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Gastro Flashcards

1
Q

What are the 4 layers of the GIT?

A

Mucosa (innermost)
Submucosa
External muscle layers
Serosa (outermost)

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2
Q

What are the layers of the mucosa?

A

Epithelium
Lamina propria
Muscularis mucosae

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3
Q

What are the layers of the external muscle of the ileum

A

Circular muscle

Longitudinal muscle

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4
Q

What are the layers of the serosa?

A

Areolar connective tissue

Epithelium

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5
Q

What is the nervous supply to the ileum?

A

Myenteric plexus - Auerbach’s plexus

Submucosal plexus - Meissner’s plexus

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6
Q

What characteristics of the epithelium makes it good for its job?

A

Selectively permeable barrier - absorption
Facilitate transport and digestion of food
Promote absorption
Produce hormones
Produce mucus

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7
Q

What characteristics of the lamina propria makes it good for its job?

A

Lots of lymphoid nodules and macrophages

Produce antibodies mainly IgA which is resistant to proteases

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8
Q

What characteristics of the muscularis mucosae makes it good for its job?

A

Layers of smooth muscle orientated in different directions
Keeps epithelium in contact with gut contents
Helps keep crypt content dynamic - stasis quickly results in infection

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9
Q

Through what layers of the GIT would be classes as a peptic ulcer?

A

Ulceration breaching the muscularis mucosae

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10
Q

In which layer of the GIT is Meissner’s plexus found?

A

Submucosal layer

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11
Q

In which layer of the GIT is Auerbach’s plexus found?

A

muscularis propria

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12
Q

What does the submucosa contain?

A

Contains:
dense connective tissue, blood vessels, glands, lymphoid tissue
Submucosal plexus - Meissner’s

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13
Q

What innervation does the inner circular muscle of the ileum contain?

A

Myenteric plexus

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14
Q

What does the serosa layer contain?

A

Blood and lymph vessels and adipose tissue

Continuous with the mesenteries

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15
Q

What types of cells are found in the GIT?

A

Stratified squamous in oesephagus and distal anus

Simple columnar everywhere else

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16
Q

What is the cell shape of the enterocyte?

A

Simple columnar epithelium

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17
Q

What is the name for the folds of the small intestine?

A

Plicae circularis

Valvulae conniventes

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18
Q

What is the base called between two villi?

A

Crypts

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19
Q

What is the subunit of a villi that gives it the brush border appearance?

A

Microvilli

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20
Q

What happens to the number of goblet cells from Duodenum to the Colon?

A

Increasing in number

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21
Q

What forces the cell nucleus to be squished to the bottom of a mucosal epithelial cell?

A

Mucous

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22
Q

What is the function of the mucus in the GIT?

A

Protect the epithelium from:
Friction - acts as a lubricant
Chemical damage - acidic environment
Bacterial inflammation - forms physical barrier

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23
Q

What is the scientific name of the gastric mucous cells?

A

Foveolar cells

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24
Q

What do gastric mucous cells do and what is their location?

A

Bottom of the pits

Secrete mucous/ HCO3 that forms a barrier to stomach acid

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25
Q

What is the name for the temporary folds in the stomach?

A

Rugae

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26
Q

What cells are found in the crypts in the GIT?

A

Stem cells - the GIT epithelium is replaced in 2-4 days
Paneth cells - look after stem cells by guarding against infection
Enteroendocrine cells

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27
Q

What is the function of the paneth cells in the GIT?

A

Secrete antibacterial proteins that protect the stem cells

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28
Q

How much saliva is produced per day?

A

1.5L

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29
Q

How much gastric secretions are produced per day?

A

2L

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30
Q

How much pancreatic secretions are produced per day?

A

1.5L

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31
Q

How much bile is produced per day?

A

0.5L

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32
Q

How much secretions are produced by the SI per day?

A

1.5L

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33
Q

What are brunners glands?

A

Found in the duodenum - neutralise acid from the stomach by releasing a hypertonic solution. Protective layer of alkaline solution lining duodenum

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34
Q

Describe the structure of the abdominal wall

A 
Skin
Fascia/ fat - superficial and deep
3x anterolateral muscles - External oblique, Internal oblique, Transverse abdominis, Rectus abdominis
Transversalis fascia
Peritoneum
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35
Q

What direction does External oblique muscle run?

A

Back to front- hands in pockets direction

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36
Q

What direction does Internal oblique muscle run?

A

Inferior to superior from iliac crest to 8th and 12th ribs

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37
Q

What direction does transversus abdominis muscle run?

A

Transverse direction - across the body

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38
Q

What direction does Rectus abdominis muscle run?

A

Up and down direction

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39
Q

What makes up the rectus sheath?

A

Aponeurosis of the external oblique muscle - makes the anterior rectus sheath layer
Aponeurosis of the internal oblique muscle - makes up the anterior and posterior layers of rectus sheath
Aponeurosis of the transversus abdominis - contributing to posterior layer of rectus sheath

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40
Q

From what rib does rectus abdominis muscle originate from?

A

5th rib

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41
Q

What is the structure separating the two verticle layers of rectus abdominis in the middle of the body?

A

Linea alba

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42
Q

What is the structure that separate the horizontal layers of the rectus abdominis muscle?

A

Tendinous intersection

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43
Q

How many muscle bellies make up rectus abdominis?

A

10 muscle bellies. 5 on each side of the linea alba

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44
Q

What bone does rectus abdominis muscle insert onto?

A

Pubic crest

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45
Q

What bone does the oblique muscles of the abdomen insert onto?

A

Iliac crest - external oblique

And 5th to 12th Ribs - internal oblique

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46
Q

What ribs does external oblique originate from?

A

5th rib to the 12th rib

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47
Q

What ribs does internal oblique originate from?

A

5th rib to the 12th rib

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48
Q

What abdominal muscle have aponeurosis?

A

External, internal obliques and transverse abdominis

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49
Q

What is the arcuate line?

A

Lower limit of the posterior layer of rectus sheath

Roughly half way between umbilicus and pubic crest

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50
Q

What is the basic histology of the peritoneum?

A

Mesothelium lined cavity
Flattened simple squamous epithelium
Basement membrane
Dense irregular connective tissue

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51
Q

What is the name given to the viscera that are not enveloped by the peritoneum?

A

Retroperitoneal viscera

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52
Q

What 5 structures are retroperiteneal?

A

Pancreas
Kidneys
Duodenum
Abdominal aorta and vena cava

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53
Q

What is the embryological development pathway of the parietal peritoneum and what type of pain is felt on insult?

A

Somatic development - sensory pain

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54
Q

What is the embryological development pathway of the visceral peritoneum and what pain is felt on insult?

A

Splanchnic development - generalised pain - referred pain

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55
Q

What is a mesentry?

A

Double fold of peritoneum that attaches certain viscera to the posterior abdominal wall

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56
Q

What is contained in a mesentry?

A

Blood vessels
Lymph vessels
Nerves
Fat

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57
Q

What GI structures are intraperitoneal?

A 
Jejunum
Ileum
Appendix
Transverse colon
Sigmoid colon
Rectum
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58
Q

What 2 sphincters are found in the oesophagus?

A

Upper oesophageal sphincter - prevents air from entering GIT

Lower oesophageal sphincter - prevents reflux from stomach into oesphagus

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59
Q

What is chyme?

A

A fluid that passes out from the stomach that consists of gastric secretions and partially digested food

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60
Q

What is the function of the terminal ileum?

A

B12 absorption

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61
Q

What is the function of jejunum?

A

Nutrient absorption

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62
Q

What is the terminal ileum?

A

End of the ileum just before the start of the large bowel/ colon

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63
Q

What is the broad function of the large bowel?

A

Final water absorption
Temporary storage
Final electrolyte absorption - some bile salt absorption and production of short chain fatty acids

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64
Q

What is the broad function of the ileum?

A

Water/ electrolyte absorption

Bile recirculation

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65
Q

What is the broad nervous control of the GIT?

A

Parasympathetic NS
Vagus nerve
Pelvic splanchnic nerves (S2-S4)
Craniosacral outflow

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66
Q

What peptides are released by the PNS in the GIT?

A

Gastrin releasing peptide

Vasoactive-inhibitory peptide

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67
Q

What nerve roots give sympathetic control of the GIT?

A

T5-L2

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68
Q

What nerve roots make up the splanchnic nerves?

A

Greater - T5-T9
Lesser - T10-11
Least - T12

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69
Q

What is the function of Meissner’s plexus?

A

Secretions and blood flow

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70
Q

What is the function of Auerbach’s plexus?

A

Motility

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71
Q

What is the greater sac/omentum of the peritoneum?

A

The peritoneum connecting the stomach to the transverse colon that acts as an apron for the GIT

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72
Q

What is the ligament that connects the stomach to the transverse colon?

A

Gastro-colic ligament

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73
Q

What is the lesser omentum?

A

The peritoneum that connects the liver anteriorly and posteriorly to the stomach

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74
Q

What is the epiploic foramen?

A

The space between the stomach and the posterior peritoneum/ abdominal wall

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75
Q

What causes visceral pain?

A

Visceral stretching, inflammation, ischaemia

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76
Q

Describe visceral pain?

A

Diffuse/ poorly defined pain

Often midline

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77
Q

What is the sympathetic outflow to the GIT?

A 
T5-L2 - preganglionic
Pass through (paravertebral) sympathetic trunk without synapsing (preganglionic)
Form (abdominopelvic) presynaptic splanchnic nerves (preganglionic) - greater, lesser, least
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78
Q

What do splanchnic nerves synapse with?

A

Prevertebral ganglia:

Coeliac, renal, superior mesenteric, inferior mesenteric plus others

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79
Q

What is a caecal volvulus?

A

Distended small bowel

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80
Q

What is the pathway of pain from the caecal volvulus to the pain perceived in its location?

A

General visceral afferents activated-> Afferent impulse goes back to superior mesenteric ganglia (prevetebral) -> continues back along least splanchnic nerve -> passes back through sympathetic chain (paravertebral) -> into dorsal horn of spine -> converge with somatic afferents at that spinal level -> brain interprets visceral afferent to be coming from the spinal level dermatomes -> peri-umbilical pain

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81
Q

What is a hernia?

A

Protrusion of part of the abdominal contents beyond the normal confines of the abdominal wall

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82
Q

What are signs and symptoms of a hernia?

A

Fullness or swelling
Gets larger when intra-abdominal pressure increases
Aches

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83
Q

What are signs and symptoms of an incarcerated hernia?

A

Pain
Cant be moved
Nausea and vomiting (and other signs of bowel obstruction)
Systemic problems if bowel has become ischaemic

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84
Q

What are the causes of hernia?

A

Congenitally related
Post surgery where wounds have not healed adequately (incisional hernia)
Normal point of weakness
Anything that increases abdominal pressure - Obesity, Weightlifting, Chronic constipation/ coughing

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85
Q

In basics what are the 3 parts of a hernia?

A

Sac
Contents of the sac
Coverings of the sac

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86
Q

What is included in the sac of a hernia?

A

Pouch of peritoneum

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87
Q

What is included in the contents of the sac?

A

Any structure found within the abdominal cavity

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88
Q

What is included in the coverings of the sac?

A

Layers of the abdominal wall through which the hernia has passed

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89
Q

Where are the anatomically normal areas of weakness in the abdominal wall?

A

Inguinal canal
Femoral canal
Umbilicus
Previous incisions

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90
Q

What is the inguinal canal?

A

Oblique passage through the lower part of the abdominal wall
In males - structure pass through from abdomen to the testis
In females - round ligament goes from uterus-labium majors

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91
Q

What is the processus vaginalis (becomes tunica vaginalis)?

A

Pouch of peritoneum

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92
Q

What is the Gubernaculum?

A

Condensed band of mesenchume that links inferior portion of testis to labioscrotal swelling

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93
Q

Why is a patent processus vaginalis a problem for hernias?

A

It is an open connection from the abdomen to the scrotum and this allows the abdominal contents to fall into the area

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94
Q

What makes up the posterior wall of the inguinal canal?

A

Transversus abdominis

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95
Q

What makes up the superior wall (roof) of the inguinal canal?

A

Internal oblique/ transversus abdominis - muscular arches

Aponeurosis

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96
Q

What makes up the anterior wall of the inguinal canal?

A

External oblique and the aponeurosis of the external oblique muscle

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97
Q

What makes up the floor of the inguinal canal?

A

Inguinal ligament + lacunar ligament (medially)

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98
Q

What two structures does the inguinal ligament join?

A

ASIS and pubic tubercle

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99
Q

What is the deep ring?

A

Hole in the transversalis fascia

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100
Q

What is the conjoint tendon?

A

Internal oblique and tranversus abdominus muscle aponeurosis that inserts into the crest of the pubis

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101
Q

What is the superficial ring?

A

A hole in the aponeurosis of the external oblique muscle

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102
Q

What is the difference between the direct and indirect inguinal hernia?

A

Indirect - through inguinal canal

Direct - through abdominal wall at Hesselbachs triangle - doesn’t go through the inguinal canal

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103
Q

What is the important landmark of the inferior epigastric vessels in the context of inguinal hernia?

