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A final year of medicine > Gastroenterology/Hepatology > Flashcards

Gastroenterology/Hepatology Flashcards

1
Q

Mortality and recurrence for SBP?

A

Both high!

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2
Q

Causative organisms for SBP?

A

90% enteric e.g. E. coil, Klebsiella, Enterococcus

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3
Q

Pathophysiology of PBC?

A

Chronic granulomatous inflammation of small intra-hepatic ducts with progressive cholestasis, cirrhosis and portal HTN. Onset of jaundice is late sign and poor prognostic factor.

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4
Q

Abs in PBC?

A

98% are positive for AMA

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5
Q

Treatment of PBC?

A

Colestyramine and UDCA; only curative is OLT. UDCA does however reduce rate of progression to liver failure (reduces total bile acid pool)

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6
Q

Patho of PSC?

A

Non-malignant, non-bacterial inflammation and fibrosis of the intra- and extra-hepatic biliary tree. Common in men, frequently in UC.

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7
Q

Diagnosis of PSC?

A

MRCP or ERCP showing beaded appearance

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8
Q

Abs in PSC?

A

ANA, ASMA and ANCA may be positive, AMA is negative (unlike PBC)

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9
Q

Presentation of AIH?

A

25% with acute hepatitis or signs of fulminant AI disease e.g. rash, fever, malaise. The remainder present insidiously

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10
Q

Abs in AIH?

A

Three subtypes.

  1. = ASMA positive
  2. = anti-LKM (liver kidney microsomal)
  3. = anti-SLA (soluble liver antigen)
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11
Q

Risk factors for ascending cholangitis?

A

Biliary instrumentation e.g. ERCP, stents

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12
Q

What are biliary stents used for?

A

Treatment of obstructive jaundice in in-operable patients

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13
Q

Most common causative organisms for ascending cholangitis?

A

E. coli, Klebsiella, Enterobacter

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14
Q

What does the marginal artery of Drummond do?

A

Connects SMA and IMA

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15
Q

Three main branches of coeliac trunk?

A
  1. Common hepatic (branches to hepatic artery proper, right gastric and gastroduodenal)
  2. Left gastric artery (oesophageal and stomach branches)
  3. Splenic artery (short gastric branches)
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16
Q

Risk factors for glutathione depletion (and therefore paracetamol OD?)

A

Malnourishment, eating disorders, FTT/CF, AIDS, cachexia, alcoholism. Also enzyme induction by regular alcohol consumption or inducing drugs

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17
Q

Patho of paracetamol OD?

A

NAPQI formed when paracetamol oxidised. Glutathione conjugates this but is depleted (is natural anti-oxidant)

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18
Q

Extra-intestinal features of IB?

A
  1. Oral (ulcers [Crohns])
  2. Eyes (anterior uveitis, conjunctivitis and episcleritis)
  3. Joints (seronegative spondyloarthritis, sacroilitis, migratory polyarthritis)
  4. Skin (pyoderma gangrenosum [UC}, erythema nodosum, erythema multiforme (not CD), clubbing)
  5. Liver (PSC [UC])
  6. Anal (fissures)
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19
Q

Features of psoriatic arthritis?

A

Bilateral, symmetrical, deforming arthopathy of hands (as with RA) Can get dactylitis and arthritis mutilans.

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20
Q

Features of rheumatoid arthritis?

A

Bilateral, symmetrical, deforming arthopathy of hands. Can get joint erosions, ulnar deviation (subluxation), Z-thumb, swan-necking and boutoniere’s

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21
Q

Pattern of pain in diverticular disease?

A

Worsened by eating, relieved after bowel emptying

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22
Q

Complications of diverticular disease?

A

Abscess, perforation, obstruction

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23
Q

Features of carcinoid syndrome?

A

Carcinoid tumours are neuro-endocrine, serotonin-secreting, most frequently in TI. Primary often asymptomatic. If serotonin produced cannot be broken down by liver, get bronchospasm, diarrhoea, facial flushing, RHS valvular disease. Diagnose with raised 5-HIAA (serotonin metabolite). Treatment includes surgery, octreotide (somatostatin analogue)

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24
Q

Innervation of lower 1/3 of oesophagus?

A

Vagus (para) and sympathetic trunks

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25
Q

Where is copper deposited in Wilson’s?

A

Liver, basal ganglia, cornea hence signs inc. tremor, dementia.

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26
Q

Investigations in Wilsons?

A

Low serum copper, low caeruloplasmin, urinary copper increased, liver biopsy shows increased leels.

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27
Q

Treatment of Wilson’s?

A

Lifelong penicillamine as chelating agent, zinc as second line

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28
Q

Patho of A1AT deficiency?

