Alimentary Pathology Flashcards
(232 cards)
1
Q
What is gastric oesophageal reflux disease?
A
Reflux of gastric acid/bile/pepsins from stomach into oesophagus –> mucosa exposure to these things –> cell loss and inflammation (can lead to erosive oesophagitis.
2
Q
How do you investigate GORD?
A
Clinical diagnosis based on symptoms. Only do endoscopy if alarm features (wt loss, vomiting, dysphagia). Oesophageal pH and manometry may be useful.
3
Q
What can cause GORD?
A
Increased transient relaxations of LOS, hypotensive LOS, delayed gastric emptying, decreased oesophageal acid clearance, decreased tissue resistance due to bile/acid, hiatus hernia.
4
Q
What are the risk factors for GORD?
A
Pregnancy, obesity, drugs lowering LOS pressure, smoking, alcoholism and hypomotility.
5
Q
What symptoms are associated with GORD?
A
Heartburn, cough, water brash, sleep disturbance (worse if lying flat).
6
Q
What complications can arise as a result of GORD?
A
Malignant/benign stricture formation (due to fibrotic healing), thickening of squamous epithelium lining, ulceration, impaired oesophageal motility, oesophageal obstruction, Barrett’s oesophagus.
7
Q
How do you manage GORD?
A
Lifestyle changes
Antacids (Maalox, contains Ag and Ml which neutralise gastric acid)
Alginates (Gaviscon, forms viscous gel over stomach)
Mucosal protectors (bismuth sucralfate, misoprostol)
H2RA (Rantidine)
PPIs (omeprazole, lanzoprazole - IRREVERSIBLY block proton pumps)
Pro-kinetic agents (e.g. metaclopramide, domperidone (dopamine antagonists - parasympathetic control of smooth muscle/sphincter tone via ACH domperidone - increase gut motility and gastric emptying).
Fundoplication (full/partial wrap) or laparoscopic hiatus hernia repair
8
Q
What are the complications associated with hiatus hernia repair?
A
Dysphagia, difficulty belching/vomiting, gas, bloating, excess flatulence, diarrhoea.
9
Q
What is a major SE of pro kinetic agents?
A
Can cause long QT syndromes.
10
Q
How is oesophageal pH measured and what is manometry?
A
A thin, pressure sensitive tube passed down nose into oesophagus. Sensory probes at level of LOS and UOS - to measure muscle contractions as patient swallows liquid. pH sensors measure acid reflux. Patient records a symptom diary to correlate with the findings.
11
Q
What areoesophageal pH and manometry used to measure?
A
Dysphagia, suspected motility disorders, spinster tonicity, relaxation of sphincters, oesophageal motility, heartburn and reflux.
12
Q
How do you investigate dysphagia?
A
Oesophagi-Gastric duodenoscopy (OGC) and upper GI endoscopy (UGIE), barium swallow (exclude pharyngeal pouch/post-cricoid web in high dysphagia before endoscopy), oesophageal pH and manometry.
13
Q
What is presbyoesophagus?
A
Age related degenerating motor function of oesophagus.
14
Q
What can cause dysphagia?
A
Benign/malignant strictures, extrinsic compression, motility disorders (presbyoesophagus, achalasia), eosinophilic oesophagitis.
15
Q
What are the two types of hiatus hernia?
A
- Sliding - fundus of stomach moves through hiatus, depends on patient position and whether eating.
- Paraoesophageal - GO position normal, but part of stomach protrudes into chest.
16
Q
What symptoms are associated with hiatus hernia?
A
Heartburn, chest pain and other GORD symptoms. Many asymptomatic.
17
Q
What risk factors are associated with hiatus hernia?
A
Obesity, ageing.
18
Q
What is Barrett’s oesophagus?
A
Type of metaplasia (whereby squamous epithelium transforms into glandular epithelium due to long term exposure to oesophageal reflux).
19
Q
What are the complications of Barrett’s oesophagus?
A
Predisposes to formation of adenocarcinoma (metaplasia –> dysplasia –> carcinoma).
20
Q
How is Barrett’s oesophagus treated?
A
Endoscopic mucosal resection (removal of nodular areas via banding and ligation), then radiofrequency ablation to allow squamous tissue to grow back through, oesophagectomy in very rare cases may be needed.
21
Q
What complications are associated with oesophageal cancer?
A
Obstruction (–> malnutrition), ulceration (tumour uses up blood supply so normal tissue necroses), BV erosion (–> anaemia/blood loss), spread (direct, lymphatic, blood or distant mets (liver, brain, lung, bone).
22
Q
What signs/symptoms are associated with oesophageal cancer?
A
Progressive dysphagia, anorexia, wt loss, odynophagia, chest pain, heart burn, cough, pneumonia, trachea-oesophageal fistula, vocal cord paralysis, haematemesis.
