Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y3 Hard Qs > GI Medicine > Flashcards

GI Medicine Flashcards

1
Q

Staph. aureus: enterotoxin from food Vomiting shortly after consumption Bacillus cereus: reheated rice Vomiting later, 1-2h hx

A

Gastroenteritis

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

Salmonella, Shigella, Campylobacter Lower abdo pain + diarrhoea

A

Dysentry

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

Baby, 3-6 weeks old, projectile vomiting Palpable mass in epigastrium, succession splash

A

Pyloric Stenosis

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

Burns, haematemesis

A

Curling’s Ulcer

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

Sepsis, IC lesion, organ failure, haematemesis

A

Cushing’s Ulcer

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

Gastrin-secreting tumour

Recurrent ulceration, high serum gastrin

A

Zollinger Ellison

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

Massive haematemesis, macrocytic anaemia, Hx of alcoholism

A

Oesophageal Varices

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

Short hx of change in bowel habit Tenesmus and mucus

A

Rectal Carcinoma

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

Reduced food intake, low fibre diet, lack of exercise/mobility, elderly

A

Simple Constipation

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

Constipation due to pain

A

Anal Fissure

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

Young, constipated, distended abdomen

A

Agangliosis

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

Hx of broad-spec abx, green diarrhoea

A

C Diff

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

Visit to Eastern Europe/Russia

Pale stool, foul flatus, watery diarrhoea

A

Giardia

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

Prev hx. of chronic constipation

A

Overflow

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

Diarrhoea, recently started OCP, diet controlled

A

Lactose Intolerance

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

Bloody diarrhoea + intense abdo pain

A

Ischaemic Colitis

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

Loose stool, weight loss, hypopigmentation, onycholysis

A

Thyrotoxicosis

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

Worse epigastric pain on meals/EtOH

A

Chronic Pancreatitis

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

Rapidly progressive dysphagia, weight loss, hypoproteinaemia

Apple core lesion on barium swallow

A

Oesophageal Carcinoma

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

Progressive difficulty with speech/ swallowing

Weak facial muscles, absent jaw jerk

A

Bulbar Palsy

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

Weight loss + anorexia + iron deficiency Signet-ring cells, leather bottle stomach

A

Adenocarcinoma

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

Immunosuppression

Generalised ulceration of oesophagus

A

Oesophageal Candidiasis

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

Infiltration of atypical lymphocytes Thickened folds

A

MALT lymphoma

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

Slit-like vascular spaces Proliferating spindle cells Purple, plaque-like lesions

A

Kaposi’s Sarcoma

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

Cholestatic jaundice, ↑ALP Beading of intrahepatic ducts Associated with UC

A

Sclerosing Cholangitis

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

Ulcer on L shin IBD/Vasculitis/haem malignancy

A

Pyoderma Gangrenosum

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

Acute illness + raised bilirubin

A

Gilbert’s Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

RNA

Jaundice, Diarrhoea + Fever

A

Hepatitis A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Thrombus in hepatic portal vein Secondary to thrombogenic disorders

A

Budd Chiari

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

Chronic liver disease + jaundice Antimitochondrial antibodies

A

Primary Biliary Cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

dsDNA

Mild fibrosis

A

Chronic Hep B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Haemosiderin within hepatocytes Darken skins

Raised transaminase

A

Genetic Haemochromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Copper accumulation

Neuro (adults), liver (children)

A

Wilson’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

In acute oesophageal variceal bleeding, what is the management?

A

Variceal band ligation is the NICE recommended method of stopping oesophageal variceal bleeding. Sengstaken-Blakemore tube and TIPSS is recommended if this fails. Propranolol is used as bleeding prophylaxis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Rules with PPI in regards to endoscopy?

A

Stop taking 2 weeks before as it can mask underlying pathology.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Inheritance pattern in hereditary haemochromatosis?

A

Haemochromatosis is an autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation. It is caused by inheritance of mutations in the HFE gene on both copies of chromosome 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Epidemiology of haemochromatosis?

A

1 in 10 people of European descent carry a mutation in the genes affecting iron metabolism, mainly HFE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Early symptoms of haemachromatosis?

A

early symptoms include fatigue, erectile dysfunction and arthralgia (often of the hands)

Bronze diabetes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the reversible complications of haemochromatosis? 2

A

Cardiomyopathy

Skin Pigmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the irreversible complications of haemochromatosis? 4

A

Diabetes Mellitus
Hypogonadotrophic hypogonadism
Arthropathy
Liver Cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Classic presentation of enterotoxigenic E.coli?

A

Watery travellers diarrhoea with stomach cramps and nausea, think Enterotoxigenic E. coli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How to rule out the causative organism in diarrhoea questions?

A

Divide into Bloody vs non bloody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Diarrhoea in Camplyobacter Jejuni?

A

Bloody diarrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Most common cause of pyogenic liver abscess?

A

S. aureus in kids

E. coli in adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Investigation + Management plan of a pyogenic liver abscess?

A

CT scan

Drainage (typically percutaneous) and antibiotics

amoxicillin + ciprofloxacin + metronidazole

if penicillin allergic: ciprofloxacin + clindamycin

Surgical resection typically used when this fails

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Features of a carcinoid syndrome?

A

Flushing (often 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is pellagra?

