Transcribed

by Ana Sangadala

October 7, 2014

General Pathology Lecture 30-Nutritional Disorders 1 by Dr. Phelan

Slide 1- Nutritional Disorders
Ok. Can you hear me in the back? Yes? In the back. Yes? Ok, good. So were going to
do 2 sessions-today and Friday on nutritional disorders and this is on our next exam
which is why there are only, what, 20 of you here. This is interesting stuff and I think
that not only for me it is, but whether it is interesting for you remains to be seen. A
number of these nutritional disorders have oral or head and neck manifestations.
Also, some of the diseases that were going to talk about, you will talk about later in
other sections of this course or in systems pathology next year. As we look at the
range of nutritional disorders

Slide 2-Nutritional Disorders
The first one are the deficiencies and there are a group of deficiencies that are
considered protein calorie malnutrition. There are vitamin deficiencies, theres
mineral deficiency. Malabsorped disorders are part of what gives us nutritional
disorders. Nutritional deficiencies. And then on Friday, we will focus at the end of
the session or the second half of the session on Friday on obesity and the issues
associated with obsesity.

Slide 3-Protein-Calorie Malnutrition
So when we talk about this issue of protein-calorie malnutrition, the definition of
malnutrition has a number of different..let me put it this way. Theres a number of
different ways of defining malnutrition. It can be defined anywhere from a
inadequate amount of calories, proteins, vitamins, it can be defined as a disorder of
intake of vitamins, proteins, calories. So the definition is varied. The definition of
protein-calorie malnutrition is a little bit more specific. That, as its written here on
your slide, is a malnutrition that results from inadequate protein, carbohydrates,
and lipids. In some developing countries, it is reported to affect up to 25% of
children in those countries. And theres 2 different reasons in that setting and you
can extrapolate those reasons to issues that might emerge in this country as well.
One is an unavailable food supply and the other is diseases that interfere with
intestinal absorption and both of those are possible here.

Slide 4-Clinical Conditions
There are two clinical conditions and two names that you need to know. One of
them is called marasmus and the other one is called Kwashiorkor. In marasmus,
there is deficiency of calories from all sources. Its a generalized deficiency of
calories. In Kwashiorkor, the malnutrition and in both of these, are disorders in
children. They are usually defined as disorders of children, is probably more
accurate. In Kwashiorkor, the malnutrition is due to a lack of protein. Those children
have a diet that is high in carbohydrates. The effects of this nutritional type of
deficiency are actually worse and severe than marasmus. Sometimes these are
considered a spectrum from marasmus to Kwashiorkor, but they really result from a
different type of intake. Where with marasmus, it is much more generalized and
there just arent enough calories. In kwashiorkor, the protein is the part of the diet

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October 7, 2014

that is primarily missing. Malnutrition is also describes as undernutrition, where

there just isnt enough food or the amount of the food that is available may have the
right components of nutrients.

