Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BRS GASTROENTEROLOGY > 1b// Upper GI Tract > Flashcards

1b// Upper GI Tract Flashcards

1
Q

What are the sphincters of the oesophagus?

A

upper and lower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Label.

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where does the oesophagus start?

A

C5, trachea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which side does the aorta lie to compared to the oesophagus?

A

to the left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where does the oesophagus end?

A

T10, diaphragm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is the oesophagus split into 2?

A

thoracic and abdominal oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the arterial and venous supply to the thoracic oesophagus?

A

arterial supply from the branches of the thoracic aorta and the inferior thyroid artery

Venous drainage into the systemic circulation occurs via branches of the azygous veins and the inferior thyroid vein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the arterial and venous supply of the abdominal oesophagus?

A

The abdominal oesophagus is supplied by the left gastric artery (a branch of the coeliac trunk) and left inferior phrenic artery.

This part of the oesophagus has a mixed venous drainage via two routes: To the portal circulation via left gastric vein. To the systemic circulation via the azygous vein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the 2 plexuses in the oesophagus?

A

myenteric and meissner

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the anatomical contributions to the lower oesophageal sphincter? (4)

A
  • 3-4 cm distal oesophagus within abdomen
  • Diaphragm surrounds LOS (Leftt & Right crux)
  • An intact phrenoesophageal ligament
  • Angle of His
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the stages of swallowing?

A

stage 0= oral phase

stage 1= pharyngeal phase

stage 2= upper oesophageal phase

stage 3= lower oesophageal phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens in stage 0 of swallowing?

A

all in mouth

  • Chewing & saliva prepare bolus
  • Both oesophageal sphincters constricted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens in stage 1 of swallowing?

A
  • Pharyngeal musculature guides food bolus towards oesophagus
  • circular and longitudinal muscle
  • Upper oesophageal sphincter opens reflexly
  • LOS opened by vasovagal reflex (receptive relaxation reflex)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens in stage 2 of swallowing?

A
  • Upper sphincter closes
  • Superior circular muscle rings contract & inferior rings
    dilate
  • Sequential contractions of longitudinal muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens in stage 3 of swallowing?

A
  • Lower sphincter closes as food passes through
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What determines oesophageal motility?

A

determined by pressure measurements (manometry)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the pressure roughly of peristaltic waves?

A

40mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the LOS resting pressure?

A

roughly 20mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

When does LOS pressure decrease?

A

decreases 5mmHg during receptive relaxation (when the bolus goes down)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What mediates the decrease in pressure of the LOS?

A

mediated by inhibitory noncholinergic nonadrenergic (NCNA) neurones of the myenteric plexus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does the myenteric plexus do?

A

motility, allows relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does Meissner’s plexus do?

A

helps with secretions, and blood supply to oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the major cause of functional disorders of the oesophagus?

A

absence of structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What causes the absence of structure in the oesophagus leading to disorders? (2)

A

abnormal oesophageal contraction

failure of protective mechanisms for reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are examples that cause abnormal oesophageal contraction?

A

hypermotility
hypomotility
disordered coordination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is an example that causes failure of protective mechanisms for reflux?

A

GastroOesophageal Reflux Disease (GORD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is dysphagia?

A

difficulty swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Why is localisation important for dysphagia?

A

it can be high or low dysphagia

high= cricopharyngeal sphincter (aka UOS)

low= distal sphincter (aka LOS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the types of dysphagia?

A

for solids or fluids

intermittent or progressive (e.g., cancer)

precised or vague in appreciation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is odynophagia?

A

pain on swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is regurgitation?

A

Regurgitation refers to return of oesophageal contents from above an obstruction

May be functional or mechanical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is reflux?

A

Reflux is passive return of gastroduodenal contents to the mouth

I.e., acidic contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is an example of hypermotility?

A

Achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What causes Achalasia?

A
  • Due to loss of ganglion cells in Auerbach’s myenteric plexus in LOS wall

→ decreased activity of inhibitory NCNA neurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the aetiology of primary achalasia?

