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GI Flashcards

0
Q

What is the fluid balance of hype GI tract?

A 
In 
1kg food
1.5 L saliva
2.5 L stomach secretions
9 L small intestine and pancreatic secretions
Total 14L

Out

  1. 5L absorbed in small intestine
  2. 35L absorbed in large intestine
  3. 15L faeces
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1
Q

What must the GI tract convert food too?

A

Sterile
Neutral
Isotonic
Small particles

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2
Q

What does the lower oesophageal sphincter comprise of?

A

Acute angle of entry of oesophagus
Oesophagus passes through oesophageal hietus and right crux of diaphragm
High pressure in abdomen collapses oesophagus
Circular muscle of oesophagus
Folds of oesophageal mucus membrane

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3
Q

What are the functions of saliva?

A 
Lubricate food
Begin digestion of carbs 
Moisten mucus membranes
Clean teeth 
Reduce breakdown of teeth
Immune response
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4
Q

Why is saliva necessary in the mouth?

A

Non keratanized epithelium so vulnerable to dehydration
Mucus membrane exposed to external environment so vulnerable to infection
Teeth would decay rapidly without protection and maintainance

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5
Q

What are the constituents of saliva that aid its function?

A 
Salivary amylase
Calcium 
Iodine
Lysozyme
Bicarbonate ions
Mucin
Hypotonic
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6
Q

What types of saliva are there?

A

Mucous - rich in mucin

Serous - rich in enzymes

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7
Q

Which salivary glands produce which types of saliva? What volume of saliva does each contribute?

A

Parotid - serous - 25%
Sublingual - mucus - 5%
Submandibular - both - 70%

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8
Q

What distinguishes the submandibular gland Histologically?

A

The presence of demilunes - serous glands that move back out of the acini during preparation.

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9
Q

What do the acinar cells secrete when making saliva?

A

An isotonic solution with normal cations, high iodine and consequently low chlorine ions.

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10
Q

How are acinar secretions modified by ductal cells?

A

Absorption of Na+ with less K+ excretion thus hypotonic

Exchange of Cl- for HCO3- thus alkali

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11
Q

How is a sodium gradient set up in saliva ductal cells?

A

Na+/K+ ATPase on basal membrane extrudes Na+ setting up a gradient in the cell drawing ductal Na+ in
Some K+ released into duct
Remainder of K+ excreted in cotransport with Cl- into the blood

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12
Q

How is HCO3- created within the ductal salivary cells?

A

Inward diffusion of CO2
Combination with H2O creating HCO3- and H+
H+ extruded into blood in exchange for Na+ down its gradient

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13
Q

How does resting saliva differ from stimulated saliva?

A 
More hypotonic (less Na+, marginally higher K+) due to longer spent in duct
Less HCO3- and less enzymes as less stimulation for their release
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14
Q

How is saliva secretion controlled?

A

Stimulation (taste, smell, reflex) trigger increased parasympathetic stimulation to the glands - this causes increased secretion. Reduced sympathetic stimulation causes vasodilation resulting in increased blood flow

Stimulation of the sympathetic NS also increases gland activity but reduces blood flow, as a result secreation decrease

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15
Q

Which cranial nerves supply which salivary glands?

A

Parotid - CN IX - glossopharangeal

Sl and SM - CN facial via the chorda tympani

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16
Q

What is the term for:
Difficulty in swallowing
Painful swallowing

A

Dysphagia

Odynophagia

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17
Q

What can cause dysphagia?

A

Neurological causes - cve, myesthenia gravis, parkinsons, MS
Oesophageal causes - tumour, stricture, right atrial hypertrophy, enlarged aorta, achalaesia (lack of peristalsis due to enteric NS destruction).

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18
Q

How does lateral folding of the embryo contribute to the formation the GI tract?

A

Somatic mesoderm that surrounds the amniotic cavity pinches the yoke sac creating a tube suspended by splanchnic mesoderm lined with ectoderm.

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19
Q

What does craniocaudal folding cause in the GI tract?

A

Cuts the connection between the GI tract and the yoke sac down to one tube - the vitelline duct

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20
Q

What occurs at either end of the primitive gut tube?

A

Direct connections between endoderm and ectoderm - the stomatodeum and proctodeum

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21
Q

What does endoderm form in the GI tract?

A

The epithelium

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22
Q

What forms the GI tract muscles? What else does this layer form?

A

The splanchnic mesoderm.

Also forms the visceral peritoneum

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23
Q

What are the divisions of the gut?

A

Foregut - oesophagus to major duodenal papilla
Midgut - major duodenal papilla to 2/3rds along transverse colon
Hindgut - last 1/3rd of transverse colon to rectal canal (pectinate line)

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24
Q

How is the gut tube suspended in its cavity?

What splits this cavity?

A

The dorsal mesentery

The diaphragm

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25
Q

Which section of the gut also has a ventral mesentery?

What does this do to the cavity?

A

Forgut - stomach to major duodenal papilla.

Divides the intraembryonic coelom into a right and left sac.

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26
Q

How do the mesenteries change around the stomach?

A

The stomach twists clockwise carrying the mesenteries with it. The stomach also tilts as the greater curvature (was posterior now right side) grows faster than the lesser. This causes the dorsal mesentery to become horizontal on its attachment to the bottom edge of the stomach.

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27
Q

What develops in the dorsal and ventral mesogastrium?

A

Dorsal - spleen

Ventral - liver

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28
Q

What does the ventral mesogastrium form in the adult?

A

The lesser omentum connecting the lesser curvature to the liver
The surroundings of the liver
The falciform ligament connecting the liver to the anterior abdominal wall

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29
Q

What does the dorsal mesogastrium form in the adult?

