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GI workbook Questions > Formative > Flashcards

Formative Flashcards

0
Q

Which veins drain blood from the liver to the IVC

Which vein drains blood from the GIT/spleen to the liver?

A

Hepatic veins

Hepatic portal vein

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1
Q

the Liver is suspended in the abdominal cavity by the Falciform, Coronary and Triangular ligaments.
How else is the Liver suspended?

A

The hepatic veins draining blood from the Liver into the IVC help to suspend the Liver in the abdominal cavity.

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2
Q

In embryological terms, what is the Falciform ligament a remnant of?

A

The Falciform ligament is a remnant of the Ventral mesogastrium of the foregut

The Liver develops in this mesentery dividing it up into the  
Falciform ligament (Anterior wall- Liver) 
Lesser Omentum (Liver-Stomach
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3
Q

What embryological remnant lies within the Falciform ligament?

A

The Umbilical vein lies within the Ventral mesogastrium during development.
It remains as the Ligamentum teres (also called the round ligament of the Liver)

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4
Q

If a gallstone were to get stuck in any structures on its way to the duodenum:
What structures would it lass through
what clinical condition might result in each case

A

Cystic duct- Cholecystitis/ Biliary colic

Common bile duct- Cholangitis/Jaundice

Ampulla de vater/sphincter of oddi- Cholangitis/Jaundice/pancreatitis/steatorrhoea

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5
Q

Name the three paired salivary glands

Which of these glands secretes a mainly serous fluid?

A

Parotid
Sublingual
Submandibular/Submaxilliary

The Parotid secretes a mainly serous fluid

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6
Q

The Acinar cells of the salivary glands produce a fluid that is initially isotonic (with plasma), but the end product is a solution that is hypotonic.
Explain the process of producing hypotonic saliva

A

Ductal modification:

More ions (Na+/Cl-) reabsorbed from saliva than secreted into saliva

Ductal cells relatively impermeable to water

Overall effect = more ions removed from saliva than water = hypotonic

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7
Q

What happens to the tonicity of saliva when the flow rate increases?
Explain why

A

Increases

Less contact time with ductal cells/ Less time for ductal modification/ reduced reabsorption of Na/Cl

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8
Q

What happens to the alkalinity of saliva as the flow rate increases?
Explain why

A

Increases

Ductal HCO3- secretion is selectively stimulated when saliva production is stimulated

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9
Q

Describe causes of dysphagia where swallowing solids is harder than
swallowing liquids

A

Dry mouth

Any physical obstruction from the oral cavity to the gastro-oesophageal junction i.e. various cancers (usually squamous cell carcinoma or adenocarcinoma)

fibrous strictures

external compression from structures surrounding the oesophagus

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10
Q

suitable investigation for Dysphagia to solid foods

A

Barium swallow
Oesophago-gastro-duodenoscopy (OGD)
Accept Videofluoroscopy
CXR- for external compression

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11
Q

What is the Peritoneal cavity?
What does it normally contain?
Is the Peritoneal cavity an enclosed space?

A

the space that lies between the Visceral and Parietal peritoneum

A small amount of fluid (normally sterile)

In males it is an enclosed space
in females it is open to the external environment via the infundibulum of the Fallopian tubes

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12
Q

What differences exist in the abdominal wall above and below the arcuate line (line of Douglas)?

A

The Rectus muscles are surrounded by the aponeurosis of the other abdominal wall muscles;

  • both anterior and posterior to them above the arcuate line
  • only anterior below it below the arcuate line
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13
Q

A patient complains of vague central (peri-umbilical) abdominal pain.
Using just this information what can you deduce about the possible location of the patients pathology.
Explain why

A

The pathology probably lies within the embryological mid-gut derivatives of the abdominal cavity.

Intra-peritoneal midgut structures will convey a vague periumbilical pain when pathology is irritating/distending their visceral peritoneum

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14
Q

What is a Meckel’s diverticulum?

Where is it normally located?

A 
a diverticulum that exists because of the incomplete obliteration of the 
vitelline duct (omphalomesenteric duct)

Usually found within 2 feet (proximal) of the Ileo-caecal valve.

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15
Q

With reference to local organs, describe the site of the lesser sac.
How does the lesser sac form during development in the human?

A

The lesser sac lies posterior to the Liver , the lesser omentum and the stomach

The foregut has both a Ventral and a Dorsal attachment to the abdominal cavity. When the foregut rotates an enclosed space is created posterior to the stomach. This becomes the lesser sac.

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16
Q

If you were to insert the tip of your finger in the epiploic foramen (foramen of Winslow or entrance to lesser sac), name three tubular structures that would be lying in the peritoneum in front (anterior to) of your finger.

A

Common Hepatic artery
common Bile duct
Portal vein

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17
Q

In pancreatitis, how does fluid come to collect in the lesser sac?

When a patient develops a large fluid collection in the general peritoneal cavity, what is the condition called?

A

The lesser sac lies immediately anterior to the Pancreas. During pancreatitis, the Pancreas releases (extravasates) pancreatic secretions into its surroundings and some move through into the lesser sac, where they collect.

Ascites

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18
Q

The Pancreas secretes both enzyme rich secretions and Bicarbonate rich secretions.
Name the hormones that are responsible for stimulating these.

A

Enzyme rich- Cholecystokinin (CCK)

Bicarbonate rich- Secretin

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19
Q

Explain why a cancer of the head of the pancreas should cause a patient to be jaundiced

A

A cancer in the head of the Pancreas can obstruct the common bile duct as it enters the duodenum.
This will stop bile from following its normal passage into the gut causing a backlog of Bile within the biliary system.
As a consequence of this, constituents of bile like Bilirubin will be reabsorbed into the blood causing a Hyperbilirubinaemia, which is
basis of Jaundice.

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20
Q

Which one of these does not contribute to the patency of the Lower oesophageal sphincter?

A The right crus of the diaphragm
B Positive intra-abdominal pressure acting on abdominal oesophagus
C Acute angle of entry (oesophagus into stomach)
D Pyloric sphincter
E Mucosal fold at Oesphagogastric junction

A

D
The Pyloric sphincter is the muscular sphincter that determines the rate that chime is delivered into the duodenum
and plays no part in the Lower oesophageal sphincter.
The other answers are all factors that help prevent reflux of gastric contents into the oesophagus.

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21
Q

If GORD continues over a period of time there is a risk that epithelial cells in the Oesophagus may
undergo Metaplasia.
Which of the following statements is true for Metaplasia?

A Irreversible 
 B Involves undifferentiated cells 
 C Always results in cancer 
 D Is synonymous with dysplasia 
 E Involves differentiated cells
A

E
This is an important term to be able to define. Metaplasia is the reversible change of one differentiated cell type with
another differentiated cell type.
The problem is that if prolonged this can lead to dysplasia and neoplasia and so metaplasia in the oesophagus is seen
as a potential precursor for oesophageal cancer. We call this Barrett’s oesophagus. The normal pinkish white
squamous epithelium is replaced with salmon pink columnar cells.

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22
Q

Ongoing Epigastric pain results in this gentleman undergoing an upper GI tract endoscopy in which
a gastric ulcer is visualised.
Statistically where is the most likely region of the stomach for an ulcer to develop?

A Cardia 
 B Fundus 
 C Body-lesser curve 
 D Body-greater curve 
 E Antrum
A

C
The most common site of gastric ulceration is the lesser curve of the body of the stomach.
The most common site of peptic ulceration overall is the first part of the duodenum as this is where the acidic chyme
enters the duodenum.
The neutralising pancreatic fluid and bile only join the duodenum later in the 2nd part so the first part is susceptible to
acidic damage and ulceration.

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23
Q

Although unlikely, if a stomach ulcer where to erode posteriorly through the body of the stomach
which major artery may be at risk from haemorrhage?

A Left gastro-epiploic 
 B Right gastric 
 C Splenic artery 
 D Gastro-duodenal 
 E Right gastro-epiploic

Which vessel would be damaged if a duodenal ulcer eroded through the first part of the duodenum?

A

C

Gastro-duodenal artery

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24
The Parietal cells in the stomach are responsible for acid production and which other important substance from the list below? ``` A Gastrin B Intrinsic factor C Histamine D Pepsinogen E Secretin ```
B Gastrin is released from G cells Histamine (in a gut context) is released by Enterochromaffin like cells (ECL cell) Pepsinogen is released by chief cells Secretin is released by S cells.
25
Which of the following blood vessels are involved in the formation of oesophageal varices? ``` A Left Gastric artery B Left Gastric vein C Left Gastro-epiploic artery D Right Gastic vein E Short Gastric vein ```
B The Left gastric vein drains into the Portal vein and is the one from this list most involved in the formation of varices. Arteries are not involved in forming varices.
26
Which of the following (plasma) test results would be the most specific indicator of Hepatocyte damage? A Raised Alanine Transaminase (ALT) B Raised Albumin levels C Raised Alkaline Phosphatase (ALP) D Raised Aspartate Aminotransferase (AST) E Raised conjugated Bilirubin levels
A There is a short podcast on LFTs which can be found on Blackboard. Alanine transaminase (ALT) is specific to hepatocytes and so if they are damaged it is released into plasma. ALP tends to rise in biliary obstruction and bone disease. AST is raised in liver damage but is also present in reasonable quantities in cardiac and skeletal muscle and so is not that specific to the liver. The healthy liver produces albumin so hepatocyte damage will not result in more albumin Raised conjugated Bilirubin levels is seen more in Biliary obstruction that occurs after conjugation has occurred (common bile duct blockage etc).
27
Which of the following (plasma) test results would be the most reliable indicator of a gallstone stuck in the common bile duct? A Raised Alanine Transaminase (ALT) B Raised Albumin levels C Raised Alkaline Phosphatase (ALP) D Raised Aspartate Aminotransferase (AST) E Raised conjugated Bilirubin levels
E There is a short podcast on LFTs which can be found on Blackboard. Alanine transaminase (ALT) is specific to hepatocytes and so if they are damaged it is released into plasma. ALP tends to rise in biliary obstruction and bone disease. AST is raised in liver damage but is also present in reasonable quantities in cardiac and skeletal muscle and so is not that specific to the liver. The healthy liver produces albumin so hepatocyte damage will not result in more albumin Raised conjugated Bilirubin levels is seen more in Biliary obstruction that occurs after conjugation has occurred (common bile duct blockage etc).
28
What is the clinical significance of the Paracolic gutters? A They allow the circulation of normal peritoneal fluid B They allow infectious fluids to travel to sites remote from the organ of origin C They stop infectious fluids from travelling to sites remote from the organ of origin D The demarcate the lateral borders of the peritoneal cavity E The provide structural support for the ascending/descending colon
B The paracolic gutters are formed between the lateral portions of the ascending and descending colon and the walls of the abdominal cavity. They are inside the peritoneal cavity. The allow infected fluid to move from the pelvis up the sides of the peritoneal cavity to the sub diaphragmatic recesses or the Hepato-renal recess (pouch of Morrison....James Rutherford!). The also allow contents from a perforated bowel to travel distant to the perforation. This is when knowledge of the recesses in the peritoneal cavity becomes useful as fluid can collect in them....please know about the pouch of Douglas and utero-vesical pouch.
29
Which of the following characteristics would indicate a diagnosis of Ulcerative colitis as opposed to Crohn’s disease? A Presence of disease in the rectum B Presence of disease in the terminal ileum C Presence of fistulas D Presence of Perianal disease E Presence of skip lesions
A
30
``` Which of the following endoscopic findings would indicate a diagnosis of Ulcerative colitis as opposed to Crohn’s disease? A Aphthous ulcers B Continuous mucosal involvement C Discontinuous mucosal involvement D Longitudinal ulcers E Normal vascular pattern ```
B
31
``` Which of the following is most directly responsible for the movement of Glucose from the lumen of the gut into the enterocyte ? Options: A GLUT2 B GLUT5 C Na/K ATPase D SGLT1 E SGLT2 ```
D This is slightly debatable as the gradient produced by the Na/K ATPase drives the movement of Na into the enterocyte (and glucose is co- transported with Na), but the question says most directly so SGLT1 is the best option. GLUT2 is the facilitated diffusion path across the basolateral membrane. GLUT5 is a fructose specific transporter (we don’t mention it in our teaching) SGLT2 is found in the kidney.
32
What does the term ‘mass movement’ describe? A The mixing of colonic content B The mixing of small intestinal content C The rapid movement of colonic content D The rapid movement of small intestinal content E The urge to defaecate
C
33
``` Blockage of which of the following arteries would have the greatest impact on the blood supply to the Appendix? A Ileocolic B Left colic C Middle colic D Right colic E Superior rectal ```
A The Appendix is located off the Caecum and lies in the right lower quadrant. The Ileocolic artery (a branch of the SMA) gives off an artery to the Appendix. The left colic (branch of IMA) supplies descending colon area. The Middle colic generally supplies transverse colon The right colic is ascending colon The superior rectal (when the IMA crosses into pelvis) supplies upper portion of rectum.
34
Describe visceral vs parietal pain
Peritoneal cavity made of visceral & parietal peritoneum But these dev from diff embryological pathways: Viscera (e.g surrounding intraperitoneal structures) don't have somatic nerve supply When viscera stretched/irritated chemically etc, pain will be referred according to whether that structured belonged to foregut (epigastric) midgut (periumbilical), or hindgut (suprapubic) Follow splanchnic nerves that exit at dermatome of these central areas Visceral peritoneum therefore refers pain along the midline Parietal peritoneum lines the body wall: has more dedicated somatic innervation and therefore is more localised
35
What can irritate the diaphragm Where is pain to the diaphragm referred to
Things that shouldn't be in the peritoneal cavity (e.g. Intraperitoneal structure bursting, resulting in faeces, pus, blood etc being present) Infection can make its way up to the diaphragm via pouches (e.g. Hepatorenal recess, pouch of Douglas, paracolic gutters). Pouches may be more prone to spreading infection when lying flat Pain referred to shoulder tip Phrenic nerve = motor supply to diaphragm The corresponding dermatomes extend to the shoulder tip (C3,4,5 keeps the diaphragm alive) Example of visceral referred pain
36
What can cause back pain
``` Retroperitoneal structures (E.g. Ruptured aorta, kidney, bladder) ```
37
Describe the pain experienced in appendicitis
Initially pain from inflamed appendix referred to periumbilical region (a midgut structure) Then inflammation of surrounding parietal peritoneum causes localised pain to RLQ Example of visceral referred pain & parietal pain
38
What are the main pouches/recesses within the peritoneal space What is their clinical significance
Pouch of Morrison/hepatorenal recess/subphrenic recess: Separates liver & right kidney (behind duodenum) Pouch of Douglas/rectouterine pouch (females): Between rectum & posterior wall of uterus Vesico-uterine pouch (uterovesical pouch of Meiring) (females): Between Uterus, bladder, part of intestinal surface (shallower) ``` Rectovesicle pouch (males): Reflects onto posterior wall of bladder ``` Paracolic gutters: Between ascending/descending colon & abdominal wall on either side Are potential spaces that can collect fluid/infection which can then travel around peritoneal cavity (Often when lying down)
39
What are the common presentations (symptoms) of gastric disorders
``` Pain Reflux Vomiting (food, haematemesis) Bloatinb Dysphagia Weight loss ```
40
Outline the investigations for common gastric disorders
``` A good history (most important) Physical exam Blood tests Urease breath test (H.Pylori) Endoscopies ```
41
List some common endoscopic studies
Oesophagogastroduodenoscopy (OGD) Endoscopic retrograde cholangiolancreatography (ERCP) (Tools are put into sphincter of oddi/amputta de vata where ducts exit to duodenum; can remove blockages but can also cause pancreatitis) Sigmoidoscoy Colonoscopy (Only way to see terminal ileum) Laptoscoppy (Inside peritoneal cavity)
42
Draw the biliary tree
http://lookfordiagnosis.com/mesh_info.php?term=biliary+tract&lang=1
43
At what spinal level do the following exit: Aortic hiatus Vena cava Oesophagus
T12 T8 T10 (Corresponds to number of letters in the name!)
44
What 4 mechanisms help prevent gastro-oesophageal reflux
Lower oesophageal sphincter Right crus of diaphragm Angle of entry of oesophagus; Oesophagus pierces at T10 Higher pressure in abdominal cavity than thorax (narrows oesophagus but stomach more muscular & resistant)
45
What is the management of peptic ulcers
antacids or H2 antagonists Review NSAIDs; may be prescribed a prostaglandin analogue (Misoprostol) to help prevent peptic ulcers H. pylori infection: triple therapy 2 antibiotics (e.g. Clarithromycin, Amoxicillin) PPI H2 antagonist Severe cases: selective vagotomy
46
What is the management of GORD
Lifestyle: weight loss, reduce alcohol, reduce aggravating foods Meds: Raft antacids (sits on top of stomach contents, preventing reflux e.g. Gaviscon) Simple antacids (neutralises acid e.g. Calcium carbonate) PPI H2 antagonist
47
Describe how the following medications work & some example names
Proton pump inhibitors (e.g. Omeprazole) Prevents H+ ions being pumped into parietal cell canniculi Reduces acid secretion by parietal cells More effective H2 antagonists (e.g. Ranitidine, simetidine) Inhibits histamine/ blocks stimulation of Gastrin/ACh Blocks H2 receptors, reducing acid secretin of parietal cell Not as effective as don't block whole system
48
Describe how a vagotomy works | & what are the potential problems
Can block stomach acid secretion By switching off number of inputs to acid secretion However, important for other functions e.g. Relaxing pyloric sphincter Can make vagotomy more selective
49
Where are parietal cells mainly found
In body & fundus of stomach
50
How is gastric acid stimulated normally?
Cephalic phase: Signt/smell/swallow Stimulates ACh release from parasympathetic neurones Binds to receptors on parietal cells = release HCl Gastric phase: Stomach distension = further release ACh Food Buffering stomach acid = increase pH = stimulates Gastrin: (From endocrine G cells in stomach) binds to receptor on parietal cell = release HCl Histamine amplifies: stimulated by Gastrin & ACh (Released by mast cells & binds to H2 receptors on parietal cells)
51
How is gastric acid inhibited normally?
Intestinal phase: Chyme leaves stomach = increase CCK, reduce Gastrin = reduce acid Stomach acid not buffered by food = reduce pH = gastrin reduced Reduced pH also stimulates D cells in stomach: release somatostatin which inhibits G cells producing Gastrin
52
How do parietal cells produce acid?
Have a proton pump in canaliculi which pumps H+ ions up a concentration gradient Energy intensive Stimulated/inhibited by hormones (Mitochondria split water to produce H+ ions: OH- combines with CO2 from metabolism to produce HCO3-, exported in blood)
53
Describe how fat is absorbed
Bile emulsifies fats Negatively charged bile salts surround lipids Are amphipathic molecules Negative ends of bile slats repel eachother = disperse lipids Increases surface area for digestive enzymes (lipase) Breakdown products of lipids remain attached to the BS These form micelles Migrate to apical membrane (brush border) of enterocyte of gut All but BS then diffuses into enterocyte (or use fatty acid transporter) BS reabsorbed at terminal ileum In enterocyte, lipid converted back to TAG & packaged with cholesterol & proteins (chylomicron) Moved to lacteal (small lymph vessel of gut) = Chyle Lacteals drain into thoracic duct Thoracic duct drains into L subclavian vein Foregut lymph nodes drain to coeliac nodes /midgut-SMN / hindgut-IMN Unite to form intestinal trunk
54
Distinguish bile acids & bile salts
Bile acids: E.g. Cholic acids, kenodeoxycolic acid (primary bile acids) Bile salts: = conjugated bile acids (with taurine & glycine) More variety Soluble at lower pH (i.e. At duodenal pH) = mor active in duodenum In ionised form at duodenal pH Amphipathic: hydrophobic ends bury into fat, leaving hydrophilic exposed to water so can dissolve Increases s/a of fats for actin of lipases
55
What is a micelle composed of
``` Bile salts Surrounding: Mono glycerides Fatty acids Cholesterol Phospholipids ```
56
In what forms are fats absorbed from the diet
Triglycerides Phospholipids Sterols (e.g. Cholesterol) Minor lipids, incl fat soluble vitamins (ADEK)
57
Describe the enterohepatic circulation of bile salts
Bile salts only reabsorbed in terminal ileum (So in high concs along small intestine; supports fat absorption) Na/bile salt co-transporter in terminal ileum Enter portal circulation (straight back to liver) Liver extracts them, so don't have to re-synthesise too much
58
How would you distinguish small bowel obstruction on an ABX
Complete circular folds More centrally placed in abdo cavity > 3cm dilation (>6 = large bowel >9 = caecum)
59
How would you distinguish small bowel obstruction from large bowel obstruction clinically?
Vomiting earlier in relation to constipation
60
What will you see on an erect CXR when the bowel has perforated?
Air underneath diaphragm: gas rises
61
Describe what a hernia is | List the common hernias
When viscera (& its coverings) protrude thru containing cavity Inguinal (indirect & direct) Femoral Umbilical Incisional
62
Describe the boundaries of the inguinal canal
Floor = inguinal ligament (lacunar ligament medially) Roof = internal oblique / transverse abdominus (musc arches & aponeurosis) Posterior wall = transversalis fascia (innermost layer; includes conjoint tendon medially) Anterior wall = aponeurosis of external oblique
63
Where is an inguinal hernia located Where is a femoral hernia located
Above inguinal ligament Below inguinal ligament (More common in women but not as common overall as inguinal) (Location of hernia = location of neck of hernia)
64
Where is the deep inguinal ring located?
In the transversalis fascia (posterior wall of inguinal canal)
65
Where is the superficial inguinal ring located?
In aponeurosis of external oblique (anterior wall of inguinal canal)
66
What are the boundaries of Hesselbach's triangle | Why is it clinically significant
Inf epigastric artery/vein Rectus abdominus Inguinal ligament Potential area of weakness (& contains superficial ring: an area of weakness)
67
Distinguish between a direct & indirect hernia | What are their routes
Direct: Protrudes straight through superficial ingunal ring contained in Hesselbach's traingle Indirect: Takes an indirect route thru deep & then superficial inguinal ring Goes through inguinal canal
68
What is included in the femoral canal anatomy (surrounding the femoral canal)
``` NAVEL: Nerve (femoral) Artery (femoral) Empty space - femoral ring (opening to femoral canal) Lacunar ligament ```
69
What is contained in the femoral canal
Lymphatic vessels Lymphatic node Areolar tissue
70
What are the key features of ulcerative colitis
More superficial: mucosal depth of inflammation Contiguous (continuous) pattern of disease Mainly located in colorectum Causes bleeding (but not usually fiatulas, granulomas, perianal disease, malnutrition) Risk colorectal cancer
71
What are the key features of crohn's disease
Deeper inflammation: transmural (poss through bowel to other structures) Skip areas (not continuous) Located anywhere mouth-anus Rectal involvement less common Causes ileal disease, fistulas, granulomas, malnutrition (bleeding less common) Risk colorectal & small bowel cancer (depending on disease location)
72
What are the peritoneal cavity subdivisions
``` Grater sac (anteriorly): Supracolic compartment (above) Infracolic compartment (below) ``` ``` Lesser sac (posteriorly) Formed by lesser & greater omentum ```
73
What connects the greater & lesser sac Where is it located
Omental foramen (epiploic foramen) Lies between inferior vena cava & portal vein
74
Describe the normal process of Bilirubin breakdown
Rbc's: completed lifespan (120days) or damages Membrane ruptures Hb phagocytosed by macrophages (globin protein broken down) Forms heme Forms unconjugated bilirubin Travels to liver via blood (not soluble: bound to albumin) In liver: conjugated with glucuronic acid (UDP glucornyl transferase) Excreted as part of bile (into biliary & cystic ducts) Converted to Urobilinogen (by intestinal bacteria) Either forms stercobilin (excreted in faeces) Or reabsorbed by intestinal cells & transported to kidneys via blood & excreted in urine (as urobilin)
75
Distinguish: Dysplasia Metaplasia Neoplasia
Dysplasia = abnormal dev of epithelial growth / differentiation Metaplasia = reversible replacement of 1 differentiated cell type with another Neoplasia = abnormal/excessive growth of tissue, usually resulting in tumour

GI workbook Questions (10 decks)

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