23
Q
Why is spread of oesophageal cancer common?
A
No peritoneal liming so invasion into adjacent structures more easy. Rich lymphatic supply in lamina propria leads to more lymph node involvement.
24
Q
What are the two types of oesophageal cancer and where on the oesophagus do they tend to arise?
A
Adenocarcinoma - distal third (from Barrett’s)
Squamous - middle/proximal third. Preceded by dysplasia and carcinoma in situ.
25
What sort of tumours to squamous cell carcinomas often form?
From squamous tissue, often large exophytic tumours.
26
What are the risk factors for developing squamous cell carcinoma?
Smoking, alcohol, dietary carcinogens (?vit deficiencies), low socio-economic status.
27
What conditions are associated with squamous cell carcinoma?
Achalasia, caustic strictures, Plummer-Vinson syndrome.
28
How do you investigate oesophageal cancer?
Endoscopy, biopsy (at leas 8), OCG???, staging (CT, endoscopic US, PET, bone scan, laparotomy).
29
What risk factors are associated with adenocarcinoma of oesophagus?
Barrett's metaplasia, abdominal obesity, male, middle aged, Caucasian.
30
How is adenocarcinoma of oesophagus treated?
Curative - oesophagectomy +/- adjuvant (after)/neoadjuvant (after) chemotherapy. Req nutritional support, long post-op recovery (10mnths).
Combined chemo and radiotherapy may improve long-term survival in advanced dx.
If mets - palliative care (dysphagia can be helped by endoscopic stunting, laser, APC, PEG, chemo, brachytherapy).
31
What are the different oesophagectomy techniques?
Ivor Lewis, trans-hiatal or left thoracic-adbominal.
32
What conduits can be used for oesophagectomy?
Stomach, colon.
33
What patients are offered curative therapy in oesophageal adenocarcinoma?
Localised dx, no com orbs, <70 usually.
34
What is APC?
Argon plasma coagulation - endoscopic procedure used to control bleeding from lesions in GIT and something to debulk tumours.
35
What is brachytherapy?
Radiotherapy, where a sealed radiation source is placed inside or next to the area requiring treatment.
36
What can oesophageal hypomotility lead to?
Failure of LOS mechanism.
37
What risk factors are associated with oesophageal hypomotility?
Connective tissue disease, e.g. scleraderma, diabetes, neuropathy.
38
What symptoms are associated oesophageal hypomotility?
Heartburn and reflux symptoms.
39
What is achalasia?
Degeneration of myenteric plexus ganglion cells in distal oesophagus and LOS (failure to relax normally during swallowing, leads to functional obstruction).
40
What investigations can you do for suspected achalasia and what results will confirm achalasia?
Xray - rat tail appearance at distal end and proximal dilation of oesophagus.
Manometry - high pressure in LOS at rest and failure of LOS to relax after swallowing, absence of useful peristaltic contractions in lower oesophagus (LAST TWO FEATURES REQUIRED FOR DIAGNOSIS).
41
What is the aetiology of achalasia?
Suspected inflammatory aetiology as histology shows lots of lymphocytes.
42
What symptoms are associated with achalasia?
Progressive dysphagia for solids, liquids, weight loss, chest pain, regurgitation, chest infections (aspiration risk).
43
What complications are associated with achalasia?
Aspiration pneumonia, lung disease, increased risk of squamous cell oesophageal carcinoma.
44
How is achalasia treated?
Nitrates, CCBs, endoscopically delivered botulinum toxin (few months relief in those unable to have definitive Rx), pneumatic balloon dilatation (lasts longer but symptoms tend to recur), myotomy (muscles of lower cardia cut allowing contents to pass into stomach).
45
What is gastritis?
Inflammation of the gastric mucosa (appears v red on endoscopy).
46
How do you investigate gastritis?
Endoscopy and biopsy to reach histological diagnosis if necessary.
47
What symptoms are associated with gastritis?
Dyspepsia, burning stomach pain, nausea and vomiting.
48
How is gastritis generally treated?
Antacids, H2RAs, PPIs.
49
What are the three different types of gastritis?
Type A - autoimmune
Type B - bacterial
Type C - chemical
B being the most common.
50
What is type A gastritis?
Organ-specific autoimmune disease. Antibodies are created against the parietal cells and intrinsic factor leading to atrophy and loss of specialised acid secreting gastric epithelium --> reduced acid secretion and loss of intrinsic factor.
51
What risk factors are associated with type A gastritis?
H. pylori exposure, NSAIDs, alcohol, aspirin, stress, acute illness. Associated with other autoimmune diseases.
52
What is type B gastritis?
H. pylori found in gastric mucous producing acute and chronic inflammatory response --> increased acid production as bacterial produces urease which catalyses urea --> ammonia, which the stomach tries to counteract.
