1-10 Flashcards
(444 cards)
1
Q
Describe the developmental malformations of the face mentioned in the content.
A
Cleft lip and cleft palate are developmental malformations that occur when the palate fails to close during embryonic life, leading to potential feeding and speech problems.
2
Q
Explain the purpose of a palatal obturator.
A
A palatal obturator is used from birth before surgery to assist with feeding and speech in infants with cleft lip or cleft palate.
3
Q
Define a thyroglossal cyst and its origin.
A
A thyroglossal cyst is a fibrous cyst that forms on the neck from leftover tissue during the development of the thyroid gland, resulting from the persistence of the thyroglossal duct.
4
Q
How can infectious inflammations in the oral cavity be caused?
A
Infectious inflammations in the oral cavity can be caused by viruses, bacteria, or fungi.
5
Q
Explain the characteristics of Herpes simplex virus 1 (HSV1).
A
HSV1, also known as labial herpes or cold sores, is the most common herpes virus in the oral region, with primary infections often occurring in early childhood.
6
Q
Describe the symptoms associated with the primary infection of HSV1.
A
The primary infection of HSV1 can be accompanied by fever, sore throat, and enlarged lymph nodes, with cold sores appearing that eventually disappear.
7
Q
How does the herpes simplex virus remain in the body after the initial infection?
A
After the initial infection, the herpes simplex virus remains dormant in the trigeminal ganglion and may reactivate periodically.
8
Q
List some triggers for the reactivation of HSV1.
A
Triggers for the reactivation of HSV1 include sunlight, fever, psychological stress, menstruation, pregnancy, upper respiratory tract infections, and immunosuppression.
9
Q
What percentage of primary attacks of HSV1 can lead to acute gingivostomatitis herpetica?
A
Primary attacks of HSV1 can cause acute gingivostomatitis herpetica in 10-20% of cases, characterized by multiple vesicles and ulcerations in the oral cavity.
10
Q
Identify the congenital malformations of the face discussed in the content.
A
The congenital malformations of the face discussed include cleft lip and cleft palate, as well as thyroglossal cysts.
11
Q
What is the significance of the age range 3-12 months in relation to cleft lip and palate surgery?
A
Surgery for cleft lip and palate is typically performed when the patient is around 3-12 months old to address feeding and speech issues.
12
Q
Describe the dormancy of Herpes Simplex virus 2.
A
Herpes Simplex virus 2 stays dormant in the sacral ganglia.
13
Q
Explain the first incidence of Varicella Zoster virus.
A
The first incidence of the Varicella Zoster virus results in chickenpox.
14
Q
How does Varicella Zoster virus behave after the initial infection?
A
After the initial infection, the Varicella Zoster virus stays dormant in the nerves.
15
Q
Identify risk factors for the reactivation of Varicella Zoster virus.
A
Risk factors for reactivation include old age, poor immune system, and getting chickenpox before the age of 18 months.
16
Q
What is the condition called when Varicella Zoster virus is reactivated?
A
When reactivated, it is called shingles.
17
Q
Describe the symptoms of shingles.
A
Shingles appears as a very painful rash along the dermatomes where the virus was dormant, usually only on one side.
18
Q
What is the Norwegian term for shingles and its meaning?
A
In Norway, shingles is called ‘fire from hell’ (helvetesild) due to the severe burning sensation it causes.
19
Q
How does vaccination affect shingles incidence?
A
The vaccine reduces the incidence of shingles.
20
Q
Define scarlet fever and its causative agent.
A
Scarlet fever is a result of group A streptococcus infection.
21
Q
List common symptoms of scarlet fever.
A
Symptoms include sore throat, fever, headaches, swollen lymph nodes, strawberry tongue, and a characteristic rash.
22
Q
What long-term complications can arise from scarlet fever?
A
Long-term complications can include kidney disease, rheumatic heart disease, and rheumatic arthritis.
23
Q
Describe the characteristic feature of diphtheria.
A
Diphtheria often results in a dense, grey pseudomembrane covering the tonsils.
24
Q
What severe complications can arise from diphtheria toxins?
A
Diphtheria toxins can result in cardiac arrhythmias, myocarditis, and cranial and peripheral nerve palsies.
25
Explain the oral manifestations of tuberculosis.
Tuberculosis can leave flat ulcers with soft edges in the oral cavity.
26
What is the historical term for syphilis?
The historical term for syphilis is 'lues'.
27
Identify the stages of syphilis.
Syphilis exists in four stages.
28
Describe the symptoms seen in primary and secondary syphilis.
In primary and secondary syphilis, ulcers and lesions can be seen around the mouth and inside the oral cavity.
29
What type of infection is characterized as lumpy jaw syndrome?
Lumpy jaw syndrome is a granulomatous infection caused by anaerobic, gram-positive filamentous bacteria.
30
What conditions can lead to the disease caused by the bacteria responsible for lumpy jaw syndrome?
The disease occurs when the bacteria find an opportunity to form in anoxic environments, such as after dental disease or mandibular osteomyelitis.
31
What are the characteristics of abscesses in lumpy jaw syndrome?
The abscesses in lumpy jaw syndrome are large and located on the head and neck, containing sulphur granules.
32
Identify the main bacteria responsible for actinomycosis.
Actinomycosis is caused mostly by anaerobic bacteria, especially fusobacteria and spirochete species.
33
List risk factors associated with actinomycosis.
Risk factors include poor oral hygiene and smoking.
34
What is acute necrotizing ulcerative gingivitis (ANUG)?
ANUG is a severe gum infection characterized by painful ulcers and necrosis of the gum tissue.
35
Describe the common condition affecting 20% of the general population involving mouth ulcers.
It consists of repeated formation of benign and non-contagious mouth ulcers in healthy individuals, caused by a T-cell mediated immune response triggered by factors like nutritional deficiencies, local trauma, stress, hormonal influences, allergies, and genetic predisposition.
36
Explain the chronic blistering skin disease classified as type II hypersensitivity.
This condition involves antibodies attacking the desmosomes that hold different layers of skin together, resulting in large blisters, while basal keratinocytes remain attached to the basement membrane, a phenomenon known as tombstoning.
37
Identify the demographic most affected by the chronic blistering skin disease associated with type II hypersensitivity.
It mostly affects middle-aged and older patients.
38
Define epulis and its characteristics.
Epulis means growth in Greek and refers to enlargements of tissue located on the gingiva or the alveoli of the oral cavity, which can be fibromatous, ossifying, or acanthomatous.
39
Describe the lobulated capillary haemangioma found in the gingiva.
It grows rapidly and appears as a red lump.
40
Explain the association of tumors with human papilloma virus (HPV).
Many tumors in the oral cavity are associated with HPV, particularly squamous cell hyperplasia found mostly on the gums.
41
What is papillomatosis in the context of oral health?
Papillomatosis refers to the presence of multiple papillomas in the oral cavity, which are similar to genital warts but larger.
42
Differentiate between leukoplakia and erythroplakia.
Leukoplakia is an unbrushable white lesion, while erythroplakia is a fiery red lesion, both associated with an increased risk of cancer.
43
List the risk factors for leukoplakia and erythroplakia.
The risk factors include smoking, chewing tobacco, and excessive alcohol intake.
44
What is the risk of progression to invasive squamous cell carcinoma for leukoplakia and erythroplakia?
The risk is 3-25% for leukoplakia and more than 50% for erythroplakia.
45
Explain the importance of distinguishing leukoplakia and erythroplakia from benign oral lesions.
It is crucial to differentiate them from benign lesions like oral candidiasis due to their associated cancer risks.
46
What percentage of oral cancers are squamous cell carcinomas?
90% of oral cancers are squamous cell carcinomas.
47
Identify the risk factors for squamous cell carcinoma.
The risk factors include smoking, alcohol consumption, and HPV16.
48
Describe the characteristics of the HPV-associated type of squamous cell carcinoma.
This type affects younger patients who have no history of smoking or drinking alcohol.
49
Describe the most frequent locations for aggressive tumors in the oral cavity.
The most frequent locations are the lower lip, base of the mouth, or both sides of the tongue.
50
Explain the spread of aggressive tumors in the body.
These tumors spread to the lymph nodes in the neck, mediastinum, retropharyngeal lymph nodes, and to the liver, lung, and bones through hematogenic spread.
51
How does the stage of detection affect the survival chances of aggressive tumors?
If detected early, the 5-year survival chances are 80%, but if the tumor is advanced, the chances drop to only 20%.
52
Define cachexia and its relation to aggressive tumors.
Cachexia is a complication that can arise from aggressive tumors, characterized by weight loss and muscle wasting.
53
What are some complications associated with aggressive tumors?
Complications include cachexia, arrosion bleedings, and aspiration pneumonia.
54
Describe a cyst in the context of odontogenic cysts.
A cyst is a pathological cavity lined by epithelium and contains an accumulation of fluid or gaseous content, which is not pus.
55
Explain the origin and characteristics of a dentigerous cyst.
A dentigerous cyst is a type of odontogenic cyst of developmental origin that involves the crown of an unerupted or partially erupted tooth.
56
How does pressure from an erupting tooth affect a dentigerous cyst?
The pressure from the erupting tooth may obstruct venous flow, resulting in exudate between the reduced enamel epithelial cells and the crown of the tooth.
57
Define the characteristics of a rare, benign but aggressive cyst affecting the posterior mandible.
This cyst usually presents in patients around their 30s and is characterized by its aggressive nature despite being benign.
58
What is the most common type of odontogenic cysts and where is it typically found?
The most common type of odontogenic cysts surrounds the apex of the root of a tooth and occurs mostly in the anterior region of the maxilla.
59
Explain how dental caries and trauma can lead to the formation of cysts.
Dental caries and trauma to the teeth can lead to pulpal necrosis, which forms the cyst from the epithelial cells’ rests.
60
Identify the demographic most affected by odontogenic cysts.
Odontogenic cysts are more common in men and individuals between 20 and 60 years.
61
Describe the origin of odontogenic tumors.
Odontogenic tumors are derived from odontogenic epithelium (ameloblast), ectomesenchyme, or both.
62
What is an ameloblastoma and its characteristics?
An ameloblastoma is a tumor derived from ameloblast that does not cause chondroid or osseous differentiation, is cystic, infiltrates local tissue, and is slow-growing.
63
Explain the characteristics of odontomas.
Odontomas arise from epithelium and show deposition of enamel and dentin, and the tumor can be either hard or soft.