A

unk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the aetiology of secondary achalasia? (4)

A
  • Diseases causing oesophageal motor abnormalities similar to primary achalasia
  • Chagas’ Disease (a parasitic infection)
  • Protozoa infection
  • Amyloid/Sarcoma/Eosinophilic
    Oesophagitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How could you check for secondary achalasia cause?

A

serum blood sample

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Do you understand this proposed model for achalasia?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What happens to the pressure of the LOS in hypermotility/ achalasia?

A

increased resting pressure

during reflex phase pressure in LOS is markedly higher than stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What happens to the oesophagus during hypermotility/ achalasia?

A

swallowed food collects in oesophagus causing increased pressure throughout with dilation of the oesophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What happens to the “waves” in achalasia/ hypermotility?

A

propagation of peristaltic waves cease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the symptoms of achalasia/ hypermotility and why? (5+extra)

A

weight loss
trouble swallowing
pain

esophagitis
pneumonia

during swallowing, due to achalasia, excitation of the NCNA (nonadrenergic noncholinergic) neurones decrease
causing the sphincter pressure to be too high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the disease course of achalasia/ hypermotility?

A

has insidious onset- symptoms for years prior to seeking help

without treatment=> progressive oesophageal dilation of oesophagus

risk of oesophageal cancer increased x28

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is a non-surgical treatment for achalasia/ hypermotility?

A

pneumatic dilation (PD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What does pneumatic dilation do?

A

PD weakens LOS by circumferential stretching and in some cases, tearing of its muscle fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the efficacy of pneumatic dilation?

A

71-90% of patients respond initially but many patients subsequently relapse, need repeat dilation

it is almost never a definite treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Can achalasia/ hypermotility be treated surgically?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How do you treat achalasia/ hypermotility surgically?

A

Heller’s Myotomy and then Dor fundoplication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is Heller’s Myotomy?

A

a continuous myotomy performed for 6cm on the oesophagus and 3cm onto the stomach

50
Q

What is Dor fundiplication?

A

anterior fundus folded over oesophagus and sutured to right side of myotomy

51
Q

What type of surgery is it normally for achalasia/ hypermotility?

A

laparoscopic

52
Q

What is the risk of surgery for achalasia/ hypermotility?

A

oesophageal and gastric perforation

division of vagus nerve- rare

splenic injury

53
Q

What is a type of hypomotility called?

A

scleroderma

54
Q

What is scleroderma?

A

autoimmune disease

hypomotility in its early stages due to neuronal defects=> atrophy of smooth muscle of oesophagus

peristalsis in the distal portion ultimately ceases altogether

55
Q

What happens to the pressure of the LOS in scleroderma and what does it lead to?

A

decreased resting pressure of LOS

leading to gastrooesophageal reflux disease develops
- often associated with CREST syndrome

56
Q

What is the mechanism of scleroderma?

A

neuronal defects
-> muscle atrophia
-> no peristalsis in smooth muscles
-> hypomotility
-> gostrooesophageal reflux disease

57
Q

What is the treatment for slceroderma?

A
  • Exclude organic obstruction 40
  • Improve force of peristalsis with prokinetics (cisapride)
  • Once peristaltic failure occurs → usually irreversible
58
Q

What is an example of a disorders coordination disease?

A

corkscrew oesophagus

59
Q

What does corkscrew oesophagus cause?

A

diffuse oesophageal spasm

60
Q

What does diffuse oesophageal spasm cause?

A
  • Incoordinate contractions → dysphagia & chest pain
  • Pressures of 400-500 mmHg
  • Marked hypertrophy of circular muscle
  • Corkscrew oesophagus on Barium
61
Q

What is the treatment for corkscrew oesophagus?

A

may respond to forceful pneumatic dilation of cardia

results not as predictable as achalasia

62
Q

How do you see a corkscrew oesophagus?

A

endoscopy

63
Q

What is the anatomy of oesophageal perforation?

A

3x areas of anatomical constriction

Pathological narrowing (cancer, foreign body, physiological dysfunction)

64
Q

What are the 3 areas of constriction in the oesophagus?

