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What is inflammation of the lamina propria?

Chronic Gastritis – Chronic gastritis is a persistent inflammatory reaction in the gastric mucosa that is characterized by the accumulation of lymphocytes and plasma cells in the lamina propria. Chronic active gastritis implies that ongoing active inflammation is causing damage to epithelial cells.

On gastric biopsy, chronic active gastritis shows acute inflammatory cells infiltrating gastric epithelium in addition to a chronic inflammatory cell infiltrate in the lamina propria (see Fig.9-4B ). By far the most common cause of chronic gastritis in the United States is chronic bacterial infection of the stomach by Helicobacter pylori (see Fig.9-4C ).H.

pylori is adapted to live in the low pH environment of the gastric lumen, and infection is common and often persists throughout life unless it is eradicated by treatment with antibiotics (often a combination of three antibiotics is employed).H. pylori initiates a chronic immunoreaction that usually results in the formation of germinal centers in the gastric mucosa (antrum and fundus).

• While the bulk of organisms remain extracellular in the mucous layer adherent to gastric mucosa, the ongoing immunoreaction results in persistent acute and chronic inflammation with ongoing injury to the gastric epithelium.
• Over time, infection can result in metaplasia of the gastric mucosa to small intestinal type mucosa or loss of specialized gastric epithelium (atrophy).

Some strains of Helicobacter are associated with a more intense immune response, but host factors are probably also important. Eradication of the bacterium usually terminates the chronic gastritis but does not result in the regeneration of normal mucosa if atrophy has developed.

• Chronic Helicobacter gastritis and the resulting oxygen free radicals and inflammatory mediators predispose to the development of adenocarcinoma that can arise in metaplastic gastric mucosa.
• Chronic gastritis can also result from autoimmune gastritis (e.g., pernicious anemia) that specifically destroys parietal cells and can ultimately result in gastric atrophy with the loss of all acid-producing parietal cells.

Since the stomach is no longer acidified, gastrin levels increase markedly in an attempt to stimulate acid secretion. High gastrin levels drive the hyperplasia of neuroendocrine cells in the gastric mucosa. Neuroendocrine hyperplasia is very prominent in pernicious anemia and may form microscopic neuroendocrine tumors (microcarcinoids).

What medications cause colon inflammation?

2. Drug induced inflammatory bowel like diseases. Drugs that have been linked to cause or worsen IBD like conditions include isotretinoin, antibiotics, non-steroidal anti-inflammatory drugs (NSAIDs), oral contraceptives, mycophenolate mofetil, etanercept, ipilimumab, rituximab and sodium phosphate.

What are the symptoms of ileitis?

Cytomegalovirus – Cytomegalovirus (CMV) infection of the GI tract most frequently causes esophageal ulcers and colitis, whereas small bowel involvement occurs in only 4% of GI cases, Disease usually occurs in immunosuppressed patients, including those with AIDS or transplant recipients.

Of note, AIDS patients with CMV often have concurrent infections (eg, MAC). Symptoms include fever, abdominal pain, watery diarrhea, or bleeding. Endoscopic findings include erosions, ulceration, and mucosal hemorrhage; a mass lesion may also occur. The prototypical ulceration has a well-defined, punched-out appearance.

The pathogenesis involves ischemic mucosal injury secondary to infection of the vascular endothelial cells. The diagnosis is by demonstration of typical CMV inclusion bodies by routine histologic examination, culture, staining for CMV antigen, or DNA,

What is lamina propria associated with?

Hence, Lamina propria is connected with ‘ Intestine ‘.

Why is the lamina propria important?

Lamina propria – The epithelium attaches to a loose connective tissue called the lamina propria. This is the middle layer of the mucosa. The lamina propria is composed of structural protein molecules, nerves and veins. It carries blood supply to the epithelium while holding the cells in place and binding them to the smooth muscle below.

Can intestine inflammation go away?

Is there a cure? No, IBD cannot be cured. There will be periods of remission when the disease is not active. Medicines can reduce inflammation and increase the number and length of periods of remission, but there is no cure. How long will IBD last? IBD is a lifelong (chronic) condition.

1. A few patients find their disease becomes milder (“burned out”) after age 60, but many do not.
2. Do I have to take medicine forever? Probably.
3. IBD is a chronic disease, and most patients need a maintenance medicine to ease symptoms and reduce the number and severity of flares.
4. Most maintenance medicines act fairly slowly, so if you have an active flare, you may need to take additional medicine temporarily.

Are there some medicines that can get me out of a flare quickly? Yes. These are not necessarily used long term because of side effects. Patients will often change over from rescue medicines to long-term maintenance medicines. Rescue medicines include steroids such as prednisone and cyclosporine.

• Why do I need to keep taking medicines when I feel well? It’s important to keep taking maintenance medicines because they reduce the recurrence of flares.
• For biologic medicines (like infliximab, adalimumab, and certolizumab) it is important to keep taking them to prevent the formation of antibodies against the medicine.

The formation of antibodies can lead to allergic reactions and loss of benefit from the medicine. Taking biologic medicines regularly can maintain their good effect. Why might I need a colonoscopy? A colonoscopy is used to make the initial diagnosis of Crohn’s disease or ulcerative colitis.

A colonoscopy can also assess the symptoms of IBD flares and the response to treatment. A third important use of a colonoscopy is to screen for early colon cancer or to look for abnormal cells that may turn into cancer cells. Will surgery cure my IBD? No, but surgery can be very helpful. For patients with ulcerative colitis, removal of 97% of the colon dramatically reduces symptoms.

Surgery is no picnic, but it can often dramatically improve the quality of life of someone with severe colitis. There are several ways to reconnect the intestine after the colon is removed, each of which has pros and cons. The effect of surgery for Crohn’s disease can often be like pushing a giant reset button, as surgery can remove scarred tissue and strictures, fistulas and abscesses that cause a lot of symptoms for which medicines are not very effective.

1. After surgery for Crohn’s disease, maintenance medicines are often more effective and help prevent further complications that lead to requiring further surgery in the future.
2. Is it dangerous to suppress (weaken) the immune system for the rest of my life? There are some risks in suppressing or weakening your immune system.

Viruses that stay in your body, like the chicken pox virus, are more likely to be activated (cause shingles) in people taking immunosuppressives such as azathioprine and methotrexate. Bacterial infections of the skin and soft tissues are more likely in people taking anti-TNF medicines.

However, for many, all these risks are outweighed by the risks of complications of IBD, which accumulate over time. You can reduce some of these risks. You can discuss early vaccination with your doctor. Also, after some years in remission some patients take a “drug holiday” and stop the immunosuppressive medicine with close monitoring by their doctor for any recurrence of inflammation.

If you are on anti-TNF therapy and you are in the final trimester of pregnancy or going to have an operation, your doctor may adjust your dosing schedule to minimize complications. Could any condition other than IBD be causing my symptoms? Yes. Patients with IBD can get IBD-like symptoms for other reasons.

• Infections can cause diarrhea.
• Previous inflammation can cause increased sensitivity of the nerves in the intestine and make you very sensitive to intestinal cramping.
• Overgrowth of bacteria in the small intestine can cause cramping and gas.
• This is why you should visit a health care provider if there is a change in your symptoms because it might not be a flare of IBD.

Why shouldn’t my pain be treated with narcotics? Narcotics treat the symptoms, not the cause (inflammation) of IBD. Narcotics can make the inflammation worse. Research has shown that patients with IBD who use narcotics are more likely to have severe abdominal infections (abscesses), strictures and intestinal obstruction.

We try to avoid prescribing narcotics for IBD because they seem to be harmful. Why not just take prednisone whenever I have a flare? Prednisone has many side effects, including bone loss, diabetes, cataracts, emotional distress and severe acne, which make us want to minimize the use of prednisone as much as possible.

In addition, the longer prednisone or other steroids are used, the less likely they are to work. That’s why we like to save prednisone for when (and if) you really need it to rescue you from a flare. Maintenance medicines are designed to reduce your flares in both number and severity.

