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Gastroenterology Flashcards

1
Q

definition of 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

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2
Q

clinical features of achalasia

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

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3
Q

investigation findings in achalasia

A

oesophageal manometry
excessive LOS tone which doesn’t relax on swallowing

barium swallow
shows grossly expanded oesophagus, fluid level
‘bird’s beak’ appearance

chest x-ray
wide mediastinum
fluid level

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4
Q

treatment of achalasia

A

pneumatic (balloon) dilation

surgical intervention with a Heller cardiomyotomy should be considered if recurrent or persistent symptoms

intra-sphincteric injection of botulinum toxin - high surgical risk

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5
Q

causes of abdominal pain

A

infective
inflammatory
vascular
traumatic
metabolic

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6
Q

causes of RUQ pain

A

biliary colic

acute cholecystitis - fever, raised inflammatory markers

ascending cholangitis - RUQ pain, fever, jaundice

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7
Q

causes of epigastric or central pain

A

acute pancreatitis - tenderness, ileus, fever

peptic ulcer disease

ruptured AAA - shock

mesenteric ischaemnia - metabolic acidosis, diarrhoea, rectal bleeding

intestinal obstruction - tinkling bowels, vomiting

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8
Q

causes of iliac fossa pain

A

ectopic pregnancy

appendicitis

acute diverticulitis - LLQ - diarrhoea, fever, raised inflammatory markers

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9
Q

causes of loin pain

A

renal colic - may cause haematuria

acute pyelonephritis - fever, rigors, vomiting

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10
Q

causes of acute liver failure

A

rapid onset of hepatocellular dysfunction leading to a variety of systemic complications

paracetamol overdose
alcohol
viral hepatitis (usually A or B)
acute fatty liver of pregnancy

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11
Q

features of acute liver failure

A

jaundice
coagulopathy: raised prothrombin time
hypoalbuminaemia
hepatic encephalopathy
renal failure is common (‘hepatorenal syndrome’)

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12
Q

how to manage acute upper GI bleed

A

ABC
platelet transfusion if active bleeding and platelets <50
FFP if fibrinogen <1g/l or prothrombin 1.5x normal
prothrombin complex if bleeding and on warfarin

endoscopy - immediately in severe bleed, <24h for all pt

variceal bleeding - terlipressin and prophylactic antibiotics
band ligation
ransjugular intrahepatic portosystemic shunts

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12
Q

clinical features of upper GI bleeding

A

haematemesis - bright red or coffee ground

melena - passage of altered blood PR, black and tarry

urea++ due to protein meal

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13
Q

scoring systems used in acute upper GI bleeding

A

the Glasgow-Blatchford score at first assessment
helps clinicians decide whether patient patients can be managed as outpatients or not

the Rockall score is used after endoscopy
provides a percentage risk of rebleeding and mortality

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14
Q

features of alcoholic ketoacidosis

A

Metabolic acidosis
Elevated anion gap
Elevated serum ketone levels
Normal or low glucose concentration

infusion of saline & thiamine

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15
Q

investigation findings in alcoholic hepatitis

A

gamma-GT is characteristically elevated

the ratio of AST:ALT is normally > 2

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16
Q

management of alcoholic hepatitis

A

acute - glucocorticoids (e.g. prednisolone)

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17
Q

moa of aminosalicylate drugs

A

5-aminosalicyclic acid (5-ASA) is released in the colon and is not absorbed. It acts locally as an anti-inflammatory

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18
Q

features of angiodysplasia

A

vascular deformity of the gastrointestinal tract which predisposes to bleeding and iron deficiency anaemia

Features
anaemia
gastrointestinal (GI) bleeding
if upper GI then may be melena
if lower GI then may present as brisk, fresh red PR bleeding

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19
Q

diagnosis and management of angiodysplasia

A

diagnosis
colonoscopy
mesenteric angiography if acutely bleeding

management
endoscopic cautery or argon plasma coagulation
antifibrinolytics e.g. Tranexamic acid

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20
Q

causes of high SAAG >11g/L ascites

A

high SAAG = portal hypertension

liver disorder - cirrhosis/alcoholic liver disease
acute liver failure
liver metastases

cardiac - RHF, constrictive pericarditis

Budd-Chiari syndrome
portal vein thrombosis
veno-occlusive disease
myxoedema

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21
Q

causes of low SAAG <11g/L ascites

A

Hypoalbuminaemia
nephrotic syndrome
severe malnutrition (e.g. Kwashiorkor)

