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Diabetes
Reasons & definitions of
main complications
Uploaded on Slideshare on
Saturday /24/06/2014: At 10:05PM
Dr. Amit Gangwal
Smriti college of pharmaceutical
education, Indore
Amit Ka PPT
DisclaimerSome of the contents have been as such taken
from reputed website Wikipedia besides other useful
and original websites. All the contents have been
taken from various web sources as mentioned in
reference. I do not claim on these contents. Images
have been taken from internet. These are of original
creator/photographer. I am thankful to these
men/women and websites. This PPT is on
Slideshare and I am not making any money by this
PPT. This is available for public free of cost. I do
not want to make money by these slides.
Polyuria
http://insulin-glucagon-and-diabetes.blogspot.in/2009/10/polyuria-polydipsia-
and-polyphagia.htmla
Excess glucose (solute molecule) in the
filtrate, (by kidney) causes more amount of
water to be flushed out in urine as part of
osmosis.
Diabetic, in turns, discharges more water
and urinates more frequently.
Polydipsia
The polyuria results in decreased blood
volume and dehydration. That is why a
diabetic experiences excessive thirst and
this is called polydipsia.
Polydipsia Continue
Along with water loss, which is a solvent, there is also
electrolyte losses as the body rids itself of excess ketones.
The ketone bodies are negatively charged ions. To maintain
positive and negative ions balance, ketone bodies attract
and carry positive charged ions like sodium (Na+) and
potassium (K+) out of the body fluids as well.
This creates an electrolyte imbalance in diabetic. It leads to
abdominal pains and vomiting, and the stress reaction
("flight, fright and frolic").
Vomiting expels even more water from the body and carries
with it more important electrolytes. This rapid water loss, or
dehydration, stimulates the hypothalamic thirst center
causing polydipsia or frequent desire to consume water.
Diabetic ketoacidosis (DKA)
en.wikipedia.org/wiki/Diabetic_ketoacidosis
Diabetic ketoacidosis arises because of a lack of insulin in the body. The lack of insulin
and corresponding elevation of glucagon leads to increased release of glucose by
the liver (a process that is normally suppressed by insulin) from glycogen via
glycogenolysis and also through gluconeogenesis. High glucose levels spill over into the
urine, taking water and solutes (such as sodium and potassium) along with it in a
process known as osmotic diuresis. This leads to polyuria, dehydration, and
compensatory thirst and polydipsia. The absence of insulin also leads to the release of
free fatty acids from adipose tissue (lipolysis), which are converted, again in the liver,
into ketone bodies (acetoacetate and β-hydroxybutyrate). β-Hydroxybutyrate can serve
as an energy source in the absence of insulin-mediated glucose delivery, and is a
protective mechanism in case of starvation. The ketone bodies, however, have a low pKa
and therefore turn the blood acidic (metabolic acidosis). The body initially buffers the
change with the bicarbonate buffering system, but this system is quickly overwhelmed
and other mechanisms must work to compensate for the acidosis. One such mechanism
is hyperventilation to lower the blood carbon dioxide levels (a form of compensatory
respiratory alkalosis). This hyperventilation, in its extreme form, may be observed as
Kussmaul respiration.
• DKA is common in type 1 diabetes as this form of diabetes is associated with an absolute
lack of insulin production by the islets of Langerhans. In type 2 diabetes, insulin production
is present but is insufficient to meet the body's requirements as a result of end-organ insulin
resistance. Usually, these amounts of insulin are sufficient to suppress ketogenesis. If DKA
occurs in someone with type 2 diabetes, their condition is called "ketosis-prone type 2
diabetes“. The exact mechanism for this phenomenon is unclear, but there is evidence both
of impaired insulin secretion and insulin action. Once the condition has been treated, insulin
production resumes and often the patient may be able to resume diet or tablet treatment as
normally recommended in type 2 diabetes.
