Gastroenterology Flashcards
if someone has an autoimmune condition, what are they more likely to have?
another autoimmune condition e.g.
T1DM and coeliac’s disease, thyroid disease, autoimmune hepatitis
pathophysiology of coeliac disease
autoantibodies created in response to gluten that target the epithelial cells of the small intestine, leading to inflammation
particularly of the jejunum, leading to villus atrophy = malabsorption of nutrients & symptoms of disease
investigations for coeliac disease
need to be eating gluten for at least 6 weeks
anti-TTG and anti-EMA (endomysial) both IgA
** need to check for IgA deficiency beforehand
endoscopic intestinal biopsy (gold standard - duodenal)
-villous atrophy
-crypt hyperplasia
presentation of coeliac disease
failure to thrive in children
diarrhoea
abdominal pain/bloating
weight loss
fatigue
anaemia
mouth ulcers
dermatitis herpetiformis (itchy blistering skin rash typically on the abdomen)
complications of coeliac disease
hyposplenism
anaemia: iron, folate, B12 (folate more common than b12)
osteoporosis
lactose intolerance
enteropathy-associated T-cell lymphoma of small intestine
subfertility
non-hodgkin lymphoma
oesophageal cancer
what are all new cases of T1DM tested for
coeliac disease
what is haemochromatosis
an autosomal recessive condition
iron storage disorder that results in excessive total body iron and deposition in tissues
mutation in HFE gene on chromosome 6
presentation of haemochromatosis
early symptoms: fatigue, arthralgia, erectile dysfunction
bronze skin pigmentation
diabetes mellitus
liver: chronic liver disease, hepatomegaly, cirrhosis
cardiac failure
amenorrhoea, infertility, reduced libido
reversible vs irreversible complications of haemochromatosis
reversible: cardiomyopathy, skin pigmentation
irreversible: diabetes, cirrhosis, arthropathy, hypogonadotrophic hypogonadism
significance of HBsAg in interpreting hepatitis B serology
if positive, ongoing infection
1-6 months = acute
>6 months = chronic
significance of anti-HBs and anti-HBc in interpreting hepatitis B serology
anti-HBs = implies immunity (either exposure/vaccination), negative in chronic disease
anti-HBc = negative if immunised
IgM anti-HBc appears during acute/recent HB infection and lasts for around 6 months
IgG persists
symptoms of scurvy
follicular hyperkeratosis & perifollicular haemorrhages
easy bruising
poor wound healing
Gingivitis with bleeding and receding gums
Sjogren’s syndrome
generalised symptoms = weakness, malaise, anorexia, depression
what is pseudomembranous colitis
inflammation of the colon due to overgrowth of c.diff bacteria
develops when the normal gut flora are suppressed
due to broad spectrum antibiotics
risk factors: PPIs, clindamycin, 2nd and 3rd generation cephalosporins
side effects of PPIs
hyponatremia, hypomagnasaemia
increased risk of osteoporosis
microscopic colitis
increased risk of c.diff infections
causes of vitamin b12 deficiency
pernicious anaemia
Diphyllobothrium latum infection
Crohn’s disease
atrophic gastritis (Secondary to h.pylori infection)
gastrectomy
malnutrition e.g. alcoholism
Ulcerative colitis - CLOSE UP
continuous inflammation
limited to colon & rectum
only superficial mucosa affected
smoking is protective
excrete blood & mucus
use aminosalicylates
primary sclerosing cholangitis
different types of autoimmune hepatitis
type 1 = affects women in lates 40s/50s, fatigue & features of liver disease, less acute
type 2 = affects teenagers/early twenties, more acute picture of raised transaminases & jaundice
autoantibodies involved in autoimmune hepatitis
type 1 - ANA, SMA
type 2 - Anti-liver/kidney microsomal type 1 antibodies (LKM1)
features of autoimmune hepatitis
may present with signs of chronic liver disease
acute hepatitis: fever, jaundice
amenorrhoea
ANA/SMA/LKM1 antibodies, raised IgG levels
management of autoimmune hepatitis
steroids e.g. prednisolone, azathioprine
liver transplantation
scoring systems used for liver cirrhosis
Child-Pugh classification: albumin, bilirubin, prothrombin time, encephalopathy, ascites
Model for End-Stage Liver Disease (MELD): bilirubin, creatinine, INR
