GASTRO: BOARDS AND BEYOND Flashcards

1
Q

What condition is characterized by endometrial cancer, colon cancer, and a family history of endometrial and ovarian cancer?

A

Lynch syndrome (hereditary nonpolyposis colorectal cancer).

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1
Q

What is the “3-2-1 Rule” in relation to Lynch syndrome?

A

Requires 3 or more Lynch-associated cancers (2 of whom are first-degree relatives) over 2 or more generations, with at least 1 person affected by age 50.

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2
Q

What type of genetic inheritance pattern does Lynch syndrome follow?

A

Autosomal dominant.

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3
Q

What is the underlying cause of Lynch syndrome?

A

A DNA mismatch repair gene defect leading to microsatellite instability.

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4
Q

How does Lynch syndrome affect the development of cancer?

A

It causes dysplasia in multiple organs that becomes malignant faster than typical lesions.

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5
Q

At what age do patients with Lynch syndrome typically develop cancers compared to the general population?

A

Patients develop cancers at a much younger age than would typically occur.

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6
Q

What role do genetic counseling and screening play in managing Lynch syndrome?

A

They are crucial for early detection and prevention strategies in affected individuals and families.

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7
Q

What gene mutation is associated with familial adenomatous polyposis (FAP)

A

Mutations in the APC gene.

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8
Q

What is the primary cancer risk associated with familial adenomatous polyposis?

A

Increased risk of colorectal cancer.

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9
Q

Why is “polyposis” included in the name familial adenomatous polyposis?

A

Because the APC gene leads to the development of multiple colonic polyps.

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10
Q

Does familial adenomatous polyposis increase the risk of breast or ovarian cancers?

A

No, it does not increase the risk of breast or ovarian cancers

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11
Q

How many colon polyps do patients with familial adenomatous polyposis typically develop?

A

Patients can develop hundreds to thousands of colon polyps.

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12
Q

At what age do patients with familial adenomatous polyposis typically start developing polyps?

A

Often by adolescence.

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13
Q

What is Gardner’s syndrome?

A

An autosomal dominant condition characterized by adenomatous polyposis and soft-tissue tumors.

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14
Q

Which gene mutation is responsible for Gardner’s syndrome?

A

APC gene mutation on chromosome 5.

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15
Q

How many colonic polyps do patients with Gardner’s syndrome typically develop?

A

Hundreds of colonic polyps.

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16
Q

What is the malignancy potential of the colonic polyps in Gardner’s syndrome?

A

Although benign, they have a strong malignancy potential.

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17
Q

What is the risk of developing colorectal cancer for patients with Gardner’s syndrome or familial adenomatous polyposis (FAP) by age 50?

A

100% chance if the colon is not removed.

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18
Q

What are some extra-colonic features associated with Gardner’s syndrome?

A

Osteomas, congenital hypertrophy of retinal pigment epithelium (CHRPE), and epidermoid cysts.

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19
Q

Where do osteomas commonly develop in patients with Gardner’s syndrome?

A

In the mandible.

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20
Q

Where do epidermoid cysts typically occur in Gardner’s syndrome?

A

In locations such as the face, scalp, and extremities.

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21
Q

How does classic familial adenomatous polyposis (FAP) differ from Gardner’s syndrome?

A

FAP is restricted to the colon and does not involve the development of epidermoid cysts, fibromas, or osteomas.

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22
Q

What common genetic mutation is found in both Gardner’s syndrome and familial adenomatous polyposis (FAP)?

A

APC gene mutation.

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23
Q

Why are the terms Gardner’s syndrome and FAP sometimes used interchangeably?

A

Because some FAP patients have limited extra-colonic features similar to those in Gardner’s syndrome.

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24
Q

In a patient with osteomas and cysts, which syndrome is the more accurate diagnosis: Gardner’s syndrome or classic FAP?

A

Gardner’s syndrome is the better answer.

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25
Q

Is a variant of Lynch syndrome (hereditary non-polyposis colorectal cancer) with sebaceous skin tumors.

A

Muir-Torre syndrome

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26
Q

Is a variant of familial adenomatous polyposis with malignant central nervous system tumors.

A

Turcot’s syndrome

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27
Q

What is juvenile polyposis syndrome (JPS)?

A

An autosomal dominant condition involving numerous hamartomatous polyps in the GI tract, primarily in the colon and rectum.

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28
Q

What types of polyps are most commonly found in JPS?

A

Hyperplastic, adenomatous, and hamartomatous polyps.

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29
Q

At what age can polyps in JPS begin to develop?

A

As early as the first decade of life.

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30
Q

What does the term “juvenile” refer to in juvenile polyposis syndrome?

A

It refers to the histological characterization of the polyps, not the age of the patient.

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31
Q

What is the most common clinical manifestation of JPS?

A

Rectal bleeding

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32
Q

What are some other symptoms that can occur in JPS?

A

Prolapsing polyps, pain, diarrhea, and iron-deficiency anemia

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33
Q

What is the risk of colorectal cancer in patients with JPS by age 35?

A

About 20%, increasing to 68% by age 60.

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34
Q

What is the lifetime risk of gastric cancer in patients with JPS?

A

20% to 30%

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35
Q

What is required for a clinical diagnosis of JPS?

A

At least one of the following:

  • Five or more juvenile polyps in the colorectum
  • Multiple juvenile polyps throughout the GI tract
  • Any number of juvenile polyps in someone with a known family history of the disease.
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36
Q

How is JPS managed?

A

Routine screening for colorectal cancer with colonoscopy and gastric cancer with upper endoscopy.

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37
Q

Is an autosomal dominant syndrome associated with hamartomatous polyps of the GI tract, mucosal hyperpigmentation, and increased risk of cancer. Although this patient has hamartomatous lesions of the GI tract, he does not have the pigmented macules seen in more than 95% of PJS.

A

Peutz-Jeghers syndrome (PJS)

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38
Q

What is a common site for distant metastases of colon cancer?

A

The liver.

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39
Q

Why does colon cancer commonly metastasize to the liver?

A

Because of the portal venous drainage from the intestinal tract to the liver.

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40
Q

Besides the liver, what are other potential sites of metastasis for colon cancer?

A

The lungs and peritoneum.

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41
Q

How do most carcinomas, including colonic adenocarcinoma, primarily spread?

A

Via lymphatics.

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42
Q

What are the alternative routes of metastasis for colon cancer?

A

Through the bloodstream (hematogenous spread via the portal system), direct extension of the tumor, and seeding of peritoneal fluid.

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43
Q

What are the most common sites of metastasis for colon cancer?

A

Regional lymph nodes, the liver, lungs, and the peritoneum.

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44
Q

Intraperitoneal seeding refers to the spread of tumors via intraperitoneal fluid. Ovarian tumors in women often spread through this mechanism. Colon cancer can spread via intraperitoneal seeding. When it does, lesions appear on the outside of the liver, since this is the area in contact with intraperitoneal fluid. In addition to the exterior of the liver, seeding from colon cancer often leads to abdominal lesions in specific areas with stasis of peritoneal fluid (normally this fluid moves with position and bearing down). These include

A

The pouch of Douglas, the right lower quadrant mesentery, and the peritoneum of the sigmoid colon.

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45
Q

Develops in the setting of cirrhosis and chronic infection by hepatitis B or C.

A

A primary liver cancer or hepatocellular carcinoma

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46
Q

Occurs in immunocompromised patients (e.g., recipients of solid organ transplants, allogeneic hematopoietic cell transplants, etc.).

A

Systemic or invasive aspergillosis

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47
Q

What is the progression of mutations in colon cancer called?

A

The adenoma-carcinoma sequence (chromosomal instability pathway).

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48
Q

Which gene is the first to mutate in the adenoma-carcinoma sequence?

A

The APC gene (a tumor suppressor gene).

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49
Q

What is the significance of a mutation in the KRAS gene?

A

It is a proto-oncogene mutation found in the majority of hyperplastic colon polyps and is essential for neoplastic progression.

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50
Q

What is the third mutation that cells acquire to become malignant in colon cancer?

A

A mutation in the p53 gene (another tumor suppressor gene).

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51
Q

What does the presence of all three mutations (APC, KRAS, p53) indicate?

A

The cells are malignant.

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52
Q

How does familial adenomatous polyposis (FAP) affect the adenoma-carcinoma sequence?

A

n FAP, germline mutations in the APC gene are inherited, leading to numerous polyps due to the mutation being present from the start.

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53
Q

What characterizes a sporadic polyp in colon cancer?

A

A negative family history for colon cancer and no inherited gene mutations.

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54
Q

What deficiency is this woman experiencing in the context of carcinoid syndrome?

A

Niacin deficiency

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55
Q

What symptoms are associated with elevated serotonin levels in carcinoid syndrome?

A

Flushing, palpitations, abdominal pain, and diarrhea

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56
Q

What is the precursor molecule to serotonin?

A

Tryptophan

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57
Q

How much of tryptophan is normally utilized for serotonin production?

A

About 1%

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58
Q

In carcinoid syndrome, what percentage of tryptophan may be used for serotonin synthesis?

A

Up to 70%

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59
Q

What deficiency can result from the increased use of tryptophan for serotonin synthesis?

A

Tryptophan deficiency

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60
Q

How is niacin (vitamin B3) produced in the body?

A

From tryptophan

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61
Q

What are the primary symptoms of Sjögren’s syndrome?

A

Dry mouth (xerostomia) and dry eyes (xerophthalmia).

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62
Q

How does diminished saliva production affect oral health in Sjögren’s syndrome?

A

It frequently leads to an increased risk of dental caries (cavities).

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63
Q

What is the mechanism of action of pilocarpine in treating Sjögren’s syndrome?

A

Pilocarpine stimulates muscarinic receptors (M1, M2, M3) to increase oral and ophthalmic secretions.

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64
Q

Why is pilocarpine often intolerable for many patients?

A

Its nonselective action on muscarinic receptors causes cholinergic side effects.

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65
Q

What are some common cholinergic side effects of pilocarpine?

A

Sweating, urinary frequency, diarrhea, bradycardia, nausea, weakness, flushing, and hypotension.

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66
Q

What eye effect is caused by pilocarpine?

A

Miosis (pupillary constriction).

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67
Q

Anticholinergic drugs include atropine and scopolamine. Some side effects include:

A

Hypertension, constipation, urinary retention and mydriasis.

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68
Q

What is the most common type of salivary gland tumor?

A

Pleomorphic adenomas.

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69
Q

Where are pleomorphic adenomas typically located?

A

In the superficial lobes of the parotid glands.

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70
Q

Are pleomorphic adenomas benign or malignant?

A

They are usually benign, but they can undergo malignant transformation.

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71
Q

What is a potential complication of pleomorphic adenomas regarding facial anatomy?

A

They can invade the facial nerve.

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72
Q

Why are pleomorphic adenomas described as “biphasic”?

A

They contain glandular epithelial cells surrounded by supportive stroma.

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73
Q

What types of supportive tissue can be found in pleomorphic adenomas?

A

Cartilage, hyaline, or bone.

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74
Q

What term is sometimes used to describe the composition of pleomorphic adenomas?

A

“Chondromyxoid,” due to the presence of cartilage (chondroid tissue) and mucous cells (myxoid tissue).

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75
Q

What is a common issue associated with the surgical removal of pleomorphic adenomas?

A

Local recurrence.

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76
Q

What are Type I branchial cleft cysts, and where do they form?

A

They are cavities near the parotid gland caused by incomplete regression of ectodermal structures in the embryo.

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77
Q

What is the most common malignant salivary gland tumor?

A

Mucoepidermoid carcinoma.

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78
Q

What cell types are found in mucoepidermoid carcinoma?

A

A mixture of mucin-producing columnar cells and epidermoid cells.

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79
Q

What viral infection is caused by paramyxovirus and characterized by bilateral parotid gland swelling?

A

Mumps.

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80
Q

What would be seen on biopsy in a case of mumps?

A

A lymphocytic infiltrate consistent with viral infection.

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81
Q

What type of tumors are Warthin’s tumors, and are they benign or malignant?

A

Warthin’s tumors are benign salivary gland tumors.

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82
Q

What is the histological characteristic of Warthin’s tumors?

A

Fluid-filled cysts surrounded by lymphoid infiltrates.

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83
Q

What are Warthin’s tumors also known as?

A

Papillary cystadenoma lymphomatosum.

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84
Q

What is the second most common type of salivary gland tumor?

A

Warthin’s tumors.

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85
Q

Where do Warthin’s tumors almost always occur?

A

In the parotid glands.

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86
Q

Why should both parotid glands be examined in clinical practice?

A

Because Warthin’s tumors can be multifocal and bilateral.

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87
Q

In which gender do Warthin’s tumors occur more commonly?

A

Males

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88
Q

How much more likely are smokers to develop Warthin’s tumors?

A

Smokers are 8 times more likely to develop this tumor.

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89
Q

What are the histological features of Warthin’s tumors?

A

They are composed of fluid-filled cystic spaces lined with epithelial cells and dense lymphoid infiltrates, sometimes forming germinal centers.

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90
Q

Is the most common salivary gland malignancy in adults. It is composed of a variable mixture of squamous, mucus-secreting, and intermediate cells.The cystic appearance of this man’s tumor is not consistent with mucoepidermoid carcinoma.

A

Mucoepidermoid carcinoma

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91
Q

Represent 60% of parotid tumors and present as painless, slow-growing, discrete masses. Histologically, pleomorphic adenomas are called “biphasic,” because they contain glandular epithelial cells surrounded by stroma (supportive tissue) with cartilage, hyaline, or bone. The tumor is sometimes described as “chondromyxoid,” because it contains cartilage (chondroid tissue) and mucous cells (myxoid tissue).

A

Pleomorphic adenomas

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92
Q

Are rare and aggressive salivary tumors that occur in older men and have distant metastases at the time of presentation.

A

Small-cell carcinomas

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93
Q

Adenoid cystic carcinoma (ACC) is a locally aggressive tumor with three growth patterns: ?. This tumor is more common in the submandibular, sublingual, and minor salivary glands. ACC is not associated with smoking.

A

Tubular, cribriform, and solid.

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94
Q

What is the most common malignant salivary gland tumor in all age groups?

A

Mucoepidermoid carcinoma.

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95
Q

What types of cells compose mucoepidermoid carcinoma?

A

Variable mixtures of squamous, mucus-secreting, and intermediate cells

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96
Q

How do low-grade mucoepidermoid carcinoma lesions typically appear histologically?

A

They are cystic and have a higher percentage of squamous and mucus-producing cells than intermediate cells.

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97
Q

How do high-grade mucoepidermoid carcinoma lesions differ from low-grade lesions?

A

High-grade lesions are more solid, have more squamous and intermediate cells, show signs of anaplasia in the squamous component, and contain fewer mucus-producing cells.

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98
Q

What percentage of all salivary gland tumors do mucoepidermoid carcinomas represent?

A

Approximately 15%.

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99
Q

Where do mucoepidermoid carcinomas typically occur?

A

In the parotid glands or minor salivary glands.

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100
Q

What are some potential complications of mucoepidermoid carcinoma?

A

They can invade the facial nerve and present with pain and paralysis.

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101
Q

What is Meckel’s diverticulum a remnant of?

A

The embryonic vitelline duct (or yolk stalk).

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102
Q

What is a diverticulum?

A

An outpouching of the intestines.

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103
Q

In which part of the intestine does Meckel’s diverticulum occur?

A

In the small intestine.

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104
Q

What type of tissue can be found in Meckel’s diverticulum?

A

Gastric mucosa (or, rarely, pancreatic tissue).

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105
Q

What do the parietal cells in the gastric mucosa of Meckel’s diverticulum produce?

A

Acid.

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106
Q

How can gastric mucosa in Meckel’s diverticulum lead to complications?

A

It may cause ulceration in the adjacent small bowel, resulting in bleeding.

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107
Q

What is the “rule of twos” regarding Meckel’s diverticulum?

A

It occurs in about 2% of the population, is about 2 inches long, found about 2 feet from the ileocecal valve, 2% of patients develop complications, and has a male-to-female ratio of 2:1.

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108
Q

Lymphocytes are found in ? of the intestines. These cells are not responsible for the bleeding in Meckel’s diverticulum.

A

Peyer’s patches

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109
Q

Chief cells are found in the stomach and produce ? for digestion of proteins.

A

pepsin

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110
Q

Are glandular cells present in epithelial coatings of the mucous membranes of the respiratory tract and the digestive system. These cells produce mucus to protect the digestive or respiratory tubes.

A

Goblet cells

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111
Q

Are found in the jejunum and duodenum. They release secretin when stimulated by a fall in pH to 4 or below in the small intestinal lumen. Secretin increases the secretion of bicarbonate (HCO3-) from the pancreas.

A

S cells

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112
Q

What findings during pregnancy are consistent with Down syndrome (trisomy 21)?

A

Elevated serum β-HCG concentrations and fetal nuchal translucency detected on ultrasound.

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113
Q

What is duodenal atresia?

A

A complete obstruction of the duodenum by an atretic (closed) lumen.

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114
Q

What is duodenal stenosis?

A

A narrowed duodenal lumen that causes partial obstruction, allowing some bile and intestinal contents to flow.

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115
Q

How do duodenal atresia and stenosis commonly present in newborns?

A

With bilious vomiting due to backup of intestinal contents.

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116
Q

What classic sign is seen on an abdominal X-ray for duodenal atresia?

A

The “double-bubble” sign, showing a pocket of air before and after the duodenum.

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117
Q

What is the initial treatment for duodenal atresia or stenosis?

A

Nasogastric decompression and fluids, followed by surgical intervention.

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118
Q

Jejunal atresia involves a failure of the jejunum to canalize. This can be indistinguishable from duodenal atresia with abdominal distension and bilious vomiting. The ? on x-ray is classically associated with jejunal atresia. In addition, duodenal stenosis is more likely in a baby with Down syndrome.

A

“triple bubble” sign

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119
Q

Is a condition that affects premature infants. The intestinal wall develops necrosis, and symptoms start within 2 weeks of birth including fever, vomiting, and diarrhea with abdominal distension.

A

Necrotizing enterocolitis

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120
Q

Is characterized by narrowing of the lumen of the pylorus due to smooth muscle hypertrophy. Babies present with nonbilious vomiting after eating, and a palpable mass in the right upper quadrant classically described as “olive-shaped.”

A

Pyloric stenosis

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121
Q

Result from a failure of the trachea to completely separate from the esophagus, leaving a connection between these structures. This results in aspiration of stomach contents into the lungs when infants attempt to feed.

A

Tracheoesophageal fistulas

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122
Q

What is duodenal atresia?

A

A congenital failure of the duodenum in the small intestine to canalize.

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123
Q

What are the clinical features of duodenal atresia?

A

Distension of the stomach with bilious vomiting.

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124
Q

What does the “double bubble” sign indicate on X-ray?

A

A blind loop of the duodenum and gastric dilatation associated with duodenal atresia.

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125
Q

How common is duodenal atresia?

A

It occurs in about 1 in every 5,000 to 10,000 live births.

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126
Q

What percentage of infants with duodenal atresia have Down syndrome?

A

20% to 40%.

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127
Q

What condition can result from any process that disrupts swallowing in the womb?

A

Polyhydramnios (excess amniotic fluid).

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128
Q

How can pregnancy be affected by a fetus with duodenal atresia?

A

It is often complicated by polyhydramnios due to disrupted swallowing.

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129
Q

Is a life-threatening complication of pregnancy. It occurs in the 3rd trimester with abrupt onset of painful vaginal bleeding. Abruption is not associated with duodenal atresia.

A

Placental abruption

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130
Q

Is a complication of pregnancy that leads to hypertension, proteinuria, edema, and seizures. This is not associated with duodenal atresia.

A

Eclampsia

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131
Q

In placenta previa, the placenta attaches to the lower uterus over the cervix. ? can be life-threatening in this situation. Placenta previa is not associated with duodenal atresia.

A

Vaginal delivery

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132
Q

How is amniotic fluid produced and removed?

A

It is produced by fetal kidneys (fetal urine) and removed by fetal swallowing and intestinal absorption.

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133
Q

What can cause excess amniotic fluid?

A

Increases in urinary excretion or impaired swallowing/digestion.

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134
Q

What physical changes might a woman with polyhydramnios experience?

A

A rapidly expanding abdomen.

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135
Q

What is the amniotic fluid index (AFI)?

A

The sum of the measurement of the maximal depth of the amniotic fluid pocket in all four quadrants of the abdomen.

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136
Q

Which condition is specifically associated with polyhydramnios?

A

Esophageal atresia.

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137
Q

What occurs in esophageal atresia?

A

The esophagus ends in a blind pouch, preventing appropriate swallowing of amniotic fluid by the fetus.

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138
Q

Refers to poor growth of a fetus during pregnancy. It can be caused by poor maternal nutrition or lack of adequate oxygen supply to the fetus. It is associated with oligohydramnios (decreased amniotic fluid).

A

Intrauterine growth restriction

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139
Q

Refers to pulmonary hypoplasia and limb abnormalities that occur in the fetus due to oligohydramnios (decreased amniotic fluid). The amniotic fluid index is low in oligohydramnios.

A

Potter’s syndrome

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140
Q

Pulmonary agenesis

A

It is associated with oligohydramnios.

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141
Q

Is the failure of one or both kidneys to form. The absence of normal fetal renal function causes oligohydramnios.

A

Renal agenesis

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142
Q

What is malrotation?

A

A condition where the cecum is positioned in the right mid- to upper quadrant instead of the right lower quadrant due to improper rotation of the midgut during development.

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143
Q

What causes volvulus in the context of malrotation?

A

The twisting of the intestines around the mesentery due to abnormal positioning during peristalsis.

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144
Q

What symptoms may develop in a baby with malrotation and volvulus?