64
List the types of odontogenic cysts mentioned.
The types of odontogenic cysts mentioned are dentigerous or follicular cyst, odontogenic keratocyst, and periapical cyst (or radicular cysts or inflammatory cyst).
65
What are the types of odontogenic tumors?
The types of odontogenic tumors include ameloblastoma and odontomas.
66
Describe the condition of sialadenitis.
Sialadenitis is the inflammation of the salivary glands, which can occur due to various causes, including bacterial infections, viral infections, and autoimmune disorders.
67
Explain the differences between bacterial and viral sialadenitis.
Bacterial sialadenitis is an acute purulent inflammation often found in elderly patients, caused by bacteria such as Staphylococcus aureus. Viral sialadenitis, more common in children, is typically caused by viruses like mumps and can lead to swelling of the parotid glands.
68
Identify the risk factors for bacterial sialadenitis.
Risk factors for bacterial sialadenitis include dehydration, sialolithiasis (stones in the salivary glands), malnutrition, and immunosuppression.
69
List the typical viruses that cause viral sialadenitis.
Typical viruses causing viral sialadenitis include Paramyxoviridae (mumps), Epstein-Barr virus, Coxsackie A, Cytomegalovirus, and Influenza.
70
Discuss the complications associated with viral sialadenitis.
Complications from viral sialadenitis can include deafness and, in cases of mumps, inflammation of the testis.
71
Define Sjögren syndrome and its association with sialadenitis.
Sjögren syndrome is an autoimmune condition characterized by the swelling of the parotid glands, dry mouth, dry eyes, and rheumatoid arthritis, often associated with anti-SSA and SSB antibodies.
72
How does Sjögren syndrome affect the salivary and lacrimal glands?
Sjögren syndrome attacks both the salivary and lacrimal glands, leading to symptoms such as dry mouth and dry eyes.
73
Describe the typical demographic affected by Sjögren syndrome.
Sjögren syndrome is typically found in middle-aged women.
74
Explain the term sialolithiasis.
Sialolithiasis refers to the presence of stones in the salivary glands, which can lead to inflammation and infection.
75
What are tumorlike lesions in the context of salivary glands?
Tumorlike lesions in the salivary glands refer to abnormal growths that may resemble tumors but are not necessarily malignant.
76
Identify the common bacteria responsible for bacterial sialadenitis.
Common bacteria responsible for bacterial sialadenitis include Staphylococcus aureus, streptococcus viridians, and intestinal bacteria.
77
Describe the symptoms of Sjögren syndrome.
Sjögren syndrome leads to bilateral swelling of the salivary and lacrimal glands, which is painless. It can also present symptoms similar to other autoimmune diseases.
78
Explain what secondary Sjögren syndrome is.
Secondary Sjögren syndrome occurs when typical symptoms are observed in conjunction with other autoimmune diseases such as scleroderma, myasthenia gravis, and systemic lupus erythematosus (SLE).
79
How is Sjögren syndrome diagnosed?
A diagnosis of Sjögren syndrome can be made by taking a biopsy from the lip.
80
Define Heerfordt syndrome and its symptoms.
Heerfordt syndrome is a rare manifestation of sarcoidosis affecting the salivary glands, characterized by granulomatous parotitis, inflammation of the eyes, fever, and potentially facial nerve palsy.
81
What is sialolithiasis and where does it commonly occur?
Sialolithiasis refers to the presence of stones in the salivary glands, most commonly occurring in the main duct of the submandibular glands.
82
Describe the symptoms experienced by patients with sialolithiasis.
Patients with sialolithiasis experience pain and swelling when thinking about food, smelling delicious food, or during meals and hunger.
83
Explain the appearance and characteristics of salivary stones in sialolithiasis.
Salivary stones are bright yellow with a granular surface and can lead to ulceration of the mucosa and fistulation.
84
How does sialolithiasis relate to long-term inflammation of the salivary glands?
Sialolithiasis is considered a rare condition that occurs due to long-term inflammation of the salivary glands.
85
What is Küttner’s tumor?
Küttner’s tumor refers to a condition where stones in the submandibular gland present as hard, indurated, and large masses that are clinically indistinguishable from salivary neoplasms and tumors.
86
List some tumor-like lesions associated with salivary gland conditions.
Tumor-like lesions include Mikulicz syndrome, Heerfordt syndrome, sialolithiasis, chronic sclerosing sialadenitis, and mucocele.
87
Discuss the etiology of sialolithiasis.
The etiology of sialolithiasis is unknown, but it is associated with long-term inflammation of the salivary glands.
88
What are the potential complications of sialolithiasis?
Complications of sialolithiasis can include ulceration of the mucosa and fistulation.
89
Explain the benign nature of sialolithiasis.
Sialolithiasis is considered benign, despite presenting as hard masses that can mimic tumors.
90
Describe the two forms of mucoceles.
Mucoceles exist in two forms: the retention/obstructive type, which has squamous epithelial lining and is caused by obstruction, and the extravasation/pseudocystic type, which is more common in children and young adults.
91
Explain the common locations for mucoceles.
Mucoceles are often located on the inner side of the lower lip and the base of the mouth.
92
Define pleomorphic adenoma.
Pleomorphic adenoma is the most frequent benign tumor of the salivary glands, usually appearing in the parotid gland at any age, characterized by slow growth and painless neoplasm.
93
How does a pleomorphic adenoma affect the facial nerve?
Due to its growth in the parotid gland, a pleomorphic adenoma can compress the facial nerve, potentially causing facial nerve palsy.
94
Do most salivary gland tumors tend to be benign or malignant?
Most salivary gland tumors are benign, although some can be malignant.
95
Explain the significance of the Warthin tumor.
Warthin tumor, also known as papillary cystadenoma lymphomatosum, is a benign cystic tumor of the salivary glands that contains lymphocytes and is more common in men, with a strong association to smoking.
96
Describe the characteristics of malignant salivary gland tumors.
Malignant salivary gland tumors often appear as mixed tumors with histological features including squamous cells, mucus-secreting cells, and undifferentiated cells, and they typically originate from the duct of the gland.
97
How does radiation exposure relate to salivary gland tumors?
Radiation exposure is a risk factor for developing malignant tumors in the salivary glands.
98
Define the prognosis for poorly differentiated salivary gland tumors.
The prognosis for survival is very low for poorly differentiated salivary gland tumors.
99
Explain the common demographic affected by salivary gland tumors.
Salivary gland tumors predominantly affect women and are most commonly found in the parotid gland.
100
Describe the common locations where a rare cancer can occur.
This rare cancer can occur in the breasts, lacrimal glands, lung, brain, and most commonly in the salivary glands.
101
Explain the prognosis for the rare cancer mentioned.
The prognosis for this rare cancer is poor.
102
Define congenital malformations of the esophagus.
Congenital malformations of the esophagus occur when the congenital segmental closure fails, often resulting in fistulas connecting the esophagus to the trachea or bronchus.
103
How are congenital malformations of the esophagus typically discovered in infants?
These malformations are usually discovered when the baby experiences repeated aspiration pneumonia from breastfeeding.
104
What surgical intervention is needed for congenital malformations of the esophagus?
Surgery is needed to fix the problem of congenital malformations of the esophagus.
105
Describe achalasia and its impact on esophageal motility.
Achalasia is a rare disorder characterized by inadequate relaxation of the lower esophageal sphincter, preventing food from passing to the stomach and leading to dilation of the esophagus.
106
Differentiate between primary and secondary achalasia.
Primary achalasia is idiopathic and caused by degeneration of distal inhibitory neurons, while secondary achalasia (pseudoachalasia) is caused by mechanical obstruction, such as a tumor or Chagas disease.
107
Explain gastroesophageal reflux disease (GERD) and its symptoms.
GERD is a common condition where gastric contents reflux into the esophagus, causing symptoms like heartburn, regurgitation, and potential severe complications.
108
What causes gastroesophageal reflux disease (GERD)?
GERD is caused by excessive relaxation of the lower esophageal sphincter, making it the opposite disorder of achalasia.
109
Identify risk factors that can contribute to GERD.
Risk factors for GERD include smoking, coffee consumption, alcohol consumption, obesity, pregnancy, and scleroderma.
110
List the types of disorders that can affect the esophagus.
Disorders affecting the esophagus include congenital malformations, functional disorders, vascular diseases, inflammations, and neoplasms.
111
What complications can arise from untreated achalasia?
Untreated achalasia can lead to severe complications such as esophageal dilation and perforation.
112
Describe the types of gastroesophageal reflux disease (GERD).
GERD is classified into three types: Non-erosive reflux disease (NERD), which has a normal gastroesophageal mucosa; Erosive reflux disease (ERD), characterized by erosions on the mucosa; and Complicated erosive reflux disease, which includes complications like ulcers, stenosis, or Barrett oesophagus.
113
Explain the difference between sliding and rolling hiatal hernias.
Sliding hiatal hernia, which accounts for 95% of cases, involves the gastroesophageal junction and gastric cardia sliding into the posterior mediastinum. In contrast, rolling hiatal hernia is more severe, with a portion of the gastric fundus herniating through the oesophageal hiatus while the gastroesophageal junction remains in place.
114
How is sliding hiatal hernia typically treated?
Sliding hiatal hernia is often treated conservatively, while paraesophageal hiatal hernia is usually treated surgically.
115
Define diverticulum in the context of the esophagus.
A diverticulum is a circumscribed outpouching of the wall of a hollow organ, such as the esophagus. It can be a true diverticulum, where all layers of the wall are involved, or a pseudodiverticulum, where only the mucosa and submucosa herniate through a weakness in the muscularis propria.
116
What complications can arise from living with an esophageal diverticulum?
Living with an esophageal diverticulum can lead to food getting stuck, causing dysphagia, aspiration, vomiting, and bad breath (halitosis). It may also result in inflammation of the diverticulum, known as diverticulitis, and the presence of diverticula is referred to as diverticulosis.
117
Describe Zenker’s diverticulum and its potential complications.
Zenker’s diverticulum is a pseudodiverticulum located above the upper esophageal sphincter and is the most common type. It protrudes posteriorly and can lead to mediastinitis if it becomes inflamed (diverticulitis).
118
Explain the term 'diverticulitis'.
Diverticulitis refers to the inflammation of a diverticulum, which can occur when food or bacteria become trapped inside the diverticulum, leading to infection and discomfort.
