Esophagus Flashcards
(21 cards)
1
Q
3 Phases of Swallowing
A
- 1- Oral Prep Phase (Primary vol control)
- Chew into bolus –> move to back of tongue –> tongue forms cups/trough –> elevated mylohyoid and soft palate to seal nasopharynx –> anterior tongue lifts and retracts to force food into pharynx
- 2- Pharyngeal Phase (reflex - medulla/pons)
- Pharyngal peristalsis (while closing vocal cords) then UES reflexively relaxes –> bolus into esophagus
- Contract superior pharyngeal constrictor muscles and arytenoids to close vocal cords and draw epiglottis down to protect larynx from aspiration
- Pharyngal peristalsis (while closing vocal cords) then UES reflexively relaxes –> bolus into esophagus
- 3- Esophageal Phase (also involuntary -ANS)
- Slower than thru pharynx
- Peristaltic contractions of esophagus and relaxation of LES to allow food to pass into stomach
2
Q
Oropharyngeal Dysphagia
Esophageal Dysphagia
Odynophagia
A
- Oropharyngeal Dysphasia - cannot initiate or transfer bolus to esophagus –> choking/aspiration (common in those w/ neuromuscular prob or stroke)
- Esophageal Dysphagia - sensation of food or liquid stuck in chest right after swallowing
- If solid food…often means there is esophagus lumen narrowing
- Odynophagia - pain when swallowing (in esophageal phase)
- Can be due to reflux, infections, inflammation
- Pill esophagitis - pills stuck in mucosa –> chemical burns
3
Q
GERD (what is it? + causes and risk factors)
A
- Abnormal reflux of gastric contents into esophagus (esp HCl and pepsin + some damage from bile and pancreatic enzymes)
- Often due to hypotensive LES OR more commonly, LES relaxes inappropriately
- Can also be due to poor salivation and/or delayed emptying of esophagus
- Risk Factors - eating before bed, obesity, carbonation/coffee, H pylori
4
Q
4 Histo Characteristics of GERD
A
- Basal zone hyperplasia (see prominent nuclei several cells away from base)
- Elongation of lamina propria papillae into top 1/3 of epithelium
- Intercellular edema (may see white lines outlining ea cell -b/n cells)
- Inflammation - mild inc in # eosinophils (red granules in cyto and bi-lobe nucleus), neutrophils and lymphocytes
5
Q
3 Normal Protections Against GERD
A
- 1- LES - esp when reinforced by diaphragm (lost if hiatal hernia)
- 2- Luminal clearance of contents (requires saliva and motility)
- 3- Epithelial resistance to injury
6
Q
GERD Eval
A
- Endoscopy - will be normal if non-erosive; used if alarming symptoms to r/o tumor AND used if persistence after 2 PPI trials BUT may see red/ulcers
- pH Testing - transnasal cath OR new wireless system in which small monitor is placed in esophagus mucosa via scope (can monitor control on PPI therapy)
- Esophagram - barium swallow to see stricture or hiatal hernia AKA check anatomy
- Manometry - trans-nasal cath to check strength of esophageal contractions, resting tone and sphincter relaxation
- Done pre-operatively b/f antireflux surgery
- Done if suspect hypotensive sphincter
7
Q
GERD Tx
A
- Lifestyle Mod - smaller portions/less fat, dec choc, mints, EtOH, caffeine, carbonated drinks; loose clothing; weight loss; stop smoking; sleep w/ elevated head and do not lay down w/in 2-3 hrs of meal
- PPIs»_space; H2 receptor blockers
- Anti-reflux Surgery - reserved for those who do not want meds or cannot control GERD w/ meds; Neissen fundoplication (wrap fundus around LES/gastro-eso junction/cardia to create barrier (may loosen in 10-15 yrs)
8
Q
Barrett’s Esophagus
A
- Change in esophageal epithelium in response to acid injury in some w/ chronic reflux
- Risk Factors = 50+ yo, >5 yrs GERD symptoms, white, male, inc BMI, inc intra-abdominal fat
- “Pre-malignant” so do surveillance scopes (every 3-5 yrs if no dysplasia yet)
- Metaplasia –> dysplasia –> cancer sequence
9
Q
BE on Pathology (gross and histo)
A
- Grossly - normal white squamous mucosa of esophagus replaced by velvety, tan BE mucosa b/c actual esophageal-gastric junction
- Histo - starts to look glandular w/ pits of columnar epithelium & glands like stomach AND goblet cells sprinkled throughout b/n epithelial cells
- Once dysplasia - see dark, prominent, large nuclei BUT no invasion yet
10
Q
BE Tx
A
- Endoscopic ablation - radio frequency burns 1 mm deep
- OR cryotherapy uses liquid nitrogen to freeze and slough epithelium
- Must use high dose PPI at same time so new epithelial growth is not BE during healing
- If nodule or superficial adenocarcinoma then resect w/ scope and biopsy for diagnosis and staging if malignant
11
Q
Squamous Cell Carcinoma
A
- Alcohol and smoking are major risk factors (male > female)
- Usually >50-60 yo
- Tends to affect upper/mid esophagus
- Most common worldwide
- Keratin pearls and intracellular bridges
12
Q
Adenocarcinoma
A
- BE/ GERD is major risk factor
- Thus tends to affect lower esophagus (more white males)
- Usually > 40 yo
- Incidence rising in US (now more common than squamous cell in US but not world)
- glandular cells that have invaded past BM`
13
Q
EoE Pathophysiology
A
- chronic eosinophilic inflammation –> loss of mucosa elasticity, subepithelial fibrosis, loss of wall compliance, esophageal strictures
- Likely allergic response to food allergy or aeroallergen (often co-occurs w/ asthma, eczema, allergic rhinitis)
14
Q
How does EoE present clinically? W/ scope? On histo?
