DIABETES MELLITUS, IT

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DIABETES MELLITUS, ITS MANAGEMENTANDINSUL
IN,ITS MANAGEMENT

• BY
•  
• ELAINE P. JAVIER

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DIABETES a condition in which theres too
many excretion of urine and can be caused by a
lack of hormone called antidiuretic or ADH that
limits the amount of urine made as in Diabetes
Insipidus or it can also result from a higher
blood sugar level as in Diabetes Mellitus.
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DIFFERENT KINDS OF DIABETES

• 1) Diabetes Insipidus decrease of anti-diuretic
  hormone
• 2) Syndrome of Inappropriate Anti-diuretic
  Hormone. Secretion ( SIADH ) increase of
  anti-diuretic hormone resulting in water
  intoxication.
• 3) Diabetes Mellitus chronic disorder of
  carbohydrates, protein and fat metabolism
  characterized by an imbalance between the
  insulin supply and demand.

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Diabetes mellitus , often referred to simply as
diabetes , pass through urine, is a syndrome of
disordered metabolism, usually due to a
combination of hereditary and environmental
causes, resulting in abnormally high blood sugar
levels (hyperglycemia). Blood glucose levels are
controlled by the hormone insulin made in the
beta cells of the pancreas.Diabetes and its
treatments can cause many complications and may
occur if the disease is not adequately
controlled.
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DIFFERENT TYPES OF DIABETES MELLITUS a) D M
Type 1 Insulin Dependent Diabetes Mellitus
(IDDM ) b) D M Type 11 Non-Insulin
Dependent Diabetes (NIDD )c) D M Type 111
Gestational Diabetes
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Diabetes Mellitus Type 1

• Diabetes mellitus type 1 Type 1 diabetes (
  formerly known as "childhood", "juvenile" or
  "insulin-dependent" diabetes) or juvenile
  diabetes) is a form of diabetes mellitus. Type 1
  diabetes is an autoimmune disease that results
  in destruction of insulin-producing beta cells of
  the pancreas. Glycosuria or glucose in the urine
  causes the patients to urinate more frequently,
  and drink more than normal (polydipsia). Type 1
  has been lethal unless treatment with exogenous
  insulin, usually via injections which replaces
  the missing hormone formerly produced by the now
  non-functional beta cells in the pancreas.

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Pathophysiology of D. M. Type 1
Virally triggered Autoimmune Response

• Immune Systems attack on virus
• Infected cells

Directed against the beta cells in the pancreas
Infection of a virus Ex. Coxsackie virus, German
measles
Pancreatic Beta Cells in the Islets of Langerhans
are destroyed or damaged sufficiently thus
abolish endogenous Insulin production.
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• Signs and Symptoms
• Kussmaul breathing ( outstanding sign )
• Polydipsia too much thirst
• Polyphagia too much eating
• Polyuria too much urination
• Hypoglycemia or Hypergycemia
• Weakness and warm skin
• Emotionally lability
• Abdominal discomfort
• Ketoacidosis
• Muscle cramps
• Irritability
• Nausea
• Glycosuria
• Weight loss
• Anxiety attacks
• Loss of Na and K
• Ketonuria

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• Diagnosis
•  
• 1) C-peptide Assay The most definite
  laboratory test to distinguish Type 1 from Type 2
  diabetes , which is a measure of endogenous
  insulin production since external insulin has
  included C-peptide.
•  
• 2) Glutamic Acid Decarboxylase 65 Antibodies
  has been proposed as an improved test for
  differentiating between Type 1 and Type 2
  diabetes as it appears that the immune system
  malfunction is connected with their
  presence.
•  
• 3) Glucose Tolerance Test a test of the
  bodys ability to process carbohydrate by giving
  a dose of glucose and then measuring the blood
  and urine for glucose. ( blood drawn then drink
  concentrated glucose solution then blood drawn
  again ).
• ORAL BASELINE FASTING 70 TO 110
• 30 minutes fasting 110 to 170 mg/dL
• 60 minutes fasting ( 1 hr ) 120 to 170 mg/dL
• 90 minutes fasting 100 to 140 mg/dL
• 120 minutes fasting (2 hrs) 70 to 120 mg/dL
•  
• 4) Hemoglobin A1C glycocylate hemoglobin
  value is the most accurate diagnostic tool in
  determining the current glucose within 60 to 100
  days. It asses blood glucose control prior to the
  current status.
• a. 5 to 8 -- mild, good
  control
• b. 9 -- fair control
• c. Above 10 -- poor control
  