53
How do you treat type B gastritis?
Antibx.
54
What cause type C gastritis?
Drugs (e.g. NSAIDs), alcohol and bile reflux.
55
Where can peptic ulceration affect?
Lower oesophagus, body, antrum of stomach, 1st and 2nd part of duodenum.
56
Are duodenal ulcers more common than gastric ulcers?
Yes.
57
How must you investigate a suspected peptic ulceration?
Endoscopy to identify those at risk of a bleed.
58
What can cause peptic ulceration?
Imbalance between acid secretion and mucous barrier.
May be associated with H. pylori (remember urease produced catalyses: urea --> ammonia + CO2, ammonia buffers acid and stomach tries to counteract).
NSAID use (trigger prostaglandin production which leads to reduced mucus and bicarbonate excretion).
Rarely due to other conditions, e.g. Zollinger-Ellison syndrome (gastrin-secreting pancreatic tumour - causes recurrent, poor healing ulcers), hyperparathyroidism, Crohn's disease and stress.
59
What are the risk factors for developing a peptic ulcer?
Smoking, alcohol excess, ulcer may sit over carcinoma.
60
What are the signs of peptic ulcers?
Maelena, haematemesis, Fe deficient anaemia.
61
What symptoms are associated with peptic ulcers?
Burning/gnawing pain in stomach, indigestion, heartburn, nausea, haematemesis.
62
What complications are associated with peptic ulcers?
Bleeding (acute = haemorrhage, chronic = anaemia), perforation (peritonitis - medical emergency req. surgery), healing by fibrosis (--> strictures), gastric outlet obstruction (oedema/stricture near pylorus).
63
How do you manage peptic ulcers?
PPIs, endoscopic injection of adrenaline (1:10, 000), thermal contact (gold standard), mechanical (clip) haemospray. Combination therapy most effective (adrenaline + thermal or clips). If bleeding uncontrollably - endoscopic angiography with embolisation/laparotomy.
64
What are the differences in symptoms between a gastric and duodenal ulcer?
If gastric ulcer - pain not relieved by eating, haematemesis and pain occurs 1-2h after eating.
If duodenal ulcer - pain relieved by eating, melon and pain 3-4h after eating.
65
What BMI is considered overweight?
25-29.9
66
What BMI is considered obesity I?
30-34.9
67
What BMI is considered obesity II?
35-39.9
68
What BMI is considered obesity III?
40+
69
What are the complications of obesity?
Shorter life-expectancy, increased risk of: strokes, cataracts, coronary heart disease, diabetes, dislipidaemia, hypertension, severe pancreatitis, cancer, phlebitis, gout, skin problems, osteoarthritis, gynaecological abnormalities, gallbladder disease, NAFLD, pulmonary disease and idiopathic intracranial hypertension...
70
How can be surgically managed?
Bariatric surgery:
- Restrictive Surgery (decrease stomach size --> increased satiety with smaller portions, e.g. laparoscopic ajustable gastric banding, laparasopic sleeve gastrectomy
- Malabsorptive Surgery
(bypassing bowel, causing malabsorption of nutrients e.g. laparoscopic gastric bypass).
- Combination surgery
(e. g. Roux-en-Y gastric bypass (gold standard)).
71
How is BMI calculated?
Weight (kg)/Height (m) squared
72
What are the complications of bariatric surgery?
Anastomatic leak, CVT/PE, infection, malnutrition, vit/mineral deficiency, hair loss, excess skin.
73
What are the advantages and disadvantages of laparoscopic adjustable gastric banding?
Adv: relatively minor surgery, reversible/adjustable. lower op complication rate and mortality.
Disadv: requires implanted medical device, easier to cheat, risk of prolapse and slippage. 15% require revision surgery.
74
What is the mechanism of laparoscopic adjustable gastric banding?
Hollow silicone band placed around stomach near upper end, creating pouch and narrow passage into remainder of stomach. Band inflated with isotonic fluids (can be tighter or looser).
75
What are the advantages and disadvantages of laparoscopic gastric bypass?
Adv: quick, dramatic weight loss, pedigree, causes dumping syndrome.
Disadv: surgery more complex, requires revision, and life-long supplements.
76
What is the mechanism of laparoscopic gastric bypass?
Small pouch is created to restrict food intake, a Y shaped section of small intestine is attached to the pouch to allow for food to bypass to the lower stomach, duodenum and first portion of the jejunum.
77
What are the advantages and disadvantages of laparoscopic sleeve gastrectomy?
Adv: good medium term outcomes, no dumping syndrome, no small bowel manipulation or foreign body.
Disadv: more invasive surgery, long staple line, short pedigree.
78
What is laparoscopic sleeve gastrectomy?
