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Gastrointestinal System Step 1 > Pathology > Flashcards

Pathology Flashcards

1
Q

MC location of salivary gland tumours

A

parotid (and most are benign)

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2
Q

Likelihood of a tumour in a smaller gland to be malignant

A

High

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3
Q

Typical presentation of a salivary gland tumor (benign)

A

painless mass/swelling

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4
Q

What does facial pain/paralysis suggest for a salivary gland tumor?

A

malignan involvement of CN7

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5
Q

MCC Salivary Gland Tumor

A

Pleiomorphic Adenoma

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6
Q

Composition of Pleiomorphic Adenoma

A

Chondromyxoid stroma and epithelium

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7
Q

What must the surgeon pay attention to, when excising a pleiomorphic adenoma?

A

To resect it completely and not to rupture intraoperatively, so as it does not recurr.

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8
Q

MC malignant salivary gland tumor

A

Mucoepidermoid carcinoma

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9
Q

What is the real name of Warthin tumor?

A

Papillary Cystadenoma lymphomatosum

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10
Q

Warthin tumor- Malignant or Benign?

A

Benign (90%)

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11
Q

Warthin tumor associations

A

Typically found in smokers
Bilateral 10%
Malignant 10%

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12
Q

Tonicity of saliva

A

Hypotonic

nacl comes in, attracts H2O, but then leaves and H20 stays

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13
Q

Cause of achalasia

A

Failure of LES to relax due to loss of myenteric plexus of Auerbach.
( Loss of postganglionic inhibitory neurons, which contain NO and VIP)

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14
Q

Dysphagia in Achalasia

A

both solids and liquids

obstruction–> solids only

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15
Q

Secondary Achalasia causes

A 
Chagas disease
Extraesophageal malignancies (mass effect or paraneoplastic)
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16
Q

Patient population with eosinophilic esophagitis

A

Usually atopic patients

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17
Q

What is the problem in eosinophilic esophagitis?

A

Food allergens cause dysphagia and food impaction

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18
Q

eosinophilic esophagitis- endoscopic findings

A

Esophagela rings and linear furrows

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19
Q

What are esophageal varices?

A

Dilated submucosal veins in lower one third of esophagus, secondary to portal HTN.

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20
Q

Dx of esophagitis based on morphology macroscopically in an immunocompromised patient

A

white pseudomembrane–> Candida
punched-out ulcers—> HSV1
linear ulcers–> CMV

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21
Q

Pills that cause esophagitis

A 
biphosphonates
tetracycline
NSAIDS
Iron
Potassium Chloride
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22
Q

Causes of esophagitis

A

Reflux
Infection in immunocompromised
caustic ingestion
Pill esophagitis

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23
Q

What is Mallory-Weiss syndrome?

A

Partial thickness mucosal lacerations at gastroesophageal junction due to severe vomiting.

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24
Q

Plummer-Vinson syndrome Triad

A

Dysphagia
Iron Deficiency Anemia
Esophageal webs

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25
Q

Plummer-Vinson syndrome risk

A

Squamous cell carcinoma of the esophagus

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26
Q

Sclerodermal Esophageal Dysmotility pathophysiology

A

esophageal smooth muscle atrophy—> decreased LES pressure and dysmotility–> acid reflux and dysphagia–> stricture, Barett, aspiration

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27
Q

SCC VS Adenocarcinoma of the Esophagus

  1. Site
  2. Risk Factors
  3. Prevalence
A

SCC affects upper 2/3 its risk factors: alcohol, ot liquids, caustic strictures, smoking, achalasia and is more common worldwide

Adeno:affects lower one third, its risk factors are: GERD, BArett, Obesity, Smoking, Achlasia and is more common in America

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28
Q

What is Tylosis?