A

cricopharyngeal constriction

aortic and bronchial constriction

diaphragmatic and sphincter constriction

65
Q

What is the aetiology of oesophageal perforations?

A
  • iatrogenic (OGD) >50%
  • Spontaneous (Boerhaave’s)- normally secondary to alcohol intake - 15%
  • Foreign body - 12%
  • Trauma - 9%
  • Intraoperative - 2%
  • Malignant - 1%
66
Q

What is the most common cause of iatrogenic oesophageal perforation?

A

OGD OesophagoGastroDuodenoscopy
- more common in presence of diverticula or cancer

67
Q

What happens in Boerhaave’s (oesophageal perforation)?

A

sudden increase in intra-oesophageal pressure with negative intrathoracic pressure

vomiting against a closed glottis

left posterolateral aspect of the distal oesophagus

68
Q

What can the foreign bodies be for foreign body oesophageal perforation?

A
  • Disk batteries growing problem
  • Cause electrical burns if embeds in mucosa
  • Magnets
  • Sharp objects
  • Dishwasher tablets
  • Acid/Alkali

*risk of attaching to mucosa= perforation
*mostly in children

69
Q

What type of trauma causes oesophageal perforation in the neck?

A

penetrating

70
Q

What type of trauma causes oesophageal perforation in the thorax?

A

blunt force

71
Q

What are symptoms of oesophageal perforation caused by trauma?

A

*can be difficult to diagnose

dysphagia
blood in saliva
haematemesis (vomiting blood)
surgical emphysema

72
Q

What is the presentation of oesophageal perforation? (4)

A
  • Pain 95 %
  • Fever 80 %
  • Dysphagia 70 %
  • Emphysema 35 %
73
Q

What type of imaging do you do for oesophageal perforation?

A

chest x ray

CT (computed tomography) scan

swallow gastrografin (contrast dye)

OGD
(OesophagoGastroDuodenoscopy)

74
Q

What is the primary management of oesophageal perforation?

A

Surgical emergency (2x increased mortality if 24h delay in diagnosis)

75
Q

What is the initial management of oesophageal perforation?

A

Nil by mouth (NBM)

IV fluids

Broad spectrum anti-b and antifungals

ITU (intensive unit)/ HDU (high dependency unit) level care

bloods (including G&S Group and Save is the sample processing that determines the patient blood group (ABO and RhD) and screens for any atypical antibodies)

tertiary referral centre

76
Q

What is the definitive management of oesophageal perforation?

A

conservative management with covered metal stent (completely blocks off hole and patient can still eat)

77
Q

What is the default for oesophageal perforation?And what is the surgery called?

A

operative management

primary repair is optimal

oesophagectomy- definitive solution

78
Q

What is a protective mechanism against reflux?

A

LOS usually closed as barrier against reflux of harmful gastric juice (pepsin and HCl)

79
Q

What is a risk factor that increases LOS pressure?

A

obesity

80
Q

What decreases LOS pressure?

A

Smoking

81
Q

What type of reflux is normal?

A

sporadic reflux

82
Q

What is sporadic reflux?

A

1)pressure on full stomach
2)swallowing
3)transient sphincter opening

83
Q

What are mechanisms to protect after reflux? (3)

A
  • Volume clearance - oesophageal peristalsis reflex
  • pH clearance - saliva
  • Epithelium - barrier properties
84
Q

What in the stomach promotes and inhibits reflux? (that picture w lots of info)

A
85
Q

What does the failure of the protective mechanisms for reflux cause?

A

GORD (gastro oesophageal reflux disease)

86
Q

What is the major thing that GORD can lead to?

A

carcinoma

87
Q

What two things from GORD causes carcinomas?

A

reflux oesophagitis

Epithelial metaplasia

88
Q

Do you understand these mechanisms for GORD?

A
89
Q

What types of hernias are there?

A

sliding and rolling

sliding hiatus hernia
and
rolling/ paraoesophageal hiatus hernia

90
Q

Picture of sliding hernia

A

picture of rolling hernia

91
Q

What types of imaging and tests do you do for GORD and why?

