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Y2B1 - GIT 📕 > Pathology 🩺 > Flashcards

Pathology 🩺 Flashcards

1
Q

what are the types of inflammation of the lips (cheilitis)?

A
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2
Q

what are the causes of inflammation of the mouth (Stomatitis)?

A
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3
Q

what are the types of inflamation of the tongue (Glossitis)?

A
  • Acute glossitis
  • chronic glossitis
  • Chronic atrophic glossitis
  • plummer vinson syndrome
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4
Q

what is acute glossitis charachterized by?

A

characterised by swollen papillae occurs in eruptions of measles and scarlet fever.

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5
Q

what is choronic glossitis charachterized by?

A

the tongue is raw and red without swollen papillae and is seen in malnutrition.

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6
Q

what is choronic atrophic glossitis charachterized by?

A

characterised by atrophied papillae and smoth muscle tongue.

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7
Q

what are the symptoms of Plummer Vinson Syndrome?

A

(anaemia, oesophageal obstruction, Pharyngitis and atrophic glossitis)

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8
Q

what are the types of tongue ulcers?

A

1- Dental (traumatic) ulcer
2- Dyspeptic ulcer
3- Syphilitic ulcers
4- Tuberculous ulcer
5- Malignant ulcer
6- aphthous ulcers

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9
Q

what are the types of inflammation of the oropharynx?

A
  1. Catarrhal pharyngitis
  2. Acute septic pharyngitis
  3. plummer–vinson syndrome
    -anaemia
    -oesophageal obstruction
    -Pharyngitis and atrophic glossitis
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10
Q

what are the types of Non-neoplastic diseases of Salivary glands?

A

(Inflammation = sialadenitis Common in the parotid gland (parotitis))

1. Acute sialadenitis (Mumps, acute Suppurative, sialadenitis)

  1. Chronic inflammation (Non specific - specific (T.B, actinomucosis))
  2. Immue mediated sialadenitis (Mickulicz Disease)
    
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11
Q

what are the complications of mumps?

A
  1. Orchitis “Inflamation of testis”
  2. Pancreatitis
  3. Mastitis “inflammation of breast”
  4. Meningitis
  5. Encephalitis and Neuritis (8th cranial neve).
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12
Q

what are the causes of esophagitis?

A

Non-Infective:
- Surface irritation
- Reflux oesophagitis.“very common in egypt”
- Alcohol, corrosives, drugs, smoking, cytotoxic drugs, Radiation.
- Vit A,C deficiency.

Infective:
- Herpes Simplex and Candidiasis

Idiopathic

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13
Q

what are the causes of reflux esophagitis?

A
  • Incompetence of the lower oesophageal sphincter.
  • Hiatus hernia.
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14
Q

what is the N/E of Reflux oesophagitis?

A

Hyperemic mucosa with superficial erosions.

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15
Q

what is the M/E of Reflux oesophagitis?

A
  • Present of inflammatory cells (eosinophils neutrophils and lymphocytes) in the epithelial layer.
  • Basal hyperplasia.
  • Congested lamina propria.
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16
Q

what are the complications of Reflux oesophagitis?

A
  1. Barrett’s oesophagus
  2. peptic ulcerations
  3. fibrous stricture.
  4. Hematemesis
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17
Q

what is the cause of Pulsion Diverticulate?

A

Congenital weakness of inferior constrictor muscle of the pharynx

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18
Q

what is the pathology “or characters” of Pulsion Diverticulate?

A
  • Protrusion of mucosa and submucosa though the posterior pharyngeal muscles of the pharynx
  • Present in posterior wall of oesophagus at upper oesophagus.
  • Directed downwards.
  • Distended with food.
  • Compress oesophagus
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19
Q

what are the effects of Pulsion diverticulae

A

Compress oesophagus
- dysphagia
- diverticulitis

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20
Q

what is the cause of Traction Diverticulate?

A

Traction by fibrosed L.N (T.B)

“due to fibrous adhesion”

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21
Q

what is the pathology ”or characters” of Traction Diverticulate?

A
  • Consists of all layers of oesophagus wall ( true divert) In the anterior wall at the level of tracheal bifurcation
  • Directed upwards
  • No food enters it
  • Symptomless
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22
Q

what are the causes of Oesophageal Obstruction?

A

Organic and functional

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23
Q

What are the causes of organic obstruction of espohagus?

A

A. Congenital absence of lumen (atresia) or congenital stricture.

B. Acquired:- due to causes in :
In the Lumen: Contains foreign body, bulging tumor, ring and webs (Plummer- Vinson Syndrome)

In the Wall of oesophagus: strictures (Congenital, post– inflammatory or malignant)

Outside the oesophagus: (compression from outside) goiter, aortic aneurysm and tumours.

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24
Q

what are the causes of the functional obstruction to the esophagus?

A

It is due to neuromuscular incoordination as in:
1. Plummer – Vinson syndrome
2. Acalasia of lower oesophagus

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25
Q

what is Acalasia of lower oesophagus? and what causes it?

A
  • It is a functional disturbance characterized by loss of peristalsis of lower esophageal segment and incomplete relaxation of lower oesophageal sphincter muscle .
  • It is due to absence ( or destruction ) of myenteric ganglion cells in lower oesophagus .
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26
Q

what are the pathological changes in the case of Functional Obstruction?