119
What is the significance of Barrett metaplasia in chronic GERD?
Barrett metaplasia is a condition that can develop from chronic GERD, where the normal esophageal lining is replaced with a type of tissue similar to that of the intestinal lining, increasing the risk of esophageal cancer.
120
How does increased abdominal pressure contribute to hiatal hernia?
Increased abdominal pressure can cause a portion of the stomach to herniate through the hiatus in the diaphragm, leading to a hiatal hernia, particularly when the esophageal hiatus is lax.
121
What are the symptoms associated with diverticulosis?
Symptoms of diverticulosis can include discomfort from food getting stuck, dysphagia, aspiration, vomiting, and bad breath (halitosis), and it may lead to diverticulitis if inflammation occurs.
122
Describe oesophageal varices and their significance in medical emergencies.
Oesophageal varices are enlarged blood vessels that develop due to portocaval shunts in patients with portal hypertension. They are significant because they can rupture and cause massive bleeding, particularly in alcoholics with alcoholic liver cirrhosis.
123
Explain Mallory-Weiss syndrome and its cause.
Mallory-Weiss syndrome is characterized by severe upper gastrointestinal bleeding resulting from longitudinal tears in the oesophageal mucous membrane, typically caused by high intraluminal pressure due to severe vomiting.
124
Define Boerhaave syndrome and its implications.
Boerhaave syndrome refers to a rupture of the oesophagus due to severe vomiting, leading to severe pain and mediastinal emphysema. It is a medical emergency that can be fatal without surgical intervention.
125
How does reflux oesophagitis occur and what are its risk factors?
Reflux oesophagitis occurs due to the reflux of acidic gastric contents into the lower oesophagus, causing chemical irritation to the mucosa. Risk factors include those associated with gastroesophageal reflux disease (GERD) and factors that increase stomach acidity.
126
Describe the types of infectious oesophagitis and their common causes.
Infectious oesophagitis is rare and most common in immunosuppressed patients. Types include Soor oesophagitis (oesophageal candidiasis) caused by Candida, Herpes oesophagitis causing pouched-out ulcers, and Cytomegalovirus oesophagitis characterized by shallow ulcers and an 'Owl-eye' appearance in histology.
127
Explain eosinophilic oesophagitis and its underlying mechanisms.
Eosinophilic oesophagitis is a recent disease characterized by pronounced eosinophilic infiltration in the oesophagus, often triggered by food or other allergens. It involves Th2-activation and may have a genetic predisposition.
128
What is Barrett oesophagus and how does it develop?
Barrett oesophagus is a condition that arises from chronic gastroesophageal reflux disease (GERD), where chronic acid exposure leads to intestinal metaplasia in the oesophageal mucosa, identifiable by the presence of goblet cells in histology.
129
Identify the most frequent cause of esophagitis and its relation to GERD.
The most frequent cause of esophagitis is reflux oesophagitis, which is directly related to chronic gastroesophageal reflux disease (GERD) due to the exposure of the oesophageal mucosa to acidic gastric contents.
130
Describe Barrett oesophagus and its significance in cancer progression.
Barrett oesophagus is a precancerous lesion that can progress into adenocarcinoma, necessitating treatment or frequent monitoring.
131
Explain the two major types of oesophageal cancer.
The two major types of oesophageal cancer are adenocarcinoma, which is more common in the Western world and evolves from Barrett mucosa, and squamous cell carcinoma (SCC), which is more prevalent in developing countries.
132
How does the location of oesophageal adenocarcinoma differ from squamous cell carcinoma?
Oesophageal adenocarcinoma is usually found in the lower part of the oesophagus, while squamous cell carcinoma is typically located in the middle and upper parts.
133
Define the prognosis of squamous cell carcinoma compared to adenocarcinoma.
The prognosis of squamous cell carcinoma is worse than that of adenocarcinoma.
134
What are common symptoms of late-stage oesophageal cancer?
In the late stages, oesophageal cancer may present with non-specific symptoms such as weight loss, dysphagia, and dyspepsia.
135
Discuss the typical demographic affected by oesophageal cancer.
Both types of oesophageal cancer typically affect elderly men.
136
Identify the risk factors associated with oesophageal adenocarcinoma.
The risk factors for oesophageal adenocarcinoma are the same as those for GERD, particularly smoking.
137
List the risk factors for squamous cell carcinoma of the oesophagus.
Risk factors for squamous cell carcinoma include alcohol consumption, smoking, a diet low in fruits and vegetables, exposure to nitrosamines in the diet, and frequent consumption of very hot beverages.
138
How does the incidence of oesophageal adenocarcinoma trend in recent years?
The incidence of oesophageal adenocarcinoma is rising.
139
Explain why oesophageal cancer is often diagnosed at an advanced stage.
Oesophageal cancer is usually asymptomatic in the early stages, leading to late discovery when most patients already have advanced cancer.
140
Describe the difference between an erosion and an ulceration in the gastric mucosa.
An erosion never goes deeper than the muscularis mucosae, affecting only the mucosa, while an ulceration goes deeper, affecting the submucosa and can even perforate the wall.
141
Explain the condition of hypochlorhydria.
Hypochlorhydria is the condition where the level of stomach acid is lower than normal.
142
Define achlorhydria.
Achlorhydria is the condition where there is no stomach acid present.
143
How does the mucus layer protect the gastric mucosa?
The mucus layer contains bicarbonate on the surface of the mucosa, which helps to neutralize gastric acid and protect the mucosa from injury.
144
What role does good mucosal circulation play in gastric mucosa protection?
Good mucosal circulation allows for 'washing out' the acid, helping to maintain a healthy environment for the gastric mucosa.
145
Explain the significance of tight junctions between epithelial cells in the gastric mucosa.
Tight junctions between epithelial cells help to maintain the integrity of the mucosal barrier, preventing harmful substances from penetrating deeper into the tissue.
146
Describe the importance of prostaglandin production in the gastric mucosa.
Prostaglandin production maintains good perfusion, stimulates bicarbonate production, and suppresses gastric acid production, all of which protect the gastric mucosa.
147
What is the function of secretory mucosal IgA in the gastric mucosa?
Secretory mucosal IgA plays a role in immune defense, helping to protect the gastric mucosa from pathogens.
148
List some aggressive factors that increase stress on the gastric mucosa.
Aggressive factors include secretion of HCl, secretion of pepsin, Helicobacter pylori, NSAIDs, ischaemia and hypoxia, smoking, alcohol, and steroids.
149
How does the balance between protective and aggressive factors affect the gastric mucosa?
A constant balance exists between protective and aggressive factors; if the balance tips towards increased stress, it can lead to acid-induced injury, including erosions and ulcers.
150
What can happen if protective factors of the gastric mucosa decrease?
If protective factors decrease, it can lead to increased stress on the gastric mucosa, resulting in acid-induced injuries such as erosions and ulcers.
151
Identify the role of Helicobacter pylori in gastric mucosa health.
Helicobacter pylori is an aggressive factor that can contribute to gastric mucosal injury and is associated with conditions like ulcers.
152
Describe the appearance of acute erosive gastritis macroscopically.
Acute erosive gastritis is characterized by multiple petechial haemorrhages, which appear as black dots, and small erosions in the stomach.
153
Explain the role of Helicobacter pylori in gastric inflammation.
Helicobacter pylori is a spiral-shaped bacterium that resides in the gastric mucus, adhering to the epithelial cells of the gastric mucosa and causing local inflammation.
154
Define the virulence factor produced by H. pylori and its effect.
H. pylori produces urease, which forms ammonia to neutralize stomach acid, allowing the bacterium to survive in the acidic environment, but this activity is toxic to epithelial cells.
155
How does H. pylori affect somatostatin production in the gastric antrum?
H. pylori destroys somatostatin-producing D-cells in the gastric antrum, leading to decreased somatostatin production, which reduces inhibition of gastrin production and increases gastric acid production.
156
What is the consequence of increased gastric acid production due to H. pylori infection?
Increased gastric acid production may predispose individuals to the formation of duodenal ulcers.
157
Explain the long-term effects of inflammation caused by H. pylori.
Chronic inflammation can lead to atrophy of the local mucous membrane, including acid-producing parietal cells, and intestinal metaplasia, which increases the risk of developing cancer.
158
Describe the typical location of inflammation in acute erosive gastritis.
Inflammation predominantly affects the gastric antrum but may spread to other parts of the stomach if left untreated.
159
What are the common causes of erosive gastritis?
The most common causes of erosive gastritis include heavy use of NSAIDs, alcoholism, and heavy smoking.
160
How does erosive gastritis lead to bleeding?
Erosive gastritis causes multiple haemorrhagic erosive lesions in the stomach, which frequently bleed, leading to haematemesis.
161
What is the significance of AMAG in the context of atrophic gastritis?
Autoimmune Metaplastic Atrophic Gastritis (AMAG) occurs in only 1% of the population and is caused by anti-parietal cell antibodies, making it one of the two causes of atrophic gastritis, the other being H. pylori.
162
Describe the relationship between parietal cells and gastric acid secretion.
Parietal cells contain the proton pump responsible for gastric acid secretion, and their destruction can lead to reduced acid production.
163
Explain why the term 'gastritis' may not be entirely accurate for erosive gastritis.
Erosive gastritis often presents with minimal or no inflammation, making the term 'gastritis' somewhat misleading, but it remains in clinical use.
164
What is another name for acute erosive gastritis?
Acute erosive gastritis is also referred to as acute haemorrhagic erosive gastropathy.
165
Describe the potential long-term consequences of H. pylori infection.
H. pylori infection may eventually lead to gastric adenocarcinoma or carcinoid tumors.
166
Explain the term 'H. pylori gastritis'.
H. pylori gastritis, also known as bacterial gastritis or environmental metaplastic atrophic gastritis (EMAG), is a form of chronic atrophic gastritis caused by H. pylori infection.
167
How prevalent is H. pylori infection worldwide?
H. pylori infection is present in approximately 2/3 of the population worldwide, with a prevalence of 90% in developing countries.
168
What factors contribute to the decreasing prevalence of H. pylori infection?
The decreasing prevalence of H. pylori infection is attributed to improvements in sanitation and the use of antibiotics.
169
Identify when H. pylori infection typically occurs in developing versus industrialized countries.
In developing countries, H. pylori infection usually occurs in childhood, while in industrialized countries, it typically occurs in adulthood.
