cvs

1. CVS

2. ENDOCARDITIS
• 1. It is defined as infection of endocardial
surface of heart , which may include one or
more heart valves, the mural endocardium or
septal defect .
• 2. May be classified as follows:
• (a) Subacute bacterial endocarditis .
• (b) Acute bacterial endocarditis .

3. • Bacteremia and septicemi during :
• 1. During dental procedures (streptococcus viridans
• 2. Colorectal cancer and surgeries of bowel and
biliary tract (staphylococcus bivis ).
• 3. Urinary tract infection (mostly enterococci).
• 4. Pneumonia and lung abscess .
• 5. Drug injections (s. aureus) .
• 6. Cardiac catheterization and cardiac surgery.
• 7. Heart conditions like RHD, congenital anomalies
like tetralogy of fallot, atrial septal defect ,
ventricular septal defect, etc.

4. • 8. Immunodeficiency or immunosuppressive states
.
• 9. Malignancy .
• 10. Diabetes .
• Main Causative Organisms
• Bacterial Causative Organisms :
• 1. Staphylococcus aureus and staphylococcus
epidermidis .
• 2. Staphylococcus viridians and bovis .
• 3. Enterococci .
• 4. Pseudomonas aeruginosa (through food
punctures) .

5. • 5. Group of bacteria called HACEK (‘HACEK’
stand for Haemophilus , Actinobacillus,
Cardiobacterium hominis, Eikenella corrodens
and kingella).
• Fungi and Viral :
• 1. Candida albicans .
• 2. Aspergillus and Histoplasma capsulatum .
• 3. Viral infection of the heart.

6. Pathogenesis
• Bacteria may enter from the above mentioned
routes and can get implanted on the cardiac valves
and mural endocardium.
• 1. Destruction of previously damaged valnes heart
diseases like RHD or due to congenital anomalies .
• 2. Conditions producing hemodynamic stress on
the valves cause damage to the endothelium,
favoring the formation of platelet thrombi, which
get infected from circulating thrombi.

7. Pathological Changes
• Typical vegetations of verrucae can be seen
deposited on the valve cusps and leaflets and less
commonly on the mural endocardium.
• Microscopically: The vegetation consist of three
zones –composed of fibrin and platelets, colonies, of
bacteria and acute and chronic inflammatory cell
infiltration .
• Clinical Manifestation
• 1. Malaise, weakness and fatigue .
• 2. Weight loss and anorexia .
• 3. Arthralgia, night sweats, chills and intermittent
fever that may reoccur for weeks .

8. • 4. Loud, regurgitant murmur in the presence
of fever is a classical physical sign .
• 5. Other signs include splenomegaly .
• 6. Other like painful raised lesions in hands
and feet (Osler’s node), splinter hemorrhages
(Roth’s spot) under nail bed , painful
hemorrhagic lesions in palm and sole (Janeway’s
lesion).
• 7. Petechiae of skin, buccal, pharyngeal or
conjunctive mucosa.

9. ATHEROSCLEROSIS
• 1. Atherosclerosis is characterized by intimal lesions
called atheromas or atheromatous or fibrofatty
plaques, that protrude and obstructs the vascular
lumens.
• 2. An atheromatous plaque consists of raised lesion
with soft, yellow core of lipid convered by a firm,
white fibrous cap.
• Natural History of Atherosclerosis :
• 1. Atherosclerosis mainly can be seen into the
intima of large and medium sized muscular arteries.
In small arteries, atheromas can gradually occlude
lumina, compromising blood flow to distal organs
and cause ischemic injury .

10. • 2. Symptomatic atherosclerotic disease most
often involves the arteries supplying the heart,
brain, kidneys and lower extremities. Myocardial
infarction (MI), cerebral infarction, aortic
aneurysms .
• Etiological Factors
• 1. Major Constitutional Risk Factors :
• 1. Age .
• 2. Gender .
• 3. Genetic factors .
• 4. Familial and racial factors .

11. • 2. Major Acquired Risk Factors :
• 1. Hyperlipidemia .
• 2. Hypertension .
• 3. Smoking .
• 4. Diabetes mellitus .
• 3. Minor Risk Factors :
• 1. Obesity .
• 2. Oral contraceptives .
• 3. Lack of exercise .
• 4. Type a behavior pattern or stress .

