Gastro Ix Mx Flashcards
Spontaneous bacterial peritonitis (sbp)
Ascites due to cirrhosis + these sx;
Fever, abdominal pain or tenderness, and confusion
Ix = paracentesis
paracentesis: neutrophil count > 250 cells/ul
the most common organism found on ascitic fluid culture is E. coli
Mx = IV cefotaxime (+diuretics?)
Achalasia
Ix: 1st = Oesophageal manometry - excessive LOS tone which doesn’t relax on swallowing
Barium swallow (w X-Ray) - ‘bird’s beak’ + fluid level
Chest x-ray = wide mediastinum + fluid level
Mx: 1st = pneumatic (balloon) dilation
Persistent sx = Surgery + Heller cardiomyotomy
High surgical risk = intra-sphincteric injection of botulinum toxin
Pts for PBD should be a low surgical risk as surgery may be required if complications occur
Surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms
Acute (ascending) cholangitis
(gallstones -> E.coli infection of the biliary tree)
Ix: 1st = USS (bile duct dilation/stones)
Mx = IV antibiotics + ERCP
(ERCP) after 24-48 hours to relieve any obstruction
Charcot’s triad = RUQ pain + fever + jaundice*
fever is the most common feature, seen in 90% of patients
RUQ pain 70%
jaundice 60%
Hypotension and confusion are also common (the additional 2 factors in addition to the 3 above make Reynolds’ pentad)
*Jaundice is only visible when bilirubin is >35
Alcoholic hepatitis
Ix = GGT, AST:ALT>2 (3=alcoholic hepatitis!)
Mx = Pred
Maddrey’s discriminant function (DF) is often used during acute episodes to determine who would benefit from glucocorticoid therapy
It is calculated by a formula using prothrombin time and bilirubin concentration
Anal fissure
Acute <6 weeks<chronic
Risk factors
constipation
inflammatory bowel disease
sexually transmitted infections e.g. HIV, syphilis, herpes
Features
painful, bright red, rectal bleeding
around 90% of anal fissures occur on the posterior midline.
if the fissures are found in alternative locations then other underlying causes should be considered e.g. Crohn’s disease!
Acute (<1week) Mx:
1st = Bulk forming laxative (2nd = lactulose)
Mx of a chronic anal fissure:
1st = Topical GTN
2nd = surgery/botulinum toxin
- Dietary advice: high-fibre diet with high fluid intake
- Lubricants such as petroleum jelly may be tried before defecation
- Topical anaesthetics
- Analgesia
The above techniques should be continued
If topical GTN is not effective after 8 weeks then secondary care referral should be considered for surgery (sphincterotomy) or botulinum toxin
Appendicitis
Examination
Generalised peritonitis if perforation has occurred or localised peritonism
Rebound and percussion tenderness, guarding and rigidity
Digital rectal examination may reveal boggy sensation if pelvic abscess is present, or even right-sided tenderness with a pelvic appendix
Psoas sign = pain on extending hip if retrocaecal appendix. Retrocaecal appendicitis may have relatively few signs
Ix = Raised inflammatory markers + history + Urinalysis
Urinalysis (B-hcg, UTI, renal colic)
a neutrophil-predominant leucocytosis is seen in 80-90%!
In patients with appendicitis, urinalysis may show mild leucocytosis but no nitrites
thin, male patients with a high likelihood of appendicitis may be diagnosed clinically
USS is useful in females where pelvic organ pathology is suspected. Although it is not always possible to visualise the appendix on ultrasound, the presence of free fluid (always pathological in males) should raise suspicion
Mx = Laproscopic Appendicectomy + prophylactic antibiotics
Perforated appendicitis (15-20% of pt’s) = Copious abdominal lavage
Appendix mass but no peritonitis = Broad-spectrum antibiotics and consideration given to performing an internal appendicectomy
Be wary in the older patients who may have either an underlying caecal malignancy or perforated sigmoid diverticular disease
Autoimmune hepatitis
Ix = ANA/SMA/LKM1/SLA ab’s, raised IgG levels, biopsy
Liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis
Acute hepatitis = Fever, jaundice etc (only 25% present in this way)
Amenorrhoea is v common!
Mx = Steroids,
also other immunosuppressants e.g. azathioprine
liver transplantation
Barrett’s oesophagus
Dyspepsia/dysphagia ix flow chart??
Histological features
the columnar epithelium may resemble that of either the cardiac region of the stomach or that of the small intestine (e.g. with goblet cells, brush border)
Risk factors
gastro-oesophageal reflux disease (GORD) is the single strongest risk factor
male gender (7:1 ratio)
smoking
central obesity
Interestingly alcohol does not seem to be an independent risk factor for Barrett’s although it is associated with both GORD and oesophageal cancer.