Slide 5-Marasmus/Kwashiorkor
These are the two of the description of marasmus and kwashiorkor. The findings in
each. I put them here because they are important in, youll see them described in
newspaper articles. Youll see them described in the whole area of nutrition and
nutritional disorders. In marasmus and kwashiorkor, in both of them, there is
growth failure in children. In marasmus and kwashiorkor, there is a decrease in
body weight. Its not enormously different between the two. Theres usually, as
described a bit more intense, a bit more extensive, decreased body weight in
kwashiorkor than marasmus with kwashiorkor being the more severe of the two. In
marasmus, there is a decrease in subcutaneous fat. The body is attempting in
marasmus to compensate for the, whoops! What did I do? I dont think I did
anything. Ok. The body is intending to, or attempting to compensate for the lack of
calories. In Kwashiorkor, the body doesnt have this same need to compensate so
there is normal. It doesnt use the fat stores in kwashiorkor. In marasmus, the kids
are usually alert and they may not be a major effect on intelligence and
development. In kwashiorkor, there is. There is an effect on mental development in
those children. Usually there is permanent disabilities in mental state. In marasmus,
there is usually described, a protuberant abdomen. You see illustrations of kids in
areas where there is famine. You will see the children with these very very large
abdomens and that is usually at least as severe in kwashiorkor. So you see it in both
of them. In kwashiorkor, theres a problem with severe edema. The edema in
kwashiorkor, it probably is related to the serum protein. But there are a number of
controversies over exactly what causes that edema so were not going into the
pathogenesis of the edema here. Except to recognize that between the two: in
marasmus, where you dont have the protein deficiency, you have normal serum
albumin. In kwashiorkor, you have low serum albumin. In marasmus, you dont have
the edema and in kwashiorkor, you have severe edema. In marasmus, you have
muscle wasting and muscle atrophy because again, its a mechanism of the body
attempting to compensate for the calorie loss. In kwashiorkor, there is a
hepatosplenomegaly that occurs and there is a fatty infiltration that occurs of the
liver and the spleen. And there is wrinkling of the skin that occurs in marasmus and
thats related to something thats a little bit up higher. The diminished subcutaneous
fat. Where instead of having the fat support for the skin, the skin wrinkles. We see
something like that and well talk about it a little later in the course when we talk
about neoplasia. But in cancer patients, you can see some of that wasting with a
wrinkling of the skin that is not the same wrinkling that you see in aging. In
marasmus, so let me go across the two so we do the two. In both of them, theres
edema. In both of them, theres an impaired ability fo the immune response to
function normally so kids in both categories have a problem that infections, and
were going to see one of those specific infections in a few minutes. Also, in both of
these, and I didnt put it on the list because it isnt as prominent and as I looked
through all of the medical textbooks, I dont see it but I do see it in the oral textbooks

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October 7, 2014

and the head and neck textbooks that there is a parotid enlargement that sometimes
occurs in both of these. Its described in both marasmus and kwashiorkor. And you
know we talked about asadinosis (sp? At 10:40) in a previous course as something
that is associated with malnutrition. So its not just associated with just this
malnutrition state, but also a number of other malnutritional states. But we can get a
parotid enlargement and Ill show you that in just a little bit.

Slide 6- Pictures
Ok. The picture on the right is marasmus. The picture on the left is kwashiorkor.
There is no way I would ever ask you as a dental student learning about this to ever
be able to distinguish between the two just on the basis of what the kids look like.
Thats far beyond what I would expect of you. Yes? (student asks question) No, I
didnt. Im sorry, if I said that, I misspoke. There is severe edema in kwashiorkor and
there isnt edema in marasmus. Im sorry if I said that. I misspoke.

Slide 7-NOMA
Ok. There is a condition known..yes?

(student asks question) Oh, I dont know. I mean thats pushing it for me, ok? There
really is in marasmus, there really is normal serum albumin. So if you want to blame
the edema totally on the issue of protein in albumin, then the answer would be no. If
you read the literature in both of these, there is a question on what the pathogenesis
of the edema is and it might be related to electrolyte balance which is a problem that
can occur in both of them. So lets put it this way, the edema is more prominent in
kwashiorkor but I cannot tell you it never occurs in marasmus. Unless you are going
to another country and you might be a pediatric dentist and you might get into an
outreach that actually will involve this, but you can work on it when you get there.
So I expect you to know the differences and I expect you to be able to compare the
two in this description, but I dont expect you to diagnose it. I think thats beyond
what we need for this course.

Ok. NOMA. The term NOMA is, if you look it up. If you google it, what you will get is a
whole lot of websites for the Christmas tree lights that are called NOMA. But in the
middle of those, there are a number of websites that talk about managing this
problem of NOMA. In a number of developing countries, not something that we see
here. I have never seen it. I have only seen it in pictures. I have talked to people who
have done certain kinds of outreaches and have seen it. There are surgeons who
travel the world repairing the faces of kids that have had this destructive disease
called NOMA. I think you already know about necrotizing ulcerative gingivitis. No? Is
that something thats been discussed anywhere? Oh ok. We have in the oral cavity, a
condition known as necrotiing ulcerative gingivitis. It is a bacterial infection. Its a
fusospirochetal dominantly caused infection. It is characterized by pain and
ulceration and in some patients, some destruction of the periodontal attachment
structures. In some people, it just remains as a gingival condition, but as an
ulcerating gingival condition. As a plaque related or microformulated plaque and
gingivitis is not painful and you dont get ulceration, but in necrotizing ulcerative

