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Phase 2a Flashcards > GI > Flashcards

GI Flashcards

1
Q

What is helicobacter pylori? Key biochem feature? Spread? Higher colonisation where?

A

Gram -ve, curve motile rod, microaerophilic, related–> campylobacter genus and spirochetes, polar sheathed flagella= corkscrew motion
Urease positivity- used in testing, person-to-person spread
In developing countries

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2
Q

Pathogenesis of helicobacter pylori?

A

Adapted to living gastric mucus–> microaerophilic, motile, urease generates ammonium to buffer acidity, need ectopic gastric mucosa for duodenal/ oesophgeal colonisation, induces inflammation–> mononuclear and neutrophilic cellular infiltrate in lamnia propria, Treg and Th17 responses, stimulates increased gastrin–> increased parietal mass but may also modulate gastric acid production

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3
Q

Natural history of campylobacter pylori?

A

Acquisition usually asymptomatic- may cause nausea and epigastric pain, chronic diffuse superficial gastritis, followed by period of achlrorrydria
Persistent colonisation in most, might clear if not host adapted or antibiotics, eradication if HP+ controversial often no benefit and might only benefit select sub-population

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4
Q

% duodenal ulcers associated with HP? Duodenal colonisation associated with what? Increased with what strains? % gastric ulcers? What increases healing and reduces relapse?

A 
90%
Gastric metaplasia and duodenitia
cagA+ strains
50-80% gastric ulcers
Antimicrobials
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5
Q

Gastric cancer associated with reduced what? What does this? Gastric lymphoma leads to what? Other disease associations?

A

Gastric acid
H.pylori
Chronic antigen stimulation causing mucosal associated lymphoid tumours
Oesophageal disease–> gastro-oesophageal reflux, Barrett’s oesophagus and oesophageal adenocarcinoma, increased asthma, height and ITP all linked

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6
Q

Investigation for h.pylori?

A

Serology- rapid but no assessment of clinical state, lower sensitivity
Stool antigen- can assess response to therapy after 6-8 weeks, urea breath test- only 60% sensitivity- need equipment, more invasive but quantitative and rapidly responsive to Tx, endoscopy with urease test, histology +/- culture= best if symptoms, more invasive, can allow culture and antibiotic sensitivity but not widely available

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7
Q

Tx for h.pylori?

A

Omeprazole, amoxicillin IV/oral- inhibits enzymes for peptidoglycans in bacterial cell walls–> lysis, clarithromycin ORAL/IV- inhibit protein synthesis–> 50S subunit of ribosome and block translocation- stops bacterial growth

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8
Q

Causes of infectious diarrhoea (gastroenteritis)? How will c.diff infection differ? Pt w/ severe B cell immunodeficiency may get what? Transplant pt may get what? Non-infectious causes? Diagnose in stool by what for what and what?

A

Viral (rotavirus,) foodborne (s.aureus,) travel related (e.coli, giardiasis)–> watery diarrhoea, bloating and malabsorption
More severe/ prolonged
Severe giardiasis
Cytomegalovirus/ parasites or feature of systemic infection with sepsis or malaria, potential HIV infection
Malignancy, overflow with constipation, endocrine
Microscopy for ova and parasites or antigen, Tx= metronidazole

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9
Q

History for infectious diarrhoea?

A

Work, acute/ chronic- acute< 2 weeks, risk factors, HIV, may be non-infectious, achlorhydia- absence of HCl in gastric secretions, on PPIs, travel, diet change, contact with D&V, any fever/ pain, chronic diarrhoea alternating with constipation= irritable bowel, weight loss, nocturnal diarrhoea and anaemia= close follow-up

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10
Q

Bloody diarrhoea also known as what? Organisms? Diagnosis? Tx?

A

Dysentry
Shigella/ salmonella, campylobacter, e.coli, amoebiasis, abdo pain
Examination of cysts in stool, antigen, PCR or serology
Metronidazole and intraluminal agent, UC, Crohn’s, colorectal cancer, colonic polyps, pseudomembranous colitis, ischaemic colitis

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11
Q

Mucus in stool occurs in what conditions? Frank pus suggests what? White cells are microscopically absent in what 4 things?

A

IBS, colorectal cancer and polyps
IBD, diverticulitis or a fistula/ abscess
Amoebiasis, cholera, e.coli and viruses

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12
Q

Explosive diarrhoea in what? Large bowel diarrhoea organisms? Features?

A

Cholera, giardia, yersinia; rotavirus
Salmonella, shigella, c.diff and entamoeba
Watery stool+/- blood/ mucus; pelvic pain relieved by defecation; tenesmus; urgency

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13
Q

Small bowel symptoms? Travellers diarrhoea most commonly due to what? Also caused by what? Symptoms?

A

Periumbilical/ RIF pain not relieved by defecation
Salmonella/ campylobacter/ shigellosis, also cryptosporidiosis, giardiasis, amoebiasis
Dehydration, decreased skin turgor, capillary refill>2s, shock, fever, weight loss, clubbing, anaemia, oral ulcers, rashes, abdo masses
Do rectal exam for masses/ impacted faeces, any goitre?

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14
Q

Investigations for travellers diarrhoea?

A

FBC- decreased MCV/ Fe deficiency, increased if alcohol abuse or B12 absorption decreased, eosinophilia if parasites, ESR/CRP raised- infection, Crohn’s/ UC, cancer
U&E- K+ decreased= severe D&V, TSH decreased–> thyrotoxicosis, coeliac serology
Stool: MC&S–> bacterial pathogens, ova cysts, parasites C.diff toxin, faecal fat excretion or chiolein breath test

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15
Q

Other investigations for infective diarrhoea?

A

Rigid sigmoidoscopy- with biopsy of normal and abnormal looking mucosa- 15% of patients with Crohn’s disease have macroscopically normal mucosa
Colonoscopy/ barium enema- avoid if acute, normal= consider small bowel radiology (Crohn’s) +/- ERCP (chronic pancreatitis)

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16
Q

Management of infectious diarrhoea?

A

Treat cuases, food handlers- no work until stool samples -ve, close wards, oral rehydration better than IV, if dehydrated and bloody diarrhoea> 2 weeks= IV fluids may be needed
Codeine phosphate PO or loperamide PO after each loose stool decrease stool freq- avoid in colitis
Avoid antibiotics unless systemic upset
Antibiotic associated may respond to probiotics (lactobacilli)

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17
Q

What is deontology based on? May compile what? What about consequentialism?

A

Based on belief that we owe a duty of care to each other
Telling of whole truth in a way which is unkind
Consequences matter- how you get there doesn’t
Hard to know what they will be, some actions= wrong, even if consequences good

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18
Q

What are virtue ethics? Centres ethics on what? Cons? 5 Cs of ethical duties?

A

Characteristics that promote human flourishing: compassion, patience, kindness, fidelity
Centres ethics on whole person and what it means to be human
No clear guidance for moral dilemmas, no agreement on what virtues are, relative to culture
Candour, consent, capacity, confidentiality, communication

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19
Q

What is the clinical truth? Truth-telling needs to be sensitive to what things?

A

Contextual, circumstantial and personal, cannot ignore objective truth, must be relegated to it either
Culture, time, person and amount

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20
Q

What is teamwork? What are the Belbin team roles?

A

Work done by several associates with each doing a part but all subordinating personal prominence to the efficiency of the whole
Plant- creative, imaginative, unorthodox
Resource- extrovert, enthusiastic, develops contacts
Coordinator- mature, chairperson
Shaper- dynamic, challenging
Monitor evaluator- strategic
Teamworker- cooperative
Implementer- disciplined
Completer- painstaking, conscientious
Specialist- single-minded, skill and knowledge

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21
Q

Teamwork issues? 6 components of teamwork?

A

Lack of teamwork- lack of working together, lack of leadership, lack of effort- ‘social loafing’
Communication/SBARR, leadership, authority gradient, situational awareness, declaring an emergency, training together- stimulation

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22
Q

What is a doctor’s obligations? What is Hippocratic paternalism?

