What Is Helicobacter Pylori (H. Pylori) Infection? H elicobacter pylori infection is a potentially deadly stomach disease characterized by chronic superficial inflammation and ulcerations in 100% of infected patients. This infection disrupts normal defense and…
M acroamylasemia is an acquired enzyme disorder that causes elevated levels of the enzyme amylase (hyperamylasaemia) in the bloodstream. It is characterized by altered amylase molecules that have become abnormally bound with plasma proteins in the bloodstream, commonly IgG (immunoglobulin G) and/or IgA (immunoglobulin A).
The resulting molecule is too large to be properly filtered by the kidneys and excreted in the urine as would be normal unbound amylase, causing sustained elevation of amylase levels in the plasma.
With normal kidney function, a hyperamylasemia without an increase in urine amylase suggests the diagnosis of macroamylasemia, and is confirmed by identifying the macromolecular components.1
Amylase is a an enzyme produced by the pancreas and the parotid glands to digest starch in the diet. Comparatively small amounts are also produced by other organs.
Q: How do the pancreas and parotid glands deliver their amylase for digestion of starch?
A: The parotid glands deliver their amylase into the mouth. The action of amylase in the mouth starts the breakdown of starch as it is chewed and moistened with saliva.
After the starchy food is liquified in the stomach, the mass empties into the duodenum. Here pancreatic amylase is delivered through the common bile duct into the duodenum where it turns starch into maltose sugar. The next step to final digestion of starch is carried out by enzymes in the small intestinal lining that split maltose into its component sugar which is glucose.
Glucose is a simple sugar that can be absorbed into the bloodstream for use in the body. Humans cannot live without adequate glucose.
Distinquishing macroamylasemia from hyperamylasemia due to pancreatic disease is necessary to prevent needless treatment and investigation for pancreatitis.2
P ruritic skin is a symptom of a primary disease that may involve only the skin or a systemic disorder with other features and is characterized by chronic itching.
Q: What part of skin is affected by itchiness?
A: Itching may arise from any layer of skin, depending on the cause.
In the image to the right, the outermost protective surface layer, or stratum cornem, is shown as a thin tan line. It is the top dead layer of the epidermis that normally sloughs off as new cells move up to replace it. The epidermis is shown as a dark pink layer. It is composed of five layers of keratinocytes that flatten as they move upward.
The pink layer under the epidermis is the dermis, or true skin, which is composed of collagen and elastin tissue. It contains oil glands that lubricate skin, sweat glands, blood vessels, nerve endings, lymphatics, and hair follicles. Under the dermis is subcutaneous tissue containing fat cells here colored yellow on the bottom of the image.
Adenocarcinomas are malignant tumors, or cancer, of the small bowel arising out of glandular tissue. They fall in the category of rare neoplasm, comprising only 3% of all gastrointestinal malignancies.
Primary adenocarcinoma is the most common histological (cell) subtype constituting 35–50% of cases.1
Q: What does adenocarcinoma look like?
A: Adenocarcinoma may manifest as strictures, nodules, excavating masses, or annular lesions.2
L ymphadenopathy is an alteration of lymph nodes that is characterized by enlargement of lymph nodes greater than 1.5 cm caused by proliferation (increased production) of lymphocytes within the node.
Q: What are lymph nodes?
A: Lymph nodes are part of the lymphatic system, acting to protect body fluids by filtering out and destroying bacteria and other harmful substances from lymph that is continually carried to them by lymph vessels.
Cleaned lymph is carried away from the nodes by lymph vessels to the bloodsteam where it helps forms blood plasma. Lymph nodes produce various blood cells needed to fight infection which includes lymphocytes.
Lymphocytes are small white blood cells that plays a major role in defending the body against disease. There are two types of lynphocytes: B cells, which make antibodies that attack bacteria and toxins, and T cells which attack body cells themselves when they have been taken over by viruses or become cancerous.
Lymph nodes that become enlarged doing battle with an infection or as a result of injury nearby usually resolve with treatment of the infection or injury. However, if the cause is cancer, the nodes would need to be treated as well as the cancer.
S eborrhea dermatitis is a recurring inflammatory disorder of sebaceous glands characterized by scaly patches of skin, often with bumps.
Seborrhea dermatitis results from the body’s inflammatory reaction to invasion by pityrosporum yeast that naturally inhabits the scalp and skin.1 Inflammation is the normal response to tissue injury and germ invasion.
Pityrosporum is a yeast that is commonly present worldwide. Its development depends on various factors that predispose to pityriasis versicolor, a chronic and mild superficial yeast infection. These infections usually are asymptomatic without itching or pain and without cellular and/or antibody responses.2
Q: Why are the sebaceous glands particularly affected by this yeast?
A: Pityrosporum yeast is an organism that needs oil produced by sebaceous glands to grow. If conditions permit, this yeast invades the superficial layer of skin and hair shafts to reproduce, causing infection. Such conditions include weakened skin due to nutritional deficiencies, excessive build-up of oil on skin, and altered immunity due to systemic disease such as psoriasis.
In adults, areas of skin that are the most affected have the greatest number of sebaceous glands especially the scalp, back, underarms, and the face including the eyelids, eyebrows and side folds of the nose.
All ages are subject to seborrhea dermatitis, and males have a higher occurence than females.
F ollicular hyperkeratosis is an abnormal skin condition characterized by disordered overgrowth of the horny layer of the epidermis with horny plugs filling the openings of hair follicles. The plugs look like bumps in hair follicles.
Follicular hyperkeratosis with corkscrew hairs (coiled hairs in the follicles) appears in scurvy, which is advanced vitamin C deficiency.1
Typical hyperkeratotic papules first appear on the extensor surfaces of the extremities (e.g. the back of upper arms), shoulders, and buttocks.
Phrynoderma is a distinctive form of follicular hyperkeratosis with papule formation in dilated hair follicles believed to be a manifestation of severe malnutrition.
Q: Why does hyperkeratosis develop?
A: Follicular hyperkeratosis develops from lack of necessary nutrients to support healthy skin. Although originally thought to represent only vitamin A deficiency or vitamin C in the case of scurvy, several studies have demonstrated deficiencies of B vitamins and vitamin E. General malnutrition seems to be the strongest association. The clinical picture typically improves with enhanced nutritional status.2
What Is Vitiligo? V itiligo is a pigmentation disorder of the skin characterized by permanent loss of melanocytes in defined areas and, in some patients, antibodies to melanin. Vitiligo has significant psychological impact if occurring before…
Sucrose intolerance is the inability to digest sucrose, a widely available sugar, while sucrosemia is the abnormal presence of sucrose in the bloodstream.
Q: Why cannot the body digest sucrose?
A: Sucrose, such as cane or beet sugar, is a double molecule sugar which must first be digested before being absorbed from the gut into the bloodstream. That is, sucrose must be split into its component single molecules of fructose and glucose, which are then properly absorbed.
The inability to properly digest sucrose results directly from low production and activity of sucrase in the small intestine. Sucrase is the specific enzyme that splits or digests sucrose.
Undigested sucrose does not remain idle. Its presence acts osmotically to draw water from the body into the intestine, causing watery diarrhea.
Meanwhile, microbiota (normal bacteria) in the colon eagerly ferment the abnormally present sucrose that arrives from the small intestine. Fermentation generates short-chain fatty acids and hydrogen gas, which results in bloating pain.1
In sucrosemia, sucrose molecules abnormaly pass through an unhealthy small intestinal lining and enter the bloodstream where there presence is abnormal. Sucrose in the blood is filtered out by the kidneys and excreted in urine.
Positive response to a breath hydrogen test (BHT), involving 1 – 3 hours of time post ingestion of sucrose test dose, signifies malabsorption in the small intestine and fermentation in the colon. If BHT is positive before 60 minutes, the result implies bacteria is abnormally present in the small intestine, causing fermentation there. Endoscopy is used to measure sucrase activity in tissue samples.
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What Is Small Bowel Intussusception?Small bowel intussusception is a bowel derangement that is characterized by the slipping of one section of intestine into another, leading to bowel obstruction.
Acute bowel intussusception is a rare manifestation in adults, which mainly involves the small intestine.1