170
Discuss the typical symptoms of H. pylori infection.
In most cases, H. pylori infection is asymptomatic and can last a lifetime; however, in symptomatic cases, the consequences can be severe.
171
What is the lifetime risk of developing peptic ulcer disease due to H. pylori infection?
H. pylori infection gives a 15-20% lifetime risk of developing peptic ulcer disease.
172
Link H. pylori infection to gastric cancer.
H. pylori infection has been linked to 70% of gastric cancers, particularly intestinal types and gastric MALT lymphoma.
173
What are some bacterial toxins associated with H. pylori infection?
Bacterial toxins associated with H. pylori infection include cagA, VacA, urease, and ammonia, which are toxic to epithelial cells.
174
How is H. pylori infection diagnosed?
Diagnosis of H. pylori infection is based on the visualization of the bacterium on biopsy.
175
What is the treatment for H. pylori infection?
Treatment for H. pylori infection involves the use of proton pump inhibitors (PPIs) and antibiotics.
176
Define peptic ulcer disease (PUD).
Peptic ulcer disease (PUD) refers to the presence of peptic ulcers in the stomach and/or duodenum.
177
Compare the occurrence of duodenal ulcers to gastric ulcers.
Duodenal ulcers are approximately three times more common than gastric ulcers.
178
Identify the primary risk factors for developing PUD.
The primary risk factors for developing PUD are H. pylori infection and long-term use of NSAIDs.
179
What types of factors can cause gastritis?
Gastritis can be caused by various factors, including chemical, toxic, or reactive agents that destroy the gastric mucosa.
180
Differentiate between endogenic and exogenic factors in gastritis.
Endogenic factors include bile acid or pancreatic fluid reflux, while exogenic factors include alcohol and drugs like NSAIDs and steroids.
181
Describe the typical location of injuries in mild gastritis.
Injuries in mild gastritis are almost always found in the antrum and can be seen as foveolar hyperplasia with hyperemia.
182
List some types of opportunistic gastritides.
Opportunistic gastritides include those caused by cytomegalovirus (CMV) or yeast infection.
183
What are some specific types of gastritis mentioned?
Specific types of gastritis include granulomatous gastritis, lymphocytic gastritis, collagenous gastritis, eosinophilic gastritis, gastritis cystica profunda, graft vs. host gastritis (GVH-gastritis), and allergic gastritis.
184
Describe the differences between acute and chronic ulcers.
Acute ulcers are mostly smaller than 1 cm, often multiple, round or oval, located at the level of the mucosa with a base covered by fibrin or hematin, and have grayish, yellow, flat edges. Chronic ulcers are 2-4 cm, often just one, have radiating mucosal folds around them, a clear ulcer base, and hyperemic, straight walls.
185
Explain the complications associated with peptic ulcers.
Peptic ulcers may bleed, obstruct the gastric outlet, or perforate. Perforation can lead to peritonitis.
186
Define Zollinger-Ellison syndrome.
Zollinger-Ellison syndrome is a rare cause of peptic ulcer disease characterized by multiple peptic ulcerations in the stomach, duodenum, and jejunum, caused by neuroendocrine tumors that produce gastrin, often located in the pancreas, duodenum, or lymph nodes of the abdomen.
187
How is peptic ulcer disease (PUD) treated?
PUD is treated with proton pump inhibitors and by addressing the underlying causes, including avoiding risk factors. Surgery may be necessary if conservative treatment is insufficient.
188
Explain the role of the Sydney system in gastritis classification.
The Sydney system is used to combine topography, morphology, and etiological information to facilitate diagnosis of gastritides.
189
Describe the aggressive and protective factors related to gastric acidity.
The red factors on the left protect against acidity, while the green factors on the right are aggressive factors that can lead to ulcer formation.
190
Identify the common locations for ulcers in the gastrointestinal tract.
Ulcers may occur in any part of the GI tract exposed to acidic gastric juices, but are most commonly found in the minor curvature of the stomach, gastric antrum, and the first portion of the duodenum.
191
What are the potential complications of chronic ulcers?
Chronic ulcers can lead to bleeding, perforation, penetration, and scarring formation.
192
Do acute ulcers have a specific appearance?
Yes, acute ulcers typically have grayish, yellow, flat edges and a base covered by fibrin or hematin.
193
How do the sizes of acute and chronic ulcers differ?
Acute ulcers are mostly smaller than 1 cm, while chronic ulcers range from 2 to 4 cm.
194
Describe the OLGA grading system.
The OLGA grading system uses at least five biopsies from five different parts of the stomach to establish the stage of gastritis.
195
Explain the significance of congenital pathologies of the stomach in the context of exams.
Congenital pathologies of the stomach are rare and not part of the topic for the exam.
196
Define atresia in relation to the stomach.
Atresia refers to the complete occlusion of the pyloric outlet in the stomach.
197
How does microgastria affect infants?
Microgastria is a condition where babies are born with an abnormally small stomach and limbs.
198
What is duplication in the gastrointestinal context?
Duplication refers to the abnormal growth of a solid tumor or cyst in the gastrointestinal tract, which can also present as bleeding or perforations.
199
Describe gastric diverticulum.
Gastric diverticulum is a rare condition involving the formation of a pouch in the stomach wall.
200
Explain infantile hypertrophic pyloric stenosis.
Infantile hypertrophic pyloric stenosis is a condition where the mucosa of the pylorus is hypertrophied, obstructing the gastric outlet, leading to projectile vomiting after meals.
201
What are the symptoms of infantile hypertrophic pyloric stenosis?
Symptoms include projectile vomiting after meals, edematous mucosa, patchy erosions, and ulcers.
202
Define pancreas heterotopy.
Pancreas heterotopy is a condition where pancreatic tissue is found outside the pancreas, occurring in approximately 1-2% of the population, sometimes in the stomach.
203
How is the grading of atrophy related to the OLGA system?
The grading of atrophy is assessed using the OLGA classification system.
204
Describe the types of polyps that can occur in the stomach.
There are several types of polyps in the stomach, including hyperplastic polyps, fundic gland polyps, and hamartomatous polyps. Hyperplastic polyps are commonly associated with chronic gastritis, while fundic gland polyps can occur sporadically or in patients with familial adenomatous polyposis (FAP). Hamartomatous polyps are part of polyposis syndromes.
205
Explain the characteristics of hyperplastic polyps in the stomach.
Hyperplastic polyps are usually 1-2 cm in size, located in the antrum, and are associated with chronic gastritis. The risk of these polyps developing into malignancy is low, but it increases if they exceed 2 cm.
206
How do fundic gland polyps develop and what is their association with proton-pump inhibitors?
Fundic gland polyps can develop sporadically or in individuals with familial adenomatous polyposis (FAP). Their occurrence has increased due to the use of proton-pump inhibitors, which lead to increased gastrin release and glandular hyperplasia.
207
Define adenomas in the context of stomach polyps.
Adenomas are rare stomach polyps that are more likely to occur with age and in certain populations, particularly in men who have a three times higher risk. They are often found in patients with chronic gastritis and show morphology similar to intestinal columnar epithelium, indicating epithelial dysplasia.
208
What is the clinical significance of xanthomas found in the stomach?
Xanthomas, described as 'lipid islands', are clinically insignificant when found in the stomach, although they are more common in Japan and can be associated with bile reflux.
209
Do hamartomatous polyps have any specific characteristics?
Hamartomatous polyps consist of disorganized cells and tissue, often found at the site of the polyps. They are typically associated with polyposis syndromes, such as Peutz-Jeghers syndrome.
210
Explain the relationship between chronic gastritis and adenomas in the stomach.
Adenomas are more likely to occur in patients with a history of chronic gastritis, particularly those with atrophy and intestinal metaplasia, and are usually located in the antrum.
211
Describe the appearance and composition of fundic gland polyps.
Fundic gland polyps are well circumscribed and composed of dilated irregular glands lined by parietal and chief cells.
212
How does the size of polyps affect the risk of malignancy?
The risk of polyps developing into malignancy is generally low, but it increases significantly if the polyps are larger than 2 cm.
213
What are the common locations for different types of stomach polyps?
Hyperplastic polyps are usually found in the antrum, while fundic gland polyps are located in the fundus and corpus of the stomach.
214
Describe the relationship between lesion size and the risk of adenocarcinoma.
The risk of it turning into adenocarcinoma increases when the lesions are bigger than 2 cm.
215
Explain the demographics most affected by gastric cancer.
Gastric cancer primarily affects the elderly, mostly men, and is the fifth most common cancer worldwide.
216
Identify regions where gastric cancer is more prevalent.
Gastric cancer is more common in Asian countries like Japan and Korea, as well as certain regions in Africa and South America.
217
Discuss the early symptoms of gastric cancer.
In the early stages, gastric cancer causes no or only nonspecific symptoms such as dyspepsia, abdominal pain, and nausea.
218
How does early diagnosis affect the prognosis of gastric cancer?
If diagnosed early, the prognosis for gastric cancer is excellent.
219
What percentage of gastric cancers have already spread by the time of diagnosis?
At the time of diagnosis, 50% of gastric cancers have already spread and are incurable.
220
Explain the impact of screening on gastric cancer mortality rates.
The mortality of gastric cancer is higher in countries with low prevalence because screening is not performed as often, leading to late discovery.
221
List some risk factors associated with gastric cancer.
Risk factors include H. pylori gastritis, a diet rich in nitrates or salts, alcohol consumption, nicotine use, Epstein-Barr virus, gastric adenomas, and previous partial gastric resection.
222
What dietary factor is considered protective against gastric cancer?
A plant-based diet is protective against gastric cancer.
223
Describe the classification of gastric cancer based on its stage.
Gastric cancer is classified as 'early' if it infiltrates no deeper than the submucosa, and 'advanced' if it infiltrates the muscularis propria and deeper.
224
What is the Lauren classification in gastric cancer?
The Lauren classification separates gastric cancers into intestinal and diffuse types based on their location in the stomach and their gross and histological morphology.
225
Compare the prognosis of intestinal and diffuse types of gastric cancer.
The intestinal type has a better prognosis than the diffuse type.
226
Define the characteristics of the intestinal type of gastric cancer.
The intestinal type has glandular structures and can be classified as high grade or low grade based on differentiation.
227
What are signet ring cells and their significance in gastric cancer?
Signet ring cells are a special cell type in the diffuse type of gastric cancer, characterized by compressed nuclei and large mucin-containing vacuoles, making them hard to find on biopsy.