A

1- Narrow lower end of oesophagus in which ganglion cells are absent.

2- The oesophagus above the narrow part is dilated , elongated with hypertrophy of muscular wall (megaoesophagus). The mucosa may show ulceration and leukoplakia .

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27
Q

what is the definition of gastritis?

A

inflammation of gastric mucosa

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28
Q

what are the types of gastritis?

A

1) Acute gastritis
2) Chronic gastritis

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29
Q

For healthy mucosa, what balance should be found?

A

balance between:

  • protective factors: (Bicarbonate, Prostaglandins (Pgs), Mucus Production, & Blood Flow to Mucosa)
  • hostile factors: (gastric acid, pepsin, helicobacter pylori infection, and NSAID)

“NSAIDs Inhibit COX which deceases PGs leading to decrease mucosa”

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30
Q

what are the charachters of acute gastritis?

A

1) Short Duration
2) Neutrophilic infiltration
3) Mucosal erosions in severe cases.

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31
Q

what is the etiology of acute gastritis?

A

Infective
- Salmonellosis & staph.
- Food poisoning

Non infective
- Drugs: NSAID and cortisone “stronger” (decrease mucosal PGs)
- Alcoholism.
- Smoking (↑ acid secretion, & ↓ mucus and PGs secretion)
- Shock (decrease mucosal blood flow)
- Chemical irritation: alkalies, acids.
- Mechanical trauma: during endoscope
- Idiopathic

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32
Q

what is the pathogenesis of acute gastritis?

A

By one or more of the following:

1) Increase acid secretion.
2) Decrease blood flow.
3) Decrease the adherent mucous layer.
4) Direct damage to surface epithelium.
5) Decrease PGs secretion from the mucosa.

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33
Q

what is the N/E of acute gastritis?

A

the mucosa is hyperemic, edematous, shows erosions (in severe cases)

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34
Q

what is the M/E of acute gastritis?

A

The lamina propria shows edema, hyperemia, neutrophilic infiltration, and erosion of surface epithelium in severe cases

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35
Q

what are the charachteristcs of chronic gastritis?

A

1) long duration
2) mononuclear infiltration (lymphocytes, plasma cells, and macrophages),
3) usually no mucosal erosions. “but there is ulcers”

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36
Q

what are the types of chronic gastritis?

A

Type A (autoimmune gastritis)
Type B (Antral gastritis)

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37
Q

compare between Types of choronic gastritis

A
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38
Q

compare between the morphological features of the stages of chronic gastritis

A
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39
Q

what are the complications of gastritis?

A

1) Hemorrhage

2) Peptic ulcer

3) Malignancy due to:
- intestinal metaplasia and dysplasia
- H.pylori infection → gastric carcinoma and lymphoma

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40
Q

what is the definition of peptic ulcer?

A

defect in the mucosa that develops at any portion of gastrointestinal tract exposed to acid pepsin secretion of gastric glands.

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41
Q

what are the types of peptic ulcer?

A

1) Acute peptic ulcers (stress ulcers):
- Superficial erosion
- Minimal erosion

2) Chronic peptic ulcer disease:
- Muscular wall erosion with formation of fibrous tissue
- Present continuously for many months or intermittently

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42
Q

what causes acute peptic ulcer?

A

It occurs within hours of:
- Cases of stress (as shock, burn)
- Cases of severe acute gastritis.

“prophylaxis from ulcers should be done before risky surgries as the pathient has high stress (sympathatic stimulation) which leads to VC and decrease Blood supply leading to acute ulcers”

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43
Q

what are the sites of acute peptic ulcer?

A

stomach and first part of duodenum

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44
Q

what are the morphological features of acute peptic ulcer?

A
  • hemorrhagic inflammation and ulcers.
  • These ulcers are multiple small (less than 1 cm) and superficial.
  • They heal by regeneration.
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45
Q

what are the sites of chronic peptic ulcer?

A

1) Duodenum: first part (98%), anterior or posterior.

2) Stomach: pyloric antrum on lesser curvature.

3) Lower1/3 of esophagus: as in reflux esophagitis.

4) Other sites:
- Margin of gastrojejunostomy
- Meckel’s diverticulum

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46
Q

what is the etiology of chronic peptic ulcers?

A

1) Genetic factors. “people who are tall,thin with O blood type”

2) Hormonal factors:
- Zollinger Ellison Syndrome: gastrin → stimulate parietal cells → acid pepsin

3) Environmental factors

4) Alcohol, smoking, coffee…

5) H. Pylori infection (100% of duodenal ulcers, and 75% of gastric ulcers)

6) Emotional stress.

7) Associated diseases (chronic Bronchitis, emphysema.)

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47
Q

what is the pathogenesis of peptic ulcer?

A

An imbalance between increased acid pepsin secretion and decreased mucosal defense

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48
Q

what is the pathogenesis of duedenal ulcer?

A

due to ↑ acid pepsin + rapid emptying of gastric juice into duodenum

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49
Q

what is the pathogenesis of gastric ulcer?