Malignancy
peritoneal carcinomatosis

Infections
tuberculous peritonitis

Other causes
pancreatitis
bowel obstruction
biliary ascites
postoperative lymphatic leak
serositis in connective tissue diseases

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22
Q

managing ascites

A

reducing dietary sodium
fluid restriction is sometimes recommended if the sodium is < 125 mmol/L

aldosterone antagonists

drainage if tense ascites - large volume paracentesis

prophylactic cipro to reduce the risk of spontaneous bacterial peritonitis

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23
Q

features of autoimmune hepatitis

A

commonly seen in young females

signs of chronic liver disease
acute hepatitis: fever, jaundice etc (only 25% present in this way)
amenorrhoea (common)
ANA/SMA/LKM1 antibodies, raised IgG levels
liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis

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24
Q

type I AI hepatitis antibodies

A

Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA)

Affects both adults and children

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25
Q

type II AI hepatitis antibodies

A

Anti-liver/kidney microsomal type 1 antibodies (LKM1)

Affects children only

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26
Q

type III AI hepatitis antibodies

A

Soluble liver-kidney antigen

Affects adults in middle-age

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27
Q

RF for barrett’s oesophagus

A

gastro-oesophageal reflux disease (GORD) is the single strongest risk factor
male gender (7:1 ratio)
smoking
central obesity

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28
Q

management of barrett’s oesophagus

A

high-dose proton pump inhibitor - ability to suppress progression limited

endoscopic surveillance with biopsies
for patients with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years

if dysplasia identified - endoscopic intervention (radiofrequency ablation, endoscopic mucosal resection)

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29
Q

causes of bile acid malabsorption

A

primary - due to excessive production of bile acid

secondary - due to an underlying gastrointestinal disorder ( ileal disease e.g., crohn’s, cholecystectomy, coeliac disease)

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30
Q

management of bile acid malabsorption

A

bile acid sequestrants e.g. cholestyramine

can lead to steatorrhoea and vitamin A, D, E, K malabsorption.

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31
Q

definition and causes of budd-chiari syndrome

A

hepatic vein thrombosis - due to underlying haem disease or procoagulant condition

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

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32
Q

features of budd-chiari syndrome

A

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

ultrasound with Doppler flow studies

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33
Q

diagnosis of carcinoid tumours

A

usually occurs with liver metastases releasing serotonin into the systemic circulation or lung carcinoid as mediators are not ‘cleared’ by the liver

check urinary 5-HIAA

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34
Q

features of carcinoid syndrome

A

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

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35
Q

management of carcinoid syndrome

A

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

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36
Q

side effects of cholestyramine

A

abdominal cramps and constipation
decreases absorption of fat-soluble vitamins
cholesterol gallstones
may raise level of triglycerides

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37
Q

features of clostroidiodes difficile

A

anaerobic gram-positive, spore-forming, toxin-producing bacillus transmitted via faecal oral route, releases exotoxins causing colitis

Features
diarrhoea
abdominal pain
a raised white blood cell count (WCC) is characteristic
if severe toxic megacolon may develop

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38
Q

diagnosis and management of c diff

A

detecting C. difficile toxin (CDT) in the stool
C. difficile antigen positivity only shows exposure to the bacteria

management
oral vancomycin for 10 days
second-line therapy: oral fidaxomicin

recurrent - <12w - fidaxomicin, >12 oral vanc

life threatening - oral vanc and IV metronidazole

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39
Q

isolation period for c diff patients

A

until no diarrhoea for 48h

all staff should wear disposable gloves and an apron during any contact with patients known to have C. difficile
hand washing is also essential

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40
Q

pathophysiology of coeliac disease

A

autoimmune condition caused by sensitivity to the protein gluten
Repeated exposure leads to villous atrophy which in turn causes malabsorption

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41
Q

features of coeliac disease

A

Chronic or intermittent diarrhoea
Failure to thrive or faltering growth (in children)
Persistent or unexplained gastrointestinal symptoms including nausea and vomiting
Prolonged fatigue (‘tired all the time’)
Recurrent abdominal pain, cramping or distension
Sudden or unexpected weight loss
Unexplained iron-deficiency anaemia, or other unspecified anaemia

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42
Q

complications in coeliac disease

A

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

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43
Q

investigation findings in coeliac disease

A

tissue transglutaminase (TTG) antibodies (IgA) are first-choice according to NICE
endomyseal antibody (IgA) - for selective IgA deficiency

