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Pathology for Health Professionals > Chapter.10- The G.I System > Flashcards

Chapter.10- The G.I System Flashcards

1
Q

What are the most common type of non-neoplastic polyp?

A

Hyperplastic polyps

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2
Q

What are hyperplastic polyps?

A

Benign lesions most often found in rectosigmoid region

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3
Q

What are hamartomas?

A

Developmental abnormalities in which the normal components of the tissue aggregate in an abnormal manner. These involve Peutz-Jeghers polyps and Juvinile polyps

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4
Q

Classification of Intestinal Tumors

A
  1. ) Non-neoplastic polyps: hyperplastic polyp, inflammatory polyp, juvinile polyp, Peutz-Jeghers polyp, lymphoid polyp
  2. ) Benign neoplasms: tubular adenoma, villious adenoma, benign stromal tumors
  3. )Malignant neoplasms: adenocarcinoma, carcinoid lymphoma, sarcoma
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5
Q

What are inflammatory polyps?

A

Known as pseudopolyps. Represent multiple fragments or regenerating mucosa surrounded by broad ulcers

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6
Q

What do neoplastic polyps consist of?

A

Neoplastic epithelium that show no evidence of differentiation

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7
Q

What are neoplastic polyps classified as?

A

Tubular, villous, and tubulovilous adenomas

All are considered pre-malignant because they can progress to adenocarcinoma

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8
Q

What are tubular adenomas?

A

Most common, account for 75% of neoplastic polyps.

Typically attached to the stoma by a stalk

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9
Q

What are villious adenomas?

A

Sessile, broad based tumors, composed of epithelial cells alligned into elongated villi. They project into the lumen of the intestine. forming finger like protrusions. Invasive carcinoma is found in alomst 50% of these tumors.

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10
Q

Peak incidence (age) for colorectal cancer

A

Between 50-70 years of age

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11
Q

Adenocarcinoma accounts for % of intestinal cancers

A

95%

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12
Q

Incidence of colorectal cancer

A
  • 10x more common in USA and Western countries than in Asia
  • Most cases occur spontaneously with no identifyable risk factor
  • 20% genetic
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13
Q

Where are adenocarcinomas found in the intestine?

A

-May develop in any part, but most commonly found in the left part of the intestinal loops

  • 45% in recto-sigmoid area
  • 25% in cecum an ascending colon
  • 30% in remaining part of the colon
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14
Q

Most adenocarcinomas originate as

A

neoplastic polyps

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15
Q

Tumors from the right colon tend to grow as…

A

fungating masses, or ulcerated, shallow cratorlike lesions

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16
Q

How do adenocarcinomas of the sigmoid or rectum present?

A

They infiltrate the intestine circumferentially, producing “napkin ring” circumferential narrowing

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17
Q

What is the 5 year survival rate for stage 4 colorecta cancer?

A

Less than 10%

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18
Q
A
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19
Q

Early symptoms of adenocarcinoma

A

May produce no symptoms at all, may be diagnosed by screening (endoscopy, biopsy, or occult blood)

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20
Q

Clinical symptoms of left sided adenocarcinoma of the colon

A

Left sided lesions, especially the rectum, tend to narrow the passage of stool=constipation, thin pencil like stools

Hematochezia may occur, but in advanced lesions

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21
Q

Symptoms of adenocarcinoma of the right colon and cecum

A

Tend to be silent or non specific (weakness or fatigue)

Chronic blood loss may cause anemia

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22
Q

What tumor marker is used in the monitoring of patients with colorectal cancer?

A

CEA (Carcino-embryonic antigen)

Not useful in diagnosis since it can be released by non-specific intestinal inflammations, but

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23
Q

What are carcinoids?

A

term used for neuroendocrine tumors of low malignancy

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24
Q

Where are carcinoids located in the GI tract?

A

Can occur in all intra-abdominal parts of the GI tract

Most common in the small intestine

located in the sub-mucosa where they form nodules, elevating the lower mucosa

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25
Q

Genetic factors in colon cancer etiology

A

-Can account for 20%

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26
Q
A
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27
Q

Where do carcinoids of the GI tract tend to metastisize?

A

Tumors larger than 2cm tend to matastaize the lymph nodes and liver

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28
Q

What is carcinoid syndrome?

A

Carcinoids that have metastesized to the liver release their secretory products into the blood.

