Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MHD2 > Block 7 (GI) - L1 to L3 > Flashcards

Block 7 (GI) - L1 to L3 Flashcards

1
Q

True or false - the tongue and the major salivary glands are part of the oral cavity.

A

False - the major salivary glands are NOT part of the oral cavity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The ___ protects the airway during swallowing to avoid aspiration.

A

Epiglottis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 3 major exocrine salivary glands (in order from largest to smallest) and what do they secrete?

A
  1. Parotid
  2. Submandibular
  3. Sublingual

Saliva (enzymes + mucus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the composition of the saliva secreted from each of the 3 major glands.

A
  1. Parotid: purely serous
  2. Submandibular: mixed (serous>mucinous)
  3. Sublingual: mixed (mucinous>serous)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The parotid gland drains via the ___ duct.

A

Stensen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

The submandibular gland drains via the ___ duct.

A

Wharton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

The sublingual gland drains via the ___ ducts, which terminate in the submandibular duct.

A

Bartholin and Rivunus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What comprises the salivary unit?

A

Acinus and draining duct system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which of the salivary glands is the only one to have intraparenchymal lymph nodes?

A

Parotid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is sialadenitis?

A

Inflammation of the salivary glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Discuss acute sialadenitis.

A

Typically caused by an ascending bacterial infection (S. aureus, S. viridans) and secondary to sialolithiasis and reduced saliva flow.

Typically unilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are obstructive causes of chronic/recurrent sialadenitis?

A
  1. Stenosis
  2. Chronic sialolithiasis
  3. Mucus retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are non-obstructive causes of chronic/recurrent sialadenitis?

A

Sjogren’s syndrome, sarcoidosis, TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the symptoms of sialadenitis?

A
  1. Swelling and pain in the affected gland
  2. Fever (acute)
  3. Dry mouth
  4. Fibrosis leading to a hard salivary gland
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the most common cause of acute, painful bilateral parotid swelling?

A

Mumps sialadenitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What population is most affected by mumps?

A

Children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What causes mumps?

A

Paramyxovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are conditions associated with mumps?

A

Orchitis (can lead to sterility), pancreatitis, or aseptic meningitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

___ is elevated when the salivary gland or pancreas is involved in mumps.

A

Serum amlyase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the treatment for mumps?

A

Supportive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the most common benign salivary gland neoplasm?

A

Pleomorphic adenoma (60% of parotid, submandibular, and minor salivary gland neoplasms)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Discuss the epidemiology of pleomorphic adenoma.

A

Adults: F>M, peaks in 4th/5th decades

Children (5-15): M>F

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Describe the tumor of a pleomorphic adenoma.

A

Painless, slow-growing, well-circumscribed mass

Composed of glandular/ductal epithelial structures and myoepithelial cells with variable morphology present within a mesenchymal stroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is a pleomorphic adenoma treated?

A

Surgical excision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the second most common benign salivary gland tumor (most commonly involving the parotid gland)?

A

Warthin tumor (papillary cystadenoma lymphomatosum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the appearance of a Warthin tumor.

A

Biphasic tumor composed of bilayered oncocytic cells forming cysts and papillary fronds within a dense lymph node-like stroma (tram track)

Cyst fluid is brown and viscous, like used motor oil

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Discuss the epidemiology of the Warthin tumor.

A

M>F, 6th and 7th decades

Smoking is an associated etiologic factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How is a Warthin tumor treated?

A

Surgical excision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the most common malignant salivary gland tumor in children and adults?

A

Mucoepidermoid carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Discuss the epidemiology of mucoepidermoid carcinoma.

A

F>M (mean age - 47)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Describe the composition of a mucoepidermoid carcinoma.

A

Painless, fixed, slow-growing mass

Mucus cells, intermediate cells, and epidermoid cells with variable cystic/solid components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the treatment for a mucoepidermoid carcinoma?

A

Surgical excision +/- neck dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What prevents reflux of gastric contents and acid back into the esophagus?

A

Lower esophageal sphincter (LES)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe the different mucosa in the esophagus and the stomach.

A

Esophagus: squamous mucosa

Stomach: glandular mucosa

Separated by GEJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the layers of the esophagus?