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October 7, 2014

gingivitis, you do. It used to be called ANUG (sp?) or acute necrotizing ulcerative
gingivitis, but we learned that more recently there really isnt acute. Its something
that can be chronic and persist for quite a long time. Its treated with antibiotics and
usually with antibiotics, it responds very very quickly. And then following that, the
rest of the treatment involves the usual dental prophylaxis and home care. And then
also evaluating the overall health of the patient. Yes? (student question) Actually
theyre there already. Thats actually where I was going-thank you for asking. Acute
necrotizing ulcerative gingivitis or necrotizing ulcerative gingivitis in HIV patients
begins with something we call necrotizing ulverative periodontisis. They are caused
again my fusospirochetal (sp? 16:08) bacteria that are already there. So were
looking at an opportunistic. You havent had-did you do opportunistic organisms in
micro? Opportunistic infections are infections by organisms that are part of us and
would normally not cause infection but if you make the circumstances right, they
cause a problem. So necrotizing ulcerative gingivitis is an unusual kind of gingivitis
that occurs in interesting settings, but its not very common. 25-30 years ago, it was
pretty common and there were studies that were done on necrotizing ulcerative
gingivitis. We cant even do the studies anymore because you just dont have enough
of it around. After the Vietnam war, military people would come back to the united
states and develop necrotizing ulcerative gingivitis. It might have been related to the
stress of being part of the military. The other name for that is trench mouth, first
described in the first world war where soldiers got it in the trenches. There seems to
be a relationship, I really am going someplace with ulcerative gingivitis. You will get
it later as a separate entity. Im not really asking you to know about it at this point
and I certainly am not going to ask you a question about that one. Its an important
way in understanding NOMA. So it was thought that trench mouth or necrotizing
ulcerative gingivitis was either due to nutritional deficiency or stress or some kind
of relationship with the stresses of war. NOMA is caused by the same bacteria, the
fusospirochetal. And its polymicrobial. Its multiple different organisms that get
together to cause this very destructive oral condition in children. It is again very
descructive. It destroys tissues. Even when it is treated and the ulceration heals, the
children are left with disfiguring defects. If you look at the websites of the soldiers
that are off repairing the faces of kids as a result of NOMA, its that disfiguration that
is happening. This happens when children have nutritional deficiencies and there is
some suggestion that it happens when in addition to the nutritional deficiencies, the
kids develop any of the childhood diseases like measles, would be one. Where it
seems that it decreases the childs resistance to infection even more. So, NOMA is
not something that we see in this country. We have one of our faculty members here
who was doing a search to see whether or not this was something that was
reemerging in Haiti. We have actually collected a number of photographs and he
was out in the far reaches of Haiti showing the photographs to the local healthcare
workers to see whether or not he was able to find an emergence of this condition.
Some of the parts of Haiti that we expected to see malnutrition and vitamin
deficiencies and a number of other issues. I will tell you, he really was not able to
identify an emergence of this condition in Haiti. There are parts of Africa where it
still exists and again if youre really interested in this, take a look at the website and
you can find it. But NOMA is again our area. It is an issue that is only related to the

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October 7, 2014

oral, the area around the oral cavity. The organisms that are responsible for this are
oral organisms. Just to give you an example of these organisms that are there. The
organism that causes syphilis is the spirochete. If a person has, again, this is just an
aside to help you understand this. Its not something Im going to test you on right
now. Maybe later, but not now. The organism is the spirochete and in making the
diagnosis of skin ulcers in syphilis, you can take a sample and do something called a
dark field examination. In the dark field examination, it will actually show up the
spirochetes. For a person that might get an oral ulcer from syphilis, we cant do that
because there are spirochetes in the oral cavity and you really cannot get a reliable
dark field examination of an oral ulcer related to the presence of spirochetes. We
dont have spirochetes normally on skin. You have spirochetes normally in the oral
cavity. Its just the relationship of those organisms to this opportunistic very
destructive oral ulceration is something thats been well described. So thats NOMA.
As far as I know, if NOMA stands for something, Im not sure what it is. I think we
have looked in the past. Somebody in one of the classes did a search to see where
NOMA comes from. The name that you will see in textbooks is cancrum oris which
relates the oral cavity and cancers, another term for an ulcer. We dont use it often
because its a little confusing, but its something that I dont expect you to see here in
this country. But if you are involved in any outreaches in other countries, its
possible you may see it or the results of it.

