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upper git Flashcards

1
Q

what vertebral level does oesophagus start and end at

A

start: C5 end T10

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2
Q

what are the 4 sections of oesophagus

A

cervical esophagus, upper thoracic esophagus, mid thoracic esophagus, lower thoracic esophagus

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3
Q

what are three structures the esophaguis is closely associated with? how is this clinically relevant?

A

trachea, diaphragm, aorta. due to close/ tight contact these areas in oesophagus are more anatomically constricted - more likely to have PERFORATIONS

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4
Q

what type of muscle is there mainly in the cervical esophagus

A

skeletal muscle

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5
Q

main type of muscle in upper and mid thoracic esophagus

A

skeletal muscle
and smooth muscle

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6
Q

main muscle type in lower thoracic esophagus

A

smooth muscle

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7
Q

what is the arterial supply of the oesophagus

A

thoracic oesophagus : by branches of aorta,

superior aspect( i think cervical oesophagus) :by superior thyroid artery (branches of the thyrocervical trunk)

abdominal oesophagus: left gastric artery + inferiro phrenic artery

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8
Q

what is the venous drainage of oesophagus

A

thoracic oesophagus;
azygos vein

portal circulation: portal vein

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9
Q

what are anatomical features that help the LOS do its job

A

4) 3-4 cm distal esophagus in abdomen

1) diaphragm surrounds LOS - LEFT AND RIGHT CRUX

2) intact oesophageal ligament

3) angle of his - angle between oesophagus and stomach

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10
Q

describe the 4 phases of swallowing (think of bolus, muscles, sphincters

A

0: oral phase: sphincters closed, bolus preped by chewing and saliva
1: pharyngeal phase: UOS - reflexively and LOS open - vasovagal reflex (receptive relaxation reflex)
2: upper oesophageal phase: UOS closes LOS remains open
upper circular muscle rings contracts lower dilates, smooth muscle contracts sequentially
3: lower oesophageal phase: LOS closes as bolus passes though

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11
Q

what reflex opens the LOS during phase 1 of swallowing? what kind of reflex is that?

A

the vasovagal reflex- receptive relaxation reflex

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12
Q

what determines the motility in the oesophagus? how do we measure it?

A

the pressure (measured by manometry)

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13
Q

what is the pressure of peristaltic waves?

A

40mmHg

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14
Q

what is the pressure of LOS- resting and during receptive relaxation

A

20mmHg resting and <5 relaxation

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15
Q

what nerve innervates LOS

A

vagus nerve

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16
Q

what neurons are responsible for LOS relaxation? how do they achieve that?

A

NCNA neurons: inhibitory noncholinergic nonadrenergic neurons of myenteric plexus,

they inhibit vagus nerve which innervates LOS

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17
Q

When the LOS shuts after bolus passes through it does it go back to resting pressure or higher? what neurons activate the closing?

A

higher pressure, cholinergic fibres excite vagus nerve: shortening

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18
Q

what is the result problem in functional disorders of the esophagus

A

absence of a stricture (meaning food is not kept down )

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19
Q

what are the two causes of functional oesophageal disorders

A

either abnormal oesophageal contraction: hyper/ hypomootility/ disordered coordination
or
failure of protective mechs for reflux:
GORD

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20
Q

what are important classifications for dysphagia

A

1) WHERE
a) is it percise or vague
b) if its percise is it up or low= (cricopharyngeal or distal whether they feel it stuck on throat or low)

2) WHAT (gets stuck)
fluids or solids

3) PROGRESSION
intermittent or porgressive

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21
Q

what do we call pain onswallowing

A

odynophagia

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22
Q

name for difficulty swallowing

A

dysphagi a

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23
Q

difference between regurgitation and reflux

A

regurgitation is return of oesophageal contents from above an obstruction- functional or mechanical VS reflux is return of GASTRODUODENAL contents to mouth

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24
Q

what is achalasia

A

hypermotility of oesophagus

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25
pathophysiology of primary achalasia
unknown but theres a proposed mechanism involving ( i dont think i need to know this perfectly just have an idea) a) environment trigger b) genetic factors c) non autoimmune inflammatory infiltrates d) extracellular turnover wound repair fibrosis e) loss of immune tolerance (autoimmune infiltrates) f) Apoptosis of neurons g) humoral responce h) myenteic neuron abnormalities
26
what is the reason for hypermotility in achalasia?
1) loss of ganglion cells in Aurebach's plexus in LOS wall 2) decreased activity of inhibitory NCNA neurones
27
what are some pathologies linked with secondary achalasia
diseases causing oesophageal motor abnormalities similar to 1o achalasia chaga's disease protozoa infection amyloidosis, sarcoma, eosinophilic oesophagitis
28
how does the pressure of the LOS change in achalasia
LOS resting pressure: higher than normal LOS during reflex relaxation: 1) late onset, 2) pressure higher than stomach - reflex is too weak= LOS doesn't relax enough
29
what eventually happens to the pressure in the oesophagus in achalasia and why? what does this lead to?
incr pressure in oesophagus due to food collected there. causing: 1) dilation of oesophagus 2) ceasation of propagation of peristaltic wave
30
what are some secondary symptoms and conditions in achalasia and why
weight loss and disphagia bc food stuck in oesophagus, can get oesophagitis or even right sided pneumonia: rare but be aware of it
31
onset of achalasia
insidious: symptoms for years prior to seekig help
32
what happens when you dont treat achalasia
progressive oesophageal dilatation of oesophagus
33
what are achalasia patients at increased risk for? what does this mean for clinical management?
oesophageal cancer - 28fold incr in risk need to do and OGD- oesophageogastroduodenoscopy to check for cancer.
34
are oesophageal cancers common? how common? (in general) what kind of cancer is it
not rl 0.34% yearly incidence squamous cell cancer
35
what is the leading treatment fir achalasia right now
pneumatic dilatation (PD)
36
HOW DOES PD work and how effective
weakens LOS by circumferential stretching and sometimes tearing of its muscle fibres 71-90 % respond initially but many relapse
37
what is an alternative treatment to achalasia, more old school
surgery: 2 examples of procedures: 1) Hellers myotomy: continuous myotomy performed 6 cm on the oesophagus and 3 on stomach 2) dor fundoplication: anterior fundus folded over oesophagus and sutured to right side of myotomy ( to recreaate angle of his and help sphincterfunction normally)
38
risks of surgery for achalasia
oesophageal/ gastric perforation 10-16% division of vagus nerve- rare splenic injury- 1-5%
39
what is scleroderma
it is an autoimmune disease causing oesophageal hypomotility
40
what happens to oesophageal motility in scleroderma and why
in early stages scleroderma presents as hypomotility due to atrophy of smooth muscle in oesophagus eventually peristalsis in the distal portion ceases alltogether
41
what happens to LOS resting pressure in scleroderma
decreases
42
what pathology is common secondary to scleroderma
GORD
43
what is CREST syndrome
a lighter version of scleroderma, often associated with scleroderma
44
what are 2 problems with scleroderma treatment? what are the treatments
bc hypomotility there is no procedure, needs to be med treatment Once peristaltic failure occurs → usually irreversible Exclude organic obstruction Improve force of peristalsis with prokinetics (cisapride)
45
what is another name for disordered coordination?
Corkscrew oesophagus
46
what does disordered coordination of oesophagus refer to?
it refers to diffuse oesophageal SPASMS: incoordinate contractions
47
what symptoms do incoordinate oesophageal contractions lead to?
dysphagia and chest pain
48
what workup findings do incoordinate oesophageal contractions lead to?
pressures in oesophagus 400-500mmHg marked hypertrophy of circular muscle corkscrew oesophagus on Barium
49
treatment of corkscrew oesophagus and what is something to note about the outcomes
may respond to forceful PD (pneumatic dilatation) of cardia results not as predictable as achalasia
50
what areas are more prone to perforations
either anatomical contriction areas or pathological narrowing arreas (cancer, foreign body ect.)
51
MOST COMMON cause of perforations of oesophagus
Iatrogenic (OGD-oesophagogastroduodenoscopy) >50% especially if someone has diverticula or cancer other iatrogenic: stricture dilatation, sclerotherapy, achalasia dilatation
52
what is it called when you get spontaneous perforation of oesophagus?onset and causes
boerhaave's syndrome- 15% is usually secondary to vommiting sometimes from alchohol ect. its sudden
53
what happens in the body psysiologically during borhaaves
sudden increase in intra oesophageal pressure and negative pressure intra thoracically and vomiting against a closed glottis
54
where is boerhaaves on oesophageus STRICTLY?
Left posterolateral aspect of the distal oesophagus – 2cm above goj – its only there if its not there its not boerhaave’s
55
what is the prevalence of borhaaves
3.1 per 1,000,000
56
examples of foreign body causing oesophageal perforation
Disk batteries growing problem ---Cause electrical burns if embeds in mucosa Magnets Sharp objects Dishwasher tablets Acid/Alkali
57
what traumas commonly cause oesophageal perforation
neck trauma leading to penetration thorax trauma- blunt force
58
what are the symptoms of trauma caused oesophageal perforation
Can be difficult to diagnose Dysphagia Blood in saliva Haematemesis Surgical empysema
59
presentation of oesophageal perforation
pain 95% fever 80% dysphagia 70% emphysema 35%
60
investigations to do for oesophageal perforation
swallow (gastrograffin)before doing CXR or CT OGD
61
What is the treatment of oesophageal perforation?
surgery: its a surgical emergency , 2x mortality if 24 delay in diagnosis
62
initial management of oesophageal perforation before surgery
NBM (nil by mouth) IV fluids Broad spectrum A/Bs & Antifungals ITU/HDU level care Bloods (including G&S) Tertiary referral centre
63
what is an alternative of surgery used as a more conservative management in oesophageal perforation
management with covered metal stent- it’s a sponge that collects the fluid or smth
64
what surgical procedures can be used to treat oesophageal perforation
primary repair is optimal thorocotomy on other side to that of problem (this means doing some procedure that involves cutting through thorax, the soecific procedure is decided after seeing the perforation in surgery) one example is: oesophagectomy- stomach elongated and linked to oesophagus
65
what are the barriers against reflux
LOS remaining closed: pressure
66
is sporadic reflux normal ?
yes: pressure on full stomach swallowing transient sphincter opening
67
what are 3 protective mechanisms after reflux has happened
Volume clearance - oesophageal peristalsis reflex pH clearance - saliva Epithelium - barrier properties
68
what is usually the patholophysiology in GORD
failure of some protective mechanism(s) such as incr transient sphincter opening, reduced saliva production reduced buffering capacity of saliva reduced sphincter pressure abnormal peristalsis hiatus hernia defective mucosal protective mechanism (eg to alchohol)
69
what can GORD lead to
epithelial metaplasia and then carcinoma
70
what are the types o hernias
sliding hiatus hernia and rolling/ paraoesophageal hiatus hernia
71
what are the investigations done for GORD
OGD - to check for barrets, exclude cancer, oesophagitis, peptric stricture, oesophageal manometry 24h ph recording (press a button every time they have reflux and measures ph and if matches- diagnose)
72
treatments for GORD
medical 1) lifestyle 2) PPIs surgical depending on cause i guess -dilatation peptic strictures -laparoscopic nissen's fundoplication
73
role of stomach
**breaks ** food in smaller pieces: pepsin and acid **holds** food and releases slow into duodenum **kills** parasites and certain bacteria
74
parts of stomach and what is produced in each
cardia and pyloric region: mucus only (they are the rings up and down linking to other organs) body and fundus: mucus, HCL, pepsinogen pyloric antrum: gastrin (its pyloric antrum then pyloric canal then pylorus --and then duodenum)
75
what are the types of gastritis
erosive + haemorrhagic gastritis nonerosive, chronic active gastritis Atrophic (fundal gland) gastritis Reactive gastritis
76
causes and consequences of erosive and haemorrhagic gastr
Numerous causes consequences: Acute ulcer – gastric bleeding & perforation
77
in which part does Nonerosive, chronic active gastritis usually happen in stomach
antrum
78
common cause of Nonerosive, chronic active gastritis and tretment
hellicobacter pylori (amoxicillin, clarithromycin, pantoprazole) for 7-14 days
79
atrophic gastritis location
Atrophic (fundal gland) gastritis Fundus
80
cause of Atrophic (fundal gland) gastritis
Autoantibodies vs parts & products of parietal cells ---> Parietal cells atrophy ---> ↓acid & IF secretion
81
mechanisms of stimulation of gastric acid secretion
Neural ACh - postganglionic transmitter of vagal parasympathetic fibres Endocrine Gastrin (G cells of antrum) Paracrine Histamine (ECL cells & mast cells of gastric wall).
82
mechanisms of inhibition of gastric acid secretion
Endocrine Secretin (small intestine) Paracrine Somatostatin (SIH) Paracrine & autocrine PGs (E2 & I2), TGF-α & adenosine
83
what happens when theres no balance between gastric acid secretion stimulation and inhibition
risk of ulcers
84
what are the protective mechanisms to ulcer formation?
basically things that protect stomach from acid : mucus, HCO3- : it neutralises acid epithleial barrier
85
Mechanisms repairing epithelial defects
Migration Adjacent epithelial cells **flatten** to close gap via sideward migration along BM Gap closed by **cell growth** Stimulated by EGF, TGF-α, IGF-1, GRP & gastrin **Acute wound healing** **BM destroyed** - attraction of *leukocytes & macrophages*; phagocytosis of necrotic cells; -angiogenesis; repair of BM, regeneration of ECM epithelial closure by restitution & cell division.
86
what are the steps of ulcer formation
1) hellicobacter pylori infection 2) secretino of gastric juice incr 3) decr in bicarb secr 4) decr in cell formatin 5) decr in blood perfusion: full depth ulcer then can become perforation
87
what are the possibel clinical outcomes form h pylori infection
**gastritis related:** asymptomatic or chronic gastritis chronic atrophic gastr gastric or duodenal **ulcer** **cancer related**: gastric cancer MALT lymphoma intestinal metaplasia
88
ulcer treatment
its primarily medical: PPI or H2 blocker Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days)
89
when do we give elective surgical ulcer treatments
Rare - most uncomplicated ulcers heal within **12 weeks** If don’t, **change medication**, observe additional **12 weeks** Check **serum gastrin** (antral G-cell hyperplasia or gastrinoma [Zollinger-Ellison syndrome]) **OGD:** *biopsy* all 4 quadrants of ulcer (rule out malignant ulcer) if refractory (persistent)
90
indications for ulcer surgery
-Intractability (after medical therapy) -Relative: continuous requirement of steroid therapy/NSAIDs -Complications: Haemorrhage Obstruction Perforation

gastro yr 2 (9 decks)

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