Gastro 2 Flashcards
Types o/f bariatric surgery
Primarily restrictive operations
laparoscopic-adjustable gastric banding (LAGB)
it is normally the first-line intervention in patients with a BMI of 30-39kg/m^2
produces less weight loss than malabsorptive or mixed procedures but as it has fewer complications
sleeve gastrectomy
stomach is reduced to about 15% of its original size
intragastric balloon
the balloon can be left in the stomach for a maximum of 6 months
Primarily malabsorptive operations
biliopancreatic diversion with duodenal switch
usually reserved for very obese patients (e.g. BMI > 60 kg/m^2)
Mixed operations
Roux-en-Y gastric bypass surgery
is both restrictive and malabsorptive in action
What is the urea breath test?
patients consume a drink containing carbon isotope 13 (13C) enriched urea
urea is broken down by H. pylori urease
after 30 mins patient exhale into a glass tube
mass spectrometry analysis calculates the amount of 13C CO2
should not be performed within 4 weeks of treatment with an antibacterial or within 2 weeks of an antisecretory drug (e.g. a proton pump inhibitor)
sensitivity 95-98%, specificity 97-98%
may be used to check for H. pylori eradication
What is the CLO test?
Rapid urease test (e.g. CLO test)
biopsy sample is mixed with urea and pH indicator
colour change if H pylori urease activity
sensitivity 90-95%, specificity 95-98%
what is haemochromatosis?
Haemochromatosis is an autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation. It is caused by the inheritance of mutations in the HFE gene on both copies of chromosome 6.
How is Haemochromatosis investigated?
There is continued debate about the best investigation to screen for haemochromatosis.
general population
transferrin saturation is considered the most useful marker
ferritin should also be measured but is not usually abnormal in the early stages of iron accumulation
testing family members
genetic testing for HFE mutation
These guidelines may change as HFE gene analysis become less expensive
Typical iron study profile in patient with haemochromatosis
transferrin saturation > 55% in men or > 50% in women
raised ferritin (e.g. > 500 ug/l) and iron
low TIBC
Further tests - LFTs, MRI, liver biopsy
How is haemacromatosis managed?
venesection is the first-line treatment
monitoring adequacy of venesection: transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l
desferrioxamine may be used second-line
Investigations for pancreatic cancer?
ultrasound has a sensitivity of around 60-90%
high-resolution CT scanning is the investigation of choice if the diagnosis is suspected
imaging may demonstrate the ‘double duct’ sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts
features of pancreatic cancer?
painless jaundice
pale stools, dark urine, pruritus
cholestatic liver function tests
the following abdominal masses may be found (in decreasing order of frequency)
hepatomegaly: due to metastases
gallbladder: Courvoisier’s law states that in the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones
epigastric mass: from the primary tumour
many patients present in a non-specific way with anorexia, weight loss, epigastric pain
loss of exocrine function (e.g. steatorrhoea)
loss of endocrine function (e.g. diabetes mellitus)
atypical back pain is often seen
migratory thrombophlebitis (Trousseau sign) is more common than with other cancers
what is Zollinger-Ellison syndrome?
Zollinger-Ellison syndrome is a condition characterised by excessive levels of gastrin secondary to a gastrin-secreting tumour. The majority of these tumours are found in the first part of the duodenum, with the second most common location being the pancreas.
Around 30% of gastrinomas occur as part of MEN type I syndrome.
what are the features of Zollinger Ellison syndrome?
And how is it diagnosed?
Features
multiple gastroduodenal ulcers
diarrhoea
malabsorption
Diagnosis
fasting gastrin levels: the single best screen test
secretin stimulation test
How do you diagnose bile acid malabsorption
the test of choice is SeHCAT
nuclear medicine test using a gamma-emitting selenium molecule in selenium homocholic acid taurine or tauroselcholic acid (SeHCAT)
scans are done 7 days apart to assess the retention/loss of radiolabelled 75SeHCAT
how is bile acid malabsorption managed?
bile acid sequestrants e.g. cholestyramine
Prophylaxsis against variceal haemorrhage?
Propranolol - reduced rebreeding and mortality - non selective beta blocker which decreases portal venous pressure by reducing cardiac output and splanchnic blood flow
Endoscopic variceal band ligation (superior to endoscopic sclerotherapy)
Offer endoscopic variceal band ligation for the primary prevention of bleeding for people with cirrhosis who have medium to large oesophageal varices.’
it should be performed at two-weekly intervals until all varices have been eradicated
proton pump inhibitor cover is given to prevent EVL-induced ulceration
Transjugular Intrahepatic Portosystemic Shunt (TIPSS) may be used if the above measures are unsuccessful in preventing further episodes
what are the causes of Budd-Chiari syndrome?
polycythaemia rubra vera
thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies
pregnancy
combined oral contraceptive pill: accounts for around 20% of cases
features of Budd chairi syndrome?