228
Explain the symptoms that may appear in later stages of gastric cancer.
In later stages, symptoms may include weight loss, different bowel habits, anemia, and hemorrhage.
229
Describe the polypoid type of gastric cancer.
The polypoid type of gastric cancer protrudes into the lumen like a polyp.
230
Explain the characteristics of the fungative type of gastric cancer.
The fungative type of gastric cancer protrudes and has an ulcerative surface.
231
Define the ulcerative type of gastric cancer.
The ulcerative type of gastric cancer is non-protruding and has an ulcerative surface.
232
How does the diffuse growth type of gastric cancer affect the stomach?
The diffuse growth type of gastric cancer leads to a diffusely thickened gastric wall, known as linitis plastica, resulting in a rigid, non-distensible, 'leather bottle-like' stomach.
233
What is linitis plastica?
Linitis plastica is the end-stage of diffuse type gastric cancer, where the entire stomach is affected by cancer.
234
Identify the common sites of metastasis for gastric adenocarcinoma.
Gastric adenocarcinoma often spreads to the skeleton, liver, lung, brain, and the peritoneum.
235
Describe the Virchow lymph node's significance in gastric cancer.
The Virchow lymph node, located in the left supraclavicular area, is the most common site of gastric cancer metastasis.
236
What is a Krukenberg tumor?
A Krukenberg tumor is a type of tumor that may form when the diffuse type of gastric adenocarcinoma metastasizes to both ovaries.
237
Explain the origin and common location of gastrointestinal stromal tumors (GIST).
GISTs are the most common mesenchymal tumors originating from interstitial Cajal-cells and can occur anywhere in the GI tract, but are most commonly found in the stomach.
238
What role does the C-kit gene play in GIST?
The C-kit gene encodes for a tyrosine kinase that is often mutated in GIST patients, leading to constitutive activation and progression to cancer.
239
Describe the morphological types of GIST tumors.
GIST tumors can be submucous, subserous, or intramural, with the submucous type often being ulcerated and polypoid.
240
What is the primary treatment for GIST?
The primary treatment for GIST is surgery, with or without the addition of the tyrosine kinase inhibitor imatinib, which blocks the mutated tyrosine kinase.
241
Identify the most common site for extranodal lymphoma.
The stomach is the most common site for extranodal lymphoma.
242
What are the two types of lymphomas discussed in relation to gastric cancer?
The two types of lymphomas discussed are MALT lymphoma and diffuse large B-cell lymphoma (DLBCL).
243
Explain the risk factor associated with MALT lymphoma.
The risk factor for MALT lymphoma is H. pylori infection, which secretes the endotoxin CagA, leading to B-cell proliferation and autoreactive B-cells.
244
How is MALT lymphoma treated?
MALT lymphoma is treated by addressing the H. pylori infection, which can cause the lymphoma to regress.
245
Compare MALT lymphoma and DLBCL in terms of aggressiveness.
DLBCL is more aggressive than MALT lymphoma and can be either primary (de novo) or secondary following the transformation of a MALT lymphoma.
246
Describe Meckel's diverticulum and its prevalence in the population.
Meckel's diverticulum is a remnant of the omphaloenteric/vitellointestinal duct, found in approximately 2% of the population. It is a true diverticulum, containing all three layers of the intestinal wall.
247
Explain the typical location and size range of Meckel's diverticulum.
Meckel's diverticulum is usually located as an outpouching from the ileum on the antimesenteric side, about half a meter proximal to the ileocecal valve. It can range in length from 1 to 12 cm.
248
What types of ectopic tissues can be found in Meckel's diverticulum?
In about 10% of cases, ectopic gastric or pancreatic tissues can be found within Meckel's diverticulum.
249
How does ectopic gastric tissue in Meckel's diverticulum lead to complications?
Ectopic gastric tissue can produce acid, which may cause ulceration of the ileum, leading to complications such as bleeding and perforation.
250
Define malrotation of the small intestine and its physiological basis.
Malrotation of the small intestine occurs when the normal physiological herniation and rotation of the intestines, which should rotate 270 degrees counterclockwise, fails to happen.
251
What are the potential causes of bowel infarction?
Potential causes of bowel infarction include Meckel's diverticulum, atresia and stenosis, malrotation, and mesenteric infarction.
252
Explain the significance of mesenteric arteries in the context of small intestine health.
The small intestine is supplied by the mesenteric arteries, and any occlusion of these arteries or their branches can lead to serious conditions, including bowel infarction.
253
Differentiate between mucosal, mural, and transmural infarction in the bowels.
Mucosal infarction affects only the mucosa, mural infarction involves both the mucosa and submucosa, while transmural infarction affects all layers of the bowel wall and is often caused by acute obstruction of an artery.
254
What complications can arise from Meckel's diverticulum?
Complications from Meckel's diverticulum can include ulceration, bleeding, and perforation, particularly due to the presence of ectopic gastric tissue.
255
Describe the role of the mesenteric arteries in bowel health.
The mesenteric arteries supply blood to the small intestine, and any blockage can lead to ischemia and potentially fatal bowel infarction.
256
Describe severe atherosclerosis and its potential impact on blood flow.
Severe atherosclerosis is a condition characterized by the buildup of plaques in the arteries, which can lead to reduced blood flow and increase the risk of cardiovascular events.
257
Explain the role of oral contraception in hypercoagulative states.
Oral contraception can increase the risk of hypercoagulative states by altering hormone levels, which may lead to increased clotting factors and a higher likelihood of thrombosis.
258
Define short bowel syndrome and its causes.
Short bowel syndrome is a malabsorption disorder resulting from the surgical resection of significant portions of the small intestine, often due to conditions like Crohn’s disease or trauma.
259
How do the intestines adapt after resection in short bowel syndrome?
After resection, the intestines undergo morphological and functional changes such as enlargement and lengthening of villi and slower peristalsis, mediated by hormones, cytokines, and growth factors.
260
What dietary adjustments are necessary for patients with short bowel syndrome?
Patients with short bowel syndrome must take supplementary vitamins and consume small, low-fat meals to ensure adequate nutrient absorption.
261
Describe the symptoms of enterocolitis.
Enterocolitis can manifest with a range of symptoms including diarrhea, abdominal pain, urgency, perianal discomfort, incontinence, and hemorrhage.
262
Identify common viral causes of enteritis.
Common viral causes of enteritis include Rota- and Noroviruses.
263
List some bacterial enteritides and their implications.
Bacterial enteritides include Cholera, Salmonella, intestinal tuberculosis, Whipple’s disease, and pathogenic E. coli enteritis, which can lead to severe gastrointestinal symptoms.
264
Explain non-occlusive intestinal ischemia and its potential causes.
Non-occlusive intestinal ischemia occurs when there is decreased blood flow to the intestines without a physical blockage, often due to conditions like shock, cardiac failure, or the use of vasoconstrictors.
265
What is the significance of systemic vasculitis in relation to intestinal blood flow?
Systemic vasculitis can lead to inflammation of blood vessels, potentially causing reduced blood flow to the intestines and contributing to ischemic conditions.
266
Describe the impact of cirrhosis or portal hypertension on intestinal blood flow.
Cirrhosis or portal hypertension can compress the portal drainage system, leading to decreased blood flow to the intestines and potentially causing ischemic symptoms.
267
Describe the common pathogenic parasitic infection that causes giardiasis.
Giardia lambia is the most common pathogenic parasitic infection causing giardiasis, which spreads through fecally contaminated water and food.
268
Explain the resistance of Giardia lambia to chlorine.
Giardia lambia is resistant to chlorine, making it a concern for contamination in water sources.
269
Define Whipple’s disease and its causative agent.
Whipple’s disease is an extremely rare chronic multisystem disease affecting the small intestine, caused by the bacterium Tropheryma Whipplei.
270
List the classic triad of symptoms associated with Whipple’s disease.
The classic triad of symptoms includes abdominal pain and diarrhea, weight loss, and arthritis.
271
How can Whipple’s disease affect other organs in the body?
Whipple’s disease can also affect the heart, lungs, brain, and eyes.
272
Describe the treatment for Whipple’s disease.
Whipple’s disease is curable with long-term antibiotic treatment.
273
What histological feature is observed in patients with Whipple’s disease?
In histology, sickle particle containing cells can be seen in patients with Whipple’s disease.
274
Define celiac disease and its alternative names.
Celiac disease, also known as celiac sprue or gluten-sensitive enteropathy, is an immune-mediated enteropathy triggered by the ingestion of gluten-containing foods.
275
Identify the foods that trigger celiac disease.
Gluten-containing foods that trigger celiac disease include wheat, rye, and barley.
276
Explain the role of gluten in celiac disease.
Gluten is a complex protein that, when ingested, is partially digested; the gliadin molecule is not fully digestible and becomes deaminated.
277
What genetic factors are associated with celiac disease?
The genes HLA-DQ2 and HLA-DQ8 are associated with celiac disease, although it can occur in individuals without these alleles.
278
List other immune diseases that can cause celiac disease.
Other immune diseases that can cause celiac disease include diabetes mellitus type 1, Sjögren disease, and thyroiditis.
279
Describe the immune response triggered by gliadin in individuals with specific alleles.
In individuals with the HLA-DQ2/HLA-DQ8 alleles, deaminated gliadin is recognized as a pathogen by CD4+ cells, initiating an immune response.
280
What are the consequences of the immune response in celiac disease?
The immune response leads to damage of the mucosa, accumulation of CD8+ cells, and formation of anti-deaminated gliadin antibodies.
281
List the symptoms of celiac disease in children.
In children, celiac disease manifests with diarrhea, weight loss, abdominal pain, anorexia, muscle wasting, bloating, and nausea.
282
What skin condition may occur in some individuals with celiac disease?
Some individuals with celiac disease may develop blistering skin lesions known as dermatitis herpetiformis.
283
Describe the symptoms of celiac disease in adults.
In adults, celiac disease can be symptomless or cause anemia, diarrhea, bloating, and fatigue.
284
What is the risk associated with celiac disease regarding cancer?
Patients with celiac disease are prone to enteropathy-associated T-cell lymphoma, which is an aggressive cancer.
285
Describe lymphomatous polyposis and its prognosis.
Lymphomatous polyposis is a rare condition found in the ileocecum, characterized by the presence of polyps. It has a poor prognosis.
