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DERS (GIT) > L2- GIT Pathology I (esophagus) > Flashcards

L2- GIT Pathology I (esophagus) Flashcards

1
Q

define Oral Leukoplakia (include specific oral locations)

A
  • well-defined white patch / plaque caused by epidermal thickening / hyperkeratosis
  • not removed by scraping
  • buccal mucosa, tongue, floor of mouth can all be affected
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2
Q

Oral Leukoplakia:

  • (1) common group affected (age/sex)
  • (2) associations, hint- 3
A

1- older men

2- tobacco (pipe and smokeless tobacco), chronic frictions (i.e. poor fitting dentures), HPV infection

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3
Q

Oral Leukoplakia:

  • (1) clinical manifestations
  • 3-7% become (2), all though (3) is the assumption
A

1- range: benign epithelial lesion –> highly dysplastic lesions

2- malignant transformation

3- considered precancerous until proven otherwise via histological evaluation

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4
Q

Oral Leukoplakia:

  • (1) gross appearance
  • (2) histological appearance
A

1- variable, but often a smooth with well-demarcated borders

2- dysplasia- cellular and nuclear pleomorphism + loss of normal maturation

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5
Q

Erythroplakia (oral) = (1):

  • (more/less) common than leukoplakia
  • (more/less) ominous than leukoplakia, mainly due to (4) reason
A

1- erythroplasia
2- less common
3- more ominous
4- 50% have malignant transformation (compared to 3-7%)

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6
Q

Erythroplakia (oral) = (1):

  • (2) gross appearance
  • (3) histological appearance
A

1- erythroplasia

2- red velvety eroded area (compared to white leukoplakia), poorly-circumscribed

3- more atypical epithelial changes, usually marked dysplasia

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7
Q

Oral Hairy Leukoplakia:

  • (1) commonly affected patients
  • (2) is the main cause
  • (3) describe malignant potential
A

1- HIV pts
2- EBV (majority of cases)
3- none

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8
Q

Oral Hairy Leukoplakia:

  • (1) gross appearance
  • (2) histological appearance
A

1- white, confluent, fluffy, hairy hyperkeratotic thickenings

2- layers of keratotic squames over underlying mucosal acanthosis (= hyperkeratotic)

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9
Q

(1) is the most popular cancer of the head and neck. (1) has a (2) type of survival.

A

(95% of head/neck CAs)
1- HNSCC (head and neck squamous cell carcinoma)
2- <50% long-term survival

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10
Q

define cancerization

A

multiple primary tumors

-may be seen in HNSCC

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11
Q

HNSCC:

  • progresses from (1) lesions
  • (2) risk factors
A

1- erythroplakia > leukoplakia > other lesions

2- tobacco, alcohol, poor fitting dentures (chronic friction), HPV infections

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12
Q

SCC of the tongue:

  • (more/less) likely to metastasize
  • (2) describe metastasis
  • (3) discuss survival rate, including the importance of (4) factor
A

1- more likely (70% have metastasis at presentation)
2- from tongue –> floor of mouth and root of tongue

3/4- (5 yr survival rate):
Anterior tongue ~60%
Posterior tongue ~40% (harder to see, therefore harder to diagnose)

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13
Q

HNSCC / SCC of the tongue progression….

A

1) normal
2) hyperplasia / hyperkeratosis
3) mild/moderate dysplasia
4) severe dysplasia / CIS
5) SCC

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14
Q

(1) is the result of non-canalization of portion of the esophagus, it is commonly associated with (2) and sometimes associated with (3)

A

1- esophageal atresia (or stenosis)
2- tracheoesophageal fistula
3- heart, neurologic, genitourinary congenital abnormalities

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15
Q

list the symptoms of esophageal atresia

A
  • excess drooling (saliva)
  • aspiration => pneumonia
  • choking and cyanosis
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16
Q

(1) are protrusions of mucosa into esophageal lumen. (1) are typically (2) in size and have (3) clinical presentations.

A

1- esophageal webs/rings

2- <5mm (rarely more), 2-4 mm thick

3- episodic dysphagia, infrequent pain

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17
Q

Esophageal (webs/rings) are found in the upper esophagus and covered with (2).

Esophageal (webs/rings) are found in the lower esophagus and are made out of (4).