Removal of most of the stomach with the remainder resembling a banana. Stomach becomes fuller quicker and leads to decreased appetite.
79
Why is bariatric surgery useful?
Can decrease risk of death, cancer and MI related deaths.
80
What is pernicious anaemia?
Autoimmune condition whereby the body produces antibodies against the parietal cells producing intrinsic factor in the stomach.
81
How can pernicious anaemia be investigated?
Bloods.
82
What symptoms are associated with pernicious anaemia?
Liver has 3y store of B12 so present 3y after antibodies start attacking.
Fatigue, lethargy, breathlessness, feeling faint, headaches, pale skin, palpitations, tinnitus, appetite, weight loss, mouth ulcers, pins and needles, disturbed vision, irritability, depression...
83
How is vit B12 treated?
B12 injections 3monthly.
84
What is gastric outlet obstruction?
Aka. pyloric obstruction. Any disease impending gastric emptying.
85
How do you investigate gastric outlet obstruction?
UGIE (prolonged fast/aspiration of gastric contents), FBC.
86
What can cause gastric outlet obstruction?
Strictures, ulcers, tumours etc.
87
What are the signs of gastric outlet obstruction?
Gastric splash (lots of material in stomach that can't go anywhere), metabolic alkalosis, FBC shows low Cl, Na, K, renal impairment.
88
What are the symptoms of gastric outlet obstruction?
If obstruction at pylorus, no bile in vomit. Vomiting fermented foodstuffs, abdominal distension, early satiety, wt loss, dehydration (loss of chlorine and hydrogen ions in vomit).
89
What are the two types of peritonitis?
Generalised
- represents failure of localisation, occurs when contamination too rapid/can't produce inflammatory response (e.g. immuncomp/taken a lot of bacteria in). Consider role of adjuvants, e.g. faecal matter.
Localised
90
Why do penetrating injuries increase the chance of generalised peritonitis?
A vacuum is created to suck material in.
91
In investigation what are you wanting to find out if patient presents with peritonitis?
Where tract as perforated to consider what bacteria has leaked out to help to choose antibx.
92
What are the different routes of infection in peritonitis?
Perforation of GI/biliary tract, female genital tract, penetration of abdominal wall, haematogenous spread (more common in paeds/oncology), trauma.
93
What complications can result from peritonitis?
Fluid loss, bacteraemia/endotoxinaemia leading to circulatory collapse and death.
94
How do you treat peritonitis?
IV antibx. May have to give anaerobic cover after a few days. Abscesses must be drained.
95
What is intestinal obstruction?
Blockage that keeps food from passing through the small intestine into the colon.
96
What can cause intestinal obstruction?
Hernias. Intestine blocked because there is something inside it, something wrong with the wall or something pressing on the wall, e.g. strictures, meconium iris (immobile gut, more seen in paeds).
97
What are the cardinal features of intestinal obstruction?
Pain, vomiting, distension, constipation, borborygmi (rumbling/gurgling noise) made by movement of fluid/gas in intestine. Dependent on site, e.g. if just at duodenum patients will be vomiting, if large bowel may result in change in bowel habits, bloating and borborygmi.
98
What complications can arise as a result of intestinal obstruction?
Fluid loss, bacteraemia/endotoxinaemia leading to circulatory collapse and death.
99
What are the majority of gastric cancers? And what are some rare types?
Adenomas.
Others include MALT, GIST.
100
What is the appearance of the gastric tumours?
Red and haemorrhagic.
101
How do you investigate gastric cancer?
UGIE, biopsies.
Staging - CT chest/abdo (contrast meal), lymph nodes/liver/lung/peritoneal/bone marrow.
102
What is the aetiology behind gastric cancer?
Develops through phases of intestinal metaplasia and dysplasia. Associated with previous H. pylori infection.
103
What risk factors are associated with developing gastric cancer?
Processed food, meats, genetics, smoking, FH, previous gastric resection, biliary reflux, premalignant gastric pathology.
104
What symptoms are associated with gastric cancer?
Non-specific presentation - alarm features: dyspepsia, evidence of GI blood loss, wt loss, vomiting, upper abdominal mass. Other symptoms: heart burning, farting/belching frequently, persistent stomach pain, blood in stools/black stools.
105
What sort of spread can occur in gastric cancer?
Direct, lymphatic, blood (mostly to liver), transcolemic (spread within peritoneal cavity). Can often spread and reside in pelvis.
106
How is gastric cancer treated?
Surgery (subtotal gastrectomy and Roux en Y reconstruction, laparoscopic distal gastrectomy or open gastrectomy), chemotherapy.
107
What are MALT tumours?
Tumours develop from lymphatic tissue draining the stomach.
108
What are GIST tumours?
Gastrointestinal stromal tumours that develop in the muscle and connective tissue of the stomach wall.
109
What is dyspepsia?