A

A direct hernia will be medial to the inferior epigastric vessels and does not traverse the epigastric vessels.
Indirect will be lateral to the inferior epigastric vessels.

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104
Q

What are the landmarks of Hesselbachs triangle?

A

Medial border - Rectus abdominis muscle lateral wall
Superior border - Inferior epigastric vessels
Lower border - Inguinal ligament

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105
Q

What is the purpose of the deep inguinal ring?

A

It allows ductus deferens to pass through it with blood vessels

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106
Q

What does incarcerated refer to in hernias?

A

Stuck hernia that cant be reducible - strangulated

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107
Q

What is an omphalocele and why does it happen?

A

Failure of the midgut to return to the abdomen during development
Viscera persist outside the abdominal cavity within umbilical ring - abdominal cavity may not grow to correct side to accommodate viscera
Viscera are covered in peritoneum - gut has a chance to develop relatively normally - then feeding can commence
It is often associated with other genetic problems - mortality rate is high

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108
Q

What is gastroschisis and when do problems arise?

A

Defect in ventral abdominal wall
Abdominal viscera not covered in peritoneum - exposed amniotic fluid
Tend to get problems with gut development (intestinal atresia, short/ inflamed gut) - problems arise around feeding

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109
Q

What has a better survival omphalocele or gastroschisis?

A

Gastroschisis - because there is less of a genetic component to it which can be closed at birth

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110
Q

Describe a umbilical hernia?

A

Commonly found in infants
Hernia at the site of the umbilicus
Not usually painful
80-90% close by age 3

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111
Q

Describe a paraumbilical hernia?

A

Central midline hernia
Goes through linea alba in region of umbilicus
F>M
Obesity
Risk of strangulation as defect is often small

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112
Q

What are symptoms of a hernia?

A

Based around if the bowel loop gets trapped:

Pain, Vomiting, Sepsis

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113
Q

What is a problem with strangulated hernia?

A

Blood supply is disrupted - can lead to tissue necrosis

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114
Q

In what week of the embryonic period does the embryo fold?

A

4th week

Laterally and cephalocaudally

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115
Q

Describe in embryological terms what the gut tube is

A 
Endoderm lined tube
Runs the length of the body
Blind pouches at the head and tail end
Opening at the umbilicus
Splanchnic mesoderm covering
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116
Q

Embryonically what is classed as the foregut, midgut and hindgut?

A

Foregut - oesophagus, stomach, pancreas, liver, gall-bladder, duodenum (proximal to entrance of bile duct)
Midgut - duodenum (distal to entrance of bile duct), jejunum, ileum, cecum, ascending colon, proximal 2/3 transverse colon
Hindgut - Distal 1/3 transverse colon, descending colon, sigmoid colon, rectum, upper anal canal, internal lining of bladder and urethra

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117
Q

What does the classification system of foregut, midgut and hindgut help us understand?

A

The blood supply to the gut - each embryonic segment receives blood supply from a distinct branch of the abdominal aorta.
Foregut - coeliac trunk
Midgut - Superior mesenteric artery
Hindgut - Inferior mesenteric artery

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118
Q

What is the caveat to the blood supply to the foregut, midgut and hindgut?

A

The structures that develop close to the junction between the foregut and midgut will have a mixed blood supply

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119
Q

What is the blood supply to the duodenum proximal entry of bile duct?

A

Gastroduodenal artery and superior pancreaticoduodenal artery (CT)

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120
Q

What is the blood supply to the duodenum distal to the entry of the bile duct?

A

inferior pancreaticoduodenal artery (SMA)

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121
Q

What is the difference in blood supply to the pancreas?

A

Head - superior pancreacticoduodenal artery (CT) AND inferior pancreacticoduodenal artery (SMA)

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122
Q

What two embryonic mesentries are attached to the gut tube?

A

Dorsal mesentery - the whole gut tube

Ventral mesentery - only foregut

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123
Q

Embryonically what do the dorsal and ventral mesentries in the foregut help to form?

A

Form a left and right sac
Left sac - greater sac
Right sac - lesser sac - comes to lie behind the stomach

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124
Q

Describe the greater and lesser omenta

A

Omenta are specialised regions of peritoneum
Greater omentum - formed from the dorsal mesentery and is the first structure seen when the abdominal cavity is opened anteriorly
Lesser omentum - formed from the ventral mesentery - lesser curve of the stomach - free edge conducts the portal triad

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125
Q

What is a secondarily retroperitoneal structure?

A

The structure began development invested by the peritoneum, had a mesentery but with successive growth and development the mesentery is lost through fusion at the posterior abdominal wall

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126
Q

How does the GI and resp tracts separate?

A

Had 2 buds - lung bud and liver bud

Separation occurs in 4th week to form a respiratory diverticulum and the oesophagus

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127
Q

What are the potential problems seen with abnormal positioning of the tracheosophageal septum?

A
  • Proximal blind-end oesphagus with tracheosophageal fistula
  • Blind ended oesophagus and trachea
  • Distal blind ended oesophagus and tracheoesophageal fistula proximally
  • Tracheosophageal fistula in both proximal and distal oesophagus
  • Incomplete separation of both pathways
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128
Q

What mesentery in development derives the liver and biliary system?

A

Ventral mesentery

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129
Q

What mesentery in development derives the pancreas?

A

Components develop in both ventral and dorsal mesenteries
Uncinate process and inferior head = ventral
Superior head, neck, body and tail = dorsal

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130
Q

What is the falciform ligament?

A

AKA round ligament

Is the ligament that is vertical in its line along the liver

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131
Q

What is the primary intestinal loop?

A

The midgut elongates enormously
Runs out of space
Makes a loop that has the SMA as its axis - is connected to the yolk sac by the vitelline duct and has cranial and caudal limbs

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132
Q

During which week of gestation does the primary intestinal loop elongate?

A

6th week

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133
Q

Why do intestines loop out of the body during growth?

A

Liver grows rapidly and so there is less space to accommodate the small intestine

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134
Q

How does the midgut rotate and in which direction?

A

Rotation along the superior mesenteric artery
The cranial and caudal limbs rotate in an anticlockwise direction
From a cranial and caudal orientation it changes to a lateral orientation

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135
Q

What are the risks associated with midgut defects?

A

Volvulus - strangulation/ ischaemia
Volvulus= twisting on itself
Obstruction

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136
Q

What is a vitelline cyst?

A

Vitelline duct forms fibrous strands but leaves a fluid-filled cyst in the band

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137
Q

What is a vitelline fistula?

A

Gut is open to the outside. Therefore contents leak out

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138
Q

What is a Meckel’s diverticulum?

A

Ileal diverticulum +/- the vitelline duct may or may not be patent

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139
Q

What is a vitelline duct?

A

A tube that connects the yolk sac to the midgut lumen of the developing foetus. This is usually only present from the 4th week and obliterates in 9th week

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140
Q

What is the rule of 2’s in Meckel’s diverticulum?

A 
2% of population
2:1 Males to females
2 feet from the ileocaecal valve
Usually detected in under 2's
2inches long
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141
Q

What type of tissue is usually found in a Meckel’s diverticulum?

A

Ectopic gastric or pancreatic tissues

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142
Q

Why is recanalisation of the gut tube important for later life?

A

Primitive gut is a simple tube -> but cell growth becomes so rapid that the lumen is partially or completely obliterated (oesophagus, bile duct, small intestine)
Recanalisation occurs to restore the lumen
If recanalisation is wholly or partially unsuccessful, atresia or stenosis of the structure

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143
Q

Where is recanalisation least likely to occur successfully?

A

Duodenum - due to vascular accidents

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144
Q

What is a common abnormality of the stomach in infants?

A

Pyloric stenosis

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145
Q

What causes pyloric stenosis?

A

Hypertrophy of the circular muscle in the pyloric sphincter region

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146
Q

What is a symptom of pyloric stenosis?

A

Projectile vomiting in infants

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147
Q

What is the pectinate line?

A

Anal canal is divided by the pectinate line into histologically distinct superior and inferior parts
Indicates difference in arterial supply, venous and lymphatic drainage and innervation

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148
Q

What is the blood supply, innervation, histological features and lymphatic drainage of the anal canal above the pectinate line?

A

Blood supply - IMA
Innervation - S2,3,4 pelvic parasympthetics
Histological features - Columnar epithelium
Lymph drain= internal iliac nodes

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149
Q

What is the blood supply, innervation, histological features and lymphatic drainage of the anal canal below the pectinate line?

A

Blood supply - pudendal artery
Innervation - S2,3,4 pudendal nerve
Histological features - Stratified epithelium
Lymph drainage - superficial inguinal nodes

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150
Q

What is the difference in the sensory afferents of the areas above and below the pectinate line?

A

Above the pectinate line - sensation only to stretch

Below the pectinate line - temperature, touch and pain

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151
Q

What are the names of the areas of pain felt by the foregut, midgut and hind gut?

A

Foregut - epigastrium
Midgut - periumbilical
Hindgut - suprapubic

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152
Q

What structures in the GIT retain mesenteries?

A 
Jejunum
Ileum
Appendix
Transverse colon
Sigmoid colon
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153
Q

What structures in the GIT are secondarily retroperitoneal?

A

Duodenum
Ascending colon
Descending colon
Rectum (no peritoneal covering in distal 1/3)

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154
Q

What structures of the GIT are in the cranial and caudal limbs of the primary bowel loops?

A

Cranial - distal duodenum, jejunum, proximal ileum

Caudal limb - distal ileum, cecum, appendix, ascending colon, proximal 2/3 transverse colon

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155
Q

What parts of the GIT are more commonly found to have atresia?

A

Duodenum> Jejunum = Ileum > colon

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156
Q

What nerve innervates the midgut?

A

Parasympathetic - vagus

Sympathetic - superior mesenteric ganglion and plexus

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157
Q

What nerve innervates the hindgut?

A

PNS - pelvic - S2,3,4

SNS - Inferior mesenteric ganglion and plexus

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158
Q

What is the composition of saliva?

A

Mostly water
Hypotonic - depending on flow rate - not enough time to make ionic changes
Rich in potassium and bicarbonate (pH slightly acidic to 8)
Mucins help with lubrication
Amylase - secrete by salivary glands
Lingual lipase - secreted by lingual glands
Immune proteins - IgA, lysozyme, lactoferrin - sequesters iron because bacteria need iron to grow

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159
Q

What is xerostomia?

A

Dry mouth

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160
Q

What is the problem with dry mouth?

A

Decreased antibacterial properties therefore increased likelihood of getting dental carries, ulcers and bad breath

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161
Q

What are the salivary glands?

A

Parotid gland
Submandibular gland
Sublingual gland

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162
Q

What does the parotid gland lie on top of?

A

Masseter muscle

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163
Q

What is interesting about the parotid gland duct in its pathway?

A

Penetrates the buccinator muscle opposite the crown of the 2nd upper molar tooth

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164
Q

What is the difference in the innervation of the glands of the mouth?

A

Above oral fissure - greater petrosal nerve of facial nerve (CN VII)
Below oral fissure - chordates tympani of facial nerve (CN VII)
Parotid gland - innervated by CN IX - glossopharyngeal nerve

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165
Q

What is the big problem with mumps and the face?

A

Parotitis - very painful as there is a capsule therefore can’t swell appropriately.
Trigeminal nerve is sensory to parotid gland

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166
Q

What imaging method is used to check the parotid gland function?

A

Parotid sialography

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167
Q

What are the 3 phases of swallowing

A

Oral preparatory phase
Pharyngeal phase
Oesophageal phase

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168
Q

Of the oral preparatory phase of swallowing what are the 3 main features of it?

A

Voluntary
Pushes bolus back towards the pharynx
Once bolus touches pharyngeal wall the pharyngeal phase begins

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169
Q

Of the pharyngeal phase of swallowing what are the 6 main features of it?

A

Involuntary
Soft palate seals off nasopharynx
Pharyngeal constrictors push bolus downwards
Larynx elevates, closing epiglottis
Vocal cords adduct (protecting airway) and breathing temporarily ceases
Opening of the upper oesophageal sphincter

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170
Q

Of the oesophageal phase of swallowing what are the 3 main features of it?

A

Involuntary
Closure of the upper oesophageal sphincter
Peristaltic wave carries bolus downwards into oesphagus

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171
Q

What is the neural control of swallowing and the gag reflex?

A 
Mechanoreceptors in pharyngeal wall ->
Glossopharyngeal nerve (sensory CN IX) ->
Medulla in brain stem ->
Vagus nerve (motor to pharynx CN X) ->
Pharyngeal constrictors
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172
Q

What could be the problem if swallowing solid foods is a problem?

A

Oesophageal stricture/ physical mass

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173
Q

What could be the problem is swallowing liquids is a problem?

A

Stroke - muscles of facial expression for example can prevent food staying in the mouth therefore liquid falls out of the mouth

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174
Q

What happens to the muscle type as you go from oesophagus to stomach?

A

Skeletal muscle transitions to smooth muscle

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175
Q

What factors help prevent gastro-oesophageal reflux?

