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