Endoscopic duodenal biopsy
villous atrophy
crypt hyperplasia
increase in intraepithelial lymphocytes
lamina propria infiltration with lymphocytes

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43
Q

management of coeliac disease

A

gluten free diet - no wheat, barley, rye, oats

5 yearly pneumococcal infection

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44
Q

types of colon cancer

A

sporadic (95%)
hereditary non-polyposis colorectal carcinoma (HNPCC, 5%)
familial adenomatous polyposis (FAP, <1%)

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45
Q

features of lynch syndrome (HNPCC)

A

autosomal dominant condition

most common form of inherited colon cancer - 90% develop cancer, proximal colon, poorly differentiated and highly aggressive

The most common genes involved are:
MSH2 (60% of cases)
MLH1 (30%)

increased risk of endometrial cancer

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46
Q

amsterdam criteria

A

aids diagnosis of lynch syndrome HNPCC

at least 3 family members with colon cancer
the cases span at least two generations
at least one case diagnosed before the age of 50 years

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47
Q

features of familial adenomatous polyposis

A

rare autosomal dominant condition
leads to the formation of hundreds of polyps by the age of 30-40
inevitably develop carcinoma

due to a mutation in a tumour suppressor gene called adenomatous polyposis coli gene (APC) Chr5

also at risk from duodenal tumours

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48
Q

features of gardner’s syndrome

A

osteomas of the skull and mandible, retinal pigmentation, thyroid carcinoma and epidermoid cysts on the skin

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49
Q

management of constipation

A

investigate and exclude any secondary causes, consider red flag symptoms

exclude any faecal impaction
advice on lifestyle measures

first-line laxative: bulk-forming laxative first-line, such as ispaghula

second-line: osmotic laxative, such as a macrogol

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50
Q

features of crohns syndrome

A

form of inflammatory bowel disease
commonly affects the terminal ileum and colon

inflammation occurs in all layers, down to the serosa - strictures, fistulas and adhesions

pt present with non-specific sx, diarrhoea (crohns colitis - bloody diarrhoea), abdo pain, perianal disease, extra-intestinal features

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51
Q

investigation findings in crohns disease

A

raised CRP
anaemia
low vitamin B12 and vitamin D

increased faecal calprotectin

colonoscopy - deep ulcers, skip lesions
histology - goblet cells, granulomas

small bowel enema
strictures: ‘Kantor’s string sign’
proximal bowel dilation
‘rose thorn’ ulcers
fistulae

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52
Q

management of crohns disease

A

induce remission
glucocorticoids
enteral feeding
5-ASA - second line to glucocorticoids
azathioprine/mercaptopurine - add on to induce remission

maintaining
stop smoking
azathioprine, mercaptopurine to maintain remission

surgery

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53
Q

causes of diarrhoea

A

acute - gastroenteritis, diverticulitis, abx, constipation overflow

chronic - IBS, IBD, colorectal cancer, coeliac

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54
Q

features of diverticulitis

A

left iliac fossa pain and tenderness
anorexia, nausea and vomiting
diarrhoea
features of infection (pyrexia, raised WBC and CRP)

Complications of diverticulitis include:
abscess formation
peritonitis
obstruction
perforation

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55
Q

management of diverticulitis

A

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

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56
Q

drugs which may induce liver disease

A

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

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57
Q

drugs which cause cholestasis

A

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

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58
Q

indications for urgent referral to endoscopy

A

All patients who’ve got dysphagia

All patients who’ve got an upper abdominal mass consistent with stomach cancer

Patients aged >= 55 years who’ve got weight loss, AND any of the following:
upper abdominal pain
reflux
dyspepsia

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59
Q

indications for non-urgent referral to endoscopy

A

Patients with haematemesis

Patients aged >= 55 years who’ve got:
treatment-resistant dyspepsia or
upper abdominal pain with low haemoglobin levels or
raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain

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60
Q

managing patients with undiagnosed dyspepsia

A
  1. Review medications for possible causes of dyspepsia
  2. Lifestyle advice
  3. Trial of full-dose proton pump inhibitor for one month OR a ‘test and treat’ approach for H. pylori
    (carbon-13 urea breath test or a stool antigen test)
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61
Q

causes of dysphagia

A

Extrinsic
Mediastinal masses
Cervical spondylosis

Oesophageal wall
Achalasia
Diffuse oesophageal spasm
Hypertensive lower oesophageal sphincter

