Special Pathology
Most common diseases of the intestine are dyskinesia, inflammatory affections (enteritis, colitis, enterocolitis) and tumours (mostly cancer of the large intestine).
According to their clinical course, inflammation of the small intestine (enteritis) and of the large intestine (colitis) may be acute or chronic.
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Acute Enterocolitis
Acute inflammation of the small and large intestine usually combines with affection of the gastric mucosa and arises after ingestion of spoiled food infected with microorganisms or after ingestion of a large amount of hardly digestable or incompatible foods (gastroenterocolitis).
Clinical picture. The clinic of acute enterocolitis varies from mild illness to fatal outcomes. The onset of the disease is sudden (3—4 hours following ingestion of inadequate food). Its first symptom is dyspepsia (diarrhoea). The body temperature is subfebrile or higher. The tongue is dry and the abdomen distended, tenderness is diffuse. Acute symptoms subside in 8—12 hours and the patient's condition improves in few days. Collapse may occur in severe cases due to poisoning.
Treatment. The stomach should be lavaged and purgative salts given. Sulpha drugs are given with a special diet; subcutaneous injections of sodium chloride are useful in marked dehydration.
Prophylaxis. This consists in adequate hygiene of nutrition, thorough inspection of cooking and foods storage conditions, especially during hot seasons.
Chronic Enteritis
Aetiology and pathogenesis. Chronic enteritis arises due to various causes. These are (1) infection: typhoid fever, dysentery, salmonellosis, etc.; (2) acute enteritis (a forerunner); (3) dysbacteriosis: upset microbial equilibrium in the intestine; (4) alimentary factor: irregular meals, ingestion of cold food, chronic overeating of poorly digestable foods; (5) radioactive exposure; (6) alcohol abuse; (7) allergic factors; (8) congenital enzymopathy; deficient quantity of enzymes responsible for absorption of foods (gluten and lactase deficiency); (9) endocrine factors (diarrhoea in thyrotoxicosis); (10) diseases of other alimentary organs (stomach, hepatobiliary system, pancreas). For example, in the presence of achlorhydria, insufficiently digested food enters the small intestine to irritate its mucosa and to provoke inflammation.
Pathological anatomy. Mucosa of the small intestine is oedematous and hyperaemic. Haemorrhage and ulceration are possible. In grave cases, inflammation may involve all layers of the intestinal wall to cause its perforation.
Clinical picture. The patient usually complains of pain in the umbilical region and distension of the abdomen. Stools are not formed; constipations are alternated with diarrhoea. Nutrition is impaired, the skin is pallid. Signs of polyhypovitaminosis are present: dry skin, brittle and laminated nails. Splashing and rumbling sounds are heard in the right iliac region. Stools contain mucus; microscopy of faeces reveals the presence of drops of neutral fat and muscle fibres. Specific X-ray signs are hypotonia, the
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presence
of gas and liquid in the small intestine, and level relief or
feather-like pattern of its mucosa.
Course. Chronic enteritis can be complicated by involvement of the pancreas, the liver, the large intestine, by development of hypochromic anaemia, and polyhypovitaminosis.
Treatment. Complex therapy is required. It is necessary to take into account the degree of the peptic disorder, complications if any, and the general condition of the patient. In exacerbations of the disease, sulpha preparations, eubiotics, and enzyme preparations (abomin, pancreatin, pansinorm, festal, and others) are indicated.
Prophylaxis. This consists in eradication of possible causes of the disease and timely and thorough treatment of acute enterocolitis, chronic gastritis, diseases of the liver and the pancreas.
Chronic Colitis
Aetiology and pathogenesis. Causes of inflammatory affections of the large intestine are quite varied. Most frequent causes of chronic colitis are infections (dysentery, salmonellosis, tuberculosis, syphilis, etc.), parasites (helminths, protozoa, etc.), and toxic effects (poisoning with arsenic, phosphorus, mercury, etc.). Irregular nutrition, overeating, and chronic constipations can account for development of colitis as well.
In the presence of motor hyperfunction of the small intestine, the ingested food is not processed sufficiently before it enters the large intestine, and it thus irritates its mucosa. Long-standing kinetic disorders cause colitis. Persistent constipations can provoke chronic colitis. Mucosa of the large intestine has the excretory function. It releases microbes and their toxins, i.e. toxic products that circulate in the body in cases with upset metabolism. These factors can become the cause of chronic colitis, e.g. renal dysfunction causes development of colitis. And finally, auto-infection (e.g. coli bacilli which become pathogenic under certain conditions) can stimulate the onset of colitis.