A

The splenorenal ligament anchoring the spleen to the posterior abdo wall
The greater omentum from the greater curvature of the stomach draping down then back up attaching to the transverse colon

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30
Q

What attaches the transverse colon to the posterior abdominal wall?
What does this form?

A

The mesocolon

This forms the lesser sac in conjunction with the greater and lesser omentum

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31
Q

What is the communication between the greater and lesser sac called?

A

The epiploic foramen of Winslow (omental foramen)

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32
Q

What is the function of the lesser sac?

A

Gives the stomach room to expand

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33
Q

What abdominal organs are retroperitoneal?

A 
Kidneys 
Aorta
Pancreas
Most of the duodenum
Acending and descending colon
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34
Q

What occurs with the mesentery of secondary retroperitoneal organs?

A

Fuses with the posterior abdominal wall becoming fusion fascia

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35
Q

What are the anterior abdominal wall muscles and where do the hey attach attach from superficial to deep

A

External oblique - runs inferiomedially from lower ribs to central aponeurosis
Internal oblique - runs superiomedially from iliac spine to central aponeurosis
Transverse abdominus - runs around the trunk from the transverse processes of the vertebra to the central aponeurosis

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36
Q

What two layers sit behind the 3 layers of anterior abdominal muscles?

A

The transversalis fascia

The parietal peritoneum

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37
Q

What muscles are found within the central aponeurosis? What lines border them?

A

The rectus abdominus
Laterally bound by Lina semilunaris
Centrally divided by Lina alba
Divided horizontally by tendinous intersections

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38
Q

What is the difference between superior and inferior to the arcuate line of Douglass?

A

Superior to it the tendons forming the aponeurosis pass either side of rectus abdominus
Below it all fibres of the aponeurosis pass in front of rectus abdominus leaving just the transversalis fascia behind.

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39
Q

Where is the arcuate line of Douglass?

A

1/3rd of the distance from the umbilicus to the pubis symphysis

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40
Q

Describe with an example, referred pain on a somatic nerve

A

Stimulation of a proximal part of the nerve causing pain to be perceived at the distal part of the nerve - e.g shingles

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41
Q

What fibres do visceral sensory fibres follow back to the spine?
What does this cause?

A

Afferent sympathetics

Perception of sensation of the dermatome at the level that the sympathetic fibres left the cord.

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42
Q

What stimulates visceral sensation?

A

Ischemia
Inflammation
Stretching
Strong muscle contraction

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43
Q

Roughly where do the 3 gut regions refer pain?

A

Foregut - epigastric
Midgut - umbilical
Hindgut - suprapubic

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44
Q 
Where does pain from 
Appendix
Liver
Spleen
Retroperitoneal 
Renal colic 
Gall bladder
Diaphragm 
Refer?
A

Appendix - umbilicus
Liver - right hypochonrium
Spleen - left hypochonrium
Retroperitoneal - central back to umbilical
Renal colic - flank to groin
Gall bladder - right hypochondriac to epigastric to right scapula tip
Diaphragm - left shoulder

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45
Q

What is a connection between the umbilicus and bladder called? How does it present?

A

Patent urachus
Failure of closure of alantosis
Urine from umbilicus either at birth, or in later life when obstruction (e.g. Enlarged prostate) causes raised pressure.
Can cause an umbilical cyst

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46
Q

What is a patent vitelline duct? How does it present? He can it be differentiated from a Urachal problem?

A

Failure of the vitelline duct to close
Connection between bowel and umbilicus
Causes an umbilical cyst
Differentiate from Urachal cyst by injecting die and seeing if it goes to bowel or bladder.

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47
Q

What is the rule applied to merkals diverticulum?

A

2% of population
2” long
2’ from the cecum within the ilium
2 types of tissue (gastric and intestinal)

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48
Q

Differentiate the types of congenital GI content herniation

A

Exampholos (omphalocele) - herniation of abdo contents including peritoneum - high rates of mortality due to concurrent abnormalities
Gastroschisis - abdominal contents without peritoneum off midline. No usual concurrent abnormalities so low mortality

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49
Q

What is divarication of recti?

A

Midline bulge due to weakness in Lina alba. Evident when sitting up.

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50
Q

What is the commonest abdominal hernia?

A

Inguinal hernia

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51
Q

Which sex gets more femoral hernias?

A

Women

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52
Q

What are the two sorts of inguinal hernia? Differentiate them.

A

Direct - bowel passes medial to the inferior epigastric vessels through a weakness in hesselbachs triangle. It passes out of the superficial inguinal ring external to the spermatic cord.

Indirect - bowel passes through the internal inguinal ring lateral to the inferior epigastric vessels, through the inguinal canal and out through the external inguinal ring within the spermatic cord. As a result can enter the scrotum.

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53
Q

What triangle do direct inguinal hernias pass through?

A

Hesselbachs triangle

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54
Q

Where do femoral hernias pass?

A

Inferior to the inguinal ligament through the femoral canal

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55
Q

Why are femoral hernias more serious than inguinal hernias?

A

They are more likely to strangulate

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56
Q

What is a spigelian hernia?

A

A hernia medial to the Lina semilunaris at or below the arcuate line of Douglas.
Rare!

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57
Q

What is the term for a partial hernia? What are the risks associated with this?

A

A richters hernia

Can strangulate without obstructing the bowel so harder to detect

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58
Q

What is a common complication of any operation to the abdo?

A

Incisional hernia

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59
Q

What are the main complications of a hernia?

A

Incarceration (not reducible)

Strangulation (painful, red, hard, non reducible mass - causes ischemic bowel)

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60
Q

What size of hernia is more likely to strangulate?

A

Small - they have a smaller opening!