A
  1. Epithelium
  2. Lamina propria
  3. Submucosa
  4. Muscularis mucosa
  5. Muscularis externa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is atresia?

A

Rare congenital defect composed of a discontinuous segment of esophagus associated with a terminal blind pouch proximally and a lower blind pouch distally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is typically associated with atresia?

A

Fistula between the trachea and the lower discontinuous segment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How does a baby with atresia present?

A

Regurgitation shortly after birth with poor feeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are complications of atresia?

A

Aspiration +/- pneumonia, paroxysmal suffocation, and fluid/electrolyte disturbances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is achalasia?

A

Failure of the LES to relax due to degeneration of the myenteric plexus with muscle denervation and increase LES resting tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the symptoms of achalasia?

A

Odynophagia

Impaired peristalsis with progressive dysphagia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is seen when a Barium swallow is done to detect achalasia?

A

“Bird’s beak” deformity and proximal dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the etiology of achalasia?

A

Unknown, but autoimmune or viral etiologies are suspected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are some causes of secondary achalasia?

A
  1. Trypanosoma cruzi infection (Chagas disease)
  2. Mass effect from extraesophageal tumors
  3. Diabetes, sarcoidosis, amyloidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Achalasia is associated with an increased risk of ___.

A

Carcinoma (especially squamous cell carcinoma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is scleroderma?

A

Autoimmune mediated chronic connective tissue disorder; can be localized or systemic (two types of systemic - CREST or systemic sclerosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the symptoms of CREST?

A
  1. Calcinosis (calcium deposits in skin)
  2. Raynaud’s phenomenon (spasm of blood vessels in response to cold or stress)
  3. Esophageal dysfunction (acid reflux and decrease in motility of esophagus)
  4. Sclerodactyly (thickening and tightening of the skin on the fingers and hands)
  5. Telangiectasis (dilation of capillaries causing red marks on the surface of the skin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What GI involvement is seen in scleroderma?

A
  1. Progressive dysphagia due to damage of esophageal tissues and fibrosis; can lead to acid reflux and secondary Barrett’s
  2. Aspiration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is Plummer-Vinson Syndrome?

A

Triad of dysphagia, iron deficiency anemia, and esophageal webs; +/- glossitis and stomatitis/angular cheilitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the epidemiology of Plummer-Vinson Syndrome?

A

Rare, typically affects middle-aged women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is a hiatal hernia?

A

Herniation of the GEJ and/or proximal stomach into the chest cavity as a result of the separation or widening of the diaphragmatic crura

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the cause of a hiatal hernia?

A

Exact cause unknown, but thought to be associated with increased abdominal pressure (obesity, pregnancy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the two types of hiatal hernia?

A
  1. Sliding: GEJ and proximal stomach are pulled up into the mediastinal space
  2. Rolling: proximal stomach herniates through the crura
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are complications of a hiatal hernia?

A

Strangulation/obstruction +/- perforation, bleeding, GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is a Mallory-Weiss tear?

A

Longitudinal mucosal lacerations or tears occuring at the GEJ in association with severe retching and vomiting (people with bulimia and alcohol use disorder)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is a predisposing factor for a Mallory-Weiss tear?

A

Hiatal hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is Boerhaave Syndrome?

A

Distal esophageal transmural rupture in association with violent retching

58
Q

What can be seen on CT in Boerhaave Syndrome?

A

Pneumomediastinum (air in the mediastinum), sometimes a hemomediastinum - this is a surgical emergency

59
Q

What are esophageal varices?

A

Dilated submucosal veins in the lower 1/3 of the esophagus, GEJ, and proximal stomach; appear as mucosal bumps on endoscopy

60
Q

What causes esophageal varices?

A

Portal HTN leads to diversion of portal blood flow through the veins of the stomach and into the plexus of the lower esophageal veins

61
Q

Esophageal varices are common in patients with ___.

A

Cirrhosis

62
Q

What are some causes of esophagitis?

A
  1. GERD
  2. Infection (fungal, HSV, CMV)
  3. Eosinophilic Esophagitis
  4. Other (ingestion of caustics, pills/medications, chemo)
63
Q

What are the general symptoms of esophagitis?