A

1/2- Webs: squamous mucosa with vascularized core (possible submucosal involvement)

3/4- Schatzki Rings: undersurface of epithelium

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18
Q

Plummer-Vinson Syndrome, aka (1):

  • (2) triad of symptoms
  • (3) other symptoms
A

1- Kelly Patterson Syndrome

2- esophageal webs, glossitis, Fe deficient anemia

3- [via IDA] koilonychia (spoon nails), splenomegaly

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19
Q

Plummer-Vinson Syndrome, aka (1):

  • (congenital/acquired) cause
  • high risk of (3) to develop
  • (4) Tx
A

1- Kelly Patterson Syndrome
2- acquired / developmental
3- SCC of esophagus
4- Fe, endoscopic dilatation

20
Q

Hiatal Hernia:

  • (1) definition
  • (2) types (include distribution)
  • (3) key feature
A

1- herniation of stomach through enlarged esophageal hiatus in diaphragm
2- sliding (95%), para-esophageal / rolling type
3- LES incompetence (worse in sliding type)

21
Q

Hiatal Hernia:

  • (1) sliding type symptoms and mechanism
  • (2) para-esophageal / rolling type symptoms and mechanism
A

Sliding: reflux of gastric contents => epigastric pain, heartburn

Para-esophageal: volvulus, strangulation, perforation

22
Q

describe the main features of Achalasia (hint- 3; also include definition)

A

(Defn: functional esophageal obstruction)

  • partial / incomplete LES relaxation with swallowing
  • aperistalsis
  • inc resting LES tone
23
Q

Achalasia:

  • (1) primary causes
  • (2) secondary causes
A

1- [local nerve issue] loss of intrinsic inhibitory innervation in LES, loss/absence of ganglion cells in myenteric plexus

2- [pseudoachalasia] Chaga’s (T. cruzi), DM neuropathy, malignancies, sarcoidosis, amyloidosis polio, surgical ablation, Down syndrome, Autoimmune diseases

24
Q

Achalasia:

  • (1) clinical features
  • (2) is seen above obstruction
  • small risk of developing (3)
A

1- dysphagia, odynophagia, reflux, vomiting, aspiration pneumonia
2- progressive esophageal dilatation above LES
3- SCC (5%)

25
Q

Mallory Weiss Syndrome:

  • (1) definition, involving (2) layers of esophagus
  • frequently seen in (3) patients due to (4)
  • (5) is the main symptom
  • (6) is the general outcome
A

1- longitudinal mucosal tear at esophageal junction
2- only mucosal layer (rarely transmural / Boerhaave syndrome)
3- alcoholics (after bouts of severe retching)
4- inadequate relaxation of LES during vomiting
5- hematemesis
6- usually heals, may be fatal sometimes

26
Q

Esophageal Varices:

  • (1) definition, include status of overlying mucosa, (2)
  • associated with (3) and sometimes (4)
  • has a (5) risk in association with (4)
  • (6) clinical presentation
A

1- dilated tortuous veins in mucosa and submucosa of lower esophagus (/proximal stomach)
2- normal, inflamed, or ulcerated
3- portal HTN
4- cirrhotic pts (30-60%): decompensated cirrhosis, HCC
5- cause of death in 50% of cirrhotic patient
6- asymptomatic until rupture

27
Q

list the many general causes of esophagitis

A
  • reflux esophagitis
  • irritants: EtOH, acids, alkalis
  • infections: HSV, CMV, candidiasis
  • allergic (eosinophilic esophagitis)
  • uremia
  • drugs: NSAIDs/ASA, anticancer therapy, bisphosphates
28
Q

list the 4 factors that affect / cause GERD (include the many causes for the *one particular factor)

A

i) delayed esophageal clearance
ii) inc gastric volume
iii) dec reparative capacity of esophagus
iv) dec LES tone: CNS depressants, hypothyroidism, pregnancy, alcohol, tobacco, nasogastric intubation

29
Q

Reflux Esophagitis (GERD):

  • (1) symptoms
  • (2) complications
A

Sxs: dyspepsia, burning sensation, nocturnal cough, Sxs worse after lying down / after big meal

Complications: bleeding, stricture, aspiration pneumonia, Barrett esophagus, adenocarcinoma

30
Q

Reflux Esophagitis pathology / histology:

  • (1) reactive changes
  • (2) involved infiltrating cells
A

Reactive changes:

  • basal zone hyperplasia
  • hyperemia
  • elongation of lamina propria papillae

Intraepithelial Inflammatory cells: eosinophils (scattered), neutrophils, lymphocytes

31
Q

(1) is the result from the replacement of esophageal squamous mucosa with metaplastic columnar epithelium containing many (2). The progression to (1) stems from (3) causing changes in (4) in order to resist (5).

