration of action.
What type of patients are more susceptible to hypoglycemia
Underweight older patients with cardiovascular, liver, or kidney impairment
Oral Blood Glucose–Lowering Agents SULFONYLUREAS
Acetohexamide (Dymelor), Chlorpropamide (Diabinese), Tolazamide (Tolinase), Tolbutamide (Orinase, Mobenol)
SECOND-GENERATION SULFONYLUREA AGENTS
Glipizide (Glucotrol), Glyburide (DiaBeta/Micronase), Glimepiride (Amaryl)
MEGLITINIDE ANALOGUES
Repaglinide (Prandin), Nateglinide (Starlix),
BIGUANIDES
Metformin (Glucophage)
ALPHA-GLUCOSIDASE INHIBITORS
Acarbose (Precose), Miglitol (Glyset)
THIAZOLIDINEDIONES
Pioglitazone (Actose), Rosiglitazone (Avandia
FIXED COMBINATIONS
are combinations of metformin and other drugs
Post-meal glucose levels (postpradial)
Under 180 mg/dl (6.6 mmol/L) one or two hours after a meal.
Pre-meal glucose leves (prepradial)
70-130 mg/dL
Blood glucose values at bedtime should be between
100 and 140 mg/dL
Signs and symptoms of hypoglycemia
sweating, hunger, weakness, dizziness, tremor, tachycardia, anxiety
Meglitinide analogues are classified as
insulin secretagogues and have actions and adverse effects similar to those of sulfonylureas
Repaglinide (Prandin) and Nateglinide (Starlix)
lower blood glucose by triggering insulin secretion from pancreatic beta cells
These drugs were designed to increase meal-related insulin secretion. They are rapidly absorbed and have a short duration of action
Repaglinide (Prandin) and Nateglinide (Starlix)
____________ is taken before meals, has a rapid onset w/limited duration of action,is used to treat fasting and postprandial hyperglycemia.
Repaglinide (Prandin)
_____________is rapidly absorbed and stimulates insulin secretion within 20 minutes of ingestion. It is taken just before meals to control mealtime hyperglycemia and improves overall glycemic control in patients with type 2 diabetes.
Nateglinide (Starlix)
________________are antihyperglycemic agents and insulin sensitizers.
Biguanides
Metformin (Glucophage) is the major drug in this class.
Biguanides
Metformin’s action
It does not increase insulin secretion. It decreases liver glucose production, →↓FPG release, and improves insulin receptor sensitivity.
The ADA recommends metformin as
initial therapy for DMII b/c drug does not induce weight gain/hypoglycemia, low cost,few adverse effects.
The most common side effects of metformin are
abdominal discomfort and diarrhea.
Metformin should not be used in conditions that decrease drug clearance, such as
renal insufficiency, liver disease, alcoholism, or severe congestive heart failure or in patients older than 80 years.
Patient teaching for metformin
to report symptoms of fatigue, unusual muscle pain, difficulty breathing, unusual or unexpected stomach discomfort, dizziness, lightheadedness, or irregular heartbeats to the primary care provider.
Alpha-glucosidase inhibitors are agents that
prevent hyperglycemia by delaying absorption of carbohydrate from the small intestine. These drugs inhibit enzymes in the intestinal tract, reducing the rate of digestion of starches and the absorption of glucose.
Acarbose does what
delays rather than prevents glucose absorption and does not cause weight loss.
The most common side effects of Acarbos and Miglitol are
flatulence, diarrhea, and abdominal discomfort. These drugs do not cause hypoglycemia unless given with sulfonylureas or insulin.
Patient teaching for acarbose and miglitol
use oral glucose tablets, glucose gel, or low-fat milk to treat hypoglycemia. Severe hypoglycemia may require glucose infusion or glucagon injection.
_____________________ improve insulin sensitivity/reduce liver glucose production. ↑insulin action in muscle, fat, and liver tissue by stimulating an enzyme receptor that regulates glucose and lipid metabolism (peroxisome proliferator activated receptor
Thiazolidinediones (TZDs)
antihyperglycemic agents and insulin sensitizers
Although______________ is available, its use has been associated with an increased risk for heart-related deaths, bone fractures, and macular edema.
rosiglitazone
All Thiazolidinedions (TZDs) reduce blood lipid levels. Major side effects of TZD treatment are
an increase in adipose tissue and fluid retention, infection, headache, peripheral edema, and pain
Teach patients taking TZDs drugs
have periodic liver function studies because of the potential for liver damage.