A group of symptoms. Means - bad digestion.
110
How do you investigate dyspepsia?
Diagnostic and therapeutic endoscopy (under LA/sedation - patient swallows camera, can see all way to duodenum, day case, fasted), FBC, ferritin (for Fe deficiency), LFTs (gallstones or liver problems), U&Es (renal function), Ca (excess can cause dyspepsia), glucose (diabetes), coeliac serology/serum IgA.
111
What are the risks of diagnostic or therapeutic endoscopy?
Perforation, bleeding, ADRs.
112
What risk factors are associated with dyspepsia?
Alcohol, diet, smoking, exercise, weight.
113
What symptoms define dyspepsia?
Pain (upper abdomen/retrosternal), anorexia, vomiting, nausea, bloating, fullness, early satiety, heartburn.
114
What is non-ulcer dyspepsia?
Dyspepsia where there is no proper cause to be found.
115
What findings may you find when investigating non-ulcer dyspepsia?
No ulcers on endoscopy. H pylori status varies. Watch out for alarm symptoms.
116
What can cause non-ulcer dyspepsia?
Probably not a single disease (reflux, low grade duodenal ulceration, delayed gastric emptying (autonomic neuropathy), IBS.
117
What stages of investigation should you follow if patient presents with dyspepsia?
```
Alarm symptoms -
Yes = UGIE
No -
<55. no UGIE -
test for H. pylori -
positive - PPIs, H2RA
```
if >55 - UGIE
118
Where can H. pylori colonise in the body?
Only in the gastric type mucosa. Residing in surface layer and not penetrating epithelium. But this evokes host immune response in underlying mucosa (dependent on host genetic factors, and bacteria-host interactions).
119
What bacteria is present in almost all patients with active, chronic gastritis and in those with duodenal ulcers?
H. pylori.
120
How do you investigate a suspected H. pylori infection?
Non-invasive serology (IgG against H. pylori)
C12/C14 urea breath test
Stool antigen test - ELISA
Endoscopy (if <50 not usually done) to check for cancer cells (biopsy for malignant or benign ulcers)
Histology of gastric biopsies which can be stained for HR
rapid slide urea test (CLO - bacteria change colour of slide as use up foodstuff)
121
What signs and symptoms are associated with H. pylori infection?
Wt loss, anorexia, N&V, epigastric pain/tenderness, nocturnal/hunger pain (more common in DU), back pain may suggest penetration of posterior DU, if ulcer bleeds --> haematemesis +/- maelena or anaemia.
122
What complications are associated with H. pylori infection?
Duodenal ulcers due to increased acid production, stomach cancer.
123
How do you treat ulcers caused by H. pylori?
Antacid meds (PPI, H2RAsO, stop NSAIDs, continue to receive protective agents.
124
What is involved in eradication of H. pylori?
Triple therapy for 7 days (clarithromycin, amoxicillin, metronidazole or tetracyclin if penicillin allergic), PPI (e.g. omeprazole).
125
What is a side effect of omeprazole?
Can cause stomach upset.
126
What kind of bacteria is H. pylori?
Gram negative, spiral-shaped, flagellated bacteria.
127
When is H. pylori acquired?
During childhood. Infects 50% of world population.
128
What is the outcome of H. pylori infestation dependent on?
Site of colonisation, characteristics of bacteria, host factors, e.g. genetic susceptibility, environmental factors, e.g. smoking. In some people can be asymptomatic, in others can cause ulcers. Denoted a primary carcinogen.
129
What are functional GI disorders?
No detectable structural pathology. Related to gut function. Diagnosis via history and examination. HUGE impact on QoL, reassurance is so important.
130
What is the biggest functional GI disease?
Irritable Bowel Syndrome.
131
What investigations can you do if you suspect IBS to rule out other diagnoses?
FBC, U&Es, LFTs, Ca, CRP, TFTs, coeliac serology, stool culture (?travelling, ?parasitic infection), calprotectin, rectal examination and OFC, ?colonscopy if concerning features.
132
What are the two diagnostic criteria for IBS?
ROME II
- Recurrent ab pain/discomfort for >3 days/month in the past 3 months, associated with 2+ of: improvement with defaecation, onset assoc. with change in stool frequency/form.
NICE
- Ab pain/discomfort relieved by defaecation or assoc. with change in stool frequency/form + 2+ of: altered stool passage, ab bloating/distension, symptoms made worse by eating, passage of mucus.
133
What can cause IBS?
Altered motility, visceral hypersensitivity, stress, anxiety, depression.
134
What can trigger contractions in IBS?
Walking/eating.
135
What is the explanation behind IBS?
Brain able to hear messages from the gut too loudly and they often have excessive awareness of normal digestive processes.
136
What symptoms are associated with IBS?