A

Duty to patient, accountable–> employer and regulator, responsible to each other, profession, matters of public health, moral obligations
Medicine had little to offer but hope, ‘bad news’ destroyed hope, concealment= was in patient’s best interests, doctors and medicines rep was at stake

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23
Q

Examples of end of life care? What is whistleblowing?

A

Euthanasia, DNAR, advance directives, withholding and withdrawing Tx, assisted suicide
Raising concerns about a person, practise/ organisation, GMC= patient care first concern, duty to report- harm to pt may occur

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24
Q

What are Immanuel Kent’s 2 formulas?

A

1) Of universal law- before acting, consider whether could live in world where everyone acted in this way
2) Formula of humanity- people are always treated as ends in themselves, never as means to an end

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25
Q

What is the gut? GIT occupies where? What is an intestinal obstruction? A Volvus? Adhesions?

A

Digestive tract mouth–>anus
Through head, neck, thorax and abdomen
Blockage to the transit of intestinal contents through the gut
Twist/ rotation of segment of bowel
Sticking together- abdominal structures, bowel loops or omentum, other solid organs, abdominal wall

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26
Q

What is intesussuption? Atresia? Hernia?

A

Telescoping of one hollow structure into its distal hollow structure
Absence of opening or failure of development of hollow structure
Abnormal protrusion through normal/ abnormal defects of body cavity

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27
Q

Features of obstruction? Fermentation of the intestinal contents in established obstruction causes what? Colic occurs when? May be absent in what? Constipation need not be what?

A

Vomiting, nausea and anorexia
‘Faeculent’ vomiting- when there is a colonic fistula with the proximal gut
Early- absent in long-standing complete obstruction
Absolute if obstruction is high- i.e. no faeces or flatus passed- one off movement doesn’t exclude SBO

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28
Q

In distal obstruction what will happen? Abdominal distension is more marked as what happens? There are what sounds? 3 key decisions in intestinal obstruction?

A

Nothing will be passed
As the obstruction progresses
Active, ‘tinkling’ bowel sounds
1) Is obstruction small or large bowel? 2) Is there an ileus or mechanical obstruction? 3) Is the obstructed bowel simple/ closed loop/ strangulated?

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29
Q

What happens in SBO? What is shown on AXR? What is ileus obstruction?

A

Vomiting occurs earlier, distension is less, pain higher in abdomen
AXR= central gas shadows with valvulae conniventes that completely cross the lumen and no gas in large bowel, LBO= pain is more constant

Functional obstruction from reduced bowel motility, no pain and bowel sounds= absent

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30
Q

What are simple, closed loop and strangulated obstructions?

A

Simple= one obstructing point and no vascular compromise, closed loop= at 2 points, risk of perforation usually at caecum, strangulated= blood supply compromised and patient is more ill than expected, sharper more localised pain, peritonism= cardinal sign, may be fever and WCC increase with other mesenteric ischaemia signs

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31
Q

SBO causes?

A 
SBO= adults= adhesion- previous surgery, increased incidence= pelvic, gynaec, colorectal surgery, hernia, strangulation groin hernia, Crohn's, malignancy, children= appendicitis, intesussuption, volvulus, atresia, hypertrophic pyloric stenosis 
Uncommon= radiation, gallstones, diverticulitis, appendicitis, sealed small perforation, intraabdominal collection/ abscess, foreign bodies
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32
Q

LBO causes? Pathophysiology?

A

Age and race dependent- US/Europe= 90% colorectal malignancy, Africa= 50% volvulus, paed= anatomical development, diverticular stricture, volvulus
Colon proximal to obstruction dilates- increased colonic pressure w/ decreased mesenteric blood flow, mucosal oedema, arterial blood supply compromised

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33
Q

Bacterial translocation causes what? If ileocaecal valve competent? If ileocaecal valve incompetent? Management of obstruction?

A

Sepsis
Caecum is the usual site of perforation
There is faeculent vomiting

General principles= cause, site, speed of onset, completeness of obstruction
Strangulation and LBO= surgery, ileus and incomplete SBO= managed conservatively at least initially

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34
Q

Immediate action for obstruction? Further imaging? Surgery?

A

‘Drip and suck’- NGT and IV fluids, analgesia, blood tests, AXR, erect CXR, catheterise to monitor fluid status
Early CT if clinical and radiographic= inconclusive, case for LBO by colonoscopy
Oral gastrografin= partial SBO, mild action against mechanical obstruction
Strangulation= emergency and closed loop, stents= obstructing large bowel malignancies in palliation/ bridge to surgery

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35
Q

Untreated obstruction–>? Intestinal obstruction can be what, what or what? 3 causes of intraluminal obstruction?

A

Ischaemia, necrosis, perforation
Intraluminal, intramural or extraluminal
Tumours (carcinoma, lymphoma,) diaphragm disease- can be NSAIDs caused, gallstone ileus

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36
Q

4 causes of intramural obstruction? What is diverticulosis? Diverticular disease? Diverticulitis? Diverticulum?

A

Inflammation–> Crohn’s disease, diverticular disease, tumours, Hirschsprung’s disease
Outpouching of gut wall, usually at sites of entry of perforating arteries
Diverticula= present, disease= symptomatic
Inflammation of the diverticulum
Can be acquired/ congenital, may occur elsewhere, most important= acquired colonic diverticula

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37
Q

Pathology of diverticulosis? Diagnosis?

A

Most in sigmoid colon, lack of dietary fibre–> high intraluminal pressure, force mucosa to herniate through muscle layers of gut at weak points adjacent to penetrating vessels, majority= asymptomatic
Incidental at colonoscopy, barium enema if altered bowel habit and abdominal pain, CT abdomen= confirm acute diverticulitis, extent and complications, AXR= obstruction, free air or vesicle fistulae

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38
Q

Complications of diverticulosis?

A

Altered bowel habit+/- left-sided colic received by defecation; nausea and flatulence, high fibre diet try, antispasmodics may help, surgical resection resorted to
Diverculitis, perforation, haemorrhage, fistulae, abscesses

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39
Q

4 causes of extraluminal obstruction? 2 volvulus types?

A

Adhesions, volvulus, peritoneal tumour, ovarian carcinoma
Sigmoid- bowel twists on its mesentery–> strangulated obstruction, AXR= ‘inverted U’ loop of bowel looks like coffee bean
Gastric- rare, typically 180 degrees rotation–> pylorus and oesophagus–> incarceration and strangulation–> vomiting, pain and failed attempts to pass an NG tube

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40
Q

Presenation of hernias? What does irreducible and incarceration mean? Obstructed and strangulated hernias?

A

Straining event, sensation of discomfort, appearance of lump, discovery of painless lump
Can’t be pushed back into the right place
Contents of the hernia sac are stuck inside by adhesions
GI hernias obstructed if bowel contents can’t pass through due to pressure of hernia edges
Blood supply to hernia contents= impaired–> gangrene and perforation of hernia contents (urgent surgery!)

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41
Q

Where does an inguinal hernia pass through? Pre-disposing factors? Examination?

A

Through the deep inguinal ring (midway between pubic tubercle and anterior superior iliac spine) & through the external ring and present above and medial to the pubic tubercle
Male, age, chronic cough, constipation, urinary obstruction, heavy lifting, ascites, past abdominal surgery
Look for previous scars, feel the other side, examine external genitalia, ask:
is lump visible, pt to cough, repeat with pt standing

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42
Q

How do you distinguish between direct and indirect inguinal hernia? Management?

A

Reduce the hernia and occlude the deep ring w/ 2 fingers (add pressure,) ask pt to stand/ cough–> hernia restrained= indirect, if not= direct
Advise pt to diet if overweight and stop smoking pre-op, warn of recurrence, laparoscopic repair

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43
Q

Where does femoral hernia travel? Presdisposing factors? Diff diagnosis? Tx?

A

Bowel enters femoral canal- presents as mass in upper medial thigh points down leg, likely to be irreducible and to strangulate due to rigidity of canal’s borders
Women, Middle Ages, elderly
Inguinal hernia, Saphena varix, enlarged Cloquet’s node, lipoma, femoral aneurysm, psoas abscess
Tx= surgical repair recommended= herniotomy–> ligation& excision of the sac, herniorrhaphy- repair of hernia defect

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44
Q

Where does umbilical hernia travel? Risk factors? Tx?