Combining drugs with different mechanisms of action may be
highly effective in maintaining desired blood glucose control. Some patients may need a combination of oral agents and insulin to control blood glucose levels.
Drugs are started
at the lowest effective dose and increased every 1 to 2 weeks until the patient reaches desired blood glucose control or the maximum dosage
Insulin therapy is indicated when
blood glucose cannot be controlled after the use of two or three different oral agents.
Antidiabetic drugs are not a substitute for dietary modification and exercise. Teach the patient
about the need for continuing dietary restrictions and regular exercise.
To avoid adverse drug interactions, teach the patient to
consult with the primary care provider or pharmacist before using any over-the-counter drugs.
The choice of oral antidiabetic drug is based on
cost, the patient's ability to manage multiple drug doses, age, and response to the drugs.
Shorter-acting agents (e.g., glipizide) are preferable in
older patients, those with irregular eating schedules, or those with liver, kidney, or cardiac dysfunction
Longer-acting agents (e.g., glyburide, glimepiride) with once-a-day dosing are better for
adherence. Beta-cell function in type 2 diabetes often declines over time, reducing the effectiveness of some oral agents. The treatment regimen for the patient with type 2 diabetes may eventually require insulin therapy either alone or with oral agents.
Insulin therapy is needed for
type 1 diabetes and also may be used for type 2 diabetes.
The safety of insulin therapy in older patients may be affected by
reduced vision, mobility and coordination problems, and decreased memory.
Insulin is manufactured using DNA technology to synthesize
pure human insulin.
Insulin analogues are
genetically engineered human insulins in which the structure of the insulin molecule is altered to change the rate of absorption and duration of action within the body
Lispro insulin,
a rapid-acting insulin analogue that is created by switching the positions of lysine and proline in one area of the insulin molecule
Patient teaching for insulin
insulin types, injection tecs/sites. Patient response can all affect the absorption, onset, degree, and duration of insulin activity. Reinforce that changing insulins may affect blood glucose control and should be done only under supervision of the HCP
A usual insulin starting dose is
between 0.5 and 1 unit/kg of body weight per day.
What factors influence insulin absorption & availability
injection site; timing, type, or dose of insulin used; and physical activity.
Absorption is fastest in the
abdomen, followed by the deltoid, thigh, and buttocks
What is the preferred site for insulin injections
the abdomen, because it provides the most rapid insulin absorption.
Absorption rate is determined by
insulin properties. The longer the duration of action, the more unpredictable is absorption. Larger doses of insulin also prolong the absorption.
What increases insulin absorption
Factors that ↑blood flow from the injection site, such as local application of heat, massage of the area, and exercise of the injected area
Injection depth
changes insulin absorption
Timing of injection affects
blood glucose levels
The interval between premeal injections and eating, known as “lag time,” affects
blood glucose levels after meals.
Insulin lispro, insulin aspart, and insulin glulisine have rapid onsets of action and should
be given within 10 minutes before mealtime when blood glucose is in the target range.
Regular insulin should be given at least
20 to 30 minutes before eating when glucose levels are within the target range.
Mixing insulins can
change the time of peak action.
When rapid-acting (Humalog or NovoLog) or short-acting (regular) insulin is mixed with a longer-acting insulin, draw the
shorter-acting dose into the syringe first
No other insulin should be mixed with insulin glargine or insulin detemir. Mixing
clouds the solution and makes the onset of action and peak effect time less predictable.
Lipoatrophy is
a loss of fat tissue in areas of repeated injection that results from an immune reaction to impurities in insulin. Treatment consists of injection of insulin at the edge of the atrophied area.
