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GI 2 Flashcards

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1
Q

How strong is the contraction in the different areas of the stomach?

A

Body - thin muscle so weak contraction. No mixing caused
Antrum - thick muscle = powerful contraction
>Causes mixing
Pyloric sphincter if contracted leads to a small amount of chyme entering duodenum
>Further mixes antral contents back into body

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2
Q

What produces peristaltic waves?

A

Peristaltic rhythm (~3/min) generated by pacemaker cells in longitudinal muscle
Slow waves – spontaneous depolarisation/repolarisation
Slow wave rhythm is base electrical rhythm (BER)
Slow waves conducted through gap junction along longitudinal muscle
Depolarisation is sub-threshold, requiring futher depolarisation to induce action potential for contraction
Number of Aps/wave determines strength of contraction

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3
Q

What is the neural/hormonal control of gastric peristalsis?

A

Gastrin – increases contractions
Distension of stomach wall – long/short reflexes increase contractions
Fat/acid/amino acid/hypertonicity in duodenum – inhibition of motility

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4
Q

How is acid neutralised in the duodenum?

A

Bicarbonate secretion from Brunner’s gland duct cells (submucosal)
Acid in duodenum:
Controlled by long vagal and short ENS reflexes
Release of secretin from S cells secretes bicarbonate from pancreas and liver
Acid neutralisation inhibits secretin release (negative feedback)

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5
Q

What is the function of the exocrine pancreas?

A

Secretion of bicarbonate by duct cells

Secretion of digestive enzymes by acinar cells

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6
Q

What are zymogens and what is their function?

A

Innactive digestive enzymes, stored as granules
Prevents auto-digestion of pancreas
Enterokinase (bound to duodenal enterocytes brush border) converts trypsinogen to tripsin, which converts all other zymogens to active forms.

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7
Q

What types of enzymes are found in the pancreas?

A

Proteases – cleave peptide bonds
Nucleases – hydrolyse DNA/RNA
Elastases – collagen digestion
Phospholipases – phospholipids to fatty acids
Lipases – triglycerides to fatty acids + glycerol
a-Amylase – starch to maltose + glucose

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8
Q

How is pancreatic function controlled?

A

Secretin released in response to acid in duodenum
Bicarbonate secretion stimulated by secretin
CCK (cholecystokinin) released in response to fat/amino acids in duodenum
Zymogen secretion stimulated by CCK
Also under neural control (vagal/local reflexes) – triggered by organic nutrients in duodenun

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9
Q

What are the lobes of the liver?

A

Right/left
Caudate
Quadrate

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10
Q

What enters/leaves the porta of the liver?

A

Blood vessels (hepatic portal vein, hepatic artery),
lymphatic vessels,
bile ducts (right/left hepatic ducts –>common hepatic duct),
nerve (hepatic plexus)

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11
Q

How are the hepatic cords laid out?

A 
Hepatic cords radiate from central veins, and are composed of hepatocytes
Bile canaliculus (cleft like lumen) lies between cells within each cord. 
Spaces between hepatic cords = hepatic sinusoids (blood channels)
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12
Q

What are the six components of bile?

A

Bile acids
Lecithin
Cholesterol (all three synthesised in liver and solubilise fat)
Bile pigments (bilirubin – from haemoglobin)
Toxic metals (detoxified in liver)
Bicarbonate (neutralisation of acid chyme (only one secreted by duct cells)

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13
Q

How does the bile in different parts of the body change colour?

A

Extracted from blood by hepatocutes + secreted into bile – yellow bile
Bilirubin modified by bacterial enzymes – brown pigments, so brown faeces
Reabsorbed bilirubin excreted in urine, yellow bile

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14
Q

How are bile acids formed?

A

Synthesised in liver from cholesterol
Before secretion, they are conjugated with glycine or taurine –> bile salts (increase solubility)
Secreted bile salts recycled via enterohepatic circulation
Liver –> bile duct –> duodenum –> Ileum –> hepatic portal vein

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15
Q

How is bile secretion controlled?

A

Sphincter of Oddi – controls release of bile and pancreatic juice into duodenum
Fat in duodenum stimulates release of CCK
CCK causes sphinter of oddi to relax and gallbladder to contract
Discharge of bile into duodenum –> fat solubilisation
CCK causes Pancreatic enzyme secretion + bile secretion

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16
Q

When does the gallbladder concentrate bile?

A

When the spinchter of Oddi is contracted, bile forced back to gallbladder
Gallbladder concentrates bile 5-20 times (absorbs sodium and water)

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17
Q

How can oesophageal cancer spread?

A

Direct – to surrounding structures (diaphragm, heart, lungs etc)
Lymphatic spread – regional lymph nodes
Blood spread – liver

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18
Q

What is autoimmune gastritis?

A

Organ specific autoimmune disease – autoantibodies to parietal cells and intrinsic factor.
>Associated with other autoimmune disease
Atrophy of specialised acid secretion gastric epithelium
Leading to loss of the specialised cells, and a loss in acid secretion and intrinsic factor
>leading to B12 deficiency

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19
Q

What is bacterial gastritis?

A

Most common type – H.pylori related
>Gram negative
>Increased acid production

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20
Q

What causes chemical gastritis?

A

Drug related – NSAIDs
Alcohol
Bile reflux

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21
Q

What are the complications of peptic ulceration?

A

Bleeding (acute/chronic)
Perforation – peritonitis
Healing by fibrosis – obstruction

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22
Q

What does oesophageal reflux lead to?

A

Thickening of squamous epithelium
Ulceration of oesophagus if severe
Can lead to barret’s oesophagus

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23
Q

What are the complications of oesophageal reflux?

A 
Healing by fibrosis
>Stricture formation
>Impaired oesophageal motility
>Oesophageal obstruction
Barretts oesophagus
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24
Q

What is barrett’s oesophagus?

A

A type of metaplasia where squamous epithelium are transformed into glandular epithelium (in the oesophagus)
Response to oesophageal reflux
A pre-malignant condition

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25
What are the two types of oesophageal cancer?
Squamous carcinoma | Adenocarcinoma
26
What are the risk factors for squamous carcinoma of the oesophagus?
Smoking Alcohol Dietary carcinogens
27
What are the risk factors of adenocarcinoma of the oesophagus?
Barrett's metaplasia | Obesity
28
What are the local effects of oesophageal cancer?
Obstruction Ulceration Perforation
29
How does oesophageal cancer spread?
Direct Lymphatic Blood (to liver)
30
What is the prognosis of oesophageal cancer?
Very poor - 5yr = 15%
31
What areas can be affected by peptic ulceration?
Oesophagus Stomach Duodenum
32
What bacteria is associated with peptic ulceration?
H. Pylori
33
What are the complications of peptic ulceration?
Bleeding Perforation (and then peritonitis) Healing by fibrosis = obstruction
34
What is the most common histological type of gastric cancer?
Adenocarcinoma
35
How can gastric cancer spread?
Direct Lymphatic Blood Transcoelomic (within peritoneal cavity)
36
What is the prognosis of stomach cancer?
5yr less than 20% | Very poor
37
What is absorbed and secreted by the small intestine villi?
``` Villus cell absorbs: NaCl/water Monosaccarides, amino acids, peptides, fats Vitamins/minerals Crypt cell – secretes cl + water ```
38
How much fluid does the small intestine secrete daily, where does it come from?
Secretes ~1500ml/day Comes from the epithelial cells lining the crypts of lieberkuhn Secreted passively due to active secretion of cl into the intestinal lumen Normally reabsorbed by villi
39
Why is fluid secretion important to the small intestine?
Maintains luminal contents in liquid state Promotes mixing of nutrients with digestive enzymes Aids nutrient presentation to absorbing surface Dilutes and washes away potentially injurious substances
40
How do crypt cells excrete chlorine ions? How is the process controlled?
Sodium potassium pump brings potassium in to the cell Potassium leaves from leaky channel Causes chlorine to be pumped into the cell This then leaves via a CFTR protein into the intestine Controlled by ATP being converted to cAMP by adenylate cyclase Turns to PKA which stimulates the CFTR protein.
41
What is segmentation?
Most common during a meal It is the contraction and relaxation of short intestinal segments Moves chyme up and down into adjacent areas of relaxation Relaxed areas then contract and push chyme back Thoroughly mixes contents with digestive enzymes and brings chyme into contact with absorbing surface
42
How are segmentation contractions generated?
Initiated by depolarisation generated by pacemaker cells in longitudinal muscle layer (cf gastric motility) Intestinal basic electrical rhythm (BER) produces oscillations in membrane potential --> threshold leads to action potential and then contraction AP frequency determines strength of contraction Frequency of segmentation determined by BER BER decreases from intestine --> rectum Produces slow migration of chyme towards large intestine
43
What effect do the nervous systems have on segmentation contractions?
Parasympathetic (vagus) leads to increased contraction Sympathetic decrease. No effect of autonomic NS
44
What is the migrating motility complex?
Pattern of peristaltic activity travelling down small intestine (starts in gastric antrum) As one MMC ends (terminal ileum) another begins Arrival of food in stomach -> cessation of MMC and initiation and segmentation
45
What does the migrating motility complex do?
It: Moves undigested material into large intestine Limits bacterial colonisation of small intestine Motilin hormone involved in initiation of MMC
46
What is the law of the intestine?
If intestinal smooth muscle is distended (ie by bolus of chyme) Muscle on oral side of bolus contracts Muscle on anus side of bolus relaxes Results in bolus moving into area of relaxation towards colon Mediated by neurones in myenteric plexus
47
What is the gastroileal reflex?
Gastric emptying results in increase in segmentation activity The ileocaecal valve (sphincter) opens Chyme enters into large intestine Distension of colon Reflex contraction of ileocaecal sphincter (prevents backflux into small intestine)
48
What are the four parts of the large intestine?
asc, transverse, desc, sigmoid
49
How is the large intestine arranged?
Two layers of muscle: Circular muscle layer complete, longitudinal not Three bands – teniae coli for length of colon Contractions of these create puches Mucosa comprised of simple columnar epithelieum Large, straight crypts lined with large number of goblet cells allow for lubrication of faeces
50
What are the features of the rectum?
Straight muscular tube (between end of sigmoid colon and anal tube) Mucosa – simple columnar epithelium Muscularis externa – thick compared to other regions of alimentary canal
51
What is the anatom of the anal canal?
Muscularis thicker than rectum – internal anal sphincter External anal sphincter – skeletal muscle Epithelium – simple columnar -> stratified squamous
52
What are the functions of the colon?
Actively transports sodium from lumen into blood causes osmotic absorption of water  dehydrates chyme and causes solid faecal pellets Bacteria colonised Bacteria ferment undigested carbohydrates into Short chain fatty acids (energy source in ruminants) Vitamin K (blood clotting) Gas – nitrogen, CO2, hydrogen, methane, hydrogen sulphide
53
What causes the defaecation reflex?
Following a meal, a wave an intense contraction (mass movement contraction) from colon to rectum Distension of rectal wall produced by mass movement of faecal material into rectum. Innervates mechanoreceptors causing the defaecation reflex (giving the urge)
54
How is the defaecation reflex
Under parasympathetic control via pelvic splanchnic nerves Contraction of rectum Causes relaxation of internal and contraction of external sphinters Increased peristaltic activity n colon Leads to inc. pressure on external anal sphincter – relaxes under voluntary control allowing for expulsion of faeces Voluntary delay of defaecation leads to descending pathways
55
What is constipation?
It is due to distension of the rectum Frequency of bowel movements vary from person to person, so decrease from normal Long periods of retention Systemic, neurogenic, organic or functional causes Can be associated with headaches, nausea, loss of appetite and abdominal distension
56
What is diarrhoea?
Stools more frequent and liqudy than normal | Major killer of children under 5
57
What can cause diarrhoea?
Can be caused by: | Viruses, toxins, food, protozoans, pathogenic bacteria
58
What are enterotocigenic bacteria?
Bacteria that produce protein enterotoxins which maximally turn on intestinal chloride secretion rom crypt cells increasing water secretion Act by elevating intracellular messengers (cAMP, cGMP, calcium) Water secretions swamps absorptive capacity of villus cells – so profuse watery diarrhoea Examples include vibrio cholera, E. Coli
59
How do you treat secretory diarrhoea?
As enterotoxins don’t damage cells, just treat symptoms Give sodium/glucose solution to drive water absorption and rehydration Secretion still washes away infection
60
What is a functional bowel disorder?
``` No detectable pathology Related to gut function Good long term prognosis V common - Have large impact on QOL – leads to work absences Psychological factors important ```
61
What are some examples of functional bowel disorders?
``` Oesophageal spasm Non-ulcer dyspepsia Biliary dyskinesia IBS Slow transit constipation Drug related effects ```
62
What is non-ulcer dyspepsia?
Dyspeptic type pain with no ulcers. H. Pyrlori status varies Probably not a single disease >Reflux, low grade duodenal ulcers >Delayed gastric emptying, IBS
63
How do you diagnose non-ucler dyspepsia?
Careful history/examination – family history Check for gastric cancer, H.pylori + alarm symptoms If all negative treat symptoms If H.pylori – eradication therapy If doubt endoscopy
64
What causes vomiting?
Sympathetic and vagal components Vomiting centre (may not exist as entity) Chemoreceptor trigger zone with receptors for: >Opiates >Digoxin >Chemo >Uraemia
65
What do the different timings of vomiting suggest?
Immediate = psychogenic 1hr+ = pyloric obstruction, motility disorders (diabetes, post gastrectomy) 12hrs – obstruction
66
What is psychogenic vomitting, who is likely to get it?
Often young women, often for years No preceeding nausea May be self-induced (overlap with bulimia) Appetite usually not disturbed, but may lose weight Often stops shortly after admission
67
What are hte GI alarm symptoms?
``` Over 50 Short symptom history Unintentional weight loss Nocturnal symptoms Male Family history of bowel/ovarian cancer Anaemia Rectal bleeding Recent antibiotics Abdominal mass ```
68
What investigations do you do into GI disorders?
``` FBC Blood glucose U+E Thyroid status Coeliac serology Proctoscopy Sigmoidoscopy Colonoscopy ```
69
What are organic causes of constipation?
``` Strictures Tumours Diverticular disease Proctitis Anal fissure ```
70
What are the functional causes of constipation?
``` Megacolon Idiopathic Depression Psychosis Institutionalised patients ```
71
What are the systemic causes of constipation?
Diabetes mellitus Hypothyroidism Hypercalcaemia
72
What are the neurogenic causes of constipation?
``` Autonomic neuropathies Parkinsons Strokes MS Spina bifida ```
73
What are the clinical features of IBS?
Abdominal pain (varies – often vague. Bloating, burning or sharp – occ radiates to lower back) Altered bowel habit Abdominal bloating Belchin wind + flatus Mucus Made worse by eating Diagnose if correct history + normal examination!
74
What do you investigate in IBS?
Bloods – FBC, UE, LFTs, ca, CRP, Thyroids, coeliac serology Stool culture (bacterial infection) Calprotectin
75
What is the calprotectin test?
Faecal test Calprotectin is released by inflamed gut mucosa Present in neutrophil cytosol, indicates presence of neutrophil infiltration in gut (differentiates IBS from IBD and monitoring IBD) Monitoring IBD
76
How do you treat IBS?
``` Education Review diet – tea, coffee, alcohol, sweeteners Lactose, gluten exclusion trials FODMAP Drug therapy ```
77
In IBS, what drugs are used for pain management?
``` Antispasmodics Linaclotide (constipation) Antidepressants (TCAs – diarrhoea, SSRIs constipation) ```
78
In IBS, what drugs are used for bloating management?
Some probiotics | Linaclotide (constipation)
79
In IBS, what drugs are used for constipation management?
Laxatives | Avoid TCAs + FODMAP
80
In IBS, how do you treat dirrhoea?
Antimotility agents + FODMAP | Avoid SSRIs
81
What is dyspepsia?
``` “Bad digestion” - Pain or discomfort in upper abdomen Can have: nausea, vomiting, bloating, fullness, early satiety heartburn ```
82
What are the causes of dyspepsia?
``` Upper GI – peptic ulcer, gastritis, gastric cancer, non-ulcer dyspepsia Hepatic causes Pancreatic disease Lower GI – IBS, colonic cancer Coeliac disease Other systemic disease – metabolic, cardiac Drugs Psychological ```
83
When do you refer to endoscopy?
``` Anorexia Loss of weight Anaemia Recent onset >55 yrs or persistent despite treatment Melaena/haematemesis or Mass Swallowing problems ```
84
What are the risks of endoscopy?
risk perforation, bleeding, reaction to drugs
85
What investigations should you do into gastric ulcers?
Bloods – FBC, ferritin, LFTs, U&Es, calcium, glucose, coeliac serology/serum IgA Drug history – NSAODs, steroids, bisphosphates, Ca antagonists, nitrates, theophyllines Lifestyle – alcohol, diet, smoking, exercise, weight reduction
86
When do you take action with dyspepsia?
Alarm features – yes --> Upper GI endecopy If not, then over 55 yrs, UGIE If under, no UGIE and test for helicobacter pylori If positive, eradication therapy, symptomatic treatment with PPIs or H2R antagonists and lifestyle factors. Refer if persist
87
What is H.pylori?
Gram negative, spiral shaped microaerophilic flagellated bacteria. >Infects 50% of world population Only colonoise gastric type mucosa, in surface layer. No penetration to epithelial layer. Evokes immune response in mucosa- dependent on host genetics Produces acute and chronic inflammatory response Increased acid production
88
How do you diagnose H. pylori?
Non-invasive – serology for IgG against H. pylori >13C/14C urea breath test >Stool antigen test – ELISA Invasive – endoscopic Histology (gastric biopsies stained for HP) – cultured Rapid slide urease test (CLO)
89
What is gastritis?
Inflammation of gastric mucosa
90
What are the risk factors of a peptic ulcer, what type is most common?
NSAIDs, smoking, male, age, (rarely): Zollinger-Elison syndrome, hyperparathyroidism, crohn’s disease Duodenal >gastric
91
What are the clinical features of a peptic ulcer?
``` Epigastric pain Nocturnal hunger/pain (more common GU) Back pain Nausea/occasional vomiting Weight loss/anorexia Might only have epigastric tenderness If ulcer bleeds then haematemesis and/or melaena/anaemia may be present ```
92
How do you treat peptic ulcers?
H.pylori treated by eradication therapy Antacid medication otherwise, PPIs or H2R NSAIDs stopped if possible, restarted after therapy if needed, alternative if available Surgery indicated only in complicated cases
93
What is eradication therapy?
Triple therapy for 7 days Clarithromycin 500mg bd Amoxycillin 1g bd (or metronidazaole 400mg bd) >Tetracycline given if penicillin allergy PPI eg omeprazole 20mg bd Effective 90% cases, resistance and poor compliance main reasons for failure
94
What are the complications of peptic ulcer?
Acute bleeding – melaena and haematemsis Chronic bleeding – iron deficiency anaemia Perforation Fibrotic stricture Gastric outlet obstruction -> oedema or stricture
95
What are the signs/symptoms of gastric outlet obstruction?
Vomiting – lacks bile or fermented foodstuffs Early satiety, abdominal distension, weight loss, gastric splash Dehydration and loss of H+ and Cl- in vomit. Metabolic alkalosis Bloods – low Cl, Na, K and renal impairment
96
How do you diagnose gastric outlet obstruction?
UGIE Then identify cause A prolonged fast is needed
97
What are the main problems associated with gastric cancer?
Poor prognosis as presents late Majority are adenocarcinomas (epithelial cells) – associated with H.Pylori Second most common GI malignancy
98
What are the risk factors for gastric cancer?
``` Family history, previous gastric resection, biliary reflux, premalignant pathology Smoking, high salt diet, nitrate high food, H.P infection ```
99
How do you manage gastric cancer?
UGIE and biopsies, CT chest/abdo– staging investigations | Surgical and chemo treatment
100
Where can gastric cancer spread to?
``` Lymph nodes, liver, lungs, peritoneum, bone marrow ```

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