A
- Clinical - solid food dysphagia in adults AND not eating/vomiting, failure to thrive in children); may have heartburn or chest pain (does not respond to PPIs)
- Scope - see mucosal rings (corrugated) –> narrow lumen OR long, linear furrows; may see white/yellow papules representing eosinophilic micro-abscesses; PROXIMAL esophageal constriction (whereas GERD is mainly all distal)
- Histo - EOSINOPHILIC infiltrate (inflammation w/ numerous eosinophils - way more than GERD and throughout whole esophagus not just eosinophils in distal portion like GERD)
15
Q
EoE Tx (3)
A
1- Allergy avoidance - do formal allergy testing to find possible cause
2- Immune modulation - swallowed steroids or spray back of throat and swallow
3- Endoscopic dilation to expand lumen
16
Q
PPI Responsive EoE (2 theories)
A
- If have same clinical picture as EoE but respond to PPIs and exclude GERD (pH monitoring and no metaplasia)
- 2 Theories
- GERD reflux causes EoE like reaction despite normal pH and scope
- OR just a variant of EoE that responds to PPIs b/c of PPI’s anti-inflammatory effects not anti-acid effects (may block cytokine -stimulate release of eotacin-3 by esophagus that normally occurs in EoE)
17
Q
Achalasia
A
- Insufficient LES relaxation and no esophageal peristalsis
- Unknown etiology but purely motor
- Path - see inflammation w/in myenteric plexus, loss of ganglionic cells and myenteric neural fibrosis AND LES has selective loss of inhibitory neurons (NO, VIP) so unopposed cholinergic high basal pressures
18
Q
Achalasia Dx
A
- “Birds beak” appearance of LES on barium esophagram b/c persistent spasm
- Loss of peristalsis and incomplete relaxation of LES on manometry
- Scope to r/o gastro-esophageal junction tumor (presents w/ pseudoachalasia)
19
Q
3 Achalasia Tx
A
GOAL = relax LES b/c cannot regain peristalsis
- Laparoscopic myotomy - cut LES muscle fibers plus must add anti-reflux wrap to re-create reflux barrier
- Endoscopic dilation - stick balloon cath in LES to tear it (8-10% perforation rate)
- Botox injections if high risk for surgery - prevents Ach release at LES (80% effective but only lasts 6-12 mo then repeat not as effective b/c make antibodies against toxin)
20
Q
Esophageal Infections in General
A
- Usually in immune-comp host
- Can have multiple infectious entities at once
- 3 most common = HSV-1, CMV and Candida
- Present w/ dysphagia or odynophagia; systemic (fever), retrosternal pain; may have oral manifestation (vesicles in mouth for HSV-1 or thrush in Candida)
21
Q
HSV-1 v. CMV v. Candida
A
- HSV-1 (esp transplant) = vesicles in squamous cells coalesce –> punched out ulcerations + cherry red viral inclusion in nuclei of epithelial cells + multi-nuclei clumped together in cells at EDGE of ulcer
- CMV (esp in HIV) = “punched out ulcerations” but cherry red viral inclusion in cells at base of ulcer (granulation tissue) + marked enlargement of some cells
- Candida (MOST COMMON) = white plaques with red, inflamed mucosa between + ulceration + intraepithelial neutrophils + squamous epithelial cells at surface flake off
- Can use brown viral immunostain for CMV or HSV-1
- *Can see yeast and pseudo-hyphae form of Candida w/ special stains