12. Pathogenesis
• 1. Atherosclerosis is a chronic inflammatory
response of arterial wall, which is initiated by injury
to the endothelium and further interaction between
lipoproteins, monocyte-derived macrophages, T-
lymphocytes and normal cellular constituents of
arterial wall leading to progression of lesion .
• 2. Various aspects of atherogenic process are :
• Role of endothelial injury .
• 3. Intimal smooth Muscle Cell Proliferation :
Stimulated by platelet derived growth factor (PDGF),
fibroblast growth factor, epidermal growth factor,
transforming growth factor - (TGF- ),and losses of
growth inhibitors like TGF- .

13. • 4. Role of blood monocytes .
• 5. Role of hyperlipidemia .
• 6. Thrombosis .
• Pathologic Changes
• There are various morphological forms of
atherosclerosis.
• 1. Fatty streak : There are harmless and are the
precursor lesions of atheromatous plaques .
• Grossly : lesions appear yellowish .
• Microscopically : formed of closely packed
foam cell’s lipid containing elongated smooth
muscle cells and few lymphoid cells .

14. • 2. Gelatinous lesion : There are round or oval lesion
with circumscribed gray elevations about 1cm in
diameter which usually develop in the intima of
aorta .
• 3. Atheromatous plaque : these lesion develop from
the progression of the above stated lesion .
• Grossly : - White to yellowish white lesions (1-
2cm in diameter with raised surface) cut section
shows firm luminal surface with white fibrous cap
and a central core composed of yellow to yellowish-
white porridge like material .
• Microscopically : 1. Superficial luminal part of
fibrous cap is covered by endothelium, which is
composed of smooth muscle cells, dense connective
tissue, extracellular matrix .

15. • 2. Cellular area under fibrous cap is composed of
macrophages, form cells, lymphocytes, smooth
muscle cells and lipid .
• 3. Deeper core consist of extracellular lipid
material, cholesterol, fibrin, necrotic debris and
lipid laden form cells .
• INFARCTION
• Infarction refers to death of tissue called necrosis
caused by an obstruction of tissues blood supply,
which eventually leads to lack of oxygen and the
resulting lesion is referred as an infarct .

16. • Etiology : 1. Thromboembolism or
atherosclerotic plaque .
• 2. Mechannical obstruction .
• 3. Vasoconstriction .
• ANEURYSM
• An aneurysm is a localized abnormal dilatation
of blood vessel occurring due to congenital or
acquired weakening or destruction of the
vessel wall

17. Classification
I. Depending Upon the Composition of the
Wall -
1. True aneurysm : When an aneurysm
involves all three layers of the arterial wall or
the attenuated wall of the heart .
2. False aneurysm : Have fibrous wall and
often occur from trauma to the vessel
leading to an extravascular hematoma that
freely communicates with the intravascular
space .

18. • 2. Depending Upon the Macroscopic Shape and
Size .
• 1. Saccular aneurysms .
• 2. Fusiform aneurysms .
• 3. Cylindrical aneurysms .
• 4. Varicose .
• 5. Racehorse .
• 3. Based on Etiology :
• 1. Atherosclerosis (atherosclerotic aneurysm)
• 2. Syphilis (syphilitic aneurysm)
• 3. Aortic dissecting (dissecting aneurysm)
• 4. Infective (mycotic aneurysm)

19. Atherosclerotic aneurysm
• 1. Most common type of aneurysm, mainly seen in
males above age of 50 years .
• 2. Common site of occurrence is abdominal aorta,
thoracic aorta, iliac and other systemic arteries.
• 3. Macroscopic pathology changes: Lesionscan be
variable in size, usually larger then 5-6cm in
diameter .
• 4. Microscopically pathological changes : Fibrous
tissue can be seen in media and adventitia with
mild inflammatory reaction. The media and inner
part of the media shows remnants of
atherosclerotic plaques and mural thrombus .

20. Syphilitic Aneurysm
• 1. Syphilitic aneurysm is seen in patients suffering
from tertiary stages of syphilis. They usually
develop arteritis , syphilitic aortitic and cerebral
arteritis to development of syphilitic aneurysm .
• 2. Sites mainly involved are ascending part and
arch of aorta; and aortic valve causing aortic
incompetence and left ventricular hypertrophy due
to volume overload resulting in enlarged heart
called ‘cor bovinum’ .
• 3. Pathogenesis : The common cause for
aneurysmal dilatation is inflammation mediated
thinning of tunica media .