Whilst Barrett’s oesophagus itself is asymptomatic clearly patients will often have coexistent GORD symptoms.
Management
high-dose proton pump inhibitor
whilst this is commonly used in patients with Barrett’s the evidence base that this reduces the change of progression to dysplasia or induces regression of the lesion is limited
endoscopic surveillance with biopsies
for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years
if dysplasia of any grade is identified endoscopic intervention is offered. Options include:
1st = radiofrequency ablation: particularly for low-grade dysplasia
2nd = endoscopic mucosal resection
Cholecystitis (gallbladder inflammation)
RUQ pain
May radiate to the right shoulder
Fever and signs of systemic upset
Murphy’s sign - inspiratory arrest upon palpation of the right upper quadrant
LFTs are normal
Ix: 1st = USS
2nd = Cholescintigraphy (HIDA scan)
Mx = IV ab’s + cholecystectomy
Deranged LFTs may indicate Mirizzi syndrome - a gallstone impacted in the distal cystic duct causing extrinsic compression of the common bile duct
HIDA scan = Technetium-labelled HIDA (hepatobiliary iminodiacetic acid) is injected IV and taken up selectively by hepatocytes and excreted into bile
In acute cholecystitis there is cystic duct obstruction (secondary to odema associated with inflammation or an obstructing stone) and hence the gallbladder will not be visualised
NICE now recommend early laparoscopic cholecystectomy, within 1 week of diagnosis!
Cirrhosis
Ix: 1st = Transient elastography 2nd = Acoustic radiation force impulse imaging
Then enhanced liver fibrosis score
Mx = ?
Coeliac disease
Caused by sensitivity to the protein gluten. Repeated exposure leads to villous atrophy which in turn causes malabsorption
Which conditions are associated with coeliac disease?
Ix:
If patients are already taking a gluten-free diet they should be asked, if possible, to reintroduce gluten for at least 6 weeks prior to testing!
Ix: GS = Endoscopic duodenal biopsy 2nd = anti-TTG 3rd = endomyseal, gliadin
findings supportive of coeliac disease:
villous atrophy
crypt hyperplasia
increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes
Mx = gluten-free diet + pneumococcal vaccine (every 5yrs) + influenza vaccine
Some notable foods which are gluten-free include:
rice
potatoes
corn (maize)
TTG-abs may be checked to check compliance with a gluten-free diet.
Immunisation = Patients with coeliac disease often have a degree of functional hyposplenism so should therefore be immunised
Conditions associated with coeliac disease :
Dermatitis herpetiformis (a vesicular, pruritic skin eruption)
+ AI disorders (type 1 diabetes mellitus and autoimmune hepatitis).
Crohn’s disease
Ix = Colonoscopy
Mx:
Maintaining remission: S-A-S 1st = stop smoking 2nd = purine synth antagonist (aza/mercaptopurine) 3rd = surgery, what type?
Acute: mind the GAP! (Crohns - skip lesions)
1st = Glucocorticoids (hydro/pred/dex)
2nd = Aminosalicyclates (mesalazine)
3rd = Purine synth anatagonists (aza/mercaptopurine) + Infliximab
Perianal = metronidazole
CRP correlates well with disease activity
Histology
inflammation in all layers from mucosa to serosa
goblet cells
granulomas
Small bowel barium enema
high sensitivity and specificity for examination of the terminal ileum;
strictures: ‘Kantor’s string sign’
proximal bowel dilation
‘rose thorn’ ulcers + cobblestoning
fistulae
Diverticular disease
Ix:
X-Ray = identifies perforation
CT = identifies acute inflammation + abcess formation
Confirmatory Ix = colonoscopy, CT cologram or barium enema
Mx = Increase dietary fibre intake
- Mild = conservatively with antibiotics
- Peri colonic abscesses = drain (surgically or radiologically)
- Recurrent episodes requiring hospitalisation = segmental resection
- Hinchey IV perforations (generalised faecal peritonitis) = resection + stoma + HDU admission
- Less severe perforations = Laparoscopic washout and drain insertion.
Irritable bowel syndrome (IBS)
what are the red flag sx?