Classification of colites. The following colites are distinguished: I, infectious colites: (1) specific, and (2) non-specific; II, parasitary colites: (1) protozoal (amoebic, trichomonal, lambliogenic), (2) helminthic; III, toxic colites: (1) exogenous and (2) endogenous; IV, alimentary colites; V, symptomatic or secondary colites; and VI, colites of mixed aetiology.
Pathological anatomy. The entire large intestine or its separate sections may be affected by inflammation. Catarrhal, follicular, infiltrative, purulent, ulcerative, and gangrenous colites are differentiated from the standpoints of pathological anatomy.
Clinical picture. The patient with chronic colitis complains of local and general disorders. Local complaints include pain in the lower abdomen or the iliac region, distension of the abdomen, tenesmus, constipation and diarrhoea. General complaints are irritability, deranged sleep, headache, and low moods. Appetite is decreased, nausea and sometimes vomiting occur. Objective examination shows that nutrition is adequate. The study of the abdominal cavity reveals pain by the course of the large intestine and rumbling. Protozoa or helminths can be found in faeces. Stools may also contain traces of blood and mucus; dysbacteriosis is also possible. X-ray examination may reveal spasms, atonia of separate portions of the large intestine, and changes in the relief of the intestinal mucosa. Rec-tosigmoidoscopy and colonoscopy are valuable diagnostic techniques.
According to the clinical course of the disease, mild, medium gravity and grave chronic colites are distinguished. Mild forms of colitis have no pronounced symptoms; only occasional diarrhoea or constipations are observed; the general condition of the patient is not affected substantially.
Signs of the disease are pronounced in chronic colitis of medium gravity. Grave forms of the disease are marked by fever, headache, asthenia, disability, involvement of other organs, and complications (haemorrhage, perforation).
Treatment. A correct treatment is only possible if the cause of chronic colitis has been discovered. Changes in other organs of the digestive system and the presence of complications should also be taken into account. The appropriate diet should be prescribed along with symptomatic therapy (spasmolytics, analgesics, etc.).
Prophylaxis. Prophylactic measures are quite varied; this agrees with the variety of causes that provoke development of chronic colitis. Labour hygiene, sanitary conditions at home, and adequate nutrition are of primary importance. Patients with acute intestinal disorders should be thoroughly examined and treated. Regular out-patient observation of population is also important (control of intestinal parasitosis, treatment of constipation and other diseases of the digestive system that may cause pathologies in the large intestine, e.g. peptic ulcer, chronic gastritis, etc.).
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LIVER AND BILE DUCTS
Methods of Examination
Inquiry
Complaints. Patients with disorders of the hepatobiliary system usually complain of abdominal pain, dyspepsia, skin itching, jaundice, enlargement of the abdomen, and fever.
Pain is localized in the right hypochondrium and sometimes in the epigastrium and differs depending on the cause. Pain may be persistent and dull, or it may be severe and occur in attacks. Persistent pain is usually boring, or the patient feels pressure, heaviness, or distension in the right hypochondrium. Pain may radiate to the right shoulder, scapula, and in the interscapular space (in chronic cholecystitis, perihepatitis and pericholecystitis, i.e. when the process extends onto the peritoneum overlying the liver and the gall bladder, and also in rapid and considerable enlargement of the liver which causes distension of Glisson's capsule). This radiation of pain is quite characteristic of many diseases of the liver and gall bladder, because the right phrenic nerve, innervating the capsule in the region of the falciform and the coronary ligaments of the liver and the ex-trahepatic bile ducts, originates in the same segments of the spinal cord where the nerves of the neck and shoulder originate as well. Pain usually becomes more severe in deep breathing; in adhesion of the liver or the gall bladder to the neighbouring organs, pain is also intensified when the patient changes his posture, and sometimes during walking.
Attacks of pain (biliary or hepatic colics) develop suddenly and soon become quite severe and unbearable. The pain is first localized in the right hypochondrium but then spreads over the entire abdomen to radiate upwards, to the right, and posteriorly. An attack of pain may continue from several hours to a few days during which pain may subside and then intensify again; the attack ends as suddenly as it arises; or pain may lessen gradually. Attacks of pain occur mostly in cholelithiasis. They are provoked by jolting (as in riding) or by fatty food. Pain attacks occur also in hypermotoric dyskinesia of the gall bladder and bile ducts. Pain usually develops quite unexpectedly due to spastic contractions of muscles of the gall bladder and large bile ducts caused by irritation of their mucosa by a stone, and due to comparatively rapid distension of the gall bladder in congestion of bile (e.g. due to obstruction of the common bile duct by a stone). Warmth applied to the liver (provided the attack is not attended by considerable fever) and also administration of cholino- and myospasmolytics
Chapter 7. Digestive System
(atropine sulphate, papaverin hydrochloride, etc.) remove pain characteristic of the colic. An attack of hepatic colic can be attended by subfebrility (fever develops with pain and subsides with alleviation of pain), which is followed by a slight transient subicteric colour of the sclera Or pronounced jaundice in obstruction of the common bile duct by a stone.
Pain developing in dyskinesia of the bile ducts is associated with upset coordination between contractions of the gall bladder and of the Oddi sphincter under the effect of increased tone of the vagus nerve. As a result, bile congests in the ducts, and the gall bladder is no longer emptied. This causes its convulsive contraction. Dyskinetic pain is characterized by the absence of signs of inflammation (leucocytosis, ESR, etc.).
Dyspeptic complaints include decreased appetite, often bitter taste in the mouth, eructation, nausea, vomiting, distension of the abdomen and rumbling, constipations or diarrhoea. These complaints are characteristic not only of diseases of the hepatobiliary system but also of other parts of the digestive system. Causes of these symptoms in diseases of the liver and bile ducts are explained by deranged secretion of bile (and hence impaired digestion of fats in the intestine) and derangement of the detoxicating function of the liver.
Fever occurs in acute inflammatory affection of the gall bladder and bile ducts, in abscess and cancer of the liver, in hepatitis, and active cirrhosis.
Skin itching attends hepatic or obstructive jaundice. It can develop without jaundice, as an early forerunner of the liver disease. Itching is caused by accumulation in the blood of bile acids which are otherwise excreted together with bile, or by stimulation of sensitive nerve endings in the skin. Itching is usually persistent and is a great annoyance to patients during night sleep (to cause insomnia). Severe itching causes scratching of the skin with its subsequent infection.
Icteric colouration of the skin and the visible mucosa (jaundice) is due to accumulation of bile pigments in the blood and tissues. Jaundice may develop unnoticeably to the patient and only the surrounding people may pay attention to the icteric colouration of the sclera and then the skin. In other cases jaundice can occur all of a sudden, following an attack of hepatic colics (in obstruction of the common bile duct by a stone in cholelithiasis). Jaundice may persist for months or even years, only slightly changing in intensity (chronic hepatitis and cirrhosis of the liver, benign bilirubinaemia). For details of the mechanism of developing jaundice and its diagnostic importance see below.
Enlargement of the abdomen (sometimes rapid) can be due to accumulation of ascitic fluid in the abdominal cavity (in obstructed blood
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outflow from the intestine via the portal vein), in considerable meteorism (due to deranged digestion in the intestine in upset bile excretory function), or in pronounced hepato- or splenomegaly. Many chronic diseases are attended by general weakness, non-motivated fatigue, and decreased work capacity.
History of the present disease. When collecting anamnesis, it is necessary to find out if the patient had in his past history jaundice or acute diseases of the liver or the gall bladder (Botkin's disease, acute cholecystitis, cholangitis), attacks of hepatic colics, enlargement of the liver or the spleen, which might be an early symptom of the present disease (chronic hepatitis, liver cirrhosis, chronic cholecystitis, cholangitis, cholelithiasis).
Life history of patient. When inquiring the patient it is necessary to establish factors that might be important for the aetiology of the present disease of the liver or bile ducts: liking for fat and meat foods, exposure to chemical and vegetable poisons (alcohol, carbon tetrachloride, compounds of phosphorus, copper, lead, arsenic, dichloroethane, etc.), poisoning with mushrooms containing strong hepatotropic poisons (e.g. helvellic acid, amanitotoxin, etc.), some infectious diseases (Botkin's disease, lambliosis, typhoid fever, malaria, syphilis, etc.), diseases of the gastro-intestinal tract (gastritis, colitis), and diabetes mellitus. Familial predisposition is also important in the development of some liver diseases (e.g. congenital benign hyperbilirubinaemia) and diseases of the gall bladder (cholelithiasis).
Physical Examination