286
Explain the types of tumors that can occur in the small intestine.
All tumors in the small intestine are very rare, but various types of GI-tract neoplasms can occur, including adenoma, adenocarcinoma, neuroendocrine tumors (NET), gastrointestinal stromal tumors (GIST), and intestinal lymphomas.
287
Do adenocarcinomas in the small intestine have any associations with other conditions?
Yes, adenocarcinomas in the small intestine are often associated with Crohn’s disease.
288
How common are tumors in the small intestine compared to other gastrointestinal tumors?
Tumors in the small intestine are very rare compared to other gastrointestinal tumors.
289
Define lymphomatous polyposis and its location in the body.
Lymphomatous polyposis is a rare condition that occurs in the ileocecum, characterized by the formation of polyps.
290
What dietary restrictions might someone with lymphomatous polyposis face?
Individuals with lymphomatous polyposis may need to avoid certain foods, such as McDonald's milkshakes and McFlurries, due to dietary intolerances.
291
Describe a colonic diverticulum.
A colonic diverticulum is a sac-like protrusion of the colonic wall, classified as a false diverticulum (pseudodiverticulum) because it involves only the mucosa and submucosa, not the other layers of the colonic mucous membrane.
292
Explain the condition known as diverticulosis.
Diverticulosis is the presence of many diverticula in the colon, which is usually asymptomatic but may cause symptoms like abdominal pain or lower GI tract bleeding.
293
Define diverticulitis and its prevalence among people with diverticulosis.
Diverticulitis is the inflammation of diverticula and occurs in approximately 10% of people with diverticulosis.
294
How does diverticular disease differ from diverticulosis?
Diverticular disease refers to symptomatic diverticulosis or diverticulitis, while diverticulosis itself is often asymptomatic.
295
Discuss the demographic most affected by diverticular disease.
Diverticular disease predominantly affects the elderly, with 60% of people at the age of 60 having diverticulosis.
296
What dietary factors contribute to the development of diverticulosis?
A diet low in fiber can lead to exaggerated peristaltic contractions, resulting in high intraluminal pressure that contributes to the development of diverticulosis.
297
Explain the geographical differences in the prevalence of diverticulosis.
Diverticulosis is more common in Western countries, likely due to dietary habits, while in Asia, it predominantly affects the right colon.
298
Describe the role of intraluminal pressure in the formation of colonic diverticula.
Colonic diverticula develop under conditions of high intraluminal pressure in the sigmoid colon, particularly in areas where the muscle layer is absent.
299
What lifestyle changes can help prevent diverticulosis?
To avoid the development of diverticulosis, it is recommended to eat dietary fiber (such as fresh fruits and vegetables) and to change the way of sitting on the toilet.
300
How does diverticulitis occur?
Diverticulitis occurs due to micro- or macroscopic perforation of a diverticulum, often caused by erosion of the diverticular wall from increased pressure and food particles.
301
What is diverticular bleeding and its cause?
Diverticular bleeding occurs when the vessels of the diverticula become stretched and weakened, leading to bleeding.
302
Explain the difference between simple diverticulitis and more severe cases.
Simple diverticulitis is characterized by localized inflammation contained by pericolic fat and mesentery, while more severe cases may involve complications such as perforation.
303
Describe the prevalence of colon polyps in adults over 50 years.
Colon polyps affect 30% of adults over 50 years.
304
Explain the classification of non-neoplastic polyps.
Non-neoplastic polyps include inflammatory polyps (pseudopolyps), hyperplastic polyps, and mucosal polyps.
305
Define adenomatous polyps and their significance.
Adenomatous polyps, also known as colorectal adenomas, are significant because they have the highest malignant potential, ranging from 5% to 50% depending on subtype.
306
How are colonic polyps classified based on their macroscopic appearance?
Colonic polyps can be classified as pedunculated (having a stalk), sessile (no stalk), or semisessile (a mix of both).
307
Explain the relationship between lifestyle factors and the development of colonic polyps.
Colonic polyps are highly related to a Western, obesogenic lifestyle, including a diet high in meat and low in vegetables and fruits, obesity, lack of exercise, smoking, and alcohol consumption.
308
Describe the types of hereditary polyposis syndromes associated with adenomatous polyps.
Hereditary polyposis syndromes associated with adenomatous polyps include Familial adenomatous polyposis (FAP) and Gardner syndrome.
309
What are the characteristics of inflammatory polyps?
Inflammatory polyps are consequences of mucosal ulceration and regeneration, often present in inflammatory bowel disease (IBD), and they do not have malignant potential.
310
Define hyperplastic polyps and their potential for malignancy.
Hyperplastic polyps are consequences of idiopathic mucosal hyperplasia and do not have malignant potential.
311
Explain the importance of screening for adenomatous polyps after age 50.
Screening for adenomatous polyps is important after age 50 because they are known to develop into malignancies, and as many as 50% of the Western population over 50 years may have these polyps.
312
Describe the morphology of colorectal polyps.
The morphology of colorectal polyps can vary, including pedunculated polyps with a stalk, sessile polyps with a broad base, and semisessile polyps that are a mix of both.
313
What factors indicate a higher malignant risk for adenomatous polyps?
Factors indicating a higher malignant risk for adenomatous polyps include having multiple polyps, specific classifications, and their etiology.
314
Describe Familial Adenomatous Polyposis (FAP).
FAP is an autosomal dominant condition caused by a mutation in the adenomatous polyposis coli gene (APC), characterized by the development of hundreds to thousands of polyps in the colon and rectum, starting in the teenage years.
315
Explain the risk associated with untreated FAP.
Patients with untreated FAP have a 100% risk of developing colorectal adenocarcinoma.
316
Define the histological characteristics of serrated polyps.
Serrated polyps exhibit a characteristic 'sawtooth' morphology and have a moderate malignant potential of about 5%.
317
How are hamartomatous polyps characterized histologically?
Hamartomatous polyps are characterized by branching and cystically dilated crypts and are comprised of normal tissue with disorganized growth.
318
Do sporadic hamartomatous polyps have malignant potential?
Sporadic hamartomatous polyps have no malignant potential, while syndromic hamartomatous polyps do.
319
Explain Peutz-Jeghers syndrome and its associated risks.
Peutz-Jeghers syndrome is a rare autosomal dominant disorder characterized by hamartomatous polyps throughout the GI tract and mucocutaneous hyperpigmentation, with increased risks for various malignancies including breast, colorectal, pancreatic, ovarian, lung, and stomach cancers.
320
Describe the symptoms of Hirschsprung’s syndrome.
The most prominent symptom of Hirschsprung’s syndrome is constipation, followed by vomiting, abdominal pain, diarrhea, and slow growth.
321
What is the significance of the number of polyps in diagnosing FAP?
The diagnosis of FAP is confirmed by the presence of more than 100 polyps, as they are morphologically indistinguishable from colorectal adenomas.
322
How does the morphology of hamartomatous polyps appear macroscopically?
Macroscopically, hamartomatous polyps are typically pedunculated, round, lobulated, and may also be eroded.
323
What are the variants of Familial Adenomatous Polyposis (FAP)?
Variants of FAP include Gardner syndrome and Turcot syndrome.
324
What is the treatment recommendation for patients with FAP?
All patients with FAP are recommended to have their colon removed to prevent cancer.
325
Describe the genetic inheritance pattern of Peutz-Jeghers syndrome.
Peutz-Jeghers syndrome is inherited in an autosomal dominant manner.
326
Explain the role of the adenomatous polyposis coli gene (APC) in FAP.
The APC gene is mutated in Familial Adenomatous Polyposis, leading to the development of numerous polyps in the colon and rectum.
327
How does the presence of hamartomatous polyps differ in idiopathic versus syndromic cases?
Idiopathic hamartomatous polyps have no malignant potential, while syndromic hamartomatous polyps are associated with conditions that may carry malignant potential.
328
Describe the demographic most affected by ischemia in patients.
90% of all cases occur in patients over 60 years old, often with other morbidities such as cardiovascular disease.
329
Explain the relationship between abdominal surgery and ischemia in younger patients.
Younger people may be affected by ischemia if they have had abdominal surgery.
330
Define angiodysplasia and its significance in gastrointestinal health.
Angiodysplasia is a small vascular malformation in the gut and is the second most common cause of bleeding from the lower GI tract after diverticulitis.
331
How does the incidence of angiodysplasia change with age?
The incidence of angiodysplasia increases with age.
332
Identify the common location of angiodysplasia in the gastrointestinal tract.
Angiodysplasia usually affects the right colon but can occur anywhere in the bowels.
333
What is the primary manifestation of angiodysplasia in patients?
Angiodysplasia manifests as lower GI tract bleeding.
334
Differentiate between occlusive and non-occlusive ischemia.
Ischemia can be classified as occlusive or non-occlusive, depending on the underlying cause.
335
Discuss the relationship between angiodysplasia and diverticulitis.
Angiodysplasia is the second most common cause of bleeding from the lower GI tract, following diverticulitis.
336
Describe the two idiopathic conditions included under inflammatory bowel disease (IBD).
The two idiopathic conditions included under inflammatory bowel disease (IBD) are Crohn disease (CD) and ulcerative colitis (UC). Both are chronic diseases of the gastrointestinal tract characterized by inappropriate immune activation of the mucosa.
337
Explain the difference between remission and flares in IBD.
Remission refers to the asymptomatic periods in IBD where the patient does not experience symptoms, while flares are the symptomatic periods where the disease is active.
338
Identify factors that may provoke a flare-up of IBD.
Factors that may provoke a flare-up of IBD include stress, specific types of food, and cigarette smoking, although many flares occur without an apparent trigger.
339
How does the incidence of IBD vary by age and geography?
IBD usually presents during adolescence or young adulthood, with a second peak of incidence around the age of 50. It is most prevalent in Western countries, particularly in northern regions compared to southern regions.
340
Define the risk factors associated with IBD.
Risk factors for IBD include family history, genetic predisposition (such as NOD2 mutation and HLA-B27), a diet poor in fiber and rich in total fat and animal fat, white or Jewish ethnicity, absence of breastfeeding, NSAID use, and previous gastrointestinal infections.
341
Explain the relationship between smoking and the risk of ulcerative colitis and Crohn disease.
Interestingly, the risk of ulcerative colitis (UC) is decreased in people who smoke, while the risk for Crohn disease (CD) is increased. However, it is advised not to start smoking due to the increased risk for CD.
342
Describe the known causes of IBD.
The causes of IBD are not fully understood, but it is known that multiple factors, both genetic and environmental, contribute to the disease. Pathogenesis involves defects in mucosal immunity, epithelium, and intestinal microbiota, leading to chronic inflammation.
343
How do epithelial defects contribute to the pathogenesis of IBD?
Epithelial defects in individuals with IBD allow bacterial components to cross the epithelial barrier and enter the mucosa, activating both adaptive and innate immune responses, which leads to the release of TNF by immune cells.
344
What role do genetic defects play in IBD?
Genetic defects in individuals with IBD can lead to an increased response to TNF, which further increases epithelial permeability, contributing to the chronic inflammation characteristic of the disease.
345
Summarize the importance of understanding IBD for medical exams.
IBD is commonly asked about in medical exams and is repeated in various later subjects, making it advantageous for students to have a thorough understanding of the condition.
346
Describe the extraintestinal manifestations associated with IBD.
IBD carries the risk for several extraintestinal manifestations, including uveitis, primary sclerosing cholangitis, arthritis, erythema nodosum, pyoderma gangrenosum, ankylosing spondylitis, and aphthous stomatitis.
347
Explain the genetic factors involved in Crohn's disease.
In homozygotic twins, if one twin has Crohn's disease (CD), the other has a 50% risk of developing it, indicating a strong genetic component. The gene NOD2 is particularly implicated in the development of CD.
348
Define the term 'skip lesions' in the context of Crohn's disease.
Skip lesions refer to the presence of multiple, separate lesions in Crohn's disease, where inflammation appears to 'skip' some parts of the mucosa, creating sharp borders between diseased and healthy areas.
349
How do the lesions in Crohn's disease differ from healthy mucosa?
Lesions in Crohn's disease are deep, depressed compared to healthy mucosa, and often have a cobblestone-like appearance due to their morphology.
350
Describe the progression of aphthous ulcers in Crohn's disease.
Aphthous ulcers in Crohn's disease begin as deep but narrow lesions, sometimes described as knife-like cuts, which can develop into fissures that may extend through the entire wall of the intestine.
351
What complications can arise from strictures in Crohn's disease?
Strictures in Crohn's disease can lead to narrowing of the intestinal lumen, potentially causing bowel obstruction due to transmural edema, inflammation, submucosal fibrosis, and hypertrophy of the muscularis propria.
352
Explain the phenomenon of 'creeping fat' in Crohn's disease.
Creeping fat refers to the gradual extension of mesenteric fat that covers the serosal surface of the intestine in Crohn's disease, contrasting with healthy intestines where mesenteric fat is separated from the serosa.
353
What histological changes are typical in Crohn's disease?
Histological changes in Crohn's disease include infiltration by lymphocytes, plasma cells, eosinophils, and neutrophils, as well as cryptal distortion where colonic crypts take on abnormal branching shapes.
354
Define cryptitis and cryptal abscess in the context of Crohn's disease.
Cryptitis is the infiltration of immune cells into the walls of colonic crypts, while cryptal abscess occurs when immune cells infiltrate into the lumen of the crypt.
355
What percentage of Crohn's disease patients exhibit noncaseating granulomas?
Noncaseating granulomas are found in approximately 35% of patients with Crohn's disease.
356
Describe the treatment approach for severe strictures in Crohn's disease.
Treatment for severe strictures in Crohn's disease may involve surgical resection, but this is not curative as the disease often recurs at the site of anastomosis. Therefore, conservative treatment with immune-suppressing drugs is usually preferred to prolong asymptomatic periods and prevent flare-ups.
357
Explain the complications that may arise from Crohn's disease.
Complications of Crohn's disease can include the development of fistulas between the bowel and other organs such as the bladder, vagina, or skin, as well as perforations and peritoneal abscesses.
358
Define the main difference between ulcerative colitis (UC) and Crohn's disease (CD).
The main difference is that ulcerative colitis can only affect the colon and the inflammation is never deeper than the submucosa, while Crohn's disease can affect any part of the gastrointestinal tract and can penetrate deeper.
359
How does ulcerative colitis (UC) typically start and progress?
Ulcerative colitis always starts in the rectum and may spread proximally. If it only affects the rectum, it is called ulcerative proctitis; if it affects the whole colon, it is referred to as ulcerative pancolitis.
360
Explain the condition known as backwash ileitis in the context of ulcerative colitis.
Backwash ileitis occurs when there is a small 'spill-over' of inflammation into the terminal ileum in cases of pancolitis.
361
Describe the characteristics of ulcers found in ulcerative colitis.
The ulcers in ulcerative colitis are broad with a large diameter and are superficial, penetrating mostly the mucosa and submucosa without being transmural.
362
What are pseudopolyps and how do they form in ulcerative colitis?
Pseudopolyps are formed due to the regeneration of ulcers in ulcerative colitis, where the regenerating mucosa bulges into the lumen.
363
Discuss the risk of colonic adenocarcinoma in ulcerative colitis compared to Crohn's disease.
Ulcerative colitis carries a higher risk for colonic adenocarcinoma than Crohn's disease because it always affects the colon.
364
How does ulcerative colitis affect the muscularis propria of the bowel?
The inflammatory process in ulcerative colitis may damage the muscularis propria, preventing it from functioning properly, which can lead to loss of muscular tone and dilation of the bowel, potentially resulting in toxic megacolon.
365
What is toxic megacolon and what risk does it pose in ulcerative colitis?
Toxic megacolon is a condition where the affected bowel loses its muscular tone and dilates, posing a significant risk of perforation.
366
Identify the histological difference between ulcerative colitis and Crohn's disease.
The histology of ulcerative colitis is similar to that of Crohn's disease, but a key difference is that there are no granulomas present in ulcerative colitis.
367
Describe the primary treatment approach for Ulcerative Colitis (UC).
UC is primarily treated conservatively with immunosuppressant drugs, but total colectomy can cure UC if conservative treatment is insufficient.
368
Explain the affected regions in Crohn's disease compared to Ulcerative Colitis.
Crohn's disease can affect anywhere in the GI tract, commonly the terminal ileum, while Ulcerative Colitis only affects the colon.
369
Define the distribution pattern of lesions in Crohn's disease.
Crohn's disease is characterized by skip lesions, which are patches of inflammation, whereas Ulcerative Colitis has a diffuse distribution.
370
How does the inflammation differ between Crohn's disease and Ulcerative Colitis?
In Crohn's disease, inflammation is transmural, affecting all layers of the bowel wall, while in Ulcerative Colitis, it is limited to the mucosa and submucosa.
371
Describe the characteristics of ulcers in Crohn's disease versus Ulcerative Colitis.
Crohn's disease features deep, knife-like ulcers (aphthous ulcers), while Ulcerative Colitis has superficial, broad-based ulcers.
372
Explain the occurrence of strictures in Crohn's disease and Ulcerative Colitis.
Strictures are common in Crohn's disease but rare in Ulcerative Colitis.
373
Do Crohn's disease and Ulcerative Colitis lead to fibrosis?
Yes, fibrosis is common in Crohn's disease, while it is rarely seen in Ulcerative Colitis.
374
How do fistulas differ between Crohn's disease and Ulcerative Colitis?
Fistulas are common in Crohn's disease but do not occur in Ulcerative Colitis.
375
Discuss the impact of Crohn's disease and Ulcerative Colitis on fat and vitamin absorption.
Crohn's disease can lead to fat and vitamin malabsorption, whereas Ulcerative Colitis does not typically cause these issues.
376
Explain the recurrence of disease after surgery in Crohn's disease compared to Ulcerative Colitis.
Recurrence after surgery is common in Crohn's disease, while it is not seen in Ulcerative Colitis.
377
Describe the association of toxic megacolon with Ulcerative Colitis and Crohn's disease.
Toxic megacolon is associated with Ulcerative Colitis but not with Crohn's disease.
378
Describe colorectal carcinoma (CRC) and its significance in the gastrointestinal tract.
Colorectal carcinoma (CRC) refers to all cancers affecting the colon and rectum, accounting for 95% of all GI cancers. It is the third most common type of cancer and the second leading cause of cancer-related death, representing 10% of the world's cancers.
379
Explain the relationship between adenomatous polyps and colorectal cancer.
Over 90% of colorectal cancers develop from adenomatous polyps of the colon, making these polyps a significant precursor to CRC.
380
How does screening impact the incidence of colorectal cancer?
Screening is crucial in reducing the incidence of colorectal cancer. In Europe, programs for CRC screening are being developed or have recently launched, with recommendations for individuals over 50/55 to undergo colonoscopy or faecal occult blood tests.
381
Identify major dietary risk factors for colorectal cancer.
A low intake of vegetable fiber and a high intake of refined carbohydrates and fats are major dietary risk factors for colorectal cancer, contributing to its higher prevalence in Western countries.
382
List other risk factors associated with colorectal cancer.
Other risk factors for colorectal cancer include family history, older age, consumption of red and processed meats, alcohol use, obesity, smoking, and lack of physical activity.
383
What protective role do NSAIDs, particularly aspirin, play in colorectal cancer?
NSAIDs, especially aspirin, are protective against colorectal cancers as they inhibit the enzyme cyclooxygenase-2 (COX-2), which is highly expressed in carcinomas.
384
Define the different types of colorectal cancer based on their causes.
Colorectal cancer can be categorized into sporadic CRC (95% of cases), hereditary CRC, HNPCC (Hereditary Nonpolyposis Colorectal Cancer), FAP (Familial Adenomatous Polyposis), and IBD-associated CRC (Inflammatory Bowel Disease-associated CRC).
385
What is the most common histological type of colorectal carcinoma?
Adenocarcinoma is the most common type of colorectal carcinoma, accounting for 95% of cases, with other types including adenosquamous carcinoma and spindle cell carcinoma.
386
Discuss the age demographic most affected by colorectal cancer.
Colorectal cancer primarily affects the elderly, particularly individuals in their 60s and 70s.
387
Explain the paradox of tumor accumulation in the colon despite the small intestine's length.
Despite the small intestine accounting for 75% of the overall length of the GI tract, tumors accumulate in the colon, which is the most common site for gastrointestinal malignancies.
388
Describe the typical characteristics of adenocarcinomas.
Adenocarcinomas are usually solitary masses that can be either polypoid or ulcerated.
389
Explain the concept of synchronous tumors in adenocarcinomas.