• Cerebral edema, which is the most dangerous DKA complication, is probably the result of a
number of factors. Some authorities suggest that it is the result from over vigorous fluid
replacement, but the complication may develop before treatment has been commenced. It
is more likely in those with more severe DKA, and in the first episode of DKA. Likely factors
in the development of cerebral edema are dehydration, acidosis and low carbon dioxide
levels; in addition, the increased level of inflammation and coagulation may, together with
these factors, lead to decreased blood flow to parts of the brain, which then swells up once
fluid replacement has been commenced. The swelling of brain tissue leads to raised
intracranial pressure ultimately leading to death.
• The main aims in the treatment of
diabetic ketoacidosis are replacing the
lost fluids and electrolytes while
suppressing the high blood sugars and
ketone production with insulin.
Admission to an intensive care unit or
similar high-dependency area or ward
for close observation may be necessary.
Polyphagia
In diabetics there is glucose in blood but if
the general body cells cannot take up
glucose for metabolism to take place, he
develop excessive hunger pangs and he
likes to eat more. This is
called Polyphagia. Despite of ample
glusoce in his body, it cannot be used,
and the body begins to use the fat and
protein stores for metabolism.
Retinopathy as such taken from
wikipedia (not a single word is mine)
• Diabetic retinopathy often has no early warning signs. Even
macular edema, which may cause vision loss more rapidly, may not
have any warning signs for some time. In general, however, a
person with macular edema is likely to have blurred vision, making it
hard to do things like read or drive. In some cases, the vision will get
better or worse during the day.
• In the first stage which is called non-proliferative diabetic retinopathy
(NPDR) there are no symptoms, it is not visible to the naked eye
and patients will have 20/20 vision. The only way to detect NPDR is
by fundus photography, in which microaneurysms (microscopic
blood-filled bulges in the artery walls) can be seen. If there is
reduced vision, fluorescein angiography can be done to see the
back of the eye. Narrowing or blocked retinal blood vessels can be
seen clearly and this is called retinal ischemia (lack of blood flow).
• Diabetic retinopathy is the result of microvascular retinal changes.
Hyperglycemia-induced intramural pericyte death and thickening of the
basement membrane lead to incompetence of the vascular walls. These
damages change the formation of theblood-retinal barrier and also make the
retinal blood vessels become more permeable.[8]
• mall blood vessels – such as those in the eye – are especially vulnerable to
poor blood sugar (blood glucose) control. An overaccumulation
of glucose and/or fructose damages the tiny blood vessels in the retina.
During the initial stage, called nonproliferative diabetic retinopathy (NPDR),
most people do not notice any change in their vision. Early changes that are
reversible and do not threaten central vision are sometimes termed simplex
retinopathy or background retinopathy.[10]
• Some people develop a condition called macular edema. It occurs when the
damaged blood vessels leak fluid and lipids onto the macula, the part of the
retina that lets us see detail. The fluid makes the macula swell, which blurs
vision.
http://media-cache-
ec0.pinimg.com/originals/5a/6b/44/5a6b4
447acc9699f5fbc903694869060.jpg.
http://scrubs-and-
pearls.tumblr.com/post/41960410108/dia
betes-mellitus-type-1
Nephropathy
• Nephropathy means kidney ailments or damage to
kidney. Diabetic nephropathy is damage to diabetic’s
kidneys as kidneys have to do more work and have
to pass jumbo molecules of sugar.
• In severe cases it can lead to kidney failure. But not
everyone with diabetes has kidney damage.
• The kidneys have many tiny blood vessels that filter
waste from our blood. High blood sugar in diabetics
can destroy these blood vessels. Over time, the
kidney is not able to do its job in a routine manner.
Depending on sugar level and work load on kidney,
kidney may stop working completely. This is called
kidney failure.
Neuropathy
http://diabetes.niddk.nih.gov/DM/pubs/neuropathies/
• Diabetic neuropathies are a family of nerve disorders
caused by diabetes. People with diabetes can, over time,
develop nerve damage throughout the body. Some people
with nerve damage have no symptoms. Others may have
symptoms such as pain, tingling, or numbness—loss of
feeling—in the hands, arms, feet, and legs. Nerve problems
can occur in every organ system, including the digestive
tract, heart, and sex organs.