A

When tissue protrudes around the umbilicus, momentum/ bowel herniates through the defect
Obesity, heavy lifting, persistent coughing, multiple pregnancies, ascites
Tx= surgery involving repair of the rectus sheath

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45
Q

Where does epigastric hernia travel? Incisional? Spigelian? Lumbar? Richter’s?

A

Through linea alba above the umbilicus
Follows breakdown of muscle closure after surgery, obese= repair isn’t easy, mesh repair= decreases recurrence but increases infection
Occurs through the linea semilunar is at the lateral edge of the rectus sheath, below and lateral to the umbilicus
Through the inferior/ superior lumbar triangles in posterior abdominal wall
Involves bowel only

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46
Q

What does Maydl’s hernia involve? Littre’s? Obturator? Sciatic? Sliding?

A

Herniating double loop of bowel, strangulated portion may reside as single loop inside abdominal cavity

Hernial sacs containing strangulated Meckel’s diverticulum

Through obturator canal, typically pain along medial side of thigh in thin woman

Through lesser sciatic foramen

A partially exztraperitoneal structure- caecum on R, sigmoid colon on L

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47
Q

What does sliding and rolling hiatus hernias involve? Imaging and tx?

A

Sliding= where GO junction slides up into chest, acid reflux, rolling= GO remain, bulge of stomach herniates up into chest alongside oesophagus, gross acid reflux= uncommon
30% pt> 50 y/o, 50%= symptomatic GO reflux
Barium swallow= best diagnostic test, upper GI endoscopy= visualises mucosa but can’t reliably exclude hiatus hernia
Tx= lose weight, treat reflux, surgery if symptomatic despite meds, repair rolling hiatus hernia prophylactically as it may strangulate

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48
Q

3 types of mesenteric ischaemia? What does acute almost always involve? Causes and most common?

A

1) Acute mesenteric ischaemia
2) Chronic mesenteric ischaemia
3) Chronic colonic ischaemia
Superior mesenteric artery thrombosis/ embolism, mesenteric vein thrombosis/ non-occlusive disease
Arterial thrombosis= becoming most common, venous= more in younger patients with hyper coagulable states and tends to affect smaller lengths of bowel
Non-occlusive disease= low-flow states, reflects poor CO, recent cardiac surgery or renal failure

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49
Q

Presentation, tests and Tx of acute mesenteric ischaemia?

A

Acute severe abdominal pain, no abdominal signs, rapid hypovolaemia–> shock, pain= constant, central or around RIF, degree of illness often far out of proportion with clinical signs
May be Hb increase, WCC increase, modestly raised amylase, persistent metabolic acidosis, early on= ‘gas-less’ abdomen, arteriography, CT/ MR angiography- provides a non-invasive alternative to simple arteriography
Resuscitation with fluid, antibiotics and usually heparin required, thrombolytics via catheter if arteriography, surgery= remove dead bowel, maybe revascularisation

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50
Q

Prognosis for acute mesenteric ischaemia? Presentation and tests for chronic mesenteric ischaemia?

A

Poor for arterial thrombosis and non-occlusive disease<40% survive, though not so bad for venous and embolic ischaemia
Triad of severe, colicky post-prandial abdominal pain, decreased weight (eating hurts,) upper abdominal bruit may be present+/- PR bleeding, malabsorption, nausea and vomiting, AF
CT angiography and contrast enhanced MR angiography replacing traditional angiography, Doppler USS may be useful

Surgery considered due to ongoing risk of acute infarction
Perc transluminal angioplasty and stent= replacing open revascularisation= less post-op morbidity and mortality, higher restenosis rates

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51
Q

Chronic colonic ischaemia usually follows what? Presentation, tests and tx?

A

Low flow in inferior mesenteric artery territory and from mild ischaemia–> gangrenous colitis
Lower left-sided abdominal pain+/- bloody diarrhoea
CT may be helpful, colonoscopy and biopsy= ‘gold-standard’, barium enema= ‘thumb-printing’ of submucosal swelling
Usually conservative with fluid replacement and antibiotics, strictures common but most recover
Gangrenous ischaemic colitis= prompt resuscitation followed by resection of affected bowel and stoma formation, mortality= high

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52
Q

Epidemiology of colorectal carcinoma? Risk factors? Reduce risk?

A

Usually adenocarcinoma, 3rd most common worldwide, majority= distal colon, those >60 y/o, more in males than females, in Western countries than in Asia or Africa

Increasing age, low fibre diet, saturated animal fat and red meat, sugar consumption, colorectal polyps, alcohol and smoking, obesity, adenomas, UC, family history, genetic disposition: FAP, HNPCC, 1st degree relative<40 y/o

Veg, garlic, milk, exercise, low-dose aspirin

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53
Q

Pathophysiology of colorectal carcinoma? Clinical presentation of L and R-sided?

A

Normal epithelium–> adenoma–> adenocarcinoma
Nearly all= adenocarcinoma, polypoid mass with ulceration, spreads by direct infiltration through bowel wall then to lymphatic and blood vessels and metastasis to liver and lung
Closer cancer to outside= more blood and mucus visible
Left-sided= altered bowel habit, PR mucus/ bleeding or obstruction, pass PR, tenesmus
Right-sided= weight loss, low Hb, abdominal pain, blood with poo so can’t see if you see pt w/ iron deficiency anaemia, colonoscopy? Anaemia and mass

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54
Q

Emergency presentation of colorectal carcinoma? Diff diagnosis? Investigations?

A

Obstruction (absolute constipation- no air coming out, Colicky abdominal pain, abdominal distension, vomiting)
Anorectal pathology- haemorrhoids, anal fissure etc, colonic pathology- polyp/ cancer, diverticulitis, colitis
SI and stomach pathology- massive upper GI bleed, Meckel’s diverticulum, small bowel angiodysplasia

Faecal occult blood following symptoms- good for screening, not diagnosis- dietary restrictions 3 days before
Tumour markers, colonoscopy- gold standard, double contrast barium enema, CT colonoscopy

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55
Q

2 types of hereditary polyps? Reasons for identifying HNPCC cancers? Macroscopic features of colorectal cancer?

A

1) Familial adenomatous polyposis- normal colon born, teens= 1000s polyps, few/1000 become cancerous
2) Hereditary non-polyposis colorectal cancer HNPCC- mutation in one of mismatch repair genes- earlier age onset cancer, DNA damage not recognised
Risk of further cancers in index patient and relatives, possible therapy implications, apoptosis not activated
38% in rectum, anus, recto-sigmoid junction–> all palpated with finger, all adenocarcinoma from glandular epithelium

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56
Q

If you find a cancer, who in MDT meeting? Spread via what in colorectal carcinoma? Staging? Prognosis?

A

Colorectal surgeon, oncologist, radiologist, gastroenterologist, colorectal nurse practitioner, stomatherapist
Local, lymphatic, by blood- to liver, blood, bone or transcolemic
TNM preferred to old Dukes’ criteria
A= restricted to muscularis mucosae, B= extension through this, C= involvement of regional lymph nodes
5 yr for stage 1 75%, drops to 5% for stage 4 - hence imperative for screening

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57
Q

Staging investigations for colorectal carcinoma? Operative technique?

A

Bloods, CT chest, abdomen and pelvis, surgery or no surgery? Only if chance of cure, offered if no metastatic spread and no inoperable intraperitoneal disease
Laparoscopic= as safe as open, same survival, shorter length of stay
R hemicolonectomy- for caecal, ascending, proximal transverse
L hemicolectomy- distal transverse or descending colon
Sigmoid colectomy- for sigmoid tumours
Anterior resection- for low sigmoid/ high rectal
Abdomen-perineal resection for tumours low in rectum

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4
5
Perfectly
58
Q

Post-op procedure for colorectal carcinoma? Radiotherapy usually for who?

A

Review histology, TNM, Dukes staging, patients with stable liver metastases delayed liver surgery, stage C= adjuvant chemo to increase life expectancy
Palliation for colonic cancer, pre-op in rectal cancer to allow resection, post-op in rectal tumours at high risk local recurrence

59
Q

What are colonic polyps? Adenomas?

