Gastro Flashcards
what is the pathogenesis behind ulcerative colitis?
Ulcerative colitis is an autoimmune condition of unknown cause (genetics and environment)
There is chronic inflammation of the bowl mucosa which starts in the rectum and spreads proximally through the colon (and rarely terminal ileum) but no further.
Ulcers appear on the surface of the mucosa
what is it called when ulcerative colitis affects the terminal ileum
backwash ilietus
caused by a leaky ileocaecal valve
what are the main clinical features of UC (not including extra intestinal)?
increased frequency of passing stools bloody diarrhoea urgency abdominal pain systemic upset - malaise, fever and weight loss
shows a remitting and relapsing pattern
what is the peak incidence for UC?
20s-40 yrs
what are the extra-intestinal manifestations of UC?
MSK: arthritis, clubbing, osteoporosis, sacroilitis
Skin: erythema nodusum and apthous ulcers
Eyes: Uveitis, iritis, episcleritis - sore eye
primary sclerosing cholangitis
what is primary sclerosing cholangitis?
autoimmune condition resulting in inflammation and fibrosis of the bile duct. Can lead to gall stones or and increases risk of cholangiocarcinoma
Does perianal disease occur in UC or Crohns?
Crohns - perianal abscess’s, skin tags and anal strictures
what are the complications of UC?
Toxic megacolon
increased risk of CRC
pouchitis
osteoporosis
Anaemia
perforation of ulcers and bleeding
prothrombotic state
what is toxic megacolon?
dilation of the colon >/=6cm
inflammation is so severe that nerve endings have been damaged and thus the bowel looses tone.
bowel wall becomes stretched and thin which leads to ischaemia and increases risk of perforation
what are the signs of toxic megacolon?
pain,
systemic upset: fever and tachycardia
how is toxic megacolon treated?
bowel decompression surgery is required ASAP
what is pouchitis? how is it treated?
To cure UC the colon and rectum can be removed and the terminal ileum can be used to make an artificial rectum. this can become inflamed
treat with metronidazole and ciprofloxacin
what are the risk factors for UC?
family history
certain unknown environmental factors
ethnicity
smoking is protective.
what is the treatment for UC?
mild to moderate (proctitis):
- topical mesalazine/sulfasalazine
- add oral prednisolone and oral tacrolimus if no response after 2-4 weeks
mild -moderate (diffuse inflammation):
- oral high dose sulfasalazine/mesalazine
- add oral prednisolone and tacrolimus if no response after 2-4 weeks
severe:
- IV corticosteroids and assess need for surgery
- add IV ciclosporin and infliximab if no short term response to steroids
remission maintained using sulphasalazine and mesalazine
other drugs: 5-ASA
thromboprophylaxis due to prothrombotic state
what drugs belong to the group aminosalicyclates?
sulphasalazine
mesalazine
what surgery is offtered to UC patients?
removal of the colon - total proctocolectomy
- curative
- need to have an ileostomy bag or make an ileoanal pouch (i.e. artificial rectum)
when is surgery in UC indicated?
failed medical management severe symptoms >8 times a day extra intestinal symptoms are bad likely perforation/toxic megacolon so want to reduce risk early signs of CRC e.g. polyp
what surviellence is offered to UC and crohns patients?
CRC via colonoscopy
what advice can be given to UC patients?
small meals
keep a log book of meals so you can find what makes it worse
reduce stress
exercise
avoid caffeine
plenty of fluid/hydrate due to diarrhoea
avoid anti motility drugs - can induce acute attacks and toxic megacolon
what is the pathogenesis behind crohns disease?
chronic inflammation with remitting and relapsing pattern that affect the whole thickness of the bowel wall.
mainly occurs at the terminal ileum but can occur at any point along GIT
autoimmune - cause unknown
what are the causes/risk factors of crohns disease?
family history ethnicity appendectomy - after this surgery can trigger crohns changes to gut flora smoking
what advice can be given to those with crohns?
stop smoking
small more frequent meals
avoid foods that lead to flares
avoid anti motility drugs - can induce acute attacks and toxic megacolon
what are the symptoms of crohns (not including extra intestinal) ?
vague symptoms watery non-bloody diarrhoea abdominal pain - most commonly in RLQ malaise, weight loss, tired, fever , anorexia perianal disease
what is the peak age of onset for crohns?
2 peaks: 15 to 30 , and at 60yrs
what is more common crohns or UC?
UC
what are the extra-intestinal manifestations of crohns?
MSK: arthritis, clubbing, metabolic bone disease, sacroilitis
Eyes: Uveititis, iritis, episcleritis
skin: erythema nodusum, pyoderma gangrenosum and mouth ulcers
renal stones
uncommon to get primary sclerosing cholangitis
what are the complications of crohns disease?
inflammation leads to fibrosis and strictures which can lead to bowel obstruction and perforation
fistulas - enterovesicle (UTIs), rectovaginal, enterocutaneous (can fix fistula by fistulotomy)
perianal abscess and sepsis
toxic megacolon - but not as likely as UC
malabsorption - weight loss, growth delays, anaemia (terminal ileum needed for B12) , osteoporosis
CRC
thrombolembolic disease - high platelets and thus DVT risk
what is the pharmacological treatment for crohns?
mild attacks: prednisolone 30mg for 1 week and then 20mg for 4 weeks. If resolves reduce by 5mg every 2-4weeks.
severe: IV hydrocortisone, nil by mouth, IV fluids. metronidazole esp in perianal disease/infection.
nutritional support and prophylactic heparin
maintaining remission = azathioprine and stop smoking
azathioprine can be used instead of steroids if not tolerated.
others:
TNFa inhibitors
methotrexate - can be used to maintain remission
is surgical treatment available for crohns?
yes but not as curative as for UC because crohns can affect any of the GIT and cant remove the whole thing.
most common procedure is an ileocaecal resection. ileum is then anatomosed to ascending colon.
what is the risk of removing bowel in crohns disease?
risk of short bowel syndrome
crohns can come back and just affect a different part
what are the indications for surgery in crohns?
failure to respond to medical therapy signs of CRC strictures fistula haemorrhage/perforation if it only appears to be affecting distal ileum to treat extra intestinal symptokms.
explain the differences between UC and crohns by history taking and examination
UC: bloody stools with urgency and abdopain
Crohns: more vague symptoms
on examination normal mainly but tenderness of abdomen. in crohns most likely to be right hand side and in UC left hand side. both will have extraintestinal features e.g. skin changes
Describe which blood tests you would take in crohns/UC and why?
FBC: both UC and crohns cause anaemia but for different reasons. UC due to blood loss and thus normocytic anaemia. crohns due to folate/iron/B12 deficiency and thus either macro or microcytic
CRP - inflammatory marker so should be very high if UC/crohns
LFTS: cirrhosis can also lead to rectal bleeding (portal hypertension) so rule this out
U&E: diarrhoea leads to dehydration and thus need to ensure kidney function is ok.
what is the faecal calprotectin test?
faecal calprotectin is a marker for bowel inflammation and thus will be very high in UC/crohns
why are stool cultures taken for someone presenting with symptoms of IBD?
rule out gastroenteritis
other than blood and faecal tests what other investigations would you want to do in crohns/UC?
colonscopy
AXR with barium enema for contrast
biopsy
test for autoantibodies
what auto antibodies are associated with UC and crohns?
UC - ANCA
Crohns - ASCA
what is found via colonscopy in crohns disease?
skip lesions (i.e. non continuous) cobble stone appearance - due to granulomas ulcers - white areas strictures fistulas rectal sparring mainly affecting ileum
what is found via colonscopy in UC?
continuous pattern of inflammation/ulcers
mainly rectum and colon
other than colonoscopy what is another method of endoscopy used for UC?
flexible sigmoidoscopy - only to the splenic flexure
only used if UC is likely
what is found on AXR for crohns?
fistulas
strictures give a ‘string sign of kantor’ sign
skin lesions - i.e. areas that are not affected
what is found on AXR for UC?
lead pipe colon - loss of haustra
continuous pattern - affecting rectum and colon
what could you see on plain abdo Xray (i.e. no barium) for IBD?
thumb printing sign and mural thickening - sign of inflammation
what is found on biopsy in crohns?
non-caesating granuloma (specific to crohns, but if not present doesn’t rule out crohns)
transmural inflammation
what is found on biopsy in UC
crypt abscesses and goblet cell hyperplasia
pseudopolyps = from repeated inflammation
mucosal inflammation only.
what general advice can be given to all IBD patients about their mental health, family planning and treatment?
depression - IBD affects life and so if depressed encourage to see GP
pregnancy - some medication is dangerous in preg so need to change. need to have IBD controlled before pregnancy because flares can lead to premature birth
warn of side effects e.g. any signs of infection and seek advice.
what is intussusception?
the bowel gets dragged in on its self. I.e. there is a polyp sticking out which gets dragged through the lumen of the bowel and that part of the bowel wall gets dragged with it.
what is an adhesion?
fibrous tissue resulting from previous trauma/surgery or intra abdominal infedctions. can hold two parts together in a way that can lead to bowel obstruction
who is a volvulus more likely to occur in?
neurological patients: MS and parkinsons.
Africans
chronic constipation
what is the difference between gastric vomit, bilious vomit and feculent vomit and faecal vomit?
gastric - gastric content
bilious - bile - green vomit
feculent - is due to stasis in small bowel and bacterial overgrowth producing a brown smelly vomit (looks like faeces but not)
faecal vomit - faeces
what is irritable bowel syndrome? who is it most common in?
a relapsing functional bowel disorder where there is abdominal pain associated with defaecation/change in bowel habit. more common in women aged 20-30
what is the cause of IBS?
unknown cause but there is increased smooth muscle activity and visceral hypersensitivity.
linked to stress and poor coping strategies
how does IBS present?
abdominal pain which is associated with bowel habits which may be constipation, diarrhoea or both.
distention and bloating.
examination usually normal but some tenderness
what investigations can be carried out in someone you suspect has IBS?
mainly to rule other causes of change in bowel habit out:
- FBC: ensure no infections, anaemia (IBD/CRC)
- LFTs
- TFTs : hypo/hyper thyroid
- U&Es: electrolyte disturbances can alter bowel habit
- ESR/CRP - infection/IBD
- coeliac screen
- Ca125 in women - if suspect ovarian cancer
faecal calprotectin - IBD
faecal occult blood - CRC
stool culture - infection
colonoscopy if CRC/IBD suspected
how do we diagnose IBS?
atleast 12 weeks (do not have to be consecutive) out 12 months of abdominal pain/discomfort which is associated with 2 of the following:
- increased stool frequency - change in stool appearance - relieved by constipation
AND >2 of:
urgency, incomplete evacuation, PR mucus, bloating/distention, worse after food and worse when stressed
when do we refer suspected IBS patient to secondary care?