Ix = FBC + ESR/CRP + anti-TTG (to exclude coeliacs)
Red flag features should be enquired about:
rectal bleeding
unexplained/unintentional weight loss
family history of bowel or ovarian cancer
onset after 60 years of age
Mx:
First-line pharmacological treatment - according to predominant symptom;
pain: antispasmodic agents
constipation: laxatives but avoid lactulose. 1st = Laxatives 2nd = ->12 months-> Linaclotide
3rd = amitriptyline ->12 months->4th = psych (CBT etc)
diarrhoea: loperamide is first-line
constipation:
General dietary advice
have regular meals and take time to eat
avoid missing meals or leaving long gaps between eating
drink at least 8 cups of fluid per day, especially water or other non-caffeinated drinks such as herbal teas
restrict tea and coffee to 3 cups per day
reduce intake of alcohol and fizzy drinks
consider limiting intake of high-fibre food (for example, wholemeal or high-fibre flour and breads, cereals high in bran, and whole grains such as brown rice)
reduce intake of ‘resistant starch’ often found in processed foods
limit fresh fruit to 3 portions per day
for diarrhoea, avoid sorbitol
for wind and bloating consider increasing intake of oats (for example, oat-based breakfast cereal or porridge) and linseeds (up to one tablespoon per day).
Gallstones (cholelithiasis) & biliary colic
RF’s - Fat, Female, Fertile(pregnant), Forty
Oestrogen increases activity of HMG-CoA reductase
other notable risk factors include:
diabetes mellitus
Crohn’s disease
rapid weight loss e.g. weight reduction surgery
drugs: fibrates, combined oral contraceptive pill
Ix = USS
Mx = Elective laparoscopic cholecystectomy
Reassure people with asymptomatic gallbladder stones (found incidentally)
↑ cholesterol -> ↓ bile salts and biliary stasis
The pain occurs due to the gallbladder contracting against a stone lodged in the cystic duct
Features
colicky right upper quadrant abdominal pain
worse postprandially, worse after fatty foods
the pain may radiate to the right shoulder/interscapular region
nausea and vomiting are common
In contrast to other gallstone-related conditions, in biliary colic there is NO FEVER and LFTs + inflamm markers are normal
Around 15% of patients are found to have gallstones in the common bile duct (choledocholithiasis) at the time of cholecystectomy, This can result in obstructive jaundice in some patients
Gastro-oesophageal reflux disease (GORD)
Ix: GI endoscopy -> oesophageal pH monitoring(GS!)
Indications for upper GI endoscopy*. Must have all of the following;
>55yo
sx > 4 weeks or persistent symptoms despite treatment
dysphagia
relapsing symptoms
weight loss
Mx = PPI
Endoscopically proven oesophagitis
full dose proton pump inhibitor (PPI) for 1-2 months
if response then low dose treatment as required
if no response then double-dose PPI for 1 month
Endoscopically negative reflux disease
full dose PPI for 1 month
if response then offer low dose treatment, possibly on an as-required basis, with a limited number of repeat prescriptions
if no response then H2RA or prokinetic for one month
*High urea levels can indicate an upper GI bleed due to the ‘protein meal of the blood’. This dos not occur in a lower GI bleed
Gastroenteritis & infectious colitis (c.diff)
Ix = stool sample
Mx = stop any current antibiotics
1st episode:
1st = oral vanc 2nd = oral fidax 3rd = oral vanc/Iv metro
Recurrent episode:
Within 12 weeks of sx resolution = oral fidax
after 12 weeks = oral vanc OR fidax
Life-threatening:
oral vanc + IV metro
specialist advice - surgery may be considered
Other therapies = Faecal microbiota transplant
may be considered for patients who’ve had 2+ recurrent episodes
Gastrointestinal perforation
Haemochromatosis
Increased chance of developing which cancer?
Ix = Transferrin saturation, TIBC, ferritin
Transferrin saturation > 55% in men or > 50% in women
Raised ferritin (e.g. > 500 ug/l) and iron
low TIBC
Further tests and diagnosis
Genetics = C282Y and H63D mutations
MRI is generally used to quantify liver and/or cardiac iron
LFT’s
liver biopsy is now generally only used if suspected hepatic cirrhosis
Mx: 1st = venesection (monitored w transferrin saturation)
2nd = desferrioxamine
Transferrin saturation should be kept <50%
and
Serum ferritin concentration <50 ug/l
Ca = Hepatocellular carcinoma
Haemorrhoids
Mx = soften stools + local anaesthetics + rubber-band ligation
Newer treatments: Doppler guided haemorrhoidal artery ligation, stapled haemorrhoidopexy
Surgery is reserved for large symptomatic haemorrhoids which do not respond to outpatient treatments
Acutely thrombosed external haemorrhoids
Typically present with significant pain and a purplish, oedematous, tender subcutaneous perianal mass
Pt presents <72 hours = refer for excision
Otherwise mx = stool softeners, ice packs and analgesia
Symptoms usually settle within 10 days
Femoral Hernia
Only 5% of abdominal hernias are femoral
More common in women (M:F 1:3)
More common in multiparous women due to increased abdominal pressure
Ix = Clinical exam 2nd = USS
Mx = Surgical repair (given the risk of strangulation)
Features:
Non-reducible, although can be reducible in a minority of cases
Given the small size of the femoral ring, a cough impulse is often absent
Complications;
Incarceration = where the herniated tissue cannot be reduced
Incarceration -> Strangulation
These hernias will be tender and likely non-reducible, and may also present with a systemically unwell patient
The risk of strangulation is much higher with femoral hernias (the strangling female!) than inguinal hernias and increases as the time from diagnosis rises;
Bowel obstruction, again a surgical emergency
Bowel ischaemia and resection due to the above, which may lead to significant morbidity and mortality for the patient.