A

Bilious emesis (vomiting) and abdominal pain.

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145
Q

Is an abdominal X-ray reliable for diagnosing malrotation with volvulus?

A

No, it is often unreliable and can be normal.

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146
Q

What is the test of choice for diagnosing malrotation with volvulus?

A

Upper GI contrast study with fluoroscopy.

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147
Q

What is the primary treatment for malrotation with volvulus?

A

Surgical intervention.

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148
Q

Is characterized by absence or underdevelopment of the bile ducts. This leads to biliary obstruction with jaundice, dark urine, and acholic stools.

A

Biliary atresia

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149
Q

Why is reflux of stomach contents common in neonates?

A

The lower esophageal sphincter is not completely developed.

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150
Q

How is regurgitation in neonates typically characterized?

A

It is effortless and without vomiting, often referred to as “happy spitters.”

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151
Q

When does regurgitation usually occur in neonates?

A

Typically occurs more than 10 minutes after feeding

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152
Q

Is bilious vomiting common in neonates with reflux?

A

No, bilious vomiting does not occur in these cases.

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153
Q

In atresia, there is no lumen for intestinal flow. This leads to vomitting shortly after the baby first begins to feed. The fact that this baby was feeding normally during his first week of life makes intestinal obstruction from atresia

A

Very unlikely.

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154
Q

The pylorus is the opening of the stomach into the duodenum. Pyloric stenosis is characterized by narrowing of the lumen of the pylorus due to smooth muscle hypertrophy. Babies present with ? after eating, and a palpable mass in the right upper quadrant, classically described as “olive-shaped.”

A

Non-bilious vomiting

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155
Q

What is a hiatal hernia?

A

A protrusion of the stomach through the diaphragm and into the thoracic cavity.

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156
Q

What causes hiatal hernias?

A

Progressive disruption of the gastroesophageal junction (GEJ) over time.

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157
Q

Where does the gastroesophageal junction (GEJ) normally reside?

A

Below the diaphragm.

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158
Q

What happens to the hiatal tunnel in patients with a hiatal hernia?

A

It widens, allowing the GEJ to slide upward.

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159
Q

What happens to the phrenoesophageal membrane in hiatal hernias?

A

It becomes lax, failing to tether the esophagus to the diaphragm.

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160
Q

What are the two main types of hiatal hernias?

A

Sliding (type I) and paraesophageal (type II, III, and IV) hernias.

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161
Q

Which type of hiatal hernia is the most common?

A

Sliding hernias (90 percent).

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162
Q

Can hiatal hernias be asymptomatic?

A

Yes, they may be asymptomatic.

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163
Q

What are common clinical features of hiatal hernias?

A

Symptoms of gastroesophageal reflux disease (GERD) such as pain after eating, regurgitation, and dysphagia.

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164
Q

What can a chest x-ray show in large sliding hiatal hernias?

A

A retrocardiac mass with an air-fluid level, indicating gastric cardia protrusion into the thoracic cavity.

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165
Q

What is achalasia?

A

A condition characterized by increased tone of the lower esophageal sphincter (LES), making it difficult to relax.

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166
Q

What causes the increased tone of the LES in achalasia?

A

Absence of inhibitory innervation to the LES, such as that seen in Chagas disease.

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167
Q

Where is Chagas disease common?

A

South America.

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168
Q

What are common symptoms of achalasia?

A

Progressive dysphagia, regurgitation, and aspiration of undigested food.

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169
Q

How might a patient with achalasia present in terms of x-ray findings?

A

Evidence of a hiatal hernia may be present alongside classic symptoms.

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170
Q

What is gastroparesis?

A

A condition characterized by delayed emptying of gastric contents.

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171
Q

What is a common cause of gastroparesis?

A

Many cases are idiopathic, but it can be associated with diabetes.

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172
Q

What are common symptoms of gastroparesis?

A

Early satiety, nausea, abdominal pain, bloating, and weight loss.

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173
Q

How might a patient with gastroparesis present in relation to hiatal hernia?

A

They may have classic hiatal hernia symptoms and evidence of a hiatal hernia on x-ray.

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174
Q

What are mediastinal lymphomas?

A

They are a type of lymphoma that can present as a mediastinal mass.

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175
Q

What is an important consideration in the differential diagnosis of a mediastinal mass?

A

Mediastinal lymphomas are part of the differential diagnosis.

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176
Q

What findings indicate that a patient does not have a mediastinal mass?

A

A chest X-ray showing no mediastinal mass.

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177
Q

What systemic symptoms do patients with lymphoma commonly present with?

A

Fevers, weight loss, and night sweats.

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178
Q

Do symptoms of GERD typically occur in mediastinal lymphoma?

A

No, symptoms of GERD generally do not occur in mediastinal lymphoma.

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179
Q

Zenker’s diverticulum is an outpouching of the mucosa and submucosa between the cricopharyngeus muscle and lower inferior constrictor muscles. This creates an outpouching in the pharynx. Zencker’s diverticulum is characterized by

A

Transient dysphagia, pulmonary aspiration, foul breath, and appearance of a neck mass.

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180
Q

What is congenital diaphragmatic hernia (CDH)?

A

A condition where abdominal contents pass into the thoracic cavity through a hole in the diaphragm.

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181
Q

What characteristic appearance does a baby with CDH often have at birth?

A

A “scaphoid-shaped” (curved inward) abdomen due to abdominal contents in the chest.

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182
Q

Why does herniation of abdominal contents occur more often on the left side in CDH?

A

The liver provides relative protection of the diaphragm on the right side.

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183
Q

What complication can result from intestinal structures herniating into the chest cavity?

A

Pulmonary hypoplasia due to lack of space for normal lung development.

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184
Q

What is believed to cause congenital diaphragmatic hernia?

A

Defective formation of the pleuroperitoneal membranes, which separate the thoracic and peritoneal cavities.

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185
Q

How is CDH often diagnosed in modern medicine?

A

By ultrasound during pregnancy.

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186
Q

What findings on a chest X-ray indicate CDH?

A

Air- or fluid-filled structures in the thorax due to herniation of bowel.

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187
Q

What is the primary treatment for congenital diaphragmatic hernia?

A

Surgery to reposition the abdominal organs and seal the diaphragm.

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188
Q

What factors influence the prognosis of CDH?

A

The degree of organ hypoplasia, especially pulmonary hypoplasia.

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189
Q

What are foregut defects?

A

Congenital abnormalities of the upper GI tract, including various malformations.

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190
Q

Name some congenital abnormalities caused by foregut defects

A

Esophageal atresia and stenosis, pyloric stenosis, atresia of the gallbladder and bile ducts, liver malformations, and pancreatic malformations.

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191
Q

What results from the persistence of the second pharyngeal cleft or pouch?

A

A branchial fistula, which is an abnormal tract on the side of the neck and in the pharynx.

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192
Q

What causes tracheoesophageal fistulas?

A

Incomplete separation of the esophagus and trachea by the tracheoesophageal septum during week 4 of development.

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193
Q

What is esophageal atresia?

A

A congenital condition where the esophagus ends in a blind pouch and does not connect to the stomach.

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194
Q

What is pyloric stenosis?

A

A condition where the pylorus (the opening from the stomach to the duodenum) is narrowed, causing obstruction.

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195
Q

What is a femoral hernia?

A

A herniation of bowel through the femoral ring.

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196
Q

What causes the femoral ring to widen and weaken?

A

Aging, injury, or frequent exposure to high intra-abdominal pressure (e.g., from constipation).

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197
Q

Where is a femoral hernia typically located?

A

Under the inguinal ligament, producing a mass or bulge.

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198
Q

How can a femoral hernia be identified during an examination?

A

By a line drawn between the anterior superior iliac spine and the pubis.

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199
Q

In which population is femoral hernia more common?

A

In woman’s

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200
Q

What is an indirect inguinal hernia?

A

A type of hernia where bowel herniates above the inguinal ligament.

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201
Q
A
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202
Q

In which population do indirect inguinal hernias most commonly occur?

A

Males

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203
Q

Where does the bowel herniate in an indirect inguinal hernia?

A

Laterally in relation to the inferior epigastric vessels and into the scrotum.

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204
Q

What causes indirect inguinal hernias?

A

Patency of the processus vaginalis.

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205
Q

How can indirect inguinal hernias be distinguished from direct inguinal hernias?

A

Indirect hernias occur lateral to the inferior epigastric vessels, while direct hernias occur medial to them.

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206
Q

What is a direct inguinal hernia?

A

A type of hernia that passes through the inguinal triangle above the inguinal ligament.

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207
Q

Where is a direct inguinal hernia located in relation to the inferior epigastric vessels?

A

Medially in relation to the inferior epigastric vessels.

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208
Q

In which population are direct inguinal hernias more common?

A

Older men

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209
Q

What causes direct inguinal hernias?

A

Weakness of the inguinal canal floor.

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210
Q

How can direct inguinal hernias be distinguished from indirect inguinal hernias?

A

Direct hernias occur medial to the inferior epigastric vessels, while indirect hernias occur lateral to them.

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211
Q

Occurs when a portion of the intestines is pushed through the umbilical opening in the abdominal wall. Umbilical hernias may occur from the persistence of the umbilical fibromuscular ring in newborns or as a consequence of increased intra-abdominal pressure due to many different causes in adults (obesity, pregnancy, etc.).

A

An umbilical hernia

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212
Q

The classic imaging finding of a sliding hiatal hernia is ?. This is indicated by the short white arrow above, which points to the GEJ, located above the diaphragm (long white arrow).

A

An hourglass sign (also called “collar sign”).

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213
Q

What are esophageal varices?

A

Dilated veins in the esophagus caused by portal hypertension, leading to gastrointestinal bleeding in patients with cirrhosis.

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214
Q

What complication of cirrhosis leads to the formation of esophageal varices?

A

Portal hypertension.

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215
Q

What is Boerhaave’s syndrome?

A

Effort ruptures of the esophagus due to increased intraesophageal pressure relative to intrathoracic pressure.

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216
Q

What are common causes of Boerhaave’s syndrome?

A

Straining and vomiting.

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217
Q

What are clinical features of Boerhaave’s syndrome?

A

Retrosternal chest pain, dyspnea, and subcutaneous emphysema.

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218
Q

What is achalasia?

A

The failure of the lower esophageal sphincter (LES) to relax due to the absence of ganglion cells in the esophagus.

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219
Q

What are clinical features of achalasia?

A

Dysphagia, regurgitation, food aspiration, and inflammation of the esophageal myenteric plexus.

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220
Q

What is eosinophilic esophagitis (EoE)?

A

An inflammatory condition of the esophagus causing dysphagia, especially in individuals with allergies or asthma.

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221
Q

What are common clinical features of eosinophilic esophagitis?

A

Dysphagia, vomiting, abdominal pain, and food impaction.

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222
Q

How is eosinophilic esophagitis diagnosed?

A

Diagnosis is made via histologic findings, as endoscopic findings are not always present.

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223
Q

What factors are involved in the pathogenesis of eosinophilic esophagitis?

A

Genetic, environmental, and host immune system factors.

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224
Q

What are common symptoms of GERD?

A

Heartburn, hoarseness, sore throat, regurgitation, and cough.

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225
Q

What occurs in a sliding hiatal hernia?

A

The gastroesophageal junction (GEJ) slides to a position above the diaphragm.

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226
Q

What characterizes a paraesophageal hiatal hernia?

A

The gastric fundus herniates upward into the thorax next to the esophagus, while the GEJ may remain in its usual position.

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227
Q

Through what structure does the gastric fundus herniate in a paraesophageal hiatal hernia?

A

Through a defect in the phrenoesophageal membrane.

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228
Q

What is the function of the phrenoesophageal membrane?

A

It is a connective tissue structure that anchors the esophagus to the esophageal hiatus in the diaphragm.

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229
Q

In the sliding or type I hiatal hernia, the gastric cardia protrudes above the diaphragm. In a paraesophogeal hernia,

A

The cardia (the point where the esophagus enters the stomach) remains below the diaphragm

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230
Q

What characterizes a direct inguinal hernia?

A

Protrusion of abdominal contents into Hesselbach’s triangle.

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231
Q

What are the borders of Hesselbach’s triangle?

A

Medially by the rectus abdominis, laterally by the inferior epigastric artery, and inferiorly by the inguinal ligament.

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232
Q

What is the most common type of inguinal hernia?

A

Indirect inguinal hernias, occurring in both men and women.

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233
Q

How does an indirect inguinal hernia occur in males?

A

The processus vaginalis fails to close, allowing a loop of bowel to enter the scrotum via the inguinal canal.

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234
Q

What is the processus vaginalis?

A

An embryonic outpouching of the parietal peritoneum that descends with the testes into the scrotum.

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235
Q

What happens to the processus vaginalis normally after descent of the testes?

A

It closes, preventing any connection to the abdomen.

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236
Q

What forms the tunica vaginalis in males?

A

Some tissue from the processus vaginalis that remains surrounding the testes.

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237
Q

Where do indirect inguinal hernias pass in relation to the inferior epigastric vessels?

A

Laterally to the inferior epigastric vessels and through both the deep and superficial inguinal rings.

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238
Q

What are potential complications of groin hernias?

A

Trapping of herniated intestine, bowel obstruction, and bowel ischemia.

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239
Q

What does tenderness on exam suggest in a patient with a hernia?

A

It may indicate a strangulated hernia, which requires immediate surgery.

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240
Q

How is the pathogenesis of an indirect inguinal hernia similar to that of a hydrocele?

A

Both conditions involve fluid or contents entering the incompletely closed processus vaginalis.

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241
Q

Is a superficial, subcutaneous connective tissue layer of the scrotum. The dartos muscle within the dartos fascia assists with scrotal elevation.

A

Dartos fascia

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242
Q

Is a connective tissue structure in the midline of the abdomen through which umbilical hernias may protrude.

A

Linda alba

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243
Q

What is the external spermatic fascia?

A

The outermost layer of fascia that covers the spermatic cord.

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244
Q

From which muscle is the external spermatic fascia derived?

A

It is derived from the external oblique muscle and its aponeurosis.

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245
Q

What is the internal spermatic fascia?

A

The innermost layer of fascia that covers the spermatic cord.

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246
Q

From which fascia is the internal spermatic fascia derived?

A

It is derived from the transversalis fascia.

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247
Q

What is the significance of the spermatic fascia?

A

It provides protection and support to the spermatic cord structures, including blood vessels and nerves.

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248
Q

What is Hirschsprung’s disease?

A

A condition caused by failure of neural crest cell migration to the intestinal wall, leading to aganglionosis.

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249
Q

What does “aganglionosis” mean?

A

A lack of neurons in the colon wall, specifically in Auerbach’s plexus and Meissner’s plexus.

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250
Q

What plexuses are absent in patients with Hirschsprung’s disease?

A

Both the myenteric (Auerbach’s) plexus and the submucosal (Meissner’s) plexus.

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251
Q

How does the absence of innervation affect intestinal function in Hirschsprung’s disease?

A

It causes a “functional” blockage due to lost intestinal motility.

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252
Q

What can be seen on a barium study in patients with Hirschsprung’s disease?

A

Recto-sigmoid narrowing with proximally distended bowel loops.

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253
Q

How can Hirschsprung’s disease be differentiated from functional constipation?

A

Presence of a tight anal sphincter and an empty rectum.

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254
Q

What is the typical presentation of Hirschsprung’s disease?

A

Chronic constipation.

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255
Q

When is Hirschsprung’s disease usually diagnosed?

A

Most patients are diagnosed in the neonatal period, but milder cases may be diagnosed later in infancy or childhood.

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256
Q

What are the crypts of Lieberkühn?

A

Glandular structures in the mucosal layer of the small intestine that contain goblet cells.

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257
Q

What are goblet cells responsible for?

A

They produce mucus, which helps lubricate and protect the intestinal lining.

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258
Q

What can a biopsy showing crypt abscess indicate?

A

It can be seen in ulcerative colitis but would not explain findings in Hirschsprung’s disease.

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259
Q

What are the components of the mucosa?

A

The epithelium (including the basement membrane), lamina propria, and muscularis mucosae

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260
Q

What are Peyer’s patches?

A

Masses of lymphatic tissue found in the lamina propria and submucosa of the ileum.

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261
Q

What is the primary function of Peyer’s patches?

A

They play a role in the immune response by monitoring intestinal bacteria and preventing the growth of pathogenic bacteria.

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262
Q

What is Hirschsprung’s disease?

A

A congenital disorder where neural crest cells fail to migrate to the intestinal wall, causing a functional blockage due to lack of innervation.
Chronic constipation and failure to pass meconium.

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263
Q

What two disorders should be considered in a case of failure to pass meconium?

A

Hirschsprung’s disease and cystic fibrosis.

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264
Q

What is the gold standard for diagnosing Hirschsprung’s disease?

A

A deep rectal suction biopsy.

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265
Q

What does a biopsy in Hirschsprung’s disease reveal?

A

Lack of ganglion cells (aganglionosis) in the colon wall.

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266
Q

What is the treatment for Hirschsprung’s disease?

A

Surgical resection of the aganglionic portions of the colon.

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267
Q

Are commonly associated with Crohn’s disease, which does not present in neonates.

A

Granulomas and transmural ulcers

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268
Q

What is observed in biopsy specimens from patients with Hirschsprung’s disease?

A

Absence of ganglion cells and hypertrophy of nerve fibers.

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269
Q

Where do the hypertrophied nerve fibers in Hirschsprung’s disease derive from?

A

Autonomic and sensory nerves outside the affected area.

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270
Q

Why do nerve fibers show hypertrophy in Hirschsprung’s disease?

A

As a compensatory response to the absence of ganglion cells, as these nerves attempt to integrate with the aganglionic segment.

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271
Q

Is the classic finding in celiac disease

A

Numerous lymphocytes with villous atrophy

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272
Q

Is characterized by transmural intestinal ganglioneuromas, a rare benign tumor of neural crest cells.

A

Multiple endocrine neoplasia type 2B (MEN 2B)

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273
Q

What is achalasia?

A

A disorder of esophageal motility characterized by an inability to relax the lower esophageal sphincter (LES).

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274
Q

What causes achalasia?

A

Damage to ganglion cells in the myenteric plexus (Auerbach’s plexus).

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275
Q

Where are the ganglion cells that are affected in achalasia located?

A

Between the inner circular and outer longitudinal layers of the muscularis propria of the esophagus.

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276
Q

What is the consequence of the loss of esophageal motility in achalasia?

A

Dysphagia for both solids and liquids due to the requirement of peristalsis for swallowing.

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277
Q

What does the inability to relax the LES lead to in achalasia?

A

Dilatation of the esophageal wall.

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278
Q

What is the classic radiological finding associated with achalasia on a barium swallow study?

A

The “bird beak” sign.

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279
Q

What are G cells?

A

Gastrin-producing cells located in the stomach and duodenum.

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280
Q

In which conditions might gastrin concentrations be elevated?

A

Zollinger-Ellison syndrome and autoimmune gastritis.

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281
Q

What do parietal cells in the stomach produce?

A

Hydrochloric acid (HCl) and intrinsic factor.

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282
Q

What can intrinsic factor deficiency lead to?

A

Pernicious anemia.

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283
Q

What is the underlying issue in achalasia related to the lower esophageal sphincter?

A

An inability of the smooth muscle to relax, but it is not the muscle cells themselves that are damaged.

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284
Q

What are common clinical findings in cirrhotic liver disease?

A

Jaundice, abdominal pain, and hematemesis from bleeding varices.

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285
Q

What structures are contained within the hepatoduodenal ligament?

A

The hepatic artery, the portal vein, and the common bile duct.

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286
Q

Why is lymphadenopathy common in patients with end-stage liver disease?

A

It usually results from lymphatic hyperplasia.

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287
Q

Where is the hepatic bile duct located?

A

Inferior to the liver and superior to the gallbladder.

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288
Q

Is the hepatic bile duct contained within the hepatoduodenal ligament?

A

No, it is not contained within the hepatoduodenal ligament.

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289
Q

Why is the gallbladder less likely to be compressed by lymphadenopathy of the hepatoduodenal ligament?

A

Because it is not contained within the hepatoduodenal ligament.

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290
Q

What is the remnant of the umbilical vein called?

A

The ligamentum teres of the liver.

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291
Q

Where is the ligamentum teres located?

A

At the free end of the falciform ligament, and it is not contained within the hepatoduodenal ligament.

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292
Q

What is Superior Mesenteric Artery (SMA) syndrome?

A

A condition characterized by compression of the third portion of the duodenum between the aorta and the superior mesenteric artery.

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293
Q

What can lead to the development of SMA syndrome?

A

Significant weight loss, which causes loss of mesenteric fat.

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294
Q

What are common clinical manifestations of SMA syndrome?

A

Postprandial epigastric pain, early satiety, and occasionally bowel obstruction.

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295
Q

How does SMA syndrome cause duodenal obstruction?

A

The compression of the duodenum leads to intermittent obstruction.

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296
Q

Hypertrophy of the gastric pylorus causes ?. This is a congenital anomaly that presents in infants with projectile vomiting.

A

Pyloric stenosis

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297
Q

Meissner’s plexus is located in the ? of the intestines. It is involved in the pathogenesis of Hirschsprung’s disease, a disorder of the colon that occurs predominantly in young children.

A

Submucosal layer

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298
Q

What two arteries supply blood to the large colon?

A

The superior mesenteric artery (SMA) and the inferior mesenteric artery (IMA).

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299
Q

Where is the watershed region located in the colon?

A

At the splenic flexure.

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300
Q

Why does the watershed area become vulnerable to ischemia during shock?

A

Because under-perfusion occurs, reducing blood flow through the sparse collateral circulation.

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301
Q

What are the primary clinical features of ischemic colitis?