A
  • Functional sphincter formed from smooth muscle of distal oesophagus - LOS
  • Diaphragm - contracting around the oesophagus prevents food entering the stomach on inhalation
  • Intra-abdominal oesophagus gets compressed when intra-abdominal pressure rises
  • Mucosal rosette at cardia of stomach
  • Acute angle of entry of oesophagus
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176
Q

What cells aid in secretion of HCl in the stomach?

A

Enterochromaffin - like cells.

Release histamine

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177
Q

What is paracrine secretion?

A

Hormone has effects only in the vicinity of the gland secreting it

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178
Q

What do D- cells in the stomach do?

A

Acid stimulates somatostatin release to inhibit meal-stimulated gastrin secretion from the G-cell

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179
Q

Give an example of a neuroendocrine cell in the stomach?

A

Gastrin releasing peptide - released by neurones in the GIT

It is released from the post-ganglionic fibres of the vagus nerve - which causes release of gastrin from G cells.

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180
Q

Where are the majority of G- cells found in the stomach?

A

Antrum on the greater curvature

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181
Q

Where are the majority of the parietal cells found in the stomach?

A

Fundus/ body of the stomach on the greater curvature

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182
Q

What neurotransmitter is released from the vagus nerve in the stomach to cause release of gastrin?

A

ACh

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183
Q

What is cholecystokinin?

A

Hormone that translates directly into bile sac move

Causes release of bile into the CBD

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184
Q

What cell is responsible for releasing cholecystokinin?

A

I cells

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185
Q

Where are I cells found and why?

A

Duodenum and jejunum

Once food has been digested the cells are stimulated to cause immediate release of bile salts and pancreatic secretions

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186
Q

What prevents pancreatic and bile secretions being released into the duodenum?

A

Sphincter of Oddi

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187
Q

Through which structure does bile and pancreatic secretions leave from the major papilla?

A

Ampulla of Vater

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188
Q

What is the name of the two tubes that connect the ducts from the pancreas and bile duct to the duodenum?

A

Minor and major papilla

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189
Q

What are the two pancreatic ducts?

A

Main pancreatic duct

Accessory pancreatic duct

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190
Q

What are the two broad families of gastrointestinal hormones?

A

Secretin and Gastrin

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191
Q

What cells release secretin?

A

S cells

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192
Q

What is the location of the S cells?

A

Duodenum

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193
Q

What do S cells do?

A

Increase HCO3 secretion from the pancreas/ gallbladder

Decreases gastric acid secretion

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194
Q

What stimulates S cells to release secretin?

A

H+ concentration and fatty acids

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195
Q

What stimulates cells to release gastric inhibitory peptide?

A

Sugars
Amino acids
Fatty acids

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196
Q

What is the problem with GIP release?

A

Increases insulin which is a problem for diabetics

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197
Q

What is the function of GIP?

A

Decreases gastric acid secretion

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198
Q

Where in the GIT can GIP secreting cells be found?

A

Duodenum and jejunum

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199
Q

What are the 4 main basic functions of the stomach?

A

Receive food - short term storage
Disrupt food - vigorous contractions of the smooth muscle
Continue/ commence digestion - mainly proteins
Disinfect

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200
Q

Why can epigastric pain be confused for a heart attack?

A

The heart sits close to the cardia of the stomach which is the area with the LOS
If the patient has reflux then pain will be felt in this location and can be confused for a heart attack hence why history and type of pain is important to differentiate

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201
Q

What is the longer and short edges of the stomach called?

A

Greater and lesser curvature of the stomach

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202
Q

What is the folds in the stomach called?

A

Rugae

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203
Q

What is the location of the LOS called in the stomach?

A

Cardia

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204
Q

What is the highest point of the stomach called?

A

Fundus

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205
Q

What is the last part of the stomach called which has the sphincter?

A

Pylorus

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206
Q

What is the part of the stomach between the pylorus and the body of the stomach called?

A

Antrum

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207
Q

What is the largest part of the stomach in the middle of it called?

A

Body

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208
Q

What is the part of the lesser curvature of the stomach called where it curves sharply towards the pylorus?

A

Angularis

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209
Q

Which part of the stomach gets free gas and can be seen on x-ray?

A

Fundus

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210
Q

What is the basic histology of the epithelium from lower oesophagus to the stomach?

A

Abrupt transition of stratified squamous epithelium to columnar
Mucosa/submucosa has folds - rugae

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211
Q

What 4 basic cells are in the stomach epithelium?

A

Mucous cells
Parietal cells
Chief cells
G cells

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212
Q

Describe the contraction types between the upper and lower stomach?

A

Upper stomach - sustained contractions creating a basal tone
Lower stomach - Strong peristalsis mixes stomach contents. Coordinated movements with contractions every 20 seconds in a proximal to distal direction.

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213
Q

Why is the shape of stomach good for its function of moving food along?

A

Larger proximally getting smaller in the distal direction
Contents accelerates towards pylorus but only smaller particles of food is allowed to exit into the duodenum.
Lumps are left behind and so this helps separate out the food and concentrate digestion on the larger food particles.

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214
Q

How many times per minute is chyme ejected from the stomach?

A

3 times a minute

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215
Q

What is the blood supply to the stomach and what are the branches?

A

Coeliac trunk to the stomach generally
Lesser curvature proximal 1/2 = left gastric artery
Lesser curvature distal 1/2 = right gastric artery branch off the common hepatic artery
Greater curvature proximal 1/3 = short gastric artery from the splenic artery
Greater curvature middle 1/3 = left gastroepiploic artery from splenic artery
Greater curvature distal 1/3 = right gastroepiploic artery from gastroduodenal artery

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216
Q

What is important about the gastroduodenal artery and its location?

A

It sits behind the pylorus which is a location of potential gastric ulceration and hence it can cause a hole in this artery which could lead to internal bleeding quickly as the blood supply is directly off the coeliac trunk

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217
Q

What is the venous drainage to the stomach and what are the branches?

A

Lesser curvature posterior part = left gastric vein drains into splenic vein
Lesser curvature anterior part = right gastric vein drains into portal vein directly
Fundus = Short gastric vein -> splenic vein
Body = left gastro-omental vein
Antrum = Right gastro-omental vein
Pylorus = Pancreaticoduodenal vein -> SMA OR Pre-pyloric vein-> right gastric vein -> portal vein

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218
Q

With all of the drainage from the stomach where does the blood all end up in?

A

Hepatic portal vein

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219
Q

What feature of the stomach allows expansion to facilitate the consumed food?

A

Gastric mucosal folds - rugae

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220
Q

What cells release pepsinogen into the stomach?

A

Chief cells

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221
Q

What happens to pepsinogen in the stomach?

A

It interacts with the acidic environment and as it is a proenzyme prior to entry into the stomach it becomes an enzyme which is then able to break down proteins

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222
Q

What do D cells release?

A

Somatostatin

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223
Q

What is pernicious anaemia caused by?

A

Antibodies against the parietal cells causes them to be destroyed
The patient then produces less intrinsic factor and so then less B12 is absorbed further down the GIT

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224
Q

What cells make up a gastric gland?

A

Mucous neck cells
Parietal cells
Chief cells
Enteroendocrine cells

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225
Q

Where are chief cells mainly found in the stomach?

A

Body

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226
Q

What hormones are mainly released from the pylorus of the stomach?

A

Gastrin and somatostatin

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227
Q

What stimulates the release of HCl in the stomach?

A

Gastrin released from G cells into the blood supply
Histamine from ECL-cells
ACh from vagus nerve

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228
Q

What receptor does gastrin act on in the stomach?

A

CCK receptors as there is cross reactivity

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229
Q

What is the control mechanism for gastrin secretion?

A
  • Peptides and amino acids stimulate the release of gastrin
  • Vagal stimulation via ACh and Gastrin-releasing peptide (GRP)
  • Somatostatin acts on S receptor on the G cell
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230
Q

What inhibits HCl production?

A

When food leaves stomach pH drops (food is a buffer)
Low pH activates D cells which release somatostatin
Somatostatin inhibits G cells and ECL cells
Stomach distension reduces which then reduces vagal activity

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231
Q

Where are D cells located?

A

Antrum of the stomach at the lesser curvature

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232
Q

How is HCO3- made in the stomach epithelium?

A

CO2 from the blood enters the cells and they then have carbonic anhydrase in them which then produces HCO3-

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233
Q

Why is carbonic anhydrase in the stomach important?

A

It converts CO2+ H2O into H+ and HCO3-
H+ is then used to make stomach acid
HCO3- is used later in the duodenum to neutralise this acid

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234
Q

What is the process of acid release into the lumen of the stomach?

A

H+ made using carbonic anhydrase is exchanged for K+ in the lumen using the H+/K+ ATPase anti-porter.
K+ enters the cell but is then goes down conc gradient through K channels into the stomach lumen

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235
Q

How does the chloride part of HCl in stomach acid end up in the lumen of the stomach?

A

Cl- is exchanged for HCO3- in the basolateral membrane of the stomach. Cl- enters the cells and HCO3- leaves the cells. Cl- then passes through the Cl- channel on the apical membrane into the lumen of the stomach

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236
Q

What are the 3 phases of digestion?

A

Cephalic phase
Gastric phase
Intestinal phase

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237
Q

What happens in the cephalic phase of digestion?

A
  • Vagus nerve stimulates gastric secretion even before food is swallowed
  • 30% of total HCl is released during this phase
  • Direct stimulation of parietal cells via vagus nerve
  • Stimulation of G cells vagus (GRP released)
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238
Q

What happens in the gastric phase of digestion?

A
  • Food stretches the stomach and activates myenteric and vagovagal reflexes - stimulates parietal cells and G cells.
  • Histamine and gastrin also stimulate acid and enzyme secretion
  • 60% of total HCl is released during this phase
  • Amino acids and small peptides stimulate G cells
  • Food acts as buffer in stomach: removes inhibition on gastrin production
  • Enteric NS and gastrin: cause strong smooth muscle contractions
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239
Q

what 4 actions does the vagus nerve have on the secretion of acid?

A

1 - acts on Chief cells to release Pepsinogen
2 - acts on G cells to release gastrin -> Parietal cells to release H+
3 - acts on parietal cells to release H+ directly
4 - acts on ECL-cells to release histamine -> Parietal cells to release H+

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240
Q

What happens in the intestinal phase of digestion?

A
  • Intestinal gastrin briefly stimulates the stomach (chyme is acidic and hypotonic) but then secretin, GIP, CCK, and the enterogastric reflex inhibit gastric secretion and motility while the duodenum processes the chyme already in it. Sympathetic nerve fibres suppress gastric activity, while vagal stimulation of the stomach is now inhibited
  • 10% of total HCl production during this phase
  • Lipids activate enterogastric reflex which reduces vagal stimulation
  • Chyme stimulates CCK and secretin (helps suppress secretion of acid)
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241
Q

What cells produce and release mucin?

A

Foveolar cells

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242
Q

What is the function of mucin in the stomach?

A
  • Prevent self digestion by proteases

- Mucous adhere to the epithelium - prevents physical damage

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243
Q

What is the function of HCO3- in the stomach?

A
  • Secreted into mucous layer

- Buffer against H+

244
Q

Why is a rich gastric blood supply good for breached acid from the mucous layer?

A

Blood removes acid and buffers it

245
Q

Why are prostaglandins good in breaches of stomach acid?

A

NSAID’s prevent prostaglandins synthesis
Prostaglandins improve blood flow to the stomach and therefore protects the breached acid by removing it and bringing HCO3-

246
Q

Why is alcohol bad for the stomach defences?

A

Dissolves mucous layer - thinning it - less protection

247
Q

Why is H. pylori bad for the stomach defences?

A

Chronic active gastritis will cause an increase in H+ production and increased risk of damage and breach of the mucous layer

248
Q

Define dyspepsia?

A

Describe a complex of upper gastrointestinal tract symptoms which are typically present for four or more weeks including upper abdominal pain or discomfort, heartburn, acid reflux, nausea and/or vomiting

249
Q

What is GORD?

A

Gastro-oesophageal reflux disease

250
Q

What are symptoms of GORD?

A

Chest pain
Acid taste in mouth
Cough - H+ refluxing into trachea

251
Q

What are 4 main consequences of GORD?

A

Nothing
Oesophagitis
Strictures
Barrett’s oesophagus

252
Q

What 5 triggers of GORD?

A

Obesity - increased abdominal pressure
Pregnancy - Inc. intra-abdominal pressure
Hiatus hernia
LOS function
Delayed gastric emptying - increased likelihood for contents to reflux

253
Q

Describe the LOS in terms of GORD

A

LOS - muscular element
Located at right crus of diaphragm
Angle of entry of oesophagus into stomach
Intra-abdominal pressure

LOS consists of distal 4cm of oesophagus
Resting pressures vary: lowest after meals - small amount of pressure to overcome, highest at night

254
Q

How do you treat GORD?

A

Lifestyle modifications
Pharmacological - antacids, H2-antagonists, PPI’s
Surgery - fundoplication

255
Q

How is a hiatus hernia increasing the risk of oesophagi’s?

A
  • Moving LOS into thorax reduces basal tone and the normal increase in LOS tone when straining
  • Loss of diaphragmatic support for LOS
  • Retention of gastric fluid in hernia
256
Q

What is gastritis?