A

1- Barrett Esophagus
2- goblet cells
3- prolonged injury (to LES, i.e. long h/o GERD)
4- progenitor/stem cells (programming switch columnar cells)
5- acid peptic injury

32
Q

Barrett’s esophagus:

  • (1) most affected group (age/sex)
  • development is related to (2) risk
  • risk of development into (3), therefore (4) is required
A

1- white men
2- length of Barrett’s mucosa
3- adenocarcinoma (inc x30-40)
4- serial endoscopic biopsies for screening

33
Q

Barrett’s esophagus: discuss appearance on endoscopy (describe the difference between short and long segments)

A

‘serpiginous salmon colored patch’
-normal pearly-white esophageal mucosa (bluish squamous mucosa) replaced by velvety pink columnar mucosa (tan colored ectopic mucosa)

Long segment >3cm
Short segment <3cm

34
Q

discuss the AGA requirement for diagnosis of Barrett’s esophagus

A

upon biopsy (histology) –> presence of columnar mucosa and goblet cells is necessary for DDx of Barrett’s

35
Q

Barrett’s esophagus symptoms

A
  • heartburn, dyspepsia
  • epigastric pain
  • substernal discomfort
36
Q

discuss Barrett’s esophagus management (post endoscopy)

A

(always continue antacid Tx)
1- no dysplasia –> continue screening

2- low grade dysplasia –> more frequent screening

3- high grade dysplasia –> definitive therapy, resection / ablation required

4- adenocarcinoma –> resection required

37
Q

Eosinophilic Esophagitis:

  • related to ingestion of (1), typically without (2)
  • (3) are the related disorders
  • (4) definition
A

1- food allergens
2- GERD
3- Atopic disorders: dermatitis, allergic rhinitis, asthma, peripheral eosinophilia

4:

i) dysphagia, food impaction
ii) feeding intolerance, GERD-like
iii) trachealization on endoscopy (circumferential rings)

38
Q

discuss histological appearance of Eosinophilic Esophagitis

A
  • marked inc in eosinophils in squamous mucosa

- involves distal, mid, proximal esophagus (more severe in proximal segment)

39
Q

Infectious Esophagitis:

  • affects mainly (1) people
  • (2) and (3) type infections (provide examples and include the histological appearance for (3))
A 
1- immunocompromised
2- fungal: candida
3- viral:
-HSVs: multinucleated squamous cell with herpes virus nuclear inclusions
-CMV: nuclear and cytoplasmic inclusions
40
Q

list the neoplasms of the esophagus- indicate if benign or malignant tumors are more common

A

Benign (rare): papilloma, leiomyoma, lipoma, hemangioma, granular cell tumors

Malignant (common): SCC, adenocarcinoma

41
Q

Esophageal SCC:

  • (1) affected age group
  • affects (males/females) most
  • (3) geographical area with highest incidences
  • affects (blacks/whites) more
A

1- >50y/o
2- males > females
3- central Asia, northern China
4- blacks > whites

42
Q

Esophageal SCC:

  • (1) diet risk factors
  • (2) lifestyle (non-diet) factors
A

1- vitamin deficiency (A, C, B1, B2, B6), fungal contamination, high nitrate content

2- EtOH, tobacco, HPV

43
Q

Esophageal SCC:

  • (1) genetic factors
  • (2) disease factors
A

1- celiac’s, Tylosis / Ectodermal dysplasia, racial factors

2- (esophageal disease) long-standing esophagitis, achalasia, Plummer-Vinson syndrome

44
Q

Esophageal SCC:

  • (1) describe distribution along the esophagus (by segment)
  • (2) describe possible growth patterns
A

1- 20% upper 1/3, 50% middle 1/3, 30% lower third

2- exophytic, diffusely infiltrative, ulcerated / excavated

45
Q

esophageal SCC commonly affects (1) part of the esophagus most, which can lead to (2)

A

1- middle third (50%)

2- strictures

46
Q

describe the metastasis of esophageal SCC

A

Direct: extension to mediastinal structures- heart, trachea

Lymphatic: cervical, mediastinal, paratracheal, tracheobronchial, gastric/celiac nodes

47
Q

Esophageal Adenocarcinoma:

  • mostly affects (1- age, sex, race)
  • mostly affect (2) portion of the esophagus
  • (3) is the common precursor lesion
  • (4) is key histological sign
A

1- ~50y/o white men
2- lower third
3- Barrett’s esophagus: inc risk x30-60, requires multi-step process thru dysplasia
4- back-to-back glands

DERS (GIT) (21 decks)

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