Gastro - general do not use this Flashcards

1
Q

Portal HTN mx

A
  • Lifestyle advice
    Salt restriction
    stop drinking + smoking
  • Keep BP low
    Propanolol, Carvediol
    Isosobride mononitrate
  • TIPS (transjugular intrahepatic portosystemic shunt)
    Passing a catheter down the jugular vein + creating a shunt from the hepatic vein to the portal vein to relieve portal HTN
    Ascites, oesophageal variceal bleeding refractory to medical treatment, bleeding from non-oesophageal varices e.g. gastric varices
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2
Q

Barrett’s oesophagus mx

A
  • Regular endoscopic surveillance
  • Radiofrequency ablation (downgrades dysplasia)
  • Endoscopic mucosal resection
  • Oesophagectomy – if high-grade dysplasia persists after intensive acid suppression
  • Aspirin

Controversial treatments
• Lifelong acid-suppressing therapy (PPI)
• Anti-reflux surgery

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3
Q

Gastritis mx

A

• PPI (lansoprazole, omeprazole) or ranitidine (H2 antagonist)
• Triple therapy for H. pylori
PPI + Amoxicillin + Clarithromycin/Metronidazole – all 3 given BD x7 days
or
PPI + clarithromycin + metronidazole – all three given BD x 7 days
• Antacids (Magnesium carbonate, Aluminium hydroxide, alginates)

• Endoscopic cautery may be needed

Lifestyle modification
•	Smaller + more frequent meals
•	Stop alcohol
•	Stop smoking
•	Reduce stress
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4
Q

Peptic ulcer disease mx

A

• Active bleeding ulcer
- OGD
Adrenaline injection/thermal coagulation/endoclips/ haemostatic powder spray
- PPI (IV for 72h, then PO)
- +/- Blood transfusion (aim for Hb 70)
if bleeding persists: transcatheter arterial embolization

• Healing ulcers H. pylori +ve
Triple therapy
PPI (omeprazole/lansoprazole) + Clarithromycin + Amoxicillin/Metronidazole – all 3 BD x7 days
or
PPI + clarithromycin + metronidazole – all 3 BD x 7 days

• Healing ulcers H. pylori -ve
o Stop NSAIDs
o Full dose PPIs for 2 months

•	Modification of behaviour 
o	Stop or replace drugs that cause peptic ulcers (e.g. replace NSAIDs with paracetamol)
o	Stop smoking
o	Stop alcohol
o	Weight reduction

o Patients with high CV risk - should continue to receive prophylactic low-dose aspirin and full-dose naproxen (preferred NSAID) + PPI or misoprostol

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5
Q

GORD mx

A
Lifestyle
•	Lose weight
•	Stop smoking
•	Stop alcohol 
•	Small, regular meals
•	Avoid hot drinks/alcohol/eating during the 3h before going to bed
•	Raise head at night
•	Avoid drugs which a) Affect oesophageal motility (nitrates, anticholinergics, TCAs), b) Damage the mucosa (NSAIDs, potassium salts, alendronate)

Pharmacological treatment
• PPIs (e.g. omeprazole) More effective + safer than H2RA (e.g. ranitidine) in relieving heartburn
• Prokinetic drugs (e.g. metoclopramide) – promote gastric emptying + increase the tone in the cardiac sphincter
• Antacids (Magnesium carbonate, Aluminium hydroxide)
• Alginates

Surgery
• Laparoscopy fundoplication (magnetic beads in distal oesophagus at the gastro-oesophageal junction)

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6
Q

Oesophageal spasm treatment

A

CCB

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7
Q

Active severe UC management

A

IV hydrocortisone to induce remission

ciclosporini n pt who cant tolerate IV steroids
(infliximab in pt who can’t tolerate ciclosporin)

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8
Q

Leaking AAA emergency management

A
  • 2 large bore IV cannulae
  • Cross match 10 units of blood (=5L, enough to replace the entire circulating volume)
  • Urinary catheter (to monitor renal function)
  • Immediately notify the vascular surgeon + anaesthetist on call
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9
Q