A

Severe abdominal pain and the passage of blood and mucus from the rectum.

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302
Q

What radiographic findings may be seen in ischemic colitis?

A

Thumb-printing and dilation of the bowel proximal to the area of ischemia.

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303
Q

Is predominantly supplied by the superior mesenteric artery and does not lie within the watershed region. Hypotension does not easily cause ischemia in this segment of the colon.

A

The ascending colon

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304
Q

What arteries supply blood to the rectum?

A

The internal iliac artery and the inferior mesenteric artery.

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305
Q

Why is the rectum infrequently involved in colonic ischemia?

A

Due to its dual blood supply from the internal iliac artery and the inferior mesenteric artery.

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306
Q

What symptoms are associated with upper gastrointestinal bleeding?

A

Hematemesis (vomiting blood) or melena (black, tarry stools), but not bright red blood from the rectum.

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307
Q

What is a classic finding in acute mesenteric ischemia?

A

Pain that is out of proportion to the physical examination.

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308
Q

What might a patient with acute mesenteric ischemia report about their abdominal pain?

A

Severe abdominal pain (e.g., “10/10”) despite only mild tenderness on examination.

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309
Q

What is a common finding in patients with bowel ischemia?

A

Blood in the stool.

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310
Q

What laboratory findings might be present in a patient with acute mesenteric ischemia?

A

Elevated white blood cell count and elevated lactate.

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311
Q

In patients with atrial fibrillation, what is a likely cause of acute mesenteric ischemia?

A

Formation of a clot in the left atrium that embolizes to the bowel.

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312
Q

Which vessel is most commonly involved in acute mesenteric ischemia?

A

The superior mesenteric artery.

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313
Q

What are colonic diverticula?

A

Outpouchings of the bowel wall that form at natural areas of weakness in the muscular layer.

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314
Q

Are diverticula usually symptomatic?

A

No, they are generally asymptomatic unless complications develop.

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315
Q

What complications can arise from diverticula?

A

Inflammation (diverticulitis), perforation, or bleeding.

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316
Q

What is diverticulitis?

A

Inflammation of the diverticula, which can lead to symptoms such as abdominal pain, fever, and changes in bowel habits.

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317
Q

What is diverticulitis?

A

A complication of diverticular disease (diverticulosis) characterized by inflammation of the diverticula. Largely asymptomatic, but may become symptomatic due to inflammation or complications.

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318
Q

What complications can arise from diverticulitis?

A

Abscess, bleeding, obstruction, and perforation.

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319
Q

What are common symptoms of diverticulitis?

A

Constipation and left lower quadrant pain.

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320
Q

What type of granulomas are associated with Crohn’s disease?

A

Noncaseating granulomas.

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321
Q

What is Crohn’s disease?

A

A form of inflammatory bowel disease (IBD) that can affect any part of the gastrointestinal tract.

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322
Q

What is the most common symptom of Crohn’s disease?

A

Recurrent diarrhea (which may or may not be bloody).

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323
Q

Can Crohn’s disease cause symptoms other than diarrhea?

A

Yes, it can also cause abdominal pain, weight loss, and fatigue, among others.

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324
Q

Perforation of the colon is characterized by acute abdominal pain and systemic inflammatory response. Abdominal examination shows

A

Rebound tenderness, guarding, and abdominal distention

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325
Q

What is the Pringle maneuver?

A

A surgical technique involving the placement of a vascular clamp across the hepatoduodenal ligament.

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326
Q

What does the Pringle maneuver accomplish?

A

It interrupts blood flow to the liver through the hepatic artery and portal vein.

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327
Q

If bleeding continues after the Pringle maneuver, what are the likely sources of blood loss?

A

The inferior vena cava or the hepatic vein.

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328
Q

When is the Pringle maneuver typically used?

A

During liver surgery or trauma to assess the source of bleeding

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329
Q

What condition is suggested by a baby’s anal dimple and inability to pass meconium in the first 24 hours?

A

Imperforate anus

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330
Q

What should children born with an imperforate anus be evaluated for?

A

Vertebral and renal abnormalities

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331
Q

What does the VACTERL association stand for?

A

Vertebral anomalies, Anal atresia, Cardiac defects, Tracheoesophageal fistula/Esophageal atresia, Renal and Radial anomalies, and Limb defects.

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332
Q

What are common cardiac abnormalities associated with the VACTERL association?

A

Ventricular septal defect, atrial septal defect, and tetralogy of Fallot.

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333
Q

What are other common findings in the VACTERL association besides anal atresia?

A

Tracheoesophageal fistulas and renal agenesis.

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334
Q

What is holoprosencephaly?

A

A failure of the brain to divide into two hemispheres.

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335
Q

In what genetic condition is holoprosencephaly most commonly seen?

A

Trisomy 13 (Patau’s syndrome), occurring in about 50% of cases

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336
Q

What sequence is typically associated with pulmonary hypoplasia?

A

Potter’s sequence.

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337
Q

What are the key features of Potter’s sequence?

A

Pulmonary hypoplasia, clubbed feet, and cranial abnormalities.

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338
Q

What are the key features of Potter’s sequence?

A

Pulmonary hypoplasia, clubbed feet, and cranial abnormalities.

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339
Q

What does the pectinate line mark?

A

The transition from the rectum to the anus.

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340
Q

What type of epithelium is found above the pectinate line?

A

Columnar epithelium, similar to that of the digestive tract.

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341
Q

Which arteries supply blood to the tissues above the pectinate line?

A

The superior and middle rectal arteries.

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342
Q

How are hemorrhoids occurring above the pectinate line classified?

A

Internal hemorrhoids.

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343
Q

Are internal hemorrhoids usually painful?

A

No, they are generally not painful but are prone to bleeding.

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344
Q

Where does lymph drainage above the pectinate line flow to?

A

The internal iliac lymph nodes.

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345
Q

Which lymph nodes receive drainage from below the pectinate line?

A

The superficial inguinal lymph nodes.

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346
Q

Why is the pectinate line clinically significant in terms of lymphatic drainage?

A

It marks the division between different lymphatic drainage pathways and associated lymph nodes.

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347
Q

What type of innervation do tissues below the pectinate line have?

A

Somatic innervation.

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348
Q

What type of innervation do tissues above the pectinate line have?

A

Visceral innervation.

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349
Q

Are lesions below the pectinate line typically painful?

A

Yes, pain is common in lesions below the pectinate line.

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350
Q

Are hemorrhoids arising below the pectinate line generally painful or prone to bleeding?

A

They are generally painful and less prone to bleeding.

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351
Q

What artery supplies blood to tissues below the pectinate line?

A

The inferior rectal artery.

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352
Q

What artery provides blood supply to tissues above the pectinate line?

A

The superior rectal artery.

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353
Q

What are hemorrhoids?

A

Vascular structures that drain blood into the venous system.

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354
Q

What can cause engorgement and bleeding of hemorrhoids?

A

Any cause of venous hypertension.

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355
Q

How does pregnancy contribute to the development of hemorrhoids?

A

The growing fetus compresses the inferior vena cava, raising venous pressure.

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356
Q

What type of hemorrhoids are commonly associated with painful rectal bleeding during pregnancy?

A

External hemorrhoids.

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357
Q

Why are hemorrhoids a common problem among pregnant women?

A

Due to increased venous pressure from compression of the inferior vena cava.

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358
Q

How can disorders of coagulation affect pregnancy?

A

They may increase the risk of bleeding during pregnancy and delivery.

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359
Q

Which disorders are examples of coagulation disorders?

A

Hemophilia and von Willebrand’s disease.

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360
Q

Do coagulation disorders typically present as isolated hemorrhoidal bleeding during pregnancy?

A

No, they do not commonly present as isolated hemorrhoidal bleeding.

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361
Q

What is a common complication of pregnancy related to hemorrhoids?

A

Painful rectal bleeding, especially from external hemorrhoids.

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362
Q

What are gallstones, and what symptoms do they typically cause?

A

Gallstones can produce right upper quadrant pain, especially after fatty meals.

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363
Q

What structures are found in the portal triad of the liver lobule?

A

Bile duct, portal vein, and hepatic artery.

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364
Q

How does the size of the bile ducts compare to the portal veins and hepatic arteries in the portal triad?

A

Bile ducts are smaller than portal veins and usually larger than hepatic arterial branches.

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365
Q

What is pancreas divisum?

A

A developmental anomaly characterized by two pancreatic ducts (a dorsal and a ventral duct) instead of a single duct.

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366
Q

From which embryonic structure does the pancreas develop?

A

The pancreas derives from the foregut.

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367
Q

Which other structures also develop from the foregut?

A

Esophagus, stomach, liver, gallbladder, and the upper portion of the duodenum.

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368
Q

What percentage of embryos develop pancreas divisum?

A

Approximately 10%.

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369
Q

What causes pancreas divisum?

A

Fusion failure of the dorsal and ventral pancreatic ducts.

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370
Q

Are most individuals with pancreas divisum symptomatic or asymptomatic?

A

Most individuals are asymptomatic, but some may develop pancreatitis.

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371
Q

The hindgut gives rise to the

A

Distal one-third of the transverse colon, the descending colon, and the rectum.

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372
Q

The intermediate mesoderm gives rise to the

A

Kidneys, lower urinary tract, and reproductive system.

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373
Q

The midgut gives rise to the

A

Distal duodenum, jejunum, ileum, ascending colon, and proximal two-thirds of the transverse colon.

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374
Q

Normally disappears before birth but may persist as an anomaly called Meckel’s diverticulum.

A

The yolk sac

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375
Q

What is annular pancreas?

A

A rare congenital anomaly where pancreatic tissue surrounds the duodenum, leading to potential obstruction.

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376
Q

What are common symptoms of annular pancreas in infants?

A

Nonbilious vomiting and poor weight gain.

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377
Q

What is the estimated prevalence of annular pancreas?

A

Approximately 5 to 15 per 100,000 births.

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378
Q

How does the pancreas normally develop?

A

From two outpouchings of the duodenum called the ventral and dorsal buds.

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379
Q

What does the dorsal bud of the pancreas become?

A

The tail and body of the pancreas.

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380
Q

What does the ventral bud of the pancreas become?

A

The head and uncinate process of the pancreas.

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381
Q

What typically happens during normal gut rotation regarding the pancreatic buds?

A

The ventral bud passes behind the duodenum to fuse with the dorsal bud.

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382
Q

What percentage of patients with annular pancreas are asymptomatic?

A

About two-thirds (or approximately 66%).

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383
Q

What complications can arise from annular pancreas?

A

Impaired flow through the duodenum due to constriction by pancreatic tissue.

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384
Q

How does the pancreatic duct connect to the digestive system?

A

The pancreatic duct joins the pancreas to the common bile duct.

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385
Q

What complication can arise from obstruction of the pancreatic duct in patients with annular pancreas?

A

Obstruction can lead to fibrosis and potentially result in pancreatitis.

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386
Q

Does the obstruction of the pancreatic duct describe the embryological cause of annular pancreas?

A

No, obstruction of the pancreatic duct is a complication, not the embryological cause of the condition.

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387
Q

What potential impact does fibrosis have in patients with annular pancreas?

A

Fibrosis can obstruct the pancreatic duct, leading to pancreatitis.

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388
Q

What is Zone 3 of the liver also known as?

A

The centrilobular zone.

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389
Q

What major function occurs in Zone 3 of the liver?

A

Drug metabolism, including the metabolism of cytochrome P-450 drugs.

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390
Q

Which drugs are metabolized in Zone 3 of the liver?

A

Phenytoin, macrolides, rifampin, warfarin, and others.

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391
Q

Why is the oxygen content lower in Zone 3 compared to Zones 1 and 2?

A

Because Zone 3 is farthest from the hepatic artery.

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392
Q

What is the significance of the lower oxygen content in Zone 3?

A

It affects the metabolic processes and susceptibility to injury in this area.

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393
Q

What are the five structures included in the portal triad?

A

The proper hepatic artery, the hepatic portal vein, the bile ductules, lymphatic vessels, and a branch of the vagus nerve.

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394
Q

What is the function of the proper hepatic artery within the portal triad?

A

It supplies oxygenated blood to the liver.

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395
Q

What role does the hepatic portal vein play in the portal triad?

A

It carries nutrient-rich blood from the gastrointestinal tract to the liver.

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396
Q

What is the function of the bile ductules in the portal triad?

A

They collect bile produced by the liver and transport it to larger bile ducts.

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397
Q

What is the role of the vagus nerve branch in the portal triad?

A

It provides autonomic innervation to the liver, influencing various functions.

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398
Q

What is a gastrinoma?

A

A gastrin-secreting tumor usually found in the pancreas or duodenum.

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399
Q

What does gastrin do?

A

It stimulates the release of gastric acid from parietal cells in the stomach.

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400
Q

What are common symptoms of gastrinoma?

A

Abdominal pain from peptic ulcers, diarrhea (either watery or fatty), and high-volume gastric secretions.

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401
Q

How does gastrin affect pancreatic enzymes?

A

Gastrin creates a low-pH environment that can inactivate pancreatic enzymes.

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402
Q

In which patients should gastrinoma be suspected?

A

In patients with multiple peptic ulcers, especially those refractory to standard therapy.

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403
Q

What is the first step in evaluating a suspected gastrinoma?

A

Measurement of serum gastrin levels.

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404
Q

What are the normal serum gastrin levels?

A

0 to 100 pg/mL.

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405
Q

What serum gastrin level indicates a gastrinoma?

A

Levels greater than 1,000 pg/mL.

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406
Q

What is the primary function of cholecystokinin (CCK)?

A

CCK stimulates contraction of the gallbladder and promotes the release of digestive enzymes from the pancreas.

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407
Q

Would elevated cholecystokinin explain symptoms of gastrinoma?

A

No, elevated CCK levels would not explain the clinical presentation of a gastrinoma.

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408
Q

What role does secretin play in digestion?

A

Secretin increases bicarbonate release from the pancreas, neutralizing gastric acid in the duodenum.

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409
Q

How is secretin used in the diagnosis of gastrinomas?

A

In gastrinomas, secretin injection causes a paradoxical increase in gastrin release, aiding in diagnosis.

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410
Q

What is the function of somatostatin in the gastrointestinal system?

A

Somatostatin inhibits the release of many gastrointestinal hormones and reduces gastric acid secretion.

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411
Q

What symptoms are associated with VIPomas?

A

VIPomas cause watery diarrhea, hypokalemia, and achlorhydria.

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412
Q

What is the effect of vasoactive intestinal peptide (VIP)?

A

VIP stimulates pancreatic bicarbonate and fluid secretion, among other functions.

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413
Q

What condition can lead to elevated levels of gastrin?

A

Gastrinomas, which are gastrin-secreting tumors.

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414
Q

What is a somatostatinoma?

A

A rare pancreatic tumor that secretes excess somatostatin, inhibiting the secretion of other gastrointestinal hormones.

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415
Q

Which cells produce somatostatin?

A

Delta cells (D cells) in the pancreas and intestines.

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416
Q

What are the effects of excess somatostatin in the body?

A

It inhibits the release of secretin, insulin, cholecystokinin, and gastrin, leading to achlorhydria, gallstones, steatorrhea, and hyperglycemia.

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417
Q

What is achlorhydria?

A

A condition characterized by a lack of hydrochloric acid in the gastric secretions, resulting in a high gastric pH.

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418
Q

What laboratory findings may be associated with cholestasis in somatostatinoma?

A

Elevated alkaline phosphatase and bilirubin levels.

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419
Q

What symptoms can arise from a somatostatinoma?

A

Symptoms include steatorrhea (greasy stools), hyperglycemia, abdominal pain, and weight loss.

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420
Q

How is somatostatinoma diagnosed?

A

Diagnosis is made by identifying elevated fasting plasma somatostatin levels.

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421
Q

What genetic condition is associated with somatostatinomas?

A

Multiple endocrine neoplasia type 1 (MEN 1), which is characterized by pituitary adenoma, parathyroid adenoma, and pancreatic tumors.

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422
Q

What are the “3 P’s” of MEN 1?

A

Pituitary adenoma, parathyroid adenoma, and pancreatic tumors.

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423
Q

Why can recognizing somatostatinoma be challenging?

A

Its key features, such as steatorrhea and hyperglycemia, overlap with conditions like chronic pancreatitis, requiring careful clinical evaluation.

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424
Q

What condition do gastrinomas cause?

A

Zollinger-Ellison syndrome, characterized by excessive gastrin production leading to peptic ulcers.

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425
Q

What are the typical symptoms of a gastrinoma?

A

Abdominal pain and watery diarrhea, often accompanied by multiple or refractory peptic ulcers.

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426
Q

Do gastrinomas cause hyperglycemia?

A

No, hyperglycemia does not occur with gastrinomas.

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427
Q

What is a glucagonoma?

A

A tumor of the pancreatic alpha cells that leads to hyperglycemia, necrolytic migratory erythema, and weight loss.

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428
Q

What symptoms are associated with glucagonomas?

A

Hyperglycemia/diabetes, necrolytic migratory erythema, and weight loss. Steatorrhea does not occur.

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429
Q

What do insulinomas produce?

A

Excess insulin, leading to hypoglycemia that is relieved by glucose administration.

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430
Q

What is a VIPoma?

A

A tumor that secretes vasoactive intestinal peptide (VIP), causing WDHA syndrome (watery diarrhea, hypokalemia, achlorhydria)

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431
Q

What are the symptoms of WDHA syndrome caused by VIPomas?

A

Watery diarrhea, hypokalemia, and achlorhydria; the diarrhea is not steatorrhea.

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432
Q

Does hyperglycemia occur with VIPomas?

A

No, hyperglycemia does not occur with VIPomas.

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433
Q

What is Zollinger-Ellison syndrome (ZES)?

A

A disorder characterized by gastrin-producing tumors that lead to increased gastric acid production, resulting in ulcers.

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434
Q

What causes the abdominal pain in ZES?

A

Abdominal pain is caused by peptic ulcers due to excessive gastric acid.

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435
Q

What types of diarrhea are associated with ZES?

A

Diarrhea may be watery (from high-volume gastric secretions) or fatty (from steatorrhea due to inactivated pancreatic enzymes).

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436
Q

Where are gastrin-secreting tumors typically located in ZES?

A

Tumors may be found in the duodenum or pancreas.

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437
Q

How is Zollinger-Ellison syndrome treated?

A

It is treated with proton pump inhibitors (PPIs) like omeprazole, which decrease gastric acid secretion.

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438
Q

What is the mechanism of action of proton pump inhibitors?

A

PPIs inhibit the H+/K+ ATPase on the luminal surface of parietal cells, reducing gastric acid secretion.

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439
Q

Acinar cells in the pancreas produce enzymes that enter the duodenum to assist in the digestion of food.

A

Ductal cells of the pancreas line the pancreatic ducts. They produce bicarbonate-rich pancreatic juice in response to secretin.

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440
Q

? of the duodenum and jejunum produce cholecystokinin. This hormone increases pancreatic secretions and causes gallbladder contraction.

A

I cells

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441
Q

Are found in the duodenum. They produce the hormone secretin, which increases pancreatic bicarbonate secretion and decreases gastric acid secretion.

A

S cells

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442
Q

What is pernicious anemia?

A

An autoimmune disorder caused by the destruction of gastric parietal cells, leading to vitamin B12 deficiency.

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443
Q

What do parietal cells produce that is essential for vitamin B12 absorption?

A

Intrinsic factor.

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444
Q

What are the typical laboratory findings in B12 deficiency due to pernicious anemia?

A

Macrocytic anemia (low hemoglobin and hematocrit, high MCV).

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445
Q

What are common symptoms of pernicious anemia?

A

Fatigue, neurologic dysfunction, and difficulty walking due to loss of proprioception.

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446
Q

How does pernicious anemia affect gastric acid production?

A

Parietal cell atrophy leads to decreased gastric acid production.

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447
Q

What happens to serum gastrin levels in pernicious anemia?

A

Serum gastrin levels rise (hypergastrinemia) due to decreased acid production.

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448
Q

What histological finding might be seen on gastric biopsy in pernicious anemia?

A

Hyperplasia of G cells

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449
Q

What is a VIPoma?

A

A rare tumor of the non-beta islet cells of the pancreas that produces vasoactive intestinal peptide (VIP).

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450
Q

What are the primary symptoms of VIPoma?

A

Profuse watery diarrhea (10 or more times per day) resembling cholera, non-anion gap acidosis, and hypokalemia.

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451
Q

How does VIP contribute to diarrhea in VIPoma patients?

A

VIP stimulates pancreatic bicarbonate secretion, leading to watery diarrhea

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452
Q

What electrolyte imbalances are commonly seen in VIPoma?

A

Hypokalemia due to loss of potassium in the stool and acidosis due to loss of bicarbonate.

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453
Q

What clinical signs might indicate volume depletion in a VIPoma patient?

A

Tachycardia and dry mucous membranes.

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454
Q

What type of acidosis is typically associated with VIPoma?

A

Non-anion gap metabolic acidosis.

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455
Q

Typically presents with weight loss, hyperglycemia, and necrolytic migratory erythema, a papular rash of the face, perineum, and extremities.

A

Glucagonoma

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456
Q

Common clinical features of an ? include hypoglycemia, leading to confusion, altered mental status, palpitations, sweating, and tremulousness. About one-fifth of patients will experience weight gain.

A

Insulinoma

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457
Q

What LFT patterns are typically seen in acute hepatitis C infection?

A

Elevated AST and ALT levels, with AST typically being less than or equal to ALT, and Alk Phos levels often normal.

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458
Q

What are the common liver function tests (LFTs) mentioned?

A

AST (aspartate aminotransferase), ALT (alanine aminotransferase), Alk Phos (alkaline phosphatase).

