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USMLE GAME TIME > GI - Pictures > Flashcards

GI - Pictures Flashcards

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USMLE® Step 1 flashcards
1
Q
A

Barrett’s esophagus

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2
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Squamous cell carcinoma of the esophagus

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3
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Signet cell adenocarcinoma

This is a signet ring cell pattern of adenocarcinoma in which the cells are filled with mucin vacuoles that push the nucleus to one side, as shown at the arrow.

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4
Q

What kind of cancer is stomach cancer?

A

Almost always adenocarcinoma

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5
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Normal intestinal villi

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6
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Celiac sprue - note the villous atrophy

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7
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The images show the characteristic feature of Whipple’s disease; foamymacrophages are present in the lamina propria.

I honestly don’t know what I’m looking at here. …

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8
Q

What will the villi look like in lactase deficiency?

A

Normal

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9
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MALT lymphoma

[MALT LYMPHOMA, COLON]. Colon is the 2nd most common site, after stomach, to be involved by non-Hodgkin lymphoma and B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) is the most common primary non-Hodgkin lymphoma in this location. This photomicrograph shows MALT lymphoma extending from mucosa (top arrow) to the subserosa (bottom arrow). Extensive mural involvement may cause colonic perforation and present as acute abdomen.

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10
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MALT lymphoma

[MALT LYMPHOMA, COLON]. Note the lymphoid infiltrate piercing through the muscularis mucosa (thin long arrow). The bulk of the tumor is in the submucosa (big arrow). By definition, MALT lymphoma is thought to arise from mucosa-associated lymphoid tissue wherever they are found. In colon abundant mucosa-associated lymphoid tissue is present including benign lymphoid follicles.

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11
Q
A

MALT lymphoma

Note heavy plasma cell infiltrate in the mucosa and a predominant lymphocyte infiltrate in the submucosa. The muscularis mucosa is disrupted and overrun by neoplastic lymphoid infiltrate. Benign lymphoid infiltrate generally respect normal anatomical boundaries but neoplastic infiltrates show aggressive behavior without regard to normal architecture.

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12
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[MALT LYMPHOMA, COLON]. Note back-to-back neoplastic lymphoid follicles with expanded marginal zones in this image. Normally, lymphoid follicles are separated by a population of interfollicular T-cells. The germinal centers might get overrun by neoplastic marginal zone B-cells and may leave only nodules.

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13
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[BARRETT’S METAPLASIA]. Barrett’s metaplasia of esophagus is defined as replacement of the normal squamous epithelium of distal esophagus by metaplastic glandular epithelium containing intestinal-type goblet cells. Note the squamous epithelium on the left (arrowhead) is continuous with the metaplastic epithelium containing goblet cells (long thin arrow) on the right. The transition is shown by downward arrow on the top.

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14
Q
A

Whipple’s disease

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15
Q

replacement of the normal squamous epithelium of distal esophagus by metaplastic glandular epithelium containing intestinal-type goblet cells

A

Barrett’s esophagus

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16
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[ADENOCARCINOMA, SIGNET-RING CELL TYPE]. Gastric adenocarcinoma of the signet-ring cell type is one of the most elusive malignancies histologically, especially when the tumor burden is low. These tumors grossly appear flat or excavating and may permeate full-thickness into the wall. Microscopically, diffuse growth pattern and presence of chronic inflammatory cells and hitiocytes may mask the individual tumor cells (lower arrowhead). It takes an eye of suspicion and vigilance to identify cases with low tumor cell burden in between normal gastric glands (top arrow).

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17
Q
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Gastric signet ring adenocarcinoma

I honestly can’t see the signet rings in this picture though.

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18
Q

This picture isn’t appearing in full for some reason

A

… this doesn’t really have a question but seemed a useful picture

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19
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There is seen plenty of mononuclear inflammatory cells in the mucosa of large intestine. In addition, round granulomas (*) in the mucosa are visible. In addition, there can be granulomas on the other wall layers. 40x magnification, HE-staining.

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20
Q
A

There is hemorrhage in the mucosa of large intestine and the surface is ulcerated. The gland ducts are doformated by inflammation.In the lamina propria plenty of inflammatory cells. 40x magnification, HE-staining.

Ulcerative colitis

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21
Q
A

ULCERATIVE COLITIS (COLITIS ULCEROSA) 100X

There is hemorrhage in the mucosa of large intestine and the surface is ulcerated. The gland ducts are doformated by inflammation.In the lamina propria plenty of inflammatory cells. 40x magnification, HE-staining.

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22
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A

Stomach layers

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23
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Normal jejunum

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24
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Colon histology

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25
Q
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Stomach histology

26
Q

**

A

Again, just seemed like a useful picture

27
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Duodenum histology

28
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A

More duodenum histology

29
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A

Jejunum histology

30
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More jejunum histology

31
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Colon histology

32
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A

More colon histology

33
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A

Anao-rectal junction

34
Q

Macroscopically visible, crescent-shaped folds of the mucosa and submucosa which extend around one-half to two-thirds of the circumference of the lumen of the small intestine.