Lipohypertrophy is
an increased swelling of fat that occurs at the site of repeated insulin injections. Treatment consists of rotating the injection site among different body areas
Dawn phenomenon
results from a nighttime release of growth hormone that causes blood glucose elevations at about 5 to 6 AM fasting hyperglycemia. Give more insulin in night time
Somogyi phenomenon is
morning hyperglycemia from the counterregulatory response to nighttime hypoglycemia. Teach adequate dietary intake at bedtime and evaluating the insulin dose and exercise programs to prevent conditions that lead to hypoglycemia
Three blood glucose phenomena in diabetic patients.
lack of insulin, dawn phenom, somogyi phenom
This method is more effective in controlling blood glucose levels than a multiple-injection schedule
Continuous subcutaneous infusion (CSII)
Teaching for CSII
adjust the #of insulin received based on data from blood glucose monitoring, monitor ketones when BGL’s are over 300mg/dL. Monitor the pump for problems, clogs/kinks. Do not abruptly d/c (hyperglycemia results). provide supplemental insulin schedule.
___________insulin analogues are used with insulin infusion pumps
Rapid-acting
Problems with CSII include
skin infections that can occur when the infusion site is not cleaned or the needle is not changed every 2 to 3 days.
CSII may lead to more frequent and more severe ketoacidosis than other methods of insulin delivery because of
inexperience in pump use, infection, accidental cessation or obstruction of the infusion, or mechanical pump problems.
Patient education for diabetic drugs
store according to manufacture’s instructions, always have a spare bottle of each type of insulin used. inspect the insulin before each use for changes, always buy the same type of syringe, don’t reuse needles. Assess pt ability to administer
Amylin analogues are drugs similar to
amylin, a naturally occurring hormone produced by beta cells in the pancreas, that works with and is co-secreted with insulin in response to blood glucose elevation.
Pramlintide (Symlin), an analogue of amylin, is approved for patients with
either type 1 or type 2 diabetes treated with insulin. It is indicated as adjunct therapy for patients who use mealtime insulin delivery and have not achieved desirable glucose control despite optimum insulin therapy
Pramlintide works by three mechanisms:
delaying gastric emptying, reducing after-meal blood glucose levels, and by triggering satiety (in the brain), which leads to decreased caloric intake and weight loss.
Pramlintide alters
gastric uptake
Patient teaching for pramlintide
to take oral drugs in which rapid onset of action is important (e.g., analgesics) either 1 hour before or 2 hours after eating, inject pramlintide into a site different from where insulin is injected
Pramlintide and insulin are
NOT to be mixed in the same syringe because the pH of the two drugs is not compatible.
Common side effects of pramlintide
Nausea, vomiting, and anorexia. It should not be used for patients with symptomatic gastroparesis
Incretin agents are natural
“gut” hormones that, in addition to insulin, also lower plasma glucose levels
GLP-1 (incretin agent) has many effects on the stomach, liver, pancreas, and brain to work together to regulate blood glucose. It lowers
glucagon secretion from the pancreas, leading to reduced liver glucose production. It also delays gastric emptying, slows the rate of nutrient absorption into the blood, and reduces food intake, all of which lower blood glucose levels
Exenatide (Byetta) is a
long-acting analogue of GLP-1. It mimics the actions of GLP-1, stimulating insulin secretion only when blood glucose is high
The main side effect of exenatide
is nausea. It stimulates insulin secretion and may cause hypoglycemia when given with sulfonylurea drugs (which also stimulate insulin secretion) but not with metformin alone.)
Teach patients not to administer exenatide
after a meal and to keep the pen injectors refrigerated.
DPP-IV inhibitors work by
slowing the inactivation of incretin hormones
Sitagliptin (Januvia) increases
the body's active incretin hormone levels, reducing both before- and after-meal blood glucose levels. It works only when blood glucose is elevated.
Januvia is approved as single agent for patients with
type 2 diabetes unable to manage diabetes with diet and exercise alone and as add-on therapy for those patients with inadequate blood glucose control taking metformin or thiazolidinediones
Side effects of Januvia include
stuffy or runny nose, sore throat, upper respiratory infection, and GI effects of abdominal pain, nausea, and diarrhea. Monitor for symptoms of renal insufficiency.
Adverse effects include hypoglycemia, GI disturbances, upper respiratory tract infection, arthralgia or back pain, and headache
Repaglinide (Prandin)
The major adverse effect is hypoglycemia. Patients who skip meals should also skip their scheduled dose of Starlix to reduce the risk for hypoglycemia
Nateglinide (Starlix)
ADA recommends that metformin should not
be given to anyone with kidney disease and elevated blood creatinine levels. The drug should be withheld for 48 hours before and after using contrast material and surgical procedures requiring anesthesia.
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