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ESA 3 > GI > Flashcards

GI Flashcards

1
Q

What are the circular folds of mucosa in the jejenum called?

A

Plicae circulares, increase SA for absorption

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2
Q

Where in the GI tract has somatic control?

A

Mouth and first 1/3rd oesophagus, and last sphincter of the anus

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3
Q

Which plexuses of the autonomic nervous system control the GI tract?

A

Submucosal plexus and the myenteric plexus.

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4
Q

What is dysphagia?

A

Difficulty swallowing

Either due to neurological deficit or musculature problems/ obstruction of oesophagus

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5
Q

What are the regions of the stomach?

A

Cardia, fundus, body, antrum and pylorum

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6
Q

What is the normal epithelium of the oesophagus?

A

Stratified squamous

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7
Q

What is Barrett’s oesophagus?

A

Chronic reflux of acidic stomach contents causing metaplasia of oesophagus mucosa from stratified squamous to gastric columnar.
This can predispose to adenocarcinoma within the oesophagus.

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8
Q

Via which veins does blood normally drain from the oesophagus?

A

Via left gastric into the portal venous system, and via azygos vein to the systemic system.

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9
Q

Which mechanism of the lower oesophageal sphincter prevent reflux of stomach contents?

A
  • acute angle of entry
  • mucosal folds at end of oesophagus
  • higher abdominal pressure than thoracic pressure
  • right crus of the diaphragm acts as a sling round the oesophagus
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10
Q

If an ulcer erodes posteriorly through the first part of the duodenum, what can be damaged?

A

Gastroduodenal artery

Can haemorrhage and result in haematemesis and malaena

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11
Q

Which part of the GI tract absorbs the majority of fluid?

A

Small intestine (approx 12.5l while larger intestine absorbs approx 1.35l)

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12
Q

What is the dentate (penctinate) line?

A

Junction in the anal canal with columnar epithelia above and stratified squamous epithelia below. Hence above dentate line can get adenocarcinoma and squamous cell carcinoma below.

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13
Q

What is Meckel’s diverticulum?

A

Remnant of embryonic Vitelline duct, bulging from ilium. Causes bleeding and inflammation. Rule of 2s (2 inches long, 2 ft from iliocaecal valve, 2% of population).

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14
Q

What are some functions of saliva?

A 
Speaking
Antimicrobial 
Oral hygiene
Lubricates food
Begins digestion of carbohydrates 
Enables taste
Disease transmission
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15
Q

What is the clinical term for a dry mouth, and how does it present?

A

Xerostomia:
Red inflamed tongue, sore lips, difficulty breathing, less taste
Due to insufficient salvia production

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16
Q

What are the components of saliva?

A 
Mostly water (hypotonic solution)
K+ and bicarbonate (alkaline compared to plasma)
Mucus
Enzymes eg amylase
Immune proteins eg lysozyme, IgA
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17
Q

What are the 3 paired salivary glands?

A

Submandibular (secretes most volume, both serous and viscous)

Parotid (serous salvia, rich in enzymes but little mucus)

Sublingual (viscous salvia, rich in mucus but little enzymes)

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18
Q

What is the mechanism of saliva secretion?

A

Saliva is hypotonic, but no mechanism for water secretion.

So, acinar cells secrete water, mucus and enzymes (isotonic to plasma)
Ductal cells modify solution by reabsorbing Na and Cl out of saliva, and insert HCO3- & K+
Tights junctions means water cannot be reabsorbed too

(Net effect is hypotonic salvia as more Na & Cl out than HCO3- & K+ in)

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19
Q

What is the neural control of salivary glands?

A

Mainly stimulated by parasympathetic (increase saliva production), but also slight sympathetic stimulation (reduces blood flow, less salvia, nervous dry mouth)

Parotid by glossopharyngeal nerve (9th cranial nerve), submandibular & sublingual by branches of facial nerve.

No hormonal influence, only ANS.

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20
Q

How does high flow rate of saliva affect its composition?

A

Fast flow rate = less modification, except bicarbonate that gets secreted at great quantities at higher flow rate

So saliva would have more Na, Cl and HCO3- but less K+. Hence saliva becomes less hypotonic but more alkaline!!!

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21
Q

What are the 3 phases of swallowing?