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61
Q

What are the functions of the stomach? How does it meet them?

A

Store food between meals - expandable
Sterilise food - acidic
Digest food - secretes enzymes, mechanical churning, acidic

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62
Q

What enzyme does the stomach secrete? What cell type secretes it?

A

Pepsinogen from chief cells, cleaved to pepsin

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63
Q

Why does pepsin have an action large than just the individual breakdown of proteins in the stomach?

A

Proteins tend to be structural - holding other substances together, thus breaking down proteins causes the food to disintegrate increasing surface area

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64
Q

Where is acid secreted into the stomach (region, cell and region of cell) ?

A

From parietal cells located in gastric pits. Components are secreted into cannuliculi

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65
Q

How is acid secreted in gastric cells?

A

Mitochondria split h2o to h+ and oh-
oh- combined with co2 to hco3-
hco3- secreted into blood in exchange for Cl-
H+ pumped into canaliculus in exchange for K+ using ATP.
Cl- also secreted

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66
Q

What does the production of h+ in parietal cells of the stomach do to the blood?

A

Alkali tide

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67
Q

How is acid secretion controlled in the stomach? What triggers/inhibits each modality?

A

A combination of the vagus nerve releasing ach, mast cells releasing histamine and g cells releasing gastrin.
All three methods stimulate parietal cells.
Vagus activity is triggered stomach distension, anticipation etc.
Gastrin activity is triggered by sensing polypeptides in the lumen and inhibited by sensing of low pH and by somatostatin release.
Histamine is stimulated ach and gastin, thus serves to amplify the effects of there other two.

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68
Q

What are the phases of control during stomach acid secreation?

A

Cephalic - feel, smell, taste all trigger CNx stimulation releasing acid

Gastric - stomach distension triggers CNx stimulation, peptides in lumen trigger gastrin secretion, food buffers stomach raising pH triggering gastrin secretion

Intestinal phase - stomach empties - pH drops reducing gastrin secretion, chyme enters duodenum, initially increases acid secretion then triggering somatostatin release inhibiting gastrin. Decreased stomach stretch lowers CNx activity.

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69
Q

Which stomach cells secrete mucus?

A

Neck cells

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70
Q

Why does mucus stay in position around the stomach?

A

Sticky so hard to displace

Thixotrophic (if disturbed becomes more runny so fills any gaps)

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71
Q

How does gastric mucus protect against acid?

A

Contains HCO3- and basic groups which buffer the acid
Constantly replaced so as it becomes saturated new is produced below.
Unstirred thus h+ has to diffuse right through to reach stomach wall

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72
Q

What controls gastric mucus secretion?

A

Prostaglandins

These increase in response to the same stimuli as acid secretion so attack is matched with defence.

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73
Q

What drugs increase stomach defence?

A

H2 receptor antagonists - eg ranitidine - inhibit the actions of histamine preventing amplification of CNx and gastrin

Proton pump inhibitors - inhibit the H+/K+ synporter a in the caniculus.

H-pylori elimination therapy

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74
Q

Drugs that harm stomach defences

A

NSAIDs - inhibit COX reducing prostaglandins decreasing mucus production

Aspirin - as per NSAIDs non-ionised in stomach so absorbed into lining then ionises causing damage

Alcohol - irritates stomach causing gastritis

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75
Q

How does the stomach expand?

What is the advantage of this method?

A

Actively relaxes under vagus nerve control

No pressure increase therefore decreased reflux

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76
Q

How do stomach contractions move food?

A

Pacemaker in cardia fires 3/minute initiates wave of contraction
Slows as stomach widens then accelerates as it narrows towards the pyloric antrum
Small particles are pushed ahead of the wave but larger ones are overtaken sorting food ready to be squirted into the duodenum
When the wave reaches the pylorus it causes contraction closing the sphincter.

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77
Q

What slows emptying of the stomach?

A

Lipids in duodenum
Low pH in duodenum
Hypertonicity in duodenum.

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78
Q

What is the timeframe for physiological herniation?

A

Week 6 to week 10

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79
Q

Why does the midgut herniate?

A

The entire GI tract expands out of proportion to the rest of the body, the midgut most of all

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80
Q

How can the midgut be subdivided?

On which subdivision is the cecum located?

A

The vitelline duct divides the midgut into a cranial and caudal limb
The cecum is on the caudal limb

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81
Q

What rotations does the midgut undergo? On what axis?

A

On the axis of the SMA
3 x 90 degree anticlockwise rotations, 1 on herniation, 2 on return

The rotation brings the caudal limb in front of the cranial (colon in front of duodenum

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82
Q

How does the midgut return to the abdominal cavity?

A

The jejunum first moving to the left side then successive return of the rest to the right side. The cecum returns to the right upper quadrant the decends.

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83
Q

What are the devisions of the peritoneum? What is the mobility of each?

A

Superior, descending, inferior, ascending.

First 3cm of superior is intraperiotoneal
. Rest of duodenum is retroperitoneal

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84
Q

What problems can arise from physiological herniation?

A

All malrotations increase risk of volvulus

Only one 90 degree turn - the colon returns first and all sits on the left with the small intestine on the right

The first turn is clockwise - the duodenum and SMA sit anterior to the transverse colon - risk of compression

Sub hepatic cecum - failure of cecum to decend - appendix then also in this region!

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85
Q

What effect does cell proliferation have in the GI tract?

A

Blocks the lumen of the oesophagus, bile duct and proximal small intestine.

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86
Q

What is recanalisation?

What happens if it fails?

A

The reopening of the areas of the GI tract that became obstructed.
Atresia (obstruction) or stenosis (narrowing) of the tract

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87
Q

What is the main cause of atresia in the jejunum, ilium and large bowel?

A

Vascular accident causing necrosis - can cause unjointed sections, holed sections or sections joined by a fibrous band.

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88
Q

How does the hindgut contribute to the urinary system?

A

Forms the epithelium. Of. The. Bladder

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89
Q

What forms the end. Of the hindgut?

A

The cloacal membrane with the proctodeum

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90
Q

What separates the hindgut from the alantosis?

A

The urorectal septum

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91
Q

What is the innervation to the proctodeum?

A

Somatic sensation

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92
Q

What divides the region derived from the proctodeum and that derived from the hindgut in the adult?

A

The pectinate line

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93
Q

What pathologies can effect the anal canal/rectum?

A

Imperforate anus - failure of the cloacal membrane to rupture
Hind gut fistula - failure of the urorectal septum to fully separate the hindgut from the alantosis (bladder)

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94
Q

What sort of bacteria causes stomach ulcers, what is its specifics?

A

Helicobacter pylori
Gram -ve flagellated, helical aerobe.
Produces urease breaking down urea to co2 and ammonia to produce alkali environment in stomach

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95
Q

How do h pylori protect themselves from stomach acid?

A

Produce ammonia from urea making CO2 using urease

Live under the stomach mucus layer

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96
Q

How is h pylori transmitted?

Who is most at risk?

A

Oral oral and faeco oral routes
Percentage increases with age - thought to be due to more chance of transmission when the older generation were children rather than more risk as elderly. Cohort effect!
More effected in developing countries.

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97
Q

What does h pylori cause?

A

Peptic ulcers (implicated in 95%)
Gastritis (implicated in 80%)
Small implication in GI cancer

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98
Q

What are the two sorts of GI ulcer?

A

Peptic ulcer - ulcer in the stomach or duodenum

Duodenal ulcer - ulcer of the duodenum only

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99
Q

What is the effect of an antral h pylori infection?

A

Increased acid secretion due to increased parietal cells and gastrin
Metaplasia of duodenum to stomach like columnar cells
H pylori colonise proximal duodenum
Formation of duodenal ulcers

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100
Q

Where do h pylori settle to cause gastric ulcers?

A

In the body of the stomach reducing mucus secretion (and acid secretion)

101
Q

What are complications of ulcers?

A

Perforation
Erosion through blood vessel (gastric - splenic artery, duodenal - gastroduodenal artery)
Obstruction (if near pyloric sphincter)

102
Q

What are other risk factors for peptic ulcer disease?

A

NSAIDs
Smoking
Alcohol
Zollinger-Ellison syndrome (gastrin secreting tumor of the pancreas)

103
Q

What is gastritis?

A

Inflammation of the stomach. With signs of. Inflammation on biopsy, not just a red. Stomach!

104
Q

What are the main branches of the coeliac trunk?

A

Left gastric, splenic and common hepatic

105
Q

What forms the circulation to the greater curve of the stomach? What do these arteries branch off?

A

The right and left gastroepiploic from the gastroduodenal and splenic respectively

106
Q

What does the common hepatic artery branch into?

A

The right gastric, proper hepatic and gastroduodenal

107
Q

What state is chyme in when it reaches the duodenum?

A

Acidic, hypertonic and partially digested

108
Q

How is chyme made isotonic?

A

Water moves from interstitial space between the cells

109
Q

What is the exocrine pancreas Histologically?

A

Compound branched acinar glands
Acini drain into intercalated duct
Intercalated duct drains to intralobular duct (simple cuboidal)
Intralobular duct drains to interlobular duct (stratified cuboidal)
Interlobular ducts into major or minor pancreatic duct

110
Q

What enzymes do acinar cells secrete?

A 
Trypsinogen
Chemotripsinogen 
Pancreatic prolipase
Pancreatic propeptidase
Pancreatic amylase
Proelastase
Procarboxypeptidase
111
Q

What are the vesicles containing the pancreatic enzymes called in the acinar cells?

A

Zymogen granules

112
Q

What triggers the release of zymogen granules?

A

CNx, hypertonic chyme and lipids stimulate APUD cells in the duodenum to release cholecystokinin (cck)
Cck stimulates zymogen granule release

113
Q

How are pancreatic enzymes activated?

A

Enterokinase in intestinal brush border cleaves trypsinogen into trypsin. Trypsin cleaves all the others.

114
Q

How is premature activation of trypsin prevented?

A

Alpha 1 antitrypsin, a protease inhibitor, stops its activation within the pancreas.

115
Q

Other than zymogen granules what else dose the pancrease release?
Where from?
How?

A

Hco3- from duct cells
After alkali tide hco3- is high in the blood
Forms co2 and water
Co2 enters cell and recombines with water forming h and hco3
H+ extruded in exchange for sodium (using the sodium gradient from Na/Katpase)
Hco3- extruded into duct

116
Q

How are pancreatic duct cells regulated?

A

Increased production at alkali tide

Secretin released from terminal jejunum in response to lowered pH enhanced by cck

117
Q

What are the two broad functions of the liver?

What are examples of each?

A

Effecting the blood - plasma protiens, cholesterol synthesis, metabolism and detoxification)
Effecting the gut - bile production

118
Q

What are the functions of bile?

A

Raising pH
Emulsifying lipids
Excretion of waste products

119
Q

How is the liver structured on a macroscopic scale?

A

Anatomically divided into four lobes, the left, the right, the Quadrate and the caudate
Surgically (functionally) has 8 lobes each with its own blood supply

120
Q

Which of the caudate and the quadrate lobes is superior? Which of the main lobes do they belong too?

A 
Caudate superior (posterior)
Quadrate inferior 
Belong to the left
121
Q

What are the two microscopic structures of the liver?

A

Hepatic acini model (functionally)

Hepatic lobule model (structurally)

122
Q

What is the hepatic lobule model of the liver?

A

The structural model
Central branch of hepatic vein
Surrounding branches of portal triad (portal vein, bile duct and hepatic artery).
Blood flows from portal vein and merges with that from hepatic artery providing oxygenation. Passes through sinosoid lined with hepatocytes to hepatic vein. Bile drains in reverse back down blind ended canals to the bile duct.

123
Q

What is the hepatic acini model of the liver?

A

Portal triad centrally with hepatic vein branches peripherally
Zones away from the triad towards the hepatic vein 1-2-3
Zone 3 most vulnerable to injury as further from O2 supply

124
Q

What vessels converge to form the portal vein?

A

Splenic (which also includes inferior mesenteric), superior mesenteric, right gastric and left gastric (which also includes oesophageal)

125
Q

What are the components of bile? What produces each?

A

Bile acid dependant components from acinar like cells - bile acids and pigments
Bile acid independent components from duct cells - HCO3-

126
Q

What are bile acids?
What are examples?
How are they altered and why?

A

Cholesterol derivatives
Eg. Cholic acid or Chenodeoxycholic acid
Conjugated to glycine or taurine to form bile salts to produce amphipathic structure.

127
Q

What are bile pigments?

A

Mainly bilirubin

128
Q

Describe the cycle of bilirubin

A

Haemoglobin to biliverdin to bilirubin in body
Transported to liver on albumin as insoluble
In liver bilirubin undergoes glucuronidation making it soluble
Conjugated bilirubin excreted in bile
Not reabsorbed due to large size
In terminal ilium bacteria convert some into urobilogen
Urobilogen reabsorbed and excreted by kidneys

129
Q

What enzyme causes glucuronidation of bilirubin?

In which disease is it deficient?

A

Udp glucuronosyl transferase

130
Q

How does bile increase the efficiency of lipid breakdown?

A

Amphipathic bile salts emulsify lipids increasing surface area
Colipase links bile salts to lipase for maximal efficiency

131
Q

What occurs with cleaved fatty acids in the GI tract?

A

Micelles formation with cholesterol and bile salts
Fatty acids absorbed in proximal small intestine
Bile salts continue to terminal ileum where they are absorbed, some are lost in the gut.

132
Q

How does the body deal with the timing of the return of bile acids to the liver?

A

Reabsorbed bile acids return to the liver after several hours prior to the next meal. As a result they are not immediately required so are stored in the gallbladder. Cck causes release from the gallbladder when chyme stimulates apud cells.

133
Q

How does the gallbladder condense bile?

A

Na and Cl ions are removed with concurrent osmotic movement of water out of the bile.

134
Q

What sort of gallstones are there? Why do they form? What other diseases may bring about gallstones?

A 
Pigment stones (increased bilirubin, reduced bile salts)
Cholesterol stones (excess cholesterol, reduced bile salts)

High bilirubin can result from haemolytic anaemia
Low bile salts can result from absorption disorders such as chrones

135
Q

What are the three classifications of jaundice?
Example of each
Blood test result of each

A

Pre-hepatic - e.g. Haemolytic anaemia - liver overwhelmed with bilirubin and unable to conjugate it all. Shows: raised unconjugated bilirubin, raised lactate dehydroginase

Hepatic - e.g. Hepatitis - liver non functioning. Shows: Mixed conjugated and unconjugated bilirubin, raised AST and ALT, deranged INR

Post hepatic - e.g. Gallstones - bile unable to leave. Shows: raised conjugated bilirubin, raised ALP, no urobilogen

136
Q

Where can gallstones obstruct - what conditions are associated with each obstruction?

A

Cystic duct - cholecystitis
Common bile duct - billary colic, ascending cholangitis
Pancreatic duct - pancreatitis

137
Q

What are the 3 main classifications for GI toxin defence?

A

Innate physical
Innate cellular
Adaptive

138
Q

Give some examples of innate physical defences of the GI tract

A 
Sight 
Smell
Memory
Saliva 
Gastric acid
Intestinal secretion 
Anaerobic environment
Deification and vomiting
139
Q

Describe salvias protective role against toxins?

A 
Washes toxins to stomach
Contains lysozymes
Contains IgA reducing adherence of pathogens
Alkali neutralising pathogen acid
Lactoperoxidase
140
Q

What pathogens can survive stomach acid?

A

Mycobacterium tuberculosis

Helicobacter pylori

141
Q

How do intestinal secretions protect against toxins?

A

Bile acts as a detergent reducing adherence and pancreatic enzymes contain proteases

142
Q

Which regions of the GI tract are anaerobic?

A

Large and small intestine

143
Q

What is the lack of saliva called? What infection can it lead to? What causes this?

A

Xerostomia
Parotitis
Staphylococcus aureus (gram +ve aerobic cocci)

144
Q

What is the infection risk of anti acids?

A

Decrease stomach acidity increasing risk of
Cholera
Salmonella
Clostridium difficile

145
Q

How can mycobacterium be cultured from the stomach? Why?

A

Stomach washes in the morning as overnight pt coughs up and swallows mucus. Mycobacterium tuberculosis is acid fast.

146
Q

Do you get bacteria in the small bowel? If not why not?

A

The small bowel is normally sterile due to
Secretions containing proteases and detergents
Lack of nutrients
Anaerobic environment
Shedding of epithelium cells
Rapid transit

147
Q

What specific mechanisms aid innate cellular defences protect the GI tract?

A 
The portal system brining all absorbed substances to the liver
Kupffer cells (fixed macrophages) in the liver
148
Q

Where are the main aggregations of GALT in the GI tract?