pathophysiology of pernicious anaemia
antibodies against intrinsic factor/parietal cells
parietal cells release intrinsic factor, essential for the absorption of vitamin b12 in the ileum
role of vitamin b12
production of blood cells & myelination of nerve cells
features of pernicious anaemia
anaemia features: fatigue, pallor, dyspnoea
peripheral neuropathy
glossitis
neuropsychiatric: depression, memory loss, confusion, poor concentration, irritability
management of pernicious anaemia
no neurological features: 3 injections per week for 2 weeks followed by 3 monthly treatment of vitamin B12 injections (1mg of intramuscular hydroxycobalamin)
more frequent doses are given for patients with neurological features
complications of pernicious anaemia
subacute combined degeneration of the spinal cord
gastric malignancy
symptoms that should suggest IBS
functional bowel disorder, symptoms present for 6 months
not common after 60yrs
abdominal pain/discomfort:
relieved on opening bowels
associated with a change in bowel habit
and 2 of the following:
abnormal stool passage (urgency, incomplete stool evacuation, straining)
bloating
worse after eating
mucus
lethargy, nausea, backache and bladder symptoms may also support the diagnosis
symptoms that should suggest IBS
abdominal pain/discomfort:
relieved on opening bowels
associated with a change in bowel habit
and 2 of the following:
abnormal stool passage
bloating
worse after eating
mucus
pathology to rule out with IBS
faecal calprotectin (IBD)
coeliac disease
malignancy
management of IBS
first line:
loperamide for diarrhoea
laxatives for constipation (avoid lactulose, linaclotide is used 2nd line)
Antispasmodics for cramps e.g. hyoscine butylbromide (Buscopan)
2nd line:
tricyclic antidepressants (better for diarrhoea)
psychological interventions e.g. CBT, psychologically manage condition & reduce distress
regular small meals
adequate fluid intake
avoid caffeine & alcohol
low FODMAP diet (FODMAPs are short-chain carbohydrates that are poorly absorbed in the small intestine, they then encourage the intake of water into the small intestine causing diarrhoea or when reaching the large bowel they are prone to fermentation by bacteria causing bloating)
what causes flares of UC
stress
NSAIDs, antibiotics
stopping smoking
flare severity criteria for UC
mild:
<4 stools a day, with or without blood
no systemic upset
moderate:
4-6 stools a day, with blood, minimal systemic upset
severe:
>6 bloody stools, systemic upset (fever, tachycardia, abdominal tenderness)
urgent referral for endoscopy criteria
dysphagia
upper abdominal mass consistent with stomach cancer
> 55, weight loss AND:
upper abdominal pain
dyspepsia
reflux
non-urgent referral for endoscopy criteria
patients with haematemesis
Patients aged >= 55 years who’ve got:
treatment-resistant dyspepsia or
upper abdominal pain with low haemoglobin levels or
raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain
pathophysiology of h.pylori
gram negative aerobic bacteria
forces its way into gastric mucosa, the break it makes exposes gastric epithelium to acidic environment
produces ammonia to neutralise acid, which also directly damages epithelial cells
results in gastritis, ulcers, malignancy
what is essential before a h.pylori test (urea breath test)
no antibiotics for 4 weeks
no PPIs for 2 weeks
used as test of eradication after therapy
stages of non-alcoholic fatty liver disease
steatosis
steatohepatitis
Fibrosis
Cirrhosis
associated features of non-alcoholic fatty liver disease
T2DM
obesity
hyperlipidaemia
low activity levels
high cholesterol
jejunoileal bypass
sudden weight loss/starvation
differentials for abnormal liver function tests
USS (non-alcoholic fatty liver disease)
Hepatitis B & C serology
Autoantibodies (autoimmune hepatitis, primary biliary cirrhosis, primary sclerosing cholangitis)
caeruloplasmin (Wilson’s)
Alpha 1 Anti-trypsin levels
transferrin & ferritin (haemochromatosis)
presentation of NAFLD
asymptomatic
hepatomegaly
ALT is typically greater than AST
increased echogenicity on ultrasound
investigation in NAFLD
enhanced liver fibrosis blood test
management of NAFLD
Weight loss
