gastro conditions Flashcards
what are haemorrhoids
they are vascular cushions on the anus that help the sphincters constrict
however we only say someone has haemorrhoids when these cushions become inflamed
presentation of haemorrhoids
usually PAINLESS fresh blood from back passage
NOT mixed in stool
pruritus may be present!!!
explain clock positions for pR exam and locations of haemorrhoids on this
clock times allocated with patient flat on back and open legs (like in surgery) and 12 is tomards belly 6 is towards back
however pr exam is not done in this position so it can be confusing
haemorrhoids in 3, 7 and 11 oclock position
haemorrhoids 2 types
internal: above dentate line in anal canal- less likely to be painful
external: below dentate line: more likely to be thrombosed and painful
haemorrhoids grades of classification
grade 1: do not prolapse out of the anal canal
grade 2: prolapse out of anal canal only in defecation
grade 3: prolapse out of anal canal in defecation and stay there but can be reduced
4: cannot be reduced
haemorrhoids diagnosis
a rigid anoscope, proctoscope, or rectoscope
when suspecting haemorrhoids what fo you do?
abdo exam and inspect rectum and PR exam to RULE OUT other pathology eg fissures or other sinister pathology
haemorrhoids management
prevention: preventing constipation: high fibre, liquids and laxatives when needed
pharmacological treatment: bunch of creams and stuff you can use
non surgical treatments: BAND LIGATION: killing the supply to haemorrhoids> injection sclerotherapy
management of acute thrombosed external haemorrhoids
veery painful
patients may benefit from admission if presentation within 72 hours for procedure
otherwise stool softeners ice packs and analgesia will do the trick
colon cancer non acute presentation
blood in stool, unexplained weight loss, change in bowel habit (usually more lose stool),
iron def anaemia, unexplained ABDO PAIN!!!!
screening bowel cancer programme ENgland and scotland
FIT test sent out to everyone 60-74 in england and 50-74 in scotland
positive fit test patients are offered a colonoscopy
risk factors for bowel cancer
diet- high in meat low in fiber
obesity
how are the genetics of bowel cancer classified
1) SPORADIC 95%
2- hereditary non-polyposis colorectal carcinoma 5%– isolated cancer
3- familial adenomatous polyposis 1%
- familial adenomatous polyposis pathology and management
patients are full of polyps by age of 30-40 and need total proctocolectomy
any age person single symptom indicator for FIT test
change in bowel habit
iron def anaemia!!!!!!
abdo mass
over 50 single symptom FIT indicators
rectal bleeding
abdo pain
weight loss
40+ 2 symptom combo FIT indicator
unexplained weight loss and abdominal pain,
under 50 2 symptoms combos FIT indicators
rectal bleeding and either of the following unexplained symptoms:
abdominal pain
weight loss,
60+ person (low threshold) FIT indicator
anaemia even if not iron def
what symptoms can indicate direct referral even without FIT testing
anal mass
rectal mass and
anal ulcer
post fit test result approach
if positive 2 week wait and if negative can still be considered for referral if symptoms presist and no other expl is found
coloractal cancer management
palliative
chemo
surgery - palliative (symptom control) or curative intent
what is the CEA
carcino embryonic antigen is a blood test used in staging and looking for reccurance of colon cacner not for screening though
other staging investigation of colon cancer
CT of the chest, abdomen and pelvis
anal fissure presentation
bright red blood, painful with defecation
risk factors for anal fissure
constipation, IBD, STI!!
Acute management of anal fissure
dietary advice high fibre and fluids
bulk forming laxative if needed and lactulose if that doesnt work
lubricants before defecation
topical anaesthetics and analgesia
chronic management of anal fissure
same as acute and additional topical GTN if needed and if that doesnt work then referral for anal sphincterotomy
diverticular disease presentation
altered bowel habit, rectal bleeding, abdo pain
pathophysiology of diverticular disease
outpouchings on the bowel wall - usually happen between taenia coli where vessels pierce muscle to supply the mucosa fo rthis reason the rectum which lacks taenia is often sparred
complications of diverticular disease
diverticulitis
perforation
abscess
peritonitis
fistula
haemorrhage
diagnosis of patients presenting in clinic with suspected diverticular disease
colonoscopy or CT cologram or barium enema
diagnosis of patients acutely unwell with diverticular disease
plain xray will show perforation
then if needed abdo CT with IV and oral contrast to identify inflammation of bowel and local complications such as abscess formation.
severity classification tool for diverticular disease complications
Hinchey classificatoin
management of diverticular disease stable disease
high fibre and liquid diet
diverticulitis management
sometimes people have rescue pack AB but may need surgical involvement if recurrent acute diverticulitis attacks, if hinchley class 4: faecal peritonitis- needs resection and maybe stoma- bad prognosis
ulcerative colitis presentation
bloody diarrhoea, abdo pain, younger patients, left abdo pain> right
diagnostics for UC when stable and if diagnosis being made in flare
colonoscopy with biopsy are usually diagnostic,
raised faecal calprotectin in IBD
NO colonoscopy when flare- flexi sigmoidoscopy preferred
pathophysiological features of UC including histology
- red raw mucosa that easily bleeds
- only past ileocoecal valve so only large bowel
- inflammation doesnt go past submucosa (nooot all layers)
- depleted goblet cells and mucin form gland epithelium
- pseudopolyps since theres ulcerated mucosa with adjacent unaffected mucosa making it look like polyps (in lumen)
- crypt abscesses filled with neutrophils
most common site of UC
rectum since this is where the inflammation always starts from
conditions commonly associate with UC
primary sclerosing colangitis, arthritis, uveitis
vit b12 deficiency causes
1) pernicious anaemia most common
other causes: malnutrition, gastrectomy, atrophic gastritis
pernicious anaemia pathophysiology
autoimmune condition leading to destruction of gastric mucosa
what leads to vit b12 deficiency
1) IF antibodies
2) destruction of gastric mucosa so less production oF IF
presentation of pernicious anaemia
1) anaemia since b12 not produced
2) neuro symptoms since b12 is critical in myelination of neurones so tingling, confusion, concentration problems,
- other: jaundice with pallor: “lemon tinge”
atrophic glossitis
management of pernicious anaemia
-IM b12 3/ week initially then 1 every 3 months
-oral b12 not commonly used but may be evidence suggesting it helps maintenance of levels
-folate supplements may also be needed
which cancer does pernicious anaemia predispose to
gastric cancer
pancreatic cancer presentation
unspecific symptoms: weight loss, anorexia, epigastric pain, atypical back pain
PAINLESS!!! jaundice, abdo mass, hepatomegaly
SPECIFIC potential symptoms:
steatorrhoea due to exocrine function loss, Diabetes due to endocrine function loss
pancreatic cancer LFTs picture
obstructive picture (ALP> ALT)
pancreatic cancer diagnostics and sign on high reso CT
high resolution CT (double duct sign)- can also do a uss
management of pancreatic cancer
less than 20% of cases are operable at diagnosis
whipple procedure: pancreaticoduodenectomy
is performed for resectable lesions in the head of pancreas.
adjuvant chemotherapy used AFTER surgery
ERCP with stenting can be used palliatively
alcoholic liver disease stages
healthy-> fatty liver->hepatitis-> fibrotic liver-> cirrhosis
alcoholic liver disease LFT picture
AST/ ALT ration HIGH
gamma GT raised
management of acute alcoholic heptitis
glucocorticoid
(phentoxyphiline sometimes used but research says is not that good)
c dif infection most common triggers
used ot be clyndamycin now its cephalosporins
PPIs are also triggering
micorbiology of c dif
gram positive, anaerobic, spore forming, toxin producing, bacillus
spreads faecal oral route by spread of the spores
complications of c dif
toxic megacolon
how is c dif diagnosis made
CDT (meanig from the cc dif toxin and NOT the anitgen - that would just so exposure rather than infection
management of C dif
1) stop current ab is possible
2) start ORAL VANCOMYCIN
fidaxomycin- second line
vancomycin and iV mtroonidazole is third line
isolate patient in ward - hand washing!! (alcohol doesnt kill )
if reccurent infections consider microbiota transplant
what LFT picture does paracetamol, sodium valporate and anti TB drugs cause?
hepatocellular picture so ALT> ALP
What LFT picture does combined oral contraceptive pill cause
cholestasic picture so ALP> ALT
femoral henrnia presentation is it painful and is it reducible?
usually painless and usually non reducible
complications of femoral hernia
striangulation and bowel obstruction: both are surgial emergencies
important DDx to exclude for femoral hernias
femoral artery aneurism
inguinal hernia
lymphadenopahty
abscess
lipoma
hydrocoele
Most common type of bowel cancer
Adenocarcinoma
meaning of incarcerated hernia
when its non reducible- stuck hernia essentially but not yet STRIANGULATED
how to differentiate incarcerated from striangulated hernia
PAIINNN!! incarcerated hernia is typically painless vs striangulated is painful
difference in management of an incarcerated vs striangulated hernia
striangulated hernia needs IMMEDIATE surgery vs incarcerated just elective
what advice is given to a patient while waiting to get surgery for striangulated hernia
DONT try to reduce it - can exacerbrate peritonitis
OTHER NAME FOR VIT B12
hy
coeliac disease pathophysiology
the protein gluten causes villous atrophy and this in turn causes malabsorption
coeliac disease presentation
- chronic or intermittent diarrhoea
- Persistent or unexplained gastrointestinal symptoms including nausea and vomiting
- prolonged fatigue
- recurrent abdo pain, cramping or distension
- sudden or unexpected weight loss
- unexplained iron deficiency anaemia
- sudden or unexpected weigh loss
coeliac disease associated conditions
autoimmune diseases
dermatitis herpetiformis (doesnt happen much independently to coeliac disease- mostly with it)
diagnosis of coeliac disease
–serology - TTG!! and IgA
—and endoscopic intestinal biopsy is the golden standard!!!!!– form duodenym> jejenum
—main findings of the biopsy: crypt hyperplasia, villous atrophy, increase in intraepithelial lymphocytes
(Also a lot of the cases are associated with HLA-DQ2 or HLA-DQ8)
For the endoscopic intestinal biopsy, what is true regarding the patients consumption of gluten in the 6 weeks prior?
patient needs to have been consuming gluten for at least 6 weeks prior
management of coeliac disease
–no gluten in diet
–this reverses the atrophy usually
– (pasta bread, beer ect have gluten, –RICE does not, potatoes dont corn doesnt)
what is another important aspect of management of coeliac disease?
pneumococcal vaccine and booster every 5 years because all coeliac disease patients have a degree of functional hyposplenism
and flu vaccine on an individual basis
Ascending cholangitis pathophysiology and cause
ascending cholangitis is caused by a combination of outflow obstruction and infection of the billiary tree most commonly caused by e coli
most common predisposing factor to ascending cholanfitis
gallstone disease
two types of gallstone disease progression leading to ascending cholangitis
Mirizi syndrome - gallstones in gallbladder externally compress the common bile duct
or
- cholidocholithiasis- gallstones move down to the common bile duct
presentation of ascending cholangitis
charcot’s triad: jaundice, fever, RUQ pain
if also HYPOTENSIVE and CONFUSED (think SYSTEMIC symptoms) then its reynold’s pentad
blood results of ascending cholangitis
infective markers raised and obstructive pattern LFTs alp> alt + GGT (also raised but less) and also billirubin raised
diagnostic golden standard of ascending cholangitis and findings
abdo USS - stones are seen AND dilation of the bile ducts
crohns disease causes
generally unknown but strong genetic component
crohns disease ages peak incidnce
20-30 can happen in adolescence too!
presentation of Crohn’s - most common symptom in adults and children
adults: diarrhoea (can be bloody but this is more characteristic of UC)
CHILDREN; abdo pain
other: weight loss, lethargy,
perianal disease: skin tags and ulcering
extra-intestinal features (more common in crohns colitis)
most common sites of Crohns
terminal ileum and colon!
ileum involvement in 80%
ileum + colon= 50%
ileum only 30%
colon only 20%
30% perianal
investigations for crohns
bloods:
- inflammatory markers, CRP good correlation with disease progress
- faecal calprotectin
- ANAEMIA
- DECREASED B12 AND FOLATE!
colonoscopy + biopsy for histology
crohns histology + colonoscopy findings
skip lesions, deep perforation till serosa, ulcers
what bowel loop complications are crohns patients at risk of and why
due to the lesions that are very deep (reach serosa layer) thiings like adhesions, strictures and fistulas
additional specific and sensitive investgations to small bowel crohns and its findings
small bowel enema
strictures: kantors string sign
proximal bowel dilation
rose thorn ulcers
fistulae
extra-enteral manifestations equally likely in uc and crohn’s that are DEPENDEDNT on disease activity
pauciarticular arthritis asymetrical
osteoporosis
erythema nodosum
extra enteral manifestations of IBD unrelated to disease activity (equal in UC AND Crohns)
polyarticular arthritis -
clubbing
pyoderma gangrenosum
extra enteral manifestations more likely in crohns
episcleritis
extra-enteral manifestations more likely in UC
primary sclerosing cholangitis
uveitis
crohns management to induce remission (acute management)
glucocorticoids - first line!
potential additions/ alternatives
enteral feeding additionally or as an alternative where steroids will cause bad side effects eg children
5 ASA drugs - used as ALTERNATIVE to glucocorticoids but not as effective
azathiorprine used IN ADDITION to glucocorticoid
management of crohns to maintain remission
azathioprine or mercaptopurine is first line
methrotrexate is used second line
WHAT Needs to be measured before starting azathioprine or mercaptopurine?
+TPMT activity- its the liver enzyme that breaks these drugs down so if its low there is risk of toxicity
how common is surgery in crohns and what are some of its uses?
80% of patients with crohn’s will require some form of surgery
examples:
stricturing terminal ileal disease: ileocaecal resection
segmental small bowel resections
stricturoplasty
crohns disease and GI cancers association
small bowel cancer (standard incidence ratio = 40)
colorectal cancer (standard incidence ratio = 2, i.e. less than the risk associated with ulcerative colitis)
what is trousseau’s syndrome and which cancer is it most associated with
its a paraneoplastic phenomenin associated iwth pancreatic cancer causing migratory thrombophlebitis (eg red painful swellings on fingers)
presentation of perianal abscess
pain around the anus, worse on sitting,
may have noticed hardening tissue around anus,
puss like discharge from anus
if its long standing there may be features of systemic infection eg fever ect
epidemiology of perianal abscess
2:1 more men, and average age is 40
what is a perianal abscess
meaning:
The infection usually starts deeper, in the glands near the anal sphincter
From there, the infection spreads through the tissue planes until it reaches the more superficial layers (under the skin), where it forms an abscess.
management of perianal abscess
incision + drainage under local anaesthetic if its superficial and no involvement of sphincter or
general anaesthetic if sphincter is involved and more complicated
antibiotic only if systemic upset - hasnt been proven to hlep with healing of wound post- drainage
common investigations to help diagnose perianal abscess
- bloods:
-infection markers - blood cultures
- can isually be diagnosed by inspecting hte areaor a DRE
- golden standard for anorectal abscesses is an MRI!!!!
-(other useful: transperineal USS)
-(but these are rarely used- more in complicated disease process such as underlying IBD or complications)
conditions commonly associated with perianal abscess
Crohn’s
Diabetes mellitus due to poor wound healing
underlying malignancy
what bacteria commonly cause perianal abscesses
e coli if from GI tract
s. aureus if skin is the source
what is a Fistula
an abnormal connection between two epithelial surfaces
what general body area are fistulas more common in in gen surg and commonest causes of it
abdomen
crohn’s and diverticular disease are common causes of it
general principle about resolution of fistulas?
they generally resolve spontaneously unless there is something blocking them distally
what are the four types of fistulae in abdomen
enterocutaneous
enterovesicular
enterovaginal
enteroenteric or enterocolic
characteristic of enterocutaneous
they have excretions onto skin
duodenal and jejenal have HIGHer output excretions and more acidic that may excoriate the skin compared to
colo- enteric fistulae that have more faecal secretions
problem with enteroenteric fistulas
overgrowth of bacteria may lead to malabsoprtion syndromes- particularly bad in IBD
enterovesicular fistulas presentations
frequent UTI OR PASSING GASS FROM fwhen peeing
management of fistula when no IBD or obstruiction
conservative as it will heal by itslef
management when there is Where there is skin involvement
protect the overlying skin, often using a well-fitted stoma bag- skin damage is difficult to treat
medicine to use in high output fistula
octreotide, this will tend to reduce the volume of pancreatic secretions.
when are nutritional complcations more common and how to manage in fistulas
Nutritional complications are common especially with high fistula (e.g. high jejunal or duodenal) these may necessitate the use of TPN to provide nutritional support together with the concomitant use of octreotide to reduce volume and protect skin.
what should surgeons avoid doing to fstulas as it worsens outcomes
probing it
what is THE MOST EFFECTIVE treatment For simple perianal fistulae, such as partial intersphincteric types,
fistulotomy is generally the most effective treatment.
(Deeper fistulae may be better managed with a seton drain in order to preserve continence and reduce the risk of sphincter injury)_
When perianal fistulae occur secondary to Crohn’s disease whatis the best management
often to drain acute sepsis and maintain that drainage through the judicious use of setons whilst medical management is implemented.
what are some good tools to help delineate the fistula anatomy, for abscesses and fistulae that have an intraabdominal source?
barium and CT studies