  • release seratonin, bradykinin, histamine
  • therefore bronchial wheezing, diarrhea
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29
Q

Long lasting carcinoid syndrome results in

A

fibrosis of right ventricle and tricuspid valve

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30
Q

Components of upper GI tract

A

Mouth, Pharynx, esophagus, stomach, and dudenum

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31
Q

In the uppder GI tract the epithelium of the mucosa is

A

Squamous

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32
Q

Components of lower GI tract

A

small and large intestine, appendix, rectum, anus

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33
Q

In the lower GI tract (stomach to anus) the epithelium of the mucosa is

A

Cuboidal gladular epithelium

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34
Q

In the lower part of the anus, the epithelium is

A

Squamous

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35
Q

Describe the musuclar component of the GI tract, in terms of structure

A

Above the diaphragm the muslce is covered by adventitia, and below the diaphragm the muscle is covered peritoneum.

This is important because the upper parts (such as esophagus) does not have a mesothelial lining, therefore it is much easier for cancer to spread into the wall of the esophagus and spread into adjacent tissues

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36
Q

Blood supply of the GI system

A
  • supplied by the mesenteric arteries
  • Recives 1/6 of cardiac output, but this depends on the needs are the GI tract (ex. digestion vs. rest)
  • Portal system drains the venous blood fro the intestines
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37
Q

What are the 4 layers of the GI tract?

A

muscosa, submucosa, muscularis, serosa

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38
Q

Lymphatic Supply of the GI system

A

Intestines habe a rich supply of lymphatics

Begins at lacteals at mucosal wall, and drains to lynph nodes and lymphatic channels that drain into the throacic duct

These lymphatics play a role in absorbing nutritients, and in the immune response

Significant route for the spread of cancer

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39
Q

Innervation of the GI Tract

A

-Mostly derived from the autonomic nervous system

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40
Q

Main functions of the GI Tract

A

Ingestion

Mastication (chewing)

Deglutition (swallowing)

Digestion: beings in mouth with saliva

Absorption

Excretion

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41
Q

Main exocine and endoctine functions of the GI tract

(table: organ, secretory product, function)

A
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42
Q

Diseases of the oral cavity

A

Developmental abnormalities

Inflamation

Dental Carries

Periodontal disease (bacterial infection the gums and tissues around the mouth)

Stomatitis (inflammation of roal mucosa)

Oral Cancer

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43
Q

Most common developmental abnormality of the oral cavity

A

Cleft lip: lack of fusion from the fetal nasal and maxilliary processes that form the upper lip

May be associated with cleft palate

Cleft lip more common in males

44
Q

What are dental carries?

A
  • Most common in children and adolescents
  • Begins as a bacterial plaque which then leads to a defect in the enamel
  • Deeper defects allow bacteria to enter the pulp cavity (pulpitis), where people experience pain
  • Influenced by lifestyle and diet (high sugar)
  • Saliva and fluoride are protective
45
Q
A
46
Q

What is stomatitis?

A
  • Inflammatio of the mouth
  • Can ocurr in the setting of systemic disease

Ex. Herpes infection (vesicles), and candida (immunompromised, bronchodilators/steroids)

Ex. Aphthous stomatits (canker sores): Uknown etiology, health spontanously

47
Q

Oral Cancer

A

Can occur anywhere in the oral cavity

Most are squamous cell carcinoma

Risk factors: Tobacco (smoking and chewing), chronic alcoholism

Males > females: 10:1 Lip, 2:1 oral cavity

Mean age of dx.: 55-60yo

48
Q

Oral cancer is morphologically present as

A

Leukoplakia: white elevated plaque that covers the mucosal surgafe

Erythroplakia: Red plaque that appears distinct

Ulcer: disruption of mucosa

crater: deeper depression

Nodule

49
Q

Salivary gland disease

A

Inflammation of the salivary glands: sialadenitis

Iinfectious:

  • Suppurative: stapyloccocus A or Streptococcus B,
  • Viral: mumps virus common in children

Autoimmune:

  • Sjogrens disease: Presents as systemic, but affets the salivary and lacrimal. Enlargement of gland is attributed to infiltrates of plasma cells and lympthocytes. Increased risk of lymphoma.

