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Muscle Spasm And Muscle Cramps 

Photo by gastroscopy showing ulcer in the antrum area of the stomach.
Photo by gastroscopy showing ulcer in the antrum area of the stomach (lower area).

What Is A Gastric Ulcer?

[dropcap]G astric ulcer is a painful stomach disorder characterized by an open sore involving the mucosa lining and deeper muscle layer of the stomach.

Gastric ulcer is associated with lymphocytic gastritis which is inflammation of the mucosal lining of the stomach. The thick mucosal lining normally protects the stomach from the erosive action of stomach acid.

Q: How do ulcers develop?

A: Ulcers develop if  hydrochloric acid secreted by the gastric glands of the stomach for the purpose of digesting food damages the normally resistant mucosal walls of the stomach. In the reverse, ulcers may be accompanied by achlorhydria (insufficient acid production).

Damage occurs when there is a predisposing factor that alters the health of the mucosal lining. The most common cause is infection with a bacteria called h. pylori bacter, stress and chronic use of the pain relievers aspirin and non-steroidal drugs like ibuprofen.

Smoking tocacco and consuming alcohol aggravate an ulcer but do not cause it to develop.

The most common location for ulcer formation is along the stomach antrum which is the area of the stomach before the pylorus, the lower region that empties liquid stomach contents into the small intestine.

What Is A Gastric Ulcer In Celiac Disease and/or Gluten Sensitivity?

Chronic Fatigue Syndrome 

Intestinal Edema in an 11 Month Old Baby. Courtesy: Nature.com
Intestinal Edema of Duodenum in an 11 Month Old Baby. Courtesy: Nature.com

What Is Small Intestinal Edema?

[dropcap]S mall intestinal edema is characterized by fluid accumulation within the intestinal mucosa so that the intestinal wall appears thick and swollen.

Intestinal edema hampers peristalsis that can result in pain and gas build-up. Peristalsis is the normal rhythmic muscular wave-like action that moves residue along the gastrointestinal tract.

Q: What part of the small intestinal lining is swollen?

A: Any part of the small intestine may be affected. Some causes of edema include allergic reactions, enteropathies such as celiac disease, cow milk enteropthy, yeast infection, parasite infection, inflammatory bowel disease such as Crohn’s disease, and certain medications.

For example, the anti-hypertensive drugs known as Angiotension Converting Enzyme (ACE) inhibitors can cause intestinal angioedema and therefore the patient may present with gastrointestinal complaints.1

What Is Small Intestinal Edema In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. LoCascio E J,  Mahler  S A, and  Arnold TC. Intestinal Angioedema Misdiagnosed as Recurrent Episodes of Gastroenteritis. West J Emerg Med. Sep 2010; 11(4): 391–394. [↩]

Gluten Sensitive Enteropathy (Active Celiac Disease)

canstockphoto17997339What Is Gluten Sensitive Enteropathy?

Gluten sensitive enteropathy is active celiac disease characterized by inflammation of the small intestinal mucosa that results from an inherited immunologic intolerance to ingested gluten.

Q: What does the inflammation do to the mucosa in the small intestine?

A: Inflammation is a cell level immune response to gluten that has these effects on the mucosa:

  • Damages the barely visible villi (multitudinous finger-like structures) by causing atrophy or loss.
  • Likely affects the structural support and microcirculation of the villus, leading to collapse of the villus.
  • Elongates the crypts between villi. The thickening of the crypt is not so much a response to loss of surface enterocytes but represents inflammation of the mucosa.1
  • Increases round cells in the lamina propria and surface epithelial cells leaving few, irregular microvilli (brush border) on the surface of villi.
  • Damage is most intense in the duodenum and decreases toward the large intestine.
  • The extent of the damage to the intestine determines the malabsorptive consequences of the disease. Both gastric and small intestinal permeability are disrupted in patients with celiac disease.2
  • Relationship between active celiac disease and intestinal permeability: There is a clear association between degree of mucosal damage and the intestinal-permeability ratio, and a normal ratio generally implies near-normal small intestinal structure. A raised intestinal permeability of the mucosal lining (leaky gut) could predispose to a high absorption of gluten and exacerbate an existing lesion and hence convert a latent to an overt enteropathy.3
  • Relationship between active celiac disease and tight junction proteins: A study of intestinal permeability showed that the expression of all junction proteins of the small intestinal lining (occludin, claudin 3, zonula occludens 1, and E-cadherin) was already decreased in early stage celiac disease when compared with non-celiac controls, showing leaky gut and confirming the above earlier study by Johnston et al. Junction protein expression correlated positively with mucosal villus structure and negatively with the number of intraepithelial lymphocytes (IELs), the intensity of small-intestinal autoantibody deposits, and serum autoantibodies. The expression of claudin 3 showed a negative correlation with diarrheal score.4
  • Relationship between active celiac disease and inflammation. In celiac disease there is an over production of inflammatory interleukin-15 (IL-15) which inhibits the correct removal of damaged intraepithelial lymphocytes caused by the reaction to gluten. Serum levels of IL-15 are directly correlated with the seriousness of tissue damage.5