Hernia support belts/trusses should NOT be used for femoral hernias due to the risk of strangulation;
In an emergency situation, a laparotomy may be the only option
Hiatus hernias
Protrusion of the stomach through the LOS
Sx = heartburn, dysphagia, regurgitation, chest pain
Ix: 1st = Endoscopy
Barium swallow = most sensitive test!
Mx = weight loss + PPI
Symptomatic paraesophageal hernias = surgery
There are two types:
Sliding (95%) = The gastroesophageal junction slides above the diaphragm
Rolling (paraoesophageal) = The gastroesophageal junctions remains below the diaphragm but a separate part of the stomach herniates through the oesophageal hiatus
RFs = Obesity + increased intraabdominal pressure (e.g. ascites, multiparity)
Mesenteric ischaemia
Acute mesenteric ischaemia = embolism of an artery which supplies the small bowel (e.g. superior mesenteric artery)
Classically patients have a history of AF
Chronic mesenteric ischaemia is a relatively rare clinical diagnosis due to it’s non-specific features and may be thought of as ‘intestinal angina’. Colickly, intermittent abdominal pain occurs.
Acute:
The abdominal pain is typically severe, of sudden onset and out-of-keeping with physical exam findings.
Mx = urgent surgery is usually required
poor prognosis, especially if surgery delayed
Chronic:
The abdominal pain is typically severe, of sudden onset and out-of-keeping with physical exam findings
Mx = Immediate laparotomy is usually required, particularly if signs of advanced ischemia e.g. peritonitis or sepsis
Poor prognosis, especially if surgery delayed
Large bowel obstruction
Tumour = 60%
More distal colonic/rectal tumours present with obstruction, as these tend to obstruct earlier due to the smaller lumen diameter
Ix: 1st = X-ray 2nd = CT scan
Mx = NBM + IV fluids + NG tube
Peritonitis/Perforation = IV antibiotics for surgery
If the cause of obstruction itself does not require surgery, conservative management for up to 72 hours can be trialled, after which further management may be required if there is no resolution
Nausea and vomiting are late symptoms that may suggest a more proximal lesion
Perforation presents with peritonism (free intra-peritoneal gas)
Normal diameter limits;
Caecum = 10-12 cm
Ascending colon = 8 cm
Recto-sigmoid = 6.5 cm
Anything bigger is diagnostic of obstruction
Around 75% of LBO’s will eventually require surgery
Liver abscesses
Children = S. aureus
Adults = E. coli
Mx = drainage (typically percutaneous) + antibiotics
amoxicillin + ciprofloxacin + metronidazole
if penicillin allergic: ciprofloxacin + clindamycin
Liver cysts
Liver failure
Causes
paracetamol overdose
alcohol
viral hepatitis (usually A or B)
acute fatty liver of pregnancy
Features*
jaundice
coagulopathy: raised prothrombin time
hypoalbuminaemia
hepatic encephalopathy
renal failure is common (‘hepatorenal syndrome’)
*remember that ‘liver function tests’ do not always accurately reflect the synthetic function of the liver. This is best assessed by looking at the prothrombin time and albumin level.
Mallory–Weiss tear
Non-alcoholic steatohepatitis (NASH)
Obesity + abnormal LFTs = NASH
T2DM + abnormal LFTs = NASH
Ix:
1st = USS (increased echogenecity) + ALT>AST
2nd = ELF blood test
3rd = FIB4 score/NALFD fibrosis score/transient elastography)
4th = Biopsy
Mx: 1st = weight loss 2nd = Gastric banding + metformin/piaglitazone etc
ELF blood test = a combination of hyaluronic acid + procollagen III + tissue inhibitor of metalloproteinase 1.
An overweight(mx) big eared(ultra-sound) elf finishing last(L>AST) in the biopsy race
Pancreatitis (acute and chronic)
Acute:
Ix = Pain + serum amylase (x3 upper limit) + lipase (good for >24hrs)
Optional = USS + CT for gallbladder obstruction
Mx = Fluids (crystalloid) + IV opioids!