Clinically can present as swelling of glands or xerostomia

50
Q

Salivary gland neoplasms

A

Can affect major or minor salivary glands

More than 60% are benign

Frequently occur if not removed completely

Most Common tumor is pleomorphic adenoma (70%)

51
Q

Diseases of the esophagus: Clinical Presentation

A
  • Dysphagea
  • Esophageal (retrosternal pain)
  • Aspiration or regurgitation
52
Q

Esophageal Atresia

A

Developmental

lack of lumen with or without esophageal fistula

babies will vomit ingested milk

without repair, babies will die of starvation or aspiration pneumonia

53
Q

Hiatal hernia

A

most common cause of reflux

Alterns function of lower esophageal sphincter and facilitates reflux of gastric juice into the esophagus

Sliding vs. paraesophageal

Displacement of gastric cardia from abdominal cavity into the thoracic cavity through diphragmatic hiatus

tone of LES decreased by smoking, caffeine, pregnancy

54
Q

Achalasia

A

Spasm of LES and dilation proximal to the site of spasm

Results in dysphagia

Most cases idiopathic, but can be secondary to chagas, cancer, amyloidosis, scleroderma

55
Q
A
56
Q

Esophagitis

A
  • Reflux of gastric juice (peptic esophagitis) with pepsin and HCL-leadinging to ulcerations; defects repaired by metastatic epithelium (Barretts esophagus)

Can be caused by infections: Viruses (herpes, cytomegalo virus), fungi, or bacterial superinfection

Can be caused by chemical irritants: (lye)

57
Q

Esophageal varicies

A
  • Typically caused by cirrhosis of the liver, marked by portal HTN
  • May cause hematemesis
  • most common cause of GI bleeds, high mortality rate

Mallory-Weiss: laceration of small blood vessels @ gastro-esophageal junction during strenuous vomiting. More common is alcoholics. Marked by hematoemesis

58
Q

Carcinoma of the esophagus

(incidence, risk factors, prognosis, clinical presentations)

A

Accounts for 4% of all cancers

higher incidence in Asian and Africa (carcinogen in soil or food?)

Correlates with alcohol, tobacco abuse

more common in men

3x more common in blacks than whites

poor prognisis: average survival <2years, 5year<25%

Clinical: present with pain, bleeding, malodorous breath

59
Q

Carcinoma of the esophagus

A

Locally invasive, at dx. most have spread to adjacent organs

Upper and lower: Swquamous cell carcinoma

Lower Esophagus: Adenocarcinoma (developig in Barretts)

Most carcinomas originate from lower esophagus

60
Q

Diseases of the Stomach: Symptoms

A

Pain: Midline, upper abdomen, due to ulceration of mucosa and HCL

Vomitting: obstruction of pylorus

Bleeding: acute with hematoemesis or chronic with melena

Dyspepsia: nausea, lack of appetitie, food aversion

Systemic consequences: iron deficiency anemia caused by chronic blood loss, vitamin B12 malabsorption

61
Q

Congenital abnormality of stomach

A

-Most common: Pyloric stenosis, occurs in pre-natal period

boys more affected

projectile vomiting.

62
Q

Gasrtitis

A

Acute (erosive): stress, shock, food, exogenous chemicals

  • Erosions
  • Ulcerations

Chronic:Atropic gastritis with or without intestinal metaplasia

  • etiology unknown
  • H.Pylori
  • Autoimmune (with pernicious anemia)- impaired absorption of B12

Increased risk for gastric cancer

63
Q

Peptic Ulcer disease

A
  • Multifactorial
  • Mucusal ulceration that extends to the gastric epithelium into muscularis

Contributing factors include:

  • Gastric juice: HCL, pepsin
  • Mucusal barrier defects: stress, shock, NSAIDS, smoking reduces resistance
  • H.Pylori
64
Q

Clincial Features of Pepic Ulcers

A

Mostly distal stomach and proximal duodenum

Duodenal 4x more common than gastric

Gastric >40, Duodenal any agea

Presentation: 1-3hours after a meal or at night

Mid-epigastric

Nausea, vomiting, weight loss, melena, iron-deficiency

65
Q

Peptic Ulcers: appearance

A

-punched out, round defects

bottom of the ulcer consists of glandular amorphous material, HCL keeps clean

margins of the ulcer are sharp

66
Q

Complications of peptic ulcer disease

A

Hemmorrhage (most common): hematemesis, melena, iron deficient anemia

Penetration into the pancreas: acute pancreatitis

Perforation: Peritonitis (duodenal ulcers may extend to the intestinal wall and form a hole, leaking contents into the peritoneum)

Cicatrization: stenosis (may be caused by scarring)

67
Q

Gastric Neoplasms

A

Benign epithelial tumors: polyps (hyperplastic, tubular, vilious)

