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Gastrointestinal Module > Pathology GIT > Flashcards

Pathology GIT Flashcards

1
Q

Dysphagia

A

Difficulty swallowing

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2
Q

Odynophagia

A

Pain on swallowing

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3
Q

Heart burn

A

Burning sensation behind sternum not due to heart issue

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4
Q

Main reason of acid regurgitation into mouth

A

Gastro esophageal reflux disease

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5
Q

Second name of ectopic gastric mucosa

A

Inlet patch

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6
Q

Where can you mostly find an ectopic gastric mucosa

A

Upper third of Esophagus

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7
Q

Complications of ectopic gastric mucosa

A

Dysphagia
Esophagitis
Barrett esophagus
Adenocarcinoma (worst case)

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8
Q

Which one is more common
A. Ectopic gastric mucosa
B. Ectopic pancreatic mucosa

A

A

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9
Q

Pulmonary sequestration

A

Lung Parenchymal tissue in esophagus

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10
Q

Atresia definition

A

Thin non canalized cord replaces a segment of the esophagus

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11
Q

Is atresia compatible with life ?

A

Incompatible without repair

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12
Q

Why does atresia occur mostly with fistula ?

A

Because most atresia occur near the tracheal bifurcation

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13
Q

Atresia symptoms

A

Cyanosis of baby when first feeding
Chocking, coughing
Respiratory distress
Baby vomits after feeding

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14
Q

Fistula definition

A

Abnormal connection between 2 organs

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15
Q

Tracheoesophageal fistula symptoms

A

Aspiration
Suffocation
Pneumonia
Severe fluid and electrolytes imbalance

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16
Q

Esophageal Stenosis

A

Narrowing of the lumen after fibrous thickening of the wall

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17
Q

What is the cause of congenital esophageal stenosis ?

A

Due to partial apoptosis of the lumen

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18
Q

How can increase peristalsis cause esophageal stenosis ?

A

Muscle hypertrophy due to high demand causing partial obstruction

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19
Q

Causes of esophageal stenosis

A 
Congenital 
Increased peristalsis causing muscle hypertrophy 
Inflammatory scarring ( chronic GERD)
Irradiation 
Systemic sclerosis 
Caustic ingestion
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20
Q

Mucosal webs

A

Semi circumferential Protusion of mucosa into lumpen ~5mm

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21
Q

Mucosal webs composition

A

Fibrovascular connective tissue

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22
Q

Which population is more at risk of mucosal webs

A

Women over 40 year old

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23
Q

What diseases are associated with mucosal webs

A

GERD
Chronic graft versus host
Blistering skin diseases

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24
Q

When can you see the

  • Patterson brown Kelly syndrome
  • Plummer vinson syndrome
A

Mucosal webs associated with
Cheilosis
Iron deficiency anemia
Glossitis

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25
Q

Symptoms of mucosal webs

A

Non progressive dysphagia ( solid food )

Incomplete chewed food

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26
Q

Rings definition

A

Circumferential protusion of mucosa submucosa into the lumen and sometimes muscularis proprio hypertrophy

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27
Q

Where do you find A rings

A

Above gastroesophageal junction with squamous mucosa

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28
Q

Where do you find B rings

A

At squamocolumnar junction with gastric cardia type mucosa

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29
Q

How can you assess esophageal dysmotility

A

Esophageal manometry

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30
Q

Three forms of dismotility

A

Nutcracker esophagus
Diffuse esophageal spasm
Hypertensive lower esophageal sphincter

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31
Q

Nutcracker esophagus

A

High amplitude contractions with loss of coordination between inner circular and outer longitudinal

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32
Q

Diffuse esophageal spasm

A

Repetitive, silmutaneous contractions of distal smooth muscle

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33
Q

Diverticulae definition

A

Outpouch of wall due to weakness

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34
Q

Epiphrenic diverticulum

A

Diverticulum above lower esophageal sphincter

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35
Q

Zenker diverticulum

A

Impaired relaxation and spasm of cricropharyngeus muscle causing outpouch just above it

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36
Q

Complications of zenker diverticulum

A

Regurgitation

Halitosis

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37
Q

Achalasia

A

Impaired smooth muscle relaxation increasing tone of lower esophageal sphincter preventing passage of food into stomach with possible obstruction

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38
Q

Achalasia triad

A

Incomplete LES relaxation
Increased LES tone
Aperistalsis of esophagus

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39
Q

Symptoms of achalasia

A

Progressive dysphagia ( food and liquid)
Chest pain
Regurgitation

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40
Q

Primary achalasia cause

A

Ganglion cell degeneration

Vagus nerve degeneration

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41
Q

Secondary achalasia cause

A

Chagas’s disease with destruction of myenteric plexus

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42
Q

Achalasia like disease

A 
Diabetic neuropathy
Malignancy 
Amyloidosis 
Sarcoidosis 
Polio
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43
Q

Hiatal hernia

A

Protusion of stomach above diaphragm

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44
Q

2 forms of hiatal hernia

A

Axial/sliding hernia

Non axial/paraesophageal hernia

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45
Q

Which form of hiatal hernia has higher incidence ?