A

Abnormal growth of tissue projecting from colonic mucosa, single/ multiple, most asymptomatic and found by chance, removed at colonoscopy, in rectum/ sigmoid colon= with bleeding

Precursor lesion in most cases of colon cancer
Benign, dysplastic tumour of columnar cells or glandular tissue, vast= sporadic and not inherited , presence increases with age, rare before 30 y/p

60
Q

Epidemiology of small intestine tumours? Risk factors? Presentation and diagnosis?

A

Relatively resistant to development of neoplasia
Quite rare for cancer to develop- 1% of all malignancies
Adenocarcinoma= most common, lymphomas= most in ileum
Coeliac disease, Crohn’s disease
Pain, diarrhoea, anorexia, weight loss, anaemia, may be palpable mass
USS, endoscopic biopsy to histologically confirm diagnosis, CT= wall thickening and lymph nodes involvement- seen in lymphoma
Tx= surgical resection, radiotherapy

61
Q

Risk factors for oesophageal cancer? % in upper, middle and lower parts? May what 2 types? Presentation?

A

Diet, alcohol excess, smoking, achalasia, reflux oesophagitis, Barrett’s oesophagus, obesity, hot drinks, nitrosamine exposure, Plummer-Vinson syndrome
20% upper, 50% middle, 30% lower, proximal= SCC, distal= adenocarcinoma
SCC or adenocarcinoma
Dysphagia, reduced weight, retrosternal chest pain, upper 1/3= hoarse voice, cough

62
Q

Tests and Tx for oesophageal cancer?

A

Oesophagoscopy with biopsy+/- EUS/CT/MRI for staging
Survival poor with/without Tx, if localised T1/T2, radical curative oesophagectomy may be tried, pre-op chemo- can cause morbidity
Chemoradio better than radio alone
Palliation to restore swallowing in advanced disease with chemo/radiotherapy, stunting and laser use

63
Q

Epidemiology and causes of stomach cancer?

A

At gastrooesophageal junction incidence dropped, gastric body and distal = increased, poor prognosis
4th most common worldwide, most common in males, 50-70, Eastern Asia, Eastern Europe, South America
Smoking, H.pylori infection- chronic gastritis, high salt and nitrates, non-starchy veg, fruit, garlic= reduce risk, loss of p53 genes and APC genes, first degree relative- CDH1 gene, pernicious anaemia- atrophic gastritis

64
Q

Pathophysiology of stomach cancer? Presentation?

A

Normal mucosa—> h.pylori infection–> acute gastritis–> chronic active gastritis–> atrophic gastritis–> intestinal metaplasia–> dysplasia–> advanced gastric cancer
Most= advanced presentation
Epigastric pain indistinguishable from peptic ulcer disease, constant and severe
Nausea, anorexia, dyspepsia, dysphagia, anaemia, liver metastasis–> jaundice, also in bone, brain and lung
Palpable lymph node in supraclavicular fossa- Virchow’s node- usually on left side

65
Q

Diagnosis and Tx for stomach cancer?

A

Gastroscopy and biopsy- confirm adenocarcinoma, EUS- evaluate depth of invasion, CT/ MRI to help staging, staging laparoscopy for locally advanced tumours
Early= resect endoscopically, partial gastrectomy for advanced distal, proximal= total gastrectomy may be needed
Combination chemo shown to improve survival in advanced
Surgical palliation needed for pain, obstruction or haemorrhage
Locally advanced and metastatic= chemo increases quality of life and survival
Prognosis better for early gastric carcinoma

66
Q

Why are notifiable diseases notifiable?

A

Stuff that makes you very scared- anthrax, cholera, plague, rabies, SARs, smallpox, viral haemorrhage fever, yellow fever
Stuff that is nasty- acute encephalitis, botulism, brucellosis, enteric fever
Vaccine preventable diseases- acute poliomyelitis, diphtheria, measles, mumps, rubella, tetanus, whooping cough
Diseases that need specific control measures- acute infectious hepatitis, food borne, scarlet fever, TB

67
Q

Why notify about notifiable diseases?

A

Detection of any changes in a disease- outbreak detection, early warning, forecasting
Track changes in disease- extent and severity of disease, risk factors
Allows development of interventions targeted at vulnerable groups

68
Q

How to protect community from notifiable diseases?

A

Investigate: contact tracing, partner notification
Identify and protect vulnerable persons e.g. chemoprophylaxis
Exclude high risk persons or from high risk settings
Educate, inform, raise awareness, health promotion
Coordinate multi-agency responses

69
Q

What is derived from the pooled plasma of donors and contains antibodies to infectious agents that are currently prevalent in the current population? Used to protect immunocompromised children exposed to what and of individuals after exposure to what? Specific Igs available for what diseases?

A

HNIG
Measles, hepatitis A
Tetanus, hep B, rabies and varicella zoster

70
Q

Vaccines made from what things? Polysaccharide not as what as protein antigens? Protection lasts how long? Response in what is often poor? What helps to improve immunogenicity?

A 
Inactivated (killed), attenuated live organisms, secreted products, constituents of cell walls/ subunits, recombinant components
Immunogenic 
Not long-lasting 
Infants and young children 
Conjugation- e.g Hib, Men C
71
Q

What is primary vaccine failure? Secondary vaccine failure? Meningococcal infection can present as what or what? Caused by what? Spread how? What is usually required?

A

Person doesn’t develop immunity from vaccine
Initially responds but protection wanes over time

Meningitis or septicaemia 
Neisseria meningitidis
Infection not easily spread, by inhaling respiratory secretions from the mouth and throat or by direct contact (kissing)
Close prolonged contact 
Don't live long outside the body
72
Q

Epidemiology of the meningococcal infection? Most common pathogenic serogroups of neisseria meningitis? Most disease in UK caused by what serogroups? Sig fewer cases by serogroup C since what was introduced?

A

Distinct serogroups- according to their polysaccharide outer capsule
B, C, A, Y and W135
B and C
Routine vaccination

73
Q

Sequalae from neisseria meningitidis infection?

A

Brain abscess, brain damage, seizure disorders, hearing impairment, focal neurological disorders, organ failure, gangrene, auto-amputation, death

74
Q

Meningococcaemia causes what? Management? Outcomes?

A

Arterial occlusions–> gangrene of extremities and auto-amputations
Cefotaxime or Ceftriaxone, supportive Tx
More from septicaemia than by meningitis

75
Q

What is contact tracing for meningitis? Close contact includes what? Once contacts identified can be offered what?

A

Any person having close contact with a case in the past 7 days
Kissing, sleeping with, spending the night together or spending in excess of 8 hours in same room
Advice- warn about symptoms and signs, glass test, contact telephone number

76
Q

Prophylaxis for meningitis?

A

Close, usually household contacts
Ciprofloxacin- older children and adults or rifampicin (not pregnant women)
For nasal carriage, reduces spread, does not stop disease if already incubating it
If serotype= vaccine preventable, may be offered to unprotected contacts
Neither vaccine efficacy nor coverage is ever 100%

77
Q

Routine childhood immunisations for meningitis? Travel vaccination? What is a key guidance reference for all immunisations in the UK? Lists what and what?

A

Men C since 1999
Men B vaccine rolled out 2015
Quadrivalent (A, C, W135, Y) for Year 9s (pre-university)
Men A&C or quadrivalent vaccine
Green Book- indications and contraindications

78
Q

What to know regarding immunisation? What is GORD caused by? Causes?

A

Childhood immunisation schedule and the notifiable diseases
Reflux of stomach contents–> troublesome symptoms >2 heartburn episodes/ week and/or complications
May cause oesophagitis, benign oesophageal stricture of Barrett’s oesophagus
Lower oesophageal sphincter hypotension, hiatus hernia, loss of peristaltic function, obesity, slow gastric emptying, overeating, smoking, alcohol, pregnancy, drugs,, H.pylori, surgery in achalasia, systemic sclerosis

79
Q

Symptoms of GORD? Complications? Diff diagnosis?