21. • 4. Pathologic changes:
• Grossly : The intimal surface is wrinkled
and show tree bark appearance
• Microscopically :
• 1. Adventitia shows fibrous thickening with
endarteritis obliterans of vasavasorum .
• 2. Fibrous scar tissue may extend into
media and intima .

22. Dissecting aneurysm
• 1. It is an aneurysm in which the wall of the artery
dissects longitudinally and blood penetrated the
intima and enters the media layer and dissects the
separated wall of the media and spreads for varying
distance longitudinally . Mainly affects the ascending
and the descending aorta.
• 2. Pathogenesis :
• 1. Hypertension .
• 2. Marfans syndrome (genetic defect in which
a connective tissue protein , fibrillin required for
formation of elastic tissue is not formed).
• 3. Iatrogenic trauma during cardiac surgeries .
• 4. Vasculitis .

23. • 5. During pregnancy
• 6. Turners syndrome .
• 3. Pathological changes :
• Grossly : 1. This type of aneurysm do not
have significant dilatation therefore referred as
dissecting homatoma .
2. Dissection is usually seen between
the outer and the middle third of the aortic
media , as a result the column of blood
separated the intima and inner two-third of the
media on one side and outer one-third of the
media and adventitia on other .

24. • Microscopically :
• 1. Focal separation of fibromuscular and
elastic tissue of media .
• 2. Elastic tissue fragmentation can be seen .
• 3. Increased fibrosis of media .

25. GIT

26. PEPTIC ULCER DISEASE
• A peptic ulcer disease refers to the condition
in which the superficial layers of the stomach
get eroded due to excessive acid ancd pepsin
activity.
• Type of Peptic Ulcers :- Peptic ulcer disease
may be classified in two broad categories, i.e.
acute peptic ulcer disease and chronic peptic
ulcer disease .

27. 1. Acute peptic ulcers (stress Ulcers )
• (a). Occurs mostly in stomach and present in the
form of small, multiple mucosal erosions.
• (b). Can be due to psychological or physical stress
response in the body (mainly seen in cases of shock,
trauma, burns and in people, who consume excessive
drugs like non-steroidal anti-inflammatory drugs
(NSAIDS), Aspirin, steroids and in cases of excessive
smoking or alcohol usage).
• (c). Pathological changes :
• Grossly : Ulcers are oval or circular in shape
with size usually <1cm in diameter .

28. • Microscopically :
• a. They are shallow and do not invade the
muscular layer .
• b. Ulcers usually heal by re-epithelization without
any scar formation at the end .
• 2. Chronic Ulcers
• Usually gastric and duodenal ulcers come under
this category and involve the deeper layers of the
stomach and the duodenum .
• Etilogical Factors
• 1. Presence of Helicobacter pylori .
• 2. Increased stimulation of vagus nerve .
• 3. Decreased inhibtion of gastric secretions .

29. Pathological Changes
• Grossly :
• 1. Peptic ulcers are commonly solitary, small,
round to oval and characteristically punched
out .
• 2. Benign ulcers have flat margins with
mucosal folds converging toward the ulcer.
• 3. Malignant ulcers are larger, bowl-shaped
with elevated mucosa at the margin .

30. • Histologically
• Chronic peptic ulcers are composed of four
layers from inside to outside as listed below:
• 1. Necrotic
• 2. Superficial exudative
• 3. Granulation tissue
• 4. Cicatrization (thick layer of granulation
tissue).

31. Clinical Manifestations
• 1. Abdominal pain: In gastric ulcer pain soon after
eating while in duodenal ulcer pain may occur or
worsen .
• 2. Dull or burning (most common symptom)
• 3. Bloating and abdominal fullness .
• 4. Water brash .
• 5. Nausea and copious vomiting
• 6. Loss of appetite and weight loss.
• 7. Others signs and symptoms such as:
• a. Hematemesis
• b. Melena
• c. Heartburn
• d. Belching .