  • Relationship between active celiac disease and gut microbiota. Results of a study investigating intestinal microbiota (normal bacterial residents) in patients with celiac disease suggest that with lower levels of the genus bifidobacteria, celiac patients have an imbalance in the intestinal microbiota even while on a gluten-free diet. This fact could favor the pathological process of the disorder. The concentration of bifidobacteria per gram of feces was significantly higher in healthy subjects (2.5 ± 1.5 x107 CFU/g) when compared to celiac patients (1.5 ± 0.63 x108 CFU/g).6

  • Relationship between active celiac disease and endoscopy technique. The most severe degree of villous atrophy was detected when distal duodenal biopsy specimens were taken in addition to a duodenal bulb biopsy specimen from either the 9- or 12-o’clock position (96.4% sensitivity; 95% CI, 79.7%-100%). The difference between the 12-o’clock position biopsy and the 3-o’clock position biopsy in detecting the most severe villous atrophy was 92% (24/26 patients) versus 65% (17/26 patients).7
  • Relationship between active celiac disease and diet adherence. Patients with consistent gluten free diet adherence experience symptomatic responses to dietary gluten (SRDG) faster and more severe in comparison to their prior gluten exposure possibly demonstrating an adept immunological response. Anxiety and depression also enhance the speed of symptom onset and co-existing visceral hypersensitivity is a risk factor for severe reactions to dietary gluten.8
  • Relationship between active celiac disease and atrial fibrillation: Patients with celiac disease, verified by intestinal biopsy, are at increased risk of atrial fibrillation. This observation is consistent with previous findings that elevation of inflammatory markers predicts atrial fibrillation.9

How Prevalent Is Gluten Sensitive Enteropathy?

Sources:
  1. Murray JA, the widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999; 69(3):354-365. [↩]
  2. Murray JA, the widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999; 69(3):354-365. [↩]
  3. Johnston SD, Smye M, Watson RGP. Intestinal permeability and morphometric recovery in coeliac disease. Lancet. Jul 28, 2001;358(9278):259, 2p. [↩]
  4. Rauhavirta T, Lindfors K, Koskinen O, Laurila K, Kurppa K, Saavalainen P, Mäki M, Collin P, Kaukinen K. Impaired epithelial integrity in the duodenal mucosa in early stages of celiac disease. Transl Res. 2014 Sep;164(3):223-31. doi: 10.1016/j.trsl.2014.02.006 [↩]
  5. Stazi AV, Trinti B. Selenium status and over-expression of interleukin-15 in celiac disease and autoimmune thyroid diseases. Ann Ist Super Sanita. 2010;46(4):389-99.DOI: 10.4415/ANN_10_04_06. [↩]
  6. Golfetto L, de Senna FD, Hermes J, Beserra BT, França Fda S, Martinello F. Lower bifidobacteria counts in adult patients with celiac disease on a gluten-free diet. Arq Gastroenterol. 2014 Apr-Jun;51(2):139-43. [↩]
  7. Kurien M, Evans KE, Hopper AD, Hale MF, Cross SS, Sanders DS. Duodenal bulb biopsies for diagnosing adult celiac disease: is there an optimal biopsy site? Gastrointest Endosc. 2012 Jun;75(6):1190-6. doi: 10.1016/j.gie.2012.02.025. [↩]
  8. Barratt SM, Leeds JS, Sanders DS. Factors influencing the type, timing and severity of symptomatic responses to dietary gluten in patients with biopsy-proven coeliac disease. J Gastrointestin Liver Dis. 2013 Dec;22(4):391-6. [↩]
  9. Emilsson L, Smith JG, West J, Melander O, Ludvigsson JF. Increased risk of atrial fibrillation in patients with coeliac disease: a nationwide cohort study. Eur Heart J. 2011 Oct;32(19):2430-7. doi: 10.1093/eurheartj/ehr167. [↩]

Cancer Predisposition In Children 

Mesenteric Lymph Node Cavitation. Courtesy
Mesenteric Lymph Node Cavitation.  Courtesy McBride OM, Skipworth RJ, Leitch D, Yalamarthi S.