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459
Q

In chronic hepatitis C, what are the expected LFT findings?

A

Mild to moderate elevations in AST and ALT, with Alk Phos usually normal.

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460
Q

What is a common mode of transmission for hepatitis C virus (HCV)

A

Exposure often occurs through dirty needles among IV drug users and at tattoo parlors.

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461
Q

What percentage of initial hepatitis C infections progress to chronic liver disease?

A

Greater than 90%.

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462
Q

What are the potential outcomes of chronic hepatitis C infection?

A

Scarring of the liver (fibrosis) and cirrhosis.

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463
Q

In chronic HCV, how do the levels of AST and ALT compare to alkaline phosphatase?

A

AST and ALT are elevated relative to alkaline phosphatase.

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464
Q

In all forms of viral hepatitis, which enzyme is typically elevated more, AST or ALT?

A

ALT is usually elevated to a greater degree than AST.

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465
Q

How does the AST
ratio differ in alcoholic hepatitis compared to viral hepatitis?

A

In alcoholic hepatitis, AST is usually greater than ALT (AST ratio > 1.5), whereas in viral hepatitis, ALT is typically greater than AST.

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466
Q

What are the expected serum levels of AST and ALT in chronic hepatitis C?

A

Usually less than 500 U/L.

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467
Q

What are alkaline phosphatase levels typically like in chronic hepatitis C?

A

Alkaline phosphatase levels are often within normal limits.

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468
Q

What is intrahepatic cholestasis of pregnancy (ICP) also known as?

A

Pruritus gravidarum.

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469
Q

During which trimester does ICP typically occur?

A

In the second or third trimester of pregnancy.

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470
Q

What causes ICP?

A

High levels of estrogen and progesterone during pregnancy, which decrease bile flow in the liver.

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471
Q

What is the hallmark symptom of ICP?

A

Pruritus (itching) of the skin.

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472
Q

What leads to the pruritus experienced in ICP?

A

Elevated bile acids in the bloodstream.

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473
Q

Can jaundice occur in cases of ICP?

A

Yes, jaundice may rarely develop in cases of severe cholestasis.

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474
Q

Is ICP a permanent or reversible condition?

A

It is a reversible form of cholestasis.

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475
Q

What is the effect of ICP on bile flow?

A

It leads to a lack of bile flow (cholestasis) in the liver.

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476
Q

In a patient with itching in absence of a rash, think of ?. This is seen in pruritus gravidarum as well as other biliary disorders, such as primary biliary cholangitis.

A

Cholestasis

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477
Q

What does the absence of urine urobilinogen suggest?

A

It indicates that bile (including bilirubin) is not reaching the intestines due to hepatic or biliary obstruction.

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478
Q

Conjugated hyperbilirubinemia: How elevated are the liver enzymes (AST and ALT) in this case?

A

They are twice the upper limit of normal.

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479
Q

Conjugated hyperbilirubinemia: How does alkaline phosphatase compare to AST and ALT in this patient?

A

Alkaline phosphatase is elevated to a much greater degree than AST and ALT.

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480
Q

What is the term for the pattern of liver test abnormalities characterized by greater alkaline phosphatase elevation?

A

Cholestatic pattern.

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481
Q

In which conditions is the cholestatic pattern typically seen?

A

It is seen in cases of biliary obstruction.

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482
Q

What are the typical liver enzyme levels (AST, ALT, alkaline phosphatase) in a patient with cholestatic liver disease?

A

AST and ALT are moderately elevated, while alkaline phosphatase is significantly elevated.

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483
Q

What type of bilirubin is released in extravascular hemolysis?

A

Unconjugated bilirubin.

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484
Q

What are the typical AST and ALT levels in isolated hemolysis?

A

They are normal.

485
Q

What is the primary mechanism of bilirubin release in extravascular hemolysis?

A

It occurs when red blood cells are broken down outside of the blood vessels, typically in the spleen and liver.

486
Q

How does the absence of unconjugated hyperbilirubinemia help differentiate between hemolytic anemia and other conditions?

A

It indicates that the hemolysis is not the primary issue, as hemolysis typically leads to increased unconjugated bilirubin.

487
Q

What types of inherited liver diseases are associated with unconjugated bilirubinemia?

A

Crigler-Najjar syndrome and Gilbert’s syndrome.

488
Q

What are the liver function test results (AST and ALT) in patients with Crigler-Najjar and Gilbert’s syndromes?

A

Liver function tests (AST and ALT) are normal.

489
Q

What are common disorders that lead to marked elevations of AST and ALT (greater than 1,000)?

A

Acute hepatitis B, acute hepatitis A, acetaminophen toxicity, and ischemic liver disease (shock liver).

490
Q

What is primary biliary cholangitis (PBC)?

A

An autoimmune condition causing destruction of intrahepatic bile ducts, leading to intrahepatic cholestasis.

491
Q

In which demographic is PBC most commonly seen?

A

Women in their 40s or 50s.

492
Q

What are common symptoms of PBC?

A

Fatigue and pruritus (itching).

493
Q

What does serum liver testing typically show in PBC?

A

Marked elevation of alkaline phosphatase (2 to 4 times the upper limit of normal) with normal or mildly elevated AST and ALT.

494
Q

What other autoimmune diseases are commonly associated with PBC?

A

Sjögren’s syndrome.

495
Q

What percentage of PBC patients may experience Raynaud’s phenomenon?

A

About 5% to 15%.

496
Q

What causes bile salt deposition in the skin?

A

Cholestasis.

497
Q

What are the major bile acids mentioned in relation to PBC?

A

Chenodeoxycholic acid and cholic acid.

498
Q

What happens to serum alkaline phosphatase levels in cholestasis?

A

They rise in the setting of impaired bile flow.

499
Q

In primary biliary cholangitis (PBC), how does alkaline phosphatase behave?

A

Alkaline phosphatase levels rise significantly.

500
Q

Histamine is produced by

A

Mast cells, basophils, neutrophils, and platelets.

501
Q

The end product of heme catabolism, gives the brown color to human feces.

A

Stercobilin

502
Q

Where does most lipid reabsorption occur in the gastrointestinal tract?

A

In the jejunum.

503
Q

What percentage of bile acids are reabsorbed in the terminal ileum?

A

95%.

504
Q

What is bile primarily composed of?

A

Cholesterol and bile acids.

505
Q

What can lead to gallstone formation?

A

Disruption in bile composition, including decreased availability of bile acids.

506
Q

How can surgical resection or Crohn’s disease affect gallstone formation?

A

They interfere with the absorption of bile acids in the terminal ileum, leading to gallstones.

507
Q

What happens to bile when there is a loss of bile salts?

A

The liver has fewer bile salts to add to new bile, resulting in bile that becomes overloaded with cholesterol.

508
Q

What type of gallstones can form as a result of bile overload with cholesterol?

A

Cholesterol gallstones.

509
Q

Folate is absorbed in the

A

Jejunum

510
Q

May cause microcytic anemia. However, iron is absorbed in the duodenum.

A

Iron deficiency

511
Q

Is absorbed in the duodenum and jejunum.

A

Vitamin B2 (riboflavin)

512
Q

Of note, vitamin B12 absorption occurs in the ileum and will be impaired following ileal resection.

A

Ileal resection.

513
Q

What digestive issue may develop after ileal resection?

A

Diarrhea due to fat malabsorption and steatorrhea.

514
Q

How does diarrhea from ileal resection affect potassium levels?

A

It can cause hypokalemia, as potassium is lost in the stool.

515
Q

What are the physiological consequences of ileal failure?

A

Loss of bile salts leading to gallstones, fat malabsorption, loss of vitamin B12 absorption, and decreased fluid absorption.

516
Q

What vitamin absorption is affected by ileal resection?

A

Vitamin B12 absorption.

517
Q

What happens to fluid absorption after ileal resection?

A

There is decreased fluid absorption.

518
Q

It is high yield to know the physiologic consequences of ileal failure that occur after surgery or in Crohn’s disease. These include

A

Loss of bile salts leading to gallstones and fat malabsorption, loss of vitamin B12 absorption, and decreased fluid absorption

519
Q

How can elevated serum bilirubin (hyperbilirubinemia) be categorized?

A

Unconjugated (>85% of total), conjugated (>50% of total), or mixed (20% to 50% conjugated).

520
Q

What is the normal distribution of serum bilirubin?

A

About 75% unconjugated and about 25% conjugated.

521
Q

What typically causes mixed bilirubin elevations?

A

Primary liver diseases (e.g., hepatitis).

522
Q

What are the main causes of unconjugated hyperbilirubinemia?

A

Hemolysis, drugs impairing the conjugation process, and inherited disorders (e.g., Gilbert’s syndrome, Crigler-Najjar syndrome).

523
Q

What indicates that this man has unconjugated hyperbilirubinemia?

A

No evidence of hemolysis and no medications, suggesting an inherited disorder.

524
Q

What enzyme is involved in conjugating unconjugated bilirubin?

A

Glucuronyl transferase.

525
Q

What is the effect of Gilbert’s syndrome on bilirubin levels?

A

It leads to unconjugated hyperbilirubinemia due to decreased glucuronyl transferase activity (about 30% of normal).

526
Q

Under what conditions might jaundice develop in a patient with Gilbert’s syndrome?

A

Stressors like fasting, febrile illness, heavy physical exertion, or menses.

527
Q

How is Gilbert’s syndrome diagnosed?

A

Based on mild unconjugated hyperbilirubinemia in the absence of liver disease or hemolysis.

528
Q

Is treatment necessary for Gilbert’s syndrome?

A

Usually not necessary.

529
Q

What occurs in Crigler-Najjar syndrome regarding glucuronyl transferase activity?

A

There is a complete absence of glucuronyl transferase activity.

530
Q

What is the consequence of the absence of glucuronyl transferase in Crigler-Najjar syndrome?

A

A complete inability to conjugate bilirubin, leading to markedly elevated unconjugated bilirubin.

531
Q

In any case of unconjugated hyperbilirubinemia, what should be included in the differential diagnosis?

A

Hemolysis.

532
Q

What findings suggest the absence of hemolysis in this patient?

A

A normal peripheral blood smear and normal markers of hemolysis (LDH, haptoglobin).

533
Q

What describes the pathophysiology of Dubin-Johnson syndrome?

A

A defect in the excretion of bilirubin, causing elevated conjugated bilirubin.

534
Q

What is the pathophysiology of Rotor’s syndrome?

A

Defective storage of bilirubin, characterized by conjugated hyperbilirubinemia.

535
Q

What is Crigler-Najjar syndrome?

A

A rare autosomal recessive condition caused by the absence of glucuronyl transferase activity in the liver. Lack of conjugation of bilirubin and high levels of unconjugated bilirubin.

536
Q

When does Crigler-Najjar syndrome typically appear?

A

In the first few days of life.

537
Q

What serious condition can result from elevated bilirubin in Crigler-Najjar syndrome?

A

Kernicterus, a form of brain damage associated with elevated bilirubin.

538
Q

What are the typical liver function test results in Crigler-Najjar syndrome?

A

Usually normal.

539
Q

What treatments are used for Crigler-Najjar syndrome?

A

Exchange transfusion and phototherapy while awaiting liver transplantation.

540
Q

How does newborn jaundice differ from adult jaundice?

A

Newborn jaundice has a unique differential diagnosis, with most cases being benign “physiologic” unconjugated hyperbilirubinemia.

541
Q

When does physiologic jaundice typically develop in newborns?

A

1 to 2 days after birth.

542
Q

What indicates that jaundice in a newborn is usually pathological?

A

Jaundice occurring within the first 24 hours of life.

543
Q

What serum bilirubin level in a newborn is always considered pathologic?

A

Greater than 17 mg/dL.

544
Q

Aside from Crigler-Najjar syndrome, what are other causes of early jaundice in newborns?

A

Congenital infections (syphilis, cytomegalovirus, rubella, toxoplasmosis), sepsis, and other causes.

545
Q

What leads to physiologic jaundice in full-term babies at birth?

A

Increased bilirubin production and decreased ability to excrete bilirubin.

546
Q

When do bilirubin levels typically peak in newborns with physiologic jaundice?

A

About 4 days after birth.

547
Q

What is the usual peak bilirubin level in physiologic jaundice?

A

About 5 to 6 mg/dL.

548
Q

How does physiologic jaundice usually resolve?

A

Most cases resolve without intervention, but some may require phototherapy.

549
Q

How can breast-fed newborns experience an exaggerated form of physiologic jaundice?

A

Inadequate food and water intake can delay meconium passage, reducing bilirubin excretion.

550
Q

What is the effect of decreased oral intake in breast-fed newborns on bilirubin levels?

A

It may lead to mild dehydration, concentrating serum bilirubin.

551
Q

What condition can arise from Rh incompatibility between an Rh-negative mother and Rh-positive fetus?

A

Hemolytic disease of the newborn (HDN), which can manifest as jaundice.

552
Q

What test would be positive in cases of Rh incompatibility, indicating hemolysis?

A

A positive Coombs test.

553
Q

How can Rh-negative mothers avoid hemolytic disease of the newborn?

A

By receiving Rhesus antibodies during pregnancy.

554
Q

Why can the normal levels of haptoglobin and the fact that this is the first pregnancy exclude the diagnosis of Rh incompatibility?

A

These findings suggest there is no hemolysis occurring.

555
Q

What is Dubin-Johnson syndrome?

A

An autosomal recessive condition characterized by mild jaundice and elevated bilirubin due to impaired transfer of conjugated bilirubin into bile ducts.

556
Q

When can Dubin-Johnson syndrome present?

A

It can present shortly after birth or after an inciting incident, such as the use of oral contraceptives or during pregnancy.

557
Q

How do sex steroids in oral contraceptives affect patients with Dubin-Johnson syndrome?

A

They can reduce hepatic excretory function, transforming mild hyperbilirubinemia into jaundice in susceptible patients.

558
Q

What laboratory results are typical in Dubin-Johnson syndrome?

A

An increase in conjugated bilirubin without elevation of liver enzymes like ALT and AST.

559
Q

What physical exam finding may be present in Dubin-Johnson syndrome?

A

Hepatomegaly.

560
Q

What macroscopic liver change is associated with Dubin-Johnson syndrome?

A

A black discoloration of the liver from the accumulation of bilirubin.

561
Q

What is the classic laboratory profile of alcoholic hepatitis?

A

An AST to ALT ratio usually >2.

562
Q

In alcoholic hepatitis, what is the typical AST level?

A

AST is usually about 500 U/L and almost never greater than 1000 U/L.

563
Q

What other liver enzyme may be elevated in alcoholic hepatitis?

A

Gamma-glutamyl transpeptidase (GGT) concentrations may be elevated up to 8 to 10 times normal.

564
Q

What symptoms might patients with alcoholic hepatitis present with?

A

Patients are often asymptomatic but may present with jaundice and hepatomegaly.

565
Q

In which population does alcoholic hepatitis typically occur?

A

In chronic alcohol users after heavy alcohol consumption.

566
Q

What are the potential consequences of acetaminophen overdose?

A

Liver tenderness and jaundice.

567
Q

What is a hallmark laboratory finding in acetaminophen toxicity?

A

Markedly elevated levels of plasma aminotransferases (AST and ALT usually both > 1,000 IU/L)

568
Q

What severe complication can arise from acetaminophen toxicity?

A

Fulminant liver failure and a rising prothrombin time (PT).

569
Q

What are other classic causes of marked elevation of AST and ALT?

A

Ischemic/shock liver and acute hepatitis A or B.

570
Q

What is ascending cholangitis?

A

An infection of the biliary tree occurring in the setting of biliary obstruction.

571
Q

What laboratory finding is typical in ascending cholangitis?

A

Elevated alkaline phosphatase concentrations.

572
Q

What is non-alcoholic steatohepatitis (NASH)?

A

Fat accumulation in the liver not caused by alcohol consumption, often associated with obesity.

573
Q

How are AST and ALT levels typically affected in NASH?

A

Elevated 2 to 5 times the upper limit of normal, with an AST to ALT ratio usually less than 1.

574
Q

What are the typical AST and ALT levels in acute hepatitis B?

A

Marked elevations of 1,000 to 2,000 IU/L.

575
Q

Often present with isolated hyperbilirubinemia in the absence of other liver test abnormalities.

A

Inborn errors of bilirubin metabolism

576
Q

What are the key differential diagnoses for conjugated hyperbilirubinemia?

A

Biliary obstruction, liver disease, or an inherited disorder of bilirubin metabolism.

577
Q

What findings would exclude biliary obstruction or liver disease in this case?

A

Normal liver enzymes and alkaline phosphatase.

578
Q

Family history is significant for a “liver problem” disease in the baby’s grandmother. Given the family history, which two syndromes are most likely in this baby?

A

Dubin-Johnson syndrome or Rotor’s syndrome.

579
Q

What causes Dubin-Johnson syndrome?

A

Defective liver excretion of conjugated bilirubin.

580
Q

What is the mechanism of Rotor’s syndrome?

A

Defective hepatic storage of conjugated bilirubin leads to leakage of bilirubin into the plasma, causing hyperbilirubinemia.

581
Q

What characterizes Arias’s syndrome (Crigler-Najjar syndrome type 2)?

A

An autosomal recessive disorder with unconjugated hyperbilirubinemia, jaundice, and serum bilirubin ranging from 6 to 20 mg/dL.

582
Q

What is the UDP-glucuronosyltransferase activity in children with Arias’s syndrome?

A

Less than 10% of normal.

583
Q

What characterizes Crigler-Najjar syndrome type I?

A

An autosomal recessive disorder with severe unconjugated hyperbilirubinemia and serum bilirubin ranging from 18 to 44 mg/dL.

584
Q

What is the UDP-glucuronosyltransferase activity in children with Crigler-Najjar syndrome type I?

A

Absence of UDP-glucuronosyltransferase activity.

585
Q

What is primary biliary cholangitis?

A

A chronic biliary disorder characterized by selective destruction of biliary epithelial cells of small and medium-sized hepatic ducts.

586
Q

Who is primarily affected by primary biliary cholangitis?

A

Mainly women between 30 and 65 years.

587
Q

What is kernicterus?

A

A form of permanent brain damage from exposure to high levels of bilirubin.

588
Q

What are some symptoms of kernicterus?

A

Abnormal movements, sensorineural hearing loss, and gaze abnormalities.

589
Q

What is a characteristic feature of kernicterus related to brain structures?

A

Yellow staining of central nervous system structures due to hyperbilirubinemia.

590
Q

Which specific areas of the brain are affected by kernicterus?

A

Basal ganglia, hippocampus, lateral thalamic nucleus, geniculate bodies of the thalamus, and some brainstem nuclei.

591
Q

Why are the basal ganglia significant in kernicterus?

A

They are involved in motor coordination, which explains the involuntary movements observed in affected children.

592
Q

What are the common symptoms of acute pancreatitis?

A

Severe upper abdominal pain, nausea, and vomiting.

593
Q

When do serum levels of pancreatic enzymes (amylase and lipase) typically elevate after the onset of acute pancreatitis symptoms?

A

Within 4 to 8 hours.

594
Q

What is the function of pancreatic amylase?

A

To cleave starch into smaller polysaccharides at the internal 1 to 4 alpha linkage during digestion.

595
Q

What are the main sources of amylase in humans?

A

The pancreas and salivary glands, with small quantities found in other tissues.

596
Q

Is an enzyme synthesized in the pancreas and secreted into the small intestine. This enzyme hydrolyzes (adds water to) proteins, leading to protein breakdown.

A

Carboxypeptidase

597
Q

The main function of pancreatic lipase is to

A

Hydrolyze triglycerides into glycerol and free fatty acids.

598
Q

Is made in the stomach and breaks down proteins into smaller peptides. Is most efficient in cleaving peptide bonds between hydrophobic and aromatic amino acids such as phenylalanine, tryptophan, and tyrosine.

A

Pepsin i

599
Q

Catalyzes the hydrolysis of peptide bonds in the duodenum, breaking down proteins into smaller peptides. Trypsin cleaves peptide chains mainly at the carboxyl side of the amino acids lysine and arginine.

A

Trypsin

600
Q

What is the hallmark symptom of acute pancreatitis?

A

Upper abdominal pain, often radiating to the back, with associated nausea and vomiting.

601
Q

What is trypsin and how is it activated?

A

Trypsin is an enzyme derived from the inactive precursor trypsinogen, activated by enteropeptidase (enterokinase) in the duodenum.

602
Q

In acute pancreatitis, where does trypsin activation occur?

A

n the pancreas itself, leading to auto-digestion of pancreatic tissue.

603
Q

What is believed to be the initiating event of acute pancreatitis?

A

The activation of trypsin within the pancreas.

604
Q

What happens once trypsin is activated in acute pancreatitis?

A

It can activate other pancreatic enzymes, leading to a cascade of enzyme activity and causing acute pancreatitis.

605
Q

What is the function of amylase?

A

Amylase breaks down long-chain carbohydrates.

606
Q

Why is amylase significant in the context of pancreatitis?

A

It is an important marker for pancreatitis, indicating pancreatic inflammation.

607
Q

What are transaminase enzymes?

A

Enzymes, such as aspartate transaminase (AST), that play a role in amino acid metabolism.

608
Q

What is the function of elastase?

A

Elastase is an enzyme that degrades elastic fibers.

609
Q

Where is pancreatic elastase produced?

A

In the acinar cells of the pancreas.

610
Q

How is pancreatic elastase activated?

A

It is initially produced as an inactive zymogen and later activated in the duodenum by trypsin.

611
Q

What gastric pH level stimulates secretin release?

A

A gastric pH below 4.5.

612
Q

Where is secretin released from?

A

Duodenal S cells into the bloodstream.

613
Q

What is the major function of secretin?

A

It is the major stimulus for pancreatic HCO3- (bicarbonate) secretion.