A

Pellagra is a disease caused by low levels of niacin, also known as vitamin B-3. It’s marked by dementia, diarrhea, and dermatitis, also known as “the three Ds”. If left untreated, pellagra can be fatal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Investigations and management for carcinoid tumours?

A

Investigation
urinary 5-HIAA
plasma chromogranin A

Management
somatostatin analogues e.g. octreotide
diarrhoea: cyproheptadine may help

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Best tests to assess synthetic function of the liver?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is H. pylori primarily associated with?

A

Main : 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Biggest modifiable risk factor for reducing episodes in Crohns?

A

Stop smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

How to induce remission in Crohn’s Disease?

A

Glucocorticoids (oral, topical or intravenous) are generally used to induce remission. Budesonide is an alternative in a subgroup of patients

5-ASA drugs (e.g. mesalazine) are used second-line to glucocorticoids but are not as effective

azathioprine or mercaptopurine* may be used as an add-on medication to induce remission but is not used as monotherapy.

infliximab is useful in refractory disease and fistulating Crohn’s.
Patients typically continue on azathioprine or methotrexate.
metronidazole is often used for isolated peri-anal disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How do you maintain remission in Crohn’s?

A

Azathioprine or mercaptopurine is used first-line to maintain remission

Methotrexate is used second-line

5-ASA drugs (e.g. mesalazine) should be considered if a patient has had previous surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Complications of Crohn’s Disease?

A

small bowel cancer
colorectal cancer
Osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What do you need to do before giving Azathioprine or Mercaptopurine for Crohn’s ?

A

Assess thiopurine methyltransferase (TPMT) activity before offering azathioprine or mercaptopurine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the single laboratory finding that should prompt an immediate consideration of liver cirrhosis and urgent review by hepatology?

A

Thrombocytopenia (platelet count <150,000 mm^3) is the most sensitive and specific lab finding for diagnosis of liver cirrhosis in those with chronic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How do you diagnose liver cirrhosis?

A

Other techniques such as transient elastography (Fibroscan) and acoustic Radiation force impulse imaging are increasingly used and were recommended by NICE in their 2016 guidelines

For patients with NAFLD, NICE recommend using the enhanced liver fibrosis score to screen for patients who need further testing

Liver biopsy used to be used however this has a bleeding risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is transient elastography (Fibroscan)?

A

Uses a 50-MHz wave is passed into the liver from a small
transducer on the end of an ultrasound probe

Measures the ‘stiffness’ of the liver which is a proxy for fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Epidemiology and aetiology of cyclical vomiting syndrome?

A

Epidemiology
Rare
More common in children than adults
Females are slightly more affected than males

Aetiology
Unknown
80% of children and 25% of adults who develop CVS also have migraines

Presentation
Severe nausea and sudden vomiting lasting hours to days
Prodromal intense sweating and nausea
Well in between episodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Investigations and management for cyclical vomiting syndrome?

A

Investigations
Clinical Diagnosis
A pregnancy test may be considered in women
Routine blood tests to exclude any underlying conditions

Management
Avoidance of triggers
Prophylactic treatments include amitriptyline, propranolol and topiramate.
Ondansetron, prochlorperazine and triptans in acute episodes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What can cause Budd-Chiari Syndrome?

A

Polycythaemia rubra vera
Thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies
Pregnancy
Oral contraceptive pill

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

How can you investigate Budd-Chiari syndrome?

A

Ultrasound with Doppler flow studies is very sensitive and should be the initial radiological investigation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

A transjugular intrahepatic portosystemic shunt procedure connects which two vessels?

A

Hepatic Vein and Portal vein

However it can connect the hepatic vein to IVC

Ultimately bypassing the liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Investigations and Management for C. difficile?

A

Diagnosis
is made by detecting Clostridium difficile toxin (CDT) in the stool
Clostridium difficile antigen positivity only shows exposure to the bacteria, rather than current infection

Management
first-line therapy is oral metronidazole for 10-14 days
if severe or not responding to metronidazole then oral vancomycin may be used
fidaxomicin may also be used for patients who are not responding , particularly those with multiple co-morbidities.
For life-threatening infections a combination of oral vancomycin and intravenous metronidazole should be used

Typically isolate for 48 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Management for pharyngeal pouch

A

Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Management for autoimmune hepatitis?

A

Steroids, immunosuppressants like azathioprine can also be used.

Liver transplantation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Amenorrhoea
ANA/smooth muscle antibodies/LKM1 antibodies, raised IgG levels
liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis

A

Autoimmune hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How many types of autoimmune hepatitis are there and describe them?

A

3

Type 1: Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA). Affects both adults and children

Type 2: Anti-liver/kidney microsomal type 1 antibodies (LKM1)
Affects children only

Type 3: Soluble liver-kidney antigen
Affects adults in middle-age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How is Hepatitis A transmitted?

A

Shellfish, in particular, are common sources of hepatitis A infections, as the virus is transmitted via the faecal-oral route. It is usually self-limiting and is not associated with chronicity. Importantly, Hepatitis A can be prevented through vaccinations.

Incubation period of 2-4 weeks.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the drugs that can cause pancreatitis?

A 
Azathioprine
mesalazine
didanosine
bendroflumethiazide
furosemide
pentamidine
steroids
sodium valproate

My Drug bendroflumethiazide finds APVs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

First line investigations in Coeliac?