What Is Mesenteric Lymph Node Cavitation And Hyposplenism?

[dropcap]M esenteric lymph node cavitation and hyposplenism combination is a rare lymphatic entity. It is characterized by involution (degeneration) of a mesenteric lymph node (abdominal) and absence of functional spleen tissue.

Q: What is happening to the lymph nodes?

A: Lymph nodes are enlarged with central, partly cystic degeneration. When cut open either at surgery or autopsy, milky fluid exudes from the cut surface.

In regards to absent spleen function, the body is highly susceptible to bacterial invasion such as pneumonia because tissues of the spleen, called the pulp, produce specialized white blood cells that protect the body against bacterial invasion and trap foreign antigens.

What Is Mesenteric Lymph Node Cavitation And Hyposplenism In Celiac Disease and/or Gluten Sensitivity?

Muscle Pain and Tenderness, Chronic 

Reproduction of a lithograph plate showing inside of the stomach from Gray's Anatomy. Courtesy Wikipedia Commons.
Reproduction of a lithograph plate showing inside of the stomach from Gray’s Anatomy. Courtesy Wikipedia Commons.

What Is Delayed Gastric Emptying?

[dropcap]D elayed gastric emptying is a stomach motility or movement disorder characterized by abnormally slow movement of gastric contents from the stomach through the pyloric sphincter into the duodenum, causing dyspepsia.

Q: What determines how fast the stomach empties?

A: How fast the stomach empties depends on the pressure of strong coordinated muscle contractions in the top region of the stomach propelling chyme against resistance at the pylorus (base region of the stomach).

Chyme is food that has been dissolved and thoroughly mixed with stomach secretions.

In the digestion of carbohydrate, protein and fat, protein leaves the stomach first (1 hour), then carbohydrates (1 1/2 to 2 hours), and fat takes longest to digest (2-4 hours). Plain water is able to pass through the pylorus within 5 minutes.

What Is Delayed Gastric Emptying In Celiac Disease and/or Gluten Sensitivity?

Lymphoma, Enteropathy-Associated T-Cell (EATL) 

A real photomicrograph of carcinoma of the esophagus. Panorama of 6 photos of a slide at 40x through the microscope. Some areas may appear blurry due to shallow DOF.
A real photomicrograph of carcinoma of the esophagus. Panorama of 6 photos of a slide at 40x through the microscope. Some areas may appear blurry due to shallow DOF.

What Is Cancer Of The Esophagus?

[dropcap]C ancer of the esophagus is a malignancy arising in the stratified squamous cell lining of any part of the esophagus and having a poor prognosis.

This tumor first invades the deeper layers of the esophagus which includes the layer beneath the mucosa (submucosa) and muscle before it may invade structures close to it including the aorta and trachea. Later, it may spread to organs further away such as the liver, lungs and bones.

Q: What is the stratified squamous cell lining of the esophagus?

A: Stratified squamous cells are flat epithelial cells that are composed of several layers, called the epithelium. This type of epithelium forms the surface mucosa that lines the inside of the esophagus.

The esophagus itself is a muscular tube that transports swallowed substances to the stomach. It begins at the cricoid cartilage (Adam’s apple) as a continuation of the pharynx in the throat and ends at the lower esophageal sphincter (LES).

The LES is a circular muscle surrounding the junction of the esophagus and stomach. The LES opens to allow swallowed food and liquids to enter the stomach and closes to prevent their travelling back into the esophagus.

Who is Affected in the General Population?

Esophageal cancer is the fifth leading cause of death in men from cancer worldwide.1

What Is Cancer Of The Esophagus In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Feldman M, Friedman LS, Brandt LJ. Sleisenger & Fordtran’s Gastrointestinal and Liver Disease. ed 9. Philadelphia: Saunders; 2010. pp. 745–767. [↩]

Cancer Of The Pharynx 

Areas of the Pharynx Where Cancer May Occur. Courtesy Wikimedia.
Areas of the Pharynx Where Cancer May Occur. Courtesy Wikimedia.

What Is Cancer Of The Pharynx?

[dropcap]C[/dropcap]ancer of the pharynx is a malignant growth of stratified squamous cells that line the pharynx, or throat.

Q: What are stratified squamous cells that line the pharynx?

A: Stratified squamous cells are thin, flat epithelial cells consisting of several layers forming the surface mucosa that protects underlying layers of the pharynx. These cells lie very close together and have no blood vessels.

The pharynx is the upper passageway of the throat where swallowing food and fluids from the mouth first pass on the way to the esophagus and breathing air passes from the nose and mouth to and from the lungs.

The pharynx provides for speech production, adequate taste reception, and proper hearing through equalization of air pressure in the eustachian tubes.

The pharynx has three areas and pharyngeal cancer can occur in any of them: the nasopharynx behind the nose, the oropharynx behind the mouth, and the hypopharynx or laryngopharynx, just above the larynx. Tonsils, adenoids, and other lymph tissue lie at the back of the throat.

Unfortunately, cancers of the pharynx tend not to be detected until late in their course when symptoms become evident. This makes the prognosis poor. See symptom below.

What Is Cancer Of The Pharynx In Celiac Disease and/or Gluten Sensitivity?

Seborrhea Dermatitis

Swollen Tongue Causing Tooth Indentations. GFW
Swollen Tongue Causing Tooth Indentations. Notice the Accompanying Denuded Area Due to Riboflavin Deficiency and Mild Candida Overgrowth. GFW

What Is A Pale, Smooth, Burning Tongue?

[dropcap]A pale, smooth, burning tongue is an alteration in tongue tissue characteristic of iron deficiency. The tongue is also swollen.1

Additionally, the sore tongue surface may be invaded by candida yeast which takes advantage of the sore tissue.

Iron deficiency itself increases susceptibility to infection.

Q: What is iron deficiency?

A: Iron deficiency results when the level within cells is too low to meet metabolic needs of the body for this mineral.

Deficiency is characterized by impaired red blood cell formation, free-radical disposal, oxygenation of cells, immune response to infection, enzyme activity, cognitive performance, digestion, nail structure, and fetal health.2

Iron is an essential mineral that is required for normal body function. Almost two-thirds of iron in the body is found in hemoglobin, the protein in red blood cells that carries oxygen to tissues. Smaller amounts of iron are found in myoglobin, a protein that helps supply oxygen to muscle, and in enzymes that assist biochemical reactions.

Iron is also found in proteins that store iron for future needs and that transport iron in blood. Iron stores are regulated by intestinal iron absorption.3

What Is A Pale, Smooth, Burning Tongue In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Krause’s Food, Nutrition, & Diet Therapy. 10th Edition. Kathleen Mahan, Sylvia Escott-Stump. 2000. W.B. Saunders Company. [↩]
  2. Kathleen Mahan and Sylvia Escott-Stump, ed. Krause’s Food, Nutrition & Diet Therapy, 10th Edition. Philadelphia, PA. USA: W.B. Saunders Company, 2000. [↩]
  3. http://ods.od.nih.gov/factsheets/Iron-HealthProfessional accessed 12/11/12 [↩]

Progressive Myoclonic Ataxia 

biliary system primary biliary cirrhosisWhat Is Primary Biliary Cirrhosis?

[dropcap]P rimary biliary cirrhosis (PBC) is a biliary tract disease characterized by chronic cholestasis (build-up of bile) and gradual destruction of bile ducts within the liver, called intrahepatic bile ducts, caused by chronic inflammation.

Primary biliary cirrhosis comes under the umbrella term autoimune liver disease in which the end result is immune-mediated hepatocellular (liver cell) or hepatobiliary (bile duct) injury.1

Q: What is the end result of destruction of bile ducts?

A: The end result of destruction of bile ducts is liver damage.

Injured liver tissue from chronic inflammation and the buildup of bile leads to cirrhosis, a condition in which the liver slowly deteriorates and malfunctions.

Scar tissue replaces healthy liver tissue, partially blocking the flow of blood through the liver. Scarring also impairs the liver’s normal ability to control infections, remove bacteria and toxins from the blood, process nutrients, hormones, and drugs, make proteins that regulate blood clotting, produce bile, and effectively replace its own cells when they become damaged.2

The liver is the largest organ within the body. It lies mostly in the upper part of the abdomen on the right side just under the diaphragm. About 70% of liver tissue is made up of cube shaped cells called hepatocytes that do the main work of the liver. Other cells (epithelial) form structure and are arranged in single layers around blood vessels, sinusoids, and bile ducts.

Bile ducts carry bile, a greenish brown liquid made by the liver to the gall bladder for storage until needed to aid in the digestion and absorption of fat and fat-soluble vitamins A, D, E, and K from the small intestine. Bile emulsifies fat eaten in the diet so that the pancreatic enzyme called lypase can break it down into its fatty acid and glycerol components which can then be absorbed into the body.

Bile also carries away waste products produced by normal metabolism and toxic substances that are removed by the liver for eventual elimination in stool. Bile is continually made by the liver from phospholipids, bile acids, cholesterol, and aging blood cells it removes from circulation. As such, bile must continually flow out of the liver to prevent build-up in the liver.

There is no cure for primary biliary cirrhosis.

What Is Primary Biliary Cirrhosis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Trivedi PJ, Adams DH. Mucosal immunity in liver autoimmunity: a comprehensive review. J Autoimmun. 2013 Oct;46:97-111. doi: 10.1016/j.jaut.2013.06.013. [↩]
  2. http://digestive.niddk.nih.gov/ddiseases/pubs/primarybiliarycirrhosis/ [↩]

Angina Pectoris

What Is Angina Pectoris?Coronary Artery Lesion

[dropcap]A[/dropcap]ngina pectoris, or simply angina, is a coronary syndrome characterized by an oppressive substernal pain (pain under breastbone) or pressure brought on by exertion and relieved by rest that results from failure of coronary arteries to deliver adequate oxygen to heart tissue due to ischemic heart disease.

Q: Why do coronary arteries fail to deliver adequate oxygen to heart tissue?

A: Coronary arteries are the blood vessels that serve the heart. In angina, these vessels fail to deliver adequate oxygen to heart tissue because they are narrowed or blocked by fatty buildups, called atherosclerotic plaques or by a blood clot which impair their ability to carry adequate blood that carries the oxygen. Diseased coronary arteries cannot deliver adequate oxygenated blood pumped by the heart to its own muscle cells.

The heart is a muscular organ that is working all the time without rest, so it needs a constant supply of oxygen. When heart muscle has to work harder, it needs more oxygen. Lack of oxygen causes pain which makes the affected person stop activity and rest.

Angina can be stable or unstable. Unstable angina is much more serious and can be life-threatening.

  • Stable angina produces predictable pain and responds to rest and/or medication. It is less serious than unstable angina but can be very painful or uncomfortable. Anything that makes the heart muscle need more oxygen can cause an angina attack in someone with heart disease, including: smoking, cold weather, exercise, emotional stress, obesity, and large meals. Other causes of angina include: abnormal heart rhythms (usually ones that cause the heart to beat quickly), anemia, coronary artery spasm, heart failure, heart valve disease, and hyperthyroidism (overactive thyroid).1
  • Unstable angina produces unpredictable pain that may occur at rest, lasting more than 20 minutes. It is more severe than stable angina and less responsive to medication. Atherosclerosis is by far the most common cause of unstable angina. Oxidized low-density lipoprotein, so-called bad cholesterol, and oxysterols play an important role in atherogenesis, the development of atherosclerosis. Coronary arteries that are narrowed by atherosclerotic plaques can rupture causing injury to the coronary blood vessel resulting in blood clotting which blocks the flow of blood to the heart muscle. Blood clots may form, partially dissolve, and later form again and angina can occur each time a clot blocks blood flow in an artery. People with unstable angina are at increased risk of having a heart attack.2

What Is Angina In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001247/ [↩]
  2. http://www.heart.org/HEARTORG/Conditions/HeartAttack/SymptomsDiagnosisofHeartAttack/Unstable-Angina_UCM_437513_Article.jsp# [↩]