Gastro 3 Flashcards

1
Q

Who is FIT screen offered to?

A

the NHS now has a national screening programme offering screening every 2 years to all men and women aged 60 to 74 years in England, 50 to 74 years in Scotland. Patients aged over 74 years may request screening

a type of faecal occult blood (FOB) test which uses antibodies that specifically recognise human haemoglobin (Hb)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Outcomes of colonoscopy following FIT screening?

A

5 out of 10 patients will have a normal exam
4 out of 10 patients will be found to have polyps which may be removed due to their premalignant potential
1 out of 10 patients will be found to have cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Clincial features of acute upper GI bleeeding?

A

Haematemesis
coffee gorund vomit
Melena
raised urea

features associated with a particular diagnosis e,g,
oesophageal varices: stigmata of chronic liver disease
peptic ulcer disease: abdominal pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Oesophageal causes for UGIB?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Gastric causes of upper GI Bleed?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Duodenal causes of upper GI bleed?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Risk assessment in UGIB?

A

the Glasgow-Blatchford score at first assessment
helps clinicians decide whether patients can be managed as outpatients or not
the Rockall score is used after endoscopy
provides a percentage risk of rebleeding and mortality
includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Management of upper GI bleed?

A

Reusciation - A-E
IV access
Endoscopy -if svere bleed immediately after resusitation, all other patients within 24 hours

Management of non-variceal bleeding
NICE do not recommend the use of proton pump inhibitors (PPIs) before endoscopy to patients with suspected variceal upper gastrointestinal bleeding although PPIs should be given to patients with non-variceal upper gastrointestinal bleeding and stigmata of recent haemorrhage shown at endoscopy
if further bleeding then options include repeat endoscopy, interventional radiology and surgery

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

platelet transfusion if actively bleeding platelet count of less than 50 x 10*9/litre
fresh frozen plasma to patients who have either a fibrinogen level of less than 1 g/litre, or a prothrombin time (international normalised ratio) or activated partial thromboplastin time greater than 1.5 times normal
prothrombin complex concentrate to patients who are taking warfarin and actively bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

management of Upper GI bleed when endoscoic magement has failed?

A

Refer to surgeons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

causes of threadworms?

A

Enterobius vermicularis,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Symptoms of thread worms?

A

perianal itching, particularly at night
girls may have vulval symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Management of threadworms?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

causes of dysphagia?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Drug indiced liver disease
causes of hepatocellular picture?

A

paracetamol
sodium valproate, phenytoin
MAOIs
halothane
anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
statins
alcohol
amiodarone
methyldopa
nitrofurantoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Drug indiced liver disease
causes of cholestasis picture?

A

combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates
rare reported causes: nifedipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

causes of drug induced liver cirrhosis?

A

methotrexate
methyldopa
amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is microscopic colitis?

A

Microscopic colitis is a chronic inflammatory condition of the gut. It is approximately as common as the ‘classic’ inflammatory bowel diseases (ulcerative colitis and Crohn’s disease) and is considered a separate entity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

causes of microscopic colitis?

A

smoking
drugs: NSAIDs, PPIs and SSRIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the two types of microscopic colitis?

A

Collagenous colitis (CC)
Lymphocytic colitis (LC)

For both types of MC, there is an increased number of intraepithelial and lamina propria lymphocytes seen on microscopy. In CC specifically, there is a thickened subepithelial collagen band.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Features of microscopic colitis?

A

Diarrhoea (watery, non-bloody)
Abdominal pain
Faecal urgency and incontinence
Bloating and flatulence
weight loss
noctural diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Extraintestinal manifestations of microscopic collitis?

A

Joint pain: Arthralgia or arthritis may occur in patients with microscopic colitis, particularly in those with underlying autoimmune disorders.
Dermatological manifestations: Skin conditions such as erythema nodosum and pyoderma gangrenosum have been reported in association with microscopic colitis.
Autoimmune diseases: There is an increased prevalence of concomitant autoimmune disorders including celiac disease, thyroid dysfunction, rheumatoid arthritis, and type 1 diabetes mellitus among patients with microscopic colitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Investigations for microscopic colitis?