A

Axial hernia (95% cases)

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46
Q

Axial hernia presentation

A

Circumferential and bell shaped dilation

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47
Q

False diverticulum

A

Outpouching of mucosa and submucosa

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48
Q

True diverticulum

A

Outpouching of all parts of the GIT zone concerned

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49
Q

Traction diverticulum

A

Diverticulum near midpoint of esophagus

Tb like Scarring due to mediastinal lymphadenitis

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50
Q

Mallory Weiss syndrome

A

Longitudinal tear at esophagogastric junction

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51
Q

Mallory Weiss syndrome most common in

A

Alcoholics because of excessive vomiting and gastric reflux

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52
Q

What would happen in case of infection in Mallory Weiss syndrome

A

Inflammatory ulcer

Mediastinitis

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53
Q

Which one is most severe
Mallory Weiss syndrome
Boerrhave syndrome

A

Boerrhave syndrome

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54
Q

Why do you do ECG in boerrhave syndrome

A

Because ressembles myocardial infarction

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55
Q

Boerthave syndrome

A

Transmural tearing with rupture of distal oesophagus

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56
Q

Complication of boerrhave syndrome

A

Severe mediastinitis

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57
Q

Symptoms of boerrhave syndrome

A

Severe chest pain
Tachypnea
Shock

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58
Q

What are some factors that can injure oesophagus

A

Irritants ( alcohol, corrosive acids, hot fluids, smoking)
Chemical injury in children
Attempted suicide in adults

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59
Q

What are the desquamative diseases of esophageal injuries

A

chron’s disease
Bullous pemphigoid
Epiderm

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60
Q

How does stenosis manifest in adulthood

A

Progressive dysphagia

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61
Q

What do you see in X ray of achalasia patient

A

Bird beak sign

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62
Q

Most important cause of acute esophagitis

A

Viral and fungal infections in immunocompromised patient

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63
Q

Most common infection of esophagus

A

Candidiasis

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64
Q

Complication of candidiasis in esophagus

A

Dysphagia

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65
Q

How do you recognize candidiasis

A

White plaque with hemorrhagic margins

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66
Q

What are the diseases under chronic esophagitis

A

GERD

Barrets esophagus

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67
Q

How is the esophagus protected from abrasion

A

Stratified squamous epithelium

Mucin and bicarbonate secretions

Constant LES tone

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68
Q

What is the most common cause of GERD

A

LES incompétence

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69
Q

Symptoms of GERD

A

Acid awareness
Heartburn
Odynophagia
Dysphagia

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70
Q

Morphology of GERD

A 
Cell injury 
Accelerated desquamation
Basal cell hyperplasia 
Immature cell predominance in epithelium 
Low grade inflammation
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71
Q

Severe GERD presentation

A

Ulceration

Possible hemorrhages

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72
Q

GERD Healing process

A

Fibrosis

Epithelial regeneration

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73
Q

What disease is Barrett’s disease a complication of ?

A

GERD

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74
Q

Barrett’s esophagus

A

columnar metaplasia in esophagus

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75
Q

Two criteria to diagnose Barrett’s esophagus

A

Endoscopy evidence of columnar epithelium ( appear as tongue of red mucosa)

Histologic evidence with biopsy to find columnar cell

Goblet cells - stain pale blue by H&E

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76
Q

What is the single most important factor to develop esophagus adenocarcinoma

A

Barrett’s esophagus

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77
Q

Why do you put patient with barrets esophagus disease on regular endoscopic surveillance ?

A

They have 100 more chances of developing cancer

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78
Q

Are benign tumors of esophagus common ?

A

No

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79
Q

Most common type of benign tumor of esophagus

A

Leiomyoma ( smooth muscle)

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80
Q

Type of benign tumors of esophagus

A 
Leiomyomas ( smooth muscle)
Hemangiomas ( blood vessels) 
Neurofibromas (nerves)
Lymphangiomas (lymphatic vessels) 
Fibrovascular polyps/pedunculated lipomas 
Squamous papillomas 
Inflammatory polyps
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81
Q

Fibrovascular polyps morphology

A

Mucosal polyps with conbination of fibrous, vascular, or adipose tissue covered with normal mucosa

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82
Q

Squamous papillomas morphology

A

Sessile lésions with connective tissue core , and hyperplastic pappiliform squamous mucosa

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83
Q

What population most affected by malignant tumors of esophagus ?

A

Adult male (4x more than female)

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84
Q

Etiology of malignant esophageal tumor

A

Riboflavin, vit À, C, thiamine, pyridoxine deficiencies in diet

Zinc, molybdenum deficiencies

Fungal contamination

Opium usage

Thermal injury

Smoking

Alcohols

Viruses ( HPV)

Genetic alterations (p161NK4 mutation, cyclin D1, c-MYC, EGFR amplification)

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85
Q

Morphology of malignant cancer of esophagus

A

Pleomorphism ( disordered maturation, mitotis at surface)

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86
Q

Most common type of carcinoma in lower third of esophagus

A

Adenocarcinoma

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87
Q

Most common type of carcinoma in esophagus

A

Squamous type

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88
Q

How do squamous carcinoma start

A

As ulcer

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89
Q

Main presentation of esophagus carcinoma

A

Dysphagia

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90
Q

Main Treatment of esophagus carcinoma

A

Radiotherapy

Laser therapy

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91
Q

How is long term survival of esophagus carcinoma

A

Poor - 5% survival in 5 years

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92
Q

Congenital anomalies of stomach

A

Heterotopic rest

Pyloric stenosis

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93
Q

Pancreatic heterotopia

A

Pancreatic tissue in gastric submucosa , subserosal

Pancreatic tissue in intestinal submucosa, subserosal

Pancreatic tissue on pylorus with risk of obstruction

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94
Q

Which population is more affected by the congenital hypertrophic pyloric stenosis

A

Infants especially boys

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95
Q

What disease are associated with congenital hypertrophic pyloric stenosis

A

Turner syndrome, trisomy 18, esophageal atresia

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96
Q

Congenital hypertrophic pyloric stenosis clinical presentation

A

Regurgitation

Vomiting (persistent, projectile, non bilious)

Visible Peristalsis and mass in pyloric region or distal stomach

Edema

Inflammatory changes

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97
Q

Curative measure of Congenital hypertrophic pyloric stenosis

A

Surgical muscle split

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98
Q

Possible complications of peptic ulcer near pylorus

A

Acquired pyloric stenosis

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99
Q

Possible causes of acquired pyloric stenosis

A

Carcinoma, lymphomas, inflammatory fibrosis, malignant infiltration, chronic pyloric spasm

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100
Q

Two types of gastritis

A

Acute or chronic

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101
Q

Acute gastritis is an important cause of..

