(This is part of Inflammatory Bowel Disease (IBD) along with Ulcerative Colitis and Whipples)

• Chron’s, or Iliocolitis are the aka’s

• Regional Enteritis starts at the distal ileum

• 40% involve cecum at the beginning; however it can be anywhere from mouth to anus.

• This is not the same as ulcerative colitis even though they are related

• Know Dif bet. UC, RE, and Whipples

• It is a full thickness IBD

• It involves very big holes

• Leads to perforations

• Can have long periods of remission

• Skip lesions seen on endoscopic exam and contrast.

• In remissive tissue lesions fill in with adhesion (scar tissue) that shrinks down over time

• Can decrease peristaltic wave through that region

• Can get low grade obstruction from narrowed lumen

• Can happen at any age though 2^nd and 3^rd decade is most common

• RE has no gender bias

• More Caucasians of Jewish descent get RE (chron’s)

• Chron’s is 2-3x more common in blood relatives.

• Diarrhea followed by constipation is a major sign of RE

• The lesion is dominated by immune globulins

• Milk and dairy are trigger foods, however they don’t cause the disease

• The cause seems to be genetic predisposition with viral trigger

• Once the skip lesions reach the capillary bed you will begin to see blood in the stool of RE patients (hemocult = positive)

• RE can cause anemia but so can menstruation so RE in women can be missed especially since it is prime in the 2^nd and 3^rd decade.

• If the SI isn’t absorbing appropriately RE people will see weight loss

• THE stool of RE patients will have stuff in it that should have been absorbed

• Retrograde endoscopy is the best way to diagnose it (contrast shows decrease peristaltic wave

• If it goes through one loop, it can go into another causing a fistula

• Additionally, it can also break through to surrounding organs (i.e. bladder) and urine will smell like caca (that means poop)

• TREATMENT of REGIONAL ENTERITES a.k.a. chron’s/iliocolitis

  • the most successful drugs claim 40% success rate, barely beating placebo

  • we (chiropractors) can help 40-50% without the side effects of drugs so we are better tx.

  • Cutting out/ avoiding trigger foods (i.e. dairy) is a good form of treatment

  • During inflammation consume highly absorbable foods

  • Avoid raw vegetables and fruits b/c the bulk of it will not get absorbed and will speed through the SI and not get absorbed.

  • Corticosteroids – are advised if the flare up is very bad

(NOT A FULL THICKNESS IBD)

• UC starts in the rectum and works its way backwards, skipping nothing in between

• It starts later than chron’s 3^rd, 4^th, and 5^th, decade

• Emotional stress is trigger for new round of inflammation.

• Since the first (most mature) lesion is at the rectum, the blood in the stool wil be painted on, unlike chron’s which will have blood mixed in.

• Alternating Diarrhea and constipation like Chron’s is present

• Weight loss is not a problem as it does not affect SI where nutrient absorption takes place

• 50%=mild 35%=moderate 15%=severe (bloody b.m.. daily, tachycardia w/ Low B.P. , inflammation involving JELS (joints,eyes, liver, skin), iron deficiency anemia is contracted due to bleeding, peripheral arthropathy, sacroilitis,

• Complications of UC

  • Toxic megacolon (septicemia) – 40%

  • Stricture

  • Massive Hemorrhage

  • Perforation is not as likely as Chron’s b/c UC is NOT A FULL THICKNESS DX LIKE CHRON’S

  • All the different ulcers in Ulcerative colitis are rare

  • UC AND CHRON’S ARE THE 2 MOST COMMON IBD’S

1. Volvulus – a twisting or folding over onto itself ( Small intestine) like a balloon artist with the long thing balloons.

• Closed Loop = High Grade

• Open Loop = Low Grade

• Volvulus is seen in premature infants.

• If there is an adhesion anchoring the bowels it causes a pivot point allowing for twisting.

2. Intusseception – is a telescoping or invagination

   • The most common cause of this in adults is a tumor!!!

3. Perforation – is the worst case scenario of obstruction as it leads to peritonitis.

4. Functional Obstruction (a.k.a. Adynamic Ileus, Paralytic Ileus)

• Whereas other obstructions maintain intact neurological tracts Functional Obstructions have inhibited motor function.

• Any “itis” in the abdomen can cause decreased motor function (i.e. Cholecystitis, Meckel’s diverticulitis, hepatitis, appendicitis, peritonitis.

• KUB is usually normal

• Bolus clears in a Functional Obstruction because of the work of more proximal parts of the Small Intestine.

• The area of functional obstruction just does not contract

• Functional obstruction can cause severe back pain

• Surgery can produce Functional Obstruction

• If an ITIS caused it take care of the IT IS!

• If back pain is decreased function is restored.

1. The most common obstruction of the GI is ABDOMINAL ADHESIONS which occur as a result of:

   • pancreatitis, surgery, etc.

   • old time migraine medications which lead to fibrosis in the abdomen.

2. The 2^nd most common GI obstruction is Hernia (it was the former #1 but now is #2)

High Grade vs. Low Grade GI Obstruction

High Grade (early vs. late)

Early

• In a high grade GI obstruction nothing gets past a certain portion of bowel.

