Diabetes Lecture 1 – April 4th
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Transcript of Diabetes Lecture 1 – April 4th
7/26/2019 Diabetes Lecture 1 – April 4th
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Diabetes Lecture 1 – April 4th, 2013
Diabetes
Diabetes is an epidemic; it’s exploding everywhere
Fat (obesity) & diabetes: they are always fighting each other because the moresubcutaneous body fat an individual has, the harder it is for your own insulin to
bring your blood sugar (glucose) down and put it in the cell
Glucose needs to be put into the cell because it gives you energy
o Glucose is the body’s fuel
Definition of diabetes: elevated blood glucose
o Two problems:
Problem with secretion and/or
Problem with utilization
FYI: Diabetes is Greek; it means to siphon and that refers to the amount of urine
because with certain types of diabetes you are going to have an increase in urineo Mellitus is Latin; it means “outpouring of sweet urine”
o The take home message from the slide: excess urination – excess
urination from a problem
Diabetes is a chronic problem; it’s increasing in the country and it is very costly
o The amount of people diagnosed are increasing so the healthcare
industry is initiating procedures and policies to prevent and/or stop
diabetes that’s already happening for those in the country that have
diabetes
Diabetes is an increase in blood sugar from a defect in secretion and/or
utilization of insulin
What happens with insulin: insulin comes from your pancreas from the beta
cells
o When you ingest the food, the beta cells recognize that food is coming
and in response, the beta cells squirt out/push out insulin into the
vascular system
o Insulin takes the food and brings into the cell (glucose) and we use it as
energy
When we don’t eat, or when we are sleep deprived and we eat something – no
matter what it is – 10 minutes after you feel as if you have more energy
o
This is because whatever you ingested – nutritious or not – insulin is
being secreted and it’s bringing that food into the cell and giving youenergy that’s the normal response
Your pancreas secretes it’s own insulin approximately 1 to 2 units per hour –
secreting, secreting, secreting
o Whether you are eating or not, the pancreas is secreting insulin
o You have so many locks and keys in your body that if you haven’t eaten
for 8, 10, 12 or 24 hours – your pancreas is still secreting insulin
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o
There is check and balance however; it never lets anything get too high
or too low until you are diagnosed with diabetes
Then the problem is secretion and/or utilization
As we covered, insulin is the hormone that is produced from the pancreas by the
beta cells and the insulin is what controls your blood sugar/blood glucose
o
Insulin regulates the blood glucose by: Producing
Storing
o With increased blood sugar/blood glucose, insulin gets secreted to bring
the blood sugar/blood glucose down, and put the blood sugar/blood
glucose back into the cell
o However, in diabetes, the body has a difficult time with utilization and
secretion of this insulin, depending on whether you are Type 1 or Type 2
Overall, Diabetes is a group of metabolic diseases characterized by high levels of
blood glucose resulting from defects in secretion or insulin action (utilization), or
both Three organs involved in the regulation and utilization of glucose:
o Liver
The liver stores and releases glucose ingested from our diet
The liver also makes its own glucose in a process called
gluconeogenesis
When the blood sugar is down, the liver releases glucose
When the blood sugar is up, the liver stops releasing and
producing glucose because it recognizes that there is
enough in the serum to do what it needs to do
So when you think of the liver think of: storage of extra glucose
and release of glucose as needed
o Pancreas
The pancreas is where the beta cells are
The beta cells release insulin
The pancreas also has alpha cells; the alpha cells release
glucagon
Here is how you know when the alpha cells are working:
Glucagon gets released when the sugar is gone
So in cases of hypoglycemia – low blood sugar – the alpha
cells in the pancreas will “spit out” glucagon to raise the
serum blood sugar to keep it at about 70 to 110/70 to 120
Once again, the pancreas supplies two hormones: insulin and
glucagon
Beta cells release insulin
o
Insulin allows the glucose to enter into the cell,
where it is used for fuel and energy for the body
Alpha cells release glucagon
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o
Glucagon gets released to increase blood sugar
levels in periods of hypoglycemia
o
Skeletal muscle tissue
Glucose is stored in your muscle cells
The muscles are the place where there are the most insulin
receptor sites – two-thirds of the receptor sites are located there
Insulin has to bind to a receptor in the muscle and then it
allows it to enter into the cell except if there is insulin