- family history of bowel or ovarian cancer
- PR bleeding
- unintentional weight loss
- change in bowel habit and >60yrs
- anaemia
- abdo/rectal mass
- raised inflammatory markers
what advice is given to patients with IBS i.e. conservative management?
explain condition and reassure
encourage to keep a log book so can make correlations of what makes them worse. Get dietician to help. e.g. reduce caffeine, alcohol and fizzy drinks.
everyone is different so some remedies e.g. high fibre may help those with constipation but not others.
in general reduce sorbital intake for diarrhoea and stay hydrated for constipation
increase sleep and exercise
reduce stress
how can we treat constipation in IBS?
sometimes high fibre can be problematic and increase flatulence and bloating.
laxative:
- bisacodyl and sodium picosulphate
- isphagula
- not lactulose - bloating gets worse
how can we treat diarrhoea in IBS?
loperamide
bulking agents
how can we treat colic pain/bloating in IBS?
antispasmodics - mebeverine
peppermint oil
how can we treat psychological symptoms and visceral hypersensitivity in IBS?
tricyclic antidepressants - amitriptyline
SSRIs
psychotherapy
what is the pathogenesis behind appendicitis?
there is inflammation caused by: infection, faecolith, worm, tumour, foreign body, lymphodenitis
this inflammation leads to increased intraluminal pressure and swelling
the appendicular artery is an end artery and can become blocked due to reduced venous drainage
moreover thrombosis is more likely
Therefore can lead to ischaemia/necrosis and gangrene
the stasis can also promote bacterial growth which can lead to sepsis/abscess
overall there is an increased risk of perforation and peritonitis
how does someone with acute appendicitis present?
abdominal pain:
- initially vague and central (visceral in origin - appendix is a midgut organ during development)
- localises to right iliac fossa (parietal peritoneum) and now more sharp
fever if systemic upset/infection
malaise and anorexia
sometime N&V
Rarely constipations
is the pain in appendicitis always felt in the RLQ?
no sometimes the appendix can be located in abnormal places e.g. RUQ in pregnancy and sometimes retroperitoneal and thus can be felt in slightly different places. Makes it more difficult to diagnose.
what are the signs on clinical examination in appendicitis?
localised tenderness in RLQ
rebound tenderness and guarding - peritonititis
Rovsing sign
Psoas sign
McBurneys point tenderness
tachycardic and low BP
shallow breaths to reduce pain
what is the Rovsing sign?
seen in patients with acute appendicitis
continuous deep palpation of the left iliac fossa causes more pain in the right iliac fossa
what is the Psoas sign?
seen in patients with acute appendicitis
patient is asked to lie on their left with legs straight. the right leg is then extended back, stretching the right psoas muscle
this creates pain in the right iliac fossa
where is McBurneys point?
1/3 ASIS to umbilicus
What investigations would you do if you suspected acute appendicitis and why?
FBC - infection, anaemia
amylase - pancreatitis
LFTs
U&Es
urine - pregnancy test (ectopic pregnancy)
urine - sugars, ketones, protein - AKI/DKA
How would you manage someone presenting with appendicitis?
acutely unwell so ABCDE investigations IV access, fluids and nil by mouth analgesia Abx - metronidazole and cefuroxime/gentamicin
Laproscopic appendectomy
what is a laproscopic appendectomy?
operation used to remove appendix
find McBurney’s point and carry out Gridiron incision (cut bowel wall layers in different direction to ensure strong scar). find caecum and cut off appendix. ligate blood supply. close layers
what are the complications of Appendectomy?
infections of wound collection of fluid due to surgery - can lead to infection sepsis bleeding fistula
(sometimes onset of crohns disease)
what is Alvarado’s score?
Scoring system for the likelihood of appendicitis
symptoms:
- N&V 1 point
- anorexia 1 point
- migration of pain to RLQ 1 point
signs:
- rebound tenderness 1 point
- >38.5 degrees 1 point
- tenderness in RLQ 2 point s
labs:
- leucocyte shift >75% neurtrophils 1 point
- raised WCC (more than 10x10^9) 2 points
1-4 points = low risk
5-6 = moderate
>7 = high risk
what are the differentials to appendicitis?
children: ovarian cyst, meckels diverticulum
adults: ectopic pregnancy, ovarian cyst , pancreatitis, renal colic, crohns/UC, perforated ulcer, cholecystitis, meckels diverticulum, food poisoning
older adults - caecal tumour, diverticular disease
how can you differentiate renal colic from appendicitis ?
renal colic - patient will be moving around in pain
appendicitis/peritonitis - patient is very rigid to reduce pain.
what is acute mesenteric ischaemia?
sudden decrease of blood supply to bowel which if not treated can lead to necrosis, infection and death
what are the causes of acute mesenteric ischaemia?
thrombosis in situ - atherosclerosis
emboli - e.g. cardiac arrhythmia, post MI , prosthetic heart valve
venous occlusion - coagulopathy/malignancy
hypovolemic shock
cardiogenic shock
what are the risk factors for acute mesenteric ischaemia?
risk factors that are the same for atherosclerosis - smoking, hypertension and hyperlipidaemia
what are the clinical features of acute mesenteric ischaemia?
generalised abdominal pain
usually more on the left hand side (because the transverse colon/descending colon junction has the poorest blood supply so most likely to become ischaemic)
bloody diarrhoea
N&V
bowel perforation can occur
tachycardia , tachypnoea, delirium
what investigations would you carry out for acute mesenteric ischaemia?
FBC , U&E, clotting, amylase
LFTs (incase coeliac trunk is affected and liver necrosis)
ABG - assess lactate and degree of acidosis
Group and save
imaging:
- AXR and erect CXR
- CT with contrast
- CT angiography for definitive diagnosis
how would you manage acute mesenteric ischaemia?
ABCDE
IV fluid resus and urinary catheter to monitor fluid balance
broad spec Abx - metronidazole/gentamicin due to risk of perforation
ITU input due to acidosis and multiorgan failure
surgery - bowel resection
how is acute mesenteric ischaemia fixed surgically?
bowel resection
revascularise - remove thrombus and stent - angioplasty
laproscopically check 24-48 hours later to make sure necrotic bowel has gone
majority of patients will have a stoma and possibly short bowel syndrome
what are the differentials for raised amylase
pancreatitis
however also : ectopic pregnancy, mesenteric ischaemia, bowel perforation and DKA
what is a Mallory Weiss tear?
tearing of oesophagus due to bulimia or vomiting due to alcohol
a.k.a. Boerhaave syndrome
what are the types of diarrhoea?
- watery/osmotic a.k.a functional - seen in IBS and after laxitives
- steatorrhoea - increased gas, float and offensive smell
- inflammatory - blood, pus or mucus - UC , crohns, bacterial infection
what are the clinical features of diarrhoea?
watery stools at least 3 times in 24 hours
may be blood /mucus
tummy cramps
may have fever
symptoms of dehydration: tired, dizzy, headache, muscle cramps, dry mouth and weakness. confusion and increased HR when severe.
what are the causes of diarrhoea?
bloody:
- campylobacter, salmonella, shigella and Ecoli
- UC
- CRC
- Diverticulitis
- ischaemic colitis
- pseudomembranous colitis
mucus:
- IBD, CRC and polyps
common causes of diarrhoea:
gastroenteritis, IBS, IBD, CRC and coeliacs
less common:
chronic pancreatitis, laxative abuse, lactose intolerance, diverticular disease, thyrotoxicosis, drugs
what drugs can cause diarrhoea?
Abx laxatives PPI metformin propanol NSAIDs
what is clostridium difficile
gram positive bacterium that lives in the bowel. Can overgrow if other bacteria are killed by Abx use.
it has very resilient spores and have toxin A and B which lead to diarrhoea and pseudomembranous colitis with a risk of toxic megacolon
what are the symptoms of C.difficile infection? what is found on blood tests?
fever, colic pain, mild to severe bloody diarrhoea
raised CRP and WCC
how is C.difficile infection treated?
stop causative Abx
may need to treat with metronidazole or vancomycin
what questions are important in the history of someone with diarrhoea?
acute or chronic ?
- acute - gastroenteritis - then ask about fever, recent travel, contacts with diarrhoea, risk factors (HIV, PPI) , any recent Abx
- chronic: IBS/ cancer - ask about weight loss/other symptoms
blood or mucus in stools
recent stress / worse with stress / change in diet - IBS
medication e.g. metformin can cause diarrhoea
what are you expecting to find on examination of someone with diarrhoea?
signs of dehydration: dry mucus membranes, reduced cap refil, oral ulcers/skin changes
may be fever
may be signs of anaema
may be goitre - if hyperthyroid
what blood tests would you want to do in someone with diarrhoea and why?
FBC - anaemia (CRC, IBD, coeliac) and WCC (infection)
raised ESR - IBD, infection, cancer
TFTs - check for hyperthyroid
coeliac serology
U&Es - check kidneys aren’t damaged due to dehydration
what would you need to test from a stool sample in someone with diarrhoea?
MC&S - infection, C diff spores /toxin
faecal calprotectin - IBD
faecal occult blood - CRC, UC, infection
faecal fat excretion
how is diarrhoea managed?
treat cause e.g. stop Abx
fluids - oral or IV
eat as normal as possible
pharmacology
- codeine phosphate
- loperamide - avoid in colitis as it may lead to toxic megacolon
avoid Abx unless systemic upset from infection
prevent spread to others.
what are the complications of diarrhoea?
dehydration (esp old/frail/pregnant) which can lead to AKI
electrolyte imbalance
reactive arthritis (infective causes)
triggers IBS
reduces effectiveness of COCP, anti-empileptic medication and diabetic medication
what are the general symptoms of malabsorption?
diarrhoea, steatorrhoea, weight loss, lethargy, bloating/flatulence
signs of vitamin deficiency’s
what are the different signs of deficiencies that may be seen in malabsorption?
anaemia (B12, folic acid and iron) bleeding (vit K) osteoporosis and bone pain /metabolic bone disease (vit D) neurological (B vitamins) oedema (proteins)
if someone is showing signs of malabsorption, what tests can you do?
FBC - see if they are anaemia
test vitamin/mineral levels: Ca, Vit D, Fe, B12 and folate
INR is increased if vit K deficient
coeliacs test
stool: sudan stain for fat globules
- faecal elastase
AXR with barium
endoscopy
hydrogen breath test
ERCP - incase pancreatitis
MRI/CTwhat is the hydrogen breath test?
radioactive glucose is eaten and then radioactive hydrogen is measured in someones breath. if raised it is suggestive that there is an overgrowth of bacteria in the small bowel
what does faecal elastase suggest?
if reduced it suggests a pancreatic deficiency
what are the causes of malabsorption?
coeliacs
chronic pancreatitis
crohns
others: CF, metformin, short bowel syndrome, infection (Giardia), dumping syndrome, reduced bile (primary biliary cholangitis, ileal resection, removal of gallbladder), bacterial overgrowth and alcohol.
what is coeliacs disease?
type IV hypersensitivity reaction to gluten and related prolamins in genetically susceptible individuals
which allele is coeliacs associated with?
HLA DQ2
who does coeliacs affect?
mainly females
can present in children OR at age 50-60yrs
what is the pathogenesis behind coeliacs?
upon exposure to gliadin and 3 peptides in prolamins the enzyme tissue transglutaminase modifies the protein and there is cross reaction with the bowel tissue causing inflammation (CD8 T cells)
there is villous atrophy leading to malabsorption because villi are needed for absorption
what is the presentation of coeliacs disease?
foul smelling, pale stools which float. diarrhoea, bloating, abdominal pain, mouth ulcers, weight loss, tiredness. signs of anaemia (angular stomatitis)
what are all the effects of coeliacs disease (Pneumonia GLIAD)?