Intrinsic
Tumours
Strictures
Oesophageal web
Schatzki rings

Neurological
CVA
Parkinson’s disease
Multiple Sclerosis
Brainstem pathology
Myasthenia Gravis

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62
Q

role of ferritin

A

binds iron and stores it to be released in a controlled fashion at sites where iron is required

may be synthesised in increased quantities in situations with inflammation

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63
Q

causes of increased ferritin

A

> 300 µg/L in men/postmenopausal women and > 200 µµg/L in premenopausal women

ferritin++ with iron overload (10%) - primary iron overload (hereditary haemochromatosis), secondary iron overload (following repeated transfusions)

ferritin++ without iron overload - Inflammation (due to ferritin being an acute phase reactant)
Alcohol excess
Liver disease
Chronic kidney disease
Malignancy

64
Q

action of transferrin

A

best test to see whether iron overload is present is transferrin saturation
normal transferrin of < 45% in females and < 50% in males exclude iron overload.

Transferrin is a protein produced by the liver. It regulates the absorption of iron into the blood. TIBC relates to the amount of transferrin in your blood that’s available to attach to iron

65
Q

investigating gallstones

A

colicky right upper quadrant pain that occurs postprandially

abdominal ultrasound - may be repeated

liver function tests

for bile duct stones - MRCP, intraoperative imaging

66
Q

managing gallstones

A

asymptomatic gallstones in gallbladder - common, dont require treatment

symptomatic gallstones - lap cholecystectomy

bile duct stones - surgical management - ERCP

67
Q

features of gastric cancer

A

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)

68
Q

investigation findings of gastric cancer

A

diagnosis: oesophago-gastro-duodenoscopy with biopsy - signet ring cells

staging - CT

69
Q

management of gastric cancer

A

surgical options depend on the extent and side but include:
endoscopic mucosal resection
partial gastrectomy
total gastrectomy
chemotherapy

70
Q

management for oesophagitis on endoscopy

A

full dose proton pump inhibitor (PPI) for 1-2 months
if response then low dose treatment as required
if no response then double-dose PPI for 1 month

71
Q

features of gilbert syndrome

A

autosomal recessive condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase

unconjugated hyperbilirubinaemia
jaundice if intercurrent stress

72
Q

investigations and management of gilberts syndrome

A

rise in bilirubin following prolonged fasting or IV nicotinic acid

no treatment required

73
Q

definition and features of haemochromatosis

A

autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation - HFE gene, Ch6

fatigue, erectile dysfunction and arthralgia
‘bronze’ skin pigmentation
diabetes mellitus
liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
cardiac failure (2nd to dilated cardiomyopathy)
hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)

74
Q

complications of haemochromatosis

A

reversible
Cardiomyopathy
Skin pigmentation

irreversible
Liver cirrhosis**
Diabetes mellitus
Hypogonadotrophic hypogonadism
Arthropathy

75
Q

iron profile in haemochromatosis

A

transferrin saturation > 55% in men or > 50% in women
raised ferritin (e.g. > 500 ug/l) and iron
low TIBC

transferrin saturation - most useful marker

76
Q

management of haemochromatosis

A

venesection is the first-line treatment
monitoring adequacy of venesection: transferrin saturation kept below 50%, serum ferritin concentration below 50 ug/l
desferrioxamine may be used second-line

77
Q

eradication of helicobacter pylori

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

78
Q

tests used in helicobacter pylori

A

urea breath test - consume a drink containing carbon isotope 13 enriched urea

rapid urease test (CLO) - mix biopsy sample with urea and pH indicator

serum antibody - positive after eradication

culture of gastric biopsy

stool antigen test

79
Q

features of hepatic encephalopathy

A

confusion, altered GCS (see below)
asterix: ‘liver flap’, arrhythmic negative myoclonus with a frequency of 3-5 Hz
constructional apraxia: inability to draw a 5-pointed star
triphasic slow waves on EEG
raised ammonia level (not commonly measured anymore)

80
Q

grades of hepatic encephalopathy

A

Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma

81
Q

management of hepatic encephalopathy

A

treat any underlying precipitating cause

lactulose first-line (promotes excretion of ammonia)

addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy

82
Q

hepatitis b serology

A

HBsAG - acute disease
HBsAG >6m - chronic disease
anti HBs - implies immunity, negative in chronic disease
anti HBc - previous or current infection
HbeAg - marker of HBV replication and infectivity

83
Q

features of biliary colic

A

RUQ pain, intermittent, usually begins abruptly and subsides gradually. Attacks often occur after eating. Nausea is common.