Anal fissures mx

Conservative
Medical
Surgical

On presentation
Resistant fissures

A
•	Conservative management
o	High fibre diet
o	Good hydration
o	Warm baths 
o	Softening the stool (laxatives)
•	Medical management
o	High fibre diet + laxatives +/or non-constipating analgesics (i.e. avoid opioids) 
o	Topical anaesthetics (e.g. lidocaine) 
o	GNT – increases local blood flow + relaxes internal anal sphincter 
o	Diltiazem (CCB) – relaxes the anal sphincter 
o	Chronic fissures - Botox injections into anal sphincter - relieve spasm + promote healing 

• Surgical management
o Lateral internal sphincterotomy (Need to check integrity of external anal sphincter first)
o Anal advancement flap
Adjacent well vascularised tissue is advanced into the defect left following fissure excision
o Fissurectomy

On presentation

  • Conservative management alone (1st line)
  • Topical GTN
  • Topical diltiazem

Refractory fissures

  • Botox injection (1st line)
  • Surgical sphincterectomy (1st line)
  • Anal advancement flap
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10
Q

Haemorrhoids management

Conservative
Medial
Non-surgical
Surgical

A

• Conservative management – Lifestyle modification –o Increase dietary fibre
o Keep well hydrated
o Avoid straining at stool

• Medical management
o Local anaesthetic (e.g. lidocaine)
o Steroidal creams/suppositories – decrease local inflammation
o Laxative if constipation causes straining, hard stool, bleeding
Lactulose, sodium docusate, ispaghula husk, sterculia

• Non-surgical management – Grade 2
o Rubber band ligation
o Injection sclerotherapy
o Infrared coagulation/photocoagulation

• Surgical management – for large symptomatic haemorrhoids that do not respond to other treatments
o Haemorrhoidectomy
o Stapled haemorrhoidopexy –
o Haemorrhoidal artery ligation (doppler guided) + rectoanal repair (DG-HAL-RAR)

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11
Q

Summary of management of haemorrhoids for Grade 1, 2, 3, 4

A

Grade 1
Dietary + lifestyle modifications
Topical corticosteroids

Grade 2
Dietary + lifestyle modifications
Rubber band ligation / sclerotherapy / Infrared photocoagulation / haemorrhoid arterial ligation / stapled haemorrhoidopexy

Grade 3
Dietary + lifestyle modifications
Rubber band ligation

Grade 4
Dietary + lifestyle modifications
Surgical haemorrhoidectomy

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12
Q

Appendicitis mx

A
  • IVF
  • Analgesia (opioids)
  • Anti-emetics
First line treatment
- Appendicectomy 
   NBM solids - 6h
   NMB clear fluids - 2h
- Abx after surgery (e.g. cefoxitin)
- DVT prophylaxis
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13
Q

Constipation

give examples of stool softners

A

Sodium docusate, liquid paraffin, arachis oil enema, poloxamer

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14
Q

Constipation

Give examples of osmotic laxatives

A

Lactulose
Macrogols (Movicol)
Polyethene glycols (e.g. laxido)
Magnesium salts

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15
Q

Constipation

give examples of peristalsis stimualnts

A

Senna, docusate, glycerol suppositories, bisacodyl, dantron

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16
Q

Constipation

Give examples of bulking agents

A

Ispaghula husk (Fybogel)

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17
Q

Constipation

Give examples of drug used for opioid induced constipation

A

Methynaltrexone

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18
Q

Constipation

What kind of drug is co-danthamer

A

Dantron (peristalsis stimulant) + poloxamer (stool softner)

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19
Q

Severe acute gallstone pancreatitis with evidence of biliary obstruction +/or cholangitis management

A
  • IVF
  • Analgesia
  • ERCP + sphnincterectomy + stone extraction within 72h of admission
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20
Q