resistance
o Insulin resistance is where the body has a problem
utilizing the insulin
Looking at slide 7:
o Glucose enters the blood stream and blood sugar levels rise
You eat food, glucose goes in, your blood sugar starts to go up
o The pancreas is signaled to release INSULIN into the blood
Immediately your pancreas is going to squirt out insulin (inresponse)
o INSULIN is the key to unlock the cells & allow the glucose to enter the
cells
o The blood sugar levels drop
o Glucose yields energy for the body cells
You are able to carry on with your activities except with insulin
resistance where you have a secretion problem
Euglycemia
o Normal blood sugar range
Want to keep it 70-110 or 80-120
o
What happens: When you eat, your blood sugar level starts to go up As your blood sugar goes up, the pancreas squirts out insulin
Insulin then comes and takes the glucose and brings it into the
cell to use for fuel or energy that you need to sustain daily
activities
This is a normal process with meals – whatever you happen to eat
o When you eat a fast-acting carbohydrate, such as Snickers bar, M&Ms,
Milky Way – essentially candy bars that are loaded with processed
sugar – immediately your blood sugar starts to go up but the insulin is
squirted out and it brings back into the vascular cell – this goes on all day
long EXCEPT when you have: Lack of insulin, either because it’s not being secreted or it’s not
being utilized properly because those receptors sites in your
muscles – where two-thirds of them are – are not letting the
insulin in
Insulin is being secreted but the receptor sites are closed
and not letting the insulin in
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As a result the insulin is continuing to rise in your
bloodstream as opposed to being let in
o What happens in diabetes with secretion and utilization is:
You eat food and the beta cells squirt out just a little bit of insulin
– not enough for the big meal that you have just eaten
So instead of the blood sugar level rising and then coming backdown, the blood sugar level continues to rise
That little bit of insulin that the beta cells squirted out
might bring it down a little bit but not enough
The blood sugar as a result is constantly elevated
The food and nutrition is not being brought into the body
because it is circulating in the vascular system
The blood sugar levels aren’t consistent
o The goal in diabetes is to become euglycemic
Euglycemia is blood sugar levels between 70-110 or 80-120 pre-
meal
Post-prandial (post-meal)
When you hear someone say “do a 2-hour post-prandial
on him” it means give him a normal amount of carbs,
proteins, fats, and 2 hours later draw a glucose on him and
let’s see where he is
Review:
o Insulin helps the glucose get into the cell to use it for fuel and energy
o
Three organs involved in the utilization of insulin
Liver
Pancreas
Muscles
Key place because two-thirds of the insulin receptor sites
are located there
Types of Diabetes
o
Type 1 (slide 9): 5-10% of people have Type 1
A small portion of people have Type 1 Diabetes; the vast majority
of people who have diabetes, have Type 2 Diabetes
When you think if Type 1 Diabetes, you think of subQ
insulin; when you think of Type 2, you think of oral
meds/oral control
o
Remember: an oral controlled diabetic can also beon subQ insulin at some point
50% of Type 2 orally controlled diabetics
will go on to use insulin at some point in
their life
Auto-immune
The body is attacking itself
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With any auto-immune disease, your body is attacking
itself
Complete insulin deficiency (insulinopenic)
The pancreas can’t produce or secrete enough of it’s own
insulin
o
Why: because it’s an auto-immune illness It could also be partial insulin deficiency
o Type 1 diabetics could start with partial insulin
deficiency and as the disease progresses, less and
less of their own inherent insulin is made
Absolute dependence upon exogenous (outside) insulin
Type 1 diabetics need exogenous insulin to live; they
cannot live without the administration of insulin
Prone to Diabetic Keto-Acidosis
The take home word here is acidosis
Ketosis-prone when insulin is absento If there is no insulin, the body has to attack it’s own
stores and ingest its own stores
Where are the “storage units”: muscles and
liver
o Ketosis-prone meaning that they produce ketones
When you think of ketones, think
immediately acid; ketone is an acid
With decreased insulin – because it’s a
secretion or utilization problem, and
increased glucose, the body goes to break
down it’s own fat because it needs to feed
the cells – the cells are starving
Where is the glucose? Not in the cell but
circulating in the bloodstream
When this starts to happen, Diabetic Keto-
acidosis begins
One of the things that patients with DKA get is
dehydration (see polyuria)
Review:
o Type 1 diabetics have an insulin secretion and
utilization problem – they rely on insulin to live;they cannot live without insulin
o It is a genetic predisposition that these patients
have
Lean; recent weight loss
These patients usually look slender
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Very often what will bring them to the doctor is a recent
weight loss – a significant weight loss of 10 to 15 lbs and
they will come in with the three Ps:
o Polyuria
When your blood sugar is approximately
180 and above, the glucose spills out intoyour urine
ADH (anti-diuretic hormone) is released
from the brain and ADH tells the body to
get rid of the water so you start to pee
When you pee, out goes the water and out
goes the glucose – that’s a good thing
However, polyuria can lead to dehydration
for these patients with DKA
o Polydipsia
Excessive thirst o
Polyphagia
Eat abnormally excessive amounts of food
due to the decreased storage of calories
Abrupt onset, usually before age 40
Comes on suddenly; this is the guy that goes to the doctor
because he feels bad – something is not right
Traditionally we see this in the younger client
May occur in elderly
Patients with Type 1 diabetes usually have a genetic
predisposition – meaning it can be inherited
If you have a parent that has Type 1 or Type 2, they areprone to having a child with diabetes
There is also a viral theory but that is still being worked
on; the genetic predisposition is more significant
There is no prevention for Type 1 diabetes but the history of the
parents can certainly help – not help prevent it but help watch for
symptoms should it occur in the patient
Diagnosis of Type 1 diabetes is usually with the signs and
symptoms which usually brings the patient in
Review:
Type 1 diabetics have an insulin secretion and utilizationproblem – they rely on insulin to live; they cannot live
without insulin
It is a genetic predisposition that these patients have
The symptoms occur quickly bringing them to a medical
practitioner who does a blood test and diagnosis them
with Type 1 diabetes
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Usually this is a younger client
They are prone to DKA (Diabetic Keto-Acidosis) or
Ketosis-prone
o With a decrease in insulin – because their pancreas
is either squirting it little bits at a time, not at all, or
inconsistently – the glucose is rising o The body cells are starving; the body says “I have
to feed the cells!”
Where does it go for food? To your stored
subcutaneous fat
When that stored subcutaneous fat is
broken down, ketones or acids are
released, putting the patient and making
them prone to Diabetic Keto-Acidosis
DKA is something that happens over a
period of hours – you just don’t go into it in5 minutes
The glucose rises, the insulin isn’t
secreted – it happens over a period
of hours
How we monitor that is serum blood
glucose levels
Primary concern with Type 1 Diabetes is insulin
deficiency
Symptoms (slide 11):
o Extreme fatigue
o
Polyuria
o Polydipsia
o
Polyphagia
o
Unusual weight loss
o Irritability
o Type 2 (slide 14) – 80-85% have Type 2
Two problems with Type 2: impaired insulin secretion or insulin
resistance
Insulin resistance = no binding at the receptor site
o Decreased sensitivity to insulin so the blood sugar
does not come down as much as it should/down toa normal number
Impaired secretion: meaning that the pancreas is putting
out some insulin but it’s not enough or it’s inconsistent
Not absolutely dependent upon exogenous (outside) insulin
The key here is that the pancreas produces some insulin
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If there is a non-compliance however, Type 2 diabetics
may be dependent on exogenous insulin
Progressive condition
Type 2 diabetes is usually present years before it is
diagnosed because these beta cells start to stop
producing insulin, the receptor sites start to close off By the time someone is diagnosed with Type 2 diabetes,
they say that it is really 3 to 5 years that they’ve had it and
just have not been diagnosed
Diabetes is a condition for life; it’s not something that can
be reversed – it has to be managed
May be relatively free of classical symptoms (three Ps)
Symptoms (slide 11):
o Any of Type 1
o Frequent infections
Sometimes with patients that havefrequent infections, all of a sudden we do a
fasting glucose on them, we see an
elevated number and it all starts to make
sense as to why they keep having these
frequent infections
o Blurred vision
o Cuts/bruises slow to heal
o Tingling or numbness in hands/feet
o Recurring skin, gum, or vaginal/bladder infection
The symptoms are more subtle with Type 2 diabetes
What usually gets the Type 2 diagnosed is a yearly
physical because Type 2 diabetics feel okay – they don’t
feel great but they don’t go to the doctor for a checkup
Come in for the yearly physical and a serum fasting blood
glucose is done
o Magic number for diagnosis of diabetes = 126
Not prone to DKA (Diabetic Keto-Acidosis)
Not prone because Type 2 diabetics have some insulin;
maybe not a lot but they are not prone to DKA
Not breaking down or eating their own fat
Strong family history of diabetes mellitus Not genetic, but family history
o Family history: parents
Usually obese or history of obesity
Again, obesity is an antagonist to insulin; the fatter you
are, the more subcutaneous body fat you have, the harder
it is for that insulin to work
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Usually diagnosed after age 40
Traditionally we see this in the older client
Usually peaks in the 50s
Primary concern is insulin resistance
With insulin resistance: insulin is being secreted but the
receptors at the site on the muscles are not letting theinsulin in
The receptor sites are shutting down and not letting the
insulin in so the glucose is then circulating in the
bloodstream and it’s rising
o Is it going into the cell? With Type 2 diabetes,
sometimes yes and sometimes no
We treat Type 2 diabetics with diet and exercise to try and bring
the blood glucose down
If we can’t get into a normal range, we begin oral therapy
with Type 2 diabetics 50% of diabetics will eventually go on to add insulin to
their regime if they are not compliant
Really the major way that we control blood glucose in
Type 2 is through weight loss because again think of fat
and insulin – the more weight you have; they are
antagonists
o Just by losing 10 lbs, it can bring down your blood
pressure, your blood sugar and that antagonist
effect between fat and insulin lessens
First thing we try is we try to put the Type 2 diabetics on a
diet and weight loss
o This is not as easy as it sounds, however, so the
potential for noncompliance is there
Going over slide 13: Type 2 Diabetes
The stomach changes food into glucose
o You eat, food goes in
Glucose enters the bloodstream
The pancreas makes insulin
o As soon as the food goes in, the pancreas squirts
out insulin as a response
Insulin goes into the bloodstream Glucose can’t get into the cells of the body (resistance);
glucose builds up in the blood vessels
The problem here is either not enough insulin is secreted
or we give you plenty of insulin but there’s a resistance
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o
Glucose levels in the blood increase and eventually
patients start to experience the signs and
symptoms
In response to Gasha’s question: Type 2 Diabetics are
metabolically prone, while Type 1 Diabetics are auto-
immune o Type 2’s are prone to cardiovascular disease
Prone to an MI, prone to a CVA, prone to
PVD
o Type 2’s tend to have the lifestyle of “the rich and
famous”
Meaning: they eat a lot of refined sugars,
processed foods – that leads to obesity
Remember, obesity is the
antagonist to insulin
They are inactive Inactivity leads to increased blood
sugar; this is why the first thing that
Type 2 diabetics are put on is a diet
and are also told to move – be active
o Get the weight off, exercise,
get the circulation going and
get another serum blood test
to see how you are doing
African-Americans, Hispanics, Native Americans are much more
prone to Type 2 genetically than the other races and cultures
Diagnosis of Diabetes (slide 15): Non-pregnant adult:
FPG (fasting plasma glucose) ≥ 126 mg/dL (fasting = 8 hours) OR
o Fasting = NPO after midnight, 8 hours
OGTT (oral glucose tolerance test; pregnancy) ≥ 200 mg/dL in 2 hr sample OR
(75-g glucose)
Repeat on a different day in absence of unequivocal hyperglycemia
Casual BG ≥ 200 mg/dL w/symptoms
o In other words: right now, you do a serum blood glucose on Prof. Molloy
casually – nobody is asking what she ate, when she ate, etc – and it’s 200and above
From that point on, the diagnosis of diabetes is made
We have to know these numbers
o
You have to know:
Fasting – 8 hours in, NPO – 126 and above and we have a problem
Casual blood glucose - 200 and above, and we have a problem
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Remember it is casual blood glucose with symptoms – the
symptoms brought you in
This is serum – not fingerstick
Risk Factors for Diabetes(slide 17): Obesity (any age)
o BMI > 25
o American kids are obese because of inactivity
Heredity
Viruses
o With Type 1
Stress
Diet
o Refined sugar
o
Fast foodso “life of the rich and famous” – not cooking, always eating out
Aging (> 45 years old)
o With Type 2
Race:
o African-American
o Latino
o Native American
o Asian-American
o
Pacific Islanders
o
Alaska Native
Going over slide 19: Diabetes Mellitus – Type 1 Signs & Symptoms
The three Ps:
o Polyuria:urination
o Polydipsia:thirst
o Polyphagia:hunger
Weight loss
Fatigue
Frequency of infections
Rapid onset
Insulin dependent
Familial Tendency
Peak incidence from 10 to 15 years
Going over slide 20: Management – Type 1
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Goal: To keep blood sugar in normal range (aka: tight control)
Dependent on insulin for life
American Diabetes Association recommends blood sugar levels between:
o
80 – 120 before meals – Tight control
o
100 – 180 postprandial (after meals)