Severe = NG tube nutrition <72hrs after presenting
Acute pancreatitis due to gallstones = cholecystectomy
Obstructed biliary system due to stones = early ERCP
Infected necrosis = Antibiotics + Debridement and either radiological drainage or surgical necrosectomy
Other causes of raised amylase include: pancreatic pseudocyst, mesenteric infarct, perforated viscus, acute cholecystitis, diabetic ketoacidosis
Aim for a urine output of > 0.5mls/kg/hr - may also help relieve pain by reducing lactic acidosis
Parental (through a vein) nutrition should only be used if enteral nurition has failed or is contraindicated
Peptic ulcer disease and gastritis
perforated = sudden epigastric pain, later becoming more generalised. Patients may describe syncope.
The #1 cause of upper GI bleeding!!
Peptic ulcer:
Ix: 1st = Urea breath test* + Stool antigen test
Mx:
if H pylori -ve = PPI’s until the ulcer is healed
if H pylori +ve = Triple therapy (PPI+amox+clarithro) .
penallergy = metro instead of amox
Acute bleeding:
Mx = ABC + IV PPI
1st = endoscopic intervention
2nd = urgent interventional angiography with transarterial embolization or surgery
remember long-term PPI’s cause hyponatraemia!
Perforated:
Ix: 1st = X-Ray (free air under diaphragm)
Most common = duodenal (relieved by eating)
*only test recommended to check eradication post treatment
Perineal abscesses and fistulae
Pilonidal sinus = sinuses and cysts form near the upper part of the natal cleft of the buttocks. It is more common in men and typically presents around the age of 20 years
Pathophysiology
it is thought to develop as a result of hair debris collecting in intergluteal pores that become stretched when a person sits or bends
over a period of time, this may lead to sinus formation, with further hairs become trapped within the sinus
the opening of the sinus is lined by squamous epithelium, but most of its wall consists of granulation tissue
Ix:
Acute inflammation -> an abscess
pain (may be severe)
purulent discharge
fluctuant swelling at the site
patients may describe cycles of being asymptomatic and periods of pain and discharge from the sinus
Mx:
Asymptomatic patients = conservative (hygiene focus)
symptomatic patients:
Acute = incision + drainage
Chronic/recurrent = Excision of the pits and obliteration of the underlying cavity
Primary biliary cirrhosis
?
Primary biliary cholangitis
seen in middle aged females (F:M is 9:1!)
Ix: 1st = AM-ab’s (M2-subtype
2nd = SM-ab’s + IgM
Then MRCP/USS to exclude biliary obstrucion
Mx: 1st = Ursodeoxycholic acid
Pruritus = cholestyramine
Also,
Fat-soluble vitamin supplementation
Liver transplantation
e.g. if bilirubin > 100 (PBC is a major indication)
Primary sclerosing cholangitis
80% of pts w PSC have UC
Also, which cancer is PSC most associated with?
Ix = MRCP (iMvestigation)
Showing multiple biliary strictures giving a ‘beaded’ appearance
p-ANCA may be positive
Rarely - liver biopsy = ‘onion skin’ fibrous obliterative cholangitis
Mx = Observe
cancer = cholangiocarcinoma
Rectal prolapse
?
Ulcerative colitis
Severe = 6 stools per day plus 1 of;
> 37.8°C
HR>90
Anaemia (Hb<105g/ L)
ESR>30 mm/hour
Ix:
1st = Colonoscopy + biopsy
Severe = Flexisig (to prevent perforation)
2nd = Barium enema
Positive faecal calprotectin = IBD
Mx:
Acute:
mild/mod: topical mesal -4weeks-> +oral mesal-> +pred
severe: IV pred or ciclosprin -72hrs-> both together/surgery!
If the disease has reached the ascending colon then start with topical+oral mesal!
Ongoing: UC+ tomyum soup
mild/mod: top/oral mesal, extensive = oral mesal
severe (>2flares/yr): oral aza/mercaptopurine
TOM YUM - Topical/Oral Mesal, Yikes UC! Mercapto!
Ix:
U ntrue polyps/Ulcers
L ow amount of of goblet cells
C rypt abscess’
Barium enema:
loss of haustrations
superficial ulceration, ‘pseudopolyps’
long standing disease: colon is narrow and short -‘drainpipe colon’
Viral hepatitis (A-E?)