Benign Stromal Tumors (ex.leiomyoma)

Malignant Tumors

  • Adenocarcinoma (most common, 90%)
  • lymphoma (stomach most common site of GI lymphomas)
68
Q

Carcinoma of the stomach incidence and etiology

A

90% of gastric malignancies

8x more common in Japan and Chile (diet, soil)

Incidence has decreased last 70 years in USA

Etiology is unknown, suspect H.Pylori, and nitrosamines in food

69
Q

Macroscopic features of gastric carcinoma

A

Forms: 75% in distal part of the stomach

  • Superficial: flat, resembling early stages
  • Polypoid: protrude into lumen of the stomach
  • Ulcerated: resemble peptic ulcers, but increased irregulartity
  • Diffuse infiltrating: permeate gastric wall and “linitis plastica” leather like bottle
70
Q

Histology of gastric carcinoma

A
  • Adenocarcinoma
  • Metastasize to regional lymph nodes, to liver and lungs
  • Virchows node: left supraclavicular lymph node
  • Krunkenburgs tumor: bilateral ovarian involvement
71
Q

Clinical Features of Gastric Carcinoma

(Symptoms, prognosis)

A

Symptoms: non-specific, weight loss, anemia, weakness, vomiting, loss of appetite, dysphagia, bleeding

  • ditant metastases
  • most tumors are at advanced stage at dx.

Poor prognosis 5year<25%

72
Q

Gastrointestinal Lymphoma

A

May be secondary (from lymph nodes or bone marrow)

Primary GI lymphoma

  • Originate in mucosa-associated lymphoid tissue
  • localized masses
  • most MALTomas related to h.Pylori

**stomach most common site of GI lymphomas**

73
Q

Hirschsprung’s Disease

A

Abnormality of inervatio in the rectum and sigmoid colon

Intramural ganglion cells do not develop -

  • segment lacking inervation is in spasm
  • segment proxmial dilates and causes megacolon.
74
Q

Diseases of the Intestines

A

Developmental: Hirschsprungs, congenital diverticula (Meckels)

Diverticulosis, hernias, obstructions

Vascular Disorders

Inflammatory bowel

Infections: peritonitis

Malabsorption

Neoplasm

75
Q

Congenital Diverticula

A

Best known: Meckels

  • incompletely obliterated omphalomesenteric duct (small intesting to umbilical)
  • meckels diverticulitis is similar to acute appendicitis, except LLQ pain instead of RLQ pain
76
Q

Diverticulosis of the Colon

A

Can be solitary or multiple

Any part of the GI tract

Sigmoid most clinically significant

Older persons with chronic constipation

weakneing of intestinal wall at any point of arterial entry through muscle

77
Q

Hemmorrhoids: what are they and what causes them?

A
78
Q

Angiodysplasia: What is it, what does it cause?

A

Localized vacular lesion of the colon

may cause unexplained bleeding-dilated thin walled blood vessels

79
Q

Mesenteric Thrombosis

A

Common complication of atherosclerosis

most important cause of transmural infarction

typically affects small intestines

80
Q

Inflammatory Bowel Disease: Incidence

A

Ulcerative Colitis: incidence 70-100 per 100,000 persons per year in USA

Crohns: incidence 20-40 per 100,000, per persons per year

Cause unknown, may be stress or genetics

more common in whites

81
Q

Crohns VS. Ulcerative Colitis: Comparison Chart

A
82
Q

Crohns Disease: What is it, what % of colon is involved, what does it lead to

A

-Chronic inflammation of the Gi tract: terminal ileum and colon

50% both ilium and colon, 30% just ilium, 20% just colon

  • 1/3 have extraintestinal involvement
  • Terminal ilium aphtous ulcers, typically overlie lymphoid aggregates
  • inflammation extends through the wall of the mucosa,
  • Chronic inflammation is associated with fibrosis-cobblestone mucusa
  • Fibrotic intestine may be narrowed
  • inflammation of serosa leads to adhesions with adjacent intestinal loops which may lead to fistulas
  • 50% associated with granuloma
83
Q

Clinical Presentation of Crohns disease

A

Presentation varies- common is diarrhea, abd. pain, weight loss

Later stages:

  • constipation because of narrowing
  • malabsorption- weight loss, vitamin deficiency

1/3 extraintestinal symptoms: arthritis, skin lesions, liver disease, eye lesions

84
Q

Ulcerative Colitis: what is it? where in the intestine is it most commonly seen?