83
Q

features of acute cholecystitis

A

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)

84
Q

features of ascending cholangitis

A

fever (rigors are common)
RUQ pain
jaundice

85
Q

features of cholangiocarcinoma

A

Persistent biliary colic symptoms, associated with anorexia, jaundice and weight loss. A palpable mass in the right upper quadrant (Courvoisier sign), periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen

86
Q

features of acute pancreatitis

A

Usually due to alcohol or gallstones
Severe epigastric pain
Vomiting is common
Examination may reveal tenderness, ileus and low-grade fever
Periumbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign) is described but rare

87
Q

features of hepatocellular carcinoma

A

ends to present late
features of liver cirrhosis or failure may be seen: jaundice, ascites, RUQ pain, hepatomegaly, pruritus, splenomegaly
possible presentation is decompensation in a patient with chronic liver disease
raised AFP

88
Q

risk factors for developing hepatocellular carcinoma

A

liver cirrhosis, for example secondary to hepatitis B & C, alcohol, haemochromatosis and primary biliary cirrhosis
alpha-1 antitrypsin deficiency
hereditary tyrosinosis
glycogen storage disease
aflatoxin
drugs: oral contraceptive pill, anabolic steroids

89
Q

management of hepatocellular carcinoma

A

early disease: surgical resection
liver transplantation
radiofrequency ablation
transarterial chemoembolisation
sorafenib: a multikinase inhibitor

90
Q

causes of hepatomegaly

A

Cirrhosis: if early disease, later liver decreases in size. Associated with a non-tender, firm liver
Malignancy: metastatic spread or primary hepatoma. Associated with a hard, irregular. liver edge
Right heart failure: firm, smooth, tender liver edge. May be pulsatile

91
Q

definition of hepatorenal syndrome

A

vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance causing underfilling of kidneys, activating RAAS, causing renal vasoconstriction

92
Q

classification of hepatorenal syndrome

A

type 1
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

type 2
Slowly progressive
Prognosis poor, but patients may live for longer

93
Q

management of hepatorenal syndrome

A

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

94
Q

main differences between crohns and UC

A

crohns - weight loss, upper GI symptoms, gallstones, fistulas, perianal signs, increased goblet cells, granulomas, deep ulcers, skip lesions

UC - bloody diarrhoea, LLQ pain, tenesmus, PSC, colorectal ca risk, continuous disease, no inflammation beyond submucosa, crypt abscesses , pseudopolyps

95
Q

inherited causes of jaundice

A

Unconjugated hyperbilirubinaemia
Gilbert’s syndrome
Crigler-Najjar syndrome

Conjugated hyperbilirubinaemia Dubin-Johnson syndrome
Rotor syndrome

96
Q

iron studies interpretation

A

Total iron binding capacity (TIBC)
transferrin
raised in iron deficiency anaemia (IDA)
raised in pregnancy and by oestrogen

Transferrin saturation
calculated by serum iron / TIBC

Ferritin
raised in inflammatory disorders
low in IDA

97
Q

features of acute mesenteric ischaemia

A

typically caused by an embolism resulting in occlusion of an artery which supplies the small bowel, for example the superior mesenteric artery

hx AF

abdo pain severe, of sudden onset and out-of-keeping with physical exam findings.

98
Q

management of acute mesenteric ischaemia

A

urgent surgery is usually required
poor prognosis, especially if surgery delayed

99
Q

features of chronic mesenteric ischaemia

A

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.

100
Q

features of ischaemic colitis

A

cute but transient compromise in the blood flow to the large bowel - may lead to inflammation, ulceration and haemorrhage.

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.

