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NYCC Visceral Pathology > Lab 6&7 Gastrointestinal Pathologies > Flashcards

Lab 6&7 Gastrointestinal Pathologies Flashcards

1
Q

What is an Achalasia?

A

“failure to relax” lower esophageal sphincter

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2
Q

What is an Esophageal Web/Ring?

A

concentric, smooth, thin (3-5mm) extension of normal esophageal tiss. into lumen (all 3 layers)

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3
Q

What pathology is the loss/absence of ganglion cells in the esophageal myenteric plexus assocaited with?

A

Achalasia

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4
Q

what features are visualized on a barium swallow for Achalasia?

A
  • megaesophagus: widened esophagus: absent peristalsis = food retention
  • “birds beak”/”rat tail” deformity: tonic contraction of pyloric sphincter
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5
Q

what are the clinical features of an Achalasia?

A
  • odynophagia (pain swallowing)
  • regurgitation (tends after meals
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6
Q

what is the etiology of an Esophageal Web/Ring?

A

often idiopathic, but predisposing factors include:
- Plummer-Vinson Syndrome: severe iron deficiency
- autoimmune/inflammatory disorders

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7
Q

what is the preferential location of Esophageal Rings?

A

usually distal esophagus (but anywhere along esophagus)

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8
Q

what diet is prescribed to those with an Esophageal Web?

A

gradullay convert to semi-solid, followed by liquid diets

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9
Q

what are the clinical features of an Esophageal Ring?

A
  • asymptomatic
  • Intermintent dysphagia
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10
Q

What condition may be visualized on a upper GI biopsy sample in a patient with chronic heartburn?

A

Barrett Esophagus

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11
Q

what is the normal epithelia of the esophagus?

A

stratified squamous

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12
Q

what gross characteristics would be visualized at the gastro-esophageal jct. in a patient with Barrett Esophagus?

A

columnar epithelium creeps upward above the GE jct. (normally a straight line)

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13
Q

what is Barrett Esophagus? what are the cellular events?

A

columnar metaplasia of the esophagus:
- stratified squamous epithelium replaced w/ simple columnar epithelium w/ goblet cells

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14
Q

what is the etiology of Barrett Esophagus?

A

gastroesophageal reflux

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15
Q

why is treatment of Barrett Esophagus important?

A

it’s a risk factor for Adenocarcinoma

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16
Q

what cellular events occur in Barrett Esophagus as GERD continues?

A

dysplastic cell changes:
- decrease goblet cells
- ^hyperchromatic cells
- hyperplasia

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17
Q

what histological feature is indicative of the malignant transformation of Barrett Esophagus into frank Adenocarcinoma?

A

invasive glands deep to basement membrane (“fern-leaf” glandular pattern)

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18
Q

what is a potentially disastrous complication of ^portal venous hypertension?

A

Esophageal Varices

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19
Q

what is the gross view of Esophageal Varices?

A

dilated veins on the external surface of the esophagus

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20
Q

massively dilated veins often accompany what pathology?

A

Liver Cirrhosis

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21
Q

what is the etiology of portal vein hypertension?

A

Hepatic Cirrhosis (alcoholism)

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22
Q

what is the pathogenesis of Chronic Hepatic Cirrhosis?

A

alcoholism -> hemochromatosis (build up iron) -> extensive scarring

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23
Q

what is a clinical feature of Esophageal Varices?

A

massive hematemesis (vomit blood)

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24
Q

why does massive hematemesis create a high mortality statistic for Esophageal Varices?

A
  • high % develop fatal bleed = Hypovolemic shock
  • those who survive often re-bleed w/in 1 yr w/ same mortality rate
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25
Q

massively dilated veins below the mucosa are prone to ____.

A

rupture & hemorrhage into the lumen

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26
Q

what feature of Liver Cirrhosis makes Esophageal Varices especially fatal?

A

hypofunctioning liver can’t produce clotting factors (vomit blood)

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27
Q

what is the pathogenesis of Mallory-Weiss Tear/Syndrome?

A
  • a single episode of severe retcing results in sudden ^intra-esophageal pressure
  • mechanically tears the gastro-esophageal jct. = small linear fissure of lower esophagus
  • trend toward minor anemia
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28
Q

what population is Mallory-Weiss Syndrome seen in?

A

alcoholics

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29
Q

what pathology is demonstrated in a patient who feels ill and has an episode of vomiting that resembles “coffee grounds”

A

Acute Gastritis

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30
Q

tiny hemorrhages seen in an edoscope of Acute Gastritis are termed ____.