A

A1AT inhibits enzymes from inflammatory cells. Get cirrhosis and respiratory pathology

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29
Q

Inheritance of haemochromatosis?

A

AR

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30
Q

Rx of haemochromatosis?

A

Venesection, OLT eventualy if severe

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31
Q

Penetrance of haemochromatosis?

A

Low. Few homozygotes will show symptoms, fewer still get cirrhosis

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32
Q

Treatment for NAFLD?

A

Weight loss, but not rapid as this increases fibrosis

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33
Q

Treatment of AIH?

A

Oral steroids, can add in azathioprine

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34
Q

What should be suspected in coeliac patients who initially respond to gluten-free diet then recur?

A

T-cell intestinal lymphoma

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35
Q

McBurney’s point is where?

A

A third of the way from ASIS to umbilicus. Landmark for location of appendix in most people. May not have tenderness here if appendix is retrocaecal or pelvic

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36
Q

Tinkling vs absent bowel sounds?

A

Tinkling suggests mechanical obstruction, absent suggests ileus

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37
Q

Features of Plummer-Vinson?

A

Progressive dysphagia, IDA, glossitis (get oesophageal webs). Treatment is iron replacement

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38
Q

Conditions predisposing to B12 deficiency?

A

Strict vegans and those with terminal ileum disease e.g. Crohns, coeliac, PA, chronic pancreatitis

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39
Q

Presentations of B12 deficiency?

A

Glossitis (beefy red tongue), jaundice, depression, psychosis, neuro e.g. peripheral neuropathy and combined degen. of SC

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40
Q

Management of b12 def?

A

If cause is dietary, then oral B12 supps; if malabsorption then IM

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41
Q

Which patients get hypomagnasaemia?

A

Severe diarrhoea, diuretic use, alcoholism, long-term PPI

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42
Q

Presentation of hypomagnasaemia?

A

Ataxia, parasthesia, seizures, tetany

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43
Q

Crypt abscesses are associated with?

A

UC!

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44
Q

Complications of long-term UC?

A

Colorectal cancer, toxic megacolon, PSC

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45
Q

Microscopic appearance of Crohns?

A

Mixed acute and chronic transmural inflammatory infilitrate with non-caseating granulomas

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46
Q

2ww for oesophageal/gastric cancer?

A
  1. Dysphagia

2. 55 and over, with weight loss and one of upper abdomina pain, reflux, dyspepsia

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47
Q

Management of Mallory-Weiss?

A

If stable and improves, can discharge. Do not need further investigation

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48
Q

Rule of 2s for Meckel’s?

A 
2% of population
2 inch-long diverticulum projecting from ileum
2 feet from IC valve
2 times more common in men than women
2 or more types of tissue can be present
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49
Q

What is Meckel’s a remnant of?

A

Vitello-intestinal duct

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50
Q

How does Meckel’s present?

A

Mostly asymptomatic, but can cause bowel obstruction, perforation or bleeding. This occurs because contains ectopic tissue such as gastric mucosa so secretes acid and ulcerates. DD appendicitis; must be excluded if appendix normal.

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51
Q

Raised anti-endomysial antibody?

A

Seen in coeliac

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52
Q

How does coeliac present?

A

Bloating, diarrhoea, weight loss, anorexia

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53
Q

Patho of coeliac?

A

Get chronic inflammation causing flattened villi and malabsorption, as have cross-reactivity between Abs to gluten and gliadin and SB antigens

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54
Q

What are anti-Jo Abs associated with?

A

Dermatomyositis and polymyositis

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55
Q

RFs for oesophageal cancer?

A

Smoking, alcohol, Barrett’s, Plummer-Vinson

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56
Q

What are the three Hep B antigens?

A

Surface (HBsAg), core (HBcAg), envelope (HBeAg). Surface tells you about disease/immunity, core not involved in active infection. Envelope results from breakdown of core antigen. Thought to imply high infectivity

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57
Q

Hep B serology?

A

Positive HBsAg titre means acute or chronic infection. Anti-HBs = immunised or resolved infection.
Anti-HBc is not protective but useful for timing. Anti-HBc IgM rises after 2 months and drops after six; IgG becomes positive after 4-6 months an remains positive lifelong i.e. chronic infection

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58
Q

Difference between incubation and chronic infection profiles for Hep B?

A

Both would have positive HBsAg and HBeAg, negative anti-HBsAg and anti-HBeAg. But IgG and IgM to HBcAg negative in incubation, while IgG is positive in chronic infection

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59
Q

What are ASCA and pANCA and relation to IBD?