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• Laboratories
• Blood glucose normal is 70 to 110 mg/dL
• Electrolytes
• Venous pH
• Urine analysis for glucose and ketones
• Hemoglobin A1C level
• C-peptide insuin level
• Islet-cell antibodies
• T4 and thyroid antibodies

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Acute complications

• 1) Diabetic ketoacidosis
• Diabetic ketoacidosis (DKA) is an acute and
  dangerous complication that is always a medical
  emergency. no insulin levels cause the liver to
  turn to fat for fuel On presentation at hospital,
  the patient in DKA is typically dehydrated, and
  breathing rapidly and deeply. Abdominal pain is
  common and may be severe. The level of
  consciousness is typically normal until late in
  the process, when lethargy may progress to coma.
  Ketoacidosis can easily become severe enough to
  cause hypotension, shock, and death. Ketoacidosis
  is much more common in type 1 diabetes than
  type 2. Hyperglycemia,
• Signs and Symptoms of DKA
• Dull headache warning sign
• Dehydration 1st sign of DKA
• Ketonemia/ketonuria
• Kussmaul breathing
• Polydipsia , Polyuria
• Fatigue
• Dry lips
• Nausea
• Sunken eyes , blurred vision
• Pain below the breastbone
• Temperature rises and falls
• Acetone or fruity breath odor
• Metabolic Acidosis

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• 2) Hypoglycemia
• Hypoglycemia, or abnormally low blood glucose,
  is an acute complication of several diabetes
  treatments. It is rare otherwise, either in
  diabetic or non-diabetic patients. The patient
  may become agitated, sweaty, and have many
  symptoms of sympathetic activation of the
  autonomic nervous system resulting in feelings
  akin to dread and immobilized panic. In most
  cases, hypoglycemia is treated with sugary drinks
  or food. In severe cases, an injection of
  glucagon (a hormone with the opposite effects of
  insulin) or an intravenous infusion of dextrose
  D50/50 via fast drip (microset) is used for
  treatment, but usually only if the person is
  unconscious.
• 3) Diabetic coma deep unconsciousness leading
  to death

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• Treatment
• Type 1 is treated with insulin replacement
  therapy usually by injection or insulin pump,
  along with attention to dietary management,
  typically including carbohydrate tracking, and
  careful monitoring of blood glucose levels using
  Glucose meters.
• Untreated Type 1 diabetes can lead to one form
  of diabetic coma, diabetic ketoacidosis, which
  can be fatal. At present, insulin treatment must
  be continued for life this may change when
  better treatment, or a cure, becomes clinically
  available. Continuous glucose monitors have been
  developed which can alert patients to the
  presence of danger.
•  
• Insulin
• Pancreas Transplantation through surgery
• Islet Cell Transplantation

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Gene therapy approach
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• "Immunization" Approach
•   A substance designed to cause lymphocyte cells
  to cease attacking beta cells, DiaPep277 is a
  peptide fragment of a larger protein called
  HSP60. Given as a subcutaneous injection
• Intra-nasal insulin
• There is pre-clinical evidence that a Th1-Th2
  shift can be induced by administration of insulin
  directly onto the immune tissue in the nasal
  cavity.
• Diamyd
• Diamyd is the name of a vaccine being developed
  by Diamyd Medical. Injections with GAD65, an
  autoantigen involved in type 1 diabetes.

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Diabetes Mellitus Type 2

• Type 2 diabetes mellitus is characterized
  differently due to insulin resistance or reduced
  insulin sensitivity, combined with reduced
  insulin secretion. The defective responsiveness
  of body tissues to insulin almost certainly
  involves the insulin receptor in cell membranes.
  At this stage hyperglycemia can be reversed by a
  variety of measures and medications that improve
  insulin sensitivity or reduce glucose production
  by the liver. As the disease progresses the
  impairment of insulin secretion worsens, and
  therapeutic replacement of insulin often becomes
  necessary and is usually seen in adult.

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• Signs and Symptoms
• Poydipsia
• Polyphagia
• Polyuria
• Hyperglycemia
• Hyperosmolar
• Glycosuria
• Chronic fatigue
• Weakness
• Paresthesia
• Skin infection

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• Laboratories
•  
• Fasting Blood Sugar normal is 70 to 110 mg/100
  mL or 3.8 to 6.1 mmol/L
• Oral Glucose Tolerance Test
• Random Plasma Glucose normal gt 200 mg/d/L
• Fasting Plasma Glucose normal gt 126 mg/dL,
  then will be given oral glucose with 75 g glucose
  load , after 2 hours, blood sugar will go up. On
  the 3rd hour, it will go to back to normal.
•  
• Hemoglobin A1C glycocylate hemoglobin value,
  usually a measurement of blood glucose for the
  past 3 months.
• a. 5 to 8 -- mild, good
  control
• b. 9 -- fair control
• c. Above 10 -- poor
  control

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• Chronic complications
•  
• 1) Nonketotic hyperosmolar coma
• Hyperosmolar nonketotic state (HNS) or
  Hyperosmolar Hyperglycenia State ( HHS) is an
  acute complication sharing many symptoms with
  DKA, but an entirely different origin and
  different treatment. A person with very high 600
  and above mmol/dl blood glucose levels, water is
  osmotically drawn out of cells into the blood and
  the kidneys eventually begin to dump glucose into
  the urine. This results in loss of water and an
  increase in blood osmolarity. If fluid is not
  replaced (by mouth or intravenously), the osmotic
  effect of high glucose levels, combined with the
  loss of water, will eventually lead to
  dehydration. The body's cells become
  progressively dehydrated as water is taken from
  them and excreted. Electrolyte imbalances are
  also common and are always dangerous. As with
  DKA, urgent medical treatment is necessary,
  commonly beginning with fluid volume replacement.
  Lethargy may ultimately progress to a coma,
  though this is more common in type 2 diabetes
  than type 1.

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• 2) Vascular disease
• Chronic elevation of blood glucose level leads
  to damage of blood vessels (angiopathy). The
  endothelial cells lining the blood vessels take
  in more glucose than normal. They then form more
  surface glycoproteins than normal, and cause the
  basement membrane to grow thicker and weaker. In
  diabetes, the resulting problems are grouped
  under "microvascular disease" (due to damage to
  small blood vessels) and "macrovascular disease"
  (due to damage to the arteries).

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• Image of fundus showing scatter laser surgery for
  diabetic retinopathy
•  

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The damage to small blood vessels leads to a
microangiopathy, which can cause one or more of
the following

• Diabetic retinopathy, growth of friable and
  poor-quality new blood vessels in the retina as
  well as macular edema (swelling of the macula),
  which can lead to severe vision loss or
  blindness.
• Diabetic neuropathy, abnormal and decreased
  sensation, usually in a 'glove and stocking'
  distribution starting with the feet but
  potentially in other nerves, later often fingers
  and hands. When combined with damaged blood
  vessels this can lead to diabetic foot (see
  below). Diabetic amyotrophy is muscle weakness
  due to neuropathy.
• Diabetic nephropathy, damage to the kidney which
  can lead to chronic renal failure, eventually
  requiring dialysis.
• Diabetic cardiomyopathy, damage to the heart,
  leading to diastolic dysfunction and eventually
  heart failure.

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• 2) Macrovascular disease leads to cardiovascular
  disease, to which accelerated atherosclerosis is
  a contributor
• Coronary artery disease, leading to angina or
  myocardial infarction ("heart attack")
• Stroke (mainly the ischemic type)
• Peripheral vascular disease, which contributes to
  intermittent claudication (exertion-related leg
  and foot pain) as well as diabetic foot.
• Diabetic myonecrosis ('muscle wasting') Diabetic
  foot, often due to a combination of sensory
  neuropathy (numbness or insensitivity) and
  vascular damage, increase rates of skin ulcers
  and infection and, in serious cases, necrosis and
  gangrene.
• Carotid artery stenosis does not occur more often
  in diabetes, and there appears to be a lower
  prevalence of abdominal aortic aneurysm.
• Diabetic encephalopathy is the increased
  cognitive decline and risk of dementia observed
  in diabetes. Various mechanisms are proposed,
  including alterations to the vascular supply of
  the brain and the interaction of insulin with the
  brain itself.

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• HYPERGLYCEMIA 3 Ps
• Polyuria too much urination
• Polydyspsia too much thirst
• Polyphagia too much eating

• HYPOGLYCEMIA
• Cold and Clamy to touch
• Early sign is tremulousness
• Confusion
• Headache
• Extreme fatigue
• Shakiness, Sweating
• Tremor , Tachycardia,
• Tingling sensation around the mouth
• Diaphoresis
• Restlessness
• Irritability
• Pallor
• Seizure

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S/S Plasma Glucose Serum Na Potassium Bicabonate
Ketones Fruity/Aceton breath odor pH Serum
Osmolality Menthol states Dehydration Prognosis
HHS Above 600 mg/dl High/Normal H/normal High Abs
ent Absent Norma Above 320 mOsm/kg Mental
Status Changed SEVERE 15 mortality
DKA 300 to 600 mg/dl Low/normal H/L or
normal Low Present Present Low Below 320
mOsm/kg Mental Status Changed Mild to moderate lt
10 mortality
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Management of Diabetes Mellitus

• Diet 50 to 60 of carbohydrates , 20 to 30
  Fats, 10 to 20 of cholesterol
• Insulin
• Antidiuretic Agents
• Blood sugar monitoring
• Exercise
• Transplant of pancreas or insulin
• Ensure adequate food intake
• Scrupulous foot care

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GESTATIONAL DIABETES

• Gestational Diabetes Mellitus (GDM) resembles
  type 2 diabetes in several respects, involving a
  combination of relatively inadequate insulin
  secretion and responsiveness. It occurs in about
  25 of all pregnancies and may improve or
  disappear after delivery. Gestational diabetes is
  fully treatable but requires careful medical
  supervision throughout the pregnancy. About
  2050 of affected women develop type  2
  diabetes later in life.
• Risks to the baby include macrosomia (high birth
  weight), congenital cardiac and central nervous
  system anomalies, and skeletal muscle
  malformations. Increased fetal insulin may
  inhibit fetal surfactant production and cause
  respiratory distress syndrome. Hyperbilirubinemia
  may result from red blood cell destruction. In
  severe cases, perinatal death may occur, most
  commonly as a result of poor placental profusion
  due to vascular impairment. Induction may be
  indicated with decreased placental function. A
  cesarean section may be performed.

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• Signs and Symptoms
• Polydipsia
• Polyphagia
• Polyuria
• Weight loss
• Fatigue
• Nuasea and vomiting common symptoms

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• Laboratory Data Elevated FBS usually on the 2nd
  3rd trimster , GTT
• Treatment and Management
• High protein diet
• Exercise is squatting
• Monitor blood glucose leves
• Allow calcium 300 mg/day
• Ist Trimester has decrease need of insulin
• 2nd Trimester has increase demand of insulin
• Use only Regular and NPH A.M. dose is 21 /
  P.M. dose is 11.
• Signs Symptoms of Hypoglycemic New Born
• Jittery , Tremors
• Irritability , Irregular respiration
• Letargic
• Shaky

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I N S U L I N
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• WHAT IS INSULIN ?
• Insulin is a hormone. And like many hormones,
  insulin is a protein.   Insulin is secreted by
  groups of cells within the pancreas called islet
  cells. The pancreas is an organ that sits behind
  the stomach and has many functions in addition to
  insulin production. Carbohydrates (or sugars) are
  absorbed from the intestines into the bloodstream
  after a meal. Insulin is then secreted by the
  pancreas in response to this detected increase in
  blood sugar.

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• Where Does Commercial Insulin Come From?
• The first successful insulin preparations came
  from cows (and later pigs). The bovine (cow) and
  porcine (pig) insulin worked very well for the
  vast majority of patients, but some could develop
  an allergy or other types of reactions to the
  foreign protein.  In the 1980's technology had
  advanced to the point where we could make human
  insulin.  The advantage would be that human
  insulin would have a much lower chance of
  inducing a reaction because it is not a foreign
  protein.

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Normal Regulation of Blood Glucose
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• Many Type 1 treatments include combination use
  of regular or NPH insulin, and/or synthetic
  insulin analogs (eg, Humalog, Novolog or Apidra)
  in combinations such as Lantus/Levemir and
  Humalog, Novolog or Apidra. Another treatment
  option is the use of the insulin pump (eg, from
  Deltec Cozmo, Animas, Medtronic Minimed, Insulet
  Omnipod, or ACCU-CHEK). A blood lancet is used to
  pierce the skin (typically of a finger), in order
  to draw blood to test it for sugar levels.