A

Oesophageal–> heartburn, belching, acid brash, water brash, odynophagia, nocturnal asthma, chronic cough, laryngitis, sinusitis

Oesophagitis, ulcers, benign stricture, iron-deficiency
Metaplasia–> dysplasia–> neoplasia
Barrett’s oesophagus= distal epithelium undergoes metaplasia from squamous–> columnar

Oesophagitis from corrosives, NSAIDs, herpes, Candida, duodenal or gastric ulcers or cancers, non-ulcer dyspepsia, sphincter of Oddi malfunction, cardiac disease

80
Q

Tests and Tx for GORD?

A

Endoscopy for symptoms>4 weeks, barium swallow may show hiatus hernia, 24h oesophageal pH monitoring +/- manometry help diagnose GORD when endoscopy is normal

Encourage raising the bed head +/- weight loss, smoking cessation, small regular meals, avoid- hot drinks, citrus, tomatoes, onion, fizzy drinks, spicy foods, coffee, tea, chocolate, eating< 3h before bed
Avoid nitrates, anticholinergics, Ca2+ channel blockers- relax lower oesophageal sphincter, or damage mucosa- NSAIDs, K+ salts, bisphosphonates

81
Q

Drugs for GORD? Surgery?

A

Antacids, alginates relieve symptoms, PPI–> oesophagitis, metoclopramide as mono- or adjunctive therapy is discouraged (dopamine D2 receptors antagonists–> promote gastric emptying and stimulate chemoreceptor trigger zone–> reduced gut motility)

Laparoscopic aims to increase resting lower oesophageal sphincter- consider in severe if drugs not working
Atypical symptoms less likely to improve with surgery- cough, laryngitis

82
Q

4 grades Los Angeles classification of GORD?

A

Minor diffuse changes are not included, mucosal break= used to encompass the old terms erosion and ulceration
1= >1 mucosal break <5mm long not extending beyond 2 mucosal fold tops
2= >5mm long limited to space between 2 mucosal fold tops
3= mucosal break continuous between tops of 2 or more mucosal folds, less than 75% oesophageal circumference
4= >75% of the oesophageal circumference

83
Q

What is a peptic ulcer? What is dyspepsia? Risk factors?

A

A break in the continuity of an epithelial surface
1+ of following: postprandial fullness, early satiation, epigastric pain/ burning, affects 25% population

Increasing age, smoking, HTN, DM, NSAIDs, anaemia, tachycardia

84
Q

Diff diagnosis for dyspepsia? Symptoms? Red flag symptoms?

A

Non ulcer dyspepsia, duodenal/ gastric ulcer, duodenitis, oesophagitis/ GORD, gastric malignancy, gastritis
Epigastric pain often related to hunger/ specific foods or time of day, reflux indigestion, heartburn, acid taste, bloating, tender epigastrium

Unexplained weight loss, anorexia, anaemia, dysphagia, meleana/ haematemesis, swallowing difficulty, upper abdo mass, persistent vomiting, recent onset/ progressive symptoms

85
Q

H.pylori and dyspepsia?

A

If <55y/o then do test and treat w/ lansoprazole for 4 weeks to reduce symptoms and recurrence more than acid suppression alone
If 55 y/o and new dyspepsia not from NSAID use, persisting for >4-6 weeks/ alarm symptoms–> urgent endoscopy

86
Q

What things can a duodenal ulcer do? Risk factors?

A

Can hit artery–> pulsatile spurting of blood–> haemorrhage–> HTN, tachycardia, huge loss of blood volume
Erode through muscle–> hole between stomach/ duodenum and peritoneal cavity- air seen under diaphragm
Can cause pancreatitis by eroding backwards through tissue

H.pylori, drugs, increased gastric acid secretion, increased gastric emptying

87
Q

Signs and symptoms of duodenal ulcer? Diff diagnosis and diagnosis?

A

Epigastric tenderness, typically before meals/ at night, relieved by eating/ drinking milk, 1/2= asymptomatic
Upper GI endoscopy- stop PPT 2 weeks prior, test for H.pylori, measure gastrin conc when off PPIs if Zollinger-Ellison syndrome is suspected
Non-ulcer dyspepsia, duodenal Crohn’s, TB, lymphoma, pancreatic cancer

88
Q

Gastric ulcers mainly in who? Elsewhere most often what? Risk factors? Symptoms and tests?

A

Elderly, malignant
H.pylori, smoking, NSAIDs, reflux of duodenal contents, delayed gastric emptying, stress
Asymptomatic/ epigastric pain- related to meals relieved by antacids +/- decreased weight
Upper endoscopy to exclude malignancy- stop PPI 2 weeks before
Multiple biopsies from ulcer rim and base, repeat endoscopy to check healing

89
Q

Clinical approach to peptic ulcers? Investigations? Complications?

A

History- classic symptoms, red flag, alternative diagnosis
Endoscopy- can find Barrett’s oesophagus, bleeding ulcer, oesophagitis, gastritis, gastric cancer, barium enema, non oesophageal catheter, Bravo capsule- detect pH changes
Bleeding, perforation, malignancy, decreased gastric outflow

90
Q

Risk stratifying pt for gastric ulcers management? Any person high risk? Low risk? Lifestyle modifications?

A

Pre-endoscopy; Glasgow Blatchord–> using Hb, high urea, initial systolic BP/HR, presence of maelaena (black poo,) syncope, hepatic disease/ heart failure, score of 1+= investigation as in-patient
Investigation for h.pylori and eradication and IV PPI infusion for 72 hours
H.pylori test and eradication, oral PPI–> discharge with plan to re-scope all ulcers in 6-8 weeks, non healing= malignancy?

Reduced alcohol, tobacco, weight loss

91
Q

Medication for peptic ulcers? Further management?

A

a) Lifelong PPIs- oral/ injectable- tx/ prevention, of peptic ulcers/ dyspepsia, GORD and eradication of H.pylori infection in combo with antibiotics
b) Histamine H2 receptor antagonists: oral (Ranitidine)- PPIs= alternative

H.pylori detection- breath test, stool antigen test and eradication
Stop offending drug, give PPI, re-endoscope if symptoms persist, recheck H.pylori
Surgery- haemorrhage, perforation and pyloric stenosis

92
Q

Tx for functional non ulcer dyspepsia? What is gastritis? Causes? What can cause too much acid? What can mucosal ischaemia lead to?

A

Lifestyle measures, reassurance, dietary review, antidepressants, H.pylori eradication
Inflammation of stomach lining
Reflux, hiatus hernia, atrophic gastritis, granulomas
Stress, H.pylori
Fewer blood supply, won’t produce mucin, exposure to acid, gastric cells attacked, ulcer can form- treat them to raise BP, get rid of acid- PPI

Sphincter between pylorus and duodenum= bile reflux, bile acid overcome mucin
Alcohol–> direct toxic effect on stomach

93
Q

Presentation, diagnosis, prevention and tx of gastritis?

A

Epigastric pain, vomiting(haematemesis)
Endoscopy and biopsy
Give PPI gastroprotection with NSAIDs
H2 receptor antagonist or PPI, eradicate H.pylori, endoscopic cautery may be needed

94
Q

What is malabsorption? What must be ruled out before diagnosis? Causes?

A

Failure to fully absorb nutrients, either due epithelium destruction/ issue in lumen
Disorders of SI= coeliac disease, tropical sprue, Crohn’s, parasite infection
Insufficient intake

Defective intraluminal digestion, insufficient absorptive area, lack of digestive enzymes, defective epithelial transport, lymphatic obstruction

95
Q

What may cause defective intraluminal digestion?

A

Pancreatic insufficiency- pancreatitis- reduced enzyme release, CF= blocks pancreatic duct
Defective bile secretion- biliary secretion e.g. gallstone, ideal resection- bile salt reuptake reduced
Bacterial overgrowth

96
Q

What may cause insufficient absorptive area causing malabsorption?