A 
Auto dominant syndrome.
Its phenotypic hallmarks are:
1. oral leukoplakia
2.hyperkeratosis of palms and soles
3. SCC of esophagus (95%)
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29
Q

Acute Gastritis- Causes

A
  1. NSAIDs–>lower PGE2
  2. Burns(curling Ulcer)–>hypovolemia–> mucosa ischemia
  3. Brain injury (Cushing ulcer)–> incr. vagal stimulation–> incr. Ach–> incr H+
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30
Q

Chronic Gastritis pathophysiology

A

Mucosal inflammation–> atrophy
(hypochloridria–>hypergastrinemia) and
intestinal G cell metaplasia (incr risk of gastric cancers)

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31
Q

MC chronic gastritis

A

H.pylori gastritis

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32
Q

H.pylori chronic gastritis

Site and risks

A

Affects antrum first and spreads to the body of the stomach

Incr risk of MALToma and Pept Ulcer Disease

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33
Q

Autoimmune Chronic Gastritis

site and risk

A

Affects body and fundus

Pern anemia

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34
Q

Autoimmune Chronic Gastritis Targets of ABs

A

parietal cells and IF

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35
Q

What is Menetrier disease?

A

Hyperplasia of gastric mucosa–>
hypertrophied rugae (that look like brain gyri),
excess mucous production with resultant protein loss and parietal cell atrophy with lower acid production.

It is precancerous

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36
Q

Paraneo of gastric cancer

A
  1. acanthosis nigricans

2. Leser-Trelat sign

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37
Q

Gastric cancer types and associated risk factors, site

A

Intestinal: associated with H. Pylori, dietary nitrosamines, smoking, achlorydria, chronic gastritis, blood type A
Commonly in lesser curvature

Diffuse: not associated with H. pylori
Signet ring cells, linitis plastica

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38
Q

What is linitis plastica?

A

Stomach wall grossly thickened and leathered

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39
Q

What are signet ring cells?

A

Mucin filled cells with peripheral nuclei

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40
Q

What is Virchow node?

A

Involvement of left supraclavicular node by meta from stomach

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41
Q

What is Kruckenberg tumor?

A

Bilateral meta to ovaries. Abundant mucin secreting, signet ring cells

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42
Q

What is the Sister Mary Joseph nodule?

A

Subcutanous periumbilical metastasis

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43
Q

Pain of peptic ulcer disease

A

Gastric–> Greater with meals

Duodenal–> Decreases with meals

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44
Q

Which Peptic Ulcer is more common?

A

Duodenal

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45
Q

Duodenal Peptic Ulcer- Risk of cancer

A

Generally benign

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46
Q

Associations/Causes of Duodenal Peptic Ulcer

A

ZES
MEN1
Cirrhosis
COPD

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47
Q

Which Peptic Ulcer is more commonly associated with H. Pylori?

A

Duodenal (90%) vs gastric (70%)

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48
Q

MC complication of Peptic Ulcer

A

Hemorrhage

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49
Q

Peptic Ulcer Hemorrhage- Artery involved based on site

A

lesser curvature–> Left Gastric Artery

Posterior Wall of duodenum–> gastroduodenal artery

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50
Q

Risk of cancer with gastric ulcer

A

High

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51
Q

Which duodenal Peptic Ulcer more commonly hemorrhages?

A

posterior> anterior

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52
Q

Gastroparesis Tx

A

Metoclopramide

Erythromycin

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53
Q

How do we screen for fecal fat?

A

Sudan stain

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54
Q

Celiac Diseases- HLA associations

A

HLA-DQ2

HLA-DQ8

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55
Q

Celiac Disease- pathophysiology

A

Autoimmune mediated intolerance of gliadin–> malabsorption and steatorrhea

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56
Q

Celiac Disease Antibodies

A

IgA anti-tissue transglutaminase Abs
antiendomysial Abs
anti-deaminated gliadin pepride Abs

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57
Q

Celiac Disease Microscopic Findings

A

Villous Atrophy
Crypt Hyperplasia
Intraepithelial lymphocytosis

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58
Q

Celiac Disease risk of malignancy

A

moderately incr–> T cell lymphoma

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59
Q

Celiac Disease- Sites

A

Primarily affects distal duodenum and/or proximal jejunum.

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60
Q

What is a D-xylose test?

A

D-xylose is a monosaccharide, or simple sugar, that does not require enzymes for digestion prior to absorption. Its absorption requires an intact mucosa only and then it is excreted by the urine.

Blood and urine low levels—> mucosa defects/ bacterial overgrowth

It is normal in pancreatic insufficiency.

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61
Q

Lactose intolerance- Histology

A

Normal, exc when lactose intolerance is secondary to injury at tips of villi (eg viral enteritis)

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62
Q

Lactose Hydrogen Breath Test

A

It is positive for lactose malabsorption if prolactose breath hydrogen value>20ppm compared with baseline.

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63
Q

Stool pH with lactose intolerance

A

lower than normal.

Colonic bacteria ferment lactose

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64
Q

Pancreatic Insufficiency Findings

A

Lower duodenal pH and fecal elastase

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65
Q

Tropical Sprue-histology

A

Similar findings as celiac sprue but responds to Abx.

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66
Q

Tropical Sprue associations

A

Associated with megaloblastic anemia due to folate deficiency and then b12

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67
Q

Whipple Disease cause

A

Tropheryma whipplei

intracellular Gram +

68
Q

Whipple Disease Histological findings

A

PAS+ foamy macrophages in intestinal lamina propria

69
Q

Whipple Disease symptomatology

A

Cardiac Symptoms
Arthralgias
Neurologic symptoms
Diarrhea and steatorrhea occur later in disease course

70
Q

IBD Histology

A

Crohn nonceaseting granulomas and lymphoid aggregates

UC: crypt abscesses and ulcers, bleeding, Th2 mediated

71
Q

IBD Extraintestinal manifestations

A

Rash (pyoderma gangrenosum, erythema nodusum)
Eye inflammation (episcleritis, uveitis)
Oral ulcerations (apthous stomatitis)
Arthritis (peripheral, spondylitis)

72
Q

IBD- Chrohn specific Extraintestinal manifestations

A

Kidney stones, usually calcium oxalate
Gallstones
may be postive for anti- Saccharomyces cervisiae antibodies (ASCA)

73
Q

IBD- UC specific Extraintestinal manifestations

A

Primary sclerosing cholangiitis

p-ANCA positive

74
Q

Genetic Associations of Crohn

A

NOD-2

75
Q

Genetic Association of UC

A

HLA-B27

76
Q

Crohn- Gross Morphology

A 
Transmural inflammation---> fistulas
Cobblestone mucosa
Creeping fat
Bowel wall thickening (string sign on barium swallow)
linear ulcers
Fissures
77
Q

UC- Gross Morphology

A

Mucosal and Submucosal Inflammation only
Friable mucosa with suerficial and/or deep ulcerations

Loss of haustra—> lead pipe on imaging

78
Q

Where do false diverticula usually occur?

A

where vasa recta perforate muscularis externa

79
Q

Zenker Diverticulum Location

A

Phryngoesophangeal false diverticulum
Herniation of mucosal tissue at Killian triangle between thyropharyngeal and cricopharyngeal parts of the inferior pharyngeal constrictor

80
Q

Meckel’s diverticulum

A

Persistence of vitteline duct

81
Q

MC congenital anomaly of GI tract

A

Meckel diverticulum

82
Q

Meckel diverticulum- Rule of 2

A

2 times as likely in males
2 inches long
2 feet from ileocecal valve
2% of population
Commonly presents in first 2 years of life
May have 2 types of epithelia (gastric/pancreatic)

83
Q

meckel diverticulum diagnosis

A

Pertechnetate study for uptake by ectopic gastric mucosa

84
Q

Hirschprung-what is missing

A

ganglion cells/enteric nervous plexuses(meissner and Auerbach) in distal segment of colon.

85
Q

Hirschprung- associated mutations/ conditions

A

RET

Risk of Hirschprung is increased with Down syndrome.

86
Q

Hirschprung- Clinical picture

A 
bilious emesis
abdominal distention
failure to pass meconium within 48h
Explosive expulsion of feces (squirt sign)
Empty rectum on DRE
87
Q

What are Ladd bands?

A

They are fibrous stalks of peritoneal tissue that attach the cecum to the retroperitoneum in the right lower quadrant (RLQ). Obstructing Ladd’s Bands are associated with malrotation of the intestine,

88
Q

Volvulus- axon of twisting

A

bowel twists around its mesentery

89
Q

Intussusception MC site

A

ileocecal valve

Meckel is MC lead point

90
Q

Stools in intussusception

A

Currant Jelly Stool

91
Q

Intussusception- Associated conditions

A

Recent viral infection as adenovirus–>Peyer patch hypertrophy–> lead point
Associate with Rotavirus vaccine

92
Q

What is a thumbprint sign?

A

Colonic ischemia–> mucosal edema/hemorrhage –>protrude in the lumen like thumbs

93
Q

Ileus associations

A

abdominal surgery
opiates
hypokalemia
sepsis

94
Q

Necrotizing Enterocolitis

A

Seen in premies, formula-fed infants with immature immune system. Primarily necrosis of colonic mucosa with possible perforation which can lead to pneumatosis intestinalis
free air in abdomen
portal venous gas

95
Q

Categories of generally non neoplastic polyps

A 
hamartomatous
mucosal
inflammatory pseudopolyps
submucosal
hyperplastic
96
Q

Condition where inflammatory pseudopolyps are notices

A

IBD

97
Q

Which is the most dangerous polyp of the benign category?

A

hyperplastic. may evolve into serrated polyps and more advanced lesions

98
Q

Categories of polyps with malignant potential

A

Adenomatous

Serrated

99
Q

Pathway, via which adenomatous polyps are neoplastic

and mutations

A

Chromosomal instability pathway with mutations in APC and KRAS

100
Q

Adenomatous polyps. Villous or tubular is worse= more malignant?

A

Villous

101
Q

Pathway, via which serrated polyps are neoplastic

and mutations

A

CpG hypermethylation phenotype pathway with microsattellite instability and mutations in BRAF

102
Q

How many cases of sporadic adenoca are attributed to serrated polyps?

A

20%

103
Q

Means of inheritance of polyposis syndromes?

A

all dominant exc. Turcot

104
Q

FAP mutation- what gene

what chromosome

A

APC tumor suppressor gene on Chr 5q

105
Q

FAP- cancers

A

colorectal(100%)
duodenal adenoca
ca of ampulla of vater

106
Q

Gardner clinical picture

A

FAP +
osseus and soft tissue tumors+
congenital hypertrophy of retinal pigmented epithelium+
impacted/supernumerary teeth

107
Q

Turcot clinical picture

A

FAP/GARDNER and malignant CNS tumor

108
Q

Peutz Jeghers

A

hamartomas through GI trct
hyperpigmented mouth lips hands genitalia
Incr risk of breast and GI cancers

109
Q

Juvenile polyposis syndrome
age
findings

A

usually in children

Numerous hamartomatous polyps in the colon stomach small bowel

110
Q

Lynch syndrome mutation

A

DNA mismatch repair genes and microsatellite instability

111
Q

Lynch syndrome associated cancers

A

endometrial
ovarian
skin

112
Q

Carcinoid tumors of the GI tract

A

neuroendocrine tumors that produce serotinin
Sites: appendix, terminal ileum
If meta to liver–> carcinoid syndrome

113
Q 
GIST
What is it?
Mutation?
Age?
Tx?
A

MC sarcoma of the GI tract
KIT mutation
Peak at 70 years
Tx: resection and tyrosine kinase inh.

