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gastro yr 2 > upper git > Flashcards

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
Q

pathophysiology of primary achalasia

A

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

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26
Q

what is the reason for hypermotility in achalasia?

A

1) loss of ganglion cells in Aurebach’s plexus in LOS wall

2) decreased activity of inhibitory NCNA neurones

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27
Q

what are some pathologies linked with secondary achalasia

A

diseases causing oesophageal motor abnormalities similar to 1o achalasia

chaga’s disease

protozoa infection

amyloidosis, sarcoma, eosinophilic oesophagitis

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28
Q

how does the pressure of the LOS change in achalasia

A

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

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29
Q

what eventually happens to the pressure in the oesophagus in achalasia and why? what does this lead to?

A

incr pressure in oesophagus due to food collected there. causing:
1) dilation of oesophagus
2) ceasation of propagation of peristaltic wave

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30
Q

what are some secondary symptoms and conditions in achalasia and why

A

weight loss and disphagia bc food stuck in oesophagus,

can get oesophagitis or even right sided pneumonia: rare but be aware of it

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31
Q

onset of achalasia

A

insidious: symptoms for years prior to seekig help

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32
Q

what happens when you dont treat achalasia

A

progressive oesophageal dilatation of oesophagus

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33
Q

what are achalasia patients at increased risk for? what does this mean for clinical management?

A

oesophageal cancer - 28fold incr in risk

need to do and OGD- oesophageogastroduodenoscopy to check for cancer.

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34
Q

are oesophageal cancers common? how common? (in general) what kind of cancer is it

A

not rl 0.34% yearly incidence squamous cell cancer

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35
Q

what is the leading treatment fir achalasia right now

A

pneumatic dilatation (PD)

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36
Q

HOW DOES PD work and how effective

A

weakens LOS by circumferential stretching and sometimes tearing of its muscle fibres

71-90 % respond initially but many relapse

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37
Q

what is an alternative treatment to achalasia, more old school

A

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
Q

risks of surgery for achalasia

A

oesophageal/ gastric perforation 10-16%

division of vagus nerve- rare
splenic injury- 1-5%

39
Q

what is scleroderma

A

it is an autoimmune disease causing oesophageal hypomotility

40
Q

what happens to oesophageal motility in scleroderma and why

A

in early stages scleroderma presents as hypomotility due to atrophy of smooth muscle in oesophagus

eventually peristalsis in the distal portion ceases alltogether

41
Q

what happens to LOS resting pressure in scleroderma

A

decreases

42
Q

what pathology is common secondary to scleroderma

A

GORD

43
Q

what is CREST syndrome

A

a lighter version of scleroderma, often associated with scleroderma

44
Q

what are 2 problems with scleroderma treatment? what are the treatments

A

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
Q

what is another name for disordered coordination?

A

Corkscrew oesophagus

46
Q

what does disordered coordination of oesophagus refer to?

A

it refers to diffuse oesophageal SPASMS: incoordinate contractions

47
Q

what symptoms do incoordinate oesophageal contractions lead to?

A

dysphagia and chest pain

48
Q

what workup findings do incoordinate oesophageal contractions lead to?

A

pressures in oesophagus 400-500mmHg
marked hypertrophy of circular muscle
corkscrew oesophagus on Barium

49
Q

treatment of corkscrew oesophagus and what is something to note about the outcomes

A

may respond to forceful PD (pneumatic dilatation) of cardia

results not as predictable as achalasia

50
Q

what areas are more prone to perforations

A

either anatomical contriction areas or pathological narrowing arreas (cancer, foreign body ect.)

51
Q

MOST COMMON cause of perforations of oesophagus

A

Iatrogenic (OGD-oesophagogastroduodenoscopy) >50%
especially if someone has diverticula or cancer

other iatrogenic: stricture dilatation, sclerotherapy, achalasia dilatation

52
Q

what is it called when you get spontaneous perforation of oesophagus?onset and causes

A

boerhaave’s syndrome- 15% is usually secondary to vommiting sometimes from alchohol ect. its sudden

53
Q

what happens in the body psysiologically during borhaaves

A

sudden increase in intra oesophageal pressure and negative pressure intra thoracically
and
vomiting against a closed glottis

54
Q

where is boerhaaves on oesophageus STRICTLY?