A

Guidelines written by the British Society for Gastroenterology advise that when microscopic colitis is suspected, patients should be referred for colonoscopy even before assessing faecal calprotectin levels.

Microscopic colitis can only be diagnosed by histology examination of biopsied tissue taken during colonoscopy. Macroscopic changes are not usually seen unlike in other types of IBD. The characteristic microscopic findings are:
Lymphocytic colitis: increased number of intraepithelial and lamina propria lymphocytes (>20 per 100 cells)
Collagenous colitis: as above, along with a thickened collagenous band in the subepithelial layer (>10µm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Management of microscopic colitis?

A

Lifestyle factors that can exacerbate MC should first be addressed. These include:
Stopping smoking, Stopping medications such as NSAIDs, PPIs and SSRIs where possible
Decreasing caffeine intake, Decreasing dairy intake (in patients with lactose intolerance)
Decreasing alcohol consumption

if lifestyle fails
mid cases - trial of loperamide

Budenoside - shown to be effective in the induction and maintenance of remission. A typical dosage is 9mg daily for 8 weeks and the medication then stopped to assess response. If symptoms recur, then re-initiation of budesonide may be necessary.

In patients who do not respond to budesonide, other medications that may be tried include immunomodulators (e.g. azathioprine) and biologics (e.g. anti-TNF-alpha drugs).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

mechanism of action of PPI?

A

Proton pump inhibitors (PPI) cause irreversible blockade of H+/K+ ATPase of the gastric parietal cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

adverse effects of PPI?

A

hyponatraemia, hypomagnasaemia
osteoporosis → increased risk of fractures
microscopic colitis
increased risk of C. difficile infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is intrahepatic cholestasis of pregnancy?

A

A liver disease occurring in around 1% of pregnancies, typically in the third trimester.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the common features of intrahepatic cholestasis of pregnancy?

A
  • Pruritus, often in the palms and soles
  • No rash (skin changes may be present due to scratching)
  • Raised bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the primary management for intrahepatic cholestasis of pregnancy?

A
  • Ursodeoxycholic acid for symptomatic relief
  • Weekly liver function tests
  • Induction at 37 weeks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is a significant complication of intrahepatic cholestasis of pregnancy?

A

Increased rate of stillbirth.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Is intrahepatic cholestasis of pregnancy associated with increased maternal morbidity?

A

No, it is not generally associated with increased maternal morbidity.

31
Q

What is acute fatty liver of pregnancy?

A

A rare complication that may occur in the third trimester or immediately after delivery.

32
Q

What are the features of acute fatty liver of pregnancy?

A
  • Abdominal pain
  • Nausea & vomiting
  • Headache
  • Jaundice
  • Hypoglycaemia
  • Severe disease may result in pre-eclampsia
33
Q

What laboratory finding is typically elevated in acute fatty liver of pregnancy?

A

ALT is typically elevated, e.g., 500 u/l.

34
Q

What is the management approach for acute fatty liver of pregnancy?

A

Support care and delivery once stabilized.

35
Q

What syndromes may be exacerbated during pregnancy?

A

Gilbert’s and Dubin-Johnson syndrome.

36
Q

What does HELLP stand for?

A

Haemolysis, Elevated Liver enzymes, Low Platelets.

37
Q

What is Whipple’s disease?

A

Whipple’s disease is a rare multi-system disorder caused by Tropheryma whippelii infection. It is more common in those who are HLA-B27 positive and in middle-aged men.

38
Q

Features of Whipple’s disease?

A

malabsorption: diarrhoea, weight loss
large-joint arthralgia
lymphadenopathy
skin: hyperpigmentation and photosensitivity
pleurisy, pericarditis
neurological symptoms (rare): ophthalmoplegia, dementia, seizures, ataxia, myoclonus

39
Q

Inestigations for Whipples disease?

A

jejunal biopsy shows deposition of macrophages containing Periodic acid-Schiff (PAS) granules

40
Q

Managment of Whipple’s disease?

A

guidelines vary: oral co-trimoxazole for a year is thought to have the lowest relapse rate, sometimes preceded by a course of IV penicillin

41
Q

What is Peutz Jeghers syndrome?