114
Q

Molecular pathogenesis of colorectal cancer sequence

A

normal colon–LOSS OF APC GENE—> Colon at risk—KRAS MUTATION—> Adenoma–LOSS OF TUMOR SUPRESSOR GENES(p53,DCC)—> carcinoma

115
Q

Cirrhosis that alcohol causes

A

Micronodular

116
Q

Diagnois of Spontaneus Bacterial peritonitis

A

paracentesis–> PLMN>250 cells/ml

117
Q

Liver disease: AST> ALT suggests what

A

alcoholic liver disease

EXC. when non alcoholic liver disease progresses to advanced fibrosis, this pattern can be noticed

118
Q

Reyes

Pathologoanatomic picture of the liver

A

Microvesicular fatty change

119
Q

Reyes mechanism of disease

A

Aspirin metabolites lower b-oxidation by reversible inhibition of mitochondrial enzymes

120
Q

Amebic liver abscess associations

patient population and color of aspirate

A

Rare in the US–think of trevvellers

Brown material on aspiration

121
Q

Alchoholic hepatitis Micro image

A

Swollen and necrotic hepatocytes with PLMN infiltration

and MAllory bodies

122
Q

What are Mallory bodies?

A

Intracytoplasmic eosinophilic inclusions of damaged keratin filaments

123
Q

Alcoholic cirrhosis Microscopic picture

A

Regenerative nodes wurrounded by fibrous bands.

Sclerosis around central vein may be seen in early disease.

124
Q

NAFLD

Microscopic pic

A

Fatty infiltration of hepatocytes and cellular ballooning and eventually necrosis
ALT>AST

125
Q

Tx of hepatic encephalopathy

A

lactulose (NH4 generation)

rifamixin or neomycin( lowers NH3 producing gut bacteria)

126
Q

Causes of hepatic encephalopathy

A

Increased NH3 production (diet, GI bleed, constipation, infection)
Decreased NH3 removal (TIPS, ESRD,Diuretics)

127
Q

How does hepatocellular carcinoma spread?

A

hematogenously

128
Q

Variant of HCC with a better prognosis?

A

Fibrolamellar

129
Q

How is aflatoxin carcinogenic?

A

Mutates p53

130
Q

How is a hepatic adenoma different from normal liver tissue?

A

They look the same exc. adenoma has no portal tracts

131
Q

Angisarcoma Associations

A

Exposure to arsenic, vinyl chloride

132
Q

Focal Nodular Hyperplasia- cause and radiological picture

A

nodular proliferation in response to vascular anomaly

Central stellate scar

133
Q

Microscopic Picture of Budd Chiarri

A

centrilobular congestion adn necrosis

May cause nutmeg liver

134
Q

a1 antithrypsin deficiency Mutation

A

a1 antithrypsin in produced by SERPINA gene on Chr 14

135
Q

a1 antithrypsin deficiency Microscop. Picture

A

Misfolded gene products aggragates in hepatocellular ER–> cirrhosis with PAS+ lobules in liver

136
Q

a1 antithrypsin deficiency lung pathology

A

low a1 antithrypsin –> un inhibited elastase–> lower elastic tissue–> panacinar emphysema

137
Q

Physiologic neonatal jaundice Mechanism

A

immature UDP-glycurosyltransferase—-> high indirect bilirubin

138
Q

Hereditary hyperbilirubinemias

Way of inheritance

A

All autosomal recessive

139
Q

Gilbert syndrome mechanism

A

low UDP-glycurosyltransferase conjugation and impaired bilirubin uptake—-> high indirect bilirubin

140
Q

Crigler Najjar syndrome

A

ABSENT UDP-glycurosyltransferase –> early death Type1)

Type 2 is less severe and responds to phenobarbital which increases liver enzyme synthesis.