A

Tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE

Endomyseal antibody (IgA)

anti-gliadin antibody (IgA or IgG) tests are not recommended by NICE
anti-casein antibodies are also found in some patients

Make sure the patient has gluten in their diet ( you might need to ask them to reintroduce it to their diet)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is intussuception?

A

Intussusception is a condition in which one segment of intestine “telescopes” inside of another, causing an intestinal obstruction (blockage).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Inheritance pattern of Peutz- Jeghers syndrome and patterns?

A

Autosomal dominant - responsible gene encodes serine threonine kinase LKB1 or STK11.

Features
hamartomatous polyps in GI tract (mainly small bowel)
pigmented lesions on lips, oral mucosa, face, palms and soles
intestinal obstruction e.g. intussusception
gastrointestinal bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the main benefit of prescribing albumin when treating large volume ascites’?

A

An albumin infusion is used when draining large volumes of fluid via paracentesis as it has benefit in reducing paracentesis-induced circulatory dysfunction and mortality when compared to alternative treatments.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is used to group the causes of ascites?

A

Serum albumin ascites gradient (SAAG):
<11 g/L or a gradient >11g/L

SAAG > 11g/L indicates portal hypertension but also can point to cirrhosis, Budd- Chiari, Alcoholic hepatitis…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the management of ascites?

A

Management
Reducing dietary sodium

Fluid restriction is sometimes recommended if the sodium is < 125 mmol/L

Aldosterone antagonists: e.g. spironolactone

Drainage if tense ascites (therapeutic abdominal paracentesis): large-volume paracentesis for the treatment of ascites requires albumin ‘cover’.

Prophylactic antibiotics to reduce the risk of SBP.
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’
a transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Dysphagia that affects both solids and liquids from the start

A

Achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Signs and symptoms of scurvy?

A

Vitamin C deficiency

Ecchymosis, easy bruising
Poor wound healing
Gingivitis with bleeding and receding gums
Sjogren's syndrome
Arthralgia
Oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Abdominal pain, rectal bleeding and diarrhoea
Pain worse after eating a larger meal

History of HTN/IHD

A

Ischemic colitis

Particularly at the splenic flexure (watershed area)
near where the SMA blood supply changes to the IMA. Add to this the pain gets worse after eating, when the bowel requires more blood flow for its increased energy demands for digestion and ischaemic colitis would be the diagnosis to investigate first.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Investigation of choice for ischaemic colitis?

A

CT (gold standard)

‘thumbprinting’ may be seen on abdominal x-ray due to mucosal oedema/haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Chronic liver failure who then progresses to develop renal failure.

A

Hepatorenal syndrome

Hepatorenal syndrome is split into type 1 and 2. Type 1 is a rapid onset hepatorenal syndrome (less than two weeks). This typically occurs following an acute event such as an upper GI bleed. Type 2 is a more gradual decline in renal function and is generally associated with refractory ascites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Pathophysiology of Hepatorenal syndrome?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Management of hepatorenal syndrome?

A

Management options
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

84
Q

Investigations + Management of primary biliary cirrhosis?

A

Diagnosis
anti-mitochondrial antibodies (AMA) M2 subtype are present in 98% of patients and are highly specific
smooth muscle antibodies in 30% of patients
raised serum IgM

Management
pruritus: cholestyramine
fat-soluble vitamin supplementation
ursodeoxycholic acid
liver transplantation e.g. if bilirubin > 100 (PBC is a major indication) - recurrence in graft can occur but is not usually a problem
85
Q

Why do coeliacs people have to keep very upto date with their vaccinations?

A

Functional hyposplenism

86
Q

Triad of acute liver failure?

A

Triad of encephalopathy, jaundice and coagulopathy

87
Q

Liver failure vs chronic liver cirrhosis?

A

The key differentiating features between a chronic liver disease and acute failure is the raised prothrombin time, the very high bilirubin and the presence of encephalopathy, all of which you would not expect to see in a stable chronic liver disease picture.

88
Q

How do you grade hepatic encephalopathy?

A 
Grading of hepatic encephalopathy
Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma
89
Q

Management of hepatic encephalopathy?

A

Management
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

90
Q

Pain relief on eating?

A

ddx: Duodenal ulcer?

91
Q

How does significant bleeding occur in PUD?

A

Bleeding in peptic ulcer disease (PUD) occurs when the base of the ulcer erodes into a vessel supplying the muscles of the stomach or duodenal wall. This man has a duodenal ulcer, as his pain is relieved by eating. Classically, posterior duodenal ulcers erode the gastroduodenal artery, which can cause significant bleeding.

92
Q

Management of acute bleeding in PUD?

A

Management
ABC approach as with any upper gastrointestinal haemorrhage
IV proton pump inhibitor

The first-line treatment is endoscopic intervention
if this fails (approximately 10% of patients) then either:
urgent interventional angiography with transarterial embolization or
surgery

93
Q

How can you differentiate between primary Sjogrens and Primary biliary cholangitis?

A

Primary Bilary Cholangitis can cause sicca syndrome in 70% of cases so if the ALP is raised, the dry mouth is more likely to be due to PBC than to a primary Sjogren

94
Q

What are adverse risks associated with PPIs?