Synchronous tumors refer to the presence of more than one primary tumor at the same time in a few percent of adenocarcinoma cases.
390
Define the grading system for adenocarcinomas based on differentiation.
Adenocarcinomas are graded as well differentiated (low grade), moderately differentiated (most frequent type), and poorly differentiated (few glands, mostly sheets of cells).
391
How is colorectal cancer (CRC) staged?
CRC is staged as follows: Stage 0 - carcinoma in situ; Stage I - cancer invades muscularis mucosa; Stage II - cancer invades beyond muscularis mucosa; Stage III - cancer spreads to regional lymph nodes; Stage IV - cancer spreads distally.
392
Explain the lymphogenic and hematogenous spread of colorectal cancer.
Colorectal cancer can metastasize through lymphogenic spread to regional lymph nodes, or through portal circulation to the liver, and caval circulation to the lung if originating in the lower third of the rectum.
393
Describe the two major molecular pathways involved in colorectal carcinoma development.
The two major pathways are the chromosomal instability pathway, occurring in 80% of cases, and the microsatellite instability pathway, occurring in 15% of cases.
394
What is the adenoma-carcinoma sequence?
The adenoma-carcinoma sequence is a well-studied multistep process where there is a progression from normal epithelium to an adenomatous polyp to invasive cancer.
395
How long does the progression from normal epithelium to invasive cancer typically take in sporadic colorectal cancers?
The progression typically takes 10 to 15 years.
396
What role does the APC gene play in the adenoma-carcinoma sequence?
The APC gene is mutated and inactivated early in the sequence, coding for a protein that inhibits the proto-oncogene β-catenin.
397
What mutations occur late in the adenoma-carcinoma sequence?
Inactivation of k-RAS and p53 occurs late in the adenoma-carcinoma sequence.
398
Define microsatellite instability (MSI) in the context of colorectal carcinoma.
MSI is a condition where the DNA repair mechanism is impaired, leading to easier mutations in genes, commonly due to mutations in MLH1 and MSH2.
399
How can the presence of microsatellite instability be detected?
The presence of microsatellite instability can be shown using PCR (polymerase chain reaction).
400
Describe the role of immunotherapy in treating colorectal cancer.
Immunotherapy involves using specific drugs that target and bind to cell surface proteins like EGFR and PD-1, which are important for cancer cells that express them.
401
Explain the genetic basis of HNPCC.
HNPCC, or Hereditary Nonpolyposis Colorectal Cancer, is caused by germline mutations in genes responsible for DNA error detection, excision, and repair, primarily MSH2 and MLH1.
402
How does HNPCC affect cancer risk in patients?
Patients with HNPCC have an 80% risk of developing colorectal cancer in their lifetime and are also at increased risk for cancers in other organs such as the endometrium and ovaries.
403
Define the typical age of colorectal cancer onset in HNPCC patients compared to sporadic cases.
Patients with HNPCC tend to develop colorectal cancer at much younger ages than those with sporadic colon cancer.
404
What is the significance of aspirin in the context of HNPCC?
Taking small doses of aspirin daily may help in the prevention of colorectal cancer in individuals with HNPCC.
405
Describe the recommended surgical intervention for females with HNPCC.
Females with HNPCC are advised to undergo prophylactic surgery, including hysterectomy and removal of the ovaries, due to the high risk of cancer in these organs.
406
List some types of tumors that can occur in the colon and rectum.
Common tumors include lipomas, leiomyomas, GIST, leiomyosarcoma, angiosarcoma, Kaposi sarcoma, and lymphoma.
407
Explain how other cancers can affect the colon.
Cancers from the stomach, lungs, prostate, breasts, and ovaries can metastasize to the colon, and melanoma can also spread to this area.
408
What is anal intraepithelial neoplasia (AIN)?
AIN is a condition in the anal canal induced by HPV, characterized by lesions similar to those seen in CIN III of the cervix, and it has a poor prognosis.
409
Define the term 'non-epithelial colorectal tumors.'
Non-epithelial colorectal tumors refer to tumors that do not originate from the epithelial tissue of the colon, including various rare types.
410
Describe the vermiform appendix and its role in the human body.
The vermiform appendix is a true diverticulum of the cecum, which can be prone to acute and chronic inflammations.
411
Explain the most common pathology associated with the appendix.
The most common pathology in the appendix is acute appendicitis, which refers to the acute inflammation of the vermiform appendix.
412
How important is rapid management in cases of acute appendicitis?
Rapid management is crucial to prevent complications such as perforation of the appendix.
413
What is the lifetime incidence of appendicitis in men and women?
The lifetime incidence of appendicitis is 9% for men and 7% for women.
414
Identify the peak incidence age range for acute appendicitis.
The peak incidence of acute appendicitis occurs in the second and third decades of life.
415
Discuss the trend in the incidence of acute appendicitis since the 1970s.
The incidence of acute appendicitis has been decreasing since the 1970s, for reasons that are not well understood.
416
Define the etiology of acute appendicitis.
The etiology of acute appendicitis is largely unknown, and it frequently occurs in healthy, young individuals.
417
What are some identified causes of obstruction leading to acute appendicitis?
Obstruction may be caused by hard fecal masses, calculi, lymphoid tissue hyperplasia, or tumors.
418
Explain the physiological consequences of obstruction in the appendix.
Obstruction can lead to increased luminal and intramural pressure, thrombosis in small vessels, localized edema, ischemic injury, and stasis of luminal contents.
419
How does bacterial proliferation relate to acute appendicitis?
The obstruction creates an environment conducive to bacterial proliferation, which triggers inflammatory responses.
420
What is the pathological criterion for diagnosing acute appendicitis?
The pathological criterion for diagnosing acute appendicitis is neutrophilic infiltration of the muscularis propria.
421
Describe the progression of acute appendicitis in severe cases.
In severe cases, focal abscesses may form, leading to acute suppurative appendicitis, which can progress to hemorrhagic ulceration and gangrenous necrosis, resulting in acute gangrenous appendicitis.
422
What symptoms are associated with localized appendiceal edema?
Localized appendiceal edema stimulates visceral afferent pain fibers, initially causing vaguely localized periumbilical abdominal pain.
423
How does inflammation of the appendix affect surrounding tissues?
As inflammation progresses, it can involve the adjacent parietal peritoneum, causing characteristic peritonitic pain.
424
Describe the appearance and location of a carcinoid tumor in the appendix.
A carcinoid tumor in the appendix typically appears yellow and solid, and is usually located at the distal tip of the appendix.
425
Explain the treatment for carcinoid tumors of the appendix.
The treatment for carcinoid tumors of the appendix is surgical removal of the appendix, known as an appendectomy, which is usually performed laparoscopically.
426
Define chronic appendicitis and its symptoms.
Chronic appendicitis shows symptoms similar to acute appendicitis but is much milder, with symptoms that can come and go over weeks, months, or even years.
427
How are carcinoid tumors of the appendix typically discovered?
Carcinoid tumors of the appendix are usually discovered during resection surgery of the appendix.
428
Explain the rarity of metastasis in carcinoid tumors of the appendix.
Metastasis to lymph nodes and more distant sites is very rare in carcinoid tumors of the appendix, even though intramural and transmural invasion is often seen.
429
What hormones are produced by well-differentiated carcinoid tumors?
Well-differentiated carcinoid tumors produce hormones such as histamine, kallikrein, prostaglandins, and serotonin.
430
Describe the characteristics of mucocele in the appendix.
Mucocele is a dilated appendix filled with mucus, which can be caused by an obstruction and may contain thickened mucus.
431
Explain the potential consequences of mucinous cystadenocarcinoma in the appendix.
Mucinous cystadenocarcinoma can invade through the wall of the appendix and lead to intraperitoneal seeding, potentially resulting in pseudomyxoma peritonei.
432
Define peritonitis and its clinical diagnosis.
Peritonitis is the inflammation of the peritoneum, diagnosed clinically by the presence of typical findings such as rebound tenderness, guarding, and pain on gentle percussion.
433
What is rebound tenderness and how is it assessed?
Rebound tenderness is the pain felt by a patient when pressure is quickly removed from the abdomen, indicating irritation of the peritoneum.
434
Describe guarding in the context of peritonitis.
Guarding refers to the involuntary contraction of abdominal wall muscles when palpating the abdomen, often seen in patients with peritonitis.
435
What is the typical cause of peritonitis?
The typical cause of peritonitis is infectious, usually caused by bacteria.
436
Describe Ormond's disease and its characteristics.
Ormond's disease, also known as retroperitoneal fibrosis, is characterized by the development of extensive fibrosis throughout the retroperitoneum, often beginning around a severely atherosclerotic aorta.
437
Explain the potential causes of Ormond's disease.
The exact pathogenesis of Ormond's disease is unknown but may be related to an immune response against atherosclerotic plaques. It can also be associated with autoimmune disorders like Sjögren's and Crohn's disease, as well as trauma, radiation, or certain drugs.
438
How does Ormond's disease present clinically?
Ormond's disease typically presents with nonspecific symptoms such as dull pain in the back, and the fibrosis may envelop retroperitoneal structures like the inferior vena cava or ureter, potentially leading to renal failure.
439
Define pseudomyxoma peritonei (PMP) and its origin.
Pseudomyxoma peritonei (PMP) is a rare condition of the peritoneum that begins with an adenocarcinoma or mucinous cystadenocarcinoma in the appendix, which perforates the appendix wall and spreads to the peritoneum.
440
Explain the progression of pseudomyxoma peritonei.
In pseudomyxoma peritonei, tumor cells multiply and produce mucin, which fills the peritoneal cavity, leading to increased abdominal pressure that can obstruct the intestines.
441
How common is pseudomyxoma peritonei in the general population?
Pseudomyxoma peritonei is a rare condition, occurring in approximately 1-2 cases per million people.
442
Describe the relationship between Ormond's disease and autoimmune disorders.
Ormond's disease is associated with certain autoimmune disorders, including Sjögren's syndrome and Crohn's disease, which may contribute to its development.
443
What complications can arise from Ormond's disease?
Complications from Ormond's disease can include renal failure due to the fibrosis enveloping retroperitoneal structures like the ureter.
444
Identify the symptoms associated with pseudomyxoma peritonei.
Symptoms of pseudomyxoma peritonei may include abdominal distension, pain, and intestinal obstruction due to increased abdominal pressure from mucin accumulation.
