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Gastro Flashcards

0
Q

Why do you bleed in liver disease?

A
  1. Reduced number and function of platelets
  2. Increased fibrinolytis
  3. Clotting factors defective synthesis
    - increase in factor 8 for some reason but decrease in all the others especially factor seven which has a really short half life

Leads to prolonged PT - aptt and thrombin clotting time may be long too THE MIXING STUDY FOR APTT WILL CORRECT THIS TOTALLY

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1
Q

How would you differentiate urine of hepatorenal syndrome from ATN?

A

Urine sodium low (less than 20) and is hyperosmolar compared with ATN

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2
Q

What does OLT stand for?

A

Orthotopic liver transplant

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3
Q

What is terlipressin and how does it work?

A

Long acting vasopressin analogue
Mediates vasoconstriction by activation of the V1 receptor
Preferentially expressed on vascular smooth muscle cells within the splanchnic bed and thus reverses vasodilation

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4
Q

What bugs are responsible for SBP?

A

50% will be culture positive
50% gram pos
50% gram neg

** should be a trigger for referral for transplant- 1 year mortality is 40% after the first episode.

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5
Q

What was the study that showed effect of terlipressin in HRT?

A 
OT-0401
Sanyal 2008
Terlipressin + albumin vs albumin alone
Higher chance of reversal in tx group
Optimal if treated for three days
No difference in overall or transplant free survival
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6
Q

What is the cause of acute liver failure is the AST:ALT ratio is greater than 2.2 and ALP:bilirubin less than 4?

A

100% specific for Wilson disease in acute liver failure

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7
Q

How does HDV work?

A

Needs coinfection with HBV for transmission.
If get both B and D at same time- higher mortality, worse acute hepatitis.
HDV presence will supress HBV load in chronic infection
Treatment is pegIFN for 48 weeks.

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8
Q

How does HEV work?

A

RNA virus, genotype 3 most common
Diagnose via Ab however in the immunosupressed need to directly look for RNA
Can have chronic infection in immunocompromised patient.
Get from food, esp pig meat.

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9
Q

What evidence based therapy is there for fatty liver disease?

A

Weight loss 7%

Mediterranean diet

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10
Q

Which is worse for HCC risk in the setting of cirrhosis?

HCC/HBV/alcoholic cirrhosis?

A

HBV and alcoholic cirrhosis- 3-4% per year as opposed to 2% per year

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11
Q

What is the only oral chemo for HCC?

A

Sorafenib

  • lots of s/e and poorly tolerated eg hand foot skin reaction, diarrhoea
  • candidates if Child Pugh A but not for surgery, transplant or ablative therapy
  • Improves survival and progression free survival
  • Inhibits multiple tyrosine kinases and Raf kinases
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12
Q

Which SNp makes you more prone to developing fibrosis in alcoholic liver disease?

A

PNPLA3

Not sure what the gene normally does!

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13
Q

Mallory hyaline what significance on hist?

A

Red material in cells in clouds…
most often seen with chronic alcoholism

Remember that fatty liver and alcoholic fatty liver look just the same.

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14
Q

Acute alcoholic hepatitis histo?

A 
Mallory's hyaline
Neutrophils
Hepatocyte necrosis
Collagen deposition
Fatty change
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15
Q

What are the only two therapies shown to be of benefit in alcoholic hepatitis in selected cases?

A

Corticosteroids

Pentoxifylline- competitive nonselective phosphodiesterase inhibitor

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16
Q

When would you use Steroids or pentoxifilline in alcoholic hepatitis.

A 
If MDF is 32 or more
or
MELD is 18 or more
or 
presence HE

–>prednisolone or if steroids C/I or early renal failure penoxifilline

Otherwise, nutritional support and close follow up

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17
Q

What is the half life of ALT?

A

24 hours- so if more gradual decrease, then potentially ongoing injury.

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18
Q

Explain paracetamol metabolism-

A

Mostly metabolised to inactive glucuronide or sulphate conjugates and excreted in urine.

The 10% remainder is metabolised via P-450 producing NAPQI- if this is bound by glutathione can be excreted in the urine. Free= toxic.

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19
Q

What are some rules of thumb for panadol overdose and NAC?

A

Less than 1 hour: activated charcoal and measure level within 4-8 hours of ingestion

1-8 hours: measure level and plot on nomogram

Over 8 hours: commence NAC then get panadol and ALT levels. If ALT not normal at the end of the NAC infusion then KEEP GOING UNTIL panadol level undetectable and ST AND ALT are normal or trending well.

If over 24 hours post infusion or under treatment line and ALT is normal then stop NAC

Watch for hypos and do not treat hyperglycaemia unless very high. Do not give FFP unless active bleeding. Vit K does not normally work.

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20
Q

Kings college criteria for PANADOL

A

pH less than 7.3

OR all of:

INR over 6.5
encephalopathic 3-4
Creatinine over 300

21
Q

Kings college criteria NOT panadol

A

3 of:

INR over 6.5
Age under 10 or over 40
Caused by hep C, idiosyncratic reaction, halothane
Jaundice more than 7 days before encephalopathy
INR over 3.5
Bili over 300

22
Q

Most high risk drug induced cholestasis

A

Anti-androgens (CPA, flutamide)

23
Q

Recommendations in chronic liver disease mx

  • nutritional
  • coagulopathy
  • ascites
  • renal dysfunction
  • portosystemic encephalopathy
  • pulmonary hepatic vascular disorders
A

Nutritional: maintain adequate protein intake 1-1.5 g/kg

Coagulopathy: vit k supplementation, FFp transfusions, IV cryoprecipitate, IV recomb factor VIIa, plt transfusions

Ascites: paracentesis, salt restrict less than 2g, spiro/frusemide, fluid restrict IF Na under 120, avoid saline, avoid NSAIDs

Renal: avoid nephrotoxins, albumin infusion if over 5L paracentesis

Encephalop: avoid sedatives and opiates, lactulose titrated, nonabsorbable oral abx, restrict protein

Pulmonary: supportive care, supplemental oxygen

24
Q

What transferrin saturation makes you think haemochromatosis?

A

45% or more

Cirrhosis unusual if ferritin less than 1000
Aim for 50-100 within 3-6 months of venesection

25
Q

Treatment for wilsons disease

A

Zinc
Penicillamine
Trientine

26
Q

How are AST and ALT independently useful?

A

ALT more specific than AST

AST:ALT= 1 is associated with ischaemia of the liver whatever cause. Note ALT not related to DEGREE of necrosis, no prognostic significance

AST:ALT over 2.5 = associated with alcoholic hepatitis

AST:ALT

27
Q

What are the transferrin saturation cutoffs when considering haemochromatosis

A

Over 50% in women
Over 55% in men

Venesect ferritin to 50, saturation to below 50%

28
Q

What does the joint X ray look like in haemochromatosis?

A

Chondrocalcinosis

29
Q

H Pylori increases risk of what things?

A 
Duodenal ulceration (strongest association)
Gastric ulceration
Gastric adenoca
MALT
Atrophic gastritis

NOT GORD

30
Q

What are the two antibiotics that typically cause obstructive LFTs?

A

Flucloxacillin
Augmentin

also erythromycin

31
Q

What are the gastro implications of Peutz-Jeghers syndrome?

A

Autosomal dominant condition with numerous hamartomatous polyms in the GIT. Pigmented freckes on face, lips, soles and palms. 50% die from GI cancer by age 60.

Genes are LKB1 and STK11
(serine threonine kinase)

Polyps GIT
intestinal obst from intussusception
GI bleeding from cancer

32
Q

Achalasia: what does the classic barium swallow show?

A

Dilated oesophagus
Birds beak appearance at LES
air fluid level due to lack of peristalsis
Can also see tertiary contractions giving a corkscrew appearance

33
Q

Gilbert’s…bilirubin conjugated or unconjugated?

A

Unconjugated (dipstick negative for bilirubin)

34
Q

Causes of solid and liquid dysphagia?

A

Achalasia
GERD with weak peristalsis
Diffuse oesophageal spasm
scleroderma

35
Q

Causes of intermittent solid dysphagia (2)

A 
Schatzki ring (mucosal thickening- recurs only occasionally, not daily)
Oesophageal web
36
Q

What are the main neuro causes of oropharyngeal dysphagia?

A 
CVA
PD
ALS
GBS
HD
post polio
MS
Cerebral palsy 
myasthenia
37
Q

What is the best way to treat PTLD? (livers)

A

Management : reduction in immunosuppression + treatment with acyclovir.

Occasionally: aggressive monoclonal lesion may requires antilymphoma therapy.

38
Q

Campylobacter diarrhoea over 48 hours or need hospitalisation- what antibiotic?

A

Erythromycin

20% resistance to fluoroquinolones

39
Q

What do you give for salmonella needing hospitalisation, bacteraemia, over 50, cellular immunity impaired, malignancy, prosthetic valve, or significant atherosclerotic disease (risk of aortitis)?

A

Azithromycin or ciprofloxacin.

40
Q

Vibrio cholerae treatment if severe illness or liver disease?

A

Fluoroquinolones or doxycycline

41
Q

Shigella- 48 hours duration or needing hospitalisation what abx?

A

Norfloxacin

42
Q

Bloody diarrhoea but few polymorphs…? consider what?

A

Amoebiasis

43
Q

What is the treatment for entamoeba histolytica?

A

Need to DOCUMENT eradication!

Metronidazole and diloxamide or paromomycin

44
Q

Immunocompetent person with cryptosporidium?

A

Nitazoxanide

45
Q

How do you make sure you don’t transmit C diff?

A

Wash your hands!

Aqium does not kill spores

46
Q

Giardia and asymptomatic cyst shedding?

A

Don’t need to treat

47
Q

Why do you worry about giving loperamide or diphenoxylate in a patient with E Coli diarrhoea?

A

Both may precipitate HUS in patients with enterohaemorrhagic E coli

48
Q

Mechanism of loperamide in hepatic encephalopathy? (Main proposed)

A

In the colon, lactulose undergoes bacterial degradation results in an acidic pH (lowers colonic pH to approx. 5.0) which inhibits the diffusion of NH3 into the blood by promoting the conversion of NH3 to non-absorbable NH4+ NH4+ trapped in the colon and not absorbed reduced plasma ammonia concentration reduced hepatic encephalopathy

49
Q

What are the amsterdam criteria for suspecting HNPCC?

A

3-2-1

3 relatives
2 generations
1 diagnosed before age 50

50
Q

What is the gold standard diagnosis for bacterial overgrowth?

A

The gold standard investigation of bacterial overgrowth is small bowel aspiration and culture

Hydrogen breath test or trial of antibiotics often used in practice.

51
Q

What is the relationship between Wilson’s disease related cirrhosis and HCC?

A

Is none! Does not increase risk

Gastro (12 decks)

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