A

HYPONATREMIA and hypomagnesemia

Increased risk of fractures
Increased risk of C. Difficile

95
Q

How to maintain remission in ulcerative colitis?

A

Maintaining remission

Following a mild-to-moderate ulcerative colitis flare

Proctitis and proctosigmoiditis:
topical (rectal) aminosalicylate alone (daily or intermittent) or
an oral aminosalicylate plus a topical (rectal) aminosalicylate (daily or intermittent)
or
an oral aminosalicylate by itself: this may not be effective as the other two options

Left-sided and extensive ulcerative colitis
low maintenance dose of an oral aminosalicylate

Following a severe relapse or >=2 exacerbations in the past year
oral azathioprine or oral mercaptopurine

96
Q

How do you manage severe colitis?

A

Severe colitis

Should be treated in hospital
IV steroids are usually given first-line

intravenous ciclosporin may be used if steroid are contraindicated
if after 72 hours there has been no improvement, consider adding intravenous ciclosporin to intravenous corticosteroids or consider surgery

97
Q

How do you induce remission in mild-moderate colitis?

A

Proctitis
1. Topical (rectal) aminosalicylate: for distal colitis rectal mesalazine has been shown to be superior to rectal steroids and oral aminosalicylates

If remission is not achieved within 4 weeks, add an oral aminosalicylate

If remission still not achieved add topical or oral corticosteroid

proctosigmoiditis and left-sided ulcerative colitis
1. Topical (rectal) aminosalicylate

  1. If remission is not achieved within 4 weeks, add a high-dose oral aminosalicylate OR switch to a high-dose oral aminosalicylate and a topical corticosteroid
  2. If remission still not achieved stop topical treatments and offer an oral aminosalicylate and an oral corticosteroid

extensive disease
topical (rectal) aminosalicylate and a high-dose oral aminosalicylate:
if remission is not achieved within 4 weeks, stop topical treatments and offer a high-dose oral aminosalicylate and an oral corticosteroid

98
Q

RUQ pain, itching.

Sweet smelling breath

A

Acute liver failure

Breath is a sign called Fetor hepaticus which is a late sign in hepatic encephalopathy

99
Q

Patient has a worsening severe flare up of ulcerative colitis. Bloods show systemic disturbance. What investigation would you like to do ?

A

Abdominal X ray

This patient may go on to develop toxic megacolon

100
Q

Features of NASH and first line management?

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

Management: Lifestyle changes (particularly weight loss)

101
Q

Negative AMA
ERCP shows strictures having a beaded appearance
Postive pANCA

A

Primary Sclerosing cholangitis
Although not all patients with primary sclerosing cholangitis (PSC) with have positive pANCA, if you see it in a question with negative antimitochondrial antibodies (which would suggest primary biliary cirrhosis if positive) think PSC. This is backed up by the classic ‘beaded’ strictures on ERCP

UC Beads

102
Q

First line investigations for primary sclerosing cholangitis?

A

Investigation
Endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopancreatography (MRCP) are the standard diagnostic investigations, showing multiple biliary strictures giving a ‘beaded’ appearance
ANCA may be positive
There is a limited role for liver biopsy, which may show fibrous, obliterative cholangitis often described as ‘onion skin’

103
Q

First line investigation for oesophageal carcinoma?

A

Upper GI endoscopy

CT can help stage after the diagnosis is made

104
Q

A 4-year-old presents with sudden onset of dysphagia. He undergoes an upper GI endoscopy and a large bolus of food is identified in the mid oesophagus. He has no significant history, other than a tracheo-oesophageal fistula repair soon after birth.

A

Benign oesophageal stricture

105
Q

What is courvoisier’s law?

A

Courvoisier’s sign states that in a patient with a painless, enlarged gallbladder and mild jaundice the cause is unlikely to be gallstones. Furthermore, it is more likely to be a malignancy of the pancreas or biliary tree.

106
Q

Investigations + Management of Wilson’s disease?

A

Diagnosis
reduced serum caeruloplasmin
reduced serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
increased 24hr urinary copper excretion

Management
penicillamine (chelates copper) has been the traditional first-line treatment

107
Q

What is one of the most useful tests to differentiate IBS and IBD?

A

Faecal Calprotectin

108
Q

Droopy eyelid, difficulty swallowing and facial weakness. Double vision

A

Myasthenia gravis

109
Q

What are the symptoms of hypomagnesemia ?

A 
Features may be similar to hypocalcaemia:
paraesthesia
tetany
seizures
arrhythmias
decreased PTH secretion → hypocalcaemia
110
Q

What is Rovsing’s Sign?

A

If palpation of the left lower quadrant of a person’s abdomen increases the pain felt in the right lower quadrant, the patient is said to have a positive Rovsing’s sign and may have appendicitis.

111
Q

Name 3 drugs that can cause drug induced cirrhosis?

A

Liver cirrhosis

methotrexate
methyldopa
amiodarone

112
Q

Name 6 types of drugs that can cause drug induced cholestasis/ hepatitis?

A

The following drugs tend to cause cholestasis (+/- hepatitis): CAFASP

Combined oral contraceptive pill
Antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
Anabolic steroids, testosterones
Phenothiazines: chlorpromazine, prochlorperazine
Sulphonylureas
Fibrates

113
Q

What is the scoring system used to first assess an Upper GI bleed?

