2. Type 1 DM
⢠Type 1 diabetes (formerly known as insulin-
dependent) in which the pancreas fails to produce
the insulin which is essential for survival.
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3. Type 2 DM
⢠Type 2 diabetes (formerly named non-insulin-
dependent) which results from the body's inability to
respond properly to the action of insulin produced by
the pancreas.
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4. Hyperglycaemia
⢠Hyperglycaemia, or high blood sugar is a condition in which an
excessive amount of glucose circulates in the blood plasma.
⢠It is caused by a decrease in the production of insulin, a decrease
in the action of insulin, or a combination of the two
abnormalities.
⢠Mild hyperglycemia- no symptoms
⢠Severe hyperglycemia- increase in urine volume and thirst, fatigue
and weakness, and increased susceptibility to infection.
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5. Hyperglycaemia
⢠The hyperglycemia of diabetes mellitus causes an osmotic diuresis, leading
to large deficits of water, sodium and potassium during acute loss of
control, e.g., diabetic ketoacidosis.
⢠An osmotic diuresis may also result from excessive urea production owing to
excessive protein administration.
⢠Osmotic diuresis occurs when substances in the blood accumulate in the tubules of the
kidney, reducing reabsorption of water in the kidneys, thereby increasing urine output.
Osmosis refers to the movement of fluids through membranes.
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6. Hypoglycaemia
⢠Low blood sugar, the body's main source of energy.
⢠Hypoglycemic symptoms are related to sympathetic activation and
brain dysfunction.
⢠Stimulation of the sympatho adrenal nervous system leads to
sweating, palpitations, tremulousness, anxiety, and hunger.
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7. Glycogenolysis and Gluconeogenesis
⢠Glycogenolysis and Gluconeogenesis are two types of processes
occurring in the liver to release glucose into blood.
⢠Glycogenolysis, as name specifies is the breakdown of glycogen to
release glucose molecules.
⢠Gluconeogenesis is the process which results in the formation of
glucose from non-carbohydrate sources.
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8. What is insulin?
⢠Insulin is a hormone made by the pancreas that allows your body to use
sugar (glucose) from carbohydrates in the food that you eat for energy or to
store glucose for future use.
⢠Insulin is needed to move blood sugar into cells throughout the body.
⢠The resulting insulin deficiency leaves too much sugar in the blood and not
enough in the cells for energy.
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9. What is acidosis?
⢠Insulin deficiency causes the body to break down proteins and fat for
energy.
⢠These are organisms known as ketones and are excreted in urine and via
the lungs.
⢠The breath of the patient therefore has a fruity smell.
⢠Ketosis causes nausea & vomiting, which increases dehydration.
⢠An increase of ketones in the extracellular fluid causes transcellular shifts
of potassium ions from out of the cells into the extracellular fluid where
they are excreted by the kidneys in the urine.
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10. What is acidosis?
⢠KETOACIDOSIS:
⢠The production of ketones
which is normal in the individual
free of diabetes.
⢠The bodyâs normal adaptation to
starvation.
⢠Production is regulated.
⢠when the body produces
excessive quantities of acid or
when the kidneys are not
removing enough acid from the
body.
⢠DIABETIC KETOACIDOSIS:
⢠Insufficient insulin to help fuel
the bodyâs cells.
⢠Ketosis is the presence of
ketones. It's not harmful. You can
be in ketosis if you're on a low-
carbohydrate diet or fasting. If
you're in ketosis, you have a
higher than usual level of ketones
in your blood or urine, but not
high enough to cause acidosis.
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11. Carbohydrates, Proteins, and Fats
⢠The human body is remarkable at making do with whatever type of food is
available.
⢠From the moment a bite of food enters the mouth, nutrition within starts to
be broken down for use by the body.
⢠So begins the process of metabolism, the series of chemical reactions that
transform food into components that can be used for the body's basic
processes.
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12. Carbohydrates, Proteins, and Fats
⢠Proteins, carbohydrates, and fats move along sets of metabolic
pathways.
⢠Fundamentallyâif all three nutrients are abundant in the dietâ
carbohydrates and fats will be used primarily for energy while
proteins provide the raw materials for making hormones, muscle,
and other essential biological equipment.
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13. Carbohydrates
⢠Carbohydrates, on the other hand, can only be stored in limited quantities,
so the body is eager to use them for energy.
⢠The carbohydrates in food are digested into small pieces- glucose.
⢠Glucose enters the circulatory system, causing blood glucose levels to rise.
⢠Once the cells have had their fill of glucose, the liver stores some of the
excess for distribution between meals should blood glucose levels fall below
a certain threshold.
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14. Carbohydrates
⢠If there is leftover glucose beyond what the liver can hold, it can be turned
into fat for long-term storage so none is wasted.
⢠When carbohydrates are scarce, the body runs mainly on fats. If energy
needs exceed those provided by fats in the diet, the body must liquidate
some of its fat tissue for energy.
⢠These cells could easily run on glucose from the diet, but they can't run on
fatty acids directly.
⢠So under low-carbohydrate conditions, these cells need the body to make
fat-like molecules called ketone bodies.
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15. Carbohydrates
⢠This is why a very-low-carbohydrate diet is sometimes called
"ketogenic."
⢠Ketone bodies could alone provide enough energy for the parts of the
body that can't metabolize fatty acids, but some tissues still require
at least some glucose, which isn't normally made from fat.
⢠Instead, glucose can be made in the liver and kidneys using protein
from elsewhere in the body.
⢠But take care: If not enough protein is provided by the diet, the body
starts chewing on muscle cells.
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16. Fat
⢠Fats typically provide more than half of the body's energy needs.
⢠Fat from food is broken down into fatty acids, which can travel in
the blood and be captured by hungry cells.
⢠Fatty acids that aren't needed right away are packaged in bundles
called triglycerides and stored in fat cells, which have unlimited
capacity.
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17. Proteins
⢠Proteins in food are broken down into pieces (called amino acids)
that are then used to build new proteins with specific functions.
⢠When there is a shortage of fats or carbohydrates, proteins can
also yield energy.
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18. What Is Diabetic Ketoacidosis (DKA)?
⢠Diabetic ketoacidosis (DKA) results from a state of relative insulin
deficiency, associated with hyperglycaemia and hyperketonaemia (elevated
concentrations of ketone bodies in the blood) & metabolic acidosis (a
condition in which too much acid accumulates in the body).
⢠DKA is associated with significant disturbances of the body's chemistry, which
resolve with proper therapy.
⢠Diabetic ketoacidosis usually occurs in people with type 1 DM but DKA can
develop in any person with diabetes.
⢠Since type 1 diabetes typically starts before age 25 years, DKA is most
common in this age group, but it may occur at any age.
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19. Pathophysiology of DKA
⢠The patient experiencing DKA presents significantly different from one
who is hypoglycaemic.
⢠(Below 4 mmol/L Hgt, Sweating, Fatigue, Feeling dizzy, Being
pale, Feeling weak, Feeling hungry, A higher heart rate than usual,
Blurred vision, Confusion, Convulsions, Loss of consciousness,
Coma & Headache)
⢠This is due to the variation in the pathology of the condition.
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20. Pathophysiology of DKA
⢠Unlike hypoglycemia, where the insulin level is in excess and the
blood glucose level is extremely low, DKA is associated with a relative
or absolute insulin deficiency and a severely elevated blood glucose
level.
⢠Due to the lack of insulin, tissue such as muscle, fat and the liver are
unable to take up glucose.
⢠Even though the blood has an extremely elevated amount of
circulating glucose, the cells are basically starving.
⢠Because the blood brain barrier does not require insulin for glucose to
diffuse across, the brain cells are receiving more than an adequate
amount of glucose. 2018/07/24Compiled by C Settley
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21. Pathophysiology of DKA
⢠Basically, the general body tissue is starving while the brain has more
than an adequate supply of glucose.
⢠Thus, the patient does not experience the sudden onset of signs and
symptoms associated with hypoglycaemia.
⢠There are three major pathophysiologic syndromes associated with an
excessively elevated blood glucose level in DKA:
⢠Metabolic acidosis
⢠Osmotic diuresis
⢠Electrolyte disturbance
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22. Pathophysiology of DKA
⢠Due to the lack of insulin, cells are not receiving an adequate fuel source to
produce energy.
⢠Even though the blood is loaded with glucose, the cells go into a starvation
mode.
⢠This triggers the release of glucagon and other counter-regulatory hormones that
promote the breakdown of triglycerides into free fatty acids and initiate
gluconeogenesis to produce more glucose for the starving cells.
⢠Glucagon is a peptide hormone. It works to raise the concentration of glucose and fatty acids
in the bloodstream.
⢠This further elevates the blood glucose level as the body begins to metabolize
protein and fat to produce a source of energy.
⢠Due to the insulin deficiency and release of large amounts of glucagon, free fatty
acids circulate in abundance in the blood and are metabolized into acetoacetic
acid and B-hydroxybutric acid - both of which are strong organic acids and are
referred to as ketones. 2018/07/24Compiled by C Settley
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23. Pathophysiology of DKA
⢠As acetoacetic acid is metabolized it produces acetone, which begins
to accumulate in the blood.
⢠Small amounts of acetone are released in respiration and produce the
characteristic âfruity breathâ odour.
⢠In normal metabolism, ketones would be used as fuel in the peripheral
tissue; however, due to the starvation state of the cells, the ketones
are not used.
⢠An increase in ketone production and a decrease in peripheral cell use
lead to metabolic acidosis â also called ketoacidosis.
⢠This is reflected in a decreasing pH value typically less than 7.40.
⢠The patient will also begin to eliminate large amounts of ketones
through excretion in the urine.
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24. Pathophysiology of DKA
⢠Typically, when the blood glucose level reaches approximately 12,5
mmol/l a significant amount of glucose spills over into the urine.
⢠A glucose molecule produces an osmotic effect by drawing water
across a semipermeable membrane.
⢠As an excessive amount of glucose enters the renal tubules, it draws
a large amount of water that ends up producing a significant amount
of urine.
⢠This is known as osmotic diuresis and leads to volume depletion and
dehydration in the patient.
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25. Pathophysiology of DKA
⢠Large amounts of ketones also collect in the urine.
⢠Because ketones are strong organic acids, they must be buffered in
order to be excreted.
⢠Sodium is typically used as the buffer. As we have been instructed,
where sodium goes, water follows. Thus, the sodium used to buffer
the ketones also draws a large amount of water into the renal
tubules, which produces excessive urine and leads to further volume
depletion and dehydration.
⢠The loss of large amounts of fluid also leads to the excretion of
other electrolytes, such as potassium, calcium, magnesium and
phosphorous.
⢠This produces electrolyte imbalance and disturbances.
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28. DKA emergency care and management
⢠Ensure an adequate airway, ventilation, oxygenation and circulation.
⢠Based on the physiologic syndromes of osmotic diuresis â leading to dehydration,
ketoacidosis and electrolyte disturbances â the primary goal of prehospital treatment of a
DKA patient is rehydration with isotonic fluids.
⢠Normal saline is an acceptable fluid.
⢠Administer the normal saline based on the blood pressure and other indicators of tissue
perfusion.
⢠It would be acceptable to bolus the fluid in cases of severe hypovolemia and hypotension.
⢠Also be sure to place the patient on a continuous cardiac monitor and obtain and record the
blood glucose level.
⢠Continuously reassess the patient for improvement or deterioration.
⢠By understanding the pathophysiology of diabetic ketoacidosis, you should be better
prepared to recognize the clinical presentation more promptly, differentiate the condition
from other diabetic emergencies and have a good foundation for understanding the
emergency care necessary to manage the patient effectively. 2018/07/24Compiled by C Settley
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29. DKA emergency care and management
⢠Solutions were classified as isotonic if they had the same or near
osmotic pressure as blood (eg, 0.9% saline, Hartmann's solution, or
Ringer's solution) or hypotonic if they had a lower osmotic
pressure than blood (eg, 0.45% saline, 0.3% saline, or 0.18%
saline).
⢠IV insulin (as long as serum potassium is ⼠3.3 mEq/L)
⢠Milliequivalents Per Litre
⢠Rarely IV sodium bicarbonate (if pH < 7 after 1 h of treatment)
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31. INSULIN
INSULIN TYPE ONSET PEAK DURATION
Intermediate acting:
- NPH
- Lente
- Pre mixed
(combination of
short &
intermediate
acting insulins)
2-4 hours
3-4 hours
15 minutes- 1 hours
4-10 hours
4-12 hours
3-4 hours;
8-12 hours
3-6 hours
10-16 hours
12-18 hours;
16-24 hours
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32. INSULIN
INSULIN TYPE ONSET PEAK DURATION
Long acting:
- Ultralente 6-10 hours None 18-20 hours
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33. INSULIN
⢠Other combination treatments:
⢠NovoLog Mix 70/30 (insulin aspart protamine-insulin aspart)
⢠Humalog Mix 75/25 (insulin lispro protamine-insulin lispro)
⢠Humalog Mix 50/50 (insulin lispro protamine-insulin lispro)
⢠Humulin 70/30 (human insulin NPH-human insulin regular)
⢠Novolin 70/30 (human insulin NPH-human insulin regular)
⢠Ryzodeg (insulin degludec-insulin aspart)
⢠Pramlintide (SymlinPen 120, SymlinPen 60) is an amylinomimetic drug. Itâs an
injectable drug used before meals. It works by delaying the time your stomach
takes to empty itself. It reduces glucagon secretion after meals. This lowers
your blood sugar. It also reduces appetite through a central mechanism.
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35. Medication for type 2 diabetes
⢠Most medications for type 2 diabetes are oral drugs. However, a
few come as injections. Some people with type 2 diabetes may
also need to take insulin.
⢠Alpha-glucosidase inhibitors:
⢠These medications help your body break down starchy foods and table
sugar. This effect lowers your blood sugar levels. For the best results, you
should take these drugs before meals. These drugs include: Arcarbase &
Meglitnides
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36. Medication for type 2 diabetes
⢠Biguanides: Biguanides decrease how much sugar your liver makes.
They decrease how much sugar your intestines absorb, make your
body more sensitive to insulin, and help your muscles absorb
glucose. The most common biguanide is metformin (Glucophage,
Metformin Hydrochloride ER, Glumetza, Riomet, Fortamet).
⢠Sulfonylureas: They work by stimulating the pancreas with the
help of beta cells. This causes the body to make more insulin.
These drugs include:glimepiride (Amaryl), glimepiride-
pioglitazone (Duetact), glimeperide-rosiglitazone (Avandaryl),
gliclazide & glipizide (Glucotrol)
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37. Medication for type 2 diabetes
⢠Thiazolidinediones: These medications work by decreasing glucose
in your liver. They also help your fat cells use insulin better. These
drugs come with an increased risk of heart disease. If your doctor
gives you one of these drugs, they will watch your heart function
during treatment. These drugs include:rosiglitazone (Avandia) &
rosiglitazone-glimepiride (Avandaryl).
⢠See https://dtc.ucsf.edu/types-of-diabetes/type2/treatment-of-
type-2-diabetes/medications-and-therapies/type-2-non-insulin-
therapies/table-of-medications/ (additional information)
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38. Reference list
⢠http://www.diabetesforecast.org/2011/mar/how-the-body-uses-
carbohydrates-proteins-and-fats.html
⢠https://www.slideshare.net/allerasic/urinalysis-45789342
⢠Dalton AL, Limmer D, Mistovich JJ, Werman HA. Advanced Medical Life
Support: A Practical Approach to Adult Medical Emergencies, 3nd edition.
Upper Saddle River, NJ: Prentice Hall, 2007.
⢠Guyton, A.C., and J.E. Hall. Textbook of Medical Physiology. 10th ed.
Philadelphia: W.B. Sauders, 2001.
⢠Marx, J.A., R.S. Hockberger, R.M. Walls. Rosenâs Emergency Medicine:
Concepts and Clinical Practice. 5th ed. St. Louis: Mosby, Inc., 2002.
⢠https://www.healthline.com/health/diabetes/medications-list#type-2-
diabetes
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