A
  • intestinal inflammation of unknown etiology
  • most often involves large intestine
  • From initial rectal lesions, inflammation spreads proximal, involving the entire colon
  • does not involve ileum, involves the appendix in 30%
85
Q

Ulcerative Colitis: Patho

A

Limited to colonic mucusa.

Starts as edematous patch - sandpapered

As disease progresses mucosal lesions become more prominent.

Crypts and aggregates of leukocytes in lesions (crypt abscess)

ulcerations bleed easily and become infected

Colonic ulcerations spread leaving behind small remnants of mucosa - inflammatory pseudopolyps- some polyps are foci of regeneration, some may undergo malignant transformation

86
Q

Ulcerative Colitis: Clinical Manifestations

A

Mild symptoms to evolve in chronic diarrhea, rectal pain, bleeding

70% chronic, 20% resistive to tx., 10% single episode

87
Q

Gastrointestinal Infections:

A

Caused by

  • a disturbed balance of colonic flora: pseudomembranous colitis from overgrowth c.diff as a result of abx.
  • Introduction of pathogens: food poisoning, bacteral toxins,

Infectious diarrhea in small intestine: ecoli, vibrio cholerae, giardia, rotovirus

Infectious diarhhea in large intestine: ecoli, norwalk, shigella

88
Q

Comparison of Diarrhea between small and large intestine

Stool characteristic table: volume, appearance, blood, leukocytes, proctoscopy

A
89
Q

Causes of Diarrhea

A

a. ) ingested toxin
b. )toxins formed by bacteria colonising the intestine
c. ) bacteria that invade the wall of the intestine

90
Q

Pseudomembranous Colitis:

What is the cause?

A
91
Q

Acute Appendicitis: Caused by

A
  • one of the most common acute intestinal infection
  • caused by enterogenic bacteria of normal intestinal flora that becomes pathologic after obstruction of the lumen of the appedix (feces, lymphnode, intramural tissue, worm).
92
Q

Acute appendicitis Clinical features

A

Sudden pain, fever leukocytosis

Pain strongest in RLQ (McBurneys Point), may be referred to umbilican area-peritonitis

tenderness/Rebound pain

Appendectomy is only tx.

93
Q

Acute peritonitis:

Defined as, types

A

Inflammation of the peritoneal lining

local or diffuse

sterile or infectious

94
Q

Acute Sterile Peritonitis caused by

A
  • Acute pancreatitis with spill of enzymes
  • Rupture of gallbladder with bile entry to peritoneum
95
Q

Acute infectious peritonitis caused by

A
  • rupture of stomach (PUD) or intestines (appy)
  • Spread of infection from fallopian tubes
  • rupture of abscess
  • Infection of pre-existing ascites
96
Q

Clinical Features of Acute Peritonitis

A
  • sharp abdominal pain
  • rebound tenderness
  • voluntary guarding
  • intestinal peristalsis slows down-intestinal paralysis
  • treatment- surgical exploratio to remove puss and repair rupture site
  • All forms high mortality
97
Q

Causes of intestinal obstruction

A
98
Q

Intestinal Obstruction: Hernia

Defined as, types, most common, and if left untreated

A

*see slide

Inguinal is most common

If left untreated- leads to adhesions and subsequent incarceration. The neck of the hernia may compromise blood flow causing strangulation and gangrene of intestinal loop.

99
Q

Intestinal Obstruction: Intussusception

Definted as, causes in children and adults, complication

A

-bloodflow of invaginated segment may become compromised b/c constriction of outside segment, and could lead to necrosis

100
Q

Volvulus: Defined as, involves, can lead to

A
101
Q

Pathogenesis of Malabsorption

A

*usually caused by more than 1 mechanism

102
Q

Malabsorption is characterized by

A

Deficency of nutrients- most prominent are protein and lipids

  • Protein deficiency leads to anemia, decreased iron, hypoalbumin -edema
  • Decreased fat absorption: fatty stools (steatorrhea), decreased absorption of fat soluble vitamins. low k =bleeding disorders, low vitD= osteomalacia, hypocalcemia
103
Q

Malabsorption: Intraluminal digestion may be impaired by

A

*deficiency of gastric juices* - these patients do not absorb b12 and can present with anemia

*deficiency with bile- impaired fat absorption

104
Q

Celiac Sprue:

A
105
Q

Whipple’s disease

A

Pathology for Health Professionals (14 decks)

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