A

Anything damaging microvilli
Coeliac disease= villous atrophy and crypt hyperplasia, lots of lymphocytes in the epithelium, Crohn’s inflame damage to lining of the bowel –> cobblestone mucosa
Giardia lamblia- surface parasitisation of villi and microvilli
Surgery- SI resection, bypass by small bowel infarction

97
Q

What may cause a lack of digestive enzymes causing malabsorption? What may cause defective epithelial transport or lymphatic obstruction?

A

Disaccharidase deficiency- undigested lactose eaten by bacteria and CO2 released–> wind and diarrhoea
bacterial overgrowth–> brush border damage

Abetalipoproteinaemia- lack of transporter protein to transport lipoprotein across cell
Primary bile acid malabsorption- mutations in bile acid transporter protein

Lymphoma, TB

98
Q

Symptoms and deficiency signs of malabsorption? What is tropical sprue and caused by what organisms? What may help?

A

Weight loss, diarrhoea, steatorrhoea, lethargy, bloating
Anaemia, bleeding disorders, oedema, metabolic bone disease, neurological features
Disease of the SI causing malabsorption of food via villous atrophy and malabsorption in far and Middle East and Caribbean- cause unknown
Giardia, cryptosporidium, isospora belli, cyclosporine cayetanensis, microsporidia

Tetracycline PO + folic acid PO+ optimum nutrition

99
Q

2 types of IBD? What is IBD defined as? Where can Crohn’s occur?

A

Crohn’s disease and ulcerative colitis
Chronic idiopathic inflammatory bowel disease
Anywhere from mouth to anus
Deep ulcers/ granulomas (in TB/ leprosy) going through bowel wall

100
Q

Unaffected bowel in Crohn’s known as what? Epidemiology? Risk factors?

A 
Skip lesions 
Highest in Northern Europe, UK and North America 
Lowe than UC per year 
Prevalence less if Asian 
More females affected 
Cause= unknown 
Smoking increases risk by x3-4 
1/5 if first-degree relative 
Presentation= mostly 20-40 y/o

Genetic association stronger than in UC, mutations on NOD2 gene on chromosome 16 increases risk, smoking, NSAIDs may exacerbate, family history, chronic stress and depression–> flares, good hygiene, appendicectomy may increase risk

101
Q

Pathophysiology of Crohn’s disease? Signs and symptoms?

A

Transmural granulomatous inflammation affecting any part of the gut, skip lesions, thickened and often narrowed bowel, cobblestone appearance due to ulcers and fissures in mucosa
Microscopic= inflammation through all layers, increases in chronic inflammatory cells and lymphoid hyperplasia, goblet cells, less crypt abscesses than UC

Diarrhoea with urgency, bleeding and pain due to defecation, acute RIF pain mimicking appendicitis, weight loss, malaise, lethargy, anorexia, abdo tenderness/ mass, perianal abscess, anal strictures

102
Q

Complications of Crohn’s disease? Diff diagnosis? Diagnosis?

A

Perforation and bleeding, fistula formation, anal; skin tags, fissure, fistula, malabsorption, SBO, toxic dilatation of colon, colorectal cancer, venous thrombosis, amyloidosis
Salmonella spp, guardia intestinali and rotavirus, chronic diarrhoea

RIF tenderness, anal examination
Anaemia common, B12 anaemia= unusual, raised ESR and CRP, WBC and platelets, hypoalbuminaemia, liver biochem may be abnormal, negative pANCA, stool to exclude c.difficile and campylobacter, faecal calprotectin- indicates IBD, not specific
Colonoscopy- spot lesions from biopsy, upper GI endoscopy= exclude oesophageal and gastroduodenal disease

103
Q

Tx for Crohn’s disease?

A

Smoking cessation, replacement for anaemia, mild attacks= controlled-released corticosteroids e.g. BUDESONIDE
Moderate- severe attakcs= ORAL PREDNISOLONE- reduce dose every 2-4 weeks if symptoms resolve
Severe= IV HYDROCORTISONE per rectum (enema,) IV metronidazole for perianal disease and abscesses
Infliximab if no improvement
Maintain remission= AZATHIOPRINE, intolerant= METHOTREXATE, INFLIXIMAB to induce remission if resistant

104
Q

Surgery for Crohn’s disease?

A

80% need at some point, avoided and only minimal resection, indicated in medical therapy failure, failure to thrive and perianal sepsis
Temporary ileostomy- allow time for affected areas to rest
Resection at worst areas- can result in short bowel syndrome–> diarrhoea

105
Q

Where does ulcerative colitis affect? Epidemiology? Risk factors?

A

Entire colon up to ileocaecal valve= 20%, rectum- proctitis (50%,) rectum and left colon- left-sided colitis (20%)
Highest incidence= Northern Europe, UK and North America, more than Crohn’s, males and females equally, mostly 15-30 years, 3x more in non-ex smokers, cause= unknown, 1/6= 1st degree relative, appendicectomy= protective
Family history, NSAIDs, chronic stress and depression–> flares

106
Q

Pathophysiology of UC? Presentation?

A

Macroscopic= starts in rectum and extends, circumferential, mucosal disease= differentiates from Crohn’s, looks reddened and inflamed, bleeds easily, ulcers pseudo-polyps in severe disease, microscopic= mucosal inflammation NOT DEEPER, no granulomata, depleted goblet cells, increased crypt abscesses

Course of remissions and exacerbations, restricted pain usually in lower left quadrant, episodic/ chronic diarrhoea with blood and mucus, cramps, bowel frequency linked with severity, acute= fever, tachycardia and tender distended abdomen, acute attack= bloody diarrhoea, at night, urgency, incontinence severely disabling
Clubbing, aphthous oral ulcers, erythema nodusum and amyloidosis

107
Q

Complications, diff diagnosis and diagnosis of UC?

A

Liver= fatty change, chronic pericholangitis, sclerosing cholangitis
Colon= blood loss, perforation, toxic dilatation, colorectal cancer
Skin= erythema nodusum, pyoderma gangrenous, joints= ankylosing spondylitis, arthritis
Eyes= iritis, uveitis, episcleritis
Alternative diarrhoea causes should be excluded

WBC count, platelets raised in moderate/ severe attacks
Iron def anaemia, ESR and CRP raised, liver biochem may be abnormal, hypoalbuminaemia, pANCA may be positive, stool samples, faecal calprotectin, colonoscopy with mucosal biopsy: gold standard, assess activity and extent
Abdo Xray to exclude colonic dilatation
Useful when too severe for colonoscopy

108
Q

Tx for UC?

A

Induce remission= AMINOSALICYLATE- topically in colonic lumen, absorbed in SI, deliver active 5-ASA to colon= sulfasalazine, mesalazine, olsalazine
Mild/moderate= ORAL 5-ASA- left-sided/ extensive, rectal 5-ASA= proctitis, oral prednisolone not respond to 5-AS
Severe= oral prednisolone, systemic features= hydrocortisone, cyclosporin, infliximab
Maintain remission= 5-ASA, azathioprine

109
Q

Surgery for UC? What is panproctocolectomy with ileostomy?

A

Not responding to tx, colectomy with ileoanal anastomosis
Whole colon removed and rectum–> ileum
Terminal ileum= ‘reservoir pouch’ to store faeces and patients remain continent
Whole colon and rectum removed, ileum onto abdominal wall as stoma

110
Q

What is gluten sensitive enteropathy? Intolerance to what leads to villous atrophy and malabsorption? Prolamin examples x3? Component of what protein?

A

Inflammation of mucosa of upper small bowel that improves when gluten is withdrawn from diet and relapses when reintroduced
Prolamin
Gliadin in wheat, hordeins in barley and secalins in rye
Gluten protein

111
Q

Epidemiology of coeliac disease? Risk factors?

A

1% population, any age but peaks in infancy and 50-60 years, males and females equally, 10% in first degree relatives and 30% risk in siblings
Other AI diseases: type 1 diabetes, thyroid disease, Sjorgens, IGA deficiency, breast feeding, age of introduction of gluten into diet, rotavirus infection in infancy increases risk

112
Q

Pathophysiology of coeliac disease?

