Gastroenterology Flashcards

(161 cards)

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
type I AI hepatitis antibodies
Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA) Affects both adults and children
25
type II AI hepatitis antibodies
Anti-liver/kidney microsomal type 1 antibodies (LKM1) Affects children only
26
type III AI hepatitis antibodies
Soluble liver-kidney antigen Affects adults in middle-age
27
RF for barrett's oesophagus
gastro-oesophageal reflux disease (GORD) is the single strongest risk factor male gender (7:1 ratio) smoking central obesity
28
management of barrett's oesophagus
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)
29
causes of bile acid malabsorption
primary - due to excessive production of bile acid secondary - due to an underlying gastrointestinal disorder ( ileal disease e.g., crohn's, cholecystectomy, coeliac disease)
30
management of bile acid malabsorption
bile acid sequestrants e.g. cholestyramine can lead to steatorrhoea and vitamin A, D, E, K malabsorption.
31
definition and causes of budd-chiari syndrome
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
32
features of budd-chiari syndrome
polycythaemia rubra vera thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies pregnancy combined oral contraceptive pill: accounts for around 20% of cases ultrasound with Doppler flow studies
33
diagnosis of carcinoid tumours
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
34
features of carcinoid syndrome
flushing (often the earliest symptom) diarrhoea bronchospasm hypotension right heart valvular stenosis (left heart can be affected in bronchial carcinoid) other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing's syndrome pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tumour
35
management of carcinoid syndrome
somatostatin analogues e.g. octreotide diarrhoea: cyproheptadine may help
36
side effects of cholestyramine
abdominal cramps and constipation decreases absorption of fat-soluble vitamins cholesterol gallstones may raise level of triglycerides
37
features of clostroidiodes difficile
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
38
diagnosis and management of c diff
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
39
isolation period for c diff patients
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
40
pathophysiology of coeliac disease
autoimmune condition caused by sensitivity to the protein gluten Repeated exposure leads to villous atrophy which in turn causes malabsorption
41
features of coeliac disease
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
42
complications in coeliac disease
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
43
investigation findings in coeliac disease
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
43
management of coeliac disease
gluten free diet - no wheat, barley, rye, oats 5 yearly pneumococcal infection
44
types of colon cancer
sporadic (95%) hereditary non-polyposis colorectal carcinoma (HNPCC, 5%) familial adenomatous polyposis (FAP, <1%)
45
features of lynch syndrome (HNPCC)
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
46
amsterdam criteria
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
47
features of familial adenomatous polyposis
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
48
features of gardner's syndrome
osteomas of the skull and mandible, retinal pigmentation, thyroid carcinoma and epidermoid cysts on the skin
49
management of constipation
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
50
features of crohns syndrome
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
51
investigation findings in crohns disease
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
52
management of crohns disease
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
53
causes of diarrhoea
acute - gastroenteritis, diverticulitis, abx, constipation overflow chronic - IBS, IBD, colorectal cancer, coeliac
54
features of diverticulitis
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
55
management of diverticulitis
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
56
drugs which may induce liver disease
paracetamol sodium valproate, phenytoin MAOIs halothane anti-tuberculosis: isoniazid, rifampicin, pyrazinamide statins alcohol amiodarone methyldopa nitrofurantoin
57
drugs which cause cholestasis
combined oral contraceptive pill antibiotics: flucloxacillin, co-amoxiclav, erythromycin* anabolic steroids, testosterones phenothiazines: chlorpromazine, prochlorperazine sulphonylureas fibrates rare reported causes: nifedipine
58
indications for urgent referral to endoscopy
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
59
indications for non-urgent referral to endoscopy
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
60
managing patients with undiagnosed dyspepsia
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)
61
causes of dysphagia
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
62
role of ferritin
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
63
causes of increased ferritin
> 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
action of transferrin
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
investigating gallstones
colicky right upper quadrant pain that occurs postprandially abdominal ultrasound - may be repeated liver function tests for bile duct stones - MRCP, intraoperative imaging
66
managing gallstones
asymptomatic gallstones in gallbladder - common, dont require treatment symptomatic gallstones - lap cholecystectomy bile duct stones - surgical management - ERCP
67
features of gastric cancer
abdominal pain typically vague, epigastric pain may present as dyspepsia weight loss and anorexia nausea and vomiting dysphagia: particularly if the cancer arises in the proximal stomach overt upper gastrointestinal bleeding is seen only in a minority of patients if lymphatic spread: left supraclavicular lymph node (Virchow's node) periumbilical nodule (Sister Mary Joseph's node)
68
investigation findings of gastric cancer
diagnosis: oesophago-gastro-duodenoscopy with biopsy - signet ring cells staging - CT
69
management of gastric cancer
surgical options depend on the extent and side but include: endoscopic mucosal resection partial gastrectomy total gastrectomy chemotherapy
70
management for oesophagitis on endoscopy
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
features of gilbert syndrome
autosomal recessive condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase unconjugated hyperbilirubinaemia jaundice if intercurrent stress
72
investigations and management of gilberts syndrome
rise in bilirubin following prolonged fasting or IV nicotinic acid no treatment required