A

Plicae circulares

are permanent structures, i.e. their presence does not depend on the state of distension of the small intestine.

are absent from the first few centimetres of the duodenum and the distal part of the ileum.

Are particularly well developed in the jejunum.

increase the surface area of the mucosa by a factor of ~ three.

35
Q

Occur most frequently in the neck of the glands, where they reach the lumen of the gland. They are situated deeper, between and below chief cells, in lower parts of the gland.

A

Parietal cells secrete the hydrochloric acid of the gastric juice. Aside from activating the pepsinogen the hydrochloric acid also effectively sterilizes the contents of the stomach.

36
Q

The most numerous of the four types of cells in the stomach. They occur primarily in the body of the glands. They produce pepsinogen, which is a precursor of the proteolytic enzyme pepsin.

A

Chief cells

37
Q
A
38
Q
A

Gastroschis

39
Q
A

Omphalocele

40
Q
A

Apple peel atresia

Jejunal, ileal, colonic atresia due to vascular accident.

41
Q
A

Double bubble sign associated with duodenal atresia

42
Q

M cells

A

Specialized cells in Peyer’s patches, found in lamina propria and submucosa of the ileum. Present antigens to immune cell.s

Selectively endocytose antigens, transport them to macrophages and lymphocytes which migrate to lymph nodes.

43
Q
A

Gastric antral vascular ectasia (GAVE) is an uncommon cause of chronic gastrointestinal bleeding or iron deficiency anemia.[1][2][3] The condition is associated with dilated small blood vessels in the antrum, or the last part of thestomach.[1] The dilated vessels result in intestinal bleeding.[4] It is also calledwatermelon stomach because streaky long red areas that are present in the stomach may resemble the markings on watermelon

GAVE is characterized by dilated capillaries in thelamina propria with fibrin thrombi.

44
Q
A

Micrograph of a tubular adenoma (left of image), a type of colonic polyp and a precursor of colorectal cancer. Normal colorectal mucosa is seen on the right of the image.

45
Q
A

Villous adenoma - note the long finger like villi

46
Q
A

Apple core lesion

On the left side, cancers are more likely to infilrate the intestinal wall and encircle the lumen.

47
Q
A

Porcelain gallbladder - calcified gallbladder due to chronic cholecystitis. Treat with prophylactic cholecystectomy due to high rates of gallbladder carcinoma

48
Q
A

Mallory bodies are highly eosinophilic and thus appear pink on H&E stain. The bodies themselves are made up of intermediate keratin filament proteins that have been UBIQUINATED, or bound by other proteins such as heat shock proteins, or p62.

49
Q
A

Menetrier’s disease - gastric hypertrophy with protein loss, parietal cell atrophy, and increased mucou cell. Precancerous. Rugae of the stomach are so hypertrophied that they look like brain gyri.

50
Q

Menetrier’s disease - more details

A

Menetrier’s disease

Note the giant rugal folds.

Patients lose protein in the mucus secretions.

Hyperplasic gastropathy

Increased proliferation of mucus-producing cells => huge rugal folds!

Increased mucus prod. => protein loss from excessive gastric secretions

Consequences: hypoalbuminemia, edema

51
Q
A

Herniation proximal to cricopharyngeus.

Occur due to cricopharyngeal muscle dysfunction (weakness)

False diverticulum = herniation of mucosa and submucosa through muscular layer

52
Q

![Cronic Hepatitis (>6 months)
Hep B => ground glass hepatocytes (black arrows)

Persitent: inflammation confined in portal tracts
Active: inflammation in parenchima](http://38.media.tumblr.com/83fb719ae60856b5474c35e1fa477b6c/tumblr_mhomgjTpdl1rsdqvqo1_400.jpg)

A

Ground glass hepatocytes, associated with Hep B

53
Q
A

Councilman bodies, associated with acute viral hepatitis

These are apoptotic hepatocytes

54
Q
A

Primary sclerosing cholangitis with onion skin fibrosis

55
Q
A

Primary sclerosing cholangitis

56
Q

GI Tract

INNERVATION

A

Intrinsic: Auerbach & Meissner Plexus (*)

Extrinsic: Autonomic Parasympathetic (stimulatory: sensory fibers) & Sympathetic (inhibitory: pain fibers)

(*) mutation of neural crest cells, affects its migration into the gut, hence no Auerbach or Meissner plexus => HIRSCHPRUNG DISEASE

57
Q
A

Hirschprung’s baby

58
Q

A transmural (affecting all layers of the bowel wall), dense infiltration of lymphocytes and macrophages; presence of granulomas in up to 60% of patients; fissuring ulceration and submucosal fibrosis (see left-hand figure).

A
59
Q

Inflammation affects superficial (mucosal) layers with infiltration of lymphocytes and granulocytes and loss of goblet cells. Presence of ulcerations and crypt abscesses (see right-hand figure).

A
60
Q

Liver blood flow

A

Blood flow into thee liver: 75% PORTAL VEIN, 25% Hepatic Artery

Blood flow out of the liver: Hepatic Veins + IVC

61
Q

**

A

Liver zones

62
Q

*

A

Liver portal triad

USMLE GAME TIME (46 decks)

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