A

Wheat: a-Gliadin= toxic, resistant to pepsin and chymotrypsin digestion because of high glutamine and proline- remain in intestinal lumen
Are deaminated through epithelium by tissue transglutaminase- increases immunogenicity
Bind to APC cells–> CD4 T cells in lamina propria via HLA class II molecules DQ2(95%) / DQ8
Pro-inflam cytokines and inflam cascade
Metaloproteinkinases and other mediators released–>villous atrophy, crypt hyperplasia and intraepithelial lymphocytes–> malabsorption
Mucosa of proximal small bowel= predom affected
Aanaemia results, damage decreases in severity towards ileum as gluten digested into small ‘non-toxic fragments’

113
Q

Presentation of coeliac disease? Diagnosis?

A

1/3= asymptomatic- on routine blood tests, stinking/ fatty stools (steatorrhoea), diarrhoea, abdominal pain, bloating, nausea, vomiting, angular stomatitis- inflam of one/ both mouth corners, weight loss, fatigue, anaemia, osteomalacia–> osteoporosis, dermatitis heptiformis- red raised patches, often with blisters that burst on scratching- elbows, knees, buttocks

Maintain gluten for 6 weeks before testing, low Hb, B12, ferritin, duodenal biopsy= gold standard, villous atrophy, crypt hyperplasia and increase intraepithelial white cell count- histologically, all reverse on gluten free diet
Serum antibody testing: 95% sensitive unless pt= IgA deficient, EMA, tTG, both= IgA antibodies, correlate with severity of muscosal damage- used for dietary monitoring

114
Q

Complications and tx of coeliac disease?

A

Lifelong gluten free diet i.e. no prolamins, eliminate wheat, barley and rye
Oats= tolerated unless flour during production, eat meat, dairy and fruit and veg, correction of vit and min deficiencies, DEXA- osteoporotic risk
Few don’t improve on strict diet, anaemia, secondary lactose intolerance, T-cell lymphoma, increased risk of malignancy due to increased cell turnover, osteoporosis

115
Q

What is IBS? 3 types? What things can contribute to IBS symptoms? Only diagnose if what?

A

A functional bowel syndrome. Diarrhoea predominant, constipation predominant, mixed
Multifactorial; visceral hypersensitivity(more sensitive to pain,) abnormal gut motility–> diarrhoea, autonomic nerve dysfunction(mood/ stress affects this,) altered gut flora–> IBS symptoms
Recurrent abdo pain/ discomfort at least 3 days/ month in last 3 months w/ improving pooing, altered stool passage/ frequency (constipation then diarrhoea,) and >2 of; urgency, incomplete evacuation, mucus in stool, worsening of symptoms after food, abdominal bloating/ distension

116
Q

Symptoms, examination and investigations for IBS? Diff diagnosis if aged >40, male, history <6m, anorexia, reduced weight, waking at night w/ pain/ diarrhoea, mouth ulcers, abnormal CRP/ ESR/ Hb, coeliac serology?

A

Nausea, back pain, lethargy, bladder symptoms, abdominal pain/ discomfort, unexplained weight loss, family history of bowel/ ovarian cancer, change in bowel habit- straining, urgency, incomplete evacuation, mucus in stool, nocturnal symptoms

Examination often normal, bloating= common

FBC, U&E- should be normal, LFT, CRP, ESR, coeliac serology

Coeliac disease, lactose intolerance, bile acid malabsorption, IBD, colorectal cancer, anaemia

117
Q

Further investigations for IBS? Management- mild, moderate, severe?

A

Colonoscopy= if >50 y/o and high temp, blood in stool, decreased weight, faecal calprotectin, CA125, TSH, upper GI endoscopy, small bowel radiology, duodenal biopsy, giardiasis test, ERCP, MRCP

Education, reassurance, diet modification
Education, reassurance, diet modification, pharmacotherapy, psychological treatments to control symptoms
Education, reassurance, diet modification, pharmacotherapy, psychological treatments, MDT approach, referral to pain tx centre

118
Q

Diet modification and pharmacotherapy for IBS? Psychological tx?

A

Regular/ small frequent meals, plenty of fluids, reduce caffeinated/ fizzy/ alcoholic drinks, reduce sorbitol sweeteners, insoluble fibre intake, restrict starch intake, fruit to 3/ day
Wind/ bloating= increase soluble fibre- avoid insoluble fibre, FODMAP diet= many foods however

Pain= antispasmodics- PRN MEBEVERINE, BUSCOPAN, constipation= laxatives, linaclotide, diarrhoea= anti motility agents- loperamide= opioid agonist in GIT, low dose tricyclic antidepressants to dampen down IBS pain, SSRIs if CI

If symptoms not responded to drugs for 12 months–> cognitive therapy, hypnotherapy (relaxation technique)

119
Q

What is a fissure-in-ano? Causes? Tx?

A

Painful tear in the squamous lining of the lower anal canal- often, if chronic, with ‘sentinel pile’ or mucosal tag at the external aspect, 90%= posterior
Most= due to hard faeces, spasm may constrict inferior rectal artery–> ischaemia, making healing difficult
Syphilis, herpes, trauma, Crohn’s, anal cancer, psoriasis

5% LIDOCAINE ointment and GTN ointment (0.2-0.4%) or topical DILTIAZEM (2%), increased dietary fibre, fluids +/- stool softener and hygiene advice
BOTULINUM toxin infection and topical diltiazem= as effective as GTN with fewer side effects
Lateral partial internal sphincterotomy

120
Q

What is a fistula-in-ano? Causes? Tests and tx?

A

A track communicated between skin and anal canal/ rectum, blockage of deep IM gland ducts–> abscesses, discharge to form fistula
Anterior- path= in straight line, posterior- internal opening is at 6 o’clock position
Perianal sepsis, abscesses, Crohn’s, TB, diverticular disease, rectal carcinoma, immunocompromised

MRI, endoanal US scan

Fistulotomy+ excision, high fistulae= require ‘seton suture’ tightened over time to maintain continence, low fistulae= ‘laid open’ to heal by secondary intention

121
Q

Anorectal abscesses usually caused by what? More common in who? Types and %s? Tx? Associations?

A

Gut organisms, in women
Perianal (45%), ischiorectal (<30%), intersphincteric (>20%), supralevator (5%)
Incise and drain under GA
DM, Crohn’s, malignancy, fistulae

122
Q

What is a pilonidal (buttock sinus)? More common in who? Tx>

A

Obstruction of natal cleft hair follicles- 6cm above anus
In-growing hair excites a foreign body reaction and may cause secondary tracks to open laterally +/- abscesses, with foul-smelling discharge
Male, obese Caucasians, those from Asia, Middle East and Mediterranean

Excision of sinus tract +/- primary closure, consider pre-op antibiotics, complex tracks can be laid open and packed individually or skin flaps can be used to cover defect, hygiene and hair removal advice

123
Q

What are haemorrhoids? From childbirth (lithotomy) position, where are the 3 anal cushions, what is also here? Attached by what but prone to what? What may make them bulky and loose–> protrude to form piles? Vulnerable to what? Bleed readily from what?

A

Disrupted and dilated anal cushions
3, 7 and 11 oclock–> anal closure
3 major arteries feed vascular plexuses enter the anal canal
Smooth muscle and elastic tissue- displacement and disruption, singly or together

Effects of gravity, increased anal tone- stress?, effect of straining at stool

Trauma e.g. hard stools
From the capillaries of the underlying lamina propria= bright red

124
Q

Why are piles not painful unless what? Diff diagnosis?

A

No sensory fibres above the dentate line (squamomucosal junction,) unless they thrombus when they protrude and are gripped by the anal sphincter, blocking venous return
Perianal haematoma, anal fissure, abscess, tumour, proctalgia fugas–> never ascribe rectal bleeding to piles without adequate examination or investigation

125
Q

Causes of haemorrhoids? Pathogenesis? Symptoms?

A

Constipation with prolonged straining, many= bowel habit may be normal, congestion from a pelvic tumour, pregnancy, CCF, portal HTN

Vascular cushions through a tight anus, become more congested and hypertrophy to protrude again more readily, these protrusions may then strangulate

Bright red rectal bleeding, often coating stools, on the tissue or drip-pig into the pan after defecation, may be mucous discharge and pruritus ani, severe anaemia may occur

126
Q

What symptoms should prompt thoughts of other pathology other than haemorrhoids? In all rectal bleeding do what investigations?

