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Keratomalacia

Image From Gray's Anatomy. Courtesy Wikipedia.org
Image  of Pancreas From Gray’s Anatomy. Courtesy Wikipedia.org

What Is Pancreatic Insufficiency?

P ancreatic insufficiency is a disorder characterized by insufficient exocrine production of pancreatic enzymes for normal digestion of fats, proteins, and carbohydrates that results in maldigestion of these foodstuffs.

Pancreatic insufficiency also causes malabsorption of the fat-soluble vitamins: vitamin A, vitamin D, vitamin E, and vitamin K.

Q: What are the exocrine enzymes produced by the pancreas?

A: Exocrine enzymes produced by the pancreas include amylase for the digestion of carbohydrates, lipase for the digestion of fats, and protease for the digestion of proteins.

While lipases and amylase are secreted in the active form, proteases are secreted as pro-enzymes (need to be activated). Trypsinogen is converted to its active form trypsin in the duodenum by enterokinase, a protease secreted by the enterocytes (surface cells that line the duodenum), and trypsin in turn activates the other pancreatic proteases.1

Pancreatic enzymes are released by the pancreas into the internal pancreatic duct that empties into the common bile duct from which they are pumped through the Sphincter of Odi directly into the duodenum as needed. Tthe Sphincter of Odi is a strong circular muscle that controls the entrance of pancreatic enzymes into the duodenum.

After a meal, enzyme secretion into the duodenum increases quickly reaching peak output within the first 20 to 60 minutes, then decreasing to a stable level before reaching an interdigestive level at the end of the digestive period, that is, about 4 hours after meal intake.2

Medical treatment is with medication that contains enzymes to break down carbohydrates, fats, and protein in food at mealtime. This treatment is safe, effective, and has few side effects.

What Is Pancreatic Insufficiency In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Fieker A, Philpott J, Armand M. Enzyme replacement therapy for pancreatic insufficiency: present and future. Clin Exp Gastroenterol. 2011;4:55-73. doi: 10.2147/CEG.S17634. [↩]
  2. Fieker A, Philpott J, Armand M. Enzyme replacement therapy for pancreatic insufficiency: present and future. Clin Exp Gastroenterol. 2011;4:55-73. doi: 10.2147/CEG.S17634. [↩]

Dyspareunia (Painful Intercourse), Primary

Koilonychia (Hordinsky, Sawaya, and Scher, 2000)

What Is Koilonychia?

K oilonychia is a feature of an iron deficiency state characterized by abnormally shaped nails, called spoon shaped nails, meaning that the normal downward curve is reversed.

Depending on the inadequacy of iron, nails may simply remain flat or with a slight dip without progressing to a reversed curve.

These nails develop vertical ridges from the base to the nail tip that can become deep, called washboard nails.

Q: Are all nails affected?

A: All nails are affected in varying degrees. The small finger shows the least effect while the thumb shows the greatest change which begins as flattening before scooping upward.

Nail Anatomy. Nail Anatomy. A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.org.

A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.

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

Night Blindness – Nyctalopia

What Is Steatorrhea?

S teatorrhea is a condition of abnormal stool composition and consistency that is due to high fat content because fat from food is not  digested and absorbed into the body but rather passes out with stool.1

Q: How does fatty stool look?

A: The stool in steatorrhea appears pale, bulky and may float in the toilet. If stool is loose, it varies from a pudding consistency to whipped cream. If it is solid, it can vary from thin sqiggles to big turds that smear the sides of the toilet bowl. All types have a foul smell.

Fat of any kind must be digested, or broken down, by enzymes into fatty acids and glycerol and then these parts only are absorbed through the small intestinal lining into the body. The failure to digest or absorb fats deprives the body of these foodstuffs needed for many functions such as blood clotting and vital cell parts such as eye and brain structure.

Fat malabsorption produces malabsorption of vitamins A, D, E, and K because these vitamins can only be absorbed along with fatty acids.

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

Sources:
  1. Murray JA, The widening spectrum of celiac disease. American Journal of Clinical Nutrition. Mar 1999;69 (3):354-365. [↩]

Inflammatory Vaginitis

The tiny brown streak is a splinter hemorrhage.
The tiny brown streak is a splinter hemorrhage.

What Are Splinter Hemorrhages In Nails?

S ubungual (under the nail) splinter hemorrhage is characterized by fragility of the underlying capillaries resulting in bleeding under the nail . Bleeding that results looks like a brown streak or splinter.1

Because the streak of blood is not in the nail but under the nail, it does not grow out with the nail. It can be a feature of vitamin C deficiency which resolves with adequate nutrition.

Nail Anatomy. Nail Anatomy. A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.org.

A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.

Splinter hemorrhage can be seen in a diet poor in vitamin C, disorders of food absorption, systemic disease such as psoriasis, nail lichen planus, an aggressive disease that may destroy the nail plate, and endocarditis. Some drugs, such as oral contraceptives, cause vitamin C deficiency.

Who is Affected in the General Population? Both sexes are commonly affected, though it occurs significantly more frequently in males. Where present in females, they were confined to a single digit.2

What Are Splinter Hemorrhages In Nails 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. Monk BE. The prevalence of splinter haemorrhages. Br J Dermatol. 1980 Aug;103(2):183-5. [↩]

Ocular Myopathy

What Is Primary Hyperparathyroidism?

Tissue changes in hyperparathyroidism. Courtesy Quizlet.com
Tissue Changes in Hyperparathyroidism Causing Brown Tumor. Courtesy Quizlet.com

P rimary hyperparathyroidism is a parathyroid disorder characterized by excessive secretion of parathyroid hormone by one or more parathyroid glands for more than 6 months.

In primary hyperparathyroidism, blood calcium levels are high while phosphorus levels are decreased due to the action of parathyroid hormone.

Parathyroid hormone is produced by the four pea sized parathyroid glands that are located on the thyroid gland in the front of the neck. Partly because the thyroid and parathyroid glands share the same anatomic place in the body and partly because they have similar names, they are often confused although they have completely different actions.

Parathyroid hormone normally keeps calcium and the opposing mineral phosphorus levels in balance by drawing calcium as needed from bones to increase it in blood and releasing excess phosphorus through the kidneys to decrease blood levels.

Primary hyperparathyroidism is commonly caused by an adenoma (tumor) in a parathyroid gland (80%) or 15% due to hyperplasia of gland tissue (overgrowth). It is seldom associated with autoimmune disorders. However, cancer is a  possibility.

Q: What is a parathyroid adenoma?

A: A parathyroid adenoma is usually a solitary, well circumscribed, soft, tan reddish-brown nodule with a capsule. Gland tissues outside of the adenoma are normal or slightly shrunken (not needed anymore).1

Untreated, primary hyperparathyroidism results in cyst formations in bone marrow (osteitis fibrosa cystica) and brown tumors in bone tissue. Cysts contain large amounts of fibrous tissue with areas of hemorrhage. Brown tumors contain aggregates of osteoclasts (bone cells), hemorrhage and giant cells resembling neoplasms.2

Here is the symptomatolgy: “Painful Bones, Renal Stones, Abdominal Groans, and Mental Moans.”

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

Sources:
  1. http://quizlet.com/32428692/pathology-of-parathyroid-and-bone-flash-cards [↩]
  2. http://quizlet.com/32428692/pathology-of-parathyroid-and-bone-flash-cards/ [↩]

Hypogonadism In Adult Males That Is Unexplained  

Nail Anatomy. A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.org
Nail Anatomy. A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikimedia.org

What Are Rounded Nails With Curved Ends?

R ounded, curved, dark and dry nails are a well known feature of vitamin B12 deficiency.

Q: How does vitamin B12 deficiency cause the nails to grow this way?

A: Vitamin B12 deficiency affects the nail plate. The nail plate is the hard keratin cover of the finger tip and toe tip, simply called “the nail.” The nail plate is produced by the living nail matrix at its base.

What Are Rounded Nails With Curved Ends In Celiac Disease and/or Gluten Sensitivity?

Dysgeusia (Impaired Taste)

DyspareuniaWhat Is Autoimmune Thyroiditis (Hypothyroidism)?

A utoimmune thyroiditis, also called Hashimoto’s thyroiditis or Hashimoto’s Disease, is an autoimmune destruction of thyroid tissue characterized by insufficient thyroid hormone circulating in the body that causes formation of a goiter (enlarged thyroid gland) and hypothyroidism.

Hypothroidism refers to the condition of markedly reduced secretion of thyroid hormone. There are other causes of hypothyroidism besides Hashimoto’s thyroiditis.

Hashimoto’s thyroiditis is often associated with other autoimmune diseases such as celiac disease.

In Hashimoto’s thyroiditis, a profusion of antibodies are produced, which build up in the blood. Left untreated so that much of the thyroid gland is destroyed, this condition may progress to the very serious and life-threatening condition called myxedema.

Note: In myxedema, protein, electrolytes, and water abnormally accumulate in between cells which produce firm, inelastic puffy skin that is cool, dry, rough, scaly, and may appear yellow; in some people, areas such as the ankles become crusty with a look of tree bark. Many systemic changes develop shown by significant slowing of mental and physical functions. Please see below.

Q: What thyroid tissue is targeted for destruction?

A: In Hashimoto’s thyroiditis, high levels of autoantibodies target thyroglobulin and thyroid peroxidase, leading to inflammation and destruction of the thyroid gland. The resulting fibrosis or scarring of the gland results in lack of thyroid hormone production.