G = GI malabsorption - overall result in fatigue and weakness - low carbs - low energy, N/V/D, flatulence, distention, colic pain - fats - steatorrhoea, hyperoxaluria (renal stones) - protein - oedema - Fe/Folate/B12 = anaemia - Vit D/Ca - bone pain/osteoporosis - vit K - bleeding, petechiae - B1 and 6 - polyneuropathy - B2 - angular stomatitis L = lymphoma and carcinoma - increased risk of GI T cell lymphoma - increased risk of adenocarcinoma of small bowel I = immune associations - IgA deficiency - type 1 diabetes - primary biliary cholangitis A= anaemia D = Dermatological - dermatitis herpetiforms - aphthous ulcers
what is dermatitis herpetiforms?
symmetrical vesicles on extensor surface esp elbows
vey itchy
on biopsy show granular deposition of IgA
responds to gluten free diet
seen in coeliacs disease
what are the specific autoantibodies found in coeliacs disease?
anti tissue transglutaminase (anti TTG igA)
endomysial Ab IgA
IgG to Gliadin peptides
what would be deficient in a blood test in someone with coeliacs? what would be raised?
vit D, ferritin, B12, albumin all low
transglutaminases would be raised on LFTs
what can be seen on a duodenal biopsy in someone with coeliacs disease?
the patient must be consuming gluten for the biopsy to be positive
villous atrophy, crypt hyperplasia and inflammatory cell infiltration
how can you manage someone with coeliacs disease?
gluten free diet - no barley, rye or oats or wheat
can eat soya and rice
add supplements to diet e.g. vitamin D and iron to prevent osteomalacia and anaemia
follow up 3 and 6 months after diagnosis and starting a gluten free diet and there should be no symptoms
keep a record of BMI, Weight and height.
Repeat blood tests to check for deficiencies
check Ab titres to confirm their new diet is good
what are the complications of coeliac’s disease?
anaemia secondary lactose intolerance osteoporosis GI malignancy risk T cell lymphoma risk bleeding disorders
what is the clinical syndrome for vitamin A deficiency?
xeropthalmia - dry conjunctiva, cloudy cornea, can lead to blindness
what is the clinical syndrome for vitamin B1 (thiamine) deficiency?
Beri Beri - heart failure
Wernickes encephalopathy
what is the clinical syndrome for B2 (riboflavin) deficiency?
angular stomatitis
what is the clinical syndrome for B6 (pyridoxine) deficiency?
polyneuropathy
what is the clinical syndrome for B12 deficiency
anaemia - macrocytic
neuropathy
glossitis
what is the clinical syndrome for vitamin C deficiency
scurvy
what is the clinical syndrome for vitamin D deficiency ?
osteomalacia/rickets
what is the clinical syndrome for vitamin K deficiency?
bleeding
what is the clinical syndrome for folic acid deficiency ?
macrocytic anaemia
what is the clinical syndrome for iron deficiency?
microcytic anaemia
what is the clinical syndrome for selenium deficiency?
cardiomyopathy
what is the clinical syndrome for vitamin E deficiency?
haemolysis, neurological deficit
what are the causes of upper GI bleeding?
- first consider it could be from oral cavity/nasopharynx
oesophagus: tumour, varices, Mallory Weiss tear, oesophagitis
stomach: peptic ulcer, tumour
duodenum: peptic ulcer (first part can lead to gastroduodenal artery bleed)
haemobilia: fistula between biliary system and vessel from splanchnic circulation
what are the causes of small bowel bleeding?
tumour ulcer IBD meckles diverticulum infectious - shigella and salmonella
what are the causes of large bowel bleeding?
tumour IBD diverticular disease AV malformations piles and varices
what are the signs and symptoms of an upper GI bleed?
haematemesis - vomiting blood
melaena - black blood stools
signs of hypovolaemia - hypotensive, pale, clammy, tachycardia, cold, reduced capillary refil time
signs of cause e.g. infectious (fever), ischaemia (pain)
signs of liver disease (varies)
what are the signs and symptoms of a lower GI bleeds?
rectal/left colon - bright red blood in stools
right colon - maroon blood
small intestine - melaena
signs of hypovolaemia - hypotensive, pale, clammy, tachycardia, cold, reduced capillary refil time
signs of cause e.g. infectious (fever), ischaemia (pain). angiodysplasia is painless. signs of liver disease (varies)
what investigations are carried out in someone with a GI bleed?
Bloods - find cause/ state of other organs - FBC, U&Es, LFTs, clotting profile
Cross match/group and save
Endoscopy - upper or lower to find the source of the bleed
CT mesenteric angiography - gold standard but only used if bleed is not found by endoscopy
what are the classes of hypovolaemic shock?
class I: - <15 % blood loss, no change in BP, not tachycardic class II: - 15-30% blood loss, raised diastolic pressure, >100bpm
class III: - 30-40% blood loss, reduced BP (both systolic and diastolic), >120bpm, high resp rate
class IV: - more than 40%, very low BP, >140bpm, >35 resp rate
urine output also falls from class I to IV
how is someone with a GI bleed managed (if they are haemodynamically stable)?
- take a good history to find cause e.g. peptic ulcer history, liver disease, weight loss/dysphagia
insert 2 large bore canulae
start IV fluids
get blood results and monitor vital signs
cross match/ group and save in case they deteriorate
how is someone with a GI bleed managed (if they are in shock)?
ABCDE
- airways: protect if vomiting blood, NBM
- Breathing - likely to have increased resp rate - high flow O2
- C: hypotensive and tachycardic: insert 2 large bore cannulae and give IV crystalloid infusion. if class III or IV hypovolaemia give O type blood until cross match is ready. catheterise to measure urine output.
ABG, FBC, LFTs, U&Es, glucose, Cross match/group and save ready for transfusion, clotting screen
- disability - Correct any abnormalities e.g. clotting abnormalities - fresh frozen plasma/ vitamin K
vital signs every 15 mins
urgent endoscopy to find cause
ECG - massive bleed can cause angina/MI
broad spectrum Abx if lower GI and perforation suspected
what scorring system is used to predict prognosis after an acute GI bleed?
Rockall scoring system
how would you manage someone presenting with acute abdomen?
history
examination
investigation:
- amylase (pancreatitis)
- FBC, U&Es (bowel obstruction can disturb electrolytes), LFTs - try find cause
- ABG - lactate - signs of hypoperfusion
- CRP
- urinalysis - rule out ectopic pregnancy
- INR
- erect CXR - perforation
- AXR/ CT - obstruction
- ECG to rule out MI
- USS of kidneys and bladder, biliary tree, ovaries and ovarian tube
- frequent obs
treat:
- NBM
- IV fluids + catheterise
- analgesia and anti emetic
- thromboprophylaxis
- deduce cause and treat
- broad spec Abx if suspect peritonitis/perforation
why may the INR of someone be altered?
liver disease, sepsis, DIC and warfarin
how high does amylase have to be to diagnose pancreatitis?
x3 upper limit
how is renal colic differentiated from peritonitis?
renal colic - wriggling around
peritonitis - very rigid and still to reduce pain
if someone presents as acutely unwell, why is it important to know if they are on B blocker?
may be septic/shock but not show tachycardia
what are the causes of bowel obstruction?
extramural:
-adhesions, hernia, compression by tumour, volvulus
intramural:
- strictures (tumour, IBD), turmours, intussusception
intraluminal:
- faecal compaction, gall stone ileus
what are the symptoms of small and large bowel obstruction?
both: pain, distention, visible peristalsis, obstipaion (complete constipation), failure to pass wind, high pitched tinkling bowel sounds, tachycardia and hypotension
small bowel:
- colicky pain 2-3 min intervals
- vomiting and eventually feculent
- pain localised centrally
large bowel:
- colicky pain 10-15 mins
- vomiting is a late sign
- pain in lower abdomen
if pain starts to be constant - sign of ischaemia - red flag
focal tenderness, rebound tenderness and guarding - peritonitis and sign of perforation
what is the pathophysiology behind bowel obstruction?
blockage of the bowel results in increased peristalsis
this leads to increased fluid secretion and electrolytes
this can lead to electrolyte imbalances and metabolic alkalosis (esp small bowel)
what is closed loop obstruction?
when both ends of the bowel are obstructed
the bowel segment continues to dilate and content cant go anywhere so high risk of perforation and thus is a medical emergency
may be due to competent ileocaecal valve
what are the commonest causes of small bowel obstruction
adhesions
hernias
cancer
what are the commonest causes of large bowel obstruction?
cancer
diverticular disease and strictures
volvulus - sigmoid colon
constipation
how can you confirm bowel obstruction?
AXR:
- small bowel >3 cm , central dilation, valvulae coniventes
- large bowel >6cm, peripheral, haustra
barium meal - in some patients
CT scan
PR exam - may allow you to feel the mass
what is the difference between simple, closed loop and strangulated bowel obstruction
simple: at one end obstructed and no vascular compromise
closed: both ends , usually at caecum
strangulated: blood supply is compromised and patient is very ill. sharper, constant localised pain - signs of ischaemia.
how would you manage someone with large bowel obstruction?
bloods - U&Es (due to electrolyte disturbances), ABG (incase of ischaemia)
immediate:
- NGT and IV fluids - rehydrate and correct electrolytes
- urinary catheter to monitor output.
- analgesia, antiemetic
small bowel:
- non opetative: adhesional obstruction unless they don’t get better in 48 hours or peritonitis s
- operate for non-adhesional obstruction
large bowel
- don’t operate for sigmoid volvulus - instead sigmoidoscopy
- operative /stenting for other causes
strangulation and closed loop need emergency surgery
what is paralytic ileus?
absent peristalsis and thus can appear as obstruction.
caused by hypokalaemia, hypoNa, Tricyclic antidepressants/ AntiAch, spinal injury, any localised peritonitis (pancreatitis) , post op. mesenteric ischaemia
can lead to ..
pseudo obstruction - no clear mechanical cause but appears to be obstructed
treat by decompression and correction of the cause
what are the complications of bowel obstruction?
bowel ischaemia
perforation and peritonitis
dehydration and electrolyte disturbances
intra-abdominal abscess
what are the differentials for bowel obstruction?
toxic megacolon and paralytic ileus
what is SIRS?
systemic inflammatory response syndrome
can occur when there is massive systemic upset e.g. acute pancreatitis
temperature less than 36 or more than 38
tachycardia
high resp rate
raised WCC
what are the causes of GI perforation?
ulcer - first part of duodenum is most common
small bowel - cancer, obstruction or trauma
larger bowel- cancer, IBD, obstruction, iatrogenic
appendicitis, cholecystitis
meckels diverticulum
toxic megacolon - C.diff/UC
what ae the signs and symptoms of GI perforation?
acute abdomen - severe pain, worse with movement/breathing. may radiate to back/shoulders
peritonitis: fever, tachycardia, hypotensive, focal tenderness, rebound tenderness and guarding. rigid abdomen
reduced/absent bowel sounds.
look for signs of cause e.g. weight loss in cancer. copious vomiting and abdo distention - volvulus
lower GI perforation, patient will be much more sick because not sterile
how does retroperitoneal perforation present?
insidious onset
right shoulder tip pain, back pain or right iliac fossa
e.g. posterior duodenal ulcer
what questions could you ask in the history of someone with suspected perforation to deduce the cause?
peptic ulcer history
medication - NSAIDs/steroids
smoking/alcohol
symptoms associated with appendicitis etc
signs associated with obstruction
weight loss
what are the XRAY signs for abdominal perforation?
riglers sign - air on both sides of bowel wall
psoas sign - loss of sharp delination of psoas muscle border - secondary to fluid in peritoneum
what are the complications of bowel perforation
faecal peritonitis - 50% mortality
sepsis
haemorrhage
how would you manage a bowel perforation?