A

Weight loss, tenesmus, change in bowel habit

An abdominal examination, PR exam- prolapsing piles= obvious, internal= not palpable, proctoscopy to see internal haemorrhoids, sigmoidoscopy to identify rectal pathology higher up- no higher than rectosigmoid junction

127
Q

Tx for haemorrhoids- medical and non-operative?

A

Medical= increased fluid and fibre +/- topical analgesics and stool softener, topical steroids for short periods only
Non-operative- rubber band ligation- banding–> ulcer to anchor the mucosa, low recurrence rate
Sclerosants= 2ml of 5% phenol in almond/ arches oil–> pile above the dentate line, recurrence= higher
Infra-red coagulation- applied to localised areas of piles, coagulating vessels and tethering mucosa to subcut tissue, as successful as banding and may be less painful
Cryotherapy- high complication rate, not recommended, in all but 4th-degree piles- may obviate need for surgery

128
Q

Surgical tx for haemorrhoids? Surgical complications?

A

Excisional haemorrhoidectomy- most effective tx, excision of piles +/- ligation of vascular pedicles, day-case surgery needing 2 weeks off work (scalpel, electrocautery or laser may be used)
Stapled haemorrhoidopexy- for prolapsing haemorrhoids–> less pain, shorter hospital stay and quicker return to normal activity, when large internal component, higher recurrence and prolapse rate than excision
Constipation, infection; stricture; bleeding
Prolapse, thromboses piles= analgesia, ice packs and stool softeners, pain= resolves in 2-3 weeks, some advocate early surgery

129
Q

What is a varices? If portal pressure rises above what value, compliant venous system does and varices form? Can form where?

A

Dilated vein at risk of rupture–> haemorrhage, in GI system can result in GI bleeding
10-12 mmHg–> dilates
Gastro-oesophageal junction, rectum, left renal vein, diaphragm, anterior abdominal wall via the umbilical vein

130
Q

Gastro-oesophageal varices are what and tend to rupture resulting in what? Usually when pressure exceeds what? Epidemiology?

A

Superficial–> GI bleeding
12mmHg
90% of cirrhosis patients–> GO varices over 10 years- only third will bleed
Bleeding likely with large varices, those with red signs at endoscopy and in severe liver disease
Tend to develop in lower oesophagus and gastric cardia

131
Q

Risk factors and pathophysiology of GI varices?

A

Cirrhosis, portal HTN, schistosomiasis infection, alcoholism
Liver injury and fibrogenesis, contraction of activated myofibroblasts–> increased resistance to blood flow–> portal HTN–> splanchnic vasodilation–> drop in BP–> increased CO to compensate for BP–> salt and water retention to increase blood volume and compensate–> hyper dynamic circulation/ portal flow–> formation of collateral between portal and systemic systems–> varices above 10mmHg and bleed above 12mmHg
Can occur rapidly and could result in major haemorrhage

132
Q

Presentation of GO varices?

A

Ruptured= haematemesis, abdominal pain, shock- if major blood loss, fresh rectal bleeding- shock in acute massive GI bleed, hypotension and tachycardia, pallor, suspect varices as cause of GI bleeding if alcohol abuse/ cirrhosis
Signs chronic liver damage e.g. jaundice, increased bruising and ascites, splenomegaly, ascites, hyponatraemia

133
Q

Diagnosis and tx of GO varices?

A

Endoscopy for bleeding source
Resuscitate until haemodynamically stable
If anaemic= blood transfusion aiming to get Hb to 80g/L
Vit K and platelet transfusion for clotting abnormalities
IV TERLIPRESSIN- cause vasoconstriction, IV SOMATOSTATIN if CI e.g. in IHD
Prophylactic antibiotics
Vatical banding- using endoscope, few days vary falls off leaving scar
Balloon tamponade- reduce bleeding by placing pressure on avarice if banding fails
TIPS- only when bleeding cannot be controlled
PROPANOLOL- reduce resting pulse rate
Vatical banding repeatedly to obliterate varices
Liver transplant- best when poor liver function

134
Q

What is achalasia? Tests and tx?

A

Lower oesophageal sphincter fails to relax–> dysphagia, regurgitation, substernal cramps and weight loss
CXR- fluid in dilated oesophagus, barium swallow–> dilated tapering oesophagus

Tx= endoscopic balloon dilatation or Heller’s cardiomyotomy-then PPIs
Botulinum toxin injection if non-invasive is needed, CCBs and nitrates also relax sphincter, longstanding achalasia may cause O-cancer

135
Q

What is anorexia nervosa? Subtypes?

A

Restriction of energy intake relative to requirements leading–> sig low body weight in context of age, sex, dev trajectory, physical health- often <17.5 BMI, intense fear gaining weight/ becoming fat, disturbance in which one’s body weight/ shape experienced, influence on self-evaluation, denial of seriousness of current low body weight
Restricting/ binge-eating/ purging

136
Q

What is bulimia nervosa?

A

Recurrent episodes binge eating: eating in discrete time (within 2 hours) large amounts, sense of lack of control, purging
Binge eating and compensatory= at least once week for 3 months
Self-evaluation= influenced by body shape and weight, disturbance= not exclusively during episodes of anorexia nervosa

137
Q

What is a binge-eating disorder? Episodes= associated with 3 or more of what?

A

Recurrent episodes, episode= eating, in discrete period of time, amount that is larger than most in similar period, lack of control
Eating more rapidly than normal, until feeling uncomfortable, when not hungry, alone as embarrassed, disgust, depressed, guilty afterwards, marked distress= present
Once week for 3 months, not compensatory behaviour- purging, not exclusively during course anorexia, bulimia or avoidant intake disorder

138
Q

Other specified feeding and eating disorders (OFSED)?

A

Atypical anorexia nervosa- despite sig weight loss, in normal range
Bulimia nervosa- low freq/ limited duration
Binge-eating disorder- low freq/ limited duration
Purging disorder- still absorb some of huge amount, less weight loss, fewer symptoms thus not recognised
Night eating syndrome

139
Q

Diagnosis of eating disorders? Factors leading to onset? Summarised by what model?

A 
Most don't fit into diagnoses, atypical presentation, want to move away from rigid diagnoses- focus more on symptoms and attitudes 
Genes/ nature, family interaction, social pressures, trauma 
Core model (Slade, 1982), low self esteem+ perfectionism--> need for control
140
Q

Maintaining factors for eating disorders?

A

Initially= positive reinforcement for weight loss/ control (enhances overvaluation of eating, shape and weight as ways of defining oneself,) then terror at losing control –>
starvation, body image disturbance, cognitive rigidity, emotional instability, own body family and professionals try to take control make you eat, enhances overvaluation even more and reduce ability to respond well

141
Q

Risk assessment and management of eating disorders?

A

Important issues look for: severe restriction of food/ fluid, electrolyte imbalance, bone deterioration, physical damage- tears to oesophagus, blood in vomit, alcohol/ drug intake
Urgent signs in session- muscular weakness, problems with breathing, deterioration of consciousness, cardiac signs, rapid weight loss, risky behaviours

142
Q

Motivation for change eating disorders- they are what? What aren’t helpful? Accommodation by who doesn’t help? What is more positive?

A

‘Ego-syntonic’- makes them feel good, pros outweigh cons
Motivational interventions
Carers and loved ones
Early behavioural change w/ reinforcement for doing well

143
Q

Responsibility of doctor with eating disorders? Psychological disorders?

A

For physical and mental health, clashes with forming ‘good relationship,’ has to deal with hostility from parents and patients

‘Doing’ rather than talking therapies- diaries, weighing regularly, food
Bulimia and binge eating= CBT, can try self-guided first but not as effective, alternatives= interpersonal psychotherapy, dialectical behaviour therapy
Anorexia- family therapy for adolescent cases, anything for adults
Meds not widely supported- apart from SSRIs to reduce bulimic symptoms in limited number of patients

Phase 2a Flashcards (14 decks)

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