Vitamin deficiency (A, B, C, D, E, K)
A (Retinoids) = Night-blindness (nyctalopia)
B1 (Thiamine) = Beriberi*/polyneuropathy/Wernicke-Korsakoff syndrome/heart failure
B3 (Niacin) = Pellagra (dermatitis/diarrhoea/dementia->death)
B6 (Pyridoxine) = Anaemia, irritability, seizures
B7 (Biotin) = Dermatitis, seborrhoea
B9 (Folic acid) = Megaloblastic anaemia, deficiency during pregnancy - neural tube defects
B12 (Cyanocobalamin) = Megaloblastic anaemia, peripheral neuropathy
C (Ascorbic acid) = Scurvy/gingivitis
D (Ergocalciferol, cholecalciferol) = Rickets, osteomalacia
E (Tocopherol, tocotrienol) = Mild haemolytic anaemia in newborn infants, ataxia, peripheral neuropathy
K (Naphthoquinone) = Haemorrhagic disease of the newborn, bleeding diathesis
*beriberi can be wet/dry -
Wet beriberi = tachypnoea, dyspnoea and pedal oedema
Dry beriberi = pain, paresthesia and confusion. Wernicke–Korsakoff syndrome is a subtype of dry beriberi.
Volvulus = obstruction caused by twisting of the stomache/intestines
Features
constipation
abdominal bloating
abdominal pain
nausea/vomiting
Ix = X-ray/CT
Sigmoid volvulus: large bowel obstruction (large, dilated loop of colon, often with air-fluid levels) + coffee bean sign
Caecal volvulus: small bowel obstruction may be seen
M:
sigmoid volvulus = Rigid sigmoidoscopy with rectal tube insertion
caecal volvulus = Right hemicolectomy
Wilson’s disease
Features result from excessive copper deposition in the tissues, especially the brain, liver and cornea:
liver: hepatitis, cirrhosis
neurological:
basal ganglia degeneration: in the brain, most copper is deposited in the basal ganglia, particularly in the putamen and globus pallidus
speech, behavioural and psychiatric problems are often the first manifestations
also: asterixis, chorea, dementia, parkinsonism
Kayser-Fleischer rings
present in 90% of those who have neurological involvement
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails
Ix = Slit lamp + serum caeruloplasmin & copper
Confirmation = ATP7B gene
Mx = penicillamine (chelates copper)
2nd = trientine hydrochloride
Slit lamp examination for Kayser-Fleischer rings
reduced serum caeruloplasmin
reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
free (non-ceruloplasmin-bound) serum copper is increased
increased 24hr urinary copper excretion
Inguinal Hernia = groin lump, superior and medial to the pubic tubercle
Larger and more noticeable than a femoral hernia, so less likely to strangulate
Ix = disappears on pressure or when the patient lies down
Discomfort and ache: often worse with activity, severe pain is uncommon
strangulation is rare
Mx = surgery (mesh repair)
unilateral = open
bilateral = laproscopic
Not fit for surgery = truss (frame)
Return to work:
Laparoscopic repair = 1-2 weeks
Non-manual work = 2-3 weeks
Ischaemic Colitis = acute but transient compromise to GI blood flow
Ischaemia to the lower gastrointestinal tract can be:
- acute mesenteric ischaemia
- chronic mesenteric ischaemia
- ischaemic colitis
Common features in bowel ischaemia
Common predisposing factors
increasing age
AF = mesenteric ischaemia
other causes of emboli: endocarditis, malignancy
cardiovascular disease risk factors: smoking, hypertension, diabetes
cocaine + young = ischaemic colitis
Common features
abdominal pain - in acute mesenteric ischaemia this is often of sudden onset, severe and out-of-keeping with physical exam findings
rectal bleeding
diarrhoea
fever
bloods typically show an elevated white blood cell count associated with a lactic acidosis
If unsure which GI ischaemia = CT
If ischaemic colitis = X-Ray
Investigations
‘thumbprinting’ may be seen on abdominal x-ray due to mucosal oedema/haemorrhage
Mx: 1st = Supportive 2nd = Surgery
Indications for surgery = generalised peritonitis, perforation or ongoing haemorrhage
Ischaemic colitis is more likely to occur in ‘watershed’ areas such as the splenic flexure that are located at the borders of the territory supplied by the superior and inferior mesenteric arteries.
Small bowel obstruction
Adhesions (e.g. following previous surgery) are the most common cause of small bowel obstruction, followed by hernias.
Typically bilious vomiting
‘constipation’ with complete obstruction and lack of flatulence
Lower level obstruction = abdominal distension
Early bowel obstruction = ‘tinkling’ bowel sounds
Ix: 1st = Abdominal x-ray
Definitive = CT
Distended small bowel loops with fluid levels
considered dilated if small bowel is >3cm diameter
Mx = same as LBO;
Intial steps: NBM + IV fluids + NG tube
Some patients settle with conservative management but otherwise will require surgery
CT is the definitive investigation and is more sensitive, particularly in early obstruction
Chronic Pancreatitis
Ix: 1st = CT 2nd = faecal elastase
Mx = pancreatic enzyme supplements + analgesia
analgesia
Abdominal x-ray shows pancreatic calcification in 30% of cases
CT is more sensitive at detecting pancreatic calcification. Sensitivity is 80%, specificity is 85%
functional tests: may be used to assess exocrine function if imaging inconclusive
Ascites = the abnormal accumulation of fluid in the abdomen. I don’t understand the SAAG groupings yet.