73
definition and features of haemochromatosis
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
complications of haemochromatosis
reversible Cardiomyopathy Skin pigmentation irreversible Liver cirrhosis** Diabetes mellitus Hypogonadotrophic hypogonadism Arthropathy
75
iron profile in haemochromatosis
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
management of haemochromatosis
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
eradication of helicobacter pylori
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
tests used in helicobacter pylori
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
features of hepatic encephalopathy
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
grades of hepatic encephalopathy
Grade I: Irritability Grade II: Confusion, inappropriate behaviour Grade III: Incoherent, restless Grade IV: Coma
81
management of hepatic encephalopathy
treat any underlying precipitating cause lactulose first-line (promotes excretion of ammonia) addition of rifaximin for the secondary prophylaxis of hepatic encephalopathy
82
hepatitis b serology
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
features of biliary colic
RUQ pain, intermittent, usually begins abruptly and subsides gradually. Attacks often occur after eating. Nausea is common.
83
features of 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)
84
features of ascending cholangitis
fever (rigors are common) RUQ pain jaundice
85
features of cholangiocarcinoma
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
features of acute pancreatitis
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
features of hepatocellular carcinoma
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
risk factors for developing hepatocellular carcinoma
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
management of hepatocellular carcinoma
early disease: surgical resection liver transplantation radiofrequency ablation transarterial chemoembolisation sorafenib: a multikinase inhibitor
90
causes of hepatomegaly
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
definition of hepatorenal syndrome
vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance causing underfilling of kidneys, activating RAAS, causing renal vasoconstriction
92
classification of hepatorenal syndrome
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
management of hepatorenal syndrome
vasopressin analogues, for example terlipressin, have a growing evidence base supporting their use. They work by causing vasoconstriction of the splanchnic circulation volume expansion with 20% albumin transjugular intrahepatic portosystemic shunt
94
main differences between crohns and UC
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
inherited causes of jaundice
Unconjugated hyperbilirubinaemia Gilbert's syndrome Crigler-Najjar syndrome Conjugated hyperbilirubinaemia Dubin-Johnson syndrome Rotor syndrome
96
iron studies interpretation
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
features of acute mesenteric ischaemia
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
management of acute mesenteric ischaemia
urgent surgery is usually required poor prognosis, especially if surgery delayed
99
features of chronic mesenteric ischaemia
Chronic mesenteric ischaemia is a relatively rare clinical diagnosis due to it's non-specific features and may be thought of as 'intestinal angina'. Colickly, intermittent abdominal pain occurs.
100
features of ischaemic colitis
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
cause of ischaemic hepatitis
diffuse hepatic injury resulting from acute hypoperfusion has inciting event e.g., cardiac arrest market increase in aminotransferase >1000
102
diagnosis of liver cirrhosis
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
definition of malnutrition
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
management of malnutrition
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
what is melanosis coli
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
mechanism of metabolic alkalosis
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
features of oesophageal adenocarcinoma
most common in UK/US affects lower third RF - GORD Barrett's oesophagus smoking obesity
108
features of oesophageal SCC
common in developing world affects upper 2/3 RF smoking alcohol achalasia Plummer-Vinson syndrome diets rich in nitrosamines
109
investigation findings of oesophageal carcinoma
Upper GI endoscopy with biopsy Endoscopic ultrasound - for locoregional staging CT CAP - initial staging
110
management of oesophageal carcinoma
operable disease T1N0M0 - managed by surgical resection risk - anastomotic leak adjuvant chemotherapy
110
features of plummer vinson syndrome
Triad of: dysphagia (secondary to oesophageal webs) glossitis iron-deficiency anaemia Treatment includes iron supplementation and dilation of the webs
111
features of pancreatic cancer
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
investigations in pancreatic cancer
high res CT 'double duct' sign - the presence of simultaneous dilatation of the common bile and pancreatic ducts
113
management of pancreatic cancer
a Whipple's resection (pancreaticoduodenectomy) is performed for resectable lesions in the head of pancreas adjuvant chemo ERCP with stenting for palliation
114
management of acute peptic ulcer disease
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
investigating perforated peptic ulcers
erect CXR - when pt presents with acute upper abdo pain free air under diaphragm
116
causes of pernicious anaemia
antibodies to intrinsic factor +/- gastric parietal cells RF - autoimmune disorders: thyroid disease, type 1 diabetes mellitus, Addison's, rheumatoid and vitiligo, females
117
features of pernicious anaemia
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
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investigation findings in pernicious anaemia
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%)
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management of pernicious anaemia
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
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features of peutz-jeghers syndrome
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
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features of pharyngeal pouch
dysphagia regurgitation aspiration neck swelling which gurgles on palpation halitosis seen via barium swallow combined with dynamic video fluoroscopy
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pathophysiology of primary biliary cholangitis
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
