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Semester 3 - me > GI > Flashcards

GI Flashcards

0
Q

What does the mucosa consist of?

A

Epithelia
Lamina propria
Muscularis mucosa

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1
Q

What is the general layers of the GI tract?

A

Mucosa
Submucosa
Muscularis externae
Adventitia

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2
Q

What does the submucosa consist of?

A

Loose connective tissue
Blood vessels
Lymphatics

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3
Q

What does the Muscularis externa consist of?

A

Inner circular layer

Outer longitudinal layer

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4
Q

What is the adventitia?

A

Supporting tissue lining the external surface

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5
Q

What epithelia is in the oesophogus?

A

Stratified squamous

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6
Q

How is reflux of food prevented from the stomach to the oesophogus?

A

Diaphragm pinch cock
Angle of his
Lower oesophogeal spinchter
Intra abdominal pressure collapses the oesophogeal wall

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7
Q

What epithelium does the stomach have and where does it start?

A

Simple columnar

Gastro-oesophogeal junction

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8
Q

What is there to allow chyme to pass through to the duodenum?

A

Pylorus spinchter

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9
Q

What specialised adaptations does the small intestine have?

A

Villi
Microvilli
Plicae circulares
Inner and outer muscular layers

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10
Q

Where does the common bile duct enter the duodenum?

A

Ampulla

Second part of the duodenum

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11
Q

What specialisations does the large intestine have?

A

Inner and outer layers
Mucous secretions
Taeniae coli - 3 distinct bands of outer muscle

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12
Q

What epithelium is below the pectin ate line?

A

Stratified squamous

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13
Q

Why is there a change between upper and lower pectinate lines?

A

In embryo the mesoderm cells died off to make a hole for the anus

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14
Q

What specialised features are below the pectinate line?

A

Sebaceous glands

Sweat glands

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15
Q

Name the processes of the GI Tract

A

Digestion
Absorption
Excretion

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16
Q

Name where the sequence events occur in order

A 
Mouth
Saliva
Pharynx
Oesophogus 
Stomach
Duodenum
Small intestine 
Large intestine
Anus
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17
Q

Where does the most amount of absorption occur?

A

Small intestine

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18
Q

What is chyme?

A 
Food turns into this in the stomach
Neutral
Low pH
Hypertonic 
Sterile
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19
Q

Describe where fluid is added to GI

A 
1l in 1kg food each day
1.5l saliva 
2.5l gastric secretions 
9l isotonic and neutral
12.5l absorbed on small intestine
1.35l absorbed in large intestine 
Remaining in faeces
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20
Q

What controls the GI system?

A

Enteric nervous system

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21
Q

What function does the mouth have?

A

Disrupts food to form a bolus

Allowing swallowing food without choking

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22
Q

Why does the mouth require protection?

A

Teeth
Microbes
Mucosa
Stratified squamous epithelium

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23
Q

What is mastication?

A

The disruption of food by teeth

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24
Q

What is the main muscle involved in mastication?

A

Masseter

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25
Q

What nerve innervates the masseter?

A

Trigeminal nerve

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26
Q

What are the 3 salivary glands?

A

Sub mandibular glands
Sublingual
Parotid

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27
Q

How much saliva is used every day?

A

1.5l

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28
Q

What is the function of saliva?

A 
Make a food bolus
Keeps the mucosa wet
Protects against microbes 
Washes the teeth 
Maintains an alkaline environment 
High calcium for teeth 
Digestion of carbohydrates
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29
Q

What is xerostomia?

A

Inability to produce saliva due to nerve damage or a tumour.
Microbes grow and teeth and mucosa degenerate and they also cannot swallow so results in dysphasia

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30
Q

What are the main consistuents of saliva?

A 
Water
Electrolytes
Enzymes
Alkali
Mucous
Bacteriostats
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31
Q

What type of glands are the salivary glands?

A

Paired tubuloacinar compound exocrine

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32
Q

What are the glands composed of?

A

Tubes which are blind ended with acini at the end which secrete merocrine secretions
They have myoepithelia which contract and push saliva down the duct

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33
Q

What are serous demilunes?

A

Shrinkage artefacts that salivary glands appear as when fixed because they are capable of mucous and serous secretions

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34
Q

How much does the sublingual glands contribute and what do their secretions consist of?

A

5%
No enzymes
Mucous

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35
Q

How much does the sublmandibular glands contribute and what do their secretions consist of?

A

25% mostly serous secretions

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36
Q

How much does the parotid glands contribute and what do their secretions consist of?

A

75% serous and mucous secretions

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37
Q

What is saliva mostly when resting?

A

Mucous

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38
Q

What is saliva mostly when stimulated?

A

Serous

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39
Q

What is the volume of saliva controlled by?

A

Acinar cells

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40
Q

What is the composition of saliva determined by?

A

The ducts

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41
Q

What are the 3 properties of chyme?

A

Hypertonic
Partially digested
Acidic

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42
Q

What is bile made from?

A

Acid independent - mainly alkali juice
Acid dependent - bile acids,bile pigment, cholesterol

Water, phospholipids

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43
Q

What are the 2 main bile acids?

A

Cholic acid

Chenodeoxycholic acid

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44
Q

Where is the bile dependent secreted from?

A

Canaliculi

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45
Q

Where is the bile acid independent secreted from?

A

Ducts

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46
Q

Describe the structure of the liver

A

It has lobules surrounding central lobes
The hepatic arteries and hepatic portal vein enter the central vein via sinusoids which are surrounded by hepatocytes
Hepatic triad - bile duct, artery, vein

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47
Q

Describe the entero-hepatic circulation of bile acids

A

Gastric emptying stimulates cck which causes gall bladder to contract and bile acids to be secreted
They come out of the ampulla of vater and enter the duodenum and the terminal ileum is where they are actively reabsorbed through the epithelium on entering the hepatic portal vein
They are then secreted into the canaliculi

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48
Q

Are all bile acids reabsorbed again?

A

No, some are unconjugated by bacteria and lost

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49
Q

Describe the function of the gall bladder

A

The gall bladder stores bile acids and it contracts on stimulation of cck
They are concentrated and therefore sodium and chloride diffuse in and therefore so does water

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50
Q

Explain the formation of gall stones

A

Gall stones are formed due to the water and salt entering the epithelium, this can lead to precipitation which can form gall stones.
They can be symptomatic but if in the neck or on gall bladder contraction they can lead to billary cholic and cholecystits

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51
Q

Name the secretions from the exocrine pancreas

A 
Lipases
Anylases
Proteases:
- elastin 
- carboxypeptidase
- chymotrypsin 
- trypsin
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52
Q

Explain the function of acini of the pancreas

A

They secrete enzymes into vacuoles as zymogens granules which are then cleaved in the intestine to their active form.
Acinar secretions are Stimulated by cck, released from APUD duodenal cells and stimulated by hypeprtonicity and fats

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53
Q

Explain the function of the ducts in the pancreas

A

Secrete an alkaline juice.

Stimulated by secretin, released from jujenal cells in response to a low pH

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54
Q

Describe the mechanism of the secretion of alkaline juice

A

Na-K-ATPase sets up a concentration gradient
Na-H and H+ binds with HCO3- in the ECF to make water and carbon dioxide which is transported back into the cell and reforms as H+ and HCO3- which is then secreted across the lumen

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55
Q

Describe the digestion of fats

A

The bile acids are in a miscelle configuration and this allows fatty acids to enter the hydrophobic entity. They are then transported and once they go through the unstirred layer they diffuse slowly into epithelia cells where they then become triaclglycerols and can be transported in the lymphatics by chylomicrons into the systemic veins

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56
Q

What is steatorrhoea?

A

An inadequate amount of bile salts are produced and therefore fat appears in the stools and they are pale and float and very foul smelling

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57
Q

What is jaundice?

A

Bilirubin accumulates in the body as it cannot be excreted as there is a problem, giving rise to jaundice.

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58
Q

What does the upper stomach secrete?

A

Acid and pepsinogen

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59
Q

What does the lower third of the stomach secrete?

A

Mucous and gastrin

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60
Q

What anatomy makes up the stomach?

A

2 spinchters - lower oesophogeal and pyloric
Antrum, body, cardia, pylorus, fundus, lesser curvature, greater curvature
Mucous bicarbonate barrier

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61
Q

What epithelium lines the stomach?

A

Simple columnar

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62
Q

What is a hiatus hernia?

A

A little bit of the stomach gone above the diaphragm

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63
Q

What are the preventative measures of stopping gastric contents refluxing back into the oesophagus?

A 
Angle of his
Diaphragm acts as a pinch cock
High intra abdominal pressure compresses the oesophagus 
The lower oesophogeal spinchter 
Gravity
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64
Q

Some reflux is normal, how is this dealt with?

A

Gravity, salivary bicarbonate, peristaltic waves

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65
Q

When do the clinical features of gastro-oesophogeal reflux disease occur?

A

Prolonged contacts of stomach with the oesophagus

Anti reflux mechanisms fail

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66
Q

What are the clinical features of GORD?

A

Dyspepsia - heartburn

Worse lying down, bending over and drinking hot drinks

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67
Q

What investigations would you usually do for GORD?

A

None usually unless you suspect cancer or hiatus hernia then you would do an endoscopy
But you can usually diagnose based on history.

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68
Q

How do you manage GORD?

A

Raft antacids which sit on top of stomach contents
Simple antacids such as calcium carbonate
PPIs eg omeprazole
H2 antagonists eg, ranitidine
Both lower inhibit acid secretion
Diet and lifestyle - stop eating fatty foods/alcohol/smoking/lose weight

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69
Q

What is a major complication of GORD?

A

Barrett’s oesophagus - a metaplastic change of oesophageal epithelium converted to gastric epithelium

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70
Q

What is a peptic ulcer?

A

A break in the superficial epithelia cells penetrating down into the muscularis mucosa of the stomach or the duodenum

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71
Q

What are the causes of peptic ulcers?

A

H pylori
NSAID’s
Alcohol

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72
Q

How does the use of NSAIDs cause gastric ulcers?

A

They inhibit prostaglandins which prevents the production of the unstirred layer

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73
Q

What is the epidemiology of peptic ulcers?

A

Decreasing in young, esp men
Increasing in elderly, esp women
10% of population (duodenal, 3x more common than gastric)
Decreased h pylori cause and increased NSAIDs cause in developed world

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74
Q

What are the clinical features of peptic ulcers?

A

Recurrent, burning epigastric pain, nausea, vomitting, weight loss, anorexia, back pain, severe persistent pain

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75
Q

What investigations would you do for peptic ulcers?

A

H pylori by C13 urease test
See if on NSAIDs
Endoscopy in the elderly

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76
Q

Management of peptic ulcers

A

Stop NSAIDs (if on)
Antibiotics (if h pylori) - amoxicillin or clarythromycin
PPI
H2 antagonist

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77
Q

What are some complications of peptic ulcers?

A

Haemorrhage
Perforation
Gastric outlet obstruction

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78
Q

What type of bacterium is h pylori?

A

Helical
Gram negative
Urease producing
Aerobic

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79
Q

How does h pylori cause pud?

A 
Invades epithelium releasing ammonium to get through unstirred layer and causes a neural environment 
Release cytotoxins causing apoptosis 
Affects gastrin secretion 
In Antrum - DU
Antrum and body - a symptomatic 
Body - GU
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80
Q

How do you detect H pylori?

A

C13 urea breath test as it produces urease which breaks down to form co2
IgG detected in serum
Gastric sample and culture

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81
Q

What is gastritis?

A

Inflammation of the stomach

Chronic causes chronic hypergastraemia due to increased gastrin and increased Gastrin production

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82
Q

What is gastric cancer survival like?

A

5 year survival has not changed much over 40 years
Late diagnosis usually
Poor survival rates

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83
Q

What are the functions of the stomach?

A

Disinfection
Store food
Break down food into chyme

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84
Q

What product does parietal cells produce?

A

Acid - HCL

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85
Q

What product does chief cells produce?

A

Enzymes

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86
Q

What product does neck cells produce?

A

Mucous

Alkali

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87
Q

What do G cells produce?

A

Gastrin

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88
Q

Where do secretions of the stomach come from?

A

Gastric pits

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89
Q

How is stomach acid secreted?

A

Mitochondria of partial cells
Splitting water
Proton pumps which pump H+ onto the canaliculi and then these H+ sit on top of the bicarbonate layer of the stomach so that the epithelia is protected

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90
Q

Why are the proton pumps of the canaliculi key targets for drug action?

A

Because this will inhibit the production of stomach acid

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91
Q

How is gastric acid secretion controlled?

A

Ach
Histamine
Gastrin

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92
Q

Explain the mechanism of Ach controlling acid secretion

A

Ach is released from the gastric distension. They act on muscurinic receptors of parietal cells. Stimulated by the parasympathetic nervous system.

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93
Q

Explain how gastrin controls stomach acid release

A

Gastrin is stimulated by peptides and disinhibited by neutral pH
It acts on parietal cells to stimulate the release of gastrin
Stimulated by Ach additionally.
Intrinsic factor is also stimulated by gastrin which is important for absorption of vitamin B12 for production of RBC

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94
Q

Explain how histamine controls stomach secretion

A

Acts as a second messenger pathway, acts on h2 receptors of parietal cells and then acid secretion is done via c-amp
Released from mast cells
Amplified by gastrin and Ach as these stimulate mast cells

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95
Q

What are the 3 phases of gastric control?

A

Ceohalic
Gastric
Interstitial

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96
Q

Explain the cephalic phase of gastric secretion

A

Your body responds to the sight and smell of food by releasing Ach
Also responds to swallowing
Stimulates parietal cells directly

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97
Q

Explain the gastric phase of acid secretion

A

At first, gastrin is inhibited by the food neutralising the stomach
The distension of the stomach releases Ach
The release of peptides releases gastrin

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98
Q

Explain the interstitial phase of gastric secretion

A

Once chyme has entered the duodenum, CCK and gastric inhibitory peptide are released to inhibit gastrin
Low ph inhibits gastrin as food is no longer buffering the stomach
This low pH Inbetween meals can lead to stomach ulcers and the no buffering action of food at night is why they are so painful

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99
Q

How can gastric acid secretion be inhibited by drugs?

A

PPI which stops the production of acid
Eg. Omeprazole
H2 receptor antagonists such as cimetidine which removes the signal from gastrin and Ach

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100
Q

Describe the stomachs defences to acid

A

Mucous - sticky, bicarbonate layer with acidic layer on top and the acid cannot pass through
Mucous and hco3- are produced by prostaglandins acting on neck cells

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101
Q

Name some ways in which the stomach cells can be breeched

A

Alcohol - dissolves
H pylori - cytotoxins and neutralise
NSAIDs - get into the epithelia layer and cause apoptosis
Inhibit prostaglandins

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102
Q

What does breaching of the stomachs defences result in?

A

Peptic ulcers

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103
Q

Describe receptive relaxation

A

In order for us to be able to eat big meals, we have to reduce the stomachs pressure and so it does this via the vagus nerve causing the relaxation of the stomach

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104
Q

Describe the contractions of the stomach

A

Peristaltic waves are produced which allows the mixing of the stomach contents with chyme. Allows chyme to go to the bottom and larger particles to stay on top. Chyme leaves via the pyloric spinchter and the contractions relate to the stomach emptying and are usually 3 per minute.

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105
Q

Describe the control of gastric emptying

A

Controlled via:
Peristalsic waves
Squirt volume affected by rate of digestion
Low ph, fat and hypertonicity slow gastric emptying

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106
Q

What’s the 4 muscles in the abdominal wall?

A

External oblique
Internal oblique
Transversalis abdominis
Rectus abdominis

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107
Q

What are the next layers in the abdomen?

A

Transversalis fascia
Peritoneum
Greater omentum

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108
Q

What is the function of the greater omentum?

A

To stop the spread or the infection in appendicitis

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109
Q

What is the significance of Douglas line?

A

It’s where the rectus sheath disappears underneath the umbilicus and pubic symphysis
Important for caesarians - phannestiel incision

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110
Q

What is a patent urachus?

A

Where the urachus has become again and you excrete urine out of your umbilicus

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111
Q

What is a patent vitellointestinal duct?

A

Diverticulum of small intestine, reminent of yolk stalk, can excrete pancreatic enzymes
Occurs in 2% of pop, 2 inches long, 2 feet away from ilicoecal valve, 2 tissues involved

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112
Q

How would you diagnose a patent urachus and patent vitellointestinal duct?

A

MRI and see if dye comes out of the GI or the urinary tract - they present the same and are hard to diagnose

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113
Q

What tissue are sutures usually done through in the abdomen?

A

Linea alba because it is strong.
Cannot do through muscle or it will just rip through it

Or transverse incision where you suture the external oblique aponeurosis

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114
Q

At what anatomical landmark do you perform an Appendicecromy?

A

McBurney’s point which is 2/3 way between umbilicus and ASIS
Grid on incision

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115
Q

Define referred pain

A

Pain which is perceived at a distant site from that causing it

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116
Q

Define somatic referred pain

A

Pain caused by a noxious stimulus to the proximal part of the somatic nerve that is perceived in the distal dermatome of that nerve

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117
Q

What is the dermatomal level of the umbilicus?

A

T10

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118
Q

What is the dermatomal level of the pelvis?

A

T12

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119
Q

Give 2 examples of somatic referred pain

A

Shingles - RIF pain but a lower back rash

Right lower lobe pneumonia - RIF

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120
Q

Causes of pain in the abdomen

A

Inflammation
Ischaemia
Stretching
Abnormally strong muscle contractions

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121
Q

Why can’t you feel touch, burning, cutting or crushing in your abdomen?

A

No reason as there is no protective mechanism

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122
Q

Where do you get pain for foregut derivatives?

A

Epigastric

123
Q

Where do you get pain for midgut derivatives?

A

Peri umbilical

124
Q

Where do you get pain for hindgut derivatives?

A

Supra pubic

125
Q

Explain phrenic nerve referred pain

A

C3, C4, C5 innervate the shoulder too so pain from your diaphragm standing up presents as shoulder pain on lying down

126
Q

Explain where you get cardiac pain

A

Either side of mouth, left ear, either side of neck, right shoulder, left arm, epigastric

127
Q

Where is the arcuate line?

A

1/3 way between pubis and umbilicus

128
Q

What are the 4 common types of abdominal hernia?

A

Inguinal
Umbilical
Femoral
Incisional

129
Q

Where do direct inguinal hernias occur?

A

Through Hesselbach’s triangle
Supra inguinal ring
Through muscle

130
Q

What are the borders of Hesselbach’s triangle?

A

Inferior epigastric vessels inguinal ligament, rectus abdominis

131
Q

Where does an indirect inguinal hernia occur?

A

Through the deep inguinal ring, within the transversalis fascial sling

132
Q

Explain the epidemiology of femoral hernias

A

More common in women
More likely to strangulate
Bowel obstruction
Through the femoral canal

133
Q

List the 4 types of hernia in order of prevalence with most prevalent first

A

Inguinal
Incisional
Umbilical
Femoral

134
Q

What is a Richters hernia?

A

Where only part of the bowel is strangulated through the abdomen
Does not present with bowel obstruction
Through the femoral canal

135
Q

What is a Spigelian hernia?

A

An area of weakness vaguely in the abdomen
Presents with a lump
Lateral border of rectus muscle and arcuate line

136
Q

What does incarnated mean?

A

Stuck, not strangulated

137
Q

Where is the mid point of the inguinal ligament?

A

Palate for the femoral artery

138
Q

Where is the mid inguinal point?

A

Between the ASIS and the pubic symphysis

139
Q

Where is the femoral canal?

A

Below the inguinal ligament and next to the femoral vein

140
Q

Why would you operate on a hernia?

A

Worrying
Strangulation
Bowel obstruction
Painful or aching

141
Q

Name the range of toxins that the GI tract and the liver may be exposed to

A 
Chemical
Bacteria
Worms
Viruses
Protozoa
142
Q

How much of the worlds population do not have access to clean water?

A

1 billion

143
Q

What are the physical/innate defences of the GI tract?

A 
Sight/smell
Memory
Mucous
Anaerobic conditions
Peristalsis 
Stomach acid 
Small intestine secretions
144
Q

What are the cellular innate defences of the GI tract?

A 
Eosinophils
Tissue mast cells
Natural killer cells
Macrophages
Neutrophils
145
Q

What is a guinea worm?

A

Goes from the duodenum to the foot
Wants to get back into water
Need to wind it out each day with a match stick
Causes a lot of suicides

146
Q

What are the adaptive defences of the GI tract?

A

B lymphocytes which present antigens
T lymphocytes which deal with intracellular organisms
GALT

147
Q

Explain what happens when salivary defences fail

A

Xerostima which is the inability to produce saliva and causes mucous destruction, bacterial overgrowth
Parotitis caused by staph aureus which has a 25% mortality rate

148
Q

What happens when you have a decrease in acid production?

A

More susceptible to cholera, salmonella and shigelosis

In a hosp environment, patients on PPI are more susceptible to clostridium difficile

149
Q

Which organisms are resistant to stomach acid?

A 
Norovirus
TB
Hep A
Polio
Coxsackie
150
Q

Is H pylori resistant to stomach acid?

A

No it produces ammonia which neutralises the stomach acid

151
Q

What do mast cells do?

A 
Release histamine 
Cause major dehydration
Vasodilation and decreases in blood volume 
Rice stools
Washer woman's hands
152
Q

What are the causes of appendicitis?

A

Lymphoid hyperplasia
Faecal obstruction
Chickenpox
Worm

153
Q

What is mesenteric adenitis caused by and what is it commonly mistaken for?

A

Right iliac fossa pain mistaken for appendicitis

Coxsackie or adenovirus

154
Q

Why is there a lot of lymphoid tissue in the gut?

A

To protect from bacteria as the iliocaecal valve allows bacteria into the small bowel

155
Q

What can gut Ischaemia be causes by?

A

Hypotension
Arterial disease
Venous thrombosis

156
Q

What are the causes of liver failure?

A 
Hepatitis
Alcohol
Drugs
Mushrooms
Industrial solvents
157
Q

What does hepatic fibrosis lead to?

A

Portal hypertension
Portosystemic shunting
Oesophogeal varicies, haemorrhoids, caput medusa
Toxin shunting

158
Q

What are the functions of the liver?

A 
Carb metabolism
Lipid metabolism
Detoxification
Vit d metabolism
Storage of vitamins
Produces bile
159
Q

At what bilirubin concentration is jaundice?

A

> 40 micromol/L

160
Q

What is the normal bilirubin concentration?

A

<22 micromol/L

161
Q

What blood proteins does the liver produce?

A

Clotting factors
Thromboprotein
Amino acid synthesis
Albumin

162
Q

What proteins are used for liver function tests?

A

Bilirubin
Albumin
ALTS/ASTS
Alkaline phosphatase

163
Q

What are the effects of jaundice?

A

Yellow sclerae
Yellow mucous
Yellow skin

164
Q

What is the definition of pre hepatic jaundice?

A

Excessive bilirubin production, usually due to an increased breakdown of RBC
Liver is unable to cope with excess bilirubin

165
Q

What are the lab findings with pre hepatic jaundice?

A

Anaemia
Unconjugated bilirubin
Reticulolysis
Increased LDH

166
Q

What are the causes of pre hepatic jaundice?

A 
Gilbert's syndrome
Crigler Najjar syndrome 
Dublin Johnson syndrome
Immune 
Mechanical
Drugs
Infections
Burns
167
Q

What is hepatic jaundice?

A

A reduced capacity of liver cells to secrete conjugated bilirubin
Dysfunction

168
Q

What are the lab findings of hepatic jaundice?

A

Increased ALT
Swollen cells
Abnormal clotting
Mixed unconjugated and conjugated bilirubin

169
Q

What are the causes of hepatic jaundice?

A 
Gilbert's syndrome
Crigler Najjar syndrome
Viral
Autoimmune hepatitis
Alcohol
Wilson's disease
Cirrhosis
Hepatic tumours
170
Q

What is post hepatic jaundice?

A

Obstruction to drainage of bile, causing a back up of bile acids into the liver
Can be intra hepatic or extra hepatic
Conjugated bilirubin passage is blocked

171
Q

What are the lab findings of post hepatic jaundice?

A

Urine is dark
Increased liver enzymes
Pale stools
Increased Canalicular enzymes

172
Q

What are the causes of post hepatic jaundice?

A 
Drugs 
Hepatitis
Cirrhosis
Biliary colic
Gallstones 
Pancreatitis
Carcinoma
173
Q

What are the causes of hepatitis?

A 
Viral: hep ABCD, yellow fever, EBV
Autoimmune
Hereditary - alpha 1 antitrypsin deficiency
Drugs
Alcohol
174
Q

What are the symptoms of hepatitis?

A

Decreased albumin
Decreased clotting factors
Jaundice
Raised liver enzymes

175
Q

Describe the key features of alcoholic liver disease

A

Fatty liver
Cirrhosis
Alcoholic hepatitis
Complications such as liver failure, carcinoma etc

176
Q

What are the causes of cirrhosis of the liver?

A

Wilson’s disease
Alcohol
Alpha 1 antitrypsin deficiency
Hepatitis

177
Q

What are the clinical features of cirrhosis?

A 
Liver dysfunction
Jaundice
Palpable liver
Anaemia
Bruising
Palmar erythema
Portal hypertension
178
Q

What would you find on investigation with cirrhosis?

A 
Low albumin
Decreased clotting
Raised liver enzymes
Raised bilirubin 
Decreased sodium
179
Q

What is portal hypertension defined as?

A

Hypertension of >20mmHg
Intra hepatic or extra hepatic
Obstruction of portal vein or an obstruction in liver

180
Q

What is Ascites?

A

Increased tension in portal veins and then this causes less fluid in the circulation and for it to back up in the abdomen

181
Q

How can splenomegaly occur?

A

Subsequent increased BP in spleen

182
Q

Where are the main sites of Porto-systemic anastomoses?

A

Oesophagus
Anus as haemorrhoids
Caput medusa near the umbilicus

183
Q

What is fulminant hepatic failure?

A

Hepatic encephalopathy within 2 months of liver failure diagnosis

184
Q

What is hepatic encephalopathy?

A

Confusion
Reversible
Tremor, personality changes, intellectual deterioration

185
Q

What are the causes of pancreatitis?

A 
Gallstones
ECRP
Trauma
Steroids
Mumps
Autoimmune
Scorpion bite
Hyperlipidaemia
Ethanol
Drugs
186
Q

What are the symptoms of acute pancreatitis?

A 
Pain
Nausea/vomiting
Oedema or haemorrhage
Dehydration
Shock
187
Q

What are the symptoms of chronic pancreatitis?

A

Calcification fibrosis
Pain
Malabsorption
Jaundice

188
Q

What percentage of cancer deaths do pancreatic tumours account for?

A

5%

Mostly ductal

189
Q

What are the causes of pancreatic tumours?

A

Smoking
Benzedrine
Familial pancreatitis
Beta napthylamine

190
Q

How does the duodenum make chyme less acidic?

A

HCO3- is added to it from the pancreas, liver and mucosa

191
Q

How does the duodenum deal with chyme being hypertonic?