A

Acute gastrointestinal bleeding

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102
Q

Acute gastritis possible causes

A 
Heavy use of NSAIDs
Alcohol 
smoking 
chemotherapy 
ureamia 
Systemic bacterial or viral infections 
heavy stress ischemia
 shock 
suicide attempts 
mechanical trauma 
gastrectomy
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103
Q

Gastritis pathophysiology

A 
Increased acid secretion 
Decreased bicarbonate 
Reduced blood flow 
Mucus layer disruption 
Epithelium damage 
Acid bile regurgitation 
Low PG 
Lysolecithins
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104
Q

Acute Gastritis morphology

A

Moderate Edema lamina propria

Vascular congestion

Neutrophils in epithelium

Erosion ( fibrin, infiltrate)

hemorrhage (dark spots) in severe cases

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105
Q

Is acute gastritis a major cause of massive hemorrhage in alcoholics

A

Yes

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106
Q

Acute gastritis symptoms

A 
May be asymptomatic
Nausea 
pain 
vomiting 
hemorrhage massive 
haematemesis 
melaena
Fatal blood loss
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107
Q

Chronic gastritis presentation

A

Chronic mucosal inflammatory changes
Mucosal atrophy
Epithelial metaplasia
No erosion

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108
Q

Major cause of chronic gastritis

A 
Chronic infection by H pylori 
Autoimmunity - pernicious anemia 
Toxic ( smoke and alcohol) 
Post surgery 
Motor and mechanical 
Radiation 
Granulomatous
Miscellaneous ( amyloidosis, graft versus host )w
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109
Q

Percentage of patients with chronic gastritis affected by h pylori

A

90%

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110
Q

H pylori specialized traits

A

Motility in viscous mucus ( flagella)

Urease which buffers acids around parasite

Adhésins ( especially in O patients)

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111
Q

What type of h pylori associated with duodenal ulcer

A

Cag A gene

Vac A gene

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112
Q

2 patterns of h pylori chronic gastritis

A

Antral type gastritis

Pan gastritis

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113
Q

Antral type gastritis

A

H pylori gastritis with high acid production and high risk of duodenal ulcer

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114
Q

Pam gastritis

A

Lower acid secretion , high risk of adenocarcinoma

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115
Q

Autoimmune chronic gastritis

A

Autoantibodies against gastric parietal cells which prevent acid production.

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116
Q

Autoimmune chronic gastritis presentation

A

Hypoclorrhydria

Macrocytic anemia with vit B12 deficiency because no intrinsic factor

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117
Q

Pernicious anemia

A

Autoimmune gastritis + macrocytic anemia

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118
Q

Autoimmune gastritis morphology

A 
Glandular atrophy 
Fibrosis of lamina propria 
Intestinal metaplasia with goblet cells replacing mucin cells 
Absortive cells
Paneth cells
119
Q

Reflux gastritis

A

Regurgitation of bile and alkaline duodenal juice in stomach

120
Q

Reflux gastritis presentation

A

Epithelial desquamation
Compensatory Hyperplasia
Vasodilation and edema of lamina propria

121
Q

When does reflux gastritis occur

A

Post operative stomach with bypass of pylorus

Failure in pyloric competence

122
Q

Types of chronic gastritis

A

Type a - immune gastritis ( less frequent) affect fundus, antibodies to parietal cells (achlorrydria and high gastrin serum)

Type b- infectious disease ( more frequent) mostly h pylori

123
Q

Ulcers

A

Breach in mucosa of GIT from muscularis mucosa to submucosa or deeper

124
Q

Most common type of ulcer

A

Chronic
Solitary
Présent in any part of GIT exposed to acid or peptic juices

125
Q

Which type of peptic ulcer pénétrâtes the full thickness of muscularis propria and has base in serosal layer of organ

A

Chronic peptic ulcer

126
Q

Most common location of peptic ulcer

A

Duodenum first part

Stomach ( antrum)

Gastro esophageal junction ( barrets esophagus)

Within margins of gastrojejunostomy

Duodenum,stomach or/and jéjunum of patient with zollinger Ellison syndrome

Within or adjacent to iléal Meckel diverticulum with ectopic gastric mucosa

127
Q

Which type of peptic ulcer pénétrâtes muscularis mucosa but does not extend further than submucosa ?

A

Acute peptic ulcer

128
Q

Main cause of acute peptic ulcer

A

Stress

Analgesic drugs

129
Q

Curling ulcers

A

Ulcers with severe burns

130
Q

Cushing’s ulcer

A

Ulcers occurring in brain damage

131
Q

Main presentation of acute peptic ulcer

A

Gastric hemorrhage

132
Q

Acute peptic ulcer heals. Scar or no ?

