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ESA 3 > Gastrointestinal System > Flashcards

Gastrointestinal System Flashcards

1
Q

What are some functions of the alimentary tract?

A 
Entry point for food
Break up
Storage
Chemical digestion
Kill pathogens
Move along tract
Absorb nutrients
Eliminate residual waste
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2
Q

What are the contents of saliva (apart from water)?

A

Amylase
Lipase
Bacteriostatic agents (IgA)
High calcium to protect teeth

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3
Q

What is the difference between the upper and lower oesophageal muscles?

A

Upper - striated (voluntary control)

Lower - smooth (not voluntary)

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4
Q

What are rugae in the stomach?

A

Longitudinal folding of the mucosa

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5
Q

What is receptive relaxation in the stomach?

A

Relaxation of the walls as food enters to stop a rise in pressure

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6
Q

What is the function of parietal cells, chief cells and G-cells in the stomach?

A

Acid and intrinsic factor
Pepsin
Gastrin

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7
Q

What is the function of Brunner’s gland in the duodenum?

A

Produce bicarbonate-rich mucus to neutralise stomach acid

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8
Q

What is the function of bile salts?

A

Emulsify fats

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9
Q

In the alimentary tract, when does absorption begin?

A

Duodenum

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10
Q

What are plicae circularis in the small intestine?

A

Circular folds in the mucosa and submucosa

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11
Q

What key things are actively absorbed in the duodenum, jejunum and ileum?

A

Duodenum - iron

Jejunum - sugar, amino acids, fatty acids

Ileum - vitamin B12, bile acid, nutrients

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12
Q

What type of epithelia is found in the colon?

A

Simple columnar

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13
Q

What areas of the alimentary tract are under somatic control?

A

Mouth, first third of the oesophagus, last anal sphincter

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14
Q

What two plexuses are found in the gut?

A

Submucosal plexus - beneath submucosa (plexus of Meissner)

Myenteric plexus.p - between muscle layers

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15
Q

What sphincter is at the top of the oesophagus and relaxes on swallowing?

A

Cricopharyngeal sphincter (upper oesophageal sphincter)

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16
Q

What type of cancer would you see in the top part of the oesophagus?

A

Squamous cell carcinoma

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17
Q

What type of cancer would you see in the bottom part of the oesophagus?

A

Adenocarcinoma

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18
Q

What is Barrett’s oesophagus?

A

A pre malignant condition caused by chronic acid reflux.

Metaplasia to cuboidal epithelium, appears red and inflamed.

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19
Q

From top to bottom, what are the areas of the stomach?

A

Fundus
Cardia
Body
Pylorus

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20
Q

What is the significance of the incisura angularis of the stomach?

A

An anatomical notch indicating the boundary between the body and pylorus

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21
Q

What is the omentum?

A

Layers of peritoneum attaching the stomach to other abdominal organs

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22
Q

What is a peptic ulcer?

A

Lesion in the mucosa caused by the digestive action of pepsin and stomach acid. Frequently due to a loss of mucosal protection.

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23
Q

What valve separates the ileum and colon?

A

Ileocaecal valve

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24
Q

Briefly, what is ulcerative colitis?

A

Chronic ulceration which begins in the rectum then continues up the colon. Causes diarrhoea, often bloody. Can predispose to cancer.

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25
Q

What is a colonic volvus?

A

A twist in the colon which can cut off the blood supply and cause necrosis. Needs a colostomy.

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26
Q

What are colonic diverticulae?

A

Pouches which form in the wall of the colon.
Can cause bleeding and obstruction, may become infected and perforate.
Associated with left iliac fossa pain.

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27
Q

What are the layers that make up the musosa of the gut, from lumen out?

A

Epithelia
Lamina propria (mucus cells, Peyer’s patches)
Muscularis mucosa

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28
Q

When is peak salivary production?

A

In the afternoon

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29
Q

Give some substances which are found in saliva.

A 
Mainly water 
May have mucus
Antibodies
Electrolytes
Lymphocytes
Amylase/lipase
Bacterial flora
Neutrophils
Epithelial cells
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30
Q

What does the duodenum detect to slow gastric emptying?

A

Lipids
pH
Hypertonicity

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31
Q

What are the large salivary glands?

A

Sublingual
Parotid
Submandibular

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32
Q

What is the affect of having low ANS stimulation of the salivary glands?

A

Dry mouth
Halitosis
Poor dental hygeine

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33
Q

What are the three types of saliva and where are they mainly produced?

A

Serous - thin and watery. From parotid gland

Mucus - thick, mucinous and viscid. Sublingual

Mixed - submandibular

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34
Q

Describe the location if the parotid gland.

A

In front of and level with the external ear, within the parotid fascia

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35
Q

What duct drains the parotid gland?

A

Stenson’s duct

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36
Q

What is the major salivary gland?

A

Submandibular gland

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37
Q

Where is the submandibular gland located?

A

In the floor of the mouth

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38
Q

What duct drains the submandibular gland?

A

Wharton’s duct

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39
Q

Histologically, how can you differentiate between serous and mucus cells in a mixed acinus?

A

Serous have faint nuclei

Mucus have large, rounded nuclei

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40
Q

What cells surround secretory units in salivary glands and what is their function?

A

Myoepithelial cells

Pump secretions into the intercalated ducts

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41
Q

What are the primary and secondary stages of plasma production?

A

Primary - occurs in the acini, which secretes fluid which is isotonic with plasma

Secondary - undergoes modification in the striated duct

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42
Q

Give some conditions which can cause problems swallowing from the mouth to oesophagus.

A 
Cleft palate
Cleft uvula
Stroke (paralysis of nerves supplying soft palate)
Hypertrophy of pharyngeal tonsils
Drug overdose with CNS depression
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43
Q

Describe the tonsillar pillars and the location of the tonsils in relation to them.

A

Anterior tonsillar pillar has the palatoglossal arch

Posterior tonsillar pillar has the palatopharyngeal arch

The palatine tonsils are between the pillars

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44
Q

Describe the oral phase of swallowing.

A

Voluntary formation of a bolus
Activates receptors in the anterior tonsillar pillars and pharyngeal phase of tongue
Initiates swallowing

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45
Q

Describe the pharyngeal phase of swallowing.

A

Soft palate closes the border with the nasal/oropharynx

Hyoid bone and larynx are raised

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46
Q

Describe the oesophageal phase of swallowing.

A

Controlled by swallowing centres of the brain
Upper oesophageal sphincter relaxes
Reflex peristalsis initiated

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47
Q

What muscle forms the upper oesophageal sphincter?

A

Cricopharyngeal muscle

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48
Q

What is a hiatus hernia?

A

When the upper stomach herniates into the thoracic cavity through the lower oesophageal sphincter. Causes reflux.

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49
Q

What is the somatodeum of the gut tube?

A

Future mouth

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50
Q

What is the proctodeum of the primitive gut tube?

A

Future anus

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51
Q

What embryonic layer does the inner lining of the gut tube arise from?

A

Endoderm

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52
Q

What embryonic layer is the outer lining of the gut tube derived from?

A

Splanchnic mesoderm

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53
Q

What suspends the gut tube in the intraembryonic coelom?

A

Double layer of splanchnic mesoderm

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54
Q

What are the adult derivatives of the foregut?

A 
Oesophagus
Stomach
Pancreas
Liver
Gall bladder
Proximal duodenum (to the entrance of the bile duct)
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55
Q

What are the adult derivatives of the midgut?

A 
Distal 2/3 of the duodenum
Jejunum
Ileum
Caecum
Ascending colon
Proximal 2/3 of the transverse colon
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56
Q

What are the adult derivatives of the hindgut?

A 
Distal 1/3 of transverse colon
Descending colon 
Rectum
Upper anal canal
Inner lining of the urethra and bladder
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57
Q

Give the main arterial supply for each embryonic segment of the gut.

A

Foregut - coeliac trunk
Midgut - superior mesenteric artery
Hindgut - posterior mesenteric artery

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58
Q

What is the significance of an organ being close to the junction between different sections of the primitive gut, in terms of its blood supply?

A

It will have a dual blood supply

E.g. Pancreas, duodenum

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59
Q

What is the difference between the dorsal and ventral mesentry?

A

The ventral mesentry is only in the region of the foregut, so has a free edge at the liver.

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60
Q

What happens to the right and left sacs in development of the gut?

A

The left sac contributes to the greater sac

The right sac contributes to the lesser sac

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61
Q

What is mesentry?

A

A double layer of peritoneum, suspending the gut tube from the abdominal wall.
Gives a conduit for blood and nerve supply, allows mobility when required.

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62
Q

What are the omenta?

A

Specialised areas of peritoneum which allow the neurovasculature to pass along them.

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63
Q

What is located at the free edge of the lesser omentum?

A

Portal triad

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64
Q

What mesentry does the liver develop within?

A

Ventral

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65
Q

What is the difference between retroperitoneal and secondary retroperitoneal structures?

A

Retroperitoneal - the organ was never suspended in the peritoneal cavity
Kidneys, aorta

Secondary retroperitoneal - the organ began as part of the primitive gut tube, but became pushed against the abdominal wall and lost its mesentry.
Pancreas, duodenum

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66
Q

What has gone wrong in development to allow a tracheoesophageal fistula to form?

A

Incorrect formation or the absence of the tracheoesophageal septum.

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67
Q

What are the symptoms of a tracheoesophageal fistula?

A

Newborn unable to swallow.
Choking, coughing, vomiting, cyanosis when trying to feed
Polyhydramnios

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68
Q

What attaches the liver to the stomach?

A

Lesser omentum

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69
Q

What is the bare area of the liver?

A

Where it is attached to the diaphragm, with no peritoneal lining

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70
Q

What is the cause of duodenal atresia?

A

Failure to recanalise during development.

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71
Q

What are the symptoms of duodenal atresia?

A

Intestinal obstruction in the newborn

Polyhydramnios

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72
Q

How is chyme altered in the duodenum?

A

Adds water from the ECF/circulation using the osmotic gradient and CFTR
Pancreatic secretions such as enzymes and HCO3-
Liver secretions such as bile and HCO3-

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73
Q

What is the function of the centroacinar cells in the pancreatic exocrine system?

A

Produce enzymes

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74
Q

Describe the passage that pancreatic secretions take to enter the duodenum.

A

Enters the major pancreatic duct
Joins with the common bile duct at the ampulla of Vater
Common bile duct enters the duodenum at the duodenal papilla
The sphincter of Oddi controls entry into the duodenum

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75
Q

What stimulates the acinus to produce more enzymes?

A

Vagus nerve

CCK

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76
Q

What causes CCK release in the duodenum and jejunum?

A

Hypertonic chyme

Lipids

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77
Q

What active enzymes are secreted by the pancreas?

A

Amylase

Lipase

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78
Q

What inactive enzymes are secreted by the pancreas?

A

Trypsin
Chemotrypsin
Carbopeptidase
Elastase

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79
Q

Describe the formation and storage of inactive enzymes.

A 
Formed on RER
Modified in golgi
To condensing vacuoles
Made into zymogen granules for storage
Release
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80
Q

What are zymogen granules?

A

Membrane-bound inactive enzyme precursors.

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81
Q

What would a high plasma amylase indicate?

A

Pancreatic damage, most likely pancreatitis

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82
Q

What is the function of duct cells in the exocrine pancreas?

A

Produce an isotonic aqueous solution with Na+, Cl-, K+, HCO3-

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83
Q

What stimulates ductal cells of the exocrine pancreas to increase their production of HCO3-?

A

Secretin

Increased flow rate

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84
Q

What are the functions of the liver?

A

Energy metabolism
Detoxification
Plasma protein production
Bile secretion

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85
Q

What blood vessel takes blood from the gut to the liver?

A

Portal vein

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86
Q

What divides the liver into structural units?

A

Liver capsule

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87
Q

What is the functional unit of the liver?

A

Acinus

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88
Q

What are the short and long axes of the acini of the liver?

A

Short - between portal triads

Long - to the central vein

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89
Q

Describe the significance of the different zones around each portal triad in an acinus.

A

1 - closest to the triad and therefore closest to the blood supply. Will be first affected by toxins

3 - furthest from the triad. Will be worst affected by hypoxia

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90
Q

What is the hepatic sinusoid?

A

Convergence of the portal vein and hepatic artery in the liver

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91
Q

What is a Kupffer cell?

A

A macrophage in the liver

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92
Q

What is the vessel called which transports bile from hepatocytes to the bile duct?

A

Bile canaliculi

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93
Q

Give an example of a primary bile acid

A

Cholic acid

Chenodeoxycholic acid

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94
Q

Why must primary bile acids be modified before entry to the duodenum?

A

They aren’t soluble at duodenal pH.

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95
Q

How are primary bile acids modified to bile salts?

A

Conjugation with amino acids e.g. Glycine/taurine

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96
Q

What is a micelle?

A

Bile salts surrounding the breakdown products of fat in the intestine

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97
Q

What happens to the contents of a micelle after absorption into enterocytes?

A

Re-esterised to form triglycerides, phospholipids, and cholesterol.

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98
Q

What happens to lipids after re-esterification to allow them to be transported around the body?

A

Packaged with apoproteins to form chylomicrons.

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99
Q

Describe the path chylomicrons take from the gut into the venous system.

A

Absorbed into lacteals
Travel to thoracic duct
Left subclavian vein

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100
Q

Where are bile salts reabsorbed?

A

Terminal ileum

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101
Q

What is the function of the gall bladder?

A

Store and concentrate bile.

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102
Q

What is the effect of CCK on the gall bladder?

A

Stimulates contraction

Relaxes the sphincter of Oddi

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103
Q

Describe the basic cause and presentation of steatorrhoea

A

Inadequate bile salts or lipase production

Pale, foul smelling, floating faeces

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104
Q

What is bilirubin?

A

Bile pigment

Breakdown product of haemoglobin

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105
Q

Where is bilirubin conjugated?

A

Liver

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106
Q

Give a cause and symptoms of a blockage in the biliary tree

A

Pre-hepatic jaundice
Pale stools
Dark urine

Pancreatic cancer
Gall stones

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107
Q

What vein drains the small intestine?

A

Superior mesenteric vein

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108
Q

What vein drains the large intestine?

A

Inferior mesenteric vein

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109
Q

What vein does the superior and inferior mesenteric veins drain into?

A

Splenic vein

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110
Q

What veins drain into the portal vein?

A

Splenic

Right and left gastric

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111
Q

Give the branches of the superior mesenteric artery.

A 
Inferior pancreatoduodenal artery
Middle colic artery
Ileocolic artery
Right colic artery
Ileal artery
Duodenal artery
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112
Q

What are the branches of the inferior mesenteric artery?

A

Left colic
Sigmoid
Superior rectal (continuation)

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113
Q

Why is the splenic flexure at especially high risk of ischaemia in a person with hypoxia?

A

It is a ‘watershed area’ where the anastamosis of arteries is poor

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114
Q

Describe the difference between a direct and indirect inguinal hernia.

A

Indirect

  • hernial sac enters the inguinal canal through the deep inguinal ring
  • lateral to the epigastric vessels
  • may extend into the scrotum
  • more common in males

Direct

  • common in older men
  • hernial sac bulges forwards through the posterior wall of the inguinal canal
  • medial to the inferior epigastric vessels
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115
Q

Describe a femoral hernia.

A

The hernial sac descends through the femoral canal, within the femoral sheath.
More common in women
The lacunar ligament can cause strangulation by compressing the blood vessels.

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116
Q

What is an incarcerated hernia?

A

When a loop of intestine becomes trapped in a weak point of the abdominal wall, obstructing the bowel.
Causes pain, nausea, vomiting, and constipation

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117
Q

What is a strangulated hernia?

A

When the blood supply is cut off to tissue in the hernia

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118
Q

What is exomphalos?

A

A congenital umbilical hernia caused by failure of the midgut to return to the abdomen.

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119
Q

What is a Spigelian hernia?

A

Herniation through the aponeurosis of the transverse abdominis, lateral to the lateral edge of the rectus sheath.
Strangulation is a common complication.

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120
Q

What are the basic functions of the stomach?

A

Receive and disrupt food
Continue chemical digestion
Disinfection

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121
Q

What are the orad and caudad regions of the stomach?

A

Orad - fundus and proximal body. Dilates and receives food.

Caudad - distal body and antrum. Constricts and regulates gastric emptying

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122
Q

What is receptive relaxation?

A

Vagally mediated relaxation of the orad stomach which stops the pressure rising too much when food enters, preventing reflux.

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123
Q

What area of the stomach does peristalsis mainly happen in?

A

Antrum

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124
Q

Why is it important for the pyloric sphincter to maintain a small exit from the stomach?

A

To force pieces of food which are too large back into the body of the stomach to be further digested

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125
Q

Where are parietal cells of the stomach mainly found?

A

Fundus and body

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126
Q

What is the function of gastric parietal cells?

A

Secrete HCl and intrinsic factor

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127
Q

Why is intrinsic factor essential?

A

For the absorption of vitamin B12.

Causes pernicious anaemia if absent.

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128
Q

In what region of the stomach are G cells mainly found?

A

Antrum

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129
Q

What is the function of G cells?

A

Secrete gastrin

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130
Q

What is the function of enterochromaffin-like cells in the stomach?

A

Produce histamine

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131
Q

What is the function of Chief cells?

A

Secrete pepsinogen

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132
Q

What is the function of D cells?

A

Secrete somatostatin

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133
Q

What is the function of mucous cells?

A

Secrete mucus and bicarbonate

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134
Q

What is the basic order of cells in a gastric gland from top to bottom?

A

Mucus cells
Parietal cells
Chief cells
Enteroendocrine cells

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135
Q

What substances stimulate parietal cells?

A

Gastrin (on CCK receptor)
Histamine
Acetylcholine (vagus nerve)

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136
Q

What substances stimulate G cells?

A

Digestive breakdown products

Vagus nerve

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137
Q

What stimulates D cells?

A

Drop in pH of the stomach as it empties

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138
Q

Describe the production of acid in the stomach.

A

H+ and Cl- are moved into the stomach lumen by parietal cells. They combine to form HCl.
Intracellular CO2 combines with OH- to form HCO3-, which moves into the bloodstream and creates an alkaline tide.

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139
Q

Describe the cephalic stage of digestion.

A

Activated by smelling, tasting, chewing and swallowing food.
The vagus nerve stimulates parietal cells and releases gastrin related peptide to stimulate G cells.

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140
Q

Describe the gastric stage of digestion.

A

Produces 60% of the total HCl.
Distention of the stomach stimulates the vagus nerve, which stimulates parietal and G cells.
The presence of small peptides and amino acids also stimulates G cells
Food acting as a buffer removes inhibition on gastrin production.

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141
Q

Describe the intestinal stage of digestion.

A

Produces 10% of the total HCl.
Chyme initially stimulates gastrin secretion, but this phase is short and is soon overtaken by the inhibition of G cells.

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142
Q

How does the stomach protect itself from damage?

A

Production of mucus and bicarb which adheres to the lining, keeping epithelial cells at a higher pH.
High turnover of epithelial cells
Prostaglandins cause vasodilation, sustaining good blood flow for repair and regeneration.

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143
Q

Give an example of something which removes the protective layer in the stomach.

A

Alcohol
Heliobacter pylori
NSAIDs

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144
Q

What drugs can be used to reduce acid production in the stomach, and how?

A

H2 inhibitors - cimetidine. Inhibits histamine action on parietal cells

Proton pump inhibitors - omeprazole. Reduces hydrogen ion movement into the stomach lumen.

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145
Q

What connects the gut loop to the yolk sac?

A

Vitelline duct

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146
Q

What rotations does the gut go through during development?

A

3 90 degree turns anti-clockwise

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147
Q

Describe what would happen with incomplete rotation of the midgut.

A

Only one 90 degree rotation occurred so the limbs don’t cross. Will have a left-sided colon.

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148
Q

Describe what would happen with reversed rotation of the midgut in development.

A

The transverse colon will be posterior to the duodenum.

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149
Q

What causes a sub-hepatic caecum?

A

Failure of the caecal bud to descend.

No ascending colon.

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150
Q

Describe a vitelline cyst.

A

The middle of the vitelline duct remains patent and fluid filled.
Fibrous strands form at either end.

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151
Q

Describe a vitelline fistula.

A

Abnormal opening of the bowel causing a leak of intestinal contents through the umbilicus.

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152
Q

Describe Meckel’s diverticulum.

A

May be attached via a fibrous cord to the anterior abdominal wall.
More common in males and may contain ectopic gastric or pancreatic tissue. (If it has this, can have inflammation of the bowel).

Rule of 2’s.

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153
Q

Describe pyloric stenosis.

A

Common in infants
Causes projectile vomiting
Caused by muscle overgrowth

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154
Q

Describe gastroschisis

A

Intestinal loops are outside the body wall because the wall doesn’t close and there is regression of the left umbilical vein.
Linear defects in the anterior abdominal wall
Isolated defect with good prognosis if the bowel loops are healthy.
Has skin cover

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155
Q

Describe omphalocoele.

A

Persistence of the physiological herniation

No skin cover

156
Q

What divides the anal canal and what is its significance?

A

Pectineal line

Above - columnar epithelium, visceral innervation (detects stretch), superior rectal artery supply, internal haemorrhoids

Below - stratified epithelium, somatic innervation (range of feeling), middle and inferior rectal artery supply, external haemorrhoids

157
Q

What is an imperforate anus?

A

Congenital defect where the opening to the anus is missing or blocked.

158
Q

What is anorectal agenesis?

A

Failure of the anus or rectum to form

159
Q

What is a hindgut fistula?

A

A failure of the urogenital sinus and anorectal canal to separate fully, creating abnormal communication.

160
Q

What parts of the gut retain their mesentry?

A 
Jejunum
Ileum
Appendix
Transverse colon
Sigmoid colon
161
Q

What are the adult derivatives of the dorsal mesentry?

A 
Greater omentum
Gastrolineal ligament (stomach to spleen)
Lienorenal ligament (kidney to spleen)
Mesocolon (colon to posterior abdominal wall)
Mesentry proper
162
Q

What are the adult derivatives of the ventral mesentry?

A

Lesser omentum

Falciform ligament

163
Q

What blood vessel supplies the midgut?

A

Superior mesenteric artery

164
Q

What is the innervation of the midgut?

A 
Vagus nerve (parasympathetic)
Superior mesenteric ganglion and plexus (sympathetic)
165
Q

What is the blood supply of the hindgut?

A

Inferior mesenteric artery

166
Q

What is the innervation of the hindgut?

A 
Pelvic nerve (S2,3,4)
Inferior mesenteric ganglion
167
Q

What is secreted by the duodenum when chyme enters?

A

Cholecystekinase
Secretin
Gastrin inhibitory peptides

168
Q

Explain the change in pain location with appendicitis.

A

Pain is initially felt in the midgut region as the appendix has autonomic innervation.
Then the inflammation spreads into the peritoneum, which causes pain to localise due to somatic innervation.

169
Q

What is dyspepsia?

A

A collection of upper GI symptoms

170
Q

Describe the symptoms of gastro-oesophageal reflux disease.

A 
Cough
Wheeze
Burning
Sore throat
Dysphagia
Regurgitation of solids if strictures form
171
Q

Give an example of a condition which can cause gastro-oesophageal reflux disease.

A

Lower oesophageal sphincter problem
Delayed gastric emptying with increased pressure
Hiatus hernia
Obesity

172
Q

What are the treatments for gastro-oesophageal reflux disease?

A

Lifestyle changes e.g small spaced out meals
Antacids
H2 antagonists
Proton pump inhibitors

173
Q

Describe what acute gastritis is.

A

Transient inflammation of the stomach epithelium

174
Q

What can cause acute gastritis?

A

Chronic use of NSAIDs/alcohol
Chemotherapy
Bile reflux (uncommon)

175
Q

What are the symptoms of acute gastritis?

A

Mainly asymptomatic

Nausea
Vomiting
Discomfort
Bleeding

176
Q

Give a cause of chronic gastritis.

A

Heliobacter pylori infection
Autoimmune
Chronic alcohol/NSAID use

177
Q

What are the symptoms of chronic gastritis?

A

Can be asymptomatic

Anorexia
Glossitis
Peptic ulcer
Cancer
Nausea
Vomiting
Bleeding
Neurological (altered gait) and lethargy if autoimmune
178
Q

Describe the causes of peptic ulcer disease.

A

Defects in the gastric or duodenal mucosa, most common in the first part of the duodenum or the lesser curve of the stomach.
Occurs when the normal defence mechanism is breached
E.g. Excess stomach acid, NSAIDs, H pylori, smoking (causes relapse), massive physiological stress.

179
Q

What are the symptoms of peptic ulcer disease?

A

Burning or gnawing pain in the epigastric region or back
Bleeding, melaena, anaemia, haematemesis
Early satiety
Weight loss

If it perforates, leads to peritonitis

180
Q

What tests can you do in dyspepsia?

A

Upper GI endoscopy
Urease breath test for H pylori
Blood test for anaemia
Erect chest x-ray to check for perforation

181
Q

What are the treatments for dyspepsia?

A 
Stop the insulting factor
Eradicate H. pylori (amoxicillin, clathromycin, omeprazole)
Endoscopy to stop bleeding ulcers
Proton pump inhibitor (omeprazole)
H2 blocker (cimetidine/ranitidine)
182
Q

What is the significance of H. pylori producing urease?

A

It converts urea to ammonia, creating an alkali region around it to protect it against stomach acidity.

183
Q

What type of bacteria is Heliobacter pylori?

A

Gram negative

Helical rod

184
Q

Give some ways in which Heliobacter pylori directly damages the gastric epithelium.

A

Cytokines cause epithelial damage
Ammonia is directly toxic
May erode mucus
Promotes inflammatory response (self injury)

185
Q

What is the difference in the effect of Heliobacter pylori when it colonises the antrum in comparison to the body of the stomach?

A

Antrum - stimulates G cells and/or inhibits D cells, producing more acidic chyme. Can cause duodenal metaplasia. This may allow H pylori to also colonise the duodenum, causing duodenal ulceration.

Body - atrophy of parietal cells, leading to gastric ulcers and metaplastic changes. Can cause dysplasia and eventually cancer

186
Q

Describe Zollinger-Ellison syndrome.

A

Non-beta islet cell gastrin-secreting tumour.
Can be part of multiple endocrine neoplasia type I.
Proliferation of parietal cells increases acid secretion, causing severe ulceration of the stomach and small bowel, leading to diarrhoea and abdominal pain.

187
Q

What are the symptoms of stomach cancer?

A 
Dysphagia if in the cardia
Decreased appetite
Weight loss
Malaena if eroded
Nausea and vomiting
Virchow's nodes in left clavicular region.
188
Q

What increases the risk of stomach cancer?

A

High salt intake
Male
Heliobacter pylori
Smoking

189
Q

What type of cancer is stomach cancer normally?

A

Adenocarcinoma

Small number of lymphoma

190
Q

Where does the liver begin to develop?

A

Ventral mesentry

191
Q

What is the falciform ligament?

A

Attaches the anterior surface of the liver to the anterior abdominal wall
Free edge contains the ligamentum teres

192
Q

What are the coronary ligaments of the liver?

A

Attach the superior surface to the diaphragm

193
Q

What are the four anatomical lobes of the liver?

A

Caudate
Left
Right
Quadrate

194
Q

What suspends the liver in the abdomen?

A

Inferior vena cava

195
Q

What is contained in the porta hepatis?

A

Hepatic artery and vein

Common bile duct

196
Q

Draw the biliary tree.

A

Right and left hepatic ducts come from the liver, merge to form the common hepatic duct.
The cystic duct comes from the gall bladder, meets the common hepatic duct, then becomes the common bile duct.
The common bile duct then joins with the pancreatic duct

197
Q

What is divarification of the recti?

A

The linea alba is weak and stretchy, allowing abdominal organs to push through. Not a hernia.

198
Q

When would you perform a grid-iron incision?

A

Appendiectomy

199
Q

Where is foregut pain felt?

A

Epigastric region

200
Q

Where is midgut pain felt?

A

Periumbilical

201
Q

Where is oesophageal pain generally felt?

A

Retrostna

202
Q

Where is hindgut pain generally felt?

A

Suprapubic pain

203
Q

Where can diaphragmatic pain be referred to?

A

Left shoulder tip

204
Q

What is xerostomia?

A

Reduced salivary flow
Causes microbial overgrowth in the mouth and dental caries. Can lead to parotitis if Staphylococcus aureus enters Wharton’s duct.
Caused by dehydration

205
Q

What is achlorhydria?

A

The stomach isn’t able to produce hydrochloric acid.
Seen in pernicious anaemia
Can be caused by H2 antagonist use and proton pump inhibitors

206
Q

What features of the small intestine protect against bacterial colonisation?

A 
Bile
Proteolytic enzymes
Lack of nutrients
Anaerobic environment
Shedding epithelia
Rapid transit
207
Q

What are the innate cellular defences of the gut?

A

Neutrophils
Macrophages
Natural killer cells (kills virally infected cells)
Tissue mast cells
Eosinophils (protect against parasitic infections)

208
Q

Briefly, how can bacterial infections in the gut cause diarrhoea?

A

The bacteria activate the complement pathway, which recruits mast cells. They release histamine causing huge vasodilation, leading to massive water loss.

209
Q

Where is gut associated lymphoid tissue (GALT) mainly found?

A

Tonsils
Peyer’s patches
Appendix

210
Q

What tonsils drain into the cervical lymph nodes?

A

Nasopharyngeal
Linguinal
Pallatine

211
Q

What is the importance of the ileocaecal valve in GI infection?

A

Stops reflux of bacteria into the small intestine from the colon.

212
Q

What is present in the terminal ileum to stop infection?

A

Peyers patches

213
Q

Describe mesenteric adenitis.

A

Right ileac fossa pain in children under 12 which mimics appendicitis.
Cocksackie virus or adenovirus take over Peyers patches

214
Q

What effect can typhoid fever have on the ileum?

A

Cause Peyers patches to become inflamed and may perforate.

215
Q

How can lymphoid hyperplasia precipitate appendicitis?

A

It can trap bacteria in the appendix, allowing them to proliferate and cause infection.

216
Q

Give a cause of appendicitis

A

Lymphoid hyperolasia
Chicken pox
Faecoliths

217
Q

What can cause gut ischaemia?

A

Embolus
Heavy haemorrhage
Systemic hypotension
Arterial disease

218
Q

How can gut ischaemia lead to potentially fatal bacteraemia?

A

It breaks down the gastrointestinal tract’s defensive mechanisms which allows bacteria to invade the bloodstream

219
Q

Give the liver function tests and what functions they are testing.

A 
Hepatocellular damage
  ALT/AST
  Y-GT
Cholestasis
  Bilirubin
  ALP
Synthetic function
  Albumin
  Prothrombin
220
Q

Describe pre-hepatic jaundice.

A

The patient has excessive haemolysis and the liver is unable to cope with the huge load of bilirubin

221
Q

What are the lab findings in pre-hepatic jaundice?

A 
Unconjugated hyperbilirubinaemia
Reticulocytosis
Anaemia
High lactate dehydrogenase
Low haptoglobin
222
Q

Give a cause of pre-hepatic jaundice.

A 
RBC membrane defects (spherocytosis)
Haemoglobin abnormalities (sickle cell)
Metabolic defects
Congenital hyperbilirubinnaemias
Infection
Drugs
Burns
Acquired RBC membrane defects
Immune destruction of RBC
Mechanical destruction of RBC
223
Q

Describe hepatocellular jaundice.

A

Deranged hepatocyte function with an element of cholestasis.

224
Q

What are the lab findings in hepatocellular jaundice?

A

Raised AST/ALT
Normal or raised ALP
Mixed conjugated and unconjugated hyperbilirubinaemia
Abnormal clotting

225
Q

Give a cause of hepatocellular jaundice.

A 
Gilbert's syndrome (jaundice)
Hepatitis A, B, C, E
Autoimmune hepatitis
Alcohol
Wilson's disease
Haemochromatosis
Paracetamol overdose
Cirrhosis
Hepatocellular carcinoma
Metastases
226
Q

What type of virus is hepatitis A and what infectious route does it take?

A

RNA

Faecal-oral

227
Q

What type of virus is hepatitis B and what infectious route does it take?

A

DNA

Blood, saliva, sexual, vertical

228
Q

What type of virus is hepatitis C and what infectious route does it take?

A

RNA

Blood

229
Q

Aside from the viruses, what can cause hepatitis?

A

Drugs (methyl DOPA, isoniazid)
Alpha-1 antitrypsin disease
Wilson’s disease
Autoimmune

230
Q

Give some consequences of alcoholic liver disease.

A 
Alcoholic hepatitis
Cirrhosis
Hepatocellular carcinoma
Liver failure
Wernicke-Korsakoff syndrome
Encephalopathy
Dementia
Epilepsy
231
Q

What is liver cirrhosis?

A

Cell necrosis with nodular regeneration which contains fibrosis.

232
Q

What are the symptoms of liver cirrhosis?

A 
Jaundice
Anaemia
Bruising
Palmar erythema
Duputrens contracture
Flapping tremor
Portal hypertension
Spontaneous bacterial peritonitis
233
Q

What are the lab findings of liver cirrhosis?

A 
Normal or raised AST/ALT
Raised ALP
Raised bilirubin
Low albumin
Deranged clotting
Low sodium
234
Q

How do you manage liver cirrhosis?

A

Stop drinking alcohol
Treat complications
Transplant (if they fit strict criteria)

235
Q

Describe primary biliary cirrhosis and its complications.

A

An autoimmune condition which mainly affects women

Jaundice, pruritis, xanthelasma, hepatosplenomegaly, portal hypertension

236
Q

Describe hereditary haemochromatosis and its complications.

A

An autosomal recessive disorder causing abnormal iron transport and therefore deposits in organs.

Cardiomyopathy, hyperpigmentation, diabetes, hypogonadism

237
Q

Describe Wilson’s disease and its complications.

A

Autosomal recessive disorder causing abnormal copper transport and therefore deposit it in organs.

Hepatitis, cirrhosis, tremor, dysarthria, dementia, renal tubular degeneration, Kayser-Fleischer rings around the eyes

238
Q

Give some causes of portal hypertension

A 
Congenital obstruction
Thrombosis
Tumour
Cirrhosis
Hepatoportal sclerosis
Schistosomiasis
Sarcoidosis
239
Q

Where are there porto-systemic anastamoses?

A 
Oesophagus
Rectum
Mesentry + retroperitoneal veins
Liver to anterior abdominal wall
Liver to diaphragm
240
Q

What is the significance of porto-systemic anastamoses in the rectum and oesophagus in portal hypertension?

A

It causes venous dilations which can protrude into the lumen and become ruptured or ulcerated, causing extreme haemorrhage.

241
Q

What are the signs or symptoms of portal hypertension?

A

Splenomegaly
Ascites
Spider naevi
Caput medusae

242
Q

What is fulminant hepatic failure?

A

Acute decompensation of hepatic function due to increased metabolic demand

243
Q

What are the causes of fulminant hepatic failure?

A 
Hepatitis A, D, E
Drugs (isoniazid, paracetamol, ecstasy)
Wilson's disease
Pregnancy
Reye's syndrome
Alcohol
244
Q

What are the symptoms and signs of fulminant hepatic failure?

A 
Jaundice
Encephalopathy
High ammonium
Hypoglycaemia
Haemorrhage
Low potassium and calcium
245
Q

What is hepatic encephalopathy

A

A reversible neuropsychiatric deficit due to the inability of the liver to remove toxic substances

246
Q

What precipitates hepatic encephalopathy?

A 
Sepsis or infection
Constipation
Diuretics
GI bleeding
Alcohol withdrawal
247
Q

What are the clinical features of hepatic encephalopathy?

A

Raised ammonia
Flapping tremors
Intellectual deterioration

248
Q

Give some examples of benign tumours of the liver

A 
Haemangioma
Focal nodular hyperplasia
Liver cell adenoma
Liver cysts
Polycystic liver disease
Cystadenoma
249
Q

What is the most common malignancy in the liver?

A

Colorectal carcinoma (secondary metastases)

250
Q

What is post-hepatic jaundice?

A

Caused by obstruction in the biliary tree

251
Q

What will a patent with post-hepatic jaundice complain of?

A

Dark urine

Pale, fatty, offensive faeces

252
Q

What are the lab findings in post-hepatic jaundice?

A

Conjugated hyperbilirubinaemia
Raised ALP
Normal or high AST/ALT

253
Q

Give some intrahepatic causes of post-hepatic jaundice.

A

Hepatitis
Drugs
Cirrhosis
Primary biliary cirrhosis

254
Q

Give some extrahepatic causes of post-hepatic jaundice

A 
Gallstones
Biliary stricture or atresia
Carcinoma (e.g. head of pancreas or cholangiocarcinoma)
Pancreatitis
Sclerosing cholangitis
255
Q

What are the risk factors for gallstones?

A 
Female
Increasing age
Obesity
Diet
Developed country
Ileal disease or resection
Haemolytic disease (sickle cell)
256
Q

When can gallstones cause biliary colic?

A

If they are impacted into the wall of the gall bladder. The muscle contracts around it, pain mainly after eating

257
Q

What is the cause of ascending cholangitis?

A

A gallstone blocking the duct, causing infection.

258
Q

What is the triad of symptoms in ascending cholangitis?

A

Right upper quadrant pain
Fever
Jaundice

259
Q

What are the main close anatomical relations to the pancreas?

A

Duodenum
Common bile duct
Portal vein
Coeliac trunk

260
Q

What are the lab findings in a patient with pancreatitis?

A 
High amylase
Low calcium
Hyperglycaemia
High ALP
High bilirubin
261
Q

What are the signs and symptoms of pancreatitis?

A 
Severe pain
Vomiting
Dehydration
Shock or SIRS
Ecchymosis
Ileus
262
Q

What are the effects on the pancreas in chronic pancreatitis?

A

Parenchymal destruction
Fibrosis
Loss of acini
Duct stenosis

263
Q

What are the causes of chronic pancreatitis?

A

Chronic alcoholism
Cystic fibrosis
Biliary disease

264
Q

What are the causes of acute pancreatitis?

A

Excessive alcohol consumption
Gallstones

GET SMASHED

265
Q

What is the main type of pancreatic carcinoma?

A

Ductal adenocarcinoma

266
Q

What are some causes of pancreatic carcinoma?

A

Smoking
Beta-napthylamine
Benzidine
Familial pancreatitis

267
Q

What are the signs and symptoms of pancreatic carcinoma?

A 
Obstructive jaundice
Pain
Vomiting
Carcinomatosis
Gastric outlet obstruction
Malabsorption
Diabetes
268
Q

From superior to inferior, what are the anterolateral abdominal muscles?

A

External oblique
Internal oblique
Transversus abdominis

269
Q

What are the borders of Hesselbach’s triangle?

A

Inguinal ligament
Inferior epigastric vessels
Lateral border of rectus abdominus

270
Q

What type of hernia passes through Hesselbach’s triangle?

A

Direct inguinal hernia

271
Q

What structure does an indirect inguinal hernia pass beneath?

A

Inguinal ligament

272
Q

What structure separates the supracolic and infracolic compartments of the greater sac?

A

Transverse mesocolon

273
Q

Below the arcuate line, what is the posterior surface of the rectus abdominis muscles in contact with?

A

Transversalis fascia

274
Q

What artery does the left gastroepiploic artery branch off?

A

Splenic artery

275
Q

Is the caudate or quadrate lobe more anterior on the inferior side of the liver?

A

Caudate

276
Q

What structure is in the free edge of the lesser omentum?

A

Hepatic artery

277
Q

What is the role of the intestines?

A

Absorb nutrients, water, and electrolytes

278
Q

What factors increase the surface area of the intestines for absorption?

A

Plicae circularis - permanent mucosal folds (villi) in the small intestine
Microvilli

279
Q

Describe the different areas of the intestinal glands.

A

Stem cells at the bottom which are constantly dividing.
Cell amplification just up from the base
Stem cells migrate and differentiate up the crypt

280
Q

What is the function of paneth cells in the crypts of the intestine?

A

Produce antibacterial and antiviral toxins as part of the innate immune system

281
Q

What is anoikis?

A

Programmed cell death when they detach from the intestinal epithelia.

282
Q

What monosaccharides are absorbed by the gut?

A

Fructose
Galactose
Glucose

283
Q

Describe the molecular structure of starch.

A

Amylose (linear glucose, alpha 1-4) and amylopectin (branched glucose, alpha 1-6)

284
Q

What is the function of amylase?

A

Breaks alpha 1-4 bonds in starch to make glucose and maltose from amyloses, and alpha dextrins from amylopectins.

285
Q

What is the function of isomaltase?

A

Breaks alpha 1-6 bonds in starch

286
Q

What enzymes involved in breaking things down into monosaccharides are found on the brush border?

A

Maltase (to glucose)
Alpha dextrinase (to glucose)
Sucrase (to glucose and fructose)
Lactase (to glucose and galactose)

287
Q

Describe the transport of monosaccharides across the epithelia of the intestines?

A

SGLT-1 on the apical membrane to transport glucose/galactose and sodium
GLUT5 on the apical membrane to transport fructose

Na/K ATPase on the basolateral membrane for gradient
GLUT2 on the apical membrane to transport fructose, glucose, and galactose

288
Q

Why is it important to drink sports drinks rather than just water when heavily exercising?

A

They are high in sugar and salt.
The uptake of sodium generates and osmotic gradient and glucose uptake stimulates sodium uptake via SGLT-1.
This allows maximum water absorption

289
Q

What protein breakdown products can be absorbed by the intestine?

A

Amino acids
Dipeptides
Tripeptides

290
Q

What enzyme breaks down proteins in the stomach?

A

Pepsin (from pepsinogen)

Protein to oligopeptides or aa

291
Q

What activates trypsinogen?

A

Enteropeptidase (on the brush border)

292
Q

What produces trypsinogen?

A

Pancreas

293
Q

What is the function of trypsin?

A

Activate proteases

294
Q

What are the important proteases in the small intestine?

A

Chemotrypsin and elastase (endopeptidases)

Carboxypeptidase A/B (exopeptidase)

295
Q

What allows amino acid uptake into epithelial cells of the small intestine?

A

Na-aa cotransporters

296
Q

What allows dipeptide and tripeptide uptake in the small intestine?

A

H+ cotransporter

297
Q

What happens to dipeptides and tripeptides when they are absorbed into intestinal epithelial cells?

A

Broken down to amino acids by cytosolic peptidases

298
Q

What is the difference in sodium absorption between the small and large intestines?

A

Large - sodium channels (induced by aldosterone)

Small - sodium cotransporters

299
Q

How is calcium absorbed in the intestine?

A

Enters the cells by facilitated diffusion
Ca+ATPase removes it on the basolateral membrane
Vitamin D allows calbindin to transport calcium across the cell

Passive paracellular absorption in the distal part of the intestine

300
Q

Describe how iron is absorbed in the intestine.

A

Mostly as haem or Fe2+. Gastric acid is important.
Absorbed across the apical membrane
Binds apoferritin to move across the basolateral membrane
Binds transferrin in the circulation.

301
Q

What vitamins can be absorbed using sodium cotransport in the intestine?

A

B and C

They are water soluble

302
Q

What is vitamin B12 absorption dependent on?

A

Intrinsic factor

303
Q

Where does vitamin B12 absorption occur?

A

Terminal ileum

304
Q

Describe the three types of motility seen in the small intestine.

A

Intestinal gradient - between meals, pacemakers have a higher frequency proximally. Drives slow caudal progression of contents

Segmentation - occurs following meals, causing a back-and-forth movement to mix contents and allow absorption.

Peristalsis - serves to move contents down the intestine

305
Q

What are the two types of motility seen in the large intestine?

A

Segmentation - also known as haustral shuttling. Occurs in the proximal colon due to the 3 bands of muscle going in different directions. Agitates and mixes the contents to absorb most of the remaining water.

Mass movement - gastrocolic reflex. Occurs 1-3 times a day, moving contents rapidly from transverse colon to rectum.

306
Q

What is the taenia coli?

A

Longitudinal muscle in the large intestine

307
Q

What is the difference between the internal and external anal sphincters?

A

Internal - smooth muscle, parasympathetic control

External - striated muscle, voluntary control

308
Q

Where in the GI tract can Crohn’s disease occur?

A

Anywhere

309
Q

Where in the GI tract can ulcerative colitis occur?

A

Rectum and/or colon

310
Q

Is there rectal involvement in Crohn’s disease?

A

No

311
Q

Is there rectal involvement in ulcerative colitis?

A

Yes

312
Q

Is there gross bleeding in Crohn’s disease?

A

25% of the time

313
Q

Is there gross bleeding in ulcerative colitis?

A

Yes

314
Q

Is there perianal disease in Crohn’s disease?

A

75% of the time

315
Q

Is there perianal disease in ulcerative colitis?

A

Rarely

316
Q

Is there fistula formation in Crohn’s disease?

A

Yes

317
Q

Is there fistula formation in ulcerative colitis?

A

No

318
Q

Is there malnutrition in Crohn’s disease?

A

Potentially

319
Q

Is there malnutrition in ulcerative colitis?

A

No

320
Q

Is there transmural inflammation in Crohn’s disease?

A

Yes

321
Q

Is there transmural inflammation in ulcerative colitis?

A

Rarely

322
Q

Are there granulomas in Crohn’s disease?

A

Up to 75% of the time

323
Q

Are there granulomas in ulcerative colitis?

A

No

324
Q

Is there fibrosis in Crohn’s disease?

A

Commonly

325
Q

Is there fibrosis in ulcerative colitis?

A

No

326
Q

Are there crypt abcesses in ulcerative colitis?

A

Yes

327
Q

Are there crypt abscesses in Crohn’s disease?

A

Rarely

328
Q

What mucosal involvement is there in Crohn’s disease?

A

Skip lesions

329
Q

What mucosal involvement is there in ulcerative colitis?

A

Continuous

330
Q

Are there apthous ulcers in Crohn’s disease?

A

Yes

331
Q

Are there apthous ulcers in ulcerative colitis?

A

Rarely

332
Q

Are there linear ulcers in Crohn’s disease?

A

Yes

333
Q

Are there linear ulcers in ulcerative colitis?

A

Rarely

334
Q

Is there friable mucosa in Crohn’s disease?

A

Rarely

335
Q

Is there friable mucosa in ulcerative colitis?

A

Yes

336
Q

Is there cobblestone mucosa in Crohn’s disease?

A

Yes if severe

337
Q

Is there cobblestone mucosa in ulcerative colitis?

A

No

338
Q

Is there narrowing in Crohn’s disease?

A

Yes

339
Q

Is there narrowing in ulcerative colitis?

A

Rarely

340
Q

What investigations would you do in suspected ulcerative colitis?

A 
Bloods - anaemia/serum markers
Stool cultures
Plain abdominal radiographs
Barium enema if mild
CT/MRI if complicated 
Colonoscopy
341
Q

What is inflammatory bowel disease?

A

A group of conditions characterised by idiopathic inflammation of the GI tract.

342
Q

What is the presentation of Crohn’s disease?

A 
Tender mass in the right lower quadrant
Mild perianal inflammation or ulceration
Low grade fever
Weight loss
Mild anaemia
Joint pains
343
Q

What is the gross pathology of Crohn’s disease?

A 
Hyperaemia
Mucosal oedema
Discrete superficial ulcers
Deeper ulcers
Transmural inflammation (thickened bowel wall with narrowed lumen)
Cobblestone appearance
Fistulae
344
Q

What investigations would you do in suspected Crohn’s disease?

A

Bloods - anaemia
CT/MRI scans - bowel wall thickening, obstruction, extramural problems
Barium enema - stricture problems
Colonoscopy

345
Q

What is the presentation of ulcerative colitis?

A 
Mildly tender abdomen
No perianal disease
Normal temperature
Weight loss
Mild lower abdominal cramps
Mucus and blood in stools
346
Q

What are the pathological changes in ulcerative colitis?

A 
Chronic inflammatory filtrate of the lamina propria
Crypt abscesses 
Low number of goblet cells
Pseudopolyps
Loss of haustra
347
Q

Where does ulcerative colitis begin?

A

In the rectum

348
Q

What extraintestinal problems can be seen in ulcerative colitis and Crohn’s disease?

A

MSK pain - arthritis
Skin - erythema nodosum, pyoderma gangrenosum, psoriasis
Liver and biliary tree - primary sclerosing cholangitis
Eye problems

349
Q

What pharmacological treatments are there for ulcerative colitis and Crohn’s disease?

A

Aminosalicylates (sulphasalazine) for flares and remission
Steroids (prednisolone) for flares only
Immunomodulators for fistulas/remission

350
Q

What effect can surgery have in Crohn’s disease?

A

Correct strictures and fistulas
Can’t treat
As little bowel must be removed as possible

351
Q

What effect can surgery have in ulcerative colitis?

A

Colectomy can cure it.

Used when there are precancerous changes or toxic megacolon

352
Q

What is Zollinger-Ellison syndrome?

A

A gastrin secreting tumour or hyperplasia of islet cells in the pancreas, leading to peptic ulcers

353
Q

What is mass movement?

A

Rapid movement of colonic content

354
Q

What can be caused by a stone blocking the cystic duct?

A

Cholecystitis

Biliary colic

355
Q

What can be caused by a stone blocking the common bile duct?

A

Cholangitis

Jaundice

356
Q

What can be caused by a stone blocking the ampulla of Vater or sphincter of Oddi?

A

Cholangitis
Jaundice
Pancreatitis
Steatorrhoea

357
Q

What salivary gland mainly secretes serous fluid?

A

Parotid gland

358
Q

When can swallowing solids be harder than liquids?

A

Any physical obstruction
Cancer
Fibrous strictures
External compression

359
Q

What are the investigations for dysphagia?

A

Barium swallow
OGD

CXR for external compression

360
Q

What is the difference in opening of the peritoneal cavity in males and females?

A

Males - enclosed

Females - open via the ifundibulum of the fallopian tube

361
Q

What causes Meckel’s diverticulum?

A

Incomplete obliteration of the vitelline duct

362
Q

What lies in front of the lesser sac in the abdomen?

A

Liver
Lesser omentum
Stomach

363
Q

What structures lie anteriorly to the foramen of Winslow (epiploic foramen)?

A

Common hepatic artery
Common bile duct
Portal vein

364
Q

What hormone stimulates enzyme rich pancreatic secretions?

A

Cholecystikinin

365
Q

What hormone stimulates bicarbonate rich secretions from the pancreas?

A

Secretin

366
Q

What are obligate anaerobes?

Give an example.

A

Bacteria which die in the presence of oxygen.

Clostridial organisms.

367
Q

What are facultative anaerobes?

Give an example.

A

Organisms which prefer oxygen but can live without it.
E. Coli
Staphylococcu

368
Q

What are obligate aerobes?

Give an example.

A

Organisms which must have oxygen to survive.
Pseudomonas
Mycobacterium tuberculosis

369
Q

What are the anaerobic zones of the gastrointestinal tract?

A

Parts of the mouth (deep in taste buds, biofilm around teeth, peridontal pockets in peridontal disease)
Small bowel
Colon

370
Q

What are the functions of human colonic bacteria?

A

Synthesise and excrete vitamins K, B12, thiamine
Prevent colonisation by pathogens
Kill non-indigenous bacteria
Stimulate MALT development
Stimulate production of natural antibodies

371
Q

Describe noma oris.

A

An oro-facial gangrene caused by commensal organisms in the mouth when the person is malnourished, dehydrated, immunocompromised, or systemically unwell.

372
Q

Describe oral thrush.

A

Candida albicans infection in the mouth creating white plaques which can be easily removed, leaving red, sore areas.
Seen in patients taking antibiotics, diabetes, inhaled steroids, newborns

373
Q

Why are people with prosthetic heart valves at greater risk of endocarditis due to Strep viridans?

A

Strep viridans causes transient bacteraemia in many people when they brush their teeth. It is unable to stick to cells due to their protective membranes.
Prosthetic heart valves don’t have these membranes, so the bacteria can more easily stick to them and colonise, causing endocarditis.

374
Q

What is the difference between bacteraemia and septicaemia?

A

Bacteraemia - bacteria are cleared quickly from the bloodstream.
Septicaemia - bacteria multiply in the bloodstream, symptoms of sepsis develop.

375
Q

What are the principles in prophylactic antibiotic treatment for surgery on the gut?

A

An antibiotic which kills anaerobes with a broad-spectrum antibiotic

376
Q

How does lactobacillus in the vagina prevent colonisation by other bacteria?

A

Converts glycogen to lactic acid, creating an acidic environment which other bacteria can’t grow in.

377
Q

What is the most common cause of urinary tract infections?

A

E. coli

378
Q

What types of bacteria don’t cause urinary tract infections?

A

Gram positive bacilli (lactobacillus)

Gram negative cocci (gonococci)

379
Q

Which organisms causing a urinary tract infection would you expect to have underlying pathology associated with?

A

Klebsiella
Proteus
Pseudomonas

380
Q

What are the symptoms of tetanus?

A 
Muscle spasm
Risus sardonicus (sardonic smile)
Lockjaw
Opisthotomas
Spasm of the larynx
381
Q

What makes up the superior wall of the inguinal canal?

A

Internal oblique and transversus abdominis muscles

382
Q

What makes up the anterior wall of the inguinal canal?

A

Aponeurosis of the external oblique and internal oblique.

383
Q

What makes up the lower wall of the inguinal canal?

A

Inguinal and lacunar ligaments

384
Q

What makes up the posterior wall of the inguinal canal?

A

Transversalis fascia and the conjoint tendon

385
Q

Give the borders of Hesselbach’s triangle.

A

Medial: lateral margin of the rectus sheath (Linea semilunaris)
Inferior: inguinal ligament
Superolateral: inferior epigastric vessels

ESA 3 (5 decks)

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