614
Q

When do plasma secretin levels rise?

A

After a meal.

615
Q

How do plasma secretin levels correlate with bicarbonate secretion?

A

Plasma secretin levels rise and correlate with increased HCO3- secretion.

616
Q

Inhibits the release of other gastrointestinal hormones (gastrin, secretin). It is not a major stimulus for pancreatic bicarbonate secretion.

A

Somatostatin

617
Q

Is the major stimulus for the release of pancreatic enzymes. Also stimulates the gallbladder. Alone has a weak effect on pancreatic fluid and bicarbonate secretion. It can potentiate (increase) the effects of secretin.

A

Cholecystokinin (CCK)

618
Q

Can stimulate pancreatic bicarbonate release but has only a small effect, much smaller than secretin.

A

The vagus nerve

619
Q

What do lipases catalyze?

A

The breakdown of lipids.

620
Q

What is the role of pancreatic lipases?

A

They convert triglycerides into glycerol and fatty acids.

621
Q

Increases glycogenolysis and relaxes the smooth muscle of the stomach and gallbladder.

A

VIP

622
Q

Zollinger-Ellison syndrome due to a gastrin-producing tumor (gastrinoma). These tumors occur in the duodenum or pancreas, and secrete gastrin. Gastrin is a hormone normally secreted by G cells that stimulates secretion of gastric acid from parietal cells. Excess gastric acid leads to ulcers. The main clinical features of Zollinger-Ellison disease are

A

peptic ulcers, diarrhea, weight loss, and abdominal pain. The majority (80%) of gastrinomas occur sporadically. About 20% are linked with multiple endocrine neoplasia type 1 (MEN 1) syndrome.

623
Q

What are some indications for proton pump inhibitors (PPIs) like omeprazole?

A

Treatment of peptic ulcer disease, gastroesophageal reflux disease (GERD), and Zollinger-Ellison syndrome.

624
Q

How do PPIs block gastric acid secretion?

A

By inhibiting the hydrogen-potassium ATPase pump on the luminal surface of the parietal cell membrane.

625
Q

What happens to gastrin levels when PPIs are used?

A

Gastrin levels increase as a compensatory response to decreased stomach acid production.

626
Q

What role does carbonic anhydrase play in gastric acid secretion?

A

It generates gastric acid in parietal cells.

627
Q

How does PPI therapy affect carbonic anhydrase activity?

A

The activity of carbonic anhydrase decreases in patients taking PPIs who cannot secrete acid normally.

628
Q

What effect does histamine binding to H2 receptors have on cAMP levels?

A

It increases intracellular cyclic adenosine monophosphate (cAMP) levels.

628
Q

Where do histamine molecules bind in the stomach?

A

To H2 receptors located on acid-secreting gastric parietal cells.

629
Q

How does cyclic AMP affect gastric acid secretion?

A

It activates the hydrogen-potassium pump, leading to the release of hydrogen ions into the stomach.

630
Q

What is the mechanism of action of ranitidine?

A

Ranitidine is an H2 receptor antagonist that competitively inhibits H2 receptors, reducing acid secretion.

631
Q

What happens to intracellular cAMP levels when ranitidine blocks histamine activity?

A

There is a fall in intracellular cAMP levels.

632
Q

Is a membrane-associated enzyme that cleaves phospholipids. It is a second messenger for several G-protein associated receptors including those for acetylcholine and gastrin.

A

Phospholipase C (PLC)

633
Q

Is a lipid second messenger that is converted to inositol triphosphate (IP3) by PLC. This second messenger system is associated with receptors for acetylcholine and gastrin.

A

Phosphatidylinositol 4,5-bisphosphate (PIP2)

634
Q

The main function of ? is to mobilize Ca2+ from storage organelles. Calcium then regulates other processes. This is part of the PLC-IP3 system associated with acetylcholine and gastrin.

A

IP3

635
Q

What is aluminum hydroxide commonly used for?

A

Relief of gastroesophageal reflux disease (GERD) symptoms.

636
Q

How does aluminum hydroxide neutralize stomach acid?

A

By forming aluminum chloride and water.

637
Q

What is a common adverse reaction to aluminum hydroxide?

A

Constipation, Hypophosphatemia.

638
Q

Why does aluminum hydroxide cause constipation?

A

It decreases gastrointestinal motility.

639
Q

How does aluminum hydroxide lead to hypophosphatemia?

A

By binding phosphate in the gut.

640
Q

What can hypophosphatemia lead to?

A

Muscle weakness.

641
Q

How does sodium bicarbonate neutralize acid?

A

It forms salt, water, and carbon dioxide.

642
Q

What side effects can result from the formation of carbon dioxide when using sodium bicarbonate?

A

Bloating and belching.

643
Q

What can absorption of bicarbonate lead to?

A

Alkalosis.

644
Q

What can the formation of salt from sodium bicarbonate lead to?

A

Fluid retention.

645
Q

How does magnesium hydroxide neutralize acid?

A

By forming magnesium chloride and water.

646
Q

What is a common side effect of magnesium hydroxide?

A

Diarrhea.

647
Q

What can excessive use of magnesium hydroxide lead to?

A

Hypermagnesemia, which can cause bradycardia, hypotension, and death.

648
Q

What is famotidine classified as?

A

A histamine 2 (H2) blocker.

649
Q

How does famotidine work?

A

By blocking histamine receptors in parietal cells.

650
Q

What are common side effects of famotidine?

A

Generally well tolerated; rare confusion in the elderly, elevation of AST and ALT, and cardiac arrhythmias.

651
Q

What is omeprazole classified as?

A

A proton pump inhibitor (PPI).

652
Q

How does omeprazole work?

A

By inhibiting the hydrogen-potassium pump in parietal cells.

653
Q

What are some long-term adverse reactions of omeprazole?

A

Increased risk of Clostridioides difficile infection, pneumonia, osteopenia, and decreased levels of calcium, magnesium, iron, and B12.

654
Q

What rare side effect can omeprazole cause?

A

Constipation.

655
Q

What side effects can occur after administering metoclopramide?

A

Restlessness and dystonia (spasms).

656
Q

What type of side effects are caused by metoclopramide?

A

Extrapyramidal side effects.

657
Q

How does metoclopramide function pharmacologically?

A

It is a dopamine (D2) receptor antagonist.

658
Q

What area of the brain does metoclopramide primarily affect to decrease nausea and vomiting?

A

The chemoreceptor trigger zone in the central nervous system.

659
Q

What movement symptoms can metoclopramide induce due to altered dopamine activity?

A

Restlessness, akathisia, dystonia, and rarely tardive dyskinesia.

660
Q

What is tardive dyskinesia and how is it related to metoclopramide?

A

A movement disorder that can occur with long-term use of metoclopramide.

661
Q

How does metoclopramide affect the seizure threshold?

A

It lowers the seizure threshold and should be avoided in patients with epilepsy.

662
Q

What type of medication is ondansetron?

A

A 5-hydroxytryptamine (5-HT3) receptor antagonist.

663
Q

Where are 5-HT3 receptors located?

A

In the vomiting center of the medulla and in the vagal and spinal nerves of the GI tract.

664
Q

What effect does ondansetron have when it blocks 5-HT3 receptors?

A

Relief of nausea.

665
Q

What are common side effects of ondansetron?

A

Headache and constipation.

666
Q

What is lactulose primarily used for?

A

Treatment of constipation.

667
Q

How does lactulose benefit patients with hepatic encephalopathy?

A

It promotes the excretion of ammonia via the GI tract.

668
Q

What is the function of calcium carbonate?

A

It is an antacid that neutralizes stomach acid by forming calcium chloride.

669
Q

What side effects can result from calcium carbonate use?

A

Bloating and belching due to carbon dioxide formation, as well as constipation from calcium ingestion.

670
Q

What is sodium polystyrene sulfonate primarily used for?

A

Management of hyperkalemia by binding and excreting potassium through the GI tract.

671
Q

What type of laxative is sodium polystyrene sulfonate?

A

An osmotic laxative.

672
Q

What are magnesium hydroxide and magnesium citrate used for?

A

Management of constipation as osmotic laxatives.

673
Q

What is polyethylene glycol commonly used for?

A

As an osmotic laxative for bowel preparation prior to colonoscopy.

674
Q

What is the classic presentation of ulcerative colitis?

A

Bloody diarrhea.

675
Q

How does diarrhea in Crohn’s disease differ from that in ulcerative colitis?

A

While diarrhea and gastrointestinal bleeding can occur in Crohn’s disease, grossly bloody stools are rare; usually, only microscopic amounts of blood are detected.

676
Q

What serum antibody is strongly associated with ulcerative colitis?

A

Elevated levels of serum p-ANCA antibodies.

677
Q

What is pyoderma gangrenosum?

A

A painful skin lesion characterized by ulceration and necrosis, common in ulcerative colitis.

678
Q

Name some extraintestinal manifestations of ulcerative colitis.

A

Primary sclerosing cholangitis, ankylosing spondylitis, and uveitis.

679
Q

What are pseudopolyps in the context of ulcerative colitis?

A

Masses of scar tissue that project into the intestinal lumen, developing from the healing of colonic ulcerations.

680
Q

Are pseudopolyps more common in ulcerative colitis or Crohn’s disease?

A

Pseudopolyps are a common manifestation of ulcerative colitis.

681
Q

Is an abnormal connection between two body structures. Intestinal fistula formation is common in Crohn’s disease. Examples of fistulas in Crohn’s disease include connections between the intestines and anus (perianal), abdomen, or bladder (enterovesical). Treatment is usually with surgery.

A

A fistula

682
Q

Is a feature of long-standing Crohn’s disease. Inflammation leads to excess fat deposition within the mesentery. This can lead to extension of the mesentery around the entire surface of the bowel. Other pathological features of Crohn’s disease include stricture formation and transmural inflammation

A

Creeping fat

683
Q

Are a common extraintestinal manifestation of Crohn’s disease, specifically due to involvement of the terminal ileum. Patients with Crohn’s disease often have malabsorption of fat due to small bowel inflammation. Free fat in the gut binds calcium. Normally, calcium binds oxalate in the gut, limiting oxalate absorption. When less calcium is available due to fat malabsorption, oxalate absorption increases. This leads to increased urinary oxalate excretion and increases the risk of kidney stones.

A

Calcium oxalate kidney stones

684
Q

Are a pathological hallmark of Crohn’s disease.

A

Non-caseating granulomas

685
Q

What are classic symptoms of ulcerative colitis?

A

Abdominal pain and bloody diarrhea

686
Q

What is the “lead pipe” appearance in ulcerative colitis?

A

The distal colon shows smooth intestinal walls lacking the normal haustra indentations.

687
Q

What type of antibodies are often elevated in ulcerative colitis?

A

Perinuclear antineutrophil cytoplasmic antibodies (p-ANCA).

688
Q

What is the sensitivity and specificity of p-ANCA for ulcerative colitis?

A

55% sensitivity and 88% specificity.

689
Q

What characterizes toxic megacolon?

A

Abrupt onset of colon inflammation and dilation without obstruction (non-obstructive dilation).

690
Q

How can toxic megacolon be differentiated from other causes of colon dilation?

A

Toxic megacolon is associated with systemic toxicity (fever, tachycardia) in addition to colon dilation.

691
Q

In which other conditions might you see dilated bowel without obstruction?

A

Hirschsprung’s disease, impaired gastrointestinal motility, and chronic constipation.

692
Q

Are found in patients with granulomatosis with polyangiitis.

A

Cytoplasmic antineutrophil cytoplasmic antibodies (c-ANCA)

693
Q

Are found in patients with Crohn’s disease with a 55% sensitivity and 92% specificity.

A

Anti-Saccharomyces cerevisiae antibodies (ASCA)

694
Q

Are elevated in patients with autoimmune hepatitis.A

A

Anti-smooth muscle antibodies

695
Q

Are elevated in patients with primary biliary cholangitis.

A

Anti-mitochondrial antibodies

696
Q

What are common clinical findings in Crohn’s disease?

A

Abdominal pain and diarrhea.

697
Q

What portions of the GI tract can Crohn’s disease affect?

A

Any portion from “mouth to anus,” but most commonly the ileum.

698
Q

What symptoms may occur with ileal involvement in Crohn’s disease?

A

Fat malabsorption leading to steatorrhea (greasy, foul-smelling stools) and right lower quadrant abdominal pain.

699
Q

What are common extraintestinal features of Crohn’s disease?

A

Erythema nodosum, migratory polyarthritis, ankylosing spondylitis, kidney stones, and uveitis.

700
Q

What pathologic features are associated with Crohn’s disease?

A

Transmural, non-caseating granulomatous inflammation, skip lesions, cobblestone mucosa, fistula disease, strictures, and creeping fat.

701
Q

What type of immune response is associated with Crohn’s disease?

A

Th1 cell-mediated response.

702
Q

How does the immune response in Crohn’s disease differ from that in ulcerative colitis?

A

Ulcerative colitis is associated with a Th2 cell-mediated response.

703
Q

Smoking improves outcomes in ? for unclear reasons. In Crohn’s disease, smoking is associated with worsened outcomes.

A

ulcerative colitis

704
Q

Crypt abscesses caused by neutrophil inflammation are a hallmark pathological feature of ulcerative colitis.

A

Crypt abscesses caused by neutrophil inflammation

705
Q

Ulcerative colitis always involves the

A

Rectum

706
Q

Crohn’s disease most commonly involves the

A

Ileum

707
Q

How does sulfasalazine work in the treatment of ulcerative colitis?

A

It is split by bacteria in the colon into sulfapyridine and 5-aminosalicylic acid (5-ASA), with 5-ASA being the active component that limits inflammation.

708
Q

What are common side effects of sulfasalazine?

A

Nausea, vomiting, hypersensitivity, and oligospermia in men.

709
Q

Is the oligospermia caused by sulfasalazine reversible?

A

Yes, it is reversible with drug cessation.

710
Q

What is the role of methotrexate in treating inflammatory bowel disease?

A

It inhibits folate metabolism.

711
Q

What side effect is associated with methotrexate?

A

Megaloblastic anemia.

712
Q

What is infliximab and its use in inflammatory bowel disease?

A

Infliximab is an antibody that binds tumor necrosis factor alpha (TNF-alpha) and is used to treat inflammatory bowel disease, rheumatoid arthritis, ankylosing spondylitis, and psoriasis.

713
Q

What are some adverse effects of infliximab?

A

Increased risk of infection, including tuberculosis.

714
Q

What is prednisone commonly used for in inflammatory bowel disease?

A

It is used as an anti-inflammatory medication.

715
Q

What are some side effects of prednisone?

A

Cushing’s-like syndrome, gastritis, skin thinning, poor wound healing, hyperglycemia, and lipodystrophy.

716
Q

What condition is indicated by abdominal pain, distension, and failure to pass stools or flatus?

A

Small bowel obstruction.

717
Q

What is the most common cause of mechanical small bowel obstruction in adults?

A

Abdominal adhesions (fibrous scar tissue) following surgery, such as appendectomy.

718
Q

What are the initial treatment steps for small bowel obstruction?

A

Bowel rest and intestinal decompression via placement of a nasogastric tube.

719
Q

When is surgery indicated for small bowel obstruction?

A

If symptoms are severe or do not resolve with conservative treatment.

720
Q

What is the second most common cause of mechanical small bowel obstruction?

A

Hernias, often seen at the umbilicus or inguinal regions.

721
Q

How does intestinal malignancy relate to small bowel obstruction?

A

It is a rare cause and typically requires surgical removal of the affected area.

722
Q

What characterizes intussusception?

A

“Telescoping” of the intestine, where one segment folds into another, leading to obstruction and ischemia.

723
Q

What are the classic symptoms of intussusception?

A

Abdominal pain, obstruction, and potentially “currant jelly stool.”

724
Q

What are common underlying causes of intussusception in children?

A

Meckel’s diverticulum and lymphoid hyperplasia due to viral infections.

725
Q

What is volvulus, and where is it commonly located?

A

Twisting of the intestines, commonly occurring at the sigmoid colon or cecum.

726
Q

What are classic imaging findings of sigmoid volvulus?

A

A dilated sigmoid colon and an airless rectum.

727
Q

In which population is volvulus most commonly seen?

A

The elderly population, typically around age 70.

728
Q

What condition is characterized by a lack of movement in the intestines?

A

Ileus.

729
Q

What imaging findings are typical in ileus?

A

Diffuse dilation of the small bowel with air-fluid levels.

730
Q

What is the most common etiology of ileus?

A

Recent abdominal surgery or medications, particularly opioids.

731
Q

How do opioids contribute to the development of ileus?

A

They slow down intestinal motility, leading to decreased movement and potential constipation.

732
Q

What are stool softeners often prescribed alongside opioid pain medications?

A

To limit constipation and prevent ileus.

733
Q

What role does inflammation play in ileus?

A

Inflammation (e.g., from inflammatory bowel disease, appendicitis, diverticulitis) can impair the muscular function of the intestine.

734
Q

How is the ileus typically affected in cases of inflammation?

A

It is often isolated to the affected segment of bowel.

735
Q

Why is inflammation less likely in this patient, despite potential causes of ileus?

A

The patient has normal vital signs and no fever.

736
Q

Are small bowel tumors common causes of ileus?

A

No, they are rare causes of ileus and obstruction.

737
Q

Is intussusception common in adults?

A

No, it is rare but can lead to ileus involving the affected segment of the bowel.

738
Q

What is the most common cause of mechanical small bowel obstruction in adults?

A

Adhesions, but they are unlikely if there is no history of abdominal surgery.

739
Q

What is Hirschsprung’s disease?

A

A congenital disorder characterized by abnormal colonic peristalsis due to the absence of ganglion cells in the colon.

740
Q

What causes Hirschsprung’s disease?

A

Failure of neural crest cells to migrate to the colon, leading to absence of nerve cells in Meissner’s and Auerbach’s plexuses.

741
Q

What are common symptoms of Hirschsprung’s disease?

A

Failure to pass meconium, abdominal distension, bilious emesis, and absence of stool on digital rectal examination.

742
Q

What does barium imaging reveal in Hirschsprung’s disease?

A

A “transition zone” that is cone-shaped, with proximal bowel being dilated and distal bowel being narrow and compressed.

743
Q

How is Hirschsprung’s disease definitively diagnosed?

A

Through a rectal suction biopsy that demonstrates the absence of ganglion cells.

744
Q

What is the treatment for Hirschsprung’s disease?

A

Resection of the affected colon and rectum.

745
Q

Why is abdominal ultrasound important in children?

A

It does not expose them to harmful radiation and can diagnose various abdominal conditions.

746
Q

Why is a CT scan used cautiously in younger patients?

A

Due to the radiation exposure involved.

747
Q

What imaging technique is not useful for diagnosing Hirschsprung’s disease?

A

Upper endoscopy, as it affects the colon and rectum.

748
Q

What is a technetium-99m scan useful for?

A

Diagnosing Meckel’s diverticulum, characterized by ectopic gastric and pancreatic tissue in the small intestine.

749
Q

What is the classic physical exam finding in Hirschsprung’s disease?

A

Absence of stool on digital rectal examination.

750
Q

What is the likely diagnosis for a woman presenting with cystitis and pneumaturia?

A

Cystitis with pneumaturia, likely due to a colovesical fistula.

751
Q

What is a colovesical fistula?

A

An abnormal connection between the colon and bladder, often caused by diverticulitis.

752
Q

How does a colovesical fistula develop after diverticulitis?

A

Inflammation leads to adhesion of the diverticulum to the bladder wall, and necrosis can create an opening allowing air and stool to enter the bladder.

753
Q

What are the common symptoms of cystitis?

A

Dysuria, urgency, frequency, and pneumaturia (air in the urine).

754
Q

What is the definitive management for a colovesical fistula?

A

Surgery to remove the affected colon segment and repair the bladder

755
Q

What is a common complication of acute diverticulitis?

A

Abscess formation, often presenting with persistent symptoms despite antibiotic treatment.

756
Q

What clinical features indicate perforation of the colon due to diverticulitis?

A

Severe abdominal pain, rebound tenderness, fever, chills, leukocytosis, and often hemodynamic instability.

757
Q

What symptoms can occur if diverticulitis leads to bowel obstruction?

A

Nausea, vomiting, abdominal distension, and obstipation.

758
Q

When is lower gastrointestinal bleeding most common in diverticular disease?

A

Significant bleeding generally occurs in the absence of acute diverticulitis.

759
Q

What are the key features of diverticulitis?

A

Symptoms include abdominal pain, fever, changes in bowel habits, and potentially complications like abscesses or perforation.

760
Q

What is the primary characteristic of irritable bowel syndrome (IBS)?

A

IBS is defined as a functional bowel disorder characterized by chronic abdominal pain and altered bowel habits with no structural cause

761
Q

How frequently must abdominal pain occur for a diagnosis of IBS?

A

Abdominal pain must occur at least 3 days per month over the last three months.

762
Q

What additional features are required for the diagnosis of IBS?

A

Improvement of pain with defecation, change in stool frequency, or onset of symptoms associated with change in stool appearance.

763
Q

What types of bowel habits can IBS involve?

A

IBS can involve diarrhea, constipation, or both.

764
Q

In which demographic is IBS slightly more common?

A

IBS has a slightly higher incidence among women.

765
Q

What are telangiectasias, and in which condition can they be found?

A

Telangiectasias are dilated submucosal capillaries with flattened endothelia, commonly seen in hereditary hemorrhagic telangiectasia.

766
Q

What complications can arise from telangiectasias in the gastrointestinal tract?

A

They can lead to gastrointestinal bleeding and iron deficiency anemia.

767
Q

What are common causes of duodenal ulcers?