A

Due to ↓ mucosal defense which is due to:

  • Chronic gastritis
  • Cigarette smoking
  • Local ischemia
  • Deficiency of mucosal cytoprotective as normal mucous film, buffers e.g bicarbonate, and PGs which help maintenance of blood supply
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50
Q

what is the N/E of peptic ulcer?

A

Shape: rounded or oval

Size: 2-4 cm

Margin: flattened with blurring of mucosal folds.

Edge: sharp deep penetrating to the muscle coat

Floor: clean and smooth due to peptic digestion of inflammatory exudate.

Base: indurated due to fibrosis.

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51
Q

what is the M/E of peptic ulcer?

A
  • The mucosa surrounding the ulcer shows chronic atrophic gastritis.
  • Inner zone: debris, neutrophils, and fibrinoid necrosis
  • Intermediate zone: chronic non specific inflammation and granulation tissue.
  • Outer zone: fibrosis
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52
Q

what are the complications of peptic ulcer?

A

1) Hematemesis.

2) Perforation → Peritonitis “fatal”

3) Fibrosis:(Hour glass Stomach - Pyloric or Duodenal Stenosis).

4) Duodenal diverticulum.

5) Malignant change: in 1% of gastric ulcers only

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53
Q

what is the definition of inflammatory bowel disease?

A

chronic Prolonged inflammation of the intestine results in damage to the GI tract leading to impaired absorption of nutrients.

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54
Q

what do inflammatory bowel disease include?

A

1) Ulcerative Colitis
2) Crohn’s disease(regional ileitis)

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55
Q

what is the definition of Ulcerative Colitis?

A

Chronic non specific inflammation of large intestine characterized by severe ulceration.

“comes in the form of recurrent attacks”

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56
Q

what is the cause of Ulcerative Colitis?

A

Idiopathic, but it can be:
- genetic predisposition
- Psychosomatic
- virus, amoebiasis, diet
- Allergic

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57
Q

what is the N/E of ulcerative colitis?

A

Site: “left side of the body”
- sigmoid colon & rectum.
- No skip lesions
- The lesion occurs only in mucosa and submucosa (No serositis)

Appearence:
The mucosa:
- appears deeply congested associated with:
 muco- purulent discharge
 superficial irregular ulcers

  • the mucosa in between the ulcers is swollen producing pseudopolyposis
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58
Q

what is the M/E of ulcerative colitis?

A

Mucosa:
- It is congested and infiltrated by inflammatory cells (neutrophils and plasma cells).
- The mucosa at the margins of the ulcers shows mucus depletion, metaplasia (gastric) and hyperplasia.

Crypt abscess:
- They are in the lumen of the crypt
- They fuse to form large abscess which may rupture causing mucosal ulcerations.

Pseudopolyps: consists of hyperplastic mucosa and granulation tissue.

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59
Q

what are the complications of ulcerative colitis?

A
  1. Perforations: rare “as they are superficial ulcers”
  2. Stricture: rare
  3. Toxic megacolon
  4. Malignancy: more common 1/100 (10folds) than crohn’s disease.
  5. Associated disease: more common
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60
Q

what are the diseases that may be associated with ulcerative colitis?

A
  • Iridocyclitis
  • Vasculitis
  • Fatty change liver & cirrhosis
  • Arthritis
  • Erythema nodosum
  • Secondary amyloidosis
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61
Q

what is the prognosis of ulcerative colitis?

A

Chronic course with exacerbation & remission.

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62
Q

what is the definition of Crohn’s disease (regional ileitis)?

A

Non caseating granuloma of alimentary tract

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63
Q

what is the cause of crohn’s disease?

A

Idiopathic but it can be:
- Genetic predisposition
- Virus or bacteria
- Autoimmune

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64
Q

what is the N/E of crohn’s disease?

A

Site: “in the right side of the body”
- terminal ileum and Right colon but any part can be affected.
- Skip lesions: The affected segments are separated by normal tissue
- The lesion occurs in all layers (serositis is present)

Appearence:
- The affected segments show intense edema of the mucosa leading to thickening of the wall and narrowing of the lumen
- Linear deep penetrating ulcers (fissures) are present giving cobble stone appearance.
- The mesentery is thickened and mesenteric LNs are enlarged.
- Fibrosis.

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65
Q

what is the M/E of crohn’s disease?

A

Inflammatory reaction:
1. extends through whole wall of intestine reaching the serosa and the mesentery.
2. consists of lymphocytes, plasma cells, eosinophils and mast cells.

  • Some cases show non caseating granuloma and fibrosis.
  • Mucosa shows metaplasia (to mucus secreting pyloric cells), hyperplasia and dysplasia.
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66
Q

what are the complications of crohn’s disease?

A
  • Intestinal obstruction due to stricture
  • Perforation:
     peritoneal abscess
     fistula with nearby organs (intestine, U.B, Peri-anal skin and Rectovaginal)
  • Secondary malabsorption syndrome.
  • Carcinoma: Rare 1/1000
  • Toxic megacolon
  • Associated diseases: rare
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67
Q

compare between ulcerative colitis according to clinical features

A
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68
Q

compare between ulcerative colitis according to macroscopic features

A
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69
Q

compare between ulcerative colitis according to microscopic features

A
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70
Q

what are the tumors of lips, mouth & tongue?