Slide 8-Undernutrition
Ok, then. The other area that we could talk about is undernutrition. Usually in our
country, were looking more at overnutrition than undernutrition but it is a way of
comparing body weight to the standard tables. In different tables, the standard
tables are somewhat different, but not dramatically different. There are a number of
different ways to do that. One of the ways is to actually measure skin folds. Theirs is
a caliper where you actually hold the skin fold and you estimate the amount of fat.
Its also a way of looking at obesity as well as undernutrtion. Another way of looking
at undernutrition is in reduced muscle mass. Remember I said before, in the
example that I gave you in marasmus, theres muscle wasting. And in
undernutrition, there would also be muscle wasting and one way of testing that is to
measure the circumference of the arm. There are tables that will guide you or the
person thats doing it to what the normal range is. You could also measure serum
proteins and thats sometimes helpful in trying to assess whats happening.

Slide 9-Sialadenosis
Ok. In our area, weve talked before about something called sialadenosis and it
comes into play here again. Sialadenosis is defined as bilateral. Could it be
unilateral? Probably, but it usually isnt and its not inflammatory. There are a
number of enlargements. I think I gave you a list of bilateral salivary gland
enlargements. Sialadenoses are a group of those but every bilateral salivary
enlargement is not a sialadenosis. If it is bilateral, enlarged, painful, and all the kids,
they wouldnt get it anymore because they get a vaccine usually, but all the kids in a
class got it, what would it be? Mumps. That is not sialadenosis, but its a bilateral
salivary gland enlargement. Another condition in which you get a bilateral salivary

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gland enlargement is an autoimmune disease in which there is a bilateral salivary

enlargement, dry mouth, dry eyes, and that ones called Sjogrens syndrome. Its not
a sialadenosis. Those are bilateral diagnoses that have a very different pathogenesis.
In sialadenoses, again there is an enlargement. Its not neoplastic, its not
inflammatory. Its usually soft, its usually painful. And there is persistant
enlargement of the salivary glands. In most of these, the histophathologic
appearance is acinar hypertrophy. We get sialadenoses in the malnutrition
disorders. In many of them, but sialadenosis is involved. The response of the
salivary gland to this phenomenon of malnutrition is to produce larger acini so we
have acinar hypertrophy. We dont have that many good examples. I mentioned it
before when we talked about hypertrophy, but we dont have that many good
examples of hypertrophy. This is one. In long standing diabetics and alcoholics, the
phenomenon is still called sialadenosis, but in some of the studies that have looked
at the salivary gland, it appears that it can be in some patients, a bit different where
youre getting an atrophy of the acini and replacement with that. Youre not going to
know by looking at the salivary glands what it is. However, if you have a person who
has salivary enlargement and has been an alcoholic for many many many years,
there is actually no reason for us to explore it, unless it is enlarging and we think it
may be a tumor or a lymphoma. We wouldnt actually go in and look at the salivary
glands. In those patients, you might find fatty infiltration. Instead of seeing acinar
hypertrophy, its almost as if the acini got tired and became atrophied instead of
hypertrophy. I made that up. Thats not a pathogenesis.

Slide 10-Nutritional Etiology of Sialadenosis
Ok. So, nutritional etiology of these that we actually recognize and there are some
examples of this. In general malnutrition, its been described. In marasmus and
kwashiorkor, its been described. In alcoholics and as alcoholics get to be very long
term alcoholics, its still sialadenosis, but exactly what the histopathological makeup
of the salivary glands is may change over time. In the eating disorders and anorexia
nervosa and bulimia, you can also get sialadenosis. It is usually more likely to be
associated with anorexia nervosa than it is with bulimia but its been described in
both.