A

Peutz-Jeghers syndrome is an autosomal dominant condition characterised by numerous hamartomatous polyps in the gastrointestinal tract. It is also associated with pigmented freckles on the lips, face, palms and soles. Although the polyps themselves don’t have malignant potential, around 50% of patients will have died from another gastrointestinal tract cancer by the age of 60 years.

42
Q

genetics in Peutz jeghers syndrome?

A

autosomal dominant
responsible gene encodes serine threonine kinase LKB1 or STK11

43
Q

Features of Peutz Jeghers syndrome?

A

hamartomatous polyps in the gastronintestinal tract (mainly small bowel)
small bowel obstruction is a common presenting complaint, often due to intussusception
gastrointestinal bleeding
pigmented lesions on lips, oral mucosa, face, palms and soles

44
Q

what is Pseudomembranous colitis?

A

This condition is characterised by the presence of multiple white plaques or pseudomembranes on the gastrointestinal mucosa, typically as a result of overgrowth of the bacterium Clostridium difficile following antibiotic use.

45
Q

what are the two types of oesophageal cancer?

A

The majority of adenocarcinomas are located near the gastroesophageal junction whereas squamous cell tumours are most commonly found in the upper two-thirds of the oesophagus.

46
Q

Features of oesophageal cancer?

A

dysphagia: the most common presenting symptom
anorexia and weight loss
vomiting
other possible features include: odynophagia, hoarseness, melaena, cough

47
Q

How is oesophageal cancer diagnosed?

A

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

48
Q

why does TIPs procedure lead to increased risk of hepatic encephalopethy?

A

The hepatic vein is cannulated percutaneously via the internal jugular vein, using a needle under radiological guidance. A connection is created and a stent is inserted through the liver from the hepatic to the portal vein, thereby reducing portal pressure and reducing the risk of a bleed. Encephalopathy is found in up to 25% of cases as blood normally detoxified in the liver, now bypasses this stage and toxins are delivered in greater quantity to the cerebral circulation.

49
Q

Features of NAFLD?

A

usually asymptomatic
hepatomegaly
ALT is typically greater than AST
increased echogenicity on ultrasound

50
Q

Pathophysiology - H.pylori?

A

Helicobacter pylori has 2 main mechanisms to survice in the acidic gastric environment:
chemotaxis away from low pH areas, using its flagella to burrow into the mucous lining to reach the epithelial cells underneath
secretes urease → urea converted to NH3 → alkalinization of acidic environment → increased bacterial survival
pathogenesis mechanism:
Helicobacter pylori releases bacterial cytotoxins (e.g. CagA toxin) → disruption of gastric mucosa

51
Q

what is assoicated with H.pylori?

A

peptic ulcer disease
95% of duodenal ulcers
75% of gastric ulcers
gastric cancer
B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
atrophic gastritis

The role of H pylori in Gastro-oesophageal reflux disease (GORD) is unclear - there is currently no role in GORD for the eradication of H pylori

52
Q

Managament of H.pyloir?

A

eradication may be achieved with a 7-day course of
a proton pump inhibitor + amoxicillin + (clarithromycin OR metronidazole)
if penicillin-allergic: a proton pump inhibitor + metronidazole + clarithromycin

53
Q

Primary biliary cholangitis - the M rule

A

IgM
anti-Mitochondrial antibodies, M2 subtype
Middle aged females

54
Q

Serology testing in coeliac?

A

tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE
endomyseal antibody (IgA)
needed to look for selective IgA deficiency, which would give a false negative coeliac result
anti-gliadin antibody (IgA or IgG) tests are not recommended by NICE
anti-casein antibodies are also found in some patients

55
Q

Biopsy findings in coeliac?

A

the ‘gold standard’ for diagnosis - this should be performed in all patients with suspected coeliac disease to confirm or exclude the diagnosis
traditionally done in the duodenum but jejunal biopsies are also sometimes performed
findings supportive of coeliac disease:
villous atrophy
crypt hyperplasia
increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes

56
Q

side effects of sulphasalazine?

A

many side-effects are due to the sulphapyridine moiety: rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, lung fibrosis
other side-effects are common to 5-ASA drugs (see mesalazine)

57
Q

side effects of mesealazine?

A

ulphapyridine side-effects seen in patients taking sulphasalazine are avoided
mesalazine is still however associated with side-effects such as GI upset, headache, agranulocytosis, pancreatitis*, interstitial nephritis

*pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine

58
Q

most common causes of HCC?

A

Hepatocellular carcinoma
hepatitis B most common cause worldwide
hepatitis C most common cause in Europe

59
Q

Management of pyogenic liver abscess?

A

drainage (typically percutaneous) and antibiotics
amoxicillin + ciprofloxacin + metronidazole
if penicillin allergic: ciprofloxacin + clindamycin

60
Q

What is the most appropriate test for post eradication therapy for hypyloria?

A

the only recommended test for H. pylori post-eradication therapy, is urea breath test. The others are either too invasive, remain positive, or are not sensitive and specific enough.

61
Q

Indicators of severe pancreatitis?

A

age > 55 years
hypocalcaemia
hyperglycaemia
hypoxia
neutrophilia
elevated LDH and AST

62
Q

what is plummer vinson syndrome?

A

Triad of:
dysphagia (secondary to oesophageal webs)
glossitis
iron-deficiency anaemia

Treatment includes iron supplementation and dilation of the webs

63
Q

What are the causes of increased ferritin?

A

We can split the causes of increased ferritin levels into 2 distinct categories
The best test to see whether iron overload is present is transferrin saturation. Typically, normal values of < 45% in females and < 50% in males exclude iron overload.

64
Q

Management of IBS?

A

First-line pharmacological treatment - according to predominant symptom
pain: antispasmodic agents
constipation: laxatives but avoid lactulose
diarrhoea: loperamide is first-line

Second-line pharmacological treatment
low-dose tricyclic antidepressants (e.g. amitriptyline 5-10 mg) are used in preference to selective serotonin reuptake inhibitors

psychological interventions - if symptoms do not respond to pharmacological treatments after 12 months and who develop a continuing symptom profile (refractory IBS), consider referring for cognitive behavioural therapy, hypnotherapy or psychological therapy

65
Q

Dietary advice in IBS?

A

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).

66
Q

Associations of pancreatic cancer?

A

increasing age
smoking
diabetes
chronic pancreatitis (alcohol does not appear an independent risk factor though)
hereditary non-polyposis colorectal carcinoma
multiple endocrine neoplasia
BRCA2 gene
KRAS gene mutation

67
Q

Features of pancreatic cancer?

A

classically painless jaundice
pale stools, dark urine, and 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

68
Q

Investigations for pancreatic cancer?

A

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

69
Q

Management for pancreatic cancer?

A

less than 20% are suitable for surgery at diagnosis
a Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas. Side-effects of a Whipple’s include dumping syndrome and peptic ulcer disease
adjuvant chemotherapy is usually given following surgery
ERCP with stenting is often used for palliation

70
Q

what test can be used to check for H.pylor eradication?

A

Urea breath test

71
Q

What is Achalasia?

A

Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus i.e. LOS contracted, oesophagus above dilated. Achalasia typically presents in middle-age and is equally common in men and women.

72
Q

Clinical features of Achalsia?

A

dysphagia of BOTH liquids and solids
typically variation in severity of symptoms
heartburn
regurgitation of food
may lead to cough, aspiration pneumonia etc
malignant change in small number of patients

73
Q

Investigations for Achalasia?

A

oesophageal manometry
excessive LOS tone which doesn’t relax on swallowing
considered the most important diagnostic test
barium swallow
shows grossly expanded oesophagus, fluid level
‘bird’s beak’ appearance
chest x-ray
wide mediastinum
fluid level

74
Q

I

Treatment for achalaisa?

A

pneumatic (balloon) dilation is increasingly the preferred first-line option
less invasive and quicker recovery time than surgery
patients 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
intra-sphincteric injection of botulinum toxin is sometimes used in patients who are a high surgical risk
drug therapy (e.g. nitrates, calcium channel blockers) has a role but is limited by side-effects