A

ASCA is anti-Saccharomyces cerevisiae antibodies; present in serum of Crohns. p-ANCA associated with UC. Can be useful in diagnosis (especially where unclear)

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60
Q

What is abetalipoproteinaemia

A

AR disorder where lipoprotein synthesis is defective. Get fat malabsorption so deficient in fat-soluble vitamins (A, D, E, K). Vit E deficiency gives neuro symptoms (ataxia, cognitive decline). Vit A gives visual problems too. Vit D gives low calcium and phosphate.

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61
Q

How does methanol toxicity present?

A

Neuro: drowsiness, headaches, dizziness, ataxia, confusion. Later, get visual problems. Classically from drinking antifreeze. Get metabolic acidosis with high anion gap and low bicarb.

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62
Q

Treatment of methanol toxicity?

A

Fomepizole

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63
Q

Triad of Wernicke’s

A

Ataxia, opthalmoplegia, confusion. Preservation of pupillary responses

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64
Q

Presentation of Budd-Chiari?

A

Acute abdominal pan, rapidly developing ascites, elevated liver enzymes, enlarged caudate lobe on ultrasound, tender hepatomegaly. If IVC obstructed get prominent venous collaterals in the back and bipedal oedema

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65
Q

What is Budd-Chiari?

A

Hepatic venous outflow obstruction; thrombosis usually in hepatic vein but can be from hepatic venules to IVC entrance at RA

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66
Q

Management of Budd-Chiari?

A

Less severe = anticoagulation. Second line is angioplasty/thrombolysis.
Third line is TIPSS
Severe or refractory = OLT

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67
Q

Simultaneous ?pneumonia and biliary features?

A

Biliary disease can cause reactive effusion and pneumonia secondary to atelectasis of lower airways so exclude this first

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68
Q

Three things that stimulate gastric acid secretion?

A

ACh, gastrin, histamine

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69
Q

Three things that inhibit gastric acid secretion?

A

Somatostatin, secretin, cholecystokinin

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70
Q

Most common cause of nodular hepatomegaly?

A

Liver mets (from bowel or breast). Often only affect LFTs if over 50% involved or obstruct biliary tract

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71
Q

Pseudopolyps are associated with?

A

UC

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72
Q

Anti-dsDNA?

A

Associated with SLE

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73
Q

Two regions endemic for Hep B?

A

Sub-Saharan Africa, East Asia

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74
Q

Treating bleeding ulcer?

A

Injected with adrenaline and clipped

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75
Q

Complications of ERCP?

A

Acute pancreatitis, oesophageal perforation, anaphylaxis, papillary stenosis (late complication), duodenal pneumatosis

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76
Q

Dietary advice for IBS?

A

Restrict caffeinated and fizzy drnks, no more than 3 fresh fruit, reduce insoluble fibre, eat small & frequent meals, decrease sorbitol

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77
Q

Side effects of azathioprine?

A

Pancreatitis, leukopenia, abnormal LFTs

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78
Q

Why is azathioprine a poor initial choice to induce remission?

A

Takes 6-10 weeks to take effect

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79
Q

Treating exacerbation of Crohns?

A

If systemically well, can give oral steroids. If unwell, with more abnormal inflammatory markers, then admit for IVT, IV steroids and electrolyte replacement. Surgery in patients refractory to medical management.

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80
Q

Features of dyspepsia that require urgent endoscopy referral? (ALARMS55)

A 
Anaemia
Loss of weight
Anorexia
Recent onset of progressive symptoms
Melaena
Swallowing difficulty (dysphagia)
55 = >55 years old
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81
Q

Test for SIBO and precaution? And gold standard test?

A

Small intestinal bacterial overgrowth - do hydrogen breath test. Ingest glucose (normally absorbed in SI)’ if bacteria overgrow then broken down to hydrogen and CO2 instead. Hydrogen exhaled and measured. Must not smoke before this.. Gold standard is culture of SI fluid.

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82
Q

Gold standard test for SIBO?

A

SI fluid aspiration

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83
Q

Investigations done during ascitic tap for undetermined cause of ascites?

A

Cell count, MC&S, cytology, protein and albumin, LDH, glucose, amylase

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84
Q

Key investigation for acute management of ascites?

A

Do paracentesis. If raised cell count consistent with SBP (>250cells/mm3) then give broad spectrum antibiotcs.

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85
Q

Management of ascites?

A

Firstline is spiro. Can use furosemide if refractory, or where potassium rises. If fails do therapeutic paracentesis

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86
Q

Features and presentation of scurvy?

A

Vitamin C deficiency. Relatively common in elderly and socially disadvantaged. Vit C needed to make collagen; deficiency means collagen not replaced and get these symptoms. Muscle and joint pain, fatigue, perifollicular haemorrhages, gingivitis, poor wound healing, easy bruising

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87
Q

Pellagra cause and features?