Slide 11-Picture
This is a young patient with bilateral salivary gland enlargements and I used this in
a number of different courses so I might have shown this to you before. This is a
patient that I saw in a clinic when I was a senior dental student and I was just going
into my oral pathology residency and she was seen by the clinic in which I was
taking my elective in oral pathology. I probably ended up staying there. Anyway, she
had a bilateral salivary gland enlargement. 16 years old. They questioned whats
causing this. One of the things that was done early on was again a differential
diagnosis was could she possibly have, could she be a very young Sjogrens
syndrome? So all of the workup for Sjogrens syndrome was done. One of the things
you can never get is you can never get an accurate history. Never say never, Dr.
Phelan. You almost never can get an accurate history in eating disorders from a child
or young woman when the mother is in the room. You usually are not going to get it

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October 7, 2014

unless its already diagnosed and we didnt get it from her. She went very shortly
after that to college in Maryland and she went to the oral medicine/oral pathology
group at the university of Maryland dental school and they were able to interview
her and they were also able to take a needle biopsy of the parotid gland and it
turned out that she was a young women with anorexia nervosa with associated
sialadenosis. The salivary glands showed huge acini and this is a nice well
established patient with anorexia nervosa and bilateral salivary gland enlargement.

Slide 12-Eating Disorders
Bulimia nervosa is different and these are just two of the spectrum of eating
disorders and there are other courses and there are other places where its more
appropriate to spend more time on eating disorders than this one. In bulimia
nervosa, there is binge eating followed by vomiting or by laxatives or diuretics. So
the binge eating is there and the individual eats but then the individual does
something, and its usually women more than men but not entirely. But the
individual does something to get rid of the food either one way or another. The
clinical findings are similar to what I showed you depending on what the nutritional
components are that the individual is getting to what we looked at in marasmus and
kworshiokor. Its not the same but the effects are very similar. These young women
have amenorrhea, they have low thyroid hormone, theres changes in bone density,
and there is a traumatic risk of cardiac arrhythmia and sudden death. And the
sudden death, when it occurs, is usually due to hypokalemia which is low potassium.
What happens is there is a major electrolyte imbalance that occurs. In bulimia
nervosa, those individuals are very often, not so thing. Anorexia nervosa, those
individuals are usually very very thin.

Slide 13-Bulemia Related Lingual Erosion
There is a dental change thats associated with bulimia. Not anorexia nervosa,
because the anorexia nervosa doesnt involve vomiting. The bulimia related change
is a traumatic lingual erosion. Have you talked about this elsewhere? Yeah? Just in
your dental practice, when you see this, you may be as the dentist, the first person
who has had to confront this individual with the problem. And sometimes, its very
very helpful to them because they havent been able to talk to anybody about it. You
may be the person who helps them move to some kind of help in relationship to the
bulimia. The problem can be severe. Ive seen patients who needed full coverage of
all of their teeth because of the extensive erosion of bulimia. Nothing else does this.
GERD or gastroesophageal reflux disease, patients can vomit, but its usually not
nearly as severe and not nearly as generalized as you would find in bulimia.

Slide 14-Vitamin Deficiencies
So, before we go, from there we go to the vitamin deficiencies. This is a bit of maybe
alphabet soup if you will. We are going to go through the alphabet. And youre
textbook uses one letter, but it is much easier for me to think about them in order,
so you will see that I go A, B, C and try to put the alphabet in order instead of
skipping around the way the textbook does. Im not exactly sure. I think what the
textbook does, it takes the fat soluble first, and then does the water soluble. An easy

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October 7, 2014

way of looking at vitamin deficiencies. I just, its easier for me to think about them in
order, so you get the my way, instead of the textbook way. So if you look at the
textbook, youre just not going to find them in the same order that Im giving you.

Slide 15-Vitamin A (Fat Soluble)
Vitamin A is a fat soluble vitamin and many of youve spent some time talking about
this in biology in high school. Did you talk about this in basic sciences, vitamin
deficiency? In which course? Oh ok. So, some of this, youll have to tell me just how
much of this is completely redundant from last year, but it is something that I think
we do need to cover in general pathology to remind you of whats going on. Vitamin
A when you remember, is important in maintaining normal vision in reduced light.
So sometimes, the deficiency is called night blindness. It is a very important vitamin
in making specialized epithelial cells. If you lose vitamin A, or are deficient in
vitamin A, one of the things that will happen is you will have metaplasia from the
specialized cell to the squamous cell. So the vitamin A is important for pushing the
epithelial cell to a specialized cell. Also, there is an important function of Vitamin A
in the immune response. The sources of Vitamin A come from leafy green vegetables
and from fish liver. Most of us dont eat fish liver. Do many of you eat fish liver? No,
not something that I would go at. One of the ways of developing a deficiency is if in
areas where rice is the staple food. Because it doesnt contain carotene or beta
carotene and beta carotene is the inactive form. Retinoids are a chemical that is very
similar to vitamin A and you will actually see that retinoids are used in the
management of skin diseases and there is some attempt that skin diseases that are
epithelial. There is some attempt in using retinoids in managing some mucosal
diseases as well.