The features are classically a triad of:
abdominal pain: sudden onset, severe
ascites → abdominal distension
tender hepatomegaly
what is Budd chair syndrome?
Budd-Chiari syndrome, or hepatic vein thrombosis, is usually seen in the context of underlying haematological disease or another procoagulant condition.
investigations for Budd Chiari syndrome?
ultrasound with Doppler flow studies is very sensitive and should be the initial radiological investigation
what happens in referring syndrome?
hypophosphataemia
this is the hallmark symptom of refeeding syndrome
may result in significant muscle weakness, including myocardial muscle (→ cardiac failure) and the diaphragm (→ respiratory failure)
hypokalaemia
hypomagnesaemia: may predispose to torsades de pointes
abnormal fluid balance
what is the pathophysiology of hypophosphataemia in referring syndrome?
Shift from Fat to Carbohydrate Metabolism: In refeeding syndrome, the reintroduction of carbohydrates leads to a shift from fat to carbohydrate metabolism. This switch activates insulin secretion, which in turn increases cellular uptake of glucose.
Intracellular Movement of Phosphate: Insulin and increased glucose uptake stimulate the intracellular movement of phosphate, which is used in the synthesis of ATP and 2,3-diphosphoglycerate in erythrocytes. This intracellular shift reduces serum phosphate levels.
Decreased Phosphate Stores: Patients with chronic malnutrition often have depleted phosphate stores, although their serum phosphate levels may initially be normal. When refeeding starts, the sudden demand for phosphate in anabolic processes exceeds the supply, leading to hypophosphatemia.
clinical consequences of hypophphopshataemia in referring syndrome?
Cardiac Dysfunction: Hypophosphatemia can impair myocardial contractility, leading to heart failure. It may also cause arrhythmias due to its role in maintaining normal cellular electrophysiology.
Respiratory Failure: Phosphate is essential for ATP production, necessary for respiratory muscle function. Severe hypophosphatemia can lead to muscle weakness, including the diaphragm and intercostal muscles, potentially resulting in acute respiratory failure.
Neurological Complications: These can range from confusion and seizures to coma, attributable to disturbed ATP metabolism in the central nervous system.
Haematological Effects: Reduced 2,3-diphosphoglycerate levels in erythrocytes affect oxygen release from haemoglobin, leading to tissue hypoxia. Hypophosphatemia can also result in hemolysis.
Rhabdomyolysis: Phosphate depletion impairs ATP production in muscles, which can lead to muscle breakdown and rhabdomyolysis.
how is familial adenomatous polyposis inherited?
Familial adenomatous polyposis (FAP) is an autosomal dominant disorder
what is ischaemic colitis?
Ischaemic colitis describes an acute but transient compromise in the blood flow to the large bowel. This may lead to inflammation, ulceration and haemorrhage.
what sit is most commonly affected in ischaemic colitis?
It 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.
what would an XR show in ischaemic colitis?
‘thumbprinting’ may be seen on abdominal x-ray due to mucosal oedema/haemorrhage
What is Wilson’s disease and how is is inherited?
Wilson’s disease is an autosomal recessive disorder characterised by excessive copper deposition in the tissues. Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion.
where is the gene defect located in Wilsons disease?
Wilson’s disease is caused by a defect in the ATP7B gene located on chromosome 13.
Features of Wilsons disease?
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
green-brown rings in the periphery of the iris
due to copper accumulation in Descemet membrane
present in around 50% of patients with isolated hepatic Wilson’s disease and 90% who have neurological involvement
renal tubular acidosis (esp. Fanconi syndrome)
haemolysis
blue nails
Investigations for Wilsons disease?
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
the diagnosis is confirmed by genetic analysis of the ATP7B gene
Management of Wilsons disease?
penicillamine (chelates copper) has been the traditional first-line treatment
trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future
tetrathiomolybdate is a newer agent that is currently under investigation
hepatitis B in pregnant?
Who should be offered screening?
Treatment of babies born to mothers with hep B?
Can it be transmitted via breastfeeding?
all pregnant women are offered screening for hepatitis B
babies born to mothers who are chronically infected with hepatitis B or to mothers who’ve had acute hepatitis B during pregnancy should receive a complete course of vaccination + hepatitis B immunoglobulin
studies are currently evaluating the role of oral antiviral treatment (e.g. Lamivudine) in the latter part of pregnancy
there is little evidence to suggest caesarean section reduces vertical transmission rates
hepatitis B cannot be transmitted via breastfeeding (in contrast to HIV)
what is SBP and what are the features?