A

OGD
- To exclude cancer
- Oesophagitis, peptic stricture & Barretts
oesophagus confirm narrowing

Oesophageal manometry

24-hr oesophageal pH recording

92
Q

What is prescribed for GORD?

A

Medical:
Lifestyle changes (wt loss, smoking, EtOH)
PPIs

Surgical:
- Dilatation peptic strictures
- Laparoscopic Nissen’s fundoplication

93
Q

What is the function of the stomach?

A
  • Breaks food into smaller particles (acid & pepsin)
  • Holds food, releasing it in controlled steady rate into duodenum
  • Kills parasites & certain bacteria
94
Q

What do different areas of the stomach do?

A

Cardia & Pyloric Region: Mucus only

Body & Fundus: Mucus, HCl, pepsinogen

Antrum: Gastrin (G cells)

95
Q

What is gastritis?

A

Gastritis is when the lining of your stomach becomes irritated (inflamed)

96
Q

What are the types of gastritis?

A

erosive and hemorrhagic gastritis

nonerosive, chronic gastritis

atrophic (fundal gland) gastritis

reactive gastritis

97
Q

What is erosive and hemorrhagic gastritis?

A

Numerous causes

acute ulcer- gastric bleeding and perforation

98
Q

What is nonerosive, chronic active gastritis?

A

Antrum

Helicobacter pylori - Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14/7

99
Q

What is atrophic (fundal gland) gastritis?

A
  • Fundus
  • Autoantibodies vs parts & products of parietal cells
  • Parietal cells atrophy
  • ↓acid & IF (intrinsic factor) secretion
100
Q

DO you understand this diagram of the mechanism of gastritis?

A
101
Q

What is the stimulatory regulation of gastric juices?

A

Neural
Endocrine
Paracrine

102
Q

What is the neural stimulation of gastric juices?

A

ACh- postganglionic transmitter of vagal parasympathetic fibres

103
Q

What is the endocrine stimulation of gastric juices?

A

gastrin (G cells of antrum)

104
Q

What is the paracrine stimulation of gastric juices?

A

histamine (ECL (Enterochromaffin-like) cells and mast cells of gastric wall)

105
Q

What are the inhibitory regulations of gastric regulation?

A

Endocrine
Paracrine
Paracrine and Autocrine

106
Q

What is the endocrine inhibition of gastric secretion?

A

secretin (small intestine)

107
Q

What is the paracrine inhibition of gastric secretion?

A

somatostatin (SIH)
- secreted by delta cells
- pyloric antrum, the duodenum and the pancreatic islets

108
Q

What is the paracrine and autocrine inhibition of gastric juices?

A
  • PGs (E2 & I2), TGF-α & adenosine
109
Q

Do you understand this diagram?

A

Yes

110
Q

Do you understand this diagram of mucosal protection, How is the mucosa protected?

A
  1. epithelial barrier
  2. mucus film
  3. bicarbonate
111
Q

What needs to happen after ulcer for your body?

A

epithelial repair and wound healing

112
Q

What are the 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; regeneration of ECM after repair of BM
* epithelial closure by restitution & cell division.

113
Q

What happens to the epithelial layer during an ulcer?

A

breaks mucosal epithelial layer

114
Q

What can cause gastric ulcers?

A
115
Q

Do you understand this diagram?

A

yes

116
Q

What are the clinical outcomes of infections of H.Pylori? (4)

A
117
Q

What are the treatments for Ulcers?

A

primarily medical
Elective Surgical prescription

118
Q

What is the medical treatment for ulcers?

A
  • PPI or H2 blocker
  • Triple Rx (amoxicillin, clarithromycin,
    pantoprazole) for 7-14 days)
119
Q

What do you do before surgical treatment of ulcers?

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
120
Q

What are the surgical indications of ulcers?

A

Intractability aka hard to control/ manage (after medical therapy)

Relative: continuous requirement of
steroid therapy/NSAIDs

121
Q

What are the complications of ulcer surgery?

A

haemorrhage
obstruction
perforation

122
Q

What do you measure to check pancreas function?

A

amylase

BRS GASTROENTEROLOGY (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions