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Conditions + definitions > GI 2 > Flashcards

GI 2 Flashcards

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
Q

What are the two types of oesophageal cancer?

A

Squamous carcinoma

Adenocarcinoma

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26
Q

What are the risk factors for squamous carcinoma of the oesophagus?

A

Smoking
Alcohol
Dietary carcinogens

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27
Q

What are the risk factors of adenocarcinoma of the oesophagus?

A

Barrett’s metaplasia

Obesity

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28
Q

What are the local effects of oesophageal cancer?

A

Obstruction
Ulceration
Perforation

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29
Q

How does oesophageal cancer spread?

A

Direct
Lymphatic
Blood (to liver)

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30
Q

What is the prognosis of oesophageal cancer?

A

Very poor - 5yr = 15%

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31
Q

What areas can be affected by peptic ulceration?

A

Oesophagus
Stomach
Duodenum

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32
Q

What bacteria is associated with peptic ulceration?

A

H. Pylori

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33
Q

What are the complications of peptic ulceration?

A

Bleeding
Perforation (and then peritonitis)
Healing by fibrosis = obstruction

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34
Q

What is the most common histological type of gastric cancer?

A

Adenocarcinoma

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35
Q

How can gastric cancer spread?

A

Direct
Lymphatic
Blood
Transcoelomic (within peritoneal cavity)

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36
Q

What is the prognosis of stomach cancer?

A

5yr less than 20%

Very poor

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37
Q

What is absorbed and secreted by the small intestine villi?

A 
Villus cell absorbs:
NaCl/water
Monosaccarides, amino acids, peptides, fats
Vitamins/minerals
Crypt cell – secretes cl + water
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38
Q

How much fluid does the small intestine secrete daily, where does it come from?

A

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

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39
Q

Why is fluid secretion important to the small intestine?

A

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

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40
Q

How do crypt cells excrete chlorine ions? How is the process controlled?

A

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.

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41
Q

What is segmentation?

A

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
Q

How are segmentation contractions generated?

A

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
Q

What effect do the nervous systems have on segmentation contractions?

A

Parasympathetic (vagus) leads to increased contraction
Sympathetic decrease.
No effect of autonomic NS

44
Q

What is the migrating motility complex?

A

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
Q

What does the migrating motility complex do?

A

It: Moves undigested material into large intestine
Limits bacterial colonisation of small intestine
Motilin hormone involved in initiation of MMC

46
Q

What is the law of the intestine?

A

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
Q

What is the gastroileal reflex?

A

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
Q

What are the four parts of the large intestine?

A

asc, transverse, desc, sigmoid

49
Q

How is the large intestine arranged?

A

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
Q

What are the features of the rectum?

A

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
Q

What is the anatom of the anal canal?

A

Muscularis thicker than rectum – internal anal sphincter
External anal sphincter – skeletal muscle
Epithelium – simple columnar -> stratified squamous

52
Q

What are the functions of the colon?

A

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
Q

What causes the defaecation reflex?

A

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
Q

How is the defaecation reflex

A

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
Q

What is constipation?

A

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
Q

What is diarrhoea?

A

Stools more frequent and liqudy than normal

Major killer of children under 5

57
Q

What can cause diarrhoea?

A

Can be caused by:

Viruses, toxins, food, protozoans, pathogenic bacteria

58
Q

What are enterotocigenic bacteria?

A

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
Q

How do you treat secretory diarrhoea?

A

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
Q

What is a functional bowel disorder?

A 
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
Q

What are some examples of functional bowel disorders?

A 
Oesophageal spasm
Non-ulcer dyspepsia
Biliary dyskinesia
IBS
Slow transit constipation
Drug related effects
62
Q

What is non-ulcer dyspepsia?

A

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
Q

How do you diagnose non-ucler dyspepsia?

A

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
Q

What causes vomiting?

A

Sympathetic and vagal components
Vomiting centre (may not exist as entity)
Chemoreceptor trigger zone with receptors for:
>Opiates
>Digoxin
>Chemo
>Uraemia

65
Q

What do the different timings of vomiting suggest?

A

Immediate = psychogenic
1hr+ = pyloric obstruction, motility disorders (diabetes, post gastrectomy)
12hrs – obstruction

66
Q

What is psychogenic vomitting, who is likely to get it?

A

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
Q

What are hte GI alarm symptoms?

A 
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
Q

What investigations do you do into GI disorders?

A 
FBC
Blood glucose
U+E
Thyroid status
Coeliac serology
Proctoscopy
Sigmoidoscopy
Colonoscopy
69
Q

What are organic causes of constipation?

A 
Strictures
Tumours
Diverticular disease
Proctitis
Anal fissure
70
Q

What are the functional causes of constipation?

A 
Megacolon
Idiopathic
Depression
Psychosis
Institutionalised patients
71
Q

What are the systemic causes of constipation?

A

Diabetes mellitus
Hypothyroidism
Hypercalcaemia

72
Q

What are the neurogenic causes of constipation?

A 
Autonomic neuropathies
Parkinsons
Strokes
MS
Spina bifida
73
Q

What are the clinical features of IBS?

A

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
Q

What do you investigate in IBS?

A

Bloods – FBC, UE, LFTs, ca, CRP, Thyroids, coeliac serology
Stool culture (bacterial infection)
Calprotectin

75
Q

What is the calprotectin test?

A

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
Q

How do you treat IBS?

A 
Education
Review diet – tea, coffee, alcohol, sweeteners
Lactose, gluten exclusion trials
FODMAP
Drug therapy
77
Q

In IBS, what drugs are used for pain management?

A 
Antispasmodics
Linaclotide (constipation)
Antidepressants (TCAs – diarrhoea, SSRIs constipation)
78
Q

In IBS, what drugs are used for bloating management?

A

Some probiotics

Linaclotide (constipation)

79
Q

In IBS, what drugs are used for constipation management?

A

Laxatives

Avoid TCAs + FODMAP

80
Q

In IBS, how do you treat dirrhoea?

A

Antimotility agents + FODMAP

Avoid SSRIs

81
Q

What is dyspepsia?

A 
“Bad digestion” - Pain or discomfort in upper abdomen
Can have: 
nausea, 
vomiting, 
bloating, 
fullness, 
early satiety 
heartburn
82
Q

What are the causes of dyspepsia?

A 
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
Q

When do you refer to endoscopy?

A 
Anorexia
Loss of weight
Anaemia
Recent onset >55 yrs or persistent despite treatment
Melaena/haematemesis or Mass
Swallowing problems
84
Q

What are the risks of endoscopy?

A

risk perforation,
bleeding,
reaction to drugs

85
Q

What investigations should you do into gastric ulcers?

A

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
Q

When do you take action with dyspepsia?

A

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
Q

What is H.pylori?

A

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
Q

How do you diagnose H. pylori?

A

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
Q

What is gastritis?

A

Inflammation of gastric mucosa

90
Q

What are the risk factors of a peptic ulcer, what type is most common?

A

NSAIDs,
smoking,
male, age, (rarely): Zollinger-Elison syndrome, hyperparathyroidism, crohn’s disease
Duodenal >gastric

91
Q

What are the clinical features of a peptic ulcer?

A 
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
Q

How do you treat peptic ulcers?

A

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
Q

What is eradication therapy?

A

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
Q

What are the complications of peptic ulcer?

A

Acute bleeding – melaena and haematemsis
Chronic bleeding – iron deficiency anaemia
Perforation
Fibrotic stricture
Gastric outlet obstruction -> oedema or stricture

95
Q

What are the signs/symptoms of gastric outlet obstruction?

A

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
Q

How do you diagnose gastric outlet obstruction?

A

UGIE
Then identify cause
A prolonged fast is needed

97
Q

What are the main problems associated with gastric cancer?

A

Poor prognosis as presents late
Majority are adenocarcinomas (epithelial cells) – associated with H.Pylori
Second most common GI malignancy

98
Q

What are the risk factors for gastric cancer?

A 
Family history, 
previous gastric resection, 
biliary reflux, 
premalignant pathology
Smoking, 
high salt diet, 
nitrate high food, 
H.P infection
99
Q

How do you manage gastric cancer?

A

UGIE and biopsies, CT chest/abdo– staging investigations

Surgical and chemo treatment

100
Q

Where can gastric cancer spread to?

A 
Lymph nodes, 
liver, 
lungs, 
peritoneum, 
bone marrow

Conditions + definitions (68 decks)

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