📖 General Pathology
Chronic lymphocytic leukaemia
General PathologyChronic lymphocytic leukaemia
Commoner in middle age. It starts insidiously and often runs a long chronic course
Features:
- Lymphnode enlargement.
- Anaemia (with haemolytic element).
- Moderate splenomegaly.
- Haemorrhagic tendency in late stages.
- Infection.
Blood picture:
- Anaemia with features of haemolytic anaemia
- Total leucocytic count of 50-100,OOO/cu.mm.
- Upto 90-95% cells are lymphocytes and prolymphocytes.
- Thrombocytopenia may be seen.
Bone marrow. Lymphocytic series cells-are seen. Cells of other series are reduced,
SMALL INTESTINE pathology
General PathologySMALL 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
Osteogenesis Imperfecta
General PathologyOsteogenesis Imperfecta (OI) (Brittle bone diseases)
It is a group of hereditary disorders caused by gene mutations that eventuate in defective synthesis of and thus premature degradation of type I collagen. The fundamental abnormality in all forms of OI is too little bone, resulting in extreme susceptibility to fractures. The bones show marked cortical thinning and attenuation of trabeculae.
Extraskeletal manifestations also occur because type I collagen is a major component of extracellular matrix in other parts of the body. The classic finding of blue sclerae is attributable to decreased scleral collagen content; this causes a relative transparency that allows the underlying choroid to be seen. Hearing loss can be related to conduction defects in the middle and inner ear bones, and small misshapen teeth are a result of dentin deficiency
VIRAL DISEASES -RABIES
General PathologyVIRAL DISEASES
RABIES (Hydrophobia)
An acute infectious disease of mammals, especially carnivores, characterized by CNS pathology leading to paralysis and death.
Etiology and Epidemiology
Rabies is caused by a neurotropic virus often present in the saliva of rabid animals
Pathology
The virus travels from the site of entry via peripheral nerves to the spinal cord and the brain, where it multiplies; it continues through efferent nerves to the salivary glands and into the saliva.
microscopic examination shows perivascular collections of lymphocytes but little destruction of nerve cells. Intracytoplasmic inclusion bodies (Negri bodies), usually in the cornu Ammonis, are pathognomonic of rabies, but these bodies are not always found.
Sign/Symptoms
In humans, the incubation period varies from 10 days to > 1 yr and averages 30 to 50 days.
Rabies commonly begins with a short period of depression, restlessness, malaise, and fever. Restlessness increases to uncontrollable excitement, with excessive salivation and excruciatingly painful spasms of the laryngeal and pharyngeal muscles. The spasms, which result from reflex irritability of the deglutition and respiration centers, are easily precipitated Hysteria due to fright
Prognosis and Treatment
Death from asphyxia, exhaustion, or general paralysis usually occurs within 3 to 10 days after onset of symptoms