• Parasympathetic driven persitalsis (due to stretch receptors) try to drive matter past the point of obstruction

• Multiple spinal levels get involved and as a result overlapping peristaltic waves that can be heard as increase peristaltic sounds (HYPERPERISTALSIS)

• Colicky pain – signifies an “unsatisfied contraction” meaning the neurological system is intact

• The colicky pain gets, bad, worse, worst, then goes way, only to return again and get even worse.

• The patient with a high grade obstruction will be normal for a while until it gets completely compacted up to that point; The individual may have a couple of Bowel movements after it happens b/c there was fecal matter distal to the site of obstruction.

• The obstruction may be palpable

Late

• At this phase of obstruction the area of involvement is very dilated. The muscular wall of the Small intestine is stretched so much that it is not very contractile.

• There is difficulty draining blood which causes obstruction, which then leads to no blood coming in

• No bowel sounds may be present for up to 5 minutes

• NO bowel movements will be present in Late High Grade Obstruction.

• Contrast is a contraindication in viewing a Late High Grade Obstruction as barium is in suspension when the patient drinks it. The patient will absorb the water and the Barium will be left behind forming a cement plug. A water soluble contrast agent is needed for a High Grade Obstruction so that the vascular tree can take it away.

• Upright KUB shows multiple air fluid levels due to the layering of feces

• Normal air fluid levels

• Stomach, cecum, hepatic flexure, splenic flexure will not be visible.

• 3 or more air fluid levels on a KUB is abnormal and is considered an obstruction unless proven otherwise.

KEY QUESTIONS

1. Is the Bowel movement schedule normal?

2. Is there a decrease in fecal bulk volume?

LOW GRADE

• The low grade GI Obstruction is like a toothpaste tube. It is a big tube with a small opening.

• Transient dilation (painful) occurs proximal to the partial obstruction.

• Low grade Obstruction is less severe than high grade obstruction

• The pain of a Low grade occurs a certain time after the meal.

• The pain occurs specifically when the area proximal to the obstruction dilates. The pain dissipates as some matter goes through the little hole, and the pain decreases as the stretch decreases.

• It is safe to perform a contrast study here

Chronic – Chronic Mesenteric Vascular lesion will progress over time as blood supply decreases

• These patients will present in the Chiropractic Office and can be treated as it is a vascular compromise.

• Chronic Mesenteric Vascular Lesion is a consequence of atherosclerotic disease.

• These individuals will eat and at a fixed time interval after the meal, they start to hurt.

• The blood supply can keep up with normal activity, but when you add a bolus of food and the activity of the Small Intestine increases with peristaltic waves, these individuals exceed the capacity of the vasculature and the muscles are demanded to contract without replacement energy .

• The muscles then become stressed because of the absence of oxygen necessary to do the work.

• The pain from Chronic Mesenteric Vascular Lesion will pass as the food passes.

• Usually as the patient decides they need a doctor, they start to feel better and don’t come in.

• An Arteriogram is the best way to observe the vasculature problems occurring in Chronic Mesenteric Vascular Lesion.

ACUTE MESENTERIC VASCULAR LESION

• AMVL presents with an abrupt vascular compromise.

• This is a patient that we as chiropractors will not treat

• The patient with AMVL will be sent directly to the Emergency Room

• Acute Mesenteric Vascular Lesion is a SURGICAL EMERGENCY!!!

• The bowels will die quickly due to vascular compromise.

• Ususally the scenario that a person with AMVL encounters is that they eat, pain emerges a fixed time after, and they describe the pain as “THE WORST PAIN I EVER FELT!!!!”

• Hopefully these patients live to make it to surgery.

• 2% have it

• There are two forms

1. Symptomatic – discovered before age 2

2. Asymptomatic

   • It is attached to the last 2 feet of the ileum

   • Meckel’s Diverticulum is the #1 cause for a bloody diaper (rectal bleeding).

   • It is a red flag for child abuse

   • Meckel’s diverticulum mimic appendicitis in its presentation of acute abdomen.

   • The appendix is also a blind sac

   • Both the appendix and Meckel’s Diverticulum can get obstructed

   • Because Meckel’s Diverticulum can be located anywhere in the last 2 feet of the ileum it is possible for it to present on the left or the right.

   • Infants with Meckel’s Diverticulum cannot afford the blood loss and as a result will not thrive.

   • Surgical repair is the treatment for Meckel’s Diverticulum

   • In adults meckel’s diverticulum is asymptomatic and because they have had it for so long the best thing to do is leave it alone and see if the individual can go the distance.

   • It is possible for these individuals to get an overlay of Zollinger-Ellison

In contrast to all of the other heart sounds so far, the gallops are low frequency events. They are much harder to hear and they are uniquely appreciated in the receiving ventricle of the pathology. For example, if you have a failing large LV and the LA is allowing blood to move into the LV causing this sound in the LV, you need to listen to the apex beat. If this is occurring due to a large failing RV, you would need to approximate the position of the RV apex, which is usually at the lower left sternal edge near the xiphoid process, to hear a right sided third heart sound. The other kind of gallop is the fourth heart sound, which is a presystolic sound. It precedes S1. The S3 is usually in the first half of diastole. Remember that S3 is a reflection of a failing ventricle or a volume overloaded ventricle such as in a ventricle of severe mitral regurgitation.

Demo of S3: you listen at the apex of the heart and hear a low frequency sound.

Demo of S4: also low frequency but it occurs right before S1.

Demo of S3 and S4 together: if the heart rate increases enough when you have both an S3 and an S4, you have a summation gallop. That is when S3 and S4 superimpose on each other, producing a loud single diastolic sound.

Hearing a third heart sound is an exceedingly important clinical observation. This is not found in normal individuals with the one exception of pregnancy. It’s found in very diseased ventricles and in very volume overloaded ventricles.

Heart murmurs have been classified in many ways, one of which is based on the timing of the murmur. Systolic murmurs have been divided into four types.

Midsystolic – occurs after S1 and before S2. This murmur usually has a shape of a crescendo/decrescendo pattern. It builds up to a max. intensity and then degrades. It has also been called a diamond shaped murmur or an ejection type systolic murmur b/c most of these murmurs are in fact ejection murmurs; they represent blood flow out of the aorta or out of the pulmonary artery. However, other valvular abnormalities can produce crescendo/decrescendo murmurs so that it is not particularly useful to call something an ejection murmur when it may not be. It’s best to call it a midsystolic murmur. This is the most common type of murmur that is appreciated clinically. It can represent a normal state, a so called innocent or benign murmur, simply due to increased velocity of blood flow or it can represent a structural abnormality of the heart.

Holosystolic (Pansystolic) – The second most common type of murmur. These begin with S1 and end with S2. If they originate in the left side of the heart they end with aortic closure. If they originate in the right side of the heart, they end with pulmonic closure. These murmurs remain relatively constant in intensity. They usually represent murmurs of AV (atrioventricular)valve regurgitation i.e. mitral or tricuspid insufficiency. They may also occur in ventricular septal defects or other congenital heart defects, but they are typically murmurs of AV valve regurgitation.

Early Systolic – Rare event. Begins with S1 and is a decrescendo murmur ending before S2. Usually occurs in one or two very different settings. It occurs in individuals with ventricular septal defects that are small and are physiologically closing. That is, as systole continues, there’s a gradient btwn. the left and right ventricles, hence a murmur is generated due to velocity. As the defect becomes smaller with systole (if it is a muscular VSD vs. a membranous VSD), you get a decrescendo murmur. Paradoxically, you can also hear these murmurs in the opposite extreme case, the so called Eisenmenger syndrome, where you have right sided pressures at systemic levels (almost equal pressure in RV and LV). During systole, these murmurs can abate simply b/c of equalization of pressures in the RV and LV. This is an extreme end- stage condition in patients with large VSDs.

Late Systolic – Also rare. Begins after S1 and goes into S2. This is the murmur of mitral valve prolapse that occurs due to a valve becoming incompetent during systole and allowing a gradient of pressure btwn the LV and LA until the end of systole.

There are three types of diastolic murmurs

1. Early Diastolic Murmur (EDM). These are the most common type. It is a decrescendo murmur initiated by the (incomplete) closure of the aortic (or pulmonary on the right) valve. This is a high frequency murmur because of the high pressure gradient between the aorta and the left ventricle during diastole. This high frequency is unique among diastolic murmurs. To refresh your memory, the high frequency sounds kind of like the shooshing of Darth Vader breathing. Since the blood is flowing from the aorta back into the left ventricle you would listen for this along the lower left sternal border. They are best heard with patient sitting up, leaning forward, in held expiration. He did not say what it would sound like on the right.

2. Mid Diastolic Murmur (MDM). These tend to be low frequency sounds that develop as blood flows through the A/V valves. They are described as “rumbles”. They can be caused by either a restrictive valve (mitral stenosis) or sheer volume such a large left to right shunt. In this case, so much blood (the normal atrial return plus the added volume from the previous systole) is flowing over the tricuspid it causes a rumble. As you can guess, the same type of rumble will develop over the mitral valve in severe, chronic mitral regurgitation.

3. Pre-Systolic Murmurs. It would be too sensible to call these late diastolic murmurs, but know that that is essentially what they are. These are murmurs that run into the first heart sound. Early closure of the mitral valve during severe aortic regurgitation will show this (the murmur runs into S1 here because the murmur is basically causing S1 if the flow is big enough).

4. Continuous Murmurs. The definition of this is a little tricky. The murmur does not have to be constantly present to be termed continuous. It is a continuous murmur if it can be heard during systole and diastole. If it runs through S2, it is a continuous murmur. It is also to be distinguished from “to and fro” murmurs. These can appear to run through S2, but are actually two distinct murmurs, one of them ending at S2 while the other starts. An example of a to and fro murmur would be combined mitral regurgitation (systolic) and aortic regurgitation (diastolic). Continuous murmurs are rare and usually occur in the context of congenital heart disease. The typical one is caused by a patent ductus arteriosus. It produces a loud murmur in the second left intercostal space and will follow the pulmonary artery out toward the left lung. This can strange sounding if the murmur is loud enough to obscure S2.

- Rheumatic heart disease (caused by Rheumatic Fever - RF) and Scarlet Fever ( SF ):

Most people believe that their decline was the result of antibiotics, which is in part true. Moreover, RF as well as scarlet fever began declining even before the advent of Penicillin.

Some believe this is due to a less virulent Streptococcus.

In recent years there has been periodic upswings in the appearance of rheumatic heart disease. This resurgence has been isolated to certain geographic areas. It tended to occur in different socioeconomic groups. In the past it was seen in poorer and more crowded areas whereas now rheumatic heart disease is being found in the more affluent community.

- Cause: Streptococcus

- Mechanism: A temperate bacteriophage infects and causes Streptococcus to produce a specific toxin. This Toxin causes what is known as SF.

- Clinical: A red rash.

Once an individual mounts an immune response to the Strep, a person can never develop the red rash of SF again, but one can still be reinfected.

Does SF have anything to do with RF?

No, they are not the same. Many people associate SF with heart disease and RF, but this is not the case.

- Cause: occurs after infection with Streptococcus. It need not be the Strep that produces a toxin.

- Mechanism: antibody - antigen cross reactivity. The body mounts a reaction to the Strep and it also as an innocent bystander, damages the heart, brain , skin. joints etc. in RF. These various body structures look to the immune system as does the Strep - called Molecular Mimicry.

How do you make a diagnosis of group B hemolytic strep?

Based on microbiology - Its hemolytic on a blood culture agar.

For a quick diagnosis:

Based on ab- ag complex - A quickey strep test- a Q test.

After a cotton swab test you look for the antigen of the strep - an immunologic diagnosis. Your substrate also includes the antibody and if the two are there you get a reaction.

Why the big fuss over whether a child has strep throat? - because of the possible consequence of RF:

The Jones criteria: Major manifestations of RF:

- carditis - pancarditis involving all layers of the heart

- polyarthritis

- Sydenham's chorea

- erythema marginatum

- subcutaneous nodules

Minor manifestations:

- fever

- arthralgia

- previous RF

- increased erythrocyte sedimentation rate or positive C-reactive protein.

- prolonged P-R interval

RF has a relation to the different parts of the strep wall:

- the so called M protein ( involved in the virulence on the strep) cross reacts with the sarcolemma and myosin in the human cardiac muscle.

- Cell membrane lipoproteins cross react with antigens in neurons and the caudate nucleus which is responsible for the chorea (abnormal movements) seen in a child with RF.

- Cell wall CHO react with glycoproteins in the heart valve.

Here we see the way Molecular Mimicry of the cross reacting ab - ag complexes can cause the various manifestations of RF.

The pathonamonic inflammatory lesion in the myocardium is the aschoff body. This is the localized aggregate of inflammation in the intersitium, not within the muscle cells but in the connective tissue between the muscle cells. They tend to be around blood vessels and are composed of characteristic cells, some of which may be multinucleated giant cells( the aschoff giant cells), histiocytes , and modified muscle cells. Some of the cells have elongate "caterpillar" nuclei. See figure #1.

.

What does RF do?

- During the acute phase - can cause arrhymias, heart failure, and occasionally a person dies in the acute phase of left ventricular failure. Essentially RF is a pancarditis , or an immunologically mediated inflammation, involving all levels of the heart - peri, myo, and endocardiums as well as the valvular endocardium.

- The main worry is the chronic sequelae of the recurrent attacks of RF that lead to a

scarred deformed valve - most commonly the mitral valve. In the slide we know the mitral valve is being depicted because we see the smooth left atrium compared to the rough right atrium. The valve is stenotic. ** RF is the only factor that can cause mitral stenosis as opposed to the many factors that cause mitral valve insufficiency.**

It is fusion of the commissures ( The analogy that was used - imagine that you sewed together the corners of your mouth and also that the valve resembles the mouth of a fish- hence the name fish mouth valve). There is scarring of the valve that inhibits the valve's fused commissures to allow it to open to its fullest extent. This fusion is the classic post inflammatory RF lesion.

The commissures are once again fused but now the valve also has a fixed opening. The insufficiency is the consequence of the rolling back of the edges of the valve leading to a permanent somewhat rectangular opening. This picture has already been presented with the aortic valve as well, but the difference lies in the fact that the mitral valve has other components that the aortic does not have. Namely, the cordae tendini and papillary muscles which can of course be affected in mitral valve disease.

The valve appears to have had molten candle wax drip down over it. The cordae become thick, fused, and shortened as a consequence of the damage. Therefore, the leaflet of the valve almost seems to directly insert into the top of the papillary muscle. The consequences of this retraction of the cordae are the insufficient closure of the valve.

Old replacements:

- Caged ball valve - there were a variety of problems associated with theses valves:4

- Thrombus formation of the prosthetic valve was too common.

Newer valves:

1) St. Jude mechanical valve- It is a double flap closure valve and does not always have part of the prosthesis (the occluder) in the way of blood flow as in the caged ball valve does. This gives a relatively unimpeded laminar flow of blood as compared to the other.

2) The porcine valve prosthesis ( pig valve) -

The pig aortic valve's leaflets are actually sewn into a cloth covered material called a stent . (This is all factory produced.) The valve is then sewn into the heart of a patient. The valve is completely self supporting - mimicking the original anatomy of the aortic valve.

The great thing about the pig valve is that its self supporting valve can be used for any valve replacement (mitral, tricuspid, and also rarely in the pulmonic valve as well) in the heart, not just the aortic. Of course, the valve has to be placed in the right direction for all of these different replacements, and the appropriate size must be used as well.

Bovine valves have also began to be manufactured now as well.

These newer valves are also prone to problems- but not as great as the caged ball model.

- These valves could also develop thrombosis

- The valves are subjected to the same wear and tare as the native aortic valve experienced and therefore have a tendency to deteriorate - they may calcify and become stiff. They can break apart and become insufficient.

In general problems related to prosthesis:

- prosthesis endocarditis

- prosthesis dehiscence

- prosthesis dysfunction

a. obstruction

- thromboembolus

- hemorrhage

Question -What is the average life span of these newer valves?

The pig valve has an anticipated failure of 1/3 after about 10 years, so that this would not be the choice valvular replacement for a child or young adult. The St. Jude's valve could last a lifetime if the patient is also kept on anticoagulants. The trade off lies in the idea that with the pig valve one might not have to be maintained on a lifetime anticoagulant regime.

How is it that humans accept pig or cow tissue without rejection?

In general you can not. Gradual deterioration of the porcine valve does not relate to immunologic factors . Curiously, these substances are not antigenic, partly because of the way they are treated or manufactured. The pig aortic valve is not implanted as a living metabolically active tissue. The pig tissue is treated with glutaraldehyde which is essentially a "tanning process". So, basically you are inserting a piece of tanned shoe leather into a patient. Due to this process the foreign tissue is rendered non - antigenic. It is believed that the treatment somehow binds up haptens that would have been immumologic determinants. Therefore, there is no antibody reaction to the tissue.

Gortex (?) was also used in an attempt to construct prosthetic heart valves - this was not a success.

Question - Is there any predisposition to survival of heart valves in certain individuals?

Answer - In general no. In the past, some young children seem to have a predisposition to valve calcification. The age cut off for what is considered young in the literature is <>

Question - Is there a problem with valve replacement in people with tissue diseases? ( as in Lupus, rheumatoid arthritis etc.)

Answer- In general no.

Mechanical valves can have a blender effect on RBC's, and unless this occurs to a great extent the body's bone marrow can compensate.

With a severely dysfunctional valve, a problem with hemolytic valve can become a problem.

The incidence of different problems with bioprosthetic v.s. mechanical valves:

• Paravalvular leaks
• endocarditis
• degeneration
• thrombosis

A disease in which there are certain cardiovascular problems. Namely, a prolapsed mitral valve, and an aortic dissection and then a patient could subsequently suffer from actasia (?) of the aorta somewhat similar to the syphilitic abnormality where the aortic root just dilates up leading to aortic insufficiency because the valve no longer closes.

Cause and mechanism: An abnormality in fibrilin production because of a genetic defect on chromosome 15.

Fibrilin is normally made as a monomer that goes on to form multimers. In Marfan's disease a defective fibrilin monomer is formed which in turn fails to create viable multimers.

Not all symptoms of the disease are all manifested in one individual with the disease.

Characteristics of Marfan's disease:

- Tall stature - height mostly due to long legs while the torso looks disproportionately short relative to the rest of the body.

- Long arms and digits

- Deformed anterior chest structure - either an inward chest deformity or a pigeon chest deformity (outward chest).

- Thin

- Palate tends to be high and arched.

- Joints tend to be hyperextendable

- a displacement of the lens of the eye - lentis ectopia.

All of these deformities relates to the defect in fibrilin.

Basic structural features of hyaline cartilage:

1. Perichondrium:

• outer fibrous layer of dense IR CT (usual components of CT including capillaries)

• inner cellular (protochondral/chondrogenic) layer populated by mesenchymal cells that can produce fibro/chondroblasts

2. types of cells and arrangement:

• chondrocytes—fill lacunae and maintain matrix; are not replaced

• chondroblasts—actively produce cartilage (GAGS and type 2 collagen)

• chondrocytes are found embedded in lacunae in isogenic cell nests (2-4 cells) at regular intervals

3. components of matrix:

• type 2 and small type 11 collagen

• 75% tissue fluid: hyaluronic acid backbone with proteoglycan bottle brushes; chondroitin sulfate binds to type 2 collagen via chondronectin

• territorial matrix—high concentration of GAGS and low collagen

4. nourishment:

• cartilage is not vascularized; cells obtain nutrients via diffusion through the matrix

• if diffusion is poor or is blocked,the cells hypertrophy, die and the matrix calcifies

5. Types of cartilage:

• Hyaline—most common, glassy

• Articular—hyaline cartilage at joints where synovial fluid (provides nutrients) is present; has no perichondrium

• Fibrocartilage—contains type 1 collagen as well as type 2; collagen oriented in one direction; does not have perichondrium

• Elastic—similar to hyaline but has elastic fibers replace some of type 2 collagen

2. Development and growth of cartilage

1. chondroblasts come from mesenchymal stem cells; also produce fibroblasts that produce fibrous perichondrium; some stem cells remain to form chondrogenic layer

2. an avascular mesenchymal membrane forms and then cartilage forms within it

3. interstitial—cartilage grows from within so it rises like bread dough: chondroblasts divide and secrete more matrix

4. appositional—adds on to outer surface: chondroblasts are generated by perichondrium and secrete matrix near the outside

5. these two mechanisms are not separate and a cell can participate in both. Ex. A chondroblast generated by perichondrium participates in appositional, but if it divides again it can contribute to interstitial

6. isogenic cells nests in adult cartilage is evidence of interstitial growth; small chondroblasts in lacunae near edge of cartilage is evidence of appositional

3. Development of flat bone

   1. develop via intramembranous ossification

   2. initiated in mesenchymal membrane of pluripotential mesenchyme cells surrounded by GAGS and ground substance similar to cartilage except it is vascularized.

   3. development starts when mesenchyme cells near capillary convert to osteoblasts and produce bone matrix—forms spicules

   4. cells lay bone down on surface of spicules by appositional method—makes trabeculae

   5. trabeculae are enlarge in close relationship to BV and grow to encircle them—makes 1 (woven) bone

   6. mesenchyme also generates fibroblasts to make periosteum and some mesenchymal cells remain to form the osteogenic layer or periosteum

   7. diploe—spongy bone, contains marrow

   8. BONE MUST GROW AROUND CAPPILARIES!

4. development of long bone

   1. grow by endochondral ossification

   2. production of cartilage model would be the same as how hyaline cartilage develops since the model for a long bone is hyaline (see B)

   3. mesenchyme converts to chondroblasts and fibroblasts; fibroblasts and mesenchymal cells within perichondrium convert to osteoblasts

   4. vessel penetrates outside of cartilage—converts perichondrium to periosteum—produces osteoblasts

   5. osteoblasts form bony collar underneath periosteum on outside of cartilage (via intramembranous oss)

   6. bony collar blocks diffusion, chondroblasts die, matrix calcifies

   7. calcified cartilage causes more degeneration

   8. dead cells cause osteoclasts to come clean up and BV follow

   9. pluripotential cells make osteoblasts which make bone on surfaces of calcified cartilage near BV

   10. 1⁰ center of ossification—diaphysis

   11. 2^o center of ossification--epyhysis

   12. BONE MUST GROW AROUND CAPILLARIES

1. A break damages the blood supply to the area – avascular

2. Periosteum converts back to Perichondrium

3. Hyaline collagen collar forms

4. Degenerating bone near area of break attracts a blood supply

5. Perichondrium converted back to Periosteum

6. Periosteum starves the chondrocytes => hypertrophy => death => cartilage calcifies

7. Phagocytes, blood supply, osteoblasts attracted to clean up and convert calcified cartilage to bone

8. Immature bone forms on the cartilage scaffolding => compact bone replaces immature

9. Cartilage bump is removed by remodeling

10. Benefit of cartilage is that it holds the two broken ends together in the right place so that the bone mends properly

1. Epiphyseal plate cartilage dies, calcifies  converted to bone

2. Epiphysis and diaphysis welded together

3. Remodeling  conversion of immature to mature Haversian Systems

4. Inner and outer cortex smoothed: inner and outer circumferential lamellae.

In flat bones, sutures close and the plates are welded together.

Bone quality is maintained by continuous remodeling and replacement of Haversian Systems.

Adjustment to physical stress - bone is formed on the side where traction is applied, and resorbed where pressure is exerted.

1. Slow, continuous growth of the epiphyseal plate cartilage

   1. Chondrocytes near the diaphysis hypertrophy  die  calcified

   2. CARTILAGE GROWS AWAY FROM DIAPHYSIS

   3. Metaphysis—conversion of cartilage to bone

2. Elongation of the diaphysis

3. Replacement of cartilage with bone.

4. Can tell difference in H&E because calcified cartilage is basophilic and bone is acidophilic

Appositional growth also occurs to maintain constant diameter.

Stages of Chondrocyte Development

1. Uppermost – resting

2. Dividing cells – isogenic nests

3. Mature Chondroblasts – produce cartilage

4. Hypertrophied and dying cells – larger lacunae

5. Calcified matrix surrounding cells - Metaphysis

6. Replacement of cartilage by bone

Blood Vessel Involvement

1. Chondroclasts drill into calcified matrix

2. Blood vessels follow

3. Osteoblasts form

4. Bone deposited on calcified cartilage

Flat Bones Grow in Thickness, Flat Bones in Diameter

The outer surface enlarges by intramembranous ossification

(osteoblasts)

Osteoclasts on the inside break down bone => enlarging the

medullary cavity

Thickness of cortex increases slightly as bone thickens

Blood vessels that enter the Periosteum become incorporated

into Volksman’s canals

Remodeling converts immature bone into compact bone

Sutures are DICT

Fontanelles are mesenchymal membranes that have not been

converted to bone

Remodeling must occur in the skull because the curvature must

be reduced to accommodate the growing brain.

Long bones must be remodeled as the individual grows.

1. Whipple’s is the 3^rd most common IBD

2. Whipple’s can associate itself with EA

3. Older white men mostly get this dx

4. Mr. Whipple from the Charmin commercial needed soft TP for his diarrhea

5. Bowel ds. And joint disease occur – treating 1 gets rid of the other

• Lots of problems come from sx of IBD,

• Chiropractic has 40% success rate w/ IBD, which is same as medical, but no side effects

• IBD - malabsorption, need smaller meals more often, supplement vit & minerals

• A variable combination of chronic or recurrent GI symptoms (attributed to pharynx, esophagus, stomach, SI, etc…) Not explained by structural or biomechanical abnormalities
• Chronic or recurrent
• Lower abdomin pain
• Disturbed defecation – diarrhea or constipation
• Bloating
• NOT EXPLAINED by structural (anatomical) or biomechanical abnormality
• Nervous system seems to be major playor
• So if IBS, that means that all anatomical biomechanical problems have been excluded

• We even know what neuro tracks are involved
• Genetics and environment play a role
• Bowel symptom improvement parallels psychological improvement
• Stress, anxiety

• Adjustments / acupuncture help
• Education of pt - it is not cancer
• Focus on health, not illness
• Some may get antidepressants, but then that can cause more problems for pt
• Exercise can help mental health
• There is not usually a trigger food w/ IBS, but if there is something that bothers them, just avoid that

• Digestive ds that damages SI and decreases absorption
• Essentially have an allergy to gluten (protein in wheat, rye, barley)
• When they eat it, their immune system damages SI
• Starts in jejunum
• Immune system attaches villi (velvety) and leaves behind bowel wall that is flat with no villli - wall is featureless or moonfaced
• No villi = no absorption - malnourished, regardless of quanity of food eaten
• Gold standard for dx is endoscopy w/ biopsy
• Unlike crohn's , no hole developes through the mucosa
• They have eosinophelia (sign of hypersensitivity rxn)
• Signs and symptoms
• Recurring abdominal bloating and pain
• Tough to dx because symptoms look like other ds of GI
• Good test is blood test to see if they have antibodies to gluten - 3 of them
• Screening is not a bad idea
• They screen in Italy - dx comes 2-3 weeks after symptoms start
• In US dx comes > 10 yrs after symptoms
• Tx
• Gluten free diet - can be difficult

• Small bowel vs Large bowel
• Short bowel syndrome - not much bowel left to absorb
• Gall bladder removed - liver empties directly into duodenum, if you eat a huge fatty meal, the liver can’t keep up with enough bile and fat goes by unprepared for absorption….poop out fat
• Disacharidase insufficiency - ex is lactose intolerance
• Lymph obstruction
• Infection of cells of SI or LI - ex is Tropical Sprue
• Excess laxatives
• Some things are global malabsorption, some are just one (think lactose or fat)
• Steatorrhea - fatty stool, common in people w/ cholecystectomy that eats fatty meal, stool floats even after a few minutes
• Need to eat less fat at servings
• Lactose intolerance - eliminated lactose or take an enzyme or take in prepared lactose
  

3 M/c enteritis for malabsorption (if it is global malabsorption - - need lots of diff nutrients)

1. Celiac sprue - m/c

2. Crohn's

3. Chronic pancreatitis

4. Whipples could produce EA

5. Diverticulitis of SI

6. Tropical sprue - they have to have visited to tropics

7. Sx of stomach or SI

• Cholera
  

• People lie and get sick from dehydration causing the electrolyte imbalance
• You must replace fluid and electrolytes to keep people healthy

• The E. coli strain that is in water in foreign place is new to your system and makes you sick
• Nursery diarrhea - epidemic at one time
• Changing diaper after diaper without washing hands gets organism transferred between infants - introduction of the next strain
• Travelers diarrhea

• Custard is essentially a good culture media
• Pastries , processed meats, fish
• It produces a toxin that stimulates vomiting center,

• Neurotoxin that has broader effect then the toxin of staph
• Highest mortality rate of all these even with care
• Sustained heat is only way to kill it, microwave leaves pockets that survive

• Found in poultry
• Self limiting
• Can be carrier without being very sick
• Blood testing for antibodies is negative b/c it collects in the feces
• Montezuma's revenge - testing differentiates between the travelers diarrhea

• More often in 3rd trimester pregnancy

• Prolonged sitting can cause more

• Valsalva manuever

• This is a dialation of veins due to increased systemic or portal pressure

  • The veins have no valves

• Decreases with age

• Caucasion

• Higher income and education levels

• More often sitting

• Puritis - burning and itching (EDUCATE THEM)

  • Anesthetics will help for some time, but does not heal the problem

  • Sitz bath - hypertonic solution - this may pull out some fluid

    • The warmer the water the more blood that comes to the party

  • Donut - NOT GOOD

  • Try foam pillow

  • Standing up

  • Avoid tight fitting clothing

• Hemorrhoidectomy - remove and cauterize

  • Anal plasty may occur later on

• • 75% of the carcinoma of the colon can be found in the last 18 inches of the colon

    • 50% can be reached with your finger

  • Painted blood on fecal matter look

  • Lumbar spine radiographs show signs of carcinoma

    • Paravertebral area

    • Distance between the back of the rectal air shadow and sacrum should be 20mm unless morbidly obese (30mm)

  • Screening

    • Colonoscopy

      • Begin treatment in polyp stage

    • Digital rectal exam

• Blood on the fecal matter

• Check films to see if there is enlargement

• Weight loss is a common finding for colon cancer

• Barium? - high rate of false negatives

• Benign lesion above the surface and surrounded by mucous membranes

• They start their life benign

• Familial polyposis - colonic polyps…concentrated presence in the colon

  • High malignant potential

• Gardeners syndrome - colonic polyps…it is assumed that they will go malignant

  • Frontal sinus for tumor (benign osteomas)

  • Skin lesions

• Peutz-jegher syndrome - there are two things that get tested

  • Low malignant potential

  • Pigmentation around the mouth usually (perioral)

• Juvenile polyposis - classic colorectal disease

  • Low malignant potential

• Chronkite-canada syndrome

  • NO malignant potential

  • Skin pigmentation - but not as specifically located as puetz-jegher (perioral)

    • WIDELY DISSEMINATED OR DISTRIBUTED

• Diverticulum are most often found in the sigmoid colon. This is most likely because of the high pressure zone.
• The sigmoid colon has to work more to empty its self with a highly refined diet
• The diverticulum can be quiet at first, but then when obstruction or proliferation of bacteria begin to start. This might remind you of meckles or appendicitis
• This is the smallest of obstruction that leads to sequestration

• Diverticulitis - this can spread
  Blood supply is compromised, swelling occurs
• It is the most common cause of free air in the abdomen *

  • These will not get golf ball size

  • The wall is thin and there is opportunity for rupture

    • If gas is released it will be seen easily in the upper right quadrant

• This can occur form the esophagus to the sigmoid colon

  • More often the sigmoid

  • Symptoms will be bad enough to go to the hospital

  • May be on antibiotic therapy

  • LLQ pain **

  • Most common cause of free air in the abdomen is a RUPTURED DIVERTICULUM

• MANAGEMENT

  • Early recognition - send to hospital

  • Observation and prevention is what you can assist with.

  • Once the out pocketing occurs you have it forever

  • Anything with small seeds - ELEMINATE from diet

    • No popcorn, or peanut shell

  • The older the patient the more often the deconditioning of the bowel may occur - so you may create a high grade obstruction if there is a significant increase in fiber too quickly

• Why does fiber work?

  • It increases the fecal bulk

• Either meisners or Aurebachs plexus, or both, doesn't appear congenitally

• Without the neural network, colon size won't change

• It is stricture that causes huge dilation behind it

• So the problem is at the stricture ( no manual network)

• Premature infants can have underdevelopment of neural network, it just needs time to mature, smaller needs more often until then

• Biopsy is best diagnosis - flexible fiber optics

• Vestibular apparatus maintains the body (mainly the head) at equilibrium (at balance) and stabilizing the eyes relative to the environment

• Static equilibrium- maintenance of the position of the body (mainly the head) relative to the force of gravity

• Dynamic equilibrium- maintenance of the position of the body (mainly the head) in response to sudden movements such as rotation, acceleration, and deceleration.

• Consists of 2 parts:

• Otolithic organs

• Utricle and saccule- static equilibrium

• Semicircular canals- dynamic equilibrium

• Bony labyrinth surrounds membranous labyrinth filled with endolymph (like ECF).

• Between bony labyrinth and membrane of membranous labyrinth is perilymph (like CSF)

Otolithic organs

• Utricle and saccule

• Saccule connected to utricle by duct.

• Each sensory area consist of a macule that contains the sensory mechanisms

Utricle

• an irregular, oblong membranous sac located on the medial wall of the vestibule.

• lies horizontally

• More sensitive to horizontal acceleration.

• macula consist of sensory hair cells and supporting cells (sustentacular cells)

• Each sensory hair cell has one kinocilium and many stereocilia

• The stereocilia and kinocilium are embedded in a gelatinous membrane, the otolithic membrane, which sits on top of the sensory cells.

• The membrane is produced by the sustentacular cells.

• On the surface of the otolithic membrane are otoliths (or otoconia), crystals of Ca⁺⁺ carbonate which are composed of calcium carbonate and protein.

• These otoliths sensitive to horizontal movements

Saccule

• a flattened, irregularly-shaped membranous sac also located in the medial wall of the bony vestibule.

• saccular macula, having the same struture as the utricle, lies perpendicular and verticle to the macula of the utricle.

• More sensitive to vertical (saggital plane, up and down forward and back) acceleration.

• has two small openings are present in the saccule.

• One is the opening of a duct, called the endolymphatic duct, that communicates with the utricle.

• The other opening communicates with the duct of the cochlea via the ductus reuniens.

Semicircular Canals

• Provide information about rotational acceleration.

• Project in 3 different planes.

• Each canal contains a semicircular duct. At the base is the crista ampullaris.

• = enlarged swellings at base of each canal communicating with utricles

Endolymph Movement in Canals

Movement of Cupula Relative to Body Movement