A
  1. Chest pain/heartburn (retrosternal burning pain)
  2. Dysphagia (difficulty swallowing)
  3. Odynophagia (pain with swallowing)
  4. Hematemesis
  5. Coughing and hoarseness
64
Q

What is GERD and what are its causes?

A

Reflux of gastric acid contents into the esophagus, leading to mucosal inflammation and injury

  1. Incompetent LES
  2. Hiatal hernia
  3. Delayed gastric emptying/increased gastric volume
65
Q

What are complications of GERD?

A
  1. Ulcerations and bleeding

2. Barrett’s esophagus

66
Q

What is seen on histology in GERD?

A
  1. Variable inflammation
  2. Basal cell hyperplasia
  3. Elongation of vascular papillae
67
Q

How does fungal esophagitis appear?

A

Limited to the epithelium, appears at white mucosal plaques

68
Q

How does esophagitis with Herpes simplex virus appear?

A

Virus vesicles form in the epithelium, squamous cell becomes infected, can also cause ulcers in the subepithelial layers

69
Q

How does esophagitis with CMV appear?

A

Deep linear ulcers, infecting deeper stromal or vascular endothelial cells, viral “owl eye nuclear inclusions”

70
Q

What are the three M’s of HSV esophagitis?

A
  1. Multinucleation of cells
  2. Molding of nuclei
  3. Margination of chromatin
71
Q

What is eosinophilic esophagitis?

A

Formation of esophageal rings and linear furrows +/- white mucosal discolorations due to chronic inflammation secondary to food allergen exposure

72
Q

What are typical causes of pill esophagitis?

A

NSAID’s, bisphosphanates, antibiotics, potassium

73
Q

What is Barrett’s Esophagus?

A

Complication of long-standing GERD; chronic acid reflux injury leads to intestinal metaplasia

74
Q

Discuss the epidemiology of Barrett’s Esophagus.

A

Occurs in ~10% of symptomatic patients, 40-60 y/o, M>F

75
Q

Describe the gross and histologic appearance of Barrett’s Esophagus.

A

Gross: salmon colored metaplastic epithelium
Histology: intestinal metaplasia and goblet cell metaplasia

76
Q

Barrett’s Esophagus is the single most important risk factor for ___.

A

Adenocarcinoma

77
Q

What is the most common benign esophageal tumor?

A

Leiomyoma

78
Q

What are the molecular abnormalities associated with squamous cell carcinoma?

A
  1. p53 point mutations

2. P16/INK4a mutation

79
Q

Describe the histology of squamous cell carcinoma.

A

Infiltrating islands of malignant squamous cells, keratin pearls, abnormal keratinization

80
Q

Where does esophageal squamous cell carcinoma tend to occur? Adenocarcinoma?

A

Sq: proximal 2/3 of esophagus
Ac: distal 1/3 of esophagus + GEJ

81
Q

What are some mutations associated with adenocarcinoma?

A
  1. p53
  2. Amplification of c-ERB-B2, cyclin D1, cyclin E
  3. RB gene
  4. Allelic loss of cyclin dependent kinase inhibitor p16/INK4a
  5. Hypermethylation of p16/INK4a
  6. Increased epithelial expression of TNF and NF-kB

(Stepwise)

82
Q

What is omphalocele?

A

Persistent herniation of the bowel into the umbilical cord COVERED by peritoneum and amnion of cord - failure of abdominal wall to return to body cavity during development

83
Q

What is gastroschisis?

A

Malformation of abdominal wall causing exposure of abdominal contents, not covered by peritoneum

84
Q

What is pyloric stenosis?

A

Congenital hypertrophy of smooth muscle of pylorus

85
Q

How does pyloric stenosis present?

A

Projectile vomiting in first 2-6 weeks of life, visible peristalsis, olive-like mass in abdomen

86
Q

Pyloric stenosis is more common in ___ (M or F).

A

Males

87
Q

What is the pH of the stomach?

A

1

88
Q

What are the 4 parts of the stomach?

A
  1. Cardia
  2. Fundus
  3. Body
  4. Antrum
89
Q

What are the cells contained in each of the 4 parts of the stomach?