ABCDE
- high flow oxygen
- IV fluids and catheter (possible blood transfusion if signs of haemorrhage)
- broad spec Abx (metronidazole and gentamicin)
- analgesia and anti-emetic
- NBM and NGT
- PPI if due to ulcer
non-surgical:
- if no sepsis/peritonitis
- oesophageal perforation can be treated endoscopically with stent or just bowel rest (NGT)
surgical:
- small bowel and colonic perforations usually require surgical intervention
- usually result in stoma formation
- requires intra-op washout with saline to reduce risk of infection.
how is an NG tube inserted?
put it atleast 40cm in
check by draw back of fluid and test pH
if pH is >6 need a CXR to check not in lungs
- should be below diaphragm
where is the incision made for oesophageal surgery?
neck incision, thoracotomy or upper abdo
where is the incision made for stomach/duodenal surgery?
upper midline incision
where is incision made for small bowel/large bowel surgery?
midline laparotomy
how can a perforated peptic ulcer be treated surgically?
patch of omentum (Graham patch)
what is the advantage of laproscopic surgery over open?
quicker healing time
reduced post op pain
reduced risk of infection
what is meant by an irreducible hernia?
cannot be pushed back in
what is meant by an incarcenated hernia?
contents of hernia are stuck in by adhesions
what is meant by an obstructed hernia?
bowel content cannot pass through
what is meant by a strangulated hernia?
blood supply stopped, ischaemia, necrosis and systemic toxicity
describe the path of a femoral hernia?
through the femoral canal into upper medial thigh. Ends lateral and inferior to the pubic tubercle
borders of femoral canal:
- anterior: inguinal ligament
- medial: lacunar ligament
- lateral : femoral vein
- posterior : pectineal ligament and pectinus
who are femoral hernias most common in?
middle aged - old women
which hernia is most likely to strangulate?
femoral hernia is more likely to strangulate and be irreducible due to the rigid borders of the femoral canal (lacunar ligament)
surgical repair is recommended to prevent this occurring.
what is an umbilical hernia? who is it most common in?
gut content pushes through the umbilical ring and appears either below or above umbilicus
can occur in children or adults (ascites or obesity)
how does the treatment of umbilical hernias differ in children and adults?
in children it is not a problem and usually resolves spontaneously
in adults there is risk of strangulation and thus needs to be repaired
what symptoms may be associated with an umbilical hernia?
vomtting and pain
what is a hernia?
abnormal protrusion of an organ through its containing wall. usually through a weak point in the wall. often reduces when lay down.
what is an epigastric hernia? what are the risk factors?
hernia passes through the linea alba above umbilicus.
obesity and pregnancy are risk factors for this.
what is the commonest type of hernia?
inguinal
who does inguinal hernias most commonly affect?
men
what are the risk factors for inguinal hernias?
male, chronic cough, constipation, heavy lifting, previous abdominal surgery
what is an indirect inguinal hernia?
part of the bowel penetrates through the deep inguinal ring and through the inguinal ligament and the superficial inguinal ring.
the herniation therefore occurs laterally in relation to the inferior epigastric vessels.
what is a direct inguinal hernia?
The bowel penetrates directly into the inguinal canal through a region known as the hesselbach triangle (posterior surface of inguinal canal) and through the superficial ring.
thus it penetrates medially in relation to the inferior epigastric vessels.
which type of inguinal hernia is most common?
direct
where do inguinal hernias appear? (how does this compare to femoral hernias)?
medial and superior to the pubic tubercle.
Femoral hernias appear inferior and lateral to the pubic tubercle
when examining an inguinal hernia how can you help exaggerate the hernia?
ask the patient to cough and the hernia should pulsate (get bigger transiently)
how can you distinguish a direct from an indirect inguinal hernia?
ask the patient to reduce the hernia e.g. lie down etc
place 2 fingers over the region of the deep inguinal ring and obstruct this passage way. now ask patient to cough/stand.
if indirect - hernia is restrained and wont appear
otherwise the hernia is direct.
what are the complications of inguinal hernias?
they can strangulate - must more common in indirect ones.
can lead to bowel obstruction etc.
what are the borders of the hesslebach triangle?
rectus abdominis.
inferior epigastric vessels
inguinal ligament
what are the contents of the inguinal canal normally?
in men spermatic cord (vas deferens, vessles and nerves)
in women - round ligament of uterus.
ilioinguinal nerve
how are inguinal hernias repaired?
mesh technique to reinforce the posterior wall of inguinal canal:
- cut through external oblique
- separate hernia from spermatic cord
- push back bowel content
- cut off excess peritoneum
- put mesh in region of herniation
mesh may be porcine, bovine or plastic
can be done laproscopically or open
advise patient to loose weight
4 weeks of rest
when are open hernia repairs chosen and when are laproscopic hernia repairs chosen?
open for one off hernias
laproscopic for recurrent hernias, bilateral or in younger people
what are the complications after surgically repairing an inguinal hernia?
pain, bruising, infection, haemorrhage
reoccurance
damage to vas deferens - infertility
what is a hiatus hernia?
protrusion of bowel through the diaphragmatic junction (oesophageal hiatus) into the thorax
what is the name of the 2 types of hiatus hernias?
sliding
rolling
what is a sliding hiatus hernia?
the gastro-duodenal junction and often the cardia slide upwards through the diaphragmatic junction
what is a rolling hiatus hernia?
the fundus moves upwards through diaphragmatic junction to made a sac in the thorax
what are the risk factors for hiatus hernia?
age - loss of diaphragmatic tone and increased intra-abdominal pressure
obesity, ascites and pregnancy - all increase intra-abdominal pressure
what are the clinical features associated with a hiatus hernia?
often asymptomatic
symptoms of GORD
bleeding and anaemia - oesophageal ulceration
hiccups and palpitations - irritation of diaphragm and pericardial sac
vomiting and weight loss - gastric outflow is blocked
dysphagia
what are the complications of hiatus hernia?
incarceration and strangulation - more so for rolling type
gastric volvulus - necrosis and prompt surgery required. more likely for rolling type
what is borchardts triad?
epigastric pain, retching without vomiting and failure to pass NG tube
indicates gastric volvulus
what investigations could you carry out if you suspected a hiatus hernia?
endoscopy - oesophagogastroduodenoscopy (OGD) is gold standard - shows upward displacement of oesophago-duodenal junction
CT/CXR
- CXR will show dark semicircle over heart region.
how would you manage a hiatus hernia?
PPIs and weight loss
surgery - curoplasty or fundoplication
what is curoplasty?
surgery for hiatus hernia
hernia is reduced from thorax back into abdominal cavity
mesh is used to correct defect /weakness
what is fundoplication?
surgery for hiatus hernias
gastric fundus is wrapped around the lower oesophagus to tighen it. this strengthens the LOS to prevent reflux and keeps the gastroduodenal junction below the diaphragm
what are the indications for surgery for hiatus hernias?
remaining symptoms despite conservative management
risk of strangulation/volvulus
nutritional failure
what are the complications of surgery for hiatus hernias?
reoccurance
dysphagia if fundoplication is too tight
abdominal bloating due to reduced ability to belch
fundal necrosis - If blood supply via left gastric artery is disrupted - emergency
what is an incisional hernia?
hernia due to previosu surgery.
can reduce the risk of this by using mesh during surgery
can repair these also with mesh
whats a richters hernia?
part of gut lumen has herniated and part hasn’t.
what are the general complications of hernias?
obstruction - can lead to perforation
strangulation can lead to ischaemia and necrosis
- more likely if neck of hernia is narrow
- can lead to perforation and sepsis
what Is a peptic ulcer?
an imbalance between acid production and mucus production leads to breakdown of the epithelial lining down into the muscularis mucosa
this can occur in stomach or duodenum.
where do peptic ulcers mainly affect?
first part of duodenum
lesser curve of stomach
what is Helicobacter pylori? (type of organisms and adaptations)
gram negative helical bacterium
colonises the gastric epithelium (mainly the antrum)
by its enzyme urease which breakdown urea into ammonia to neutralise acid around it. Also has a flagellum to swim
Describe the effect of H.pylori in the antrum and in the body of the stomach
Antrum:
- increases gastrin release (by increasing histamine release) and reduces somatostatin. therefore acid production increases. leads to a duodenal ulcer
body:
- produces toxins and induces apoptosis leading to atrophy of the stomach lining. this reduces the acid secretion but also less mucus so less protection from acid (produced by other regions). leads to stomach ulcer
how do NSAIDs lead to peptic ulcers?
inhibit COX enzyme which results in less prostaglandin production which reduces blood flow and mucus production
list the causes/risk factors of peptic ulcers
H.pylori NSAIDs alcohol - dissolves mucus stress hiatus hernia genetic variations (FHx) zollinger elison syndome
what is zollinger elison syndrome?
non B cell islet cell tumour (pancreatic tumour) secreting gastrin (gastrinoma). results in parietal cell hyperplasia.
other: smoking, chemo/radiotherapy and steroid use
what are the symptoms of peptic ulcers
may be asymptomatic
gastric ulcer:
- epigastric pain
- worse after food
- N&V
- weight loss
duodenal ulcer:
- epigastric pain (2-5 hours after eating)
- often pain allievated by eating (esp milk)
other:
- oral flatulence, bloating
- posterior ulcer may cause back pain
- symptoms get better/worse with certain foods.
what are the ALARMS symptoms associated with peptic ulcers?
A - anaemia L - loss of weight A - anorexia R - recent rapid onset M - melaena S - swallowing difficulties
what are the complications of peptic ulcers?
perforation and bleeding - anaemia (can be a massive haemorrhage too)
pyloric stenosis - gastric outlet obstruction - weight loss
MALT lymphoma - b cell
adenocarcinoma
How can we test for H.pylori?
Urease breath test:
- give 13C urea and measure CO2 in breath. if 13CO2 is present suggests H.pylori has digested the urea
serum Ab (igG) for H.pylori
stool antigen
can do histology test (CLO test) on biopsy sample
CLO = campylobacter like organism
why is GI endoscopy performed on someone with symtpoms of gastric ulcer?
exclude malignancy (if patient is >55 with ALARM symptoms do endoscopy)
need to stop PPIs 2 weeks before endoscopy
how can zollinger elison syndrome be diagnosed?
measure fasting gastrin levels
if >1000pg/L = positive test
what is the management for H.pylori ?
triple therapy for 7-14 days:
- PPI
- H2 antagonist
- clarithromycin and amoxicillin
(metronidazole instead of amoxicillin in pen allergy)
how can we conservatively manage peptic ulcers?
avoid citric foods avoid alcohol and smoking avoid NSAIDs (take with food) reduce stress
what pharmacological treatment is available for peptic ulcers?