Spontaneous bacterial peritonitis (SBP) is a form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis.
Features
ascites
abdominal pain
fever
how do you diagnose SBP?
Diagnosis
paracentesis: neutrophil count > 250 cells/ul
the most common organism found on ascitic fluid culture is E. coli
Management of SBP?
intravenous cefotaxime is usually given
when should abx prophylaxis be given in SBP?
cpatients who have had an episode of SBP
patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
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’
HIV - common biliary and pancreatic disease?
The most common cause of biliary disease in patients with HIV is sclerosing cholangitis due to infections such as CMV, Cryptosporidium and Microsporidia
Pancreatitis in the context of HIV infection may be secondary to anti-retroviral treatment (especially didanosine) or by opportunistic infections e.g. CMV
risk factors for gastric cancer?
Risk factors
Helicobacer pylori
triggers inflammation of the mucosa → atrophy and intestinal metaplasia → dysplasia
pernicious anaemia, atrophic gastritis
diet
salt and salt-preserved foods
nitrates
ethnicity: Japan, China
smoking
blood group A
features of gastric cancer?
abdo pain
dyspepsia
weight loss
N&V
dysphagia
GI bleeding
if lymphatic spread:
left supraclavicular lymph node (Virchow’s node)
periumbilical nodule (Sister Mary Joseph’s node)
what is seen on biopsy of gastric cancer?
signet ring cells may be seen in gastric cancer. They contain a large vacuole of mucin which displaces the nucleus to one side. Higher numbers of signet ring cells are associated with a worse prognosis
what is Barrett’s oesophagus?
Barrett’s refers to the metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium. There is an increased risk of oesophageal adenocarcinoma, estimated at 50-100 fold.
what are the histological features of Barrett’s?
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)
what are the risk factors for Barret’s?
gastro-oesophageal reflux disease (GORD) is the single strongest risk factor
male gender (7:1 ratio)
smoking
central obesity
How is Barret’s managed?
High dose PPI
Endoscopic surveillance with biopsy
If dysplasia of any grade is identified endoscopic intervention is offered. Options include:
radiofrequency ablation: preferred first-line treatment, particularly for low-grade dysplasia
endoscopic mucosal resection
investigations for chronic pancreatitis?
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: faecal elastase may be used to assess exocrine function if imaging inconclusive
who requires screening for hepatocellular carcinoma?
patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis
men with liver cirrhosis secondary to alcohol
what is the management of variceal bleeding?
terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy)
band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices
transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures
what is primary biliary cholagnitis?
> chronic liver disorder
middle aged females
Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis which may eventually progress to cirrhosis. The classic presentation is itching in a middle-aged woman
associations with primary Biliary cholagitis?
Sjogren’s syndrome (seen in up to 80% of patients)
rheumatoid arthritis
systemic sclerosis
thyroid disease
clinical features with primary Biliary cholangitis?
early: may be asymptomatic (e.g. raised ALP on routine LFTs) or fatigue, pruritus
cholestatic jaundice
hyperpigmentation, especially over pressure points
around 10% of patients have right upper quadrant pain
xanthelasmas, xanthomata
also: clubbing, hepatosplenomegaly
late: may progress to liver failure
how is primary biliary cholangitis diagnosed?
AMA - 98% of patients
SMA
raised IgM
MRCP
management of primary biliary cholangitis ?
ursodeoxycholic acid
pruritus: cholestyramine
fat-soluble vitamin supplementation
liver transplantation
e.g. if bilirubin > 100 (PBC is a major indication)
recurrence in graft can occur but is not usually a problem
complications of primary biliary cholangitis?
cirrhosis → portal hypertension → ascites, variceal haemorrhage
osteomalacia and osteoporosis
significantly increased risk of hepatocellular carcinoma (20-fold increased risk)
what biologic therapy can be used in C.dfff?
bezlotoxumab is a monoclonal antibody which targets C. difficile toxin B
What is Villous adenoma?
Villous adenomas are colonic polyps with the potential for malignant transformation. They characteristically secrete large amounts of mucous, potentially resulting in electrolyte disturbances.
what are the features of villous adenoma?
The vast majority are asymptomatic. Possible features:
non-specific lower gastrointestinal symptoms
secretory diarrhoea may occur
microcytic anaemia
hypokalaemia
What causes ascending cholangitis?