Ascites causes are grouped by 11<(SAAG) <11 g/L.
SAAG>11 (trans - pushed through due to portal hypertension, proteins build up in capillaries) High pressure, forcing proteins out, high SAAG.
Liver disorders are the most common cause
cirrhosis/alcoholic liver disease
acute liver failure
liver metastases
Cardiac
right heart failure
constrictive pericarditis
Other causes
Budd-Chiari syndrome
portal vein thrombosis
veno-occlusive disease
myxoedema
SAAG<11 (exudative - causes holes in the capillaries so proteins leave, so serum albumin will be low) low pressure leaking from damage, low SAAG.
Hypoalbuminaemia
nephrotic syndrome
severe malnutrition (e.g. Kwashiorkor)
Malignancy
peritoneal carcinomatosis
Infections
tuberculous peritonitis
Other causes
pancreatitisis
bowel obstruction
biliary ascites
postoperative lymphatic leak
serositis in connective tissue diseases
Mx =
1. Reducing dietary sodium
- Fluid restriction is sometimes recommended if the sodium is < 125 mmol/L
- Aldosterone antagonists: e.g. spironolactone -> +loop diuretics are often added.
- Drainage if tense ascites (therapeutic abdominal paracentesis) + ‘Albumin cover’ + antibiotics (oral cip)
Albumin cover is to reduce the risk of paracentesis induced circulatory dysfunction can occur due to large volume paracentesis (> 5 litres). It is associated with a high rate of ascites recurrence, development of hepatorenal syndrome, dilutional hyponatraemia, and high mortality rate
prophylactic antibiotics to reduce the risk of spontaneous bacterial peritonitis. NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has resolved’
How do you assess an acute abdomen post-surgery?
CT abdo
Familial adenomatous polyposis
Mutation of APC gene (80%) cases, dominant Typically over 100 colonic adenomas
Cancer risk of 100%
20% are new mutations If known to be at risk then predictive genetic testing as teenager
Annual flexible sigmoidoscopy from 15 years
If no polyps found then 5 yearly colonoscopy started at age 20
Mx:
Polyps found = resectional surgery (resection and pouch Vs sub total colectomy and IRA)
Mesenteric adenitis = inflammed lymph nodes in the mesentery
Ix: post viral infection with RLQ pain (presents similar to appendicitis)
Mx = no treatment required
Hepatic encephelopathy
Features
confusion, altered GCS (see below)
asterix: ‘liver flap’, arrhythmic negative myoclonus with a frequency of 3-5 Hz
constructional apraxia: inability to draw a 5-pointed star
triphasic slow waves on EEG
raised ammonia level (not commonly measured anymore)
Grading of hepatic encephalopathy
Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma
Precipitating factors
infection e.g. spontaneous bacterial peritonitis
GI bleed
post transjugular intrahepatic portosystemic shunt
constipation
drugs: sedatives, diuretics
hypokalaemia
renal failure
increased dietary protein (uncommon)
Mx:
treat any underlying precipitating cause
NICE recommend lactulose first-line, with the addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy
lactulose is thought to work by promoting the excretion of ammonia and increasing the metabolism of ammonia by gut bacteria
antibiotics such as rifaximin are thought to modulate the gut flora resulting in decreased ammonia production
other options include embolisation of portosystemic shunts and liver transplantation in selected patients
Drugs which cause cholestasis? and cirrhosis?
Drugs which are known to cause cholestasis include:
can’t COPE-estasis
C lavulanic acid/Chlorpromazine
O estrogens
P enicillins
E rythromycin
Cirrhosis;
MAM
M ethotrexate
A miodarone
M ethyldopa
Laxative examples for;
Osmotic
Stimulant
Bulk-forming
Osmotic laxatives (used for LBO) work by retaining fluid within the bowel. Examples
include;
- Lactulose (a semi-synthetic dissacharide which produces an osmotic diarrhoea),
- Magnesium salts which are used when rapid bowel
evacuation is required, - Sodium salts and phosphate enemas which are also
used for rapid bowel evacuation.
stimulant laxatives which work by increasing
intestinal motility. Stimulant laxatives are not indicated in intestinal
obstruction and should not be used for a long duration of time as this may
give rise to colonic atony and hypokalaemia. Examples include;
- Senna and docusate sodium
- bisacodyl,
- glycerin suppositories
Bulking agents which
increase faecal mass resulting in an increase in peristalsis. They are usually
mixed with water before ingestion and are contraindicated in patients with
intestinal obstruction, faecal impaction and swallowing difficulty. Examples include;
- Ispaghula husk
- Methylcellulose
Causes of clubbing?