Chronic, relapsing, remitting manner. Mucus in stool, ab pain (bloating, burning, sharp, often radiates to back (can be replicated with balloon inflation suggesting its to do with bowel distension). Altered bowel habits (rarely occurs at night), belching, wind, flatus.
137
What are the three types of IBS?
IBS-D - diarrhoea.
IBS-C - constipation.
IBS-M - both.
Altered bowel habits assoc. with urgency and variability.
138
What are the complications of IBS?
Significant impact on QoL. But must reassure that it is not assoc. with serious pathology.
139
How is IBS managed?
Obtain firm diagnosis, dietetic review: tea, coffee, alcohol, sweetener, lactose, glucose exclusion trial (FODMAP may be helpful).
Symptomatic therapy may also be helpful.
Psychological therapies - relaxation, hypnotherapy, CBT (find triggers).
140
What can be used to help bloating in IBS?
Probiotics, linaclotide (IBS-C), avoid bulking agents/fibre.
141
What can be used to help constipation in IBS?
Laxatives, bulking agents, fibre (episodic), softeners (adjuvant), stimulants (occasional), osmotic (rare), avoid TCAs, FODMAP.
142
What can help with diarrhoea in IBS?
Antimotility agents, FODMAP, avoid SSRIs.
143
What class of drugs can reduce symptoms due to IBS?
Anti-spasmodics -
1. cholingeric muscarinic antagonists (hyoscine buscopan, nebeverine) inhibit smooth muscle contractions in gut wall, producing muscle relaxation and reduction in spasm
2. direct smooth muscle relaxants
3. CCBs (peppermint oil) reduce Ca required for smooth muscle contraction.
144
What is diffuse oesophageal spasm?
Hypermotility disorder.
145
What will you find when you're investigating diffuse oesophageal spasm?
Corkscrew appearance on barium swallow, manometry shows exaggerated uncoordinated hypertonic contractions.
146
What causes diffuse oesophageal spasm?
Idiopathic in most, can be secondary to GORD.
147
What symptoms are associated with diffuse oesophageal spasm?
Severe, retrosternal episodic chest pain +/- dysphagia. Often confused with angina or MI.
148
How is diffuse oesophageal spasm managed?
Smooth muscle relaxants.
149
What can cause oesophagi's?
Reflux oesophagitis, bisphosponates, alcohol, hiatus hernia, systemic illness.
150
What symptoms are associated with oesophagitis?
Bloating, belching, acid taste in mouth, odynophagia.
151
What complications can arise from oesophagitis?
Barrett's, stricture formation or cancer.
152
Define nausea.
Sensation of sickness without actually vomiting.
153
Define vomiting.
Expelling of stomach contents.
154
Define retching.
Antrum contracts but glottis is closed, so no expelling of stomach contents.
155
What are the different nervous components of vomiting?
Sympathetic and vagal components. Chemoreceptor trigger zone (CTZ) is for opiates, digoxin, chemotherapy and uraemia.
156
What causes would you consider if an individual is vomiting immediately after eating?
Psychogenic vomiting.
157
What causes would you consider if an individual is vomiting over an hour after eating?
Pyloric obstruction, motility disorders, diabetes, post-gastrectomy.
158
What causes would you consider if an individual is vomiting over 12h after eating?
Obstruction, hernias, strictures.
159
What are functional causes of nausea and vomiting?
Pregnancy, drugs, migraine, cyclical vomiting syndrome (onset in childhood, recurrent episodes 2-3x a year - 2-3x a month), alcohol.
160
In which group of people is psychogenic vomiting most common?
What does it involve?
Young women. May be self-induced, overlap with bulimia. May have no preceding nausea and appetite not usually disturbed. Often stops shortly after admission.
161
What factors can cause you to vomit?
Smell, sight etc. to cerebral cortex.
Motion to the vestibular nuclei.
Drugs or toxins to the chemoreceptor trigger zone (CTZ).
Information from the pharynx and GIT.
Which all can impact on the vomiting centre in the medulla.
162
Define constipation.
Bowel movements that are infrequent or hard to pass.
163
What can cause constipation?
DM (autonomic neuropathy), hypothyroidism, hypercalcaemia, neurogenic, autonomic neuropathies, Parkinson's, strokes, MS, spina bifida, organic strictures, tumours, diverticular disease, prothesis, anal fissure, megacolon, idiopathic, depression, psychosis.
Mostly arises when patients aren't drinking/eating enough because they're tense.
164
What symptoms are associated with constipation?
Abdominal pain, bloating, bowel movements too infrequently/too hard to pass.
165
What does treatment of constipation involve?
BULKING AGENTS (e.g. isphagula) - increase faecal mass to stimulate peristalsis
OSMOTIC AGENTS (e.g. lactulose) - only work with adequate fluid intake.
STIMULANTS (e.g. Senna) - stimulates muscles in gut to increase peristalsis.
SOFTENERS (e.g. Arachis oil(.
166
What issues may you encounter in treating constipation?
Obstruction, route of admission (oral or rectal), need other measures (hydration), addiction to laxatives, overdoing it with laxatives --> continence issues.
167
What is slow transit constipation?
Reduced motility (spontaneous movement) within large intestine, caused by abnormalities to the enteric nerves. Usually slow passage of waste leads to chronic problems, e.g. constipation and uncontrollable soiling. No cure.
168
What is biliary dyskinesia?
Disorder in which bile cannot physically move normally int he proper direction through the biliary tract (improper peristalsis).
169
What is duodenitis? What can cause it?
Inflammation of duodenum.
H. pylori, NSAIDs/aspirin, alcohol.
170
What is a Mallory-Weiss tear?
Tear at the gastro-oesophageal junction following prolonged periods of vomiting and retching.
171
What can cause a Mallory-Weiss tear?
Retching and vomiting, gastritis, trauma, severe/prolonged hiccups, intense coughing, heavy lifting/straining.
172
What are the symptoms of a Mallory-Weiss Tear?
Abdominal pain, haematemesis, involuntary retching, bloody/black stools.
173
How is a Mallory-Weiss Tear treated?
Spontaneous resolution of bleeding in up to 90%. Some have threatening bleeds and require Rx via endoscopy.
174
What is diuelafoy?
Submucosal arteriolar vessel eroding through mucosa. can occur at any point in GIT and bleeds like a tap on and off. Rarely can cause gastric haemorrhage.
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How do you treat diuelafoy?
Endoscopically.
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What is angiodysplasia?
Vascular malformations due to degeneration that can occur anywhere in the GIT. Frequent cause of chronic occult or overt bleeding.
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What conditions are associated with angiodysplasia?
Chronic conditions, incl. heart valve replacement.
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What can commonly make the bleeding worse in angiodyplasia?
Anti-coagulants or anti-platelets.
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How is angiodyplasia managed?
Argon phototherapy.
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What is acute liver failure?
Loss of liver function that occurs rapidly (days-weeks). Less common than chronic liver failure.
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What can cause acute liver failure?
Viruses, alcohol, toxins, drugs, bile obstruction.
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What symptoms are associated with acute liver failure?
Jaundice, pain in upper right quadrant of abdomen, abdominal swelling, nausea, vomiting, malaise, encephalopathy.
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What is hepatitis?
Inflammation fo the liver. Loss of liver cells in severe hepatitis can lead to liver failure.
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What types of viral hepatitis are there?
A, B, C, D, E.
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What is hepatitis A?
Causes self-limiting acute infection.
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How is hepatitis A normally contracted?
Low incidence in UK, usually contracted abroad and occurs in epidemics.
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How is hepatitis A investigated?
Rise and fall of IgM, shape rise and fall of ALT, continuous steady rise of IgG in patient serology. Acute disease diagnosed by IgM antibodies.
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How is hepatitis A spread?
Faecal-oral route. Can also be transferred by sexual, blood contact.
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What signs and symptoms and are associated with hepatitis A?
Jaundice, high liver enzymes. Liver failure only if severe damage.
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How is hepatitis A prevented? How is it treated?
Vaccination of travellers or patients with chronic liver dx (HCV, HBV), haemophiliacs, homosexual men or those with occupational exposure.
No treatment as self-limiting.
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What is the virus structure of hepatitis B?
Shell - inactive carrier of virus
DNA - for replication
Antigen - coating, inner part is the core antigen, outer part is the surface antigen.
Genetic makeup -
surface antigen gene, polymerase gene (makes DNA), core antigen (produces A antigen - important for detection of virus and release when actively dividing), core antigen makes inner shell.
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How can Hepatitis B be investigated?
E antigen as a marker of viral replication via blood test. Core antigen never leaves liver so can only be picked up in liver biopsy.
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What antigens can be picked up in the blood if someone is infected with hepatitis B and what do these mean?
Anti-HBs - protection
IgM anti-HBc - acute infection (first one to go up, if IgM positive, virus has been acquired in the last 6m, 90% of chance clearing virus)
IgG anti-HBc - chronic infection/exposure (IgG positive, IgM negative - no longer able to clear virus themselves)
Anti-HBe - inactive virus
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What complications are associated with Hep B?
Further progression and liver cirrhosis.
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How is hepatitis B treated?
Pegylated interferon, oral antiviral drugs (adeflovir, entecavir).
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What is the route of transmission in hepatitis C?
Blood route - needle sharing commonest.
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What might you find when you investigate hepatitis C?
May have normal LFTs, diagnostic test is to look for antibodies against hepatitis C.
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What symptoms are experienced in hepatitis C?
10% have acute jaundice. Most asymptomatic until cirrhotic.
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How is hepatitis C managed?
Lifestyle changes to prevent further live damage. Pegylated interferon (encourages immune system to fight virus), ribacvarin (antivirals).
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What can result from hepatitis C infection?
Liver cancer and cirrhosis.
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What is hepatitis D?
Small RNA virus that doesn't code for its own protein coat, eveloped by BHaAg, co-infection or super-infection with HBV (parasite of HBV). Very resistant to Rx.
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What is infection with hepatitis E like?
Self-limiting, acute infection. No long term sequelae.
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What is the commonest source of hepatitis E infection in the UK?
Infected pork meat.
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How is hepatitis E spread?
Faecal-oral route.
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How do you treat hepatitis E?
Don't - it's self-limiting.
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What symptoms can you experience in hepatitis?
Muscle/joint pain, fever, nausea, fatigue, anorexia, abdominal pain, dark urine, jaundice, itch.
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Which people get autoimmune hepatitis?
Females.
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What will investigations show in autoimmune hepatitis?
Abnormal LFTs, elevated IG, three types of antibodies (ANA, SMA - type 1, LKM1 - type 2, SLA - type 3).
Liver biopsy will show lymphocyte infiltration and inflammation of the liver.
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How do you treat autoimmune hepatitis?
Steroids, long term azathioprine.
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What other viruses can be involved in liver disease?
Hepatitis F - probably variant of B
Hepatitis G - related to HCV
Hepatitis GB - ?cause liver disease
EBV - cause mildly deranged LFTs only in immunocomp
CMV
Herpes simplex - rare severe acute hepatitis
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What is non-alcoholic fatty liver disease?
Umbrella term encompassing:
- Simple steatosis
- Non-alcoholic steatohepatitis (NASH)
- Fibrosis and cirrhosis
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What is simple steatosis?
A largely harmful build up of fat in the liver cells.
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What is NASH?
A more serious form of NAFLD, where the liver has become inflamed.
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What is fibrosis?
Persistent inflammation causes scarring of liver and nearby BVs - but liver still able to function normally.
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What is cirrhosis?
Most severe stage, happens years after inflammation. Liver shrinks and becomes lumpy and scarred. Damage permanent and leads to liver failure.
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What investigations can you do in NAFLD?
AST/ALT ratio, enhanced liver fibrosis panel (ELD), hyaluronic acid, TIMP,-1, PIINP, cytokeratin-18, USS, fibroscan (distinguish between cirrhosis and non-cirrhosis), MRI/CT, NE spectroscopy (quantify fat), liver biopsy.
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What causes NAFLD?
Assoc. with metabolic syndrome (DM, obesity, hypertriacylglyceridaemia, HTN).
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What are risk factors for NAFLD?
Age, ethnicity (e.g. hispanics), genetic factors (e.g. PNPLA3 gene).
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What symptoms are associated with NAFLD?
Dull/aching pain in top right quadrant, fatigue, unexplained wt loss, weakness.
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What is the progression of NAFLD?
Normal liver --> steatosis --> NASH +/- fibrosis --> cirrhosis.
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How is NAFLD treated?
Diet, weight loss, insulin sensitisers (metformin, pioglitazone, glucagon like peptide-1 analogues, farnesoid X nuclear receptor ligand, e.g. obeticholic acid, vitamin E. Bariatric surgery may be needed
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What are the main autoimmune liver diseases?
Autoimmune hepatitis
Primary biliary cholangitis
Primary sclerosing cholangitis
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What is primary biliary cholangitis?
Organ specific autoimmune disease leading to granulomatous inflammation involving the intrahepatic bile ducts. Loss of intrahepatic bile ducts makes secretion of bile difficult.
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In which group of people is PBC and PSC mostly found?
Females in PBC, males in PSC.
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What would you find when you investigate PBC?
IgM elevated, antimitochondrial antibody positive (this is diagnostic), raised serum alkaline phosphatase v. helpful in diagnosis. Biopsy rarely done, would show bile duct inflammation.
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What symptoms are associated with PBC?
Pruritus, fatigue, dry mouth and eyes, pain/discomfort in upper right quadrant.
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What can PBC progress to?
Cirrhosis.
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How do you treat PBC?
Ursodeoxycholic acid (bile acid) helps flush out bile salts from the liver.
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What is primary sclerosing cholangitis?
Chronic inflammation and fibrous obliteration of bile ducts. Sclerosing = structuring, narrowing of intrahepatic and extra hepatic ducts.
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What would you find when investigating patients with PSC?
pANCA postiive, MRCP test of choice.
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What disease is PSC associated with?
IBD.
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What are the signs and symptoms of PSC?
Jaundice, pruritus, fever, fatigue, upper right quadrant discomfort.