PPIs - lansoprazole (30mg/day), omeprazole
H2 antagonists - ranitidine /cimetidine
PPIs much more effective - they block final step of acid production whereas H2 blockers only block on of the pathways leading to acid production.
what surgical treatment is offered for peptic ulcers?
rarely done.
partial gastrectomy - remove ulcer and G cells in the antrum. followed by bilroth I or II procedure
selective vagotomy: remove parts of vagus nerve to reduce acid secretion
what is a bilroth I and II procedure?
bilroth I: gastroduodenal anatomoses
bilroth II gastrojejunal anastomoses
after removal of part of the stomach
what are the complications of the surgical repair of ulcers?
reduced bowel transit time - diarrhoea
dumping syndrome
alkaline reflux gastritis - reflux of duodenal contents into stomach
what is dumping syndrome
post surgical complication (gastrectomy)
less time in stomach (rapid gastric emptying) so hyperosmotic chyme enters duodenum and water shift and thus can result in bowel distention and faintness,
cramping, nausea, vomiting and sweating
what is achlorhydria?
low stomach acid production.
autoimmune condition against parietal cells.
how do gall stones form?
bile is made up of many different components including cholesterol, phospholipids and different pigments.
if these imbalance, the one in excess can supersaturate in solution and become a solid stone.
alternatively if there is stasis within the biliary tree this can aid the solidification of bile into stones
what are the different types of gall stones?
pigmented - very black
cholesterol - big and yellow
mixed - small and brown - most likely to get into cystic duct.
what conditions predispose someone to pigmented stones?
haemolytic anaemia - sickle cell etc
what are the risk factors for gall stones?
5 Fs: Fat, Female, Forty, fertile, fair others: - FHx - COCP and pregnancy - Crohns - diabetes - haemolytic anaemia - cirrhosis of the liver - loss of bile salts - terminal ileitis /resection
what are the symptoms of gall stones?
often asymptomatic
biliary colic:
- due to gall stones in cystic duct/ampulla of Vater - RUQ/epigastric pain which is worse after eating esp fats (CCK leads to gall bladder contraction) - may radiate to back - associated with N&V
cholecystitis:
- now inflamed and involves parietal peritoneum
- localised tenderness - peritonism
- similar symptoms to above
- associated with systemic response - fever, malaise
other:
- obstructive jaundice
- dark urine and pale stools (Steatorrhoea)
what is murpheys signs?
indicates inflamed gall bladder
2 fingers are placed on RUQ and pressure is applied. ask the patient to take a breath in and this will elicit pain for a positive result.
for a true positive result need a negative result on the other side
what investigations would you carry out if you suspected gall stones.
- FBC, U&Es, LFTs, amylase, - get a better picture to rule out differentials/ find cause
e.g. raised WCC indicates acute cholecystitis
e.g. raised ALP may indicate obstruction (however not definite)
amylase and U&Es (dehydration) to rule out complications of gallstones
pregnancy test, urinalysis - rule out ectopic/renal problem
transabdominal USS - confirms diagnosis - stones are visible and there is a thickened inflamed wall
MRCP - gold standard
what does MRCP stand for?
magnetic resonance cholangiopancreatography
how would you manage someone with gall stones
don’t treat asymptomatic ones
biliary colic:
- analgesics, antiemetic, bed rest
- advice on life style - loose weight, reduce fat
- may need to make them NBM and IV fluids
acute cholecystitis:
- Abx (Co-amoxiclav and metronidazole ) + fluids
ERCP to remove stones - can use a stent to keep ducts open
cholecystectomy - definitive treatment - open or laproscopic
others:
- lithotripsy
- percutaneous drainage of gall bladder - mainly in elderly who are not fit for surgery
manage complications
what are the indications for cholecystectomy?
failure to respond to conservative management
repeated stones
what should you warn the patient after a cholecystectomy?
low fat diet is required because no gall bladder means no store of bile and instead low amount of continuous bile from the liver.
should take fat soluble vitamin supplements
what are the complications of cholecystectomy?
infection
bile leak
gall bladder bed haemotoma
bile duct injury
what are the complications of gall stones?
mucocele (dilation and mucus)
- due to failure to relieve cystic duct obstruction
- can lead to gall bladder necrosis, gangrene and perforation
empyema: same as above but infective - can become septic
fibrosis of gall bladder wall
fistula formation - into duodenum or colon
mirizzi syndrome
common bile duct obstruction - jaundice, cholangitis risk
pancreatitis - block pancreatic duct and enzymes attack pancreas
chronic cholecystitis can increase risk of gall bladder carcinoma
what is bouveret syndrome?
fistula formed between gall bladder and duodenum and stone obstructs the duodenum
what is gall stone ileus?
gall stone impacts the terminal ileum
what is mirizzi syndrome?
gall stone is found withing the hartmanns pouch which pushes on the biliary tree externally
in terms of pain, WCC and jaundice compare biliary colic, acute cholecystits and cholangitis.
biliary colic - RUQ pain
Acute cholecystitis - RUQ pain and raised WCC
cholangitis - RUQ pain, raised WCC and jaundice
what is acalculous cholecystitis?
inflammatory disease of the gall bladder with no evidence of gall stones of cystic duct obstruction
can you get gall stones after the gall bladder has been removed?
yes - very rare. Either by:
= pre-existing stone within the bile duct that grows (if the stone presents <2 yrs after surgery)
= made by bile from liver (if found >2 yrs after surgery)
what is cholangitis ?
infection of the biliary tract associated with high mortality if left untreated
describe the pathogenesis behind cholangitis.
obstruction to biliary tree results in stasis of fluid and bacterial growth.
commonly caused by gall stones but also by ERCP, pancreatitis, cholangiocarcinoma and malignant strictures.
main organism is E.coli, then klebsiella and then enterococcus
what symptoms will you get with cholangitis?
charcots triad: RUQ pain, fever and jaundice
pruritis - due to bile accumulation
tenderness
sepsis signs
rynolds pentad: charcots triad + hypotension (shock) and mental obtundation (indicates sepsis)
what are the risks for cholangitis?
history of gall stones/ ERCP
COCP and fibrates
how do we manage cholangitis?
Co-amoxiclav and metronidazole
sepsis 6
ERCP - remove obstruction/stent
may require cholecystectomy if gall stones are underlying cause.
how does acute pancreatitis present?
epigastric pain that radiates to back
nausea and vomiting
aggravated by movement , relieved by sitting up
abdominal distension
what are the causes of acute pancreatitis?
GET SMASHED:
- gall stones
- ethanol
- trauma
- steroids
- mumps
- autoimmune
- scorpion bite
- hyperlipidaemia, hyperCa, hypothermia
- ERCP
- drugs - NSAIDs, diuretics and azothioprine
what is the pathogenesis behind acute pancreatitis?
e.g. gall stone blocks pancreatic duct
pancreatic enzymes build up and self activate and start to digest pancreatic tissue resulting in inflammation
pancreatic enzymes are released into the circulation
autodigestion of fats by pancreatic enzymes - results in fat necrosis. Free fatty acids react with calcium and result in hypocalcaemia
enzymes can erode blood vessels - haemorrhage
also autodigestion means increased oncotic pressure –> fluid shift –> 3rd space loss –> hypovolaemia (especially alongside vomiting and haemorrhage)
what are the signs of acute pancreatitis?
Grey turner sign - bruising over flanks
Cullens sign - bruising around the belly button
both of the above is due to digestion of blood vessels and peritoneal haemorrhage
tetany - due to low Ca signs of shock due to - pancreatic autodigestion results in fluid shifts - vomiting - haemorrhage
jaundice if obstructive cause
epigastric tenderness
ilieus
what tests would you do if you suspected pancreatitis?
serum pancreatitic enzymes will be raised:
- amylase needs to be x3 upper limit for diagnosis - this isn’t very specific because amylase is also raised in other conditions (ectopic pregnancy, DKA etc)
- lipase is more specific
FBC, U&Es, LFTs - bleeding? how other organs are working
ABG
calcium levels
AXR - sentineal loop sign - dilated proximal bowel adjacent to pancreas
CXR - perforation
USS - rule out gall stones
CT - assess necrosis
how can we manage pancreatitis?
ABCDE
- high flow oxygen
- fluids + catheter to monitor urine output.
analgesia and anti-emetic (morphine however this can cause sphinter of oddi to contract)
IV Abx if severe due to infection risk (due to necrosis)
feeding patients is good if tolerated (may require nasojejunal tube)
treat cause
long term - reduce alcohol intake and reduce risk of gallstones.
what are the early complications of pancreatitis?
shock renal failure ARDS DIC metabolic disturbances (calcium and high glucose) SIRS
what are the late complications of pancreatitis?
pancreatic necrosis - if infective need to remove otherwise treat conservatively
pancreatic fistula or duct stricture- treat with stenting
pancreatic abscess - sepsis - drain
pseudocyst - fluid in lesser sac - can cause pressure symptoms - gastric outflow obstruction and jaundice
pancreatic ascites - usually secondary to pseudocyst or duct obstruction
thrombosis and bowel necrosis - due to DIC
haemorrhage
when are the peaks of mortality in acute pancreatitis?
2 peaks
- within first week - from multiorgan failure and systemic upset
- within week 2-4 due to complications e.g. pancreatic necrosis
name different scoring systems that predict likelihood for acute pancreatitis
APACHE II, ranson and Glasgow (Imrie)
ranson criteria is only applicable to ethanol and can only be applied 48 hours later
is amylase a good marker for pancreatitis outcome?
no
what is the Glasgow scoring system for severity of pancreatitis?
P - PO2 arterial <8kpa A - age >55 N - neutrophils (WCC >15 x10^9) C - calcium <2mM R - renal (urea >16mM) E - endocrine (LDH > 160ml) A - albumin <32g S - sugar (glucose >10mM)
score of 3 or more - severe pancreatitis - ITU referral
how does the ranson score for pancreatitis work?
score of 3 or more makes pancreatitis likely
what is the pathogenesis behind chronic pancreatitis?
progressive fibrosis and destruction of both endocrine and exocrine glands. caused by:
- chronic alcohol - pancreas divisum - congenital abnormalities of ducts - CF - Neoplasm - Trauma - inherited
what are the clinical features of chronic pancreatitis?
recurrent epigastric back pain radiating to back
anorexia and weight loss
evidence of exocrine and endocrine insufficiency
- steatorrhoea and malabsorption
- diabetes
signs - erythema ab igne - from chronic use of hot water bottle.
how can you confirm diagnosis of chronic pancreatitis?
CT or MRCP shows pancreatic calcifications
what will the faecal elastase test show in someone with chronic pancreatitis?
it will be low
how can we treat chronic pancreatitis?
analgesia / nerve block (coeliac plexus)
reduce alcohol intake
creon - pancreatic enzyme supplements
fat soluble vitamins
insulin
treat any strictures - ERCP and stenting
surgery to resect abnormal part of pancreas
steroids for autoimmune cause
what are the complications of chronic pancreatitis?
acute on chronic pancreatitis
malabsorption - deficiencies - clotting abnormalities, metabolic bone disease
ascites
pancreatic malignancy
how does someone with right sided CRC present?
usually presents with symptoms associated with chronic anaemia - tiredness, malaise
although bleeding occurs it is not noticed because mixed in with faeces
change in bowel habit - more likely to be diarrhoea
weight loss and anorexia
sometimes abdo pain and mass
how does someone with left sided CRC present?
diarrhoea and bleeding - no time for blood to mix with faeces so it is noticed. the colon thinks the colon is faeces and so increased peristalsis and fluid secretion leads to diarrhoea
Eventually this can lead to complete obstruction (cancer occludes lumen)
weight loss
tenesmus
bloating and flatulence
mass may be felt
anaemia can occur however usually diagnosed before anaemic
which side of the colon will CRC more commonly lead to bowel obstruction and why?
left side - because there is a smaller lumen
how does rectal cancer present?
bleeding altered bowel habits tenesmus - feeling of incomplete evacuation, pain and urge to strain (tenesmus is highly indicative of rectal C) urgency wet wind incomplete evacuation mass of PRE
discuss some emergency presentations associated with CRC.
bowel obstruction - patient may describe this as constipation. you need to determine whether it is constipation (hard infrequent stools) or obstipation (no stools). Ask them about wind too. ask them about symptoms prior - usually in someone with CRC obstipation will be preceeded by diarrhoea
perforation and peritonitis - guarding, tenderness and rebound tenderness. systemically unwell
acute PR bleed - may show signs of shock
what are the risk factors associated with CRC?
usually sporadic - no obvious risk factors FHx low fibre diet crohns/UC smoking red meets/processed meats high alcohol intake age
where in the bowel is it most common to find CRC?
rectosigmoid colon - 70%
Then ascending colon
then transverse
then descending colon
(therefore overall left side if more common due to sigmoid colon)
what are the complications of CRC?
bleeding and anaemia (microcytic)
obstruction and perforation
fistula
who is CRC more common in?
colon - women
rectum - men
what is the pathology behind the development of CRC?