32. • e. General discomfort in the abdomen .
• f. Feeling sick .
• Diagnostic Methods
• a. Barium swallow .
• b. Esophagogastroduodenoscopy .
• c. Stool analysis .
• d. Gastric secretory studies .
• e. Urea breath test .
•

33. Pathogenesis
• TYPHOID FEVER OR ENTERIC FEVER
• Typhoid fever is an acute systemic disease resulting from
infection with salmonella typhi or salmonella paratyphi .
• 1. Ingestion typhoid bacilli through contaminated food and
water .
• 2. Bacteria invade the lyphoid follicles and peyers pathes
and proliferatetheir .
• 3. Then, bacteria invade the blood stream causing
bacterimea .
• 4. Leads to appearnce of red sporits on skin hyperpyrexia
.
• 5. Finally bacteria localize themselves in interstinal
lymphoid tissue, mesenteric lymph nodes liver gall bladder
and spleen .

34. Pathologic Changes
• Macroscopically :
• 1. Mainly seen in terminal ileum .
• 2. Peyer’s patches show oval ulcers with long axis
along the length of the bowel .
• 3. Base of the ulcer is black due to sloughed
mucosa with raised margins due to inflammatory
edema and cellular proliferation.
• Microscopically :
• 1. Cellular proliferation consists of phagocytic
histiocytes, lymphocytes and plasma cells appear
with hyperemia and edema .
• 2. Peripheral blood smear reflects lymphocytosis
with leukopenia and neutropenia .

35. Clinical Manifestations
• Proliferation of large mononuclear cells in many
different tissue leads to :
• 1. Lymphadenopathy .
• 2. Splenomegaly.
• 3. Enlargement of lymphoid tissue in intestine, bone
marrow, liver and lungs.
• 4. Lesions may extend deep into the intestinal wall
and cause perforation of the bowel, late in the disease
usually in the distal ileum .
• Diagnostic Methods
• 1. Leukopenia
• 2. Occult blood test .
• 3. Widal test .
• 4. Blood culture .

36. ESOPHAGEAL CARCINOMA
• The primary malignant tumors of the esophagus are
squamous cell carcinoma and adenocarcinoma .
• Etiopathogenesis
• 1. Gender (male)
• 2. Age (greater risk in fifth decade or life).
• 3. Chronic esophageal irritation .
• 4. Use of alcohol and tobacco .
• 5. Gastroesophageal reflux disorder (GERD).
• 6. Heavy smoking and alcohol consumption .
• 7. Genetic factors and family .
• 8. Molecular level abnormality in TP53 tumor
suppressor gene .

37. Clinical Manifestations
• 1. No early symptoms .
• 2. Progressive dysphagia and weight loss of
short duration .
• 3. Dysohagia begins with solid foods and
gradually progresses to semisolid and liquid .
• 4. Ulceration and subequal hemorrhage from
erosive effects of tumor .
• 5. Fistula formation and possible aspiration
secondary to continued erosive tumor effects .
• 6. Feeling of lump in the throat and painful
swallowing
• 7. Substernal pain or fullness, regurgitation of
undigested food with foul breath and hiccups .

38. Pathological Changes
• Squamous cell Carcinoma : Half of squamous cell
carcinoma (90% of the primary esophageal
cancers) occurs in the middle third of the
esophagus followed by lower third and then upper
third of esophagus.
• 1. Macroscopically : Basically following three
types of gross changes may observed:
• A . Polyploid fungating type (commonest,
appears as cauliflower-like friable mss in the
lumen).
• B . Ulcerating type (appears as necrotic ulcer with
everted edges).
• C. Diffuse infiltrating type .

39. • 2. Microscopically :
• A. Squamous cell carcinoma are well-
differentiated carcinomas.
• B. Prickle cells, keratin formation and
epithelial pearls are also seen.
• Adenocarcinoma
• Adenocarcinoma (less then10% of the primary
esophageal cancers) commonly occur in lower or
middle third esophagus).
• 1. Macroscopically : Appears as nodular and
elevated mass .
• 2. Microscopically : Generally following three
types of patterns are seen

40. • A. Intestinal type-pattern seen similar to
adenocarcinoma of intestine or stomach .
• B . Adenosquamous type- pattern seen as an
irregular mixture of adenocarcinoma and squamous
cell carcinoma.
• C. Adenoid cystic type- uncommon cribriform
appearance in epithelial tumor .
• Spread of Esophageal Tumor
• 1. Locally .
• 2. Hematogenous .
• 3. Lymphatic spread .