‘thumbprinting’ on AXR due to mucosal oedema/haemorrhage

supprotive management

101
Q

cause of ischaemic hepatitis

A

diffuse hepatic injury resulting from acute hypoperfusion

has inciting event e.g., cardiac arrest
market increase in aminotransferase >1000

102
Q

diagnosis of liver cirrhosis

A

transient elastography - fibroscan - measures the ‘stiffness’ of the liver which is a proxy for fibrosis

fibroscan offered to:
people with hepatitis C virus infection
men drinking >50 units of alcohol per week
women drinking >35 units of alcohol per week
people diagnosed with alcohol-related liver disease

upper endoscopy - check for varices in new cirrhosis diagnoses
liver USS + AFP every 6m to check for HCC

103
Q

definition of malnutrition

A

a Body Mass Index (BMI) of less than 18.5; or
unintentional weight loss greater than 10% within the last 3-6 months; or
a BMI of less than 20 and unintentional weight loss greater than 5% within the last 3-6 months

screening using MUST

104
Q

management of malnutrition

A

dietician support if the patient is at high-risk
a ‘food-first’ approach with clear instructions (e.g. ‘add full-fat cream to mashed potato’), rather than just prescribing oral nutritional supplements (ONS) such as Ensure
if ONS are used they should be taken between meals, rather than instead of meals

105
Q

what is melanosis coli

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

106
Q

mechanism of metabolic alkalosis

A

activation of renin-angiotensin II-aldosterone (RAA)

aldosterone causes reabsorption of Na+ in exchange for H+ in the distal convoluted tubule

ECF depletion (vomiting, diuretics) → Na+ and Cl- loss → activation of RAA system → raised aldosterone levels
in hypokalaemia, K+ shift from cells → ECF, alkalosis is caused by shift of H+ into cells to maintain neutrality

107
Q

features of oesophageal adenocarcinoma

A

most common in UK/US
affects lower third
RF -
GORD
Barrett’s oesophagus
smoking
obesity

108
Q

features of oesophageal SCC

A

common in developing world
affects upper 2/3

RF
smoking
alcohol
achalasia
Plummer-Vinson syndrome
diets rich in nitrosamines

109
Q

investigation findings of oesophageal carcinoma

A

Upper GI endoscopy with biopsy

Endoscopic ultrasound - for locoregional staging

CT CAP - initial staging

110
Q

management of oesophageal carcinoma

A

operable disease T1N0M0 - managed by surgical resection

risk - anastomotic leak

adjuvant chemotherapy

110
Q

features of plummer vinson syndrome

A

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

Treatment includes iron supplementation and dilation of the webs

111
Q

features of pancreatic cancer

A

classically painless jaundice
(pale stools, dark urine, and pruritus
cholestatic liver function tests)
abdominal masses:
hepatomegaly: due to metastases
gallbladder
epigastric mass
non-specific - anorexia, weight loss, epigastric pain
loss of exocrine function - steatorrhoea
loss of endocrine function (e.g. diabetes mellitus)

112
Q

investigations in pancreatic cancer

A

high res CT
‘double duct’ sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts

113
Q

management of pancreatic cancer

A

a Whipple’s resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas
adjuvant chemo
ERCP with stenting for palliation

114
Q

management of acute peptic ulcer disease

A

presenting features include haematemesis, melaena, hypotension, tachycardia

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

115
Q

investigating perforated peptic ulcers

A

erect CXR - when pt presents with acute upper abdo pain
free air under diaphragm

116
Q

causes of pernicious anaemia

A

antibodies to intrinsic factor +/- gastric parietal cells

RF - autoimmune disorders: thyroid disease, type 1 diabetes mellitus, Addison’s, rheumatoid and vitiligo, females

117
Q

features of pernicious anaemia

A

fx of anaemia

neurological features
peripheral neuropathy: ‘pins and needles’, numbness. Typically symmetrical and affects the legs more than the arms
subacute combined degeneration of the spinal cord: progressive weakness, ataxia and paresthesias that may progress to spasticity and paraplegia
neuropsychiatric features: memory loss, poor concentration, confusion, depression, irritabiltiy

mild jaundice: combined with pallor results in a ‘lemon tinge’
glossitis → sore tongue

118
Q

investigation findings in pernicious anaemia

A

macrocytic anaemia
hypersegmented polymorphs on blood film
low WCC and platelets may also be seen

a vitamin B12 level of >= 200 nh/L is generally considered to be normal

anti intrinsic factor antibodies: sensivity is only 50% but highly specific for pernicious anaemia (95-100%)