A
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71
Q

what are the predisposing factors of cancer tongue?

A
  1. Chronic irritation. “like a broken tooth”
  2. Oncogenic viruses as HPV
  3. precancerous lesions as leukoplakia.
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72
Q

what is the site of cancer tongue?

A

more common on anterior 2/3 than posterior 1/3 at the lateral edge.

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73
Q

what is the N/E of cancer tongue?

A

mass: fungating, ulcerative or infiltrative.

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74
Q

what is the M/P of cancer tongue?

A

Squamous cell carcinoma.

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75
Q

what is leukoplakia?

A

Leukoplakia is defined by the World Health Organization as a white lesion of the oral mucosa that cannot be scraped off and cannot be attributed to another definable lesion.

random adherent white lesion

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76
Q

what is the microscopic picture of Squamous cell carcinoma?

A

- Ulcerated surface epithelium.

——–

- The subepithelial tissue shows :

➢ sheets of Malignant squamous epithelial cells separated by desmoplastic stroma.
➢ The periphery of the sheets consists of layer of basaloid cell, inner to this are polyhedral cells resemble the prickle cell layer.
➢ The central area consists of keratin.
➢ The cells show the cytologic criteria of malignancy (describe).

77
Q

border’s grading of SCC

A
  • Grade I: 75-100% of tumor consists of cell nests.
  • Grade II: 50-75% cell nests.
  • Grade III: 25-50% cell nests.
  • Grade IV: 0-25% cell nests.
78
Q

what are the tumors of salivary glands?

A
79
Q

what is the incidence, age, site & cell of origin of Pleomorphic adenoma (B. mixed salivary tumor)?

A
80
Q

what is the N/E of Pleomorphic adenoma (B. mixed salivary tumor)?

A
  • Rounded, well- demarcated masses with mal-developed capsule allowing tongue-like projections of the tumor into the adjacent salivary tissue.
  • The tumor is firm, grayish white with areas of cartilaginous or osseous tissues.
81
Q

at is the M/P of Pleomorphic adenoma (B. mixed salivary tumor)?

A
  • The epithelial component is formed of benign epithelial cells arranged in ducts, acini, tubules, strands or sheets.
  • The mesenchymal component is formed of loose myxoid tissue contain islands of cartilage and rarely bone
82
Q

what is the behaviour of Pleomorphic adenoma (B. mixed salivary tumor)?

A
  • High recurrence rate.
  • Malignant transformation: evidenced by rapid rate of growth, facial nerve paralysis, induration and fixation and enlarged regional lymph nodes
83
Q

what is the incidence, age, site & cell of origin of (Papillary cystadenoma lymphomatosum - adenolymphoma - Warthin tumor)?

A
84
Q

what is the N/E of (Papillary cystadenoma lymphomatosum - adenolymphoma - Warthin tumor)?

A
  • Round to oval, capsulated mass usually located in the superficial part of parotid.
  • Cut section shows pale gray surface with cleft- like spaces filled with mucinous or serous secretion.
85
Q

what is the M/P of (Papillary cystadenoma lymphomatosum - adenolymphoma - Warthin tumor)?

A
  • Cystic spaces with papillary ingrowth lined by two layers of epithelial the cells, the outer layer is formed of tall columnar cells and secretory cells and the inner layer is formed of oncocytic cells.
  • The stroma : lymphoid aggregates up to follicle formation with germinal centers.
86
Q

what is the behaviour of (Papillary cystadenoma lymphomatosum - adenolymphoma - Warthin tumor)?

A
  • No recurrence.
  • No malignant transformation
87
Q

what is the incidence, age, site & cell of origin of oncocytoma?

A
88
Q

what is the N/E of Oncocytoma?

A
  • Rounded or oval surrounded by complete capsule.
  • Cut section is solid and homogenous, light brown in color.
89
Q

what is the M/P of Oncocytoma?

A

Solid sheets of large cells with abundant bright red granular cytoplasm, The fibrous stroma is scanty and hyalinized

90
Q

what is the behaviour of Oncocytoma?

A
  • No recurrence.
  • No malignant transformation.
91
Q

what are the malignant salivary gland tumors?

A
  • Adenoid cystic carcinoma
  • Mucoepidermoid carcinoma
  • Acinic adenocarcinoma
92
Q

what is the site of malignant salivary gland tumors?

A

parotid, sublingual and minor salivary glands

93
Q

what are the characters of malignant salivary gland tumors?

A
  • Hard fixed mass.
  • Cut surface is grayish white with areas of hemorrhage and necrosis.
94
Q

what is the M/P of Adenoid cystic
carcinoma?

A

Sheets of small and dark stained cells showing microcystic spaces containing PAS positive material and the stroma is hyalinized

95
Q

what is the prognosis of Adenoid cystic carcinoma?

A

Highly malignant

96
Q

what is the M/P of Mucoepidermoid carcinoma?

A

Mixed tumor: Adenocarcinoma with mucus secretion + sheets of squamous cell carcinoma

97
Q

what is the prognosis of Mucoepidermoid carcinoma?

A

Intermediate

98
Q

what is the M/P of Acinic adenocarcinoma?