Ascending cholangitis is a bacterial infection (typically E. coli) of the biliary tree. The most common predisposing factor is gallstones.
what are the features of ascending cholangitis?
Charcot’s triad of right upper quadrant (RUQ) pain, fever and jaundice occurs in about 20-50% of patients
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)
investigations for ascending cholangitis?
ultrasound is generally used first-line in suspected cases to look for bile duct dilation and bile duct stones
management of ascending ascending cholangitis?
intravenous antibiotics
endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve any obstruction
How is C.diff spread?
spreads via the faecal-oral route by ingestion of spores
What is Cholestyramine?
Cholestyramine is a bile acid sequestrant used in the management of hyperlipidaemia. It decreases bile acid reabsorption in the small intestine, therefore upregulating the amount of cholesterol that is converted to bile acid. The main effect it has on the lipid profile is to reduce LDL cholesterol. It is also occasionally used in Crohn’s disease for treatment diarrhoea following bowel resection.
what is ocreotide used for?
Overview
long-acting analogue of somatostatin
somatostatin is released from D cells of pancreas and inhibits the release of growth hormone, glucagon and insulin
Uses
acute treatment of variceal haemorrhage
acromegaly
carcinoid syndrome
prevent complications following pancreatic surgery
VIPomas
refractory diarrhoea
what is steatosis and what is steatohepatitis?
steatosis - fat in the liver
steatohepatitis - fat with inflammation, non-alcoholic steatohepatitis (NASH), see below
progressive disease may cause fibrosis and liver cirrhosis
what is NAFLD?
NAFLD is thought to represent the hepatic manifestation of the metabolic syndrome and hence insulin resistance is thought to be the key mechanism leading to steatosis.
what is NASH?
Non-alcoholic steatohepatitis (NASH) is a term used to describe liver changes similar to those seen in alcoholic hepatitis in the absence of a history of alcohol abuse. It is relatively common and thought to affect around 3-4% of the general population.
what is associated with NAFLD?
obesity
type 2 diabetes mellitus
hyperlipidaemia
jejunoileal bypass
sudden weight loss/starvation
COntraindications of liver biopsy?
deranged clotting (e.g. INR > 1.4)
low platelets (e.g. < 60 * 109/l)
anaemia
extrahepatic biliary obstruction
hydatid cyst
haemoangioma
uncooperative patient
ascites
What symptoms should be present for at least 6 months to consider a diagnosis of IBS?
Abdominal pain, and/or bloating, and/or change in bowel habit
These symptoms are essential for the initial consideration of IBS.
What is required for a positive diagnosis of IBS?
Abdominal pain relieved by defecation or associated with altered bowel frequency/stool form, plus 2 of the following:
* altered stool passage (straining, urgency, incomplete evacuation)
* abdominal bloating, distension, tension or hardness
* symptoms made worse by eating
* passage of mucus
These criteria help differentiate IBS from other gastrointestinal disorders.
What additional features may support the diagnosis of IBS?
Lethargy, nausea, backache, and bladder symptoms
While not definitive, these features can provide supportive evidence for IBS.
What are the red flag features to inquire about in a potential IBS diagnosis?
Red flag features include:
* rectal bleeding
* unexplained/unintentional weight loss
* family history of bowel or ovarian cancer
* onset after 60 years of age
These features may indicate a more serious underlying condition.
What primary care investigations are suggested for IBS?
Suggested investigations include:
* full blood count
* ESR/CRP
* coeliac disease screen (tissue transglutaminase antibodies)
These tests help rule out other conditions that may mimic IBS symptoms.
What kind of bacteria is C.diff?
anaerobic gram-positive, spore-forming, toxin-producing bacillus
Risk factors for gastric cancer?
Helicobacer pylori
triggers inflammation of the mucosa → atrophy and intestinal metaplasia → dysplasia
pernicious anaemia, atrophic gastritis
diet
salt and salt-preserved foods
nitrates
ethnicity: Japan, China
smoking
blood group A
what is the most common type of gastric cancer?
Gastric adenocarcinoma, the most prevalent type of gastric cancer, arises from the glandular epithelium of the stomach lining.
Features of gastric cancer?
abdominal pain
typically vague, epigastric pain
may present as dyspepsia
weight loss and anorexia
nausea and vomiting
dysphagia: particularly if the cancer arises in the proximal stomach
overt upper gastrointestinal bleeding is seen only in a minority of patients
if lymphatic spread:
left supraclavicular lymph node (Virchow’s node)
periumbilical nodule (Sister Mary Joseph’s node)
what is the pathophsyiology of hepatorenal syndrome?