A

Left posterolateral aspect of the distal oesophagus – 2cm above goj – its only there if its not there its not boerhaave’s

55
Q

what is the prevalence of borhaaves

A

3.1 per 1,000,000

56
Q

examples of foreign body causing oesophageal perforation

A

Disk batteries growing problem

—Cause electrical burns if embeds in mucosa

Magnets

Sharp objects

Dishwasher tablets

Acid/Alkali

57
Q

what traumas commonly cause oesophageal perforation

A

neck trauma leading to penetration
thorax trauma- blunt force

58
Q

what are the symptoms of trauma caused oesophageal perforation

A

Can be difficult to diagnose
Dysphagia
Blood in saliva
Haematemesis
Surgical empysema

59
Q

presentation of oesophageal perforation

A

pain 95%
fever 80%
dysphagia 70%
emphysema 35%

60
Q

investigations to do for oesophageal perforation

A

swallow (gastrograffin)before doing
CXR
or
CT

OGD

61
Q

What is the treatment of oesophageal perforation?

A

surgery: its a surgical emergency , 2x mortality if 24 delay in diagnosis

62
Q

initial management of oesophageal perforation before surgery

A

NBM (nil by mouth)
IV fluids
Broad spectrum A/Bs & Antifungals
ITU/HDU level care
Bloods (including G&S)
Tertiary referral centre

63
Q

what is an alternative of surgery used as a more conservative management in oesophageal perforation

A

management with covered metal stent- it’s a sponge that collects the fluid or smth

64
Q

what surgical procedures can be used to treat oesophageal perforation

A

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
Q

what are the barriers against reflux

A

LOS remaining closed: pressure

66
Q

is sporadic reflux normal ?

A

yes:
pressure on full stomach
swallowing
transient sphincter opening

67
Q

what are 3 protective mechanisms after reflux has happened

A

Volume clearance - oesophageal peristalsis reflex
pH clearance - saliva
Epithelium - barrier properties

68
Q

what is usually the patholophysiology in GORD

A

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
Q

what can GORD lead to

A

epithelial metaplasia and then carcinoma

70
Q

what are the types o hernias

A

sliding hiatus hernia and rolling/ paraoesophageal hiatus hernia

71
Q

what are the investigations done for GORD

A

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
Q

treatments for GORD

A

medical
1) lifestyle
2) PPIs

surgical depending on cause i guess
-dilatation peptic strictures
-laparoscopic nissen’s fundoplication

73
Q

role of stomach

A

**breaks ** food in smaller pieces: pepsin and acid

holds food and releases slow into duodenum

kills parasites and certain bacteria

74
Q

parts of stomach and what is produced in each

A

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
Q

what are the types of gastritis

A

erosive + haemorrhagic gastritis

nonerosive, chronic active gastritis

Atrophic (fundal gland) gastritis

Reactive gastritis

76
Q

causes and consequences of erosive and haemorrhagic gastr

A

Numerous causes

consequences: Acute ulcer – gastric bleeding & perforation

77
Q

in which part does Nonerosive, chronic active gastritis usually happen in stomach

A

antrum

78
Q

common cause of Nonerosive, chronic active gastritis and tretment

A

hellicobacter pylori (amoxicillin, clarithromycin, pantoprazole) for 7-14 days

79
Q

atrophic gastritis location

A

Atrophic (fundal gland) gastritis
Fundus

80
Q

cause of Atrophic (fundal gland) gastritis

A

Autoantibodies vs parts & products of parietal cells —> Parietal cells atrophy —>
↓acid & IF secretion

81
Q

mechanisms of stimulation of gastric acid secretion

A

Neural
ACh - postganglionic transmitter of vagal parasympathetic fibres
Endocrine
Gastrin (G cells of antrum)
Paracrine
Histamine (ECL cells & mast cells of gastric wall).

82
Q

mechanisms of inhibition of gastric acid secretion

A

Endocrine
Secretin (small intestine)
Paracrine
Somatostatin (SIH)
Paracrine & autocrine
PGs (E2 & I2), TGF-α & adenosine

83
Q

what happens when theres no balance between gastric acid secretion stimulation and inhibition

A

risk of ulcers

84
Q

what are the protective mechanisms to ulcer formation?

A

basically things that protect stomach from acid :
mucus,
HCO3- : it neutralises acid
epithleial barrier

85
Q

Mechanisms repairing epithelial defects

A

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
Q

what are the steps of ulcer formation

A

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
Q

what are the possibel clinical outcomes form h pylori infection

A

gastritis related:
asymptomatic or chronic gastritis
chronic atrophic gastr

gastric or duodenal ulcer

cancer related:
gastric cancer MALT lymphoma
intestinal metaplasia

88
Q

ulcer treatment

A

its primarily medical: PPI or H2 blocker
Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days)

89
Q

when do we give elective surgical ulcer treatments

A

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
Q

indications for ulcer surgery

A

-Intractability (after medical therapy)

-Relative: continuous requirement of steroid therapy/NSAIDs

-Complications:
Haemorrhage
Obstruction
Perforation

gastro yr 2 (9 decks)

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