A

Blatchford Score

Rockall Score - after endoscopy

114
Q

What are the components and uses of the Blatchford score?

A 
8 Different Factors:
Urea (mmol/l):
6·5 - 8 = 2
8 - 10 = 3
10 - 25 = 4
> 25 = 6
Haemoglobin (g/l):
Men
12 - 13 = 1
10 - 12 = 3
< 10 = 6

Women
10 - 12 = 1
< 10 = 6

Systolic Blood Pressure (mmHg)
100 - 109 = 1
90 - 99 = 2
< 90 = 3

Pulse >=100/min = 1
Presentation with melaena  = 1
Presentation with syncope  = 2
Hepatic disease  = 2
Cardiac failure  = 2
115
Q

What are the treatments for IBS?

A

First-line pharmacological treatment - according to predominant symptom

pain: antispasmodic agents
constipation: laxatives but avoid lactulose
diarrhoea: loperamide is first-line

For patients with constipation who are not responding to conventional laxatives linaclotide may be considered, if:
optimal or maximum tolerated doses of previous laxatives from different classes have not helped and
they have had constipation for at least 12 months

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

116
Q

What are the complications of coeliac disease?

A

Complications (6)
Anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)

Hyposplenism

Osteoporosis, osteomalacia

Lactose intolerance

Enteropathy-associated T-cell lymphoma of small intestine

Subfertility, unfavourable pregnancy outcomes
rare: oesophageal cancer, other malignancies

117
Q

How much weight loss is malnutrition?

A

Unintentional weight loss greater than 10% within the last 3-6 months is diagnostic of malnutrition

118
Q

What is the main risk factor for hepatocellular carcinoma?

A

Chronic hepatitis B is the most common cause of HCC worldwide with chronic hepatitis C being the most common cause in Europe.

The main risk factor for developing HCC is liver cirrhosis, for example secondary* to hepatitis B & C, alcohol, haemochromatosis and primary biliary cirrhosis.

119
Q

What are the management plans for hepatocellular carcinoma?

A 
Management options
early disease: surgical resection
liver transplantation
radiofrequency ablation
transarterial chemoembolisation
sorafenib: a multikinase inhibitor
120
Q

Hepatocellular carcinoma screening?

A

Screening with ultrasound (+/- alpha-fetoprotein) should be considered for high risk groups such as:
patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis
men with liver cirrhosis secondary to alcohol

121
Q

What are the investigations and management for haemochromatosis?

A

Diagnostic tests
Molecular genetic testing for the C282Y and H63D mutations
liver biopsy: Perl’s stain

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

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

122
Q

Describe the pathophysiology of Gilbert’s and the features?

A

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
unconjugated hyperbilirubinaemia (i.e. not in urine)
jaundice may only be seen during an intercurrent illness, exercise or fasting
123
Q

What is the investigations and management for Gilbert’s Syndrome?

A

Investigation: rise in bilirubin following prolonged fasting or IV nicotinic acid

Management: no treatment required

124
Q

Why does Crohn’s disease lead to gallstones?

A

Crohn’s disease can result in terminal ileitis, this is the section of the bowel where bile salts are reabsorbed. When this area is inflamed and the bile salts are not absorbed and people are prone to development of gallstones.

125
Q

What are the risk factors for the development of gallstones?

6

A

Other risk factors for the development of gallstones include

Increasing age
Family history.
Sudden weight loss - eg, after obesity surgery.
Loss of bile salts - eg, ileal resection, terminal ileitis. (Crohn’s disease)
Diabetes - as part of the metabolic syndrome.
Oral contraception - particularly in young women

126
Q

What is the use of chlordiazepoxide?

A

Alcoholic withdrawal

127
Q

What is the management of acute severe alcoholic hepatitis?

A

Oral prednisone

128
Q

What is Spontaneous bacterial peritonitis and what are the features?

A

Spontaneous bacterial peritonitis (SBP) is a form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis.

Features
Ascites
abdominal pain
fever

129
Q

Investigations and Management of SBP?

A

Diagnosis
Paracentesis: neutrophil count > 250 cells/ul
the most common organism found on ascitic fluid culture is E. coli

Management
intravenous cefotaxime is usually given

130
Q

Why is ferritin not used to assess if a patient is anaemic in infection?

A

During infection, ferritin is an unreliable indicator of iron stored in the body as it is an acute phase protein. Transferrin saturation should be used instead

131
Q

In what diseases is metaclopramide contraindicated in?

A

Parkinson’s

Bowel Obstruction

132
Q

What is refeeding syndrome?

A

Refeeding syndrome describes the metabolic abnormalities which occur on feeding a person following a period of starvation. It occurs when an extended period of catabolism ends abruptly with switching to carbohydrate metabolism. The metabolic consequences include:

Hypophosphataemia
Hypokalaemia
Hypomagnesaemia: may predispose to torsades de pointes
Abnormal fluid balance

These abnormalities can lead to organ failure.

133
Q

What are the recommendations in refeeding syndrome?

A

NICE recommend that if a patient hasn’t eaten for > 5 days, aim to re-feed at no more than 50% of requirements for the first 2 days.

134
Q

What is small bowel bacterial overgrowth syndrome and what are the risk factors and features?

A

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

135
Q

Investigations and Management in SBBOS?

A

Diagnosis
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 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.

136
Q

Treatment with Isoniazid leads to what vitamin deficiency? What are the complications of this deficiency?

A

Vitamin B6 (pyridoxine)

Vitamin B6 is a water soluble vitamin of the B complex group. It is converted to pyridoxal phosphate (PLP) which is a cofactor for many reactions including transamination, deamination and decarboxylation.

Causes of vitamin B6 deficiency
isoniazid therapy

Consequences of vitamin B6 deficiency
peripheral neuropathy
sideroblastic anemia

137
Q

A 62-year-old presents with upper abdominal pain. She has recently been discharged from hospital where she underwent an ERCP to investigate cholestatic liver function tests. The pain is severe. On examination she is apyrexial and has a pulse of 96 / min.

A

Acute pancreatitis

138
Q

What is the most common organism in ascending cholangitis?

A

E. coli

139
Q

What is ascending cholangitis?

A

Ascending cholangitis is a bacterial infection (typically E. coli) of the biliary tree. The most common predisposing factor is gallstones.

140
Q

Features of ascending cholangitis?

A

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)

Other features
Raised inflammatory markers

141
Q

What are the features of Reynold’s Pentad?

A 
RUQ pain
Fever
Jaundice
Hypotension
Confusion
142
Q

What is the management for ascending cholangitis?

A

Management

Intravenous antibiotics
Endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve any obstruction

143
Q

What is gallstone ileus?

A

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.

144
Q

What is the management of gallstone ileus?

A

Laparotomy and removal of the gallstone from small bowel, the enterotomy must be made proximal to the site of obstruction and not at the site of obstruction. The fistula between the gallbladder and duodenum should not be interfered with.

145
Q

What is the mechanism of action of loperamide?

A

Opioids agonist

Diphenoxylate is another example

146
Q

What antibiotics can lead to C. difficile?

A

Clindamycin is historically associated with causing Clostridium difficile but the aetiology has evolved significantly over the past 10 years. Second and third generation cephalosporins are now the leading cause of Clostridium difficile.

147
Q

What drugs can affect the accuracy of a urea breath test?

A

Urea breath test - no antibiotics in past 4 weeks, no antisecretory drugs (e.g. PPI) in past 2 weeks

148
Q

Liver failure that follows a cardiac arrest?

A

Ischaemic hepatitis

Very high aminotransferase levels (over 1000)

149
Q

What is alcoholic ketoacidosis and how does it occur?

A

Alcoholic ketoacidosis is a non-diabetic euglycaemic form of ketoacidosis. It occurs in people who regularly drink large amounts of alcohol. Often alcoholics will not eat regularly and may vomit food that they do eat, leading to episodes of starvation. Once the person becomes malnourished, after an alcohol binge the body can start to break down body fat, producing ketones. Hence the patient develops a ketoacidosis.

150
Q

How does alcoholic ketoacidosis present?

A 
It typically presents with a pattern of:
Metabolic acidosis
Elevated anion gap
Elevated serum ketone levels
Normal or low glucose concentration
151
Q

Management of alcoholic ketoacidosis?

A

The most appropriate treatment is an infusion of saline & thiamine. Thiamine is required to avoid Wernicke encephalopathy or Korsakoff psychosis.

152
Q

What does a barium swallow show in oesophageal cancer?

A

The film shows narrowing and irregularity with hold-up of contrast noted in the mid thoracic oesophagus consistent with oesophageal cancer.

153
Q

What is kantor’s string sign?

A

There is a long segment of narrowed terminal ileum in a ‘string like’ configuration in keeping with a long stricture segment.

Crohn’s Disease

154
Q

Investigations in Crohn’s disease?

A

Bloods
C-reactive protein correlates well with disease activity

Endoscopy
colonoscopy is the investigation of choice
features suggest of Crohn’s include deep ulcers, skip lesions

Small bowel enema
Kantor string sign

155
Q

What is HNPCC?

A

HNPCC, an autosomal dominant condition, is the most common form of inherited colon cancer. Around 90% of patients develop cancers, often of the proximal colon, which are usually poorly differentiated and highly aggressive

156
Q

What is the most common association with HNPCC?

A

Endometrial cancer

Pancreatic cancer in males

157
Q

What is diverticulosis?

A

Diverticulosis is an extremely common disorder characterised by multiple outpouchings of the bowel wall, most commonly in the sigmoid colon. Strictly speaking the term diverticular disease is reserved for patients who are symptomatic - diverticulosis is the more accurate term for diverticula being present

158
Q

How does diverticulosis present?

A

Diverticulosis can present in a number of ways:
painful diverticular disease: altered bowel habit, colicky left sided abdominal pain. A high fibre diet is usually recommended to minimise symptoms

159
Q

How does diverticulitis present?

A

One of the diverticular become infected. The classical presentation is:
Left iliac fossa pain and tenderness
anorexia, nausea and vomiting
diarrhoea
features of infection (pyrexia, raised WBC and CRP)

160
Q

How do you manage Diverticulitis?

A

Management:
mild attacks can be treated with oral antibiotics
more significant episodes are managed in hospital. Patients are made nil by mouth, intravenous fluids and intravenous antibiotics (typical a cephalosporin + metronidazole) are given

161
Q

What are some complications of diverticulitis?

A 
Complications of diverticulitis include:
abscess formation
peritonitis
obstruction
perforation
162
Q

What is the most common cause of inherited colorectal cancer?

A

HNPCC

(FAP is 2nd most common)

Gardner’s Syndrome is a variant of FAP

163
Q

RUQ pain, fatigue and dizziness.

Tender hepatomegaly. Pulsatility.

A

Right heart failure

The real clue in this question is that it is also pulsatile, which is due to the back-up of blood due to the failure of the right side of the heart to work effectively. The fact that it is pulsatile, distinguishes it from the other possible answers.

164
Q

What are the classical symptoms of gallstones?

A

The classical symptoms are of colicky right upper quadrant pain that occurs postprandially. The symptoms are usually worst following a fatty meal when cholecystokinin levels are highest and gallbladder contraction is maximal.

165
Q

What is a good investigation when you suspect gall stones?

A

Abdominal Ultrasound

166
Q

What is the biggest cancer risk from primary sclerosing cholangitis?

A

Cholangiocarcinoma (around 10%)

167
Q

Whats the scoring system that can be used to assess severity of pancreatitis?

A

Modified Glasgow Score: PANCREAS

Pa02	<8kPa
Age	>55 years
Neutrophilia	WBC >15x10^9
Calcium	<2mmol/L
Renal function	Urea >16mmol/L
Enzymes	LDH >600 ; AST >200
Albumin	<32g/L
Sugar	Blood glucose >10mmol/L
168
Q

A woman who is know to have gallstones presents with pain in her right upper quadrant. On examination she is not jaundiced and has a temperature of 37.8C. Palpating under the right costal margin causes her to catch her breath.

A

Acute Cholecystitis
Pain similar to biliary colic but more severe and persistent. The pain may radiate to the back or right shoulder.

The patient may be pyrexial and Murphy’s sign positive (arrest of inspiration on palpation of the RUQ)

169
Q

A 72-year-old man who is known to have heart failure and type 2 diabetes mellitus presents with a persistent dull ache in his right upper quadrant. Blood tests show a mild elevation of the alanine aminotransferase level.

A

Congestive hepatomegaly

The liver only usually causes pain if stretched. One common way this can occur is as a consequence of congestive heart failure. In severe cases cirrhosis may occur.

170
Q

What is melanosis coli?

A

Melanosis coli is a disorder of pigmentation of the bowel wall. Histology demonstrates pigment-laden macrophages

It is associated with laxative abuse, especially anthraquinone compounds such as senna

171
Q

Increased Goblet cells.

UC/Crohn’s

A

Crohn’s

172
Q

What is acute cholecystitis and describe the pathophysiology??

A

Inflammation of the gallbladder.

Pathophysiology

  • Develops secondary to gallstones in 90% of patients (acute calculous cholecystitis)
  • the remaining 10% of cases are referred to as acalculous cholecystitis
173
Q

Where is acalculous cholecystitis seen?

A

Typically seen in hospitalised and severely ill patients

Multifactorial pathophysiology: gallbladder stasis, hypoperfusion, infection

In immunosuppressed patients it may develop secondary to Cryptosporidium or cytomegalovirus
associated with high morbidity and mortality rates

174
Q

Features of cholecystitis?

A

Features

Right upper quadrant pain

May radiate to the right shoulder

Fever and signs of systemic upset

Murphy’s sign on examination: inspiratory arrest upon palpation of the right upper quadrant
Occasionally mildly deranged LFT’s (especially if Mirizzi syndrome)

175
Q

Investigations of choice in acute cholecystitis?

A

Investigation

Ultrasound is the first-line investigation of choice

If the diagnosis remains unclear then cholescintigraphy (HIDA scan) may be used
technetium-labeled 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

176
Q

What is the management of acute cholecystitis?

A

Treatment

Intravenous antibiotics
NICE now recommend early laparoscopic cholecystectomy, within 1 week of diagnosis. Previously, surgery was delayed for several weeks until the inflammation has subsided

177
Q

Endoscopy in upper GI bleed timing?

A

All patients should have endoscopy within 24 hours

178
Q

What medications should you consider stopping in C. difficile and why?

A

Anti-peristaltic and anti- motility medications
e.g Opioids

It will reduce the clearance of C. difficile and increase the chance of toxic megacolon occurring

179
Q

What Hep B serology results would show acute infection?

A

HBsAg positive, anti-HBs negative, IgM anti-HBc positive

180
Q

What Hep B serology results would show previous vaccination?

A

HBsAg negative, anti-HBs positive and anti-HBc negative

181
Q

What Hep B serology results would show chronic infection?

A

Chronic infection would result in IgG anti-HBc positive status.

If the patient has positive IgM, indicating an acute infection, rather than chronic.

182
Q

What is Zollinger - Ellison syndrome, what are the features and how do you diagnose it?

A

Zollinger-Ellison syndrome is condition characterised by excessive levels of gastrin, usually from a gastrin secreting tumour usually of the duodenum or pancreas. Around 30% occur as part of MEN type I syndrome

Features
multiple gastroduodenal ulcers
diarrhoea
malabsorption

Diagnosis
fasting gastrin levels: the single best screen test
secretin stimulation test

183
Q

Hepatitis D?

A

Hepatitis D superinfection is an differential for chronic hepatitis B patients with acute flare up

184
Q

Obese T2DM with abnormal LFTs

A

non-alcoholic fatty liver disease

185
Q

Which vitamin, if taken in high doses, can be teratogenic?

A

Vitamin A is teratogenic in high doses, and pregnant women should not exceed a daily intake of >10,000IU. Women are therefore advised to avoid any supplements containing vitamin A, such as normal multivitamin tablets, in pregnancy (NHS Choices)

186
Q

What is used as prophylaxis for variceal bleeding?

A

propranolol: reduced rebleeding and mortality compared to placebo

187
Q

Patients with Barrett’s metaplasia are at higher risk of?

A

Adenocarcinoma of the oesophagus

Adenocarcinoma is also related to GORD

188
Q

According to the Truelove and Witts’ severity index, which of the following is most likely to indicate severe colitis??

A

The Truelove and Witts’ severity index is recommended by NICE when assessing the severity of ulcerative colitis in adults. Ulcerative colitis is classified as ‘severe’ when the patient has blood in their stool, or is passing more than 6 stools per day plus at least one of the following features:

Temperature greater than 37.8°C
Heart rate greater than 90 beats per minute
Anaemia (Hb less than 105g/ L)
Erythrocyte sedimentation rate greater than 30 mm/hour

189
Q

How would the LFTs change in autoimmune hepatitis?

A

Autoimmune hepatitis is more likely to show predominantly raised ALT / AST on LFTs than ALP

Autoimmune hepatitis predominantly involves inflammation in the liver and thus ALT / AST are likely to be raised

190
Q

What is the management of appendicitis?

A

Laparoscopic appendicectomy is now the treatment of choice

Administration of prophylactic intravenous antibiotics reduces wound infection rates
patients with perforated appendicitis (typical around 15-20%) require copious abdominal lavage.

Patients without peritonitis who have an appendix mass should receive broad-spectrum antibiotics and consideration given to performing an interval appendicectomy.

191
Q

What is Sister Mary Joseph’s node?

A

Sister Mary Joseph node is a palpable nodule in the umbilicus due to metastasis of malignant cancer within the pelvis or abdomen

192
Q

Uses of the midline incision?

A

Commonest approach to the abdomen

Structures divided: linea alba, transversalis fascia, extraperitoneal fat, peritoneum (avoid falciform ligament above the umbilicus)

Bladder can be accessed via an extraperitoneal approach through the space of Retzius

193
Q

Uses of Kocher incision?

A

Incision under right subcostal margin e.g. Cholecystectomy (open)

194
Q

Use of the lanz incision?

A

Appendicectomy

195
Q

Use of Gridiron incision?

A

Oblique incision centered over McBurneys point- usually appendicectomy (less cosmetically acceptable than Lanz)

196
Q

Use of Pfannenstiel incision?

A

Transverse supra pubic, primarily used to access pelvic organs

197
Q

Use of Mcevedy incision?

A

Groin incision e.g. Emergency repair strangulated femoral hernia

198
Q

Use of Rutherford Morrison incision?

A

Extraperitoneal approach to left or right lower quadrants. Gives excellent access to iliac vessels and is the approach of choice for first time renal transplantation.

199
Q

What is the most appropriate tool to screen for malnutrition?

A

MUST

200
Q

What is antiphospholipid syndrome?

A

Antiphospholipid syndrome is an acquired disorder characterised by a predisposition to both venous and arterial thromboses, recurrent fetal loss and thrombocytopenia. It may occur as a primary disorder or secondary to other conditions, most commonly systemic lupus erythematosus (SLE)

A key point for the exam is to appreciate that antiphospholipid syndrome causes a paradoxical rise in the APTT. This is due to an ex-vivo reaction of the lupus anticoagulant autoantibodies with phospholipids involved in the coagulation cascade

201
Q

What are gluten containing cereals?

A 
The management of coeliac disease involves a gluten-free diet. Gluten containing cereals include:
wheat: bread, pasta, pastry
barley*: beer
rye
oats**
202
Q

What are gluten free?

A

Some notable foods which are gluten-free include:
rice
potatoes
corn (maize)

203
Q

CDT negative
CD antigen positive
What do you do?

A

Reassure and continue monitoring.

Clostridium difficile antigen positivity only shows exposure to the bacteria, rather than current infection

204
Q

What increases the risk of squamous cell carcinoma of the oesophagus?

A

Achalasia

205
Q

A 41-year-old man with cerebral palsy is admitted with abdominal pain and diarrhoea. His carers report him passing 5-6 watery stools per day for the past four days. On examination he has a mass in the left side of the abdomen.

A

Constipation causing overflow

206
Q

Which drugs paint a hepatocellular picture?

A

SPAM MAVAH

Paracetamol
Sodium valproate, phenytoin
MAOIs
Halothane

Anti-tuberculosis: isoniazid, rifampicin, Pyrazinamide

Statins
Alcohol
Amiodarone
methyldopa

207
Q

What is the triad for Boerhaave’s Perforation?

A

The Mackler triad for Boerhaave syndrome:

Vomiting, thoracic pain, subcutaneous emphysema. It typically presents in middle aged men with a background of alcohol abuse.

Y3 Hard Qs (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions