SMALL INTESTINE 

Congenital anomalies 

1. Meckel's diverticulum (a true diverticulum) is due to persistence of the omphalomesenteric vitelline duct. 
2. Atresia is a congenital absence of a region of bowel, leaving a blind pouch or solid fibrous cord. 
3. Stenosis refers to a narrowing of any region of the gastrointestinal tract, which may cause obstruction. 
4. Duodenal diverticula are areas of congenital weakness permitting saccular enlargement. The duodenum is the most common region of the small bowel to contain diverticula. 
5. Diverticula of jejunum and ileum are herniations of mucosa and submucosa at points where the mesenteric vessels and nerves enter. 

Infections

1. Bacterial enterocolitis may be caused by the ingestion of preformed bacterial toxins, producing symptoms ranging from severe but transient nausea, vomiting, and diarrhea (Staphylococcus aureus toxin) to lethal paralysis (Clostridium botulinum toxin). Ingestion of toxigenic bacteria with colonization of the gut (e.g., Vibrio cholera, toxigenic E. coli, various species of Campylobacter jejuni, Shigella, salmonel
Yersinia, and many others) is another potential cause. 

2. Nonbacterial gastroenterocolitis
a. Viral 
(1) Rotavirus (children)
(2) Parvovirus (adults) 
b. Fungal-Candida 
c. Parasitic 
(1 ) Entamoeba histolytica 
(2) Giardia lamblia 

3. In HIV patients. Causes of infectious diarrhea in HIV patients include Cryptosporidium, Microsporidia, isospora belli, CMV, and M. avium-intracellulare. 

C. Malabsorption is defined as impaired intestinal absorption of dietary constituents. 
Clinical features include diarrhea,steatorrhea, weakness, lassitude, and weight loss. Steatorrhea results in deficiency of fat-soluble vitamins (A, D, E, K) and calcium. 

1. Celiac sprue
a. Etiology. Celiac sprue (nontropical sprue or gluten enteropathy) is caused by an allergic, immunologic, or toxic reaction to the gliadin component of gluten. There is a genetic predisposition. 

Symptoms:
– Steatorrhea, abdominal distention, flatulence, fatigue, and weight loss

Complications:
– Iron and vitamin deficiency
– Risk of lymphoma (T-cell type)

Extraintestinal manifestation:
– Dermatitis herpetiformis (a pruritic papulovesicular rash with IgA deposits at the dermoepidermal junction) 

2. Tropical sprue

Etiology. Tropical sprue is of unknown etiology, but may be  caused by enterotoxigenic E. coli. 

3. Disaccharidase deficiency is due to a deficiency of brush border enzymes. Lactase deficiency is most common. 

4. Diverticulosis Coli

- Acquired colonic diverticula are present in nearly half of the population over the age of 50
- Diverticula are associated with low-fiber, low-residue diets
- Etiology is most likely high intraluminal pressure required for propulsion of hard, small stools
- Complications include hemorrhage, acute diverticulitis, perforation, fistula formation 

Obstructive lesions

Hernias cause 15% of small intestinal obstruction. They are due to a protrusion of a serosa-lined sac through a weakness in the wall of the peritoneal cavity. They occur most commonly at the inguinal and femoral canals, at the umbilicus, and with scars. They may lead to entrapment, incarceration, and strangulation of the bowel. 

Tumors of the small bowel account for only 5% of gastrointestinal tumors. 

Benign tumors in descending order of frequency include:
leiomyomas, lipomas, adenomas (polyps), angiomas, and fibromas. Adenomatous polyps are most common in the stomach and duodenum and may be single or multiple, sessile or pedunculated. The larger the polyp, the greater the incidence of malignant transformation. 

Malignant tumors, in descending order of frequency, include: endocrine cell tumors, lymphomas, adenocarcinomas, and leiomyosarcomas. 

Idiopathic Inflammatory Bowel Disease (IBD)

- Chronic, relapsing, idiopathic inflamamtory disease of the GI tract
Crohn’s Disease
– Transmural granulomatous disease affecting any portion of the GI tract
Ulcerative Colitis
– Superficial, non-granulomatous inflammatory disease restricted to the colon

Ulcerative Colitis
- Bloody mucoid diarrhea, rarely toxic megacolon
- Can begin at any age, peaks at 20-25 years
- Annual incidence of ~10 per 100,000 in US
- Negligible risk of cancer in the first 10 years, but 1% per year risk of cancer thereafter
- Good response to total colectomy if medical therapy fails

Macroscopic
- Normal serosa
- Bowel normal thickness
- Continuous disease
- Confluent mucosal ulceration
- Pseudopolyp formation

Microscopic
- Crypt distortion + shortening
- Paneth cell metaplasia
- Diffuse mucosal inflammation
- Crypt abscesses
- Mucin depletion
- Mucosal ulceration

Crohn’s Disease

- Variable and elusive clinical presentation with diarrhea, pain, weight loss, anorexia, fever
- Can begin at any age, peaks at 15-25 years
- Annual incidence of ~3 per 100,000 in US
- Many GI complications and extracolonic manifestations
- Risk of cancer less than in UC
- Poor response to surgery 

Macroscopic
Fat wrapping
Thickened bowel wall
Skip Lesions
Stricture formation
Cobblestoned mucosa
Ulceration

Microscopic
- Cryptitis and crypt abscesses
- Transmural inflammation
- Lymphoid aggregates +/- granulomas
- “Crohn’s rosary”
- Fissuring
- Neuromuscular hyperplasia

THE THYROID GLAND

The thyroid gland develops embryologically from the developing pharyngeal epithelium that descends from the foramen cecum at the base of the tongue to its normal position in the anterior neck. This pattern of descent explains the occasional presence of ectopic thyroid tissue, most commonly located at the base of the tongue (lingual thyroid) or at other sites abnormally high in the neck. 

Glycogen storage diseases (glycogenoses)

1. Genetic transmission: autosomal recessive.

2. This group of diseases is characterized by a deficiency of a particular enzyme involved in either glycogen production or degradative pathways.

Diseases include:
on Gierke disease (type I)
(a) Deficient enzyme: glucose-6-phosphatase.
(b) Major organ affected by the buildup of glycogen: liver.

Pompe disease (type II)

(1) Deficient enzyme: α-glucosidase(acid maltase).
(2) Major organ affected by the buildup of glycogen: heart.

Cori disease (type III)
(1) Deficient enzyme: debranching enzyme (amylo-1,6-glucosidase).
(2) Organs affected by the buildup of glycogen: varies between the heart, liver, or skeletal muscle.

Brancher glycogenosis (type IV)
(1) Deficient enzyme: branching enzyme.
(2) Organs affected by the buildup of glycogen: liver, heart, skeletal muscle, and brain.

McArdle syndrome (type V)
(1) Deficient enzyme: muscle phosphorylase.
(2) Major organ affected by the buildup of glycogen: skeletal muscle.

Anemia (Disorder of Hematopoietic System) - Probably the most common effect of nutritional deficiency. Any factor that decreases hematopoiesis can cause an anemia.

A. Iron deficiency - Widely recognized as the most important cause of anemia, It is indicated that ½ of all pregnant women and infants are affected, as are ~13% of all adult women.

1. Dietary factors - Availability of iron from different food sources and mixtures.
2. Malabsorption – One third of patients with inflammatory bowel disease (IBD) have recurrent anemia and 30% or more of patients who have had partial gastrectomy will develop iron deficiency anemia.
3. Blood loss - Menses, gastrointestinal bleeding 
4. Increased demand - Pregnancy, growth in children.
5. Congenital - Atransferrinemia
6. Importance of multiple factors.
7. Pathophysiology - Initially iron is mobilized from reticuloendothelial stores and increased intestinal absorption occurs. Total iron stores are depleted, serum iron levels fall. In severe cases in peripheral blood, the red cells become smaller (microcytic) and their hemoglobin content is reduced (hypochromic).  

B. Megaloblastic anemias- Characterized by the presence of abnormal WBCs and RBCs. In severe cases, megaloblasts (abnormal red cell precursors) may be present. These anemias are a consequence of disordered DNA synthesis.
1. Folate deficiency - Can be caused by:
a. Dietary deficiency
b. Malabsorption (celiac disease)
c. Increased demand (pregnancy & lactation)
d. Drugs - methotrexate, anticonvulsants, oral contraceptives, alcoholism.
e. Liver disease

2. Cobalamin (vitamin B12) deficiency - Almost always a secondary disorder that can  be caused by:

a. Intrinsic factor deficiency (pernicious anemia due to autoimmune destruction of the gastric mucosa)

b. Malabsorption

3. Pyridoxine (vitamin B6) deficiency- most commonly associated with alcoholism.

C. Other factors known to be frequently associated with anemia would include protein-calorie malnutrition, vitamin C deficiency, and pyridoxine deficiency (usually associated with alcoholism).

D. Other anemias not particularly associated with nutritional disease would include hemolytic anemia
(decreased red cell life span) and aplastic anemia (failure of marrow to produce new cells).  

Acne vulgaris is a chronic inflammatory disorder usually present in the late teenage years characterized by comedones, papules, nodules, and cysts.
 - subdivided into obstructive type with closed comedones (whiteheads) and open comedones (blackheads) and the inflammatory type consisting of papules, pustules, nodules, cysts and scars.
 - pathogenesis of inflammatory acne relates to blockage of the hair follicle with keratin and sebaceous secretions, which are acted upon by Propionibacterium acnes (anaerobe) that causes the release of irritating fatty acids resulting in an inflammatory response.
 - pathogenesis of the obstructive type (comedones) is related to plugging of the outlet of a hair follicle by keratin debris.
 - chocolate, shellfish, nuts iodized salt do not aggravate acne.
 - obstructive type is best treated with benzoyl peroxide and triretnoin (vitamin A acid)
 - treatment of inflammatory type is the above plus antibiotics (topical and/or systemic; erythromycin, tetracycline, clindamycin).

 LUNG ABSCESS  Lung abscess is a localised area of necrosis of lung tissue with suppuration.

 It is of 2 types:

 - Primary lung abscess that develops in an otherwise normal lung. The commonest cause is aspiration of infected material.

 - Secondary lung abscess that develops as a complication of some other disease of the lung or from another site

ETIOPATHOGENESIS.

 The microorganisms commonly isolated from the lungs in lung abscess are streptococci, staphylococci and various gram-negative organisms. These are introduced into the lungs from one of the following mechanisms:

 1.   Aspiration of infected foreign material.

 2. Preceding bacterial infection.

 3.  Bronchial obstruction.

 4. Septic embolism.

 5. Miscellaneous (i) Infection in pulmonary infarcts, (ii) Amoebic abscesses, (iii) Trauma to the lungs. (iv) Direct extension from a suppurative focus.

Abscesses may be of variable size from a few millimeters to large cavities, 5 to 6 cm in diameter. The cavity often contains exudate. An acute lung abscess is initially surrounded by acute pneumonia and has poorly-defined ragged wall. With passage of time, the abscess becomes chronic and develops fibrous wall.

Microscopic Examination

The characteristic feature is the destruction of lung parenchyma with suppurative exudate in the lung cavity. The cavity is initially surrounded by acute inflammation in the wall but later there is replacement by exudate of lymphocytes, plasma cells and macrophages. In more chronic cases, there is considerable fibroblastic proliferation forming a fibrocollagenic wall.