A
  1. Cardia - foveolar cells
  2. Fundus and Body -
    parietal cells and chief-cells
  3. Antrum - G-cells and mucin-secreting cells
90
Q

What is the differential diagnosis of upper abdominal pain?

A
  1. Gastritis
  2. Peptic ulcer disease
  3. GERD
  4. Biliary colic
  5. IBS
  6. Pancreatitis
91
Q

What are the symptoms of gastritis?

A
  1. Nausea
  2. Epigastric pain
  3. Vomiting
  4. Hematemesis
92
Q

What are the normal damaging forces in the stomach?

A
  1. Gastric acidity

2. Peptic enzymes

93
Q

What are the normal defensive forces in the stomach?

A
  1. Surface mucus secretion
  2. Bicarbonate secretion into mucus
  3. Mucosal blood flow
  4. Apical surface membrane transport
  5. Epithelial regenerative capacity
  6. Elaboration of prostaglandins
94
Q

What are possible injuries to the stomach?

A
  1. H. pylori infection
  2. NSAIDs
  3. Aspirin
  4. Cigarettes
  5. Alcohol
  6. Gastric hyperacidity
  7. Duodenal-gastric reflux
95
Q

What are possible causes of impaired defenses in the stomach?

A
  1. Ischemia
  2. Shock
  3. Delayed gastric emptying
  4. Host factors
96
Q

What causes stress-related gastric injury?

A

Local ischemia in patients with critical illness/injury

97
Q

What are three examples of stress-related gastric injury?

A
  1. Stress ulcers (patients in shock, sepsis, severe trauma)
  2. Curling ulcers
  3. Cushing ulcers
98
Q

What are Curling ulcers?

A

Ulcers located in the proximal duodenum, seen in patients with severe burns or trauma

99
Q

What are Cushing ulcers?

A

Ulcers located in the stomach, duodenum, or esophagus, seen in patients with intracranial disease

100
Q

Describe the features of acute gastritis.

A

Transient process involving nausea, vomiting, and epigastric pain.

Superficial, erosive, ulcerative, may have hemorrhage

Often an impairment of protective systems (NSAIDs, ingestion, direct injury)

101
Q

How is acute gastritis treated?

A

Stress ulcer prophylaxis with PPI or H2 blockers in at-risk patients

Treatment with acid blocking agents

Treat underlying condition

102
Q

What are the features of chronic gastritis?

A

Similar symptoms as acute, but hematemesis is uncommon

Symptoms less severe, but more persistent

Most common cause is H. pylori infection; other causes include autoimmune, radiation injury, chronic bile reflux, mechanical injury

103
Q

How is H. pylori visualized?

A
  1. Methylene blue stain

2. Warthin-Starry silver stain

104
Q

H. pylori is a Gram ___ bacteria.

A

Negative

105
Q

What are the four modes of virulence of H. pylori?

A
  1. Flagella
  2. Secretion of urease
  3. Adhesins
  4. Toxins
106
Q

How is infection with H. pylori treated?

A

PPI + antibiotics

107
Q

How is chronic gastritis caused by autoimmune processes different from that caused by H. pylori?

A

Autoimmune - spares the antrum

H. pylori - primarily affects the antrum

108
Q

What happens in autoimmune chronic gastritis?

A

Ab to parietal cells and IF lead to Vitamin B12 deficiency (and pernicious anemia), as well as decreased pepsinogen I levels (due to loss of chief cells). This leads to impaired gastric acid secretion (achlorhydria). Gastrin release increases and antral G cells undergo hyperplasia.

109
Q

What are the symptoms of peptic ulcer disease?

A

Epigastric burning or aching pain occurring 1-3 hours after eating, worse at night, relieved by alkali or food; may also have nausea, bloating, belching

110
Q

What are the most common causes of peptic ulcer disease?

A

H. pylori or NSAIDs

111
Q

Where is peptic ulcer disease most common in the body?

A

Proximal duodenum and antrum

112
Q

Food ___ pain with duodenal ulcers; pain ___ with gastric ulcers.

A

Decreases; increases

113
Q

How is peptic ulcer disease treated?