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features of primary biliary cholangitis
early: may be asymptomatic (e.g. raised ALP on routine LFTs) or fatigue, pruritus cholestatic jaundice hyperpigmentation, especially over pressure points around 10% of patients have right upper quadrant pain xanthelasmas, xanthomata also: clubbing, hepatosplenomegaly late: may progress to liver failure
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investigation findings in primary biliary cholangitis
anti-mitochondrial antibodies (AMA) M2 anti smooth muscle antibodies raised serum IgM
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management of primary biliary cholangitis
ursodeoxycholic acid - slows disease progression and improves symptoms cholestyramine for pruritis fat-soluble vitamin supplementation liver transplant
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pathophysiology of primary sclerosing cholangitis
biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts.
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features and investigation findings of primary sclerosing cholangitis
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
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action of PPI
Proton pump inhibitors (PPI) cause irreversible blockade of H+/K+ ATPase of the gastric parietal cell.
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management of pyogenic liver abscesses
causative organisms: Staphylococcus aureus in children, Escherichia coli in adults management percutaneous drainage amoxicillin + ciprofloxacin + metronidazole if penicillin allergic: ciprofloxacin + clindamycin
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metabolic abnormalities seen in refeeding syndrome
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
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pathophysiology of refeeding syndrome
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 >> supply, leading to hypophosphatemia
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scoring systems used in liver cirrhosis
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
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features and diagnosis of small bowel bacterial overgrowth syndrome
excessive amounts of bacteria in the small bowel causing chronic diarrhoea, bloating, flatulence, abdo pain diagnosed by hydrogen breath test treat with rifamixin
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features of spontaneous bacterial peritonitis
usually seen in patients with ascites secondary to liver cirrhosis Features ascites abdominal pain fever
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diagnosis of spontaneous bacterial peritonitis
paracentesis - neutrophils >250 cells/ul usually caused by E. coli - treat with IV cefotaxime
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indications for spontaneous bacterial peritonitis prophylactic therapy
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'
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endoscopy findings in ulcerative colitis
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
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barium enema findings in ulcerative colitis
loss of haustrations superficial ulceration, 'pseudopolyps' long standing disease: colon is narrow and short -'drainpipe colon'
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classification of severity of ulcerative colitis
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)
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inducing remission in ulcerative colitis
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
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maintaining remission in ulcerative colitis
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
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prophylactic measures for variceal haemorrhage
propranolol reduced rebleeding and mortality compared to placebo endoscopic variceal band ligation (EVL) TIPSS
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managment of variceal haemorrhage
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
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function of vitamin A and deficiency
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
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function of vitamin B1 (thiamine) and deficiency
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
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function of vitamin B3 (niacin) and deficiency
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
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function of vitamin B6 (pyridoxine) and deficiency
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
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functions of vitamin C (ascorbic acid)
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
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features of vitamin C deficiency
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
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features of whipple's disease
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
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investigations and management of whipple's disease
jejunal biopsy - macrophages containing Periodic acid-Schiff (PAS) granules management - oral co-trimoxazole 1 year has lowest relapse rate
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definition of wilson's disease
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
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features of wilson's disease
Features result from excessive copper deposition in the tissues, especially the brain, liver and cornea: liver: hepatitis, cirrhosis neurological: basal ganglia degeneration - 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
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investigation findings for wilson's disease
slit lamp examination for Kayser-Fleischer rings reduced serum caeruloplasmin reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin) free serum copper is increased increased 24hr urinary copper excretion the diagnosis is confirmed by genetic analysis of the ATP7B gene
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treatment of wilson's disease
penicillamine - copper chelator
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features of zollinger ellison syndrome
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
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investigations for zollinger ellison syndrome
fasting gastrin levels: the single best screen test secretin stimulation test