A

No scar

133
Q

Population more at risk of gastric ulcer

A

Older group , females

134
Q

Clinical presentation of chronic peptic ulcer

A

Dyspepsia when chronic gastric ulcer

Odynophagia that improves when eating in duodenal

135
Q

Classic peptic ulcer appearance

A

Circular or oval
Punched out
Gastri rugae converging near ulcer margin

136
Q

Most common location of chronic gastric ulcer

A

Along the lesser curvature

137
Q

Most common location of chronic duodenal ulcer

A

1st part of duodenum

138
Q

Kissing ulcers

A

Ulcers on both posterior and anterior part of duodenum. Common in chronic peptic ulcer

139
Q

Chronic peptic ulcer morphology

A

Usually solitary
Gastric ulcer can coexist with duodenal ulcer
Kissing ulcers
Circular or oval
Gastric rugae converge upon ulcer margin
Base of ulcer in gastric or duodenal mucosa

140
Q

Microscopic feature of chronic peptic ulcer

A

Surface layer with neutrophils and structure less harmatoxyphilic bodies

Under : fibrinoid necrosis organized by granulation in deeper areas

Granulation tissue become fibrous scar

Small inflammation with lymphocytes eosinophils plasma

Endarteritis obliterans in arterial lesions (thrombosis and inflammation of small vessels)

141
Q

Complication of chronic peptic ulcers

A

Healing and scarring ( scarring invariable can lead to pyloric stenosis which can cause gastric outlet obstruction)

Perforation when ulceration faster than repair ( gut content into peritoneal cavity)

Hemorrhage ( erosion of small blood vessels leading to iron deficiency anemia, when large blood vessels haematemesis and melaena visible)

Carcinoma ( 1% of chronic gastric ulcer)

142
Q

Gastric outlet obstruction presentation

A 
Recurrent vomiting 
Dehydration
Chloride depletion
Rise in plasma bicarbonate 
Hypokalemic alkalosis
143
Q

Arteries involved in life threatening hemorrhage due to peptic ulcer

A

Left gastric artery

Gastro duodenal artery

144
Q

Ethipathogenesis of chronic gastric ulcer

A 
Environment (h pylori)
Stress psychological 
Cigarette 
Anelgesic
Genetics ( especially O blood group) 
Familial ( monozygotic twin)
145
Q

Pathogenesis of peptic ulcer

A

Imbalance between mucosal defense and damaging forces (pepsin, gastric acid )

In gastric ulcer : impaired mucosal difference with in most cases h pylori present (70%)

Un duodenal ulcers : high gastric levels at night with in most cases h pylori present (90 x%)

Gastrinomas like zollinger Ellison syndrome stimulate acid secretion

146
Q

Polyp in git

A

Any mass or nodule that projects above the level of the surrounding mucosa

147
Q

2 forms of polyps

A

Neoplastic

Form because of excess reparative/regenerative process

148
Q

Commonest form of polyp

A

Simple elongation of gastric pits separated by fibrous tissue or musky inflamed lamina propria

149
Q

What form of polyp is unusual

A

True benign neoplastic epithelial polyp

150
Q

Commonest connective tissue gastric neoplasm

A

Smooth muscle tumor

151
Q

Morphology of smooth muscle tumor of stomach

A

Intramural tumor projecting into lumen
Sometimes presence of ulcer crater ( source of hemorrhage)

Interwoven bundles of spindle cells
Variable amount of eosinophils in cytoplasm

All of this can be seen in neural tumors too

152
Q

Gastric strolls tumors

A

Unpredictable behaviors
Difficult to say if benign or malignant
(Benign would have small size, encapsulation, low mitosis, no necrosis)

153
Q

Most common type of malignancy in stomach

A

Carcinoma (90-95%)

Then lymphomas (4%)
Carcinoid ( 3%)
Malignant stromal cell tumor (2%)

154
Q

Second most common fatal malignancy in the world

A

Gastric cancer

155
Q

Factors increasing gastric carcinoma

A

Diet ( nitrites , smoked food, salted food, pickled vegetables)
Low socioeconomic
Cigarette

Chronic gastritis (hypochlorridria which favors h pylori) 
H pylori infection

Partial gastrectomy ( favors duodenal excretion reflux

Gastric adenomas ( 40% have cancer when diagnosed )

Barrett’s esophagus (gastro esophageal junction tumors )

Genetic (increased risk in group A blood , family history of gastric cancer, hereditary non polyposis colon cancer syndrome)

156
Q

Dysplasia-carcinoma sequence in gastric cancer

A

Chronic gastritis to atrophy and intestinal metaplasia to pre malignant dysplasia

157
Q

Percentage of cases where curative operation still possible

A

45%

158
Q

Prognosis of gastric cancer

A

10-15% survival rate in 5 years

159
Q

Basis of classification of gastric cancer

A

Depth of invasion

Macroscopic growth pattern

Histologic subtype

160
Q

Depth of invasion of gastric cancer

A

Early or advanced based on direct spread into stomach wall

When early => mucosa of submucosa only ( 90% survival in 5 years)

When advanced => extend into or beyond main muscle coats

161
Q

Growth pattern of gastric cancer (3 patterns)

A

Exophytic ( Protusion of tumor mass into lumen)

Flat or depressed (no obvious tumor mass in mucosa )

Excavated ( shallow or deep erosive crater present in wall )

162
Q

Linitis plastica

A

Uncommon
Broad region of gastric wall or entire stomach infiltatred by malignancy

Rigid and thick leather bottle like stomach

163
Q

Histological pattern of gastric cancer

A

Intestinal type => neoplastic intestinal glands in gastric wall

Diffuse type => gastric type mucous cell permetjfn mucosa and wall ( they are individual or in small clusters) with signet ring conformation ( peripheral nucleus)

164
Q

First clinical presentation of gastric carcinoma

A

Metastasis to supraclavicular sentinel node (virchow node)

165
Q

Location of body invaded by gastric carcinoma

A

Duodenum
Pancreas
retroperitoneum

166
Q

Krukenberg tumor

A

Gastric carcinoma metastasis that reached one or both ovaries

167
Q

Is gastric carcinoma insidious ?