A

Duodenal ulcers can occur due to Helicobacter pylori infection or Zollinger-Ellison syndrome (ZES).

768
Q

How does abdominal pain typically present in patients with duodenal ulcers?

A

Abdominal pain is worse at night and improved with eating.

769
Q

What is the role of Brunner’s glands in the duodenum?

A

Brunner’s glands produce alkaline fluid in response to acidified conditions, often hypertrophying in cases of peptic ulcer disease.

770
Q

What is KRAS, and where is it located?

A

KRAS is a GTPase proto-oncogene located on the short arm of chromosome 12.

771
Q

What is the consequence of a mutation in KRAS?

A

A point mutation in KRAS leads to increased expression and uncontrolled cellular division, resulting in dysplasia.

772
Q

Which malignancies are commonly associated with KRAS mutations?

A

KRAS mutations are implicated in pancreatic, lung, and colonic adenocarcinomas.

773
Q

What is BCR-ABL, and what condition is it associated with?

A

BCR-ABL is a mutated tyrosine kinase inhibitor associated with chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL).

774
Q

Which malignancy is primarily associated with mutations in the BRAF gene?

A

BRAF mutations are primarily associated with melanoma.

775
Q

What other malignancies can BRAF mutations be implicated in?

A

BRAF mutations are also associated with non-Hodgkin’s lymphoma and papillary thyroid cancer.

776
Q

What is the MYC proto-oncogene, and with which cancer is its amplification associated?

A

MYC is a transcription factor, and its amplification is associated with small cell lung cancer.

777
Q

What syndromes are associated with mutations in the RET oncogene?

A

The RET oncogene is associated with multiple endocrine neoplasia (MEN) types 2A and 2B.

778
Q

What type of cancer is linked to MEN 2A and 2B?

A

MEN 2A and 2B are associated with medullary thyroid cancer.

779
Q

What condition is this woman likely experiencing due to pancreatic cancer?

A

Splenic vein thrombosis.

780
Q

Where does the splenic vein course in relation to the pancreas?

A

The splenic vein courses along the posterior aspect of the pancreas.

781
Q

What happens to the spleen when the splenic vein is thrombosed?

A

Splenomegaly occurs due to the obstruction of blood flow.

782
Q

Which veins does the splenic vein drain?

A

The splenic vein drains blood from the spleen and the short gastric veins of the stomach.

783
Q

What is a potential consequence of splenic vein thrombosis in terms of gastric veins?

A

Congestion of the short gastric veins can lead to gastric varices along the greater curvature of the stomach.

784
Q

What syndrome can also cause gastric varices along the greater curvature of the stomach?

A

Budd-Chiari syndrome, characterized by thrombosis of the hepatic veins.

785
Q

What is the hallmark of hepatic cirrhosis related to varices?

A

Esophageal varices, which develop from collateral formation between esophageal veins and the left gastric vein.

786
Q

How do umbilical veins become enlarged in relation to hepatic conditions?

A

They become enlarged due to elevated portal venous pressures, typically seen in hepatic cirrhosis.

787
Q

Which rectal veins are affected by increased portal venous pressure in hepatic cirrhosis?

A

The superior rectal vein, which drains into the inferior mesenteric vein, can dilate and lead to internal hemorrhoids.

788
Q

Why are internal hemorrhoids a concern in patients with hepatic cirrhosis?

A

Increased portal venous pressure can cause dilation of the superior rectal vein, leading to potential rupture and bleeding.

789
Q

What condition is this man likely suffering from due to chronic pancreatitis?

A

Pancreatic insufficiency.

790
Q

What are the classic findings in the pancreas associated with chronic pancreatitis?

A

White calcifications due to chronic inflammation.

791
Q

What is a common symptom of pancreatic insufficiency?

A

Diarrhea associated with malabsorption of fat, known as steatorrhea.

792
Q

How is steatorrhea characterized?

A

Greasy, foul-smelling stools that float.

793
Q

What can chronic pancreatitis lead to in terms of blood sugar regulation?

A

Diabetes from destruction of insulin-producing pancreatic beta cells.

794
Q

What symptoms may indicate hyperglycemia in this patient?

A

Excessive thirst and frequent urination.

795
Q

What does an elevated Hemoglobin A1C indicate?

A

Chronically elevated serum glucose levels.

796
Q

Why is Hemoglobin A1C important in managing diabetes?

A

It provides an average of blood glucose levels over the past 2-3 months.

797
Q

What blood count finding is commonly associated with acute pancreatitis but not chronic pancreatitis?

A

Leukocytosis (elevated white blood cell count).

798
Q

How do blood counts, electrolytes, and liver function tests typically present in chronic pancreatitis?

A

They are usually normal.

799
Q

What may happen to serum lipase and amylase levels in chronic pancreatitis?

A

They may be normal or low due to fibrotic changes in the pancreas.

800
Q

What does serum creatinine indicate, and how is it affected in chronic pancreatitis?

A

Serum creatinine is a marker of kidney function and is not directly affected by chronic pancreatitis.

801
Q

What conditions could cause an increase in serum creatinine if the patient had chronic pancreatitis?

A

Poorly controlled hypertension or volume depletion.

802
Q

What is alkaline phosphatase, and when are its levels elevated?

A

Alkaline phosphatase is secreted by bile duct epithelium, and elevated levels occur in cholestasis (bile duct obstruction, inflammation, or tumor).

803
Q

What common nutritional deficiencies occur in patients with chronic pancreatitis?

A

Deficiencies of fat-soluble vitamins A, D, E, and K.

804
Q

What does the acronym CREST stand for?

A

Calcinosis, Raynaud’s phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasias.

805
Q

What form of scleroderma is associated with CREST syndrome?

A

Limited cutaneous scleroderma.

806
Q

What is a characteristic feature of sclerodactyly?

A

Thickening and tightening of the fingers and toes due to collagen buildup in the skin.

807
Q

What are telangiectasias?

A

Spider veins, often seen on the face, associated with conditions like CREST syndrome.

808
Q

What does the acronym CREST stand for?

A

Calcinosis, Raynaud’s phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasias.

809
Q

What form of scleroderma is associated with CREST syndrome?

A

Limited cutaneous scleroderma.

810
Q

What is a characteristic feature of sclerodactyly?

A

Thickening and tightening of the fingers and toes due to collagen buildup in the skin.

811
Q

What are telangiectasias?

A

Spider veins, often seen on the face, associated with conditions like CREST syndrome.

812
Q

What specific antibodies are characteristic of CREST syndrome?

A

Anticentromere antibodies.

813
Q

What contributes to loss of tone in the lower esophageal sphincter (LES) in scleroderma?

A

Esophageal smooth muscle atrophy.

814
Q

How does LES hypotension in scleroderma differ from classic gastroesophageal reflux disease (GERD)?

A

LES hypotension in scleroderma is persistent, while GERD typically involves intermittent/transient hypotension.

815
Q

What symptoms can persistent LES hypotension in scleroderma cause?

A

Severe reflux symptoms.

816
Q

Which feature of CREST syndrome can be visibly noted during a physical exam?

A

Sclerodactyly and telangiectasias.

817
Q

What is the primary virus associated with esophagitis in immunocompromised patients?

A

Herpes simplex virus type 1 (HSV-1).

818
Q

What common symptoms are associated with HSV-1 esophagitis?

A

Dysphagia and chest pain.

819
Q

What does endoscopy typically reveal in HSV-1 esophagitis?

A

Numerous ulcers with a “punched-out” appearance that often coalesce.

820
Q

How is the diagnosis of HSV-1 esophagitis confirmed?

A

By biopsy.

821
Q

What do the pathology findings show in HSV-1 esophagitis?

A

Squamous epithelial cells with dense eosinophilic intranuclear inclusion bodies.

822
Q

What is a key endoscopic finding in cytomegalovirus (CMV) esophagitis?

A

One or more deep linear ulcers.

823
Q

What condition is associated with gastroesophageal reflux disease (GERD) and can lead to Barrett’s esophagus?

A

Reflux esophagitis.

824
Q

What are the typical symptoms of reflux esophagitis?

A

Long-standing history of GERD symptoms like heartburn.

825
Q

What does endoscopy reveal in Candida esophagitis?

A

Glossy white lesions lining the esophagus.

826
Q

What is eosinophilic esophagitis?

A

A hypersensitivity reaction of the esophageal mucosa, presenting with GERD-like symptoms or dysphagia.

827
Q

A key difference from HSV-1 esophagitis is that endoscopy in ?shows one or more deep linear ulcers.

A

CMV

828
Q

What are the initial symptoms of esophageal cancer?

A

Dysphagia (difficulty swallowing), initially to solids and then to liquids, often associated with weight loss.

829
Q

What is the 5-year survival rate for esophageal cancer?

A

Approximately 15%.

830
Q

Which gender is more affected by esophageal cancer?

A

Men, who are affected three times more than women.

831
Q

What are the two main types of primary esophageal cancers?

A

Squamous cell carcinoma (SCC) and adenocarcinoma.

832
Q

Where is squamous cell carcinoma (SCC) more commonly found?

A

More commonly seen in the developing world.

833
Q

What is the common treatment approach for esophageal cancer?

A

A combination of surgery, radiation, and chemotherapy.

834
Q

What lifestyle factor is strongly associated with adenocarcinoma?

A

Obesity.

835
Q

How does untreated gastroesophageal reflux disease (GERD) contribute to adenocarcinoma?

A

It can cause metaplasia of esophageal stratified squamous epithelium to gastric columnar epithelium (Barrett’s esophagus), increasing the risk of adenocarcinoma.

836
Q

What type of epithelium is normally found in the esophagus?

A

Stratified squamous epithelium, not glandular cells.

837
Q

What can lead to malignant transformation of normal squamous mucosa in the esophagus?

A

Other esophageal injuries that are not associated with metaplasia.

838
Q

What long-term habit is a risk factor for squamous cell carcinoma (SCC) of the esophagus?

A

Consumption of very hot liquids, such as tea.

839
Q

Where are approximately half of the reported new cases of esophageal cancer each year located?

A

In China, where hot tea consumption is common.

840
Q

What type of caustic ingestions can increase the risk of esophageal strictures and SCC?

A

Ingestions of substances like lye and battery acid.

841
Q

How does alcohol abuse affect the risk of esophageal SCC?

A

Alcohol abuse confers an increased risk of esophageal SCC.

842
Q

Besides esophageal SCC, what other cancers are associated with alcohol consumption?

A

SCC of the head and neck, breast, liver, and colon cancer.

843
Q

What type of esophageal cancer is associated with alcohol consumption?

A

Squamous cell carcinoma (SCC).

844
Q

Why might the lack of association between alcohol and esophageal adenocarcinoma be counterintuitive?

A

Because alcohol is associated with gastroesophageal reflux disease (GERD), which can lead to adenocarcinoma.

845
Q

What is “steakhouse syndrome”?

A

Acute, complete obstruction of the esophagus by a food bolus, often a large piece of meat.

846
Q

What is the most common cause of “steakhouse syndrome”?

A

The presence of a Schatzki ring, a benign stricture that narrows the lumen of the esophagus.

847
Q

Where is a Schatzki ring typically located?

A

Just above or at the squamocolumnar (SC) junction.

848
Q

What is the primary risk factor for developing a Schatzki ring?

A

Gastroesophageal reflux disease (GERD).

849
Q

What type of epithelium lines rings at the squamocolumnar (SC) junction?

A

Stratified squamous epithelium proximally (toward the mouth) and gastric epithelium distally (toward the stomach).

850
Q

How are rings located above the squamocolumnar junction lined?

A

Entirely with stratified squamous epithelium.

851
Q

What are esophageal webs associated with?

A

Plummer-Vinson syndrome.

852
Q

Where are esophageal webs typically found?

A

Mostly in the proximal esophagus.

853
Q

What are the key features of Plummer-Vinson syndrome?

A

Dysphagia, iron deficiency anemia, and an increased risk of squamous cell carcinoma (SCC) of the esophagus.

854
Q

What are the two main types of esophageal neoplasms?

A

Esophageal squamous cell carcinoma and esophageal adenocarcinoma.

855
Q

How do patients with esophageal cancer typically present?

A

Chronic, progressive dysphagia initially to solids and then liquids, along with appetite change, weight loss, and night sweats.

856
Q

What are the characteristic features of eosinophilic esophagitis?

A

Esophageal strictures, linear furrows, whitish papules, or esophageal rings.

857
Q

In which patients is eosinophilic esophagitis often seen?

A

Those with asthma or food allergies.

858
Q

What complication can arise from portal hypertension in the setting of cirrhosis?

A

Esophageal varices.

859
Q

In addition to cirrhosis, what other condition can lead to esophageal varices?

A

Portal venous thrombosis.

860
Q

What is achalasia?

A

A rare disorder of the esophagus characterized by abnormal smooth muscle tone and obstruction to flow.

861
Q

What causes achalasia?

A

Loss of ganglion cells in the myenteric plexus due to inflammation, thought to be autoimmune in nature.

862
Q

What is the usual age of diagnosis for achalasia?

A

Between 25 and 60 years.

863
Q

How does achalasia affect the distal esophagus?

A

It develops high smooth muscle tone (spasm), obstructing flow.

864
Q

What compensatory changes occur in the esophagus due to flow obstruction in achalasia?

A

Hypertrophy and thickening of smooth muscle cells in the circular muscle layer.

865
Q

What type of dysphagia is associated with achalasia?

A

Dysphagia that affects solids and liquids equally.

866
Q

What are the conventional findings on esophageal manometry in achalasia?

A

Absence of peristaltic waves in the distal two-thirds of the esophagus and elevated relaxed lower esophageal sphincter (LES) pressure (often >100 mmHg).

867
Q

What does a biopsy of the distal esophagus in achalasia reveal?

A

Inflammatory changes and absence of ganglion cells in the myenteric plexus.

868
Q

What does a barium esophagram show in cases of achalasia?

A

Distal tapering and proximal dilatation of the esophagus.

869
Q

What causes transient relaxations of the lower esophageal sphincter (LES)?

A

Gastroesophageal reflux disease (GERD).

870
Q

What is the motility status of the esophagus in conventional GERD?

A

Esophageal motility is normal; however, the LES inappropriately relaxes.

871
Q

What are the three criteria for diagnosing acute pancreatitis?

A

1) Characteristic abdominal pain, nausea, vomiting
2) Elevation of serum amylase/lipase at least 3 times the upper limit of normal
3) CT findings consistent with acute pancreatitis.

872
Q

How many criteria must be met to diagnose acute pancreatitis?

A

Two out of the three criteria must be met.

873
Q

What are the characteristic symptoms of acute pancreatitis?

A

Abdominal pain, nausea, and vomiting.

874
Q

In this case, what is the level of serum amylase, and is it sufficient for diagnosis?

A

Serum amylase is elevated at 349 U/L, but it is not elevated to greater than 3 times the upper limit of normal (125 U/L).

875
Q

What is the next step required for diagnosis in this patient?

A

An abdominal CT is required to make a diagnosis of acute pancreatitis.

876
Q

What imaging study can be used to evaluate for underlying causes of pancreatitis?

A

Right upper quadrant ultrasound.

877
Q

What may an ultrasound reveal in cases of gallstone pancreatitis?

A

Gallstones or common bile duct dilation.

878
Q

What liver function test abnormalities may indicate gallstone pancreatitis?

A

Elevations in aspartate aminotransferase (AST), total and direct bilirubin, and alkaline phosphatase.

879
Q

How useful is an abdominal radiograph in diagnosing acute pancreatitis?

A

It is generally not helpful for diagnosing acute pancreatitis and is more useful if bowel obstruction is suspected.

880
Q

What are common causes of acute pancreatitis?

A

Gallstones, alcohol, trauma, toxins, hypertriglyceridemia, endoscopic manipulation of the common bile duct (e.g., during ERCP), and rarely, medications.

881
Q

Name some medications that may cause pancreatitis

A

Sulfa drugs and 6-mercaptopurine (6-MP).

882
Q

What class of medications for type 2 diabetes has been associated with pancreatitis?

A

Glucagon-like peptide 1 (GLP-1) agonists.

883
Q

Give examples of GLP-1 agonists.

A

Liraglutide and exenatide.

884
Q

What effects do GLP-1 agonists have on insulin secretion and gastric emptying?

A

They increase insulin secretion after meals, delay gastric emptying, and decrease post-prandial glucagon secretion.

885
Q

What is the primary action of metformin in diabetes management?

A

It inhibits hepatic gluconeogenesis.

886
Q

What are common side effects of metformin?

A

Diarrhea, nausea, vomiting, and flatulence.

887
Q

Why should metformin not be prescribed in patients with chronic kidney disease?

A

There is an increased risk of lactic acidosis.

888
Q

What class of medications do SGLT2 inhibitors belong to?

A

Sodium/glucose cotransporter 2 (SGLT2) inhibitors.

889
Q

What is the mechanism of action of SGLT2 inhibitors like gliflozin and canagliflozin?

A

They block reuptake of glucose by the kidneys, leading to glucose excretion in the urine.

890
Q

What are common side effects of SGLT2 inhibitors?

A

Increased risk of urinary tract infections and yeast infections.

891
Q

What do alpha-glucosidase inhibitors do?

A

They inhibit the brush border enzyme alpha-glucosidase, inhibiting the absorption of glucose in the GI tract.

892
Q

Name two examples of alpha-glucosidase inhibitors.

A

Acarbose and miglitol.

893
Q

What is the most common side effect of alpha-glucosidase inhibitors?

A

Osmotic, watery diarrhea.

894
Q

What condition is this patient experiencing?

A

Acute pancreatitis secondary to hypertriglyceridemia.

895
Q

What serum triglyceride level is associated with causing pancreatitis?

A

Greater than 1000 mg/dL.

896
Q

How does blood appear when triglyceride levels are significantly elevated

A

Thickened and milky-white color.

897
Q

What are some potential causes of hypertriglyceridemia in this patient?

A

Poorly controlled diabetes, beta blocker therapy, and hydrochlorothiazide.

898
Q

What is the pathophysiology behind triglyceride-induced pancreatitis?

A

Increased circulating levels of chylomicrons obstruct small capillaries within the pancreas, leading to ischemia.

899
Q

What happens when excessive chylomicrons obstruct capillaries in the pancreas?

A

This leads to damaged capillary endothelium, exposure of circulating triglycerides to pancreatic lipase, formation of free fatty acids, decreased pH, and tissue injury resulting in pancreatitis.

900
Q

What type of cell destruction occurs in autoimmune pancreatitis?

A

Antibody-mediated destruction of pancreatic exocrine cells.

901
Q

What is the typical presentation of autoimmune pancreatitis?

A

Recurrent pancreatitis with enlargement of the pancreas over time.

902
Q

What laboratory finding is often associated with autoimmune pancreatitis?

A

Elevated IgG4 levels.

903
Q

What is the first-line treatment for autoimmune pancreatitis?

A

Steroids.

904
Q

What is the mechanism of action in pancreatitis secondary to hypercalcemia?

A

Calcium deposition in pancreatic ducts.

905
Q

What does calcium deposition in the pancreatic ducts lead to?

A

Inappropriate activation of trypsinogen.

906
Q

What happens after the inappropriate activation of trypsinogen?

A

It initiates a cascade of activation of pancreatic enzymes.

907
Q

What is the result of pancreatic auto-digestion?

A

Development of pancreatitis.

908
Q

Is a rare cause of pancreatitis. This can be seen in children with abdominal pain following a car accident with restraint by a seat belt.

A

Trauma

909
Q

Obstruction of the main pancreatic duct leading to decreased flow of pancreatic secretions is the cause of

A

Gallstone pancreatitis.

910
Q

What is a pancreatic pseudocyst?

A

A collection of fluid with a well-defined inflammatory wall usually located outside the pancreas.

911
Q

How is a pancreatic pseudocyst diagnosed?

A

By CT or MRI imaging of the abdomen.

912
Q

What distinguishes pseudocysts from true cysts?

A

Pseudocysts contain no epithelium or endothelium.

913
Q

What is a pancreatic pseudocyst composed of?

A

Pancreatic fluid surrounded by a thin fibrous layer.

914
Q

When should suspicion for a pancreatic pseudocyst be raised?

A

When pancreatitis does not resolve with conventional therapy, such as when amylase or lipase fail to normalize, or when abdominal pain persists or returns.

915
Q

How do pancreatic pseudocysts typically resolve?

A

They generally resolve without intervention.

916
Q

When might a pancreatic pseudocyst require drainage?

A

Occasionally, if symptoms persist or complications arise.

917
Q

What risks are associated with the drainage of a pancreatic pseudocyst?

A

It can lead to infection or rupture, resulting in peritonitis.

918
Q

A pancreatic abscess can result from infection of pseudocyst. This generally occurs within 10 days of development of acute pancreatitis. This is unlikely in this patient, as he does not have signs of infection (fevers, severe pain, etc.). Causative organisms include

A

E. coli, Pseudomonas, Klebsiella, and Enterococcus.

919
Q

Occurs in the setting of acute pancreatitis via inflammation of fat surrounding the pancreas. Formation of free fatty acids combined with calcium leads to calcium saponification, which can be seen on abdominal imaging.

A

Pancreatic fat necrosis

920
Q

What does hypocalcemia in the setting of acute pancreatitis suggest?

A

Extensive involvement of the surrounding fat.

921
Q

Is characterized by right upper quadrant pain that typically occurs after eating and lasts for 2 to 3 hours. There is often associated nausea and vomiting.

A

Biliary colic

922
Q

What serum glucose level is one of Ranson’s criteria indicating a poor outcome in pancreatitis?

A

Serum glucose greater than 200 mg/dL.

923
Q

What factors contribute to hyperglycemia in severe cases of pancreatitis?

A

Impaired insulin release and activation of the sympathetic nervous system.

924
Q

What age is associated with a poor prognosis in acute pancreatitis?

A

Age greater than 55 years.

925
Q

What laboratory finding is associated with a poor prognosis in acute pancreatitis?

A

Elevated serum lactate dehydrogenase (LDH).

926
Q

What causes hypocalcemia in acute pancreatitis?

A

Marked inflammation of pancreatic fat, which binds with calcium (saponification), pulling calcium from the plasma.

927
Q

Patients with acute and chronic pancreatitis can have

A

Reduced duodenal pH after meals.

928
Q

A fall in hematocrit by ? at 48 hours after admission predicts a worse prognosis among patients with acute pancreatitis.

A

10%

929
Q

What is celiac sprue also known as?

A

Celiac disease or gluten sensitivity.

930
Q

What triggers the autoimmune response in celiac disease?

A

Gluten exposure, specifically the deamidated form of gliadin.

931
Q

Which enzyme catalyzes the deamidation of gliadin?

A

Tissue transglutaminase (tTG).

932
Q

What type of hypersensitivity reaction is associated with celiac disease?

A

Type IV hypersensitivity reaction.

933
Q

Which human leukocyte antigens (HLA) are strongly associated with celiac disease?

A

HLA-DQ2 and HLA-DQ8.

934
Q

What are the pathological hallmarks of celiac sprue observed in small intestine biopsy?

A

Blunting (atrophy) of villi, crypt hyperplasia, and increased intraepithelial lymphocytes.

935
Q

What are common symptoms of celiac disease?

A

Bloating, flatulence, diarrhea, and weight loss.

936
Q

What rash is associated with celiac disease, and where does it typically occur?

A

Dermatitis herpetiformis, commonly on the buttocks, knees, and elbows.

937
Q

What is the first-line antibody test for celiac sprue?

A

IgA anti-tissue transglutaminase (anti-tTG).

938
Q

What are the sensitivity and specificity of the IgA anti-tTG test?

A

Sensitivity is 95% and specificity is 97%.

939
Q

What is done after a positive IgA anti-tTG screening?

A

A duodenal biopsy is performed to confirm the diagnosis.

940
Q

What is the exception to the IgA anti-tTG testing algorithm?

A

In patients deficient in IgA antibodies, the IgG anti-tTG level can be measured instead.

941
Q

What condition is characterized by persistent, watery diarrhea after traveling to the Caribbean?

A

Tropical sprue.

942
Q

What causes tropical sprue?

A

An unknown infectious agent leading to malabsorption.

943
Q

How does tropical sprue progress in the small intestine?

A

It begins in the duodenum and progresses to affect the entire small bowel.

944
Q

What vitamin deficiency commonly occurs in tropical sprue?

A

Folate deficiency.

945
Q

Why can B12 deficiency occur in tropical sprue?

A

It can occur if the disease progresses to involve the ileum, but this is less common than folate deficiency.

946
Q

What are the hematological features of megaloblastic anemia due to vitamin deficiencies?

A

Reduced hemoglobin, reduced hematocrit, and elevated mean corpuscular volume.

947
Q

What do peripheral blood smears typically show in megaloblastic anemia?

A

Hyper-segmented neutrophils.

948
Q

What is the typical treatment for tropical sprue?

A

Tetracycline and folate supplementation.

949
Q

An elevated serum ferritin can be seen in primary and secondary hemochromatosis, both disorders of

A

Iron overload.

950
Q

Decrease serum lipase occurs in pancreatic insufficiency. Predisposing factors include

A

Chronic pancreatitis, cystic fibrosis, and obstruction.

951
Q

Mesenteric lymphadenopathy is seen in Whipple’s disease. Whipple’s disease is characterized by four cardinal features:

A

Abdominal pain, diarrhea, weight loss, and migratory arthralgias of the large joints.

952
Q

Patients with IgA deficiency have decreased serum IgA antibodies. When screening these patients for celiac sprue, IgA tissue transglutaminase (tTG) antibodies cannot be used, and

A

IgG tissue transglutaminase antibodies must be measured instead.

953
Q

Celiac sprue and tropical sprue can have similar clinical presentations. Because this man recently traveled to the Caribbean, tropical sprue is likely, but celiac disease still must be ruled out. To do this, testing for tissue ? should be performed. These antibodies are not present in tropical sprue.

A

Transglutaminase antibodies

954
Q

What is Whipple’s disease caused by?

A

Tropheryma whipplei, a gram-positive rod related to actinomycetes.

955
Q

Who is most commonly affected by Whipple’s disease?

A

Middle-aged Caucasian males of European descent.

956
Q

What are the cardinal signs of Whipple’s disease?

A

Diarrhea from malabsorption of fats and sugars, abdominal pain, weight loss, and migratory joint pains.

957
Q

What percentage of patients with Whipple’s disease experience arthralgias?

A

Up to 80%.

958
Q

What other clinical features may be present in Whipple’s disease?

A

Mesenteric lymphadenopathy, encephalopathy, and darkened skin (hyperpigmentation).

959
Q

What is the treatment for Whipple’s disease?

A

Antibiotics, commonly ceftriaxone.

960
Q

What is the pathologic hallmark of Whipple’s disease observed on biopsy?

A

Foamy macrophages in the lamina propria of the small intestine.

961
Q

How do foamy macrophages stain in Whipple’s disease?

A

They turn red when stained with periodic acid-Schiff (PAS) stain.

962
Q

What condition is associated with normal fecal fat excretion?

A

Lactose intolerance.

963
Q

What causes lactose intolerance?

A

Deficient activity of lactase, the enzyme that breaks down lactose into galactose and glucose.

964
Q

What type of diarrhea is associated with lactose intolerance?

A

High-volume, watery diarrhea.

965
Q

What mechanism causes the diarrhea seen in lactose intolerance?

A

Osmotic diarrhea, where undigested lactose draws water into the intestines.

966
Q

What is a positive fecal fat test indicative of?

A

Inability to break down and/or absorb fat, leading to steatorrhea.

967
Q

What fecal fat level is considered abnormal?

A

Greater than 7 g of stool fat per day.

968
Q

Chronic pancreatitis and pancreatic insufficiency lead to impaired pancreatic function including the secretion of enzymes such as lipase and colipase. These enzymes are necessary for breaking down fat for absorption. Patients with chronic pancreatitis or pancreatic insufficiency develop

A

Steatorrhea (greasy, foul-smelling stools that float) by this mechanism.

969
Q

Short gut syndrome occurs following bowel resections where more than 100 cm of bowel are removed, for conditions like Crohn’s disease. Bile acids emulsify fats to improve digestion and absorption. Bile acids are reabsorbed in the terminal ileum, then recycled into the bile for emulsification of dietary fats. Following ileal resection, fat malabsorption and steatorrhea develop due to

A

Insufficient enterohepatic circulation of bile acids.

970
Q

Occurs in pancreatic and biliary cancer, autoimmune conditions such as primary biliary sclerosis and primary sclerosing cholangitis, and gallstone disease. These conditions lead to impaired secretion of bile acids necessary for emulsification of fats.

A

Biliary obstruction

971
Q

Normal digestion of fats requires three elements: ?. Loss of any of these elements may lead to steatorrhea.

A

Pancreatic enzymes, bile acids from the liver, and bile acid reabsorption in the ileum.

972
Q

What does the D-xylose test evaluate?

A

Carbohydrate absorption in the small intestine.

973
Q

Does D-xylose require enzymatic modification for digestion?

A

No, it does not require enzymatic modification.

974
Q

What is necessary for the absorption of D-xylose?

A

An intact mucosa in the small intestine.

975
Q

What should happen to D-xylose in a normal small intestine?

A

It should appear in the bloodstream and urine in normal amounts.

976
Q

What conditions can lead to an abnormal D-xylose test result?

A

Small intestinal bacterial overgrowth and Whipple’s disease.

977
Q

How do small intestinal bacterial overgrowth and Whipple’s disease affect D-xylose absorption?

A

They disrupt the integrity of the small intestinal mucosa, impairing absorption.

978
Q

How is the small intestinal mucosa in lactose intolerance?

A

It is normal, except for the absence of the enzyme lactase.

979
Q

What condition leads to impaired secretion of pancreatic enzymes necessary for fat absorption?

A

Pancreatic insufficiency.

980
Q

Why is D-xylose absorption unaffected by pancreatic enzyme deficiency?

A

D-xylose is a monosaccharide and does not require pancreatic enzymes for absorption.

981
Q

What is irritable bowel syndrome (IBS)?

A

A functional bowel disorder characterized by chronic abdominal pain and altered bowel habits with no structural cause.

982
Q

What condition affects the stomach and can lead to malabsorption of vitamin B12?

A

Atrophic gastritis, due to impaired secretion of intrinsic factor.

983
Q

Where are the majority of peptic ulcers located?

A

In the duodenum (over 90%).

984
Q

How does food affect the pain associated with duodenal ulcers?

A

Pain often improves with food due to alkaline fluid production that raises duodenal pH.

985
Q

When do symptoms of duodenal ulcers typically worsen?

A

About 2 to 3 hours after eating when pH falls again and symptoms worsen in the acidic environment.

986
Q

What type of pain is associated with gastric ulcers?

A

Epigastric pain that worsens with food, as food stimulates gastric acid production.

987
Q

What is the rule of thumb for distinguishing between duodenal and gastric ulcer pain?

A

Duodenal Ulcers: Pain decreases with meals.
Gastric Ulcers: Pain increases with meals.

988
Q

What are common risk factors for duodenal ulcers?

A

Helicobacter pylori infection, NSAID use, and smoking.

989
Q

Does alcohol have a consistent association with peptic ulcer disease?

A

No, alcohol has no consistent association, though it can cause gastritis.

990
Q

What is autoimmune gastritis also known as?

A

Atrophic gastritis or type A chronic gastritis.

991
Q

What causes autoimmune gastritis?

A

Autoimmune destruction of gastric parietal cells.

992
Q

What physiological change occurs due to the loss of parietal cells in autoimmune gastritis?

A

Hypochlorhydria (high luminal pH) with reflex hypergastrinemia.

993
Q

What complication arises from impaired intrinsic factor release?

A

Impaired absorption of vitamin B12 in the terminal ileum, leading to pernicious anemia.

994
Q

What type of anemia is caused by vitamin B12 deficiency due to autoimmune gastritis?

A

Megaloblastic anemia (characterized by elevated mean corpuscular volume, MCV).

995
Q

What is the increased risk associated with atrophic gastritis?

A

Increased risk for gastric adenocarcinoma.

996
Q

With which HLA antigens is autoimmune gastritis associated?

A

HLA-DR antigens, and it may run in families.

997
Q

Which parts of the stomach are affected in autoimmune gastritis?

A

The gastric body and fundus.

998
Q

Risk of MALT lymphoma is increased in the setting of chronic gastritis from

A

Helicobacter pylori (H. pylori) infection.

999
Q

H. pylori infection is diagnosed via breath test as well as detection of H. pylori stool antigen. This typically causes

A

Type B chronic gastritis that affects the antrum (portion of stomach nearest the duodenum).

1000
Q

What is the most common cause of duodenal ulcers?

A

H. pylori infection (over 90% of cases).

1001
Q

Where do duodenal ulcers typically occur?

A

On the anterior wall of the duodenum, less often on the posterior wall.

1002
Q

How do patients with duodenal ulcers typically present?

A

With epigastric pain that improves with eating and worsens at night.

1003
Q

Why does pain from a duodenal ulcer improve after meals?

A

Food stimulates bicarbonate secretion in the duodenum, creating an alkalotic environment that decreases irritation from stomach acid.

1004
Q

What are Brunner’s glands, and where are they located?

A

Brunner’s glands are located in the submucosa of the duodenum and secrete alkaline fluid to protect the mucosa from acidic chyme.

1005
Q

What occurs to Brunner’s glands in the setting of a duodenal ulcer?

A

They undergo hypertrophy, increasing the thickness of the submucosal layer of the duodenum.

1006
Q

Are seen in diffuse gastric cancer. When this cancer metastasizes to the ovaries, the ovarian tumors are termed Krukenberg’s tumors. Patients generally present with early satiety.

A

Signet ring cells

1007
Q

May be seen in duodenal ulcers, but eosinophils are uncommon.

A

Surface neutrophils

1008
Q

The muscularis mucosa is a thin layer of smooth muscle below the submucosa. In the setting of ulcers, the muscularis mucosa is

A

Eroded and becomes thinner.

1009
Q

What type of bacteria is Helicobacter pylori (H. pylori)?

A

A curved, gram-negative bacillus.

1010
Q

Why is H. pylori often described as “triple positive”?

A

Because it is catalase, oxidase, and urease positive.

1011
Q

What is a key pathogenic mechanism of H. pylori?

A

It uses flagella for motility.

1012
Q

What conditions are associated with H. pylori infection?

A

Acute and chronic gastritis, peptic ulcers, gastric adenocarcinoma, and MALT lymphoma.

1013
Q

What is the standard treatment for H. pylori infection?

A

Triple therapy consisting of a proton pump inhibitor (PPI), clarithromycin, and either amoxicillin or metronidazole.

1014
Q

hat should be done after initial treatment of H. pylori?

A

Repeat testing is indicated, as the initial therapy is only about 80% effective.

1015
Q

What is a concerning sign if ulcers do not resolve with H. pylori treatment?

A

It may indicate gastric malignancy.

1016
Q

Does H. pylori have a type III secretion system?

A

No, it does not; this system is found in some other gram-negative rods like E. coli, Salmonella, and Shigella.

1017
Q

Is H. pylori a lactose-fermenting bacteria?

A

No, H. pylori does not ferment lactose.

1018
Q

Which gram-negative rods are known to ferment lactose?

A

E. coli, Enterobacter, Klebsiella, Citrobacter, and Serratia species.

1019
Q

From where does the gastroduodenal artery most commonly arise?

A

The common hepatic artery.

1020
Q

What is a significant complication of a posterior duodenal ulcer?

A

Bleeding due to erosion into the gastroduodenal artery.

1021
Q

What are the branches of the gastroduodenal artery?

A

The retroduodenal artery, right gastroepiploic artery, and superior pancreaticoduodenal artery.

1022
Q

What does the gastroduodenal artery supply blood to?

A

The pylorus and proximal duodenum, and indirectly to the pancreatic head.

1023
Q

The proper hepatic artery is also a branch of the common hepatic artery, and branches to the

A

Right and left hepatic arteries.

1024
Q

Where does the left gastric artery run, and what does it anastomose with?

A

It runs along the lesser curvature of the stomach and anastomoses with the right gastric artery

1024
Q

What are the three main branches of the celiac trunk?

A

Left gastric artery, splenic artery, and common hepatic artery.

1025
Q

What is a common cause of bleeding from the left gastric artery?

A

Perforated gastric ulcers.

1026
Q

What does the splenic artery supply, and what branches does it give off?

A

It runs along the greater curvature of the stomach and gives off short gastric branches that supply the fundus and upper part of the greater curvature.

1027
Q

What are gastric varices, and what condition can cause them?

A

Gastric varices result from dilation of the short gastric vessels, often caused by cirrhosis and portal hypertension.

1028
Q

What is the role of the superior mesenteric artery (SMA)?

A

It supplies the gut distal to the ampulla of Vater, through the mid-transverse colon.

1029
Q

What arteries are branches of the superior mesenteric artery?

A

Inferior pancreaticoduodenal artery, right colic artery, middle colic artery, and ileocolic artery.

1030
Q

What type of cancer comprises approximately 95% of gastric cancers?

A

Gastric adenocarcinoma.

1031
Q

What are common symptoms of gastric adenocarcinoma?

A

Weight loss, abdominal pain, and early satiety.

1032
Q

What is Virchow’s node, and what does its presence indicate?

A

Virchow’s node is an enlarged left supraclavicular lymph node, and its presence may indicate gastric adenocarcinoma.

1033
Q

What is a Sister Mary Joseph’s nodule?

A

A palpable periumbilical nodule that may indicate metastatic gastric cancer.

1034
Q

What is the five-year survival rate for localized gastric adenocarcinoma?

A

Approximately 95%.

1035
Q

What is the five-year survival rate for metastatic gastric adenocarcinoma?

A

Approximately 15%.

1036
Q

What are nitrosamines, and where can they be found?

A

Nitrosamines, such as N-Nitrosodimethylamine (NDMA), are found in preserved meats, cheeses, and are components of tobacco.

1037
Q

What are important risk factors for gastric adenocarcinoma?

A

H. pylori infection, smoking, obesity, and consumption of nitrosamines.

1038
Q

Is a risk factor for angiosarcoma of the liver, a rare but highly malignant tumor.

A

Polyvinyl chloride

1039
Q

Is a risk factor for adenocarcinoma of the stomach.

A

Type A blood

1040
Q

Which are produced by Aspergillus species, are a risk factor for hepatocellular carcinoma.

A

Aflatoxins

1041
Q

Chewing tobacco is a risk factor for

A

oral-pharyngeal squamous cell carcinoma.

1042
Q

Achalasia is a risk factor for

A

esophageal squamous cell carcinoma.

1043
Q

Although NSAIDs may cause gastritis and peptic ulcers, these drugs have never been associated with gastric cancer.

A

In fact, some studies have found a decreased risk (“protective effect”) of gastric cancer among patients that take NSAIDs.

1044
Q

What is Ménétrier’s disease?

A

A form of hypertrophic gastropathy characterized by hyperplasia of mucous cells and excessive gastric mucous secretion.

1045
Q

What physiological change occurs in Ménétrier’s disease that leads to achlorhydria?

A

Excessive gastric mucous secretion neutralizes gastric acid.

1046
Q

What is “protein-losing enteropathy” and how is it related to Ménétrier’s disease?

A

A condition where proteins are lost in the stool due to improper protein breakdown, leading to total-body protein depletion.

1047
Q

What are the clinical manifestations of hypoalbuminemia in Ménétrier’s disease?

A

Lower-extremity edema and facial swelling.

1048
Q

In which demographic is Ménétrier’s disease more commonly found?

A

More common in men (3:1 ratio), typically between ages 30 and 60.

1049
Q

What endoscopic or imaging finding is characteristic of Ménétrier’s disease?

A

Striking enlargement of gastric folds, often seen on endoscopy or abdominal imaging.

1050
Q

How does Ménétrier’s disease affect the gastric antrum?

A

Ménétrier’s disease usually spares the antrum.

1051
Q

What is the risk associated with Ménétrier’s disease?

A

An increased risk of gastric adenocarcinoma.

1052
Q

What is the main consequence of protein-losing nephropathies?

A

They lead to proteinuria and are a significant renal cause of hypoalbuminemia.

1053
Q

Name some examples of protein-losing nephropathies.

A

Acute poststreptococcal glomerulonephritis, rapidly progressive glomerulonephritis, IgA nephropathy (Berger’s disease), Alport’s syndrome, and membranoproliferative glomerulonephritis.

1054
Q

What condition is associated with duodenal ulcers and characterized by excess gastric acid?

A

Zollinger-Ellison syndrome.

1055
Q

What is linitis plastica?

A

A variant of diffuse gastric cancer characterized by thickened and rigid gastric walls.

1056
Q

How does linitis plastica differ from most gastric cancers regarding Helicobacter pylori?

A

It is not associated with Helicobacter pylori infection or chronic gastritis.

1057
Q

What is a key pathological finding in linitis plastica?

A

The presence of signet ring cells.

1058
Q

Linitis plastica, also known as ? is a variant of diffuse gastric cancer characterized by thickened and rigid gastric walls.

A

Brinton’s disease or “leather bottle stomach,”

1059
Q

What are Curling’s ulcers?

A

They are stomach ulcers that occur in the setting of extensive burn injuries.

1060
Q

What causes Curling’s ulcers?

A

Skin damage from burns leads to fluid volume loss, decreased plasma volume, gastric mucosal ischemia, and necrosis.

1061
Q

How is the treatment for Curling’s ulcers primarily approached?

A

Treatment involves fluid resuscitation to maintain adequate perfusion.

1062
Q

What is the primary mechanism behind stress ulcers?

A

Ischemia due to under-perfusion of the stomach, often seen in shock, sepsis, and trauma.

1063
Q

What are Cushing’s ulcers, and what causes them?

A

Cushing’s ulcers result from increased intracranial pressure, leading to increased vagal tone.

1064
Q

What is the primary mechanism of NSAID-induced gastritis?

A

Decreased prostaglandin synthesis, which leads to increased acid production and loss of mucus and bicarbonate production.

1065
Q

What is acalculous cholecystitis?

A

A type of acute cholecystitis that occurs without the presence of gallstones.

1066
Q

In which patient population is acalculous cholecystitis commonly seen?

A

It is often seen in critically ill patients due to gallbladder ischemia and bile stasis.

1067
Q

What is biliary sludge?

A

Thickened bile that forms due to bile stasis in the gallbladder.

1068
Q

What is the preferred treatment for acalculous cholecystitis in unstable patients?

A

Drainage via a percutaneous cholecystostomy.

1069
Q

Why might patients with acalculous cholecystitis be too unstable for surgery?

A

Critical illness often leads to overall instability, making surgical procedures risky.

1070
Q

What are black stones, and what causes them?

A

Black stones are pigmented gallstones composed of unconjugated bilirubin, caused by increased bilirubin secretion (hemolysis) or decreased bilirubin excretion (cirrhosis).

1071
Q

What conditions are associated with brown stones?

A

Brown stones are often found in conditions of infected bile, typically in settings of infection or sepsis.

1072
Q

What is the most common type of gallstone?

A

Cholesterol stones are the most common type of gallstones.

1073
Q

What are some risk factors for cholesterol gallstones?

A

Risk factors include female gender, pregnancy or history of multiple pregnancies, obesity, rapid weight loss, and impaired bile salt synthesis/resorption.