119
Q

management of pernicious anaemia

A

IM vitamin B12 replacement

no neurological features: 3 injections per week for 2 weeks followed by 3 monthly treatment of vitamin B12 injections
more frequent if with neurological features

folic acid supplementation

120
Q

features of peutz-jeghers syndrome

A

AD condition

numerous hamartomatous polyps in the gastrointestinal tract - may cause small bowel obstruction or GI bleeds

pigmented freckles on the lips, face, palms and soles

conservative mx

121
Q

features of pharyngeal pouch

A

dysphagia
regurgitation
aspiration
neck swelling which gurgles on palpation
halitosis

seen via barium swallow combined with dynamic video fluoroscopy

122
Q

pathophysiology of primary biliary cholangitis

A

chronic liver disorder of middle-aged females

interlobular bile ducts are damaged by chronic inflammation -> progressive cholestasis, may cause cirrhosis

assx
Sjogren’s syndrome (seen in up to 80% of patients)
rheumatoid arthritis
systemic sclerosis
thyroid disease

123
Q

features of primary biliary cholangitis

A

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

124
Q

investigation findings in primary biliary cholangitis

A

anti-mitochondrial antibodies (AMA) M2
anti smooth muscle antibodies
raised serum IgM

125
Q

management of primary biliary cholangitis

A

ursodeoxycholic acid - slows disease progression and improves symptoms

cholestyramine for pruritis

fat-soluble vitamin supplementation

liver transplant

126
Q

pathophysiology of primary sclerosing cholangitis

A

biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts.

127
Q

features and investigation findings of primary sclerosing cholangitis

A

cholestasis
jaundice, pruritus
raised bilirubin + ALP
right upper quadrant pain
fatigue

ERCP/MRCP show multiple biliary strictures giving a ‘beaded’ appearance
pANCA+

risk of cholangiocarcinoma

128
Q

action of PPI

A

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

129
Q

management of pyogenic liver abscesses

A

causative organisms: Staphylococcus aureus in children, Escherichia coli in adults

management
percutaneous drainage

amoxicillin + ciprofloxacin + metronidazole

if penicillin allergic: ciprofloxacin + clindamycin

130
Q

metabolic abnormalities seen in refeeding syndrome

A

hypophosphataemia - hallmark symptom of refeeding syndrome - causes significant muscle weakness, including myocardial muscle (→ cardiac failure) and the diaphragm (→ respiratory failure)

hypokalaemia

hypomagnesaemia: may predispose to torsades de pointes

abnormal fluid balance

131
Q

pathophysiology of refeeding syndrome

A

Shift from Fat to Carbohydrate Metabolism - reintroduction of carbohydrates leads to a shift from fat to carbohydrate metabolism - activates insulin secretion, increases cellular uptake of glucose

IC movement of phosphate - insulin stimulates IC movement of phosphate

reduced phosphate stores - chronic malnutrition causes depletion of phosphate stores - refeeding increases demand for phosphate&raquo_space; supply, leading to hypophosphatemia

132
Q

scoring systems used in liver cirrhosis

A

child-pugh - bilirubin, albumin, PT, encephalopathy, ascites - to severity of liver cirrhosis

MELD - combination of a patient’s bilirubin, creatinine, and the international normalized ratio (INR) to predict survival - increasing use for those on transplant waiting list

132
Q

features and diagnosis of small bowel bacterial overgrowth syndrome

A

excessive amounts of bacteria in the small bowel causing chronic diarrhoea, bloating, flatulence, abdo pain

diagnosed by hydrogen breath test

treat with rifamixin

133
Q

features of spontaneous bacterial peritonitis

A

usually seen in patients with ascites secondary to liver cirrhosis

Features
ascites
abdominal pain
fever

134
Q

diagnosis of spontaneous bacterial peritonitis

A

paracentesis - neutrophils >250 cells/ul

usually caused by E. coli - treat with IV cefotaxime

135
Q

indications for spontaneous bacterial peritonitis prophylactic therapy

A

patients 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’

136
Q

endoscopy findings in ulcerative colitis

A

colonoscopy + biopsy is generally done for diagnosis - avoid if severe colitis due to perforation risk

red, raw mucosa, bleeds easily
no inflammation beyond submucosa (unless fulminant disease)
widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (‘pseudopolyps’)
inflammatory cell infiltrate in lamina propria
neutrophils migrate through the walls of glands to form crypt abscesses
depletion of goblet cells and mucin from gland epithelium
granulomas are infrequent

137
Q

barium enema findings in ulcerative colitis

A

loss of haustrations
superficial ulceration, ‘pseudopolyps’
long standing disease: colon is narrow and short -‘drainpipe colon’

138
Q

classification of severity of ulcerative colitis

A

The severity of UC is usually classified as being mild, moderate or severe:
mild: < 4 stools/day, only a small amount of blood
moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)