A
  1. Oral (voluntary)
    Tongue pushes bolus to pharynx
  2. Pharyngeal (involuntary)
    Soft palate seals off nasopharynx, epiglottitis shuts, vocal cords adduct, breathing temporarily stops, upper oesophageal sphincter opens
  3. Oesophageal (involuntary)
    Peristalsis sweeps bolus down oesophagus to stomach
    Upper oesophageal sphincter shuts & lower sphincter opens
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22
Q

What are the terms for dysphagia for solids and dysphagia for fluids.

A

Difficulty swallowing foods = oesophageal dysphagia

Difficulty swallowing liquids = oropharyngeal dysphagia

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23
Q

What are the layers of the abdominal wall?

A

Rectus abdominis and external obliques -> internal obliques -> transversalis abdominis -> transversalis fascia -> peritoneum

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24
Q

What is the arcuate (douglas’s) line?

A

1/3rd from the umbilicus to pubic symphysis. Represents when sheath is only anterior

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25
Q

Where is an incision for an appendicectomy done?

A

At McBurney’s point, 2/3rds from the umbilicus to ASIS via a grid iron incision

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26
Q

What is a patent urachus?

A

When allantois remains open, forming an open channel between bladder and umbilicus.
Can present at birth or later in life in men which bladder outflow obstruction/ prostatic hypertrophy that will increase bladder pressure and force urine out of umbilicus.

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27
Q

What is the difference between exampholos and gastroschisis?

A

Both are umbilical defects.
Exampholos is when the viscera is covered by peritoneum and amnion. Gastroschisis is when viscera is not covered. Gastroschisis is the the right of the umbilicus.

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28
Q

What causes visceral pain?

A

Stretch, ischamia, abnormally strong muscle contraction, inflammation.

NOT touch/burning/crushing.

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29
Q

Where is visceral pain from the foregut, midgut and hindgut felt?

A

Foregut: epigastric
Midgut: periumbilical
Hindgut: suprapubic

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30
Q

What are the borders of the inguinal canal?

A 
Floor = inguinal ligament (& lacunae ligament medially)
Posterior = transversalis fascia 
Anterior = aponeurosis of external oblique
Roof = internal oblique/ transversalis muscle
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31
Q

Failure of which embryonic structure to degenerate can lead to an indirect inguinal hernia?

A

Processus vaginalis

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32
Q

What is the different between the mid point of the inguinal ligament and the mid inguinal point?

A

Mid point of inguinal ligament = from ASIS to pubic tubercle

Mic inguinal point = ASIS to pubic symphysis (femoral artery just below)

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33
Q

What are the borders of Hesselbachs triangle?

A 
Medial = rectus abdominis
Lateral = epigastric vessels
Floor = inguinal ligament
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34
Q

Which type of inguinal hernia begins medial to the epigastric vessels?

A

Direct

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35
Q

What is the difference between indirect and direct inguinal hernias?

A

Direct is through weakness in Hesselbachs triangle, near superficial ring, medial to epigastric vessels

Indirect is lateral to inferior epigastric vessels, through deep then superficial rings

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36
Q

What is the difference between the terms incarcerated and strangulated?

A

Incarcerated means irreducible, stuck

Strangulated means blood supply is disrupted and can lead to necrosis

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37
Q

What are the greater and lesser omentum?

A

Omentum is a double layer of peritoneum that attaches the stomach to another viscus.

Greater omentum from greater curvature like an apron

Lesser omentum from lesser curvature to liver (forms hepatoduodenal ligament at its free edge)

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38
Q

What are the branches of the coeliac trunk?

A

Left gastric, splenic and common hepatic

Stomach is supplied by all 3!!!

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39
Q

Describe the blood supply to the stomach

A

L gastric artery for coeliac trunk runs along lesser curvature and anastomoses to R gastric artery which branches from common hepatic (from coeliac trunk).

R gastro-omental (terminal branch of gastroduodenal from common hepatic a.) along greater curvature anastomoses with L gastro-omental (branch of splenic a.)

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40
Q

What are sliding and rolling hiatus hernias?

A

Sliding is when lower oesophageal sphincter slide superior (more common and cause reflux!)

Rolling is when part of stomach herniates into chest

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41
Q

What separates the supra and infra colic regions?

A

Transverse mesocolon

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42
Q

A gastric ulcer would rupture which artery compared to a duodenal ulcer?

A

Gastric ulcer would rupture splenic artery

Duodenal artery would rupture gastroduodenal artery

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43
Q

What is the passage between the greater and lesser sac known as?

A

Epiploic foramen

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44
Q

How is HCl secretion controlled?

A

Parietal cell is stimulated by:

  • gastrin from G cells
  • histamine from ECL cells
  • ACh from parasympathetic stimulation via vagus nerve
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45
Q

How is HCl production inhibited?

A

Food leaves stomach causing its pH to drop, low pH activates D cells to produce somatostatin which inhibits G cells

Food leaving also reduces stomach distension so vagal activity is reduced

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46
Q

What is the first phase of digestion?

A

Cephalic

Smell and taste of food will stimulate parietal cell by vagal nerve (parasympathetic stimulation)

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47
Q

What is the second phase of digestion?

A

Gastric
Distension of stomach due to food stimulates parietal and G cells
Presence of AA and small peptides stimulates G cells
Food acts as a buffer to remove inhibition of gastrin production

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48
Q

What is the third phase of digestion?

A

Intestinal

Chyme initially stimulates gastrin secretion
Overtaken by inhibition of G cells ( presence of lipids activates enterogastric reflex, reduces vagal stimulation )
Chyme stimulates secretin and CCK

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49
Q

How is the stomach itself protected from the acidic conditions?

A

Mucous cells secrete mucus to form thick alkaline layer
Prostaglandins maintain mucosal blood flow
Also high turnover of epithelial cells

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50
Q

What can breach stomach defences?

A
  • alcohol dissolves mucus layer
  • NSAIDS inhibit prostaglandin
  • H pylori causes chronic gastritis
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51
Q

What pharmacological intervention can be used to reduce stomach acid secretion?

A 
PPIs eg Omeprazole 
H2 antagonists (block affect of histamine) eg ranitidine
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52
Q

What is the different between the foregut, midgut and hindgut in terms of mesentery?

A

Forget has both ventral and dorsal mesentery

Mid but and hindgut only have dorsal mesentery

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53
Q

How does the liver attach to the anterior abdominal wall?

A

Falciform ligament
(remnant of ventral mesentery of foregut, also separates right and left lobes)

Falciform ligament branches into R&L coronary ligaments (attach liver to diaphragm) then reflects into R&L triangular ligaments

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54
Q

What lies within the free edge of the lesser omentum?

A

(Free edge forms because only the forgot has ventral mesentery hence free edge below where midgut and hindgut do not have this ventral mesentery)

Portal vein
Common bile duct
Hepatic artery

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55
Q

Is the duodenum retroperitoneal?

A

First part is intra peritoneal

Rest of it is retroperitoneal

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56
Q

Is the duodenum in the foregut or midgut?

A

First half in foregut

Second half in midgut

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57
Q

What are the divisions of the biliary tree?

A

At liver, R&L hepatic ducts converge to form common hepatic duct. Cystic duct connects to gallbladder from common hepatic duct.
Common hepatic duct then becomes the common bile duct, where the pancreatic duct later joins into.

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58
Q

What anatomical structure determines the control of secretions from the biliary tree into the duodenum?

A

Sphincter of Oddi

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59
Q

What is Zollinger Ellison syndrome?

A

Non-beta islet cell gastrin secreting tumour of the pancreas that stimulates proliferation of stomachs parietal cells, hence a high acid production.

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60
Q

What are some causes of acute gastritis?

A

Alcohol
NSAIDs
Chemotherapy
Bile reflux

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61
Q

What are causes of chronic gastritis?

A
  • Helicobacter pylori infection
  • Autoimmune (antibodies attack parietal cells, can lead to pernicious anaemia in which intrinsic factor cannot be produced so vitamin B12 cannot be absorbed)
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62
Q

Where must peptic ulcers extend through?

A

Muscularis mucosa

63
Q

What can cause peptic ulcers?

A 
Stomach acid
H pylori
NSAIDs
Smoking
Severe stress (ie burns, sepsis, organ failure)
64
Q

How can GI pathology be investigated?

A 
Endoscopy
Biopsy
Urease breath test 
Blood test for anaemia
Chest x Ray for perforation
65
Q

How does the urease breath test work?

A

Indicates H pylori presence as H pylori can convert urea to CO2 and ammonia via urease enzyme, so after swallowing radioactivively labelled urea the patient will breath out the CO2 isotope if H pylori is present

66
Q

What treatment can be used for gastritis and a H pylori infection infection?

A
  • eradicate H pylori with triple therapy of PPI+amoxicillin+clarithromycin
  • stop NSAIDs
  • PPIs
67
Q

What is H pylori and how is it transmitted?

A
  • Faecal oral/ oral route
  • Gram negative
  • Survives acidic conditions by converting urea to CO2 and ammonia via urease to form alkaline cloud around itself
  • Ammonia produced is toxic to stomach epithelium
  • H pylori is also cytotoxic
  • Promotes inflammation and may degrade mucous layer
68
Q

What is an example of a PPI?

A

Omeprazole

69
Q

What is an example of a H2 antagonist?

A

Ranitidine

70
Q

What is the tonicity of chyme entering the duodenum from the stomach and when it leaves the duodenum?

A

Hypertonic but becomes isotonic

(Because food produces lots of solutes and stomach is largely impermeable to water, unlike duodenum where it can become isotonic)

71
Q

What stimulates the acinus of the pancreas?

A

Vagus and CCK

due to hypertonicity, fats and peptides detected in duodenum

72
Q

After stimulation, what does the pancreas acinus release?

A

Enzymes:

  • amylases and lipases in active form
  • proteases in inactive form (zymogens), Trypsin activates other proteases
73
Q

After stimulation, what do the pancreatic ductal cells release?

A
  • Isotonic solution

- HCO3- (to neutralise acidic chyme)

74
Q

What stimulates pancreatic ductal cells to release HCO3-?

A

Secretin

75
Q

At higher flow rates, does secretion of HCO3- increase or decrease?

A

Increase

76
Q

The functional unit of the liver is the acinus, if there is a drop in oxygen high zone will undergo hypoxic damage and why?

A

Zone 3 as it is furthest away from the portal triad where oxygenated blood comes into the liver via hepatic artery and portal vein

77
Q

The functional unit of the liver is the acinus, if there is toxic damage which zone will undergo most damaged and why?

A

Zone 1 as it is closest to the portal triads

78
Q

What are bile salts?

A

Bile acids conjugated with an amino acid
Ampithatic structure
Used because bile salts are not always soluble at duodenal pH

79
Q

What is the function of bile acids?

A

Lipids form large globules at the end of the duodenum so have low SA for enzymes to act
Bile acids emulsify fats into smaller units to increase SA for lipases to act
Bile acids then form micelles to carry products of fat breakdown to intestinal epithelial cells
Lipids here are re-esterified (to phospholipids, cholesterol, triglycerides) and packaged with apoplipoproteins to form chylomicrons and enter lymphatic system then rejoin vascular circulation
Bile salts resorbed in ileum, return to liver and are reused

80
Q

What stimulates the gallbladder to contract and release bile?

A

CCK from duodenum causes Sphincter of Oddi

81
Q

What happens if bile acids or pancreatic lipases are not release in adequate amounts?

A

Steatorrhea (fat in faeces, pale, foul smelling and floats)

82
Q

What is the inferior mesenteric artery renamed as it crosses into the pelvis?

A

Superior rectal artery

83
Q

What are the specialised liver macrophages that line the sinusoids?

A

Kupffer cells

84
Q

Ammonia produced by bacteria can accumulate in liver failure if it not cleared by the urea cycle. What can this cause?

A

Hepatic encephalopathy

Ammonia can cross blood brain barrier

85
Q

What affect can portal hypertension have?

A 
Portal systemic shunting
Leading to:
 -haemorrhoids 
 -caput medusa
 -oesophageal varices
86
Q

Where is gut associated lymphoid tissue?

A
  • tonsils
  • Peyer’s patches
  • appendix
87
Q

What are Peyer’s patches?

A

Patches of lymphoid tissue in the small intestine, especially the ileum.
Form part of the immune system to prevent the growth of pathogens.

(Become inflamed in typhoid fever)

88
Q

What can cause appendicitis?

A
  • lymphoid hyperplasia -> obstructs outflow -> stasis and infection
  • faecolith (calcified faeces in the colon that can obstruct the appendix)
89
Q

What are the functions of the liver?

A
  • detoxification (drugs, toxins)
  • glycogen storage (gluconeogenesis)
  • bile production
  • production of plasma proteins (clotting factors, albumin)
  • metabolism (alcohol, proteins, lipids)
90
Q

How does liver disease lead to ascites?

A

Less production of plasma proteins -> low oncotic pressure in plasma -> draws fluid into peritoneal cavity

91
Q

What is pre hepatic jaundice?

A

Increased bilrubin overwhelms liver (eg haemolytic anaemia causing excessive RBC breakdown)
Liver unable to conjugate all of the bilirubin
Hence rise in unconjugated levels

92
Q

What is hepatic jaundice?

A

Reduced rate of conjugation due to liver injury/ damage (eg Gilberts disease)
Causes a rise in both conjugated and unconjugated bilrubin

93
Q

What is post-hepatic jaundice?

A

Obstruction to the biliary tree (eg gallstones in common bile duct) means conjugated bilirubin cannot drain into duodenum
Instead the bilirubin refluxes into circulation and is not excreted in stool, hence pale fatty stool (steatorrhea)

94
Q

What enzymes can show on liver function tests?

A

Enzymes can leak from damaged hepatocytes:

  • AST & ALT
  • ALP (alkaline phosphatase)
  • GGT (gamma glutamyltransferase)
  • bilirubin
95
Q

What is a better measure of true liver function (rather than damage)?

A

Levels of albumin and clotting factors

96
Q

What are the possible sites of porto-systemic anastomoses and what are the veins involved?

A

“butt, gut and caput”, distended veins at these sites

  • oesophageal varices (left gastric vein -> oesophageal branches of azygos)
  • anorectal varices (superior rectal -> middle and inferior rectal veins)
  • caput medusa (paraumbilical to superficial and inferior epigastric veins)
97
Q

Other than porto-systemic anastomoses, what else can portal hypertension lead to?

A

Ascites and splenomegaly

98
Q

What is the most common cancer of the pancreas?

A

Ductal adenocarcinoma

99
Q

What is acute pancreatitis?

A

Damaged acinar cells release their enzymes and cause inflammation of pancreatic tissue.
Eg due to gallstones or alcohol

100
Q

What is a common cause of portal hypertension?

A

Cirrhosis

Fibrotic nodular changes in liver can cause narrowings in hepatic veins and portal vein

101
Q

What is a portal systemic anastomoses?

A

Due to portal hypertension in the portal veins, blood is shunted away from the portal vein and to the systemic circulation. This leads to enlarged, distended veins (butt gut and caput).

102
Q

Name one bacteria that is resistant to stomach acid

A

Mycobacterium tuberculosis

103
Q

What is mesenteric adenitis and what is its importance?

A

Self limiting inflammatory response when mesenteric lymph nodes in lower right quadrant become inflamed.
Can mimic late stage appendicitis.

104
Q

Is AST or ALT better to specifically indicate liver damage?

A

ALT as it is specific to the liver, whereas AST is present in other parts of the body.

105
Q

What are the circular folds of the small intestines called?

A

Plicae circulares, contain villi and Microvilli to further increase SA for absorption

106
Q

Why must carbohydrates be broken down?

A

Because only monosaccharides can be absorbed

107
Q

What is starch composed of, what are the binds between them and what can break down these bonds?

A
  • 20% amylose which is glucose monomers joined by alpha-1,4 bonds. Can be broken by amylase.
  • 80% amylopectin which has alpha-1,4 bonds along the chains (can be broken by amylase), and alpha-1,6 bonds between the chains (can be broken my isomaltase to break the alpha dextrins)
108
Q

How is glucose or galactose reabsorbed from the intestines?

A

Can only be coabsorbed with Na!!!

Na/K-ATPase on basolateral membrane sets up concentration gradient
SGLT1 on apical allows Na and glucose to enter
Exits down conc gradient via GLUT2 on basolateral membrane, into blood

109
Q

What is the principle behind oral rehydration therapy?

A

Give a mixture of Na with glucose to allow maximum water reabsorption as water will follow Na (and the Na is absorbed along with the glucose)

110
Q

How is trypsin oven converted to trypsin?

A

By enteropeptidase

111
Q

What happens to pepsinogen released from chief cells in the stomach?

A

Converted to pepsin by HCl

Pepsin can then act on proteins

112
Q

What is the difference between endopeptidase and exopeptidases, with examples?

A

Exopeptidases act on the ends of proteins to produce individual amino acids or dipeptides. Eg carboxypeptidase A B

Endopeptidase so act within the protein chain to form shorter peptides. Eg trypsin, elastase, chymotrypsin

113
Q

How does Ca reabsorption in the intestines differ when intake is low or normal/ high?

A

Low intake: Ca enters on apical membrane via facilitated diffusion. Leaves on basolateral via Ca-ATPase. This process requires vitamin D (calbindin) and is stimulated by PTH.

Normal intake: passive paracellular uptake through tight junctions

114
Q

How is the contents of the small intestines moved?

A
  • intestinal gradient between meals, set by intestinal pacemakers
  • segmentation following meals
  • peristalsis
115
Q

How is the contents of the large intestine moved?

A
  • segmentation (haustral shuffling) in the proximal colon which allows most of remaining water to be absorbed so faeces can form
  • mass movement 1-3 times per day can rapidly move food from transverse colon to rectum
116
Q

What are the taenia Coli?

A

3 longitudinal bands of muscle that run all along the large intestine

117
Q

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

A

Internal: parasympathetic control, smooth muscle

External: voluntary control, striated muscle

118
Q

What are common health problems that affect patients with IBD?

A

Arthritis!

Also possible skin problems eg psoriasis, liver problems or eye problems although rare

119
Q

What are the key difference between ulcerative colitis and Crohn’s?

A

Crohn’s:

  • anywhere in GI tract
  • transmural (deep)
  • skip lesions
  • cobblestone appearance with discrete ulcers
  • fistulae
  • granulomas

UC:

  • usually begins in rectum and can work proximally to involve colon
  • continuous
  • superficial
  • Crypt abscesses
  • friable
120
Q

How can IBD be investigated?

A
  • colonoscopy
  • bloods (anaemia)
  • stool cultures
  • barium enema
  • CT/MRI
121
Q

How is glucose or galactose reabsorbed from the intestines?

A

Can only be coabsorbed with Na!!!

Na/K-ATPase on basolateral membrane sets up concentration gradient
SGLT1 on apical allows Na and glucose to enter
Exits down conc gradient via GLUT2 on basolateral membrane, into blood

122
Q

What is the principle behind oral rehydration therapy?

A

Give a mixture of Na with glucose to allow ,animus water reabsorption as water will follow Na

123
Q

How is trypsin oven converted to trypsin?

A

By enteropeptidase

124
Q

What happens to pepsinogen released from chief cells in the stomach?

A

Converted to pepsin by HCl

Pepsin can then act on proteins

125
Q

What is the difference between endopeptidase and exopeptidases, with examples?

A

Exopeptidases act on the ends of proteins to produce individual amino acids or dipeptides. Eg carboxypeptidase A & B

Endopeptidase so act within the protein chain to form shorter peptides. Eg trypsin, elastase, chymotrypsim

126
Q

How does Ca reabsorption in the intestines differ when intake is low or normal/ high?

A

Low intake: Ca enters on apical membrane via facilitated diffusion. Leaves on basolateral via Ca-ATPase. This process requires vitamin D (calbindin) and is stimulated by PTH.

Normal intake: passive paracellular uptake through tight junctions

127
Q

What are the pharmacological treatments available for IBD?

A
  • aminosalicylates
  • corticosteroids (flares only, don’t give steroids long term)
  • immune modulators
128
Q

Can Crohn’s and UC be treated by surgery?

A

Crohn’s not curative, remove as little bowel as possible

UC curative via colectomy

129
Q

What is strep Viridans?

A

Non pathogenic commensal in throat
Can enter blood stream in dental procedures -> bacteriaemia
Can stick to prostheses

130
Q

What is the difference between bacteriaemia and septicaemia?