A

Solid acini of large round or polygonal cells with basophilic cytoplasmic granules

99
Q

what is the prognosis of Acinic adenocarcinoma?

A

Less malignant

100
Q

what are the tumors of the esophagus?

A
101
Q

what are the presdisosing factors of esophagus carcinoma?

A
  • Age: old age
  • Sex: males
  • Genetic susceptibility.
  • Diet.
  • GERD
  • Alcohol and smoking.
  • Precancerous lesions.
102
Q

what is the site of carcinoma of the esophagus?

A

common in middle 1/3 then lower 1/3 then upper 1/3.

103
Q

N/E of carcinoma of the esophagus

A

polypoid fungating mass, malignant ulcer or infiltrative growth (annular stricture).

104
Q

M/P of carcinoma of the esophagus

A
  • Squamous cell carcinoma (95%).
  • Adenocarcinoma (5%) when develops on top of barrette’s esophagus.
  • Rarely small cell undifferentiated carcinoma.
105
Q

what are the prognostic factors of carcinoma of the esophagus?

A
  • Tumor stage
  • Tumor grade
  • Lymphovascular tumor emboli
  • Perineural invasion.
  • Tumor thickness.
  • Involved resection margins.
106
Q

what is Barrett esophagus?

A
  • there is an abnormal (metaplastic) change in
    the mucosal cells lining the lower portion of the esophagus, from normal stratified squamous epithelium to simple columnar epithelium with interspersed goblet cells that are normally present only in the stomach, small intestine, and large intestine.
107
Q

what is Barrett esophagus considered?

A

considered to be a premalignant condition because it is associated with a high incidence of further transition

108
Q

what are the cells of Barrett esophagus classified into?

A

classified into four categories:
- nondysplastic
- low-grade dysplasia
- high-grade dysplasia
- frank carcinoma.

109
Q

what are the tumors of the stomach?

A
110
Q

Adenomatous polyps

A
  • Precursor lesion of gastric adenocarcinoma
  • Up to 30 - 40% contain focus of carcinoma at time of diagnosis, risk higher in larger tumors, especially if > 2cm, flat or depressed
  • Up to 30% risk of carcinoma in adjacent mucosa
111
Q

N/E of Adenomatous polyps

A

single, small or large, sessile or pedunculated, firm, pink, with corrugated outer surface.

112
Q

M/P of Adenomatous polyps

A
  • Polypoid projections of dysplastic epithelium (by definition) with pseudostratification, nuclear abnormalities, mitotic figures overlying cystically dilated glands without dysplastic changes
113
Q

prognosis of Adenomatous polyps

A

malignant transformation.

114
Q

at what age does gastric carcinoma usually occur?

A

over 50 years

115
Q

where is gastric carcinoma more common?

A

in males

116
Q

what are the precancerous lesions of gastric carcinoma?

A
  • Adenomatous polyps (gastric adenoma)
  • Chronic gastritis associated with intestinal metaplasia and dysplasia
  • Gastric peptic ulcer
117
Q

risk factors for gastric carcinoma

A
118
Q

what is the site of gastric carcinoma?

A

Commonest site is pyloric antrum but can occur anywhere in the stomach.

119
Q

N/E of gastric carcinoma

A
  1. Fungating type: large polypoid mass
  2. Ulcerating type: malignant ulcer
  3. Infiltrating type: infiltrate deep to the musculosa, 2 Patterns
120
Q

what are the patterns of infiltrating type of gastric carcinoma?

A

localized infiltrating: The pyloric region is thick rigid and narrow (stricture)

Diffuse infiltrating: affect the whole stomach leading to small rigid, thick walled stomach with narrow lumen (Linitis plastica, leather bottle stomach)

121
Q

M/P of gastric carcinoma

A
  • Adenocarcinoma
  • Mucoid adenocarcinoma.
  • Signet ring carcinoma.
122
Q

spread of gastric carcinoma

A
  • Local.
  • Lymphatic: Lt. supraclavicular L.Ns (Virchow’s sign).
  • Blood: to liver.
  • Transcoelomic spread: to peritoneum (hemorrhagic ascitis), ovaries (Krukenberg’s tumor) and to rectovesical & rectovaginal pouches.
123
Q

what are the complications of gastric carcinoma?

A
  • Haematemesis and melena
  • Iron deficiency – anaemia
  • Hypochlorhydria due to mucosal destruction.
  • Pyloric obstruction.
  • Cachexia
124
Q

what are the tumors of the small intestine?

A
125
Q

where does Carcinoid tumor arise from?

A

Arises from Argentafin cells of gastrointestinal mucosa.

126
Q

what is the behaviour of Carcinoid tumor?

A

locally malignant or malignant.

127
Q

what is the site of Carcinoid tumor?

A
  • appendix and terminal ileum (most common site)
  • Rectum & sigmoid: less common
  • Esophagus & stomach: rare.
128
Q

N/E of Carcinoid tumor

A

firm yellowish submucosal nodule or multiple nodules.

  • in the appendix: few mm, near its tip obliterates its lumen.
  • Small intestine: multiple, polypoidal masses that can ulcerate.
129
Q

M/P of Carcinoid tumor

A
  • Neuroendocrine growth pattern (organoid, trabecular, rosette formation, nested) or pseudoglandular, follicular and papillary growth
  • Tumor cells are uniform with a polygonal shape, round to oval nuclei with salt and pepper chromatin and inconspicuous nucleoli, along with moderate to abundant eosinophilic cytoplasm
  • Stroma is fine and highly vascularized; hyalinization, cartilage or bone formation are possible
130
Q

what are the complications of Carcinoid tumor?

A
  1. Partial intestinal obstruction: due to muscle hypertrophy of the affected segment.
  2. Hepatomegaly
  3. Carcinoid syndrome: occurs only when there is liver and lung metastasis
131
Q

what are the bioactive products secreted by carcinoid tumor?

A

serotonin & histamine

132
Q

what are the effects of serotonin secreted by Carcinoid tumor?

A
  • hypertrophy of intestinal muscle … obstruction
  • increase intestinal motility … diarrhea
  • stimulate fibroblastic proliferation in Rt side of heart … tricuspid and pulmonary valve stenosis
133
Q

what are the effects of histamine secreted by Carcinoid tumor?

A
  • Bronchospasm (asthmatic attacks)
  • flushing of face, and edema.
134
Q

what are the tumors of large intestine?

A
135
Q

what are the types of Neoplastic (Adenomatous) polyps?

A

1- Tubular adenoma
2- Villous adenoma
3- Tubulo - villous adenoma
4- Familial polyposis syndromes

136
Q

compare between tubular adenoma & villous adenoma according to N/E & M/E

A
137
Q

what is Familial polyposis syndromes?

A

A hereditary (autosomal dominant) disease, young age, Hundreds of adenomatous polyps are present in GIT. Precancerous -> malignant change within 10-20 years (multicentric carcinoma).

138
Q

what are the syndromes associated with Familial polyposis syndromes?

A

Multiple familial polyposis:
- Multiple colonic adenomatous polyps.

Gardener’s syndrome:
- Triad -> colonic adenomatous polyps, soft tissue tumors of small intestine & osteoma of mandible.

Turcot’s syndrome:
- colonic polyps & brain tumors.

Peutz-Jegher’s syndrome

139
Q

what is Multiple familial polyposis?

A
  • is an autosomal dominant inherited condition in which
    numerous adenomatous polyps form mainly in the epithelium of the large intestine.
  • While these polyps start out benign, malignant transformation into colon cancer occurs when they are left untreated.
140
Q

what is the site of Multiple familial polyposis?

A
  • Polyps are usually more proximal (i.e., right sided) than in classic FAP
  • Rectum often spared
141
Q

what is the incidince of carcinoma of large intestine (colorectal carcinoma)?

A
  • It represents 95% of malignancy of LI
  • occurs in old age
  • equal in both sexes.
142
Q

what are the predisposing factors for carcinoma of large intestine (colorectal carcinoma)?

A
  1. Genetic factors: an in multiple familial polyposis
  2. Diet: high protein and low fiber diet (Processed meat).
  3. Precancerous lesions:
    * adenomatous polyps
    * ulcerative colitis & crohn’s disease
    * Multiple familial polyposis
143
Q

what is the site of carcinoma of large intestine (colorectal carcinoma)?

A
  • Recto-sigmoid: commonest site 75%
  • Other parts of colon: 25%
144
Q

what is the gross appearence of carcinoma of large intestine (colorectal carcinoma)?

A
  • infiltrating (annular types): produce early obstruction
  • ulcerating type: Irregular margin, everted edge, indurated base and necrotic floor.
  • fungating type: cauliflower mass
145
Q

M/E of carcinoma of large intestine (colorectal carcinoma)

A
  • Adenocarcinoma,
  • mucoid adenocarcinoma
  • Signet ring cell carcinoma.
146
Q

M/P of carcinoma of adenocarcinoma of large intestine (colorectal carcinoma)

A
  • Infiltration of the wall by malignant tumoral proliferation formed of malignant acini, irregular in outline with no basement membrane and variable in size and shape.
  • Lined by multiple layers of malignant columnar cells that show cytologic criteria of malignancy.
147
Q

spread of carcinoma of large intestine (colorectal carcinoma)

A
  • local spread: in the wall of intestine -> surroundings
  • lymphatic spread: para-colic lymph nodes
  • Blood spread: liver, lung, brain.
  • Transcoelomic ->Hemorrhagic ascites, peritoneal nodules and ovarian krukenberg tumor.
148
Q

what are the prognostic factors of carcinoma of large intestine (colorectal carcinoma)?

A
  • Tumor stage.
  • Tumor grade.
  • Tumor type.
149
Q

grading of adenocarcinoma of carcinoma of large intestine (colorectal carcinoma)

A
  • Glandular differentiation.
  • Nuclear pleomorphism.
  • Mitotic activity.
150
Q

staging of cancer colon (Duke’s staging)

A
151
Q

TNM staging of cancer colon

A
152
Q

what is the histological structure of the parenchyma of hepatic lobules?

A

Cords (plates) of hepatocytes run in radial pattern between the central vein and portal areas. The plates are one cell thick and are separated by sinusoids lined by endothelial cells and macrophages (Von Kupffor cells).

153
Q

what is the limiting plate of hepatocytes?

A

The hepatocytes that lie at the interface between the lobule and the portal area is called the limiting plate

154
Q

patterns of liver cell injury (necrosis)

A

i- Apoptosis: councilman body
ii- Interface hepatitis
iii- Focal necrosis
iv- Bridging, (confluent) necrosis

“The reticular framework is intact”

155
Q

what is the definition of apoptosis?

A

single cell death

156
Q

what is the M/E of apoptosis?

A
  • Cell undergoes acidophilic necrosis
  • Cytoplasm is granular & dense
  • Nucleus is pyknotic.
  • When the nucleus is extruded, Councilman body is produced.
157
Q

what is the definition of Interface hepatitis?

A

Apoptosis of peripheral hepatocytes resulting in irregular appearance of the limiting plate.

158
Q

what is the M/E of Interface hepatitis?

A

Irregular appearance of the limiting plate

159
Q

what is the definition of Focal (Spotty) necrosis?

A

Necrosis of small groups of hepatocytes within the lobule.

160
Q

what is the M/E of Focal (Spotty) necrosis?

A

Necrotic foci accumulate macrophages, lymphocytes and may be neutrophils

161
Q

what are the characters of Bridging (Confluent) necrosis?

A
  • Involves large groups of hepatocytes in more than one lobule resulting in collapse of reticulin framework of the affected lobules and connection between liver structures.

“due to distruction of cells that they support”

162
Q

what is the definition of acute hepatitis?

A
  • Acute parenchymal liver damage can be caused by many agents.
  • Hepatitis is acute when it lasts less than six months
163
Q

what are the causes of acute hepatitis?

A
  1. Viral hepatitis: Hepatitis A ,E (>95% of viral cause),B,C
  2. Herpes simplex, Cytomegalovirus, Epstein-Barr.
  3. Alcohol .
  4. Toxins: Amanita toxin in mushrooms, carbon tetrachloride,
  5. Drugs: Paracetamol
  6. Metabolic diseases, e.g., Wilson’s disease “Disturbance in metabolism of copper”
164
Q

what is the pathology (microscopic picture) of acute hepatitis?

A

1- Hepatocytes
* Lobular disarray
* Hepatocellular necrosis
* Cholestasis

2- Inflammatory cellular infiltrate
* Lobular inflammation
* Portal inflammation

3- Acute cholestasis

165
Q

what causes acute cholestasis?

A

Due to obstruction of bile canaliculi which is caused by:

  1. Swollen, degenerated necrotic hepatocytes.
  2. Cholangiolitis i.e. inflammation of intralobular bile canaliculi.
166
Q

what are the characters of acute cholestasis?

A
  • Bile canaliculi above the obstruction are dilated and filled with bile. It may form bile plugs or thrombi.
  • Intracytoplasmic bile droplets accumulate in hepatocytes (feathery degeneration) and in von-Kupffor cells

“Due to accumilation of bile within hepatocytes”

167
Q

recovery of the liver

A
  • Active von Kupffer cells show hypertrophy and hyperplasia with increased phagocytosis.
  • Regeneration of hepatocytes begins after 3 weeks and continues for weeks to few months. It is complete regeneration.
  • The surviving hepatocytes show hypertrophy, hyperplasia and increased mitotic activity with occasional binucleated and multinucleated cells.
168
Q

what is the fate of acute viral hepatitis?

A

1. Typical (classical) cases:-
a) Complete recovery after 4 weeks to 4 months.
b) Chronicity that may progress to cirrhosis
c) Chronic carriers in whom the viral antigens are excess in hepatocytes and may reach the blood.

——–

2. Cases with panacinar necrosis:-
a) Death rate 70-90 %.
b) Post necrotic scarring may result in: portal hypertension, liver failure, & increased risk of hepatocellular carcinoma.

169
Q

what is the definition of chronic hepatitis?

A

It is the continuity of hepatitis symptomatic or biochemical (elevated enzymes or presence of viral antigens) without steady improvement for more than 6 months.

170
Q

what are the causes of chronic hepatitis?

A
  1. Viral hepatitis: B,C
  2. Herpes simplex, Cytomegalovirus, Epstein-Barr.
  3. Autoimmune: due to auto-antibodies
  4. Alcohol .
  5. Toxins: Amanita toxin in mushrooms, carbon tetrachloride,
  6. Drugs: Paracetamol
  7. Metabolic diseases, e.g., Wilson’s disease
  8. Cryptogenic: idiopathic
171
Q

what is the pathology of chronic hepatitis?

A
  • N/E: liver slightly enlarged
  • Surface: may be smooth or nodular.
  • M/E: liver biopsy remains the standard in the evaluation of the etiology and extent of diseases of the liver.
172
Q

what is chronic hepatitis analyzed according to?

A

1) the grade ( degree of inflammation) range from very mild to severe

  • Considering the presence or absence and the extent of
    a. Piecemeal necrosis
    b. Lobular necrosis
    c. Bridging necrosis
    d. Portal inflammation
  • These items correlate to the activity of the lesion.
  • Each of these item is given a score number (0- 4 or 6).
  • The sum of score (overall score) is evaluated

2) the stage (extent of fibrosis) divided to a spectrum of 6

173
Q

what is the microscopic picture of chronic hepatitis B?

A
  • Microscopic appearance of Hepatitis B characterized by Ground glass hepatocytes due to the presence of cytoplasmic hepatitis B surface antigen
174
Q

what is the microscopic picture of chronic hepatitis C?

A
  • Predominantly sinusoidal lymphocytic infiltrate, often with lymphoid follicles
  • Lymphoid aggregates are specific for hepatitis C but only 50% sensitive
  • mild and focal macrovesicular steatosis
175
Q

what is the microscopic picture of autoimmune hepatitis?

A
  • Autoimmune Hepatitis
  • Portal plasma cell rich inflammation Interface hepatitis
  • Hepatocyte rosettes
176
Q

what is the prognosis of chronic hepatitis?

A

1- Remission especially with hepatitis C, It occurs with lower grades and stages of chronic hepatitis.

2- Severe disease with high mortality especially with hepatitis B or Delta agent.

3- Cirrhosis (end stage liver).

4- Hepatocellular carcinoma especially with hepatitis B.

177
Q

compare between acute and chronic hepatitis

A
178
Q

CDIP

what is the definition of liver cirrhosis?

A

Chronic Diffuse Irreversible Progressive liver disease characterized by hepatocellular necrosis, hyperplasia of the surviving hepatocytes forming regenerating nodules lacking normal lobular architecture, vascular derangement (Disturbance) and diffuse fibrosis.

179
Q

what are the characteristics of regenerating nodules?

A

An abnormal mass of liver cells without a normal cord pattern nor a central vein and surrounded by fibrous tissue.

180
Q

what are the gross features of cirrhosis?

A

The liver is shrunken, firm and nodular

  • According to the size of the nodules, cirrhosis is classified into:
    1. Micronodular cirrhosis: the nodules are less than 3 mm. in diameter.
    2. Macronodular cirrhosis: the nodules are more than 3 mm. in diameter (poor prognosis)
    3. Mixed micro & macronodular cirrhosis.
181
Q

what are the microscopic features of cirrhosis?

A
  • Loss of the normal hepatic architecture and replacement by regenerative nodules, which is surrounded by fibrous tissue septa.
  • The regenerative nodules: consist of proliferating hepatocytes arranged in thick plates and separated by sinusoidal spaces. The central veins are eccentric or absent, The regenerating hepatocytes may be small, large, uni or binucleated.
  • The fibrous tissue septa: the fibrous tissue replace the damaged hepatocytes and develops at certain sites e.g. perivenular, persinusoidal, pericellular and in relation to portal tracts, The fibrous septae contains proliferating bile ductules and chronic inflammatory cells.

(fibrosis everywhere)

182
Q

what is the definition of hepatocellular carcinoma?

A

Primary carcinoma formed of cells resembling hepatocytes.

This disease is FATAL

183
Q

incidence of hepatocellular carcinoma

A
  • 80-85% of primary malignant liver tumors, in high incidence areas (Africa & Asia) it affects young adults.
  • In low incidence areas (USA& Europe), it occurs after 50 years.
  • Males > females
184
Q

predisposing factors of hepatocellular carcinoma

A
  • HBV.
  • Regenerating nodules of cirrhosis
  • Diet
    1. Poor protein and vitamins
    2. Experimentally, Aflatoxin B1 produces mycotoxin that contaminates badly stored food & cereals.
    3. Nitrosamines.
  • Hormones e.g estrogen and androgen.
185
Q

what are the gross features of hepatocellular carcinoma?

A

- May take one of three forms:

1- Single large, well-defined mass with areas of hemorrhage and necrosis.

2- Multiple small nodules scattered all over the liver sparing its periphery.

3- Diffuse infiltration of the entire liver.

  • Tumor tissue is yellow-white and may be bile stained (green).
186
Q

what are the microscopic features of hepatocellular carcinoma?

A

1.Well differentiated carcinoma: Tumor cells resemble hepatocytes. They are arranged in trabeculae separated by sinusoids & pseudo-glandular, Bile may be present.

2. Poorly differentiated carcinoma: Large anaplastic cells, may be bi or multinucleated giant cells or clear cell type.
Stroma is scanty and poorly vascular.

3. Fibrolamellar carcinoma: cords of polygonal cells with acidophilic cytoplasm. They are separated by Lamellated fibrous stroma.

187
Q

spread of hepatocellular carcinoma

A
  • Direct in the liver
  • Lymphatic to L.N of porta hepatic
  • Blood: Intrahepatic by branches of portal vein and extrahepatic by hepatic vein.
188
Q

what are the symptoms of hepatocellular carcinoma?

A
  1. Silent hepatomegaly.
  2. Rapid increase in size of a cirrhotic liver with hemorrhagic ascites.
  3. Paraneoplastic syndrome (difficulity maintaining balance)
  4. Increased level of α fetoprotein (1000 ng/ml)
189
Q

prognosis of hepatocellular carcinoma

A
  • Poor, most patients die within one year from liver cell failure or metastasis.
  • 5 years survival rate is 5%.

Y2B1 - GIT 📕 (9 decks)

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