41. Diagnostic Mathods
• 1. Esophageal X-ray with barium swallow and
motility studies.
• 2. Endoscopi examination with punch and brush
biopsies confirm cancer cell type.
• TUMORS OF STOMACH
• The tumors of the stomach may be classified as
follows : 1. Tumor like lesions(gastric polyps)
• 2. Benign tumors .
• 3. Malignant tumors :
• a. Adenocarcinoma
• b. Leiomyosarcoma.
• c. Leiomyoblastoma

42. 1. Gastric Polyps
• Any nodule or mass that projects above the level of
the surrounding mucosa is known as polyps .
• polyps are of two types, i.e. Inflammatory
polyps and hyperplastic polyps.
• 2. Benign Tumors :
• a. The benign tumors of the stomach are gastric
• b. Incidence of gastric adenoma increases with
age, most common in seventh decade .
• c. Male to female ratio is 2:1 .
• d. Gastric adenoma arises in the background of
chronic gastritis and intestinal metaplasia

43. • e. The gastric adenoma are also referred to as
adenomatous or neoplastic polyps, which are
commonly seen in colon and are also located in the
distal portion of the stomach particularly the antrum.
Gastric adenomas may be sessile or pedunculated .
contain proliferative dysplastic epithelium and has
malignant potential.
• 3. Malignant Tumors
• Malignant tumors of stomach are:
• a. Gastric carcinoma (90%95%)
• b. Lymphomas (4%)
• c. Carcinoids(3%)
• d. Mesenchymal tumors (rare)

44. Gastric Carcinoma
• Gastric carcinoma is the most common tumor of
stomach. The highest incidence is in fourth to sixth
decades of life.
• 1. Intestinal type, which arises from gastric mucosa
cells that have undergone intestinal metaplasia.
• 2. Diffuse type, which arises from native gastric
mucosa cells.
• Etiology
• 1. Diet : a. Nitrites in diet.
• b. Smoked and salted food .
• c. Tobacco smoke, tobacco juice and
consumption of alcohol have carcinogenic effect on
gastric mucosa .

45. • 2. Host factors : a. Ch. Atrophic gastritis .
• b. Infection by H. pylori.
• c. Partial gastrectomy .
• d. Gastric adenoma .
• e. Genetic factors.
• Morphology
Located in stomach at following sites :
• 1. Pylorus and Antrum (50%-60%)
• 2. Cardia (25%)
• 3. Body and fundus (15%-25%)
• 4. Favored location is the lesser curvature of
stomach .

46. Classification
• Gastric carcinoma is classified based on :
• 1. Depth of invasion :
• a. Early gastric carcinoma .
• b. Advanced gastric carcinoma .
• 2. Macroscopic growth pattern : Three
morphological growth patterns of gastric
carcinoma .
• a. Exophytic
• b. Flat.
• c. Excavated .
• d. Linitis plastica

47. • 3. Histological subtypes: Two most important
histological subtypes are:
• a. Intestinal type : This is composed of neoplastic
intestinal glands penetrating the wall of stomach
and resemble adenocarcinoma.
• b. Diffuse type : this is composed of gastric type
mucous cells and dose not form glands .
• Spread of gastric carcinoma
• 1. Lymphatic : Paragastric , paraaortic .
• 2. Virchow’s node : Supraclavicular lymph node

48. • 3. Hematogenous : Liver, lungs, brain and bones .
• 4. Transcelomic : Peritoneal cavity, ascites, pouch
of Dougals, pelvic and ovaries .
• 5. Krukenberg tumors .
• Clinical Manifestations
• 1. Chronic dyspepsia and epigastric discomfort
related to tumor growth in gastric cells and
destruction of mucosal barrier .
• 2. Persistent abdominal pain .
• 3. Gastric distension and vomiting .
• 4. Loss of weight .

49. • 5. Loss of appetite .
• 6. Anemia, weakness and malaise .
• 7. Postprandial fullness .
• 8. Hematemesis, melena and alteration in bowel
habits
• 9. Blood in stools from erosion of gastric mucosa
from tumor .
• Diagnostic Methods
• 1. Barium X-ray fluoroscopy shows tumor or
filling defects in outline of stomach, loss of flexibility
and distensibility and abnormal mucosa with or
without ulceration .