CRC develops from the epithelial lining of the gut through a series of steps: hyperplasia, polyp and then adenocarcinoma.
during this procession a number of mutations are accumulated.
1. APC and MSH genes mutated in normal epithelial cells.
2. drives their proliferation and genetic instability.
3. leads to hyperproliferation and polyp formation
3. further mutations (KRAS, P53) result in an adenocarcinoma
is there a way to predict if a polyp will become an adenocarcinoma?
if >1.5cm it is likely
certain types of polyps are more likely to
what gene mutation is associated with CRC on left and right colon?
left - APC
right- MMR
(therefore most CRC are via APC)
once CRC has developed how can it progress?
ulceration and stenosis of the colon
infiltrate the bowel wall and spread to..
- hepatic portal system - to the liver
- via vena cava and pulmonary artery to lungs
- locally to bladder
is the prognosis of CRC good?
yes relatively good because good treatment options
for each of the following tests explain why they are indicated if you suspect CRC:
- FBC
- LTF
- DRE
FBC - microcytic anaemia in CRC (particularly if right sided on diagnosis)
LFTS - may be deranged if liver metastasis
DRE - if you suspect rectal exam to check for any masses
what is the gold standard for diagnosis of CRC ?
What would you do after diagnosis?
colonoscopy and biopsy
after CT chest-abdo-pelvis: To stage - look for local invasion and distal metastasis
MRI for rectal cancers to assess the depth of invasion
barium enema Xray - look for stenosis/obstruction
what marker can be used to monitor the progression of CRC treatment?
carcinoembryogenic antigen - tumour marker
what two staging systems can be used for CRC?
TNM and dukes
describe the TNM staging system
T = degree of invasion T1 = invades submucosa T2 = invades muscularis propria T3 = into subserosa T4 = perforates visceral peritoneum N: nodes N1: 1-3 nodes N2: >4 N3: distant lymph nodes M: metastasis (M1) or not (M0)
describe the dukes staging system for CRC
dukes A = confined to bowel wall - up to muscularis propria
Dukes B = through muscle layers
Dukes C: into lymph nodes
-C1 =only lymph nodes near tumour
- C2 = lymph nodes away from tumour (more proximal)
Dukes D = distant metastasis.
what surgery is indicated in right sided CRC?
right hemicolectomy
- ileocaecal, right colic and right branch of middle colic vessels removed (branches of SMA)
what surgery is indicated for CRC in transverse colon?
extended right hemicolectomy
what surgery is indicated in CRC in left sided colon
left hemicolectomy
- left branch of middle colic (SMA) and left colic vessels (IMA) are removed
what are the two surgical proceedures available for rectal cancers and when are they indicated?
anterior resection (if cancer is >5cm from anus) abdomino-perineal resection (if cancer is <5cm from anus)
Describe an anterior resection (surgical procedure)
for rectal cancers
anal sphincter is left in tact and anastomoses are made with colon and anus - bowel works normally
sometimes a defunctioning loop ileostomy is performed to allow anastomoses to heal and reduce complications. reversed after 4-6 weeks
IMA removed as well for rectal cancers
describe an abdomino-perineal resection (surgical procedure)
remove distal colon, rectum and anal sphincter
permanent colostomy bag required.
what is a Hartmanns procedure?
used in emergency bowel surgery e.g. obstruction or perforation where anatomoses of the bowel is not possible at that time.
complete removal of rectosigmoid colon with formation of end colostomy and closure of the rectal stump.
can be versed in the future
used for CRC and diverticulitis
why is hartmanns preffered over abdominoperineal resection?
if it is possible to perform hartmans this is better because APR can lead to damage of pelvic floor and also having an anus is more normal for patients.
what is the difference between an anterior resection and hartmanns?
anterior resection - anastomoses are made between proximal colon and rectum
hartmanns - rectal stump and end colonstomy bag
why is it important to remove adjacent colon that is not affected by a tumour when treating CRC?
ensure all fragments of the tumour have been removed
vessels are usually removed with tumour so need to remove other areas of bowel supplied by that vessel to reduce ischaemia/necrosis of colon
what determines if 2 ends of a bowel will make healthy anastomoses?
good blood supply
reach one another.
better success in younger patients.
lower down the blood supply is poorer so anastomoses are worse.
when is radiotherapy used in rectal cancers? why cant it be used in the same way for Colon cancers?
rectal cancers to shrink down the tumour before surgical resection
not in colon because risk of damage to small bowel. can instead be used for palliative care for colon cancers.
what palliative treatment is available for CRC?
endoluminal stenting - relieves obstruction
stoma for acute obstruction.
what are the complications of stenting the bowel open in CRC?
perofration of bowel
migration of stent
incontinence
if used low down for rectal cancers it can lead to tenesmus - not used for this reason.
how can we screen for CRC?
foecal occult blood test
- if positive , repeat the test
- if still positive - endoscopy
why is CRC a good disease to screen for?
common
good treatment available
easy test available
which side of the colon has better prognosis for CRC?
left side because it presents quicker.
- right side has larger lumen so longer to obstruct
- left side blood is visible (not mixed in with faeces)
name two forms of inherited CRC.
familial adenomatous polyposis coli
hereditary non-polyposis CRC
what gene is affected in familial adenomatous polyposis coli?
APC (chrom 7)
- helps maintain cell morphology and chrom number in cell division
what gene is affected in hereditary non-polyposis CRC?
MMR leading to genetic instability
what are piles/haemorrhoids?
Haemorrhoids are part of normal bowel function. There are internal and external ones. the internal ones sit just above the anal margin and act as cushions helping to maintain continence. the external ones sit just below the anal margin. They are also involved in sensing presence of faeces to initiate defaecation.
however with straining and constipation haemorrhoids can prolapse down and become more dilated and cause problems such as bleeding, pain, itching.
are piles painful?
internal haemorrhoids are above the pectinate/dentate line and thus do not have somatic innervation. Therefore unless they strangulate and thrombose they should not be painful.
external haemorrhoids are below the pectinate line and thus have more of a tendency to be painful
what are the symptoms of piles?
bright red blood , mucus
itching
sometimes pain
feeling of a lump when they go to the loo.
what investigations could be carried out in someone presenting with symptoms of piles?
with all rectal bleeding:
- an abdo examination
- PR examination
proctoscopy - to see internal haemorrhoids
sigmoidoscopy - to identify rectal pathology higher up and exclude CRC in older patients.
what treatment is available for piles?
usually no treatment is offered - just topical analgesics and bed rest until pain subsides. high fibre diet and laxatives
However other treatment options include:
- banding - strangulate the herniated haemarrhoid so it falls off
- injection - sclerosants injected to bulk out and prevent prolapse
- haemorrhoidectomy - surgically remove them. very successful and haemorrhoids rarely come back. only indicated in those with reoccurring haemorrhoids.
what is a perianal haematoma?
A thrombosed pile - it has been strangulated
what are the complications of a haemorrhoidectomy?
stricture and constipation
infection
bleeding
how can we grade haemorrhoids?
grade 1: remains in rectum
grade 2: prolapses through anus on defaecation but then reduces spontaneously
grade 3: as for grade 2 but requires digital reduction
grade 4: remains persistently prolapsed.
what is a perianal abscess? what is it associated with? how does it present and how should it be managed?
abscess around the anus usually associated with diabetes, crohns, malignancy or fistula
presents as red swollen abscess, pain (esp on sitting) and patient is acutely unwell - may show signs of sepsis
need to drain the abscess and give Abx
otherwise can need to sepsis or necrotising fasciitis
what is a perianal fistula?
connection between anal canal/ rectum and skin. there are a number of different pathways a fistula can form
what are perianal fistulas caused by?
perianal abscess, crohns, TB, diverticular disease, rectal carcinoma
how can you treat a perianal fistula?
lay open the fistula - cut through the tunnel and skin to leave a big opening. for this you need to know the direction of the tunnel. The position of the opening can help determine this and also USS
what is an anal fissure?
A painful tear in the squamous lining of the anocutaneous junction (also causes bleeding and pruritus)
what causes an anal fissure?
usually hard stools
other causes: crohns, anal cancer, trauma, psoriasis
why do anal fissures take time to heal?
every time you defecate, opens up the cut again
the internal sphincter will contract and reduce blood supply which slows down the healing process
how can we treat an anal fissure?
stool softeners
GTN cream and diltiazem - relax muscle of the internal sphincter (GTN can give headaches so diltiazem is better)
inject botox to relax the anal sphincter
last resort: surgery - lateral sphincterotomy
what is the problem with a lateral sphinchterotomy (treatment for anal fissure)?
can lead to incontinence especially in women after birth and pelvic floor weakening
what type of cancers are anal cancer?
majority are squamous cell carcinomas arising from below the dentate line.
the remainder are adenocarcinomas from above the upper anal epithelium
overall anal cancer is rare
what is intreaepithelial anal neoplasia?
metaplastic change that precedes the development of invasive squamous anal cancer.
usually occurs on perianal skin or the anal canal.
strongly associated with HPV infection.
graded from low to high - high grade is premalignant and can progress to cancer.
what are the risk factors for anal cancer?
HPV, HIV, immunosuppression, age, crohns and smoking
what are the clinical features of anal cancer?
pain and rectal bleeding - most common symptoms
anal discharge
pruritus
palpable mass - DRE
stricture
local invasion can lead to perianal infections, fistula, and if sphincter is involved tenesmus or incontinence
what investigations would you do if you suspected anal cancer?
DRE, examine inguinal lymph nodes, GI exam
proctoscopy
smear test to exclude CIN
biopsy - USS guided fine needle aspiration
CT thorax-abdo-pelvis - distant metastasis
MRI or pelvis to assess local invasion
how would you treat anal cancer?
chemo-radiotherapy - first lijne
surgical:
- indicated when very early disease to avoid complications of chemoradiotherapy
- abdominoperineal resection
patients are under regular surveillance for next 5 years
what is angiodysplasia?
most common vascular abnormality of the GIT. caused by the formation of arteriovenous malformations between healthy blood vessels most commonly in caecum and ascending colon.
what are the two most common causes of rectal bleeding in over 60s?
- DIVERTICULAR DISEASE
2. ANGIODYSPLASIA
what is the pathophysiology of acquired angiodysplasia?
reduced submucosal venous drainage of colon
results in dilated tortuous veins
the precapillary sphincter competency is lost due to pressure and thus there is an arteriovenous communication
what is congenital angiodysplasia?
hereditary haemorrhagic telangiectasia or Heyde’s syndrome
what are the clinical features of angiodysplasia?
rectal bleeding - main presenting feature
could be asymptomatic (however occult blood test may be positive i.e. non visible blood)
iron deficient anaemia
acute haemorrhage
upper GI lesions - melena or haematemesis
what investigations would you do with someone presenting with symptoms of angiodysplasia?
blood tests - anaemia
endoscopy - capsule endoscopy (swallow camera)
may need to confirm location of the bleed with mesenteric angiography
how is angiodysplasia treated?
usually self limiting so fluids and bed rest is sufficient
however in persistent/sever cases:
- endoscopy and subject the bleeding to electrical current and argon - argon plasma coagulation
- mesenteric angiography - for small bowel lesions that cannot be treated endoscopically. involves embolization of bleeding vessel.
- surgical resection of affected bowel segment - indicated for severe bleeding, life threatening, or multiple angiodysplastic lesions
what are the complications of angiodysplasia?
anaemia
in severe bleeds - hypovolemic shock
complications from treatment - perforation and endoscopy
how does pancreatic cancer spread?
local invasion to spleen, transverse colon and adrenal glands
lymphatic metastasis to regional lymph nodes, liver, lung and peritoneum
is metastasis common at the time of diagnosing pancreatic cancer?
yes and therefore very poor prognosis
what type of cancers are pancreatic cancers?
majority are ductal adenocarcinomas (majority arise from the head of the pancreas)
the remainder can be divided into exocrine and endocrine tumours
what are the risk factors to pancreatic cancer?
family history, smoking, chronic pancreatitis, recent late onset diabetes.
increasing age
hereditary non-polyposis colorectal carcinoma
multiple endocrine neoplasia
BRCA2 gene
how does pancreatic cancer present clinically?
cancers affecting the head:
- painless obstructive jaundice
- sometimes abdo pain
- gastric outflow obstruction and vomiting
cancers affecting the tail: insidious onset and not symptomatic till late. but present with epigastric pain which radiates to back and relieved by sitting forward.
other: anorexia, weight loss, diabetes, acute pancreatitis , steatorrhoea
epigastric mass, palpable gallbladder
usually between age 60-80
what investigations would you carry out for someone presenting with symptoms of pancreatic cancer?
bloods: FBC, LFTS (raised bilirubin) , CA19-9 tumour marker - high selectivity and specificity
USS/ CT scan - show pancreatic mass, dilated biliary tree
endoscopic USS Guided fine needle aspiration biopsy
ERCP for biopsy and stenting (therapeutic too)
what marker is good at assessing response to treatment in pancreatic cancer?
CA19-9
how would you manage pancreatic cancer?
only curative option is radial resection.
surgery
chemotherapy
palliative care
what surgical options are available for pancreatic cancer?
tumours of the head of the pancreas: pancreatoduodenectomy - whipples procedure
tumour of body = distal pancreatectomy
what is whipples procedure?
remove head of pancreas, antrum of stomach and 1st/2nd part of duodenum, common bile duct and gall bladder.
all removed due to common supply by the gastroduodenal artery
tail of pancreas and hepatic duct and stomach are joined to the jejunum allowing pancreatic juices to drain here
what are the contraindications to surgery in pancreatic cancer?
peritoneal, liver and distant metastasise
what are the complications of surgery for pancreatic cancer?
pancreatic insufficiency
delayed gastric emptying
pancreatic fistula
what chemotherapy is available for pancreatic cancer?
Adjuvant (after surgery) chemotherapy - 5 fluorouracil
what does palliative care for pancreatic cancer consist of?
ERCP and stenting - for obstructive jaundice - improves pruritus
if exocrine insufficiency - creon can be given
opiates for pain
describe the classification of the endocrine pancreatic cancers
functional - produce hormones
non-functional - no hormones
list some of the functional endocrine pancreatic tumours and their syndromes.
G cells - gastrinoma - Zollinger elison syndrome
a cells - glucagonoma - increased glucose and diabetes
B cell - insulinoma - hypoglycaemia and neuroglycopenic symptoms
g cell - somatostatinoma - mild diabetes, steatorrhoea, gall stones (reduced CCK), achlorhydria (low gastrin)
non-islet cell - vasoactive intestinal peptide - watery diarrhoea and hypokalaemia
what is zollinger elison syndrome?
caused by excess gastrin (gastrinoma of pancreas) leads to excess acid production and peptic ulcers refractory to medication. also diarrhoea and steatorrhoea
what are the effects of increased somatostatin (somatostatinoma)?
mild diabetes
steatorrhoea
gall stones (reduced CCK)
achlorhydria (reduced stomach acid due to less gastrin)
inhibits TSH and prolactin from anterior pituitary
what are the majority of gastric cancers?
adenocarcinomas arising from the gastric mucosa
what are the risk factors for gastric cancer?
male H.pylori smoking, alcohol, heavy salt in diet FHx age pernicious anaemia
what are the symptoms of gastric cancer?
dysphagia dyspepsia N&V melena and hematemesis anaemia, weight loss, malaise
what are the signs of gastric cancer?
Trossiers sign - enlarged virchows node palpable epigastric mass Acanthous nigricans - hyperpigmentation of skin creases pale conjunctiva (anaemia) hepatomegaly/splenomegaly (if mets)
what are the complications of gastric cancer?
gastric outlet obstruction
- leads to iron deficient anaemia
- perforation
- malnutrition
what investigations should we carry out for gastric cancer?
FBC, LFTs
CEA - Carcinoembryonic antigen - marker
endoscopy and biopsy
CT chest, abdo, pelvis
what would we test for in a biopsy of a suspected gastric cancer?
CLO test for H.pylori
Grade neoplasm
HER2 expression for targeted therapies
what is the curative management for gastric cancer?
peri operative chemotherapy and 3 cycles of adjuvant chemo after surgery.
surgery involves:
- proximal gastric cancer - total gastrectomy
- distal gastric cancer - subtotal gastrectomy
followed by Roux en Y reconstruction.
what is a Roux en Y procedure?
small bowel reconnected to oesophagus
distal duodenum is reconnected to small bowel
what is the palliative treatment for gastric cancer?
chemotherapy stenting (if gastric outlet obstruction) bypass surgery if stenting fails
what are the complications of gastrectomy?
dumping syndrome
anastomotic leak
vit B12 deficiency (due to low intrinsic factor)
what is dysphagia? and odynophagia?
dysphagia = difficulty swallowing odynophagia = pain on swallowing
how can the causes of dysphagia be categorised?
mechanical: luminal, intramural and extramural
neuromuscular
what are the luminal causes of dysphagia?
diverticulum / pharyngeal pouch
foreign body
what are the intraluminal causes of dysphagia?
benign oesophageal stricture
oesophageal/gastric malignancy
what are the extraluminal causes of dysphagia?
extrinsic compression - goitre, cervical spondylosis, bronchogenic CA, enlarged left atria
what are the neuromuscular causes of dysphagia?
Stroke achalasia diffuse oesophageal spasm myasthenia gravis myotonic dystrophy
how can you tell if the dysphagia is due to a neuromuscular problem?
difficulty initiating swallowing
worse on liquids
what investigations would you carry out for someone presenting with dysphagia?
endoscopy +/- biopsy to exclude malignancy
FBC and LFTs
for motility disorder: barium swallow, video fluoroscopy or maometry
what is a diverticulum?
out pouching of the bowel wall
what are the different types of diverticulum?
pulsion: pressure within the gut causes outpouching
traction: outpouching due to external adhesions e.g. TB, adenitis
what are the different types of oesophageal pulsion diverticulum?
pharyngeal pouch - zenkers pouch
epiphrenic pouch - near LOS
what is zenkers diverticulum?
a pharyngeal pouch
most common diverticulum of the oesophagus
uncoordinated contractions of oesophagus causes outpouching of all layers (true diverticulum) through the killian dehiscence
how does a zenkers diverticulum present?
food sticking
regurgitation
aspiration pneumonia
bad breath
how would you manage a zenkers diverticulum?
cricopharyngeal myotomy +/- diverticulectomy
endoscopic diverticulectomy
what is diverticulitis ?
inflammation of diverticulum
what is diverticular disease?
symptomatic diverticulum. with age the bowel wall becomes weaker and less able to with stand pressure and thus outpouches occur. bacteria can accumulate within these leading to inflammation.
what are the complication of diverticular disease?
inflammation/infection can lead to increased pressure and perforation - peritonitis
bleeding
fistula: colovesicle, colovaginal,
bowel obstruction (secondary to stricture formation )
pericolic abscess
sepsis
what are the risk factors for diverticular disease?
smoking obesity low fibre diet NSAIDs FHx
how does diverticular disease usually present?
may be asymptomatic
simple disease: left lower colicky pain - worse after eating and better after defaecation
diverticulitis - abdo pain and localised tenderness. PR bleeding, anorexia, nausea and vomiting
how would you investigate diverticular disease?
endoscopy - however not if you suspect diverticulitis due to risk of perforation
ERECT AP CXR - if perforation is suspected
CT scan - for accurate diagnosis
how is diverticular disease managed?
paracetamol and fluid
hospitalised if significant bleed/sepsis - may need fluid resuscitation
diverticulitis - broad spec Abx
pericolic abscess - CT guided drain, bowel rest, Abx
may do hartmans procedure if perforation/sepsis
what are the two types of oesophageal cancer ?
adenocarcinoma - mainly lower 1/3
squamous cell carcinoma - mainly upper/middle third
what is squamous cell carcinoma of the oesophagus associated with?
smoking
alcohol
achalasia
low vitamin A
what is adenocarcinoma of the oesophagus associated with?
long standing GORD
obesity
high fat intake
who is oesophageal cancer more common in?
x3 men
what is the pathogenesis behind adenocarcinoma oesophageal cancer?
damage to the lower oesophagus due to acid (GORD) results in metaplasia (stratified squamous to simple columnar with goblet cells). Barret oesophagus is strongly linked to the development of adenocarcinoma
what are the symptoms of oesophageal cancer?
majority of patients present late in a vague way dysphagia (solids > liquids) retrosternal pain dyspepsia weight loss - due to dysphagia and cancer cough hoarseness of voice choking
what are the complications of oesophageal cancer?
metastasis - supraclavicular node, coeliac node, lung, liver, bone
pneumonia
cord palsy - hoarsness
fistula
how does the treatment for adenocarcinoma and squamous cell carcinoma of the oesophagus differ?
squamous cell carcinoma is difficult to operate on because of location - chemo radiotherapy
adenocarcinoma - surgical treatment is more likely to be available
what surgical treatment is available for adenocarcinoma of the oesophagus?
oesophagectomy - remove tumour, top part of stomach and surrounding lymph nodes.
the stomach is made into a tube and brought up into the stomach to replace the oesophagus
right thoracotomy and laparotomy = Ivor lewis
right thoracotomy and abdominal incision and neck incision = McKeown
left thoracotomy +/- neck incision
left thoracoabdominal incision
what are the complications of an oesophagectomy?
- during the procedure one lung is deflated - can lead to pneumonia, atelectasis and ARDS
- post nutrition problem - smaller more frequent meals because stomach is smaller
- delayed gastric emptying - adds to feeding problem
- anastomotic leak
- gastric necrosis
- strictures later (struggle to eat )
- recurrent laryngeal nerve palsy
what palliative treatment is available for oesophageal cancer?
stent to ease swallowing
nutritional support
can we treat barrets oesophagus?
yes for high grade we can use endoscopic mucosal resection to remove part of it. followed by radiofrequency ablation - destroys malignant cells.
what is ERCP?
endoscopic retrograde cholangiopancreatography - scope is inserted down the oesophagus , all the way down to the duodenum into the common bile duct.
contrast is added and Xrays are taken while scope is in to view the biliary tree
what blood results are important before ERCP and why?