A

Yes
Slow growing
No symptoms at first

168
Q

Symptoms of gastric cancer

A 
Weight loss
Abdominal pain
Anorexia 
Vomiting 
Altered bowel habits

Less frequent:
Dysphagia
Anemia
Hemorrhage

169
Q

Idiopathic inflammatory bowel disease

A

Chronic inflammatory conditions due to persistent action of mucosal immune system because of strong response to normal intramural flora

170
Q

2 disorders of idiopathic inflammatory bowel disease

A

Crohn’s disease

Ulcerative colitis

171
Q

Pathogenesis of inflammatory bowel disease

A

Failure of immune regulation
Genetic susceptibility
Environnemental triggers

172
Q

Cronhs disease

A

Autoimmunity against any portion of GIT from mouth to anus

Most often at distal small intestine and colon

173
Q

Crohn’s disease characteristics

A

Sharply delimited
Transmural involvement of bowel
Non caseating granulomas
Fissuring with fistulae

174
Q

Peak of detection of Crohn’s disease

A

2nd and 3rd decades

175
Q

Clinical features of Crohn’s disease

A 
Intermittent attacks with : 
Mild diarrhea 
Fever 
Abdominal pain  
Physical and emotional stress can trigger them

Fecal blood loss leading to anemia sometimes

In some patients => mimic acute appendicitis or acute bowel perforation with right lower quadrant pain

176
Q

Complications of Crohn’s disease

A

Intestinal obstruction

177
Q

Organs involvement stats in Crohn’s disease

A

Small intestine involvement in 40% cases

Small intestine and colon 30%

Colon alone 30%

178
Q

Morphology of Crohn’s disease

A

Granular and dull gray serosa

Mesenteric fat around bowel surface

Thick, edematous, fibrotic Mesentery

Aphtous ulcers - small discrete shallow ulcers with hemorrhagic rims

Coarsely textured mucosa - cobblestone appearance

Longitudinal ulcers which progress into narrow deep fissures

Subsequent fibrosis leading to string sign because of narrowing ( only small amount of contrast passes through affected segment)

Fissure may cause rose thorn appearance of lumen with contrast medium

Enlarged reactive hyperplasia which contain granulomas

179
Q

Skip lesions in Crohn’s disease

A

Disease separated by normal tissue

180
Q

Earliest evidence of Crohn’s disease with naked eye

A

Aphtous ulcers

181
Q

Microscopic feature of Crohn’s disease

A

Early => neutrophilic infiltration in epithelium which progresses to crypts

Crypt abscesses

Chronic mucosal damage with architectural distortion

Blunting of villi in small intestine

Crypts irregular and branching in colon

Mucosa metaplasia ( Paneth cell metaplasia or pyloric metaplasia in colon )

Transmural collection of lymphocytes and plasma cells

Granulomas ( non caseated ) With giant cells ( langhans type)

Réduplication,thickening and irregularity of the muscularis mucosa

Fibrosis of the submucosa muscularis propria and mucosa

Mucosal and submucosa lymphangiectasia, hypertrophy of mural nerve fibers , localized vasculitis

182
Q

Classical Microscopic feature of Crohn’s disease

A

Granulomas ( only in 60% of patients tho so use summation of other histologicak findings to Diagnose patients without granulomas)

183
Q

Complication of Crohn’s disease

A

Malabsorption syndrome ( due to Small intestine involvement and resection of bowel)

Fistula formation ( Between loops of bowel or enterocutaneous fistula)

Anal lesions ( 60% of patients)

Perforation , hemorrhage , toxic dilatation => rare

Malignancy over long-term

Systemic amyloidosis

184
Q

More or less risk of malignancy in Crohn’s disease compared to ulcerative colitis

A

Less

185
Q

Ulcerative colitis

A

Ulcero inflammatory disease which involves the mucosa the submucosal of the large intestine

186
Q

Main location where ulcerative colitis starts

A

Rectum

187
Q

Main differences between Ulcerative colitis and Crohn’s disease

A

Confined to the colon

No granulomas

188
Q

Backwash ileitis

A

Sometimes in ulcerative colitis involvement of the terminal ileum is seen

Maybe due to the incompetence of the ileocecal valve

189
Q

Which disease is more common, ulcerative colitis or Crohn’s disease

A

Ulcerative colitis

190
Q

What population is more at risk of ulcerative colitis

A

Females with an onset at 20 and 25 year old

191
Q

Etiology of ulcerated colitis

A

Obscure causes so three theories ( Infection psychosomatic factors and Immunological factors)

Due to atypical immune response triggered by an infection (enteropathogenic E. coli)

192
Q

Presentation of ulcerative colitis

A

Attacks of persistent bloody mucoid diarrhea which appear after long period without no symptoms

Initial attack can be explosive with serious bleeding and fluids and electrolytes imbalance

Can have sudden cessation of bowel function and toxic megacolon

Cramps relieved by defecation

Constipation in small number of patients

Stress can cause an attack

193
Q

First manifestation of ulcerative colitis

A

Bloody diarrhea with mucus

lower abdominal pain and cramps relieved by defecation

194
Q

Morphology of ulcerative colitis

A

Continues in distribution
Disease maximal In the rectum

Severe active inflammation
Extensive broad-based ulceration of mucosa in distal colon or throughout its length