Exercise
Stop smoking
Control of diabetes, blood pressure and cholesterol
Avoid alcohol
what drugs tend to cause cholestasis
COCP
antibiotics e.g. flucloxacillin, co-amoxiclav, erythromycin
sulfonylureas
anabolic steroids, testosterones
raised ALP, GGT
what should happen to males drinking >50 units a week & females >35 with normal LFTs
should be referred for ELF test or fibroscan, even if liver function tests are normal
investigations for haemochromatosis
general population: transferrin saturation
family members: HFE mutation
**ferritin is an acute phase reactant, transferrin will indicate if ferritin is high due to inflammation/NAFLD or iron overload
Liver biopsy with Perl’s stain can be used to establish the iron concentration in the parenchymal cells
management of haemochromatosis
venesection - transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l
desferrioxamine may be used second-line
complications of haemochromatosis
chronic liver disease/carcinoma
cardiomyopathy
T1DM
hypothyroidism
Chrondocalcinosis / pseudogout (calcium deposits in joints) causing arthritis
Iron deposits in the pituitary and gonads lead to endocrine and sexual problems (hypogonadism, impotence, amenorrhea, infertility)
features of c.diff infection
diarrhoea
abdominal pain
raised WCC
if severe, toxic megacolon can develop
criteria for varying severities of c.diff infection
mild:
normal WCC
moderate:
raised WCC
3-5 loose stools a day
severe:
raised WCC
temp >38.5, evidence of severe colitis (abdominal/radiological signs)
life-threatening:
hypotension
partial/complete ileus
toxic megacolon
diagnosis of c.diff infection
Clostridium difficile toxin (CDT) in the stool
management of c.diff infection
first-line therapy is oral vancomycin for 10 days
second-line therapy: oral fidaxomicin
third-line therapy: oral vancomycin +/- IV metronidazole
recurrent episode:
within 12 weeks of symptom resolution: oral fidaxomicin
after 12 weeks of symptom resolution: oral vancomycin OR fidaxomicin
Life-threatening Clostridium difficile infection:
oral vancomycin AND IV metronidazole
specialist advice - surgery may be considered
criteria for same day admission for someone presenting with jaundice
acutely unwell
fever
encephalopathy (confusion, ataxia)
cholangitis
dehydrated
bilirubin >100
abnormal coagulation
abnormal kidney function
suspected paracetamol overdose
frail/significant co-morbidities
differentials for dysphagia
oesophageal cancer
oesphagitis
oesophageal candidiasis
achalasia
pharyngeal pouch
systemic sclerosis
myasthenia gravis
globus hystericus
what is primary sclerosing cholangitis
biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts
associations of primary sclerosing cholangitis
UC
crohn’s
HIV
presentation of PSC
cholestasis: jaundice, raised ALP, bilirubin, pruritus
RUQ pain
fatigue
investigation for PSC
ERCP/MRCP - beaded appearance
complications of PSC
cholangiocarcinoma
increased risk of colorectal cancer
what is Peutz Jeghers syndrome
autosomal dominant condition characterised by numerous hamartomatous polyps in the GI tract (mainly small bowel) & pigmentation of lips, face, palms & soles
**can present with small bowel obstruction often due to intussusception
GI bleeding
management of Peutz Jeghers syndrome
conservative unless complications develop
what to think with T2DM and abnormal LFTs
non alcoholic fatty liver disease
symptoms of oesphageal cancer
dysphagia
weight loss
anorexia
vomiting
odynophagia, hoarse voice, cough, melaena
features of cyclical vomiting syndrome
severe nausea and vomiting lasting hours to days
Prodromal intense sweating and nausea
Well in between episodes
might have:
weight loss
reduced appetite
abdominal pain
diarrhoea
photophobia
headache
what is cyclical vomiting syndrome
rare
seen in children more than adults
seen in females more than males
associated with migraines
investigations of cyclical vomiting syndrome
clinical diagnosis
pregnancy test to exclude in women
routine blood tests to identify any underlying condition
management of cyclical vomiting syndrome
avoidance of triggers
Prophylactic treatments include amitriptyline, propranolol and topiramate.