LFTs, amylase INR so we can assess for any changes
LFTs will tell you if procedure was successful
amylase will tell you if any pancreatitis
how is patient prepped for ERCP?
no eating 4 hours before
lidocaine throat spray
midazolam 5mg for sedation
analgesic - fentanyl /pethidine - sometimes
buscapan - antimuscarinic - stops smooth muscle contraction
what are the indications for ERCP?
looking at the biliary tree for strictures, stones etc
balloon out stones
stent insertion
sphincterectomy - if sphincter needs to be dilated for big stones to pass
biopsies
how does ballooning out gall stones work?
with ERCP put an undilated balloon past the stones and then inflate balloon and pull stone out with balloon
what are the complications of ERCP?
pancreatitis - check amylase before and after , avoid going into pancreatic duct with scope
perforation N&V bleeding - due to sphincterectomy cholangitis allergies to meds/resp depression from opioids
what is an external biliary drain?
after ERCP the contrast medium needs to be drained otherwise it will be toxic to the liver. usually this occurs via the ampula of Vater and into the bowel etc. however if this is blocked and the spinchterectomy failed it need to be drained via an external biliary drain
how is colonoscopy performed?
midazolam can be given prior to the procedure to sedate the patient. alternatively gas and air can be given.
the procedure involves inserting the scope via the anus and all the way to the caecum whilst inserting air to open up the colon.
the practitioner looks for pathologies and takes biopsies on the way out.
what are the indications for colonoscopy
diagnostic: symptoms of cancer, suspect UC/crohns, biopsies to be taken
therapeutic: volvulus (untwist), polypectomy, decompression, stenting, stop bleeds
what are the contraindication to colonoscopy?
risk of current perforation
haemorrhoifs/varices - risk of bleeding
obstruction
a lot of stricture/adhesions - the procedure will be too difficult/uncomfortable
what are the risks of colonoscopy?
pain
perforation
bleeding - when taking biopsies/removing polyps
can cause sigmoid colon/transverse colon to twist
what are the indications of oesophagogastroduodenoscopy (OGD)?
investigations for dysphagia, dyspepsia, reflux, acute/chronic GI bleeding, iron deficient anaemia
therapeutic:
- balloon dilation for benign strictures
- endoluminal stenting for malignant stricture
- coagulation, banding of bleeding sources e.g. ulcers, varices and tumours.
describe the preparation for OGD?
NMB for 4 hours
lidocaine throat spray
midazolam is offered or gas and air
what are the risks/complications of OGD?
perforation - most likely to occur in upper region (against cervical spine)
bleeding
overmedication from midazolam and respiratory depression/arrest
what are the principles behind weight loss surgery?
reduce stomach size - feel fuller quicker so eat less
reduce absorption area - less food is absorbed
a combination of the above 2 can also be used
who is considered for weight loss surgery?
BMI >40
OR BMI between 35-40 where comorbidities would be improved with weight loss e.g. sleep apnoea
tried other ways to loose weight
what are the benefits of weigh loss surgery?
increases life expectancy
helps with diabetes and hypertension
what are the risks of weight loss surgery?
anaesthetic risks are greater in those who are obese
higher risk of DVT/P.E in those who are obese
gall stones risk with rapid weight loss
excess skin
what is gastric band surgery?
a band is placed around the top part of the stomach to create a smaller stomach pouch - feel fuller quicker (i.e. stomach is divided into two
what is gastric bypass surgery?
roux en Y procedure
- stomach is divided into two and the top part is attached to the jejunum. the bottom part of the stomach, duodenum and proximal jejunum are bypassed
mainly done by key hole surgery
stomach is smaller AND less food absorbed
what are the advantages of gastric band surgery?
can be reversed later in life
can be adjusted
can be done laproscopically (heal quicker)
what are the complications of gastric band surgery?
band can slip out of place and become ineffective
infection
pouch enlargement
what are the complications of gastric bypass surgery?
anastomotic leak
micro deficiencies - e.g. less intrinsic factor (anaemia), and vitamins - need regular blood tests
dumping syndrome
wound infection
what is a sleeve gastrectomy?
one side of the stomach is removed so you are left with a narrow tube
less can be eaten (reduced stomach size)
how does the bowel content in an ileostomy and a colostomy compare?
ileostomy is more liquid like
colostomy - more solid and faeces like
what is an end stoma and a loop stoma?
end stoma: the intestine has been cut in transverse and proximal end empties into a bag
loop: a loop of the intestine goes into the stoma bag and there is an opening via the side of the bowel wall. some fluid will still go into the distal end of the bowel but majority leaves via the stoma bag.
can both loop and endo stomas be reversed?
yes
what is a pouch ileostomy?
ileum is joined to the anus.
using the distal part of the ileum, it is folded over and a pouch is created - J pouch
it is then linked to the anus so the ileum is acting as a rectum
used for UC when colon and rectum have been removed
what is a cholangiocarcinoma?
a cancer of the bilary system.
where do cholangiocarcinomas normally occur?
mainly in the extra-hepatic biliary tree
most commonly at the bifurcation of the left and right hepatic duct (klatskin tumours)
what types of tumours are cholangiocarcinomas?
mainly adenocarcinomas
remaining are squamous cell carcinomas
what are the causes of cholangiocarcinomas?
primary sclerosing cholangitis - UC infection - HIV, hepatitis, liver flukes toxins congenital - choledochal cyst alcohol abuse diabetes
what are the clinical features of cholangiocarcinomas?
generally asymptomatic until later stage jaundice and pruritis pale stools, dark urine RUQ pain, early satiety weight loss, anorexia, malaise
what is Courvoisiers law?
in the presence of jaundice and an enlarged palpable gallbladder, malignancy of biliary tree or pancreas should be strongly suspected
what are the complciations of cholangiocarcinomas?
obstruction and stasis of biliary tract - cholangitis and sepsis
secondary biliary cirrhosis
what tumour markers may be present in cholangiocarcinomas?
CEA
CA 19-9
what investigations would you suggest for someone presenting with cholangiocarcinoma ?
LFTs - raised ALP and a-GT confirm obstructive jaundice screen for tumour markers USS followed by CT MRCP - optimal imaging for diagnosis ERCP
what is the progression of klatskin tumours?
slow growing, invade lymph nodes then peritoneal cavity, then lung and liver.
what is the surgical management of cholangiocarcinomas?
surgery - complete surgical resection. however most are inoperable at time of presentation.
intrahepatic and klatskin tumours: require partial hepatectomy and reconstruction of biliary
Distal bile duct tumours: whipples procedure.
what is the palliative management of cholangiocarcinoma?
stenting with ERCP
radiotherapy to prolong survival
chemotherapy to slow tumour growth
what are the 3 types of jaundice?
pre-hepatic
hepatic
post hepatic
what are the causes of pre-hepatic jaundice?
increased breakdown of RBC - malaria, spherocytosis
reduced uptake by liver = Gilberts, rifampicin
reduced conjugation due to enzyme defect - Crigler-Nagler disease
what are the causes of hepatic jaundice?
hepatocyte damage with some cholestasis - both conj and unconj bilirubin raised
viral hepatitis
alcoholic hepatitis
cirrhosis and liver cancer
A1 antitrypsin deficiency
Amoxicillin
Wilsonswhat type of bilirubin is present in pre-hepatic jaundice?
unconjugated is high
which type of jaundice will present with dark urine?
hepatic and post hepatic where conjugated bilirubin is raised (unconj is not soluble)
what signs may be associated with pre hepatic , hepatic and post hepatic jaundice (other than jaundice)?
pre hepatic - possible anaemia if due to haemolysis
hepatic - other signs of liver failure e.g. bruising and ascites.
post hepatic - dark urine
what are the causes of post hepatic jaundice?
biliary cirrhosis, sclerosing cholangitis, gall stones in common bile duct , pancreatic cancer (compression of bile duct), cancer of gall bladder, cholangiocarcinoma.
what drugs can cause jaundice?
TB drugs: rifampicin, isoniazid, pyrazinamide anti-malarials amoxicillin sodium valproate statins paracetamol overdose
define sensitivity
the proportion of people with the disease who get a positive test result (how well does it detect those with the disease)
define specificity
the proportion of people without the disease who get a negative result (how well does it detect those without the disease)
define positive predicted value
the number of people with an abnormal result that actually have cancer
define negative predicted value
the number of people with a negative result that actually are disease free
what are the principles behind a good screening programme?
Disease: high mortality/incidence etc, known aetiology,
Test: simple, acceptable, valid and reliable
Treatment: available and acceptable, benefit from early detection
programme: cost effective, agreed protocol
what is length time bias?
A screening programme is more likely to pick up less aggressive cancers that do not progress fast anyway. naturally longer survival time which will now be correlated to screening.
what is lead time bias?
by screening we will detect the cancer earlier which will lengthen the time between diagnosis and death. this will look like survival time is longer which will correlate with screening
what is the hydrogen breath test?
anaerobic bacteria are able to break down unabsorbed food and produce hydrogen
if there is a problem with digestion/absorption the amount of hydrogen increases
the hydrogen is absorbed by the blood and excreted in lungs so picked up by a breath test.
e.g. lactulose malabsorption or bacterial overgrowth in small bowel
what is oesophageal manometry?
assess’s oesophageal motility disorders e.g. sphincter disorders, achalasia, nutcracker oesophagus
what is nut cracker oesophagus?
motility disorder of the oesophagus where there is increased pressure created from muscular contractions
leads to dysphagia and chest pain
what is a barium enema used for?
allows imaging to be more visible. colon is filled with barium and thus any areas that don’t fill with barium could suggest cancer, polyps, obstruction of spasms.
could also see diverticular , volvulus and strictures
which area of the GIT is a capsule endoscopy mainly used for?
small bowel because cant get to this as easily with OGD or colonoscopy
which side of CRC (left or right ) is more likely to present with bowel obstruction?
left because sigmoid colon has a relatively narrow lumen
what diets can be used to help IBS?
gluten free
fod map diet
what are the complications of high output stoma?
dehydration (can lead to kidney damage) and weight loss
how does the region of bowel affected by crohns alter prognosis?
terminal ileum responds best to treatment
anal disease is worst.
what proceedures should be avoided in toxic megacolon and why?
endoscopy
barium swallow
due to risk of perforation
what should be given to a patient that is found to have less than or equal to 15g/L protein on an ascetic tap?
oral ciprofloxacin or norfloxacin as prophylaxis against spontaneous bacterial peritonitis
criteria for prophylaxis:
- patients who have had an episode of SBP
- or patients with fluid protein <15 g/l and either - - Child-Pugh score of at least 9 or hepatorenal syndrome
what are risk factors for oral candidiasis ?
HIV
inhaled steroids
Abx
what is the difference between dry and wet beri beri?
wet beri beri
- vasodilation, high out put HF, oedema
dry beriberi
- peripheral motor and sensory neuropathy
both are caused by B1 deficiency
what is the rose thorn appearance suggestive of?
crohns
on AXR with barium can see sharp lines along bowel wall due to ulcers
what investigations can you do in chronic pancreatitis?
faecal elastase - raised USS - pseudocyst glucose levels AXR - speckled calcifications CT: pancreatic calcifications (also seen by MRCP)