A

Inflammation of the stomach mucosa on endoscopic appearance

257
Q

What are the symptoms of gastritis?

A

Abdominal pain
Nausea
Vomiting
Bleeding

258
Q

What are 4 risk factors for gastritis?

A

Heavy NSAID use
Lots of alcohol
Chemotherapy
Bile reflux

259
Q

What is the histological reason for gastritis?

A

Exposure of mucosa to chemical injury -> damaged epithelium > reduced mucous production > vasodilation/ oedema + inflammatory cells in mucosa

260
Q

How do you treat gastritis?

A

Removal of irritant

261
Q

What are 2 causes of chronic gastritis?

A

H. pylori infection

Autoimmune - antibodies to gastric parietal cells - leads to pernicious anaemia

262
Q

What is a symptom of H pylori infection?

A

Asymptomatic or similar to acute gastritis

Symptoms may develop due to complications - peptic ulcer, adenocarcinoma, MALT lymphoma

263
Q

What is a symptom of autoimmune chronic gastritis?

A

Symptoms of anaemia
Glossitis
Anorexia
Neurological symptoms - due to B12 deficiency

264
Q

What are 3 microbiological features of Helicobacter pylori?

A 
Helix shaped
Gram negative
Microaerophilic
Flagellum - for motility in mucous layer
Adhesins - resistance to peristalsis
265
Q

What test is used to detect H. pylori and why?

A

Urea breath test - bacteria produces urease - urea-> ammonia
Stool antigen test
Upper GI endoscopy

266
Q

Why are H. pylori infections bad for the host?

A

1 - Releases cytotoxins - direct epithelial damage
2 - Expresses urease - urea to ammonia - toxic to epithelium
3 - Degrades mucous layer
4 - Promotes inflammatory response - self injury

267
Q

Where is H. pylori most often found?

A

Antrum (home of G cells)

Asymptomatic then antrum/ body of stomach

268
Q

How does H. pylori cause ulceration?

A

Inc. gastrin secretion (or Dec. D cell activity) ->
Increased parietal cell acid secretion ->
Duodenal epithelial metaplasia - >
Colonisation of duodenum ->
Duodenal ulceration as little mucous

269
Q

What problems does H. pylori cause in the body of the stomach?

A

Atrophy - inc tissue breakdown and therefore ulceration more likely
Intestinal metaplasia -> Dysplasia -> Cancer

270
Q

How do you treat a H. pylori infection

A

PPI + 2x ABx

Omeprazole/ Lansoprazole + Amoxicillin + Clarithromycin/ Metronidazole

271
Q

Define peptic ulcer disease?

A

Defects in gastric/ duodenal mucosa
Extends through muscularis mucosa
D1 most commonly affected
Commonly affects lesser curve/ antrum of stomach

272
Q

What are the 4 main causes of peptic ulcer disease?

A

H. pylori
NSAIDs
Smoking
Stress

273
Q

Where are chronic gastric ulcers more commonly found?

A

Mucosal junctions
Antrum meets body on lesser curve
In duodenum where antrum meets small intestine

274
Q

What is the morphology of a peptic ulcer?

A

<2cm but <10cm in severe cases
Base of ulcer = necrotic/ granulation tissue
Muscularis propriety can be replaced by scar tissue

275
Q

What are clinical consequences of peptic ulcer disease?

A 
Scar tissue - pyloric stenosis
Perforation -> peritonitis
Erosion to adjacent structures
Haemorrhage
Malignancy
276
Q

What are the symptoms of peptic ulcer disease?

A 
Epigastric pain (sometimes back pain - dermatomal distribution)
Burning/ gnawing
Follows meal times - increased acid production/ physically irritating. 
Immediate pain after eating - gastric
Delayed pain after eating - duodenal
Often at night
Haematemesis/ Malaena- Bleeding/ anaemia
Early satiety due to stricture
Weight loss
277
Q

How do you manage peptic ulcer disease?

A 
Lifestyle modification
Stopping exacerbating medications
Testing for H. pylori - eradication
PPI's
Endoscopy - haemostasis of bleed
278
Q

How do you test for gastric pathology?

A

Upper GI endoscopy - biopsies
Urease breath test
Erect chest X-ray - perforation
Blood test - anaemia

279
Q

What is Zollinger-Ellison syndrome?

A

Non-beta islet cell gastrin secreting tumour of the pancreas
Proliferation of parietal cells due to increased gastrin
Lots of acid production
Severe ulceration of the stomach and small bowel - abdominal pain and diarrhoea

280
Q

What is stress related mucosal damage?

A

Spectrum of pathology attributed to the acute, erosive, inflammatory insult to the upper GIT associated with critical illness

281
Q

What could cause stress related mucosal damage?

A 
Severe burns
Raised intracranial pressure
Sepsis
Severe trauma
Multiple organ failure
282
Q

What are symptoms of gastric cancer?

A 
Dysphagia
Loss of appetite
Malaena
Weight loss
N+V
Virchow's nodes (left supraclavicular node)
283
Q

What are 4 risk factors for gastric cancer?

A

Male
H. pylori
Dietary factors
Smoking

284
Q

What is the difference between the jejunum and the ileum in terms of location, intestinal wall thickness, vasa recta, and arcades (arterial loops)?

A

Location - jejunum- upper left quadrant, ileum - lower right quadrant
Intestinal wall - Jejunum - thick, ileum - thin
Vasa recta- Jejunum - long, ileum - short
Arcades - Jejunum - less, ileum - more arcades

285
Q

What are the branches of the SMA and what structures do they supply?

A

In order superior to inf along SMA:
1 - Middle colic artery - Transverse colon
2 - Right colic - Ascending colon
3 - Jejunal and ileal arteries
4 - Ileocolic artery - Ascending colon, appendix, cecum, proximal ileum

286
Q

What structures drain into the SMV?

A

Superior and inferior mesenteric veins

287
Q

What is the final vein that drains the blood from the gut?

A

Portal vein - into the liver

288
Q

What vein becomes IMV as it enters the abdomen?

A

Superior rectal vein

289
Q

What is the name of the artery that is formed with the merging of Middle colic, Right colic and Ileocolic arteries?

A

Marginal artery

290
Q

What is plicae circulares?

A

Permanent folds of the ileum

291
Q

What are the 3 main cells of the ileal epithelium?

A

Enterocytes - absorptive cells
Goblet cells - mucous producing - more mucous further down GI
Enteroendocrine cells - produce hormones

292
Q

What is the name of the intestinal glands?

A

Crypts of Lieberkuhn

293
Q

What 2 cells are found at the base of the intestinal glands (crypts of Lieberkuhn)

A

Stems cells at base

Paneth cells - innate mucosal defence cells - produce antimicrobial peptides

294
Q

How long does it take to replace the intestinal mucosa?

A

3-6 days

295
Q

In IBD where are the inflammatory cells?

A

Deep in the crypts

296
Q

What size of carbohydrate is absorbable?

A

Only monosaccharides

297
Q

What do carbohydrates need to be absorbed through the GIT?

A

Sodium in the SGLUT

298
Q

What is the difference between amylose and amylopectin?

A

Amylose - straight chain of glucose

Amylopectin - Branches chains of glucose

299
Q

What enzyme breaks down carbohydrates?

A

Salivary and pancreatic amylase

300
Q

What are short chains of branched starch called?

A

Alpha dextrins

301
Q

What enzyme is required to break down branched alpha 1-6 bonds?

A

Isomaltase

302
Q

How does the body maintain a low luminal sodium?

A

Na/K ATPase on the basolateral membrane - keeps intracellular Na low and so brings Na into the cell

303
Q

Through which channel does glucose enter the enterocyte?

A

SGLT-1 with sodium

304
Q

What channel does glucose leave the enterocyte?

A

GLUT-2 - diffusion down gradient

305
Q

What channel does fructose enter the enterocyte?

A

GLUT-5 facilitated diffusion

306
Q

How is protein digested in the stomach -> brush border?

A

Stomach - H+ / Pepsinogen -> Pepsin
Intestinal lumen - Trypsin, chymotrypsin, Elastase ->
Brush border: Amino-oligopeptidase (3-8 aa long) to di,tri peptides or amino acids. Dipeptidyl aminopeptidase (penultimate proline or alanine AA) to di,tri peptides.

307
Q

What ileal transporters allows amino acids and peptides to be absorbed?

A

A.A. transport proteins

Protein transport protein (Peptide transport 1) - di and tri-peptides

308
Q

What cytosolic peptidases make A.A from peptides?

A

Prolidase, dipeptidase, tripeptidase

309
Q

What is a zymogen?

A

A substance that is converted into an enzyme once it has been activated by another enzyme

310
Q

What is important about the proteases the pancreas released?

A

Released as inactive zymogens which are then activated once they reach the intestinal lumen
Trypsinogen is converted to trypsin by enteropeptidase (brush border enzyme)
Trypsin will activate other proteases

311
Q

What are the two classes of peptidases?

A

Endopeptidases - produce shorter polypeptides

Exopeptidases - produce dipeptides or AA

312
Q

Through which mechanism are amino acids transported?

A

Co-transporters with sodium through amino acid transporter protein

313
Q

How is water absorbed through the intestine?

A

Na/K ATPase on basolateral membrane
Na diffusion lumen-> epithelial cell
Water follows Na
Osmotic gradient from all absorption leads to uptake of water

314
Q

Apart from SGLUT transporters how else is sodium reabsorbed from the lumen of the intestine?

A

Through a Na/H exchange transporter

315
Q

How does the small intestine and large intestine vary in their water absorption?

A

Apical membrane:
SI - Na co-transported
LI - Na channels. Aldosterone induced.

316
Q

How is water secreted into the gut?

A

Basolateral membrane:
Cl- enters epithelial cell via NKCC2 channel
Na/K ATPase working
Cytosol:
Inc levels of cAMP -> activation of CFTR channel -> Cl- secretion
Na drawn into lumen across tight junctions
NaCl secretion creates osmotic gradient - water moves into lumen

317
Q

What are the GI causes of B12 deficiency?

A

Lack of intrinsic factor released by parietal cells - B12 bound to IF in SI and transported to distal ileum for absorption
Hypochlorhydria (inadequate HCl) - acid is important in initially releasing cobalamin - gastric atrophy and PPI’s
Inadequate intake in food (vegetarian)
Inflammatory disorders of ileum (site of absorption) - Crohn’s disease

318
Q

What is a lactose intolerance?

A

Deficiency of lactase enzyme in brush border
>2years less expression
Lactose -> not broken down -> remains in lumen -> high osmotic effect -> diarrhoea + bloating (bacteria ferment lactose)

319
Q

What are the symptoms of IBS?

A 
Abdominal pain
Bloating
Flatulence
Diarrhoea/ constipation
Rectal urgency
320
Q

What demographic is more affected by IBS?

A

2:1 F:M
20-40 yr olds
Associated with psychological disorders - depression/ anxiety - hence serotonin

321
Q

What is coeliac disease?

A

Immunological response to the gliadin fraction of gluten
Found in wheat, rye and barley
Damage to mucosa of intestines - absence of villi, hypertrophy of intestinal crypts, lymphocyte infiltration of epithelium and lamina propria, impaired digestion and malabsorption

322
Q

What are the symptoms of coeliac disease?

A

Malabsorption - diarrhoea, weight loss, flatulence, abdominal pain
Anaemia - impaired iron absorption, neurological symptoms (hypocalcaemia)

323
Q

What investigations are done in coeliac disease?

A

IgA antibodies to smooth muscle endomyseium and tissue transglutaminase
Upper GI endoscopy + biopsies of duodenum = absent villi or reduced

324
Q

How do you treat coeliac disease?

A

Gluten avoidance

325
Q

What are the features of chyme?

A

Low pH
Hypertonic
Partially digested food

326
Q

How is hypertonicity of chyme dealt with in the duodenum?

A

Water from ECF/ circulation is slowly released into the duodenum by the hypertonic chyme solution

327
Q

Describe the permeability of the stomach and duodenum to water

A

Stomach - largely impermeable to water

Duodenum - relatively permeable to water

328
Q

Do enzymes come from the liver for digestion?

A

No

329
Q

What hormones are secreted from the duodenum in response to chyme?

A

Secretin - released due to low pH of chyme - acts on pancreas to release aqueous bicarbonate part of pancreatic solution
CCK - acts on pancreas to release enzyme component of pancreatic solution
CCK also acts on the gallbladder to contract and also relaxes the sphincter of Oddi

330
Q

Apart from hormones what else stimulates the pancreas to secrete (exocrine function)

A

Sympathetic inhibits

PNS via vagus stimulates

331
Q

Within the pancreas in general where are enzymes stored?

A

In granules within acinar cells

332
Q

What is important about the enzymes released from the pancreas?

A

Amylases and lipase are already active

Proteases - inactive zymogen granules

333
Q

What happens if the proteases are activated too early in the pancreas?

A

Pancreatitis

334
Q

What cells of the pancreas release aqueous component?

A

Duct cells secrete aqueous bicarbonate isotonic solution

335
Q

What are the liver secretions in response to chyme?

A

Liver secretes bile into the duodenum 250ml- 1L/day

336
Q

What does bile consist of?

A

Bile acids and bile pigments

Alkaline solution

337
Q

What is the role of bile?

A

Emulsifying fats in duodenum so that they can be readily digested by lipases

338
Q

What is the macro anatomy of the liver?

A

Left and right lobes + caudate and quadrate lobes of the right lobe of the liver

339
Q

What is the micro anatomy of the liver in gastro detail?

A

Lobules are arranged in a hexagonal configuration of cells, bile ducts and blood vessels
Sheets of hepatocytes arranged towards a central hepatic vein
Liver acinus = sinusoid, Kupffer cells, Heptatocyte (80% of mass)
Hepatic artery and portal vein branches into the acinus from outside into a central hepatic vein

340
Q

What is the blood flow of the hepatic acinus?

A

Blood flows in from hepatic artery and portal vein towards the central vein via sinusoids
Blood flows out along canilucili
Bile acids flow out along bile duct

341
Q

What pathological processes affect hepatocytes in the acinar structure?

A

Zones 1 - 3 corresponding distance away from blood supply
Zone 1 - toxic injury
Zone 3 - ischaemic injury

342
Q

What part of the biliary try produces the alkaline juices?

A

Bile duct cells stimulated by secretin produce the alkaline solution

343
Q

What are bile salts?

A

Conjugated bile acids
Bile salts are more soluble than bile acids at duodenal pH
Bile acids - cholic acid and chenodeoxycholic acid
Bile acids are synthesised in the liver and then conjugated to amino acids
Bile salts have amphipathic structure = hydrophilic and hydrophobic ends

344
Q

What structures do bile salts create in the SI?

A

Micelles transport hydrophobic lipids towards enterocytes

345
Q

What is the enterohepatic circulation of bile salts?

A
  • Lipids diffuse into enterocytes but bile salts remain in gut
  • Reabsorbed in terminal ileum when combined with fat (also when not combined)
  • Returned to liver in portal blood
  • Liver recycles the bile salts (does not have to re-synthesise large volumes)
346
Q

How are chylomicrons formed in enterocytes?

A

Inside enterocyte lipid molecules built back up to triglycerides, phospholipids and cholesterol
Packed with apoproteins within enterocytes - Chylomicron
Chylomicron exocytosed from basolateral membrane of enterocyte - too large to enter capillaries so enter lymphatic capillaries -> thoracic duct

347
Q

What is steatorrhoea?

A

Bile acids/ salts pancreatic lipases not secreted in adequate amounts
Undigested fat appears in faeces- pale, floating, foul smelling

348
Q

What does the liver store?

A

Glycogen
Vitamins
Iron
Copper

349
Q

Generally what does the liver synthesise?

A 
Glucose
Protein
Lipids and cholesterol
Bile
Coagulation factors
Albumin
350
Q

What does the liver metabolise/ detoxify?

A 
Bilirubin
Ammonia
Drugs
Alcohol
Carbohydrates/ lipids
351
Q

What is the reason for a patient having jaundice?

A

Metabolic function: bilirubin is not being metabolised therefore raised serum bilirubin

352
Q

What is the reason for a patient having oedema/ ascites?

A

Synthetic function: albumin not occuring

353
Q

What is the reason for a patient having bleeding/ easy bruising?

A

Synthetic function: Clotting factors

354
Q

What is the reason for a patient having confusion with liver impairment?

A

Metabolic function: ammonia

355
Q

What is cirrhosis and why does it occur?

A

End result of a lot of conditions
Develops in response to any chronic liver injury:
ongoing inflammation causes fibrosis associated with hepatocyte necrosis which results in architectural changes (nodules)
-Irreversible condition that ends up with impaired liver function and distorted architecture - hepatomegaly then liver shrinks

356
Q

What are the 5 groups of causes of cirrhosis?

A

Drugs - alcoholic liver disease, iatrogenic
Infection - EBV, HCV
Deposition - Fat, Iron, Copper
Autoimmune - Autoimmune hepatitis, PBC, PSC
Other - Alpha1 anti-trypsin, glycogen storage disease, Budd-Chiari

357
Q

What are the 3 main ways alcohol causes alcoholic liver disease?

A

Fatty change - weeks - initially reversible
Alcoholic hepatitis - years - initially reversible although takes time
Cirrhosis - years - end stage, irreversible damage

Partly due to build up of acetaldehyde

358
Q

How is alcoholic liver disease identified?

A

Hx
Asymptomatic or general symptoms of liver disease
Fatty liver - hepatomegaly on examination
Alcoholic hepatitis - rapid onset jaundice, tender hepatomegaly (RUQ pain)
Severe liver disease symptoms: N+V, oedema, ascites, splenomegaly

359
Q

In terms of cure and vaccine which of Hep B and C have them?

A

Hep B - vaccine no cure - symptoms during acute infection

Hep C - no vaccine but cure - asymptomatic during acute infection

360
Q

Apart from acute infection what does Hepatitis B/C increase the chance of getting?

A

Hepatocellular carcinoma

361
Q

How does fat cause liver problems?

A

Non-alcoholic fatty liver disease (NAFLD)
Similar pathogenesis to Alcoholic liver disease (but without alcohol) - Link to insulin resistance!
Accumulation of triglycerides and other lipids in hepatocytes - inflammation present = non-alcoholic steatohepatitis (NASH)

362
Q

What 4 conditions increase risk of Non-alcoholic liver disease?

A

Obesity
Diabetes - treatable with oral hypoglycaemic drugs
Metabolic syndrome (dyslipidaemia)
Familial hyperlipidaemia

363
Q

What is the name of the condition where there is liver dysfunction in iron metabolism and copper metabolism?

A

Iron metabolism - hereditary haemochromatosis

Copper metabolism - Wilson’s disease

364
Q

Describe hereditary haemochromatosis

A

Abnormal iron metabolism
Increase absorption of iron from SI -> excess deposition
Autosomal recessive
Increased ferritin
Risk of developing hepatocellular carcinoma
Tx - venesection for life

365
Q

Describe Wilson’s disease

A

Abnormal copper metabolism
Reduced secretion of copper from biliary system -> accumulation in tissues
Autosomal recessive
Low caeruloplasmin - if not secreting copper therefore less protein carrying copper around

366
Q

What two blood tests can be done to help identify autoimmune hepatitis?

A

Anti-smooth muscle antibodies

Anti-nuclear antibody

367
Q

What is different in the antimitochondrial antibodies detection in primary biliary cholangitis and primary sclerosis cholangitis

A 
PBC = AMA +ve
PSC = AMA +ve
368
Q

Describe what happens in portal hypertension due to liver disease

A

Inc blood in portal system - fibrotic liver is not very expansive
Compresses veins entering the liver from the portal veins = ascites
Also causes a build up of pressure in the splenic circulation = splenomegaly
Blood shunts from portal system to systemic venous circulation via anastomoses that are not usually used - distended veins at anastomoses - varices

369
Q

Where are the sites of varices in portal hypertension?

A

Oesophageal - distal 1/3 portion drains to left gastric - mucosal varices - rupture= haematemesis
Anorectal - between superior and middle/ inferior rectal veins - typically painless (above pectinate line) - rarely bleed.
Umbilical - ligamentum teres (round ligament) - normally no blood flow - caput medusa

370
Q

What is hepatorenal syndrome?

A

Development of AKI in presence of cirrhosis.
Portal hypertension -> Arterial vasodilation (splanchnic) -> RAAS activated -> Renal artery vasoconstriction (reduce blood flow to kidney)
-Pooled blood in venous system, body thinks hypovolaemia -> RAAS activated
Kidney improves if patients liver failure is reversed.

371
Q

Describe the biliary tree

A

Liver -> left and right hepatic duct -> common hepatic duct
Gallbladder -> Cystic duct
Pancreas -> pancreatic duct
Common hepatic duct + cystic duct = common bile duct
CBD + Pancreatic duct = CBD
D2 insertion of Ampulla of Vater

372
Q

What imaging technique would be done for gallstones?

A

Ultrasound.

Stones are radiolucent

373
Q

What are 5 risk factors for developing gallstones?

A 
Diet and lifestyle
Age
Gender
Pregnancy
Pre-existing liver disease
374
Q

What are complications of gallstones?

A

Biliary colic pain - on/off pain worse a few hours after eating a fatty meal - RUQ
No features of inflammation

375
Q

How would you treat a gallstone complication?

A

Analgesia

Elective cholecystectomy

376
Q

How do patients present with acute cholecystitis?

A

Initial presentation similar to biliary colic
Impaction of stone in cystic duct - permanent blockage
Inflammatory features (fever) - thickened gallbladder wall
Murphy’s sign positive - breath in and put hand under ribs if pain on inspiration then test +ve

377
Q

How would you manage acute cholecystitis?

A

Initially conservative the cholecystectomy

378
Q

What is acute (ascending) cholangitis?

A

Infection of the biliary tree - blockage permanently of bile duct therefore backing up of bile
Present with RUQ pain, features of inflammation (fever) and jaundice = Charcot’s triad
Typically due to an impacted CBD stone or other obstruction

379
Q

How would you manage acute cholangitis?

A

IV ABx
Fluids
Relieve obstruction

380
Q

What is acute pancreatitis?

A

Acinar cell injury and necrosis = blockage of pancreatic duct
Inflammatory response
Autodigestion of pancreas
Presentation - acute epigastric pain radiating to back - pancreas is retroperitoneal
Associated with vomiting
Cullens and Grey Turner’s sign position
Bruising around belly button and bruising around flanks

381
Q

What is Cullens and Grey Turner’s sign?

A

Bruising around belly button and bruising around flanks

382
Q

What is acute pancreatitis and how is it managed?

A

Release of pancreatic enzymes locally ->
Amylase and lipase detected in serum
Fluids, manage gallstones, organ support

383
Q

What is bilirubin and how does the liver handle it?

A

Bilirubin - breakdown product of harm - unconjugated
Liver conjugates - excretion - water soluble - renally
Spleen breaks down haemoglobin into haem and globin

384
Q

How is conjugated bilirubin removed from the body?

A

Through the gut as urobilinogen and removed in faeces (majority) some renally
Due to enterohepatic circulation some is reabsorbed into the blood and removed in the kidneys/ removed via the bile again

385
Q

What are the 3 broad classifications of jaundice?

A

Pre-hepatic - too much haem
Hepatic - reduced hepatocyte function
Post-hepatic - obstructive causes

386
Q

Describe pre-hepatic jaundice

A

Increased degradation of haemoglobin
Liver conjugating ability is fine and excretion pathway is fine
Too much demand on the liver
Therefore levels of serum bilirubin rise

387
Q

Describe the pre-hepatic causes of jaundice

A

Haemoglobinopathies - sickle cell, thalasseamia, spherocytosis
Damage to red blood cells - haemolysis - most likely immune causes

388
Q

Describe hepatic causes of jaundice

A

Reduced conjugating ability of the liver
Damage to hepatocytes, amount of bilirubin is fine and excretion pathway is usually fine therefore you get a:
mix of conjugated and unconjugated bilirubin as some parts of the liver are fine and others that aren’t
Causes : Fatty liver disease, Alcohol, Wilson’s disease, Hereditary haemochromatosis, drugs, autoimmune, hepatitis, infections, deposition disorders

389
Q

State 3 common causes of acute liver damage

A

Paracetamol toxicity
Viral hepatitis
Other infections

390
Q

Describe post-hepatic jaundice

A

Obstruction to excretion pathway
Amount of bilirubin is fine
Conjugating ability of liver is usually fine
Therefore the raised bilirubin tends to be conjugated i.e. water soluble -> more excreted by the kidneys
Bilirubin is pigmented therefore leads to Dark urine and pale coloured stools

391
Q

Describe common causes of post-hepatic jaundice

A

Gallstones
Biliary stricture
Pathology of the head of the pancreas
Intrahepatic pathology can compress the intrahepatic bile ducts

392
Q

What intra-hepatic pathologies can cause post-hepatic and hepatic jaundice?

A

Oedema e.g. inflammation (autoimmune conditions)
Growth e.g. primary or metastatic malignancy
Scarring e.g. cirrhosis

393
Q

What are the anatomical divisions of the pancreas?

A

Head
Body
Tail

394
Q

What liver function tests can be done?

A 
Metabolism: Conjugated and unconjugated bilirubin
Synthesis: Albumin
Markers of liver damage directly:
Alanine transaminase (ALT)
Asparate aminotransferase (AST)
Alkaline phosphatase (ALP)
395
Q

What is albumin and what happens if it is low?

A

Major serum protein
Assessment of liver synthetic function - usually reduced in chronic cases
Low albumin contributes to ascites
Nephrotic syndrome - loss of albumin not attributed to liver synthetic function being impaired

396
Q

What happens to the ALT and AST in liver damage?

A

ALT is liver specific
AST found in cardiac, skeletal muscle and RBC’s

ALT>AST acute liver damage
AST>ALT in cirrhosis and alcoholic hepatitis

397
Q

Where is ALP released from?

A

Cells lining the bile ducts - levels go up in cholestasis (bile duct obstruction - post hepatic jaundice)

398
Q

Apart from ALP what other enzyme tests gives an indication of liver damage vs bone turnover?

A

GGT
ALP and GGT raised - liver dysfunction/ damage
ALP and normal GGT - not liver could be bone

399
Q 
From the following blood tests what can be identified as a problem?
Total bilirubin 46 (3-22)
ALT 245 (5-35)
AST 114 (7-40)
ALP 120 (30-130)
A

Acute hepatic damage
ALT>AST - acute
No details of bilirubin and normal level so not pre-hepatic
ALP within normal limits therefore not post-hepatic

400
Q 
From the following blood tests what can be identified as a problem?
Epigastric pain, N+V
Total bilirubin 38 (3-22)
ALT 35 (5-35)
AST 46 (7-40)
ALP 265 (30-130)
A

All LFT’s apart from ALP NAD
ALP raised significantly therefore post hepatic cause
Gall stone as obstructive picture
Would do GGT, pancreatic lipase and amylase to see if pancreas affecting the biliary tree

401
Q 
From the following blood tests what can be identified as a problem? PMHx - breast cancer, whites of eyes becoming more yellow
Total bilirubin 46 (3-22)
ALT 275 (5-35)
AST 618 (7-40)
ALP 140 (30-130)
A

AST>ALT - chronic cause
Hepatic cause of the problem
Slightly raised ALP therefore some biliary tree problem
Liver metastases most likely diagnosis

402
Q

What happens to the liver morphology from acute to chronic liver damage?

A 
Acute= Yellow/ Tan, Fatty, Enlarged
Chronic = Brown, Non-fatty, Shrunken
403
Q

What landmarks of the GIT indicate the start and end of the large intestines?

A

Caecum to anal canal

404
Q

What epithelium is found in the large intestines?

A

Columnar epithelium

405
Q

What are 3 basic features of the large intestine?

A

Production of some vitamins
Microbiome - contains lots of commensal bacteria
Acts as a temporary storage until defection (distal)

406
Q

What is interesting about the colonic mucosa and its nutrients?

A

Colonic mucosa does not get majority of nutrients from blood

Short chain fatty acids derive from the fermentation of dietary fibre - binds cholesterol and bile salts

407
Q

What part of the colon are peritoneal and retroperitoneal?

A

Ascending and descending colon are retroperitoneal
Transverse colon has its own mesentery - intraperitoneal
Sigmoid colon has its own mesentery
Rectum - upper 1/3- intraperitoneal middle 1/3- retroperitoneal lower 1/3- no peritoneum

408
Q

What is the blood supply to the Hind gut?

A

Left colic - descending colon
Sigmoid - descending colon
Superior rectal artery - upper 1/3 rectum

409
Q

What blood vessel does the hind gut drain into?

A

Inferior mesenteric vein

410
Q

What blood vessel does the rectum drain into?

A

Upper 1/3 - superior rectal vein

Middle and lower 1/3 - systemic venous

411
Q

What are the folds in the colon called?

A

Haustra

412
Q

Sacculations of what muscle causes haustra to be formed?

A

Teniae coli the longitudinal muscle

413
Q

What is the line along the colon which does not have any muscle running longitudinally?

A

Colic band

414
Q

How is water absorbed through the colon?

A

ENaC channels
Induced by aldosterone
ENaC channels allows sodium to enter the cells down its concentration gradient set up by the Na/K ATPase pump on the basolateral side

415
Q

Why is the presence of tighter tight junctions important in the colon?

A

Less back diffusion of ions allowing a bigger ionic gradient to form

416
Q

What diseases are classed together as IBD?

A

Crohn’s disease and Ulcerative colitis

417
Q

What is the basic difference between UC and Crohn’s disease?

A

Crohns - Whole GI can be affected, ileum involved in most cases, transmural (through the wall of the bowel), skip lesions
UC - continuous colonic involvement beginning in the rectum. Extends to entire colon. Continuous pattern. Mucosal inflammation

418
Q

Apart from the GIT what else could be affected indicating IBD?

A

MSK pain up to 50% - arthritis
Skin up to 30% - erythema nodosum/ pyoderma gangrenosum/ psoriasis
Liver- primary sclerosing cholangitis
Eye problems - uvitis

419
Q

What are possible causes of IBD?

A

Genetic - 1st degree relative
Gut organism (altered interaction)
Immune response - trigger could be ABx, Infections, Smoking (helps in UC, worse in Crohn’s), Diet

420
Q

What is a common presentation of someone with Crohn’s?

A 
Young female - previous fit and healthy
Hx of multiple loose stools/ day
Weight loss
RLQ pain
Joint pains
Smoker 
Perianal inflammation/ ulceration
Fever (inflammatory symptoms)
Anaemia
421
Q

What is the gross pathology of Crohn’s?

A 
Skip lesions
Hyperaemia
Mucosal oedema
Discrete superficial ulcers
Deeper ulcers
Transmural inflammation - thickening of bowel wall leading to narrowing of lumen
Cobblestone appearance
Fistulae - bowel -bowel/ bladder/ vagina/ skin
422
Q

Microscopically what is a sign that the specimen is showing Crohn’s?

A

Granuloma formation - organised collection of epithelioid macrophages

423
Q

How would you investigate Crohn’s?

A

Bloods - anaemia
CT/MRI - bowel wall thickening, obstruction, extramural problems
Barium enema/ swallow - Used less as may end up elsewhere due to fistulae. Shows- strictures/ fistulae
Colonoscopy - cobblestone appearance, skip lesions, fistulae, strictures

424
Q

What is a common presentation of UC?

A 
Young female
Multiple blood stools/ day
Weight loss
Abdo pain/ cramping
Painful red eye
Perianal disease - not usually found
Normal temperature - unless advanced disease
425
Q

Why is blood stools more commonly seen in UC rather than Crohn’s?

A

UC the mucosal epithelial layer sloughs off leaving a fresh layer of blood vessels which bleed.
Crohn’s is is transmural so can produce bloody diarrhoea but the blood is tamponaded by the oedema

426
Q

What are the pathological microscopic appearances of UC?

A

Chronic inflammatory infiltrate of lamina propriety
Crypt accesses (neutrophilic exudate in crypts)
Crypt distortion - irregular shaped glands and darker crowded nuclei
Reduced number of goblet cells

427
Q

Why do pseudopolyps develop after repeated episodes of UC?

A

Inflammation then healing - superficial scarring and redness around the site
Non-neoplastic
Most common in UC vs Crohn’s
Loss of haustra - inflammation reduces the appearance of hasutra on imaging

428
Q

How do you investigate UC?

A 
Bloods - anaemia, serum markers
Stool cultures
Colonoscopy
Pain abdominal radiographs
Barium enema
CT/MRI - less useful in diagnosing uncomplicated UC
429
Q

In which condition are aphthous ulcers more common Crohn’s or UC?

A

Crohn’s disease

430
Q

What is a barium swallow appearance in UC?

A

Fluffy because the barium has gone into the ulcers

431
Q

What are the 3 medical treatments for IBD?

A

Aminosalicylates - sulfasalazine (5-ASA) for flares and remission
Corticosteroids - for flares only
Azathioprine - Fistulas/ maintenance of remission

432
Q

What are the surgical managements for IBD?

A

Crohn’s- not curative as whole GIT. Strictures/ fistulas. As little bowel removed as possible
UC - Curable (colectomy)
Precancerous changes, but can get toxic megacolon - vast distension of the whole colon and potentially perforate

433
Q

Define diarrhoea

A

Symptoms of loose or watery stools

>3x/ day

434
Q

What time frame is acute diarrhoea?

A

<2weeks

435
Q

What is the pathophysiology of diarrhoea?

A

Unwanted substance in GIT that stimulate secretion and motility to remove it
Primarily down to epithelial secretory function rather than inc motility
Colon overwhelmed - can’t absorb all fluid

436
Q

What are the two broad categories of diarrhoea?

A

Osmotic and secretory
Osmotic - Food is hypertonic -> draws water into the gut creating a liquid stool
Secretory - Ions secreted into ileum -> draws water into the lumen

437
Q

Of the two categories of diarrhoea which ones are responsive to fasting?

A

Osmotic - reduced food - the stimulus is removed

Secretory - no change

438
Q

Describe secretory diarrhoea

A

Too much secretion of ions (Cl-) into GI lumen

Too little absorption of sodium due to reduced surface area, mucosal disease, surgery, reduced contact time

439
Q

Describe osmotic diarrhoea

A

Gut contains osmotic material - malabsorption
Ingestion of poorly absorbed material - magnesium sulphate
Inability to absorb nutrients - lactose

440
Q

Define constipation

A

Suggestive if hard stools, difficulty passing stools or inability to pass stools
Straining during ≥25% defecations
Lumpy of hard ≥25% defecations
Feeling of incomplete evacuation ≥25% of defecations
Feeling of obstruction/ blockage ≥ 25% of defecations
Having fewer than three unassisted bowel movements a week

441
Q

What are risk factors for constipation?

A 
Female to male 3:1
Medications
Low physical activity
Increasing age
Poor diet
442
Q

What is the pathophysiology of constipation?

A

Slow colonic transport - large colon, poor peristalsis, fewer intestinal pacemaker cells (interstitial cells of Canal), systemic disorders (hypothyroidism, diabetes), Nervous system disorder (Parkinson’s, MS)
Defaecation muscle problems with poor coordination

443
Q

How do you treat constipation?

A 
Inc activity
Improve diet - more fibre
Stop offending medications
Inc fluid intake
Inc fibre intake
Laxatives
Psychological support
444
Q

What is the appendix and what is its blood supply?

A

Appendix is diverticulum of caecum
Complete longitudinal layer of muscle
Separate blood supply to caecum through mesentery from ileocolic branch of SMA

445
Q

What locations of the appendix are there?

A

Retro-caecal
Pelvic
Sub-caecal
Para-ileal (pre/ post)

446
Q

What are the broad categories of appendicitis?

A

Acute - mucosal oedema
Gangrenous - transmural inflammation and necrosis
Perforated - peritonitis

447
Q

What could be causes of appendicitis?

A

-Blockage of appendicaecal lumen creates higher pressure in appendix (faecolith, lymphoid hyperplasia, foreign body)
Pressure rises - oedema - reduced blood supply - ischaemia - bacterial invasion
-Viral/ bacterial infection causes mucosal changes that allows bacterial invasion of appendicaecal walls

448
Q

What are the classic presentations of appendicitis?

A

Poorly localised peri-umbilical pain
Anorexia
N+V
Low grade fever
After 12-24 hours pain is felt more intensely in right iliac fossa
If appendix is retro-caecal or pelvic = may not get RIF pain. Parietal peritoneum in RIF not in contact with appendix. Therefore suprapubic pain, right sided rectal or vaginal pain

449
Q

What are signs of appendicitis?

A 
Patients appears ill
Slight fever/ tachycardia
Generally lie still due to pain
Localised right quadrant tenderness
Rebound tenderness in RIF
450
Q

What is McBurney’s point?

A

2/3 from umbilicus to ASIS - check for rebound tenderness

451
Q

How is appendicitis diagnosed?

A 
Bloods - raised WBC
Hx/ Examination
Rebound tenderness in RIF
Pregnancy ruled out
CT - distended appendix
452
Q

How do you treat appendicitis?

A

ABx

Open/ laparoscopic appendicectomy

453
Q

What is diverticulosis?

A

Asymptomatic outpouchings of mucosa and submucosa through muscularis layers
They occur along where nutrient vessels (vasa recta) penetrate the bowel wall
Caused by increased intra-luminal pressure (low fibre diet)
85% in sigmoid colon

454
Q

What is acute diverticulitis?

A

Diverticula become inflamed or perforate (+/- bleeding and abscess formation)
Entrance to diverticula becomes blocked - inflammation allows bacterial invasion of diverticular wall - perforation

455
Q

What is the difference between a complicated and uncomplicated diverticula?

A

Uncomplicated - inflammation and small abscess confined to colonic wall
Complicated - larger abscess, fistula, perforation

456
Q

What are signs and symptoms of acute diverticulitis?

A 
Abdo pain at site of inflammation - usually left lower quadrant
Fever - inflammation and infection
Bloating
Constipation
Haematochezia - Large amounts of blood loss in stool
Distension of abode
Reduced bowel sounds
Signs of peritonitis
457
Q

What tests are done to diagnose diverticulitis?

A

Bloods - raised WCC, pregnancy test to exclude ectopic
USS/ CT
Colonoscopy if large haematochezia

458
Q

How do you treat acute diverticulitis?

A

ABx, fluids, analgesia

Surgery if perforation or large abscess needs draining

459
Q

What are some features of the rectum?

A

12-15cm long passing through pelvic floor
Continuous band of outer longitudinal muscles
Curved shape anterior to sacrum
Parts are peritoneal and retroperitoneal
Temporary storage of faeces prior to defaecation

460
Q

What is the blood supply and drainage of the rectum and anal canal?

A

Arteries: Superior rectal artery (

461
Q

What factors are involved in anal canal continence?

A 
Distensible rectum
Firm bulky faeces
Normal anorectal angle
Anal cushions
Normal anal sphincters
462
Q

What is the outer most part of the anal canal?

A

Anal verge

463
Q

What are the anal sphincters?

A

Internal and external

464
Q

Explain the internal and external anal sphincters

A 
Internal - 
involuntary, 
thickened circular smooth muscle - under autonomic control - 80% of resting anal pressure
External - 
striated muscle, 
deep section- upper anal canal, mixed fibres from levator ani,  joins with pubo-rectalis muscle to form a sling, 
Pudendal nerve 
20% resting pressure
465
Q

What happens in the defaecation response in terms of muscles and sphincters?

A

Relaxation of external anal sphincter
Relaxation of puborectalis muscle
Forward peristalsis in rectum, sigmoid colon
Valsalva maneuver (inc abdo pressure)

466
Q

What happens if defaecation needs to be delayed in terms of muscles and sphincters?

A

Contraction of external anal sphincter
Contraction of puborectalis muscle
Reverse peristalsis in rectum

467
Q

What is the dentate line?

A

Anal canal contains it

Junction of handgun and proctodaeum (ectoderm)

468
Q

What cells are found and what pain is felt above and below the dentate line?

A 
Above:
Cells - columnar epithelium
Pain - visceral pain
Below:
Cells - stratified squamous
Pain - somatic pain
469
Q

What are anal cushions?

A

Anal cushions contains complex venous plexus which drains blood away from the anal canal
3 anal cushions: Rt anterior anal cushion, Lt anal cushion, Rt posterior anal cushion

470
Q

What are internal haemorrhoids?

A

Symptomatic anal cushions
Loss of connective tissue support, above dentate line, relatively painless, enlarge and prolapse through anal canal, bleed bright red blood/ pruritis

471
Q

What is the treatment for internal haemorrhoids

A

Increased hydration, fibre
Avoid straining
Rubber band ligation
Surgery

472
Q

What are external haemorrhoids?

A

Haemorrhoids below dentate line
Swelling of anal cushions which then thrombus
Painful ++
Surgery is the treatment - thrombosis

473
Q

What is an anal fissure?

A

Linear tear in the anoderm (posterior midline usually)

474
Q

What causes anal fissures?

A 
Passing of hard stools
Pain on defeacation ++ (passing of razor blades)
Haematochezia
High internal anal sphincter tone
Reduced blood flow to anal mucosa
475
Q

What is the treatment for anal fissure?

A

Hydration, dietary fibre, analgesia
Warm baths
Medication to relax internal anal sphincter

476
Q

What are common causes for haematochezia?

A

Diverticulitis
Angiodysplasia (vascular malformation in bowel wall)
Colitis - IBD, infective
Colorectal cancer
Anorectal disease - haemorrhoids, anal fissure
Upper GI bleed - large bleed with fast transit

477
Q

What is melaena?

A

Black tarry stools
Offensive smelling
Due to haemoglobin digested by digestive enzymes and gut bacteria

478
Q

What are common causes of melaena?

A 
Upper GIB
Peptic ulcer
Variceal bleeds
Upper GI malignancy
Oesophageal/ gastric cancer
479
Q

What are uncommon causes of melaena?

A

Gastritis
Meckel’s diverticulum
Iron supplements

480
Q

What are the 3 ways dysphagia can be caused by an obstruction?

A

Extraluminal
Luminal
Intraluminal

481
Q

What are dysphagia red flags?

A 
ALARM mnemonic
A- anaemia
L- loss of weight
A - anorexia
R - recent onset of symptoms
M - masses/ melaena
482
Q

What type of carcinoma can occur in the oesophagus?

A

Stratified squamous epithelium -> squamous cell carcinoma
Columnar epithelium -> adenocarcinomas
BUT in the oesophagus due to metaplasia -> dysplasia due to Barrett’s the cancer in the distal 1/3 could be adenocarcinoma

483
Q

What would happen in dysphagia with advancing oesophageal carcinoma?

A

Progressive dysphagia

484
Q

What is the problem with progressive dysphagia in oesophageal carcinoma?

A

Once the dysphagia is symptomatic it indicates to a more progressive disease

485
Q

What are epigastric pain red flags?

A

Haematemesis

Melaena

486
Q

What are major differentials for epigastric pain?

A

Oesophageal varices
Acute gastritis
Duodenal ulcer
Gastric ulcer

487
Q

Typically where can gastric cancers be found in the stomach?

A

Cardia or antrum

Adenocarcinomas

488
Q

What are the risk factors for gastric cancer?

A

Smoking
High salt diet
FMHx
H. pylori

489
Q

What is the general prognosis of gastric cancer?

A

10% 5 year survival

50% after curative surgery

490
Q

What are 2 uncommon types of gastric cancer?

A

Gastric lymphoma - MALT tissue - similar presentation to gastric carcinoma - associated with H. pylori - Prognosis better than gastric cancer
Gastrointestinal stromal tumours - sarcomas (not epithelial) - tend to be incidental findings on OGD

491
Q

What are red flags for jaundice?

A

Hepatomegaly - irregular border
Unintentional weight loss
Painless
Ascites

492
Q

Why are hepatic malignancies rare?

A

Primary malignancy is rare and usually linked to underlying disease - hereditary haemochromatosis
GI cancers - drains entirety of GI tract - malignant cells pass through

493
Q

What malignancies commonly metastasise to the liver?

A

Lung
Breast
Skin
Renal

494
Q

What is a common presentation for pancreatic cancer and what are the risk factors?

A

Head: jaundice
Body/ tail: symptoms more vague, relate to function of pancreas
80% ductal adenocarcinomas
Risk factors: FMHx, Smoking, men>women, increasing age, chronic pancreatitis

495
Q

What are 3 key symptoms in lower GI malignancies?

A

Obstruction
PR bleeding
Change in bowel habit

496
Q

What are 2 symptoms of GI obstruction?

A

Abdo distension

Abdo pain

497
Q

What are differentials for benign GI obstruction?

A 
Volvulus - twisting
Diverticular disease
Hernias
Strictures - inflammation
Intussusception - small intestine into the large intestine
Pyloric stenosis - projectile vomiting
Malignant: Small vs large bowel
498
Q

What are obstruction red flags?

A

Unintential weight loss

Unexplained abdominal pain

499
Q

What are PR bleeding differentials?

A 
Haemorrhoids
Anal fissure
Infective gastroenteritis
IBD
Diverticular disease
Malignant: Small vs large bowel cancer
500
Q

What are PR bleeding red flags?

A 
Age dependent
Iron deficient anaemia
Unexplained weight loss
Change in bowel habit
Tenesmus - feeling of needing to evacuate but nothing comes out
501
Q

What are differentials for change in bowel habit?

A 
Bening: 
Thyroid disorder
IBD
Medication related
IBS
Coeliac disease
502
Q

What are red flags for change in bowel habit?

A

Age dependent
Iron deficient anaemia
Unexplained weight loss
PR blood loss

503
Q

How is large bowel cancer screened for?

A

Faecal occult blood samples

504
Q

What are risk factors for large bowel cancer?

A

FHx
IBD
Polyposis syndromes - FAP, HNPCC
Diet and lifestyle

505
Q

How does a polyp become an adenocarcinoma?

A 
Hyperproliferation of cells ->
Adenomatous polyp (small) ->
Adenomatous polyp (large) ->
Severe dysplasia (precancerous polyp) ->
Adenocarcinoma ->
Invasive cancer
506
Q

What are the similarities and differences between left and right sided colon cancer?

A 
RHS:
Weight loss
Anaemia - occult bleeding
Less likely to have bowel obstruction
Mass in RIF
Late change in bowel habit
More advanced disease at presentation
Fungating - growth and has a stalk
LHS:
Weight loss
Rectal bleeding
Bowel obstruction
Tenesmus
Mass in LIF
Early change in bowel habit
Less advanced disease at presentation
Stenosing - causing and obstruction
507
Q

When would you see the apple core sign?

A

Large bowel growth that is around the whole circumference

508
Q

What are 5 rare small bowel cancer?

A 
Stromal
Lymphoma
Adenocarcinoma
Sarcoma
Carcinoid tumours - neuroendocrine tumours - secretory
509
Q

What are risk factors for small bowel cancer?

A

IBD
Coeliac disease
FAP
Diet

510
Q

What is the staging used in GI malignancies?

A

Dukes staging - colon

and TNM staging - rest

511
Q

What are the stages in Dukes’ staging?

A

Dukes A - confined to inner mucosal lining
Dukes B - affects musculature of bowel
Dukes C - dukes B + lymph nodes
Dukes D - dukes C + more lymph nodes and mets

512
Q

How would you manage a GI malignancy?

A

Blood tests - FBC, Tumour markers e.g. CEA, CA 19-9
CT/MRI
Endoscopy/ Colonoscopy
Treatment - chemo, radio, surgery

513
Q

What does microbiome mean?

A

Refers to all the genome within the gut environment

514
Q

What does microbiota mean?

A

Refers to all the organisms within the gut environment

515
Q

What are the stool types?

A

Type 1 - separate hard lumps to pass like nuts
Type 2 - Sausage shaped but lumpy
Type 3 - Sausage but with cracks on surface
Type 4 - Sausage or snake, smooth and soft
Type 5 - Soft blobs with clear cut edges
Type 6 - Fluffy pieces with ragged edges - mushy stools
Type 7 - Watery, no solid pieces, entirely liquid

516
Q

What investigations are carried out on stool samples?

A

Stool culture - E. coli 0156, Salmonella, Shigella, Campylobacter
PCR - Clostriodioides, Entamoeba histolytia, Norovirus, Rotavirus,
Enzyme immunoassay - Cryptosporidium, Giadia, Clostridioides difficule
Microscopy - Ova, cysts, parasites

517
Q

What bacteria/ viruses are causes for acute infectious watery diarrhoea?

A

Norovirus, rotavirus, Clostridioides, difficile, Entertoxigenic E. coli, Giorgia lamblia, Cryptosporidium parvum

518
Q

What bacteria cause inflammatory diarrhoea?

A

Non-typhoidal salmonella, campylobacter, Clostridioides difficile, Shigella, E. coli 0157, Entamoeba histolytica

519
Q

What are the 2 divisions of salmonella and what disease do they cause?

A

Typhoidal salmonella - Enteric fever

Non-typhoidal salmonella - Primarily gastroenteritis

520
Q

How are non-typhoidal salmonella transmitted and what is their incubation period?

A

Incubation period - 8-72 hours

Transmission route: Food, Faeco-Oral route

521
Q

What would you use to treat non-typhoidal salmonella infections?

A

Usually self limiting
Fluoroquinolones - ciprofloxacin
Azithromycin
Ceftriaxone

522
Q

What is the incubation period of Campylobacter and what is the transmission route?

A

Incubation period - 3 days

Transmission - food, water, animal contact

523
Q

What is the treatment for campylobacter GI infections?

A

Macrolides/ Fluoroquinolones

524
Q

What is a complication of Campylobacter infection?

A

Reactive arthritis

Guillain-Barre Syndrome (GBS)

525
Q

What is the transmission route and incubation period for Shigella?

A

Transmission route: Faeco-Oral, food and water. Person-person. Low infective dose
Incubation period: 1-7days

526
Q

What are the treatments for Shigella infection?

A

Self limiting in immunocompetent

Ciprofloxacin, azithromycin, ceftriaxone

527
Q

What are complications of shigella infections?

A

Intestinal: Proctitis, rectal prolapse, toxic megacolon, perforation, obstruction
Systemic: bacteraemia, seizures (children), reactive arthritis, Haemolytic uraemia syndrome

528
Q

What are complications of non-typhoid salmonella GI infections

A

Bacteraemia, endovascular infections, abscesses, osteomyelitis, septic arthritis

529
Q

What are the E. coli bacteria associated with diarrhoea?

A 
Enterotoxigenic E. coli
Enterpathogenic E. coli
Enterinvasive E. coli
Enteraggregative E. coli
Shiga toxin-producing E. coli (E. coli 0157)
530
Q

What are symptoms of Shiga toxin-producing E. coli infections?

A

Painful bloody diarrhoea and haemolytic uraemic syndrome

Very contagious bacteria

531
Q

What is the incubation period for Shiga toxin producing E. coli (E. coli 0157)?

A

1-10 days

532
Q

What is haemolytic uraemic syndrome characterised by?

A

Nonimmune-mediated haemolytic anaemia, thrombocytopenia and acute kidney injury

533
Q

What is a problem with treating E. coli 0157 with antibiotics?

A

Worsening infection with antibiotics as the E. coli will produce more toxin as a result

534
Q

Describe Clostridiodes difficile

A

Anaerobic gram negative bacilli
Most common nosocomial infections
Cause of antibiotic associated colitis -> toxic megacolon
Colonisation - faecal oral route
Produces spores which are very resistant to the environment
Children have lots of C. diff in GI but don’t get infections due to them not having receptors for the toxin

535
Q

What are risk factors for C. diff infection?

A

Antibiotic therapy
PPI therapy
Prolonged hospitalisation
Age >65years

536
Q

How do you treat C. diff infection?

A

Metronidazole, Vancomycin, Fidaxomycin, Microbiota transplant

537
Q

What are the symptoms of norovirus infection, incubation period and transmission?

A

Profuse -diarrhoea, vomiting
Incubation period- 12-48 hours
Transmission - faeco-oral route, direct contact, aerosol

538
Q

How do you treat norovirus infection?

A

highly infectious

Self limiting - resolves 1-2 days but excrete for longer than this

539
Q

What are the symptoms, incubation period and transmission of rotavirus?

A

Symptoms: diarrhoea, vomiting, fever
Incubation period: <48hours
Transmission: faeco-oral route. Highly infective

540
Q

What is important about rotavirus infection?

A

Gastroenteritis in young children is severe hence why we get vaccinated
Complications: Seizures, encephalopathy, acute encephalitis

541
Q

How do you treat rotavirus infection?

A

Self limiting - supportive

542
Q

What are the symptoms, incubation period and transmission routes of cryptosporidium?

A

Symptoms: watery diarrhoea, stomach cramps
Incubation period: 10-14 days but can cause debilitating disease
Transmission route: Faeco-oral route, person-person, animals, food, water

543
Q

What are symptoms and transmission routes for Giardia?

A

Symptoms: malaise, steatorrhoea, abdo cramps, bloating, asymptomatic. Malabsorption, weight loss.
Transmission: faeco-oral route

544
Q

Who is most likely to get a giardia infection?

A

Travellers

Associated wit sporadic or epidemic infection linked to water, food, childcare settings and international travel

545
Q

Who is at high risk of Giardia infections?

A

Children, infants, immunocompromised, travellers and CF patients

546
Q

What are the symptoms, transmission route and incubation period of Entamoeba histolytica?

A

Symptoms: Diarrhoea (bloody), abode pain. Fulminant colitis with necrosis and perforation can occur. Can mimic IBD.
Transmission: Faeco-oral. Highly transmissible.
Incubation: 2 weeks to years

547
Q

What is a complication of Entamoeba histolytica infection?

A

Majority of infections asymptomatic but can cause amoebic dysentery, or infection at extra-intestinal sites such as the liver.

548
Q

What is peritonitis and what causes it?

A

Inflammation of the serial membrane that lines the abdominal cavity
Can occur spontaneously or through trauma causing foreign substances to enter the normally sterile space

549
Q

What causes primary peritonitis?

A

Spontaneous bacterial peritonitis
Most commonly seen in patients with end stage liver disease
Infection of the ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory or surgically correctable condition

550
Q

What are the symptoms of primary peritonitis?

A

Abdo pain
Fever
Vomiting

551
Q

How is primary peritonitis diagnosed?

A

Aspiration of ascitic fluid - neutrophil count >250 cells/mm3

552
Q

Define secondary peritonitis

A

result of inflammatory process in the peritoneal cavity secondary to inflammation, perforation, or gangrene of an intra-abdominal or retroperitoneal structure

553
Q

What are common causes of secondary bacterial peritonitis?

A

Peptic ulcer disease (perforated)
Appenditicits (perforated)
Diverticulitis (perforated)
Post surgery

554
Q

What are non bacterial causes of secondary peritonitis?

A

Tubal pregnancies that bleeds
Ovarian cyst
Blood

555
Q

What is the clinical presentation of peritonitis?

A

Abdo pain - gradual or acute
Diffuse pain in perforated viscera
Patients lie still and shallow breath due to pain of viscera

556
Q

What are treatments for peritonitis?

A

Control infection source
Eliminate bacteria and toxins - antibiotics
Maintain organ system function - intensive care

557
Q

What is bowel obstruction?

A

Mechanical or functional problem that inhibits the normal movement of gut contents
Can be large or small bowel
All ages affected

558
Q

What are common causes of bowel obstruction in children and in adults?

A

Children: intussusception, intestinal atresia
Adults: adhesions, incarcerated hernias

559
Q

Define intussusception

A

One part of the gut tube telescopes into an adjacent section

560
Q

What is the problem with intusesception if left untreated?

A

Extend far as the SI extends into the LI and can even prolapse out of the rectum
Lymphatic and venous drainage impaired - oedema occurs - impede arterial supply - infarction - ischaemia - necrosis

561
Q

What are the symptoms of intussusception?

A

Abdo pain, vomiting and haematochezia

562
Q

What are the treatments of intusscesception?

A

Air enema

Surgery - removal of necrotic tissue

563
Q

What symptoms are due to small bowel obstruction?

A 
Abdo distension
Absolute constipation (late)
564
Q

What causes small bowel obstruction?

A
  • Intra-abdominal adhesions - abnormal fibrous bands between organs or tissues that are normally separated.
    Surgery is the biggest cause of these adhesions - greater omentum is commonly involved
  • Hernias - narrowing of lumen - incarcerated worse
  • IBD - Crohn’s - repeated inflammation/healing - narrowing
    -Tumours
    -Inflammation
565
Q

How do you diagnose small bowel obstruction?

A

Hx - cramps intermittent pain
OE - abdo distension, increased/ absent bowel sounds, presence of hernia
Imaging - X-ray - the permanent folds appear the traverse the whole length of the lumen

566
Q

What are the 5 main causes of large bowel obstruction?

A 
Colonrectal carcinoma
Diverticular disease (stricture)
Volvulus - sigmoid, caecal
Hernia
Pseudo-obstruction
567
Q

What are symptoms of large bowel obstruction?

A

Change in bowel habit
Abdo distension - ileocaecal valve prevents faeces moving backwards initially - therefore less chance of N+V initially
Crampy abdo pain
N+V - later stages

568
Q

What is a volvulus?

A

Twisting of the bowel around its mesentery
Most common is sigmoid colon and caecum - but occurs anywhere
Results in obstruction

569
Q

What is one big common cause of a volvulus?

A

Overloaded sigmoid colon - constipation
Extra mass predisposes of elongation of sigmoid relative to mesenteric attachment
High fibre diets add to this problem

570
Q

What is a coffee bean sign on x-ray indicative of?

A

Volvulus

571
Q

What is different in the time of the colicky pain in small and large bowel obstruction?

A

Small bowel - 3-4mins

Large bowel - 10-15mins

572
Q

What is different in the ages affected in small and large bowel obstruction?

A

Small - younger

Large - older

573
Q

If the ileocaecal valve is tightly closed what problems can that cause in large bowel obstruction?

A

Colon can’t decompress and therefore can cause ischaemia and perforation eventually

574
Q

What is the difference in pathophysiology in an acute occlusion and non-occlusive mesenteric ischaemia?

A

Occlusive - arterial thrombus in SMA (50%)
Non-occlusive - low cardiac output - drop in BP - watershed area the splenic flexure - least collateral blood supply - affected the worst

575
Q

What are the symptoms of acute mesenteric ischaemia?

A

Abdo pain disproportionate to clinical findings
Pain comes on 30mins after eating and last for 4 hours - when blood goes to GI
N+V
Pain often left sided due to splenic flexure

576
Q

What investigations would be done for acute mesenteric ischaemia?

A

Bloods - metabolic acidosis/ inc lactate levels
Erect chest x-ray for perforation
CT angiogram

577
Q

What is the treatment for acute mesenteric ischaemia?

A

Surgery - resection of ischaemic bowel
Thrombolysis/ angioplasty
Mortality is high

578
Q

How does a peptic ulcer potentially lead to an upper GIB?

A

Ulceration that erodes through the layers of the organ wall
Duodenal ulcers most common
Duodenal ulcer can erode through all the layers of the muscle into the surrounding structures
Gastroduodendal artery sits just behind D1 and so erosion goes through blood vessel

579
Q

How do oesophageal varices form?

A

Increased portal pressure prevents blood from easily entering the liver
Blood backs up and uses other routes to get back to circulation and tends to use veins not normally used
Normally - Portal drainage-oesophageal veins ->left gastric vein -> portal vein
Abnormally - Systemic drainage - oesophageal vein -> azygous vein -> SVC

580
Q

How do you treat oesophageal varices?

A

1 - Endoscopic band ligation
2 - Transjugular intrahepatic portosystemic shunt - stent placed within liver that was occluded to regain blood drainage -> decompresses portal vein pressure -> reduction in vatical pressure -> reduction in ascites
3 - Terlipressin - reduces portal venous pressure

581
Q

What is an abdominal aortic aneurysm?

A

Permanent pathological dilation of the aorta with a diameter >1.5x the expected AP diameter of that segment
Most aneurysms originate below the renal arteries
Degeneration of media layer of the arterial wall elastin and collagen - lumen gradually dilates

582
Q

What are risk factors for AAA?

A

Male
Inherited risk
Increasing age
Smoking

583
Q

What is a typical presentation of AAA rupture?

A

Abdo, flank, back and groin pain
Pulsatile abdo mass
Transient hypotension- syncope - retroperitoneum can temporarily tamponade the bleed
Sudden cardiovascular collapse

584
Q

How is AAA diagnosed?

A

Physical examination
Ultrasonography
CT
Plain X-rays - if calcification

585
Q

What is the treatment for AAA?

A

HTN control, smoking cessation
Surveillance <5.5cm - grow slowly, >5.5cm refer to vascular
Surgery
Endovascular repair - relining aorta with endograft/ stent - inserted through femoral artery
Open surgical repair - covering of aorta

586
Q

What gastro reasons would you request an abdominal x-ray?

A 
Acute abdo pain
Small or large bowel obstruction
Acute exacerbation of IBD
Renal colic (CT now first line)
587
Q

What mnemonic helps with not missing any diagnosis of abdomen in an x-ray?

A

A-E approach
A- Air/gas - where it should and shouldn’t be
B- Bowel - size and wall thickness
C- Calcification/ stones -
D- Dem bones
E- Everything else - organs and soft tissues - liver, spleen, kidneys, objects, artefacts

588
Q

What features of the gas or fluid in the GIT would allow the structures around it to be seen?

A

Gas or gas+fluid filled - easily seen
Low density gas - acts as contrast
Fluid filled only - NOT visible

589
Q

What are classed as small and large bowel obstruction in terms of gas sizes?

A

Rules of 3’s (3,6,9)
Small bowel obstruction >3cm
Large bowel obstruction >6cm - competent ileocaecal valve (caecum >9cm), incompetent ileocaecal valve

590
Q

What is toxic megacolon?

A 
Acute deterioration with UC or colitis
Colonic dilation
Oedema
Pseudopolyps
Toxic implies patient unwell
591
Q

What is a lead pipe colon?

A

Featureless colon
Loss of haustra
UC - chronic inflammation

592
Q

What is thumb printing?

A

Radiographic sign of large bowel wall thickening - caused by oedema, infective or inflammatory process (colitis). The normal haustra become thickened at regular intervals appearing like thumbprints projecting into the aerated lumen.

593
Q

Why do we do erect chest x-ray?

A

To see if free gas under the diaphragm can be seen and this could be related to perforation/ normal

594
Q

What fluoroscopic contrast studies can be done to diagnose GI problems?

A

Contrast - barium, water soluble contrast

Common GI contrast studies - Swallow, Meal, Follow through, Enema

595
Q

What are the layers of the small and large intestine?

A

Mucosa:
Epithelium
Lamina Propria
Muscularis Mucosa

Submucosa:
Meissner’s Plexus

Muscularis Propria:
Circular muscle
Auerbach’s Plexus
Longitudinal muscle

Serosa or Adventitia

596
Q

At what vertebral level do the coeliac trunk, SMA and IMA exit the abdominal aorta?

A

Coeliac trunk - T12
SMA - L1
IMA - L3

597
Q

What is the drainage of blood from the middle and lower oesophagus?

A

Middle and lower - azygous vein -> SMV

Lower - left gastric vein -> portal vein

598
Q

What was the ligamentum teres before?

A

Umbilical vein

599
Q

What is the mental bursa?

A

Behind leser Momentum space

600
Q

Why does the lesser sac form?

A

The rotation of the stomach creates a lesser sac behind the stomach

601
Q

What is the epileptic foramen?

A

The hole where the epiploic vessels enter the lesser sac

602
Q

What do the myenteric plexus and the submucosal plexus control in the GIT?

A

Myenteric plexus - controlling GI movement

Submucosal plexus - controlling GI secretion

603
Q

What are distinguishing features of the myenteric and submucosal plexuses?

A

Myenteric - lies between circular and longitudinal layers,
liner chain of interconnecting neurones, spans the whole GIT, controls muscle activity, unmyelinated neurones

Submucosal - lies between mucosal layer, function within the inner wall, intestinal secretion, local absorption and local contraction of the submucosal muscle, finer neurones

604
Q

What is Charcot’s triad in acute cholangitis?

A

RUQ pain
Fever
Jaundice

605
Q

What is Reynold’s pentad in acute suppurative cholangitis?

A

Charcots Triad - RUQ pain, fever and jaundice
+
Altered consciousness, hypotension

606
Q

What is acute suppurative cholangitis?

A

Presence of pus in the biliary ducts may result in Reynold’s Pentad

607
Q

What are some causes for acute pancreatitis?

A 
IGETSMASHED
Idiopathic
Gall stones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion poison
Hypertriglyceridaemia, Hypercalcaemia
ERCP
Drugs

Medicine (15 decks)

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