Ulcers with irregular outline and orientation

Pseudopolyps ( Protusion of regenerating mucosa )
No mural thickening
Normal serosal surface

195
Q

Proctitis

A

Ulcerative colitis confined to the rectum

196
Q

Distal colitis

A

Ulcerative colitis confined to the rectosigmoid

197
Q

Pancolitis

A

Ulcerative colitis extending to the cecum

198
Q

Presentation of ulcerative colitis in severe cases

A 
Muscularis propria damage 
Neural plexus damage 
progressive dilatation 
swelling 
gangrene of the colon 
mixed acute and chronic inflammatory cell infiltration in mucosa 
Crypts abscesses
Goblet cell depletion
199
Q

Rectal biopsy in long-standing ulcerative colitis

A

Crypt atrophy
shortfall and distortion
metaplastic (paneth cells)
Dysplasia and progression to Franck carcinoma on epithelium

200
Q

Ulcerative colitis complications

A

Locally :
Malignancy (2% but 10% if disease for more than 25years)
Hemorrhage (generally chronic blood loss with iron deficiency anemia)
electrolyte disturbances due to severe diarrhea toxic dilatation ( leading to perforation and fecal peritonitis)

Systemic :
Skin lesions with pigmentation erythema nodosum and pyoderma gamgrenosum

Liver with fatty change

Chronic Pericholangitis ( Can lead to sclerosing cholangitis and biliary obstruction and cirrhosis)

Eyes complications with iritis, uveitis, episcleritis

Joints complications (Arthritis , spinal disease, ankylosing spondylitis)

201
Q

Higher risk of cancer in ulcerative colitis associated with

A

Onset of disease in childhood severe first attack
pancolitis
continuous symptoms rather than intermittent

202
Q

Population more at risk of appendicitis

A

Adolescents and young adults

203
Q

Sequence of events in appendicitis

A

Pain from Periumbilical region to the right lower quadrant

Nausea / vomiting

Abdominal tenderness

Mild fever

High WBC

Right flank or pelvic pain in retoceacal appendix

Left upper quadrant pain in mal rotated colon

204
Q

Predisposing factors to appendicitis

A

Faecoliths/faecalith - hard pellets of feces due to dehydration and compaction

Food residue

Enterobius worm

Lymphoid hyperplasia

appendix diverticulum

Tumor

Sometime no evident obstruction

Specific inflammation ( yersinia pseudotunerculosis, typhoid, actinomycoses)

UC and CDs

205
Q

Appendicitis morphology

A

Bridge in epithelium and acute inflammation of mucosa

Neutrophilic exudate in mucosa ( can spread)

Congestion of subserosal vessels

Dull granular red membrane serosal of appendix (early stage)

Fibrino purulent exudate over serosa ( later stage )

Infection by bowel flora so mucosal ulcers with exudate and fibrin into lumen

Abscess formation in wall ( suppurative necrosi in mucosa) can cause peritonitis if affect all layers

Superimposed ischaemia (caused by build up of fluid exudate + blood vessel damage + thrombosis)

Distal part of appendix can become gangrenous and perforate

206
Q

Histology of appendicitis

A

Neutrophilic infiltration of muscularis propria

207
Q

Complications of acute appendicitis

A 
Perforation leading to peritonitis
Abscess and fistula
Bacteremia
Inflammation thrombosis septicemia
Portal vein and liver abscess 
Fibrosis and obstruction of neck of appendix forming mucocele which can rupture => Mucus can get into the peritoneal cavity
208
Q

Appendicitis like diseases

A 
Mesenteric lymphadenitis (virus etiology )
Acute salpingites 
Ectopic pregnancy
Mittelschmerz 
CF 
Meckels diverticulitis
209
Q

Colonic diverticulosis

A

Outpouching of the mucosa and submucosa due to weakness in muscularis propria

210
Q

Meckel diverticulum

A

Congenital diverticulae of all three layers of the bowel wall due to failure of involution of the vitelline duct

50% cases with heterotopic rest of gastric mucosa or pancreatic tissue

211
Q

Diverticula of jéjunum and ileum, rare or common ?

A

Rare

212
Q

Population at risk of colonic diverticulae

A

Above 60 years old , 50% prevalence

Rate under 30

213
Q

Morphology of colonic diverticulum

A

Flask like or spherical outpouching

Majority in sigmoid colon

Appear alongside teniae coli

Elastic

Compressible

Easily emptied of fecal contents

214
Q

Histology of colonic diverticulum

A

Thin wall
Flat or atrophied mucosa
Attenuated or absent musucularis propria
Inflammation due to obstruction and or perforation
Fibrotic thickening ( can ressemble colonic cancer)

215
Q

Complication of colonic diverticulum

A

Pericolic abscess

Sinus tracts

Pelvic peritonitis

Generalized peritonitis

216
Q

Cholera pathogen involved

A

Comma shaped gram negative vibrio cholera

217
Q

Number of great long lasting cholera epidemics

A

7

218
Q

Which aero type of cholera associated with severe diarrhea

A

01 serotype

219
Q

Pathogenesis of cholera disease

A

Invade lumen and secrete enterotoxin ( cholera toxin)

cAMP increases in cell which promote chloride and bicarbonate secretion with sodium and water secretion

Water secreted with small mucus ( 14L/day) leading to severe dehydration and electrolyte imbalance