A

small petechial hemorrhages

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31
Q

what are the etiologies of Acute Gastritis?

A
  • infection
  • insult
  • NSAIDs
  • overindulgence of alcohol/caffeine
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32
Q

what is the MC etiology of Chronic Gastritis? what is another etiology of this condition/

A
  • Helicobacter Pylori MC
  • Autoimm. destruction of gastric parietal cells (in stomach body & fundus)
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33
Q

what are the clinical features of Chronic Gastritis?

A
  • mucosal atrophy w/ intestinal metaplasia
  • achlorhydria w/ ^gastrin & antral G-cell hyperplasia
  • lack of intrinsic factor = megaloblastic (pernicious) anemia
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34
Q

what pathology does Chronic Gastritis predisope an individual to?

A

^risk of gastric adenocarcinoma (intestinal type)

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35
Q

what are the 2 locations of Peptic Ulcers? which is MC?

A
  • Gastric Ulcer (stomach)
  • Duodenal Ulcer MC (1st part / distal to pyloric sphincter)
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36
Q

what is the MC etiology of Peptic Ulcer disease?

A

Helicobacter Pylori MC

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37
Q

describe the appearance of a Gastric Ulcer.

A

rugae surrounding lesion

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38
Q

what are the characteristic clinical features of Gastric Ulcers?

A

symptomatic w/:
- mere contemplation of food (added hylochloric acid)
- immediately after eating
- aversion to food
- weight loss

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39
Q

what are the characteristic clinical features of Duodenal Ulcers?

A
  • symptomatic relief immediately after eating (produce bicarbonate)
  • ^symptoms 2-3 hours after eating
  • snacking (constant bicarbonate production)
  • weight gain
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40
Q

what feature of Gastric Ulcers can be visualized on and endoscope?

A

zone of hyperemia surrounding lesion

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41
Q

what event can result in a Gastric Ulcer surgical emergency?

A

ulcer can borrow thru mucosa, submucosa, & deeper = perforation (uncommon)

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42
Q

what is visualized on a microscopic preperation of an Ulcer?

A

epithelia loss extending into submucosa + muscularis externa (punched out area)

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43
Q

what are the 2 types of Gastric Carcinomas?

A

both adenocarcinomas:
- intestinal type
- diffuse type

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44
Q

what is the preferential location of Intestinal type Gastric Carcinomas?

A

lesser curvature of the stomach

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45
Q

what is the gross appearance of Diffuse type Gastric Carcinomas?

A

Linitis Plastica “Leather Bottle”
- overall thickening of stomach wall w/o stretch during digestion

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46
Q

how is Diffuse adenocarcinoma of the stomach unlike typical adenocarcinomas

A
  • Signet-Ring appearance (rather than glandular)
  • invade submucosal & muscular layers of the stomach
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47
Q

what is the histological appearance of Intestinal type adenocarcinoma?

A

glandular “fern leaf” pattern

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48
Q

a patient presents w/ change in eating habits as well as conspicuous weight loss, biopsy would most likely reveal ___.

A

Diffuse or Intestinal type Adenocarcinomas

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49
Q

what is the etiology of Diffuse adenocarcinoma of the stomach?

A

bacterial infection leads to peptic ulcer disease + neoplasm

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50
Q

how would an Intestinal type adenocarcinoma present grossly?

A

ulceration of gastric mucosal
- result of tumor growth
- central zone of necrosis
- bleeding ulcerated area surrounded by raised lesion

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51
Q

biopsy of Intestinal type adenocarcinoma would most likely display what?

A

glandular epithelium of mucosa extending throughout deeper layers

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52
Q

invasion of glands strongly suggests ____

A

Gastric adenocarcinoma

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53
Q

what condition is characterized by mucosal changes that occur in longstanding inability to tolerate wheat-containing foods?

A

Celiac disease

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54
Q

what is Celiac disease?

A

production of Ab against wheat proteins (hypersensitivity)

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55
Q

what immunoglobulin is generated & deployed at the intestinal mucosa in Celiac disease?

A

IgA

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56
Q

describe the histological mucosal changes that occur in Celia disease.

A

inflammatory reaction in small intestine:
- loss of microvilli brush border
- infiltration of many plasma cells

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57
Q

what are the normal characteristics of intestinal mucosa?

A
  • microvilli brush border (nutrient absorption)
  • simple columnar epithelium
  • normal intraepithelial lymphocytes
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58
Q

what clinical features will present in an individual w/ Celiac disease?

A
  • pain
  • gas
  • bloating
  • weight loss
  • Dermatitis Herpetiformis
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59
Q

what is the cutaneous complication of Celiac disease?

A

Dermatitis Herpetiformis:
- IgA immune complexes deposit in skin creates vesicular pattern in non-dermatomal fashion

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60
Q

cutaneous depostion resulting in a dermatomal vesicular pattern is associated w/ what condition?

A

Herpes Voster infection (chicken pox)

61
Q

cutaneous depostion resulting in a non-dermatomal vesicular pattern is associated w/ what condition?

A

Celiac disease

62
Q

A hospitalized 57-year-old male is in declining health. An alcoholic for 25 years, his skin has taken on a yellowish cast. His abdomen is distended and demonstrates dilated per umbilical veins and has had his abdomen aspirated three times to reduce pressure on his organs. Marked bilateral pitting edema can be seen on his lower extremities. Immediately following lunch he feels a searing pain in the lower part of his chest. He also begins to feel as though his “stomach is expanding”, and he feels nauseated. He begins to gag and vomits an enormous amount of blood. He manages to press the nurse call button next to his bedside prior to losing consciousness.
A. what is responsible for the dilated priumbilical veins, distended abdomen, & bilateral pitting edema?
B. where is blood originating?

A

A. Cirrhosis of the Liver
B. Ruptured Esophageal Veins

63
Q

what pathology is often called “left-sided appendicitis”?

A

Diverticulosis

64
Q

histologically what lesions are found in Diverticulosis?

A

diverticula (outpouchings)

65
Q

what is the preferential location of Diverticulosis outpouchings?

A

anywhere along GI tract, but very common in distal colon, specifically Sigmoid colon

66
Q

outpouchings of Diverticulosis are prone to ____ + ____.

A

obstruction + inflammation

67
Q

what is the etiology of Diverticulosis?

A

interplay btwn diet & genetics

68
Q

what dietary restriction would you place your Diverticulosis patient on?

A
  • eliminate nuts & seeds
  • ^fiber intake
69
Q

patient presents with excruciating lower-right quadrant abdominal pain, what is this area called?

A

McBurney’s Point

70
Q

McBurney’s point pain is a clinical feature of what condition?

A

Acute Appendicitis

71
Q

what are the clinical features of Acute Appendicitis?

A
  • extreme lower R. quadrant pain (McBurney’s point pain)
  • reflex tenderness
  • ^WBC (>35000 in some cases)
  • fever
  • nausea + vomitting
72
Q

what is a common etiology of McBurney’s point pain? what might this lead to?

A

fecalith impaction obstructs the lumen of the appendix
- leads to microbial overgrowth & potential perforation

73
Q

an infant with a dilated sigmoid colon may present with what clinical symptoms? how is this assessed?

A

inability to pass meconium (fetal feces)
- assessed w/in first 24hrs postnatally thru passing of meconium

74
Q

a pediatric barium study shows massively dilated sigmoid (distal) colon. what condition is most likely?

A

Hirschsprung’s Disease

75
Q

a congenital absence of myenteric ganglia leading to an area of aperistalsis in the colon is associated with what coedition?

A

Hirschsprung’s disease

76
Q

inflammatory infiltrate is seen spanning the entire thickness of the gut wall in what disease?

A

Chron’s Disease

77
Q

what is the preferential location of Chron’s disease?

A

predilection to terminal ileum, can appear anywhere along GI

78
Q

what term is given for the histological appearance of Chron’s disease? what are the characteristics of this appearance?

A

Transmural inflammation
- basophilic cell patches along entire cross-section thickness of intestinal wall, including mucosa + submucosa

79
Q

“skip lesions” are characteristic of what pathology? what are skip lesions?

A

Chron’s Disease
- may leave parts of the GI intact

80
Q

which condition has a higher incidence of neoplastic trasnformation and why?
- Chron’s disease or Ulcerative Colitis

A

Ulcerative Colitis
- chronic inflammation w/in unique area of gut leads to successive ulcerations
- ulcerative healing = ^mucosal cell turnover = ^colon cancer incidence

81
Q

what charcteristics of Ulcerative Colitis make it’s gut involvement more predicatble?

A
  • exclusively starts at distal colon, moving proximally
  • inflammation limited to mucosa, sometimes submucosa
  • Crypt abscesses
82
Q

areas of neutrophils occupying intestinal crypts of Lieberkuhn are visulaized histologically in what condition?

A

Ulcerative Colitis

83
Q

what are crypt abscesses?

A

neutrophils occupying intestinal crypts of Lieberkuhn

84
Q

describe the progression of the adenoma-carcinoma sequence.

A

Benign: hyperproliferation -> small adenomatous polyps -> large adenomatous polyps -> severe dysplasia (pre-cancerous polyp) ->
Malignant: adenocarcinoma -> cancer

85
Q

a colonoscopy visualizes a mass connected to the colon wall via a stalk. what is this termed?

A

Solitary Polyp (pedunculated)

86
Q

what is fAPC?

A

familial adenomatous polyposis coli
- inheritance of a non-functional allele of the APC gene

87
Q

what is the APC gene?

A

tumor supressor gene which is the only exception to the two-hit hypothesis

88
Q

Numerous Polyps visualized on a colonoscopy are most commonly due to what?

A

fAPC MC

89
Q

how would you describe the histological appearance of a (solitary) colon polyp?

A

well-defined glandular architecture confined to the epithelia

90
Q

numerous well-differentiated glands throughout a histological view of a polyp is indicative of ____.

A

Benign adenoma

91
Q

colonoscopy shows an ill-defined mass obstructing the lumen, what is this termed? what pathology is suspected? what additional finding could also be visualized on a colonoscopy to confirm your suspicion?

A

“napkin-ring” lesion: L. sided colon carcinoma
- spontaneous hemorrhaging of the mass is common in Colon Cancer

92
Q

what are the conspicuous signs of an individual presenting with L. sided colon carcinoma?

A
  • “napkin ring” lesion
  • decreased stool caliber
  • lower L. quadrant pain
  • blood-streaked stool
93
Q

blood streaked stool could present in a patient whose colonoscopy displays what characteristic?

A

a spontaneously hemorrhaging napkin-ring lesion

94
Q

the general rule in elderly patients is that cancer must be ruled out in those w/ ____ that are also co-presenting w/ ____

A
  • iron deficient anemia
  • hematochezia/hematuria
95
Q

what is Hematochezia?

A

bright red blood in stool

96
Q

what is hematuria?

A

blood in urine

97
Q

what are the conspicuous signs of an individual presenting with R. sided colon carcinoma?

A
  • raised lesion
  • iron deficiency anemia (occult bleeding)
  • vague pain
98
Q

bleeding in the GI tract that is not visible can be due to ___. what condition is this a sign of?

A

iron deficiency anemia (occult bleeding) = R. sided colon carcinoma

99
Q

histologically, Invasive adenocarcinom of the colon will show what?

A

abnormal glands deep to the submucosa of the colon wall

100
Q

intracellular accumulations w/in the parenchyma of the liver are found in what conditions?

A
  • Hemochromatosis
  • Steatosis of the liver
101
Q

what will be visualized in a histological Prussian blue staining of Hemochromatosis?

A

hemosiderin granules w/in hepatocytes

102
Q

what will be visualized in a histological Hematoxylin + Eosin (H&E) staining of Hemochromatosis?

A

rusty brown clusters of granules w/in hepatocytes

103
Q

what are the potential complications of Hemochromatosis?

A

long-term excess iron favors free radical production, damaging hepatocytes =
- Cirrhosis +/or
- Hepatocellular carcinoma

104
Q

what is “fatty liver disease” termed?

A

Steatosis of the liver

105
Q

what are accumulations composed of in Hemochromatosis?

A

abnormal iron deposition w/in tissues

106
Q

what are accumulations composed of in Steatosis of the liver?

A

intracellular fatty acid (FA) accumulation

107
Q

what is the etiology of Hemochromatosis?

A

autosomal dominant disease
- other conditions: multiple blood transfusions, excess medicinal iron intake

108
Q

what is the etiology of Steatosis of the liver?

A

excess alcohol consumption MC
- also possible: hypoxia & certain toxins

109
Q

what characteristic histological appearance is visualized in Steatosis of the liver?

A

peripheral nucleus indicating fat accumulation

110
Q

what is the gross appearance of Fatty Liver disease?

A

normally fleshy red-brown liver takes on a more yellow appearance due to ^fat

111
Q

what is a possible consequence of iron or fat accumulations in the liver?

A

Cirrhosis

112
Q

describe the histologically appearance of liver cirrhosis that is visualized using trichrome staining.

A
  • bridging fibrous septa disrupt normal hepatic lobular architecture (function decreases)
  • hepatocytes w/in remaining lobules are not uniform in color, some appear more pale due to atrophy
113
Q

how would Cirrhosis be visualized grossly?

A

fine, diffuse, CT-filled nodular appearance of lesions throughout the liver’s surface

114
Q

what is a dark brown ring in the iris termed?

A

Kayser-Fleischer ring

115
Q

yellow discoloration of the sclera is seen in what condition?

A

Jaundice (Cirrhosis of the liver)

116
Q

Kayser-Fleischer ring is seen in what condition?

A

Wilson’s disease

117
Q

what deficit is characteristic of Hepatolenticular disease?

A

Ceruloplasmin - a copper-excreting protein

118
Q

what is Wilson’s disease?

A

abnormal, toxic levels of Copper (Cu) deposition in body tissue

119
Q

Kayser-Fleischer ring is will co-resent w/ what?

A

Parkinson’s traits

120
Q

Wilson’s disease is also known as ____.

A

Hepatolenticular disease

121
Q

how would you differentiate between Hepatobiliary conditions & endocrine conditions?

A

observe eyes in context of skin pigmentation changes
- endocrine conditions may cause skin coloration changes such as in Addison’s disease

122
Q

what may cause yellow discolorated body secretions such as tears and glandular products?

A

Hyperbilirubinemia

123
Q

Hyperbilirubinemia may result in what presentation?

A

Jaundice

124
Q

what are the risk factors of Cholelithiasis?

A

four F’s:
- Female
- Forty (40)
- Fatty
- Fertile

125
Q

what are Gallstones also known as?

A

Cholelithiasis

126
Q

what is pain in the upper R. quadrant termed?

A

Murphy’s point

127
Q

what is pain in the lower R. quadrant termed?

A

McBurney’s point

128
Q

why are females considered at risk for Cholelithiasis?

A

generally ^cholesterol excreted into bile = low cholesterol

129
Q

why are people age 40+ considered at risk for Gallstones?

A

longer exposure to estrogen (middle age females)

130
Q

why is an ^BMI considered a risk for Cholelithiasis? what are some other ways this risk manifests?

A

more fat
- significant loss in weight can release fat into blood stream, as can a high fat meal

131
Q

why are mothers considered at risk for Gallstones?

A

more children = more fertile = ^estrogen

132
Q

patient presents w/ a R. Scapular/shoulder colicky pain. what do you suspect the cause is?

A

Cholelithiasis which occludes the cystic duct

133
Q

refered pain to the R. Scapula/Shoulder may originate where?

A

Murphy’s point

134
Q

Gall stones which occlude the cystic duct may produce what?

A

Murphy’s point colicky pain

135
Q

Why would a patient present with Jaundice & acute pancreatitis?

A

small gall stones travel to the common bile duct, occluding the duodenum enterance

136
Q

generally ____ stones can’t be passed

A

large

137
Q

what is the most common gross presentation of Cholelithiasis?

A

Unpigmented stones MC

138
Q

what is the chief presenting complaint of Acute Cholelithiasis?

A

Murphy’s point pain

139
Q

which gall stones often present in industrialized nations?

A

Unpigmented

140
Q

Unpigmented gall stones are primarily composed of ____.

A

Cholesterol salts

141
Q

what is a less common gross presentation of Cholelithiasis?

A

Pigmented stones

142
Q

Pigmented gall stones are darker b/c ____.

A

Crystallized bilirubin makes up a ^proportion

143
Q

what is the chemical composition of Gall stones?

A

cholesterol + bilirubin

144
Q

what are common bile duct stones termed

A

Choledocholithiasis

145
Q

what is Cholecystitis? what symptom does it produce?

A

inflammation creates right upper quadrant pain - Murphy’s point

146
Q

Choledocholithiasis can also be described as ____.

A

Post-Hepatic Jaundice

147
Q

what are the 5 main causes of Liver Cirrhosis? what can this result in?

A
  • Steatosis (due to alcholism)
  • Viral hepatitis
  • Hemachromatosis
  • Wilson’s disease
  • a-antitrypsin deficiency
    can result in Liver Carcinoma
148
Q

what condition presents w/ Parkinson’s traits?

A

Wilson’s disease

149
Q

A 43 year old female complains of sharp pains in her abdomen every time she has her favorite meal of fettucine alfredo. After her most resent “attack,” her pain increased dramatically and she felt as though her skin started to take on a different hue. She presents to her primary care physician who orders some radiographs and bloodwork. Small calcific densities are visualized in the area of complaint and increased bilirubin is indicated in her bloodwork. She is referred to a surgeon.
A. what is the exact location of the pain?
B. what is the most likely diagnosis?

A

A. Murphy’s point pain (R^Q)
B. Cholecystitis

NYCC Visceral Pathology (36 decks)

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