The thyroid gland consists of a large number of closed vesicles that contain a homogenous substance called colloid, which contains the thyroglobulin. Thyroglobulin is an iodine-containing protein secreted by the thyroid gland and stored within its colloid, from which the thyroid hormones thyroxine (T4) and triiodothyroinine (T3) are derived.1

T3 is the active hormone and is made from T4. Thyroid hormones affect metabolism, brain development, breathing, heart and nervous system functions, body temperature, muscle strength, skin dryness, menstrual cycles, weight, and cholesterol levels.

Thyroid hormone production is regulated by thyroid-stimulating hormone (TSH), which is made by the pituitary gland in the brain. Normally, when thyroid hormone levels in the blood are low, the pituitary releases more TSH. When thyroid hormone levels are high, the pituitary decreases TSH production.

Hashimoto’s disease, with or without the development of hypothyroidism, is treated with synthetic thyroxine, which is man-made T4. Health care providers prefer to use synthetic T4, such as Synthroid® (Levothyroxine), rather than synthetic T3, because T4 stays in the body longer, ensuring a steady supply of thyroid hormone throughout the day. The thyroid preparations made with animal thyroid are not considered as consistent as synthetic thyroid.2

What Is Autoimmune Thyroiditis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Taber’s Cyclopedic Medical Dictionary. 19th ed. F.A. Davis Company. Philadelphia, PA. [↩]
  2. National Endocrine and Metabolic Diseases Information Service. [↩]

Impotence

This White Spot Is A Feature of Zinc Deficiency.
This White Spot Is A Feature of Zinc Deficiency.

What Are White Spots And White Bands In Nails?

W hite spots in the nails is a feature of zinc deficiency and white bands signify protein deficiency characterized by abnormal appearance anywhere in one or more nails.

White spots and bands can appear separately or together in nails. There may be just one mark or many marks depending on the level of deficiency.

Q: What part of the nail is affected by zinc and/or protein deficiency?

A: Zinc and protein deficiencies affect the nail plate.

The nail plate is the hard keratin cover of the finger tip and toe tip, simply called “the nail.” The nail plate is produced by the living nail tissue at its base. Here is an illustration of the parts that make up a fingernail:

Nail Anatomy. Nail Anatomy. A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.org.

A. Nail plate; B. lunula; C. root; D. sinus; E. matrix; F. nail bed; G. hyponychium; H. free margin. Courtesy Wikipedia.

What Are White Spots And White Bands In Nails In Celiac Disease and/or Gluten Sensitivity?

Bone Pain

This is a depiction of immunoglobulin E (IgE) antibody which is elevated in allergic reactions.
This is a depiction of immunoglobulin E (IgE) antibody which is elevated in allergic reactions.

What Is Allergic Rhinitis?

A llergic rhinitis is an immune disorder characterized by inflammation of the nasal mucosa by an IgE antibody reaction to an allergen.

An allergen is something that triggers an allergic immune response.

Q: What is the immune response?

A: Implicated in the response is an increase in T gamma-delta intraepithelial lymphocytes (IELs), which is a subset of pro-inflammatory T-cells located in the respiratory mucosa.  Lymphocytes are white blood cells.

When a person with allergic rhinitis breathes in an allergen such as pollen or dust, the body releases chemicals, including histamine that cause allergy symptoms. For example, hay fever involves an allergic reaction to pollen. A similar reaction occurs with allergy to mold, animal dander, dust, and other allergens that are breathed in.

What Is Allergic Rhinitis In Celiac Disease and/or Gluten Sensitivity?

Infertility In Males

Cutaneous Vasculitis. Courtesy quizlet.com
Cutaneous Vasculitis. Courtesy quizlet.com

What Is Cutaneous Vasculitis?

Cutaneous vasculitis is a vascular disease of small blood vessels serving the skin that is characterized by segmental (spotty) inflammation of affected vessel walls resulting in their necrosis (destruction). Scarring is seen in the affected skin that lies over the destroyed blood vessels.

Skin appearance varies from small flat, purplish spots to raised purplish areas over damaged vessels.

In most cases, cutaneous vasculitis results from deposits of toxic immune complexes in the affected vessel walls that is caused by autoimmune activity targeting small blood vessels.1

Cutaneous vasculitis can also result from infection, drug reactions, or malignancies.

Who is Affected in the general Population? Cutaneous vasculitis affects all ages.

The overall annual incidence of cutaneous vasculitis was 38.6 persons per million in 1998.2

What Is Cutaneous Vasculitis In Celiac Disease and/or Gluten Sensitivity?

Sources:
  1. Abenavoli L, Proietti I, Leggio L, Ferrulli A, Vonghia L, Capizzi R, Rotoli M, Amerio PL, Gasbarrini G, Addolorato G. Cutaneous manifestations in celiac disease. World J Gastroenterol. 2006 Feb 14;12(6):843-52. [↩]
  2. Watts RA, Jolliffe VA, Grattan CE, Elliott J, Lockwood M, Scott DG. Cutaneous vasculitis in a defined population–clinical and epidemiological associations. J Rheumatol. 1998 May;25(5):920-4. [↩]