1074
Q

What condition is indicated by gallbladder findings on hospital day 4 in a critically ill patient?

A

Gallbladder sludge (acalculous cholecystitis) is the likely explanation for gallbladder findings in this context.

1075
Q

What causes bile duct strictures?

A

Bile duct strictures can occur due to neoplasia (cholangiocarcinoma, pancreatic adenocarcinoma) or autoimmune conditions (e.g., primary biliary cholangitis, sclerosing cholangitis).

1076
Q

What is ascending cholangitis?

A

Ascending cholangitis is a life-threatening infection of the biliary tract that can lead to septic shock and death.

1077
Q

What is the typical treatment for ascending cholangitis?

A

Treatment involves fluid resuscitation, antibiotics, and biliary drainage, usually via endoscopic retrograde cholangiopancreatography (ERCP).

1078
Q

What are the most common causative organisms of ascending cholangitis?

A

The most common organisms are gastrointestinal flora, particularly gram-negative rods like Klebsiella pneumoniae and Enterobacter.

1079
Q

Why is it important to treat for anaerobes in ascending cholangitis?

A

Obstruction and ischemia create a hypoxic environment, making anaerobic bacteria significant contributors to infection.

1080
Q

What are common antimicrobial regimens for treating ascending cholangitis?

A

Common regimens include ceftriaxone or ciprofloxacin (for gram-negative rods) and metronidazole (for anaerobes), or a single broad-spectrum agent.

1081
Q

A rare cause of ascending cholangitis is ?, a helminth found in infected fish. Blood work in these cases will show eosinophilia. Praziquantel is the drug of choice for treatment. Although this woman ate sushi recently, her neutrophil-predominant leukocytosis indicates bacterial infection, not helminth infection.

A

Clonorchis sinensis (Chinese liver fluke)

1082
Q

Chronic infection of the biliary tree with a virus can be seen in the setting of AIDS due to infection with ?. This is rarely seen in the modern era with widespread use of antiretroviral therapy.

A

Cytomegalovirus (CMV)

1083
Q

What does the X-ray finding of calcification along the perimeter of the gallbladder indicate?

A

This finding is known as “porcelain gallbladder,” associated with chronic gallbladder inflammation.

1084
Q

What symptoms may be associated with porcelain gallbladder?

A

Patients may be asymptomatic or present with right upper quadrant abdominal pain, and occasionally a palpable mass.

1085
Q

What complications can arise from common bile duct stones in patients with porcelain gallbladder?

A

Complications include jaundice, fever, cholangitis, or pancreatitis.

1086
Q

Why is porcelain gallbladder concerning in elderly patients?

A

It indicates an increased risk of gallbladder carcinoma, which is a rare cancer with a poor prognosis.

1087
Q

What causes chronic gallbladder inflammation that can lead to porcelain gallbladder?

A

Prolonged, untreated gallstone disease or chronic infection with Salmonella typhi, particularly in endemic regions.

1088
Q

Which countries are known for high rates of Salmonella typhi gallbladder infections?

A

Endemic areas include South American countries like Chile, Bolivia, Ecuador, and Asian countries like India, Pakistan, Japan, and Korea.

1089
Q

What is choledocholithiasis?

A

Choledocholithiasis is the presence of a gallstone in the common bile duct (CBD) that obstructs bile flow into the duodenum.

1090
Q

What are the clinical signs of choledocholithiasis?

A

Signs include jaundice (yellowing of the skin and sclera), dark urine, and elevated serum bilirubin.

1091
Q

How does choledocholithiasis affect liver function tests?

A

It leads to elevated serum alkaline phosphatase due to obstruction of bile flow, but it typically does not cause severe liver failure or elevated INR.

1092
Q

What major causes of acute liver failure are associated with elevated INR?

A

Major causes include acetaminophen toxicity and ischemic hepatitis.

1093
Q

What ultrasound findings would be expected in a case of acute pancreatitis?

A

Ultrasound would show an enlarged pancreas with heterogeneous tissue due to edema.

1094
Q

What is ascending cholangitis, and how does it present?

A

Ascending cholangitis is an infection of the bile duct that presents with Charcot’s triad: jaundice, right upper quadrant pain, and fever.

1095
Q

What is Reynolds’ pentad?

A

Reynolds’ pentad includes Charcot’s triad plus hypotension and altered mental status, indicating severe sepsis.

1096
Q

What is pneumobilia?

A

Pneumobilia is the presence of air in the biliary tree, often indicated by radiologic findings.

1097
Q

What condition is associated with pneumobilia and intestinal obstruction?

A

Gallstone ileus, which occurs when a gallstone erodes into the bowel, causing obstruction.

1098
Q

How does gallstone ileus develop?

A

It typically occurs after chronic cholecystitis leads to the formation of a fistula between the gallbladder and the small intestine, allowing gallstones to enter the intestines.

1099
Q

Which part of the intestine is most commonly obstructed in gallstone ileus?

A

The ileum, as it is the narrowest section of the intestines.

1100
Q

What clinical findings are consistent with gallstone ileus?

A

Evidence of intestinal obstruction (nausea, vomiting, abdominal fullness, lack of bowel movements) combined with pneumobilia.

1101
Q

What does “ileus” mean?

A

“Ileus” refers to a lack of movement of the intestines.

1102
Q

How does gallstone ileus occur?

A

A large gallstone erodes into the bowel, causing intestinal obstruction and forms a fistula between the bowel and bile ducts.

1103
Q

In what condition does gallstone ileus typically occur?

A

Gallstone ileus generally occurs in the setting of chronic cholecystitis.

1104
Q

Why does gallstone ileus happen in the ileum?

A

The ileum is the narrowest section of the intestines; a large stone that cannot pass through leads to obstruction.

1105
Q

Why might pneumobilia be present after ERCP or biliary surgery?

A

It is a normal consequence of the procedure and typically resolves on its own.

1106
Q

What are other causes of pneumobilia?

A

Mesenteric ischemia, gastric ulcers, diverticulitis, or post bowel surgery.

1107
Q

What might a woman’s history of recurrent abdominal pain suggest in relation to gallstone ileus?

A

It may indicate untreated gallstone disease that has led to gallstone ileus.

1108
Q

What is primary sclerosing cholangitis (PSC)?

A

PSC is an autoimmune disorder of the biliary tree associated with ulcerative colitis, characterized by immune-mediated fibrosis

1109
Q

What happens to the bile ducts in PSC?

A

Immune-mediated fibrosis leads to narrowing (stenosis) or obliteration of the bile ducts, causing dilation behind these areas.

1110
Q

What is the classic imaging finding in PSC?

A

Numerous intra- and extra-hepatic bile duct strictures, often described as “beads on a string” or a “chain of lakes.”

1111
Q

How many patients with PSC are asymptomatic at diagnosis?

A

Up to half of patients with PSC may be asymptomatic at the time of diagnosis.

1112
Q

What are the most common symptoms of PSC?

A

Fatigue and pruritus are the most common symptoms.

1113
Q

What rare symptoms may occur due to cholestasis in PSC?

A

Symptoms like jaundice and dark urine may occur due to impaired bile flow.

1114
Q

What does pathology reveal in patients with PSC?

A

Pathology typically shows periductal fibrosis of the bile ducts.

1115
Q

What is the risk associated with PSC?

A

Patients with PSC are at increased risk of cholangiocarcinoma and should be screened every 6-12 months.

1116
Q

What are the treatment options for PSC?

A

Treatment options include endoscopic stenting and liver transplant.

1117
Q

How is autoimmune hepatitis often discovered?

A

It is often found incidentally through blood work showing transaminitis (increased ALT and AST).

1118
Q

Is autoimmune hepatitis typically acute or chronic?

A

Autoimmune hepatitis is a chronic disease.

1119
Q

Does autoimmune hepatitis commonly progress to cirrhosis?

A

It rarely progresses to cirrhosis.

1120
Q

What is the hallmark of diagnosis for autoimmune hepatitis?

A

The presence of anti-smooth muscle antibodies is the hallmark for diagnosis.

1121
Q

Primary biliary cholangitis (PBC; also called primary biliary cirrhosis) is an autoimmune disorder of the biliary tree. It typically affects middle-aged women and presents with symptoms consistent with biliary obstruction, including fatigue, pruritis, pale stools, jaundice, and bilirubinuria. Lab findings include elevated AST, ALT, total bilirubin, and direct bilirubin. Markedly elevated alkaline phosphatase is a classic finding.

A

PBC is distinguished from PSC by imaging. In PBC, there is no extrahepatic bile duct obstruction. The serum hallmark of diagnosis is presence of anti-mitochondrial antibodies. PBC patients often have additional autoimmune disorders such as Sjögren’s syndrome. Serum lipids can be markedly elevated (>1,000). Ursodeoxycholic acid is the only effective pharmaceutical agent for this disease. The definitive treatment is liver transplant.

1122
Q

Is a clinical feature of many disorders of cholestasis (obstructed bile flow). Itching is a classic feature of primary biliary cirrhosis where it occurs in up to 80% of patients, but may also occur in other biliary disorders including PSC.

A

Itching (pruritus)

1123
Q

Is characterized by a long history of intermittent right upper quadrant pain, nausea, and vomiting. Left untreated, it can increase the risk of gallbladder carcinoma.

A

Chronic cholecystitis

1124
Q

What is primary biliary cholangitis (PBC)?

A

PBC is an autoimmune disease of the biliary tree, also known as primary biliary cirrhosis.

1125
Q

Who is typically affected by PBC?

A

PBC primarily affects middle-aged women.

1126
Q

What are common symptoms of PBC?

A

Symptoms include fatigue, pruritus, pale stools, jaundice, and bilirubinuria.

1127
Q

What laboratory findings are indicative of PBC?

A

Elevated transaminases (AST and ALT), total and direct bilirubin, and markedly elevated alkaline phosphatase.

1128
Q

How is PBC distinguished from primary sclerosing cholangitis?

A

PBC shows no extrahepatic bile duct obstruction on imaging.

1129
Q

What is the serum hallmark for diagnosing PBC?

A

The presence of anti-mitochondrial antibodies.

1130
Q

What does a liver biopsy reveal in PBC?

A

A dense lymphocytic infiltrate with granulomatous inflammation, known as a “florid duct lesion.”

1131
Q

What characterizes late-stage PBC?

A

Late disease is characterized by direct hyperbilirubinemia.

1132
Q

Why might a patient have normal bilirubin levels in early PBC?

A

Normal bilirubin levels indicate that the disease is relatively mild at that point.

1133
Q

Hepatic fibrosis is characteristic of cirrhosis. This patient’s presentation does not fit cirrhosis. She has no history of chronic liver disease or alcohol use. Also, AST and ALT are often normal or even decreased in cirrhosis because the normal hepatic parenchyma has been replaced by fibrous tissue. Key lab findings in cirrhosis include

A

Low platelets, decreased albumin, and elevated prothrombin time and INR.

1134
Q

Are eosinophilic intracytoplasmic inclusions in hepatocytes that occur in alcoholic hepatitis.

A

Mallory bodies

1135
Q

What are classic features of ulcerative colitis?

A

Abdominal pain, bloody diarrhea, fatigue, weight loss, arthralgias, and a family history of gastrointestinal disease.

1136
Q

What is the “lead pipe” appearance in X-ray imaging?

A

A smooth colon with a lack of haustra, typically seen in chronic ulcerative colitis.

1137
Q

What lab findings are consistent with primary sclerosing cholangitis?

A

Elevations in AST and ALT in a ~1:1 pattern, along with elevated alkaline phosphatase and total bilirubin.

1138
Q

What percentage of patients with PSC have coexisting inflammatory bowel disease?

A

The majority, most commonly ulcerative colitis.

1139
Q

What symptoms indicate a patient with ulcerative colitis may have PSC?

A

Evidence of cholestasis such as hyperbilirubinemia, jaundice, and elevated alkaline phosphatase.

1140
Q

What antibodies are found in up to 80% of patients with PSC?

A

Perinuclear antineutrophil cytoplasmic antibodies (p-ANCAs).

1141
Q

What conditions are associated with p-ANCA antibodies?

A

Ulcerative colitis (without PSC), microscopic polyangiitis, crescentic glomerulonephritis, and rheumatoid arthritis.

1142
Q

What imaging study should be performed to confirm the diagnosis of PSC?

A

A cholangiogram to image the biliary tree.

1143
Q

What does a cholangiogram typically show in PSC?

A

Numerous strictures and dilatations of the extrahepatic bile ducts.

1144
Q

Are a diagnostic marker of primary biliary cholangitis

A

Anti-mitochondrial antibodies

1145
Q

Occur in granulomatosis with polyangiitis (formerly known as Wegener’s granulomatosis).

A

Cytoplasmic antineutrophil cytoplasmic antibodies (c-ANCAs)

1145
Q

Occur in autoimmune hepatitis.

A

Anti-smooth muscle antibodies

1146
Q

Anti-double-stranded DNA antibodies are highly specific for

A

Systemic lupus erythematosus

1147
Q

What is biliary atresia?

A

A congenital abnormality of the biliary ducts where the biliary tree fails to develop or develops abnormally.

1148
Q

What are common signs of cholestasis in infants with biliary atresia?

A

Hyperbilirubinemia, dark urine, and pale (“acholic”) stools.

1149
Q

What is the appearance of vomitus in a baby with biliary atresia?

A

Non-bilious vomitus (clear to light yellow), as bile is absent in the intestinal lumen.

1150
Q

What is a classic finding on a cholangiogram in biliary atresia?

A

Failure to visualize the biliary tree, indicating it is not present.

1151
Q

How might the gallbladder appear in biliary atresia?

A

The gallbladder may be absent or have an irregular shape.

1152
Q

What is the etiology of biliary atresia?

A

Biliary atresia is idiopathic, meaning its exact cause is unknown.

1153
Q

What is the surgical management for biliary atresia?

A

The Kasai procedure, which aims to restore bile flow.

1154
Q

Does not result in absence of one or more lobes of the liver, as it affects the biliary tract itself and not the surrounding liver parenchyma.

A

Biliary atresia

1155
Q

A blind jejunal pouch is consistent with jejunal atresia. This is associated with ?use during pregnancy.

A

Maternal cocaine

1156
Q

Is consistent with renal hypoplasia.

A

A shrunken kidney at birth

1157
Q

What is autoimmune hepatitis (AIH)?

A

AIH is an inflammatory liver condition that primarily affects women in their forties and fifties.

1158
Q

How is AIH often discovered?

A

AIH is often asymptomatic and identified through incidental findings of elevated AST and ALT on blood work.

1159
Q

What can AIH lead to if left untreated?

A

It can lead to chronic liver disease and, rarely, cirrhosis.

1160
Q

What are key diagnostic criteria for AIH?

A

Presence of antinuclear antibodies (ANA) and anti-smooth muscle antibodies (ASMA), which are specific for type I AIH.

1161
Q

How does type 2 AIH differ from type 1?

A

Type 2 AIH is often ASMA negative and is far less common than type 1.

1162
Q

What is the management for acute episodes of AIH?

A

Management typically involves steroids and immunosuppressants.

1163
Q

Are highly specific for systemic lupus erythematosus (SLE) and are believed to be implicated in the pathogenesis of lupus nephritis.

A

Anti-double stranded DNA antibodies

1164
Q

Are specific for CREST syndrome

A

Anti-centromere antibodies

1165
Q

Are associated with drug-induced lupus. Common drugs implicated include procainamide, penicillamine, isoniazid, and methyldopa.

A

Anti-histone antibodies

1166
Q

Are found in patients with anti-phospholipid syndrome, a hypercoagulable state that causes thrombosis in arteries and veins. It causes a number of pregnancy-related complications, including miscarriage, stillbirth, preterm delivery, and preeclampsia.

A

Anti-cardiolipin antibodies

1167
Q

What is a pyogenic liver abscess?

A

A walled-off infection of the liver.

1168
Q

What is the most likely etiology of a pyogenic liver abscess in a patient with diverticulitis?

A

Seeding of the portal venous system with bacteria from diverticulitis.

1169
Q

What are the common causative organisms of a pyogenic liver abscess?

A

Enteric flora, including gram-negative rods like E. coli and Klebsiella pneumoniae.

1170
Q

Why are gram-positive cocci like Staphylococcus aureus and Staphylococcus epidermidis unlikely causes of liver abscess?

A

They generally do not lead to intra-abdominal infections except in the setting of abdominal surgery.

1171
Q

What role do mycobacteria, such as tuberculosis, play in liver abscess formation?

A

They are a rare cause of liver abscess, unlikely in patients with recent diverticulitis.

1172
Q

Are spirochetes like Treponema pallidum common causes of liver infection?

A

No, they are very rare causes of liver infection and unlikely in this patient.

1173
Q

What is acute alcoholic hepatitis?

A

Hepatitis occurring in the setting of acute binge drinking in individuals with a history of alcohol-use disorder.

1174
Q

What are common symptoms of acute alcoholic hepatitis?

A

Right-upper-quadrant abdominal pain, fever, and jaundice.

1175
Q

What is the pathophysiology of acute alcoholic hepatitis?

A

It is caused by the toxic effects of acetaldehyde, a metabolic by-product of alcohol.

1176
Q

How does acetaldehyde affect hepatocytes?

A

Acetaldehyde damages intermediate filaments within hepatocytes.

1177
Q

What is the classic histopathological finding in acute alcoholic hepatitis?

A

The presence of “Mallory bodies,” which are cytoplasmic inclusions within hepatocytes representing damaged intermediate filaments.

1178
Q

In alcoholic liver disease, nuclei may be pushed aside by fat accumulation with cells, but nuclear abnormalities are

A

Not a classic feature of alcoholic hepatitis.

1179
Q

An overabundance of microtubules can be seen in cardiac myocytes in patients with

A

Hypertrophic cardiomyopathy.

1180
Q

Structural and functional alterations of the Golgi apparatus are seen in several neurodegenerative, diseases including

A

Amyotrophic lateral sclerosis (ALS), Parkinson’s disease, Alzheimer’s dementia, and Huntington’s disease

1181
Q

In ?, AAT builds up in the endoplasmic reticula of hepatocytes. AAT polymers can be seen on periodic acid-Schiff (PAS) staining of hepatocytes of affected individuals.

A

Alpha-1 antitrypsin (AAT) deficiency

1182
Q

What is Budd-Chiari syndrome?

A

A rare condition caused by hepatic vein thrombosis.

1183
Q

What are common clinical features of Budd-Chiari syndrome?

A

Abdominal pain, ascites, and hepatomegaly.

1184
Q

What does Doppler imaging show in Budd-Chiari syndrome?

A

Obstruction in the outflow of the hepatic vein.

1185
Q

What underlying conditions are associated with Budd-Chiari syndrome?

A

Hepatocellular carcinoma, polycythemia vera, and hypercoagulable states.

1186
Q

What structures make up the portal triad in the liver?

A

A single bile duct, hepatic artery, and portal vein.

1187
Q

How is the liver organized in terms of zones?

A

Zone I (periportal zone), Zone II (midzone), and Zone III (centrilobular zone).

1188
Q

How does blood flow through the liver zones?

A

Blood from the portal vein and hepatic artery moves from Zone I to Zone III, draining into the hepatic vein.

1189
Q

What occurs in Zone III during hepatic vein thrombosis?

A

Backflow of blood leads to congestion and subsequent hepatic necrosis in Zone III.

1190
Q

What other conditions can affect Zone III of the liver?

A

Ischemic insult from shock liver, fatty infiltration in alcoholic liver disease, and fibrosis in cirrhosis.

1191
Q

What is hepatic cirrhosis?

A

A condition characterized by liver fibrosis with loss of normal liver architecture and function.

1192
Q

What are common etiologies of cirrhosis?

A

Alcoholic liver disease, viral hepatitis, autoimmune conditions (autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis).

1193
Q

What physiological functions does cirrhosis impair?

A

The liver’s ability to perform synthetic functions, such as producing albumin and clotting factors.

1194
Q

What would serum albumin levels be in a patient with cirrhosis?

A

Serum albumin would be decreased.

1195
Q

How does cirrhosis affect clotting factors?

A

Reduced levels of clotting factors prolong prothrombin time (PT), partial thromboplastin time (PTT), and international normalized ratio (INR).

1196
Q

What is the status of Factor VIII levels in chronic liver disease?

A

Factor VIII levels are usually normal or increased.

1197
Q

Where is Factor VIII synthesized?

A

It is synthesized by hepatic sinusoidal endothelial cells and also by endothelial cells in other organs (kidney, spleen, lungs, brain).

1198
Q

What other factor is synthesized outside the liver?

A

von Willebrand factor (VWF) is also synthesized by endothelial cells outside the liver.

1199
Q

What is Wilson’s disease?

A

An autosomal recessive disorder of copper metabolism characterized by impaired copper transport and excretion in bile.

1200
Q

What gene is mutated in Wilson’s disease?

A

The ATP7B gene on chromosome 13.

1201
Q

What is the role of the ATP7B protein?

A

It incorporates copper into ceruloplasmin and transports copper into bile for excretion.

1202
Q

What are the consequences of impaired ATP7B function?

A

Accumulation of copper in the liver and other organs, leading to free radical production and tissue damage.

1203
Q

What is a Kayser-Fleischer ring?

A

A pathological hallmark of Wilson’s disease, representing corneal copper deposits along Descemet’s membrane at the limbus of the eye.

1204
Q

What neurological symptoms are associated with Wilson’s disease?

A

Ataxia and difficulty speaking due to copper accumulation in the brain.

1205
Q

How does total body copper levels compare to normal in Wilson’s disease?

A

Total body copper is increased, but the majority is trapped in organs.

1206
Q

What do liver biopsy specimens show in Wilson’s disease?

A

Increased copper content.