50. • 2 . Gastroscopy with fiberoptic endoscopy .
• 3. Computed tomography scan, X-rays, liver and
bone scans and liver biopsy reveal metastasis .
• TUMORS OF SMALL AND LARGE INTESTINE
• Cancer of the large bowel is the second most
common cause for carcinoma in both males and
females. Majority of tumors are epithelial in origin .
• ETIOPATHOGENESIS
• The cause of colon cancer is unknown . The various
risk factors can be suggested as:
• 1. Advancing age .
• 2. Family history of colon cancer or polyps, history
of inflammatory bowel disease
• 3. A diet in fat, protein, beef and low in fiber .

51. Classifications of intestinal tumors
• 1.Non – neoplastic polyps :
• a. Hyperplastic polyps
• b. Hamartomatous polyps
• c. Inflammatory polyps
• d. Lymphoid polyps
• 2. Neoplastic polyps :
• a. Adenoma
• -Tubular adenoma
• - Tubulovillous
• adenoma
• -Villous adenoma

52. • 3. Familial polyposis syndromes :
• a. Gardner’s syndrome
• b. Turcot’s syndrome
• c. Juvenile polyposis syndrome
• Malignant Tumor
• Colorectal carcinoma :
• 1. The 98% of all cancers in large intestine are
adenocarcinomas.
• 2. Incidence is highest in US, Canada, Australia
and other affluent countries .

53. • Etiology
• 1. Environmental and dietary factors:
• 2. Dietary factors that predispose to carcinoma are :
• a . Low content of unobservable vegetable
fibers.
• b. A high content of refined carbohydrate diet .
• c. A high fat content (as from meat).
• d. Decreased intake of protective
micronutrients, e.g. vitamin A,C,E .
• Morphology
• 1. The location of carcinoma are as follows :
• a . Cecum and ascending colon (25%)
• b . Rectum and sigmoid colon (25%)
• c . Descending colon (25%)
• d . Rest is scattered elsewhere in the colon .

54. • 2. tumors in proximal colon tend to grow as
polypoid, fungating masses. In distal colon
they tend to be annular, encircling lesions that
produce so called napkin ring constriction of
the bowel. Both the forms penetrate the
bowel wall to produce serosal or subserosal
firm masses. Circumferential growth around
the bowel wall result in stricture formation .
• 3. Microscopically : The features are those of
adenocarcinoma, which may be from well 10%
of tumors show foci of neuroendocrine
differentiation .

55. • Spread of Tumor :
• a. Hematogenous spread .
• b. Lymphatic spread .
• c. Transcelomic spread .
• Carcinoid Tumors :
• The tumors of neuroendocrine cells are called
carcinoids . Neuroendocrine cells are normally
dispersed along the length of GI tract mucosa,
lungs, pancreas, biliary tract . They are specialized
cells that secrete hormones :
• 1. About 60%-80% arises in tip of appendix .
• 2. 10%-20% in terminal ileum, remaining in rest of
the gut .

56. • 3. Can occur at any age, peak incidence in
sixth decade of life .
• 4. About 90% of gastric, ileal and colonic
carcinoids spread to lymph node and distant
sites at diagnosis .
• 5. Cells of carcinoids tumor can able to
synthesize and secrete a variety of hormonal
products .
• 6 . cells of origin of carcinoids is functionally
uncommitted gut endocrine cell that undergo
differentiation during tumorigenesis .

57. • Morphology :
• 1. Most common site for gut carcinoid is
appendix .
• 2. Elsewhere in the gut, small yellow-orange
nodule present in submucosa, overlying
mucosa may be normal or ulcerated .
• 3. Microscopic examination shows the
neoplastic cell form islands, trabeculae, glands
or sheets .

58. Clinical Manifestation
• 1. Changes in bowel habits Diarrhea, constipation
and sensation of incomplete rectal emptying .
• 2. Many patients are asymptomatic for long
periods .
• 3. Black tarry stools secondary to tumor erosion .
• 4 Anemia secondary to increased tumor growth
needs and blooding .
• 5. Abdominal aching, pressure or cramps
secondary to pressure from tumor .
• 6. Weakness, fatigue, anorexia, weight loss
secondary to increased tumor growth needs .
• 7. Vomiting as disease progresses related to
possible obstruction .

59. • Diagnostic methods :
• 1. Digital rectal examination reveals mass.
• 2. Hemoccult test detects blood in stool .
• 3. Proctoscopy and sigmoidoscopy reveals
tumor mass .
• 4. colonoscopy reveals tumor location .
• 5. Barium X-ray .
• 6. Carcinoembryonic antigen may be elevated
.