Mild gallstone pancreatitis management

A
  • IVF

- Supportive care

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21
Q

ERCP assosciated pancreatitis management

A
  • IVF
  • Analgesia
  • Bowel rest
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22
Q

Asymptomatic cholelithiasis management

A

Observation

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23
Q

Symptomatic cholelithiasis management

A

Laparoscopic cholecystectomy

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24
Q

Choledocholithiasis +/- symptoms management

A

ERCP w biliary sphincterectomy + stone extraction

if stone is large (>1.5cm) –> lithotripsy, papillary ballon dilation, long-term biliary stenting

Following extraction, cholecystectomy represents definitive treatment to reduce the risk of recurrent biliary events (e.g. cholangitis, pancreatitis)

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25
Q

Cholecystitis management

A
  • NBM
  • IVF
  • NSAID analgesia (diclofenac, indometacin)
  • Abx IV (ampicillin/ceftriaxone/ertapenem)
  • Early laparoscopic cholecystectomy

If surgically high risk patient
- Pre-cutaneous transhepatic gallbadder drainage

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26
Q

Acute cholangitis mx

A
  • IV abx - piperacillin/tanzobactam or imipenem/cilastatin
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27
Q

Mallory Weiss tear mx

A
•	IVF
•	Blood transfusion if
   Hb <80g/L 
   Hb <100g/L with comorbidities 
•	Platelet transfusion if 
   Plt <50 x 10^9/L
•	FFP +/or vitamin K (phytomenadione) if
   Prolonged PT/INR

• OGD
o Adrenaline + thermocoagulation/band ligation
o Haemoclip +/- adrenaline

If bleeding can’t be stopped using endoscopic treatments - Angiography with VP injection or embolization

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28
Q

Toxic megacolon mx

A
  • IVF
  • IV steroids
  • NG decompression
  • Abx (broad spectrum - piperaccilin/tanzobactam (If C. difficile suspected/confirmed - vancomycin)
  • IV ciclosporin
  • Total colectomy with end-ileostomy (if no improvemet with medical treatment after 72h)
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29
Q

Acute exacerbation of UC treatment

A
  • IVF
  • IV steroids
  • Abx
  • Bowel rest
  • TPN might be required
  • DVT prophylaxis
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30
Q

Mild UC

What does it mean (6)
Management

A
Mild UC
<4 stools per day
no more than small amount of blood in stools
no anaemia
pulse rate <90
no fever
N ESR/CRP

oral/rectal 5-ASA derivatives (melsalazine, olsalazine, sulfalazine)
+/- rectal steroids (prednisilone, methylprednisilone)

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31
Q

Moderate UC

What does it mean (6)
Management

A
Moderate UC
4-6 stools per day
more blood than mild
no anaemia
pulse rate <90
no fever
N ESR/CRP (<30)

oral/rectal 5-ASA derivatives (melsalazine, olsalazine, sulfalazine)
+ oral steroids (prednisilone, methylprednisilone) + immunosuppresants (azathioprine, mercaptopurine, cyclosporin, infliximab)

32
Q

Severe UC

What does it mean (6)
Management

A
Severe UC
>6 stools per day
Visible blood in stools
\+ 1 or more systemic upsets:
anaemia
pulse rate >90
fever >37.8
raised ESR/CRP (>30)

oral/rectal 5-ASA derivatives (melsalazine, olsalazine, sulfalazine)
+ oral steroids (prednisilone, methylprednisilone) + immunosuppresants (azathioprine, mercaptopurine, cyclosporin, infliximab)

ciclosporin - pt w severe refractory colitis, rapid onset of action, reduced colectomy rate by 50%

33
Q

Surgical UC therapy

A

Past: protocolectomy with ileostomy

Now: IPAA - ileal-pouch anal anastomosis

34
Q

Acute exacerbation of Crohn’s disease mx

A
  • IVF
  • IV steroids
  • 5-ASA (melsalazine, sulfalazine, olsalazine)
  • Analgesia
  • TPN might be neccessary
  • Monitor markers of disease activity
35
Q

To induce remission in Crohns

A

Budesonide or 5-ASA (melsalazine, olsalazine)

Budesonide less effective than conventional steroids but fewer SE

In 1000 SBAs+ EMQs they say that to induce remission in Crohn’s flare up you use steroids

36
Q

Crohn’s first, second, third line treatment

A

1st line
Budesonide +/or 5-ASA (melsalazine, olsalazine) or oral corticosteroids (prednisilone, 2nd line)

2nd line
Immunomodulator therapy (azathiorpine, mercaptopurine) + oral corticosteroids

Methotrexate second line if unable to tolerate azathioprine or mercaptopurine

3rd line
Biological therapies
anti-TNFa (infliximab, adalimumab) - used in refractory Crohn’s +/- azathioprine +/- oral corticosteroids

Surgery - removing affected part of bowel + stoma formation

37
Q

Cirrhosis mx

A

1st line
• Treatment of underlying chronic liver disease
Hep C - Oral direct antivirals

• Prevention of superimposed hepatic insult
o No alcohol, no hepatotoxic drugs
o Immunisation against hep A + B, influenza and pneumococci
o Management of metabolic RF – e.g. preventative treatment for osteoporosis
o Maintenance of adequate nutrition
o Regular exercise to prevent muscle wasting

• Monitoring for complications

• Na restriction + diuretic therapy for ascites
o Spironolactone – to maintain normal serum K
o Frusemide – if pt don’t respond to spironolactone

2nd line
• Liver transplantation

38
Q

Ascites mx

A

• Treatment of underlying cause

Medical treatment – sodium restriction + diuretic therapy
• Restricted salt intake <90mmol/day (<5.2 g salt/day)

• Spironolactone - increase Na excretion + increase K absorption (with K sparring diuretics,Na reabsorption and K excretion are prevented)
- Needs monitoring because of risk of hyperkalaemia

• Loop diuretics (e.g. frusemide) – if pt don’t respond to spironolactone
- Higher doses cause severe electrolyte disturbance, particularly hyponatraemia

Therapeutic paracentesis
• Large/refractory ascites
• Large-volume paracenteses should be followed by volume expansion using human albumin solution

Surgical
• TIPS (transjugular intrahepatic portosystemic shunt) – refractory ascites needing frequent paracentesis

39
Q

UC role of

corticosteroids 
aminosalicylates 
thiopurines
ciclosporin
TNFa antibodies
A

corticosteroids - to induce remission

aminosalicylates - 5- ASA to induce + maintain remission 1ST LINE) (mild to moderate)
Melsalazine - to maintain remission

thiopurines (azathioprine, 6-mercaptopurine) - if intolerant to corticosteroids

ciclosporin - severe refractory colitis, rapid onset of action

TNFa antibodies (infliximab, adalimumab, golimumab) -severely active UC in adults whose disease has responded inadequately to conventional therapy (moderate to severe UC)

40
Q

Mx of liver failure for all patients

A

o ICU – mandatory once hepatic encephalopathy is present
o Intubation once advanced encephalopathy develops
o Neurological status monitoring for advanced encephalopathy – associated with a greater risk of cerebral oedema + intracranial HTN
o Monitoring of blood glucose, electrolytes, cultures (high risk of bacterial + fungal infection)
o Liver transplantation assessment (all pt should be considered for liver transplantation)

41
Q

Mx of causes of liver failure

Acute hep B
Autoimmune hepatitis
HSV
Budd-Chiari syndorme
Wilson's disease
A
  • Acute hepatitis B – entecavir or tenofovir disoproxil (oral nucleoside or nucleotide analogue)
  • Autoimmune hepatitis - methylprednisolone
  • Herpes Simplex hepatitis – acyclovir
  • Budd- Chiari syndrome – anticoagulation (LMWH), TIPS
  • Wilson’s disease – measures to decrease serum copper (plasmapheresis, continuous veno-venous hemofiltration, album dialysis, plasma exchange, chelation therapy for Wilson’s in the setting of AFP is generally ineffective + may be associated with hypersensitivity)
42
Q

Management of complications of liver failure

  • To decrease ammonia production
  • ICP
  • Cerebral oedema
  • AKI
  • Treat + prevent abnormal clotting
  • Paracetamol overdose
  • Monitor glucose
  • Liver transplantation
A
  • To decrease ammonia production – Lactulose (w neomycin)
  • ICP – Mannitol
  • Cerebral oedema – therapeutic hypothermia (when medical treatments are not successful)
  • AKI – haemodialysis, hemofiltration
  • Treat + prevent abnormal clotting – FFP, platelet concentrates, antifibrinolytic drugs, prothrombin complex concentrates, recombinant activated factor 7
  • Paracetamol overdose – acetylcysteine therapy should be administered in all suspected cases, regardless of the dose/timing of paracetamol ingestion
  • Monitor glucose – IV glucose may be required
  • Liver transplantation – all patients should be considered
43
Q

SBO - partial or complete or complicated poor surgical candidate management

A
  • IVF + correct electrolyte imbalances
  • NG decompression
  • Analgesia – morphine sulfate
  • Anti-emetic – ondansetron (metoclopramide is contraindicated in patients with bowel obstruction as it’s a pro-kinetic)
  • Correction of underlying cause
44
Q

SBO-complete or complicated, surgical candidate

A
  • IVF + correct electrolyte imbalances
  • Emergency laparotomy
  • Abx – ampicillin + gentamicin or cefoxitin
  • NG decompression
  • Analgesia
  • Correction of underlying cause
45
Q

LBO acutely ill mx

A
•	Supportive measures
o	NBM
o	O2
o	IVF + correct electrolyte imbalances
o	NG decompression 
o	Abx pre-operatively (broad spectrum: amoxicillin, metronidazole, gentamycin) 
\+/-
o	Blood transfusion to correct anaemia +/- coagulopathy

• Emergency surgery – if suspected/impending perforation, peritonitis, irreducible hernia

46
Q

HAV mx

A
  • Supportive treatment (no specific anti-viral available)
  • Post-exposure (<2 weeks) prophylaxis in unvaccinated people - Active/passive immunisation
  • With worsening jaundice and encephalopathy - liver transplant
47
Q

HBV mx

A
  • Supportive care – most will achieve seroconversion with appearance of ab to HBsAg in the absence of treatment
  • HBeAg +ve/-ve chronic hepatitis B + compensated liver disease – 1) peginterfeon alpha 2a, 2) tenofovir disoproxil or entecavir
  • Liver transplant
48
Q

HCV mx

A

• Oral direct-acting antiviral therapies – elbasvir+grazoprevir

49
Q

HDV mx

A
  • Supportive care
  • Pegylated interferon alfa
  • Liver transplantation
50
Q

HEV mx

A

Supportive care

51
Q

Autoimmune hepatits mx

A

• Corticosteroids – if treatment <6 months
o Prednisolone
o Budesonide if intolerant to prednisolone

• Corticosteroids + Immunosuppressants – if treatment >6m (corticosteroid sparring effect), if at risk of corticosteroid-related complications (e.g. post-menopausal women, pt w osteoporosis, DM, glaucoma, cataracts, arterial HTN, major depression, emotional lability)
o Prednisolone/budesonide + Azathioprine/Mercaptopurine

• Liver transplantation indicated in
o Pt with advanced liver disease who are refractory/intolerant to corticosteroid therapy

52
Q

AAA seen on US (AA >3cm in diameter) + pt has abdominal pain mx

A

Stable pt - CT angiogram

Unstable pt - surgery to rule out ruptured AAA

53
Q

Perforated peptic ulcer emergency mx (resuscitation + treatment until surgery)

A
  • IVF
  • O2
  • Analgesia
  • NBM
  • Abx
  • NG tube (so that gastric contents dont come up the G tube rather than the perforated ulcer)
  • Monitor UO

Surgical emergency

54
Q

Acute pancreatitis mx

A
  • IVF
  • Analgesia (morphine sulfate, fentanyl)
  • Oxygen
  • Anti-emetics (ondansentron)
  • DVT prophylaxis
  • Nutritional support (low fat diet, might need an NJ tube)
  • Tight glucose control (might need to give insulin)
55
Q

Chronic pancreatitis mx

A
  • No definitive therapy
  • Acute episodic pain – analgesics (paracetamol/ibuprofen + tramadol)

• Chronic symptoms
o Lifestyle modifications – (decrease smoking+ alcohol)
o Dietary modifications (e.g. low fat diet) + enteral feeding
o Analgesia
o Octreotide – SS analogue, may relieve pain
o Pancreatic enzymes (pancreatin)
o PPI (omeprazole)

56
Q

How to manage

Pancreatic endocrine insufficiency
Pancreatic exocrine insufficiency

as a result of chronic pancreatitis

A

Pancreatic endocrine insufficiency (DM)
- insulin
But be careful - chronic pancreatitis patients are at risk of hypoglycameia due to imapired hepatic gluconeogenesis and hypoglycaemia

Pancreatic exocrine indufficiecy (enzymes e.g. lipase, amylase, protease)- pancreatic enzyme supplementation (.e.g pancreatin)

57
Q

Which enzymes does pancreatin include?

A

Amlylase
Protease
Lipase

58
Q

Peritonitis management

A
  • IVF
  • Analgesia
  • Broad spectrum abx
  • NG tube
  • Blood transfusion
  • Surgery
    Exploratory laparotomy
    Correct cause of peritonitis
59
Q

If you suspect varices you should include the following in your initial (pre-endoscopy) management

A
  • Terlipressin
    ADH agonist, causes splanchnic vasoconstriction and decreases mesenteric blood flow and portal pressure
  • Prophylactic abx
    Increased risk of translocation of bacteria from gut into systemic circulation
60
Q

Alcoholic hepatitis mx

A
•	Alcohol abstinence + alcohol withdrawal management
o	Benzodiazepines (oxazepam, diazepam, lorazepam) 
   Long acting (diazepam) – provide greater protection against seizures + delirium
   Short acting (oxazepam, lorazepam) – safer in older adults + those with hepatic dysfunction 

• Weight reduction + smoking cessation
o Careful with orlistat – might lead to acute liver failure, cholelithiasis, cholestatic hepatitis

• Nutritional supplementation + multivitamins
o At risk of developing “re-feeding syndrome” –> Monitor for hypokalaemia, hypophosphatemia, hypomagnesaemia

• Immunisation
o Influenza + pneumococcal vaccine recommended in patients with chronic ALD
o Hep A + Hep B vaccination if Anti-HBs (Hep B surface antibody) + HAIgG are negative

• Corticosteroids
o Prednisolone
o If patients have hepatic encephalopathy

• Sodium restriction +/- diuretics
o Frusemide + spironolactone
o Treatment for ascites

• Liver transplant
o Second line
o For patients with end-stage ALD

61
Q

NASH/NAFLD mx

A

With no end-stage liver disease
• Lifestyle modification – first line therapy
o Weight loss through diet + exercise
o Diet should have a high protein: calorie ratio
o Exercise with diet increases muscle mass + insulin sensitivity
o Abstinence from alcohol + hepatotoxic drugs

• Vitamin E (alpha tocopherol)
o Vitamin E significantly improves liver function + histological changes in patients with NASH

• Gastric bypass with Roux-en-Y
o Patients with a BMI >40 kg/m² or
o Patients with a BMI >35 kg/m² and at least one or more obesity-related comorbidity

With diabetes
• Insulin sensitiser
o Metformin – does not improve histological scores or fibrosis but leads to weight reduction, reduced HbA1c, reduced plasma glucose

With dyslipidaemia
• Statins

With end-stage liver disease secondary to NASH
• Liver transplantation
• TIPS

62
Q

Which abx is the first line treatment for C. difficile infection?

A

Metronidazole

63
Q

How to maintain remission in UC?

A
  • Low dose oral ASA (e.g. melsalazine)

- Second line - oral azathioprine/mercaptopurine

64
Q

Types of hepatitis that cause chronic liver disease vs acute hepatitis

A

Chronic - B,C - can cause cirrhosis and HCC

Acute - A, D, E

65
Q

Congenital/genetic causes of chronic liver disease

A

Wilson’s
Haemochromatosis
A1 antitrypsin deficiency

all are AR

66
Q

What are the causes of tranaminits in the 1000s?

A

Paracetamol overdose
Acute viral hepatitis (not B)
Ischaemic hit

67
Q

Ratio of transaminits in alcoholic hepatitis

A

2:1

68
Q

Pathophysiology of Wilson’s disease

A

ATP7B mutation on Chr 13
codes for transporters that excrete copper form liver into bile

• ATP7B encourages:
o Production of the ferroxidase caeruloplasmin (in which copper is incorporated)
o Excretion of copper into bile

69
Q

Presentation of Wilson’s disease in

Children, adolescents
vs
Young adults

A
  • Usually presents as liver disease in children + adolescents - acute hepatitis - cirrhosis - liver failure
  • Usually presents as a neuropsychiatric illness in young adults
70
Q

Pathophysiology of haemochromatosis

A

Deficiency of hepcidin HFE gene mutations on the short arm of Chr 6
Known mutations of the HFE gene are C282Y and H63D (must be homozygous)
Increased intestnal absorption of iron causes accumulation in tissues , esp liver
Increased iron release from macrophages
This can lead to organ damage
Deposits in liver, pancreas, pituitary gland

iron in enterocytes wants to be released into the hepatic portal system
ferroprotin is responsible for transferring the iron out of the cells into the blood
Hepcidin inhibits ferrportin –> iron stays in enterocytes, is not released into the blood and is excreted
Hepcidin mutation means ferroportin is uninhibited –> increased release of iron from entercytes to blood

71
Q

Difference bn PBC and PSC

A

PBC
Pathology of intra-hepatic bile ducts by antibodies
Anit-mitochondrial antibody 95%
ANA 35%
Females
Assosciated with other autoimmune conditions (thyroid, sjogrens syndrome, systemic sclerosis, coeliac disease)
“Buzzwords” – Hypercholestrolaemia: tendon xanthomata, xanthelasma peri-ocular

PSC
Pathology of intra+extra hepatic bile ducts
MRCP - beads on a string
Males
Assosciated with IBD (UC specifically)
“Buzzwords” – UC, cholangiocarcinoma
72
Q

Which patients are likely to develop cholangiocarcinoma?

A

Pt w UC who develop PSC

73
Q

Commonest abscesses in developed world vs worldwide

A
  • Developed countries – pyogenic (bacterial) abscesses most common
  • Worldwide – amoebae most common
74
Q

Liver cyst vs liver abscess

A

Liver cyst - not infetious
Lined with biliary-type epithelium but cyst fluid does not contain bile
F>M

Liver abscess - infectious 
Mass filled with pus in liver 
Pyogenic = polymicrobial (80%) 
Amoebic = Entamoeba histolytica (10%) 
Fungal = Candida (10%)
75
Q

What is the difference between a sliding hiatus hernia and a para-oesophageal (rolling) hiaus hernia?

A
  • Sliding hiatus hernia [85-95%] – the gastro-oesophageal junction slides up into the thoracic cavity
  • Para-oesophageal (rolling) hiatus hernia [5-15%] – the gastro-oesophageal junction remains in place but part of the stomach (or colon, spleen, pancreas, small intestine) herniates into the chest next to the oesophagus