Slide 16-Vitamin A Deficiencies
So, if we have a deficiency, we will have impaired vision at night. There is something
called xeropthalmia which you should know at this point and that is dry eyes and
dryness of the conjunctiva. It is build up of keratin and erosion of the corneal
surface. And thats partly because of the lack of lubrication and irritation of the
cornea. The final result if this goes on for a very long time can lead to blindness.
Squamous metaplasia and hyperkeratosis are both components or results of
Vitamin A deficiency. Again, squamous metaplasia is metaplasia of a specialized
mucosa to a squamous epithelium and again these individuals with long standing
vitamin A deficiency may be at risk of developing some increased risk of infections
because their immune response is not as efficient as its supposed to be.

Slide 17-Picture
And if you look carefully at this child, you can see that there is some whiteness in the
eye. You can see a little bit over here (corner of iris), which is keratin that is forming
on the eye.

Slide 18-Picture
This is an example of the skin keratosis that can be seen in vitamin A deficiency.

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Slide 19-Picture
This is just a cartoon that includes the list of problems that is associated with
vitamin A deficiency. There is again, the eye problem that is a number of different
problems in the eye. These individuals may have problems with the
bronchopneumonia and I think you could probably figure that out. Whats
happening is that the epithelium in the pulmonary tract is then changing from
pseudostratified ciliated columnar epithelium and also the mucin producing cells to
squamous cells, so losing the functional, the normal functional epithelium in the
lungs. The changes in the pancreatic ducts, again because you have a problem with
maintaining the epithelial integrity and you have columnar and cuboidal cells that
are becoming squamous cells and not functioning the same way. There are problems
with kidney stones and follicular hyper-keratosis of the skin was the example that I
showed you in the arm of the patient just before.

Slide 20-Vitamin A Toxicity
Since vitamin A is a fat soluble vitamin, those vitamins are often potentially able to
cause a toxic response. In hypervitaminosis, A is what the vitamin A toxicity is
called. There are two forms, acute and chronic. And again its dependant on whats
going on with the vitamin A. In a normal intake of vitamin A, would give you a
chronic form of vitamin A toxicity. And chronic would be of course, less severe. You
talked about the terms acute and chronic, and again this is not in terms of any
histopathological change. Its in terms of timings. Acute is what would happen if you
took a lot of vitamin A all at once. I think its what would happen if you ate polar
bear liver. Its one of those trivias out there that polar bear liver is toxic. And one of
the students at one point picked up a study and actually described why and what
basis its known that polar bear liver is toxic and again its because of acute
vitaminosis. My only example of telling you is saying a lot at one time. Chronic
means that there has been an overintake of vitamin A over a long time, but not
enough to actually be so severe that we get the signs and symptoms in the acute.
Usually, chronic toxicity is because people are trying to do too much of a good thing.
You see it in this country, its just because somebody has decided they need more
vitamin and they increase dramatically their vitamin A over a long time. We begin to
see the problems due to overdoing certain vitamins.

Slide 21-Vitamin B Complex
And then we go to the vitamin B complex. Now, its also in your textbook, they dont
go through the vitamin Bs 1, 2, 3, 4. And I just cant remember them that way, so I
give them to you in order. Im not..I understand the reason for doing the fat soluble
and doing the water soluble. I really dont understand the reason for mixing up the
vitamin Bs, so anyway, you are getting them from me in order 1, 2, 3, and we are
only doing 6 and 12. Those are the only ones that usually designated by numbers.
Theres also a number 2 folic acid, but its usually not what is used. These numbers
and these names at this point, you do need to know. Thiamine, riboflavin, niacin,
pyridoxine, cianocobalamin, which is almost always called B12, and the last one folic
acid, we can all try to pronounce it is pteroylmonoglutamic acid. Again, folic acid is
the way I would expect you to remember it. I dont think that you need to memorize

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pteroylmonoglutamic acid. I will not give it to you that way. If you remember folic
acid, I will be thrilled. Again, its a long one. Its not the way its usually designated. If
we ever need to worry about it, I will tell you. For now, you do need to know, if you
look it up, that there is another name for it.