A

Eradicate H. pylori, remove offending agent, surgery for bleeding or perforation

114
Q

What is the key issue in peptic ulcer disease?

A

Gatric hyperacidity

115
Q

What is Zollinger-Ellison Syndrome?

A

Multiple ulcerations in GI tract due to hypersecretion of gastrin by a tumor

116
Q

What are other risk factors for peptic ulcer disease?

A

NSAIDs, smoking, high-dose corticosteroids, alcoholic cirrhosis, COPD, chronic renal failure, hyperparathyroidism, psychological stress

117
Q

What are the 5 common neoplasms of the stomach?

A
  1. Gastric polyps
  2. GIST
  3. Lymphoma
  4. Carcinoid tumor
  5. Gastric adenocarcinoma
118
Q

What is a polyp?

A

Nodule or mass that projects above the level of the surrounding mucosa, due to hyperplasia, inflammation, ectopia, or neoplasia

119
Q

Which type of polyp makes up 75% of polyps?

A

Inflammatory and hyperplastic polyps

120
Q

Which type of polyp occurs more in males (versus evenly in M/F)?

A

Gastric adenoma

121
Q

Which type of polyp has no neoplastic potential?

A

Fundic gland polyp

122
Q

Where are fundic gland polyps located? Gastric adenomas?

A

Fundic gland polyp: body and fundus

Gastric adenoma: antrum

123
Q

How does gastric adenoma appear on histology?

A

Intestinal-type epithelium with variable degrees of dysplasia

124
Q

Which polyp is sporadic or associated with familial adenomatous polyposis?

A

Fundic gland polyp

125
Q

Carcinoid tumors arise from neuroendocrine tumors; in the stomach, they arise from ___.

A

G-cells

126
Q

Location determines the prognosis of a carcinoid tumor - which location is most aggressive?

A

Midgut

127
Q

What is a GIST (gastrointestinal stromal tumor)?

A

Mesenchymal neoplasm of the interstitial cells of Cajal (pacemaker cells of gut peristalsis)

128
Q

75-80% of people with GIST have a gain-of-function mutation in the gene encoding ___.

A

Tyrosine kinase c-KIT

129
Q

How is GIST treated?

A

Surgical resection if possible + Imatinib (inhibits tyrosine kinase activity); resistance to this drug does exist

130
Q

Where is gastric adenocarcinoma most common in the world?

A

Eastern Asia

131
Q

What are the early and late symptoms of gastric adenocarcinoma?

A

Early: nausea, dyspepsia, dysphagia

Late: weight loss, anorexia, bowel habit changes, anemia, hemorrhage

132
Q

What are risk factors for gastric adenocarcinoma?

A
  1. Geography
  2. Low SES
  3. Multifocal mucosal atrophy and intestinal metaplasia in the setting of chronic gastritis
  4. History of partial gastrectomy for PUD
  5. Blood type A
133
Q

What are some causes of gastric adenocarcinoma?

A
  1. H. pylori infection
  2. Epstein Barr Virus
  3. Mutations of CHD1 causing loss of E-cadherin function and mutations in APC genes (familial adenomatous polyposis)
134
Q

What are the 2 categories of gastric adenocarcinoma in the Lauren classification?

A
  1. Intestinal

2. Diffuse

135
Q

Describe the structure and epidemiology of intestinal gastric adenocarcinoma.

A

Bulky, glandular structures, exophytic mass or ulcerated tumor

Mean age 55, M>F (2:1), incidence higher in high-risk areas

136
Q

Describe the structure and epidemiology of diffuse gastric adenocarcinoma.

A

Infiltrative growth, discohesive cells with large mucin vacuoles (signet ring cells)

Linitis plastica (gross)

M=F, incidence the same regardless of geography

137
Q

What is a Virchow node?

A

Metastatic gastric adenocarinoma in the left supraclavicular node

138
Q

What is a common location of distant metastases of gastric adenocarcinoma?

A

Liver

139
Q

What is a Sister Mary Joseph nodule?

A

Metastatic gastric adenocarinoma in the periumbilical region (intestinal type)

140
Q

What is a Krukenberg tumor?

A

Metastatic gastric adenocarinoma in bilateral ovaries (diffuse type)

MHD2 (34 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions