GI system Flashcards

1
Q

How is oesophageal reflux from the stomach prevented?

A
  • Oesophageal sphincter
  • Acute angle of entry of oesophagus into stomach producing a valve like effect.
  • Mucosal folds at oesophagogastric junction act as a valve.
  • Right crus of diaphragm acts as a ‘pinch cock’.
  • +ve intra-abdominal pressure compresses walls of intra-abdominal oesophagus, helping to collapse it.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define dysphagia

A

Difficulty swallowing

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

What may cause dysphagia?

A
  • Neuro-muscular dysfunction, may be due to a stroke, parasitic infections.
  • Oesophageal tumour
  • Obstruction
  • May be congenital
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is peristalsis?

A

a coordinated wave of contraction behind bolus of food, with relaxation ahead, to propel bolus forward. Involuntary- from intrinsic neuromuscular reflexes.

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

What is Odynophagia?

A

pain on swallowing

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

What is a stricture?

A

narrowing

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

What can cause odynophagia?

A

Severe oesophagitis, a stricture

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

Name some mechanical causes of dysphagia

A

enlarged aorta, mediastinal tumour, enlarged LA, oesohpageal or stomach tumours, hiatal hernia (all of these are oesophageal lesions)

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

Name some neurological oropharyngeal causes of dysphagia

A

stroke, MS, myasthenia gravis, Parkinson’s disease

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

What nerve innervates the Masseter muscle and what is this muscle responsible for?

A

Trigeminal (5th cranial), mastication (chewing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which parasympathetic nerve controls salivary secretion and where does this nerve synapse?

A

Glossopharyngeal nerve (9th cranial), otic ganglion.

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

Where does the sympathetic nerve controlling salivary secretion synapse?

A

Superior cervical ganglion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe parasympathetic stimulation to salivary glands.

A

ACh release, acts on M3 receptor, Gq, PLC cleaves PIP2 to IP3 and DAG.
Secretion is watery.
Parasympathetic control responsible for volume (mainly).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why does water not pass from the saliva into the duct cells during duct cell modification?

A

Duct cells relatively impermeable to water as tight junctions and lack of aquaporins, so hypotonic saliva produced.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Define a mesentery

A

a double layer of peritoneum that connects portions of the gut tube or other viscera to the body wall or to each other.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

In the developing embryo, how does the mid gut communicate with the yolk sac?

A

Via the vitteline duct.

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

What is a Meckels diverticulum?

A

a vestigial remnant of the vitellointestinal duct (connecting gut tube to yolk sac), forming an outpouching. Rule of 2: 2 inches long, 2 ft from ilio-caecal junction, and 2 types of tissue: small bowel epithelium, and gastric tissue, occurs in 2% of pop.

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

How are the greater and lesser sacs, and greater and lesser omenta formed?

A

By rotation of the stomach

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

What does rotation of stomach achieve?

A
  • vagus nerves put ant. and post. rather than left and right.
  • cardia and pylorus shifted from midline, stomach lies obliquely
  • contributes to lesser sac lying behing stomach
  • forms greater omentum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Name 2 secondarily retroperiotneal organs

A

Most of duodenum, pancreas

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

Which part of the duodenum is intraperitoneal?

A

Duodenal cap

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

Name 3 retroperitoneal structures

A

Aorta, IVC, kidneys

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

How is a structure retroperitoneal?

A

It never had a mesentery, so never were within the periotneal cavity, and so lie against the post. abdominal wall, with periotneum covering its anterior surface only, and are not suspended in abdominal cavity.

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

How does duodenum become secondarily retroperitoneal?

A

Stomach rotation moves duodenum to the right, along with rapid growth of head of pancreas and rapid growth of liver. Duodenum then pressed against post. body wall, and dorsal mesoduodenum fuses with peritoneum.

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

Define mid-inguinal point and what is found there.

A

Midpoint between ASIS and pubic symphysis. Femoral artery can be palpated.

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

Define mid-point of inguinal ligament and what is found there.

A

Midpoint between ASIS and pubic tubercle. Femoral nerve found here. Deep inguinal ring found just above this point, though now been found to lie just medial to it, so closer to where femoral artery located, which is why may be said to lie at mid-inguinal point.

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

What is the deep inguinal ring?

A

Entrance to the inguinal canal.

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

Why might liver cirrhosis result in tortuous mucosal oesophageal veins?

A

Liver cirrhosis can cause portal hypertension, and oesophageal varices may result from this due to porto-systemic anastomosis. The L gastric vein drains blood from the oesophagus, and leads into the hepatic portal vein to the portal system, and the azygos vein, into the systemic system. With portal hypertension, blood normally passing through L gastric vein is redirected through oesophageal veins, into the azygos vein, causing dilation of veins in oesophageal mucosa.

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

What are diverticula and where do they develop?

A

Out-pouchings of a hollow or fluid filled structure in the body, related to pressure changes. Most common site= sigmoid colon, as has highest intra-luminal pressure.

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

Where is the dentate (pectinate) line?

A

Divides hind gut from procto-deum, dividing upper 2/3 of anal canal with columnar epithelium, from lower 1/3 with stratifies squamous epithelium. Blood supply and venous drainage also different between the 2, and pathology below line will be painful.

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

What are haemorrhoids?

A

vascular structures in anal canal which swell to stop faecal material from leaking out when it shouldn’t and so help with stool contro. Problems occur if distend beyond normal limits, and become pathological when symptoms produced e.g. bright red bloody stools, pain of defecation, itching and prolapse of haemorrhoidal tissue.

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

At what point is an incision made for an appendicectomy?

A

McBurney’s point- 2/3rds of distance between the umbilicus and the right ASIS. Incisions have to be able to close, and provide long-lasting strength, so minimise incidence of incisional hernias.

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

What is a hernia?

A

Protrusion of visceral contents through a cavity that normally contains it because of increased pressure or a weakened abdominal wall.

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

Where are the paired rectus abdominis muscles?

A

enclosed within rectus sheath- (fibrous CT, sheet of fascia), extends from thoracic cage to pubic bones. Tendinous intersections within muscles attach to deep surface of anterior side of the rectus sheath.

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

What is the linea alba?

A

fibrous line formed from midline fusion of aponeuroses of all 6 antero-lateral abdominal muscles.

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

What are the linea semilunares?

A

the sites of fusion of the aponeuroses of the 3 antero-lateral abdominal muscles per side at the lateral margin of the rectus sheath.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Describe the structure of the anterolateral abdominal wall, from superficial to deep.

A
  • skin
  • superficial fascia (fatty layer of subcutaneous tissue)
  • deep, membranous layer of subcutaneous tissue
  • deep fascia
  • external oblique
  • internal oblique
  • transversus abdominis
  • transversalis fascia
  • extraperitoneal fat
  • parietal peritoneum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Describe external oblique muscle

A
  • Most superficial muscle of antero-lateral abdominal wall
  • Muscle fibres run inferiorly and anteriorly from origin on thoracic cage (5th to 12th ribs)
  • Inserts onto linea alba, pubic tubercle and anter. half of iliac crest.
  • Lower, inferior margin of aponeurosis forms the inguinal ligament- extends from ASIS to pubic tubercle.
  • thoracoabdominal nerves (T7-T11) and subcostal nerve.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How is the rectus sheath formed?

A

By decussation and interweaving of aponeuroses of flat abdominal muscles. External oblique aponeurosis contributes to ant. wall of sheath throughout its length. Internal oblique aponeurosis contribute to ant. and post. rectus sheaths. Aponeurosis of transversus abdominis forms post. layer of rectus sheath.

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

Describe internal oblique muscle

A
  • muscle fibres run anteriorly and superiorly from origin on anter. 2/3 of iliac crest, thoracolumbar fascia and CT deep to lateral 1/3 of inguinal ligament.
  • inserts into linea alba, 10th-12th ribs.
  • Thoracoabdominal nerves (A.rami of T6-T12 spinal nerves) and 1st lumbar nerves.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What would happen if the muscle fibres of 1 abdominal wall muscle abutted the fibres of another.

A

The muscle fibres would tear themselves apart. Instead, each muscle is covered in epimysium.

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

Describe transversus abdominis muslce

A
  • fibres run transversely/horizontally from internal surfaces of 7-12th costal cartilages, thoracolumbar fascia, iliac crest, and CT deep to lateral 1.3 of inguinal ligament.
  • inserts into linea alba
  • Same innervation as internal oblique.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the arcuate(Douglas’ line)?

A

Line marking the disapperance of the posterior rectus sheath below the umbilicus, resulting in inferior 1/4 of rectus abdominis muscle lying directly on transversalis fascia. Disappears about 1/3 of way between umbilicus and the pubic symphysis. So in pfannenstiel incision, there would be no post. sheath to look out for. Also, below this line, the rectus abdominis muscle lies directly on the transversalis fascia.

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

Where post. rectus sheath is absent., what does rectus abdominis lie on?

A

The transverslais fascia.

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

Describe rectus abdominis

A

-muscle fibres travel from pubic symphysis and pubic crest to the xiphoid process and the 5th-7th costal cartilages.

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

Describe inguinal canal structure

A

oblique passage directed inferomedially through inferior part of anterolateral abdominal wall. Lies parallel and superior to medial half of inguinal ligament. Spermatic cord occupies canal in males, round ligament of uterus in females. Also blood and lymphatic vessels, and the ilioinguinal nerve.
2 walls, roof and floor: Anter. wall- external oblique aponeurosis, lateral part reinforced by muscle fibres of internal oblique
Post.- transversalis fascia
Roof- laterally by transversalis fascia, centrally by musculoaponeurotic arches of internal oblique and transversus abdominis, and medially by medial crus of external oblique aponeurosis.
Floor- laterally by iliopubic tracr, centrally by gutter formed by infolded inguinal ligament, and medially by lacunar ligament.

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

Where does the greater omentum extend to?

A

From stomach to transverse colon.

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

What is the falciform ligament?

A

A peritoneal ligament, formed from the ventral mesogastrium, which connects the liver to the ventral body wall, as attached to visceral peritoneum of liver and parietal periotneum on deep surface of anterior body wall.

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

What connects the greater and lesser sacs?

A

The foramen of Winslow (epiploic foramen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How are the greater and lesser curvatures of the stomach formed?

A

During longitudinal axis rotation, the posterior wall of the stomach grows more quickly and larger than the anterior part, forming the curvatures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Why are inguinal hernias more common in males?

A

Due to passage of spermatic cord through inguinal canal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Why are femoral hernias more common in females?

A

Due to wider pelves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Why might strangulation of a femoral hernia occur?

A

As sharp, rigid boundaries of femoral ring, part. the concave margin of the lacunar ligament.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Describe differences between direct and indirect inguinal hernias.

A

Direct- herniation passing medial to inferior epigastric vessels, pushing through peritoneum and transversalis fascia in inguinal triangle to enter inguinal canal. Acquired hernia. Passes through Hesselbach’s triangle.
Indirect- herniation passing lateral to inferior epigastric vessels, to enter deep inguinal ring at the opening of the inguinal canal. Passes lateral to Hesselbach’s triangle. Congenital- failure of processus vaginalis to close properly. This is part of the peritoneum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What are the borders of Hesselbach’s triangle and what is its clinical relevance?

A

Inferiorly- inguinal ligament
Laterally- inferior epigastric vessels
Medially- rectus abdominis muscle (lateral border of)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Before longitudinal axis rotation, the stomach comprises anterior and posterior sides, which after rotation faces right or left and is now the greater or lesser curvatures?

A

Anterior side now faces right, forming the lesser curvature.

Posterior side now faces left, forming the greater curvature.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is the dentate/pectinate line?

A

Line demarcating the 2 different parts of the anal canal, the part above the anal canal has simple columanar epithelium and is derived from endoderm, the part below had stratified squamous epithelium, and is derived from ectoderm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Give the name of the part of the lesser curvature which marks the start of the pyloric antrum.

A

Angular notch/ angular incisure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is achalasia?

A

Problem with enteric NS resulting in failure of lower oesophageal sphincter to relax, and so stomach unable to accomodate food from oesophagus.
Cause of dysphagia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the transverse mesocolon?

A

An expanse of peritoneum connecting the transverse colon to the posterior abdominal wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Where is the fundus of the stomach located?

A

Directly below the diaphragm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Where does the liver develop?

A

In the ventral mesetery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Where does the spleen develop?

A

In the dorsal mesentery (mesogastrium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is the hepatoduodenal ligament part of?

A

The lesser omentum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Where does the duodenum end?

A

At the duodenojejunal flexure, at L2 vertebral level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the axis of the primary intestinal loop?

A

The SMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the derivatives of the cranial limb of the primary intestinal loop?

A

Distal duodenum, jejunum and proximal ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Where is visceral pain felt if foregut derived?

A

Epigastric region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Where is visceral pain felt if midgut derived?

A

Peri umbilical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Where is visceral pain felt if hindgut derived?

A

Supra public region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What level is the celiac trunk at?

A

T12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What ligaments does the greater omentum form?

A

Gastrocolic ligament
Gastrosplenic ligament
Gastrophrenic ligament

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Where does a direct inguinal hernia push through in Hesselbach’s trinagle most commonly, and why?

A

The superficial inguinal ring as further area of weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Describe difference between an incarcerated and a strangulated hernia?

A

Incarcerated- stuck, cannot go back to where it came from, but blood supply intact, though can become strangulated.
Strangulated- blood supply compromised.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is the saphenous opening?

A

An opening in the deep fascia (fascia lata) of the thigh, which allows the ascent of the great saphenous vein, which once through opening joins the femoral vein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the dermatomal level of the umbilicus?

A

T10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Where does the celiac trunk originate from?

A

The abdominal aorta, immediately after thoracic aorta descends behind the diaphragm to enter the abdomen. Diaphragm- aortic hiatus- level of T12.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Where does the left gastric artery run and what branch does it give off? Also, what artery does it anastomose with?

A

To the left side of the lesser curvature of the stomach.
Oesophageal branch
R gastric artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is the left gastric vein a tributary of?

A

The portal hepatic vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Where does the splenic artery run?

A

Retroperitoneally along superior border of pancreas to spleen from celiac trunk.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What anastomoses form along the greater curvature of the stomach?

A

Right and left gastro-epiploic arteries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Which arteries supply upper body and fundus of stomach?

A

Short and posterior gastric arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the hepatic portal vein formed from?

A

The splenic vein and SMV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Which arteries does the splenic artery give rise to?

A

Left gastroepiploic, the short gastric and the posterior gastric arteries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is a peritoneal ligament?

A

A double layer of peritoneum that connects an organ with another organ or to the abdominal wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

How is the liver connected to other organs and the abdominal wall by peritoneal ligaments?

A

-falciform ligament- to anterior body wall
-hepatogastric ligament- to stomach
-hepatoduodenal ligament- to duodenum. This ligament is the thickened free edge of the ventral mesentery, which conducts the portal triad.
All part of lesser omentum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

How is the stomach connected to other organs and the abdominal wall by peritoneal ligaments?

A
  • gastrophrenic ligament-to diaphragm
    -gastrosplenic ligament-to spleen
    -gastrocolic ligament- to the transverse colon.
    All have a continuous attachment along greater curvature, and are all part of greater omentum.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Clinical significance of gastroduodenal artery

A

Duodenal ulcers may erode posteriorly into the gastroduodenal artery, causing extensive bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What is the dermatomal level of the pubis

A

T12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Treatment for H.pylori infection

A

2 antibiotics and a proton pump inhibitor- combination of clarithromycin with either amoxicillin or metronidazole, +PPI e.g. lansoprazole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

How does H.pylori survive in acid environ. of stomach?

A

It produces urease- converts urea to ammonia- this buffers gastric acid with concurrent production of CO2. Bacterium has urea channels which open at pH less than 6.5, so urea delivered to enzyme.
Basis for urease breath test for bacterium detection.
H pylori can then live within the mucous gel of the barrier, its motility-flagellum and chemotaxis, allowing it to penetrate close to epithelium.
Also, it produces adhesins so can attach to mucosa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is GORD?

A

A digestive disorder where there is regurgitation of stomach contents into lower oesophagus through an effective lower oesophageal sphincter, and the associated symptoms and pathology that this produces.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What structures does celiac trunk supply?

A

Foregut derived:

so oesophagus, liver/biliary apparatus, spleen, stomach, proximal duodenum and pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

At what vertebral level does the caval opening, oesophageal opening and aortic hiatus in diaphragm occur?

A

Vena cava- T8
Oesophagus- T10
Aortic hiatus- T12

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

At what vertebral level is the cardial orifice?

A

T11

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is dyspepsia?

A

A variety of symptoms including upper abdominal pain, acid reflux, heartburn and nausea/vomiting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Describe H.pylori

A

A gram -ve bacterium which is helical in shape and highly motile. Major cause of peptic ulcers. Urease producing and ability to penetrate gastric mucosa enables its survival in acidic stomach environment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Importance of alkaline tide

A

HCO3- readily available in blood to be subsequently re-secreted into GI tract by pancreas and liver to neutralise acid as it leaves the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

How can we detect H.pylori in a patient?

A

Urease breath test- give patient radioactively labelled urea, and then see if 20 mins later, radioactively labelled CO2 is produced as this would mean urease has acted upon the urea given, and urease is produced by H.pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Why is a PPI more effective than a H2 antagonist at reducing stomach acid production?

A

Stomach acid produced by parietal cells which have receptors for gastrin, Ach, and histamine which all stimulate acid production via the proton pump. A histamine antagonist will only block the input of histamine to acid production, with receptors for gastrin and Ach still being able to stimulate acid prod., whereas a PPI will block all receptor inputs to acid prod. as it blocks the proton pump necessary for any acid production from the parietal cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Why might NSAIDs lead to peptic ulcer formation?

A

COX1 inhibitors, COX1 being the enzyme responsible for prostaglandin synthesis from arachidonic acid- an eicosanoid, and prostaglandin E increases mucus and alkali prodcution, mucus being produced by neck cells at surface of mucosa, which protects the stomach mucosa from gastric acid, and also increases mucosal blood flow, which again is protective, so inhibition of PG production inhibits these protective mechanisms against harsh acidic environment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Give 3 causes of oesophageal atresia

A
  • tracheo-oesophageal septum misplacement
  • rencanalisation failure
  • ischaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What is polyhydamnios and why might it occur with oesophagel atresia?

A

accumulation of amniotic fluid

Atresia results in upper GI obstruction that will prevent normal amniotic fluid swallowing by the fetus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What is the common bile duct formed from?

A

The cystic duct from the gallbladder and the common hepatic duct from the R and L hepatic ducts from the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What prevents reflux of duodenal contents into ampulla of Vater (hepatopancreatic ampulla)?

A

Sphincter of Oddi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Give 2 functions of mesenteries

A
  • Attach organs to body wall

- Provide a conduit for nerves and blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

During physiological herniation, if the midgut rotates once clockwise, what would happen?

A

The cranial limb would still enter abdominal cavity 1st and so reside to the left, but would now be anterior rather than posterior to the caudal limb.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is omphalocele?

A

Incomplete physiological herniation where primary intestinal loop resides outside of body, with a covering of amnion. Contrast with covering of subcutaneous tissue in an umbilical hernia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

List functions of saliva

A
  • start digestion with secretion of salivary amylase
  • protection of oral mucosal environment via bacteriostatic actions, and alkaline secretion- Ca2+ unable to dissolve, protects the teeth.
  • Lubrication of food bolus for swallowing and passage down the oesophagus.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What are the 3 phases of swallowing?

A

Voluntary, pharyngeal and oesophageal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

List the key functions of the digestive tract

A

DAMES

Digestion, absorption, motility, excretion and secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

How might xerostomia result?

A
  • salivary gland tumour
  • calculus blocking saliva outflow from salivary gland
  • side effect of anti-muscarinics, inhibit parasympathetic innervation controlling saliva secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What might be the causes for a difficulty in swallowing food, and a difficulty in swallowing liquids.

A

food- mechanical causes of dysphagia e.g. large oesophageal tumour
liquids- problem with neural control e.g. stroke.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

How might haematemesis result?

A

peptic ulcer, gastric cancer, oesophageal varices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Describe chyme

A

acidic
hypertonic
partially digested

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What controls pancreatic enzyme secretion?

A

CCK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What controls pancreatic alkaline secretion?

A

Secretin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

When in bile released from gallbladder?

A

When CCK secreted by duodenum during gastric emptying. Stimulates smooth muscle of gallbladder to contract and release bile. CCK also relaxes sphincter of Oddi so bile can pass into duodenum. Vagal stimulation can also cause weak gallbladder contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

During what phase of are most pancreatic secretions released?

A

Intestinal phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What is cholecystitis?

A

gallbladder inflammation as result of gallstone impaction in neck of gallbladder, (or cystic duct?) which may cause continuous epigastric pain, vomiting and fever. If stone moves to common bile duct, obstructive jaundice and cholangitis may occur- infection of common bile duct.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What is biliary colic?

A

Symptomatic gallstones with cystic duct obstruction or bypassing into common bile duct.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

How might pancreatitis be caused by gallstones?

A

Galllstone obstruction of outflow of pancreatic duct, if travel down common bile duct, blocking enzyme release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Why is liver larger in mature fetus?

A

Serves as a haematopoietic organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What is the only nutrient absorbed not to be initially conveyed to liver by portal venous system?

A

Fat- absorbed into lymphatic system which bypasses liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Where does liver lie anatomically?

A

R hypochondrium, where protected by thoracic cage and diaphragm, deep to ribs 7-11 on R side and crosses midline toward left nipple, so also occupies upper epigastrium and extends into left hypochondrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Where are the sub-phrenic recesses?

A

These are sup. extensions of greater sac existing between diaphragm and ant. and sup. aspects of diaphragmatic surface of liver. Separated into R and L by falciform ligament.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What is the subhepatic space?

A

portion of supracolic compartment of peritoneal cavity, immediately inferior to liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Describe the heptaorenal recess (hepatorenal pouch/Morison pouch)

A

posterosuperior expansion of subhepatic space, lying between R part of visceral surface of liver and R kidney and suprarenal gland. In supine position, fluid drains from lesser sac into this recess. Communicates anter. with R subphrenic recess.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Why is liver susceptible to scarring from cellular damage?

A

As primary site for detoxification of substances absorbed by digestive system. Hepatocytes=stable cells- good regenerative capacity, in G0 of cell cycle so can reenter when needed if receive growth stimulus, this requires activation of proto-oncogenes.
Fibrous tissue surrounds intra-hepatic blood vessels and biliary ducts, making liver firm, and impeding circulation of blood through it when liver cirrhosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Describe the bare area of liver

A

Posterior part of diaphragmatic surface not covered with visceral peritoneum and so in direct contact with diaphragm. Demarcated by reflection of peritoneum from diaphragm to it as anterior and posterior layers of the coronary ligament. These layers meet on R to form R triangular ligament.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Describe triangular ligaments of liver

A

Result from convergence of anterior and posterior parts of coronary ligament from reflection of peritoneum from diaphragm. A and P layers meet on R to form R triangular ligament. A layer continuous on L with R layer of falciform ligament, and P layer continuous with R layer of lesser omentum. L triangular ligament formed near apex where A and P layers of L part of coronary ligament meet.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Describe relationship of IVC to liver

A

IVC traverses a deep groove for the vena cava within bare area of liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What is the fibrous remnant of the ductus venosus

A

ligamentum venosum
DV was a fetal shunt where blood from umbilical vein bypassed liver to enter IVC as liver not needed to detoxify blood as carried from mother’s placenta.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What is the fibrous remnant of the umbilical vein?

A

Round ligament/ ligamentum teres hepatis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Where does hepatoduodenal ligament (thickened free edge of lesser omentum) extend from?

A

from porta hepatis to duodenum, and encloses structures passing through porta hepatis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Where does hepatogastric ligament extend?

A

from groove for ligamentum venosum to lesser curvature of stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Impressions on visceral surface of liver reflect liver’s relationship to which structures?

A
  • stomach- R side of ant. part so pyloric and gastric areas
  • duodenum- S.part (duodenal area)
  • lesser omentum, which extends into groove for ligamentum venosum
  • gallbladder-fossa
  • colon-(colic area)- R colic flexure and R transverse colon
  • R kidney and suprarenal gland (renal and suprarenal areas).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

How is liver divided into 2 anatomical lobes and 2 accessory lobes?

A

By reflections of periotneum from its surface, fissures formed in relation to those reflections and the vessels serving liver and gallbladder.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

How is essentially midline plane separating R and L lobes of liver defined?

A

By attachment of falciform ligament and left sagittal fissure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Where are the 2 accessory lobes of liver located?

A

These are parts of anatomic R lobe and lie on slanted visceral surface, with R and L sagittal fissures on each side, and are separated from each other by porta hepatis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Why can hepatic lobectomies where R or L part of liver removed, occur without excessive bleeding?

A

Because liver divisions, as R and L hepatic arteries and ducts, + branches of R and L hepatic portal veins, do not communicate. Most liver injuries involve R part. Can now perform hepatic segmentectomies so remove only those segments with severe injury or affected by tumor. R, intermediate, and L hepatic veins serve as guides to planes between hepatic divisions but also provide major source of bleeding. each hepatic resection requires ultrasonography to establish patient’s segmental pattern as differ in size and shape as result of variation in branching of hepatic and portal vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Where is portal vein formed?

A

Anterior to IVC and posterior to neck of pancreas, close to L1 vertebra and transpyloric plane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Where do hepatic veins open into IVC?

A

Just inferior to diaphragm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

What are kupffer cells?

A

specialised macrophages of liver found along sinusoids, and perform phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What are the main tributaries of hepatic portal vein?

A

SMV, splenic vein, gastric veins, cystic veins and IMV- drains into HPV directly in 1/3 of people, but in most enters splenic vein, or SMV.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

Where is the gallbladder?

A

Lies in fossa for gallbladder on visceral surface of liver. Fossa at junction of R and L parts of liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Describe relationship of gallbladder to duodenum

A

Gallbladder lies anterior to superior part of duodenum, and its neck and cystic duct are immediately superior to duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

How does hepatic surface of gallbladder attach to liver?

A

Via CT of fibrous capsule of liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Describe the 3 parts of the gallbladder

A

Fundus: wide blunt end that usually projects from Inf. liver border at tip of R 9th costal cartilage in MCL
Body: main portion contacting visceral liver surface, transverse colon and superior part of duodenum
Neck: narrow, tapering end, opp. fundus, and directed toward porta hepatis, typically makes an S-shaped bend and joins cystic duct runnning from gallbladder to meet common hepatic duct from liver, to form common bile duct.

Peritoneum completely surrounds fundus and binds its body and neck to liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

How is cystic duct helped to be kept open?

A

By spiral fold formed by spiralling of mucosa of neck of gallbladder. This means bile can be easily re-directed into gallbladder when distal end of bile duct closer by sphincter of bile duct and/or hepatopancreatic spincter, or bile can pass into duodenum as gallbladder contracts- stimulated by CCK released on gastric emptying, by I cells.
Spiral fold also offers additional resistance to sudden damping of bile when sphincters closed, and intra-abdominal pressure suddenly increased, e.g. in cough.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

Describe cystic duct course

A

Passes between layers of lesser omentum, usually parallel to common hepatic duct, which it then joins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Describe arterial supply of cystic duct and gallbladder

A

Cystic artery, commonly from R hepatic artery from hepatic artery proper, in triangle between common hepatic duct, cystic duct, and visceral liver surface= cystohepatic triangle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Describe venous drainage of gallbaldder and cystic duct

A

Cystic veins-enter liver directly or drain through hepatic portal vein, after joining veins draining hepatic ducts and proximal bile duct. Veins from fundus and body enter visceral liver surface directy and drain into hepatic sinusoids= drainage from 1 capillary bed to another, so additional portal sytem.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Lynphatic drainage of gallbladder

A

Hepatic lymph nodes, often through cystic lymph nodes near neck of gallbladder. Efferent lymphatic vessels from nodes pass to celiac LNs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Nerves to GB and CD?

A

From celiac plexus, vagus nerve and R phrenic nerve.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Describe relations of spleen

A

Anteriorly: stomach
Posteriorly: L part of diaphragm, separating it from pleura, lung and ribs 9-11
Inferiorly: L colic flexure
Medially: L kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Arterial supply of spleen

A

Splenic artery from celiac trunk. Follows tortuous course along superior border of pancreas, posterior to lesser sac and anterior to L kidney. Divides into 5 or more branches between layers of splenorenal ligament. Lack of anastomosis between branches within spleen so vascular segments of spleen formed- 2 in most, 3 in others, with relatively avascular segments between, so allows subtotal splenectomy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Venous drainage of spleen

A

Splenic vein- formed by several tributaties emerging at hilum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What toxins must GI tract cope with?

A
bacteria
viruses
chemical
protozoa
nematodes/roundworms
cestodes/tapeworms
trematodes/flukes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

What innate physical defences protect GI tract from toxins?

A
  • saliva
  • colonic mucus
  • sight
  • smell
  • memory
  • gastric acid
  • small intestinal secretions
  • anaerobic environ. in small bowel and colon
  • peristalsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

Give 3 viruses resistant to stomach acid

A

hepatitis A- RNA non-enveloped
polio-picornavirus, RNA non-enveloped
coxsackie

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Where is gut associated lymphoid tissue (GALT) found in concentrated nodules?

A
  • tonsils
  • peyer’s patches-in ileum
  • appendix
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

A 50 yr old man with liver cirrhosis presents with hand problems- 4th and 5th digits pulled into partial flexion at MP and proximal IP joints, what is this presentation called?

A

Dupuytren’s contracture- disease of palmar fascia resulting in progressive shortening, thickening and fibrosis of palmar fascia and aponeurosis. Fibrous degeneration of longitudinal bands of palmar aponeurosis on medial side of hand pulls 4th and 5th digits into partial flexion at MP and proximal IP joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

What is mesenteric adenitis?

A

Enlargement of mesenteric lymph nodes as become inflamed, common cause of RIF pain in children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

What investigations may be done in appendicits?

A

CRP

FBC, look at neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Describe a femoral hernia

A

bowel enters femoral canal, presenting as a mass in upper medial thigh or above inguinal ligament, where it points down the leg, unlike an inguinal which point to groin. Neck of hernia felt inferior and lateral to pubic tubercle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Describe epigastric hernias

A

pass through linea alba above umbilicus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

Describe true umbilical hernias

A

result of perisitent defect in transversalis fascia- umbilical ring, through which umbilical vessels passed to reach the foetus. Can recur in adulthoood e.g. in pregnancy, or gross ascites.
Paraumbilical occur just above of below umbilicus and are found in a canal bordered by umbilical fascia posteriorly, linea alba anteriorly and rectus sheath laterally.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Why is surgical repair less urgent in omphalocoele than in gastroschisis?

A

Bowel protrusion protected by membranes e.g. amnion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

Give 3 causes of appendicits

A

Faecoliths
Worms
Lymphoid hyerplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

Why does alcoholic liver injury produce a ‘fatty’ liver?

A

Cellular energy diverted away from fat metabolism to alcohol metabolism, so fat accumulates as globules within liver cells.
Toxic acetaldehyde damages liver cells so unable to produce lipoproteins necessary to transport TAGs away from liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

What is liver cirrhosis?

A

Hepatic fibrosis with nodular regenration producing a shrunken liver. Results from recurrent loss of liver cells or severe tissue architectural damage. Irreversible. Liver cells no loner arranged in acini or lobules, but as nodules. Blood perfuses nodules in haphazard fashion as well-organised zonal structure lost, so organ prone to failure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

Why can excess ammonia cause mental confusion?

A

NH3 reacts with and removes alpha ketoglutarate from TCA cycle, so diminished energy supply to brain cells. Also increases pH of cells of CNS, interfering with neurotransmitter synthesis and release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

Where in body can ruptured varices as result of porto-systemic anastomosis occur?

A
  • oesophagus
  • ano-rectal junction
  • umbilical vein in falciform ligment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

How does paracetemol overdose lead to liver failure?

A

Phase II conjugation pathways become saturated so paracetemol undergoes phase I metabolism, producing the metabolite NAPQI which is toxic to hepatocytes. Can give N-acetyl cysteine.
Then undergoes phase II with glutathione, depleting cell of important anti-oxidant for protection against ROS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

Why can alcohol lead to acute pancreatitis?

A

Results in hyper-stimulation of pancreatic secretions so enzymes produced by acinar cells activated prematurely in pancreatic ducts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

Enzyme responsible for bilirubin conjugation?

A

UDP-glucoronyl transferase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

Liver cirrhosis can result in oesophageal varices, which may present with very significant blood loss with vomiting of blood, why is so much blood lost?

A

Varices rupture and deficient clotting ability due to liver cirrhosis, so increased PTT, and LOTS of bleeding!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

Give 4 key functions of the liver (blood and gut related)

A

Energy metabolism
detoxification
production of plasma proteins e.g. albumin
Bile production and secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

What does bile comprise?

A
Bile acids (salts)
Bile pigments
Cholesterol
Phosopholipids
electrolytes
water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

What 2 important functions of bile acids can be carried out due to amphipathic nature of molecules?

A
  • emulsification of lipid aggregates

- transport and solubilization of lipids in an aq environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

What part of duodenum most prone to peptic ulcers and why?

A

First part=duodenal cap, as this is the first place that chyme enters once it leaves the stomach and at this point, alkaline secretions have not yet been able to act on the chyme to neutralise it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

Gallbladder functions?

A

Store, concentrate, and release bile when needed i.e. when chyme enters duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

How is liver helped to be suspended in abdominal cavity?

A

Hepatic veins
R and L triangular, and coronary ligaments
Tone of anterior abdominal wall muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

Xerstomia may result in parotitis, what bacterial organism causes this infection?

A

Staphylococcus aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

Give an example of a H2 antagonist used to reduce gastric acid production

A

Cimetidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

Which cells of stomach produce histamine?

A

Enterochromaffin-like cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

Which clotting factors depend on Vit.K for their synthesis?

A

II(pro-thrombin), VII, IX and X (2,7,9 and 10)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

Which organ is the only one that can, in effect, release glucose into the bloodstream to maintain blood sugar levels, and why?

A

Liver

Contains enzyme glucose 6-phophatase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

Where is intrinsic factor produced?

A

Parietal cells of stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

Where is most Vit B12 absorbed?

A

Terminal ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

Why might someone with Crohn’s disease experience pernicious anaemia?

A

Chronic inflammation of terminal ileum reduces ability to absorb vitamin B12 necessary for erythropoiesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

If parietal cell destruction, why might patient have pernicious anaemia?

A

As intrinsic factor not produced as normally produced by parietal cells, and this factor is necessary for VitB12 absorption from the terminal ileum, in order to have erythropoiesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

Which part of GI tract does Crohn’s disease normally affect?

A

Terminal ileum or proximal colon, but can occur anywhere from mouth to anus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

Which part of GI tract does ulcerative colitis normally affect?

A

Rectum and sigmoid colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

Differences between Crohn’s and ulcerative colitis

A

Crohn’s: transmural, skip lesions as patch mucosal involvement, granulomas

Ulcerative colitis: Only mucosa affected, inflammation continuous in distribution, increases risk of colon cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

Describe the distribution of the SMA

A

Supplies duodenum distal to entry on common bile duct, jejunum, ileum, ascending colon and proximal 2/3 of transverse colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

Where does the ileocolic artery run?

A

From SMA to caecum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

Where do R colic and middle colic arteries run?

A

From SMA to ascending colon (R colic) and transverse colon (middle colic)
R colic commonly originates from ileocolic artery but may arise as a direct branch of the SMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

At what level is the IMA?

A

L3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

Describe path of L colic artery?

A

Originates from IMA and supplies ascending colon and distal part of transverse colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

How is arcade of arteries formed in transverse mesocolon?

A

Anastomosis of L colic artery and middle colic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

What artery supplies proximal part of rectum ?

A

Superior rectal artery from IMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

How is blood supplied to sigmoid colon?

A

Sigmoid branches of IMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

What are the main functions of bile acids?

A

Emulsification of lipids so large SA prod. for digestion
Lipid transport- micelles
Induction of bile flow
Regulation of bile acid synthesis- normal reabsorption inhibits hepatic synthesis
Water and electrolyte secretion- if bile acids present in colon, can result in diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

What regualtes platelet prod. by BM?

A

Thrombopoietin- a glycoprotein hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

When might alkaline phosphatase levels be elevated?

A

Cholestasis- obstruction of bile ducts so enzyme released from liver into blood.
Paget’s disease- active bone formation, enzyme released as by-product of osteoblast activity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
208
Q

Vertebral level of SMA?

A

L1, originates from anterior surface of abdominal aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
209
Q

What are vasa recta?

A

Straight arteries, * seen in juxtamedullary nephrons of kidney, run from arcade of arteries see in mesentery of small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
210
Q

What does the ileocolic artery bifurcate into close to ileocaecal junction?

A

Ileal and cecal branches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
211
Q

What does descending branch of R colic artery anastomose with?

A

Cecal branch of ileocolic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
212
Q

Where does middle colic artery arise from and ascend to?

A

Proximal part of SMA

Ascends into transverse mesocolon where it gives off R and L branches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
213
Q

Major blood supply of transverse colon?

A

Middle colic artery from SMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
214
Q

Anastomosis of ascending branch of R colic artery?

A

With R branch of middle colic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
215
Q

Anastomosis of L branch of middle colic artery?

A

with ascending branch of L colic artery from IMA-L3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
216
Q

Describe the marginal artery

A

A summation of the anastomoses of adjacent colic branches of SMA and IMA. Lies along inner perimeter of colon, extending from cecum to the sigmoid colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
217
Q

Describe relationship of SMA to pancreas

A

Originates posterior to neck of pancreas, then descends and passes anterior to uncinate process of pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
218
Q

Where does the inferior pancreaticodudenal artery originate and what does it supply?

A

SMA, supplies head of pancreas and duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
219
Q

In addition to its bacteriostatic and immune actions, how else does saliva defend GI tract against toxins?

A

It washes bacteria and toxins into stomach where acidic environment plays an important defensive role

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
220
Q

What is the 1st line of defence of the colon against its contents?

A

Colonic mucus layer
Colonic microflora drive maturation of colonic mucosa and mucus prod. Mucus barrier can act as an energy source or support medium for growth to intestinal microflora.
Barrier effectively separates microbes from epithelium of colonic wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
221
Q

Where are the main locations of portosystemic anastomoses?

A
  1. Between the oesophageal tributaries of the left gastric vein and the veins draining the rest of the oesophagus- SM oesophageal veins, draining into the azygos system.
  2. Between the superior rectal veins from the SMV and the middle & inferior rectal veins
    draining into the internal iliac vein.
  3. Between the portal tributaries of retro-peritoneal organs (such as ascending and descending colon, kidney, etc.) and the lumbar veins draining eventually into the inferior vena cava.
  4. Between the veins in and around the falciform ligament-hepatic portal veins, and the veins of the anterior abdominal wall- anterior abdominal veins, draining into the epigastric veins.
  5. Between the veins of the posterior abdominal wall and bare area of the liver
    draining into the inferior vena cava.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
222
Q

Which aminotransferase is specific to the liver?

A

ALT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
223
Q

Treatment options for viral hepatitis?

A

Alpha interferon- inhibits viral replication

Antivirals to reduce viral load, e.g. ribavirin and lamivudine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
224
Q

Why might post-hepatic jaundice be associated with slow blood clotting?

A

Obstruction in biliary tree means bile salts don’t enter the bowel where required for absorpion of fats, so fats, and subsequently fat soluble vits not abdorbed. Vit K=fat soluble, so Vit K deficiency, and Vit K essential for synthesis of clotting factors II, VII, IX and X.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
225
Q

Describe symptoms of hepatic encephalopathy that may occur in liver failure, and can be potentiated by hypokalemia

A

Disturbances in consciousness- confusion to coma or death
Asterixis- flapping tremor of outstretched hands
Fluctuating neurological signs- muscualar rigidity and hyperreflexia
Intellectual deterioration- constructional apraxia and slow, slurred speech

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
226
Q

Treatment of hepatic encephalopathy?

A

Reduce protein intake to reduce uraemia and endogenous protein b.down, treat any infection, empty bowel of N-containing material and correct metabolic and coagulation disturbances.
Flumazenil- benzodiazepine receptor antagonsit, can improve condition in ST.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
227
Q

What is hepatic encephalopathy precipitated by?

A
Sepsis/infection
Diuretics e.g. loops and thiazides
GI bleeding
Alcohol withdrawal
Constipation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
228
Q

Features of fulminant hepatic failure

A
Jaundice
Encephalopathy
Reduced level of consciousness
Hypoglycaemia-renal failure
Decrease K+/Ca2+
Haemorrhage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
229
Q

Which metastasis makes up 50% of secondary liver metastases?

A

Colorectal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
230
Q

What are majority of liver metastases due to?

A

Portal venous drainage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
231
Q

What does upper 2/3 of stomach secrete?

A

Pepsin and HCL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
232
Q

What does lower 1/3 of stomach secrete?

A

Mucus and gastrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
233
Q

Relations of the inguinal canal?

A

Anteriorly: external oblique aponeurosis and internal oblique muscle fibres reinforce lateral 1/3
Posteriorly: transversalis fascia laterally, conjoint tendon medially
Roof: fibres of transversalis fascia laterally, internal oblique and transversus abdominis centrally, medially by medial crus of external oblique aponeurosis
Floor: laterally by iliopubic tract, inguinal ligament infolded to form a gutter centrally and lacunar ligament medially

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
234
Q

Where is C reactive protein produced?

A

Liver- hepatocytes produce this inflammatory marker in response to factors secreted by macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
235
Q

L gastric vein blood diverted to oesophageal mucosal veins when portal hypertension. Where does blood in this vein normally come from and how does it drain into the liver?

A

L gastric vein drains blood from oesophagus via and oesophageal vein: along with the R gastic vein, they enter the portal vein, which takes blood the the liver for detoxification before it enters the systemic circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
236
Q

Where is the portal vein formed?

A

Posterior to neck of pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
237
Q

What name is given to the smooth surface of the liver?

A

Diaphragmatic surface, separated from visceral surface by sharp inferior border

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
238
Q

How are the L and R functional parts of the liver demarcated?

A

By a line extending along the fossa for the IVC and the gallbladder on the visceral surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
239
Q

How are shallow depressions created on visceral liver surface?

A

By organs related to the liver e.g. stomach, oesophagus, R kidney and adrenal gland, duodenum and colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
240
Q

What name is given to the procedure of endoscopy used to look at the upper GI tract?

A

Oesophagogastricduodenoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
241
Q

Name the 2 flexures of the colon, located between the ascending and transverse parts, and the transverse and descending parts

A

Hepatic and splenic flexures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
242
Q

What are intestinal crypts?

A

Glands lining intestinal epithelia, situated at base of villi. Secrete various enzymes and site of enterocyte multiplication. Enterocytes then migrate along villi, maturing as they go and gaining the capacity to absorb. They are then shed from the tips of the villi, so mucosa is continually renewed by the process of enterocyte multiplication in the crypts and subsequent ascent of the villi.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
243
Q

What is the ‘unstirred layer’?

A

A layer of mucus and water adjacent to the intestinal wall. Here, enzymes secreted by the enterocytes are trapped and can act on nutrients in the small intestinal lumen as their diffusion is slowed, and so they can be further broken down, completing digestion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
244
Q

Hoe are the alpha 1,6 glycosidic linkages in amylopectin broken down?

A

By isomaltase present in the unstirred layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
245
Q

Why do oral rehydration therapies contain glucose and salt?

A

In diseased states if you just put water into the gut, it would simply pass through without being absorbed as an osmotic gradient generated by altering osmolarity is necessary as we can’t actively move H20.
If you put water and salt into a solution and ingested this, there would be very limited absorption of Na into the enterocyte and hence very little movement of water across the cell membrane of the enterocyte.
If you add glucose to the solution, even in a disase state, the gut will absorb this.
Net movement of both Glucose and Na into the enterocyte as use of SGLUT1 cotransporter. The movement of Na sets up the movement of water and so water moves into the enterocyte.
So will be greater absorption of water.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
246
Q

Describe how chymotrypsinogen released by pancreatic acinar cells is activated to produce chymotrypsin

A

Trypsinogen released from pancreatic acinar cells is converted to its active form trypsin by enterokinase. Trypsin then activates chymotrypsinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
247
Q

What is ‘mass movement’

A

Peristaltic movements once or twice a day in transverse and descending colon which rapidly move faeces into the rectum. Resulting stretch of rectum causes urge to defecate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
248
Q

What is the gastrocolic reflex?

A

Urge to defecate produced on stomach distension after eating a meal, as stretching of stomach initiates peristalsis, which involves mass movement, so rapid faeces movement into rectum, stimulating defecation urge.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
249
Q

What is classical pernicious anaemia?

A

Vitamin B12 deficiency resulting specifically from a lack of intrinsic factor production by parietal cells of stomach, hence inability to absorb Vit B12 from terminal ileum. Vit B12 necessary for erythropoiesis and so in its absence, erythropoiesis is ineffective as dysfunctional thymidine synthase, causing a megaloblastic anameia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
250
Q

Cause of pernicious anaemia?

A

AI atrophic gastritis, causing destruction of parietal cells, hence reduction in intrinsic factor prod.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
251
Q

What term is given when ulcerative colitis affects the terminal ileum due to a defective ileo-caecal valve?

A

Backwash ileitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
252
Q

Potential cure for ulcerative colitis?

A

Total colectomy
Would result in a stoma (Terminal ileum brought to the surface of abdominal wall, on the right side). Options include an ileoanal or ileorectal anastomosis with an Ileal reservoir. This avoids the need for a permanent stoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
253
Q

Other than an oesophageal cancer, what causes of dysphagia make swallowing solids harder than swallowing liquids?

A

External compression of oesophagus e.g. hiatal hernia, aortic aneurysm
Fibrous stricture
Anything causing a physical obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
254
Q

Is the peritoneal cavity an enclosed space?

A

Yes in males, but no in females- open to external environment via the infundibulum of the fallopian tubes

255
Q

where is the most likely region in the stomach for an ulcer to develop?

A

Lesser curvature

256
Q

Describe the gram staining process which would differentiate between gram +ve staph aureus and gram -ve pseudomonaa aeruginosa

A

+vly charged crystal violet binds to -vly charged cell components. Iodine added which binds to the complex formed. Acetone or methanol is used to extract the complexes through the gram -ve cell walls, but is unable to do so for the gram +ves due to thick peptidoglycan cell wall, so gram +ves stain blue/purple, and a red dye is then used to stain the now unstained gram-ve bacteria, so these stain red.

257
Q

Examples of obligate aerobes

A

Mycobacterium TB

Pseudomonas aeruginosa

258
Q

Examples of obligate anerobes

A

C.difficile

Bacteroides fragilis

259
Q

Clostridia bacteria are unable to live in an environement with O2. However, what aids their survival?

A

Spore-forming

260
Q

Where are the anaerobic zones in the GI tract?

A

Parts of mouth- on the tongue deep in taste buds, fluid films including biofilms between teeth, gingival crevice areas and in people with peridontal disease they live in peridontal pockets
Small bowel
Colon

261
Q

Give 5 beneficial reasons for human colonic bacteria

A

Synthesise and excrete Vits that are absorbed by host. Vit K- necessary for blood clotting, Vit B12- necessary for erythropoiesis- thymidylate synthase activity?, thiamine and many other B-Vits
Prevent colonisation by pathogens
Kill non-indigenous bacteria
Stimulates production of natural antibodies
Stimulate devlopment of MALT- in caecum and Peyer’s patches- terminal ileum in case of defective ileo-caecal valve- can result in backwash ileitis in ulcerative colitis

262
Q

Aerobic gram +ve cocci?

A

Staphylococcus
Streptococcus
Enterococcus

263
Q

Aerobic gram -ve cocci?

A

Neisseria meingitidis and gonorrhoeae

264
Q

Aerobic gram +ve bacilli?

A

Lactobacillus
Bacillus anthrax
Corynebacterium (diptheria)

265
Q

Anaerobic gram +ve bacilli?

A

Clostridium

266
Q

Aerobic gram -ve enteric (bacteria of intestines) bacilli?

A
E coli
Proteus mirabilis
Pseudomonas
Klebsiella
Salmonella
Shigells
Vibrio cholerae
Campylobacter
H pylori
267
Q

Anaerobic gram -ve enteric bacill?

A

Bacteroides fragilis

268
Q

Aerobic gram -ve bacilli non-enteric?

A

H.influenzae
Bordatella pertussis- whooping cough
Brucella

269
Q

Where does helicobacter pylori colonise?

A

The mucous layer of the pyloric antrum in the stomach, and in areas of duodenum where gastric metaplasia

270
Q

How does H pylori cause peptic ulcers to form?

A

Release of enzymes and induction of apoptosis through binding to MHC class II molecules. Urease prod. allows NH3 and Cl- production, which are directly cytotoxic. Expression of CagA- cytotoxic assoc. protein and VacA-vacuolating toxin, genes assoc. with greater induction of IL-8- potent mediator of gastric inflammation

271
Q

Describe Ludwig’s angina

A

Cellulitis (infection of deeper skin layers) of neck as streptococcal bacteria causing a sore throat e.g. strep. pyogenes, spread in the body. Huge inflammation of neck, with vast oedema, can result in airway obstruction so patient may have their neck stretched back in order to keep the airway open.

272
Q

Where would you swab for MRSA?

A

Nose, throat and perineum

273
Q

Describe the difference between bacteraemia and septicaemia

A

Bacteraemia: bacteria only transiently present in the bloodstream, asymptomatic, rapidly cleared by liver/spleen macrophages
Septicaemia: bacteria not cleared and multiply in the bloodstream, sepsis symptoms develop.

274
Q

Why are antibitoics not commonly prescribed for tonsillitis?

A

As 70% are viral e.g. rhinovirus, adenovirus and epstein-barr virus

275
Q

What microbe most commonly causes appendicitis when stasis in the appendix?

A

Bacteroides fragilis

276
Q

What prophylaxis can be given in gut surgery to reduce surgical wound infections?

A

Metronidazole- kills anaerobes e.g. bacteroides fragilis, and a broad-spectrum e.g. gentamicin or a cephalosporin.
Alternative- co-amoxiclav

277
Q

How does lactobacillus prevent candida albicans from growing in the vagina?

A

Converts glycogen to lactic acid, creating an acidic environment. Lactobacillus acidophilus- gram +ve bacillus.

278
Q

What produces the peritoneal fluid that lines the peritoneal cavity?

A

The parietal peritoneum

279
Q

Complications of acute pancreatitis?

A
  • abscess or pseudocyst formation- collection of fluid in lesser sac
  • renal failure due to shock- reduced renal perfusion
  • DIC
  • relapses and DM if severe and necrosis ensues
280
Q

Symptoms of acute pancreatitis?

A

Sudden onset of severe abdominal or epigastric pain, which may radiate to the back, along with nausea and vomiting

281
Q

Why might morphine not be used for pain relief in acute pancreatitis?

A

may cause spasm of the Sphincter of Oddi, which can worsen the pain

282
Q

What type on incision can be made at McBurney’s point?

A

a gridiron incision

283
Q

What region of parietal peritoneum is an exception to the rule that pain from the parietal peritoneum is generally well localised?

A

Inferior surface of central part of diaphragm, where innervation provided by the phrenic nerves (C3,C4,C5), irritation here is often referred to the C3-C5 dermatomes over shoulder.
Pain generally well localised as somatic NS innervation, same as supply to region of wall it lines

284
Q

Why might someone with a prosthetic heart valve receive prophylactic antibiotics before dental surgery?

A

To reduce risk of infective endocarditis. Lots of bacteria in mouth, and in dental surgery, may cause bleeding, so bacteria can enter blood- bacteraemia, and then may undergo haematogenous spread and can colonise heart valves. Prosthetic heart valves are colonised more easily as bacteria can more readily adhere, so there is an increased risk of an infection of the endocardial heart surface- infective endocarditis. Prophylactic antibiotics reduce the duration of the bacteraemia, hence reduce the likelihood of valve colonisation.

285
Q

How might you assess dehydration of a patient?

A

Common simple ones include the assessment of mucous membranes, skin turgor and whether or not the person has sunken eyes. Signs of shock in severely dehydrated patients will include tachycardia and tachypnoea. May mention that they have not passed much urine.

286
Q

Describe the mechanism by which enterotoxigenic E coli produces diarrhoea

A

ETEC bacteria colonize the mucosal surface of the small intestine. The bacteria use pili to bind enterocyte cells in the small intestine. Adhesion to the mucosal epithelial cells allows for transfer of enterotoxins produced by ETEC bacteria which stimulate the release of liquid from the cells lining the intestinal walls. ETEC make two toxins, heat-labile (LT) and heat-stable (ST), that cause intestinal epithelial cells to secrete excess fluid. Some strains produce only one of the toxins while others produce both.
ETEC infection results in the production of abundant watery diarrhea and abdominal cramping. Other symptoms such as fever, vomiting, chills, headache, muscle aches, and bloating can also occur but are less common. Illness usually lasts 3-4 days following exposure to the bacteria but can persist for up to 3 weeks. Supportive measures including rehydration tend to be sufficient for recovery, and hospitalization or antibiotics are usually not required.

287
Q

Define metaplasia

A

The change from one differentiated cell type to a different differentiated cell type, and is a reversible process

288
Q

What is coeliac disease?

A

An abnormal reaction to gluten which damages surface enterocytes of SI

289
Q

What is rebound tenderness a sign of?

A

Peritoneal irritation

290
Q

3 risk factors for pancreatic cancer?

A

Smoking
Chronic pancreatitis
Diabetes of at least 5 yrs duration

291
Q

What technique is good for screening intra or extra hepatic bile duct dilation?

A

Transcutaneous ultrasound scan

292
Q

Potential side effects of ERCP (endoscopic retrograde cholangipancreatography)

A

Biliary tree perforation, cholangitis, pancreatitis, haemorrhage

293
Q

3 reasons why pancreatic cancer has poor prognosis?

A

Vague and late presentation
Local spread can involve many structures
Resection complicated and largely unsuccessful in terms of being curative

294
Q

Tumour markers in pancreatic carcinoma?

A

Carcino-embryonic antigen- not specific

Ca19-9

295
Q

What vessel does the azygos vein drain into?

A

SVC

296
Q

What marks the boundary between the abdominal and pelvic cavities?

A

The pelvic brim
* ureters cross pelvic brim at birfurcation of common iliac artery and this is a point of ureteric constriction where renal stones may lodge.

297
Q

In addition to most of the duodenum and the pancreas, what other GI structures are secondarily retroperitoneal?

A

Ascending and descending colon

298
Q

Functions of the greater omentum?

A

Prevents visceral peritoneum from adhering to parietal peritoneum
Considerable mobility and can form adhesions adjacent to inflamed organs e.g. appendix, to localise infection, preventing spread and so protecting other viscera.
So may enter abdominal cavity and find greater omentum isn’t in it’s normal position
Cushions abdominal organs against injury and forms insulation against loss of body heat

299
Q

Clinical importance of paracolic gutters (part of infracolic compartment below transverse mesocolon)?

A

Provide pathways for flow of ascitic fluid and spread of intraperitoneal infections e.g. purulent material can pass down into pelvic cavity where slow absorption of toxins if patient made to sit upright. Infections in pelvis may extend superiorly to a subphrenic recess. Abscesses may form in peritonitis, and pus may then collect in subphrenic recesses.
Provide pathways for spread of cancer cells that have entered peritoneal cavity.

300
Q

Innervation of visceral peritoneum?

A

Visceral afferent nerves

301
Q

Parietal peritoneum innervation?

A

Somatic NS

302
Q

How do abdominal viscera become intraperitoneal?

A

They completely protruded into the peritoneal sac during development, and so are almost completely invested by visceral peritoneum. These organs are connected to the abdominal wall by a mesentery.

303
Q

How does the oesophagus terminate?

A

By entering the stomach at the cardial orifice of the stomach, to L of midline, at level of 7th left costal cartilage and T11 vertebra.

304
Q

What are the submandibular and sublingual glands innervated by (parasympathetic)?

A

Facial nerve (submandibular ganglion)

305
Q

Parasympathetic Innervation of parotid glands?

A

Glosspharyngeal nerve

306
Q

What might leukonychia be a sign of?

A

hypoalbuminaemia in liver disease

307
Q

Importance of anterolateral abdom. wall muscles?

A

Coughing, micturition, defecation, posture, lifting, parturition, flexing, twisting and lateral flexion of trunk

308
Q

Why is a direct inguinal hernia usually seen as only a bulge in inguinal region?

A

strong conjoint tendon covers post. wall where hernia passes into ingunal canal

309
Q

What is a sliding hiatus hernia?

A

Gastrooesophageal junction may slide through diaphragm into chest, where oesophagus passes through diaphragm at level of T10

310
Q

What is a rolling hiatus hernia?

A

Fundus of stomach may pass into chest alongside oesphagus

311
Q

Which hormone stimulates transaminase synthesis by liver?

A

cortisol

312
Q

The ovaries are a recognised site of metastasis of gastic cancer. What name is given to the tumour when it affects the ovaries?

A

Krukenberg tumour

313
Q

What is a carcinoid tumour?

A

Slow growing neuroendocrine tumour of gut which can produce 5-HT

314
Q

What are the 9 abdominal wall surface regions and what are they demarcated by?

A

R and L hypochondriac regions, epigastric, unbilical, pubic/hypogastric, R and L flanks, R and L inguinal

2 sagittal planes: midclavicular planes passing from mpoint of clavicles to midingunal points
2 transverse planes: subcostal- passes through inf. border of 10th costal cartilage on each side, transtubercular- passes through iliac tubercles and body of L5 vertebra

315
Q

How is anterolateral abdom. wall bounded?

A

Superiorly by cartilages of 7th to 10th ribs and xiphoid process, and infer. by inguinal ligament, and superior margins of anterolateral aspects of pelvic girdle- iliac and pubic crests, and pubic symphysis.

316
Q

2 core functions of stomach?

A

store food as we ingest food much more quickly than we can digest it
disinfects food- production of acid by parietal cells

317
Q

how does acid produced by parietal cells of stomach affect pro-enzymes?

A

it activates them

318
Q

what substances secreted by stomach prevent ulceration?

A

HCO3-

mucus

319
Q

describe effect of food entering stomach on gastrin production during gastric phase

A

food buffers acid so disinhibits gastrin secretion which was inhibited by somatostatin released from D cells of endocrine pancreas
dietary peptides in lumen stimulate G cells
stomach distension stimulatates ACh release from vagal pre-ganglionic nerve fibres, which stimulates gastrin releasing hormone, which stimulates G cells.

320
Q

how is gastrin production inhibited in intestinal phase of gastric control?

A

acid accumulates in empty stomach and is unbuffered as no food, so stimulates D cells to produce somatostatin, which inhibits gastrin prod. by G cells

321
Q

what slows rate of gastric emptying if detected in duodenum?

A

FA, low pH, hypertonicity

322
Q

2 significant consequences of abdom. stab wound?

A

shock

peritonitis

323
Q

potential clinical consequences of incarcerated hernia?

A

strangulation, causing tissue death
bowel obstruction if bowel herniated, can lead to vomiting, colicky abdominal pain, electrolyte imbalance problems, bowel perforation.

324
Q

blood supply to oesophagus?

A

cervical part- inferior thyroid artery
thoracic- oesophageal branches of aorta
abdominal- oesophageal branches of L gastric artery

325
Q

borders of epiploic foramen?

A

A: hepatoduodenal ligament
P :IVC and R crus of diaphragm
S: liver, covered with visceral periotneum
I: superior duodenum

326
Q

why are internal haemorrhoids painless and external haemorrhoids painful?

A

external occur below pectinate line where innervation via pudendal nerve (S2-S4)= somatic nerve, but innervation above line where internal haemorrhoids= autonomic

327
Q

3 mechanisms of GI control?

A

neural
paracrine
endocrine

328
Q

what are the 2 plexuses of the enteric NS?

A

Myenteric plexus: lies between circular and longitudinal muscle layers and mainly regulates intestinal motility and sphincter function.
Submucosal plexus: mainly responds to and regulates epithelial cell and SM blood vessel function.
Nerves respond to stimuli from enteric nerves, ANS nerves and from epithelial cells e.g. entero-endocrine cells
enteric NS also receives innervation from S and P divisions of ANS
nerve plexuses may act independently of CNS- short reflex pathway, but activity may be altered by both branches of ANS- long reflex pathway

329
Q

how does somatic NS contribute to GI tract?

A

ingestion and excretion: lips, tongue, muscles of mastication- masseter muscle- trigeminal nerve (5th cranial), external anal sphincter- skeletal muscle- voluntary

330
Q

describe sympathetic control of GI tract

A

thoracolumbar origin, those from cervical chain and travelling in spanchnic nerves via coeliac and other ganglia innervate entire GI system. NA- alpha 2- reduced gut motility, sphincter contraction and inhibited secretion.

331
Q

describe parasympathetic control of GI tract

A

most important, craniosacral origin. Glossopharyngeal (synapses in otic ganglion, saliva secretion from parotid gland) and vagus cranial nerves. Submandibular and sublingual glands- facial cranial nerve- submandibular ganglion. Sacral part provides innervation distally beyond hepatic flexure of colon.
ACh- M3- stimulates gut secretion, increase gut motility and relax sphincters

332
Q

Neurotransmitters of enteric nerves?

A

ACh, NO, peptides
enteric NS results in peristalsis- intrinsic NM reflex, and secretion and regulation of blood flow when intermittent feeding

333
Q

why is it important to know distance from incisor teeth to oesophago-gastric junction?

A

to know how far you can advance a naso-gastric tube before it enters the stomach
38-40cm

334
Q

why does achalasia cause dyphagia?

A

problem with inhibitory neurones of lower oesophageal sphincter, so sphincter fails to relax, food can’t enter stomach, enteric NS problem

335
Q

problem with sigmoid colon being mobile?

A

volvulus- can twist on its mesentery to cause obstruction and potential necrosis if it cuts off its blood supply

336
Q

why do some structures in the GI tract e.g. oesophagus, have adventitia in their walls, whereas other structures e.g. stomach, have serosa?

A

dependent on if intra-periotneal- structure invaginated into peritoneal cavity during development, or retroperiotneal- have parietal peritoneum on anterior surface only. intraperitoneal- have serosa- mesothelium and subtending CT, retroperiotneal- adventitia- just CT, no epithelium

337
Q

What demarcates the thoracic cavity from the abdominal cavity?

A

costal margin, separated from each other by diaphragm

338
Q

What demarcates the abdominal cavity from the pelvic cavity?

A

pelvic brim

339
Q

what must our bolus of food become in order for absorption to take place in SI?

A

isotonic, neutral and sterile

340
Q

clinical consequences of free gastrooesophageal reflux?

A

reflux oesophagitis
oesophageal strictures
Barrett’s oesophagus
Oesophageal adenocarcinoma

341
Q

where might a tumour be located to cause symtoms of dysphagia?

A

oesophagus, oropharynx and cardia of stomach

342
Q

how can we evaluate the phases of swallowing e.g. if looking for an oropharyngeal (difficulty with fluids) caused of dysphagia?

A

video fluroscopy

343
Q

causes of odynophagia?

A

oesophageal candidiasis, cancer of orophrarynx or oesophagus, oesophagitis due to reflux

344
Q

despite sympathetic, as well as parasympathetic innervation to salivary glands resulting in secretion of saliva, why do we get a dry mouth when we are anxious?

A

as sympathetic stimulation slows blood flow through the salivary glands, blood vessels shut down

345
Q

what is bulbar palsy?

A

medulla problems, so lower CNS, can cause dysphagia

346
Q

what is pseudo bulbar palsy?

A

bilateral lesions of connections between cerebral cortex and medulla, can cause dysphagia

347
Q

blood supply of duodenum?

A

proximally- from celiac trunk- foregut, gastroduodenal and superior pancreaticoduodenal arteries
distally- midgut, inferior pancreaticoduodenal artery from SMA

348
Q

blood supply of pancreas?

A

head- superior (celiac trunk) and inferior (SMA) pancreaticoduodenal arteries

349
Q

what does the splanchnic (visceral) mesoderm (from LP mesoderm) give rise to?

A

smooth gut musculature

visceral peritoneum

350
Q

what is the dorsal mesentery formed from?

A

condensation of splanchnic (visceral) mesoderm

351
Q

what does the free margin of the falciform ligament contain in the adult?

A

the ligamentum teres hepatis

352
Q

what does invagination into the peritoneal cavity result in?

A

intra-peritoneal structures- enveloped in visceral peritoneum

353
Q

what are the lungs derived from?

A

endoderm- as bud off from the foregut

354
Q

what structures are formed within the ventral mesentery?

A

liver, biliary tree, uncinate process and inferior head of pancreas
rest of pancreas formed in dorsal mesentery

355
Q

describe how the fascial and muscular layers of the abdominal wall are formed in embryological devlopment

A

lateral folding of embryo, results in the 2 sides of the develoing anterolateral abdominal wall meeting in the midline, forming the linea alba. An opening is left at the ubiliicus where the connecting stalk connects the foetus to the placenta. Each wall side is formed from 3 muscle layers. Muscles and fascia develop from somatic (parietal) mesoderm

356
Q

what does the inguinal canal allow for during devlopment in males?

A

the passage of the developing testis into the scrotum in males.

357
Q

describe a congenital inguinal hernia

A

this is an indirect inguinal hernia that occurs due to failure of the processus vaginalis to close- within scrotal sac in males, intestinal loops can descend down into the scrotum

358
Q

what is the processus vaginalis

A

embryonic outpouching of peritoneum

359
Q

where does the fundus of the stomach lie in the supine postion?

A

lies posteriorly to 6th rib, in plane of the mid-clavicular line

360
Q

describe the cephalic phase of gastric secretion

A

stomach prepares for food entry with secretion of acid and mucus. stimulated by sight, smell and taste of food. Vagus nerve releases ACh- acid prod. directly, and indirectly via release of histamine and gastrin.

361
Q

what mediates the cephalic phase of gastric secretion entirely?

A

vagus nerve

362
Q

why are the reflexes in the gastric phase of gastrc secretion termed vago-vagal?

A

both afferent and efferent impulses are carried by neurones in vagus nerve

363
Q

describe the gastric phase of gastric secretion

A

food enters stomach- alkaline- buffers stomach acid, disinhibits gastrin. food broken down, proteins to peoptides by pepsin, then appear in lumen, stimualte gastrin release. distension of stomach causes ACh release, stimulates parietal cells directly, and indirectly via gastin and histamine release, histamine also stimulated by gastrin.

364
Q

longest phase of gastric secretion?

A

gastric

365
Q

phase where most acid secreted in gastric secretion?

A

gastric

366
Q

how does mucus secreted by gastric pit neck cells protect stomach mucosa from acid which would otherwise dissolve mucosa?

A

mucus-sticky- adheres to stomach lining, and basic- mucins- heavily glycosyalted proteins- basic amine groups- can bing H+- neutralise acid.

367
Q

how does alcohol damage the stomach mucosa?

A

it dissolves the mucus and hence protection against stomach acid, so mucosa exposed to acid, resutling in gastritis and this leads to vomiting

368
Q

how can aspirin kill cells of stomach?

A

aspirin converted into a non-ionised form by stomach acid, can then pass into cells where neutral, and is re-ionised, producing acid in the cells, which kills them

369
Q

in between meals, what is the muscle doing in the upper part of the stomach?

A

it is strongly contracted

370
Q

what is receptive relaxation of the stomach mediated by and coordinated by?

A

NO and VIP

coordinated by vagus nerve (10th cranial nerve)

371
Q

benefit of stomach relaxing when filling?

A

prevents pressure increase that would lead to oesophageal reflux

372
Q

describe the process of gastric emptying

A

APs generated by pacemaker cells in cardia of stomach, result in peristaltic wave propelled from cardia to pylorus via circular and longitudinal muscle cell contraction. Wave propels food ahead of it until reaches narrower pyloric part where food slowed down, and chyme can move faster. APs sent to a smaller muscle mass, so peristaltic wave is sped up and overtakes the slower food bolus, sending food back into the body of the stomach for further mixing and breakdown. Chyme ahead of wave- squirted into duodenum, until wave rapidly progresses to pylorus and shuts the pylorus off, so remaining chyme returns to stomach.

373
Q

describe control of gastric emptying

A

Three peristaltic waves- three ejected squirts of chyme a minute.
Squirt volume affected by the rate of acceleration of peristaltic wave and hormones from the intestine.
Gastric Emptying is slowed by fat, low pH and hypertonicity in the duodenum.

374
Q

what structure anatomically marks the boundary between the foregut and the midgut?

A

the ampulla of Vater

375
Q

problem with malrotation in physiological herniation if there is 1 clockwise rotation only?

A

cranial structures placed anteriorly to caudal structures, so increased motility, susceptible to voluvus

376
Q

complications of chronic peptic ulcer disease?

A

perforation, leading to peritonitis e.g. if anterior dudodenal ulcer
haemorrhage e.g. perforation into blood vessel, causing haematemesis and malaena
penetration- can get into pancreas and liver
stricture- causing pyloric stenosis or oesophageal stricture
malignant change

377
Q

how does gastric outlet obstruction normally present? How is it caused?

A

vomiting without pain

can occur with peptic ulcers, either due to inflammation with oedema, or healing with fibrosis

378
Q

Neuropeptide Y is released from primary neurones and acts on secondary nerurone within arcuate nucleus of hypothalamus to stimulate appetite. what effect does neuropeptide Y have on intestinal secretions?

A

it is released by sympathetic nerve terminals and decreases intestinal secretions

379
Q

where is CCK released from?

A

I cells throughout small intestine

380
Q

where are intersitial cells of Cajal found and what tumour can be derived from them?

A

pacemakers located in body of stomach

GI stromal tumour- soft tissue sarcoma

381
Q

how does somatostatin affect gastric acid production?

A

it inhibits acid production by parietal cells

382
Q

how is the duodenum protected against ulcer formatino?

A

by S cells which release secretin when acid detected, and secretin stimulates alkaline juice release from ductal cells of the pancreas, which neutralises the acidic chyme

383
Q

what nerve innervates the external anal sphincter?

A

pudendal nerve (S2-S4)

384
Q

what 2 attachments does the duodenum exhibit?

A

the lesser omentum- derived from ventral mesentery and attaches from lesser curvature of stomach to liver and the duodenum.
the ligament of Treitz (suspensory ligament) * which supports the duodenum and is found at the duodenojejunal flexure- L1

385
Q

how are the blood vessels of the mesentery of the small intestine arranged?

A

in arcades

386
Q

why is the mucosa of the colon smoothe?

A

no villi

387
Q

which part of the greater omentum attaches the stomach to the transverse colon?

A

gastrocolic ligament

388
Q

where does the transverse colon end?

A

at the splenic (L colic) flexure

389
Q

where does the sigmoid colon end?

A

at the level of S3 where it merges with the rectum

390
Q

how is the internal anal sphincter formed?

A

by a continuation of the circular smooth muscle of the anal canal

391
Q

how is the lesser omentum formed?

A

by rotation of the stomach during the 4th wk of embryonic development: AP axis rotation results in ventral mesentery coming to lie along lesser curvature of the stomach

392
Q

describe formation of lesser sac

A

rotation of stomach: L axis rotation pulls the dorsal mesogastrium to the L, creating a space behind the stomach

393
Q

how does the greater omentum become attached to the transverse colon?

A

during development, the greater omentum grows downwards, and the greater omentum then comes together with the transverse mesocolon, the double layers are absorbed, leaving the greater omentum stuck to the transverse colon.

394
Q

where does the falciform ligament run down to?

and what does it separate?

A

the hepatic notch

the anatomical L and R lobes of the liver

395
Q

list the peritoneal attachments of the liver

A

the falciform ligament
the lesser omentum- hepatoduodenal and hepatogastric ligaments
the coronary ligament
the R and L triangular ligaments

396
Q

how is the bare area of the liver enclosed?

A

by divergence of the anterior and posterior layers of the coronary ligament- a peritoneal reflection, towards the left.

397
Q

which surface of the liver is the bare area part of?

A

the diaphragmatic surface

398
Q

which areas of the visceral surface of the liver are absent of peritoneum?

A

porta hepatis and fossa for gallbladder

399
Q

how is the acidity of chyme corrected?

A

HCO3- from blood, secreted by liver, pancreas and duodenal mucosa

400
Q

high incidence where of oesophageal carcinoma?

A

china, parts of caspian sea

401
Q

age group where oseophageal carcinoma most prevalent?

A

60-70yrs

402
Q

clinical features of oesophageal carcinoma?

A

dysphagia- progressive and persistent-solids to liquids
weight loss- cancer and dysphagia
anorexia
lympadenopathy
retrosternal chest pain
hoarseness and cough if upper 1/3 but less likely

403
Q

what can be used to try and prevent the progression of Barrett’s to adenocarcinoma?

A

aspirin

404
Q

where is gastric cancer more common?

A

finland, colombia and japan

405
Q

which blood group is gastric cancer commoner in?

A

blood group A- genetic predispos. to GC?

406
Q

what is linitis plastica?

A

macroscopic appearance of gastric cancer where uniform thickening of stomach wall

407
Q

2 microscopic appearances of gastric cancer?

A

intestinal- tubules

diffuse- signet ring cells- mucus in cell pushes nucleus to 1 side

408
Q

clinical presentation of gastric cancer?

A

late presentation, non-specific- epigastric pain, vomiting and nausea espec. if pyloric- obstrucution, weight loss, palapable epigastric mass
anaemia- Fe deficinet from bleeding- haematemesis

signs of metastases: ascites, hepatomegaly, jaundince, large virchow’s node

409
Q

when can herceptin be used in gastric cancer?

A

if HER2 gene amplification- proto-oncogene

410
Q

what is gardner’s syndrome?

A

similar to FAP as APC gene mutated- TSG, but also other mutations, resulting in bone and soft tissue tumours

411
Q

how is HNPCC caused?

A

mutation in DNA mismatch repair gene

412
Q

when might an apple core stricture be seen on barium enema?

A

colorectal adenocarcinoma

413
Q

what can TNM staging tell you about colorectal adenocarcinoma which Duke’s staging can’t?

A

if peritoneum involvement- T4- increases risk of metastasis

414
Q

why can a carcinoid tumour cause diarrhoea?

A

as local stimulation of contractility of intestine by 5-HT

415
Q

what is Trosseau’s sign?

A

thrombophlebitis- dark red patch on skin indicative of internal malignancy e.g. pancreatic carcinoma

416
Q

Key presentation of pancreatic carcinom?

A

painless, obstructive jaundice

417
Q

how can we diagnose pancreatic mass?

A

ultrasound or CT

418
Q

what are 80% of pancreatic carcinomas?

A

ducatal adenocarcinomas- well-fromed glands with or without mucin

419
Q

acinar pancreatic tumour?

A

rarer, cells contain zymogen granules

420
Q

most common malignant neoplasm of stomach?

A

gastric adenocarcinoma

421
Q

what is meant by ‘early’ in context of gastric adenocarcinoma?

A

confined to mucosa or SM, not spread through muscularis propria

422
Q

how is FAP likely to be identified?

A

following screening of an affected individual’s family

423
Q

how does FAP arise?

A

autosomal dominant inheritence pattern- APC gene mutation on chromosome 5

424
Q

prophylaxis for colorectal cancer when FAP?

A

colectomy in 20s

425
Q

what types of adenoma are recognised?

A

tubular

villous tubulovillus

426
Q

what histological features of an adenocarcinoma might influence prognosis?

A

degree of differentiation-anaplastic?
edges
inflammatory infiltrate

427
Q

what types of tumour affect the SI?

A

lymphoid
carcinoid
carcinoma-rare
smooth muscle tumour

428
Q

symptoms of a carcinoid tumour

A

hot flushes
watery diarrhoea
bronchoconstriction

429
Q

5 most common cancers in males?

A
lung
prostate
colorectal 
bladder 
non-hodkins lymphoma
430
Q

5 most common cancers in females?

A
breast
lung
colorectal
uterus
ovarian
431
Q

describe the journey of TAGs from duodenum to AT

A

bile acids- TAGs- acted upon by lipases- FA and glycerol- enterocyte- reassoc TAGs- transported by chylomicrons- AT- liproprotein lipase- broken down, then reassoc in cell to be stored as TAGs in AT

432
Q

what family is CCK a member of?

A

gastrin family

433
Q

describe amino acid deamination by liver*

A

glutamate converted to glutamine by reaction with NH3. Glutamine tranported to liver where broken down via glutaminase to NH3 and glutamate. NH3 then forms urea via urea cycle in liver, urea- H20 soluble so can be excreted in urine by kidneys

434
Q

when might albumin be deficient in blood?

A

liver cirrhosis
nephrotic syndrome
kwashiorkor

435
Q

functional unit of the liver?

A

hepatic acinus

436
Q

define a hepatic lobule

A

area of liver based on organisation of hepatocytes around liver vascular elements. central vein at central axis with portal triads at its periphery

437
Q

Other than statins and lifestyle modification, how else can high cholesterol be treated?

A

bile acid sequestrants- bindd bile salts so preventing their reabsorption for use in lipid emulsification and transport

438
Q

why are bile acids conjugated to aa?

A

to make them water soluble for movements and travel as micelles

439
Q

what happens when gallstones get to a certain size?

A

new bile entering GB doesn’t dissolve them so they stay there

440
Q

what is bile acid secretion inhibited by?

A

somatostatin and NA

441
Q

characterisitcs of steatorrhoea?

A

undigested fat in faeces- pale, floating as less dense than water, and foul-smelling due to action of gut bacteria
occurs if bile acids or pancreatic enzymes not secreted in adequate amounts

442
Q

venous drainage of neck and cystic duct of gallbladder

A

cystic veins into hepatic PV or liver directly

443
Q

venous drainage of fundus and body of gallbladder

A

pass directly into visceral surface of the liver, into the hepatic sinusoids, drain into CV, hepatic veins, IVC

444
Q

describe the anatomical location of the pancreas

A

retroperitoneal, crosses L1 and L2 vertebra, on post. abdom wall, posterior to stomach, between duodenum on the right and spleen on the left, with transverse mesocolon attached to its anterior margin

445
Q

4 parts of the pancreas?

A

body
head
neck
tail

446
Q

describe the head of pancreas

A

The expanded part of the gland, embraced by the C-shaped curve of the duodenum, to the right of the superior mesenteric vessels and just inferior to the transpyloric plane.

most common site of panceas for carcinoma- non-specific present.-weigh loss, pain, obstructive jaundice

447
Q

describe the neck of the pancreas

A

Short, and overlies the superior mesenteric vessels, which form a groove in it’s posterior surface.
The anterior surface of the neck is covered with peritoneum and adjacent to the pylorus of the stomach.
The SMV joins the splenic vein posterior to the neck to form the hepatic portal vein.

448
Q

describe the body of the pancreas

A

Continues from the neck and lies to the left of the superior mesenteric vessels, passing over the aorta and L2 vertebra, continuing just above the transpyloric plane posterior to the omental bursa.
The anterior surface is covered with peritoneum and forms part of the stomach bed.
The posterior surface is devoid of peritoneum and is in contact with the aorta, SMA, left suprarenal gland, left kidney and renal vessels.

449
Q

describe the tail of the pancreas

A

Lies anterior to the left kidney, where it is closely related to the splenic hilum and the left colic flexure. The tail is relatively mobile and passes between the layers of the splenorenal ligament with the splenic vessels.

450
Q

describe the main pancreatic duct

A

The main pancreatic duct begins at the tail of the pancreas and runs through the gland to the head. It then turns inferiorly, and is closely related to the bile duct. The two usually unite to form to short, dilated hepatopancreatic Ampulla of Vater, which opens into the descending part of the duodenum.

451
Q

describe the arterial supply of the pancreas

A

The arterial supply of the pancreas is derived mainly from the branches of the Splenic Artery. Multiple Pancreatic arteries from several arcades with pancreatic branches of the Gastroduodenal and Superior Mesenteric arteries.

Celiac trunk gives rise to splenic artery which supplies the body and tail of the pancreas

The Anterior and Posterior Superior Pancreaticoduodenal Arteries (branches of the Gastroduodenal Artery) and the Anterior and Posterior Inferior Pancreaticoduodenal Arteries (branches of the SMA) form anteriorly and posteriorly placed arches that supply the head.

452
Q

venous drainage of the pancreas?

A

pancreatic veins- tributaries of splenic and superior mesenteric parts of the hepatic portal vein, most empty into splenic

453
Q

describe the anatomical location of the spleen

A

The spleen is an ovoid, usually purplish, pulpy mass about the size and shape of a fist. It is relatively delicate and considered the most vulnerable abdominal organ.

The spleen is located in the left hypochondrium of the abdomen, resting on the left colic flexure. It is entirely covered by a layer of visceral peritoneum, except at the splenic hilum, where the splenic branches of the splenic artery and vein enter and leave.

454
Q

what are the relations of the spleen

A
The relations of the spleen are:
o	Anteriorly
o	The stomach
o	Attached by the Gastrosplenic Ligament- part of greater omentum
o	Posteriorly 
o	The left part of the diaphragm, which separates it from the pleura, lung and ribs 9-11
o	Inferiorly 
o	The left colic flexure
o	Medially 
o	The left kidney
o	Attached by the Splenorenal ligament
455
Q

arterial supply of spleen?

A

splenic artery from celiac trunk
between layers of splenorenal ligament, it divides into 5 or more branches entering hilum to supply different vascular segements of the spleen

456
Q

venous drainage of the spleen?

A

The venous drainage of the spleen flows via the Splenic Vein, formed by several tributaries that emerge from the hilum.

It is joined by the Superior Mesenteric Vein and runs posterior to the body and tail of the pancreas throughout most of its course.

SMV and SV unite posterior to neck of pancreas to form the hepatic PV

457
Q

patient receiving treatment after an MI (MONA), why might they be susceptible to gastric ulcer formation?

A

aspirin tmen=NSAID- inhibts COX1 necessary for PGE prod.- increases HCO3- and alkali, and mucosal blood flow, which protects mucosal environm of stomach from damaging effects of gastric acid

458
Q

what does lysozyme in saliva do?

A

breaks down peptidoglycan cell walls in gram +ve bacteria

459
Q

what breaks down cell walls of gram -ve bacteria, in saliva?

A

oxidases

460
Q

why is the SI normally sterile?

A

bile- detergent, proteolytic enzymes, anaerobic, rapid transit- peristalsis, nutrient lack, epithelial cell shredding

461
Q

what infections might a patient on proton pump inhibitors be susceptible to and why?

A

shigellosis, cholera, salmonella

as reduced gastric acid prod- necessary for sterilisation in stomach- kills bacteria

462
Q

why are eosinophils capable of killing worms?

A

granules contain perforins- punch holes in walls of worms

also peroxidase, major basic protein and cationic protein help with killing

463
Q

what colour do eosinophilic granules stain?

A

intense orange

464
Q

when does eosinophilia occur?

A

parasitic infections, asthma, hayfever

465
Q

where do the tonsils drain into?

A

cervical LNs

466
Q

differences in mobility between S and LIs?

A

jejunum and ileum= mobile= mesentery of SI, but duodenum= fixed=secondarily retroperitoneal apart from duodenal cap=intraperitoneal

ascending and descending colon= secondarily retroperiotneal= not mobile
transverse colon= transverse mesocolon= mobile, transverse colon usually hangs down to L3 vertebral level- level of umbilicus
sigmoid colon= sigmoid mesocolon= mobile
caecum= no mesentery but is mobile because it is almost entirely enveloped by peritneum, but commonly bound to lateral abdom. wall by cecal folds of peritoneum
appendix= mesoappendix, and appendix= blind intestinal diverticulum

467
Q

diameter of S and LIs?

A

smaller diameter of SI

468
Q

differences between longitudinal muscle of S and LIs?

A
small= continuous
large= longitudinal muscle of ME reduced to 3 narrowed, thickened, equally spaced bands= teniae coli
469
Q

distinctive small, fatty projections of serosa on outer surface if colon, not seen in SI?

A

omental appendices

470
Q

differences between mucosa of S and LIs?

A

SI= plicae circulares- transverse folds with core of SM
villi
microvilli

LI= smooth surface of mucosa as no villi or plicae circulares present. numerous straight tubular intestinal glands= crypts of Lieberkuhn

471
Q

4 key distinguishing features between SI and LI?

A

omental appendices
haustra- sacculations of wall of colon between teniae coli
teniae coli
diameter

472
Q

lymphoid tissue in S and LIs?

A
SI= peyer's patches in terminal ileum (GALT)
LI= appendix GALT
473
Q

Describe the 4 parts of the duodenum

A
  1. Superior part. Short, (5cm) and lies anterolateral to the body of the L1 vertebra
  2. Descending part. Longer (7-10cm) and descends along the right sides of L1-L3 vertebrae.
  3. Inferior part. 6-8cm long and crosses the L3 vertebra.
  4. Ascending part. Short (5cm) and begins at the left of L3 vertebra and rises superiorly as far as the superior border of the L2 vertebra.
474
Q

How can H pylori cause duodenal ulceration?

A

result of gastric metaplasia
H pylori colonises pyloric antrum, stimulating increased gastrin prod. hence acid production by parietal cells, causing duodenal cap damage and gastric metaplasia, so H pylori can now colonise duodenal cap, and response to this is duodenitis

475
Q

Describe the superior part of the duodenum

A

The superior part of the duodenum ascends from the pylorus and is overlapped by the liver and gallbladder. Peritoneum covers its anterior aspect, but it is bare of peritoneum posteriorly (except for the duodenal cap). The proximal part has the hepatoduodenal ligament (part of the lesser omentum) which conducts portal triad, attached superiorly, and the greater omentum attached inferiorly.

476
Q

Describe the descending part of the duodenum

A

The descending part of the duodenum runs inferiorly, curving around the head of the pancreas. The Bile and Main pancreatic ducts enter its posteromedial wall via the Ampulla of Vater. The descending part of the duodenum is entirely retroperitoneal. The anterior surface of its proximal and distal thirds is covered with peritoneum; however the peritoneum reflects in its middle third to form the double-layered mesentery of the transverse colon, the Transverse Mesocolon.

477
Q

Describe the inferior part of the duodenum

A

The inferior (horizontal) part of the duodenum runs transversely right to left, passing over the IVC, aorta and L3 vertebra. The Superior Mesenteric Artery and Vein and the root of the mesentery of the jejunum and ileum cross it. Where these structures cross is the only part of its anterior surface not covered with peritoneum. Posteriorly it is separated from the vertebral column by the right psoas major, IVC, aorta and the right testicular/ovarian vessels.

478
Q

Describe the ascending part of the duodenum

A

The ascending part of the duodenum runs superiorly and along the left side of the aorta to reach the inferior border of the body of the pancreas. Here it curves anterior to join the jejunum at the duodenojejunal flexure- L2, supported by the attachment of a suspensory muscle of the duodenum (Ligament of Treitz). Contraction of this muscle widens the flexure, facilitating movement.

479
Q

Describe the jejunum and the ileum

A

The jejunum is the second part of the small intestine, beginning at the duodenojejunal flexure where the digestive tract resumes an intraperitoneal course. The third part of the small intestine, the ileum, ends at the ileocaecal junction.

Together, the jejunum and ileum are 6-7 metres long, the jejunum constituting approximately two fifths and the ileum three fifths of the intraperitoneal section of the small intestine.

Most of the Jejunum lies in the left upper quadrant (LUQ) of the Infracolic compartment- part of greater sac below transverse mesocolon, whereas most of the ileum lies in the right lower quadrant (RLQ).
The terminal ileum usually lies in the pelvis, from which it ascends, ending in the medial aspect of the cecum.

The mesentery is a fan-shaped fold of peritoneum that attaches the jejunum and ileum to the posterior abdominal wall. Between its two layers are the superior mesenteric vessels, lymph nodes, a variable amount of fat and autonomic nerves.
The root of the mesentery crosses the ascending and inferior parts of the duodenum, abdominal aorta, IVC, right ureter, right psoas major, and right testicular/ovarian vessels.

480
Q

distinguishing features between jejunum and ileum in living body?

A

Colour: J=deeper red, I=paler pink
Caliber: J=2-4cm, I=2-3cm
Wall: J=thick and heavy, I= thin and light
Vascularity: J=greater, I=less
Vasa recta: J=long, I=short
Arcades: J= few large loops, I= many short loops
Fat in mesentery: J=less, I=more
Circular folds: J=large, tall, closely packed, I= low and sparse, absent in terminal ileum
Lymphoid nodules: J=few, I= many

481
Q

How does blood supply change between in duodenum from entry of common bile duct?

A

proximal- foregut- celiac trunk- superior pancreaticoduodenal artery

distal- midgut- SMA- inferior pancreaticoduodenal artery

both arteries lie in curve between duodenum and the head of the pancreas and supply both structures

482
Q

venous drainage of duodenum?

A

pancreaticoduodenal veins that follow the arteries and drain into the hepatic portal vein, some directly, others indirectly through SM and splenic veins

483
Q

arterial supply to jejunum and ileum?

A

jejunal and ileal arteries from SMA- midgut, from abdominal aorta at L1
SMA runs between layers of mesentery, and sends 15-18 branches to the jejunum and ileum.

These arteries unite to form loops or arches called arterial arcades, which gives rise to vasa recta.

484
Q

Where do the teniae coli begin?

A

appendix

485
Q

Where do the teniae coli merge together?

A

Merge together again at the rectosigmoid junction into a continuous layer around the rectum

486
Q

arterial supply of cecum and appendix?

A

cecum- ileocolic artery from SMA

appendix- appendicular artery from ileocolic artery

487
Q

venous drainage of cecum and appendix?

A

ileocolic vein- tributary of SMV

488
Q

arterial supply to ascending colon and R colic flexure?

A

ileocolic and R colic arteries

arteries anastmose with 1 another and with R branch of middle colic artery- from SMA

489
Q

venous drainage of ascending colon?

A

ileocolic and R colic veins- tributaries of SMV

490
Q

arterial supply of transverse colon?

A

mainly middle colic artery from SMA

blood may also come from R and L colic arteries via anastomoses, part of arcades forming the marginal artery

491
Q

venous drainage of transverse colon?

A

SMV

492
Q

arterial supply of descending and sigmoid colon?

A

L colic and sigmoid arteries- both from IMA

493
Q

venous drainage of descending and sigmoid colon?

A

IMV

494
Q

2 portal systems in body?

A

hepatic, and hypothalamo-hypophyseal

represent 2 capillary systems in series

495
Q

how are many toxins ejected from liver once detoxification occurred?

A

in bile

then ejected in faeces

496
Q

what are found in the sinusoid spaces?

A

hepatocytes, kupffer cells, endothelial cells, veins

497
Q

microscopic changes in Crohn’s disease?

A

transmural inflammation
non-caseating granulomas with Langhan’s giant cells
chronic inflammatory cells increased and lymphoid hyperplasia

498
Q

microscopic changes in ulcerative colitis?

A

Superficial inflammation
Chronic inflammatory cell infiltrate in the lamina propria
Crypt abscesses-neutrophils
Goblet cell depletion

499
Q

what can cause intestinal inflammation and infection?

A
Ulcerative Colitis
Crohn’s Disease
Diversion Colitis
Diverticular colitis
Radiation, Drug, Infectious, Ischaemic Colitis
500
Q

treatment for Crohn’s disease?

A

induction of remission: glucocorticosteroids IV or oral
anti-TNF antibodies-infliximab- bind to membrane bound TNF-α and induce immune cell apoptosis.
enteral nutrition

maintenance of remission:
Methotrexate, Azathioprine
Anti-TNF antibodies (Infliximab)

Perianal Disease
Ciprofloxacin and Metronidazole
Azathioprine
Anti-TNF antibodies (Infliximab)

501
Q

when is surgery indicated in Crohn’s disease?

A

Failure of therapy with acute or chronic symptoms
Complications, e.g.toxic dilatation, obstruction, perforation, abscesses
Failure to grow in children despite treatment
Presence of a perianal abscess

if colonic CD involves entire colon, with no or minimal rectal involvement, a subtotal colectomy with an ileorectal anastomosis may be performed

502
Q

tment of ulcerative colitis?

A

Distal Disease (Proctitis)- topical or suppository corticosteroids
Left Sided Colitis- Topical corticosteroid enema
Extensive Colitis- oral corticosteroids, Infliximab

Surgical Management
Patients with complications e.g. toxic megacolon / Corticosteroids dependence

In acute disease, subtotal colectomy with end ileostomy and preservation of the rectum is the operation of choice.

503
Q

diagnostic difficulties with CD and UC?

A

must look at histological differences seen on biopsies
It is occasionally not possible to distinguish between the two disorders, particularly if biopsies are obtained in the acute phase. Such patients are considered to have Colitis of Undetermined Type and aEtiology (CUTE).
Serological testing for anti-neutrophil cytoplasmic antibodies (ANCA) in UC and anti-Saccharomyces cervisiae antibodies (ASCA) in CD may be of value in differentiating the two conditions.

Sometimes, an exact diagnosis can only be made after examining a surgical colectomy specimen.

504
Q

use of an abdominal X ray?

A

acute abdominal pain
small or large bowel obstruction
acute exacerbation of IBD- CD or UC- must exclude colonic dilatation, perforation and obstruction
renal colic-radioopaque stones*

505
Q

arterial supply of the rectum?

A

superior rectal artery from the IMA supplies priximal rectum

R and L middle rectal arteries from internal iliac arteries supply middle and inferior parts

506
Q

arterial supply of anorectal junction and anal canal?

A

inferior rectal arteries from internal pudendal arteries in perineum

507
Q

venous drainage of rectum?

A

superior (portal), middle and inferior rectal veins (systemic)

508
Q

what is bilirubin transported by to the liver?

A

albumin

as insoluble, must be made soluble by conjugation at the liver

509
Q

2 mechanisms of elimination in phase III drug metabolism?

A

via blood so excretion by kidneys, or via bile through the intestines.
ATPase pumps necessary for AT out of the hepatocyte

510
Q

important blood proteins produced by liver?

A
albumin
transferrin
alphafetoprotein
alpha 1 antitrypsin
blood clotting factors
complement
lipoprotein
globulins
511
Q

when is jaundice clinically detectable?

A

> 40micromol/L

512
Q

what gives our stools colour?

A

stercobilinogen

513
Q

what happens to bilirubin in bile when it reaches the terminal ileum?

A

intestinal flora convert it 1st to urobilinogen, and then to stercobilinogen, some urobilinogen is reabsorbed at terminal ileum and then excreted in the urine

514
Q

why is a pre-heptic jaundice particularly dangerous in neonates?

A

unconjugated hyperbilirubinaemia, and unconjugated bilirubin can cross the BB barrier, causing brain damage- kernicterus

515
Q

why might a patient with post-hepatic jaundice experience pruritis?

A

cholestasis means bile salts also escape into circulation

516
Q

How is Hep A transmitted?

A

faecal-oral-contaminated shellfish

517
Q

How is Hep B transmitted?

A

blood-bourne virus- contam. blood/bodyfluids/sex.contact/vertical transmission

518
Q

What can Hep B infection of liver causing hepatitis lead to?

A

chronic carrier state, liver cancer or cirrhosis

519
Q

symptoms of hepatitis?

A

fever
cough
headache
gastroenteritis

520
Q

what is the final result of alcohol damage to the liver?

A

cirrhosis

521
Q

3 major complications of liver cirrhosis?

A

portal hypertension
hepatocellular carcinoma
liver failure

522
Q

what type of jaundice does alcoholic liver disease cause?

A

hepatic jaundice- unconjugated and conjugated hyperbilirubinaemia

523
Q

how might wernicke-korsakoff syndrome resulting from alcoholic liver disease present?

A

mental confusion and an unsteady gait

result of thiamine deficiency

524
Q

describe the microscopic appearance of the liver with alcoholic hepatitis

A

inflammation! Mallory’s hyalin: intracytoplasmic aggregates of altered, ubiquitinated keratin filaments. Neutrophils aggregate around damage, and lymphocyte and macrophage entry. Lipid peroxidation and prod. by phagocytes result in free radicals which form a focal necrosis. protein and water retained by hepatocytes after injury so they balloon. Collagen deposited

525
Q

consequences of alcoholic liver disease

A
fasting hypoglycaemia- can't activate gluconeogenesis
wernicke-korsakoff syndrome
hepatic encephalopathy- reduced ability to produce urea, hyperammoniaemia
lactic acidosis, gout- urate crystals 
fatty liver- reversible, steatosis
jaundice
ketoacidosis
oedema
dementia
epilepsy
cirrhosis
blood tests: increase ALT, AST, AP, bilirubin, and PTT, plus low serum albumin
526
Q

describe liver cirrhosis

A

IRREVERSIBLE response of liver to cell damage. Liver cell necrosis followed by hepatic fibrosis and nodular regeneration, so loss of organised zonal structure, blood perfuses nodules in haphazard fashion, so organ prone to failure, and also problem of portal hypertension as fibrous tissue compresses PV, and hepatocellular carcinoma.

527
Q

clinical features of liver cirrhosis?

A

PH: oesophageal varices, rectal varices, caput medusae
hypoalbuminaemia- pitting/ankle oedema and ascites- PH and low albumin and RAAS stimulation*
jaundince- hyperbilirubinaemia
duputren’s contracture-thickening of palmar fascia, so 4th and 5th digits are pulled into partial flexion at MCP joints
anaemia- spleen enlarged due to PH, so starts to filter normal aswell as abnormal rbc
bruising- clotting factors not working properly
spider naevia
gynaecomastia
palmar erythema
muscle wasting
spontaneous bacteria peritonitis

528
Q

management of liver cirrhosis?

A

stop drinking
treat underlying cause- antivirals
treat complication e.g. ascitic taps
transplantation

529
Q

how is early detection of hepatocellular carcinoma development enabled in a patient with cirrhosis?

A

6mnthly check ups involving ultrasound and serum alpha fetoprotein measurements

530
Q

if alpha 1 antitrypsin deficiency is causative of liver cirrhosis, what treatment is required?

A

liver transplant

liver= site of alpha 1 antitrypsin prodcution

531
Q

after how many counter clockwise turns of 90 degrees does the midgut return to the abdominal cavity after herniating through the umbilical cord?

A

3

532
Q

what is the cause of pyloric stenosis?

A

hypertrophy of the circular muscle in the region of the pyloric sphincter
NOT a recanalisation failure

common abnormality of stomach in infants, causing projectile vomiting

533
Q

how is the caecum moved to the R lower quadrant?

A

on return to the abdominal cavity after herniation through the umbilical cord, cecal bud returns last.

When the cecal bud has returned to the abdomen, it descends, moving the caecum to the right lower quadrant

534
Q

result of incomplete gut rotation?

A

L sided colon

535
Q

result of reversed gut rotation?

A

Midgut makes one 90 degress rotation clockwise
Transverse colon passes posterior to the duodenum. (Can wrap around and occlude it)
so cranial strucures anterior to caudal
trasnverse colon normally keep parts in place to prevent volvulus, so susceptible to obstruction and strangulation-ischaemia

incomplete or reversed rotation leads to hypermobile guts

536
Q

describe supply above and below pectinate line

A

above: IMA, S2-S4 pelvic parasympathetics-ANS, columnar epithelium-hindgut-endoderm, internal iliac nodes lymph drainage
below: pudendal artery, S2-S4 pudendal nerve-somatic NS, stratified epithelium- proctodeum- ectoderm, superficial inguinal nodes=draiange

only stretch sensation above line
below= pain, temp and touch

537
Q

problem with gastric tissue in meckel’s diverticulum

A

small bowel not adapted, causes ulceration

538
Q

what does a vitelline fistula result in?

A

faecal matter coming out of umbilicus as abnormal connection with intestinal tract

539
Q

PS anastomoses other than those responsible for causing oesophageal and rectal varices, and caput medusae if PH?

A

bare areas of GI tract and related organs: veins between bare area of liver and diaphragm

portal tributaries of mesentery and retroperitoneal organs

540
Q

describe all the mechanisms behind ascites in PH

A

ascites= abnormal fluid collection in peritoneal cavity. increased hydrostatic pressure within splanchnic circulation, so transudation of fluid. Hypoalbuminaemia so reduced oncotic pressure of blood in capillaries so more fluid enters the peritoneal cavity. Blood pooling in splanchinc vasculature with peripheral arterial vasodilatation so decrease effective blood vol, RAAS avtivation and SNS so water and Na+ retention, so further fluid accumulation. NO elevated in liver disease, so vasodilation of splanchnic vasculature, so RAAS and fluid movement

541
Q

RFs of gallstones?

A
female
increase age
multiparity
obesity- rapid weight loss
diet
drugs-OCP
ileal disease/resection e.g. Crohns
haemolytic disease
542
Q

why is pain intermittent in symptomatic gallstones?

A

stone impact in cystic duct/neck of GB, pain produced on gallbladder contraction when stimulated by CCK during intestinal phase of gastric secretion, so pain after eating, so biliary colic

543
Q

describe acute cholecystitis

A

inflammation of GB wall and infection, oedema causes mucosal ulceration which causes fibropurulent exudate production, causing pain, SIRS, pyrexia and sepsis, antibiotics can be given to treat

544
Q

complications of gallstones

A

acute pancreatitis
gallbladder carcinoma, gallbladder perforation
empyema
mucocoele- impaction of stone, mucus secretion as GB empty, painful distension
obstructive jaundice
ascending cholangitis- charcot’s triad- RUQ pain, jaundice, fever
biliary-enteric fistula/gallstone ileus- fistula between GB and ileum, large stone obstructs ileum

545
Q

how is the inflammatory process of acute pancreatitis caused?

A

effects of enzymes released from pancreatic acini into the pancreas itself in active form

546
Q

how can epigastric pain in acute pancreatitis be relieved by the patient?

A

by sitting forward

547
Q

how is chronic pancreatitis diagnosed?

A

CT scan - chronic= fibrosis, calcification

contrast to acute- greatly elevated serum amylase- blood test

548
Q

how can severity of pancreatitis be assessed?

A

Glasgow criteria

549
Q

causes, apart from acute pancreatitis, for an elevated serum amylase?

A

intestinal obstruction and trauma

perforated peptic ulcer

550
Q

what investigation can be used to see whether gallstones are the causes of acute pancreatitis?

A

abdominal ultrasound

551
Q

extravasation of blood in acute pancreatitis?

A

elastates cause blood vessel destruction- blood vessel autodigestion and retroperitoneal haemorrhage
periumbilical brusing= cullen’s sign
flank brusing- grey turner’s sign

552
Q

why is obstructive jaundice in head of pancreas carcinoma usually painless?

A

no inflammation

553
Q

why might the GB be palpable with head of pancreas carcinoma?

A

bile accumualtes in proximal biliary tree

554
Q

investigation of head of pancreas carcinoma?

A

abdominal CT

555
Q

signs of acute pancreatitis?

A
upper abdomen tender to palpation
cullens of grey turner's sign
fever
jaundice
tachpnoea
shock
SIRS
tachycardia
556
Q

tment of acute pancreatitis

A

treat precipitant
pain relief with opiate analgesisa
IV fluids and electrolytes as vomiting, hypotensive
supplemental O2
antibiotics- acute infections or assoc cholangitis
early nutritional support- enteral feeding- tybe put in nose and down to stomach, parenteral feeding- peripheral line used

557
Q

antibiotics for H pylori?

A

clarithromycin

metronidazole or amoxicillin

558
Q

what test might be done to look for peptic ulceration if upper GI bleeding occurring?

A

upper GI endoscopy

559
Q

which midgut structure returns to the abdominal cavity 1st?

A

jejunum

560
Q

what occurs if the caecal bud fails to descend?

A

subhepatic caecum

561
Q

where is the caecum initially?

A

in the right upper quadrant, below liver

descends to the RIF

562
Q

management of appendicitis?

A

appendicectomy
analgesia
antibiotics- bacteroides fragilis- obligate anaerobe, metronidazole?

563
Q

what may be found on examination of a patient with appendicits?

A

rebound tenderness
fever
psoas sign- supine, actively flex R hip against resistance, producing pain

564
Q

transporter vital for absorption in SI?

A

Na+-K+-ATPase

as most absorption is an active process so Na+ gradient is essential

565
Q

what are villi separated by in SI?

A

intestinal glands- simple tubular structures extend from muscularis mucosae through LP thickness, where then open onto luminal surface at base of villi

566
Q

in which layer of the mucosa are Peyer’s patches founf in terminal ileum?

A

lamina propria

567
Q

how is striated appearance of SI created under microscopy?

A

microvilli on luminal surface of enterocytes to increase SA

568
Q

what can damage to unstirred layer result in?

A

malabsorption

569
Q

function of mucus small intestinal secretion?

A

lubricates chyme for intestinal protection and can be better propelled

570
Q

what is amylose broken down into by action of alpha amylases?

A

maltose and glucose

571
Q

what is amylopectin broken down into by alpha maylases?

A

alpha limit dextrins

572
Q

why is a patient with Crohn’s disease susceptible to lactose intolerance?

A

chronic inflammation of terminal ileum, and SI is site of major absorption of nutrients via action of enzymes found within the unstirred layer e.g. lactases- brush border enzymes- membrane bound. Low activity of lactase so lactose fermented by gut bacteria to lactic acid, methane gas and H2. water potential of gut lowered, so fluid and electrolytes secreted, producing diarrhoea, and gases cause stomach cramps.

573
Q

why do monosaccharides require transporters for absorption in SI?

A

as hydrophilic, so can’t simply diffuse through lipid bilayer

574
Q

which other sugar is absorbed in the same way as glucose in the SI? (SGLUT 1 co-transporter using Na+ gradient from Na+ pump)

A

galactose

575
Q

where does glucose travel once it has passed across the BL membrane of the enterocyte via GLUT2?

A

from ECF into the PV, where it can then be carried to the liver

576
Q

transporter on enterocyte apical membrane for fructose and lactose absorption?

A

GLUT5

FD so can’t reduce their concentrations in lumen as much as for glucose

577
Q

contents of oral rehydration fluid?

A

NaCl and glucose in water

578
Q

what are proteins broken down into in the stomach?

A

oligopeptides via pepsin released by chief cells

pepsin acts on bonds near aromatic aa side chains

579
Q

describe which parts of aa are acted upon by proteases released from acinar cells of pancreas

A

trypsin- likes bonds near basic side chains
chymotrypsin- likes bonds near aromatic side chains
carboxypeptidase- likes C terminal aa with basic side chains

580
Q

describe aa uptake by enterocytes in SI

A

aa produced from oligopeptides acted upon by brush border enzymes. Na+ pump on BL memebrane creates Na+ gradient for active absorption of aa across apical membrane via Na+/aa co-transporter

some by FD- passive process, aa in high enouch conc in lumen, but AT resorted to as conc decreases with absoprtion

aa transporters found on BL membrane

581
Q

describe peptide uptake by enterocytes in SI?

A

dipeptides and tripeptides taken up by active mechanism assoc with active pumping of H+ into lumen, with return of H+ into cell by co-transport with a peptide= H+-oligopeptide co-transporter

582
Q

what happens to FA and glycerol within the enterocyte?

A

reassociate to form TAGs which then form apoprotein vesicles, which are exocytosed through BL membrane. Then moved into lymphatic system for transportation as chylomicrons as chylomicrons can’t pass into the circulation due to capillary fenestration size restrictions

583
Q

which FA enter portal system?

A

medium and short chain as more water soluble so not transported via chylomicrons

584
Q

function of colipase?

A

helps to position and stabilise pancreatic lipase to act on fats in micelles

585
Q

describe the uptake of calcium by enterocytes

A

FD across apical membrane through calcium channel as low IC calcium, then pumped out across BL membrane via Ca ATPase and NCX. calbindin transports calcium in cell

calcitriol- increases synthesis of calbindin, and both apical and BL transporters

duodenal absorption- transcellular, but also paracellular route throughout the SI

586
Q

why might stomach pathology cause Fe deficiency anaemia?

A

gastric acid prod by parietal cells if stomach solubilises Fe complexes into a form that can be absorbed by the duodenum, and stomach also secretes gastroferrin that solubilises Fe as transports Fe2+ and keeps it in this ferrous form, so poor Fe absorption may result if these substances are not produced by a problem with stomach functioning

587
Q

what from of iron is better absorbed by enterocytes?

A

Fe2+

588
Q

what happens to Fe2+ once uptaken by RME in enterocyte?

A

oxidised to Fe3+, and may then be released into plasma where binds to transferrin for uptake into rbc, or is stored in enterocyte bound to ferritin

589
Q

describe vit absorbtion by GI tract

A

water soluble e.g. vit C, B vits- passive diffusion
fat soluble- A,D,E and K- incorporated into micelles, then absorbed similarly to LCFAs and packaged into chylomicrons
B12- absorbed with intrinsic factor at terminal ileum

590
Q

describe segmentation in SI

A

back and forth mixing movement between adjacent segments, so mixing of secretions and slow transit time for sufficient absorption.
intestinal pacemakers-located at intervals along length of SI, so can initiate own contractions. AP frequency highest at stomach end so contract more, so intestinal gradient produced, AP 12 to 8 per min at distal end, gradient causes differential segmenting rates in adjoining sections, so more rapidly segementing cephalic segment squirts more frequently into adjacent caudal segment, than that segment does into it, so there is a net movement of material in caudal direction, though slow rate, as more squirts go caudally.

segments formed as intermittent contraction of smooth muscle along length as each pacemaker drives its own section, so contents can be mixed in region where muscle not contracted.

nerve plexuses: PNS post-ganglionic neurones in muscle layer, electrical activity propagates along nerves rather than SMCs, and escapes intermittently, so result in only certain points of contraction where lumen closed, so mixing in adjacent non-contracted segments, so opportunity for luminal contents intestinal epithelia contact maximised

591
Q

describe haustral shuffling

A

haustra located between taenia coli. circular smooth muscle contracts, to shuffle contents back and forth so propelled very slowly towards sigmoid colon

592
Q

describe defecation

A

rectum filled by mass movement. pressure receptors in rectal wall activated as wall stretched, so wave of contraction in rectal muscle, forcing faeces towards anus. external anal sphincter- voluntary-somatic NS< relaxes, causing reflex relaxation of internal sphincter-ANS-PNS.
control via sacral reflexes modified by higher centres, and these centres are overidden if pressure too high, producing defecation.

593
Q

what is absorbed in terminal ileum?

A

Vit B12
bile acids
anything not absorbed in jejunum

594
Q

describe absorption in LI

A

remaining water
absorbable nutrients
Vits produced by colonic bacteria e.g. vit K and B12, thiamine and riboflavin

faeces then enters rectum where it is stored and compacted

movements: haustral shuttling and mass movement

595
Q

2 key functions of LI?

A

water absorption

mucus secretion- protection of colonic mucosa

596
Q

3 modifications of SI to maximise SA?

A

villi
microvilli
plicae circulares

597
Q

2 examples of scenarios with referred pain?

A

appendicitis initially- visceral referred- epigastric as foregut derivative

diaphrgmatic irritation- shoulder pain as phrenic nerve C3, C4, C5, pain referred to these dermatomes of the shoulder

598
Q

what organisms are present in the mouth?

A
streptococci
staphylococci
candida
lactobacillus
enterococcus
anaerobes
599
Q

what name is given to the infection caused by mouth bacteria is person manourished, dehydrated, IC of systemically unwell?

A

noma/cancrum oris

600
Q

which 3 bacteria are found in the throat of all people?

A

Strep viridans
staphylococci
N.meningitidis

601
Q

name given to swelling seen around tonsils?

A

quinsy

602
Q

which vitamin can inhibit gastric cancer cell growth?

A

Vit C

603
Q

causes of peptic ulcers?

A
H pylori
NSAIDs
smoking
alcohol
ZE syndrome
604
Q

3 bacteria always present in colon?

A

bacteroides fragilis
E coli
enterococcus faecalis

605
Q

surgical wound infection prophylaxis?

A

metronidazole and BS e.g. gentamicin or a cephalosporin

606
Q

2 features of patient in tetanus?

A

lack jaw- risus sardonicus

back muscles in spasm- opisthotonus

607
Q

how does C perfingens causes gas gangrene?

A

glucose- anerobi met., produces ethanol and CO2, so fluid lous gas, so wet or gas gangrene

608
Q

difference between a urachal fistula and a patent urachus?

A

fistula- abnormal connection between the bladder and the umbilicus, so urine passes out of the belly button, can causes severe infection and sepsis if not treated

a fistula is a type of patent urachus- urachus is completely open

609
Q

complications of a meckel’s diverticulum?

A

haemorrhage
diverticulitis
neoplasm
intestinal obstruction

610
Q

why might pain in the back occur with a ruptured aorta?

A

aorta is retroperitoneal

611
Q

what is referred pain?

A

pain perceived at a site distant from the site causing the pain

612
Q

what is visceral referred pain?

A

ischaemia, stretch, inflammation or abnormally strong muscle contract affects the viscera, pain is a vague pain felt either in the epigastric, periumbilical or hypogastric regions depending on embryological derivative. Visceral afferent pain fibres in thorax and abdomen follow sympathetic fibres back to same SC segments that gave rise to the preganglionic sympathetic fibres, so CNS perceives visceral pain as coming from the somatic portion of the body supplued by the relevant SC segements

613
Q

why can an ectopic pregnancy cause shoulder pain?

A

blood can travel along the paracolic gutters to the shoulder

614
Q

why do neurological problems causing dysphagia cause difficulty in swallowing liquids?

A

very coordinated process

615
Q

what is ERCP used to to look at?

A

the biliary tree

616
Q

what is laparoscopy?

A

going into the peritoneal cavity, air is put in, so if do CXR than air would be seen under the diaphragm

617
Q

what is it called when air enters the peritoneal cavity?

A

pneumoperitoneum

618
Q

why is chyme not neutralised in duodenal cap?

A

this is proximal to the entry of the bile duct in the region of the ampulla of vater, which is at the second part of the duodenum, and so this is the region most prone to peptic ulcers

619
Q

where is the most common place for peptic ulcers to occur?

A

duodenal cap

620
Q

difference between bile acids and salts?

A

acids= cholic acid and chenodeoxycholic acid, become conjugated with glycine or taurine to form bile salts, and bile salts work better in the duodenal pH

621
Q

when is a micelles formed by bile salts?

A

when they are still in association with the FA and monoglycerides produced from the bdown of TAGs by pancreatic lipase

622
Q

how is a chylomicron formed in enterocytes?

A

TAGs associate with apoprotein

623
Q

what happens to the transversalis fascial sling during coughing?

A

tightens as intra abdominal pressure is increased, protecting the deep inguinal ring

624
Q

how is the peritoneal cavity open in females?

A

via infundibulum of the fallopian tubes

625
Q

what is the peritoneal cavity divided into?

A

greater and lesser sacs

communicate via foramen of Winslow

626
Q

define a hernia?

A

a protrusion of viscera through the wall of the cavity which normally contains it, which can be the result of weakness or an increase in pressure

627
Q

what remnants of the yolk sac can occur?

A

vitelline fistula
vitelline cyst
meckel’s diverticulum

628
Q

what happens to the midgut during development?

A

forms a primary intestinal loop as growing too rapidly for the trunk of the body, and then as liver grwoing rapidly too, it runs out of room in the abdominal cavity and so herniates out into teh umbilical cord. Undergoes 3 90 degree counterclockwise roatations to result in caudal limb behind cranial, and cranial reenters abdominal cavity first.

629
Q

negatives of using a CT scan to produce a cross sectional image?

A

high dose radiation- can cause carcinogenesis, genetic risks and developmental risks to foetus

630
Q

when might a paralytic ileus occur?

A

after surgery

631
Q

how can the small bowel become obstructed?

A

hernias
tumours
inflammation
adhesions

632
Q

causes of large bowel obstruction?

A

volvulus- sigmoid- mesentery
colorectal carcinoma
hernia
diverticular stricture

633
Q

what can cause a perforated bowel?

A
trauma
obstruction
tumour
diverticular
peptic ulcer

view on erect CXR- air under the diaphragm

634
Q

when are barium studies used?

A
contrast studies for:
dysphagia- swallow- if barium seen in airways then know patient aspirating
stomach- meal
SI- follow through
colon- enema