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• There are several problems with insulin as a
  clinical treatment for diabetes
• Mode of administration.
• Selecting the 'right' dose and timing.
• Selecting an appropriate insulin preparation
  (typically on 'speed of onset and duration of
  action' grounds).
• Adjusting dosage and timing to fit food intake
  timing, amounts, and types.
• Adjusting dosage and timing to fit exercise
  undertaken.
• It is dangerous in case of mistake (most
  especially 'too much' insulin).

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• The commonly used types of insulin are
• Rapid-acting types are presently insulin analogs,
  such as the insulin analogs aspart or lispro.
  these begin to work within 5 to 15 minutes and
  are active for 3 to 4 hours. Most insulins form
  "clumps" which delay entry into the blood in
  active form.
• Short-acting, such as regular insulin starts
  working within 30 minutes and is active about 5
  to 8 hours.
• Intermediate-acting, such as NPH, or semilente
  insulin starts working in 1 to 3 hours and is
  active 16 to 24 hours.
• Long-acting, such as ultralente insulin starts
  working in 4 to 6 hours, and is active well
  beyond 32 hours.
• Insulin glargine and Insulin detemir both
  insulin analogs which start working within 1 to 2
  hours and continue to be active, without major
  peaks or dips, for about 24 hours, although this
  varies in many individuals.
• A mixture of NPH and regular insulin starts
  working in 30 minutes and is active 16 to 24
  hours. There are several variations with
  different proportions of the mixed insulins.
• A mixture of Semilente and Ultralente (typically
  in the proportion 30 Semilente to 70
  Ultralente), known as Lente, is typically active
  for an entire 24 hour period. Beef Lente, in
  particular, has a very 'flat' profile.

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• Modes of administration
• Unlike many medicines, insulin cannot be taken
  orally. Like nearly all other proteins introduced
  into the gastrointestinal tract, it is reduced to
  fragments (even single amino acid components),
• Subcutaneous
• Insulin is usually taken as subcutaneous
  injections by single-use syringes with needles,
  an insulin pump, or by repeated-use insulin pens
  with needles.
• Insulin pump
• Insulin pumps are a reasonable solution.
  Advantages to the patient are better control over
  background or 'basal' insulin dosage, bolus doses
  calculated to fractions of a unit, and
  calculators in the pump that may help with
  determining 'bolus' infusion dosages.
• Inhalation
• In 2006 the U.S. Food and Drug Administration
  approved the use of Exubera, the first inhalable
  insulin

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Injection Site Selection

• The most common injection site is the abdomen (or
  stomach). The back of the upper arms, the upper
  buttocks or hips, and the outer side of the
  thighs are also used. These sites are the best to
  inject into for two reasons
• They have a layer of fat just below the skin to
  absorb the insulin, but not many nerves - which
  means that injecting there will be more
  comfortable than injecting in other parts of your
  body.
• They make it easier to inject into the
  subcutaneous tissue, where insulin injection is
  recommended.

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• Rotating Your Injection Sites
•  
• If you inject insulin three or more times a day
  then its a good idea to rotate your injection
  sites. Injecting in the same place much of the
  time can cause hard lumps or extra fat deposits
  to develop. These lumps are not only unsightly
  they can also change the way insulin is absorbed,
  making it more difficult to keep your blood
  glucose on target.
• Follow these two rules for proper site rotation
• Same general location at the same time each day.
• Rotate within each injection site.
•  
•  

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•  
•  Most insulin enters the blood
• Fastest from the abdomen (stomach)
• A little slower from the arms
• Even slower from the legs
• Slowest from the buttocks

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• COMPLICATIONS OF INSULIN
• SOMOGYI PHENOMENON EFFECTS (Sa Gabi) rebound
  hypoglycemia during the night until morning
  Reduced or adjust insulin and give snack.
• INSULIN WANING (In bed Time until inumaga)
  hyperglycemia from bedtime until morning
  Increase NPH dose in the evening.
• Dawn Phenomenon hyperglycemia at dawn due to
  too early administration of insulin Delay the
  insulin in the evening dose .

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The End...?