• Treatment: Bring blood glucose levels within the normal
range.
People with neuropathy need to inspect their feet daily
for any injuries.
Untreated injuries increase the risk of infected foot
sores and amputation.
Diabetes

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Diabetes

  • 1. Diabetes Reasons & definitions of main complications Uploaded on Slideshare on Saturday /24/06/2014: At 10:05PM Dr. Amit Gangwal Smriti college of pharmaceutical education, Indore Amit Ka PPT
  • 2.
  • 3. DisclaimerSome of the contents have been as such taken from reputed website Wikipedia besides other useful and original websites. All the contents have been taken from various web sources as mentioned in reference. I do not claim on these contents. Images have been taken from internet. These are of original creator/photographer. I am thankful to these men/women and websites. This PPT is on Slideshare and I am not making any money by this PPT. This is available for public free of cost. I do not want to make money by these slides.
  • 4. Polyuria http://insulin-glucagon-and-diabetes.blogspot.in/2009/10/polyuria-polydipsia- and-polyphagia.htmla Excess glucose (solute molecule) in the filtrate, (by kidney) causes more amount of water to be flushed out in urine as part of osmosis. Diabetic, in turns, discharges more water and urinates more frequently.
  • 5. Polydipsia The polyuria results in decreased blood volume and dehydration. That is why a diabetic experiences excessive thirst and this is called polydipsia.
  • 6. Polydipsia Continue Along with water loss, which is a solvent, there is also electrolyte losses as the body rids itself of excess ketones. The ketone bodies are negatively charged ions. To maintain positive and negative ions balance, ketone bodies attract and carry positive charged ions like sodium (Na+) and potassium (K+) out of the body fluids as well. This creates an electrolyte imbalance in diabetic. It leads to abdominal pains and vomiting, and the stress reaction ("flight, fright and frolic"). Vomiting expels even more water from the body and carries with it more important electrolytes. This rapid water loss, or dehydration, stimulates the hypothalamic thirst center causing polydipsia or frequent desire to consume water.
  • 7. Diabetic ketoacidosis (DKA) en.wikipedia.org/wiki/Diabetic_ketoacidosis Diabetic ketoacidosis arises because of a lack of insulin in the body. The lack of insulin and corresponding elevation of glucagon leads to increased release of glucose by the liver (a process that is normally suppressed by insulin) from glycogen via glycogenolysis and also through gluconeogenesis. High glucose levels spill over into the urine, taking water and solutes (such as sodium and potassium) along with it in a process known as osmotic diuresis. This leads to polyuria, dehydration, and compensatory thirst and polydipsia. The absence of insulin also leads to the release of free fatty acids from adipose tissue (lipolysis), which are converted, again in the liver, into ketone bodies (acetoacetate and β-hydroxybutyrate). β-Hydroxybutyrate can serve as an energy source in the absence of insulin-mediated glucose delivery, and is a protective mechanism in case of starvation. The ketone bodies, however, have a low pKa and therefore turn the blood acidic (metabolic acidosis). The body initially buffers the change with the bicarbonate buffering system, but this system is quickly overwhelmed and other mechanisms must work to compensate for the acidosis. One such mechanism is hyperventilation to lower the blood carbon dioxide levels (a form of compensatory respiratory alkalosis). This hyperventilation, in its extreme form, may be observed as Kussmaul respiration.
  • 8. • DKA is common in type 1 diabetes as this form of diabetes is associated with an absolute lack of insulin production by the islets of Langerhans. In type 2 diabetes, insulin production is present but is insufficient to meet the body's requirements as a result of end-organ insulin resistance. Usually, these amounts of insulin are sufficient to suppress ketogenesis. If DKA occurs in someone with type 2 diabetes, their condition is called "ketosis-prone type 2 diabetes“. The exact mechanism for this phenomenon is unclear, but there is evidence both of impaired insulin secretion and insulin action. Once the condition has been treated, insulin production resumes and often the patient may be able to resume diet or tablet treatment as normally recommended in type 2 diabetes. • Cerebral edema, which is the most dangerous DKA complication, is probably the result of a number of factors. Some authorities suggest that it is the result from over vigorous fluid replacement, but the complication may develop before treatment has been commenced. It is more likely in those with more severe DKA, and in the first episode of DKA. Likely factors in the development of cerebral edema are dehydration, acidosis and low carbon dioxide levels; in addition, the increased level of inflammation and coagulation may, together with these factors, lead to decreased blood flow to parts of the brain, which then swells up once fluid replacement has been commenced. The swelling of brain tissue leads to raised intracranial pressure ultimately leading to death.
  • 9. • The main aims in the treatment of diabetic ketoacidosis are replacing the lost fluids and electrolytes while suppressing the high blood sugars and ketone production with insulin. Admission to an intensive care unit or similar high-dependency area or ward for close observation may be necessary.
  • 10. Polyphagia In diabetics there is glucose in blood but if the general body cells cannot take up glucose for metabolism to take place, he develop excessive hunger pangs and he likes to eat more. This is called Polyphagia. Despite of ample glusoce in his body, it cannot be used, and the body begins to use the fat and protein stores for metabolism.
  • 11. Retinopathy as such taken from wikipedia (not a single word is mine) • Diabetic retinopathy often has no early warning signs. Even macular edema, which may cause vision loss more rapidly, may not have any warning signs for some time. In general, however, a person with macular edema is likely to have blurred vision, making it hard to do things like read or drive. In some cases, the vision will get better or worse during the day. • In the first stage which is called non-proliferative diabetic retinopathy (NPDR) there are no symptoms, it is not visible to the naked eye and patients will have 20/20 vision. The only way to detect NPDR is by fundus photography, in which microaneurysms (microscopic blood-filled bulges in the artery walls) can be seen. If there is reduced vision, fluorescein angiography can be done to see the back of the eye. Narrowing or blocked retinal blood vessels can be seen clearly and this is called retinal ischemia (lack of blood flow).
  • 12. • Diabetic retinopathy is the result of microvascular retinal changes. Hyperglycemia-induced intramural pericyte death and thickening of the basement membrane lead to incompetence of the vascular walls. These damages change the formation of theblood-retinal barrier and also make the retinal blood vessels become more permeable.[8] • mall blood vessels – such as those in the eye – are especially vulnerable to poor blood sugar (blood glucose) control. An overaccumulation of glucose and/or fructose damages the tiny blood vessels in the retina. During the initial stage, called nonproliferative diabetic retinopathy (NPDR), most people do not notice any change in their vision. Early changes that are reversible and do not threaten central vision are sometimes termed simplex retinopathy or background retinopathy.[10] • Some people develop a condition called macular edema. It occurs when the damaged blood vessels leak fluid and lipids onto the macula, the part of the retina that lets us see detail. The fluid makes the macula swell, which blurs vision.
  • 14. Nephropathy • Nephropathy means kidney ailments or damage to kidney. Diabetic nephropathy is damage to diabetic’s kidneys as kidneys have to do more work and have to pass jumbo molecules of sugar. • In severe cases it can lead to kidney failure. But not everyone with diabetes has kidney damage. • The kidneys have many tiny blood vessels that filter waste from our blood. High blood sugar in diabetics can destroy these blood vessels. Over time, the kidney is not able to do its job in a routine manner. Depending on sugar level and work load on kidney, kidney may stop working completely. This is called kidney failure.
  • 15. Neuropathy http://diabetes.niddk.nih.gov/DM/pubs/neuropathies/ • Diabetic neuropathies are a family of nerve disorders caused by diabetes. People with diabetes can, over time, develop nerve damage throughout the body. Some people with nerve damage have no symptoms. Others may have symptoms such as pain, tingling, or numbness—loss of feeling—in the hands, arms, feet, and legs. Nerve problems can occur in every organ system, including the digestive tract, heart, and sex organs. • Treatment: Bring blood glucose levels within the normal range. People with neuropathy need to inspect their feet daily for any injuries. Untreated injuries increase the risk of infected foot sores and amputation.