C: cardiac. subacute infective endocarditis. cyanotic heart disease. atrial myxoma
L: Lungs/Liver. lung abscess. empyema. Liver disease
U: ulcerative colitis.
B: biliary cirrhosis.
B: bronchogenic carcinoma (most commonly small cell)
I: idiopathic.
N: NOT COPD.
G: gastrointestinal malabsorption (e.g. coeliac disease) Crohn disease.
functional dyspepsia (indigestion)
Urgent and non urgent referral criteria?
mx?
Red flag features should be enquired about:
rectal bleeding
unexplained/unintentional weight loss
family history of bowel or ovarian cancer
onset after 60 years of age
Urgent
- All patients who’ve got dysphagia (painful swallowing)
- All patients who’ve got an upper abdominal mass consistent with stomach cancer
- Patients aged >= 55 years who’ve got weight loss, AND any of the following:
upper abdominal pain
reflux
dyspepsia
Non-urgent
- 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
Dyspepsia + reflag(weight loss) = urgent endoscopy referral
When treating dyspepsia, if either a PPI or ‘test and treat’ approach has failed then the other approach should be tried next (ie. after omeprazole doesn’t work, then investigate h.pylori urea breath test)
Variceal haemorrhage
Patients with liver cirrhosis are at risk of developing portal hypertension (increased portal venous system pressure). One of the most significant complications of portal hypertension is oesophageal varices.
These are at risk of rupturing leading to a potentially severe and life-threatening upper gastrointestinal bleed.
Mx:
Acute mx;
ABC
patients should be resuscitated prior to endoscopy
blood transfusion may be needed (if Hb <70g/L)
correct clotting: FFP, vitamin K, platelet transfusions may be required (if plt <30 * 109/L)
Both terlipressin and prophylactic IV antibiotics(quinolones) should be given before endoscopy in patients with suspected variceal haemorrhage
1st = Endoscopic variceal band ligation (EVL)
2nd = endoscopic sclerotherapy
3rd = sendstaken blakemore tube
4th = TIPSS*
Uncontrolled variceal haemorrhage = Sengstaken-Blakemore tube
EVL is 1st line once haemorrhaging is controlled
EVL should be performed at two-weekly intervals until all varices have been eradicated and PPI is given as cover to prevent ulceration
TIPSS is the definitive management once the pt is fit for surgery
Prophylaxis;
Propranolol then above 4 steps^
*Transjugular Intrahepatic Portosystemic Shunt commonly causes an exacerbation of hepatic encephalopathy
Transjugular Intrahepatic Portosystemic Shunt causes blood from the portal system to bypass the liver and enter the systemic circulation without the metabolism of nitrogenous waste products such as ammonia. As these build up in the systemic circulation, increased ammonia is able to cross the blood brain barrier resulting in hepatic encephalopathy
How to differentiate between B12 and iron deficiency based on sx?
B12 deficiency cause glossitis, but iron deficiency can be involved in;
Plummer Vinson syndrome, this is a triad of dysphagia (due to the oesophageal webs), glossitis and iron-deficiency anaemia (some definitions additionally include cheilitis in the syndrome).
Gallstone ileus Ix?
This describes small bowel obstruction secondary to an impacted gallstone.
It may develop if a fistula forms between a gangrenous gallbladder and the duodenum.
Abdominal pain, distension and vomiting are seen.
In gallstone ileus, a plain abdominal film classically shows small bowel obstruction and air in the biliary tree
Pernicious anaemia
PA is a disease of the stomach that results in vitamin B12 deficiency and macrocytic anaemia.
Intrinsic factor antibodies are highly specific but only present in 50-60% of cases. These are the main investigation
A positive result is diagnostic of PA but is not necessary for a diagnosis.
Gastric parietal cell antibodies, whilst highly sensitive for PA, have a low specificity and are not generally tested for.
Small bowel bacterial overgrowth syndrome (SBBOS) is a disorder characterised by excessive amounts of bacteria in the small bowel resulting in gastrointestinal symptoms
Risk factors for SBBOS;
neonates with congenital gastrointestinal abnormalities
scleroderma
diabetes mellitus
It should be noted that many of the features overlap with irritable bowel syndrome:
chronic diarrhoea
bloating, flatulence
abdominal pain
Ix = hydrogen breath test
small bowel aspiration and culture: this is used less often as invasive and results are often difficult to reproduce
clinicians may sometimes give a course of antibiotics as a diagnostic trial
Management
correction of the underlying disorder
antibiotic therapy: Rifaximin is now the treatment of choice due to relatively low resistance.
Co-amoxiclav or metronidazole are also effective in the majority of patients.