A

Water reabsorpbed through the duodenum wall

192
Q

How does the duodenum deal with chyme being partially digested?

A

It digests it via enzymes from the mucosa and bile acids from the liver

193
Q

What properties does the small intestine have for absorption?

A

Microvilli
Brush border
High surface area

194
Q

What properties does the large intestine have?

A

Teniae coli which is 3 muscular layers

Run the length of the intestine

195
Q

What is the function of the large intestines?

A

It absorbs water and any remaining nutrients

Stores faeces

196
Q

What does the duodenum secrete?

A 
Bile acids
Water
HCO3-
Proteases, carbohydrase
Secretin, gastrin, cholecystokinin
197
Q

What does the duodenum absorb?

A

Iron

198
Q

What does the Jujenum secrete?

A

Carbohydrase, proteases, cholecystokinin, secretin, gastrin

199
Q

What does the Jujenum absorb?

A 
Carbohydrates
Fatty acids 
Amino acids 
Vitamins 
Minerals 
Electrolytes
Water
200
Q

What does the ileum secrete?

A

Proteases, carbohydrase, gastrin, secretin, cholecystokinin

201
Q

What does the ileum absorb?

A

Bile
Remaining nutrients
B1

202
Q

What does the large intestine secrete?

A

Nothing

203
Q

What does the large intestine absorb?

A

Water
Anything remaining
Bacteria vitamins - k, b12, thiamine, riboflavin

204
Q

What bonds does amylose have?

A

Alpha 1,4

205
Q

What bonds does amylopectin have?

A

Alpha 1,6

206
Q

What do alpha amylases act upon?

A

1,4 bonds
Yield glucose and maltose from amylose
Alpha dextri a from amylopectin

207
Q

What does isomaltase do?

A

Breaks down branched molecules at alpha 1,6 bonds

208
Q

What does maltase do?

A

Breaks down maltose into glucose

209
Q

What does sucrase do?

A

Breaks down sucrose into glucose and fructose

210
Q

What does lactase do?

A

Breaks down lactose into glucose and galactose

211
Q

Explain how glucose is absorbed

A

Na-K-ATPase driving force
Sglut1 on apical membrane
Glut2 on basolateral membrane

212
Q

What does pepsin do?

A

Breaks down peptides near aromatic AA side chains

213
Q

What does chymotrypsin do?

A

Breaks down peptides near AA aromatic chains

214
Q

What does trypsin do?

A

Breaks down peptides near basic AA chains

215
Q

What does carboxypeptidase do?

A

Breaks down peptides near basic AA chains

216
Q

What specialisation do neonates have in terms of proteins in the gut?

A

Absorb whole proteins as their gut is open
Allows passage of immune system proteins so innate immune system is set up
Passive immunity

217
Q

How are amino acids absorbed?

A

Na+ co transporter

Na-K-ATPase

218
Q

How are fats absorbed?

A

Bile salts ingest them into their miscelle

Then once though epithelia they go into triacylglycerols so can be transported by chylomicrons

219
Q

How is NaCl absorbed?

A

Diffusion into cell
Active transport by Na-K-ATPase and chloride follows
Sets up an osmotic gradient

220
Q

How is calcium absorbed?

A

Vitamin d binds to it in the gut
Stimulated by parathyroid hormone
Enters by facilitated diffusion and pumped out by ca-ATPase

221
Q

How is iron absorbed?

A

Has to be absorped as ferrous form (2+)
Gastric acid makes it ferrous, and gastroferrin keeps it ferrous
Absorbed via transferrin endocytosis and then splits and then binds to transferrin in the blood again

222
Q

What type of vitamins are c and b and how are they absorbed?

A

Water soluble

Passive diffusion

223
Q

How is vitamin b12 absorbed?

A

Co factor - intrinsic factor which keeps it soluble

224
Q

What occurs with vitamin b12 deficiency?

A

Pernicious anaemia - damage to stomach and intrinsic factor is not secreted

225
Q

What is oral rehydration therapy?

A

Uptake of Na creates an osmotic gradient
Glucose uptake stimulates Na uptake
Osmotic gradient also
Stimulates maximum water uptake and this is oral rehydration

226
Q

What is segmenting?

A

The intestines move slowly to move the food along and agitation for absorption
Must move very slowly
Each section of small intestine has a pacemaker and an interstitial gradient
More mixing rather than moving along

227
Q

What is haustral shunting?

A

Shuffles the contents of the large intestine back and forth for slow reabsorption and formation of faeces

228
Q

What is mass movement?

A

1-2 times a day, especially when you’ve eaten, the faeces moves along the transverse and ascending colon to the rectum, producing the urge to defecate

229
Q

What are the 2 anal spinchters?

A

Internal which is smooth muscle and involuntary

External which is skeletal muscle and voluntary

230
Q

Explain the excretion of faeces

A

The spinchters relax which creates a high pressure

Forces faeces out

231
Q

What are the different types of IBD?

A

Crohns
Ulcerative colitis
Diversion colitis
Diverticular colitis

232
Q

Explain ulcerative colitis

A

Superficial
Bleeding, diarrhoea
Continuous and starts off in the rectum
TH2 cells which produce TGF and IL5

233
Q

Explain Crohn’s disease

A

Transmural
Patchy
Anywhere between mouth and anus
TH1 cells which produce IL2 and IFN gamma

234
Q

What are the presentations of Crohn’s?

A

Upper GI: nausea, indigestion, small bowel obstruction, anorexia, loose stools
Colonic GI: diarrhoea passage of blood
Terminal ileum: anaemia

235
Q

What are the causes of Crohn’s?

A 
Genetic
NSAIDs
Diet 
Smoking 
Acute infections
236
Q

Explain common methods used for IBD

A 
Colonoscopy
Stool analysis
Barium radiographs
Ct scan 
X ray
237
Q

What are the macroscopic changes with Crohn’s?

A

Thickened
Ulcers
Fissures
Cobblestone

238
Q

What is the macroscopic appearance of uc?

A

Reddened mucosa
Bleeds easily
Polyps

239
Q

What are the microscopic changes of Crohn’s?

A

Lymphoid hyperplasia

Granulomas

240
Q

What are the microscopic changes with uc?

A

Crypt abscesses

Goblet cell depletion

241
Q

What is CUTE?

A

Colitis of undetermined type and aetiology

242
Q

What is the treatment for Crohn’s?

A 
Oral or IV glucosteroids
Nutrition
anti TNF antibodies 
Methotrexate, azathiorpine
Ciprofloxacin or metronidazole 
Surgery
243
Q

What is the treatment for uc?

A

Corticosteroids
Anti TNF antibodies
Surgery

244
Q

What are the functions of the normal flora in the GI tract (5)?

A

synthesise vitamines (thiamine, b12, k)
produce GALT in peyers patchers and cecum
prevent colonisation
kill non indigenous bacteria
stimulate production of natural antibodies

245
Q

What are obligate aerobes and give an example?

A

Die without O2

pseudomonas and myobacterium TB

246
Q

What are obligate anaerobes and give an example?

A

Die in the presence of O2

Clostridia, bacteriodes fragillis

247
Q

What are facultative anaerobes and give an example?

A

Prefer O2 but can live without it

eg. E. coli

248
Q

Where are the anaerobic zones of the GI tract?

A

Mouth - deep in taste buds and tongue, gingival crevices
Small bowel
Colon

249
Q

Give some examples of bacteria in the mouth and what they can cause

A

Streptococci - strep mutans causes dental cavities/gingivitis
Staphylococci aureus - parotitis
Candida albicans (fungi) causes oral thrush
Lactobacillus
Enterococcus

250
Q

What is noma/cancrum oris?

A

This is tissue degradation in the mouth which is caused by streptococcus and staphylococcus especially in immunocompromised, malnourished and dehydrated patients

251
Q

What bacteria is particularly known for being in the nose?

A

MRSA (1 of 3 screening sites)
staphylococcus
streptococcus

252
Q

What bacteria in the throat are present in 100% of people?

A

strep viridians
staphylococci
neisseria meningitidus

253
Q

Name some throat bacteria and what they can cause?

A 
Strep pyogenes - tonsillitis
Candida albicans - oral thrush
Haemophillus influenza - pneumonia 
Strep pneumonia - pneumonia 
Strep viridians - bacteraemia after dental procedures
Corneybacterium Diptheriae
254
Q

What is the ratio between viral causes of tonsillitus and bacterial and what organisms are responsible?

A

70% viral - adenovirus, rhinovirus, EBV

30% bacterial - strep pyogenes

255
Q

What organisms are present in the stomach and what can they cause?

A

H pylori

Causes stomach ulcers, duodenal ulcers and gastritis

256
Q

Give some examples of colonic bacteria

A 
Bacteriodes fragilis
Bacteriodes oralis
Bacteriodes melaninogenicus
E coli
Enterococcus faecialis
257
Q

Name some colonic bacteria that aren’t very common

A 
Pseudomonas
Campylobacter
Salmonella
Shigella
Vibrio cholera 
Proteus
258
Q

What is ‘dirty surgery’?

A

When there may be small bowel bacteria
Most surgery opening the small bowel is dirty surgery
Treat with prophylactic antibiotics such as metronidazole and gentamicin

259
Q

Explain faecal peritonitis

A

This is when bacteria from the abdomen gets into the peritoneum which can cause peritonitis and this has a high mortality even in the fit and healthy

260
Q

Explain perianal abscesses

A

These are formed when the glands in the anus which produce lubrication for expulsion of faeces get infected, forming an abscess

261
Q

Explain the development of vaginal thrush and how this is usually presented

A

Lactobacilli usually prevent thrush by excreting an acid, this is part of vaginal normal flora. When this is depressed, candida albicans can grow to form thrush. Antibiotics can do this

262
Q

Where is the perineal skin?

A

Below the anus

263
Q

What organisms can survive in the perineal skin?

A

E coli
Enterococcus faecialis
Lactobacillus

264
Q

What are the common organisms causing urinary tract infections?

A

E coli
Enterococci faecialis
Gram negative enterococci

265
Q

What are the 3 common clostridia organisms and what do they cause?

A

Difficile - diarrhoea - endospores which spread through hospital. can be associated with antbiotics
Tetani - cause tetanus (lock jaw) especially in women who bite the umbilical cord and elderly women who prune their roses
Perfingens - causes gas gangrene -> cardiac arrest

266
Q

What does norovirus cause?

A

Vomitting and diarrhoea

267
Q

What is gastroenteritis?

A

Food poisoning
D+V, stomach cramps
Caused by raw food or contaminated water
salmonella, campylobacter, listeria, clostridium, staphylococcus all common

268
Q

What is cholera?

A

Generally from contaminated water from vibrio cholera, causes rice water stools, severe dehydration, diarrhoea

269
Q

Give some examples of interstitial parasites

A

Giardia and cryptosporidium cause gastroenteritis

Hemlinth causes malabsorption

270
Q

What is the difference between bacteraemia and septicaemia?