141
Q

Dubin Johnson syndrome

A

direct hyperbilirubinemia
due to defective liver excretion
Grossly black liver

142
Q

Rotor

A

Similar with Dubin Johnson but milder

and without black liver

143
Q

Wilson disease- Hepatolenticular degeneration

way of inheritance

A

auto recessive

144
Q

Wilson disease- Hepatolenticular degeneration

mutation

A

hepatocyte copper transporting ATPase (ATP7b gene, Chrom 13)—->

lower copper excretion in bile and incorporation in apoceruloplasmin—>

lower serum ceruloplasmin

145
Q

Wilson disease- Hepatolenticular degeneration

Pathophysiology

A

ATP7B protein deficiency impairs biliary copper excretion,resulting in positive copper balance, hepatic copper accumulation,and copper toxicity from oxidant damage.
Excess hepatic copper is initially bound to metallothionein, but as this storage capacity
is exceeded, liver damage begins as early as 3 years of age.

Defective copper incorporation into apoceruloplasmin leads to excess catabolism and low blood levels of ceruloplasmin.

Serum copper levels are usually lower than normal because of low blood ceruloplasmin, which normally binds 90% of serum copper.

As the disease progresses, non-ceruloplasmin serum copper (“free” copper) levels increase, resulting in copper buildup in other parts of the body, such as the brain, leading to neurologic and psychiatric disease.

146
Q

What is a Kaiser- Fleischer Ring?

A

deposits in Descemet membrane of cornea

147
Q

Laboratory findings in Wilson disease

A

low serum ceruloplasmin levels
high tissue levels of copper (bipsy)
increased urinary copper secretion

148
Q

Hemochromatosis mutation

A

Recessive mutations in HFE gene( C282Y>H63D), chromosome 6, associated with HLA-A3

149
Q

Classic triad of hemochromatosis and clinical picture

A

Cirrhosis
DM
skin pigmentation

also causes restrictive myocardiopathy, hypogonadism, arthropathy and HCC (200x normal risk)

150
Q

Hemochromatosis Arthropathy cause

A

Calcium pyrophosphate deposition, especially metacarpophalangeal joints

151
Q

PSC pathology

A

Concentric onion skin bile duct fibrosis—> alernating strictures and dilatation with beading of intra and extrahepatic bilde ducts on ERCP, MRCP

152
Q

PSC epidemiology

A

middle aged men with IBD

153
Q

PSC associations

A

UC
pANCA +
Incr IgM

154
Q

PBC pathology

A

autoimmune reaction–> lympho infiltrate and granulomas–> destruction of intralobular bile ducts

155
Q

PBC associations

A

AMA +
asso. with
Sjogren Hashimoto CREST RA celiac disease

156
Q

Infections that cause cholelithiasis

A

Ascaris

Clonorchis

157
Q

Acalculus cholecystitis causes

A

gallbladder stasis

hypoperfusion

infection (CMV)

Seen in critically ill

158
Q

HIDA scan(cholescintigraphy and hepatobiliary scintigraphy) in cholecystitis

A

Failure to visualise GB in HIDA scan suggests obstruction

Inability to see the radioactive tracer in your gallbladder might indicate acute inflammation (acute cholecystitis).

159
Q

When do we see a strawberry like Gallbladder?

A

Cholesterolosis—> accumulation of cholesterol lades macrophages within the mucosa of GB wall

160
Q

Drugs that cause pancreatitis

A

sulfa
NRTI
protease inhibitors

161
Q

Pseudocyst pathology

A

Lined by granulation tissue not epithelium

162
Q

Best screen for chronic pancreatitis

A

Secretin stimulation test

The health care provider inserts a tube through your nose and into your stomach. The tube is then moved into the first part of the small intestine (duodenum). You are given secretin through a vein (intravenously). The fluids released from the pancreas into the duodenum are removed through the tube over the next 1 to 2 hours.
Sometimes, the fluid can be collected during an endoscopy.

163
Q

Microscopic Picture of Pancreatic Cancer

A

cancer arises from ductal epithelium
tumor desmoplasia
perineural invasion

164
Q

Intraductal papillary mucinous neoplasms mutations

A

GNAS

165
Q

Cystic neoplasms of the pancreas mutations

A

VHL

Most are benign

Gastrointestinal System Step 1 (5 decks)

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