How long can your intestines stay inflamed?

What is ulcerative colitis? – Ulcerative colitis is an IBD that causes your colon (large intestine) to become red and swollen. The redness and swelling can last for a few weeks or for several months. Ulcerative colitis always involves the last part of the colon (the rectum).

Does ibuprofen help intestinal inflammation?

What to expect from your doctor – Your provider is likely to ask you a number of questions. Being ready to answer them may reserve time to go over points you want to spend more time on. Your provider may ask:

When did you first begin experiencing symptoms? Have your symptoms been continuous or intermittent? How severe are your symptoms? Do you have abdominal pain? Have you had diarrhea? How often? Do you awaken from sleep during the night because of diarrhea? Is anyone else in your home sick with diarrhea? Have you lost weight unintentionally? Have you ever had liver problems, hepatitis or jaundice? Have you had problems with your joints, eyes or skin — including rashes and sores — or had sores in your mouth? Do you have a family history of inflammatory bowel disease? Do your symptoms affect your ability to work or do other activities? Does anything seem to improve your symptoms? Is there anything that you’ve noticed that makes your symptoms worse? Do you smoke? Do you take nonsteroidal anti-inflammatory drugs (NSAIDs), for example, ibuprofen (Advil, Motrin IB, others), naproxen sodium (Aleve) or diclofenac sodium (Voltaren)? Have you taken antibiotics recently? Have you recently traveled? If so, where?

Sept.03, 2022

Why does my intestines keep getting inflamed?

What causes IBD? – The exact cause of IBD is unknown, but IBD is the result of a weakened immune system. Possible causes are:

The immune system responds incorrectly to environmental triggers, such as a virus or bacteria, which causes inflammation of the gastrointestinal tract. There also appears to be a genetic component. Someone with a family history of IBD is more likely to develop this inappropriate immune response.

What makes colon inflammation worse?

Dear @, Your healthcare team has discussed the following subject with you: causes of flares in inflammatory bowel disease. Here is some additional information. Let us know if you have any questions regarding this information. A flare is a period of time when symptoms and inflammation from ulcerative colitis or Crohn’s disease become active.

Missing medication doses: Even when symptoms are in remission, people with inflammatory bowel disease need to continue to take their medications. Missing doses or taking the medication incorrectly can result in flares of symptoms Non-steroidal anti-inflammatory drugs (NSAIDs): NSAIDs include aspirin, naproxen, and ibuprofen – with brand names that include Aleve, Motrin, Aleve. These medications can cause flares and should generally be avoided. For pain, acetaminophen (Tylenol) can be used up to 3000mg per day. Antibiotics: In some circumstances, antibiotics can cause flares of symptoms. If you are prescribed antibiotics, confirm that this is for a bacterial infection and make your gastroenterologist aware before using the therapy. Smoking: Smoking can increase the possibility of a flare in Crohn’s disease. Keep in mind that this could include prolonged exposure to second-hand smoke. Infections: Sometimes, infection of the gastrointestinal tract (such as c. difficile) can cause flares of symptoms. Your doctor will oftentimes check for this in your stool if you have flares of symptoms.

Other factors can worsen symptoms, without necessarily worsening inflammation:

Stress: Stress can worsen symptoms in patients with inflammatory bowel disease. These symptoms include diarrhea and abdominal pain. Foods: Certain foods can cause symptoms in patients with inflammation in inflammatory bowel disease. There is no direct evidence currently that food can cause a flare in IBD.

For further information, please check out https://www.crohnscolitisfoundation.org/sites/default/files/2019-07/managing-flares-brochure-final-online.pdf

Can colonoscopy detect ileitis?

Conclusions: Ileoscopy during colonoscopy may identify an ulcerative ileitis. This lesion likely contributes to gastrointestinal blood loss and other clinical manifestations, and likely is caused by NSAID use, including those usually associated with low toxicity or at low doses.

What does ileitis pain feel like?

RLQ or Middle Lower Abdominal Pain – The right lower quadrant or middle of your lower abdomen are common Crohn’s disease pain locations. It’s often described as a cramping pain. Pain in this location is most common with subtypes of CD called ileocolitis and ileitis. Together, these subtypes account for 75% of all diagnosed cases of CD.

• Ileocolitis involves inflammation in two places: the ileum (last section of the small intestine ) and part of the colon (large intestine).
• Ileitis, which is about half as common as ileocolitis, affects only the ileum.

This pain often comes on within a few hours of eating a meal.

What is lamina propria in colon?

(LA-mih-nuh PROH-pree-uh) A type of connective tissue found under the thin layer of tissues covering a mucous membrane.

What is another term for lamina propria?

Overview – The lamina propria is a constituent of the moist linings known as mucous membranes or mucosa, which line various tubes in the body (such as the respiratory tract, the gastrointestinal tract, and the urogenital tract). The lamina propria (more correctly lamina propria mucosae ) is a thin layer of loose connective tissue which lies beneath the epithelium and together with the epithelium constitutes the mucosa,

• As its Latin name indicates it is a characteristic component of the mucosa, “the mucosa’s own special layer”.
• Thus the term mucosa or mucous membrane always refers to the combination of the epithelium plus the lamina propria.
• The lamina propria contains capillaries and a central lacteal (lymph vessel) in the small intestine, as well as lymphoid tissue.

Lamina propria also contains glands with the ducts opening on to the mucosal epithelium, that secrete mucus and serous secretions.

What is specific about colon lamina propria?

Abstract – The lamina propria of colonic mucosa normally contains eosinophils, lymphocytes, plasma cells, and a few neutrophils. If the number of such cells is judged to be increased, colonic inflammation is said to be present. However, the number of cells present in normal mucosa has not been clearly established.

1. Mild abnormalities are difficult to identify, yet might be associated with colonic dysfunction.
2. We therefore developed a morphometric point-counting method to quantitatively analyze the areas occupied by different structures in the mucosa of the human colon.
3. A computer was used to move a dot in a rectilinear pattern over the X400 magnified image of biopsy specimens obtained from throughout the colon by colonoscopy.

The structure on which the dot landed was identified and tabulated by a pathologist. In preliminary studies, we established counting parameters that would yield the most representative results. Based on statistical analysis, it was decided to count 98 points in each of seven regions of six biopsy specimens, i.e., over 4000 points per subject.

Results were expressed as percentages of counts landing on a given item, and represented the area of the biopsy specimen covered by that item. Using this method, we determined the range of normal in healthy volunteers. The sensitivity of this method was tested by studying patients with chronic diarrhea previously diagnosed as having or not having mild to moderate mucosal inflammation.

In the patient group, colonic fluid absorption measured by a perfusion technique was directly correlated with epithelial cell counts and inversely correlated with lamina propria cellularity and with the counts of lamina propria neutrophils and plasma cells.

Does lamina propria have gut immune cells?

In the intestinal lamina propria, various kinds of myeloid and lymphoid cells are present. These cells orchestrate gut immune system by communicating with one another through cytokine production or cell-cell contact. There are numerous CD4 + T cells in the lamina propria, most of which are effector or memory T cells.

Are gastric glands in lamina propria?

Gastric Glands in the fundus (body) of the stomach – The epithelium of the mucosa of the fundus and body of the stomach forms invaginations called gastric pits, The lamina propri a contains gastric glands, which open into the bases of the gastric pits, This diagram shows the structure of a gastric gland, a simple tubular gland. The isthmus and neck contain dividing cells (stem cells) immature cells and maturing neck mucous cells, The mature cells move up to replace the surface mucous cells. These mucous cells are very pale staining.

1. Parietal (oxyntic) cells are also concentrated in the isthmus region, but also found in the base and neck of the glands.
2. These are large pale staining cells with a central spherical nucleus.
3. Can you identify them in these sections? (They have a ‘fried egg’ appearance).
4. Parietal cells make hydrochloric acid, and intrinsic factor, which is needed for absorption of vitamin B12 in the terminal ileum.

Chief/Peptic/zymogenic cells are found in the bases of gastric glands. They have a stongly basophilic granular cytoplasm, as they have lots of rER for production of peptin, which is secreted (as precursor pepsinogen), and basally located nuclei. Neuroendocrine cells in the bases of the glands secrete serotonin and other hormones.

1. Look at this high power image of the gastric mucosa from the fundus (main body of the stomach) showing the numerous gastric pits.
2. Can you identify Parietal cells and Peptic cells, surface mucous cells, gastric pits, and the base of the pits,
3. Now take a look at this eMicroscope of the gastric pits and glands in the fundus.

Toggle labels This image may also be viewed with the Zoomify viewer.

What is lamina propria fibrosis?

INTRODUCTION – Eosinophilic esophagitis (EoE) is an antigen-mediated esophageal disease in which esophageal mucosal biopsies reveal an eosinophil-predominant inflammation.1 With chronic eosinophilic inflammation, esophageal fibrosis and remodeling develop and underlie the serious adverse events of EoE.2 – 5 In adults, the signs of EoE remodeling can be quite obvious with fibrostenotic features such as rings and strictures that cause food impactions.6, 7 In children, who often lack these obvious fibrostenotic features, assessing for early evidence of esophageal remodeling can be challenging.

• Endoscopic pinch biopsy specimens reliably sample the esophageal epithelium, but remodeling takes place in the deeper, subepithelial layers of the esophagus that might be beyond the reach of standard endoscopic biopsy techniques.
• Fibrosis within the lamina propria (LP) is evidence of remodeling, and LP can be included in standard endoscopic esophageal biopsy specimens.

However, those specimens often contain only esophageal epithelium either with no associated LP or with LP in quantities insufficient for assessment of subepithelial fibrosis. Indeed, insufficient LP in esophageal biopsies has limited a number of studies that have attempted to evaluate fibrosis in children with EoE.8 – 14 Criteria that have been used to define “adequate” LP in esophageal biopsy specimens are quite variable, and research in this area would benefit considerably from consensus among investigators on these criteria.12 – 15 The mere presence of LP does not guarantee adequacy for assessing fibrosis, because crush artifact is common, and it can render biopsy specimens uninterpretable in this regard.

Studies that have assessed LP fibrosis in EoE biopsy specimens have found that fibrosis is strongly associated with epithelial eosinophilic inflammation, and the authors of one report speculated that, in EoE esophageal biopsies that have no associated LP, the absence of epithelial eosinophilic inflammation implies that the esophagus is not fibrotic.14 The validity of this assumption has not been established, however, and it is not even clear how often LP is included in esophageal biopsies taken from patients without esophageal eosinophilia.

Few studies have focused specifically on the presence and adequacy of LP in esophageal biopsies, with the exception of some studies on post-ablation surveillance of patients with Barrett’s esophagus (in whom detection of subsquamous intestinal metaplasia requires adequate LP).16 We hypothesized that the frequency of obtaining esophageal biopsy specimens with LP adequate for fibrosis evaluation would be higher in patients with EoE than in those without esophageal eosinophilia.

What is the lamina propria of the intestine?

Lamina Propria – The lamina propria constitutes the layer of loose connective tissue and interstitial matrix located just below the epithelium. In the stomach, the lamina propria tends to be relatively inconspicuous, filling the interstitial spaces between the tubular gastric glands.

It is more expansive in the small intestine, where it occupies the cores of the villi and envelops the crypts. In the colon, it again becomes more retracted based on morphology, restricted largely to the regions between crypts. The structural composition of this zone differs fundamentally from that of the basement membrane in terms of its high content of fibrillar collagens and proteoglycans.

However, as shown in Fig.2, there is some overlap in terms of content with basement membrane-associated proteins. Notably, in addition to their reciprocal expression pattern seen in the basement membrane, both tenascin and fibronectin are found as part of the meshwork of the lamina propria interstitial matrix.

• Functionally, this region provides the structural support for the lymphatics and vasculature.
• Furthermore, the lamina propria of the stomach and intestine is also particularly cell-rich, including fibroblasts, lymphocytes, macrophages, plasma cells, and mast cells.
• This large proportion of cells with immune function provides an effective secondary line of defense against potential invading microorganisms and aggregations of lymphoid nodules within the lamina propria of the small intestine give rise to the specialized areas known as Peyer’s patches.

The lamina propria extends to the thin layer of smooth muscle, or muscularis mucosae, which together with the epithelium and basement membrane constitutes the mucosa of the gastrointestinal tract. FIGURE 2, Summary of the major extracellular matrix protein components and their distribution within the basement membrane and lamina propria. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B0123868602003257

What is another term for lamina propria?

Overview – The lamina propria is a constituent of the moist linings known as mucous membranes or mucosa, which line various tubes in the body (such as the respiratory tract, the gastrointestinal tract, and the urogenital tract). The lamina propria (more correctly lamina propria mucosae ) is a thin layer of loose connective tissue which lies beneath the epithelium and together with the epithelium constitutes the mucosa,

1. As its Latin name indicates it is a characteristic component of the mucosa, “the mucosa’s own special layer”.
2. Thus the term mucosa or mucous membrane always refers to the combination of the epithelium plus the lamina propria.
3. The lamina propria contains capillaries and a central lacteal (lymph vessel) in the small intestine, as well as lymphoid tissue.

Lamina propria also contains glands with the ducts opening on to the mucosal epithelium, that secrete mucus and serous secretions.

What is the lamina propria of the colon?

The histology of the wall of the small intestine differs somewhat in the duodenum, jejunum, and ileum, but the changes occur gradually from one end of the intestine to the other.1. Duodenum Slide 162 40x (pyloro-duodenal junct, H&E) View Virtual Slide Slide 161 40x (pylorus, duodenum, pancreas, H&E) View Virtual Slide Look at slide 162 first.

Locate the duodenal portion in this slide and notice the presence of submucosal mucous glands ( Brunner’s glands ). Observe that the ducts of these glands (and, occasionally, some acini) penetrate the muscularis mucosae and open into a crypt of Lieberkühn, After viewing slide 162, move to slide 161 and try to find the duodenal region in this tissue section.2.

Jejunum and ileum Slide 29 40x (jejunum, monkey, H&E) View Virtual Slide Slide 168 40x (ileum, H&E) View Virtual Slide Slide 169 40x (jejunum, H&E) View Virtual Slide Slide 170 40x (ileum, H&E) View Virtual Slide Slide 165 40x (ileum, Alcian blue PAS stain) View Virtual Slide Slide 171 20x (jejunum, vascular inj) View Virtual Slide Slide UCSF 246 40x (jejunum, human, H&E stain) View Virtual Slide Slide UCSF 247 40x (jejunum, human, H&E and silver stain) View Virtual Slide View these sections with the low power objective and identify the mucosa, submucosa and the muscularis externa.

epithelium lamina propria ( or lamina propria mucosa –”propria” means “belonging to” muscularis mucosae ( or lamina muscularis mucosae –”mucosae” here is not plural, but genitive, so this literally means “muscular layer of the mucosa” )

The mucosa, which is clearly demarcated from the submucosa by the prominent muscularis mucosae layer, frequently shows heavy lymphocytic infiltration in the lamina propria. The appearance of the submucosa layer is a bit variable, but, in general, it’s best considered as irregular connective tissue: in slide 29 the submucosa appears more “loose” whereas in slides 168 and 170 it is more dense, and, in slide 169, here the submucosa is edematous and exhibits unusually dilated blood vessels.

You can see the intestinal villi and intestinal glands (crypts of Lieberkühn). Examine the villi at a higher magnification and note that the lining epithelium consists of simple columnar cells (aka enterocytes ) with a brush border and interspersed goblet cells, particularly well-demonstrated in slide 168.

You can observe the distribution of goblet cells in the intestinal epithelium stained with PAS ( slide 165 ). The epithelium lining the villi continues into the intestinal glands. Examine several of these glands in slide 169 and note that goblet cells and enterocytes similar to those lining the villi, cover the upper portions of the gland.

Also, notice that there are many mitotic figures View Image, The cells which line the lower portions of the crypts are less well differentiated. You may be able to see the enteroendocrine cells View Image in this region. These are the cells with spherical nuclei and clear cytoplasm -the secretory granules of these cells are not always stained very well, but, if they are, you should note that the granules are oriented basally.

Slides 246 View Virtual Slide and 247 View Virtual Slide from the UCSF collection have some excellent examples of enteroendocrine cells View Image, Again, the enteroendocrine cells have a clear cytoplasm and, if visible, basally-oriented granules. Slide 247 in particular has been stained with ammonium silver nitrate to demonstrate so-called “argentaffin” cells View Image (which, incidentally, are now known to be “S” or serotonin-secreting enteroendocrine cells -the serotonin in these cells reacts with the silver causing a black precipitate to form).

• Note that there are about 20 different types of enteroendocrine cell, and you are NOT expected to be able to identify a specific type of enteroendocrine cell (e.g.
• The “S” cells described above), but you should know the general histological characteristics and functions of enteroendocrine cells as a whole.

Paneth cells View Image occupy the base of the intestinal cypts/crypts of Lieberkühn. They are not well preserved in slide 169, somewhat better in slide 168, and quite good in slides 29 and 170, These cells are pyramidal shaped with round nuclei located near their base.

They contain brightly eosinophilic (almost orange) secretory granules in the apical cytoplasm. In slide 168, the secretory granules in the Paneth cells stain a refractory brown or green. Just under the mucosal epithelium is the lamina propria (or lamina propria mucosa), which consists of loose connective tissue that fills the spaces between the intestinal glands and forms the cores of the intestinal villi.

Within the core of each villus is a central lacteal, capillaries, and delicate wisps of smooth muscle that extend from the muscularis mucosae below. However, in some regions, the lamina propria may be so packed with a heavy infiltration of lymphoid cells that these finer structures may not be visible.

1. You may hear the term “Peyer’s patches” used to describe such regions in the GI tract.
2. However, technically, Peyer’s patches are found ONLY in the ileum and they are big enough to be visible with the naked eye.
3. The muscularis mucosae (or laminae muscularis mucosae) consists of smooth muscle fibers.
4. Observe that strands of smooth muscle fibers from the muscularis mucosae extend into the cores of the intestinal villi along the central axis.

Contractions of this muscle layer are controlled by ganglion cells and nerve fibers of the submucosal (Meissner’s) plexus View Image located in the submucosa. The muscularis externa consists of two layers of smooth muscle: inner circular and outer longitudinal.

What is normal lamina propria?

Abstract – The lamina propria of colonic mucosa normally contains eosinophils, lymphocytes, plasma cells, and a few neutrophils. If the number of such cells is judged to be increased, colonic inflammation is said to be present. However, the number of cells present in normal mucosa has not been clearly established.

Mild abnormalities are difficult to identify, yet might be associated with colonic dysfunction. We therefore developed a morphometric point-counting method to quantitatively analyze the areas occupied by different structures in the mucosa of the human colon. A computer was used to move a dot in a rectilinear pattern over the X400 magnified image of biopsy specimens obtained from throughout the colon by colonoscopy.

The structure on which the dot landed was identified and tabulated by a pathologist. In preliminary studies, we established counting parameters that would yield the most representative results. Based on statistical analysis, it was decided to count 98 points in each of seven regions of six biopsy specimens, i.e., over 4000 points per subject.

Results were expressed as percentages of counts landing on a given item, and represented the area of the biopsy specimen covered by that item. Using this method, we determined the range of normal in healthy volunteers. The sensitivity of this method was tested by studying patients with chronic diarrhea previously diagnosed as having or not having mild to moderate mucosal inflammation.

In the patient group, colonic fluid absorption measured by a perfusion technique was directly correlated with epithelial cell counts and inversely correlated with lamina propria cellularity and with the counts of lamina propria neutrophils and plasma cells.