220
Q

Histology of cholera

A

Congestion of mucosal lamina propria

Moninuclear inflammatory cells infiltration

Hyperplasia of peyers patches

221
Q

Thyphoid fever pathogen involved

A

Salmonellae typhi

222
Q

Epidemiology of thyphoid fever

A

Underdeveloped countries

Sanitary conditions insufficient

223
Q

Presentation of thyphoid fever

A 
Bacteremia 
Fever 
Chills
Reticuloendothelial involvement
Rash 
Abdominal pain
Prostration
Intestinal bleeding 
Shock
224
Q

Typhoid fever pathogenesis

A

Salmonella invade epithelial cells and tissue macrophages

Proteins for adhesions and recruitment of host cytoskeletal proteins

225
Q

Morphology of typhoid fever

A

Phagocytes proliferation

Reticuloendothelial and lymphoid tissue enlargement

Payers patches in terminal ileum

Oval ulcers with long axis in direction of bowel flow to

Enlarged, soft, bulging spleen ( pale red pulp)

Liver with parenchymal necrosis with phagocytiez mononuclear cell replacing hepatocytes forming typhoid module

Hall bladder colonized

226
Q

Microscopy of typhoid fever

A

Macrophages withbbacteria and erythrocytes and nuclear debris

Lymphocytes and plasma cells with paucity of neutrophils

227
Q

Ameobiasis pathogen

A

Entamoeba hystolitica

228
Q

Presentation of amoeobiasis

A

Dysentery
Liver abscess
Intestinal pain
Fever

229
Q

Ameobiasis payhogenesis

A

Cyst form release trophozoites

Attach colonic epithelium (lectin, channel forming protein, cysteine proteinases)
lyse colonic epithelial cells

230
Q

Morphology of amoebiasis

A

Involves mostly caecum and ascending colon

Invade crypts

Flask shaped ulcers at muscularis mucosa

231
Q

Microscopy of amoebiasis

A

Neutrophilic infiltrâtes in mucosa

Ulcers with few inflammatory hosts

Areas of liquefactive necrosis

Ameboema - napkin like constrictive lesion, profuse granulation

Parasite can embolies to the liver and produce liver absces

232
Q

Bacterial enterocolitis

A

Various entities causing diarrheal illnesses

233
Q

Pathogens involved in diarrhea caused by ingestion of preformed toxin

A

Staph aureus
Vibrios
Clostridium perfringens

234
Q

Pathogens involved in diarrhea caused by toxigenic organism

A

E. coli
Shigella
They release enterotoxins

235
Q

Pathogens involved in diarrhea caused by entrain as I’ve organism that destroy mucosal epithelial cells

A

Yersinia enterocolitica

236
Q

Presentation of ingestion of preformed bacterial toxins

A

Symptoms in matter of hours
Explosive diarrhea
Acute abdominal distress

237
Q

Presentation of infection with enteric pathogens

A

Incubation from hours to days
Diarrhea
Dehydration
Disentery

238
Q

Presentation of insidious infections

A

Can present as subacute disease resembling CD

239
Q

Bacterial enterocolitis complications

A

Dehydration
Sepsis
Perforation
Death

240
Q

Necrotizing enterocolitis

A

Acute necrotizing inflammation of small and large intestine

241
Q

What is most common acquired GIT energy of neonates

A

Necrotizing enterocolitis

242
Q

Peak incidence of necrotizing enterocolitis

A

When infants start on oral food

243
Q

Etiology of necrotizing enterocolitis

A 
Combination of : 
Ischemic injury 
Pathogenic colonization 
Excess proteins in lumen 
Immaturity of neonate gut
244
Q

Is necrotizing enterocolitis most prevalent in formula fed infants ?

A

Yes

245
Q

Primary location affected by necrotizing enterocolitis

A

Terminal ileum

Ascending colon

246
Q

Necrotizing enterocolitis presentation

A

Early => bowel mucosa with edema, hemorrhage, necrosis

After

Full thickness is hemorrhagic, inflamed, grangenous

Bacterial overgrowth
Mural gas formation

Features of repairs ( epithelial regeneration, granulation, fibrosis)

Can have sepsis , perforation and shock

Distended tender abdomen
Ileus
Diarrhea with frank blood

247
Q

Long term complications of necrotizing enterocolitis

A

Short bowel syndrome

Malabsorption

248
Q

Main origin of tumors in small and large intestine

A

Epithelial

249
Q

Most common host of primary neoplasm in body

A

Colon

250
Q

70% of all malignancies in GIT are

A

Adenocarcinoma

251
Q

Main classification of intestinal tumors

A

Non neoplastic polyps

Neoplastic epithelial lesion

Neoplastic mesenchymal lesions

Other

252
Q

Types of non neoplastic polyps

A

Hyperplastic polyps

Harmatomatous polyps

Inflammatory polyps

Lymphoid polyps

253
Q

Type of neoplastic epithelial lesions

A

Benign ( tubular adeno ma, tubulovillous adenoma, villous)

Malignant ( adenocarcinoma, carcinoid tumors, anal zone carcinoma)

254
Q

Type of neoplastic mesenchymal lesions

A

Benign ( leiomyoma, lipoma, neuroma, angioma)

Malignant ( leiomyosarcoma, liposarcoma, malignant spindle cel tumor, kaposis sarcoma)

Lymphoma

255
Q

Hyperplastic polyps

A

Epithelial polyps
Seems mostly in 6th and 7th decade
Nipple like , hemispheric, moist protrusions of mucosa
Common in recto segmoid colon

Formed Glands and crypts with non neoplastic epithelial cells

256
Q

Harmatomous polyps

A

Juvenile polyps ( sporadic or due to rare autosomal dominant juvenile polyposis syndrome)
80% in rectum
Large, round , smooth, slightly lobulated, stalked
Bulk of polyp with lamina propria enclosing abundant cystically dilated glands
Congested or ulcerated surface

Peutz jeghers polyps
Rare autosomal dominant syndrome
Multiple harmatomatous polyps in entire GIT
Melanotic mucosa
Cutaneous pigmentation around lips , oral mucosa, face, genitalia , palms
Large , pedunculated, firm lobulated contour
Connective tissue and well formed smooth muscle into polyp

257
Q

Inflammatory polyps

A

Inflamed regenerating and reparative mucosa after ulceration

Granulation tissue

Seen in long CD and UD

258
Q

Lymphoid polyps

A

Mucosal bumps with intra mucosal lymphoid tissue

259
Q

Neoplastic epithelial lesions incidence

A

20-30% before 40 yo

40-50% after 60

260
Q

most common type of neoplastic epithelial lesions

A

Tubular

261
Q

Interdépendant features of malignancy risk of adenomatous polyp

A

Polyp size
Histologic architecture
Severity of epithelial dysplasia

262
Q

In what type of neoplastic epithelial lesions is cancer more common

A

40% - sessile villous adenoma bigger than 4 cm

263
Q

Colorectal tubular/tubulovillous adenoma mostly asymptomatic. So how is discovered

A

During anemia or occult bleeding evaluations

264
Q

Why are villous adenoma more frequently symptomatic?

A

Associated with overt rectal bleeding

265
Q

Majority of tubular adenoma located in

A

Colon (90%)

Rectosigmoid (1/2)

266
Q

Tubular adenoma microscopy

A

Stalk - fibromuscular tissue , prominent blood vessels, non neoplastic mucosa cover

Raspberry like head- neoplastic epithelium, all degree of dysplasia,

267
Q

Villous adenoma major location

A

Rectum

Rectosigmoid

268
Q

Villous adenoma morphology

A

Sessile
Cauliflower like masses
Finger like Projection in surrounding normal mucosa with dysplatic columnar epithelium

269
Q

Tubulovillous adenoma

A

Intermediate adenoma between tubular and villous lesions

270
Q

Familial adenomatous polyposis

A

Lot of adenomatous polyps

Mostly always progress to colon adenocarcinoma

271
Q

Number of polyps required for FAP diagnosis

A

At least 100 polyps

272
Q

Gardners syndrome

A 
Variant of FAP with same polyps but with on top : 
Multiple osteomas 
Epidermal cysts 
Fibromatosis
Dental abnormalities 
Duodenal and thyroid cancer
273
Q

Turcot syndrome

A

Multiple adenomatous polyps + CNS tumor

274
Q

Major type of cancer in large intestine

A

Adenocarcinoma(95%)

275
Q

Adenocarcinoma of large intestine characteristics

A

Arise in polyps

Symptoms early when still curable by resection

276
Q

Adenocarcinoma of large intestine incidence

A

60-70 yo
UC or one polyposis syndrome preexisting in young people
Affect men and women the same

277
Q

Make:ratio in rectal cancer

A

2:1

278
Q

Rectal adenocarcinoma etiology

A

Dietary ( low insoluble vegetables fiber , high CHO, high fat, low protective micronutrient

279
Q

Cæcal and right colonic cancers clinical characteristics

A 
Fatigue 
Weakness 
Iron deficiency anemia 
Bulky and bleeding 
Discovered at early stage
280
Q

Left sided colonic cancers characteristics

A

Occult bleeding
Changes in bowel habit
Cramps lower quadrant discomfort

281
Q

Why do cancer of rectum and sigmoid have poorer prognosis

A

More infiltrative at time of diagnosis

282
Q

What does iron deficiency anemia in an old man means

A

Git cancer until proven otherwise

283
Q

Sites of metastasis spread of colorectal tumors

A

Regional lymph nodes
Liver
Lungs
Bones

284
Q

colorectal carcinoma classification

A

By stages
A- mucosa limited
B1- stops at muscularis propria (nodes neg)
B2- penetrates muscularis propria
C1- stops at muscularis propria (nodes pos)
C2- penetrates muscularis propria
D- distant metastatic spread

285
Q

Proximal colon Colorectal carcinoma morphology

A

Polypoid

Fungating masses

286
Q

Distal colon Colorectal carcinoma morphology

A

Annular
Encircling lesions that produce constrictions
Napkin rings - mid region ulcerated , beaded, firm, heaped

287
Q

Carcinoid tumors

A

Tumors of neuroendocrine cells

Slow growing mostly arising from gut

288
Q

Most common site of gut carcinoid

A

Appendix

289
Q

Appendix carcinoid tumor morphology

A

Bulbous swelling of tip which can obliterate lumen

290
Q

carcinoid tumor morphology

A

Appendix -> Bulbous swelling of tip which can obliterate lumen

in other part of the gut -> Intramural or submucosa masses / Small polypoid or plateau like elevations

Overlying intact or ulcerated mucosa

Solid yellow tan appearance or transection

291
Q

Histology of carcinoid tumor morphology

A

Cells from discrete islands , trabeculae, glands, or undifferentiated sheets

Monotonous similar cells
Scant pink granular cytoplasm
Round to oval stipples nucleus

292
Q

What type of tumors can produce gastrinoma, somatostatinoma, vipoma, insulinoma?

A

Carcinoïd tumors

293
Q

Cause of carcinoid syndrome

A

Excess serotonin production

294
Q

Clinical features of carcinoid syndrome

A 
Vasomotor disturbances (cutaneous flushes) 
Intestinal hypermotility 
Asmathic broncho constrictive attack 
Hepatomegaly 
Systemic fibrosis

Gastrointestinal Module (15 decks)

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