Download DIABETES MELLITUS, IT`S MANAGEMENT AND INSULIN, IT`S

BY :
ELAINE P. JAVIER
DIABETES = a condition in which there’s 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.
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.
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.
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
Diabetes Mellitus Type 1
Diabetes mellitus type 1 Type 1 diabetes ( formerly
known as "childhood", "juvenile" or "insulindependent" diabetes) or juvenile diabetes) is a form of
diabetes mellitus. Type 1 diabetes is an autoimmune
disease
that results in destruction of insulinproducing 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.
Pathophysiology of D. M. Type 1:
Virally triggered Autoimmune Response
Immune System’s 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.
Signs and Symptoms:
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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
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 body’s 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
Laboratories :
1. Blood glucose = normal is 70 to 110 mg/dL
2. Electrolytes
3. Venous pH
4. Urine analysis for glucose and ketones
5. Hemoglobin A1C level
6. C-peptide insuin level
7. Islet-cell antibodies
8. T4 and thyroid antibodies
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:
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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
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
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.
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Insulin
Pancreas Transplantation through surgery
Islet Cell Transplantation
Gene therapy approach:
"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.
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.
Signs and Symptoms:
Poydipsia
Polyphagia
Polyuria
Hyperglycemia
Hyperosmolar
Glycosuria
Chronic fatigue
Weakness
Paresthesia
Skin infection
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 > 200 mg/d/L
Fasting Plasma Glucose = normal > 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
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.
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).
Image of fundus showing scatter laser surgery for
diabetic retinopathy
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.
2) Macrovascular disease leads to cardiovascular disease, to
which accelerated atherosclerosis is a contributor:
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Coronary artery disease, leading to angina or myocardial
infarction ("heart attack")
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Stroke (mainly the ischemic type)
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Peripheral vascular disease, which contributes to
intermittent claudication (exertion-related leg and foot
pain) as well as diabetic foot.
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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.
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Carotid artery stenosis does not occur more often in
diabetes, and there appears to be a lower prevalence of
abdominal aortic aneurysm.
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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.
 HYPOGLYCEMIA:
 Cold and Clamy to touch
 Early sign is
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tremulousness
Confusion
Headache
Extreme fatigue
Shakiness, Sweating
Tremor , Tachycardia,
Tingling sensation around
the mouth
Diaphoresis
Restlessness
Irritability
Pallor
Seizure
HYPERGLYCEMIA: 3 P’s
•Polyuria = too much
urination
•Polydyspsia = too much thirst
•Polyphagia = too much eating
S/S
DKA
HHS
Plasma Glucose
Serum Na
Potassium
Bicabonate
Ketones
Fruity/Aceton breath
odor
pH
Serum Osmolality
Menthol states
Dehydration
Prognosis
300 to 600 mg/dl
Low/normal
H/L or normal
Low
Present
Present
Above 600 mg/dl
High/Normal
H/normal
High
Absent
Absent
Low
Below 320 mOsm/kg
Mental Status Changed
Mild to moderate
< 10% mortality
Norma;
Above 320 mOsm/kg
Mental Status Changed
SEVERE
15% mortality
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
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 2%–5% of all pregnancies and may improve or disappear
after delivery. Gestational diabetes is fully treatable but requires
careful medical supervision throughout the pregnancy. About
20%–50% 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.
Signs and Symptoms:
Polydipsia
Polyphagia
Polyuria
Weight loss
Fatigue
Nuasea and vomiting = common symptoms
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 2:1 / P.M. dose is 1:1.
Signs & Symptoms of Hypoglycemic New Born:
Jittery , Tremors
Irritability , Irregular respiration
Letargic
Shaky
I N S U L I N:
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.
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.
Normal Regulation of Blood Glucose
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.
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).
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.
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
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
Rotating Your Injection Sites
 If you inject insulin three or more times a day then it’s 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.
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
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 .
The End...