The most accepted theory regarding the pathophysiology of HRS is that vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance. This results in ‘underfilling’ of the kidneys. This is sensed by the juxtaglomerular apparatus which then activates the renin-angiotensin-aldosterone system, causing renal vasoconstriction which is not enough to counterbalance the effects of the splanchnic vasodilation.
What are the two categories of hepatorenal syndrome?
Type 1 HRS
Rapidly progressive
Doubling of serum creatinine to > 221 µmol/L or a halving of the creatinine clearance to less than 20 ml/min over a period of less than 2 weeks
Very poor prognosis
T2 HRS
Slowly progressive
Prognosis poor, but patients may live for longer
Management of hepatorenal syndrome?
vasopressin analogues, for example terlipressin, have a growing evidence base supporting their use. They work by causing vasoconstriction of the splanchnic circulation
volume expansion with 20% albumin
transjugular intrahepatic portosystemic shunt
what is acute mesenteric ischaemia?
Acute mesenteric ischaemia is typically caused by an embolism resulting in occlusion of an artery which supplies the small bowel, for example the superior mesenteric artery. Classically patients have a history of atrial fibrillation.
The abdominal pain is typically severe, of sudden onset and out-of-keeping with physical exam findings.
Management
urgent surgery is usually required
poor prognosis, especially if surgery delayed
what is chronic mesenteric ischaemia?
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.
What are the diffent types of oesophageal cancer?
Until recent times oesophageal cancer was most commonly due to a squamous cell carcinoma but the incidence of adenocarcinoma is rising rapidly. Adenocarcinoma is now the most common type of oesophageal cancer and is more likely to develop in patients with a history of gastro-oesophageal reflux disease (GORD) or Barrett’s.
Features of oesophageal cancer?
dysphagia: the most common presenting symptom
anorexia and weight loss
vomiting
other possible features include: odynophagia, hoarseness, melaena, cough
How is oesophageal cancer diagnosed?
Upper GI endoscopy with biopsy is used for diagnosis
Endoscopic ultrasound is the preferred method for locoregional staging
CT scanning of the chest, abdomen and pelvis is used for initial staging
FDG-PET CT may be used for detecting occult metastases if metastases are not seen on the initial staging CT scans.
Laparoscopy is sometimes performed to detect occult peritoneal disease
How is oesophageal cancer managed?
Operable disease (T1N0M0) is best managed by surgical resection - the most common procedure is an Ivor-Lewis type oesophagectomy
The biggest surgical challenge is that of anastomotic leak, with an intrathoracic anastomosis resulting in mediastinitis
In addition to surgical resection many patients will be treated with adjuvant chemotherapy
what is carcinoid syndrome?
usually occurs when metastases are present in the liver and release serotonin into the systemic circulation
may also occur with lung carcinoid as mediators are not ‘cleared’ by the liver
Features of carcinoid syndrome?
flushing (often the earliest symptom)
diarrhoea
bronchospasm
hypotension
right heart valvular stenosis (left heart can be affected in bronchial carcinoid)
other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing’s syndrome
pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tumour
Investigations for carcinoid syndrome?
urinary 5-HIAA
plasma chromogranin A y
Management of carcinoid syndrome?
somatostatin analogues e.g. octreotide
diarrhoea: cyproheptadine may help
what is Gilbert’s syndrome?
Gilbert’s syndrome is an autosomal recessive* condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase. The prevalence is approximately 1-2% in the general population.
Features of Gilbert’s ?
unconjugated hyperbilirubinaemia (i.e. not in urine)
jaundice may only be seen during an intercurrent illness, exercise or fasting
Investigations in Gilbert’s?
rise in bilirubin following prolonged fasting or IV nicotinic acid
what are threadworms?
Infestation with threadworms (Enterobius vermicularis, sometimes called pinworms) is extremely common amongst children in the UK. Infestation occurs after swallowing eggs that are present in the environment.
Features of threadworms?
Threadworm infestation is asymptomatic in around 90% of cases, possible features include:
perianal itching, particularly at night
girls may have vulval symptoms
Diagnosis of threadworms?
Diagnosis may be made by the applying Sellotape to the perianal area and sending it to the laboratory for microscopy to see the eggs. However, most patients are treated empirically and this approach is supported in the CKS guidelines.
Managment of threadworms?
CKS recommend a combination of anthelmintic with hygiene measures for all members of the household
mebendazole is used first-line for children > 6 months old. A single dose is given unless infestation persists
NICE bariatric referral cut-offs
with risk factors (T2DM, BP etc): > 35 kg/m^2
no risk factors: > 40 kg/m^2