Ondansetron, prochlorperazine and triptans in acute episodes
management of GORD
endoscopically negative:
full dose PPI for one month
if response = offer low dose treatment
no response = offer H2RA e.g. ranitidine
endoscopically proven oesphagitis:
full dose PPI 1-2 months
if response: lower dose
no response: double dose PPI for 1 month
lifestyle:
weight loss
smaller, lighter meals
avoid heavy meals before bed
sit upright after eating
stop smoking
reduce tea, coffee, caffeine
complications of GORD
oesphagitis
ulcers
anaemia
benign strictures
Barrett’s oesphagus
carcinoma
what can often be used to test for H.pylori
stool test
management of patients with a raised ALT
all patients should be investigated with a raised ALT with a liver screen including USS
presentation of UC
bloody diarrhoea
urgency
tenesmus
abdominal pain, particularly in the LLQ
investigations for UC
colonoscopy + biopsy
** if severe colitis use flexible sigmoidoscopy to prevent perforation
findings:
red, raw mucosa that bleeds easily
no inflammation beyond submucosa
pseudopolyps
barium enema:
loss of haustrations
narrowing of colon if long standing disease
investigations for UC
colonoscopy + biopsy
** if severe colitis use flexible sigmoidoscopy to prevent perforation
findings:
red, raw mucosa that bleeds easily
no inflammation beyond submucosa
pseudopolyps
barium enema:
loss of haustrations
narrowing of colon if long standing disease
what is melanosis coli
disorder of pigmentation of the bowel wall
histology shows pigment laden macrophages
associated with laxative abuse
what is melanosis coli
disorder of pigmentation of the bowel wall
histology shows pigment laden macrophages
associated with laxative abuse
presentation of crohn’s
non-specific e.g. fatigue, weight loss
diarrhoea
abdominal pain
perianal disease e.g skin tags, ulcers
Is small bowel or large bowel obstruction more common
Small bowel
Pathophysiology of bowel obstruction
Obstruction of food, fluids and gas results in a build up proximal to the obstruction, resulting in back pressure which causes vomiting & dilatation of intestines proximal to the obstruction
GI tract secretes fluid later absorbed in the colon, when there is an obstruction & fluid can’t be absorbed, fluid loss from intravascular space leads to hypovolaemia and shock = third spacing
The higher up the intestine the obstruction, the greater the fluid loss as there is less bowel for fluid to be reabsorbed
Causes of bowel obstruction
Adhesions and hernias (small bowel)
Malignancy (large bowel)
Other causes: intussusception, strictures, diverticular disease, volvulus
What causes adhesions
Abdominal or pelvic surgery
Peritonitis
Endometriosis
Abdominal or pelvic infections e.g. PID
Can be congenital or secondary to radiotherapy
What is closed loop obstruction
Two points of obstruction along the bowel, middle section sandwiched between 2 points of obstruction
E.g. adhesions
Hernias
Volvulus
Single point of obstruction with competent ileocaecal valve (does not allow any movement back into ileum)
Consequences of a closed loop obstruction
Do not have an open end where they can drain and decompress
Will continue to expand, leading to ischaemia and perforation
EMERGENCY SURGERY
Presentation of bowel obstruction
Vomiting (green bilious vomiting)
Abdominal distension
Diffuse abdominal pain
Constipation and lack of flatulence
Tinkling bowel sounds in early bowel obstruction
How to tell the difference between small and large bowel on X-ray
Small bowel = valvulae conniventes
Mucosal folds extending full width of the bowel
Large bowel = haustra
Pouches formed by muscles in walls of large bowel, do not extend full width of bowel
Investigation for bowel obstruction
Abdominal X-RAY = initial
>3cm diameter small bowel
>6cm colon
>9cm caecum
Free intraperitoneal gas might indicate perforation
Erect CXR can demonstrate air under the diaphragm if intra-abdominal perforation
Contrast abdominal CT scan
Initial management of bowel obstruction
ABCDE approach:
May be haemodynamically unstable if hypovolaemic shock, bowel ischaemia or perforation, or sepsis
Nil by mouth
IV fluids to hydrate and correct any electrolyte abnormalities
NG tube with free drainage (reduce risk of vomiting and aspiration)
Key blood findings in bowel obstruction
U&Es
Metabolic alkalosis (vomiting)
Bowel ischaemia (raised lactate)
Further management of bowel obstruction
Conservative management if patient stable and secondary to adhesions/volvulus
If this fails, definitive management anyway is surgery
Exploratory surgery
Adhesiolysis
Hernia repair
Emergency resection of tumour
Stents may be inserted during colonoscopy
When will IV ABx be started during bowel obstruction
Perforation suspected or surgery planned
Role of mesentery
Membranous peritoneal tissue that creates a connection between the bowel and posterior abdominal wall
Bowel gets its blood supply via the mesentery through the mesenteric arteries
What is a volvulus
Condition where the bowel twists around itself and the mesentery it is attached to
Leads to a closed bowel obstruction
Bowel vessels might be involved, leading to ischaemia, necrosis and bowel perforation
What are the 2 types of volvulus
Sigmoid
Caecal
Associations of sigmoid volvulus
More common (80%), affects older individuals
Associated with chronic constipation (becomes overloaded with faeces, sinks downwards and causes a twist)
Chagas’ disease
Neurological conditions e.g. Parkinson’s, duchenne muscular dystrophy
Psychiatric e.g. scizhophrenia
Associations of caecal volvulus
All ages
Pregnancy
Adhesions
Presentation of volvulus
Same as bowel obstruction
Investigations of volvulus
Abdominal X-ray - coffee bean sign
Contrast CT to confirm
what type of peptic ulcer are more common
duodenal > gastric
pathophysiology of peptic ulcers
stomach mucosa is prone to ulceration from breakdown of the protective layer of the stomach/duodenum or an increase in the production of stomach acid
protective layer can be broken down due to: medications (steroids/NSAIDs) or H.pylori
increase in production of stomach acid: caffeine, stress, alcohol, smoking, spicy foods
presentation of peptic ulcers
epigastric pain
nausea and vomiting
dyspepsia
haematemesis, coffee ground vomit, melaena
iron deficiency anaemia
*** eating typically worsens the pain of gastric ulcers and improves the pain of duodenal ulcers.
investigations for peptic ulcers
endoscopy
- rapid urease test (CLO) can be performed to check for H.pylori
- biopsy should be considered to check for malignancy
management for peptic ulcers
high dose PPIs
endoscopy can be used for monitoring
complications of peptic ulcers
bleeding - most common complication, with the gastroduodenal artery being a source of significant GI bleeding
perforation - epigastric pain that becomes generalised due to peritonitis
can be diagnosed with an erect CXR indicating air under the diaphragm
scarring and strictures of the muscle and mucosa, which can lead to pyloric stenosis