A

Vitamin B3 deficiency (niacin) Get diarrhoea, dermatitis and dementia. Treat with vitamin replacement.

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88
Q

Red cell distribution width and MCV?

A

High RDW and low MCV indicates IDA; normal RDW and low MCV indicates anaemia cause by chronic disease or thalassaemia

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89
Q

Cholestasis/ALP in AI liver disease?

A

Cholestasis dominant in PBC or PSC, less so in AIH.

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90
Q

Presentation and treatment of botulinum poisoning?

A

Eat improperly stored/pickled fish or food, or wound infection. Get GI disorder with neuro symptoms: lethargy and weakness, difficulty seeing and speaking, descending paralysis. Pupils dilated and non-reactive. No sensory symptoms! Caused by Clostridium botulinum. Rx is trivalent antitoxin

91
Q

Risk factors for haemorrhoids?

A

Obesity, chronic constipation and coughing e.g. COPD

92
Q

Causes of met. acidosis (UKSLAMS)?

A 
Uraemia
Ketoacidosis
Salicylates
Lactic acidosis
Alcohol
Methanol
Sepsis
93
Q

Phosphate in alcohol withdrawal?

A

Commonly get hypophosphataemia in alcohol withdrawal therefore wary of re-feeding

94
Q

Treating seizures in alcohol withdrawal?

A

No need for AED, just benzos

95
Q

Features of modified Glasgow severity score for pancreatitis? (PANCREAS)

A 
P02 (<8kPa)
Age (>55)
Neutrophils (WCC >15)
Calcium <2)
Renal (urea >16)
Enzymes (LDH or AST)
Albumin (<32)
Sugar (glucose >10)

(3 or more indicates severe episode and consider ITU transfer)

96
Q

Other causes of raised amylase?

A

Acute cholecystitis, aortic aneurysm, intestinal obstruction, perforated PUD, ruptured ectopic

97
Q

Markers for serial progression of pancreatitis?

A

CRP good, amylase bad

98
Q

Do you need endoscopy for GORD?

A

Not if no alarm symptoms e.g. weight loss, IDA, anorexia, dysphagia, recent onset or progressive symptoms

99
Q

Features of GORD?

A

Burning, retrosternal pain that does not radiate, post-prandial. May get globus sensation, acid brash/water brash (hypersalivation), nocturnal cough

100
Q

Triple therapy for H. pylori eradication?

A

7 days of PPI, amoxicillin (or clarithromycin if penicillin allergic) and metronidazole (all BD)

101
Q

Jaundice and urine/stools?

A

Pre-hepatic does not affect urine or stools.

102
Q

Risk factors for cholangiocarcinoma?

A

Men, over 50, IBD/PSC. Can cause hepatomegaly.

103
Q

CFs of localised/generalised peritonitis?

A

Both inc. guarding, pain worse on inspiration/movement, rebound tenderness, pneumoperitoneum. Generalised alone = absent bowel sounds, tenderness to percussion, “board-like abdomen”

104
Q

Three causes of absent bowel sounds?

A

Complete obstruction, ileus, generalised peritonitis

105
Q

Causes of pneumoperitoneum?

A

Perforated viscus, bowel obstruction, NEC, peritoneal dialysis, post-laparoscopy/laparotomy

106
Q

What does 1 unit =?

A

10mls of 100% alcohol i.e. one 25ml measure of 40% alcohol

107
Q

Most common mechanism of transmission for Hep C and B?

A

C = Exposure to infected blood (mostly IVDU). B = mainly sexual, vertical/perinatal common.

108
Q

What is Pemberton’s sign?

A

Patient with SVC obstruction raises hands above head, gets venous congestion in face and neck

109
Q

Named signs in acute appendicitis?

A

Rovsing’s (palpate LLQ, pain in RLQ)
Psoas (passively extend leg when lying on side, get pain [friction between appendix and psoas])
Cope’s/obturator (flex and internally rotate hip. Positive shows appendix lies close to obturator)

110
Q

Two causes for psoas sign?

A

Appendicitis and psoas abscess

111
Q

What is the PABA test?

A

Used to diagnose pancreatic insufficiency. Signs or symptoms of this include weight loss and steatorrhoea (exocrine) or DM (endocrine)

112
Q

What is the H in IGETSMASHED?

A

Hypertriglyceridaemia or hypercalcaemia. Elevated triglycerides cause 5% of acute pancreatitis.

113
Q

Get difference for investigations in triglyceride-induced pancreatitis?

A

May have low levels of amylase and lipase, so if triglycerides are above ~11 and these are normal, do not exclude pancreatitis

114
Q

Key serum test for gastrinoma?

A

High serum gastrin not suppressed by test meal

115
Q

Treating gastrinoma?

A

Somatostatin analogue i.e. octreotide

116
Q

Two reasons why UGI bleed patients get high urea?

A

Blood in lumen digested and urea absorbed, and reduced perfusion of kidneys

117
Q

Causes of hyperkalaemia? WEAKER

A 
Whack (i.e. tissue injury/burns/rhabdo)
Extracting blood with clenched fist/Excess K+ therapy
ACEI/Addisons/met. acidosis
K+ sparing diuretics
Exchange of blood (massive transfusion)
Renal failure
118
Q

Amylase and disease severity?

A

No correlation!

119
Q

Course of amylase in acute panc?

A

Rises 2 hours after symptom onset, peaks between 12 and 48 hours, normal in 3-7. Lipase stays high for longer. May be no peak in chronic or acute-on-chronic. Lipase or CT needed.

120
Q

Propanolol in variceal bleed?

A

Useful prophylactically, less so acutely as will not affect bleeding

121
Q

PUD and post-prandial pain?

A

Duodenal improves when eating, worsens two hours later. Occurs before meals and at night. Better with milk.

122
Q

Risk factors for gastric cancer?

A

H. pylori, pernicious anaemia, blood group A, smoking, diet (high nitrates and salt bad, citrus and leafy greens good)

123
Q

H. pylori and gastric cancer?

A

Increases risk, except in gastric cardia (more RFs allied with oesophageal adenocarcinoma)

124
Q

Openings at diaphragm and levels?

A

IVCA at T8 (eight letters), oesophagus at T10 (and vagus) (10 letters), aorta at 12

125
Q

Defective enzyme in Gilbert’s?

A

Bilirubin UDP glucuronyl transferase; unable to conjugate bilirubin. AR.

126
Q

Triggers for bilirubin rise in Gilbert’s?

A

Fasting, fatigue, stress, viral illness

127
Q

Investigating achalasia?

A

Manometry is best test. Barium swallow inferior. Do endoscopy mainly to rule out differentials. CXR may show widened mediastinum

128
Q

Diagnosing toxic megacolon?

A

Suspect in patients with UC, fever, acute abdomen. Do erect AXR: show colon dilated >6cm (3, 6, 9) and loss of haustra, may show perforation.

129
Q

Precipitating factors for toxic megacolon in UC?

A

Electrolyte disturbance, anti-motility agents e.g. loperamide, opiates, barium enemas, colonoscopy

130
Q

When might azathioprine toxicity occur?

A

Concomitant use of allopurinol, or patients lacking TPMT

131
Q

How does aspirin damage gastric mucosa?

A

Reduces surface mucus/HCO3- secretion by preventing PGE2 (prostaglandin E2) production (by inhibiting COX). Increases gastric acid production as prostaglandins inhibit this.

132
Q

Treating apthous ulcers?

A

Firstline is topical steroids and topical lidocaine for pain control. Oral steroids if refractory.

133
Q

What renal disease is associated with Wilson’s?

A

Membranous nephropathy

134
Q

Normal bilirubin metabolism?

A

Conjugated and excreted in bile into SI, where some is converted to urobilinogen, reabsorbed (EHC) and excreted via kidney, remainder converted to stercobilinogen and excreted in stool

135
Q

Raised urine urobilinogen?

A

Haemolysis

136
Q

Low urine urobilinogen?

A

Complete obstructive jaundice

137
Q

Four features of Gilbert’s?

A

Unconjugated hyperbilirubinaemia, normal LFTs, no haemolysis, no evidence of liver disease

138
Q

Two methods of ensuring safe NG placement?

A

CXR and pH; CXR is mainstay (pH between 1 and 5.5 exclude pulmonary but not oesophageal placement)

139
Q

The five things to see on CXR for NGT placement?

A
  1. Passes down midline
  2. Past carina
  3. Past diaphragm
  4. Deviates to the left
  5. Tip seen in stomach
140
Q

Causes of Wernicke’s?

A

(All relate to thiamine depletion). Alcohol excess, anorexia nervosa, hyperemesis gravidarum, prolonged TPN w/out B1 supps.

141
Q

Why does glucose administration precipitate Wernicke’s?

A

B1 is cofactor for enzymes in energy metabolism so needed more with high glucose intake

142
Q

Management of C. diff?

A
  1. First episode, mild-to-moderate = oral metro for 10-14
  2. Second or subsequent, severe, not responding, intolerant to metro = oral vanc 10-14 days
  3. Life-threatening, not responding = oral vanc and IV metro, or faecal transplant.
    Never a role for IV vanc!
143
Q

Characteristic finding of achalasia on barium swallow?

A

‘Bird’s beak’ tapering of distal oesophagus

144
Q

Neuro vs mechanical dysphagia?

A

Neuro/motility e.g. achalasia = problems with liquids and solids; mechanical e.g. tumour progresses eventually to include liquids

145
Q

Risk of CRC in HNPCC?

A

50-70% (and up to 40% chance of endometrial cancer, and up to 20% ovarian). FAP is 100%.

146
Q

Screening in HNPCC?

A

Start at 25. Do annual colonoscopy, and annual pelvic USS and serum Ca-125 in women

147
Q

First-line therapy for moderate exacerbation of distal UC?

A

Topical aminosalicylate, topical and oral aminosalicylate, oral alone e.g. mesalazine or sulfasalazine.
Second line is corticosteroids.
After that, can try infliximab or cyclosporin

148
Q

Side effects of aminosalicylates (mesalazine and sulfasalazine)?

A

Diarrhoea, vomiting, abdominal pain. Rarely, peripheral neuropathy and blood disorders (agranulocytosis, aplastic anaemia, leucopenia). Infertility in males.

149
Q

Ciclosporin side effects?

A

Anorexia, nausea and vomiting, diarrhoea, gingival hyperplasia, hepatic dysfunction, HTN, tremor

150
Q

Infliximab side effects?

A

Diarrhoea, dyspepsia, GI bleed, HTN, tachycardia, sleep disturbances. Hepatitis and ILD. Can reactive Tb and Hep B.

151
Q

Investigating obscure GI bleeding?

A

Do capsule endoscopy. Can go small bowel angiography after capsule endoscopy has shown site

152
Q

Dual therapy in Hep C?

A

PEG-interferon and ribavirin (plus new -evirs). Must do genotype before starting treatment

153
Q

Key symptoms of DTs?

A

Agitation, hyperthermia, visual hallucinations, seizures. Tends to be 24-36 hours after acute cessation of alcohol. Oral lorezepam first line

154
Q

Features of Korsakoff’s?

A

Irreversible condition caused by chronic thiamine deficiency. Get anterograde amnesia, and confabulation.

155
Q

How does primary hyperparathyroidism cause dyspepsia?

A

High calcium causes excess gastric acid secretion and PUD

156
Q

Rapid urease test and results? (Aka CLO test)

A

Diagnoses H. pylori, as this organism produces urease that converts urea to ammonia and CO2 unlike normal mucosa. Biopsy antrum in endoscopy, then place in medium containing urea and pH indicator. Ammonia increases pH and becomes red. If positive, eradicate with 7 day triple therapy.

157
Q

How can H. pylori be diagnosed?

A

Urease test after OGD, or faecal stool antigen, CLO breath test, blood serology.

158
Q

Features of ZES?

A

Get gastrinoma, usually in D1/D2. Excessive gastrin release acts on stomach to cause parietal cell hyperstimulation and therefore multiple GASTRIC ulcers, refractory to PPI. Associated with MEN1. Symptoms are those of pUD.

159
Q

Key investigation for ZES?

A

Elevated fasting serum gastrin (serial). Then EUS, then CT. Either surgically resect or aggressive PPI and ocetrotide for symptoms

160
Q

Work-up for new Px of IBD?

A

Bloods, stool sample, C. diff testing, then AXR (essential, can exclude colonic dilatation, may show extent of disease, identify proximal constipation, small bowel dilatation). Do sigmoidoscopy etc. after

161
Q

Colonoscopy in acute IBD?

A

Useful in mild-moderate disease to show extent of disease; higher risk of perf in moderate to severe so considered after resolution

162
Q

Patho of Crohns?

A

Present with R sided abdo pain, watery diarrhoea, weight loss. Bloody diarrhoea less prominent than UC. Get bowel wall thickening on BE. Colonoscopy shows skip lesions, cobblestone mucosa, multiple ulcers. Get acute and chronic mixed transmural inflammation with non-caseating granulomas. Get strictures and fistulas as a result of transmural inflammation.

163
Q

Malignancy in IBD?

A

Higher risk in UC than Crohns!

164
Q

Apthous ulcers in IBD?

A

Can occur in both. Not helpful diagnostically

165
Q

Firstline for oral candida?

A

Nystatin topically

166
Q

Who gets oral candida?

A

Infants, elderly people wearing dentures, diabetics, IC atients

167
Q

CRC surveillance in UC?

A

High risk get annual colonoscopy, intermediate three years, low risk every five years. Based on FHx and disease activity

168
Q

Management of asymptomatic (incidental) gallstones?

A

No intervention required

169
Q

What causes Cullen’s/Greyturner’s?

A

Retroperitoneal haemorrhage

170
Q

Secondary prophylaxis for variceal bleed?

A

Propnaolol or nadolol (non-selective B-blockade)

171
Q

Condition caused by prolonged laxative abuse on colonoscopy?

A

Melanosis coli; incidental finding caused by lipofuscin overload, giving reticulated black appearance in proximal colon

172
Q

How does bacterial overgrowth syndrome present?

A

Get diarrhoea, steatorrhoea and macrocytic anaemia. Bacteria proliferate in SB (usually caused by SB diverticula). Get macrocytic anaemia as B12 is used up by bacteria, steatorrhoea as reduced concentration of conjugated bile acids, leading to diarrhoea. This occurs as Bacteroides conver conjugated BAs to unconjugated

173
Q

What does the presence of HBeAg indicate?

A

Current infection, either acute or chronic state with high infectivity

174
Q

Why avoid opiates in biliary colic?

A

Can cause sphincter of Odd dysfunction

175
Q

Cause of SIBO?

A

Diverticulae, decreased gastric acid secretion, gut motility diosrders, immunodeficiency, procedures such as Roux-en-Y that creates blind loop, or any intestinal surgery as creates blind loop

176
Q

Treating SIBO?

A

Antibiotics e.g. co-amox

177
Q

Grading oesophagitis?

A

A-D using LA classification

178
Q

Causes of oesophagitis?

A

GORD, infections (HSV/CMV/candida), radiation, medication e.g. bisphosphonates, alcohol abuse, eosinophilic oesophagitis

179
Q

Morphological criteria for coeliac disease?

A

Marsh criteria

180
Q

Signs of infective endocarditis?

A

Murmur, fever, arthritis, splinter haemorrhages, Osler’s nodes, Janeway lesions, petechiae, Roth spots

181
Q

Most common cause of acute infective endocarditis in patients with IVDU?

A

S. aureus

182
Q

Most common cause of endocarditis in patients with prosthetic valves or CVCs?

A

S. epidermidis

183
Q

Key organism for subacute endocarditis?

A

S. viridens

184
Q

Cholangiocarcinoma presenting symptoms?

A

Jaundice, abdominal pain, pruritus

185
Q

What does chronic idiarrhoea and steatorrhoea imply?

A

Malabsorption of some cause

186
Q

Initial investigation in suspected coeliac and key variable?

A

Anti-TTG, and check IgA concurrently as anti-TTG is a type of IgA and may not be elevated if IgA deficient. Gold standard is small bowel biopsy

187
Q

Complications of coeliac?

A

Small bowel lymphoma, oesophageal carcinoma, malabsorption of iron, fat-soluble vitamins etc, osteoporosis, dermatitis herpetiformis. Anaemia initially caused by low folate (jejunal), then more uncontrolled leads to iron deficiency (duodenum) and B12.

188
Q

Expected electrolytes in coeliac?

A

Low K+, low Ca2+, low albumin, low Mg2+, anaemia with iron/B12/folate deficiency

189
Q

Most specific Ab for AIH?

A

ASMA

190
Q

Causes of achalasia?

A

Normally idiopathic, can be secondary to Chagas’ or oesophageal cancer. Reduced secretion of NO implicated

191
Q

Treatments for achalasia?

A

Mainstay is surgical i.e. Hellers myotomy. Can do endoscopic dilatation.
If not fit or unwilling, can do botox injection, or drugs e.g. CCBs, nitrates, sildenafil

192
Q

Chest pain in achalasia vs GORD?

A

Pain in achalasia is severe and occurs while eating, while in GORD is less severe, typically comes after large meals and on lying down (and responds to PPI)

193
Q

Treating toxic megacolon?

A

(Tachycardia, fever, hypotension, dilatation of colon). If not perforated or peritonitic, try IV steroids, LMWH, IVT. If doesn’t respond after 2 hours, may need urgent surgery (usually subtotal colectomy with end ileostomy)

194
Q

Wilsons patho?

A

Disordered copper metabolism, get copper retained and accumulated in various organs

195
Q

What does Ziehl-Neelsen positivity suggest?

A

Present of mycobacteria, not necessarily TB

196
Q

Features of Hep A?

A

Acute viral, common in North Africa, faecal-oral spread. 2-week prodrome of flu-like illness, nausea and vomiting, then acute hepatitis with RUQ pain, jaundice. Raised ALT.

197
Q

Two main malabsorptions in SIBO?

A

B1 and fat, with B12 deficiency secondary to utilisation by

198
Q

Risk factors for Budd-Chiari?

A

Prothrombotic conditions e.g. APLS, Factor V Leiden.
Myeloproliferative e.g. polycythaemia rubra vera.
Hormonal treatment, pregnancy and puerperium, infections in liver, malignancy, trauma, AI conditions e.g. sarcoid

199
Q

Risk factors for PUD?

A

H. pylori, NSAIDs, steroids, aspirin, ZES. Chronic gastric ischaemia in critical care can cause gastric ulcers.

200
Q

Dermatitis herpetiformis features?

A

Itchy, vesicular, on extensor surfaces of limbs, buttocks and back. Resolves with gluten-free diet

201
Q

Two features needed for coeliac diagnosis?

A

SI biopsy showing lymphocyte infiltration, villous atrophy, crypt hyperplasia (non-specific) and bloods showing gluten sensitivity (anti-TTG, anti-endomysial, anti-gliadin)

202
Q

Key electrolyte to monitor when treating alcohol dependency?

A

Phosphate. Can plummet during re-feeding and may need IVI of dipotassium hydrogen phosphate.

203
Q

RFs for pancreatic cancer?

A

Chronic pancreatitis, smoking, alcohol, DM

204
Q

Features of diffuse oesophageal spasm?

A

Intermittent dysphagia for solids and liquids (not intermittent in achalasia), with no blood test abnormalities or constitutional symptoms. Get increased contractions of distal oesophagus. Get heartburn, globus, retrosternal chest pain. Key investigation is manometry (excludes achalasia), second-line is barium swallow showing “corkscrew”

205
Q

Investigating diffuse oesophageal spasm?

A

Manometry (shows simultaneous contractions with normal LOS tone). Second line includes barium swallow (shows corkscrew oesophagus)

206
Q

Oral hairy leukoplakia?

A

History of immunosuppression, then get white mass on lateral aspect of tongue that cannot be scraped off. Caused by EBV

207
Q

What is pancreatin?

A

Mix of amylase, lipase, protease, given in states like CF, chronic pancreatitis to supplement

208
Q

Complications post-gastrectomy?

A

No IF means low B12, get early satiety and bloating, increased upper GI transit (diarrhoea and weight loss), achlorohydria (loss of parietal cells) which can lead to SIBO

209
Q

Two antibodies implicated in PA?

A

Antibodies to parietal cells or IF

210
Q

Treating PA?

A

Vitamin B12 injections for life

211
Q

Treating diffuse oesophageal spasm?

A

Antacids e.g. PPIs, relaxants such as CCBs, nitrates, buscopan

212
Q

Pathophysiology of Barret’s?

A

Columnar metaplasia in squamous cells in response to chronic acid reflux, pre-malignant

213
Q

Diagnosing IBS?

A

Rome criteria. Recurrent abdominal pain or discomfort, classically improves with defecation, altered stool frequency and appearance. Treat with mebeverine (anti-spasmodic). Can use loperamide if diarrhoea predominant

214
Q

What are the highly eosinophilic, irregularly shaped hyaline bodies seen in fibrotic liver cells?

A

Mallory bodies (intracytoplasmic eosinophilic inclusions). Derived from endoderm

215
Q

When is exploratory laparatomy indicated?

A

Patients who are haemodynamicaly unstable with rigid, peritonitic abdomen

216
Q

Exam findings for ascites?

A

Distended abdomen with shifting dullness

217
Q

Pathophysiology of ascites/peripheral oedema in CLD, and therefore choice of diuretic?

A

Get ascites because fibrosis causes portal hypertension, increased hydrostatic pressure so get transudate in peritoneum. However, haemodynamic changes from cirrhosis also cause peripheral vasodilatation, so get RAAS activation to maintain MAP, and renal vasoconstriction, so reduced GFR and increases sodium reabsorption (aldosterone action) and therefore water, causing oedema. This is why spironolactone is firstline diuretic in ascites caused by cirrhosis!

218
Q

Chance of progression to cirrhosis with acute Hep A?

A

Approx 0%

219
Q

Acute Hep B vs acute Hep C?

A

Acute hep C usually asymptomatic, while up to 50% of acute hep B get jaundice

220
Q

Causes of ALT >1000?

A

Viral, ischaemic or drug-induced hepatitis?

221
Q

Best investigation to check H. pylori eradication?

A

13C urea breath test. Do not want anything invasive e.g. CLO/rapid urease, and serology stays high for months

222
Q

Investigating IBS?

A

Good history and exam, bloods for FBC, CRP, ESR, coeliac screen. Endoscopy or imaging not needed unless symptoms of organic disease present

223
Q

What should be co-prescribed with codeine?S

A

Stimulant laxative i.e. senna

224
Q

Side effects and indications of phosphate enemas?

A

Can cause fluid shifts, ascites and heart failure. Indicated for faecal impaction, and will otherwise not benefit

A final year of medicine (20 decks)

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