A

Bacteriaemia is when the bacteria are rapidly cleared from the blood (by liver/ spleen macrophages), so NO symptoms are produced

Septicaemia is when bacteria are not cleared from the blood and so multiply and produce symptoms

131
Q

What are the most common organisms causing UTIs?

A

E. coli, then enterococcus faecalis

132
Q

Which parts of the GIT are predominantly anaerobic?

A

Parts of the mouth (eg deep in taste buds), small bowel, colon

133
Q

What are benefits are some bacteria in the GIT?

A
  • produce vitamins (K, B12)
  • prevent pathogen colonisation
  • stimulate development of mucosal associated lymphoid tissue ie Peyer’s patches and in caecum
  • kill non-indigenous bacteria
  • produce natural antibodies
134
Q

Should a patient with tonsillitis receive antibiotics?

A

Most cases are viral

Only give antibiotics if have tonsillar exudate/ secondary pharyngitis

135
Q

What are some causative organisms of travellers diarrhoea?

A

E Coli
Shigella
Salmonella

136
Q

What is lactobacillus?

A

Normal vaginal commensal that converts glycogen to lactic acid.
Acidic environment prevents other bacteria and Candida albicans growing.
(Broad spectrum antibiotic can kill lactobacillus and cause vaginal thrush)

137
Q

Which antibiotic is capable of killing anaerobes?

A

Metronidazole

138
Q

What are the types of oesophageal carcinoma and where can they occur?

A
  • squamous cell carcinoma can occur anywhere in oesophagus

- adenocarcinoma occurs in the lower third, is associated with Barrett’s oesophagus, more uncommon

139
Q

What are symptoms of oesophageal carcinoma?

A

Dysphagia

Weight loss

140
Q

How can cancers of the GI tract be investigated?

A

Biopsy
Barium swallow
Endoscopy

141
Q

Gastric cancer is often associated with infection from which organsim?

A

H Pylori causing gastritis

142
Q

How is colorectal adenocarcinoma staged?

A

Dukes Staging:
A: confined to bowel wall
B: through bowel wall, lymph nodes clear
C: spread to lymph nodes

143
Q

What tumours can occur in the large intestine?

A
  • adenomas
  • adenocarcinomas
  • polyps
  • anal carcinoma
144
Q

What are adenomas?

A

Benign neoplastic legions in the large bowel
Can be due to familial adenomatous polypsosis (FAP) where there become 1000s of adenomas on the large intestine, giving a high risk of cancer
Or due to Gardners syndrome which is a type of FAP, with bone and soft tissue tumours

145
Q

Is a rise in ALT and AST indicative of hepatocyte damage?

A

Yes, but ALT release is due to direct hepatocyte damage while AST is not specific as it is also released from skeletal and cardiac muscle.

146
Q

When would alkaline phosphatase rise?

A

Damage to bile canaliculi or blocking of bile duct eg stones.

Is also present in bones so is not specific to biliary tree.

147
Q

Where is a Volvulus common?

A

In the sigmoid colon

Twist around mesentery so the enclosed bowel loop could perforate or become ischaemic

148
Q

What is lead pipe colon?

A

Featureless colon with loss of haustra often seen in ulcerative colitis

149
Q

What is an advantage of MRIs?

A

No radiation required, unlike CT!

But are more time consuming

150
Q

What features on plain radiography can differentiate between small and large bowel obstruction?

A
  • SBO more central, LBO more peripheral
  • SB has valvulae going all the way across, LB haustra only partially cross
  • Dilated loops in SB 3-5cm, >5cm in LB
  • SB would have many loops, LB few loops
151
Q

Why may a patient with pancreatic cancer present with pale stool?

A

If tumour in head of pancreas may block common bile duct and prevent bile reaching the colon. Bile is meant to be broken down in the colon and gives faeces its colour, but would be unable to.

152
Q

Why would a patient with pancreatic cancer present with dark urine?

A

Compression of common bile duct would lead to jaundice as bile accumulates and bilirubin reabsorbed into the blood.
Bilirubin has been conjugated by the liver so is soluble and can be excreted by kidneys.

153
Q

MRSA screening involves 3 swabs from which locations?

A

Throat
Nose
Peritoneum

154
Q

Which organism is capable of causing parotitis?

A

Staph aureus

ESA 3 (6 decks)

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