A

Bacteraemia is just the presence of bacteria in the blood

Septicaemia is this with the clinical presentation

271
Q

What is the common cause of travellers diarrhoea?

A

ETEC (enterotoxinogenic E coli)
Heat stable or labile toxins produced from this
Severe cholera like watery diarrhoea

272
Q

What does the gram stain consist of?

A

Crystal violet and iodine

273
Q

What are the common GI malignancies?

A 
Oesophagus
Stomach
Large Intestine
Pancreas
Liver
274
Q

What is the epidemiology of oesophogeal carcinoma?

A

2% of malignancies in the UK
Males more than females
Low incidence in USA
High incidence in China

275
Q

What are the most common GI malignancies?

A 
Oesophogeal
Stomach
Large intestine
Pancreatic 
Liver
276
Q

Explain the prevalence of oesophogeal cancers

A

2% of UK population

High incidence in China

277
Q

What are the clinical features of oesophogeal cancer?

A

Dysphagia, starting off with dry food

Weight loss

278
Q

How can you investigate oesophogeal cancer?

A

Endoscopy
Barium swallow
Biopsy

279
Q

What are the 2 types of oesophogeal cancer and where do they occur?

A

Squamous cell carcinoma - anywhere, most common

Adenocarcinoma - lower third of the oesophagus, associated with Barrett’s oesophagus

280
Q

What is the prognosis of oesophageal cancer?

A

presents at an advanced stage
5% 5 year survival
direct spread through oesophogeal wall means that only 40% are operable
many patients have a tube down through the tumour to allow passage of food and drink

281
Q

What is the prevalence of gastric cancer?

A 
15% of worldwide cancer deaths
associated with H pylori 
Poor prognosis
<20% 5 year survival
More common in men 
More common in Japan, Finland and Columbia
Associated with gastritis
More common in blood group A
282
Q

What are the clinical features of gastric cancer?

A 
Dysphagia
Dyspepsia
Weight loss
Vomiting 
Anaemia 
Epigastric pain
283
Q

What investigations would you do for gastric cancer?

A

Biopsy
Barium swallow
Endoscopy

284
Q

What are the macroscopic features of gastric cancer?

A

Fungating
Ulcerating
Linitis plastica
Early

285
Q

What are the microscopic features of gastric cancer?

A

Variable degree of gland formation

Single cells - signet ring cells

286
Q

What is the prognosis for gastric cancer?

A

If caught early, the prognosis is good
If caught late, there is a 10% 5 year survival
Late - spread through bowel wall, to liver, to lymph nodes and possibly ovaries

287
Q

Explain gastric lymphoma

A 
It is the most common GI lymphoma
Starts as a low grade lesion
Prognosis better than gastric cancer 
Strong association with h pylori 
Can potentially be cured by antibiotics because H pylori maintains control over the tumour and therefore you can technically cure it with antibiotics but realistically it slows it
288
Q

Explain a little about gastro-intestinal stromal tumours

A

Relatively uncommon, derived from the interstitial cells of Cajal
CD117 mutation
Highly specific treatment
Unpredictable behaviour - pleomorphisms, mitoses, necrosis

289
Q

Name the tumours of the large intestine

A

Adenoma
Adenocarcinoma
Polyps
Anal carcinoma

290
Q

Explain intestinal adenomas

A

Present as polyps which stick out into the lumen
Macroscopic - sessile or pedunculated
Microscopic - variable degree of dysplasia - all large bowel adenomas are dysplastic
Definite malignant potential
Increases with age, FAP, Gardeners syndrome

291
Q

Explain colorectal adenocarcinomas

A 
60-70% are retrosigmoid 
Fungating
Stenotic 
Can usually see the pectinate line
Signet cells, mucinous
292
Q

Explain how colorectal adenocarcinomas spread

A

Through bowel wall to organs
Via hepatic portal system to liver
Via lymph nodes
High risk of metastasis

293
Q

What staging is used for colorectal cancer?

A

Dukes OR TNM
Dukes - A confined to bowel wall
B - through bowel wall
C1/C2 - lymph nodes involved

TNM - considers peritoneum

294
Q

What is the incidence of colorectal cancer?

A

60-70
High UK/USA
polyposis syndromes
UC

295
Q

What genetic factors increase the risk of colorectal cancer?

A

FAP
RAS
DCC deletion
p53 loss

296
Q

What are the outcomes of colorectal cancer?

A

Decrease in survival with an increase in Duke’s staging
Liver metastasis is common in advanced stages and taking out bits of liver can prolong life
Local radiotherapy
Bowel cancer screenings

297
Q

What are some other rare tumours of the GI tract?

A

Carcinoid tumour
Lymphoma
Smooth muscle/stromal tumour

298
Q

Explain a little about pancreatic tumours

A

Early symptoms are vague

Presents with Jaundice, weight loss, trousseaus sign

299
Q

Explain the histology of pancreatic tumours

A

80% ductal
well formed glands
some acinar cells with zymogen granules
+/- mucins

300
Q

What is the prognosis for pancreatic cancer?

A

Poor

301
Q

Explain about a carcinoma of the ampulla of Vater

A

Dilation of gallbladder
Presents with jaundice
Tumour blocks the bile duct
Pale stools, dark urine

302
Q

Name some islet cell tumours

A

Insulinoma
Glucagonoma
VIPoma
Gastinoma

303
Q

Name some benign tumours of the liver

A

Hepatic adenoma
Bile duct adenoma
Haemangioma

304
Q

Name some malignant tumours of the liver

A

Hepatocellular carcinoma
Cholangiocarcinoma
Hepatoblastoma

Semester 3 - me (8 decks)

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