139
Q

inducing remission in ulcerative colitis

A

proctitis - topical (rectal) aminosalicylate (+ oral aminosalicylate after 4w, add topical/oral corticosteroid if still not effective)

left sided - topical aminosalicylate, + high dose oral aminosalicylate after 4w, add oral corticosteroid and stop topical tx if remission not achieved

extensive - topical aminosalicylate + high dose oral aminosalicylate, add oral corticosteroid and stop topical tx if remission not achieved
severe colitis - IPT, IV steroids

140
Q

maintaining remission in ulcerative colitis

A

Following a mild-to-moderate ulcerative colitis flare
proctitis and proctosigmoiditis -
topical aminosalicylate or
oral aminosalicylate or both

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

141
Q

prophylactic measures for variceal haemorrhage

A

propranolol
reduced rebleeding and mortality compared to placebo
endoscopic variceal band ligation (EVL)
TIPSS

141
Q

managment of variceal haemorrhage

A

ABC
patients should be resuscitated prior to endoscopy
blood transfusion may be needed
correct clotting: FFP, vitamin K, platelet transfusions may be required
vasoactive agents: terlipressin
prophylactic IV antibiotics
give terlipressin and abx before endoscopy
endoscopic variceal band ligation
Sengstaken-Blakemore tube if uncontrolled haemorrhage

142
Q

function of vitamin A and deficiency

A

Vitamin A is a fat soluble vitamin - retinol

Functions
converted into retinal, an important visual pigment
important in epithelial cell differentiation
antioxidant

Consequences of vitamin A deficiency
night blindness

143
Q

function of vitamin B1 (thiamine) and deficiency

A

important in the catabolism of sugars and aminoacids

Conditions associated with thiamine deficiency:
Wernicke’s encephalopathy: nystagmus, ophthalmoplegia and ataxia
Korsakoff’s syndrome: amnesia, confabulation
dry beriberi: peripheral neuropathy
wet beriberi: dilated cardiomyopathy

144
Q

function of vitamin B3 (niacin) and deficiency

A

a water soluble vitamin of the B complex group. It is a precursor to NAD+ and NADP+ and hence plays an essential metabolic role in cells.

Consequences of niacin deficiency:
pellagra: dermatitis, diarrhoea, dementia

145
Q

function of vitamin B6 (pyridoxine) and deficiency

A

water soluble vitamin of the B complex group
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

146
Q

functions of vitamin C (ascorbic acid)

A

antioxidant
collagen synthesis: acts as a cofactor for enzymes that are required for the hydroxylation proline and lysine in the synthesis of collagen
facilitates iron absorption
cofactor for norepinephrine synthesis

147
Q

features of vitamin C deficiency

A

Vitamin C deficiency (scurvy) leads to defective synthesis of collagen resulting in capillary fragility (bleeding tendency) and poor wound healing

Features vitamin C deficiency
gingivitis, loose teeth
poor wound healing
bleeding from gums, haematuria, epistaxis
general malaise

148
Q

features of whipple’s disease

A

a rare multi-system disorder caused by Tropheryma whippelii infection

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

149
Q

investigations and management of whipple’s disease

A

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

management - oral co-trimoxazole 1 year has lowest relapse rate

150
Q

definition of wilson’s disease

A

autosomal recessive disorder characterised by excessive copper deposition in the tissues

increased copper absorption from the small intestine and decreased hepatic copper excretion

defect in the ATP7B gene, Chr13

151
Q

features of wilson’s disease

A

Features result from excessive copper deposition in the tissues, especially the brain, liver and cornea:

liver: hepatitis, cirrhosis

neurological:
basal ganglia degeneration - speech, behavioural and psychiatric problems are often the first manifestations
also: asterixis, chorea, dementia, parkinsonism

Kayser-Fleischer rings - green-brown rings in iris peripheral due to copper deposition

RTA

haemolysis

blue nails

152
Q

investigation findings for wilson’s disease

A

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 serum copper is increased

increased 24hr urinary copper excretion

the diagnosis is confirmed by genetic analysis of the ATP7B gene

153
Q

treatment of wilson’s disease

A

penicillamine - copper chelator

154
Q

features of zollinger ellison syndrome

A

excessive levels of gastrin secondary to a gastrin-secreting tumour, usually in 1st part of duodenum or pancreas

assx MEN type 1

multiple gastroduodenal ulcers
diarrhoea
malabsorption

155
Q

investigations for zollinger ellison syndrome

A

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

Finals (27 decks)

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