A

Tonsils (pharangeal, palatine, linguinal)
Payers patches in small intestine mucosa, becoming more common the more distal travelled.
Appendix

149
Q

How does GALT work?

A

Covered in a specialised epithelium that samples lumen (essentially the afferent lymph vessel)
Centre is many B cells surrounded by lymphocytes and macrophages
Activated B cells travel to nearby lymph nodes exaggerating any response.

150
Q

What can cause appendicitis?

A

Lymphoid hyperplasia
Faecolith
Any obstruction

151
Q

What is the inflammation of a lymph node of the mesentery called?
What causes it?
What can it be confused with?
What is the main complication

A

Mesenteric adenitis
Adenovirus
Acute appendicits
Intussusception

152
Q

What is typhoid?

A

Salmonella typhi
Fever, headache, abdo pain, hepatosplenomegaly, lymphadonopathy, macupapular rash
Infects payers patches in terminal ilium which can cause perforation,

153
Q

Why does alcohol damage the liver?

A

Build up of acetylaldehyde (midstep of metabolism) damages cells

NADP - NADPH favours increased fatty acid synthesis

Fat deposited in zone 3

154
Q

What are causes of hepatitis?

A 
Viral
Wilson's disease
Alcohol
Inflammatory bowel disease
Alpha 1 antitrypsin deficiency 
Paracetamol overdose
155
Q

What is fulminant hepatic failure?

A

Failure of the liver within two weeks causing encephalopathy

156
Q

What is liver cirrhosis?

A

Stellate cells in the space of diss secrete collagen
This causes fibrosis of the liver causing necrosis of hepatocytes
It is irreversible

157
Q

What is the cause of portal hypertension?

A

Increased resistance to blood flow increasing pressure in the venous system.

158
Q

Where are risks of portosystemic anastamosis formation in oesophageal hypertension?

A

Umbilicus - caput medusae following recannulisation of ligamentum teres

Rectum - haemorrhoids

Oesophagus - oesophageal varacies

159
Q

What are other causes of portal hypertension other than cirrhosis?

A

Portal vein thrombosis
Schistosomiasis (Shistosoma mansoni)
Hepatic vein obstruction

160
Q

What causes ascites?

A

Low albumin lowering oncotic pressure
Renal sodium retention causing water retention
Increased hydrostatic pressure due to portal hypertension

161
Q

What are liver signs (other than portal hypertension and ascites) and why

A

Puritis - bilirubin itches
Spider naevi - high oestrogen due to decreased metabolism
Palmer erythema - high oestrogen due to decreased metabolism
Leukonychia - hypoalbumaemia
Clubbing - unknown mechanism
Encephalopathy - build up of ammonia due to reduced action of liver and from diet in portosystemic shunts.

162
Q

What is Wilson’s disease?

What is the pathomomonic sign

A

Autosomal recessive disease
Inappropriate deposition of copper during transport
Causes hepatitis, dementia
Kayser fleischer rings

163
Q

What is the cause of most liver tumours?

A

Secondaries to colorectal cancer

164
Q

What is the cause of pancreatitis (the common link to all causes)
What are the acute and chronic effects

A

Innapropriate digestion of its own tissues by pancreatic enzymes.
Causes necrosis, oedema and haemorrhage acutely
Causes fibrosis and calcification chronically

165
Q

What are the causes of pancreatitis?

A 
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpions
ERPC
Cystic Fibrosis
166
Q

What general adaptions do the intestines have to maximise absorption?

A

Large surface area

Slow movement

167
Q

How is surface area maximised in the small and large bowels?

A

Small - valvular conniventes, folding of the mucosa into villi, brush borders of microvilli

Large - crypts of leiberkuhn, microvilli

168
Q

How does the small intestine move?

A

Segmenting
Contraction of smooth muscle intermittently along the course controlled by pacemakers activating different sections at different times. Faster proximally then slowing distally. Food pushed both ways but as faster proximally then general movement distal.

Mass movement
True peristalsis once or twice a day to clear the intestine of debris

169
Q

How does the large intestine move?

A

Houstral shuffling
Much like segmenting moving contents back and fourth but faster proximally so moves distally.

Mass movement
Propels faeces into rectum, usually following a meal

170
Q

How are muscles organised in the large intestine?

A

Circular layer contracted permanently at set points creating houstra
Longitudinal layer condensed into the three taenia coli

171
Q

How is deification controlled?

A

Two sphincters internal and external (NOTE, internal next to bowel, external behind internal, not further out)
Internal under autonomic parasympathetic control
External under voluntary control
Pressure receptors sense increasing faeces - sacral reflex that can be modified by higher centres - overridden if pressure is too high!

172
Q

What are the parts of the end of the colon

A

The sigmoid colon, the rectum (the pelvic part of the GI tract), the anal canal, the anus

173
Q

What are the components of carbohydrates?

A

Amylose (alpha 1-4 chains)

Amylopectin (alpha 1-4 and alpha 1-6 chains)

174
Q

What are the subcategories of the amylases?

A

Alpha amylase - alpha 1.4 bonds between glucose
Isomaltase - alpha 1.6 bonds between glucose
Maltese - maltose to 2 glucose
Sucrase - sucrose to glucose and fructose
Lactase - lactose to glucose and galactose

175
Q

How are glucose monomers transported into enterocytes? Through what channels?

A

Synport using a sodium ion gradient set up by Na/KATPase on the basal membrane
SGLT1

176
Q

How is glucose expelled from the basal cell membrane of enterocytes?

A

GLUT2 channels

177
Q

How do fructose and galactose enter the enterocytes?

A

Facilitated diffusion

178
Q

Explain the principle of oral rehydration salts

A

Giving sodium and glucose together at optimal concentrations maximises absorption and osmotic pressure drawing water with it out of hitherto GI tract.

179
Q

What is special about a neonatal Gi tract re. Proteins?

A

It is open - IgG from mothers milk can pass between enterocytes

180
Q

In non-neonates how are proteins broken down in the GI tract by specific proteases?

A

Pepsin - nr aromatic amino acids
Trypsin - nr basic amino acids
Chemotrypsin - nr aromatic amino acids
Carboxypeptidase - c terminal

181
Q

Where is protein breakdown completed?

A

The brush border

182
Q

How can amino acids be absorbed into enterocytes?

A

Facilitated diffusion
Alongside Na gradient
Active pumping of h+ into lumen

183
Q

How are electrolytes absorbed in the GI tract? (Na, Cl, Ca, Fe)

A

Na - gradient set up by active pumping on basal membrane
Cl - follows Na to equalise charge
Ca - active transport on basal membrane creating gradient
Fe - combines with gastroferrin, then transferrin, into enterocytes, back to free ion, into blood then back onto another transferrin

184
Q

How is vit b12 absorbed?

A

Combination with intrinsic factor in stomach then absorbed in terminal ilium

185
Q

What areas of the GI tract may damage result in vit b12 deficiency?

A

Stomach

Terminal ilium

186
Q

What is absorbed of note in the terminal ilium?

A

Vit b
Urobilogen
Bile salts

187
Q

What changes in the small intestine between the three areas?

A

Less villi / valvulae conniventes distally
More payers patches distally (max in terminal ilium)

Duodenum - APUD cells, brunners glands
Jejunum - secretin releasing cells
Ilium - absorption of bile salts, urobilogen and vit. B12

188
Q

What deficiencies could result from surgical removal of the stomach?

A 
Iron (no gastroferrin)
Vit b12 (no intrinsic factor)
189
Q

What artery connects the inferior and superior mesenteric arteries?

A

The marginal branch

190
Q

What are the branches of the SMA

A

Inferior parncratoduodenal
Middle colic
Right colic
Ileocolic

191
Q

What are the branches of the IMA?

A

Left colic
Superior sigmoid
Sigmoid
Superior rectal

192
Q

The major specific symptoms of chrones are:

A

Perianal disease
Infrequent gross bleeding
Fistulation
Aphthous ulcer

193
Q

The major specific symptoms of UC are

A

Always gross bleeding

Rare perianal disease

194
Q

Which IBD is improved by smoking?

A

UC

195
Q

What are the usual ages and genders for IBD

A

Chrones - 15 to 30 or over 60

UC young adult females

196
Q

Other than chrones and UC what other IBDs are there?

A

Microscopic colitis
Diverticular colitis
Ischemic colitis
Infectious colitis

197
Q

What are the specific signs of chrones?

A 
Patchy damage
Mouth to anus distribution
Granuloma formation
Cobble stoning
Lines of ulcers
Fibrosis
198
Q

The major signs of UC are

A

Continuos from rectum inwards

No fistulation, granulomas, cobble stoning, fibrosis

199
Q

What are the radiological signs of chrones and UC?

A

Chrones - string sign of kantor

UC - collar button ulcer

200
Q

What are general symptoms of IBD

A 
Abdo pain
Cramps
Bloody diarrhoea (more UC) 
Weight loss
Faecal urea / pneumaturea (chrones)
Fever (UC)
201
Q

What are differentials for IBD

A

Lymphoma

Tb

202
Q

What are extra intestinal symptoms of IBD

A 
Increased cancer risk
Primary sclerosing cholangitis 
Bone disease
Arthritis
Erythema nodosum
Ophthamlmological issues
203
Q

How to Dx IBD

A

Colonoscopy
Biopsy
Stool analysis
Ct enterography

204
Q

What is the progression of UC

A 
Proctitis
Proctosigmoiditis
Left sided
Extensive
Pancolitis
205
Q

What are treatments for IBD

A

Oral steroids
IV steroids
Infliximab
Topical therapy for proctitis

206
Q

What are some benefits of commensal GI bacteria?

A 
Vitamine synthesis (K, B12, thiamine)
Prevent colonisation by pathogens
Kill non indigenous bacteria
Stimulate malt development
Stimulate natural antibodies
Alter environment (e.g. Lactobacilli in vagina convert glycogen to lactic acid)
207
Q

What is the main bacteria in the GI tract? What is its classification?

A

Bacteroides fragalis - anaerobic gram -ve. Bacilli

208
Q

Give an example of a gram +ve anaerobic bacilli from the GI tract?

A

Clostridia sp. (e.g. Clostridium difficile / tetani)

209
Q

What are some gram +ve cocci associated with the GI tract

A

Staphylococcus
Streptococcus
Enterococcus

210
Q

What are some gram -ve cocci associated with the gi tract

A

Neisseria meningitidis

Neisseria gonorrhoeae

211
Q

What gram +ve aerobic bacilli are associated with the GI tract?

A

Bacillus
Lactobacillus
Mycobacterium

212
Q

Give a few gram -ve bacillus aerobics associated with the GI tract

A 
Escherichia coli 
Salmonella
Cholera
Campylobacter
H pylori
213
Q

What causes oral thrush?

Tx?

A

Candida albicans
Fluconazole
Nystatin suspension

214
Q

Which bacteria is associated with infective endocarditis post dental procedures? What makes this mores likely?

A 
Streptococcus viridans (gram +ve aerobic cocci)
Prosthetic valve
215
Q

What is the most common cause of tonsillitis? What percentage?

A

Virus (70%)

216
Q

What is the most commonest cause of bacterial tonsillitis?

A

Streptococcus pyrogens (gram +ve aerobic cocci)

217
Q

What is the risk of GI surgery?

What abx mitigates this?

A

Peritonitis from GI bacteria
Most GI bacteria are anaerobic therefore treat with metronidazole
Gentamicin as a general broad spectrum

218
Q

Commonest causes of uti

A 
Escherichia coli (gram -ve aerobic bacilli)
Enterococcus faecalis (gram +ve aerobic cocci)
219
Q

On a uti culture you find a gram -ve aerobic bacillus, what is it likely to be?

A

Escherichia coli

220
Q

On a uti culture you find a gram +ve aerobic bacillus, what is it likely to be?

A

Lactobacillus - not the causitive organism!

221
Q

On a uti culture you find a gram -ve aerobic cocci, what is it likely to be?

A

Neisseria gonorrhoeae - not a uti!

222
Q

On a uti culture you find a gram +ve aerobic cocci, what is it likely to be?

A

Enterococcus faecalis

223
Q

There is a green pus covering someone’s legs, what is the likely cause?

A

Pseudomonas aeruginosa (gram -ve aerobic bacilli)

224
Q

A patient has truisms and an arching back. What is the infection. What is the term for the arching back. What is the treatment?

A

Clostridium tetani
Opisthotonos
Airway and ventilation if RS involvement
Benzos for spasm

225
Q

What is the causitive organism for gas gangrene?

A

Clostridium perfringens (gram +ve anaerobic bacilli)

226
Q

What is the big complication of clostridium difficile infection, what sort of bacteria is it?

A

Pseudo membranous colitis

Gram +ve anaerobic bacilli

227
Q

What are the two main types of oesophageal cancer? In what part of the oesophagus is each more common? What risk factors are associated with each?

A

Squamous cell carcinoma - upper 2/3rds - associated with red meat, tannin, HPV, smoking and geography (China)

Adenocarcinoma - lower 1/3rd - associated with barrets oesophagus (and therefor GORD) progressing through metaplasia then dysplasia.

228
Q

What are symptoms of oesophageal cancer?

A 
Dysphagia (solids, progressive)
Odynophagia 
Constant pain (suggests invasion)
Aspiration
Weight loss
229
Q

What is the prognosis of oesophageal cancer?

A

Around 5% 5 year survival due to late presentation.

230
Q

What is the general classification of stomach tumours? What are the subdivisions?how do they appear Histologically?

A

Adenocarcinoma
Intestinal (well differentiated - glands like)
Diffuse (poorly differentiated - signet ring cells poor cohesion)

231
Q

What are macroscopic signs of stomach cancer?

A

Ulceration
Fungating
Linitis plastica

232
Q

How is gastric cancer staged?

A

Early (localised to mucosa / submucosa) vs late (

TNM score

233
Q

How does gastric cancer present?

A 
Epigastric pain
Vomiting
Weight loss
Haematemasis 
Palpable mass
Virchows node enlargement
234
Q

What drugs other than standard chemo may be of use in gastric adenocarcinoma?

A

Herceptin if her2 expressed

235
Q

Other than adenocarcinomas what other cancers can effect the stomach?how are they treated?

A

Gastrointestinal stromal tumours from the mesenchyme. Treated with surgery and imatanib
Gastric lymphomas. H pylori eradication can be curative if don early enough! Otherwise surgery.

236
Q

What do most tumours of the large intestine develop from? What implication does this have?

A

Benign polyps

More polyps means more cancer risk

237
Q

What are most large intestine polyps?

A

Benign spontaneous adenomas

238
Q

What signs on an adenoma polyp in the large bowel make it more likely to become malignant?

A

Large
Sessile
Dysplastic

239
Q

What genetic conditions raise risk of colon cancer?

A

Familial adenomatous polyposis - autosomal dominant. 100s to 1000s of adenomas thus high risk of one becoming malignant

Gardeners syndrome - like fap but also ostomas of skull

Hereditary non polyposis colon cancer (HNPCC) - autosomal dominant, polyps form and progress rapidly to cancer, preference for right colon so hard to see.

240
Q

What mutations are required for a colonic adenoma to mutate into an adenocarcinoma?

A

APC
KRAS
DCC
P53

241
Q

Are most colorectal cancers sporadic or inherited?

A

65 - 90% sporadic

242
Q

What are risk factors for colon cancer?

A 
High fat diet
Slow gut transit time
Low fibre diet
Genetics
Western
243
Q

What are symptoms of colorectal cancer?

A 
Altered bowel habits
Obstruction 
Pr bleeding / occult blood
Anaemia
Weight loss
Palpable mass
Tenesmus
244
Q

What is the term for feeling incomplete emptying of bowels post deification?

A

Tenesmus

245
Q

What ct scan sign may show?

A

Apple core stricture

246
Q

How can colorectal cancers be staged?

A

TNM
Dukes score - A (confined to wall) B (local spread clear lymphatics) C1 (lymph nodes involved) C2 (highest lymph nodes involved)

247
Q

What are most pancreatic cancers?

A

Adenocarcinoma

Most are ductal

248
Q

What are risk factors for pancreatic cancer?

A 
Chronic pancreatitis (therefore, alcohol, CF etc)
Smoking
249
Q

Where do most cases of pancreatic cancer occur?

A

Head or ampulla of vater

250
Q

How can pancreatic cancer present?

A 
Billary obstruction
Abdominal pain
Weight loss
Anorexia 
Jaundice
251
Q

What are unusual tumours of the pancreas?

A 
Neuroendocrine tumours. 
Insulomas
Glucagonomas
Vipomas
Gastrinomas

PPE (12 decks)

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