L2- GIT Pathology I (esophagus) Flashcards by Connor Patrick

define Oral Leukoplakia (include specific oral locations)

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

How well did you know this?

Not at all

Perfectly

Oral Leukoplakia:

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

1- older men

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

How well did you know this?

Not at all

Perfectly

Oral Leukoplakia:

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

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

2- malignant transformation

3- considered precancerous until proven otherwise via histological evaluation

How well did you know this?

Not at all

Perfectly

Oral Leukoplakia:

(1) gross appearance
(2) histological appearance

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

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

How well did you know this?

Not at all

Perfectly

Erythroplakia (oral) = (1):

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

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

How well did you know this?

Not at all

Perfectly

Erythroplakia (oral) = (1):

(2) gross appearance
(3) histological appearance

1- erythroplasia

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

3- more atypical epithelial changes, usually marked dysplasia

How well did you know this?

Not at all

Perfectly

Oral Hairy Leukoplakia:

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

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

How well did you know this?

Not at all

Perfectly

Oral Hairy Leukoplakia:

(1) gross appearance
(2) histological appearance

1- white, confluent, fluffy, hairy hyperkeratotic thickenings

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

define cancerization

multiple primary tumors

-may be seen in HNSCC

How well did you know this?

Not at all

Perfectly

HNSCC:

progresses from (1) lesions
(2) risk factors

1- erythroplakia > leukoplakia > other lesions

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

How well did you know this?

Not at all

Perfectly

SCC of the tongue:

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

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)

How well did you know this?

Not at all

Perfectly

HNSCC / SCC of the tongue progression….

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

list the symptoms of esophageal atresia

excess drooling (saliva)
aspiration => pneumonia
choking and cyanosis

How well did you know this?

Not at all

Perfectly

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

1- esophageal webs/rings

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

3- episodic dysphagia, infrequent pain

How well did you know this?

Not at all

Perfectly

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).

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

3/4- Schatzki Rings: undersurface of epithelium

How well did you know this?

Not at all

Perfectly

Plummer-Vinson Syndrome, aka (1):

(2) triad of symptoms
(3) other symptoms

1- Kelly Patterson Syndrome

2- esophageal webs, glossitis, Fe deficient anemia

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

How well did you know this?

Not at all

Perfectly

Plummer-Vinson Syndrome, aka (1):

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

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

Hiatal Hernia:

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

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

Hiatal Hernia:

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

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

Para-esophageal: volvulus, strangulation, perforation

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

(Defn: functional esophageal obstruction)

partial / incomplete LES relaxation with swallowing
aperistalsis
inc resting LES tone

Achalasia:

(1) primary causes
(2) secondary causes

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

Achalasia:

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

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

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

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

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

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

list the many general causes of esophagitis

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

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

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

Reflux Esophagitis (GERD): - (1) symptoms - (2) complications

Sxs: dyspepsia, burning sensation, nocturnal cough, Sxs worse after lying down / after big meal Complications: bleeding, stricture, aspiration pneumonia, Barrett esophagus, adenocarcinoma

Reflux Esophagitis pathology / histology: - (1) reactive changes - (2) involved infiltrating cells

Reactive changes: - basal zone hyperplasia - hyperemia - elongation of lamina propria papillae Intraepithelial Inflammatory cells: eosinophils (scattered), neutrophils, lymphocytes

(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).

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

Barrett's esophagus: - (1) most affected group (age/sex) - development is related to (2) risk - risk of development into (3), therefore (4) is required

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

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

'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

discuss the AGA requirement for diagnosis of Barrett's esophagus

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

Barrett's esophagus symptoms

- heartburn, dyspepsia - epigastric pain - substernal discomfort

discuss Barrett's esophagus management (post endoscopy)

(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

Eosinophilic Esophagitis: - related to ingestion of (1), typically without (2) - (3) are the related disorders - (4) definition

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)

discuss histological appearance of Eosinophilic Esophagitis

- marked inc in eosinophils in squamous mucosa | - involves distal, mid, proximal esophagus (more severe in proximal segment)

Infectious Esophagitis: - affects mainly (1) people - (2) and (3) type infections (provide examples and include the histological appearance for (3))

``` 1- immunocompromised 2- fungal: candida 3- viral: -HSVs: multinucleated squamous cell with herpes virus nuclear inclusions -CMV: nuclear and cytoplasmic inclusions ```

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

Benign (rare): papilloma, leiomyoma, lipoma, hemangioma, granular cell tumors Malignant (common): SCC, adenocarcinoma

Esophageal SCC: - (1) affected age group - affects (males/females) most - (3) geographical area with highest incidences - affects (blacks/whites) more

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

Esophageal SCC: - (1) diet risk factors - (2) lifestyle (non-diet) factors

1- vitamin deficiency (A, C, B1, B2, B6), fungal contamination, high nitrate content 2- EtOH, tobacco, HPV

Esophageal SCC: - (1) genetic factors - (2) disease factors

1- celiac's, Tylosis / Ectodermal dysplasia, racial factors 2- (esophageal disease) long-standing esophagitis, achalasia, Plummer-Vinson syndrome

Esophageal SCC: - (1) describe distribution along the esophagus (by segment) - (2) describe possible growth patterns

1- 20% upper 1/3, 50% middle 1/3, 30% lower third 2- exophytic, diffusely infiltrative, ulcerated / excavated

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

1- middle third (50%) | 2- strictures

describe the metastasis of esophageal SCC

Direct: extension to mediastinal structures- heart, trachea Lymphatic: cervical, mediastinal, paratracheal, tracheobronchial, gastric/celiac nodes

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

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