Slide 22-Vitamin B Deficiencies
Vitamin B deficiencies. We do see vitamin B deficiencies and we see them in people
who are alcoholics and thats usually because people who are alcoholics usually
have nutritional deficiency of a number of different types. Usually they are
malnourished individuals. And so, you will see nutritional deficiencies in alcoholics,
particularly vitamin B deficiencies. Of course, in people with overall nutrition, you
can see it. In people with special diets, particularly Vitamin b12. Vitamin b12 is only
naturally available from animal sources. So you have to supplement diets that are
not using any animal sources with vitamin B12 so you may see vitamin B12
deficiencies in that setting. And then there are a number of diseases that are called
malabsorptive diseases. As you go through this year, you will know about those
diseases. You will know a lot more about them. Im going to give you the names of
them because I think those are important. The pathogenesis of those diseases is
going to come later in your year, particularly in systems pathology. Yes? (student
question) Um, usually, and actually vegetarians can tell me more than I know, my
assumption is that its taken by a vitamin B 12 supplement. And actually if you think
about it, its not all vegetarians because some vegetarians will have some of their
nutrition from animal sources, just not meat. Again, it depends on what your diet is.
The vegan diet, you really do have to figure out some way of supplementing B12. In
this country, its usually over the counter B12 because the individual has no
problem absorbing vitamin B12. There is a problem that we will talk about a little
bit later where that is. At this point, I dont know, anybody vegetarian want to tell
me if there is another way of supplementing? But you see again, thats animal
protein and thats animal source. So I think again that it depends on the diet,
whether or not there is vitamin B12 in the diet. So people who are on special diets,
just have to be careful. Usually this is the one they have to be careful about. Vegan,
people that are vegan are the ones who have to be more conscious about
supplementation. There are vegetarian cultures all over the world that do not take
Vitamin B12 supplements because they are getting some vitamin B12 from animal
sources. Where are you? Say it again? (student question) Some vegetarians do
supplement with eggs and do eat some animal products. Others dont eat any and if
you dont eat any animal products, you have to worry about B12. Now, I mean, its
an interesting subject. I dont know how everybody supplements with vitamin B12,
but if you dont theres going to be a vitamin B12 deficiency. And those cultures that
are vegetarian cultures have figured out how to do it and their diet may be
vegetarian but its a healthful diet. Its not an unhealthy diet, and maybe more
healthful than those of us that are getting our vitamin B12 form meat.

Slide 23-Malabsorptive Disorders
Here are the malabsorptive disorders that are..there are more of them, but these are
the important ones I think for you to know at this point. There is something called

Transcribed by Ana Sangadala

October 7, 2014

Celiac disease. Celiac disease is a gluten intolerance disease, but it is a very well
defined gluten intolerance disease. And we know now that there are many people
that appear to have gluten intolerance that doesnt match the definition of celiacs
disease, but they are sensitive to gluten and have absorptive problems and have GI
problems related to the intake of gluten. Lactose intolerance is another
malabsorptive disorder. Cystic fibrosis, we talked about a little bit, where there is a
change in the intestinal absorption process. And then two inflammatory bowel
diseases: Crohn disease and ulcerative colitis. And again, you will spend some time
with those when we get to systems pathology later in the year. But these are all
disease and Ive put them on the list because theyre the ones that are the most
common. Theyre the ones that your patients may tell you about. And the other
malabsorptive disorders are really pretty rare. Doesnt mean they dont exist or that
theyre not important, but these are the ones that I think youre most likely to bump
into and have patients that may have these disorders.

Slide 24-Thiamin (B1) Deficieny (Beri-beri)
And so, it is 3:53. Lets stay on schedule and lets take a break until 4 oclock.